Vasopressin therapy

Vasopressin and its derivatives are used in die treatment of diabetes insipidus, a disease resulting from die failure of the pituitary to secrete vasopressin or from surgical removal of die pituitary. Diabetes insipidus is characterized by marked increase in urination (as much as 10 L in 24 hours) and excessive tiiirst by inadequate secretion of die antidiuretic hormone or vasopressin. Treatment with vasopressin therapy replaces die hormone in the body and restores normal urination and thirst Vasopressin may also be used for die prevention and treatment of postoperative abdominal distention and to dispel gas interfering with abdominal roentgenography. 

Skin necrosis is often reported after vasopressin therapy. In a retrospective study, two of five patients treated with a continuous infusion of terlipressin developed skin necrosis at the infusion site and a third developed scrotal necrosis (15). 

There are two types of disturbances in vasopressin secretion. In central diabetes insipidus, vasopressin secretion is reduced it can be treated by giving vasopressin or desmopressin, which has a longer half-life, by mouth or intranasally. In nephrogenic diabetes insipidus, the plasma vasopressin concentration may be normal but the kidney fails to respond. The latter type of diabetes insipidus does not respond to vasopressin therapy but, paradoxically, can be managed by giving a thiazide diuretic, for example chlortalidone, at a maintenance dose of 50 mg daily. 

Hyponatremia (normal sodium 135-145 mEq/L) may occur when the client is taking vasopressin therapy. This sodium level is within normal limits therefore, the nurse would not question administering this medication. 

Davalos MC, Barrett R, Seshadri S, Walters HL, Delius RE, Zidan M, et al. H)fponalremia during arginine vasopressin therapy in children following cardiac surgery. Pediatr Crit Care Med 2013 14(3) 290-7. 

Primary therapy is based on disease severity and type of hemorrhage.7 Most patients with mild to moderate disease and a minor bleeding episode can be treated with l-desamino-8-D-arginine vasopressin [desmopressin acetate (DDAVP)], a synthetic analog of the antidiuretic hormone vasopressin. DDAVP causes release of von Willebrand factor (vWF) and factor VIII from endogenous storage sites. This formulation increases plasma factor VIII levels by three- to fivefold within 30 minutes. The recommended dose is 0.3 mcg/kg intravenously (in 50 mL normal saline infused over 15 to 30 minutes) or subcutaneously or 300 meg intranasally via concentrated nasal spray every 12 hours. Peak effect with intranasal administration occurs 60 to 90 minutes after administration, which is somewhat later than with intravenous administration. Desmopressin infusion may be administered daily for up to 2 to 3 days. Tachyphylaxis, an attenuated response with repeated administration, may occur after several doses.8... 

Li+ also inhibits several hormone-stimulated adenylate cyclases which, in some cases, appear to be related to side effects of Li+ therapy. For instance, Li+ inhibits the hydro-osmotic action of vasopressin, the antidiuretic hormone which increases water resorption in the kidney [136]. This effect is associated with polyuria, a relatively harmless side effect sometimes experienced with Li+ treatment, which arises from the inability of the kidney to concentrate urine. Li+ has been shown to inhibit vasopressin-stimulated adenylate cyclase activity in renal epithelial cells. Additionally, Li+ is reported to enhance the vasopressin-induced synthesis of prostaglandin E2 (PGE2) in vitro in kidney. PGE2 inhibits adenylate cyclase activity by stimulation of Gj, and, therefore, this effect may contribute to the Li+-induced polyuria. 

Vasopressin, alone or in combination with nitroglycerin, can no longer be recommended as first-line therapy for the management of variceal hemorrhage. Vasopressin causes nonselective vasoconstriction and can result in hypertension, severe headaches, coronary ischemia, myocardial infarction, and arrhythmias. 

Nondialytic therapies that may temporarily shorten increased bleeding time include cryoprecipitate, desmopressin (l-deamino-8-D-arginine vasopressin), and estrogens. 

The cornerstone of therapy for ventricular fibrillation is electrical deflbrillation. In the acute setting, defibrination is first-line therapy. Intravenous bretylium can occasionally contribute to conversion, but this is infrequent. In the management of out-of-hospital cardiac arrest, high-dose epinephrine (5 mg intravenously) improves the rate of successful resuscitation in patients with asystole, but not in those with ventricular fibrillation, when compared with the standard dose of 1 mg. Vasopressin (40 U intravenously) may more effective than 1 mg intravenous epinephrine in out-of-hospital patients with ventricular fibrillation that is resistant to electrical defibrillation. The OPTIC smdy (see Connolly et al., 2006) showed that amiodarone plus jS-blocker is superior than sotalol or jS-blocker alone for reducing ICD shocks in patients with reduced left ventricular function and history of sustained VT, VF, or cardiac arrest. 

