When a person with diabetes stops taking insulin, they initiate a rapid, life-threatening chain of events. Insulin acts as a key, unlocking cells to allow glucose, the body’s primary fuel, to enter and be used for energy. Without this hormone, cells are locked off from their fuel source, which is immediately serious for anyone requiring insulin, especially those with Type 1 diabetes who produce none. The consequences are swift, often leading to medical emergencies within hours or days as the body attempts to find alternative ways to power itself.
The Initial Response: Cellular Starvation and Hyperglycemia
The absence of insulin prevents glucose from moving out of the bloodstream and into muscle, fat, and liver cells. This leads to a rapid accumulation of sugar in the blood, known as hyperglycemia, which quickly climbs to high levels. Despite the high concentration of glucose, the cells are starved of energy, prompting the body to signal a state of famine.
This perceived starvation triggers a surge of counter-regulatory hormones, including glucagon, epinephrine, cortisol, and growth hormone, designed to raise blood sugar further. Glucagon signals the liver to produce more glucose by breaking down stored glycogen (glycogenolysis) and creating new glucose from non-carbohydrate sources (gluconeogenesis). Epinephrine also intensifies hyperglycemia by signaling the liver and kidneys to produce glucose and inhibiting glucose uptake in muscle tissue.
With glucose unavailable, the body switches metabolism to stored fat. The lack of insulin activates lipolysis, breaking down fat tissue and releasing free fatty acids into the bloodstream. The liver processes these fatty acids, converting them into ketone bodies to provide energy for tissues like the brain and muscles. This metabolic shift establishes the foundation for the most immediate and dangerous complication of stopping insulin.
Acute Danger for Type 1: Diabetic Ketoacidosis (DKA)
Diabetic Ketoacidosis (DKA) is the primary and most rapid life-threatening consequence of stopping insulin for a person with Type 1 diabetes. The excessive production of acidic ketone bodies, such as beta-hydroxybutyrate and acetoacetate, overwhelms the body’s buffering system. This causes a drop in the blood’s pH, resulting in metabolic acidosis, the defining feature of DKA.
The body attempts to eliminate excess sugar and ketones through osmotic diuresis. This results in frequent urination (polyuria) and extreme thirst (polydipsia), leading to severe dehydration and electrolyte loss. Dehydration causes symptoms like dry skin, a rapid heart rate, and can impair kidney function, worsening hyperglycemia.
To compensate for increasing acidity, the respiratory system attempts to restore pH balance by expelling carbon dioxide. This results in Kussmaul respirations, characterized by deep, labored, and rapid breaths. Acetone, a volatile ketone body, is exhaled through the lungs, giving the breath a characteristic fruity odor.
As DKA progresses, the combination of acidosis, dehydration, and electrolyte imbalance leads to severe systemic symptoms. Patients often experience nausea, vomiting, and abdominal pain, which contribute to fluid loss. If left untreated, the accumulation of acid and profound dehydration can cause lethargy, confusion, and eventually progress to a coma and death. Severe symptoms often appear within 24 hours of insufficient insulin.
Acute Danger for Type 2: Hyperosmolar Hyperglycemic State (HHS)
While Type 1 diabetics face DKA, Type 2 diabetics who stop insulin are more likely to develop Hyperosmolar Hyperglycemic State (HHS). HHS is characterized by extremely high blood sugar levels, often exceeding 600 mg/dL, and profound dehydration. Because Type 2 diabetics still produce some endogenous insulin, this small amount usually prevents the massive fat breakdown that causes DKA’s severe acidosis.
The immense hyperglycemia pulls water from the body’s cells into the bloodstream, which the kidneys rapidly excrete, causing significant fluid loss. This dehydration makes the blood highly concentrated, a state called hyperosmolarity, which is the hallmark of HHS. Hyperosmolarity draws water out of brain cells, leading to severe neurological symptoms.
HHS typically develops more slowly than DKA, often over several days or weeks, but it is equally life-threatening. Symptoms include extreme thirst, frequent urination, and severe mental changes, ranging from confusion and disorientation to seizures and coma. HHS often presents with more severe dehydration and higher blood glucose levels than DKA, carrying a high risk of death if not promptly treated.
Emergency Treatment and Recovery
Both DKA and HHS are medical emergencies requiring immediate hospitalization. Treatment focuses on reversing metabolic derangements through fluid replacement, insulin therapy, and electrolyte management.
The initial step is aggressive intravenous (IV) fluid replacement to correct severe dehydration. Saline solutions restore blood volume and dilute the high concentration of glucose and other substances. For DKA, IV fluids are typically administered at high rates initially; for HHS, the rate is often individualized.
Once rehydration begins, an insulin infusion is started intravenously to lower blood glucose. In DKA, insulin halts the production of acidic ketones and is administered until acidosis resolves. For HHS, the primary role of insulin is to normalize the extremely high glucose levels.
Electrolyte replacement, particularly potassium management, is essential. Patients with DKA or HHS often have a total body potassium deficit due to fluid loss, even if initial blood levels are normal or high. As insulin is administered, it causes potassium to shift rapidly back into the cells, which can lead to dangerously low blood potassium (hypokalemia) if not monitored. Close monitoring of fluid status, electrolytes, and glucose levels is required throughout recovery.