Vasopressin Levels and Pediatric Head Trauma

PEDIATRICS ◽  
1989 ◽  
Vol 83 (5) ◽  
pp. 700-705
Author(s):  
Guadalupe Padilla ◽  
John A. Leake ◽  
Robert Castro ◽  
M. Gore Ervin ◽  
Michael G. Ross ◽  
...  
Keyword(s):  
Antidiuretic Hormone ◽  
Head Trauma ◽  
Pediatric Patients ◽  
Urine Osmolality ◽  
Sodium Concentration ◽  
Clinical Syndrome ◽  
Serum Osmolality ◽  
Fluid Restriction ◽  
Healthy Children ◽  
Inappropriate Secretion

The syndrome of inappropriate secretion of antidiuretic hormone is associated with head trauma; however, there are no reports concerning vasopressin levels in pediatric patients with head trauma. Urine vasopressin in eight children (mean ± SEM, age 7.5 ± 1.6 years, range 1 to 15 years) was measured by radio-immunoassay during their hospitalization for head trauma. Urine vasopressin values for ten healthy children (mean age 5.4 ± 1.3 years) and for eight children hospitalized for systemic antibiotic treatment of infections (age 5.9 ± 1.8 years) also were obtained. Urine vasopressin, urine and serum sodium concentration and osmolality, urea nitrogen, creatinine, and fluid intake were measured within 24 hours of admission and daily for the following two days. For the first three days following head trauma, mean urine vasopressin levels in pediatric patients with head trauma were increased (P < .05) compared with those of healthy children. Despite fluid restriction to 85% of maintenance level, 25% of patients with head trauma exhibited the clinical syndrome of inappropriate secretion of antidiuretic hormone (hyponatremia, increased urinary sodium, diminished serum osmolality, and urine osmolality greater than serum osmolality). Urine osmolality greater than 800 mosm/kg was associated with markedly increased urine vasopressin levels (200 to 1,650 pg/mL); children with this finding may be at particular risk for the syndrome of inappropriate secretion of antidiuretic hormone without restrictive water intake.

scholarly journals Syndrome of Inappropriate Secretion of Antidiuretic Hormone due to Selective Serotonin Reuptake Inhibitors After Pancreaticoduodenectomy for Carcinoma of the Ampulla of Vater: Case Report

2013 ◽  
Vol 98 (4) ◽  
pp. 289-291
Author(s):  
Ryota Iwase ◽  
Hiroaki Shiba ◽  
Takeshi Gocho ◽  
Yasuro Futagawa ◽  
Shigeki Wakiyama ◽  
...  
Keyword(s):  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Ampulla Of Vater ◽  
Serum Sodium Concentration ◽  
Selective Serotonin ◽  
Inappropriate Secretion

Abstract A 68-year-old man underwent pancreaticoduodenectomy with lymph nodes dissection for carcinoma of the ampulla of Vater. The patient had anxiety neurosis and had been treated with a selective serotonin reuptake inhibitor (SSRI). Postoperatively, SSRI was resumed on postoperative day 2. His serum sodium concentration gradually decreased, and the patient was given a sodium supplement. However, 11 days after the operation, laboratory findings included serum sodium concentration of 117 mEq/L, serum vasopressin of 2.0 pg/mL, plasma osmolality of 238 mOsm/kg, urine osmolality of 645 mOsm/kg, urine sodium concentration of 66 mEq/L, serum creatinine concentration of 0.54 mg/dL, and serum cortisol concentration of 29.1 μg/dL. With a diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH), the antianxiety neurosis medication was changed from the SSRI to another type of drug. After switching the medication, the patient made a satisfactory recovery with normalization of serum sodium by postoperative day 20.

Neurosurgical hyponatremia: the role of inappropriate antidiuresis

1971 ◽  
Vol 34 (4) ◽  
pp. 506-514 ◽  
Author(s):  
John L. Fox ◽  
Joel L. Falik ◽  
Robert J. Shalhoub
Keyword(s):  
Differential Diagnosis ◽  
Sodium Concentration ◽  
Fluid Restriction ◽  
Urine Sodium ◽  
Content Type ◽  
Inappropriate Secretion ◽  
Neurosurgical Patients ◽  
Inappropriate Antidiuresis ◽  
Fine Print

✓ Of 80 consecutive neurosurgical patients, 23 exhibited inappropriate secretion of the antidiuretic hormone (ISADH); 11 of these patients required marked fluid restriction. Sodium concentration in the urine characteristically increased as serum values decreased. Only by following the urine sodium concentrations could the differential diagnosis of nutritional hyponatremia and ISADH be made. The role of ISADH in cerebral edema is stressed. The treatment recommended for ISADH is marked fluid restriction, whereas in nutritional hyponatremia, saline replacement is indicated.

