Osmolal Gap Research Articles

HOW LOW CAN YOU GO: RECOVERY AFTER A SERUM PH OF 6.62 DUE TO ETHYLENE GLYCOL POISONING

HOW LOW CAN YOU GO: RECOVERY AFTER A SERUM PH OF 6.62 DUE TO ETHYLENE GLYCOL POISONING

A False-Positive Gamma-Hydroxy Butyric Acid Urine Screening in a Patient with High Anion Gap Metabolic Acidosis Due to Ethylene Glycol Poisoning.

A young woman with a history of several suicide attempts was admitted to the hospital after suspicion of a new intoxication without definite identification of the causing agent. The patient had a high anion gap metabolic acidosis (HAGMA) with respiratory compensation, a lactate gap and an osmolar gap at admission. Initial toxicological screening showed no abnormalities except for a weak positive gamma-hydroxy butyric acid (GHB) enzymatic screen in urine. This finding could not be confirmed using chromatographic analysis nor be explained by the presence of known cross-reacting substances like ethanol. In this case, falsely elevated urinary GHB screening was caused by the ingestion of ethylene glycol. To confirm that the interference was due to ethylene glycol or its metabolites, we performed a spiking experiment. Cross reactivity was linked to ethylene glycol and was low in our experiments (0.1-0.2%). Substantial amounts of ethylene glycol are required to slightly elevated GHB results, depending on the endogenous cutoff used. We can conclude that ethylene glycol can give rise to falsely elevated urinary GHB levels at ethylene glycol concentrations that are typically found in intoxications.

Elevated Anion Gap Metabolic Acidosis With High Osmolar Gap and Increased Serum Acetone Level: A Case Report

Acetone poisoning, although not very common, can present with varied signs and symptoms. High acetone levels in serum can be due to exogenous exposure or endogenous production of acetone. Unlike certain alcohol toxicities, acetone does not cause high anion gap metabolic acidosis.A 69-year-old male presented to our service with shock and acute encephalopathy and required intensive care support. Initial laboratory investigation showed high anion gap metabolic acidosis with high osmolar gap. Serum acetone level was elevated. Clinicians need to be aware of how to elucidate such metabolic disturbances and associated toxicities.

Distal renal tubular acidosis presenting with an acute hypokalemic paralysis in an older child with severe vesicoureteral reflux and syringomyelia: a case report

BackgroundDistal renal tubular acidosis (dRTA) is the most common type of renal tubular acidosis (RTA) in children. Pediatric dRTA is usually genetic and rarely occurs due to acquired issues such as obstructive uropathies, recurrent urinary tract infections (UTIs), and chronic kidney disease (CKD). Although persistent hypokalemia frequently occurs with dRTA, acute hypokalemic paralysis is not frequently reported, especially in older children.Case presentationAn eight-year-old girl presented with an acute first episode of paralysis. A physical examination revealed normal vital signs, short stature consistent with her genetic potential, and decreased muscle strength of her upper and lower extremities. Preexisting conditions included stage 4 CKD due to recurrent UTIs, severe vesicoureteral reflux and bilateral hydronephrosis, neurogenic bladder, and multisegment thoracic syringomyelia. Her laboratory work-up revealed hypokalemic, hyperchloremic metabolic acidosis with a normal anion gap. She also had a urine osmolal gap of 1.9 mOsmol/kg with a high urine pH. Intravenous potassium replacement resulted in a complete resolution of her paralysis. She was diagnosed with dRTA and discharged with oral bicarbonate and slow-release potassium supplementation.ConclusionsThis case report highlights the importance of considering dRTA in the differential diagnosis of hypokalemic acute paralysis in children. Additionally, in children with neurogenic lower urinary tract dysfunction and recurrent UTIs, early diagnosis of spinal cord etiology is crucial to treat promptly, slow the progression of CKD, and prevent long-term complications such as RTA.

