WHITE CLOT SYNDROME

Citation
Cr. Canova et al., WHITE CLOT SYNDROME, Schweizerische medizinische Wochenschrift, 127(18), 1997, pp. 762-765
Citations number
18
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00367672
Volume
127
Issue
18
Year of publication
1997
Pages
762 - 765
Database
ISI
SICI code
0036-7672(1997)127:18<762:WCS>2.0.ZU;2-X
Abstract
A 75-year old female underwent coronary angiography for chest pain. Si gnificant proximal stenosis of the left coronary artery was found. Dur ing the waiting time for bypass surgery, intravenous heparin treatment was established for several days because of recurrent unstable angina pectoris. 10 days after coronary angiography an acute event with ches t pain, hypotension, tachycardia and a new right bundle branch block s uspect for myocardial infarction occurred, which was treated with rt-P A. Fever, persistent hypotension, acute progressive renal failure and thrombocytopenia suggested septic shock, and the patient was transferr ed to our hospital. A pulmonary artery catheter could not be advanced beyond the main stem of the pulmonary artery. The patient died suddenl y 24 hours later from acute right ventricular failure. Autopsy demonst rated multiple white clots in both pulmonary arteries. The histologica l finding of clots rich in leukocytes and fibrin was compatible with t he diagnosis of heparin-induced thrombosis-thrombocytopenia or white c lot syndrome. Heparin-induced thrombocytopenia may occur after about 5 days of treatment. Two distinct types have been described. The first type occurs in up to 25% of patients receiving heparin and is a result of temporary platelet aggregation, margination and peripheral sequest ration. The less common second type of thrombocytopenia is thought to be mediated by a heparin-dependent IgG antibody inducing platelet aggr egation and may be associated with thromboembolic events leading to th e white clot syndrome, which is rarely reported in the literature. In these cases heparin should be stopped immediately and replaced by oral anticoagulation. Other therapies such as low molecular weight heparin , synthetic heparinoids, hirudin, fibrinolytic agents, plasmapheresis and intravenous immunoglobulins are discussed. Monitoring of the plate let count every 5 days in patients receiving heparin for any extended period should become standard medical practice to avoid potential fata l complications.