Refractory Metabolic Acidosis Research Articles

Prognostic Factors in Children with Acute Kidney Injury Requiring Continuous Renal Replacement Therapy

Introduction: This study aimed to evaluate prognostic factors and outcomes in a single-center PICU cohort that received continuous renal replacement therapy (CRRT). Methods: This retrospective study analyzed clinical characteristics, laboratory data, and outcomes. Ninety-day mortality and advanced chronic kidney disease (CKD) (eGFR <60 mL/min/1.73 m2) were defined as primary and secondary outcomes, respectively. Results: Seventy-five patients were enrolled, all of whom received CRRT for indications including acute kidney injury with complicated refractory metabolic acidosis, electrolyte derangement, and existed or impending fluid overload. The 90-day mortality and advanced CKD were 53% and 29%, respectively. Multivariate Cox regression analysis demonstrated that only underlying bone marrow transplantation (BMT) (HR 4.58; 95% CI: 2.04–10.27) and a high pSOFA score (HR 1.12; 95% CI: 1.01–1.23) were independent risk factors for 90-day mortality. Among survivors, ten developed advanced CKD on the 90th day, and this group had a higher serum fibrinogen level (OR 1.01; 95% CI: 1.01–1.03) at the start of CRRT. Conclusion: In critically ill children with AKI requiring CRRT, post-BMT and high pSOFA scores are independent risk factors for 90-day mortality. Additionally, a high serum fibrinogen level at the initiation of CRRT is associated with the development of advanced CKD.

Persistent pulmonary hypertension of the newborn due to methylmalonic acidemia: a case report and review of the literature

BackgroundPersistent pulmonary hypertension of the newborn manifesting with refractory and severe cyanosis is the consequence of high pulmonary vascular resistance causing extrapulmonary right-to-left shunt. Acidosis and hypoxemia produce pulmonary vasoconstriction. Persistent pulmonary hypertension of the newborn occurs due to numerous disorders and has been rarely reported as a manifestation of methylmalonic acidemia. We report a newborn with methylmalonic acidemia who presented with persistent pulmonary hypertension of the newborn.Case presentationA 1-day-old Iranian girl presented with respiratory distress and refractory metabolic acidosis. She was born at 39 + 5 weeks gestational age with Apgar scores of 8 and 9 in the 1st and 5th minutes, respectively, and was in good condition up to 10 hours of life. After that, she presented with cyanosis, tachypnea, retraction, and hypotonia. Despite receiving oxygen, she had low oxygen saturation. Echocardiography revealed severe pulmonary hypertension and right-to-left shunt through patent ductus arteriosus and foramen ovale. Her acidosis worsened despite receiving full support and medical therapy. So, she was started on peritoneal dialysis. Unfortunately, she did not respond to treatment, and after she had died, biochemical tests confirmed methylmalonic acidemia.ConclusionPersistent pulmonary hypertension of the newborn is a very rare manifestation of methylmalonic acidemia. Severe inborn errors of metabolism may cause irreversible damage with adverse lifelong morbidity, and early diagnosis may help to prevent such complications. Furthermore, diagnosis of these disorders aids in prenatal diagnosis through the use of cultured amniocytes or chorionic villi to detect gene mutations, as well as biochemical analyses of amniotic fluid for subsequent pregnancies.

Persistent acidosis and chronic kidney disease in a patient with type 1 glycogen storage disease.

Type 1 glycogen storage disease (GSDI) is a rare autosomal recessive disorder caused by glucose-6-phosphatase (G6Pase) deficiency. We discuss a case of a 29-year-old gentleman who had GSDI with metabolic complications of hypoglycemia, hypertriglyceridemia, hyperuricemia, and short stature. He also suffered from advanced chronic kidney disease, nephrotic range proteinuria, and hepatic adenomas. He presented with acute pneumonia and refractory metabolic acidosis despite treatment with isotonic bicarbonate infusion, reversal of hypoglycemia, and lactic acidosis. He eventually required kidney replacement therapy. The case report highlights the multiple contributing mechanisms and challenges to managing refractory metabolic acidosis in a patient with GSDI. Important considerations for dialysis initiation, decision for long-term dialysis modality and kidney transplantation for patients with GSDI are also discussed in this case report.

