Hypertensive encephalopathy: what is it, symptoms, treatment, prognosis

What is hypertensive encephalopathy?

Hypertensive encephalopathy - This is a less common type of urgent hypertension, manifested by changes in mental status and severely high blood pressure. This is a condition that is one of the manifestations of urgent hypertension that requires rapid but careful treatment.

Urgent hypertension (hypertensive crisis) Is a life-threatening condition in which permanent damage to a target organ occurs as a result of a significant, sudden increase in blood pressure. Edema lung, ischemic heart events, acute renal failure, aortic dissection, eclampsia, retinopathy, and encephalopathy are conditions that can result from organ damage due to hypertension.

Hypertensive encephalopathy is a less common type of urgent hypertension. It is characterized by signs of cerebral edema that occur after a severe episode of hypertension. This condition is usually diagnosed by doctors retrospectively after symptoms have abruptly disappeared with lowering the patient's blood pressure, and other causes of neurological disease will excluded. Symptoms of hypertensive encephalopathy include the gradual onset of headache, nausea and vomiting, over followed by neurological symptoms such as anxiety, confusion, seizures and, possibly a coma. If hypertension is treated quickly, symptoms of encephalopathy are usually reversible.

Signs and symptoms

Hypertensive encephalopathy most often occurs in young and middle-aged people with hypertension. In general, this condition rarely occurs even among people with hypertension. Studies report that 0.5 to 15% of people with malignant hypertension develop hypertensive encephalopathy. With the development of methods for the detection and treatment of hypertension, hypertensive encephalopathy is becoming increasingly rare.

Symptoms of hypertensive encephalopathy usually begin 12–48 hours after a sudden and sustained increase in blood pressure (BP). The first manifestation of these symptoms is severe headache. Headache occurs in more than 75% of patients. The patient becomes restless. Changes in consciousness may follow after several hours, including impaired judgment and memory, confusion, drowsiness, and stupor. If the condition is left untreated, these neurological symptoms can worsen and eventually develop into a coma.

Other symptoms may include:

• increased irritability;
• vomiting;
• diplopia;
• epilepsy;
• jerking and myoclonus limbs.

Visual impairment (blurred vision, defects in the semi-visual field, color blindness, cortical blindness). They occur in 4 out of 11 cases. Hemiparesis may occur, intracerebral hemorrhage, aphasiabut they are less common.

Causes and risk factors

Hypertensive encephalopathy is most often caused by inadequately controlled primary hypertension. Secondary causes of hypertension can also predispose patients to this condition.

Hypertensive encephalopathy shares many characteristics with other syndromes that cause cerebral edema, such as posterior reversible encephalopathy syndrome (PCOE), brainstem hypertensive encephalopathy, and eclampsia.

If primary hypertension has not been previously diagnosed, testing for chronic or chronic hypertension should be considered. acute renal failuretaking sympathomimetics (amphetamines, cocaine), side effects from medications such as immunosuppressants, preeclampsia and eclampsia.

Epidemiology

In the world, approximately 50% of the adult population suffers from hypertension to one degree or another. Emergency cases of hypertension account for a small percentage (less than 2%) of hypertension cases in emergency departments. Hypertensive encephalopathy accounts for 15% of all cases of hypertension.

Pathophysiology

Typically, the brain maintains blood flow in a narrow range of perfusion pressure without being influenced by fluctuations in systemic blood pressure. For healthy people, the pressure range is 50-150 mm Hg. Art. cerebral perfusion pressure (CPP) or 60 to 160 mm Hg. Art. mean arterial pressure (MAP). CPP = GARDEN - intracranial pressure (ICP).

With an increase in SBP, vasoconstriction of the cerebral arterioles occurs, and, conversely, with a decrease in SBP, the arterioles expand in order to maintain a constant CPP. This adaptive process maintains constant brain perfusion despite systemic changes in blood pressure. However, sudden and severe increases in blood pressure can overwhelm this autoregulatory mechanism because arterioles are limited in their ability to constrict. The increased intracerebral blood pressure then causes the blood-brain barrier to be disrupted and the vascular fluid diffuses through the capillary membranes into the brain parenchyma. This leads to the development of cerebral edema, increased intracranial pressure and neurological disorders such as impaired thinking, blurred vision and seizures.

In patients with chronic arterial hypertension, the cerebral vessels undergo adaptations, such as arteriolar hypertrophy, to provide a wider range of autoregulation. A too rapid decrease in blood pressure in these patients can cause cerebral ischemia at higher blood pressure than in patients with normal blood pressure.

