Refractory Shock Research Articles

Multidisciplinary approach and early use of percutaneous mechanical circulatory support devices in patients with cardiogenic shock

Abstract Background Despite progresses in the reperfusion strategies, the prognosis of patients with cardiogenic shock (CS) remains poor with a high in-hospital mortality rate. Percutaneous mechanical circulatory support systems (pMCS) reducing afterload, preload and myocardial oxygen demand, preventing compensatory tachycardia and increasing mean arterial pressure, lead to improve end-organ perfusion. Since CS progression to a refractory shock state is deleterious, timing of treatment represents a crucial issue in these patients. Purpose The aim of our study was to assess whether a multidisciplinary approach and an early use of pMCS could be safe and effective in improving CS patients' outcome. Methods We examined the outcome in terms of one-month survival of 62 patients (75.8% males, mean age 67.7±12.2 years) admitted between January and December 2018 to our Cardiac Intensive Care Unit (CICU) with cardiogenic shock due to acute coronary syndrome (ACS), acute heart failure (AHF) and other causes in 43.5%, 21.6%, 35.4% of cases respectively. For each patient, a Multidisciplinary Shock Team (CS-Team) including critical care specialists, interventional cardiologists and advanced heart failure specialists, was involved and the early use of pMCS was considered. Results Overall, 52 (83.9%) CS patients underwent pMCS implant, including intra-aortic ballon pump counterpulsation (IABP), Impella system (Impella), venous-arterial extracorporeal membrane oxygenation (VA ECMO) in 67.7%, 46.7%, 11.3% of cases respectively. Median time from the first CS-Team contact to the pMCS implantation was 32.5 (30–60) minutes. Among ACS-CS group, AHF-CS group and CS-due to other causes group, pMCS were implanted in 25 (92.5%), 12 (92.3%) and 15 (68.1%) patients respectively. Lower extremities ischemia, gastrointestinal/intracerebral and life-threatening bleeding and ischemic stroke were observed as pMCS related adverse events in 9.7%, 6.4%, 1.6%, 3.2%, 6.4% of cases respectively. At one month, 56 (90.3%) CS patients were discharged alive while 6 (9.7%) CS patients died during the CICU stay. Conclusion A multidisciplinary approach of CS patients, contemplating an early and extensive use of pMCS, may be effective in the reduction of in-hospital mortality rate with a low and acceptable occurrence of pMCS related adverse events. Funding Acknowledgement Type of funding source: None

Non-catecholamine vasopressors in the treatment of adult patients with septic shock—evidence from meta-analysis and trial sequential analysis of randomized clinical trials

BackgroundNorepinephrine (NE) has currently been the first-choice vasopressor in treating septic shock despite generally insufficient for patients with refractory septic shock. The aim of this update meta-analysis was to assess the safety and efficacy of a combination of non-catecholamine vasopressors (vasopressin/pituitrin/terlipressin/selepressin/angiotensin II) and NE versus NE in managing adult septic shock patients.MethodsWe conducted this study of literatures published from the inception to April 30, 2020, using PubMed, Embase, and the Cochrane Library databases without language restriction. Randomized controlled trials comparing NE with non-catecholamine vasopressors among adult septic shock patients were included in this meta-analysis. Pooled effects of relative risk (RR) or standard mean difference (SMD) and corresponding 95% confidence interval (CI) were calculated using a random-effects model.ResultsTwenty-three studies covering 4380 participants were finally enrolled. The combined analysis of non-catecholamine vasopressors resulted in a nonsignificant reduction in 90-day/ICU/hospital mortality except for a decreased in 28-day mortality (n = 4217; RR, 0.92; 95% CI 0.86–0.99; P = 0.02). This favorable result was subsequently verified by the subgroup analyses of low risk of bias studies (RR = 0.91, 95% CI = 0.84 to 0.98; P = 0.02) and catecholamine-resistant refractory shock patients group (RR, 0.84; 95% CI = 0.70–1.00; P = 0.048). The pooled analysis of non-catecholamine vasopressors showed a 14% higher success rate of shock reversal at 6 h, a 29% decreased risk of continuous renal replacement therapy, but a 51% increased risk of hyponatremia and a 2.43 times higher risk of digital ischemia. Besides, the pooled data showed that non-catecholamine vasopressors decreased heart rate (HR) (SMD, − 0.43; 95% CI − 0.66 – − 0.19; P < 0.001), serum creatinine (− 0.15; 95% CI − 0.29 – − 0.01; P = 0.04), and the length of mechanical ventilation (MV) (− 0.19; 95% CI − 0.31 – − 0.07; P < 0.01, but there was no significant difference in other parameters.ConclusionsCurrent pooled results suggest that the addition of NE to non-catecholamine vasopressors was associated with a marginally significant reduction in 28-day mortality. Moreover, they were able to shorten the length of MV, improved renal function, decreased HR, and increased the 6-h shock reversal success rate at the expense of increased the risk of hyponatremia and digital ischemia.

