Guillain–Barré Syndrome Presenting as Acute Flaccid Paralysis in a Child A Case Report

Guillain-Barré syndrome (GBS) is an uncommon, acute, inflammatory, immune-mediated disorder affecting the nerve roots and peripheral nerves, and it can be potentially life-threatening. It is recognized worldwide as a neuromuscular emergency and represents the most frequent cause of acute flaccid paralysis unrelated to poliovirus infection. Clinically, GBS commonly presents as a symmetrical, ascending sensorimotor weakness that begins with distal paraesthesia’s, progresses to weakness in the lower limbs, and may extend to the upper limbs and cranial nerves¹.

Acute flaccid paralysis (AFP) is a neurological condition marked by the sudden onset of weakness or paralysis in one or more limbs, and in some cases, the respiratory or bulbar muscles, along with reduced muscle tone, without any clear identifiable cause².

Most studies that estimate incidence rates of Guillain-Barré syndrome were done in Europe and North America, and showed a similar range of 0·8–1·9 (median 1·1) cases per 100?000 people per year.¹⁵ The annual incidence rate of Guillain-Barré syndrome increases with age (0·6 per 100?000 per year in children and 2·7 per 100?000 per year in elderly people aged 80 years and over) and the disease is slightly more frequent in males than in females. Seasonal fluctuations, presumably related to variations in infectious antecedents, have been reported, but these observations are rarely statistically significant³.Top of Form

Guillain–Barré syndrome (GBS) is suspected in patients presenting with rapidly progressive bilateral limb weakness, often accompanied by sensory disturbances and diminished or absent deep tendon reflexes. Cranial nerve involvement, including facial weakness or bulbar palsy, as well as ophthalmoplegia and ataxia, may further support the clinical suspicion⁴

Guillain–Barré syndrome demonstrates considerable clinical variability in its presentation. In most patients, symptoms develop approximately 1–2 weeks following a preceding event, commonly an infectious illness, and progress to peak severity within two weeks. A very rapid progression within 24 hours or continued worsening beyond four weeks should prompt consideration of alternative diagnoses. Typically, the disease enters a plateau phase within one to four weeks after onset¹.

The diagnosis of GBS is primarily clinical and is established by fulfilling recognized diagnostic criteria while carefully excluding alternative causes of acute flaccid paralysis. Supportive investigations include routine laboratory tests to rule out other etiologies, cerebrospinal fluid (CSF) examination demonstrating characteristic findings, and electrophysiological studies to confirm peripheral nerve involvement and determine the subtype⁴.

Intravenous immunoglobulin and plasma exchange are equally efficacious treatments for GBS⁵

Case Presentation

Patient Information

A 12-year-old male child was admitted to the Pediatrics Department at Karnataka Medical College and Research Institute (KMCRI), Hubballi on 2 January 2026 with complaints of weakness in both lower limbs for 2 days.

History of Presenting Illness

The child was apparently normal two days prior to admission. Subsequently, he developed sudden onset weakness in both lower limbs which gradually progressed. Initially, he experienced pain in both lower limbs, followed by difficulty in walking. By the day of admission, the child was unable to stand independently.

The weakness gradually progressed and involved the right upper limb, resulting in difficulty climbing stairs. There was a history of fever one week before the onset of weakness, which lasted for one day and subsided with symptomatic treatment. After the febrile episode, the child experienced difficulty in getting up from a sitting position and climbing stairs.

There was no history of vomiting, loose stools, headache, convulsions, slurred speech, deviation of mouth angle, abnormal movements, loss of consciousness, head injury, or limb trauma. The child had no bowel or bladder incontinence, no recent vaccination, and no history of drug intake. There was no difficulty in breathing or performing fine motor activities such as writing or buttoning clothes. No diurnal variation of symptoms was reported.

Clinical Examination

Vital Signs

On admission, the patient’s vital parameters were stable:

• Temperature: 36.8°C
• Pulse rate: 96 beats/min
• Respiratory rate: 24 breaths/min
• Blood pressure: 94/60 mmHg
• Oxygen saturation: 99% on room air
• Glasgow Coma Scale: E4 V5 M6 (15/15)

General Physical Examination

The child was conscious, cooperative, and oriented to time, place, and person. No pallor, icterus, cyanosis, clubbing, lymphadenopathy, or edema were observed.

Anthropometric measurements:

• Height: 130 cm
• Weight: 24.9 kg
• BMI: 14.7 kg/m²

No skeletal abnormalities were noted. Developmental milestones were appropriate for age, and immunization status was up to date.

Systemic Examination

Neurological Examination

• Cranial nerves: Normal
• Motor power:

• Upper limbs: 4/5
• Lower limbs: 2/5

• Muscle tone: Decreased
• Deep tendon reflexes: Diminished

Cardiovascular, respiratory, and abdominal examinations were within normal limits.

Investigations

Cerebrospinal Fluid Analysis

CSF examination revealed clear and colorless fluid with normal glucose levels, elevated protein (226 mg/L), and a normal cell count (3 cells/cumm), indicating albuminocytological dissociation, a characteristic finding in Guillain–Barré syndrome.

Gram stain, AFB stain, and CSF culture were negative, ruling out bacterial and tubercular meningitis.

Routine hematological and biochemical investigations were within normal limits except for mild hyponatremia, which may occur due to syndrome of inappropriate antidiuretic hormone secretion (SIADH) in Guillain–Barré syndrome.

Nerve Conduction Study

Nerve conduction study demonstrated reduced compound muscle action potential (CMAP) amplitude in the right peroneal nerve with preserved conduction velocity and distal latency. Sensory nerve conduction parameters were normal, and F-wave latencies were within normal limits. These findings suggested right peroneal motor axonopathy without evidence of demyelination.

CT Cerebral and Neck Angiography

CT cerebral and neck angiography revealed patent extracranial and intracranial vessels without evidence of stenosis, occlusion, or aneurysm. No intracranial hemorrhage or acute infarction was observed, thereby excluding a vascular cause of acute limb weakness.

Management

The patient was treated with intravenous immunoglobulin (IVIG) at a dose of 400 mg/kg/day for 5 consecutive days. The infusion was administered over six hours with close monitoring of vital parameters. No infusion-related adverse reactions were observed.

During the first 48–72 hours of therapy, the patient showed progression of flaccid weakness predominantly affecting the lower limbs. However, there was no respiratory compromise, bulbar weakness, or significant autonomic instability.

Due to the risk of autonomic complications, the patient was monitored in the High Dependency Unit (HDU) but did not require ventilatory support.

Table 1: Management and Clinical Course of the Patient

Table 2: Clinical Course During Hospital Stay