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Spontaneous hepatic rupture in pregnancy
Spontaneous Hepatic Rupture in Pregnancy Edward W. Nelson, MD, Salt Lake City, Utah Lyle Archibald, MD, Salt Lake City, Utah Dominic Albo, Jr, MD, Salt Lake City, Utah
Spontaneous rupture of the liver is a rare but well documented complication of late pregnancy and delivery, usually associated with pre- or true eclampsia. Since first described by Abercrombie in 1844 [I], isolated reports and reviews have appeared primarily in obstetric literature. Although these patients present first to the obstetrician with toxemia of pregnancy, the recognition and management of their life-threatening hepatic injury often involves a general surgeon. Material and Methods Over a three year period (1973-1976), the general surgery service at the University of Utah affiliated hospitals has been involved in the successful management of four cases of hepatic rupture in toxemia of pregnancy. A review of this experience with emphasis on the pathogeneses of the hepatic injury and its recognition and management is presented. Two illustrative cases follow. Patient 4. A thirty-five year old white female, gravida 8, presented at thirty-four weeks’ gestation with complaints of shortness of breath, headache, and blurred vision for one week. Blood pressure on admission was 190/140, with +3 proteinuria. There was tenderness to palpation over the liver and generalized edema. She was placed on bed rest, treated with magnesium sulfate, and 11 hours after admission, she delivered a viable premature female infant. Immediately after delivery, the patient complained of acute right upper quadrant pain and was noted to have a blood pressure of 100/60 supine and a hematocrit of 22 per cent. Laboratory studies included a platelet count of 22,000, an elevated fibrinogen level of 536 mg/lOO ml, and a negative protamine sulfate test. At laparotomy, an extensive subcapsular hematoma of the right hepatic lobe with free rupture into the peritoneal cavity was discovered. This was evacuated and drained externally. A total of 25 units of blood were given during the pre- and intraoperative period. In the immediate postoperative period, the patient required an additional 18 units of blood for continued hemorrhage from the hepatic drain sites. Eventually, she underwent reexploration for infected subphrenic, subFrom the Department of Surgery, University of Utah Medical Center, Salt Lake Citv. Utah. Reprini requests should be addressed to Edward W. Nelson, MD, Dapartment of Surgery, University of Utah Medical Center, 50 North Medical Drive, Salt Lake City, Utah 84132. Presented at the Twenty-Ninth Annual Meeting of the Southwestern Surgical Congress, Acapulco, Mexico, April 25-28. 1977.
Volume 134, December 1977
hepatic, and pleural spaces. She was discharged on the thirty-ninth postoperative day and found to be doing well several months later when readmitted for elective tubal ligation.
Patient 1. A twenty-one year old female, para 0, presented at thirty-five weeks’ gestation with a four day history of headache. On admission, her blood pressure was 220/135, +3 proteinuria was present, and she complained of right upper quadrant pain. After 5 hours of treatment with bed rest, magnesium sulfate, and morphine, her blood pressure suddenly dropped to 130/80, and fetal heart rate slowed to 60. Laboratory studies at that time showed a platelet count of 27,000, fibrinogen level of less than 100 mg/lOO ml, and a positive protamine sulfate test. Shd underwent immediate laparotomy and caesarean section with delivery of a viable infant girl. At that time, a large rent in the left lobe of the liver and a secondary hemoperitoneum were discovered. During partial resection of the left lobe, she was transfused with 1,500 cc whole blood. An additional 5 units of blood were required for postoperative losses from the hepatic drainage sites. She left the hospital nineteen days after admission without further complications. Results
