High Anion Gap Acidosis Research Articles

Approach to poisoned patients with high anion gap metabolic acidosis in the emergency department - a case series

Toxicology cases are frequent presentations in the emergency department (ED) and often their presentation can vary from a straightforward manner to a complex manner. In this case series we will discuss three cases that presented to the ED with a known, suspected, and unknown toxicological substance ingestion with the common denominator being high anion gap metabolic acidosis (HAGMA). HAGMA is a subcategory of metabolic acidosis. Categorizing metabolic acidosis as a high anion gap aids in identifying the underlying disease process and subsequently initiating appropriate treatment. There have been many broadly inclusive mnemonics used to list the common causes of High anion gap acidosis such as CAT MUDPILES which correspond to Carbon monoxide, Cyanide, Congenital heart disease, Aminoglycosides, Theophylline, Toluene, Methanol, Uremia, Diabetic ketoacidosis, Alcoholic ketoacidosis, Starvation, Acetaminophen, Phenformin, Paraldehyde, Iron, Isoniazid, Inborn errors of metabolism, Lactic acidosis, Ethanol, Ethylene glycol, and Salicylates, respectively. It is not uncommon to be faced with patients with an unclear clinical picture and a lack of clear toxicological ingestion. In such circumstances, the presence of a high anion gap acidosis is an important clue that should prompt investigating for uncommon toxicological causes not listed in the forementioned mnemonics, such as metformin, beta blockers, and CCBs.

Approach To Poisoned Patients with High Anion Gap Metabolic Acidosis in The Emergency Department – A Case Series

Toxicology cases are frequent presentations in the emergency department (ED) and often their presentation can vary from a straightforward manner to a complex manner. In this case series we will discuss three cases that presented to the emergency department with a known, suspected, and unknown toxicological substance ingestion with the common denominator being high anion gap metabolic acidosis (HAGMA). High Anion Gap Metabolic acidosis is a subcategory of metabolic acidosis. Categorizing metabolic acidosis as high anion gap aids in identifying the underlying disease process and subsequently initiating appropriate treatment. There have been many broadly inclusive mnemonics used to list the common causes of High anion gap acidosis such as CAT MUDPILES which correspond to Carbon monoxide, Cyanide, Congenital heart disease, Aminoglycosides, Theophylline, Toluene, Methanol, Uremia, Diabetic ketoacidosis, Alcoholic ketoacidosis, Starvation, Acetaminophen, Phenformin, Paraldehyde, Iron, Isoniazid, Inborn errors of metabolism, Lactic acidosis, Ethanol, Ethylene glycol and Salicylates respectively. It is not uncommon to be faced with patients with an unclear clinical picture and a lack of clear toxicological ingestion. In such circumstances, the presence of a high anion gap acidosis is an important clue that should prompt investigating for uncommon toxicological causes not listed in the forementioned mnemonics, such as metformin, beta blockers and calcium channel blockers.

A Fatal Case of 3‐Hydroxyisobutyryl‐CoA Hydrolase Deficiency in a Term Infant with Severe High Anion Gap Acidosis and Review of the Literature

3‐hydroxy isobutyl‐CoA hydrolase (HIBCH) deficiency is a recently described, rare inborn error of valine metabolism associated with a Leigh syndrome‐like phenotype, neurodegenerative symptoms, and caused by recessive mutations in the HIBCH gene. We report the most severe case to date of an intrauterine growth‐restricted term male who presented with severe acidosis and a high anion gap soon after birth. The manifestation was fatal that led to death within 36 hours of life. The diagnosis was made postnatally by Whole Genome Sequencing (WGS). We report a rapid and fatal event of HIBCN in a neonate and review of the literature.

A Literature Review of the Therapeutic Perspectives of Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitor-Induced Euglycemic Diabetic Ketoacidosis.

