Acute Cyanide Toxicity and Emergency Management in a Goldsmith: A Case Report.

Acute cyanide toxicity is very rare but it is almost always associated with fatal outcomes. Here we describe the case of a 43-year-old healthy male who worked in a jewelry factory and presented with acute cyanide toxicity. He was successfully managed with all the supportive measures and an appropriate antidote kit containing amyl nitrite, sodium nitrite, and sodium thiosulfate. We also describe the relevant importance of knowing the history of easy access to cyanide as a part of the patient's profession, the critical nature of the patient at presentation, as well as the efforts needed to procure the antidote.

Polyethylene Glycol Misuse Causing Acute Renal Failure and Metabolic Acidosis Requiring Dialysis: A Case Report.

Laxative misuse is a well-known occurrence, most often identified in patients struggling with eating disorders. Polyethylene glycol (PEG) 3350 is a readily available, well-tolerated osmotic laxative. High doses of PEG 3350 may cause gastrointestinal upset, diarrhea, dehydration, and electrolyte imbalance, although systemic toxicity is infrequently reported. This case report highlights the exceedingly rare metabolic derangements associated with profound levels of protracted PEG misuse. A 60-year-old female presented to the emergency department with altered mental status. She was found to have acute renal failure (ARF), anion gap metabolic acidosis (AGMA), and rhabdomyolysis secondary to excessive PEG 3350 use, requiring continuous renal replacement therapy (CRRT). Renal function improved after three days of CRRT, and no alternative causes beyond PEG ingestion were found to account for her mental status changes or metabolic anomalies. This report illustrates the importance of considering osmotic laxative misuse in the setting of pre-renal and intrinsic renal failure.

Empagliflozin-Associated Euglycemic Diabetic Ketoacidosis Masked by Urinary Tract Infection.

Sodium-glucose co-transporter 2 (SGLT2) inhibitors have demonstrated efficacy in slowing the progression of chronic kidney disease (CKD), managing conditions such as congestive heart failure (CHF), and reducing cardiovascular and overall mortality in patients with type 2 diabetes mellitus (T2DM). However, their use is associated with complications, including euglycemic diabetic ketoacidosis (euDKA), genital fungal infections, and urinary tract infections (UTIs). Although rare, complications like euDKA can lead to serious consequences if not promptly addressed, as illustrated by this case report of a 90-year-old man with ischemic cardiomyopathy and type 2 diabetes who developed both euDKA and a UTI while on SGLT2 inhibitor therapy. Early identification of euDKA from SGLT2 inhibitor usage prompted cessation of the SGLT2 inhibitor and administration of insulin infusion, ultimately resolving the life-threatening condition.

Using Acidosis as a Surrogate for or Supplement to the Bedside Index of Severity in Acute Pancreatitis Scoring Prediction System Has a Nonsignificant Effect.

Currently, risk stratification calculators for acute pancreatitis (AP) can at best predict acute pancreatitis mortality at 12 hours from the presentation. Given the severe morbidity associated with AP, the identification of additional prognostic indicators, which may afford earlier prediction in length of stay (LOS) and mortality, is desired. Metabolic acidosis can be a prognostic marker for the severity of AP, and venous bicarbonate can reliably and accurately be substituted for arterial base deficit to detect metabolic acidosis. Since serum bicarbonate, anion gap (AG), and corrected AG (CAG) are routinely obtained upon presentation to the emergency department and often daily in the hospital, we conducted a retrospective analysis of 443 patients, evaluating if venous bicarbonate could predict the severity of pancreatitis as well as mortality, admission to the ICU, ICU LOS, and hospital LOS. The inclusion of venous bicarbonate, AG, and CAG in the first 12 hours only slightly improved the predictive capabilities of the Bedside Index for Severity in Acute Pancreatitis (BISAP) score for these secondary outcomes. None of our incorporations of acidemia improved severity predictions more than the BISAP alone. Adding CAG to BISAP scoring had the largest effect on predicting ICU admission and hospital LOS (area under the curve (AUC): 1.12 (confidence interval (CI) 95%: 1.06-1.19), p <.001 and AUC 1.02 (CI 95% 1.01-1.04), p <.001; respectively). ICU LOS was not impacted by the addition of AG, CAG, or venous bicarbonate. In-hospital death (n=12) was too small to be determined.

A case report of Paracetamol related pyroglutamic acidosis: mind the gap in a malnourished patient.