Various reviews of spontaneous hepatic rupture in toxemic pregnancy place the total number of reported cases at less than fifty [l-3]. Previous authors emphasize that this condition most often presents in women more than thirty years old of multiparity who present with signs and symptoms of eclampsia [I]. The lesion most often described has been a subcapsular hematoma of the right hepatic lobe which has carried up to a 70 per cent mortality in these review series [l-3]. Without prompt recognition and surgical intervention, it has proven universally fatal. Our four cases represent one of the largest groups seen and reported by a single institution. (Table I.) Although the average age of this group is lower than that previously reported and gestation periods were variable, all but one of our patients were multiparous. Universal in these patients was the triad of toxemia (manifested by hypertension and proteinuria), right upper quadrant pain, and sudden unexplained shock. Two patients were explored after delivery, and two discovered to have liver injury at the time of emer-
817
Nelson, Archibald,
TABLE I
and Albo
Manifestations of Preeclampsla, Right Upper Quadrant Pain, and Shock in Present Series
Parity and Gestation
Age W 21 26 22 35
TABLE II
Preeclampsia Blood Proteinuria Pressure
Gravida Gravida Gravida Gravida
1, 3, 2, 8,
35 40 37 34
wk wk wk wk
Surgical Factors (Intraoperatlve)
2201135 170196 210/130 190/130
:“2 +4 +3
Right Upper Quadrant Pain
Shock
i-36 hr l t24 hr +9 hr i-12 hr
130160 lOOl60 60160 lOOl60
In Present Serles Blood Replacement
Patient
Exploration
Hepatic Lesion
Treatment
1 2 3 4
Caesarean section After delivery-8 hr Caesarean section After delivery-7 hr
Left lobe hematoma with laceration Right lobe subcapsular hematoma Right lobe subcapsular hematoma Right lobe subcapsular hematoma
3/4Lobectomy, Drainage Evacuation, Suture, Drainage Evacuation, Gelfoam, Drainage Evacuation, Drainage
TABLE III
Postoperative Complications and Results In Present Series
Fluid PostOverload/ operative Pleural RespiraBlood Effusion tory Replace- on Side of InsuffiPatient ment Lesion ciency
Intraabdominal Abscess
1
5 units
+
2
11 units
+
+
-
3
30 units
+
+
-
4
18 units
+
+
+
Fetus Premature female Normal female Stillborn female Premature female
gency caesarean section. (Table II.) In three patients, the hepatic injury presented as a subcapsular hematoma of the right lobe which was treated with evacuation and drainage. One patient with hematoma and laceration of the left lobe underwent partial resection and drainage. Initial blood replacement varied from 4 to 25 units, and all patients required significant blood replacement postoperatively for continued bleeding from hepatic drains. (Table III.) All patients developed pleural effusions on the side of hepatic injury. The three patients who had required most massive transfusions were treated for fluid overload with mild secondary respiratory insufficiency. Intraabdominal abscesses and empyema were treated in one patient and ruled out in a second. A single stillborn infant was removed in a case where right upper quadrant pain and shock developed before emergency caesarean section could be completed. There was no maternal mortality.
818
4 15 4 25
units units units units
Comments
Since a multitude of physiologic changes occur in normal pregnancy, it is predictable that a variety of endocrine, metabolic, and hemodynamic factors have been mentioned in the pathogenesis of toxemia. Although the toxemia complex of hypertension, proteinuria, and convulsions remains a disease of many theories, an intermediate role of disseminated intravascular coagulation (DIC), either as a cause or effect, has continuously appeared in the literature since the 1950s [2-g]. Current reports stress that the degree and manifestations of the consumptive coagulopathy present in these patients are proportional to the severity of their toxemic state [5,6,10-151. In a recent large review series [B], DIC was shown to be present in 9.1 per cent of eclamptic patients and 2.1 per cent of severely preeclamptic patients. The deposition of microembolic fibrin and fibrinogen breakdown products seen on the basement membrane of glomerular capillary endothelium, and in the capillaries and sinusoids of the liver supports a DIC-mediated mechanism for the renal and hepatic damage sometimes seen in toxemia [4,9,15,16]. It has also been postulated that similar lesions in the central nervous system, pituitary, adrenals, and cardiopulmonary system explain the damage occasionally seen in these areas [4,9,15]. Various factors including poor diet, diabetes, obesity, hypertension, renal disease, sodium overload, and first pregnancy are all known to statistically increase therisk of toxemia. Current theories relate the coagulation abnormalities seen in toxemia to inadequate placental perfusion and secondary “uteroplacental dysfunction” perhaps caused by one or
