Endocrine Alterations

Endocrine Alterations
Chapter 18 Endocrine Alterations Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Introduction Endocrine system regulates physiological processes
Metabolic processes Energy production Fluid and electrolyte balance Bone health Stress reactions Growth and reproduction The endocrine glands form a communication network linking all body systems. Hormones from these glands control and regulate metabolic processes such as energy production, fluid and electrolyte balance, response to stress, reproduction, and growth. This system is closely linked to, and integrated with, the nervous system. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Introduction (continued)
Hypothalamus Conveyed to pituitary Pituitary Response to hypothalamus Increased or decreased secretion of hormone Controlled by feedback loops Hormone low: stimulus to release more Hormone high: stimulus to limit production The hypothalamus manufactures and secretes several releasing or inhibiting hormones that are conveyed to the pituitary. Positive feedback stimulates release of a hormone when serum hormone levels are low. Negative feedback inhibits the release of hormones when serum hormone levels are high. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Feedback System Figure 18-1. Feedback system for cortisol regulation.
The hypothalamic/pituitary communication mechanism participates in regulation of the following hormones: cortisol, thyroid hormone, growth hormone, and sex hormones. Low circulating hormone levels result in release of hypothalamic release hormones which, in turn, stimulate the anterior pituitary gland to release a stimulating hormone which, in turn, results in release of the final hormone by the target endocrine gland. When circulating levels of the end hormone are elevated, negative feedback results in decreases in secretion of hypothalamic and pituitary hormones. Figure 18-1. Feedback system for cortisol regulation. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Feedback Abnormalities
Primary Endocrine Disorders End gland is not responsive to hormone signals of pituitary hormone Example primary hypothyroidism ↓ T3 and T4 and Free T4 ↑ TSH and TRH End hormone and release hormones in opposite directions With primary endocrine diseases, the gland itself is nonresponsive to negative feedback controls. Hormone levels of release and stimulating hormones are opposite those of the final endocrine gland. For example, in primary hypothyroidism, levels of T3,T4, and Free T4 are decreased while TSH and TRH are increased. Alternately, in primary hyperthyroidism, the gland produces excess hormone and is not responsive to feedback control mechanisms. T3, T4, and Free T4 hormone levels will be elevated while TSH and TRH levels will be greatly reduced. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Feedback Abnormalities (continued)
Secondary Endocrine Disorders End gland is responsive to stimulating hormones but there is problem with pituitary or hypothalamus Example secondary hypothyroidism ↓ T3 and T4 and Free T4 ↓ TSH and TRH End hormone and release hormones in same direction. With secondary endocrine diseases, the gland itself is capable of eliciting a response to negative feedback controls. Hormone levels of release and stimulating hormones are in same direction as those of the final endocrine gland. For example, in secondary hypothyroidism, levels of T3, T4, and Free T4 are decreased because the gland is receiving insufficient pituitary stimulation. In secondary hyperthyroidism, the gland produces excess thyroid hormone because of overstimulation by pituitary hormone. Clinically, primary and secondary endocrine disorders manifest the same. Hormone testing is required to identify the cause of the hormone derangement. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Stress and Critical Illness
Hyperglycemia Excessive hepatic glucose production Relative hypoinsulinemia Adrenal insufficiency Primary and/or secondary dysfunction Thyroid dysfunction The stress of critical illness provokes a significant response by the endocrine system. Excess glucose in the blood occurs as a result of release of counterregulatory hormones and resultant excessive hepatic output of glucose through glycolysis and gluconeogenesis with resulting relative hypoinsulinemia. Relative adrenal insufficiency may occur in critically ill patients whenever elevated cortisol levels are inadequate for the demand. Thyroid hormone balance is disrupted by changes in peripheral metabolism that cause a decrease in triiodothyronine (T3) levels. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Pancreatic Disorders in the Critically Ill Patient
Stress-induced hyperglycemia Diabetic ketoacidosis (DKA) Hyperosmolar hyperglycemic state (HHS) Hypoglycemia Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Stress-Induced Hyperglycemia
Risk Factors Diabetes (diagnosed or undiagnosed) Advancing age Administration of exogenous catecholamines Glucocorticoid therapy Enteral or parenteral nutrition therapy Medications Obesity Pancreatitis, cirrhosis Stress response release of cortisol, growth hormone, catecholamines (including epinephrine and norepinephrine), glucagon, glucocorticoids, and the cytokines interleukin-1, interleukin-6, and tumor necrosis factor creates relative insulin deficiency and may raise glucose in the critically ill patient. Insulin coverage is frequently required. Whereas stress-induced hyperglycemia is a normal physiological response related to the fight-or-flight mode, glucose elevation has been associated with poor outcomes in hospitalized patients with and without a formal diagnosis of diabetes. Box 18-1 provides a list of risk factors of hyperglycemia in critically ill patients. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Stress-Induced Hyperglycemia (continued)
Potential adverse consequences Immune suppression Cerebral ischemia/stroke Dehydration/osmotic diuresis Impaired wound healing Endothelial dysfunction/thrombosis Decreased erythropoiesis Impaired gastric motility Whereas stress-induced hyperglycemia is a normal physiological response related to the fight-or-flight mode, glucose elevation has been associated with poor outcomes in hospitalized patients with and without a formal diagnosis of diabetes. Poor glycemic control affects multiple organs and is particularly problematic to endothelial and nervous tissues. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Stress-Induced Hyperglycemia (continued)
Clinical Management Establish euglycemia Target glucoses of mg/dL Insulin protocol Critically ill patients with diabetes are most effectively managed with insulin therapy regardless of their usual home self-management regimen. The degree of glycemic control desired in critically ill patients is a source of debate. Ask students what protocols they have seen in the clinical setting. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Hyperglycemic Crises Reduction in circulating insulin with concurrent elevation of counterregulatory hormones Occurrence DKA: Type 1 diabetes HHS: Type 2 diabetes Increasing incidence of both DKA and HHS in same patient The basic underlying mechanism for both DKA and HHS is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (cortisol, epinephrine, glucagon). Together, this hormonal mix leads to increased hepatic and renal glucose production, but it prevents utilization of glucose in the peripheral tissues. Box 18-3 describes physiological activity of insulin. Reinforce with students that alterations in glucose, protein, and fat metabolism will occur with uncontrolled diabetes and diabetic emergencies. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Diabetic Ketoacidosis
Pathophysiology Relative or absolute insulin deficiency Increase in counterregulatory hormones: glucagon, cortisol, catecholamines, and growth hormone The basic underlying mechanism for DKA is a reduction in the net effective action of circulating insulin coupled with elevation of counterregulatory hormones. This creates an absolute or relative insulin deficiency with the net effect of deranged glucose metabolism. In an individual with previously diagnosed diabetes, there is a need to increase insulin delivery as insulin needs increase with the stress of illness. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Physiological Changes in DKA
Hyperglycemia due to increased glucose production and decreased utilization Osmotic diuresis and dehydration Hyperlipidemia due to increased lipolysis Metabolic acidosis/ketosis When serum glucose levels exceed the renal threshold (approximately 200 mg/dL), glucose is lost through the kidneys (glycosuria). As glycosuria and osmotic diuresis progress, urinary losses of water, sodium, potassium, magnesium, calcium, and phosphorus occur. This cycle of osmotic diuresis worsens dehydration. Hyperosmolarity further impairs insulin secretion and a state of insulin resistance. The absolute or relative insulin deficiency that precipitates DKA causes derangement of carbohydrate, protein, and fat metabolism. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Physiological Changes in DKA (continued)
Altered potassium balance Excess acids result in increased anion gap Altered consciousness related to acidosis and dehydration Total body potassium deficits are common in DKA. Because of the fluid volume shifts and potassium shifts, serum potassium values must be interpreted with caution in patients with DKA. Excess lactic acid results in an increased anion gap (increased body acids). Inadequate buffering of the excess ketone acids by bicarbonate results in metabolic acidosis. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DKA: Etiology Initial presentation of type 1 diabetes Infections
Insufficient insulin relative to need Severe stress—trauma, surgery, acute myocardial infarction (AMI) Pregnancy in type 1 diabetes mellitus (DM) Table 18-3 outlines common events or physical changes that may precipitate DKA and HHS. Many of the causes are shared by both disorders. Have students describe factors that are common to and unique to both disorders. Patients with undiagnosed type 1 diabetes often present with DKA. Physiological events that increase glucose and insulin demands and are not accompanied by an increase in insulin delivery may precipitate DKA. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DKA: Etiology (continued)
Missed or reduced insulin Nonadherence to insulin regimen Insulin pump failure Intentional omission Eating disorders Behavioral health issues Medications Glucocorticoids Mismanagement of sick days Interruption of insulin delivery or failure to meet physiological insulin demands may precipitate DKA. Eating disorders are more common in people with type 1 diabetes and often may manifest as failure to take required insulin doses (insulin promotes fat storage and weight gain). Glucocorticoid therapy promotes gluconeogenesis and glycolysis by the liver and may result in significant increases in insulin requirements. Failure to effectively manage sick days is a common cause of DKA. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Clinical Presentation of DKA
Classic signs of dehydration Orthostasis Polyuria Polydipsia Polyphagia Hyperventilation/Kussmaul’s respirations Fruity odor to breath Flushed/dry skin Individuals with DKA may lose 6 liters of fluid, resulting in classic signs of dehydration. Polyuria, polydipsia, and polyphagia are the classic “three P’s” of diabetes. Polyuria is a result of the osmotic diuresis that accompanies the condition. Polydipsia results as a compensatory response to dehydration. Polyphagia occurs in response to the starvation state. Hyperventilation and Kussmaul’s respirations occur as the respiratory system attempts to compensate with the acidosis by “blowing off” carbonic acid. The fruity odor or acetone odor of the breath results from the ketosis, as does the flushing. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Clinical Presentation of DKA (continued)
Lethargy/altered consciousness Abdominal pain/nausea/vomiting Blood glucose greater than 250mg/dL May be lower in pregnancy Ketonuria/glucosuria Weight loss (may be profound) Blood gas changes (metabolic acidosis) Dehydration, electrolyte, and blood gas disturbances contribute to changes in mental status and may induce coma. Blood glucose levels of over 250 mg/dL are characteristic of DKA but may be lower in pregnancy. Weight loss is a product of profound osmotic diuresis. Blood gas disturbances are a result of the metabolic acidosis that accompanies DKA. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Sources of Fluid and Electrolyte Loss in Hyperglycemic States
The clinical presentation of hyperglycemic emergencies (DKA and HHS) is a product of fluid volume losses related to osmotic diuresis caused by hyperglycemia, ketosis (DKA), and respiratory losses (DKA). Sodium, potassium, and phosphate losses may accompany fluid losses. Figure 18-4. Intracellular/extracellular shifts in hyperglycemic crises. DKA, Diabetic ketoacidosis. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Electrolyte Imbalances in DKA
Hypokalemia (even if serum K+ is normal or high) - Will progress with addition of insulin to treatment regimen Insulin “pushes” potassium INTO CELLS Phosphate depletion Enhanced by insulin administration Mild hyponatremia Elevated BUN/creatinine Secondary to profound dehydration Serum electrolyte levels, particularly potassium, may be falsely elevated in relation to the actual intracellular level. Total body potassium deficits are common and must be considered in the overall management of DKA. Administration of insulin will further lower potassium. Total body phosphorus levels are also depleted by osmotic diuresis, but serum phosphate levels may remain in the normal range. BUN and creatinine levels and the BUN/creatinine ratio rise due to dehydration. A BUN/creatinine ratio of greater than 1:20 is suggestive of dehydration. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Hyperosmolar Hyperglycemic State
This condition most commonly occurs in individuals with type 2 diabetes. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

