Glomerulonephritis is typically associated with dysmorphic red blood cells and hematic casts in the sediment (option 1 correct). Proteinuria can also appear in variable range, although it is not usual in the form of isolated microalbuminuria (incorrect option 2), and hematuria with pyuria although it is not characteristic (incorrect option 3). Clots usually appear in the context of alterations of the lower urinary tract (option 4 incorrect).

Glomerulonephritis is typically associated with dysmorphic red blood cells and hematic casts in the sediment ([HIDDEN]). Proteinuria can also appear in variable range, although it is not usual in the form of isolated microalbuminuria ([HIDDEN]), and hematuria with pyuria although it is not characteristic ([HIDDEN]). Clots usually appear in the context of alterations of the lower urinary tract ([HIDDEN]).

A 28-year-old man comes to the hospital emergency room with gross hematuria. Which of the following urinalysis abnormalities would support a diagnosis of glomerulonephritis?

Dysmorphic red blood cells and/or hematic casts.

Proteinuria of 1 g/day, with negative test strip result and with microalbuminuria greater than 300 mg/24 hours.

Coexistence of hematuria with pyuria without bacteriuria.

Microhematuria

Microhematuria, also called microscopic hematuria (both usually abbreviated as MH), is a medical condition in which urine contains small amounts of blood; the blood quantity is too low to change the color of the urine (otherwise, it is known as gross hematuria). While not dangerous in itself, it may be a symptom of kidney disease, such as IgA nephropathy or Sickle cell trait, which should be monitored by a doctor. The American Urological Association (AUA) recommends a definition of microscopic hematuria as three or more red blood cells per high-power microscopic field in urinary sediment from two of three properly collected urinalysis specimens. Microhematuria is usually asymptomatic, and there are medical guidelines on how to handle asymptomatic microhematuria (AMH) so as to avoid problems such as overtreatment or misdiagnosis. See also Proteinuria Hematuria Myoglobinuria Hemoglobinuria References External links 2012 AUA Guidelines

Renal biopsy findings and clinical indicators of patients with hematuria without overt proteinuria.

Whether to perform a renal biopsy for isolated hematuria remains a matter of controversy. We performed renal biopsy in hematuria without overt proteinuria patients and reported the proportion of glomerulonephritis, pathological activities, and statistical analysis of indicators associated with glomerulonephritis. Among 203 patients who underwent renal biopsy in Okubo Hospital, Japan, between January 2008 and October 2013, we identified 56 patients who fulfilled the criteria: (1) urine dipstick examination shows equal to or greater than ± blood on three or more visits, (2) proteinuria <0.3 g/day (g/g Cr), (3) eGFR ≧60 ml/min/1.73 m(2), and (4) no current medication for renal disease. We investigated biopsy findings and compared the clinical indicators in the IgA nephropathy (IgAN) and non-IgAN group. The pathological diagnosis was IgAN in 35 cases (62 %), thin basement membrane disease (TBMD) in 7 (13 %), minor glomerular abnormality (MGA) in 6 (11 %), glomerular basement membrane (GBM) abnormality in 5 (9 %), and others in 3 (5 %). The histological grade of IgAN was I in 90 % and II in 10; 31 % of patients had some crescentic lesions. Comparisons between the IgAN and non-IgAN group revealed significant differences in age of onset (26 ± 13 vs. 34 ± 17 years, p = 0.04), serum IgA (340 ± 114 vs. 220 ± 101 mg/dl, p < 0.01), proteinuria (0.08 [0-0.25] vs. 0 [0-0.23] g/day [g/gCr], p < 0.01), and the presence of poikilocytes (40 vs. 10 %, p = 0.02). The proportion of IgAN in hematuria without overt proteinuria was high and the pathological activities were variable. Patients with hematuria without overt proteinuria should continue their medical follow-up and the best timing of biopsy may be controversial for these patients who have multiple risk factors of IgAN.

Clinical urine tests

Urine test strip A urine test strip can quantify: Leukocytes – with presence in urine known as leukocyturia Nitrite – with presence in urine known as nitrituria Protein – with presence in urine known as proteinuria, albuminuria, or microalbuminuria Erythrocytes – with presence in urine known as hematuria Specific gravity Glucose - with presence in urine known as glucosuria Bilirubin - with presence in urine known as bilirubinuria Ketones - with presence in urine known as ketonuria Microscopic examination

Hematuria

The first step in evaluation of red or brown colored urine is to confirm true hematuria with urinalysis and urine microscopy, where hematuria is defined by three of more red blood cells per high power field. Although a urine dipstick test may be used, it can give false positive or false negative results. In gathering information, it is important to inquire about recent trauma, urologic procedures, menses, and culture-documented urinary tract infection. If any of these are present, it is appropriate to repeat a urinalysis with urine microscopy in 1 to 2 weeks or after treatment of the infection. If the results of the urinalysis and urine microscopy reveal a glomerular origin of hematuria (indicated by proteinuria or red blood cell casts), consultation of a nephrologist should be made. If the results of the urinalysis indicate a non-glomerular origin, a microbiological culture of the urine should be performed, if it has not been done already. If the culture is positive, treatment of the

IgA nephropathy

For an adult patient with isolated hematuria, tests such as ultrasound of the kidney and cystoscopy are usually done first to pinpoint the source of the bleeding. These tests would rule out kidney stones and bladder cancer, two other common urological causes of hematuria. In children and younger adults, the history and association with respiratory infection can raise the suspicion of IgA nephropathy. A kidney biopsy is necessary to confirm the diagnosis. The biopsy specimen shows proliferation of the mesangium, with IgA deposits on immunofluorescence and electron microscopy. However, patients with isolated microscopic hematuria (i.e. without associated proteinuria and with normal kidney function) are not usually biopsied since this is associated with an excellent prognosis. A urinalysis will show red blood cells, usually as red cell urinary casts. Proteinuria, usually less than 2 grams per day, also may be present. Other renal causes of isolated hematuria include thin basement

Nephritic syndrome

Signs and symptoms that are consistent with nephritic syndrome include: Hematuria (red blood cells in the urine) Proteinuria (protein in the urine) ranging from sub-nephrotic (<3.5 g/day) to >10 g/day, although it is rarely above nephrotic range proteinuria levels. Hypertension resting blood pressure is persistently at or above 130/80 or 140/90 mmHg. Blurred vision Azotemia (increased plasma Urea and Creatinine) Oliguria (low urine output <400 ml/day) Red blood cell casts (seen with urine analysis and microscopy) Pyuria (white blood cells or pus in the urine) Causes

Refined microscopic urinalysis for red blood cell morphology in the evaluation of asymptomatic microscopic hematuria in a pediatric population.

The use of refined microscopic urinalysis for the presence of dysmorphic red blood cells (RBCs) has been evaluated in children and adults with a known source of hematuria. We examined the clinical usefulness of this study in a pediatric population with an unknown source of hematuria. Children 12 years old or younger referred for evaluation of asymptomatic microscopic hematuria exhibiting 4 or more RBCs per high power field were enrolled in this study. Patients provided a first morning urine sample subjected to refined urinalysis for RBC morphology. Standard evaluation of patients was performed until a final diagnosis of the hematuria source was identified. A total of 44 patients completed the study. Refined urinalysis revealed pure dysmorphic RBCs in 22 patients, pure isomorphic RBCs in 8 and mixed isomorphic/dysmorphic RBCs in 14. The presence of dysmorphic RBCs correctly predicted a glomerulotubular source of hematuria in 29 of 36 patients (sensitivity 83%, specificity 81%), while the presence of isomorphic RBCs predicted a uroepithelial source of hematuria in 2 of 8 patients (sensitivity 25%, specificity 22%). Hematuria and 2+ proteinuria (100 mg./dl.) were more sensitive (100%) and specific (83%) than the presence of dysmorphic RBCs in predicting glomerulotubular hematuria. We believe that this is a costly test offering little additional information to the evaluation of microscopic hematuria in children. A thoughtful history and physical examination with microscopic urinalysis and dipstick for proteinuria provide an equal amount of diagnostic information. We do not recommend its routine use in the evaluation of microscopic hematuria in children.

Urine test strip

Blood Blood may be present in the urine either in the form of intact red blood cells (hematuria) or as the product of red blood cell destruction, hemoglobin (hemoglobinuria). Blood present in large quantities can be detected visually. Hematuria produces cloudy red urine, and hemoglobinuria appears as a clear red specimen. Any amount of blood greater than five cells per microliter of urine is considered clinically significant; visual examination cannot be relied upon to detect the presence of blood. Microscopic examination of the urinary sediment shows intact red blood cells, but free hemoglobin produced either by hemolytic disorders or lysis of red blood cells is not detected. Therefore, chemical tests for hemoglobin provide the most accurate mean for determining the presence of blood. Once blood has been detected, the microscopic examination can be used to differentiate between hematuria and hemoglobinuria.

