INTRODUCTION: Pembrolizumab, an anti-programmed death 1 receptor monoclonal antibody, increases survival in non-small cell lung cancer (NSCLC). It causes less toxicity than traditional chemotherapy, however it can induce autoimmune adverse events including pneumonitis and colitis. There have been a limited number of case reports chronicling myositis with respiratory distress as an adverse effect of pembrolizumab. We present a case of a patient with NSCLC being treated with pembrolizumab, which induced respiratory failure secondary to myositis. CASE PRESENTATION:A 77-year-old man with metastatic NSCLC status post right upper lobectomy on carboplatin/ paclitaxel/pembrolizumab started 10/26/20, with recent hepatitis diagnosed one week prior to admission and identified as secondary to pembrolizumab, on treatment with prednisone (1 mg/kg), presented with proximal weakness and progressive exertional dyspnea over the last three weeks. Vital signs were remarkable for tachypnea and tachycardia. Physical exam showed 2/ 5 proximal muscle strength in upper and lower extremities, absent deep tendon reflexes, and no skin rash. Labs revealed CK 1567, LDH 889, SARS-CoV2 PCR negative. CT pulmonary arteries was negative for acute lung processes. The patient required noninvasive positive pressure ventilation (NIPPV) for respiratory distress. Treatment was initiated with pyridostigmine (60mg QID PO) and pulsed glucocorticoids (methylprednisolone 1 g daily). He remained NIPPV dependent so pyridostigmine was increased to 90mg QID PO and IV immunoglobulin (IVIG) 85 g QD was added for refractory respiratory failure and muscle weakness. Acetylcholine receptor antibodies, ANA, anti SSA/SSB, anti-Jo1 were negative. Lumbar puncture was performed with normal opening pressure, CSF cell count, and chemistry. The clinical diagnosis was myositis attributed to pembrolizumab. The patient responded to a week of continued IVIG (30 g QD for 5 more days) and tapering steroids, with improvement in proximal muscle strength and was weaned off NIPPV.DISCUSSION: Pembrolizumab works as an immune checkpoint inhibitor, which may cause an autoimmune effect. One study identified 5 patients with pembrolizumab induced myositis. Our patient, presented with proximal muscle weakness and respiratory distress requiring NIPPV, two months after starting pembrolizumab. His respiratory distress was not due to lung disease. Autoimmune workup was negative. He underwent a lumbar puncture which ruled out Guillain-Barre syndrome. He was diagnosed with pembrolizumab induced myositis. A limitation in our case was that a biopsy never confirmed the diagnosis as he responded to pulsed steroids and IVIG. In other cases, the myositis has been treated by plasma exchange or immunosuppression.CONCLUSIONS: Pembrolizumab can induce potentially fatal myositis. It is crucial that clinicians are aware of this so prompt treatment can be initiated.

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INTRODUCTION: Mitragyna speciosa (MS) also known as Kratom is a synthetically derived opioid that is easily available for purchase on the internet and not federally regulated. MS is mostly found in Southeast Asia and used for medicinal purposes, such as curing viral illness, herpes zoster, diabetes, hypertension, decreased libido and depression [4]. Traditionally, it is ingested by chewing raw, boiled in water and drank as a beverage or inhaled as a vapor. It has surpassed its use in Southeast Asia and reached consumers all over the world as a recreational drug. We present a case of a young male with kratom toxicity.CASE PRESENTATION: 31-year-old male with history of substance abuse and low testosterone levels, who was taking kratom and alprazolam for many years, presented to the emergency department with altered mental status, hallucinations; progressively became incoherent and combative, requiring intubation for airway protection. His laboratory revealed rhabdomyolysis with creatinine kinase level of 3000 U/L in addition to urine drug screen positive for barbiturates and tetrahydrocannabinol. Continuous video electroencephalogram showed no seizure activity.DISCUSSION: In 2016, The American Kratom Association estimated there was approximately 3-5 million active kratom users in the United States [4]. Kratom is a mu opioid receptor agonist. When ingested orally, there is approximately 3% bioavailability with onset of action within 5 to 10 minutes [2]. If given at a lower dose, Kratom acts like a stimulant, meanwhile higher doses emit analgesic and euphoric effects [1]. In a survey with active kratom users for recreational purposes, 85% used it for decreased pain, 84% for increased energy and 80% for depressed mood [3]. Adverse effects of Kratom include acute respiratory distress syndrome, Kratom induced hepatotoxicity, hypothyroidism, rhabdomyolysis and hypogonadism. Central nervous system effects include seizure, coma and posterior reversible encephalopathy syndrome. Our review of literature of 42 cases from 2008 to 2020, showed only one reported case of rhabdomyolysis secondary to kratom abuse [2]. CONCLUSIONS:As the number of substances abused are growing, critical care providers should be aware of this drug and its pharmacological toxicity profile for optimal management.

INTRODUCTION:Myocarditis is an inflammatory condition of the myocardium. Legionella is a known rare infectious cause of myocarditis. Additionally, it has been implicated with pericarditis and prosthetic valve endocarditis. We present a case of a 39year-old male with legionella pneumonia with myocarditis, acute renal failure, and rhabdomyolysis. CASE PRESENTATION:A 39-year-old male with no known past medical history presented to the emergency department with worsening dyspnea after a viral syndrome for 3 weeks. He was intubated in the emergency department for respiratory failure. Chest x-ray showed multifocal atypical infiltrates. Electrocardiogram significant for diffuse ST depressions. Echocardiogram revealed severe left ventricular systolic dysfunction with ejection fraction of 30% with no valvular abnormalities. Lab analysis revealed hyponatremia, elevated troponins and acute renal failure with rhabdomyolysis requiring hemodialysis. Atypical serology was positive for Legionella which was treated with levofloxacin and azithromycin. SARS-CoV-2 PCR was negative and urine drug screen was negative. He was diagnosed with myocarditis given the legionella culture, elevated troponins, significant for electrocardiogram and echocardiogram findings. DISCUSSION:The first case of Legionella myocarditis was reported in 1981 by Gross [1]. Symptoms of myocarditis can range from a mild flu-like illness to cardiogenic shock or sudden death. Myocarditis is the cause of 12% of sudden deaths in young adults [2]. Diagnosis is typically made clinically with non-diagnostic exams, as endomyocardial biopsy is only used for special circumstances when other testing are non-diagnostic. A literature review of Legionella myocarditis as of 2017 portrayed ten patients with positive Legionella urine antigens, with eight having reduced left ventricular ejection fraction on echocardiogram. Only two of those cases were based on cardiac biopsy [3].CONCLUSIONS: Extrapulmonary manifestations of Legionella such as myocarditis have been reported even in the absence of overt pneumonia, and most often in immunocompromised patients. Clinicians should be aware of Legionella in the setting of unexplained myocarditis with findings as above. Treatment should be initiated for this reversible cause of myocarditis without delay, resulting in favorable prognosis.

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