Endocrine organs produce hormones that are secreted into the bloodstream to act on distant target tissues.
The endocrine system as a whole regulates the functions of the body and maintains homeostasis throughout the body. It consists of about half a dozen different glands scattered throughout the body. These endocrine glands manufacture and secrete hormones directly into the bloodstream, which carries the hormone to the cells of the target organ. Exocrine glands secrete hormones and other products through a duct directly to their site of action. Once the hormone arrives at the target organ, the hormone can exert its effects in 1 of 2 primary ways: (1) it can attach to a receptor on the cell membrane, and a secondary messenger inside the cell will carry the “message” of altering the cell’s activity, or (2) it can pass through the cell membrane and directly exert its effects on the enzyme or protein in the cell.
This section of the chapter will discuss issues related to the glands of the endocrine system. Each gland will be presented in a similar manner. First, the anatomy and physiology of the gland, including the hormones that the gland primarily produces and their actions on the body, will be discussed. This is followed by syndromes resulting from dysfunction of that hormone or gland and the emergency treatment for that dysfunction as it relates to the paramedic. The most common endocrine emergency that paramedics must know how to treat is diabetes, particularly low blood sugar.
The pituitary gland hangs off the base of the brain and is attached directly to the hypothalamus. It is known as the master gland because the hormones it releases control the release of hormones from other endocrine glands. The 2 lobes of the pituitary gland are the posterior lobe and the anterior lobe.
The posterior lobe of the pituitary gland does not manufacture or secrete its own hormones; rather it stores and secretes oxytocin and antidiuretic hormone (ADH), both of which are made in the hypothalamus. Oxytocin is responsible for the initiation of contractions for and throughout childbirth, and it stimulates milk production in the breasts. ADH is released when the sodium concentration is too high and stimulates water reabsorption in the kidneys. It also stimulates thirst and increases blood pressure.
The anterior lobe of the pituitary gland manufactures and releases 6 different hormones.
Panhypopituitarism is the major syndrome associated with pituitary gland malfunction. Although often the result of an abnormal hypothalamus, this condition results in an inadequate or a complete lack of pituitary hormone production. This patient will be followed closely by a pediatric endocrinologist, and a paramedic will not likely see this patient for anything acute, and it will considerably alter the paramedic’s course of treatment for other problems.
The pineal gland is located near the posterior portion of the thalamus in the brain. It is responsible for circadian rhythms. Melatonin is secreted from this gland when light entering the eye decreases, which helps us fall asleep. No significant medical conditions that the paramedic would encounter are associated with this gland .
The thyroid gland is located in the neck, anterior to the trachea at the level of the thyroid cartilage. The thyroid produces triiodothyronine (T3) and thyroxine (T4), known collectively as thyronines, which are responsible for increasing metabolism. These hormones increase the basal metabolic rate at a cellular level and regulate fat, protein, and carbohydrate metabolism. An increase in these hormones increases body heat. These hormones are important in normal neurological and physical development in children.
The thyroid gland also produces calcitonin, which is responsible for decreasing the blood calcium level. Calcitonin decreases calcium levels in the following 3 ways: increases calcium excretion in the kidneys, increases calcium storage in the bones, and decreases the amount of dietary calcium that is absorbed in the intestines. Remember, calcitonin tones it down!
Medical conditions can result from too much or too little production of thyronines. Hyperthyroidism results from overproduction of thyroid hormones, and hypothyroidism comes from too little production.
| System | Hypothyroidism | Hyperthyroidism |
|---|---|---|
| Cardiovascular | Slow heart rate | Tachycardia and hypertension |
| Metabolic | Decreased metabolism and weight gain | Increased metabolism, hyperthermia, and weight loss |
| Muscular | Weakness | Tremor and hyperactive reflexes |
| Neurological | Decreased level of consciousness and sleepiness | Restlessness and irritability |
| Integumentary | Dry, cold skin | Hot, flushed skin and diaphoresis |
| Gastrointestinal | Constipated | Diarrhea |
Graves disease or hyperthyroidism is the most common and most severe form of hyperthyroidism, which can be fatal if left untreated. In Graves disease, the thyroid increases in size as its activity increases. This enlarged thyroid is called a goiter and is visible on the anterior neck of the patient. Patients suffering from Graves disease have an increased appetite combined with weight loss, excessive thirst (polydipsia) from excessive sweating, and diarrhea. Another classic finding in Graves disease is exophthalmos, which is the protrusion of the eyeballs from their sockets, giving these patients a perpetual surprised look.
