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Critical care management of severe burns and inhalational injury
TRAUMA
Critical care management of severe burns and inhalational injury
Learning Objectives After reading this article, you should be able to: C
C
Andrew Clarey Dominic Trainor
C
C
Abstract Anaesthetists and critical care physicians involved in emergency care provision, must be equipped with the knowledge and skills to accurately assess and initiate treatment in patients with severe burns. This summary aims to review airway management and fluid resuscitation in addition to sedation and analgesic choices. Some of the dogma involved in current aspects of modern burns care will also be questioned.
C
List clinical features that indicate the presence of an inhalational injury Identify risk factors for and signs of noxious agent involvement in a severe burn Outline the key aspects of severe burn pathophysiology including burn shock Apply evidence-based practice to commence resuscitation of severe burns patients Understand the role of the multi-disciplinary team in burns patient care
The effects on the cardiovascular system in response to burns are divided into acute and hypermetabolic phases. Hypovolaemia dominates the acute phase, generated by increased capillary permeability resulting in losses of both protein and fluid volume to the extravascular space. The hypermetabolic phase results in hypoproteinaemia causing gross tissue oedema, whilst excess catecholamine synthesis can lead to cardiac dysfunction and acute kidney injury secondary to ischaemia or infarction.6 Thermal injury results in multiple gastrointestinal tract complications. Reduced nutritional intake, increased incidence of gastric mucosal ulceration and bowel wall ischaemia may all result in gastrointestinal haemorrhage. Translocation of bacteria across the mucosal wall may also result in sepsis. There are two aspects to inhalational injury pathophysiology: direct thermal inflammatory response and smoke inhalation. Local cellular inflammation occurs throughout the entire respiratory tract including the parenchyma, resulting in oedema,
Keywords Critical care medicine; inhalational injury; resuscitation; severe burns Royal College of Anaesthetists CPD Matrix: 1A01, 1A02, 1C01, 1C02, 1D02, 1E01, 2A02, 2A05, 2C01, 2C02, 2C05
Introduction Throughout one year in England, 116,588 patients attended Emergency Departments with a burn or scald, 12,667 of whom required inpatient treatment.1,2 A specialized multidisciplinary team with an enhanced understanding of severe burns pathophysiology helps ensure the delivery of safe, high quality care to this specific subgroup. Gender, age, size and depth of burn are all important factors in prognostication. Between 5% and 35% of burns patients suffer inhalational injury which is associated with significant complications.3,4 The need for a co-ordinated approach via a strategically developed burns network is fundamental to reducing morbidity and mortality, whilst promoting high quality specialist care.5
Jackson’s burn zones and their relevance in calculating total body surface area (TBSA) of any burn 3 1
Pathophysiology Irrespective of burn modality, local (Table 1) and systemic effects ensue. The systemic response begins immediately and is driven by the release of both inflammatory mediators and oxygen radicals. This inflammatory response creates both the hyperdynamic and hypermetabolic phases, driving multi-organ failure.
Andrew Clarey BSc MBChB MRCEM is an Emergency Medicine Trainee, Regional Intensive Care Unit, The Royal Victoria Hospital, Belfast, UK. Conflicts of interest: none declared. Dominic Trainor BSc MB MRCP FCARCSI DICM is Consultant in Anaesthesia and Intensive Care Medicine at The Royal Victoria Hospital, Belfast, UK. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
2
1) Zone of Total and coagulation irreversible tissue destruction 2) Zone of Damaged tissue stasis suffering reduced perfusion. Salvageable and main target in resuscitative therapy for healing 3) Zone of Outermost zone hyperaemia with increase in perfusion and is highly likely to recover from the original insult
Include in TBSA calculation
Not included in TBSA calculation
Table 1
1
Ó 2017 Published by Elsevier Ltd.
Please cite this article in press as: Clarey A, Trainor D, Critical care management of severe burns and inhalational injury, Anaesthesia and intensive care medicine (2017), http://dx.doi.org/10.1016/j.mpaic.2017.05.009
TRAUMA
intubate, can’t ventilate’ scenario must be planned for with equipment prepared in advance. Suxamethonium use should be limited to within the first 24 hours of injury due to the risk of hyperkalaemia caused by the increase in extrajunctional nicotinic acetylcholine receptors. Increased receptor numbers can also promote a resistance to non-depolarizing agents, requiring higher doses. The endotracheal tube (ETT) must have a sufficient internal diameter to allow passage of a fibreoptic bronchoscope. The ETT should never be cut short as facial oedema may increase. Bronchoscopy must be carried out post-intubation in order to fully assess the presence of inhalational injury and/or burns to the lower airway.
irritation and raised airway pressures that can cause challenges during positive pressure ventilation (PPV). Smoke inhalation can cause either direct asphyxiation with O2 displacement in the alveoli, or systemically via carboxyhaemoglobinaemia.
