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Coagulopathy and abdominal aortic aneurism
Eur J VascSurg 4, 557-562(1990)
R E V I E W ARTICLE
Coagulopathy and Abdominal Aortic Aneurism E. J. Gibney and D. Bouchier-Hayes Department of Surgery, RCS1, Beaumont Hospital, Dublin 9, Ireland Coagulopathy has been described in association with intact, ruptured and repaired abdominal aortic aneurysm. This review examines the relationshipand its clinicalsignificanceand outlines current management strategies. Key Words: Coagulopathy;Disseminated intravascularcoagulation;Aneurysm; Abdominal; Aortic; Ruptured.
Introduction In 1967 Fine and his colleagues described a patient who presented with a dissecting aneurysm of the aorta and multiple coagulation defects suggestive of disseminated intravascular coagulation (DIC). 1 Coagulopathy was manifest clinically as gingival bleeding, petechiae, and prolonged bleeding from venipuncture sites. Since then numerous reports have appeared documenting an association between coagulopathy and a number of vascular disorders, particularly aneurysms. Bieger et al.2 described three patients (one with a large femoral artery aneurysm, another with an aneurysm of the aortic arch, and a third with a dissecting aneursym) with clinical coagulation disorders, and laboratory evidence of DIC. Fisher and associates, in a prospective study of 76 patients with aortic aneurysms 3 detected three patients with DIC, all of w h o m had thoraco-abdominal aneurysms. Disseminated intravascular coagulation has been described in association with dissecting aneurysms, 1-5 thoraco-abdominal aneurysms 3,6,7, and abdominal aortic aneurysms which are either intact, 8-12 ruptured, 5"13"14 or post-repair. 14 Peripheral aneurysms (particularly femoral2"12), and arterio-venous fistula and false aneurysm 15 have also been described in association with DIC. The present report reviews the relationship between DIC and abdominal aortic aneurysm (AAA).
Disseminated intravascular coagulation Disseminated intravascular coagulation, also referred Please address all correspondence to: E. J. Gibney, Department of Surgery, RCSI,BeaumontHospital, Dublin 9, Ireland. 0950-821X/90/060557+06$03.00/0© 1990Grune & Stratton Ltd."
to as consumptive coagulopathy or defibrination syndrome, represents a disturbance of the normal fine balance between coagulation and fibrinolysis, which preserves homeostasis by preventing excessive bleeding without hypercoagulability. It occurs in a wide variety of clinical conditions including: (1) obstetrical complications (abruptio placentae, amniotic fluid embolism, retained dead fetus); (2) infections (particularly meningococcal septicaemia); (3) following trauma and shock; and (4) in association with malignant disease. It may also occur with giant haemangioma--the Kasabach-Merritt syndrome.16 Hardaway, 17"~8 has postulated that two conditions are necessary for DIC to occur (1) a stagnant acid capillary flow and (2) the presence of a thromboplastic agent in the blood stream. Acute and chronic forms of DIC have been described. The clinical manifestations of DIC include spontaneous bleeding, organ dysfunction due to capillary obstruction, and sometimes haemolysis. Straub 19 points out that even in the absence of spontaneous bleeding, diagnostic or therapeutic procedures may lead to life threatening haemorrhagic complications. Several authors have noted a strong association between DIC and organ dysfunction and failure, particularly renal, respiratory and hepatic, and often multiple organ failure. 6,12,14 The relationship between DIC and liver function is complex, with a well-recognised but poorly defined association between the two. Liver dysfunction has often been implicated as a contributary aetiological factor, l' 4,20,2 with central hepatic necrosis 1,4 or cirrhosis 21 being the usual histological findings. The reticuloendothelial system is known to play a major role in clearing activated coagulation factors, thromboplastic material and fibrin degradation products (FDP) from
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the blood. Thompson and colleagues 22 postulated the existence of a "compensated state" of "low grade" DIC with laboratory evidence of consumptive coagulopathy but no clinical bleeding. This reflected adequate reticuloendothelial function in clearance of FDPs, and increased production of consumed coagulation factors and platelets. They suggested that this balance could be disturbed by additional factors such as hepatic or renal insufficiency, or rapid aneurysm expansion. Bieger and co-authors '2 findings in a patient whose coagulopathy appeared to be related to the growth of a femoral aneurysm tend to support this hypothesis. In addition, both liver dysfunction and DIC have been postulated as important aetiological factors in adult respiratory distress syndrome (ARDS). 17,23,24 The diagnosis of DIC is usually made by finding the combination of the following: low fibrinogen, elevated FDPs, low platelet count, and prolongation of one or more coagulation function tests (prothrombin time, activated partial thromboplastin time). Clinical manifestations include petechiae, ecchymosis, prolonged bleeding from veni- or arterial-puncture sites, and excessive intra-operative or postoperative bleeding. However, the diagnosis is not always as clear cut as the above clinical and laboratory features suggest. Fisher et al. 3 point out that fibrinogen and FDP levels correlate poorly with clinical DIC, but that the combination of elevated FDPs, reduced platelet count and a bleeding tendency give a good indication of the presence or absence of clinically significant DIC. Fibrinogen synthesis may or may not keep pace with consumption, so fibrinogen levels may be elevated, reduced or normal, 3 and the findings of isolated elevated FDP levels have been shown not to predict greater operative blood lOSS. 3"2s Thrombocytopaenia appears to be the single most reliable abnormality that predicts blood IOSS. 3'13 The finding of fibrin microthrombi histologically is supportive evidence of DIC, but is reliable only when positive, 19 because clearance of microthrombi can occur in vivo by fribinolysis and via the reticulo-endothelial system.
