Pre-hospital assessment and management of high-voltage electrical burns in a 58-year-old male

Pre-hospital assessment and management of high-voltage electrical burns in a 58-year-old male

Electrical burns are relatively rare among all age groups but constitute some of the most devastating burns, as well as danger to first responders; thus, they demand special considerations (1,2). Electricity either flows in direct current (DC) or alternating current (AC) (3). When a victim is electrified by DC, continuous muscle tetany is induced, while AC causes cyclical tetanic muscle contractions; both forms often preventing the victim from releasing themselves from the electrical source (3,4). The strength of induced muscle contractions in upper limbs have been known to cause dislocations, muscular injury, and even bone fractures (4). The characteristics and severity of electrical injuries are determined by several variables, including the form and strength of current flow, its pathway, site of contact, and duration of exposure (3). Electrical burns caused by voltages greater than 1000 (i.e. transmission lines) are classified high-voltage electrical burns (HVEBs), and account for 6% of hospitalised burns in Australia (1,3). Mortality rates from electrical burns have been reported as high as 59% of cases (5). Acute arrhythmias are the most frequent cause of death in electrical injuries (1,6). Damage to deep tissue from electrical conduction can cause several sequelae in survivors, including compartment syndrome, which, without timely intervention, can lead to amputations (1,7). Because of the nature of electrical conduction through the body, the size of external burns does not necessarily equate to the extent of internal damage (7).

In this article, the case of a 58-year-old male linesman who received arm-to-arm electrification while working on an adjacent line will be discussed. Firstly, the anatomical pathophysiology of the organs and tissues affected by a HVEB will be explored, followed by a discussion on the pre-hospital assessment and management of HVEBs.

Case Study

Steven Burundi (fictional name and character), a 58-year-old indigenous male, was employed as a linesman and has a history of depression, heart disease, type-2 diabetes, and chronic renal impairment. His medications include a monoamine oxidase inhibitor, a calcium channel blocker, aspirin, metformin, and a thiazide diuretic. Steven was doing maintenance on high-voltage powerlines in rural Victoria during midday with an ambient temperature of 36°C. During his work, he lost balance while reaching for the back of his tool-belt. Subsequently, he fell, accidentally brushing his left elbow and right forearm against an adjacent powerline of 50,000V. Falling from his position, he swung from his harness, and struck his head on the powerline frame, losing consciousness. Upon retrieval by local State Emergency Service personnel, paramedics assessed him. Steven had regained consciousness and was alert and oriented, sitting upright with a Glasgow Coma Scale (GCS) of 15. He had a total of 3.5% body surface area (BSA) 3rd-degree burns to posterior and lateral regions of his left elbow and right forearm and complained of a headache. Steven appeared diaphoretic and slightly flushed, though he stated he had been that way all day on account of the heat. He was tachycardic with a heart rate (HR) of 128 beats per minute, blood pressure (BP) of 142/76mmHg, haemoglobin oxygen saturation (SpO2) of 96%, and a temperature of 37.2°C. A 12-lead electrocardiograph (ECG) showed sinus tachycardia with intermittent multifocal PVCs averaging four per minute. The incident occurred one-and-a-half hours by land from the nearest clinical facility, and three hours by land to the nearest burns centre.

Pathophysiology of electrothermal injury

Skin

Damage to the skin results in multiple system disturbances due to its integration with various other body systems such as nerves, vasculature, structural fascia, and the lymphatic system (8–10). Skin has variable thickness depending on its location and purpose (i.e. soles and palms have thicker and tighter skin for protection) and is comprised of three layers: the epidermis, dermis, and hypodermis (9,11). HVEBs penetrate all three layers and are therefore classified as 3rd-degree burns (7,11–13). Skin serves the rest of the body through multiple roles; it’s durability and slight acidity protects against trauma and infection, it regulates water absorption and transpiration, protects internal organs and tissues from harmful radiation, is involved with vitamin D production, provides us with knowledge of our surroundings through sensation, and assists thermo-regulative function through monitoring environmental temperature and altering skin circulation (11). Thus, perturbations in the skin’s integrity can negatively affect the protection and function of other organs and body systems opening the way for pathogens to enter and infect, impair blood flow and cellular respiration, negatively affect thermoregulation, and destroy glands associated with homeostasis (9).

