FATALHIY FROM DISSEMINATED INTRAVASCULAR COAGUIATIONCOMPLICATING TOTAL HIP ARTHROPIASTY:

A CASE REPORT

Scott M. Sporer, B.S.John J. Callaghan, M.D.

ABSTRACrFollowing a routine hybrid total hip arthroplasty

in an eighty-two year-old female, profuse bleedingoccurred through the suction drain immediatelypostoperatively. The patient was found to haveacute disseminated intravascular coagulation.Despite early recognition and treatment the pa-tient died fourteen days later.

Disseminated intravascular coagulation (DIC) can bea fatal disorder with mortality rates approaching 80percent in severe disease'. DIC has been reported tooccur as a result of numerous diverse etiologies, buthas rarely been reported as a complication of total hiparthroplasty. The following is a case of a healthy, eld-erly woman who underwent elective total hip arthro-plasty and developed DIC postoperatively and subse-quently died.

Case ReportAn eighty-two year-old white female underwent elec-

tive right total hip arthroplasty for increasing pain sec-ondary to degenerative arthritis which was refractoryto conservative treatment. She also had radiographicevidence of degenerative changes in her knees and herspine. Her past medical history was remarkable for con-trolled hypertension, mildly elevated liver enzymes,hematuria with a negative urological work-up, vasova-gal syncope, gout and a previous left knee Baker's cyst.She denied a history of cardiovascular, pulmonary orbleeding disorders, and at the time of surgery was with-out complaints other than right hip pain. Her medica-tions included: Monopril 20 mg daily, enteric coatedaspirin 80 mg daily, colchicine 0.6 mg daily, Motrin 400mg daily, vitamin D 600 mg twice daily, vitamin C 500mg daily, and a multivitamin. The patient had been un-der general anesthesia in the past without complications

Reprints to: John J. Callaghan, M.D., University of Iowa, Departmentof Orthopaedics, Iowa City, Iowa 52242-1088

for an appendectomy and a tonsillectomy/adenoidec-tomy. She had no known drug allergies.

Laboratory studies at the time of admission revealeda hemoglobin level of 12.7 g/dl, a prothrombin time(PT) of 11.0 seconds, a partial thromboplastin time(PIT) of 25.0 seconds, and a platelet count of 138,000/mm3. Her general screen was remarkable for an in-creased alkaline phosphatase of 156, lactate dehydro-genase of 239 and AST of forty. The remainder of herpresurgical blood work was within normal limits.The patient was anesthetized under general anesthe-

sia and was monitored intraoperatively via ECG moni-toring, indirect blood pressure monitoring, pulse oxim-etry, and serial arterial blood gas measurements. Herintraoperative course was relatively stable with- the ex-ception of several episodes of hypotension to 90/50mmHg which responded adequately to fluids (one unitpacked red blood cells, 500 cc colloid and 500 cc Lac-tated Ringers) and two 100 mg boluses of phenyleph-rine. A hybrid total hip replacement was performed, andthe patient was taken postoperatively to the Post Anes-thesia Critical Care Unit (PACCU) with a hematocrit of28 pecent and an arterial blood gas of 7.43/35/149/0/24. Operative time was 105 minutes and blood loss wasestimated at 600 cc. No anticoagulant therapy was ad-ministered intraoperatively other than pneumatic com-pressive stockings.

Upon arrival to the PACCU, her blood pressure re-mained stable for a few minutes before suddenly drop-ping to 80/60 mmHg. A normal blood pressure wasrestored with fluids (two units of packed red blood cellsand 1000 cc of Lactated Ringers), two doses of phenyl-ephrine (100 mg) and two doses of ephedrine (five mg).The patient remained stable for approximately forty-fiveminutes. A chest x-ray was unremarkable, an ECGshowed no acute changes, and an arterial blood gasrevealed 7.40/26/167/-2/23. Her ConstavacR drain wasnoted to have significant (700 cc) sanguinous outputover the forty-five minutes, urine output was minimal,and her platelets had fallen to 116,000/mm3. Suction tothe ConstavacR drain was stopped to avoid further bloodloss. The presumptive diagnosis was DIC; there was nosuspicion of trauma to a major vessel during the sur-gery. A right subclavian line was placed which revealed

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S. M. Sporer, J. J. Callaghan

Figure 1. Incision site at the time ofhematoma evacuation, post-operative day three. Note the edema and hemorrhagic blistering of the skinover the incision site due to the acute accumulation of blood and expansion of the thigh circumference.

a central venous pressure of negative four centimetersof water. A dopamine drip was started but was quicklydiscontinued due to severe tachycardia. A phenyleph-rine drip was then begun at 125 gcg/hr to maintain asystolic blood pressure greater than 90 mmHg.The patient was transferred to the Surgical Intensive

