Adipsia, or absence of thirst, is a rare condition caused by lesions in the hypothalamus that impair thirst perception. This can lead to life-threatening dehydration and hypernatremia. Diagnosis involves finding elevated sodium levels and low urine osmolality. Treatment requires slow correction of sodium and lifelong management of fluid intake through behavioral changes, nasogastric tubes, or institutional care. Prognosis is generally unfavorable as the underlying hypothalamic damage cannot be reversed.
Diabetes insipidus is an uncommon disorder that causes an imbalance of fluids in the body. This imbalance makes you very thirsty even if you've had something to drink. It also leads you to produce large amounts of urine
Concept Map of Syndrome of Inappropriate (ly high) Anti-Diuretic Hormone (SIADH)riddler2008
Optimized for the BlackBerry, iPhone, Windows mobile phone, Symbian smartphone screen as a reviewer on-the-go.
Write to riddler2008@msn.com for similar slideshows.
09.30.08(b): Approach to the Patient with Disorders of OsmoregulationOpen.Michigan
Slideshow is from the University of Michigan Medical School's M2 Renal sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Renal
Buoni leader non si diventa per caso. La lista delle personali 12 "regole" per il successo stilata da Bill Marriott, Executive Chairman dell'omonima catena di Hotel. Buona lettura.
Diabetes insipidus is an uncommon disorder that causes an imbalance of fluids in the body. This imbalance makes you very thirsty even if you've had something to drink. It also leads you to produce large amounts of urine
Concept Map of Syndrome of Inappropriate (ly high) Anti-Diuretic Hormone (SIADH)riddler2008
Optimized for the BlackBerry, iPhone, Windows mobile phone, Symbian smartphone screen as a reviewer on-the-go.
Write to riddler2008@msn.com for similar slideshows.
09.30.08(b): Approach to the Patient with Disorders of OsmoregulationOpen.Michigan
Slideshow is from the University of Michigan Medical School's M2 Renal sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Renal
Buoni leader non si diventa per caso. La lista delle personali 12 "regole" per il successo stilata da Bill Marriott, Executive Chairman dell'omonima catena di Hotel. Buona lettura.
DITA Quick Start: System Architecture of a Basic DITA ToolsetSuite Solutions
Presenter: Joe Gelb, President, Suite Solutions
Abstract: In this webinar, you will learn about the software, integration and customization which enable you to effectively author, manage, localize, publish and share your DITA XML content. We will review how each tool fits into the content lifecycle and discuss options for an incremental DITA XML implementation using a basic toolset as the starting point.
Converteo Forum E Marketing 2009 Prendre des décisions en période de criseRaphaël Fétique
Intervention de Raphaël FETIQUE, directeur associé de Converteo au forum emarketing 2009 sur le thème "Prendre les bonnes décisions en période de crise".
Une analyse et des méthodes pour rester optimiste et saisir les opportunités nombreuses de gagner des parts de marché à moindre coût.
Demarrer et developper une activite e commerce 2014 (support d'atelier)SID-Networks
Support d'atelier permettant à un entrepreneur ou un porteur de projet e-commerce de connaitre et comprendre les points indispensables à ne pas oublier pour démarrer et développer son activité e-commerce.
Définitions,
Quelques chiffres,
Du besoin à la demande (cahier des charges),
Sur votre Site e-commerce : (vente et communication),
Chaland - prospect - client – référent : méthode,
Un site e-commerce à son image,
ergonomie et utilisabilité d'un site,
Moyens de paiement et implications,
Merchandising et e-logistique,
Visibilité, e-marketing référencement et implication sociale,
Obligations légales,
Résumé des coûts à prévoir et/ou envisager.
Questions / réponses.
N'est utile qu'accompagné du discours adapté.
Téléchargement sur demande via contact.
Landing page con WordPress: come ottenere di più dal tuo sitoTiziano Fogliata
Cos’è una landing page, a cosa ti può servire e perché è importante. Gli strumenti per realizzare landing page con WordPress. Indicazioni e metodi per evitare gli errori più comuni in fase di realizzazione, monitoraggio e ottimizzazione.
La presentazione è stata realizzata in occasione del WordCamp Torino 2016.
Ulteriori info sulle landing page: http://www.motoricerca.net/landing-page/
Ulteriori info sgli strumenti per creare landing page: http://www.fogliata.net/landing-page-wordpress/
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
2. Overview
• Adipsia or hypodipsia: absence of thirst even
in the presence of body water depletion or
salt excess.
• Rare condition presented as: Na +
dehydration.
• The cause is usually a hypothalamic lesion,
which can be congenital or acquired.
3.
4. Pathophysiology 1
• Thirst center: anterior hypothalamus.