Symptomatic Diethylene Glycol Ingestion Successfully Treated with Fomepizole Monotherapy

BackgroundDiethylene glycol (DEG) is an industrial solvent with many uses, including brake fluids. It has also caused mass poisonings after use as an inappropriate substitute for propylene glycol or glycerin, though individual ingestions are rare. Like other toxic alcohols, DEG is metabolized by alcohol dehydrogenase and aldehyde dehydrogenase, with toxicity likely mediated by the resulting metabolites. Fomepizole, an alcohol dehydrogenase inhibitor, is used to prevent metabolite formation with other toxic alcohol exposures. Fomepizole is recommended for DEG poisoning, though supporting clinical evidence is limited. Case ReportA 31-year-old man presented after ingestion of DEG-containing brake fluid and hydrocarbon-containing “octane booster.” He was noted to be clinically intoxicated, with a mildly elevated anion gap metabolic acidosis and no osmolar gap. DEG level was later found to be elevated, consistent with his ingestion. He was treated with fomepizole alone, with resolution of metabolic acidosis and clinical findings over the next 2 days. No delayed neurologic sequelae were present at 52-day follow-up. Our case provides additional evidence supporting the use of fomepizole for DEG poisoning. Consistent with other toxic alcohols, DEG poisoning, especially early presentations, may benefit from empiric fomepizole administration. Why Should an Emergency Physician Be Aware of This?DEG poisoning is potentially life threatening, but treatable if identified early. An ingestion can be toxic despite a normal osmolar gap, leading to false reassurance. Finally, it is rare, so emergency physicians must be made aware of its potential dangers.

A toxic ingestion with an elevated osmolal gap: Answers.

A toxic ingestion with an elevated osmolal gap: Answers.

A toxic ingestion with an elevated osmolal gap: Questions.

A toxic ingestion with an elevated osmolal gap: Questions.

The effect of sodium zirconium cyclosilicate on acid-base balance inchronic kidney disease.

Hyperkalemia is a common electrolyte abnormality in chronic kidney disease (CKD). Sodium zirconium cyclosilicate (SZC) is a novel selective cation exchanger that is used to treat hyperkalemia and may also capture ammonium, which is of a similar size to potassium. We investigated the effect of SZC on acid-base balance in CKD patients. This retrospective study surveyed 20 patients with CKD whose serum potassium levels were maintained within the normal range by treatment with polysulfonate resin, which was replaced with SZC during the clinical course. We compared clinical parameters before and after changing medications. Changing the potassium binder from polysulfonate resin to SZC increased serum bicarbonate (p=0.016) and decreased blood urea nitrogen (p=0.017). Serum potassium levels were maintained within the normal range. Urine pH, anion gap, and osmolality gap were unchanged during treatment. No gastrointestinal symptoms were noted during the observation period. Our data suggest that SZC may improve not only hyperkalemia but also metabolic acidosis by increasing the excretion of ammonium from the intestinal tract in patients with CKD. SZC could be a more suitable medication for CKD patients with hyperkalemia and metabolic acidosis.

Acute Kidney Injury Following Mannitol Infusion in Neurosurgical Patients

Background: To evaluate the acute kidney injury (AKI) predictors and their predictive performance during mannitol infusion, and the impact of AKI on in-hospital mortality of neurocritically ill patients.Methods: This was a retrospective, observational study of patients who were admitted at a tertiary university hospital, Seoul, Republic of Korea, neurosurgical intensive care unit (ICU) from January 2013 to December 2019. We included neurosurgical patients on mannitol infusion admitted in the ICU The primary endpoint was the occurrence of AKI.Results: A total of 3,964 patients were included in the final analysis. AKI was detected in 540 (13.6%) patients on mannitol infusion. Measured osmolality and osmolar gap were significantly higher in patients with AKI than those without (both p< 0.001). However, the predictive power of the two indicators was similar and were both weak predictors of AKI (both C-statistic <0.650). In the multivariable analysis, maximal measured osmolality, chronic kidney disease, Acute Physiology and Chronic Health Evaluation 2 score on ICU admission, use of vasopressor, use of glycerin, mechanical ventilation, and invasive ICP monitoring were significantly associated with AKI. In-hospital mortality was significantly higher in patients with AKI than those without (11.1% vs. 1.4%, p< 0.001).Conclusions: Based on our findings, kidney injury may be associated with poor clinical outcomes in neurosurgical and neurocritically ill patients, and monitoring serum osmolality and OG remains important in the prevention of kidney injury for patients on mannitol infusion. Moreover, clinical factors related to ICU management and pre-existing renal disease may aggravate AKI during mannitol infusion.