Disseminated intravascular coagulation and intact abdominal aortic aneurysm The occurence of DIC as a complication of an intact AAA has been disputed. Siebert and Natelson 21 described two p/~tients in w h o m the conditions coexisted. Their first patient had been reported previously, 26 and was widely held to have 'had DIC secondary to an AAA, which was repaired. However, Eur J VascSurg Vol4, December1990
following repair of his aneurysm he continued to exhibit clinical and laboratory manifestations of DIC and a diagnosis of pancreatic carcinoma was eventually confirmed at laparotomy 18 months later. Their second patient was more convincing, his coagulopathy was corrected by AAA repair, but he proved also to have liver cirrhosis, and in addition underwent splenectomy at the time of his aortic surgery. Because of their experience with these two cases, the authors proposed four criteria for accepting intact AAA as the primary cause of DIC: (1) the presence of a chronic acquired bleeding disorder; (2) laboratory evidence of DIC; (3) correction of haematological abnormality by successful aneurysm repair; and (4) maintenance of normal coagulation for at least 3 months after surgery. They cautioned that the discovery of DIC accompanying a stable aneurysm should prompt a search for another underlying disorder. Their last two criteria also make the diagnosis of DIC secondary to AAA "speculative" in those patients who have not undergone aneurysm repair. Applying these criteria strictly to published reports, there remain several patients who have apparently developed DIC in association with stable AAA.10,11, 22 Of the three patients described by Goto and co-workers, 9 one had a gastric carcinoma, another died within 24 h of surgery, while the third fulfilled Siebert and Natelson's criteria. A number of other cases also satisfy the diagnostic criteria but these patients were also noted to have histological evidence of liver disease. These include Siebert and Natelson's 21 second case, who had cirrhosis, and a patient described by Keagy and associates, s who had "increased fibrous connective tissue in the portal area with some bridging" on liver biopsy. Cases reported to document the association between the two conditions but failing to fulfil strict diagnostic criteria include those of Satiani, 12 Diskin, 27 and Fouser. 28 Two major prospective studies have been performed in an attempt to examine the relationship between DIC and intact AAA'more closely. In 1976 Mulcare et al. 25 reported a prospective study of all patients undergoing elective operations on the abdominal aorta over a 1 year period. This included 18 patients with AAA and 14 with aorto-occlusive disease. Although a total of 40% of patients had elevated FDP levels preoperatively, with low levels of plasminogen in 20%, the authors concluded that there was no evidence from their study that intact AAA could promote intravascular coagulation. Similarly, in the prospective study by Fisher and colleagues, 3 which included 22 patients with infrarenal AAA among the 76 patients, eight (36%) were shown to have isolated elevated FDP levels but all three cases of clinically
Coagulopathy and Abdominal Aortic Aneurysm
overt DIC detected were in the group with thoracoabdominal aortic aneurysms. In a retrospective study Getaz and Louw, 13 found that 28.2% of 57 patients with unruptured AAA had thrombocytopaenia, but otherwise demonstrated no coagulation abnormality. Full coagulation tests, however, were not done on all patients. Three of the group had documented dramatic postoperative increases in platelet count, suggesting that the aneurysm was the cause of thrombocytopaenia. Local consumption of platelet and clotting factors or at least local initiation of the coagulation process, is considered to be the most likely mechanism of coagulopathy in arterial aneurysm. It has been shown that radioactive labelled fibrinogen localises to the aneurysm wall. 5"29 Platelet consumption may be due to platelet incorporation into mural thrombus, or mechanical destruction. There have been numerous studies documenting adherance of platelets to denuded aorta, 3° collagen contact activation of the intrinsic clotting mechanism 31 and abnormal platelet adherance to atheromatous aorta. 32 Local turbulance may play a role in coagulopathy, comparable in some ways to the platelet abnormalities seen in relation to prosthetic heart valves. 33 Haemolysis may also be a feature in these circumstances as Rhodes et al. is described in their case of DIC complicating arterio-venous fistula and false aneurysm. Many authors cite the presence of fresh clot in the aneurysm sack when performing surgery on these patients, s'9" 12,19 Fisher and colleagues g felt that aneurysms with a larger surface area were more likely to be associated with coagulation abnormalities, and in the three patients with well documented DIC as a result of AAA where the aneurysm size is given 1°"11,22 all had aneurysms 8 cm or more in diameter. Given however, the high prevalence of AAA and the rarity of DIC it appears that Siebert and Natelson's 21 advice that the discovery of the DIC association with AAA should prompt a careful search for another precipitating disorder is sound. In particular occult neoplasm and liver disease must be excluded.
