Diagnosis of acute adrenal insufficiency

For the diagnosis of acute adrenal insufficiency, it is important to have anamnestic indications of the adrenal gland that were previously available in patients. More often adrenal crises occur in patients with a reduced function of the adrenal cortex for various extreme conditions of the body. Insufficient secretion of the adrenal cortex occurs with primary adrenal damage and secondary hypocorticism caused by a decrease in ACTH secretion.

Adrenal disease includes Addison's disease and congenital dysfunction of the adrenal cortex. If the patient has any autoimmune disease: thyroiditis, diabetes mellitus or anemia - one can think of Addison's autoimmune disease. Primary adrenal insufficiency or Addison's disease sometimes develops due to tuberculosis lesions.

There is a high probability of an acute crisis in patients with the disease and with Itenko-Cushing syndrome after bilateral total adrenalectomy or removal of the adrenal cortex tumor and in patients receiving inhibitors of adrenal cortex biosynthesis. To inhibit the synthesis of cortisol and aldosterone most often used drug Chloditan. Its long-term use leads to adrenal insufficiency and the potential for development in patients with acute hypocorticism. Usually, with the appointment of this drug, the addition of 25-50 mg of cortisol per day compensates for adrenal insufficiency. But under extreme conditions of the body these doses may prove inadequate.

To diagnose acute adrenal insufficiency, an important clinical sign is the increased pigmentation of the skin and mucous membranes. In some patients melasma is not pronounced, but there are only small signs: increased pigmentation of the nipples, palmar lines, increase in the number of pigment spots, birthmarks, darkening of postoperative sutures. The presence of depigmental spots - vitiligo - is also a diagnostic sign of a decrease in the function of the adrenal cortex. Vitiligo can occur both against the background of hyperpigmentation, and in its absence.

With primary adrenal insufficiency, the increase in pigmentation at the time of decompensation against a background of progressive hypotension helps to diagnose an addisonic crisis. It is much more difficult to suspect adrenal insufficiency in depigmentary forms, the so-called white addisonism. The absence of melasma in primary hypocorticism occurs in approximately 10% of cases and in all patients with secondary adrenal insufficiency. Hyperpigmentation is characteristic for patients with congenital dysfunction of the adrenal cortex. It is associated with increased secretion of ACTH in response to a decreased production of cortisol.

Characteristic in the diagnosis of acute adrenal insufficiency is a progressive decrease in blood pressure. The peculiarity of the addisonian crisis is the lack of compensation for hypotension from various drugs that affect vascular tone. Only the appointment of adrenal hormones - hydrocortisone, cortisone and DOXA - leads to an increase and normalization of pressure. But it should be remembered that in patients after removal of the adrenal glands in connection with the Itenko-Cushing's disease or adrenal corticosteroid and with the hypertonic form of congenital adrenal cortex dysfunction, acute adrenal insufficiency occurs in a number of cases with an increase in blood pressure. Sometimes it is necessary to differentiate the addisonian crisis in such patients with hypertensive crisis.

Diagnosis of secondary adrenal insufficiency is assisted by anamnestic data on the transferred diseases or traumas of the central nervous system, on operations on the pituitary or radiotherapy on the hypothalamic-pituitary region, on the intake of corticosteroids for various autoimmune diseases. Among diseases and damages of the pituitary gland the most frequently occurs postpartum partial necrosis of the pituitary (Shien syndrome), craniopharyngiomas, tumors that cause a decrease in the secretion of pituitary hormones. Basal meningitis, encephalitis, gliomas of the optic nerve can also cause secondary adrenal insufficiency.

Isolated decrease in ACTH secretion in diseases of the pituitary gland is extremely rare, and usually its deficiency is accompanied by a drop in the level of other trophic hormones - thyreotropic, somatotropic, gonadotropins. Therefore, with secondary adrenal insufficiency, along with adrenal hypofunction, hypothyroidism is noted, growth retardation if the disease develops in childhood, menstrual cycle disorders in women, hypogonadism in men. Sometimes, when the posterior lobe of the pituitary gland is damaged, symptoms of diabetes insipidus are added to it.

Laboratory methods for diagnosing acute adrenal insufficiency are rather limited. The determination of cortisol, aldosterone and ACTH in plasma can not always be studied quickly enough. In addition, a single indicator of the level of hormones does not accurately reflect the functional state of the adrenal cortex. Diagnostic tests used for chronic adrenal insufficiency in the acute addisonic crisis are contraindicated.

For the diagnosis of acute adrenal insufficiency, changes in electrolyte balance are more important. In a state of compensation in patients, the level of electrolytes, as a rule, can not be changed. During the addison's crisis and the state of dehydration, the content of sodium and chlorides decreases: the sodium level is below 142 meq / l, and during the crisis this level can be 130 meq / l and lower. Characteristic is a decrease in the release of sodium in the urine - less than 10 g / day. Important for the diagnosis of acute adrenal insufficiency is an increase in blood potassium to 5-6 meq / l; sometimes this figure reaches 8 meq / l. As a result of an increase in the content of potassium in blood and a decrease in sodium, the sodium / potassium ratio is changing. If this coefficient is 32 in healthy people, then acute hypokorticism is characterized by a drop of up to 20 or less.

Hyperkalemia has a toxic effect on the myocardium, and ECG often shows a high pointed T-tooth, as well as a slowing of conduction. In addition, in conditions of insufficiency of the function of the adrenal cortex, the elongation of the S-T interval and the QRS complex, the low-voltage ECG, can be revealed.

In addition to a significant loss of water and salts, hypoglycaemia is a significant hazard during the addisonic crisis. The determination of the sugar content in the blood should be controlled. But the hypoglycemic crisis can be an independent manifestation of decompensation of chronic adrenal insufficiency during fasting and infectious diseases. During acute hypocorticism, the level of glucose in the blood can be very low, but hypoglycemic manifestations are absent.

The loss of sodium and water during a crisis leads to a true blood thickening and an increase in the hematocrit number. If the blood thickening does not depend on adrenal insufficiency, but is caused by diarrhea, vomiting, the concentration of sodium and chloride can be normal, increased or decreased, and potassium does not increase.

During the development of acute adrenal insufficiency, the level of urea and residual nitrogen often increases significantly, different degrees of acidosis appear, as evidenced by a decrease in the alkalinity of the blood.

The differential diagnosis between addisonic crisis, vascular collapse, shock of various origin and hypoglycemic coma is complex. The unsuccessful application of vascular agents and anti-shock measures usually indicates an adrenal nature of the crisis.

At present, corticosteroids are included in the arsenal of means for removing patients from shock. Therefore, in these cases, an overdiagnosis of the addisonian crisis is possible. But this is justified by the immediate appointment of patients along with anti-shock treatment of corticosteroids.

[1], [2], [3], [4], [5], [6], [7], [8],