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Cerebral Embolization Presenting as Delayed, Severe Obtundation in the Postanesthesia Care Unit After Total Hip Arthroplasty
Cerebral Embolization Presenting as Delayed, Severe Obtundation in the Postanesthesia Care Unit After Total Hip Arthroplasty MICHAEL C.
OTT, MD; JAMES F. MESCHIA, MD;
DAVID
C.
MACKEY, MD; MARK
CHARLES BURGER, MD; J. DAN ECHOLS, MD; AND DOUGLAS
status after pelvic or long bone fracture or lower extremity major joint replacement, and this condition may occur despite normal pulmonary function and no patent foramen ovale or right-to-Ieft intracardiac shunt. Magnetic resonance imaging with T 2-weighted sequences is the cranial imaging study of choice for early evaluation of patients with sudden multifocal neurologic deficits and suspected fat embolism syndrome. Mayo Clin Proc. 2000;75:1209-1213
Catastrophic neurologic events occur rarely postoperatively and must be diagnosed quickly. A 63-year-old woman who had undergone uneventful total hip arthroplasty experienced obtundation after admission to the postanesthesia care unit. Cranial magnetic resonance imaging revealed multiple lesions consistent with ischemia or infarction, and fat cerebral embolism was diagnosed. We describe the numerous complications that may occur in patients in the postanesthesia care unit and review the differential diagnosis of altered mental status in such patients. Paradoxical cerebral fat embolization must be considered in the differential diagnosis of altered mental
CT = computed tomography; MRI = magnetic resouance imaging; PACU =postanesthesia care unit
A
preoperative laboratory investigation revealed normal findings on electrocardiography and chest radiography, as well as normal serum electrolytes. The preoperative hemoglobin concentration was 11.0 g/dL after she was given 2 U of autologous blood. Spinal anesthesia was established with hyperbaric bupivacaine, 12mg, epinephrine, 0.2 mg, and preservativefree morphine, 0.25 mg. General endotracheal anesthesia was induced with propofol, 140 mg, and maintained with isoflurane (0.6%-1.2%) and nitrous oxide-oxygen (0%66%). Continuous intraoperative monitoring included electrocardiography, pulse oximetry, capnography, oscillometric blood pressure determinations, and esophageal temperature. The cardiac rhythm remained in normal sinus, and the oxygen saturation was 100% throughout the intraoperative anesthetic course. The systolic blood pressure ranged from 90 to 120 mm Hg, the mean blood pressure ranged from 60 to 80 mm Hg, and the heart rate ranged from 52 to 72 beats/min. Crystalloid, 1300 mL, was administered, and the estimated blood loss was 300 mL during the operative procedure, which lasted 1 hour and 27 minutes. While awake, the patient was taken to the PACU and extubated; she responded appropriately to verbal stimuli. Throughout the PACU stay, her blood pressure, monitored at 5-minute intervals, and findings on continuous electrocardiography remained normal; the oxygen saturation by pulse oximetry ranged from 96% to 100%. She complained of nausea and was given intravenous ondansetron, 4.0 mg on 2 occasions. The patient was noted to be lethargic 2 112 hours after PACU admission, and over the following 50 minutes, obtundation progressed to the point that reintu-
dverse events occur commonly in the postanesthesia care unit (PACU), with a complication rate that may exceed 23% to 30%.1-3 Pain (16%) and nausea-vomiting (8%) are the most common complications. Altered mental status is seen in 3% to 9% of cases (Table 1).2.4 Delayed emergence and emergence delirium secondary to anesthetic and analgesic medication administered preoperatively and intraoperatively are the principal causes of postoperative mental status changes, but the differential diagnosis is broad (Table 2). We describe a patient who underwent total hip arthroplasty and experienced obtundation after admission to the PACU. Cerebral fat embolization was detected subsequently. REPORT OF A CASE
A 63-year-old woman who weighed 65 kg and had a history of hypertension controlled with amlodipine-benazepril, idiopathic hypothyroidism treated with levothyroxine, and seasonal asthma underwent total hip arthroplasty for degenerative osteoarthritis; a combination of spinal and general anesthesia was used. A preoperative medical evaluation disclosed no evidence of coronary artery or neurologic disease. Her preoperative blood pressure was 110/70 mm Hg. The From the Division of Pulmonary Medicine (M.C.O.• C.B.), Department of Neurology (J.F.M.), Department of Anesthesiology (D.C.M.), Department of Orthopedic Surgery (M.P.B.), Division of Community Internal Medicine (J.D.E.), and Department of Diagnostic Radiology (D.S.F.), Mayo Clinic, Jacksonville, Fla. Address reprint requests and correspondence to James F. Meschia, MD, Department of Neurology, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224-1865 (e-mail: [email protected]).
