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Electrical Injuries

Author: Jonathan Baird / Editor: Adrian Boyle / Codes: Trauma / Published: 20/03/2014 / Review Date: 20/03/2017

 

Introduction

Electric shocks can cause death by inducing ventricular arrhythmia or asystole. Tetany of respiratory muscles can also induce hypoxic cardiac arrest. Much of the morbidity resulting from electrical injury relates to burns and neurological dysfunction.

 

Clinical assessment

Cardiac dysrhythmias

Asystole (DC) and VF/VT (AC) are the most sinister cardiac dysrhythmias. Numerous other dysrhythmias may occur. These include atrial fibrillation and atrial tachycardia, junctional rhythms, SVT, 1st and 2nd degree heart block and premature ventricular beats. ST segment abnormalities may be evident and usually resolve spontaneously. Coronary artery spasm and thrombosis can cause myocardial ischaemia and infarction.

Post mortem studies demonstrate a variety of anatomical cardiac changes following electrocution including widespread focal necrosis of the myocardium and specialized tissue such as the atrio-ventricular and sino-atrial nodes [1].

Respiratory system

Electrical current can induce apnoea through tetany of the respiratory muscles or through disruption of the normal cyclical output of the respiratory centre in the brainstem.

Cutaneous burns

Cutaneous burns are often full thickness involving typical entrance and exit sites of the current pathway such as the hands and feet. Cutaneous burns may have a relatively small surface area and can lead to underestimation of internal burns produced by the current pathway.

Peripheral neurological features

Nerves have a small cross sectional diameter. Electrical exposure can result in high current density within nervous tissue producing significant damage. Effects can be immediate or delayed with paraesthesia and weakness. The ulnar and median nerves are commonly involved with injuries to the hand.

Central Nervous System features

Application of electrical current to the brain can cause loss of consciousness, confusion and amnesia. Siezures may occur. A wide variety of neurological findings may be present such as hemiparesis, speech and visual disturbance. Involvement of the spinal cord can result in tetraplegia and paraplegia which may be transient or permanent. The incidence of spinal cord injury following high voltage electrical accidents varies between 2 and 27% [2].

Musculoskeletal features

Deep muscle burns can give rise to contractures and deformity. Marked skeletal muscle necrosis can produce electrolyte abnormalities, myoglobinuria and renal impairment. Muscle oedema within myofascial sheaths may produce compartment syndrome.

feet

A picture showing a classic burn injury. There are two entry burns on the palms from holding an electrical source and an exit burn on the foot.

Secondary trauma can result as a consequence of being thrown from the electrical source. Violent muscle contraction can produce fractures and dislocations particularly around the shoulder girdle (e.g. the characteristic posterior shoulder dislocation). Opisthotonus may produce vertebral fractures with secondary damage to the cord or cauda equina.

xray

A posterior dislocation of the shoulder with an associated fracture

Ocular features

Passage of current through or adjacent to the eye may produce burns to the cornea, sclera or deeper structures. Cataract formation is a delayed consequence of lens involvement.

Vascular injuries

Involvement of blood vessels in the current pathway can produce vascular spasm and thrombosis with potential distal ischaemia. Delayed aneurysm formation may result from damage to the vessel wall.

Intramural burns

Intra oral burns are more common in young children. The characteristic patient is the toddler who explores domestic electrical appliances or cables by placing them in his or her mouth. Current conduction may be aided by electrolyte rich saliva.

Delayed haemorrhage is a recognised feature of intra oral electrical burns. Haemostasis may initially appear satisfactory but as temporary vasospasm induced by the current resolves severe haemorrhage may result. Contraction of scar tissue has the potential to make intra oral burns particularly disfiguring.

Effects upon the foetus

Amniotic fluid readily conducts electrical current. If the gravid uterus is involved in the electrical pathway the effects on the foetus may be devastating. Maternal cardiac arrest and dysrhythmias also compromise uteroplacental blood flow.

 

Differential Diagnosis

The diagnosis of an electrical injury is rarely difficult. The exception is a patient who has been struck by lightning. These patients may appear confused and have been found outside in stormy weather.

 

Investigation Strategies

Many individuals attend the emergency department following an electrical shock from a low voltage source. Such patients have often sustained little or no thermal injury. Debate exists about the need for ECG monitoring of such patients. The risk of malignant dysrhythmias, such as ventricular fibrillation or ventricular tachycardia, is greatest at the time of injury. The incidence of late dysrhythmia is not known but is thought to be very low. A six year review of fatal electrocutions in Delhi found that 150 of the 153 fatalities died at the scene. A further two died of septicaemia and one died of a dysrhythmia that was present on admission [3].

By the time of presentation to the emergency department the risk of a malignant dysrhythmia is low. An Australian study of 212 consecutive presentations of low voltage electrical injury demonstrated transient conduction abnormalities in only 4% of patients following 6 hours of ECG monitoring. The authors went on to develop a protocol whereby patients who sustained a low voltage injury and had a normal baseline ECG did not undergo further monitoring. No ill effects resulting from this policy were observed [4].

Traditionally, patients who sustain high voltage injuries (>1000volts), lose consciousness, have a transthoracic current pathway or an abnormal baseline ECG are thought to be at higher risk of dysrhythmia and consequently undergo cardiac monitoring. The necessity and duration of cardiac monitoring in this so called high risk group is subject to debate. A Canadian study performed 24 hours of continuous cardiac monitoring on 134 high risk patients. No lethal dysrhythmias were observed during the 24 hour monitoring period [5].

