Question: crest syndrome esophageal dysfunction

CREST syndrome - Wikipedia CREST syndrome
CREST syndrome
Contents
Signs and symptoms
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Other
Cause
Diagnosis
Treatment
Epidemiology
History
See also
References
External links
 Underlying this transition is pallor and cyanosis of the digits, followed by a reactive hyperemia as they rewarm. When extreme and frequent, this phenomenon can lead to digital ulcerations, gangrene, or amputation. Ulceration can predispose to chronic infections of the involved site. Esophageal dysmotility
Presents as a sensation of food getting stuck ( dysphagia) in the mid- or lower esophagus, atypical chest pain, or cough. People often state they must drink liquids to swallow solid food. This motility problem results from atrophy of the gastrointestinal tract wall smooth muscle. This change may occur with or without pathologic evidence of significant tissue fibrosis. Sclerodactyly
Though it is the most easily recognizable manifestation, it is not prominent in all patients. Thickening generally only involves the skin of the fingers distal to the metacarpophalangeal joints in CREST. Early in the course of the disease, the skin may appear edematous and inflamed.

CREST syndrome - Wikipedia

CREST syndrome
CREST syndrome
Contents
Signs and symptoms
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Other
Cause
Diagnosis
Treatment
Epidemiology
History
See also
References
External links

Underlying this transition is pallor and cyanosis of the digits, followed by a reactive hyperemia as they rewarm. When extreme and frequent, this phenomenon can lead to digital ulcerations, gangrene, or amputation. Ulceration can predispose to chronic infections of the involved site. Esophageal dysmotility
Presents as a sensation of food getting stuck ( dysphagia) in the mid- or lower esophagus, atypical chest pain, or cough. People often state they must drink liquids to swallow solid food. This motility problem results from atrophy of the gastrointestinal tract wall smooth muscle. This change may occur with or without pathologic evidence of significant tissue fibrosis. Sclerodactyly
Though it is the most easily recognizable manifestation, it is not prominent in all patients. Thickening generally only involves the skin of the fingers distal to the metacarpophalangeal joints in CREST. Early in the course of the disease, the skin may appear edematous and inflamed.

CREST Syndrome Clinical Presentation: History, Physical Examination, Complications CREST Syndrome Clinical Presentation
CREST Syndrome Clinical Presentation
History
Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectases
Other manifestations
 Rarely, the nose and ears can be affected. Involved skin is cool during the attack, but the proximal skin is warm. Color changes are often accompanied by symptoms that can include pain and paresthesias. The phenomenon lasts minutes to hours, and the patient is symptom-free between episodes. Esophageal dysmotility
While the entire intestine can be involved in scleroderma, esophageal involvement is most common and most often clinically relevant. According to Akesson and Wollheim from 1989, [ 44] dysmotility is common. Cine-esophagram and radionuclide transit time studies demonstrate hypomotility in as many as 75-86% of patients with CREST syndrome. All patients have normal motility of the proximal esophagus, which primarily is striated muscle. In 1987, Zamost et al [ 45] correlated esophageal symptoms with anatomic and physiologic measurements in 53 patients with scleroderma. The prevalence of esophagitis and strictures (41%) in this patient population is higher than in otherwise healthy patients with gastroesophageal reflux disease.

CREST Syndrome Clinical Presentation: History, Physical Examination, Complications

CREST Syndrome Clinical Presentation
CREST Syndrome Clinical Presentation
History
Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectases
Other manifestations

Rarely, the nose and ears can be affected. Involved skin is cool during the attack, but the proximal skin is warm. Color changes are often accompanied by symptoms that can include pain and paresthesias. The phenomenon lasts minutes to hours, and the patient is symptom-free between episodes. Esophageal dysmotility
While the entire intestine can be involved in scleroderma, esophageal involvement is most common and most often clinically relevant. According to Akesson and Wollheim from 1989, [ 44] dysmotility is common. Cine-esophagram and radionuclide transit time studies demonstrate hypomotility in as many as 75-86% of patients with CREST syndrome. All patients have normal motility of the proximal esophagus, which primarily is striated muscle. In 1987, Zamost et al [ 45] correlated esophageal symptoms with anatomic and physiologic measurements in 53 patients with scleroderma. The prevalence of esophagitis and strictures (41%) in this patient population is higher than in otherwise healthy patients with gastroesophageal reflux disease.

CREST Syndrome - Clinical Features, Diagnosis, Self-Care Tips and Treatment | medcaretips.com CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
Clinical Features
Cause of CREST Syndrome
Risk Factors
Complications
Gastrointestinal complications
Lung complications
Heart Complications
Kidney complications
Ulcers on fingers and toes
Endocrinal complications
Other complications
Diagnosis and Investigations
Clinical evaluation
Autoantibody tests
Complete blood counts
Nonspecific indicators of inflammation
Serum calcium and phosphorus levels
Renal function tests
Thyroid function tests
X-ray of extremities
Doppler ultrasonography or angiography
Electromyogram/nerve conduction velocity test
Pulmonary function tests
Electrocardiography and Holter monitoring
Upper GI endoscopy, esophageal manometry, barium swallow studies
CT scan
Skin biopsy
Self –Care Tips
Keep warm
Quit smoking
Exercise regularly
Healthy eating habits
To prevent acid reflux
Take care of your skin
Practice good oral hygiene
Treatment
Medicinal treatment
Pain relief medication
Antibiotics
Antacids
Medicines to treat dry mouth
Immunosuppressive drugs
Penicillamine
Calcinosis
Raynaud’s phenomenon
E sophageal dysfunction
Sclerodactyly
Telangiectasias
Treatment of complications
References
About Dr Surbhi Mahajan
 Exposure to toxins like polyvinyl chloride, benzene, silica, etc can trigger CREST syndrome in people who have a genetic predisposition for the disease. Complications
In contrast with diffuse scleroderma, CREST syndrome is associated with better survival rates and a lower incidence of complications. Mortality in patients with limited skin involvement is a result of pulmonary, cardiac, and gastrointestinal causes. Gastrointestinal complications
Fibrosis of the distal esophagus may lead to dysphagia (difficulty in swallowing), chronic heartburn, esophageal strictures and even bleeding. Involvement of the stomach can lead to delayed gastric emptying resulting in early satiety. Intestinal involvement can cause bloating, constipation, diarrhea, nausea, vomiting, and anorexia leading to malnutrition and weight loss. Lung complications
It is the leading cause of deaths in patients of CREST syndrome as it may cause progressive respiratory failure. The deposition of excess collagen in between the air sacs of the lungs makes the lung tissue stiffer resulting in reduced functioning of the lungs. It may also cause pulmonary artery hypertension (increased blood pressure in the arteries between the heart and lungs) which may ultimately lead to cor pulmonale (heart failure). Heart Complications
Fibrosis and scarring of heart tissue can result in arrhythmias (abnormal heart rhythms) or dilated cardiomyopathy (enlargement and weakening of the heart).

CREST Syndrome - Clinical Features, Diagnosis, Self-Care Tips and Treatment | medcaretips.com

CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
Clinical Features
Cause of CREST Syndrome
Risk Factors
Complications
Gastrointestinal complications
Lung complications
Heart Complications
Kidney complications
Ulcers on fingers and toes
Endocrinal complications
Other complications
Diagnosis and Investigations
Clinical evaluation
Autoantibody tests
Complete blood counts
Nonspecific indicators of inflammation
Serum calcium and phosphorus levels
Renal function tests
Thyroid function tests
X-ray of extremities
Doppler ultrasonography or angiography
Electromyogram/nerve conduction velocity test
Pulmonary function tests
Electrocardiography and Holter monitoring
Upper GI endoscopy, esophageal manometry, barium swallow studies
CT scan
Skin biopsy
Self –Care Tips
Keep warm
Quit smoking
Exercise regularly
Healthy eating habits
To prevent acid reflux
Take care of your skin
Practice good oral hygiene
Treatment
Medicinal treatment
Pain relief medication
Antibiotics
Antacids
Medicines to treat dry mouth
Immunosuppressive drugs
Penicillamine
Calcinosis
Raynaud’s phenomenon
E sophageal dysfunction
Sclerodactyly
Telangiectasias
Treatment of complications
References
About Dr Surbhi Mahajan

Exposure to toxins like polyvinyl chloride, benzene, silica, etc can trigger CREST syndrome in people who have a genetic predisposition for the disease. Complications
In contrast with diffuse scleroderma, CREST syndrome is associated with better survival rates and a lower incidence of complications. Mortality in patients with limited skin involvement is a result of pulmonary, cardiac, and gastrointestinal causes. Gastrointestinal complications
Fibrosis of the distal esophagus may lead to dysphagia (difficulty in swallowing), chronic heartburn, esophageal strictures and even bleeding. Involvement of the stomach can lead to delayed gastric emptying resulting in early satiety. Intestinal involvement can cause bloating, constipation, diarrhea, nausea, vomiting, and anorexia leading to malnutrition and weight loss. Lung complications
It is the leading cause of deaths in patients of CREST syndrome as it may cause progressive respiratory failure. The deposition of excess collagen in between the air sacs of the lungs makes the lung tissue stiffer resulting in reduced functioning of the lungs. It may also cause pulmonary artery hypertension (increased blood pressure in the arteries between the heart and lungs) which may ultimately lead to cor pulmonale (heart failure). Heart Complications
Fibrosis and scarring of heart tissue can result in arrhythmias (abnormal heart rhythms) or dilated cardiomyopathy (enlargement and weakening of the heart).

CREST syndrome - Wikipedia CREST syndrome
CREST syndrome
Contents
Signs and symptoms
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Other
Cause
Diagnosis
Treatment
Epidemiology
History
See also
References
External links
 X-ray of subtle calcifications in CREST syndrome. Calcinosis
CREST causes thickening and tightening of the skin with deposition of calcific nodules ("calcinosis"). Raynaud's phenomenon
Raynaud's phenomenon is frequently the first manifestation of CREST/lcSSc, preceding other symptoms by years. Stress and cold temperature induce an exaggerated vasoconstriction of the small arteries, arterioles, and thermoregulatory vessels of the skin of the digits. Clinically this manifests as a white-blue-red transition in skin color. Underlying this transition is pallor and cyanosis of the digits, followed by a reactive hyperemia as they rewarm. When extreme and frequent, this phenomenon can lead to digital ulcerations, gangrene, or amputation. Ulceration can predispose to chronic infections of the involved site. Esophageal dysmotility
Presents as a sensation of food getting stuck ( dysphagia) in the mid- or lower esophagus, atypical chest pain, or cough. People often state they must drink liquids to swallow solid food.

CREST syndrome - Wikipedia

X-ray of subtle calcifications in CREST syndrome. Calcinosis
CREST causes thickening and tightening of the skin with deposition of calcific nodules ("calcinosis"). Raynaud's phenomenon
Raynaud's phenomenon is frequently the first manifestation of CREST/lcSSc, preceding other symptoms by years. Stress and cold temperature induce an exaggerated vasoconstriction of the small arteries, arterioles, and thermoregulatory vessels of the skin of the digits. Clinically this manifests as a white-blue-red transition in skin color. Underlying this transition is pallor and cyanosis of the digits, followed by a reactive hyperemia as they rewarm. When extreme and frequent, this phenomenon can lead to digital ulcerations, gangrene, or amputation. Ulceration can predispose to chronic infections of the involved site. Esophageal dysmotility
Presents as a sensation of food getting stuck ( dysphagia) in the mid- or lower esophagus, atypical chest pain, or cough. People often state they must drink liquids to swallow solid food.

CREST Syndrome - Clinical Features, Diagnosis, Self-Care Tips and Treatment | medcaretips.com CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
Clinical Features
Cause of CREST Syndrome
Risk Factors
Complications
Gastrointestinal complications
Lung complications
Heart Complications
Kidney complications
Ulcers on fingers and toes
Endocrinal complications
Other complications
Diagnosis and Investigations
Clinical evaluation
Autoantibody tests
Complete blood counts
Nonspecific indicators of inflammation
Serum calcium and phosphorus levels
Renal function tests
Thyroid function tests
X-ray of extremities
Doppler ultrasonography or angiography
Electromyogram/nerve conduction velocity test
Pulmonary function tests
Electrocardiography and Holter monitoring
Upper GI endoscopy, esophageal manometry, barium swallow studies
CT scan
Skin biopsy
Self –Care Tips
Keep warm
Quit smoking
Exercise regularly
Healthy eating habits
To prevent acid reflux
Take care of your skin
Practice good oral hygiene
Treatment
Medicinal treatment
Pain relief medication
Antibiotics
Antacids
Medicines to treat dry mouth
Immunosuppressive drugs
Penicillamine
Calcinosis
Raynaud’s phenomenon
E sophageal dysfunction
Sclerodactyly
Telangiectasias
Treatment of complications
References
About Dr Surbhi Mahajan
 Race: It is more common and severe in blacks and Native Americans than in whites. Genetic factors: Presence of any autoimmune disease in the family increases the risk of developing CREST syndrome. Environmental factors: Exposure to toxins like polyvinyl chloride, benzene, silica, etc can trigger CREST syndrome in people who have a genetic predisposition for the disease. Complications
In contrast with diffuse scleroderma, CREST syndrome is associated with better survival rates and a lower incidence of complications. Mortality in patients with limited skin involvement is a result of pulmonary, cardiac, and gastrointestinal causes. Gastrointestinal complications
Fibrosis of the distal esophagus may lead to dysphagia (difficulty in swallowing), chronic heartburn, esophageal strictures and even bleeding. Involvement of the stomach can lead to delayed gastric emptying resulting in early satiety.

Race: It is more common and severe in blacks and Native Americans than in whites. Genetic factors: Presence of any autoimmune disease in the family increases the risk of developing CREST syndrome. Environmental factors: Exposure to toxins like polyvinyl chloride, benzene, silica, etc can trigger CREST syndrome in people who have a genetic predisposition for the disease. Complications
In contrast with diffuse scleroderma, CREST syndrome is associated with better survival rates and a lower incidence of complications. Mortality in patients with limited skin involvement is a result of pulmonary, cardiac, and gastrointestinal causes. Gastrointestinal complications
Fibrosis of the distal esophagus may lead to dysphagia (difficulty in swallowing), chronic heartburn, esophageal strictures and even bleeding. Involvement of the stomach can lead to delayed gastric emptying resulting in early satiety.

CREST Syndrome Clinical Presentation: History, Physical Examination, Complications CREST Syndrome Clinical Presentation
CREST Syndrome Clinical Presentation
History
Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectases
Other manifestations
 According to Akesson and Wollheim from 1989, [ 44] dysmotility is common. Cine-esophagram and radionuclide transit time studies demonstrate hypomotility in as many as 75-86% of patients with CREST syndrome. All patients have normal motility of the proximal esophagus, which primarily is striated muscle. In 1987, Zamost et al [ 45] correlated esophageal symptoms with anatomic and physiologic measurements in 53 patients with scleroderma. The prevalence of esophagitis and strictures (41%) in this patient population is higher than in otherwise healthy patients with gastroesophageal reflux disease. Abnormal motility was a significant predictor of erosive esophagitis; 70% of patients with dysmotility had gross or microscopic evidence of erosive esophagitis. No patients with normal motility had erosive esophagitis. Symptoms of heartburn and dysphagia were more common in patients with erosive esophagitis. Heartburn alone did not predict esophagitis;

According to Akesson and Wollheim from 1989, [ 44] dysmotility is common. Cine-esophagram and radionuclide transit time studies demonstrate hypomotility in as many as 75-86% of patients with CREST syndrome. All patients have normal motility of the proximal esophagus, which primarily is striated muscle. In 1987, Zamost et al [ 45] correlated esophageal symptoms with anatomic and physiologic measurements in 53 patients with scleroderma. The prevalence of esophagitis and strictures (41%) in this patient population is higher than in otherwise healthy patients with gastroesophageal reflux disease. Abnormal motility was a significant predictor of erosive esophagitis; 70% of patients with dysmotility had gross or microscopic evidence of erosive esophagitis. No patients with normal motility had erosive esophagitis. Symptoms of heartburn and dysphagia were more common in patients with erosive esophagitis. Heartburn alone did not predict esophagitis;

CREST Syndrome - Clinical Features, Diagnosis, Self-Care Tips and Treatment | medcaretips.com CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
Clinical Features
Cause of CREST Syndrome
Risk Factors
Complications
Gastrointestinal complications
Lung complications
Heart Complications
Kidney complications
Ulcers on fingers and toes
Endocrinal complications
Other complications
Diagnosis and Investigations
Clinical evaluation
Autoantibody tests
Complete blood counts
Nonspecific indicators of inflammation
Serum calcium and phosphorus levels
Renal function tests
Thyroid function tests
X-ray of extremities
Doppler ultrasonography or angiography
Electromyogram/nerve conduction velocity test
Pulmonary function tests
Electrocardiography and Holter monitoring
Upper GI endoscopy, esophageal manometry, barium swallow studies
CT scan
Skin biopsy
Self –Care Tips
Keep warm
Quit smoking
Exercise regularly
Healthy eating habits
To prevent acid reflux
Take care of your skin
Practice good oral hygiene
Treatment
Medicinal treatment
Pain relief medication
Antibiotics
Antacids
Medicines to treat dry mouth
Immunosuppressive drugs
Penicillamine
Calcinosis
Raynaud’s phenomenon
E sophageal dysfunction
Sclerodactyly
Telangiectasias
Treatment of complications
References
About Dr Surbhi Mahajan
 Clinical Features
Image credit: medlineplus.gov
C alcinosis – thickening and tightening of the skin with painful nodules of calcium in the skin. It can involve the fingers or other parts of the body. R aynaud’s phenomenon – White, blue, cold, or numb skin on the hands and feet in response to cold or emotional stress. It occurs due to the spasm of the blood vessels which causes blockage of the flow of blood. Once the blood circulation improves, the skin becomes reddened and painful. It is usually the first manifestation of CREST syndrome. E sophageal dysfunction – Poor functioning of the muscles of the esophagus (the tube that connects the mouth to the stomach) results in difficulty in swallowing food, chest pain, or cough. It may also cause acids from the stomach to enter back into the esophagus, resulting in heartburn or inflammation and scarring of the esophagus. S clerodactyly – Thickening and tightening of the skin of fingers or toes which makes bending of the fingers difficult.

Clinical Features
Image credit: medlineplus.gov
C alcinosis – thickening and tightening of the skin with painful nodules of calcium in the skin. It can involve the fingers or other parts of the body. R aynaud’s phenomenon – White, blue, cold, or numb skin on the hands and feet in response to cold or emotional stress. It occurs due to the spasm of the blood vessels which causes blockage of the flow of blood. Once the blood circulation improves, the skin becomes reddened and painful. It is usually the first manifestation of CREST syndrome. E sophageal dysfunction – Poor functioning of the muscles of the esophagus (the tube that connects the mouth to the stomach) results in difficulty in swallowing food, chest pain, or cough. It may also cause acids from the stomach to enter back into the esophagus, resulting in heartburn or inflammation and scarring of the esophagus. S clerodactyly – Thickening and tightening of the skin of fingers or toes which makes bending of the fingers difficult.

CREST Syndrome - Clinical Features, Diagnosis, Self-Care Tips and Treatment | medcaretips.com CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
CREST Syndrome – Clinical Features, Diagnosis, Self-Care Tips and Treatment
Clinical Features
Cause of CREST Syndrome
Risk Factors
Complications
Gastrointestinal complications
Lung complications
Heart Complications
Kidney complications
Ulcers on fingers and toes
Endocrinal complications
Other complications
Diagnosis and Investigations
Clinical evaluation
Autoantibody tests
Complete blood counts
Nonspecific indicators of inflammation
Serum calcium and phosphorus levels
Renal function tests
Thyroid function tests
X-ray of extremities
Doppler ultrasonography or angiography
Electromyogram/nerve conduction velocity test
Pulmonary function tests
Electrocardiography and Holter monitoring
Upper GI endoscopy, esophageal manometry, barium swallow studies
CT scan
Skin biopsy
Self –Care Tips
Keep warm
Quit smoking
Exercise regularly
Healthy eating habits
To prevent acid reflux
Take care of your skin
Practice good oral hygiene
Treatment
Medicinal treatment
Pain relief medication
Antibiotics
Antacids
Medicines to treat dry mouth
Immunosuppressive drugs
Penicillamine
Calcinosis
Raynaud’s phenomenon
E sophageal dysfunction
Sclerodactyly
Telangiectasias
Treatment of complications
References
About Dr Surbhi Mahajan
 Once the blood circulation improves, the skin becomes reddened and painful. It is usually the first manifestation of CREST syndrome. E sophageal dysfunction – Poor functioning of the muscles of the esophagus (the tube that connects the mouth to the stomach) results in difficulty in swallowing food, chest pain, or cough. It may also cause acids from the stomach to enter back into the esophagus, resulting in heartburn or inflammation and scarring of the esophagus. S clerodactyly – Thickening and tightening of the skin of fingers or toes which makes bending of the fingers difficult. Initially, the skin appears edematous and inflamed while in later stages, the skin becomes tightened. Many patients may develop ulcers on the distal fingers. T elangiectasias — Swelling of small blood vessels near the skin’s surface results in small red spots or lines on the skin. They are painless and occur mainly on the hands and face. Cause of CREST Syndrome
The exact cause of CREST syndrome is not known.

Once the blood circulation improves, the skin becomes reddened and painful. It is usually the first manifestation of CREST syndrome. E sophageal dysfunction – Poor functioning of the muscles of the esophagus (the tube that connects the mouth to the stomach) results in difficulty in swallowing food, chest pain, or cough. It may also cause acids from the stomach to enter back into the esophagus, resulting in heartburn or inflammation and scarring of the esophagus. S clerodactyly – Thickening and tightening of the skin of fingers or toes which makes bending of the fingers difficult. Initially, the skin appears edematous and inflamed while in later stages, the skin becomes tightened. Many patients may develop ulcers on the distal fingers. T elangiectasias — Swelling of small blood vessels near the skin’s surface results in small red spots or lines on the skin. They are painless and occur mainly on the hands and face. Cause of CREST Syndrome
The exact cause of CREST syndrome is not known.

CREST Syndrome Clinical Presentation: History, Physical Examination, Complications CREST Syndrome Clinical Presentation
CREST Syndrome Clinical Presentation
History
Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectases
Other manifestations
 half the patients without this complication still experienced heartburn. Additionally, dysphagia did not predict the presence of stricture. Barrett esophagitis, a complication of gastroesophageal reflux, has been found in scleroderma patients, perhaps at a higher rate (37% in patients with scleroderma vs 4-13% in patients without scleroderma). Esophageal adenocarcinoma, a malignant transformation of Barrett esophagitis, has also been documented in scleroderma patients. Another potential complication of esophageal dysmotility and gastroesophageal reflux is occult aspiration and pulmonary disease. In 1989, Johnson et al [ 46] examined 13 patients with systemic sclerosis using endoscopy, laryngoscopy, esophageal manometry, 24-hour esophageal pH monitoring, pulmonary function testing, and aspiration scanning. All 13 patients had endoscopic evidence of reflux. Twelve patients had abnormal laryngeal examination findings suggestive of aspiration; however, in this group, 1 patient had no evidence of proximal reflux by pH monitoring and 2 patients had normal aspiration scan results. Nonetheless, an inverse relationship was found between diffusing capacity of lung for carbon dioxide and esophageal reflux scores, indicating that gastroesophageal reflux potentially contributes to diminished pulmonary function.

half the patients without this complication still experienced heartburn. Additionally, dysphagia did not predict the presence of stricture. Barrett esophagitis, a complication of gastroesophageal reflux, has been found in scleroderma patients, perhaps at a higher rate (37% in patients with scleroderma vs 4-13% in patients without scleroderma). Esophageal adenocarcinoma, a malignant transformation of Barrett esophagitis, has also been documented in scleroderma patients. Another potential complication of esophageal dysmotility and gastroesophageal reflux is occult aspiration and pulmonary disease. In 1989, Johnson et al [ 46] examined 13 patients with systemic sclerosis using endoscopy, laryngoscopy, esophageal manometry, 24-hour esophageal pH monitoring, pulmonary function testing, and aspiration scanning. All 13 patients had endoscopic evidence of reflux. Twelve patients had abnormal laryngeal examination findings suggestive of aspiration; however, in this group, 1 patient had no evidence of proximal reflux by pH monitoring and 2 patients had normal aspiration scan results. Nonetheless, an inverse relationship was found between diffusing capacity of lung for carbon dioxide and esophageal reflux scores, indicating that gastroesophageal reflux potentially contributes to diminished pulmonary function.

CREST syndrome - Wikipedia CREST syndrome
CREST syndrome
Contents
Signs and symptoms
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Other
Cause
Diagnosis
Treatment
Epidemiology
History
See also
References
External links
 The number of telangiectasias and the sites involved tend to increase over time. Other
Other symptoms of CREST syndrome can be exhaustion, weakness, difficulties with breathing, pain in hands and feet, dizziness and badly healing wounds. Patients with lcSSc commonly induce pulmonary artery hypertension which may result in cor pulmonale ( heart failure due to increased pulmonary artery pressure). Cause
Crest syndrome involves the production of autoimmune anti-nuclear and anti-centromere antibodies, though their cause is not currently understood. There is no known infectious cause. Diagnosis
CREST is not easily diagnosed as it closely mimics symptoms of other connective tissue and autoimmune diseases. Diagnoses are usually given when a patient presents two or more of the five major clinical symptoms. Additionally, blood exams can be given to test for a positive ANAs and ACAs or skin biopsies can be given to help confirm a diagnosis. Treatment
Disease progression may be slowed with immunosuppressives and other medications, and esophageal reflux, pulmonary hypertension and Raynaud phenomenon may benefit from symptomatic treatment. However, there is no cure for this disease as there is no cure for scleroderma in general.

CREST syndrome - Wikipedia

The number of telangiectasias and the sites involved tend to increase over time. Other
Other symptoms of CREST syndrome can be exhaustion, weakness, difficulties with breathing, pain in hands and feet, dizziness and badly healing wounds. Patients with lcSSc commonly induce pulmonary artery hypertension which may result in cor pulmonale ( heart failure due to increased pulmonary artery pressure). Cause
Crest syndrome involves the production of autoimmune anti-nuclear and anti-centromere antibodies, though their cause is not currently understood. There is no known infectious cause. Diagnosis
CREST is not easily diagnosed as it closely mimics symptoms of other connective tissue and autoimmune diseases. Diagnoses are usually given when a patient presents two or more of the five major clinical symptoms. Additionally, blood exams can be given to test for a positive ANAs and ACAs or skin biopsies can be given to help confirm a diagnosis. Treatment
Disease progression may be slowed with immunosuppressives and other medications, and esophageal reflux, pulmonary hypertension and Raynaud phenomenon may benefit from symptomatic treatment. However, there is no cure for this disease as there is no cure for scleroderma in general.

CREST Syndrome Clinical Presentation: History, Physical Examination, Complications CREST Syndrome Clinical Presentation
CREST Syndrome Clinical Presentation
History
Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectases
Other manifestations
 Color changes extend proximally from the tips of digits to various levels, with a well-demarcated border. Raynaud phenomenon showing pallor of most of the finger tips with a violaceous discoloration (hyperemia) of the thumb tip. View Media Gallery
Esophageal dysmotility
The earliest change in the distal esophagus (primarily smooth muscle) is an uncoordinated disorganized pattern of contractions resulting in low amplitude or absent peristalsis. Lower esophageal sphincter (LES) pressure typically is lower than in healthy controls, and incomplete relaxation of the LES occurs. [ 30]
Sclerodactyly
The process typically begins in the distal fingers and advances proximally. The process also may occur on the face, over the forehead, and around the mouth. Facial involvement can lead to a mauskopf (mouse head) appearance. Lips become thinner, and radial furrowing develops around the mouth. The oral aperture is reduced in size (microstomia). Wrinkles over the forehead diminish.

Color changes extend proximally from the tips of digits to various levels, with a well-demarcated border. Raynaud phenomenon showing pallor of most of the finger tips with a violaceous discoloration (hyperemia) of the thumb tip. View Media Gallery
Esophageal dysmotility
The earliest change in the distal esophagus (primarily smooth muscle) is an uncoordinated disorganized pattern of contractions resulting in low amplitude or absent peristalsis. Lower esophageal sphincter (LES) pressure typically is lower than in healthy controls, and incomplete relaxation of the LES occurs. [ 30]
Sclerodactyly
The process typically begins in the distal fingers and advances proximally. The process also may occur on the face, over the forehead, and around the mouth. Facial involvement can lead to a mauskopf (mouse head) appearance. Lips become thinner, and radial furrowing develops around the mouth. The oral aperture is reduced in size (microstomia). Wrinkles over the forehead diminish.

CREST syndrome - Wikipedia CREST syndrome
CREST syndrome
Contents
Signs and symptoms
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Other
Cause
Diagnosis
Treatment
Epidemiology
History
See also
References
External links
 Diagnosis
CREST is not easily diagnosed as it closely mimics symptoms of other connective tissue and autoimmune diseases. Diagnoses are usually given when a patient presents two or more of the five major clinical symptoms. Additionally, blood exams can be given to test for a positive ANAs and ACAs or skin biopsies can be given to help confirm a diagnosis. Treatment
Disease progression may be slowed with immunosuppressives and other medications, and esophageal reflux, pulmonary hypertension and Raynaud phenomenon may benefit from symptomatic treatment. However, there is no cure for this disease as there is no cure for scleroderma in general. Epidemiology
CREST syndrome can be noted in up to 10% of patients with primary biliary cholangitis. History
The combination of symptoms was first reported in 1964 by R.H. Winterbauer, at that point a medical student at Johns Hopkins School of Medicine. See also
Scleroderma
References
^ RESERVED, INSERM US14-- ALL RIGHTS. " Orphanet: CREST syndrome".

CREST syndrome - Wikipedia

Diagnosis
CREST is not easily diagnosed as it closely mimics symptoms of other connective tissue and autoimmune diseases. Diagnoses are usually given when a patient presents two or more of the five major clinical symptoms. Additionally, blood exams can be given to test for a positive ANAs and ACAs or skin biopsies can be given to help confirm a diagnosis. Treatment
Disease progression may be slowed with immunosuppressives and other medications, and esophageal reflux, pulmonary hypertension and Raynaud phenomenon may benefit from symptomatic treatment. However, there is no cure for this disease as there is no cure for scleroderma in general. Epidemiology
CREST syndrome can be noted in up to 10% of patients with primary biliary cholangitis. History
The combination of symptoms was first reported in 1964 by R.H. Winterbauer, at that point a medical student at Johns Hopkins School of Medicine. See also
Scleroderma
References
^ RESERVED, INSERM US14-- ALL RIGHTS. " Orphanet: CREST syndrome".

CREST syndrome - Wikipedia CREST syndrome
CREST syndrome
Contents
Signs and symptoms
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Other
Cause
Diagnosis
Treatment
Epidemiology
History
See also
References
External links
 Eventually, dermal fibroblasts overproduce extracellular matrix leading to increased tissue collagen deposition in the skin. Collagen cross-linking then causes a progressive skin tightening. Digital ischemic ulcers commonly form on the distal fingers in 30-50% of patients. Telangiectasias
Marked telangiectasias (dilated capillaries) occur on the skin of the face, the palmar surface of the hands, and the mucous membranes. Telangiectasias tend to be more numerous in people with other scleroderma related vascular disease (i.e., pulmonary arterial hypertension). The number of telangiectasias and the sites involved tend to increase over time. Other
Other symptoms of CREST syndrome can be exhaustion, weakness, difficulties with breathing, pain in hands and feet, dizziness and badly healing wounds. Patients with lcSSc commonly induce pulmonary artery hypertension which may result in cor pulmonale ( heart failure due to increased pulmonary artery pressure). Cause
Crest syndrome involves the production of autoimmune anti-nuclear and anti-centromere antibodies, though their cause is not currently understood. There is no known infectious cause.

CREST syndrome - Wikipedia

Eventually, dermal fibroblasts overproduce extracellular matrix leading to increased tissue collagen deposition in the skin. Collagen cross-linking then causes a progressive skin tightening. Digital ischemic ulcers commonly form on the distal fingers in 30-50% of patients. Telangiectasias
Marked telangiectasias (dilated capillaries) occur on the skin of the face, the palmar surface of the hands, and the mucous membranes. Telangiectasias tend to be more numerous in people with other scleroderma related vascular disease (i.e., pulmonary arterial hypertension). The number of telangiectasias and the sites involved tend to increase over time. Other
Other symptoms of CREST syndrome can be exhaustion, weakness, difficulties with breathing, pain in hands and feet, dizziness and badly healing wounds. Patients with lcSSc commonly induce pulmonary artery hypertension which may result in cor pulmonale ( heart failure due to increased pulmonary artery pressure). Cause
Crest syndrome involves the production of autoimmune anti-nuclear and anti-centromere antibodies, though their cause is not currently understood. There is no known infectious cause.

CREST syndrome - Wikipedia CREST syndrome
CREST syndrome
Contents
Signs and symptoms
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Other
Cause
Diagnosis
Treatment
Epidemiology
History
See also
References
External links
 CREST syndrome - Wikipedia
CREST syndrome
From Wikipedia, the free encyclopedia
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Medical condition
CREST syndrome
Other names
Calcinosis-Raynaud phenomenon-esophageal involvement-sclerodactyly-telangiectasia syndrome

CREST syndrome (calcinosis and sclerodactyly)
Specialty
Rheumatology
CREST syndrome, also known as the limited cutaneous form of systemic sclerosis (lcSSc), is a multisystem connective tissue disorder. The acronym "CREST" refers to the five main features: calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. CREST syndrome is associated with detectable antibodies against centromeres (a component of the cell nucleus ), and usually spares the kidneys (a feature more common in the related condition systemic scleroderma ). If the lungs are involved, it is usually in the form of pulmonary arterial hypertension . Contents
1 Signs and symptoms
1.1 Calcinosis
1.2 Raynaud's phenomenon
1.3 Esophageal dysmotility
1.4 Sclerodactyly
1.5 Telangiectasias
1.6 Other
2 Cause
3 Diagnosis
4 Treatment
5 Epidemiology
5.1 History
6 See also
7 References
8 External links
Signs and symptoms
CREST syndrome (calcinosis and sclerodactyly)
X-rays showing calcinosis in a woman with CREST syndrome.

CREST syndrome - Wikipedia

CREST syndrome - Wikipedia
CREST syndrome
From Wikipedia, the free encyclopedia
Jump to navigation Jump to search

This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. Find sources: " CREST syndrome" – news · newspapers · books · scholar · JSTOR (February 2009) ( Learn how and when to remove this template message)
Medical condition
CREST syndrome
Other names
Calcinosis-Raynaud phenomenon-esophageal involvement-sclerodactyly-telangiectasia syndrome

CREST syndrome (calcinosis and sclerodactyly)
Specialty
Rheumatology
CREST syndrome, also known as the limited cutaneous form of systemic sclerosis (lcSSc), is a multisystem connective tissue disorder. The acronym "CREST" refers to the five main features: calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. CREST syndrome is associated with detectable antibodies against centromeres (a component of the cell nucleus ), and usually spares the kidneys (a feature more common in the related condition systemic scleroderma ). If the lungs are involved, it is usually in the form of pulmonary arterial hypertension . Contents
1 Signs and symptoms
1.1 Calcinosis
1.2 Raynaud's phenomenon
1.3 Esophageal dysmotility
1.4 Sclerodactyly
1.5 Telangiectasias
1.6 Other
2 Cause
3 Diagnosis
4 Treatment
5 Epidemiology
5.1 History
6 See also
7 References
8 External links
Signs and symptoms
CREST syndrome (calcinosis and sclerodactyly)
X-rays showing calcinosis in a woman with CREST syndrome.