Mayo Clin Proc. 2000;75: 1209-1213
P. BRODERSEN, MD;
S. FENTON, MD
1209
© 2000 Mayo Foundation for Medical Education and Research
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
1210
Cerebral Embolization After Total Hip Arthroplasty
Table I. Complications in the Postanesthesia Care Unit* Complication
Rate (%)t
Pain Nauseaand vomiting Alteredmentalstatus Hypoxemia or hypercapnia Hypotension Cardiacdysrhythmias Upperairwayobstruction Hypertension Oliguria Major cardiacevent Hypothermia Hyperglycemia
16 8 7 7
6 4 4 2 I
<1
*Datafrom Hineset al,' Zelcer and Wells,' and de Melloet al.' tUnweighted averages. bation was required for airway protection. Before reintubation, arterial blood gas determinations obtained while the patient was receiving supplemental oxygen via an updraft face tent at 10 L/min revealed a pH of 7.35, Pco, of 39 mm Hg, POz of91 mm Hg, and oxygen saturation of 96%. The patient exhibited spontaneous eye opening but did not follow commands. Pupillary light and corneal reflexes were preserved, but a left lower facial droop, leftward gaze preference, and minimal withdrawal from painful stimulus were noted. The patient exhibited diffuse hyporeflexia and bilateral extensor plantar reflexes. No skin, conjunctival, or funduscopic abnormalities were found. Intravenous administration of 100 ug of naloxone resulted in no clinical improvement. Electrocardiographic findings, serum electrolytes, and glucose level were normal. Chest radiography showed prominent bilateral interstitial markings. ElectroTable 2. Differential Diagnosis of Altered Mental Status in the Postanesthesia Care Unit Residual or prolongedanesthetic effect or overdose (including vapor agents, sedative-hypnotic agents, barbiturates, opioids, musclerelaxants) Hypoxemia and/orhypercarbia Hypotension Fluid and electrolyte imbalance (including hyperosmolar syndrome, waterintoxication) Metabolic encephalopathy (hepatic, renal,endocrine) Hypothermia or hyperthermia Intraoperative complication (air or particulate embolism, cerebral ischemia, intracranial hemorrhage, hypoxic encephalopathy, hypotension) Preexisting alteredmental status Emergence delirium Interaction with preoperative medications or illicit drugs Alcoholand drug withdrawal Atypical or allergicmedication reaction Seizure(statusepilepticus or postictal state)
Mayo Clin Proc, November 2000, Vol7S
encephalography showed diffuse slowing but no ictal discharges. Findings on cranial computed tomography (CT) without contrast were normal, as were those on cerebral digital subtraction arteriography performed 5 hours after onset of symptoms. Cranial magnetic resonance imaging (MRI) with Tz-weighted sequences performed the following morning revealed multiple cortical and subcortical lesions in both cerebral and cerebellar hemispheres, highly suggestive of an embolic event (Figure 1), and probable cerebral fat embolism was diagnosed. Transesophageal echocardiography with a contrast agent disclosed no patent foramen ovale, intrapulmonary shunting, or cardiac abnormality. Subsequent electroencephalography revealed diffuse slowing, and MRI performed 12 days postoperatively revealed resolution of many of the brain lesions (Figure 2). The patient gradually regained consciousness and her ability to communicate, and she was transferred to a rehabilitation facility 19 days after her initial hospital admission. DISCUSSION Differential Diagnosis of Altered Mental Status Delayed emergence from general anesthesia due to the residual effects of oral, intravenous, and inhalational sedative, analgesic, and anesthetic medications is a frequent cause of mental status alteration found in patients in the PACU. This situation may be complicated by preexisting mental dysfunction, postoperative hypothermia, or unrecognized preoperative ingestion of alcohol, opioids, benzodiazepines, and other prescription and illicit drugs that potentiate the effects of anesthesia-related medications (Table 2). Emergence delirium, a behavioral manifestation of recovery from general anesthesia ranging from mild confusion and lethargy to extreme excitement and combativeness, is the second most common mental status abnormality found in patients in the PACU. Return of cognitive function after general anesthesia may be slower in the elderly population in the immediate postoperative period, whereas agitation and combativeness are more frequently observed in children and young adults.' Emergence delirium may also be produced by perioperative administration of ketamine or an anticholinergic medication such as scopalomine or atropine and by postoperative withdrawal from alcohol or illicit drugs. Moreover, it may be seen preoperatively in patients receiving long-term meperidine. Emergence delirium may be amplified by anxiety and by discomfort such as surgical pain, nausea, pruritis, and gastric or urinary bladder distention. Abnormal mental status after surgery may be an indication of hypoxemia and/or hypercarbia due to residual effects of anesthetic agents, incomplete reversal of neuromuscular blockade, airway obstruction, pneumothorax, or pulmonary aspiration.v" Rarely, metabolic derangements such as hypoglycemia or hyperglycemia, hyponatremia,
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
Mayo Clin Proc, November 2000, Vol 75
Cerebral Embolization After Total Hip Arthroplasty
1211
Figure 1. Cranial magnetic resonance images reveal multiple regions of abnormally increased signal intensity. Left, Multiple focal abnormalities in the cerebellum, especially on the left. Right, Multiple cortical and subcortical abnormalities in watershed distributions (regions between large vascular territories) bilaterally and in the left periventricular region.