Alpha Lipoic Acid Toxicity: The First Reported Mortality in an Adult Patient After Multiorgan Failure

BackgroundAlpha lipoic acid (ALA) is an anti-oxidant found in many over-the-counter supplements and is used in treatments for diabetes, hypertension, and obesity. Although it is a safe oral molecule, there have been eight cases of ALA toxicity reported. Three reported cases were among adult patients and five were among pediatric patients. A 14-year-old girl died after ingestion of 6 g of ALA leading to multi-organ failure. Case ReportA 42-year-old woman presented to the emergency department 4 h after an intentional overdose of 10 tablets of ALA 600 mg each (6 g, 92.3 mg/kg). She developed refractory seizures, metabolic acidosis, thrombocytopenia, rhabdomyolysis, depressed cardiac contractility, kidney injury, and supraventricular tachycardia. Her condition deteriorated and she developed multi-organ failure. The patient was started on dual pressors, anti-epileptic medications, high-dose insulin and euglycemia protocol, and methylene blue (1 mg/kg). Despite aggressive resuscitation, she required intubation and died. Why Should an Emergency Physician Be Aware of This?This was the ninth case and the first reported adult mortality from ALA toxicity with multi-organ failure. Our case shared some similar findings with previously reported cases, including refractory seizures, metabolic acidosis, thrombocytopenia, and rhabdomyolysis. Refractory supraventricular tachycardia and severe agitation have not been reported with ALA toxicity previously. The range of toxicity of ALA is not well established. A reported dose of 6 g caused death in a pediatric patient as well as our patient, but others survived doses of 6 g and 18 g. Toxicologists and emergency physicians should be prepared for clinical deterioration and consider aggressive resuscitation in severe ALA toxicity.

Metastatic mixed VIPoma/PPoma-induced diarrhoea causing renal failure.

SummaryVasoactive intestinal peptide-secreting tumours (VIPomas) are an extremely rare form of functional pancreatic neuroendocrine tumour with an estimated annual incidence of 1 in 10 million. Associated tumour hypersecretion of other peptides, including pancreatic polypeptide (PPomas), may also be seen. These malignancies classically present with a defined triad of refractory diarrhoea, hypokalaemia and metabolic acidosis known as Verner–Morrison syndrome. Diagnosis is frequently delayed, and the majority of patients will have metastatic disease at presentation. Symptoms are usually well controlled with somatostatin analogue administration. Here we report a case of metastatic mixed VIPoma/PPoma-induced diarrhoea causing renal failure so severe that ultrafiltration was required to recover adequate renal function.Learning pointsProfuse, watery diarrhoea is a common presenting complaint with a multitude of aetiologies. This, combined with the rarity of these tumours, makes diagnosis difficult and frequently delayed. A functional neuroendocrine tumour should be suspected when diarrhoea is unusually extreme, prolonged and common causes have been promptly excluded.These patients are likely to be profoundly unwell on presentation. They are extremely hypovolaemic with dangerous electrolyte and metabolic abnormalities. Aggressive initial rehydration and electrolyte replacement are imperative. A somatostatin analogue should be commenced as soon as the diagnosis is suspected.This is an extreme example of Verner–Morrison syndrome. We are unaware of another case where renal failure secondary to diarrhoea and dehydration was so severe that renal replacement therapy was required to restore adequate renal function, further emphasising how critically unwell these patients can be.Both the primary tumour and metastases showed a remarkably good and rapid response to somatostatin analogue administration. Cystic change and involution were noted on repeat imaging within days.Prior to his illness, this patient was extremely high functioning with no medical history. His diagnosis was an enormous psychological shock, and the consideration and care for his psychological well-being were a crucial part of his overall management. It highlights the importance of a holistic approach to cancer care and the role of the clinical nurse specialist within the cancer multidisciplinary team.

A Term Neonate with Multiorgan Dysfunction, Severe Metabolic Acidosis, and Hyperkalemia.

A Term Neonate with Multiorgan Dysfunction, Severe Metabolic Acidosis, and Hyperkalemia.

Vasoactive intestinal peptide secreting tumour: An overview.

Vasoactive intestinal peptide (VIP) secreting tumour (VIPoma) is a rare functional neuroendocrine tumour that typically arises from pancreatic islet cells. These present as sporadic, solitary pancreatic neoplasias with an estimated incidence of one in ten million individuals per year. Only around 5% of VIPomas are associated with multiple endocrine neoplasia type I syndrome. Excessive VIP secretion produces a clinical syndrome characterized by refractory watery diarrhoea, hypokalemia and metabolic acidosis. These coupled with elevated plasma levels of VIP are diagnostic. The majority of VIPomas are malignant and have already metastasized at the time of diagnosis (60%). Metastases occur most frequently in the liver, or regional lymph nodes, lungs, kidneys and bones. Some reports of skin metastases have been documented. Complete surgical resection continues to be the only potentially curative treatment. However, when the neoplasia cannot be excised completely, surgical debulking may provide palliative benefit. Other palliative options have included recently the peptide receptor radionuclide therapy which has shown to be effective and well-tolerated. This article will review all aspects of pancreatic VIPomas highlighting aspects such as clinical presentation, diagnosis and management.