The role of troponin or CK MB measurement in electrical injury is unclear. Baseline and 12 hour troponin measurement may be carried out if high risk features are present. The clinical significance of elevated troponin is uncertain.

Monitoring of the foetus by cardiotochography (CTG) is advisable for pregnant women over 22 weeks gestation. An obstetric consultation should also be obtained.

 

Management

The management of electrical injuries within the emergency department and the prehospital setting can be complex. Patients may require advanced life support with immediate treatment of cardiac dysrhythmias In addition simultaneous treatment and assessment is required for associated injuries.

Pre-hospital

Switching off the current source is essential to prevent further injury to the patient and would be rescuers. In the pre hospital setting this responsibility usually falls upon the fire brigade or employees of the regional electrical authority. Great care is required particularly with high voltage sources which may produce arcing of electrical current. When faced with multiple casualties who have sustained electrical injury those who are apparently lifeless should receive priority. Victims are often fit young individuals who may respond to simple measures such as ventilation and defibrillation.

Management of cardio respiratory arrest

Initial management follows standard basic advanced life support principles. Likely causes may include:

  • Current induced dysrhythmia (ventricular fibrillation or ventricular tachycardia)
  • Hypoxic cardiac arrest (respiratory muscle tetany, centrally mediated apnoea)
  • Hypovolemia from associated injuries
  • Hyperkalaemia secondary to rhabdomyolysis
  • Intravenous cannulation should be in a limb not involved in the current pathway. Damage to the vascular structures (e.g. vasospasm/thrombosis) of a limb may prevent systemic circulation of resuscitative drugs and fluids.

Management of thermal injury

Simply considering surface burns may result in gross underestimation of the extent of internal thermal injury. Prediction of the current pathway by examining entrance and exit burns allows appreciation of which internal structures may have been involved.

Adherence to traditional resuscitation formulae for thermal burns can result in insufficient fluid administration. Administration of large volumes of fluid (often much larger than initially appreciated) may be required to compensate for large internal fluid losses into damaged tissues. Haemodilution from aggressive administration of crystalloid may require blood transfusion to ensure adequate circulating haemoglobin

Early establishment of invasive monitoring is useful to assess and guide fluid resuscitation.

Analgesia is required for all patients with electrical thermal injuries. Cutaneous burns should be photographed, dressed and were appropriate elevated. Plastic surgical consultation is required but should not delay or interfere with ongoing resuscitation.

Compartment syndrome should be actively sought but can be difficult to distinguish from muscle ischaemia secondary to vascular injury. Vasospasm of limb arteries may be transient but arterial thrombosis may present with distal ischaemia and infarction. Distal pulses, limb temperature and pain should be assessed regularly. Vessel injury requires vascular surgery consultation.

Skeletal muscle damage results in electrolyte derangement and myoglobin release. Serum potassium, phosphate, calcium and creatine phosphokinase measurements are necessary and should be repeated if rhabdomyolysis is a possibility. Hyperkalaemia poses the main threat to myocardial stability.

Myoglobin release produces a brown discolouration of the urine and impairs renal tubular function. Dipstick analysis of urine will demonstrate a false positive finding for haematuria in the presence of myoglobin. Maintenance of adequate renal perfusion by restoring circulating volume and blood pressure helps to prevent renal failure. Alkalisation of the urine may also have a role. Ultimately if renal failure ensues, haemofiltration may be required.

Severely burned patients demonstrate evidence of the systemic inflammatory response syndrome (SIRS). SIRS may develop with resulting multi organ dysfunction. Early effective resuscitation of the patient with severe electrical injury may reduce the severity of multi organ dysfunction and failure.

 

Prognosis & Followup strategies

Patients who have suffered a domestic shock, without visible injury and have a normal ECG can be safely discharged from the emergency department.

The presence of arrhythmias should lead to a period of monitored observation. Women who are more than 22 weeks pregnant should undergo obstetric assessment.

Electrical burns should be managed like any other burn, but the threshold for admission and review should be lower as the burns are often deeper than purely thermal burns.

 

Safety pearls and Pitfalls

  1. The extent of injury underneath an electrical burn is often under-estimated.
  2. A patient who has suffered a lightning strike can be difficult to diagnose. These are usually golfers who are found outside in an acutely confused state in stormy weather

 

MedicoLegal and other considerations

Occupational injuries may lead to investigation by the Health and Safety Executive, or similar regulatory bodies. Good note keeping is essential in case statements are required.

 

References

  1. James TN, Riddick L, Embry JH. Cardiac abnormalities demonstrated post-mortem in four cases of accidental electrocution and their potential significance relative to nonfatal electrical injuries of the heart. Am Heart J. 1990; 120(1): 143-57.
  2. Lammerste D. Neurorehabilitation of spinal cord injuries following lightning and electrical trauma. NeuroRehabilitation. 2005; 20: 9-14.
  3. Rautji R, Rudra A, Behera C. Electrocution in South Dehli: A retrospective study. Med Sci Law. 2004; 43: 350-2.
  4. Blackwell N, Hayllar J. A three year prospective audit of 212 presentations to the emergency department after electrical injury with a management protocol. Postgrad Med J. 2002; 78: 283-285.
  5. Bailey B, Gaudereault P, Thivierge R. Cardiac monitoring of high-risk patients after an electrical injury: a prospective study. Emerg Med J. 2007; 24: 348-352.

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