Deep tissue

An important consideration when assessing HVEBs is that the appearance of the external burn does not necessarily correlate with the extent of internal injury (4). Notice the small entry wound in Figure 1 which is associated with significant collateral and deep tissue injury requiring fasciotomy. Massive coagulation and necrosis of subcutaneous tissue can cause the skin injury to appear severe, while it is the underlying tissue which is causing the appearance (14). Skin condition can affect the severity of thermal injury (4). Water offers low resistance to electrical current, as does thin skin, therefore such skin conducts electricity more readily, resulting in a less significant cutaneous burn, but greater conduction of electricity with subsequent damage to deeper tissues. Whereas dry or thicker skin has greater resistance, and therefore retards electrical conduction to deeper tissue, but results with greater cutaneous burns (4). Thus, the greater the resistance of a tissue, the greater the severity of thermal injury suffered.

The greatest resistance of all human tissues is found in bone; therefore, bones suffer the most severe thermal injuries, often resulting in osteonecrosis (6,15). Aside from direct thermal injury to bones, victims of HVEBs have a high risk of vertebral fracture and spinal cord injury due to muscle tetany (15). Electrical injury to muscle tissue can cause rhabdomyolysis necrosis and oedema, leading to a high risk of compartment syndrome and renal damage due to a huge release of myoglobin (6).

Figure 1. Note entry wound on palm and fasciotomy to decompress forearm musculature.

Cardiorespiratory

Myocardial tissue damage can occur when electricity is conducted through the mediastinum (16). Pulmonary tissue damage is rarely seen in electrical injuries (14). However, apnoea can be caused by inhibition of diaphragmatic innervation, or diaphragmatic tetany (14). Normal cardiac electrical conduction can be disrupted, and pathways damaged by electrical shock (17). Though not always lethal, cardiac arrhythmias are the most common cause of death following electrical injury; ECG changes occur in close to one-third of victims and generally occur within a few hours (4,6,16). The most common arrhythmias observed post HVEBs include premature ventricular contractions (PVCs) and sinus tachycardia, and more rarely, but more likely with HVEBs, atrial fibrillation (AF), ventricular fibrillation (VF), ventricular tachycardia (VT), and asystole (6,7,18).

Other injuries caused by falling from the point of electrification may be present in areas unaffected electrothermally; traumatic spinal, cranial, and limb injuries may be distracted from by external thermal injuries (7).

Pre-hospital assessment and management

Primary and secondary surveys

The ‘DRABC’ approach should be the first component of a systematic approach to this case; that is, check for danger and ensure sources of electricity have been removed from the scene and patient, check for responsiveness, airway patency, adequate breathing, and circulation, intervening where any of these checks elicit abnormal findings (16). A further ‘head-to-toe’ investigation is important to identify any traumatic injuries associated with his fall, and to identify other potential burn sites (16,19). Due to the high-voltage of the line he was electrified by, as well as Steven’s head-strike and fall, immobilisation is required until spinal injuries, joint dislocations, and bone fractures due to tetany can be assessed and ruled out (4,15). Appropriate splinting and traction should be applied as required for suspected fractures and joint dislocations (19).

Steven’s cervical vertebrae should be assessed for tenderness by palpation, followed by a full neurological examination involving sensory and motor nerve testing of the cervical, thoracic, lumbar, and spinal dermatomes (19,20). I if Steven were unconscious, airway support should be maintained using a jaw thrust and chin lift (19). If Steven’s breathing is inadequate, there is a chance that either his respiratory innervation has been interrupted, or his respiratory muscles have been paralysed, putting him in danger of subsequent cardiac arrest (14). In this case, intermittent positive pressure ventilation should occur and his SpO2 monitored (19,21). If Steven goes into cardiac arrest, then this should be managed the same way as an acute myocardial infarction (AMI) (6).

A vital signs survey should include respiratory rate, HR including pulse quality, BP, SpO2, and temperature. Pain should be frequently monitored, as should changes in BP, HR, and GCS; Steven is at risk of an intracranial bleed following his head-strike as he is on aspirin, complains of a headache, and lost consciousness (19).

First aid

The next treatment priority consists of providing first aid and pain relief (13). Generally, contact points of HVEBs develop 3rd degree burns and require treatment as such (22). Stopping the burning process and providing pain relief are priorities in this phase of care (22,23). Bilateral large-bore intravenous (IV) access should be achieved early to administer analgesia and fluid (15,21,24). Cool running water should be applied to cutaneous burn sites for up to 20 minutes, while ensuring the patient is kept otherwise warm to avoid hypothermia; if signs of hypothermia begin, cooling should cease (4,16). Once cooled, any further pain-relief should be restricted to pharmacological means (13,16). The injury sites should then be cleaned with normal saline or 0.1% chlorohexidine, and covered with clingfilm (16,23,25). Clingfilm should be applied lengthways, rather than circumferentially, to avoid impeding blood and lymph flow as swelling increases (16). Steven’s arms should then be elevated to slow swelling (25).