Blocking vicious cycle of cardiac dysfunction by external cardiopulmonary resuscitation is the key to rescue acute aluminium phosphide poisoning.

Aluminium phosphide (ALP) and aluminium zinc phosphide (ZnP), the two main ingredients of fumigation drugs, are commonly used to kill insects or rodents in grain. When exposed to water, highly toxic phosphine gas is released and absorbed through the respiratory or digestive tract. Phosphine gas could non-selectively block cytochrome oxidase, inhibit electron transfer and suppress oxidative phosphorylation, leading to cellular hypoxia and organ dysfunction. The characteristic clinical manifestations are refractory shock and metabolic acidosis with high mortality. However, patients with ALP poisoning have a chance to be cured. Here, we report a case of oral ALP poisoning that was successfully treated by extracorporeal membrane oxygenation (ECMO) combined with continuous renal replacement therapy (CRRT) during frequent ventricular fibrillation and cardiac dysfunction.

IN-HOSPITAL MORTALITY OF ACUTE KIDNEY INJURY: AN EXPERIENCE FROM SOUTH RAJASTHAN.

INTRODUCTION: There are few studies on in-hospital mortality among medical intensive care unit (MICU) patients with acute kidney injury (AKI). We assessed the clinical characteristics of AKI at MICU admission, its impact on mortality during the current hospitalization, and whether the inuence of AKI varied in subgroups of AKI patients. METHODS: We identied all adult aged 12 years and above having medical etiology related community acquired AKI who were admitted to MICU at Pacic Medical College and Hospital, Udaipur, India; from 2015 to 2019. AKI was dened based on the Kidney Disease Improving Global Outcomes (KDIGO) criteria; based on serum creatinine (SCr). Dialysis requiring AKI (D-AKI) was dened as needing acute dialysis at or after MICU admission. Among 2440 MICU patients; 516 patients (21.1%) had AKI. We analyzed in-hospital mortality for subgroups of AKI: stage1, stage2 and stage3: with different etiology, comorbidity levels, acute risk factors, primary hospital diagnosis, and treatment with mechanical ventilation, vasopressors and dialysis. RESULTS: Maximum number of AKI patients (57.8%) were in KDIGO Stage3, while stage1 and stage2 had 17.8% and 24.4% respectively. 51.4% patients were male, median age was 54.81 years and average length of ICU stay was 11.73 days. The most common primary diagnosis and etiology was sepsis (31.4%), the most common acute risk factor was hypovolemia (18.8%), the common chronic comorbidity were diabetes (17.0%) and hypertension (10.0%). The most common presenting symptoms was oliguria (43.8 %), while commonest sign on admission was edema (28.1%). Common indications for dialysis were oliguria (75%), hyperkalemia (38.2%), refractory uid overload (36.2%) and metabolic acidosis (35.2%). Overall common critical care treatment required in AKI patients were acute dialysis (58.9%), vasopressor support (16.5%) and ventilator support (14%). The requirement of dialysis was 0.0%, 4.8% and 100%; among stage1, stage2 and stage3 respectively. The overall AKI mortality was 9.9% (95% condence interval (CI) 7% to 12% ). The associations between AKI and mortality were 10.87% (95% CI 5% to 17%) for the AKI-stage1, 13.49% (95% CI 8% to 19% ) for the AKI-stage2 and 8.05% (95% CI 5% to 11%) for the AKI-stage3. The mortality in D-AKI group was 8.6% (95% CI 5 % to 12 %) compared to the mortality in ND-AKI group 11.8% (95% CI 7 % to 16 %). The association between AKI and in-hospital mortality was evident in all subgroups of AKI; association was more pronounced in stage2 AKI, mostly due to worsening of complications which suggests that KDIGO stage2 AKI is a transition zone among D-AKI and ND-AKI groups. Further, it may be needed to lower the threshold for dialysis criteria in AKI. CONCLUSIONS: Any degree of AKI was associated with increased mortality. Timely and early initiation of dialysis in AKI was an important prognostic factor for the reduction of in-hospital mortality.