CREST Syndrome Clinical Presentation: History, Physical Examination, Complications CREST Syndrome Clinical Presentation
CREST Syndrome Clinical Presentation
History
Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectases
Other manifestations
 Abnormal motility was a significant predictor of erosive esophagitis; 70% of patients with dysmotility had gross or microscopic evidence of erosive esophagitis. No patients with normal motility had erosive esophagitis. Symptoms of heartburn and dysphagia were more common in patients with erosive esophagitis. Heartburn alone did not predict esophagitis; half the patients without this complication still experienced heartburn. Additionally, dysphagia did not predict the presence of stricture. Barrett esophagitis, a complication of gastroesophageal reflux, has been found in scleroderma patients, perhaps at a higher rate (37% in patients with scleroderma vs 4-13% in patients without scleroderma). Esophageal adenocarcinoma, a malignant transformation of Barrett esophagitis, has also been documented in scleroderma patients. Another potential complication of esophageal dysmotility and gastroesophageal reflux is occult aspiration and pulmonary disease.

Abnormal motility was a significant predictor of erosive esophagitis; 70% of patients with dysmotility had gross or microscopic evidence of erosive esophagitis. No patients with normal motility had erosive esophagitis. Symptoms of heartburn and dysphagia were more common in patients with erosive esophagitis. Heartburn alone did not predict esophagitis; half the patients without this complication still experienced heartburn. Additionally, dysphagia did not predict the presence of stricture. Barrett esophagitis, a complication of gastroesophageal reflux, has been found in scleroderma patients, perhaps at a higher rate (37% in patients with scleroderma vs 4-13% in patients without scleroderma). Esophageal adenocarcinoma, a malignant transformation of Barrett esophagitis, has also been documented in scleroderma patients. Another potential complication of esophageal dysmotility and gastroesophageal reflux is occult aspiration and pulmonary disease.

CREST syndrome - Wikipedia CREST syndrome
CREST syndrome
Contents
Signs and symptoms
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Other
Cause
Diagnosis
Treatment
Epidemiology
History
See also
References
External links
 The acronym "CREST" refers to the five main features: calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. CREST syndrome is associated with detectable antibodies against centromeres (a component of the cell nucleus ), and usually spares the kidneys (a feature more common in the related condition systemic scleroderma ). If the lungs are involved, it is usually in the form of pulmonary arterial hypertension . Contents
1 Signs and symptoms
1.1 Calcinosis
1.2 Raynaud's phenomenon
1.3 Esophageal dysmotility
1.4 Sclerodactyly
1.5 Telangiectasias
1.6 Other
2 Cause
3 Diagnosis
4 Treatment
5 Epidemiology
5.1 History
6 See also
7 References
8 External links
Signs and symptoms
CREST syndrome (calcinosis and sclerodactyly)
X-rays showing calcinosis in a woman with CREST syndrome. X-ray of subtle calcifications in CREST syndrome. Calcinosis
CREST causes thickening and tightening of the skin with deposition of calcific nodules ("calcinosis"). Raynaud's phenomenon
Raynaud's phenomenon is frequently the first manifestation of CREST/lcSSc, preceding other symptoms by years. Stress and cold temperature induce an exaggerated vasoconstriction of the small arteries, arterioles, and thermoregulatory vessels of the skin of the digits. Clinically this manifests as a white-blue-red transition in skin color.

CREST syndrome - Wikipedia

The acronym "CREST" refers to the five main features: calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. CREST syndrome is associated with detectable antibodies against centromeres (a component of the cell nucleus ), and usually spares the kidneys (a feature more common in the related condition systemic scleroderma ). If the lungs are involved, it is usually in the form of pulmonary arterial hypertension . Contents
1 Signs and symptoms
1.1 Calcinosis
1.2 Raynaud's phenomenon
1.3 Esophageal dysmotility
1.4 Sclerodactyly
1.5 Telangiectasias
1.6 Other
2 Cause
3 Diagnosis
4 Treatment
5 Epidemiology
5.1 History
6 See also
7 References
8 External links
Signs and symptoms
CREST syndrome (calcinosis and sclerodactyly)
X-rays showing calcinosis in a woman with CREST syndrome. X-ray of subtle calcifications in CREST syndrome. Calcinosis
CREST causes thickening and tightening of the skin with deposition of calcific nodules ("calcinosis"). Raynaud's phenomenon
Raynaud's phenomenon is frequently the first manifestation of CREST/lcSSc, preceding other symptoms by years. Stress and cold temperature induce an exaggerated vasoconstriction of the small arteries, arterioles, and thermoregulatory vessels of the skin of the digits. Clinically this manifests as a white-blue-red transition in skin color.

CREST syndrome - Wikipedia CREST syndrome
CREST syndrome
Contents
Signs and symptoms
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Other
Cause
Diagnosis
Treatment
Epidemiology
History
See also
References
External links
 medlineplus.gov. ^ "CREST syndrome - Genetic and Rare Diseases Information Center (GARD) – an NCATS Program". rarediseases.info.nih.gov. ^ Talwalkar, JA; Lindor, KD (Jul 5, 2003). " Primary biliary cirrhosis". Lancet. 362 (9377): 53–61. doi:

CREST syndrome - Wikipedia

medlineplus.gov. ^ "CREST syndrome - Genetic and Rare Diseases Information Center (GARD) – an NCATS Program". rarediseases.info.nih.gov. ^ Talwalkar, JA; Lindor, KD (Jul 5, 2003). " Primary biliary cirrhosis". Lancet. 362 (9377): 53–61. doi:

CREST Syndrome Clinical Presentation: History, Physical Examination, Complications CREST Syndrome Clinical Presentation
CREST Syndrome Clinical Presentation
History
Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectases
Other manifestations
 54]
Deposits typically are found in the flexor surfaces of the hands and the extensor surfaces of the forearms and knees. The deposits rest in the dermis but can be found in deeper periarticular tissues. Calcinosis on dorsal forearm. View Media Gallery
Close-up view of calcinosis. View Media Gallery
Raynaud phenomenon
Triphasic color changes of pallor, cyanosis, and erythema represent phases of vasoconstriction, slow blood flow, and reperfusion, respectively. Color changes extend proximally from the tips of digits to various levels, with a well-demarcated border. Raynaud phenomenon showing pallor of most of the finger tips with a violaceous discoloration (hyperemia) of the thumb tip. View Media Gallery
Esophageal dysmotility
The earliest change in the distal esophagus (primarily smooth muscle) is an uncoordinated disorganized pattern of contractions resulting in low amplitude or absent peristalsis. Lower esophageal sphincter (LES) pressure typically is lower than in healthy controls, and incomplete relaxation of the LES occurs. [ 30]
Sclerodactyly
The process typically begins in the distal fingers and advances proximally.

54]
Deposits typically are found in the flexor surfaces of the hands and the extensor surfaces of the forearms and knees. The deposits rest in the dermis but can be found in deeper periarticular tissues. Calcinosis on dorsal forearm. View Media Gallery
Close-up view of calcinosis. View Media Gallery
Raynaud phenomenon
Triphasic color changes of pallor, cyanosis, and erythema represent phases of vasoconstriction, slow blood flow, and reperfusion, respectively. Color changes extend proximally from the tips of digits to various levels, with a well-demarcated border. Raynaud phenomenon showing pallor of most of the finger tips with a violaceous discoloration (hyperemia) of the thumb tip. View Media Gallery
Esophageal dysmotility
The earliest change in the distal esophagus (primarily smooth muscle) is an uncoordinated disorganized pattern of contractions resulting in low amplitude or absent peristalsis. Lower esophageal sphincter (LES) pressure typically is lower than in healthy controls, and incomplete relaxation of the LES occurs. [ 30]
Sclerodactyly
The process typically begins in the distal fingers and advances proximally.

CREST Syndrome: Background, Pathophysiology, Etiology CREST Syndrome
CREST Syndrome
Background
 Jeanie C Yoon, MD; Chief Editor: Dirk M Elston, MD more...
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CREST Syndrome
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Overview
Background
CREST ( calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome is a member of the heterogeneous group of sclerodermas, and its name is an acronym for the cardinal clinical features of the syndrome. [ 1, 2]
In 1910, Thibierge and Weissenbach described the first case report of what was later called CRST (calcinosis cutis, Raynaud phenomenon, sclerodactyly, and telangiectasia) syndrome in English by Winterbauer who, in 1964, described a series of 8 patients with the features that make up the abbreviation CRST. [ 3, 4] Although he noted esophageal dysmotility in 4 of 8 patients, he did not include this feature in his original description of CRST syndrome. Frayha et al [ 5] noted the frequent occurrence of esophageal dysmotility and suggested that the acronym CREST may be more appropriate. Velayos et al [ 6] reviewed 13 patients with CREST and CRST syndromes and found the syndromes equivalent. The 1980 American College of Rheumatology Classification Criteria for Rheumatic Diseases is the most widely used system for systemic scleroderma. Because it was designed for research applications and not for clinical diagnosis, it has been criticized for its low sensitivity in identifying early disease and milder forms of systemic scleroderma such as CREST syndrome. Several authors recognized this limitation and responded by categorizing patients with scleroderma syndromes into 2 groups:

CREST Syndrome: Background, Pathophysiology, Etiology

CREST Syndrome
CREST Syndrome
Background

CREST syndrome | definition of CREST syndrome by Medical dictionary CREST syndrome
CREST syndrome
CREST syndrome
CREST syn·drome
CREST syn·drome
CREST syndrome
Thibierge,
CREST syn·drome
Mentioned in ?
References in periodicals archive ?
Medical browser ?
Full browser ?
 CREST syndrome | definition of CREST syndrome by Medical dictionary
CREST syndrome
Also found in: Dictionary, Thesaurus, Financial, Encyclopedia. Related to CREST syndrome: Scleroderma, Raynaud's syndrome, Sjogren's syndrome
CREST syndrome
one of the less severe forms of systemic scleroderma, consisting of calcinosis of the skin, raynaud's phenomenon, esophageal dysfunction, sclerodactyly, and telangiectasia. When esophageal dysfunction is not prominent, it is known as CRST syndrome. Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved. CREST syn·drome
a variant of systemic sclerosis characterized by calcinosis, Raynaud phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia. Farlex Partner Medical Dictionary © Farlex 2012
An acronym for the pentad of clinical signs seen with a limited form of scleroderma: Calcinosis cutis
Raynaud’s phenomenon—at least a 2-phase colour change
Esophageal distal hypomotility or reflux esophagitis
Sclerodactyly or nonpitting digital edema
Telangiectasia;

CREST syndrome | definition of CREST syndrome by Medical dictionary

CREST syndrome
CREST syndrome
CREST syndrome
CREST syn·drome
CREST syn·drome
CREST syndrome
Thibierge,
CREST syn·drome
Mentioned in ?
References in periodicals archive ?
Medical browser ?
Full browser ?

CREST syndrome | definition of CREST syndrome by Medical dictionary
CREST syndrome
Also found in: Dictionary, Thesaurus, Financial, Encyclopedia. Related to CREST syndrome: Scleroderma, Raynaud's syndrome, Sjogren's syndrome
CREST syndrome
one of the less severe forms of systemic scleroderma, consisting of calcinosis of the skin, raynaud's phenomenon, esophageal dysfunction, sclerodactyly, and telangiectasia. When esophageal dysfunction is not prominent, it is known as CRST syndrome. Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved. CREST syn·drome
a variant of systemic sclerosis characterized by calcinosis, Raynaud phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia. Farlex Partner Medical Dictionary © Farlex 2012
An acronym for the pentad of clinical signs seen with a limited form of scleroderma: Calcinosis cutis
Raynaud’s phenomenon—at least a 2-phase colour change
Esophageal distal hypomotility or reflux esophagitis
Sclerodactyly or nonpitting digital edema
Telangiectasia;

Esophageal motility disorder - Wikipedia Esophageal motility disorder
Esophageal motility disorder
Contents
Symptoms
Types
See also
References
External links
 The most prominent one is dysphagia . Esophageal motility disorder may be a result of CREST syndrome, referring to the five main features: calcinosis, Raynaud syndrome, esophageal dysmotility, sclerodactyly and telangiectasia. Contents
1 Symptoms
1.1 Types
2 See also
3 References
4 External links
Symptoms
There are contractions along the lower esophagus when this condition happens. These contractions prevent the passage of food. Types
Dysphagia could be for solid only or for solid and liquid. Solid dysphagia is due to obstruction such as esophageal cancer, esophageal web, or stricture. Solid plus liquid dysphagia is due to esophageal motility disorder (or dysmotility) either in the upper esophagus ( myasthenia gravis, stroke, or dermatomyositis) or lower esophagus ( systemic sclerosis, CREST syndrome, or achalasia ). If there is a food allergy causing an EMD, then physicians recommend an elimination diet. If this fails, then physicians will prescribe special types of Medication to help resolve this problem.

Esophageal motility disorder - Wikipedia

Esophageal motility disorder
Esophageal motility disorder
Contents
Symptoms
Types
See also
References
External links

The most prominent one is dysphagia . Esophageal motility disorder may be a result of CREST syndrome, referring to the five main features: calcinosis, Raynaud syndrome, esophageal dysmotility, sclerodactyly and telangiectasia. Contents
1 Symptoms
1.1 Types
2 See also
3 References
4 External links
Symptoms
There are contractions along the lower esophagus when this condition happens. These contractions prevent the passage of food. Types
Dysphagia could be for solid only or for solid and liquid. Solid dysphagia is due to obstruction such as esophageal cancer, esophageal web, or stricture. Solid plus liquid dysphagia is due to esophageal motility disorder (or dysmotility) either in the upper esophagus ( myasthenia gravis, stroke, or dermatomyositis) or lower esophagus ( systemic sclerosis, CREST syndrome, or achalasia ). If there is a food allergy causing an EMD, then physicians recommend an elimination diet. If this fails, then physicians will prescribe special types of Medication to help resolve this problem.

Esophageal motility disorder - Wikipedia Esophageal motility disorder
Esophageal motility disorder
Contents
Symptoms
Types
See also
References
External links
 Esophageal motility disorder - Wikipedia
Esophageal motility disorder
From Wikipedia, the free encyclopedia
Jump to navigation Jump to search

This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. Find sources: " Esophageal motility disorder" – news · newspapers · books · scholar · JSTOR (February 2017) ( Learn how and when to remove this template message)
Esophageal motility disorder
Other names
Esophageal dysmotility (ED)
Diagnostic method
Esophageal motility study
Functional Lumen Imaging Probe
Treatment
treatment depends on cause
An esophageal motility disorder ( EMD) is any medical disorder causing difficulty in swallowing, regurgitation of food and a spasm -type pain which can be brought on by an allergic reaction to certain foods. The most prominent one is dysphagia . Esophageal motility disorder may be a result of CREST syndrome, referring to the five main features: calcinosis, Raynaud syndrome, esophageal dysmotility, sclerodactyly and telangiectasia. Contents
1 Symptoms
1.1 Types
2 See also
3 References
4 External links
Symptoms
There are contractions along the lower esophagus when this condition happens. These contractions prevent the passage of food.

Esophageal motility disorder - Wikipedia
Esophageal motility disorder
From Wikipedia, the free encyclopedia
Jump to navigation Jump to search

This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. Find sources: " Esophageal motility disorder" – news · newspapers · books · scholar · JSTOR (February 2017) ( Learn how and when to remove this template message)
Esophageal motility disorder
Other names
Esophageal dysmotility (ED)
Diagnostic method
Esophageal motility study
Functional Lumen Imaging Probe
Treatment
treatment depends on cause
An esophageal motility disorder ( EMD) is any medical disorder causing difficulty in swallowing, regurgitation of food and a spasm -type pain which can be brought on by an allergic reaction to certain foods. The most prominent one is dysphagia . Esophageal motility disorder may be a result of CREST syndrome, referring to the five main features: calcinosis, Raynaud syndrome, esophageal dysmotility, sclerodactyly and telangiectasia. Contents
1 Symptoms
1.1 Types
2 See also
3 References
4 External links
Symptoms
There are contractions along the lower esophagus when this condition happens. These contractions prevent the passage of food.

CREST Syndrome - What is?, Pictures, Symptoms, Treatment, Diagnosis CREST Syndrome
CREST Syndrome
Definition
Symptoms
Tight hardened skin
Raynaud’s phenomenon
Red spot marks on the skin
Lumps beneath the skin
Difficulty in swallowing
Classification
Causes of CREST Syndrome
Risk factors
Complications
Diagnosis
Blood test
Biopsy of the skin sample
Heart, lung and gastrointestinal tests
CREST Syndrome Treatment
Antibiotics
Antacids
Antihypertensive drugs
Immunosuppressive medications
Rehabilitation Therapy
References
 These lumps may be infected and tenderness also develop. Difficulty in swallowing
In CREST syndrome, people often face swallowing difficulties, due to their problem in the esophagus. The loss of control over the esophageal muscles at the upper and lower end can cause difficulty in swallowing and let back flow the acidic content of the stomach into the esophagus. This leads to heartburn, irritation and scarring of the esophagus. ( 1,2,3,4)
Classification
In medical science, depending upon the sign and symptoms, CREST syndrome is further divided into two forms: “Pure”CREST — it means when the diagnostic reports reveled that patient have two or more than two symptoms of CREST and not associated with diffuse scleroderma or other autoimmune disease. Plus CREST – It means when the patient has CREST syndrome along with another form of scleroderma, including diffuse scleroderma or other types of autoimmune disease symptoms. In diffuse scleroderma the involved skin is not localized in a particular area and the involvement of the internal organs like the digestive system, heart, lungs and kidney. ( 2,4)
Causes of CREST Syndrome
It assumed that CREST syndrome is developed due to an autoimmune disorder, means the immune system of one’s body can act against own body. This assumption comes from the pathophysiology involved in developing the CREST Syndrome.

CREST Syndrome - What is?, Pictures, Symptoms, Treatment, Diagnosis

CREST Syndrome
CREST Syndrome
Definition
Symptoms
Tight hardened skin
Raynaud’s phenomenon
Red spot marks on the skin
Lumps beneath the skin
Difficulty in swallowing
Classification
Causes of CREST Syndrome
Risk factors
Complications
Diagnosis
Blood test
Biopsy of the skin sample
Heart, lung and gastrointestinal tests
CREST Syndrome Treatment
Antibiotics
Antacids
Antihypertensive drugs
Immunosuppressive medications
Rehabilitation Therapy
References

These lumps may be infected and tenderness also develop. Difficulty in swallowing
In CREST syndrome, people often face swallowing difficulties, due to their problem in the esophagus. The loss of control over the esophageal muscles at the upper and lower end can cause difficulty in swallowing and let back flow the acidic content of the stomach into the esophagus. This leads to heartburn, irritation and scarring of the esophagus. ( 1,2,3,4)
Classification
In medical science, depending upon the sign and symptoms, CREST syndrome is further divided into two forms: “Pure”CREST — it means when the diagnostic reports reveled that patient have two or more than two symptoms of CREST and not associated with diffuse scleroderma or other autoimmune disease. Plus CREST – It means when the patient has CREST syndrome along with another form of scleroderma, including diffuse scleroderma or other types of autoimmune disease symptoms. In diffuse scleroderma the involved skin is not localized in a particular area and the involvement of the internal organs like the digestive system, heart, lungs and kidney. ( 2,4)
Causes of CREST Syndrome
It assumed that CREST syndrome is developed due to an autoimmune disorder, means the immune system of one’s body can act against own body. This assumption comes from the pathophysiology involved in developing the CREST Syndrome.

Scleroderma Esophagus (Throat) Involvement Scleroderma Esophageal (Throat) Involvement
SCLERO.ORG
Scleroderma Esophageal (Throat) Involvement
Overview
Air Esophagogram
Barrett's Esophagus
Candida Esophagitis
Correlation with Lung Disease
Dysphonia (Hoarseness, Loss of Voice)
Dysphonia (Hoarseness, Loss of Voice) Personal Stories
Esophageal Diseases
Esophageal Motility Disorders
Esophageal Motility Stories
Esophageal Spasm
Esophageal Stricture
Esophageal Stricture Personal Stories
Esophageal Ulcer
Gastric MALT Lymphoma
Reflux (Heartburn)
References
 Carol Langenfeld: Diffuse Scleroderma People tell me that I have earned my credentials as a "certified patient" the hard way…
Don Alfera: CREST, Pulmonary Fibrosis and Sjögren's I entitled this "My Time So Far" since this has been a journey unlike any that I could have ever tried to imagine in my life…
Jerri: CREST Syndrome I was twenty-one years of age when I first noticed that my fingers, toes and lips were turning colors…
Sharon: CREST with Limited Scleroderma, Sjögren's and Pulmonary Hypertension (Australia) Day by day I discover another food I cannot eat …
Candida Esophagitis
The "Foamy" Esophagus A Radiographic Sign of Candida Esophagitis. Shows sophagrams of scleroderma patients. American Journal of Roentgenology. Correlation with Lung Disease
Relationship Between Interstitial Lung Disease (ILD) and Oesophageal Dilatation on Chest High-Resolution Computed Tomography (HRCT) in Patients With Systemic Sclerosis: A Cross-Sectional Study. An increased oesophageal diameter ( ≥ 11 mm) on chest HRCT is associated with pulmonary and oesophageal symptoms, more severe ILD, and lower DLco.

Scleroderma Esophagus (Throat) Involvement

Scleroderma Esophageal (Throat) Involvement
SCLERO.ORG
Scleroderma Esophageal (Throat) Involvement
Overview
Air Esophagogram
Barrett's Esophagus
Candida Esophagitis
Correlation with Lung Disease
Dysphonia (Hoarseness, Loss of Voice)
Dysphonia (Hoarseness, Loss of Voice) Personal Stories
Esophageal Diseases
Esophageal Motility Disorders
Esophageal Motility Stories
Esophageal Spasm
Esophageal Stricture
Esophageal Stricture Personal Stories
Esophageal Ulcer
Gastric MALT Lymphoma
Reflux (Heartburn)
References

Carol Langenfeld: Diffuse Scleroderma People tell me that I have earned my credentials as a "certified patient" the hard way…
Don Alfera: CREST, Pulmonary Fibrosis and Sjögren's I entitled this "My Time So Far" since this has been a journey unlike any that I could have ever tried to imagine in my life…
Jerri: CREST Syndrome I was twenty-one years of age when I first noticed that my fingers, toes and lips were turning colors…
Sharon: CREST with Limited Scleroderma, Sjögren's and Pulmonary Hypertension (Australia) Day by day I discover another food I cannot eat …
Candida Esophagitis
The "Foamy" Esophagus A Radiographic Sign of Candida Esophagitis. Shows sophagrams of scleroderma patients. American Journal of Roentgenology. Correlation with Lung Disease
Relationship Between Interstitial Lung Disease (ILD) and Oesophageal Dilatation on Chest High-Resolution Computed Tomography (HRCT) in Patients With Systemic Sclerosis: A Cross-Sectional Study. An increased oesophageal diameter ( ≥ 11 mm) on chest HRCT is associated with pulmonary and oesophageal symptoms, more severe ILD, and lower DLco.

CREST Syndrome - What is?, Pictures, Symptoms, Treatment, Diagnosis CREST Syndrome
CREST Syndrome
Definition
Symptoms
Tight hardened skin
Raynaud’s phenomenon
Red spot marks on the skin
Lumps beneath the skin
Difficulty in swallowing
Classification
Causes of CREST Syndrome
Risk factors
Complications
Diagnosis
Blood test
Biopsy of the skin sample
Heart, lung and gastrointestinal tests
CREST Syndrome Treatment
Antibiotics
Antacids
Antihypertensive drugs
Immunosuppressive medications
Rehabilitation Therapy
References
 Regional blood circulation can totally obstruct in case of a severe Raynaud’s phenomenon and ulcer may develop. Usually fingers and toes often get affected and delayed healing leads to increase the chance of gangrene of fingers or toes due to narrowed blood vessels. Stiffness of the lung tissue lead to a lower functioning capability of the lungs and can cause an increase work load of the heart and heart muscle becomes weakened. Cardiac problem like arrhythmias and myocarditis gradually develop due to progression of the CREST syndrome. Severe contraction of the facial skin leads to difficulty in opening and widening mouth and it may create difficulty in brushing of the teeth. Due to esophageal impairment can cause acid reflux and that able to obliterate tooth enamel, and alteration of the gum muscles may lead to loosen tooth hold. In severe CREST syndrome patient also complain about dry eyes and mouth. ( 1)
Diagnosis
The CREST syndrome diagnosis is based on symptomatic examination and medical history analysis. In addition following tests are also conducted for determination of the underlying cause and severity judgment: Blood test
Analysis of the involve antibodies is assessed through a blood test, though this is not provided confirmatory result, as every individual has not contain the suspected identified antibodies.

Regional blood circulation can totally obstruct in case of a severe Raynaud’s phenomenon and ulcer may develop. Usually fingers and toes often get affected and delayed healing leads to increase the chance of gangrene of fingers or toes due to narrowed blood vessels. Stiffness of the lung tissue lead to a lower functioning capability of the lungs and can cause an increase work load of the heart and heart muscle becomes weakened. Cardiac problem like arrhythmias and myocarditis gradually develop due to progression of the CREST syndrome. Severe contraction of the facial skin leads to difficulty in opening and widening mouth and it may create difficulty in brushing of the teeth. Due to esophageal impairment can cause acid reflux and that able to obliterate tooth enamel, and alteration of the gum muscles may lead to loosen tooth hold. In severe CREST syndrome patient also complain about dry eyes and mouth. ( 1)
Diagnosis
The CREST syndrome diagnosis is based on symptomatic examination and medical history analysis. In addition following tests are also conducted for determination of the underlying cause and severity judgment: Blood test
Analysis of the involve antibodies is assessed through a blood test, though this is not provided confirmatory result, as every individual has not contain the suspected identified antibodies.

CREST Syndrome - What is?, Pictures, Symptoms, Treatment, Diagnosis CREST Syndrome
CREST Syndrome
Definition
Symptoms
Tight hardened skin
Raynaud’s phenomenon
Red spot marks on the skin
Lumps beneath the skin
Difficulty in swallowing
Classification
Causes of CREST Syndrome
Risk factors
Complications
Diagnosis
Blood test
Biopsy of the skin sample
Heart, lung and gastrointestinal tests
CREST Syndrome Treatment
Antibiotics
Antacids
Antihypertensive drugs
Immunosuppressive medications
Rehabilitation Therapy
References
 Due to esophageal impairment can cause acid reflux and that able to obliterate tooth enamel, and alteration of the gum muscles may lead to loosen tooth hold. In severe CREST syndrome patient also complain about dry eyes and mouth. ( 1)
Diagnosis
The CREST syndrome diagnosis is based on symptomatic examination and medical history analysis. In addition following tests are also conducted for determination of the underlying cause and severity judgment: Blood test
Analysis of the involve antibodies is assessed through a blood test, though this is not provided confirmatory result, as every individual has not contain the suspected identified antibodies. Biopsy of the skin sample
Doctors can take a small skin sample of the affected area, for biopsy test. This may not helpful to determine the CREST symptom, but it confirms that malignancy is not involved in the alteration of the skin structure. Heart, lung and gastrointestinal tests
The different test related to heart, lungs and gastrointestinal tract also conduct to estimate the internal organ involvement and severity of the CREST syndrome. ( 1)
CREST Syndrome Treatment
CREST syndrome is incurable condition, the available treatment options help to reduce the symptomatic manifestations and restrict probable complications. Pharmaco-therapies
Antibiotics
Topical antibiotics are prescribed to apply the affected area, if the superficial skin surface become infected.

Due to esophageal impairment can cause acid reflux and that able to obliterate tooth enamel, and alteration of the gum muscles may lead to loosen tooth hold. In severe CREST syndrome patient also complain about dry eyes and mouth. ( 1)
Diagnosis
The CREST syndrome diagnosis is based on symptomatic examination and medical history analysis. In addition following tests are also conducted for determination of the underlying cause and severity judgment: Blood test
Analysis of the involve antibodies is assessed through a blood test, though this is not provided confirmatory result, as every individual has not contain the suspected identified antibodies. Biopsy of the skin sample
Doctors can take a small skin sample of the affected area, for biopsy test. This may not helpful to determine the CREST symptom, but it confirms that malignancy is not involved in the alteration of the skin structure. Heart, lung and gastrointestinal tests
The different test related to heart, lungs and gastrointestinal tract also conduct to estimate the internal organ involvement and severity of the CREST syndrome. ( 1)
CREST Syndrome Treatment
CREST syndrome is incurable condition, the available treatment options help to reduce the symptomatic manifestations and restrict probable complications. Pharmaco-therapies
Antibiotics
Topical antibiotics are prescribed to apply the affected area, if the superficial skin surface become infected.

CREST Syndrome: Background, Pathophysiology, Etiology CREST Syndrome
CREST Syndrome
Background
 CREST Syndrome: Background, Pathophysiology, Etiology
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Drugs & Diseases > Dermatology
CREST Syndrome
Updated: Oct 05, 2020
Author: Jeanie C Yoon, MD; Chief Editor: Dirk M Elston, MD more...
Sections
CREST Syndrome
Sections CREST Syndrome
Overview
Background
Pathophysiology
Etiology
Epidemiology
Prognosis
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Presentation
History
Physical Examination
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DDx
Workup
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References
Overview
Background
CREST ( calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome is a member of the heterogeneous group of sclerodermas, and its name is an acronym for the cardinal clinical features of the syndrome. [ 1, 2]
In 1910, Thibierge and Weissenbach described the first case report of what was later called CRST (calcinosis cutis, Raynaud phenomenon, sclerodactyly, and telangiectasia) syndrome in English by Winterbauer who, in 1964, described a series of 8 patients with the features that make up the abbreviation CRST. [ 3, 4] Although he noted esophageal dysmotility in 4 of 8 patients, he did not include this feature in his original description of CRST syndrome.

Scleroderma Esophagus (Throat) Involvement Scleroderma Esophageal (Throat) Involvement
SCLERO.ORG
Scleroderma Esophageal (Throat) Involvement
Overview
Air Esophagogram
Barrett's Esophagus
Candida Esophagitis
Correlation with Lung Disease
Dysphonia (Hoarseness, Loss of Voice)
Dysphonia (Hoarseness, Loss of Voice) Personal Stories
Esophageal Diseases
Esophageal Motility Disorders
Esophageal Motility Stories
Esophageal Spasm
Esophageal Stricture
Esophageal Stricture Personal Stories
Esophageal Ulcer
Gastric MALT Lymphoma
Reflux (Heartburn)
References
 PubMed, Am J Gastroenterol, 2021 Mar 1;116 (3):517-521. Acceptability and Adequacy of a Non-endoscopic Cell Collection Device for Diagnosis of Barrett's Esophagus (BE): Lessons Learned. Diagnostic characteristics suggest that non-endoscopic assessment of BE deserves further development as an alternative to endoscopy. PubMed, Dig Dis Sci, 02/03/2021. Carol Langenfeld: Diffuse Scleroderma People tell me that I have earned my credentials as a "certified patient" the hard way…
Don Alfera: CREST, Pulmonary Fibrosis and Sjögren's I entitled this "My Time So Far" since this has been a journey unlike any that I could have ever tried to imagine in my life…
Jerri: CREST Syndrome I was twenty-one years of age when I first noticed that my fingers, toes and lips were turning colors…
Sharon: CREST with Limited Scleroderma, Sjögren's and Pulmonary Hypertension (Australia) Day by day I discover another food I cannot eat …
Candida Esophagitis
The "Foamy" Esophagus A Radiographic Sign of Candida Esophagitis.

PubMed, Am J Gastroenterol, 2021 Mar 1;116 (3):517-521. Acceptability and Adequacy of a Non-endoscopic Cell Collection Device for Diagnosis of Barrett's Esophagus (BE): Lessons Learned. Diagnostic characteristics suggest that non-endoscopic assessment of BE deserves further development as an alternative to endoscopy. PubMed, Dig Dis Sci, 02/03/2021. Carol Langenfeld: Diffuse Scleroderma People tell me that I have earned my credentials as a "certified patient" the hard way…
Don Alfera: CREST, Pulmonary Fibrosis and Sjögren's I entitled this "My Time So Far" since this has been a journey unlike any that I could have ever tried to imagine in my life…
Jerri: CREST Syndrome I was twenty-one years of age when I first noticed that my fingers, toes and lips were turning colors…
Sharon: CREST with Limited Scleroderma, Sjögren's and Pulmonary Hypertension (Australia) Day by day I discover another food I cannot eat …
Candida Esophagitis
The "Foamy" Esophagus A Radiographic Sign of Candida Esophagitis.

CREST syndrome | definition of CREST syndrome by Medical dictionary CREST syndrome
CREST syndrome
CREST syndrome
CREST syn·drome
CREST syn·drome
CREST syndrome
Thibierge,
CREST syn·drome
Mentioned in ?
References in periodicals archive ?
Medical browser ?
Full browser ?
 The word forming the third letter of the acronym is spelt ‘esophageal’ in the USA. Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005
Thibierge,
Georges, French physician, 1856-1926. Thibierge-Weissenbach syndrome - calcinosis, Raynaud phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia. Synonym (s): CREST syndrome
Medical Eponyms © Farlex 2012
CREST syn·drome
( krest sin'drōm)
Acronym for variant of systemic sclerosis characterized by calcinosis, Raynaud phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia. Medical Dictionary for the Dental Professions © Farlex 2012
Want to thank TFD for its existence? Tell a friend about us, add a link to this page, or visit the webmaster's page for free fun content . Link to this page: CREST syndrome
Mentioned in ? acroscleroderma
acrosclerosis
Antinuclear antibodies
autoantibody
Autoimmune Disorders
Brown
Brown Syndrome
Brown, Jason W.
circumscribed scleroderma
crest
crista
CRST syndrome
dermatosclerosis
diffuse scleroderma
generalized scleroderma
intimal sclerosis
linear scleroderma
Localized scleroderma
MS
References in periodicals archive ?

The word forming the third letter of the acronym is spelt ‘esophageal’ in the USA. Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005
Thibierge,
Georges, French physician, 1856-1926. Thibierge-Weissenbach syndrome - calcinosis, Raynaud phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia. Synonym (s): CREST syndrome
Medical Eponyms © Farlex 2012
CREST syn·drome
( krest sin'drōm)
Acronym for variant of systemic sclerosis characterized by calcinosis, Raynaud phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia. Medical Dictionary for the Dental Professions © Farlex 2012
Want to thank TFD for its existence? Tell a friend about us, add a link to this page, or visit the webmaster's page for free fun content . Link to this page: CREST syndrome
Mentioned in ? acroscleroderma
acrosclerosis
Antinuclear antibodies
autoantibody
Autoimmune Disorders
Brown
Brown Syndrome
Brown, Jason W.
circumscribed scleroderma
crest
crista
CRST syndrome
dermatosclerosis
diffuse scleroderma
generalized scleroderma
intimal sclerosis
linear scleroderma
Localized scleroderma
MS
References in periodicals archive ?

CREST Syndrome | Sunridge Medical Center Symptoms of CREST Syndrome
CREST Syndrome
Symptoms of CREST Syndrome
Contact Us
Address
Phone
Email
Have A Question Or Just Need More Information?
Don’t hesitate to contact us at anytime. we are here to help
Call Toll Free
1-800-923-7878
 CREST Syndrome | Sunridge Medical Center
CREST Syndrome
CREST syndrome is a slow form of scleroderma, an autoimmune disease causing abnormalities in the blood vessels, degenerative changes, and the scarring of internal organs and joints. Women are four times more likely to develop CREST syndrome. Though this disease is slow moving and the prognosis for CREST syndrome is better than that of Scleroderma, it is still very damaging over time—causing the skin to darken and tighten. This can result in an over-all stiffness or difficulty forming facial expressions. It can cause problems with swallowing or digestion owing to the scar tissue that can form in the esophagus. Symptoms of CREST Syndrome
Some symptoms of CREST syndrome are aches and pains in joints, heartburn, trouble swallowing that can lead to weight loss, and shortness of breath sometimes develops after scar tissue has built up in the esophagus. Other symptoms may include the swelling and thickening of the fingers or tingling and paling of fingers. There is sometimes scarring present around the joints that can cause fingers, wrists, and other joints to stay in a flexed position. Sometimes sufferers experience a grating sound made by joints that are inflamed. Typically, as fingers warm they become bluish in color.