The American Journal of Surgery
Hepatic Rupture in Pregnancy
more of these factors [15]. Whether the DIC seen in toxemia is triggered by the release of some thromboplastic or vasoactive agent from the placenta [15,17] or is secondary to platelet consumption at sites of vascular endothelial damage caused by toxemic hypertension [14] is not known. Although workup for DIC is not routine in all toxemic patients, all patients in this series were suspected of DIC and evaluated with appropriate studies. (Table IV.) As noted in the literature, the earliest and most reproducible abnormality seen was acute thrombocytopenia [18]. Fibrinogen levels, normally elevated in pregnancy, varied widely as did other, more specific tests including fibrin split products and protamine sulfate tests. Only one patient was believed clinically to have diffuse bleeding from sites other than the liver and was therefore transiently treated with heparin, although its usefulness in this setting is debated in the literature [12,14,19]. All patients did receive platelet transfusions and other blood products postoperatively. Whatever the mechanism of injury, the histopathology of the liver in toxemia has been consistently described as showing the fibrin emboli in the sinusoids and hepatic arterioles with resultant areas of periportal necrosis [1,2,4,9,15]. (Figure 1.) Many toxemic patients probably have subclinical hepatic damage manifested only by distension of Glisson’s capsule and resultant right upper quadrant tenderness, which spontaneously resolves after delivery. However, in the rare patient, the coalescence and enlargement of these microscopic areas into a subcapsular hematoma may occur. (Figure 2.) The impaired coagulation and hypertension in toxemia as well as external trauma of diaphragm and uterine movement during labor and delivery may influence the further enlargement and eventual rupture of such lesions.
TABLE IV
Figure 7. Pafhologic specimen from patlent 1 showing
Figure 2. Periporfal hemorrhagk necroses and s&capsular
periportal hemorrhage and surrounding necrosis.
hematoma formafion in specimen from patient 1.
Volume 134, December 1977
Patient
Coagulation Defects in Present Series
Platelet Count
Diffuse Hemorrhage
Fibrinogen
Other Tests
No
1
27,000
PT = l7fll PTT = 39130 PS = -
2
40,000
155 mgl100 ml
PT = 18113 PI-r = 44130
No
3
70,000
175 mg/lOO ml
PT = 18113 PTT = 83 i42 FSP = +
Yes
4
22,000
538 mg/ 100 ml
PS = PTlPTT = WNL
No
Note: PT = prothrombin time; PlT = partial thromboplastin time; PS = protamine sulfate; FSP = fibrin split products; WNL = within normal limits.
Surgical Management
When the triad of toxemia, right upper quadrant pain, and sudden hypotension present in the pregnant patient, early recognition with rapid termination of pregnancy and prompt surgical exploration are the keys to successful management. As previously noted, the hepatic lesion is usually a subcapsular hematoma of the right lobe with free rupture into the peritoneal cavity and an underlying raw bleeding liver surface. (Figure 3.) Evacuation of the hematoma, individual ligation of any discrete bleeding sites, if present, and wide, dependent drainage was the most successful approach in our experience. This is consistent with the management of these lesions suggested in large reviews of liver trauma [20-221. Although it was not used in any of our cases present or those reviewed, microcrystalline collagen (Avitenea) may be an ideal local hemostatic agent for large surface areas of the liver without discrete
819
Nelson, Archibald, and Albo
organs has been discussed. Basic surgical principles in the management of hepatic subcapsular hematomas, and the prolonged postoperative course and frequent complications in these patients have been stressed. References
Figure 3. Artist’s conception of right hepatlc lobe subcapsular hematoma involving a large area of the liver surface.
