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Diabetes Insipidus Management Guidelines

Diabetes Insipidus -post-neurosurgical Management Of Acute

Diabetes Insipidus -post-neurosurgical Management Of Acute

Diabetes Insipidus -post-neurosurgical management of acute Diabetes Insipidus -post-neurosurgical management of acute This document is only valid for the day on which it is accessed. Please read our disclaimer . Management guideline specifically for new onset ortransient diabetes insipidus (DI) followingneurosurgery in Starship Children's Hospital A Paediatric Endocrinologist must be consulted in allchildren with post neurosurgical diabetes insipidus(DI) Acute DI may develop after injury or surgery to thehypothalamic-pituitary region For established DI or treatment of DI due to chemotherapy,brain death or other aetiologies, see other guidelines Mild-moderate hypernatraemia (Na of 145 to <155mmol/l) is the intended target range, i.e. notdangerous. It is relatively easy to treat hypernatraemia > targetrange However acute hyponatraemia is life-threatening and mustbe actively avoided DI is not life threatening unless the followingoccurs: The child is prevented from drinking when severelythirsty The child has an impaired thirst mechanism(hypodipsia/adipsia) The child is unable to access water when they need to, e.g. veryyoung or altered level of consciousness, NBM The child is over treated with AVP analogues (DDAVP etc). The tri-phasic response is relativelycommon This is immediate DI (hours to days), a variable period of SIADH(days), followed by permanent DI Avoid over-treatment with AVP analogues until DI is permanent(earn each dose of DDAVP) A number of factors can complicate peri-operative fluidbalance: Large volumes of saline or other isotonic fluids resultin obligate diuresis (mimicking DI). Mannitol or similar osmotic agents also lead to large volume urineoutput. Cortisol and T4 deficiency can result in reduced free waterexcretion, with DI unmasked by hormone replace Continue reading >>

Diabetes Insipidus: The Other Diabetes

Diabetes Insipidus: The Other Diabetes

Go to: Abstract Diabetes insipidus (DI) is a hereditary or acquired condition which disrupts normal life of persons with the condition; disruption is due to increased thirst and passing of large volumes of urine, even at night. A systematic search of literature for DI was carried out using the PubMed database for the purpose of this review. Central DI due to impaired secretion of arginine vasopressin (AVP) could result from traumatic brain injury, surgery, or tumors whereas nephrogenic DI due to failure of the kidney to respond to AVP is usually inherited. The earliest treatment was posterior pituitary extracts containing vasopressin and oxytocin. The synthetic analog of vasopressin, desmopressin has several benefits over vasopressin. Desmopressin was initially available as intranasal preparation, but now the oral tablet and melt formulations have gained significance, with benefits such as ease of administration and stability at room temperature. Other molecules used for treatment include chlorpropamide, carbamazepine, thiazide diuretics, indapamide, clofibrate, indomethacin, and amiloride. However, desmopressin remains the most widely used drug for the treatment of DI. This review covers the physiology of water balance, causes of DI and various treatment modalities available, with a special focus on desmopressin. Keywords: Antidiuretic hormone, desmopressin, polydipsia, polyuria, vasopressin Go to: Diabetes insipidus (DI) is part of a group of hereditary or acquired polyuria and polydipsia diseases. It is associated with inadequate arginine vasopressin (AVP) or antidiuretic hormone (ADH) secretion or renal response to AVP, resulting in hypotonic polyuria and a compensatory/underlying polydipsia.[1] Polyuria (>50mL/kg), dilute urine (osmolality <300 mOsm/L), and increas Continue reading >>

