Table of Contents  
Year : 2016  |  Volume : 9  |  Issue : 1  |  Page : 122-125

Unique cardiac injury after high-voltage electrical burn

Department of Anesthesiology, Intensive Care and Pain Management, Faculty of Medicine, Ain Shams University, Cairo, Egypt

Date of Submission01-Dec-2015
Date of Acceptance09-Dec-2015
Date of Web Publication17-Mar-2016

Correspondence Address:
Yasser A Salem
Department of Anesthesiology, Intensive Care and Pain Management, Faculty of Medicine, Ain Shams University, Cairo - 11371
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1687-7934.178891

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Patients of high-voltage injury commonly present with devastating burns requiring prolonged hospitalization with multiple complications. Crossing of sufficient current flow through cardiac tissue can cause lethal arrhythmia. This may lead to immediate cardiac arrest. In the following case report we described a condition of probable anatomic disfigurement of the endocardium and intracardiac structures secondary to high-voltage electrical burn.

Keywords: cardiac, electric burn, high voltage, left atrial

How to cite this article:
Salem YA, Hassan R. Unique cardiac injury after high-voltage electrical burn . Ain-Shams J Anaesthesiol 2016;9:122-5

How to cite this URL:
Salem YA, Hassan R. Unique cardiac injury after high-voltage electrical burn . Ain-Shams J Anaesthesiol [serial online] 2016 [cited 2023 Sep 24];9:122-5. Available from:

  Introduction Top

Electrical injuries represent 2-7% of all admissions to burn units. Patients with electrical injuries represent a special challenge because they encompass a wide spectrum of presentations - from thermal burns to arrhythmias to spinal cord injuries - which the emergency clinician, by definition, must know how to assess and treat [1] . Both direct effect of electrical current and its conversion from electric to thermal energy can result in tissue damage. The extent of damage from electrical injury ranges from mild superficial skin burns to severe multiple-organ dysfunction and death [2] . The most destructive indirect injury occurs when a victim becomes a part of an electrical arc. The temperature of an electrical arc is ~2500°C; it causes very deep thermal burns at the point where it comes in contact with the skin [3] . In arcing circumstances, burns may be caused by the heat of the arc itself, electrothermal heating due to current flow, or by flames that result from the ignition of clothing.

Cardiac injury can occur from coronary artery spasm, cell death through electroporation, as well as arrhythmia. Ventricular fibrillation can occur with low-voltage alternating current, whereas asystole is more common with direct current or high-voltage alternating current [4] . Cardiac arrest, either from asystole or ventricular fibrillation, is a common presenting condition in electrical accidents [5] . Other ECG findings include sinus tachycardia, transient ST segment elevation, reversible QT segment prolongation, premature ventricular contractions, atrial fibrillation, and bundle branch block [6] . Acute myocardial infarction is reported in the literature but is relatively rare [7] . The mechanism behind electrically induced cardiac arrhythmias is not entirely clear but may involve patchy areas of myocardial necrosis, which serve as arrhythmogenic foci, as well as increased cardiac sodium-potassium pump activity [6] . Electrical exposure may cause direct myocardial tissue damage through transcardiac passage of the electric current or indirect damage through ischemic injury precipitated by arrhythmia-induced hypotension or coronary artery spasm. Direct myocardial damage is thought to be caused by electric current flowing vertically (head to foot), whereas arrhythmias are more likely to be caused by electric current flowing horizontally (hand to hand) [4] . To our knowledge, there has been no previous recording of a possibility of cardiac tissue affection by arcing, with the current passing through the myocardium, although it was described theoretically.

Injury to the lungs may occur because of associated blunt trauma but is rare from electrical current, perhaps because air is a poor conductor. Injury to solid visceral organs also is rare, but damage to the pancreas and liver has been reported [8] . Injuries to hollow viscera, including the small intestine, large intestine, bladder, and gallbladder, have also been reported [9] .

  Case report Top

A 40-year-old man was admitted to the burn ICU at Galaa Military Hospital with combined high-voltage electrical burn and flash electrical burn with an estimated total burn surface area of 65% of second and third degree. Third degree areas were concise: to left pectoral and axillary area plus suprapubic area, which were considered as source and ground sites, respectively.

General assessment started immediately by performing trauma survey and bone scan, which was negative for any combined injuries other than burn insult.

