Clinical and Laboratory Aspects of Disseminated Intravascular Coagulation (DIC): A Study of 118 Cases^[*]

Summary

The medical records of 118 cases who met laboratory criteria of DIC were studied. The most frequent etiologies were: Generalized infection (39.8%), trauma (16.9%), malignancy (6.8%) and surgical cases (6.8%). The main clinical manifestations which appeared to be related solely to DIC were (in a decreasing order of frequency): Bleeding (64.4%), renal dysfunction (24.6%), liver dysfunction (18.6%), respiratory dysfunction (16.1%), shock (14.4%), thromboembolic phenomena (6.8%) and central nervous system involvement (1.7%). In 26 patients none of these manifestations were observed. In patients with infection, liver and renal dysfunction were frequent and respiratory dysfunction rare, whereas in trauma cases, liver and renal dysfunctions were rare and respiratory dysfunction frequent. This variability indicates that the clinical manifestations are affected not only by the process of intravascular coagulation but also by the underlying clinical disorders.

The most impaired coagulation tests were prothrombin time, partial thromboplastin time, platelet count and thrombin time. The degree of abnormality of these coagulation tests was found to be related to the extensiveness of organ involvement.

The mortality (overall 54.7%) increased independently with age, with the number of clinical manifestations and with the degree of abnormality of the above-mentioned four most impaired coagulation tests. In addition, older patients were more likely to have an increased number of clinical manifestations and more impaired coagulation tests. Mortality was similar in the various etiologies except for trauma patients in whom it was lower (30%).

• References

• 1 Al-Mondhiry H. 1975; Disseminated intravascular coagulation in a major cancer center. Thrombosis et Diathesis Haemorrhagica 34: 181
• 2 Alving BM, Bell WR. 1976; Methods for correcting inhibitory effects of fibrinogen degradation products in fibrinogen determinations. Thrombosis Research 9: 1
• 3 Collins RC, Al-Mondhiry H, Chernik NL, Posner JB. 1975; Neurologic manifestations of intravascular coagulation in patients with cancer. A clinico pathologic analysis of 12 cases. Neurology 25: 795
• 4 Colman RW, Robboy SJ, Minna JD. 1972; Disseminated intravascular coagulation (DIC). An approach. American Journal of Medicine 52: 679
• 5 Hardisly RM, Ingram GIC, Sharp AA. 1964. The Association of Clinical Pathologists Broadsheet no 48 new series.
• 6 Kidder WR, Logan LJ, Rapaport SI, Patch MJ. 1972; The plasma protamin paracoagulation test. A clinical and laboratory evaluation. American Journal of Clinical Pathology 58: 675
• 7 Merskey C, Johnson AJ, Kleiner GJ, Wohl H. 1967; The defibrination syndrome; clinical features and laboratory diagnosis. British Journal of Haematology 13: 528
• 8 Minna JD, Robboy SJ, Colman RW. 1974. Disseminated Intravascular Coagulation in Man. Charles C. Thomas, Springfield, Illinois; U.S.A:
• 9 Mckay DG. 1965. Disseminated Intravascular Coagulation New York. Harper and Row; New York:
• 10 Proctor RR, Rapaport SI. 1961; The partial thromboplastin time with Kaolin. A simple screening test for first stage plasma clotting factor deficiencies. American Journal of Clinical Pathology 36: 212
• 11 Quick AJ. 1966. Hemorrhagic Diseases and Thrombosis 2nd edition, Lea and Febiger. Philadelphia; U.S.A:
• 12 Rampling MW, Gaffney PJ. 1976; The sulphite precipitation method for fibrinogen measurement; its use on small samples in the presence of fibrinogen degradation products. Clinica Chimica Acta 67: 43