Assessment and management The consideration of and transfer to a specialist burns centre is often managed regionally or nationally and local referral guidelines should be consulted. Airway Cespine protection must be implemented if there is a suspicion of trauma. Immediate application of supplemental oxygen therapy with high-flow humidified oxygen inhibits secondary injury and provides prompt treatment of smoke inhalation. Risk factors and clinical signs indicating inhalational injury must be recognized early (Table 2). No guideline exists to instruct on what collective features require a definitive airway. The progressive and potentially fatal complications of an insecure, obstructed or oedematous airway, especially in those requiring transfer, often generates an indoctrinated reaction e intubation. The dogma of endotracheal intubation has to be questioned considering 31% of intubated patients are extubated within the first twenty-four hours of admission at burns centres.7 Fibreoptic nasendoscopy can help to further stratify the presence of or risk of inhalational injury and help guide decision making on whether to proceed with intubation or opt instead for a period of close observation in a high dependency unit. Should intubation of the trachea be required, a clear airway plan must be made and communicated to all members of the emergency team. Consideration should be given to awake fibreoptic intubation versus sedation and muscle relaxation. Restricted mouth opening, oedema of the face and upper airways and carbonaceous deposits within the oropharynx mean a ‘can’t
Breathing A lung protective ventilatory (LPV) strategy (Table 3) should be implemented in those who require intubation. Between 40% and 54% of patients requiring mechanical ventilation will develop acute respiratory distress syndrome (ARDS).4 Rescue interventions including muscle relaxation, prone positioning and extracorporeal membrane oxygenation (ECMO) may be required in cases of refractory hypoxaemia. Rising plateau pressures and inadequate ventilation should prompt consideration of either circumferential burns of the thorax and abdomen or abdominal compartment syndrome. The affinity of haemoglobin (Hb) for carbon monoxide (CO) is approximately 200 times that for oxygen (O2), thus hypoxaemia results from displacement of O2 from the Hb molecule by CO. A carboxyhaemoglobinaemia (COHb) of >30% requires rapid treatment; increasing the alveolar partial pressure of oxygen by instigating a FiO2 of 1.0 whilst optimizing ventilation. This reduces the half-life of COHb from four hours to approximately one hour. Hyperbaric oxygen treatment is rarely required. Circulation Peripheral venous access with two large-bore catheters via unburnt skin is a priority. An arterial line and central-venous catheter, inserted through unburnt skin, should be considered early. A urinary catheter must be inserted and hourly urometer commenced as urinary output is a useful measure of the adequacy of perfusion. A balanced crystalloid solution should be used for initial resuscitation; however, the optimal fluid choice continues to be debated. Packed red cells and coagulation products may be required as bleeding from excised wounds can be significant. Hypertonic solutions such as albumin are also showing
Risk factors and clinical signs that indicate inhalational injury Risk factors
Clinical signs
Exposure to smoke, flames or chemicals and whether these were either industrial or household Duration of time exposed and whether this was in an enclosed space Burning substances such as plastics or fabrics Obtunded consciousness at scene At scene fatalities or cardiac arrests
Carbonaceous sputum Evidence of burns to the face or neck Oropharyngeal burns (e.g bulla and/or erythema) Respiratory embarrassment Singed facial or nasal hair Added sounds (wheeze or stridor) Haemoptysis Altered voice Odynophagia or dysphagia Reduced Glasgow Coma Scale (GCS)
Lung protective ventilation strategy criteria determined by the ARDS network Tidal volume
Plateau pressure FiO2
Table 2
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
6 ml/kg (range 4e8 ml/kg titrated against plateau pressures and blood pH) predicted body weight 30 cm H2O Wean as low as tolerated to achieve PaO2 55e80 mmHg (7.3e10.7 kPa)
Table 3
2
Ó 2017 Published by Elsevier Ltd.
Please cite this article in press as: Clarey A, Trainor D, Critical care management of severe burns and inhalational injury, Anaesthesia and intensive care medicine (2017), http://dx.doi.org/10.1016/j.mpaic.2017.05.009
TRAUMA
movement in the ICU bed through to surgical procedures and dressing changes, the nociceptive stimulation can be immense. Inadequate analgesia results in both short and long-term deterioration; raised inflammatory response and increased risk of posttraumatic stress disorder, respectively.4 A multi-modal analgesic approach is required to adequately cover background, breakthrough and procedural pain. Reliance on opioid only protocols must be avoided. Agents which exert their effects by modifying different pain pathways, such as ketamine (the NMDA receptor antagonist) and pregabalin (GABA analogue) will help improve analgesia. It is important to avoid agents that may promote or worsen AKI, such as non-steroidal anti-inflammatory drugs. Whilst no strong evidence supports any single sedative agent, ketamine can act as both sedative and analgesic without the risks of haemodynamic instability that other agents carry. Combination with an anxiolytic is required to reduce the incidence of emergence phenomenon. Sedation requires regular assessment using a recognized sedation scale which will assist in ventilator weaning.