Diabetes Insipidus

Diabetes Insipidus

Diabetes insipidus (DI) is an uncommon condition with either relative or absolute lack of anti-diuretic hormone (ADH) leading to inability to concentrate the urine and subsequent polyuria/polydypsia and potentially fluid and electrolyte imbalance. This can be seen in a variety of conditions in the paediatric population, most commonly in patients post neurosurgery or with cerebral malformations. Consideration should be given to: Hydration status/fluid balance/urine output Presence of intercurrent illness eg UTI Causes of excess fluid loss eg gastro, surgical drains Past history of DI with similar episode Change in weight as marker of fluid status Baseline investigations should include urea and electrolytes, full ward test of urine and paired serum and urine osmolality. Diabetes insipidus is present when the serum osmolality is raised (>295milliOsmol/kg) with inappropriately dilute urine (urine osmolality < 700milliOsmol/kg). The serum sodium is often elevated due to excess free water losses. After assessment of level of dehydration and ongoing losses, adequate rehydration therapy should be commenced. If the serum Na is > 150mmol/L, rehydration should occur over 48 hours (see hypernatraemia guideline). If Na >170mmol/L, contact ICU. Discussion with the endocrinologist on call is advised prior to the commencement of Desmopressintherapy Desmopressin (DDAVP, trade name: Minirin(R)) acts on the distal tubules and collecting ducts of the kidney to increase water reabsorption, as a long acting analog of anti-diuretic hormone (ADH). There are several formulations available: Intranasal solution - 100 micrograms/mL Intranasal spray (10 micrograms/spray) Parenteral (IM/IM) - 4 micrograms/ml - used rarely Oral - 200 micrograms/tablets (roughly 10 micrograms intranasal is approximate Continue reading >>

Clinical Guidelines For Management Of Diabetes Insipidus And Syndrome Of Inappropriate Antidiuretic Hormone Secretion After Pituitary Surgery

Clinical Guidelines For Management Of Diabetes Insipidus And Syndrome Of Inappropriate Antidiuretic Hormone Secretion After Pituitary Surgery

Clinical guidelines for management of diabetes insipidus and syndrome of inappropriate antidiuretic hormone secretion after pituitary surgery Gua clnica de manejo de la diabetes inspida y del sndrome de secrecin inapropiada de hormona antidiurtica en el postoperatorio de la ciruga hipofisaria , Carlos del Pozo b , Carles Villabona c , on behalf of the Neuroendocrinology Group of the SEEN a Servicio de Endocrinologa, Complejo Hospitalario Universitario de Albacete, Albacete, Spain b Servicio de Endocrinologa y Nutricin, Hospital Universitari Mtua de Terrassa, Terrassa, Barcelona, Spain c Servicio de Endocrinologa, Hospital Universitari de Bellvitge, L Hospitalet de Llobregat, Barcelona, Spain Changes in water metabolism and regulation of vasopressin (AVP) or antidiuretic hormone (ADH) are common complications of pituitary surgery. The scarcity of studies comparing different treatment and monitoring strategies for these disorders and the lack of prior clinical guidelines makes it difficult to provide recommendations following a methodology based on grades of evidence. This study reviews the pathophysiology of diabetes insipidus and inappropriate ADH secretion after pituitary surgery, and is intended to serve as a guide for their diagnosis, differential diagnosis, treatment, and monitoring. Las alteraciones en el metabolismo del agua y en la regulacin de la vasopresina (AVP) u hormona antidiurtica (ADH) son complicaciones frecuentes de la ciruga hipofisaria. La escasez de estudios que comparen diversas estrategias de tratamiento y monitorizacin de estos trastornos, as como la falta de guas clnicas previas, hace difcil hacer recomendaciones siguiendo la metodologa basada en grados de evidencia. Este trabajo revisa la fisiopatologa de la diabetes inspida y la secrecin inade Continue reading >>

Treatment Of Central Diabetes Insipidus In Adults And Children With Desmopressina Synthetic Analogue Of Vasopressin

Treatment Of Central Diabetes Insipidus In Adults And Children With Desmopressina Synthetic Analogue Of Vasopressin

Modification of the natural vasopressin molecule to form desmopressin acetate (DDAVP) resulted in a compound with prolonged antidiuretic activity and virtual elimination of vasopressor activity. Twenty-one patients with central diabetes insipidus who ranged in age from 3 to 68 years were treated with DDAVP, which was administered intranasally in a dosage ranging from 10 μg every 12 hours to 20 μg every eight hours. Effective control of symptoms was obtained in all cases. There were no consequential toxic effects. As previously reported, DDAVP appears to be the preferred drug for the management of central diabetes insipidus. Biochemical alteration of hormones may enhance desired therapeutic activity and eliminate toxic effects. The development of DDAVP is an example of the potential for development of useful therapeutic peptides. (Arch Intern Med 138:1382-1385, 1978) Continue reading >>

Diabetes Insipidus Treatment & Management: Approach Considerations, Postoperative Setting, Consultations

