diabetestalk.net

Diabetes Insipidus Hypernatremia

Hyponatremia And Hypernatremia

Hyponatremia And Hypernatremia

Physiology of Water and Body Fluids Disorders of sodium concentration result from a perturbation in water balance. Water is the most abundant body fluid. In lean individuals, water accounts for 60% of total body weight, with approximately two thirds residing intracellularly and one third in the extracellular space. Of the water in the extracellular space, approximately 75% is in the interstitium and 25% in the intravascular space. Because fat contains less water than lean muscle, water accounts for a lower percentage of total body weight in women, older adults, and obese persons. Additionally, water can move between these compartments, resulting in changes in plasma sodium concentration. Water movement between body fluid compartments is regulated by the effective osmolality of the solutes within each compartment. Sodium is the main determinant of plasma osmolality, and water moves toward body compartments with higher osmolality and away from those with lower osmolality. Plasma water is regulated by an interaction between sensory organs (e.g., carotid body and hypothalamus), antidiuretic hormone (ADH or vasopressin), and the kidney. Although the gastrointestinal tract, skin, and bronchial tree are capable of sodium and water loss, the kidney is the only organ able to conserve or excrete sodium and water under tight regulatory control. Alterations in arterial blood pressure and plasma osmolality are the main physiologic signals regulating ADH secretion. As plasma water decreases, increases in plasma sodium concentration and osmolality are sensed by nuclei in the hypothalamus, with a resultant increase in production of ADH by the supraoptic and paraventricular nuclei. ADH acts to increase renal free water reabsorption in the collecting tubule to restore plasma water, resul Continue reading >>

Life-threatening Hypernatremia In A Case Of Diabetes Insipidus/panhypopituitarism

Life-threatening Hypernatremia In A Case Of Diabetes Insipidus/panhypopituitarism

Management of diabetes insipidus (DI) accompanied by panhypopituitarism requires understanding of the relationships between ADH and thyroid/glucocorticoid tone. Low thyroid/glucocorticoid tone decreases free water clearance which protects against DI and may lead to hyponatremia while high thyroid/glucocorticoid tone may unmask DI and facilitate hypernatremia. A 31 year-old man with DI/panhypopituitarism was stable until his levothyroxine was incorrectly lowered based on TSH levels. He became hypothyroid and was hospitalized 3 times over 1 month for recurring altered mental status and mild hyponatremia. DDAVP was repeatedly held with rapid onset of polyuria resulting severe hypernatremia. On the last admission, he presented with altered mental status from sepsis. Serum sodium was 135 mmol/l. He was made NPO and treated with stress dose hydrocortisone and fludrocortisone. DDAVP was held for the mild hyponatremia. Serum sodium rapidly elevated to 168 mmol/l after only 12 hours. DDAVP was restarted with liberalization of diet to unlimited free water access causing rapid downward sodium correction. Hypernatremia almost always results from iatrogenic causes. In our case, holding DDAVP for hyponatremia resulted in rapid onset of hypernatremia and volume depletion. Stress dose glucocorticoids further unmasked DI. Thirst and free access to water which typically protects patients with un-replaced DI were not operational due to his NPO status which contributed to the rapid rise in serum sodium. Water balance is controlled by thyroid, glucocorticoid, and principally ADH working at the renal effector level while the RAAS principally controls sodium balance. Together these hormones tightly regulate serum sodium concentration. Managing hospitalized patients with DI/panhypopituitarism Continue reading >>

Gestational Diabetes Insipidus, Severe Hypernatremia And Hyperemesis Gravidarum In A Primigravid Pregnancy

Gestational Diabetes Insipidus, Severe Hypernatremia And Hyperemesis Gravidarum In A Primigravid Pregnancy

