Diabetic ketoacidotic coma
This emergency condition develops against the background of absolute (less often relative) insulin deficiency. As a rule, the complication arises due to delayed diagnosis of type 1 diabetes mellitus. Triggering factors may also include situations that sharply increase the body's demand for the hormone: acute infections, trauma, poisoning, surgical interventions, or pregnancy.
The pathogenesis is based on a specific triad: hyperglycemia, metabolic acidosis, and electrolyte disturbances. These shifts cause severe impairment of water-electrolyte metabolism, dehydration, and a pathological increase in intracellular osmotic pressure.
Clinical presentation
Symptoms develop in stages. In the prodromal period, the patient notes increased thirst and polyuria. Later, the following appear:
- Gastrointestinal syndrome: dyspeptic symptoms and epigastric pain.
- Neurological manifestations: insomnia, headache, and occasionally clonic seizures.
As it progresses, consciousness becomes depressed, passing through phases from pronounced drowsiness and complete apathy to coma. A specific sign is the sharp smell of acetone (rotting apples) in the exhaled air. Objectively, dry skin, soft eyeballs, and decreased muscle tone and tendon reflexes are revealed. Hemodynamically, there is a drop in blood pressure against the background of a rapid, thready pulse.
Laboratory diagnostics and treatment
- Blood: glucose within 25–50 mmol/L, pronounced leukocytosis, pH drop below 7.2 (metabolic acidosis).
- Urine: massive glucosuria and the presence of ketone bodies.
Treatment tactics are based on massive insulin therapy (regular insulin intravenously, sometimes over 100 IU/day). An isotonic sodium chloride solution is used for rehydration. Acidosis is managed with sodium bicarbonate solution, and electrolyte shifts are corrected by administering potassium chloride.
Hyperosmolar (non-ketotic) coma
This type of complication develops predominantly in patients with type 2 diabetes mellitus and is characterized by marked dehydration and a spike in plasma osmolarity without signs of ketoacidosis (ketone bodies are absent in lab tests). Triggers include severe stress, acute infectious processes, surgeries, and exacerbations of chronic pathologies.
The disease begins with increasing thirst, polydipsia, and polyuria, which, as it progresses, are replaced by oliguria and the development of azotemia. The patient's status is dominated by signs of severe dehydration, tachycardia, hypotension, and neurological deficits.
The biochemical profile includes hyperglycemia (glucose exceeding 40 mmol/L), hyperchloremia, and hypernatremia. The main directions of emergency care are urgent insulin administration and the infusion of significant fluid volumes to restore water balance.
Hypoglycemic coma
Unlike hyperglycemic states, hypoglycemia develops due to an insulin overdose or against the background of increased (sometimes irregular) physical exertion. The main feature of the condition is its extremely rapid onset, measured in minutes.
Stages of development
- Precursors: the patient suddenly experiences an acute sensation of hunger, severe weakness, and tremors throughout the body. Pronounced sweating and motor agitation occur.
- Comatose state: consciousness is lost, and seizures may begin against the background of psychomotor agitation.
Upon examination, dilated pupils and moist skin are noteworthy, which serves as a crucial differential sign compared to ketoacidosis.
Blood tests record a drop in glucose levels, while glucose and acetone are absent in the urine, and its specific gravity remains within the normal range. The sudden onset of an attack outside a hospital setting (on public transport or in the street) greatly complicates diagnosis. In such situations, discovering a "diabetic patient's booklet" helps the physician. Emergency care consists of the urgent intravenous infusion of a hypertonic glucose solution.
Briefly: answers to topical questions
What specific type of breathing develops in a patient with severe diabetic ketoacidosis?
In severe diabetic ketoacidosis, Kussmaul breathing ("air hunger") develops. This deep, noisy breathing appears against the background of a drop in blood glucose pH and an increase in CO₂ levels.
Characteristics of this pathological rhythm:
- Kussmaul breathing — regular cycles characterized by an infrequent yet deep and noisy inspiration followed by a forced expiration.
This type of breathing is usually observed against the background of severe impaired consciousness and is accompanied by a specific smell of acetone (stale apples) from the mouth. Its presence is a prognostic sign indicating an extremely severe patient condition requiring emergency medical care.
To what exact numerical values does plasma osmolarity rise in hyperosmolar coma?
In hyperosmolar diabetic coma, blood osmolarity rises to values above 310–320 mOsm/L. This condition is characterized as a progressive increase in plasma osmolarity (hyperosmia).
The pathogenesis of this disorder includes:
- Extreme hyperglycemia (glucose levels rising above 40 mmol/L).
- Absence of concomitant ketoacidosis.
- Increased permeability of blood-tissue barriers.
It is reaching and exceeding the threshold of 310–320 mOsm/L that triggers the development of pronounced neurological symptoms in the patient.
To quickly distinguish hypoglycemia from ketoacidosis during the examination stage, pay attention to the skin. In hypoglycemia, the skin is MOIST (like after physical exertion), whereas in ketoacidosis, it is completely DRY due to systemic dehydration.
Class and exam questions
Which of the diabetic comas develops the fastest?
Hypoglycemic coma develops the fastest — from the appearance of precursor symptoms to loss of consciousness, only a few minutes may pass.
What eye symptoms are characteristic of ketoacidosis?
During an objective examination of a patient with diabetic ketoacidosis, palpation reveals soft eyeballs, which is associated with a marked drop in intracellular osmotic pressure and severe dehydration.
What else to study on this topic
- Pathophysiology of gastrointestinal syndrome in ketoacidosis (causes of abdominal pain).
- Mechanisms of metabolic acidosis formation in absolute insulin deficiency.
- Features of electrolyte shifts (sodium and potassium) in different stages of coma.
- Algorithms and formulas for calculating infusion therapy in severe dehydration.
Master the entire topic in the "Propaedeutics" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Acute Complications of Diabetes Mellitus (Comas)" and 3,152 other subject pages
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 113 video lessons on the subject
Other topics in the section "Endocrine System and Metabolism"
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.