A 59-year-old Sinhalese female with poorly controlled type 2 diabetes mellitus, hypertension, and dyslipidemia resulting from non-adherence of medication use, presented to a peripheral base hospital in Sri Lanka (primary level of care) with sudden onset right-sided upper and lower limb weakness associated with slurring of speech, mouth deviation, vertigo, and emesis of yellowish content with undigested food particles. On direct inquiry, she complained of an intermittent, vague anterior chest pain over the preceding 12 hours that worsened to agonizing angina pectoris associated with autonomic symptoms, presyncope, and sweating within a few minutes of the acute neurological event. She had no fever, cough, pleurisy, palpitations, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, headache, syncope, or suggestive features for deep vein thrombosis.
Her poor insight about the underlying comorbidities and prevailing social restrictions associated with the COVID-19 pandemic had made her non-adherent to treatments during the previous three months. Nevertheless, she did not have any history of ischemic cardiac or cerebral vascular events. Her family history was negative for any acute premature cardiac or cerebrovascular events. She was a non-smoker, non-alcoholic, consumed a high fat and salt content diet, and led a sedentary lifestyle pattern.
On arrival at the primary level of care, approximately 2 hours from the neurological event, she was ill, and in pain with a temperature of 36 ˚C, of GCS of 13/15, pulse rate of 90/minute with a regular rhythm, blood pressure of 240/130 mmHg, a left-sided pyramidal weakness of grade 3/5 and aphasia. ECG changes were suggestive of an acute inferior ST-elevation myocardial infarction (STEMI). Intravenous morphine 3 mg and metoclopramide 10 mg, supplemental oxygen via face mask was given, and a nasogastric tube was placed. An infusion of glyceryl trinitrate (GTN) at 10ug/kg was commenced. Subsequently, she was transferred via ambulance to the tertiary care center located 1 ½ hour away for an NCCT brain and further care.
She arrived at the emergency treatment unit of the tertiary care center approximately 6 ½ hours from the neurological event. The physical examination at the tertiary care center presentation revealed a pulse rate of 79 beats per minute (regular), blood pressure of 182/102 mmHg, respiratory rate of 20 cycles per minute, and SpaO2 of 97%. The eye-opening was spontaneous; she obeyed commands; however, she was confused, giving rise to a GCS of 14/15. Bilateral pupils were equal in size (3 mm) and reactive to light. Neurological examination of the limbs revealed spastic hemiparesis with power MRC grade of 3, hyperreflexia, positive Babinski sign of right upper and lower limbs, and a right-side upper motor type facial nerve palsy. Neurological examination of the left upper and lower limbs was unremarkable. The sensorium and the coordination of the limbs were difficult to assess, given the patient’s debilitating condition. The initial NIHSS was at 12. The rest of the cardiovascular, respiratory, and abdominal system-related examinations were unremarkable.
A repeated ECG revealed inferior and new additional posterior and right ventricular STEMI (Figure 1). Non-contrast CT (NCCT) of the brain showed a focal hypodense lesion in the right centrum semiovale with multiple lacunar infarctions in the right temporoparietal region (Figure 2), suggesting an AIS.
Opinions of the cardiology team and the neurology team were taken. Thrombolysis and mechanical thrombectomy for AIS was not indicated as the patient presented beyond the recommended time window. Also, an adequate facility for mechanical thrombectomy was unavailable in the institution. Coronary revascularization by the primary percutaneous coronary intervention (PCI) was deemed impossible because peri-procedural heparinization was presumed to carry an increased risk of a secondary cerebral hemorrhage. Therapy with fibrinolytic agents given at doses recommended for thrombolysis in AMI was contraindicated in a setting of a recent stroke.
Subsequently, the patient was transferred to the high dependency unit of a general medical unit for medical management of the acute STEMI and acute ischemic stroke (CCI). The initial clinical decision was to manage with a single antiplatelet (aspirin 75 mg nocte) and a statin (atorvastatin 40 mg nocte) sublingual glyceryl trinitrate 0.5 mg as needed and ISMN 30mg mane, considering the possible risk of intracranial bleeding. For pain management, intravenous morphine 2.5 mg and metoclopramide 10 mg were given as needed. Additional general and supportive care included oxygen supplementation during the initial hours, timely nasogastric enteral feeding, urinary catheterization, and avoidance of constipation with stool softeners. Troponin I level on admission was 57.1 ng/mL, which gradually came down to 26.1 ng/mL by day three. The 2D echocardiogram revealed global wall hypokinesia with an ejection fraction of 35%. The patient was neurologically non-progressing during the first two days of admission, and the repeat brain NCCT scan performed 48 hours after the AIS revealed an extension of the cerebral infarction to the right frontal region (Figure 3).
After discussing with the cardiology team, we started clopidogrel 75 mg nocte and a total of 10 doses of subcutaneous enoxaparin 60 mg 12 hourly along with bisoprolol 1.25 mg mane and enalapril 1.25 mg nocte. With that, the patient had a remarkable clinical improvement. Troponin I level came down to 6.96 ng/mL by day seven of admission. However, after ten days of admission, the repeat ECG showed q waves in previously affected territories, and T inversions in anterior and lateral chest leads (Figure 4).
On day one, the patient’s clinical picture was complicated with fluid responsive hypotension, possibly due to right ventricular infarction and ischaemic hepatitis. On admission, the liver enzymes were high; alanine aminotransferase (ALT) of 1067.5 U/L, aspartate aminotransferase (AST) of 1088.9 U/L. Intravenous N-acetylcysteine (NAC) regimen was prescribed at 150 mg/kg with 5% dextrose over 15 mins, followed by 50 mg/kg over 4 hours and 100 mg/kg after that. The levels came down to ALT 226.4 U/L and AST 142.1 U/L by two days, and the NAC infusion was withheld. However, after another two days, the liver enzyme levels were again elevated to ALT 569.9 U/L and AST 180 U/L, and another NAC infusion was started 100 mg/kg 24 hours, and the ALT level came down to 196.4 U/L with an AST level of 66.6 U/L. On admission, the alkaline phosphatase level was 121.5 U/L (44 – 147) with a total bilirubin level of 33.94 µmol/L (1.71 – 20.5), direct bilirubin 24.22 µmol/L and indirect bilirubin 9.7 µmol/L.
On admission, the capillary blood sugar level was 406 mg/dL, with positive urine ketone bodies and was treated with intravenous infusion of soluble insulin 5 units per hour, which was gradually tailed down over a day and converted to soluble subcutaneous pre-meal insulin 10 units three times a day, following which she had a satisfactory glycemic control.
There was initial hematological and biochemical evidence of infection; white cell count was 23.26 × 109/L with neutrophil predominance, blood picture showing evidence of bacterial infections, and elevated inflammatory markers; c-reactive protein 119.6 mg/dL and erythrocyte sedimentation rate of 49 mm per hour. However, the urine culture and blood culture showed no growth, and the urine full report only showed 6 to 8 pus cells per high power field. However, there was no clinical evidence of any other infective focus. Nevertheless, a broad-spectrum antibiotic cover with intravenous meropenem 1 g 8 hourly for 7 days was given until the inflammatory markers came down to baseline.
By day seven, the patient had a remarkable clinical improvement. By day five, she could sit on the bed and walk with support by day seven. The nasogastric tube was removed on day five, and oral feeds were commenced as she showed good oral tolerance. The cognitive impairment was minimal, and she was discharged after eleven days of admission with a plan of reviewing at the outpatient clinic. A routine coronary angiogram was arranged to be done in a few months. Outpatient neurorehabilitation was also arranged. Modified Rankin score at discharge was 3.