Nephritic syndrome

Blood urea nitrogen (BUN) - Also measured using a BMP or CMP, blood urea nitrogen is an indicator of how much nitrogen is in the blood at the time of the phlebotomy. The kidney is responsible for excreting nitrogenous substances in the urine, so an elevated BUN usually indicates that the kidney is not functioning appropriately. Urine Analysis (Urinalysis) - After the patient provides a urine specimen, it is sent to the lab for analysis using a variety of methods including urine dipstick testing and microscopic examination. Because the kidney is responsible for making urine, analyzing the urine directly can provide crucial data that can help the physician diagnose nephritic syndrome. Some findings on urinalysis that are consistent with nephritic syndrome include red blood cells (hematuria), red blood cell casts, proteinuria, and possibly white blood cells (pyuria).

Hematuria

a female less than 50 years old or a male less than 40 years old; has 3-10 red blood cells per high power field; has not had microscopic hematuria before; and has no other risk factors for urothelial cancer. To be in the intermediate risk category, one must satisfy any of the following criteria: Has smoked 10-30 pack-years; is a female 50-59 years old or a male aged 40-59 years old; has 11-25 red blood cells per high power field; or was previously a low-risk patient with persistent microscopic hematuria and has 3-25 red blood cells per high power field. To be in the high risk category, one must satisfy any of the following criteria: Has smoked more than 30 pack-years; is older than 60 years of age; or has above 25 red blood cells per high power field on any urinalysis. For the low risk category, the next step is to either repeat a urinalysis with urine microscopy in 6 months or perform a cystoscopy and renal ultrasound. For the intermediate risk category, the next step is to perform a

Hematuria -- Evaluation

Urinalysis is the initial and most useful test to perform. Although urine dipstick is widely available and can be performed quickly, it can give false-positive or false-negative results and warrants urinalysis and urine microscopy to establish the diagnosis. Presence of 3 or more RBCs per High Power Field on urine sediments is defined as microscopic hematuria although there is no "safe" lower limit of hematuria. [2] Urine appearance, pH, the presence of proteins, WBCs, nitrites, leukocyte esterase, crystals, and casts is helpful. A dirty urine specimen with significant WBCs and positive nitrites and leukocyte esterase suggests urinary tract infection and a likely cause of hematuria. The presence of excessive proteins with hematuria favors glomerulonephritis.

IgA nephropathy

A smaller proportion (20–30%), usually the older population, have microscopic hematuria and proteinuria (less than 2 gram/day). These patients may be asymptomatic and only picked up due to urinalysis. Hence, the disease is more commonly diagnosed in situations where screening of urine is compulsory (e.g., schoolchildren in Japan). Very rarely (5% each), the presenting history is: Nephritic syndrome Acute kidney failure (either as a complication of the frank hematuria, when it usually recovers or due to rapidly progressive glomerulonephritis which often leads to chronic kidney failure) Chronic kidney failure (no previous symptoms, presents with anemia, hypertension and other symptoms of kidney failure, in people who probably had longstanding undetected microscopic hematuria and/or proteinuria)

The presence of microscopic hematuria detected by urine dipstick test in the evaluation of patients with renal colic.

Urolithiasis is a common diagnosis in patients presenting at our hospital with flank pain. One of the most important steps in the diagnostic algorithm of renal colic is the presence of hematuria, but this fact has been challenged by authors reporting a negative urinalysis for microscopic hematuria in about 9-18% of such patients. Our aim was to investigate whether the same results are obtained when a sample of urine is tested with a urine dipstick test (UDT) at the time of the initial examination. Data from patients with the clinical diagnosis of renal colic examined at the emergency department of our hospital were reviewed, and the sensitivity of hematuria in urine samples tested by UDT was recorded in a group consisting of patients for whom imaging showed evidence of a stone >3 mm in size. In cases in which UDT was negative, or showed only traces of red blood cells (RBCs), a formal urinalysis was performed. A total of 609 patients were finally included in the study, with a mean age of 49.2 years. Average stone size was 5.8 mm, located mainly in the lower part of the ureter. Dipstick analysis was positive for hematuria in 92.9%. A urinalysis, with a cut-off point of less than three red blood cells per high power field, was used as a means to verify the results of the UDT in 17.8% of cases: in 7.1% of UDT negative patients and 10.7% of patients with traces of blood. The urinalysis was negative in 5.1% of patients, adding only 2% to the diagnostic accuracy of UDT. Therefore, our findings suggest that the sensitivity of a UDT for hematuria in cases of suspected renal colic has a high degree of accuracy when performed at the emergency department, and can be used as a first-line, low cost examination. A microscopic analysis may be useful when the UDT is negative or not clear enough, to verify the results.

Hematuria (Nursing) -- Evaluation

Hematuria

Hematuria or haematuria is defined as the occurrence of blood or red blood cells in the urine. The word hematuria is derived from Greek haima (αἷμα) "blood" and ouron (οὖρον) "urine". Hematuria can be visible to the naked eye (termed "gross hematuria") and may appear red or brown (sometimes referred to as tea-colored), or it can be microscopic (i.e. not visible to the eye but detected with a microscope or laboratory test). The origin of the blood that enters and mixes with the urine can arise from any anatomical site within the urinary system, including the kidney, ureter, urinary bladder, and urethra, and in men, the prostate. Common causes of hematuria include urinary tract infection (UTI), kidney stones, viral illness, trauma, bladder cancer, and exercise. The underlying causes of hematuria can be divided into glomerular and non-glomerular causes, referring to the involvement of the glomerulus of the kidney. Notably, not all red urine is hematuria. Other substances such as certain

Clinical urine tests

Microscopic examination The numbers and types of cells and/or material such as urinary casts can yield a great detail of information and may suggest a specific diagnosis. Hematuria – associated with kidney stones, infections, tumors and other conditions Pyuria – associated with urinary infections Eosinophiluria – associated with allergic interstitial nephritis, atheroembolic disease Red blood cell casts – associated with glomerulonephritis, vasculitis, or malignant hypertension White blood cell casts – associated with acute interstitial nephritis, exudative glomerulonephritis, or severe pyelonephritis (Heme) granular casts – associated with acute tubular necrosis Crystalluria – associated with acute urate nephropathy (or acute uric acid nephropathy, AUAN) Calcium oxalatin – associated with ethylene glycol, kidney stone disease Waxy casts – associated with chronic renal disease

Minimal Change Disease -- Evaluation -- Basic labs:

Urine collection: A spot protein/creatinine ratio greater than 200 mg/mmol in children and protein/creatinine ratio>300-350mg/mmol in adults is consistent with nephrotic syndrome, as is a 24-hour urine collection that reveals a total protein greater than 3 to 3.5 g/24hour in adults. A report of measuring protein output as gms/m2/hr accounts for differences in body mass. A measurement of 40mg/m2/hour or greater (1gm/m2/24hour) is indicative of proteinuria consistent with nephrotic syndrome in children. Microscopic hematuria is present in 10% to 30% of adults. [13]

Hematuria

After detecting and confirming hematuria with urinalysis and urine microscopy, the first step in evaluation of microscopic hematuria is to rule out benign causes. Benign causes include urinary tract infection, viral illness, kidney stone, recent intense exercise, menses, recent trauma, or recent urological procedure. After benign causes have resolved or been treated, a repeat urinalysis and urine microscopy is warranted to ensure cessation of hematuria. If hematuria persists (even if there is a suspected cause), the next step is to stratify the risk of the person for urothelial cancer into low, intermediate, or high risk to determine next steps. To be in the low risk category, one must satisfy all of the following criteria: Has never smoked tobacco or smoked less than 10 pack-years; is a female less than 50 years old or a male less than 40 years old; has 3-10 red blood cells per high power field; has not had microscopic hematuria before; and has no other risk factors for urothelial

False 'hematuria' due to bacteriuria.

To determine the effects of bacteriuria on dipstick urinalysis for microhematuria. Selection of urine samples with dipstick readings of at least one plus (+) for blood, followed by microscopic examination and bacterial culture, from patients with signs and symptoms of urinary tract diseases. A large teaching hospital in Melbourne, Australia. Two hundred forty-six inpatients and outpatients being investigated for signs and symptoms of urinary tract diseases. Seventeen (7%) of 246 patients having within-reference erythrocyte counts had polymicrobic cultures. One hundred nine patients had slight hematuria (1 x 10(7) to 6 x 10(7) cells/L). Of these, 21 bacteriuric patients had significantly higher dipstick findings than 88 abacteriuric patients (P < .005, Fisher's Exact Probability Test, two-tailed). Hydroperoxidase was detected in 80% of isolates (in 27 of 27 gram-negative bacilli cultures, in 6 of 6 staphylococci cultures, and in 3 of 12 streptococci cultures) on agar medium and in 69% of isolates in urine. These results show that patients without hematuria but with bacteriuria may give a false-positive dipstick reading for blood.

