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.