Aetiology

Essential hypertension that is either undiagnosed or inadequately treated is a common cause of hypertensive emergency.[12][21][22][23] Another common cause is secondary and resistant hypertension.

System disorders that can lead to a presentation of hypertensive emergency include:

  • Renal disease (underlying chronic disease, renal artery stenosis, acute glomerulonephritis, collagen-vascular diseases, kidney transplantation)[24][25][26][27][28][29][30]

  • Neurological (head trauma, spinal cord injury, autonomic dysfunction)[31]

  • Respiratory (obstructive sleep apnoea)[32][33][34]​​

  • Immunological (scleroderma, vasculitis)[31]

  • Endocrine (primary aldosteronism, phaeochromocytoma, thyroid disorder, Cushing's syndrome, acromegaly, hyperparathyroidism, carcinoid tumour, congenital adrenal hyperplasia, or renin-secreting tumour).[31][35][36]​​[37]

Pregnancy-related pre-eclampsia, HELLP (haemolysis, elevated liver enzymes, low platelets) syndrome, and eclampsia are also important causes of hypertensive emergency in women.[31]

Lifestyle choices should also be considered when trying to determine the potential cause of a hypertensive emergency as excessive dietary salt intake, obesity, and/or alcohol consumption can all contribute to hypertension.[38]​ A thorough medication history must also be obtained as hypertension can be induced or exacerbated by certain medications, including non-steroidal anti-inflammatory drugs, oral contraceptives, sympathomimetics, illicit drugs, glucocorticoids, mineralocorticoids, calcineurin inhibitors, erythropoietin, herbal supplements, vascular endothelial growth factor inhibitors, and inadvertent drug or food interactions with monoamine oxidase inhibitors.[7]​[31][39]

Pathophysiology

The factors that lead to the development of hypertensive emergency are poorly understood. A rise in systemic vascular resistance, resulting from a combination of humoral vasoconstrictor increase and autoregulatory failure, initiates the cycle. The subsequent increase in blood pressure generates mechanical stress and endothelial injury leading to increased permeability, activation of the coagulation cascade and platelets, deposition of fibrin, and inflammatory cytokine induction. These processes result in ischaemia and the release of additional vasoactive mediators, generating ongoing injury. Volume depletion caused by pressure natriuresis and activation of the renin-angiotensin system often leads to further vasoconstriction. Systemic vasoconstriction leads to decreased blood flow to vital organs and the subsequent end-organ injury that is the hallmark of hypertensive emergency. End-organ injury primarily affects the neurological, cardiac, and renal systems.[39][40][41][42][43][44][45]

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