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So-called “liver death” syndrome following thoracostomy
SOCALLED
“LIVER DEATH” SYNDROME THORACOSTOMY JOHN
GEORGE SLEVIN, M.D.
Assistant
Surgeon, Grace HospitaI
DETROIT,
I
FOLLOWING
T was in rgzq. that CharIes Gordon Heyd* first announced the syndrome which has since been termed “Iiver death.” As SuttonI describes it, “the so-caIIed high temperature, Iiver death syndrome is a cI;nicaI entity characterized by rapid progressive deveIopment of high fever, faI1 in bIood pressure, circuIatory coIIapse, coma and death, with temperature rising as high as 109’~. within thirty-six to forty-eight hours after operation.” So-called “Iiver deaths” with few reported exceptions have occurred after surgery on the biliary tract. Although it is only thirteen years since the syndrome of “ Iiver death ” was first recognized as a cIinical entity, there have accumuIated in the literature more than IOO cases of this kind. A search of the Iiterature does not revea1 a singIe case of high temperature death foIIowing thoracic surgery. The onIy demonstrabIe pathoIogy in “Iiver deaths,” as determined at postmortem examination, is passive congestion, softening and diffuse disorganization of the Iiver cords with widespread foca1 necrosis of the liver. Experimenta work done on dogs by Sutton14 showed that simiIar cIinicai causes and Iiving changes were produced in six of fourteen dogs by the Iigation of the hepatic arteries. In eight dogs which did not die, adequate coIIatera1 circuIation to a11 Iobes of the Iiver was found and there was no hepatic necrosis. CriIe5 beIieves that there is also interference with the heat reguIating mechanism of the body. However, this has not been proved. The foIlowing case fits the definition of “high temperature, Iiver death syndrome” in that thirty-one hours after operation the temperature began to rise rapidly, there
MICHIGAN
was circuIatory coIlapse, foIIowed by coma and death occurred just thirty-five and three-quarter hours after operation. CASE
REPORT
J. B., male, aged 60 years, white, Polish, a baker by trade, contracted dry pIeurisy of the lower right pleura on November g, 1936, and was treated symptomaticahy. Three weeks Iater (December 3), he developed a right Iobar pneumonia. He was treated at home and was making a norma recovery unti1 December 15, when his temperature began to rise and he complained of pain in the right chest at the base. A diagnosis was made of delayed resoIution of the pneumonia associated with an encapsuIated empyema of the right pIeura. The patrent was admitted to the Grace Hospital, Detroit, on December 22, 1936. X-rays taken on admission confirmed the diagnosis of pIeural empyema and unresolved pneumonia. On admission the chest showed some swelhng of the Iower right waI1 with obIiteration of interspaces. The Iungs exhibited diminished escursion on the right side and absent fremitus at the right base. FIatness on percussion was noted from the eighth right rib to the base with absent breath sounds in the same area. Above the eighth rib right posteriorIy, breathing was vesicuIar. BronchovesicuIar breathing and many crepitant rbIes were heard over the Ieft Iower Iobe. The heart was negative except for a slight shift to the left. Hemoglobin was 13 Gm. (go per cent); erythrocytes numbered 4380,000; Ieucocytes, I 1,400, with poIymorphonucIear ceI1.s 81 per cent, (filaments $5 per cent, non-fitaments 25 per cent), small Iymphocytes 15 per cent, monocytes I per cent, and metamyeIocytes 3 per cent. No abnormal red bIood ceIIs were seen. Sputum showed no pneumococci present. Culture of pus from thoracentesis was positive for 594
NEW SERIES VOL. XLV,
No.
