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T Hau

Publications and source records attributed to T Hau.

At least 55 records · Page 3Linked to original sources

The effect of bacterial trapping by fibrin on the efficacy of systemic antibiotics in experimental peritonitis.

Sixty Sprague-Dawley rats were inoculated with 10(9) Escherichia coli either suspended in 2 milliliters of normal saline solution or incorporated in a 2 milliliter 0.4 per cent fibrin clot. One hour after inoculation, one-half of the rats in each group received gentamicin, 12.5 milligrams per kilogram, intramuscularly. Escherichia coli suspended in normal saline solution was uniformly lethal. Incorporation of the bacteria and fibrin resulted in a survival of 13 of 15 rats (p = less than 0.002), but in abscess formation in all survivors. Treatment with gentamicin nearly abolished the mortality of Escherichia coli suspended in normal saline solution (14 of 15 rats survived, p = less than 0.002) but did not prevent abscess formation when bacteria were incorporated into fibrin. The gentamicin level exceeded the minimal inhibitory concentration (0.98 microgram per milliliter) for the strain of Escherichia coli used in serum (15.84 micrograms per milliliter after one hour) and peritoneal fluid (14.75 micrograms per milliliter after one hour) but never reached inhibitory levels in the fibrin clot (0.75 microgram per milliliter after one hour). We conclude that entrapment of bacteria by fibrin abolishes systemic sepsis but also protects bacteria against the action of systemic antibiotics and favors abscess formation.

Abscess↗

Irrigation of the peritoneal cavity and local antibiotics in the treatment of peritonitis.

Peritonitis was induced in the Sprague-Dawley rats by the implantation of gelatin capsules containing 0.3 milliliter of human fecal suspension into the peritoneal cavity. The rats were then treated with systemic antibiotics or peritoneal irrigation with normal saline solution alone or cephalotin solution, 2,000 micrograms per liter, or both. The results show that peritoneal irrigation with normal saline solution or with cephalotin alone was ineffective, even though the cephalotin concentration used inhibited the growth of all bacterial species isolated during the free stage of peritonitis in vitro. Systemic antibiotics alone as well as in combination with peritoneal irrigation significantly improved the survival rate, p less than or equal to 0.05 and p less than or equal to 0.02, respectively. However, only systemic antibiotics in combination with peritoneal irrigation resulted in a significant cure rate compared with the control group and the group treated with systemic antibiotics alone, p less than or equal to 0.002. There was no increase in the cure or survival rates when antibiotics were added to the peritoneal irrigation fluid. In the second experiment, seven of ten rats treated with systemic antibiotics survived, but only two rats had no intraperitoneal abscesses at autopsy. Intraperitoneal application of antibiotics did not improve these results: six rats survived, and one rat was cured. We conclude that peritoneal irrigation alone is ineffective in the treatment of peritonitis. The addition of peritoneal irrigation to systemic antibiotic therapy, however, resulted in a significantly increased cure rate. The addition of antibiotics to the irrigant does not further improve the results, and local antibiotics are not more effective than systemic antibiotics. We believe that benefit of peritoneal irrigation is due to its mechanical effect.

Animals↗

Amebic liver abscess.

Amebic liver abscess was seen in 35 patients over a ten-year period at Cook County and the University of Illinois hospitals, Chicago; 32 had immigrated from an area of endemic amebiasis, but three were natives of Chicago. Typically they had right upper-quadrant abdominal pain and fever of short duration (nine days); on physical examination, upper abdominal tenderness and hepatomegaly were usually present. The diagnosis was confirmed by liver scan, serologic studies, aspiration of "anchovy paste" from the abscess, and/or a favorable response to specific antiamebic therapy. Most were solitary abscesses in the right lobe of the liver. Metronidazole treatment alone was adequate in 24 of 29 patients (83%). Nine patients underwent percutaneous or surgical drainage of the abscess owing to incorrect diagnosis (three), persistent pain and fever after medical treatment (three), expanding left lobe abscess (two), and for diagnosis (one). Mortality was 5.7% (two patients). Owing to current immigration patterns amebic liver abscess should be considered in the differential diagnosis of patients with right upper-quadrant pain and fever. The diagnosis should be confirmed with a liver scan and serologic study for amebiasis.

Adolescent↗

[Intraperitoneal infections and immunosuppression (author's transl)].