Nephritic syndrome

Signs and symptoms Historically, nephritic syndrome has been characterized by blood in the urine (hematuria), high blood pressure (hypertension), decreased urine output <400 ml/day (oliguria), red blood cell casts, pyuria, and mild to moderate proteinuria. If the condition is allowed to progress without treatment, it can eventually lead to azotemia and uremic symptoms. This constellation of symptoms contrasts with the classical presentation of nephrotic syndrome (excessive proteinuria >3.5 g/day, low plasma albumin levels (hypoalbuminemia) <3 g/L, generalized edema, and hyperlipidemia).

InternalMed_Harrison

Patients with glomerular disease usually have some hematuria with varying degrees of proteinuria. Hematuria is typically asymptomatic. As few as three to five red blood cells in the spun sediment from first-voided morning urine is suspicious. The diagnosis of glomerular injury can be delayed because patients will not realize they have microscopic hematuria, and only rarely with the exception of IgA nephropathy and sickle cell disease is gross hematuria present. When working up microscopic hematuria, perhaps accompanied by minimal proteinuria (<500 mg/24 h), it is important to exclude anatomic lesions, such as malignancy of the urinary tract, particularly in older men. Microscopic hematuria may also appear with the onset of benign prostatic hypertrophy, interstitial nephritis, papillary necrosis, hypercalciuria, renal stones, cystic kidney diseases, or renal vascular injury. However, when red blood cell casts (see Fig. 62e-34) or dysmorphic red blood cells are found in the sediment,

Hematuria -- Introduction

Hematuria is the presence of blood in the urine. Hematuria can be gross or microscopic. Gross hematuria is visible blood in the urine. Microscopic hematuria refers to the detection of blood on urinalysis or urine microscopy. Hematuria can be intermittent or persistent. Hematuria is defined as the presence of at least 5 red blood cells/HPF in 3 of 3 consecutive centrifuged specimens obtained at least 7 days apart. Hematuria may be asymptomatic or symptomatic and may be associated with other urinary tract abnormalities. Hematuria is often first encountered by the primary care provider.

Proteinuria

Protein dipstick measurements should not be confused with the amount of protein detected on a test for microalbuminuria which denotes values for protein for urine in mg/day versus urine protein dipstick values which denote values for protein in mg/dL. That is, there is a basal level of proteinuria that can occur below 30 mg/day which is considered non-pathology. Values between 30 and 300 mg/day are termed microalbuminuria which is considered pathologic. Urine protein lab values for microalbumin of >30 mg/day correspond to a detection level within the "trace" to "1+" range of a urine dipstick protein assay. Therefore, positive indication of any protein detected on a urine dipstick assay obviates any need to perform a urine microalbumin test as the upper limit for microalbuminuria has already been exceeded. Analysis It is possible to analyze urine samples in determining albumin, hemoglobin and myoglobin with an optimized MEKC method.

Is the red cell morphology really useful to detect the source of hematuria?

Morphological analysis of urinary red blood cells by phase-contrast microscopy to identify the source of bleeding was, and still is, widely used also as a starting point for workup. To evaluate the reliability of this approach, we studied 129 outpatients presenting with persistent isolated microhematuria; 31 subjects also had mild proteinuria (1 g/day), while 21 had pathological albumin levels. All patients were followed for a period of 6 years. During this time, 6 patients underwent renal biopsy for the onset of macrohematuria episodes and proteinuria of 2-3 g/day. Glomerular bleeding was identified in only 14.7% of the patients, despite the persistent microhematuria and the presence of proteinuria or microalbuminuria. The renal origin of the urinary erythrocytes correlated with histological findings in only 2 of 6 patients with dysmorphic erythrocytes who developed proteinuria (exceeding 1 g/day), and none with isomorphic erythrocytes showed urological abnormalities. These results challenge the validity and reliability of morphological analysis to identify the source of bleeding along the urinary tract.

Hematuria

can be divided into glomerular and non-glomerular causes, referring to the involvement of the glomerulus of the kidney. Notably, not all red urine is hematuria. Other substances such as certain medications and foods (e.g. blackberries, beets, food dyes) can cause urine to appear red. Menstruation in women may also cause the appearance of hematuria and may result in a positive urine dipstick test for hematuria. Additionally, a urine dipstick test may be falsely positive for hematuria due to other substances in the urine such as myoglobin during rhabdomyolysis. A positive urine dipstick test should be confirmed with microscopy, where hematuria is defined by three of more red blood cells per high power field. When hematuria is detected, a thorough history and physical examination with appropriate further evaluation (e.g. laboratory testing) can help determine the underlying cause.

Hematuria

In terms of the visibility, hematuria can be visible to the naked eye (termed "gross hematuria") and may appear red or brown (sometimes referred to as tea-colored), or it can be microscopic (i.e. not visible to the eye but detected with a microscope or laboratory test). Microscopic hematuria is present when there are three of more red blood cells per high power field.

Hemoglobinuria

Causes Acute glomerulonephritis Burns Renal cancer Malaria Paroxysmal nocturnal hemoglobinuria Microangiopathies, e.g. hemolytic-uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP) leading to microangiopathic hemolytic anemia Transfusion reactions IgM autoimmune hemolytic anemia Glucose-6-phosphate dehydrogenase deficiency Pyelonephritis Sickle cell anemia Tuberculosis of the urinary tract March hemoglobinuria secondary to repetitive impacts on the body, usually the feet Athletic nephritis secondary to strenuous exercise Acute lead poisoning Diagnosis The diagnosis is often made based on the medical history, blood samples, and a urine sample. The absence of urine RBCs and RBC casts microscopically despite a positive dipstick test suggests hemoglobinuria or myoglobinuria. The medical term for RBCs in the urine is hematuria. See also Hematuria References External links Abnormal clinical and laboratory findings for urine

Hypertensive kidney disease

Malignant nephrosclerosis is where hypertensive nephrosclerosis occurs in presence of malignant hypertension (when DBP > 130mmHg). Vessels feature intimal thickening, fibrinoid necrosis, red blood cell fragmentation, extravasation, thrombosis. These changes create an exaggerated layered appearance (onion skinning). Urine test Microalbuminuria (moderate increase in the levels of urinary albumin) is a non-specific finding in patients with vascular disease that is associated with increased risk of cardiovascular events. The majority of patients with benign nephrosclerosis have proteinuria in the range from 0.5 to 1 g/ 24hr. In the case of glomerular damage occurring in HN, hematuria can occur as well.

Crescentic Glomerulonephritis -- Evaluation

Complete blood count may show leukocytosis and anemia; inflammatory markers such as ESR and C-reactive protein, as are urea and serum creatinine, are usually elevated. Urinalysis shows modest proteinuria (1 to 4 g/d), microscopic hematuria, RBCs, and RBC and WBC casts. Rarely, urine findings may be minimal, and an absence of active urine sediment does not exclude a diagnosis of RPGN. [8] [9] [10] [11]

Loin pain hematuria syndrome

Diagnosis LPHS is considered a diagnosis of exclusion. The syndrome presents with hematuria (blood in the urine) and flank (a region of the lower back beneath the ribs and above the ilium) pain which can result from a number of causes. Nonglomerular causes of bleeding (e.g., urinary infection, tumor, or nephrolithiasis) must be excluded. Obstruction of the urinary tract should not be present, confirmed by at least two imaging procedures while pain is present. Diagnosis of loin pain-hematuria syndrome (LPHS) occurs when hematuria is present, recurrent or persistent pain is severe, and other causes of bleeding are excluded. Urine testing can be performed to detect microscopic levels of hematuria. Protein is also commonly found in the urine of patients with LPHS. Kidney biopsies are sometimes performed to look for evidence of glomerular hematuria, excess red blood cells in the kidney tubules, and to assess the width of the glomerular basement membrane.

Atypical Presentation of IgA Nephropathy Mimicking Acute Pyelonephritis.

IgA glomerulonephritis may present with hematuria, flank pain, and fever. This clinical presentation may be easily confused with acute pyelonephritis. We present the case of a 25-year-old female with a typical clinical presentation for acute pyelonephritis (high fever, left flank pain, left costovertebral angle tenderness, hematuria, elevated inflammatory markers, and a hypoenhancing region in the left kidney on contrast-enhanced computed tomography). However, urine and blood cultures were both negative, the serum creatinine was elevated, and the urinalysis revealed significant proteinuria and dysmorphic red blood cells. A kidney biopsy confirmed a diagnosis of IgA nephropathy. She was treated with a combination of lisinopril and methylprednisolone, with good response. Gross hematuria, especially in the absence of pyuria or bacteriuria, should raise the suspicion for underlying IgA nephropathy, even if the rest of the clinical presentation is typical for a urinary tract infection. The presence of significant proteinuria, red blood cell casts, and dysmorphic red blood cells are useful clues suggesting glomerular disease.

