Frontiers in Medical Case Reports (FMCR)
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Pages: 1-15

Date of Publication: 30-Nov--0001

Management of Severely Burned Adult Patients: From Sedation to Organ Dysfunction

Author: Nissar Shaikh, Shoaib Nawaz, Arshad Chanda, Naiathramveetil MM, Rahman MA, Muhammad Zubair, Qazi Zeeshan, Mathais R, AR. Raju Vegesna, Thomas J

Category: Surgical Case Reports

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Abstract:

Burns are devastating and debilitating injuries leading to high morbidity and mortality, emotional stress and they add to the financial burden. Severely burned patients should preferably be managed in burn centre with dedicated intensive care unit (ICU). Severity of burns are classified according to the degree of burns and total body surface area (TBSA) with burns. Rule of nine is used for calculation of TBSA with burn. Severe burns will cause cellular leak, hypovolemia, storm of proinflammatory markers and cardiovascular impairment leading to the burn shock and multiple organ dysfunction.

Intensive care management of severe burns includes resuscitation and organ supportive care. There are number of formulae for fluid resuscitation in these patients, these formulas give initial guidance for fluid resuscitation and further fluid therapy should be guided by dynamic preload parameters. The opioids and benzodiazepines are frequently used for analgesia and sedation respectively whereas ketamine and dexmedetomidine have added advantage of opioid and benzodiazepine sparing effects. In these patient’s hyperglycaemia and hypercatabolism should be controlled. ARDS (acute respiratory distress syndrome) occurs in up to 50% of the ventilated burns patient. High frequency percussive ventilation and use of ARDS adjuvant therapies will have better outcome. Acute kidney injury occurs in 30% of severe burns, renal replacement therapy should be started early. Early enteral feeds, gastric ulcer prophylaxis and adequate fluid resuscitation will prevent the GI dysfunction. Burns shock will improve with adequate fluid resuscitation and supportive care. The common neurological dysfunction in burns is delirium. Delirium should be managed with pharmacological and non-pharmacological therapies. There is a decreasing trend in the mortality of severely burns patients and it is around 10%.

Keywords: Airway, Burn shock, Multiorgan dysfunction, Sedation, Sepsis

Full Text:

Although majority of burns are preventable, burns remained 4th major trauma related injuries. The burn injuries are difficult and devastating injuries. They are more common in low socioeconomic group and in lesser developed countries. These injuries cause high morbidity and mortality, emotional imbalance, additional socioeconomic burden and can be stressful (Smolle, 2017). Severe burns are the burns involving more than 20% of the body surface area or inhalational injury, chemical, electric burns, lightening injury and burns associated with other traumatic injuries.

In October 2012 a fire broke out in a marriage party in which 25 people were killed and 30 people sustained injuries (Kattan et al., 2016). In Kuwait in 2009 electric short circuit and fire led to death of 57 people and caused injuries to 90 more people (Shih et al., 2017). Both these major fire accidents were preventable and use of fire alarms and exist doors decreased the incidence of burn injuries (Sheridan, 2016). Coconut Grove pub fire raised the initial alarm to have a better preventive measures and the recent advances in the medical science namely in resuscitation, wound care, infection control and management of inhalation injuries improved the care of severely burned patients. The complex metabolic and glycaemic changes, multiple organ dysfunction, repeated long term interventions remained worrisome factors (Herndon and Thompkins, 2004).

Epidemiology

World Health Organization (WHO), reports that more than 300,000 people per year die from burn injuries all over the world, the highest deaths are from Southeast Asia and the Middle East. Majority of burn (90%) related fatalities occur in moderate and low income countries due to a lack of medical and resuscitative facilities (Seyed-Forootan et al., 2016). Smolle C, et al. reviewed 46 burn publications, majority of studies come from highly developed (HD) countries, few from medium developed (MD) and no reports from low developed (LD) countries. Australia, Bulgaria, China, the Czech Republic, Finland, Iran, Israel, the Netherlands, the Oman and the United Kingdom are reporting an increasing trend in burn incidence and hospital admissions. Austria, Canada, Chile, China, Germany, Hong Kong, India, Japan, Mexico, Netherlands, Singapore, South Africa, South Korea, Sweden and the United States are showing decreasing trend in burn incidences (Smolle et al., 2017). Studies from Australia, Austria, Bulgaria, Chile, China, Germany, Israel, Netherlands, Taiwan and the United States are showing a decreasing trend in severity of burns (Smolle et al., 2017).

Burn injuries are frequent in younger age group, the average age of patients with burn injuries was 30.38 years. The hip is the most frequently burned area (45.9%), followed by thigh (22%) and wrist and hand (19%) (Sarbazi et al., 2019).

The common traumatic injuries associated in burns patients are multiple fractures (64%), complex soft tissue injuries (52%), head injuries (26%) and thoraco-abdominal injuries in 24% (Table 1) (Santaniello et al., 2004).

