In this question, they give an important piece of information when it comes to suspecting a diagnosis, which is the antitransglutaminase antibodies that must lead you to suspect celiac disease. The rest of the symptoms fall perfectly within the picture and although probably several of the tests that it says will be done, the answer that will give us the diagnosis is 4 (intestinal biopsy).

In this question, they give an important piece of information when it comes to suspecting a diagnosis, which is the antitransglutaminase antibodies that must lead you to suspect celiac disease. The rest of the symptoms fall perfectly within the picture and although probably several of the tests that it says will be done, [HIDDEN].

A 27-year-old woman under study in the dermatology department for recurrent episodes of oral aphthous ulcers. She was referred to the gastrointestinal department for a blood test showing Hb 11.5 gr/dl Fe 38 AST 52 ALT 64 Ac antitrasglutaminase IgA 177. The patient reported only occasional diffuse abdominal discomfort. She reports no signs of hemorrhage or jaundice. The physical examination is normal. Which of the following tests do you consider to be the most appropriate to make the diagnosis?

Epstein-Barr Virus Hepatitis Masquerading as Painless Jaundice.

Epstein-Barr virus (EBV) infection typically presents with pharyngeal symptoms and subclinical transaminitis. We present a case of a 27-year-old woman with no known past medical history who presented with painless jaundice and dark-colored urine for three days. Her review of systems was negative for fever, sore throat, nausea, vomiting, pruritus, or rash. Her last sexual contact was six months ago with a male partner, and she only drank alcohol socially. Family and surgical history were non-significant. Physical examination revealed 3+ bilateral conjunctival icterus without abdominal tenderness or organomegaly. She had elevated transaminases: alanine transaminase (ALT) of 1287U/L and aspartate aminotransferase of (AST) 1057U/L but her alkaline phosphatase (ALP) was only slightly above normal at 109U/L (normal range 35-104U/L), with a direct hyperbilirubinemia - total bilirubin 9.5mg/dl, direct bilirubin 6.8mg/dl; the abdominal ultrasound revealed non-dilated bile ducts. Hepatitis A, B, and C serology was negative, but her EBV serology showed an infection. She had incidental thalassemia minor without splenomegaly or asterixis. She was managed conservatively, and her liver enzymes trended down with supportive management. Although EBV is an uncommon cause of painless jaundice, this diagnosis should be considered, especially when other more common causes of jaundice have been ruled out. A high index of suspicion should be maintained to detect EBV hepatitis as it can easily be diagnosed through serological testing.

[Bleeding gastric ulcers and acute hepatitis: 2 simultaneous adverse reactions due to nimesulide in a case].

A 66 year-old obese woman with arthrosis, self-medicated with oral nimesulide, 200 mg daily. After 6 weeks she developed nausea, jaundice and dark urine. Two weeks later she had recurrent hematemesis and was hospitalized. Besides obesity and anemia her physical examination was unremarkable. An upper GI endoscopy revealed 3 acute gastric ulcers and a 4th one in the pyloric channel. Abdominal ultrasonogram showed a slightly enlarged liver with diffuse reduction in ecogenicity; the gallbladder and biliary tract were normal. Blood tests demonstrated a conjugated hyperbilirubinemia (maximal total value: 18.4 mg/dl), ALAT 960 U/l, ASAT 850 U/l, GGT 420 U/l, alkaline phosphatases mildly elevated, pro-time 49% and albumin 2.7 mg/dl. Serum markers for hepatitis A, B and C viruses were negative. ANA, AMA, anti-SmA, were negative. Ceruloplasmin was normal. A liver biopsy showed bridging necrosis and other signs of acute toxic liver damage. Gastric ulcers healed after conventional treatment and hepatitis subsided after 2 months leaving no signs of chronic liver damage. The diagnosis of toxic hepatitis due to nimesulide was supported by the time-course of drug usage, sex, age, absence of other causes of liver disease, a compatible liver biopsy and the improvement after drug withdrawal. Peptic ulcers or toxic hepatitis have been previously described as independent adverse reactions in patients taking nimesulide or other NSAIDs but their simultaneous occurrence in a single patient is a unique event that deserves to be reported.

Chronic GI bleeding in a middle-aged woman.

A middle-aged woman without any underlying systemic disease was referred to our hospital due to a 1-month history of recurrent black diarrhoea and anaemia. At presentation, her vital signs were stable and the physical examination was unremarkable except for pale conjunctiva. Laboratory tests showed iron-deficiency anaemia with a haemoglobin concentration of 7.3 g/dL (reference range, 11.1-15.1 g/dL). As she had no severe symptoms of anaemia, we administered oral iron preparations without blood transfusion and her anaemia was gradually corrected. Oesophagogastroduodenoscopy, colonoscopy and contrast-enhanced abdominal CT revealed no cause of bleeding, so obscure GI bleeding was suspected. Capsule enteroscopy revealed black fluid in the proximal small intestine, and subsequent peroral double-balloon enteroscopy detected a 1 cm diameter hemispheric elevated lesion at the upper jejunum (figure 1A, B). The lesion was non-pulsatile and hard in consistency, appearing as a submucosal tumour (SMT). An ulcer was located at the top of the lesion, suggesting the source of bleeding, although no blood clot was present around the site.gutjnl;68/8/1385/F1F1F1Figure 1Endoscopic findings of the jejunum on white light endoscopy (A) and chromoendoscopy with indigo carmine dye (B). What is your diagnosis? Do you try to obtain biopsy specimens from this lesion?

A Case of Brucellosis with Possible Ileal Involvement.

Brucellosis is a zoonotic disease that can involve different organs and tissues. Fever, fatigue, lymphadenopathy, hepatosplenomegaly, cytopenia, and arthritis are the usual modes of presentation. Gastrointestinal manifestations of human brucellosis are common but documented ileal involvement is extremely rare. A 68-year-old female presented with a history of 10 days of intense temporal migraine, photophobia, and phonophobia with partial response to paracetamol. The patient referred night sweats, anorexia, and colicky abdominal pain after her meals for the past 4 months followed by diarrhea. She denied nausea, vomiting, hypersensitivity of the scalp, blurry vision, melena, or rectal bleeding. She denied travelling or contact with animals. Physical examination revealed fever (38.3°C) and splenomegaly. Laboratory workup revealed Hb 7.8 g/dL, leukopenia (3.47 × 10<sup9</sup/L), C-reactive protein 5.94 mg/dL, and erythrocyte sedimentation rate 23 mm/h. Abdominal ultrasound showed hepatic steatosis and mild homogeneous splenomegaly. Chest radiography was normal. Lumbar puncture; transcranial, carotid, and temporal arteries Doppler, and head computed tomography (CT) did not show any significant changes. Abdominal CT showed diffuse thickening of the ileum and some mildly swollen locoregional lymph nodes. Fecal calprotectin was not elevated. Blood cultures and serologies were positive for <iBrucella</i (positive Rose-Bengal test, ELISA IgM-positive, IgG-negative anti-brucella antibody serology and positive Huddleson reaction - titer 1:320). The patient was started on rifampicin 600 mg/day and doxycycline 100 mg q. 12 h for 10 weeks with good clinical and analytical response. Upper and lower gastrointestinal endoscopy were normal, although the last was done already under antibiotic treatment. Although gastrointestinal manifestations of brucellosis are quite common, ileitis is thought to be extremely rare. In countries where brucellosis is endemic, doctors must consider this diagnosis when faced with patients with systemic symptoms and diarrhea or abdominal pain. Early recognition of brucellosis and institution of appropriate therapy usually leads to a good recovery without complications.

Jaundice

Diagnosis Most people presenting with jaundice have various predictable patterns of liver panel abnormalities, though significant variation does exist. The typical liver panel includes blood levels of enzymes found primarily from the liver, such as the aminotransferases (ALT, AST), and alkaline phosphatase (ALP); bilirubin (which causes the jaundice); and protein levels, specifically, total protein and albumin. Other primary lab tests for liver function include gamma glutamyl transpeptidase (GGT) and prothrombin time (PT). No single test can differentiate between various classifications of jaundice. A combination of liver function tests and other physical examination findings is essential to arrive at a diagnosis. Laboratory tests

Hepatitis B -- Introduction

Initial symptoms are nonspecific and may include anorexia, nausea, vomiting, abdominal pain, and jaundice. In cases of severe liver damage, patients can develop jaundice, hepatic encephalopathy, ascites, gastrointestinal bleeding secondary to esophageal varices, coagulopathy, or infections. Diagnosis is based on serologic blood tests in patients with suspected signs and symptoms and associated risk factors for viral hepatitis. This will be discussed in more detail below.

Megaduodenum

Acute pancreatitis, adhesions, aneurysm all clinically lead to Megaduodenum. Diagnosis Diagnostic tests and procedures can vary for different types of intestinal disorders. These can include colonoscopy, upper GI endoscopy, capsule endoscopy, endoscopic ultrasound. Since patients with megaduodenum often have atypical symptoms such as hematemesis, steatorrhea, and acute pancreatitis. Therefore, physical and histological examination helps demonstrate the grade of distention and the nutritional status of the patient. Many of the physical examinations include: blood pressure, bowel sounds, blood tests, and thyroid function. In addition, a histological examination such as upper endoscopy, an X-ray of the abdomen, and biopsies can also be performed to diagnose megaduodenum efficiently.