A 27 years old primigravid lady presented with nausea and recurrent vomiting at 35 weeks gestation. She was diagnosed with hyperemesis gravidarum at 5 weeks gestation. TPN was commenced but she continued vomiting. On examination, foetal size was normal for gestational age, BP was 105/70 mmHg. Electrolytes were normal except potassium of 2.7 mmol/l, LFT was normal, albumin 29 g/l and uric acid 307 umol/l. 16 days after admission, she rapidly deteriorated with weakness and plasma sodium rose from 137 to 187mmol/l in 2 days. She was transferred to ICU. Further investigations revealed rise in AST (124U/l) and ALT (87U/l) and uric acid (557 umol/l). Acid base balance was deranged with pH 7.16, pCO2 8.2 kPa, pO2 28.5 kPa, and bicarbonate 21.4 suggesting mixed respiratory and metabolic acidosis. Serum osmolality was 381mOsm/l and corresponding urinary osmolality was 142 mOsm/l which was suggestive of diabetes insipidus. Emergency Caesarean section was performed due to foetal distress. Sadly, the baby died on day 3 after cardiac arrest. The patient's sodium was gradually reduced from 192 to 144 mmol/l over 5 days with hourly electrolyte monitoring. However, she developed nystagmus on day 3 in ITU and later developed dysmetria, left heel shin ataxia and tandem gait ataxia. MRI brain showed changes consistent with myelinolysis of pons and cerebellar peduncles. Water deprivation test on days 12 and 17 post partum failed to concentrate serum osmolality beyond 290mOsm/l but urinary osmolality rose to 470 and 585mOsm/l respectively excluding diabetes insipidus at that stage. Summary: this 27 years old lady had hyperemesis gravidarum which was complicated by transient diabetes insipidus of pregnancy with rapid onset hypernatremia which resulted in central pontine myelinolysis, and bab Continue reading >>

Why Does Diabetes Insipidus Cause Hypernatremia?

Why Does Diabetes Insipidus Cause Hypernatremia?

Sodium is the main extracellular ion that regulates the osmotic pressure in the cells and body fluids. Water and sodium interact to control intravascular volume. Water balance usually determines the concentration of sodium and sodium acts as a buffer to prevent an excessive loss of water from the tissues. Hypernatremia is defined as an elevation in the concentration of serum sodium above 145 mEq/L and is always indicative of dehydration. Signs and symptoms of hypernatremia include irritability, restlessness, weakness, lethargy, fever, hyperglycemia, headache, and seizures. Hypernatremia has also been associated with adipsia in 50% of patients with hypothalamic tumors. Thirst, however, usually prevents severe hypernatremia unless water intake is restricted or water resorption is reduced (Behrman, Kleigman, & Jenson, 2004; Workeneh, Balakumaran, Bichet & Mitch, 2004). Hypernatremic dehydration can develop in patients with central diabetes insipidus when the patient does not drink adequately. An elevated osmolality (> 295) normally causes the secretion of antidiuretic hormone (ADH). Diabetes insipidus (DI) is an ADH deficiency disorder of the hypothalamus. The hypothalamus, which is responsible for regulating water balance, secretes ADH that is subsequently released from the pituitary gland into the bloodstream. ADH tells the body to conserve the right amount of water to prevent dehydration. Causes of deficient amounts of ADH secretion include: (a) a malfunctioning hypothalamus or pituitary gland, (b) damage to the hypothalamus or pituitary gland during surgery, (c) endocrine and metabolic disorders, (d) brain injury, (e) tumor, (f) tuberculosis, and (g) meningitis. Disturbances and disorders of the hypothalamus result in insufficient secretion of ADH. If too little ADH is Continue reading >>