Elective aneurysm repair and coagulopathy It is well recognised that DIC may complicate major surgery and elective repair of an AAA is no exception. In a retrospective study of patients undergoing repair of AAA, Mulcare and colleagues 14 described three cases of elective aneurysm repair which were complicate~t by DIC. Two of these patients had significant hypotension intra-operatively. A subsequent report
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from the same group 25 examined coagulation function tests prospectively in patients undergoing aortic surgery. They concluded that elective aortic grafting procedures may produce low grade intravascular coagulation, either locally or disseminated. The fibrinolytic system normally prevents the development of clinical sequelae. One of their 32 patients developed clinical evidence of DIC which was successfully treated with heparin. Collins et aI. 6 reported a series of cases where coagulopathy was associated with arterial disease and its treatment, and one of their patients, having had a normal coagulation profile preoperatively, developed laboratory evidence of DIC after AAA repair. This patient developed multiple areas of infarcted skin, eventually progressing to gangrene of the right foot. Two further patients had severe bleeding requiring reexploration, and laboratory evidence of DIC, after otherwise uncomplicated abdominal aortic surgery. In Johnston and Scobie's 34 large series the incidence of postoperative coagulopathy was noted to be significantly higher in those with an inflammatory aneurysm (6.7%) than in those with a standard aneurysm (0.8%). By contrast; many series describing large numbers of patients undergoing elective aortic aneurysm repair do not mention coagulopathy as a commonly significant postoperative complication. B5 It is well recognised that coagulopathy and subsequent bleeding does play a major role in morbidity and mortality from thoraco-abdominal aneurysm repair, B6 with operative and postoperative bleeding being responsible for 25% of early deaths following the procedure. Cohen and colleagues B7induced DIC in a dog model by supracoeliac cross-clamping of the aorta for 90 min, and from their study concluded that clamping at this level could produce DIC, the severity of which was related to the duration of clamping. A number of theories were proposed to account for the phenomenon. Ischaemic hepatic damage might be an important factor, and if this is so then it is hardly surprising that elective infrarenal AAA repair is associated with a low incidence of DIC, since cross-clamping is generally below the origin of the blood supply to the liver. Nevertheless, as Mulcare's studies suggest, 14 the conditions which might lead to a clinically apparent DIC exist as a result of elective AAA repair, particularly if aggravating factors are also present. Postulated aetiological factors in these circumstances include sluggish acidotic flow in tissues distal to the aortic claml~, vascular and tissue injury, mechanical injury to platelets as a result of cross-clamping, and the formation of microaggregates and microembolisation with the release of procoagulants.
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Ruptured aneurysm and coagulopathy The association between abnormal coagulation and ruptured AAA is an important and clinically relevant one. Getaz and Louw 13, described a group of 27 patients with ruptured aneurysms in which 50% of those in whom platelet counts were performed had abnormally low values. Fifty-six per cent of the same group had evidence of abnormal coagulation, while two patients fulfilled the diagnostic criteria for DIC. Mortality in the group with coagulopathy was 70%, compared to 56% in the group as a U?hole, and it was noted that coagulopathy was second only to shock as a factor associated with mortality. In Marsh's series 38 of 29 patients, nine had coagulation disorders and only one of these patients survived. Graft haemorrhage due to coagulopathy was found to be a major complicating factor in 25% of the postoperative deaths. High coagulation factor consumption in the haematoma was considered to be the primary cause. FDP levels were not apparently measured. Mulcare et a]. 14 described four patients with ruptured AAA who developed DIC postoperatively, all of w h o m exhibited clinically excessive bleeding, and developed renal shutdown. None survived. All three reports concluded that coagulation abnormalities were a far more significant problem in ruptured AAA than had previously been suspected. Other authors have since confirmed the significance of this association. Wakefield e t a [ . 39 e n c o u n t e r e d coagulopathy in eight of 92 patients (9%), and detected abnormalities of prothrombin time, partial thromboplastin time and other liver function tests in 30% of patients. Hiatt et al. 40 identified coagulopathy as contributing to poor outcome in six of 29 patients who died as a result of ruptured AAA. In a study of ruptured AAA, Hoffman's group 41 found that postoperative haemorrhage occurred in 37 patients (24.3%), with a mortality rate of 89.2%. Moreover Diehl et al. 42 noted that postoperative haemorrhage was the second leading cause of early mortality (after myocardial infarction) because of its incidence among patients with ruptured aneurysms. It is clear therefore that coagulopathy plays a major role in postoperative morbidity and mortality in patients with ruptured aneurysms who survive long enough to undergo surgery. Many of the factors known to precipitate or promote the development of DIC are present in patients with a ruptured aneurysm--shock, stasis, endothelial damage, depressed reticulo-endothelial function, and blood lOSS. 38" 42 It is tempting to speculate that myocardial infarction, secondary to coronary artery thrombosis, a leading cause of mortality after aneurysm repair, might result Eur J VascSurg Vol4, December1990
from a low grade hypercoagulability, and thus bear a close relationship to DIC in these patients.
Management Definitive management of DIC is best accomplished by correction of the underlying cause. Thus, in those cases of subacute or chronic DIC where AAA alone is considered to be the cause, and other contributory factors have been excluded or treated, aneurysm repair is indicated. Whether or not an attempt should be made preoperatively to correct the coagulopathy is controversial. A number of authors have observed spontaneous correction of the coagulopathy. 2'11 Heparin has had its advocates and opponents, while antifibrinolytics have no place in the management of DIC. Experimentally heparin has been shown to be of benefit only if given prophylactically. 18 Theoretically heparin could reduce the thrombotic tendency but increase the risk of bleeding. In practice, many authors have used heparin, 2'7"8'9'21'22"27 in doses usually ranging from 300-600 units per hour as preoperative preparation or treatment of DIC and have been successful in improving coagulation status. Heparin treatment is not always successful however, 3"1°'5 and an alternative approach has been suggested by Fisher et al., 3 and supported by Macneily and Graham. 11 These authors advocate a direct surgical approach to the problem, aiming to correct the coagulopathy by aneurysm repair. A large intra-operative blood loss is anticipated, and a high speed autotransfuser should be available in addition to adequate amounts of platelets, fresh frozen plasma, and cryoprecipitate. Meticulous surgical technique is essential at all stages, and minim u m aneurysm dissection, the use of a woven graft, and wrapping the old aneurysm sac around the graft are all suggested as ways to minimise blood loss. The coagulopathy associated with ruptured aneurysm is an acute one, precipitated by shock, consumption of coagulation factors and tissue trauma. The emphasis on management is on replacement of clotting factors and platelets, and restoration of circulating blood volume. Early diagnosis and prompt surgery are essential to limit mortality. 4°'41"43 Lambert and associates 44 found that administration of fresh frozen plasma preoperatively in ruptured aneurysm significantly increased survival. Woven Dacron grafts are preferred to knitted grafts in ruptured aneurysms because they are less porous.
