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 >>
Hypernatremia And Central Diabetes Insipidus Following Neurosurgical Procedure Of Trauma
Dialysis Access Center of Pittsburgh, PA, USA *Address for Correspondence: Dr. Awad Magbri, Dialysis Access Center of Pittsburgh, PA, USA, Email: [email protected] How to cite this article: Magbri A, El-Magbri E, Hershit S. Hypernatremia and central Diabetes Insipidus following Neurosurgical procedure of Trauma. Arch Pathol Clin Res. 2017; 1: 005-008. Copyright: © 2017 Magbri A. 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. Keywords: Hypernatremia; Central diabetes insipidus; Pituitary adenoma; Traumatic brain injury; Urine and Plasma osmolality; dDAVP; Triphasic or Adepsic DI The greater risk of hypernatremia in patients over 65 years old are associated with impaired mental status and physical disability which may result in impaired sensation to thirst, impaired ability to express thirst, and/or decrease access to water [1,2]. Normally, anti-diuretic hormone (ADH, also known as arginine-vasopressin, AVP) is secreted in response to 1-2% increase in osmolality which stimulate thirst, as do hypovolemia and hypotension. Broadly, speaking hypernatremia is due to hypotonic fluid loss or hypertonic sodium gain. Hypotonic fluid loss is mainly caused by diabetes insipidus. There are many causes of central diabetes incipidus (CDI). Pituitary and hypothalamus injuries caused by trauma, neurosurgical procedures, hemorrhage, ischemia, autoimmune diseases e.g. hypophysitis, IgG4 related disease or tumors involving hypothalamic-pituitary axis (HPA) are but few causes of CDI. Central diabetes incipidus is also reported with traumatic brain injuries causing ischemia to the HPA [3] and presented with exertion of larg Continue reading >>
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Skip to content Hypernatremia is most often due to unreplaced water that is lost from the gastrointestinal tract (vomiting or osmotic diarrhea), ... diagnosis, or treatment. Diagnosis of Hypernatremia. DIABETES INSIPIDUS AND HYPERNATREMIA ] The REAL cause of ... Diabetes Diagnosis Emedicine@ Diabetes Insipidus And Hypernatremia @ Diabetes Insipidus And Hypernatremia Diabetes Diagnosis Medscape The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. Hypernatremia is most often due to unreplaced water that is lost from the gastrointestinal tract (vomiting or osmotic diarrhea), ... diagnosis, or treatment. @ Nursing Diagnosis For Diabetes Insipidus Diabetes Insipidus Hypernatremia The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. 3 Diagnosis and treatment of hypernatremia Saif A. Muhsin, MBChB a, David B. Diagnostic approach. DIABETES INSIPIDUS AND HYPERNATREMIA ] The REAL cause of Diabetes ... Diabetes Insipidus And Hypernatremia 5) A diagnosis of diabetes is Hypernatremia is defined as plasma sodium concentration of >145 mEq/L. Hyperosmolality and hypernatremia. @ Diabetes Insipidus Hypernatremia Diagnosing Diabetes The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. @ Diabetes Insipidus Hypernatremia Diabetes Diagnosis And Treatment The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. Hypernatremia is a common electrolyte problem and is defined as a rise in serum sodium concentration to a value exceeding 145 mmol/L. 2016 2017 2018 Billable/Specific Code. March 1, 2015 Volume 91, Number 5 www.aafp.org/afp American Family Physician 299 Diagnosis and Management of Sodium Disorders: Hyponatremia and Hypernatremia Learn about the causes, symptoms, diagnosis & treatment of Electro Continue reading >>
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 >>
[diabetes Insipidus And Adipsic Hypernatremia In A Patient With A Craniopharyngioma].
