Neurogenic Pulmonary Oedema
Dr John Griffiths DICM MRCP FRCA MA
Neurogenic pulmonary oedema is a widely recognised complication of major neurological events in both adults and children. Neurogenic pulmonary oedema was first reported in association with status epilepticus in 1908 and with head injury in 1918. It is most frequently associated with intracranial haemorrhage, notably subarachnoid haemorrhage (SAH).
Focus on neurogenic pulmonary oedema in association with SAH
In one large study of SAH associated with aneurysmal rupture, neurogenic pulmonary oedema was reported in 23% of patients, the majority developing oedema between days 0-7. This value was comparable to the proportion of deaths attributed to the direct effects of the initial haemorrhage (19%), rebleeding (22%) or vasospasm (23%). Those patients who were greater than 30 years old had an increased frequency of pulmonary oedema but there was no correlation with previous lung or cardiac disease or with the use of “triple H therapy” (Hypertension, Hypervolaemia and Haemodilution). Poor clinical grade at the time of admission was also associated with a higher frequency of respiratory dysfunction, suggesting that neurogenic influences are involved in the aetiology of the pulmonary oedema.
Focus on the pathophysiology of neurogenic pulmonary oedema
Neurogenic pulmonary oedema is characterised by fulminant pulmonary oedema that develops rapidly after CNS injury. Proposed pathophysiological mechanisms involve massive central sympathetic neural discharge, causing peripheral vasoconstriction and displacement of blood from the periphery to the heart and pulmonary vascular bed. The resultant increase in pulmonary capillary pressure predisposes to oedema formation. The effect of hydrostatic pressure is then compounded by pressure-induced endothelial damage. Hence, pulmonary oedema may be due to either increased pulmonary capillary permeability with normal pulmonary artery occlusion pressure or to left ventricular dysfunction with increased pulmonary artery occlusion pressure, or a mixture of the two.
Focus on myocardial dysfunction in association with neurogenic pulmonary oedema
Various reports in the literature suggest that patients who develop profound myocardial dysfunction (e.g. ejection fraction <20-30%) merit active and aggressive early treatment and invasive monitoring, as a good clinical outcome is likely. Hypotension and hypoxaemia may aggravate the neurological injury and must be rapidly corrected. Reports exist in the literature of the successful use of inotropes, pulmonary artery flotation catheters and serial TOE in the management of profound myocardial dysfunction in association with neurogenic pulmonary oedema. Measurement of pulmonary artery occlusion pressure and cardiac output permits logical selection and titration of inotropes, and may prevent inappropriate fluid restriction and diuretic therapy, both of which may further reduce cardiac output. Careful monitoring of haemodynamic variables also allows “triple H” therapy for the treatment of vasospasm while monitoring myocardial function.
The reported duration of myocardial dysfunction associated with neurogenic pulmonary oedema varies enormously. Inotropic therapy has been required for 3-29 days. However, good recovery of myocardial function occurred in all cases. One report describes the use of an intra-aortic balloon pump to facilitate the discontinuation inotropes and vasopressors within 24 hours. Prone ventilation has been used successfully to treat life-threatening hypoxia and in optimising neurological recovery.
Focus on myocardial dysfunction associated with SAH
SAH is often associated with significant ECG changes. Symmetrical T wave inversion and severe QTc prolongation (>500 ms) have been reported and are associated with left ventricular dysfunction (100% sensitivity, 81% specificity). Abnormal wall motion is also associated with borderline CKMB elevation (2-5%) and poor neurological grade.
Contraction band necrosis and myofibrillar degeneration are common cardiac pathological findings in patients with SAH. Contraction band necrosis involves the left ventricle in a diffuse pattern, with multifocal microscopic lesions that primarily involve the endocardium. Contraction band necrosis is rarely found if the patient survives longer than 2 weeks, presumably because the changes are reversible. Contraction band necrosis is indicative of a hyper-contracted state. Catecholamine infusions, CNS stimulation, autonomic discharge associated with stress and reperfusion of transiently ischaemic muscle have all been shown to give rise to identical lesions. Echocardiogram studies in SAH patients with evidence of myocardial dysfunction have demonstrated the development of widespread areas of hypokinesia or akinesia that extend beyond the territory of a single coronary artery. All akinetic or hypokinetic segments progressively normalise over a period of weeks. Figure 1 provides an example of a management algorithm for the management of myocardial dysfunction associated with SAH.
Figure 1. Example of clinical algorithm for the management of left ventricular dysfunction in patients with SAH
(Adapted from Mayer et al 1995)
Key learning points
• Neurogenic pulmonary oedema is commonly seen in association with neurological insult
• Neurogenic pulmonary oedema is associated with various degrees of myocardial dysfunction
• Myocardial dysfunction associated with neurogenic pulmonary oedema should be managed aggressively, as cardiovascular and neurological recovery is likely
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