Diagnose It Answer — April 29, 2026
ALL CLUES
31-year-old female presents with progressive bilateral leg weakness over the past 5 days that has now spread to her arms and hands. She states she 'can barely walk' and dropped her phone this morning because she couldn't grip it. She also reports tingling and numbness in her feet and fingertips. She came in today when she noticed she was having difficulty swallowing.
Three weeks ago she had a 4-day illness with diarrhea, cramping, and low-grade fever that resolved on its own — she did not seek treatment. No recent travel outside the country, but she attended a beach barbecue where she ate undercooked chicken. No significant past medical history. No current medications. No family history of neurological disease.
BP 138/86 mmHg (lying), 112/72 mmHg (standing) — significant orthostatic drop of 26 mmHg systolic, consistent with autonomic dysfunction. HR 108 bpm (sinus tachycardia with HR variability noted on monitor). RR 18 breaths/min, SpO2 97% on room air. Patient is in no acute respiratory distress currently, but is visibly frightened. Bedside spirometry: FVC 2.4L (normal predicted 3.6L — 67% of predicted).
Ascending symmetrical weakness on neurological exam: lower extremity strength 2/5 proximally and distally, upper extremity 3/5 bilateral. Deep tendon reflexes absent bilaterally — areflexia throughout. Cranial nerve exam: dysarthria (CN X) and mild bilateral facial weakness (CN VII). Sensory: stocking-glove distribution numbness. No bladder/bowel involvement. Neurology consulted immediately. ICU admission planned for respiratory and autonomic monitoring. Serial FVC every 4 hours — intubation threshold: FVC <20 mL/kg, NIF weaker than -25 cmH2O, or SpO2 decline.
CSF analysis (lumbar puncture): protein 186 mg/dL (markedly elevated; normal 15–45 mg/dL), WBC 2 cells/µL (normal), glucose normal — the classic albuminocytologic dissociation of GBS. Stool culture: Campylobacter jejuni identified (likely antecedent trigger). Anti-ganglioside antibodies (anti-GM1): positive. Nerve conduction studies: markedly reduced motor nerve conduction velocities and absent F-waves — consistent with demyelinating neuropathy. MRI spine: no cord compression or intrinsic cord lesion. IVIG 0.4 g/kg/day x5 days initiated.
Guillain-Barré Syndrome is an acute immune-mediated polyneuropathy most commonly triggered by Campylobacter jejuni enteritis, influenza, or other infections. The hallmark is ascending symmetrical flaccid weakness with areflexia, and the CSF shows elevated protein with a normal white cell count — the albuminocytologic dissociation. The most feared complication is respiratory failure from intercostal and diaphragm weakness, occurring in up to 30% of patients; serial FVC measurement and autonomic monitoring are the most critical nursing responsibilities. IVIG and plasmapheresis are equally effective treatments; there is no role for corticosteroids.
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