Severe Hyponatremia and Bradycardia Associated with Intravenous Vasopressin Therapy for Variceal Hemorrhage

Melo, Jairo; Lee, Makau; Muñoz, J; Levine, Stephanie M.

doi:10.1097/00004836-199504000-00028

Cited by 12 publications

(9 citation statements)

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“…7 In addition, one case report described a 35-year-old pregnant woman receiving vasopressin 0.4 U/minute for esophageal varices who developed hyponatremia (her sodium concentration was 116 mEq/L). 8 Her sodium levels 8 and 24 hours after discontinuing vasopressin were 129 and 142 mEq/L, respectively.…”

Section: Discussionmentioning

confidence: 96%

Transient Diabetes Insipidus After Discontinuation of Therapeutic Vasopressin

Kristeller

Sterns²

2004

Pharmacotherapy

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The use of vasopressin for the treatment of septic shock is increasing. Few reports of fluid and electrolyte complications of this therapy have been reported. A neurologically impaired, 53-year-old man with a history of syndrome of inappropriate antidiuretic hormone developed apparent transient diabetes insipidus and acute hypernatremia after being treated with vasopressin. He was treated for presumed septic shock with intravenous vasopressin 0.01-0.10 U/minute. His blood pressure did not improve with this therapy, and his course was complicated by hyponatremia during the vasopressin infusion. Discontinuation of the infusion was followed by a profound (8.4 L) diuresis and rapid onset of hypernatremia (serum sodium concentration increased from 132 to 157 mEq/L over 8 hrs). Although urine osmolality was not measured during the patient's diuresis, the rapid changes in serum sodium concentration can be explained only by an inappropriate water diuresis. The diuresis ceased when the vasopressin infusion was resumed. We concluded that these findings are most consistent with transient diabetes insipidus. The safety and efficacy of intravenous vasopressin have not been established in patients with septic shock and underlying disorders of water homeostasis. The drug may have diminished vasoconstrictive effects in this patient population. Careful monitoring of water and sodium balance is warranted in all patients treated with vasopressin for septic shock.

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Section: Discussionmentioning

confidence: 96%

Transient Diabetes Insipidus After Discontinuation of Therapeutic Vasopressin

Kristeller

Sterns²

2004

Pharmacotherapy

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“…22 Similarly, a case report described the development of severe hyponatremia (serum sodium 116 mEq/mL from baseline of 141 mEq/mL) in a 35-year-old woman after 3 days of vasopressin infusion for variceal hemorrhage at 0.4 units/min. 23 Prompt diuresis and subsequent normalization of serum sodium occurred in this patient within 24 hours of discontinuing vasopressin.…”

Section: Literature Reviewmentioning

confidence: 69%

“…However, several high rates of hyponatremia have been reported in studies where vasopressin is used for indications other than vasodilatory shock. [21][22][23] For example, in a pilot safety study, 24 critically ill but hemodynamically stable children were administered either low-dose vasopressin (0.005 units/kg/min) or normal saline placebo. 21 In all, 8 (66%) children in the vasopressin group developed hyponatremia versus 1 (8%) in the control group despite a trend toward higher sodium intake in the vasopressin group and no differences in fluid intake between the groups.…”

Section: Literature Reviewmentioning

confidence: 99%

Exogenous Vasopressin-Induced Hyponatremia in Patients With Vasodilatory Shock

Salazar

Vázquez

et al. 2013

J Intensive Care Med

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Vasopressin has gained wide support as an adjunct vasopressor in patients with septic shock. This agent exerts its vasoconstriction effects through smooth muscle V1 receptors and also has antidiuretic activity via renal V2 receptors. This interaction with the renal V2 receptors results in the integration of aquaporin 2 channels in the apical membrane of the renal collecting duct leading to free water reabsorption. Thus, water intoxication with subsequent hyponatremia, although rare, is a potentially serious side effect of exogenous vasopressin administration. We present 2 patients who developed hyponatremia within hours of initiation of vasopressin infusion. Extensive diuresis followed its discontinuation with subsequent normalization of serum sodium. One of the patients required the use of hypertonic saline for more rapid normalization of serum sodium due to concerns for potential seizure activity. A review of the literature relevant to the incidence of vasopressin-induced hyponatremia is provided as well as discussion on additional factors relevant to septic shock that should be considered when determining the relative risk of hyponatremia in patients receiving vasopressin.

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“…Significant hyponatremia was also observed following high dose (0.4 units/min) of vasopressin administration in a small study comparing somatostatin with vasopressin for the treatment of acute variceal hemorrhage [19]. Similarly, a case report described the development of severe hyponatremia (serum sodium 116 mEq/ mL from baseline of 141 mEq/mL) in a 35-year-old woman after 3 days of vasopressin infusion for variceal hemorrhage at 0.4 units/min [20]. Prompt diuresis and subsequent normalization of serum sodium occurred in this patient within 24 hours of discontinuing vasopressin.…”

Section: Discussionmentioning

confidence: 92%

“…A search of the literature did not yield any peer-reviewed publications reporting significant rates of hyponatremia when vasopressin is used for vasodilatory shock. Although, several high rates of hyponatremia have been reported in studies where vasopressin is used for indications other than vasodilatory shock [18][19][20]. For example, in a pilot safety study, 24 critically ill but hemodynamically stable children were administered either low-dose vasopressin (0.005 units/kg/min) or normal saline placebo [18].…”

Section: Discussionmentioning

confidence: 99%

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2021

NCP

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Arginine Vasopressin (AVP), also known as antidiuretic hormone, is a endogenously secreted peptide by the posterior pituitary in response to hyperosmolar plasma or systemic hypoperfusion states. Patients in refractory shock associated with severe sepsis, cardiogenic or vasodilatory shock, or cardiopulmonary bypass have inappropriately low plasma levels of AVP ('relative vasopressin deficiency') and supersensitivity to exogenously-administered vasopressin. Low doses of vasopressin can restore vasomotor tone in conditions that are resistant to catecholamines, with preservation of renal blood flow and urine output. This agent exerts its vasoconstriction effects through smooth muscle V1 receptors and also has antidiuretic activity via renal V2 receptors. This interaction with the renal V2 receptors results in the integration of aquaporin 2 channels in the apical membrane of the renal collecting duct leading to free water reabsorption. Thus, water intoxication with subsequent hyponatremia, although rare, is a potentially serious side effect of exogenous vasopressin administration. We present 1 patient who developed hyponatremia with initiation of vasopressin infusion. The patient required the use of hypertonic saline for more rapid normalization of serum sodium due to her seizure.

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Severe Hyponatremia and Bradycardia Associated with Intravenous Vasopressin Therapy for Variceal Hemorrhage

Cited by 12 publications

References 0 publications

Transient Diabetes Insipidus After Discontinuation of Therapeutic Vasopressin

Transient Diabetes Insipidus After Discontinuation of Therapeutic Vasopressin

Exogenous Vasopressin-Induced Hyponatremia in Patients With Vasodilatory Shock

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