COVID-19 Infection with Refractory Diabetic Ketoacidosis- A case Report

Diabetic ketoacidosis is an acute life-threatening complication of type 1 diabetes. Sometimes it is the first presentation in an undiagnosed child. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) and diabetes mellitus are very much interrelated as diabetes mellitus is associated with an increased risk of severe COVID19 at the same time, many cases of new-onset diabetes had been diagnosed. Hyperglycemia, metabolic acidosis, and ketonemia are classical presentations. It is essential to correct the acidosis and fluid correction and insulin therapy in these patients, leading to vital organ dysfunction. In refractory metabolic acidosis, renal replacement therapy may help

Succinyl-CoA: 3-Ketoacid CoA-Transferase Deficiency in a Saudi Girl

Objective: Succinyl-CoA:3-ketoacid CoA transferase (SCOT) deficiency is a rare genetic disorder of ketone utilization and isoleucine catabolism caused by mutations in the OXCT1 gene,&#x0D; Case: A Saudi girl case of SCOT deficiency confirmed by genetic analysis has been reported in this study. A 5-year-old girl presented to the emergency with the first episode of severe metabolic ketoacidosis after a febrile illness. On admission, she was drowsy lethargic, and severely dehydrated needs to admit in a highly dependent area. Initial investigations were done during the crisis showed refractory severe metabolic acidosis (pH of 7.18, HCO3- of 7.4 mmol/L), normal ammonia, lactic acidosis, and urine organic acid profile revealed elevations in 3-hydroxybutyrate and acetoacetate. Genetic analysis was done by CentoMito Comprehensive (Large extended screening panel), sequencing of OXCT1 gene revealed that the proband is homozygous for the missense likely pathogenic variant c.1402C&gt;T p.(Arg468Cys) confirming the diagnosis of SCOT deficiency.&#x0D; Conclusion: This is the first Saudi child with succinyl-CoA:3-ketoacid CoA transferase (SCOT) deficiency case report as searched in the literature. This case highlights the importance of suspecting SCOT deficiency in the differential diagnosis of pediatric metabolic ketoacidosis in preventing life-threatening of severe Metabolic ketoacidosis

228 Unique Case of Refractory Metabolic Acidosis in Continuous Kidney Replacement Therapy

228 Unique Case of Refractory Metabolic Acidosis in Continuous Kidney Replacement Therapy

A woman with abdominal pain while being treated with steroid

Introduction/Background Saccharomyces cerevisiae is a yeast of the phylum Ascomycota which can be used in food production. It has rarely been mentioned in the literature as a cause of human disease. Various types of infections have been reported, primarily bloodstream infections. Whether Saccharomyces is a cause of true infection in other sites as compared to a culture contaminant is controversial, as it is considered a normal part of the gastrointestinal (GI), vaginal, and respiratory mucosal flora. The main risk factors for infection with Saccharomyces are immunodeficiency including chemotherapy, history of a central venous catheter, gastroenterological surgery, and use of antibiotics or probiotics. We present the case of an 80-year-old woman who, after five days of dexamethasone treatment for COVID-19 pneumonia, presented with worsening abdominal pain. The patient was diagnosed with perforated diverticulitis, complicated by Saccharomyces cerevisiae fungemia. We will discuss the management of Saccharomyces cerevisiae fungemia and other infections to highlight the difficulty in management and high mortality risk associated with similar infections. Case Presentation An 80-year-old woman with no known medical history was admitted for COVID-19 pneumonia and hypoxia, for which she required four liters of oxygen. She was initially treated with dexamethasone, remdesivir, cefepime, and azithromycin. On the fifth day of hospitalization, she developed acute generalized abdominal pain. Computed tomography of the abdomen and pelvis (figure 2) showed pneumoperitoneum, sigmoid versus terminal ileum perforation, and two abscesses (measuring 5.5 cm and 8 cm in the largest diameters) in the pelvis. Surgical team recommended non-operative management. On days eight and ten of illness, blood cultures were obtained and grew Saccharomyces cerevisiae. Piperacillin-tazobactam was started for empiric GI coverage. Micafungin was started when yeast was identified in blood cultures and was subsequently switched to oral voriconazole once the yeast was identified as Saccharomyces. Blood cultures cleared four days after first positive. Due to persistently worsening leukocytosis, an exploratory laparotomy with sigmoidectomy and end colostomy was performed on day twelve of hospitalization. Intraoperative diagnosis of Hinchey stage IV diverticulitis (diverticulitis with generalized fecal peritonitis) was made. A drain was placed, and cultures from the abscess fluid grew Saccharomyces cerevisiae. In addition to the Saccharomyces isolate, a Mucor species grew in the abscess culture after four days, and the patient was transitioned to liposomal amphotericin B. Two days after amphotericin was started, the patient developed acute encephalopathy to the point where she was non-responsive to pain, believed to be secondary to amphotericin B neurotoxicity. She required transfer to a surgical intensive care unit. Liposomal amphotericin B was changed to intravenous posaconazole. Within 48 hours of stopping amphotericin, the patient's mental status showed moderate improvement and she was disoriented but conversive. She then developed refractory hypoxia and progressive kidney dysfunction, and ultimately required intubation and continuous renal replacement therapy. Surgical team questioned posaconazole as a cause for her worsening renal function, and she was subsequently switched to intravenous Isavuconazole. The patient continued to decline, requiring vasopressor support. She developed refractory metabolic acidosis and lactic acidosis, and hypoxia uncorrected with maximum ventilatory support. The patient's family requested to transition to comfort measures, and the patient expired on day 21 after initial COVID-19 admission. Discussion In one study, Saccharomyces cerevisiae was considered one of the nosocomially acquired infections. It has been reported to cause an average of 1.7% of all fungal cases. Our patient developed Saccharomyces cerevisiae after evidence of diverticulitis complicated by bowel perforation in the setting of being treated with broad-spectr m antibiotics and while not being known to use probiotics. Various types of GI infections have been reported in Saccharomyces cerevisiae, including esophagitis, peritonitis, liver abscess and a link to Crohn's disease, where antibodies to Saccharomyces cerevisiae are a sensitive and specific test. A key element in the management of Saccharomyces cerevisiae is the removal of the infected foreign bodies and the purification of the source. There are no guidelines for dealing with Saccharomyces cerevisiae infections, it is well known that it is susceptible to amphotericin B. Several different types of azole drugs have been investigated, resistance to itraconazole and fluconazole have been reported. Better susceptibility Results were observed with voriconazole and posaconazole. The mortality rate of Saccharomyces cerevisiae fungemia remains high and was reported in one study as 29.5%. Saccharomyces cerevisiae fungemia is a rare, lifethreatening disease with no clearly defined treatment guidelines. Further studies are needed to better understand the therapeutic antifungals options. (Table Presented).