Patients with Graves disease are not usually treated by paramedics because it tends to be more of a chronic condition. That said, Graves disease, among other causes including cancer and drug overdoses, can cause a condition known as thyrotoxicosis or thyroid storm. In this condition, excessive circulating thyroid hormones increase metabolism to unmaintainably high levels, resulting in a critically ill patient. Here, patients have an extremely high fever, diaphoresis, tachycardia, and possibly nausea and vomiting. Patients also can be irritable, be in an agitated delirium, have seizures, or be unconscious. Patients also may be hypoglycemic, which can reoccur after initial treatments as a result of the hypermetabolic state.
Thyroid storm needs to be aggressively managed to avoid death in this patient. Monitoring and continuous treatment of low blood sugar should be a concern, especially during long transport times. This patient may require abnormally high doses of benzodiazepines to achieve sedation, sometimes in excess of 3 times the normal dose. Tachycardia could be a result of the agitation, excessive dehydration from the sweating and hyperpyrexia, or some combination of both. Therefore, fluid should be aggressively administered to these patients as long as they are normotensive or hypotensive. Initiating beta-blocker treatment is recommended where available. Atenolol or metoprolol may be used; however, 0.5–1 mg propranolol as an intravenous piggyback over 10 minutes is the preferred choice. Finally, patients should be actively cooled using cold packs to the axillae and groin or intravenous cold saline to reduce their core temperature, especially if their temperature exceeds 103°F.
Hypothyroidism, sometimes called myxedema coma, is a slow-to-develop condition related to a decline in the production of thyroid hormones. Myxedema coma begins slowly and has subtle changes that may be mistaken for other problems or even just the general effects of aging. Symptoms of the initial onset of hypothyroidism include fatigue, dry skin, weight gain, and feeling cold all the time. The continued decline in the thyroid hormone can lead to deterioration of the patient’s mental status, at which point the family may call for an ambulance. The patient can then quickly decline further from altered mental status to unconsciousness and death if not treated. Once patients have reached the stage of myxedema coma heralded by an altered mental status, they are very likely to also be hypothermic, sometimes with core temperatures <90°F.
Treatment for myxedema coma is largely supportive, with goals focused on maintaining oxygenation, cardiovascular function, and temperature. Patients should receive supplemental O2 if the SpO2 is <95%, and intubation and ventilation should be considered in those patients without a gag reflex who also are breathing inadequately. Monitor the ECG and blood glucose level and give D50 if <60 mg/dL. For patients who are hypothermic, begin passive rewarming methods, including blankets and hot packs to the groin, axillae, and neck. Patients who are severely hypothermic or are hemodynamically unstable and requiring aggressive cardiovascular management or CPR should receive warmed fluids as well.
Located on the posterior side of the thyroid gland are 4 small glands that make up the parathyroid gland. These glands produce 1 hormone aptly named the parathyroid hormone (PTH). PTH also is involved in regulation of the blood calcium level, but in opposition to calcitonin. Calcitonin tones calcium levels down, whereas PTH increases calcium levels. It accomplishes this by limiting the excretion of calcium in the kidneys and increasing reabsorption of bone (dissolving bone to its components of calcium and phosphate).
Hyperparathyroidism is a condition where the parathyroid glands secrete excess amounts of the hormone for long periods of time. Because of increased calcium levels, the patient can be prone to kidney stones resulting from the amount of calcium and phosphorus in the blood. Patients also can have pathologic fractures—fractures not caused by an obvious traumatic event such as standing up—caused by continuous bone reabsorption. Treatment for any of these conditions is largely supportive.
The thymus gland is located in the chest of children. During adolescence, the thymus atrophies and essentially disappears, so adults do not actually have a thymus. During childhood, this gland produces thymosin, which stimulates the development of T-lymphocytes, a family of white blood cells essential in cell-mediated immunity. Cytotoxic T-cells, or killer T-cells, attack the antigen—virus, fungus, parasite, tumor cell, or bacterium—directly by engulfing it through a process called phagocytosis and killing it. Helper T-cells secrete chemical mediators called lymphokines that alert other lymphocytes to the presence of an invader and signal the thalamus to raise the body temperature. After the invader is cleared from the body, suppressor T-cells contain the immune response. It is thought that the failure of suppressor T-cells is a factor in allergic reactions and autoimmune diseases. A paramedic will seldom encounter a thymus-related problem.