Table1: The traumatic injuries associated with burns

Type of Injuries

%

Multiple skeletal fractures

64%

Soft tissue injuries

52%

Traumatic brain injuries

26%

Thoraco-abdominal injuries

24%

Types of Burn

The following are the common types of burns (Yasti et al., 2015).

Flame burn: Common type of burn, caused by burning flames.

Electric burn: This burn injury occurs due to the electric current causing arc burns. These patients will have entry and exit points. This type of burns is known to cause high cardiac and muscular injuries.

Chemical burn: It occurs when skin or eyes comes in contact with chemical irritants acid or base.

Thermal burn: It is the burns caused by heated objects or liquids.

Inhalation injuries: These are the burns causing injury to the upper and lower airway (Yasti et al., 2015).

Severity of Burn

Severity of burns is classified as follows

The 1st degree burns injuries epidermis is intact, there is erythema. In 2nd degree burns, the epidermal integrity is lost. When all the layers of dermis are involved, it is 3rd degree burns. In 4th degree burns all layers of skin, subcutaneous tissues and muscles are injured and there is carbonised appearance (Santaniello et al., 2004; Yasti et al., 2015).

Minor burns are the 2nd degree burns involving less than 10% of total body surface area (TBSA) in adults. Moderate burns are the 2nd degree burns involving 15 to 20% TBSA. Major or severe burns are when burn injury occurs to more than 20% of the TBSA (Sarbazi et al., 2019; Santaniello et al., 2004; Yasti et al., 2015).

Calculation of Percentage of Burns

The extent of burns is described by the percentage of burns involving total body surface area (TBSA). TBSA is important to calculate TBSA for prescribing the required amount of fluids and to decide the need to transfer the patient to specialized burn centres (Kagan and Smith, 2000). There are three methods to calculate the TBSA with burns 1. Wallace rule of nine 2. Palm method 3. Lund and Browder chart.

Wallace rule of Nine: In this formula various body sections represent 9% each of the TBSA. It is the most commonly used formula for calculation of burn percentage in adult, it is not accurate in pediatric population. In Palm method, each palm including fingers represents 1% of TBSA. Lund and Browder chart is used in pediatric population as the surface area of the neck and head is much larger compared to the limbs in children (Kagan and Smith, 2000).

Pathophysiology of Shock in Severe Burns

When the burns are severe or involve more than 1/3rd of the TBSA leading to typical derangements of cardiovascular functions and shock, it is commonly called as burn shock (Figure1). The etiopathology of burn shock is combination of direct tissue injury, hypovolemia and the storm of pro-inflammatory mediators generated by burn injuries. The strong negative interstitial fluid pressure, capillary leak, loss of glycocalyx and endothelial activation lead to rapid edema formation in burn patients. Although the colloids are blamed for the increased edema formation in burns, the recent study showed that the use of crystalloid fluids in resuscitation increases the glycocalyx damage and shock thus increasing the cellular leak and more edema formation (Wurzer et al., 2018).

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Figure 1: Pathophysiology of edema and shock in burns

Indications for Intensive Care Unit (ICU) Admission of Burn Patients

Following burn patients should be admitted to intensive care unit (ICU) for monitoring and /or management (Spiro and Lambert, 2015),

  1. Patients with chemical and electric burns
  2. Inhalation injury patients
  3. Burns involving more than 20% of the TBSA
  4. Patients with burns shock and organ dysfunction
  5. Burns involving extremities, genitalia and major joints.

Burn patient management in ICU

Moderate to severe burns and above-mentioned patients are better managed in a specialized burn centre with dedicated burns ICU as multidisciplinary teamwork and skilful management in the intensive care unit is essential for outcome of severely injured patients (Schiefer et al., 2016).

Airway management: Inspite of recent developments in airway management and ventilation, the inhalation injuries remained a leading cause of morbidity and mortality in burn patients. The risk of inhalation injury increases with percentage of burns and approximately 2/3rd of patients with 70% of TBSA burns will have inhalation injuries (Lpaktchi and Arabi, 2006). Oxygen supplementation should be started as early as possible to neutralize the effects of toxic gases in these patients. The involvement of upper airway in inhalation injury can progress rapidly and lead to airway catastrophes, concomitant fluid resuscitation can exacerbate the laryngeal edema making endotracheal intubation difficult or even impossible. Hence the ATLS (advance trauma life support) course advice that patient with inhalation injury should be intubated early. Other indications in inhalation and major burn injury patients are before transferring them to the specialised burn centre or anticipated to develop ARDS (acute respiratory distress syndrome) (Lpaktchi and Arabi, 2006).These patients should be intubated with a larger possible size ETT (endotracheal tube) to facilitate bronchoscopy and the ETT should be secured well to avoid any dislodgments. Initial mode of ventilation should be the one which the treating physicians are familiar with, using100% oxygen. After obtaining the ABG (Atrial blood gas) and the levels of carbon monoxide we can titrate the Ventilatory setting accordingly. Lpaktchi K, et al. found that the lung protective ventilation reduces the ventilator associated events in burn patients (Oribabor et al., 2018). Chung KK, et al. suggested that the high frequency percussion and high frequency oscillatory ventilation are useful in ventilating major burn patients (Lpaktchi and Arabi, 2006). Aerosol heparin and N-acetylcysteine nebulisations are found to reduce ventilator days in the inhalation injury patients (McIntire et al., 2017).