Care Unit (SICU) three hours postoperatively with sys-tolic blood pressures in the sixties and seventies. Shehad received seven units of packed red blood cells andfour units of fresh frozen plasma (FFP)to replace her2375 cc ConstavacR drain output. Overnight she devel-oped worsening metabolic acidosis with a blood gas of7.12/48/207/-12, and her PIT and fibrin degradationproducts (FDP) remained elevated at sixty-eight sec-onds and greater than eighty mg/dl respectively. Alongwith a decreased fibrinogen level of 121 mg/dl (normal160-340 mg/dl), her hematocrit dropped to 24 percentand her platelets to 33,000/mm3. Heparinization was be-gun at that time. She continued to require phenyleph-rine to maintain a blood pressure of 90/60 mm Hg, and

repeated attempts to start a dopamine infusion for re-nal protection continued to produce excessive tachycar-dia and atrial fibrillation. Due to the patient's worsen-ing acid-base balance and to protect her airway, she wasre-intubated with an oral endotracheal tube. The patientwas noted to have a sciatic nerve palsy, most likely fromthe massive hematoma.

Over the course of the next three days, the patientrequired nineteen units of packed red blood cells,twenty units of FFP and five packs of platelets in orderto maintain a hematocrit greater than 30 percent, PTless than fifteen seconds, and platelets greater than75,000/mm3. She continued to have significant outputin her drains, and ooze from her central and peripheralintravenous line insertion sites. Her renal function re-mained poor with a urine output of twenty cc/hr underforced diuresis with Lasix, and her BUN and creatinewere elevated at twenty-one and 2.1 secondary to myo-globinuria induced acute renal failure. The patient's ASTand ALT were also elevated at 3326 and 1527 respec-

54 The Iowa Orthopaedtc Journal

Fatalityfrom Disseminated Intravascular Coagulation Complicating Total Hip Arthroplasty: A Case Report

TABLE 1Coagulation Studies and Factor Levels in the Immediate Postoperative Period

Normal Preop Immed. Postop 3 Hrs. Postop 5 Hrs. Postop 24 Hrs. PostopHct (%) 35-40 36 28 24 16 23

Platelets (K/mm3) 151-400 138 116 33 120 73

PT (sec.) 9-13 11 15 16 15 14FIT (sec.) 22-37 25 - 77 63 39

FDP (gg/ml) 0-9 - - >80 >80 >80

D-Dimer (pcg/ml) 0-0.1 | - - - 4.0

tively, and were believed to be due to "shock liver" fromthe prior episodes of hypotension. Her diminished re-nal function, excessive fluid from transfusion, and poornutritional status presented clinically as anasarca whichwas treated with continuous veno-venous hemofiltration,central venous nutrition and nasogastric tube placement.On postoperative day three, she was taken back to

the operating room for evacuation of the wound he-matoma which had caused the sciatic nerve palsy (Fig-ure 1). The procedure was without complications. Ap-proximately eight liters of consolidated hematoma wereevacuated, and her bleeding was adequately controlled.However, upon return to the SICU her blood pressurewas 90/50 mmHg. A 500 cc bolus of Plasmanate pre-cipitated a sudden drop in blood pressure to 53/31mmHg. A normal blood pressure was restored with 500mg boluses of phenylephrine, and the patient wasstarted on a Levophed drip. Throughout the day, sherequired six units of FFP, one pack of platelets and fourunits of packed red blood cells every eight hours inorder to maintain adequate hematologic parameters.(Table 1 illustrates the first twenty-four hour coagula-tion studies.)

By the sixth postoperative day, her PIT had im-proved to forty-five seconds, PT to thirteen seconds andfibrinogen level to 382 mg/dl. There was no evidenceof clinically significant bleeding, and the patient did notrequire further blood transfusions. However, she hadbecome markedly obtunded, icteric, anuric and re-mained ventilator and vasopressor dependent. Seriallabs showed increasing direct and indirect bilirubin, PT,PIT and ammonia levels which suggested that she wasdeveloping worsening hepatic function. Despite aggres-sive therapy, care was withdrawn on postoperative dayfourteen at the request of the family, and the patientdied. A postmortem examination was not performed.

DISCUSSIONDeep venous thrombosis and subsequent pulmonary

embolism is the most common cause of death in theimmediate postoperative period following total hip re-placement. Deep vein thrombosis has been reported inup to 70 percent of patients in the absence of anti-coagulation therapy2. The hypercoagulable state and in-creased circulating tissue thromboplastins followingroutine total hip arthroplasty contribute to this occur-rence. Although the exact etiology of DIC remains un-known, it is believed that the release of tissue throm-boplastins into the systemic circulation or diffuseendothelial damage is the common triggering factor asdemonstrated in Figure 23. However, an autoimmunereaction to the acrylic bone cement has also been hy-pothesized4. The inciting event of this patient's courseof DIC can only be postulated. In retrospect, it was sus-pected that intermittent intraoperative hypotensive epi-sodes combined with the release of tissue thromboplas-tin during the total hip replacement procedure (i.e.femoral and acetabular reaming) and preexisting mildhepatic dysfunction triggered this event. Her progres-sive hepatic and renal insufficiency were undoubtedlydue to microthrombus-induced, end-organ ischemia.The diagnosis of DIC can usually be made from the

patient's systemic signs and symptoms as well as theirabnormal laboratory profile. These patients often havefever, hypotension, acidosis, proteinuria, hypoxia, pete-chia and purpura, and are bleeding from at least threeunrelated sites. Due to systemic microvascular throm-bosis, the cardiovascular, pulmonary, renal and centralnervous systems are especially prone to ischemic epi-sodes with their resulting sequelae5. While the PT, PIT,fibrinogen and FDP levels have traditionally been fol-lowed, it is currently recommended that the D-dimer,Antithrombin III (AT-Ill), Fibrinopeptide A and FDPlevels be monitored in order to maximize diagnostic re-liability6. The D-dimer is specific for fibrin degradation,whereas the FDP is derived from either fibrin or fibrino-