bleeding points [23]. Right hepatic artery ligation, omental or other viable packs, and resection are also technics available but generally not required to control hepatic bleeding in this condition [21,22]. Temporizing measures, such as packing the bleeding surface of the liver for 24 hours to allow coagulation abnormalities to correct, might even be helpful in certain patients. Postoperatively, care should be directed toward the prevention of continued hemorrhage with adequate replacement of blood and coagulation factors, and prolonged, wide dependent drainage of the hematoma site. Since pulmonary and infectious complications have been noted in these patients and similar patients presented in the literature [22], vigorous respiratory care and careful surveillance for the development of intraabdominal abscess should be stressed. Summary
Hepatic rupture as a late complication of toxemic pregnancy is a rare yet lethal condition requiring rapid recognition and surgical management. The clinical triad of toxemia, right upper quadrant pain, and sudden hypotension is the diagnostic hallmark of presentation. Most patients present near the time of delivery and are found to have subcapsular hematomas of the right hepatic lobe with free rupture into the peritoneal cavity and resultant exsanguinating hemorrhage. The association of toxemia and disseminated intravascular coagulation with secondary microembolic damage to the liver and other
820
1. Hakim-Elahi: Spontaneous rupture of the liver in pregnancy. Obsfet Gynecol26: 435, 1965. 2. Castaneda H, Garcia-Romero H, Canto M: Hepatic hemorrhage in toxemia or pregnancy. Am J Obstet Gynecol 107: 578, 1970. 3. Utley JR: Spontaneous rupture of the liver during pregnancy. Surg Gynecol Obstet 133: 250, 1971. 4. Coopland AT: Blood clotting abnormalities in relation to preeclampsia: a review. Can Med Assoc J 150: 121, 1969. 5. Smith H,.Gregori CA, Breen JC: Disseminated intravascular coaaulation in oreanancv. J Med Sot NJ 71: 729. 1974. 6. Bellar FK, Uszynski G ‘disseminated intravascular coagulation in pregnancy. C/in Obstet Gynecoll7: 250, 1974. 7. Youssef AH: Proceedings: disseminated intravascular coagulation (DIC) and toxemia or pregnancy in Kuwait. Thromb Diath Haemorrh 34: 569, 1975. 8. Roberts JM, May WJ: Consumptive coagulopathy in severe preeclampsia. Obstet Gynceo/ 125: 747, 1976. 9. McKay DG: Hematologic evidence of disseminated intravascular coagulation in eclampsia. Obstet Gynecol Surv 27: 399, 1972. 10. Howie PW, Begg CB, Purdie DW, Prentice CR: Use of coagulation tests to predict the clinical progress of preeclampsia. Lancet 2: 323, 1976. 11. McKillop C, Forbes CD, Howie PW, Prentice CM: Soluable fibrinogen/fibrin complexes in preeclampsia. Lancet 1: 56, 1976. 12. Beecham JB: Association of microangiopathic hemolytic anemia with severe preeclampsia. Am J Obstet Gynecol 121: 292,1975. 13. McKay DG: Intravascular coagulation-acute and chronicdisseminated and local. Proc lnst Med Chicago 29: 159, 1972. 14. Prichard JA, Cunningham FG, Mason RA: Coagulation changes in ectampsia: their frequency and pathogenesis. Am J Obstet Gynecoll24: 855, 1976. 15. Page E: On the pathogenesis of pre-eclampsia and eclampsia. J Obstet Gynecol Br Commonw 79: 883, 1972. 16. Kinkaid-Smith P: Participation of intravascular coagulation in the pathogeneses of glomerular and vascular lesions. Kidney Int 7: 242, 1975. 17. Speroff L: Toxemia of pregnancy. Mechanism and therapeutic management. Am J Cardiol32: 582, 1973. 18. Beecham JB, Watson W, Clapp JF: Eclampsia, preeclampsia and DIC. Obstet Gynecol43: 576, 1974. 19. Howie DW, Prentice CR, Forbes CD: Failure of heparin therapy to affect the clinical course ef severe preeclampsia. Br J Obstet Gynecol82: 711, 1975. 20. Longmire WP, McArthur MS: Occult injuries of the liver, bile ducts, and pancreas after blunt abdominal trauma. Am J Surg 125: 661, 1973. 21. Lucas CE, Ledgerwood AM: Prospective evaluation of hemostatic techniques for liver injuries. J Trauma 16: 442, 1976. 22. Defore WW, Mattox KL, Jordan GL. Beau AC: Management of 1,590 consecutive cases of liver trauma. Arch Surg 111: 493, 1976. 23. Hait MR. Robb CA, Baxter CR, Borgmann AR, Tippett LO: Comparative evaluation of Avitene microcrystallene coltagen hemostat in experimental animal wounds. Am J Surg 125: 284, 1973.
