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Lateral Medullary Syndrome After Prone Position for General Surgery

Chu, Ya-Chun, MD, PhD; Tsai, Shen-Kou, MD, PhD; Chan, Kwok-Hon, MD; Kao, Sheng-Chin, MD; Liang, Ching-Huang, MD; Lin, Su-Man, MD

doi: 10.1097/00000539-200211000-00065
CASE REPORTS: Case Report
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Department of Anesthesiology, Taipei-Veterans General Hospital and National Yang-Ming University, School of Medicine, Taipei, Taiwan

July 9, 2002.

Address Correspondence and reprint requests to Su-Man Lin, MD, Department of Anesthesiology, Veterans General Hospital-Taipei, 11221, Taiwan. Address e-mail to sm_lin@vghtpe.gov.tw.

Complications associated with positioning a patient for surgery are not rare. The main complications associated with the prone position include ocular and auricular injury, musculoskeletal injuries, venous air embolism, compression of limb neurovascular bundles, ischemia of skin at pressure points, and excessive joint flexion and extension (1). However, complications associated with the central nervous system, especially the vertebral arterial territory, have not been reported. We report a case of postoperative lateral medullary syndrome with myoclonus after prone position for general surgery. The mechanism and successful management are discussed.

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Case Report

A 40-yr-old, 86-kg man was admitted for surgical removal of a soft tissue mass, 8 × 8 cm, over the right middle back area. He had a history of cervical spinal whiplash injury 2 yr previously during an accident and received C4-5 and C5-6 discectomy, anterior fusion with bone graft, and Orion plate fixation.

Routine preoperative clinical assessment and investigations were all normal, except that movements of the neck were very limited because of a previous operation. After topical spraying with 8% lidocaine over his entire oral airway, tracheal intubation via fiberoptic bronchoscope was performed smoothly while the patient was conscious. General anesthesia was augmented with IV thiopental 240 mg, rocuronium 50 mg, and isoflurane in oxygen (Fio2 0.5). Then the patient was carefully turned onto the prone position with the body supported by blanket rolls from the clavicle to iliac crest. The head was retained by a horseshoe-shaped pad and faced downward without turning. The arms were anteriorly flexed and abducted. The eyes and ears were examined and freed from pressure. Elbows and knees were all padded. Arms were checked to ensure that the contents of axilla were neither compressed nor under tension. The tumor mass was smoothly excised within 100 min. The patient was changed to the supine position at the end of the surgery. Heart rate and noninvasive blood pressure were maintained at preoperative value during the whole course of operation. After reversing of the residual neuromuscular blockade, the patient was awake and tracheally extubated in the operating room.

As soon as the patient was transported to the postanesthesia care unit, the anesthesiologist first noticed involuntary myoclonic movements of the patient’s left arm and leg. Meanwhile, the patient also complained of dizziness, headache, and painful numbness of the right face. His speech was slurred. The myoclonic spasms of his left side extremities occurred every 3–5 min and lasted approximately 5 s. Hip flexor contraction dominated, resulting in a marked lifting of the leg off the bed approximately 15–20 cm. A neurologic examination demonstrated hypalgesia in the ipsilateral side of the face and contralateral limbs and trunk. The patient was completely awake during and after the spasms. Vital signs were normal. Arterial blood gases, serum electrolytes, and ionized calcium and magnesium were all within normal limits.

The patient was treated with supplemental oxygen and incremental doses of midazolam to a total of 4 mg. Myoclonic movements subsided immediately but reappeared when the patient regained consciousness. Brain computed tomography scan was immediately performed and showed negative findings. Doppler ultrasonography revealed decreased flow in the intracranial portion of the right vertebral artery. Magnetic resonance (MR) angiography, performed 24 h later, demonstrated relative stenosis in the right distal vertebral artery (Fig. 1). No brain infarction or intravascular lesions of the large arteries was noted. In addition, the electroencephalogram was normal. Under the impression of lateral medullary syndrome, he was transferred to the neurology ward and received heparin and regular rehabilitation therapy. Further examination with echocardiography showed no intracardiac emboli or shunt. There was considerable improvement in his neurologic status during the admission. The symptoms subsided gradually. He had minimal weakness of the left side limbs and sensation returned to normal. He was discharged with stable and satisfactory recovery after 40 days.

