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Chapter 1. Endocrine Emergencies Free To View

Robert C Hyzy, MD, FCCP
DOI: 10.1378/critcare.21.1
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Objectives 
  • Recognize the clinical presentations of endocrine emergencies involving the pancreas, thyroid, adrenal, and pituitary glands.

  • Learn the approach to laboratory testing necessary for the diagnosis and management of these conditions in the ICU.

  • Understand the treatment for each endocrine emergency.

Synopsis 

Many endocrine emergencies require admission to the ICU. Although not necessarily common as a primary diagnosis requiring ICU admission, many endocrine emergencies occur in the context of ongoing illness and comorbidities, where the stress of intercurrent illness serves to exacerbate and unmask the underlying condition. Hence, the practicing intensivist needs not only to be able to diagnose and manage these conditions as presenting diagnoses but also to recognize endocrine emergencies in the context of critical care more generally.

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Diabetic Ketoacidosis

Clinically significant hyperglycemic syndromes consist of diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmotic state (HHS), frequently also referred to as hyperosmotic nonketotic syndrome. The American Diabetes Association definitions for these conditions are given in Table 1. Serum glucose level is usually below 800 mg/dL in DKA, whereas in HHS a glucose level in excess of 1,000 mg/dL is not uncommon. DKA is characterized by a syndrome of hyperglycemia, ketonemia, and an anion gap metabolic acidosis, usually in excess of 20.
Anion gap=serum sodium(serum chloride+serum bicarbonate) 
The degree of acidosis and magnitude of the increase in anion gap are contingent on the rate of ketoacid production and urinary excretion. Hyperglycemia produces glycosuria and an osmotic diuresis, resulting in extracellular fluid volume depletion, which can be profound and result in hypotension. Many of the symptoms of DKA result in large measure from this: polyuria, polydipsia, tachycardia, and lethargy. The degree of acidosis is the primary determinant of depressed sensorium. In addition, other symptoms such as nausea, vomiting, abdominal pain, and Kussmaul respirations with a characteristic fruity breath may be present.
Table Graphic Jump LocationTable 1 Diagnostic Criteria for Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar Syndrome (HHS)

DKA is usually diagnosed in known diabetics who present to the emergency room with either noncompliance or with a concomitant stressful illness, especially infection, which has resulted in progressively worsened glycemic control and the onset of ketogenesis. Occasionally, a patient, usually an adolescent or young adult, will present with DKA as the initial presentation of their diabetes. Other causes of ketoacidosis include alcohol and starvation, which should be in the differential diagnosis in patients without a known history of diabetes.

Besides elevations in serum glucose and the presence of ketones in serum in urine, laboratory abnormalities seen at presentation in DKA include: a low serum bicarbonate, elevated anion gap, leukocytosis, hyperkalemia, elevated BUN and creatinine (suggesting prerenal azotemia), and elevated amylase and lipase. Leukocytosis is proportionate to the degree of acidemia and can confuse the clinical picture as regards the presence of infection. Hyperkalemia, due to extracellular osmotic shifting and insulin deficiency, is common despite a deficit in total body potassium, largely from urinary losses. Serum sodium is variable in DKA and reflects a balance between osmotic dilution in the serum from hyperglycemia and urinary losses due to osmotic diuresis. Pseudohyponatremia may be seen in patients with concomitant hyperlipidemia. Although pancreatitis is uncommon, patients with elevations of amylase and lipase should have pancreatitis ruled out. Arterial blood gas shows acidosis with a compensatory respiratory alkalosis and hypocapnia. Acidemia is usually present.

Treatment of DKA is centered on expanding intravascular volume and is best performed utilizing normal saline solution. As patients are usually several liters down, there is little risk in administering normal saline solution in large quantity. Regular insulin is administered as an IV bolus of 0.10 to 0.15 U/kg/h, followed by a continuous IV infusion at 0.10 U/kg/h. Blood glucose should be lowered by about 50 mg/dL/h and assessed hourly, with downward adjustments made in the insulin drip as blood glucose lowers. Clinicians should recognize that fingerstick capillary blood glucose measurements can be inaccurate in critically ill patients. Fingerstick glucose measurements are lower than glucose measured from venous blood in hypotensive patients but at other times may be found to be higher than venous blood. Serum electrolytes should be assessed q2-4h.

