Hypertension ascites and

Lieberman, F.L., Denison, E.K., Reynolds, T.B. The relationship of plasma volume, portal hypertension, ascites, and renal sodium retention in cirrhosis the overflow theory of ascites formation. Ann. N. Y Acad. Sci. 1970 170 202-206... 

The pathophysiologic mechanisms of portal hypertension and of cirrhosis itself are entwined with the mechanisms of ascites (Fig. 19-3). Cirrhotic changes and the subsequent decrease in synthetic function lead to a decrease in production of albumin (hypoalbuminemia). Albumin is the major intravascular protein involved in maintaining oncotic pressure in the vascular system low serum albumin levels and increased capillary permeability allow fluid to leak from the vascular space into body tissues. This can result in peripheral edema, ascites, and fluid in the pulmonary system. The obstruction of hepatic sinusoids and... 

Garcia-Tsao G Current management of the complications of cirrhosis and portal hypertension Variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology 2001 120 726-748. 

Bumetanide is used for relieving edema associated with cardiac insufficiency, for liver and kidney diseases including nephrotic syndrome, for ascites, and hypertension. Synonyms of this drug are bumex and others. 

Both drugs are gastric irritants and should probably be avoided in patients with varices or a history of variceal bleeding or coagulopathy, or a risk thereof. Niacin can also cause thrombocytopenia. This patient has a varix and would be at risk of a variceal bleed if decompensation occurred. Niacin and acipimox also commonly cause pruritus. They are also vasodilators and may potentiate the effect of drugs that lower blood pressure (spironolactone, propranolol, furosemide), which are used to treat ascites and portal hypertension. 

Ascites and oedema are due to portal venous hypertension together with decreased plasma colloid osmotic pressure causing hyperalodosteronism as with nephrotic oedema (above). Furthermore, diversion of renal blood flow from the cortex to the... 

An increase in the retention of sodium occurs in the early stages of severe liver disease, particularly in liver cirrhosis, without any disruption of the water balance. This early tendency towards sodium retention can be detected using the NaCl-tolerance test. The retention of sodium reduces the sodium excretion rate in the urine to < 10 mval/day (normal rate 120 to 220 mval/day). Diuresis is not primarily restricted patients with ascites and oedema react to an excessive intake of water with an adequate excretion of diluted urine, albeit in the virtual absence of sodium excretion. The limited sodium excretion derives from increased, mainly proximal tubular reabsorption of sodium and not from diminished glomerular filtration. Overall maintenance of the liver architecture is usually accompanied by undisturbed sodium excretion, despite existing portal hypertension (such as in primary biliary cirrhosis). Marked sodium retention is, however, usually found in alcoholic-toxic cirrhosis. For this reason, such patients are not only the ones most frequently affected by ascites and oedema, but as a rule they display the most serious forms. This is probably also due to additional biochemical and hormonal factors which are present to a greater degree in patients with alcohol-related liver disease. 

It is not clearly understood why in some cases oedema without ascites and in other cases ascites without oedema as well as ascites together with oedema or even pleural effusion without ascites occur. Ascites develops most frequently during the course of liver disease (= hepatogenic ascites), in particular in chronic liver diseases with portal hypertension (= portal ascites), (s. tab. 16.7) Various mechanical, biochemical and neural disorders overlap in their effects and pathways, depending on the underlying liver disease. Only rarely is ascites found in diseases with presinusoidal localization of portal hypertension (such as portal vein thrombosis) or with minor restrictions in the synthesis of albumin (as in biliary cirrhosis). Formation of ascites occurs in about 50% of all cirrhotic patients within 10 years of... 

In a South African study 20 children were identified as suffering from hepatic veno-occlusive disease thought to be caused by the administration of traditional remedies (3). The predominant clinical presentation was ascites and hepatomegaly. Nine children died. The surviving patients progressed to cirrhosis and portal hypertension. In four cases early urine specimens were available, and in all of these the presence of pyrrolizidine alkaloids was confirmed. 

Ascites is the effusion and accumulation of fluid in the abdominal cavity. Ascites is the most common chnical finding in patients with portal hypertension. Ascites itself is not life threatening, but is uncomfortable and may compromise respiration (from upward displacement of the diaphragm and compression of the lungs). It also predisposes individuals to spontaneous bacterial peritonitis, which is life threatening. 