CREST Syndrome | Sunridge Medical Center

Symptoms of CREST Syndrome
CREST Syndrome
Symptoms of CREST Syndrome
Contact Us
Address
Phone
Email
Have A Question Or Just Need More Information?
Don’t hesitate to contact us at anytime. we are here to help
Call Toll Free
1-800-923-7878

CREST Syndrome | Sunridge Medical Center
CREST Syndrome
CREST syndrome is a slow form of scleroderma, an autoimmune disease causing abnormalities in the blood vessels, degenerative changes, and the scarring of internal organs and joints. Women are four times more likely to develop CREST syndrome. Though this disease is slow moving and the prognosis for CREST syndrome is better than that of Scleroderma, it is still very damaging over time—causing the skin to darken and tighten. This can result in an over-all stiffness or difficulty forming facial expressions. It can cause problems with swallowing or digestion owing to the scar tissue that can form in the esophagus. Symptoms of CREST Syndrome
Some symptoms of CREST syndrome are aches and pains in joints, heartburn, trouble swallowing that can lead to weight loss, and shortness of breath sometimes develops after scar tissue has built up in the esophagus. Other symptoms may include the swelling and thickening of the fingers or tingling and paling of fingers. There is sometimes scarring present around the joints that can cause fingers, wrists, and other joints to stay in a flexed position. Sometimes sufferers experience a grating sound made by joints that are inflamed. Typically, as fingers warm they become bluish in color.

2021 ICD-10-CM Diagnosis Code M34.1: CR (E)ST syndrome
2021 ICD-10-CM Diagnosis Code M34.1
CR (E)ST syndrome
 sclerodactyly, and telangiectasis. When the defect in esophageal function is not prominent, it is known as crst syndrome. A variant of systemic sclerosis characterized by calcinosis, raynaud phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia. ICD-10-CM M34.1 is grouped within Diagnostic Related Group (s) (MS-DRG v38.0): 545 Connective tissue disorders with mcc
546 Connective tissue disorders with cc
547 Connective tissue disorders without cc/mcc
Convert M34.1 to ICD-9-CM
Code History
2016 (effective 10/1/2015): New code (first year of non-draft ICD-10-CM)
2017 (effective 10/1/2016): No change
2018 (effective 10/1/2017): No change
2019 (effective 10/1/2018): No change
2020 (effective 10/1/2019): No change
2021 (effective 10/1/2020):

2021 ICD-10-CM Diagnosis Code M34.1: CR (E)ST syndrome

2021 ICD-10-CM Diagnosis Code M34.1
CR (E)ST syndrome

sclerodactyly, and telangiectasis. When the defect in esophageal function is not prominent, it is known as crst syndrome. A variant of systemic sclerosis characterized by calcinosis, raynaud phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia. ICD-10-CM M34.1 is grouped within Diagnostic Related Group (s) (MS-DRG v38.0): 545 Connective tissue disorders with mcc
546 Connective tissue disorders with cc
547 Connective tissue disorders without cc/mcc
Convert M34.1 to ICD-9-CM
Code History
2016 (effective 10/1/2015): New code (first year of non-draft ICD-10-CM)
2017 (effective 10/1/2016): No change
2018 (effective 10/1/2017): No change
2019 (effective 10/1/2018): No change
2020 (effective 10/1/2019): No change
2021 (effective 10/1/2020):

Esophageal Dysmotility | Loma Linda University Health Esophageal Dysmotility
Esophageal Dysmotility
Esophageal Dysmotility
WHAT IS ESOPHAGEAL DYSMOTILITY?
WHAT ARE THE SYMPTOMS OF ESOPHAGEAL DYSMOTILITY?
WHAT CAUSES ESOPHAGEAL DYSMOTILITY?
HOW IS ESOPHAGEAL DYSMOTILITY DIAGNOSED?
HOW IS ESOPHAGEAL DYSMOTILITY TREATED?
WHO IS AT RISK FOR ESOPHAGEAL DYSMOTILITY?
NEXT STEPS
 This causes problems swallowing. The board-certified gastrointestinal specialists at Loma Linda University Health provide advanced care for the most complex conditions, including esophageal dysmotility. We treat more people with esophageal conditions than any center in the region. WHAT ARE THE SYMPTOMS OF ESOPHAGEAL DYSMOTILITY? The symptoms of esophageal dysmotility may include: Heartburn
Regurgitation
Chest pain
Difficulty swallowing
The feeling that food is stuck in the throat or chest
Weight loss and malnutrition
Recurrent bouts of pneumonia
WHAT CAUSES ESOPHAGEAL DYSMOTILITY? Esophageal dysmotility may be caused by: An ulcer, stricture, irritation, infection, inflammation, or cancer in the esophagus
Uncoordinated or abnormal muscles in the mouth, throat or esophagus
A nerve or brain problem (such as a stroke) that leaves the mouth, tongue or throat muscles weak (or changes how they coordinate)
HOW IS ESOPHAGEAL DYSMOTILITY DIAGNOSED? If a doctor suspects esophageal dysmotility, the diagnosis will begin with a physical examination and discussion of health history. Tests and imaging techniques used to diagnose esophageal dysmotility might include:

Esophageal Dysmotility | Loma Linda University Health

Esophageal Dysmotility
Esophageal Dysmotility
Esophageal Dysmotility
WHAT IS ESOPHAGEAL DYSMOTILITY?
WHAT ARE THE SYMPTOMS OF ESOPHAGEAL DYSMOTILITY?
WHAT CAUSES ESOPHAGEAL DYSMOTILITY?
HOW IS ESOPHAGEAL DYSMOTILITY DIAGNOSED?
HOW IS ESOPHAGEAL DYSMOTILITY TREATED?
WHO IS AT RISK FOR ESOPHAGEAL DYSMOTILITY?
NEXT STEPS

This causes problems swallowing. The board-certified gastrointestinal specialists at Loma Linda University Health provide advanced care for the most complex conditions, including esophageal dysmotility. We treat more people with esophageal conditions than any center in the region. WHAT ARE THE SYMPTOMS OF ESOPHAGEAL DYSMOTILITY? The symptoms of esophageal dysmotility may include: Heartburn
Regurgitation
Chest pain
Difficulty swallowing
The feeling that food is stuck in the throat or chest
Weight loss and malnutrition
Recurrent bouts of pneumonia
WHAT CAUSES ESOPHAGEAL DYSMOTILITY? Esophageal dysmotility may be caused by: An ulcer, stricture, irritation, infection, inflammation, or cancer in the esophagus
Uncoordinated or abnormal muscles in the mouth, throat or esophagus
A nerve or brain problem (such as a stroke) that leaves the mouth, tongue or throat muscles weak (or changes how they coordinate)
HOW IS ESOPHAGEAL DYSMOTILITY DIAGNOSED? If a doctor suspects esophageal dysmotility, the diagnosis will begin with a physical examination and discussion of health history. Tests and imaging techniques used to diagnose esophageal dysmotility might include:

CREST syndrome | definition of CREST syndrome by Medical dictionary CREST syndrome
CREST syndrome
CREST syndrome
CREST syn·drome
CREST syn·drome
CREST syndrome
Thibierge,
CREST syn·drome
Mentioned in ?
References in periodicals archive ?
Medical browser ?
Full browser ?
 4 (3):132-135. From autoimmune thyroid disease and CREST syndrome to incidental discovery of incipient gastric carcinoma: a case report
To improve sensitivity for milder forms of disease, the condition is often divided into diffuse systemic scleroderma (dSSc) or limited systemic scleroderma (lSSc) (TABLE 1), with CREST syndrome being a variant of the limited form. If CREST syndrome is suspected, it is important to look for its cardinal features. Our patient had all the cardinal features of CREST syndrome on history and physical exam. Elbow nodules: the nodules on the patient's elbow prompted her visit. The fact that she also had frequent heartburn provided an important diagnostic clue
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Esophageal dysmotility, esophageal motility disorder, causes, symptoms, diagnosis & treatment Esophageal dysmotility
Esophageal dysmotility
Esophageal motility disorder
Esophagus anatomy
Figure 1. Esophagus
Figure 2. Esophagus anatomy
Figure 3. Cross section view of the esophagus
Esophagus physiology
Figure 4. How the esophagus works
Upper esophageal sphincter
Peristalsis
Lower esophageal sphincter
Esophageal motility disorder causes
Primary esophageal causes of esophageal dysmotility include:
Systemic disorders causing esophageal dysmotility include:
Esophageal motility disorder symptoms
Achalasia
Spastic esophageal motility disorders
Scleroderma esophagus
Esophageal motility disorder diagnosis
Esophageal motility disorder treatment
Esophageal strictures treatment
Achalasia treatment
Medications
Botulinum toxin injection
Mechanical dilation
Surgery
Common pitfalls and side-effects of management
Esophageal motility disorder prognosis
Achalasia
Scleroderma esophagus
Spastic esophageal motility disorders
Mortality and morbidity
Complications
Achalasia and squamous cell carcinoma
MOST POPULAR
 Oropharyngeal dysfunction may result from certain surgeries, such as tracheostomy, laryngectomy or cervical dissection. There are primary idiopathic motor disorders that include achalasia, diffuse esophageal spasm, nutcracker esophagus, hypertensive lower esophageal sphincter and nonspecific esophageal motility disorders. Reflux disease is associated with an lower esophageal sphincter that is not sufficiently tight allowing gastric acid to wash back into the esophagus. The contractions of the esophagus in patients with reflux are generally not abnormal, but with long-standing reflux disease, they may decrease in amplitude. The esophagus is lined by both circular and longitudinal muscles that terminate at a 2- to 4-cm circular muscle layer called the lower esophageal sphincter. The lower esophageal sphincter accounts for approximately 90% of the basal pressure at the gastroesophageal junction, and functions as an anti-reflux barrier. Esophageal peristalsis is a very synchronized action regulated by the vagus nerve that both stimulates and inhibits neurons in the esophageal myenteric plexus. The disruption of coordination between excitatory and inhibitory signals to myenteric neurons results in esophageal motility disorder. Hypomotility of the esophageal body ranges from low wave amplitude to complete peristaltic failure, and etiologies include rheumatologic (scleroderma, connective tissue disorders), endocrinologic (diabetes mellitus, hypothyroidism) and other diseases (alcoholism, amyloidosis). The shared symptom of these disorders of hypomotility is gastroesophageal reflux disease (GERD).

Esophageal dysmotility, esophageal motility disorder, causes, symptoms, diagnosis & treatment

Esophageal dysmotility
Esophageal dysmotility
Esophageal motility disorder
Esophagus anatomy
Figure 1. Esophagus
Figure 2. Esophagus anatomy
Figure 3. Cross section view of the esophagus
Esophagus physiology
Figure 4. How the esophagus works
Upper esophageal sphincter
Peristalsis
Lower esophageal sphincter
Esophageal motility disorder causes
Primary esophageal causes of esophageal dysmotility include:
Systemic disorders causing esophageal dysmotility include:
Esophageal motility disorder symptoms
Achalasia
Spastic esophageal motility disorders
Scleroderma esophagus
Esophageal motility disorder diagnosis
Esophageal motility disorder treatment
Esophageal strictures treatment
Achalasia treatment
Medications
Botulinum toxin injection
Mechanical dilation
Surgery
Common pitfalls and side-effects of management
Esophageal motility disorder prognosis
Achalasia
Scleroderma esophagus
Spastic esophageal motility disorders
Mortality and morbidity
Complications
Achalasia and squamous cell carcinoma
MOST POPULAR

Oropharyngeal dysfunction may result from certain surgeries, such as tracheostomy, laryngectomy or cervical dissection. There are primary idiopathic motor disorders that include achalasia, diffuse esophageal spasm, nutcracker esophagus, hypertensive lower esophageal sphincter and nonspecific esophageal motility disorders. Reflux disease is associated with an lower esophageal sphincter that is not sufficiently tight allowing gastric acid to wash back into the esophagus. The contractions of the esophagus in patients with reflux are generally not abnormal, but with long-standing reflux disease, they may decrease in amplitude. The esophagus is lined by both circular and longitudinal muscles that terminate at a 2- to 4-cm circular muscle layer called the lower esophageal sphincter. The lower esophageal sphincter accounts for approximately 90% of the basal pressure at the gastroesophageal junction, and functions as an anti-reflux barrier. Esophageal peristalsis is a very synchronized action regulated by the vagus nerve that both stimulates and inhibits neurons in the esophageal myenteric plexus. The disruption of coordination between excitatory and inhibitory signals to myenteric neurons results in esophageal motility disorder. Hypomotility of the esophageal body ranges from low wave amplitude to complete peristaltic failure, and etiologies include rheumatologic (scleroderma, connective tissue disorders), endocrinologic (diabetes mellitus, hypothyroidism) and other diseases (alcoholism, amyloidosis). The shared symptom of these disorders of hypomotility is gastroesophageal reflux disease (GERD).

Belching and Heartburn: Common Related Medical Conditions Belching and Heartburn
Belching and Heartburn Esophagitis
Esophagitis, an inflammation of the lining of the esophagus, causes chest pain, nausea, and more. Eating certain foods
Certain foods can cause unusual and sometimes unpleasant side effects, such as bad breath and heartburn. Obesity
Obesity is having too much body fat, marked by a BMI of 30 or higher. Esophageal spasm
Esophageal spasms are sudden, painful contractions in the muscles of the esophagus. Barrett esophagus
Barrett's esophagus occurs when the lining of the esophagus is damaged, usually by acid reflux. Hyperparathyroidism
Hyperthyroidism causes weight loss, shakiness, tiredness, sensitivity to heat, insomnia, and more. CREST syndrome
CREST syndrome is a rare autoimmune disease that causes tissues to harden throughout the body. Advertisement
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Belching and Heartburn: Common Related Medical Conditions

Belching and Heartburn
Belching and Heartburn

Esophagitis
Esophagitis, an inflammation of the lining of the esophagus, causes chest pain, nausea, and more. Eating certain foods
Certain foods can cause unusual and sometimes unpleasant side effects, such as bad breath and heartburn. Obesity
Obesity is having too much body fat, marked by a BMI of 30 or higher. Esophageal spasm
Esophageal spasms are sudden, painful contractions in the muscles of the esophagus. Barrett esophagus
Barrett's esophagus occurs when the lining of the esophagus is damaged, usually by acid reflux. Hyperparathyroidism
Hyperthyroidism causes weight loss, shakiness, tiredness, sensitivity to heat, insomnia, and more. CREST syndrome
CREST syndrome is a rare autoimmune disease that causes tissues to harden throughout the body. Advertisement
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Esophageal dysmotility, esophageal motility disorder, causes, symptoms, diagnosis & treatment Esophageal dysmotility
Esophageal dysmotility
Esophageal motility disorder
Esophagus anatomy
Figure 1. Esophagus
Figure 2. Esophagus anatomy
Figure 3. Cross section view of the esophagus
Esophagus physiology
Figure 4. How the esophagus works
Upper esophageal sphincter
Peristalsis
Lower esophageal sphincter
Esophageal motility disorder causes
Primary esophageal causes of esophageal dysmotility include:
Systemic disorders causing esophageal dysmotility include:
Esophageal motility disorder symptoms
Achalasia
Spastic esophageal motility disorders
Scleroderma esophagus
Esophageal motility disorder diagnosis
Esophageal motility disorder treatment
Esophageal strictures treatment
Achalasia treatment
Medications
Botulinum toxin injection
Mechanical dilation
Surgery
Common pitfalls and side-effects of management
Esophageal motility disorder prognosis
Achalasia
Scleroderma esophagus
Spastic esophageal motility disorders
Mortality and morbidity
Complications
Achalasia and squamous cell carcinoma
MOST POPULAR
 Esophageal dysmotility, esophageal motility disorder, causes, symptoms, diagnosis & treatment
Esophageal dysmotility
Contents [ hide]
Esophageal motility disorder
Esophagus anatomy
Esophagus physiology
Upper esophageal sphincter
Peristalsis
Lower esophageal sphincter
Esophageal motility disorder causes
Esophageal motility disorder symptoms
Achalasia
Spastic esophageal motility disorders
Scleroderma esophagus
Esophageal motility disorder diagnosis
Esophageal motility disorder treatment
Esophageal strictures treatment
Achalasia treatment
Common pitfalls and side-effects of management
Esophageal motility disorder prognosis
Mortality and morbidity
Complications
Esophageal motility disorder
Esophageal dysmotility also called esophageal motility disorder are abnormal contractions occurring in the esophagus, which propel the food bolus forward toward the stomach, causing symptoms such as difficulty in swallowing (dysphagia), heartburn, and chest pain 1). When contractions in the esophagus become irregular, unsynchronized or absent, the patient is said to have esophageal dysmotility. The areas of dysfunction in the esophagus may be in the upper esophageal sphincter, the body of the esophagus or the lower esophageal sphincter (LES). The esophagus functions solely to deliver food from the mouth to the stomach where the process of digestion can begin. Efficient transport by the esophagus requires a coordinated, sequential motility pattern that propels food from above and clears acid and bile reflux from below. Disruption of this highly integrated muscular motion limits delivery of food and fluid, as well as causes a bothersome sense of dysphagia and chest pain. Disorders of esophageal motility are referred to as primary or secondary esophageal motility disorders and categorized according to their abnormal manometric patterns. The spectrum of these disorders ranges from the well-defined primary esophageal motility disorders to very nonspecific disorders that may play a more indirect role in reflux disease and otherwise be asymptomatic. Esophageal motility disorders may occur as manifestations of systemic diseases, referred to as secondary motility disorders. Disorders of esophageal motility can also be divided into two categories:

Ear ache and Heartburn: Common Related Medical Conditions Ear ache and Heartburn
Ear ache and Heartburn Barrett esophagus
Barrett's esophagus occurs when the lining of the esophagus is damaged, usually by acid reflux. Hyperparathyroidism
Hyperthyroidism causes weight loss, shakiness, tiredness, sensitivity to heat, insomnia, and more. CREST syndrome
CREST syndrome is a rare autoimmune disease that causes tissues to harden throughout the body. Advertisement
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©2005-2015 WebMD, LLC. All rights reserved. WebMD does not provide medical advice, diagnosis or treatment. See additional information.

Ear ache and Heartburn: Common Related Medical Conditions

Ear ache and Heartburn
Ear ache and Heartburn

Barrett esophagus
Barrett's esophagus occurs when the lining of the esophagus is damaged, usually by acid reflux. Hyperparathyroidism
Hyperthyroidism causes weight loss, shakiness, tiredness, sensitivity to heat, insomnia, and more. CREST syndrome
CREST syndrome is a rare autoimmune disease that causes tissues to harden throughout the body. Advertisement
Learn about WebMD Apps
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Esophageal dysmotility - MediGoo - Health Medical Tests | Information Esophageal dysmotility
Esophageal dysmotility
Esophageal dysmotility: Description, Causes and Risk Factors:
Symptoms:
Diagnosis:
Treatment:
 Occasionally, epiphrenic diverticula are noted immediately above the LES. Hiatal hernia reportedly is observed in 10-20% of patients with achalasia. In patients with DES, the classic esophagram findings are of a "corkscrew" or "rosary bead" esophagus. Pseudodiverticula and curling also suggest DES. In patients with scleroderma esophagus, the esophagram shows a slightly dilated esophagus, weak or absent peristalsis, and free reflux often is demonstrated. Other Tests: Esophageal manometry evaluates esophageal motor pattern, contraction amplitude, and LES pressure and function. Treatment: Dysmotility disorders of the esophagus are generally incurable. The main objective of treatment is, therefore, symptom management and relief.

Esophageal dysmotility - MediGoo - Health Medical Tests | Information

Esophageal dysmotility
Esophageal dysmotility
Esophageal dysmotility: Description, Causes and Risk Factors:
Symptoms:
Diagnosis:
Treatment:

Occasionally, epiphrenic diverticula are noted immediately above the LES. Hiatal hernia reportedly is observed in 10-20% of patients with achalasia. In patients with DES, the classic esophagram findings are of a "corkscrew" or "rosary bead" esophagus. Pseudodiverticula and curling also suggest DES. In patients with scleroderma esophagus, the esophagram shows a slightly dilated esophagus, weak or absent peristalsis, and free reflux often is demonstrated. Other Tests: Esophageal manometry evaluates esophageal motor pattern, contraction amplitude, and LES pressure and function. Treatment: Dysmotility disorders of the esophagus are generally incurable. The main objective of treatment is, therefore, symptom management and relief.

CREST syndrome | definition of CREST syndrome by Medical dictionary CREST syndrome
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Heartburn, Numbness or tingling, Numbness or tingling and Numbness or tingling: Common Related Medical Conditions Heartburn, Numbness or tingling (Upper arm (tricep)), Numbness or tingling (Forearm (extensor)) and Numbness or tingling (Hand (back))
Heartburn, Numbness or tingling (Upper arm (tricep)), Numbness or tingling (Forearm (extensor)) and Numbness or tingling (Hand (back)) Barrett esophagus
Barrett's esophagus occurs when the lining of the esophagus is damaged, usually by acid reflux. CREST syndrome
CREST syndrome is a rare autoimmune disease that causes tissues to harden throughout the body. Advertisement
Learn about WebMD Apps
Find WebMD on: Facebook
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View Site: Mobile | Desktop
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©2005-2015 WebMD, LLC. All rights reserved. WebMD does not provide medical advice, diagnosis or treatment. See additional information.

Heartburn, Numbness or tingling, Numbness or tingling and Numbness or tingling: Common Related Medical Conditions

Heartburn, Numbness or tingling (Upper arm (tricep)), Numbness or tingling (Forearm (extensor)) and Numbness or tingling (Hand (back))
Heartburn, Numbness or tingling (Upper arm (tricep)), Numbness or tingling (Forearm (extensor)) and Numbness or tingling (Hand (back))

Barrett esophagus
Barrett's esophagus occurs when the lining of the esophagus is damaged, usually by acid reflux. CREST syndrome
CREST syndrome is a rare autoimmune disease that causes tissues to harden throughout the body. Advertisement
Learn about WebMD Apps
Find WebMD on: Facebook
Twitter
Pinterest
View Site: Mobile | Desktop
About WebMD
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©2005-2015 WebMD, LLC. All rights reserved. WebMD does not provide medical advice, diagnosis or treatment. See additional information.

Esophageal dysmotility - MediGoo - Health Medical Tests | Information Esophageal dysmotility
Esophageal dysmotility
Esophageal dysmotility: Description, Causes and Risk Factors:
Symptoms:
Diagnosis:
Treatment:
 Patients with spastic esophageal motility disorders show no abnormalities on chest radiographs. Esophagram: Advanced achalasia produces a dilated intrathoracic esophagus with an air-fluid level. The classic sign is a tapering of the LES, creating the characteristic "bird-beak" appearance. Early achalasia would reveal a normal anatomical esophagus with loss of peristalsis and transient stasis just above the GEJ. Occasionally, epiphrenic diverticula are noted immediately above the LES. Hiatal hernia reportedly is observed in 10-20% of patients with achalasia. In patients with DES, the classic esophagram findings are of a "corkscrew" or "rosary bead" esophagus. Pseudodiverticula and curling also suggest DES. In patients with scleroderma esophagus, the esophagram shows a slightly dilated esophagus, weak or absent peristalsis, and free reflux often is demonstrated.

Patients with spastic esophageal motility disorders show no abnormalities on chest radiographs. Esophagram: Advanced achalasia produces a dilated intrathoracic esophagus with an air-fluid level. The classic sign is a tapering of the LES, creating the characteristic "bird-beak" appearance. Early achalasia would reveal a normal anatomical esophagus with loss of peristalsis and transient stasis just above the GEJ. Occasionally, epiphrenic diverticula are noted immediately above the LES. Hiatal hernia reportedly is observed in 10-20% of patients with achalasia. In patients with DES, the classic esophagram findings are of a "corkscrew" or "rosary bead" esophagus. Pseudodiverticula and curling also suggest DES. In patients with scleroderma esophagus, the esophagram shows a slightly dilated esophagus, weak or absent peristalsis, and free reflux often is demonstrated.

Disorders of the Esophagus - About GI Motility Disorders of the Esophagus
Disorders of the Esophagus
Dysphagia
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 Disorders of the Esophagus - About GI Motility
Home » About GI Motility
Disorders of the Esophagus
The function of the esophagus (food tube) is to transport food from the mouth to the stomach. Synchronized (peristaltic) contractions follow each swallow to accomplish this task. Between swallows, the esophagus usually does not contract. The lower esophageal sphincter (or LES) is a muscle that separates the esophagus from the stomach. It acts like a valve that normally stays tightly closed to prevent contents in the stomach from backing up into the esophagus. When we swallow, the LES opens up (the muscle relaxes) so that the food we swallow can enter the stomach. Difficulty swallowing liquids or solids, heartburn, regurgitation, and atypical (or non-cardiac) chest pain may be symptoms of an esophageal motility disorder. Examples of motility disorders of the esophagus that are described below include gastroesophageal reflux disease (GERD), dysphagia, achalasia, and functional chest pain. Gastroesophageal reflux disease (GERD)
The most common symptom that occurs in the esophagus is heartburn. It happens when stomach contents washes up into the esophagus repeatedly (gastroesophageal reflux) and irritates the lining of the esophagus.

Disorders of the Esophagus - About GI Motility

Disorders of the Esophagus
Disorders of the Esophagus
Dysphagia
Was this article helpful?
If you found this article helpful, please consider supporting IFFGD with a small tax-deductible donation.

Disorders of the Esophagus - About GI Motility
Home » About GI Motility
Disorders of the Esophagus
The function of the esophagus (food tube) is to transport food from the mouth to the stomach. Synchronized (peristaltic) contractions follow each swallow to accomplish this task. Between swallows, the esophagus usually does not contract. The lower esophageal sphincter (or LES) is a muscle that separates the esophagus from the stomach. It acts like a valve that normally stays tightly closed to prevent contents in the stomach from backing up into the esophagus. When we swallow, the LES opens up (the muscle relaxes) so that the food we swallow can enter the stomach. Difficulty swallowing liquids or solids, heartburn, regurgitation, and atypical (or non-cardiac) chest pain may be symptoms of an esophageal motility disorder. Examples of motility disorders of the esophagus that are described below include gastroesophageal reflux disease (GERD), dysphagia, achalasia, and functional chest pain. Gastroesophageal reflux disease (GERD)
The most common symptom that occurs in the esophagus is heartburn. It happens when stomach contents washes up into the esophagus repeatedly (gastroesophageal reflux) and irritates the lining of the esophagus.

Esophageal dysmotility, esophageal motility disorder, causes, symptoms, diagnosis & treatment Esophageal dysmotility
Esophageal dysmotility
Esophageal motility disorder
Esophagus anatomy
Figure 1. Esophagus
Figure 2. Esophagus anatomy
Figure 3. Cross section view of the esophagus
Esophagus physiology
Figure 4. How the esophagus works
Upper esophageal sphincter
Peristalsis
Lower esophageal sphincter
Esophageal motility disorder causes
Primary esophageal causes of esophageal dysmotility include:
Systemic disorders causing esophageal dysmotility include:
Esophageal motility disorder symptoms
Achalasia
Spastic esophageal motility disorders
Scleroderma esophagus
Esophageal motility disorder diagnosis
Esophageal motility disorder treatment
Esophageal strictures treatment
Achalasia treatment
Medications
Botulinum toxin injection
Mechanical dilation
Surgery
Common pitfalls and side-effects of management
Esophageal motility disorder prognosis
Achalasia
Scleroderma esophagus
Spastic esophageal motility disorders
Mortality and morbidity
Complications
Achalasia and squamous cell carcinoma
MOST POPULAR
 Disruption of this highly integrated muscular motion limits delivery of food and fluid, as well as causes a bothersome sense of dysphagia and chest pain. Disorders of esophageal motility are referred to as primary or secondary esophageal motility disorders and categorized according to their abnormal manometric patterns. The spectrum of these disorders ranges from the well-defined primary esophageal motility disorders to very nonspecific disorders that may play a more indirect role in reflux disease and otherwise be asymptomatic. Esophageal motility disorders may occur as manifestations of systemic diseases, referred to as secondary motility disorders. Disorders of esophageal motility can also be divided into two categories: hypomotility and hypermotility, either of which can affect the lower esophageal sphincter (LES) and/or the esophageal body. Dysphagia is a condition affecting over 9 million individuals in the United States. Oropharyngeal dysphagia, specifically, happens in as much as 50% of the elderly and 50% of patients with neurological pathologies. Clinically, oropharyngeal dysphagia can present with severe symptoms such as aspiration and death. Esophageal dysphagia, on the other hand, is a rarer condition with less severe symptoms but is easier to recognize due to symptoms arising from diseases of the enteric nervous system or esophageal muscular layers.

Disruption of this highly integrated muscular motion limits delivery of food and fluid, as well as causes a bothersome sense of dysphagia and chest pain. Disorders of esophageal motility are referred to as primary or secondary esophageal motility disorders and categorized according to their abnormal manometric patterns. The spectrum of these disorders ranges from the well-defined primary esophageal motility disorders to very nonspecific disorders that may play a more indirect role in reflux disease and otherwise be asymptomatic. Esophageal motility disorders may occur as manifestations of systemic diseases, referred to as secondary motility disorders. Disorders of esophageal motility can also be divided into two categories: hypomotility and hypermotility, either of which can affect the lower esophageal sphincter (LES) and/or the esophageal body. Dysphagia is a condition affecting over 9 million individuals in the United States. Oropharyngeal dysphagia, specifically, happens in as much as 50% of the elderly and 50% of patients with neurological pathologies. Clinically, oropharyngeal dysphagia can present with severe symptoms such as aspiration and death. Esophageal dysphagia, on the other hand, is a rarer condition with less severe symptoms but is easier to recognize due to symptoms arising from diseases of the enteric nervous system or esophageal muscular layers.

Esophageal dysmotility, esophageal motility disorder, causes, symptoms, diagnosis & treatment Esophageal dysmotility
Esophageal dysmotility
Esophageal motility disorder
Esophagus anatomy
Figure 1. Esophagus
Figure 2. Esophagus anatomy
Figure 3. Cross section view of the esophagus
Esophagus physiology
Figure 4. How the esophagus works
Upper esophageal sphincter
Peristalsis
Lower esophageal sphincter
Esophageal motility disorder causes
Primary esophageal causes of esophageal dysmotility include:
Systemic disorders causing esophageal dysmotility include:
Esophageal motility disorder symptoms
Achalasia
Spastic esophageal motility disorders
Scleroderma esophagus
Esophageal motility disorder diagnosis
Esophageal motility disorder treatment
Esophageal strictures treatment
Achalasia treatment
Medications
Botulinum toxin injection
Mechanical dilation
Surgery
Common pitfalls and side-effects of management
Esophageal motility disorder prognosis
Achalasia
Scleroderma esophagus
Spastic esophageal motility disorders
Mortality and morbidity
Complications
Achalasia and squamous cell carcinoma
MOST POPULAR
 Diffuse esophageal spasm is characterized by uncoordinated or simultaneous contractions of the esophagus with abnormal peristalsis following swallowing. The other disorders may show abnormalities in the amplitude, frequency or duration of contractions and/or a hypertensive lower esophageal sphincter. One subgroup of spastic disorders is “nutcracker esophagus”, characterized by contractions of high amplitude with otherwise normal peristalsis. Presenting symptoms of all hypermotility disorders include chest pain (in 80-90% of cases), dysphagia, regurgitation, and heartburn. A barium swallow and/or manometry are the preliminary diagnostic tests. The significance of these disorders is not fully understood however, as abnormal results can be seen in patients with and without symptoms, and the pain may not be directly attributable to dysmotility. Fortunately, these spastic disorders are not typically progressive or fatal. Treatment risks must therefore be especially weighed against potential benefits, with consideration of low-risk treatments (e.g., proton pump inhibitor to rule out possible GERD) first. Other options range from swallowing warm liquids with meals to invasive treatments used for achalasia (see below). Bougienage and serial dilation with increasing sizes of bougies may be effective for some patients.

Diffuse esophageal spasm is characterized by uncoordinated or simultaneous contractions of the esophagus with abnormal peristalsis following swallowing. The other disorders may show abnormalities in the amplitude, frequency or duration of contractions and/or a hypertensive lower esophageal sphincter. One subgroup of spastic disorders is “nutcracker esophagus”, characterized by contractions of high amplitude with otherwise normal peristalsis. Presenting symptoms of all hypermotility disorders include chest pain (in 80-90% of cases), dysphagia, regurgitation, and heartburn. A barium swallow and/or manometry are the preliminary diagnostic tests. The significance of these disorders is not fully understood however, as abnormal results can be seen in patients with and without symptoms, and the pain may not be directly attributable to dysmotility. Fortunately, these spastic disorders are not typically progressive or fatal. Treatment risks must therefore be especially weighed against potential benefits, with consideration of low-risk treatments (e.g., proton pump inhibitor to rule out possible GERD) first. Other options range from swallowing warm liquids with meals to invasive treatments used for achalasia (see below). Bougienage and serial dilation with increasing sizes of bougies may be effective for some patients.

Esophageal Motility Disorders - American Family Physician Esophageal Motility Disorders
Esophageal Motility Disorders
This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions.
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Classification and Epidemiology
Classification of Esophageal Motility Disorders
ACHALASIA
HYPERCONTRACTILE MOTILITY DISORDERS
FUNCTIONAL ESOPHAGEAL DISORDERS
Clinical Features
Enlarge Print
DYSPHAGIA
CHEST PAIN
Testing
Esophageal Conditions That Cause Pain or Dysphagia
MANAGEMENT OF COMMON CONDITIONS
ESOPHAGOGASTRODUODENOSCOPY
BARIUM ESOPHAGOGRAPHY
HIGH-RESOLUTION ESOPHAGEAL MANOMETRY
Management
LIFESTYLE MODIFICATIONS
MEDICATIONS
ENDOSCOPIC AND SURGICAL THERAPIES
The Authors
References
6.00 CME Credits Available
CME expires 09-01-2021
Editor's Collections
Email Alerts
 1, 4 – 7
Enlarge Print
TABLE 1. Classification of Esophageal Motility Disorders
Disorder
Lower esophageal sphincter tone
Peristalsis
Comments
Achalasia
Type I (classic)
Fails to relax
100% failed (no contractility)
Responds to laparoscopic Heller myotomy, less so to pneumatic dilation
Type II (with esophageal compression)
Fails to relax
Some pressurization, but no normal peristalsis
All treatments are effective
Type III (spastic)
Fails to relax
No normal peristalsis and spastic contractions distally in more than 20% of swallows
Poor response to treatment
Esophagogastric junction outflow obstruction
Fails to relax
Some preserved
May reflect a physical obstruction at the level of the lower esophageal sphincter rather than early achalasia
Major disorders of peristalsis *
Absent contractility
Normal
Failed
Relatively rare; easily diagnosed but treatments are only minimally effective; common in patients with systemic sclerosis (scleroderma); included among the major motility disorders but typically manifests with reflux, not dysphagia or chest pain 1
Distal esophageal spasm
Normal
Premature distal contraction with poor peristalsis
Relatively rare; diagnosis is difficult and treatments are only minimally effective
Hypercontractile (jackhammer) esophagus
Normal
Abnormally forceful contractions
Relatively rare; diagnosis is difficult and treatments are only minimally effective
Minor disorders of peristalsis†
Fragmented peristalsis
Normal
> 50% fragmented contractions
—
Ineffective esophageal motility
Normal
> 50% ineffective swallows
—
*—The term nutcracker esophagus is no longer used; the manometric pattern in this condition is common in asymptomatic people and is not thought to cause symptoms. †—Food bolus transit is impaired, but clinical significance is unclear; may occur in people without esophageal disorders.