[Critical study of microscopic hematuria disclosed by screening tests].

Asymptomatic microscopic haematuria detected by dipstick in 0.28 p. 100 of 95,200 men was confirmed in only 0.11 p. 100. These results lead to the study of 272 cases to determine the value of dipsticks as a screening test and the benefits of complementary investigations to exclude symptomless diseases. Microscopic haematuria was confirmed in 65 p. 100 but results of other tests reduce the false positive screening results to 25.3 p. 100. Addis counting of at least 5,000 RBC/min is preferable to RBC count/ml which is dilution dependent. 77 p. 100 of microscopic haematuria are intermittent and can only be diagnosed by repeated Addis counts. In the absence of confirmed haematuria, only investigations to exclude proteinuria and urinary infections are justified.


Urgent surgical treatment by thromboembolectomy.

An 85-year-old man in permanent atrial fibrillation consults for abrupt pain and coldness in the right foot for 6 hours. On examination he presents plantar cyanosis with partial sensory and mobility deficit. The femoral pulse is palpable, while the popliteal and distal pulses of this extremity are absent. Which of the following is the best therapeutic approach?

Discourage revascularization surgery because of prolonged ischemia time.

Apply heat and notify the on-call vascular surgeon.

Urgent surgical treatment by thromboembolectomy.

Urgent medical treatment with intravenous prostaglandins.

Acute limb ischemia: surgical thromboembolectomy and the clinical course of arterial revascularization at ankle.

Surgical thromboembolectomy for acute limb ischemia using Fogarty catheter is basically a blind procedure. Therefore, the complete removal of thromboemboli in all calf arteries is difficult even if completion angiography or radiological intervention is performed. The purpose of this study is to identify whether limb salvage could be achieved if at least one ankle artery was revascularized by surgical thromboembolectomy. We also observed the effectiveness of below-knee popliteal approach. Over 1 year, surgical thromboembolectomy via below-knee popliteal artery was performed on 18 acutely ischemic limbs in 14 consecutive patients. All patients were diagnosed based on clinical symptoms and computed tomography (CT) angiography. Surgical thromboembolectomy was terminated when a pulse was detected by a handheld vascular Doppler device in at least one ankle artery after closing the arteriotomy. Patients were observed during postoperative anticoagulation therapy. Of the 14 patients, 1 died and 1 underwent amputation due to the already necrotized lesion in the foot. After 1 week of anticoagulation therapy, two or more arterial pulses were detected at the ankles in all 15 limbs from the remaining 12 patients. During the 6 to 18 months of follow-up, all 15 limbs were salvaged successfully. In acute limb ischemia, successful limb salvage could be achieved by the revascularization of at least one ankle artery by surgical thromboembolectomy with concomitant anticoagulation therapy. Below-knee popliteal approach is an effective method and is worth for further study compared with other approaches.

Successful Conservative Treatment of an Acute Arterial Occlusion After Total Knee Arthroplasty: Report of 2 Cases and Review of the Literature.

BACKGROUND Acute arterial occlusion after total knee arthroplasty (TKA) is a rare but occasionally limb-threatening complication. Successful outcomes of surgical treatment for acute arterial occlusion after TKA have been frequently reported in the literature; however, few reports have described conservative treatment. This case report describes the successful conservative treatment of popliteal artery occlusion after TKA. CASE REPORT We report 2 cases of popliteal artery occlusion after TKA that were managed with conservative treatment. In Case 1, a 68-year-old woman presented with a weak dorsalis pedis pulse in the foot and weakness to dorsiflexion of the toe on the operative side immediately after TKA. The operative lower extremity arterial ultrasonography and computed tomography angiography demonstrated the popliteal artery occlusion. In Case 2, a 79-year-old woman presented a cold right foot and lack of popliteal and dorsalis pedis pulse in the operated extremity immediately after TKA, and Doppler ultrasound did not reveal a flow for the dorsalis pedis artery. In both patients, urgent angiographies showed popliteal artery occlusion, and blood flow was observable in the anterior tibial, peroneal, and foot arteries collateral perfusion. Thus, conservative treatments were chosen, and anticoagulant and vasodilator therapies were undergone in both patients. At 6 months after surgery, they were able to walk without intermittent claudication. CONCLUSIONS Conservative treatment can be a good option for popliteal artery occlusion after TKA in cases of rich collateral circulation.

Hyperbaric oxygenation combined with streptokinase for treatment of arterial thromboembolism of the lower leg.

Thromboembolic occlusion of peripheral arteries is a common problem in patients referred to vascular surgery departments. Standard treatments include catheter aspiration techniques, use of fibrinolytic agents and surgical thrombendarterectomy. Recent reports have described the use of hyperbaric oxygen therapy in patients with limb ischemia, yet their main focus has been on patients with chronic disorders. We present the case of a 74-year-old woman with atrial fibrillation and acute thromboembolic occlusion of the posterior tibial artery. The patient presented with severe pain in the right calf, unresponsive to non-opioid parenteral analgesia and accompanied by coldness, numbness and partial motor palsy of the right foot. After 60 minutes of oxygenation in a hyperbaric chamber with a pressure of 2.2 bar, the pain receded, although without signs of restored blood flow in the occluded artery. After fibrinolytic therapy with streptokinase, patency of the posterior tibial artery was verified by return of palpable pulsations and color Doppler ultrasonography. By combining hyperbaric oxygenation and streptokinase in the treatment of lower-leg arterial thromboembolism we achieved regression of ischemic pain, prolongation of the survival time of tissues compromised by ischemia and resolved the cause of the ischemia. We believe the use of this therapeutic strategy in selected cases of peripheral arterial thromboembolism is justified.

Acute Limb Ischemia: A Rare Complication of COVID-19.

A 60-year-old male with a history of primary hypertension presented to the emergency department of a tertiary care hospital, in Pakistan, with complaints of fever, cough, and shortness of breath. He tested positive for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) polymerase chain reaction, with bilateral infiltrates found in chest X-ray. At admission, oxygen saturation was 80% on room air; hence, he was immediately put on non-invasive ventilation. Laboratory investigation revealed elevated D-dimer, international normalized ratio, and total leukocyte count. C-reactive protein was markedly elevated (82.5 mg/L), indicating the state of a cytokine release syndrome (CRS). Treatment started with antibiotics, prophylactic enoxaparin (40-mg subcutaneous once daily), methyl prednisone 60 mg BD and multivitamins. Intravenous tocilizumab (TCZ) 6 mg/kg was started from Day 1 to address the CRS. On Day 3, he complained of pain in the right lower limb with signs of hypothermia, numbness, and slight blackening of the right foot. Peripheral pulses were not palpable, and vascular ultrasound showed no vascular flow in the popliteal, anterior and posterior tibial, and dorsalis pedis artery. The Vascular Surgery department declared the limb unsalvageable and right limb above-knee amputation. On Day 9, the right foot was blackened and atrophied extending up to the knee. Above-knee amputation was done, and he was discharged on rivaroxaban after 48 hours of observation. We conclude that heparin is effective in treating coronavirus disease 2019-associated coagulopathy, while TCZ, simultaneously, decreases the severity of CRS. Our case suggests that the concomitant use of TCZ and anticoagulation therapy can be beneficial in patients presenting with arterial and venous thrombosis.

Surgery_Schwartz

manifests with the “five Ps”: pain, pallor, paresthesias, paralysis, and pulselessness, to which some add a sixth “P”—poikilothermia or “perishing cold.” Pain is the usual symptom that causes a patient to present to the emergency room. The most common location for an embolus to lodge in the leg is at the common femoral bifurcation. Typically, a patient will complain of foot and calf pain. Pulses are absent, and there may be diminution of sensation. Inability to move the affected muscle group is a sign of very severe ischemia and necessitates urgent revascularization. During evaluation of the affected extremity, it is important to compare findings with the contralateral limb. Clinical evaluation is extremely important in determining the etiology and location of the obstruction. One of the most important pieces of information to obtain is whether the patient has had prior vascular procedures or if there is a history of lower extremity claudication. Either of these features suggests

[Acute limb ischemia from the general surgeon's point of view. How much knowledge of vascular surgery is necessary?].