Bi-atrial thrombosis in a patient with SARS-CoV-2 infection: a case report.

BackgroundCoronavirus disease 2019 (COVID-19) is a rapidly spreading pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It is a multisystemic disease associated with micro- and macrovascular thrombo-embolic complications, including intracardiac thrombosis, which has not been previously reported in the literature.Case summaryWe report a case of a 68-year-old woman with COVID-19 admitted to our intensive care unit with acute respiratory distress, undifferentiated shock, hyperkalaemia, acute kidney injury, and coagulopathy. She received crystalloid infusion, broad-spectrum antibiotics, hydroxychloroquine, insulin–dextrose, calcium gluconate, sodium bicarbonate, and i.v. vasopressors. Continuous renal replacement therapy (CRRT) was started for refractory hyperkalaemia and metabolic acidosis. Transthoracic echocardiogram obtained for concern of pulmonary embolism found bi-atrial thrombosis with normal bi-ventricular dimensions and function. Systemic anticoagulation was provided, but this was stopped soon afterwards due to worsening coagulopathy and bleeding. Despite intensive measures and supportive therapy, the patient developed worsening hypoxia, refractory shock, and multiorgan failure. After discussion of goals of care with her family, a decision was made to initiate hospice care. The patient died within 72 h of hospital admission.DiscussionInfection with SARS-CoV-2 is a multisystemic disease that primarily affects the lungs, but also predisposes to rare thrombo-embolic phenomena such as intracardiac thrombosis.

