Burns And Fluid Management in Major Burn Injuries.

 

 

Overview

Burn injuries lead to a fluid loss which is a problem that leads to morbidity and death. Thus, fluid replacement should form the bases for the modern burn treatment. This paper focuses on treatment of burns and management of fluids as well as reviewing approaches in fluid management to adults with burn injuries.

Aims

The objectives of this paper are addressed in a fourfold base. The first objective focuses on addressing the pathophysiology of burns. From this, the reader can understand the clinical progression of the injuries. Secondly, the paper aims at addressing the treatment methods which provides the necessary steps for management of the patient in general and fluid in specific. Finally, the paper aims at creating awareness of the increased demand for more research, publication, and funding to build a clear understanding of burns and fluid loss management.

Background

In 2004 the World Health Organization reported that the rate of deaths resulting from injuries including burns is increasing. Thus, this raises the alarm for fire prevention such as smoke detectors and fire response, i.e., firefighters’ personnel. All these together with health care cost, create an economic burden. Moreover, a fluid loss that accompanies these burns needs to be adequately managed to increase survival of burn patients directly. However, there are controversies in regards right type of fluid management approach for the first 24 hours of a burn injury (Landry et al. 2013). Today, the accepted guidelines being used are liquid replacement formulas that were developed some decades ago.  To this end, current research focuses on the issue of burn patients being over or under fluid resuscitated (Haberal, Abali, & Karakayali 2010).

 

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Pathophysiology of burn shock

Severe burns occur in necrotic zone area beneath which lies the zone of statist lies. This result to production of inflammation mediators that contribute to increased permeability of the capillary leading to localized burn wound edema. This happens within minutes or hours and presumes the production of reactive oxygen species (Scott et al. 2005). These reactive oxygen species are very toxic cell metabolites which cause the local cellular membrane to dysfunction leading to an immune response. Consequently, decreased Transmembrane cellular potential occurs in both injured and uninjured tissues. Sodium ATPase is disrupted as a result of Cellular membrane dysfunction leading to Sodium ATPase activity. This causes a shift in intracellular sodium contributing to hypovolemic as well as cellular edema. Vasoactive mediators are also activated during heat injury. This causes vasoconstriction of the local surface, vasodilation and increased capillary permeability (Tricklebank 2009).This result to improved transfer of water, plasma proteins and inorganic solutes between the cellular spaces. Also, intravascular hypovolemic and haemoconcentration get to their maximum levels. This leads to fluid loss that needs sustained replacement to prevent end-organ hypoperfusion and ischemia. During this early stage several pathophysiology changes occur, and thus, appropriate fluid management needs implementation (Haberal, Abali, & Karakayali 2010).

Attempts to explain why there are high mortality and morbidity due to fire are being conducted. According to World Health Organization, the common risk factors are alcohol, smoke, cooking ground level stoves, open fires close to homes, setting water heaters to high temperatures and improper electrical wiring (Ahrens 2009)

 

Recommendations

Due to insufficient data on the right fluid management for burn patients, The American Burn Association provides the guidelines to resuscitative burn shock as they undertake their investigations (Singer, Brebbia, & Soroff 2007).These and other recommendations are discussed below.