Place de la corticothérapie dans le choc septique

Le sepsis est un problème de santé publique majeur, associé à une morbi-mortalité conséquente. La forme la plus sévère du sepsis, le choc septique, a une physiopathologie complexe, associant entre autres anomalies une insuffisance corticotrope et une réponse inflammatoire exagérée. Les corticoïdes, médicaments aux effets pléiotropes, corrigent cette insuffisance corticotrope et exhibent un effet anti-inflammatoire. Les corticoïdes sont à l’heure actuelle un des rares médicaments possiblement capables de réduire la mortalité dans le choc septique. S’ajoute à cet effet bénéfique sur la mortalité un effet hémodynamique favorable. L’administration de corticoïdes à faibles doses et sur une courte période est associée à remarquablement peu d’effets secondaires. Un traitement par hydrocortisone 200mg/j peut être administré chez les patients en choc septique. Nous suggérons l’administration de ce traitement en bolus intraveineux intermittent pendant sept jours sans sevrage progressif à la fin de cette période. Un minéralocorticoïde, la fludrocortisone, peut être associée au traitement par hydrocortisone dans les états de choc réfractaire. La recherche de biomarqueurs permettant d’identifier précisément une population répondant aux corticoïdes dans le choc septique est une thématique porteuse.

Utility of Low Dose Vasopressin for Persistent Pulmonary Hypertension of Newborn with Catecholamine Refractory Shock.

To evaluate the effect of low dose vasopressin on the hemodynamics of neonates with persistent pulmonary hypertension and catecholamine refractory shock. This retrospective study was conducted in a level III NICU of a tertiary care teaching hospital, south India. Eighteen neonates with hypoxemic respiratory failure due to persistent pulmonary hypertension of newborn with catecholamine refractory shock were studied. Neonates were managed for hypotension with conventional inotropic support with the additional use of low dose vasopressin (LDV). Effect of vasopressin on oxygenation index (OI), blood pressure, duration of inotropic usage and survival was evaluated. Mean OI was 38.2 ± 4.9, and mean blood pressure was 30.7 ± 5.3mmHg before the start of vasopressin. Initiation of LDV (0.0003 ± 0.0001IU/kg/min) for a median duration 36.4 ± 17.9h was followed by a reduction in OI (p < 0.001), control of hypotension (p < 0.001), reduction in lactic acidosis (p < 0.001) and decline in inotropic support. In resource-restricted settings, LDV may be useful as a rescue therapy for persistent pulmonary hypertension of newborn with catecholamine refractory shock.

UNCOMMON AMONGST COMMON: ANGIOTENSIN II-INDUCED PERIPHERAL ISCHEMIA IN REFRACTORY SEPTIC SHOCK

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Angiotensin (AT) II, a naturally occurring hormone, modulates blood pressure through direct vasoconstriction of the circulatory system and through stimulation of various catecholamines and vasopressin. Derived from the hydrolysis of AT I via the AT-converting enzyme (ACE) in the pulmonary & renal endothelium, AT II has been studied for cases of vasodilatory shock since the 1930’. Most recently, the ATHOS-3 trial demonstrated AT II’s utility as a rescue vasopressor agent, highlighting its catecholamine-sparing effects. CASE PRESENTATION: 34-year-old African American male presented with 3-day history of dyspnea, productive cough and an episode of hemoptysis. Upon presentation, he was febrile, tachycardic, hypotensive and hypoxic prompting endotracheal intubation and vasopressor support. Laboratory studies were significant for leukocytosis with bandemia, lactic acidosis, acute kidney injury, transaminitis & positive for influenza A. Despite aggressive critical care management with maximum ventilator requirements, broad-spectrum antibiotics, renal replacement therapy & proning, his overall condition continued to worsen. AT II was initiated on Day 2 of ICU admission for refractory hypotension secondary to septic shock. Approximately 48-72 hours after the initiation of AT II, he developed skin discoloration and blistering in all extremities secondary to both arterial and venous thromboemboli despite prophylaxis. The lesions ultimately progressed leading to gangrenous necrosis extending proximally to the torso. Unfortunately, on day 7 of ICU admission, patient suffered a cardiac arrest and expired despite ACLS efforts. DISCUSSION: In our patient, we exhibited similar results to those described in the ATHOS-3 trials. Administration of the AT II resulted in an overall improvement in the patient’s mean arterial pressure, systemic vascular resistance and reduced norepinephrine requirements. We also observed a concomitant improvement in serum lactate, indicating improvement in overall organ perfusion. There are no absolute contraindications to AT II administration, but ATHOS-3 did report an increased incidence of both venous and arterial thromboembolic events in patients who received AT II. Although AT II has been FDA approved for the management of refractory septic shock, more studies are necessary to define those populations most at risk of the adverse effects. CONCLUSIONS: AT II is an important vasopressor agent used in refractory shock; however, more studies are needed to understand the adverse effects in populations most at risk. Reference #1: National Center for Biotechnology Information. PubChem Database. Angiotensin II, CID=172198, https://pubchem.ncbi.nlm.nih.gov/compound/Angiotensin-II (accessed on Mar. 26, 2020) DISCLOSURES: No relevant relationships by Krupa Gandhi, source=Web Response No relevant relationships by Mohit Mody, source=Web Response