BACKGROUND: Pyroglutamic acidosis is a rare cause of high anion gap metabolic acidosis. Most cases of paracetamol related pyroglutamic acidosis are described in malnourished women and patients with kidney/liver failure, alcohol use or severe sepsis. In this report, we describe how pyroglutamic acidosis could be related to the use of chronic therapeutic paracetamol with only malnutrition as an associated risk factor. CASE PRESENTATION: We report a case of a 67-year-old male patient developing a pyroglutamic acidosis. The patient was initially admitted to hospital for infectious osteoarthritis and developed a metabolic acidosis during his hospital stay. Analgesics included daily therapeutic doses of paracetamol. What makes our case unusual is that our malnourished male patient did not have renal or hepatic failure. The diagnosis of paracetamol related pyroglutamic acidosis was made after ruling out the main causes of metabolic acidosis. It was further confirmed by urine organic acids measurement showing a markedly elevated level of pyroglutamic aciduria. Paracetamol was discontinued allowing a prompt correction of the anion gap. CONCLUSION: This case is a representative of pyroglutamic acidosis related to chronic therapeutic paracetamol with only malnutrition as an associated risk factor. Physicians should be aware of such unusual cause of metabolic acidosis, which may be more common than expected in hospitalized patients. A high clinical suspicion is needed when urine organic acids analysis is not available.

Diabetic Ketoacidosis Presenting as Abdominal Pain in a Two-Year-Old Female: A Case Report.

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes and can sometimes be the first indication of undiagnosed type 1 diabetes mellitus (T1DM). Our case presents a unique scenario in which a two-year-old female presented to her pediatrician with persistent abdominal pain, along with fatigue and tachypnea. On physical examination, she was mildly distressed, tachypneic, and utilized accessory muscles during respiration. Subsequent urinalysis indicated elevated glucose levels of 500 milligrams/deciliter (mg/dL). She was promptly referred to the emergency department to be treated for DKA. Upon arrival, the patient's glucose level was elevated at 533 mg/dL, with an anion gap of 25. She was stabilized and admitted to the pediatric intensive care unit (PICU) with a new diagnosis of T1DM with ketoacidosis. Given the emergent nature of DKA and the need for immediate treatment, physicians should consider DKA as a potential diagnosis for any pediatric patient presenting with abdominal pain.

A Case of Metformin-Associated Lactic Acidosis Complicated by Acute Liver Failure, Acute Renal Failure, and Shock.

Metformin is an oral antihyperglycemic agent used for type 2 diabetes mellitus (T2DM) management and is considered to be the first-line treatment for diabetic patients. It works by improving insulin sensitivity, reducing intestinal absorption, and decreasing glucose production in the liver, leading to decreased blood glucose levels. It is generally considered a safe drug; however, it is associated with an uncommon but serious side effect known as metformin-associated lactic acidosis (MALA), a potentially life-threatening condition. Patients with renal failure and liver disease are at high risk of developing MALA; therefore, the medication should be used cautiously in these patients. The diagnosis of MALA requires high suspicion from the physician of this specific entity; otherwise, it may be easily missed. Herein, we report a case of a 63-year-old female with alcoholic liver disease on metformin who was found to have MALA complicated by acute decompensated liver failure, renal failure, and shock.

Mind the Anion Gap: 5-Oxoproline-Induced High Anion Gap Metabolic Acidosis in End-Stage Renal Disease.

A rare complication, 5-oxoproline-induced high anion gap metabolic acidosis (HAGMA) is associated with chronic acetaminophen use, predominantly reported in outpatient settings. However, its occurrence in hospitalized patients, particularly those with end-stage renal disease (ESRD), remains underreported. We present a case of a 74-year-old female with ESRD on hemodialysis who developed HAGMA highly suspicious for 5-oxoproline toxicity from acetaminophen usage following cardiac surgery. Despite a standard analgesic dose, the patient's renal impairment likely predisposed her to 5-oxoproline accumulation, resulting in severe metabolic acidosis. Discontinuation of acetaminophen led to the resolution of HAGMA, highlighting the importance of recognizing this rare but potentially life-threatening complication in the inpatient and critical care setting. This case suggests a potential interaction between acetaminophen metabolism and renal dysfunction in the pathogenesis of 5-oxoproline-induced HAGMA.

Ethylene Glycol Poisoning: A Case Study of a 71-Year-Old Male with a History of Alcohol Abuse and Suicide Attempts.

