The epidemiology of thromboembolic disorders: a review.

Abstract The thromboembolic disorders (exclusive of cerebral and coronary thrombosis) were responsible for over 12,000 deaths in 1962 for a rate of 6.6 per 100,000 population. Though constituting less than 1 per cent of the gross total mortality in this country, these disorders actually claimed about as many lives as did such diseases as the leukemias or acute rheumatic fever and chronic rheumatic heart disease combined. More than half of these deaths were in the specific categories of pulmonary embolism and infarction and other venous embolism and thrombosis. In succeeding order, mesenteric infarction and thrombophlebitis each accounted for 17 per cent of the total load of thromboembolic mortality. Available data on age-distribution of mortality for selected types of thromboembolic disorders (ISC Codes 454, 463, 464, 465, 466, 570.2) for 1959 and 1962 reveal a distinct positive gradient with increasing age; the rates for some of these doubling and tripling in the successive age intervals from the 25–34 year through the 35–44 year to the 45–54 year age groups. Sex differences in mortality were noted for the majority of the thromboembolic disorders, though most of these differences were not large. A male excess of mortality was noted for arterial embolism (454), hemorrhoids (461), varicose veins of sites other than the lower extremities (462), thrombophlebitis (463, 464) in non-white only, and pulmonary embolism (465). Female excess mortality was noted for thrombophlebitis of the intracranial venous sinuses (341), varicose veins of the lower extremities (460) and for thrombophlebitis of the lower extremities and other sites (463, 464) among whites only. No sex differences in mortality were noted for venous embolism and thrombosis other than pulmonary (466) and for mesenteric infarction (570.2). Racial differences in mortality were observed for the majority of thromboembolic disorders also, but these differences were much more marked than the sex differences. Arterial embolism and thrombosis (454) was responsible for 50 per cent more deaths among whites. Varicose veins of sites other than the lower extremities (462) and mesenteric infarction (570.2) claimed 30 per cent and 40 per cent excess deaths, respectively, among whites. On the other hand, excess mortality among non-whites was noted for thrombophlebitis of the intracranial venous sinuses (341), thrombophlebitis of the lower extremities (463) and other sites (464), pulmonary embolism (465) and puerperal phlebitis (682) and puerperal pulmonary embolism (684). These nonwhite excesses ranged from 5 per cent for thrombophlebitis of the lower extremities to twofold excesses for the two peuperal causes. No racial differences in mortality were noted for varicose veins of the lower extremities (460), hemorrhoids (461) and other venous embolism and thrombosis (466). Distinct trends in mortality have been noted for almost all the specific thromboembolic causes of death during the period 1950–1962. Pronounced, steadily increasing trends have been observed for arterial embolism and thrombosis, phlebitis and thrombophlebitis of all sites, pulmonary embolism and infarction, other venous embolism and thrombosis and mesenteric infarction. These are the entities which constitute the bulk of recorded mortality from thromboembolic disease. Death rates for phlebitis and thrombophlebitis of the intracranial sinuses and for varicose veins have remained virtually stable in the 13-year period. On the other hand, death rates for hemorrhoids, for puerperal phlebitis and thrombosis and puerperal pulmonary embolism have declined steadily with the puerperal conditions having approximately a 70 per cent reduction. Mordidity data are seriously deficient . No rigidly designed population surveys other than those in prospective studies of cardiovascular disease (Framingham) have been undertaken for thromboembolic disorders and these data are limited in their interpretations because of difficulties in diagnosis. Thromboembolic phenomena are protean in their clinical manifestations and range over a broad spectrum of severity. Estimates of incidence of the major thromboembolic disorders have ranged from a minimum of 698 cases of thrombophlebitis per million population per year in the Saskatchewan Hospital Services Plan in 1960, to 1600 such cases per million enrollees in the Health Insurance Plan of New York in 1951, and to 2060 first visits for this disorder per million population in the National Disease and Therapeutic Index (annual probability sample of private physicians in U.S.) for 1962. These sources estimate the incidence of pulmonary embolism variously as 100 cases per million enrollees (HIP, New York), 135 cases per million population (Saskatchewan) and 148 first visits per million population (NDTI). These same sources indicate that the incidence of thrombophlebitis among the female population (all ages) is approximately twice that in the male. This is far greater than the sex ratio in mortality from these same disorders. Most other sources of morbidity data are unfortunately based on hospital populations with varying demographic compositions and reasons for patient admission which prevent reliable projections to the general population. Sound epidemiological studies of the thromboembolic disorders with respect to associations with environmental and host factors are conspicuous by their absence . The total lack of such information obviously spells the priority of research needs in this disease area. Both the accurate measurement of morbidity and the execution of epidemiological studies of association with selected environmental and host factors demand immediate attention. These, and particularly morbidity measurement, are in turn contingent upon improved and uniform definitions and diagnostic criteria of the several thromboembolic phenomena. Also, in view of the frequency of elicitation of previously undiagnosed thromboembolism at autopsy in cases certified as dying of other causes, death certificate data on all conditions with which individuals die should be made available for study. This implies re-design of the certificate and tabulation of all conditions present at death irrespective of contribution to cause of death. Such improvement in vital statistics practices would be particularly helpful in this category of diseases which not only appear as sequelae to other underlying disease processes but as idiopathic phenomena without apparent antecedents. Sub-classification of mortality data with idiopathic forms as separate categories might prove helpful.