Euglycemic diabetic ketoacidosis (DKA), a side effect of sodium-glucose cotransporter-2 (SGLT2) inhibitors, is a triad of high metabolic anion gap acidosis, raised serum and urine ketones, and serum glucose <250 mg/dl. SGLT2 inhibitors cause a carbohydrate deficit by glucosuria, which leads to an increased glucagon/insulin ratio, the metabolic shift from glucose to lipid utilization causing ketogenesis, and hence euglycemic DKA. Additional factors like the ketogenic diet, illness, surgery, and pregnancy contribute to precipitating these episodes. Keywords searchincluded "Euglycemic DKA and SGLT2 inhibitors" in PubMedand Google Scholar, to compile data from existing articles that provide information on the withholding and restarting period of the drug after a euglycemic DKA episode. SGLT2 inhibitors, used in the treatment of type 2 DM, have an average half-life of 11-13 hours, so most articles suggested withholding the drug three days before any elective surgery but some articles suggested a longer withholding period based on other precipitating factors contributing to euglycemic DKA. Hence, we came up with patient inclusion criteria and concomitant therapies review that we need to consider in making this decision. In addition, a multidisciplinary approach is required when laying out guidelines for restarting the drug to have a unanimous approach. After reviewing the existing literature, it is clear that concrete guidelines are required to decide on drug withholding and restarting periods after a euglycemic DKA episode, as they vary among different institutions and different specialties. We believe it is crucial to consider patient inclusion criteria and concomitant therapies in forming those guidelines.

Time-updated anion gap and cardiovascular events in advanced chronic kidney disease: a cohort study.

ABSTRACTBackgroundStudies examining associations between metabolic acidosis and cardiovascular events in chronic kidney disease (CKD) have shown conflicting results and have not differentiated between normal anion gap (hyperchloremic) acidosis and high anion gap acidosis. We aimed to examine the impact of normal and high anion gap acidosis, separately, on the risk of cardiovascular events among patients with CKD.MethodsThis retrospective cohort study included 1168 patients with an estimated glomerular filtration rate (eGFR) of 10–60 mL/min/1.73 m2 and available data on anion gap. We analyzed the association of time-updated high anion gap (anion gap ≥9.2) with the rate of cardiovascular events using marginal structural models (MSMs) to account for time-dependent confounding. We also analyzed the association between time-updated normal anion gap acidosis (anion-gap-adjusted bicarbonate level ≤22.8 mEq/L) and cardiovascular events.ResultsThe mean baseline eGFR of the cohort was 28 mL/min/1.73 m2. The prevalence rates of high anion gap in CKD stages G3a, G3b, G4 and G5 were 20%, 16%, 27% and 46%, respectively. During a median follow-up period of 2.9 years, 132 patients developed cardiovascular events (3.3/100 patient-years). In MSMs, high anion gap was associated with a higher rate of cardiovascular events [hazard ratio (HR) 1.87; 95% confidence interval (95% CI) 1.13‒3.09; P = 0.02] and the composite of cardiovascular events or all-cause death (HR 3.28; 95% CI 2.19‒4.91; P < 0.001). Normal anion gap acidosis was not associated with cardiovascular events (HR 0.74; 95% CI, 0.47‒1.17; P = 0.2).ConclusionsAmong patients with advanced CKD, high anion gap was associated with an increased risk of cardiovascular events.

Association of Time-Updated Anion Gap With Risk of Kidney Failure in Advanced CKD: A Cohort Study