Analgesia

IV administration of analgesia provides the most effective relief due to its rapid absorption (16). Conventional locations for IV administration consist of upper limb sites, such as the cephalic, median cubital, basilic, and metacarpal veins (26). However, because of the potential for oedema to occur in, or proximal to, these areas due to Steven’s burns, other routes should be explored (26). External jugular cannulation is an alternative to conventional sites, and could be considered in Steven’s case (26,27).

Morphine is the preferred analgesic for burns, and ondansetron is commonly administered prophylactically alongside it to counter its commonly induced nausea (28,29). However, ondansetron can cause QT prolongation, and is a contraindication for amiodarone (see section: ‘Cardiac monitoring’) (21,30,31). Therefore, fentanyl is a more appropriate alternative, having lower associations with developing nausea (32). An initial dose of up to 50 mcg of IV fentanyl with repeats of at least five minute intervals should be administered with a maximal does of 200mcg (consult for further) (21). If antiemetics are indicated, prochlorperazine should be administered as it does not affect QT-segments, and lacks the cardiovascular adverse effects of metoclopramide (21).

Upon completion of primary and secondary surveys, and first aid, there are four priorities identified by the Victorian Adult Burns Service for managing electrical burn victims, these are: cardiac monitoring, fluid resuscitation,  management of myoglobinaemia, and management of compartment syndrome (13). These priorities will be discussed below considering Steven’s case.

Cardiac monitoring

There is a high chance that Steven has suffered myocardial injury, as electricity was conducted arm-to-arm via the mediastinum (16). Steven presented with sinus tachycardia and multifocal PVCs;  arrhythmias produced by electrification should be treated the same as those produced by an AMI (17). However, Steven’s HR of 128 and the frequency of PVCs does not warrant immediate intervention (33). Because of his history of heart disease, and the high risk of VT and VF developing from arm-to-arm electrification, continuous cardiac monitoring via a 12-lead ECG is essential (6,16,34). Additionally, an infusion of amiodarone at 5mg/kg with a maximal does of 300mg should be prepared in case Steven suffers an episode of VT lasting more than 30 seconds (21). If Steven’s cardiac condition remains unstable or rapidly deteriorates towards pulseless ventricular arrhythmias synchronised cardioversion should occur by a skilled clinician (21).

Fluid management

Assessing the extent of external thermal injury using the Rule of Nines or the Parkland formula is conventionally conducted to determine the amount of fluid resuscitation (35). However, external burn size does not indicate the extent of internal injury in HVEBs, and as Steven was already diaphoretic at the time of electrification, there is likely more extensive injury internally than is externally indicated (4,13,14). The Parkland formula can thus leave damaged muscle and rhabdomyolysis unaccounted for, resulting in un-anticipated fluid shifts (16,24). Therefore, an indicator other than the size of Steven’s external burns is required (4,13,24).

Muscle breakdown products can lead to myoglobinaemia, putting an immense strain on the kidneys, which would severely exacerbate Steven’s renal failure and cause acute kidney injury (AKI)(6). Increased diuresis can prevent circulating myoglobin from damaging renal tubules (16). Therefore, fluid resuscitation should be commenced to ‘flush’ the renal tubules, being titrated to a urinary output goal of 75-100mls/hr (16). Measurement of urinary output is not generally done using a catheter in pre-hospital care, therefore a vessel of known volume, such as a saline bottle should be used to collect all urinary output and provide estimates of urinary volume to determine flow rate of IV fluid. Diuretics may also be used as a pharmacological adjunct (16).

Steven’s pre-existing renal disease can make management of myoglobinuria fraught with problems (36). The development of an AKI in Steven’s case may cause a relative hypervolaemia without a commensurate increase in urine output, further exacerbating his renal failure (24).

Management of compartment syndrome

Swelling of the burn sites can cause compartment syndrome, impeding blood flow distally (4,15). Throughout transport and care, areas distal to Steven’s burns should be frequently assessed for perfusion (capillary refill time and pulses), temperature, pallor, and neurological function (4,15,24). If compartment syndrome develops, Steven risks necrosis and amputation of distal portions of his upper limbs, therefore, fasciotomy and, potentially, escharotomy will be required to restore distal perfusion (7). This heavily influences decisions regarding transport solutions (37). Due to the nature of Steven’s burns, he must receive rapid care at a burns centre such as the Alfred in Melbourne (16,25). Due to the cardiac, renal, and compartment syndrome risks faced by Steven, air transport is preferred to expedite hospital care.