The diagnosis of acute peripheral ischemia can be obtained based on clinical presentation, inspection, and palpation of the affected extremity. Unfractionated heparin as a single shot is immediately given followed by continuous infusion when diagnosis is clinically evident and contraindications are excluded. Thromboembolectomy using a Fogarty catheter is immediately performed in patients with evidence of arterial embolization and signs of advanced ischemia (TASC IIb/III) followed by intraoperative angiography. Patients with evidence of arterial thrombosis require urgent angiography followed by thrombectomy and probably subsequent endovascular or surgical interventions and vascular reconstruction. For patients with moderate ischemia (TASC IIa), initial diagnostic angiography is recommended followed by primary thrombectomy with subsequent intraoperative angiography and immediate endovascular or operative treatment of remaining vascular problems. As an alternative therapeutic option initial catheter-guided local thrombolysis can be performed in selected patients with the intention of subsequent limb revascularization or unmasking relevant vessel alterations leading to specific endovascular or surgically performed vascular reconstruction. Possible development of muscle ischemia because of increased compartment pressure should be considered and fasciotomy performed when indicated. Primary amputation of the severely ischemic limb after initial thrombectomy might be recommended in patients with life-threatening organ failure related to muscle necrosis.

Mobile biatrial thrombus in a patient with mitral stenosis under heparin infusion.

A 58-year-old female patient with complaints of sudden presenting pain and pallor on her left foot was referred to our clinic for urgent embolectomy. On her cardiovascular examination there was an apical grade 2/6 systolic murmur and a grade 2/4 diastolic murmur. The presenting electrocardiography revealed atrial fibrillation with rapid ventricular response. She underwent emergent femoro-popliteal embolectomy. Transthoracic echocardiography showed a mobile 1.4 x 1.7-cm sized left atrial thrombus, mild mitral regurgitation and 9 mmHg mean gradient on mitral valve after embolectomy. Unfractioned (UF) heparin infusion was initiated immediately after surgery. After three days, the control transthoracic echocardiography revealed left atrial thrombus and also a large 'snake-like' thrombus waving in right atrium. The patient underwent biatrial thrombectomy and mitral valve replacement. When she became haemodynamically stable, a bilateral lower limb venous Doppler ultrasonographic study was performed. This study indicated a thrombus formation in the deep veins of the left leg. The origin of the right atrial thrombus was probably a snapped piece of thrombus from the calf deep-veins after the initiation of intravenous UF heparin. In summary, we have reported an extremely rare case of biatrial thrombus in a patient under UF heparin infusion.

Surgery_Schwartz

an initiating event. While the instances of acute leg ischemia caused by emboli have decreased due to more effective treatment of rheumatic fever and atrial fibrillation, the incidence of thrombotic acute leg ischemia has increased. Even with the extensive use of newer endovascular techniques including thrombolysis, most published series report a 10% to 30% 30-day amputation rate.115 The short-term mortal-ity of patients presenting with acute ischemia is 15% to 20%. The most common etiologies of ALI include embolism, native vessel thrombosis, reconstruction thrombosis, trauma, and com-plications of peripheral aneurysm. Most cases of lower extrem-ity ALI are the result of thrombosis of a prosthetic conduit. This stems from increased use of prosthetic conduits to address CLI.Presenting symptoms in ALI are pain and loss of sensory or motor function. The abruptness and time of onset of the pain, its location and intensity, and change in severity over time should all be taken into

Dick Cheney

On September 24, 2005, Cheney underwent a six-hour endo-vascular procedure to repair popliteal artery aneurysms bilaterally, a catheter treatment technique used in the artery behind each knee. The condition was discovered at a regular physical in July, and was not life-threatening. Cheney was hospitalized for tests after experiencing shortness of breath five months later. In late April 2006, an ultrasound revealed that the clot was smaller. On March 5, 2007, Cheney was treated for deep-vein thrombosis in his left leg at George Washington University Hospital after experiencing pain in his left calf. Doctors prescribed blood-thinning medication and allowed him to return to work. CBS News reported that during the morning of November 26, 2007, Cheney was diagnosed with atrial fibrillation and underwent treatment that afternoon.

Surgical Thrombectomy, Fibrinolysis, Angioplasty and Stenting: A Combined Approach for Treatment of a May-Thurner Syndrome Presenting as Phlegmasia Cerulea Dolens.

Phlegmasia cerulea dolens (PCD) is a rare complication of deep venous thrombosis (DVT). Massive ileo-femoral DVT is usually the cause and prompt treatment is mandatory as it represents a medical emergency. Reported amputation rates range from 12% to 25% and mortality ranges from 25% to 40%. Limb ischemia results from obstruction to arterial inflow secondary to extreme levels of venous hypertension. Primary treatment goal is restoration of venous outflow and can be achieved by endovascular or surgical techniques. After thrombus removal an underlying iliac vein stenosis may be present. May-Thurner syndrome, a condition where the left common iliac vein is compressed by the right iliac artery, is the most prevelant iliac stenotic lesion. We report a case of a 57 years-old male, smoker, with no significant medical history, who presented to the emergency department with excruciating sudden left limb pain and swelling, with no trauma history, with a 2-hour onset. On physical examination he showed significant edema, purplish discoloration of the entire leg and absent dorsalis pedis artery pulse. Hipocoagulation with intravenous heparin was immediately initiated and emergent surgical venous thrombectomy was performed associated with direct intravenous fibrinolytic agent injection. Postprocedure phlebography showed a left common iliac vein lesion which was treated with angioplasty and venous stent placement. Pain, edema and coloration improved markedly after procedure without any complications. The patient was discharged home with anticoagulation treatment and compression stocking. Endovascular approaches such as catheter-directed thrombolysis (CDT) or pharmacomecanical thrombolysis (PMT) are becoming the treatment of choice to achieve venous outflow in DVT. In cases of PCD, when rapid restauration of venous outflow is mandatory, CDT has the disadvantage of having a long mean treatment time. This way, surgical thrombectomy still plays an important role in cases of PCD, especially if PMT is not available. In our case, the combined used of surgical thrombectomy with direct intravenous thrombolytic infusion provided effective treatment of PCD and uncovered an underlying left common iliac vein stenosis, which was successfully managed by angioplasty and stenting.

Acute Thromboembolism from Trauma in a Patient with Abdominal Aortic Aneurysm.

A 64-year-old man with a history of a 5.5-centimeter (cm) abdominal aortic aneurysm (AAA) presented to the emergency department (ED) complaining of severe back pain after climbing over a fence and falling a distance of eight feet. Prior to arrival, the prehospital paramedics reported that the patient did not have palpable pulses in either lower extremity. The initial physical examination in the ED was significant for absent dorsalis pedis pulses bilaterally as well as absent posterior tibialis pulses bilaterally and cold, insensate lower extremities. Point-of-care ultrasound identified an approximate 7-cm infrarenal AAA with a mural thrombus present. After receiving several computed tomography (CT) studies including CT head without contrast and CT angiography of the chest, abdomen and pelvis, the patient was diagnosed with acute thrombosis of AAA and associated thromboembolic occlusion of both his right and left distal iliac vessels causing bilateral acute limb ischemia. He immediately received unfractionated heparin and was admitted to the hospital for embolectomy and intra-arterial tissue plasminogen activator. Acute thrombosis of AAA and subsequent thromboembolic events are a rare but significant complication that can occur in patients with a history of AAA. Thromboembolic events may occur spontaneously or in the setting of blunt abdominal trauma. Common presenting signs and symptoms include distal limb ischemia and absent femoral pulses. Timely management and recognition of this rare complication is vital as this condition can ultimately result in limb loss or death if not treated in a timely manner. Heparinization after confirmation of non-ruptured AAA as well as vascular surgery, and therapeutic and vascular interventional radiology consultations are key steps that should be taken to decrease patient morbidity and mortality.

[Septic splenic infarction after acute arterial embolism].

A 62-year-old woman was admitted because of sudden onset of increasingly severe pain in the left lower leg and foot. She also reported having had diarrhoea for the past few days. Physical examination revealed a cold and pale left leg below the knee joint. Peripheral sensory and motor functions were normal. While femoral and popliteal arterial pulses were normally palpable, foot pulses were not felt. Magnetic resonance angiography of the pelvic and leg arteries showed an embolic occlusion of the left popliteal artery extending to the arteries of the lower leg. Because of the acute embolic occlusion of the deep femoral and popliteal arteries an embolectomy of the deep and superficial femoral arteries was performed. The source of the emboli had been a free-floating thrombus in the descending aorta. Subsequently a persistent fever and leukocytosis occurred which had been cause by a septic splenic infarction. A conventional splenectomy was done. The postoperative was protracted, because of the development of a pancreatic fistula, which responded to treatment. Anticoagulation treatment started. The patient was finally discharged after more than five weeks. After urgent surgical treatment of an acute peripheral arterial occlusion its cause needs to be identified. Transthoracic echocardiography, computed tomography and magnetic resonance angiography are the methods of choice. If there is a floating aortic thrombus further embolizations, including septic splenic emboli may occur.

Vascular obstruction at the level of the ankle joint as a complication of hip arthroscopy.