HHS: Pathophysiology Decreased use of glucose and/or increased production Hyperglycemia; increased extracellular osmolality Osmotic diuresis Profound dehydration No ketoacidosis—hyperglycemia with hyperosmolarity blocks lipolysis Pathophysiology of HHS is similar to that of DKA. However, in HHS, there are significantly lower levels of free fatty acids, resulting in a lack of ketosis but even higher levels of hyperglycemia, hyperosmolality, and severe dehydration secondary to osmotic diuresis. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

HHS: Etiology Inadequate insulin secretion; usually with type 2 diabetes Often in geriatric patients with decreased compensatory mechanisms Stress response Box 18-4 lists common causes of DKA and HHS. Again, discuss common causes and those specific to HHS. Most commonly, patients who develop HHS are older and have other medical problems such as renal insufficiency, heart failure, myocardial ischemia, and chronic lung disease. Mortality is very high. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Medications Affect blood glucose levels
Thiazides Phenytoin Glucocorticoids Beta-blockers Calcium channel blockers Enteral and parenteral nutrition A variety of medications, particularly glucocorticoids and nutrition support therapies may precipitate the condition. A complete list of medications that may induce hyperglycemia is included in Box Discuss how these agents may impact glucose control in both type 1 and type 2 diabetes. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DKA Versus HHS Pathophysiology
Both HHS and DKA arise from insulin deficiency relative to insulin need. Both conditions are characterized by hyperglycemia (more severe in HHS), osmotic diuresis, and electrolyte derangement. Acidosis occurs in all cases of DKA but may also be present in severe cases of HHS, although to a lesser degree. Figure 18-3. Pathophysiology of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DKA and HHS: Assessment
Based on severity of presentation Dehydration and hypovolemia Nausea and vomiting Classic polyuria, polyphagia, and polydipsia Decreased level of consciousness (LOC) Table 18-3 provides a comparison of DKA and HHS clinical manifestations. Emphasize those that are specific or unique to each condition. Review Laboratory Alert: Pancreatic Endocrine Disorders – pay attention to glucose levels, ketones, blood gasses, and anion gap differences between the conditions. Signs of DKA and HHS are related to the degree of dehydration present and the electrolyte imbalances. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DKA Versus HHS HHS Blood sugar >DKA; average >1000 mg/dL
More “normal” arterial blood gases (ABGs) More electrolyte imbalances and renal dysfunction Higher serum osmolarity than DKA Ketosis absent or mild Review Laboratory Alert: Pancreatic Endocrine Disorders In HHS, the laboratory results are similar to those in DKA, but with four major differences: 1) Serum glucose concentration in HHS is generally significantly more elevated. 2) Plasma osmolality is higher than in DKA and is associated with the degree of dehydration. 3) Acidosis is not present or very mild compared with DKA. 4) Ketosis is usually absent or very mild in comparison with DKA. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DKA and HHS: Interventions
Manage airway (DKA and HHS) Fluid replacement (DKA and HHS) First use 0.9% NS, then 0.45% NS Dextrose added when glucose approaches 200mg/dL Monitor closely for signs of fluid volume overload and cerebral edema Airway and breathing may be supported through the use of oral airways and oxygen therapy; intubation and ventilatory support may be needed. Isotonic fluid replacement is first used to restore vascular volume and perfusion. A rapid decrease in the plasma glucose level, combined with rapid fluid administration and concurrent insulin therapy (see next section), may lead to movement of water into brain cells, resulting in brain edema which may be fatal. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DKA and HHS: Interventions (continued)
Insulin therapy (DKA and HHS) Fluid replacement initiate first; monitor K+ Loading dose (not in children) Continuous infusion Hourly glucose monitoring Decrease glucose by 50 to 75 mg/dL/hr When glucose is less than 200 mg/dL, adjust infusion to maintain values of 150 to 200mg/dL Before starting insulin therapy, fluid replacement therapy must be under way and the serum potassium level must be greater than 3.3 mEq/L. It is important that serum glucose levels not be lowered too rapidly, not more than 50 to 75 mg/dL per hour, to avoid the potential for cerebral edema, which could result in seizures and coma. When the plasma glucose approaches 200 mg/dL, 5% dextrose is added to fluids to prevent hypoglycemia and assist in the resolution of ketosis. Components of an inpatient glucose management protocol are outlined in Table 18-2. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Insulin therapy – transitioning to subcutaneous therapy Blood glucose < 200 mg/dL Two of the following criteria met (DKA): pH > 7.30 HCO3 > 15 mEq/L Anion gap ≤ 12 mEq/L Ketosis must be resolved before transition Patients may be transitioned to subcutaneous insulin when blood glucose is < 200mg/dL and when two of the following criteria are met: 1) venous pH > 7.30 2) serum bicarbonate level > 15 mEq/L 3) calculated anion gap of < 12 mEq/L Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Insulin therapy – transitioning therapy Basal/bolus insulin regimen preferred Long-acting/short- or rapid-acting insulin Insulin pump Administer subcutaneous insulin prior to discontinuing IV insulin with attention to insulin action profile Monitor at least every 6 to 8 hours Determined by meal schedule If NPO, then every 6 hours A basal/bolus insulin regimen is preferred to most closely mimic physiological insulin delivery. This may be accomplished through a combination of a long-acting (glargine or detemir) insulin or intermediate insulin (NPJ) with a rapid-acting (aspart, lispro, glulisine) or short-acting (regular) insulin. Continuous subcutaneous insulin infusions via pump may also be a preferred insulin delivery method. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Insulin action curves Figure 18-2 provides a review of insulin action curves. Students should be aware of the onset, peak, and duration of action of each insulin product and the implication with timing of administration and assessment for hyperglycemia and hypoglycemia. Insulin transition is to be timed with attention to the insulin action curve of the subcutaneous insulin. The infusion should be discontinued following the onset of action of the subcutaneous insulin. The peak of insulin action is associated with the highest risk of hypoglycemia. Durations of action may be extended in patients who delayed renal clearance of insulin (renal insufficiency or renal failure). Individuals with delayed gastric emptying (gastroparesis) also may be at a higher risk for hypoglycemia, as glucose absorption by the gut and insulin action will not match. Figure 18-2. Commercially available insulin preparations showing onset, peak, and duration of action. (From Michel B. Nursing management of diabetes. In Lewis SL, Dirksen SR, Heitkemper MM, et al, eds. Medical-Surgical Nursing: Assessment and Management of Clinical Problems. 8th ed. St. Louis: Mosby ) Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Common insulin regimens All patients with type 1 diabetes require basal/bolus regimens. Individuals with type 2 diabetes who are responsive to oral agents may not require insulin or may benefit from basal therapy only in combination with oral agents once glycemic control has been attained. Table Unnumbered Figure. Common Insulin Regimens. Once a day. Single dose (From Michel B. Nursing management of diabetes. In Lewis SL, Dirksen SR, Heitkemper MM, eds. Medical-Surgical Nursing: Assessment and Management of Clinical Problems. 8th ed. St. Louis: Mosby ) Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

All patients with type 1 diabetes require basal/bolus regimens. Individuals with type 2 diabetes who are responsive to oral agents may not require insulin or may benefit from basal therapy only in combination with oral agents once glycemic control has been attained. Table Unnumbered Figure. Common Insulin Regimens. Twice a day. Split-mixed dose (From Michel B. Nursing management of diabetes. In Lewis SL, Dirksen SR, Heitkemper MM, eds. Medical-Surgical Nursing: Assessment and Management of Clinical Problems. 8th ed. St. Louis: Mosby ) Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