Figure 1

Figure 1

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Discussion

Most postoperative strokes involve the carotid artery territory, most often in the territory of a middle cerebral artery (2,3). It causes unilateral weakness and cognitive, language, and behavioral changes that are easy to recognize. Vertebrobasilar strokes are more heterogeneous and often incorrectly diagnosed. Lateral medullary syndrome, also known as “posterior inferior cerebellar artery syndrome,” or “Wallenberg’s syndrome,” is one of the best recognized among the several syndromes of brainstem strokes. Although originally described as secondary to occlusion of the posterior inferior cerebellar artery, the vertebral artery is more often involved (4). The age at onset is most often in the sixth or seventh decade of life, and concomitant risk factors, such as hypertension, diabetes, and vascular atherosclerosis are frequent (5). However, there are increasing reports that young adults are also susceptible when there is neck trauma or manipulation (6,7). Tettenborn et al. (8) also suggested that potentially embolic material is deposited within the vertebral system as a result of extension and rotation of the neck in the anesthetized patients. Postoperatively, the material is dislodged, carried intracranially, and causes strokes. However, there is no convincing evidence that vertebral artery disease or occlusion occurs more often in patients who have degenerative cervical spine disease. Our report suggests that repositioning in those with a history of cervical trauma or pathology can exacerbate vertebral arterial insufficiency.

The vertebral arteries are vulnerable to mechanical injury at three sites: during ascent in the foramina of the cervical vertebrae, at the junction of the axis and the atlas, and as they pass over the atlas at the cervicocranial junction to enter the skull (9). Here the arteries are especially susceptible to stretching and shearing forces. Thus, sudden rotation of the head, hyperextension, and sudden acceleration-deceleration movements are likely to cause injury or obstruction. In the present case, Doppler ultrasonography and MR angiography demonstrated only decreased flow and relative stenosis in the intracranial portion of the right vertebral artery without evidence of cardioemboli or vertebral artery atheroma. Therefore, we presume that during repositioning, head rotation or hyperextension obstructed the flow of the vertebral artery at the neck and led to hypoperfusion of the areas supplied by the previously asymptomatic stenosis. In addition, vasoconstriction and relative hypoperfusion related to general anesthesia might have aggravated the overall perfusion.

The triad of Horner’s syndrome, ipsilateral ataxia, and ipsilateral hypalgesia clinically identify patients with lateral medullary syndrome (5). Nevertheless, the manifestation is broad and includes numbness, dysphagia, vertigo, nausea-emesis, hoarseness, hiccups, facial pain, visual disturbance, etc. The clinical features of lateral medullary syndrome are so dramatic that the diagnosis usually is straightforward. But diagnosis can be confounded in the postoperative period. Decreased alertness, bilateral or diffuse weakness, dizziness, dysarthria, nausea-emesis, hoarseness, and ataxia are common postoperative problems and are often explained by anesthetic, metabolic, and drug-related causes. Our patient initially presented with the astonishing myoclonus. This prompted a detailed neurologic physical examination and led to the suspicion of lateral medullary syndrome. Brainstem infarction has been reported to evoke myoclonus (10,11). Although MR imaging was normal in our patient, clinical presentation and noninvasive tests, such as Doppler ultrasonography and MR angiography, provided reliable criteria for the diagnosis.

In summary, we report a case of lateral medullary syndrome with myoclonic spasms. The patient had a history of cervical spinal injury and received general surgery in the prone position. Whether vertebral arterial disease is more frequent in this group of patients cannot be concluded, but the prone position and general anesthesia potentially increase the incidence of complications. Anesthesiologists should be aware of this hazard and make a quick diagnosis. Once the diagnosis is established, anticoagulation therapy should be instituted accordingly. The outcome of our patient was favorable.

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References

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© 2002 International Anesthesia Research Society