We report a case of foot vascular obstruction as a complication of hip arthroscopy. A 23-year-old female patient underwent hip arthroscopy for femoroacetabular impingement. The duration of the procedure was 80 minutes, including 20 minutes with traction for arthroscopy of the central compartment and 60 minutes without traction for cam treatment in the peripheral compartment. Three days postoperatively, the patient complained of a cold foot and pain and paresthesia during leg and foot elevation with continuous passive motion therapy. With persisting symptoms, she was seen by the referring physician 4 days postoperatively. Pulselessness at the level of the ankle and reduced capillary perfusion were observed. Doppler sonography and magnetic resonance angiography showed an occlusion of the peroneal, posterior tibial, and anterior tibial arteries at the level of the right ankle. The patient was readmitted to the hospital and underwent intravenous prostaglandin E1 therapy for 9 days, followed by oral clopidogrel treatment for 6 weeks. After 8 weeks, follow-up Doppler sonographic findings were normal. Subjective paresthesia and sensation of coldness resolved completely after 6 months. Possible theories for this complication and strategies on how to avoid it are discussed.

Central Nervous System and Limb Embolism Concurrence due to Atrial Myxoma: A Case Report.

Cardiac myxomas are the most common cardiac tumors with diverse nonspecific clinical manifestations. A 78-year-old man presented to the emergency department with complaints of pain and coldness of the left lower extremity. The left femoral artery pulse was detected, while the pulses of the left popliteal, dorsalis pedis, and posterior tibialis arteries were absent. No blood inflow was detected in the superficial and deep femoral, popliteal, and anterior and posterior tibialis arteries. Thrombectomy was performed, and a fatty-like mass from the bifurcation of the common femoral artery and a thrombotic mass from the proximal portion of the superficial and deep femoral arteries were removed. The pulsatile inflow and palpable pulses of the left femoral, popliteal, dorsalis pedis, and posterior tibialis arteries were restored after surgery. The histological findings of the embolus were suggestive of a cardiac myxoma. The patient's consciousness and lower limb blood flow improved gradually. He was discharged from the hospital with full awareness and improved lower extremity muscle function 2 weeks after surgery.

[Arterial embolisms of the lower extremities].

Embolism is one of the most frequent causes of lower limbs acute arterial occlusion [1]. Of the total number of peripheral embolism 56% of cases involve lower limbs arteries [2]. Inadequate and late treatment of the lower limbs embolism is associated with high morbidity and mortality rate. The aim of this paper was to study the aetiology of lower limbs embolism and to detect factors influencing early and late results after the operative treatment. The study included 204 patients with 224 lower limbs embolism, treated surgically at the Institute of Cardiovascular Diseases of the Clinical Centre of Serbia in Belgrade in the period between 1993 and 1997. There were 107 (52.2%) female and 97 (47.8%) male patients. Thirty two (14.3%) patients were younger than 50 years, 64 (28.6%) were between 51 and 65, 101 (45.1%) between 66-75, while 27 patients (12.1%), were older than 75. Twenty (8.9%) patients were admitted less than 6 hours before the operation, 79 (33.3%) between 6 and 24 hours, and 125 (55.8%) more than 24 hours before the operation (Table 1). One hundred (53.6%) patients had motor and 133 (59.4%) sensor paralysis on admission. Table 2 shows arterial localization of the lower limbs embolism. The popliteal artery was involved in most cases. During the operation transfemoral arterial approach was used in 132 (58.9%) cases, while transpopliteal in 92 (41.1%) cases. Fourteen cases required bypass surgery, 43 fasciotomy, 2 intraoperative streptokinase and 4 intraoperative angiography. All patients were controlled using physical and CW Doppler ultrasonographic examinations immediately after the operation, and then one, six and 12 months, as well as every year. In 173 (84.4%) patients cardiac causes of embolism were found, in 8 (3.9%) noncardiac, while in 8 (3.9%) the cause could not be established. Of all cardiac causes absolute arrhythmia was most frequent. Table 3 and Table 4 show the aetiology of the lower limb embolism. The early amputation rate was 23 (10.3%) cases, while limb salvage was recorded in 174 (77.7%) patients. Of all saved limbs complete recovery was noted in 162 (72.4%) cases and peroneal nerve paresis in 12 (5.3%) cases. The early postoperative mortality rate was 27 (12.0%). Table 5 shows early results of embolectomy. The early results (limb salvage, complete recovery, rethrombosis, early reoperations, amputations rate, morbidity and mortality rate) of embolectomy were statistically significant: worse in cases when the embolus was located in the abdominal aorta and popliteal artery; in cases with a long time interval before the operation as well as in patients with sensor-motoric paralysis on admission (Tables 6-8). Of the total number of patients in 87 (56.5%) cases a late control examination was carried out. Forty nine (31.8%) patients died before the late control, while 18 (11.7%) did not come to control examination. Late recidivation of embolism was found in 3 cases. In these patients the cause could not be found, and they were treated by anticoagulant drugs.

Surgery_Schwartz

the most important pieces of information to obtain is whether the patient has had prior vascular procedures or if there is a history of lower extremity claudication. Either of these features suggests preexisting vascular disease, renders revasculariza-tion more complicated, and usually mandates angiography to permit surgical planning. On the contrary, in a patient with no history suggestive of prior vascular disease, the etiology is most likely embolic, and simple thrombectomy is more likely to be successful.Absent bilateral femoral pulses in a patient with bilateral lower extremity ischemia is most likely due to saddle embolus to the aortic bifurcation. A palpable femoral pulse and absent popliteal and distal pulses may either be due to distal common femoral embolus (the pulse being palpable above the level of occlusion) or embolus to the superficial femoral or popliteal arteries. Typically, emboli lodge at arterial bifurcations where they are trapped due to sudden reductions in

Vascular evaluation and arterial reconstruction of the diabetic foot.

Findings of diminished or absent pulses, pallor on elevation, redness of the foot on lowering of the leg, sluggish refilling of the toe capillaries, and thickened nails or absence of toe hair are consistent with impaired arterial perfusion to the foot. When ischemia is recognized as contributing to pedal ulceration and infection in the diabetic foot, quantitation of its severity may be difficult. Standard clinical evaluation of trophic changes is limited in an infected foot with its accompanying swelling, edema, and erythema. A palpable pedal pulse does not preclude the possibility of the presence of limb-threatening ischemia. Additional non-invasive vascular studies should be undertaken for these patients. Management of the diabetic foot is often a complex clinical problem. However, the principles of care are simple, including correction of systemic factors, such as blood glucose control, cardiovascular risk factor management, and smoking, as well as local factor correction, such as debridement, pressure relief, infection control, and revascularization when indicated. When a patient presents with evidence of infection, adequate drainage and antibiotic therapy are mandatory. The next step should be performed to differentiate the more common neuropathic ulcerations from the truly ischemic ulceration. Symptoms of rest pain or claudication are not often helpful because many of these patients are asymptomatic as a result of the presence of their neuropathy and inactivity. If an infected foot requires debridement or open partial forefoot amputation, observing the wound on a daily base is also important. Once infection is eradicated, there should be prompt signs of healing, including the development of wound granulation within several days. If wounds are not showing signs of prompt healing, arteriography is necessary. Early aggressive drainage, debridement, and local foot amputations combined with liberal use of revascularization results in cumulative limb salvage of 74% at 5 years in high-risk groups. Others report that pedal bypass to the ischemic infected foot is effective and safe as long as infection adequately controlled. These studies strongly suggest that early recognition and aggressive surgical drainage of pedal sepsis followed by surgical revascularization is critical to achieving maximal limb salvage in the high-risk population. Patients who have diabetes present a unique challenge in lower extremity revascularization because of the distal origination of many bypasses, distal distribution of the occlusive disease, and the frequently calcified arterial wall. An aggressive multidisciplinary approach to foot disease associated with diabetes involving the primary care provider, medical specialists, interventional radiology, and podiatric, plastic, and vascular surgeons will provide optimal medical and surgical care. Peripheral vascular disease is highly treatable if intervention is instituted in a timely and collegial fashion.

[Surgical therapy of acute and chronic arterial occlusions below the inguinal ligament].

The history and physical examination are extremely important in the management of vascular surgical patients because a correct diagnosis can usually be made on the basis of information obtained from these two modalities. The severity of the chronic occlusive process leads to characteristic symptoms in the extremity: claudication, rest pain, skin ulcerations and gangrene. Chronic progressive lesions permit enlargement of collateral blood supply which, for a time, minimizes the severity of symptoms. Milde degrees of arterial insufficiency (claudication) can be treated conservatively. Unreconstructed chronic critical ischemia predicts a poor outcome in terms of survival and limb salvage. The outlook with arterial reconstructive surgery is by far better. Arteriography ist the most reliable diagnostic test for occlusive lesions. It ist essential for the operative planning. Vein-bypass procedures are, if feasible, very effective in most cases. Acute embolic occlusion: Sudden occlusion of a previously patent artery is usually a dramatic event producing severe ischemia of the distal tissue. The characteristic symptoms and signs are the 5 P's: pallor, pain, paresthesia, paralysis, pulselessness. Emergent restoration of blood flow by operation may be essential to prevent limb loss. Milder forms of ischemia (acute thrombosis--acute or chronic disease) can be treated initially with intravenous heparin if the extremity is not threatened (minimal sensory loss, no muscle weakness). Elective surgery at a later date is highly successful.