EFFECTS OF DISCONTINUING VS TAPERING VASOPRESSIN INFUSION ON HEMODYNAMIC RECOVERY IN VASODILATORY SHOCK

SESSION TITLE: Critical Care Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: October 18-21, 2020 PURPOSE: Vasopressin (AVP) discontinuation strategies vary significantly despite its widespread use as an adjunctive agent in the treatment of vasodilatory shock. Several studies have looked at clinical outcomes associated with the discontinuation sequence of norepinephrine and AVP; however, these studies do not specify AVP de-escalation strategy. The purpose of our study is to compare the effect of gradual taper (GT) versus abrupt discontinuation (ADC) on the rates of clinically significant hypotension in patients recovering from vasodilatory shock. METHODS: This is a single-center, retrospective chart review of critically ill adult patients admitted to medical and surgical intensive care units from January 2016 to December 2019. The inclusion criterion was the confirmed administration of AVP infusion as an adjunct to catecholamine-based vasopressor therapy for at least one hour. Exclusion criteria included a primary diagnosis of cardiogenic shock, treatment with vasopressin as a sole vasopressor agent, vasopressin use for diabetes insipidus or organ donation, or transition to comfort care. The primary endpoint was the incidence of clinically significant hypotension after the initiation of vasopressin titration. Clinically significant hypotension was defined as hypotension requiring an increase or re-initiation of vasopressin, increase or re-initiation of catecholamine vasopressor, administration of fluid bolus, or a combination of these interventions. Secondary endpoints included duration of therapy and the number of vasopressors required. Additionally, ICU length of stay (LOS) and in-hospital mortality were evaluated. RESULTS: Of the 259 patients screened, a total of 46 patients were analyzed (15 in GT and 31 in ADC). Overall, the ADC group had a higher incidence of clinically significant hypotension, but this difference did not reach statistical significance (51.6% vs 26.7%, p = 0.11). While there were no differences in demographics or SOFA scores, the GT group tended to be on more vasopressors (3 vs 2, p = 0.05). In addition, of the 11 patients who received phenylephrine, the duration of therapy (59 hours vs 5 hours, p = 0.008) and the maximum dose (380 mcg/min vs 100 mcg/min, p = 0.0226) was higher in the GT group. There were no differences in ICU LOS or mortality between the two groups. CONCLUSIONS: Our study shows that, upon shock recovery, the abrupt discontinuation of vasopressin infusion was associated with numerically higher rates of clinically significant hypotension than gradual taper, although not statistically significant. There were no significant differences in LOS or in-hospital mortality. A larger study is needed to confirm these findings. CLINICAL IMPLICATIONS: The abrupt discontinuation of vasopressin may be relatively safe as it did not increase LOS or mortality. However, a gradual taper approach may be preferred in more profound shock, given the reduced rate of rebound hypotension. DISCLOSURES: No relevant relationships by Ola Elnadoury, source=Web Response No relevant relationships by Bhaskara Garimella, source=Web Response No relevant relationships by Andrew Lehr, source=Web Response No relevant relationships by Anthony Lubinsky, source=Web Response

BILIOPTYSIS: AN UNUSUAL CLINICAL FINDING

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Bilioptysis means presence of bile in the sputum. It has been previously identified in the setting of acute chest syndrome, hepatic infections such as echinococcosis and amebiasis, and bronchobiliary fistulae.1 We discuss a rare case of bilioptysis in the setting of fulminant liver failure, of which only one other case has been reported.2 This unique clinical constellation is one that likely portends a poor prognosis among those critical. CASE PRESENTATION: 47-year-old man with significant alcohol abuse was admitted to the ICU for fulminant liver failure and lacticemia. He presented with two episodes of hemoptysis and worsening jaundice. He took no pertinent medications. Exam was notable for ascites, severe jaundice, hepatosplenomegaly and spider angiomas. Labs were remarkable for AST 244, ALT 78, bilirubin 26.8, albumin 2.1, platelets 134, INR 2.2, hemoglobin 12.6, creatinine 3.14 and lactic acid 5.0. ICU course was complicated by worsening mental status, vasodilatory shock, renal failure requiring continuous renal replacement therapy, and acute hypoxemic respiratory failure requiring mechanical ventilation. He had increasing yellowish-green secretion on endotracheal suction with worsening infiltrates on chest X-ray. Bronchoscopy demonstrated copious yellowish fluid in the lower airway. BAL also showed biliary-tinged fluid. Despite aggressive management, he died in the setting of multiorgan failure from severe liver failure. DISCUSSION: We believe that bilioptysis in our patient was secondary to increased alveolar permeability causing bilirubin leakage. The patient did not have sickle cell disease and had no imaging evidence of fistulae. The secretions were unlikely of gastric origin given the presence of intact endotracheal tube cuff and intermittent suction on the orogastric tube. Bilirubin with molecular weight of 584 acts similar to high molecular weight serum proteins. Pleural fluid to serum bilirubin ratio >0.6 has been used for differentiating exudative from transudative effusion, especially in resource limited settings where LDH is difficult to obtain to meet Light’s criteria.3 Systemic inflammation generated by decompensated liver disease increases the permeability of capillary alveolar membrane, causing the diffusion of bilirubin according to concentration gradient. This can be seen as worsening infiltrates on chest X-ray. The unusual discoloration of the BAL should prompt a dipstick test for bilirubin, which can help differentiate between cardiac and non-cardiac causes of pulmonary edema and assess the prognosis in critically ill patients. CONCLUSIONS: In fulminant liver failure, this rare finding of bile in sputum or tracheal secretions could potentially be useful in establishing the diagnosis of the underlying pathology and assessing the prognosis in the critically ill patient. Reference #1: 1. Saraya, T. et al. A new diagnostic approach for bilious pleural effusion. Respir. Investig. 54, 364–368 (2016). Reference #2: 2. Choong, C. V., Chai, G. T., Lew, S. J. W. & Lim, A. Y. H. Bilioptysis: A Rare Finding with Valuable Information. in C52. CRITICAL CARE CASE REPORTS: UNUSUAL GI CAUSES OF CRITICAL ILLNESS A5805–A5805 (American Thoracic Society, 2017). doi:10.1164/ajrccm-conference.2017.195.1_MeetingAbstracts.A5805 Reference #3: 3. Agrawal, P., Shrestha, T. M., Prasad, P. N., Aacharya, R. P. & Gupta, P. Pleural Fluid Serum Bilirubin Ratio for Differentiating Exudative and Transudative Effusions. JNMA J. Nepal Med. Assoc. 56, 662–665 (2018). DISCLOSURES: No relevant relationships by Eric Ahlstrom, source=Web Response No relevant relationships by Kejal Gandhi, source=Web Response No relevant relationships by Khushali Jhaveri, source=Web Response No relevant relationships by Emil Oweis, source=Web Response