InternalMed_Harrison

Symptom No. of Patients (%) No symptom 129 (24) Abdominal pain 219 (40) Other (workup of anemia and various 64 (12) diseases) Routine physical exam finding, elevated LFTs 129 (24) Weight loss 112 (20) Appetite loss 59 (11) Weakness/malaise 83 (15) Jaundice 30 (5) Routine CT scan screening of known cirrhosis 92 (17) Cirrhosis symptoms (ankle swelling, 98 (18) abdominal bloating, increased girth, pruritus, GI bleed) Diarrhea 7 (1) Tumor rupture 1 Mean age (yr) 56 ± 13 Male:Female 3:1 Ethnicity Abbreviations: CT, computed tomography; GI, gastrointestinal; LFT, liver function test. esophageal varices from the underlying portal hypertension. Bone pain is seen in 3–12% of patients, but necropsies show pathologic bone metastases in ∼20% of patients. However, 25% of patients may be asymptomatic.

Single organ hepatic artery vasculitis as an unusual cause of epigastric pain: A case report.

Single-organ vasculitis (SOV) is characterized by inflammation of a blood vessel, affecting one organ, such as the skin, genitourinary system, or the aorta without systemic features. Gastrointestinal SOV is rare, with hepatic artery involvement reported only in two prior published cases. Herein, we presented a case of isolated hepatic artery vasculitis presenting after Pfizer-BioNTech mRNA corona virus disease 2019 (COVID-19) vaccination. A 50-year-old woman with hypertension presented to our Emergency Department with recurrent diffuse abdominal pain that localized to the epigastrium and emesis without diarrhea that began eight days after the second dose of the Pfizer-BioNTech COVID-19 vaccine. Blood work revealed an elevated C-reactive protein (CRP) of 19 mg/L (normal < 4.8 mg/L), alkaline phosphatase 150 U/L (normal 25-105 U/L), gamma-glutamyl transferase (GGT) 45 U/L (normal < 43 U/L) and elevated immunoglobulins (Ig) G 18.4 g/L (normal 7-16 g/L) and IgA 4.4 g/L (normal 0.7-4 g/L). An abdominal computed tomography revealed findings in keeping with hepatic artery vasculitis. A detailed review of her history and examination did not reveal infectious or systemic autoimmune causes of her presentation. An extensive autoimmune panel was unremarkable. COVID-19 polymerase chain reaction nasopharyngeal swab, human immunodeficiency virus, viral hepatitis and <iHeliobacter pylori</i serology were negative. At six months, the patient's symptoms, and blood work spontaneously normalized. High clinical suspicion of SOV is required for diagnosis in patients with acute abdominal pain and dyspepsia.

InternalMed_Harrison

attendant expense. Decision-analysis studies show that serology testing for celiac sprue in patients with IBS-D has an acceptable cost when the prevalence of celiac sprue is >1% and is the dominant strategy when the prevalence is >8%. In patients with concurrent symptoms of dyspepsia, upper GI radiographs or esophagogastroduodenoscopy may be advisable. In patients with postprandial right upper quadrant pain, an ultrasonogram of the gallbladder should be obtained. Laboratory features that argue against IBS include evidence of anemia, elevated sedimentation rate, presence of leukocytes or blood in stool, and stool volume >200–300 mL/d. These findings would necessitate other diagnostic considerations.

Duodenal Ulcer -- History and Physical

Patients who initially present with ulcer-related complications may present with symptoms suggestive of upper GI bleed, including melena, hematemesis, elevated BUN, and anemia of varying degrees in severity with associated fatigue. Patients who present with more alarming symptoms such as anemia, melena, or hematemesis, which may represent perforation or bleeding, will likely require more invasive forms of evaluation. The patient's history and age should also be considered when considering duodenal ulcers as part of the differential diagnosis, especially when patients present with more non-specific symptoms such as epigastric abdominal pain. Duodenal ulcers may occur in any age group. However, they are most commonly diagnosed in patients aged 20 to 45 and are more common in men than women. Most patients will have a history of presenting symptoms consistent with peptic ulcer disease (PUD) associated with a previous diagnosis of H. pylori and/or heavy NSAID use. Other elements of the history to consider include smoking history, daily aspirin use, and history of GI malignancy. On physical examination, patients may have epigastric abdominal tenderness, and if presenting with complications, they may demonstrate signs of anemia such as pale skin and positive fecal occult blood test.

InternalMed_Harrison

Discriminating functional and organic causes of indigestion man dates excluding certain historic and exam features. Odynophagia suggests esophageal infection. Dysphagia is concerning for a benign or malignant esophageal blockage. Other alarm features include unexplained weight loss, recurrent vomiting, occult or gross bleed ing, jaundice, palpable mass or adenopathy, and a family history of gastrointestinal neoplasm. Because indigestion is prevalent and most cases result from GERD or functional dyspepsia, a general principle is to perform only lim ited and directed diagnostic testing of selected individuals.

Acute cytomegalovirus hepatitis in an immunocompetent host.

A 52-year-old woman presented with a 1-week history of recurrent fevers and joint pains accompanied by abdominal and low back discomfort. She has a history of hypoparathyroidism and is on calcium supplements. Physical examination revealed fever and tachycardia. The rest of the examination was normal. Laboratory tests showed newly increased transaminase activity. Serum bilirubin and prothrombin time were normal. She was admitted for evaluation of acute hepatitis. Serology for hepatitis A, B, C and HIV were negative. Her serum acetaminophen and alcohol were undetected. Abdominal imaging was normal. Cultures were sterile. Additional tests for uncommon viral hepatitis included herpes simplex virus, cytomegalovirus and Epstein-Barr virus. Liver biopsy revealed non-specific inflammation. Subsequently, cytomegalovirus serology showed an IgM positive and negative IgG titre. Cytomegalovirus DNA qualitative PCR was also positive. No antiviral medication was given. She continued to have intermittent daily fever but reported no associated symptoms. She was discharged 9 days after admission in stable condition per her request with the advice to follow-up in the clinic in 1 week. Her serum hepatic profile returned to normal and she reported no more episodes of fever. Repeated titres of cytomegalovirus serology showed seroconversion.

Evaluation of jaundice in general practice.

Though there are many causes of jaundice, the GP's role is to differentiate that which is secondary to obstruction from that which is caused by viral hepatitis. Useful laboratory tests for both have changed in recent years and the diagnosis and treatment of extrahepatic obstruction has been revolutionised by endoscopic techniques.

Abdominal mass

Diagnosis The first steps in diagnosis are a medical history and physical examination. Important clues during history include weight loss, diarrhea and abdominal pain. During physical examination, the clinician must identify the location of the mass, as well as characterize its location (usually specified in terms of quadrants). The mass should be assessed for whether it is rigid or mobile. It should also be characterized for pulse or peristalsis, as these would help in further identifying the mass. Routine blood tests are usually the next step in diagnosis after a thorough medical history and physical examination. They should include a full blood count, blood urea nitrogen (BUN), creatinine, and liver function tests such as albumin, international normalized ratio (INR), partial thromboplastin time (PTT), serum amylase and total bilirubin (TBIL). If late-stage liver disease is suspected, then a serum glucose may be appropriate.

Sister Mary Joseph's nodule as a presenting sign of internal malignancy.

