COMPLICACIONES DE PARACENTESIS PDF

Royal Infirmary of Edinburgh and the Department of Medicine. University of Edinburgh. Scotland, United Kingdom. Hepatic cirrhosis is the most common cause of ascites. It is caused by liver failure leading to complex interrelated circulatory and renal changes resulting in retention of sodium and water and portal hypertension localising that sodium and water in the peritoneum. Ascites is an important development in cirrhosis as it implies a generally poor long term prognosis.

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Royal Infirmary of Edinburgh and the Department of Medicine. University of Edinburgh. Scotland, United Kingdom. Hepatic cirrhosis is the most common cause of ascites.

It is caused by liver failure leading to complex interrelated circulatory and renal changes resulting in retention of sodium and water and portal hypertension localising that sodium and water in the peritoneum. Ascites is an important development in cirrhosis as it implies a generally poor long term prognosis. Investigation is important as ascites is not always dueto cirrhosis, may bethe consequence of complications of cirrhosis such as hepatocellular carcinoma, and may be associated with infection which is fatal if untreated.

Most patients respond to treatment with sodium restriction and diuretic drugs. This treatment takes time, and increasingly doctors use therapeutic paracentesis with sodium restriction and diuretics to prevent recurrence of ascites. Paracentesis, however, is not without complications, and it is particularly important to give colloid replacement to prevent hypovolaemia which can lead to renal failure. Patients who do not respond to this treatment may be helped by a TIPSS procedure or a peritoneovenous shunt.

However, these patients usually have very poor liverfunction and the possibility of fiver transplantation should be considered. Infection is a very serious complication of ascites spontaneous bacterial peritonitis and carries a generally poor prognosis. Antibiotic prophylaxis is important to prevent recurrence and liver transpiantation shoulcl be considered. Key words: Ascites, cirrhosis, detection, diagnosis, prognosis, complications, treatment.

Ascites, free fluid in the peritoneal cavity, indicates the presence of serious disease. This paper considers the ascites of chronic liver disease, including its detection, diagnosis, prognosis, complications and treatment. Ascites in hepatic cirrhosis develops because of a considerable increase of total body sodium and water, and portal hypertension which localises much of that sodium and water to the peritoneal cavity Arroyo et al Retention of sodium by the kidneys is the main reason for this increase though renal water retention does occur in more advanced dasease table 1.

Water retention occurs primarily as a consequence of sodium retention. Three general theories have been proposed to explain renal retention of sodium in hepatic cirrhosis Ring-Larsen and Henriksen, One suggests that portal hypertension causes a loss of fluid into the peritoneun and leads to depletion of the intravascular volume underfilling theory with secondary and compensatory renal retention of sodium and water; another suggests that the fiver disease itself causes primary renal sodium and water retention leading to expansion of the vascular volume and hence the ascites overflow theory ; a third theory proposes a primary circulatory derangement resulting in a reduced effective arterial plasma volume with consequent renal retention of sodium and water Henriksen et al The mechanisms underlying these theories are complex, poorly understood, and beyond the scope of this paper as they do not yet have important implications for the management of hepatic ascites.

All, however, are associated with poor liver function and include activation of the renin-angiotensin-aldosterone system with high plasma and urine aldosterone, increased sympathetic activity possibly via a hepatorenal reflex arc, and the actions of such agents as arterial natriuric peptide, kallikrein-kinin prostaglandins, nitrous oxide, endothelin, and endotoxin.

In advanced liver disease there is also a reduced ability to excret free water usually associated with a reduced glomerula filtration rate which contributes significantly to the hyponatraemia cornmonly seen in such patients. As would expected, impaired free water clearance is associated with hyponatraemia and a poor prognosis Table 2. Portal hypertension is caused primarily by an increased resistance to blood flow which, in hepatic cirrhosis, occurs in the hepatic parenchyma.

In addition, there is an increased portal blood flow which acts to maintain and aggravate portal hypertension Bosch et al These factors cause an increased filtration pressure in the hepatic sinusoids and in the mesenteric capillaries leading to increased passage of fluid into the peritoneal cavity Witte et al Once the transport capacity of the lymphatics is exceeded fluid accumulates in the peritoneal cavity and eventually ascites becomes evident.

Most of the peritoneal fluid originates from the hepatic sinusoids which are high1y permeable and produce protein-rich interstitial fluid explaining the high ascites protein content in acute obstruction of the hepatic venous outflow e.

