Updated June 13, 2017
If any patient presents with an altered mental status or any type of bizarre or uncharacteristic behavior, the EMS practitioner must consider a diabetic emergency as a possibility during his or her critical thinking process when developing a differential field diagnosis. Encountering a patient in the prehospital environment with a medical history of diabetes mellitus (DM) is a very common event for EMS.
Initially, the conditions that must be considered and eventually ruled out are hypoglycemia, diabetic ketoacidosis (DKA), and hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Even though all of these conditions are related to a disturbance in the blood glucose level, each presents with a different set of signs and symptoms that can be explained based on basic pathophysiology.
Understanding the basic pathophysiology will explain the etiology of the signs and symptoms and will preclude the EMS practitioner from having to memorize clinical presentations.
Diabetes mellitus is a condition in which the patient experiences a chronically elevated blood glucose level. Although EMS frequently responds to those with a low blood glucose level (hypoglycemia), most DM patients struggle on a daily basis to decrease their blood glucose level down to a normal range.
However, it is the occasional acute hypoglycemic event that carries a high risk of morbidity and mortality. Thus, it is imperative that the EMS practitioner quickly recognize the signs and symptoms of hypoglycemia and manage the patient accordingly to prevent any lasting long-term effects.
Physiology and pathophysiology
To understand the signs and symptoms of hypoglycemia, one must comprehend some basic normal physiology and pathophysiology. The primary energy fuel for cells is glucose. Glucose is a simple sugar that accounts for approximately 95 percent of the sugar in the blood after gastrointestinal absorption. Thus, it is the blood glucose level that EMS and other health care practitioners are most interested in determining.
Insulin is a hormone secreted by the beta cells in the pancreas. The primary function of insulin is to move glucose from the blood into the cells where it can be used for energy. However, insulin does not directly carry glucose into the cell. It triggers a receptor on the plasma membrane to open a channel allowing a protein helper, through the process of facilitated diffusion, to carry the glucose molecule into the cell.
As long as insulin is available in the blood — and is active, effective, and able to stimulate the receptor — it will continue to move glucose into cells, even if the blood glucose level falls below the normal range. When this occurs, a large amount of glucose is moved out of the blood leaving an inadequate supply for the brain cells. If the pancreas is functioning normally, insulin secretion will decrease as the blood glucose level drops.
Approximately 60 percent of a person’s blood glucose after eating a meal will be sent to the liver to be stored in the form of glycogen. Glycogen is a complex carbohydrate molecule that is broken down through a process known as glycogenolysis and returned back to the blood as free glucose. This allows a person to maintain a near-normal blood glucose level between meals. Glucagon is a hormone released by the alpha cells in the pancreas that stimulates glycogenolysis and the conversion of non-carbohydrate substances into glucose (gluconeogenesis), subsequently raising the blood glucose level.
As the blood glucose level decreases to approximately 70 mg/dL, insulin secretion will cease. As a result, glucagon will be released to maintain a normal level of glucose and constant supply to the brain cells.
Once in the cell, the glucose is then metabolized and produces energy in the form of adenosine triphosphate (ATP). ATP is necessary for cells to maintain a normal function. Without an adequate blood glucose level, alternative energy sources must be used by the cells. As a result, ATP production and cellular function may be altered.
Blood-brain barrier
The brain cells, unlike many other cells in the body, can not effectively use any other energy source for ATP production but glucose. Interestingly, the blood-brain barrier does not require the presence of insulin to move glucose across the brain cell membrane.
The brain cannot synthesize glucose, store it for extended periods of time, or concentrate it from the blood. Thus, a decrease in the blood glucose level below normal may result in brain cell dysfunction from a lack of ATP production, a decrease in oxygen uptake, and a decrease in cerebral blood flow. A prolonged and severe decrease in the blood glucose level could result in brain cell death.
A decrease in the blood glucose level below a normal range is known as hypoglycemia. Hypoglycemia is precipitated by having too much insulin or not enough glucose in the blood. This may result from the following:
- taking too much insulin
- missing a meal or not eating enough calories to match the insulin dose
- increasing energy output through exercise or work related activities and not increasing caloric intake
- from an increased dose of oral hypoglycemic agents (sulphonylureas or meglintides)
- or from other unknown causes
Alcohol ingestion inhibits the gluconeogenesis and glycogenolysis, which may predispose the patient to hypoglycemia.
Presentation thresholds
Most DM patients become symptomatic when the blood glucose level decreases to 40 - 50 mg/dL; however, this varies among patients. Patients have different thresholds and may present with severe signs and symptoms with reported blood glucose levels that are higher or lower than 50 mg/dL, which may also vary within the same individual on repeated episodes of hypoglycemia.
The onset and severity of signs and symptoms also depends on how quickly the glucose level fell, how low it fell, and the typical level for the patient.
When the blood glucose level decreases beyond the normal range, the body will secrete counter regulatory hormones in an attempt to increase it. Glucagon is secreted from the alpha cells and epinephrine is released from the adrenal medulla. Both glucagon and epinephrine stimulate gluconeogenesis and glycogenolysis in the liver.
Epinephrine will also cause the breakdown of proteins into amino acids for conversion to glucose and will decrease the secretion of insulin from the pancreas. Growth hormone, cortisol and vasopressin are also secreted as counter regulatory hormones; however, they do not have as significant an effect.
Insulin shock
The signs and symptoms the hypoglycemic patient exhibits are due to an activated sympathetic nervous system, epinephrine circulating throughout the body in an attempt to increase the blood glucose level, and brain cells that are dysfunctioning due to the lack of glucose.
Hypoglycemia was once referred to as “insulin shock” due to the similarities of the signs exhibited by both hypovolemic shock and the hypoglycemic patient. The primary hormone that produces tachycardia and pale, cool and clammy skin in the shock patient is epinephrine, which is also released in the hypoglycemic patient producing similar signs.
The signs and symptoms of hypoglycemia can be categorized as being either hyperadrenergic, which is associated with an increase in the sympathetic nervous system activity or circulating epinephrine; or, neuroglucopenic, which is a result of direct brain cell dysfunction from the lack of glucose.
| Typical hyperadrenergic signs and symptoms: Neuroglucopenic signs and symptoms: |
Severe episodes of hypoglycemia may cause hemiplegia, making the patient present as a potential stroke. Thus, be sure to assess the blood glucose level in a suspected stroke patient; but never administer glucose without a confirmed low blood glucose level, typically less than 60 mg/dL.
By understanding that the signs and symptoms of hypoglycemia are a result of increased sympathetic nervous system activity and circulating epinephrine (hyperadrenergic), and from brain cell dysfunction (neuroglucopenic), there is no need to memorize signs and symptoms of the condition.
Just use knowledge of sympathetic nervous system stimulation and circulating epinephrine in order to envision how a patient would present if his or her brain cells were dysfunctioning. This understanding will equip EMS providers with the tools to accurately and efficiently assess a diabetic emergency.
