Metabolic coma, why, what e who

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Coma due to metabolic disorders

Many systemic metabolic alterations cause a coma status due to the interruption of energy substrates (hypoxia, ischemia, hypoglycemia) or altered neuronal excitability (drug intoxication, alcohol intoxication, anesthesia, epilepsy) .The same metabolic abnormalities that induce the coma may, in a milder form, cause widespread cortical dysfunction and an acute confusional state. Therefore, in the metabolic encephalopathies the phenomena of obfuscation of consciousness and the coma represent a continuum.

The brain neurons are totally dependent on the cerebral blood flow and the relative supply of oxygen and glucose. The cerebral blood flow is approximately 75 ml / min per 100 g in the gray substance and 30 ml / min per 100 g in the white matter (on average 55 ml / min per 100 g); the oxygen consumption is 3.5 ml / min per 100 g and the glucose utilization is 5 mg / min per 100 g. Glucose cerebral reserves supply energy for about 2 minutes after the interruption of the blood flow and the oxygen reserves are sufficient for 8-10 seconds after cessation of flow. The simultaneous presence of hypoxia and ischemia depletes glucose deposits more rapidly.

In these circumstances the rhythm of the electroencephalogram (EEG) becomes diffusely slow (typical condition of the metabolic encephalopathies) and, with the worsening of the contribution of substrates, eventually the adjustable cerebral electrical activity ceases completely. In almost all metabolic encephalopathy situations, the global metabolic activity of the brain is reduced proportionally to the extent of loss of consciousness.
Pathological conditions such as hypoglycemia, hyponatraemia, hyperosmolarity, hypercarbia, hypercalcaemia and hepatic failure and renal failure are associated with a wide variety of alterations of neurons and astrocytes. Unlike hypoxia-ischemia, which causes neuron destruction, metabolic disorders generally only cause minor neuropathological changes. The reversibility of the effects of these conditions on the brain has not been clarified, but they can in different circumstances compromise the supply of energy, modify the ionic flows through the neuronal membranes and cause neurotransmitter abnormalities.
For example, the high cerebral concentration of detectable ammonia during hepatic coma interferes with energy metabolism and with the Na +, K + -ATPase pump, increases the number and size of astrocytes, alters the functions of nerve cells and causes an increase in concentrations of potentially toxic metabolic products of ammonia; Neurotransmitter abnormalities may also occur, including the possibility of "false" neurotransmitters acting at the receptor sites.

Except for hyperammonemia, it is not clear which of these mechanisms is critical. The pathogenetic mechanism of encephalopathy in renal failure is also unknown. Unlike ammonia, urea is not, in itself, a cause of intoxication of the central nervous system. A multifactorial aetiology has been hypothesized, including an increase in the permeability of the blood-brain barrier to toxic substances, such as organic acids, and an increase in the cerebral content of calcium or of the phosphate liquor concentration.

Coma, epilepsy and alteration of electrolytes

Coma epileptic ecrisis are manifestations common to any significant variation in the water balance and sodium in the brain. These changes in osmolarity may be the consequence of many systemic medical disorders, such as diabetic ketoacidosis, non-ketotic hyperosmolar status and hyponatraemia due to various causes (eg, water intoxication, excessive secretion of antidiuretic hormone or peptide atrial natriuretic).
Sodium levels of less than 125 mmol / L induce confusion and less than 115 mmol / L are associated with coma and convulsions. In the hyperosmolar coma the osmolarity of the serum is generally higher than 350 mosmol / L. Hypercignia decreases the levels of consciousness in proportion to the increase in the C02 tension in the blood. In all these metabolic encephalopathies, the degree of neurological changes depends, in most cases, on the rapidity with which changes occur in the serum. The pathophysiology of other metabolic encephalopathies, such as hypercalcaemia, hypothyroidism, vitamin B12 deficiency and hypothermia, has not been fully specified, but also in these cases there must be alterations in the CNS biochemistry and membrane functions.