Fluid therapy: In patients with severe burns and burn shock due to capillary and cellular leakage, there will be depletion of the intravascular volume, hence aggressive fluid resuscitation is required for initial 48 hours to replenish the intravascular volume status and to maintain the end organ perfusion. Any delay or inadequate resuscitation in severely burn patients will increase the morbidity and mortality (Spiro and Lambert, 2015). At the same time one must be careful as over resuscitation can complicate into compartment syndromes, pneumonia and ARDS. A survey of burn resuscitation revealed that up to 58% patients receive more than recommended fluids (Oribabor et al., 2018).

There are number of formulas available to estimate the initial fluid requirement in severely burned patients. Unfortunately, any of these formulae will not provide precise method to determine the fluid requirement, but they describe the starting points and initial guidelines for fluid management (Schiefer et al., 2016). We should tailor the fluid therapy in severely burn patients according to the age, associated injuries and comorbidities by using dynamic parameters of preload namely ITBVI (Intrathoracic blood volume index) and GEDVI (Global end diastolic volume index) to avoid the complications of under or over resuscitation.

European burn association found a wide variation in the formulas for initial fluid resuscitation in burn patients. Parkland formula was preferred by 69.3% and others used Brook 6 to 9%, Galveston 8.9%, Warden 5.9% and colloids by 11.9% (Greenhalgh, 2010). The difference between the Parkland and modified Brook formula is the amount of crystalloid prescription, in former it is 4ml/kg, in latter formula it is 2ml/kg (Table 2a __ampersandsign b). Commonly used crystalloid fluid is ringer lactate and out of the total calculated fluid requirement, half amount should be given in the initial 8 hours and remaining half in the next 16 hours. (Table 2a __ampersandsign b) Additional daily maintenance fluid should run separately.

US army institute of surgical research (USAISR) proposed rule of 10 (ISR rule of 10) for the resuscitation of severe burn patients (Table 2c). Most of the care givers also use 5% albumin as colloid resuscitation decreases the requirement of the crystalloids. The use of albumin in initial 12 hours is discouraged due to the cellular leak and creep out of the albumin, decreasing the intravascular volume (Lundy et al., 2016). However a recent meta-analysis showed decrease in mortality in burn patients with use of albumin (Navickis et al., 2014). USAISR and modified Brook formula advice to use 5% albumin as shown in Table 2.

Adjuvant for fluid therapy: The use of vitamin C in high dosage reduces the endothelium dysfunction and reduces the fluid requirement and increases the urine output. The risk of acute kidney injury and formation of renal stones limit routine use of vitamin c (Buehner et al., 2016).

Table 2: Formulas for fluid resuscitation in severe burns

Formulae

Total Volume and Plan of administration

Parkland Formula

Volume: 4ml/kg Lactated Ringer/% TBSA

Plan administration: 50% to be given in 8 hours __ampersandsign 50% to be given in next 16 hours

MODIFIED BROOKE’S Formula

Volume: 2ml/kg Lactated Ringer/% TBSA

Plan administration: 50% to be given in 8 hours __ampersandsign 50% to be given in next 16 hours

Rule of 10

Estimates Burn Area to nearest of 10%

Initial rate (ML/Hour) equal to TBSA×10 (Body weight 40-80 kgs)

Adult >80 kgs: Increase rate of infusion by 100 ml/hour for every 10 kg above 80

USAISR MODIFIED BROOKE’S Formula

TBSA burn 0-29%: No albumin

TBSA burn 30-49%: 0.3ml/kg/% of burn

TBSA burn 50-69%: 0.4ml/kg/% of burn

TBSA burn 70-100%: 0.5ml/kg/% of burn

Analgesia and Sedation

A recent survey about analgesia and sedation in critically ill burn patients showed that opioids are commonly used analgesic and 45% of the care givers use morphine analgesia (Depetris et al., 2018). The Society of Critical Care Medicine (SCCM) guidelines for management of analgesia in ICU patients heavily rely on narcotic / opioids, but there is awareness about opioid induced hyperalgesia where opioids are increasingly blamed for hyperalgesia (Holtman and Jellish, 2012). The opioid sparing effects of dexmedetomidine, ketamine, NSAID (non-steroidal anti-inflammatory drugs) and paracetamol are well described in the literature (Asmussen et al., 2013). Hence we should maximise the use of opioid sparing agents to reduce the requirement of opioids.