High anion gap acidosis frequently develops in patients with advanced chronic kidney disease (CKD) and might be involved in kidney injury. Its impact on kidney outcomes, however, has not been well studied. We sought to examine the association between time-updated anion gap and the risk of kidney failure with replacement therapy (KFRT) among patients with advanced CKD. Retrospective cohort study. 1,168 patients with CKD glomerular filtration rate categories 3b-5 (G3b-G5) who had available data on anion gap. High time-updated anion gap defined as values ≥ 9.2 (top 25th percentile). KFRT and death. Marginal structural models were fit to characterize the association between anion gap and study outcomes while accounting for potential time-dependent confounding. The mean baseline estimated glomerular filtration rate (eGFR) of the study participants was 28 mL/min/1.73 m2. Over a median follow-up period of 3.1 years, 317 patients progressed to KFRT (7.5 per 100 patient-years), and 146 died (3.5 per 100 patient-years). In the marginal structural models, a high anion gap was associated with a higher rate of KFRT (HR, 3.04 [95% CI, 1.94-4.75]; P < 0.001). This association was stronger in patients with a baseline eGFR of <30 mL/min/1.73 m2 (P for interaction = 0.05). High anion gap was also associated with a higher mortality rate (HR, 5.56 [95% CI, 2.95-10.5]; P < 0.001). Sensitivity analyses with different definitions of high anion gap showed similar results. Observational study design and selection bias due clinical indications for measuring anion gap. Among patients with advanced CKD, high anion gap was associated with an increased risk of progression to KFRT and death.

Hyperchloremic acidosis develops at the stage G4 and shifts to high anion gap acidosis at the stage G5 in chronic kidney disease.

Amelioration of hyperchloremic acidosis (Cl-Ac), a common complication in chronic kidney disease (CKD), could preserve renal function in chronic kidney disease (CKD). However, the development of Cl-Ac in CKD has not been clarified yet. The degree of Cl-Ac, which is indicated as the bicarbonate concentration decrease with serum chloride concentration increase (∆[HCO3-]Cl), was compared with the estimated glomerular filtration rate (eGFR) by using CKD patient records. In 307 records with metabolic acidosis, a spline curve obtained from the plot comparing ∆[HCO3-]Cl with eGFR showed that ∆[HCO3-]Cl did not change, increased, and decreased during eGFR decrease until 27, from 27 to 17.5, and from 17.5mL/min/1.73m2, respectively. By CKD progression, Cl-Ac progressed and regressed at the CKD stages G4 and G5, respectively. The regression would have reflected the shift of Cl-Ac to high anion gap acidosis.

Pancreatic ketoacidosis-a rare case report

Euglycemic Pancreatic Ketoacidosis is a syndrome of high anion gap acidosis in which the high anion gap is due to elevated serum ketone bodies comprising of acetone, aceto- acetate and beta hydroxyl-butyrate, due to increased peripheral adipose tissue breakdown by elevated serum lipase as a consequence of acute pancreatitis with normal blood glucose levels. There are multiple causes for ketonuria and/or ketonemia with or without acidosis like uncontrolled diabetes mellitus, usually of the insulin dependent type (diabetic ketoacidosis), lactic acidosis, prolonged starvation (starvation ketosis), ethanol ingestion (alcoholic ketoacidosis), sepsis, pregnancy and vomiting. Our patient was not a known diabetic and his blood glucose were always within normal limits, so this ketoacidosis cannot be attributed to Diabetes Mellitus. It cannot be attributed to starvation as our patient was not fasting when he got admitted and furthermore ketoacidosis is not a frequent manifestation of starvation adding to it that we transfused adequate amount of DNS and resumed oral intake during our observation period. It cannot be attributed to vomiting as our patient had only two episodes of vomiting. Our patient does not have any liver or kidney pathology and there is no history or evidence of alcohol intoxication. But, acute pancreatitis without diabetes-mellitus, causing ketoacidosis is a very rare presentation which is caused by high levels of pancreatic lipase in the circulation.

