deamino-arginine-vasopressin and Hypernatremia

The authors report permanent central diabetes insipidus (CDI) in a patient after severe traumatic brain injury (TBI) in traffic accident. A 16-year-old boy entered to a medical facility in coma (GCS score 6) with the following diagnosis: acute TBI, severe cerebral contusion, subarachnoid hemorrhage, depressed comminuted cranial vault fracture, basilar skull fracture, visceral contusion. CDI was diagnosed in 3 days after injury considering polyuria and hypernatremia (155 mmol/l). Desmopressin therapy was initiated through a feeding tube. Thirst appeared when a patient came out of the coma after 21 days despite ongoing desmopressin therapy. Considering persistent thirst and polyuria, we continued desmopressin therapy in a spray form. Under this therapy, polyuria reduced to 3-3.5 liters per a day. Symptoms of CDI persisted in long-term period (2 years after TBI) while function of adenohypophysis was intact. This case demonstrates a rare development of permanent diabetes insipidus after TBI. CDI manifested only as polyuria and hypernatremia in coma. Thirst joined after recovery of consciousness. Probable causes of CDI were damage to neurohypophysis and partially injury of pituitary stalk because of extended basilar skull fracture and/or irreversible secondary lesion of hypothalamus following diffuse axonal damage after TBI.. В статье представлен клинический случай развития постоянной формы центрального несахарного диабета (ЦНД) у пациента после тяжелой черепно-мозговой травмы (ТЧМТ) в результате дорожно-транспортного происшествия. Подросток 16 лет поступил в лечебное учреждение в состоянии комы (6 баллов по шкале комы Глазго) с диагнозом: сочетанная травма; острая ТЧМТ; ушиб головного мозга тяжелой степени; субарахноидальное кровоизлияние; вдавленный многооскольчатый перелом свода черепа справа; протяженный перелом основания черепа; ушиб внутренних органов. На 3-и сутки развились полиурия и гипернатриемия (155 ммоль/л); диагностирован ЦНД и начата терапия десмопрессином в таблетированной форме через зонд. При выходе из комы (21-е сутки) отмечено появление жажды на фоне продолжения терапии. В связи с сохраняющейся жаждой и полиурией произведен перевод на терапию десмопрессином в виде спрея, на этом фоне отмечено уменьшение выделения мочи до 3—3,5 л в сутки. Симптоматика ЦНД наблюдалась и через 2 года после ТЧМТ, при этом функция аденогипофиза оставалась сохранной. Представленный случай является примером развития постоянного несахарного диабета у подростка с ТЧМТ, находившегося под длительным наблюдением. Клиническая картина ЦНД в состоянии комы проявлялась только полиурией и гипернатриемией, а по мере повышения уровня сознания присоединилась жажда. Вероятными причинами развития ЦНД явились повреждение нейрогипофиза и частичное повреждение стебля гипофиза в результате протяженного перелома основания черепа и/или необратимого вторичного повреждения гипоталамуса вследствие диффузного аксонального повреждения головного мозга после ТЧМТ.

Topics: Adolescent; Brain Injuries, Traumatic; Coma; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Hypernatremia; Male; Polyuria

The treatment of central diabetes insipidus has not changed significantly in recent decades, and dDAVP and replacement of free water deficit remain the cornerstones of treatment. Oral dDAVP has replaced nasal dDAVP as a more reliable mode of treatment for chronic central diabetes insipidus. Hyponatraemia is a common side effect, occurring in one in four patients, and should be avoided by allowing a regular break from dDAVP to allow a resultant aquaresis. Hypernatraemia is less common, and typically occurs during hospitalization, when access to water is restricted, and in cases of adipsic DI. Management of adipsic DI can be challenging, and requires initial inpatient assessment to establish dose of dDAVP, daily fluid prescription, and eunatraemic weight which can guide day-to-day fluid targets in the long-term.

Topics: Body Weight; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Humans; Hypernatremia; Hyponatremia; Neurophysins; Protein Precursors; Vasopressins

Diabetes insipidus and the syndrome of inappropriate antidiuretic hormone secretion lie at opposite ends of the spectrum of disordered renal handling of water. Whereas renal retention of water insidiously causes hypotonic hyponatremia in syndrome of inappropriate antidiuretic hormone secretion, diabetes insipidus may lead to free water loss, hypernatremia, and volume depletion. Hypernatremia and hyponatremia are associated with worse outcomes and longer intensive care stays. Moreover, pathologies causing polyuria and hyponatremia in patients in intensive care may be multiple, making diagnosis challenging. We provide an approach to the diagnosis and management of these conditions in intensive care patients.

Topics: Antidiuretic Agents; Critical Care; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Male; Practice Guidelines as Topic; Water-Electrolyte Balance

Hyponatremia causes significant morbidity, mortality, and disability. This review considers the literature of the past 18 months to improve understanding of these complications and to identify therapeutic strategies to prevent them.. Acute hyponatremia causes serious brain swelling that can lead to permanent disability or death. A 4-6 mEq/l increase in serum sodium is sufficient to reverse impending herniation. Brain swelling is minimal in chronic hyponatremia, and to avoid osmotic demyelination, correction should not exceed 8 mEq/l/day. In high-risk patients, correction should not exceed 4-6 mEq/l/day. Inadvertent overcorrection of hyponatremia is common and preventable by controlling unwanted urinary water losses with desmopressin. Even mild chronic hyponatremia is associated with increased mortality, attention deficit, gait instability, osteoporosis, and fractures, but it is not known if the correction of mild hyponatremia improves outcomes.. Controlled trials are needed to identify affordable treatments for hyponatremia that reduce the need for hospitalization, decrease hospital length of stay, and decrease morbidity. Such trials could also help answer the question of whether hyponatremia causes excess mortality or whether it is simply a marker for severe, lethal, underlying disease.

Topics: Animals; Brain Edema; Cognition Disorders; Deamino Arginine Vasopressin; Fractures, Bone; Gait Disorders, Neurologic; Humans; Hypernatremia; Hyponatremia; Osteoporosis; Saline Solution, Hypertonic; Sodium; Sodium Chloride

Hypernatremia is a common electrolyte disorder that reflects an imbalance in the water balance of the body, often resulting from an increased loss of free water compared to sodium excretion. It is rarely based on excessive sodium intake. The clinical presentation is often characterized by a central nervous system dysfunction (confusion, coma) and pronounced thirst (in awake patients). In addition to medical history, the volume status of the patient and the osmolality of urine are leading in the differential diagnosis. Usually, the treatment of hypernatremia - in addition to addressing the underlying cause - is replacing the (absolute or relative) loss of free water by hypotonic infusions, or in case of diabetes insipidus, by application of Desmopressin (Minirin). As rapid changes in serum sodium concentration may have deleterious consequences (osmotic demyelinsiation syndrome), preexisting hypernatremia (>48h) should not be reduced by more than 8-10 mmol/l/day. Close laboratory controls are important. For acute hypernatremia (< 24 hours), hemodialysis is an effective option to rapidly normalize the serum sodium levels. To avoid a rapid drop in sodium concentration that must also be considered when starting a renal replacement therapy in patients with chronic hypernatremia.

Topics: Antidiuretic Agents; Deamino Arginine Vasopressin; Diagnosis, Differential; Fluid Therapy; Humans; Hypernatremia; Renal Dialysis; Sodium; Treatment Outcome

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Deamino Arginine Vasopressin; Humans; Hyperkalemia; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Membrane Potentials; Morpholines; Osmolar Concentration; Potassium; Randomized Controlled Trials as Topic; Sodium; Spiro Compounds; Survival Rate; Tolvaptan; Water-Electrolyte Imbalance

