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Learning Scope #404
1 contact hour
Expires Oct. 22, 2014
You can earn 1 contact hour of continuing education credit in three ways: 1) Grade and certificate are available immediately after taking the online test. 2) Send the answer sheet (or a photocopy) to ADVANCE for Nurses, Learning Scope, 2900 Horizon Dr., King of Prussia, PA 19406. 3) Fax the answer sheet to 610-278-1426. If faxing or mailing, allow 30 days to receive certificate or notice of failure. A certificate of credit will be awarded to participants who achieve a passing grade of 70 percent or better.
Merion Matters is an approved provider of continuing nursing education by the Pennsylvania State Nurses Association (No. 221-3-O-09), an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation.
Merion Matters is also approved as a provider by the California Board of Registered Nursing (No. 13230) and by the Florida Board of Nursing (No. 3298).
The goal of this continuing education article is offer the latest information on the endocrine system and the critical abnormalities that can occur. After reading this article, you will be able to:
1. List the organs that comprise the endocrine system.
2. Identify the critical diseases of the endocrine system.
3. Explain the major functions of the endocrine system.
* The author has completed a disclosure form and reports no relationships relevant to the content of this article.
A patient reacts both psychologically and physically to the stress of being critically ill. One such response is releasing a long list of hormones, including adrenocorticotropin, cortisol, aldosterone, growth hormone, prolactin, glucagon, renin and angiotensin II (see Table).1-2
The stress response is identified by the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is the part of the neurologic/endocrine system comprising the brain and the pituitary and adrenal glands that responds to stressors. The hypothalamus is the first to react to the stressor by releasing the compound corticotropin-releasing factor (CRF). The CRF travels to the pituitary gland, where it triggers the release of adrenocorticotrophic hormone (ACTH). ACTH is discharged into the bloodstream, causing the cortex of the adrenal gland to release stress hormones, particularly cortisol. Cortisol increases the availability of the body's fuel supply (carbohydrate, fat and glucose), which is used by the body in respond to stress. If cortisol levels remain elevated for too long, then muscle breaks down, there is a decreased inflammatory response and suppression of the immune system occurs. If the body continues to act under the influence of cortisol, it will begin to break down.3
Decades before the theory just described was generated, endocrinologist Hans Seyle introduced the world to the general adaptation syndrome model, which states there are three phases of effects that stress has on the body. Seyle also described the HPA axis, which prepares the body to cope with stress.4
The first stage is the alarm stage, which occurs when the body initially encounters the stressor and reacts with the "fight-or-flight" response that includes activating the nervous system and the release of hormones such as cortisol and adrenalin into the bloodstream.5
The second stage is the resistance stage, where the parasympathetic nervous system acts to return many physiologic functions to normal while the body focuses against the stressor. During this stage, blood glucose, cortisol and adrenalin levels remain high, and there is an increase in heart rate, blood pressure and breathing.5
The third stage is the exhaustion stage. Here, if the stressor continues, the body runs out of its adaptation abilities and the body exhausts itself and becomes susceptible to disease and death.4,5
Normally, the endocrine system plays a major role in the establishment and maintenance of the fluid and electrolyte, acid-base and energy balance.6 In the critically ill patient, there may be abnormalities that occur to these basic functions. If left unchecked, these abnormalities can become life threatening.
The following seven syndromes are endocrine emergencies that bring patients into the critical care unit or occur as a response to the care being administered to the patient.
Diabetes insipidus (DI) is characterized by either an insufficient production of antidiuretic hormone (ADH, vasopressin) by the posterior pituitary lobe or renal resistance to this hormone. It occurs when an organic lesion of the hypothalamus, infundibular stem or posterior pituitary partially or completely blocks ADH synthesis, transport or release.
ADH secretion is dictated by the hypophysial-posterior pituitary system. The hypophysial-posterior pituitary system regulates ADH release based on feedback from receptor cells known as osmoreceptors, which alters the impulse to the posterior pituitary in response to changes in body tonicity or hyperosmolality. This explains the neurogenic causes of DI.
The most common presentation of patients with DI to the critical care unit is for acute traumatic head injury, craniotomy or cerebral infarctions.
There are three forms of DI: neurogenic (i.e., neurologic trauma, brain tumors), nephrogenic and psychogenic. Inadequate renal response to ADH causes nephrogenic DI. The collecting duct permeability to water doesn't increase in response to ADH. Nephrogenic DI is generally related to disorders and drugs that damage the renal tubules or decreased renal responsiveness to ADH, including pyelonephritis, amyloidosis, destructive uropathies, polycystic disease, intrinsic renal disease, lithium and general anesthetics. Psychogenic DI may be idiopathic or related to psychosis or sarcoidosis.
