Laparoscopy for diagnosis and treatment of recurrent abdominal pain in children.

Extensive radiographic evaluation of children with recurrent abdominal pain (RAP) is rarely diagnostic or cost-effective. The authors sought to define the role of laparoscopy in the evaluation of children with RAP. Fifteen children underwent laparoscopy for RAP in a 2-year period. Their mean age was 12 years (range, 6 to 16 years), 13 (87%) were female, and the mean duration of symptoms was 11 months (range, 2 to 60 months). Thirty-eight imaging studies (excluding plain films) had been obtained before laparoscopy, including 19 abdominal sonograms, 9 upper gastrointestinal series, four abdominal computed tomography scans, 3 barium enemas, 2 isotope scans, and 1 magnetic resonance examination of the head. Only two (5%) of these studies provided an accurate diagnosis. Eleven of the 15 children (73%) had positive findings diagnosed and treated laparoscopically. These included eight appendiceal abnormalities (in six patients), three Meckel's diverticula, one inguinal hernia, one urachal cyst, one para-fallopian tube cyst, and one adhesion to an appendectomy stump. Eight of 11 (73%) children with positive findings had immediate resolution of symptoms after laparoscopic treatment. Three children with pathological findings at the time of laparoscopy had persistent symptoms, which resolved completely within 4 months of the laparoscopy. Laparoscopy is an accurate technique for the evaluation and treatment of children with RAP. Its early application could provide economic benefit by eliminating many low-yield imaging studies and minimizing lost time from school.

Thoracic aortic dissection with renal artery involvement following blunt thoracic trauma: case report.

Blunt thoracic aortic injury most often occurs beyond the left subclavian artery with subsequent transection and exsanguination. We present a case of an unrestrained driver involved in a high-speed motor vehicle crash who had a traumatic mid-thoracic aortic dissection involving the orifices of both renal arteries, resulting in anuria. This diagnosis should be considered in the presence of anuria following chest trauma.

Intravascular IL-8. Inhibitor of polymorphonuclear leukocyte accumulation at sites of acute inflammation.

IL-8 has been characterized primarily as a polymorphonuclear leukocyte (PMN) chemoattractant and proinflammatory mediator. Recently, we have reported that [Ala-IL-8]77 is secreted by activated cultured human endothelial cells and can function as a potent inhibitor of PMN adhesion to these monolayers. The pathophysiologic relevance of this in vitro observation was examined by determining the effects of intravascular or extravascular administration of IL-8 on PMN emigration at sites of acute inflammation in the skin of NZW rabbits. An i.v. bolus of [Ala-IL-8]77 (12 micrograms/kg) produced a marked and selective reduction of circulating PMN within 3 min, which returned toward preinjection levels within 30 min, and subsequently exceeded this level. A similar response was observed for circulating radiolabeled PMN, and gamma-scintigraphy determined that the lungs were the primary site of leukosequestration. During the 30- to 150-min interval after i.v. infusion of [Ala-IL-8]77, PMN emigration into acute inflammatory sites, elicited by various chemoattractants or cytokines, was significantly reduced, as judged histologically and quantitated with 51Cr-labeled PMN and myeloperoxidase measurements. Intravenous administration of [Ser-IL-8]72 yielded similar results. This inhibitory effect of i.v. IL-8 was transient and reinducible and did not reflect a suppression of the responsiveness of circulating PMN to chemoattractants. Intradermal injections of [Ala-IL-8]77 or [Ser-IL-8]72 induced dose-dependent PMN accumulation, which also was significantly reduced by i.v. administration of either form of IL-8. These results indicate that i.v. IL-8 can function as a PMN-directed leukocyte adhesion inhibitor and suggest that local secretion of IL-8 by activated endothelium may differentially modulate leukocyte-endothelial interactions at sites of acute inflammation.

Platelet interaction with vascular smooth muscle in synthesis of prostacyclin.

Because vascular smooth muscle cells (SMC) can be exposed to platelets at sites of significant arterial injury, we studied whether cultured rat aorta SMC can utilize platelet-derived arachidonate and prostaglandin (PG) endoperoxides (PGG2/PGH2) in the synthesis of prostacyclin (PGI2). SMC converted exogenous PGH2 to PGI2, measured by radioimmunoassay (RIA) of 6-keto-PGF1 alpha, despite cyclooxygenase inhibition or PGH2-receptor blockade. SMC produced increasing amounts of PGI2 in the presence of an increasing number of platelets when the two cell types were coincubated with arachidonate. Furthermore, aspirin-pretreated SMC produced PGI2 in response to arachidonate, ionophore A23187, or thrombin in the presence of platelets but not in their absence. SMC, by themselves unresponsive to thrombin, produced PGI2 during coincubation with thrombin-stimulated aspirin-pretreated platelets. Separation of the SMC monolayer and platelets with a filter did not prevent platelet-dependent PGI2 formation by the SMC. Finally, aspirin-pretreated SMC, in cosuspension with platelets, inhibited platelet aggregation in association with PGI2 production. These data indicate that 1) SMC can synthesize PGI2 from exogenously added PGH2 and from platelet-derived arachidonate or endoperoxides, 2) direct cell-cell contact is not required for intercellular endoperoxide transfer, and 3) SMC can inhibit platelet aggregation possibly through PGI2 production from platelet-derived endoperoxides.

Inhibition of cold-induced vasoconstriction with ketanserin.

The role of serotonin, thromboxane A2, and prostacyclin in cold-stimulated vasoconstriction was studied in 11 volunteers randomly pretreated with placebo, antagonists to serotonin (ketanserin, 40 mg), cyclooxygenase (ibuprofen, 800 mg), or thromboxane synthetase (ketoconazole, 400 mg). With an ambient temperature of 27 degrees, the hand and distal arm of one side were immersed in iced slush for 2 min. At the end of this time there was a fall in skin temperature from 31.2 to 12.2 degrees. Six minutes later with ketanserin treatment, temperature rose 4.5 degrees above placebo (P less than 0.05). In the noncooled side, ketanserin led to a rise in baseline temperature of 2.3 degrees (P less than 0.05), and increased plethysmographic finger flow to 2.08% delta vol/sec contrasted with 1.00% delta vol/sec in the placebo group (P less than 0.05). During cold immersion, temperature of this side fell 0.5 degrees, and flow decreased to 0.17% delta vol/sec. With ketanserin, temperature did not fall and flow was 0.85% delta vol/sec (P less than 0.05). Ketanserin accelerated recovery of temperature and flow (P less than 0.05). Plasma serotonin levels were constant. Ibuprofen and ketoconazole reduced baseline thromboxane B2 levels from 30 pg to 18 and 20 pg/ml (P less than 0.05), respectively, but did not influence temperature or flow. Results show that serotonin and perhaps alpha-adrenoreceptors, but not prostanoids, modulate resting skin flow and cold-induced vasoconstriction.