IV fluid resuscitation aimed at expanding intravascular volume is essential, and several liters may be required. Although hypernatremia is frequently present, normal saline solution should be administered IV until the intravascular volume deficit is corrected, as normal saline solution is hypotonic relative to the patient's serum and is more effective at expanding plasma volume than the administration of hypotonic saline solution such as 0.45 NaCl. Once intravascular volume has been restored and the patient's glucose has lowered to the 200 range, glucose and hypotonic saline solution, in the form of dextrose 5 in 0.45 NaCl, should be administered until the DKA has resolved. This serves to avoid hypoglycemia in the context of not as yet resolved DKA and permits the continued administration of IV insulin. IV insulin should be continued until ketogenesis has resolved, as reflected in normalization of the anion gap.

The routine treatment of metabolic acidosis with IV sodium bicarbonate has been largely abandoned, in recognition that vigorous volume expansion alone is generally sufficient. Nevertheless, patients presenting with a pH <7.00 can be considered for this if tissue perfusion is compromised or life-threatening hyperkalemia is present. The management of serum potassium levels in DKA requires careful attention, with frequent monitoring necessary. Despite initial hyperkalemia, with the administration of insulin and the correction of metabolic acidosis, hypokalemia develops and should be treated with IV potassium supplementation. Usually 20 to 30 mEq/L is added to 0.45 saline solution, as the addition of potassium to normal saline solution would result in the administration of hypertonic fluids. Hypophosphatemia often develops during treatment of DKA, but it seldom requires supplementation, which should be administered only if clinically significant or severe (<1.0 mg/dL).

Clinical resolution of DKA can be monitored via venous pH and serum anion gap. Repeat arterial blood gases are not required. After the normalization of the anion gap has occurred, the patient should receive subcutaneous regular insulin. The administration of IV dextrose is stopped, and IV insulin is discontinued 30 min later. These changes are best made once the patient has resumed oral nutrition, otherwise ketogenesis may resume.

Cerebral edema can occur as a complication of DKA treatment in patients under 20 years of age, but the risk is mitigated if rapid correction of sodium and water deficits are avoided and glucose is added to IV fluids once serum glucose level has dropped to the low 200 range.

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Hyperosmolar Nonketotic Dehydration Syndrome

HHS, also often referred to as the hyperosmolar nonketotic syndrome, occurs when hyperglycemia occurs with little or no ketoacidosis. HHS occurs in patients who are only partially insulin deficient, and hence HHS is more common among older, type 2 diabetics. While the usual symptoms of hyperglycemia such polyuria, polydipsia, dehydration, and tachycardia are present, an anion gap metabolic acidosis from ketogenesis is not. The severity of hyperglycemia is often quite significant (>1,000 mg/dL). The resultant hyperosmolality produces depression of the CNS, which, when severe, can cause coma. HHS is contrasted with varying degrees of DKA in Table 1.

Serum sodium is often low in HHS due to osmotic shifting of water from the intracellular compartment. That is, water enters the extracellular compartment, following the gradient created by the osmotically active glucose molecules. As serum glucose levels tend to be higher in HHS than in DKA, this effect can be quite profound. In addition, just as in DKA, plasma volume is contracted at the same time, owing to osmotic diuresis from glucosuria. If, however, the glucosuria effect predominates, hypernatremia may be observed. In either circumstance, the serum sodium level is fictitiously altered by hyperglycemia. A common correction factor to determine the actual serum sodium is: Na corrected = Na measured + [0.016 × (Glucose in mg/dL − 100)] The corrected sodium is used to determine free water deficit, which can serve as a guide to the amount of volume resuscitation required: Free water deficit (men) = (Weight in kg × 0.6) − (Na/140 − 1) Free water deficit (women) = (Weight in kg × 0.5) − (Na/140 − 1) The treatment of HHS involves the same management principles as DKA: vigorous volume replacement and an IV insulin drip. The amount of normal saline solution required to restore extracellular fluid tends to be greater in HHS than in DKA. Half normal saline solution is administered once this has been achieved.