The growing number of patients showing a restricted immune defence, also causes the surgeon to be faced with big problems; particularly in the case of intraperitoneal infections. In case of peritonitis the organism may dispose of various opportunities of immune defence involving the local limitation by adhesions, phagocyte activity, humoral and cellular immunity. Deficiencies in immune defence (congenital, acquired or iatrogenically induced) will change symptoms, diagnosis and therapy of intraperitoneal infections. Due to the lack of segmental granulocytes in patients with restricted immune defence there are frequently no symptoms of intraperitoneal infections, such as abdominal tenderness and pain. The diagnostic lavage of the abdominal cavity should be applied early. The therapy hardly differs from the general treatment of peritonitis in normal patients. The changed germ spectrum among them opportunistic germs, viruses, parasites amd mycetes, required a modified application of antibiotics. The prognosis of peritonitis in patients with restricted immune defence depends on the etiology of the infection and the degree of immunosuppression. At present a mortality rate of up to 70% is still registered.

Antibody Formation↗

[Peritonitis following kidney transplantation].

Twenty of 322 renal allograft recipients developed intraperitoneal infections. The mortality was 70% and responsible for 20% of all transplant deaths. Wound infections were the source of the peritonitis in over 50% of the patients, 40% were on high-dose immunosuppression. In contradistinction to the patients who died, the clinical picture of the survivors was characterized by: (1) localized peritonitis, (2) no high-dose immunosuppression, (3) absence of uncommon pathogens like C. albicans and S. marcescens, (4) radical peritoneal debridement with irrigation of the abdominal cavity at the time of surgery.

Humans↗

Mechanisms of the adjuvant effect of hemoglobin in experimental peritonitis. IV. The adjuvant effect of hemoglobin in granulocytopenic rats.

Intraperitoneal inocula of pure Escherichia coli do not produce lethal peritonitis unless adjuvant materials are present. We have previously presented evidence that hemoglobin acts as an adjuvant in experimental Escherichia coli peritonitis by interfering with antibacterial neutrophil function. The hypothesis was further tested in normal Sprague-Dawley rats and rats depleted of granulocytes by pretreatment with busulfan and cyclophosphamide. Hemoglobin increased the lethality of Escherichia coli peritonitis in both neutropenic and normal rats. Furthermore, the early clearance of bacteria from the peritoneal cavity was equally depressed by hemoglobin in neutropenic and normal rats. We conclude that hemoglobin has some effect on intraperitoneal infections beyond its suppression of granulocyte function. This additional effect may represent interference with bacterial lymphatic absorption or peritoneal or systemic macrophage function or may be a manifestation of a nutritional effect of hemoglobin on bacterial growth.

Adjuvants, Immunologic↗

Chemotactic substances in the treatment of experimental intraperitoneal infections.

Since peritonitis remains a serious clinical problem, we have evaluated the prophylactic efficacy of intraperitoneally administered chemotactic substances in murine intraperitoneal infections. The injection of 10 ml of 3% thioglycollate increased the peritoneal white blood cell count of rats from 1.3 +/- 0.1 X 10(6) (mean +/- SEM) to 1.1 +/- 0.1 X 10(7) (mean +/- SEM) cells/ml. This increase in the number of intraperitoneal phagocytes resulted in reduction in mortality caused by an inoculum consisting of E. coli and hemoglobin from 68% in the control group to 29% in the thioglycollate pretreated group (p less than or equal to 0.02). Intraperitoneal injection of N-formyl-methionyl-phenylalanine (FMP), a chemotactically active oligopeptide, increased the intraperitoneal granulocyte count from virtually 0 to 1 X 1.9 +/- 0.53 X 10(4) (mean +/- SEM) cells/ml after 90 minutes. The rats pretreated in such a manner showed a mortality of 51% after an intraperitoneal challenge with an E. coli/hemoglobin inoculum as compared to a mortality of 72% in control animals (p less than or equal to 0.025). Thus, chemotactic substances can effectively increase the number of phagocytes and concurrently induce resistance to an intraperitoneal bacterial challenge.

Animals↗

Mechanisms of the adjuvant effect of hemoglobin in experimental peritonitis. III. The influence of hemoglobin on phagocytosis and intracellular killing by human granulocytes.

The effect of hemoglobin on the ability of polymorphonuclear granulocytes (PMNs) to phagocytize and kill opsonized E. coli was measured. Results show that the addition of hemoglobin in a concentration of 0.1% inhibititis phagocytotic activity of PMNs from 68% to 13% after 30 minutes and from 73% to 45% after 60 minutes. The rate of intracellular killing after the addition of hemoglobin in the concentration of 0.5% declined from 63% to 21%. Though these experiments do not allow any conclusions as to the exact mechanism of action of hemoglobin in inhibition of phagocytosis, it seems likely from other data that the inhibitory activity resides in the heme part of the molecule. We conclude that hemoglobin inhibits phagocytotic activity and the ability to kill ingested bacteria of human polymorphonuclear granulocytes. This provides an additional mechanism for the adjuvant action of hemoglobin in intraperitoneal infections and supports the theory that hemoglobin acts directly on the granulocyte to impair the essential host defenses.