MASSIVE AIR PULMONARY EMBOLISM: IS IT REAL?

SESSION TITLE: Fellows Pulmonary Vascular Disease Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Air embolism is a rare but potentially catastrophic condition that occurs when air enters into the vasculature. Here we present a case of venous- air-embolism causing hemodynamic compromise that was treated with hyperbaric oxygen. CASE PRESENTATION: 63 years old female with COPD on LTOT presented at an outside hospital with worsening shortness of breath, found to be in hypercarbic respiratory failure presumable from acute exacerbation of COPD. Peripheral iv lines were placed, she was given fluids and placed on antibiotics, nebulizers and steroids. Patient rapidly deteriorated into refractory shock requiring pressors and hypoxia needing endotracheal intubation. Patient was also noted to have a seizure while in the ED. On transfer to our hospital, patient continued to remain in refractory shock and refractory hypoxia with PaO2/FiO2 ratio of 150. CXR showed changes consistent with obstructive lung disease. CT scan of chest was performed given unexplained hypoxia and shock which showed evidence of air in the main pulmonary artery extending into the segmental and subsegmental arteries with air also tracking from left subclavian vein into SVC. CT scan of head was unremarkable. Diagnosis of venous air embolism was made, and patient was placed in left lateral decubitus, Trendelenburg position with 100% FiO2 on the ventilator. Decision was made to proceed with hyperbaric oxygen therapy (HBO) due to severe hemodynamic instability. ENT was consulted for bilateral myringotomies prior to the therapy. Patient successfully received hyperbaric oxygen therapy for almost 7 hours, with complete resolution of air embolism on repeat CT scan of chest. Patient came off of vasopressors immediately after completion of treatment. She was extubated on day 4 of mechanical ventilation. DISCUSSION: Air embolism is a rare but potentially catastrophic condition that occurs when the air enters into the vasculature. It can be venous and arterial. Common causes include vascular intervention, surgery, trauma, barotrauma from mechanical ventilation and diving. Diagnosis require high clinical suspicion and imaging evidence. Treatment options are limited including positioning, HBO and direct removal of air. Venous embolisms are self-limiting if volume of air is <50 ml, beyond which patients can have direct and indirect effect of embolism. Based on indications different treatment tables are used for HBO therapy. It was thought that our patient had iatrogenic air embolism from IV access placed on the left arm. She was appropriately started on HBO as she was hemodynamically unstable. There is limited literature about direct removal of air using catheters and it is typically performed when catheters are already in place. CONCLUSIONS: Air embolism, especially pulmonary air embolism, is life threatening and prompt intervention with appropriate positioning and HBO are life saving measures. Reference #1: King, Melissa B., and Keith R. Harmon. “Unusual forms of pulmonary embolism.” Clinics in chest medicine 15.3 (1994): 561-580. Reference #2: Leach, R. M., P. J. Rees, and P. Wilmshurst. “Hyperbaric oxygen therapy.” Bmj 317.7166 (1998): 1140-1143. Reference #3: Bessereau, Jacques, et al. “Long-term outcome of iatrogenic gas embolism.” Intensive care medicine 36.7 (2010): 1180-1187. DISCLOSURES: No relevant relationships by Hassan Yousaf, source=Web Response