All patients with type 1 diabetes require basal/bolus regimens. Individuals with type 2 diabetes who are responsive to oral agents may not require insulin or may benefit from basal therapy only in combination with oral agents once glycemic control has been attained. Table Unnumbered Figure. Common Insulin Regimens. Basal-bolus. Multiple dose (From Michel B. Nursing management of diabetes. In Lewis SL, Dirksen SR, Heitkemper MM, eds. Medical-Surgical Nursing: Assessment and Management of Clinical Problems. 8th ed. St. Louis: Mosby ) Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Treatment of acidosis (DKA) Assess respiratory compensation and LOC Usually corrected by fluids and insulin Bicarbonate only if pH is less than 6.9 Administered by infusion until pH is 7.0 Multiple studies have shown that treatment with sodium bicarbonate is often not beneficial and may pose increased risk of hypoglycemia, cerebral edema, cellular hypoxemia secondary to decreased uptake of oxygen by body tissues, worsening hypokalemia, and development of central nervous system acidosis. Sodium bicarbonate is not routinely used to treat acidosis unless the serum pH is less than 6.9. Bicarbonate replacement is used only to bring the pH up to 7.0, but not to normal levels. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Electrolyte replacement (DKA and HHS) Potassium Establish renal function first Maintain between 4 and 5 mEq/L Phosphorus Magnesium Monitor ECG Insulin replacement and monitoring begin after the first liter of IV fluid has been administered, the serum potassium level is greater than 3.3 mEq/L, and the patient is producing urine. Serum potassium levels should be maintained between 4 and 5 mEq/L during the course of therapy. Potassium may be added to maintenance IV fluids or may be administered by intermittent infusions. The IV site should be monitored closely. Electrocardiographic (ECG) monitoring for cardiac dysrhythmias and assessment of respiratory status is also important during potassium administration, phosphate and magnesium replacement. Potassium phosphate can be administered to treat part of the potassium deficit in a concentration of 20 to 30 mEq/L. Phosphate replacement is used with extreme caution in patients with renal failure because these patients are unable to excrete phosphate and typically have underlying hyperphosphatemia. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Survival Skill Education (Hospital) Insulin/medication management Blood glucose monitoring Personal targets/recordkeeping Sick day management Hypoglycemia prevention, recognition, and treatment Basic meal planning Referral to diabetes self-management education program for follow-up A primary intervention to prevent DKA and HHS is diabetes self-management education. Survival education should be initiated/reinforced in the hospital and continued in an outpatient setting. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Critical Thinking Challenge
Why is the insulin drip decreased when the blood sugar reaches 250 mg/dL? Why is regular insulin used? What is the most efficient way to test blood sugar hourly? The insulin drip is decreased when the glucose reaches 250 mg/dL in order to prevent development of cerebral edema, which can be promoted by rapid declines in glucose levels. Regular insulin is the preferred insulin product for IV administration. Bedside glucose monitoring using point-of-care testing procedures is most effective for frequent blood glucose testing. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Hypoglycemia Pathophysiology Glucose production below utilization
Glucose lower than 70 mg/dL Rise in counterregulatory hormones to compensate – stress response Classic symptoms and physiological response may be blunted in individuals with autonomic neuropathy A hypoglycemic event activates the sympathetic nervous system, causing a rise in counterregulatory hormones, including glucagon, epinephrine, cortisol, and growth hormone. Those at highest risk for hypoglycemia are patients taking insulin, children and pregnant women with type 1 DM, patients with autonomic diabetic neuropathy, and elderly persons with type 1 or type 2 DM. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Hypoglycemia: Etiology
Excess insulin/oral agents Alcohol potentiates hypoglycemic effects Insufficient nutrition intake Excess exercise Medications (e.g., beta-blockers) Renal impairment Diabetic neuropathy Hypoglycemia unawareness Gastroparesis Box 18-8 describes common causes of hypoglyemia. Emphasize that students should be aware of diabetes and non-diabetes agents that may induce hypoglycemia. They also should know insulin action curves and oral agents and other diabetes medications that may induce hypoglycemia. Table 18-2 provides an overview of common medications used in diabetes treatment. Students should be directed to review these. Stress that medications that result in increased levels of circulating insulin may cause hypoglycemia. Other agents, when combined with an agent that directly causes hypoglycemia, may potentiate hypoglyecemia. Patients receiving insulin therapy must be closely monitored for hypoglycemia. Hypoglycemia unawareness, also known as hypoglycemia-associated autonomic failure, is a term used to describe a diabetes-related condition where a patient does not recognize the onset of hypoglycemic signs and symptoms. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Hypoglycemia: Assessment
Rapid decrease in serum glucose levels Activation of sympathetic nervous system (epinephrine release) Tachycardia Diaphoresis Pallor Dilated pupils Clinical signs of hypoglycemia by etiology are outlined in Table 18-4. With a rapid decrease in serum glucose levels, there is activation of the sympathetic nervous system, mediated by epinephrine release from the adrenal medulla, and a rise in counterregulatory hormones, including glucagon, epinephrine, cortisol, and growth hormone. This compensatory “fight-or-flight” mechanism may result in symptoms such as tachycardia; palpitations; tremors; cool, clammy skin; diaphoresis; hunger; pallor; and dilated pupils. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Hypoglycemia: Assessment (continued)
Slow decrease in serum glucose levels Neuroglucopenia Restlessness Difficulty thinking and speaking Visual disturbances Paresthesias Change in LOC Clinical signs of hypoglycemia by etiology are outlined in Table 18-4. Because the brain is an obligate user of glucose, the first clinical sign of hypoglycemia is a change in mental status. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Laboratory evaluation Blood glucose level less than 70 mg/dL May vary in the following patient groups: Hypoglycemia unawareness Cognitive impairment Older adults at risk for falls If recurrent and DM long-standing, evaluate renal function In most patients, the confirming laboratory test for hypoglycemia is a serum or capillary blood glucose level less than 70 mg/dL. Adults with a history of hypoglycemia unawareness, cognitively impaired elders, and older adults at high risk for falls may have higher target glucose ranges. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Glucose production falls behind glucose utilization, resulting in decrease in blood glucose. Because the brain is an obligate user of glucose, the first clinical sign of hypoglycemia is a change in mental status, which could lead to seizures and brain damage. A hypoglycemic event activates the sympathetic nervous system causing a rise in counterregulatory hormones, including glucagon, epinephrine, cortisol, and growth hormone. Figure 18-5. Pathophysiology of hypoglycemia. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Hypoglycemia: Interventions
Treat hypoglycemia 15 g carbohydrate orally 50% dextrose (EMS, ED, ICU settings) Glucagon Oral glucose Assess response: should improve rapidly Adjust insulin regimen temporarily Prevention and teaching Hypoglyecemia management by degree of hypoglycemia is outlined in Box Box provides 15-gram carbohydrate replacement equivalents. After serum or capillary glucose levels have been confirmed, carbohydrates must be replaced. The patient’s neurological status and ability to swallow without aspiration determine the route to be used. In the event of hypoglycemia, rapid- and short-acting insulin should be withheld temporarily. If the patient has an insulin pump, it should be suspended for moderate or severe hypoglycemia. Longer-acting basal insulin should typically not be withheld in patients on subcutaneous insulin therapy who are experiencing hypoglycemia, as this will increase the risk for DKA in patients with type 1 diabetes and hyperglycemia in all insulin-treated patients with diabetes. Patients at risk for severe hypoglycemia should be prescribed a glucagon emergency kit, and family and significant regular contacts should be instructed in its use. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Quick Quiz! An 72-year-old patient is admitted after being found unresponsive by a caregiver. The following laboratory findings are reported: glucose 628 mg/dL; BUN 62 mg/dL; creatinine 3.8 mg/dL; sodium 130 mEq/L; potassium 3.1 mEq/L; pH 7.2; CO2 28 mm Hg; HCO3 8 mEq/L; anion gap 18 mEq/L. These findings are consistent with which of the following? Adrenal crisis Diabetes insipidus Diabetic ketoacidosis Hyperosmolar hyperglycemic state Answer: C. Diabetic ketoacidosis The patient has a very elevated glucose in combination with a partially compensated metabolic acidosis characterized by a low pH, low CO2, low bicarbonate, and elevated anion gap. The patient’s renal markers are consistent with acute renal failure. Ketones would contribute to the anion gap elevation. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Acute Adrenal Insufficiency