hypercalcemia, or hypermagnesemia may contribute to abnormal mental status in patients in the PACU. Finally, once reversible causes of acutely altered sensorium are excluded, neurologic events such as seizure activity and embolic or hemorrhagic stroke must be considered. Diagnostic and Therapeutic Approach to SuddenOnset Altered Mental Status Our patient received naloxone in the PACU because of concerns that her respiratory depression might be in part related to her having received intrathecal morphine. Prior studies suggest that naloxone can prevent? and reverse'? respiratory depression due to intrathecal morphine. We did not think that intrathecal morphine caused obtundation in our patient. However, administration of naloxone enabled us to exclude an adverse drug effect as a contributing factor in our patient's altered mental status. Spinal anesthesia with intrathecal morphine, in combination with light general anesthesia, was used because of reported benefits of spinal anesthesia, including less blood loss and lower risk of thrombophlebitis. We have also found that patients return more rapidly to a normal mental status with light general anesthesia than with deeper sedation, particularly elderly patients. However, general anesthesia alone and spinal anesthesia alone are widely accepted techniques for total hip arthroplasty . We do not believe that the choice of anesthesia had a bearing on our patient's postoperative condition.
The diagnosis of basilar artery thrombosis should be considered in a patient who becomes unresponsive suddenly and spontaneously and has signs of bilateral corticospinal tract dysfunction, including quadriparesis with or without spasticity, ankle clonus, and extensor plantar responses. In the early period after a brainstern stroke, patients may have spinal shock consisting of hypotonic quadriparesis, absent muscle stretch reflexes, and absent plantar responses. Our patient had sudden unresponsiveness and bilateral extensor plantar responses, suggesting basilar artery thrombosis; however, other findings on the neurologic examination, such as lower facial paresis, suggested multifocal bihemispheric dysfunction. Ischemic stroke is a complication of general surgery in 0.08% to 2.9% of cases and typically occurs within the first 2 weeks after the procedure. II Findings on CT without contrast and on digital subtraction angiography were normal in our patient, but results of MRI were strikingly abnormal and supportive of the diagnosis of cerebral fat embolism. Other investigators have found that T2-weighted MRI is sensitive for detecting cerebral fat embolism, even in the acute stage.":" Magnetic resonance imaging is more sensitive than CT in detecting cerebral fat embolism.I-" and the extent of T2-weighted abnormalities correlates with the severity of neurologic impairment. 12 We suggest that, when feasible, an emergent brain MRI with T2-weighted sequences be the first cranial imaging study performed in patients with sudden multifocal neurologic deficits after total hip arthroplasty. Magnetic
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
1212 Cerebral Embolization After Total Hip Arthroplasty
Mayo Clin Proc, November 2000, Vol 75
Figure 2. Cranial magnetic resonance images obtained 12days later,demonstrating resolution of a substantial majority of the abnormal signals, suggesting that mostof the abnormalities seeninitially were areasof transient ischemia. resonance imaging may be particularly useful in patients with fat embolism who demonstrate only neurologic signs." Transcranial Doppler ultrasonography is also helpful in diagnosing fat emboli. In the case of long bone fractures, transcranial Doppler ultrasonography can detect transient microemboli resolving within 4 days after injury. 17 Fat Embolism Syndrome
Systemic embolization associated with lower extremity intramedullary operative procedures may not become evident clinically until several hours postoperatively and may present as mental status change without associated pulmonary dysfunction. 18-21 Embolic showers of medullary contents occur in almost all cases of pelvic and long bone fractures and lower extremity major joint replacement.v" However, the fat embolism syndrome, characterized by progressive respiratory dysfunction, petechiae, thrombocytopenia, and mental status deterioration, is uncommon.P->" Respiratory insufficiency may occur and is generally manifested as dyspnea and hypoxemia. The most likely pathogenesis of respiratory insufficiency in the fat embolism syndrome is noncardiac pulmonary edema secondary to lung injury from fat deposition in the pulmonary circulation. In the general population, a patent foramen ovale has an incidence of approximately 25% in the 4th through 8th decades of life, and paradoxical embolization of fat, air, microthrombi, spicular bones, and other intramedullary debris may occur via this passage.":" Transpulmonary systemic embolization may also occur. In an animal orthopedic sur-