A Rare Case of Elevated Osmolar Gap in Diabetic Ketoacidosis/Hyperosmolar Hyperglycaemic State in the Absence of Concomitant Toxic Alcohol Ingestion

The serum osmolar gap, defined as the difference between measured osmolality and calculated osmolarity, is a convenient method to screen for toxins in serum. In normal circumstances, the difference between the two is 6–10 mol/kg. Typical contributors to serum osmolarity are sodium bicarbonate, sodium chloride, glucose and urea. An elevated gap, defined as a difference >10 mol/kg, can occur if a sufficient quantity of an additional solute other than those mentioned above is present in the serum or there are inaccuracies in sodium measurement secondary to hyperlipidaemia and hyperproteinaemia. An elevated serum osmolar gap should thus prompt clinicians to check for toxic alcohol levels. Treatment with fomepizole should not be delayed if suspicion is high. Isolated diabetic ketoacidosis can occasionally present with an elevated osmolar gap in the absence of concomitant alcohol ingestion. This finding is attributed to the production of acetone and glycerol.We describe the case of a 62-year-old man presenting with diabetic ketoacidosis/hyperosmolar hyperglycaemic state and an elevated osmolar gap in the absence of toxic alcohol ingestion.LEARNING POINTSThe osmolar gap is the difference between the measured and the calculated serum osmolarity and should be calculated in all patients presenting with elevated serum osmolarity; if elevated, toxic alcohol ingestion should be considered and prophylactic treatment with fomepizole immediately administered if the index of suspicion is high.Although toxic alcohol ingestion is one of the common causes of an elevated osmolar gap, hyperlipidaemia, hyperproteinaemia and less occasionally lactic acidosis and ketoacidosis have also been implicated.In the setting of ketoacidosis, the osmolar gap can be elevated in the absence of toxic alcohol ingestion, is attributed to increased production of acetone and glycerol, and is responsive to treatment with insulin and intravenous fluids.

Hyperosmolar Therapy in the Management of Intracranial Hypertension.

Hyperosmolar Therapy in the Management of Intracranial Hypertension.

Methanol Intoxication After Suicidal Ingestion of Liquid Rodenticides: A Report of Two Cases.

Methanol is highly toxic to humans. Although methanol poisoning is not uncommon in developing countries, poisoning caused by ingestion of commercial products containing undeclared methanol has rarely been reported. Herein, we describe two patients who experienced methanol poisoning after ingestion of liquid rodenticides. A 39-year-old woman attempted suicide by ingesting liquid rodenticide which contained bromadiolone. She developed high anion gap metabolic acidosis and coagulopathy. Methanol poisoning was confirmed 20 hours later. She received oral ethanol therapy and hemodialysis. Vitamin K1 was also administered. She did not develop any hemorrhage or visual impairment and was discharged after 11 days. The rodenticide sample was tested and found to have a methanol concentration of 324 g/L. In another case, a 62-year-old man ingested the same brand of rodenticide. Laboratory data showed mild metabolic acidosis with an increased osmol gap, suggestive of methanol poisoning. He received hemodialysis and eventually recovered without sequelae. Liquid rodenticide may contain methanol as a solvent. Ingestion of a methanol-containing commercial product without a clear label can result in a considerable delay in diagnosis and management. Methanol poisoning should be considered for patients who present with unexplained metabolic acidosis following exposure to liquid rodenticides or other liquid commercial products.

Comparison of 1.0 g/kg of 20% mannitol initiated at different time points and effects on brain relaxation in patients with midline shift undergoing supratentorial tumor resection: a randomized controlled trial.

Previous studies have suggested the use of 1.0 g/kg of 20% mannitol at the time of skin incision during neurosurgery in order to improve brain relaxation. However, the incidence of brain swelling upon dural opening is still high with this dose. In the present study, the authors sought to determine a better timing for mannitol infusion. One hundred patients with midline shift who were undergoing elective supratentorial tumor resection were randomly assigned to receive early (immediately after anesthesia induction) or routine (at the time of skin incision) administration of 1.0 g/kg body weight of 20% mannitol. The primary outcome was the 4-point brain relaxation score (BRS) immediately after dural opening (1, perfectly relaxed; 2, satisfactorily relaxed; 3, firm brain; and 4, bulging brain). The secondary outcomes included subdural intracranial pressure (ICP) measured immediately before dural opening; serum osmolality and osmole gap (OG) measured immediately before mannitol infusion (T0) and at the time of dural opening (TD); changes in serum electrolytes, lactate, and hemodynamic parameters at T0 and 30, 60, 90, and 120 minutes thereafter; and fluid balance at TD. The time from the start of mannitol administration to dural opening was significantly longer in the early administration group than in the routine administration group (median 66 [IQR 55-75] vs 40 [IQR 38-45] minutes, p < 0.001). The BRS (score 1/2/3/4, n = 14/26/9/1 vs 3/25/18/4, p = 0.001) was better and the subdural ICP (median 5 [IQR 3-6] vs 7 [IQR 5-10] mm Hg, p < 0.001) was significantly lower in the early administration group than in the routine administration group. Serum osmolality and OG increased significantly at TD compared to levels at T0 in both groups (all p < 0.001). Intergroup comparison showed that serum osmolality and OG at TD were significantly higher in the routine administration group (p < 0.001 and = 0.002, respectively). Patients who had received early administration of mannitol had more urine output (p = 0.001) and less positive fluid balance (p < 0.001) at TD. Hemodynamic parameters, serum lactate concentrations, and incidences of electrolyte disturbances were comparable between the two groups. Prolonging the time interval between the start of mannitol infusion and dural incision from approximately 40 to 66 minutes can improve brain relaxation and decrease subdural ICP in elective supratentorial tumor resection.