Esophageal Motility Disorders - American Family Physician

Esophageal Motility Disorders
Esophageal Motility Disorders
This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions.
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Classification and Epidemiology
Classification of Esophageal Motility Disorders
ACHALASIA
HYPERCONTRACTILE MOTILITY DISORDERS
FUNCTIONAL ESOPHAGEAL DISORDERS
Clinical Features
Enlarge Print
DYSPHAGIA
CHEST PAIN
Testing
Esophageal Conditions That Cause Pain or Dysphagia
MANAGEMENT OF COMMON CONDITIONS
ESOPHAGOGASTRODUODENOSCOPY
BARIUM ESOPHAGOGRAPHY
HIGH-RESOLUTION ESOPHAGEAL MANOMETRY
Management
LIFESTYLE MODIFICATIONS
MEDICATIONS
ENDOSCOPIC AND SURGICAL THERAPIES
The Authors
References
6.00 CME Credits Available
CME expires 09-01-2021
Editor's Collections
Email Alerts

Esophageal Motility Disorders - American Family Physician Esophageal Motility Disorders
Esophageal Motility Disorders
This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions.
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Classification and Epidemiology
Classification of Esophageal Motility Disorders
ACHALASIA
HYPERCONTRACTILE MOTILITY DISORDERS
FUNCTIONAL ESOPHAGEAL DISORDERS
Clinical Features
Enlarge Print
DYSPHAGIA
CHEST PAIN
Testing
Esophageal Conditions That Cause Pain or Dysphagia
MANAGEMENT OF COMMON CONDITIONS
ESOPHAGOGASTRODUODENOSCOPY
BARIUM ESOPHAGOGRAPHY
HIGH-RESOLUTION ESOPHAGEAL MANOMETRY
Management
LIFESTYLE MODIFICATIONS
MEDICATIONS
ENDOSCOPIC AND SURGICAL THERAPIES
The Authors
References
6.00 CME Credits Available
CME expires 09-01-2021
Editor's Collections
Email Alerts
 Information from references 1 and 4 – 7. TABLE 1. Classification of Esophageal Motility Disorders
Disorder
Lower esophageal sphincter tone
Peristalsis
Comments
Achalasia
Type I (classic)
Fails to relax
100% failed (no contractility)
Responds to laparoscopic Heller myotomy, less so to pneumatic dilation
Type II (with esophageal compression)
Fails to relax
Some pressurization, but no normal peristalsis
All treatments are effective
Type III (spastic)
Fails to relax
No normal peristalsis and spastic contractions distally in more than 20% of swallows
Poor response to treatment
Esophagogastric junction outflow obstruction
Fails to relax
Some preserved
May reflect a physical obstruction at the level of the lower esophageal sphincter rather than early achalasia
Major disorders of peristalsis *
Absent contractility
Normal
Failed
Relatively rare; easily diagnosed but treatments are only minimally effective; common in patients with systemic sclerosis (scleroderma); included among the major motility disorders but typically manifests with reflux, not dysphagia or chest pain

Information from references 1 and 4 – 7. TABLE 1. Classification of Esophageal Motility Disorders
Disorder
Lower esophageal sphincter tone
Peristalsis
Comments
Achalasia
Type I (classic)
Fails to relax
100% failed (no contractility)
Responds to laparoscopic Heller myotomy, less so to pneumatic dilation
Type II (with esophageal compression)
Fails to relax
Some pressurization, but no normal peristalsis
All treatments are effective
Type III (spastic)
Fails to relax
No normal peristalsis and spastic contractions distally in more than 20% of swallows
Poor response to treatment
Esophagogastric junction outflow obstruction
Fails to relax
Some preserved
May reflect a physical obstruction at the level of the lower esophageal sphincter rather than early achalasia
Major disorders of peristalsis *
Absent contractility
Normal
Failed
Relatively rare; easily diagnosed but treatments are only minimally effective; common in patients with systemic sclerosis (scleroderma); included among the major motility disorders but typically manifests with reflux, not dysphagia or chest pain

Esophageal dysmotility, esophageal motility disorder, causes, symptoms, diagnosis & treatment Esophageal dysmotility
Esophageal dysmotility
Esophageal motility disorder
Esophagus anatomy
Figure 1. Esophagus
Figure 2. Esophagus anatomy
Figure 3. Cross section view of the esophagus
Esophagus physiology
Figure 4. How the esophagus works
Upper esophageal sphincter
Peristalsis
Lower esophageal sphincter
Esophageal motility disorder causes
Primary esophageal causes of esophageal dysmotility include:
Systemic disorders causing esophageal dysmotility include:
Esophageal motility disorder symptoms
Achalasia
Spastic esophageal motility disorders
Scleroderma esophagus
Esophageal motility disorder diagnosis
Esophageal motility disorder treatment
Esophageal strictures treatment
Achalasia treatment
Medications
Botulinum toxin injection
Mechanical dilation
Surgery
Common pitfalls and side-effects of management
Esophageal motility disorder prognosis
Achalasia
Scleroderma esophagus
Spastic esophageal motility disorders
Mortality and morbidity
Complications
Achalasia and squamous cell carcinoma
MOST POPULAR
 The lower esophageal sphincter accounts for approximately 90% of the basal pressure at the gastroesophageal junction, and functions as an anti-reflux barrier. Esophageal peristalsis is a very synchronized action regulated by the vagus nerve that both stimulates and inhibits neurons in the esophageal myenteric plexus. The disruption of coordination between excitatory and inhibitory signals to myenteric neurons results in esophageal motility disorder. Hypomotility of the esophageal body ranges from low wave amplitude to complete peristaltic failure, and etiologies include rheumatologic (scleroderma, connective tissue disorders), endocrinologic (diabetes mellitus, hypothyroidism) and other diseases (alcoholism, amyloidosis). The shared symptom of these disorders of hypomotility is gastroesophageal reflux disease (GERD). Food impaction and slow transit of pills may result in caustic esophageal damage as well. Barium esophagogram and manometry are the main diagnostic tools, and treatment varies with the etiology of the hypomotility. Hypermotility of the lower esophageal sphincter is most commonly seen in achalasia, which is discussed in detail throughout the rest of this chapter. Hypertensive disorders of the esophageal body (which may or may not involve the lower esophageal sphincter) are termed spastic disorders. They can be further categorized as diffuse esophageal spasm and non-specific spastic disorders, and are almost universally idiopathic.

The lower esophageal sphincter accounts for approximately 90% of the basal pressure at the gastroesophageal junction, and functions as an anti-reflux barrier. Esophageal peristalsis is a very synchronized action regulated by the vagus nerve that both stimulates and inhibits neurons in the esophageal myenteric plexus. The disruption of coordination between excitatory and inhibitory signals to myenteric neurons results in esophageal motility disorder. Hypomotility of the esophageal body ranges from low wave amplitude to complete peristaltic failure, and etiologies include rheumatologic (scleroderma, connective tissue disorders), endocrinologic (diabetes mellitus, hypothyroidism) and other diseases (alcoholism, amyloidosis). The shared symptom of these disorders of hypomotility is gastroesophageal reflux disease (GERD). Food impaction and slow transit of pills may result in caustic esophageal damage as well. Barium esophagogram and manometry are the main diagnostic tools, and treatment varies with the etiology of the hypomotility. Hypermotility of the lower esophageal sphincter is most commonly seen in achalasia, which is discussed in detail throughout the rest of this chapter. Hypertensive disorders of the esophageal body (which may or may not involve the lower esophageal sphincter) are termed spastic disorders. They can be further categorized as diffuse esophageal spasm and non-specific spastic disorders, and are almost universally idiopathic.

Esophageal Motility Disorders - American Family Physician Esophageal Motility Disorders
Esophageal Motility Disorders
This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions.
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Classification and Epidemiology
Classification of Esophageal Motility Disorders
ACHALASIA
HYPERCONTRACTILE MOTILITY DISORDERS
FUNCTIONAL ESOPHAGEAL DISORDERS
Clinical Features
Enlarge Print
DYSPHAGIA
CHEST PAIN
Testing
Esophageal Conditions That Cause Pain or Dysphagia
MANAGEMENT OF COMMON CONDITIONS
ESOPHAGOGASTRODUODENOSCOPY
BARIUM ESOPHAGOGRAPHY
HIGH-RESOLUTION ESOPHAGEAL MANOMETRY
Management
LIFESTYLE MODIFICATIONS
MEDICATIONS
ENDOSCOPIC AND SURGICAL THERAPIES
The Authors
References
6.00 CME Credits Available
CME expires 09-01-2021
Editor's Collections
Email Alerts
 Classification and Epidemiology
Jump to section +
Abstract
Classification and Epidemiology
Clinical Features
Testing
Management
References
When normal swallowing (deglutition) is initiated, the upper esophageal sphincter relaxes, followed within one to two seconds by the lower esophageal sphincter, allowing a food bolus from the oropharynx to be propelled by peristalsis through the esophagus and into the stomach. In normal peristalsis, excitatory neurons cause contraction of one segment of smooth muscle as inhibitory neurons relax the segment below. Achalasia is the esophageal motility disorder of greatest clinical significance. Hypercontractile motility disorders, although seemingly well-defined, may overlap with functional esophageal disorders to a greater degree than previously recognized. Several other conditions are classified among the esophageal motility disorders but are much less relevant ( Table 1). 1, 4 – 7
Enlarge Print
TABLE 1. Classification of Esophageal Motility Disorders
Disorder
Lower esophageal sphincter tone
Peristalsis
Comments
Achalasia
Type I (classic)
Fails to relax
100% failed (no contractility)
Responds to laparoscopic Heller myotomy, less so to pneumatic dilation
Type II (with esophageal compression)
Fails to relax
Some pressurization, but no normal peristalsis
All treatments are effective
Type III (spastic)
Fails to relax
No normal peristalsis and spastic contractions distally in more than 20% of swallows
Poor response to treatment
Esophagogastric junction outflow obstruction
Fails to relax
Some preserved
May reflect a physical obstruction at the level of the lower esophageal sphincter rather than early achalasia
Major disorders of peristalsis *
Absent contractility
Normal
Failed
Relatively rare; easily diagnosed but treatments are only minimally effective; common in patients with systemic sclerosis (scleroderma); included among the major motility disorders but typically manifests with reflux, not dysphagia or chest pain 1
Distal esophageal spasm
Normal
Premature distal contraction with poor peristalsis
Relatively rare;

5 Signs you may have an esophageal motility disorder - RefluxMD 5 Signs you may have an esophageal motility disorder
5 Signs you may have an esophageal motility disorder
Variations and causes of an esophageal motility disorder exist?
Symptoms of an esophageal motility disorder
#1 Difficulty swallowing
#2 Heartburn that often leads to acid reflux
#3 Chest pressure that sometimes becomes painful
#4 Frequent coughing
#5 Previous history of diabetes or immune diseases
Resolving an esophageal motility disorder
Resources used for this article
Most viewed articles
 5 Signs you may have an esophageal motility disorder - RefluxMD
5 Signs you may have an esophageal motility disorder
By Bruce Kaechele, The GERD Guide
Last updated on June 17th, 2019 at 08:27 pm
This Article is Written and/or Reviewed by RefluxMD Medical Authors Team and Reviewers
You can’t treat a disorder if you don’t know you have it. It’s common to feel some slight discomfort after eating. Frequent distress could be a sign of a disorder. The esophagus allows food to pass from your mouth into the stomach. An esophageal motility disorder occurs when muscles are not working together. John’s Hopkins Health System has a clear explanation of this: “An esophageal motility disorder refers to contractions occurring in the esophagus, which propel the food bolus forward toward the stomach. When contractions in the esophagus become irregular, unsynchronized or absent, the patient is said to have esophageal dysmotility.” Muscle groups that don’t work together can create major digestive problems. Those suffering from a motility disorder of the esophagus often experience many symptoms.

5 Signs you may have an esophageal motility disorder - RefluxMD

5 Signs you may have an esophageal motility disorder
5 Signs you may have an esophageal motility disorder
Variations and causes of an esophageal motility disorder exist?
Symptoms of an esophageal motility disorder
#1 Difficulty swallowing
#2 Heartburn that often leads to acid reflux
#3 Chest pressure that sometimes becomes painful
#4 Frequent coughing
#5 Previous history of diabetes or immune diseases
Resolving an esophageal motility disorder
Resources used for this article
Most viewed articles

5 Signs you may have an esophageal motility disorder - RefluxMD
5 Signs you may have an esophageal motility disorder
By Bruce Kaechele, The GERD Guide
Last updated on June 17th, 2019 at 08:27 pm
This Article is Written and/or Reviewed by RefluxMD Medical Authors Team and Reviewers
You can’t treat a disorder if you don’t know you have it. It’s common to feel some slight discomfort after eating. Frequent distress could be a sign of a disorder. The esophagus allows food to pass from your mouth into the stomach. An esophageal motility disorder occurs when muscles are not working together. John’s Hopkins Health System has a clear explanation of this: “An esophageal motility disorder refers to contractions occurring in the esophagus, which propel the food bolus forward toward the stomach. When contractions in the esophagus become irregular, unsynchronized or absent, the patient is said to have esophageal dysmotility.” Muscle groups that don’t work together can create major digestive problems. Those suffering from a motility disorder of the esophagus often experience many symptoms.

Esophageal dysmotility - MediGoo - Health Medical Tests | Information Esophageal dysmotility
Esophageal dysmotility
Esophageal dysmotility: Description, Causes and Risk Factors:
Symptoms:
Diagnosis:
Treatment:
 In some cases, a hypertensive lower esophageal sphincter can paradoxically occur in the setting of reflux disease. If the lower esophageal sphincter tone is too low, uncontrolled reflux of gastric contents may occur. Other than in the setting of GERD, this finding may occur with some connective tissue disorders, such as scleroderma. Esophageal dysmotility disorder may also be the result of the build-up of scar tissue in the esophagus. Symptoms: These problems can lead to symptoms such as chest pain, pain when swallowing or the feeling of a permanent lump in the throat. Diagnosis: A chest radiograph is not required to establish the diagnosis. In patients with long-standing achalasia, the esophagus dilates and exhibits a sigmoid appearance. An air-fluid level, a widened mediastinum, and the absence of a gastric air bubble often are observed.

In some cases, a hypertensive lower esophageal sphincter can paradoxically occur in the setting of reflux disease. If the lower esophageal sphincter tone is too low, uncontrolled reflux of gastric contents may occur. Other than in the setting of GERD, this finding may occur with some connective tissue disorders, such as scleroderma. Esophageal dysmotility disorder may also be the result of the build-up of scar tissue in the esophagus. Symptoms: These problems can lead to symptoms such as chest pain, pain when swallowing or the feeling of a permanent lump in the throat. Diagnosis: A chest radiograph is not required to establish the diagnosis. In patients with long-standing achalasia, the esophagus dilates and exhibits a sigmoid appearance. An air-fluid level, a widened mediastinum, and the absence of a gastric air bubble often are observed.

Esophageal Motility Disorders: Background, Etiopathophysiology, Epidemiology Esophageal Motility Disorders
Esophageal Motility Disorders
Background
Anatomy
Esophageal peristalsis
Esophageal motility disorders
 Peristalsis is a sequential, coordinated contraction wave that travels the entire length of the esophagus, propelling intraluminal contents distally to the stomach. The LES relaxes during swallows and stays opened until the peristaltic wave travels through the LES, then contracts and redevelops resting basal tone. Low peristaltic amplitudes normally occur at the transition zone between the striated and smooth muscle portions; however, the peristalsis is uninterrupted. Primary peristalsis is the peristaltic wave triggered by the swallowing center. The peristaltic contraction wave travels at a speed of 2 cm/s and correlates with manometry-recorded contractions. The relationship of contraction and food bolus is more complex because of intrabolus pressures from above (contraction from above) and the resistance from below (outflow resistance). The secondary peristaltic wave is induced by esophageal distension from the retained bolus, refluxed material, or swallowed air. The primary role is to clear the esophagus of retained food or any gastroesophageal refluxate. Tertiary contractions are simultaneous, isolated, dysfunctional contractions.

Esophageal Motility Disorders: Background, Etiopathophysiology, Epidemiology

Esophageal Motility Disorders
Esophageal Motility Disorders
Background
Anatomy
Esophageal peristalsis
Esophageal motility disorders

Peristalsis is a sequential, coordinated contraction wave that travels the entire length of the esophagus, propelling intraluminal contents distally to the stomach. The LES relaxes during swallows and stays opened until the peristaltic wave travels through the LES, then contracts and redevelops resting basal tone. Low peristaltic amplitudes normally occur at the transition zone between the striated and smooth muscle portions; however, the peristalsis is uninterrupted. Primary peristalsis is the peristaltic wave triggered by the swallowing center. The peristaltic contraction wave travels at a speed of 2 cm/s and correlates with manometry-recorded contractions. The relationship of contraction and food bolus is more complex because of intrabolus pressures from above (contraction from above) and the resistance from below (outflow resistance). The secondary peristaltic wave is induced by esophageal distension from the retained bolus, refluxed material, or swallowed air. The primary role is to clear the esophagus of retained food or any gastroesophageal refluxate. Tertiary contractions are simultaneous, isolated, dysfunctional contractions.

Esophageal Motility Disorders - American Family Physician Esophageal Motility Disorders
Esophageal Motility Disorders
This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions.
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Classification and Epidemiology
Classification of Esophageal Motility Disorders
ACHALASIA
HYPERCONTRACTILE MOTILITY DISORDERS
FUNCTIONAL ESOPHAGEAL DISORDERS
Clinical Features
Enlarge Print
DYSPHAGIA
CHEST PAIN
Testing
Esophageal Conditions That Cause Pain or Dysphagia
MANAGEMENT OF COMMON CONDITIONS
ESOPHAGOGASTRODUODENOSCOPY
BARIUM ESOPHAGOGRAPHY
HIGH-RESOLUTION ESOPHAGEAL MANOMETRY
Management
LIFESTYLE MODIFICATIONS
MEDICATIONS
ENDOSCOPIC AND SURGICAL THERAPIES
The Authors
References
6.00 CME Credits Available
CME expires 09-01-2021
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 Esophageal Motility Disorders - American Family Physician
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Esophageal Motility Disorders
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JOHN M. WILKINSON, MD, and MAGNUS HALLAND, MD, Mayo Clinic Alix School of Medicine, Mayo Clinic College of Medicine and Science, Rochester, Minnesota
Am Fam Physician. 2020 Sep 1;102 (5):291-296. This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions. Author disclosure: No relevant financial affiliations. Article Sections
Abstract
Classification and Epidemiology
Clinical Features
Testing
Management
References
Esophageal motility disorders can cause chest pain, heartburn, or dysphagia. They are diagnosed based on specific patterns seen on esophageal manometry, ranging from the complete absence of contractility in patients with achalasia to unusually forceful or disordered contractions in those with hypercontractile motility disorders. Achalasia has objective diagnostic criteria, and effective treatments are available. Timely diagnosis results in better outcomes.

Esophageal Motility Disorders - American Family Physician
<< Previous article
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Sep 1, 2020 Issue
Esophageal Motility Disorders
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COMMENTS
6.00 CME Credits Available
Take
JOHN M. WILKINSON, MD, and MAGNUS HALLAND, MD, Mayo Clinic Alix School of Medicine, Mayo Clinic College of Medicine and Science, Rochester, Minnesota
Am Fam Physician. 2020 Sep 1;102 (5):291-296. This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions. Author disclosure: No relevant financial affiliations. Article Sections
Abstract
Classification and Epidemiology
Clinical Features
Testing
Management
References
Esophageal motility disorders can cause chest pain, heartburn, or dysphagia. They are diagnosed based on specific patterns seen on esophageal manometry, ranging from the complete absence of contractility in patients with achalasia to unusually forceful or disordered contractions in those with hypercontractile motility disorders. Achalasia has objective diagnostic criteria, and effective treatments are available. Timely diagnosis results in better outcomes.

Heartburn and Palpitations (fluttering in chest): Common Related Medical Conditions Heartburn and Palpitations (fluttering in chest)
Heartburn and Palpitations (fluttering in chest) Hyperthyroidism
Hyperparathyroidism can cause fatigue and weakness, increased thirst, impaired thinking, and bone fractures. Obesity
Obesity is having too much body fat, marked by a BMI of 30 or higher. Barrett esophagus
Barrett's esophagus occurs when the lining of the esophagus is damaged, usually by acid reflux. Hyperparathyroidism
Hyperthyroidism causes weight loss, shakiness, tiredness, sensitivity to heat, insomnia, and more. CREST syndrome
CREST syndrome is a rare autoimmune disease that causes tissues to harden throughout the body. Advertisement
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Heartburn and Palpitations (fluttering in chest): Common Related Medical Conditions

Heartburn and Palpitations (fluttering in chest)
Heartburn and Palpitations (fluttering in chest)

Hyperthyroidism
Hyperparathyroidism can cause fatigue and weakness, increased thirst, impaired thinking, and bone fractures. Obesity
Obesity is having too much body fat, marked by a BMI of 30 or higher. Barrett esophagus
Barrett's esophagus occurs when the lining of the esophagus is damaged, usually by acid reflux. Hyperparathyroidism
Hyperthyroidism causes weight loss, shakiness, tiredness, sensitivity to heat, insomnia, and more. CREST syndrome
CREST syndrome is a rare autoimmune disease that causes tissues to harden throughout the body. Advertisement
Learn about WebMD Apps
Find WebMD on: Facebook
Twitter
Pinterest
View Site: Mobile | Desktop
About WebMD
|
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|
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|
Contact Us
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©2005-2015 WebMD, LLC. All rights reserved. WebMD does not provide medical advice, diagnosis or treatment.

Esophageal Motility Disorder - an overview | ScienceDirect Topics Esophageal Motility Disorder
Esophageal Motility Disorder
Esophageal Motility Disorders
Introduction
Mixed Connective Tissue Disease and Undifferentiated Connective Tissue Disease
Gastrointestinal System
Techniques of High-Resolution Esophageal Manometry, Classification and Treatment of Spastic Esophageal Motility Disorders
Conclusions
Stable Angina Pectoris
Esophageal Motility Disorders
High-Resolution Esophageal Manometry
Conclusion
Alimentary System and the Peritoneum, Omentum, Mesentery, and Peritoneal Cavity1
Achalasia.
Motility Disorders of the Esophagus
Nonspecific Esophageal Motility Disorder
Esophageal body motility disorders
Symptoms
The Upper Gastrointestinal Tract
DIFFUSE ESOPHAGEAL SPASM
Inflammatory Disorders of the Esophagus
ACHALASIA
 In addition, reports in the literature describe chronic active hepatitis, biliary cirrhosis, and Budd-Chiari syndrome in patients with MCTD. View chapter Purchase book
Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9781437718935000418
Techniques of High-Resolution Esophageal Manometry, Classification and Treatment of Spastic Esophageal Motility Disorders
Sabine Roman, ... John E. Pandolfino, in Shackelford's Surgery of the Alimentary Tract (Seventh Edition), 2013
Conclusions
Esophageal motility disorders are diagnosed and classified using esophageal manometry, with high-resolution manometry now being the gold standard. The Chicago Classification is an evolving classification scheme based on the consensus of an international working group that periodically meets for updates and clarifications.50 The major recognized disorders are the three subtypes of achalasia, distal esophageal spasm, jackhammer esophagus, absent peristalsis, weak peristalsis, and frequent failed peristalsis. The most common symptoms associated with these conditions are dysphagia and chest pain. Among esophageal disorders, only achalasia has well-established treatments. Further studies utilizing the improved diagnostic accuracy of HRM are required to improve management of patients with spastic disorders. View chapter Purchase book
Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9781437722062000099
Stable Angina Pectoris
Charalambos Vlachopoulos, ... Dimitris Tousoulis, in Coronary Artery Disease, 2018
Esophageal Motility Disorders
Esophageal motility disorders are not uncommon in patients with retrosternal chest pain of unclear cause and should be specifically excluded or confirmed, if possible [10]. In addition to chest pain, the majority of such patients have dysphagia.

Esophageal Motility Disorder - an overview | ScienceDirect Topics

Esophageal Motility Disorder
Esophageal Motility Disorder
Esophageal Motility Disorders
Introduction
Mixed Connective Tissue Disease and Undifferentiated Connective Tissue Disease
Gastrointestinal System
Techniques of High-Resolution Esophageal Manometry, Classification and Treatment of Spastic Esophageal Motility Disorders
Conclusions
Stable Angina Pectoris
Esophageal Motility Disorders
High-Resolution Esophageal Manometry
Conclusion
Alimentary System and the Peritoneum, Omentum, Mesentery, and Peritoneal Cavity1
Achalasia.
Motility Disorders of the Esophagus
Nonspecific Esophageal Motility Disorder
Esophageal body motility disorders
Symptoms
The Upper Gastrointestinal Tract
DIFFUSE ESOPHAGEAL SPASM
Inflammatory Disorders of the Esophagus
ACHALASIA

Iliac crest syndrome: Description, Causes and Risk Factors Iliac crest syndrome
Iliac crest syndrome
Iliac crest syndrome Symptoms:
 Osteoarthritis. Psoriatic arthritis. Rheumatoid arthritis. Septic arthritis. Injuries: Bursitis. Dislocation. Hip fracture. Hip labral tear. Inguinal hernia.

Iliac crest syndrome: Description, Causes and Risk Factors

Iliac crest syndrome
Iliac crest syndrome
Iliac crest syndrome Symptoms:

Osteoarthritis. Psoriatic arthritis. Rheumatoid arthritis. Septic arthritis. Injuries: Bursitis. Dislocation. Hip fracture. Hip labral tear. Inguinal hernia.

Esophageal motility disorder - Wikipedia Esophageal motility disorder
Esophageal motility disorder
Contents
Symptoms
Types
See also
References
External links
 PMID 14171636. ^ Medicine, UW. " Esophageal Motility Disorders - UW Medicine". www.uwmedicine.org. Archived from the original on 2018-09-27. Retrieved 2015-01-10. External links
Classification
D
MeSH: D015154
External resources
eMedicine: article/174783
v
t
e
Diseases of the digestive system
Upper GI tract
Esophagus
Esophagitis
Candidal
Eosinophilic
Herpetiform
Rupture
Boerhaave syndrome
Mallory–Weiss syndrome
UES
Zenker's diverticulum
LES
Barrett's esophagus
Esophageal motility disorder
Nutcracker esophagus
Achalasia
Diffuse esophageal spasm
Gastroesophageal reflux disease (GERD)
Laryngopharyngeal reflux (LPR)
Esophageal stricture
Megaesophagus
Esophageal intramural pseudodiverticulosis
Stomach
Gastritis
Atrophic
Ménétrier's disease
Gastroenteritis
Peptic (gastric) ulcer
Cushing ulcer
Dieulafoy's lesion
Dyspepsia
Pyloric stenosis
Achlorhydria
Gastroparesis
Gastroptosis
Portal hypertensive gastropathy
Gastric antral vascular ectasia
Gastric dumping syndrome
Gastric volvulus
Buried bumper syndrome
Gastrinoma
Zollinger–Ellison syndrome
Lower GI tract
Enteropathy
Small intestine
( Duodenum / Jejunum / Ileum)
Enteritis
Duodenitis
Jejunitis
Ileitis
Peptic (duodenal) ulcer
Curling's ulcer
Malabsorption: Coeliac
Tropical sprue
Blind loop syndrome
Small intestinal bacterial overgrowth
Whipple's
Short bowel syndrome
Steatorrhea
Milroy disease
Bile acid malabsorption
Large intestine
( Appendix / Colon)
Appendicitis
Colitis
Pseudomembranous
Ulcerative
Ischemic
Microscopic
Collagenous
Lymphocytic
Functional colonic disease
IBS
Intestinal pseudoobstruction / Ogilvie syndrome
Megacolon / Toxic megacolon
Diverticulitis / Diverticulosis / SCAD
Large and/or small
Enterocolitis
Necrotizing
Gastroenterocolitis
IBD
Crohn's disease
Vascular:

Esophageal motility disorder - Wikipedia

Esophageal motility disorder
Esophageal motility disorder
Contents
Symptoms
Types
See also
References
External links

PMID 14171636. ^ Medicine, UW. " Esophageal Motility Disorders - UW Medicine". www.uwmedicine.org. Archived from the original on 2018-09-27. Retrieved 2015-01-10. External links
Classification
D
MeSH: D015154
External resources
eMedicine: article/174783
v
t
e
Diseases of the digestive system
Upper GI tract
Esophagus
Esophagitis
Candidal
Eosinophilic
Herpetiform
Rupture
Boerhaave syndrome
Mallory–Weiss syndrome
UES
Zenker's diverticulum
LES
Barrett's esophagus
Esophageal motility disorder
Nutcracker esophagus
Achalasia
Diffuse esophageal spasm
Gastroesophageal reflux disease (GERD)
Laryngopharyngeal reflux (LPR)
Esophageal stricture
Megaesophagus
Esophageal intramural pseudodiverticulosis
Stomach
Gastritis
Atrophic
Ménétrier's disease
Gastroenteritis
Peptic (gastric) ulcer
Cushing ulcer
Dieulafoy's lesion
Dyspepsia
Pyloric stenosis
Achlorhydria
Gastroparesis
Gastroptosis
Portal hypertensive gastropathy
Gastric antral vascular ectasia
Gastric dumping syndrome
Gastric volvulus
Buried bumper syndrome
Gastrinoma
Zollinger–Ellison syndrome
Lower GI tract
Enteropathy
Small intestine
( Duodenum / Jejunum / Ileum)
Enteritis
Duodenitis
Jejunitis
Ileitis
Peptic (duodenal) ulcer
Curling's ulcer
Malabsorption: Coeliac
Tropical sprue
Blind loop syndrome
Small intestinal bacterial overgrowth
Whipple's
Short bowel syndrome
Steatorrhea
Milroy disease
Bile acid malabsorption
Large intestine
( Appendix / Colon)
Appendicitis
Colitis
Pseudomembranous
Ulcerative
Ischemic
Microscopic
Collagenous
Lymphocytic
Functional colonic disease
IBS
Intestinal pseudoobstruction / Ogilvie syndrome
Megacolon / Toxic megacolon
Diverticulitis / Diverticulosis / SCAD
Large and/or small
Enterocolitis
Necrotizing
Gastroenterocolitis
IBD
Crohn's disease
Vascular:

Esophageal Motility Disorder - an overview | ScienceDirect Topics Esophageal Motility Disorder
Esophageal Motility Disorder
Esophageal Motility Disorders
Introduction
Mixed Connective Tissue Disease and Undifferentiated Connective Tissue Disease
Gastrointestinal System
Techniques of High-Resolution Esophageal Manometry, Classification and Treatment of Spastic Esophageal Motility Disorders
Conclusions
Stable Angina Pectoris
Esophageal Motility Disorders
High-Resolution Esophageal Manometry
Conclusion
Alimentary System and the Peritoneum, Omentum, Mesentery, and Peritoneal Cavity1
Achalasia.
Motility Disorders of the Esophagus
Nonspecific Esophageal Motility Disorder
Esophageal body motility disorders
Symptoms
The Upper Gastrointestinal Tract
DIFFUSE ESOPHAGEAL SPASM
Inflammatory Disorders of the Esophagus
ACHALASIA
 Although barium studies may reveal motility problems, esophageal manometry may show diffuse esophageal spasm, increased pressure at the lower esophageal sphincter, and other motility disorders. Provocative pharmacological agents such as metacholine may provoke esophageal pain and manometric signs of spasm. A more complex problem is determining whether part or all of the symptoms in patients with known CAD are due to esophageal disease. Both CAD and esophageal disease are common clinical entities that may coexist. Diagnostic evaluation for an esophageal disorder may be indicated in patients with CAD who have a poor symptomatic response to antianginal therapy in the absence of documentation of severe ischemia or in patients with persistent symptoms despite adequate coronary revascularization. View chapter Purchase book
Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9780128119082000118
High-Resolution Esophageal Manometry
Ezra N. Teitelbaum, Christy M. Dunst, in Shackelford's Surgery of the Alimentary Tract, 2 Volume Set (Eighth Edition), 2019
Conclusion
Esophageal motility disorders are diagnosed and classified using esophageal manometry, with HRM now being the gold standard. The Chicago Classification is an evolving classification scheme based on the consensus of an international working group that periodically meets for updates and clarifications, with v3.0 serving as the most current edition.6 The major recognized disorders are the three subtypes of achalasia, EGJ outflow obstruction, DES, jackhammer esophagus, absent contractility, with IEM and fragmented peristalsis now categorized as minor motility disorders. HRM serves an important role, not only in the diagnosis of these disorders, but also in prognostication and guiding the most appropriate treatment option. In addition, HRM forms an important component in the preoperative evaluation of patients undergoing laparoscopic antireflux surgery and can help to guide the choice of fundoplication in a patient-specific manner.

Esophageal Motility Disorders - American Family Physician Esophageal Motility Disorders
Esophageal Motility Disorders
This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions.
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Classification and Epidemiology
Classification of Esophageal Motility Disorders
ACHALASIA
HYPERCONTRACTILE MOTILITY DISORDERS
FUNCTIONAL ESOPHAGEAL DISORDERS
Clinical Features
Enlarge Print
DYSPHAGIA
CHEST PAIN
Testing
Esophageal Conditions That Cause Pain or Dysphagia
MANAGEMENT OF COMMON CONDITIONS
ESOPHAGOGASTRODUODENOSCOPY
BARIUM ESOPHAGOGRAPHY
HIGH-RESOLUTION ESOPHAGEAL MANOMETRY
Management
LIFESTYLE MODIFICATIONS
MEDICATIONS
ENDOSCOPIC AND SURGICAL THERAPIES
The Authors
References
6.00 CME Credits Available
CME expires 09-01-2021
Editor's Collections
Email Alerts
 diagnosis is difficult and treatments are only minimally effective
Hypercontractile (jackhammer) esophagus
Normal
Abnormally forceful contractions
Relatively rare; diagnosis is difficult and treatments are only minimally effective
Minor disorders of peristalsis†
Fragmented peristalsis
Normal
> 50% fragmented contractions
—
Ineffective esophageal motility
Normal
> 50% ineffective swallows
—
*—The term nutcracker esophagus is no longer used; the manometric pattern in this condition is common in asymptomatic people and is not thought to cause symptoms. †—Food bolus transit is impaired, but clinical significance is unclear; may occur in people without esophageal disorders. Information from references 1 and 4 – 7. TABLE 1. Classification of Esophageal Motility Disorders
Disorder
Lower esophageal sphincter tone
Peristalsis
Comments
Achalasia
Type I (classic)
Fails to relax
100% failed (no contractility)
Responds to laparoscopic Heller myotomy, less so to pneumatic dilation
Type II (with esophageal compression)
Fails to relax
Some pressurization, but no normal peristalsis
All treatments are effective
Type III (spastic)
Fails to relax
No normal peristalsis and spastic contractions distally in more than 20% of swallows
Poor response to treatment
Esophagogastric junction outflow obstruction
Fails to relax
Some preserved
May reflect a physical obstruction at the level of the lower esophageal sphincter rather than early achalasia
Major disorders of peristalsis *
Absent contractility
Normal
Failed
Relatively rare; easily diagnosed but treatments are only minimally effective; common in patients with systemic sclerosis (scleroderma);

diagnosis is difficult and treatments are only minimally effective
Hypercontractile (jackhammer) esophagus
Normal
Abnormally forceful contractions
Relatively rare; diagnosis is difficult and treatments are only minimally effective
Minor disorders of peristalsis†
Fragmented peristalsis
Normal
> 50% fragmented contractions
—
Ineffective esophageal motility
Normal
> 50% ineffective swallows
—
*—The term nutcracker esophagus is no longer used; the manometric pattern in this condition is common in asymptomatic people and is not thought to cause symptoms. †—Food bolus transit is impaired, but clinical significance is unclear; may occur in people without esophageal disorders. Information from references 1 and 4 – 7. TABLE 1. Classification of Esophageal Motility Disorders
Disorder
Lower esophageal sphincter tone
Peristalsis
Comments
Achalasia
Type I (classic)
Fails to relax
100% failed (no contractility)
Responds to laparoscopic Heller myotomy, less so to pneumatic dilation
Type II (with esophageal compression)
Fails to relax
Some pressurization, but no normal peristalsis
All treatments are effective
Type III (spastic)
Fails to relax
No normal peristalsis and spastic contractions distally in more than 20% of swallows
Poor response to treatment
Esophagogastric junction outflow obstruction
Fails to relax
Some preserved
May reflect a physical obstruction at the level of the lower esophageal sphincter rather than early achalasia
Major disorders of peristalsis *
Absent contractility
Normal
Failed
Relatively rare; easily diagnosed but treatments are only minimally effective; common in patients with systemic sclerosis (scleroderma);

Esophageal dysmotility - MediGoo - Health Medical Tests | Information Esophageal dysmotility
Esophageal dysmotility
Esophageal dysmotility: Description, Causes and Risk Factors:
Symptoms:
Diagnosis:
Treatment:
 For food to be transported efficiently and correctly, the muscles of the esophagus must coordinate in a very structured fashion to transport food to the stomach while ensuring that the stomach contents do not escape. An esophageal dysmotility disorder is one in which this process has been disrupted. These types of disorders can prevent food from being delivered to the stomach or cause stomach contents to be regurgitated. These problems can lead to esophageal dysmotility symptoms such as chest pain, pain when swallowing or the feeling of a permanent lump in the throat. Disorders related to the upper esophageal sphincter or cricopharyngeal muscle are usually related to extremely high contraction of this muscle. This leads to difficulty swallowing, and over time can lead to an out-pouching above this sphincter known as a Zenker's diverticulum. Disorders related to the lower esophageal sphincter can be due to either extremely high muscle contraction tone or extremely low contraction tone. If the sphincter tone is too high and does not open with swallowing, patients often experience difficulty passing food. This may be associated with complete loss of peristalsis in the body of the esophagus in a condition known as achalasia. It may also be an isolated disorder that can be associated with an out-pouching of the esophagus above it, known as an epiphrenic diverticulum.