gery model, fat globules were observed to traverse the pulmonary circulation readily, and transesophageal Doppler echocardiography in 6 patients who had developed the fat embolism syndrome after long bone fractures showed no evidence of an intracardiac right-to-left shunt or patent foramen ovale.":" Contrast echocardiography may not detect transpulmonary migration of fat emboli. We suspect that the different rheological properties of air and fat may explain the lack of detection of a shunt on air-contrast echocardiography in our patient. The diagnosis of the fat embolism syndrome is usually presumptive in the setting of severe trauma and/or orthopedic surgery. It should be considered in any patient who develops confusion, respiratory distress, and/or petechiae within 3 days of such an event. Our patient had a delayed onset of neurologic symptoms despite the fact that embolization likely began intraoperatively. The most plausible explanation for this delayed presentation is from a study by Forteza et al'? who demonstrated that, in patients with long bone fractures, fat microembolization occurs 3 to 4 days after the fracture. Neurologic symptoms probably appear only after a threshold lesion burden has developed within the central nervous system. Treatment of the fat embolism syndrome is generally supportive and directed at management of the arterial hypoxemia. Such support ranges from supplemental oxygen to full mechanical ventilation depending on the severity of lung injury. Prophylactic corticosteroids have been used successfully to reduce the incidence of the fat embolism
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Mayo Clin Proc, November 2000, Vol 75
syndrome in patients with skeletal trauma.t-" The indications for corticosteroids, mechanism of protection, and dose range remain ill defined. In addition, concerns of increased infection rates and poor wound healing limit the widespread use of corticosteroids in this setting. CONCLUSIONS Although delayed emergence from general anesthesia and/ or sedatives and emergence delirium are the most common causes of mental status changes found in the PACU setting, immediate evaluation must also include consideration of potentially catastrophic conditions such as hypoxemia, incomplete reversal of neuromuscular blockade, and pulmonary aspiration. Cerebral fat embolization is unusual, but it must always be considered in the differential diagnosis of mental status changes in the setting of pelvic and long bone fractures as well as lower extremity major joint replacement because embolic showers of medullary debris occur in virtually all these cases. The diagnosis is clinical, and no specific test is conclusive. Cerebral fat embolization may occur without associated pulmonary dysfunction and is not ruled out by lack of a patent foramen ovale. Emergent brain MRI with T2-weighted sequences is the cranial imaging study of choice for early evaluation of patients with sudden multifocal neurologic deficits after pelvic or long bone fracture or lower extremity major joint replacement.
Cerebral Embolization After Total Hip Arthroplasty
10. II. 12. 13. 14. 15. 16.
17. 18. 19. 20. 21. 22. 23.
ACKNOWLEDGMENT We thank Dr Frank W. Rubino for providing clinical follow-up information.
24.
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Hines R, Barash PG, Watrous G, O'Connor T. Complications occurring in the postanesthesia care unit: a survey. Anesth Ana/g. 1992;74:503-509. Zelcer J, Wells DG. Anaesthetic-related recovery room complications. Anaesth Intensive Care. 1987;15:168-174. de Mello WF, Tully A, Restall J. Morbidity in the postanesthesia care unit [letter]. Anesth Ana/g. 1992;75:640. Van der Walt JH, Webb RK, Osborne GA, Morgan C, Mackay P, The Australian Incident Monitoring Study: recovery room incidents in the first 2000 incident reports. Anaesth Intensive Care, 1993;21:650-652. Mecca RS. Postoperative recovery. In: Barash PG, Cullen BF, Stoelting RK, eds. Clinical Anesthesia. 3rd ed. Philadelphia, Pa: Lippincott-Raven; 1997:1279-1303. Mathew JP, Rosenbaum SH, O'Connor T, Barash PG. Emergency tracheal intubation in the postanesthesia care unit: physician error or patient disease? Anesth Analg. 1990;71:691-697. Daley MD, Norman PH, Colmenares ME, Sandler AN. Hypoxaemia in adults in the post-anaesthesia care unit. Can 1 Anaesth. 1991;38:740-746. Rose DK, Cohen MM, Wigglesworth DF, DeBoer DP. Critical respiratory events in the postanesthesia care unit: patient, surgical, and anesthetic factors. Anesthesiology. 1994;81:410-418. Johnson A, Bengtsson M, Soderlind K, Lofstrom 18. Influence of intrathecal morphine and naloxone intervention on postoperative ventilatory regulation in elderly patients. Acta Anaesthesiol Scand. 1992;36:436-444.
