Laboratory Variations In

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A. Culture-Negative SBP (CNSBP) and Culture-Negative Neutrocytic Ascites (CNNA)

CNSBP is defined as the presence of the clinical picture of SBP, ascites that contains more than 250 polymorphonuclear leukocytes (PMNs) per cubic millimeter, a sterile ascitic fluid culture, and no explanation for the abdominal finding (50). In the most simple sense it represents culture-negative SBP. How can such a syndrome develop? What does it signify? First, it may represent SBP at an early phase in its course, prior to the peritoneal infection becoming fully developed. Second, it may represent SBP at a late stage in its course, after the body's defenses have defeated the invading organisms, when the bacteria are too inhibited or too few in number to show a positive culture. Third, organisms may be too fastidious to grow on the culture media employed or on a culture medium that is for any reason not as hospitable to bacteria as it usually is. Conceivably, the patient may have received an antibiotic substance that is too small to eradicate the infection, but is large enough to suppress the growth of the organism in vitro. Fourth, the number of bacteria may be so small that the inoculum contains "no" bacteria. If, for example, the number of organisms in the ascitic fluid were less than 1 per ml, inocula of 1 ml of ascitic fluid would sometimes be free of bacteria and would consequently show no growth. (See Table 2.1.)

In an attempt to assess the situation, Pelletier et al. compared 38 cirrhotic patients with SBP and 15 with CNSBP selected especially by virtue of their

Table 2.1 Clinical Variants of the Spontaneous Bacterial Peritonitis Syndrome

1. Spontaneous bacterial peritonitis (culture-positive SBP)

2. Culture-negative SBP (false-negative SBP or "probable SBP")

3. Asymptomatic bacterascites (ABA)

4. Symptomatic bacterascites (SBA)

not having received any antibiotic agents for at least one month, and, of course, of not having any intra-abdominal source of infection (51). Most of the patients had alcoholic cirrhosis. The majority of their patients with SBP were infected with E. coli. The two groups were similar in clinical and laboratory features. The only statistically significant differences were a higher mean serum creatinine concentration (1.6 vs. 1.3 mg%; p < 0.03), a higher mean serum bilirubin concentration, and a higher percentage of positive blood cultures (39 vs. 13%; p < 0.05) in those with SBP (see Table 3.3). In addition, the mean leukocyte and PMN counts in the ascitic fluid were lower in the CNSBP group than in the SBP group (3177 vs. 8064 per cubic millimeter; and 2367 vs. 6663, respectively; p < 0.02). Recovery rates were higher and 30 day mortality rates were lower in the CNSBP than in the SBP group (87 vs. 69%; p < 0.05 and 20 vs. 50%; p < 0.05, respectively). Although the exact explanation is not known, it is reasonable to accept the original hypothesis that CNSBP is a more serious variant of SBP than ABA, which may equally well be called culture-positive, neutrocytic ascites (CPNA). The cirrhosis was less severe in CNSBP than in CPNA according to Pugh's criteria (52).

Tam and associates published an almost identical paper (53) in which the patients with CNSBP responded to antibiotic therapy in terms of a decrease in the numbers of WBCs and PMNs in the ascitic fluid. They, too, believe that CNSBP is a less severe type of SBP, and one that requires antibiotic therapy.

A very similar quandary exists for culture-negative bacterial endocarditis (54), which, like CNSBP, occurs in about 20% of patients with bacterial endocarditis (55).

B. Other Variants of SBP

Another syndrome that appears to be related pathogenetically to acute scrotal edema, which occasionally occurs after paracentesis (47), is unilateral abdominal or chest wall edema that follows laparotomy or thoracotomy in ascitic cirrhotic patients (56). In principle, such patients suffer from fistulae between the peritoneal cavity and the subcutaneous tissues of the body wall. The ascitic fluid dissects into the subcutaneous spaces where its distribution is determined by the site of incision and by gravity. Because subcutaneous fluids do not cross the midline freely, the fluid is usually localized to the side of the incision. When the incision crosses the midline, the fluid may be distributed bilaterally. Occasionally, such collections of edema may dissect into the subcutaneous tissue of the lower extremity if the attachments of Scarpa's fascia to the fascia lata are incom plete, and may give rise to edema of the lower extremity and/or the scrotum and penis. When the ascitic fluid is infected by bacteria in SBP, either spontaneously or secondarily, one may see the "erysipelas" described in Beethoven after his paracentesis (see Chap. 1) (57) because the infected ascitic fluid may induce a severe, erysipelas-like erythemia.

Secondary "complications" of unilateral trunkal edema, such as unilateral jaundice, may occur when the accumulated fluid is ascitic in origin (56). This phenomenon occurs because ascitic fluid is high in albumin concentration and because bilirubin binds to albumin. Subcutaneous dissections of ascitic fluid in which the albumin concentrations is high, tend to be brightly jaundiced if the serum bilirubin concentrations are elevated whereas collections of edema fluid in patients with heart disease or nephrosis, in which the albumin concentrations are low, do not. Edema associated with burns or allergic reactions have a high albumin concentration and appear jaundiced. Indeed, this is the basis of the histamine wheal test for jaundice, in which wheals induced by subcutaneous injections of histamine appear jaundiced whereas the surrounding tissue does not.

C. Spontaneous Eosinophilic Bacterial Peritonitis

This rare syndrome is of little clinical importance. Eosinophilic ascites, i.e., ascitic fluid with a high concentration of eosinophilic leukocytes, has been reported in patients with eosinophilic gastroenteritis or the hypereosinophilic syndrome (58), and may occur in patients with progressive cardiac failure. The mechanism of the eosinophilia is unknown. It is assumed that allergy may be responsible, but the cause has never been elucidated. Eosinophilic SBP appears to be typical SBP in which the polymorphonuclear response to the infection is primarily eosinophilic for unknown reasons. Apparently, these eosinophilic polymorphonuclear leukocytes function well. Rowland described an alcoholic cirrhotic patient who developed the classical syndrome of SBP except that 80% of the 12,400 leukocytes per cubic millimeter of ascitic fluid were eosinophilic (59). Surprisingly, there were no eosinophilic leukocytes among the 7000 WBC per cubic millimeter in the patient's blood. The patients responded promptly to conventional antibiotic therapy with the disappearance of the peritoneal leukocytosis and the peritoneoeosinophilocytosis.

Eosinophilic peritonitis of unknown cause may be associated with chronic ambulatory peritoneal dialysis (60), and may be rapidly corrected by the administration of intraperitoneal hydrocortisone (61).

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