Acute Subdural Hematoma Causing Neurogenic Pulmonary Edema Following Lumbar Spine Surgery

Delayed onset of neurogenic pulmonary oedema following an evolving ischaemic stroke

“…NPO usually arises rapidly within the first few hours of presentation, particularly in the setting of traumatic brain injury and acute intracranial haemorrhage, as highlighted in table 1 3 11 12 14. We found one case report of delayed NPO occurring 4 days after the onset of subarachnoid haemorrhage; however, at that time, there was angiographic evidence of significant cerebral arterial spasm which could have triggered the NPO 10.…”

“…Severe traumatic brain injury, intracranial haemorrhage and seizures are the commonly reported neurological insults associated with NPO (table 1). 9–17 On the other hand, ischaemic stroke is a relatively rare trigger. The provoking infarction is usually large and clinically significant, often requiring intravenous thrombolysis or neurosurgical intervention 18–20.…”

“…NT-proBNP levels in the setting of NPO has been reported either as normal, moderately raised between 350 and 480 pmol/L similar to our case or above 900 pmol/L (table 1). 13 14 20 Indeed, Takotsubo cardiomyopathy (ie, stress-induced or broken-heart syndrome) can also occur concurrently with NPO since it also shares the pathophysiology of sympathetic overactivation and catecholamine surge, which can cause direct myocardial toxicity. This was illustrated in a case following right insular cortex infarction 27.…”

Ictal Mammalian Dive Response: A Likely Cause of Sudden Unexpected Death in Epilepsy

“…If this is true, the possibility arises that “spontaneous” neurogenic pulmonary edema is not actually spontaneous, but instead, is triggered by unwitnessed , prolonged apneic GTCS. After all, this form of pulmonary edema is often reported in patients who are found unconscious or with different degrees of altered mentation (i.e., possibly postictal) before being transported to the hospital, and who harbor epileptogenic pathologies, such as brain tumors ( 119 ), hydrocephalus ( 120 ), subdural hematomas ( 121 ), strokes ( 122 ), and subarachnoid hemorrhages ( 123 , 124 ). Similarly, GTCS often induce a short-lived lactic acidosis ( 101 , 102 ), which is comparable to that displayed by air-breathing aquatic mammals ( 34 ), and humans ( 61 ), surfacing from long dives.…”