Coagulopathy and Abdominal Aortic Aneurysm
Conclusion
Disseminated intravascular coagulation rarely results primarily from an intact AAA, and its finding in association with AAA should prompt a careful search for contributory causes, particularly occult neoplasia or liver disease. Similarly, DIC following elective aneurysm repair is an unusual event and additional factors are usually at play if it occurs. Isolated abnormalities of coagulation function tests are not however unusual. Coagulopathy, including DIC, are not all uncommon after ruptured AAA, and often play a leading role in postoperative morbidity and mortality from this condition. A more widespread recognition of its occurrence and appropriate aggressive management might therefore lead to a reduction in the risk of mortality from ruptured aneurysm.
References 1 FINE NL, APPLEBAUMJ, ELGUEZABALA, CASTLEMANL. Multiple coagulation defects in association with dissecting aneurysm. Arch Intern Med 1967; 119: 522-526. 2 BIEGERR, VREEKENJ, STIBBEJ, LOELIGEREA. Arterial aneurysm as a cause of consumption coagulopathy. N EngI J Med 1971; 285: 152-154. 3 FISHERDF, YAWNDH, CRAWFORDES. Preoperative disseminated intravascular coagulation associated with aortic aneurysm. A prospective study of 76 cases. Arch Surg 1983; 118: 1252-1255. 4 SCOTTJ, HUMPHREYsDR. Dissectingaorticaneurysmanddiseminated intravascular coagulation. Br Med J 1977; 1: 24. 5 TENCATEJW, TIMMERSH, BECKERAE. Coagulopathy in ruptured or dissecting aortic aneurysm. Am J Med 1975; 59: 171-176. 6 COLLINS GJ, RICH NM, SCIALLA S, ANDERSEN CA, McDONALD PT. Pitfalls in peripheral vascular surgery: disseminated intravascular coagulation. Am J Surg 1977; 134: 375-380. 7 SCHNETZER GW, PENNER JA. Chronic intravascular coagulation syndrome associated with atherosclerotic aortic aneurysm. South MedJ 1973; 66: 264-268. 8 KEAGY BA, PHARR WF, BOWLS DE. Unusual presentations of abdominal aortic aneurysms. J Cardiovasc Surg 1981; 22: 41-46. 9 GOTO H, KIMOTO A, KAWAGUCHIH, et al. Surgical treatment of abdominal aortic aneurysm complicated with chronic disseminated intravascular coagulopathy. J Cardiovasc Surg 1985; 26: 280-282. 10 MIYATAT, TADAY, TAKAGIA, OSHIMAA, SHIRAKAWAM, IDEZUKI Y. Disseminated intravascular coagulation caused by abdominal aortic aneurysm. J Cardiovasc Surg 1988; 29: 494-497. 11 MACNEILYAE, GRAHAMAM. Coagulopathyinduced by aortoiliac aneurysms. Can J Surg 1988; 31: 27-30. 12 SATIANI B, SAVRIN R, EVANS WE. Consumption coagulopathy associated with arterial aneurysms. J Cardiovasc Surg 1979; 20: 273-278. 13 GETAZ EP, Louw JH. The coagulopathy associated with aortic aneurysms. Postgrad Med J 1977; 53: 668-671. 14 MULCARERJ, ROYSTERTS, WEISS HJ, PHILLIPS LL. Disseminated intravascular coagulation as a complication of abdominal aortic aneurysm repair. Ann Surg 1974; 180: 343-349. 15 RHODES GR, Cox CB, SILVER D. Arteriovenous fistula and false aneurysm as the cause of consumption coagulopathy. Surgery 1973; 73: 535-540. 16 RODRIGUEZ-ERDMANNF, BUTTONL, MURRAYJE, et al. Kasabach-
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Merritt syndrome: Coagulo-analytical Observations. Am J Med Sci 1971; 261: 9-15. 17 HARDAWAY RIV[. Disseminated intravascular coagulation as a possible cause of acute respiratory failure. Surg Gynecol Obstet 1973; 137: 419-423. 18 HARDAWAYRM. Disseminatedintravascular coagulation. Surgery 1974; 76: 682-684. 19 STRAUBPW. Chronic intravascular coagulation. Acta Med Scand 1971; 526 (Suppl): 1-95. 20 COLMANRW, RO~BOYSJ, MINNAJD. Disseminatedintravascular coagulation (DIC): an approach. Am J Med 1972; 52: 679-689. 21 SIEBERTWT, NATELSONEA. Chronic consumption coagulopathy accompanying abdominal aortic aneurysm. Arch Surg 1976; 111: 539-541. 22 THOMPSON RW, ADAMS DH, COHEN JR, MANNICK JA, WHITTEMORE AD. Disseminated intravascular coagulation caused by abdominal aortic aneurysm. J Vasc Surg 1986; 4: 184-186. 23 SCHUMACKERPR, SARATM. Pulmonary gas exchange abnormalities following intravascular coagulation. Reticuloendothelial involvement. Ann Surg 1980; 192: 95-102. 