RETURN TO LIFE: A CASE OF THE LAZARUS PHENOMENON

SESSION TITLE: Shock and Sepsis in the ICU Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: The Lazarus Phenomenon, also known as auto-resuscitation, is a rare event where cessation of CPR results in a delayed return of spontaneous circulation (ROSC). The phenomenon was named after the story of Lazarus, who was restored to life four days after death. We present a case of a 78-year-old male who presented to the hospital for septic shock and had intra-hospital cardiac arrest with ROSC after cessation of CPR. CASE PRESENTATION: 78 year old male with a medical history of paroxysmal atrial fibrillation, stage IIIA NSCLC and COPD, presented for progressive dyspnea. He complains of feeling weak with loss of appetite and had a recent mechanical fall. Initial vital signs were temperature 96F, BP 141/78, HR 75 bpm, RR 18/min, SaO2 100% on 2LNC. Initial labs showed lactic acid 11.6, BUN 55, creatinine 3.7, CO2 9, anion gap 25, AST 2654, ALT 2120, ALP 159, total bilirubin 0.8, troponin <0.1, CK 399, INR 4.2, PTT 36, WBC 16.5, Hb 10.8, and plt 202. COVID-19 testing was negative. CXR demonstrated a retro-cardiac opacity consistent with previous diagnosis of lung cancer versus a dense consolidation. He was started on antibiotics for sepsis and admitted to the ICU for his metabolic status and shock liver. He remained hemodynamically stable for a few hours until a he had sudden onset of unresponsiveness with asystole. Code blue was called. Repeat labs demonstrated lactic acid 15.5, potassium 6.3, CO2 9. He underwent resuscitation for 32 minutes when compressions were stopped. Within 5 minutes post arrest, sinus activity was noted on the cardiac monitor. The patient had a radial pulse on evaluation. Manual blood pressure measurement was 119/71 with a HR of 99. Arterial blood gas after ROSC showed a pH 7.0, pCO2 68, pO2 273, HCO3 16, lactic acid 19. A few hours later, the patient rapidly de-compensated and underwent resuscitation for a second time. Efforts were deemed futile and the patient expired. DISCUSSION: The physiologic description of the Lazarus phenomenon is yet to be fully elucidated. Hypotheses include auto-PEEP due to rapid manual ventilation generating increased intrathoracic pressure and decreased venous return, delayed drug effect and stunned myocardium during active chest compressions (1). Once chest compressions and positive pressure ventilation via manual bag-mask stops, sudden decrease in intrathoracic pressure allows for sudden venous return and re-perfusion of cardiac tissue, resulting in ROSC in some cases. A recent literature review cited 65 published cases over the past 30 years with the most common rhythm being asystole (2). Most cases of auto-resuscitation occurred between 5-10 minutes post stopping of chest compressions (2). Mortality of these cases were 70% post resuscitation (2). CONCLUSIONS: It is important for clinicians to be aware of the Lazarus phenomenon post resuscitative efforts and to observe patients carefully post resuscitation. Reference #1: Adhiyaman V, Adhiyaman S, Sundaram R. The Lazarus phenomenon. J R Soc Med. 2007;100(12):552-557. doi:10.1177/0141076807100012013 Reference #2: Gordon, L., Pasquier, M., Brugger, H. et al. Autoresuscitation (Lazarus phenomenon) after termination of cardiopulmonary resuscitation - a scoping review. Scand J Trauma Resusc Emerg Med 28, 14 (2020). https://doi.org/10.1186/s13049-019-0685-4 DISCLOSURES: No relevant relationships by Vincent Chan No relevant relationships by Mackenzie Kramer No relevant relationships by Nathaniel Rosal No relevant relationships by Laura Walters No relevant relationships by William Ward

