A 82-year-old woman underwent a total hip arthroplasty and developed acute disseminated intravascular coagulation postoperatively. She experienced profuse bleeding through her surgical drain and had a precipitous drop in blood pressure. Despite aggressive treatment including blood transfusions, coagulation factor replacements, and hemodynamic support, her condition deteriorated over the next two weeks with multi-organ dysfunction. She ultimately died from her disseminated intravascular coagulation 14 days after her surgery. Disseminated intravascular coagulation is a life-threatening condition with high mortality that can rarely complicate total hip arthroplasty as seen in this case.

1. FATALHIY FROM DISSEMINATED INTRAVASCULAR COAGUIATION
COMPLICATING TOTAL HIP ARTHROPIASTY:
A CASE REPORT
Scott M. Sporer, B.S.
John J. Callaghan, M.D.
ABSTRACr for an appendectomy and a tonsillectomy/adenoidec-
Following a routine hybrid total hip arthroplasty tomy. She had no known drug allergies.
in an eighty-two year-old female, profuse bleeding Laboratory studies at the time of admission revealed
occurred through the suction drain immediately a hemoglobin level of 12.7 g/dl, a prothrombin time
postoperatively. The patient was found to have (PT) of 11.0 seconds, a partial thromboplastin time
acute disseminated intravascular coagulation. (PIT) of 25.0 seconds, and a platelet count of 138,000
Despite early recognition and treatment the pa- /mm3. Her general screen was remarkable for an in-
tient died fourteen days later. creased alkaline phosphatase of 156, lactate dehydro-
genase of 239 and AST of forty. The remainder of her
Disseminated intravascular coagulation (DIC) can be presurgical blood work was within normal limits.
a fatal disorder with mortality rates approaching 80 The patient was anesthetized under general anesthe-
percent in severe disease'. DIC has been reported to sia and was monitored intraoperatively via ECG moni-
occur as a result of numerous diverse etiologies, but toring, indirect blood pressure monitoring, pulse oxim-
has rarely been reported as a complication of total hip etry, and serial arterial blood gas measurements. Her
arthroplasty. The following is a case of a healthy, eld- intraoperative course was relatively stable with- the ex-
erly woman who underwent elective total hip arthro- ception of several episodes of hypotension to 90/50
plasty and developed DIC postoperatively and subse- mmHg which responded adequately to fluids (one unit
quently died. packed red blood cells, 500 cc colloid and 500 cc Lac-
tated Ringers) and two 100 mg boluses of phenyleph-
Case Report rine. A hybrid total hip replacement was performed, and
An eighty-two year-old white female underwent elec- the patient was taken postoperatively to the Post Anes-
tive right total hip arthroplasty for increasing pain sec- thesia Critical Care Unit (PACCU) with a hematocrit of
ondary to degenerative arthritis which was refractory 28 pecent and an arterial blood gas of 7.43/35/149/0/
to conservative treatment. She also had radiographic 24. Operative time was 105 minutes and blood loss was
evidence of degenerative changes in her knees and her estimated at 600 cc. No anticoagulant therapy was ad-
spine. Her past medical history was remarkable for con- ministered intraoperatively other than pneumatic com-
trolled hypertension, mildly elevated liver enzymes, pressive stockings.
hematuria with a negative urological work-up, vasova- Upon arrival to the PACCU, her blood pressure re-
gal syncope, gout and a previous left knee Baker's cyst. mained stable for a few minutes before suddenly drop-
She denied a history of cardiovascular, pulmonary or ping to 80/60 mmHg. A normal blood pressure was
bleeding disorders, and at the time of surgery was with- restored with fluids (two units of packed red blood cells
out complaints other than right hip pain. Her medica- and 1000 cc of Lactated Ringers), two doses of phenyl-
tions included: Monopril 20 mg daily, enteric coated ephrine (100 mg) and two doses of ephedrine (five mg).
aspirin 80 mg daily, colchicine 0.6 mg daily, Motrin 400 The patient remained stable for approximately forty-five
mg daily, vitamin D 600 mg twice daily, vitamin C 500 minutes. A chest x-ray was unremarkable, an ECG
mg daily, and a multivitamin. The patient had been un- showed no acute changes, and an arterial blood gas
der general anesthesia in the past without complications revealed 7.40/26/167/-2/23. Her ConstavacR drain was
noted to have significant (700 cc) sanguinous output
over the forty-five minutes, urine output was minimal,
and her platelets had fallen to 116,000/mm3. Suction to
the ConstavacR drain was stopped to avoid further blood
loss. The presumptive diagnosis was DIC; there was no
Reprints to: John J. Callaghan, M.D., University of Iowa, Department suspicion of trauma to a major vessel during the sur-
of Orthopaedics, Iowa City, Iowa 52242-1088 gery. A right subclavian line was placed which revealed
Volume 17 53

