Case Report (n=1)
Absolute Event Rate: 3% vs 49%
In a patient with severe diabetic autonomic neuropathy, conventional treatments for postural hypotension failed, but hypoglycaemia effectively abolished the blood pressure fall on standing by increasing plasma catecholamines.
Hypoglycaemia may mitigate orthostatic hypotension in diabetic autonomic neuropathy but should not change practice; leaves open mechanistic and therapeutic validation.
A 35-year-old Type 1 diabetic man with severe disabling postural hypotension was studied for physiological abnormalities, precipitating factors, and effect of current treatment. A 24-h blood pressure profile indicated a diurnal variation in systolic blood pressure with the lowest values recorded between 0100 and 0600 h, during which the patient often lost consciousness on standing (mean standing systolic pressure 78 mmHg at night vs 105 mmHg in the afternoon, p less than 0.001). Food induced a profound fall in systolic pressure, both while supine and while standing erect. The systolic pressure fall during euglycaemia was 49 mmHg vs 3 mmHg during hypoglycaemia. Plasma noradrenaline and adrenaline levels were low during euglycaemia, but increased during hypoglycaemia. Therapeutic manoeuvres aimed at increasing heart rate (by atrial tachypacing) and reducing the peripheral pooling of blood (vasoconstricting drugs and gravity suit), together with the somatostatin analogue octreotide, proved ineffective. These observations demonstrate the phenomenon of post-prandial exacerbation of postural hypotension in a Type 1 diabetic patient, and indicate that despite failure of conventional methods of treatment, hypoglycaemia increased plasma catecholamines and was effective in abolishing the blood pressure fall on standing.
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Stevens et al. (1991) conducted a case report in Type 1 diabetes with severe disabling postural hypotension (n=1). Hypoglycaemia vs. Euglycaemia was evaluated on Systolic pressure fall on standing.
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