Endocrine/​Hematology/​Gastrointestinal/​Renal/​Integumentary Study Guide for the CCRN

General Information

Since five different topics are covered in this section, there is a lot to know to be successful at answering a question on this content. About 21% of the exam covers these areas, so use this study guide to help you know what to study. Remember, you’ll not only need to know the construction of the various systems but also how they function and, especially, how to care for a patient whose condition is critical and who has problems with any of these body functions.

Endocrine

The endocrine system is responsible for maintaining and regulating numerous hormones and bodily systems. While the most common endocrine disease is diabetes, many other conditions can cause dysregulation across the bodily system. Review the following critical conditions and the role the nurse plays in monitoring for and managing these.

Adrenal Insufficiency

Adrenal insufficiency is a critical medical condition that occurs when cortisol production in the body is significantly decreased or absent. Adrenal insufficiency can quickly progress to adrenal crisis, which, if left untreated, is fatal.

Three types of adrenal insufficiency have been identified.

• Addison’s disease, noted by autoimmune destruction of the adrenal gland, is the most common primary cause of adrenal insufficiency.

• Secondary adrenal insufficiency is the most common and can develop when the pituitary gland is compromised and unable to produce ACTH to stimulate cortisol release from the adrenal glands.

• Tertiary adrenal insufficiency involves dysfunction of the hypothalamus and subsequent disruption of the ACTH release process. Common examples of these types are chronic corticosteroid use (*Glucocorticoid-induced adrenal insufficiency) and tumors with the classified type depending on where the disruption occurs.

Cushing syndrome is the opposite condition and causes hypercortisolism or too much cortisol in the body. Symptoms and lab values are often opposing those of adrenal insufficiency described below. Treatment would focus on decreasing cortisol production instead of increasing.

Symptoms

Adrenal insufficiency can go unnoticed until it becomes an adrenal crisis. Many patients will present to an emergency department or critical care unit in acute shock, unresponsive to IV fluids or vasopressors. Earlier symptoms of this condition are vague and include weakness, fatigue, decreased appetite, and weight loss. Late symptoms include hypotension, cardiovascular collapse, and neurologic changes.

Diagnosis

Diagnostic labs can identify electrolyte imbalances, including hyponatremia, hypoglycemia, hyperkalemia, hypercalcemia, decreased ACTH levels, elevated creatinine, low aldosterone, high renin, and elevated TSH levels.

Treatment

Treatment of any underlying cause is crucial to recovery. Treatment includes administration of hydrocortisone (given as an initial bolus followed by daily or more frequent dosing), IV fluid resuscitation, correction of hypoglycemia, and slow correction of hyponatremia. Patients must understand that long-term corticosteroid medication cannot be abruptly stopped. Any withdrawal of these medications must be done in slowly tapered increments to prevent a crisis. Adrenal crises can also be precipitated by dehydration, infection, surgery, or stress.

Diabetes Insipidus

Diabetes insipidus (DI) is a condition that is classified by a deficiency of antidiuretic hormone (ADH). ADH is also known as vasopressin. ADH/vasopressin is a hormone that works by maintaining peripheral vascular resistance, increasing arterial blood pressure, and determining water reabsorption in the kidneys. When this hormone is absent or deficient, the body struggles to regulate its osmolality. Osmolality refers to how concentrated a fluid is based on the amount of dissolved particles. A high osmolality means the fluid is more concentrated and a low osmolality means it is more dilute. The body must carefully balance fluid concentration to maintain hemostasis. In DI the serum (blood) osmolality is high, but the urine osmolality is low.

Causes

DI usually develops as secondary to other conditions. Head trauma, primary brain tumor, meningitis, encephalitis, metastatic tumors, or surgical removal/irradiation of the pituitary gland may all cause DI. Sometimes the cause is unknown (idiopathic). Rarely, patients may experience congenital nephrogenic diabetes insipidus, which results from the absence of renal tubule response rather than decreased ADH production.

