Case report

A 12-year-old male was struck by lightning during a football match. Instantaneous collapse was witnessed, cardiac arrest was confirmed, and cardiopulmonary resuscitation with an automated defibrillator was initiated within 5 minutes. He received one DC shock for a “shockable rhythm” of unclear aetiology then remained in pulseless electrical activity. A prehospital emergency medical team arrived and resuscitation continued according to European Resuscitation Council guidelines. ^{Reference Van de Voorde, Turner and Djakow1} He had return of spontaneous circulation 38 minutes after the initial strike. He was intubated, ventilated, and transferred by air ambulance to our hospital.

Examination revealed reactive pupils, superficial partial thickness burns over chest and abdomen (Fig 1), burns to extremities with a likely exit wound on the right heel, and total area of burns <10%.

Figure 1.

Burns to anterior torso and neck.

On electrocardiography, he had frequent premature ventricular contractions with short runs of non-sustained ventricular tachycardia lasting up to 10 beats. 12-lead electrocardiogram showed inferolateral Q waves and ST segment elevation (Fig 2). Magnesium, calcium, and potassium levels were actively optimised, and no antiarrhythmic infusion was required. Initial CT brain showed normal appearances with preserved grey-white differentiation. CT chest, abdomen and pelvis showed no evidence of traumatic injury.

Figure 2.

Electrocardiogram 8 hours post arrest.

On the paediatric intensive care unit, he remained mechanically ventilated for five days, with a neuroprotective strategy for the initial 48 hours to maximise neurological recovery, including targeted temperature management to maintain normothermia.

Initial echocardiography demonstrated severely impaired systolic function with paradoxical septal motion. Cardiac index was evaluated to be 2.44 L/min/m. ^{Reference Deep, Goonasekera and Wang2} Proximal coronary artery anatomy appeared normal, with no evidence of thrombus.

Clinically, he had profound peripheral vasoconstriction with cold extremities, poor peripheral pulses, and hypertension with a blood pressure of 150/110. After discussion with the regional Paediatric Cardiology Unit, milrinone was started at 0.5 mcg/kg/minute for lusitropic and inotropic effects and to reduce afterload by systemic vasodilation. ^{Reference Deep, Goonasekera and Wang2} Nitroglycerin was considered but not used as the hypertension improved with milrinone and the index of suspicion for an anatomical coronary lesion was low. Following the introduction of milrinone, the clinical picture improved. Captopril was introduced and milrinone was discontinued after 72 hours.

Cardiac troponin I was above the limit of the assay at >25000 ng/L (reference range 0–54 ng/L) for 5 days before falling to a measurable level. Electrocardiography remained abnormal, with ST segment changes and inferolateral Q waves for several days after admission. CT angiogram one day post injury demonstrated patent coronary arteries.

He had mild acute kidney injury with elevated urea and creatinine. Maximum creatine kinase was 10,805 U/L one day post injury, indicating a degree of rhabdomyolysis. Renal support was not required.

Post extubation, neurological examination revealed normal motor and sensory function, but significant cognitive impairment with agitation, confusion and memory loss. He was transferred to the paediatric ward for ongoing neurorehabilitation 8 days after admission.

He was discharged home six weeks post cardiac arrest on oral captopril with continued outpatient rehabilitation and review with the Paediatric Cardiology and Neurology teams.

At that point, cognitive function and neurological status were on an improving trajectory. He had ongoing fatigue, memory loss, and limb pain but was able to talk and was mobilising independently.

24-hour electrocardiogram showed sinus rhythm with infrequent ventricular ectopics. Echocardiography showed some resolution of the previously noted abnormalities, with fractional shortening of 35% and normalising regional wall dyskinesia.

Cardiac MRI at 9 weeks post injury showed akinesia and thinning of the infero-lateral left ventricular wall from mid-base to apex, likely consistent with infarction, and moderately impaired global systolic function with a left Ventricular Ejection Fraction (LVEF) of 40%. There was also a large right antero-lateral pericardial collection with a small pericardial tear.

At 5 months post event, echocardiography showed significant improvement with only mild hypokinesia of the posterior mid-ventricular segment but an overall ejection fraction of 51% and global strain of −19%. A 2-week rhythm monitor showed a ventricular ectopic burden of 2.9% with ventricular ectopic couplets at <1% and episodes of bigeminy. Repeat cardiac MRI at 7 months post injury demonstrated resolving pericardial collection in the anterior mediastinum, improved systolic function (LVEF 54%), with mild regional wall motion abnormality, thinning, and transmural scar. Despite these changes, clinically, he continues to improve and is returning to mainstream education and sport.