3
SIevin-“Liver
pneumococci. UrinaIyses on December 22 and 24 were essentiatly negative. On December 24, under novocaine infihration anesthesia, thoracostomy was done. The empyema cavity was opened and two soft rubber drains inserted. About 400 C.C. of thick pus was drained off at the time of operation. For the next twenty-hours the patient’s condition was satisfactory. The folIowing morning, however, the patient was cyanotic and required oxygen therapy. His p&e was 128 and was weak. He was miIdIy deIirious. He was catheterized at I ~30 P.M. and 300 C.C. of urine was obtained. This was a11 the urine passed in sixteen and one-haIf hours and the patient did not void thereafter. Coma deveIoped about 3 P.M., and shortIy thereafter puImonary edema appeared. The patient’s temperature rose rapidIy. At 8 A.M. it was 102’F.i at noon 102.8~~.; at 4 P.M. it was 107; and just before death it was 108. At noon the puIse was ISO per minute. DigaIen was given without effect. Thereafter, the puIse was too weak to count. The patient expired in coma at 8:44 P.M. DISCUSSION
Heyd,” in his most recentIy pubhshed articIe on this subject, gives a revised cIassification of Iiver deaths, viz: “ I. Those associated with hyperpyrexia and coma-a rapidIy developing lethargy, stupor and coma, death terminates the picture in from eighteen to thirty-six hours. “2. Liver deaths in the presence of a constantIy diminishing jaundice-sIowIy deveIoping stupor and coma; fina cIinica1 picture is simiIar to ‘choIemia death’ from cirrhosis of the Iiver. “ 3. Liver deaths associated with some unreIated kidney disease-anuria is a factor in the termina1 picture. Forty-eight hours after operation the cIinica1 picture is not dissimiIar to shock, with coId, cIammy skin; faiIure in water eIimination and a marked rise in non-protein nitrogen.” Thus, according to Heyd’s cIassification the case herein reported readiIy faIIs into group I. As has been said, most of the cases of “ Iiver deaths ” foIIow biliary surgery. But in 1935 ConneI14 reported five instances of high temperature deaths occurring after
Death”
American
Journal
of Surgery
595
operations other than on the biIiary tract. And in 1937 De Courcy6 reported two cases of “ Iiver death,” one foIIowing coIostomy and the other after hysterectomy for simpIe fibroid. Boyce and McFetridge’ recentIy reviewed a number of casuaIIy seIected autopsies covering burns, intestina1 obstruction and thyroid disease and were struck with the resembIance of these cases to the hyperpyrexic and hepatorena1 deaths foIIowing biIiary surgery. The fact that “high temperature, Iiver deaths” can occur foIIowing surgery other than on the biIiary tract, brings up for consideration the factor or factors responsibIe for this fata syndrome. LIVER
DEATHS
OF
TOXIC
ORIGIN
The prevaiIing opinion regarding the cause of “ Iiver death ” is that it is of toxic origin. Boyce and McFetridge,2 studied thirty-four cases of this type and performed experiments on animaIs, which included the injection into dogs of saIine and aqueous extracts made from the Iiver of patients who died with the typica “Iiver death” syndrome. As a resuIt they came to the foIIowing concIusions : “ I. The underIying factor is some degree of hepatic damage, either pregxistent or the resuIt of direct trauma; “2. When the added strain of operation is superimposed on the existing hepatic disabiIity, the damaged Iiver ceIIs reIease into the circuIation some potent, water soIubIe toxic substance.” If we accept this theory as a working hypothesis, is it the fina explanation of the underIying factor of Iiver death? It is possibIe that another factor enters into the picture, a factor, perhaps, which exists onIy in vivo, not discernibIe at autopsy. What caused the “Iiver death” in the case herein presented? As far as couId be determined cIinicaIIy, there being no autopsy, there was a minimum of Iiver damage such as might be expected foIIowing a protracted pneumonia and concomitant emr>vema. The oDerative Drocedure I.2 I I
596
American Journal of Surgery
SIevin-“Liver
