Anion Gap Metabolic Acidosis Research Articles

THE CLUE IS IN THE BLOOD GAS: A RARE MANIFESTATION OF LACTIC ACIDOSIS

THE CLUE IS IN THE BLOOD GAS: A RARE MANIFESTATION OF LACTIC ACIDOSIS

S3621 Imaging Finding as a Clue for Accidental Salicylate Toxicity

Introduction: The rise of acetaminophen use as an antipyretic in children dramatically decreased the incidence of salicylate toxicity in children. However, it is still relatively common in adults and usually overlooked by physicians especially in elderly patients due to non-specific presentation and unawareness of salicylate-containing medications. We present a case of salicylate toxicity secondary to Pepto-Bismol abuse. Suspicion was raised after a radiopaque density was found in a non-contrast CT abdomen. Case Description/Methods: A 62-years-old female with a history of compensated heart failure, COPD, and hypertension presented with lethargy, diaphoresis, and epigastric pain. The pain was associated with nausea and occasional vomiting. Vital signs showed HR 105, BP 110/60, RR 18, and oxygen saturation of 94 % on ambient air. Physical exam was remarkable for scattered mild expiratory wheezes. Lab results were significant for high anion gap metabolic acidosis with HCO3 16 mmol/L, Creatinine 1.4 mg/dL, and BUN 30 mg/dL. Non-contrast CT abdomen showed a contrast material in the stomach (Figure). Further history was then taken from the patient who reported ingestion of around 60 tablets of Pepto-Bismol over the last 48 hours trying to relieve her stomach pain. Salicylate toxicity was then suspected, and the salicylate level was checked and it was 26 mg/dl. The patient was then treated with activated charcoal and supportive IV fluids. The patient’s symptoms were resolved and she was discharged home. Discussion: Diagnosis of salicylate toxicity is challenging, specifically in the elderly with the non-specific presentation. In addition, salicylate is an ingredient of many over-the-counter (OTC) medications, that many physicians are not aware of, such as Alka-seltzer, Bufferin, Vanquish, Pepto-Bismol, etc. Our patient had salicylate toxicity after ingestion of around 60 tablets of Pepto-Bismol. Suspicion was raised after finding a picture of oral contrast in the patient’s stomach in a non-contrast study. Pepto-Bismol (bismuth subsalicylate) can appear as a contrast on imaging due to the hyperdense property of the bismuth ingredient. The property of this medicine should be taken into consideration. Otherwise, such incidental findings can be missed as a clue for a certain condition (as in our patient) or lead to unnecessary workup, patient anxiety, and waste of resources in other situations. Our case also demonstrates the importance of taking a thorough history including OTC medications.Figure 1.: Non-contrast CT abdomen shows a picture similar to contrast material secondary to Pepto Bismol ingestion.

S1933 Acute Pancreatitis Attributed to COVID-19: An Unusual Infectious Etiology

Introduction: COVID-19 can affect multiple organs and has various presentations, including respiratory symptoms and fever being the most common. Gastrointestinal symptoms can be reported in up to 25% of patients, with diarrhea, nausea, and emesis the usual presentation. However, abdominal pain is less than 6.8% of cases, and of those, only 27% presented with Acute Pancreatitis (AP). Here we present a case of severe AP with multiorgan involvement as the initial presentation of COVID19. Case Description/Methods: Case of a 19 y/o Female with a medical history of Obesity class I arrived at the ED with recurrent emesis and altered mental status. Symptoms began around four days prior with 6-7 episodes of non-bloody, non-bilious emesis, fatigue, subjective fever, and decreased oral intake, followed by acute onset of diffuse abdominal pain. Upon arrival, the patient was found encephalopathic with dry oral mucosa, tachycardic and tachypneic. Laboratories were remarkable for lipase 2483, amylase 382, LDH 315, ALP 219 U/L, sodium 155 mEq/L, creatinine 1.33 mg/dL, bicarbonate < 9 mmol/L, pH 7.0, pO2Sat 96%, hematocrit 51.8%, WBC 14.9 cells/L, glucose 774 mg/dL, and COVID 19 PCR positive. Abdominal US and CT with no findings suggestive of gallstones or intraabdominal pathology. Aggressive intravenous fluid, insulin, broad-spectrum antibiotics, bicarbonate replacement, analgesia, and antiemetics were implemented. Hospitalization was complicated as the patient did not tolerate PO intake, and the high anion gap metabolic acidosis was difficult to close for several days. After almost two weeks in the ICU, the patient was discharged home without apparent pancreatitis or COVID-19 repercussions. Discussion: Our case did not have any risk factors for AP, and extensive investigations did not reveal a clear etiology. Viral, bacterial, fungal, and parasitic infections are less common causes of AP. There are limited data on COVID-19 and pancreatitis; however, recent studies suggest a higher mortality rate with a 20% increased chance of dying and worse clinical outcomes. The mechanism of pancreatic injury is not well understood, but there is a link between COVID-19 and the precipitation of autoimmune and systemic diseases. Our case is an example of severe pancreatic injury with multiorgan involvement in mild symptomatic COVID 19.