Experience with nasogastric administration of oral DDAVP [desamino-D-arginine-8-vasopressin] lyophilisate (ODL) for central diabetes insipidus (CDI) in disabled children with swallowing coordination difficulties is limited.. We aimed to assess the safety and efficacy of nasogastric use of ODL in disabled children with CDI. Time to serum sodium normalisation was compared with that of children with normal intellect and CDI treated with sublingual DDAVP.. Clinical, laboratory and neuroimaging characteristics were evaluated for 12 disabled children with CDI treated with ODL through nasogastric tube at Dr Behcet Uz Children's Hospital, Turkey, between 2012 and 2022.. Six boys and six girls with a mean (±SD) age of 43 (± 40) months were evaluated. These children (mean [±SD] weight standard deviation score [SDS] - 1.2 ± 1.7; mean [±SD] height SDS - 1.3 ± 1.4) presented with failure to thrive, irritability, prolonged fever, polyuria and hypernatraemia (mean serum sodium 162 [±3.6] mEq/L). At diagnosis, mean serum and urine osmolality were 321 (± 14) mOsm/kg and 105 (± 7.8) mOsm/kg, respectively. Arginine vasopressin (AVP) levels were undetectable (< 0.5 pmol/L) at diagnosis in all patients. Nasogastric tube administration of DDAVP lyophilisate (120 µg/tablet) dissolved in water (10 mL) was commenced at a dose of 1-5 µg/kg/day in two divided doses together with controlled water intake to avoid hyponatraemia. The frequency and dose of DDAVP were titrated based on urine output and serum sodium concentration. Serum sodium declined at a rate of 0.11 ± 0.03 mEq/L/h and reached normal range in a mean duration of 174 ± 46.5 h. Serum sodium declined faster in children with normal intellect and CDI treated with sublingual DDAVP (1.28 ± 0.39 mEq/L/h; p = 0.0003). Three disabled children needed rehospitalisation because of hypernatraemia due to unintentional DDAVP omission by caregivers. No episode of hyponatraemia was observed. Weight gain and growth were normal during the median (± interquartile range) follow-up duration of 32 ± 67 months.. Nasogastric administration of oral DDAVP lyophilised formulation was safe and effective in the treatment of CDI in disabled children in this small retrospective series.

Topics: Child; Child, Preschool; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Disabled Children; Female; Humans; Hypernatremia; Hyponatremia; Male; Retrospective Studies; Sodium

Topics: Adult; Antidiuretic Agents; Deamino Arginine Vasopressin; Diabetes Insipidus; Humans; Hypernatremia; Male; Postoperative Complications; Saline Solution, Hypertonic; Sodium

A 66-year-old female patient with the initial diagnosis of acute myeloid leukemia is reported. Paraneoplastic syndrome manifested as hypernatremia due to central diabetes insipidus (CDI), which could be controlled with the administration of desmopressin. After initiation of the induction therapy, the required desmopressin administration could be reduced and terminated. In the further course, the early increasing polyuria and hypernatremia indicated the primary refractory acute myeloid leukemia.. Dargestellt wird der Krankheitsverlauf einer 66-jährigen Patientin mit der Erstdiagnose einer akuten myeloischen Leukämie. Als paraneoplastisches Syndrom zeigten sich eine Hypernatriämie sowie Polyurie infolge eines zentralen Diabetes insipidus (CDI), welcher mittels Desmopressingabe kontrolliert werden konnte. Nach Einleitung einer Induktionstherapie kam es im Verlauf nach Beendigung der Desmopressintherapie noch vor Anstieg des Blastenanteils zu einer erneuten Hypernatriämie und Polyurie als Hinweis auf eine primäre Refraktärität.

Topics: Aged; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Female; Humans; Hypernatremia; Leukemia, Myeloid, Acute; Neoplasms, Second Primary; Polyuria

Presented case demonstrates a rare diencephalic pathology - adipsic diabetes insipidus (ADI) with severe hypernatremia in a 58-year-old woman after ttranssphenoidal removal of stalk intraventricular craniopharyngioma. ADI was diagnosed because of hypernatremia (150-155 mmol/L), polyuria (up to 4 liters per day) and absence of thirst. Normalization of water-electrolyte balance occurred on the background of desmopressin therapy and sufficient hydration in postoperative period. After release from the hospital, the patient independently stopped desmopressin therapy and did not consume an adequate amount of fluid of the background of polyuria. This led to severe hypernatremia (155-160 mmol/L) and rough mental disorders.Patients with ADI need closely monitoring of medical condition and water-electrolyte parameters, appointment of fixed doses of desmopressin and adequate hydration.

Topics: Central Nervous System Cysts; Craniopharyngioma; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Mellitus; Female; Humans; Hypernatremia; Middle Aged; Neurosurgical Procedures; Polyuria; Postoperative Complications

Central diabetes insipidus (DI) is a complex disease that requires firm adherence to desmopressin therapy. There is little information on the onset of hypernatremia after withdrawal of desmopressin.. We present a case of an elderly woman with central DI whose serum sodium jumped from 141 to 171 mEq/L after 48-72 h of holding oral desmopressin. Her DI crisis resolved with intravenous desmopressin and free water administration.. Based on this precipitous onset of DI crisis, we recommend not withholding desmopressin for more than 24 h.

Topics: Administration, Intravenous; Aged; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Disasters; Female; Humans; Hypernatremia

Topics: Adult; Craniopharyngioma; Deamino Arginine Vasopressin; Drug Administration Schedule; Female; Humans; Hypernatremia; Hypopituitarism; Neurologic Examination; Pituitary Neoplasms; Postoperative Complications; Sodium; Substance Withdrawal Syndrome

COVID-19 has changed the nature of medical consultations, emphasizing virtual patient counseling, with relevance for patients with diabetes insipidus (DI) or hyponatraemia. The main complication of desmopressin treatment in DI is dilutional hyponatraemia. Since plasma sodium monitoring is not always possible in times of COVID-19, we recommend to delay the desmopressin dose once a week until aquaresis occurs allowing excess retained water to be excreted. Patients should measure their body weight daily. Patients with DI admitted to the hospital with COVID-19 have a high risk for mortality due to volume depletion. Specialists must supervise fluid replacement and dosing of desmopressin. Patients after pituitary surgery should drink to thirst and measure their body weight daily to early recognize the development of the postoperative syndrome of inappropriate antidiuresis (SIAD). They should know hyponatraemia symptoms. The prevalence of hyponatraemia in patients with pneumonia due to COVID-19 is not yet known, but seems to be low. In contrast, hypernatraemia may develop in COVID-19 patients in ICU, from different multifactorial reasons, for example, due to insensible water losses from pyrexia, increased respiration rate and use of diuretics. Hypernatraemic dehydration may contribute to the high risk of acute kidney injury in COVID-19. IV fluid replacement should be administered with caution in severe cases of COVID-19 because of the risk of pulmonary oedema.

Topics: Antidiuretic Agents; Brain Injuries; Coronavirus Infections; COVID-19; Deamino Arginine Vasopressin; Dehydration; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Disease Management; Fluid Therapy; Humans; Hypernatremia; Hyponatremia; Hypotonic Solutions; Inappropriate ADH Syndrome; Neurosurgical Procedures; Pandemics; Pneumonia, Viral; Postoperative Complications; Practice Guidelines as Topic; Saline Solution; Shock

Central diabetes insipidus (CDI) is a rare disease during the neonatal period, making it diagnosis difficult and delaying medical treatment.. We report here a case of a premature infant born at 26 weeks gestation who, during his 1st month of life, presented persistent hypernatremia with polyuria despite increased fluid supply and low sodium intake. CDI diagnosis was suspected and then confirmed by the therapeutic test with vasopressin analog, in its oral form. Electrolyte disorders were normalized after treatment, which allowed normal weight and height growth with standard fluid supply. Biological and radiological tests were all normal; this CDI was considered idiopathic.. Persistent hypernatremia with excessive diuresis should alert to CDI diagnosis.

Topics: Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Humans; Hypernatremia; Infant, Extremely Premature; Infant, Newborn; Male

We describe a three-year-old boy who had a growth and psychomotor retardation associated with inappropriate lack of thirst and vasopressin secretion in the presence of chronic plasma hyperosmolarity. Computed brain tomography revealed bilateral supratentorial sub-ependymal and cortical calcifications. Dissociation in the plasma vasopressin response to osmotic change was demonstrated in this patient. Treatment with a vasopressin analogue, desamino-D-arginine vasopressin (DDAVP) and forced intake of water restored plasma osmolality and serum sodium levels to normal.

