Coma: etiology, classification, and causes

Q: What is the detailed pathogenesis of CNS depression in coma?

Sources indicate that hypoxia and neuronal energy deficiency are the key links in the pathogenesis of coma. When cerebral circulation ceases, a critical oxygen deficit develops within 8–10 seconds, neuronal energy metabolism is disrupted, and consciousness is lost. Over the next 4–7 minutes, glucose reserves are depleted, mounting acidosis suppresses anaerobic metabolism, and irreversible ATP consumption occurs. Consequences of energy deficiency include depression of neuronal activity and complete loss of consciousness, rapidly progressive degenerative processes, breakdown of large-molecule organic compounds, accumulation of excess Na⁺ and other ions in neurons, 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 — cerebral edema and swelling. A decrease in cerebral perfusion pressure below 40 mmHg leads to catastrophic impairment of intracerebral blood flow up to its complete arrest.

Q: According to which parameters is the severity of the condition assessed using the Glasgow Coma Scale?

Severity according to the Glasgow Coma Scale is assessed based on three main parameters of patient reactivity, which are assigned points: Eye opening — response to sound (voice) or painful stimuli, as well as spontaneous eye opening (1 to 4 points). Verbal response — reflects the integrity of speech centers and cognitive functions (1 to 5 points). Motor response — reflects the integrity of motor pathways from the cortex to the brainstem; ability to follow commands, purposeful, withdrawal, or abnormal motor responses to pain is evaluated (1 to 6 points). Clinically, a total score of less than 9 indicates severe central nervous system damage.

Etiological classification of comas

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

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

Exogenous causes

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

Physical factors. Include mechanical injuries (traumatic brain injuries, electric shock), thermal influences (sunstroke, overheating, hypothermia), exposure to high-dose radiation energy (penetrating radiation), and acute barometric pressure fluctuations (decompression of aircraft at altitude, being 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 drugs, barbiturates, and sedatives.
Biological factors. Infectious agents affecting the nervous system: neurotropic viruses, bacterial toxins (botulinum, tetanus), as well as causative agents of severe infections (malaria, cholera, typhoid fever).
Gas composition of the environment. Exogenous hypoxia and anoxia.

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Endogenous causes

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

The main groups of internal pathologies capable of triggering a comatose state:

Pathological processes in the brain: ischemia, strokes, tumors, abscesses, and cerebral edema.
Circulatory failure: acute myocardial infarction, massive blood loss, progressive course of 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.

Briefly: answers to topical questions

What is the detailed pathogenesis of CNS depression in coma?

Sources indicate hypoxia and neuronal energy deficiency as the key links in the pathogenesis of coma. 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, increasing acidosis suppresses anaerobic metabolism, and an irreparable consumption of ATP occurs.

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

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

According to which parameters is the severity of the condition assessed using the Glasgow Coma Scale?

The severity of the condition on the Glasgow Coma Scale is assessed based on three main parameters of the patient's reactivity, for which points are awarded:

Eye opening — reaction to sound (voice) or painful stimuli, as well as spontaneous eye opening is assessed (from 1 to 4 points).
Verbal response — reflects the preservation of speech centers and cognitive functions (from 1 to 5 points).
Motor response — reflects the level of preservation of motor pathways from the cortex to the brainstem; the ability to follow instructions, purposeful, defensive, or pathological reactions to pain is assessed (from 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, sources describe respiratory rhythm disturbances and pathological breathing patterns. The following are distinguished:

Kussmaul breathing — deep, noisy breathing; in diabetic ketoacidotic coma, it indicates a progressive decrease in blood pH, an increase in CO₂, and the appearance of Kussmaul breathing.
Cheyne-Stokes respiration — indicated among pathological breathing patterns in coma; also described in the precoma stage of hepatic encephalopathy.

In addition, in coma, the disruption of the frequency and periodicity of the respiratory center's neurons leads to a decrease in alveolar ventilation volume, respiratory failure, and worsening hypoxia.

How to memorize

To memorize the five groups of comas by etiology, use the phrase «Ne Gubi Mozg Toksichnoy Vodoy»: Neurogenic, Hypoxic, Metabolic, Toxinemic, Water-electrolyte.

Class and exam questions

What is the difference between endogenous and exogenous toxin-induced coma?

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

How do enzyme blocks lead to the development of coma?

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

Why can prolonged vomiting trigger a coma?

Uncontrollable vomiting leads to massive loss of water and electrolytes by the body. This causes the development of severe chlorhydropenic coma.

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What else to study on this topic

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

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Coma