Excretion of aldosterone in inappropriate secretion of antidiuretic hormone following head trauma

Metabolism ◽  
1965 ◽  
Vol 14 (6) ◽  
pp. 715-725 ◽  
Author(s):  
James P. Knochel ◽  
James R. Osborn ◽  
Everett B. Cooper
Keyword(s):  
Antidiuretic Hormone ◽  
Head Trauma ◽  
Inappropriate Secretion

Delayed hyponatremia after transsphenoidal surgery for pituitary adenoma

1995 ◽  
Vol 83 (2) ◽  
pp. 363-367 ◽  
Author(s):  
Daniel F. Kelly ◽  
Edward R. Laws ◽  
Damirez Fossett
Keyword(s):  
Pituitary Adenoma ◽  
Antidiuretic Hormone ◽  
Intravenous Administration ◽  
Serum Sodium ◽  
Transsphenoidal Surgery ◽  
Fluid Restriction ◽  
Content Type ◽  
Inappropriate Secretion ◽  
Average Serum ◽  
Fine Print

✓ Hyponatremia, usually attributed to the syndrome of inappropriate secretion of antidiuretic hormone, typically occurs in a delayed fashion following transsphenoidal removal of a pituitary adenoma. In a series of 99 consecutive patients who underwent transsphenoidal surgery for pituitary adenoma, nine patients developed delayed hyponatremia, seven of whom were symptomatic. Of these seven patients, four had been discharged from the hospital and required readmission on postoperative Day 7 to 9. In the nine patients who developed hyponatremia, on the average, serum sodium levels began to fall on Day 4 and reached a nadir on Day 7 (mean serum sodium nadir 123 mmol/L). The development of delayed hyponatremia was associated with the presence of a macroadenoma in eight of the nine patients. Seven of the nine patients had serum sodium levels less than 130 mmol/L and required treatment. One patient was treated with fluid restriction alone and six were treated with both fluid restriction and intravenous urea therapy. Twenty-four and 48 hours after urea administration, serum sodium levels rose by an average of 6 and 10 mmol/L, respectively, and at discharge, levels averaged 136 mmol/L. Intravenous administration of urea provides a rapid yet safe means of correcting symptomatic hyponatremia when fluid restriction alone is inadequate. In this article, the authors discuss the pathogenesis of delayed hyponatremia.

Osmotic demyelination syndrome following slow correction of hyponatraemia

2021 ◽  
Vol 14 (8) ◽  
pp. e241407
Author(s):  
Isabel Saunders ◽  
David M Williams ◽  
Aliya Mohd Ruslan ◽  
Thinzar Min
Keyword(s):  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Inflammatory Markers ◽  
Urine Osmolality ◽  
Fluid Restriction ◽  
Osmotic Demyelination Syndrome ◽  
Electrolyte Disturbance ◽  
Osmotic Demyelination ◽  
Sodium Correction ◽  
Hospital Inpatients

Hyponatraemia is the most common electrolyte disturbance observed in hospital inpatients. We report a 90-year-old woman admitted generally unwell following a fall with marked confusion. Examination revealed a tender suprapubic region, and investigations observed elevated inflammatory markers and bacteriuria. Admission investigations demonstrated a serum sodium of 110 mmol/L with associated serum osmolality 236 mmol/kg and urine osmolality 346 mmol/kg. She was treated for hyponatraemia secondary to syndrome of inappropriate antidiuretic hormone (SIADH) and urosepsis. However, her serum sodium failed to normalise despite fluid restriction, necessitating treatment with demeclocycline and hypertonic saline. Despite slow reversal of hyponatraemia over 1 month, the patient developed generalised seizures with pontine and thalamic changes on MRI consistent with osmotic demyelination syndrome (ODS). This case highlights the risk of ODS, a rare but devastating consequence of hyponatraemia treatment, despite cautious sodium correction.

scholarly journals Challenges of Managing and Diagnosing Reset Osmostat vs SIADH in a Patient With Personal and Family History of Chronic Hyponatremia

