Hypertensive Crisis
This clinical presentation is characterised by an uncontrolled high blood pressure (BP) of systolic >180mmHg leads to progressive or impending end-organ dysfunction.
The treatment focuses on lowering BP aggressively over minutes to hours.
Neurologic end-organ damage due to uncontrolled BP may include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, cerebral haemorrhage.
Cardiovascular end-organ damage may include myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and/or aortic dissection.
Renal injury, retinopathy and even Microangiopathic Haemoliyic Anaemia can also occur.
For those being treated for essential hypertension, antihypertensives, have offered tremendous value. The advent of crisis sits at about 1% of patients with hypertension.
Before 1950, hypertension leading to crisis demonstrated a Proor prognosis with 1-year survival rate at 20%. Today with monitoring and a medicine cupboard full of innovative anti hypertensives, stats report a survival rate of more than 90%.
The most common clinical presentations of hypertensive emergencies are stroke (24.5%) and pulmonary Oedema (22.5%), but CCF and cerebral encephalopathy are in high numbers.
In pregnant patients, acute hypertensive crisis usually results from severe pregnancy induced hypertension (preeclampsia).
In assessing the presentation of hypertensive crisis, the severity of the patient’s preexisting hypertension , and the duration of their HTN needs to be factored into treatment strategy. A drug history of antihypertensives, patient compliance, use of over-the-counter (OTC) and recreational preparations such as caffeine, red bull, decongestants, Salbutamol, and , illicit drugs such as MDMA, methamphetamine and cocaine are all important, as these preps exacerbate hypertension.
The physical examination should assess whether end-organ dysfunction is present. BP should not only be measured in both the supine position and the standing position (assess volume depletion), but it should also be measured in both arms (a significant difference may suggest aortic dissection).
The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive emergency. Evaluate for the presence of heart failure, which may be indicated jugular venous distention, crackles on auscultation, and peripheral edema. Central nervous system (CNS) findings may include changes in the patient's level of consciousness and visual fields, and/or the presence of focal neurologic signs. Abdominal masses or bruits may be noted.
Renal impairment is a likely consequence of hypertensive crisis as increasing renal vessel pressure bombards the glomerulus with more molecules of protein, causing injury. Blood testing UECs to assess renal function is common. A dipstick urinalysis to detect haematuria or proteinuria and microscopic urinalysis to detect red blood cells (RBCs) is an intervention we should perform at the bedside.
A full blood cell (FBC) obtained to exclude microangiopathic anemia, and pregnancy test, and endocrine testing may be obtained.
ECG is needed if only for a baseline, and if any headache, or CNS signs are apparent , a head CT scan is considered.
One presentation is malignant hypertension.
This hypertensive emergency, always has retinal papilloedema as well as flame-shaped haemorrhages. Often there is features of LVF manifesting as pulmonary oedema which masks the initial cause.
Treatment of hypertensive crisis involves reduction of BP.
You've probably noticed that many patients have big BPs and some we treat aggressively, whereas others we tend to no be so reactive. The reality is that only a small proportion of patients will require emergency treatment. As always an important point to remember in the management of the patient with any degree of BP elevation is to "treat the patient and not the number."
We aim to identify which patients with acute hypertension have symptoms of end-organ damage. It is these that require immediate mitigation of their hypertension. Usually IV therapy is initiated with agents like sodium nitroprusside, glyceryl trinitrate or a short acting alpha and beta-blocker, or calcium channel blockers.
The aim is to increase vessel diameter to decrease vessel pressure. Reducing afterload is the target.
With patients presenting with acutely elevated BP (systolic BP [SBP] >200 mm Hg or diastolic BP [DBP] >120 mm Hg) without symptoms and whose BP stays significantly elevated should have initiation of medical therapy and close follow-up in the outpatient or GP setting.
So crisis management is really about symptoms.