Neurocognitive outcome in young child with Isovaleric Acidemia

Isovaleric Acidemia (IVA) is inherited as an autosomal recessive trait, caused by the deficiency of the enzyme isovaleryl CoA dehydrogenase. It has the prevalence of 1 in 62,500 (in parts of Germany) to 1 in 250,000 live births (in the United States). Acute episodes of metabolic decompensations may occur, which may mimic sepsis, ketosis or shock. Early diagnosis &amp; early initiation of treatment has been reported to correlate with a good neurocognitive outcome. This is case of child presenting in Paediatric emergency department with fever, vomiting, increased respiratory activity and lethargy. Child had GCS score of 8/15, acidotic breathing, hypotonia with hyporeflexia. Sepsis screen, metabolic work up and neuroimaging were all normal except for high anion Gap acidosis with ketosis. So further neurometabolic screening work up was done in view of persistent metabolic acidosis, developmental delay, and bad obstetric history in mother. It revealed increased excretion of isovalerylglycine 1(IVG 1), Isovalerylglycine 2 (IVG2) Lactate, 3-Hydroxypropionate (3HP) and 3-Hydroxybutyrate (3 HB).Serum lactate 358.54 (control 1.1-208.1) confirming the diagnosis of Isovaleric Acidemia. After recovery from the acute attack, the patient was advised low-protein diet (1.0-1.5 g/kg/24 hrs.) and carnitine (100 mg/kg/24 hrs. orally) supplements. On follow up child is asymptomatic &amp; showing neurological improvement as he started achieving further developmental milestones during 6 months follow up.Early diagnosis and early treatment of IVA cases definitely results in favorable outcome and better prognosis. But chronic intermittent cases presenting late should not be neglected, proper medical management can reverse neuromotor consequences in them also.

CRRT in critically Ill children: Clinical profile from a tertiary care hospital in South India

Background : Continuous renal replacement therapy (CRRT) is a valuable tool in a pediatric intensive care unit (PICU), however the literature available from developing countries is scarce. Methods : Retrospective analysis of children who underwent CRRT during the past 1 year (June 2016 to May 2017). 24 sessions of CRRT was performed in 22 patients using Prismaflex® Baxter. Serum levels of urea, creatinine, and liver function tests were done in all patients. Activated clotting time (ACT) was monitored in all patients every 1 hourly till target ACT was achieved (180 – 220 seconds), thereafter every 4 hourly if the ACT continues in the target range. Unfractionated heparin was used for anticoagulation. Blood priming was done in patients with hematocrit less than 30% or in infants weighing less than 10 kg. Hemodialysis catheter (8.5Fr) was used in all patients, placed in the right internal jugular vein (IJV) under ultrasound guidance. Transthoracic echocardiography was used in all patients to confirm the position of the catheter tip within the right atrium. Central venous access in the femoral vein and arterial blood pressure monitoring was done in all patients as per unit protocol. Primary outcome measure was death during the procedure. Data collected were part of PRBC transfusion in pediatric ICU study and fluid balance study at JIPMER. Results : The median age of patients was 2 years (1 to 6 IQR). Mean bodyweight was 13.4 kg, 6.6 SD. Continuous venovenous hemofiltration (CVVH) was done in 5 patients (22.7%) and 17 patients (67.3%) were started on continuous venovenous hemodiafiltration (CVVHDF). Mortality during the procedure among the patients who underwent CRRT was 50% (n=11). Mean PRISM III score was 14. Out of 22 patients, 15 patients (68.7%) were on vasoactive medications at the time of initiation of CRRT. Median fluid overload (FO%) was 0.62 (0.45 to 1.62 IQR). Average time to start CRRT since PICU admission was 55 hours. The common indications were acute kidney injury with fluid overload (n=9), acute liver failure with hyperammonemia (n=3), organic acidemia with severe high anion gap acidosis (n=1), unknown poisoning with high anion gap acidosis (n=2), pigment nephropathy following wasp sting (n=1) and electrocution (n=1). CRRT along with venovenous extra corporeal membrane oxygenation (vv ECMO) (n=1) was done in a case of hemophagolymphohistiocytosis syndrome with ARDS. Effluent dose 35ml/kg/hour in all patients except in 2 cases of acute liver failure where the effluent dose was increased up to 42ml/kg/hour due to persistent hyperammonemia. CRRT with plasma exchange using P2 plasma filter was done with CRRT circuit modification in 2 cases of thrombocytopenia associated multiorgan failure (TAMOF). Mean duration of CRRT was (55 hours, SD 23.8). Maximum circuit life with systemic heparin as anticoagulant was 92 hours. Filter clotting and new circuit requirement was encountered in 6 patients (27.7%). Conclusion : CRRT can be used safely in critically ill children. The circuit life can be prolonged with serial ACT monitoring and titration of anticoagulation.