Escherichia coli Infections↗

Enhancement of local immune response in the treatment of experimental peritonitis.

We conclude from these experiments that the host defense in peritoneal infections rests largely on the phagocytic cells attracted into the peritoneal cavity by the offending organism, and that an increase in the number of available phagocytes by pretreatment with chemotactic substances protects against lethal peritoneal infections. There seems to be a direct relationship between the number of available phagocytes in the peritoneal cavity at the time of inoculation and the reduction of mortality in experimental peritonitis (Fig. 1).

Animals↗

Fibrinolytic activity of the peritoneum during experimental peritonitis.

The effect of laparotomy, intestinal resection, heparin and bacterial peritonitis on fibrinolysis of the peritoneum was evaluated in dogs. Heparin had no effect. Sterile laparotomy and intestinal resection severely, but incompletely, reduced fibrinolytic activity measured 24 hours after operation. Fibrinopurulent peritonitis induced by creation of a 10 centimeter long ischemic loop of the terminal part of the ileum abolished the fibrinolytic activity of the peritoneum almost completely. The data are consistent with findings that adhesion formation is inversely correlated with the fibrinolytic activity of the peritoneum. Untreated peritonitis abolished that activity by mechanisms as yet not elucidated. Heparin, which has been shown to reduce both adhesion-formation and the lethality of peritonitis, apparently does so by mechanisms independent of the intrinsic fibrinolytic system of the peritoneum.

Animals↗

Heparin in the treatment of experimental peritonitis.

Two experiments were performed to determine the effect of heparin on experimental fibrinopurulent peritonitis in dogs. Peritonitis was induced by the creation of a 10 cm long isolated loop of terminal ileum. In a first experiment comprising 24 dogs the necrotic loop was removed 24 hours later without cleaning or irrigating the peritoneal cavity. All dogs showed fibrino-purulent peritonitis at that time. No antibiotics were given. All dogs received 500 ml of Ringer's lactate during surgery and were allowed p.o. fluids on the first postoperative day. At the time of excision the dogs were blindly randomized into a control group and two treatment groups receiving heparin 100 u/kg i.p. or s.c. respectively. Of the eight animals in the control group, five died of peritonitis and two showed residual intraperitoneal sepsis at the time of sacrifice 14 days after the initial surgery. Thus, only one dog cleared his peritoneal infection spontaneously. Of the heparin treated dogs six out of eight in the i.p. treated and seven out of eight in the s.c. treated group cleared their peritonitis spontaneously within 14 days (p </= 0.05 and 0.02 respectively). In a second experiment peritonitis was induced in 24 dogs as described above, but the necrotic loop was not removed. The dogs were blindly randomized to daily low dose heparin (50 u/kg s.c. b.i.d.) or no therapy. Only two out of 12 dogs of the control group survived the observation period of 14 days compared with eight out of 12 of the heparin treated group (p </= 0.05). However, in all dogs in this experiment residual i.p. sepsis was found. We conclude that heparin has a therapeutic effect in experimental canine peritonitis by preventing the additional apposition of fibrin and, thus, rendering the bacteria more susceptible to cellular and noncellular clearing mechanisms.

Animals↗

The effect of adenosine and allopurinol on the tolerance of the collapsed lung to warm ischemia.

The collapsed left lungs of dogs were subjected to 1 hour of normothermic ischemia in situ followed by immediate ligation of the contralateral pulmonary artery. Adenosine in a dose of 50 mg/kg prolonged the survival of the dogs significantly. In the survivors only transient changes in the chest x-ray were seen, and no changes in arterial oxygenation were observed. The pulmonary architecture was well preserved on histological studies 14 days after operation. Animals whose ischemic lungs were not protected by adenosine showed an immediate drop in arterial oxygenation and a massive infiltrate of the ischemic lung. Histological study of the lungs showed a complete breakdown of the capillary-alveolar barrier. Allopurinol alone was ineffective by itself and was not able to improve the survival achieved with adenosine further. We conclude that it is possible to prolong the tolerance of a deflated lung to normothermic ischemia by pretreatment with adenosine.

Adenosine↗