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Cirrhosis: Practice Essentials, Overview, Etiology. Ascites, which is an accumulation of excessive fluid within the peritoneal cavity, can be a complication of either hepatic or nonhepatic disease. The 4 most common causes of ascites in North America and Europe are cirrhosis, neoplasm, congestive heart failure, and tuberculous peritonitis.

In the past, ascites was classified as being a transudate or an exudate. In transudative ascites, fluid was said to cross the liver capsule because of an imbalance in Starling forces. In general, ascites protein would be less than 2. L in this form of ascites. A classic cause of transudative ascites would be portal hypertension secondary to cirrhosis and congestive heart failure. In exudative ascites, fluid was said to weep from an inflamed or tumor- laden peritoneum.

In general, ascites protein in exudative ascites would be greater than 2. L. Causes of the condition would include peritoneal carcinomatosis and tuberculous peritonitis.

Nonperitoneal causes. Attributing ascites to diseases of nonperitoneal or peritoneal origin is more useful. Thanks to the work of Bruce Runyon, the serum- ascites albumin gradient (SAAG) has come into common clinical use for differentiating these conditions. Nonperitoneal diseases produce ascites with a SAAG greater than 1. L. Nonperitoneal Causes of Ascites .

Chylous ascites also may be observed in the setting of cirrhosis. The triglyceride concentration of the ascites is greater than 1. L and greater than that observed in plasma. Patients should be placed on a low- fat diet that is supplemented with medium- chain triglycerides. Treatment with diuretics and large- volume paracentesis may be required. Peritoneal causes.

Peritoneal diseases produce ascites with a SAAG of less than 1. L. Peritoneal Causes of Ascites . Patients with cirrhosis are observed to have increased hepatic lymphatic flow.

Fluid and plasma proteins diffuse freely across the highly permeable sinusoidal endothelium into the space of Disse. Fluid in the space of Disse, in turn, enters the lymphatic channels that run within the portal and central venous areas of the liver. Because the trans- sinusoidal oncotic gradient is approximately zero, the increased sinusoidal pressure that develops in portal hypertension increases the amount of fluid entering the space of Disse.

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When the increased hepatic lymph production observed in portal hypertension exceeds the ability of the cisterna chyli and thoracic duct to clear the lymph, fluid crosses into the liver interstitium. Fluid may then extravasate across the liver capsule into the peritoneal cavity. The role of renal dysfunction in the pathogenesis of cirrhotic ascites.

Patients with cirrhosis experience sodium retention, impaired free- water excretion, and intravascular volume overload. These abnormalities may occur even in the setting of a normal glomerular filtration rate. They are, to some extent, due to increased levels of renin and aldosterone.

The peripheral arterial vasodilation hypothesis states that splanchnic arterial vasodilation, driven by high nitric oxide levels, leads to intravascular underfilling. This causes stimulation of the renin- angiotensin system and the sympathetic nervous system and results in antidiuretic hormone release.

These events are followed by an increase in sodium and water retention and in plasma volume, as well as by the overflow of fluid into the peritoneal cavity. Clinical features of ascites. Ascites is suggested by the presence of the following findings upon physical examination: Abdominal distention. Bulging flanks. Shifting dullness. Elicitation of a .

However, physical examination findings are much less sensitive than abdominal ultrasonography, which can detect as little as 3. L of fluid. Furthermore, ultrasonography with Doppler can help to assess the patency of hepatic vessels. Factors associated with worsening of ascites include excess fluid or salt intake, malignancy, venous occlusion (eg, Budd- Chiari syndrome), progressive liver disease, and spontaneous bacterial peritonitis (SBP). Spontaneous bacterial peritonitis. SBP is observed in 1.

The syndrome arises most commonly in patients whose low- protein ascites (< 1 g/d. L) contains low levels of complement, resulting in decreased opsonic activity. SBP appears to be caused by the translocation of gastrointestinal (GI) tract bacteria across the gut wall and also by the hematogenous spread of bacteria.

The most common causative organisms are Escherichia coli, Streptococcus pneumoniae, Klebsiella species, and other gram- negative enteric organisms. Culture- negative neutrocytic ascites is observed more commonly. Both conditions represent serious infections that carry a 2. The most commonly used regimen in the treatment of SBP is a 5- day course of cefotaxime at 1- 2g intravenously every 8 hours. Many authorities advise repeat paracentesis in 4.

PMN count to less than 2. Once SBP develops, patients have a 7.