• Thirst stimulated by hypertonicity (osmotic)
and hypovolemia.
• Osmoreceptors: anterior wall of 3rd
ventricle
• Near it secretion of AVP. This stimulus is
known as osmotic thirst.
5. Pathophysiology 2
• Thirst stimulated by:
– Hypovolemia: 4-8% .
– P. Hyperosmolarity: > 295.
– Hypotension.
• Generalized lesions that impair the cognitive
processes required for thirst perception.
• Any lesion, congenital or acquired, that
affects the anterior hypothalamus may lead to
the abolition of thirst.
6. Pathophysiology 3
• Lesions of the thirst center may also affect
AVP.
• Pts may present with a combination of
adipsia & central DI: known as adipsic DI.
• Such pts can develop Na, it is chronic &
asymptomatic in many cases.
• These pts have risk of infection & death.
7. Pathophysiology 4
• In adipsia: AVP: normal, partially abolished,
or completely abolished.
• In a normal situation, AVP acts along with
thirst to maintain S. osmolality.
• Antithyroid Abs led to hypothyroidism &
rarely adipsia: both resolved with LT4.
• Essential adipsia: no clear cause!.
• A constellation of adipsia, obesity, PRL &
hypothyroidism was reported in one child.
9. Mortality/Morbidity
• Difficulty in the management of water
balance.
• Hypernatremic dehydration: associated with
hemodynamic and CNS manifestations.
• Morbidity > DI.
10. Age
• All age groups.
– Congenital malformations, traumatic lesions
predominate in children.
– Neoplastic lesions occur in all age groups.
– Psychogenic causes are more common in adults,
particularly elderly persons.
– In children, adipsia without demonstrable
structural lesions is very rare: reported in only 6-7
pts.
11. History
• Obtundation caused by hypernatremic
dehydration.
• Lack of thirst, pointing to the diagnosis.
• Inappropriately high urinary output is highly
suggestive of concomitant central DI.
• h/o brain tumors or congenital
malformations suggests the possibility of a
hypothalamic lesion.
12. Physical
• No physical signs are specific for adipsia.
• Alterations in brain water: (due to Na):
– Hyperpnea
– Muscle weakness
– Restlessness
– High-pitched cry
– Insomnia
– Lethargy
– Coma.
– Convulsions: (rapid rehydration)
– Dehydration.
13. Physical Signs
• ! Underlying abnormality:
– Cleft palate
– Other midline facial defects
– Hydrocephalus
– A scar from a previous tumor surgery
14. Causes
• Most common neoplastic lesions are germinomas,
histiocytomas & gliomas.
• Congenital lesions that are associated with adipsia
include the following:
– Microcephaly
– Ectrodactyly-ectodermal dysplasia-cleft lip/palate (EEC)
syndrome
– Empty sella syndrome
– Malformation of the septum pellucidum
– Holoprosencephaly
15. Causes
• The following can also produce adipsia:
–Meningoencephalitis
–Subarachnoid hemorrhage
–Hydrocephalus
–Pseudotumor cerebri
–Psychogenic abnormalities
16. Laboratory
• S. electrolytes, BUN & S. Cr.
Na is a hallmark of clinically significant
water deficit that may be due to adipsia.
• Hypovolemia: BUN & Cr & BUN/Cr ratio.
• High S.osmolality: water deficit.
• Urine electrolyte levels and osmolality
• Urine electrolytes & osmolality: Central or
renal defect in water homeostasis.
18. Imaging Studies
• Brain CT scans and MRI:
– Empty sella syndrome, tumor.
– R/O complications of hypernatremia, such as
intracranial hemorrhage.
19. Other Tests
• IV AVP or nasal DDAVP required to confirm
or R/O DI.
20. Medical Care
• Slow Na correction in chronic cases: 48-72
hours: < ½ water deficit/first 24 h.
Na: 0.5 mEq/L/h or 10-12 mEq/L/d.
• Long-term therapy
• The underlying damage to the hypothalamic
area is often irreversible.
• Pt & parents education: how to maintain
adequate fluid intake.
21. Treatment options
– No drug therapy.
• Behavioral procedures are successful in
increasing water intake in some patients.
– Electroconvulsive therapy.
– When behavioral therapy fails: long-term
administration of fluids by nasogastric tube or G-
button.
– ADV: if associated DI.
– Underlying cause.
22. • Surgical Care
• Removal of tumors, hematomas, or cysts that
compress the thirst center may be curative in
selected cases.
24. • Diet
• No dietary restrictions are necessary.
• Frequent & scheduled water intake has to be
maintained.
• Activity
• No restrictions on activity are necessary.