The causes of DI may be acquired, familial, neurologic, idiopathic, nephrogenic, hypothalamic, pituitary tumors, cranial trauma or surgery, lithium, phenytoin or alcohol.
A sudden onset of polyuria (2-20 L/day of urine output) is the major sign of DI. Other symptoms include polydipsia (5-20 L/day), weight loss, dizziness, constipation, tachycardia, hypotension, urine osmolality (50-200 mOsm/kg of water, less than that of plasma) and low urine specific gravity (less than 1.005 SpG), and serum sodium greater than 147 mEq/L.
The treatment for DI is mostly pharmaceutical: desmopressin, vasopressin tannate in oil, aqueous vasopressin, hypotonic solution to replace free water loss, and thiazide diuretics for patients with nephrogenic DI. A transphenoidal hypophysectomy is recommended for patients with pituitary tumors.
Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a condition of excessive ADH that is being secreted by the hypophysial-posterior pituitary system. It is a relatively common complication after surgery or critical illness because of the stimulatory effect many medications administered have on ADH coupled with the physiologic stress response.
One of the causes of SIADH is oat cell carcinoma of the lung because it secretes excessive ADH or vasopressin-like substances; other neoplastic diseases such as pancreatic and prostatic cancer and thymoma also may trigger SIADH.
Other causes may be central nervous system disorders (brain tumors or abscesses, stroke, head injury), pulmonary disorders (pneumonia, tuberculosis, lung abscess, positive-pressure ventilation), medications (chlorpropamide, vincristine, cyclophosphamide, haloperidol, carbamazepine, morphine, thiazides) and endocrine disorders (adrenal insufficiency, myxedema, pituitary insufficiency).
The patient will have serum hyponatremia and decreased plasma osmolality (<280 mOsm/kg) and generally experiences neurologic symptoms that correspond with their level of serum sodium. Headache, anorexia, vomiting and confusion may be manifested with serum sodium levels of 115-120 mEq/L, whereas disorientation, stupor, coma, seizures and focal neurologic abnormalities seldom occur until the serum level is less than 110 mEq/L.
The treatment for SIADH is severe fluid restriction; demeclocycline or lithium may be given to inhibit renal ADH effects and phenytoin to inhibit ADH secretion. In severe hyponatremia, hypertonic sodium chloride infusions, intravenous furosemide, or osmotic diuretics such as urea or mannitol may be used to promote water excretion.
Thyroid storm, an acute manifestation of hyperthyroidism, usually occurs in patients with preexisting thyrotoxicosis. Common causes include Graves' disease, toxic adenoma and toxic multinodular goiter. Less common causes of thyroid storm are surgery, radioactive iodine therapy and severe stress. Examples of severe stressors are uncontrolled diabetes mellitus, myocardial infarction, acute infection and any critical illness.
The symptoms of thyroid storm result directly from the effects of the circulation of the excess thyroid hormone. Those symptoms are fever, flushing, sweating, marked tachycardia, atrial fibrillation, cardiac failure, agitation, nausea, vomiting and diarrhea.
Two diagnostic tests generally can be used to diagnose thyroid storm. The radioimmunoassay shows increased serum T³ and T4, and the thyrotropin-releasing hormone (TRH) stimulation test indicates hyperthyroidism if TSH fails to rise within 30 minutes after administration of TRH.
The treatment includes antithyroid drugs such as propylthiouracil (PTUI); beta-adrenergic blockers (propranolol) to block the sympathetic effects; a corticosteroid to inhibit the conversion of T³ and T4 and to replace depleted cortisol; and an iodide to block the release of the thyroid hormones. Ablation of the thyroid may be an option as well.
Myxedema coma is a condition of hypothyroidism. Primary hypothyroidism stems from a disorder of the thyroid gland. Secondary hypothyroidism is caused by a failure to stimulate thyroid function or by a failure of target tissues to respond to normal blood levels of thyroid hormones.
The symptoms of myxedema coma are pronounced hypothermia, hypercarbia and hypoventilation, hypotension, bradycardia, decreased level of consciousness, hypoglycemia, and mild-to-severe dilutional hyponatremia.
The causes of myxedema coma are not different for primary or secondary and are as follows: trauma, critical illness, exposure to cold, administration of sedatives, anesthetics, narcotics, psychotropic drugs at dosages or frequencies beyond the ability of the hypothyroid patient to metabolize, thyroid gland surgery, inflammation from irradiation therapy, chronic autoimmune thyroiditis, inflammatory conditions such as amyloidosis and sarcoidosis, and use of antithyroid medications such as propylthiouracil.
For treatment, thyroxine (T4) (levothyroxine) is given intravenously (2 microgram/kg over 5-10 minutes) followed by 100 microgram/kg intravenously once daily. Glucocorticoid support (hydrocortisone 100 mg IV bolus) is also provided for optimal physiological support for the ongoing stress response and for concurrent adrenal insufficiency, often an accompanying disorder. Respiratory hypercarbia and respiratory acidosis are treated by intubation and mechanical ventilation; hypotension is treated by volume expansion and glucocorticoids.