The American Journal of Surgery
Spontaneous rupture of the liver is a rare but well documented complication of late pregnancy and delivery, usually associated with pre- or true eclampsia. Since first described by Abercrombie in 1844 [I], isolated reports and reviews have appeared primarily in obstetric literature. Although these patients present first to the obstetrician with toxemia of pregnancy, the recognition and management of their life-threatening hepatic injury often involves a general surgeon. Material and Methods Over a three year period (1973-1976), the general surgery service at the University of Utah affiliated hospitals has been involved in the successful management of four cases of hepatic rupture in toxemia of pregnancy. A review of this experience with emphasis on the pathogeneses of the hepatic injury and its recognition and management is presented. Two illustrative cases follow. Patient 4. A thirty-five year old white female, gravida 8, presented at thirty-four weeks’ gestation with complaints of shortness of breath, headache, and blurred vision for one week. Blood pressure on admission was 190/140, with +3 proteinuria. There was tenderness to palpation over the liver and generalized edema. She was placed on bed rest, treated with magnesium sulfate, and 11 hours after admission, she delivered a viable premature female infant. Immediately after delivery, the patient complained of acute right upper quadrant pain and was noted to have a blood pressure of 100/60 supine and a hematocrit of 22 per cent. Laboratory studies included a platelet count of 22,000, an elevated fibrinogen level of 536 mg/lOO ml, and a negative protamine sulfate test. At laparotomy, an extensive subcapsular hematoma of the right hepatic lobe with free rupture into the peritoneal cavity was discovered. This was evacuated and drained externally. A total of 25 units of blood were given during the pre- and intraoperative period. In the immediate postoperative period, the patient required an additional 18 units of blood for continued hemorrhage from the hepatic drain sites. Eventually, she underwent reexploration for infected subphrenic, subFrom the Department of Surgery, University of Utah Medical Center, Salt Lake Citv. Utah. Reprini requests should be addressed to Edward W. Nelson, MD, Dapartment of Surgery, University of Utah Medical Center, 50 North Medical Drive, Salt Lake City, Utah 84132. Presented at the Twenty-Ninth Annual Meeting of the Southwestern Surgical Congress, Acapulco, Mexico, April 25-28. 1977.
Volume 134, December 1977
hepatic, and pleural spaces. She was discharged on the thirty-ninth postoperative day and found to be doing well several months later when readmitted for elective tubal ligation.
Patient 1. A twenty-one year old female, para 0, presented at thirty-five weeks’ gestation with a four day history of headache. On admission, her blood pressure was 220/135, +3 proteinuria was present, and she complained of right upper quadrant pain. After 5 hours of treatment with bed rest, magnesium sulfate, and morphine, her blood pressure suddenly dropped to 130/80, and fetal heart rate slowed to 60. Laboratory studies at that time showed a platelet count of 27,000, fibrinogen level of less than 100 mg/lOO ml, and a positive protamine sulfate test. Shd underwent immediate laparotomy and caesarean section with delivery of a viable infant girl. At that time, a large rent in the left lobe of the liver and a secondary hemoperitoneum were discovered. During partial resection of the left lobe, she was transfused with 1,500 cc whole blood. An additional 5 units of blood were required for postoperative losses from the hepatic drainage sites. She left the hospital nineteen days after admission without further complications. Results