25. Inpatient Care
• Pts with adipsia must remain in the hospital
until hypernatremia is diagnosed & corrected
& until the pt is able to maintain fluid &
electrolyte homeostasis.
26. Further Outpatient Care
• Monitor S.electrolyte
• Urine osmolality: for f/u: goal 400-600
mOsm/kg H2 O.
27. Transfer
• If pts unable to achieve an adequate fluid
intake: chronic care facility.
28. Complications
• Exacerbated existing neurological deficits by
acute episodes of Na & cerebral
hemorrhage.
• Extrarenal losses of volume during episodes
of gastroenteritis, more common in children,
may lead to rehospitalization for worsening
Na or other electrolytes disorders.
29. • Prognosis
• Unfavorable.
– Behavioral therapy.
– Most pts remain homebound or institutionalized
& may develop further neurological handicaps.
Overview
Adipsia is a disease characterized by the absence of thirst even in the presence of body water depletion or salt excess. It is a rare condition that typically presents as hypernatremic dehydration. The cause is usually a hypothalamic lesion, which can be congenital or acquired. The term hypodipsia refers to a partial deficiency of the thirst mechanism.
Pathophysiology
In humans, the thirst center is located in the anterior hypothalamus. The primary physiological stimuli for thirst are hypertonicity (osmotic) and hypovolemia. After infancy, an additional social stimulus for thirst is usually observed, which is viewed as secondary. Osmoreceptors in the anterior wall of the third ventricle, near the organum vasculosum mediate the osmotic regulation of thirst, near to or even common to the osmoreceptors that regulate secretion of aqueous vasopressin (AVP). This stimulus is known as osmotic thirst.[1]
In general, the threshold for AVP secretion is a small increase in serum osmolality from 280-290 mOsm/kg H2 O. In contrast, the stimulus for osmotic thirst stimulation is set much higher, typically when near-maximal urine concentrations are achieved (ie, at serum osmolalities around 295 mOsm/Kg H2 O). The purpose of this dichotomy appears to be so that thirst can act as a back up mechanism, when pituitary and renal mechanisms are insufficient to keep plasma osmolality within a tight 1-2% range. If thirst were the primary system, humans would need to constantly divert attention towards seeking water.
After activation of osmotic thirst, downregulation of this stimulus occurs in 2 phases: (1) an immediate but short-lived downregulation of thirst by the oropharynx and upper GI tract and (2) a less immediate but more sustained downregulation by drop in serum osmolality (negative feedback).
Hypovolemia and hypotension may also stimulate thirst through the activation of low-pressure (venous) and high-pressure (arterial) vascular stretch receptors (hypovolemic thirst). Impulses from these receptors are transmitted by the vagus and the glossopharyngeal nerves to the medulla and from there to the hypothalamus. In addition, the hypothalamus is directly stimulated by angiotensin II. Such a hypovolemic thirst occurs with depletion of plasma volume by at least 4-8% in humans and 10-15% in some species.
Thirst abnormalities may result either from specific functional lesions that impair the activation of thirst by hypertonicity or hypovolemia or from generalized lesions that impair the cognitive processes required for thirst perception.
Any lesion, congenital or acquired, that affects the anterior hypothalamus may lead to the abolition of thirst. Because the center for AVP secretion occupies a contiguous area, lesions of the thirst center may also affect AVP (also known as antidiuretic hormone [ADH]) production, storage, or secretion), leading to impaired urinary concentrating ability. Therefore, patients may present with a combination of adipsia and central diabetes insipidus (ie, absence of AVP secretion), also known as adipsic diabetes insipidus. Such patients can develop severe hypernatremia, though it is chronic and therefore asymptomatic in many cases.[2] However, these patients have a much higher risk of infection and death.[39] . In adipsia, AVP secretion may be either completely unaffected, partially abolished, or completely abolished. In a normal situation, AVP acts along with thirst to maintain serum osmolality within tight control.
In rats, areas within the caudate nucleus appear to regulate water intake through norepinephrine-sensitive alpha receptors.[3] In a single case report in a dog, antithyroid antibodies led to hypothyroidism and adipsia, both of which resolved with levothyroxine therapy.[4] &quot;Sickness behavior&quot; is a condition in animals in which systemic infection leads to a highly regulated set of responses such as fever, anorexia, adipsia, inactivity, and cachexia. The neuroimmune communication may involve the interaction of cytokines with peripheral nerves.[5] In rat models, lipopolysaccharide is used to induce adipsia as part of sickness behavior.[40]
Although many different diseases can affect the anterior hypothalamus, adipsia is seen very infrequently even among patients with known anterior hypothalamic lesions. The reason adipsia is uncommon in such situations and the instances when adipsia is more likely to occur remain unknown.