The body has 2 adrenal glands, each perched atop a kidney. The adrenal glands have 2 distinct regions: the outer part is called the adrenal cortex, and the central part is called the adrenal medulla.
The adrenal cortex produces hormones that have widely varied functions. The outermost layer of the adrenal cortex produces mineral corticoids that are responsible for maintaining the salt balance within the body. A decrease in salt concentration in the blood, a decrease in blood pressure, or an increase in potassium concentration stimulates the adrenal cortex to produce an important mineral corticoid called aldosterone. Aldosterone works on the kidneys to increase the reabsorption of sodium and instead increase the excretion of potassium. During times of stress, ACTH from the pituitary gland stimulates the middle layer of the adrenal cortex to produce the glucocorticoids. Cortisol, a prominent glucocorticoid, stimulates the body to increase its energy production and also increases the rate that fat is deposited in adipose tissue in the belly. Finally, the inner layer of the cortex is responsible for the production of the sex hormones estrogen and testosterone.
The adrenal medulla is the primary site of production in the body for epinephrine and norepinephrine, collectively known as catecholamines. These catecholamines aid in the fight-or-flight response to stress. The 3 adrenal emergencies are adrenal insufficiency, Cushing syndrome, and congenital adrenal hyperplasia.
Adrenal insufficiency can be either primary or secondary. In primary adrenal insufficiency, known as Addison disease, the patient’s adrenal cortex is no longer functioning, resulting in a deficiency of all steroid hormones. The failure can be brought on by idiopathic atrophy, an infection such as tuberculosis, adrenal cancer, or an autoimmune disease where antibodies destroy the adrenal cortex.
Secondary adrenal insufficiency is caused by a lack of production of ACTH, which results in a lack of production of all cortical steroids except aldosterone. Aldosterone is still produced because its secretion is not dependent on ACTH but rather potassium and sodium concentrations in the blood. Secondary adrenal insufficiency also may be seen in people who suddenly stop taking corticosteroid medications such as hydrocortisone or solumedrol. Because these medications suppress natural corticosteroid production by keeping blood concentrations high, the body does not catch up to the sudden drop quickly enough.
Adrenal insufficiency starts off with insidious symptoms, including unexplained weight loss, fatigue, vomiting, diarrhea, and salt craving. The patient also may have abdominal pain; back pain in the area of the kidneys; and increased pigmentation of the oral mucosa, extensor surfaces, and the palmar creases. In both primary and secondary adrenal insufficiency, the patient may experience an addisonian crisis, which occurs whenever the body is stressed and would ordinarily require corticosteroids to respond to that stress. This includes emotional or physical stress, trauma, surgery, or infection. During an addisonian crisis, what a person with normal adrenal function would handle successfully sends a person with adrenal insufficiency into catastrophic shock. The patient suddenly exhibits a change in mental status, hypotension, weakness, severe vomiting, and diarrhea. Death can follow if the hypotension and cardiac dysrhythmias caused by the excess blood potassium are not treated and reversed.
For the paramedic treating a patient in addisonian crisis, the goal is to support cardiovascular function and treat for the apparent shock with normal saline. Fluid volume expansion is usually the first line of treatment. This will help increase the sodium level in the blood and reduce the concentration of circulating potassium as well as address hypotension and dehydration. Administering several doses of 20 mL/kg NSS is not out of the question in this patient. Check the blood sugar level and administer D50 if <60 mg/dL. Consider administering 1 g calcium chloride or calcium gluconate if the cardiac rhythm reveals hyperkalemia; treat any other dysrhythmias encountered as if cardiac in nature.
Cushing syndrome is caused by an excess production of cortisol secondary to tumors of the pituitary or adrenal cortex. It is characterized by a rise in blood sugar. Protein synthesis is impaired, causing rhabdomyolysis (breakdown of skeletal muscle). Patients will complain of weakness, fatigue, depression, and mood swings. Patients also have a characteristic weight gain in Cushing syndrome. They gain weight in the belly but not the arms or legs. Fat deposits appear above the shoulders (supraclavicular), between the shoulder blades (buffalo hump), and in the face (moon face). Women will get notable facial hair in a pattern similar to that of men and will often start losing their scalp hair. Prehospital treatment involves symptomatic treatment and an evaluation of blood sugar levels.