In patients with normal blood pressure, previously acute episodes of arterial hypertension can cause hypertensive encephalopathy with diastolic blood pressure up to 100 mm Hg. This scenario can be seen in patients who develop eclampsia or in patients receiving cytotoxic and immunosuppressive therapy. It is assumed that these conditions directly cause toxic effects on the vascular endothelium and lead to dysfunction of the blood-brain barrier.

Diagnostics

Methods for diagnosing hypertensive encephalopathy include physical examination, blood pressure measurement, blood sampling, electrocardiography, electroencephalography, chest x-ray, general urine analysis, arterial blood gas analysis and head imaging (computed tomography (CT) and / or magnetic resonance imaging (MRI)). Because lowering blood pressure is important, antihypertensive drugs are given without waiting for laboratory results. An electroencephalographic study reveals the absence of alpha waves, which indicates a violation of consciousness. In people with visual impairments, slow waves are found in the occipital regions.

Treatment

The initial goal of treating hypertensive crises is to rapidly decrease diastolic blood pressure to about 100-105 mm Hg. this goal should be achieved within two to six hours, while the maximum initial drop in blood pressure should not exceed 25 percent of the current value. This level of blood pressure control will allow the necrotic vascular lesions to heal gradually. More aggressive antihypertensive therapy is unnecessary and can lower blood pressure below the autoregulatory range, which can lead to ischemic events (eg, stroke or coronary disease).

After blood pressure is controlled, the patient should be transferred to medication, gradually lowering the diastolic pressure to 85-90 mm Hg. Art. within two to three months. Initial decrease in diastolic pressure to about 100 mm Hg. Art. Often associated with mild renal impairment; this change, however, is usually temporary, as vascular disease tends to resolve and renal perfusion improves within one to three months. In this case, antihypertensive therapy cannot be abandoned unless an excessive decrease in blood pressure has occurred. However, a change in medication is indicated if decreased kidney function is temporarily associated with therapy with an angiotensin converting enzyme (ACE inhibitor) inhibitor or blocker angiotensin II receptors, which can affect renal autoregulation and cause acute renal failure in patients with bilateral renal stenosis arteries.

Several parenteral antihypertensive agents are most commonly used in the initial treatment of malignant hypertension.

• Nitroprusside is an arteriolar and venous dilator administered as an intravenous infusion. Nitroprusside acts for a few seconds and lasts only two to five minutes. Thus, hypotension can be easily reversed by temporarily stopping the infusion, which is advantageous over the drugs listed below. However, the potential toxicity of cyanide limits the long-term use of nitroprusside, especially in patients with chronic kidney disease.
• Nicardipine is an intravenous arteriolar dilator.
• Clevidipine is a short-acting dihydropyridine calcium channel blocker. It lowers blood pressure without affecting the filling pressure of the heart or inducing reflex tachycardia.
• Labetalol is an alpha and beta blocker administered intravenously or as an infusion. Bolus followed by infusion.
• Fenoldopam is a peripheral dopamine-1 receptor agonist administered by intravenous infusion.
• Oral medications - slower onset of action and inability to control degree lowering blood pressure limit the use of oral antihypertensive drugs in the treatment of hypertensive crises. However, they can be useful when there is no quick access to the parenteral drugs described above. Both sublingual nifedipine and sublingual captopril can significantly lower blood pressure within 10-30 minutes in many patients. A faster response is observed when liquid nifedipine is swallowed.

The main risk when taking oral medications is ischemic symptoms (eg angina pectoris, myocardial infarction, or stroke) due to an excessive and uncontrolled hypotensive reaction. Therefore, their use in the treatment of hypertensive crises should be avoided if more controlled drugs are available.

Forecast

In most cases, hypertensive encephalopathy can be cured by rapidly but conservatively lowering blood pressure. The prognosis for this condition may vary depending on the presence of other comorbid conditions. After being discharged from the hospital, both the patient and the doctor need to remain vigilant in the management of hypertension. These patients are at risk of others hypertensive crisesif they stop taking medication in the future.

Complications

Failure or late treatment of urgent hypertension can lead to renal failure, retinopathy, myocardial infarction and stroke. In particular, without timely treatment of high blood pressure in patients with encephalopathy, cerebral edema can progress and lead to status epilepticus, coma or death. Aggressive treatment of hypertension is not recommended and can lead to ischemic conditions in target organs, especially in patients with an adapted mechanism of autoregulation due to chronic arterial hypertension.