Rarely, some children have adipsia without a definable structural lesion (essential adipsia).[6, 7, 8] A constellation of adipsia, obesity, hyperprolactinemia, and hypothyroidism was reported in one child.[8]
In hypodipsia, the exact pathological abnormalities are not known. AVP levels are normal, suggesting that neuronal pathways affecting thirst are selectively affected, either at the osmoreceptor level or further downstream.
Pathophysiology
In humans, the thirst center is located in the anterior hypothalamus. The primary physiological stimuli for thirst are hypertonicity (osmotic) and hypovolemia. After infancy, an additional social stimulus for thirst is usually observed, which is viewed as secondary. Osmoreceptors in the anterior wall of the third ventricle, near the organum vasculosum mediate the osmotic regulation of thirst, near to or even common to the osmoreceptors that regulate secretion of aqueous vasopressin (AVP). This stimulus is known as osmotic thirst.[1]
In general, the threshold for AVP secretion is a small increase in serum osmolality from 280-290 mOsm/kg H2 O. In contrast, the stimulus for osmotic thirst stimulation is set much higher, typically when near-maximal urine concentrations are achieved (ie, at serum osmolalities around 295 mOsm/Kg H2 O). The purpose of this dichotomy appears to be so that thirst can act as a back up mechanism, when pituitary and renal mechanisms are insufficient to keep plasma osmolality within a tight 1-2% range. If thirst were the primary system, humans would need to constantly divert attention towards seeking water.
After activation of osmotic thirst, downregulation of this stimulus occurs in 2 phases: (1) an immediate but short-lived downregulation of thirst by the oropharynx and upper GI tract and (2) a less immediate but more sustained downregulation by drop in serum osmolality (negative feedback).
Hypovolemia and hypotension may also stimulate thirst through the activation of low-pressure (venous) and high-pressure (arterial) vascular stretch receptors (hypovolemic thirst). Impulses from these receptors are transmitted by the vagus and the glossopharyngeal nerves to the medulla and from there to the hypothalamus. In addition, the hypothalamus is directly stimulated by angiotensin II. Such a hypovolemic thirst occurs with depletion of plasma volume by at least 4-8% in humans and 10-15% in some species.
Thirst abnormalities may result either from specific functional lesions that impair the activation of thirst by hypertonicity or hypovolemia or from generalized lesions that impair the cognitive processes required for thirst perception.
Any lesion, congenital or acquired, that affects the anterior hypothalamus may lead to the abolition of thirst. Because the center for AVP secretion occupies a contiguous area, lesions of the thirst center may also affect AVP (also known as antidiuretic hormone [ADH]) production, storage, or secretion), leading to impaired urinary concentrating ability. Therefore, patients may present with a combination of adipsia and central diabetes insipidus (ie, absence of AVP secretion), also known as adipsic diabetes insipidus. Such patients can develop severe hypernatremia, though it is chronic and therefore asymptomatic in many cases.[2] However, these patients have a much higher risk of infection and death.[39] . In adipsia, AVP secretion may be either completely unaffected, partially abolished, or completely abolished. In a normal situation, AVP acts along with thirst to maintain serum osmolality within tight control.
In rats, areas within the caudate nucleus appear to regulate water intake through norepinephrine-sensitive alpha receptors.[3] In a single case report in a dog, antithyroid antibodies led to hypothyroidism and adipsia, both of which resolved with levothyroxine therapy.[4] &quot;Sickness behavior&quot; is a condition in animals in which systemic infection leads to a highly regulated set of responses such as fever, anorexia, adipsia, inactivity, and cachexia. The neuroimmune communication may involve the interaction of cytokines with peripheral nerves.[5] In rat models, lipopolysaccharide is used to induce adipsia as part of sickness behavior.[40]
Although many different diseases can affect the anterior hypothalamus, adipsia is seen very infrequently even among patients with known anterior hypothalamic lesions. The reason adipsia is uncommon in such situations and the instances when adipsia is more likely to occur remain unknown.
Rarely, some children have adipsia without a definable structural lesion (essential adipsia).[6, 7, 8] A constellation of adipsia, obesity, hyperprolactinemia, and hypothyroidism was reported in one child.[8]
In hypodipsia, the exact pathological abnormalities are not known. AVP levels are normal, suggesting that neuronal pathways affecting thirst are selectively affected, either at the osmoreceptor level or further downstream.