Primary: destruction of adrenal glands Secondary: interfere with secretion Deficiency of glucocorticoids (cortisol) and mineralocorticoids (aldosterone) Physiological effects of glucocorticoids are presented in Box As signs and symptoms are presented with each condition, relate them to the effects of cortisol. Hypofunction of the adrenal gland results from either primary or secondary mechanisms that suppress secretion of cortisol, aldosterone, and androgens. Primary disorders result in deficiencies of both glucocorticoids and mineralocorticoids. The most common cause of acute adrenal insufficiency is abrupt withdrawal from corticosteroid therapy. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Lack of Cortisol Decreased production of glucose
Decreased metabolism of protein and fat Decreased vascular tone Decreased effect of catecholamines Decreased intestinal motility and digestion Inability to respond to stress Box provides a list of common causes of adrenal crisis. Review primary and secondary causes with students. Adrenal crisis is a life-threatening absence of cortisol (glucocorticoid) and aldosterone (mineralocorticoid). A deficiency of cortisol results in decreased production of glucose, decreased metabolism of protein and fat, decreased appetite, decreased intestinal motility and digestion, decreased vascular tone, and diminished effects of catecholamines. Deficiency can produce profound shock due to significant decreases in vascular tone caused by the diminished effects of catecholamines. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Lack of Aldosterone Loss of sodium Loss of water
Decreased circulating volume Potassium retention (hyperkalemia) Deficiency of aldosterone results in decreased retention of sodium and water, decreased circulating volume, and increased potassium and hydrogen ion reabsorption. These effects are seen in patients with underlying primary adrenal insufficiency but not secondary adrenal insufficiency, because aldosterone secretion is not primarily dependent on adrenocorticotropic hormone (ACTH). Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Primary Acute Adrenal Insufficiency
Hypofunction Inadequate cortisol and aldosterone Autoimmune: Addison’s disease Hemorrhagic destruction Infiltration (neoplasm, amyloidosis) Infection and sepsis Medications TB in countries where endemic HIV Risk factors for adrenal crisis are described in Box Discuss how a comprehensive nursing history is needed to identify patients at risk for adrenal crisis. Primary mechanisms, resulting in Addison’s disease, are those that cause destruction of the adrenal gland itself. At least 90% of the adrenal cortex must be destroyed before clinical signs and symptoms appear. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Secondary Acute Adrenal Insufficiency
Decrease ACTH secretion or suppress production of steroids Causes Withdrawal from long-term steroid use Pituitary and hypothalamic disorders Systemic inflammatory response Inadequate steroids in highly stressed patient who has received chronic steroid therapy Secondary mechanisms that can produce adrenal insufficiency are those that decrease ACTH secretion, resulting in deficiency of glucocorticoids alone, because mineralocorticoids are not primarily dependent on ACTH secretion. Mechanisms that can produce secondary adrenal insufficiency include abrupt withdrawal of corticosteroids, pituitary and hypothalamic disorders, and sepsis. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Renin-Angiotension-Aldosterone System
Review pathophysiology of renin-angiotensin-aldosterone system (RAAS). Figure 18-6. Physiology of aldosterone release. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Adrenal Crisis Clinical Presentation
Deficiency of aldosterone results in decreased retention of sodium and water, decreased circulating volume, and increased potassium and hydrogen ion reabsorption. These effects are seen in patients with underlying primary adrenal insufficiency but not secondary adrenal insufficiency, because aldosterone secretion is not primarily dependent on ACTH. Because this condition is a medical emergency, the diagnosis should be considered in any patient acutely ill with fever, vomiting, hypotension, shock, decreased serum sodium level, increased serum potassium level, or hypoglycemia. Figure 18-7. Pathophysiological effects of adrenal insufficiency. BUN, Blood urea nitrogen; ECG, electrocardiogram; MSH, melanocyte-stimulating hormone. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Acute Adrenal Insufficiency: Assessment
Symptoms of hypovolemia Fluid and electrolyte imbalances Postural hypotension Change in LOC Hyperkalemia Fatigue, weakness Gastrointestinal complaints Decreased renal perfusion and decreased urine output See Laboratory Alert: Adrenal Disorders for Laboratory Indicators of Adrenal Crisis. Note glucose (decreased), sodium (decreased), potassium (elevated), acidosis. The manifestations of adrenal insufficiency result from a lack of adrenal cortical secretion of glucocorticoids (primarily cortisol), mineralocorticoids (primarily aldosterone), or both. The deficiency of glucocorticoids is especially significant because their influence on the defense mechanisms of the body and its response to stress makes them essential for life. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Acute Adrenal Insufficiency
Laboratory values Hyponatremia, hyperkalemia, and hypercalcemia Eosinophilia Metabolic acidosis Hypoglycemia Hyperuricemia Cortisol levels ACTH levels Cosyntropin stimulation test Laboratory findings in a patient with acute adrenal crisis include hypoglycemia, hyponatremia, hyperkalemia, eosinophilia, increased BUN level, and metabolic acidosis. The diagnosis of adrenal crisis is made by evaluating plasma cortisol levels. These levels vary diurnally in healthy individuals, but this pattern is lost in the critically ill, making the timing of the test unimportant. In crisis, plasma cortisol levels are less 10 mg/dL. Differentiating between primary and secondary adrenal insufficiency is accomplished by evaluating serum ACTH levels. ACTH levels will be elevated in primary insufficiency and normal or decreased in secondary insufficiency. The procedure for the cosyntropin stimulation test and interpretation of findings are included in Box Review with students. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Quick Quiz! Why is dexamethasone given as emergency treatment during a cosyntropin test? To reduce cerebral edema. To treat an allergic reaction. Its administration will not alter the test results. It enhances effect of cosyntropin. Answer: C. Its administration will not alter the test results. Decadron may be given in emergency situations because it will not interfere with endogenous cortisol levels and will not impact results of the cosyntropin stimulation test. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Acute Adrenal Insufficiency: Interventions
Correct fluid and electrolyte imbalances Normal saline and dextrose May need 5 liters in first 24 hours Hormonal replacement Hydrocortisone (glucocorticoid) Fludrocortisone (mineralocorticoid) Patient or family education Fluid losses should be replaced with an infusion of 5% dextrose and NS until signs and symptoms of hypovolemia stabilize. This not only reverses the volume deficit but also provides glucose to minimize the hypoglycemia. Initially, glucocorticoid replacement is the most important type of hormonal replacement. Medications used to treat adrenal crises are outlined in Table Nursing interventions in administering these therapies are described. In a patient with known adrenal insufficiency and/or receiving corticosteroid therapy, adrenal crisis is preventable. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Hyperthyroidism: Thyroid Storm
Overproduction of thyroid hormones Affected by anterior pituitary gland and hypothalamus Positive and negative feedback Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Thyroid Dysfunction in the Critically Ill
Euthyroid sick syndrome (Low T3 syndrome) Physiological adaptation to illness Thyroid storm Myxedema coma Physiological effects of thyroid hormone are outlined in Box Students should be able to relate how these effects relate to the clinical presentation of thyroid disorders. Also review Laboratory Alert: Thyroid Disorders. Table 18-6 provides a description of nursing care of patients with various thyroid crises. Thyroid storm occurs in untreated or inadequately treated patients with hyperthyroidism; it is rare in patients with normal thyroid gland function. Myxedema coma is the most extreme form of hypothyroidism and is life-threatening. Myxedema coma in the absence of an associated stress or illness is uncommon, with infection being the most frequent stressor. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Thyroid Regulation Review flow chart of thyroid regulation. Figure 18-8. Feedback systems for thyroid hormone regulation. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Hyperthyroidism: Etiology