CASE 1: A 64-year-old, otherwise healthy woman was referred to the surgery clinic for a presumed umbilical hernia. On physical examination, a cutaneous nodule was noted on the umbilical region and the patient was referred to the dermatology clinic. The patient was reexamined and an erythematous nodule was observed in the umbilicus measuring 2.5 cm in diameter. The patient denied pain, change in bowel habits, or weight loss. There were no other abdominal masses, no sign of ascites, and no regional lymphadenopathy. A skin biopsy from the nodule showed mucinous adenocarcinoma. Immunohistochemical staining was positive for carcinoembryonic antigen, and negative for cytokeratin (CK)7 and CK20. These results were consistent with a Sister Mary Joseph's nodule and led to the diagnosis of an occult colon carcinoma. The patient had no risk factors for colorectal carcinoma. The patient underwent surgery in another hospital, and died 3 months after the initial diagnosis of Sister Mary Joseph's nodule. CASE 2: A 73-year-old woman was referred to the dermatology clinic for evaluation of a painful, ulcerated, 3-cm lesion in the umbilicus (Figure 1). She was otherwise asymptomatic. A skin biopsy showed neoplastic glandular cells infiltrating among collagen bundles (Figure 2). Stainings for mucin and for CK7 were positive, while staining for CK20 was negative. An abdominopelvic CT scan demonstrated a 3.5-cm space-occupying lesion in the liver. Results of gastroscopy, colonoscopy, chest computed tomographic (CT) scan, and mammography were normal. Serum levels of the tumor-associated protein CA125 were elevated to 164 units, while those of CA 19-9 and carcinoembryonic antigen were within normal range. A gynecologic examination and a transvaginal ultrasound were normal. The patient had no personal or family history of any malignancy or any risk factors for developing a carcinoma. The patient was scheduled for a palliative resection of the umbilical nodule, combined with a laparoscopic inspection in search of the undetected primary tumor. She refused surgery and was lost to follow-up. She died 4 months after the initial diagnosis of umbilical metastasis. CASE 3: A 51-year-old man was aware of a silent mass in his umbilicus for 2 years without seeking medical advice. Following 2 weeks of increasing pain in this area, he was referred to the emergency room for a suspected incarcerated umbilical hernia. Surgery revealed a mass attached to the fascia and peritoneal fat. The mass was removed and diagnosed as a poorly differentiated adenocarcinoma, staining positively for carcinoembryonic antigen, and negatively for CK20, CK7, prostate-specific antigen, and prostatic acid phosphatase. Both gastroscopy and colonoscopy failed to detect the primary tumor. An abdominopelvic CT scan was normal, but a CT scan of the chest disclosed a nodule measuring 2.5 x 1.5 cm in the lower lobe of the right lung. On bronchoscopy, it was found to be an invasive adenocarcinoma, consistent with a primary tumor of the lung. The patient was a heavy smoker (45 pack-years). The patient received 4 cycles of combined chemotherapy with carboplatine and gemcitabine, with no improvement. A month later, the patient complained of abdominal pain. Following demonstration of intra-abdominal spread of disease by CT scan, a second line chemotherapy was instituted with paclitaxel. A month later the patient's condition deteriorated and he complained of cough, sweating, and pain along the right leg. A bone scan revealed bone metastases in the right femur and left tibia. Two weeks later he was admitted to the hospital with intestinal obstruction and underwent laparotomy. He had massive intra-abdominal spread of cancer and ascites. Only a palliative colostomy was performed. The patient died 3 weeks later, 9 months after the diagnosis of adenocarcinoma of the lung. The clinical data on the three patients are summarized in Table I.

Analysis of patients referred to the gastroenterology service of a VA medical center.

We recorded clinical information over a 12-month period on consecutive consultations to the gastroenterology service of the Durham VA Medical Center. Of 902 consultations, 789 were prospectively collected. Eighty-five percent of the patients were between 40 and 70 years old. Seventy-five percent of the referrals were from the internal medicine service. The most frequent reasons for consultation were abdominal pain (19%), GI bleeding (active, 16%; occult, 9%), abnormal results of liver tests (18%), and request for a procedure (11%). Diseases of the liver (32%) and "peptic diseases" (30%) were the most common diagnoses. One or more procedures were done in 71% of consultations. When these data are compared with those of a practicing gastroenterologist, using an identical instrument, it is apparent that trainees' experience with structurally identifiable gastroenterologic disease and with a variety of procedures was similar in scope. There were, however, differences in that the physicians at the VA saw substantially fewer patients with so-called "functional" illness. If these data are applicable to other VA Medical Centers, then the training of physicians in gastroenterology at a VA Medical Center should probably be broadened.

Masquerading in the midgut: a rare diagnosis in a patient with recurrent abdominal pain.

A 38-year-old woman who had been previously diagnosed with irritable bowel syndrome was seen in the outpatient clinic with a 2-year history of intermittent cramp-like abdominal pain which was often followed by watery diarrhoea. She had presented several times previously to the emergency department with episodes of severe pain and collapse although on arrival examination findings were mostly unremarkable other than some mild lower abdominal tenderness. On each occasion, the symptoms resolved spontaneously with conservative management. She had been extensively investigated by her general practitioner to establish the cause of her symptoms but all laboratory findings, cross-sectional imaging, ultrasound and oesophagogastroduodenoscopy to date were unremarkable. After being seen in gastroenterology outpatients' clinic, a colonoscopy was performed and was described as being macroscopically normal but microscopic evaluation of colonic biopsies suggested a possible 'resolving infection'. She was treated symptomatically, but within 6 months she represented to hospital with progressively worsening symptoms of severe abdominal pain, now associated with vomiting, followed by watery diarrhoea and then resolution of the symptoms. An abdominal CT scan was performed which showed a small intraluminal-filling defect in the mid-terminal ileum. A wireless capsule endoscopy was organised to further characterise the lesion although this was reported as showing no abnormality. Prior to any further outpatient investigations, she represented as an emergency to hospital in small bowel obstruction, underwent further cross-sectional imaging followed by surgical resection of the lesion. Histological characterisation revealed a small bowel inflammatory fibroid polyp.

A novel segmental absence of intestinal musculature with small intestinal stenosis: a case report.

Segmental absence of intestinal musculature (SAIM) is a rare cause of intestinal obstruction and perforation due to partial or complete defects in the intestinal muscularis propria in neonates and is occasionally observed in adulthood. The first case of small intestinal stenosis derived from SAIM, which was difficult to differentiate from Crohn's disease (CD), is reported. A 4-year-old girl presented with abdominal pain, anemia, and a positive fecal occult blood test. She was initially diagnosed with CD and started on treatment. Because her gastrointestinal symptoms persisted, her previous pediatricians tried to carry out capsule endoscopy, but it was not possible because the patency capsule was retained. Therefore, she was referred to our institute and re-evaluated. The patency capsule examination was repeated to re-evaluate small intestinal passage, but it stagnated again. Abdominal ultrasonography showed a poorly deformable intestinal tract that narrowed rapidly from the dilated segment and had a thin wall with an irregular laminar structure. In addition, unlike the typical ultrasonic CD findings, the power Doppler signal enhancement at the intestinal wall and "creeping fat sign" were not found. The patient was referred for laparoscopic observation to pediatric surgeons, who confirmed a prominently dilated intestinal tract 40 cm proximal to the ileocecal valve, which was resected. Histopathological findings showed longitudinal muscle hypoplasia of the resected, dilated intestinal tract and fat replacement of the muscle layer. At the stenosis site, the muscle layer was fibrotic and showed incomplete muscle arrangement. Because of these findings, she was diagnosed with SAIM. After the surgical treatment, no gastrointestinal symptoms relapsed, and the fecal occult blood test has remained negative for 2 years. Moreover, 8 months after surgery, double-balloon endoscopy showed no abnormalities, such as a longitudinal ulcer and cobblestone appearance. In the present case, SAIM involved not only intestinal ileus and perforation, but also small intestinal stenosis. Although no other reports have demonstrated the usefulness of abdominal ultrasonography for the diagnosis of SAIM, the present report suggests that ultrasonography may be useful for differentiating SAIM from CD by close observation of the area around the small intestinal stenosis.

Jaundice -- Consultations

Specific challenging patients may require specialty consultations for further workup and management. Gastroenterology specialists most frequently consult on undiagnosed cases of jaundice. [31]

Autoimmune hepatitis triggered by acute hepatitis A.

The patient was a 57-year-old woman presenting with jaundice as the chief complaint. She began vomiting on July 10, 2003. Jaundice was noted and admitted to our hospital for thorough testing. Tests on admission indicated severe hepatitis, based on: aspartate aminotransferase (AST), 1 076 IU/L; alanine aminotransferase (ALT), 1 400 IU/L; total bilirubin (TB), 20.9 mg/dL; and prothrombin time rate (PT%), 46.9%. Acute hepatitis A (HA) was diagnosed based on negative hepatitis B surface antigen and hepatitis C virus RNA and positive immunoglobulin (Ig) M HA antibody, but elevation of anti-nuclear antigen (X320) and IgG (3 112 mg/dL) led to suspicion of autoimmune hepatitis (AIH). Plasma exchange was performed for 3 d from July 17, and steroid pulse therapy was performed for 3 d starting on July 18, followed by oral steroid therapy. Liver biopsy was performed on August 5, and the results confirmed acute hepatitis and mild chronic inflammation. Levels of AST and ALT normalized, so dose of oral steroid was markedly reduced. Steroid therapy was terminated after 4 mo, as the patient had glaucoma. Starting 3 mo after cessation of steroid therapy, levels of AST and ALT began to increase again. Another liver biopsy was performed and AIH was diagnosed based on serum data and biopsy specimen. Oral steroid therapy was reinitiated. Levels of AST and ALT again normalized. The present case was thus considered to represent AIH triggered by acute HA.

Hepatitis -- History and Physical -- Viral Hepatitis

Phase 2 (prodromal phase) - Patients in this phase usually present with anorexia, nausea, vomiting, malaise, pruritus, urticaria, arthralgias, and fatigue. Many times these patients are misdiagnosed as having gastroenteritis or viral infection. Phase 3 (icteric phase) - Patients in this phase present with dark-colored urine and pale-colored stool. Some patients develop jaundice and right upper quadrant pain with liver enlargement. Phase 4 (convalescent phase) - Patients typically start noticing the resolution of symptoms, and laboratory studies show liver enzymes returning to normal levels. [32]

Ulcus vulvae acutum in a 13-year-old girl after influenza A infection.