24 PARDYBJ, DODLEYHAF. Post~traumatic pulmonary insufficiency. Surg Gynecol Obstet 1977; 144: 259-269. 25 MULCARERJ, ROYSTERTS, PHILLI~'SLL. Intravascular coagulation in surgical procedures on the abdominal aorta. Surg Gynecol Obstet 1976; 143: 730-734. 26 KAZMIER FJ, DIDISHEIM P, FAIRBANKS VF, et al. Intravascular coagulation and arterial disease. Thromb Diath Haemorrh 1969; 36: 295-303. 27 DISKIN CJ, WEITBERGAB. Minidose heparin therapy. Treatment of chronic intravascular coagulation syndrome. Arch Intern Med 1980; 140: 263-266. 28 FOUSER LS, MORROW NE, DAVIS RB. Platelet dysfunction associated with abdominal aortic aneurysm. Am J Clin Path 1980; 74: 701-715. 29 STRAUEPW, KESSLERS. Umsatz und Lokalisation yon I TM-Fibrinogen bei chronischer intravasaler Gerinnung. Schweiz Med Wochenschr 1970; 100: 2001-2003. 30 BAUMGARTNERHR, STEMERMAN MB, SPAET TH. Adhesion of blood platelets to subendothelial surface: distinct from adhesion to collagen. Experienta 1971; 27: 283. 31 NIEWlAROWSKI S, BANKOWSKI E, ROGOWICKA I. Studies on the absorption and activation of the Hageman factor (factor Xll) by collagen and elastin. Thromb Diath Haemorrh 1965; 14: 387. 32 PRENTICECRM, McNICOL GP, DOUGLASAS. Effects on blood coagulation of normal and atheromatous aortic tissue. J Clin Path 1966; 19: 154-158. 33 MYHRE E, HELLEM AJ, STORMORKENJ- Intravascular haemolysis, platelet consumption, and platelet adhesiveness in patients with prosthetic heart valves. Scand J Thorac Cardiovasc Surg 1971; 5: 13-15. 34 JOHNSTONKW, SCOBIETK. Multicenter prospective study of nonruptured aortic aneurysm. I. Population and operative management. J Vasc Surg 1988; 7: 69-81. 35 CRAWFORDES, SALEH SA, BABBJW, GLAESERDH, VACCAROPS, SILVERS A. Infrarenal abdominal aortic aneurysm. Factors influencing survival after operation performed over a 25-year period. Ann Surg 1981; 193: 699-709. 36 CI~WrORD ES, Crc~WFORDJL, SAFI HJ, et al. Thoraco-abdominal aortic aneurysms: preoperative and intra-operative factors determining immediate and long-term results of operations in 605 patients. J Vasc Surg 1986; 3: 389-404. 37 COHEN JR, ANGUS L, ASHER A, CHANG JB, WISE L. Disseminated intravascular coagulation as a result of supracoeliac clamping: implications for thoracoabdominal aneurysm repair. Ann Vasc Surg 1987; 1: 552-557. 38 MARSH CH. Experiences with abdominal aortic aneurysms in a district general hospital. Ann R Cull Surg Eng11980; 62: 294-296. 39 WAKEFIELD TW, WHITEHOUSE WM, Wu SC, et al. Abdominal aortic aneurysm rupture: statistical analysis of factors affecting outcome of surgical treatment. Surgery 1982; 91: 586-596. 40 HIATT JCG, BARKER WF, MACHLEDER HI, BAKERJD, BUSUTTIL RW, MOORE WS. Determinants of failure in the treatment of Eur J Vasc Surg Vol 4, December 1990
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ruptured abdominal aortic aneurysm. Arch Surg 1984; 119: 1264-1268. 41 HOFFMANNM, AvELLONEJC, PLECHAFR, et aI. Operation for ruptured abdominal aortic aneurysms: a community-wide experience. Surgery 1982; 91: 597-602. 42 DIEHL JT, CALl RE, HERTZER NR, BEVEN EG. Complications of aortic reconstruction. Ann Surg 1983; 197: 49-56.
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43 MANNICK JA, WHITTEMORE AD. Management of ruptured or symptomatic abdominal aortic aneurysms. Surg Clin N Am 1988; 68: 377-384. 44 LAMBERT ME, BAGULEY P, CHARLESWORTH D. Ruptured abdominal-aortic aneurysms. J Cardiovasc Surg 1986; 27: 256-261.
Accepted 15 February 1990
R E V I E W ARTICLE
Coagulopathy and Abdominal Aortic Aneurism E. J. Gibney and D. Bouchier-Hayes Department of Surgery, RCS1, Beaumont Hospital, Dublin 9, Ireland Coagulopathy has been described in association with intact, ruptured and repaired abdominal aortic aneurysm. This review examines the relationshipand its clinicalsignificanceand outlines current management strategies. Key Words: Coagulopathy;Disseminated intravascularcoagulation;Aneurysm; Abdominal; Aortic; Ruptured.
