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Diabetic Ketoacidotic Coma

Coma ketoacidoticum

For medical students2 min readUpdated 2026-10-10

Diabetic ketoacidotic coma is a severe, life-threatening complication of diabetes mellitus resulting from critical metabolic decompensation. The condition is characterized by loss of consciousness, depressed reflexes, acetone breath odor, and profound laboratory abnormalities.

Primary CauseMetabolic decompensation in diabetes mellitus
Blood GlucoseSignificant hyperglycemia, reaching 20–30 mmol/L
Ketone BodiesHigh ketonemia (10–17 mmol/L) and presence of ketonuria
DiuresisDecrease in urine output from polyuria to oliguria and complete anuria
OsmolalityIso- or mild hyperosmolality (does not exceed 310–320 mOsm/kg)

Pathology Development and the Precoma Stage

Ketoacidotic coma does not develop suddenly. It represents the predictable outcome of progressive metabolic disturbances characteristic of diabetes mellitus. When the body's compensatory mechanisms are exhausted, the patient enters a state of decompensation, clinically referred to as precoma.

At this stage, the patient is still conscious, but distinct signs of altered mental status begin to appear. The body sends warning signals that can be grouped into several categories:

Clinical Features of Fully Developed Coma

If the pathological process is not halted during the precoma stage, ketoacidotic coma ensues. This critical condition is characterized by complete unresponsiveness and profound depression of all reflexes.

Neurological status undergoes severe changes, leading to profound neurological deficits. Ocular examination reveals pronounced pupillary constriction (miosis), with complete absence of the light reflex.

Vital functions are compromised: circulatory and respiratory failure rapidly progress. Renal function continues to decline: urine output becomes extremely low and ultimately progresses to anuria (complete cessation of urine entering the bladder).

The most specific and easily recognizable symptom that suggests this type of coma even before lab results are available is a sharp, distinct acetone odor on the breath.

Laboratory Findings

Laboratory tests play a crucial role in confirming the diagnosis. Blood and urine profiles in coma ketoacidoticum exhibit clear, specific criteria:

  1. Glucose level: Significant hyperglycemia is observed, with blood sugar levels soaring to 20–30 mmol/L.
  2. Ketone bodies: High ketonemia is recorded (blood ketone concentration reaches 10–17 mmol/L). Concurrently, urinalysis consistently shows ketonuria (excretion of ketone bodies in the urine).
  3. Plasma osmolality: Unlike some other types of diabetic comas, ketoacidotic coma features a plasma osmolality not exceeding 310–320 mOsm/kg, indicating iso-osmolality or only mild hyperosmolality.

Key Diagnostic Markers

Summarizing the clinical and laboratory picture, it is essential to highlight the markers that make ketoacidotic coma recognizable.

First, respiration: the acetone odor is the hallmark of this metabolic shift. Second, renal dynamics: the transition from profuse urination to complete anuria indicates a catastrophic increase in circulatory failure. Third, the pupillary reflex: constricted pupils (miosis) unresponsive to light in an unresponsive patient indicate deep central nervous system depression. Finally, the laboratory profile featuring high ketones and glucose with normal or slightly elevated osmolality finalizes the diagnosis.

Mnemonic

How to remember the main signs of ketoacidotic coma? Use the mnemonic «DRY ACETONE»: D — Decreased consciousness and depressed reflexes. R — Restricted (narrow) pupils (miosis, no light reaction). Y — Years of diabetes in history (cause is decompensation). A — Anuria following oliguria (plus dry mucous membranes). C — Calculated osmolality normal or mild (not above 310–320 mOsm/kg). E, T, O, N — Acetone breath, ketonemia (10–17 mmol/L), and ketonuria.

Frequently asked questions

What type of abnormal breathing pattern is characteristic of fully developed ketoacidotic coma?

Fully developed ketoacidotic coma is characterized by Kussmaul breathing ("air hunger"). This is deep, labored breathing with regular cycles consisting of a deep inspiration followed by a forced expiration. The abnormality develops due to decreased blood pH and rising CO₂. This breathing pattern is accompanied by a specific acetone (fruity) odor on the breath and typically occurs alongside altered mental status, indicating an extremely severe patient condition.

How does acid-base status (blood pH) change in ketoacidotic coma?

In ketoacidotic coma, acid-base status shifts with the development of decompensated metabolic acidosis, leading to a progressive drop in blood pH. The underlying mechanism is a massive release of ketone bodies into the blood (with β-hydroxybutyrate contributing the most) due to uncontrolled fatty acid oxidation. The accumulation of acidic products depletes buffer bases in an attempt to maintain balance, resulting in decreased bicarbonate and other buffer bases.

Which condition leads to the development of ketoacidotic coma?

This condition is a direct result of worsening metabolic derangements in decompensated diabetes mellitus. It is not associated with diabetes insipidus, hypothyroidism, or Cushing syndrome.

How does diuresis change during the transition from precoma to coma?

During the precoma stage, diabetic polyuria is replaced by oliguria. With the development of fully manifested coma, urine output becomes extremely low, progressing to complete anuria.

What are the plasma osmolality values in this type of coma?

Plasma osmolality remains within normal limits or rises only slightly, not exceeding 310–320 mOsm/kg, which is considered iso- or mild hyperosmolality.

How do the patient's pupils react in ketoacidotic coma?

Pronounced miosis (small pupils) is observed, with a complete absence of the light reflex against the background of generalized reflex depression and loss of consciousness.

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