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Jones RD, Jones JG. Intrathecal morphine: naloxone reverses respiratory depression but not analgesia. Br Med 1. 1980;281:645-646. Limburg M, Wijdicks EF, Li H. Ischemic stroke after surgical procedures: clinical features, neuroimaging, and risk factors. Neurology. 1998;50:895-901. Takahashi M, Suzuki R, Osakabe Y, et al. Magnetic resonance imaging findings in cerebral fat embolism: correlation with clinical manifestations. 1 Trauma. 1999;46:324-327. Stoeger A, Daniaux M, Felber S, Stockhammer G, Aichner F, zur Nedden D. MRI findings in cerebral fat embolism. Eur Radiol. 1998;8:1590-1593. Bardana D, Rudan J, Cervenko F, Smith R. Fat embolism syndrome in a patient demonstrating only neurologic symptoms. Can 1 Surg. 1998;41:398-402. Yoshida A, Okada Y, Nagata Y, Hanaguri K, Morio M. Assessment of cerebral fat embolism by magnetic resonance imaging in the acute stage. 1 Trauma. 1996;40:437-440. Satoh H, Kurisu K, Ohtani M, et al. Cerebral fat embolism studied by magnetic resonance imaging, transcranial Doppler sonography, and single photon emission computed tomography: case report. 1 Trauma. 1997;43:345-348. Forteza AM, Koch S, Romano JG, et al. Transcranial Doppler detection offat emboli. Stroke. 1999;30:2687-2691. Heine TA, Halambeck BL, Mark 18. Fatal pulmonary fat embolism in the early postoperative period. Anesthesiology. 1998;89:15891591. Findlay JM, DeMajo W. Cerebral fat embolism. Can Med Assoc 1. 1984;131:755-757. Font MO, Nadal P, Bertran A. Fat embolism syndrome with no evidence of pulmonary involvement [letter]. Crit Care Med. 1989; 17:108-109. Jacobs S, al Thagafi MY, Biary N, HasanHA, Sofi MA, ZuleikaM. Neurological failure in a patient with fat embolism demonstrating no lung dysfunction [letter]. Intensive Care Med. 1996;22:1461. ten Duis HJ. The fat embolism syndrome. Injury. 1997;28:77-85. Christie J, Robinson CM, Pell AC, McBirnie J, Burnett R. Transcardiac echocardiography during invasive intramedullary procedures. 1 Bone loint Surg Br. 1995;77:450-455. Lafont ND, Kalonji MK, Barre J, Guillaume C, Boogaerts JG. Clinical features and echocardiography of embolism during cemented hip arthroplasty. Can J Anaesth. 1997;44:112-117. Ereth MH, Weber JG, Abel MD, et al. Cemented versus noncemented total hip arthroplasty-embolism, hemodynamics, and intrapulmonary shunting. Mayo Clin Proc. 1992;67:1066-1074. Bulger EM, Smith DG, Maier RV, Jurkovich OJ, Fat embolism syndrome: a 10-year review. Arch Surg. 1997;132:435-439. Byrick RJ. Cement implantation syndrome: a time limited embolic phenomenon [editorial]. Can J Anaesth. 1997;44:107-111. Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc. 1984;59:17-20. Etchells EE, Wong DT, Davidson G, Houston PL. Fatal cerebral fat embolism associated with a patent foramen ovale. Chest. 1993; 104:962-963. Pell AC, Hughes D, Keating J, Christie J, Busuttil A, Sutherland GR. Brief report: fulminating fat embolism syndrome caused by paradoxical embolism through a patent foramen ovale. N Engl 1 Med. 1993;329:926-929. Fabian TC. Unravelling the fat embolism syndrome [editorial]. N Engl J Med. 1993;329:961-963. Byrick RJ, Mullen 18, Mazer CD, Guest CB. Transpulmonary systemic fat embolism: studies in mongrel dogs after cemented arthroplasty. Am J Respir Crit Care Med. 1994;150(5, pt 1):14161422. Nijsten MW, Hamer JP, ten Duis HJ, Posma JL. Fat embolism and patent foramen ovale [letter]. Lancet. 1989;1:1271. Schonfeld SA, Ploysongsang Y, DiLisio R, et al. Fat embolism prophylaxis with corticosteroids: a prospective study in high-risk patients. Ann Intern Med. 1983;99:438-443. Kallenbach J, Lewis M, Zaltzman M, Feldman C, Orford A, Zwi S. 'Low-dose' corticosteroid prophylaxis against fat embolism. 1 Trauma. 1987;27:1173-1176.
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
OTT, MD; JAMES F. MESCHIA, MD;
DAVID
C.
MACKEY, MD; MARK
CHARLES BURGER, MD; J. DAN ECHOLS, MD; AND DOUGLAS
status after pelvic or long bone fracture or lower extremity major joint replacement, and this condition may occur despite normal pulmonary function and no patent foramen ovale or right-to-Ieft intracardiac shunt. Magnetic resonance imaging with T 2-weighted sequences is the cranial imaging study of choice for early evaluation of patients with sudden multifocal neurologic deficits and suspected fat embolism syndrome. Mayo Clin Proc. 2000;75:1209-1213
Catastrophic neurologic events occur rarely postoperatively and must be diagnosed quickly. A 63-year-old woman who had undergone uneventful total hip arthroplasty experienced obtundation after admission to the postanesthesia care unit. Cranial magnetic resonance imaging revealed multiple lesions consistent with ischemia or infarction, and fat cerebral embolism was diagnosed. We describe the numerous complications that may occur in patients in the postanesthesia care unit and review the differential diagnosis of altered mental status in such patients. Paradoxical cerebral fat embolization must be considered in the differential diagnosis of altered mental
CT = computed tomography; MRI = magnetic resouance imaging; PACU =postanesthesia care unit
A