MEDICATION INTERACTIONS CAUSING INSIDIOUS DIGOXIN TOXICITY IN AN ADVANCED HEART FAILURE PATIENT

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Although digoxin use has declined, its per patient toxicity incidence perhaps has not. Digoxin toxicity should be considered early in the patient presenting with gastrointestinal symptoms as they are at risk for renal dysfunction that may worsen cardiac function. CASE PRESENTATION: A 77-year-old male with a history of diabetes mellitus, atrial fibrillation, coronary artery disease, and ischemic cardiomyopathy presented with nausea, vomiting, diarrhea, and generalized fatigue worsening for one month. Presenting vitals: BP 80/60 mmHg, HR 60 bpm, temp. 34.2 C and pulse ox 99%. The patient was fully alert and oriented. Physical exam was largely unremarkable with clear lung exam, non-tender abdomen, no peripheral edema, and cardiac exam showing regular rhythm at 60 bpm. Labs showed K of 6 mmol/L, BUN of 79 mg/dL, Cr of 4.40 mg/dL, LA of 8.0 mmol/L, BNP 42000 pg/mL, and a normal CBC. Medication review significant for digoxin, amiodarone, and metformin use. Subsequently, digoxin level was found to be 6.0mcg/L and EKG showed ventricular paced rhythm. Given digoxin toxicity with hyperkalemia, digibind was administered. Patient was also found to have refractory metabolic acidosis in the setting of metformin toxicity, and so emergent sustained low efficiency dialysis was initiated. Right heart catheterization demonstrated low output heart failure, cardiac index 1.8L/min on dobutamine and norepinephrine. This low output was likely related to his renal failure and medication toxicities. The patient was sustained on inotropic agents and his pacemaker rate was increased. The patient had an aortic balloon pump placed while he and his family considered LVAD. Ultimately, the patient sustained further clinical deterioration at which time he and his family chose to pursue comfort measures. DISCUSSION: Advance heart failure is a challenging insidious disease. This is compounded by the fact that its treatments carry significant toxicities. In our case, the patient had recently reinitiated his prior amiodarone prescription. Both the prior medication discontinuation and subsequent re-initiation were unknown to his medical providers. The increase in digoxin levels when administered with amiodarone has long been observed and described. Digoxin toxicity presents with gastrointestinal symptoms as seen in our patient. Prolonged poor intake placed him at risk for renal dysfunction and perhaps subsequent worsening of his cardiac function due to the bidirectional relationship of cardiorenal syndrome. Frequent monitoring of digoxin levels is necessary in this patient population. Medication toxicities, interactions, and reconciliation are critical pieces of information in the critically ill patient. CONCLUSIONS: Drug interactions, such as the increase in serum digoxin when co-administered with amiodarone, can lead to the worsening of renal function which in the advanced heart failure patient, portends a poor prognosis. Reference #1: Haynes K, Heitjan D, Kanetsky P, Hennessy S. Declining public health burden of digoxin toxicity from 1991 to 2004. Clin Pharmacol Ther 2008;84:90-4. 10.1038/sj.clpt.6100458 Reference #2: Koonlawee Nademanee, et al. Amiodarone-digoxin interaction: Clinical significance, time course of development, potential pharmacokinetic mechanisms and therapeutic implications, Journal of the American College of Cardiology, Volume 4, Issue 1, 1984, Pages 111-116, ISSN 0735-1097. Reference #3: Forman DE, Butler J, Wang Y, Abraham WT, O’Connor CM, Gottlieb SS, Loh E, Massie BM, Rich MW, Stevenson LW, Young JB, Krumholz HM: Incidence, predictors at admission, and impact of worsening renal function among patients hospitalized with heart failure. J Am Coll Cardiol 43: 61–67, 2004 DISCLOSURES: No relevant relationships by Dustin Slagle, source=Web Response

SEVERE LACTIC ACIDOSIS CAUSED BY INGESTION OF AN UNKNOWN METFORMIN-LIKE SUBSTANCE

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Lactic acidosis is the major toxicity associated with metformin. It is a rare condition with 4.3 cases per 100,000 patient years and high mortality of 45%. This condition is most likely to occur in patient with comorbidities such as renal insufficiency, liver disease or heart failure. CASE PRESENTATION: 57-year-old male with past medical history significant for poorly controlled diabetes mellitus, CKD stage IV, hypertension and hyperlipidemia presents with nausea, vomiting, diarrhea and diffuse abdominal pain. Labs were remarkable for leukocytosis, high anion gap with severe metabolic acidosis (pH <6.82, CO2 33.3, HCO3 6, O2 87.3, AG 33), severe lactic acidosis 14, hyperkalemia 7.8, Cr 4.1, BUN 63. Urine and serum toxicology were unrevealing including volatile alcohols and metformin levels were negative. CT abdomen showed wall thickening of the small bowel suggesting of possible enteritis. As bowel ischemia was high on the differential diagnosis he underwent an exploratory laparotomy which ruled out this diagnosis. The patient was then started on antibiotics due to suspicion of sepsis, as well as IV hydration and sodium bicarbonate drip due to severe acidosis. Due to refractory metabolic acidosis and worsening kidney functions the patient underwent 2 sessions of emergent hemodialysis. After that the patient showed significant improvement and was transferred from the ICU to the medical floor. Upon further investigation, the patient’s wife revealed that he was given an unidentified Vietnamese medication for his diabetes by an acquaintance 3 days prior. We believe this medication to have similar properties to metformin. DISCUSSION: The mechanism of metformin-associated lactic acidosis is complex. It is associated with the inhibition of mitochondrial respiratory cycle and converts glucose to lactate in the small intestine. Metformin serum levels do not correlate with the severity of disease or patient outcome. It is important to have high clinical suspicion especially in patients with renal failure. Due to its high mortality rate, it is crucial to proceed with emergent hemodialysis as early as possible CONCLUSIONS: We present a case of severe lactic acidosis due to ingestion of an unknown over the counter medication. High clinical suspicion is needed to identify such cases early on in the course of the disease to initiate appropriate treatment. Reference #1: https://www.uptodate.com/contents/metformin-poisoning?search=metformin%20metabOLIC%20ACIDOSIS&source=search_result&selectedTitle=1∼150&usage_type=default&display_rank=1#H18 DISCLOSURES: No relevant relationships by Karim Anis, source=Web Response No relevant relationships by Lady Sanchez Fernandez, source=Web Response No relevant relationships by Magdi Zordok, source=Web Response