A 13-year-old otherwise healthy premenarchal girl presented with acute onset of painful vulvar ulcerations. One day before developing vulvar ulcerations, she experienced flu-like symptoms, including a low-grade fever, cough, sore throat, and myalgia. Results of a throat swab were positive for influenza A infection (polymerase chain reaction [PCR] assay), and the patient was treated with oseltamivir. The patient's constitutional symptoms improved slightly, but within 2 days after her initial presentation, she returned to her primary care provider and described 24 hours of dysuria and vulvar swelling. She had a history of herpes labialis (cold sores) and rare episodes of minor oral aphthae (canker sores) that occurred less than twice a year. The patient denied a history of sexual activity, sexual abuse, or physical trauma. Physical examination showed ulceration and swelling of the labia minora, and the patient received an empiric dose of acyclovir (200 mg 4 times daily) for presumed autoinoculated herpes simplex virus (HSV) infection. An ulcer swab was performed, and urinalysis revealed no evidence of infection. Two days later, the patient presented to the emergency department with increasing vulvar pain and vaginal discharge. The previous ulcer swab findings were negative for HSV (PCR assay), and consequently, acyclovir was discontinued after 1 day of therapy. She received topical viscous lidocaine and an empiric dose of oral fluconazole. The lidocaine provided temporary symptomatic relief. Results of DNA amplification studies were negative for Chlamydia trachomatis and Neisseria gonorrhoeae. A potassium hydroxide preparation was negative for fungi, and an ulcer swab for bacterial culture revealed usual flora. Of note, the PCR assay for Epstein-Barr virus was not performed on ulcer cells. The patient was referred to the department of dermatology, and results of a physical examination showed copious white mucoid discharge and a 2-cm ulceration of the left labia minora (Figure, panel A). Two smaller pinpoint ulcerations and swelling of the left labia minora were also noted. The lesions were clinically indistinguishable from the genital aphthous ulcers of patients with complex aphthosis (recurrent, severe aphthous ulcers on oral or genital mucosa). A diagnosis of ulcus vulvae acutum was made, and treatment was started with clobetasol 0.05% ointment (4 times daily) and lidocaine gel as needed. Four days later, the patient reported marked symptomatic improvement. Physical examination showed near resolution of the large vulvar ulceration (Figure, panel B). The patient tapered use of clobetasol ointment over the next several days until the ulcerations healed completely. Two months after her initial episode, the patient again had 3 small vulvar erosions after symptoms that included low-grade fever, malaise, and vomiting. She did not receive oseltamivir for this illness; clobetasol ointment was applied 4 times daily, and the vulvar erosions ameliorated within a few days. Her constitutional symptoms resolved without treatment. The patient has not experienced any further episodes of vulvar ulcerations in the 18 months after the most recent treatment.

InternalMed_Harrison

PART 2 Cardinal Manifestations and Presentation of Diseases A nonbloody nasogastric aspirate may be seen in up to ~18% of patients with UGIB, usually from a duodenal source. Even a bile-stained appearance does not exclude a bleeding postpyloric lesion because reports of bile in the aspirate are incorrect in ~50% of cases. Testing of aspirates that are not grossly bloody for occult blood is not useful. EVALuATION AND MANAgEMENT OF ugIB (FIg. 57-1)

Spontaneous Cure of Acute Hepatitis C.

The statistics proved that approximately 25% of the patients with acute HCV present with jaundice, and only 10-20% develop gastrointestinal symptoms. We present the case of a 58 year-old woman, with prior antecedents of arterial hypertension and diabetes mellitus since 25 years old, hypercholesterolemia and hypertriglyceridemia, psoriasis, epilepsy and depressive syndrome. She clinically presents asthenia, anorexia, itching, jaundice and choluria. The objective examination showed an orientated patient, without flapping, hemorrhagic dyscrasia or signs of chronic hepatic disease, with icteric mucosa and skin, abdominal pain, with hepatomegaly and splenomegaly. The laboratory tests have been compatible with acute hepatitis with colestatic pattern: AST/ALT 969/798 UI/ml, FA 796 UI/ml, GGT 2476 UI/ml, BT/BD 7.39/6.10, INR 0.9. The abdominal echography showed: hepatomegaly, regular borders, hepatic steatosis, splenomegaly without ascitic fluid. The viral serological tests revealed protection for hepatitis A ( IgM neg/IgG pos), negative for HVB infection (AgHBs neg, anti-HBc neg), negative for HVE and other viruses (CMV Herpes virus, Epstein Barr, HIV), positive antibodies for HCV and positive RNA VHC (164200 UI/ml), HCV genotype 3a, IL-28B CT, negative autoimmunity. The previous HCV tests were negative, sustaining the recent infection. We assumed an acute hepatitis C. The patient was symptomatically treated with hydroxyzine for the skin itch, with vitamin K for INR correction and she was closely monitored. She had good clinical and laboratorial evolution and she was discharged after one week, maintaining hepatology consultation. She spontaneously cleared HCV infection after 3 months, maintaining negative RNA VHC 6 months after infection. The patient has cured the HCV infection with no need for antiviral treatment.

InternalMed_Harrison

Any remaining symptoms are not due to H. pylori FIGuRE 188-2 Algorithm for the management of Helicobacter pylori infection. *Note that either the urea breath test or the stool antigen test can be used in this algorithm. Occasionally, endoscopy and a biopsy-based test are used instead of either of these tests in follow-up after treatment. The main indication for these invasive tests is gastric ulceration; in this condition, as opposed to duodenal ulceration, it is important to check healing and to exclude underlying gastric adenocarcinoma. However, even in this situation, patients undergoing endoscopy may still be receiving proton pump inhibitor therapy, which precludes H. pylori testing. Thus a urea breath test or a stool antigen test is still required at a suitable interval after the end of therapy to determine whether treatment has been successful (see text). †Some authorities use empirical third-line regimens, of which several have been described.

Cases from the Osler Medical Service at Johns Hopkins University.

A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen. On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. Urinalysis revealed an elevated specific gravity and numerous muddy granular casts. Hepatitis A, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm. What is the diagnosis?

[Diagnosis of jaundices in tropical practice (author's transl)].

Diagnosis of jaundices in tropical medicine complies with the same rules as in Europe. Some etiologies occur more frequently than in Europe; others, specific to tropical areas require peculiar investigations. Most jaundices observed overseas are hemolytic or hepatitic. Their diagnosis is generally easy. However, chronic viral hepatitis, a frequent infection, requires liver needle-biopsy for a valid diagnosis. The diagnosis of cholestatic jaundice must be conducted in a systematic fashion: if abdominal echotomography is not available, laparoscopy with or without liver needle-biopsy and percutaneous lateral transhepatic cholangiography (OKU-DA's technique) are easily performed in tropical countries and give a certain diagnosis.

Evolution from primary biliary cirrhosis to primary biliary cirrhosis/autoimmune hepatitis overlap syndrome.

An asymptomatic 70-year-old Hispanic woman with type 2 diabetes was found in 2004 to have an AST of 132 U/L, ALT 146 U/L, alkaline phosphatase 1107 U/L, total serum bilirubin 3.5 mg/dL, and albumin 2.9 g/dL. Viral hepatitis testing was negative. Serum IgG, IgA, and IgM were all elevated, antimitochondrial antibody was weakly positive, and antinuclear antibody was negative. Liver biopsy was reported to show "evolving cirrhosis with marked lymphoid hyperplasia." Although the indication was nowhere stated, she was prescribed ursodeoxycholic acid 500 mg b.i.d, on which her biochemical tests initially improved. One year later she developed itching and jaundice. Imaging studies revealed multiple gallstones. An MRCP was suggestive of cirrhosis with a questionable common bile duct stricture, and she underwent ERCP with removal of gallbladder and common bile duct stones and placement of a biliary stent. A periampullary mass, which proved to be a somatostatinoma, was excised in 2006 via an open laparotomy, at which the stent was removed and a second liver biopsy performed. It was reported as showing chronic active hepatitis, activity stage 2, and fibrosis grade 3 with bridging. Her subsequent course was complicated by recurrent bleeding from small bowel arteriovenous malformations. Seen for the first time at Columbia University Medical Center in January 2007, she complained of continuing pruritus. AST was 69 U/L, ALT 43 U/L, alkaline phosphatase 491 U/L, and total bilirubin 3.3 mg/dL. Serum albumin was 2.6 g/dL. Antinuclear antibodies, negative in 2004, were now positive at 1:320, and antimitochondrial M2 antibodies were strongly positive. Serum IgG and IgA, but NOT IgM, were elevated. Review of her outside liver biopsies revealed features of primary biliary cirrhosis (PBC) in the first, and of both PBC and autoimmune hepatitis (AIH) in the second. The patient exhibits an overlap syndrome, in which both histologic and serologic features of AIH evolved in a setting initially most suggestive of PBC alone. The phenomenon of autoimmune overlap syndromes is discussed.

Diagnostic Utility of Ultrasonography for Duodenal Ulcers in Pediatric Cases in Japan.

