JAMA Revisited October 1, 1927
Surgery and Fatal Pulmonary Embolism A recently published statistical summary of the occurrence of fatal pulmonary embolism among surgical cases that have come to necropsy in a large American clinic during the last ten years shows an incidence of 6 per cent.1 This is a figure of sufficient magnitude to warrant critical study. It might be expected that the formation of thrombi or other emboli is dependent primarily on the surgical interventions that have occurred in the recorded fatalities. Injuries to the walls of blood vessels with resultant thrombosis are an inevitable accompaniment of many operations. Indeed, as a surgeon has remarked, thrombosis within veins that have been cut is a normal occurrence and necessary to the completion of any surgical procedure. This should extend within the vessel to the point of entrance of the next tributary vein; when it extends beyond this point into the larger vessels, a pathologic condition of grave peril is created, as portions of the clot may become detached in the blood stream. The new study indicates, however, that frequently the site of operation is not of paramount importance in determining the site of thrombosis and the source of emboli. According to Henderson's1 observations at the Mayo Clinic, patients who die from pulmonary embolism are older than the average surgical patient; they are somewhat overweight, and, as a group, have a normal or somewhat subnormal blood pressure; a high percentage have postoperative infections. While the importance of the operative procedure in determining the site of thrombus formation and the occurrence of pulmonary embolism cannot be overlooked, he adds, other factors, such as age, weight, general condition of the patient, efficiency of the circulation, bodily inactivity incident to almost any operative procedure and infection, should also be emphasized. The circumstance that pulmonary embolism following operation seems to be a more common cause of death of the obese patient than of the average patient is apparently not due to the formation of true fat emboli, as might have been suspected. According to Snell, 2 after operation on obese patients there may be an increased liberation of thromboplastic lipoid substances such as cephalin, as a result of the extensive areas of fat invaded. True fat embolism, however, has rarely occurred in the postoperative deaths of the obese patients under observation by him. It is conceivable that
Editor’s Note: JAMA Revisited is transcribed verbatim from articles published previously, unless otherwise noted.
major operations tend to bring about changes in the blood that predispose to vascular thrombosis. Chemical investigations made by Allen3 on the blood of surgical patients of the susceptible types in fact indicate possibilities in this direction. The number of erythrocytes and leukocytes, the prothrombin time, the fibrinogen and the lipoids show definite and constant changes which may fairly be attributed to the operative interventions. Allen therefore regards it as probable that there is a nonspecific physiologic response to operation which occurs independently of the clinical or surgical status of the patient. This nonspecific physiologic change, he believes, produces definite alterations in the blood which may partially explain the relatively high incidence of pulmonary embolism occurring in surgical patients as compared with nonsurgical patients. As he interprets the condition there is probably in every surgical patient a definitely increased potentiality for intravascular coagulation by virtue of these changes, but this in all probability plays a minor part in comparison with other factors in the actual deposition of the clot and the subsequent pulmonary embolism. One feature of intravascular changes attending operations which seems to have been more definitely cleared up by the researches at the Rochester clinic concerns postoperative phlebitis. According to Brown,4 this can no longer be held responsible for the observed fatal pulmonary embolisms. Phlebitis suggests a seasonal incidence similar to that observed in duodenal ulcer. According to Brown, pulmonary infarction is a common complication, while fatal pulmonary embolism is apparently rare. This, he believes, verifies a surgical impression of the relative safety of phlebitis. The explanation for this, he adds, must rest on the fact that phlebitis is an inflammatory lesion. The clot is firmly attached to the wall of the vein, and large fragments are not easily dislodged. Thus renewed recognition of the serious importance of pulmonary embolism and the urgent necessity of further investigations become imperative. 1. Henderson, E. F.: Fatal Pulmonary Embolism, Arch. Surg. 15:231 (Aug.) 1927. 2. Snell, A. M.: The Relation of Obesity to Fatal Postoperative Pulmonary Embolism, Arch. Surg. 15:237 (Aug.) 1927 3. Allen, E. V.: Changes in the Blood Following Operation, Arch. Surg. 15:254 (Aug.) 1927. 4. Brown, G. E.: Postoperative Phlebitis, Arch. Surg. 15:245 (Aug.) 1927. JAMA. 1927;89(14):1153-1154.
Section Editor: Jennifer Reiling, Assistant Editor.