The practice pattern of sedation in burn ICU patients varies widely all over the globe. The choice of sedative agents in burns patients depends on severity, duration of mechanical ventilation, hemodynamic status and the resources available. In a recent survey about analgesia and sedation in critically ill burn patients. Depetris N, et al. (2018) found that the commonly used sedative agent was midazolam (72% of the burn patients) (Depetris et al., 2018). Inspite of strategies to use non-benzodiazepine sedatives (dexmedetomidine, ketamine and propofol) as they reduce opioid requirements and delirium. The benzodiazepine remained an important sedative agent due to deep sedation, amnesia, anxiolytic effects and sedation sparing effect. European intensivists use benzodiazepines initially and later on during weaning from the ventilator shift to other non-benzodiazepines (Barr et al., 2013). Ketamine is often used for sedation and analgesia in severely burned patients due to its favourable effects on hemodynamics, opioid sparing effects and potential to decrease the long term neurocognitive impairments (McGhee et al., 2011). The use of continuous dexmedetomidine infusion provides bridging effect during weaning from the mechanical ventilation, reduces the requirement of higher doses of opioids and benzodiazepines, decreases incidence of delirium and provides modification in hypermetabolic response similar to the b-blockers with improved nutrition support (Asmussen et al., 2013). Asmussen S, et al. in their met-analysis found that dexmedetomidine as an adjuvant in burn patients improves sedation compared to the midazolam and ketamine alone (Asmussen et al., 2013).

Wound Management

In burn patients’ eschars are formed due to deep and full thickness burns and become stiff and unyielding causing circumferential chest movement restrictions, resulting in ventilation difficulties, abdominal and extremity compartment syndromes affecting perfusion to vital organs and the extremities. Hence these burn patients should have escharotomy earlier before it complicates into the compartment syndromes (Lundy et al., 2016).

After cleaning the burn wounds, a fine non-adherent mesh should be applied over the burned area, deeper burn wounds will require multiple debridements and at a later stage skin grafting and/ or flap coverage. Various local antimicrobial creams are used in burn patients, commonly used are silver sulphadiazine, Nano crystalline silver, fucidin, bismuth impregnated petroleum gauze which improved the wound care and decreased the incidence of infection in burn patients (Norman et al., 2017).

Sepsis in Bun Patients

The loss of skin barrier, immune dysfunction and multiple invasive devices predispose these patients for higher risk for infection and sepsis and as high as 61% of the burn patients die of sepsis (Lundy et al., 2016; Navickis et al., 2014; Buehner et al., 2016; Depetris et al., 2018; Holtman and Jellish, 2012; Asmussen et al., 2013; Barr et al., 2013; McGhee et al., 2011; Norman et al., 2017; G__ampersandsignoacute;mez et al., 2009). Inappropriate use of antibiotics in burn patients will lead to development of multidrug resistant bacteria, antibiotic associated diarrhoea or clostridium difficile colitis whereas perioperative use of antibiotics will not decrease the burn wound infections (Lundy et al., 2016; Navickis et al., 2014; Buehner et al., 2016; Depetris et al., 2018; Holtman and Jellish, 2012; Asmussen et al., 2013; Barr et al., 2013; McGhee et al., 2011; Norman et al., 2017; G__ampersandsignoacute;mez et al., 2009; Barajas-Nava et al., 2013). Antibiotic should only be prescribed if patients who had raised sepsis markers associated with clinical signs and symptoms of sepsis.

Pneumonia is the common infection in patients with burns, reported to occur in 38% of the patients. Four percent of critically ill burn patients will have bacteraemia and the common bacteria is staphylococcus. Before the practice of applying the local antibiotic cream to the burns area, the invasive gram -ve burn wound infection was the common cause of death (Navickis et al., 2014; Buehner et al., 2016; Depetris et al., 2018; Holtman and Jellish, 2012; Asmussen et al., 2013; Barr et al., 2013; McGhee et al., 2011; Norman et al., 2017; G__ampersandsignoacute;mez et al., 2009; Barajas-Nava et al., 2013, Brown et al., 2004). The routine change of catheters are not recommended, the antimicrobial coated or impregnated catheters are of benefit in these patients (Ramos et al., 2006).

Nutrition, Hyperglycaemia and Hypermetabolism

Major burn injury causes hypermetabolic state resulting in protein utilization, loss of lean body mass and hyperglycaemia. This hypermetabolic state helps in providing glucose to the glucose dependent tissues but ultimately causes immune impairment, sepsis and multiorgan dysfunction leading to adverse outcome in post-burn patients (Holm et al., 2013). This post burn hyperglycaemia and hypermetabolism are associated with increased catabolism, bacteraemia, fungemia, skin graft loss and mortality. Use of intensive insulin therapy is associated with increased survival in burn patients (Swell et al., 2013). Insulin has various beneficiary effects such as immunomodulation, trophic effects on mucosa and skin barrier thus reducing the bacterial invasion as well as translocations (Swell et al., 2013). Hence the random blood sugar should be controlled between 8-10 mmols by using insulin in all these critically ill burn patients.

