Impact of Crystalloid Administration on Patients Receiving Haploidentical Allogeneic Stem Cell Transplant (Haplo SCT) with Post Transplant Cytoxan Prophylaxis (PtCy): a Quality Improvement Initiative

Background: Crystalloid fluid administration has traditionally played an important role in prevention of hemorrhagic cystitis with high dose cyclophosphamide. Cryopreservation of stem cells in the era of the COVID pandemic has further led to an increase in crystalloid use. Excess fluid administration over a short duration could lead to volume overload, respiratory failure and impact overall survival. Method(s): A retrospective chart review was conducted on patients receiving PtCy following Haplo SCT at UVA Medical Center from September 2016 through August 2022. Internal BMT quality audit in June 2021 identified increased rate of ICU transfers and respiratory failure amongst patient receiving PtCy due to fluid overload. Hence our PtCy hydration was reduced, with IV fluid administration decreasing from 200 mL/ hr over 62 hours to 100 mL/hr over 12 hours. Urine output parameters placed to administer Cytoxan were also removed. We present our quality improvement project demonstrating outcomes pre and post intervention. Result(s): All demographic patient and transplant-related data was collected during the period of hospitalization for Haplo SCT [Table 1]. Pre-intervention spanned 9/2016-8/2021. Our analysis identified higher than expected rates of respiratory (Table Presented) failure prompting intervention on 8/2021. Post-intervention spanned 8/2021-8/2022. Pre-intervention, 45% of patients receiving Haplo SCT developed respiratory failure (defined as a new hypoxia) in the 30 day post-transplant period. Of these, 93% had volume overload. Mechanical ventilation was required in 21%. Complication rates included ICU transfer - 30%, AKI - 39%, and renal replacement therapy - 18%. Three percent (1 pt) developed hemorrhagic cystitis requiring bladder irrigation. Median LOS was 31.0 days. Post-intervention, average IV crystalloid received was reduced by about 15L. Median diuretic use reduced by 40%. No instances of respiratory failure, mechanical ventilation, ICU transfer, AKI or renal replacement therapy occurred in this group. Median LOS was 26.5 days. There were no cases of hemorrhagic cystitis. Please refer Figure 1. (Figure Presented) (Figure Presented) Conclusion(s): This single center quality improvement initiative shows that reducing IV crystalloid administration with PtCy is associated with a reduction in respiratory failure and other adverse clinical outcomes, without observed increase in hemorrhagic cystitis. Larger multi-center studies are needed to validate this finding.Copyright © 2023 American Society for Transplantation and Cellular Therapy

ERS International Congress 2022 Abstracts

The proceedings contain 3270 papers. The topics discussed include: the impact of age and gender on mortality from COVID-19 at A UK hospital;vaccinated COVID-19 patients admitted in a Tunisian ICU: clinical features and outcome;pneumothorax - a life-threatening complication in patients with cystic fibrosis;impact of combined non-invasive support strategies use during acute respiratory failure due to COVID-19;early mobilization of mechanically ventilated patients in the intensive care units: results of a Saudi-wide national survey;awake prone positioning in acute hypoxemic respiratory failure from COVID-19: a randomized clinical trial;amount and distribution of parenchymal abnormalities at CT-scan do not predict awake prone position outcome in COVID-19;impact of dexamethasone on pathogen profile of COVID-19 patients requiring intensive care: a multicenter retrospective study;higher crystalloids volumes predict adverse outcomes in emergency department patients with blunt thoracic trauma;and STUMBL score for emergency department safe discharge of patients with minor blunt thoracic trauma.

