TABLE 827 Diagnosis and Treatment of Spontaneous Bacterial Peritonitis

SBP is diagnosed by sampling the ascitic fluid by paracentesis. Ideally, ascitic fluid is localized and marked for paracentesis by ultrasound to ensure fluid recovery and avoid encountering intestine during the procedure. In the absence of ultrasound, ascitic fluid can be localized with relative safety by percussion of dullness in the lateral aspects of the lower quadrants with the patient semirecumbant. Alternately, the patient is positioned supine, resting partially on the side where the paracentesis is to be performed. In choosing the site for puncture, avoid areas proximate to remote surgery. The site is prepared and draped in a sterile fashion, and lidocaine is infiltrated locally for anesthesia. An 18- or 20-gauge angiocatheter on a 20-cc syringe is adequate for fluid sampling. Postprocedural leaking of ascitic fluid can be lessened by advancing the catheter in a Z fashion through the skin, subcutaneous fat, and abdominal wall or by placing traction on the overlying skin prior to puncture so that on removing the catheter there is a lateral distance between the skin puncture and the peritoneum. Ascitic fluid is a transudate with protein content generally less than 3 g/dL. Culture results are frequently negative; however, yield can be improved by drawing 10 cc of fluid and processing it as a blood culture. Cell count with white blood cell (WBC) differential is ordered. A total WBC count in excess of 1000/mm 3 and/or neutrophil count (PMNs) greater than 250/mm3 is considered diagnostic for SBP. The Enterobacteriaceae account for 63 percent of infections, Streptococcus pneumoniae 15 percent, enteroccoci 6 to 10 percent, and anaerobes less than 1 percent. Appropriate antibiotic regimens are outlined in T.ab!e...82-7.35

Occasionally patients present with refractory and incapacitating ascites as a primary complaint. Associated symptoms include extreme fatigue, increased respiratory effort, and orthopnea. These individuals often have failed maximal diuretic therapy and have undergone high-volume paracentesis in the past. Before performing this procedure, it is useful to consult with the patient's primary care provider or hepatologist to review a protocol. As much as 6 to 8 L of ascitic fluid can be drained over a 60- to 90-min interval with the concomitant peripheral infusion of albumin (6-8 g/L of ascites collected). Many practitioners believe the albumin infusion is unnecessary when peripheral edema is present because mobilization of edema fluid attenuates intravascular volume loss. Complications of the procedure are not infrequent and include hemorrhage, infection, acute renal failure, and hemodynamic compromise. Such patients may be ideal candidates for an observation unit or short-stay admission.28

Hepatorenal Syndrome Hepatorenal syndrome is characterized by acute renal failure in the cirrhotic patient in the presence of histologically normal kidneys. The exact pathophysiology is elusive but is tied in with the metabolic derangments of end-stage liver failure, decreased effective circulating blood volume, and elevated aldosterone and antidiuretic hormone secretion. GFR drops, as does urine sodium secretion, and azotemia worsens with blood urea nitrogen-creatinine ratios usually greater than 20. This characteristic and refractory form of renal failure complicates cirrhosis with ascites and can be precipitated by any acute illness resulting in dehydration and/or sepsis or as a complication of overzealous diuresis or high-volume paracentesis. The ill cirrhotic patient with evidence of acute or worsening renal insufficiency should be hospitalized for appropriate consultation and carefully monitored intravenous fluid administration and diuretic therapy adjustment. 29

Hepatic Encephalopathy Hepatic encephalopathy is a complex syndrome that often accompanies acute or fulminant liver failure and frequently complicates the course and management of cirrhotics. In acute or fulminant liver failure, encephalopathy occurs in response to the metabolic insults of the disease and also cerebral edema. In chronic liver disease, fluctuating encephalopathy occurs in response to the accumulation of a variety of nitrogenous metabolic wastes normally cleared by the liver and also the prolonged effects of incompletely metabolized substances ingested such as prescription drugs and other more overt hepatotoxins such as acetominophen, NSAIDs, and alcohol.30

To appreciate the presence or worsening of baseline encephalopathy, one must determine the patient's underlying functional status. Questions related to changes in personality, worsening dementia, alterations in level of consciousness, and neuromuscular function should be pursued. The staging of hepatic encephalopathy is outlined in Table.82-8. Asterixis characterizes stage II and is a manifestation of neuromuscular weakness made evident when the patient tries to maintain a certain posture. Typically, the hands begin to "flap" when the patient is asked to hold the hands up and extended at the wrist ("stop traffic"). Alternately, the tongue moves back and forth like a snake when the patient is asked to keep his or her tongue extended. Serum ammonia level is often measured in this setting and is frequently significantly elevated. However, this is a nonspecific finding, and ammonia levels are notoriously inaccurate. Thus ammonia may serve as a marker but not as an index of encephalopathy. The list of potential causes of encephalopathy in the cirrhotic patient is long and includes gastrointestinal bleeding, increased dietary protein intake, constipation, infection/sepsis, drugs (frequently benzodiazepines, opiates, or commonly prescribed "muscle relaxers"), acute worsening of hepatic function, or electrolyte and acid-base disturbances. Falls are not uncommon in this population and, along with coagulopathy, place them at increased risk of head injury and intracranial bleeding. Therefore, computed tomographic (CT) imaging of the head is appropriate in the evaluation. The majority of cirrhotics presenting with acute or worsening encephalopathy are best served by hospitalization. There is the occasional patient presenting with a baseline of variable encephalopathy who appears otherwise well (stage I or II) and has an unrevealing workup for serious causes of mental deterioration who may be managed successfully as an outpatient. The cathartic lactulose is prescribed at a dose of 30 cc three times daily until one or two soft stools are produced daily. Lactulose traps ammonia within the lumen of the gut by decreasing intestinal pH and stimulates bacterial uptake of ammonia into fixed bacterial proteins. The antibiotic neomycin is an alternative therapy that decreases intestinal bacterial number, thus reducing toxic substances generated by bacterial protein degradation. Neomycin can be prescribed as 1 g four times daily; infrequent side effects include oto- and nephrotoxicity.

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