Various reviews of spontaneous hepatic rupture in toxemic pregnancy place the total number of reported cases at less than fifty [l-3]. Previous authors emphasize that this condition most often presents in women more than thirty years old of multiparity who present with signs and symptoms of eclampsia [I]. The lesion most often described has been a subcapsular hematoma of the right hepatic lobe which has carried up to a 70 per cent mortality in these review series [l-3]. Without prompt recognition and surgical intervention, it has proven universally fatal. Our four cases represent one of the largest groups seen and reported by a single institution. (Table I.) Although the average age of this group is lower than that previously reported and gestation periods were variable, all but one of our patients were multiparous. Universal in these patients was the triad of toxemia (manifested by hypertension and proteinuria), right upper quadrant pain, and sudden unexplained shock. Two patients were explored after delivery, and two discovered to have liver injury at the time of emer-
817
Nelson, Archibald,
TABLE I
and Albo
Manifestations of Preeclampsla, Right Upper Quadrant Pain, and Shock in Present Series
Parity and Gestation
Age W 21 26 22 35
TABLE II
Preeclampsia Blood Proteinuria Pressure
Gravida Gravida Gravida Gravida
1, 3, 2, 8,
35 40 37 34
wk wk wk wk
Surgical Factors (Intraoperatlve)
2201135 170196 210/130 190/130
:“2 +4 +3
Right Upper Quadrant Pain
Shock
i-36 hr l t24 hr +9 hr i-12 hr
130160 lOOl60 60160 lOOl60
In Present Serles Blood Replacement
Patient
Exploration
Hepatic Lesion
Treatment
1 2 3 4
Caesarean section After delivery-8 hr Caesarean section After delivery-7 hr
Left lobe hematoma with laceration Right lobe subcapsular hematoma Right lobe subcapsular hematoma Right lobe subcapsular hematoma
3/4Lobectomy, Drainage Evacuation, Suture, Drainage Evacuation, Gelfoam, Drainage Evacuation, Drainage
TABLE III
Postoperative Complications and Results In Present Series
Fluid PostOverload/ operative Pleural RespiraBlood Effusion tory Replace- on Side of InsuffiPatient ment Lesion ciency
Intraabdominal Abscess
1
5 units
+
2
11 units
+
+
-
3
30 units
+
+
-
4
18 units
+
+
+
Fetus Premature female Normal female Stillborn female Premature female
gency caesarean section. (Table II.) In three patients, the hepatic injury presented as a subcapsular hematoma of the right lobe which was treated with evacuation and drainage. One patient with hematoma and laceration of the left lobe underwent partial resection and drainage. Initial blood replacement varied from 4 to 25 units, and all patients required significant blood replacement postoperatively for continued bleeding from hepatic drains. (Table III.) All patients developed pleural effusions on the side of hepatic injury. The three patients who had required most massive transfusions were treated for fluid overload with mild secondary respiratory insufficiency. Intraabdominal abscesses and empyema were treated in one patient and ruled out in a second. A single stillborn infant was removed in a case where right upper quadrant pain and shock developed before emergency caesarean section could be completed. There was no maternal mortality.
818
4 15 4 25
units units units units
Comments
Since a multitude of physiologic changes occur in normal pregnancy, it is predictable that a variety of endocrine, metabolic, and hemodynamic factors have been mentioned in the pathogenesis of toxemia. Although the toxemia complex of hypertension, proteinuria, and convulsions remains a disease of many theories, an intermediate role of disseminated intravascular coagulation (DIC), either as a cause or effect, has continuously appeared in the literature since the 1950s [2-g]. Current reports stress that the degree and manifestations of the consumptive coagulopathy present in these patients are proportional to the severity of their toxemic state [5,6,10-151. In a recent large review series [B], DIC was shown to be present in 9.1 per cent of eclamptic patients and 2.1 per cent of severely preeclamptic patients. The deposition of microembolic fibrin and fibrinogen breakdown products seen on the basement membrane of glomerular capillary endothelium, and in the capillaries and sinusoids of the liver supports a DIC-mediated mechanism for the renal and hepatic damage sometimes seen in toxemia [4,9,15,16]. It has also been postulated that similar lesions in the central nervous system, pituitary, adrenals, and cardiopulmonary system explain the damage occasionally seen in these areas [4,9,15]. Various factors including poor diet, diabetes, obesity, hypertension, renal disease, sodium overload, and first pregnancy are all known to statistically increase therisk of toxemia. Current theories relate the coagulation abnormalities seen in toxemia to inadequate placental perfusion and secondary “uteroplacental dysfunction” perhaps caused by one or