Intervention	Rationale
Adults whose burns exceed 20% TBSA should go through formal fluid resuscitation based on body size and burned surface area.	Since the morbidity and mortality of burns increase with burn size, this intervention is important in helping to determine the burn surface area and put appropriate measures of control in place ( Hettiaratchy, S., & Papini, R. (2004).
Recommend the need to titrate fluid resuscitation regardless of its type, to sustain urine output to 0.5-1,0ml/kg/hr.	The second recommendation emerged from the fact that most burn patients were being overenunciated. Meta-analysis of fluid requirement illustrated that the volume administered was more than the formula estimates, and mean urine output was on the high target level. Excessive fluid resuscitation can increase infection risks and complications which can result in death. To maintain a balance between too little and too much fluid is difficult and has led to complains by clinicians that current formulas are hard to follow. Thus, fluid titration should be automated and personalized during resuscitation to achieve better burn care outcomes (Bhat et al. 2004).
During the first 24 hours, formulas used in the initiation of resuscitation should provide 2-4 ml/kg body weight % TBSA of crystalloid.	High volumes of hypertonic saline raise plasma sodium levels. This is associated with reduced urine output which is dangerous to patients. Therefore, regular sodium concentrations monitoring is essential because it helps reduce the risk of severe hypernatremia and acute renal failure.
A secondary survey should be conducted to identify other associated injuries	All burnt, constricting, or covered in chemical cloths and jewelry should be removed to avoid further injury.  Flowing water should be used to cool and clean burns. Ice water should be avoided as it increases tissue injury ( Singer &Dagum 2008)
Parkland formula should be decreased to 3ml/kg % TBSA.	Excessive fluid resuscitation is the major problem when it comes to fluid resuscitation. It can lead to pulmonary edema, acute respiratory distress syndrome, limb compartment syndrome and cerebral edema. Mostly it occurs when patients are under strict hydration and urinary output demands. Thus the need to reduce Parkland formula to 3% TBSA Pruitt Jr, B. A. (2000).  .
High lipid containing products such as Aloe Vera, lotion and honey can be used to treat superficial burns instead of antibiotics.	Topical steroids should be avoided in burn treatment as they do not help in reducing inflammation. However, all deep burns require topical antimicrobial or dressing that is absorptive (Jull, A. B., Rodgers, A., & Walker, N. 2008).
Acid burns are not to be neutralized with a base and base burn should not be neutralized with an acid	Patients who are burned with chemicals should be first brushed off the chemical and the skin flushed with running water for 30 minutes. Acid burns should not be treated with bases and vice versa. This intervention will reduce burn deterioration by limiting chemical reactions (Singer,  Brebbia, & Soroff 2007)
Initial treatment and assessment of severe burns should be done simultaneously with trauma resuscitation	This intervention focuses on making the airways, breathing, and circulation stable. This will help reduce burn morbidity and mortality, related to suffocation. The evaluation involves checking for respiratory distress, smoke inhalation, checking for other injuries and cardiovascular status and defining the level of burn (Hoffman & Weinhouse 2011).
Patients with burns that are less than 10% TBSA can be given oral hydration unless there are complications or burns in mouth or airways.	This intervention is important as it reduces the cost of care and complications related to intravenous resuscitation. It also helps to understand that all patients have different systemic responses to fluid loss. Thus, the demand for crystalloids is not the same for all patients.
Antibiotics should not be the common treatment for burns that are not deep	Only burns that are deep require antimicrobial treatments (Campbell, Alderson, Smith, & Warttig, 2015).

 

References

Bhat, S., Humphries, Y. M., Gulati, S., Rylah, B., Olson, W. E., & Twomey, J. (2004). The problems of burn resuscitation formulas: A need for a simplified guideline. J Burns Wounds, 3(7).

Campbell, G., Alderson, P., Smith, A. F., & Warttig, S. (2015). Warming of intravenous and irrigation fluids for preventing inadvertent perioperative hypothermia. status and date: New, published in, (4).

Haberal, M., Abali, A. E. S., & Karakayali, H. (2010). Fluid management in major burn injuries. Indian journal of plastic surgery: official publication of the Association of Plastic Surgeons of India, 43(Suppl), S29.

Hettiaratchy, S., & Papini, R. (2004). ABC of burns: Initial management of a major burn: II—assessment and resuscitation. BMJ: British Medical Journal, 329(7457), 101.

Hoffman, R. S., & Weinhouse, G. L. (2011). Management of moderate and severe alcohol withdrawal syndromes. UpToDate. Waltham (MA): UpToDate.

Jull, A. B., Rodgers, A., & Walker, N. (2008). Honey as a topical treatment for wounds. Cochrane Database Syst Rev, 4

Landry, A., Geduld, H., Koyfman, A., & Foran, M. (2013). An overview of acute burn management in the Emergency Centre. African Journal of Emergency Medicine, 3(1), 22-29

Pruitt Jr, B. A. (2000). Protection from excessive resuscitation:“pushingS the pendulum back”.

Scott, J. R., Muangman, P. R., Tamura, R. N., Zhu, K. Q., Liang, Z., Anthony, J., … & Gibran, N. S. (2005). Substance P levels and neutral endopeptidase activity in acute burn wounds and hypertrophic scar. Plastic and reconstructive surgery, 115(4), 1095-1102.

Singer, A. J., & Dagum, A. B. (2008). Current management of acute cutaneous wounds. New England Journal of Medicine, 359(10), 1037-1046.

Singer, A. J., Brebbia, J., & Soroff, H. H. (2007). Management of local burn wounds in the ED. The American journal of emergency medicine, 25(6), 666-671.

World Health Organization (2004). The global burden of disease

Ahrens, M. (2009). Smoke alarms in US home fires. Quincy, MA: National Fire Protection Association, Fire Analysis and Research Division.Pham, T. N., Cancio, L. C., & Gibran, N. S. (2008). American Burn Association practice guidelines burn shock resuscitation. Journal of Burn Care & Research, 29(1), 257-266.

Haberal, M., Abali, A. E. S., & Karakayali, H. (2010). Fluid management in major burn injuries. Indian journal of plastic surgery: official publication of the Association of Plastic Surgeons of India, 43(Suppl), S29.

Tricklebank, S. (2009). Modern trends in fluid therapy for burns. burns, 35(6), 757-767.

 

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