<bObjective:</b To evaluate the diagnostic utility of wall hypertrophy of the duodenal bulb with a hyperechoic lumen, designated as the "HH sign," using ultrasound sonography (US) in pediatric duodenal ulcer (DU) patients. <bStudy design:</b We performed a US for five pediatric subjects diagnosed with DU by upper gastroscopy to determine the presence of the potentially diagnostic HH sign. The sonographic images were analyzed before and after DU treatment. Computed tomography was performed in three cases and fecal occult blood test (FOBT) in all five cases. <bResults:</b Upper gastroscopy confirmed DU in all patients. While the HH sign was observed using US in four cases, with the DU located in the anterior bulb, the FOBT was positive in only one case. In these four cases, the HH sign diminished in response to treatment, as visualized by US. This was observed for both the initial as well as recurrent episodes. A mass-like region was observed in only one case, with the ulcer located in the proximity of the inferior duodenal wall. <bConclusion:</b The HH sign is useful for the follow-up of DU, and US may be a suitable modality for the follow-up. We believe that this diagnostic marker can aid in following up a greater number of DU cases.

[Capsule endoscopy for Behcet's disease-treatment: five cases reports].

Behcet's disease (BD) is a chronic vascular inflammatory disease of unknown causes. It is called intestinal BD, when digestive tract is involved. To investigate small bowel feature of intestinal BD, we now report 5 intestinal BD cases undergone capsule endoscopy from December, 2010 to April, 2014 in Peking University People's Hospital. General information, clinical feature and endoscopic feature were presented, and literatures were reviewed. There were 3 male and 2 female patients. Age range was from 23 to 55 years old (median age 40 years old). Disease course was from 3 days to 28 years (median course 9 years). 4 patients were diagnosed as systemic BD, and the rest independent intestinal BD. 4 systemic BD patients all presented as recurrent oral aphthous as initial symptom and had history of vulvar ulcer and skin lesion. They all had gastrointestinal symptoms, including retrosternal pain (2 cases), hematochezia (3 cases), diarrhea (3 cases) and abdominal pain (2 cases). 1 patient had a history of fistula of ileocecal junction and underwent caecectomy. 5 patients all underwent whole digestive tract examination by endoscopy, including gastroscopy, colonoscopy and capsule endoscopy.Except of 1 normal result of colonoscopy, all endoscopy results revealed lesions. Capsule endoscopy results of all patients were abnormal. Types of small intestinal lesion were various, including ulceration, erosion, protrusion and vasculopathy. All digestive tract can be involved in BD patients. Capsule endoscopy can evaluate lesions throughout whole digestive tract, especially in small intestine. As a consequence, it is helpful to explain gastrointestinal symptom, increase early diagnostic rate. Intestinal BD (IBD) mainly involves small bowel, and ileum is the major involved segment, not only limited in ileocecum. The updated perspective of IBD lesion distribution will contribute to differential diagnosis between IBD and Crohn's disease.This is the first time to report capsule endoscopic feature of BD patients in China.

Urea Breath Test -- Indications

The urea breath test is useful for both initial diagnosis and eradication of infection. [9] [23] Most patients with H. pylori are asymptomatic. [1] In the absence of alarm symptoms for gastric malignancy, UBT could be utilized to diagnose H. pylori . [23] Noninvasive tests, either UBT or SAT, are preferred for patients who do not need an endoscopic evaluation but have diseases strongly associated with H. pylori such as patients with a history of peptic ulcer disease (PUD), either with a history of active PUD or past medical history of PUD with no documented eradication. [5] [19] For patients less than 60 years with dyspepsia, a non-invasive H. pylori test could be offered in the absence of alarming symptoms (GI bleeding, anemia, significant weight loss, loss of appetite, dysphagia, significant emesis, family history of GI malignancy, and history of GI cancer) and if the test result is positive, H. pylori treatment could be offered. [20] [16] [5] [19] [32] For patients over 60 years with dyspepsia, an EGD is recommended to evaluate for both H. pylori and more importantly, to evaluate also other causes such as malignancy. [16] Similarly, EGD could also be considered for younger patients less than 60 years of age who have a higher risk of malignancy such as a family history of gastric cancer or living in places with a high prevalence of gastric cancer. [16] Furthermore, H. pylori infections are also associated with other conditions such as unexplained iron-deficiency anemia (after a thorough negative evaluation), and immune thrombocytopenia in adults and testing for H. pylori can be a consideration. [5] [19] Before the initiation or continuation of long-term NSAIDs or aspirin, the clinician needs to rule out H. pylori due to increased chances of development of PUD and its complications. [5] For eradication testing, UBT should be offered after 4 to 8 weeks of completion of the eradication treatment. [8] Here PPI should be discontinued at least two weeks before the testing to avoid a false negative result. [5] [7] [8]


The characteristics of the fluid described are milky, i.e., chylous ascitic fluid. Taking into account the age of the patient and the constitutional syndrome described, it is most likely to be a non-Hodgkin's lymphoma and not tuberculosis, which also presents with chylous ascitic fluid, since there is no mention of infectious symptoms. The rest of the entities offered do not present with chylous ascitic fluid.

The characteristics of the fluid described are milky, i.e., chylous ascitic fluid. Taking into account the age of the patient and the constitutional syndrome described, it is most likely to be a non-Hodgkin's lymphoma and not tuberculosis, which also presents with chylous ascitic fluid, since there is no mention of infectious symptoms. [HIDDEN].

An 80-year-old woman consults for presenting, since 1 month ago, a progressive increase in abdominal perimeter. During the previous 4-5 months she noted asthenia, anorexia and unspecified weight loss. Physical examination revealed tension ascites and malleolar edema, with no other relevant signs. An ultrasound and CT scan of the abdomen showed the presence of ascites, of homogeneous density, without peritoneal implants or abdominal or pelvic masses. Liver, pancreas, adrenal, spleen and kidneys without significant findings. Paracentesis is performed through a thick needle, obtaining with difficulty a somewhat yellowish, dense and gelatinous fluid. What is the most probable etiology?

Hydropic decompensation secondary to liver cirrhosis.

Chylous ascites due to non-Hodgkin's lymphoma.

Peritoneal metastasis of adenocarcinoma.

Ascites secondary to constrictive pericarditis.

Ascites

Ascites is the abnormal build-up of fluid in the abdomen. Technically, it is more than 25 ml of fluid in the peritoneal cavity, although volumes greater than one liter may occur. Symptoms may include increased abdominal size, increased weight, abdominal discomfort, and shortness of breath. Complications can include spontaneous bacterial peritonitis. In the developed world, the most common cause is liver cirrhosis. Other causes include cancer, heart failure, tuberculosis, pancreatitis, and blockage of the hepatic vein. In cirrhosis, the underlying mechanism involves high blood pressure in the portal system and dysfunction of blood vessels. Diagnosis is typically based on an examination together with ultrasound or a CT scan. Testing the fluid can help in determining the underlying cause.

Ascites

Ascites is detected with physical examination of the abdomen by visible bulging of the flanks in the reclining person ("flank bulging"), "shifting dullness" (difference in percussion note in the flanks that shifts when the person is turned on the side), or in massive ascites, with a "fluid thrill" or "fluid wave" (tapping or pushing on one side will generate a wave-like effect through the fluid that can be felt in the opposite side of the abdomen). Other signs of ascites may be present due to its underlying cause. For instance, in portal hypertension (perhaps due to cirrhosis or fibrosis of the liver) people may also complain of leg swelling, bruising, gynecomastia, hematemesis, or mental changes due to encephalopathy. Those with ascites due to cancer (peritoneal carcinomatosis) may complain of chronic fatigue or weight loss. Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance.

Paracentesis

Paracentesis (from Greek κεντάω, "to pierce") is a form of body fluid sampling procedure, generally referring to peritoneocentesis (also called laparocentesis or abdominal paracentesis) in which the peritoneal cavity is punctured by a needle to sample peritoneal fluid. The procedure is used to remove fluid from the peritoneal cavity, particularly if this cannot be achieved with medication. The most common indication is ascites that has developed in people with cirrhosis. Indications It is used for a number of reasons: to relieve abdominal pressure from ascites to diagnose spontaneous bacterial peritonitis and other infections (e.g. abdominal TB) to diagnose metastatic cancer to diagnose blood in peritoneal space in trauma For ascites

Hepatic hydrothorax

The most noticeable symptoms are usually those of cirrhosis and portal hypertension. Most people have signs of end-stage liver disease. pleuroperitoneal communications. The main method of diagnosis is extracting the fluid via thoracentesis. After this, the fluid is analyzed for diagnosis and to help rule out other possible causes like infection or cancer. The fluid can be analyzed for serum, protein, albumin, lactate dehydrogenase, and cell count. The fluid is a transudate and similar to fluid found in ascites. There may be a higher protein and albumin content in hepatic hydrothorax due to the pleura absorbing the water. To rule out heart-related causes of pleural effusion, an echocardiogram can be performed. Pleuroperitoneal communications are best detected by peritoneal scintigraphy. In this procedure, radioactive tracer is injected via needle into ascitic fluid, a procedure known as paracentesis. After that, a gamma camera is used to take images, showing the tracer in the pleural

Visceral scalloping on abdominal computed tomography due to abdominal tuberculosis.

