lymphadenitis. The patient was initiated on high-dose corticosteroids for KFD and hydroxychloroquine for SLE, with significant improvement in symptoms. Discussion: A well-fixed hematoxylin and eosin- stained section of a lymph node is an ideal diagnostic tool for the identification of KFD, eliminating the need for specific immunohistochemical stains. This section reveals necrosis with intense karyorrhexis and proliferating histiocytes devoid of neutrophils
or hematoxylin bodies. Histologically, SLE closely resembles KFD except for the presence of hematoxylin bodies in the former. This distinction is crucial since the diagnosis of SLE can precede, coincide, or follow that of KFD. Additionally, although SLE is associated with neurological manifestations, our patient's presenting symptoms can be attributed solely to KFD, which has been implicated in the development of aseptic meningitis, encephalitis, ataxia, and paraparesis.
FULMINANT IMMUNE CHECKPOINT INHIBITOR MYOCARDITIS Chukwunonso Ezeani MD1, Gift Echefu MD2, Ifeoluwa Stowe, MD1; Bryan Hathorn, MD3; Department of Medicine, Baton Rouge General Medical Center, Baton Rouge, LA1; Department of Cardiovascular Diseases, University of Tennessee Health Science Center, Memphis, TN2; Louisiana Cardiology Associates, Baton Rouge, LA3.
Introduction: Immune checkpoint inhibitors (ICI) Myocarditis is a rare but potentially deadly adverse event, with a prevalence of about 0.04% and mortality rate 25-50%. There is evolving data on diagnosis, choice and optimal duration of treatment. We present a case of pembrolizumab induced myocarditis in an otherwise healthy lady being treated for breast cancer. Case: A 41-year-old female presented with a one- day history of substernal chest pain. She reported associated nausea and vomiting. In the months prior to presentation, she was diagnosed with right invasive ductal carcinoma and received Carboplatinum and Paclitaxel. Afterwards, she continued Pembrolizumab. Echocardiogram prior to immunotherapy showed normal heart function. Examination revealed hypotension, bradycardia, and thready irregular pulse. Labs revealed elevated troponin (29.65 ng/mL), Brain natriuretic peptide (145 PG/mL). Electrocardiogram showed sinus waves with bigeminy and T-wave inversions in the lateral leads. Heart catheterization done due to concern for NSTEMI showed patent coronary arteries. Hypotension worsened and she was initiated on amiodarone and norepinephrine. Repeat EKG showed marked sinus bradycardia with prolonged QT interval. Hypomagnesemia (1.4 mmol/L) was noted at this time and was
repleted with 4 grams of magnesium sulphate. She subsequently went into ventricular tachycardia and was cardioverted with 200 J in a synchronized fashion. Thereafter, she converted from a rate of 150 to 100 beats per minute but had persistent wide complex tachycardia. She had a seizure which was aborted with intravenous lorazepam. The patient was intubated but unfortunately became more bradycardic and arrested despite atropine. We commenced several rounds of ACLS with epinephrine, calcium, steroids and bicarbonate. ROSC was achieved. She became bradycardic again and arrested for the second time and ACLS was reinitiated. After multiple unsuccessful attempts, the patient expired. Autopsy pathology revealed diffuse lymphocytic myocarditis with myocyte hypertrophy. Discussion: The rare and non-specific clinical presentation of ICI myocarditis poses diagnostic and therapeutic challenges for clinicians/ residents. It is challenging to distinguish other cardiovascular diseases from cardiotoxicity, but new onset acute coronary like syndrome or new onset heart failure should raise strong suspicion in patients on immunotherapy. Cardiac MRI is very helpful in diagnosis and early initiation of pulse dose steroids is recommended.
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