A 71-year-old male with a history of alcohol abuse and multiple suicide attempts was brought to the emergency department in an unconscious state. Initial assessment revealed profound obtundation and malnutrition. Laboratory findings demonstrated a significant anion gap metabolic acidosis with a high osmolar gap, suggestive of possible toxic alcohol ingestion. Despite negative serum alcohol levels, ethylene glycol poisoning was confirmed with a level of 226. Treatment included fluid resuscitation, bicarbonate therapy, and fomepizole administration. However, due to progressive multi-organ failure, continuous veno-venous hemodialysis was initiated. Despite interventions, the patient deteriorated rapidly, leading to a decision for hospice care, ultimately resulting in death. Ethylene glycol poisoning presents significant challenges in management, with potential complications including renal failure and multi-organ dysfunction. Fomepizole remains the cornerstone of treatment, but additional therapies such as ethanol administration were considered but ultimately deemed unnecessary due to associated risks. This case highlights the complexity and severity of ethylene glycol poisoning, emphasizing the need for early recognition and aggressive management strategies.

Propylene glycol toxicity in an adolescent secondary to chronic cornstarch ingestion.

Propylene glycol (PG) is a diol (a double alcohol) that is commonly used as a food additive to preserve shelf life and enhance flavors, texture, and appearance. Although PG makes up only a small percentage of cornstarch, ingestion of large doses can cause lactic acidosis leading to hyperosmolarity, high anion gap metabolic acidosis (HAGMA), and a sepsis-like syndrome. A 17-year-old female presented to our emergency department (ED) with chronic chest pain, dyspnea, nausea, and vomiting. Laboratory testing showed an elevated anion gap of 18 mEq/L with no osmolar gap. Toxicology screening was negative. Twelve hours after ED arrival, she admitted to consuming one box of cornstarch daily for the past 6 months. She was admitted to the intensive care unit (ICU) with multisystem organ failure due to propylene glycol toxicity. After empiric treatment with fomepizole and continuous renal replacement therapy, her clinical status gradually improved. This case highlights the importance of obtaining a thorough dietary history in patients with suspected toxicities, especially when laboratory values demonstrate an unexplained HAGMA and/or lactic acidosis. Prompt recognition and therapeutic intervention with fomepizole, a potent inhibitor of alcohol dehydrogenase, is essential in reducing life-threatening sequelae following toxic alcohol ingestions.

Pseudo-Hypobicarbonatemia in Patients With Hypertriglyceridemia.

Hypobicarbonatemia with an elevated anion gap on a metabolic panel is frequently the initial marker of a life-threatening condition such as diabetic ketoacidosis in a patient with epigastric pain. The two commonly used means of measuring bicarbonate levels are direct measurement from a metabolic panel and calculated measurement from arterial blood gas. In this case report, we would like to highlight a potentially serious deficiency in one of these two means and how it may lead to a dangerous misdiagnosis and subsequent mismanagement. We also shine a light on potential measures to counteract or prevent this undesirable outcome.

Profound Hypoglycemia and High Anion Gap Metabolic Acidosis in a Pediatric Leukemic Patient Receiving 6-Mercaptopurine.

A 13-year-old male undergoing maintenance chemotherapy with methotrexate and 6-mercaptopurine (6MP), for very high-risk B-cell acute lymphoblastic leukemia (ALL), presented with vomiting due to severe hypoglycemia with metabolic acidosis. While his laboratory values were concerning for a critically ill child, the patient was relatively well appearing. Hypoglycemia is a rare but serious side effect of 6MP with an unexpectedly variable presentation; therefore, a high index of suspicion is needed for its prompt detection and treatment. This patient also had severe metabolic acidosis, likely secondary to hypoglycemia, creating a serious clinical picture despite a well-appearing child. This example of incongruity between laboratory tests and clinical appearance adds nuance to the existing literature. Moreover, although 6MP-associated hypoglycemia is rare, it may be more prevalent than the literature suggests, as symptoms of hypoglycemia-nausea, vomiting, and somnolence-mirror common chemotherapy side effects. 6MP-induced hypoglycemia can be ameliorated with the addition of allopurinol to shunt metabolism in favor of the production of therapeutic metabolites over hepatotoxic metabolites. Additionally, a morning administration of 6MP and frequent snacks may also help to prevent hypoglycemia. Overall, this case adds to the literature of unusual reactions to 6MP including hypoglycemia in an older child without traditional risk factors.

Profound metabolic acidosis in association with sodium thiosulfate therapy in a patient with calcific uremic arteriolopathy: a case report and literature review.

