Intravenous Acetaminophen–Induced Hypotension: A Review of the Current Literature

Abstract

Objective: Recent literature suggests that intravenous (IV) administration may cause hypotension in hospitalized patients; data further suggest that this effect is most pronounced in the critically ill. The purpose of this review is to identify and evaluate current literature that addresses the incidence and implications of IV acetaminophen–induced hypotension. Data Sources: A literature search of MEDLINE, Cochrane, and EMBASE databases was performed (2002-2019) using the following terms: acetaminophen, paracetamol, intravenous, and hypotension. Abstracts and peer-reviewed publications were reviewed. Study Selection and Data Extraction: Relevant English-language studies conducted in humans evaluating the hemodynamic effects of IV acetaminophen were considered. Data Synthesis: A majority of the 19 studies included in this review identified a statistically significant drop in hemodynamic variables after the administration of 500 to 1000 mg IV acetaminophen as measured by changes in systolic blood pressure, diastolic blood pressure, or mean arterial pressure. Of the trials reporting vasopressor use, the authors found a significant increase in vasopressor requirements following IV acetaminophen administration. Relevance to Patient Care and Clinical Practice: This review represents the first comprehensive review of IV acetaminophen-induced hypotension. The findings raise the question of whether IV acetaminophen is an appropriate choice for inpatient pain or temperature management in the critically ill. Conclusions: Available evidence indicates that the administration of IV acetaminophen may be harmful in the critically ill. Additional monitoring is likely required when using IV acetaminophen in this specific population, particularly if a patient is hemodynamically unstable prior to administration.

A narrative review of paracetamol‐induced hypotension: Keeping the patient safe

“…Without close observation, patients may have a paracetamol‐induced trough in BP, which vastly goes undetected (Figure 2). Despite the evidence described in the literature, there are currently insufficient haemodynamic warnings available within disclosures made by pharmaceutical companies that market paracetamol (Kelly et al., 2016; Maxwell et al., 2019). Counterintuitively, such omission can influence clinical practice guidelines for safe paracetamol administration.…”

The Routes of Administration for Acute Postoperative Pain Medication

“…Recent guidelines [ 29 ] confirm the nonsignificant difference between IV and oral formulations in terms of pain scores, rescue medication, and AEs, with reduced costs of oral paracetamol. The risk of hepatotoxicity from therapeutic doses of paracetamol is extremely low, while the risk of hypotension is reported, particularly with IV formulations in critically ill patients [ 52 ].…”

Fever: Could A Cardinal Sign of COVID-19 Infection Reduce Mortality?

“…A key mechanism for lowering temperature is by initiation of cutaneous vasodilation, [50][51][52] similar to what occurs during defervescence, which facilitates arterial heat dissipation from the skin. This vasodilation can occur to varying degrees in a febrile patient, but studies in both adults [53][54][55] and children 56,57 have shown this often leads to a clinically significant fall in mean arterial pressure. The subsequent acetaminophen-induced hypotension is then countered with fluid and/or vasopressor support to maintain adequate organ perfusion.…”

“…The subsequent acetaminophen-induced hypotension is then countered with fluid and/or vasopressor support to maintain adequate organ perfusion. [53][54][55][56][57] Thus, a vicious cycle ensues as we desperately work against the normal physiology of the body to maintain blood pressure, but as total body water stores increase, oxygenation in the lungs then becomes compromised, inducing unnecessary harm. 58 The time for an evidence-based approach to fluid management in the febrile patient is long overdue.…”