Coma

*Coma*

For medical students2 min readUpdated 2026-10-10

Coma is a severe pathological state resulting from brain injury. It develops under the influence of extreme exogenous or endogenous factors leading to profound depression of central nervous system functions.

Primary TargetBrain injury is the basis of pathogenesis in any coma

Exogenous FactorsTrauma, poisons, infections, and external physical agents

Endogenous FactorsSevere internal pathologies (renal, hepatic failure)

ToxemiaIntoxication of the body by external poisons or endogenous metabolites

Etiological Classification of Comas

Depending on the underlying cause, comatose states are divided into five main groups:

Neurogenic Comas. Caused by primary lesions of the central nervous system. These result from strokes, traumatic brain injuries, epileptic seizures, as well as brain tumors and inflammatory processes of the brain and its meninges.
Hypoxic Comas. Develop due to impaired gas exchange and oxygen deficiency.
Exogenous hypoxia: normo- or hypobaric (reduced oxygen in inhaled air, drop in atmospheric pressure).
Respiratory causes: airway obstruction due to tumor growth or significant bronchial wall edema.
Circulatory causes: acute circulatory disorders in the pulmonary circulation.
Tissue/diffuse causes: significant alveolar or interstitial pulmonary edema.
Metabolic Comas. Caused by severe metabolic disorders.
Dyshormonal states: hormone deficiency or excess (in diabetes mellitus, hypothyroidism, hypocortisolism, hypopituitarism), as well as drug overdosage (thyrotoxic or hypoglycemic coma).
Enzyme inhibition: blockade of tissue respiration in mitochondria (cyanide poisoning) or blockade of glycolysis (action of monoiodoacetate).
Toxemic Comas. Caused by severe intoxication.
Endogenous: toxicoinfections, hepatic or uremic (renal) coma.
Exogenous: action of external poisons, alcohol, drugs of abuse.
Water-Electrolyte Comas. Develop with major loss of water and/or electrolytes. These include hyponatremic (in syndrome of inappropriate ADH secretion), chlorhydropenic (in prolonged intractable vomiting), and starvation-dystrophic coma.

Exogenous Causes

Exogenous factors are environmental pathogenic agents of extreme force, toxicity, or destructive nature. All of them lead to brain injury, which entails the development of a coma.

Physical factors. Include mechanical damage (traumatic brain injuries, electrical injury), thermal effects (sunstroke, overheating, hypothermia), high-dose radiation energy (penetrating radiation), and acute barometric pressure fluctuations (aircraft depressurization at altitude, presence at the epicenter of an explosion).
Chemical factors. High doses of neurotropic toxins. This includes poisoning with alcohol and its surrogates, ethylene glycol, as well as toxic doses of narcotics, barbiturates, and sedatives.
Biological factors. Infectious agents affecting the nervous system: neurotropic viruses, bacterial toxins (botulinum, tetanus), and pathogens of severe infections (malaria, cholera, typhoid fever).
Environmental gas composition. Exogenous hypoxia and anoxia.

Endogenous Causes

Endogenous factors are the result of severe disorders in the body's own vital functions. The general pathogenesis is as follows: endogenous extreme factors → brain injury → coma.

Main groups of internal pathologies capable of provoking a comatose state:

Pathological processes in the brain: ischemia, strokes, tumors, abscesses, and brain edema.
Circulatory insufficiency: acute myocardial infarction, massive blood loss, progressive shock, and collapse.
Respiratory failure: severe conditions such as pulmonary edema, asphyxia, pneumothorax.
Hepatic and renal failure: liver failure (including under the action of hepatotropic poisons—high doses of alcohol or aflatoxin) and kidney failure (acute bilateral renal ischemia, diffuse glomerulonephritis).
Blood system pathology: massive erythrocyte hemolysis, multiple thrombosis.
Digestive system disorders: malabsorption syndrome, severe intestinal autointoxication or autoinfection.
Endocrinopathies: hypoinsulinism, hypo- or hyperthyroid states, adrenal insufficiency.

Mnemonic

To remember the five etiological groups of comas, use the mnemonic: Neurogenic, Hypoxic, Metabolic, Toxemic, Water-electrolyte (No Head Metabolism Toxifies Water).

Frequently asked questions

What is the detailed pathogenesis of CNS depression in coma?

Key links in coma pathogenesis include hypoxia and neuronal energy deficiency. When cerebral blood flow ceases, critical oxygen deficiency develops within 8–10 seconds, neuronal energetics is disrupted, and consciousness is lost. Over the next 4–7 minutes, glucose stores are depleted, mounting acidosis suppresses anaerobic metabolism, and an irreparable expenditure of ATP occurs.

Consequences of energy deficiency include suppressed neuronal activity and complete loss of consciousness, rapidly progressive dystrophic processes, breakdown of high-molecular organic compounds, intracellular accumulation of excess Na⁺ and other ions, and an increase in intracellular osmotic and oncotic pressure.

Morphologically, this manifests as swelling of nerve cells combined with fluid leakage from vessels into the interstitium—brain edema-swelling. A drop in cerebral perfusion pressure below 40 mmHg leads to catastrophic impairment of intracerebral blood flow up to its complete arrest.

What parameters are used to assess severity on the Glasgow Coma Scale?

Severity on the Glasgow Coma Scale is assessed based on three main parameters of patient reactivity, assigned point values:

Eye opening — evaluates response to sound (voice) or painful stimuli, as well as spontaneous eye opening (1 to 4 points).
Verbal response — reflects the preservation of speech centers and cognitive functions (1 to 5 points).
Motor response — reflects the preservation of motor pathways from the cortex to the brainstem; evaluates the ability to follow commands, purposeful, withdrawal, or abnormal posturing responses to pain (1 to 6 points).

Clinically, a total score of less than 9 indicates a severe central nervous system lesion.

What types of pathological breathing are characteristic of comatose states?

For most comatose states, respiratory rhythm disturbances and pathological breathing patterns are described. These include:

Kussmaul breathing — deep, labored breathing; in diabetic ketoacidotic coma, it indicates a progressive drop in blood pH, rising CO₂, and the appearance of Kussmaul breathing.
Cheyne-Stokes respiration — listed among pathological breathing patterns in coma; also described in the precoma stage of hepatic encephalopathy.

Additionally, during coma, impaired frequency and periodicity of respiratory center neuronal activity leads to a decrease in alveolar ventilation volume, respiratory failure, and worsening hypoxia.

What is the difference between endogenous and exogenous toxemic coma?

Endogenous coma occurs with the accumulation of internal toxins (e.g., in hepatic or renal failure, toxicoinfections). Exogenous coma is associated with the entry of poisons from the outside (alcohol, drugs, toxic substances).

How do enzyme blocks lead to coma?

Inhibition of enzymatic processes deprives cells of energy. For example, cyanides block tissue respiration in mitochondria, and monoiodoacetate suppresses glycolysis, leading to energy starvation and brain damage.

Why can prolonged vomiting provoke a coma?

Intractable vomiting leads to massive loss of water and electrolytes by the body, causing severe chlorhydropenic coma.

Go deeper

Pathogenesis of neuronal damage in exogenous and endogenous hypoxia
Mechanisms of hepatic and uremic coma development
Dyshormonal comatose states in thyroid and adrenal pathologies
Effects of neurotropic toxins and barbiturates on the central nervous system
Syndrome of inappropriate antidiuretic hormone (ADH) secretion