The initial reduction to a diastolic pressure of approximately 100 mmHg is often associated with a modest worsening of renal function; this change, however, is typically transient as the vascular disease tends to resolve and renal perfusion improves over one to three months. Antihypertensive therapy should not be withheld in this setting unless there has been an excessive reduction in BP. A change in medication, however, is indicated if the decline in renal function is temporally related to therapy with an angiotensin (ACE) converting enzyme inhibitor or angiotensin II receptor blocker, which can interfere with renal autoregulation and produce acute kidney failure in patients with bilateral renal artery stenosis. (See "Renal effects of ACE inhibitors in hypertension". )ref
Several parenteral antihypertensive agents are most often used in the initial treatment of malignant hypertension. Nitroprusside – an arteriolar and venous dilator, given as an intravenous infusion. Nitroprusside acts within seconds and has a duration of action of only two to five minutes. Thus, hypotension can be easily reversed by temporarily discontinuing the infusion, providing an advantage over the drugs listed below. However, the potential for cyanide toxicity limits the prolonged use of nitroprusside, particularly in patients with chronic kidney disease. Nicardipine – an arteriolar dilator, given as an intravenous infusion. Clevidipine – a short-acting dihydropyridine calcium channel blocker. It reduces blood pressure without affecting cardiac filling pressures or causing reflex tachycardia. Labetalol – an alpha- and beta-adrenergic blocker, given as an intravenous bolus or infusion. Bolus followed by infusion.
With the development of methods for detection and treatment of hypertension, hypertensive encephalopathy has been becoming more rare.Symptoms of hypertensive encephalopathy typically start to occur 12–48 hours after a sudden and sustained increase in blood pressure. The first manifestation of these symptoms is a severe headache. Headache occurs in greater than 75% of patients. The patient becomes restless. Alterations in consciousness may follow several hours later, which include impaired judgement and memory, confusion, somnolence and stupor. If the condition is not treated, these neurological symptoms may worsen and ultimately turn into a coma. Other symptoms may include increased irritability, vomiting, diplopia, seizures, twitching and myoclonus of the limbs. Alterations in vision (vision blurring, hemivisual field defects, color blindness, cortical blindness) are common. They occur in  4 out of 11 cases (Jellinek et al. 1964). Hemiparesis, intracerebral hemorrhage, aphasia may also occur, but they are less common. Pathogenesis
Hypertensive encephalopathy is caused by an increase in blood pressure. Several conditions may evoke blood pressure elevation: acute nephritis, eclampsia, crises in chronic essential hypertension, sudden withdrawal of antihypertensive treatment. Additionally, hypertensive encephalopathy may occur in pheochromocytoma, Cushings syndrome, renal artery thrombosis.The impairment of cerebral blood flow that underlies hypertensive encephalopathy is still controversial. Normally, cerebral blood flow is maintained by an autoregulation mechanism that dilates arterioles in response to blood pressure decreases and constricts arterioles in response to blood pressure increases. This autoregulation falters when hypertension becomes excessive.