Reversal of ergotamine-induced vasospasm following methylprednisolone.

Ergotamine, an ergot alkaloid with partial agonist effects on alpha1 receptors and serotonin receptors, is widely used in the treatment of migraine. Ergotamine may cause severe vasospasm. A 25-year-old man was admitted to the emergency department with complaints of sudden coldness, pallor, and pain in his hands and feet for 2 days. He had been using a drug containing ergotamine for his migraine headaches for 1 week. On examination, the pulses of the radial, ulnar, popliteal, and tibial arteries were bilaterally undetectable. Treatment consisted of sodium nitroprusside and heparin. On the third day of the admission, bilateral brachial and femoral artery pulses were lost and his complaints exacerbated. Angiography revealed diffuse vasospasm of the arteries in the both lower extremities (Fig. 1A and C). Because of the lack of response to the ongoing therapy, a single dose of methylprednisolone sodium succinate (1 mg/kg) was given intravenously; the nitroprusside infusion was terminated because of the development of hypotension. The pulses were palpable 2 h after the methylprednisolone dose. Angiography done 12 h after the methylprednisolone dose showed improvement of the vasospasm in the lower extremities. Recovery was uneventful and follow-up evaluation found no abnormalities. Although vasodilator agents are first-line therapy in the treatment of ergotism, corticosteroids may be considered as an alternative therapy, especially for intractable cases. The mechanism by which corticosteroids dilate arteries is not clear. Ischemia in an extremity secondary to ergotamine-induced vasospasm unresponsive to sodium nitroprusside may be treated successfully with methylprednisolone.

Transient Monoplegia as a Result of Unilateral Femoral Artery Ischemia Detected by Multimodal Intraoperative Neuromonitoring in Posterior Scoliosis Surgery: A Case Report.

This is to report a case of 16-year-old girl with transient right lower limb monoplegia as a result of femoral artery ischemia detected by multimodal intraoperative spinal cord neuromonitoring (MISNM) during posterior correction surgery of adolescent idiopathic scoliosis.A patient with a marfanoid body habitus and LENKE IA type scoliosis with the right thoracic curve of 48° of Cobb angle was admitted for posterior spinal fusion from Th6 to L2. After selective pedicle screws instrumentation and corrective maneuvers motor evoked potentials (MEP) began to decrease with no concomitant changes in somato-sensory evoked potentials recordings.The instrumentation was released first partially than completely with rod removal but the patient demonstrated constantly increasing serious neurological motor deficit of the whole right lower limb. Every technical cause of the MEP changes was eliminated and during the wake-up test the right foot was found to be pale and cold with no popliteal and dorsalis pedis pulses palpable. The patient was repositioned and the pelvic pad was placed more cranially. Instantly, the pulse and color returned to the patient's foot. Following MEP recordings showed gradual return of motor function up to the baseline at the end of the surgery, whereas somato-sensory evoked potentials were within normal range through the whole procedure.This case emphasizes the importance of the proper pelvic pad positioning during the complex spine surgeries performed in prone position of the patient. A few cases of neurological complications have been described which were the result of vascular occlusion after prolonged pressure in the inguinal area during posterior scoliosis surgery when the patient was in prone position. If incorrectly interpreted, they would have a significant impact on the course of scoliosis surgery.

Approach to the patient with acute limb ischemia: diagnosis and therapeutic modalities.

Good patient outcomes depend on the rapidity and completeness with which re-establishment of arterial blood flow to the limbs occurs. Patients with a greater magnitude of ischemic tissue--such as with an acute aortic occlusion--have worse outcomes than patients with a segmental artery occlusion such as a popliteal arterial thrombosis. Limb loss is high in any situation in which a delay in diagnosis occurs. It is unclear whether or not endovascular therapy will supercede traditional surgery because the etiologies of ALI are too broad to make sweeping conclusions at this time. The author and others [14,15], including those who have promulgated the use of thrombolytic therapy, have come to reasonable conclusions regarding how to deal with ALI: The diagnosis of ALI should be established rapidly. Determine its classification based on the patient's history and physical examination, and promptly institute anticoagulant therapy. Determine whether or not the patient should be taken emergently for surgical thromboembolectomy or a revascularization procedure versus arteriogram and possible thrombolysis. Adjunctive therapy such as antiplatelet agents (e.g., GIIb/IIIa antagonists) and other anticoagulant agents must be better investigated before recommendations can be made. Save life over limb. Emergent guillotine amputation is sometimes required to save a patient's life.

Lift the quilt in case of atrial fibrillation and disc prolapse.

Peripheral embolism to the lower extremities may mimic disc prolapse with severe consequences. A 71-year-old male with a history of chronic alcoholism developed low back pain radiating to both lower extremities in a nonradicular distribution and bilateral dysesthesias of the distal lower legs after lifting a heavy weight. Given that magnetic resonance imaging (MRI) of the lumbar spine showed disc herniation in L3/4 and L4/5, he was scheduled for laminectomy but was unable to undergo surgery due to thrombocytopenia. After transfer to another hospital, persistence of symptoms and signs, absent pulses on the distal lower legs, and rhabdomyolysis with temporary renal insufficiency, peripheral embolism with compartment syndrome was suspected. Magnetic resonance angiography revealed occlusion of the right superficial femoral artery and long high-grade stenosis of the left superficial and profound femoral arteries and distal arteries. He successfully underwent embolectomy and fasciotomy. If lumbar pain is not radicular, peripheral pulses are minimally palpable, and distal limbs are cold and show livid decolorization, peripheral embolism is much more likely than disc herniation, particularly if the patient's history is positive for atrial fibrillation. MRI of the lumbar spine must be interpreted in conjunction with clinical presentation.

[The diagnosis of peripheral arterial embolism].

Acute embolic occlusion of a peripheral artery requires rapid and precise diagnosis in order to provide the appropriate treatment without delay. The symptoms and findings of acute arterial occlusion are characterized by "the six Ps": pain of sudden onset in the hypoperfused extremity, paleness, pulselessness, paresthesias, paralysis and, in the extreme case, prostration with the symptoms of shock. With embolization in arterial segments with only minimal residual perfusion via collaterals (for example, the femoral bifurcation), a complete ischemic syndrome is usually incurred manifesting the six Ps as delineated. If preformed collateral systems provide some perfusion distal to an arterial occlusion (for example, in the common iliac artery), there is frequently an incomplete ischemic syndrome observed which is characterized by pain, paleness and pulselessness. Peripheral arterial embolism has a predilection for the femoral bifurcation, the superficial femoral artery and the popliteal artery. In principle, however, embolization can occur in every arterial segment. The diagnosis of the acute ischemic syndrome can generally be established on the basis of the history and physical examination. Diagnostic aid can be provided by electronic segmental oscillography to demonstrate diminished or absent oscillations and with the Doppler sonographically-determined systolic arterial pressure at the ankle which, in the case of severe ischemia, is less than 50 mmHg. Arteriography provides the most accurate morphological information. Abrupt occlusion of the vessel and no collateral perfusion especially in the absence of arteriosclerotic changes are strongly indicative of embolism but not conclusive. If the clinical diagnosis is unequivocal, arteriography need not be performed prior to embolectomy with a Fogarty catheter.(ABSTRACT TRUNCATED AT 250 WORDS)

Revascularization

In medical and surgical therapy, revascularization is the restoration of perfusion to a body part or organ that has suffered ischemia. It is typically accomplished by surgical means. Vascular bypass and angioplasty are the two primary means of revascularization. The term derives from the prefix re-, in this case meaning "restoration" and vasculature, which refers to the circulatory structures of an organ. It is often combined with "urgent" to form urgent vascularization. Revascularization involves a thorough analysis and diagnosis and treatment of the existing diseased vasculature of the affected organ, and can be aided by the use of different imaging modalities such as magnetic resonance imaging, PET scan, CT scan, and X ray fluoroscopy.

[Our experience with peripheral arterial embolectomy].

34 cases of acute peripheral ischaemia examined in recent years at the University of Messina General Surgery Clinic are presented. 16 were subjected to embolectomy according to Fogarty. The remaining 18 received protracted medical therapy. Some successes were obtained. In other cases, gangrene necessitated amputation of the affected limb. Satisfactory results were observed in 70% of the operated series. Success was more marked when only a short interval was left between the embolic episode, with progressively poorer results as the penalty for delay. The long-term results of embolectomy are related to the nature of the underlying disease and the treatment given after surgery.