Symptoms

Symptoms of DI include polydipsia and polyuria. Patients with this condition may have a water deprivation test performed to determine the body’s urine output despite withholding fluids. Patients with DI will exceed 250 mL/hr of diluted urine output in this test. When water/liquid is not deprived, a patient with DI may drink 2 to 20 liters or more of fluid a day. Other diagnostic labs for DI include:

• elevated serum sodium levels
• increased BUN
• decreased ADH levels
• decreased urine osmolality (<200 mOsm/kg)
• decreased urine specific gravity (<1.005)
• increased serum osmolality

Treatment

Treatment for DI focuses on correcting the body’s fluid regulation. Vasopressin tannate provides the body with decreased or absent ADH/vasopressin and may be given either intramuscularly or subcutaneously and lasts up to 72 hours per dose. Something important to consider is that vasopressin has a more vasoconstrictive effect than desmopressin acetate (DDAVP), which helps patients to regulate fluid output and may be given via oral medication or intravenous injection two to three times a day.

One potential adverse reaction with DDAVP includes water intoxication, which can occur with medication overdose. Make sure to monitor the patients on this medication closely for neurologic status changes. Finally, some fluid deficits may be corrected with hypotonic solutions. This therapy must be conducted slowly, decreasing serum sodium levels no faster than 1 mEq/hr, to prevent cerebral edema.

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

The pituitary gland plays an important role in how the body processes fluids. If there is an increase in secretion (hypersecretion) of antidiuretic hormone (ADH) in the posterior pituitary gland, syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur. With the increase in hormones from the posterior pituitary gland, the kidneys begin to reabsorb fluid from the body. This in turn causes fluid retention and dilutional hyponatremia. Patients will have extremely concentrated urine due to the decreased fluid processing through the kidneys and drainage into the bladder.

Causes

There are many potential causes of SIADH. This includes neurologic disorders of the CNS, surgical manipulation of the brain, trauma, and tumors. Lung disorders such as pneumonia, pneumothorax, and small-cell lung cancer may precipitate SIADH. SIADH may also result from adverse reactions to vincristine, phenothiazines, tricyclic antidepressants, and thiazide diuretics. Monitor patients on these medications closely to increase early detection of symptoms.

Symptoms and Diagnosis

Common symptoms of SIADH are mostly attributed to the severe hyponatremia and include muscle cramps, nausea/vomiting, headache, irritability, and neurological changes such as confusion or hallucinations. Urine output will be severely decreased and concentrated. If left untreated, symptoms may progress into stupor and seizures. Diagnostic labs include:

• low serum sodium (<130 mEq/L),
• high urine specific gravity (>1.030)
• high urinary sodium
• high urine osmolality but low serum osmolality
• high ADH

Treatment

In patients with SIADH, fluid intake is restricted to less than 800 to 1,200 mL/day to help with the dilutional hyponatremia. In patients with concerns for cerebral vasospasms or subarachnoid hemorrhage, fluid restriction is less appropriate. Using 3% hypertonic saline may be used instead in these cases to prevent brain swelling and preserve perfusion (circulation).

Medications such as furosemide (Lasix®) may be used to promote excretion of free water. This may be used in addition to oral salt tablets to maintain appropriate serum sodium levels. Vasopressin receptor antagonists may be used to block the V2 receptors in the kidneys that are responsible for water reabsorption. While there are many supportive measures for correcting SIADH, ultimate correction occurs with treatment of the underlying condition when applicable.

Continued Care

Nurses must keep close observation of patients with SIADH. Hyponatremia must be corrected slowly. If sodium levels rise too quickly, a preventable yet fatal condition called osmotic demyelination syndrome (ODS) can occur. In this condition, water leaves the brain quickly to balance osmotic pressure, causing damage to the myelin sheaths. This can cause permanent neurological deficits such as dysarthria, paralysis, movement disorders, behavioral changes, locked-in syndrome (a fully conscious state but unable to move or speak), and even death.

Typically, sodium levels can be safely raised by 6 to 10 mEq/L within a 24-hour period. Strict monitoring of intake and output should be implemented to ensure a patient is making urine at least 0.5 to 1 mL/kg/hour. Overhydration should be avoided in patients to prevent further reuptake of fluid and resultant decreased sodium levels. Seizure precautions should be initiated to help prevent harm in the event of a hyponatremic seizure.

Diabetes Mellitus

Diabetes mellitus (DM) is a chronic illness that affects numerous patients. Patients may be admitted to critical care units due to complications with this illness or present with diabetes as a comorbid illness that impacts and often complicates medical therapies for other dominating illnesses.