was simpIe and shouId have Iessened the toxemia. NevertheIess the patient died a typica “high temperature, Iiver death.” On the basis of Sutton’s17 experimenta work on the Iigation of the hepatic artery with the production of a typical Iiver death syndrome, a thrombosis or emboIism of the hepatic artery couId be the cause of death in this case. However, thrombosis of the hepatic artery is so rare, there being onIy two authentic cases on record, that the resuIts of this sort of accident are unknown. EmboIism of the hepatic artery is aIso comparativeIy uncommon. Either thrombosis or emboIism of this artery wouId produce approximateIy the same pathoIogy as was experimentaIIy produced by Iigation, i.e., necrosis of the Iiver. Thrombosis of the hepatic veins is aIso rare and would not be Iikely to produce the same effect as we observe in “Iiver death.” WhiIe thrombosis or emboIism of the hepatic artery is a possibility, it is a rather remote IikeIihood. There is another way, however, by which the hepatic circuIation, theoreticaIIy at Ieast, couId be occIuded, nameIy, through the sympathetic nervous system. AUTONOMIC
SYSTEM’S
R6LE
IN
LIVER
DEATHS
Mann,13 in a recent review of the physioIogy of the Iiver, remarks that the sympathetic nerves are present in the Iiver in great abundance; that they reach the Iiver by accompanying the hepatic artery and seem to be mainIy for the purpose of controIIing the bIood ffow through this artery. The Iiver receives its sympathetic nerve suppIy from the ceIiac gangIion. This its branches gangIion, in turn, receives from the sixth to the tweIfth thoracic segments of the spina cord. The intercosta1 nerves invoIved at the thoracostomy operation arise from the sixth and seventh thoracic segments. Furthermore, the fibers of the intercosta1 nerves and of the sympaemerge together in the thetic system
Death” anterior nerve roots, the sympathetic Ieaving the spinaIs Iater by way of the white rami communicantes. Thus it is evident that these two systems are cIoseIy reIated. Mann further states “the arteria1 bIood flow to the Iiver is under vasomotor contro1 and is essentia1 for the existence of the organ. ” Hence, stimuli received by the intercosta1 nerves couId be reIayed to the autonomic nerves innervating the hepatic artery, by way of the sympathetic fibers which take origin from the same cord segments. If this happened the hepatic artery could undergo a massive and proIonged spasm as a resuIt of “referred stimuIi,” producing a decided diminution in bIood suppIy to the Iiver. It wiI1 be recaIIed that this patient’s Iiver was aIready damaged by proIonged infection and the diminution in bIood suppIy couId easiIy institute necrosis of the Iiver. Thus the concIusions which Boyce and McFetridge2 arrived at, are fuIfiIIed in this c&se-a damaged Iiver with the added strain of operation producing a toxin which is Iiberated into the bIood stream. The hypothesis here presented is offered as an attempt to fix the mechanism whereby “the strain of operation ” affects the “damaged Iiver ceIIs.” This is pure theory, unsupported by any cIinica1 or experimenta evidence. But if true, it wouId soIve the problem of what causes “Iiver deaths.” CONCLUSION
This, and simiIar cases of extrahepatic “Iiver deaths” shouId crystaIIize our attention on the fact that “Iiver deaths” do occur after operations on other parts of the anatomy than the biliary tract; that in preparing patients for operation we shouId consider the possibiIities of Iiver damage and give the patient a chance to buiId up a sufficient store of Iiver gIycogen to withstand the rigors of operation. AIso, where it is known that some degree of Iiver damage aIready exists, specia1 care should be taken
New SERIES VOL. XLV, No. 3
SIevin-“Liver
to prevent “ Iiver death ” by conserving the gIycogen reserve of the Iiver, especiaIIy by a more IiberaI use of intravenous gIucose solution postoperativeIy. REFERENCES I. BOYCE, F. F., and MCFETRIDGE, E. M. “Liver deaths” in surgery; analysis of 34 cases with new explanation of clinical and pathoIogica1 picture. New Orleans M. w S. J., 88: 563-567 (March) 1936. 2. BOYCE, F. F., and MCFETRIDGE, E. M. “Liver deaths,” experimental study of changes in the biliary ducts foIIowing decompression of obstructed biliary tree. Arch. Surg., 32: 1o80-1086 (June) 1936. 3. BOYCE, F. F. So-caIIed liver death syndrome in surgery. Surg., Gynec. ti O&t., 61: 122, 1935. 4. CONNELL, F. G. Liver deaths, rapid high temperature deaths. Ann. Surg., IOO: 319, 1934. 5. CRILE, G. W. CriticaI facts in surgery of the galIbIadder and ducts. South. M. J., 20: 85, 1927. 6. DKOURCY, J. L. “Liver deaths” in genera1 surgery. Ann. Surg., 106: 58-61 (July) 1937. 7. EISS, S. Conservation of hepatic function in galIbIadder operation; precautionary measures to
Death”
8. 9.