Introduction In 1967 Fine and his colleagues described a patient who presented with a dissecting aneurysm of the aorta and multiple coagulation defects suggestive of disseminated intravascular coagulation (DIC). 1 Coagulopathy was manifest clinically as gingival bleeding, petechiae, and prolonged bleeding from venipuncture sites. Since then numerous reports have appeared documenting an association between coagulopathy and a number of vascular disorders, particularly aneurysms. Bieger et al.2 described three patients (one with a large femoral artery aneurysm, another with an aneurysm of the aortic arch, and a third with a dissecting aneursym) with clinical coagulation disorders, and laboratory evidence of DIC. Fisher and associates, in a prospective study of 76 patients with aortic aneurysms 3 detected three patients with DIC, all of w h o m had thoraco-abdominal aneurysms. Disseminated intravascular coagulation has been described in association with dissecting aneurysms, 1-5 thoraco-abdominal aneurysms 3,6,7, and abdominal aortic aneurysms which are either intact, 8-12 ruptured, 5"13"14 or post-repair. 14 Peripheral aneurysms (particularly femoral2"12), and arterio-venous fistula and false aneurysm 15 have also been described in association with DIC. The present report reviews the relationship between DIC and abdominal aortic aneurysm (AAA).
Disseminated intravascular coagulation Disseminated intravascular coagulation, also referred Please address all correspondence to: E. J. Gibney, Department of Surgery, RCSI,BeaumontHospital, Dublin 9, Ireland. 0950-821X/90/060557+06$03.00/0© 1990Grune & Stratton Ltd."
to as consumptive coagulopathy or defibrination syndrome, represents a disturbance of the normal fine balance between coagulation and fibrinolysis, which preserves homeostasis by preventing excessive bleeding without hypercoagulability. It occurs in a wide variety of clinical conditions including: (1) obstetrical complications (abruptio placentae, amniotic fluid embolism, retained dead fetus); (2) infections (particularly meningococcal septicaemia); (3) following trauma and shock; and (4) in association with malignant disease. It may also occur with giant haemangioma--the Kasabach-Merritt syndrome.16 Hardaway, 17"~8 has postulated that two conditions are necessary for DIC to occur (1) a stagnant acid capillary flow and (2) the presence of a thromboplastic agent in the blood stream. Acute and chronic forms of DIC have been described. The clinical manifestations of DIC include spontaneous bleeding, organ dysfunction due to capillary obstruction, and sometimes haemolysis. Straub 19 points out that even in the absence of spontaneous bleeding, diagnostic or therapeutic procedures may lead to life threatening haemorrhagic complications. Several authors have noted a strong association between DIC and organ dysfunction and failure, particularly renal, respiratory and hepatic, and often multiple organ failure. 6,12,14 The relationship between DIC and liver function is complex, with a well-recognised but poorly defined association between the two. Liver dysfunction has often been implicated as a contributary aetiological factor, l' 4,20,2 with central hepatic necrosis 1,4 or cirrhosis 21 being the usual histological findings. The reticuloendothelial system is known to play a major role in clearing activated coagulation factors, thromboplastic material and fibrin degradation products (FDP) from
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the blood. Thompson and colleagues 22 postulated the existence of a "compensated state" of "low grade" DIC with laboratory evidence of consumptive coagulopathy but no clinical bleeding. This reflected adequate reticuloendothelial function in clearance of FDPs, and increased production of consumed coagulation factors and platelets. They suggested that this balance could be disturbed by additional factors such as hepatic or renal insufficiency, or rapid aneurysm expansion. Bieger and co-authors '2 findings in a patient whose coagulopathy appeared to be related to the growth of a femoral aneurysm tend to support this hypothesis. In addition, both liver dysfunction and DIC have been postulated as important aetiological factors in adult respiratory distress syndrome (ARDS). 17,23,24 The diagnosis of DIC is usually made by finding the combination of the following: low fibrinogen, elevated FDPs, low platelet count, and prolongation of one or more coagulation function tests (prothrombin time, activated partial thromboplastin time). Clinical manifestations include petechiae, ecchymosis, prolonged bleeding from veni- or arterial-puncture sites, and excessive intra-operative or postoperative bleeding. However, the diagnosis is not always as clear cut as the above clinical and laboratory features suggest. Fisher et al. 3 point out that fibrinogen and FDP levels correlate poorly with clinical DIC, but that the combination of elevated FDPs, reduced platelet count and a bleeding tendency give a good indication of the presence or absence of clinically significant DIC. Fibrinogen synthesis may or may not keep pace with consumption, so fibrinogen levels may be elevated, reduced or normal, 3 and the findings of isolated elevated FDP levels have been shown not to predict greater operative blood lOSS. 3"2s Thrombocytopaenia appears to be the single most reliable abnormality that predicts blood IOSS. 3'13 The finding of fibrin microthrombi histologically is supportive evidence of DIC, but is reliable only when positive, 19 because clearance of microthrombi can occur in vivo by fribinolysis and via the reticulo-endothelial system.
