Background: According to current guidelines, initial burn resuscitation should be performed with fluids alone. The aims of the study were to review the frequency of use of vasoactive and/or inotropic drugs in initial burn resuscitation, and assess the benefits and harms of adding such drugs to fluids.Methods: A systematic literature search was conducted in PubMed, Embase, Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, UpToDate, and SveMed+ through 3 December 2021. The search included studies on critically ill burn patients receiving vasoactive and/or inotropic drugs in addition to fluids within 48 h after burn injury.Results: The literature search identified 1058 unique publications that were screened for inclusion. After assessing 115 publications in full text, only two retrospective cohort studies were included. One study found that 16 out of 52 (31%) patients received vasopressor(s). Factors associated with vasopressor use were increasing age, burn depth, and % total body surface area (TBSA) burnt. Another study observed that 20 out of 111 (18%) patients received vasopressor(s). Vasopressor use was associated with increasing age, Baux score, and %TBSA burnt in addition to more frequent dialysis treatment and increased mortality. Study quality assessed by the Newcastle‐Ottawa quality assessment scale was considered good in one study, but uncertain due to limited description of methods in the other.Conclusion: This systematic review revealed that there is a lack of evidence regarding the benefits and harms of using vasoactive and/or inotropic drugs in addition to fluids during early resuscitation of patients with major burns.

Background: Vasopressors are often introduced in severe burn patients who respond poorly to fluid resuscitation to maintain adequate blood pressure and avoid fluid creep . This study aims to characterise these patients and explore potential correlations between vasopressor use and patient outcomes. Methods: Medical records from 2010 to 2023 for patients aged ≥ 18 years with burns ≥ 20% of the total body surface area (TBSA) were extracted from the TriNetX Research Network, a global federated health research platform aggregating de‐identified electronic health records. The patients were divided into two groups: those who received vasopressors within the first 2 days of hospitalisation and those who did not. Statistical analysis included Cramér–von Mises and χ ² test, with significance set at p < 0.05. Propensity score matching (PSM) in a 1:1 ratio was applied for the variables age, sex, pre‐existing comorbidities (hypertension, diabetes, chronic heart disease, chronic lung disease, chronic kidney disease, and alcohol or opioid addiction), presence of inhalation injury, %TBSA burned, and burn injury year. Odds ratios (OR) for outcomes were calculated, with p ‐values adjusted for multiple testing using the Benjamini–Hochberg correction. Results: Of 6872 included patients, 17.7% received vasopressors within the first two days of hospitalisation. These patients were older, had more comorbidities and sustained more severe burns. After PSM we included 1206 patients in both cohorts (VP+ and VP−). Acute kidney injury occurred within 3 days in 51.0% of the VP+ group and 28.4% in VP− (OR 2.62, 95% CI: 2.20–3.11). VP+ patients also had higher rates of sepsis (30.8% vs. 22.9%, OR 1.50, 95% CI: 1.25–1.81) and higher mortality (45.1% vs. 32.7%, OR 1.69, 95% CI: 1.43–2.01) within 30 days following hospitalisation. Conclusion: While vasopressors are frequently administered as part of burn resuscitation, their use was associated with higher rates of early acute kidney injury and an increased 30‐day mortality rate. Editorial Comment: Potent vasopressor use to support the circulation is commonly combined with fluid resuscitation in modern intensive care, and this is a prominent aspect of care in major burn cases. In this retrospective analysis of a commercial, de‐identified health care dataset (primarily from US hospitals or health systems), matched cases over 14 recent years were analysed by early vasopressor use (or not) and then for important outcomes including mortality. Vasopressor use was associated with some complications and negative outcomes, though there are likely many factors which may contribute to negative outcomes which were not included in this analysis.

Background: Norepinephrine is commonly used during acute burn resuscitation to maintain adequate perfusion pressure. However, its effects, together with the burn-induced catecholamine surge, on arterial α₁-adrenergic receptors (α₁-AR) remain unclear. This study examined whether burn injury and continuous norepinephrine infusion alter arterial α₁-AR subtype expression at the transcriptional and protein levels. Methods: Sprague–Dawley rats were randomized to full-thickness scald burn involving 25% total body surface area with continuous intravenous norepinephrine or sodium chloride (NaCl) infusion, sham injury with norepinephrine infusion, or untreated controls. Mean arterial pressure (MAP) was measured at baseline and before euthanasia (six or 24 h). Aorta, carotid, and renal arteries were collected for analysis of α₁-AR subtypes (Adra1a, Adra1b, and Adra1d) using quantitative PCR (qPCR) and immunohistochemistry (IHC). Results: Norepinephrine efficiently increased MAP in sham animals. In burned animals with norepinephrine, MAP increased at six hours (+10.6 mmHg) but fell below baseline at 24 h (−6.4 mmHg). Burned animals given NaCl had persistently lower MAP than those given norepinephrine, at six hours (−19.1 mmHg) and 24 h (−21.1 mmHg). qPCR demonstrated significant downregulation of Adra1b in the renal artery across all groups compared to control (7.8–16.4-fold, p < 0.001). Overall, changes in protein expression across different vascular beds and receptor subtypes were inconsistent. Conclusions: Norepinephrine increased MAP in both sham and burned animals, confirming the drug’s efficacy. Burn injury and sustained norepinephrine exposure were associated with early, vessel-specific alterations in α₁-AR mRNA expression. The absence of consistent protein-level changes within 24 h suggests a delay in receptor expression on protein level.