Isolated Colonic Histoplasmosis in Renal Transplant Recipient Post Covid-19 Infection

Introduction: Histoplasmosis is caused by the dimorphic fungus - Histoplasma capsulatum. The presentation of histoplasmosis is often disseminated, though primary intestinal involvement can rarely be seen in patients with cell mediated immune dysfunction like in patients with AIDS. We report a case of renal allograft recipient, who had history of COVID 19 infection and also underwent anti-rejection treatment for renal graft dysfunction, presented with chronic diarrhea and was diagnosed as a case of colonic histoplasmosis. Method(s): We report a case of 45 years old male who underwent renal transplant surgery one and a half year prior (February 2021) and was having stable graft function on tacrolimus, mycophenolate and steroid. He had history of fever and diarrhea in February 2022 and was diagnosed COVID-19 positive with RT-PCR, and was treated conservatively with intravenous dexamethasone and lowering of immunosuppressants. He had mild graft dysfunction in April 2022;renal graft biopsy had acute T-Cell mediated rejection (Banff Grade 1 B) and was treated with pulse steroids for 3 days. He had complaint of intermittent diarrhea, weight loss and intermittent fever since May 2022. He was evaluated and treated on outpatient basis with empirical oral antibiotics. He was admitted in June 2022 with complaint of high grade fever, loose stools leading to hypovolemic shock and renal dysfunction. He had marked thrombocytopenia and neutrophilic leukocytosis. He showed initial response to intravenous broad spectrum antibiotics and crystalloids, but intermittently symptoms of increased stool frequency and altered consistency were still persisting. Stool studies for ova, cyst, parasites and clostridium difficile were negative. Indian ink staining of stool sample had no evidence of Cryptococcosis. Serum PCR for cytomegalovirus was also negative. CT abdomen showed normal visualized bowel and other viscera. Upper GI endoscopy was unremarkable. Colonoscopy revealed multiple small ulcers with erythematous hue and clean base particularly in ceacum and along ascending colon. Multiple colonic biopsies were taken. Histopathology showed lymphoplasmacytic infilterate in the lamina propria. It also showed increased presence of foamy histiocytes, several of which also showed interacellular organism bearing a pseudocapsule. PAS stain also confirmed budding of these interacellular organisms which is consistent with Histoplasmosis. His HRCT chest revealed hyperinflated lungs, cylindrical bronchiectasis in left upper lobe. Urine for histoplasma antigenuria was negative. Result(s): He was treated with intravenous liposomal amphotericin B for initial two weeks followed by oral itraconazole. His symptoms responded remarkably to the treatment. In view of persisting thrombocytopenia and histoplasmosis his mycophenolate was stopped and tacrolimus was titrated as per trough levels Conclusion(s): Colonic histoplasmosis is associated with significant mortatlity and morbidity. Prolonged use of immunosuprresants, use of antirejection therapies (like high dose pulse methyl prednisolone and bortezomib) and even in some case reports COVID 19 infection have shown to increase the risk of histoplasmosis. Primary and isolated colonic histoplasmosis like in this case can be the atypical presentation which emphasizes the importance of maintaining a low threshold for consideration of histoplasmosis in renal allograft recipients. No conflict of interestCopyright © 2023

The triad of Legionnaires' disease: A case report

Legionnaires' disease is an atypical and severe pneumonia caused by environmental gram-negative bacteria called Legionella species. Typical symptoms include fever, cough and shortness of breath. Moreover, Legionnaires' disease can present with extrapulmonary manifestations including gastro-intestinal symptoms and rhabdomyolysis resulting in renal failure. In this case report, we describe a 43-year-old female patient with a history of HIV, latent tuberculosis and a recent covid-infection who presented with shortness of breath, chest pain, myalgias and diarrhea for 3 days. She was admitted with a left lower lobe pneumonia and acute kidney injury, initially consigned to a prerenal cause. She also had abnormal liver function tests;however, a liver ultrasound showed no dilated bile ducts or focal lesions. Empirical treatment with Amoxicillin/clavulanic acid was started at the emergency ward, besides supportive therapy with IV fluids and antipyretics. At admission, she required 2 liters of supplemental oxygen via nasal cannula and was hemodynamically stable. On day 2 of hospitalization, our patient developed oliguria. Laboratory tests revealed a serum creatinine of 6.08 mg/dL, a C-reactive protein of 528 mg/L and creatinine kinase of128100U/L. Urine analyses showed proteinuria and hematuria. The urinary Legionella Antigen test was positive. Clarithromycin was added to the treatment and aggressive IV hydration was started with crystalloids, besides the administration of sodium bicarbonate to alkalize the urine. The following days the patient's general condition improved rapidly. Eventually she could be discharged 10 days after her admission, completely recovered. This case report outlines the importance for clinicians to early recognize this rare but severe triad of Legionnaires' disease, with pneumonia, rhabdomyolysis and renal failure to reduce morbidity and mortality.

