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Treatment of Variceal Bleeding in Cirrhotic Patients
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Urgent pharmacologic intervention for emergency treatment includes the administration of splanchnic vasoconstrictors that will reduce blood flow through the portal venous system. Vasoactive agents such as octreotide and terlipressin are associated with lower 7-day all-cause mortality, improved control of acute hemorrhage, and lower transfusion requirements [5]. These medications should be administered as soon as possible. In fact, Levacher and colleagues advocate for terlipressin administration to patients by emergency medical personnel before transfer to the hospital [6].
The patient with acute gastrointestinal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Rebecca Maindonald, Adrian Jugdoyal
Patients with a variceal bleed are more likely to need further intervention due to a high risk of recurrent bleeding, with 15–30% rebleeding in the six weeks following initial bleed (Siau et al. 2017). In addition to fluid resuscitation and close monitoring, the patient with a variceal bleed is likely to require any of the following interventions: Pharmacological control with Terlipressin (NICE 2016) to reduce portal blood pressure.Prophylactic antibiotic therapy (NICE 2016) to prevent infection, which is common after upper gastrointestinal bleeding in patients with cirrhosis.Endoscopic variceal ligation (EVL), which involves rubber bands placed so that they strangulate the bleeding varices.Transjugular intrahepatic portosystemic shunt (TIPS), which is a procedure whereby a catheter is inserted into the portal vein (under radiological guidance) and a stent is then inserted between the portal vein and the systemic circulation, thereby reducing portal blood pressure. This latter intervention is reserved for patients with recurrent bleeding not controlled by band ligation (NICE 2016).
Drug therapy for portal hypertension
Published in Michael JG Farthing, Anne B Ballinger, Drug Therapy for Gastrointestinal and Liver Diseases, 2019
Terlipressin is a synthetic vasopressin analogue (triglycyl lysine vasopressin), which, in addition to an intrinsic vasoconstrictor activity, is slowly converted in vivo into vasopressin by enzymatic cleavage of the triglycyl residues. This allows a slow but continuous release of vasopressin resulting in a lower incidence of side-effects when compared with vasopressin, while maintaining a significant decrease in portal pressure. In addition, terlipressin, unlike vasopressin, does not enhance fibrinolysis and has a longer biological activity, which makes continuous intravenous infusion unnecessary.22 The preferred schedule of administration is intravenous injection of 2 mg/4 h until achieving a bleeding-free period of 24–48 h.
Renal and Hepatic Disease: Cnidoscolus aconitifolius as Diet Therapy Proposal for Prevention and Treatment
Published in Journal of the American College of Nutrition, 2021
Maria Lilibeth Manzanilla Valdez, Maira Rubi Segura Campos
The treatment with vasoconstrictors and albumin is one of the first options to choose. The goal of treatment is to produce vasoconstriction in the splenic vascular bed and reduce hypovolemia.Alpha adrenergic agonists: norepinephrine, midrodine. Norepinephrine is a catecholamine that acts on adrenergic receptors. Midodrine acts as a selective agonist of peripheral alpha-1 receptors, generating vasoconstriction and increased blood pressure (55).Somastostin analogues: Octreotide, an octapeptide analogous to somastatin with potent vasoconstrictor action on the splenic vasculature. It acts as an inhibitor of the secretion of peptides synthesized by the gastro-endocrine-pancreatic endocrine system, having the effect of decreasing splenic blood flow (55).Vasopressin analogues: ornipressin, terlipressin. Ornipressin has shown benefits in SHR, but due to its ischemic effects such as arrhythmias, myocardial ischemia and cutaneous necrosis, it has been abandoned. Terlipressin is a synthetic derivative of vasopressin, which has a dominant action on V1 receptors, with a potent vasoconstrictor effect. The administration of volume expanders such as albumin improve the effect of vasoconstrictors (54).
Development of hyponatremia after terlipressin in cirrhotic patients with acute gastrointestinal bleeding: a retrospective multicenter observational study
Published in Expert Opinion on Drug Safety, 2020
Xiangbo Xu, Su Lin, Yida Yang, Yu Chen, Bang Liu, Bimin Li, Yunhai Wu, Fanping Meng, Qiang Zhu, Yiling Li, Shanhong Tang, Shanshan Yuan, Lichun Shao, Xingshun Qi
The present study had limitations. First, because it was a retrospective study, the selection bias of patients could not be ignored. Second, because serum sodium concentration was not tested every day, the time of the development or recovery of hyponatremia during the use of terlipressin could not be accurately assessed. Third, the dosage, duration, and manufacturers of terlipressin varied. Fourth, some patients might be simultaneously treated with other drugs that might induce serum sodium concentration reduction, and others did not restrict electrolyte-free water intake during terlipressin treatment that potentially induced the confounding effect on serum sodium concentration reduction. Fifth, it is hard to evaluate the decrease in serum sodium concentration or the development of hyponatremia in predicting the risk of hepatic encephalopathy or other neurological symptoms. Such data was lacking when the study was initially designed. Sixth, the management of hyponatremia or a decrease in serum sodium concentration was unavailable. Notably, serum sodium concentration can be spontaneously reversed after withdrawing terlipressin.
Addition of terlipressin to norepinephrine in septic shock and effect of renal perfusion: a pilot study
Published in Renal Failure, 2022
Jinlong Wang, Mengjuan Shi, Lili Huang, Qing Li, Shanshan Meng, Jingyuan Xu, Ming Xue, Jianfeng Xie, Songqiao Liu, Yingzi Huang
Terlipressin is a synthetic vasopressin analog and has a great affinity for V1 receptors that are distributed in vascular smooth muscle and cause vasoconstrictive effects. However, the V1 receptor is heterogeneously distributed in the renal microcirculation. The vasoconstrictive effect of terlipressin on renal vessels is mainly concentrated on the efferent arterioles, whereas the effect on the afferent arterioles is negligible [7–9]. In addition, vasopressin is often relatively deficient in patients with septic shock [10]. Therefore, terlipressin supplementation may represent a promising method to improve renal perfusion in patients with septic shock [7].