S3259 A Case of Propofol-Induced Acute Liver Failure

Introduction: Propofol is a parenteral anesthetic routinely used for procedures given its beneficial pharmacokinetic profile of rapid onset of action and reversal. Propofol drug toxicity is rare but has been associated with idiosyncratic acute liver injury in a small number of cases. To the best of our knowledge, we present the second case of propofol-induced acute liver failure (ALF) reported in literature. Case Description/Methods: An 88-year-old male with concern for gastrointestinal bleed underwent an upper endoscopy with propofol used as the anesthetic agent. The patient tolerated the endoscopy well with no hemodynamic compromise during or afterwards. No source of bleeding was identified so the plan was to proceed with a colonoscopy the next day. Shortly after the procedure, he was noted to have altered mental status. Evaluation with routine laboratory testing revealed elevated AST of 3248 IU/L and ALT of 2411 IU/L, both increased from 35 IU/L and 24 IU/L, respectively. He was also found to have high anion gap metabolic acidosis and bicarbonate level less than 9 mEq/L. His altered mentation continued to worsen, and he became hemodynamically unstable requiring transfer to the intensive care unit. He had no history of liver disease or excessive alcohol use, no risk factors for viral hepatitis, and took no medications known to cause liver injury. Work-up was unremarkable for acute and chronic liver disease. Propofol was ultimately surmised as the cause of ALF. Unfortunately, the patient’s mental status progressively worsened despite hemodynamic stabilization and normalization of liver enzymes. His family ultimately chose to transition to comfort measures and the patient passed soon after. Discussion: The incidence of drug-induced liver injury is increasing in developed countries and is a major etiology of ALF, accounting for greater than 50% of cases. Drug toxicity secondary to an idiosyncratic reaction is unpredictable and occurs infrequently in certain individuals. While propofol is generally considered a safe agent widely used for sedation, propofol-induced acute liver injury is a rare outcome. To the best of our knowledge, it is reported to have caused five cases of acute hepatitis and one other case of ALF. We report the second case of ALF due to propofol with a lethal outcome. We recommend close monitoring of patients treated with propofol for signs of hepatitis and that ALF due to a drug insult should be considered after common causes have been excluded.

A RARE CASE OF WERNICKE'S ENCEPHALOPATHY INDUCED BY HYPEREMESIS GRAVIDARUM: A DIAGNOSTIC DILEMMA

A RARE CASE OF WERNICKE'S ENCEPHALOPATHY INDUCED BY HYPEREMESIS GRAVIDARUM: A DIAGNOSTIC DILEMMA

P.12 A case report of near normalization of serum creatine phosphokinase in a patient with Duchenne muscular dystrophy during acute pancreatitis