PVCS AND PES: A CASE OF MASSIVE PULMONARY EMBOLISM AFTER ELECTIVE RADIOFREQUENCY ABLATION

SESSION TITLE: Medical Student/Resident Pulmonary Vascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Thromboembolic events are a known but rare complication of radiofrequency ablation despite the frequent use of intra-procedural anticoagulation. CASE PRESENTATION: A 46-year-old male with history of hypertension and dilated cardiomyopathy underwent elective, repeat ablation for refractory premature ventricular contractions (PVCs) localized to the right ventricular outflow tract (RVOT). The procedure was complicated by bleeding at the groin access sites requiring pressure bandages and bed rest. Prior to discharge at 24 hours, the patient suddenly developed tachypnea, tachycardia, diaphoresis, and worsening hypoxemia. He required intubation with inotropic support; bedside echocardiogram showed a dilated right ventricle (RV). CT angiogram demonstrated extensive bilateral pulmonary emboli (PE). Intravenous heparin was started; however, refractory obstructive shock developed. Despite high minute ventilation, the patient’s hypercarbia and acidemia worsened. The decision was made to initiate veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for impending cardiovascular collapse. Transesophageal echocardiogram during cannulation revealed a hypokinetic RV with clot in transit. The patient demonstrated improved hemodynamics and RV function while on ECMO with heparin anticoagulation, and was subsequently decannulated on day 7. He required tracheostomy and prolonged mechanical ventilation secondary to ventilator associated pneumonia and critical illness myopathy, but is now fully recovered and doing well at home. DISCUSSION: Incidence of deep vein thrombosis after non-atrial fibrillation (AF) ablations is as high as 2.38%(1). Periprocedural anticoagulation is recommended in AF and left sided ablations, but expert consensus recommends its use in RV procedures only when risk of thrombosis is considered high. The duration of the procedure and number of venous catheters used may increase the risk of venous thrombosis(2). RVOT ablations can be long and technically challenging, increasing both bleeding risk and endothelial disruption. Patients with bleeding complications may require bed rest and compression leading to stasis, tipping the coagulation balance towards thrombosis. To date, use of ECMO for massive PE is limited to single center case series with promising outcomes. ECMO should be considered in cases of refractory shock or inability to ventilate due to severe V/Q mismatch, especially when further thrombolysis may exacerbate pre-existing bleeding. PE with right heart thrombi in transit are at particularly high risk for deterioration(3). Fortunately, the diagnosis was made early in our patient’s course which allowed for timely initiation of VA-ECMO. CONCLUSIONS: Providers should maintain a high index of suspicion for PE even in patients with brief hospitalizations for elective procedures. Furthermore, VA-ECMO may be especially useful in patients with both massive PE and ongoing bleeding. Reference #1: Burstein B, Barbosa RS, Kalfon E, Joza J, Bernier M, Essebag V. Venous Thrombosis After Electrophysiology Procedures: A Systematic Review. Chest [Internet]. 2017;152(3):574–86. Reference #2: Cronin EM, Bogun FM, Maury P, Peichl P, Chen M, Namboodiri N, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias. Hear Rhythm [Internet]. 2020;17(1):e2–154. Reference #3: Kronik G. The european cooperative study on the clinical significance of right heart thrombi. Eur Heart J. 1989;10(12):1046–59. DISCLOSURES: No relevant relationships by Timothy Fernandes, source=Web Response No relevant relationships by Abdurrahman Husain, source=Web Response No relevant relationships by Janna Raphelson, source=Web Response No relevant relationships by Alexandra Rose, source=Web Response

TAKOTSUBO CARDIOMYOPATHY SECONDARY TO ACUTE BACTERIAL MENINGITIS

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Infection and sepsis are not uncommon causes of cardiomyopathy due to a decrease in ventricular function. Cardiovascular dysfunction in sepsis can be seen as septic cardiomyopathy, Takotsubo cardiomyopathy, refractory shock or myocardial injury. A study showed that Takotsubo cardiomyopathy was present in 0.15% of admissions with severe sepsis. It should be considered in the differential diagnosis of acute coronary syndrome especially post-menopausal women with preceding stressful events. We present a case of bacterial meningitis leading to Takotsubo’s cardiomyopathy in the setting of CSF leak. CASE PRESENTATION: A 67-year-old woman with no past medical history presented to the emergency department with diarrhea, vomiting, and confusion. On arrival, she was hypotensive to 87/66mmHg, tachycardic 116bpm and hypoxic to 83% on room air. Laboratory evaluation was significant for leukocytosis of 29.2 k/ul, troponin 5.02 ng/ml, lactic acid 2.9 mmol/l, BNP 788 pg/ml. Cerebrospinal fluid showed a white blood cell count of 5011 (91% neutrophils), protein 791 mg/dl, glucose 95 mg/dl. She was admitted with a diagnosis of an NSTEMI, acute meningeal encephalitis and treated with aztreonam, vancomycin, doxycycline, and dexamethasone. Cultures revealed streptococcus viridians and treatment was narrowed to ceftriaxone. Facial CT showed a possible area of dehiscence concern for possible CSF leak. No significant coronary artery disease on the angiogram Echocardiogram was consistent with Takotsubo cardiomyopathy. The patient's cardiomyopathy was treated with goal-directed medical therapy with complete resolution of symptoms. DISCUSSION: Takotsubo cardiomyopathy is defined as a transient regional left ventricular systolic dysfunction without obstructive coronary artery disease and usually triggered by emotional or physical stress. During sepsis, there is an activation of the sympathoadrenergic system with rapid elevation in circulating catecholamine levels. Pathogenesis is related to myocardial stunning, catecholamine toxicity, impaired myocyte metabolism. According to Mayo Clinic criteria there should be: 1) transient hypokinetic, akinesias or dyskinesia of the LV midsegments, 2) absence of CAD, 3) EKG abnormalities or troponin elevation, 4) absence of pheochromocytoma or myocarditis. Patients can present with mild to moderate congestive heart failure or hypotension due to a reduction in stroke volume. The mean age of presentation ranges from around 60 to 75 years. The prognosis is excellent, mortality from 0%-8% and a recurrence occurs in <10% of patients. The treatment is based on the management of the underlying etiology and supportive cardiovascular care. CONCLUSIONS: Patients with suspected TTC need to be work up to rule out ACS with coronary angiogram. Takotsubo’s cardiomyopathy has a good prognosis with recovery on the EF and cardiac function once infection or physical stress disappears. Reference #1: De Giorgi, A., Fabbian, F., Pala, M., Parisi, C., Misurati, E., Molino, C., et al. (2015). Takotsubo Cardiomyopathy and Acute Infectious Diseases: A Mini-Review of Case Reports. Angiology, 66(3), 257–261. Reference #2: Pilgrim, TM, Wyss, TR. Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: a systematic review. Int J Cardiol. 2008;124(3):283–292. Reference #3: Prasad, A, Lerman, A, Rihal, CS. Apical ballooning syndrome (tako-tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J. 2008;155(3):408–417. DISCLOSURES: No relevant relationships by Daniel Colon Hidalgo, source=Web Response No relevant relationships by Diana Estefania Espinoza Barrera, source=Web Response No relevant relationships by Hugues Orozco, source=Web Response No relevant relationships by Jose Zabala-Genovez, source=Web Response