Acute Adrenal Crisis
Acute adrenal crisis is a condition of adrenal hypoperfusion. Experts believe the incidence of adrenal insufficiency in sepsis and septic shock is 30-70 percent.7
There are primary and secondary forms of acute adrenal crisis. Primary acute adrenal crisis is due to glucocorticoid insufficiency resulting from the destruction or dysfunction of the adrenal cortex. Adrenal insufficiency is frequently characterized clinically as hypotension resistant to volume resuscitation and dependent on vasopressors.7 Symptoms include weakness, fatigue, nausea, vomiting, dehydration, hypoglycemia, hypotension and hyperpigmentation (bronze color of the skin). If not treated with glucocorticoids, the patient can ultimately experience vascular collapse, renal shutdown, coma and death.
Secondary acute adrenal crisis, characterized by decreased glucocorticoid secretion, results from impaired secretion of corticotropin. The symptoms of secondary adrenal insufficiency are similar to primary, except for the hyperpigmentation. There may be fairly normal aldosterone and androgen secretion. The treatment of secondary adrenal insufficiency is small quantities of mineralocorticoids and glucocorticoids given daily as 0.1 mL of fludrocortisone and 30 mg of cortisol.
The most common cause of acute adrenal crisis is an autoimmune circulating antibody that destroys more than 90 percent of both glands. Other causes include tuberculosis, hemorrhaging into the glands, neoplasms, bilateral adrenalectomy or infections (histoplasmosis or cytomegalovirus). It can follow acute sepsis, trauma or surgery, or occur in patients on chronic steroid therapy whose treatment is stopped abruptly.
Some diagnostic results in acute adrenal crisis are decreased cortisol level, decreased sodium and fasting glucose level, increased potassium and BUN, and decreased hematocrit.
The exact causes of diabetes mellitus types 1 and 2 are unknown but are thought to be influenced by genetic factors. Type 1 also may be caused by autoimmune or infectious factors. Other risk factors for the development of diabetes mellitus include obesity; physiological or emotional stress, which may prolong elevation of stress hormones; pregnancy; and certain medications (e.g., thiazide diuretics, adrenal corticosteroids, hormonal contraceptives).
In diabetic ketoacidosis (DKA), there is an acute deficiency of insulin, which may be caused by illness, stress, infection and failure of patients to take their insulin.
Insulin deficiency causes cells to convert fats into glycerol and fatty acids for energy. These fatty acids can't be metabolized as they are released, so they accumulate in the liver, where they are converted into ketones (keto acids).8 The accumulation of acids in the body leads to the breakdown of tissue, which leads to more acidosis. Eventually, the large amount of acid in the body leads to shock, then coma and death if not treated.
The diagnosis of DKA can be made when the following criteria are met:
1. Hyperglycemic plasma glucose levels exceeds 250 mg/dL
2. Ketosis: moderate-to-severe ketonemia (ketone levels positive at a serum dilution of =1-to-2 or serum beta-hydroxybutyrate concentration greater than 0.5 mmol/L) and moderate ketonuria (2+ to 3+ by the nitroprusside method).
3. Acidosis: pH of 7.3 or less and/or bicarbonate of 15 mEq/L or less.9
The goals of treating DKA are to correct the acidosis, restore fluid and electrolyte balance; and to identify and treat the cause. Fluid replacement is critical to avoid hypovolemic shock. The fluid deficit patients usually present with is 2-4 L. Initially, an isotonic solution is given intravenously at a rate of 500-1,000 mL/hour for the first 2-3 hours. Then, the infusion rate is slowed to 250-500 mL/hour until the patient reestablishes a urine output of 50 mL/hour. Once that occurs, the infusion is slowed to 125-250 mL/hour.
Insulin corrects the acidosis by decreasing hepatic gluconeogenesis and inhibiting lipolysis. It also reduces hyperosmolality by decreasing hyperglycemia and promoting peripheral cellular utilization of glucose. Insulin can be given intravenously or intramuscularly and is based on the patient's body weight. For the intravenously treatment, a loading dose is approximately 10 units of regular insulin followed by 5-10 units/hour by continuous infusion. Intramuscular administration usually starts with a loading dose of 20 units, followed by 10 units/hour. Both regimens usually reduce the serum glucose at a rate of 75-100 mg/dL per hour.
As the acidosis is corrected, the potassium level falls, so potassium phosphate is given to replace the potassium. Potassium phosphate is effective because the reversal of phosphate enhances buffering and facilitates oxygen transport to tissues, which is adventitious to acidotic patients.