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Glucose Control in the ICU

Reports of significant benefit to patients with stress-induced hyperglycemia in the ICU treated with IV insulin to achieve blood glucose levels between 80 and 100 mg/dL were followed by others that suggested that the risk of hypoglycemia was significant, particularly among patients with sepsis. The large Normoglycemia in Intensive Care Evaluation and Survival Using Glucose Algorithm Regulation (NICE-SUGAR) trial demonstrated an increase in 90-day mortality in patients treated with this approach, sometimes called “tight glycemic control,” compared with a less aggressive approach. Only the subset of patients with trauma or those being treated with corticosteroids demonstrated a trend toward benefit with tight control. However, it should be recognized that the control group in NICE-SUGAR had a mean glucose level around 140 mg/dL; this suggests that, while practices have changed over the last decade and tight control is not warranted, patients with stress-induced hyperglycemia should still be treated with IV insulin, albeit at a more modest target of less than 150 mg/dL.

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Hypoglycemia

Hypoglycemia (blood glucose level <60 mg/dL) is seldom a cause of admission to the ICU but is seen as a consequence of other conditions, the ingestion of oral hypoglycemic agents or an overdose of long-acting insulin being exceptions. Common causes of hypoglycemia in the ICU include hepatic failure, renal failure, sepsis, adrenal insufficiency, leukemia, lymphoma, tumors including hepatoma or pancreatic islet β-cell tumor, or additional drugs such as β-blockers or pentamidine. Symptoms of hypoglycemia include nervousness, tremulousness, tachycardia, and diaphoresis, all of which are triggered by a compensatory adrenergic response to the hypoglycemia. If severe hypoglycemia is present, coma or seizures can ensue.

When clinically suspected, hypoglycemia should be promptly treated with an ampule of dextrose, containing 50 mL of 50% dextrose solution, IV push. Blood glucose should be monitored hourly via fingerstick measurements, enabling a timely therapeutic response. A second ampule may be required within an hour of treatment. Patients should also receive a dextrose drip of either 5% or 10% solution, at a rate appropriate to the clinical circumstances encountered.

Glucagon, hydrocortisone, or octreotide can be administered if hypoglycemia is profound and refractory to the above measures, but it is seldom required.

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Myxedema Coma

Myxedema coma is a severe form of hypothyroidism characterized by CNS depression and hypothermia from a low basal metabolic rate. Women are more commonly affected than men. The other manifestations common to less severe hypothyroidism may also be present. These include: lethargy, cold intolerance, delayed deep tendon reflexes, hypothermia, bradycardia, alopecia, dry, doughy skin, hoarseness, and hyperglossia. A pericardial effusion may be present, although significant cardiac compromise is uncommon. Laboratory abnormalities that are diagnostic include an elevated TSH and a low free T4. In addition, several other laboratory abnormalities can occur. These include hyponatremia, hypercapnia, a normocytic normochromic anemia, hyperlipidemia, hypoglycemia, and an elevation in creatine phosphokinase. Hyponatremia is due to an impairment in free water excretion and can result in seizure activity. Hypoglycemia can occur from hypothyroidism alone or may be due to concomitant adrenal insufficiency.

Myxedema coma is often the result of prolonged noncompliance with thyroid supplementation in the face of absent thyroid function, such as following I131 ablation. Drugs that can cause underlying hypothyroidism include amiodarone, propylthiouracil, lithium, and sulfonamides. Myxedema coma can be precipitated by cold exposure, the concomitant administration of sedative drugs, especially opioids, or stress such as infection and myocardial infarction. Infection may be masked by an inability to mount a temperature spike. Myxedema has a significant attributable mortality of almost 40%, particularly among elderly and septic patients or patients with prolonged hypothermia, cardiac compromise, or coma.