Vasopressin and desmopressin are treatments of choice for pituitary diabetes insipidus. The dosage of desmopressin is 10-40 meg (0.1-0.4 mL) in two to three divided doses as a nasal spray or, as an oral tablet, 0.1-0.2 mg two to three times daily. The dosage by injection is 1-4 meg (0.25-1 mL) every 12-24 hours as needed for polyuria, polydipsia, or hypernatremia. Bedtime desmopressin therapy, by intranasal or oral administration, ameliorates nocturnal enuresis by decreasing nocturnal urine production. Vasopressin infusion is effective in some cases of esophageal variceal bleeding and colonic diverticular bleeding. 

Watson AJ, Keogh JA. l-Deamino-8-D-arginine vasopressin as a therapy for the bleeding diathesis of renal failure. Am J Nephrol 1984 4(1) 49-51. 

Rizzo V, Albanese A, Stanhope R. Morbidity and mortality associated with vasopressin replacement therapy in children. J Pediatr Endocrinol Metab 2001 14(7) 861-7. 

Vasopressin and desmopressin are the alternative treatments of choice for pituitary diabetes insipidus. Bedtime desmopressin therapy ameliorates nocturnal enuresis by decreasing nocturnal urine production. Vasopressin infusion is effective in some cases of esophageal variceal bleeding and colonic diverticular bleeding. 

Before the introduction of specific vasopressin receptor antagonists, pharmacological treatments for hyponatremia centered on the use of loop diuretics and nonspecific inhibitors of vasopressin signaling, such as lithium carbonate and demeclocycline.11 The utility of such therapies has been limited by a range of sideeffects. Loop diuretic use can result in electrolyte imbalances and suffers from poor response predictability.11 Lithium carbonate suffers from a low therapeutic index and a risk of renal damage as well as limited effectiveness in many patients. Lithium carbonate has therefore been nearly completely supplanted by demeclocycline, a tetracycline antibiotic, in the treatment of chronic hyponatremia.12 Demeclocycline use is itself limited by its nephrotoxicity (particularly in cirrhotic patients), ability to cause reversible uremia, and ability to induce photosensitivity.1,11... 

Vasopressin is rapidly cleared from the circulation and must be given by continuous i.v. infusion. The synthetic ancJogue, terlipressin (triglycyl-lysine-vasopressin) is now preferred. This prodrug (or hormogen) is converted in vivo to the vasoactive lysine vasopressin which has biological activity for 3-4 hours, and is effective by bolus injections 4-hourly, usually for 48-72 hours. It is a useful adjunct to endoscopic therapy and reduces rebleeding. 

Medicinal therapy is similar to that used for upper GIB, e.g. vasopressin, FFP, PPSB, fibrinogen (s. p. 351) and octreotide. (248)... 

Nephrogenic diabetes insipidus, resistant to vasopressin, following damage to the distal renal tubule, may be more common than reported (103,104). Careful monitoring of electroljhes is therefore recommended in aU instances of amphotericin therapy. 

Barbonr GL, Stranb KD, O Neal BL, Leatherman JW. Vasopressin-resistant nephrogenic diabetes insipidns. A resnlt of amphotericin B therapy. Arch Intern Med 1979 139(l) 86-8. 

Current concepts of resuscitation after local anesthetic cardiotoxicity have been reviewed (17). Vasopressin may be a logical vasopressor in the setting of hypotension, rather than adrenaline, in view of the dysrhythmogenic potential of the latter. Amiodarone is probably of use in the treatment of dysrhythmias. Calcium channel blockers, phenytoin, and bretyllium should be avoided. In terms of new modes of therapy targeted at the specific action of local anesthetics, lipid infusions, propofol, and insulin/ glucose/potassium infusions may all have a role, but further research is necessary. 

Maxon HR 3rd, Rutsky EA. Vasopressin-resistant diabetes insipidus associated with short-term demethylchlor-tetracycline (declomycin) therapy. Mil Med 1973 138(8) 500-1. 

However, accumulating evidence supports the use of norepinephrine in patients with septic shock with a retrospective study demonstrating reduced mortality with norepinephrine over other vasopressors [106]. Furthermore, animal data demonstrates that reversal of septic hypotension with norepinephrine leads to increases in renal blood flow [107]. There are no studies that compare the renal outcomes between catecholamine therapy and vasopressin. 

Many studies have shown that AmB can induce a loss of concentrating ability of the kidney [18, 32, 33]. This abnormality is almost invariably present and occurs early (1-2 weeks) in the course of therapy. The impairment in concentrating ability probably reflects direct tubular toxicity since it occurs in the absence of a decrease in GFR, and is temporally unrelated to azotemia. Barbour et al. [34] reported a study of 3 patients whose inabihty to concentrate the urine was associated with a defect in free water reabsorption even under maximal stimuli, and concluded that a tubular functional abnormality was induced because of the failure of the vasopressin response in the medullary collecting tubule. 

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