Congenital adrenal hyperplasia (CAH) is the opposite of Cushing syndrome in that it is the inadequate production of cortisol as well as aldosterone. This is a lifelong problem and will require lifelong treatment with cortisol and/or aldosterone. Children with CAH appear masculine in nature, and female genitalia may resemble a penis. Male and female patients may exhibit signs of puberty as toddlers, including body hair and lowering of the voice.
The testes are the main source of testosterone and other androgens. The androgens are responsible for the development of secondary sex characteristics throughout life, especially during puberty.
The ovaries are located in the lower quadrants of the abdomen at the distal ends of the fallopian tubes. They are the primary source of estrogen in woman, which is responsible for the development of secondary sex characteristics in women.
The pancreas is centrally located in the abdomen, with part of it located in all 4 quadrants. It is both an exocrine and an endocrine gland because it delivers enzymes directly to the duodenum via the pancreatic duct and secretes hormones into the bloodstream. For our purposes here, only the endocrine properties will be addressed.
The endocrine component of the pancreas is in specific areas called the islets of Langerhans. These are groups of cells within the body of the pancreas whose sole purpose is to manufacture the hormones insulin, glucagon, and somatostatin.
Insulin is necessary for glucose in the bloodstream to be able to cross the cell membrane, where it can be properly used as cellular fuel. Insulin, which is secreted by the beta cells within the islets of Langerhans, also is required to move glucose from the blood into the liver, where it can be stored in long chains of molecules called glycogen. Once the blood glucose decreases to a normal level, the islets stop producing insulin. Glucagon, secreted by the alpha cells of the islets of Langerhans, on the other hand, stimulates the liver to convert the glycogen back to glucose during times of fasting or inadequate food consumption and release it back into circulation so it can be used by the other cells of the body. Somatostatin is released by the delta cells of the islets of Langerhans and is a potent inhibitor of both glucagon and insulin.
Diabetes is the body’s inability to metabolize glucose because it is not able to get into the cells. Insulin production in diabetes can either be nonexistent when no insulin is produced, inadequate when not enough insulin is produced to meet the needs of the body, or produced but unable to signal the cell properly to allow glucose to enter. Regardless of the reason, the glucose cannot enter the cell and cannot, therefore, be metabolized in the cells. As the glucose level continues to rise in the bloodstream, it will eventually reach a level where it spills into the urine so that it does not become a poison to the body. Diabetes is further classified into type 1 or type 2.
In type 1 diabetes, previously called juvenile diabetes because the initial onset is typically during childhood, the beta cells of the islets of Langerhans have been destroyed and no longer produce insulin. The cause still has not been conclusively determined; however, there may be a genetic cause or an autoimmune component. Because the patient no longer has functioning beta cells to produce insulin, these patients are dependent on daily insulin injections to regulate their blood sugar for the rest of their lives. The insulin prescribed to these patients is either fast acting or long acting. Fast-acting insulin is generally injected at about the time of the meal so that the increase in blood sugar is handled quickly, while the long-acting is taken once and exerts its effects equally throughout the day, resulting in fewer fluctuations of blood sugar level. For patients on long-acting insulin, they have to eat consistently throughout the day to maintain their blood sugar levels. Insulin also must be kept refrigerated to maintain its potency; if it is left out for more than a couple of days, it will be as useful as injecting saline to control blood sugar.
Type 2 diabetes was once called adult onset diabetes because it begins in late adulthood. In most people with type 2 diabetes, the pancreas produces insulin; however, the insulin it produces is either not produced in high enough quantity to be able to effectively regulate blood sugar or is produced in sufficient quantity but unable to signal the cells to allow the glucose in. Insulin resistance occurs when insulin is produced but the body cannot effectively use it. These patients often are on medications called oral antihyperglycemics that help the body use the insulin it does produce more efficiently.
In both types of diabetes, the patient can have either critically high or critically low blood sugar levels, hyperglycemia or hypoglycemia, respectively. Most commonly, hypoglycemia results from too much insulin taken for the amount of food consumed, or not consuming food often enough or in great enough quantity to keep up with the type of insulin taken. Hypoglycemia generally comes on suddenly and without obvious warning signs; the patient is suddenly found unresponsive.