A RARE FATAL CASE OF DISSEMINATED MUCORMYCOSIS IN AN IMMUNOCOMPETENT PATIENT DIAGNOSED ON AUTOPSY

SESSION TITLE: Medical Student/Resident Chest Infections Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: We present a fatal case of undiagnosed disseminated mucormycosis in an immunocompetent patient that was diagnosed on autopsy. CASE PRESENTATION: 63-year-old male with history of deep vein thrombosis/pulmonary embolism on apixaban, atrial fibrillation, hypertension and morbid obesity presented with fever, abdominal rash and malaise for 3 days. He was discharged from the ED on oral doxycycline for possible Lyme disease. Patient had worsening generalized weakness and diarrhea and presented to the ED again two days later febrile, hypotensive and tachycardic. Labs were remarkable for white cell count of 19,800 and lactic acid of 4.3 mmol/L. He was started on broad-spectrum antibiotics: piperacillin-tazobactam, vancomycin and doxycycline. Patient’s condition significantly worsened with multiorgan failure and he was started on continuous renal replacement therapy. He was placed on four inotropic agents and was started on intravenous bicarbonate infusion in the setting of severe metabolic acidosis. The patient was intubated and mechanically ventilated. Procalcitonin level was found to be 26. Serologies for Rocky Mountain spotted fever, babesiosis, anaplasmosis and ehrlichiosis were negative. Respiratory pathogen panel, hepatitis panel, EBV IgM, CMV IgM, monospot test and leptospirosis antibody, anti-double stranded DNA, anti-citrullinated peptide, anti-histone antibody, anti-neutrophilic cytoplasmic antibody were all negative. Patient had some initial improvement and was weaned off the ventilator and vasopressors. Antibiotics were discontinued after 14 days. Unfortunately, however, patient became pulseless during dialysis and was reintubated. He simultaneously began to decompensate, and vasopressors were reinitiated. IV vancomycin, cefepime, metronidazole, and acyclovir were started with suspicion for disseminated Herpes Simplex infection due to new facial eschars as shown in figure 1. Repeat CT abdomen showed progressive pancreatitis, with normal lipase levels. Patient again went into cardiac arrest. After resuscitation, however, he was found to have a bowel perforation with repeat blood cultures growing Bacteroides thetaiotaomicron. He subsequently passed away within a day. Postmortem autopsy showed disseminated mucormycosis with extensive necrosis involving lungs, spleen, bowel, kidneys as shown in figures 2 and 3. DISCUSSION: Disseminated mucormycosis is a rare fungal infection with the mortality rate of approximately 100%. It rarely occurs in immunocompetent individuals(1). The only hope for treatment is rapid diagnosis, correction of predisposing factors, surgical debridement of necrotic tissue and antifungal therapy. (2) CONCLUSIONS: Our patient, who initially presented with nonspecific symptoms, eventually progressed to refractory shock, unresponsive to broad spectrum antibiotics. The suspicion for disseminated mucormycosis should not be confined to immunocompromised patients. Reference #1: Horger M, Hebart H, Schimmel H, Vogel M, Brodoefel H, Oechsle K, et al. Disseminated mucormycosis in haematological patients: CT and MRI findings with pathological correlation. Br J Radiol. 2006;79:e88–95. Reference #2: Amir Hossein Sarrami, Mehrdad Setareh,1 Masoud Izadinejad,1 Noushin Afshar-Moghaddam,2 Mohammad Mehdi Baradaran-Mahdavi,3 and Mohsen Meidani4. Fatal Disseminated Mucormycosis in an Immunocompotent Patient: A Case Report and Literature Review. Int J Prev Med. 2013 Dec; 4(12): 1468–1471. DISCLOSURES: No relevant relationships by Marc Filstein, source=Web Response No relevant relationships by Fizza Hirani, source=Web Response no disclosure on file for Rameez Phulphoto; No relevant relationships by Emily Zagorski, source=Web Response

Treatment of Acute Hemorrhagic Shock in A Jehovah'S Witness Patient with a Heartmate 3 Left Ventricular Assist Device