Acute Esophageal Necrosis: A Case Report and Review of Literature

Acute esophageal necrosis (AEN), or “black esophagus,” is a rare phenomenon with increasing interest due to its unclear mechanism and multifactorial associated etiologies. It is an endoscopic diagnosis demonstrating proximal mucosal extension of circumferential black friable mucosa from the distal esophagus that spares the gastroesophageal junction. We present the case of a 47-year-old Caucasian male with a medical history of type 2 diabetes mellitus & compensated alcoholic cirrhosis presenting to the emergency department with abdominal pain and intractable nausea with vomiting. The patient was afebrile, hypotensive, and tachycardic, with initial blood tests demonstrating a serum glucose 1062 mg/dL, creatinine 3.12 mg/dL, and a blood gas consistent with a high anion gap acidosis with a venous pH of 7.167. The patient was treated appropriately for diabetic ketoacidosis with normalization of blood sugars, and further examination revealed a small amount of blood in the oropharynx and rectum. He was started on intravenous (IV) octreotide and an IV proton pump inhibitor (PPI). An esophagogastroduodenoscopy (EGD) was performed, which demonstrated moderate to severe circumferential esophagitis noted in the proximal esophagus with uniformly black ulcerations extending to the squamocolumnar junction with clear demarcation of this finding distal to the squamocolumnar line (Figure 1), in addition to multiple duodenal ulcers. The patient was subsequently treated with oral high dose PPI twice daily and discharged in good condition. This case illustrates the importance of including AEN in the vast differential diagnosis of gastrointestinal (GI) bleeding. The prevalence of AEN is around 0.2% and has an associated mortality as high as 36% in studies when patients have a comorbidity. AEN typically affects elderly men who commonly suffer from diabetes mellitus (specifically diabetic ketoacidosis), duodenal ulcers, malignancy, alcohol abuse, and acute renal insufficiency among other comorbidities. In addition, malnutrition can predispose patients to developing AEN due to decreased GI mucosal barrier system repair. Our report aims to explore the natural progression of AEN, potential therapeutic measures, and complications of the disease process.Figure 1

A comparison of traditional and quantitative analysis of acid-base imbalances in hypoalbuminemic dogs.

To compare the traditional (HH) and quantitative approaches used for the evaluation of the acid-base balance in hypoalbuminemic dogs. Prospective observational study. ICU of a veterinary teaching hospital. One hundred and five client-owned dogs. Jugular venous blood samples were collected from each patient on admission to determine: total plasma protein (TP), albumin (Alb), blood urea nitrogen (BUN), glucose (Glu), hematocrit (HCT), Na(+) , Cl(-) , K(+) , phosphate (Pi ), pH, PvCO2, bicarbonate (HCO3 (-) ), anion gap (AG), adjusted anion gap for albumin (AGalb ) or phosphate (AGalb-phos ), standardized base excess (SBE), strong ion difference (SID), concentration of nonvolatile weak buffers (Atot ), and strong ion gap (SIG). Patients were divided in 2 groups according to the severity of the hypoalbuminemia: mild (Alb = 21-25 g/L) and severe (Alb ≤20 g/L). All parameters were compared among groups. Patients with severe hypoalbuminemia showed significant decrease in TP (P = 0.011), Atot (P = 0.050), and a significant increase in adjusted AG (P = 0.048) and the magnitude of SIG (P = 0.011) compared to animals with mild hypoalbuminemia. According to the HH approach, the most frequent imbalances were simple disorders (51.4%), primarily metabolic acidosis (84.7%) associated with a high AG acidosis. However, when using the quantitative method, 58.1% of patients had complex disorders, with SIG acidosis (74.3%) and Atot alkalosis (33.3%) as the most frequent acid-base imbalances. Agreement between methods only matched in 32 cases (kappa < 0.20). The agreement between the HH and quantitative methods for interpretation of acid-base balance was poor and many imbalances detected using the quantitative approach were missed using the HH approach. Further studies are necessary to confirm the clinical utility of using the quantitative approach in the decision-making process of the severely ill hypoalbuminemic patients.