Topics: Antidiuretic Agents; Brain; Child, Preschool; Deamino Arginine Vasopressin; Humans; Hypernatremia; Male; Osmolar Concentration; Sodium; Syndrome; Thirst; Tomography, X-Ray Computed

Neonatal central diabetes insipidus (CDI) with or without adipsia is a very rare complication of various complex hypothalamic disorders. It is associated with greater morbidity and a high risk of developing both hypernatremia and hyponatremia, due to the condition itself or secondary to treatment with vasopressin analogs or fluid administration. Its outcomes have yet to be evaluated.. To investigate the clinical outcomes of patients with neonatal-onset CDI or adipsic CDI with hypernatremia.. All patients diagnosed with neonatal CDI in a university hospital-based observational study and followed between 2005 and 2015 were included and analyzed retrospectively.. The various causes of CDI were grouped. Clinical outcome and comorbidities were analyzed.. Ten of the 12 patients had an underlying condition with brain malformations: optic nerve hypoplasia (n = 3), septo-optic dysplasia (n = 2), semilobar holoprosencephaly (n = 1), ectopic neurohypophysis (n = 3), and unilateral absence of the internal carotid artery (n = 1). The other two were idiopathic cases. During the median follow-up period of 7.8 (4.9-16.8) years, all but one patient displayed anterior pituitary deficiency. Transient CDI was found in three (25%) patients for whom a posterior pituitary hyperintense signal was observed with (n = 2) and without (n = 1) structural hypothalamic pituitary abnormalities, and with no other underlying cerebral malformations. Patients with permanent CDI with persistent adipsia (n = 4) and without adipsia (n = 5) required adequate fluid intake and various doses of desamino-D-arginine-8-vasopressin. Those with adipsia were more likely to develop hypernatremia (45 vs 33%), hyponatremia (16 vs 4%) (P < .0001), and severe neurodevelopmental delay (P < .05) than those without adipsia. Comorbidities were common. The underlying cause remains unknown at the age of 23 years for one patient with CDI and normal thirst.. Neonatal CDI may be transient or permanent. These vulnerable patients have high rates of comorbidity and require careful monitoring.

Topics: Adolescent; Age of Onset; Child; Child, Preschool; Cohort Studies; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Drinking; Female; Humans; Hypernatremia; Hypoglycemic Agents; Hypothalamic Diseases; Infant; Infant, Newborn; Male; Pituitary Function Tests; Retrospective Studies; Sodium; Treatment Outcome

Central diabetes insipidus (CDI) is a rare cause of hypernatremia during the neonatal period. The diagnosis is particularly difficult in very low birth weight (VLBW) newborns.. We report on a preterm newborn who presented CDI soon after birth. On the third day of life, signs of dehydration were present despite normal fluid supply. The diuresis rate was 4.4 ml/kg/h. Although the fluid supply was then increased, the dehydration continued, with hypernatremia, normal glycemia, diuresis of 7.4 ml/kg/h and urine density of 1005 mOsmol/l. Thus, a diagnostic hypothesis of diabetes insipidus was raised. A test with a nasal vasopressin analogue (dDAVP) was performed and CDI was confirmed. Reduction of the fluid supply became possible through appropriate treatment.. The diagnosis of CDI is rarely made during the neonatal period, especially in VLBW newborns, because of the difficulty in detecting elevated diuresis. Persistent hypernatremia, usually accompanied by hyperthermia despite abundant fluid supply, weight loss and low urine osmolality are important signs of alert.

Topics: Administration, Intranasal; Deamino Arginine Vasopressin; Dehydration; Diabetes Insipidus, Neurogenic; Diuresis; Early Diagnosis; Female; Hemostatics; Humans; Hypernatremia; Infant, Newborn; Infant, Very Low Birth Weight; Male; Osmolar Concentration; Premature Birth; Treatment Outcome

Patients with cranial diabetes insipidus (CDI) are at risk of developing both hypernatraemia and hyponatraemia, due to the condition itself or secondary to treatment with vasopressin-analogues or during administration of i.v. fluids. We aimed to assess the frequency and impact of dysnatraemias in the inpatient (INPT) and outpatient (OPT) setting in desmopressin-treated CDI, comparing those with normal thirst with those with abnormal thirst.. The study included 192 patients with cranial diabetes, who were identified from the Beaumont Pituitary Database, a tertiary referral centre. Retrospective case note audit was performed and the clinical and biochemical information of 147 patients with CDI were available for analysis.. A total of 4142 plasma sodium measurements for 137 patients with normal thirst, and 385 plasma sodium measurements for ten patients with abnormal thirst were analysed. In those with normal thirst, the most common OPT abnormality was mild hyponatraemia (pNa(+) 131-134  mmol/l) in 27%, while 14.6% had more significant hyponatraemia (pNa(+) ≤130  mmol/l). Of those patients with normal thirst, 5.8% were admitted due to complications directly related to hyponatraemia. Compared with patients with normal thirst, those with abnormal thirst were more likely to develop significant OPT hypernatraemia (20% vs 1.4%, P=0.02) and significant INPT hyponatraemia (50% vs 11.1%, P 0.02).. OPT management of CDI is complicated by a significant incidence of hyponatraemia. In contrast, OPT hypernatraemia is almost exclusively a complication seen in adipsic CDI, who also had more frequent INPT hyponatraemia. CDI associated with thirst disorder requires increased physician attention and patient awareness of potential complications.

Topics: Adult; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hypernatremia; Hyponatremia; Male; Middle Aged; Retrospective Studies; Sodium; Young Adult

Dysnatremias are common and prognostically serious in neurocritical care. We studied whether a standardized sodium protocol would improve our neurocritical care of dysnatremias.. A 5-year prospective study of a standardized sodium protocol for 1,560 patients admitted with various brain diseases in an adult neurologic-neurosurgical intensive care unit (NNICU) was compared with a 5-year retrospective analysis of 1,440 patients without the sodium protocol. Hyponatremia was defined as serum sodium (SNa(+)) < 135 mmol/L and hypernatremia SNa(+ )> 150 mmol/L. The sodium protocol involved measuring SNa(+), serum, and urine osmolality, measured and calculated renal function parameters, fluid intake 40 mL/kg weight/day without hypotonic saline, thiazide, and desmopressin acetate in all normonatremic NNICU patients.. In the protocol study, hyponatremia occurred slightly less often (15.7 versus 16.3% of patients; p = 0.684), hypernatremia was significantly higher (respectively 8.5% versus 5.2% of patients; p < 0.001), and no differences were noted in hypo/hypernatremia (p = 0.483). There were no differences in the incidence of hypo-osmolal hyponatremia (respectively 3.5% versus 3.5% of patients; p = 0.987), cerebral salt wasting (CSW; respectively 1.7% versus 1.7% of patients; p = 0.883), syndrome of inappropriate secretion of antidiuretic hormone (SIADH; respectively 0.1% versus 0.3% of patients; p = 0.152), central diabetes insipidus (CDI; respectively 1.0% versus 0.6% of patients; p = 0.149). In hyponatremia there were no differences in the Glasgow Coma Scale (GCS) score upon onset of hyponatremia (p = 0.294), NNICU mortality (respectively 1.0% versus 0.4% patients; p = 0.074), and bad outcome upon discharge from NNICU (respectively 5.1% versus 6.5% of patients; p = 0.101), but in hypernatremia GCS score upon onset (p < 0.001), mortality (respectively 2.8% versus 1.0%; p < 0.001), and bad outcome from NNICU (respectively 6.7% versus 2.7% patients; p < 0.001) were significantly higher. Multivariate logistic regression analysis showed that hypernatremia, compared with hyponatremia, was a significant predictor of mortality during NNICU stay (respectively odds ratio [OR]: 1.14; p = 0.003 versus OR; 5.3; p = 0.002).. The standard sodium protocol lowered the frequency of SIADH, which was encountered in only one patient over 5 years. However, it did not significantly reduce the incidence and improve the outcome of hyponatremia. Hypernatremia occurred more often and had a higher mortality and worse outcome than hyponatremia, but these patients were neurologically worse upon its onset. The prospective study confirmed that CSW, SIADH, and CDI were not common in our neurocritical care.

Topics: Aged; Critical Care; Deamino Arginine Vasopressin; Diuretics; Female; Humans; Hypernatremia; Hyponatremia; Hypotonic Solutions; Iatrogenic Disease; Incidence; Male; Middle Aged; Nervous System Diseases; Osmolar Concentration; Prospective Studies; Renal Agents; Retrospective Studies; Sodium; Thiazides; Treatment Outcome

Central diabetes insipidus (CDI) is an infrequent complication of neurosarcoidosis (NS). Its presentation may be masked by adrenal insufficiency (AI) and uncovered by subsequent steroid replacement. A 45-year-old woman with a history of NS presented 2 weeks after abrupt cessation of prednisone with nausea, vomiting, decreased oral intake and confusion. She was diagnosed with secondary AI and intravenous hydrocortisone was promptly begun. Over the next few days, however, the patient developed severe thirst and polyuria exceeding 6 L of urine per day, accompanied by hypernatraemia and hypo-osmolar urine. She was presumed to have CDI due to NS, and intranasal desmopressin was administered. This eventually normalised her urine output and serum sodium. The patient was discharged improved on intranasal desmopressin and oral prednisone. AI may mask the manifestation of CDI because low serum cortisol impairs renal-free water clearance. Steroid replacement reverses this process and unmasks an underlying CDI.

