No abstract

SummaryA hypothermia-induced hemorrhagic diathesis is associated with cardiopulmonary bypass, major surgery, and multiple trauma, but its pathophysiological basis is not well understood. We examined the hypothesis that hypothermia reversibly inhibits human platelet activation in vitro and in vivo. Platelet activation was studied in normal volunteers by whole blood flow cytometric analysis of modulation of platelet surface GMP-140 and the glycoprotein (GP) Ib-IX complex in: a) shed blood emerging from a standardized in vivo bleeding time wound; b) peripheral blood activated in vitro with either thrombin (in the presence of gly-pro-arg-pro, an inhibitor of fibrin polymerization) or the stable thromboxane (TX) A2 analogue U46619. Platelets in peripheral whole blood were activated at temperatures between 22° C and 37° C. the forearm skin temperature was maintained at temperatures between 22° C and 37° C prior to and during the bleeding time incision. Platelet aggregation was studied in shed blood by flow cytometry and in peripheral blood by aggregometry. Generation of TXB 2 (the stable metabolite of TXA 2) was determined by radioimmunoassay. In vitro, hypothermia inhibited both thrombin- and U46619-induced upregulation of GMP-140, downregulation of the GPIb-IX complex, platelet aggregation, and TXB2 generation. These inhibitory effects of hypothermia were all completely reversed by rewarming the blood to 37° C. In vivo, platelet activation was inhibited by hypothermia as shown by 5 independent assays of shed blood: upregulation of GMP-140, downregulation of the GPIb-IX complex, platelet aggregate formation, TXB 2 ggeneration, and the bleeding time. In summary, by a combination of immunologic, biochemical, and functional assays, we demonstrate that hypothermia inhibits human platelet activation in whole blood in vitro and in vivo. Rewarming hypothermic blood completely reverses the activation defect. These results suggest that maintaining normothermia or rewarming a hypothermic bleeding patient may reduce the need for platelet transfusions.

We examined the effects of nitric oxide (NO)/endothelium-derived relaxing factor (EDRF) on platelet surface glycoproteins (GP). As determined by flow cytometry, in both a washed platelet system and platelet-rich plasma, the EDRF congener (S-nitroso-N-acetylcysteine) markedly inhibited both the thrombin-induced and the (stable thromboxane A2 analogue) U-46619-induced upregulation of P-selectin (alpha-granule protein), CD63 (lysosomal protein), and the GPIIb-IIIa complex (fibrinogen receptor) but minimally inhibited downregulation of the GPIb-IX complex (von Willebrand factor receptor). The inhibitory effects of EDRF were markedly reduced in whole blood or by the addition of washed erythrocytes. Platelets in whole blood were still responsive to guanosine 3',5'-cyclic monophosphate (cGMP), as shown by complete inhibition of P-selectin upregulation by the stable analogue N6,2'-O dibutyryl cGMP. These data suggests that 1) cGMP negatively regulates the platelet surface expression of P-selectin, CD63, and the GPIIb-IIIa complex but not the platelet surface expression of the GPIb-IX complex and 2) hemoglobin within erythrocytes inhibits the effects of EDRF/NO on platelet surface glycoproteins.

The efficacy of routine screening coagulation tests was studied to identify occult coagulopathies in patients prior to elective general and vascular surgery procedures. The efficacy of screening tests was compared to that of indicated tests performed for predefined clinical indications, which were elicited by history and physical examination and a detailed coagulation history questionnaire. Tests were prothrombin time (PT), partial thromboplastin time (PTT), platelet count (PC), and bleeding time (BT). Of 514 screening tests done in the 282 patients, 4.1% were abnormal, but none of them identified a clinically significant coagulopathy. Of the 605 indicated tests, 7.4% were abnormal, and all significant coagulopathies were found in this group. The study shows that preoperative screening tests for coagulopathies not suspected on the basis of detailed clinical information are unnecessary and should not be done. In the authors' institution 46% of screening coagulation tests could be eliminated.

No abstract

UGC is a safe and effective treatment for most catheter-induced femoral pseudoaneurysms with a low complication rate and excellent long-term results at a cost substantially lower than operative treatment. Because the natural history of IFP is unpredictable, UGC appears to be the preferred treatment for all IFPs persisting after cessation of heparin anticoagulation.

A 28-year-old major league baseball pitcher sustained an axillary artery thrombosis which was successfully treated with intraarterial urokinase. Subsequent angiography and duplex scanning with the arm elevated in the pitching position demonstrated inducible compression of the axillary artery by the humeral head as well as compression at the thoracic outlet. To determine the incidence of axillary and subclavian artery compression and to investigate the mechanism of injury, brachial artery blood pressures and duplex scans of the subclavian and axillary arteries were performed in both the neutral position and the throwing position in the 92 extremities of 19 major league baseball pitchers, 16 non-pitching major league players, and 11 nonathlete controls. A drop in blood pressure of greater than 20 mm Hg was noted in the position in 56% of extremities tested, with a loss of a detectable blood pressure in 13%. Compression of the axillary artery by the humeral head was documented in 83% of extremities, but in only 7.6% was a greater than 50% stenosis inducible. No statistical difference was found in the incidence of arterial compression between the three groups tested or between their dominant and nondominant extremities. Dissection of the axillary artery in two cadavers documented that abduction and external rotation of the arm causes compression of the axillary artery by the humeral head, which acts as a fulcrum. We conclude that the repetitive mechanical trauma of the throwing motion can cause intermittent compression and contusion of the axillary artery by the humeral head and predisposes the athlete who throws to thrombosis of the axillary artery.

No abstract