Merck And The Merck Manuals

Merck And The Merck Manuals

Hypernatremia is a serum sodium concentration > 145 mEq/L. It implies a deficit of total body water relative to total body sodium, caused by water intake being less than water losses. A major symptom is thirst; other clinical manifestations are primarily neurologic (due to an osmotic shift of water out of brain cells), including confusion, neuromuscular excitability, seizures, and coma. Diagnosis requires measurement of serum sodium and sometimes other laboratory tests. Treatment is usually controlled water replacement. When the response to treatment is poor, testing (eg, monitored water deprivation or administration of vasopressin) is directed at detecting causes other than decreased water intake. Hypernatremia usually involves an impaired thirst mechanism or limited access to water, either as contributing factors or primary causes. The severity of the underlying disorder that results in an inability to drink in response to thirst and the effects of hyperosmolality on the brain are thought to be responsible for a high mortality rate in hospitalized adults with hypernatremia. There are several common causes of hypernatremia (see Table: Principal Causes of Hypernatremia). Hypernatremia associated with hypovolemia occurs with sodium loss accompanied by a relatively greater loss of water from the body. Common extrarenal causes include most of those that cause hyponatremia and volume depletion. Either hypernatremia or hyponatremia can occur with severe volume loss, depending on the relative amounts of sodium and water lost and the amount of water ingested before presentation. Renal causes of hypernatremia and volume depletion include therapy with diuretics. Loop diuretics inhibit sodium reabsorption in the concentrating portion of the nephrons and can increase water clearan Continue reading >>

Exemplar: Hypernatremia- Diabetes Insipidus (di)

Exemplar: Hypernatremia- Diabetes Insipidus (di)

Sort Clinical mani FRIED SALT flushed skin, restlessness, agitation, low-grade fever, thirst, increased BP and fluid retention, edema: peripheral and pitting; decreased urine output and dry mouth primary characteristic of Di is excretion of large amount of urine (2-20 L/day) with a very low specific gravity <1.005 and urine osmolality <100 mOsm/kg) serum osmolality is elevated as a result of hypernatremia, which is caused by pure water loss in the kidney The most common s/s of DI are extreme thirst and excretion of large amount of diluted urine Continue reading >>

Diagnosis And Management Of Sodium Disorders: Hyponatremia And Hypernatremia

Diagnosis And Management Of Sodium Disorders: Hyponatremia And Hypernatremia

Hyponatremia and hypernatremia are common findings in the inpatient and outpatient settings. Sodium disorders are associated with an increased risk of morbidity and mortality. Plasma osmolality plays a critical role in the pathophysiology and treatment of sodium disorders. Hyponatremia and hypernatremia are classified based on volume status (hypovolemia, euvolemia, and hypervolemia). Sodium disorders are diagnosed by findings from the history, physical examination, laboratory studies, and evaluation of volume status. Treatment is based on symptoms and underlying causes. In general, hyponatremia is treated with fluid restriction (in the setting of euvolemia), isotonic saline (in hypovolemia), and diuresis (in hypervolemia). A combination of these therapies may be needed based on the presentation. Hypertonic saline is used to treat severe symptomatic hyponatremia. Medications such as vaptans may have a role in the treatment of euvolemic and hypervolemic hyponatremia. The treatment of hypernatremia involves correcting the underlying cause and correcting the free water deficit. Hyponatremia is a common electrolyte disorder defined as a serum sodium level of less than 135 mEq per L.1–3 A Dutch systematic review of 53 studies showed that the prevalence of mild hyponatremia was 22.2% in geriatric hospital wards, 6.0% in nongeriatric wards, and 17.2% in the intensive care unit.2 The prevalence of severe hyponatremia (serum sodium level less than 125 mEq per L) was 4.5%, 0.8%, and 10.3%, respectively. It is estimated that hyponatremia occurs in 4% to 7% of the ambulatory population, with rates of 18.8% in nursing homes.2–4 Clinical recommendation Evidence rating References Comments In patients with severe symptomatic hyponatremia, the rate of sodium correction should be 6 to Continue reading >>