Once clinically suspected, a serum TSH, free T4, and cortisol should be drawn. A cosyntropin stimulation test should also be performed whenever possible. However, treatment of myxedema coma should begin based on clinical suspicion and should not wait for laboratory confirmation. The treatment of myxedema coma is IV administration of thyroxine, starting with a loading dose of 300 μg of thyroxine followed by daily administration of doses ranging from 50 to 100 μg. As unsuspected adrenal insufficiency is frequently also in evidence, all patients with myxedema coma should be empirically treated for possible adrenal insufficiency. This can be accomplished either through the daily administration of hydrocortisone at a dose of 300 mg. Patients with myxedema coma are frequently intubated for airway protection or hypercapnia. Other supportive measures include the use of passive warming and supplemental nutrition.

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Euthyroid Sick Syndrome

Patients who are critically ill frequently manifest abnormalities in thyroid function tests, suggesting the possibility of hypothyroidism. Owing to an increased conversion of T3 to reverse T3, these patients demonstrate a low serum T3 level, a condition called euthyroid sick syndrome. T4 levels may also be low, particularly in the setting of protracted critical illness, and the TSH level can also vary, being either slightly elevated or decreased. Free T4 levels are normal, indicating the absence of clinical hypothyroidism. Hence, no thyroid supplementation is required.

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Thyroid Storm

Thyroid storm is hyperthyroidism in the presence of significant cardiac or CNS manifestations. These include cardiac dysrhythmias, such as new onset atrial fibrillation, atrial flutter, and supraventricular tachycardia, or CNS manifestations, such as tremor, delirium, stupor, or even coma. The patient may be hypertensive and tachycardic. Apathetic affect may also be present, particularly among the elderly. Other manifestations of hyperthyroidism may be present, such as exophthalmos, hyperreflexia, heat intolerance, anxiety, nausea, vomiting, diarrhea, abdominal pain, and the presence of fine hair or pretibial edema.

Graves disease, an autoimmune condition, is the most common cause of hyperthyroidism. Importantly, thyroid storm can be triggered by physiologic stress in the setting of underlying hyperthyroidism, which may have been unsuspected until that time. These can include surgery, pregnancy, trauma, or significant acute illness of any kind.

As with myxedema, the diagnosis of thyroid storm is made clinically, with treatment undertaken in anticipation of confirmatory laboratory tests. Laboratory findings in hyperthyroidism and thyroid storm include elevations in T3 and T4, with a low TSH. In an uncommon variant of thyroid storm called T3 thyrotoxicosis, T3 levels are elevated but T4 levels remain normal. Less commonly, in central hyperthyroidism, TSH, T3, and T4 are all elevated.

Treatment of thyroid storm is multifaceted and attempts to affect thyroid hormone production, release, and peripheral conversion to the physiologically more active T3 and to block the effect of thyroid hormone on the body. Thyroid hormone synthesis is inhibited by administering either propylthiouracil, 200 mg q4h, or methimazole, 20 mg q4-6h. Iodine, either saturated solution potassium iodide or Lugol solution, is administered to block thyroid hormone release from the thyroid gland. Importantly, iodine must only be administered after thyroid hormone synthesis has been blocked, in order to avoid exacerbating the problem by enhanced thyroid hormone production. Decreasing conversion of T4 into T3 is accomplished through the administration of propylthiouracil, hydrocortisone, 100 mg q8h, and propranolol. Propranolol, 60 to 80 mg q4-6h, is also administered to block the hyperadrenergic manifestations of thyrotoxicosis and to control tachyarrhythmias. IV esmolol can be used instead of propranolol.