Introduction Left ventricular assist device (LVAD) has emerged as an effective treatment of end-stage heart failure either as bridge to transplant or destination therapy. However, the need for anticoagulation with LVAD comes with the trade-off of increased bleeding risk and worsening anemia requiring blood transfusions. We describe a case of acute hemorrhagic shock in a Jehovah's Witness with a HeartMate 3 (HM3) - LVAD successfully treated without any transfusion of blood products Case A 65-year-old African American Jehovah's Witness male with a three months history of HM3 implantation for end-stage non-ischemic cardiomyopathy presented to the hospital for loss of consciousness, melanotic stool, hypotension and hemorrhagic shock. Initial laboratory included an elevated INR of 5.4 and hemoglobin of 5.4 g/dL. The LVAD remained in good function without low flow alarms at a speed of 4900 rpm and a SBP of 40mmHg. Patient's hypotension and decompensation was attributed to his acute blood loss anemia, however, given his religious beliefs, transfusion of blood products was not an option. As a result, the patient was intubated and resuscitated with IV iron, colloids and darbepoetin alfa for RBC stimulation in addition to inotropes and pressor support. Gastroenterology declined urgent endoscopic procedure due to the hemodynamic instability of this case. The patient's hemoglobin further declined to 2.4 g/dL with persistent, refractory shock. Only after an increase in LVAD speed from 4900 rpm to 5600 rpm cardiac output and overall hemodynamic status improved to MAP of 70 mmHg allowing de-escalation of inotropes and pressors. Over the next two weeks, INR corrected, bleeding subsided, and the patient was extubated without any neurological deficits or signs of mesenteric ischemia. His hemoglobin trended up to > 8 g/dL by discharge. Conclusion Bleeding is common in heart failure patients with LVADs. Blood transfusion, at times, can provide a simple and quick life-saving resolution to this problem. The severity of anemia in our case without administration of any blood products is usually not consistent with life. Our case highlights a potential role of augmenting LVAD support to maintain cardiac output in patients presenting with hypovolemic, hemorrhagic shock as a bridge to recovery of endogenous RBC mass regeneration with IV iron and darbepoetin alfa without the need of foreign blood products. Future studies are necessary to determine whether LVAD optimization is sufficient to avoid blood products and preventing the risk of sensitization BTT LVAD patients against potential future heart transplant offers.

Trends And Outcomes of The Use of Ecmo In Combined Septic And Cardiogenic Shock

Background Extracorporeal membrane oxygenation (ECMO) utilization in children is recommended in refractory septic shock. However in adults there are no official recommendation to guide this treatment. Most of the existing evidence consists of small observational and single center experiences. We aimed to investigate the trend of use and outcomes of ECMO in patients with combined septic and cardiogenic shock. Methods We queried the unweighted national inpatient sample (NIS) for patients older than 18 years old, who carried both diagnoses of septic shock and cardiogenic shock during index hospitalization and received ECMO treatment for the years 2004-2017 using ICD-9&10 codes. Results We identified 29,178 patients with combined septic and cardiogenic shock in between 2004 and 2017. Of those, 424 (0.1%) patients underwent ECMO. There was a statistically significant increasing trend of ECMO use over the years of study (Std. J-T Statistic 4.338, p Conclusion ECMO is being increasingly used in patients with combined septic and cardiogenic shock, more data is needed to further guide this treatment modality in this patient population.

Low dose corticosteroids in COVID-19 with refractory shock: We are not sure?

Low dose corticosteroids in COVID-19 with refractory shock: We are not sure?

Glucocorticoid treatment is associated with ICU-acquired hypernatremia: a nested case-control study.

BackgroundHypernatremia is a major electrolyte disorder associated with death among critically ill patients. Glucocorticoid therapy may cause hypernatremia in refractory septic shock patients, but the association between glucocorticoid and intensive care unit (ICU)-acquired hypernatremia (IAH) remains unclear. The aim of this study was to clarify whether glucocorticoid administration was associated with IAH.MethodsThis was a nested case–control study using data from an established cohort including 121 IAH cases identified from 1756 patients who were admitted to ICU in a tertiary care facility in Japan. We included patients who were admitted with a normal range of serum sodium concentrations (130–149 mEq/L) from January 1, 2013 to December 31, 2015 and remained in ICU for ≥ 2 days. Hypernatremia was defined as serum sodium concentration ≥ 150 mEq/L. Each case was matched to one control.ResultsMultivariable conditional logistic regression revealed high-dose glucocorticoid {odds ratio (OR), 4.15 [95% confidence interval (CI) 1.29–13.4]}, acute kidney injury (AKI) [OR, 2.72 (95% CI 1.31–5.62)], and osmotic diuretics [OR, 3.44 (95% CI 1.41–8.39)] to be significantly associated with IAH. The contents and amounts of fluid infusion were not significantly associated with IAH. There were also significant duration–response effects between duration of glucocorticoid use and IAH; however, pulse glucocorticoid administration was not associated with IAH.ConclusionIn this nested case–control study, we demonstrated a significant association between IAH and high-dose glucocorticoid with significant duration–response effects. Serum sodium concentrations should be monitored carefully in critically ill patients administered prolonged high-dose glucocorticoid.Electronic supplementary materialThe online version of this article (10.1007/s10157-020-01967-9) contains supplementary material, which is available to authorized users.

Critical Obstetric Patients During the Coronavirus Disease 2019 Pandemic: Operationalizing an Obstetric Intensive Care Unit.

Critical Obstetric Patients During the Coronavirus Disease 2019 Pandemic: Operationalizing an Obstetric Intensive Care Unit.

Transcriptome Analysis Revealed Inflammation Is Involved in the Impairment of Human Umbilical Vein Endothelial Cells Induced by Post-hemorrhagic Shock Mesenteric Lymph.