Type 1

Type 1 DM is often referred to as juvenile diabetes or insulin dependent. It is not as common and is most often diagnosed in early childhood following the failure of the pancreas’ ability to produce insulin. Symptoms often develop quickly and include polydipsia, polyphagia, polyuria, new onset bedwetting, unintended weight loss, irritability, fatigue, and vision changes.

Treatment

Treatment of type 1 DM focuses primarily on insulin therapy but also lifestyle factors such as a regulated (low-carb) diet and exercise. Treatment is lifelong. Patients will need to have their blood sugars monitored and corrected frequently. Patients may use insulin injections, traditional basal-bolus pumps, or closed-loop insulin delivery. Review the common insulin types and indications for use, including short-acting (regular) insulin, rapid-acting insulin, intermediate-acting (NPH) insulin, and long-acting insulin.

Type 2

Type 2 DM is more common and an acquired, chronic condition related to the inability of the body to metabolize glucose due to insulin resistance or decreased insulin production. It generally develops in adulthood. Risk factors for type 2 DM include obesity, sedentary lifestyle, abdominal fat distribution, family history, race (African American, Hispanic, American Indian, and Asian American), age greater than 45, prediabetes, and gestational diabetes.

Type 2 DM affects almost every system in the body. It can increase a patient’s risk for heart disease, atherosclerosis, renal failure, vision changes, nerve damage, hearing loss, and neurologic changes. It can also complicate therapy plans for other illnesses as patients with type 2 DM often have decreased healing ability and are at increased risk for infection.

Treatment

Treatment of type 2 DM often focuses on the prevention of the disease prior to medication or insulin. Patients can reduce their risk and treat type 2 DM by having a healthy lifestyle: exercising regularly, eating healthy and well-balanced meals, and losing weight. If these measures are not enough, patients may be prescribed oral antihyperglycemic medications such as Metformin (Glucophage®) to help decrease the body’s resistance to naturally produced insulin. Insulin therapy may be added if previous measures are not effective in reducing blood glucose and hemoglobin A1C levels. The target A1C level for adults with either type 1 or 2 diabetes is typically below 7%.

Diagnosis

Blood tests to aid in the diagnosis of type 1 DM include random blood glucose screening, fasting blood glucose testing, and hemoglobin A1C.

• A random blood sugar greater than 200 mg/dL with associated symptoms is highly indicative of diabetes.

• A fasting blood glucose greater than 126 mg/dL and/or hemoglobin A1C 6.5% or higher on two separate tests is also indicative of diabetes.

• Hemoglobin A1C, also called glycated hemoglobin, is generally considered a more accurate indicator of glucose control as it shows the average blood sugar levels over three months.

Patients with acute onset or exacerbation of type 1 DM can develop diabetic ketoacidosis. This condition is discussed later in this guide.

To help distinguish between type 1 and type 2 DM, labs are completed to help identify any presence of autoantibodies, and urinalysis is performed to determine ketonuria (less common in type 2 DM).

Hyperglycemia

Acute hyperglycemia most commonly occurs in patients with diabetes (type 1, type 2, and gestational). In acute illness or injury, patients may also have difficulties with hyperglycemia due to dysfunction of their insulin production or absorption due to other underlying conditions or extreme stress response. Medications such as corticosteroids can elevate blood sugar as well as hormonal disorders or pancreatic diseases.

Diagnosis

Acute hyperglycemia can be diagnosed by repeated testing of a patient’s blood glucose level, both fasting and non-fasting, or by way of long-term glucose regulation (hemoglobin A1C). If checking a patient’s blood glucose when fasting, levels greater than 130 mg/dL are concerning for hyperglycemia. In non-fasting patients, levels that exceed 180 mg/dL will be considered hyperglycemia. Many patients will also have their hemoglobin A1C tested. Levels greater than 5.7% are considered to be abnormal. Levels of 5.7% to 6.4% on two or more occasions are considered to be diagnostic for prediabetes. If the levels are 6.5% or higher on two different tests, this is considered diagnostic for diabetes.

Symptoms

Symptoms of acute hyperglycemia include polyuria, polydipsia, polyphagia, blurred vision, headache, and fatigue. Hyperglycemia can be asymptomatic as well. If left untreated, the hyperglycemia could develop into more serious conditions, such as diabetic ketoacidosis or hyperglycemic hyperosmolar nonketotic syndrome, which are discussed later in this study guide.