Вплив альтерації гомеостазу глюкози на водно-електролітний баланс та кислотно-основний стан у пацієнтів із цукровим діабетом

Незважаючи на успіхи в терапії цукрового діабету, частота виникнення ускладнень, зокрема порушення водно-електролітного та кислотно-основного стану, останніми роками не зменшилась. Цікаво відмітити той факт, що клінічні прояви такого грізного ускладнення, як діабетичний кетоацидоз, уперше описав Дрешфельд у 1886 році. Відтоді і до початку застосування інсуліну (в 1922 р.) смертність від цього ускладнення сягала 100 %. Широке впровадження в практику інсулінотерапії знизило смертність до 30 %, а з удосконаленням методів лікування, зокрема інфузійної терапії, відбулось подальше її зниження. На сьогодні рівень летальності пацієнтів із порушеннями водно-електролітного та кислотно-основного стану залишається високим (близько 5 % у спеціалізованих центрах). Тільки в США щорічно від цього ускладнення помирає близько 4000 хворих на цукровий діабет. Прогноз перебігу захворювання значно погіршується з віком, при розвитку коми та артеріальної гіпотензії. Поширеність цукрового діабету стрімко зростає і на сьогодні становить від 20 до 50 % випадків вперше виявленого захворювання в молодих людей. Порушення електролітів є частими в пацієнтів із даною патологією і можуть бути результатом зміненого розподілу електролітів, пов’язаного з індукованою гіперглікемією осмотичних зрушень рідини, або загального дефіциту, спричиненого осмотичним діурезом. Ускладнення від пошкодження органів-мішеней і методи лікування цукрового діабету можуть також сприяти електролітним порушенням. Порушення регуляції гомеостазу глюкози призводить до великої кількості прямих і непрямих впливів на електролітний і кислотно-основний баланс, оскільки велика поширеність діабету гарантує, що лікарі практично кожної спеціальності мають справу з пацієнтами, хворими на цукровий діабет, а знання, пов’язані зі змінами електролітів, є необхідними. У статті розглянуто, як впливають зміни гомеостазу глюкози при цукровому діабеті на водно-електролітний баланс та кислотно-основний стан пацієнта.

An unusual presentation of the chest and abdominal pain: toxic alcohol ingestion

Background: Methanol, ethylene glycol, diethylene glycol, propylene glycol, and isopropanol are common alcohols, whose consumption can lead to toxicity and significant morbidity and mortality1,2. Clinicians must often rely on clinical features and laboratory values to determine the possible causative agent. Annually, almost 95,000 people die due to alcohol and it is the third leading cause of preventable deaths in the United States of America3. Case presentation: A 53-year-old male patient reported to the Emergency Department with vomiting, severe chest, and abdominal pain for one day. He looked unwell and was unstable. The blood gases showed metabolic acidosis with lactate of 10-mmol/L. Investigations on the line of Acute Mesenteric Ischemia, Pulmonary Embolism, and Aortic Dissection were negative. With time, the patient deteriorated with severe metabolic acidosis requiring rapid sequence intubation. Blood investigations showed multi-organ failure, high serum osmolarity, and high osmolar gap. Later, he was admitted to the intensive care unit and underwent hemodialysis. His laboratory test results improved, and he was extubated. Eventually, he revealed having taken homemade alcohol. Recommendations: High Anion Gap is a hallmark of toxic alcohol poisoning. A potential toxic alcohol ingestion surrogate marker is an elevated osmol gap. Abnormal presentation and a patient hiding key information can delay the diagnosis. The key to successful early diagnosis is good history taking, patient collaboration, complete examination, and interpretation of laboratory results. Isopropyl alcohol is associated with nausea, vomiting, and abdominal pain since it is a gastrointestinal irritant. Magnetic Resonance Imaging of the brain can play a role in diagnosing toxic alcohol ingestion especially methanol, due to its characteristics findings like hemorrhagic putamen necrosis (Figure 1), however, clinical suspicion should not delay a patient&apos;s treatment. Conclusion: Abnormal presentations are quite common, and one should always keep a wide differential diagnosis in mind. Uncommon causes of severe metabolic acidosis could be easily missed. The main success factor in the management of toxic alcohol ingestion is to recognize it, do the calculations, and provide treatment.

