#3104 Is dipsogenic diabetes insipidus the same condition as psychogenic polydipsia?

Objectives/AimsTraumatic brain injury is a common cause of permanent or long-term disability,1 and up to 80% of people with moderate to severe brain injury have some degree of pituitary insufficiency. Endocrine disruption has been documented in medical literature since the 1940s,2-4 where central diabetes insipidus has been described as a common transient complication which causes polydipsia (insatiable thirst). However, polydipsia can be caused by other conditions. It is classified into dipsogenic, in a syndrome of disordered thirst-regulating mechanism in patients without psychiatric disease called dipsogenic diabetes insipidus, psychogenic, as a compulsive water drinking in patients with psychiatric conditions referred to as psychogenic polydipsia or psychogenic diabetes insipidus and iatrogenic where large quantities of water are consumed for health benefits. All of which are referred to as primary polydipsia if these conditions cannot be distinguished. Dipsogenic diabetes insipidus and psychogenic polydipsia can be easily mixed up, misdiagnosed or even unrecognised, mainly because their pathophysiology is still unclear. Are these conditions different, or is there anything that can relate them to each other? With this literature review, we are aiming to find the link between subsets of polydipsia after brain trauma, to compare proposed differential diagnosis and their functionality in clinical settings.MethodA literature review was conducted following a search of MEDLINE, CINAHL Plus, APA PsycArticles, APA PsycBooks, APA PsycInfo databases from 1858 onwards.ResultsWe will present our findings from the literature review.ConclusionPolydipsia is a common clinical problem and requires careful evaluation and management to prevent long term neurological sequelae, and there are no evidence-based treatment guidelines.References National Institute of Health and Care Excellence (NICE). (2019). Head Injury. CG176. Retrieved from: https://www.nice.org.uk/guidance/cg176 Escamilla RF, Lisser H. Simmonds disease: A clinical study with revie of the literature; Differentiation from anorexia nervosa by statistical analysis of 595 cases, 101 of which were provided pathologically. The Journal of Clinical Endocrinology & Metabolism 1942;2(2):6596. Porter RJ, Miller RA. Diabetes insipidus following closed head injury. Journal of Neurology, Neurosurgery, and Psychiatry 1946;11:528562. Webb NE, Little B, Loupee-Wilson S, Power EM. Traumatic brain injury and neuro-endocrine disruption: medical and psychosocial rehabilitation. NeuroRehabilitation (Reading, Mass.) 2014;34(4):625636.

Adult Onset Alexander Disease Presenting as Psychogenic Polydipsia Induced Recurrent Hyponatremia as the Initial Symptom: A Case Report.

BackgroundAlexander disease (AxD, OMIM 203450) is a rare and generally fatal disorder of the central nervous system associated with heterozygous mutations in glial fibrillary acidic protein (GFAP) gene. Neuroradiological and clinical features of adult onset AxD is characterized by involvement of hindbrain structures. Psychiatric manifestations and extensive white matter lesions are very sparse in adult onset AxD.Case presentationWe diagnosed a female with AxD presenting with recurrent hyponatremia caused by psychogenic polydipsia as initial symptom at the onset age of 52-year-old. Neurological examination revealed slightly cognitive decline and brisk deep tendon reflex (DTR) in bilateral lower limbs. The symptoms commonly seen in adult onset AxD such as pseudobulbar signs, ataxia and spasticity were not found in the clinical course of disease. Her mother and elder brother had a history of schizophrenia. The patient has had a history of compulsive water drinking as well as personality change in recent years. Her brain magnetic resonance imaging (MRI) showed extensive involvement of white matter without atrophy of medulla oblongata and cervical spinal cord. The next generation DNA sequencing (NGS) showed a likely pathogenic nonsense mutation C1237C>T(pR413*) in GFAP-ε isoform.ConclusionsOur report enriches the understanding of familial adult onset AxD. Our case also contributes to evidence of pathogenicity of the variants in GFAP-ε as the cause of adult onset AxD.