promising results with studies reporting a reduction in both mortality and the incidence of compartment syndrome.8 Adult patients with a TBSA >20%, or paediatric patients with TBSA >10% require formal burns resuscitation. The volume of resuscitation fluid (Ringer’s Lactate) required in the first 24 hours has historically been calculated using the Parkland formula (4 ml per kg TBSA %). Recently military physicians applied a ‘Rule of 10s’ (Table 4), which can be used to calculate initial resuscitation fluid rate. In 88% of simulated cases the calculated volume was between 2 and 4 ml/kg.4 Resuscitation requires a balance between the prevention of burn shock (caused by increased vascular permeability and intravascular depletion) and the development of fluid creep, which at its most severe results in extreme extravascular oedema causing compartment syndrome. Identifying effective resuscitation end-points are of greater significance than determining an arbitrary fluid rate. This requires regular clinical reassessment that may be supplemented by adjuvant techniques such as focused echocardiography in order to help titrate fluid resuscitation accordingly. Fluid rates may need to be adjusted by 20 e30% every 30e120 minutes, whilst regular serum electrolyte measurements are also required.4 Circumferential wounds to limbs risk perfusion and can lead to ischaemia. Rapid recognition will avoid delays in potentially limb salvaging fasciotomies. Venous thromboembolism prophylaxis (pharmacological and mechanical) should be administered in all patients unless there is a clear contraindication.
Exposure The calculation of TBSA and assessment of burn depth requires a methodical approach ensuring all areas, including the patient’s back, are reviewed without excessive total body exposure. Heat loss can be rapid. Oesophageal, bladder or nasopharyngeal probes can be used to measure core temperature. Mechanisms to prevent hypothermia via both convection and evaporation include; warmed IV fluids, forced-air heated blankets, warming blankets and temperature controlled bed spaces. Chemical contamination and/or substances which have adhered to skin must be safely, rapidly and thoroughly removed. Burn depth has four categories each with their own characteristic appearance (Table 5). TBSA is calculated by including burns of superficial partial thickness and deeper. Wallace’s Rule of Nines and Lund and Browder charts (age specific) are often used to calculate TBSA. Areas suffering contamination or devitalization require urgent surgical debridement. Bullae may benefit from prompt de-roofing or fluid evacuation. Liaising with the specialist burns surgical team is paramount for effective management of these issues. The array of dressings available for burns is vast. No single dressing is suitable for every burn; there are several biological and antimicrobial dressings available and the specialist surgical team will advise the optimum choice.5 During exposure all clothing, contact lenses and jewellery must be removed, specifically circumferential items such as rings or necklaces.
Disability A GCS of <8 or severe agitation are indications for intubation. In an obtunded patient, especially when the collateral history may be vague, consideration must be given to the need for further investigations, such as CT scan of the brain and investigation of noxious substance exposure. Hydrogen cyanide (HCN) poisoning is a significant risk for patients exposed to fires containing plastics and fabrics. The cessation of mitochondrial aerobic respiration via reversible inhibition of cytochrome C oxidase by cyanide requires rapid administration of the antidote, hydroxycobalamin, which chelates cyanide to cyanocobalamin (70 mg/kg or 5 g IV in intermediate to severe cases, 10 g IV in cardiorespiratory arrest).9 A blood glucose reading is essential given the hypermetabolic state, as is the tracking of this parameter. Both the acute and chronic pain components of burns, including a hyperalgesic state, require detailed and dynamic ICU management. A non-verbal pain score should be used to help assess and titrate analgesic requirements. From simple
Ongoing management issues Infection There is no role for prophylactic antibiotics despite the increased risk of infection. The patient should be nursed in isolation. Gloves and aprons are mandatory when handling or moving the patient. Meticulous attention to hand hygiene and application of a faecal management system (especially with burns to the buttocks and upper thighs) may all assist in limiting the risk of sepsis developing.
Rule of 10s step-wise calculation for initial fluid rate in adults weighing ‡40 kg Step 1 Step 2 Step 3
Calculate the TBSA to nearest 10% Calculate the fluid rate as 10 TBSA in ml/h If adult weighs >80 kg add an additional 100 ml/h to the fluid rate for every additional 10kg
Table 4
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
3
Ó 2017 Published by Elsevier Ltd.
Please cite this article in press as: Clarey A, Trainor D, Critical care management of severe burns and inhalational injury, Anaesthesia and intensive care medicine (2017), http://dx.doi.org/10.1016/j.mpaic.2017.05.009
TRAUMA
The appearance and features that differentiate various burn depths Burn depth
Appearance
Features
Epidermal
C C C C
Superficial partialthickness
C
Deep partialthickness
C
C C
C C C
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
4
Painful Erythematous Blanching No blisters
Blanching erythema Blisters Pain with hyperalgesia
White or yellow base Minimal to no blanching Reduced sensation Some blistering may be evident
Ó 2017 Published by Elsevier Ltd.