Osmolal and anion gaps after acute self-poisoning with agricultural formulations of the organophosphorus insecticides profenofos and diazinon: A pilot study.

Self-poisoning with organophosphorus (OP) insecticides is an important means of global self-harm. The insecticides are formulated with solvents that may also contribute to toxicity. We set up a study to detect changes in osmolal and anion gaps following ingestion of OP insecticides. We recruited consecutive patients admitted to a Teaching Hospital, Sri Lanka, with a history of OP self-poisoning. The osmolal and anion gaps were calculated on admission and at 4, 24 and 72 h post-ingestion together with ethanol concentration. Forty-nine patients were recruited (28 profenofos, 10 diazinon, one coumaphos, one chlorpyrifos, one phenthoate and eight unknown OP). Only modest increases in osmolal and anion gaps were noted. Small rises in osmolal gap above the upper limit of normal were noted in 16/49 (32.7%) of all cases, 9/28 (32.1%) profenofos cases and 4/10 (40.0%) diazinon cases. The anion gap was raised in 24/49 (49.0%) of all cases, 15/28 (53.6%) profenofos cases and 5/10 (50.0%) diazinon cases. We observed a trend for a fall in osmolal gap during the first 24 h, followed by an increase up to 72 h. There was no correlation between the anion gap and serum lactate concentration, indicating that a lactic acidosis was not responsible for the anion gap. Formate, which could have explained the increased gap, was not detected in any of the samples; ketoacids (beta-hydroxybutyrate and acetoacetate) were not measured. This pilot study found that profenofos and diazinon poisoning caused only modest increases in the osmolal and anion gaps in a minority of cases.