IO. I I. 12.
13.
14.
American
Journal of Surgery
597
prevent “liver deaths.” Ann. Surg., 98: 348-353 (Sept.) 1933. HEYD, C. G. Liver and its reIation to chronic abdomina1 infections. Ann. Surg., 79: 55, 1924. Idem. Significance of liver function from surgeon’s standpoint. New York State J. Med., 33: 1317132% 1933. Zdem. “Liver deaths” in surgery of the gall-bIadder. J. A. M. A., 97: 1847-1848 (Dec. 19) 1931. Idem. Liver deaths and the complications of gaIlbIadder surgery. Soutb. Surg., 6: 3 (June) 1937. HELWIG, F. C. Recent advances in the knowIedge of the pathology of the liver. Am. J. Surg., 19: 462 (March) 1933. MANN, F. C. Review of experimenta investigation from surgical viewpoint. Minnesota Med., 19: 695-702 (Nov.) 1936. SUTTON, JR., J. E. Acute postoperative necrosis (so-called high temperature, Iiver death syndrome). Am. J. M. SC., 192: 219-224 (Aug.)
1936. 15. Idem. “High temperature, liver death” syndrome. Proc. Sot. Exper. Biol. 13’ Med., 32: 712, 1935. 16. SCHUTZ, C. B., HELWIG, F. C., and HUHN, H. P. A contribution to study of so-caIIed liver deaths. J. A. M. A., 99: 633, 1932. 17. WALTERS, W. Function of Iiver in relation to surgery. Ann. Surg., 94: 15, 1931.
“LIVER DEATH” SYNDROME THORACOSTOMY JOHN
GEORGE SLEVIN, M.D.
Assistant
Surgeon, Grace HospitaI
DETROIT,
I
FOLLOWING
T was in rgzq. that CharIes Gordon Heyd* first announced the syndrome which has since been termed “Iiver death.” As SuttonI describes it, “the so-caIIed high temperature, Iiver death syndrome is a cI;nicaI entity characterized by rapid progressive deveIopment of high fever, faI1 in bIood pressure, circuIatory coIIapse, coma and death, with temperature rising as high as 109’~. within thirty-six to forty-eight hours after operation.” So-called “Iiver deaths” with few reported exceptions have occurred after surgery on the biliary tract. Although it is only thirteen years since the syndrome of “ Iiver death ” was first recognized as a cIinical entity, there have accumuIated in the literature more than IOO cases of this kind. A search of the Iiterature does not revea1 a singIe case of high temperature death foIIowing thoracic surgery. The onIy demonstrabIe pathoIogy in “Iiver deaths,” as determined at postmortem examination, is passive congestion, softening and diffuse disorganization of the Iiver cords with widespread foca1 necrosis of the liver. Experimenta work done on dogs by Sutton14 showed that simiIar cIinicai causes and Iiving changes were produced in six of fourteen dogs by the Iigation of the hepatic arteries. In eight dogs which did not die, adequate coIIatera1 circuIation to a11 Iobes of the Iiver was found and there was no hepatic necrosis. CriIe5 beIieves that there is also interference with the heat reguIating mechanism of the body. However, this has not been proved. The foIlowing case fits the definition of “high temperature, Iiver death syndrome” in that thirty-one hours after operation the temperature began to rise rapidly, there
MICHIGAN
was circuIatory coIlapse, foIIowed by coma and death occurred just thirty-five and three-quarter hours after operation. CASE
REPORT
J. B., male, aged 60 years, white, Polish, a baker by trade, contracted dry pIeurisy of the lower right pleura on November g, 1936, and was treated symptomaticahy. Three weeks Iater (December 3), he developed a right Iobar pneumonia. He was treated at home and was making a norma recovery unti1 December 15, when his temperature began to rise and he complained of pain in the right chest at the base. A diagnosis was made of delayed resoIution of the pneumonia associated with an encapsuIated empyema of the right pIeura. The patrent was admitted to the Grace Hospital, Detroit, on December 