Please cite this article in press as: Clarey A, Trainor D, Critical care management of severe burns and inhalational injury, Anaesthesia and intensive care medicine (2017), http://dx.doi.org/10.1016/j.mpaic.2017.05.009
TRAUMA
Table 5 (continued ) Burn depth
Appearance
Features
Full thickness
C C C C
Leathery appearance White, brown or black base No blanching No sensation
Table 5
prompt and in those with TBSA >20% a high protein diet is required. Protein requirements for adults are 1.5e2.0 g/kg/day and in children 3 g/kg/day. Use of a recognized formula to calculate calorie requirements is recommended, adjusting intake requirements based upon the TBSA involved, the patients age and weight.5 Should nasogastric feeding fail or be inadequate then consideration of either post-pyloric or total parenteral nutrition is required.10 Early engagement with the dietetics team is essential in this aspect of patient care. Interruptions to feeding should be kept to a minimum and so merely undergoing a surgical procedure should not warrant periods of fasting, unless the procedure involves airway manipulation or adjustments. Unnecessary interruption or inadequate calorific and protein provision, predisposes the patient to secondary damage of the burn and increases both the infection risk and mortality. As with other intubated ICU patients, gastric-ulcer prophylaxis should be considered.
Systemic Inflammatory Response Syndrome (SIRS) markers are commonly seen in severe burns patients, hence more specific criteria have been proposed (Box 1); however it should be recognized that the correlation of these with positive blood cultures confirming bacteraemia is poor.4 A low threshold should exist for the administration of Human Tetanus Immunoglobulin (250 iu IM, or 500 iu IM if >24 hours since burn occurred). Nutrition Given the hypermetabolic state seen in the acute phase (basal metabolic rate rises by approximately 170%), it is imperative that nutritional deprivation is avoided. Enteral rather than parenteral support is preferable and should commence as early as possible. Conversion to normal oral dietary intake should be
American Burn Association Indicators of Sepsis in Burns. Require 3 or more to indicate likely sepsis C C C C
C
C
Ophthalmological assessment Orbital or peri-orbital involvement mandates an urgent ophthalmological assessment. This reduces the risk of long-term complications and may help salvage or preserve sight.
Temperature >39 C or <36 C Progressive tachycardia (>110 beats/minute) Thrombocytopenia (<100,000/mL) Intolerance of enteral feeding for >24 hours (abdominal distension, high gastric residuals, residuals 2x the feeding rate or diarrhoea >2500 ml/day) Progressive tachypnoea (>25bpm if not ventilated, or minute volume of >12 L/minute if ventilated) Hyperglycaemia in the absence of diabetes mellitus (untreated blood glucose >11.1 mmol/L, >7 units/hour insulin infusion or >25% increase in insulin dose over 24 hours)
Palliative care Despite application of rapid assessment and advanced clinical management, severe burns carry high mortality rates. Treatment futility may, in some cases, have to be considered and discussed by the multi-disciplinary team. Should this occur then it is likely these patients will die within the ICU. High-quality end-of-life care, which may involve palliative care specialists in some institutions, should be implemented in order to ensure patient comfort and dignity is prioritized. A
Box 1
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
5
Ó 2017 Published by Elsevier Ltd.
Please cite this article in press as: Clarey A, Trainor D, Critical care management of severe burns and inhalational injury, Anaesthesia and intensive care medicine (2017), http://dx.doi.org/10.1016/j.mpaic.2017.05.009
TRAUMA
REFERENCES 1 NHS Digital. NHS accident & emergency attendances, 2014-15; Table 14, number of A&E attendances, A&E primary diagnosis 2014-15. 2016. Leeds, http://content.digital.nhs.uk/catalogue/ PUB19883/acci-emer-atte-eng-2014-15-data.xlsx (accessed 17 Jan 2017). 2 NHS Digital. NHS Hospital Episode Statistics, admitted patient care e England, 2014-15: diagnosis. 2015. Leeds, http://content. digital.nhs.uk/catalogue/PUB19124/hosp-epis-stat-admi-diag2014-15-tab.xlsx (accessed 17 Jan 2017). 3 Moore EC, Pilcher DV, Bailey MJ, et al. The Burns Evaluation and Mortality Study (BEAMS): predicting deaths in Australian and New Zealand burn patients admitted to intensive care with burns. J Trauma Acute Care Surg 2013; 75: 298e303. 4 Lundy JB, Chung KK, Pamplin JC, et al. Update on severe burn management for the intensivist. J Intensive Care Med 2016; 31: 499e510.
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
5 ISBI practice guidelines for burn care. Burns 2016; 42: 953e1021. 6 Abu-Sittah GS, Sarhane KA, Dibo SA, et al. Cardiovascular dysfunction in burns: review of literature. Ann Burns Fire Disasters 2012; 25: 26e37. 7 Romanowski KS, Palmiere TL, Sen S, Greenhalgh DG. More than one third of intubations in patients transferred to burn centres are unnecessary: proposed guidelines for appropriate intubation of the burn patient. J Burn Care Res 2016; 37: e409e14. 8 Guilabert P, Usua G, Martin N, et al. Fluid resuscitation management in patients with burns: update. Br J Anaesth 2016; 117: 284e96. 9 Anseeuw K, Delvau N, Burillo-Putze G, et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med 2013; 20: 2e9. 10 Rosseau A, Losser M, Ichai C, et al. ESPEN endorsed recommendations: nutritional therapy in major burns. Clin Nutr 2013; 32: 497e502.
