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Biomedical subjects

B A Runyon

Publications and source records attributed to B A Runyon.

80 records · Page 5Linked to original sources

Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis.

A review of the medical records of patients diagnosed as having "spontaneous bacterial peritonitis" (SBP) revealed 18 episodes of culture-negative neutrocytic ascites (CNNA) in 17 patients. The following criteria were all required in order to qualify for this diagnosis: (i) an ascitic fluid neutrophil count greater than 500 cells per mm3; (ii) negative ascitic fluid culture (5); (iii) absence of an intraabdominal source of infection; (iv) no antibiotic treatment within 30 days, and (v) no evidence of pancreatitis. Five patients had positive blood cultures. Two patients with CNNA had SBP in the past, and two other patients, who survived the episode of CNNA, subsequently developed SBP. Clinical signs and symptoms of patients with CNNA were not different from those of 32 patients with 33 episodes of culture-positive SBP. The mortality of CNNA (50%) was not different from that of SBP (70%). Because of the high mortality and because of the similarity of CNNA to SBP, it is presumed that many patients with CNNA have bacterial infection of their ascitic fluid, and it is recommended that they be treated with antibiotics.

Ascites↗

Ascitic fluid chemical analysis before, during and after spontaneous bacterial peritonitis.

A retrospective analysis of 22 patients whose ascitic fluid had been analyzed prior to the onset of spontaneous bacterial peritonitis, during infection and/or after treatment of peritonitis revealed that neither the ascitic fluid total protein nor the absolute ascitic fluid glucose changed during the infection or after treatment of the infection although the ascitic fluid/serum glucose ratio did decrease (p less than 0.001) with infection. The ascitic fluid lactate dehydrogenase increased significantly (p less than 0.05) during infection compared to the baseline value. Contrary to the typical findings in infected body fluids, the total protein content and absolute glucose content of "spontaneously" infected ascitic fluid do not measurably change.

Ascitic Fluid↗

Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis.

The opsonic activity of 60 ascitic fluids from 47 patients was measured using a standard opsonophagocytic assay. Curve analysis of the opsonic activity compared to the ascitic fluid concentration of total protein, total hemolytic complement, C3 and C4 yielded correlation coefficients of 0.84 (p less than 0.001), 0.84 (p less than 0.001), 0.94 (p less than 0.001) and 0.92 (p less than 0.001), respectively. There appeared to be a threshold of concentration for each protein below which there was no killing of bacteria. Cirrhotic ascites had significantly (all p less than 0.001) lower concentrations of total protein and complement and less opsonic activity than noncirrhotic ascites (including malignant, cardiac and miscellaneous types). Perhaps it is the dilution of crucial antimicrobial proteins below a threshold which predisposes to spontaneous bacterial peritonitis.

Ascites↗

Diuresis of cirrhotic ascites increases its opsonic activity and may help prevent spontaneous bacterial peritonitis.

Serial ascitic fluid samples were obtained during diuresis in seven patients with portal hypertension-related ascites. The samples were tested for concentrations of total protein, CH100, C3 and C4 as well as for in vitro opsonic activity. These parameters were all found to increase to a statistically significant degree when the initial specimen was compared to the final specimen: total protein = 1.5 vs. 2.7 gm per dl; CH100 = 9.3 vs. 20.2 units per ml; C3 = 13.4 vs. 23.8 mg per dl; C4 = 1.9 vs. 3.6 mg per dl, and opsonic activity = 0.8 vs. 1.9 log kill. This increased opsonic activity resulted in a greater than 10-fold increase in bacterial killing. This study demonstrates that diuresis of patients with cirrhotic ascites increases the concentrations of ascitic fluid complement components and increases the opsonic activity of ascitic fluid and may help protect patients from bacterial infection of their ascites.

Ascitic Fluid↗

Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis.

To assess the risk of development of spontaneous bacterial peritonitis in relation to ascitic fluid opsonic activity, routine admission abdominal paracentesis was performed on 119 patients during 141 hospitalizations. Paracentesis was repeated if evidence of peritonitis developed during the hospitalization. The ascitic fluid opsonic activity (0.2 +/- 0.5 log kill) of 24 spontaneously infected specimens was significantly (p less than 0.001) lower than that of the group with sterile portal hypertension-related ascites (0.8 +/- 1.1 log kill), and significantly lower than the group with ascites of miscellaneous type (2.4 +/- 1.0 log kill, p less than 0.001). The C3 and C4 concentrations of the spontaneous peritonitis specimens were also significantly lower than in the specimens from the other groups. Of the 55 patients whose initial sterile ascitic fluid opsonic activity was less than 0.2 log kill, 8 (14.5%) developed spontaneous bacterial peritonitis during the hospitalization; whereas none of the 70 patients with sterile ascitic fluid opsonic activity greater than or equal to 0.2 log kill developed spontaneous peritonitis. This difference in the risk of development of peritonitis was significant (p less than 0.01). Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis.

Ascitic Fluid↗

Ascitic fluid analysis in malignancy-related ascites.

A prospective study identified 45 patients with malignancy-related ascites among 448 ascites patients (10% of the total). Patients were categorized into five subgroups based on the pathophysiology of ascites formation. Each subgroup had a distinctive ascitic fluid analysis. Patients with peritoneal carcinomatosis but without massive liver metastases (53.3% of the patients with malignancy-related ascites) had a uniformly positive ascitic fluid cytology, high ascitic fluid protein concentration and low serum-ascites albumin gradient. Patients with massive liver metastases and no other cause for ascites formation (13.3% of the series) had a negative cytology, low ascitic fluid protein concentration, high serum-ascites albumin gradient and markedly elevated serum alkaline phosphatase. Those with peritoneal carcinomatosis and massive liver metastases (13.3% of the series) had a nearly uniformly positive ascitic fluid cytology, variable protein concentration, high serum-ascites albumin gradient and markedly elevated serum alkaline phosphatase. Chylous ascites (6.7%) was characterized by a milky appearance, negative cytology and an elevated ascitic fluid triglyceride concentration. Patients with hepatocellular carcinoma superimposed on cirrhosis (13.3%) had negative ascitic fluid cytology, low ascitic fluid protein concentration, high serum-ascites albumin gradient and elevated serum and ascitic fluid alpha-fetoprotein concentration. Two-thirds of patients with malignancy-related ascites had peritoneal carcinomatosis; 96.7% of patients with peritoneal carcinomatosis had positive ascitic fluid cytology. Ascitic fluid analysis is helpful in identifying and distinguishing the subgroups of malignancy-related ascites.

Alkaline Phosphatase↗