22, 1936. X-rays taken on admission confirmed the diagnosis of pIeural empyema and unresolved pneumonia. On admission the chest showed some swelhng of the Iower right waI1 with obIiteration of interspaces. The Iungs exhibited diminished escursion on the right side and absent fremitus at the right base. FIatness on percussion was noted from the eighth right rib to the base with absent breath sounds in the same area. Above the eighth rib right posteriorIy, breathing was vesicuIar. BronchovesicuIar breathing and many crepitant rbIes were heard over the Ieft Iower Iobe. The heart was negative except for a slight shift to the left. Hemoglobin was 13 Gm. (go per cent); erythrocytes numbered 4380,000; Ieucocytes, I 1,400, with poIymorphonucIear ceI1.s 81 per cent, (filaments $5 per cent, non-fitaments 25 per cent), small Iymphocytes 15 per cent, monocytes I per cent, and metamyeIocytes 3 per cent. No abnormal red bIood ceIIs were seen. Sputum showed no pneumococci present. Culture of pus from thoracentesis was positive for 594
NEW SERIES VOL. XLV,
No.
3
SIevin-“Liver
pneumococci. UrinaIyses on December 22 and 24 were essentiatly negative. On December 24, under novocaine infihration anesthesia, thoracostomy was done. The empyema cavity was opened and two soft rubber drains inserted. About 400 C.C. of thick pus was drained off at the time of operation. For the next twenty-hours the patient’s condition was satisfactory. The folIowing morning, however, the patient was cyanotic and required oxygen therapy. His p&e was 128 and was weak. He was miIdIy deIirious. He was catheterized at I ~30 P.M. and 300 C.C. of urine was obtained. This was a11 the urine passed in sixteen and one-haIf hours and the patient did not void thereafter. Coma deveIoped about 3 P.M., and shortIy thereafter puImonary edema appeared. The patient’s temperature rose rapidIy. At 8 A.M. it was 102’F.i at noon 102.8~~.; at 4 P.M. it was 107; and just before death it was 108. At noon the puIse was ISO per minute. DigaIen was given without effect. Thereafter, the puIse was too weak to count. The patient expired in coma at 8:44 P.M. DISCUSSION
Heyd,” in his most recentIy pubhshed articIe on this subject, gives a revised cIassification of Iiver deaths, viz: “ I. Those associated with hyperpyrexia and coma-a rapidIy developing lethargy, stupor and coma, death terminates the picture in from eighteen to thirty-six hours. “2. Liver deaths in the presence of a constantIy diminishing jaundice-sIowIy deveIoping stupor and coma; fina cIinica1 picture is simiIar to ‘choIemia death’ from cirrhosis of the Iiver. “ 3. Liver deaths associated with some unreIated kidney disease-anuria is a factor in the termina1 picture. Forty-eight hours after operation the cIinica1 picture is not dissimiIar to shock, with coId, cIammy skin; faiIure in water eIimination and a marked rise in non-protein nitrogen.” Thus, according to Heyd’s cIassification the case herein reported readiIy faIIs into group I. As has been said, most of the cases of “ Iiver deaths ” foIIow biliary surgery. But in 1935 ConneI14 reported five instances of high temperature deaths occurring after
Death”
American
Journal
of Surgery
595
operations other than on the biIiary tract. And in 1937 De Courcy6 reported two cases of “ Iiver death,” one foIIowing coIostomy and the other after hysterectomy for simpIe fibroid. Boyce and McFetridge’ recentIy reviewed a number of casuaIIy seIected autopsies covering burns, intestina1 obstruction and thyroid disease and were struck with the resembIance of these cases to the hyperpyrexic and hepatorena1 deaths foIIowing biIiary surgery. The fact that “high temperature, Iiver deaths” can occur foIIowing surgery other than on the biIiary tract, brings up for consideration the factor or factors responsibIe for this fata syndrome. LIVER