Hart, et al. found that the high carbohydrate diet and early enteral feeding in these critically ill burn patients has a beneficial effect, whereas use of selenium, zinc and other trace elements has not found to have definitive beneficial effects in burn patients (Lundy et al., 2016; David et al., 2001). In burn patients if hypermetabolic response is not controlled, it can lead to increased morbidity and mortality. Early burn wound debridement and closure, maintaining environmental temperature 30oc, use of anabolic steroids and b-blockers are associated with reduction in hypermetabolism and inflammation in severely burned patients (Herndon et al., 2001).

Acute Respiratory Distress Syndrome (ARDS)

Acute respiratory distress syndrome (ARDS) occurs in up to 17% of all burn patients, it can increase up to 40 to 50 % in severely burned patients requiring mechanical ventilation. Ventilation options for these ARDS patients are low tidal volume ventilation (LTV), high frequency ventilation and open the lung and keep it open techniques. In severely ill burn patients with increased metabolic demand, loss of chest compliance due to edema and eschar makes LTV less practical. Chung, et al. in their randomized controlled trail found that in1/3rd of patients LTV had failed to ventilate and high frequency percussion was better option for ventilating burn patients with ARDS (Chung et al., 2010). Other non-Ventilatory therapies used in burn patients are inhalation of nitric oxide, prostacyclin, fluid restriction, diuresis, prone position, ECMO (extracorporeal membrane oxygenation) (Schuster et al., 2008; Hale et al., 2012).

Acute Kidney Injury (AKI)

Acute kidney injury (AKI) occurs in up to 30% of the severe burn patients increasing the mortality from 80 to 100% if AKI requires haemodialysis (Brusselaers et al., 2010). There are various risk factors of AKI in severely burn patients namely hypovolemia, sepsis, medications and abdominal compartment syndrome (ACS). The therapeutic approaches to prevent AKI in these patients are adequate fluid resuscitation, avoiding nephrotoxic medications, early detection and treatment of sepsis and earlier escharotomy in patients with ACS. In patients with AKI haemodialysis should be initiated early without waiting for traditional indications for haemodialysis. In burn victims if renal failure is effectively predicted and promptly managed, there will be a significant reduction in morbidity and overall mortality, especially in severe burn injury (Emara and Alzalia, 2013).

Gastrointestinal Dysfunction

Various factors cause gastrointestinal dysfunction in severely burn patients leading to mucosal hypoperfusion, ileus and feed intolerance and Curling’s ulcers with increase in morbidity and mortality (LeVoyer et al., 1992). The combination of early optimal fluid resuscitation, earlier starting of enteral feeds (within 24 to 48 hours of injury), gastric ulcer prophylaxis, use of prokinetics and avoidance of NSAID and steroid will prevent gastrointestinal dysfunctions in severely burn patients (Lundy et al., 2016).

Cardiovascular Dysfunction

Burn shock, as described initially in pathophysiology, needs adequate resuscitation otherwise the combination of hypovolemia, decreased myocardial contractility and increased blood viscosity will lead to persistent shock state. Refractory shock in burns patients can be due to infections, full thickness burns, adrenal insufficiencies and vasoplegic shock. The septic shock should be managed as per the Surviving Sepsis Guidelines and in patients with vasoplegic shock the use of methylene blue may be of benefit (Shaefi et al., 2018).

Neurologic Dysfunction

Inhalational injury may cause hypoxic or anoxic brain injury which may lead to brain death in burn patients. The electric burn may cause life threatening arrhythmias and cardiac arrest may complicate into severe brain injuries (Jonathan et al., 2013). The common neurological problem in burn patient is delirium due to benzodiazepines sedation, disturbance of normal rhythm of circadian, frequent sepsis comorbidities particularly CVA (cerebro vascular accidents). Fortunately, 70% of the burn care givers assess these patients for delirium and 62.5% give combined pharmacological and non-pharmacological treatment in burn patients with delirium (Depetris et al., 2018).

Mortality in Burns

According to the estimation of WHO (World Health Organization) around 265 000 fatal burns occur annually (Lee et al., 2014). Peck, et al. reported decline in burn mortality from various regions in the world with decrease of burn incidence and burn severity as well as an overall reduction of mortality rates and LOS (Peck, 2011). Severe burn mortality is 10% (Pavoni et al., 2010).