For food to be transported efficiently and correctly, the muscles of the esophagus must coordinate in a very structured fashion to transport food to the stomach while ensuring that the stomach contents do not escape. An esophageal dysmotility disorder is one in which this process has been disrupted. These types of disorders can prevent food from being delivered to the stomach or cause stomach contents to be regurgitated. These problems can lead to esophageal dysmotility symptoms such as chest pain, pain when swallowing or the feeling of a permanent lump in the throat. Disorders related to the upper esophageal sphincter or cricopharyngeal muscle are usually related to extremely high contraction of this muscle. This leads to difficulty swallowing, and over time can lead to an out-pouching above this sphincter known as a Zenker's diverticulum. Disorders related to the lower esophageal sphincter can be due to either extremely high muscle contraction tone or extremely low contraction tone. If the sphincter tone is too high and does not open with swallowing, patients often experience difficulty passing food. This may be associated with complete loss of peristalsis in the body of the esophagus in a condition known as achalasia. It may also be an isolated disorder that can be associated with an out-pouching of the esophagus above it, known as an epiphrenic diverticulum.

Esophageal Atresia and Tracheoesophageal Fistula | Concise Medical Knowledge Esophageal Atresia and Tracheoesophageal Fistula
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Esophageal Atresia and Tracheoesophageal Fistula
Overview
Definitions
Epidemiology
Etiology
Classification of EA and TEF
Clinical Presentation and Diagnosis
Clinical presentation
Prenatal diagnosis
Diagnosis in the infant
Management and Prognosis
Management
Supportive:
Prognosis
Differential Diagnosis
References
 This condition is associated with CHARGE syndrome and is diagnosed by the inability to pass a catheter into the nasopharynx, and by CT scan. Esophageal stenosis: a rare congenital malformation that usually presents with regurgitation, weight loss, dysphagia, and refusal of solid foods. Esophagoscopy will reveal the stenosis. Esophageal achalasia: an esophageal motility disorder that presents with dysphagia, regurgitation, and occasional chest pain. The pathogenesis involves an incomplete relaxation of the lower esophageal sphincter (LES), increased LES tone, and esophageal dysmotility. Manometry and barium swallow are utilized for diagnosis. Congenital diaphragmatic hernia: caused by a failure of the pleuroperitoneal membrane to fuse, resulting in persistent communication between the thorax and the abdomen.

Esophageal Atresia and Tracheoesophageal Fistula | Concise Medical Knowledge

Esophageal Atresia and Tracheoesophageal Fistula
Learn. Apply. Retain.
Your path to achieve medical excellence.
Study for medical school and boards with Lecturio
Esophageal Atresia and Tracheoesophageal Fistula
Overview
Definitions
Epidemiology
Etiology
Classification of EA and TEF
Clinical Presentation and Diagnosis
Clinical presentation
Prenatal diagnosis
Diagnosis in the infant
Management and Prognosis
Management
Supportive:
Prognosis
Differential Diagnosis
References

This condition is associated with CHARGE syndrome and is diagnosed by the inability to pass a catheter into the nasopharynx, and by CT scan. Esophageal stenosis: a rare congenital malformation that usually presents with regurgitation, weight loss, dysphagia, and refusal of solid foods. Esophagoscopy will reveal the stenosis. Esophageal achalasia: an esophageal motility disorder that presents with dysphagia, regurgitation, and occasional chest pain. The pathogenesis involves an incomplete relaxation of the lower esophageal sphincter (LES), increased LES tone, and esophageal dysmotility. Manometry and barium swallow are utilized for diagnosis. Congenital diaphragmatic hernia: caused by a failure of the pleuroperitoneal membrane to fuse, resulting in persistent communication between the thorax and the abdomen.

Clinical disorders of oral, pharyngeal and esophageal motility : GI Motility online
Synopsis
Clinical disorders of oral, pharyngeal and esophageal motility
View article related content
Motor Disorders of the Oral Cavity, Pharynx, and Cervical Esophagus
Motor Disorders of the Thoracic Esophagus and Lower Esophageal Sphincter ( LES)
Achalasia
Diffuse Esophageal Spasm
Hypertensive Peristalsis, Hypercontracting LES, and Hypertensive LES
Inappropriate Transient LES Relaxation
Hypotensive Esophagus
Ineffective Esophageal Clearance
Gastroesophageal Reflux Disease
Heartburn and Esophageal Chest Pain
Article related content
 The most distinguishing feature of dysphagia due to pharyngeal causes is the misdirection of food into the nose or the lungs, resulting in the complaint of nasal regurgitation of food and choking and coughing during swallowing. The oral cavity, pharynx and upper esophagus are often involved together due to the underlying neuromuscular disorders. Painful swallowing or odynophagia occurs in certain inflammatory conditions of the oral, pharyngeal, or esophageal mucosa. Regurgitation of gastric contents into the esophagus suggests incompetence of the normal gastroesophageal antireflux barrier. Heartburn is a typical symptom of esophageal mucosal inflammation due to gastric acid-peptic reflux. Top
of page
Motor Disorders of the Oral Cavity, Pharynx, and Cervical Esophagus
Muscles of the oral cavity, pharynx, and cervical esophagus are of the striated variety. These disorders may manifest as oral stasis of food, inability to initiate a swallow, premature spillage of food into the pharynx, pharyngeal stasis, nasal regurgitation, or laryngeal aspiration. A large number of neuromuscular diseases are associated with dysfunction of the oropharyngeal phase of deglutition. These can be classified by whether the disease affects the central nervous system, such as stroke, cerebral palsy, head injury, amyotrophic lateral sclerosis, multiple sclerosis, and Parkinson's disease; the peripheral nervous system, such as poliomyelitis;

Clinical disorders of oral, pharyngeal and esophageal motility : GI Motility online

Synopsis
Clinical disorders of oral, pharyngeal and esophageal motility
View article related content
Motor Disorders of the Oral Cavity, Pharynx, and Cervical Esophagus
Motor Disorders of the Thoracic Esophagus and Lower Esophageal Sphincter ( LES)
Achalasia
Diffuse Esophageal Spasm
Hypertensive Peristalsis, Hypercontracting LES, and Hypertensive LES
Inappropriate Transient LES Relaxation
Hypotensive Esophagus
Ineffective Esophageal Clearance
Gastroesophageal Reflux Disease
Heartburn and Esophageal Chest Pain
Article related content

The most distinguishing feature of dysphagia due to pharyngeal causes is the misdirection of food into the nose or the lungs, resulting in the complaint of nasal regurgitation of food and choking and coughing during swallowing. The oral cavity, pharynx and upper esophagus are often involved together due to the underlying neuromuscular disorders. Painful swallowing or odynophagia occurs in certain inflammatory conditions of the oral, pharyngeal, or esophageal mucosa. Regurgitation of gastric contents into the esophagus suggests incompetence of the normal gastroesophageal antireflux barrier. Heartburn is a typical symptom of esophageal mucosal inflammation due to gastric acid-peptic reflux. Top
of page
Motor Disorders of the Oral Cavity, Pharynx, and Cervical Esophagus
Muscles of the oral cavity, pharynx, and cervical esophagus are of the striated variety. These disorders may manifest as oral stasis of food, inability to initiate a swallow, premature spillage of food into the pharynx, pharyngeal stasis, nasal regurgitation, or laryngeal aspiration. A large number of neuromuscular diseases are associated with dysfunction of the oropharyngeal phase of deglutition. These can be classified by whether the disease affects the central nervous system, such as stroke, cerebral palsy, head injury, amyotrophic lateral sclerosis, multiple sclerosis, and Parkinson's disease; the peripheral nervous system, such as poliomyelitis;

Iliac crest syndrome: Description, Causes and Risk Factors Iliac crest syndrome
Iliac crest syndrome
Iliac crest syndrome Symptoms:
 Bursitis. Dislocation. Hip fracture. Hip labral tear. Inguinal hernia. Sprains and strains. Pelvis fracture. Tendinitis. Pinched nerves: Herniated disk.

Bursitis. Dislocation. Hip fracture. Hip labral tear. Inguinal hernia. Sprains and strains. Pelvis fracture. Tendinitis. Pinched nerves: Herniated disk.

Esophageal Motility Disorders - American Family Physician Esophageal Motility Disorders
Esophageal Motility Disorders
This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions.
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Classification and Epidemiology
Classification of Esophageal Motility Disorders
ACHALASIA
HYPERCONTRACTILE MOTILITY DISORDERS
FUNCTIONAL ESOPHAGEAL DISORDERS
Clinical Features
Enlarge Print
DYSPHAGIA
CHEST PAIN
Testing
Esophageal Conditions That Cause Pain or Dysphagia
MANAGEMENT OF COMMON CONDITIONS
ESOPHAGOGASTRODUODENOSCOPY
BARIUM ESOPHAGOGRAPHY
HIGH-RESOLUTION ESOPHAGEAL MANOMETRY
Management
LIFESTYLE MODIFICATIONS
MEDICATIONS
ENDOSCOPIC AND SURGICAL THERAPIES
The Authors
References
6.00 CME Credits Available
CME expires 09-01-2021
Editor's Collections
Email Alerts
 6, 25
B
Case series and longitudinal cohort study
Patients with achalasia should undergo definitive therapy when possible. 28
C
Expert opinion and guideline
Invasive procedures are rarely needed for patients with hypercontractile motility disorders. 2
B
Small randomized controlled trial
A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort. SORT: KEY RECOMMENDATIONS FOR PRACTICE
Clinical recommendation
Evidence rating
Comments
Physicians should ensure optimal evaluation and management of common conditions such as gastroesophageal reflux disease and functional esophageal disorders before referring patients for testing for esophageal motility disorders. 1, 4 – 7
C
Consensus guideline and expert opinion
Patients with dysphagia should be asked about opioid use and helped to discontinue or taper the medication. 7
C
Disease-oriented retrospective review
High-resolution manometry is required to confirm the diagnosis of achalasia.

6, 25
B
Case series and longitudinal cohort study
Patients with achalasia should undergo definitive therapy when possible. 28
C
Expert opinion and guideline
Invasive procedures are rarely needed for patients with hypercontractile motility disorders. 2
B
Small randomized controlled trial
A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort. SORT: KEY RECOMMENDATIONS FOR PRACTICE
Clinical recommendation
Evidence rating
Comments
Physicians should ensure optimal evaluation and management of common conditions such as gastroesophageal reflux disease and functional esophageal disorders before referring patients for testing for esophageal motility disorders. 1, 4 – 7
C
Consensus guideline and expert opinion
Patients with dysphagia should be asked about opioid use and helped to discontinue or taper the medication. 7
C
Disease-oriented retrospective review
High-resolution manometry is required to confirm the diagnosis of achalasia.

Esophageal Motility Disorders - American Family Physician Esophageal Motility Disorders
Esophageal Motility Disorders
This clinical content conforms to AAFP criteria for CME. See the CME Quiz Questions.
SORT: KEY RECOMMENDATIONS FOR PRACTICE
Classification and Epidemiology
Classification of Esophageal Motility Disorders
ACHALASIA
HYPERCONTRACTILE MOTILITY DISORDERS
FUNCTIONAL ESOPHAGEAL DISORDERS
Clinical Features
Enlarge Print
DYSPHAGIA
CHEST PAIN
Testing
Esophageal Conditions That Cause Pain or Dysphagia
MANAGEMENT OF COMMON CONDITIONS
ESOPHAGOGASTRODUODENOSCOPY
BARIUM ESOPHAGOGRAPHY
HIGH-RESOLUTION ESOPHAGEAL MANOMETRY
Management
LIFESTYLE MODIFICATIONS
MEDICATIONS
ENDOSCOPIC AND SURGICAL THERAPIES
The Authors
References
6.00 CME Credits Available
CME expires 09-01-2021
Editor's Collections
Email Alerts
 For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort. SORT: KEY RECOMMENDATIONS FOR PRACTICE
Clinical recommendation
Evidence rating
Comments
Physicians should ensure optimal evaluation and management of common conditions such as gastroesophageal reflux disease and functional esophageal disorders before referring patients for testing for esophageal motility disorders. 1, 4 – 7
C
Consensus guideline and expert opinion
Patients with dysphagia should be asked about opioid use and helped to discontinue or taper the medication. 7
C
Disease-oriented retrospective review
High-resolution manometry is required to confirm the diagnosis of achalasia. 17
C
Clinical guideline
Esophageal motility disorders usually respond to lifestyle modifications, although pharmacotherapy may occasionally be needed. 6, 25
B
Case series and longitudinal cohort study
Patients with achalasia should undergo definitive therapy when possible. 28
C
Expert opinion and guideline
Invasive procedures are rarely needed for patients with hypercontractile motility disorders. 2
B
Small randomized controlled trial
A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence;

For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort. SORT: KEY RECOMMENDATIONS FOR PRACTICE
Clinical recommendation
Evidence rating
Comments
Physicians should ensure optimal evaluation and management of common conditions such as gastroesophageal reflux disease and functional esophageal disorders before referring patients for testing for esophageal motility disorders. 1, 4 – 7
C
Consensus guideline and expert opinion
Patients with dysphagia should be asked about opioid use and helped to discontinue or taper the medication. 7
C
Disease-oriented retrospective review
High-resolution manometry is required to confirm the diagnosis of achalasia. 17
C
Clinical guideline
Esophageal motility disorders usually respond to lifestyle modifications, although pharmacotherapy may occasionally be needed. 6, 25
B
Case series and longitudinal cohort study
Patients with achalasia should undergo definitive therapy when possible. 28
C
Expert opinion and guideline
Invasive procedures are rarely needed for patients with hypercontractile motility disorders. 2
B
Small randomized controlled trial
A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence;

Esophageal Motility Disorders: Background, Etiopathophysiology, Epidemiology Esophageal Motility Disorders
Esophageal Motility Disorders
Background
Anatomy
Esophageal peristalsis
Esophageal motility disorders
 The mid esophagus contains a graded transition of striated and smooth muscle types. The muscle is oriented in 2 perpendicular opposing layers: an inner circular layer and an outer longitudinal layer, known collectively as the muscularis propria. The longitudinal muscle is responsible for shortening the esophagus, while the circular muscle forms lumen-occluding ring contractions. Esophageal peristalsis
The coordination of these simultaneously contracting muscle layers produces the motility pattern known as peristalsis. Peristalsis is a sequential, coordinated contraction wave that travels the entire length of the esophagus, propelling intraluminal contents distally to the stomach. The LES relaxes during swallows and stays opened until the peristaltic wave travels through the LES, then contracts and redevelops resting basal tone. Low peristaltic amplitudes normally occur at the transition zone between the striated and smooth muscle portions; however, the peristalsis is uninterrupted. Primary peristalsis is the peristaltic wave triggered by the swallowing center.

The mid esophagus contains a graded transition of striated and smooth muscle types. The muscle is oriented in 2 perpendicular opposing layers: an inner circular layer and an outer longitudinal layer, known collectively as the muscularis propria. The longitudinal muscle is responsible for shortening the esophagus, while the circular muscle forms lumen-occluding ring contractions. Esophageal peristalsis
The coordination of these simultaneously contracting muscle layers produces the motility pattern known as peristalsis. Peristalsis is a sequential, coordinated contraction wave that travels the entire length of the esophagus, propelling intraluminal contents distally to the stomach. The LES relaxes during swallows and stays opened until the peristaltic wave travels through the LES, then contracts and redevelops resting basal tone. Low peristaltic amplitudes normally occur at the transition zone between the striated and smooth muscle portions; however, the peristalsis is uninterrupted. Primary peristalsis is the peristaltic wave triggered by the swallowing center.

Esophageal dysmotility - MediGoo - Health Medical Tests | Information Esophageal dysmotility
Esophageal dysmotility
Esophageal dysmotility: Description, Causes and Risk Factors:
Symptoms:
Diagnosis:
Treatment:
 Esophageal dysmotility - MediGoo - Health Medical Tests | Information
Esophageal dysmotility
Esophageal dysmotility: Description, Causes and Risk Factors: Esophageal dysmotility is medical disorder causing difficulty in swallowing, regurgitation of food and a spasm-type pain which can be brought on by an allergic reaction to certain foods. The most prominent one is dysphagia. The function of the esophagus is to transport food from the mouth to the stomach. For food to be transported efficiently and correctly, the muscles of the esophagus must coordinate in a very structured fashion to transport food to the stomach while ensuring that the stomach contents do not escape. An esophageal dysmotility disorder is one in which this process has been disrupted. These types of disorders can prevent food from being delivered to the stomach or cause stomach contents to be regurgitated. These problems can lead to esophageal dysmotility symptoms such as chest pain, pain when swallowing or the feeling of a permanent lump in the throat. Disorders related to the upper esophageal sphincter or cricopharyngeal muscle are usually related to extremely high contraction of this muscle.

Esophageal dysmotility - MediGoo - Health Medical Tests | Information
Esophageal dysmotility
Esophageal dysmotility: Description, Causes and Risk Factors: Esophageal dysmotility is medical disorder causing difficulty in swallowing, regurgitation of food and a spasm-type pain which can be brought on by an allergic reaction to certain foods. The most prominent one is dysphagia. The function of the esophagus is to transport food from the mouth to the stomach. For food to be transported efficiently and correctly, the muscles of the esophagus must coordinate in a very structured fashion to transport food to the stomach while ensuring that the stomach contents do not escape. An esophageal dysmotility disorder is one in which this process has been disrupted. These types of disorders can prevent food from being delivered to the stomach or cause stomach contents to be regurgitated. These problems can lead to esophageal dysmotility symptoms such as chest pain, pain when swallowing or the feeling of a permanent lump in the throat. Disorders related to the upper esophageal sphincter or cricopharyngeal muscle are usually related to extremely high contraction of this muscle.

Clinical disorders of oral, pharyngeal and esophageal motility : GI Motility online
Synopsis
Clinical disorders of oral, pharyngeal and esophageal motility
View article related content
Motor Disorders of the Oral Cavity, Pharynx, and Cervical Esophagus
Motor Disorders of the Thoracic Esophagus and Lower Esophageal Sphincter ( LES)
Achalasia
Diffuse Esophageal Spasm
Hypertensive Peristalsis, Hypercontracting LES, and Hypertensive LES
Inappropriate Transient LES Relaxation
Hypotensive Esophagus
Ineffective Esophageal Clearance
Gastroesophageal Reflux Disease
Heartburn and Esophageal Chest Pain
Article related content
 Diffuse Esophageal Spasm
Diffuse esophageal spasm ( DES) is characterized by replacement of normal peristaltic contraction by nonperistaltic contractions. Nonperistaltic contractions are not effective in causing normal esophageal transit. It is due to loss of deglutitive inhibition associated with the impairment of inhibitory nerve function that is localized to the esophageal body. The LES relaxation is normal. The impairment is usually mild, particularly in early cases. Some cases of DES may progress to achalasia. The cause of the impairment is not found in many cases (idiopathic), but it is suspected that a large number of disorders, including stress, may cause inhibitory nerve dysfunction. Dysphagia to solids and liquids and chest pain are the usual presenting symptoms. The barium swallow may be normal or show nonpropagated contractions (also called tertiary contractions). In advanced cases the barium swallow may reveal a corkscrew esophagus and pseudodiverticula.

Diffuse Esophageal Spasm
Diffuse esophageal spasm ( DES) is characterized by replacement of normal peristaltic contraction by nonperistaltic contractions. Nonperistaltic contractions are not effective in causing normal esophageal transit. It is due to loss of deglutitive inhibition associated with the impairment of inhibitory nerve function that is localized to the esophageal body. The LES relaxation is normal. The impairment is usually mild, particularly in early cases. Some cases of DES may progress to achalasia. The cause of the impairment is not found in many cases (idiopathic), but it is suspected that a large number of disorders, including stress, may cause inhibitory nerve dysfunction. Dysphagia to solids and liquids and chest pain are the usual presenting symptoms. The barium swallow may be normal or show nonpropagated contractions (also called tertiary contractions). In advanced cases the barium swallow may reveal a corkscrew esophagus and pseudodiverticula.

Update in the Diagnosis and Treatment of Esophageal Motility Disorders - Practical Gastro Update in the Diagnosis and Treatment of Esophageal Motility Disorders
DISPATCHES FROM THE GUILD CONFERENCE, SERIES #20
Update in the Diagnosis and Treatment of Esophageal Motility Disorders
INTRODUCTION
Epidemiology
Pathogenesis
Clinical Presentation
Differential Diagnosis
Testing
Treatment
Medications
Endoscopy
Surgery
Novel Treatments
CONCLUSION
 Per-oral endoscopic myotomy (POEM) represents the newest endoscopic treatment for achalasia and early data suggests efficacy comparable to that of Heller myotomy. John DeWitt MD, FACG, FACP, FASGE, AGAF Professor of Medicine, Director of Endoscopic Ultrasound , Department of Medicine, Division of Gastroenterology & Hepatology, Indiana University Health Medical Center, Indianapolis, IN. INTRODUCTION
The esophagus serves as a conduit for passage of food from the mouth to the stomach. The upper and lower esophageal sphincter, which are located on the proximal and distal ends of the esophagus, regulate passage of food into and out of the esophagus. Under normal circumstances swallowing occurs in a coordinated, sequential fashion using the musculature of the esophageal wall. This process is called peristalsis. The lower esophageal sphincter maintains a baseline tone to prevent gastroesophageal reflux disease. When peristalsis propels food to the lower esophageal sphincter, the muscle relaxes to permit food to pass into the stomach before re-establishing its baseline tone. Esophageal motility disorders (EMDs) are rare disorders of esophageal peristalsis and the lower esophageal sphincter. Although sometimes asymptomatic, they are usually characterized by symptoms of dysphagia, chest pain, regurgitation, and if severe may manifest as weight loss, aspiration pneumonia and malnutrition.

Update in the Diagnosis and Treatment of Esophageal Motility Disorders - Practical Gastro

Update in the Diagnosis and Treatment of Esophageal Motility Disorders
DISPATCHES FROM THE GUILD CONFERENCE, SERIES #20
Update in the Diagnosis and Treatment of Esophageal Motility Disorders
INTRODUCTION
Epidemiology
Pathogenesis
Clinical Presentation
Differential Diagnosis
Testing
Treatment
Medications
Endoscopy
Surgery
Novel Treatments
CONCLUSION

Per-oral endoscopic myotomy (POEM) represents the newest endoscopic treatment for achalasia and early data suggests efficacy comparable to that of Heller myotomy. John DeWitt MD, FACG, FACP, FASGE, AGAF Professor of Medicine, Director of Endoscopic Ultrasound , Department of Medicine, Division of Gastroenterology & Hepatology, Indiana University Health Medical Center, Indianapolis, IN. INTRODUCTION
The esophagus serves as a conduit for passage of food from the mouth to the stomach. The upper and lower esophageal sphincter, which are located on the proximal and distal ends of the esophagus, regulate passage of food into and out of the esophagus. Under normal circumstances swallowing occurs in a coordinated, sequential fashion using the musculature of the esophageal wall. This process is called peristalsis. The lower esophageal sphincter maintains a baseline tone to prevent gastroesophageal reflux disease. When peristalsis propels food to the lower esophageal sphincter, the muscle relaxes to permit food to pass into the stomach before re-establishing its baseline tone. Esophageal motility disorders (EMDs) are rare disorders of esophageal peristalsis and the lower esophageal sphincter. Although sometimes asymptomatic, they are usually characterized by symptoms of dysphagia, chest pain, regurgitation, and if severe may manifest as weight loss, aspiration pneumonia and malnutrition.

Clinical disorders of oral, pharyngeal and esophageal motility : GI Motility online
Synopsis
Clinical disorders of oral, pharyngeal and esophageal motility
View article related content
Motor Disorders of the Oral Cavity, Pharynx, and Cervical Esophagus
Motor Disorders of the Thoracic Esophagus and Lower Esophageal Sphincter ( LES)
Achalasia
Diffuse Esophageal Spasm
Hypertensive Peristalsis, Hypercontracting LES, and Hypertensive LES
Inappropriate Transient LES Relaxation
Hypotensive Esophagus
Ineffective Esophageal Clearance
Gastroesophageal Reflux Disease
Heartburn and Esophageal Chest Pain
Article related content
 neuromuscular transmission, such as myasthenia gravis; and striated muscles, such as muscular dystrophy, polymyositis, and metabolic myopathies including hypo- and hyperthyroidism. Stroke is the most common cause of oral and pharyngeal dysphagia. Patients with suspected oral and pharyngeal dysphagia should undergo a careful neurologic examination looking for signs of underlying neuromuscular disease. Further evaluation requires a barium videofluoroscopy. Otolaryngology evaluation and laryngoscopy may be helpful in ruling out structural abnormalities. Speech-language pathologists with special training in swallowing assessment and therapy are helpful in the evaluation and management of these patients. If the disease is severe enough to cause weight loss or aspiration pneumonia, the patient may require placement of a feeding gastrostomy or jejunostomy. Top
of page
Motor Disorders of the Thoracic Esophagus and Lower Esophageal Sphincter ( LES)
In humans, thoracic and abdominal parts of the esophagus including the LES are composed of smooth muscles and are affected by different diseases from those affecting the cervical esophagus. When used without qualification, the term esophagus implies the thoracic (smooth muscle part) esophagus.

neuromuscular transmission, such as myasthenia gravis; and striated muscles, such as muscular dystrophy, polymyositis, and metabolic myopathies including hypo- and hyperthyroidism. Stroke is the most common cause of oral and pharyngeal dysphagia. Patients with suspected oral and pharyngeal dysphagia should undergo a careful neurologic examination looking for signs of underlying neuromuscular disease. Further evaluation requires a barium videofluoroscopy. Otolaryngology evaluation and laryngoscopy may be helpful in ruling out structural abnormalities. Speech-language pathologists with special training in swallowing assessment and therapy are helpful in the evaluation and management of these patients. If the disease is severe enough to cause weight loss or aspiration pneumonia, the patient may require placement of a feeding gastrostomy or jejunostomy. Top
of page
Motor Disorders of the Thoracic Esophagus and Lower Esophageal Sphincter ( LES)
In humans, thoracic and abdominal parts of the esophagus including the LES are composed of smooth muscles and are affected by different diseases from those affecting the cervical esophagus. When used without qualification, the term esophagus implies the thoracic (smooth muscle part) esophagus.

Esophageal Motility Disorder - an overview | ScienceDirect Topics Esophageal Motility Disorder
Esophageal Motility Disorder
Esophageal Motility Disorders
Introduction
Mixed Connective Tissue Disease and Undifferentiated Connective Tissue Disease
Gastrointestinal System
Techniques of High-Resolution Esophageal Manometry, Classification and Treatment of Spastic Esophageal Motility Disorders
Conclusions
Stable Angina Pectoris
Esophageal Motility Disorders
High-Resolution Esophageal Manometry
Conclusion
Alimentary System and the Peritoneum, Omentum, Mesentery, and Peritoneal Cavity1
Achalasia.
Motility Disorders of the Esophagus
Nonspecific Esophageal Motility Disorder
Esophageal body motility disorders
Symptoms
The Upper Gastrointestinal Tract
DIFFUSE ESOPHAGEAL SPASM
Inflammatory Disorders of the Esophagus
ACHALASIA
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Motility Disorders of the Esophagus
David J. Ott MD, in Textbook of Gastrointestinal Radiology (Third Edition), 2008
Nonspecific Esophageal Motility Disorder
Nonspecific esophageal motility disorder (NEMD) is a “catchall” category used in patients with motility disturbances that are unclassified.5,7,17,18 Often, manometry reveals esophageal motility abnormalities that do not fit the criteria for specific motility disorders such as achalasia. 5,17,18,70,71 Patients with NEMD may have dysphagia or chest pain, but symptoms may be minimal or absent. These patients would now be classified as having hypocontraction abnormalities on manometric examination. 5,17,18
Manometric abnormalities are mainly of the hypocontraction type and include intermittent absence of peristalsis on 20% or more of wet swallows, low-amplitude peristalsis, prolonged duration of peristalsis, repetitive or triple-peaked contractions, or incomplete LES relaxation ( Fig. 22-15 ). 17,18,70 Radiographic findings may reflect these manometric abnormalities. 7–9 Disruption of primary peristalsis and nonperistaltic contractions are typically seen ( Fig. 22-16 ). However, the radiographic examination is often normal in patients with NEMD who have only minor manometric abnormalities.

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URL: https://www.sciencedirect.com/science/article/pii/B9780323357753000072
Motility Disorders of the Esophagus
David J. Ott MD, in Textbook of Gastrointestinal Radiology (Third Edition), 2008
Nonspecific Esophageal Motility Disorder
Nonspecific esophageal motility disorder (NEMD) is a “catchall” category used in patients with motility disturbances that are unclassified.5,7,17,18 Often, manometry reveals esophageal motility abnormalities that do not fit the criteria for specific motility disorders such as achalasia. 5,17,18,70,71 Patients with NEMD may have dysphagia or chest pain, but symptoms may be minimal or absent. These patients would now be classified as having hypocontraction abnormalities on manometric examination. 5,17,18
Manometric abnormalities are mainly of the hypocontraction type and include intermittent absence of peristalsis on 20% or more of wet swallows, low-amplitude peristalsis, prolonged duration of peristalsis, repetitive or triple-peaked contractions, or incomplete LES relaxation ( Fig. 22-15 ). 17,18,70 Radiographic findings may reflect these manometric abnormalities. 7–9 Disruption of primary peristalsis and nonperistaltic contractions are typically seen ( Fig. 22-16 ). However, the radiographic examination is often normal in patients with NEMD who have only minor manometric abnormalities.

Esophageal Motility Disorder - an overview | ScienceDirect Topics Esophageal Motility Disorder
Esophageal Motility Disorder
Esophageal Motility Disorders
Introduction
Mixed Connective Tissue Disease and Undifferentiated Connective Tissue Disease
Gastrointestinal System
Techniques of High-Resolution Esophageal Manometry, Classification and Treatment of Spastic Esophageal Motility Disorders
Conclusions
Stable Angina Pectoris
Esophageal Motility Disorders
High-Resolution Esophageal Manometry
Conclusion
Alimentary System and the Peritoneum, Omentum, Mesentery, and Peritoneal Cavity1
Achalasia.
Motility Disorders of the Esophagus
Nonspecific Esophageal Motility Disorder
Esophageal body motility disorders
Symptoms
The Upper Gastrointestinal Tract
DIFFUSE ESOPHAGEAL SPASM
Inflammatory Disorders of the Esophagus
ACHALASIA
 Among esophageal disorders, only achalasia has well-established treatments. Further studies utilizing the improved diagnostic accuracy of HRM are required to improve management of patients with spastic disorders. View chapter Purchase book
Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9781437722062000099
Stable Angina Pectoris
Charalambos Vlachopoulos, ... Dimitris Tousoulis, in Coronary Artery Disease, 2018
Esophageal Motility Disorders
Esophageal motility disorders are not uncommon in patients with retrosternal chest pain of unclear cause and should be specifically excluded or confirmed, if possible [10]. In addition to chest pain, the majority of such patients have dysphagia. Although barium studies may reveal motility problems, esophageal manometry may show diffuse esophageal spasm, increased pressure at the lower esophageal sphincter, and other motility disorders. Provocative pharmacological agents such as metacholine may provoke esophageal pain and manometric signs of spasm. A more complex problem is determining whether part or all of the symptoms in patients with known CAD are due to esophageal disease. Both CAD and esophageal disease are common clinical entities that may coexist. Diagnostic evaluation for an esophageal disorder may be indicated in patients with CAD who have a poor symptomatic response to antianginal therapy in the absence of documentation of severe ischemia or in patients with persistent symptoms despite adequate coronary revascularization.

Among esophageal disorders, only achalasia has well-established treatments. Further studies utilizing the improved diagnostic accuracy of HRM are required to improve management of patients with spastic disorders. View chapter Purchase book
Read full chapter
URL: https://www.sciencedirect.com/science/article/pii/B9781437722062000099
Stable Angina Pectoris
Charalambos Vlachopoulos, ... Dimitris Tousoulis, in Coronary Artery Disease, 2018
Esophageal Motility Disorders
Esophageal motility disorders are not uncommon in patients with retrosternal chest pain of unclear cause and should be specifically excluded or confirmed, if possible [10]. In addition to chest pain, the majority of such patients have dysphagia. Although barium studies may reveal motility problems, esophageal manometry may show diffuse esophageal spasm, increased pressure at the lower esophageal sphincter, and other motility disorders. Provocative pharmacological agents such as metacholine may provoke esophageal pain and manometric signs of spasm. A more complex problem is determining whether part or all of the symptoms in patients with known CAD are due to esophageal disease. Both CAD and esophageal disease are common clinical entities that may coexist. Diagnostic evaluation for an esophageal disorder may be indicated in patients with CAD who have a poor symptomatic response to antianginal therapy in the absence of documentation of severe ischemia or in patients with persistent symptoms despite adequate coronary revascularization.

Update in the Diagnosis and Treatment of Esophageal Motility Disorders - Practical Gastro Update in the Diagnosis and Treatment of Esophageal Motility Disorders
DISPATCHES FROM THE GUILD CONFERENCE, SERIES #20
Update in the Diagnosis and Treatment of Esophageal Motility Disorders
INTRODUCTION
Epidemiology
Pathogenesis
Clinical Presentation
Differential Diagnosis
Testing
Treatment
Medications
Endoscopy
Surgery
Novel Treatments
CONCLUSION
 This is in contrast to chest pain from angina which is often related to exercise and exertion and is a long lasting, crescendo, dull or heavy chest pain that may radiate to the jaw or left arm. Patients with esophageal motility disorders are often incorrectly diagnosed with GERD and placed on anti-secretory therapy with H2 receptor antagonists or proton pump inhibitors. These medications usually provide no benefit for the reported symptoms which may be the first clue that reflux of gastric acid is not a contributing factor to the patient’s illness. Patients with a hypertensive lower esophageal sphincter (i.e. achalasia) experience regurgitation rather than GERD and a careful history can usually distinguish between the two symptoms. Regurgitation is the effortless return of liquid or poorly digested food from the esophagus proximally higher into the upper esophagus or mouth. The contents do not have gastric acid, therefore there is usually no reported or burning sensation. GERD, on the other hand requires a loose or intermittently relaxed lower esophageal sphincter. The passage of gastric contents into the esophagus usually is accompanied by a burning sensation in the chest or mouth and is usually well controlled with the addition of H2 blockers or PPIs. Dysphagia and weight loss are common symptoms of achalasia but also primary esophageal or gastro-esophageal junction malignancy. Gastroesophageal junction malignancy can cause rapid weight loss and dysphagia and is termed pseudo-achalasia.