Topics: Adrenal Insufficiency; Antidiuretic Agents; Central Nervous System Diseases; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Female; Glucocorticoids; Humans; Hydrocortisone; Hypernatremia; Middle Aged; Polyuria; Prednisone; Sarcoidosis; Thirst

To assess the efficiency of oral desmopressin lyophilisate (ODL) in neonatal central diabetes insipidus (CDI).. The characteristics of four newborns with CDI treated with ODL were evaluated.. Four newborns with polyuria and hypernatremia were included [male, 2 (50%); mean postnatal age, 19±17 days]. At the time of hypernatremia, the mean serum and urine osmolality values were 310±16 and 179±48 mOsm/kg, respectively. Antidiuretic hormone levels were undetectable (<0.5 pmol/L) in all cases. Magnetic resonance imaging revealed anatomical malformations in all cases. ODL (60 μg/tablet) dissolved in water (3-5 mL) was initiated with a dose of 5 μg/kg/day in two equal doses, together with limitation of water intake to avoid hyponatremia. Serum sodium levels returned to normal in a mean duration of 58±9.9 h with a mean decline rate of 0.37±0.1 mEq/L/h after desmopressin administration. Rehospitalization was required for one of the infants because of hypernatremia due to non-compliance. No episode of hyponatremia was encountered. Weight gain and growth of the infants were normal during the mean follow-up duration of 8.5±1 months.. ODL appears to be practical and safe in the treatment of CDI during the first year of life.

Topics: Administration, Oral; Antidiuretic Agents; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Dose-Response Relationship, Drug; Humans; Hypernatremia; Infant; Infant, Newborn; Male; Polyuria; Treatment Outcome

Gestational diabetes insipidus is a rare, transient complication of pregnancy typically characterized by polyuria and polydipsia that may lead to mild electrolyte abnormalities. More severe sequelae of gestational diabetes insipidus are uncommon.. We present a case of a 25-year-old woman at 23 weeks of gestation in a dichorionic-diamniotic twin pregnancy who developed severe symptomatic gestational diabetes insipidus complicated by rhabdomyolysis and death of both fetuses.. Maternal rhabdomyolysis caused by gestational diabetes insipidus is extremely rare. Early recognition and treatment of gestational diabetes insipidus is necessary to prevent maternal and fetal morbidity and mortality.

Topics: Adult; Antidiuretic Agents; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Fetal Death; Humans; Hypernatremia; Polyuria; Pregnancy; Pregnancy Complications; Pregnancy, Twin; Rhabdomyolysis

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

Topics: Antidiuretic Agents; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Female; Humans; Hypernatremia; Infant; Magnetic Resonance Imaging; Osmolar Concentration

Topics: Antidiuretic Agents; Cerebral Hemorrhage; Deamino Arginine Vasopressin; Diabetes Insipidus; Humans; Hypernatremia; Infant, Newborn; Infant, Premature, Diseases; Infant, Very Low Birth Weight; Male

Topics: Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Equipment Failure; Humans; Hypernatremia; Magnetic Resonance Imaging; Nebulizers and Vaporizers; Renal Agents

Patients requiring CSF shunts frequently have comorbidities that can influence water and electrolyte balances. The authors report on a case involving a ventriculoperitoneal shunt in a patient who underwent intravenous hyperhydration and withdrawal of vasopressin substitution prior to scheduled high-dose chemotherapy regimen for a metastatic suprasellar germinoma. After acute neurological deterioration, the patient underwent CT scanning that demonstrated ventriculomegaly. A shunt tap revealed no flow and negative opening pressure. Due to suspicion of proximal shunt malfunction, the comatose patient underwent immediate surgical exploration of the ventricle catheter, which was found to be patent. However, acute severe hypernatremia was diagnosed during the procedure. After correction of the electrolyte disturbances, the patient regained consciousness and made a good recovery. Although rare, the effects of acute severe hypernatremia on brain volume and ventricular size should be considered in the differential diagnosis of ventriculoperitoneal shunt failure.

Topics: Acute Disease; Adult; Antidiuretic Agents; Antineoplastic Agents; Astrocytoma; Brain Stem Neoplasms; Cerebral Ventricles; Chemotherapy, Adjuvant; Cranial Irradiation; Deamino Arginine Vasopressin; Diagnosis, Differential; Diagnostic Errors; Equipment Failure Analysis; Fluid Therapy; Humans; Hydrocephalus; Hypernatremia; Hypertrophy; Male; Neoplasms, Multiple Primary; Pituitary Neoplasms; Postoperative Complications; Substance Withdrawal Syndrome; Tectum Mesencephali; Tomography, X-Ray Computed; Ventriculoperitoneal Shunt

Topics: Adrenal Insufficiency; Antidiuretic Agents; Breast Neoplasms; Carcinoma, Ductal, Breast; Deamino Arginine Vasopressin; Diabetes Insipidus; Diagnosis, Differential; Dizziness; Fatal Outcome; Female; Humans; Hydrocortisone; Hypernatremia; Lymphatic Diseases; Middle Aged; Muscle Weakness; Tomography, X-Ray Computed

Hyponatremic encephalopathy is a potentially lethal condition with numerous reports of death or permanent neurological injury. The optimal treatment for hyponatremic encephalopathy remains controversial. We have introduced a unified approach to the treatment of hyponatremic encephalopathy which uses 3% NaCl (513 mEq/L) bolus therapy. Any patient with suspected hyponatremic encephalopathy should receive a 2 cc/kg bolus of 3% NaCl with a maximum of 100 cc, which could be repeated 1-2 times if symptoms persist. The approach results in a controlled and immediate rise in serum sodium with little risk of inadvertent overcorrection.

Topics: Brain; Brain Diseases, Metabolic; Deamino Arginine Vasopressin; Dose-Response Relationship, Drug; Drug Overdose; Humans; Hypernatremia; Hyponatremia; Iatrogenic Disease; Sodium Chloride

Dysnatremias (hypo- and hypernatremia) are common in patients admitted to the intensive care unit (ICU) with a prevalence approaching 20-30% in some studies. Recent data reveals that both hypo- and hypernatremia present on admission to or developing in the ICU are independent risk factors for poor prognosis. The origin of hypernatremia in the ICU is often iatrogenic and due to inadequate free water replacement of ongoing water losses. The pathogenesis of hyponatremia in the ICU is more complicated but often is related to the combination of dysregulated arginine vasopressin production and concomitant inappropriate hypotonic fluid administration. Both the dysnatremia itself and the treatment of the electrolyte disturbance can be associated with morbidity and mortality making careful monitoring for and treatment of sodium disorders an imperative in the critically ill patient. Formulae have been devised to guide the therapy of severe hypo- and hypernatremia, but these formulae regard the patient as a closed system and do not take into account ongoing fluid losses that can be highly variable. Thus, a cornerstone of proper therapy is serial measurements of serum and urine electrolytes. The appropriate use of hypertonic (3%) saline in the treatment of hyponatremic encephalopathy has also shown to be very effective and the use of this therapy is reviewed here. Vasopressin receptor antagonists have also been shown to be effective at increasing serum sodium levels in patients with either euvolemic or hypervolemic hyponatremia and represent another therapeutic option. Recent data demonstrates that proper correction of hyponatremia is associated with improved short- and long-term outcomes.

Topics: Austria; Body Water; Deamino Arginine Vasopressin; Fluid Therapy; Humans; Hypernatremia; Hypertonic Solutions; Hyponatremia; Intensive Care Units; Prevalence; Prognosis; Risk Factors; Sodium

Diabetes insipidus (DI) is a well documented complication observed after traumatic head injuries. We report a case of hyperacute onset DI in a 19-year-old male who sustained a hypothalamic-pituitary injury when he was stabbed in the head with a 30-cm long thin-bladed knife. At CT, our patient showed significant hemorrhagic contusions of the lower hypothalamus. He developed polydipsia, polyuria, and mild hypernatremia in the Emergency Department. Diagnostic digital subtraction angiography showed a hypervascular congestive pituitary gland with prominent draining veins. On the third day his hypernatremia became severe (183mEq/L). He was managed with parenteral fluids and a regimen of intranasal DDAVP (1-desamino 8-d-arginine vasopressin), leading to improved plasmatic sodium levels, urine output, and urinary specific gravity. In patients presenting with hyperacute posttraumatic DI, emergency room physicians and neurosurgeons should rule out direct injury to the hypothalamus and/or the posterior lobe of the pituitary, and initiate early pharmacological treatment.