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 >>

Posterior Pituitary Hormones

Posterior Pituitary Hormones

Posterior pituitary hormones and antagonists Posterior pituitary hormones and antagonists Vasopressin (antidiuretic hormone, ADH) is used in the treatment of pituitary (cranial) diabetes insipidus as is its analogue desmopressin . Dosage is tailored to produce a slight diuresis every 24 hours to avoid water intoxication. Treatment may be required for a limited period only in diabetes insipidus following trauma or pituitary surgery. Desmopressin is more potent and has a longer duration of action than vasopressin ; unlike vasopressin it has no vasoconstrictor effect. It is given by mouth or intranasally for maintenance therapy, and by injection in the postoperative period or in unconscious patients. Desmopressin is also used in the differential diagnosis of diabetes insipidus. Following a dose intramuscularly or intranasally, restoration of the ability to concentrate urine after water deprivation confirms a diagnosis of cranial diabetes insipidus. Failure to respond occurs in nephrogenic diabetes insipidus. In nephrogenic and partial pituitary diabetes insipidus benefit may be gained from the paradoxical antidiuretic effect of thiazides. Carbamazepine is sometimes useful in partial pituitary diabetes insipidus [unlicensed]; it may act by sensitising the renal tubules to the action of remaining endogenous vasopressin . Desmopressin is also used to boost factor VIII concentration in mild to moderate haemophilia and in von Willebrands disease; it is also used to test fibrinolytic response. Desmopressin may also have a role in nocturnal enuresis. Vasopressin infusion is used to control variceal bleeding in portal hypertension, prior to more definitive treatment and with variable results. Terlipressin acetate, a derivative of vasopressin with reportedly less pressor and antid Continue reading >>

Diagnosis

Diagnosis

Print Since the signs and symptoms of diabetes insipidus can be caused by other conditions, your doctor will perform a number of tests. If your doctor determines you have diabetes insipidus, he or she will need to determine which type of diabetes insipidus you have, because the treatment is different for each form of the disease. Some of the tests doctors commonly use to diagnose and determine the type of diabetes insipidus and in some cases, its cause, include: Water deprivation test. This test confirms the diagnosis and helps determine the cause of diabetes insipidus. Under medical supervision, you'll be asked to stop drinking fluids for a time so that your doctor can measure changes in your body weight, urine output and the concentration of your urine and blood when fluids are withheld. Your doctor may also measure blood levels of ADH or administer synthetic ADH during this test. The water deprivation test is performed under close supervision in children and pregnant women to make sure no more than 5 percent of body weight is lost during the test. Urinalysis. Urinalysis is the physical and chemical examination of urine. If your urine is less concentrated — meaning the amount of water is high relative to other excreted substances — it could be due to diabetes insipidus. Magnetic resonance imaging (MRI). An MRI of the head is a noninvasive procedure that uses a powerful magnetic field and radio waves to construct detailed pictures of brain tissues. Your doctor may want to perform an MRI to look for abnormalities in or near the pituitary gland. Genetic screening If your doctor suspects an inherited form of diabetes insipidus, he or she will look at your family history of polyuria and may suggest genetic screening. Treatment Treatment of diabetes insipidus depends on Continue reading >>

2016 Endocrine Society Guidelines: Central Di

2016 Endocrine Society Guidelines: Central Di

Low ADH production by the posterior pituitary can cause excessive urination, severe dehydration and high sodium measures. The natural response is increased thirst leading to additional water intake. Polyuria could be so advanced that drinking alone would not correct dehydration or sodium anomalies. Supplementation with ADH hormone is needed in these cases. Please find below excerpts from Endocrine Society guidelines on central diabetes insipidus published in November 2016. Central DI occurs when the secretion of ADH (also called vasopressin) by the posterior pituitary is insufficient to meet urine concentration requirements. The prevalence of medically treated DI is about 100 per 1 million inhabitants. DI can be congenital or acquired; it can be secondary to a variety of pathological processes including tumors (mostly craniopharyngioma and germinomas), head trauma, and inflammatory, autoimmune, granulomatous, infectious diseases involving the hypothalamus and/or posterior pituitary. Sometimes the cause of DI is unknown (idiopathic DI) and is thought to be autoimmune in nature. In some of these cases, periodical follow-up imaging may unveil the cause, particularly in young patients. DI is very rarely encountered in nonoperated pituitary adenomas. We recommend simultaneously measuring serum and urine osmolarity in patients with polyuria (>5 L/100 kg of body weight in 24 hours). In the presence of high serum osmolarity (>295 mOsmol/L), urine osmolarity should reach approximately 600 mOsmol/L (urine/plasma osmolality ratio should be 2), whereas urine dipstick should be negative for glucose. When administering desmopressin (DDAVP) in diabetes insipidus (DI), we suggest individualized therapeutic schedules. Although clinicians should offer therapy to all patients, some patie Continue reading >>