6
Ó 2017 Published by Elsevier Ltd.
Please cite this article in press as: Clarey A, Trainor D, Critical care management of severe burns and inhalational injury, Anaesthesia and intensive care medicine (2017), http://dx.doi.org/10.1016/j.mpaic.2017.05.009
Critical care management of severe burns and inhalational injury
Learning Objectives After reading this article, you should be able to: C
C
Andrew Clarey Dominic Trainor
C
C
Abstract Anaesthetists and critical care physicians involved in emergency care provision, must be equipped with the knowledge and skills to accurately assess and initiate treatment in patients with severe burns. This summary aims to review airway management and fluid resuscitation in addition to sedation and analgesic choices. Some of the dogma involved in current aspects of modern burns care will also be questioned.
C
List clinical features that indicate the presence of an inhalational injury Identify risk factors for and signs of noxious agent involvement in a severe burn Outline the key aspects of severe burn pathophysiology including burn shock Apply evidence-based practice to commence resuscitation of severe burns patients Understand the role of the multi-disciplinary team in burns patient care
The effects on the cardiovascular system in response to burns are divided into acute and hypermetabolic phases. Hypovolaemia dominates the acute phase, generated by increased capillary permeability resulting in losses of both protein and fluid volume to the extravascular space. The hypermetabolic phase results in hypoproteinaemia causing gross tissue oedema, whilst excess catecholamine synthesis can lead to cardiac dysfunction and acute kidney injury secondary to ischaemia or infarction.6 Thermal injury results in multiple gastrointestinal tract complications. Reduced nutritional intake, increased incidence of gastric mucosal ulceration and bowel wall ischaemia may all result in gastrointestinal haemorrhage. Translocation of bacteria across the mucosal wall may also result in sepsis. There are two aspects to inhalational injury pathophysiology: direct thermal inflammatory response and smoke inhalation. Local cellular inflammation occurs throughout the entire respiratory tract including the parenchyma, resulting in oedema,
Keywords Critical care medicine; inhalational injury; resuscitation; severe burns Royal College of Anaesthetists CPD Matrix: 1A01, 1A02, 1C01, 1C02, 1D02, 1E01, 2A02, 2A05, 2C01, 2C02, 2C05
Introduction Throughout one year in England, 116,588 patients attended Emergency Departments with a burn or scald, 12,667 of whom required inpatient treatment.1,2 A specialized multidisciplinary team with an enhanced understanding of severe burns pathophysiology helps ensure the delivery of safe, high quality care to this specific subgroup. Gender, age, size and depth of burn are all important factors in prognostication. Between 5% and 35% of burns patients suffer inhalational injury which is associated with significant complications.3,4 The need for a co-ordinated approach via a strategically developed burns network is fundamental to reducing morbidity and mortality, whilst promoting high quality specialist care.5
Jackson’s burn zones and their relevance in calculating total body surface area (TBSA) of any burn 3 1
Pathophysiology Irrespective of burn modality, local (Table 1) and systemic effects ensue. The systemic response begins immediately and is driven by the release of both inflammatory mediators and oxygen radicals. This inflammatory response creates both the hyperdynamic and hypermetabolic phases, driving multi-organ failure.
Andrew Clarey BSc MBChB MRCEM is an Emergency Medicine Trainee, Regional Intensive Care Unit, The Royal Victoria Hospital, Belfast, UK. Conflicts of interest: none declared. Dominic Trainor BSc MB MRCP FCARCSI DICM is Consultant in Anaesthesia and Intensive Care Medicine at The Royal Victoria Hospital, Belfast, UK. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
2
1) Zone of Total and coagulation irreversible tissue destruction 2) Zone of Damaged tissue stasis suffering reduced perfusion. Salvageable and main target in resuscitative therapy for healing 3) Zone of Outermost zone hyperaemia with increase in perfusion and is highly likely to recover from the original insult
Include in TBSA calculation
Not included in TBSA calculation
Table 1
1
Ó 2017 Published by Elsevier Ltd.
Please cite this article in press as: Clarey A, Trainor D, Critical care management of severe burns and inhalational injury, Anaesthesia and intensive care medicine (2017), http://dx.doi.org/10.1016/j.mpaic.2017.05.009
TRAUMA
intubate, can’t ventilate’ scenario must be planned for with equipment prepared in advance. Suxamethonium use should be limited to within the first 24 hours of injury due to the risk of hyperkalaemia caused by the increase in extrajunctional nicotinic acetylcholine receptors. Increased receptor numbers can also promote a resistance to non-depolarizing agents, requiring higher doses. The endotracheal tube (ETT) must have a sufficient internal diameter to allow passage of a fibreoptic bronchoscope. The ETT should never be cut short as facial oedema may increase. Bronchoscopy must be carried out post-intubation in order to fully assess the presence of inhalational injury and/or burns to the lower airway.
irritation and raised airway pressures that can cause challenges during positive pressure ventilation (PPV). Smoke inhalation can cause either direct asphyxiation with O2 displacement in the alveoli, or systemically via carboxyhaemoglobinaemia.