Topics: Acute Disease; Brain Injuries; Confusion; Craniocerebral Trauma; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Humans; Hypernatremia; Hypoglycemic Agents; Hypothalamo-Hypophyseal System; Hypothalamus; Magnetic Resonance Angiography; Magnetic Resonance Imaging; Male; Polyuria; Tomography, X-Ray Computed; Wounds, Stab; Young Adult

Essential hypernatremia is very rare in clinical practice and the pathogenesis is unclear. We performed a set of clinical tests to a patient with chronic and sustained hypernatremia as well as absence of thirst in order to investigate the clinical characteristics and make the diagnosis, yet most importantly to analyze the possible pathogenesis and explore a possible therapy regime.. Water deprivation test and acute water intravenous loading test were performed to observe the changes of urinary osmolality, plasma osmolality and plasma sodium. Free water clearance (C(H₂O) was calculated. Osmolality was detected using the method of freezing point depression, and thirst grade using visual analogue scales. Desmopressin acetate (0.05-0.1 mg/d) was administered to the patient in order to observe the therapeutic effects to his disorder.. The patient had sustained hypernatremia over a long period of time, decreased thirst, normal renal function, as well as absence of clinical hypovoluemia. The plasma sodium was 160-190 mmol/L and plasma osmolality was 330-370 mOsm/L without any thirst perception which could not be corrected by water intake. An 18-hour period of water deprivation increased the urinary osmolality from 368 mOsm/L to 420 mOsm/L with plasma osmolality increasing from 362 mOsm/L to 369 mOsm/L and rising further to 857 mOsm/L after an injection of 5 u vasopresin. With the infusion of 1 250 ml 5%-glucose during 2 hours in an acute water loading test setting, plasma osmolality decreased from 350 mOsm/L to 334 mOsm/L associated with a plasma sodium decrease from 164.7 mmol/L to 155 mmol/L urinary osmolality dropped from a maximum of 632 mOsm/L to 135 mOsm/L urinary volume from 0.25 ml/min to 2.33 ml/min and C(H₂O) from -0.18 ml/min to 1.19 ml/min after acute water loading with 1 250 ml glucose dissolved in water. Our results reveal that treatment of the patient with Desmopressin acetate relieved the adypsia, hypernatremia and hyperosmolality effectively.. The patient was considered as suffering from essential hypernatremia which was associated with partial central diabetes insipidus and adypsia. Desmopressin acetate as a common therapeutic agent of central diabetes insipidus proved to be an effective treatment for essential hypernatremia.

Topics: Adolescent; Antidiuretic Agents; Arginine Vasopressin; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Drinking; Humans; Hypernatremia; Male; Osmolar Concentration; Severity of Illness Index; Sodium; Treatment Outcome; Water Deprivation

The study was aimed at verifying whether the occurrence of hypernatremia during the intensive care unit (ICU) stay increases the risk of death in patients with severe traumatic brain injury (TBI). We performed a retrospective study on a prospectively collected database including all patients consecutively admitted over a 3-year period with a diagnosis of TBI (post-resuscitation Glasgow Coma Score < or = 8) to a general/neurotrauma ICU of a university hospital, providing critical care services in a catchment area of about 1,200,000 inhabitants.. Demographic, clinical, and ICU laboratory data were prospectively collected; serum sodium was assessed an average of three times per day. Hypernatremia was defined as two daily values of serum sodium above 145 mmol/l. The major outcome was death in the ICU after 14 days. Cox proportional-hazards regression models were used, with time-dependent variates designed to reflect exposure over time during the ICU stay: hypernatremia, desmopressin acetate (DDAVP) administration as a surrogate marker for the presence of central diabetes insipidus, and urinary output. The same models were adjusted for potential confounding factors.. We included in the study 130 TBI patients (mean age 52 years (standard deviation 23); males 74%; median Glasgow Coma Score 3 (range 3 to 8); mean Simplified Acute Physiology Score II 50 (standard deviation 15)); all were mechanically ventilated; 35 (26.9%) died within 14 days after ICU admission. Hypernatremia was detected in 51.5% of the patients and in 15.9% of the 1,103 patient-day ICU follow-up. In most instances hypernatremia was mild (mean 150 mmol/l, interquartile range 148 to 152). The occurrence of hypernatremia was highest (P = 0.003) in patients with suspected central diabetes insipidus (25/130, 19.2%), a condition that was associated with increased severity of brain injury and ICU mortality. After adjustment for the baseline risk, the incidence of hypernatremia over the course of the ICU stay was significantly related with increased mortality (hazard ratio 3.00 (95% confidence interval: 1.34 to 6.51; P = 0.003)). However, DDAVP use modified this relation (P = 0.06), hypernatremia providing no additional prognostic information in the instances of suspected central diabetes insipidus.. Mild hypernatremia is associated with an increased risk of death in patients with severe TBI. In a proportion of the patients the association between hypernatremia and death is accounted for by the presence of central diabetes insipidus.

Topics: Brain Injuries; Deamino Arginine Vasopressin; Female; Hospitals, University; Humans; Hypernatremia; Incidence; Intensive Care Units; Male; Middle Aged; Proportional Hazards Models; Retrospective Studies; Severity of Illness Index

Adherence to therapeutic guidelines for the treatment of hyponatremia becomes difficult when water diuresis emerges during therapy. The objective of this study was to assess the effectiveness and safety of desmopressin acetate as a therapeutic agent to avoid overcorrection of hyponatremia and to lower the plasma sodium concentration again after inadvertent overcorrection.. Retrospective chart review was conducted of all patients who were given desmopressin acetate during the treatment of hyponatremia during 6 yr in a 528-bed community teaching hospital.. Six patients (group 1) were given desmopressin acetate after the 24-h limit of 12 mmol/L had already been reached or exceeded; correction was prevented from exceeding the 48-h limit of 18 mmol/L in five of the six. Fourteen patients (group 2) were given desmopressin acetate in anticipation of overcorrection after the plasma sodium concentration had increased by 1 to 12 mmol/L. In all 14 patients who were treated with desmopressin acetate as a preventive measure, correction was prevented from exceeding either the 24- or 48-h limits. After desmopressin acetate was administered, the plasma sodium concentration of 14 of the 20 patients fell by 2 to 9 mmol/L. In all six group 1 patients and in five of the group 2 patients, the plasma sodium concentration was actively lowered again by the concurrent administration of desmopressin acetate and 5% dextrose in water; no serious adverse consequences from this maneuver were observed.. Desmopressin acetate is effective in preventing and reversing inadvertent overcorrection of hyponatremia.

Topics: Adult; Aged; Aged, 80 and over; Antidiuretic Agents; Deamino Arginine Vasopressin; Female; Humans; Hypernatremia; Hyponatremia; Male; Middle Aged; Retrospective Studies

In this case report we describe the management of severe hypernatraemia following inadvertent water restriction. A 21-year-old woman with no reported medical history presented on transfer from an outside hospital with a complex volar upper extremity injury. Management both operatively and postoperatively involved a prolonged period of fasting which limited her access to drinking water Collateral history revealed that she had previously drunk copious amounts of water during the course of any given day and this had served to alleviate the dramatic symptoms of hypernatraemia that were rapidly manifest when her normal intake was curtailed. We outline the fluid management, administration of desmopressin and her subsequent recovery. A literature review of the management of central diabetes insipidus is also covered.

Topics: Adult; Brain; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hypernatremia; Intraoperative Complications; Magnetic Resonance Imaging; Osmolar Concentration; Renal Agents; Resuscitation; Sodium; Tendon Injuries

Hypernatraemia over 160 mmol/L is considered to be severe. This case reports a patient who developed extreme hypernatraemia with a serum sodium concentration of 196 mmol/L. The patient was known to have chronic renal impairment and was admitted with acute deterioration of renal function secondary to dehydration. This was considered to be secondary to poor oral fluid intake (related to depression) and lithium-induced nephrogenic diabetes insipidus with salt-losing nephropathy. The patient had a high urinary sodium excretion but was also in a pure water losing state as evidenced by an inappropriately low urine osmolality for the plasma osmolality and was successfully treated with hypotonic intravenous fluid and desmopressin.

