Causes and mechanisms of development
Globally, the causes of coma are divided into two categories:
- Primary CNS lesions. These occur with direct brain damage due to hypoxia, traumatic brain injuries, tumors, strokes, or neuroinfections. The main pathogenetic factor here is a critical decrease in cerebral perfusion pressure.
- Secondary CNS lesions. These develop against the background of severe systemic disorders: endocrine crises, hepatic or renal failure, sepsis, and exogenous poisoning.
In young children, the leading cause of coma is severe neuroinfections and generalized sepsis.
Topical diagnostics by level of lesion
The clinical picture of a coma strictly depends on how deeply the damage to brain structures has spread (rostrocaudal direction):
- Diencephalic level. The main sign is the formation of decorticate posture (pathological arm flexion).
- Midbrain level. Characterized by decerebrate posture (limb extension). The oculocephalic reflex ("doll's eyes" phenomenon) is still preserved.
- Upper brainstem level. The lower parts of the pons are affected. The "doll's eyes" reflex disappears, flaccid tetraplegia, hyperthermia, and pathological Biot's respiration develop.
- Lower brainstem level (medulla oblongata). A terminal state. Bilateral mydriasis without reaction to light, muscular atonia, absence of spontaneous breathing, and a drop in blood pressure transitioning from tachycardia to bradycardia and asystole are observed.
Differential diagnosis of metabolic comas
Assessment of the condition is based on dividing the clinical picture into a prodromal period (precoma) and a full-blown stage.
- Diabetic comas. Hyperglycemic coma develops slowly, with signs of dehydration, soft eyeballs, and the smell of acetone. Hypoglycemic coma occurs acutely, accompanied by pronounced sweating, tremor, and muscle hypertonus.
- Uremic coma. In the precoma stage, skin itching, hypertension, and nausea are noted. The full-blown stage is characterized by pale gray skin, anuria, and the smell of ammonia.
- Hepatic coma. Begins with jaundice, ascites, and adynamia. In coma, the smell of raw liver (or overripe fruit) appears, the liver decreases in size (a sign of necrosis), and anasarca and hemorrhagic syndrome occur.
- Reye's syndrome. A specific variant of hepatic coma typical for children under 12 years of age. The basis is generalized mitochondrial damage due to aspirin intake against the background of a viral infection. Characterized by a fluctuating alternation of drowsiness and agitation.
Glasgow Coma Scale and laboratory diagnostics
To objectively assess the depth of consciousness depression, the Glasgow Coma Scale is used, analyzing three parameters:
- Eye opening (from 4 points for spontaneous to 1 point for complete lack of response).
- Motor response (from 6 points for following instructions to 1 point for atonia).
- Verbal response (from 5 points for a normal conversation to 1 point for the absence of sounds.
The laboratory profile includes blood biochemistry, urinalysis, and acid-base balance (ABB). In most metabolic comas (hyperglycemic, uremic, hepatic), decompensated metabolic acidosis is detected. The exception is hypoglycemic coma, in which ABB indicators remain normal.
Tactics and emergency care
When finding an unconscious patient, it is extremely important to collect an anamnesis from indirect signs: inspect the scene for syringes or medications, and examine personal belongings. All patients are subject to immediate hospitalization in the ICU.
Emergency rule: if the physician doubts the nature of the diabetic coma (despite the presence of the smell of acetone), the patient is empirically administered a dextrose solution. Delay in stopping hypoglycemia leads to rapid irreversible brain damage and death, whereas additional glucose in hyperglycemia will not cause an immediate fatal deterioration.
For the differential diagnosis of diabetic comas: Hyperglycemia — "Dry" (dry skin, dehydration, soft eyeballs). Hypoglycemia — "Wet" (sweating, increased muscle tone).
Class and exam questions
What does the Glasgow Coma Scale assess in the motor sphere?
The GCS assesses the preservation of motor pathways: from obeying commands (6 points) to decorticate (3 points) and decerebrate rigidity (2 points), up to complete atonia (1 point).
Why administer dextrose in an unspecified coma with the smell of acetone?
Hypoglycemia carries an immediate threat of rapid destruction of brain structures. Administration of dextrose in unrecognized hyperglycemia will not lead to a fatal outcome, whereas missed hypoglycemia is fatal.
How does breathing change when the upper brainstem level of the brain is damaged?
When the lower parts of the pons (upper brainstem level) are damaged, Biot's respiration occurs—an alternation of regular respiratory movements with periods of apnea.
What else to study on this topic
- Clinical patterns of pathological breathing (Cheyne-Stokes, Kussmaul, Biot)
- Interpretation of acid-base balance (ABB) in intensive care
- Pathogenesis of Reye's syndrome at the level of mitochondrial dysfunction
- Mechanisms of formation and maintenance of cerebral perfusion pressure
- Features of taking an anamnesis in patients with impaired consciousness
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