Management of Shock in Multisystem Infammatory Syndrome Associated with COVID-19 in Children (MIS-C)

Severe infammatory state shock is commonly encountered in critically ill patients due to multisystem infammatory syndrome associated with COVID-19 (MIS-C) and is accompanied with high mortality. All four types of shock (i.e., distributive, cardiogenic, obstructive, and hypovolemic) have been observed in patients with MIS-C. Hyper-infammatory immune response with cytokine release syndrome leads to loss of vasomotor tone and higher rates of mortality. In vasodilatory shock, norepinephrine is considered as the preferred vasopressor agent and as the second line of treatment, vasopressin or epinephrine could be added. In acute cardiac injury followed by ischemia, myocarditis or cardiomyopathy, inotropic agents such as milrinone, dobutamine and epinephrine may be contemplated and in patients with hypotensive cardiogenic shock, norepinephrine is administered as the first-line vasopressor. Pneumothorax, pneumomediastinum and rarely, cardiac tamponade are etiologies of obstructive shock in COVID-19. Hypovolemia may be present due to poor oral intake, high-grade fever, diarrhea and bleeding induced by anticoagulant medications. In pediatric patients presenting with COVID-19 and shock, we suggest parenteral fuid therapy with crystalloid solutions, 10 - 20 mL/kg up to 40 - 60 mL/ kg bolus infusion in settings with pediatric intensive care unit (PICU) availability. However, in settings with inadequate pediatric critical care services, it is recommended to administer bolus fuids (10 - 20 mL/kg per bolus, up to 40 mL/kg) only in hypotensive patient. Evidences of improved outcomes with early administration of vasopressors are signifed recently. In conclusion, shock associated with COVID-19 seems to have better outcomes in children compared with adults.

Fluid Challenge in children patients with COVID-19 Disease

COVID-19 Disease is a global problem that starts with fever, anorexia, malaise and cough. In severe cases needs ICU admission. Fluid therapy in critically children with COVID-19 Disease is a concern. Conservative fuid administration with crystalloid solution is recommended. Bullous fuids are considered only if patient is fuid responsiveness based on clinical, paraclinical and laboratory parameters such as passive leg raising and stroke volume variations. The aim of this review is to study fuid therapy in critically ill pediatric patients with COVID-19 Disease admitted to ICU.