Disseminated intravascular coagulation and intact abdominal aortic aneurysm The occurence of DIC as a complication of an intact AAA has been disputed. Siebert and Natelson 21 described two p/~tients in w h o m the conditions coexisted. Their first patient had been reported previously, 26 and was widely held to have 'had DIC secondary to an AAA, which was repaired. However, Eur J VascSurg Vol4, December1990
following repair of his aneurysm he continued to exhibit clinical and laboratory manifestations of DIC and a diagnosis of pancreatic carcinoma was eventually confirmed at laparotomy 18 months later. Their second patient was more convincing, his coagulopathy was corrected by AAA repair, but he proved also to have liver cirrhosis, and in addition underwent splenectomy at the time of his aortic surgery. Because of their experience with these two cases, the authors proposed four criteria for accepting intact AAA as the primary cause of DIC: (1) the presence of a chronic acquired bleeding disorder; (2) laboratory evidence of DIC; (3) correction of haematological abnormality by successful aneurysm repair; and (4) maintenance of normal coagulation for at least 3 months after surgery. They cautioned that the discovery of DIC accompanying a stable aneurysm should prompt a search for another underlying disorder. Their last two criteria also make the diagnosis of DIC secondary to AAA "speculative" in those patients who have not undergone aneurysm repair. Applying these criteria strictly to published reports, there remain several patients who have apparently developed DIC in association with stable AAA.10,11, 22 Of the three patients described by Goto and co-workers, 9 one had a gastric carcinoma, another died within 24 h of surgery, while the third fulfilled Siebert and Natelson's criteria. A number of other cases also satisfy the diagnostic criteria but these patients were also noted to have histological evidence of liver disease. These include Siebert and Natelson's 21 second case, who had cirrhosis, and a patient described by Keagy and associates, s who had "increased fibrous connective tissue in the portal area with some bridging" on liver biopsy. Cases reported to document the association between the two conditions but failing to fulfil strict diagnostic criteria include those of Satiani, 12 Diskin, 27 and Fouser. 28 Two major prospective studies have been performed in an attempt to examine the relationship between DIC and intact AAA'more closely. In 1976 Mulcare et al. 25 reported a prospective study of all patients undergoing elective operations on the abdominal aorta over a 1 year period. This included 18 patients with AAA and 14 with aorto-occlusive disease. Although a total of 40% of patients had elevated FDP levels preoperatively, with low levels of plasminogen in 20%, the authors concluded that there was no evidence from their study that intact AAA could promote intravascular coagulation. Similarly, in the prospective study by Fisher and colleagues, 3 which included 22 patients with infrarenal AAA among the 76 patients, eight (36%) were shown to have isolated elevated FDP levels but all three cases of clinically
Coagulopathy and Abdominal Aortic Aneurysm
overt DIC detected were in the group with thoracoabdominal aortic aneurysms. In a retrospective study Getaz and Louw, 13 found that 28.2% of 57 patients with unruptured AAA had thrombocytopaenia, but otherwise demonstrated no coagulation abnormality. Full coagulation tests, however, were not done on all patients. Three of the group had documented dramatic postoperative increases in platelet count, suggesting that the aneurysm was the cause of thrombocytopaenia. Local consumption of platelet and clotting factors or at least local initiation of the coagulation process, is considered to be the most likely mechanism of coagulopathy in arterial aneurysm. It has been shown that radioactive labelled fibrinogen localises to the aneurysm wall. 5"29 Platelet consumption may be due to platelet incorporation into mural thrombus, or mechanical destruction. There have been numerous studies documenting adherance of platelets to denuded aorta, 3° collagen contact activation of the intrinsic clotting mechanism 31 and abnormal platelet adherance to atheromatous aorta. 32 Local turbulance may play a role in coagulopathy, comparable in some ways to the platelet abnormalities seen in relation to prosthetic heart valves. 33 Haemolysis may also be a feature in these circumstances as Rhodes et al. is described in their case of DIC complicating arterio-venous fistula and false aneurysm. Many authors cite the presence of fresh clot in the aneurysm sack when performing surgery on these patients, s'9" 12,19 Fisher and colleagues g felt that aneurysms with a larger surface area were more likely to be associated with coagulation abnormalities, and in the three patients with well documented DIC as a result of AAA where the aneurysm size is given 1°"11,22 all had aneurysms 8 cm or more in diameter. Given however, the high prevalence of AAA and the rarity of DIC it appears that Siebert and Natelson's 21 advice that the discovery of the DIC association with AAA should prompt a careful search for another precipitating disorder is sound. In particular occult neoplasm and liver disease must be excluded.
Elective aneurysm repair and coagulopathy It is well recognised that DIC may complicate major surgery and elective repair of an AAA is no exception. In a retrospective study of patients undergoing repair of AAA, Mulcare and colleagues 14 described three cases of elective aneurysm repair which were complicate~t by DIC. Two of these patients had significant hypotension intra-operatively. A subsequent report
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from the same group 25 examined coagulation function tests prospectively in patients undergoing aortic surgery. They concluded that elective aortic grafting procedures may produce low grade intravascular coagulation, either locally or disseminated. The fibrinolytic system normally prevents the development of clinical sequelae. One of their 32 patients developed clinical evidence of DIC which was successfully treated with heparin. Collins et aI. 6 reported a series of cases where coagulopathy was associated with arterial disease and its treatment, and one of their patients, having had a normal coagulation profile preoperatively, developed laboratory evidence of DIC after AAA repair. This patient developed multiple areas of infarcted skin, eventually progressing to gangrene of the right foot. Two further patients had severe bleeding requiring reexploration, and laboratory evidence of DIC, after otherwise uncomplicated abdominal aortic surgery. In Johnston and Scobie's 34 large series the incidence of postoperative coagulopathy was noted to be significantly higher in those with an inflammatory aneurysm (6.7%) than in those with a standard aneurysm (0.8%). By contrast; many series describing large numbers of patients undergoing elective aortic aneurysm repair do not mention coagulopathy as a commonly significant postoperative complication. B5 It is well recognised that coagulopathy and subsequent bleeding does play a major role in morbidity and mortality from thoraco-abdominal aneurysm repair, B6 with operative and postoperative bleeding being responsible for 25% of early deaths following the procedure. Cohen and colleagues B7induced DIC in a dog model by supracoeliac cross-clamping of the aorta for 90 min, and from their study concluded that clamping at this level could produce DIC, the severity of which was related to the duration of clamping. A number of theories were proposed to account for the phenomenon. Ischaemic hepatic damage might be an important factor, and if this is so then it is hardly surprising that elective infrarenal AAA repair is associated with a low incidence of DIC, since cross-clamping is generally below the origin of the blood supply to the liver. Nevertheless, as Mulcare's studies suggest, 14 the conditions which might lead to a clinically apparent DIC exist as a result of elective AAA repair, particularly if aggravating factors are also present. Postulated aetiological factors in these circumstances include sluggish acidotic flow in tissues distal to the aortic claml~, vascular and tissue injury, mechanical injury to platelets as a result of cross-clamping, and the formation of microaggregates and microembolisation with the release of procoagulants.