DEATHS
OF
TOXIC
ORIGIN
The prevaiIing opinion regarding the cause of “ Iiver death ” is that it is of toxic origin. Boyce and McFetridge,2 studied thirty-four cases of this type and performed experiments on animaIs, which included the injection into dogs of saIine and aqueous extracts made from the Iiver of patients who died with the typica “Iiver death” syndrome. As a resuIt they came to the foIIowing concIusions : “ I. The underIying factor is some degree of hepatic damage, either pregxistent or the resuIt of direct trauma; “2. When the added strain of operation is superimposed on the existing hepatic disabiIity, the damaged Iiver ceIIs reIease into the circuIation some potent, water soIubIe toxic substance.” If we accept this theory as a working hypothesis, is it the fina explanation of the underIying factor of Iiver death? It is possibIe that another factor enters into the picture, a factor, perhaps, which exists onIy in vivo, not discernibIe at autopsy. What caused the “Iiver death” in the case herein presented? As far as couId be determined cIinicaIIy, there being no autopsy, there was a minimum of Iiver damage such as might be expected foIIowing a protracted pneumonia and concomitant emr>vema. The oDerative Drocedure I.2 I I
596
American Journal of Surgery
SIevin-“Liver
was simpIe and shouId have Iessened the toxemia. NevertheIess the patient died a typica “high temperature, Iiver death.” On the basis of Sutton’s17 experimenta work on the Iigation of the hepatic artery with the production of a typical Iiver death syndrome, a thrombosis or emboIism of the hepatic artery couId be the cause of death in this case. However, thrombosis of the hepatic artery is so rare, there being onIy two authentic cases on record, that the resuIts of this sort of accident are unknown. EmboIism of the hepatic artery is aIso comparativeIy uncommon. Either thrombosis or emboIism of this artery wouId produce approximateIy the same pathoIogy as was experimentaIIy produced by Iigation, i.e., necrosis of the Iiver. Thrombosis of the hepatic veins is aIso rare and would not be Iikely to produce the same effect as we observe in “Iiver death.” WhiIe thrombosis or emboIism of the hepatic artery is a possibility, it is a rather remote IikeIihood. There is another way, however, by which the hepatic circuIation, theoreticaIIy at Ieast, couId be occIuded, nameIy, through the sympathetic nervous system. AUTONOMIC
SYSTEM’S
R6LE
IN
LIVER
DEATHS
Mann,13 in a recent review of the physioIogy of the Iiver, remarks that the sympathetic nerves are present in the Iiver in great abundance; that they reach the Iiver by accompanying the hepatic artery and seem to be mainIy for the purpose of controIIing the bIood ffow through this artery. The Iiver receives its sympathetic nerve suppIy from the ceIiac gangIion. This its branches gangIion, in turn, receives from the sixth to the tweIfth thoracic segments of the spina cord. The intercosta1 nerves invoIved at the thoracostomy operation arise from the sixth and seventh thoracic segments. Furthermore, the fibers of the intercosta1 nerves and of the sympaemerge together in the thetic system
