At 0730 hours, a 20-year-old female college student presents in an altered state, combative and struggling with campus police in her dorm room. Her roommate states the patient had been acting strangely since last night – saying things that didn’t make sense, going to the bathroom constantly and sweating a lot.
Your assessment reveals a young woman who appears to be fit, confused and disoriented. Her skin is hot, pale and diaphoretic. She is tachycardic, hypertensive and tachypneic and her pupils are dilated. The roommate doesn’t believe that the patient has any medical history, nor does she take any prescription or recreational drugs. She is on the college’s soccer team and recently strained her back, and was taking baby aspirin to ease the pain and swelling.
Endocrine system review
The endocrine system is responsible for most of the long-term processes of the human body such as sexual development and growth, and regulating the body’s internal balance of fluid, electrolytes and other chemicals to maintain homeostasis. There are several glands and other organs that secrete a variety of hormones, which are transported in the bloodstream throughout the body. Receptors in tissues detect the circulating hormones and either stimulate or block a specific action. The receptors and hormones act as a lock and key; specific hormones engage with specific receptors to elicit the appropriate response.
Endocrine emergencies are not commonly seen, yet can be one of the suspected underlying causes in many urgent presentations that EMS providers see in the field. Here are the four endocrine emergencies to know:
- Thyroid storm
- Myxedema coma
- Diabetic ketoacidosis
- Acute adrenal crisis
In many of situations, the field care is mostly supportive, focused on maintaining the patient’s airway, ventilatory ability and perfusion status. In some situations, medications and/or intravenous fluids can begin to reverse the signs and symptoms caused by the endocrine emergency.
1. Thyroid storm
The thyroid is a small gland located in the neck, just below the thyroid and cricoid cartilage. It secretes thyroxine, or thyroid hormone to control the body’s overall metabolism rate. Another structure called the pituitary gland signals the thyroid when to secrete thyroxine.
The body responds to thyroxine in many ways, including increasing heart rate (chronotropy) and contraction strength (inotropy), increasing the rate of which food passes through the gastroinstestinal tract (peristalsis), the production of blood sugar (gluconeogenesis) and the release of stored body sugar into blood sugar (glycogenolysis).
Hyperthyroidism occurs when the thyroid gland becomes hyperactive and secretes too much thyroxine. This is most commonly caused by an autoimmune disorder call Grave’s disease; other causes include thyroid or pituitary tumors, inflammation of the thyroid, and excess intake of iodine. Less common causes include myocardial infarction, major infections, thyroid trauma, salicylate overdose, diabetic ketoacidosis, congestive heart failure or pulmonary embolism.[1,2]
A thyroid storm occurs when the body is overwhelmed by very high levels of circulating thyroxine. Signs include altered mental status, hypertension, tachycardia, tachypnea, and hyperthermia with hot, diaphoretic skin. Blood sugar levels may be low, and the patient may be dehydrated due to nausea, vomiting and diarrhea associated with the thyroid storm. Supraventricular tachycardia may require vagal maneuvers or cardioversion.
EMS treatment for a thyroid storm is mostly supportive, providing intravenous fluids and dextrose as needed, cooling the body with external measures and rapid transport to an emergency department.
2. Myxedema coma
Hypothyroidism is the opposite of hyperthyroidism; the thyroid gland does not secrete enough thyroxine to support normal metabolic needs. Hypothyroidism happens eight times more frequently in women than in men.[3] Prescription thyroid medications such as Synthroid are commonly prescribed medications for hypothyroidism.
As one might expect, signs of hypothyroidism are related to slower metabolism rates: chronic fatigue, cold intolerance, weight gain, headache, and constipation. In severe hypothyroidism, or myxedema coma, the condition becomes life threatening. Patients may be profoundly bradycardic, hypotensive and hypothermic. Respirations will be slow, shallow and in extreme cases stop altogether. Their mental status might range from being confused and lethargic to deeply unconscious.
EMS treatment for myxedema coma includes supporting the patient’s airway, assisting ventilations if necessary, and support perfusion. An airway adjunct may be required to maintain airway patency. Monitor oxygen saturation (Sp02) and exhaled carbon dioxide levels (EtCO2) and provide positive pressure ventilations carefully. A parasympathetic blocker such as atropine and/or a vasopressor may be administered if heart rate does not improve after ventilation.
3. Diabetic ketoacidosis
The body balances its metabolic demand for glucose by secreting the hormone insulin from the beta cells of the islets of Langerhans, located in the pancreas. Simply, as the body’s cell requirement for glucose goes up, so does the release of insulin. In addition, glucagon is also released from alpha cells found in the islets and Langerhans, which in turn stimulates the conversion of glycogen stores in the liver and deep muscle beds to glucose, which enters the bloodstream.
Insulin assists the absorption of glucose through the cell membrane by opening channels within the membrane itself. A glucose molecule is too big to pass through the membrane by itself.
This mechanism becomes disrupted when normal insulin production or release is damaged. The beta cells in the islets of Langerhans can be permanently destroyed through an autoimmune response, resulting in little or no insulin production. This is Type I diabetes. Patients with Type I diabetes are required to self-administer artificially manufactured insulin daily.
A more common form of diabetes occurs when the amount of insulin being produced is not enough to manage the levels of glucose circulating within the body. Known as Type II diabetes, cells can also become resistant to the effects of insulin, decreasing the efficiency of glucose passing through the cell membrane. Type II diabetes can be managed through weight or diet control, and through oral hypoglycemic medications such as Diabenase, glyburide or metformin.
