Severe paradoxical intracranial embolism and pulmonary emboli during hip hemiarthroplasty

E. Narimatsu1,2, M. Kawamata2, M. Hase1, Y. Kurimoto1, Y. Asai1 and A. Namiki2

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


    Abstract
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
Both paradoxical intracranial embolism, an intracranial arterial embolism caused by venous embolic material that has passed through a right-to-left shunt, and pulmonary arterial embolism are life-threatening complications of joint arthroplasty. We report a case of severe paradoxical intracranial embolism and pulmonary embolism that occurred during hip hemiarthroplasty.

Br J Anaesth 2003; 91: 911--13

Keywords: complications, intracranial embolism; complications, embolism, paradoxical; complications, pulmonary embolism; surgery, arthroplasty, hip replacement


    Introduction
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
Both paradoxical intracranial embolism, an intracranial arterial embolism caused by venous embolic material that has passed through a right-to-left shunt,1 and pulmonary arterial embolism are life-threatening complications of joint arthroplasty. We report a case of severe paradoxical intracranial embolism and pulmonary embolism that occurred during hip hemiarthroplasty.


    Case report
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
Sudden loss of consciousness (Glasgow Coma Scale (GCS) 3) and hypoxaemia (SpO2 55%) following a brief period of central chest pain occurred in an 86-yr-old female patient undergoing left hip arthroplasty for an internal femoral neck fracture that had occurred 2 days before the operation. The patient had no varicose veins and an ultrasound examination of the femoral and popliteal veins had not revealed any deep vein thrombosis (DVT). External pneumatic compression boots providing prophylaxis against DVT had been used before the operation.

The sudden loss of consciousness and hypoxaemia occurred while the patient’s left lower leg was being passively manipulated to rasp the femoral medulla in the right lateral position under spinal anaesthesia without sedation. The patient’s 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 patient’s 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 patient’s 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 patient’s blood oxygenation satisfactorily recovered but the coma (GCS 4) persisted.




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Fig 1 Computed tomogaraphy images obtained about 90 min after the onset of embolism indicating local disappearance of cerebral gyri around the dorsal horn of the left lateral ventricle (A) and multiple deficits in a contrast medium-enhanced image of pulmonary arteries (B).

 



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Fig 2 CT images showing multiple brain infarctions (A) and disruption of the shape of the midbrain (B) obtained on the seventh day after the onset of embolism.

 

    Discussion
 Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 
It has been reported that intracranial and pulmonary emboli occur in approximately 0.5 and 0.5–2% of patients undergoing joint arthroplasties, respectively2 3 and that evidence of an embolus has been confirmed in only a few cases of arthroplasty related paradoxical intracranial embolism.4 Therefore, a paradoxical intracranial embolism with pulmonary embolism during total hip arthroplasty, as was found in our patient, is rare. However, it has been reported that embolic phenomena of varying severity were observed using transoesophageal echography in the majority of patients who underwent femoral medullary reaming and hip hemiarthroplasty.5 These findings suggest that embolic events during hip arthroplasty, including subclinical events, are actually more common than has generally been recognized.

In this case, sudden loss of consciousness and hypoxaemia occurred during manipulation of the patient’s 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.


    References
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
1 d’Audiffret A, Pillai L, Dryjski M. Paradoxical emboli: the relationship between patent foramen ovale, deep vein thrombosis and ischaemic stroke. Eur J Vasc Endovasc Surg 1999; 17: 468–71[CrossRef][ISI][Medline]

2 Giachino AA, Ostrowski J, Feibel RJ. Stroke as a complication of total joint arthropathy. J Bone Joint Surg 1998; 80B (Suppl. I): 8

3 Trowbridge A, Boese CK, Woodruff B, et al. Incidence of posthospitalization proximal deep venous thrombosis after total hip arthroplasty. A pilot study. Clin Orthop Related Res 1994; 299: 203–8[Medline]

4 Della Valle CJ, Jazrawi LM, Di Cesare PE, Steiger DJ. Paradoxical cerebral embolism complicating a major orthopaedic operation. A report of two cases. J Bone Joint Surg 1999; 81: 108–10[Free Full Text]

5 Christie J, Robinson CM, Pell AC, McBirnie J, Burnett R. Transcardiac echocardiography during invasive intramedullary procedures. J Bone Joint Surg 1995; 77B: 450–5

6 Tronzo RG, Kallos T, Wyche MQ. Elevation of intramedullary pressure when methylmethacrylate is inserted in total hip arthroplasty. J Bone Joint Surg 1974; 56: 714–8

7 Koessler MJ, Pitto RP. Fat and bone marrow embolism in total hip arthroplasty. Acta Orthop Belg 2001; 67: 97–109[Medline]

8 Scroop R, Eskridge J, Britz GW. Paradoxical cerebral arterial embolization of cement during intraoperative vertebroplasty: case report. Am J Neuroradiol 2002; 23: 868–70[CrossRef]

9 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[ISI][Medline]





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