Hypernatremia From Central Diabetes Insipidus In Acute Myelogenous Leukemia

Hypernatremia From Central Diabetes Insipidus In Acute Myelogenous Leukemia

Hypocalcemia: Sensipar® lowers serum calcium and can lead to hypocalcemia. Life threatening events and fatal outcomes associated with hypocalcemia have been reported in patients treated with Sensipar®, including pediatric patients. The safety and effectiveness of Sensipar® have not been established in pediatric patients. Decreases in serum calcium can prolong the QT interval, potentially resulting in ventricular arrhythmia. Cases of QT prolongation and ventricular arrhythmia have been reported in patients treated with Sensipar®. Patients with conditions that predispose to QT interval prolongation and ventricular arrhythmia may be at increased risk for QT interval prolongation and ventricular arrhythmias if they develop hypocalcemia due to Sensipar®. Closely monitor corrected serum calcium and QT interval in patients at risk receiving Sensipar®. Concurrent administration of Sensipar® with calcium-lowering drugs including other calcimimetics could result in severe hypocalcemia. Parsabiv™ (etelcalcetide) and Sensipar® should not be given together. Closely monitor serum calcium in patients receiving Sensipar® and concomitant therapies known to lower serum calcium levels. Serum calcium and serum phosphorus should be measured within 1 week and PTH should be measured 1 to 4 weeks after initiation or dose adjustment of Sensipar®. Once the maintenance dose has been established, serum calcium and serum phosphorus should be measured approximately monthly, and PTH every 1 to 3 months. Patients with risk factors for upper GI bleeding, such as known gastritis, esophagitis, ulcers or severe vomiting, may be at increased risk for GI bleeding with Sensipar®. Monitor patients for worsening of common Sensipar® GI adverse reactions and for signs and symptoms of GI bleeding an Continue reading >>

Transient Central Diabetes Insipidus And Marked Hypernatremia Following Cardiorespiratory Arrest

Transient Central Diabetes Insipidus And Marked Hypernatremia Following Cardiorespiratory Arrest

Copyright © 2017 Sahar H. Koubar and Eliane Younes. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Central Diabetes Insipidus is often an overlooked complication of cardiopulmonary arrest and anoxic brain injury. We report a case of transient Central Diabetes Insipidus (CDI) following cardiopulmonary arrest. It developed 4 days after the arrest resulting in polyuria and marked hypernatremia of 199 mM. The latter was exacerbated by replacing the hypotonic urine by isotonic saline. 1. Introduction Central Diabetes Insipidus (CDI) is characterized by the lack of antidiuretic hormone (ADH) causing loss of urinary concentrating ability, polyuria, thirst, and hypernatremia. ADH is an octapeptide synthesized in the supraoptic nuclei of the hypothalamus and then stored and released from the posterior pituitary gland. It maintains normal serum osmolality by promoting free water reabsorption in the collecting ducts of the nephron. The known causes of CDI include germinoma/craniopharyngioma; Langerhans cell histiocytosis; local inflammatory, autoimmune, or vascular diseases; trauma resulting from surgery or an accident; sarcoidosis; metastases; and midline cerebral and cranial malformations [1, 2]. CDI related to cardiorespiratory arrest and anoxic brain injury has been reported but appears to be an overlooked complication [3–7]. We describe a patient who experienced a transient form of CDI with marked hypernatremia following cardiorespiratory arrest and anoxic brain injury. 2. Case Presentation A 43-year-old woman with advanced amyotrophic lateral sclerosis, maintained on home ventilator, was transferre Continue reading >>

Treatment Of Central Diabetes Insipidus

Treatment Of Central Diabetes Insipidus

INTRODUCTION The major symptoms of central diabetes insipidus (DI) are polyuria, nocturia, and polydipsia due to the concentrating defect. Treatment of this disorder is primarily aimed at decreasing the urine output, usually by increasing the activity of antidiuretic hormone (ADH, also called arginine vasopressin or AVP). Replacement of previous and ongoing fluid losses is also important. Most patients with central DI have a normal or only mildly elevated plasma sodium concentration because concurrent stimulation of thirst minimizes the degree of net water loss. However, hypernatremia can occur if thirst is impaired or the patient has no access to water [1-3]. Correction of the hypernatremia requires repair of this free water deficit. (See "Treatment of hypernatremia".) The treatment of central DI will be reviewed here. The causes of this disorder and the approach to the patient with polyuria are discussed separately. (See "Clinical manifestations and causes of central diabetes insipidus" and "Diagnosis of polyuria and diabetes insipidus".) CHOICE OF THERAPY There are three main options for the treatment of polyuria in patients with central DI: Desmopressin, which is an ADH analog and is the preferred drug in almost all patients. Continue reading >>