Other adjuncts to care of the patient with thyroid storm include passive cooling if hyperpyrexia is present. Acetaminophen is preferred, as acetylsalicylate increases free thyroid hormone in the serum through displacement on plasma proteins. Thyroidectomy may be required if a patient develops life-threatening agranulocytosis from propylthiouracil or methimazole. Finally, as with myxedema, the patient should be evaluated and treated for the possibility of concomitant hypoadrenalism.

Iodine therapy is discontinued and corticosteroids may be tapered once hyperpyrexia, CNS, and cardiac manifestations have resolved. Patients with Graves disease should ultimately undergo thyroid ablation. This can be accomplished either surgically or with I131.

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Adrenal Crisis

Adrenal insufficiency can be seen in a variety of conditions and may be either primary, that is, due to insufficient production of adrenocorticotropic hormone, or secondary, usually resultant from underproduction of glucocorticoids and mineralocorticoids. Causes of primary adrenal insufficiency include autoimmune, that is, Addison's disease; bilateral adrenal hemorrhage; abrupt withdrawal of exogenously administered corticosteroids, TB; septic shock; meningococcemia; metastatic malignancy; amyloidosis; and drugs such as etomidate and ketoconazole. Causes of secondary adrenal insufficiency include pituitary tumors; craniopharyngioma; as a postoperative complication; postpartum hypopituitarism (Sheehan's syndrome); infiltrative diseases such as hemochromatosis, sarcoidosis, histiocytosis, or histoplasmosis; TB; or withdrawal of exogenously administered corticosteroids. Patients with secondary adrenal insufficiency lack hyperpigmentation, dehydration, and hyperkalemia. Hypotension is less prominent, whereas hypoglycemia is more common than in primary adrenal insufficiency.

Adrenal crisis occurs in patients with adrenal insufficiency who have hypotension and volume depletion from the absence of mineralocorticoids. Like thyroid storm, adrenal crisis is often triggered by physiologic stress such as trauma, surgery, or acute medical illness. Clinically, patients may manifest hypotension, nausea, vomiting, fatigue, anorexia, depression, and amenorrhea and may lack hyperpigmentation and/or vitiligo. Abdominal, flank, lower back, or chest pain are common in patients with bilateral adrenal hemorrhage or infarction, the main risk factors for which are anticoagulation and postoperative state. Laboratory abnormalities can include hypoglycemia, hyponatremia, hyperkalemia, and eosinophilia.

In individuals who are not stressed, a total cortisol level of >15 μg/dL is sufficient to rule out adrenal insufficiency. A level <5 μg/dL constitutes absolute adrenal insufficiency with 100% specificity but low sensitivity (36%). A cut-off level of 10 μg/dL is 62% sensitive but only 77% specific. The appropriate response of the adrenal glands in the setting of critical illness is unknown. Some authors suggest that a level <25 μg/dL may be insufficient in critical illness such as sepsis. Cortisol is protein bound, and total cortisol levels bear a variable relationship to free cortisol levels. Patients who are hypoproteinemic may have a normal total free cortisol level despite a seemingly insufficient total cortisol level. In patients who are not septic, a cosyntropin stimulation test may be useful in order to determine whether adrenal reserve is lacking and relative adrenal insufficiency is present. Thirty or 60 min after the administration of 250 μg of cosyntropin, a form of synthetic adrenocorticotropic hormone, a rise in total cortisol level <9 μg/dL or an absolute level <20 μg/dL may be indicative of relative adrenal insufficiency.

Dexamethasone, 10 mg may be administered as a single dose while a cosyntropin stimulation test is being performed as therapy for adrenal insufficiency so that the laboratory analysis is not altered, as is the case with hydrocortisone.

