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Paeds Vivasneurology-neurodisability-and-neuromuscular

Paeds Vivas · neurology-neurodisability-and-neuromuscular

Acute neuromuscular respiratory failure: Viva

Branching clinical structured oral on paediatric acute neuromuscular respiratory failure covering the respiratory pump and the two mechanisms of failure, the bedside forced vital capacity, maximum inspiratory pressure, and maximum expiratory pressure monitoring with the Lawn twenty-thirty-forty thresholds and the Durand and Sharshar predictors, the airway decision between non-invasive ventilation and intubation, the avoidance of suxamethonium and use of rocuronium, the differential across the motor unit, the disease-specific therapy for Guillain-Barre syndrome, myasthenic crisis, and infant botulism, and the long-term ventilation decision in chronic disease.

branching clinical structured oral3 min readVerification in progress

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RACP DWERACP DCEMRCPCH Clinical
Prompt
A previously well 7-year-old boy presents with progressive ascending weakness over 4 days after a viral illness. He is unable to walk, speaks in short sentences, and has a weak cough with pooled secretions. Examination shows symmetrical flaccid weakness, absent reflexes, and no sensory level. His forced vital capacity is 16 mL per kilogram, down from 24 mL per kilogram six hours ago, and his oxygen saturation is 98 percent on room air. The examiner asks why the saturation is normal, how you monitor and decide when to intubate, what drug you avoid and what you use, how you run the differential, and what you tell the family.

Q1. Why is his saturation 98 percent when he is clearly failing?

Because neuromuscular respiratory failure is a failure of the respiratory pump, not the lungs. The lung tissue is structurally normal, so the alveoli that are still ventilated continue to oxygenate the blood reaching them and the saturation stays high. What fails is the bellows: the weak diaphragm and intercostals move less air, so carbon dioxide climbs while oxygenation is preserved. The saturation is therefore reassuring in the wrong direction, and the child can arrest with a normal saturation. [4][1]

Probe: So what does the saturation tell you? It tells me almost nothing useful at this stage. I drive the decision from the bedside forced vital capacity and the bulbar assessment, never from the saturation or a single blood gas, which are both late and confirmatory. [3]

Q2. How do you monitor him, and at what point do you intubate?

I measure serial bedside spirometry every two to six hours, recording forced vital capacity, maximum inspiratory pressure, and maximum expiratory pressure, plotting them on a trend, and acting on the Lawn thresholds. A forced vital capacity under 20 mL per kilogram, a fall of over 30 percent in twenty-four hours, a maximum inspiratory pressure weaker than minus 30 cmH2O, and a maximum expiratory pressure under 40 cmH2O each predict the need for ventilation. He meets them all, so I intubate now. [1][2]

Probe: What if the bulbar function were intact? Then I could trial non-invasive bilevel positive airway pressure for pure pump failure, with cough augmentation and close spirometry, intubating only if it failed or bulbar weakness developed. But this child has bulbar weakness, so the mask will not protect his airway, and the answer is intubation. [9]

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References6ShowHide
  1. [1]Lawn ND, Fletcher DD, Henderson RD, et al. Anticipating mechanical ventilation in Guillain-Barré syndrome Arch Neurol, 2001.PMID 11405803
  2. [2]Durand MC, Porcher R, Orlikowski D, et al Clinical and electrophysiological predictors of respiratory failure in Guillain-Barré syndrome: a prospective study Lancet Neurol, 2006.PMID 17110282
  3. [3]Sharshar T, Chevret S, Bourdain F, Raphaël JC Early predictors of mechanical ventilation in Guillain-Barré syndrome Crit Care Med, 2003.PMID 12545029
  4. [4]Bach JR, Turcios NL, Wang L Respiratory Complications of Pediatric Neuromuscular Diseases Pediatr Clin North Am, 2021.PMID 33228931
  5. [9]Wijdicks EF, Roy TK BiPAP in early guillain-barré syndrome may fail Can J Neurol Sci, 2006.PMID 16583732
  6. [10]Martyn JA, Richtsfeld M Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms Anesthesiology, 2006.PMID 16394702
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