The American Journal of Surgery
Hepatic Rupture in Pregnancy
more of these factors [15]. Whether the DIC seen in toxemia is triggered by the release of some thromboplastic or vasoactive agent from the placenta [15,17] or is secondary to platelet consumption at sites of vascular endothelial damage caused by toxemic hypertension [14] is not known. Although workup for DIC is not routine in all toxemic patients, all patients in this series were suspected of DIC and evaluated with appropriate studies. (Table IV.) As noted in the literature, the earliest and most reproducible abnormality seen was acute thrombocytopenia [18]. Fibrinogen levels, normally elevated in pregnancy, varied widely as did other, more specific tests including fibrin split products and protamine sulfate tests. Only one patient was believed clinically to have diffuse bleeding from sites other than the liver and was therefore transiently treated with heparin, although its usefulness in this setting is debated in the literature [12,14,19]. All patients did receive platelet transfusions and other blood products postoperatively. Whatever the mechanism of injury, the histopathology of the liver in toxemia has been consistently described as showing the fibrin emboli in the sinusoids and hepatic arterioles with resultant areas of periportal necrosis [1,2,4,9,15]. (Figure 1.) Many toxemic patients probably have subclinical hepatic damage manifested only by distension of Glisson’s capsule and resultant right upper quadrant tenderness, which spontaneously resolves after delivery. However, in the rare patient, the coalescence and enlargement of these microscopic areas into a subcapsular hematoma may occur. (Figure 2.) The impaired coagulation and hypertension in toxemia as well as external trauma of diaphragm and uterine movement during labor and delivery may influence the further enlargement and eventual rupture of such lesions.
TABLE IV
Figure 7. Pafhologic specimen from patlent 1 showing
Figure 2. Periporfal hemorrhagk necroses and s&capsular
periportal hemorrhage and surrounding necrosis.
hematoma formafion in specimen from patient 1.
Volume 134, December 1977
Patient
Coagulation Defects in Present Series
Platelet Count
Diffuse Hemorrhage
Fibrinogen
Other Tests
No
1
27,000
PT = l7fll PTT = 39130 PS = -
2
40,000
155 mgl100 ml
PT = 18113 PI-r = 44130
No
3
70,000
175 mg/lOO ml
PT = 18113 PTT = 83 i42 FSP = +
Yes
4
22,000
538 mg/ 100 ml
PS = PTlPTT = WNL
No
Note: PT = prothrombin time; PlT = partial thromboplastin time; PS = protamine sulfate; FSP = fibrin split products; WNL = within normal limits.
Surgical Management
When the triad of toxemia, right upper quadrant pain, and sudden hypotension present in the pregnant patient, early recognition with rapid termination of pregnancy and prompt surgical exploration are the keys to successful management. As previously noted, the hepatic lesion is usually a subcapsular hematoma of the right lobe with free rupture into the peritoneal cavity and an underlying raw bleeding liver surface. (Figure 3.) Evacuation of the hematoma, individual ligation of any discrete bleeding sites, if present, and wide, dependent drainage was the most successful approach in our experience. This is consistent with the management of these lesions suggested in large reviews of liver trauma [20-221. Although it was not used in any of our cases present or those reviewed, microcrystalline collagen (Avitenea) may be an ideal local hemostatic agent for large surface areas of the liver without discrete
819
Nelson, Archibald, and Albo
organs has been discussed. Basic surgical principles in the management of hepatic subcapsular hematomas, and the prolonged postoperative course and frequent complications in these patients have been stressed. References
Figure 3. Artist’s conception of right hepatlc lobe subcapsular hematoma involving a large area of the liver surface.
