Search

Opioids are the mainstay of treatment for burn pain. However, these medications may be associated with respiratory depression and dependence. Multimodal analgesia is an alternative method that utilizes both opioid and nonopioid medications with different mechanisms. This study examines the impact of multimodal therapy for postoperative pain control in a burn intensive care unit. This was a retrospective cohort study of patients admitted to the burn unit at a tertiary medical center. Consecutively admitted patients with burns greater than or equal to 10% TBSA and intensive care unit length of stay greater than 7 days were eligible for inclusion (2012–2018). Patients were excluded if they received an opioid infusion greater than 48 hours. Patients treated with multimodal analgesia were compared to those treated with opioids alone. Data were calculated for 5 days after surgery. There were 98 patients in the nonmultimodal group and 97 in the multimodal group. Mean cumulative opioid dose was lower in the multimodal group (1028.7 mg vs 1423.2 mg, P = .0031). Patients with greater than 20% burns had a larger reduction in mean opioid equivalents in the multimodal group (1106 vs 1594 mg, P = .009) compared to patients with burns less than 20% (940 vs 1282 mg, P = .058). There was no difference in mean pain scores on postoperative day 5 (6.2 ± 2.2 vs 5.5 ± 2.3, P = .07) or at intensive care unit discharge (4.7 ± 2.4 vs 4.7 ± 2.8, P = .99). The use of multimodal analgesia significantly reduced cumulative opioid equivalent dose without compromising pain control.

Systemic anticoagulation with unfractionated heparin is standard of care for patients receiving extracorporeal life support (ECLS); however, an alternative anticoagulant may be necessary when challenges with heparin therapy arise. Evidence for alternative anticoagulation in ECLS patients is limited. This retrospective analysis evaluated the dosing and outcomes associated with bivalirudin use in 14 adult ECLS patients. Indications for bivalirudin included heparin-induced thrombocytopenia, heparin resistance, or persistent clotting or bleeding while on heparin. The median initial bivalirudin dose to achieve target activated partial thromboplastin time was 0.15 mg/kg/h (range 0.04-0.26 mg/kg/h). Dosing requirements increased by 75-125% when renal replacement was included. Median time on bivalirudin was 5.2 days (range 0.9-28 days). Five patients (36%) required a circuit change while on bivalirudin because of clotting or failing oxygenation, and four (28.6%) had bleeding significant enough to require either reduction in activated partial thromboplastin time goals or temporary holding of anticoagulation. Bivalirudin appears to be a potential option for adult patients on ECLS who are unable to receive or fail heparin therapy; however, the wide variation in dosing suggests the need for careful management.

Supplemental Digital Content is available in the text., Objectives: To determine whether the use of flumazenil reverses hypoactive delirium and increases delirium-free days in critically ill patients who were exposed to benzodiazepine therapy during the ICU admission. Design: This was a single-center, double-blinded, randomized placebo-controlled pilot study. Setting: Adult ICUs at a large academic medical center in the United States. Patients: Adult, critically ill patients with benzodiazepine exposure and hypoactive delirium based on the Confusion Assessment Method-ICU and Richmond Agitation Sedation Scale assessments were considered for enrollment. Interventions: Patients received a test dose of flumazenil starting at 0.1 mg intravenously and titrated up every 5 minutes by 0.1 mg increments up to a maximum total dose of 2 mg. Patients who demonstrated a Richmond Agitation Sedation Scale score increase of greater than 1 point were considered responders and randomized to flumazenil (0.05–0.3 mg/hr) or placebo infusion for up to 72 hours. Confusion Assessment Method-ICU scores were assessed twice daily for resolution of delirium. Measurements and Main Results: The trial was stopped early based on the observed size effect and power analysis. Twenty-two of the 25 patients responded to the flumazenil test dose (88%). The median number of delirium-free days alive without coma within 14 days of enrollment was similar between the two infusion groups (12.7 vs 9.2; p = 0.19). There was no difference in the probability of delirium resolution within the first 14 days with 90% versus 70% in the flumazenil and placebo groups, respectively (p = 0.2). There was no statistical difference (odds ratio, 0.17; 95% CI, 0.022–1.23; p = 0.079) in delirium- and coma-free days at the end of the study drug infusion. There was no difference between groups in ICU length of stay (7.8 ± 4.8 vs 7 ± 8; p = 0.74). No serious adverse events occurred. Conclusions: This study found that flumazenil test dose and infusion present a potential option for hypoactive delirium associated with benzodiazepine exposure; however, the possible benefit is unknown. Larger studies are warranted to further evaluate these findings.