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Ruptured aneurysm and coagulopathy The association between abnormal coagulation and ruptured AAA is an important and clinically relevant one. Getaz and Louw 13, described a group of 27 patients with ruptured aneurysms in which 50% of those in whom platelet counts were performed had abnormally low values. Fifty-six per cent of the same group had evidence of abnormal coagulation, while two patients fulfilled the diagnostic criteria for DIC. Mortality in the group with coagulopathy was 70%, compared to 56% in the group as a U?hole, and it was noted that coagulopathy was second only to shock as a factor associated with mortality. In Marsh's series 38 of 29 patients, nine had coagulation disorders and only one of these patients survived. Graft haemorrhage due to coagulopathy was found to be a major complicating factor in 25% of the postoperative deaths. High coagulation factor consumption in the haematoma was considered to be the primary cause. FDP levels were not apparently measured. Mulcare et a]. 14 described four patients with ruptured AAA who developed DIC postoperatively, all of w h o m exhibited clinically excessive bleeding, and developed renal shutdown. None survived. All three reports concluded that coagulation abnormalities were a far more significant problem in ruptured AAA than had previously been suspected. Other authors have since confirmed the significance of this association. Wakefield e t a [ . 39 e n c o u n t e r e d coagulopathy in eight of 92 patients (9%), and detected abnormalities of prothrombin time, partial thromboplastin time and other liver function tests in 30% of patients. Hiatt et al. 40 identified coagulopathy as contributing to poor outcome in six of 29 patients who died as a result of ruptured AAA. In a study of ruptured AAA, Hoffman's group 41 found that postoperative haemorrhage occurred in 37 patients (24.3%), with a mortality rate of 89.2%. Moreover Diehl et al. 42 noted that postoperative haemorrhage was the second leading cause of early mortality (after myocardial infarction) because of its incidence among patients with ruptured aneurysms. It is clear therefore that coagulopathy plays a major role in postoperative morbidity and mortality in patients with ruptured aneurysms who survive long enough to undergo surgery. Many of the factors known to precipitate or promote the development of DIC are present in patients with a ruptured aneurysm--shock, stasis, endothelial damage, depressed reticulo-endothelial function, and blood lOSS. 38" 42 It is tempting to speculate that myocardial infarction, secondary to coronary artery thrombosis, a leading cause of mortality after aneurysm repair, might result Eur J VascSurg Vol4, December1990
from a low grade hypercoagulability, and thus bear a close relationship to DIC in these patients.
Management Definitive management of DIC is best accomplished by correction of the underlying cause. Thus, in those cases of subacute or chronic DIC where AAA alone is considered to be the cause, and other contributory factors have been excluded or treated, aneurysm repair is indicated. Whether or not an attempt should be made preoperatively to correct the coagulopathy is controversial. A number of authors have observed spontaneous correction of the coagulopathy. 2'11 Heparin has had its advocates and opponents, while antifibrinolytics have no place in the management of DIC. Experimentally heparin has been shown to be of benefit only if given prophylactically. 18 Theoretically heparin could reduce the thrombotic tendency but increase the risk of bleeding. In practice, many authors have used heparin, 2'7"8'9'21'22"27 in doses usually ranging from 300-600 units per hour as preoperative preparation or treatment of DIC and have been successful in improving coagulation status. Heparin treatment is not always successful however, 3"1°'5 and an alternative approach has been suggested by Fisher et al., 3 and supported by Macneily and Graham. 11 These authors advocate a direct surgical approach to the problem, aiming to correct the coagulopathy by aneurysm repair. A large intra-operative blood loss is anticipated, and a high speed autotransfuser should be available in addition to adequate amounts of platelets, fresh frozen plasma, and cryoprecipitate. Meticulous surgical technique is essential at all stages, and minim u m aneurysm dissection, the use of a woven graft, and wrapping the old aneurysm sac around the graft are all suggested as ways to minimise blood loss. The coagulopathy associated with ruptured aneurysm is an acute one, precipitated by shock, consumption of coagulation factors and tissue trauma. The emphasis on management is on replacement of clotting factors and platelets, and restoration of circulating blood volume. Early diagnosis and prompt surgery are essential to limit mortality. 4°'41"43 Lambert and associates 44 found that administration of fresh frozen plasma preoperatively in ruptured aneurysm significantly increased survival. Woven Dacron grafts are preferred to knitted grafts in ruptured aneurysms because they are less porous.
Coagulopathy and Abdominal Aortic Aneurysm
Conclusion
Disseminated intravascular coagulation rarely results primarily from an intact AAA, and its finding in association with AAA should prompt a careful search for contributory causes, particularly occult neoplasia or liver disease. Similarly, DIC following elective aneurysm repair is an unusual event and additional factors are usually at play if it occurs. Isolated abnormalities of coagulation function tests are not however unusual. Coagulopathy, including DIC, are not all uncommon after ruptured AAA, and often play a leading role in postoperative morbidity and mortality from this condition. A more widespread recognition of its occurrence and appropriate aggressive management might therefore lead to a reduction in the risk of mortality from ruptured aneurysm.
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Accepted 15 February 1990