Acute Arterial Occlusion -- Treatment / Management

Cases of limb-threatening ischemia require emergent vascular surgery consult. The surgical approach is directed at the reperfusion of the affected extremity. This can be accomplished by surgical bypass, endarterectomy, or embolectomy. Results are variable and will ultimately depend on the duration of the ischemia and the extent of occlusion. Catheter-directed thrombolysis (CDT) by an interventional radiologist is becoming more common and is reserved for patients with a salvageable limb (Rutherford class II, IIa, and IIb). Patients presenting with profound paralysis and absent pain with inaudible arterial and venous pulses are considered to have irreversible damage and will require amputation. Surgical treatment options are typically reserved for more severe cases or where nonsurgical management fails. These options include the following: Open bypass surgery Endovascular therapy, such as stenting, balloon angioplasty, or atherectomy

Persistent sciatic artery aneurysm: a case report.

In early embryologic development the sciatic artery provides the blood supply to the lower limb bud. When the femoral artery develops, the sciatic artery involutes. However, in rare cases, the sciatic artery persists. It can be visualised as a prolongation of the inferior gluteal artery (branch of the internal iliac artery) and it accompanies the sciatic nerve at the posterior side of the hip. We present the case of a 47-year old woman who consulted because of a numb right foot which presented colder and paler than the left foot. She also had a right painful calf, especially after exercise. Upon physical examination and doppler ultrasound there were no popliteal nor pedal artery pulses in the right leg. CT angiography showed bilateral persistent sciatic arteries with aneurysm formation and the presence of an embolus in the popliteal artery at the right side. Treatment involved thrombolysis of the popliteal occlusion, followed by intra-aneurysmatic stent placement and embolectomy of the popliteal artery and its distal branches. Postoperative clinical results were remarkably good and the patients symptoms dissolved. A persistent sciatic artery is a rare vascular anomaly. It is more prone to vasculopathies such as aneurysm formation. In cases of acute ischemia, correct diagnosis and treatment of this anomaly can avoid serious medical consequences.

Treatment of critical limb ischemia in the elderly.

Acute critical limb ischemia (CLI) is a rather frequent clinical event in elderly patients. Atherosclerotic plaques or cardiopathies (atrial enlargement and fibrillation, ventricular thrombosis) are the most frequent clinical situations related to peripheral embolization. Rapid diagnosis followed by suitable treatment allows us to obtain good results even in elderly patients. The decision about the treatment of acute CLI is related to the clinical and functional condition of the patient. Anamnesis must inquire about recent ischemic or hemorrhagic events in the cardiovascular, gastro-intestinal and urinary apparatuses, or the presence of disorders of coagulation and fibrinolysis. An objective clinical examination and a multidimensional assessment must evaluate the degree of functional impairment and provide the basis of a therapeutic strategy (cost/benefit ratio). Diagnostic examination in the frail elderly patient (FP) involves only the ultrasonographic method, to localize the level of thromboembolic occlusion, which is followed by angiography in the non-frail patient (NFP). In the case of proximal occlusion (of the iliac or femoro-popliteal arteries), the elective treatment in both groups of patients is thromboendarterectomy, plus transcutaneous angioplastics or by-pass in NFP, followed by prostacyclin or heparin infusions. Distal occlusion (below the popliteal artery) in FP is treated only with prostacyclin or heparin, whereas in NFP, fibrinolysis is the elective treatment, followed by prostacyclin or heparin. In the cases of distal gangrene, before amputation is performed, a "limb salvage" operation must be considered. After the acute phase of medical or surgical treatment, vasoactive or antiplatelet drugs are employed in FP, whereas in NFP the use of coumadin is the preferred treatment to counteract the rethrombosis and prevent new embolizations. Antiplatelet therapy could be selected when coumadin is contra-indicated.

A successful surgical management and outcome for a young man with infrarenal aortoiliac occlusion: A rare case report of Leriche syndrome.

Leriche syndrome, also known as aortoiliac occlusive disease, is characterized by chronic obstruction of the abdominal aorta and iliac arteries. The disease was first described by Robert Graham in 1814. Leriche syndrome was named after a French surgeon, Rene Leriche, who first operated on the condition. We present a 35-year-old male patient who came to our cardiovascular polyclinic in a wheelchair. He had been complaining for a year about severe back pain, leg cramps on both sides, and weakness in both legs. Associated symptoms included fatigue, lower limb tingling, and numbness. Physical examination revealed pulselessness in the popliteal-dorsalis pedis and posterior tibial arteries in both lower extremities, and coldness and ulcers in the dorsum part of the foot. Leriche syndrome often presents with a triad of clinical symptoms: (1) intermittent lower extremity vascular claudication, (2) impotence, and (3) weak/absent femoral pulses. This case report contributes to the current literature when any patient has lower limb weakness, pain, and ulcers. It must be considered in our differential diagnosis list for Leriche syndrome. This makes us more aware of the need for early diagnosis and intervention to decrease late complications of ischemia. Leriche syndrome, also known as aortoiliac occlusive disease, is considered because of its high morbidity and mortality. This was the first case in Somalia to be successfully managed and operated on by using extra-anatomical bypass, especially axillo-bifemoral bypass, by using it as an emergency measure to save ischemic limbs and shorten the length of time in the hospital.

Does the new vascular management of acute limb ischemia have effective results with lower treatment costs.

Aim To compare hospital costs of acute limb ischemia treatment in two periods of time and to show evidence of long-term repercussions on reducing costs during successful treatment. Methods Retrospective analysis of data obtained from 100 patients' medical history in the period 2000-2016 at the Clinic of Vascular Surgery Sarajevo: group A - 60 patients with acute limb ischemia in the period 2005-2016 and group B - 40 patients with acute limb ischemia (ALI) in the period 2000-2005. From 2000 to 2005 conservative treatment method was used, invasive diagnostic and surgical procedures were often delayed for a shorter or longer period of time. During the period from 2005 to 2016, the management model and safe practice included emergency diagnostic procedures, colour-Doppler, arteriography, emergency surgery (embolectomy by Fogharty and if necessary, vascular by-pass). Results Better health service for the patients with acute limb ischemia was offered in the period 2005-2016, which relied on proven medical treatment trends. The largest share of the total costs of each patient included costs of hospital bed with significant difference between the period 2005-2016 and 2000-2005, mean of 1398.71 KM and 2480.45KM, respectively (p<0.0001), indicating rationalization of time that patients spend at the Vascular Clinic. Conclusion This trend of money/fund savings is an example of good practice, effectiveness and efficiency in the treatment of ALI and as such was used in patients with other vascular diseases.

Acute arterial thrombosis with antithrombin III deficiency in nephrotic syndrome: report of a case.

Nephrotic syndrome frequently causes venous thromboembolic complications. Arterial thrombosis has rarely been reported and is mainly observed in children. Only six cases of lower extremity arterial thrombosis in adults have been reported in the literature. The outcome in these cases was unsatisfactory because of the high rates of limb loss and recurrence of thrombosis. We report successful treatment of a 39-year-old man who suffered from right lower extremity arterial thrombosis associated with decreased levels of serum antithrombin III. He was admitted to our hospital with severe pain in his right foot. No pulse was palpable in his right dorsalis pedis or posterior tibial arteries. His right foot was cold and mottled, with a reduced sensation and motor activity. The laboratory data revealed a serum total protein concentration of 3.9g/dl and an albumin concentration of 1.5 g/dl. The coagulation profile showed a fibrinogen level of 879 mg/dl and antithrombin III value of 9.5%. Right lower extremity arteriography showed a complete occlusion of the right deep femoral artery and popliteal artery, and a filling defect in the common femoral artery. An emergency thrombectomy was performed under general anesthesia. The patient was treated successfully, and surgical treatment was followed by anticoagulant therapy with 1,000 units of antithrombin III. A renal biopsy revealed histologic evidence of minimal change of glomerulonephritis. He was discharged 3 months later, and no recurrence of thrombosis has yet been observed.

Popliteal Artery Occlusion in a Wrestler in the Absence of Known Trauma.

In brief: A college wrestler was first seen by an athletic trainer when he complained of a burning pain in his right foot. He recalled no traumatic event that might have caused the pain. He was referred to the athletic department's consulting podiatrist. An examination showed that the patient's right foot was cool and pale and that the pedal pulses were absent. Immediate referral was made to a vascular surgeon. A right femoral arteriogram showed complete occlusion of a 3.5-cm segment of the popliteal artery. A femoral popliteal artery bypass was performed. The patient recovered fully but was discouraged from participating in competitive sports.