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A576-A577
Author(s):  
Hasan Syed ◽  
Praveen Attele ◽  
Joseph Theressa Nehu Parimi ◽  
Sowjanya Naha ◽  
Timur Gusov ◽  
...  
Keyword(s):  
Family History ◽  
Serum Sodium ◽  
Compression Fracture ◽  
Urine Osmolality ◽  
Serum Osmolality ◽  
Fluid Restriction ◽  
Urine Sodium ◽  
Chronic Hyponatremia ◽  
Fluid Load ◽  
History Of

Abstract Background: Distinguishing between a reset osmostat and SIADH in a hyponatremic patient can prove to be challenging in certain circumstances. Reset osmostat is an uncommon and under recognized cause of hyponatremia. Thus, it is important to recognize it as it does not require any treatment. Clinical Case: A 48 year old male with history of chronic hyponatremia of unknown cause, fatty liver, hypertension, was in the hospital post operatively after resection of a meningioma along dura. Endocrine was consulted for management of his chronic hyponatremia. Had chronic hyponatremia for over 20 years and was always asymptomatic. Normally drank 6-7 L of water at home, mostly at night. Also found to have a spinal compression fracture of unknown cause. Both his father and brother had chronic hyponatremia of unknown cause as well, suggesting possible familial component. His baseline sodium levels were 129-133 mmol/L. In the hospital, serum sodium levels decreased to the 120s. TSH was 0.307mcunit/mL (0.27-4.2). Was also placed on 1.5 L fluid restriction. Urine osmolality was 900 mOsm/kg (500-800) with sodium of 123 mmol/L (136-145), consistent with SIADH. A rare inherited disorder, nephrogenic SIADH (NSIADH), was considered. However, it has an X-linked inheritance pattern. Fluid restriction was removed, then did fluid load with 2L of water and obtained urine sodium, serum sodium, urine osmolality, serum osmolality, Copeptin (pro-AVP) before fluid load and 1 hour after fluid load. Serum sodium level went from 127mmol/L before to 125 mmol/L after. Urine osmolality improved from 984 mOsm/kg prior to 575 mOsm/kg after. Urine sodium went from 183 mmol/L prior to 91 mmol/L after. Serum osmolality went from 278 mOsm/kg (270-310) to 268 mOsm/kg after. His co-peptin pro-AVP levels were 16.4 pmol/L (ref. <13.1). They are found to be low in NSIADH. It was decided that his chronic hyponatremia was likely due to reset osmostat. After discharge and follow up, his serum sodium was rechecked and was 128 mmol/L. It would have been challenging, but useful, to try a vaptan for diagnostic purposes and possibly to increase serum sodium. However, there are complications from overcorrection. Since patient had long standing asymptomatic chronic hyponatremia with family history, it was decided not to pursue aggressive measures just to “normalize” serum sodium. Otherwise, it would have been an example of treating the numbers and not the patient. Conclusions: Case demonstrates the importance of keeping the patient, their symptoms, and clinical picture in mind, and to not just follow numbers, as difficult as it may be, especially when managing conditions in which diagnosis may be uncertain or unclear. Sometimes no intervention is needed at all, however tempting it may be to do one, it is important to keep the former option in mind. An asymptomatic patient with longstanding chronic hyponatremia due to reset osmostat is an example of that.

Fluoxetine and the Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)

1996 ◽  
Vol 30 (2) ◽  
pp. 295-298 ◽  
Author(s):  
David Burke ◽  
Scott Fanker
Keyword(s):  
Antidiuretic Hormone ◽  
Clinical Picture ◽  
Psychiatric Inpatients ◽  
Fluid Restriction ◽  
Symptoms Of Depression ◽  
Inappropriate Secretion ◽  
Intravenous Saline ◽  
Laboratory Investigations

Objective: To report three new cases of the fluoxetine-induced syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Clinical picture: All three cases occurred in elderly psychiatric inpatients treated for depression with standard doses of fluoxetine within one month of starting the medication. All three patients were clinically symptomatic of SIADH. Treatment: In all three patients the medication was ceased and fluid restriction commenced. One patient required intravenous saline. Outcome: All three patients recovered fully within three weeks. None were rechallenged. Conclusions: The symptoms of hyponatraemia due to fluoxetine-induced SIADH may be difficult to distinguish from the symptoms of depression, unless appropriate laboratory investigations are made.

scholarly journals A Case of Miller-Fisher Syndrome with Syndrome of Inappropriate Secretion of Antidiuretic Hormone