Persistent pain: Recurrent severe subacute thyroiditis from covid 19 infection

Subacute thyroiditis is an acute inflammatory response in the thyroid which usually follows a viral infection. This report highlights a case of subacute thyroiditis in a patient with a history of benign COVID 19 infection without indication for supplemental oxygen or hospitalization. This case is unique in the fact that the patient required multiple doses of steroids for symptom control. A 36-year-old female with a past medical history of hyperlipidemia, essential hypertension, obesity, type two diabetes, and recent COVID-19 infection six months prior presented to the hospital for evaluation of persistent anterior neck pain, fevers up to 100.9- F, ten pound weight loss, and palpitations. Two months before presentation she developed anterior neck pain that radiated into the left side of her neck and jaw. This was evaluated by an outpatient otolaryngologist who performed a nasopharyngeal laryngoscopy with unremarkable findings. She was placed on a muscle relaxant, ibuprofen, and a course of steroids. She saw another physician who trialed an additional course of steroids shortly after. Unfortunately she continued to experience excruciating discomfort prompting this hospitalization. Admission labs revealed that the patient's TSH was less than 0.01 uIU/mL. Her free T4 was 1.9 ng/dL and her free T3 was 3.6 pg/mL. A CT scan of the neck showed a 1.9 x 1.0 cm hypodense lesion. Further imaging with a thyroid ultrasound showed a heterogenous thyroid with generalized hypo echogenicity, decreased blood flow, without discrete nodules, cysts, or calcifications concerning for acute thyroiditis. The patient was started on intravenous methylprednisolone with improvement in symptoms. She was subsequently transitioned to oral prednisone on discharge. Subacute thyroiditis most commonly follows a viral infection. With our patient, symptoms developed shortly after her COVID19 infection. Once a diagnosis of subacute thyroiditis is made, patients are treated with a short course of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) and occasionally oral steroids which resolves most symptoms. This case was unique in that our patient required three regimens of steroids before her symptoms improved. Given these findings, a prolonged course of steroids may be indicated for covid-19 induced subacute thyroiditis.

BRASH SYNDROME: A DOWNWARD SPIRAL

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: BRASH Syndrome is a phenomenon characterized by bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia. Literature on this syndrome is limited given its under-recognition. CASE PRESENTATION: A 77-year-old female with a past medical history of atrial fibrillation, coronary artery disease, diastolic heart failure, and chronic kidney disease (CKD) III presented with dyspnea. Her home medications included furosemide, metoprolol, spironolactone, warfarin, and rosuvastatin. Comprehensive metabolic panel was significant for an elevated creatinine from baseline. Cardiac BNP was elevated, chest X-ray demonstrated cardiomegaly, and physical exam was significant for jugular venous distention. Electrocardiogram (EKG) revealed atrial fibrillation with rapid ventricular response (Image 1). Diltiazem was added for rate control however the patient was ultimately electrically cardioverted. Post procedure EKG revealed a junctional rhythm (Image 2). Hypotension persisted however. The patient soon developed oliguric renal failure and hyperkalemia, prompting upgrade to the medical intensive care unit (ICU) for shock. The patient had persistent bradycardia with heart rates as low as 32 beats per minute (bpm). Hemodialysis was initiated the following morning and the patient's shock, bradycardia, and hyperkalemia resolved. DISCUSSION: Transient abnormal rhythms have been reported post cardioversion, however the persistence of bradycardia with our patient's other abnormal lab findings raised concerns for different etiologies. BRASH syndrome is an under recognized pathophysiological phenomenon. Patients with congestive heart failure and CKD are at risk when in an inpatient setting. Different triggers are noted in recent reports, including medications such as Ranolazine and Bactrim, anaphylaxis, and even COVID-19. These cases varied in clinical severity, ranging from asymptomatic bradycardia to multiorgan failure. The hallmark mechanism of BRASH syndrome is a synergistic effect of AV nodal blocking medications and hyperkalemia promoting bradycardia. This, in conjunction with renal injury, produces the cycle of objective findings that define BRASH syndrome. Acute kidney injury caused by renal hypoperfusion can exacerbate the effects of AV nodal blocking medications as well as worsen hyperkalemia. Profound hyperkalemia and AV nodal blockade will in turn synergistically promote and prolong bradycardia. Bradycardia can depress cardiac output and further worsen renal hypoperfusion, continuing this viscous cycle. CONCLUSIONS: We believe electrical cardioversion into a junctional rhythm caused BRASH syndrome in our patient. Treatment is tailored to correcting the individual abnormalities. Many of these case reports had favorable outcomes. This case suggests that BRASH syndrome can often go undiagnosed yet still successfully be managed with supportive care. REFERENCE #1: Farkas, J., Long, B., Koyfman, A., et al. BRASH SYNDROME: BRADYCARDIA, RENAL FAILURE, AV BLOCKADE, SHOCK, AND HYPERKALEMIA. The Journal of Emergency Medicine, 59(2):216-223, pp. 1–8, 2020. DOI: 10.1016/j.jemermed.2020.05.001 REFERENCE #2: Cakulev, I., Efimov, I., Waldo, A., et al. Cardioversion: Past, Present, and Future. Circulation. Oct 20;120(16):1623-32. 2009. DOI:10.1161/circulationaha.109.865535 REFERENCE #3: Flores, S., Anaphylaxis induced bradycardia, renal failure, AV-nodal blockade, shock, and hyperkalemia: A-BRASH in the emergency department, American Journal of Emergency Medicine 38(9), P1987.E1-1987.E3. 2020. DOI: 10.1016/j.ajem.2020.05.033 DISCLOSURES: No relevant relationships by John Madara, source=Web Response No relevant relationships by Nathaniel Rosal, source=Web Response No relevant relationships by Franklin Thelmo, source=Web Response No relevant relationships by Stephanie Tzarnas, source=Web Response