Normal blood sugar levels are generally accepted to be between 70 and 140 mg/dL; they will be higher if the blood sugar is taken within 2 hours of having eaten. Clinically significant hyperglycemia usually takes a few days to develop to the point where the patient shows signs and symptoms because blood sugar levels can easily swell to >200 mg/dL after a carbohydrate-heavy meal. Hyperglycemia is defined as sustained blood sugars despite fasting between 140 and 400 mg/dL; it is concerning when symptoms described in the next section are concurrently present. If blood sugar levels are not treated, the patient may progress to either diabetic ketoacidosis (DKA) or a state called hyperosmolar hyperglycemic nonketotic coma (HHNC), also known as hyperosmolar nonketotic coma (HONK).
DKA is typically associated with type 1 diabetes and can become a life-threatening condition as blood sugar levels rise and the acid levels in the blood exceed the body’s capacity to neutralize the acid, lowering overall pH. As the patient’s blood sugar continues to rise, the bloodstream will eventually become so concentrated that the kidneys will start to excrete the sugar in the urine, a condition known as osmotic diuresis. This requires large amounts of fluid to be able to safely excrete the glucose resulting in frequent, full bladder urination called polyuria. When a patient is in DKA, the patient’s cells turn to fat for fuel instead of glucose. This emergent type of fat metabolism results in the production of ketones (a specific group of organic compounds) that can be eliminated in both the urine and during exhalation. These ketones have a sweet or fruit-like odor to them that can be smelled on the patient’s breath.
HHNC/HONK is most often found in patients with type 2 diabetes. These patients have the same metabolic situation of hyperosmolarity (spilling sugar into the urine) and hyperglycemia; however, they lack the ketone, fruity smell to their breath. Unlike DKA, there is a high incidence of concurrent MI with patients in HHNC/HONK. There often also is a concurrent illness, commonly pneumonia or a urinary tract infection that leads to the HHNC/HONK condition.
Patients with diabetes and either hypoglycemia or hyperglycemia present with an altered mental status, but that is about where the similarities end.
| Assessment Point | Hyperglycemia | Hypoglycemia |
|---|---|---|
| Thirst | Excessive (polydipsia) | Normal |
| Hunger | Absent | Extreme |
| Vomiting | Frequently | Rarely |
| Urination frequency | Frequent (polyuria) | Normal |
| Insulin dose | Less than required | More than required |
| Onset timing | Slowly (over days) | Rapidly (minutes to hours) |
| Skin | Hot and very dry | Cool, pale, and diaphoretic |
| Respirations | Fast and deep (Kussmaul) | Normal |
| Blood pressure | Normal | Normal to low |
| Pulse | Full, bounding | Weak, thready |
| Blood sugar level | >140 | <60 |
Treatment for hypoglycemia focuses on restoring normal blood sugar levels. Depending on the patient’s level of consciousness, this can be accomplished orally or parenterally. If the patient is able to protect his or her own airway at a minimum, or better yet swallow, he or she can be given medical oral glucose or drink orange juice or regular soda to raise the blood sugar level. Patients also should be encouraged to eat complex carbohydrates after the orange juice or soda so that their blood sugar levels are more likely to be maintained. If the patient is unresponsive or unable to maintain an airway, the patient can be administered 1 mg glucagon intramuscularly if no intravenous access is readily available. If an intravenous line is available, give 25 g of D50 (1 amp) through a patent intravenous line and flush with saline. It is important to ensure that the intravenous line is not infiltrated into the soft tissue prior to administering the D50 because D50 is extremely hypertonic and could cause tissue necrosis if it extravasates.
Although the in-hospital course of treatment for hyperglycemia focuses on lowering blood sugar levels, prehospital treatment focuses on fluid replacement and beginning to correct the prevalent metabolic acidosis. Begin by establishing at least 1 intravenous line of NSS and plan to deliver 1 L of fluid during the first half hour. As with any patient receiving a hefty fluid bolus, continually evaluate lung sounds and cardiac function throughout this infusion to ensure that the patient is not getting fluid overloaded, although this is extremely unlikely in the hyperglycemic patient. Monitor the ECG rhythm and note the presence of peaked T waves that could indicate hyperkalemia, a possible complication brought about by cellular death. If this is found, consider administering 1 g calcium chloride or calcium gluconate. Although it may seem like a good idea to administer bicarbonate for the acidosis, this decision should be left up to the physician because rapid reversal of this kind of acidosis with bicarbonate could have negative effects. If employed, it must be carefully controlled, which is beyond what is capable in the field.