Balance Between Insulin and Glucagon
Both insulin and glucagon are made and released from the pancreas, an organ associated with the intestines that also makes digestive enzymes to break down food that is eaten.
Insulin: Diabetes interferes with the entrance of glucose into the cells. Normally, glucose entering from the blood into the cells (which use it for energy) is controlled by a hormone called insulin. If someone doesn’t have enough insulin, this is called diabetes mellitus, which results in a build-up of glucose in the blood that normally would have entered the cells. This increased level of glucose is called “hyperglycemia” (meaning, high glucose in the blood). With diabetes, this hyperglycemia can damage blood vessels and organs as well as mean too little getting into the cells, affecting the way they work.
Glucagon: A second hormone, glucagon, affects the liver such that it manufactures more glucose when needed. Normally, the two hormones (insulin and glucagon) are in a balance, but in diabetes, that balance is thrown off because insulin normally suppresses the release of glucagon and when there is too little insulin, glucagon is overproduced. Too little insulin makes the glucose in the blood accumulate, since it’s not getting into the cells; more glucagon makes the liver produce extra glucose. Thus, too little insulin raises the blood sugar by both mechanisms.
Another type of diabetes is “insulin-resistant” or Type II diabetes, in which—instead of not enough insulin—the cells resist the insulin’s normal functioning with the same result: not enough glucose enters cells and too much of it builds up in the blood.
Ketones: Untreated, runaway hyperglycemia can cause the acidity of the blood to increase, measured by a value called pH (how acid the blood is). Also, if the cells resort to a secondary method—a back-up method—of making their own glucose for energy, it can cause a build-up of ketones (by-products of this method). Therefore, there are two distinct types of hyperglycemia:
- Non-ketotic hyperglycemia: Also called Hyperosmolar Hyperglycemic State (HHS)
- Ketotic hyperglycemia: Also called Diabetic Ketoacidosis (DKA)
Hyperosmolar Hyperglycemic State and Diabetic Ketoacidosis (HHS and DKA)
Both HHS and DKA are endpoints in the abnormal metabolism initiated with hyperglycemia and are the most serious acute complications seen in DM. As glucose builds in the blood, its concentrations rise, making the blood “hyperosmolar” (over-concentrated). This stimulates the kidneys to compensate with excess urinary excretion of electrolytes (sodium, potassium, etc.) which causes an imbalance in them, as well.
In normal circumstances, blood sugar concentration is < 100 mg/dL. In DKA, however, the glucose concentration can be 350-400, and in HSS it can reach 1,000. DKA is a rapid sequence of events, causing nausea, vomiting, and abdominal pain, but HSS begins more slowly.
In both HSS and DKA there is a hyperosmolality (overconcentration of glucose within the blood) that causes neurologic changes, beginning as focal neurologic weakness, lethargy, and mental changes that progresses to seizures, stupor, and coma.
Diabetic coma results from these over-concentrated conditions, with neurological changes in the brain beginning with levels > 320-330 mg/dL. The coma can occur due to either a hyperosmolar hyperglycemic state (HHS) or being in diabetic ketoacidosis (DKA). Both involve a hyperglycemia state, but in HHS, glucose levels can exceed 1,000. In DKA, they are usually lower.
Identifying HHS vs. DKA as the Cause of Diabetic Coma: Blood pH
pH—a measure of the acid nature of blood, is determined by an arterial blood gas (which has the pH as one of its measurements. This measure of acidity can help distinguish between HHS vs. DKA, as DKA is an acidosis (acid-like, with a low pH) due to excess ketoacids (ketones) in the blood.
HHS, Alternately, Is a Non-Ketotic Hyperosmolar State
Determination of electrolytes levels (sodium, potassium, etc.) is important to identify life-threatening conditions that the overconcentration in the blood produces in HHS and DKA. Then when there is additional excretion by the kidneys to compensate, the lost water makes the concentration of some solutes (sugar, electrolytes, and other substances found in the blood) even higher. Therefore, testing of the following are indicated:
- Serum and urine ketones (present or absent)
- Serum sodium, potassium, chloride, bicarbonate, and other electrolytes
- ECG/EKG: Acidosis/overconcentrated states resulting in electrolyte abnormalities (too little or too much of one of them) severely impact cardiovascular status, necessitating an electrocardiogram to determine whether support for cardiac issues is warranted
- Infection can convert a well-controlled diabetic into an hyperglycemic state, so diagnostic tests for infection, such as bacterial cultures, blood counts, and chest X-rays, are indicated
Telling the difference between HHS and DKA as the cause of coma and diagnosing the types of electrolyte problems that occur allow for a rational approach to rapid treatment, which is necessary to avoid death.