Background:Self-reported and behavioral pain assessment scales are often used interchangeably in critically ill patients due to fluctuations in mental status. The correlation between scales is not well elucidated. The purpose of this study was to describe the correlation between self-reported and behavioral pain scores in critically ill patients.Methods:Pain was assessed using behavioral and self-reported pain assessment tools. Behavioral pain tools included Critical Care Pain Observation Tool (CPOT) and Behavioral Pain Scale (BPS). Self-reported pain tools included Numeric Rating Scale (NRS) and Wong-Baker Faces Pain Scales. Delirium was assessed using the confusion assessment method for the intensive care unit. Patient preference regarding pain assessment method was queried. Correlation between scores was evaluated.Results:A total of 115 patients were included: 67 patients were nondelirious and 48 patients were delirious. The overall correlation between self-reported (NRS) and behavioral (CPOT) pain scales was poor (0.30, P = .018). In patients without delirium, a strong correlation was found between the 2 behavioral pain scales (0.94, P < .0001) and 2 self-reported pain scales (0.77, P < .0001). Self-reported pain scale (NRS) and behavioral pain scale (CPOT) were poorly correlated with each other (0.28, P = .021). In patients with delirium, there was a strong correlation between behavioral pain scales (0.86, P < .0001) and a moderate correlation between self-reported pain scales (0.69, P < .0001). There was no apparent correlation between self-reported (NRS) and behavioral pain scales (CPOT) in patients with delirium (0.23, P = .12). Most participants preferred self-reported pain assessment.Conclusion:Self-reported pain scales and behavioral pain scales cannot be used interchangeably. Current validated behavioral pain scales may not accurately reflect self-reported pain in critically ill patients.

Dexmedetomidine (DEX) is a selective α2 adrenergic agonist that is commonly used for sedation in the intensive care unit (ICU). The role of DEX for adjunctive treatment of refractory intracranial hypertension is poorly defined. The primary objective of this study was to determine the effect of DEX on the need for rescue therapy (ie, hyperosmolar boluses, extraventricular drain [EVD] drainages) for refractory intracranial hypertension. Secondary objectives included the number of intracranial pressure (ICP) excursions, bradycardic, hypotensive, and compromised cerebral perfusion pressure episodes. This retrospective cohort study evaluated patients admitted to the neurosurgical ICU from August 1, 2009, to July 29, 2015, and who received DEX for refractory intracranial hypertension. The objectives were compared between the 2 time periods—before (pre-DEX) and during therapy (DEX). Twenty-three patients with 26 episodes of refractory intracranial hypertension met the inclusion criteria. The number of hyperosmolar boluses was decreased after DEX therapy was initiated. Mannitol boluses required were statistically reduced (1 vs 0.5, P = .03); however, reduction in hypertonic boluses was not statistically significant (1.3 vs 0.9, P = .2). The mean number of EVD drainages per 24 hours was not significantly different between the time periods (15.7 vs 14.0, P = .35). The rate of ICP excursions did not differ between the 2 groups (24.3 vs 22.5, P = .62). When compared to pre-DEX data, there was no difference in the median number of hypotensive (0 vs 0), bradycardic (0 vs 0), or compromised cerebral perfusion pressure episodes (0.5 vs 1.0). Dexmedetomidine may avoid increases in the need for rescue therapy when used as an adjunctive treatment of refractory intracranial hypertension without compromising hemodynamics.

Background: There is inadequate guidance for clinicians on selection of the optimal dextrose 50% (D50W) dose for hypoglycemia correction in critically ill patients. Objective: The purpose of this study was to determine the blood glucose (BG) response to D50W in critically ill patients. Methods: A retrospective analysis was conducted of critically ill patients who received D50W for hypoglycemia (BG < 70 mg/dL) while on an insulin infusion. The primary objective of this study was to determine the BG response to D50W. The relationship between participant characteristics and the dose-adjusted change in BG following D50W was analyzed using simple and multiple linear mixed-effects models. Results: There were 470 hypoglycemic events (BG < 70 mg/dL) corrected with D50W. The overall median BG response was 4.0 (2.53, 6.08) mg/dL per gram of D50W administered. Administration of D50W per protocol resulted in 32 episodes of hyperglycemia (BG > 150 mg/dL), resulting in a 6.8% rate of overcorrection; 49% of hypoglycemic episodes (230/470) corrected to a BG >100 mg/dL. A multivariable GEE analysis showed a significantly higher BG response in participants with diabetes (0.002) but a lower response in those with recurrent hypoglycemia ( P = 0.049). The response to D50W increased with increasinginsulin infusion rate ( P = 0.022). Burn patients experienced a significantly larger BG response compared with cardiac, medical, neurosurgical, or surgical patients. Conclusions: The observed median effect of D50W on BG was approximately 4 mg/dL per gram of D50W administered. Application of these data may aid in rescue protocol development that may reduce glucose variability associated with hypoglycemic episodes and the correction.