Death” anterior nerve roots, the sympathetic Ieaving the spinaIs Iater by way of the white rami communicantes. Thus it is evident that these two systems are cIoseIy reIated. Mann further states “the arteria1 bIood flow to the Iiver is under vasomotor contro1 and is essentia1 for the existence of the organ. ” Hence, stimuli received by the intercosta1 nerves couId be reIayed to the autonomic nerves innervating the hepatic artery, by way of the sympathetic fibers which take origin from the same cord segments. If this happened the hepatic artery could undergo a massive and proIonged spasm as a resuIt of “referred stimuIi,” producing a decided diminution in bIood suppIy to the Iiver. It wiI1 be recaIIed that this patient’s Iiver was aIready damaged by proIonged infection and the diminution in bIood suppIy couId easiIy institute necrosis of the Iiver. Thus the concIusions which Boyce and McFetridge2 arrived at, are fuIfiIIed in this c&se-a damaged Iiver with the added strain of operation producing a toxin which is Iiberated into the bIood stream. The hypothesis here presented is offered as an attempt to fix the mechanism whereby “the strain of operation ” affects the “damaged Iiver ceIIs.” This is pure theory, unsupported by any cIinica1 or experimenta evidence. But if true, it wouId soIve the problem of what causes “Iiver deaths.” CONCLUSION
This, and simiIar cases of extrahepatic “Iiver deaths” shouId crystaIIize our attention on the fact that “Iiver deaths” do occur after operations on other parts of the anatomy than the biliary tract; that in preparing patients for operation we shouId consider the possibiIities of Iiver damage and give the patient a chance to buiId up a sufficient store of Iiver gIycogen to withstand the rigors of operation. AIso, where it is known that some degree of Iiver damage aIready exists, specia1 care should be taken
New SERIES VOL. XLV, No. 3
SIevin-“Liver
to prevent “ Iiver death ” by conserving the gIycogen reserve of the Iiver, especiaIIy by a more IiberaI use of intravenous gIucose solution postoperativeIy. REFERENCES I. BOYCE, F. F., and MCFETRIDGE, E. M. “Liver deaths” in surgery; analysis of 34 cases with new explanation of clinical and pathoIogica1 picture. New Orleans M. w S. J., 88: 563-567 (March) 1936. 2. BOYCE, F. F., and MCFETRIDGE, E. M. “Liver deaths,” experimental study of changes in the biliary ducts foIIowing decompression of obstructed biliary tree. Arch. Surg., 32: 1o80-1086 (June) 1936. 3. BOYCE, F. F. So-caIIed liver death syndrome in surgery. Surg., Gynec. ti O&t., 61: 122, 1935. 4. CONNELL, F. G. Liver deaths, rapid high temperature deaths. Ann. Surg., IOO: 319, 1934. 5. CRILE, G. W. CriticaI facts in surgery of the galIbIadder and ducts. South. M. J., 20: 85, 1927. 6. DKOURCY, J. L. “Liver deaths” in genera1 surgery. Ann. Surg., 106: 58-61 (July) 1937. 7. EISS, S. Conservation of hepatic function in galIbIadder operation; precautionary measures to
Death”
8. 9.
IO. I I. 12.
13.
14.
American
Journal of Surgery
597
prevent “liver deaths.” Ann. Surg., 98: 348-353 (Sept.) 1933. HEYD, C. G. Liver and its reIation to chronic abdomina1 infections. Ann. Surg., 79: 55, 1924. Idem. Significance of liver function from surgeon’s standpoint. New York State J. Med., 33: 1317132% 1933. Zdem. “Liver deaths” in surgery of the gall-bIadder. J. A. M. A., 97: 1847-1848 (Dec. 19) 1931. Idem. Liver deaths and the complications of gaIlbIadder surgery. Soutb. Surg., 6: 3 (June) 1937. HELWIG, F. C. Recent advances in the knowIedge of the pathology of the liver. Am. J. Surg., 19: 462 (March) 1933. MANN, F. C. Review of experimenta investigation from surgical viewpoint. Minnesota Med., 19: 695-702 (Nov.) 1936. SUTTON, JR., J. E. Acute postoperative necrosis (so-called high temperature, Iiver death syndrome). Am. J. M. SC., 192: 219-224 (Aug.)
1936. 15. Idem. “High temperature, liver death” syndrome. Proc. Sot. Exper. Biol. 13’ Med., 32: 712, 1935. 16. SCHUTZ, C. B., HELWIG, F. C., and HUHN, H. P. A contribution to study of so-caIIed liver deaths. J. A. M. A., 99: 633, 1932. 17. WALTERS, W. Function of Iiver in relation to surgery. Ann. Surg., 94: 15, 1931.