Generally, this is symptomatic blood pressure dysregulation, due to the decrease in cerebral blood flow when passing a standing position. But sometimes it is a discovery of clinical examination. To retain the diagnosis requires a decrease in systolic blood pressure of 20 mm Hg or more and / or diastolic blood pressure of 10 mm Hg or greater when the patient is standing.
This fall in blood pressure must occur within the first 5 minutes of orthostatic (which distinguishes it from vasovagal syncope hypotension or bradycardia syndrome that is usually delayed (up to 30 min in an exploration tilting table).
The most important is to measure heart rate (HR) during the fall in blood pressure which can distinguish orthostatic hypotension (HO) asympathicotoniques (cardiac acceleration is zero or less than 15 beats / min) and orthostatic hypotension sympathicotonic.
CAUSES orthostatic hypotension:
Orthostatic hypotension causes of sympathicotonic (Table I):
They are mostly iatrogenic. Antidepressants are often involved except reuptake inhibitors of serotonergic (fluoxetine or Prozac was even recommended as a treatment for HO). Antihypertensive vasodilators and nitrates are often involved in the elderly.
In the absence of iatrogenic cause, look hypovolemia and in this framework to think about pregnancy and varicose veins that lead to storage of plasma volume in the veins of the legs. We must also look endocrinopathy. By the end of the nineteenth century, Addison noted the possibility of HO in adrenal insufficiency (the test Synacthene made the diagnosis); hypothyroidism and certain pheochromocytomas secreting especially dopamine are also causes of HO.
Guillain Barré syndrome, and early stages of alcoholic neuropathy or diabetic autonomic are also causes of HO.
Orthostatic hypotension causes of asympathicotoniques (Table I):
HO asymphaticotonique principle translated into an organic lesion baro reflex arc, involving in particular the baroreceptors of the aortic arch and carotid bifurcation, bulbar centers, vagus (X) and friendly. It is first necessary to evoke an infectious origin (botulism, Chagas disease and especially HIV infection).
We must seek pernicious anemia if there is macrocytosis, diabetes (fasting and postprandial, glycated hemoglobin) and some systemic diseases whose primary amyloidosis is. It can be an amyloidosis (by deposits of light chains) with or without myeloma or amyloidosis by mutation of the transthyretin (mainly the mutation 30) encountered especially in the Portuguese Porto. It’s biopsy (lip, digestive, liver or kidney) that can make the diagnosis. If the search is negative systemic disease, look for a purely neurological disease mainly Shy Drager syndrome or multiple system atrophy (especially olivopontocerebellar cerebellar atrophy).
If the neurological examination is normal, it can be a pure autonomic failure (Bradbury-Egglestone syndrome).
TREATMENT orthostatic hypotension:
Treatment of HO begins with some simple steps: stockings, coffee after the meal, elevation of the head of the bed to stimulate the renin-angiotensin system. If these measures are insufficient, therapeutic climbing is as follows:
– 9 α fludrohydrocortisone (Fludrocortisone) tablets 50 gamma in the absence of decubitus pressure 50 to 200 gamma / day;
– Midodrine (Gutron, 2.5 mg tablet) 2.5 to 10 mg morning, afternoon and in the evening if necessary;
– Erythropoietin (Neorecormon®, Aranesp®) if hematocrit <40%, 40 to 100 Gamma Aranesp® every fortnight for a hematocrit around 45%;
– Sandostatin® 50-100 Gamma sc 2 times / day;
– Pacemaker frequency locked to patient movement.