The hepatic sinusoids become 'capillarised', by connective tissue progressively in hepatic cirrhosis and are less permeable which accounts for the generally low protein content of ascites in this condition. The mesenteric capillaries also contribute to ascites and produce interstitial fluid with a low protein content as in other arts of the body Witte et al Local diseases in the peritoneal cavity such as TB, malignant disease,and pancreatitis, damage capillaries and produce protein-rich ascites exudates.

Clinically evident ascites causes abdominal distention and bulging of the flanks. Three bedside signs have been advocated for determining that these appearances are due to ascites. The most widely used is "shifting clullness". The "puddle sing" is said to be able to detect as little as ml of ascites Lawson and Weissbein , and a "fluid thrill" is considered very specific. It is, however, important to be realistic and recognise the limitations and practicality of these clinical signs.

Cattau et al have shown that clinical examination detects peritoneal fluid in only a half of patients with less than a litre of ascites Table 3. They found that bulging and dullness in the flanks and shifting dullness were most sensitive but of limited specifity, that a fluid thrill was specific but of limited sensitivity, and that the puddle sign in their hands was of very limited value.

In practice, shifting dullness is the sign most used though it generally requires the presence of more than a litre of fluid and probably more in obese patients.

The puddle sign is little used, and the fluid thrill is an interesting observation in patients with ascites visible even to the casual observer. Lack of flank dullness is useful as it makes ascites very unilikely. Ascites can give rise to a number of secondary abdominal features including umbilical eversion, herniae, pale abdominal striae, scrotal oedema, and meralgia paresthetica from entrapment of the lateral cutaneous nerve of the thigh. Mechanical effects on the chest impair cardiopulmonary function and can cause dyspnoea which is relieved by removal of the ascites Table 4.

Pleural effusion and hydrothorax can also occur below. Ascites can often be detected confidently from clinical examination, but in some cases the findings are equivocal usually because the amount of ascites is small or the patient is obese. In these circumstances, ultrasonography is a good noninvasive means of confirming ascites. Ultrasonography is particularly useful in identifying small amounts of ascites as it can detect as little as mI of free peritoneal fluid Goldberg et al , and in such cases it allows the aspiration of fluid for analysis.

Ascites in cirrhosis is usually clear and straw or light green in colour, but it can also be cloudy, bloo -stained chylous or bile -stained. Cloudy or slightly or opaque ascites suggests the presence of infection below and indicates the need for an immediate ascites polymorphonuclear leucocyte cell count. Ascitic fluid and blood culture shoulcl also be done below. It usually develops insidiously without causing haemodynamic instability, and is most often due to a hepatocellular carcinoma.

Bloody ascites can also be caused by rupture of intra-abdominal varices or possibly leakage from dilated liver lymphatics as liver lymph in cirrhosis contains significant numbers of red blood cells Dumont and Mulholland Hepatocellular carcinoma and ruptured intra-abdominal varices can also cause acute bleeding leading to hypovolaernic shock.

Bloody ascites can be due to trauma caused by liver biopsy, fine-needle piration, TIPPS insertion or, rarely, paracentesis. It is usually caused by malignant disease in adults but rarely it has been found in cirrhosis possibly due to leakage from lymphatics Malagelada et al It is a poor prognostic sign.

B ile-stained ascites points to a biliary communication usually caused by gallstones, neoplasia or trauma. Analysis of the ascitic fluid is helpful in identifying the cause of the ascites and in recognising complications such as infection and neoplasia Table 5. Chronic parenchymal liver disease is the most cornmon cause of ascites, and Table 6 shows the main conditions from which it needs to be differentiated.

Hepatic cirrhosis is generally regarded as giving rise to ascites which is a transudate. Furthermore, the ascites protein may rise during diuretic therapy Hoefs Blood and ascites culture should also be done, and the chance of isolating an organism from the ascites is best if the fluid is drawn into blood culture bottles Runyon et al Culture for M. Cytology of ascites is important as malignant cells can be identified reliably in ascites sediment by this technique.

Unfortunately, the sensitivity of ascites cytology for malignancy is low. The ascites amylase is high in pancreatic ascites and should be measured particularly when the protein content of ascites is high. Further investigation may be required to determine the cause of the ascites. In the case of hepatic cirrhosis, this includes imaging to detect cirrhosis, portal hypertension and complications of cirrhosis such as hepatocellular carcinoma, the causes of cirrhosis, and endoscopy for detection of oesophago-gastric varices which imply portal hypertension.

Rarely, measurement of the portal venous pressure may reveal otherwise occult hepatic cirrhosis by revealing portal hypertension. This is done most safely by measuring the wedged hepatic venous pressure. Ascites not attributed to cirrhosis is usually due to intra-abdominal malignant disease and other causes are uncommon Table 6. Ascites in hepatic cirrhosis is associated with advanced liver disease and with poor hepatic function and portal hypertension, and consequently it is also associated with a poor prognosis.