Prophylactic antibiotic therapy can reduce the recurrence rate of SBP to 2. Some of the regimens used in the prophylaxis of SBP include norfloxacin at 4. One study noted that the 3. The use of an elastic abdominal binder may protect the skin overlying a protruding umbilical hernia from maceration and may help to prevent rupture and subsequent infection. Timely, large- volume paracentesis also may help to prevent this disastrous complication.

Umbilical hernias should not undergo elective repair unless patients are significantly symptomatic or their hernias are irreducible. As with all other surgeries in patients with cirrhosis, herniorrhaphy carries multiple potential risks, such as intraoperative bleeding, postoperative infection, and liver failure, because of anesthesia- induced reductions in hepatic blood flow. However, these risks become acceptable in patients with severe symptoms from their hernia. Urgent surgery is necessary in the patient whose hernia has been complicated by bowel incarceration.

Other complications of massive ascites. Patients with massive ascites may experience abdominal discomfort, depressed appetite, and decreased oral intake. Diaphragmatic elevation may lead to symptoms of dyspnea. Pleural effusions may result from the passage of ascitic fluid across channels in the diaphragm. Paracentesis in the diagnosis of ascites. Paracentesis is essential in determining whether ascites is caused by portal hypertension or by another process.

Ascites studies also are used to rule out infection and malignancy. Paracentesis should be performed in all patients with either new onset of ascites or worsening ascites. Paracentesis also should be performed when SBP is suggested by the presence of abdominal pain, fever, leukocytosis, or worsening hepatic encephalopathy. Final Fantasy Iv Advanced Manuals. Some argue that paracentesis should be performed in all patients with cirrhosis who have ascites at the time of hospitalization, given the significant possibility of asymptomatic SBP. Ascites Tests (Open Table in a new window)Routine. Optional. Special.

Cell count. Glucose (minimal use)Cytology. Albumin. Lactate dehydrogenase. Tuberculosis smear and culture. Culture. Gram stain. Triglycerides (to rule out chylous ascites)Total protein Bilirubin (to rule out biliary leak when clinically suspected)  Amylase (to rule out pancreatic duct leak when clinically suspected)Ascitic fluid with more than 2. PMNs/mm. 3 defines neutrocytic ascites and SBP. Many cases of ascites fluid with more than 1.

PMNs/mm. 3 (and certainly > 5. PMNs/mm. 3) are associated with appendicitis or a perforated viscus with resulting bacterial peritonitis. Appropriate radiologic studies must be performed in such patients to rule out surgical causes of peritonitis. Lymphocyte- predominant ascites raises concerns about the possibility of underlying malignancy or tuberculosis. Similarly, grossly bloody ascites may be observed in malignancy and tuberculosis. This author recommends subtraction of 1 PMN for every 2. Download Option File Pes 2009 Pc.

RBCs) in ascites to ascertain a corrected PMN count. The yield of ascites culture studies may be increased by directly inoculating 1. L of ascetic fluid into aerobic and anaerobic culture bottles at the patient's bedside. Some patients with mild ascites respond to sodium restriction or diuretics taken once or twice per week. Other patients require aggressive diuretic therapy, careful monitoring of electrolytes, and occasional hospitalization to facilitate even more intensive diuresis. The development of massive ascites that is refractory to medical therapy has dire prognostic implications, with only 5.

In general, patients begin with a diet containing less than 2. Some patients with refractory ascites require a diet containing less than 5. However, ensuring that patients do not construct diets that might place them at risk for calorie and protein malnutrition is important. Indeed, the benefit of commercially available liquid nutritional supplements (which often contain moderate amounts of sodium) often exceeds the risk of slightly increasing the patient's salt intake. Diuretics. Diuretics should be considered the second line of therapy. Spironolactone (Aldactone) blocks the aldosterone receptor at the distal tubule.

It is dosed at 5. Although the drug has a relatively short half- life, its blockade of the aldosterone receptor lasts for at least 2. Adverse effects of spironolactone include hyperkalemia, gynecomastia, and lactation. Other potassium- sparing diuretics, including amiloride and triamterene, may be used as alternative agents, especially in patients complaining of gynecomastia. Furosemide (Lasix) may be used as a solo agent or in combination with spironolactone.

The drug blocks sodium reuptake in the loop of Henle. It is dosed at 4. Patients infrequently need potassium repletion when furosemide is dosed in combination with spironolactone. An Italian study by Angeli et al found sequential dosing with a potassium- sparing diuretic plus furosemide to be superior for patients with moderate ascites without renal failure when compared with potassium- sparing diuretic monotherapy.