If insulin levels fall below normal levels, the cells are unable to absorb and process glucose efficiently. Patients become hyperglycemic when the amount of glucose in the blood stream becomes elevated. In turn the body turns to metabolizing proteins and fats (lipolysis) as a primary source of energy. This mechanism creates ketone bodies as a byproduct of metabolism; acetone is an example of a ketone. Elevated levels of ketones cause an increase of acidosis in the body; combined, these effects cause a condition known as diabetic ketoacidosis or DKA.
DKA typically occurs more frequently in Type I diabetics, but Type II diabetics are susceptible during times of infection, trauma, and cardiovascular events.[4] Normal fasting blood glucose levels range from 70-100 mg/dcl; patients in DKA will have levels of 250 mg/dcl or higher.[5,6].
There is a wide range of signs and symptoms associated with DKA. A classic set of history findings includes the three “Pollys.” The body tries to remove the excess amount of blood glucose through the kidneys via increased urination (polyurea). This causes the patient to feel thirsty (polydipsia). Meanwhile, the cells continue to demand glucose; this registers as hunger (polyphagia). These symptoms may manifest themselves gradually over a period of days to weeks.
The body will try to compensate for the excess ketone bodies and the worsening acidosis by increasing the rate and depth of respirations. Known as Kussmaul breathing, this reduces the level of carbon dioxide in the bloodstream, creating an alkalosis condition that somewhat balances the metabolic acidosis temporarily. Ketone bodies are also exhaled; EMS providers may be able to detect ketone bodies by the faint smell of acetone on the patient’s breath. Be forewarned that the smell may be easily mistaken with the smell of alcohol; carefully evaluate the history of the event to discriminate between alcohol ingestion and DKA.
In severe cases of DKA, patients become altered and finally unresponsive. The skin can become warm, look flushed and feel dry as dehydration worsens. Heart rate rises dramatically and hypotension can develop.
Combined with severe dehydration, a highly metabolic acidotic condition, and serious injury to the kidneys and other organs by severe hyperglycemia, the patient is in critical condition. EMS treatment for DKA includes airway management and assisting ventilation if necessary; a large amount of crystalloid fluid (1-2 liters) administered intravenously may be necessary.
4. Acute adrenal crisis
The adrenal glands are found at the top of each kidney. They are responsible for secreting several hormones that help with overall body function. Adrenalin (epinephrine) is integral to managing normal and unusual stress levels by increasing chronotropy and inotropy. Norepinehrine causes vasoconstriction. Cortisol (hydrocortisone) regulates how the body converts fats, proteins and carbohydrates to energy.
Corticosterone works with hydrocortisone to regulate inflammatory responses associated with injury and illness. Aldosterone regulates the retention of salts and water as blood passes through the kidney, and is a major factor in regulating blood pressure.
There are several diseases and conditions that affect the adrenal glands. Addison’s disease causes decreased secretion of aldosterone and cortisol. Conversely, Cushing Syndrome is an overproduction of cortisol. Adrenal cancer and tumors can also cause alterations in hormone production.
What is likely to cause a patient with an adrenal insufficiency is acute adrenal crisis. This can occur if a patient with a condition such as Addison’s disease suddenly stops corticosteroid therapy. Sepsis, surgery or trauma to the kidneys can also initiate an acute adrenal crisis. These patients will present in a hypotensive state, with altered mental status. In addition, acute adrenal crisis can produce hyponatremia (low sodium levels) and hyperkalemia (high potassium levels), causing nausea, vomiting, weakness and/or fatigue.
EMS treatment for acute adrenal crisis is again mostly supportive. A large normal saline fluid bolus may be very helpful for both fluid and sodium replacement. For patients experiencing cardiac dysrhythmias secondary to hyperkalemia, administration of calcium chloride and nebulized albuterol can temporarily reduce blood levels of potassium. Sodium bicarbonate may be an effective treatment under emergency conditions.[7]
Summary
There are many possible conditions for the signs and symptoms presented by our case study patient. Drug reaction, overdose, hyperthermia are but a few possibilities. It turned out that she had been taking more aspirin than the recommended dose and precipitated a thyroid storm that resulted in her presentation.
There are a small number of endocrine system conditions that can mimic other more common causes of a patient’s signs and symptoms during a medical emergency. Careful evaluation of the patient’s medical history and maintaining an open view of possible conditions will help the EMS provider be more accurate in their field impressions.
References
1. Singhal, A., & Campbell, D. “Thyroid storm.” 2003. www.emedicine.com/ped/topic2247.htm retrieved 10 June 2015.
2. Dahlen, R. (2002). Managing patients with acute thyrotoxicosis. Crit Care Nurse, 22(1), 62.
3. American Association of Clinical Endocrinologists . Thyroid Awareness Month 2004: Facts About Thyroid Disease. Jacksonville, FL: American Association of Clinical Endocrinologists. September 21, 2005. http://www.aace.com/public/awareness/tam/2004/fact.php.
4. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises in patients with diabetes mellitus (technical review). Diabetes Care. 2001;24:131-153.
5. U.S. National Library of Medicine. Blood sugar test – blood. http://www.nlm.nih.gov/medlineplus/ency/article/003482.htm retrieved 20 June 2015.
6. Hamdy O. Diabetic Ketoacidosis workup. Medscape/ WedMD. http://emedicine.medscape.com/article/118361-workup retrieved 20 June 2015.
7. Kamel KS and Wei C. Controversial issue in the treatment of hyperkalemia. Nephrology Dialysis Transplantation. (2003) 18: 2215–2218.
This article, originally published Aug. 4, 2015, has been updated.