preoperative laboratory investigation revealed normal findings on electrocardiography and chest radiography, as well as normal serum electrolytes. The preoperative hemoglobin concentration was 11.0 g/dL after she was given 2 U of autologous blood. Spinal anesthesia was established with hyperbaric bupivacaine, 12mg, epinephrine, 0.2 mg, and preservativefree morphine, 0.25 mg. General endotracheal anesthesia was induced with propofol, 140 mg, and maintained with isoflurane (0.6%-1.2%) and nitrous oxide-oxygen (0%66%). Continuous intraoperative monitoring included electrocardiography, pulse oximetry, capnography, oscillometric blood pressure determinations, and esophageal temperature. The cardiac rhythm remained in normal sinus, and the oxygen saturation was 100% throughout the intraoperative anesthetic course. The systolic blood pressure ranged from 90 to 120 mm Hg, the mean blood pressure ranged from 60 to 80 mm Hg, and the heart rate ranged from 52 to 72 beats/min. Crystalloid, 1300 mL, was administered, and the estimated blood loss was 300 mL during the operative procedure, which lasted 1 hour and 27 minutes. While awake, the patient was taken to the PACU and extubated; she responded appropriately to verbal stimuli. Throughout the PACU stay, her blood pressure, monitored at 5-minute intervals, and findings on continuous electrocardiography remained normal; the oxygen saturation by pulse oximetry ranged from 96% to 100%. She complained of nausea and was given intravenous ondansetron, 4.0 mg on 2 occasions. The patient was noted to be lethargic 2 112 hours after PACU admission, and over the following 50 minutes, obtundation progressed to the point that reintu-
dverse events occur commonly in the postanesthesia care unit (PACU), with a complication rate that may exceed 23% to 30%.1-3 Pain (16%) and nausea-vomiting (8%) are the most common complications. Altered mental status is seen in 3% to 9% of cases (Table 1).2.4 Delayed emergence and emergence delirium secondary to anesthetic and analgesic medication administered preoperatively and intraoperatively are the principal causes of postoperative mental status changes, but the differential diagnosis is broad (Table 2). We describe a patient who underwent total hip arthroplasty and experienced obtundation after admission to the PACU. Cerebral fat embolization was detected subsequently. REPORT OF A CASE
A 63-year-old woman who weighed 65 kg and had a history of hypertension controlled with amlodipine-benazepril, idiopathic hypothyroidism treated with levothyroxine, and seasonal asthma underwent total hip arthroplasty for degenerative osteoarthritis; a combination of spinal and general anesthesia was used. A preoperative medical evaluation disclosed no evidence of coronary artery or neurologic disease. Her preoperative blood pressure was 110/70 mm Hg. The From the Division of Pulmonary Medicine (M.C.O.• C.B.), Department of Neurology (J.F.M.), Department of Anesthesiology (D.C.M.), Department of Orthopedic Surgery (M.P.B.), Division of Community Internal Medicine (J.D.E.), and Department of Diagnostic Radiology (D.S.F.), Mayo Clinic, Jacksonville, Fla. Address reprint requests and correspondence to James F. Meschia, MD, Department of Neurology, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224-1865 (e-mail: [email protected]).
Mayo Clin Proc. 2000;75: 1209-1213
P. BRODERSEN, MD;
S. FENTON, MD
1209
© 2000 Mayo Foundation for Medical Education and Research
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
1210
Cerebral Embolization After Total Hip Arthroplasty
Table I. Complications in the Postanesthesia Care Unit* Complication
Rate (%)t
Pain Nauseaand vomiting Alteredmentalstatus Hypoxemia or hypercapnia Hypotension Cardiacdysrhythmias Upperairwayobstruction Hypertension Oliguria Major cardiacevent Hypothermia Hyperglycemia
16 8 7 7
6 4 4 2 I
<1
*Datafrom Hineset al,' Zelcer and Wells,' and de Melloet al.' tUnweighted averages. bation was required for airway protection. Before reintubation, arterial blood gas determinations obtained while the patient was receiving supplemental oxygen via an updraft face tent at 10 L/min revealed a pH of 7.35, Pco, of 39 mm Hg, POz of91 mm Hg, and oxygen saturation of 96%. The patient exhibited spontaneous eye opening but did not follow commands. Pupillary light and corneal reflexes were preserved, but a left lower facial droop, leftward gaze preference, and minimal withdrawal from painful stimulus were noted. The patient exhibited diffuse hyporeflexia and bilateral extensor plantar reflexes. No skin, conjunctival, or funduscopic abnormalities were found. Intravenous administration of 100 ug of naloxone resulted in no clinical improvement. Electrocardiographic findings, serum electrolytes, and glucose level were normal. Chest radiography showed prominent bilateral interstitial markings. ElectroTable 2. Differential Diagnosis of Altered Mental Status in the Postanesthesia Care Unit Residual or prolongedanesthetic effect or overdose (including vapor agents, sedative-hypnotic agents, barbiturates, opioids, musclerelaxants) Hypoxemia and/orhypercarbia Hypotension Fluid and electrolyte imbalance (including hyperosmolar syndrome, waterintoxication) Metabolic encephalopathy (hepatic, renal,endocrine) Hypothermia or hyperthermia Intraoperative complication (air or particulate embolism, cerebral ischemia, intracranial hemorrhage, hypoxic encephalopathy, hypotension) Preexisting alteredmental status Emergence delirium Interaction with preoperative medications or illicit drugs Alcoholand drug withdrawal Atypical or allergicmedication reaction Seizure(statusepilepticus or postictal state)