Topics: Bipolar Disorder; Deamino Arginine Vasopressin; Dehydration; Depression; Diabetes Insipidus, Nephrogenic; Female; Humans; Hypernatremia; Hypotonic Solutions; Infusions, Intravenous; Lithium Carbonate; Middle Aged; Renal Insufficiency, Chronic; Treatment Outcome

Central pontine myelinolysis (CPM) is a serious demyelination disease commonly associated with the rapid correction of hyponatremia. Although its pathogenesis remains unclear, the disruption of the blood-brain barrier (BBB) as a consequence of a rapid increase in serum sodium concentration is considered to play a critical role. Since glucocorticoids are known to influence BBB permeability and prevent its disruption as a result of hypertension or hyperosmolarity, we investigated whether dexamethasone (DEX) could protect against osmotic demyelination in an animal model of CPM. Hyponatremia was induced in rats by liquid diet feeding and dDAVP infusion. Seven days later, the animals' hyponatremia was rapidly corrected by injecting a bolus of hypertonic saline intraperitoneally. Rats subjected to this treatment displayed serious neurological impairment and 77% died within 5 days of rapid correction of their hyponatremia; demyelinative lesions were observed in various brain regions in these animals. On the other hand, rats that were treated with DEX (2 mg/kg, 0 and 6 h after hypertonic saline injection) exhibited minimal neurological impairment and all were alive after 5 days. Demyelinative lesions were rarely seen in the brains of DEX-treated rats. A marked extravasation of endogenous IgG was observed in the demyelinative lesions in the brains of rats that did not receive DEX, indicating disruption of the BBB, but was not observed in DEX-treated rats. Furthermore, Evans blue injection revealed a significant reduction in staining in the brains of DEX-treated rats (P < 0.05). These results indicate that early DEX treatment can prevent the BBB disruption that is caused by the rapid correction of hyponatremia and its associative demyelinative changes, and suggest that DEX might be effective in preventing CPM.

Topics: Animals; Blood-Brain Barrier; Brain; Deamino Arginine Vasopressin; Dexamethasone; Disease Models, Animal; Hypernatremia; Hyponatremia; Immunoglobulin G; Male; Myelinolysis, Central Pontine; Nerve Fibers, Myelinated; Rats; Rats, Sprague-Dawley; Saline Solution, Hypertonic; Water-Electrolyte Balance

We report a 42-year-old woman with severe motor and intellectual disabilities (SMID) who showed partial central diabetes insipidus during severe pneumonia. Serum sodium levels were previously within the upper normal range from 140 to 147 mEq/L. During pneumonia, however, serum sodium rose rapidly to reach 185 mEq/L. The daily urinary volume exceeded the daily intake of water. Nasal administration of 1-desamino-8-D-arginine vasopressin (DDAVP) reduced the daily urinary volume and the serum sodium level to normal ranges. Consequently, we diagnosed her as having central diabetes insipidus (DI). She required a smaller dose of DDAVP (2.5 microg/day) than usual DI (5-15 microg/day) to maintain normal urinary volume and the serum sodium level for seven months. After the nasal administration of DDAVP was discontinued, the serum sodium levels again returned to within the upper normal range. A water deprivation study demonstrated poor elevation of both plasma antidiuretic hormone (ADH) level (range, 0.5-2.0 pg/ml) and urine osmolarity (peak level, 552 mOsm/kgH2O) despite the elevation of plasma osomolarity, suggesting latent partial central DI. Water balance and serum electrolyte levels should be closely monitored in cases of SMID.

Topics: Adult; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Female; Humans; Hypernatremia; Hypothalamic Diseases; Persons with Mental Disabilities; Pituitary Diseases; Pneumonia; Severity of Illness Index; Water-Electrolyte Balance

Transient diabetes insipidus is an uncommon complication of pregnancy, usually manifesting with polydipsia and polyuria. This condition is considered to result from excess placental vasopressinase activity and is managed with deamino D arginine vasopressin.. While on restricted oral intake after cesarean delivery, the patient gradually became disoriented and agitated in conjunction with markedly increased urine output disproportional to her intravenous crystalloid fluid intake. Marked hypernatremia of 178 mEq/dL was noted. Urine osmolality was low at 248 mOsm/L. The clinical presentation and electrolyte abnormalities were considered consistent with transient diabetes insipidus of pregnancy. The patient responded well to nasal-spray-administered deamino D arginine vasopressin and increased intravenous fluid intake, with resolution of symptoms and gradual normalization of serum sodium levels.. Transient diabetes insipidus of pregnancy should be considered in the differential diagnosis of severe hypernatremia in obstetric patients with restricted oral intake after operative delivery.

Topics: Adult; Cesarean Section; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Fluid Therapy; Humans; Hypernatremia; Postoperative Care; Postoperative Complications; Pregnancy; Pregnancy Complications

A 41-year-old woman who had undergone transfrontal craniotomy for a pituitary tumor 4 months before presentation was admitted with confusion and orientation only to self. She had a fever of 40 degrees C. Serum sodium and chloride levels on admission were 180 and 139 mEq/L, respectively. Measured serum osmolality was 380 mOsmol/L with a urine osmolality of 360 mOsmol/L. Magnetic resonance imaging revealed a 1.5-cm mass in the sella turcica, which was nonfunctioning on endocrine evaluation. The "bright spot" of a normal posterior pituitary was absent. Central diabetes insipidus was confirmed by a 300% increase in urine osmolality with desmopressin. The patient survived her severe hypernatremia, which has 70% mortality with a serum sodium level of 160 mEq/L or above. However, she developed permanent (6 months) disorientation to time and place even when hypernatremia was corrected, which has not been described previously.

Topics: Adult; Confusion; Craniopharyngioma; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Female; Humans; Hypernatremia; Magnetic Resonance Imaging; Pituitary Gland; Pituitary Neoplasms; Renal Agents; Sella Turcica

Hypodipsic hypernatremia (HH) represents a pathological increase in serum sodium due to a lack of thirst and defect in hypothalamic osmoreceptors. While 15% of patients with HH have a vascular aetiology, few cases have been described. Moreover, the presence of such abnormalities in the amnestic patient can have particularly threatening implications, as HH tends to recur unless the patient complies with a regimen of water intake. This study reports the case of a 46-year-old male admitted for rehabilitation of functional deficits following subarachnoid haemorrhage (SAH), with clipping of an anterior communicating artery (ACoA) aneurysm. Clinical examination was remarkable for profound short-term memory loss and inability to retain new information. Blood chemistry on admission showed a serum sodium level of 160 mEq/L, increasing to 167 mEq/L the following day. The patient denied thirst, and showed no clinical signs of dehydration. Neuroendocrine evaluation revealed diabetes insipidus (DI) and HH. Treatment initially included DDAVP and intravenous hydration, later supplemented with chlorpropramide. Stabilization of serum sodium and osmolality did not ensue until the treatment regimen included hydrochlorothiazide and supervision of enforced fluid intake. Endocrine abnormalities may be encountered among patients with vascular lesions adjacent to the hypothalamus. Rehabilitation interventions include establishing a structured medication regimen with fluid administration in the amnestic patient with hypothalamic dysfunction.

Topics: Amnesia, Anterograde; Chlorpropamide; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuretics; Drinking Behavior; Drug Administration Schedule; Fluid Therapy; Humans; Hydrochlorothiazide; Hypernatremia; Hypoglycemic Agents; Intracranial Aneurysm; Male; Middle Aged; Postoperative Complications; Renal Agents; Subarachnoid Hemorrhage; Thirst

We present here a case of prominent hypercalcemia accompanied by hypothalamic tumor and Graves' disease. A 24-year-old man with hypothalamic tumor showed hypopituitarism, central diabetes inspidus (DI) and hyperthyroidism. Nausea, loss of thirst and appetite, and general fatigue were found with the unveiling of hypercalcemia and hypernatremia. Parathyroid hormone (PTH) and 1alpha-dihydroxyvitamin D levels were suppressed with a normal range of PTH-related protein values. One-desamino-(8-D-arginine)-vasopressin (DDAVP) and half-saline administration normalized hypernatremia, while hypercalcemia was still sustained. Administration of cortisone acetate and thiamazole reduced the elevated serum Ca level. In the present case, concurrent hyperthyroidism was assumed to accelerate skeletal mobilization of calcium into the circulation. Hypocortisolism and central DI was also considered to contribute, to some extent, to the hypercalcemia through renal handling of Ca.