2021 ◽  
pp. 380-383
Author(s):  
Shunya Fujiwara ◽  
Yasuhiro Manabe ◽  
Yumiko Nakano ◽  
Yoshio Omote ◽  
Hisashi Narai ◽  
...  
Keyword(s):  
Antidiuretic Hormone ◽  
Immunoglobulin Therapy ◽  
Sodium Concentration ◽  
Miller Fisher Syndrome ◽  
Intravenous Immunoglobulin Therapy ◽  
Fisher Syndrome ◽  
Upper Respiratory Infection ◽  
Inappropriate Secretion ◽  
Unsteady Gait ◽  
Upper Respiratory

We report a 72-year-old woman with Miller-Fisher syndrome (MFS) with syndrome of inappropriate secretion of antidiuretic hormone (SIADH). She developed diplopia and unsteady gait a week after an upper respiratory infection. Neurologic examination revealed ophthalmoplegia, ataxia, symmetrical weakness, numbness, and areflexia. She underwent intravenous immunoglobulin therapy. Her serum sodium concentration decreased to 119 mEq/L on day 12. She had low plasma osmolarity (254 mosm/kg), high urine osmolarity (457 mosm/kg), and high urine sodium level (73 mEq/L), while the blood level of antidiuretic hormone was normal. Anti-GD1b immunoglobulin G (IgG), -GQ1b IgG, -GT1a IgG, and -Gal-C IgM antibodies were positive. We diagnosed her with MFS overlapping with SIADH. Four weeks after onset, her symptoms recovered. The elevation of anti-GD1b, -GQ1b, and -GT1a antibodies that recognize disialosyl residue may be pathologically related to SIADH.

Syndrome of Inappropriate Antidiuretic Hormone Secretion in a Cat

2010 ◽  
Vol 46 (6) ◽  
pp. 425-432 ◽  
Author(s):  
Kristin Cameron ◽  
Alexander Gallagher
Keyword(s):  
Antidiuretic Hormone ◽  
Hormone Secretion ◽  
Clinical Signs ◽  
Urine Osmolality ◽  
Electrolyte Imbalance ◽  
Fluid Restriction ◽  
Severe Hyponatremia ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Antidiuretic Hormone Secretion ◽  
Serum And Urine

A 3-year-old, spayed female, domestic shorthaired cat was presented for evaluation of liver disease. Following anesthesia, laparoscopy, and medical therapy, the cat developed severe hyponatremia that was unresponsive to fluid therapy. Further evaluation of serum and urine osmolality determined that the cat fulfilled the criteria for syndrome of inappropriate antidiuretic hormone secretion. Treatment with fluid restriction resulted in resolution of the hyponatremia and clinical signs associated with the electrolyte imbalance.

Syndrome of Inappropriate Antidiuretic Hormone Secretion Associated with Desvenlafaxine

2016 ◽  
Vol 33 (S1) ◽  
pp. S469-S469 ◽  
Author(s):  
E. García Fernández ◽  
D.M.I. Ramos García
Keyword(s):  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Antidepressant Treatment ◽  
Hormone Secretion ◽  
Urine Osmolality ◽  
Prescription Medication ◽  
Fluid Restriction ◽  
Close Monitoring ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Competing Interest

IntroductionDesvenlafaxine is a prescription medication approved for the treatment of major depressive disorder in adults. Hyponatremia secondary to inappropriate secretion of antidiuretic hormone (SIADH) is a possible side effect in patients receiving serotonin-norepinephrine reuptake inhibitors (SNRIS)MethodTo report a case of SIADH associated with desvenlafaxine.ResultsWe present a 80-year-old female patient who required hospitalization due to an episode of psychotic depression. During the hospitalization, the patient developed hyponatremia after commencing treatment with desvenlafaxine. The serum sodium at this time was 117 mmol/L, serum osmolality was 249 mosmol/kg, urine osmolality 395 mosmol/kg and urine sodium 160 mmol/L, consistent with a diagnosis of SIADH. Desvenlafaxine was ceased and fluid restriction implemented. The mental status improved, and electrolyte studies 6 days later revealed serum sodium and osmolality values of 135 mEq/L during treatment with duoxetine.ConclusionsSIADH has been reported with a range of antidepressants in elderly patients. This case report suggests that desvenlafaxine might cause clinically significant hyponatremia. Close monitoring is recommended in patients starting therapy with antidepressant treatment to study and prevent possible adverse effects.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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