Many early deaths are attributable to serious complications such as hepatocellular carcinoma and spontaneous bacterial peritonitis, but patients with severe ascites who do not have such complications also often have a poor prognosis.

About a half of patients with tense ascites who do not have gastrointestinal bleeding, infection, encephalopathy, severe renal failure or hepatocellular carcinoma at presentation die within a year, and poor prognostic factors in these patients are shown in Table 7. Prognosis is related largely to liver function, and patients with lesser degrees of ascites and better liver function respond better to treatment and survive longer.

In view of its prognostic implications, the development of ascites should always lead to consideration of liver transplantation. Mild to moderate ascites can be treated as an outpatient, but more severe ascites is treated best in hospital as these patients usually have more severe liver damage and they more often have adverse reactions to therapy. Important factors intreating ascites include removing precipitating factors, controlling sodium intake and sometimes water intake , promoting sodium excretion with diuretic drugs, removing ascites by paracentesis, and diverting ascitic fluid into the systemic circulation via a transjugular intrahepatic portal systemic stent TIPSS shunt or a Le Veen shunt lt is very doubtful whether any of this treatment prolongs life, and as the prognosis for patients with hepatic cirrhosis and ascites is generally poor, liver transplantation shoulcl be considered.

Precipitatinq Factors. Precipitating factors should be sought though in many cases none can be found. Such factors include recent heavy alcohol abuse, ingestion of unusually salty foods, and medicines.

Drugs sometimes contain significant amounts of sodium including some antacids and alginates, aspirin, fybogel, phenytoin and all effervescent preparations. Other drugs can promoje renal retention of sodium and these include nonsteroidal anti-inflammatory drugs, corticosteroids, oestrogens and metociopramide.

ACE-inhibitors reduce glomerular filtration rate and sodium excretion even in doses which do not reduce the blood pressure. Ascites arising or worsening in hospital shoulcl always lead to a review of therapy, especially the use of parenteral antibiotics and of intravenously administered fluids which often contain much sodium. Renal sodium retention is marked in ascites caused by hepatic cirrhosis above , particularly when the ascites is severe and hepatic dysfunction marked, and accordingly restriction of sodium intake is important, particulary in initial treatment.

Occasionally, sodium restriction alone will allow resolution of ascites, particularly where a precipitating cause has been found and removed, but the great majority of patients require also diuretic drugs. Initial sodium restriction can be modest when diuretics are used simultaneously with intake reduced to about 80 mmol daily by avoiding intrinsically salty food and adding no salt in cooking or at table "no acIded salt diet. Patients with cirrhosis and ascites are often malnourished, and this modest reduction in salt intake allows the diet to remain reasonably palatable which is important in maintaining nutrition.

Diuresis can then be produced by gradually increasing the dose of diuretics given. Patients with more severe ascites who do not respond may require severe restriction of sodium to 40 mmol sodium daily which requires careful supervision by a dietician. Sodium depletion Rarely, patients become truly sodium and water depleted following large fluid losses by paracentesis, diuresis or enteric losses.

These patients have lost their ascites and oedema and show clinical features of dehydration, tachycardia, hypotension and uraemia. These patients need to be given sodium and water parenterally to replace their losses. Urine sodium estimation. Measurement of the daily urine sodium output is useful in patients who do not respond to dietary salt restriction and diuretics as the finding of a good sodium excretion implies the intake of excess salt.

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Fisiopatogenia y opciones de tratamiento. Plancarte 1 , M. Guajardo2 y F. Mayer 2. Ascites in cancer patients. Physiopathology and therapeutic options. Rev Soc Esp Dolor ;

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Runyou BA. Management of adult patients with ascites due to cirrhosis: an up date. Transyugular intrahepatic portosystemic shunt for refractory ascites: a meta analysis of individual patient data. Midridines versus albumin in the prevention of paracentesis-induce circulatory dysfunction in the cirrotics: a randomized pilot study. Am J Gastroenterology. Heidelbaugh JJ, Bruderly M. Cirrhosis and chronic liver failure.

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Skip to search form Skip to main content You are currently offline. Some features of the site may not work correctly. DOI: Generalidades Las complicaciones de la cirrosis hepatica no han cambiado a lo largo del tiempo, pero si lo han hecho las opciones de tratamiento, en especial durante los ultimos ocho anos. View PDF. Save to Library. Create Alert.

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