Topics: Adult; Antithyroid Agents; Calcitriol; Calcium; Cortisone; Craniotomy; Deamino Arginine Vasopressin; Diabetes Insipidus; Drug Therapy, Combination; Germinoma; Graves Disease; Humans; Hypercalcemia; Hypernatremia; Hyperthyroidism; Hypopituitarism; Hypothalamic Neoplasms; Magnetic Resonance Imaging; Male; Methimazole; Parathyroid Hormone; Parathyroid Hormone-Related Protein; Peptide Fragments; Proteins; Renal Agents; Sodium; Teratoma

In the differential diagnosis of patients with polyuria-polydipsia one must distinguish usually between primary polydipsia (PP) and central diabetes insipidus (CDI). The first situation is a state of volume expansion and the second of volume contraction. We evaluate whether serum uric acid determination could help to differentiate between the two conditions.. We analyzed the score of 13 consecutive patients with CDI, 7 patients with PP, and 7 patients with nephrogenic diabetes insipidus (NDI). Serum uric acid concentration was available during normonatremia without treatment with 1-desamino-8-D-arginine vasopressin (dDAVP), during mild dehydration and during treatment with dDAVP. In 8 of these patients plasma renin activity (PRA), urate, urea and creatinine clearances were also available. These data were also obtained in the patients with NDI. In 1 patient with CDI, we studied the effect on urate clearance of dDAVP, which stimulates exclusively the V2 receptors, and of triglycyl-lysine-vasopressin (TGLV), a potent V1-receptor agonist.. Normonatremic polydypsic patients with CDI presented an increase in uric acid concentration (7.1 +/- 2.2 mg/dL), whereas in the PP group the value was decreased (3 +/- 0.75 mg/dL; P <0.001). All the normonatremic PP presented a serum uric acid concentration lower than 5 mg/dL, whereas all the normonatremic CDI patients, exept 1, presented a value higher than 5 mg/dL. In both groups blood urea concentration was decreased as a consequence of high renal clearances. The hyperuricemia of CDI was related to low uric acid clearances. Patients with hypernatremia and NDI presented a lower increase in serum uric acid concentration than those with similar levels of hypernatremia and CDI (NDI: 5.7 +/- 0.8 mg/dL and CDI: 7.9 +/- 2.3 mg/dL; P <0.05) and the NDI patients presented an urate clearance corrected for creatinine clearance which was significantly higher than in CDI (9% +/- 3% and 4% +/- 1.1%; P <0.01). When the patients with CDI were treated with dDAVP and normalyzed their PRA (0.9 +/- 0.4 ng/mL/h) we observed still mild hyperuricemia compared to controls (5.5 +/- 1.4 mg/dL and 4.3 +/- 0.9 mg/dL; P <0.01) and a low fractional excretion of filtered uric acid (6.5% +/- 1.7% compared to 8.2% +/- 2% in controls; P <0.05). Acute administration of dDAVP, stimulating the V2 receptors, in one patient with CDI, had no effect on urate clerance, while TGLV, which stimulates the V1 receptor, increased urate clearance.. The presence of an serum uric acid concentration higher than 5 mg/dL in polyuric polydipsic patients is highly suggestive of CDI. Even when these patients are treated with dDAVP many of them remain hyperuricemic, and this seems to be the consequence of a lack of V1 receptor stimulation.

Topics: Adult; Antihypertensive Agents; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diagnosis, Differential; Drinking; Female; Humans; Hypernatremia; Lypressin; Male; Medical Records; Renal Agents; Retrospective Studies; Sodium; Terlipressin; Uric Acid

Axonal injury to hypothalamic magnocellular vasopressin (AVP) and oxytocin (OT) neurons causes degeneration of a substantial subpopulation of these neurons. In this study, we investigated the influence of osmolality on this injury-induced cell death. Normonatremic, chronically hypernatremic, and chronically hyponatremic rats received pituitary stalk compression (SC), which causes degeneration of AVP and OT terminals in the neurohypophysis. Twenty-one days after SC, rats were perfused and hypothalami were serially sectioned and alternately stained for AVP-neurophysin and OT-neurophysin immunoreactivities. Normonatremic and hypernatremic rats exhibited a triphasic pattern of water intake after SC, with peak intakes 3 times higher than those exhibited by sham-operated normonatremic rats. In contrast, hyponatremic SC rats exhibited peak water intakes of 600 ml/24 hr, approximately 9-10 times the water intakes of sham-operated normonatremic rats. In normonatremic rats, SC caused degeneration of 65% of the AVP neuron population in the SON and 73% in the PVN, but only 31% of the OT neuron population in the SON and 35% in the PVN. Similar results were found in hypernatremic rats after SC. However, in hyponatremic rats SC caused degeneration of 97% of the AVP neuron population in the SON and 93% in the PVN, and 90% of the OT neuron population in the SON and 84% in the PVN. Our results, therefore, demonstrate that injury-induced degeneration of magnocellular AVP and OT neurons is markedly exacerbated by chronic hypo-osmolar conditions, but neuronal survival is not enhanced by chronic hyperosmolar conditions.

Topics: Animals; Axons; Cell Count; Cell Death; Cell Survival; Deamino Arginine Vasopressin; Drinking; Hypernatremia; Hyponatremia; Male; Nerve Degeneration; Neurons; Oxytocin; Rats; Rats, Sprague-Dawley; Sodium; Sodium Chloride; Time Factors; Vasopressins

Both central diabetes insipidus (DI) and a high rate of excretion of sodium (Na) and chloride (Cl) contributed to the development of polyuria and dysnatremia in two patients during the acute postoperative period after neurosurgery. To minimize difficulties in diagnosis and projections for therapy, two available (but not often used) clinical tools were helpful. First, the osmole excretion rate early on revealed the co-existence of central DI and an osmotic diuresis. The osmoles excreted were largely Na salts; after antidiuretic hormone acted, this electrolyte diuresis caused the urine flow rate to be much higher than otherwise anticipated. Interestingly, part of this saline diuresis occurred when the extracellular fluid volume was contracted. The tool to explain the basis for the dysnatremias was a tonicity balance. Hypernatremia, which developed before treatment of central DI, was primarily a result of a positive balance for Na rather than a large negative balance for water. Moreover, hyponatremia that developed once antidiuretic hormone acted was primarily a result of a negative balance for Na; the urine volume was large and its Na concentration was hypertonic. To prevent a further decline in the plasma Na concentration, either the Na concentration in the urine should be decreased by provision of urea or a loop diuretic while replacing all unwanted water and electrolyte losses; alternatively, the fluid infused should have a similar Na concentration and volume as the urine (infuse hypertonic saline).

Topics: Adult; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuresis; Female; Humans; Hypernatremia; Hyponatremia; Male; Natriuresis; Osmosis; Postoperative Complications; Sodium; Vasopressins

Topics: Adult; Blood Glucose; Brain Edema; Brain Neoplasms; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Mellitus, Type 1; Diabetic Coma; Diabetic Ketoacidosis; Diagnosis, Differential; Fatal Outcome; Female; Fluid Therapy; Headache; Humans; Hypernatremia; Insulin; Polyuria; Postoperative Complications; Radiography

We present two patients with known sarcoidosis who developed neurosarcoidosis manifested by paranoid psychosis and clinical diabetes insipidus with hypernatremia. Both had gadolinium enhanced magnetic resonance imaging which demonstrated leptomeningeal and hypothalamic enhancement. Both had elevated protein and a lymphocytosis in their cerebrospinal fluid, which improved after corticosteroid therapy. The patients improved clinically with this therapy as well. We suggest that new onset psychosis in a sarcoid patient, particularly with symptoms of hypothalamic/pituitary involvement, should be evaluated for neurosarcoidosis with an MRI and CSF examination. If the results are consistent with neurosarcoidosis, the patient should be treated promptly with corticosteroids.