This is in contrast to chest pain from angina which is often related to exercise and exertion and is a long lasting, crescendo, dull or heavy chest pain that may radiate to the jaw or left arm. Patients with esophageal motility disorders are often incorrectly diagnosed with GERD and placed on anti-secretory therapy with H2 receptor antagonists or proton pump inhibitors. These medications usually provide no benefit for the reported symptoms which may be the first clue that reflux of gastric acid is not a contributing factor to the patient’s illness. Patients with a hypertensive lower esophageal sphincter (i.e. achalasia) experience regurgitation rather than GERD and a careful history can usually distinguish between the two symptoms. Regurgitation is the effortless return of liquid or poorly digested food from the esophagus proximally higher into the upper esophagus or mouth. The contents do not have gastric acid, therefore there is usually no reported or burning sensation. GERD, on the other hand requires a loose or intermittently relaxed lower esophageal sphincter. The passage of gastric contents into the esophagus usually is accompanied by a burning sensation in the chest or mouth and is usually well controlled with the addition of H2 blockers or PPIs. Dysphagia and weight loss are common symptoms of achalasia but also primary esophageal or gastro-esophageal junction malignancy. Gastroesophageal junction malignancy can cause rapid weight loss and dysphagia and is termed pseudo-achalasia.

Esophageal dysphagia - Wikipedia Esophageal dysphagia
Esophageal dysphagia
Contents
Signs and symptoms
Causes
Differential diagnosis
Main article: esophageal web
Main article: achalasia
Rare causes of esophageal dysphagia not mentioned above
Diagnostic tools
Treatment
References
External links
 17942
External resources
MedlinePlus: 003115
eMedicine: pmr/194
v
t
e
Signs and symptoms relating to the human digestive system or abdomen
Gastrointestinal
tract
Nausea
Vomiting
Heartburn
Aerophagia
Pagophagia
Dysphagia
oropharyngeal
esophageal
Odynophagia
Bad breath
Xerostomia
Hypersalivation
Burping
Wet burp
Goodsall's rule
Chilaiditi syndrome
Dance's sign
Aaron's sign
Arapov's sign
Markle sign
McBurney's point
Sherren's triangle
Radiologic signs: Hampton's line
Klemm's sign
Accessory
liver: Councilman body
Mallory body
biliary: Boas' sign
Courvoisier's law
Charcot's cholangitis triad / Reynolds' pentad
cholecystitis ( Murphy's sign
Lépine's sign
Mirizzi's syndrome)
Nardi test
Defecation
Flatulence
Fecal incontinence
Encopresis
Fecal occult blood
Rectal tenesmus
Constipation
Obstructed def

Esophageal dysphagia - Wikipedia

Esophageal dysphagia
Esophageal dysphagia
Contents
Signs and symptoms
Causes
Differential diagnosis
Main article: esophageal web
Main article: achalasia
Rare causes of esophageal dysphagia not mentioned above
Diagnostic tools
Treatment
References
External links

17942
External resources
MedlinePlus: 003115
eMedicine: pmr/194
v
t
e
Signs and symptoms relating to the human digestive system or abdomen
Gastrointestinal
tract
Nausea
Vomiting
Heartburn
Aerophagia
Pagophagia
Dysphagia
oropharyngeal
esophageal
Odynophagia
Bad breath
Xerostomia
Hypersalivation
Burping
Wet burp
Goodsall's rule
Chilaiditi syndrome
Dance's sign
Aaron's sign
Arapov's sign
Markle sign
McBurney's point
Sherren's triangle
Radiologic signs: Hampton's line
Klemm's sign
Accessory
liver: Councilman body
Mallory body
biliary: Boas' sign
Courvoisier's law
Charcot's cholangitis triad / Reynolds' pentad
cholecystitis ( Murphy's sign
Lépine's sign
Mirizzi's syndrome)
Nardi test
Defecation
Flatulence
Fecal incontinence
Encopresis
Fecal occult blood
Rectal tenesmus
Constipation
Obstructed def

The Chicago Classification of esophageal motility disorders, v3.0 The Chicago Classification of esophageal motility disorders, v3.0
The Chicago Classification of esophageal motility disorders, v3.0
Authors
Affiliation
Abstract
Publication types
MeSH terms
 i) disorders of esophagogastric junction (EGJ) outflow (achalasia subtypes I-III and EGJ outflow obstruction), (ii) major disorders of peristalsis (absent contractility, distal esophageal spasm, hypercontractile esophagus), and (iii) minor disorders of peristalsis characterized by impaired bolus transit. EGJ morphology, characterized by the degree of overlap between the lower esophageal sphincter and the crural diaphragm and baseline EGJ contractility are also part of CC v3.0. Compared to the previous CC version, the key metrics of interpretation, the integrated relaxation pressure (IRP), the distal contractile integral (DCI), and the distal latency (DL) remain unchanged, albeit with much more emphasis on DCI for defining both hypo- and hypercontractility. New in CC v3.0 are: ( i) the evaluation of the EGJ at rest defined in terms of morphology and contractility, (ii) 'fragmented' contractions (large breaks in the 20-mmHg isobaric contour), (iii) ineffective esophageal motility (IEM), and (iv) several minor adjustments in nomenclature and defining criteria. Absent in CC v3.0 are contractile front velocity and small breaks in the 20-mmHg isobaric contour as defining characteristics. Conclusions & inferences: Chicago Classification v3.0 is an updated analysis scheme for clinical esophageal HRM recordings developed by the International HRM Working Group. Keywords: achalasia;

The Chicago Classification of esophageal motility disorders, v3.0

The Chicago Classification of esophageal motility disorders, v3.0
The Chicago Classification of esophageal motility disorders, v3.0
Authors
Affiliation
Abstract
Publication types
MeSH terms

i) disorders of esophagogastric junction (EGJ) outflow (achalasia subtypes I-III and EGJ outflow obstruction), (ii) major disorders of peristalsis (absent contractility, distal esophageal spasm, hypercontractile esophagus), and (iii) minor disorders of peristalsis characterized by impaired bolus transit. EGJ morphology, characterized by the degree of overlap between the lower esophageal sphincter and the crural diaphragm and baseline EGJ contractility are also part of CC v3.0. Compared to the previous CC version, the key metrics of interpretation, the integrated relaxation pressure (IRP), the distal contractile integral (DCI), and the distal latency (DL) remain unchanged, albeit with much more emphasis on DCI for defining both hypo- and hypercontractility. New in CC v3.0 are: ( i) the evaluation of the EGJ at rest defined in terms of morphology and contractility, (ii) 'fragmented' contractions (large breaks in the 20-mmHg isobaric contour), (iii) ineffective esophageal motility (IEM), and (iv) several minor adjustments in nomenclature and defining criteria. Absent in CC v3.0 are contractile front velocity and small breaks in the 20-mmHg isobaric contour as defining characteristics. Conclusions & inferences: Chicago Classification v3.0 is an updated analysis scheme for clinical esophageal HRM recordings developed by the International HRM Working Group. Keywords: achalasia;

Disorders of Swallowing
Oral Stage General Disorders
Pharyngeal Stage General Disorders
Neruomuscular and Anatomic Disorders of Swallowing
Inability to lateralize material with  tongue.
Reduced buccal tension
Reduced tongue coordination to form  bolus (after mastication)
Reduced oral sensation
Reduced  tongue coordination to hold  bolus ( c5 )  (for liquids and paste materials).
Reduced tongue elevation
Reduced anterior to posterior tongue  movement
Swallow apraxia (Disorganized anterior to  posterior tongue movement. Repeated tongue pumping)
Scarred tongue contour
Delayed  pharyngeal swallow ( c6 )
Absent pharyngeal swallow
Reduced  pharyngeal contraction (c2)  /tongue  base movement (c9)
Reduced  laryngeal elevation (c7)
Unilateral (c10)  or bilateral pharyngeal paralysis. Reduced tongue base movement.
Cricopharyngeal  dysfunction/Reduced laryngeal  elevation ( c1)
Reduced esophageal peristalsis or other  esophageal disorder
Reduced esophageal peristalsis or other  esophageal disorder
Esophageal diverticulum
Partial or total obstruction in  esophagus
 Residual gradually works its way  toward the airway. Dry swallows to clear residue
Delayed response
Pt 22 (CVA, Cricopharyngeal  Dysfunction)
Cricopharyngeal  dysfunction
Food does not penetrate upper  esophageal sphincter into esophagus
Aspiration after swallow because food  collected in pyriform sinuses is sucked into airway when  pt inhales after swallow. Pt 23 (CVA, Cricopharyngeal  Dysfunction)
Oral and pharyngeal swallow  normal
Residue in pyriform  sinuses
Repeated dry swallows, pt drives  residue into esophagus. Head turned to left (damaged side)  clears right pyriform sinus. Reduced esophageal peristalsis or other  esophageal disorder
Patient Description
Coughing, choking
Material catching at bottom of  throat
Clinical Symptoms
Coughingm choking after the  swallow. Gargly voice quality
Excessive secretions
Radiographic Symptoms
Aspiration after swallow
Collection of material in pyriform  sinuses
Prominant pharyngoesophageal  segment
Reduced esophageal peristalsis or other  esophageal disorder
Patient Description
Coughing, choking
Material catching at bottom of  throat
Clinical Symptoms
Coughingm choking after the  swallow. Gargly voice quality
Excessive secretions
Radiographic Symptoms
Aspiration after swallow
Collection of material in pyriform  sinuses
Prominant pharyngoesophageal  segment
Esophageal diverticulum
Patient Description
Coughing, choking after the  swallow
Regurgitation of food
Clinical Symptoms
Regurgitation of food
Coughing, choking after  swallow
Radiographic Symptoms
Collection of material in side pocket in  the pharynx or esophagus. Partial or total obstruction in  esophagus
Patient Description
Coughing, choking after the  swallow
Regurgitation of food
Clinical Symptoms
Regurgitation of food
Coughing, choking after  swallow
Radiographic Symptoms
Collection of material in side pocket in  the pharynx or esophagus
Aspiration after the swallow from  esophageal "overflow"
Tracheoesophageal fistula
Patient Description
Coughing, choking after the  swallow
Clinical Symptoms
Coughing, choking after  swallow
Radiographic Symptoms
Material leaks through skin
Video Sample
Pt 24 (Head Injury, TE Fistula)
Expectorates barium up airway  tracheoesophageal fistula
Pharyngocutaneous fistula
Patient Description
Material leaks out hole
Clinical Symptoms
Material leaks out hole onto  skin
Radiographic Symptoms
Material leaks through skin

Disorders of Swallowing

Oral Stage General Disorders
Pharyngeal Stage General Disorders
Neruomuscular and Anatomic Disorders of Swallowing
Inability to lateralize material with  tongue.
Reduced buccal tension
Reduced tongue coordination to form  bolus (after mastication)
Reduced oral sensation
Reduced  tongue coordination to hold  bolus ( c5 )  (for liquids and paste materials).
Reduced tongue elevation
Reduced anterior to posterior tongue  movement
Swallow apraxia (Disorganized anterior to  posterior tongue movement. Repeated tongue pumping)
Scarred tongue contour
Delayed  pharyngeal swallow ( c6 )
Absent pharyngeal swallow
Reduced  pharyngeal contraction (c2)  /tongue  base movement (c9)
Reduced  laryngeal elevation (c7)
Unilateral (c10)  or bilateral pharyngeal paralysis. Reduced tongue base movement.
Cricopharyngeal  dysfunction/Reduced laryngeal  elevation ( c1)
Reduced esophageal peristalsis or other  esophageal disorder
Reduced esophageal peristalsis or other  esophageal disorder
Esophageal diverticulum
Partial or total obstruction in  esophagus

Clinical disorders of oral, pharyngeal and esophageal motility : GI Motility online
Synopsis
Clinical disorders of oral, pharyngeal and esophageal motility
View article related content
Motor Disorders of the Oral Cavity, Pharynx, and Cervical Esophagus
Motor Disorders of the Thoracic Esophagus and Lower Esophageal Sphincter ( LES)
Achalasia
Diffuse Esophageal Spasm
Hypertensive Peristalsis, Hypercontracting LES, and Hypertensive LES
Inappropriate Transient LES Relaxation
Hypotensive Esophagus
Ineffective Esophageal Clearance
Gastroesophageal Reflux Disease
Heartburn and Esophageal Chest Pain
Article related content
 In advanced cases nocturnal regurgitation may lead pulmonary aspiration. Weight loss also occurs in advanced cases. Many patients also complain of chest pain, and heartburn-like symptoms may occur. Chest pain may be due to esophageal distention or excessive muscle contraction. Heartburn may be due to lactic acid formed by fermentation of stagnant food in the esophagus, esophageal distention, or esophageal muscle contraction. Gastroesophageal reflux does not occur in the presence of achalasia. Diagnosis of achalasia is often suspected by clinical symptoms. The chest x-ray may reveal a widened mediastinum and air-fluid level in the esophagus due retained food, fluid, and air. The barium swallow shows a dilated esophagus with a fluid level and characteristic bird-beak-like narrowing of the gastroesophageal junction. Administration of a smooth muscle relaxant such as sublingual nitroglycerin causes relaxation of the LES and may help distinguish achalasia from pseudoachalasia due to mechanical causes.

In advanced cases nocturnal regurgitation may lead pulmonary aspiration. Weight loss also occurs in advanced cases. Many patients also complain of chest pain, and heartburn-like symptoms may occur. Chest pain may be due to esophageal distention or excessive muscle contraction. Heartburn may be due to lactic acid formed by fermentation of stagnant food in the esophagus, esophageal distention, or esophageal muscle contraction. Gastroesophageal reflux does not occur in the presence of achalasia. Diagnosis of achalasia is often suspected by clinical symptoms. The chest x-ray may reveal a widened mediastinum and air-fluid level in the esophagus due retained food, fluid, and air. The barium swallow shows a dilated esophagus with a fluid level and characteristic bird-beak-like narrowing of the gastroesophageal junction. Administration of a smooth muscle relaxant such as sublingual nitroglycerin causes relaxation of the LES and may help distinguish achalasia from pseudoachalasia due to mechanical causes.

Esophageal Atresia and Tracheoesophageal Fistula | Concise Medical Knowledge Esophageal Atresia and Tracheoesophageal Fistula
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Esophageal Atresia and Tracheoesophageal Fistula
Overview
Definitions
Epidemiology
Etiology
Classification of EA and TEF
Clinical Presentation and Diagnosis
Clinical presentation
Prenatal diagnosis
Diagnosis in the infant
Management and Prognosis
Management
Supportive:
Prognosis
Differential Diagnosis
References
 Dysphagia
GERD
Respiratory issues (cough, wheezing, recurrent infections)
Barrett’s esophagus: 4 times greater risk than the general population
Esophageal cancer: 50 times greater risk than the general population
Differential Diagnosis
Choanal atresia: a congenital anomaly in which the nasal passage is blocked due to failure of recanalization of the nasal fossae during fetal development. The newborn presents with cyanosis that subsides when stimulated and when they cry or open the mouth. This condition is associated with CHARGE syndrome and is diagnosed by the inability to pass a catheter into the nasopharynx, and by CT scan. Esophageal stenosis: a rare congenital malformation that usually presents with regurgitation, weight loss, dysphagia, and refusal of solid foods. Esophagoscopy will reveal the stenosis. Esophageal achalasia:

Dysphagia
GERD
Respiratory issues (cough, wheezing, recurrent infections)
Barrett’s esophagus: 4 times greater risk than the general population
Esophageal cancer: 50 times greater risk than the general population
Differential Diagnosis
Choanal atresia: a congenital anomaly in which the nasal passage is blocked due to failure of recanalization of the nasal fossae during fetal development. The newborn presents with cyanosis that subsides when stimulated and when they cry or open the mouth. This condition is associated with CHARGE syndrome and is diagnosed by the inability to pass a catheter into the nasopharynx, and by CT scan. Esophageal stenosis: a rare congenital malformation that usually presents with regurgitation, weight loss, dysphagia, and refusal of solid foods. Esophagoscopy will reveal the stenosis. Esophageal achalasia:

K22.70 - ICD-10 Code for Barrett's esophagus without dysplasia - Billable ICD-10-CM Code
K22.70

ICD-10-CM Code K22.70
Coding structure:
K22 Other diseases of esophagus
K22.0 Achalasia of cardia
K22.1 Ulcer of esophagus
K22.2 Esophageal obstruction
K22.3 Perforation of esophagus
K22.4 Dyskinesia of esophagus
K22.5 Diverticulum of esophagus, acquired
K22.6 Gastro-esophageal laceration-hemorrhage syndrome
K22.7 Barrett's esophagus
K22.8 Other specified diseases of esophagus
K22.9 Disease of esophagus, unspecified
 Corkscrew esophagus
Diffuse esophageal spasm
Spasm of esophagus
K22.5 Diverticulum of esophagus, acquired
Inclusion term (s): Esophageal pouch, acquired
K22.6 Gastro-esophageal laceration-hemorrhage syndrome
Inclusion term (s): Mallory-Weiss syndrome
K22.7 Barrett's esophagus
Inclusion term (s): Barrett's disease
Barrett's syndrome
K22.70 Barrett's esophagus without dysplasia
Inclusion term (s): Barrett's esophagus NOS
K22.71 Barrett's esophagus with dysplasia
K22.710 Barrett's esophagus with low grade dysplasia
K22.711 Barrett's esophagus with high grade dysplasia
K22.719 Barrett's esophagus with dysplasia, unspecified
K22.8 Other specified diseases of esophagus
Inclusion term (s): Hemorrhage of esophagus NOS
K22.9 Disease of esophagus, unspecified
Abbreviations used here: NEC Not elsewhere classifiable
This abbreviation in the Tabular List represents “other specified”. When a specific code is not available for a condition, the Tabular List includes an NEC entry under a code to identify the code as the “other specified” code. NOS Not otherwise specified
This abbreviation is the equivalent of unspecified. This note further define, or give examples of, the content of the code or category.

K22.70 - ICD-10 Code for Barrett's esophagus without dysplasia - Billable

ICD-10-CM Code
K22.70

ICD-10-CM Code K22.70
Coding structure:
K22 Other diseases of esophagus
K22.0 Achalasia of cardia
K22.1 Ulcer of esophagus
K22.2 Esophageal obstruction
K22.3 Perforation of esophagus
K22.4 Dyskinesia of esophagus
K22.5 Diverticulum of esophagus, acquired
K22.6 Gastro-esophageal laceration-hemorrhage syndrome
K22.7 Barrett's esophagus
K22.8 Other specified diseases of esophagus
K22.9 Disease of esophagus, unspecified

Corkscrew esophagus
Diffuse esophageal spasm
Spasm of esophagus
K22.5 Diverticulum of esophagus, acquired
Inclusion term (s): Esophageal pouch, acquired
K22.6 Gastro-esophageal laceration-hemorrhage syndrome
Inclusion term (s): Mallory-Weiss syndrome
K22.7 Barrett's esophagus
Inclusion term (s): Barrett's disease
Barrett's syndrome
K22.70 Barrett's esophagus without dysplasia
Inclusion term (s): Barrett's esophagus NOS
K22.71 Barrett's esophagus with dysplasia
K22.710 Barrett's esophagus with low grade dysplasia
K22.711 Barrett's esophagus with high grade dysplasia
K22.719 Barrett's esophagus with dysplasia, unspecified
K22.8 Other specified diseases of esophagus
Inclusion term (s): Hemorrhage of esophagus NOS
K22.9 Disease of esophagus, unspecified
Abbreviations used here: NEC Not elsewhere classifiable
This abbreviation in the Tabular List represents “other specified”. When a specific code is not available for a condition, the Tabular List includes an NEC entry under a code to identify the code as the “other specified” code. NOS Not otherwise specified
This abbreviation is the equivalent of unspecified. This note further define, or give examples of, the content of the code or category.

The Chicago Classification of esophageal motility disorders, v3.0 - Kahrilas - 2015 - Neurogastroenterology & Motility - Wiley Online Library The Chicago Classification of esophageal motility disorders, v3.0
Neurogastroenterology & Motility
The Chicago Classification of esophageal motility disorders, v3.0
Abstract
Background
Methods
Key Results
Conclusions & Inferences
Abbreviations
Key Messages
Introduction
Interpreting the HRM Study
Simplifying metrics and technology‐specific adjustments to normative values
Metrics pertinent to EGJ morphology and tone
EGJ morphology
EGJ tone
Conclusions of the HRM Working Group
Simplifying the criteria for disorders (and abnormalities) of peristalsis
Contraction vigor
Contraction pattern
Intrabolus pressure pattern
Summary
The Chicago Classification v3.0
Achalasia and EGJ outflow obstruction
Update in Chicago classification v3.0
Major disorders of peristalsis
Update in Chicago classification v3.0
Minor disorders of peristalsis
Update in Chicago classification v3.0
Next Steps
Conclusion
Acknowledgments
Funding
Conflicts of Interest
Author Contribution
Supporting Information
References
Citing Literature
 Conclusions & Inferences
Chicago Classification v3.0 is an updated analysis scheme for clinical esophageal HRM recordings developed by the International HRM Working Group. Abbreviations
CC
Chicago Classification
CD
crural diaphragm
CDP
contractile deceleration point
CFV
contractile front velocity
DCI
distal contractile integral
DES
distal esophageal spasm
DL
distal latency
EGJ‐CI
EGJ contractile integral
EGJ
esophagogastric junction
GERD
gastroesophageal reflux disease
IEM
ineffective esophageal motility
IRP
integrated relaxation pressure
LES
lower esophageal sphincter
UES
upper esophageal sphincter
Key Messages
The Chicago Classification (CC) categorizes esophageal motility disorders utilizing high‐resolution manometry (HRM) imaged with pressure topography plots. This update, CC v3.0, was developed by the International HRM Working Group through an international consensus process. CC v3.0 utilizes a hierarchical approach, sequentially prioritizing: ( i) disorders of esophagogastric junction (EGJ) outflow, (ii) other major disorders of peristalsis, and (iii) minor disorders of peristalsis. Disorders of EGJ outflow obstruction are characterized by a median integrated relaxation pressure above the limit of normal. These disorders are divided into achalasia subtypes (I, II, and III) and EGJ outflow obstruction. Major motility disorders (never found in control subjects) apart from those characterized by EGJ outflow obstruction are absent contractility, distal esophageal spasm and jackhammer esophagus. Minor motility disorders, characterized by impaired esophageal bolus transit, are ineffective esophageal motility and fragmented peristalsis. Introduction
The Chicago Classification (CC) categorizes esophageal motility disorders in high‐resolution manometry (HRM) depicted with color pressure topography plots, also known as Clouse plots in honor of Ray E. Clouse (1951–2007), their key innovator.

The Chicago Classification of esophageal motility disorders, v3.0 - Kahrilas - 2015 - Neurogastroenterology & Motility - Wiley Online Library

The Chicago Classification of esophageal motility disorders, v3.0
Neurogastroenterology & Motility
The Chicago Classification of esophageal motility disorders, v3.0
Abstract
Background
Methods
Key Results
Conclusions & Inferences
Abbreviations
Key Messages
Introduction
Interpreting the HRM Study
Simplifying metrics and technology‐specific adjustments to normative values
Metrics pertinent to EGJ morphology and tone
EGJ morphology
EGJ tone
Conclusions of the HRM Working Group
Simplifying the criteria for disorders (and abnormalities) of peristalsis
Contraction vigor
Contraction pattern
Intrabolus pressure pattern
Summary
The Chicago Classification v3.0
Achalasia and EGJ outflow obstruction
Update in Chicago classification v3.0
Major disorders of peristalsis
Update in Chicago classification v3.0
Minor disorders of peristalsis
Update in Chicago classification v3.0
Next Steps
Conclusion
Acknowledgments
Funding
Conflicts of Interest
Author Contribution
Supporting Information
References
Citing Literature

Motility Disorders of the Esophagus | Radiology Key Motility Disorders of the Esophagus
Motility Disorders of the Esophagus
Chapter Outline
Normal Esophageal Anatomy
Normal Esophageal Physiology
Radiographic Evaluation
Esophageal Motility Disorders
Primary Motility Disorders
Achalasia
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 Incomplete relaxation of the UES may be manifested on barium studies by a persistent indentation on the posterior aspect of the pharyngoesophageal junction resulting from the contracted cricopharyngeal muscle (see Chapter 15 ). This finding is often associated with other signs of pharyngeal dysmotility, such as aspiration or stasis of barium within the valleculae and piriform sinuses. Motion-recording techniques (using videotape or a digital recording device) facilitate evaluation of the pharynx and UES. The fluoroscopic examination can be used to evaluate esophageal motility, but motion-recording techniques facilitate assessment of the findings. The patient is placed in the prone right anterior oblique (RAO) position and instructed to take single swallows of barium. At least five barium swallows are required for adequate evaluation of esophageal peristalsis and LES relaxation. Single swallows must be observed because a second swallow taken before completion of a primary contraction wave inhibits the propagating wave, so it can erroneously be mistaken for a peristaltic abnormality. In contrast, rapid, repetitive swallowing does not assess primary esophageal peristalsis but distends the esophagus maximally for structural evaluation ( Fig. 18-3 ). Figure 18-3
Manometric representation of normal esophageal peristalsis.

Motility Disorders of the Esophagus | Radiology Key

Motility Disorders of the Esophagus
Motility Disorders of the Esophagus
Chapter Outline
Normal Esophageal Anatomy
Normal Esophageal Physiology
Radiographic Evaluation
Esophageal Motility Disorders
Primary Motility Disorders
Achalasia
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Incomplete relaxation of the UES may be manifested on barium studies by a persistent indentation on the posterior aspect of the pharyngoesophageal junction resulting from the contracted cricopharyngeal muscle (see Chapter 15 ). This finding is often associated with other signs of pharyngeal dysmotility, such as aspiration or stasis of barium within the valleculae and piriform sinuses. Motion-recording techniques (using videotape or a digital recording device) facilitate evaluation of the pharynx and UES. The fluoroscopic examination can be used to evaluate esophageal motility, but motion-recording techniques facilitate assessment of the findings. The patient is placed in the prone right anterior oblique (RAO) position and instructed to take single swallows of barium. At least five barium swallows are required for adequate evaluation of esophageal peristalsis and LES relaxation. Single swallows must be observed because a second swallow taken before completion of a primary contraction wave inhibits the propagating wave, so it can erroneously be mistaken for a peristaltic abnormality. In contrast, rapid, repetitive swallowing does not assess primary esophageal peristalsis but distends the esophagus maximally for structural evaluation ( Fig. 18-3 ). Figure 18-3
Manometric representation of normal esophageal peristalsis.

K22.4 - ICD-10 Code for Dyskinesia of esophagus - Billable ICD-10-CM Code
K22.4

ICD-10-CM Code K22.4
Coding structure:
 Bársony (-Polgár) (-Teschendorf) syndrome (corkscrew esophagus)
Corkscrew esophagus
Curling esophagus
Esophagismus
Esophagospasm
Nutcracker esophagus
MS-DRG - Medicare Severity-Diagnosis Related Group
MDC 06 Diseases & Disorders of the Digestive System
Esophagitis, Gastroenteritis and Miscellaneous Digestive Disorders
DRG 391 - ESOPHAGITIS, GASTROENTERITIS AND MISCELLANEOUS DIGESTIVE DISORDERS WITH MCC
DRG 392 - ESOPHAGITIS, GASTROENTERITIS AND MISCELLANEOUS DIGESTIVE DISORDERS WITHOUT MCC
Coding structure: ICD-10 code K22.4 is based on the following Tabular structure: Chapter 11: Diseases of the digestive system
Section K20-K31: Diseases of esophagus, stomach and duodenum
Category K22: Other diseases of esophagus
K22.4___
Category
Etiology, Anatomic Site,
Severity, Other Vital Details
Extension
Should you use K22.4 or K224 ( with or without decimal point )? DO NOT include the decimal point when electronically filing claims as it may be rejected. Some clearinghouses may remove it for you but to avoid having a rejected claim due to an invalid ICD-10 code, do not include the decimal point when submitting claims electronically. See also: Bársony (-Polgár) (-Teschendorf) syndrome (corkscrew esophagus) K22.4
Corkscrew esophagus K22.4
Curling esophagus K22.4
Disease, diseased see also Syndrome
esophagus K22.9
functional K22.4
Disorder (of) see also Disease
esophagus K22.9
functional K22.4
Dyskinesia G24.9
esophagus K22.4
Dysphagia R13.10
spastica K22.4
Esophagismus K22.4
Esophagospasm K22.4
Nutcracker esophagus K22.4
Spasm, spastic, spasticity (s) R25.2 see also condition
esophagus (diffuse) K22.4
Syndrome see also Disease
Barsony-Polgar K22.4
Barsony-Teschendorf K22.4

K22.4 - ICD-10 Code for Dyskinesia of esophagus - Billable

ICD-10-CM Code
K22.4

ICD-10-CM Code K22.4
Coding structure:

Bársony (-Polgár) (-Teschendorf) syndrome (corkscrew esophagus)
Corkscrew esophagus
Curling esophagus
Esophagismus
Esophagospasm
Nutcracker esophagus
MS-DRG - Medicare Severity-Diagnosis Related Group
MDC 06 Diseases & Disorders of the Digestive System
Esophagitis, Gastroenteritis and Miscellaneous Digestive Disorders
DRG 391 - ESOPHAGITIS, GASTROENTERITIS AND MISCELLANEOUS DIGESTIVE DISORDERS WITH MCC
DRG 392 - ESOPHAGITIS, GASTROENTERITIS AND MISCELLANEOUS DIGESTIVE DISORDERS WITHOUT MCC
Coding structure: ICD-10 code K22.4 is based on the following Tabular structure: Chapter 11: Diseases of the digestive system
Section K20-K31: Diseases of esophagus, stomach and duodenum
Category K22: Other diseases of esophagus
K22.4___
Category
Etiology, Anatomic Site,
Severity, Other Vital Details
Extension
Should you use K22.4 or K224 ( with or without decimal point )? DO NOT include the decimal point when electronically filing claims as it may be rejected. Some clearinghouses may remove it for you but to avoid having a rejected claim due to an invalid ICD-10 code, do not include the decimal point when submitting claims electronically. See also: Bársony (-Polgár) (-Teschendorf) syndrome (corkscrew esophagus) K22.4
Corkscrew esophagus K22.4
Curling esophagus K22.4
Disease, diseased see also Syndrome
esophagus K22.9
functional K22.4
Disorder (of) see also Disease
esophagus K22.9
functional K22.4
Dyskinesia G24.9
esophagus K22.4
Dysphagia R13.10
spastica K22.4
Esophagismus K22.4
Esophagospasm K22.4
Nutcracker esophagus K22.4
Spasm, spastic, spasticity (s) R25.2 see also condition
esophagus (diffuse) K22.4
Syndrome see also Disease
Barsony-Polgar K22.4
Barsony-Teschendorf K22.4

Disorders of the Esophagus in Cats - Cat Owners - Merck Veterinary Manual Disorders of the Esophagus in Cats
Disorders of the Esophagus in Cats
Inflammation of the Esophagus (Esophagitis)
Esophageal Dysmotility
Foreign Objects in the Esophagus
Esophageal Strictures
Esophageal Diverticula
For More Information
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 Signs of esophagitis include regurgitation, drooling, difficulty or repeated swallowing, pain, depression, loss of appetite, and extension of the head and neck. Mild inflammation may produce no visible signs and often requires no treatment. Esophagitis is diagnosed by using a special camera called an endoscope that allows a veterinarian to look inside the esophagus. If your cat displays signs of esophagitis, your veterinarian will likely recommend treatment. If the problem is caused by acid reflux (a cause of heartburn in people), drugs may be prescribed to reduce stomach acid, to decrease reflux, to protect the esophagus, and to relieve pain. Your veterinarian may recommend feeding your pet a diet of soft food, low in fat and fiber, in small, frequent meals. If esophagitis is severe, a feeding tube may need to be surgically placed into the stomach, bypassing the esophagus to allow it to rest. Antibiotics are sometimes prescribed to prevent bacterial infection. Esophageal Dysmotility
Esophageal dysmotility is an abnormal movement of the esophagus. Cats can be born with esophageal dysmotility, or it can develop because of certain neurologic disorders, tumors in the chest, or narrowing of the esophagus (esophageal stricture).

Disorders of the Esophagus in Cats - Cat Owners - Merck Veterinary Manual

Disorders of the Esophagus in Cats
Disorders of the Esophagus in Cats
Inflammation of the Esophagus (Esophagitis)
Esophageal Dysmotility
Foreign Objects in the Esophagus
Esophageal Strictures
Esophageal Diverticula
For More Information
Was This Page Helpful?
Also of Interest
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Signs of esophagitis include regurgitation, drooling, difficulty or repeated swallowing, pain, depression, loss of appetite, and extension of the head and neck. Mild inflammation may produce no visible signs and often requires no treatment. Esophagitis is diagnosed by using a special camera called an endoscope that allows a veterinarian to look inside the esophagus. If your cat displays signs of esophagitis, your veterinarian will likely recommend treatment. If the problem is caused by acid reflux (a cause of heartburn in people), drugs may be prescribed to reduce stomach acid, to decrease reflux, to protect the esophagus, and to relieve pain. Your veterinarian may recommend feeding your pet a diet of soft food, low in fat and fiber, in small, frequent meals. If esophagitis is severe, a feeding tube may need to be surgically placed into the stomach, bypassing the esophagus to allow it to rest. Antibiotics are sometimes prescribed to prevent bacterial infection. Esophageal Dysmotility
Esophageal dysmotility is an abnormal movement of the esophagus. Cats can be born with esophageal dysmotility, or it can develop because of certain neurologic disorders, tumors in the chest, or narrowing of the esophagus (esophageal stricture).

Motility Disorders of the Esophagus | Radiology Key Motility Disorders of the Esophagus
Motility Disorders of the Esophagus
Chapter Outline
Normal Esophageal Anatomy
Normal Esophageal Physiology
Radiographic Evaluation
Esophageal Motility Disorders
Primary Motility Disorders
Achalasia
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 A. Barium study of an 89-year-old man with dysphagia but no chest pain. The esophagus has a corkscrew appearance because of simultaneous nonperistaltic contractions. A nonspecific esophageal motility disorder was diagnosed on manometric examination. B. Another older man without esophageal symptoms has less severe simultaneous nonperistaltic contractions. (From Ott DJ: Radiologic evaluation of esophageal dysphagia. Curr Probl Diagn Radiol 17:1–33, 1988.) Individual variations in esophageal function are primarily related to aging. In young adults, most wet swallows initiate a complete peristaltic sequence, followed invariably by LES relaxation. NPCs are rare in this age group.

A. Barium study of an 89-year-old man with dysphagia but no chest pain. The esophagus has a corkscrew appearance because of simultaneous nonperistaltic contractions. A nonspecific esophageal motility disorder was diagnosed on manometric examination. B. Another older man without esophageal symptoms has less severe simultaneous nonperistaltic contractions. (From Ott DJ: Radiologic evaluation of esophageal dysphagia. Curr Probl Diagn Radiol 17:1–33, 1988.) Individual variations in esophageal function are primarily related to aging. In young adults, most wet swallows initiate a complete peristaltic sequence, followed invariably by LES relaxation. NPCs are rare in this age group.

ICD-10-CM Code K22.4 - Dyskinesia of esophagus ICD-10-CM Code
K22.4

ICD-10-CM Code K22.4
Dyskinesia of esophagus
The ICD code K224 is used to code Diffuse esophageal spasm
Coding Notes for K22.4 Info for medical coders on how to properly use this ICD-10 code
MS-DRG Mapping
Related Concepts SNOMET-CT
ICD-10-CM Alphabetical Index References for 'K22.4 - Dyskinesia of esophagus'
Equivalent ICD-9 Code GENERAL EQUIVALENCE MAPPINGS (GEM)
 Cardiospasm - instead, use code K22.0
MS-DRG Mapping
DRG Group #391-392 - Esophagitis, gastroent and misc digest disorders with MCC. DRG Group #391-392 - Esophagitis, gastroent and misc digest disorders without MCC. Related Concepts SNOMET-CT
Diffuse spasm of esophagus (disorder)
ICD-10-CM Alphabetical Index References for 'K22.4 - Dyskinesia of esophagus'
The ICD-10-CM Alphabetical Index links the below-listed medical terms to the ICD code K22.4. Click on any term below to browse the alphabetical index. Nutcracker esophagus (K22.4)
Esophagismus (K22.4)
Esophagospasm (K22.4)
Corkscrew esophagus (K22.4)
Curling esophagus (K22.4)
Bársony (-Polgár) (-Teschendorf) syndrome (corkscrew esophagus) (K22.4)
Dysphagia +
spastica
Disease, diseased (see: Syndrome ) +
esophagus
Syndrome (see: Disease ) +
Barsony-Polgar
Barsony-Teschendorf
Dyskinesia +
esophagus
Spasm (s), spastic, spasticity (see: condition ) +
esophagus (diffuse)
Disorder (of) (see: Disease ) +
esophagus
Equivalent ICD-9 Code GENERAL EQUIVALENCE MAPPINGS (GEM)
530.5
Dyskinesia of esophagus (exact match)
This is the official exact match mapping between ICD9 and ICD10, as provided by the General Equivalency mapping crosswalk. This means that in all cases where the ICD9 code 530.5 was previously used, K22.4 is the appropriate modern ICD10 code.