Scalloping of visceral organs is described in pseudomyxoma peritonei, malignant ascites, among other conditions, but not tuberculosis. We report findings from a retrospective study of patients with abdominal tuberculosis who had visceral scalloping on abdominal computed tomography (CT). Diagnosis of abdominal tuberculosis was made on the basis of combination of clinical, biochemical, radiological and microbiological criteria. The clinical data, hematological and biochemical parameters, and findings of chest X-ray, CT, Mantoux test, and HIV serology were recorded. Of 72 patients with abdominal tuberculosis whose CT scans were included, seven patients had visceral scalloping. The mean age of these patients was 32.14 ± 8.43 years and four were men. While six patients had scalloping of liver, one had splenic scalloping. The patients presented with abdominal pain (all), abdominal distension (five patients), loss of weight or appetite (all), and fever (four patients). Mantoux test was positive in five, while none had HIV infection. The diagnosis was based on fluid (ascitic or collections) evaluation in four patients, ileo-cecal biopsy in one patient, fine needle aspiration from omental thickening in one patient, and sputum positivity for acid fast bacilli (AFB) in one patient. On CT examination, four patients had ascites, five had collections, one had lymphadenopathy, four had peritoneal involvement, three had pleural effusion, and two had ileo-cecal thickening. All except one patient received standard ATT for 6 months or 9 months (one patient). Pigtail drainage for collections was needed for two patients. This report is the first description of visceral scalloping of liver and spleen in patients with abdominal tuberculosis. Previously, this finding has been reported primarily with pseudomyxoma peritonei and peritoneal carcinomatosis. Visceral scalloping may not conclusively distinguish peritoneal tuberculosis from peritoneal carcinomatosis or pseudomyxoma peritonei.

Peritoneal lymphoma with ascites mimicking portal hypertensive ascites: A case report.

Lymphoma with an initial manifestation of ascites and peritoneal invasion is rare. A 65-year-old woman presented to the emergency department with a 3-week history of abdominal distention, anorexia, and night sweating, and a 2-week history of melena. She was a silent hepatitis B virus carrier. Abdominal ultrasound showed massive ascites without cirrhosis. Abdominal computed tomography revealed ascites, infiltrative peritoneal lesions with omental cake appearance, and lymphadenopathies. We performed paracentesis and the ascites cytology was obtained. The patient also underwent esophagogastroduodenoscopy, which showed ulcerative tumors in the stomach. Both ascites cytology and pathology of the gastric tumors confirmed the diagnosis of B-cell lymphoma. This patient received 7 cycles of chemotherapy. Follow-up imaging studies revealed partial remission of lymphoma, but an enlargement of residual tumors in omentum and mesentery, which resulted in intractable ascites and rapid deterioration of performance status. Despite a change of regimen of chemotherapy, this patient expired 10 months after diagnosis. Lymphoma should be one of the differential diagnoses in patients with intractable ascites not attributable to other comorbidities.

Abdominal tuberculosis

The definitive diagnosis can be established by demonstrating Mycobacterium tuberculosis in peritoneal fluid or in a biopsy specimen. The histopathologic findings of tuberculosis in biopsy, such as caseous granuloma, can be suggestive of tuberculosis, but is not pathognomic. CT scan offers evaluation of involvement of the liver or other organs, as well as for the presence of ascites, lymphadenopathy and peritoneal involvement. Ultrasound scan is useful for demonstrating lymphadenopathy and ascites.

The role of laparoscopy in the evaluation of ascites of unknown origin.

The role of laparoscopy in the diagnostic evaluation of ascites of unknown origin was studied in 129 patients. Laparoscopic results were as follows: (1) Carcinomatosis peritonei in 78 (60.5%). Peritoneal biopsies in 76 of these cases revealed malignancy in 67 (adenocarcinoma 62, lymphoma 4, mesothelioma 1) and tuberculosis in 5; specimens were inadequate for diagnosis in 4. (2) Tuberculous peritonitis in 26 (20.2%). Peritoneal biopsies in 24 of these cases revealed tuberculosis in 22 and non-specific chronic peritonitis in 2. (3) Cirrhosis in 7 (5.4%). (4) No gross abnormality in 18 (14.0%). Of the latter, causes of ascites had already been identified in 13 (72.2%), including chronic renal failure in 7, systemic lupus erythematosus in 2, constrictive pericarditis in 2, chronic pancreatitis with chylous ascites in 1, and retroperitoneal lymph node metastasis with chylous ascites in 1. Thus, laparoscopic observation in combination with biopsy established the cause of ascites of unknown origin in 111 (86.0%) of 129 patients. Most of the 18 patients without gross laparoscopic abnormality had underlying disease identified as a cause of ascites; laparoscopy was indicated in these cases to exclude other processes that may also cause ascites.

Peritoneal fluid

Peritoneal fluid is a serous fluid made by the peritoneum in the abdominal cavity which lubricates the surface of tissue that lines the abdominal wall and pelvic cavity. It covers most of the organs in the abdomen. An increased volume of peritoneal fluid is called ascites. Sampling of peritoneal fluid is generally performed by paracentesis. Peritoneal fluid analysis The serum-ascites albumin gradient (SAAG) is the most useful index for evaluating peritoneal fluid and can help distinguish ascites caused by portal hypertension (cirrhosis, portal vein thrombosis, Budd-Chiari syndrome, etc.) from other causes of ascites. SAAG is calculated by subtracting the albumin measure of ascitic fluid from the serum value. In portal hypertension, the SAAG is >1.1 g/dL while ascites from other causes shows a SAAG of less than 1.1 g/dL.

Peritonitis

Peritonitis is inflammation of the localized or generalized peritoneum, the lining of the inner wall of the abdomen and cover of the abdominal organs. Symptoms may include severe pain, swelling of the abdomen, fever, or weight loss. One part or the entire abdomen may be tender. Complications may include shock and acute respiratory distress syndrome. Causes include perforation of the intestinal tract, pancreatitis, pelvic inflammatory disease, stomach ulcer, cirrhosis, or a ruptured appendix. Risk factors include ascites (the abnormal build-up of fluid in the abdomen) and peritoneal dialysis. Diagnosis is generally based on examination, blood tests, and medical imaging. Treatment often includes antibiotics, intravenous fluids, pain medication, and surgery. Other measures may include a nasogastric tube or blood transfusion. Without treatment death may occur within a few days. About 20% of people with cirrhosis who are hospitalized have peritonitis. Signs and symptoms

Ascites

Causes of low SAAG ("exudate") are Cancer (metastasis and primary peritoneal carcinomatosis) – 10% Infection: Tuberculosis – 2% or spontaneous bacterial peritonitis Pancreatitis – 1% Serositis Nephrotic syndrome Hereditary angioedema Other rare causes Meigs syndrome Vasculitis Hypothyroidism Renal dialysis Peritoneum mesothelioma Abdominal tuberculosis Mastocytosis Diagnosis Routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation should be performed. Most experts recommend a diagnostic paracentesis be performed if the ascites is new or if the person with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as microbiological culture, Gram stain and cytopathology.

InternalMed_Harrison

FIguRE 59-2 CT of a patient with peritoneal carcinomatosis (white arrow) and ascites (yellow arrow). Cirrhosis accounts for 84% of cases of ascites. Cardiac ascites, peritoneal carcinomatosis, and “mixed” ascites resulting from cirrhosis and a second disease account for 10–15% of cases. Less common causes of ascites include massive hepatic metastasis, infection (tuberculosis, Chlamydia infection), pancreatitis, and renal disease (nephrotic syndrome). Rare causes of ascites include hypothyroidism and familial Mediterranean fever. Once the presence of ascites has been confirmed, the etiology of the ascites is best determined by paracentesis, a bedside procedure in which a needle or small catheter is passed transcutaneously to extract ascitic fluid from the peritoneum. The lower quadrants are the most frequent sites for paracentesis. The left lower quadrant is preferred because of the greater depth of ascites and the thinner abdominal wall.

Diagnosis of abdominal tuberculosis: experience from 11 cases and review of the literature.