Toxic diffuse goiter: most common cause Graves’ disease (autoimmune) Toxic multinodular goiter Heart failure or severe muscle weakness Amiodarone therapy Radiation therapy Interferon-alpha therapy Box outlines common causes of hyperthyroidism. What questions are critical for the nurse to include when gathering a history? The most frequent form of hyperthyroidism is toxic diffuse goiter, also known as Graves’ disease; occurs most frequently in young (ages 30 to 40), previously healthy women. Hyperthyroidism also occurs secondary to exposure to radiation, interferon-alpha therapy for viral hepatitis, and other events. Administration of amiodarone, a heavily iodinated compound, can result in either hyperthyroidism or hypothyroidism. Hyperthyroidism must be explored as a causative factor in new-onset, otherwise unexplained rapid heart rates. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Thyroid Storm Inadequately controlled hyperthyroidism
Produces a hyperdynamic and hypermetabolic state Affects many major body functions Medical emergency, death within 48 hours without treatment Thyroid storm occurs in untreated or inadequately treated patients with hyperthyroidism; it is rare in patients with normal thyroid gland function. Crisis is often precipitated by stress related to an underlying illness, general anesthesia, surgery, or infection. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Thyroid Storm: Assessment
Increased cardiac workload Increased oxygen demands and alterations in respirations Severe fever Fear, delirium, overt psychosis, convulsions, stupor, or coma Fatigue Nausea, vomiting, diarrhea, and cramps Box describes, in detail, progressive signs of hyperthyroidism. How do these relate to known actions of thyroid hormone? Thyroid storm has an abrupt onset. The most prominent clinical features of thyroid storm are severe fever, marked tachycardia, heart failure, tremors, delirium, stupor, and coma. The severity of the hyperthyroid state is not necessarily indicated by the serum levels of thyroid hormones but rather by tissue and organ responsiveness to the hormones. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Thyroid Storm: Diagnosis
Elevated T3 and T4 Elevated T3 resin intake Lowered thyroid-stimulating hormone Due to negative feedback Electrolyte imbalances Thyroid hormone levels are elevated; however, these levels are generally no higher than those normally seen. In primary glandular disease, the TSH will be exceptionally low due to negative feedback. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Thyroid Storm: Interventions
Goals of treatment Inhibit thyroid hormone biosynthesis Block thyroid hormone release Antagonize peripheral effects of thyroid hormone Provide supportive care Treat precipitating cause Educate Specific pharmacological management of thyroid storm is described in detail in Box What is the rationale for inclusion of these medications? The primary objectives in the treatment of thyroid storm are antagonizing the peripheral effects of thyroid hormone, inhibiting thyroid hormone biosynthesis, blocking thyroid hormone release, providing supportive care, identifying and treating the precipitating cause, and providing patient and family education. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Thyroid Storm: Interventions (continued)
Administer medications Inhibit thyroid hormone production and CV effects Propylthiouracil (PTU) and methimazole (Tapazole) inhibit thyroid synthesis Iodide agents retard release of hormones Medication to block effects: beta-blockers, steroids In high doses, propylthiouracil inhibits conversion of T4 to T3 in peripheral tissues and results in a more rapid reduction of circulating thyroid hormone levels. Methimazole may be used because of its longer half-life and higher potency. The disadvantage to both propylthiouracil and methimazole is that they lack immediate effect. Iodide agents inhibit the release of thyroid hormones from the thyroid gland, inhibit thyroid hormone production, and decrease the vascularity and size of the thyroid gland. Serum T4 levels decrease approximately 30% to 50% with any of these drugs, with stabilization in 3 to 6 days. The mortality rate of thyroid storm has been significantly reduced with the introduction of beta-blockers to block the effects of thyroid hormones. The drug used most frequently is propranolol (Inderal). Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Thyroid Storm: Interventions (continued)
Monitor cardiovascular status Monitor and treat hyperthermia Promote oxygenation Fluid replacement Adequate nutrition Prevent injury Patient and family education Symptoms are aggressively treated. Acetaminophen is used as an antipyretic; cooling blankets and ice packs may be used. Cardiac complications are treated with pharmacotherapy such as beta-blockers. Oxygen is administered to support the respiratory effort. The large fluid losses are replaced; hemodynamic monitoring may be required. Nutritional support is provided. Precipitating factors are identified and treated and/or removed. The patient should be kept in a cool, quiet environment with minimal stimulation. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Quick Quiz! What strategy is helpful for promoting nutrition in the patient with thyroid storm? Provide high-calorie, high-protein oral diet. Insert feeding tube for enteral nutrition. Start TPN via a central catheter. Provide Ensure or Boost supplements if the patient will not eat. Answer: A. Provide high-calorie, high-protein oral diet. The patient needs an easy-to-digest, high-calorie, high-protein diet to counteract the excessive caloric expenditures and muscle wasting that accompany thyroid storm. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Myxedema Coma Pathophysiology Hypofunction of thyroid
Hypometabolism and hypodynamic state Myxedema coma is the most extreme form of hypothyroidism and is life-threatening. Myxedema coma in the absence of an associated stress or illness is uncommon, with infection being the most frequent stressor. The addition of stress to an already hypothyroid patient accelerates the metabolism and clearance of whatever thyroid hormone is present in the body. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Myxedema Coma: Etiology
Primary disease Hashimoto’s thyroiditis Surgical or radioactive treatment for Graves’ disease with inadequate follow-up treatment Insufficient thyroid stimulation due to hypothalamus or pituitary disease Exacerbation of hypothyroid state Box provides a list of common causes of hypothyroidism. What are critical nursing elements to include in the nursing history? The underlying causes of myxedema coma are those that produce hypothyroidism. Most cases occur either in patients with long-standing autoimmune disease of the thyroid (Hashimoto’s thyroiditis) or in patients who have received surgical or radioactive iodine treatment for Graves’ disease and have received inadequate hormone replacement. The addition of stress to an already hypothyroid patient accelerates the metabolism and clearance of whatever thyroid hormone is present in the body. Thus the patient experiences increased hormone utilization but decreased hormone production, which precipitates a crisis state. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Myxedema Coma: Assessment
Cognitive changes Activity intolerance, decreased reflexes, and slow movements Cardiovascular Bradycardia, hypotension Cardiomegaly Decreased cardiac output Electrocardiogram (ECG) changes Edema Box provides a detailed list of common clinical manifestations of progressive hypothyroidism. How do these relate to the physiological effect of thyroid hormone? The patient in hypothyroid crisis may present with somnolence, delirium, seizures, or coma. Personality changes such as paranoia and delusions may be evident. Slowed motor conduction produces decreased tendon reflexes and sluggish, awkward movements. Cardiac function is depressed, resulting in decreases from baseline in heart rate, blood pressure, contractility, stroke volume, and cardiac output. The patient may develop a pericardial effusion, making heart tones distant. Many of the manifestations are attributable to the development of mucinous edema. This interstitial edema is the result of water retention and decreased protein. Fluid collects in soft tissue such as the face and in joints and muscles. Facial edema and an enlarged tongue are classic signs of myxedema. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Myxedema Coma: Assessment (continued)
Pulmonary disturbances Hypoventilation CO2 retention Pleural effusion Upper airway and tongue edema Hypothermia Respiratory system responsiveness is depressed, producing hypoventilation, respiratory muscle weakness, and CO2 retention. CO2 narcosis may contribute to decreased mentation. Patients with hypothyroidism are unable to maintain body heat because of the decreased metabolic rate and decreased production of thermal energy. Hypothermia is present in 80% of patients in myxedema coma, with temperatures as low as 80˚ F. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Myxedema Coma: Diagnosis
Primary myxedema ↓ T3 and T4; ↓ T3 resin update ↑ TSH Secondary myxedema ↓ TSH Hypoglycemia Hyponatremia Secondary to fluid retention As with other disorders that involve hypothalamic/pituitary regulation, in primary disease the end hormones (T3 and T4) are decreased while TSH increases as the pituitary gland attempts to stimulate the nonresponsive gland. In primary endocrine disorders, stimulating hormones typically are increased while the final glandular hormone levels are decreased. In secondary disorders where there is a decrease in hormone levels, the functional gland is understimulated by the pituitary gland or possibly even the hypothalamus gland. This results in a decrease in the end hormone levels (T3 and T4) due to the decreased TSH level. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Myxedema: Interventions