Conclusion

Electrothermal injuries can manifest in multiple areas depending on contact points and exit sites. Additional to cutaneous thermal injury, injury to deep tissue can be unexpectedly extensive, and progress rapidly. Skin condition can affect the extent of internal injury, and more benign external injuries tend to mask more serious internal injuries. Further to thermal injuries, dislocations and fractures may occur due to tetany induced by electrical conduction through myocytes. Therefore, c-spine precautions should always be taken, and a full neurological assessment conducted. Suspected fractures and dislocations should be splinted and immobilised. Cool running water should be used to hinder the progression of thermal injury and provide analgesia but should not occur for longer than 20 minutes to avoid hypothermia. Fentanyl is the preferred pharmacological analgesic agent, and ondansetron and metoclopramide should be avoided due to potentially detrimental interactions and cardiovascular effects; instead prochlorperazine should be administered in the case of nausea. Cardiorespiratory disturbances are also common, with arrhythmias often developing within hours. Any acute dysrhythmia and cardiac arrest should be managed as an acute myocardial infarction in normal circumstances. Internal electrothermal injury provides a high risk of acute kidney injury due to rhabdomyolysis and subsequent high plasma concentrations of myoglobin. Fluids should be given liberally to aid renal clearance of myoglobin, with a urinary output of 75-100mls/hr being the driving force behind flow rate. Compartment syndrome is a serious risk in electrothermal injury due to oedema from deep tissue destruction. This risk should expedite transport to the closest burns centre so that fasciotomy and escharotomy may be conducted. Due to multiple devastating injuries being associated with HVEBs, initial impressions of a patient’s condition may not represent the extent of actual and developing injury. The prognosis of HVEBs victims depends upon the severity of the initial injury, as well as that of subsequent injuries. Early interventions such as fluid resuscitation and surgical interventions are primary goals to reduce complications. Therefore, additional to expediting transport solutions, the first-responder must remain focussed on what they are observing, intervening as necessary, while considering likely developments in the patient’s condition and preparing appropriate interventions.

 

 References:

