PGY2 Michael Pimienta presented a case of a 66 year old M with history of chronic tinnitus and R thalamic CVA in 2018 who presents after being found unresponsive in car, slumped over, without pulses and covered in emesis. Per EMS, patient underwent CPR x3, epi x2 and defibrillation due to refractory ventricular tachycardia. The patient regained pulses in the field and was intubated en-route to the ED. Upon presentation to the ED, the patient was noted to have upper extremity generalized tonic-clonic movements, lip smacking and eye rolling back phenomenon concerning for seizure like activity.
Home medications: amlodipine 10mg qday, ASA 81mg qday, Atorvastatin 80mg qday
SH: From El Salvador and immigrated to US in the 1980s. Hospitalized around age of 8-10 y/o for a fever x14 days. No tobacco/alcohol/drug use.
Vitals: T 36.5, HR 116, RR 14, BP 147/81,O2 sat 100% on Ventilator
Physical Exam significant intubated and non-responsive male, pinpoint pupils, tachycardic, pulm and abd exam normal, no extremity edema, corneal reflex absent bilaterally, cough absent, gag absent, decreased tone throughout, no withdrawal to noxious stimuli
CBC: WBC 12.1> Hb 14.4/Hct 44.2 <Plt 209 (MCV 88.6, RDW 14.7%)
Na 140/K 2.8/Cl 103/HCO3 15/BUN 16/Cr 1.05<Glucose 252
ALP 139>T.protein 7.0/Albumin 4.3/AST 117/ALT 122/Tbili 1.1/Dbili <0.3
Ca 9.2, Mg 2.7, Phos 6.8
Coags: PT 15.2, INR 1.21, PTT 30.1
Infectious workup including BCx, UA, UCx, COVID-19, flu panel, CXR, hepatitis panel, HIV, RPR are negative.
Toxicology including Utox, ETOH, APAP and ASA all negative.
Troponin 0.19 > 0.08
Lactate elevated at 11.5, procalcitonin elevated at 1.91.
TTE: EF 60%, Grade 1 diastolic function (impaired relaxation). Hypokinesis and aneurysm of the basal-mid inferolateral and basal-mid anterolateral myocardium.
Cardiac MRI: enlarged L ventricle with multiple large areas of L ventricular wall thinning and myocardial delayed gadolinium enhancement. There is 75% thickness delayed gadolinium enhancement of the basal inferolateral and basal inferior walls and full thickness/transmural delayed gadolinium enhancement of the basal anterolateral wall and mid-inferior, mid inferolateral and mid anterolateral walls. There is severe hypokinesis and near total akinesis of these segments, with broad-based aneurysm of these segments. Calculated L ventricular EF 33%.
LV gram: LV EF around 55-60%, there is a true LV aneurysm at postero-basal location.
T. Cruzi Ab IgG reactive x2
Treatment: Patient admitted to CCU and cardiac cath done without evidence of CAD. LV angiogram remarkable for LV aneurysm in postero-basal segment concerning for Chagas disease. Peripheral smear without parasites. T. Cruzi IgG positive and ID consulted, no treatment recommended no treatment given extent of disease. Patient self-extubated on day 3 and underwent AICD placement on hospital day 4. Discharged on hospital day 5.
- Chagas disease is the most common cause of non-ischemic cardiomyopathy in Latin America.
- Sudden death, most commonly associated with ventricular arrhythmia, can interrupt the course of the disease at any time, even before the development of symptoms or heart failure.
- Implantable cardioverter-defibrillator (ICD) therapy is empirically used for primary and secondary prevention of sudden cardiac death.
- Anti-trypanosomal therapy with Benznidazole and Nifurtimox is generally not prescribed to patients with advanced Chagas cardiomyopathy as clinical benefit is likely negligible. Treatment in general is aimed towards the acute phase which presents with non-specific symptoms.
- Even with no history, a high index of suspicion is warrant for patients coming from or living in endemic regions.