Continued Care

Hyperglycemia must be addressed to prevent long-term changes to the body. These changes can cause other chronic, debilitating conditions such as cardiovascular disease, neuropathy, kidney damage/failure, diabetic retinopathy, cataracts, poor circulation and healing, and infections. Treatment for hyperglycemia usually results in the use of insulin or other medications as mentioned in the diabetes section.

Acute Hypoglycemia

Acute hypoglycemia is classified by a blood glucose level less than 50 to 60 mg/dL. This is often complicated by symptoms varying in severity. Some patients are asymptomatic until their blood sugar drops really low. Severe hypoglycemia is characterized by a blood glucose level less than 54 mg/dL, and most people will have symptoms by this point. Seizures, changes in consciousness, lethargy, vomiting, myoclonus, respiratory distress, hypothermia, diaphoresis, and cyanosis can all be central nervous system symptoms of acute hypoglycemia. The adrenergic system may also be affected and result in symptoms of diaphoresis, tremor, tachycardia, palpitations, hunger, and anxiety. These symptoms usually precede the neurological ones and, therefore, are the first signs and symptoms of hypoglycemia.

Causes

There are several possible causes of acute hypoglycemia. Pancreatic islet tumors or hyperplasia can affect how much insulin is produced in the body, driving down blood glucose levels. In patients with diabetes mellitus, overdosing on insulin correction or not maintaining appropriate dietary measures can also quickly drop blood sugars. Genetic defects, infections, sepsis, and drug or alcohol overdose may also impact the body’s blood glucose regulatory system.

Treatment

Treatment for acute hypoglycemia involves correcting the blood glucose to a more normal range. If the patient is alert and able to swallow, the first-line treatment is to give 15 grams of fast-acting carbohydrates and recheck the blood sugar in 15 minutes. Examples of this are four oz of fruit juice or three glucose tablets. If unsuccessful, repeat this process again. In the unconscious patient or one that cannot have anything by mouth, dextrose is given intravenously via push (D50%) or an infusion (D10% or D25%). It is important to note that dextrose is a vesicant, meaning it can damage veins and surrounding tissues, so ensure you have patent access and access to IV sites frequently. Nonetheless, it is the preferred treatment as it is rapidly absorbed. In patients without IV access, glucagon is often used intramuscularly to provide a blood glucose elevation. Any other treatment would be aimed at treating the root cause.

Continued Care

Patients with acute hypoglycemia need to be closely monitored for persistent symptoms and lowered blood glucose levels. What may acutely increase a patient’s blood glucose may not maintain their levels if the underlying problem (insulin production/release) is not also addressed. Nurses should especially monitor their patients for central nervous and cardiopulmonary changes, as hypoglycemia may cause damage to these systems, resulting in neurologic impairment if not corrected. Hypoglycemia is far more immediately dangerous than hyperglycemia because the brain depends on glucose to function. Without it, permanent damage can occur within minutes to hours, whereas complications from hyperglycemia develop gradually over time.

Diabetic Ketoacidosis

Diabetic ketoacidosis occurs in the event of poorly controlled diabetes mellitus, as an exacerbation of stress, or an acute illness in a patient with diabetes mellitus. In ketoacidosis, the body cannot metabolize glucose due to inadequate insulin levels. The body then looks to the breakdown of fat for energy. This process leads to ketone creation. The body can only use so many ketones, so excess ketones are released mainly through the urine (ketonuria) and a small amount through respiration (acetone/ fruity breath).

Diagnosis and Symptoms

Acute care nurses should be aware of diabetic ketoacidosis in previously known and unknown diabetics. Diabetic ketoacidosis is generally the presenting factor in children with Type 1 diabetes. Untreated illness can lead to severe reactions, such as cardiac arrhythmias, lethargy, hypotension, coma, and possibly death. Other symptoms include classic hyperglycemia signs like polyuria/ polydipsia, CNS depression, fluid imbalance, dehydration, nausea/vomiting, appetite loss, abdominal pain, and confusion. Nurses may note Kussmaul respirations, a compensatory deep, rapid breathing due to metabolic acidosis. Anion gap is another tool used to measure the severity of metabolic acidosis in DKA. It is a lab test that reflects unmeasured acids (in this case, ketoacids) in the blood. The normal range is between 8 to 12 mEq/L. In DKA, the anion gap is normally elevated and you may hear this referred to as an open gap. As DKA is treated, the anion gap decreases back toward the normal range and is called a closed gap.

