Medical Case: Infective Polyneuritis

Infective Polyneuritis

Dr. Chibitam Hope Obia., MBBS


Medical Case Details:

A 26-year-old male presented with weakness and pain in both lower limbs for 2-3 days, along with tingling and weakness sensation in his hands since this morning. His bladder and bowel habits were normal. There was no history of any recent infection or fever. HR (heart rate): 66/min, BP (blood pressure): 110/90 mmHg, SpO2 (Saturation of Peripheral Oxygen): 98%, deep tendon reflexes absent, and weakness of forehead muscles were present.

Immediate Management: On admission to the ICU, the following treatments were given: an 18-gauge IV (intravenous) catheter was secured, and NS (normal saline) was initiated at 100 ml/hr. Inj. Pantocid (Pantoprazole) 40 mg IV was administered, Inj. Methylprednisolone 1gm IV was given, and a nasogastric tube was inserted. Nerve Conduction Velocity, EMG (Electromyogram), CSF (cerebrospinal fluid), and MRI (magnetic resonance imaging) were planned, along with routine lab investigations.

Data: ABG (arterial blood gas) Value Range - Hb 14.1 (13-17 gm%), WBC 18400 (4000-11000 cells/mm3), Platelets - 1.53 (1.5-4.0 lacs/mm3), Serum Na (Sodium) 137.5 (135-145 mmol/L), Serum K (Potassium) 4.08 (3.5- 4.5 mmol/L), Serum Creatinine 0.95 (0.8-1.3 mg/dl), Random blood sugar - 86 (82 -110 mg/dL), CPK 277 (35-232 U/L), Serum Vitamin B12 494.3 (174-878 pg/ml), HIV - Negative, ESR (Erythrocyte sedimentation rate) - 06 (0-15 mm/hr). His ABG was within normal limits (no CO2 retention), MRI did not show any signs of demyelination, nerve conduction studies and EMG were suggestive of early demyelinating neuropathy, and NMJ (neuromuscular junction) disorder was ruled out. The CSF was normal.

Course in ICU: The patient was treated on the lines of GBS (Guillain–Barré syndrome) with intravenous immunoglobulin and supportive care. A careful watch was kept on his respiratory functions by daily ABGs to monitor CO2 retention, and intensive physiotherapy was administered. The facial muscle weakness continued to persist and increased for the next two days, followed by gradual improvement. The patient responded to treatment and was shifted to the ward on the 9th day.

Focused Discussion: Focus on clinical symptoms and signs, especially involvement of cranial nerves. Symmetric weakness is the major symptom of GBS (Infective polyneuritis). It may be either proximal or distal at onset and usually begins in the lower extremities. The weakness classically progresses in an ascending manner, involving first the lower and then the upper extremities, and finally the CNS (central nervous system) within 1-3 days of symptom onset. The weakness does not ascend in all cases. However, subjective and objective sensory disturbances (numbness or paresthesias) of brief duration are common initially and may be the presenting complaint. These dysesthesias most commonly occur in a distal (stocking-glove) distribution. Muscle pain or tenderness is also an early symptom in about half of cases. Absence of deep tendon reflexes (or, rarely, only distal areflexia with definite hyporeflexia of biceps and knee jerks) almost always occurs by the time of presentation to a physician. CN (cranial nerve) involvement is common. The involvement of every nerve except CNs I and II (olfactory and optic) has been described. The nerve most commonly affected is CN VII (facial); facial weakness (usually bilateral) occurs in half of the cases. CN palsies may be the most prominent feature of the illness, as in the Guillain-Barre variant of ophthalmoplegia, ataxia, and areflexia (Miller-Fisher Syndrome). Peripheral autonomic nervous system involvement may also occur and manifest as hypertension, tachycardia, facial flushing, postural hypotension, and ECG (electrocardiogram) changes. Respiratory musculature weakness requiring assisted ventilation occurs in 25% of cases.

Note: In our case, the facial nerve involvement leading to weakness of forehead muscles, which caused an inability to raise the eyebrows properly, was confused (wrongly interpreted) with ptosis, and initially, it was confused with myasthenia gravis.

Influence on Future Management: Before this case, I was of the opinion that cranial nerves are not involved in GBS. In fact, the facial weakness in our patient prompted me to consider myasthenia gravis as the first diagnosis. From the next time, I will not confuse ptosis with facial weakness.

Reference: Oh’s Intensive Care manual 6th edition, Harrison’s Principles of Internal Medicine 18th edition.


Are You a Doctor?

Please Login to comment or ask a question.

New to iCliniq? Sign Up Now