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S. M. Sporer, J. J. Callaghan

Release of tissuethromboplasti ns

Endothelial cell injury*4Ci ntravascular coagulation

Microthrombi(fi bri n) -

Plasmin

proteol !Ji3 Ofcoagulation factors

Fi bri n... degradation

products

Consumption ofclotti ng factors

Vascular Occl usion

Ischemic tissue damageand microangiopathichemolytic anemia

Inhibition of thrombin,platelet aggregation, op Bleedi ngand i mpai red fi bri npol ymerization

Figure 2. The mechanism of the thrombohemorrhagic state in Disseminated Intravascular Coagulation.

gen. The AT-III concentration will be reduced due tothe complexing of activated clotting factors with circu-lating AT-III, while the Fibrinopeptide A level will beincreased due to its liberation during fibrinogen forma-tion7.

Although therapeutic options for DIC remain contro-versial, treatment should initially be targeted at theunderlying etiology. If severe hemorrhagic or throm-botic phenomena occur, therapeutic heparin anticoagu-lation followed by aggressive replacement of specificcoagulation factors is indicated. Adequate anticoagula-tion is crucial since it is the thrombosis of small ves-sels that has the largest impact on morbidity and mor-tality. Although clinically alarming, the hemorrhagiceffects can generally be controlled7.

DIC is rarely encountered by the orthopedic surgeonperforming total hip arthroplasty, but it is a potentiallylife threatening complication which needs to be diag-nosed early in order to maximize patient outcome. Two

cases of DIC were described in patients undergoing hiparthroplasty for metastatic carcinoma of the proximalfemur. Pugh described a patient who developed DICfollowing bilateral cemented total hip arthroplasties. Afourth case of DIC after arthroplasty was documentedin a healthy patient who had a previous uncomplicatedjoint replacement of the opposite hip8 9. If aggressivetherapy is promptly instituted, small vessel thrombosiscan be prevented and the thrombohemorrhagic statereversed. However, in this case the patient was unableto be resuscitated.

If a patient presents in the early postoperative pe-riod following total hip replacement with excessivebleeding, the diagnosis of DIC in addition to the morecommon occurrence of major vessel damage should beconsidered. Appropriate lab tests should be obtained(D-dimer, Antithrombin III (AT-III), Fibrinopeptide Aand Fibrin degradation product) and early therapeuticand resuscitative efforts should be instituted. Although

56 The Iowa Orthopaedic Journal

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Fatalityfrom Disseminated Intravascular Coagulation Complicating Total Hip Arthroplasty: A Case Report

the condition is usually reversible, this case demon-strates the potential mortality from DIC following totalhip replacement in spite of early diagnosis and appro-priate treatment.

REFERENCES1. Mant, M., and King, E.: Severe, acute disseminated

intravascular coagulation: A reappraisal of its patho-physiology, clinical significance and therapy basedon 47 patients. Am. J. Med., 1979. 67:557.

2. Swayze, 0.; Nasse, S.; and Roberson, J.: Deepvenous thrombosis in total hip arthroplasty. Orthop.Clin. North Am., 1992. 23:359-364.

3. Preston, F. E.: Disseminated intravascular coagu-lation. Br Hosp. Medicine, 1982. 28(2):129-137.

4. Ling, R. S. M.: Systemic and miscellaneous com-plications. In: Complications of Total Hip Replace-ment. Edited by R. S. M. Ling. 1984. ChurchillLivingstone, New York. 204-205.

5. Muller-Berghous, G.: Pathophysiology of gener-alized intravascular coagulation. Seminars Thromb.Hemost., 1977. 3:209.

6. Feinstein, D. I.: Treatment of disseminated intra-vascular coagulation. Seminars Thromb. Hemost.,1988. 14:351.

7. Bick, R. L: Disseminated intravascular coagula-tion and related syndromes: A clinical review. Semi-nars Thromb. Hemost., 1988. 14:299.

8. Unger, A. S., and Booth, R. E.: Disseminatedintravascular coagulopathy in a patient undergoingtotal hip arthroplasty for carcinoma. Clin. Orthop.,1984. 183:76-78.

9. Pugh, S. C.: Disseminated intravascular coagulationcomplicating bilateral cemented total hip arthroplasty.Anaes. and Inten. Care, 1991. 19:106-108.

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