This text are my notes taken from the video published in the #SFAR YT channel, presented by Marie-Reine Losser, about the initial reanimation of the major burn patient. First of all, here is the video in question:
Important Links
Highlights
The initial reanimation of severely burned patients is a critical phase demanding precise assessment, aggressive yet judicious intervention, and a deep understanding of the underlying pathophysiology.
Identifying patients requiring aggressive reanimation is paramount. This extends beyond those presenting in overt shock or respiratory distress to include individuals with:
- extensive total body surface area (TBSA) burns
- significant comorbidities that may compromise their physiological reserve
- specific injury patterns such as high-voltage electrical burns
Electrical burns, in particular, warrant heightened vigilance due to the potential for significant internal tissue damage and associated complications like rhabdomyolysis, which may not be immediately apparent externally.
Airway and ventilation
While initial airway management often occurs pre-hospital, continuous reassessment is vital. Secondary decompensation, potentially due to progressive airway edema or inhalation injury, may necessitate delayed sequence intubation.
Fiberoptic bronchoscopy is not merely diagnostic but crucial for assessing the severity of smoke inhalation, guiding the need for aggressive pulmonary toilet, and identifying potential airway compromise due to soot and secretions within the bronchial tree.
Ventilatory support should adhere to lung-protective strategies, prioritizing low tidal volumes, managing plateau pressures, and titrating FiO2 to maintain adequate oxygenation while minimizing oxygen toxicity.
Antibiotic use
A key point emphasized is the current consensus against routine prophylactic antibiotic use, even in documented smoke inhalation, due to concerns about promoting resistance and the lack of clear evidence of benefit in preventing early pneumonia.
Fluid resuscitation
Fluid resuscitation in severely burned patients is guided by formulas (e.g., Parkland formula) based on weight and burn percentage, but these provide only an initial estimate. For instance, an 80 kg patient with 50% TBSA burns might initially require approximately 8 liters of fluid in the first 8 hours. However, rigid adherence to formulas without dynamic physiological assessment is strongly discouraged.
Monitoring
Monitoring goes beyond standard vital signs. While mean arterial pressure (MAP) is a necessary parameter, tachycardia is often an unreliable indicator of hypovolemia in the context of the burn-induced hyperadrenergic and inflammatory state. Urine output, targeting 0.5 to 1 mL/kg/hour, serves as a more sensitive marker of end-organ perfusion. Elevated lactate levels should prompt a critical re-evaluation of resuscitation adequacy and potential adjustments to fluid administration rates.
In cases refractory to initial fluid boluses or presenting with frank shock, advanced hemodynamic monitoring is warranted. While pulmonary artery catheters can provide comprehensive data, their use may be limited by burn locations – does anyone use them anymore outside chest and heart surgery contexts? Alternatives include central venous pressure (CVP) monitoring (are they really useful?) and non-invasive or minimally invasive stroke volume assessment tools. Fluid boluses should be administered cautiously, with a focus on documented increases in stroke volume or CVP rather than empiric administration.
Albumin
The role of albumin in resuscitation remains a topic of discussion; however, incorporating albumin into the protocol, particularly in extensive burns, should be considered . The rationale lies in the significant loss of endogenous albumin due to increased capillary permeability, contributing to decreased oncotic pressure and exacerbating edema.
Myocardial dysfunction
The complex interplay of systemic inflammation and early myocardial dysfunction, often seen in extensive burns, contributes to vasoplegia. This necessitates a delicate balance in fluid management to avoid the detrimental effects of both under-resuscitation and fluid overload, which can precipitate or worsen pulmonary edema .
Shock
Understanding the pathophysiology is key to rational management. Burn shock is a form of distributive shock driven by massive fluid shifts. The initial injury damages the extracellular matrix and increases capillary permeability, leading to rapid fluid and protein leakage into the interstitial space of the burned tissue. This is followed by a sustained systemic inflammatory response, which further compromises capillary integrity in both burned and unburned tissues. The resultant loss of plasma proteins, particularly albumin, reduces plasma oncotic pressure, further driving fluid extravasation and exacerbating edema formation . This profound hypovolemia, often occurring with burns exceeding 20-30% TBSA, necessitates aggressive fluid replacement .
Organ dysfunction
Burn injury has profound effects on multiple organ systems.
The kidneys are susceptible to acute kidney injury (AKI) from a confluence of factors including hemodynamic instability, pigment nephropathy from rhabdomyolysis (especially post-electrical injury), exposure to nephrotoxic agents, and the effects of positive pressure ventilation . Secondary insults such as systemic inflammation, surgical interventions, and septic shock further increase the risk of AKI.
The pulmonary system is particularly vulnerable. Smoke inhalation directly damages the alveolar-capillary membrane and bronchial epithelium, impairing gas exchange and increasing susceptibility to infection. Aggressive fluid resuscitation, while necessary, can exacerbate pulmonary edema in the setting of increased capillary permeability, further compromising lung function.
Prevention of complications
Prevention of complications is integral to initial management. Hypothermia must be assiduously avoided through aggressive warming measures, as it can worsen coagulopathy and metabolic acidosis.
Management of agitation and delirium requires a multifactorial approach, prioritizing adequate pain control, minimizing benzodiazepine use, and considering agents like dexmedetomidine for sedation and delirium prevention.
Pain management should employ a multimodal strategy, including regional anesthesia techniques where feasible, to reduce opioid requirements.
Early enteral nutrition, ideally initiated within 12 hours of injury, is critical for maintaining gut integrity, meeting the hypermetabolic demands of burn injury, and preventing ileus.
Given the hypercoagulable state, prophylactic low molecular weight heparin (LMWH) is recommended for venous thromboembolism prevention.
Infection remains a leading cause of morbidity and mortality; therefore, strict aseptic technique during wound care and avoiding routine antibiotics are paramount.
Urgent surgical intervention is generally limited to escharotomies to decompress constricting circumferential burns .
Multidisciplinary care
The initial 24 hours of reanimation are focused on stabilizing the patient and optimizing physiological function to bridge them to definitive care . Effective burn care is inherently multidisciplinary, requiring seamless collaboration between critical care physicians, burn surgeons, nurses, physical therapists, and other specialists. Future advancements in areas such as skin substitutes, 3D-printed skin, and immunomodulation hold promise for further improving outcomes in this complex patient population.