Reports from Iran, shows that 9% of burn victims die with annual mortality of 4.6 to 5.6 per 100,000 people (Sarbazi et al., 2019). Adolescence, illiteracy, unemployment, residing in rural areas, low socioeconomic status and percentage of TBSA burned were found to be significant factors in increasing the mortality rate (Sarbazi et al., 2019). The improvement of health care facilities and preventive measures will decrease the burns mortality. The nature of burn, burned body surface over 40% and timing of first debridement are associated with mortality (Tabiee and Nakhaee, 2004). Dastgiri, et al. found that the TBSA of more than 75% has a higher mortality risk. Burns on the head and neck, trunk and upper extremity increase the mortality risk (Dastgiri et al., 2006). The improved awareness of burns pathophysiology with the recent advances in intensive care, renal replacement therapy, and nutritional support had contributed for the reduction of burns patients’ mortality (Stylianou et al., 2015; Dokter et al., 2014). Simultaneously the improvements in infection control had added to the decline in mortality of these patients (Al-Shaqsi et al., 2013). The reduction of length of hospital stay was the main improvement in burn treatment particularly due to early surgical therapy, newer wound dressings which allow less frequent burn dressing changes, reduced infection rates in combination with above mentioned patient care developments (Harats et al., 2015; Dokter et al., 2014; Jonsson et al., 2015).

Conclusion

The overall incidence and severity of burns are showing descending trend, still burn injuries remain a major trauma related injury. Major /severe burn injuries are the injuries involving more than 20% of total body surface area (TBSA) and these severe burn injuries patients should be managed in burn centre with a dedicated ICU, where the teamwork and skillful critical management will have a better impact. Burn shock occurs due to tissue injury, hypovolemia and storm of proinflammatory markers.

The intensive care management of severely burned patients includes securing the airway and optimal ventilation, fluid therapy initially guided by various formulas and meticulously tailored by using the dynamic preload parameters, using opioid sparing sedatives to minimize use of opioids and benzodiazepines to avoid opioid hyperalgesia and delirium. Early escharotomy will prevent the occurrence of various body compartment syndromes in severely burned patients. These patients are at a higher risk for infection and sepsis due to loss of dermatological protective barrier. Early detection and appropriate management of sepsis is necessary for better outcome. Hyperglycaemia and hypermetabolism should be controlled by insulin therapy, use of dexmedetomidine and b-blockers. Severely burned patients frequently complicate into multiorgan dysfunction namely ARDS, AKI, burn shock, gastrointestinal and CNS dysfunction and should be managed as described above.

The recent advances in intensive care therapy, burn wound care, organ and nutritional support and infection control had improved the outcome in severe burn patients.

Burns injuries are preventable and impact can be minimized by using smoke alarms, exit doors and other preventive measures developed over the last few years.

References:

Al-Shaqsi S, Al-Kashmiri A, Al-Bulushi T. Epidemiology of burns undergoing hospitalization to the National Burns Unit in the Sultanate of Oman: a 25-year review. Burns J Int Soc Burn Inj 2013; 39: 1606-1611.

Asmussen S, Maybauer DM, Fraser JF, Jennings K, George S, Maybauer MO. A metanalysis of analgesic and sedative effect of dexmedetomidine. Burns 2013; 39: 625-631.

Barajas-Nava LA, Lopez-Al calde J, Roquei Figuls M, Sola I, Cospx B. Antibiotics prophylaxis for preventing burn wound infections. Cochrane Data base Syst Rev 2013; 6: CD008738.

Barr J, Fraser G L, Puntillo K, Ely EW, Gélinas C, Dasta JF, Davidson JE, Devlin JW, Kress JP, Joffe AM, Coursin DB, Herr DL, Tung A, Robinson BR, Fontaine DK, Ramsay MA, Riker RR, Sessler CN, Pun B, Skrobik Y. Clinical practice guidelines for management of pain, agitation and delirium in adult patients in the intensive care unit. Crit care Med 2013; 41: 263-306.

Brown TP, Cancio LC, McManus AT, Mason AD Jr. Survival benefits conferred by tropical antibacterial preparations in burn patients: a historical prospective. J Trauma 2004; 56: 863-866.

Brusselaers N, Monstrey S, Colpaert K, decryyenaere J, Bolt SI, Hoste EA. Outcome of acute kidney injury in severe burn: a systematic review and met analysis. Intensive Care Med 2010; 36: 915-925.

Buehner M, Pamplin J, Studer L, Hughes R L, King BT, Graybill J C, Chung K K. Oxalate Nephropathy After Continuous Infusion of High-Dose Vitamin C as an Adjunct to Burn Resuscitation. J Burn Care Res 2016; 37: e374-e379.

Chung KK, Wolf SE, Renz EM, Allan PF, Aden JK, Merrill GA, Shelhamer M C, King BT, White CE, Bell DG, Schwacha MG, Wanek S, Wade C E, Holcomb J. B, Blackbourne LH, Cancio LC. High frequency percussive ventilation and low tidal volume ventilation in burns; randomized controlled trial. Crit Care Med 2010; 38: 1970-1977.

Dastgiri S, Kalankesh LR, Pourafkary N, Vahidi RG, Mahmoodzadeh F. Incidence, survival pattern and prognosis of self-immolation: a case study in Iran. J Public Health 2006; 14: 2-6.

