Diagnosis Of Syndrome Of Inappropriate Antidiuretic Hormone Research Articles

Tolvaptan Versus Fluid Restriction in the Treatment of Hyponatremia Resulting from SIADH Following Pituitary Surgery.

Context The relevance of hyponatremia has been acknowledged by guidelines from the United States (2013) and Europe (2014). However, treatment recommendations differ due to limited evidence.ObjectiveIn hyponatremia following pituitary surgery—caused by the syndrome of inappropriate antidiuretic hormone (SIADH) secretion—we compared fluid restriction with the pharmacological increase of water excretion by blocking the vasopressin 2 receptors with tolvaptan at a low and a moderate dose.DesignProspective observational study.SettingNeurosurgical Department of a University hospital with more than 200 surgical pituitary procedures per year.PatientsPatients undergoing pituitary surgery and developing serum sodium below 136 mmol/L. The diagnosis of SIADH was established by euvolemia (daily measurement of body weight and fluid balance), inappropriately concentrated urine (specific gravity), and exclusion of adrenocorticotropic and thyroid-stimulating hormone deficiency.InterventionPatients were treated with fluid restriction (n = 40) or tolvaptan at 3.75 (n = 38) or 7.5 mg (n = 48).Main Outcome MeasuresTreatment efficacy was assessed by the duration of hyponatremia, sodium nadir, and length of hospitalization. Safety was established by a sodium increment below 10 mmol/L per day and exclusion of side effects.ResultsTreatment with 7.5 mg of tolvaptan resulted in a significant attenuation of hyponatremia and in a significant overcorrection of serum sodium in 30% of patients. The duration of hospitalization did not differ between treatment groups.ConclusionsTolvaptan at a moderate dose is more effective than fluid restriction in the treatment of SIADH. Overcorrection of serum sodium may be a side effect of tolvaptan even at low doses.

Lack of appropriate investigations in making a diagnosis of syndrome of inappropriate antidiuretic hormone.

The syndrome of inappropriate antidiuretic hormone (SIADH) is reported as the most common cause of hyponatraemia. This retrospective cross-sectional study evaluated the diagnosis of SIADH in 110 hospitalised patients in an Australian tertiary hospital with reference to recently published clinical guidelines. Investigation of SIADH was incomplete in all but 20% of cases. Adrenal insufficiency and hypothyroidism were not excluded in a significant number of cases.

Severe Symptomatic Hyponatremia Due to Syndrome of Inappropriate Antidiuretic Hormone From Mild Closed Head Trauma and Concussion

We report the first published case of severe, symptomatic hyponatremia resulting from syndrome of inappropriate antidiuretic hormone (SIADH) incurred as the result of a blow to the head inducing a concussion without any additional signs of head injury. A 38-year-old male in excellent health suffered a fall from a tree causing a right leg fracture and blunt trauma to the head with concussion but no other signs of head injury. The patient was discharged several days after surgery for repair of his leg fracture and subsequently became severely ill with nausea, vomiting, headache, and seizures. He was readmitted with a serum sodium of 114 mEq/L (mmol/L) with a presumed diagnosis of dehydration. After several days of saline administration he was discharged, but within 24 hours he again experienced severe, symptomatic hyponatremia and was admitted for the third time with a serum sodium of 110 mEq/L (mmol/L). A diagnosis of SIADH was made, and the patient was successfully treated with fluid restriction, intravenous saline, and demeclocycline resulting in a full recovery without further incident. This case emphasizes the need to consider SIADH as a possible cause of severe hyponatremia in patients sustaining relatively minor closed head trauma. J Med Cases. 2015;6(1):27-29 doi: http://dx.doi.org/10.14740/jmc2001w

Syndrome of inappropriate antidiuretic hormone secretion associated with desvenlafaxine

To report a case of syndrome of inappropriate anti-diuretic hormone (SIADH) secretion associated with desvenlafaxine. A 57-year old female with hyponatraemia. Her medications included desvenlafaxine, and symptoms included nausea, anxiety and confusion. The serum sodium at this time was 120 mmol/L, serum osmolality was 263 mosmol/kg, urine osmolality 410 mosmol/kg and urine sodium 63 mmol/L, consistent with a diagnosis of SIADH. Desvenlafaxine was ceased and fluid restriction implemented. After 4 days the sodium increased to 128 mmol/L and fluid restriction was relaxed. During her further 3 weeks inpatient admission the serum sodium ranged from 134 to 137 mmol/L during treatment with mirtazapine. SIADH has been widely reported with a range of antidepressants. This case report suggests that desvenlafaxine might cause clinically significant hyponatremia. Clinicians should be aware of the potential for antidepressants to cause hyponatremia,and take appropriate corrective action where necessary.

Hyponatraemia: etiology, management and outcome.

