Terlipressin & Lactic Acidosis: Case Report of Vasospasm in Cirrhosis

A recent case report details severe complications arising from the use of terlipressin, a vasopressor, in a patient with cirrhosis and oesophageal variceal bleeding. The incident, documented in Cureus, highlights the potential for widespread vasospasm and multi-organ dysfunction when the drug is administered, even in settings where it is increasingly used.

Terlipressin is a synthetic analogue of vasopressin, a naturally occurring hormone that constricts blood vessels. It’s gaining traction in the management of complications related to cirrhosis, particularly refractory ascites – fluid buildup in the abdomen that doesn’t respond to standard treatment – as noted in research published in HepComm. The case report details a situation where terlipressin administration led to severe lactic acidosis and multi-organ dysfunction, underscoring the need for careful monitoring and a thorough understanding of the drug’s potential adverse effects.

The patient in question suffered from liver cirrhosis and was experiencing bleeding from oesophageal varices – enlarged veins in the esophagus that are prone to rupture in individuals with portal hypertension, a common complication of cirrhosis. Terlipressin was administered to control the bleeding, but the patient subsequently developed widespread vasospasm, leading to a significant reduction in blood flow to various organs. This resulted in severe lactic acidosis, a condition where lactic acid builds up in the bloodstream, and multi-organ dysfunction.

Lactic acidosis is a particularly concerning complication. As explained in a chapter on hemodynamic optimization in anesthesia for liver transplantation, published by IntechOpen, higher doses of norepinephrine, another vasopressor, can also promote lactic acidosis through peripheral vasospasm. The case report suggests terlipressin carries a similar risk, even at doses intended to control variceal bleeding. The development of lactic acidosis indicates inadequate tissue perfusion, meaning organs aren’t receiving enough oxygenated blood to function properly.

The clinical evaluation report for Terlipressin, available from the Therapeutic Goods Administration of Australia (TGA), lists acidosis lactic as an adverse reaction observed in clinical trials, although the frequency was relatively low (2 cases). Other reported adverse reactions included haematoma, vomiting, and diarrhoea. This report, however, doesn’t detail the severity of these reactions or the specific circumstances surrounding their occurrence.

The increasing use of terlipressin is driven by its potential to improve outcomes in patients with cirrhosis. However, this case highlights the importance of recognizing and promptly addressing potential complications. Cirrhosis itself is often associated with renal dysfunction and an increased risk of acute kidney injury, as detailed in research published in Gastro. The addition of terlipressin-induced vasospasm can exacerbate these existing vulnerabilities, potentially leading to a cascade of organ failures.

While terlipressin has shown promise in certain applications, such as increasing cerebral perfusion pressure (CPP) without significantly raising intracranial pressure (ICP) – a finding reported in ScienceDirect – clinicians must remain vigilant for signs of excessive vasoconstriction. The case report serves as a stark reminder that the benefits of terlipressin must be carefully weighed against its potential risks, particularly in patients with pre-existing conditions like cirrhosis and portal hypertension.

The incident underscores the need for robust monitoring protocols when terlipressin is used. Close observation of vital signs, including blood pressure, heart rate, and oxygen saturation, is crucial. Regular assessment of lactate levels can help detect the early stages of lactic acidosis. Clinicians should be prepared to rapidly intervene with supportive care, such as fluid resuscitation and vasodilation, if signs of organ dysfunction develop. The long-term implications of such events, and the potential for lasting organ damage, require further investigation.