A Case of Chronic Ethylene Glycol Intoxication Presenting without Classic Metabolic Derangements

Acute ethylene glycol ingestion classically presents with high anion gap acidosis, elevated osmolar gap, altered mental status, and acute renal failure. However, chronic ingestion of ethylene glycol is a challenging diagnosis that can present as acute kidney injury with subtle physical findings and without the classic metabolic derangements. We present a case of chronic ethylene glycol ingestion in a patient who presented with acute kidney injury and repeated denials of an exposure history. Kidney biopsy was critical to the elucidation of the cause of his worsening renal function.

Metabolic Acidosis with a Raised Anion Gap Associated with High 5-Oxoproline Levels; An Under-Recognized Cause for Metabolic Acidosis in Intensive Care

Metabolic acidosis is a common problem in ICU patients. Frequent causes of metabolic acidosis with a raised anion gap include lactic acidosis and ketoacidosis. In recent years high anion gap acidosis due to acquired 5- oxoprolinuria has been reported in association with chronic paracetamol use 1. There have been occasional reports of acidosis due to 5-oxoproline in an ICU setting 2 but to date there does not seem to be a general awareness of this phenomonen. 5-oxoproline is an amino acid derivative within the γ-glutamyl cycle within the liver, When gluathione stores are depleted γ-glutamycycteine synthase activity increases in an attempt to replenish the glutathione stores. However in the process excess glutamylcycteine is produced which is then converted into 5-oxoproline which can accumulate and cause a metabolic acidosis. We present a case series of unexplained high anion gap metabolic acidoses in ICU associated with an acculumation of 5-oxoproline. These patients had a background history of alcohol abuse and/or malnutrition and had received paracetamol 4 g/day over periods of 2-3 weeks in ICU. Urinary 5-oxoproline levels were tested and were found to be abnormally high. In all these cases cessation of the paracetamol resulted in correction of the acidosis. It is likely that a combination of predisposing factors and prolonged paracetamol treatment resulted in depletion of glutathione stores in these patients. ICU patients may have risk factors for depletion of glutathione stores. Prolonged use of paracetamol in these patients can further deplete gluathione and introduce the risk of developing metabolic acidosis due to 5-oxoproline.

Distúrbios ácido-base em cães com cetoacidose diabética: estudo prospectivo de 60 casos

Diabetic ketoacidosis (DKA) is considered a typical high anion gap metabolic acidosis due to the retention of ketoanions. The objective of this study was to describe the acid-base disturbances of dogs with DKA and further characterize them, according to their frequency, adequacy of the secondary physiologic response, and occurrence of mixed disturbances. Sixty dogs with DKA were enrolled in the study. Arterial blood pH and gas tensions, plasma electrolytes, serum b-hydroxybutyrate (b-OHB), glucose, albumin and urea concentrations were determined for all dogs included in the study. All dogs were evaluated individually and systematically by the traditional approach to the diagnosis of acid-base disorders. Most of the dogs had a high anion gap acidosis, with appropriated respiratory response (n = 18; 30%) or concurrent respiratory alkalosis (n = 14; 23%). Hyperchloremic acidosis with moderated to marked increases in b-OHB was observed in 18 dogs (30%) and 7 of these patients had concurrent respiratory alkalosis. Hyperchloremic acidosis with mild increase in b-OHB was observed in 6 dogs (10%). Four dogs (7%) had a high anion gap acidosis with mild increase in b-OHB and respiratory alkalosis. Most of dogs with DKA had a high anion gap acidosis, but mixed acid-base disorders were common, chiefly high anion gap acidosis and concurrent respiratory alkalosis, and hyperchloremic acidosis with moderated to marked increases in serum b-OHB.