Primary management was completed using the modified Parkland formula for resuscitation along with antibiotics, proton pump inhibitors, enoxaparin as anticoagulant in a prophylactic dose, and antioxidants, with a satisfactory response to management. Patient was hemodynamically stable with normal laboratory findings except for creatinine phosphokinase (CPK) and CPK-MB, which were 5616 and 4721 IU/l, respectively. Simultaneously, troponin T (cTnT) was positive at a level of 0.65 μg/l and ECG showed mild elevation in ST segment (0.5 mm) suggesting myocardial contusion. There was neither discoloration of urine nor change in kidney function. Follow-up of cardiac enzymes revealed gradual drop of cTnT over the next 48 h by the end of which it was normalized (<0.01 μg/l) together with the normalization of ST segment in ECG. Both CPK and CPK-MB continued to drop gradually over the next 4 days, with slight fluctuations in their levels, and were normalized by the fifth day. Echocardiography was carried out on day 2 with normal echo findings.

Osmotic diuresis and alkalization of urine were adopted in the first 48 h with monitoring of urine color and output. Nutritional support was provided according to the unit protocol, depending mainly on oral feeding with partial parenteral nutritional support. Mobilization started from day 3 and continued to be satisfactory. Supportive management in the form of multivitamins and intravenous glutamine were added for 15 days with an enhancement of wound healing and a good response to grafting.

Along the next 25 days the patient had underwent two sessions of excision and grafting, one of them with biological homograft and the other with autograft after removal of the homograft at day 5 and 19, respectively. Chest radiography was normal, as shown in [Figure 1].
Figure 1: Chest radiography before the attack of respiratory failure

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By day 25, patient was almost totally healed and ready for discharge from intensive care to ward. Unfortunately, he developed sudden attack of dyspnea and tachypnea, and desaturation went down to 85% on oxygen mask Venturi 60%. Intubation was carried out to avoid exhaustion, with suction of bloody froth from the endotracheal tube indicating pulmonary edema. Mechanical ventilation was followed by hemodynamic instability in the form of severe hypotension of 70/50 mmHg. Pharmacological support was added in the form of norepinephrine (50 ng/kg/min), epinephrine (100 ng/kg/min), dopamine (3 μg/g/min), and nitroglycerin (3 μg/kg/min), aiming to keep systolic blood pressure above 90 mmHg and mean blood pressure above 55 mmHg. Chest radiography showed marked increase in bronchovascular markings and lung congestion, as shown in [Figure 2].
Figure 2: Chest radiography after the development of dyspnea and just before intubation

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Sedation policy was adopted together with lung protective strategy in mechanical ventilation with the use of ascending positive end expiratory pressure (PEEP) as far as hemodynamics permitted keeping oxygen saturation above 90%. Morphine was used to facilitate tolerance to mechanical ventilation, improve myocardial performance, and decrease cardiac work load. Forced diuresis was carried out aiming at negative fluid balance. Transthoracic echocardiography was carried out and showed impaired diastolic function, right ventricular dilatation, and straightening of the interventricular septum. Moreover, echogenic mass could be visualized traversing mitral valve, measuring 1 × 1.5 cm. In addition, there was mild mitral incompetence with a pressure gradient of 8 mmHg across the mitral valve. Narrow window did not allow a full study to the mitral valve, mostly because of the use of high PEEP and lung encroachment on the cardiac field. This picture suggested rupture chorda tendineae versus vegetation due to infective endocarditis affecting mitral valve. Transesophageal echocardiography (TEE) was planned for a more detailed study of the mitral valve, but we were reluctant in taking this decision in order not to disrupt the thrombus if present. Twelve hours later patient hemodynamics started to improve gradually with marked improvement in lung compliance and oxygenation index. Successful gradual weaning of inotropic supports and vasopressors was carried out. In addition, chest radiographs confirmed and documented this improvement, as shown in [Figure 3]. A plan for weaning was initiated.
Figure 3: Chest radiography after improvement of oxygenation showed marked resolution of pulmonary congestion

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Unfortunately, after discontinuation of sedation, deterioration in the level of consciousness was unleashed. Glasgow coma score was 4/15, which is associated with high fever (more than 39.5°C). Blood culture was drawn. Antibiotic policy was shifted to management of infective endocarditis in the form of meropenem-amikacin-vancomycin empirically, in addition to aggressive fever control. Neurological consultation recommended carrying out MRI for suspecting brain-stem affection but this could not be done for hemodynamic instability.

The next day the patient was still intubated and ventilated with the same conscious level; blood pressure was 90/60 mmHg, SpO 2 98%, and urine output was 1-2 ml/h.

TEE was carried out on the next day, which showed a definitive mass with a pedicle originating from the left atrium just above the mitral valve ring and dangling inside the valve area as shown in [Figure 4] [Figure 5] [Figure 6] [Figure 7].
Figure 4: Midesophageal long axis 2 chamber view with the mass emerging from the mitral valve

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Figure 5: Midesophageal 4 chamber view with poor visualization of the right ventricle to visualize the left atrial mass

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Figure 6: Transgastric long axis view with the mass visualized separately from papillary muscle and subvalvular apparatus

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Figure 7: Another shot to the transgastric long axis view confirming that papillary muscle is in place and not avulsed with the chordae

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From our point of view (intensivist who performed TEE), this picture suggested left atrial thrombus. The cardiologist still suspected rupture chorda tendineae. Concomitantly, the cardiac surgeon in turn suspected huge left atrial thrombus and stated that the patient was not fit for surgery. No mitral incompetence could be detected by TEE.

