AJA Asian Journal of Anesthesiology

Advancing, Capability, Improving lives

Articles in Press
Che-Hsien Chang 1 , Shiao-Pieng Lee 2 , Yi-Hsuan Huang 3 , Wei-Hung Chan 3


To the Editor,

Guillain-Barré syndrome (GBS) is an immune-related polyneuropathy typically characterized by progressive muscular weakness, paresthesia, and areflexia. It is usually precipitated by recent infection; however, it could also be an uncommon postoperative neurologic complication.1,2 Acute motor and sensory axonal neuropathy (AMSAN), which manifests additional sensory disturbance, is a rare axonal subtype of GBS with a more serious course and slow recovery. Prognosis may be poor without early diagnosis and proper treatment. To the best of our knowledge, patients with spinal, bones, or digestive organ surgeries were at increased risk for GBS.2,3 However, AMSAN following oral cavity cancer surgery was not reported previously. Here, we present a female patient with oral cavity cancer developed AMSAN after cancer surgery.

A 74-year-old female (150 cm, 56 kg) has hypertensive cardiovascular disease, type 2 diabetes mellitus with medication control and history of old cerebral infarction with right hemiparesis 5 years ago (muscle powers: grade 4 in right upper and lower limb; grade 5 in left upper and lower limb). She was diagnosed adenoid cystic carcinoma of right mouth floor and received wide excision, right suprahyoid neck dissection and radical forearm flap reconstruction under general anesthesia. Anesthesia was induced using intravenous fentanyl (2 μg/kg), 2% lidocaine (1 mg/kg) and propofol (2 mg/kg). Cisatracurium (0.15 mg/kg) was given after lost consciousness, followed by tracheal intubation. Sevoflurane (2%) was used for maintenance of anesthesia and repetitive bolus injections of cisatracurium were prescribed as required throughout the procedure. However, the patient did not receive neuromuscular monitor during the procedure. After surgery, she was transferred to the intensive care unit for the following care. She regained consciousness and four limbs movement thirty minutes later. Autonomic dysfunction (hypertension) which required intravenous calcium channel blocker treatment developed on postoperative day four. Weakness of four limb muscles developed one week later. Although the patient passed weaning profiles and was successfully extubated, quadriparesis and dysesthesia progressed. The patient was less likely to develop critical illness polyneuropathy (CIP) or critical illness myopathy (CIM) because no neuromuscular blocking agents or corticosteroids were prescribed after surgery and no obvious infection source or sepsis was identified. On neurological examination, upper and lower limbs muscle powers were estimated to be grade 1 with decreased deep tendon reflexes and absent of Babinski’s sign. Magnetic resonance image (MRI) of cervical spine revealed mild disk bulging at C4–5 and C6–7. MRI of brain showed senile brain atrophy with old lacunar infarcts. Nerve conduction velocity (NCV) and electromyogram (EMG) of upper and lower limbs indicated polyneuropathies (axonal type, no acute denervation) with chronic lower cervical and lumbar radiculopathies. She received lumbar puncture and cerebrospinal fluid (CSF) analysis. The results showed elevated protein level (66 mg/dL) and albuminocytological dissociation. The AMSAN variant of GBS was finally diagnosed by the neurologist. After intravenous immune globulin (IVIG, 0.4 g/kg bodyweight) treatment for 5 days and 5 times of plasma exchange, symptoms subsided and muscle power of all limbs regained to grade 3–4. The patient was transferred to the ordinary ward and discharged one month later.

In conclusion, postoperative AMSAN is a rare but potentially life-threatening complication without early recognition. It is easily overlooked and misdiagnosed as cerebral vascular accident, CIP/CIM,4 or cervical myelopathy in intensive care unit especially in postoperative patients presenting progressive muscular weakness. In this case, old age,2 cancer,5 and surgery1-3 may alter the balance of the immune system and predispose to the development of AMSAN. A thorough assessment of the underlying causes of neuromuscular weakness is necessary because the underline diseases may complicate a differential diagnosis and exacerbate her weakness. Investigations including MRI, NCV/EMG, and CSF studies facilitate confirming the diagnosis and early intervention. Plasma exchange and IVIG are effective treatments to relieve symptoms and shorten the clinical course.


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