Nephrogenic Diabetes Insipidus

Nephrogenic Diabetes Insipidus

Not to be confused with Neurogenic diabetes insipidus. Nephrogenic diabetes insipidus (also known as renal diabetes insipidus) is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central/neurogenic diabetes insipidus, which is caused by insufficient levels of antidiuretic hormone (ADH, that is, arginine vasopressin or AVP). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to ADH, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water. Signs and symptoms[edit] The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with excessive thirst and excretion of a large amount of dilute urine. Dehydration is common, and incontinence can occur secondary to chronic bladder distension.[1] On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, ADH levels are likely to be abnormal or raised. Polyuria will continue as long as the patient is able to drink. If the patient is unable to drink and is still unable to concentrate the urine, then hypernatremia will ensue with its neurologic symptoms.[citation needed] Causes[edit] Acquired[edit] Nephrogenic DI (NDI) is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including amyloidosis,[2] polycystic kidney disease,[3] electrolyte imbalance,[4][5] or some other kidney defect.[2] The major causes of acquired NDI that produce clinical symptoms (e.g. polyuria) in the adult are lithium toxicity and high blood calcium. Chronic lithium ingestion – appears to affect the tubules by enterin Continue reading >>

Clinical Guidelines For Management Of Diabetes Insipidus And Syndrome Of Inappropriate Antidiuretic Hormone Secretion After Pituitary Surgery - Sciencedirect

Clinical Guidelines For Management Of Diabetes Insipidus And Syndrome Of Inappropriate Antidiuretic Hormone Secretion After Pituitary Surgery - Sciencedirect

Volume 61, Issue 4 , April 2014, Pages e15-e24 Clinical guidelines for management of diabetes insipidus and syndrome of inappropriate antidiuretic hormone secretion after pituitary surgeryGua clnica de manejo de la diabetes inspida y del sndrome de secrecin inapropiada de hormona antidiurtica en el postoperatorio de la ciruga hipofisaria Author links open overlay panel CristinaLamasa Get rights and content Changes in water metabolism and regulation of vasopressin (AVP) or antidiuretic hormone (ADH) are common complications of pituitary surgery. The scarcity of studies comparing different treatment and monitoring strategies for these disorders and the lack of prior clinical guidelines makes it difficult to provide recommendations following a methodology based on grades of evidence. This study reviews the pathophysiology of diabetes insipidus and inappropriate ADH secretion after pituitary surgery, and is intended to serve as a guide for their diagnosis, differential diagnosis, treatment, and monitoring. Las alteraciones en el metabolismo del agua y en la regulacin de la vasopresina (AVP) u hormona antidiurtica (ADH) son complicaciones frecuentes de la ciruga hipofisaria. La escasez de estudios que comparen diversas estrategias de tratamiento y monitorizacin de estos trastornos, as como la falta de guas clnicas previas, hace difcil hacer recomendaciones siguiendo la metodologa basada en grados de evidencia. Este trabajo revisa la fisiopatologa de la diabetes inspida y la secrecin inadecuada de ADH en el postoperatorio de la ciruga hipofisaria, y pretende servir de gua en su diagnstico, diagnstico diferencial, tratamiento y monitorizacin. Continue reading >>

Diabetes Insipidus Diagnosis And Management (including Fluid Management In Children Following Suprasellar Tumour Surgery)

Diabetes Insipidus Diagnosis And Management (including Fluid Management In Children Following Suprasellar Tumour Surgery)