Mayo Clin Proc, November 2000, Vol7S
encephalography showed diffuse slowing but no ictal discharges. Findings on cranial computed tomography (CT) without contrast were normal, as were those on cerebral digital subtraction arteriography performed 5 hours after onset of symptoms. Cranial magnetic resonance imaging (MRI) with Tz-weighted sequences performed the following morning revealed multiple cortical and subcortical lesions in both cerebral and cerebellar hemispheres, highly suggestive of an embolic event (Figure 1), and probable cerebral fat embolism was diagnosed. Transesophageal echocardiography with a contrast agent disclosed no patent foramen ovale, intrapulmonary shunting, or cardiac abnormality. Subsequent electroencephalography revealed diffuse slowing, and MRI performed 12 days postoperatively revealed resolution of many of the brain lesions (Figure 2). The patient gradually regained consciousness and her ability to communicate, and she was transferred to a rehabilitation facility 19 days after her initial hospital admission. DISCUSSION Differential Diagnosis of Altered Mental Status Delayed emergence from general anesthesia due to the residual effects of oral, intravenous, and inhalational sedative, analgesic, and anesthetic medications is a frequent cause of mental status alteration found in patients in the PACU. This situation may be complicated by preexisting mental dysfunction, postoperative hypothermia, or unrecognized preoperative ingestion of alcohol, opioids, benzodiazepines, and other prescription and illicit drugs that potentiate the effects of anesthesia-related medications (Table 2). Emergence delirium, a behavioral manifestation of recovery from general anesthesia ranging from mild confusion and lethargy to extreme excitement and combativeness, is the second most common mental status abnormality found in patients in the PACU. Return of cognitive function after general anesthesia may be slower in the elderly population in the immediate postoperative period, whereas agitation and combativeness are more frequently observed in children and young adults.' Emergence delirium may also be produced by perioperative administration of ketamine or an anticholinergic medication such as scopalomine or atropine and by postoperative withdrawal from alcohol or illicit drugs. Moreover, it may be seen preoperatively in patients receiving long-term meperidine. Emergence delirium may be amplified by anxiety and by discomfort such as surgical pain, nausea, pruritis, and gastric or urinary bladder distention. Abnormal mental status after surgery may be an indication of hypoxemia and/or hypercarbia due to residual effects of anesthetic agents, incomplete reversal of neuromuscular blockade, airway obstruction, pneumothorax, or pulmonary aspiration.v" Rarely, metabolic derangements such as hypoglycemia or hyperglycemia, hyponatremia,
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
Mayo Clin Proc, November 2000, Vol 75
Cerebral Embolization After Total Hip Arthroplasty
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Figure 1. Cranial magnetic resonance images reveal multiple regions of abnormally increased signal intensity. Left, Multiple focal abnormalities in the cerebellum, especially on the left. Right, Multiple cortical and subcortical abnormalities in watershed distributions (regions between large vascular territories) bilaterally and in the left periventricular region.
hypercalcemia, or hypermagnesemia may contribute to abnormal mental status in patients in the PACU. Finally, once reversible causes of acutely altered sensorium are excluded, neurologic events such as seizure activity and embolic or hemorrhagic stroke must be considered. Diagnostic and Therapeutic Approach to SuddenOnset Altered Mental Status Our patient received naloxone in the PACU because of concerns that her respiratory depression might be in part related to her having received intrathecal morphine. Prior studies suggest that naloxone can prevent? and reverse'? respiratory depression due to intrathecal morphine. We did not think that intrathecal morphine caused obtundation in our patient. However, administration of naloxone enabled us to exclude an adverse drug effect as a contributing factor in our patient's altered mental status. Spinal anesthesia with intrathecal morphine, in combination with light general anesthesia, was used because of reported benefits of spinal anesthesia, including less blood loss and lower risk of thrombophlebitis. We have also found that patients return more rapidly to a normal mental status with light general anesthesia than with deeper sedation, particularly elderly patients. However, general anesthesia alone and spinal anesthesia alone are widely accepted techniques for total hip arthroplasty . We do not believe that the choice of anesthesia had a bearing on our patient's postoperative condition.