Assessment and management The consideration of and transfer to a specialist burns centre is often managed regionally or nationally and local referral guidelines should be consulted. Airway Cespine protection must be implemented if there is a suspicion of trauma. Immediate application of supplemental oxygen therapy with high-flow humidified oxygen inhibits secondary injury and provides prompt treatment of smoke inhalation. Risk factors and clinical signs indicating inhalational injury must be recognized early (Table 2). No guideline exists to instruct on what collective features require a definitive airway. The progressive and potentially fatal complications of an insecure, obstructed or oedematous airway, especially in those requiring transfer, often generates an indoctrinated reaction e intubation. The dogma of endotracheal intubation has to be questioned considering 31% of intubated patients are extubated within the first twenty-four hours of admission at burns centres.7 Fibreoptic nasendoscopy can help to further stratify the presence of or risk of inhalational injury and help guide decision making on whether to proceed with intubation or opt instead for a period of close observation in a high dependency unit. Should intubation of the trachea be required, a clear airway plan must be made and communicated to all members of the emergency team. Consideration should be given to awake fibreoptic intubation versus sedation and muscle relaxation. Restricted mouth opening, oedema of the face and upper airways and carbonaceous deposits within the oropharynx mean a ‘can’t
Breathing A lung protective ventilatory (LPV) strategy (Table 3) should be implemented in those who require intubation. Between 40% and 54% of patients requiring mechanical ventilation will develop acute respiratory distress syndrome (ARDS).4 Rescue interventions including muscle relaxation, prone positioning and extracorporeal membrane oxygenation (ECMO) may be required in cases of refractory hypoxaemia. Rising plateau pressures and inadequate ventilation should prompt consideration of either circumferential burns of the thorax and abdomen or abdominal compartment syndrome. The affinity of haemoglobin (Hb) for carbon monoxide (CO) is approximately 200 times that for oxygen (O2), thus hypoxaemia results from displacement of O2 from the Hb molecule by CO. A carboxyhaemoglobinaemia (COHb) of >30% requires rapid treatment; increasing the alveolar partial pressure of oxygen by instigating a FiO2 of 1.0 whilst optimizing ventilation. This reduces the half-life of COHb from four hours to approximately one hour. Hyperbaric oxygen treatment is rarely required. Circulation Peripheral venous access with two large-bore catheters via unburnt skin is a priority. An arterial line and central-venous catheter, inserted through unburnt skin, should be considered early. A urinary catheter must be inserted and hourly urometer commenced as urinary output is a useful measure of the adequacy of perfusion. A balanced crystalloid solution should be used for initial resuscitation; however, the optimal fluid choice continues to be debated. Packed red cells and coagulation products may be required as bleeding from excised wounds can be significant. Hypertonic solutions such as albumin are also showing
Risk factors and clinical signs that indicate inhalational injury Risk factors
Clinical signs
Exposure to smoke, flames or chemicals and whether these were either industrial or household Duration of time exposed and whether this was in an enclosed space Burning substances such as plastics or fabrics Obtunded consciousness at scene At scene fatalities or cardiac arrests
Carbonaceous sputum Evidence of burns to the face or neck Oropharyngeal burns (e.g bulla and/or erythema) Respiratory embarrassment Singed facial or nasal hair Added sounds (wheeze or stridor) Haemoptysis Altered voice Odynophagia or dysphagia Reduced Glasgow Coma Scale (GCS)
Lung protective ventilation strategy criteria determined by the ARDS network Tidal volume
Plateau pressure FiO2
Table 2
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
6 ml/kg (range 4e8 ml/kg titrated against plateau pressures and blood pH) predicted body weight 30 cm H2O Wean as low as tolerated to achieve PaO2 55e80 mmHg (7.3e10.7 kPa)
Table 3
2
Ó 2017 Published by Elsevier Ltd.
Please cite this article in press as: Clarey A, Trainor D, Critical care management of severe burns and inhalational injury, Anaesthesia and intensive care medicine (2017), http://dx.doi.org/10.1016/j.mpaic.2017.05.009
TRAUMA
movement in the ICU bed through to surgical procedures and dressing changes, the nociceptive stimulation can be immense. Inadequate analgesia results in both short and long-term deterioration; raised inflammatory response and increased risk of posttraumatic stress disorder, respectively.4 A multi-modal analgesic approach is required to adequately cover background, breakthrough and procedural pain. Reliance on opioid only protocols must be avoided. Agents which exert their effects by modifying different pain pathways, such as ketamine (the NMDA receptor antagonist) and pregabalin (GABA analogue) will help improve analgesia. It is important to avoid agents that may promote or worsen AKI, such as non-steroidal anti-inflammatory drugs. Whilst no strong evidence supports any single sedative agent, ketamine can act as both sedative and analgesic without the risks of haemodynamic instability that other agents carry. Combination with an anxiolytic is required to reduce the incidence of emergence phenomenon. Sedation requires regular assessment using a recognized sedation scale which will assist in ventilator weaning.