Metabolic Acidosis and Hyponatremia in a Patient With Metastatic Melanoma

Metabolic Acidosis and Hyponatremia in a Patient With Metastatic Melanoma

POISON IN OUR POCKETS: MANAGEMENT OF LIFE-THREATENING ISOPROPANOL INTOXICATION

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Isopropanol is a readily available substance, which can cause disastrous consequences if ingested even in a relatively small amount. High degree of suspicion is required for identification. This issue has become more concerning in light of the increasing exposure to household disinfectants and cases of toxicity in the context of the Covid-19 pandemic. CASE PRESENTATION: A 70 year-old African American woman presented after being found difficult to arouse by her son. Her last known well was 1 hour prior to presentation. She was profoundly lethargic on arrival, hypotensive and having profuse hematemesis. She was intubated for airway protection. Her hypotension did not respond to intravenous fluid and required vasopressors to maintain a mean arterial pressure of 65 mmHg. She was found to have ketonuria and severely elevated osmolar gap with no acidosis. Her mental status continued to deteriorate and she became dependent on mechanical ventilation. After further probing, her son noted he had found an empty bottle of rubbing alcohol in her room. No evidence of co-ingestion of other toxic substances were found on laboratory evaluation. She was observed for 8 hours with no discernible improvement in her mental status or hemodynamics. Hemodialysis was initiated for isopropanol clearance. Within 1 hour the patient became alert and hemodynamically stable. She was extubated without incident and mental status returned to baseline. DISCUSSION: Isopropanol is one of the most ubiquitous toxic substances, especially in the midst of the Covid-19 pandemic. Unlike ethylene glycol and methanol, isopropanol is more toxic than its metabolites. It reaches peak serum levels within minutes of ingestion. The minimum documented lethal dose is estimated at 100 ml. Isopropanol intoxication presents non-specifically, usually manifesting as central nervous system impairment and gastrointestinal upset. Most ingestion only result in mild symptoms. Massive ingestion may result in hemorrhagic gastritis or circulatory collapse. Hypotension is associated with a near 50% mortality rate. Identification of isopropanol poisoning is challenging due to its non-specific symptoms and subtle laboratory abnormalities. An increased osmolal gap and positive ketonemia are frequently the only abnormalities observed. In life threatening cases hemodialysis has been utilized with some success as a rescue therapy. CONCLUSIONS: Isopropanol intoxication requires a high degree of clinical suspicion is required for early identification and intervention in life threatening cases. In doing so significant morbidity and mortality may be prevented. No antidotes or neutralizing agents are currently available. Further study is needed to determine which patients would benefit most from hemodialysis with isopropanol intoxication. REFERENCE #1: Abramson S, Singh AK. Treatment of the alcohol intoxications: ethylene glycol, methanol and isopropanol. Curr Opin Nephrol Hypertens. 2000 Nov;9(6):695-701. doi: 10.1097/00041552-200011000-00017. PMID: 11128434. REFERENCE #2: Slaughter RJ, Mason RW, Beasley DM, Vale JA, Schep LJ. Isopropanol poisoning. Clin Toxicol (Phila). 2014 Jun;52(5):470-8. doi: 10.3109/15563650.2014.914527. Epub 2014 May 9. PMID: 24815348. REFERENCE #3: King LH Jr, Bradley KP, Shires DL Jr. Hemodialysis for isopropyl alcohol poisoning. JAMA. 1970 Mar 16;211(11):1855. PMID: 5467117. DISCLOSURES: No relevant relationships by Philip Almalouf, source=Web Response No relevant relationships by Alexander Angelidis, source=Web Response No relevant relationships by Robert Petrossian, source=Web Response No relevant relationships by Farheen Surtie, source=Web Response

SEVERE LACTIC ACIDOSIS SECONDARY TO ACUTE ALCOHOL INTOXICATION

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Alcoholic ketoacidosis is one of the several etiologies where serum lactate level rarely exceeds 3 mmol/L. We present to you an interesting case of severe lactic acidosis (24 mmol/L) in a patient with acute alcohol intoxication. CASE PRESENTATION: Patient is a 62-year male who presented with intractable abdominal pain for 2 days. Past medical history was significant for alcohol use disorder. On presentation, patient had tachycardia, tachypnea, was restless with slurred speech with mild abdominal tenderness. Laboratory findings were remarkable for leukocytosis of 22.7, serum bicarbonate of 4 mmol/L, serum glucose 104 mg/dL, serum lactate 24 mmol/L. ABG showed pH of < 7.00, pCO2 12 mmHg, HC03 4.6 mmol/L. Anion gap was 41.0. Serum ethanol level was elevated at 0.185 g/dl. Patient was started on bicarbonate infusion, IV thiamine with 5% dextrose fluid and CIWA protocol. Serum beta hydroxybutyrate was elevated at 2.9, serum osmolality was elevated at 344 with osmolar gap of 13. LFT was deranged with unremarkable liver ultrasound. Patient was admitted to the ICU. Serum isopropanol, methanol, and ethylene glycol were negative. Infectious workup including blood culture, urine culture, pneumonia workup were negative. Acetaminophen and salicylate levels were normal. Urine drug screen was unremarkable. No history of GI malabsorption (short-bowel syndrome), renal failure or recent phenobarbital administration. Lactic acidosis was therefore attributed to alcoholic ketoacidosis in a setting of alcoholic hepatitis. Patient gradually improved with final pH 7.38, lactate 1.80 and serum HC03 24.6 by day 2. DISCUSSION: Lactate level of > 4 mmol/L with arterial pH < 7.35 suggests lactic acidosis. Lactic acidosis is broadly classified into type A which occurs due to impaired systemic tissue oxygenation and type B due to toxin induced cellular metabolism impairment and regional ischemia, commonly in alcoholism, HIV, antiretroviral medications, beta adrenergic medications, D lactic acidosis (short-bowel syndrome), diabetes mellitus, metformin, malignancy. Alcoholic ketoacidosis remains important etiology as if missed may result in fatal consequences including sudden death. Occasionally, alcoholic ketoacidosis can be misdiagnosed as diabetic ketoacidosis with subsequent mismanagement resulting in increased morbidity and mortality. CONCLUSIONS: Alcoholic ketoacidosis typically presents with metabolic acidosis but rarely with lactate > 3mmol/L in absence of other contributing factors. Oftentimes, the diagnosis is missed or misdiagnosed as diabetic ketoacidosis resulting in mismanagement contributing to increased morbidity and mortality. REFERENCE #1: Adeva-Andany, M., et al. 'Comprehensive Review on Lactate Metabolism in Human Health'. Mitochondrion, vol. 17, July 2014, pp. 76–100. PubMed, doi:10.1016/j.mito.2014.05.007. REFERENCE #2: Kreisberg, R. A. 'Lactate Homeostasis and Lactic Acidosis'. Annals of Internal Medicine, vol. 92, no. 2 Pt 1, Feb. 1980, pp. 227–37. PubMed, doi:10.7326/0003-4819-92-2-227 REFERENCE #3: Madias, N. E. 'Lactic Acidosis'. Kidney International, vol. 29, no. 3, Mar. 1986, pp. 752–74. PubMed, doi:10.1038/ki.1986.62 DISCLOSURES: No relevant relationships by Luna Khanal, source=Web Response No relevant relationships by Adarsha Ojha, source=Web Response