Pathophysiology
In humans, the thirst center is located in the anterior hypothalamus. The primary physiological stimuli for thirst are hypertonicity (osmotic) and hypovolemia. After infancy, an additional social stimulus for thirst is usually observed, which is viewed as secondary. Osmoreceptors in the anterior wall of the third ventricle, near the organum vasculosum mediate the osmotic regulation of thirst, near to or even common to the osmoreceptors that regulate secretion of aqueous vasopressin (AVP). This stimulus is known as osmotic thirst.[1]
In general, the threshold for AVP secretion is a small increase in serum osmolality from 280-290 mOsm/kg H2 O. In contrast, the stimulus for osmotic thirst stimulation is set much higher, typically when near-maximal urine concentrations are achieved (ie, at serum osmolalities around 295 mOsm/Kg H2 O). The purpose of this dichotomy appears to be so that thirst can act as a back up mechanism, when pituitary and renal mechanisms are insufficient to keep plasma osmolality within a tight 1-2% range. If thirst were the primary system, humans would need to constantly divert attention towards seeking water.
After activation of osmotic thirst, downregulation of this stimulus occurs in 2 phases: (1) an immediate but short-lived downregulation of thirst by the oropharynx and upper GI tract and (2) a less immediate but more sustained downregulation by drop in serum osmolality (negative feedback).
Hypovolemia and hypotension may also stimulate thirst through the activation of low-pressure (venous) and high-pressure (arterial) vascular stretch receptors (hypovolemic thirst). Impulses from these receptors are transmitted by the vagus and the glossopharyngeal nerves to the medulla and from there to the hypothalamus. In addition, the hypothalamus is directly stimulated by angiotensin II. Such a hypovolemic thirst occurs with depletion of plasma volume by at least 4-8% in humans and 10-15% in some species.
Thirst abnormalities may result either from specific functional lesions that impair the activation of thirst by hypertonicity or hypovolemia or from generalized lesions that impair the cognitive processes required for thirst perception.
Any lesion, congenital or acquired, that affects the anterior hypothalamus may lead to the abolition of thirst. Because the center for AVP secretion occupies a contiguous area, lesions of the thirst center may also affect AVP (also known as antidiuretic hormone [ADH]) production, storage, or secretion), leading to impaired urinary concentrating ability. Therefore, patients may present with a combination of adipsia and central diabetes insipidus (ie, absence of AVP secretion), also known as adipsic diabetes insipidus. Such patients can develop severe hypernatremia, though it is chronic and therefore asymptomatic in many cases.[2] However, these patients have a much higher risk of infection and death.[39] . In adipsia, AVP secretion may be either completely unaffected, partially abolished, or completely abolished. In a normal situation, AVP acts along with thirst to maintain serum osmolality within tight control.
In rats, areas within the caudate nucleus appear to regulate water intake through norepinephrine-sensitive alpha receptors.[3] In a single case report in a dog, antithyroid antibodies led to hypothyroidism and adipsia, both of which resolved with levothyroxine therapy.[4] &quot;Sickness behavior&quot; is a condition in animals in which systemic infection leads to a highly regulated set of responses such as fever, anorexia, adipsia, inactivity, and cachexia. The neuroimmune communication may involve the interaction of cytokines with peripheral nerves.[5] In rat models, lipopolysaccharide is used to induce adipsia as part of sickness behavior.[40]
Although many different diseases can affect the anterior hypothalamus, adipsia is seen very infrequently even among patients with known anterior hypothalamic lesions. The reason adipsia is uncommon in such situations and the instances when adipsia is more likely to occur remain unknown.
Rarely, some children have adipsia without a definable structural lesion (essential adipsia).[6, 7, 8] A constellation of adipsia, obesity, hyperprolactinemia, and hypothyroidism was reported in one child.[8]
In hypodipsia, the exact pathological abnormalities are not known. AVP levels are normal, suggesting that neuronal pathways affecting thirst are selectively affected, either at the osmoreceptor level or further downstream.
Pathophysiology
In humans, the thirst center is located in the anterior hypothalamus. The primary physiological stimuli for thirst are hypertonicity (osmotic) and hypovolemia. After infancy, an additional social stimulus for thirst is usually observed, which is viewed as secondary. Osmoreceptors in the anterior wall of the third ventricle, near the organum vasculosum mediate the osmotic regulation of thirst, near to or even common to the osmoreceptors that regulate secretion of aqueous vasopressin (AVP). This stimulus is known as osmotic thirst.[1]
In general, the threshold for AVP secretion is a small increase in serum osmolality from 280-290 mOsm/kg H2 O. In contrast, the stimulus for osmotic thirst stimulation is set much higher, typically when near-maximal urine concentrations are achieved (ie, at serum osmolalities around 295 mOsm/Kg H2 O). The purpose of this dichotomy appears to be so that thirst can act as a back up mechanism, when pituitary and renal mechanisms are insufficient to keep plasma osmolality within a tight 1-2% range. If thirst were the primary system, humans would need to constantly divert attention towards seeking water.