promising results with studies reporting a reduction in both mortality and the incidence of compartment syndrome.8 Adult patients with a TBSA >20%, or paediatric patients with TBSA >10% require formal burns resuscitation. The volume of resuscitation fluid (Ringer’s Lactate) required in the first 24 hours has historically been calculated using the Parkland formula (4 ml per kg TBSA %). Recently military physicians applied a ‘Rule of 10s’ (Table 4), which can be used to calculate initial resuscitation fluid rate. In 88% of simulated cases the calculated volume was between 2 and 4 ml/kg.4 Resuscitation requires a balance between the prevention of burn shock (caused by increased vascular permeability and intravascular depletion) and the development of fluid creep, which at its most severe results in extreme extravascular oedema causing compartment syndrome. Identifying effective resuscitation end-points are of greater significance than determining an arbitrary fluid rate. This requires regular clinical reassessment that may be supplemented by adjuvant techniques such as focused echocardiography in order to help titrate fluid resuscitation accordingly. Fluid rates may need to be adjusted by 20 e30% every 30e120 minutes, whilst regular serum electrolyte measurements are also required.4 Circumferential wounds to limbs risk perfusion and can lead to ischaemia. Rapid recognition will avoid delays in potentially limb salvaging fasciotomies. Venous thromboembolism prophylaxis (pharmacological and mechanical) should be administered in all patients unless there is a clear contraindication.
Exposure The calculation of TBSA and assessment of burn depth requires a methodical approach ensuring all areas, including the patient’s back, are reviewed without excessive total body exposure. Heat loss can be rapid. Oesophageal, bladder or nasopharyngeal probes can be used to measure core temperature. Mechanisms to prevent hypothermia via both convection and evaporation include; warmed IV fluids, forced-air heated blankets, warming blankets and temperature controlled bed spaces. Chemical contamination and/or substances which have adhered to skin must be safely, rapidly and thoroughly removed. Burn depth has four categories each with their own characteristic appearance (Table 5). TBSA is calculated by including burns of superficial partial thickness and deeper. Wallace’s Rule of Nines and Lund and Browder charts (age specific) are often used to calculate TBSA. Areas suffering contamination or devitalization require urgent surgical debridement. Bullae may benefit from prompt de-roofing or fluid evacuation. Liaising with the specialist burns surgical team is paramount for effective management of these issues. The array of dressings available for burns is vast. No single dressing is suitable for every burn; there are several biological and antimicrobial dressings available and the specialist surgical team will advise the optimum choice.5 During exposure all clothing, contact lenses and jewellery must be removed, specifically circumferential items such as rings or necklaces.
Disability A GCS of <8 or severe agitation are indications for intubation. In an obtunded patient, especially when the collateral history may be vague, consideration must be given to the need for further investigations, such as CT scan of the brain and investigation of noxious substance exposure. Hydrogen cyanide (HCN) poisoning is a significant risk for patients exposed to fires containing plastics and fabrics. The cessation of mitochondrial aerobic respiration via reversible inhibition of cytochrome C oxidase by cyanide requires rapid administration of the antidote, hydroxycobalamin, which chelates cyanide to cyanocobalamin (70 mg/kg or 5 g IV in intermediate to severe cases, 10 g IV in cardiorespiratory arrest).9 A blood glucose reading is essential given the hypermetabolic state, as is the tracking of this parameter. Both the acute and chronic pain components of burns, including a hyperalgesic state, require detailed and dynamic ICU management. A non-verbal pain score should be used to help assess and titrate analgesic requirements. From simple
Ongoing management issues Infection There is no role for prophylactic antibiotics despite the increased risk of infection. The patient should be nursed in isolation. Gloves and aprons are mandatory when handling or moving the patient. Meticulous attention to hand hygiene and application of a faecal management system (especially with burns to the buttocks and upper thighs) may all assist in limiting the risk of sepsis developing.
Rule of 10s step-wise calculation for initial fluid rate in adults weighing ‡40 kg Step 1 Step 2 Step 3
Calculate the TBSA to nearest 10% Calculate the fluid rate as 10 TBSA in ml/h If adult weighs >80 kg add an additional 100 ml/h to the fluid rate for every additional 10kg
Table 4
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TRAUMA
The appearance and features that differentiate various burn depths Burn depth
Appearance
Features
Epidermal
C C C C
Superficial partialthickness
C
Deep partialthickness
C
C C
C C C
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Painful Erythematous Blanching No blisters
Blanching erythema Blisters Pain with hyperalgesia
White or yellow base Minimal to no blanching Reduced sensation Some blistering may be evident
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TRAUMA
Table 5 (continued ) Burn depth
Appearance
Features
Full thickness
C C C C
Leathery appearance White, brown or black base No blanching No sensation
Table 5
prompt and in those with TBSA >20% a high protein diet is required. Protein requirements for adults are 1.5e2.0 g/kg/day and in children 3 g/kg/day. Use of a recognized formula to calculate calorie requirements is recommended, adjusting intake requirements based upon the TBSA involved, the patients age and weight.5 Should nasogastric feeding fail or be inadequate then consideration of either post-pyloric or total parenteral nutrition is required.10 Early engagement with the dietetics team is essential in this aspect of patient care. Interruptions to feeding should be kept to a minimum and so merely undergoing a surgical procedure should not warrant periods of fasting, unless the procedure involves airway manipulation or adjustments. Unnecessary interruption or inadequate calorific and protein provision, predisposes the patient to secondary damage of the burn and increases both the infection risk and mortality. As with other intubated ICU patients, gastric-ulcer prophylaxis should be considered.