  1. Flinders University. Hospitalised burn injuries Australia. Canberra: AIHW; 2013.
  2. Buja Z, Arifi H, Hoxha E. Electrical burn injuries. An eight-year review. Ann Burns Fire Disasters. 2010;23(1):4.
  3. Edlich R, Farinholt H-MA, Winters KL, Britt LD, Long III WB. Modern concepts of treatment and prevention of electrical burns. J Long Term Eff Med Implants. 2005;15(5).
  4. Shrivastava P, Goel A. Pre-hospital care in burn injury. Indian J Plast Surg Off Publ Assoc Plast Surg India. 2010;43(Suppl):S15.
  5. Haberal M. Electrical burns: a five-year experience. J Trauma. 1986;26(2):103–9.
  6. Waldmann V, Narayanan K, Combes N, Jost D, Jouven X, Marijon E. Electrical cardiac injuries: current concepts and management. Eur Heart J. 2018;39:1459–65.
  7. Lee J, Sinno H, Perkins A, Tahiri Y, Luc M. 14,000 volt electrical injury to bilateral upper extremities: A case report. Med Hournal Malaysia. 2010;13(1):7–10.
  8. Wong R, Geyer S, Weninger W, Guimberteau J, Wong JK. The dynamic anatomy and patterning of skin. In: Skin Aging & Cancer. Singapore: Springer; 2016. p. 1–10.
  9. Yadav N, Parveen S, Chakravarty S, Banerjee M. Skin Anatomy and Morphology. In: Skin Aging & Cancer. Springer; 2019. p. 1–10.
  10. Herlin C, Subsol G, Gilles B, Captier G, Chaput B. Three-dimensional surface imaging is not enough for surgical simulation. Plast Reconstr Surg. 2016;137(1):246e-247e.
  11. Saladin KS, Gan CA, Cushman HN. Anatomy and Physiology. 8th ed. New York, USA: McGraw Hill Education; 2018.
  12. Talley NJ, O’Conner S. Clinical examination: A systematic guide to physical diagnosis. 7th ed. Canberra: Elsevier; 2019.
  13. Victorian Adult Burns Service. Electrical burns: Early management [Internet]. Burns Management Guidelines. 2017 [cited 2020 Jan 12]. Available from: http://www.vicburns.org.au/severe-burns/electrical-burns/early-management-2/
  14. Spies C, Bates A, Medical S, Trohman RG. Narrative review: Electrocution and life-threatening. Ann Intern Med. 2006;145(7):531–7.
  15. Friedstat J, Brown DA, Levi B. Chemical, electrical, and radiation injuries. Clin Plast Surg. 2018;44(3):657–69.
  16. Trauma Victoria. Burns Guideline. Melbourne, Victoria: Victorian Health Department; 2017. p. 1–24.
  17. Hocagil H, Ay D. Cardiac monitoring in patients with electrocution injury. Turkish J Trauma Emerg Surg. 2012;18(4):301–5.
  18. Perret JN, Sanders TW, d’Autremont SB, Patrick HC. Ventricular fibrillation initiated by an electrocution injury and terminated by an implantable cardioverter-defibrillator. J Louisiana State Med Soc Off organ Louisiana State Med Soc. 2009;161(6):343–7.
  19. Stanford Health Care. Trauma Guidelines. Stanford: Stanford Medicine; 2016. p. 1–156.
  20. Betts JG, Desaix P, Johnson E, Johnson JE, Korol O, Kruse D, et al. Anatomy and physiology. 1st ed. Rice University; 2017.
  21. Ambulance Victoria. Clinical practice guidelines ambulance and MICA paramedics. Melbourne: Governemnt of Victoria; 2018. 1–426 p.
  22. Kearns RD, Cairns CB, Rich PB, Cairns BA. Thermal burn care: a review of best practices. What should prehospital providers do for these patients? EMS World. 2013;42(1):43–51.
  23. Allison K, Porter K. Consensus on the prehospital approach to burns patient management. Trauma. 2003;5:97–101.
  24. Culnan DM, Farner K, Bitz GH, Capek KD, Tu Y, Jimenez C, et al. Volume resuscitation in patients with high-voltage electrical injuries. Ann Plast. 2018;80(3):1–14.
  25. Australian and New Zealand Burn Association. Initial management of severe burns. Canberra: ANZBA; 2016. p. 1.
  26. Ortega R, Sekhar P, Hansen CJ. Peripheral intravenous cannulation. N Engl J Med. 2008;359(21):e26–9.
  27. Queensland Ambulance Service. External jugular intravenous cannulation. In: Clinical Practice Procedures: Queensland Ambulance Service. Brisbane: Queensland Government; 2016. p. 348–51.
  28. Campos GO, de Jesus Martins M, Jesus GN, de Oliveira PRR, Lessa CN, de Oliveira JCMF, et al. Palonosetron versus ondansetron for prevention of nausea and vomiting after total abdominal hysterectomy under spinal anesthesia with intrathecal morphine: a double-blind, randomized controlled trial. BMC Anesthesiol. 2019;19(1):1–6.
  29. Richardson P, Mustard L. The management of pain in the burns unit. Burns. 2009;35(7):921–36.
  30. Armahizer MJ, Seybert AL, Smithburger PL, Kane-Gill SL. Drug-drug interactions contributing to QT prolongation in cardiac intensive care units. J Crit Care. 2013;28(3):243–9.
  31. McKechnie K, Froese A. Ventricular tachycardia after ondansetron administration in a child with undiagnosed long QT syndrome. Can J Anesth Can d’anesthésie. 2010;57(5):453–7.
  32. Richards T, Corso L. Management of burn wound pain in the hospital setting. Aust Med Student J. 2019;9(1):41–4.
  33. Steg P, James S, Atar D, Badano L, Lundqvist C, Borger M, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012;33:2569–619.
  34. Goldberger AL, Goldberger ZD, Shvilkin A. Sinus and Escape Rhythms. In: Goldberger AL, Goldberger ZD, Shvilkin ABT-GCE (Ninth E, editors. Goldberger’s Clinical Electrocardiography. 9th ed. Elsevier; 2018. p. 122–9.
  35. Moore RA, Waheed A, Burns B. Rule of Nines [Internet]. StatPearls [Internet]. StatPearls Publishing; 2019 [cited 2020 Jan 16]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513287/
  36. Emara SS, Alzaylai AA. Renal failure in burns patients: A review. Ann Burns Fire Disasters. 2013;26(1):12–5.
  37. Cassidy TJ, Edgar DW, Phillips M, Cameron P, Cleland H, Wood FM. Transfer time to a specialist burn service and influence on burn mortality in Australia and New Zealand: A multi-centre, hospital based retrospective cohort study. Burns. 2015;41(4):735–41.