After activation of osmotic thirst, downregulation of this stimulus occurs in 2 phases: (1) an immediate but short-lived downregulation of thirst by the oropharynx and upper GI tract and (2) a less immediate but more sustained downregulation by drop in serum osmolality (negative feedback).
Hypovolemia and hypotension may also stimulate thirst through the activation of low-pressure (venous) and high-pressure (arterial) vascular stretch receptors (hypovolemic thirst). Impulses from these receptors are transmitted by the vagus and the glossopharyngeal nerves to the medulla and from there to the hypothalamus. In addition, the hypothalamus is directly stimulated by angiotensin II. Such a hypovolemic thirst occurs with depletion of plasma volume by at least 4-8% in humans and 10-15% in some species.
Thirst abnormalities may result either from specific functional lesions that impair the activation of thirst by hypertonicity or hypovolemia or from generalized lesions that impair the cognitive processes required for thirst perception.
Any lesion, congenital or acquired, that affects the anterior hypothalamus may lead to the abolition of thirst. Because the center for AVP secretion occupies a contiguous area, lesions of the thirst center may also affect AVP (also known as antidiuretic hormone [ADH]) production, storage, or secretion), leading to impaired urinary concentrating ability. Therefore, patients may present with a combination of adipsia and central diabetes insipidus (ie, absence of AVP secretion), also known as adipsic diabetes insipidus. Such patients can develop severe hypernatremia, though it is chronic and therefore asymptomatic in many cases.[2] However, these patients have a much higher risk of infection and death.[39] . In adipsia, AVP secretion may be either completely unaffected, partially abolished, or completely abolished. In a normal situation, AVP acts along with thirst to maintain serum osmolality within tight control.
In rats, areas within the caudate nucleus appear to regulate water intake through norepinephrine-sensitive alpha receptors.[3] In a single case report in a dog, antithyroid antibodies led to hypothyroidism and adipsia, both of which resolved with levothyroxine therapy.[4] &quot;Sickness behavior&quot; is a condition in animals in which systemic infection leads to a highly regulated set of responses such as fever, anorexia, adipsia, inactivity, and cachexia. The neuroimmune communication may involve the interaction of cytokines with peripheral nerves.[5] In rat models, lipopolysaccharide is used to induce adipsia as part of sickness behavior.[40]
Although many different diseases can affect the anterior hypothalamus, adipsia is seen very infrequently even among patients with known anterior hypothalamic lesions. The reason adipsia is uncommon in such situations and the instances when adipsia is more likely to occur remain unknown.
Rarely, some children have adipsia without a definable structural lesion (essential adipsia).[6, 7, 8] A constellation of adipsia, obesity, hyperprolactinemia, and hypothyroidism was reported in one child.[8]
In hypodipsia, the exact pathological abnormalities are not known. AVP levels are normal, suggesting that neuronal pathways affecting thirst are selectively affected, either at the osmoreceptor level or further downstream.
Epidemiology
Frequency
International
Adipsia is an extremely rare condition. Fewer than 200 cases have been reported worldwide, although more cases are likely unreported. Mavrakis et al collated and described 70 reported cases in which thirst and AVP secretion were both abolished.[9]
Interestingly, a number of cases are reported in the veterinary literature, largely due to intracranial tumors, similar to causes in humans.
Mortality/Morbidity
Adipsia leads to considerable difficulty in the management of water balance. Its common consequence is hypernatremic dehydration, which, when severe, is associated with hemodynamic and CNS manifestations. Adipsia has a higher morbidity than diabetes insipidus, in which the thirst mechanism is intact.
Age
Adipsia occurs in all age groups. Congenital malformations and traumatic lesions predominate in children, neoplastic lesions occur in all age groups, and psychogenic causes are more common in adults, particularly elderly persons. In children, adipsia without demonstrable structural lesions is very rare and has been reported in only 6-7 patients.[10]
History
•In most situations, patients with adipsia present with obtundation caused by hypernatremic dehydration.
•Information regarding the quantity and type of fluid intake may reveal the lack of thirst, pointing to the diagnosis. The presence of an inappropriately high urinary output is highly suggestive of concomitant central diabetes insipidus.
•A history of brain tumors or congenital malformations suggests the possibility of a hypothalamic lesion.
Physical
•No physical signs are specific for adipsia. The most prominent physical signs are referable to alterations in brain water content due to hypernatremia. These alterations include the following:
oHyperpnea
oMuscle weakness
oRestlessness
oHigh-pitched cry
oInsomnia
oLethargy
oComa
oConvulsions (uncommon, except in cases of overly rapid rehydration)
•Loss of skin turgor and dry mucous membranes are evident but may not be commensurate with the grade of dehydration.