Systemic Inflammatory Response Syndrome (SIRS) markers are commonly seen in severe burns patients, hence more specific criteria have been proposed (Box 1); however it should be recognized that the correlation of these with positive blood cultures confirming bacteraemia is poor.4 A low threshold should exist for the administration of Human Tetanus Immunoglobulin (250 iu IM, or 500 iu IM if >24 hours since burn occurred). Nutrition Given the hypermetabolic state seen in the acute phase (basal metabolic rate rises by approximately 170%), it is imperative that nutritional deprivation is avoided. Enteral rather than parenteral support is preferable and should commence as early as possible. Conversion to normal oral dietary intake should be
American Burn Association Indicators of Sepsis in Burns. Require 3 or more to indicate likely sepsis C C C C
C
C
Ophthalmological assessment Orbital or peri-orbital involvement mandates an urgent ophthalmological assessment. This reduces the risk of long-term complications and may help salvage or preserve sight.
Temperature >39 C or <36 C Progressive tachycardia (>110 beats/minute) Thrombocytopenia (<100,000/mL) Intolerance of enteral feeding for >24 hours (abdominal distension, high gastric residuals, residuals 2x the feeding rate or diarrhoea >2500 ml/day) Progressive tachypnoea (>25bpm if not ventilated, or minute volume of >12 L/minute if ventilated) Hyperglycaemia in the absence of diabetes mellitus (untreated blood glucose >11.1 mmol/L, >7 units/hour insulin infusion or >25% increase in insulin dose over 24 hours)
Palliative care Despite application of rapid assessment and advanced clinical management, severe burns carry high mortality rates. Treatment futility may, in some cases, have to be considered and discussed by the multi-disciplinary team. Should this occur then it is likely these patients will die within the ICU. High-quality end-of-life care, which may involve palliative care specialists in some institutions, should be implemented in order to ensure patient comfort and dignity is prioritized. A
Box 1
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TRAUMA
REFERENCES 1 NHS Digital. NHS accident & emergency attendances, 2014-15; Table 14, number of A&E attendances, A&E primary diagnosis 2014-15. 2016. Leeds, http://content.digital.nhs.uk/catalogue/ PUB19883/acci-emer-atte-eng-2014-15-data.xlsx (accessed 17 Jan 2017). 2 NHS Digital. NHS Hospital Episode Statistics, admitted patient care e England, 2014-15: diagnosis. 2015. Leeds, http://content. digital.nhs.uk/catalogue/PUB19124/hosp-epis-stat-admi-diag2014-15-tab.xlsx (accessed 17 Jan 2017). 3 Moore EC, Pilcher DV, Bailey MJ, et al. The Burns Evaluation and Mortality Study (BEAMS): predicting deaths in Australian and New Zealand burn patients admitted to intensive care with burns. J Trauma Acute Care Surg 2013; 75: 298e303. 4 Lundy JB, Chung KK, Pamplin JC, et al. Update on severe burn management for the intensivist. J Intensive Care Med 2016; 31: 499e510.
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5 ISBI practice guidelines for burn care. Burns 2016; 42: 953e1021. 6 Abu-Sittah GS, Sarhane KA, Dibo SA, et al. Cardiovascular dysfunction in burns: review of literature. Ann Burns Fire Disasters 2012; 25: 26e37. 7 Romanowski KS, Palmiere TL, Sen S, Greenhalgh DG. More than one third of intubations in patients transferred to burn centres are unnecessary: proposed guidelines for appropriate intubation of the burn patient. J Burn Care Res 2016; 37: e409e14. 8 Guilabert P, Usua G, Martin N, et al. Fluid resuscitation management in patients with burns: update. Br J Anaesth 2016; 117: 284e96. 9 Anseeuw K, Delvau N, Burillo-Putze G, et al. Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med 2013; 20: 2e9. 10 Rosseau A, Losser M, Ichai C, et al. ESPEN endorsed recommendations: nutritional therapy in major burns. Clin Nutr 2013; 32: 497e502.
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Please cite this article in press as: Clarey A, Trainor D, Critical care management of severe burns and inhalational injury, Anaesthesia and intensive care medicine (2017), http://dx.doi.org/10.1016/j.mpaic.2017.05.009