Establishment of a sepsis model following implantation of Klebsiella pneumoniae-infected fibrin clot into the peritoneal cavity of mice.

Successful establishment of sepsis by entrapping a dose of 150 colony forming units of Klebsiella pneumoniae in a fibrin clot following implantation into the peritoneal cavity of mice is reported. The dose in the fibrin clot gave 50% mortality in mice, spread over a period of one week. All the infected mice showed positive blood culture up to 6 d post-infection; histopathology revealed inflammatory changes in both liver and spleen. Introduction of K. pneumoniae into experimental mice without entrapment in fibrin clot caused no mortality and blood culture remained positive only up to 2 d; histopathology of liver and spleen throughout the period of study showed relatively mild inflammatory changes, which almost cleared during 14 d post-infection. The use of the fibrin-clot model may thus be considered to be useful in studying both the initial and the persisting stage of infection in the peritoneum, whence a slow release of bacteria into the blood takes place which finally leads to sepsis and septicemia.

Congenital jejunal leiomyoma in a neonate.

Leiomyomas of the small intestine are rare in neonates. We report a neonate with jejunal leiomyoma, who presented with acute intestinal obstruction.

Bilateral proptosis due to metastatic Ewing's sarcoma of the orbit: fine needle aspiration cytology (FNAC) and histopathology of a case.

Bilateral proptosis due to metastatic Ewing's sarcoma is an extremely rare presentation and thus merits reporting. The role of fine needle aspiration cytology in the diagnosis is highlighted.

Adrenocortical involvement in aluminium phosphide poisoning.

The effect of aluminium phosphide (AlP) which is a systemic poison on the adrenal cortex was studied in 30 patients of AlP poisoning. A significant rise in the plasma cortisol level (greater than 1048 nmol/l) was observed in the twenty patients. Mortality was 50 per cent. Autopsy study could be undertaken only in 10 patients. Histopathology showed mild to moderate changes. In the rest (10 patients), the adrenal cortex was critically involved and the cortisol level failed to rise beyond normal levels (less than 690 nmol/l). The histopathology revealed severe changes (complete lipid depletion, haemorrhage, necrosis etc.) and all these patients died. In the critically ill patients, the cortisol levels remained low because of severe adreno-cortical involvement. The changes in the adrenal cortex could be due to shock or to cellular toxic effect of phosphine. The histopathological changes in various viscera showed congestion, edema and cellular infiltration. In the heart, there were patchy areas of necrosis, while the liver showed fatty changes and the lungs showed, in addition areas of gray/red hepatization. There was no adrenal apoplexy or extensive haemorrhage that could explain shock in these patients. Cardiogenic shock could not be confirmed due to lack of facilities for haemodynamic monitoring, but there was histopathological evidence in support of cardiovascular shock.

Adult respiratory distress syndrome following aluminium phosphide ingestion. Report of 4 cases.

Four cases of adult respiratory distress syndrome (ARDS) following aluminium phosphide ingestion (ALP) are being reported. The dose of the intoxicant varied from 2 tablets (6.0 gm) to 3 tablets (9.0 gm). All patients had shock at admission and developed ARDS within 6 hours. The exhalation of Phosphine, (PH3) detected by positive silver nitrate paper test, was the possible noxious triggering factor in our cases. The cases are being reported because of their rare occurrence.