Calciphylaxis, also known as Calcific uremic arteriolopathy (CUA), is a serious disorder that presents with skin necrosis due to calcification of dermal and subcutaneous adipose tissue capillaries and arterioles. The condition occurs primarily in patients with end-stage renal disease (ESRD) on dialysis, and it carries high morbidity and mortality, primarily due to sepsis, with an estimated six-month survival of approximately 50%. Although there are no high-quality studies to guide the optimal treatment approach for patients with calciphylaxis, many retrospective studies and case series support treatment with sodium thiosulfate (STS). Despite the frequent use of STS as an off-label treatment, data regarding its safety and efficacy are limited. STS has generally been considered a safe drug with mild side effects. However, severe metabolic acidosis associated with STS is a rare and life-threatening complication of STS treatment and is often unpredictable. Herein, we report a 64-year-old female with ESRD on peritoneal dialysis (PD) who presented with a profound high anion gap metabolic acidosis and severe hyperkalemia while on STS treatment for CUA. No other etiology for her severe metabolic acidosis other than STS was identified. ESRD patients receiving STS should be monitored closely for this side effect. Dose reduction, increasing the duration of infusion, or even discontinuing STS treatment should be considered if severe metabolic acidosis develops.

The Cause of Severe Metabolic Acidosis With Vomiting in a Neonate.

We present a 22-day-old male born full term who presented with worsening non-projectile, non-bilious vomiting and failure to thrive (FTT) and was admitted to the pediatric intensive care unit (PICU) for severe metabolic acidosis with an elevated anion gap. Despite changing the formula, the patient continued to have spit-ups after feeds since birth. Before this admission, his vomiting worsened with every feed, which was now forceful along with two days of loose stools. Obstructive causes of emesis were ruled out with an upper gastrointestinal series, and a decision was made to evaluate for organic causes of FTT. Transient resolution of symptoms was noticed when the patient was placed NPO (nothing by os/mouth) briefly. His symptoms returned on resuming cow milk-based formula feeds. At this time, a presumptive diagnosis of cow milk protein allergy (CMPA) was made. Positive fecal occult blood supported the diagnosis, and his formula was changed to an extensively hydrolyzed formula (eHF). This is a case of severe CMPA with prolonged vomiting and FTT presenting with severe metabolic acidosis with an elevated anion gap. This case report highlights how CMPA can lead to severe dehydration with metabolic acidosis and increased anion gap.

Assessing the Role of Initial Serum Calcium Concentration in Patients with Ethylene Glycol Poisoning.

INTRODUCTION: Assays for ethylene glycol (EG) with a rapid turn-around time are not routinely available. Clinicians must rely on historical features and readily available clinical tests, combined with clinical acumen, to guide the initial management of suspected EG poisoning. Hypocalcemia has been suggested as a clue supporting the diagnosis of EG poisoning in patients presenting with an unexplained high anion gap metabolic acidosis (HAGMA). A previous small study challenged this assumption. METHODS: This was a retrospective case series of one state's poison control system of confirmed EG-poisoned patients between September 2017 and April 2021. The definition of EG poisoning was based on suspected EG ingestion and a serum EG concentration > 5 mg/dL. Patients who were suspected to have EG toxicity but did not have a confirmed EG concentration or the EG concentration was less than 5 mg/dL were excluded. Routine laboratory studies were recorded for all patients. Comparisons between serum calcium on presentation to presenting blood pH, bicarbonate, anion gap, and creatinine were assessed for correlation. RESULTS: There was no correlation between the presenting calcium and either pH or creatinine. There was a weak positive correlation between the initial serum calcium and anion gap, a weak negative correlation between the initial serum calcium and bicarbonate. CONCLUSION: On hospital presentation, hypocalcemia was not associated with EG poisoning, even in patients with a HAGMA. A normal serum calcium on presentation does not exclude the diagnosis of EG poisoning.

Normal Anion Gap: A Knowledge Gap.

We studied with great interest the article titled "Acute diarrhea and severe dehydration in children: Does non-anion gap component of severe metabolic acidemia need more attention?" by Takia L et al. and would express our views about the same. Normal anion gap metabolic acidosis (NAGMA) is a common entity following stool loss of bicarbonate during an acute diarrheal illness. Several studies have shown that there is a higher incidence of hyperchloremic acidosis and acute kidney injury (AKI) with normal saline (NS) when compared to balanced crystalloids like Ringer's lactate (RL) or balanced salt solutions like plasmalyte. We would like to know about the type of resuscitation fluid used in the study population as it would affect the degree of resolution of acidemia. As per the World Health Organization (WHO) guidelines, rehydration therapy for children with severe acute malnutrition (SAM) is different from other children including the fluid used for bolus, i.e., RL and oral rehydration solution (ORS), i.e., rehydration solution for malnourished (ReSoMal). We would like to know if the study population included SAM children and a subgroup analysis of the same was done as SAM is an independent risk factor for mortality and morbidity. We suggest to plan studies on cognitive outcome of these children. How to cite this article: Pratyusha K, Jindal A. Normal Anion Gap: A Knowledge Gap. Indian J Crit Care Med 2023;27(4):298.

