CASE PRESENTATION
A 38-year old, previously healthy female experienced dizziness followed by loss of consciousness for a few seconds. Two days before the loss of consciousness, she experienced a gradual onset of intermittent left-sided chest pain, shortness of breath, palpitations, upper abdominal pain, and vomiting. During the initial evaluation, she became unresponsive and pulseless. Cardiopulmonary resuscitation (CPR) was initiated, and the patient was found to be in ventricular fibrillation. There was a return of spontaneous circulation after a single DC-shock and 6 minutes of CPR.
Following cardiopulmonary resuscitation, her electrocardiography showed ST-elevation in the anterolateral leads (Figure 1). Primary percutaneous coronary intervention protocol was activated; however, she developed ventricular fibrillation before she could be transferred for primary percutaneous coronary intervention. She had six cardiac arrests with ventricular fibrillation, each one lasting successively longer than the prior episode with return of spontaneous circulation between the episodes. A decision was made in conjunction with the cardiology and critical care team for thrombolytic therapy during CPR using r-tPA (recombinant-tissue plasminogen activator). She received a total of 14 DC shocks, 900 mg of amiodarone, and adrenaline and nor-adrenaline infusions. After 180 minutes of the initial arrest, veno-arterial extracorporeal cardiopulmonary resuscitation (VA e-CPR) was initiated, and clinical hypothermia was induced, leading to hemodynamic stability. The patient received aspirin, clopidogrel, atorvastatin, and heparin infusion. Repeated electrocardiography showed a complete resolution of ST-segment elevations.
Initial blood tests at time of admission were unrevealing except for a raised troponin of 189 ng/l (Table 1). On day 2 of her hospital stay, she developed non-fluid responsive hypotension requiring two concurrent vasopressors and was found to have a hemoglobin of 5.5gm/dL. Tri-phasic CT-chest, abdomen, and pelvis were suggestive of hemoperitoneum and colon ischemia. Urgent exploratory laparotomy showed multiple small omental bleeds with lacerations. Hemostasis was achieved, and two drains were applied. The patient had four re-look surgeries and was found to have dark discoloration of hepatic flexure of the colon without bowel perforation. She also developed acute kidney injury secondary to acute tubular necrosis requiring five sustained low-efficiency dialysis sessions. The patient had extracorporeal membrane oxygenation (ECMO) de-cannulation on day 6.
She developed massive gastrointestinal bleeding with a hemoglobin drop from 10.2 gm/dL to 4.1 gm/dL. A massive blood transfusion protocol was activated. Colonoscopy showed multiple large circumferential ulcers that were injected with epinephrine (Figure 2A, 2B, and 2C). Clipping attempt at the underlying vessel failed, and a right hemicolectomy with end ileostomy was performed. The biopsy of the colonic ulcers showed CMV colitis (Figure 3A,3B,3C). Intravenous ganciclovir 5mg/Kg twice daily was initiated with a positive CMV polymerase chain reaction (PCR). Two weeks later, repeated CMV-PCR was negative. The patient was switched to oral valganciclovir 900mg twice daily for 8weeks. Table 1 shows laboratory investigations during receiving antiviral therapy.
Coronary angiography revealed left anterior descending (LAD) segmental single-vessel disease with plaque. There was a successful insertion of a single drug-eluting stent in the LAD.
The patient was discharged and received twice-weekly physiotherapy sessions for 8 weeks post-discharge. A reversal of ileostomy was done at five months from its creation. Clopidogrel was discontinued at one-year post-angiography, and repeat echocardiography showed an ejection fraction of 56%. The patient retained an excellent functional status with no neurological deficit, anginal symptoms, palpitations, or dizziness. She continues to follow up with cardiology and general surgery on a 6-monthly basis.