Diabetes insipidus diagnosis and management (Including fluid management in children following suprasellar tumour surgery) Diabetes insipidus diagnosis and management (Including fluid management in children following suprasellar tumour surgery) Children with a suprasellar tumours are at risk of developing panhypopituitarism, along with diabetes insipidus. This guideline has been written to aid in the diagnosis, post-operative management, monitoring and potential complications of diabetes insipidus. It also includes an algorithm for the management of a high urine output and a four hourly fluid balance chart. Children with suprasellar tumours with the features of diabetes insidipidus. Healthcare professionals involved in the care of neurosurgical patients. Children with suprasellar tumours, particularly craniopharyngiomas, are at risk of developingpanhypopituitarism together with diabetes inspidus. Some of these children may havesymptoms at diagnosis. Baseline investigations may not always demonstrate anendocrinopathy. The patient may have inadequate ACTH and cortisol secretion, which maymask DI. This may be unmasked once hydrocortisone (dexamethasone) is started, or worsen DIrequiring a change of dose of DDAVP. Therefore close monitoring is required during this time. The diagnosis of diabetes inspidus is based on: elevated plasma osmolality due tohypernatreamia AND inappropriately dilute urine. Management is to maintain plasma Na+ in the normal range and prevent large fluctuations. The management of postoperative craniopharyngioma should take account of the triphasicpattern of vasopressin or antidiuretic hormone (ADH) secretion. This is as follows: Days 1-2 postop diabetes insipidus (DI) initial hypothalamic damage with ADH insufficiency, Days 2-8 postop syndrome of inap Continue reading >>

Treatment

Treatment

Treatments for diabetes insipidus aim to reduce the amount of urine your body produces. Depending on the type of diabetes insipidus you have, there are several ways of treating your condition and controlling your symptoms. Cranial diabetes insipidus Mild cranial diabetes insipidus may not require any medical treatment. Cranial diabetes insipidus is considered mild if you produce approximately 3-4 litres of urine over 24 hours. If this is the case, you may be able to ease your symptoms by increasing the amount of water you drink, to avoid dehydration. Your GP or endocrinologist (specialist in hormone conditions) may advise you to drink a certain amount of water every day, usually at least 2.5 litres. However, if you have more severe cranial diabetes insipidus, drinking water may not be enough to control your symptoms. As your condition is due to a shortage of vasopressin (AVP), your GP or endocrinologist may prescribe a treatment that takes the place of AVP, known as desmopressin (see below). Desmopressin Desmopressin is a manufactured version of AVP that's more powerful and more resistant to being broken down than the AVP naturally produced by your body. It works just like natural AVP, stopping your kidneys producing urine when the level of water in your body is low. Desmopressin can be taken as a nasal spray, in tablet form or as a form that melts in your mouth, between your gum and your lip. If you're prescribed desmopressin as a nasal spray, you'll need to spray it inside your nose once or twice a day, where it's quickly absorbed into your bloodstream. If you're prescribed desmopressin tablets, you may need to take them more than twice a day. This is because desmopressin is absorbed into your blood less effectively through your stomach than through your nasal passage 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 >>

Diabetes Insipidus – Diagnosis And Management

Diabetes Insipidus – Diagnosis And Management

Abstract Central diabetes insipidus (CDI) is the end result of a number of conditions that affect the hypothalamic-neurohypophyseal system. The known causes include germinoma/craniopharyngioma, Langerhans cell histiocytosis (LCH), local inflammatory, autoimmune or vascular diseases, trauma resulting from surgery or an accident, sarcoidosis, metastases and midline cerebral and cranial malformations. In rare cases, the underlying cause can be genetic defects in vasopressin synthesis that are inherited as autosomal dominant, autosomal recessive or X-linked recessive traits. The diagnosis of the underlying condition is challenging and raises several concerns for patients and parents as it requires long-term follow-up. Proper etiological diagnosis can be achieved via a series of steps that start with clinical observations and then progress to more sophisticated tools. Specifically, MRI identification of pituitary hyperintensity in the posterior part of the sella, now considered a clear marker of neurohypophyseal functional integrity, together with the careful analysis of pituitary stalk shape and size, have provided the most striking findings contributing to the diagnosis and understanding of some forms of ‘idiopathic’ CDI. MRI STIR (short-inversion-time inversion recovery sequencing) is a promising technology for the early identification of LCH-dependent CDI. © 2012 S. Karger AG, Basel Definition/Classification Diabetes insipidus is a disease in which large volumes of dilute urine (polyuria) are excreted due to vasopressin (AVP) deficiency [central diabetes insipidus (CDI)], AVP resistance [nephrogenic diabetes insipidus (NDI)], or excessive water intake (primary polydipsia). Polyuria is characterized by a urine volume in excess of 2 l/m2/24 h or approximately 150 ml/k Continue reading >>

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