2. S. M. Sporer, J. J. Callaghan
Figure 1. Incision site at the time of hematoma evacuation, post-operative day three. Note the edema and hemorrhagic blistering of the skin
over the incision site due to the acute accumulation of blood and expansion of the thigh circumference.
a central venous pressure of negative four centimeters repeated attempts to start a dopamine infusion for re-
of water. A dopamine drip was started but was quickly nal protection continued to produce excessive tachycar-
discontinued due to severe tachycardia. A phenyleph- dia and atrial fibrillation. Due to the patient's worsen-
rine drip was then begun at 125 gcg/hr to maintain a ing acid-base balance and to protect her airway, she was
systolic blood pressure greater than 90 mmHg. re-intubated with an oral endotracheal tube. The patient
The patient was transferred to the Surgical Intensive was noted to have a sciatic nerve palsy, most likely from
Care Unit (SICU) three hours postoperatively with sys- the massive hematoma.
tolic blood pressures in the sixties and seventies. She Over the course of the next three days, the patient
had received seven units of packed red blood cells and required nineteen units of packed red blood cells,
four units of fresh frozen plasma (FFP)to replace her twenty units of FFP and five packs of platelets in order
2375 cc ConstavacR drain output. Overnight she devel- to maintain a hematocrit greater than 30 percent, PT
oped worsening metabolic acidosis with a blood gas of less than fifteen seconds, and platelets greater than
7.12/48/207/-12, and her PIT and fibrin degradation 75,000/mm3. She continued to have significant output
products (FDP) remained elevated at sixty-eight sec- in her drains, and ooze from her central and peripheral
onds and greater than eighty mg/dl respectively. Along intravenous line insertion sites. Her renal function re-
with a decreased fibrinogen level of 121 mg/dl (normal mained poor with a urine output of twenty cc/hr under
160-340 mg/dl), her hematocrit dropped to 24 percent forced diuresis with Lasix, and her BUN and creatine
and her platelets to 33,000/mm3. Heparinization was be- were elevated at twenty-one and 2.1 secondary to myo-
gun at that time. She continued to require phenyleph- globinuria induced acute renal failure. The patient's AST
rine to maintain a blood pressure of 90/60 mm Hg, and and ALT were also elevated at 3326 and 1527 respec-
54 The Iowa Orthopaedtc Journal

3. Fatality from Disseminated Intravascular Coagulation Complicating Total Hip Arthroplasty: A Case Report
TABLE 1
Coagulation Studies and Factor Levels in the Immediate Postoperative Period
Normal Preop Immed. Postop 3 Hrs. Postop 5 Hrs. Postop 24 Hrs. Postop
Hct (%) 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 14
FIT (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" from DISCUSSION
the prior episodes of hypotension. Her diminished re- Deep venous thrombosis and subsequent pulmonary
nal function, excessive fluid from transfusion, and poor embolism is the most common cause of death in the
nutritional status presented clinically as anasarca which immediate postoperative period following total hip re-
was treated with continuous veno-venous hemofiltration, placement. Deep vein thrombosis has been reported in
central venous nutrition and nasogastric tube placement. up to 70 percent of patients in the absence of anti-
On postoperative day three, she was taken back to coagulation therapy2. The hypercoagulable state and in-
the operating room for evacuation of the wound he- creased circulating tissue thromboplastins following
matoma which had caused the sciatic nerve palsy (Fig- routine total hip arthroplasty contribute to this occur-
ure 1). The procedure was without complications. Ap- rence. Although the exact etiology of DIC remains un-
proximately eight liters of consolidated hematoma were known, it is believed that the release of tissue throm-
evacuated, and her bleeding was adequately controlled. boplastins into the systemic circulation or diffuse
However, upon return to the SICU her blood pressure endothelial damage is the common triggering factor as
was 90/50 mmHg. A 500 cc bolus of Plasmanate pre- demonstrated in Figure 23. However, an autoimmune
cipitated a sudden drop in blood pressure to 53/31 reaction to the acrylic bone cement has also been hy-
mmHg. A normal blood pressure was restored with 500 pothesized4. The inciting event of this patient's course
mg boluses of phenylephrine, and the patient was of DIC can only be postulated. In retrospect, it was sus-
started on a Levophed drip. Throughout the day, she pected that intermittent intraoperative hypotensive epi-
required six units of FFP, one pack of platelets and four sodes combined with the release of tissue thromboplas-
units of packed red blood cells every eight hours in tin during the total hip replacement procedure (i.e.
order to maintain adequate hematologic parameters. femoral and acetabular reaming) and preexisting mild
(Table 1 illustrates the first twenty-four hour coagula- hepatic dysfunction triggered this event. Her progres-
tion studies.) sive hepatic and renal insufficiency were undoubtedly
By the sixth postoperative day, her PIT had im- due to microthrombus-induced, end-organ ischemia.
proved to forty-five seconds, PT to thirteen seconds and The diagnosis of DIC can usually be made from the
fibrinogen level to 382 mg/dl. There was no evidence patient's systemic signs and symptoms as well as their
of clinically significant bleeding, and the patient did not abnormal laboratory profile. These patients often have
require further blood transfusions. However, she had fever, hypotension, acidosis, proteinuria, hypoxia, pete-
become markedly obtunded, icteric, anuric and re- chia and purpura, and are bleeding from at least three
mained ventilator and vasopressor dependent. Serial unrelated sites. Due to systemic microvascular throm-
labs showed increasing direct and indirect bilirubin, PT, bosis, the cardiovascular, pulmonary, renal and central
PIT and ammonia levels which suggested that she was nervous systems are especially prone to ischemic epi-
developing worsening hepatic function. Despite aggres- sodes with their resulting sequelae5. While the PT, PIT,
sive therapy, care was withdrawn on postoperative day fibrinogen and FDP levels have traditionally been fol-
fourteen at the request of the family, and the patient lowed, it is currently recommended that the D-dimer,
died. A postmortem examination was not performed. Antithrombin III (AT-Ill), Fibrinopeptide A and FDP
levels 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-
Volume 17 55

