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J C Hoefs

Publications and source records attributed to J C Hoefs.

43 records · Page 3Linked to original sources
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Ascitic fluid analysis in the differentiation of spontaneous bacterial peritonitis from gastrointestinal tract perforation into ascitic fluid.

A review of patients with bacterial peritonitis and ascites revealed six patients with gastrointestinal tract perforation into their ascitic fluid and 33 episodes of spontaneous bacterial peritonitis in 32 patients. Signs and symptoms were not helpful in differentiating the two groups; however, ascitic fluid analysis was found to be useful. All patients with perforation peritonitis fulfilled at least two of the following criteria: ascitic fluid total protein greater than 1 gm per dl, glucose less than 50 mg per dl and lactate dehydrogenase greater than 225 mU per ml. In only two episodes of spontaneous bacterial peritonitis were two of the criteria fulfilled.

Ascitic Fluid↗
PubMedDate not supplied

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↗
PubMedDate not supplied

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↗
PubMedDate not supplied

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↗
PubMedDate not supplied

Hepatofugal portal flow in cirrhosis: observations on hepatic hemodynamics and the nature of the arterioportal communications.

Six of 85 patients (7%) with alcoholic liver disease undergoing transhepatic portal pressure measurement had either stagnant (3 patients) or reversed (3 patients) portal blood flow documented by gentle hand injection of 1 to 2 ml of angiographic contrast. Portal blood flow was uniformly hepatopetal in 24 patients with nonalcoholic liver disease. Recurrent spontaneous hepatic encephalopathy and sodium retention occurred in 4 of 6 patients with stagnant or reversed portal flow; gastrointestinal bleeding was not seen. Standard laboratory tests of liver function were widely variable. Net portal pressure was lower in this group than in patients with alcoholic liver disease and forward portal flow (9.2 +/- 2.6 vs. 15.6 +/- 4.1 mm Hg, p less than 0.001). Wedged hepatic vein pressure was 1 to 7 mm Hg higher than portal vein pressure in patients with reversed portal flow. The arterioportal extraction of bile acid was calculated from the difference in concentration between artery and portal vein, and total functional hepatic blood flow was calculated from the hepatic extraction and systemic clearance of indocyanine green. Extraction was 0%, and hepatic blood flow was 0.469 liter per min in a patient with hepatofugal portal flow and recurrent encephalopathy. Extraction was 20%, and hepatic blood flow was 4.014 liters per min in a patient who had never had encephalopathy. These data indicate that arterioportal communications may be sinusoidal or presinusoidal in patients who lose forward portal flow and that the amount of flow in the arterioportal circuit, together with its efficiency, largely determine the clinical outcome.

Collateral Circulation↗
PubMedDate not supplied

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↗