David WH, Wolf SE, Xiao-Jun Z, David L C, Michael CB, Sina IM, Roy D, Meelie A, Wolfe RR, David HN. Efficacy of a high-carbohydrate diet in catabolic illness. Crit Care Med 2001; 29: 1318-1324.

Depetris N, Raineri S, Pantet O, Lavrentieva A. Management of pain, anxiety, agitation and delirium in burn patients: a survey of clinical practice and a review of the current literature. Ann Burns Fire Disasters 2018; 31: 97-108.

Dokter J, Vloemans AF, Beerthuizen G I J M, van der Vlies C H, Boxma H, Breederveld R, Tuinebreijer WE, Middelkoop E, van Baar ME, Dutch Burn Repository Group. Epidemiology and trends in severe burns in the Netherlands. Burns J Int Soc Burn Inj 2014; 40: 1406-1414.

Dokter J, Vloemans AF, Beerthuizen G I J M, van der Vlies CH, Boxma H, Breederveld R, Tuinebreijer WE, Middelkoop E, van Baar ME, Dutch Burn Repository Group. Epidemiology and trends in severe burns in the Netherlands. Burns J Int Soc Burn Inj 2014; 40: 1406-1414.

Emara SS and Alzalia AA. Renal failure in burn patients: a review. Ann Burn Fire Disaster 2013; 26: 12-15.

Gómez RM, Hospenthal C, Cancio D, Renz L, Holcomb E, Wade J, Wolf SC. Causes of Mortality by Autopsy Findings of Combat Casualties and Civilian Patients Admitted to a Burn Unit. JACS 2009; 208: 348-354.

Greenhalgh DG. Burn resuscitation: result of ISBI/AAA survey. Burns 2010; 36: 176-182

Hale DF, Cannon JW, Batchinsky AI, Cancio LC, Aden JK, White CE, Renz EM, Blackbourne LH, Chung KK. Prone positioning improves oxygenation in adult burn patients with severe acute respiratory distress syndrome. J Trauma Acute Care Surg 2012; 72: 1634-1639.

Harats M, Peleg K, Givon A, Kornhaber R, Goder M, Jaeger M, Haik J. Burns in Israel, comparative study: Demographic, etiologic and clinical trends 1997-2003 vs. 2004-2010. Burns J Int Soc Burn Inj 2015; 42: 500-507.

Herndon DN and Thompkins RG. Support of metabolic response to burn injury. Lancet 2004; 363: 1895.

Herndon DN, Hart DW, Wolf SE, Chinkes DL, Wolf RR. Reversal of catabolism by B-Blockers after severe burns. N Eng J Med 2001; 345: 123-1229.

Holm C, Horbrand F, Mayr M, von Donners Marck GH, Muhlbauer W. Acute hyperglycaemia following thermal injury: Friend or foe? Resuscitation 2004; 60: 71-77

Holtman JR and Jellish WS. Opioid induced hyperalgesia and burn pain. J Burn Care 2012; 33: 692-701.

Jonathan C, WiltonMark O, HardinJohn D, RitchieKevin K, ChungJames K, AdenLeopoldo C, CancioSteven E, WolfChristopher EW. Outcomes after cardiac arrest in adult burn centre. Burns 2013; 39: 1541-1546.

Jonsson A, Huss FRM, Svee A, Sjöberg F. Burns in Sweden: Temporal Trends 1987-2010. Ann Burns Fire Disasters 2015: 28: 1-7.

Kagan RJ and Smith SC. Evaluation and treatment of thermal injuries. Dermal Nurs 2000; 12: 334-338.

Kattan A, AlShomer F, Alhujayri AK, AddarA, Aljerian A. Current knowledge of burn injury first aid practices and applied traditional remedies: a nationwide survey. Burn Trauma 2016; 4: 37.

Lee KC, Joory K, Moiemen NS. History of burns: The past, present and the future. Burn Trauma 2014; 2: 169-180.

LeVoyer T, Cioffi WG Jr, Pratt L, Shippee R, McManus WF, Mason AD Jr, Pruitt BA Jr. Alterations in intestinal permeability after thermal injury. Arch Surg 1992; 127: 26-30.

Lpaktchi K and Arabi S. Advances in burn critical care. Crit care Med 2006; 34: S239.

Lundy JB, Chung KK, Pamplin JC, Ainsworth CR, Jeng JC, Friedman BC. Update on severe burn management for the intensivist. J Int Care Med 2016; 31: 499-501.

McGhee LL, Slater TM, Garza TH, Fowler M, DeSocio PA, Maani CV. The relationship of early pain scores and posttraumatic stress disorder in burned soldiers. J Burn Care Res 2011; 32: 46?51.

McIntire AM, Harris SA, Whitten JA, Fritschle-Hilliard AC, Foster DR, Sood R, Walroth TA. Outcomes Following the Use of Nebulized Heparin for Inhalation Injury. J Burn Care Res 2017; 38: 45-52.