ICD-10-CM Code K22.4 - Dyskinesia of esophagus

ICD-10-CM Code
K22.4

ICD-10-CM Code K22.4
Dyskinesia of esophagus
The ICD code K224 is used to code Diffuse esophageal spasm
Coding Notes for K22.4 Info for medical coders on how to properly use this ICD-10 code
MS-DRG Mapping
Related Concepts SNOMET-CT
ICD-10-CM Alphabetical Index References for 'K22.4 - Dyskinesia of esophagus'
Equivalent ICD-9 Code GENERAL EQUIVALENCE MAPPINGS (GEM)

Cardiospasm - instead, use code K22.0
MS-DRG Mapping
DRG Group #391-392 - Esophagitis, gastroent and misc digest disorders with MCC. DRG Group #391-392 - Esophagitis, gastroent and misc digest disorders without MCC. Related Concepts SNOMET-CT
Diffuse spasm of esophagus (disorder)
ICD-10-CM Alphabetical Index References for 'K22.4 - Dyskinesia of esophagus'
The ICD-10-CM Alphabetical Index links the below-listed medical terms to the ICD code K22.4. Click on any term below to browse the alphabetical index. Nutcracker esophagus (K22.4)
Esophagismus (K22.4)
Esophagospasm (K22.4)
Corkscrew esophagus (K22.4)
Curling esophagus (K22.4)
Bársony (-Polgár) (-Teschendorf) syndrome (corkscrew esophagus) (K22.4)
Dysphagia +
spastica
Disease, diseased (see: Syndrome ) +
esophagus
Syndrome (see: Disease ) +
Barsony-Polgar
Barsony-Teschendorf
Dyskinesia +
esophagus
Spasm (s), spastic, spasticity (see: condition ) +
esophagus (diffuse)
Disorder (of) (see: Disease ) +
esophagus
Equivalent ICD-9 Code GENERAL EQUIVALENCE MAPPINGS (GEM)
530.5
Dyskinesia of esophagus (exact match)
This is the official exact match mapping between ICD9 and ICD10, as provided by the General Equivalency mapping crosswalk. This means that in all cases where the ICD9 code 530.5 was previously used, K22.4 is the appropriate modern ICD10 code.

Esophageal Manometry Article Esophageal Manometry
Esophageal Manometry
Introduction
Specimen Collection
Procedures
Indications
Potential Diagnosis
Normal and Critical Findings
Interfering Factors
Complications
Patient Safety and Education
Clinical Significance
 4]
Indications
Patients that present with symptoms of dysphagia, odynophagia, gastroesophageal reflux (GERD), or noncardiac chest pain are typically worked up for esophageal pathology. Patients typically first undergo upper gastrointestinal (GI) swallow study or an EGD to rule out structural lesions or masses. [ 8] Once structural lesions or masses have been excluded, motility disorders of the esophagus are considered. The gold standard in the evaluation of esophageal motility disorders is HRM, which has replaced conventional manometry. Potential Diagnosis
Based on the results of HRM, the patient will be classified into 1 of 4 categories based on the Chicago Classification: (1) Incomplete LES relaxation (achalasia or esophagogastric junction (EGJ) outflow obstruction)
(2) Major motility disorders (distal esophageal spasm, hypercontractile or jackhammer esophagus and absent contractility)
(3) Minor motility disorders (ineffective esophageal motility or fragmented peristalsis)
(4) Normal esophageal motility [3] [9]
Normal and Critical Findings
The first category in the Chicago Classification is incomplete LES relaxation, which includes achalasia and EGJ outflow obstruction. Achalasia is defined as the absence of esophageal peristalsis with incomplete LES relaxation. In the Chicago Classification, the diagnosis of achalasia is based on an elevated median IRP in combination with failed peristalsis or spasm. [ 3] The IRP is a measure of the relaxation of the EGJ, with typical values (less than 15.0 mmHg), although this is catheter specific. [ 10] During normal swallows, the LES at the EGJ relaxes to allow the food bolus into the stomach.

Esophageal Manometry Article

Esophageal Manometry
Esophageal Manometry
Introduction
Specimen Collection
Procedures
Indications
Potential Diagnosis
Normal and Critical Findings
Interfering Factors
Complications
Patient Safety and Education
Clinical Significance

4]
Indications
Patients that present with symptoms of dysphagia, odynophagia, gastroesophageal reflux (GERD), or noncardiac chest pain are typically worked up for esophageal pathology. Patients typically first undergo upper gastrointestinal (GI) swallow study or an EGD to rule out structural lesions or masses. [ 8] Once structural lesions or masses have been excluded, motility disorders of the esophagus are considered. The gold standard in the evaluation of esophageal motility disorders is HRM, which has replaced conventional manometry. Potential Diagnosis
Based on the results of HRM, the patient will be classified into 1 of 4 categories based on the Chicago Classification: (1) Incomplete LES relaxation (achalasia or esophagogastric junction (EGJ) outflow obstruction)
(2) Major motility disorders (distal esophageal spasm, hypercontractile or jackhammer esophagus and absent contractility)
(3) Minor motility disorders (ineffective esophageal motility or fragmented peristalsis)
(4) Normal esophageal motility [3] [9]
Normal and Critical Findings
The first category in the Chicago Classification is incomplete LES relaxation, which includes achalasia and EGJ outflow obstruction. Achalasia is defined as the absence of esophageal peristalsis with incomplete LES relaxation. In the Chicago Classification, the diagnosis of achalasia is based on an elevated median IRP in combination with failed peristalsis or spasm. [ 3] The IRP is a measure of the relaxation of the EGJ, with typical values (less than 15.0 mmHg), although this is catheter specific. [ 10] During normal swallows, the LES at the EGJ relaxes to allow the food bolus into the stomach.

Diffuse Esophageal Spasm - Gastrointestinal Disorders - Merck Manuals Professional Edition Diffuse Esophageal Spasm
Diffuse Esophageal Spasm
(Corkscrew Esophagus)
Symptoms and Signs of Diffuse Esophageal Spasm
Diagnosis of Diffuse Esophageal Spasm
Treatment of Diffuse Esophageal Spasm
Drugs Mentioned In This Article
Also of Interest
Merck and the Merck Manuals
 Diffuse Esophageal Spasm - Gastrointestinal Disorders - Merck Manuals Professional Edition
Diffuse Esophageal Spasm
(Corkscrew Esophagus)
By
Kristle Lee Lynch
, MD, Perelman School of Medicine at The University of Pennsylvania
Last full review/revision Sep 2020| Content last modified Sep 2020
Click here for Patient Education
Symptomatic diffuse esophageal spasm is part of a spectrum of motility disorders characterized variously by nonpropulsive contractions and hyperdynamic contractions, sometimes in conjunction with elevated lower esophageal sphincter pressure. Symptoms are chest pain and sometimes dysphagia. Diagnosis is by barium swallow or manometry. Treatment is difficult but includes nitrates, calcium channel blockers, botulinum toxin injection, surgical or endoscopic myotomy, and antireflux therapy. (See also Overview of Esophageal and Swallowing Disorders .) Abnormalities in esophageal motility correlate poorly with patient symptoms; similar abnormalities may cause different or no symptoms in different people. Furthermore, neither symptoms nor abnormal contractions are definitively associated with histopathologic abnormalities of the esophagus. Symptoms and Signs of Diffuse Esophageal Spasm
Sometimes, diffuse esophageal spasm is asymptomatic and is found incidentally. When symptomatic, diffuse esophageal spasm typically causes substernal chest pain with dysphagia for both liquids and solids.

Diffuse Esophageal Spasm - Gastrointestinal Disorders - Merck Manuals Professional Edition

Diffuse Esophageal Spasm
Diffuse Esophageal Spasm
(Corkscrew Esophagus)
Symptoms and Signs of Diffuse Esophageal Spasm
Diagnosis of Diffuse Esophageal Spasm
Treatment of Diffuse Esophageal Spasm
Drugs Mentioned In This Article
Also of Interest
Merck and the Merck Manuals

Diffuse Esophageal Spasm - Gastrointestinal Disorders - Merck Manuals Professional Edition
Diffuse Esophageal Spasm
(Corkscrew Esophagus)
By
Kristle Lee Lynch
, MD, Perelman School of Medicine at The University of Pennsylvania
Last full review/revision Sep 2020| Content last modified Sep 2020
Click here for Patient Education
Symptomatic diffuse esophageal spasm is part of a spectrum of motility disorders characterized variously by nonpropulsive contractions and hyperdynamic contractions, sometimes in conjunction with elevated lower esophageal sphincter pressure. Symptoms are chest pain and sometimes dysphagia. Diagnosis is by barium swallow or manometry. Treatment is difficult but includes nitrates, calcium channel blockers, botulinum toxin injection, surgical or endoscopic myotomy, and antireflux therapy. (See also Overview of Esophageal and Swallowing Disorders .) Abnormalities in esophageal motility correlate poorly with patient symptoms; similar abnormalities may cause different or no symptoms in different people. Furthermore, neither symptoms nor abnormal contractions are definitively associated with histopathologic abnormalities of the esophagus. Symptoms and Signs of Diffuse Esophageal Spasm
Sometimes, diffuse esophageal spasm is asymptomatic and is found incidentally. When symptomatic, diffuse esophageal spasm typically causes substernal chest pain with dysphagia for both liquids and solids.

K21.00 - ICD-10-CM Gastro-esophageal reflux dis with esophagitis, without bleed ICD-10-CM Code
K21.00

ICD-10-CM Code K21.00
Coding structure:
 K21.00 - ICD-10-CM Gastro-esophageal reflux dis with esophagitis, without bleed
ICD-10-CM Code K21.00
Gastro-esophageal reflux disease with esophagitis, without bleeding
“Gastro-esophageal reflux dis with esophagitis, without bleed” for short Billable Code
K21.00 is a valid billable ICD-10 diagnosis code for Gastro-esophageal reflux disease with esophagitis, without bleeding . It is found in the 2021 version of the ICD-10 Clinical Modification (CM) and can be used in all HIPAA-covered transactions from Oct 01, 2020 - Sep 30, 2021 . ↓ See below for any exclusions, inclusions or special notations
K21.00 also applies to the following: Inclusion term (s): Reflux esophagitis
MS-DRG - Medicare Severity-Diagnosis Related Group
MDC 06 Diseases & Disorders of the Digestive System
Esophagitis, Gastroenteritis and Miscellaneous Digestive Disorders
DRG 391 - ESOPHAGITIS, GASTROENTERITIS AND MISCELLANEOUS DIGESTIVE DISORDERS WITH MCC
DRG 392 - ESOPHAGITIS, GASTROENTERITIS AND MISCELLANEOUS DIGESTIVE DISORDERS WITHOUT MCC
Coding structure: ICD-10 code K21.00 is based on the following Tabular structure: Chapter 11: Diseases of the digestive system
Section K20-K31: Diseases of esophagus, stomach and duodenum
Category K21: Gastro-esophageal reflux disease
↑ Parent code:

K21.00 - ICD-10-CM Gastro-esophageal reflux dis with esophagitis, without bleed

ICD-10-CM Code
K21.00

ICD-10-CM Code K21.00
Coding structure:

K21.00 - ICD-10-CM Gastro-esophageal reflux dis with esophagitis, without bleed
ICD-10-CM Code K21.00
Gastro-esophageal reflux disease with esophagitis, without bleeding
“Gastro-esophageal reflux dis with esophagitis, without bleed” for short Billable Code
K21.00 is a valid billable ICD-10 diagnosis code for Gastro-esophageal reflux disease with esophagitis, without bleeding . It is found in the 2021 version of the ICD-10 Clinical Modification (CM) and can be used in all HIPAA-covered transactions from Oct 01, 2020 - Sep 30, 2021 . ↓ See below for any exclusions, inclusions or special notations
K21.00 also applies to the following: Inclusion term (s): Reflux esophagitis
MS-DRG - Medicare Severity-Diagnosis Related Group
MDC 06 Diseases & Disorders of the Digestive System
Esophagitis, Gastroenteritis and Miscellaneous Digestive Disorders
DRG 391 - ESOPHAGITIS, GASTROENTERITIS AND MISCELLANEOUS DIGESTIVE DISORDERS WITH MCC
DRG 392 - ESOPHAGITIS, GASTROENTERITIS AND MISCELLANEOUS DIGESTIVE DISORDERS WITHOUT MCC
Coding structure: ICD-10 code K21.00 is based on the following Tabular structure: Chapter 11: Diseases of the digestive system
Section K20-K31: Diseases of esophagus, stomach and duodenum
Category K21: Gastro-esophageal reflux disease
↑ Parent code:

PROTONIX®

DESCRIPTION

CLINICAL

PHARMACOLOGY

Pharmacokinetics

AUC

(µg.hr/mL)

Cmax

(µg/mL)

Absorption

Distribution

Metabolism

Elimination

Special

Populations

Geriatric

Pediatric

Gender

Renal

Impairment

Hepatic

Impairment

Drug-Drug

Interactions

Pharmacodynamics

Mechanism

of

Action

Antisecretory

Activity

–––––––––––––––––––Median

pH

on

day

7––––––––––––––

Serum

Gastrin

Effects

Enterochromaffin-Like

(ECL)

Cell

Effects

Other

Effects

Clinical

Studies

Erosive

Esophagitis

(EE)

Associated

with

Gastroesophageal

Reflux

Disease

(GERD)

Erosive

Esophagitis

Healing

Rates

(per

protocol)

––––––––––PROTONIX––––––––––––

Nizatidine

Long-Term

Maintenance

of

Healing

of

Erosive

Esophagitis

Long-Term

Maintenance

of

Healing

of

Erosive

Gastroesophageal

Reflux

Disease

(GERD

Maintenance):

Percentage

of

Patients

Who

Remained

Healed

Number

of

Episodes

of

Heartburn

(mean

SD)

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

INDICATIONS

AND

USAGE

Short-Term

Treatment

of

Erosive

Esophagitis

Associated

With

Gastroesophageal

Reflux

Disease

(GERD)

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

CONTRAINDICATIONS

PRECAUTIONS

General

Information

for

Patients

Drug

Interactions

Carcinogenesis,

Mutagenesis,

Impairment

of

Fertility

Pregnancy

Teratogenic

Effects

Pregnancy

Category

B

Nursing

Mothers

Pediatric

Use

Use

in

Women

Use

in

Elderly

Laboratory

Tests

ADVERSE

REACTIONS

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Short-term

Domestic

Trials

Adverse

Events

in

GERD

Patients

in

Short-term

International

Trials

Most

Frequent

Adverse

Events

Reported

as

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Related

in

Long-term

Domestic

Trials

Postmarketing

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Values

OVERDOSAGE

DOSAGE

AND

ADMINISTRATION

Treatment

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Esophagitis

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

Administration

Options

Applesauce:

PROTONIX

For

Delayed-Release

Oral

Suspension

PROTONIX

For

Delayed-Release

Oral

Suspension

–

Nasogastric

Tube

Administration

HOW

SUPPLIED

Storage

 CLINICAL

PHARMACOLOGY

Pharmacokinetics

PROTONIX

Delayed-Release

Tablets

are

prepared

as

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tablets

so

that

absorption

of

pantoprazole

begins

only

after

the

tablet

leaves

the

stomach. Peak

serum

concentration

(Cmax)

and

area

under

the

serum

concentration

time

curve

(AUC)

increase

in

a

manner

proportional

to

oral

and

intravenous

doses

from

10

mg

to

80

mg. Pantoprazole

does

not

accumulate

and

its

pharmacokinetics

are

unaltered

with

multiple

daily

dosing. Following

oral

or

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the

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pantoprazole

declines

biexponentially

with

a

terminal

elimination

half-life

of

approximately

one

hour. In

extensive

metabolizers

(see

CLINICAL

PHARMACOLOGY,

Pharmacokinetics,

Metabolism)

with

normal

liver

function

receiving

an

oral

dose

of

the

enteric-coated

40

mg

pantoprazole

tablet,

the

peak

concentration

(Cmax)

is

2.5

µg/mL,

the

time

to

reach

the

peak

concentration

(tmax)

is

2.5

h

and

the

total

area

under

the

plasma

concentration

versus

time

curve

(AUC)

is

4.8

µg·hr/mL.

When

pantoprazole

is

given

with

food,

its

tmax

is

highly

variable

and

may

increase

significantly. Following

intravenous

administration

of

pantoprazole

to

extensive

metabolizers,

its

total

clearance

is

7.6-14.0

L/h

and

its

apparent

volume

of

distribution

is

11.0-23.6

L.

PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

has

been

shown

to

be

comparable

to

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

in

suppressing

pentagastrin-stimulated

maximum

acid

output

(MAO)

in

patients

with

gastroesophageal

reflux

disease

(GERD)

and

a

history

of

erosive

esophagitis

(EE)

(see

Clinical

Pharmacology,

Pharmacodynamics). PROTONIX

For

Delayed-Release

Oral

Suspension

is

bioequivalent

when

administered

orally

in

applesauce

or

apple

juice,

or

mixed

in

apple

juice

and

administered

through

a

nasogastric

tube. The

plasma

pharmacokinetic

parameters

from

a

crossover

study

in

healthy

subjects

are

summarized

in

the

table

below. In

this

study,

a

single

oral

40

mg

dose

of

Protonix

For

Delayed-
Release

Oral

Suspension

was

administered

to

healthy

subjects

(N

=

22)

as

granules

sprinkled

over

a

teaspoonful

of

applesauce,

as

granules

mixed

with

apple

juice

and,

mixed

with

apple

juice

followed

by

administration

through

a

nasogastric

tube. Pharmacokinetics

parameters

(mean

±

SD)

of

Pantoprazole

with

Administration

of

Protonix

For

Delayed-Release

Oral

Suspension

Sprinkled

on

Applesauce,

Mixed

with

Apple

Juice,

Mixed

with

Apple

Juice

and

Administered

through

a

Nasogastric

Tube

Pharmacokinetic

Granules

in

Granules

in

apple

Granules

in

Parameters

applesauce

juice

nasogastric

tube

AUC

(µg.hr/mL)

Cmax

(µg/mL)

aTmax

(hr)

2.0

0.69

±

1.97

1.53

±

4.01

a

Median

values

are

reported

for

Tmax

1.49

3.99

4.06

±

1.73

0.45

±

1.91

±

2.2

±

0.70

2.5

2.0

Absorption

The

absorption

of

pantoprazole

is

rapid,

with

a

Cmax

of

2.5

µg/mL

that

occurs

approximately

2.5

hours

after

administration

of

single

or

multiple

40

mg

doses

of

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets.

PROTONIX®

DESCRIPTION

CLINICAL

PHARMACOLOGY

Pharmacokinetics

AUC

(µg.hr/mL)

Cmax

(µg/mL)

Absorption

Distribution

Metabolism

Elimination

Special

Populations

Geriatric

Pediatric

Gender

Renal

Impairment

Hepatic

Impairment

Drug-Drug

Interactions

Pharmacodynamics

Mechanism

of

Action

Antisecretory

Activity

–––––––––––––––––––Median

pH

on

day

7––––––––––––––

Serum

Gastrin

Effects

Enterochromaffin-Like

(ECL)

Cell

Effects

Other

Effects

Clinical

Studies

Erosive

Esophagitis

(EE)

Associated

with

Gastroesophageal

Reflux

Disease

(GERD)

Erosive

Esophagitis

Healing

Rates

(per

protocol)

––––––––––PROTONIX––––––––––––

Nizatidine

Long-Term

Maintenance

of

Healing

of

Erosive

Esophagitis

Long-Term

Maintenance

of

Healing

of

Erosive

Gastroesophageal

Reflux

Disease

(GERD

Maintenance):

Percentage

of

Patients

Who

Remained

Healed

Number

of

Episodes

of

Heartburn

(mean

SD)

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

INDICATIONS

AND

USAGE

Short-Term

Treatment

of

Erosive

Esophagitis

Associated

With

Gastroesophageal

Reflux

Disease

(GERD)

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

CONTRAINDICATIONS

PRECAUTIONS

General

Information

for

Patients

Drug

Interactions

Carcinogenesis,

Mutagenesis,

Impairment

of

Fertility

Pregnancy

Teratogenic

Effects

Pregnancy

Category

B

Nursing

Mothers

Pediatric

Use

Use

in

Women

Use

in

Elderly

Laboratory

Tests

ADVERSE

REACTIONS

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Short-term

Domestic

Trials

Adverse

Events

in

GERD

Patients

in

Short-term

International

Trials

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Long-term

Domestic

Trials

Postmarketing

Reports

Laboratory

Values

OVERDOSAGE

DOSAGE

AND

ADMINISTRATION

Treatment

of

Erosive

Esophagitis

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

Administration

Options

Applesauce:

PROTONIX

For

Delayed-Release

Oral

Suspension

PROTONIX

For

Delayed-Release

Oral

Suspension

–

Nasogastric

Tube

Administration

HOW

SUPPLIED

Storage

 Each

PROTONIX

(pantoprazole

sodium)

Delayed-Release

tablet

contains

45.1

mg

or

22.6

mg

of

pantoprazole

sodium

sesquihydrate

(equivalent

to

40

mg

or

20

mg

pantoprazole,

respectively)

with

the

following

inactive

ingredients: calcium

stearate,

crospovidone,

hypromellose,

iron

oxide,

mannitol,

methacrylic

acid

copolymer,

polysorbate

80,

povidone,

propylene

glycol,

sodium

carbonate,

sodium

lauryl

sulfate,

titanium

dioxide,

and

triethyl

citrate. PROTONIX

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

contains

the

active

ingredient

pantoprazole

sodium

sesquihydrate,

in

the

form

of

enteric-coated

granules

in

unit

dose

packets. Each

unit

dose

packet

contains

enteric-coated

granules

containing

45.1

mg

pantoprazole

sodium

sesquihydrate

(equivalent

to

40

mg

pantoprazole)

with

the

following

inactive

ingredients: crospovidone,

hypromellose,

methacrylic

acid

copolymer,

microcrystalline

cellulose,

polysorbate

80,

povidone,

sodium

carbonate,

sodium

lauryl

sulfate,

talc,

titanium

dioxide,

triethyl

citrate,

and

yellow

ferric

oxide. CLINICAL

PHARMACOLOGY

Pharmacokinetics

PROTONIX

Delayed-Release

Tablets

are

prepared

as

enteric-coated

tablets

so

that

absorption

of

pantoprazole

begins

only

after

the

tablet

leaves

the

stomach. Peak

serum

concentration

(Cmax)

and

area

under

the

serum

concentration

time

curve

(AUC)

increase

in

a

manner

proportional

to

oral

and

intravenous

doses

from

10

mg

to

80

mg. Pantoprazole

does

not

accumulate

and

its

pharmacokinetics

are

unaltered

with

multiple

daily

dosing. Following

oral

or

intravenous

administration,

the

serum

concentration

of

pantoprazole

declines

biexponentially

with

a

terminal

elimination

half-life

of

approximately

one

hour. In

extensive

metabolizers

(see

CLINICAL

PHARMACOLOGY,

Pharmacokinetics,

Metabolism)

with

normal

liver

function

receiving

an

oral

dose

of

the

enteric-coated

40

mg

pantoprazole

tablet,

the

peak

concentration

(Cmax)

is

2.5

µg/mL,

the

time

to

reach

the

peak

concentration

(tmax)

is

2.5

h

and

the

total

area

under

the

plasma

concentration

versus

time

curve

(AUC)

is

4.8

µg·hr/mL.

When

pantoprazole

is

given

with

food,

its

tmax

is

highly

variable

and

may

increase

significantly.

PROTONIX®

DESCRIPTION

CLINICAL

PHARMACOLOGY

Pharmacokinetics

AUC

(µg.hr/mL)

Cmax

(µg/mL)

Absorption

Distribution

Metabolism

Elimination

Special

Populations

Geriatric

Pediatric

Gender

Renal

Impairment

Hepatic

Impairment

Drug-Drug

Interactions

Pharmacodynamics

Mechanism

of

Action

Antisecretory

Activity

–––––––––––––––––––Median

pH

on

day

7––––––––––––––

Serum

Gastrin

Effects

Enterochromaffin-Like

(ECL)

Cell

Effects

Other

Effects

Clinical

Studies

Erosive

Esophagitis

(EE)

Associated

with

Gastroesophageal

Reflux

Disease

(GERD)

Erosive

Esophagitis

Healing

Rates

(per

protocol)

––––––––––PROTONIX––––––––––––

Nizatidine

Long-Term

Maintenance

of

Healing

of

Erosive

Esophagitis

Long-Term

Maintenance

of

Healing

of

Erosive

Gastroesophageal

Reflux

Disease

(GERD

Maintenance):

Percentage

of

Patients

Who

Remained

Healed

Number

of

Episodes

of

Heartburn

(mean

SD)

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

INDICATIONS

AND

USAGE

Short-Term

Treatment

of

Erosive

Esophagitis

Associated

With

Gastroesophageal

Reflux

Disease

(GERD)

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

CONTRAINDICATIONS

PRECAUTIONS

General

Information

for

Patients

Drug

Interactions

Carcinogenesis,

Mutagenesis,

Impairment

of

Fertility

Pregnancy

Teratogenic

Effects

Pregnancy

Category

B

Nursing

Mothers

Pediatric

Use

Use

in

Women

Use

in

Elderly

Laboratory

Tests

ADVERSE

REACTIONS

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Short-term

Domestic

Trials

Adverse

Events

in

GERD

Patients

in

Short-term

International

Trials

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Long-term

Domestic

Trials

Postmarketing

Reports

Laboratory

Values

OVERDOSAGE

DOSAGE

AND

ADMINISTRATION

Treatment

of

Erosive

Esophagitis

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

Administration

Options

Applesauce:

PROTONIX

For

Delayed-Release

Oral

Suspension

PROTONIX

For

Delayed-Release

Oral

Suspension

–

Nasogastric

Tube

Administration

HOW

SUPPLIED

Storage

 Pantoprazole

sodium

sesquihydrate

is

freely

soluble

in

water,

very

slightly

soluble

in

phosphate

buffer

at

pH

7.4,

and

practically

insoluble

in

n-hexane. The

stability

of

the

compound

in

aqueous

solution

is

pH-dependent. The

rate

of

degradation

increases

with

decreasing

pH.

At

ambient

temperature,

the

degradation

half-life

is

approximately

2.8

hours

at

pH

5.0

and

approximately

220

hours

at

pH

7.8. PROTONIX

(pantoprazole

sodium)

is

supplied

as

a

delayed-release

tablet

for

oral

administration,

available

in

2

strengths

(40

mg

and

20

mg); and

as

delayed-release

granules

for

oral

administration,

available

in

the

40

mg

strength. Each

PROTONIX

(pantoprazole

sodium)

Delayed-Release

tablet

contains

45.1

mg

or

22.6

mg

of

pantoprazole

sodium

sesquihydrate

(equivalent

to

40

mg

or

20

mg

pantoprazole,

respectively)

with

the

following

inactive

ingredients: calcium

stearate,

crospovidone,

hypromellose,

iron

oxide,

mannitol,

methacrylic

acid

copolymer,

polysorbate

80,

povidone,

propylene

glycol,

sodium

carbonate,

sodium

lauryl

sulfate,

titanium

dioxide,

and

triethyl

citrate. PROTONIX

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

contains

the

active

ingredient

pantoprazole

sodium

sesquihydrate,

in

the

form

of

enteric-coated

granules

in

unit

dose

packets. Each

unit

dose

packet

contains

enteric-coated

granules

containing

45.1

mg

pantoprazole

sodium

sesquihydrate

(equivalent

to

40

mg

pantoprazole)

with

the

following

inactive

ingredients: crospovidone,

hypromellose,

methacrylic

acid

copolymer,

microcrystalline

cellulose,

polysorbate

80,

povidone,

sodium

carbonate,

sodium

lauryl

sulfate,

talc,

titanium

dioxide,

triethyl

citrate,

and

yellow

ferric

oxide.

Pantoprazole

sodium

sesquihydrate

is

freely

soluble

in

water,

very

slightly

soluble

in

phosphate

buffer

at

pH

7.4,

and

practically

insoluble

in

n-hexane. The

stability

of

the

compound

in

aqueous

solution

is

pH-dependent. The

rate

of

degradation

increases

with

decreasing

pH.

At

ambient

temperature,

the

degradation

half-life

is

approximately

2.8

hours

at

pH

5.0

and

approximately

220

hours

at

pH

7.8. PROTONIX

(pantoprazole

sodium)

is

supplied

as

a

delayed-release

tablet

for

oral

administration,

available

in

2

strengths

(40

mg

and

20

mg); and

as

delayed-release

granules

for

oral

administration,

available

in

the

40

mg

strength. Each

PROTONIX

(pantoprazole

sodium)

Delayed-Release

tablet

contains

45.1

mg

or

22.6

mg

of

pantoprazole

sodium

sesquihydrate

(equivalent

to

40

mg

or

20

mg

pantoprazole,

respectively)

with

the

following

inactive

ingredients: calcium

stearate,

crospovidone,

hypromellose,

iron

oxide,

mannitol,

methacrylic

acid

copolymer,

polysorbate

80,

povidone,

propylene

glycol,

sodium

carbonate,

sodium

lauryl

sulfate,

titanium

dioxide,

and

triethyl

citrate. PROTONIX

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

contains

the

active

ingredient

pantoprazole

sodium

sesquihydrate,

in

the

form

of

enteric-coated

granules

in

unit

dose

packets. Each

unit

dose

packet

contains

enteric-coated

granules

containing

45.1

mg

pantoprazole

sodium

sesquihydrate

(equivalent

to

40

mg

pantoprazole)

with

the

following

inactive

ingredients: crospovidone,

hypromellose,

methacrylic

acid

copolymer,

microcrystalline

cellulose,

polysorbate

80,

povidone,

sodium

carbonate,

sodium

lauryl

sulfate,

talc,

titanium

dioxide,

triethyl

citrate,

and

yellow

ferric

oxide.

The Radiology Assistant : Esophagus I: anatomy, rings, inflammation Esophagus I: anatomy, rings, inflammation
Esophagus I: anatomy, rings, inflammation
Terrence C. Demos, MD, Harold V. Posniak, MD, Wayde Nagamine, MD and Mary Olson, MD
Department of Radiology of the Loyola University Medical Center, USA
Anatomy and Function
Hypopharynx
Upper esophageal sphincter
Lower esophageal sphincter
Gastroesophageal reflux
Esophageal peristalsis
Diffuse esophageal spasm
Nutcracker esophagus
Achalasia
Lower esophageal rings
Webs and Diverticula
Esophageal web
Diverticula
Zenker's diverticulum
Hiatus hernia
Inflammation and Infection
Reflux esophagitis
Barrett's esophagus with reticular mucosa and web-like (arrow) stricture
Barrett's esophagus
Infectious esophagitis
Pseudodiverticulosis
Glycogen acanthosis
 Bulbous distention of the distal esophagus is called the vestibule and corresponds to the manometrically-defined lower esophageal sphincter. This distention is best demonstrated by breath holding in inspiration or a Valsalva maneuver. Do not mistake this for a hiatal hernia. Spontaneous reflux extends to level of aortic arch. Gastroesophageal reflux
Spontaneous gastroesophageal reflux has been demonstrated in up to 1/3 of patients with reflux esophagitis. Various maneuvers during the examination have been used to increase sensitivity, but these are generally discredited as not being physiologic. In addition many asymptomatic patients have spontaneous reflux so that reflux during an esophagram is not sensitive or specific for relating symptoms to reflux. Esophageal peristalsis
Normal: Primary contraction: Propels bolus through the esophagus
Secondary contraction:

The Radiology Assistant : Esophagus I: anatomy, rings, inflammation

Esophagus I: anatomy, rings, inflammation
Esophagus I: anatomy, rings, inflammation
Terrence C. Demos, MD, Harold V. Posniak, MD, Wayde Nagamine, MD and Mary Olson, MD
Department of Radiology of the Loyola University Medical Center, USA
Anatomy and Function
Hypopharynx
Upper esophageal sphincter
Lower esophageal sphincter
Gastroesophageal reflux
Esophageal peristalsis
Diffuse esophageal spasm
Nutcracker esophagus
Achalasia
Lower esophageal rings
Webs and Diverticula
Esophageal web
Diverticula
Zenker's diverticulum
Hiatus hernia
Inflammation and Infection
Reflux esophagitis
Barrett's esophagus with reticular mucosa and web-like (arrow) stricture
Barrett's esophagus
Infectious esophagitis
Pseudodiverticulosis
Glycogen acanthosis

Bulbous distention of the distal esophagus is called the vestibule and corresponds to the manometrically-defined lower esophageal sphincter. This distention is best demonstrated by breath holding in inspiration or a Valsalva maneuver. Do not mistake this for a hiatal hernia. Spontaneous reflux extends to level of aortic arch. Gastroesophageal reflux
Spontaneous gastroesophageal reflux has been demonstrated in up to 1/3 of patients with reflux esophagitis. Various maneuvers during the examination have been used to increase sensitivity, but these are generally discredited as not being physiologic. In addition many asymptomatic patients have spontaneous reflux so that reflux during an esophagram is not sensitive or specific for relating symptoms to reflux. Esophageal peristalsis
Normal: Primary contraction: Propels bolus through the esophagus
Secondary contraction:

PROTONIX®

DESCRIPTION

CLINICAL

PHARMACOLOGY

Pharmacokinetics

AUC

(µg.hr/mL)

Cmax

(µg/mL)

Absorption

Distribution

Metabolism

Elimination

Special

Populations

Geriatric

Pediatric

Gender

Renal

Impairment

Hepatic

Impairment

Drug-Drug

Interactions

Pharmacodynamics

Mechanism

of

Action

Antisecretory

Activity

–––––––––––––––––––Median

pH

on

day

7––––––––––––––

Serum

Gastrin

Effects

Enterochromaffin-Like

(ECL)

Cell

Effects

Other

Effects

Clinical

Studies

Erosive

Esophagitis

(EE)

Associated

with

Gastroesophageal

Reflux

Disease

(GERD)

Erosive

Esophagitis

Healing

Rates

(per

protocol)

––––––––––PROTONIX––––––––––––

Nizatidine

Long-Term

Maintenance

of

Healing

of

Erosive

Esophagitis

Long-Term

Maintenance

of

Healing

of

Erosive

Gastroesophageal

Reflux

Disease

(GERD

Maintenance):

Percentage

of

Patients

Who

Remained

Healed

Number

of

Episodes

of

Heartburn

(mean

SD)

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

INDICATIONS

AND

USAGE

Short-Term

Treatment

of

Erosive

Esophagitis

Associated

With

Gastroesophageal

Reflux

Disease

(GERD)

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

CONTRAINDICATIONS

PRECAUTIONS

General

Information

for

Patients

Drug

Interactions

Carcinogenesis,

Mutagenesis,

Impairment

of

Fertility

Pregnancy

Teratogenic

Effects

Pregnancy

Category

B

Nursing

Mothers

Pediatric

Use

Use

in

Women

Use

in

Elderly

Laboratory

Tests

ADVERSE

REACTIONS

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Short-term

Domestic

Trials

Adverse

Events

in

GERD

Patients

in

Short-term

International

Trials

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Long-term

Domestic

Trials

Postmarketing

Reports

Laboratory

Values

OVERDOSAGE

DOSAGE

AND

ADMINISTRATION

Treatment

of

Erosive

Esophagitis

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

Administration

Options

Applesauce:

PROTONIX

For

Delayed-Release

Oral

Suspension

PROTONIX

For

Delayed-Release

Oral

Suspension

–

Nasogastric

Tube

Administration

HOW

SUPPLIED

Storage

 PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

Rx

only

DESCRIPTION

The

active

ingredient

in

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

and

PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

is

a

substituted

benzimidazole,

sodium

5-(difluoromethoxy)-2-[[(3,4-dimethoxy-2-pyridinyl)methyl]

sulfinyl]-
1H-benzimidazole

sesquihydrate,

a

compound

that

inhibits

gastric

acid

secretion. Its

empirical

formula

is

C16H14F2N3NaO4S

x

1.5

H2O,

with

a

molecular

weight

of

432.4. The

structural

formula

is: Pantoprazole

sodium

sesquihydrate

is

a

white

to

off-white

crystalline

powder

and

is

racemic. Pantoprazole

has

weakly

basic

and

acidic

properties. Pantoprazole

sodium

sesquihydrate

is

freely

soluble

in

water,

very

slightly

soluble

in

phosphate

buffer

at

pH

7.4,

and

practically

insoluble

in

n-hexane. The

stability

of

the

compound

in

aqueous

solution

is

pH-dependent. The

rate

of

degradation

increases

with

decreasing

pH.