Abstract A fourteen-year male patient presented a retrochiasmatic craniopharyngioma. Aer transcranial surgical resection, the patient had diabetes insipidus, which presented an interphase with manifestations of inadequate secretion of ADH. The patient was adequately treated with intranasal desmopresin, but aer i.v. fluid replacement was withdrawn, severe dehydration occurred. This was attributed to loss of the thirst reflex, due to surgical lesion of the lamina terminalis, where the osmoreceptor neurons are located. This case underscores the complications with body fluids and osmolality which may occur after surgery of hypothalamic lesions; i.e. diabetes insipidus (which may have a triphasic course), and adipsia, an infrequent complication due to absence of thirst. Continue reading >>
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 >>
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 >>
Central Diabetes Insipidus In Infancy With Or Without Hypothalamic Adipsic Hypernatremia Syndrome: Early Identification And Outcome
Neonatal central diabetes insipidus (CDI) with or without adipsia is a very rare complication of various complex hypothalamic disorders. It is associated with greater morbidity and a high risk of developing both hypernatremia and hyponatremia, due to the condition itself or secondary to treatment with vasopressin analogs or fluid administration. Its outcomes have yet to be evaluated. All patients diagnosed with neonatal CDI in a university hospital-based observational study and followed between 2005 and 2015 were included and analyzed retrospectively. Ten of the 12 patients had an underlying condition with brain malformations: optic nerve hypoplasia (n = 3), septo-optic dysplasia (n = 2), semilobar holoprosencephaly (n = 1), ectopic neurohypophysis (n = 3), and unilateral absence of the internal carotid artery (n = 1). The other two were idiopathic cases. During the median follow-up period of 7.8 (4.9–16.8) years, all but one patient displayed anterior pituitary deficiency. Transient CDI was found in three (25%) patients for whom a posterior pituitary hyperintense signal was observed with (n = 2) and without (n = 1) structural hypothalamic pituitary abnormalities, and with no other underlying cerebral malformations. Patients with permanent CDI with persistent adipsia (n = 4) and without adipsia (n = 5) required adequate fluid intake and various doses of desamino-D-arginine-8-vasopressin. Those with adipsia were more likely to develop hypernatremia (45 vs 33%), hyponatremia (16 vs 4%) (P < .0001), and severe neurodevelopmental delay (P < .05) than those without adipsia. Comorbidities were common. The underlying cause remains unknown at the age of 23 years for one patient with CDI and normal thirst. Patients with NAFLD had severe insulin resistance, especially at the le Continue reading >>
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Hypernatremia Treatment Guidelines
If this limit is exceeded, Soo Wan Kim, M.D. Patients with chronic hyponatremia without severe or moderately severe symptoms require cause-specic treatment and avoiding an increase in serum sodium concentration . Practical Approach To Patients With Electrolyte Disorders Diabetes Insipidus Hypernatremia Treatment Diabetes ... only a few easy easy to understand guidelines. One example is the excessive administration of hypertonic sodium bicarbonate during treatment of lactic acidosis. editorial PurPoSe The Internal ... Hypernatremia Earl H. Rudolph, DO Fellow, Nephrology and Hypertension, ... fludrocortisone, sometimes used in the treatment of 2% for hypernatremia upon admission and 1% for patients devel- Diabetes Insipidus Hypernatremia Your second step is start out looking online for information belonging to best diabetes treatment functions. ACUTE HYPONATRAEMIA GUIDELINES Acute symptomatic hyponatraemia CNS disturbance Confusion Headache Drowsiness Reduced GCS Seizures Encephalopathic @ Diabetes Insipidus And Hypernatremia Treatment For Diabetic Skin Ulcers The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. Diabetes Insipidus Hypernatremia Since diabetes is a chronic disease it doesnt have any permanent a therapy. With proper care and treatment one can expect to live a long and happy life the following disease. @ Diabetes Treatment Guidelines Algorithm Diabetes Diagnostic Criteria The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. Diabetes Insipidus and SIADH Joseph G. Verbalis, MD Clinical Endocrinology: 2007 1 hyponatremia treatment guidelines: 2012 and beyond Joseph G. Verbalis, MD rapid treatment is mandatory. Recommended treatment of acute hyponatremia varies by symptom severity, as follows: It has detrimental ef Continue reading >>
Diabetes Insipidus Treatment & Management: Approach Considerations, Postoperative Setting, Consultations
Diabetes InsipidusTreatment & Management Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD more... Most patients with diabetes insipidus (DI) can drink enough fluid to replace their urine losses. When oral intake is inadequate and hypernatremia is present, replace losses with dextrose and water or an intravenous (IV) fluid that is hypo-osmolar with respect to the patients serum. Do not administer sterile water without dextrose intravenously, as it can cause hemolysis. To avoid hyperglycemia, volume overload, and overly rapid correction of hypernatremia, fluid replacement should be provided at a rate no greater than 500-750 mL/h. A good rule of thumb is to reduce serum sodium by 0.5 mmol/L (0.5 mEq/L) every hour. The water deficit may be calculated on the basis of the assumption that body water is approximately 60% of body weight. In patients with central DI, desmopressin is the drug of choice. [ 31 , 32 ] A synthetic analogue of antidiuretic hormone (ADH), desmopressin is available in subcutaneous, IV, intranasal, and oral preparations. [ 33 ] Generally, it can be administered 2-3 times per day. Patients may require hospitalization to establish fluid needs. Frequent electrolyte monitoring is recommended during the initial phase of treatment. Alternatives to desmopressin as pharmacologic therapy for DI include synthetic vasopressin and the nonhormonal agents chlorpropamide, carbamazepine, clofibrate (no longer on the US market), thiazides, and nonsteroidal anti-inflammatory drugs (NSAIDs). Because of side effects, carbamazepine is rarely used, being employed only when all other measures prove unsatisfactory. NSAIDs (eg, indomethacin) may be used in nephrogenic DI, but only when no better options exist. In central DI, the primary problem is a ho Continue reading >>