Delayed leukopenia following intentional azathioprine ingestion

Background: Azathioprine is a purine analog metabolized to 6- mercaptopurine (6-MP) utilizing glutathione. Its high oral bioavailability and longer duration of action make it viable as a treatment for ulcerative colitis or as an anti-rejection medication for renal transplant patients. Specific experience in overdose with this agent is limited although toxicity mimics 6-MP including hepatotoxicity, delayed leukopenia, and acute interstitial nephritis. Case report: A 46 year old female (64 kg) with a history of ulcerative colitis, migraines, and anxiety presented with a selfreported intentional ingestion of 1000mg azathioprine and presented to care approximately 8 h post-ingestion. Her compliance with azathioprine preceding the ingestion was unclear. She reported taking her other medications as prescribed (tadalafil, sulfasalazine, fioricet, alprazolam) the day prior to presentation. Other than one episode of emesis without pill fragments, myalgias, headache she had no other symptoms. Her presenting vital signs were HR 84, RR 22, BP 90/63, T 36.2 degreeC. Initial labs included a normal chemistry profile, undetectable serum acetaminophen and salicylates, an ethanol level of 50 mg/dL and venous lactate of 1.6mmol/L. She received a total of 3 L of crystalloid IV fluids with improvement in blood pressure to 125/66 and was transferred for higher level of care. Due to the delay in presentation and well appearance, activated charcoal and hemodialysis were considered but deferred. While inpatient she had laboratory evaluation including CBC and differential every 8 h. In the ED she developed a fever, 38.1 degreeC. PCR testing for COVID-19 was negative. Whole blood thiopurine metabolites (Prometheus Biosciences, Test 3200) were sent approximately 33 h from time of ingestion. 6-thioguanine levels were 108 pmol/8x10degree8 RBC, below the therapeutic reference range (230-400 pmol/8x10degree8 RBC). 6-methylmercaptopurine metabolites were below the lower limit of quantification (761pmol/8x10degree8 RBC). Genetic testing for thiopurine S-methyltransferase was declined by the patient. She was hospitalized for 4 days and did not develop any substantial vital sign abnormalities or creatinine elevation. Her absolute neutrophil count dropped to 500/mm3 approximately 76 h post-ingestion, but started to improve 84 h post-ingestion and granulocyte-macrophage colony-stimulating factor was deferred. Her peak AST was 113 IU/L, approximately 46 h post-ingestion and returned to normal (16 IU/L) upon follow-up 7 days postingestion. White blood cell count 7 days post-ingestion was 4.3 K/mm3. Discussion(s): Azathioprine overdose is rarely reported in the literature. Case reports describe delayed leukopenia and hepatotoxicity from repeat supratherapeutic ingestions, however, based upon limited experience serious toxicity from single acute ingestions appears rare. A report of a single acute ingestion of 7500mg of azathioprine resulted in moderate leukopenia (4.1 K/ mm3) 3 days post-ingestion. Peak immunosuppressive effects can take up to 2 weeks from initiation or change in dose. Symptoms in this case are consistent with effects from azathioprine including vomiting, transient hypotension, and myalgias. Conclusion(s): Intentional ingestions of azathioprine are infrequently reported and can result in serious delayed myelosuppression. We report a case of a single acute ingestion of >15 mg/kg resulting in delayed myelosuppression managed conservatively.

Minimal recovery of drug from extracorporeal treatment in a case of phenytoin toxicity associated with coma and hypothermia

