Key result
Autonomic dysreflexia-induced acute pulmonary oedema resolves with prompt oxygen and intravenous furosemide.
Why the study?
Autonomic dysreflexia is a life-threatening complication in spinal cord injuries at or above the sixth thoracic level that is characterized by episodic hypertension and can cause serious cardiovascular and respiratory complications.
Case Report (n=1)
No
This case highlights the importance of recognizing a clinically meaningful rise from baseline blood pressure as probable autonomic dysreflexia when a patient with high-level spinal cord injury develops acute pulmonary oedema and hypercapnic respiratory failure, particularly in the presence of underlying HFpEF and recent intravenous fluid administration.
Answers are grounded in this paper and cite their sources.
May link autonomic dysreflexia to pulmonary oedema in tetraplegia; single case leaves open need for prospective validation.
Autonomic dysreflexia is a life-threatening complication affecting individuals with spinal cord injuries at or above the sixth thoracic level.While episodic hypertension is its clinical hallmark, serious cardiovascular and respiratory complications may occur.We report the case of a 67-year-old male with long-standing C5-C6 tetraplegia and established autonomic dysreflexia who was admitted with community-acquired pneumonia (CAP).At approximately 01:00 on hospital day 4, after receiving approximately 3 L of maintenance intravenous fluid for poor oral intake over the preceding 72 hours, he developed sudden severe breathlessness and loss of consciousness despite a previously improving oxygen requirement.Oxygen saturation fell to 77% despite oxygen therapy, while systolic blood pressure rose from a baseline of approximately 125-130 mmHg to 167 mmHg.Physical examination revealed bilateral crackles and reduced air entry.Arterial blood gas analysis showed profound hypercapnic acidaemia (pH 7.009; partial pressure of carbon dioxide 18.5 kPa).A chest radiograph showed rapidly progressive bilateral airspace opacities consistent with pulmonary oedema.His blood pressure returned towards baseline, and following highconcentration oxygen and intravenous furosemide, his oxygen requirement subsequently decreased.Computed tomography pulmonary angiography excluded pulmonary embolism, and echocardiography showed low-normal left ventricular systolic function without a major structural or valvular abnormality.The sudden respiratory deterioration, clinically significant rise in blood pressure from baseline, rapid radiographic evolution, and subsequent improvement supported acute pulmonary oedema occurring during a probable autonomic dysreflexic episode.No discrete precipitating stimulus was confirmed, although concurrent pneumonia was considered the most likely trigger for autonomic dysreflexia.Recent intravenous fluid administration and underlying cardiac vulnerability may have lowered the threshold for pulmonary oedema.This case highlights the importance of recognising a clinically meaningful rise from baseline blood pressure when a patient with high spinal cord injury develops sudden respiratory deterioration.
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Ghannoum et al. (2026) conducted a case report in Acute pulmonary oedema and hypercapnic respiratory failure during a probable autonomic dysreflexic episode in chronic cervical spinal cord injury (n=1). Probable autonomic dysreflexic episode (managed with high-concentration oxygen and intravenous furosemide) was evaluated on Acute pulmonary oedema and hypercapnic respiratory failure resolution. Probable autonomic dysreflexia (SBP rising from 125-130 to 167 mmHg) coincided with acute pulmonary oedema and hypercapnic acidaemia, resolving after oxygen and furosemide.
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