Treatment

In a patient with diabetic ketoacidosis, the nurse can anticipate that the patient’s blood glucose will exceed 250 mg/dL. The patient will also have decreased sodium and increased potassium levels before treatment. This will inverse the following treatment. Arterial blood gas results will show metabolic acidosis with a pH less than 7.3 and \(HCO_3\) less than 18 mEq/L. A urinalysis will show elevated glucose and ketones.

Treatment of diabetic ketoacidosis focuses on fluid resuscitation and slow lowering of the patient’s blood glucose. One to two liters of isotonic fluids are recommended to be given within the first hour. This is followed by up to eight liters of that fluid within the first 24 hours. As the patient’s potassium begins to decrease, potassium may be added to the fluids. This generally occurs when the patient’s potassium falls below 5 mEq/L.

Continuous intravenous insulin will be initiated beginning at 0.1 unit/kg/hour. This usually does not exceed five to seven units per hour. The goal of treatment is to reduce the blood glucose slowly between 50 to 75 mg/dL per hour. Nurses should monitor for rebound hypoglycemia, and dextrose may be added to the fluids once the patient’s blood glucose decreases to less than 200 mg/dL.

Continued Care

The combination of insulin and fluid resuscitation can quickly decrease a patient’s potassium. If the patient’s potassium level falls below 3 mEq/L, the insulin infusion should be stopped and potassium corrected prior to reinitiation of insulin. The patient’s sodium level should be monitored as well. The patient may have to be decreased to fluids with 0.45% normal saline if the patient’s levels become greater than 150 mEq/L. Magnesium supplementation should be prescribed if the patient’s magnesium levels decrease, as magnesium impairs the uptake of potassium.

Patients in acute diabetic ketoacidosis are often managed in the intensive care unit due to the close monitoring needs and frequent medication/drip changes. Some patients may require mechanical ventilation due to vomitus aspiration, ARDS, or secondary respiratory alkalosis. As the patient’s electrolytes and arterial blood gas results normalize, the patient may be transitioned to a step-down or general medicine unit. These patients will likely need extensive education to help prevent future episodes of diabetic ketoacidosis throughout their hospital stay.

Hyperosmolar Hyperglycemic State (HHS)

HHS is a condition in which a patient’s increased blood sugars last so long that their body starts to have osmotic diuresis. This can occur in patients with and without a history of type 2 diabetes. Hyperglycemia causes fluid shifts within the cells to help the body maintain an osmotic equilibrium. When the hyperglycemia is not corrected, this process continues until hypernatremia occurs due to glucosuria and dehydration. The hypernatremia increases the osmotic pull from the tissues, causing adverse symptoms and HHS. Patients with HHS have enough insulin to prevent the breakdown of fats that would normally result in ketoacidosis.

Causes

HHS is most common in people between the ages of 50 and 70 years old. While patients may have had elevated blood glucose levels for a long period of time, HHS often results as an imbalance that occurs after an acute illness. Events such as strokes and cardiac events make these patients with chronic hyperglycemia more likely to develop HHS. Thiazide medications are also known to contribute to this condition.

Symptoms and Diagnosis

Patients with this condition will likely present with symptoms of polyuria, dehydration, hypotension, and tachycardia. More severe symptoms include changes in mental status, seizures, and hemiparesis. Several labs may be obtained. Essential laboratory tests include glucose, sodium, osmolality in both urine and blood, and BUN/creatinine. Blood glucose is often significantly elevated >600 mg/dL. Hypernatremia (sodium >145 mmol/L), high serum and urine osmolality, as well as elevated BUN/creatinine, can all be observed due to dehydration. Unlike DKA, HHS has minimal to no ketones or acidosis present.

Treatment

While HHS is not the same as diabetic ketoacidosis, the treatment is extremely similar. Fluid replacement is the number one priority as these patients are severely dehydrated. After rehydration, the patient with HHS will be initiated on insulin, either a low-dose continuous infusion or subcutaneous injection with an even slower correction of hyperglycemia than DKA. Electrolytes will be monitored closely for imbalances and treated appropriately; however, electrolyte issues are not as prominent in this condition.

Nurses should monitor patients for rebound hypo- or hyperglycemia and begin education on ways to prevent this from occurring in the future.