Hyponatremia caused by water intoxication: successful treatment of psychiatric disturbances with olanzapine and fluoxetine

ABSTRACT Hyponatremia is a frequent, yet often unrecognized result of water intoxication caused by psychogenic polydipsia in patients with psychiatric disorders such as schizophrenia and anorexia nervosa. The consequences of hyponatremia may include cerebral edema with tonic–clonic seizures and, in extreme cases, death. In cases of hyponatremia seen in psychiatric practices, the use of psychotropic drugs is often necessary to address both the underlying psychiatric problem and reduce the hyponatremia. Therefore, a patient’s clinical condition, the risk of side effects, the possible effect of the medication on hyponatremia and a history of prior medication use should be considered when selecting appropriate psychotropics. The present clinical case details the beneficial effects of olanzapine and fluoxetine in treating a patient with anorexia nervosa and body dysmorphic disorder experiencing acute hyponatremia, and the stable effect the medications achieved over a period of 2.5 years of maintenance therapy.

Life threatening water intoxication

Water intoxication is a fatal disorder associated with disturbance in brain function, known as hypo-osmolar syndrome which resulting from an excessive water intake, with dilutional hypernatremia leads to a potentially fatal outcome. A change in the electrolyte equilibrium such as this sudden drop in serum sodium level and then subsequent mortality. With hyponatremia, the plasma osmolality decreased leading to water movement into the brain according to the osmotic gradient, resulting in hyponatremic encephalopathy and cerebral oedema. Increased water intake such as in Psychogenic polydipsia is followed by urination of high amount of diluted urine (polyuria) which are the main initial symptoms of water intoxication with headache, blurred vision, nausea, tremor, and deterioration in psychosis. Other serious symptoms involve muscle spasms, Early detection of seizures and coma are more serious outcomes, Untreated cases may lead to death, Risk factor for water intoxication are Marathon runners, military population and athletes and due to this endurance events, these behaviors encouraging heavy sweating that result in heat exhaustion and consume large volumes of fluid, then hyponatremia developed as a result of excessive fluid substitution. Child abuse is other pediatric clinical cases reported with water intoxication. Psychogenic polydipsia which is psychiatric disorder with obsessive water drinking leading to a serious self-induced water intoxication (SIWI), water is normally metabolized and excreted by different means and it is mainly by kidneys in urine, evaporation through the skin, by respiratory system through the respired water vapor and little quantity of water was lost from the gastrointestinal tract (GI).The LD50 of water is > 90 ml/kg orally in rats. The current review illustrates the Life threatening effects of water when it is aggressively consumed.

Severe Hyponatremia Precipitated by Acute Urinary Retention in a Patient with Psychogenic Polydipsia

A woman in her late sixties presented with severe hyponatremia and acute kidney injury (AKI) as consequence of psychogenic polydipsia and acute urinary retention due to urinary tract infection. Urinary catheterization promptly drained 5.5 L of urine with resulting polyuria, leading to an initial swift raise in plasma (P) sodium concentration, disregarding the course of fluid resuscitation. After the polyuric phase, normal range P-sodium levels were reestablished by oral water restriction. Treatment with psychoactive drugs, e.g., zuclopentixol, may have contributed to the severity of the condition. There are few published reports regarding water intoxication and urinary retention, but none reflecting severe hyponatremia precipitated by acute urinary retention in a patient with polydipsia. By this report, we illustrate the detrimental consequences on water and electrolyte homeostasis of urinary retention and polydipsia resulting in acute water intoxication. The purpose of presenting this case is firstly to draw attention to the potentially fatal combination of polydipsia and postrenal acute kidney injury, where the kidneys are unable to correct the enormous excess water, then to focus on the difficulty in correcting hypervolemic hyponatraemia in the context of polyuria after relief of urinary retention, and finally, to point out that patients in treatment with antipsychotics may have further worsening of electrolyte derangement.