Two days later the patient's hemodynamics progressively deteriorated. His Glasgow coma score deteriorated to 3/15. Fever persisted, elevating sometimes to more than 40°C, with normal leukocytic count ranging between 4000 and 6000. The previous pattern suggested central fever. The patient could not respond to the elevation of inotropic supports till he developed asystole.


Our suggestion for such a scenario is that the high-voltage electric burn produced endocardial scaring at the site of pedicle attachment in the left atrium just above the mitral valve ring, as shown in [Figure 5]. This suggestion is supported by the transient mild elevation in troponin level that simulated the elevation following maze procedure and atrial ablations [10] . In addition, the imaginary arcing axis connecting the two full thickness burn areas (i.e. left pectoral and axilla at one end and suprapubic area at the other) crosses the heart perpendicularly as shown in [Figure 8].
Figure 8: The patient by the end of the second weak showing good healing power. The black line indicates the hypothetical pathway of the electric current

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This scaring creates mural thrombus formation despite prophylactic anticoagulation therapy. It gradually encroaches on the mitral valve area till it suddenly performs a picture of acute mitral stenosis. This explains the attack of pulmonary edema for which the patient was ventilated. Later on, unfortunately, part of this fresh friable thrombus was detached. This suggested accident can explain two results. The first one is the neurological manifestation in the form of fever, which mostly will be central and play a role in deteriorated conscious level. The second one is the sudden improvement in the cardiopulmonary function with improvement in hemodynamics and oxygenation index in addition to the chest radiographic picture due to the relieve of mitral stenotic effect of this thrombus.

  Conclusion and recommendation Top

Electric burn is like an iceberg. That is to say, what is evident from this injury is quite less grave than the actual in most of the cases. Single echocardiography examination after high-voltage electric burn is not sufficient even if it was initially normal. Follow-up with echocardiography is recommended especially if the contact ground vector crosses the heart perpendicularly. Therapeutic anticoagulation instead of prophylactic dose might provide more protection.[11]

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Conflicts of interest

There are no conflicts of interest.

  References Top

Price TG, Cooper MA. Electrical and lightning injuries. In: Marx JA, Hockberger RS, Walls RM, editors. Rosen's emergency medicine concepts and clinical practice. Philadelphia, PA: Mosby-Elsevier; 2006. 2267-2278.  Back to cited text no. 1
Schaefer NR, Yaxley JP, O'Donohue P, Lisec C, Jeyarajan E. Electrical burn causing a unique pattern of neurological injury. Plast Reconstr Surg Glob Open 2015; 3:e378.  Back to cited text no. 2
Jaffe RH. Electropathology: a review of the pathologic changes produced by electric currents. Arch Pathol 1928; 5:839.  Back to cited text no. 3
Spies C, Trohman RG. Narrative review: electrocution and life-threatening electrical injuries. Ann Intern Med 2006; 145:531-537.  Back to cited text no. 4
Kobernick M. Electrical injuries: pathophysiology and emergency management. Ann Emerg Med 1982; 11:633-638.  Back to cited text no. 5
Jensen PJ, Thomsen PE, Bagger JP, Nørgaard A, Baandrup U. Electrical injury causing ventricular arrhythmias. Br Heart J 1987; 57:279-283.  Back to cited text no. 6
Walton AS, Harper RW, Coggins GC. Myocardial infarction after electrocution, Med J Aust 1988; 148:365.  Back to cited text no. 7
Newsome TW, Curreri PW, Eurenius K. Visceral injuries: an unusual complication of an electrical burn. Arch Surg 1972; 105:494-497.  Back to cited text no. 8
Branday JM, DuQuesnay DR, Yeesing MT, Duncan ND. Visceral complications of electrical burn injury. A report of two cases and review of the literature. West Indian Med J 1989; 38:110-113.  Back to cited text no. 9
Yoshida K, Yui Y, Kimata A, Koda N, Kato J, Baba M, et al. Troponin elevation after radiofrequency catheter ablation of atrial fibrillation: relevance to AF substrate, procedural outcomes, and reverse structural remodeling. Heart Rhythm 2014; 11:1336-1342.  Back to cited text no. 10
Ku CS, Lin SL, Hsu TL, Wang SP, Chang MS. Myocardial damage associated with electrical injury. Am Heart J 1989; 118:621-624.  Back to cited text no. 11


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]


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