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 >>
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Diabetes Insipidus
Practice Essentials Diabetes insipidus (DI) is defined as the passage of large volumes (>3 L/24 hr) of dilute urine (< 300 mOsm/kg). It has the following 2 major forms: Two other forms are gestational DI and primary polydipsia (dipsogenic DI); both are caused by deficiencies in AVP, but the deficiencies do not result from a defect in the neurohypophysis or kidneys. Signs and symptoms The predominant manifestations of DI are as follows: The most common form is central DI after trauma or surgery to the region of the pituitary and hypothalamus, which may exhibit 1 of the following 3 patterns: In infants with DI, the most apparent signs may be the following: In children, the following manifestations typically predominate: If the condition that caused DI also damaged the anterior pituitary or hypothalamic centers that produce releasing factors, patients may present with the following: Physical findings vary with the severity and chronicity of DI; they may be entirely normal or may include the following: See Clinical Presentation for more detail. If the clinical presentation suggests DI, laboratory tests must be performed to confirm the diagnosis, as follows: Additional studies that may be indicated include the following: See Workup for more detail. Management Most patients with DI can drink enough fluid to replace their urine losses. When oral intake is inadequate and hypernatremia is present, provide fluid replacement as follows: Give dextrose and water or an intravenous fluid that is hypo-osmolar with respect to the patient’s serum; do not administer sterile water without dextrose IV Administer fluids at a rate no greater than 500-750 mL/hr; aim at reducing serum sodium by approximately 0.5 mmol/L (0.5 mEq/L) every hour Pharmacologic therapeutic options include the follo Continue reading >>
Hypernatremia/diabetes Insipidus
OVERVIEW: What every practitioner needs to know Are you sure your patient has hypernatremia/diabetes insipidus? What are the typical findings for this disease? Diabetes insipidus (DI) presents clinically as pathologic polyuria and polydipsia and if volume depletion is present, serum sodium is greater than145 mEq/L and serum osmolality is greater than 300 mOsm/kg. Infants often present with failure to thrive, irritability, and intermittent fever. DI can result from a variety of causes associated with vasopressin deficiency (central DI) or resistance (nephrogenic DI). A careful history should focus on establishing daily fluid intake and urinary output, including an assessment for nocturia and enuresis. Signs of volume depletion can be marked in patients without the ability to compensate by increasing fluid intake. In contrast, volume status may be nearly normal in patients able to increase their fluid, intake albeit at great inconvenience. Risk factors for acquired forms of central DI include conditions that impact the vasopressin-secreting neurons or their fiber tract, such as head injury (either accidental or surgical), neoplasms, and infiltrative, infectious, or autoimmune diseases. Risk factors for acquired nephrogenic DI include metabolic alterations such as hypercalcemia and hypokalemia, exposure to certain drugs, or conditions affecting renal concentrating ability. Pathologic polyuria or polydipsia (>2 L/m2/d) warrants a detailed evaluation to establish the underlying cause. What other disease/condition shares some of these symptoms? What caused this disease to develop at this time? Vasopressin gene (autosomal dominant), onset by age 5 years; defect in gene processing leads to cellular stress and death DIDMOAD syndrome (also known as Wolfram syndrome) includes dia Continue reading >>
Diabetes Insipidus And Hypernatremia
One of the most common effects of diabetes insipidus on the human body is the development of hypernatremia. This is a medical term that is used to describe the presence of elevated sodium levels within the blood because of an electrolyte imbalance. Hypernatremia is defined by having sodium serum levels measured at 145 mEq/L or above. In addition to the symptoms of diabetes insipidus, people who have hypernatremia may experience a feeling of weakness in their muscles, irritability, fever, and general restlessness. In some instances, migraine headaches may be triggered, seizures may occur, and there may be severe changes to an individual’s blood sugar levels. What Is the Danger of Hypernatremia? When people are suffering from diabetes insipidus, it means their bodies are unable to respond to commands to concentrate urine to preserve hydration. The kidneys begin to pull out all consumable fluids and prepare them to be expelled from the body. Without proper fluid intake, the end result is dehydration because the body is losing more water than what is being consumed. The danger of hypernatremia is that in up to half of all cases that occur because of diabetes insipidus, a condition called adipsia occurs. This is because the hypothalamus is responsible for the thirst mechanisms and if it is malfunctioning already by not producing the necessary levels of anti-diuretic hormone, it may also fool people into thinking that they aren’t thirsty when they really are. This means that an individual may not feel thirsty, be expelling up to 20 liters of urine per day, and wind up with severe dehydration. Many cases of diabetes insipidus involve polydipsia, which means excessive thirst, but when sodium levels are increased, the opposite effect may occur. This generally occurs with cen Continue reading >>
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 >>