Topiramate-Induced Coma in a 39-Year-Old Female Patient: Burst Suppression on EEG.

Reported cases of topiramate ingestion resulting in coma and generalized convulsive status epilepticus are very rare. Such a phenomenon of a relatively safe antiepileptic drug (AED) causing serious neurological compromise should be carefully reviewed. A 39-year-old female with a history of uncontrolled epilepsy, migraine headaches, hypothyroidism, obsessive-convulsive disorder, and depression presented with generalized tonic-clonic seizures that progressed to status epilepticus and coma thereafter. She was intubated due to a depressed level of consciousness and transferred afterward to our hospital. Electroencephalography (EEG) demonstrated a burst suppression pattern without receiving any sedating agents. The level of consciousness improved on the fourth day, and she achieved complete neurological recovery by the sixth day of hospitalization. She was offered AEDs and supportive therapy during her admission. Upon further investigation into the cause of her seizures, it was discovered that she had ingested a large dose of topiramate in a suicide attempt.

From Toxic Ingestion to Cancer: Dramatic Acidosis as a Myeloma-Defining Event.

Acute kidney failure has myriad causes and presentations. This is a case of an individual with a history of alcohol abuse and a previous suicide attempt presenting with acute kidney failure and altered mentation accompanied by an anion gap metabolic acidosis with an elevated osmolar gap. These findings were concerning for toxic alcohol ingestion, but the patient was ultimately diagnosed with multiple myeloma. This case demonstrates the multiple factors that can impact both the anion and osmolar gaps. It shows that the traditionally held dogma about the meaning of anion or osmolar gaps may cloud an otherwise more obscure etiology. It illustrates a dramatic presentation of acute myeloma, for which early recognition is essential to initiate appropriate chemotherapy for a chance at preservation of renal function.

An Unrecognized Cause of Elevated Procalcitonin Level.

Diabetic Ketoacidosis (DKA) is a preventable yet serious complication of diabetes that is commonly associated with type 1 diabetes but can also occur in other forms of diabetes, including type 2. Infection is a primary cause of DKA and can lead to elevated levels of procalcitonin (PCT), which is a biomarker used to differentiate bacterial infections from non-infectious inflammation. However, some cases of DKA have shown increased PCT levels even in the absence of bacterial infection, and the underlying mechanism of this observation is not fully understood. To gain a better understanding of how non-infectious inflammation affects PCT levels, further research is needed. While PCT is a helpful biomarker, it should be interpreted in the context of the patient's overall clinical picture, including signs and symptoms of infection or inflammation and underlying medical conditions that may be contributing to their presentation. A systematic approach to evaluating and managing patients with DKA can minimize the risk of unnecessary antibiotic use and ensure optimal treatment. We present a 31-year-old male who was admitted to the ICU with DKA, and further investigations revealed elevated PCT levels. Despite conducting several studies and cultures, including blood and urine, no infections were detected. The patient was treated for DKA with hydration and insulin administration without the use of antibiotics, and his PCT levels subsequently decreased.

A Case of Metformin-Associated Lactic Acidosis.

Metformin is a US FDA-approved oral anti-hyperglycemic medication used to treat non-insulin-dependent diabetes mellitus (NIDDM). Metformin, a biguanide drug, works by reducing glucose production in the liver, decreasing intestinal absorption, and improving insulin sensitivity, leading to lower blood glucose levels. Metformin is generally considered to be a medication with a good safety profile and high tolerability. However, metformin therapy is associated with an uncommon but potentially serious complication known as metformin-associated lactic acidosis (MALA), which is marked by severe lactic acid accumulation in the bloodstream. This case introduces an elderly female with multiple comorbidities who presented with confusion, malaise, and lethargy. Her laboratory findings revealed acute renal failure, severe metabolic acidosis, and significantly elevated lactic acid levels consistent with sepsis and possibly MALA. Aggressive resuscitation with fluids and sodium bicarbonate was initiated. Antimicrobial drugs were started for urinary tract infections. She subsequently required endotracheal intubation with invasive ventilation, pressor support, and continuous renal replacement therapy. Her condition gradually improved over several days. The patient ultimately recovered, and at the time of discharge, metformin was discontinued, and a sodium-glucose cotransporter-2 (SGLT-2) inhibitor was initiated. This case underscores the relevance of MALA as a potential complication of metformin therapy, particularly in patients with underlying kidney disease or other risk factors. Timely detection and prompt management of MALA can prevent progression to a critical stage and thus avoid potentially fatal outcomes.