To determine the etiology of hyponatraemia, the treatment instituted and the outcome of treatment in a tertiary care hospital setting. Case series. The Aga Khan University Hospital, Karachi, between January and June 2004. Case records of 220 patients admitted to the medical service were identified through computerized hospital patients' data. All patients (3) 15 years with a sodium level on admission of (2) 130 mmol/litre were included. The records of those patients were reviewed for relevant demographic, clinical and laboratory data, in addition to the diagnosis, treatment and outcome of hospitalization. The data was analyzed through SPSS software version 11.0. Over a 6-month period, 220 patients were admitted with hyponatraemia (serum sodium (2) 130 mmol/L). Of those 127 females and 93 males, the mean age was 65 + 13.29 years. Neurological symptoms were the presenting feature in 25% patients. The mean serum sodium level on admission was 119.46 mmol/L. The rate of correction was >10 mmol/L/ 24 hours in 17% patients. The average duration of stay was 4 days. The mortality was 6.8%. Medicines accounted for 30% cases of hyponatraemia, of which diuretics, angiotensin converting enzyme inhibitor (ACEI) and angiotensin receptor blockers (ARBs) were top of the list. Other causes were gastrointestinal in 25%, chest infection in 11% patients, depletional hyponatraemia in 10% patients, SIADH (Syndrome of Inappropriate Antidiuretic Hormone) in 6% patients, congestive cardiac failure and malignancy in 5% each and chronic liver disease in 3.6% patients. Hyponatraemia was seen more commonly in the elderly, major causes being gastrointestinal losses and use of drugs. Serum sodium correction should be less than 10 mmol/L/24 hours. The treatment plan be directed to correction of the underlying cause. Diagnosis of SIADH should be sought with appropriate investigation.

Syndrome of inappropriate anti-diuretic hormone (SIADH) secretion in pre-eclampsia

SIADH as a cause of hyponatremia in pre-eclampsia is rare. We present the case of a 29 year old woman with this condition and discuss the obstetric and anaesthetic challenges...

Syndrome of Inappropriate Antidiuretic Hormone in Association with Amiodarone Therapy: A Case Report and Review of Literature

Background: Amiodarone is a class III antiarrhythmic agent that is widely used in the treatment of a variety of arrhythmias. Several different systemic side effects are reported after use of this medication. In this article, we report a case that had developed syndrome of inappropriate antidiuretic hormone (SIADH) after starting treatment with this agent. Case report: The patient is a 66-year-old male with past medical history of hypertension, hyperlipidemia, coronary artery disease, and class III New York Heart Association congestive heart failure who presented with monomorphic nonsustained ventricular tachycardia. A loading dose of amiodarone followed by maintenance dose was started. Baseline serum sodium of 138 mmol/L on admission decreased to 119 mmol/L by day 7, and a diagnosis of SIADH was made. The patient was not taking any other medication known to cause SIADH, nor had any such comorbidity to explain it. Serum sodium increased to 133 and 138 mmol/L, respectively, after 16 and 33 days from discontinuation of amiodarone. Conclusion: SIADH is a rare but serious side effect of amiodarone and practicing physicians should be aware of this complication, particularly after loading dose of the medication.

Can the fractional excretion of uric acid distinguish the etiology of hyponatremia in patients taking diuretics?

Measurement of the urinary sodium concentration can often help differentiate the various etiologies of hyponatremia. An elevated urinary sodium concentration is detected in the syndrome of inappropriate antidiuretic hormone (SIADH); however, the use of diuretics confounds the validity of this measurement. In this Practice Point commentary, I discuss the findings of Fenske et al., who suggest that the fractional excretion of uric acid (FEUA) is the best biomarker to determine whether hyponatremia is caused by SIADH in patients taking diuretics. An FEUA cutoff ≥12% had a positive predictive value of 100% for a diagnosis of SIADH in patients receiving diuretics, whereas an FEUA <8% excluded SIADH in this group. Here, I place the findings of Fenske et al. into clinical context, and discuss the utility of the FEUA and other biochemical markers for the diagnosis of SIADH in the presence of diuretics.

Hyponatraemia for the clinical endocrinologist

Hyponatraemia for the clinical endocrinologist

Syndrome of inappropriate antidiuretic hormone secretion in children following spinal fusion.

a) To determine if antidiuretic hormone (ADH) is elevated in patients undergoing spinal fusion, especially in those who have clinical evidence of syndrome of inappropriate antidiuretic hormone (SIADH); b) to evaluate the relationship between ADH secretion and the secretion of atrial natriuretic peptide (ANP). Tertiary care pediatric intensive care unit (ICU) in a university hospital. A prospective cross-sectional, observational study with factorial design. Thirty patients > or = 10 yrs of age undergoing spinal fusion admitted to the ICU for postoperative care. Patients underwent anterior, posterior, or both anterior/posterior spinal fusion. Blood was collected for serial measurements of ADH, ANP and serum electrolyte levels. Heart rate, blood pressure and central venous pressure were measured. Thirty children were studied. Nineteen had idiopathic scoliosis, nine had neuromuscular scoliosis, one had Marfan's disease, and one had congenital scoliosis. Ten (33%) children met clinical criteria of SIADH. There was no difference in duration of surgery, blood loss, volume of iv fluid administration pre- and intraoperatively, or type of scoliosis between those who developed SIADH and those who did not. Hemodynamic variables were similar in both groups. ADH levels increased in both groups immediately postoperatively and at 6 hrs after surgery, but were much more elevated in those patients with SIADH. Patients with SIADH also had significantly higher ADH levels preoperatively. In relation to serum osmolality, ADH was considerably higher in those with SIADH compared with those who did not. Although ANP values tended to be higher in the group with SIADH, this did not reach statistical significance. SIADH occurs in a subset of children who undergo spinal fusion. The diagnosis of SIADH can be made easily using clinical parameters which are well-defined. In the face of SIADH, continued volume expansion may be harmful, and should therefore be avoided.