If the blood pH is 7 or less or the blood bicarbonate is below 9 mEq/L, 1-2 ampules of sodium bicarbonate (44 mEq bicarbonate per ampule) may be administered in a hypotonic (45 percent saline) solution.6
Hyperglycemic hyperosmolar nonketotic syndrome (HHNK) is an acute complication of hyperglycemia that may occur in the diabetic patient. It occurs mostly in patients with type 2 diabetes.
The causes of HHNK are similar of those of DKA, but the pathophysiologic response differs. In HHNK, inadequate insulin hinders glucose uptake by fat and muscle cells. Because the cells can't take in glucose to convert to energy, glucose accumulates in the blood. At the same time, the liver responds to the demands of the energy-starved cells by converting glycogen to glucose and releasing glycogen into the blood, further increasing the blood glucose level. Hyperglycemia is more pronounced in HHNK than in DKA. Values are typically 600-2,500 mg/dL. When the glucose level exceeds the renal threshold, excess glucose is excreted in the urine.
When the still insulin-starved cells can't get glucose, they start converting protein, which results in a loss of intracellular potassium and phosphorus, and excessive liberation of amino acids. The liver converts these amino acids into urea and glucose. As a result, blood glucose levels are grossly elevated, serum osmolarity is increased and glycosuria occurs, which leads to osmotic diuresis.
Clinical findings with these patients are an elevated serum glucose as stated above, a negative urine acetone, a serum ketone that is usually negative, positive urine glucose, serum osmolality elevated (above 350 mOsm/L), hypokalemia, hypophosphatemia, hypomagnesemia and hypochloremia.
The goals of treatment are to correct fluid and electrolyte imbalances, normalize metabolism, and identify and treat the precipitating cause(s). Replacement of fluids and electrolytes is critical in these patients. Both hypotonic and isotonic fluids are utilized. Half of the fluid that is replaced occurs in the first 12 hours, with the other half occurring in the next 24 hours. Fluid replacement is titrated using central venous access or other hemodynamic parameters. Potassium is usually added to the fluid replacement depending on the serum values and if the patient can tolerate the rate of infusion of the potassium.
Even though hyperglycemia is much higher in patients with HHNK than in patients with DKA, insulin is administered in smaller amounts, because the patient with HHNK does secrete some endogenous insulin and may be very sensitive to exogenous doses. It is recommended that when the blood glucose falls to 250-300 mg/dL and osmolality decreases to roughly 310 mOsm/kg, glucose-containing infusions are initiated to lower the chance of treatment-induced hypoglycemia.
Stress & Critical Illness
Critical illness can bring about its own critical illness. We have just learned about seven syndromes of the endocrine system that can bring a patient to the critical care unit or that can occur in the critical care unit. We also learned stress, as it relates to the endocrine system and critical illness, can bring about any of these crises.
Nurses can play an important role in helping to decrease the stress of critical illness and also to recognize the signs and symptoms of stress when they occur in the critically ill patient.
1.Guyton, A.C., & Hall, J. (2011). Textbook of medical physiology (12th ed.). Philadelphia: Elsevier.
2.VanderLaan, T., & Walker, M. The critically ill patient: Surgical intensive care. Retrieved Aug. 26, 2012 from the World Wide Web: http://www.physicianeducation.org/downloads/PDF%20Downloads%20for%20website/The%20Critically%20Ill%20Patient%20(ICU).pdf
3. WebMD. (2011). What is the role of the hypothalamus-pituitary-adrenal axis in stress? Retrieved Aug. 26, 2012 for the World Wide Web: http://answers.webmd.com/answers/1173728/what-is-the-role-of-the
4. Essence of Stress Relief. Hans Selye's general adaptation syndrome. Retrieved Oct. 3, 2012 from the World Wide Web: http://www.essenceofstressrelief.com/general-adaptation-syndrome.html
5. Current Nursing. (2011). General adaptation syndrome (GAS) - theory of stress. Retrieved Oct. 2, 2012 from the World Wide Web: http://www.currentnursing.com/nursing_theory/Selye's_stress_theory.html
6.Kinney, M.R., Packa, D.R., & Dunbar, S.B. (1988). AACN's clinical reference for critical-care nursing (2nd ed.). New York: McGraw-Hill Book Company.
7. Dubey, A., & Boujoukos, A.J. (2004). Free cortisol levels should not be used to determine adrenal responsiveness. Retrieved Aug. 24, 2012 from the World Wide Web: http://ccforum.com/content/9/1/E2
8. Kowalak, J.P. (2003). Critical care challenges: Disorders, treatments, and procedures. Philadelphia: Lippincott, Williams & Wilkins.
9. Andreoli, T.E., et al. (2010). Cecil essentials of medicine (8th ed.). Philadelphia: Elsevier.
Deanna McCarthy is lead nurse planner at ADVANCE.