The diagnosis of basilar artery thrombosis should be considered in a patient who becomes unresponsive suddenly and spontaneously and has signs of bilateral corticospinal tract dysfunction, including quadriparesis with or without spasticity, ankle clonus, and extensor plantar responses. In the early period after a brainstern stroke, patients may have spinal shock consisting of hypotonic quadriparesis, absent muscle stretch reflexes, and absent plantar responses. Our patient had sudden unresponsiveness and bilateral extensor plantar responses, suggesting basilar artery thrombosis; however, other findings on the neurologic examination, such as lower facial paresis, suggested multifocal bihemispheric dysfunction. Ischemic stroke is a complication of general surgery in 0.08% to 2.9% of cases and typically occurs within the first 2 weeks after the procedure. II Findings on CT without contrast and on digital subtraction angiography were normal in our patient, but results of MRI were strikingly abnormal and supportive of the diagnosis of cerebral fat embolism. Other investigators have found that T2-weighted MRI is sensitive for detecting cerebral fat embolism, even in the acute stage.":" Magnetic resonance imaging is more sensitive than CT in detecting cerebral fat embolism.I-" and the extent of T2-weighted abnormalities correlates with the severity of neurologic impairment. 12 We suggest that, when feasible, an emergent brain MRI with T2-weighted sequences be the first cranial imaging study performed in patients with sudden multifocal neurologic deficits after total hip arthroplasty. Magnetic
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Figure 2. Cranial magnetic resonance images obtained 12days later,demonstrating resolution of a substantial majority of the abnormal signals, suggesting that mostof the abnormalities seeninitially were areasof transient ischemia. resonance imaging may be particularly useful in patients with fat embolism who demonstrate only neurologic signs." Transcranial Doppler ultrasonography is also helpful in diagnosing fat emboli. In the case of long bone fractures, transcranial Doppler ultrasonography can detect transient microemboli resolving within 4 days after injury. 17 Fat Embolism Syndrome
Systemic embolization associated with lower extremity intramedullary operative procedures may not become evident clinically until several hours postoperatively and may present as mental status change without associated pulmonary dysfunction. 18-21 Embolic showers of medullary contents occur in almost all cases of pelvic and long bone fractures and lower extremity major joint replacement.v" However, the fat embolism syndrome, characterized by progressive respiratory dysfunction, petechiae, thrombocytopenia, and mental status deterioration, is uncommon.P->" Respiratory insufficiency may occur and is generally manifested as dyspnea and hypoxemia. The most likely pathogenesis of respiratory insufficiency in the fat embolism syndrome is noncardiac pulmonary edema secondary to lung injury from fat deposition in the pulmonary circulation. In the general population, a patent foramen ovale has an incidence of approximately 25% in the 4th through 8th decades of life, and paradoxical embolization of fat, air, microthrombi, spicular bones, and other intramedullary debris may occur via this passage.":" Transpulmonary systemic embolization may also occur. In an animal orthopedic sur-
gery model, fat globules were observed to traverse the pulmonary circulation readily, and transesophageal Doppler echocardiography in 6 patients who had developed the fat embolism syndrome after long bone fractures showed no evidence of an intracardiac right-to-left shunt or patent foramen ovale.":" Contrast echocardiography may not detect transpulmonary migration of fat emboli. We suspect that the different rheological properties of air and fat may explain the lack of detection of a shunt on air-contrast echocardiography in our patient. The diagnosis of the fat embolism syndrome is usually presumptive in the setting of severe trauma and/or orthopedic surgery. It should be considered in any patient who develops confusion, respiratory distress, and/or petechiae within 3 days of such an event. Our patient had a delayed onset of neurologic symptoms despite the fact that embolization likely began intraoperatively. The most plausible explanation for this delayed presentation is from a study by Forteza et al'? who demonstrated that, in patients with long bone fractures, fat microembolization occurs 3 to 4 days after the fracture. Neurologic symptoms probably appear only after a threshold lesion burden has developed within the central nervous system. Treatment of the fat embolism syndrome is generally supportive and directed at management of the arterial hypoxemia. Such support ranges from supplemental oxygen to full mechanical ventilation depending on the severity of lung injury. Prophylactic corticosteroids have been used successfully to reduce the incidence of the fat embolism
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Mayo Clin Proc, November 2000, Vol 75
syndrome in patients with skeletal trauma.t-" The indications for corticosteroids, mechanism of protection, and dose range remain ill defined. In addition, concerns of increased infection rates and poor wound healing limit the widespread use of corticosteroids in this setting. CONCLUSIONS Although delayed emergence from general anesthesia and/ or sedatives and emergence delirium are the most common causes of mental status changes found in the PACU setting, immediate evaluation must also include consideration of potentially catastrophic conditions such as hypoxemia, incomplete reversal of neuromuscular blockade, and pulmonary aspiration. Cerebral fat embolization is unusual, but it must always be considered in the differential diagnosis of mental status changes in the setting of pelvic and long bone fractures as well as lower extremity major joint replacement because embolic showers of medullary debris occur in virtually all these cases. The diagnosis is clinical, and no specific test is conclusive. Cerebral fat embolization may occur without associated pulmonary dysfunction and is not ruled out by lack of a patent foramen ovale. Emergent brain MRI with T2-weighted sequences is the cranial imaging study of choice for early evaluation of patients with sudden multifocal neurologic deficits after pelvic or long bone fracture or lower extremity major joint replacement.
Cerebral Embolization After Total Hip Arthroplasty
10. II. 12. 13. 14. 15. 16.
17. 18. 19. 20. 21. 22. 23.
ACKNOWLEDGMENT We thank Dr Frank W. Rubino for providing clinical follow-up information.
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