In a recent randomized, placebo-controlled trial of corticosteroids in septic patients, CORTICUS, the cosyntropin stimulation test was found to be unreliable when correlated with free cortisol levels. In addition, contrary to earlier studies, a mortality benefit was not observed in the corticosteroid group. Patients receiving corticosteroids were able to be weaned off vasopressor medications an average of 2 days sooner than the placebo group but also were found to have a threefold risk of subsequent sepsis while in the ICU. In contrast, meta-analyses suggest that a mortality benefit might be expected only among patients who are at a high risk of death. Whether or not to administer corticosteroids to patients with vasopressor-dependent shock remains an area of great controversy in critical care. The standard dose is hydrocortisone, 50 mg IV q6h for 5 days. Concomitant mineralocorticoid administration has also been advocated in this setting, but a beneficial effect may only occur if given prophylactically.

Adrenal crisis is treated with an initial dose of 200 mg of IV hydrocortisone followed by 100 mg q6h. IV administration of normal saline solution is important to correct volume contraction. Hypotonic fluids should not be administered, as they can worsen hyponatremia. Mineralocorticoid administration is not required in adrenal crisis, with the possible exception of patients with sepsis.

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Pheochromocytoma

A pheochromocytoma is a catecholamine-secreting tumor of chromaffin cells; most common in the adrenal glands, it may occur elsewhere in the body. It is an uncommon cause of secondary hypertension that may present in an accelerated form in the ICU. Symptoms, which are due to the release of catecholamines such as epinephrine, norepinephrine, and/or dopamine, include tachycardia, palpitations, diaphoresis, headache, chest pain, tremor, and flushing. The classic triad of episodic headache, sweating, and tachycardia is seldom in evidence. Episodes of catecholamine release and resultant symptoms tend to be episodic and seldom last more than a few hours at time. Other conditions resulting in increased sympathetic activity can result in BP elevations suggestive of pheochromocytoma, including autonomic dysfunction such as may be the case with spinal injury or Guillain-Barré syndrome; the use of sympathomimetic drugs such as cocaine, phencyclidine, or amphetamines; and the ingestion of tyramine-containing foods in patients taking monoamine oxidase inhibitors.

The diagnosis, once suspected, is best confirmed by obtaining plasma levels of metanephrine and normetanephrine or 24-h urine levels of metanephrines and catecholamines when the patient is stable and not critically ill, as the stress of critical illness can produce misleading values that may be false positives. The administration of tricyclic antidepressants can also result in falsely elevated results. Subsequent to a chemical diagnosis, imaging studies such as CT scan or I123-metaiodobenzylguanidine scan are performed to localize the tumor and determine resectability.

As with some other endocrinopathies, the stress of surgery can precipitate a hypertensive crisis due to catecholamine release in these patients. Patients with undiagnosed pheochromocytoma presenting with a hypertensive crisis following surgery have a high mortality. Patients with known pheochromocytoma who are scheduled to undergo surgery should receive preoperative management well in advance of surgery with an α-agent, such as phenoxybenzamine. β-Blocker administration is contraindicated unless prior α- blockade has been accomplished in order to avoid unopposed α-tone. The calcium channel blocker nicardipine can be a useful adjunct to management of these patients. Metyrosine, an inhibitor of catecholamine synthesis, may also be used.

As opposed to patients with essential hypertension who have a hypertensive crisis, the drug of choice for a patient with pheochromocytoma who develops a hypertensive crisis is phentolamine. This is administered intravenously in doses ranging from 2 to 5 mg every 5 min until the target BP is achieved. Sodium nitroprusside and nicardipine may also be considered.

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Diabetes Insipidus (DI)

DI is a condition in which water adsorption by the collecting tubules of the kidney is impaired, either from a lack of the antidiuretic hormone (ADH) arginine vasopressin (AVP), as in central DI, or due to the lack of responsiveness of the collecting tubules, as is the case in nephrogenic DI. Symptoms are driven by the loss of free water and include polyuria, polydipsia, hypernatremia, volume contraction, and hyperosmolality. Most ICU patients have intake medically determined and, as a result, cannot respond to an increased thirst drive, resulting in hypernatremia. Diagnosis is made by measuring urine specific gravity, which reveals dilute urine. In primary polydipsia a low plasma sodium concentration (<137 mEq/L) is seen with a low urine osmolality (142 mEq/L, due to water loss) is seen. Urine osmolality should be less than the plasma osmolality.