Central Diabetes Insipidus

Central Diabetes Insipidus

OVERVIEW diabetes insipidus is a condition caused by loss of the effect of antidiuretic hormone on the collecting ducts of the kidneys, resulting in loss of free water. diabetes insipidus can be central or nephrogenic This article will focus on CDI PATHOPHYSIOLOGY Normal physiology ADH is produced in the hypothalamus and travels along nerve fibers to the posterior pituitary, where it is stored and released Increased plasma osmolality stimulates release of ADH ADH promotes reabsorption of water in the collecting duct of nephrons via translocation of aquaporins (water channels) to the plasma membrane from internal sites within the cells Diabetes insipidus central DI (CDI) results from causes that impair the synthesis, transport, or release of ADH nephrogenic DI (NDI) results from receptor, or downstream, unrepsonsiveness to circulating ADH loss of ADH effect results in polyuria, dehydration, hypernatremia and a hyperosmolar state CAUSES OF CENTRAL DIABETES INSIPIDUS Acquired Surgery (transsphenoidal) – common TBI – common Idiopathic Autoimmune Tumours (suprasellar, lung, breast, lymphoma, leukaemia) Hypoxic brain injury Brain stem death Profound hyponatraemia -> cerebral oedema Radiotherapy Inflammatory conditions – sickle cell, sarcoid, Wegener’s, histiocytosis X Infections – Tb, abscess, encephalitis, meningitis Vascular disease – CVA, SAH, Sheehan’s syndrome, pituitary apoplexy Congenital Autosomal dominant mutation in ADH production Wolfram syndrome DIAGNOSIS Key findings plasma hyperosmolality (can be mild in partial DI) hypernatraemia (na >155 mM) polyuria (>3L/24h) urine osmolality < 200 mOsm/kg Water deprivation test rarely performed in the critical care setting usually 4-18h water deprivation with serial urine and plasma osmolality until: — 5% los Continue reading >>

Profound Hypernatremia Due To Central Diabetes Insipidus.

Profound Hypernatremia Due To Central Diabetes Insipidus.

Abstract Diabetes insipidus is a rare endocrine disorder in paediatric patients. Polyuria is a cardinal manifestation that is extremely difficult to recognize in diapered infants. Careful urine quantification is the key to diagnosis in appropriate clinical setting. We report a case of a 4 months old infant presenting with an acute life threatening event following an episode of vomiting and decreased oral intake. She had profound hypernatremia which persisted after stabilization. Polyuria unrecognized by the mother was revealed by 24-hour urine output measurement. A diagnosis of diabetes insipidus was made after appropriate laboratory investigations including serum and urine osmolality. The central nature of the disease was confirmed by neuroimaging which showed holoprosencephaly. Continue reading >>

Diabetes Insipidus

Diabetes Insipidus

Print Overview Diabetes insipidus (die-uh-BEE-teze in-SIP-uh-dus) is an uncommon disorder that causes an imbalance of water in the body. This imbalance leads to intense thirst even after drinking fluids (polydipsia), and excretion of large amounts of urine (polyuria). While the names diabetes insipidus and diabetes mellitus sound similar, they're not related. Diabetes mellitus — which can occur as type 1 or type 2 — is the more common form of diabetes. There's no cure for diabetes insipidus, but treatments are available to relieve your thirst and normalize your urine output. Symptoms The most common signs and symptoms of diabetes insipidus are: Extreme thirst Excretion of an excessive amount of diluted urine Depending on the severity of the condition, urine output can be as much as 16 quarts (about 15 liters) a day if you're drinking a lot of fluids. Normally, a healthy adult will urinate an average of less than 3 quarts (about 3 liters) a day. Other signs may include needing to get up at night to urinate (nocturia) and bed-wetting. Infants and young children who have diabetes insipidus may have the following signs and symptoms: Unexplained fussiness or inconsolable crying Trouble sleeping Fever Vomiting Diarrhea Delayed growth Weight loss When to see a doctor See your doctor immediately if you notice the two most common signs of diabetes insipidus: excessive urination and extreme thirst. Causes Diabetes insipidus occurs when your body can't regulate how it handles fluids. Normally, your kidneys remove excess body fluids from your bloodstream. This fluid waste is temporarily stored in your bladder as urine, before you urinate. When your fluid regulation system is working properly, your kidneys conserve fluid and make less urine when your body water is decreased, suc Continue reading >>