Background: The Extracorporeal Treatments in Poisoning (EXTRIP) workgroup provides a weak conditional recommendation in support of hemodialysis (HD) for select patients with severe phenytoin poisoning. Despite this recommendation, the HD clearance of phenytoin is poorly studied. We present a patient who developed phenytoin toxicity that was treated with hemodialysis and report on the efficacy of phenytoin removal during HD. Case report: An 87-year-old man with epilepsy who was maintained on a stable dose of 300mg phenytoin extended-release daily was admitted to the hospital for treatment of Coronavirus Disease 2019 and congestive heart failure. On hospital day 14, the patient had a gradual onset of depressed mental status with hypothermia (nadir 35 degrees Celsius). At this time, he had a rising total blood phenytoin concentration (peak 49.3 mcg/mL [therapeutic 10-20mcg/mL] with an albumin of 3.8 g/dL [normal 3.4-5.4 g/dL]). The patient's other medications included furosemide, aspirin, atorvastatin, digoxin, doxycycline, metoprolol tartrate, and warfarin;he was also receiving albumin and crystalloid for hypovolemia (albumin nadir on hospital day 14: 2.5 g/dL). Free phenytoin concentrations were not available. Alternate etiologies of hypothermia (endocrine, infectious) were excluded. The Poison Control Center was consulted and recommended HD because of the concern for prolonged coma, as per EXTRIP guidelines. The patient received three sessions of HD over a period of 6 days at 2.5-3 h per session using an F160 Optiflux membrane filter (Fresenius Medical Care, Waltham, MA, USA), with a blood flow rate of 350mL/min and a dialysate flow rate of 700mL/min. After the first session of HD (2.5 h) on hospital day 21, his hypothermia resolved and his phenytoin concentration fell from 39.2mcg/mL to 34.2 mcg/mL with only mild improvement in his mental status. After 6 days (hospital day 27), his phenytoin concentration decreased to 19.5 mcg/mL and his mental status normalized. Effluent from the first HD session had phenytoin concentrations below the limit of detection (0.50mcg/mL). Thus, no greater than 52mg of phenytoin was removed during a 2.5-h session of hemodialysis. Discussion(s): The reason for the sudden increase in blood phenytoin concentrations in this patient is unclear in the absence of drug-drug interactions or dosing changes to the phenytoin. Although uncommonly reported, patients with phenytoin toxicity can experience hypothermia. In this case, the patient's hypothermia resolved during HD, although it is unclear if this was related to changes in phenytoin concentration or (more likely) direct extracorporeal warming via the HD machine. If the patient's phenytoin clearance from the first session were extrapolated to subsequent sessions an estimated maximum of 166.4mg of phenytoin would be removed in 8 total hours of HD, which is far less than previously reported phenytoin clearances on the order of grams. This difference may be related to the use of high cutoff dialysis membranes in prior studies, which are not routinely used. Conclusion(s): Although HD rapidly resolved this patient's hypothermia, a minimal amount of phenytoin was recovered in the patient's dialysate. Prior studies suggesting consequential clearance and efficacy of phenytoin removal by extracorporeal treatment may not apply to routine HD methods. Further studies on the utility of extracorporeal treatment for phenytoin toxicity are needed.

COVID VACCINE-INDUCED RHABDOMYOLYSIS. A CASE OF RECURRENT RHABDOMYOLYSIS

CASE: A 46-year-old African-American female was evaluated for generalized body aches five days after receiving second dose of COVID mRNA-1273 (Moderna) vaccine. Six months prior, she received her first dose of Ad26 (Johnson & Johnson) vaccine without sequelae, Family history includes maternal systemic lupus erythematous. Patient has a history of cystic acne and, most notably, frequent episodes of muscle aches and weakness. In 2006 and 2016, patient was hospitalized for episodes of rhabdomyolysis after receiving influenza vaccine. Autoimmune myositis was ruled out. She has never received statin medication. In late 2017, she was admitted for rhabdomyolysis after upper respiratory tract infection. She reported dark urine but no rash or arthralgia. Patient had elevated CK 107,737 U/L, AST 379 U/L, and ALT 115 U/L. Her renal function, sed rate, TSH, HIV, influenza, direct Coombs, protein electrophoresis, and antinuclear antibodies were negative or within normal limits. She was treated with IV fluids, pain medication, and discharged. In her current admission for rhabdomyolysis, she presented with dark urine, CK 130,702 U/L, AST 692 U/L, ALT 208 U/L, and D-dimer 1,544 ng/mL. No acute renal injury was noted. Patient was treated with intravenous crystalloids and pain medication. CK and transaminases steadily trended down. Patient was discharged as she was asymptomatic and CK had dropped significantly. IMPACT/DISCUSSION: Rhabdomyolysis can be an adverse event to vaccine administration, most commonly influenza vaccination. Detection of SARS-CoV-2 inside skeletal muscle has not been documented. Reports on COVID- 19 vaccine-induced rhabdomyolysis focus on the type of vaccine the patient received, the number of doses that triggered the event, CK level, and presence of risk factors for developing rhabdomyolysis. Although no pathophysiologic mechanism has been established, several hypotheses exist to explain muscle damage including genetic factors, autoimmune reactions to the virus nucleic material, or external adjuvant. This has been described as autoimmune/inflammatory syndrome induced by adjuvants. Our patient had a history of recurrent episodes of rhabdomyolysis after receiving influenza and COVID immunizations, as well as viral infection. CONCLUSION: The mechanism of our patients' reaction is unknown. Reported cases support autoimmunity as the major risk factor for vaccinerelated rhabdomyolysis. This patient had elevated CK level on subsequent episodes of rhabdomyolysis fitting the pattern where a more exaggerated response of the immune system is observed every time patient is re-exposed to known insult. Genetic predisposition may also play a role. AfricanAmericans have higher prevalence of slow acetylation and carnitine palmitoyltransferase II deficiency, a disorder of fatty acid. The myopathic form presents with high CK values. Therefore, patients should be counseled to seek medical attention when symptoms occur and physicians should consider vaccination as a possible cause.