To analyze the experience within our hospital and to review the literature so as to establish the best means of diagnosis of abdominal tuberculosis. The records of 11 patients (4 males, 7 females, mean age 39 years, range 18-65 years) diagnosed with abdominal tuberculosis in Harran University Hospital between January 1996 and October 2003 were analyzed retrospectively and the literature was reviewed. Ascites was present in all cases. Other common findings were weight loss (81%), weakness (81%), abdominal mass (72%), abdominal pain (72%), abdominal distension (63%), anorexia (45%) and night sweat (36%). The average hemoglobin was 8.2 g/dL and the average ESR was 50 mm/h (range 30-125). Elevated levels of cancer antigen CA-125 were determined in four patients. Abdominal ultrasound showed abnormalities in all cases: ascites in all, tuboovarian mass in five, omental thickening in 3, and enlarged lymph nodes (mesenteric, para-aortic) in 2. CT scans showed ascites in all, pelvic mass in 5, retroperitoneal lymphadenopathy in 4, mesenteric stranding in 4, omental stranding in 3, bowel wall thickening in 2 and mesenteric lymphadenopathy in 2. Only one patient had a chest radiograph suggestive of a new TB lesion. Two had a positive family history of pulmonary TB. None had acid-fast bacilli (AFB) in the sputum and the tuberculin test was positive in only two. Laparotomy was performed in 6 cases, laparoscopy in 4 and ultrasound-guided fine needle aspiration in 2. In those patients subjected to operation, the findings were multiple diffuse involvement of the visceral and parietal peritoneum, white 'miliary nodules' or plaques, enlarged lymph nodes, ascites, 'violin string' fibrinous strands, and omental thickening. Biopsy specimens showed granulomas, while ascitic fluid showed numerous lymphocytes. Both were negative for acid-fast bacilli by staining. PCR of ascitic fluid was positive for Mycobacterium tuberculosis (M. tuberculosis) in all cases. Abdominal TB should be considered in all cases with ascites. Our experience suggests that PCR of ascitic fluid obtained by ultrasound-guided fine needle aspiration is a reliable method for its diagnosis and should at least be attempted before surgical intervention.

Shifting dullness

If the borders between tympanitic (resonant) and dull notes remain the same, the person probably does not have ascites, or has less than 2 litres of free fluid present. If the fluid causing the dullness was not free, then the air-fluid level would not move. Shifting dullness is usually present if the volume of ascitic fluid is up to 500 mL ml. If low volume ascites is suspected, then an attempt to elicit the puddle sign may be performed. In some cases, the ascites collide to form a bigger ascites. This creates a different kind of shifting dullness. See also Abdominal examination Fluid wave test Bulging flanks Puddle sign References Medical signs

Peritoneal mesothelioma

Diagnosis Peritoneal mesothelioma has two clinical types which can be differentiated with the help of CT findings, the "dry" type, and the "wet". It is classified as "dry" when there are multiple tiny masses or one dominant localized mass and generally little or no ascites. The "wet" type has widespread small nodules, no dominant mass, and a presence of ascites. If fluid is found, the process of eliminating it is through paracentesis; however, the analysis of this fluid has limited diagnostic significance. Normally, a definitive diagnosis may be obtained through tissue biopsy.

Ascites of Unexplained Origin: A Case Report.

Ascites is defined as a massive collection of fluid in the peritoneal cavity, and it is most commonly caused by portal hypertension due to liver cirrhosis, acute liver failure, and heart failure. We report a case of ascites in a 39-year-old male who presented to the ED complaining of abdominal distention, sporadic pain on the epigastric area, unintentional weight loss over the past two months, night sweats, and blood-mixed stool. We conducted several imaging investigations and laboratory studies and none of them revealed any significant findings except for the abdominal CT with contrast, which showed large ascites along with submucosal fat deposition in the long segment of the transverse colon, suggestive of chronic inflammation [probably inflammatory bowel disease (IBD)], omental caking, and thickening. Peritoneal malignancy was highly suspected. A diagnostic/therapeutic paracentesis was performed, through which 8 L of fluid was drained. Cytology was also performed and this showed mostly reactive mesothelial cells, negative acid-fast bacilli (AFB) culture, and negative polymerase chain reaction (PCR). We also discuss the other investigations performed, none of which helped in establishing a diagnosis.

Symptoms and investigative findings in 145 patients with tuberculous peritonitis diagnosed by peritoneoscopy and biopsy over a five year period.

This study analysed clinical features and laboratory investigations in 145 patients with tuberculous peritonitis diagnosed by peritoneoscopy at this hospital between 1984 and 1988. Tuberculous peritonitis was found in 2% of all patients with tuberculosis and in 59.8% of all those with abdominal tuberculosis admitted to the hospital during the study period. Tuberculous peritonitis was more common in women than men (1.4:1) and was most frequently encountered in the third and fourth decades of life. The commonest presenting symptoms were abdominal swelling (73.1%), fever and night sweats (53.8%), anorexia (46.9%), weight loss (44.1%), and abdominal pain (35.9%). The mean duration of symptoms was 1.5 months. Ascites was the commonest (95.2%) physical sign. Tuberculin skin testing was positive in 57.6% of patients (n = 118). The mean erythrocyte sedimentation rate was 75 mm/1st hour (n = 58). Chest radiography on 98 patients showed pleuropulmonary pathology in 40 patients (40.8%). Sputum examination confirmed active pulmonary tuberculosis in 26 patients. The ascitic fluid was an exudate in 96.4% and a transudate in 3.6% of patients, with 91.3% showing a straw coloured ascites. Cirrhosis, detected by biopsy specimen, was a finding in 6.2% of patients.

Portal hypertension

Signs and symptoms Signs and symptoms of portal hypertension include: Ascites (free fluid in the peritoneal cavity), Abdominal pain or tenderness (when bacteria infect the ascites, as in spontaneous bacterial peritonitis). Increased spleen size (splenomegaly), which may lead to lower platelet counts (thrombocytopenia) Anorectal varices Swollen veins on the anterior abdominal wall (sometimes referred to as caput medusae) In addition, a widened (dilated) portal vein as seen on a CT scan or MRI may raise the suspicion about portal hypertension. A cutoff value of 13 mm is widely used in this regard, but the diameter is often larger than this is in normal individuals as well.

Ascites

The serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites. A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive as a cause. Ultrasound investigation is often performed prior to attempts to remove fluid from the abdomen. This may reveal the size and shape of the abdominal organs, and Doppler studies may show the direction of flow in the portal vein, as well as detecting Budd-Chiari syndrome (thrombosis of the hepatic vein) and portal vein thrombosis. Additionally, the sonographer can make an estimation of the amount of ascitic fluid, and difficult-to-drain ascites may be drained under ultrasound guidance. An abdominal CT scan is a more accurate alternate to reveal abdominal organ structure and morphology.

Large hepatocellular carcinoma in a non-cirrhotic liver with peritoneal and omental metastasis in a healthy man: a case report.

Liver cancer is the second leading cause of cancer death in men worldwide. Hepatocellular carcinoma usually develops in the setting of cirrhosis or chronic inflammation. Major risk factors for developing hepatocellular carcinoma are chronic hepatitis B or C virus infection, alcoholic cirrhosis, and nonalcoholic fatty liver disease. The most frequent locations for hepatocellular carcinoma to metastasize are the lungs, portal vein, bones, and regional lymph nodes. A 41-year-old Sri Lankan man presented with progressive abdominal distension and on examination was found to have a palpable irregular mass in the left lobe of his liver with moderate ascites. His ascitic fluid was an exudate without malignant cells. An ultrasound scan and contrast-enhanced computed tomography of his abdomen showed a large contrast-enhancing lesion in the left lobe of his liver without features of cirrhosis. Laparoscopic assessment revealed peritoneal and omental deposits. Histology of the biopsies taken from the liver lesion, omental deposits, and peritoneal deposits supported a diagnosis of hepatocellular carcinoma. His liver biochemistry was normal and hepatitis serology was negative. He is abstinent from alcohol and did not have metabolic syndrome. It is rare for a young patient to develop hepatocellular carcinoma with a normal liver without chronic hepatitis B or C infection, or any other risk factors. Intraperitoneal metastasis of non-ruptured hepatocellular carcinoma is also very rare. Here we report a rare case of a 41-year-old man with a large hepatocellular carcinoma in a non-cirrhotic liver without chronic hepatitis who presented with peritoneal and omental metastasis.

Ascites

Classification Ascites exists in three grades: Grade 1: mild, only visible on ultrasound and CT Grade 2: detectable with flank bulging and shifting dullness Grade 3: directly visible, confirmed with the fluid wave/thrill test Pathophysiology Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 35 liters are possible. Roughly, transudates are a result of increased pressure in the hepatic portal vein (>8 mmHg, usually around 20 mmHg (e.g., due to cirrhosis), while exudates are actively secreted fluid due to inflammation or malignancy. As a result, exudates are high in protein and lactate dehydrogenase and have a low pH (<7.30), a low glucose level, and more white blood cells. Transudates have low protein (<30 g/L), low LDH, high pH, normal glucose, and fewer than 1 white cell per 1000 mm3. Clinically, the most useful measure is the difference between ascitic and serum albumin concentrations. A difference of less than 1 g/dl (10 g/L) implies an exudate.