RARE CAUSE OF FATAL LIVER DISEASE: A CASE OF ACUTE LIVER FAILURE IN A PATIENT WITH RECENTLY DIAGNOSED METASTATIC OVARIAN CARCINOMA

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Metastatic liver disease is a relatively common finding in autopsies of adults with aggressive tumors. In a majority of cases, affected patients do not have signs or symptoms of liver failure. CASE PRESENTATION: A 41-year-old previously healthy Caucasian female presented to our ED with worsening abdominal pain and shortness of breath. Her symptoms started about a week prior to the ED visit. Her PCP ordered a CT scan of chest, abdomen, and pelvis which showed an ovarian mass concerning for carcinoma with multiple hepatic and pulmonary metastases. In the ED, vital signs were normal. A distended non-tender abdomen was appreciated during the physical exam. Laboratory workup revealed leukocytosis (WBC 31.1K/UL), abnormal LFTs (AST 1525U/L, ALT 396U/L, bilirubin 3.6MG/DL, alkaline phosphatase 366U/L), renal failure (Crea 1.76MG/DL, BUN 47MG/DL), elevated lactic acid (8.1MEQ/L), INR (1.6). A repeat CT scan of the chest, abdomen, and pelvis was unchanged. The patient was started on broad-spectrum antibiotics. On day 2, the patient was noted to have the worsening of liver function (AST 4652U/L and ALT 907U/L) as well as the development of respiratory failure. She was placed on BiPAP for increased work of breathing. She was started on CRRT for refractory metabolic acidosis and the worsening of renal failure. On day 3, the patient became confused with visible jaundice, asterixis, worsening of LFTs with AST and ALT (20845U/L and 2441U/L, respectively), elevated ammonia level as well as coagulopathy. Her MELD score was 46. Unfortunately, the patient suffered a cardiac arrest (PEA) twice within an hour with ROSC. The family made the decision to proceed with the withdrawal of care. The patient expired soon after that. DISCUSSION: Acute (also known as fulminant) liver failure is characterized by severe acute liver dysfunction (INR ≥1.5 and hepatic encephalopathy) in the absence of preexisting liver disease within less than 26 weeks. The two most common causes of acute liver failure are viral and drug-induced hepatitis. Malignant infiltration is a rare cause of liver failure which has been increasingly recognized in recent years. Patients with acute liver failure in the setting of metastatic liver disease have a very poor prognosis. CONCLUSIONS: In patients with signs and symptoms of acute liver failure, it is important to rule out metastatic liver disease as a potential etiology. Unfortunately, no definitive treatment is available at this point in affected individuals since liver transplant is contraindicated in patients with metastatic liver disease not meeting oncologic criteria for cure. Reference #1: Polson J, Lee WM. AASLD position paper: The management of acute liver failure. Hepatology. 2005;41(5):1179-1197. Reference #2: Nazario HE, Lepe R, Trotter JF. Metastatic breast cancer presenting as acute liver failure. Gastroenterology & hepatology. 2011;7(1):65. DISCLOSURES: No relevant relationships by Vincent Chan, source=Web Response No relevant relationships by Artem Minalyan, source=Web Response No relevant relationships by Qian Zhang, source=Web Response

Challenging Management of Refractory Metabolic Acidosis and Acute Kidney Injury in a Child with Diabetic Ketoacidosis.

ABSTRACTDiabetic ketoacidosis (DKA) is the most serious complication of type I diabetes mellitus (DM) in children. Majority of these patients respond to fluid resuscitation, insulin, and supportive measures and rarely require renal replacement therapy. Here, we report the case of a young girl with DKA with severe refractory metabolic acidosis and acute kidney injury (AKI) and was successfully managed with renal replacement therapy.How to cite this article: Jain R, Kumar P. Challenging Management of Refractory Metabolic Acidosis and Acute Kidney Injury in a Child with Diabetic Ketoacidosis. Indian J Crit Care Med 2020;24(6):475–476.