Syndrome Of Hypernatremia, Hypodipsia And Partial Diabetes Insipidus: A New Interpretation

Syndrome Of Hypernatremia, Hypodipsia And Partial Diabetes Insipidus: A New Interpretation

A 17-yr-old girl is described with a space-occupying lesion in the region of the hypothalamus and evidence of secondary trophic hormone lack. Despite clinical evidence of slight dehydration and a serum sodium of 170–190 mEq/1 there was complete absence of thirst and the average fluid intake was 1200 ml per day. This abnormality persisted following replacement therapy with cortisol and thyroxine. Although plasma volume and total body water measurements were within the normal range there was evidence to suggest a deficit in both these body fluid compartments. Comparison of serum sodium and urine U/S Osm ratios indicated an impaired ADH release at all levels of serum osmolality. The maximum urine osmolality achieved following exogenous vasopressin (1200 mOsm/kg) was greater than that with fluid deprivation (720 mOsm/kg) confirming partial diabetes insipidus. Despite this, the osmotic threshold for ADH release measured during hypertonic saline infusion appeared to be normal (less than 295 mOsm/kg). Both this and lack of patient cooperation prevented a reduction in serum sodium when water loading was attempted. The disorder was effectively treated with chlorpropamide which allowed rehydration by reducing free water clearance. The term “essential hypernatremia” has previously been used to describe such hypodipsic patients and the abnormality ascribed to a resetting of the osmotic threshold for ADH release (“syndrome of hypodipsia and ADH reset”). It is apparent, however, that there is insufficient published evidence to support the concept of normal ADH release above an elevated osmotic threshold. It seems more likely that ADH secretion is impaired at all levels of serum osmolality and that urine concentration and effective water conservation is possible only when th Continue reading >>

Diabetes Insipidus

Diabetes Insipidus

OBJECTIVES After completing this article, readers should be able to: Describe the simple test that will establish the diagnosis of diabetes insipidus. Explain how to differentiate central diabetes insipidus from nephrogenic diabetes insipidus and compulsive water drinking. Delineate the inheritance pattern of central diabetes insipidus and nephrogenic diabetes insipidus. Describe the treatments of choice for central diabetes insipidus and nephrogenic diabetes insipidus. Definition and Epidemiology Polydipsia and polyuria with dilute urine, hypernatremia, and dehydration are the hallmarks of diabetes insipidus in infants and children. Patients who have diabetes insipidus are unable to conserve water and can become severely dehydrated when deprived of water. The polyuria exceeds 5 mL/kg per hour of dilute urine, with a documented specific gravity of less than 1.010. The hypernatremia is evidenced by a serum sodium concentration in excess of 145 mmol/L (145 mEq/L). Three conditions give rise to polydipsia and polyuria. The most common condition is central or neurogenic diabetes insipidus related to a deficiency of vasopressin. Less common is nephrogenic diabetes insipidus, including the X-linked recessive, autosomal recessive, and autosomal dominant types due to renal tubular resistance to vasopressin. Finally, these conditions can occur in the compulsive water drinker who demonstrates physiologic inhibition of vasopressin secretion. The incidence of diabetes insipidus in the general population is 3 in 100,000, with a slightly higher incidence among males (60%). X-linked nephrogenic diabetes insipidus is very rare, with arginine vasopressin receptor2 (AVPR2) gene mutations among males estimated to be 4 in 1,000,000. The incidence of compulsive water drinking is unknown, bu Continue reading >>

More in diabetes