Treat with replacement thyroid hormone Fluid and electrolyte replacement; thyroid replacement usually corrects sodium Monitor gas exchange and respiratory status Box details clinical management of myxedema, including thyroid replacement therapy. Discuss rationales for each nursing intervention based on known effects of thyroid hormone and the endocrine derangement. The primary objectives in the treatment of myxedema coma are identifying and treating the precipitating cause, providing thyroid replacement, restoring fluid and electrolyte balance, providing supportive care, and providing patient and family education. Levothyroxine sodium is commonly used for treatment. Symptoms are aggressively treated. Drugs that depress respirations, such as narcotics, are avoided. Mechanical ventilation is frequently required. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Myxedema: Interventions (continued)
Monitor cardiovascular status Manage hypothermia Protect from injury and infection Educate patient and family Cardiac function is assessed and treated. Hypothermia is treated by keeping the room warm and using passive rewarming methods. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Quick Quiz! A patient who has previously undergone a transphenoidal hypophysectomy has been nonadherent with hormone replacement therapies. Which of the following lab findings would be consistent with this patient’s history? Decreased T3, T4; decreased TSH Decreased T3, T4; increased TSH Decreased cortisol; increased ACTH Increased cortisol; decreased ACTH Answer: A. Decreased T3, T4; decreased TSH Removal of the pituitary gland results in an inability of the gland to produce TSH, ACTH, growth hormone, FSH, LH, and MSH hormones and would produce a secondary hormone failure. Pituitary level hormones would be decreased because the pituitary gland has been removed and will produce a resulting hypofunction at each of the target glands affected by these anterior pituitary hormones. In secondary hormone conditions, anterior pituitary hormones and end-organ hormones elevate and decrease together because negative feedback controls are lost. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Explain why narcotics are avoided or used cautiously in the patient with myxedema coma. Patients with myxedema coma may experience hypoventilation and resultant carbon dioxide retention due to weakness of respiratory muscles. Narcotics and sedatives would further decrease respiratory drive and further reduce the patient’s mental status. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Diabetes Insipidus (DI)
Pathophysiology Deficiency in synthesis or release of antidiuretic hormone (ADH) Excessive water loss Types Neurogenic (central): ADH deficiency Nephrogenic: kidneys insensitive to ADH Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Antidiuretic Hormone Disorders
Diabetes insipidus Syndrome of inappropriate secretion of antidiuretic hormone Cerebral salt wasting Two common disturbances of ADH are diabetes insipidus (DI) and the syndrome of inappropriate secretion of ADH (SIADH). A less common disorder is cerebral salt wasting (CSW). CSW is a disorder of sodium and fluid balance that occurs in patients with a neurological insult. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Antidiuretic Hormone Regulation
Review the pathophysiology of antidiuretic hormone regulation. Figure Physiology of antidiuretic hormone (ADH) release. BP, Blood pressure. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Antidiuretic Hormone Regulation (continued)
Osmoreceptors in the hypothalamus stimulate the thirst response to promote restoration of fluid volume. Stimulation of the supraoptic and paraventricular nuclei causes release of ADH from nerve endings in the posterior pituitary. Primary triggers for ADH release are increased serum osmolality, decreased blood volume (by more than 10%), or decreased blood pressure (5% to 10% drop). Other factors that stimulate ADH release are elevated serum sodium level, trauma, hypoxia, pain, stress, and anxiety. Figure 18-9. Hypothalamic–posterior pituitary system. Os, Osmoreceptor; PVN, Paraventricular nuclei; SON, Supraoptic nuclei. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DI: Neurogenic Etiology
Genetically predisposed Head trauma Neurological abnormalities Increased intracranial pressure (ICP) Pituitary surgery A specific listing of causes of neurogenic diabetes insipidus is included in Box What is common about all of these causes? Answer: They either involve direct damage to the pituitary gland or hypothalamus or increased intracranial pressure. The primary cause of neurogenic diabetes insipidus is traumatic injury to the posterior pituitary or hypothalamus as a result of head injury or surgery. Transient DI may occur after trauma to the pituitary, after manipulation of the pituitary stalk during surgery, or as a result of cerebral edema. Permanent DI occurs when more than 80% to 85% of hypothalamic nuclei or the proximal pituitary stalk is destroyed. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DI: Nephrogenic Etiology (continued)
Genetically predisposed Chronic renal disease Multisystem disorders affecting kidney Multiple myeloma, sickle cell disease, and cystic fibrosis A specific listing of causes of nephrogenic diabetes insipidus is included in Box Nephrogenic DI may occur in genetically predisposed persons. It also may be acquired from chronic renal disease, drugs, or other conditions that produce permanent kidney damage or inhibit the generation of cyclic adenosine monophosphate in the tubules. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DI: Nephrogenic Etiology (continued)
Drugs Ethanol Phenytoin (Dilantin) Lithium carbonate Demeclocycline Amphotericin Methoxyflurane (inhaled anesthetic) Medications that may affect regulation of antidiuretic hormone include ethanol, phenytoin, lithium, demeclocycline, amphotericin, and inhaled anesthetics such as methoxyflurane. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DI: Assessment High urine output Thirst and polydipsia Hypotension
Decreased skin turgor Dry mucous membranes Tachycardia Weight loss Low right atrial pressure/central venous pressure (RAP/CVP) and pulmonary artery (PA) pressure Neurological changes Hypernatremia and hypovolemia Review Laboratory Alert: Pituitary Disorders. Discuss why these assessments are done (e.g., assess fluid balance, symptoms of hypovolemia, etc.). Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DI: Diagnosis Dilute urine with low specific gravity
Increased serum osmolarity Increased blood urea nitrogen (BUN) and creatinine Hypokalemia or hypercalcemia Water deprivation test Vasopressin test (to differentiate) The classic signs of DI are an inappropriately low urine osmolality, decreased urine specific gravity, and a high serum osmolality. Corresponding with the low urine osmolality is a decreased urine specific gravity. Serum osmolality is greater than 295 mOsm/kg, and the serum sodium level is greater than 145 mEq/L. Other values such as BUN and creatinine may be elevated as a result of hemoconcentration. The presence of hypokalemia or hypercalcemia suggests nephrogenic DI. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Laboratory Indicators of DI
Sodium (serum) >145 mEq/L Free water loss due to absent or diminished release of ADH or lack of response by the kidneys results in hemoconcentration of sodium Osmolality (serum) >295 mOsm/kg H2O Free water loss due to absent or diminished release of ADH or lack of response by the kidneys increases serum osmolality; will be normal in secondary DI Osmolality (urine) <100 mOsm/kg H2O Free water loss into urine decreases urine osmolality Sodium (urine) mEq/L Urine sodium is not affected Diabetes insipidus is characterized by high serum sodium; high serum osmolality; low urine osmolality; and normal urine sodium. Excessive losses of very dilute urine occur. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Explain how the water deprivation test and vasopressin test help to diagnose the type of DI. In a person with normal ADH function, deprivation of water would result in increased levels of circulating vasopressin as the patient dehydrates. Failure to increase ADH levels in the face of known dehydration would be suggestive of a neurogenic DI. The expected response to administration of vasopressin would be a decrease in urine output and concentration of urine. An impaired urine output in response to vasopressin administration is suggestive of nephrogenic DI – ADH is present, but the collecting tubules of the nephron cannot respond to the hormone appropriately. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DI: Interventions Volume replacement Hormone replacement
Monitor for fluid overload and water intoxication once therapy has been initiated Hormone replacement Vasopressin (desmopressin) Thiazide diuretics (nephrogenic) Volume already lost must be replaced. In addition, fluid is replaced every hour to keep up with current urine losses. Correction of hypernatremia and replacement of free water are achieved by using hypotonic solutions of dextrose in water. If the patient has circulatory failure, isotonic saline may be administered until hemodynamic stability and vascular volume have been restored. Nephrogenic DI is treated with sodium restriction, which decreases the glomerular filtration rate and enhances fluid reabsorption. Administration of thiazide diuretics may increase tubular sensitivity to ADH. Neurogenic DI is controlled primarily with exogenous ADH preparations. These drugs replace ADH and enable the kidneys to conserve water. The drug most commonly used for management is desmopressin (DDAVP), a synthetic analogue of vasopressin. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