Navickis RJ, Greenhalgh, Wilkes MM. Albumin in burn shock resuscitation: a metanalysis of controlled clinical trials. J Burn care 2014; 37: e268-278.

Norman G, Christie J, Liu Z, Westby MJ, Jefferies JM, Hudson T, Edwards J, Mohapatra D, Hassan IA, Dumville JC. Antiseptics for burns. Cochrane Database Syst Rev 2017; 7: CD011821.

Oribabor C, Gulkarov I, Khusid F, Ms EF, Esan A, Rizzuto N, Tortolani A, Dattilo PA, Suen K, Ugwu J, Kenney, B. The use of high-frequency percussive ventilation after cardiac surgery significantly improves gas exchange without impairment of hemodynamics. RCTR 2018; 54: 58-61.

Pavoni V, Gianesello L, Paparella L, Buoninsegni LT, Barboni E. Outcome predictors and quality of life of severe burn patients admitted to intensive care unit. Scand J Trauma Resusc Emerg Med 2010; 18: 24.

Peck MD. Epidemiology of burns throughout the world. Part I: Distribution and risk factors. Burns 2011; 37: 1087-1100.

Ramos G, Bolgiani A, Patiño O, Prezzavento G, Guastavino P, Durlach R, Fernandez Caniggia L, Benaim F. Antiseptic-impregnated central venous catheters: their evaluation in burn patients. Ann Burn Fire Disaster 2006; 19: 63-67.

Santaniello JM, Luchette FA, Esposito T J, Gunawan H, Reed R L, Davis K A, Gamelli RL, Albrecht R M, Pruitt BA, Mendleson JA, Santaniello JM. Ten years experience of burn, trauma and combined burn/trauma injuries, comparing the outcomes. Trauma 2004; 57: 696.

Sarbazi E, Yousefi M, Khami B, Ettekal-Nafs R, Babazadeh T, Gaffari-Fam S. Epidemiology and the survival rate of burn-related injuries in Iran: a registry-based study. Ann Burns Fire Disasters 2019; 32: 3-9.

Schiefer JL, Alischahi A, Perbix W, Grigutsch D, Graeff I, Zinser M, Demir E, Fuchs P C, Schulz A. Time from accident to admission to a burn intensive care unit: how long does it actually take? A 25-year retrospective data analysis from a german burn center. Ann Burns Fire Disasters 2016; 29: 18-23.

Schuster KM, Aloiuder R, Barquist ES. Non ventilatory interventions in acute respiratory distress syndrome. J Inten Care Med 2008; 23: 19-32.

Seyed-Forootan K, Karimi H, Motevalian S, Momeni M. LA50 in burn injuries. Ann Burns Fire Disasters 2016; 29: 14.

Shaefi S, Mittel A, Klick J, Evans A, Ivascu NS, Gutsche J, Augoustides JGT. Vasoplegia after Cardiovascular Procedures-Pathophysiology and Targeted Therapy. J Cardiothorac Vasc Anesth 2018; 32: 1013?1022.

Sheridan RL. Fire-Related Inhalation Injury. NEJM 2016; 375: 464-469

Shih JG, Shahrokhi S, Jeschke MG. Review of Adult Electrical Burn Injury Outcomes Worldwide: An Analysis of Low-Voltage vs High-Voltage Electrical Injury. J Burn Care Res 2017; 38: e293-e298.

Smolle C, Cambiaso-Daniel J, Forbes AA, Wurzer P, Hundeshagen G, Branski LK, Huss F, Kamolz LP. Recent trends in burn epidemiology worldwide: A systematic review. Burns 2017; 43: 249-257.

Smolle C. Recent trends in burn epidemiology worldwide: A systematic review. Burns 2017; 43: 249-257.

Spiro MD and Lambert MW. The intensive care management of adult burn patients. Curr Anesthesiol Rep 2015; 5: 393-399.

Stylianou N, Buchan I, Dunn KW. A review of the international Burn Injury Database (iBID) for England and Wales: descriptive analysis of burn injuries 2003-2011. BMJ Open 2015; 5: e006184.

Swell JA, Loh NHW, Mahambray T, Shokrollahi K. Clinical review: The critical management of burn patients. Crit Care 2013; 17:241: 2-10.

Tabiee S and Nakhaee M. Epidemiology of burn patients in Emam Reza Hospital, Birjand, 1998-2002. J Shahrekord Univ Med Sci 2004; 6: 43-51.

Tejiram S, Romanowski KS, Palmieri T. Initial management of severe burn injury. Curr Opin Crit Care 2019; 25:647-52.

Wurzer P, Culnan D, Cancio LC, Kramer G C. Pathophysiology of burn shock and burn edema. In Total Burn Care: Fifth Edition. Elsevier Inc 2018: 66-76.

Yasti AC, Senel E, Saydam M, Ozok G, Coruh A, Yorganci K. Guidelines and treatment algorithm for burn injuries. Ulus Travna Acil Cerrahi Derg 2015; 21: 79-89.