Wooden chest syndrome: Fentanyl induced chest wall rigidity

Fentanyl induced chest wall rigidity, otherwise known as Wooden Chest Syndrome, is a rare complication of fentanyl characterized by a patient's inability to properly ventilate. We present a patient with acute respiratory distress syndrome (ARDS) who developed this syndrome in a medical intensive care unit (ICU) setting. A 61- year-old female with a history of prior episodes of pancreatitis presented with a chief complaint of left-sided, sharp, abdominal pain associated with nausea. Physical exam demonstrated epigastric tenderness without rebound or guarding. Chest exam demonstrated strong inspiratory effort and was negative for rales, rhonchi, or accessory muscle use. Vital signs demonstrated no abnormalities and she had oxygen saturation levels greater than 92% on room air. Laboratory findings revealed an elevated lipase of 1086 u/L. A diagnosis of pancreatitis was made. The patient was given intravenous fluids and made NPO. The patient developed respiratory distress and chest x-ray findings revealed bilateral infiltrates consistent with ARDS, requiring endotracheal intubation. She was sedated with intravenous fentanyl and midazolam to a Richmond Agitation-Sedation Scale (RASS) goal of -4. The fentanyl infusion was incrementally increased and maximized to 300mcg/hr. Following maximizing the fentanyl infusion, the patient began experiencing periods of hypoxia. Physical exam at this time was significant for a tense abdomen, facial cyanosis, and episodes of what appeared to be breath holding spells. Ventilator readings revealed drastically elevated airway pressures. The patient required bag valve mask ventilation which was met by strong resistance. Passage of the suction catheter revealed no obstruction or mucus. An emergent bedside bronchoscopy confirmed these findings. A repeat chest X-ray revealed no pneumothorax. This presentation raised concern for Wooden Chest Syndrome. The fentanyl infusion was titrated down and she was transitioned to dexmedetomidine. The patient exhibited no further episodes was successfully extubated three days later. Chest wall skeletal muscle rigidity is a result of fentanyl bound mu opioid receptors on the central nervous system and activation of a dopaminergic pathway. The subsequent decreased chest wall compliance results in ineffective assisted and spontaneous ventilation, translating to elevated pressures within the ventilator circuit. Management of this syndrome is with the opioid receptor antagonist Naloxone, neuromuscular blocking agents such as rocuronium, or cessation of fentanyl infusion with supportive care. Given the COVID-19 pandemic and surge in ICU admissions, analgesic fentanyl use is rising. Therefore, an understanding of this rare complication is necessary.

Ventricular ectopy with remdesivir use in COVID-19

INTRODUCTION: Remdesivir is an antiviral medication that has demonstrated improvement in time to symptom resolution in Covid-19. The side effect profile documented in literature is still developing. To date, there have been no wide scale demonstrated cardiac toxicities noted. We present a case of COVID-19 who developed ventricular ectopy suspected to be due to Remdesivir. METHODS: A 70-year-old male with a past medical history of coronary artery disease, hypertension, and recurrent aspiration events presented from a nursing home in respiratory distress. The patient initially presented with findings consistent with aspiration pneumonia, however was also found to be positive for Covid-19. Vital signs were positive for fever, tachycardia, tachypnea, and an oxygen saturation of 90% on Non-Rebreather, requiring intubation. Metabolic panel on admission showed a slightly elevated ALT, but no electrolyte abnormalities or altered renal function. A leukocytosis and mild anemia were noted on complete blood count. Admission electrocardiogram was negative for ectopy. Remdesivir therapy for COVID-19 was planned. During infusion of the first dose, the patient had multiple premature ventricular complexes (PVCs) that developed into a short run of non-sustained ventricular tachycardia. During the second dose, PVCs again were noted, and Remdesivir was stopped. After infusion was held, ectopy resolved. Echocardiogram showed an ejection fraction of 60 - 65%, mild tricuspid and mitral regurgitation, and no evidence of wall motion abnormalities. After 48 hours, ectopy was no longer observed. RESULTS: A preliminary report of the Adaptive COVID-19 Treatment Trial evaluated Remdesivir's efficacy and safety. Of the patients receiving it, 29% had grade 3 or 4 adverse reactions, though none were cardiac in nature. In our patient, the onset of ectopy was noted immediately upon infusion and resolved upon abortion of infusion. Postulated mechanisms were drug interactions (carvedilol, atorvastatin, and sertraline were considered), CAD, or underlying disease of the conduction system. Further studies investigating the association of underlying conditions and medications with Remdesivir may shed light on this occurrence.