Departments of 1 Traumatology and Critical Care Medicine and 2 Anesthesiology, Sapporo Medical University School of Medicine, South 1, West 16, Chuo-ku, Sapporo, Hokkaido 060-8543, Japan
*Corresponding author: Department of Traumatology and Critical Care Medicine, Sapporo Medical University School of Medicine, South 1, West 16, Chuo-ku, Sapporo, Hokkaido 060-8543, Japan. E-mail: enarimat@sapmed.ac.jp
Accepted for publication: July 3, 2003
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Abstract |
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Br J Anaesth 2003; 91: 911--13
Keywords: complications, intracranial embolism; complications, embolism, paradoxical; complications, pulmonary embolism; surgery, arthroplasty, hip replacement
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Introduction |
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Case report |
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The sudden loss of consciousness and hypoxaemia occurred while the patients left lower leg was being passively manipulated to rasp the femoral medulla in the right lateral position under spinal anaesthesia without sedation. The patients arterial pressure, heart rate (BP 146/76 mm Hg, HR 110), and spontaneous respiration were not obviously altered when the event occurred. Following the loss of consciousness, the patients trachea was intubated and mechanical ventilation of the lungs was commenced. This improved blood oxygenation (SpO2 94%; PaO2 78 mm Hg; PaCO2 46 mm Hg under FIO2 1.0) and the SpO2 gradually increased further but without recovery of consciousness.
When the patient arrived at our intensive care unit 65 min after the onset of the event, she was not in shock (BP 155/90 mm Hg, HR 99) but appeared to have severe neurological deficiencies (GCS 3, left conjugate deviation of the eyes, and loss of right eyelash reflex). The patients spontaneous ventilation was satisfactory but oxygen 100% was required to prevent hypoxaemia (SpO2 99%). Computed tomography (CT) was performed and revealed localized loss of distinction of the cerebral gyri in the region of the dorsal horn of the left lateral ventricle, suggesting cerebral infarction-induced oedema (Fig. 1A) and multiple deficits in a contrast medium-enhanced image of the pulmonary arteries indicating pulmonary emboli (Fig. 1B). There were no emboli in the left atrium/ventricle, aorta, and cervical arteries or interstitial pulmonary oedema observed in CT images. Trans-thoracic echocardiography showed a severely dilated right ventricle and atrium with mild tricuspid regurgitation but did not reveal right-to-left intra-cardiac shunting. No lipid particles were seen in the retinal blood vessels. An electroencephalogram showed slow waves with occasional huge spikes. The first and third waves of the auditory brainstem responses were observed only on the left. A CT scan of the brain on the seventh postoperative day showed multiple infarctions of the cortex (Fig. 2A), cerebellum, and brain stem and disruption of the normal shape of the midbrain (Fig. 2B). Evidence of the pulmonary emboli on CT images of the chest persisted for 20 days after the event. Thereafter, the patients blood oxygenation satisfactorily recovered but the coma (GCS 4) persisted.
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Discussion |
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In this case, sudden loss of consciousness and hypoxaemia occurred during manipulation of the patients left lower limb and rasping of the femoral medulla, which can trigger dissemination of concealed i.v. thrombi by physical compression and medullary contents by elevation of the internal pressure of the medullary cavity,6 respectively. As hypercoagulopathy induced by lipid particles that have migrated from bone marrow to blood can also generate macroemboli,7 we could not determine whether the origin of the embolus was deep venous thrombosis or a mixed fatty macroembolism. However, as lipid particles in the retinal vessels and interstitial pulmonary oedema, both of which suggest fatty emboli,7 were not observed, we think a venous thrombus is more likely to have been the origin of the emboli. Bone cement, which can also cause emboli,8 had not been applied when the embolism occurred.
Despite evidence indicating pulmonary embolism, that is embolic masses in pulmonary arteries, overloading of the right atrium/ventricle and impaired blood oxygenation, systemic circulatory deficiency was not obvious in this case even in the acute period of the embolism. Although an effective right-to-left shunt was presumed, the location of the shunt could not be identified. As trans-thoracic echocardiography can fail to reveal the presence of a shunt through the atrial septum,1 it is possible that a persistent foramen ovale9 or a concealed atrial septum defect was present.
In conclusion, we report a serious complication of orthopaedic lower limb surgery. Routine preoperative examination and ultrasound examination of the lower limbs did not detect the presence of a DVT, which we presume to be the source of the emboli. Furthermore, catastrophic embolization occurred despite the use of external pneumatic compression devices.
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References |
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