Cranial-entry Electrical Burns with Neurological Sequelae: A Case Report

Promise Tamunoipiriala Jaja1 and Afieharo Igbibia Michael 2,3 

 1. Department of Neurological Surgery, University College Hospital, Ibadan, Nigeria 

2. Department of Plastic, Reconstructive and Aesthetic Surgery, University College Hospital, Ibadan, Nigeria 

3. Department of Surgery, University of Ibadan, Ibadan, Nigeria 

Correspondence to: Dr. Promise Tamunoipiriala Jaja; email: projat@hotmail.com 

Received: 29 May 2021; Revised: 06 Jun 2021; Accepted: 06 Jun 2021; Available online: 27th June 2021

Summary 

Cranial-entry high-voltage electrical burn injury rarely occurs. Hence, early presentation is rare. We herein present a case of a teenage male with mainly full-thickness electrical burn injury covering 9% of the total body surface area, with gangrenous mid-fronto-parietal scalp and calvarium, moderate head injury with bi-hemispheric deficits, and left frontoparietotemporal intracerebral hematoma and exit wounds (right thumb, thigh, and toes). He underwent initial outer-strip and, later, inner-strip corticectomy, covered with split-thickness skin graft (STSG) and bilateral posterior-auricular artery-based flap, respectively, as well as tangential burn wound excisions with STSG and louvre flap cover for the digits. He also underwent right upper eyelid contracture release and tarsorrhaphy. He developed late post-traumatic seizures, which were managed with anti-epileptic drugs. Definitive calvarial reconstruction is underway. Cranial-entry electrical injury had high morbidity and mortality risks. The spectrum of nervous damage causation mimics nervous syndromes and their presentations. Although elaborate surgical and medical care offers the possibility of survival, the neurological and neuropsychological syndromes in the post-acute and rehabilitative phases of care should be taken care of. 

Keywords: Electrical burns, cranial entry, neurological sequelae, scalp reconstruction, electrical burn injury rehabilitation 


Ann Afr Surg. 2021 ; 18(4): 246-251 
DOI: http://dx.doi.org/10.4314/aas.v18i4.11 
Conflicts of Interest: None
Funding: None
© 2021 Author. This work is licensed under the Creative Commons Attribution 4.0 International License 

Introduction

High-voltage electrical burn injury is rare and potentially life-threatening, due to widespread coagulative necrosis of deep tissues from generated heat (1, 2). Ohm’s law had described the relationship among current, voltage, and tissue resistance when electricity passes through a tissue; while Joule’s heat equation calculated the heat energy produced from electricity, the Joules’ effect posited that the heat generated in a tissue by current is directly and inversely proportional to the electrical potential and tissue resistance, respectively (2–6). Tissues with excellent conductive properties (e.g., nerves, arteries) can deliver electricity to other tissues; meanwhile, in some of the deeper, poor-conductive tissues, electricity causes more injury, resulting in rhabdomyolysis, myoglobinemia, myoglobinuria, and potential interstitial nephritis causing acute kidney injury (2, 4, 6). The extent of damage from electrical injury is grossly underestimated when using standardized burns surface area estimation methods; hence, the fluid resuscitation is titrated with the desired urine output (>1.5 mL/kg/h) (7). 

Tracking of unduly large electric currents through excitable tissues (especially nerves, cardiac tissues) may offset the premorbid electrical rhythmicity of these tissues. The result is a cascade of short- and long-term conditions such as cardiac arrhythmias, altered sensorium, cognitive deficits, seizure disorder, focal brain lesions (e.g., such as infarcts, hematoma), diffuse brain lesions (e.g., cerebral edema), spinal cord or nerve lesions (presenting with varying paresis or plegia, in addition to motor or sensory unit losses), retinal detachment, etc. (3, 4, 8). 

Cranial-entry electrical burns, which are very rare, causes significant damage to the scalp, calvarium, meninges, and brain (1, 9). Scalp defect could pose a challenge for scalp reconstruction (9). Early presentation for care is a rare occurrence in Ibadan, Nigeria. This case report presents a stepwise follow-up of a high-voltage electrical burn survivor, which provided the patient a greater chance at survival from the acute and chronic sequelae. 


Case presentation

A 16-year-old right-hand dominant male, presented 2 hours post-electrical burns that were sustained while attempting to turn off power following a neighborhood power surge. He was thrown onto a nearby energized iron rod, impacting with his head, right hand, and toes. He was rescued after approximately 2 minutes with a dry wooden staff, suffering multiple burn injuries to the head, fingers, thighs, and toes as well as transient loss of consciousness, which was partially regained within 30 minutes. There were no seizures, craniofacial effluxes, bisphincteric dysfunction, or vomiting. He was able to actively move all his limbs. He had no dyspnea or limb deformity. On presentation, there was marked craniofacial edema, and his Glasgow Coma Scale score was at least 9 (best eye response, not testable; best verbal response, 2; best motor response, 6); he had marked bilateral periorbital edema, was making incomprehensible sounds, and can obey two-phased motor commands. The mid-frontoparietal scalp was charred, with exposed, denuded parietal calvarium (Figure 1). He had full-thickness burns on the exit wounds to the right thumb, index, and ring fingers, right thigh, and toes. The diagnoses were mainly full-thickness electrical burn injury on 9% of the total body surface area, gangrenous mid-frontoparietal scalp and calvarium, and moderate head injury with bihemispheric deficits and left frontoparietotemporal intracerebral hematoma. His complete blood count showed leukocytosis (22,000 cells/mm3) with relative neutrophilia. The serum electrolytes, urea and creatinine, urine analysis, and electrocardiogram were normal. A cranial computed tomographic scan showed cerebral edema, left frontoparietotemporal intracerebral hematoma with a midline shift (2mm) toward the left (Figure 1e-g). 

Click to view Figure 1. Showing areas of denuded scalp and cranial computed tomography scan images.  

He was resuscitated with the standard burn unit protocol. His neurological status on the 5th post-operative day was that of a defective Mini Mental State Examination (defects in short-term memory, calculation, sluggish speech, and neutral affect), but he had i