There are many causes of ascites, and it is important to differentiate ascites secondary to portal hypertension from ascites of other causes. This is done by analyzing ascitic fluid. The feature that best distinguishes portal hypertension is an increase in the plasma to ascitic fluid albumin gradient. A gradient greater than 1.1 g/dL is diagnostic of ascites caused by portal hypertension. ... 

The signs and symptoms are usually insidious in onset and may consist of anorexia, malaise, edema, anasarca, or ascites, and pericardial and pleural effusions may also be present. As a result of a hypercoagulable state, pulmonary embolism may develop, but rarely results in death. " The incidence of renal vein thrombosis varies from 5% to 62%, " and membranous nephropathy should be suspected when there is a sudden onset of hematuria loin pain pulmonary embolus fluctuating or worsening proteinuria or glomerular filtration rate renal tubular acidosis or an increase in leg edema. Hypertension is found in about 30% of patients and is more common in the presence of renal insufficiency or until the disease is advanced. 

Symptoms of pulmonary hypertension include dyspnea on exertion, chest pain, palpitations, syncope, ascites and lower extremity edema. Anginal symptoms may occur and are thought to be due to increased RV oxygen demand, decreased right coronary artery perfusion due to decreased pressure difference between aorta and RV end diastolic pressure, and rare instances of compression of the left main coronary artery by the dilated pulmonary trunk. Right ventricular hypertrophy (RVH) correlates with EKG findings including RV... 

Hepatic cirrhosis may be associated with portal hypertension, ascites, encephalopathy, spontaneous bacterial peritonitis, and hepatocellular carcinoma. Portal hypertension is directly responsible for the formation of esophageal varices, which may give rise to massive upper gastrointestinal bleeding. Therapy is aimed at correcting hypovolemic shock and at achieving hemostasis at the bleeding site. 

Diuretics are commonly prescribed for the management of essential hypertension, congestive heart failure, ascites, and chronic renal insufficiency. Adverse effects from chronic use or misuse (in sports, dieting, anorexia) are more frequently encountered than those from acute overdose. Overdoses are generally benign, and no serious outcomes have resulted from acute ingestion. Common currently available diuretics are listed in Table 11-23. 

Amiodarone has been associated with steatohepadtis with advanced fibrosis, presenting with hepatic decompensation and portal hypertension, with ascites and recurrent hemorrhage from esophageal varices [42 ]. There was marked histological similarity between amiodarone-induced liver disease and alcoholic and non-alcoholic steatohepatitis. 

Diuretics are one of the dmg categories most frequendy prescribed. The principal uses of diuretics are for the treatment of hypertension, congestive heart failure, and mobilization of edema fluid in renal failure, fiver cirrhosis, and ascites. Other applications include the treatment of glaucoma and hypercalcemia, as well as the alkafinization of urine to prevent cystine and uric acid kidney stones. 

Loop diuretics are used in the treatment of edema associated with CHF, cirrhosis of the liver, and renal disease, including the nephrotic syndrome. These drug s are particularly useful when a greater diuretic effect is desired. Furosemide is the drug of choice when a rapid diuresis is needed or if the patient has renal insufficiency. Furosemide and torsemide are also used to treat hypertension. Ethacrynic acid is also used for the short-term management of ascites caused by a malignancy, idiopathic edema, or lymphedema. 

O Portal hypertension is the precipitating factor for the complications of cirrhotic liver disease—ascites, spontaneous bacterial peritonitis (SBP), variceal bleeding, and hepatic encephalopathy. Lowering portal pressure can reduce the complications of cirrhosis and decrease morbidity and mortality. 

Patients with ascites or known varices must be assumed to have portal hypertension and are treated as such, even if direct measurements of portal pressure have not been made.29... 

Drug therapy for portal hypertension and cirrhosis can alleviate symptoms and prevent complications but it cannot reverse cirrhosis. Drug therapy is available to treat the complications of ascites, varices, spontaneous bacterial peritonitis, hepatic encephalopathy, and coagulation abnormalities. 

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