Thyroid Conditions

The thyroid is responsible for hormone secretion and regulation. If too many or too few thyroid hormones circulate in the system, complications can occur.

Hyperthyroidism

Hyperthyroidism is caused by an overactive thyroid gland when the thyroid produces too much triiodothyronine (T3) and/orthyroxine (T4). It can be caused by a variety of conditions, including thyroiditis, Graves’ disease, cancerous lesions, and benign enlargement of the thyroid. Patients at increased risk for hyperthyroidism include women, those with a family history of Graves’ disease or other hyperthyroid conditions, and those with chronic illness.

Symptoms

Symptoms of hyperthyroidism can be nonspecific and include unintentional weight loss, tachycardia, abnormal heart rhythm patterns, increased appetite, tremor, nervousness, sweating, heat intolerance, increased bowel motility, goiter (enlarged thyroid gland), thinning skin, brittle hair, and fatigue. Patients with Graves’ disease may develop Graves’ ophthalmopathy, which can lead to exophthalmos where protrusion of the patient’s eyeballs occurs as tissues behind the eyes swell. Eyes may become dry, reddened, swollen, and uncomfortable. Patients may experience light sensitivity, blurred vision, and reduced eye movement. Patients who smoke are more at risk for this development.

Diagnosis

Diagnosis of hypothyroidism combines the use of medical history, physical exam, and blood work. Patients will have thyroid hormones and thyroid-stimulating hormone (TSH) levels drawn. Elevated T3 and/or T4 and low or absent TSH levels indicate a hyperactive thyroid. To help identify the underlying cause of hyperthyroidism, patients may undergo a radioiodine uptake test, thyroid scan, and/or thyroid ultrasound.

Treatment

Treatment of hyperthyroidism includes correction of the underlying cause. If the thyroid is enlarged, oral radioactive iodine can be used to help shrink the thyroid. Anti-thyroid medications, such as methimazole (Tapazole®) and propylthiouracil (PTU), can be used to reduce thyroid hormone secretion. Methimazole is considered first line treatment and preferred over PTU because of the black-box warning due to the risk of severe and potentially fatal liver damage. Beta blockers may be used to help manage the symptoms of hyperthyroidism, including tremor and heart rate abnormalities. Finally, thyroidectomy may be indicated if hyperthyroidism cannot be managed with alternative therapies.

Hypothyroidism

Hypothyroidism is caused by an underactive thyroid gland. It can occur spontaneously or as a result of autoimmune disease (Hashimoto’s thyroiditis), overtreatment of hyperthyroidism, thyroid surgery, radiation therapy, or medication (such as lithium). Less common causes of hypothyroidism include pregnancy, iodine deficiency, and pituitary disorder. Risk factors for hypothyroidism include being a woman, age greater than 60, family history, autoimmune disorder, radiation to the neck or thyroid, and thyroid surgery.

Symptoms

Early symptoms of hypothyroidism may be subtle and include fatigue and weight gain. If not recognized or treated, hypothyroidism can progress with symptoms of cold intolerance, constipation, dry skin, thinning hair, muscle aches, weakness, joint pain, depression, and impaired memory. Patients may also have increased cholesterol levels and peripheral neuropathy.

Lab work is commonly used to diagnose hypothyroidism. The same laboratory values are used to assess for both underactive and overactive thyroid. In hypothyroidism, patients will likely have an elevated TSH and low T3 and/or T4.

Treatment of hypothyroidism focuses on the correction of thyroid hormone levels and resolution of any underlying disease. Patients will often be prescribed the synthetic thyroid hormone levothyroxine (Levothroid®). Patients should be educated on dietary recommendations, including the limiting of soy and fiber as excess of one or both can decrease the absorption of thyroid hormones. Additionally, education should be provided to take these medications on an empty stomach to ensure proper absorption. Signs of hyperthyroidism should be reported to the healthcare provider as the dosage may need to be decreased.

A serious complication of hypothyroidism is myxedema coma. This is life-threatening and can be characterized by hypotension, bradycardia, hypothermia, respiratory distress, and neurological changes, including coma. It is generally caused by long-standing, untreated hypothyroidism or precipitated by stress due to an illness or injury. This complication has a high mortality rate, and patients will be admitted to the ICU. Intravenous thyroid hormones and steroids are given, as well as other supportive measures such as warming blankets for hypothermia, respiratory support, and fluid/electrolyte management.