Creatine phosphokinase (CPK) is a muscle-specific protein that has served a vital role as a diagnostic biomarker for Duchenne Muscular Dystrophy (DMD). It is also often used to track disease progression in DMD. However, its role as a monitoring, or predictive biomarker is less clear. We describe a 6-year-old boy with DMD caused by duplication of exon 2 of the dystrophin gene as well at IgG deficiency. He presented acutely to the emergency department with brown colored urine in the setting of five days of non-bloody non-bilious emesis, abdominal pain and poor oral intake. His initial examination was notable for signs of moderate dehydration and a soft, non-tender abdomen. His initial laboratory evaluation was notable for anion gap metabolic acidosis, hyponatremia and hypoglycemia. He was ultimately diagnosed with acute pancreatitis after lipase was found to be 2201.0 unit/L (ref 48.0-199.0 unit/L) on day of his admission. He was placed on intravenous fluids and admitted for a total of 3 days with complete recovery. This individual had a baseline CPK of 11,000-21,000 unit/L at previous outpatient visits. Of note, CPK level was obtained on the day of his hospital admission and was found to be 284 unit/L (ref 30-250). The day after admission, CPK was rechecked twice and were 312 and 322 unit/L separately. Fourteen days after admission, CPK was rechecked and had returned to near his previous baseline at 15,496 unit/L. Pancreatitis and other acute inflammatory conditions in DMD are rare. Transient near normalization of CPK has been described previously in one patient with Becker Muscular Dystrophy patient during transient arthritis. To our knowledge, our patient is the first reported case of normalization of CPK level in DMD during acute inflammatory disease. We hypothesize the transient normalization of CPK was secondary to active systemic response during the acute inflammation. Studies to look deeper into reasons that may underlie such a phenomenon may shed light in finding protective mechanisms associated with the inflammation pathway.

A rare case report of combined metformin-associated lactic acidosis and diabetic ketoacidosis

BackgroundTriad of diabetic ketoacidosis (DKA) comprises of hyperglycemia with serum glucose > 11 mmol/L, high anion gap metabolic acidosis and ketonemia. Hyperlactemia is often noted in patients with DKA. Metformin use is one of the risk factors of hyperlactemia, resulting in high anion gap metabolic acidosis, known as metformin associated lactic acidosis (MALA). This report is of a 60-year-old woman with type 2 diabetes mellitus who presented with combined metformin-associated lactic acidosis MALA and DKA.Case presentationA 60-year-old diabetic female presented to the emergency department with complaints of abdominal pain, vomiting and diarrhea. She was on metformin for the last 10 years, but despite compliance to medications, her HbA1c was 14.1. With an aim to improve her glycemic control, linagliptin 5 mg once a day was added 1 month ago. Initial investigations in ED including arterial blood gas analysis revealed metabolic acidosis, ketosis, hyperlactemia, and acute kidney injury. In view of metabolic acidosis and ketosis with elevated blood glucose level, she was diagnosed to have DKA. Compared to isolated DKA, patients with combined MALA and DKA have severe metabolic acidosis, a greater degree of hyperlactatemia but less extensive ketoacidosis. Hence, she was diagnosed to have combined MALA and DKA. She was admitted to intensive care unit and treated with intravenous fluids, insulin infusion, and continuous renal replacement therapy. Her metabolic acidosis, hyperlactemia, and kidney injury resolved and she was discharged well.ConclusionThis report has shown the importance of rapid diagnosis and management of the rare and challenging diagnosis of combined MALA and DKA. The main goal of therapy is preventing hyperglycemia and ketosis, resolution of metabolic acidosis, and removal of accumulated metformin using intensive therapies like aggressive fluid resuscitation and early initiation of renal replacement therapy. Adjustment of dose of medications is needed to avoid this complication.

39-Year-Old Woman With Severe Weakness

39-Year-Old Woman With Severe Weakness

Methanol induced intracranial hemorrhage: A rare case report

Intracranial hemorrhage is a rare but fatal complication in methanol poisoning. We report a case of large bilateral basal ganglia hematoma in a 29-years old man with methanol poisoning. He drank alcohol, and was admitted to a tertiary level hospital 6 hours post-ingestion for depressed mental status, lower blood pressure, and high anion gap metabolic acidosis. After fourteen days of methanol exposure, he suddenly developed left sided weakness with one episode of seizure attack. MRI of brain was carried out and showed large intracerebral bleed basal ganglia, specially putaminal and brain edema with midline shift. The uncommon presentation of methanol poisoning is highlighted in this case report. Bangladesh J Medicine 2022; 33: 300-303

Pseudohypobicarbonatemia in a patient with amyloidosis.

We report a case of a patient who had critically low serum bicarbonate (HCO3 -) levels ranging from 8 to 11mmol/L on repeated venous measurements using an enzymatic/photometric assay. This prompted hospitalization and treatment with intravenous sodium bicarbonate (NaHCO3) followed by oral NaHCO3. He was evaluated for potential causes of high anion gap metabolic acidosis without any etiology found. He continued to have low serum HCO3 - levels despite maintenance oral NaHCO3 therapy and was referred for a second opinion where further laboratory work was pursued. An arterial blood gas was obtained, which revealed normal whole blood pH and HCO3 - levels. A different enzymatic/photometric assay revealed a normal serum HCO3 - level at 21mmol/L. Additional workup revealed paraproteinemia, which was thought to interfere with the enzymatic process by which his serum HCO3 - was measured, resulting in erroneous values.