Vascular endothelial injury caused by post-hemorrhagic shock mesenteric lymph (PHSML) return is an important manifestation during refractory hemorrhagic shock. Using human umbilical vein endothelial cells (HUVECs) and transcriptome analysis, this study sought to investigate the molecular mechanism underlying the adverse effect of PHSML on vascular endothelium. Post-hemorrhagic shock mesenteric lymph was collected from male rats after they underwent hemorrhagic shock and following resuscitation, while normal mesenteric lymph (NML) was harvested from sham rats. Human umbilical vein endothelial cells were incubated with the culture medium containing either 10% phosphate buffered saline (Control), NML, or PHSML for 3 h, and then were harvested for RNA sequencing. In comparison with NML treated cells, 37 genes were differentially expressed in PHSML-treated HUVECs, including 32 upregulated genes and five downregulated genes. These differentially expressed genes were mainly enriched in inflammatory pathways, including signaling pathways for activation of the NOD-like receptors, NF-κB, and TNF. Furthermore, we found that C–C motif chemokine ligand 2 (CCL2) was increased significantly after PHSML treatment, and Bindarit, a CCL2 production inhibitor, attenuated the damage of HUVECs induced by PHSML. The results provide molecular evidence on vascular endothelium damage caused by PHSML. C–C motif chemokine ligand 2 might represent a new target for reducing vascular injury after severe hemorrhagic shock.

Rescue Treatment with Terlipressin for Persistent Pulmonary Hypertension and Refractory Shock in a Preterm Infant

Rescue Treatment with Terlipressin for Persistent Pulmonary Hypertension and Refractory Shock in a Preterm Infant

Angiotensin II Infusion for Shock: A Multicenter Study of Postmarketing Use

Vasodilatory shock refractory to catecholamine vasopressors and arginine vasopressin is highly morbid and responsible for significant mortality. Synthetic angiotensin II is a potent vasoconstrictor that may be suitable for use in these patients. What is the safety and effectiveness of angiotensin II and what variables are associated with a favorable hemodynamic response? We performed a multicenter, retrospective study at five tertiary medical centers in the United States. The primary end point of hemodynamic responsiveness to angiotensin II was defined as attainment of mean arterial pressure (MAP) of≥ 65mmHg with a stable or reduced total vasopressor dosage 3h after drug initiation. Of 270 included patients, 181 (67%) demonstrated hemodynamic responsiveness to angiotensin II. Responders showed a greater increase in MAP (+10.3mmHg vs+1.6mmHg, P< .001) and reduction in vasopressor dosage (-0.20 μg/kg/min vs+0.04 μg/kg/min; P< .001) compared with nonresponders at 3 h. Variables associated with favorable hemodynamic response included lower lactate concentration (OR 1.11; 95%CI, 1.05-1.17, P< .001) and receipt of vasopressin (OR, 6.05; 95%CI, 1.98-18.6; P= .002). In severity-adjusted multivariate analysis, hemodynamic responsiveness to angiotensin II was associated with reduced likelihood of 30-day mortality (hazard ratio, 0.50; 95%CI, 0.35-0.71; P< .001). Arrhythmias occurred in 28 patients (10%) and VTE was identified in 4 patients. In postmarketing use for vasopressor-refractory shock, 67%of angiotensin II recipients demonstrated a favorable hemodynamic response. Patients with lower lactate concentrations and those receiving vasopressin were more likely to respond to angiotensin II. Patients who responded to angiotensin II experienced reduced mortality.

Vasopressor Therapy in the Intensive Care Unit

After fluid administration for vasodilatory shock, vasopressors are commonly infused. Causes of vasodilatory shock include septic shock, post-cardiovascular surgery, post-acute myocardial infarction, postsurgery, other causes of an intense systemic inflammatory response, and drug -associated anaphylaxis. Therapeutic vasopressors are hormones that activate receptors-adrenergic: α1, α2, β1, β2; angiotensin II: AG1, AG2; vasopressin: AVPR1a, AVPR1B, AVPR2; dopamine: DA1, DA2. Vasopressor choice and dose vary widely because of patient and physician practice heterogeneity. Vasopressor adverse effects are excessive vasoconstriction causing organ ischemia/infarction, hyperglycemia, hyperlactatemia, tachycardia, and tachyarrhythmias. To date, no randomized controlled trial (RCT) of vasopressors has shown a decreased 28-day mortality rate. There is a need for evidence regarding alternative vasopressors as first-line vasopressors. We emphasize that vasopressors should be administered simultaneously with fluid replacement to prevent and decrease duration of hypotension in shock with vasodilation. Norepinephrine is the first-choice vasopressor in septic and vasodilatory shock. Interventions that decrease norepinephrine dose (vasopressin, angiotensin II) have not decreased 28-day mortality significantly. In patients not responsive to norepinephrine, vasopressin or epinephrine may be added. Angiotensin II may be useful for rapid resuscitation of profoundly hypotensive patients. Inotropic agent(s) (e.g., dobutamine) may be needed if vasopressors decrease ventricular contractility. Dopamine has fallen to almost no-use recommendation because of adverse effects; angiotensin II is available clinically; there are potent vasopressors with scant literature (e.g., methylene blue); and the novel V1a agonist selepressin missed on its pivotal RCT primary outcome. In pediatric septic shock, vasopressors, epinephrine, and norepinephrine are recommended equally because there is no clear evidence that supports the use of one vasoactive agent. Dopamine is recommended when epinephrine or norepinephrine is not available. New strategies include perhaps patients will be started on several vasopressors with complementary mechanisms of action, patients may be selected for particular vasopressors according to predictive biomarkers, and novel vasopressors may emerge with fewer adverse effects.