I CANNOT SEE YOUR FACE! A CASE OF PURTSCHER DISEASE

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Purtscher-like retinopathy is an acquired form of retinopathy due to hemorrhagic or vasoocclusive vasculopathy associated with acute pancreatitis and other systemic diseases 1. It is associated with severe vision. Recent studies suggested ophthalmoscopy performed within first 24 hours of developing acute pancreatitis was a good indicator for predictor of disease evolution, outcome and overall poor prognosis 2. We present a rare case of a young African American male who had experienced acute vision loss in the setting of severe alcoholic pancreatitis. CASE PRESENTATION: 34-year-old African American male with a history of alcoholic dependence presents with abdominal pain. His last drink was 36 hours ago. It's described as sharp and radiating to his back. He denies any other ingestions or drug use. On presentation, vital signs show that he is mildly hypertensive, but otherwise within normal limits. Physical exam reveals epigastric tenderness on palpation with positive bowel signs, negative murphy sign, cullens sign and gray turners sign. Labs were significant for an elevated lipase as well as liver enzymes. No significant osmolar gap. Intravenous fluids were provided as well as pain control and patient was placed on a withdrawal assessment scale. Within 12 hours of admission, he started to experience alcoholic hallucinosis with decreased visual acuity and inability to recognize facial features. Fundoscopy revealed retinal whitening bilaterally, Intraretinal flame heme along inferior arcade of the right eye, cherry red spot of the left eye within the macula, consistent with Purtscher-like retinopathy in the setting of acute pancreatitis declaring him legally blind. Patient signed a 302 to receive further inpatient psychiatric care. DISCUSSION: The patient's acute psychosis from alcohol compounded his complaint of acute vision loss. Purtscher retinopathy is a rare complication of acute pancreatitis. The etiology is unclear, however in relation to pancreatitis, the condition may be caused by complement induced granulocyte activity causing cotton wool spots, retinal hemorrhages, and papilledema [2]. It should be suspected if patients voice concern of decreased visual acuity. Previously high dose steroids have been used but there is no evidence that this treatment improves morbidity. Recovery of visual acuity is variable with some patients regaining vision with mild loss of acuity and others remain legally blind. Certainly, a rare and interesting complication of acute pancreatitis. CONCLUSIONS: Evaluation and treatment of patients with acute pancreatitis with visual complaints should raise concern for Purtcher's retinopathy. There are no current evidence-based treatment options. Close follow up with a retinal specialist is required. Further clinical studies are required to investigate treatment options for Purtcher's retinopathy. REFERENCE #1: Bissonnette B. Purtscher Disease. AccessAnesthesiology 2019. REFERENCE #2: C; CDRABFB. [Retinopathy in severe acute pancreatitis]. Oftalmologia (Bucharest, Romania : 1990). REFERENCE #3: Buckley, S. and James, B., 2020. [online] Pmj.bmj.com. Purtschers Retinopathy. [Accessed 7 July 2020]. DISCLOSURES: No relevant relationships by Abdelrhman Abo-zed, source=Web Response No relevant relationships by Melissa Chrites, source=Web Response No relevant relationships by Erica OKane, source=Web Response No relevant relationships by Syed Arsalan Zaidi, source=Web Response