•Physical signs indicative of an underlying abnormality are often evident. Examples of such physical signs include the following:
oCleft palate
oOther midline facial defects
oHydrocephalus
oA scar from a previous tumor surgery
Physical
•No physical signs are specific for adipsia. The most prominent physical signs are referable to alterations in brain water content due to hypernatremia. These alterations include the following:
oHyperpnea
oMuscle weakness
oRestlessness
oHigh-pitched cry
oInsomnia
oLethargy
oComa
oConvulsions (uncommon, except in cases of overly rapid rehydration)
•Loss of skin turgor and dry mucous membranes are evident but may not be commensurate with the grade of dehydration.
•Physical signs indicative of an underlying abnormality are often evident. Examples of such physical signs include the following:
oCleft palate
oOther midline facial defects
oHydrocephalus
oA scar from a previous tumor surgery
Causes
•Most common neoplastic lesions are germinomas, histiocytomas, and gliomas.
•Congenital lesions that are associated with adipsia include the following:
oMicrocephaly
oEctrodactyly-ectodermal dysplasia-cleft lip/palate (EEC) syndrome
oEmpty sella syndrome
oMalformation of the septum pellucidum
oHoloprosencephaly
•The following can also produce adipsia:
oMeningoencephalitis
oSubarachnoid hemorrhage
oHydrocephalus
oPseudotumor cerebri
oPsychogenic abnormalities
Causes
•Most common neoplastic lesions are germinomas, histiocytomas, and gliomas.
•Congenital lesions that are associated with adipsia include the following:
oMicrocephaly
oEctrodactyly-ectodermal dysplasia-cleft lip/palate (EEC) syndrome
oEmpty sella syndrome
oMalformation of the septum pellucidum
oHoloprosencephaly
•The following can also produce adipsia:
oMeningoencephalitis
oSubarachnoid hemorrhage
oHydrocephalus
oPseudotumor cerebri
oPsychogenic abnormalities
Laboratory Studies
The following studi & es are indicated in patients with adipsia:
•Serum electrolytes, BUN, and serum creatinine levels
oSuspicion of adipsia frequently results from serum electrolyte abnormalities.
oHypernatremia is a hallmark of clinically significant water deficit that may be due to adipsia.
oVolume depletion that is associated with adipsia also causes elevations in BUN and creatinine levels and an increase in the BUN/creatinine ratio.
•Serum osmolality: The water deficit results in a markedly elevated serum osmolality.
•Urine electrolyte levels and osmolality
oSimultaneous measurements of urine electrolytes and osmolality are critical in determining the central, rather than renal, nature of the defect in water homeostasis.
oIn adipsia, the fractional excretion of sodium is less than 1%, unless a coexisting defect in aqueous vasopressin (AVP) secretion is present.
oUrine osmolality is very high, unless a coexisting defect in AVP secretion is present.
oIn diabetes insipidus, the concentration of urine is submaximal, even in the face of high serum osmolality. In salt intoxication, the urine sodium concentrations are very high and fractional excretion of sodium is greater than 1%.
oDifficulties in diagnosis may arise when adipsia and diabetes insipidus coexist. In these patients, initial test results may be suggestive of diabetes insipidus; however, administration of AVP increases urine osmolality and diminishes the tendency for hypernatremia. The patient&apos;s history of absence of thirst points toward the coexistence of adipsia.
•Blood hormone levels
•AVP levels: In isolated adipsia, circulating AVP levels must be high, reflecting an appropriate response of the pituitary to hyperosmolality. In patients who have defects in thirst regulation and AVP secretion, serum AVP levels are low or absent.
•Plasma renin and aldosterone levels: These are elevated secondary to hypovolemia.
Laboratory Studies
The following studi & es are indicated in patients with adipsia:
•Serum electrolytes, BUN, and serum creatinine levels
oSuspicion of adipsia frequently results from serum electrolyte abnormalities.
oHypernatremia is a hallmark of clinically significant water deficit that may be due to adipsia.
oVolume depletion that is associated with adipsia also causes elevations in BUN and creatinine levels and an increase in the BUN/creatinine ratio.
•Serum osmolality: The water deficit results in a markedly elevated serum osmolality.
•Urine electrolyte levels and osmolality
oSimultaneous measurements of urine electrolytes and osmolality are critical in determining the central, rather than renal, nature of the defect in water homeostasis.
oIn adipsia, the fractional excretion of sodium is less than 1%, unless a coexisting defect in aqueous vasopressin (AVP) secretion is present.
oUrine osmolality is very high, unless a coexisting defect in AVP secretion is present.
oIn diabetes insipidus, the concentration of urine is submaximal, even in the face of high serum osmolality. In salt intoxication, the urine sodium concentrations are very high and fractional excretion of sodium is greater than 1%.
oDifficulties in diagnosis may arise when adipsia and diabetes insipidus coexist. In these patients, initial test results may be suggestive of diabetes insipidus; however, administration of AVP increases urine osmolality and diminishes the tendency for hypernatremia. The patient&apos;s history of absence of thirst points toward the coexistence of adipsia.
