Rapid preparation of a patient with pheochromocytoma with labetolol and magnesium sulfate.

PURPOSE: To describe the rapid perioperative optimization and control of blood pressure in a young patient who presented with pheochromocytoma. He was non-compliant with phenoxybenzamine but insisted on early surgery. He was scheduled for laparoscopic resection of the tumour. CLINICAL FEATURES: This 32-yr-old man presented with uncontrolled hypertension for a few years for which he was treated with nifedipine. He subsequently defaulted follow-up. The patient presented again approximately three months from the day of surgery and was diagnosed to have a pheochromocytoma. The endocrinologist prescribed phenoxybenzamine and propanolol in addition to the nifedipine but the patient stopped taking both drugs six weeks prior to surgery due to their side effects. The patient was admitted the evening before surgery to the intensive care unit for rapid control of his blood pressure. Blood pressure was optimized with an infusion of labetolol and volume expansion titrated under central venous catheter and intraarterial blood pressure guidance throughout the night. On the morning of surgery, a magnesium sulfate infusion was started. The laparoscopic surgery proceeded uneventfully and the patient was hemodynamically stable. There were two transient periods of hypotension after induction and at removal of tumour respectively which were corrected with a brief adrenaline infusion. No adverse outcome was noted. CONCLUSION: This case highlights the possibility of a more rapid perioperative control of pheochromocytoma using high doses of labetolol and a magnesium sulfate infusion to achieve stable intraoperative hemodynamics during laparoscopic resection of pheochromocytoma.

Helicobacter hepaticus infection triggers inflammatory bowel disease in T cell receptor alphabeta mutant mice.

The T cell receptor alpha chain-deficient (TCR alpha-/-) and TCR beta chain-deficient (TCR beta-/-) mice develop chronic intestinal inflammation that resembles inflammatory bowel disease by 3 to 4 months of age. The objective of the study reported here was to determine the role of infection with the bacterial pathogen Helicobacter hepaticus in the pathogenesis of disease in TCR alphabeta mutant mice. The H. hepaticus-infected TCR alphabeta mutant mice were rederived by use of embryo transfer to produce Helicobacter-free animals. Helicobacter-free TCR alpha-/-, TCR beta-/-, and TCR alpha-/- beta-/- mice were inoculated with H. hepaticus. Experimentally infected mice and uninfected control mice were examined for intestinal lesions at 3, 6, and 9 months after inoculation. The TCR alphabeta mutant mice inoculated with H. hepaticus developed intestinal epithelial cell hyperplasia and mucosal inflammation. By 6 months after inoculation, infected animals had moderate cecal and colonic lesions. Helicobacter-free TCR alpha-/- mice, but not TCR beta-/- or TCR alpha-/- x beta-/- mice, also developed H. hepaticus-independent colitis by 9 months after inoculation. Infection with H. hepaticus is sufficient to cause chronic proliferative intestinal inflammation in TCR alphabeta mutant mice. However, H. hepaticus infection is not necessary for intestinal disease in TCR alpha-/- mice.

Denitrogenation in pregnant women.

Forty-five pregnant females were studied with respect to the effectiveness of denitrogenation by the 3, 5, 7 and 9 rapid vital capacity breaths, and 3 to 5 minutes of normal breathing. It was found that 3 to 9 vital capacity breaths cannot effectively denitrogenate a pregnant patient when a circle breathing system with a gas flow of 8 litres/min is used. At least 3 minutes of normal tidal volume breathing should be given for proper denitrogenation or preoxygenation if the circle system is used for such a purpose.

Preoxygenation in parturients: a comparison of 4, 6 and 8 vital capacity breaths to 5 minutes of tidal volume breathing.

We compared the difference in denitrogenation (by intermittent measurement of arterial tension, PaO2) in 45 parturients at term when preoxygenated with 4, 6 or 8 rapid vital capacity breaths and 5 minutes of tidal volume breathing. Oxygen, at 8 litres min-1, was delivered through a facemask via a circle absorber with a 2 litre reservoir bag. Higher PaO2 was produced with 5 minutes of tidal volume breathing. This differed significantly from the PaO2 produced by 4, 6 or 8 rapid vital capacity breaths (p less than 0.01).