General cascade of disorders
Any comatose state starts with the impact of an extreme factor that triggers a universal pathological cascade. First and foremost, the brain is damaged to the maximum extent, followed by the functional failure of other systems.
Key links of the pathogenesis include:
- Hypoxia and cellular energy deficiency.
- Intoxication (accumulation of endogenous or exogenous poisons).
- Acid-base balance disorders (most often persistent acidosis).
- Dysionia and dyshydration (water-electrolyte balance failure).
- Imbalance of biologically active substances (hormones, neurotransmitters, cytokines).
In the early stages of coma, specific symptoms depending on the cause of the disease predominate. However, as the condition worsens, the picture becomes universal: physiological systems collapse, regulation shifts to a primitive tissue level, and multiple organ dysfunction syndrome develops. Alveolar ventilation drops in the lungs, blood viscosity changes and thrombohemorrhagic syndrome is triggered, while digestion stops in the gut, leading to autoinfection.
Energy crisis and cerebral edema
Neurons are critically dependent on oxygen. If cerebral blood flow stops, events unfold rapidly:
- In 8–10 seconds, acute oxygen deficiency occurs, cellular energy drops, and the person completely loses consciousness.
- Within 4–7 minutes, glucose reserves are depleted. Increasing intracellular acidosis blocks even anaerobic metabolism, and ATP reserves disappear irreversibly.
Without energy, neurons cannot maintain the operation of ion pumps. Sodium (Na⁺) rapidly accumulates inside the cells, which sharply increases osmotic and oncotic pressure. Water rushes from the vessels into the neurons and interstitium, resulting in cerebral edema and swelling. Morphologically, this is accompanied by venous hyperemia and petechial hemorrhages in the nervous tissue.
Toxic shock and electrogenesis failure
Coma is always accompanied by severe intoxication. Toxins strike neurons, the heart, blood cells, and endocrine glands. A vicious circle arises: poisons damage the liver and kidneys, which further reduces detoxification and the excretion of waste products.
For example, in hepatic coma, intestinal protein breakdown products (putrescine, cadaverine, phenol and indole derivatives) as well as ammonia accumulate in the blood. Excess ammonia inhibits enzymes and destroys benzodiazepine receptors.
In parallel, dysionia—an imbalance of ions—develops. This disrupts normal electrogenesis in tissues:
- The formation of the membrane potential and action potential is distorted.
- The excitability of nervous and muscular tissue drops.
- Severe cardiac rhythm disturbances (up to ventricular fibrillation) and respiratory disorders occur.
Features of specific types of coma
| Type of coma | Key mechanisms and clinical manifestations |
|---|---|
| Post-traumatic | The consequence of severe concussion, contusion, and cerebral edema. Characterized by areflexia, paralysis, and convulsions. With a fracture of the skull base, the VII and VIII pairs of cranial nerves are damaged, resulting in the "raccoon eyes" sign, CSF leakage, and bleeding from the ears and nose. |
| Apoplectic | Occurs during a stroke (hemorrhage or ischemia). Microvascular permeability increases sharply, and a "penumbra" zone forms around the lesion (penumbra). It is characterized by an extremely unfavorable prognosis. |
Briefly: answers to topical questions
What stages of consciousness depression are distinguished in the dynamics of coma development?
Four successive degrees of impaired consciousness are distinguished in the dynamics of coma development:
- Dullness and somnolence—a mild degree of depression manifested by sluggishness and inconstant, shallow drowsiness.
- Delirium—a stage of agitation against the background of altered consciousness; the patient is disoriented and unable to adequately assess the surrounding environment.
- Sopor—deep depression of consciousness, outwardly resembling a state of deep sleep from which the patient cannot be fully awakened.
- Coma—total shutdown of consciousness with no reactions to external stimuli.
What is the pathogenesis of diabetic ketoacidotic coma?
The pathogenesis of diabetic ketoacidotic coma is based on an absolute or relative insulin deficiency, leading to hyperglycemia, metabolic acidosis, and electrolyte disorders.
- Hyperglycemia—causes an increase in osmotic pressure in the vascular bed.
- Dehydration—fluid moves from cells to vessels, tissues lose water and ions (cellular dehydration develops).
- Ketoacidosis—due to cellular starvation, fats are broken down and ketone bodies are formed (ketonemia), which leads to a decrease in blood pH and depletion of buffer bases.
What are the features of the pathogenesis of uremic coma in renal failure?
The main feature of the pathogenesis of uremic (azotemic) coma is severe toxic damage to the central nervous system.
- Loss of the excretory function of the kidneys—leads to the cessation of waste excretion from the body.
- Hyperazotemia—nitrogenous wastes, primarily urea and creatinine, accumulate in the blood.
- Toxic encephalopathy—nitrogenous wastes have a significant toxic effect on the nervous system, which is the main link in the development of coma.
To remember the main links of coma pathogenesis, use the "HID" rule: Hypoxia, Intoxication, Disbalance (ions, water, acids, and mediators).
Class and exam questions
Why does acidosis almost always develop in coma?
Acidosis occurs due to tissue hypoxia, impaired renal function (decreased excretion and ammoniagenesis), and liver dysfunction (accumulation of ketone bodies).
Which organs are the primary targets during energy deficiency?
First and foremost, the brain and heart suffer to the greatest extent, as their cells are most vulnerable to oxygen and ATP shortage.
What happens to respiration and circulation in a patient in a coma?
Respiratory failure develops due to the depression of the neurons of the respiratory center. Cardiovascular complications include arrhythmias, arterial hypotension, collapse, and heart failure.
What else to study on this topic
- Mechanisms of penumbra zone formation in apoplectic coma
- The role of neurotransmitter and cytokine imbalance in CNS depression
- Pathogenesis of thrombohemorrhagic syndrome in comatose states
- Specific markers of intoxication in liver failure
- ECG and EEG changes against the background of severe dysionia
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