InternalMed_Harrison

288 be measured. In contrast to “spontaneous” bacterial peritonitis, which may complicate cirrhotic ascites (see “Complications,” below), secondary peritonitis is suggested by an ascitic glucose level <50 mg/dL, an ascitic LDH level higher than the serum LDH level, and the detection of multiple pathogens on ascitic fluid culture. When pancreatic ascites is suspected, the ascitic amylase level should be measured and is typically >1000 mg/dL. Cytology can be useful in the diagnosis of peritoneal carcinomatosis. At least 50 mL of fluid should be obtained and sent for immediate processing. Tuberculous peritonitis is typically associated with ascitic fluid lymphocytosis but can be difficult to diagnose by paracentesis. A smear for acid-fast bacilli has a diagnostic sensitivity of only 0 to 3%; a culture increases the sensitivity to 35–50%. In patients without cirrhosis, an elevated ascitic adenosine deaminase level has a sensitivity of >90% when a cut-off value of 30–45 U/L is used. When

Hepatorenal syndrome

Certain precipitants of HRS have been identified in vulnerable individuals with cirrhosis or fulminant liver failure. These include bacterial infection, acute alcoholic hepatitis, or bleeding in the upper gastrointestinal tract. Spontaneous bacterial peritonitis, which is the infection of ascites fluid, is the most common precipitant of HRS in cirrhotic individuals. HRS can sometimes be triggered by treatments for complications of liver disease: iatrogenic precipitants of HRS include the aggressive use of diuretic medications or the removal of large volumes of ascitic fluid by paracentesis from the abdominal cavity without compensating for fluid losses by intravenous replacement.

Spontaneous bacterial peritonitis

Spontaneous bacterial peritonitis (SBP) is the development of a bacterial infection in the peritoneum, despite the absence of an obvious source for the infection. It is specifically an infection of the ascitic fluid – an increased volume of peritoneal fluid. Ascites is most commonly a complication of cirrhosis of the liver. It can also occur in patients with nephrotic syndrome. SBP has a high mortality rate. The diagnosis of SBP requires paracentesis, a sampling of the peritoneal fluid taken from the peritoneal cavity. If the fluid contains large numbers of white blood cells known as neutrophils (>250 cells/µL), infection is confirmed and antibiotics will be given, without waiting for culture results. In addition to antibiotics, infusions of albumin are usually administered.

InternalMed_Harrison

Jugular venous distention, a sign of right-sided heart failure, suggests hepatic congestion. Right pleural effusion in the absence of clinically apparent ascites may be seen in advanced cirrhosis. The abdominal examination should focus on the size and consistency of the liver, on whether the spleen is palpable and hence enlarged, and on whether ascites is present. Patients with cirrhosis may have an enlarged left lobe of the liver, which is felt below the xiphoid, and an enlarged spleen. A grossly enlarged nodular liver or an obvious abdominal mass suggests malignancy. An enlarged tender liver could signify viral or alcoholic hepatitis; an infiltrative process such as amyloidosis; or, less often, an acutely congested liver secondary to right-sided heart failure. Severe right-upper-quadrant tenderness with respiratory arrest on inspiration (Murphy’s sign) suggests cholecystitis. Ascites in the presence of jaundice suggests either cirrhosis or malignancy with peritoneal spread.

Hepatic hydrothorax

this procedure, radioactive tracer is injected via needle into ascitic fluid, a procedure known as paracentesis. After that, a gamma camera is used to take images, showing the tracer in the pleural cavity. Hydrothorax without ascites has been reported to occur in as many as 20% of people with cirrhosis, but only detected in 7% of cases via CT scan and ultrasound.

Hepatic hydrothorax

There are no specific symptoms, because it generally occurs with ascites and other manifestations of increased pressure in the portal vein caused by liver disease. Pleural fluid can far more easily cause symptoms than ascitic fluid, due to the lower volume of the pleural cavity as compared to the abdominal cavity. The main symptoms are usually related to the symptoms of liver cirrhosis and ascites. Less often, it may be the only manifestation of chronic liver disease. The symptoms depend on many factors, such as the effusion's volume, rate of accumulation, and the co-existence of cardiopulmonary disease. The disease may cause no symptoms and be incidentally detected by medical scans, or it may cause large pleural effusions that result in respiratory symptoms like cough, shortness of breath, low blood oxygen, and respiratory failure. Most people have progressive difficulty breathing and reduced tolerance for exercise. Rarely, there may be acute cases that accumulate fluid rapidly and

Serum-ascites albumin gradient

Differential High gradient A high gradient (> 1.1 g/dL, >11g/L) indicates the ascites is due to portal hypertension, either liver related or non-liver related, with approximately 97% accuracy. This is due to increased hydrostatic pressure within the blood vessels of the hepatic portal system, which in turn forces water into the peritoneal cavity but leaves proteins such as albumin within the vasculature. Important causes of high SAAG ascites (> 1.1 g/dL, >11 g/L) include: cirrhosis of the liver, heart failure, Budd-Chiari syndrome, portal vein thrombosis, and idiopathic portal fibrosis. Low gradient A low gradient (< 1.1 g/dL, <11 g/L) indicates causes of ascites not associated with increased portal pressure such as: tuberculosis, pancreatitis, infections, serositis, various types of peritoneal cancers (peritoneal carcinomatosis) and pulmonary infarcts. References Medical tests Hepatology

Peritonitis

the future. Computed tomography (CT or CAT scanning) may be useful in differentiating causes of abdominal pain. If reasonable doubt still persists, an exploratory peritoneal lavage or laparoscopy may be performed. In people with ascites, a diagnosis of peritonitis is made via paracentesis (abdominal tap): More than 250 polymorphonuclear cells per μL is considered diagnostic. In addition, Gram stain is almost always negative, whereas culture of the peritoneal fluid can determine the microorganism responsible and determine their sensitivity to antimicrobial agents.

Untangling the etiology of ascites.

Amyloidosis is a systemic disease known to affect a vast range of organs, including the liver, heart, and kidney. When infiltrating the liver, amyloidosis typically does not present with cirrhosis. Typical presentation includes hepatomegaly with some mild laboratory abnormalities. A 72-year-old man presented with a 2-week history of worsening abdominal, scrotal, and extremity swelling. He endorsed melanotic stools and intermittent dizziness with a 10-pound weight gain. Vitals revealed a blood pressure of 82/57 mmHg and a pulse of 83 beats/min with positive orthostatic changes. Mild bibasilar crackles were noted. His abdomen was moderately distended with a fluid wave present, but no hepatosplenomegaly was noted. He displayed anasarca with significant extremity and scrotal edema, but no jaundice, telangiectasias, or other stigmata of chronic liver disease were present. Liver function tests demonstrated a total bilirubin of 1.5 mg/dL (normal value: 0.2-1.2 mg/dL), AST 111 IU/L (normal value 5-34 IU/L), ALT 51 IU/L (normal value 5-55 IU/L), and GGT 583 U/L (12-64 U/L). Alkaline phosphatase was 645 U/L (40-150 U/L). Analysis of peritoneal fluid was consistent with portal hypertension due to liver disease. Given an atypical presentation of cirrhosis with unclear etiology, a biopsy was performed and revealed amyloid deposition. Liver disease can be due to various etiologies, many of which can present ambiguously. Although the most typical etiologies have been well defined, we present a case of an atypical presentation of hepatic amyloidosis discovered in a patient with ascites and without typical hepatomegaly.

Chylous Ascites -- History and Physical

Patients with chylous ascites (CA) usually complain of painless, progressive abdominal distention that could extend over weeks to months. This is the most common symptom in up to 81% of the patients. Less common symptoms among patients with chylous ascites include pain or peritonitis in 11%, diarrhea, dysphagia (as reported in atraumatic causes due to goiter or para-esophageal hernia compressing the thoracic duct and leading to the formation of chylothorax and CA), peripheral edema, weight gain and shortness of breath, resulting from the increased abdominal pressure. [12] Other less specific symptoms include loss of appetite, fatigue, nausea, lymph nodes enlargement, fullness, fever, and night sweats.

[Constrictive pericarditis: the story of a constrained heart].

Symptoms of constrictive pericarditis may be nonspecific, misleading and may delay or lead to an incorrect diagnosis. We present the case of a 28-year-old male who was admitted to the hospital with progressive dyspnea, thoracic pain and a history of 25 kg of weight gain during the last 2 years. He was evaluated at another facility and his clinical presentation led to an erroneous diagnosis of primary hepatic disease (cirrhosis and portal hypertension). Physical examination showed that he was dyspneic, emaciated, had marked distention of his frontal cranial veins, diminished heart sounds, massive ascites and leg edema. Laboratory tests reported abnormal liver function tests and abdominal paracentesis chylous ascites. Electrocardiogram showed sinus rhythm with generalized low voltage and nonspecific repolarization changes. Heart size was normal on chest radiography. Doppler echocardiography reported bilateral atrial dilatation, a thickened pericardium and a short deceleration time of transmitral flow. A thickened and calcified pericardium was seen on CT scan. Pericardiectomy was performed. Spontaneous polyuria was observed during and after surgery with subsequent improvement of ascites and edema. The pericardium was found to be grossly thickened and inflamed. Clinician must be aware of the slow and progressive course of right ventricular failure, as well as to recognize constrictive pericarditis as a cause of chronic ascites.The hemodynamic aspects of the disease are of paramount importance for early diagnosis and opportune treatment.