ADH is produced in the hypothalamus and released by the anterior pituitary gland. Causes of central DI include causes of panhypopituitarism, such as Sheehan's syndrome, anoxia, trauma, and tumors. In addition, infiltrative conditions including sarcoidosis and lymphoma as well as infectious diseases such as neurosyphilis or tuberculosis can result in central DI. Nephrogenic DI occurs in the setting of adequate AVP and is caused by disorders of the kidney that involve damage to the collecting tubules, where AVP would ordinarily act to promote water adsorption. Nephrogenic DI can be caused by several drugs, including lithium, demeclocycline, amphotericin B, and antiretroviral drugs such as tenofovir and indinavir. Hence, ADH levels are elevated in nephrogenic DI but are diminished or absent in central DI.

Central DI can be clinically distinguished from nephrogenic DI by administering the ADH analog desmopressin in conjunction with water restriction: administration of 1 μg desmopressin subcutaneously will cause the urine osmolality to increase by at least 50% if there is complete DI on a central basis. In partial central DI, the urine osmolality will increase by 10% to 50%. In nephrogenic DI, the urine osmolality will generally not increase after AVP administration. Water restriction is useful to determine if primary polydipsia is present. With water restriction, patients with primary polydipsia will exhibit a rise in urine osmolality, usually to above 500 mOsm/kg, but will not respond to desmopressin since endogenous release is intact.

Treatment of central DI entails correcting the free water deficit as well as prevention of ongoing polyuria through the administration of desmopressin 1 or 2 μg subcutaneously q12h. Free water deficit is calculated in the following manner:
0.6×patient's weight in kg×(patient's sodium/1401), 
where 0.6 × weight equals estimated body water, and 140 is the desired sodium. This represents total body water for young males; for females and elderly males multiply the weight in kg by 0.5. Because the urinary fluid losses in DI are hypotonic, the IV fluid is also hypotonic. Patients who are hypotensive due to hypovolemia should receive normal saline solution until intravascular volume has been replenished. Otherwise, hypotonic fluids may be administered. Careful monitoring of intake and output as well as serial electrolyte measurements are required to successfully manage these patients.

Management of nephrogenic DI is similar, although desmopression is not administered. The discontinuation of any drugs that may be causing nephrogenic DI is an important component of management. A thiazide diuretic is administered to induce mild extracellular fluid volume depletion, which causes increased water reabsorption at the proximal tubule. As a result, there is less water delivered to the distal nephron and, therefore, less urine is produced.

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Nothing to Disclose

The author has disclosed that no relationships exist with any companies/organizations whose products or services may be discussed in this chapter.

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Brewster UC, Hayslett JP. Diabetes insipidus in the third trimester of pregnancy. Obstet Gynecol. 2005;105(5 Pt 2):1173-1176. [PubMed] [CrossRef]
 
Mavrakis AN, Tritos NA. Diabetes insipidus with deficient thirst: report of a patient and review of the literature. Am J Kidney Dis. 2008;51(5):851-859. [PubMed] [CrossRef]
 
Sands JM, Bichet DG. Nephrogenic diabetes insipidus. Ann Intern Med. 2006;144(3):186-194. [PubMed] [CrossRef]
 
Table Graphic Jump LocationTable 1 Diagnostic Criteria for Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar Syndrome (HHS)

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Brewster UC, Hayslett JP. Diabetes insipidus in the third trimester of pregnancy. Obstet Gynecol. 2005;105(5 Pt 2):1173-1176. [PubMed] [CrossRef]
 
Mavrakis AN, Tritos NA. Diabetes insipidus with deficient thirst: report of a patient and review of the literature. Am J Kidney Dis. 2008;51(5):851-859. [PubMed] [CrossRef]
 
Sands JM, Bichet DG. Nephrogenic diabetes insipidus. Ann Intern Med. 2006;144(3):186-194. [PubMed] [CrossRef]
 
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