DI: Interventions (continued)
Patient education Pathogenesis of DI Dose, side effects, and rationale for prescribed medications Parameters for notifying the physician Importance of adherence to medication regimen Importance of recording daily weight measurements to identify weight gain Importance of wearing a Medic-Alert identification bracelet Importance of drinking according to thirst and avoiding excess drinking Patients who have a permanent ADH deficit require education regarding medication management and recognition of signs of inadequate or excessive therapy. Excessive therapy may produce signs of SIADH, and inadequate therapy may cause a DI condition. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)
Pathophysiology Excess ADH Plasma hypotonicity Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) results from excessive production of antidiuretic hormone with resultant retention of water and plasma hypotonicity. SIADH may be neurogenic in origin, resulting from damage to neuronal, pituitary, or hypothalamic tissue. The condition also may result from endogenous release for ADH from ectopic sources such as tumors and pulmonary disorders. This occurs when there is a failure in the negative feedback mechanism that regulates the release and inhibition of ADH. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

SIADH: Etiology Central nervous system disease Malignancy
Trauma Tumor Malignancy Small-cell lung carcinoma Hodgkin’s lymphoma Pancreatic and duodenal carcinoma Pulmonary disorders TB, lung abscess, pneumonia, COPD Box includes a list of CNS and ectopic causes of SIADH as well as a complete list of medications that may induce SIADH. Note that many common medications used in treatment of behavioral health problems may induce this disorder. CNS disorders such as head injury, infection, hemorrhage, surgery, and stroke stimulate the hypothalamus or pituitary, producing excess secretion of ADH. A common cause of SIADH is ectopic production of ADH by malignant disease, especially small-cell carcinoma of the lung. Other types of malignancies known to produce SIADH include pancreatic and duodenal carcinoma, Hodgkin’s lymphoma, sarcoma, and squamous cell carcinoma of the tongue. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