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JAMA March 19, 2014 Volume 311, Number 11
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Surgery and Fatal Pulmonary Embolism A recently published statistical summary of the occurrence of fatal pulmonary embolism among surgical cases that have come to necropsy in a large American clinic during the last ten years shows an incidence of 6 per cent.1 This is a figure of sufficient magnitude to warrant critical study. It might be expected that the formation of thrombi or other emboli is dependent primarily on the surgical interventions that have occurred in the recorded fatalities. Injuries to the walls of blood vessels with resultant thrombosis are an inevitable accompaniment of many operations. Indeed, as a surgeon has remarked, thrombosis within veins that have been cut is a normal occurrence and necessary to the completion of any surgical procedure. This should extend within the vessel to the point of entrance of the next tributary vein; when it extends beyond this point into the larger vessels, a pathologic condition of grave peril is created, as portions of the clot may become detached in the blood stream. The new study indicates, however, that frequently the site of operation is not of paramount importance in determining the site of thrombosis and the source of emboli. According to Henderson's1 observations at the Mayo Clinic, patients who die from pulmonary embolism are older than the average surgical patient; they are somewhat overweight, and, as a group, have a normal or somewhat subnormal blood pressure; a high percentage have postoperative infections. While the importance of the operative procedure in determining the site of thrombus formation and the occurrence of pulmonary embolism cannot be overlooked, he adds, other factors, such as age, weight, general condition of the patient, efficiency of the circulation, bodily inactivity incident to almost any operative procedure and infection, should also be emphasized. The circumstance that pulmonary embolism following operation seems to be a more common cause of death of the obese patient than of the average patient is apparently not due to the formation of true fat emboli, as might have been suspected. According to Snell, 2 after operation on obese patients there may be an increased liberation of thromboplastic lipoid substances such as cephalin, as a result of the extensive areas of fat invaded. True fat embolism, however, has rarely occurred in the postoperative deaths of the obese patients under observation by him. It is conceivable that
Editor’s Note: JAMA Revisited is transcribed verbatim from articles published previously, unless otherwise noted.
major operations tend to bring about changes in the blood that predispose to vascular thrombosis. Chemical investigations made by Allen3 on the blood of surgical patients of the susceptible types in fact indicate possibilities in this direction. The number of erythrocytes and leukocytes, the prothrombin time, the fibrinogen and the lipoids show definite and constant changes which may fairly be attributed to the operative interventions. Allen therefore regards it as probable that there is a nonspecific physiologic response to operation which occurs independently of the clinical or surgical status of the patient. This nonspecific physiologic change, he believes, produces definite alterations in the blood which may partially explain the relatively high incidence of pulmonary embolism occurring in surgical patients as compared with nonsurgical patients. As he interprets the condition there is probably in every surgical patient a definitely increased potentiality for intravascular coagulation by virtue of these changes, but this in all probability plays a minor part in comparison with other factors in the actual deposition of the clot and the subsequent pulmonary embolism. One feature of intravascular changes attending operations which seems to have been more definitely cleared up by the researches at the Rochester clinic concerns postoperative phlebitis. According to Brown,4 this can no longer be held responsible for the observed fatal pulmonary embolisms. Phlebitis suggests a seasonal incidence similar to that observed in duodenal ulcer. According to Brown, pulmonary infarction is a common complication, while fatal pulmonary embolism is apparently rare. This, he believes, verifies a surgical impression of the relative safety of phlebitis. The explanation for this, he adds, must rest on the fact that phlebitis is an inflammatory lesion. The clot is firmly attached to the wall of the vein, and large fragments are not easily dislodged. Thus renewed recognition of the serious importance of pulmonary embolism and the urgent necessity of further investigations become imperative. 1. Henderson, E. F.: Fatal Pulmonary Embolism, Arch. Surg. 15:231 (Aug.) 1927. 2. Snell, A. M.: The Relation of Obesity to Fatal Postoperative Pulmonary Embolism, Arch. Surg. 15:237 (Aug.) 1927 3. Allen, E. V.: Changes in the Blood Following Operation, Arch. Surg. 15:254 (Aug.) 1927. 4. Brown, G. E.: Postoperative Phlebitis, Arch. Surg. 15:245 (Aug.) 1927. JAMA. 1927;89(14):1153-1154.
Section Editor: Jennifer Reiling, Assistant Editor.
jama.com
JAMA March 19, 2014 Volume 311, Number 11
Copyright 2014 American Medical Association. All rights reserved.
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1163