Undifferentiated Shock: A Case of Idiopathic Capillary Leak Syndrome

Systemic capillary leak syndrome (SCLS or Clarkson's disease) is a rare condition characterized by episodes of vascular hyperpermeability. The extravasation of plasma to the interstitial space results in hemoconcentration, hypoalbuminemia, hypovolemia and compartment syndrome of the extremities. The disease can be idiopathic or secondary to causes including viral infections or chemotherapeutic toxicity. We present a fatal case of idiopathic SCLS which rapidly deteriorated to multiple organ failure despite initial improvement with methylene blue. A 57-year-old male presented for worsening back pain over one month. He described a flulike illness 2 weeks prior. Testing for respiratory viruses including SARS-CoV-2 was negative. He received intravenous crystalloid fluids acutely developed respiratory distress and hypotension requiring emergent intubation and initiation of norepinephrine infusion. CT angiography of the chest demonstrated pulmonary edema. Early during his hospitalization urine output ceased and body weight increased by 10 kg, developing tense anasarca. Hematocrit concentrated from 42.7 to 54.4%. Serum albumin dropped from 4.6 to 2.5 g/dL. C1 esterase inhibitor level and IgM were normal. Ferritin was elevated at 2515 ng/ml. He received cefepime and vancomycin, though infectious workup returned unremarkable. Continuous renal replacement therapy and stress dose steroids were initiated. Vasopressor requirement worsened until he was on three vasopressors at one point. Given the constellation of hemoconcentration, hypoalbuminemia, and shock a diagnosis was made of idiopathic SCLS. Treatment was started with methylene blue, montelukast, and the β-adrenergic agonist terbutaline. Blood pressure improved and patient came off pressors and lactate improved from 13 to 4. However, he later developed rising creatine kinase continued to climb to >40,000 U/L. He developed rhabdomyolysis with concern for compartment syndrome of the extremities due to third spacing of fluids. Orthopedic surgery was consulted;but did not believe a fasciotomy was indicated due to rapid decline. Lactic acidosis rose to 18 mmol/L. His family decided to transition to comfort measures. He passed with family at bedside on Day 4 of hospitalization. There are fewer than 500 cases of SCLS reported since initial discovery in 1960. Given the overlap in presentation with common causes of plasma leakage such as sepsis, it is likely that many cases are unrecognized. Patients are often mismanaged;development of severe hypovolemia despite fluids and compartment syndrome is overlooked. This case builds on our evolving recognition of this disease, and the potential for the use of methylene blue to help acute exacerbations of the disease.

Effectiveness of ketofol versus propofol induction on hemodynamic profiles in adult elective surgical patients: A Randomized Controlled Trial