4. S. M. Sporer, J. J. Callaghan
Release of tissue
thromboplasti ns
*4C Endothelial cell injury
i ntravascular coagulation
proteol !Ji3 Of ",,-IL
coagulation factors
Consumption of
clotti ng factors
Microthrombi Fi bri n
Plasmin degradation
(fi bri n) - ...
products
r
I Vascular Occl usion
Ischemic tissue damage Inhibition of thrombin,
and microangiopathic platelet aggregation, op Bleedi ng
hemolytic anemia and i mpai red fi bri n
pol ymerization
Figure 2. The mechanism of the thrombohemorrhagic state in Disseminated Intravascular Coagulation.
gen. The AT-III concentration will be reduced due to cases of DIC were described in patients undergoing hip
the complexing of activated clotting factors with circu- arthroplasty for metastatic carcinoma of the proximal
lating AT-III, while the Fibrinopeptide A level will be femur. Pugh described a patient who developed DIC
increased due to its liberation during fibrinogen forma- following bilateral cemented total hip arthroplasties. A
tion7. fourth case of DIC after arthroplasty was documented
Although therapeutic options for DIC remain contro- in a healthy patient who had a previous uncomplicated
versial, treatment should initially be targeted at the joint replacement of the opposite hip8 9. If aggressive
underlying etiology. If severe hemorrhagic or throm- therapy is promptly instituted, small vessel thrombosis
botic phenomena occur, therapeutic heparin anticoagu- can be prevented and the thrombohemorrhagic state
lation followed by aggressive replacement of specific reversed. However, in this case the patient was unable
coagulation factors is indicated. Adequate anticoagula- to be resuscitated.
tion is crucial since it is the thrombosis of small ves- If a patient presents in the early postoperative pe-
sels that has the largest impact on morbidity and mor- riod following total hip replacement with excessive
tality. Although clinically alarming, the hemorrhagic bleeding, the diagnosis of DIC in addition to the more
effects can generally be controlled7. common occurrence of major vessel damage should be
DIC is rarely encountered by the orthopedic surgeon considered. Appropriate lab tests should be obtained
performing total hip arthroplasty, but it is a potentially (D-dimer, Antithrombin III (AT-III), Fibrinopeptide A
life threatening complication which needs to be diag- and Fibrin degradation product) and early therapeutic
nosed early in order to maximize patient outcome. Two and resuscitative efforts should be instituted. Although
56 The Iowa Orthopaedic Journal

5. Fatalityfrom Disseminated Intravascular Coagulation Complicating Total Hip Arthroplasty: A Case Report
the condition is usually reversible, this case demon- 5. Muller-Berghous, G.: Pathophysiology of gener-
strates the potential mortality from DIC following total alized intravascular coagulation. Seminars Thromb.
hip replacement in spite of early diagnosis and appro- Hemost., 1977. 3:209.
priate treatment. 6. Feinstein, D. I.: Treatment of disseminated intra-
vascular coagulation. Seminars Thromb. Hemost.,
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1. Mant, M., and King, E.: Severe, acute disseminated 7. Bick, R. L: Disseminated intravascular coagula-
intravascular coagulation: A reappraisal of its patho- tion and related syndromes: A clinical review. Semi-
physiology, clinical significance and therapy based nars Thromb. Hemost., 1988. 14:299.
on 47 patients. Am. J. Med., 1979. 67:557. 8. Unger, A. S., and Booth, R. E.: Disseminated
2. Swayze, 0.; Nasse, S.; and Roberson, J.: Deep intravascular coagulopathy in a patient undergoing
venous thrombosis in total hip arthroplasty. Orthop. total hip arthroplasty for carcinoma. Clin. Orthop.,
Clin. North Am., 1992. 23:359-364. 1984. 183:76-78.
3. Preston, F. E.: Disseminated intravascular coagu- 9. Pugh, S. C.: Disseminated intravascular coagulation
lation. Br Hosp. Medicine, 1982. 28(2):129-137. complicating bilateral cemented total hip arthroplasty.
4. Ling, R. S. M.: Systemic and miscellaneous com- Anaes. and Inten. Care, 1991. 19:106-108.
plications. In: Complications of Total Hip Replace-
ment. Edited by R. S. M. Ling. 1984. Churchill
Livingstone, New York. 204-205.
Volume 17 57