Case Report: Acute isoniazid intoxication after intentional ingestion

Isoniazid is an anti-tuberculosis medication that is extensively used for treatment and prevention of tuberculosis. Acute isoniazid poisoning is characterized by a clinical triad of recurrent seizures, raised anion gap metabolic acidosis and coma. The seizures are unresponsive to standard anticonvulsant drugs, instead requiring pyridoxine administered in a dose equal to the amount of isoniazid consumed. Due to the high incidence of tuberculosis in low-income countries like Nepal, isoniazid intoxication should be considered in any patient who present with such unresponsive seizures and coma. We report a case of a 31 years old woman from Nepal, who intentionally ingested 12 grams of isoniazid and presented with generalized tonic-clonic seizures. She was successfully managed with 10 grams of pyridoxine along with other supportive management, including sodium bicarbonate for metabolic acidosis and mechanical ventilation. Doctors working in low-income countries, like Nepal, where tuberculosis is endemic, should be well acquainted with presentations and management of isoniazid intoxication.

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.

Acid–Base Abnormalities among Patients Admitted in the Intensive Care Unit of a Teaching Hospital

Abstract Acid–base abnormalities (arterial blood gas [ABG]) pose a threat to survival in intensive care unit (ICU) patients. We present a case series of 60 cases from hospital records highlighting the acid–base abnormalities among ICU patients. All standard protocols were followed in the study hospital to collect the arterial blood samples and standard procedures for measurement of ABGs. We found that 93.3% had acid–base abnormalities, 13.3% had nonanion gap metabolic acidosis, 20% had anion gap metabolic acidosis, 50% had metabolic alkalosis, 45% had respiratory acidosis, 21.7% had respiratory alkalosis, 41.7% had mixed disorders, 31.7% had double disorders, and 10% had triple disorder. We conclude that mixed disorder is common in ICU patients with alkalosis being slightly more common than acidosis. By doing ABG, we will be able to detect the underlying acid–base disorder promptly and initiate treatment immediately so that we can decrease the suffering and save the lives of the patients. Hence, a careful look at the ABG within 24 h of admission of a patient to ICU can help save lives.

Renal Tubular Acidosis in Pregnant Critically Ill COVID-19 Patients: A Secondary Analysis of a Prospective Cohort.

Background: Renal tubular acidosis (RTA) is an extremely rare cause of metabolic acidosis (10 in 100,000). RTA has been linked neither to pregnancy nor to severe coronavirus disease 2019 (COVID-19). The purpose of this study was to analyze the prevalence and clinical course of normal anion gap metabolic acidosis in critically ill pregnant COVID-19 patients and to compare them to an age-matched nonpregnant female patient cohort. Methods: Secondary analysis was conducted on a prospective observational cohort of critically ill patients suffering from COVID-19 consecutively admitted to a tertiary intensive care unit (ICU) between February 2020 and April 2021. Results: A total of 321 COVID-19 patients required admission to the ICU; 95 (30%) were female, and 18 (19%) were of childbearing age. Seven of eight (88%) pregnant women (all in the last trimester) required advanced respiratory support due to COVID-19. The estimated glomerular filtration rate was 135 (123–158) mL/min/m2 body surface area, and six pregnant women (86%) were diagnosed with a normal, respiratory compensated, anion gap metabolic acidosis (pHmin 7.3 (7.18–7.31), HCO3−min 14.8 (12.8–18.6) mmol/L, and paCO2 3.4 (3.3–4.5) kPa). Three (43%) acidotic pregnant women fulfilled diagnostic criteria for RTA. All women recovered spontaneously within less 7 days. Conclusions: Metabolic acidosis seems to be very common (85%) in pregnant critically ill COVID-19 patients, and the prevalence of RTA might be higher than normal. It remains to be demonstrated if this observation is an indirect epiphenomenon or due to a direct viral effect on the tubular epithelium.

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.

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.

