Thromb Haemost 1996; 76(06): 0909-0915
DOI: 10.1055/s-0038-1650685
Original Article
Schattauer GmbH Stuttgart

Activation of Coagulation and Fibrinolysis in Heatstroke

Abderrezak Bouchama
1   The Department of Medicine, Biomedical and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia
,
Françoise Bridey
2   Service d’Hematologie et d’lmmunologie Biologiques et INSERM U294, CHU Xavier Bichat, Paris, France
,
Muhammad M Hammami
1   The Department of Medicine, Biomedical and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia
,
Catherine Lacombe
2   Service d’Hematologie et d’lmmunologie Biologiques et INSERM U294, CHU Xavier Bichat, Paris, France
,
Essam Al-Shail
1   The Department of Medicine, Biomedical and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia
,
Yazid Al-Ohali
1   The Department of Medicine, Biomedical and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia
,
Frédéric Combe
2   Service d’Hematologie et d’lmmunologie Biologiques et INSERM U294, CHU Xavier Bichat, Paris, France
,
Sultan Al-Sedairy
1   The Department of Medicine, Biomedical and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia
,
Dominique de Prost
2   Service d’Hematologie et d’lmmunologie Biologiques et INSERM U294, CHU Xavier Bichat, Paris, France
› Author Affiliations
Further Information

Publication History

Received 15 February 1996

Accepted after resubmission 14 June 1996

Publication Date:
11 July 2018 (online)

Summary

Hemorrhagic diathesis and widespread microthrombosis are common in heatstroke. To assess the early stages of coagulopathy in heatstroke, thrombin-antithrombin III (TAT), fibrin monomers, plasmin-a2-antiplasmin (PAP), plasminogen and D-Dimer were measured in 16 heatstroke patients (means ± SE rectal temperature 42.3 ± 0.2° C) pre- and postcooling and compared with 8 heatstressed and 23 normal controls.

Comparing heatstroke patients with normal controls, TAT, fibrin monomers, PAP and D-Dimer were elevated to (median (range)) 16.5 (4-1000) versus 3.5 (2-7.2) Μg/l p<0.001,16 (4-113) versus 2 (2-9) nM p<0.001; 3300 (1000-36500) versus 255 (136-462) Μg/l p<0.001 and 0.72 (0.22-64.8) versus 0.15 (0.05-0.25) Μg/ml p<0.01 respectively. Plasminogen decreased to 81% (34-106); PAP, TAT and D-Dimer correlated significantly with hyperthermia (r = 0.577, p = 0.02; r = 0.635, p = 0.01; r = 0.76, p = 0.003). Postcooling PAP decreased to 545 (260-850) Μg/1 p<0.005, TAT 10 (6-70) |ig/l, and fibrin monomers 22 (18-86) nM remained unchanged. Heatstressed controls showed mild but significant increase in all markers.

Activation of coagulation and fibrinolysis occurs early and is profound and sustained in heatstroke. Cooling seems to attenuate the activation of fibrinolysis only, however, this requires confirmation in a larger study population.