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Three cases of splenic rupture causing cardiovascular collapse in critically ill patients are discussed. The first patient had received cardiopulmonary resuscitation (CPR) in the days before the collapse, the second patient was recovering from severe sepsis and the third patient was recovering from severe sepsis, had received CPR and had undergone percutaneous endoscopic gastrostomy (PEG). The diagnosis was made at post mortem in two of the patients, the third patient, who bled following PEG, survived after prompt surgical intervention. Splenic rupture should be considered as part of the differential diagnosis of unexpected cardiovascular collapse in patients who have received CPR or who are recovering from sepsis.

This article deals with the dilemmas in the definition, diagnostic work-up, and treatment of patients with the irritable bowel syndrome. The data presented are a blend of scientific insight to date and more than four decades of clinical experience with this disorder.

Four patients developed adrenal hemorrhage during treatment with intravenous adrenocorticotropic hormone (ACTH) for severe inflammatory bowel disease (IBD). This complication presented suddenly with upper abdominal and flank pain mimicking an acute surgical abdomen. In each patient the symptoms of the underlying bowel disease had subsided under the ACTH therapy. In our first patient the diagnosis was not made until laparotomy, but in the subsequent three patients the diagnosis was suspected by the strikingly similar clinical presentation. In each of these three latter patients the diagnosis was confirmed by sonography or computed tomography (CT) scan, and surgery was avoided. All four of our patients are doing well at 1-58 months of follow-up. Signs of adrenal insufficiency occurred only in the one of our four patients, and in those six of 11 previously reported patients, who had bilateral adrenal hemorrhage. ACTH-induced adrenal hemorrhage requires stopping ACTH and maintaining corticosteroid support. The diagnosis of adrenal hemorrhage should be considered in the patient treated with ACTH who develops unexplained acute abdominal or flank pain. Failure to recognize this complication of ACTH therapy can lead to unnecessary surgery or the dangerous continuation of the offending agent.

Spurious elevation of the serum potassium can be seen if the platelet count exceeds 1,000 x 10(9)/L in patients with myeloproliferative disease. To see if serum potassium is increased at more modest elevations of the platelet count we studied these parameters in 283 controls and 161 patients with reactive thrombocytosis. The incidence of hyperkalemia was 34% in patients with over 500 x 10(9) platelets/L compared with 9% if the platelet count was below 250 x 10(9)/L. Over this range there was a significant correlation of potassium increasing with the platelet count. The higher potassium values could not be explained on the basis of leukocytosis, renal insufficiency, or acidosis, suggesting that the elevated serum levels were often spurious. In support of this conclusion, the serum potassium exceeded plasma potassium by a larger amount in patients with thrombocytosis. We conclude that serum potassium rises in direct proportion to the platelet count in normal patients and in those with thrombocytosis, and that this increment is an artifact.

Detergents in general inhibit bacterial growth. The anionic detergent, sodium lauryl sulphate (NaLS), seems to have a more specific inhibitory effect on growth of the Gram-positive Bacillus subtilis than on growth of the Gram-negative Escherichia coli. The specificity of anionic detergent towards B. subtilis has been traced to the difference in the nature of the cell wall. The inhibitory action of the detergent is markedly increased by the presence of metal ions like Cd++ or Mg++, due probably to the increase in the micellar phase, facilitating the solubilisation of bacterial species in the inner core of micelles. While metal ions like Cu++ do not influence the activity of NaLS, Na+, Ca++ or Mn++ ions seem to act against the detergent action on bacterial growth, probably by altering the structure of micelles.