At

ambient

temperature,

the

degradation

half-life

is

approximately

2.8

hours

at

pH

5.0

and

approximately

220

hours

at

pH

7.8. PROTONIX

(pantoprazole

sodium)

is

supplied

as

a

delayed-release

tablet

for

oral

administration,

available

in

2

strengths

(40

mg

and

20

mg); and

as

delayed-release

granules

for

oral

administration,

available

in

the

40

mg

strength.

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

Rx

only

DESCRIPTION

The

active

ingredient

in

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

and

PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

is

a

substituted

benzimidazole,

sodium

5-(difluoromethoxy)-2-[[(3,4-dimethoxy-2-pyridinyl)methyl]

sulfinyl]-
1H-benzimidazole

sesquihydrate,

a

compound

that

inhibits

gastric

acid

secretion. Its

empirical

formula

is

C16H14F2N3NaO4S

x

1.5

H2O,

with

a

molecular

weight

of

432.4. The

structural

formula

is: Pantoprazole

sodium

sesquihydrate

is

a

white

to

off-white

crystalline

powder

and

is

racemic. Pantoprazole

has

weakly

basic

and

acidic

properties. Pantoprazole

sodium

sesquihydrate

is

freely

soluble

in

water,

very

slightly

soluble

in

phosphate

buffer

at

pH

7.4,

and

practically

insoluble

in

n-hexane. The

stability

of

the

compound

in

aqueous

solution

is

pH-dependent. The

rate

of

degradation

increases

with

decreasing

pH.

At

ambient

temperature,

the

degradation

half-life

is

approximately

2.8

hours

at

pH

5.0

and

approximately

220

hours

at

pH

7.8. PROTONIX

(pantoprazole

sodium)

is

supplied

as

a

delayed-release

tablet

for

oral

administration,

available

in

2

strengths

(40

mg

and

20

mg); and

as

delayed-release

granules

for

oral

administration,

available

in

the

40

mg

strength.

PROTONIX®

DESCRIPTION

CLINICAL

PHARMACOLOGY

Pharmacokinetics

AUC

(µg.hr/mL)

Cmax

(µg/mL)

Absorption

Distribution

Metabolism

Elimination

Special

Populations

Geriatric

Pediatric

Gender

Renal

Impairment

Hepatic

Impairment

Drug-Drug

Interactions

Pharmacodynamics

Mechanism

of

Action

Antisecretory

Activity

–––––––––––––––––––Median

pH

on

day

7––––––––––––––

Serum

Gastrin

Effects

Enterochromaffin-Like

(ECL)

Cell

Effects

Other

Effects

Clinical

Studies

Erosive

Esophagitis

(EE)

Associated

with

Gastroesophageal

Reflux

Disease

(GERD)

Erosive

Esophagitis

Healing

Rates

(per

protocol)

––––––––––PROTONIX––––––––––––

Nizatidine

Long-Term

Maintenance

of

Healing

of

Erosive

Esophagitis

Long-Term

Maintenance

of

Healing

of

Erosive

Gastroesophageal

Reflux

Disease

(GERD

Maintenance):

Percentage

of

Patients

Who

Remained

Healed

Number

of

Episodes

of

Heartburn

(mean

SD)

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

INDICATIONS

AND

USAGE

Short-Term

Treatment

of

Erosive

Esophagitis

Associated

With

Gastroesophageal

Reflux

Disease

(GERD)

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

CONTRAINDICATIONS

PRECAUTIONS

General

Information

for

Patients

Drug

Interactions

Carcinogenesis,

Mutagenesis,

Impairment

of

Fertility

Pregnancy

Teratogenic

Effects

Pregnancy

Category

B

Nursing

Mothers

Pediatric

Use

Use

in

Women

Use

in

Elderly

Laboratory

Tests

ADVERSE

REACTIONS

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Short-term

Domestic

Trials

Adverse

Events

in

GERD

Patients

in

Short-term

International

Trials

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Long-term

Domestic

Trials

Postmarketing

Reports

Laboratory

Values

OVERDOSAGE

DOSAGE

AND

ADMINISTRATION

Treatment

of

Erosive

Esophagitis

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

Administration

Options

Applesauce:

PROTONIX

For

Delayed-Release

Oral

Suspension

PROTONIX

For

Delayed-Release

Oral

Suspension

–

Nasogastric

Tube

Administration

HOW

SUPPLIED

Storage

 Following

intravenous

administration

of

pantoprazole

to

extensive

metabolizers,

its

total

clearance

is

7.6-14.0

L/h

and

its

apparent

volume

of

distribution

is

11.0-23.6

L.

PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

has

been

shown

to

be

comparable

to

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

in

suppressing

pentagastrin-stimulated

maximum

acid

output

(MAO)

in

patients

with

gastroesophageal

reflux

disease

(GERD)

and

a

history

of

erosive

esophagitis

(EE)

(see

Clinical

Pharmacology,

Pharmacodynamics). PROTONIX

For

Delayed-Release

Oral

Suspension

is

bioequivalent

when

administered

orally

in

applesauce

or

apple

juice,

or

mixed

in

apple

juice

and

administered

through

a

nasogastric

tube. The

plasma

pharmacokinetic

parameters

from

a

crossover

study

in

healthy

subjects

are

summarized

in

the

table

below. In

this

study,

a

single

oral

40

mg

dose

of

Protonix

For

Delayed-
Release

Oral

Suspension

was

administered

to

healthy

subjects

(N

=

22)

as

granules

sprinkled

over

a

teaspoonful

of

applesauce,

as

granules

mixed

with

apple

juice

and,

mixed

with

apple

juice

followed

by

administration

through

a

nasogastric

tube. Pharmacokinetics

parameters

(mean

±

SD)

of

Pantoprazole

with

Administration

of

Protonix

For

Delayed-Release

Oral

Suspension

Sprinkled

on

Applesauce,

Mixed

with

Apple

Juice,

Mixed

with

Apple

Juice

and

Administered

through

a

Nasogastric

Tube

Pharmacokinetic

Granules

in

Granules

in

apple

Granules

in

Parameters

applesauce

juice

nasogastric

tube

AUC

(µg.hr/mL)

Cmax

(µg/mL)

aTmax

(hr)

2.0

0.69

±

1.97

1.53

±

4.01

a

Median

values

are

reported

for

Tmax

1.49

3.99

4.06

±

1.73

0.45

±

1.91

±

2.2

±

0.70

2.5

2.0

Absorption

The

absorption

of

pantoprazole

is

rapid,

with

a

Cmax

of

2.5

µg/mL

that

occurs

approximately

2.5

hours

after

administration

of

single

or

multiple

40

mg

doses

of

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets. Pantoprazole

is

well

absorbed; it

undergoes

little

first-pass

metabolism

resulting

in

an

absolute

bioavailability

of

approximately

77%. Pantoprazole

absorption

is

not

affected

by

concomitant

administration

of

antacids. Administration

of

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

with

food

may

delay

its

absorption

up

to

2

hours

or

longer; however,

the

Cmax

and

the

extent

of

pantoprazole

absorption

(AUC)

are

not

altered.

Dyskinesia of the esophagus | Competently about health on iLive Dyskinesia of the esophagus
Health
Dyskinesia of the esophagus
Classification of esophagus dyskinesia
Hypermotor disorders of the peristalsis of the thoracic esophagus
Segmental esophagospasm (the "esophagus of the nutcracker")
Diffuse esophagospasm
Nonspecific motor disorders of the esophagus
Hypomotor disorders of the peristalsis of the thoracic esophagus
Cardiospasm
Achalasia cardia
What do need to examine?
How to examine?
What tests are needed?
 Segmental esophagospasm (the "esophagus of the nutcracker")
With this variant of esophageal dyskinesia spasm of limited areas of the esophagus is observed. The main symptoms are: dysphagia - is characterized primarily by the difficulty of the passage of semi-liquid food (sour cream, wiped cottage cheese) and rich in fiber (fresh fruit, vegetables), dysphagia can occur when consuming juices; pain of moderate intensity in the middle and lower third of the sternum without irradiation begin and stop gradually; spasm of restricted areas of the esophagus; spastic contractions of the limited sections of the walls of the esophagus lasting longer than 15 s with an amplitude of 16-18 mm Hg. ( according to the data of the esophagothicography)
Diffuse esophagospasm
Characteristic manifestations of diffuse esophagospasm are: extremely severe pain in the sternum or epigastrium, rapidly spreading upward, as well as irradiating on the front surface of the chest, in the lower jaw, shoulders. The pains occur suddenly, often associated with swallowing, last long (from half an hour to several hours), in some patients may disappear after a sip of water. Pain is caused by prolonged non-peristaltic contractions of the thoracic esophagus;

Dyskinesia of the esophagus | Competently about health on iLive

Dyskinesia of the esophagus
Health
Dyskinesia of the esophagus
Classification of esophagus dyskinesia
Hypermotor disorders of the peristalsis of the thoracic esophagus
Segmental esophagospasm (the "esophagus of the nutcracker")
Diffuse esophagospasm
Nonspecific motor disorders of the esophagus
Hypomotor disorders of the peristalsis of the thoracic esophagus
Cardiospasm
Achalasia cardia
What do need to examine?
How to examine?
What tests are needed?

Segmental esophagospasm (the "esophagus of the nutcracker")
With this variant of esophageal dyskinesia spasm of limited areas of the esophagus is observed. The main symptoms are: dysphagia - is characterized primarily by the difficulty of the passage of semi-liquid food (sour cream, wiped cottage cheese) and rich in fiber (fresh fruit, vegetables), dysphagia can occur when consuming juices; pain of moderate intensity in the middle and lower third of the sternum without irradiation begin and stop gradually; spasm of restricted areas of the esophagus; spastic contractions of the limited sections of the walls of the esophagus lasting longer than 15 s with an amplitude of 16-18 mm Hg. ( according to the data of the esophagothicography)
Diffuse esophagospasm
Characteristic manifestations of diffuse esophagospasm are: extremely severe pain in the sternum or epigastrium, rapidly spreading upward, as well as irradiating on the front surface of the chest, in the lower jaw, shoulders. The pains occur suddenly, often associated with swallowing, last long (from half an hour to several hours), in some patients may disappear after a sip of water. Pain is caused by prolonged non-peristaltic contractions of the thoracic esophagus;

PROTONIX®

DESCRIPTION

CLINICAL

PHARMACOLOGY

Pharmacokinetics

AUC

(µg.hr/mL)

Cmax

(µg/mL)

Absorption

Distribution

Metabolism

Elimination

Special

Populations

Geriatric

Pediatric

Gender

Renal

Impairment

Hepatic

Impairment

Drug-Drug

Interactions

Pharmacodynamics

Mechanism

of

Action

Antisecretory

Activity

–––––––––––––––––––Median

pH

on

day

7––––––––––––––

Serum

Gastrin

Effects

Enterochromaffin-Like

(ECL)

Cell

Effects

Other

Effects

Clinical

Studies

Erosive

Esophagitis

(EE)

Associated

with

Gastroesophageal

Reflux

Disease

(GERD)

Erosive

Esophagitis

Healing

Rates

(per

protocol)

––––––––––PROTONIX––––––––––––

Nizatidine

Long-Term

Maintenance

of

Healing

of

Erosive

Esophagitis

Long-Term

Maintenance

of

Healing

of

Erosive

Gastroesophageal

Reflux

Disease

(GERD

Maintenance):

Percentage

of

Patients

Who

Remained

Healed

Number

of

Episodes

of

Heartburn

(mean

SD)

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

INDICATIONS

AND

USAGE

Short-Term

Treatment

of

Erosive

Esophagitis

Associated

With

Gastroesophageal

Reflux

Disease

(GERD)

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

CONTRAINDICATIONS

PRECAUTIONS

General

Information

for

Patients

Drug

Interactions

Carcinogenesis,

Mutagenesis,

Impairment

of

Fertility

Pregnancy

Teratogenic

Effects

Pregnancy

Category

B

Nursing

Mothers

Pediatric

Use

Use

in

Women

Use

in

Elderly

Laboratory

Tests

ADVERSE

REACTIONS

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Short-term

Domestic

Trials

Adverse

Events

in

GERD

Patients

in

Short-term

International

Trials

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Long-term

Domestic

Trials

Postmarketing

Reports

Laboratory

Values

OVERDOSAGE

DOSAGE

AND

ADMINISTRATION

Treatment

of

Erosive

Esophagitis

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

Administration

Options

Applesauce:

PROTONIX

For

Delayed-Release

Oral

Suspension

PROTONIX

For

Delayed-Release

Oral

Suspension

–

Nasogastric

Tube

Administration

HOW

SUPPLIED

Storage

 Although

these

sub-populations

of

slow

pantoprazole

metabolizers

have

elimination

half-life

values

of

3.5

to

10.0

hours,

they

still

have

minimal

accumulation

(≤

23%)

with

once

daily

dosing. Elimination

After

a

single

oral

or

intravenous

dose

of

14C-labeled

pantoprazole

to

healthy,

normal

metabolizer

volunteers,

approximately

71%

of

the

dose

was

excreted

in

the

urine

with

18%

excreted

in

the

feces

through

biliary

excretion. There

was

no

renal

excretion

of

unchanged

pantoprazole. Special

Populations

Geriatric

Only

slight

to

moderate

increases

in

pantoprazole

AUC

(43%)

and

Cmax

(26%)

were

found

in

elderly

volunteers

(64

to

76

years

of

age)

after

repeated

oral

administration,

compared

with

younger

subjects. No

dosage

adjustment

is

recommended

based

on

age. Pediatric

The

pharmacokinetics

of

pantoprazole

have

not

been

investigated

in

patients

<

18

years

of

age. Gender

There

is

a

modest

increase

in

pantoprazole

AU

Although

these

sub-populations

of

slow

pantoprazole

metabolizers

have

elimination

half-life

values

of

3.5

to

10.0

hours,

they

still

have

minimal

accumulation

(≤

23%)

with

once

daily

dosing. Elimination

After

a

single

oral

or

intravenous

dose

of

14C-labeled

pantoprazole

to

healthy,

normal

metabolizer

volunteers,

approximately

71%

of

the

dose

was

excreted

in

the

urine

with

18%

excreted

in

the

feces

through

biliary

excretion. There

was

no

renal

excretion

of

unchanged

pantoprazole. Special

Populations

Geriatric

Only

slight

to

moderate

increases

in

pantoprazole

AUC

(43%)

and

Cmax

(26%)

were

found

in

elderly

volunteers

(64

to

76

years

of

age)

after

repeated

oral

administration,

compared

with

younger

subjects. No

dosage

adjustment

is

recommended

based

on

age. Pediatric

The

pharmacokinetics

of

pantoprazole

have

not

been

investigated

in

patients

<

18

years

of

age. Gender

There

is

a

modest

increase

in

pantoprazole

AU

PROTONIX®

DESCRIPTION

CLINICAL

PHARMACOLOGY

Pharmacokinetics

AUC

(µg.hr/mL)

Cmax

(µg/mL)

Absorption

Distribution

Metabolism

Elimination

Special

Populations

Geriatric

Pediatric

Gender

Renal

Impairment

Hepatic

Impairment

Drug-Drug

Interactions

Pharmacodynamics

Mechanism

of

Action

Antisecretory

Activity

–––––––––––––––––––Median

pH

on

day

7––––––––––––––

Serum

Gastrin

Effects

Enterochromaffin-Like

(ECL)

Cell

Effects

Other

Effects

Clinical

Studies

Erosive

Esophagitis

(EE)

Associated

with

Gastroesophageal

Reflux

Disease

(GERD)

Erosive

Esophagitis

Healing

Rates

(per

protocol)

––––––––––PROTONIX––––––––––––

Nizatidine

Long-Term

Maintenance

of

Healing

of

Erosive

Esophagitis

Long-Term

Maintenance

of

Healing

of

Erosive

Gastroesophageal

Reflux

Disease

(GERD

Maintenance):

Percentage

of

Patients

Who

Remained

Healed

Number

of

Episodes

of

Heartburn

(mean

SD)

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

INDICATIONS

AND

USAGE

Short-Term

Treatment

of

Erosive

Esophagitis

Associated

With

Gastroesophageal

Reflux

Disease

(GERD)

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

CONTRAINDICATIONS

PRECAUTIONS

General

Information

for

Patients

Drug

Interactions

Carcinogenesis,

Mutagenesis,

Impairment

of

Fertility

Pregnancy

Teratogenic

Effects

Pregnancy

Category

B

Nursing

Mothers

Pediatric

Use

Use

in

Women

Use

in

Elderly

Laboratory

Tests

ADVERSE

REACTIONS

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Short-term

Domestic

Trials

Adverse

Events

in

GERD

Patients

in

Short-term

International

Trials

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Long-term

Domestic

Trials

Postmarketing

Reports

Laboratory

Values

OVERDOSAGE

DOSAGE

AND

ADMINISTRATION

Treatment

of

Erosive

Esophagitis

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

Administration

Options

Applesauce:

PROTONIX

For

Delayed-Release

Oral

Suspension

PROTONIX

For

Delayed-Release

Oral

Suspension

–

Nasogastric

Tube

Administration

HOW

SUPPLIED

Storage

 Pantoprazole

metabolism

is

independent

of

the

route

of

administration

(intravenous

or

oral). The

main

metabolic

pathway

is

demethylation,

by

CYP2C19,

with

subsequent

sulfation; other

metabolic

pathways

include

oxidation

by

CYP3A4. There

is

no

evidence

that

any

of

the

pantoprazole

metabolites

have

significant

pharmacologic

activity. CYP2C19

displays

a

known

genetic

polymorphism

due

to

its

deficiency

in

some

sub-populations

(eg,

3%

of

Caucasians

and

African-Americans

and

17%-23%

of

Asians). Although

these

sub-populations

of

slow

pantoprazole

metabolizers

have

elimination

half-life

values

of

3.5

to

10.0

hours,

they

still

have

minimal

accumulation

(≤

23%)

with

once

daily

dosing. Elimination

After

a

single

oral

or

intravenous

dose

of

14C-labeled

pantoprazole

to

healthy,

normal

metabolizer

volunteers,

approximately

71%

of

the

dose

was

excreted

in

the

urine

with

18%

excreted

in

the

feces

through

biliary

excretion. There

was

no

renal

excretion

of

unchanged

pantoprazole. Special

Populations

Geriatric

Only

slight

to

moderate

increases

in

pantoprazole

AUC

(43%)

and

Cmax

(26%)

were

found

in

elderly

volunteers

(64

to

76

years

of

age)

after

repeated

oral

administration,

compared

with

younger

subjects. No

dosage

adjustment

is

recommended

based

on

age.

Pantoprazole

metabolism

is

independent

of

the

route

of

administration

(intravenous

or

oral). The

main

metabolic

pathway

is

demethylation,

by

CYP2C19,

with

subsequent

sulfation; other

metabolic

pathways

include

oxidation

by

CYP3A4. There

is

no

evidence

that

any

of

the

pantoprazole

metabolites

have

significant

pharmacologic

activity. CYP2C19

displays

a

known

genetic

polymorphism

due

to

its

deficiency

in

some

sub-populations

(eg,

3%

of

Caucasians

and

African-Americans

and

17%-23%

of

Asians). Although

these

sub-populations

of

slow

pantoprazole

metabolizers

have

elimination

half-life

values

of

3.5

to

10.0

hours,

they

still

have

minimal

accumulation

(≤

23%)

with

once

daily

dosing. Elimination

After

a

single

oral

or

intravenous

dose

of

14C-labeled

pantoprazole

to

healthy,

normal

metabolizer

volunteers,

approximately

71%

of

the

dose

was

excreted

in

the

urine

with

18%

excreted

in

the

feces

through

biliary

excretion. There

was

no

renal

excretion

of

unchanged

pantoprazole. Special

Populations

Geriatric

Only

slight

to

moderate

increases

in

pantoprazole

AUC

(43%)

and

Cmax

(26%)

were

found

in

elderly

volunteers

(64

to

76

years

of

age)

after

repeated

oral

administration,

compared

with

younger

subjects. No

dosage

adjustment

is

recommended

based

on

age.

PROTONIX®

DESCRIPTION

CLINICAL

PHARMACOLOGY

Pharmacokinetics

AUC

(µg.hr/mL)

Cmax

(µg/mL)

Absorption

Distribution

Metabolism

Elimination

Special

Populations

Geriatric

Pediatric

Gender

Renal

Impairment

Hepatic

Impairment

Drug-Drug

Interactions

Pharmacodynamics

Mechanism

of

Action

Antisecretory

Activity

–––––––––––––––––––Median

pH

on

day

7––––––––––––––

Serum

Gastrin

Effects

Enterochromaffin-Like

(ECL)

Cell

Effects

Other

Effects

Clinical

Studies

Erosive

Esophagitis

(EE)

Associated

with

Gastroesophageal

Reflux

Disease

(GERD)

Erosive

Esophagitis

Healing

Rates

(per

protocol)

––––––––––PROTONIX––––––––––––

Nizatidine

Long-Term

Maintenance

of

Healing

of

Erosive

Esophagitis

Long-Term

Maintenance

of

Healing

of

Erosive

Gastroesophageal

Reflux

Disease

(GERD

Maintenance):

Percentage

of

Patients

Who

Remained

Healed

Number

of

Episodes

of

Heartburn

(mean

SD)

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

INDICATIONS

AND

USAGE

Short-Term

Treatment

of

Erosive

Esophagitis

Associated

With

Gastroesophageal

Reflux

Disease

(GERD)

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

CONTRAINDICATIONS

PRECAUTIONS

General

Information

for

Patients

Drug

Interactions

Carcinogenesis,

Mutagenesis,

Impairment

of

Fertility

Pregnancy

Teratogenic

Effects

Pregnancy

Category

B

Nursing

Mothers

Pediatric

Use

Use

in

Women

Use

in

Elderly

Laboratory

Tests

ADVERSE

REACTIONS

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Short-term

Domestic

Trials

Adverse

Events

in

GERD

Patients

in

Short-term

International

Trials

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Long-term

Domestic

Trials

Postmarketing

Reports

Laboratory

Values

OVERDOSAGE

DOSAGE

AND

ADMINISTRATION

Treatment

of

Erosive

Esophagitis

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

Administration

Options

Applesauce:

PROTONIX

For

Delayed-Release

Oral

Suspension

PROTONIX

For

Delayed-Release

Oral

Suspension

–

Nasogastric

Tube

Administration

HOW

SUPPLIED

Storage

 Pantoprazole

is

well

absorbed; it

undergoes

little

first-pass

metabolism

resulting

in

an

absolute

bioavailability

of

approximately

77%. Pantoprazole

absorption

is

not

affected

by

concomitant

administration

of

antacids. Administration

of

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

with

food

may

delay

its

absorption

up

to

2

hours

or

longer; however,

the

Cmax

and

the

extent

of

pantoprazole

absorption

(AUC)

are

not

altered. Thus,

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

may

be

taken

without

regard

to

timing

of

meals. PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

should

be

taken

approximately

30

minutes

before

a

meal. Distribution

The

apparent

volume

of

distribution

of

pantoprazole

is

approximately

11.0-23.6

L,

distributing

mainly

in

extracellular

fluid. The

serum

protein

binding

of

pantoprazole

is

about

98%,

primarily

to

albumin. Metabolism

Pantoprazole

is

extensively

metabolized

in

the

liver

through

the

cytochrome

P450

(CYP)

system.

Pantoprazole

is

well

absorbed; it

undergoes

little

first-pass

metabolism

resulting

in

an

absolute

bioavailability

of

approximately

77%. Pantoprazole

absorption

is

not

affected

by

concomitant

administration

of

antacids. Administration

of

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

with

food

may

delay

its

absorption

up

to

2

hours

or

longer; however,

the

Cmax

and

the

extent

of

pantoprazole

absorption

(AUC)

are

not

altered. Thus,

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

may

be

taken

without

regard

to

timing

of

meals. PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

should

be

taken

approximately

30

minutes

before

a

meal. Distribution

The

apparent

volume

of

distribution

of

pantoprazole

is

approximately

11.0-23.6

L,

distributing

mainly

in

extracellular

fluid. The

serum

protein

binding

of

pantoprazole

is

about

98%,

primarily

to

albumin. Metabolism

Pantoprazole

is

extensively

metabolized

in

the

liver

through

the

cytochrome

P450

(CYP)

system.

PROTONIX®

DESCRIPTION

CLINICAL

PHARMACOLOGY

Pharmacokinetics

AUC

(µg.hr/mL)

Cmax

(µg/mL)

Absorption

Distribution

Metabolism

Elimination

Special

Populations

Geriatric

Pediatric

Gender

Renal

Impairment

Hepatic

Impairment

Drug-Drug

Interactions

Pharmacodynamics

Mechanism

of

Action

Antisecretory

Activity

–––––––––––––––––––Median

pH

on

day

7––––––––––––––

Serum

Gastrin

Effects

Enterochromaffin-Like

(ECL)

Cell

Effects

Other

Effects

Clinical

Studies

Erosive

Esophagitis

(EE)

Associated

with

Gastroesophageal

Reflux

Disease

(GERD)

Erosive

Esophagitis

Healing

Rates

(per

protocol)

––––––––––PROTONIX––––––––––––

Nizatidine

Long-Term

Maintenance

of

Healing

of

Erosive

Esophagitis

Long-Term

Maintenance

of

Healing

of

Erosive

Gastroesophageal

Reflux

Disease

(GERD

Maintenance):

Percentage

of

Patients

Who

Remained

Healed

Number

of

Episodes

of

Heartburn

(mean

SD)

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

INDICATIONS

AND

USAGE

Short-Term

Treatment

of

Erosive

Esophagitis

Associated

With

Gastroesophageal

Reflux

Disease

(GERD)

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

CONTRAINDICATIONS

PRECAUTIONS

General

Information

for

Patients

Drug

Interactions

Carcinogenesis,

Mutagenesis,

Impairment

of

Fertility

Pregnancy

Teratogenic

Effects

Pregnancy

Category

B

Nursing

Mothers

Pediatric

Use

Use

in

Women

Use

in

Elderly

Laboratory

Tests

ADVERSE

REACTIONS

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Short-term

Domestic

Trials

Adverse

Events

in

GERD

Patients

in

Short-term

International

Trials

Most

Frequent

Adverse

Events

Reported

as

Drug

Related

in

Long-term

Domestic

Trials

Postmarketing

Reports

Laboratory

Values

OVERDOSAGE

DOSAGE

AND

ADMINISTRATION

Treatment

of

Erosive

Esophagitis

Maintenance

of

Healing

of

Erosive

Esophagitis

Pathological

Hypersecretory

Conditions

Including

Zollinger-Ellison

Syndrome

Administration

Options

Applesauce:

PROTONIX

For

Delayed-Release

Oral

Suspension

PROTONIX

For

Delayed-Release

Oral

Suspension

–

Nasogastric

Tube

Administration

HOW

SUPPLIED

Storage

 Thus,

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

may

be

taken

without

regard

to

timing

of

meals. PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

should

be

taken

approximately

30

minutes

before

a

meal. Distribution

The

apparent

volume

of

distribution

of

pantoprazole

is

approximately

11.0-23.6

L,

distributing

mainly

in

extracellular

fluid. The

serum

protein

binding

of

pantoprazole

is

about

98%,

primarily

to

albumin. Metabolism

Pantoprazole

is

extensively

metabolized

in

the

liver

through

the

cytochrome

P450

(CYP)

system. Pantoprazole

metabolism

is

independent

of

the

route

of

administration

(intravenous

or

oral). The

main

metabolic

pathway

is

demethylation,

by

CYP2C19,

with

subsequent

sulfation; other

metabolic

pathways

include

oxidation

by

CYP3A4. There

is

no

evidence

that

any

of

the

pantoprazole

metabolites

have

significant

pharmacologic

activity. CYP2C19

displays

a

known

genetic

polymorphism

due

to

its

deficiency

in

some

sub-populations

(eg,

3%

of

Caucasians

and

African-Americans

and

17%-23%

of

Asians).

Thus,

PROTONIX®

(pantoprazole

sodium)

Delayed-Release

Tablets

may

be

taken

without

regard

to

timing

of

meals. PROTONIX®

(pantoprazole

sodium)

For

Delayed-Release

Oral

Suspension

should

be

taken

approximately

30

minutes

before

a

meal. Distribution

The

apparent

volume

of

distribution

of

pantoprazole

is

approximately

11.0-23.6

L,

distributing

mainly

in

extracellular

fluid. The

serum

protein

binding

of

pantoprazole

is

about

98%,

primarily

to

albumin. Metabolism

Pantoprazole

is

extensively

metabolized

in

the

liver

through

the

cytochrome

P450

(CYP)

system. Pantoprazole

metabolism

is

independent

of

the

route

of

administration

(intravenous

or

oral). The

main

metabolic

pathway

is

demethylation,

by

CYP2C19,

with

subsequent

sulfation; other

metabolic

pathways

include

oxidation

by

CYP3A4. There

is

no

evidence

that

any

of

the

pantoprazole

metabolites

have

significant

pharmacologic

activity. CYP2C19

displays

a

known

genetic

polymorphism

due

to

its

deficiency

in

some

sub-populations

(eg,

3%

of

Caucasians

and

African-Americans

and

17%-23%

of

Asians).

Search Page 1/20: erosive esophagitis
Search Results
500 results found. Showing 1-25:
 Esophagitis due to chemotherapy; Esophagitis due to corrosive agent; Esophagitis due to radiation therapy; Herpes simplex esophagitis; Radiation esophagitis
ICD-10-CM Diagnosis Code K20.8
Other esophagitis
2016 2017 2018 2019 2020 2021 - Converted to Parent Code Non-Billable/Non-Specific Code
ICD-10-CM Diagnosis Code K21.00
Gastro- esophageal reflux disease with esophagitis, without bleeding
Gastro-esophageal reflux dis with esophagitis, without bleed; Reflux esophagitis
ICD-10-CM Diagnosis Code K21.00
Gastro-esophageal reflux disease with esophagitis, without bleeding
2021 - New Code Billable/Specific Code
Applicable To
Reflux esophagitis
ICD-10-CM Diagnosis Code K20.80
Other esophagitis without bleeding
Abscess of esophagus; Other esophagitis NOS
ICD-10-CM Diagnosis Code K20.80
Other esophagitis without bleeding
2021 - New Code Billable/Specific Code
Applicable To
Abscess of esophagus
Other esophagitis NOS
ICD-10-CM Diagnosis Code K21.01
Gastro- esophageal reflux disease with esophagitis, with bleeding
Gastro-esophageal reflux dis with esophagitis, with bleed
ICD-10-CM Diagnosis Code K21.01
Gastro-esophageal reflux disease with esophagitis, with bleeding
2021 - New Code Billable/Specific Code
ICD-10-CM Diagnosis Code K22.11 [convert to ICD-9-CM]
Ulcer of esophagus with bleeding
Bleeding due to ulcerative esophagitis; Bleeding esophageal ulcer; Bleeding ulcer of esophagus; Upper gastrointestinal bleed due to ulcerative esophagitis;

Search Page 1/20: erosive esophagitis

Search Results
500 results found. Showing 1-25:

Esophagitis due to chemotherapy; Esophagitis due to corrosive agent; Esophagitis due to radiation therapy; Herpes simplex esophagitis; Radiation esophagitis
ICD-10-CM Diagnosis Code K20.8
Other esophagitis
2016 2017 2018 2019 2020 2021 - Converted to Parent Code Non-Billable/Non-Specific Code
ICD-10-CM Diagnosis Code K21.00
Gastro- esophageal reflux disease with esophagitis, without bleeding
Gastro-esophageal reflux dis with esophagitis, without bleed; Reflux esophagitis
ICD-10-CM Diagnosis Code K21.00
Gastro-esophageal reflux disease with esophagitis, without bleeding
2021 - New Code Billable/Specific Code
Applicable To
Reflux esophagitis
ICD-10-CM Diagnosis Code K20.80
Other esophagitis without bleeding
Abscess of esophagus; Other esophagitis NOS
ICD-10-CM Diagnosis Code K20.80
Other esophagitis without bleeding
2021 - New Code Billable/Specific Code
Applicable To
Abscess of esophagus
Other esophagitis NOS
ICD-10-CM Diagnosis Code K21.01
Gastro- esophageal reflux disease with esophagitis, with bleeding
Gastro-esophageal reflux dis with esophagitis, with bleed
ICD-10-CM Diagnosis Code K21.01
Gastro-esophageal reflux disease with esophagitis, with bleeding
2021 - New Code Billable/Specific Code
ICD-10-CM Diagnosis Code K22.11 [convert to ICD-9-CM]
Ulcer of esophagus with bleeding
Bleeding due to ulcerative esophagitis; Bleeding esophageal ulcer; Bleeding ulcer of esophagus; Upper gastrointestinal bleed due to ulcerative esophagitis;

Treacher Collins Syndrome - NORD (National Organization for Rare Disorders) Rare Disease Database
Rare Disease Database
Treacher Collins Syndrome
Synonyms of Treacher Collins Syndrome
General Discussion
Summary
Introduction
Signs & Symptoms
Causes
Affected Populations
Diagnosis
Standard Therapies
Investigational Therapies
NORD Member Organizations
Other Organizations
References
Years Published
 Additional abnormalities that may contribute to respiratory or feeding difficulties include narrowing or obstruction of the nasal airways (choanal stenosis or atresia). Some children may be described as having features of “Pierre Robin sequence” which include severe micrognathia, a tongue that is displaced farther back in the mouth than normal (glossoptosis) with or without incomplete closure of the roof of the mouth (cleft palate). Even in patients where the palate fuses, it may remain high arched which can still affect feeding and respiration. In addition, malformations of the mouth and the jaw may result in dental abnormalities, such as teeth that are underdeveloped (hypoplastic) and/or misaligned (malocclusion). Additional dental abnormalities have also been reported including missing teeth (tooth agenesis), clouding or discoloration of the enamel of teeth (enamel opacity), and improper (ectopic) eruption of certain upper teeth (maxillary molars). Individuals with TCS may develop hearing loss due to the failure of sound waves to be conducted through the middle ear (conductive hearing loss). Conductive hearing loss usually results from abnormalities affecting structures within the middle ear and individuals with TCS may also have malformed or absent ossicles, the three small bones through which sound waves are transmitted in the middle ear (i.e., incus, malleus, and stapes). In addition, the external ear structures are often absent, small or malformed (microtia), with narrowing (stenosis) or blockage (atresia) of the external ear canals. The outer ears may be crumpled or rotated. In contrast, the inner ear is usually unaffected, although malformation of the bony spiral organ in the inner ear (cochlea) and the structures within the inner ear that play a role in balance (vestibular apparatus) have been reported.

Treacher Collins Syndrome - NORD (National Organization for Rare Disorders)

Rare Disease Database
Rare Disease Database
Treacher Collins Syndrome
Synonyms of Treacher Collins Syndrome
General Discussion
Summary
Introduction
Signs & Symptoms
Causes
Affected Populations
Diagnosis
Standard Therapies
Investigational Therapies
NORD Member Organizations
Other Organizations
References
Years Published