Topics: Adult; Benzothiadiazines; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuretics; Female; Humans; Hypernatremia; Magnetic Resonance Imaging; Male; Nervous System Diseases; Paranoid Disorders; Sarcoidosis; Sodium Chloride Symporter Inhibitors

Topics: Acute Disease; Adult; Arginine Vasopressin; Deamino Arginine Vasopressin; Female; Humans; Hypernatremia; Postpartum Period; Pregnancy; Pregnancy Complications

Hypothalamic osmoreceptor dysfunction resulting in hypodipsia and altered regulation of vasopressin secretion is well established as the pathogenetic mechanism in the syndrome of 'essential hypernatremia'. However, little is known about the secretory pattern of atrial natriuretic peptide (ANP) in this syndrome. Therefore, we assessed ANP regulation by determining ANP concentrations in a patient manifesting this syndrome of essential hypernatremia during several well-established experimental protocols. The serum ANP level was within normal limits despite severe euvolemic hypernatremia (serum Na+ 163 mEq/l) during one of the many admissions and remained unchanged following normalization of serum Na+. Furthermore, a decline in serum ANP instead of an appropriate rise was noted when hypernatremia (serum Na+ 152 mEq/l) was induced by either hypertonic (3%) saline infusion or following a high-Na+ (300 mEq/day) diet for several days (serum Na+ 161 mEq/l). Similarly, exogenous pitressin administration failed to cause a rise in ANP, although an appropriate fall in ANP concentration occurred following fluid deprivation. Therefore, it is apparent that ANP regulation may be significantly altered in essential hypernatremia. However, further studies are required to define whether it plays a role in the pathogenesis of hypernatremia in this syndrome.

Topics: Adult; Arginine Vasopressin; Atrial Natriuretic Factor; Deamino Arginine Vasopressin; Fluid Therapy; Humans; Hypernatremia; Hypothalamus; Male; Saline Solution, Hypertonic; Sodium; Sodium, Dietary; Thirst; Water-Electrolyte Balance

Vasopressin is synthesized in the perikarya of magnocellular neurons and is transported down long axons to the storage terminals of the posterior pituitary. To maintain stable pituitary stores following vasopressin secretion, the hypothalamus must synthesize and transport an amount of new vasopressin, equivalent to the amount released. Vasopressin release and synthesis rate can be chronically upregulated or suppressed relative to basal levels, depending on the demand for vasopressin. We studied whether vasopressin transport was similarly regulated during situations of varying demand. During chronic hyponatremia, when synthesis of vasopressin was reduced to undetectable levels, transport of vasopressin was also markedly decreased, as evidenced by continued presence of vasopressin in the transport system. Upregulation of transport was demonstrated by measuring pituitary accumulation of vasopressin in rats whose pituitary stores were initially depleted by hypernatremia and in whom subsequent release was suppressed by hyponatremia. In hypernatremic rats, transport of vasopressin was increased fivefold over baseline as determined by pituitary accumulation, and this elevated rate persisted for 7 days in the absence of release. This study demonstrates that axonal transport of vasopressin is a regulated process and is linked to synthesis rate rather than release.

Topics: Animals; Biological Transport; Colchicine; Deamino Arginine Vasopressin; Hypernatremia; Hyponatremia; Hypothalamus; Male; Pituitary Gland; Rats; Rats, Inbred Strains; Sodium Chloride; Vasopressins

Topics: Adolescent; Brain Neoplasms; Child; Child, Preschool; Craniopharyngioma; Craniotomy; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuresis; Female; Humans; Hypernatremia; Male; Osmolar Concentration

The clinical and neuroradiological findings in a case of semilobar holoprosencephaly associated to hypernatremia behaving like diabetes insipidus are described. The differential diagnosis with a neurogenic hypernatremia is discussed. The advantages of ultrasounds in the diagnosis of this malformation are pointed out. So are the characteristics which differentiate it from other neurological malformations and the importance of a dorsal sac to delimitate the more serous clinical forms.

Topics: Abnormalities, Multiple; Brain; Deamino Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hypernatremia; Infant; Sodium; Tomography, X-Ray Computed; Ultrasonography

A male, aged 16, with chronic hypernatremia, adipsia, polyphagia, and poikilothermia was studied regarding regulation and secretion of arginine vasopressin. During recumbency at night, low plasma arginine vasopressin levels and increased volumes of dilute urine were found; whereas plasma arginine vasopressin levels and urine osmolalities rose and urine volumes decreased during ambulation in the daytime. Neither a 25% reduction of mean arterial pressure nor hypertonic saline infusion increased plasma arginine vasopressin or urine osmolalities. Treatment with 1-desamino-D-arginine-vasopressin at 6 p.m. and a scheduled fluid intake according to actual body weight eradicated hypernatremia and hyperosmolality. These data demonstrate a complete loss of arginine vasopressin secretion to osmotic stimulation, a partial defect of arginine vasopressin secretion to non-osmotic stimulation, an abolished response to stimulation of high-pressure-baroreceptors, but an intact responsiveness to stimulation of low-pressure-baroreceptors.

Topics: Adolescent; Arginine Vasopressin; Body Temperature Regulation; Deamino Arginine Vasopressin; Diabetes Insipidus; Feeding and Eating Disorders; Humans; Hypernatremia; Hyperphagia; Male; Obesity; Thirst

Patients with essential hypernatremia maintain urinary concentrating ability despite plasma hyperosmolality and low plasma vasopressin concentrations. We investigated renal sensitivity to ultralow dose vasopressin infusions in two patients with a syndrome of hypodipsia, hypernatremia with selective osmoreceptor dysfunction, early puberty, and aggressive behavior. The patients were water loaded until a hypotonic diuresis was established. Vasopressin was infused in stepwise increments from 0.4-12 fmol/kg X min. Both patients had increased renal sensitivity to vasopressin, achieving negative free water clearance at infusion rates of 0.4 and 4 fmol/kg X min (normal greater than or equal to 6). Treatment for 3 months with 1-desamino-8-D-arginine vasopressin (DDAVP) led to an improvement in behavior and the reporting, for the first time, of a sensation of thirst. After DDAVP therapy both patients had a reduction of their renal sensitivity to infused vasopressin. We conclude that untreated patients with essential hypernatremia have increased renal sensitivity to vasopressin which is reduced by DDAVP administration.

Topics: Adolescent; Adult; Deamino Arginine Vasopressin; Dose-Response Relationship, Drug; Drug Therapy, Combination; Humans; Hypernatremia; Kidney; Male; Osmolar Concentration; Vasopressins; Water-Electrolyte Balance

A 24 year old man developed partial central diabetes insipidus with impaired thirst and an elevated osmotic threshold to the release of arginine vasopressin (AVP). Plasma AVP was present in inappropriately small concentrations despite severe hyperosmolality. In addition, marked hypertension accompanied this disorder and all abnormalities, including the hypertension, responded to 1-desamino-8-D-arginine vasopressin therapy. Several lines of evidence suggest this disorder may be a disturbance of hypothalamic function.

Topics: Adult; Arginine Vasopressin; Deamino Arginine Vasopressin; Diabetes Insipidus; Glucose; Humans; Hypernatremia; Hypertension; Infusions, Parenteral; Male; Radioimmunoassay; Sodium Chloride; Thirst; Water

An infant with microcephaly and delayed development was found to have chronic asymptomatic hypernatremia. Computerized brain tomography disclosed dysplasia of the midline structures, septum pellucidum and corpus collosum. Evaluation revealed defective osmoregulation, hypothalamic hypothyroidism, and hypogonadotropinism. He showed no desire to drink at plasma osmolalities over 330 mOsm/kg. His plasma vasopressin levels (less than or equal to 1.4 pg/ml) were inappropriately low relative to his high levels of plasma osmolality (greater than or equal to 310 mOsm/kg), which might be accounted for by either deficient neurohypophyseal vasopressin stores or disturbance of the hypothalamic osmoreceptors governing vasopressin. The first possibility was ruled out by demonstrating normal vasopressin response (167 pg/ml) to nonosmotic (emetic) stimulation. Under baseline conditions, his urine was concentrated up to 747 mOsm/kg and urine volume was low. With water loading, maximal water diuresis developed (urine osmolality 68 mOsm/kg), but his plasma osmolality remained in the hyperosmolar range (312 mOsm/kg). Treatment with a vasopressin analogue, desamino-D-arginine vasopressin, and forced hydration restored plasma osmolality and plasma sodium to normal. These findings indicate a severe defect in the hypothalamic osmoreceptors controlling thirst and vasopressin secretion with normal vasopressin stores and preserved vasopressin responsiveness to nonosmotic stimuli. To our knowledge, this report provides the first documentation of selective osmoreceptor defect in conjunction with congenital dysplasia of midline brain structures.

Topics: Brain; Deamino Arginine Vasopressin; Dehydration; Developmental Disabilities; Humans; Hypernatremia; Infant; Male; Microcephaly; Osmolar Concentration; Thirst; Vasopressins

Topics: Arginine Vasopressin; Body Water; Deamino Arginine Vasopressin; Diabetes Insipidus; Humans; Hypernatremia; Hypoglycemia; Hyponatremia; Inappropriate ADH Syndrome; Pharmacology; Radioimmunoassay; Vasopressins; Water-Electrolyte Imbalance