Background: Most of the time propofol and ketamine have been used as an induction agent in adult surgical patients but propofol may cause cardiorespiratory depression while ketamine increases heart rate and arterial blood pressure. On the other hand, the clinical effects of propofol and ketamine seem to be complementary. Ketofol is most commonly used for procedural sedation hence exploring its effectiveness for induction will be paramount for the clinical care of surgical patients. Objective: This study aims to compare the hemodynamic changes between ketofol and propofol within 30 min after induction of general anesthesia for elective surgical patients. Methodology: A Double-blind Randomized Controlled Trial was done on 62 patients aged between 18 and 65 years and the American Society of Anesthesiologist class I & II those have been allocated randomly into ketofol and propofol groups. A change in systolic blood pressure, mean arterial pressure, and heart rate within 30mins was followed for both groups. After the normal distribution of data was tested analytic statistics were calculated for variables in the study using Mixed ANOVA, Independent samples T-test, and Mann Whitney U test as appropriate, and for categorical data Chi-square test or fisher's exact test was used for analysis. P-value < 0.05 is considered statistically significant with a power of 90%. Results: Both the mean systolic blood pressure and mean arterial pressure were significantly decreased in the propofol group immediately after induction, at 5th minute, 10th minute, and 15th minute compared to the baseline value with a statistically significant value of (p < 0.05). There was a significant increase in mean heart rate in the ketofol group immediately after induction and on the 5th minute after induction compared to the baseline value (p = 0.001 and p = 0.022 respectively). Conclusion and recommendations: We conclude the administration of ketofol (0.75 mg/kg of ketamine and 1.5 mg/kg of propofol) for induction of general anesthesia has better hemodynamic stability than propofol during the first 30 min after induction. We recommend to researchers to do further randomize controlled trials, with invasive blood pressure measurement and multicenter study.

A Rare Case of Concurrent New-Onset Microscopic Polyangiitis and Thrombotic Thrombocytopenic Purpura in a 77-Year-Old Woman

Introduction: Microscopic polyangiits (MPA) is a rare ANCA-associated necrotizing vasculitis that affects the small vessels, often involving the lung or kidney. When presenting with diffuse alveolar hemorrhage, this disease warrants emergent treatment, often with plasma exchange. Here, we present a rare case of a patient presenting with alveolar hemorrhage in the setting of MPA and concurrent thrombotic thrombocytopenic purpura (TTP) with an extremely reduced ADAMTS13 activity. Case Report: A 77 y/o woman with HTN and PUD presented to outside facility with new onset anemia (Hb 6.3 g/dL). Positive Coombs test gave her a tentative diagnosis of hemolytic anemia, and she was transfused 2 U RBCs. Ten days later, she presented to our hospital with respiratory distress. Hb remained stable at 10.7 but had leukocytosis with WBC 22,000 with left shift, platelets 439. Vitals not consistent with sepsis though saturating 70-80% on room air. In the ED, she developed frank hemoptysis and was emergently intubated. CTA chest was negative for pulmonary embolus but demonstrated diffuse ground-glass opacities. COVID test negative. Bronchoscopy was consistent with diffuse alveolar hemorrhage (DAH), and she received tranexamic acid, crystalloids, 1 U RBCs. Suspicious for underlying vasculitic process, she was given pulse dose IV steroids (1 g methylprednisolone daily) and started plasma exchange. Creatinine on presentation was elevated at 1.77 but she continued to have adequate urine output and appropriate volume status. Her hospital course was marked by progressive thrombocytopenia with schistocytes appreciated on peripheral smear. ADAMTS13 activity <5% with inhibitor detected, consistent with TTP. Vasculitic workup revealed positive myeloperoxidase antibodies and p-ANCA consistent with MPA. Other rheumatologic workup ANA positive 1:640 and positive IgM cardiolipin antibodies;she had no personal autoimmune history but some family autoimmune disease including one daughter with systemic lupus erythematosus and another relative with Guillian-Barre. She remained intubated for 4 days and post-extubation experienced some short-lived ICU delirium but after made a remarkable recovery. She completed 12 total sessions of of plasma exchange and 3 of 4 planned doses of rituximab, to continue on oral steroids outpatient and prophylactic TMP-SMX. She was discharged to rehab facility on hospital day 20. Discussion: With diffuse alveolar hemorrhage on presentation, initial differential remained broad including delayed presentation of transfusion-related lung injury (TRALI) given recent history of transfusion. She had recently started hydralazine outpatient. Along with positive ANA, this could suggest drug-induced lupus. However, histone antibodies were negative, but results may have been compromised by steroids and plasma exchange. Both MPA and TTP can be deadly but are managed with similar treatment. Luckily, our patient was rapidly initiated on plasma exchange following hospitalization. Although further workup including ADAMTS13 and vasculitis labs were pending at the time, it is important to not delay treatment while awaiting results. Cased of concurrent TTP and ANCA-associated vasculitis have been described in the literature, but the full relationship between these two entities remains unclear. TTP may develop after starting glucocorticoids in the setting of ANCA vasculitis, so close monitoring is recommended. Disclosures: No relevant conflicts of interest to declare.