54-Year-Old Woman With Altered Mental Status and Abdominal Pain

54-Year-Old Woman With Altered Mental Status and Abdominal Pain

Diabetic ketoacidosis as a complication of methanol poisoning; a case report

IntroductionDiabetic ketoacidosis (DKA) is a complication of diabetes presenting with high anion gap metabolic acidosis. Methanol poisoning, on the other hand, is a toxicology emergency which presents with the same feature. We present a case of methanol poisoning who presented with DKA.Case presentationA 28-year-old male was referred to us with blurred vision and loss of consciousness three days after ingestion of 1.5 L of an unknown mixture of bootleg alcoholic beverage. He had history of insulin-dependent diabetes and had neglected his insulin shots on the day prior to hospital admission due to progressive loss of consciousness. Vital signs were normal and venous blood gas analysis showed severe metabolic acidosis and a methanol level of 10.2 mg/dL. After eight hours of hemodialysis, he remained unresponsive. Diabetic ketoacidosis was suspected due to positive urine ketone and blood sugar of 411 mg/dL. Insulin infusion was initiated which was followed by full awakening and extubation. He was discharged completely symptom-free after 4 weeks.ConclusionsDiabetic ketoacidosis and methanol poisoning can happen simultaneously in a diabetic patient. Given the analogous high anion gap metabolic acidosis, physicians should pay particular attention to examination of the diabetic patients. Meticulous evaluation for both conditions is highly recommended.

THE SWEETEST TOOTH: A CASE OF PULMONARY MUCORMYCOSIS IN A PATIENT WITH COVID-19

TYPE: Case Report TOPIC: Chest Infections INTRODUCTION: COVID-19 has been associated with opportunistic bacterial and fungal infections. Both aspergillus and candida have been reported as the main fungal pathogens for coinfection but there has been an increasing number of cases of mucormycosis as the fungus thrives in low oxygen states and high glucose environments. CASE PRESENTATION: A 51-year-old with the past medical history of type 2 diabetes with glycohemoglobin A1C of 16. Seven days post Covid 19 diagnosis, she presented due to altered mentation and hypotension. Found to have DKA, with concomitant hypovolemic and septic shock. Noted to have profound anion gap metabolic acidosis and acute kidney injury. Initial infective pathogens included candidemia, with pulmonary aspergillosis and mucormycosis. Subsequently developed MSSA and stenotrophomonas pneumonia. Her course was complicated by acute renal failure requiring dialysis, large tracheal pleural fistula with tension pneumothorax and empyema. Bronchoscopy (Image 1) showed grossly necrotic trachea, right mainstem and right upper lobe segments. Despite timely appropriate treatment, she expired. DISCUSSION: Immunocompromised individuals such as uncontrolled diabetics, organ transplants, prolonged neutropenia and steroid use are prone to Mucormycosis infections. Sites include sinus, lungs, skin and mediastinum. Several triggers precipitate Mucormycosis in the setting of active infection along with steroid use. CONCLUSIONS: Increasing co infections including mucormycosis have been noted in COVID 19 patients due to uncontrolled diabetes and with steroid treatment. Efforts should be made to maintain euglycemia and judicious steroid use while remaining vigilant for unusual coinfections. DISCLOSURE: Nothing to declare. KEYWORD: mucor

Tenofovir-induced distal renal tubular acidosis: A rare cause of recurrent hypokalaemic paralysis

Tenofovir disoproxil fumarate was the first nucleotide analogue reverse transcriptase inhibitor to be approved for treatment of human immunodeficiency virus infection. It is a relatively safe drug but can present with nephrotoxicity. We report a case of 36-year-old male who presented with acute onset flaccid paraparesis. He was a diagnosed case of acquired immunodeficiency syndrome for 9 years ago and was on tenofovir-based antiretroviral therapy for last 6 months. As the patient had normal anion gap metabolic acidosis, hypokalaemia and urine pH > 5.5, distal renal tubular acidosis (RTA) was suspected. He improved dramatically within 24 h of hospitalisation after potassium correction to regain normal power. Tenofovir-induced distal RTA presenting as hypokalaemic paralysis is a very rare complication of tenofovir; hence, we are reporting this case. In addition, we suggest regular follow-up of patients taking tenofovir with urine analysis and serum potassium to detect this complication earlier as it is reversible.