SIADH: Etiology (continued)
Medications Many medications can result in SIADH. Many medications are associated with development of SIADH. See Box Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

SIADH: Assessment Central nervous system Pulmonary system
Confusion, headache, seizures, and weakness Pulmonary system Increased respiration, dyspnea, and adventitious lung sounds Cardiovascular Hypertension and elevated CVP and PA pressures, edema GI system Anorexia, nausea, vomiting, muscle cramps, and decreased bowel sounds Neurological manifestations such as weakness, lethargy, mental confusion, difficulty concentrating, restlessness, headache, seizures, and coma may occur in response to hyponatremia and hypo-osmolality. If the serum sodium level decreases to less than 120 mEq/L in 48 hours or less, serious neurological symptoms and a mortality rate as high as 50% can result. Fluid overload in the pulmonary system produces increased respiratory rate; dyspnea; adventitious lung sounds; and frothy, pink sputum. Water retention produces edema, increased blood pressure, and elevated central venous and pulmonary artery occlusion pressures. Congestion of the GI tract and decreased motility occur because of hyponatremia. This is manifested by nausea and vomiting, anorexia, muscle cramps, and decreased bowel sounds. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

SIADH: Diagnosis Hyponatremia Decreased serum osmolarity
High urine sodium Concentrated urine Decreased BUN and creatinine Decreased albumin The hallmark of SIADH is hyponatremia and hypo-osmolality in the presence of concentrated urine. High urinary sodium levels (>20 mEq/L) help to differentiate SIADH from other causes of hypo-osmolality, hyponatremia, and volume overload (such as congestive heart failure). Hemodilution may decrease other laboratory values such as BUN, creatinine, and albumin. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Laboratory Indicators of SIADH
Sodium (serum) <135 mEq/L Free water retention due to oversecretion of ADH dilutes sodium Osmolality (serum) <280 mOsm/kg H2O Free water retention due to oversecretion of ADH decreases osmolality Osmolality (urine) >100 mOsm/kg H2O Lack of water excretion increases urine osmolality Sodium (urine) >200 mEq/L Sodium excretion in an attempt to excrete excess water Review Laboratory Alert: Pituitary Disorders. Note labs characteristic of SIADH, including low serum sodium, low serum osmolality, high urine osmolality, and high urine sodium. These findings will be in combination with low output of concentrated urine. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

SIADH: Interventions Fluid restriction ( mL/day), including fluids high in sodium content If needed, hypertonic saline and diuretics Intake and output, serum sodium, urine and serum specific gravity, and daily weights Loop diuretics Mouth and skin care Patient and family education The primary goals of therapy are to treat the underlying cause, eliminate excess water, and increase serum osmolality. Treatment of SIADH is outlined in Box Note that demeclocycline and lithium, both of which may induce diabetes insipidus, are used in the treatment of SIADH. Fluid intake is restricted to 800 to 1000 mL/day, with liberal dietary salt and protein intake. In severe, symptomatic cases (coma, seizures, serum sodium level <110 mEq/L), very small amounts of hypertonic 3% saline may be given following rigorous guidelines. Correction of the serum sodium level must be done slowly, no more than 12 mEq within the first 24 hours. Box describes nursing care of the patient receiving hypertonic saline. Stress the need to monitor the patient for fluid balance overload and the need to slow the increase in sodium levels. A diuretic such as furosemide may be given during hypertonic saline administration to promote diuresis and free water clearance. The patient’s response is evaluated by monitoring serum sodium levels, serum osmolality, and weight loss for a gradual return to baseline. In some patients, SIADH may require long-term treatment, ongoing monitoring, or both. These patients and their families require instruction regarding the following: Early signs and symptoms to report to the healthcare provider: weight gain, lethargy, weakness, nausea, mental status changes The significance of adherence to fluid restriction Dose, side effects, and rationale for prescribed medications Importance of daily weights Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Cerebral Salt Wasting (CSW)
Result of serious brain injury Disorder of sodium or fluid balance Similar to SIADH Pathophysiology not understood Defect sodium transport The exact pathophysiology of CSW is unknown. A defect in renal sodium transport has been suggested, and a change from cerebral to renal salt wasting has been suggested as a more accurate term. Natriuretic peptides, commonly released in severe brain injury, and impaired aldosterone have been implicated as factors in defective renal sodium transport. The patient presents with signs of hypovolemia in combination with hyponatremia. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

CSW: Assessment Tachycardia Weight loss Hypotension
Dry mucous membranes; poor skin turgor Lethargy and weakness Mental status changes Seizures and coma The clinical presentation of CSW results from hypovolemia and hyponatremia. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Laboratory Indicators of CSW
Sodium (serum) <135 mEq/L Inability of kidneys to conserve sodium Osmolality (serum) >295 mOsm/kg Inability of kidneys to conserve water Osmolality (urine) <100 mOsm/kg H2O Free water loss into urine decreases urine osmolality Sodium (urine) >200 mEq/L Sodium wasting through renal tubules Review Laboratory Alerts: Pituitary Disorders. An increased serum osmolality, decreased serum sodium, and increased urine sodium characterize CSW. Hemoconcentration may increase other laboratory values such as BUN, creatinine, and albumin. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

CSW: Interventions Restore sodium and fluid volume
Isotonic saline Hypertonic saline Oral or IV fludrocortisone The primary goals of treatment are to simultaneously restore both sodium and fluid volume. Replacing fluids without sodium may worsen the hyponatremia, resulting in life-threatening consequences. Both isotonic saline and hypertonic saline (3%) are used. Isotonic saline is administered to replace volume at a rate to match urine output, and 3% saline is given to increase sodium levels at a rate of no more than 12 mEq/hr. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Comparison of ADH Disorders
Understanding of the laboratory presentation of individuals with ADH disorders is critical and is a pertinent element of clinical management of the patient. See Table 18-7. Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Quick Quiz! The following findings are reported on a patient who suffered a traumatic brain injury: serum Na+ 120 mEq/L; BUN 34 mg/dL; creatinine 1.1 mg/dL; urine sodium 60 mmol/L; urine output 175 mL/hr; pulse 112 beats/min; BP 96/58 mm Hg; dry mucous membranes. These findings are consistent with: Cerebral salt wasting Diabetes insipidus Diabetic ketoacidosis SIADH Answer: A. Cerebral salt wasting CSW is most commonly seen in patients with serious brain injury and is a product of renal losses of sodium. The condition is accompanied by hyponatremia and elevated urine sodium and osmolaity in combination with high urine output, hypovolemia, elevated urine sodium, elevated serum osmolality, and classic signs of dehydration, including changes in renal markers of dehydration (elevated BUN/creatinine ratio); tachycardia; hypotension; and dry mucous membranes. The BUN/creatinine ratio in the above case is 30.9, which is consistent with dehydration (ratio > 20). Copyright © 2013, 2009, 2005, 2001, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

Endocrine Alterations

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Endocrine Alterations

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