•Blood hormone levels
•AVP levels: In isolated adipsia, circulating AVP levels must be high, reflecting an appropriate response of the pituitary to hyperosmolality. In patients who have defects in thirst regulation and AVP secretion, serum AVP levels are low or absent.
•Plasma renin and aldosterone levels: These are elevated secondary to hypovolemia.
Imaging Studies
•Brain imaging studies, such as CT scans and MRI studies, are indicated if the underlying cause for adipsia needs to be determined (eg, empty sella syndrome, tumor). They may also help to rule out complications of hypernatremia, such as intracranial hemorrhage.
Other Tests
•Therapeutic challenge with intravenous AVP or nasal desmopressin acetate (DDAVP) is often required to confirm or rule out the diagnosis of diabetes insipidus. Perform these tests in consultation with experts in water metabolism.
Medical Care
Do not rapidly correct chronic hypernatremia in patients with adipsia. Correct hypernatremia over 48-72 hours, with no more than half of the calculated water deficit replaced during the first 24 hours of therapy. Drop in serum sodium level should be at rate of approximately 0.5 mEq/L/hour or 10-12 mEq/L/day.
•Long-term therapy
oThe underlying damage to the hypothalamic area is often irreversible.
oThe goal of medical care is to teach the patient and parents how to maintain adequate fluid intake.[11]
•Treatment options
oNo pharmacological therapy is currently available.
oBehavioral procedures are successful in increasing water intake in some patients.
oElectroconvulsive therapy has been used, with mixed results, in patients in whom the underlying cause is psychogenic.
oWhen behavioral therapy fails, the only remaining option is long-term administration of fluids by nasogastric tube or G-button.
oNasal desmopressin acetate (DDAVP) therapy to limit urine output is useful in patients with coexisting central diabetes insipidus.
oIn adipsic diabetes insipidus, recovery of thirst function after removal of underlying cause can be assessed by a visual analog scale after hypertonic saline infusion.{{Ref38}
Medical Care
Do not rapidly correct chronic hypernatremia in patients with adipsia. Correct hypernatremia over 48-72 hours, with no more than half of the calculated water deficit replaced during the first 24 hours of therapy. Drop in serum sodium level should be at rate of approximately 0.5 mEq/L/hour or 10-12 mEq/L/day.
•Long-term therapy
oThe underlying damage to the hypothalamic area is often irreversible.
oThe goal of medical care is to teach the patient and parents how to maintain adequate fluid intake.[11]
•Treatment options
oNo pharmacological therapy is currently available.
oBehavioral procedures are successful in increasing water intake in some patients.
oElectroconvulsive therapy has been used, with mixed results, in patients in whom the underlying cause is psychogenic.
oWhen behavioral therapy fails, the only remaining option is long-term administration of fluids by nasogastric tube or G-button.
oNasal desmopressin acetate (DDAVP) therapy to limit urine output is useful in patients with coexisting central diabetes insipidus.
oIn adipsic diabetes insipidus, recovery of thirst function after removal of underlying cause can be assessed by a visual analog scale after hypertonic saline infusion.{{Ref38}
Surgical Care
•Removal of tumors, hematomas, or cysts that compress the thirst center may be curative in selected cases.
Consultations
•Obtain the opinion of an oncologist, a neurosurgeon, or both for patients with space-occupying lesions.
•Obtain the opinion of an endocrinologist in patients with associated central diabetes insipidus.
Further Inpatient Care
•Patients with adipsia must remain in the hospital until hypernatremia is diagnosed and corrected and until the patient is able to maintain fluid and electrolyte homeostasis.
Further Outpatient Care
•Monitor the serum electrolyte levels in order to ensure adequate fluid intake. The level of comprehension and compliance of the patient and parents determines the frequency of the visits.
•In children with normal aqueous vasopressin (AVP) secretion, measuring urine osmolality may be sufficient for follow-up care. The goal of a urine osmolality is 400-600 mOsm/kg H2 O.
Transfer
•Patients who are unable to achieve an adequate fluid intake may be transferred to a chronic care facility where they can be kept under close supervision and receive behavioral therapy.
Complications
•Existing neurological deficits can be exacerbated by acute episodes of severe hypernatremia and cerebral hemorrhage.
•Extrarenal losses of volume during episodes of gastroenteritis, more common in children, may lead to rehospitalization for worsening hypernatremia or other disorders of serum electrolytes.