Ultrasound in CoViD-19 not only for the lung: work-up of a case of acute kidney injury

Background: Acute kidney failure (AKI) is not an infrequent complication of CoViD 19 infection, especially in severe forms. Several pathogenic mechanisms could provoke AKI in CoViD 19: some aspecific (dehydratation, post-renal, rhabdomyolisis), other directly related to virus toxicity (tubulopathy, endothelial damage, coagulopathy), other to immune response. Ultrasound findings in AKI in CoViD 19 are poorly reported in literature at this moment and could help in diagnostic workup. Description of clinical case: A 72-year old hypertensive man born in Senegal was admitted for respiratory failure from CoViD-19, requiring NIV support. Starting creatinine levels slightly elevated (1,25 mg/dl) rapidly grew in the next days (2,74 mg/dl), although adequate crystalloid support;micro-hematuria and glycosuria were present with absence of relevant proteinuria;glycemic levels were high and HBA1c (7%) revealed previous diabetes. Ultrasound reveals normal dimension kidneys with preserved parenchymal thickness, but diffused hyper-echogenicity;Doppler study showed parenchymal IR in the upper range of normality (0,67-0,70). Renal function gradually improved with respiratory condition and patient was discharged 28 days after admission. Conclusions: AKI in CoViD-19 has relevant prognostic implications and ultrasound evaluation could inform about previous nephropathy, current renal damage and prognostic prevision through measurement of parenchymal IR, known to be related in several AKI conditions with prognosis and reversal of AKI condition.

Physical compatibility of Normosol-R with critical care medications used in patients with COVID-19 during simulated Y-site administration.

PURPOSE: Guidelines from the National Institutes of Health support the use of balanced crystalloid solutions such as Normosol-R (Hospira, Lake Forest, IL) for patients with coronavirus disease 2019 (COVID-19). However, their clinical utility is hindered by a lack of Y-site compatibility data that is essential for use in patients with limited intravenous access. The objective of this study was to determine the physical compatibility of selected intensive care unit medications with Normosol-R. METHODS: The study involved laboratory simulation of Y-site compatibility. Medications tested included amiodarone, caspofungin, dexmedetomidine, dobutamine, dopamine, epinephrine, levofloxacin, norepinephrine, pantoprazole, phenylephrine, piperacillin/tazobactam, vancomycin, and vasopressin. Tests performed were visual assessment with Tyndall light, turbidity measurement, and pH assessment. Tests were performed immediately after mixing (with the exception of turbidity testing) and after 1 hour and 4 hours. RESULTS: Incompatibility was defined as observation of haze, gas, particulate, or color change or admixture turbidity above 0.3 or above 0.5 nephelometric turbidity unit (NTU), depending on whether the baseline turbidity was less than or greater than 0.5 NTU, respectively. Analysis of solubility and compatibility based on change from baseline to admixture pH in relation to the reported -log of the acid dissociation constant (pKa) was performed. There was no evidence of visual incompatibility for any of the admixtures when mixed with Normosol-R. Turbidity exceeded the defined threshold with pantoprazole, phenylephrine, and highly concentrated norepinephrine. Pantoprazole was the only test medication with a significant pH change when compared to its pKa. CONCLUSION: Normosol-R is compatible for Y-site administration with all tested medications except for pantoprazole, phenylephrine, and highly concentrated norepinephrine, allowing for potential increased use in patients with COVID-19.