Diagnosis of acute adrenal insufficiency

For the diagnosis of acute adrenal insufficiency, anamnestic indications of previously existing adrenal diseases in patients are important. Adrenal crises most often occur in patients with reduced adrenal cortex function in various extreme conditions of the body. Insufficiency of adrenal cortex secretion occurs with primary adrenal damage and secondary hypocorticism caused by decreased ACTH secretion.

Diseases of the adrenal glands include 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 about autoimmune Addison's disease. Primary adrenal insufficiency or Addison's disease sometimes develops as a result of tuberculosis.

There is a high probability of acute crisis in patients with Cushing's disease and syndrome after bilateral total adrenalectomy or adrenal cortex tumor removal and in patients receiving adrenal cortex biosynthesis inhibitors. Chloditan is the most commonly used drug to inhibit cortisol and aldosterone synthesis. Its long-term use leads to adrenal insufficiency and the potential for acute hypocorticism in patients. Usually, when prescribing this drug, adding 25-50 mg of cortisol per day compensates for adrenal insufficiency. However, in extreme conditions of the body, these doses may be inadequate.

An important clinical sign for diagnosing acute adrenal insufficiency is increased pigmentation of the skin and mucous membranes. In some patients, melasma is not clearly expressed, but there are only minor signs: increased pigmentation of the nipples, palmar lines, an increase in the number of pigment spots, moles, darkening of postoperative sutures. The presence of depigment spots - vitiligo - is also a diagnostic sign of decreased function of the adrenal cortex. Vitiligo can occur both against the background of hyperpigmentation, and in its absence.

In primary adrenal insufficiency, increased pigmentation at the time of decompensation against the background of progressive hypotension helps to diagnose Addisonian crisis. It is much more difficult to suspect adrenal insufficiency in depigmented 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 also characteristic of patients with congenital dysfunction of the adrenal cortex. It is associated with increased secretion of ACTH in response to reduced production of cortisol.

A characteristic feature of the diagnosis of acute adrenal insufficiency is a progressive decrease in blood pressure. A feature of the Addisonian crisis is the lack of compensation for hypotension from various drugs that affect vascular tone. Only the administration 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 due to Itsenko-Cushing's disease or adrenal corticosteroma and with a hypertensive form of congenital dysfunction of the adrenal cortex, acute adrenal insufficiency occurs in some cases with an increase in blood pressure. Sometimes it is necessary to differentiate an Addisonian crisis in such patients from a hypertensive crisis.

The diagnosis of secondary adrenal insufficiency is aided by anamnestic data on previous diseases or injuries of the central nervous system, operations on the pituitary gland or radiation therapy to the hypothalamic-pituitary region, and the use of corticosteroids for various autoimmune diseases. Among the diseases and injuries of the pituitary gland, the most common are postpartum partial necrosis of the pituitary gland (Sheehan's syndrome), craniopharyngiomas, and tumors that cause a decrease in the secretion of pituitary hormones. Basal meningitis, encephalitis, and gliomas of the optic nerve can also cause secondary adrenal insufficiency.

Isolated decrease in ACTH secretion in pituitary diseases is extremely rare, and usually its deficiency is accompanied by a drop in the level of other tropic hormones - thyrotropic, somatotropic, gonadotropins. Therefore, in secondary adrenal insufficiency, along with adrenal hypofunction, hypothyroidism is observed, growth retardation if the disease developed in childhood, menstrual irregularities in women, hypogonadism in men. Sometimes, when the posterior lobe of the pituitary gland is damaged, symptoms of diabetes insipidus join it.

Laboratory methods for diagnosing acute adrenal insufficiency are quite limited. Determination of plasma cortisol, aldosterone, and ACTH levels cannot always be tested quickly enough. In addition, a single hormone level does not accurately reflect the functional state of the adrenal cortex. Diagnostic tests used in chronic adrenal insufficiency are contraindicated in acute Addisonian crisis.

Changes in electrolyte balance are more important for diagnosing acute adrenal insufficiency. In a state of compensation, the level of electrolytes in patients, as a rule, may not change. During an Addisonian crisis and a state of dehydration, the content of sodium and chlorides decreases: the sodium level is below 142 meq/l, and during a crisis this level can be 130 meq/l and lower. A characteristic feature is a decrease in sodium excretion in the urine - less than 10 g / day. An increase in potassium in the blood to 5-6 meq/l is important for diagnosing acute adrenal insufficiency; sometimes this figure reaches 8 meq/l. As a result of an increase in potassium in the blood and a decrease in sodium, the sodium/potassium ratio changes. If in healthy people this ratio is 32, then in acute hypocorticism it is typical for it to fall to 20 and below.

Hyperkalemia has a toxic effect on the myocardium, and the ECG often shows a tall, peaked T wave, as well as conduction slowing. In addition, in conditions of adrenal cortex insufficiency, prolongation of the S-T interval and QRS complex, and a low-voltage ECG may be detected.

In addition to significant loss of water and salts, hypoglycemia is a significant danger during an Addisonian crisis. Blood sugar levels should be determined under control. But a hypoglycemic crisis can be an independent manifestation of decompensation of chronic adrenal insufficiency during starvation and infectious diseases. During acute hypocorticism, blood glucose levels can be very low, but there are no hypoglycemic manifestations.

The loss of sodium and water during a crisis leads to true thickening of the blood and an increase in the hematocrit number. If the thickening of the blood does not depend on adrenal insufficiency, but is caused by diarrhea, vomiting, then the concentration of sodium and chlorides may 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, and various degrees of acidosis occur, as evidenced by a decrease in blood alkalinity.

Differential diagnosis between Addisonian crisis, vascular collapse, shock of various origins and hypoglycemic coma is complex. Failure of vascular agents and anti-shock measures usually indicates an adrenal nature of the crisis.

Currently, corticosteroids are included in the arsenal of means for bringing patients out of shock. Therefore, in these cases, hyperdiagnosis of the Addisonian crisis is possible. But this is justified by the immediate prescription of corticosteroid drugs to patients along with anti-shock treatment.

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