الفهرس 
LIVER CIRRHOSIS (CAUSES AND PATHOPHYSIOLOGYOnly 14 pages are availabe for public view
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Abstract
Liver disease is not an infrequent condition for patients admitted to ICUs. Cirrhosis represents the final evolution of advanced liver disese. Outcomes for critically ill patients with cirrhosis remain poor, with mortality rates exceeding 40%. When organ system complications of cirrhosis develop (most notably, acute renal failure, mortality rates can reach 80%.
In this review, we will examine the hemodynamic derangements peculiar to patients with cirrhosis and ascites. We will outline the response of their cardio-vascular systems to volume expansion and - eventually - discuss the specific role of albumin in this regard.
Patients with cirrhosis have total extracellular fluid overload but central effective circulating hypovolaemia. The resulting neurohumoral compensatory response favours the accumulation of fluids into the peritoneal cavity (ascites) and may hinder renal perfusion (hepatorenal syndrome). Their deranged systemic haemodynamics (hyperdynamic circulatory syndrome) is characterized by elevated cardiac output with decreased systemic vascular resistance and low blood pressure.
Molecular and biological mechanisms determining cirrhosis-induced haemodynamic alterations are prog-ressely being elucidated. The need for a goal-directed assessment of volume resuscitation especially with volumetric techniques) in patients with cirrhosis is becoming more and more evident. The role of fiuid expansion with albumin and the use of splanchnic vasopressors in a variety of cirrhosis-related conditions has recently been investigated.
The response to fluid loading in patients with advanced cirrhosis is abnormal, primarily resulting in expansion of their noncentral blood volume compartment. Colloid solutions, in particular albumin, are best used in these patients. Albumin may be effective in preventing the haemodynamic derange-ments associated with large-volume paracentesis (paracentesis-induced circulatory dysfunction), in preventing renal failure during spontaneous bacterial peritonitis and, in association with splanchnic vasopressors, in caring for patients with the hepatorenai syndrome.
The administration of intravenous fluids is one of the most common and universal interventions in medicine. Crystalloid solutions are the most frequently chosen, by far, with normal saline (NS) and lactated Ringer’s (LR) both being frequent choices in the United States. Colloids are an alternative to crystalloids, with highly variable use depending on a myriad of clinical variables. Of interest, the choice of intravenous fluids has remained one of the most controversial subjects in critical care over the past half a century.
Administration of plasma expanders has been used extensively in clinical practice to improve renal function in patients with cirrhosis and ascites despite the lack of available evidence supporting such an indication. The circulatory dysfunction causing impairment in effective arterial blood volume and subsequent renal dysfunction in cirrhosis with ascites is not a fixed, unalterable disorder. Rather its intensity may increase as a consequence of the evolution of the disease or by intercurrent processes.
Plasma volume expansion with albumin, as well as other procedures that cause expansion of total blood volume (infusion of ascitic fluid or peritoneovenous shunting), have traditionally been used in the management of patients with hepatorenal syndrome with little success.
Albumin infusion plus administration of vasoactive drugs such as octreotide and midodrine should be considered in the treatment of type I hepatorenal syndrome (Grade II-1).
Patients with cirrhosis, ascites, and type I hepatorenal syndrome should have an expedited referral for liver transplantation (Grade II-3).
One controlled trial randomized patients with SBP to receive cefotaxime alone versus cefotaxime plus 1.5g albumin per kg body weight within 6hrs of enrollment and 1.0g/kg on day 3. A decrease in mortality from 29% to 10% was reported. This is the lowest hospitalization mortality ever reported in a randomized trial of SBP.
Protein requirements in end stage hepatic failure remain a matter of controversy. Conventional wisdom and textbook information continue to include protein restriction to reduce hepatic encephalopathy. However, controlled trials have demonstrated that patients with hepatic failure not only require increased protein intake to maintain nitrogen balance, but commonly tolerate normal or increased protein intake without exacerbating encephalopathy.
Current recommendations are to provide adequate medication (lactulose, Neomycin, Metronidazole) to control encephalopathy, and optimize protein to as much as the patient is able to tolerate.
In practice, it is clear that that an acute worsening of encephalopathy or mental status is invariably related to infections, GI bleeding, medications, or missed doses of lactulose regardless of protein intake.
PN is indicated in moderately or severely malnourished cirrhotics who cannot be nourished sufficiently by either oral or enteral route. Cirrhotics who can be fed sufficiently either by the oral or enteral route but who have to abstain from food temporarily (including nocturnal fasting!) for more than 12hrs should be given i.v. glucose at 2-3g/kg-1d1. When this fasting period lasts longer than 72hrs total PN is required. PN should be considered in patients with unprotected airways and encephalopathy (HE) when cough and swallow reflexes are compromised.