bleeding points [23]. Right hepatic artery ligation, omental or other viable packs, and resection are also technics available but generally not required to control hepatic bleeding in this condition [21,22]. Temporizing measures, such as packing the bleeding surface of the liver for 24 hours to allow coagulation abnormalities to correct, might even be helpful in certain patients. Postoperatively, care should be directed toward the prevention of continued hemorrhage with adequate replacement of blood and coagulation factors, and prolonged, wide dependent drainage of the hematoma site. Since pulmonary and infectious complications have been noted in these patients and similar patients presented in the literature [22], vigorous respiratory care and careful surveillance for the development of intraabdominal abscess should be stressed. Summary
Hepatic rupture as a late complication of toxemic pregnancy is a rare yet lethal condition requiring rapid recognition and surgical management. The clinical triad of toxemia, right upper quadrant pain, and sudden hypotension is the diagnostic hallmark of presentation. Most patients present near the time of delivery and are found to have subcapsular hematomas of the right hepatic lobe with free rupture into the peritoneal cavity and resultant exsanguinating hemorrhage. The association of toxemia and disseminated intravascular coagulation with secondary microembolic damage to the liver and other
820
1. Hakim-Elahi: Spontaneous rupture of the liver in pregnancy. Obsfet Gynecol26: 435, 1965. 2. Castaneda H, Garcia-Romero H, Canto M: Hepatic hemorrhage in toxemia or pregnancy. Am J Obstet Gynecol 107: 578, 1970. 3. Utley JR: Spontaneous rupture of the liver during pregnancy. Surg Gynecol Obstet 133: 250, 1971. 4. Coopland AT: Blood clotting abnormalities in relation to preeclampsia: a review. Can Med Assoc J 150: 121, 1969. 5. Smith H,.Gregori CA, Breen JC: Disseminated intravascular coaaulation in oreanancv. J Med Sot NJ 71: 729. 1974. 6. Bellar FK, Uszynski G ‘disseminated intravascular coagulation in pregnancy. C/in Obstet Gynecoll7: 250, 1974. 7. Youssef AH: Proceedings: disseminated intravascular coagulation (DIC) and toxemia or pregnancy in Kuwait. Thromb Diath Haemorrh 34: 569, 1975. 8. Roberts JM, May WJ: Consumptive coagulopathy in severe preeclampsia. Obstet Gynceo/ 125: 747, 1976. 9. McKay DG: Hematologic evidence of disseminated intravascular coagulation in eclampsia. Obstet Gynecol Surv 27: 399, 1972. 10. Howie PW, Begg CB, Purdie DW, Prentice CR: Use of coagulation tests to predict the clinical progress of preeclampsia. Lancet 2: 323, 1976. 11. McKillop C, Forbes CD, Howie PW, Prentice CM: Soluable fibrinogen/fibrin complexes in preeclampsia. Lancet 1: 56, 1976. 12. Beecham JB: Association of microangiopathic hemolytic anemia with severe preeclampsia. Am J Obstet Gynecol 121: 292,1975. 13. McKay DG: Intravascular coagulation-acute and chronicdisseminated and local. Proc lnst Med Chicago 29: 159, 1972. 14. Prichard JA, Cunningham FG, Mason RA: Coagulation changes in ectampsia: their frequency and pathogenesis. Am J Obstet Gynecoll24: 855, 1976. 15. Page E: On the pathogenesis of pre-eclampsia and eclampsia. J Obstet Gynecol Br Commonw 79: 883, 1972. 16. Kinkaid-Smith P: Participation of intravascular coagulation in the pathogeneses of glomerular and vascular lesions. Kidney Int 7: 242, 1975. 17. Speroff L: Toxemia of pregnancy. Mechanism and therapeutic management. Am J Cardiol32: 582, 1973. 18. Beecham JB, Watson W, Clapp JF: Eclampsia, preeclampsia and DIC. Obstet Gynecol43: 576, 1974. 19. Howie DW, Prentice CR, Forbes CD: Failure of heparin therapy to affect the clinical course ef severe preeclampsia. Br J Obstet Gynecol82: 711, 1975. 20. Longmire WP, McArthur MS: Occult injuries of the liver, bile ducts, and pancreas after blunt abdominal trauma. Am J Surg 125: 661, 1973. 21. Lucas CE, Ledgerwood AM: Prospective evaluation of hemostatic techniques for liver injuries. J Trauma 16: 442, 1976. 22. Defore WW, Mattox KL, Jordan GL. Beau AC: Management of 1,590 consecutive cases of liver trauma. Arch Surg 111: 493, 1976. 23. Hait MR. Robb CA, Baxter CR, Borgmann AR, Tippett LO: Comparative evaluation of Avitene microcrystallene coltagen hemostat in experimental animal wounds. Am J Surg 125: 284, 1973.
The American Journal of Surgery