P0637SAFETY, EFFICACY AND OUTCOMES OF SLOW LOW EFFICIENCY DIALYSIS (SLED) IN CRITICALLY ILL PATIENTS WITH ACUTE KIDNEY INJURY (AKI) IN MEDICAL INTENSIVE CARE UNITS (ICU)- A PROSPECTIVE STUDY IN A TERTIARY CARE HOSPITAL IN INDIA

Abstract Background and Aims Slow low efficiency dialysis (SLED) is increasingly being used as a renal replacement therapy in hemodynamically unstable, critically ill patients with acute kidney injury (AKI). SLED may reduce intradialytic hemodynamic instability as compared with conventional intermittent haemodialysis, while reducing resource demands of continuous renal replacement therapies (CRRT). There are very few studies which have evaluated its safety, efficacy and outcome despite its increasing use, especially in Indian subcontinent. Method We conducted a single centre, prospective study to demonstrate safety, efficacy and outcome of SLED.. Net fluid removal and duration of SLED were based on need and hemodynamic status of the individual patient as decided by treating nephrologist. SOFA score was used as severity illness score. Efficacy of SLED was studied in terms of ability to achieve ultrafiltration goal, correction of acidosis and urea reduction ratio. Safety was studied in terms of hemodynamic and cardiovascular stability and complications during and after SLED. Outcomes were noted at time of discharge and six months later in terms of dialysis dependence, renal parameters (if dialysis independent) and mortality (In hospital and 6 months following discharge). We included hemodynamically unstable patients with AKI from medical ICUs with age &amp;gt;18 years of either gender. We excluded patients with AKI who could tolerate conventional haemodialysis or ESRD on maintenance haemodialysis. Results We analysed 228 patients with AKI in medical ICUs who underwent 576 SLED sessions over period of six months. Mean age was 57.48 ± 15.67 years and 74% (n=169) were male. Comorbidities were hypertension (56%), diabetes mellitus (43%), CKD (33%) and cardiovascular diseases (28%). Sepsis (93%) and hypoperfusion (68%) were most common causes for AKI. Refractory fluid overload (91%) and refractory metabolic acidosis (79%) were most common indications for SLED. Mean SOFA score was 12.2 ± 7.75 with 61 % patients had SOFA score more than 11. 66% were on mechanical ventilator. Out of 576 sessions, 555 sessions (96%) completed the planned duration without any adverse event. Planned ultrafiltration goal was achieved in 94%. SLED was able to correct metabolic acidosis in majority (86.1%). 68% SLED sessions required a vasopressor support and 34.8 % of SLED sessions were associated with hemodynamic instability. Total 14(6.2 %) patients died during SLED session. No documented arrhythmias developed after starting SLED. In-hospital mortality occurred in 61% patients. At 6 months follow up, another 13% patients died. In subgroup analysis, mortality was significantly higher in patients with SOFA score more than 11 (P&amp;lt;0.0001). Ventilatory requirement was also significantly high in non-survivors(P&amp;lt;0.0001). Univariate logistic regression analysis showed that inotropic requirement, higher SOFA severity score, acidosis with pH &amp;lt;7.25 and presence of underlying CKD were associated with significant mortality. Conclusion Our study demonstrated efficacy and safety of SLED in critically ill AKI patients in medical ICU. SLED was able to achieve planned ultrafiltration goal and correct metabolic acidosis in majority of patients. SLED had good hemodynamic tolerability. Mortality was noted in 61 % of patients (not attributable to SLED per se). High SOFA score, underlying co morbidities, vasopressor requirement and severe acidosis (pH &amp;lt;7.25) were associated with high mortality. SLED is a reasonable cost-effective option of RRT in hemodynamically unstable patients with AKI especially in developing countries.

Extracorporeal Membrane Oxygenation for Coronavirus Disease 2019 in Shanghai, China.

Severe cases of coronavirus disease 2019 (COVID-19) cannot be adequately managed with mechanical ventilation alone. The role and outcome of extracorporeal membrane oxygenation (ECMO) in the management of COVID-19 is currently unclear. Eight COVID-19 patients have received ECMO support in Shanghai with seven with venovenous (VV) ECMO support and one veno arterial (VA) ECMO during cardiopulmonary resuscitation. As of March 25, 2020, four patients died (50% mortality), three patients (37.5%) were successfully weaned off ECMO after 22, 40, and 47 days support, respectively, but remain on mechanical ventilation. One patient is still on VV ECMO with mechanical ventilation. The partial pressure of oxygen/fractional of inspired oxygen ratio before ECMO initiation was between 54 and 76, and all were well below 100. The duration of mechanical ventilation before ECMO ranged from 4 to 21 days. Except the one emergent VA ECMO during cardiopulmonary resuscitation, other patients were on ECMO support for between 18 and 47 days. In conclusion, ensuring effective, timely, and safe ECMO support in COVID-19 is key to improving clinical outcomes. Extracorporeal membrane oxygenation support might be an integral part of the critical care provided for COVID-19 patients in centers with advanced ECMO expertise.