Clinical utility of anion gap in deciphering acid-base disorders

The anion gap (AG) measurement is a very useful tool in the evaluation of patients with acid-base disorders. Once metabolic acidosis is identified, AG will provide the important first step in the differential diagnosis of disorders that either increase the AG and those that leave the AG unchanged. Delta gap is the comparison between change (delta) in the AG and the change (delta) in bicarbonate (HCO(3)(-)). Delta ratio, defined as delta AG:delta HCO(3)(-) is usually 1:1 in patients with an uncomplicated high AG acidosis. A value below 1:1 suggests a combined high and normal AG acidosis. A value above 2:1 suggests a combined metabolic alkalosis and a high AG acidosis. Urine AG (unmeasured anions-unmeasured cations) is an indirect estimate of the urine NH(4)(+) excretion. It is typically negative in patients with normal AG metabolic acidosis secondary to diarrhoea. Utilisation of AG calculations helps clinicians in identifying and treating acid-base disorders.

Metabolic acidosis in the critically ill: Part 2. Causes and treatment

The correct identification of the cause, and ideally the individual acid, responsible for metabolic acidosis in the critically ill ensures rational management. In Part 2 of this review, we examine the elevated (corrected) anion gap acidoses (lactic, ketones, uraemic and toxin ingestion) and contrast them with nonelevated conditions (bicarbonate wasting, renal tubular acidoses and iatrogenic hyperchloraemia) using readily available base excess and anion gap techniques. The potentially erroneous interpretation of elevated lactate signifying cell ischaemia is highlighted. We provide diagnostic and therapeutic guidance when faced with a high anion gap acidosis, for example pyroglutamate, in the common clinical scenario 'I can't identify the acid--but I know it's there'. The evidence that metabolic acidosis affects outcomes and thus warrants correction is considered and we provide management guidance including extracorporeal removal and fomepizole therapy.

South Beach Diet associated ketoacidosis: a case report

IntroductionIt has been previously unclear whether a "mild" degree of low carbohydrate or "starvation" ketonemia and acidosis induced by a low carbohydrate diet is clinically relevant to a patient.Case presentationA 30-year-old Caucasian male on a low carbohydrate diet presented with nausea, vomiting and abdominal pain. The patient's bicarbonate level was 12 and he had hyperglycemia and ketonemia. He was felt to be in diabetic ketoacidosis and was started on intravenous insulin and isotonic saline infusions and responded well. Following cessation of insulin therapy, the patient remained normoglycemic for the remainder of his hospital stay. He later admitted to having been on the South Beach Diet, which is a low carbohydrate diet, for the three weeks prior to his presentation and during which time he had lost 16 pounds. On admission his BMI was 27.1. On presentation, the patient was felt to be in diabetic ketoacidosis but, interestingly, he was subsequently euglycemic without therapy. Following discharge, the patient discontinued the diet plan and he has remained asymptomatic and euglycemic over the following two years.ConclusionThe hyperglycemic ketoacidosis in this patient may have been caused by increased concentrations of free fatty acids in the absence of carbohydrate-induced inhibition of beta-oxidation of fatty acids and in the presence of an abnormally high ratio of glucagons to insulin. Given the present day popularity of low-carbohydrate diet plans, healthcare providers should be aware of the apparent association between such diets and symptomatic ketoacidosis. In a patient with ketoacidosis suspected to be secondary to a low carbohydrate diet, all other causes of high anion gap acidosis should be ruled out before attributing the acidosis to the low carbohydrate diet.

Metabolic acidosis in childhood: why, when and how to treat

To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies. Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines. There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies. Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in the presence of high anion gap acidosis, especially lactic acidosis, diabetic acidosis and cardiopulmonary resuscitation, the use of sodium bicarbonate is not beneficial and has potential adverse effects, limiting its indication. The only points of agreement in the literature refer to the early treatment of the underlying disease and the mechanisms generating metabolic acidemia. Other promising treatment alternatives have been proposed; however, the side effects and absence of controlled studies with pediatric populations translate into lack of evidence to support the routine use of such treatments.

Rhabdomyolysis and Acute Renal Failure After Fire Ant Bites

We describe a 59-year-old patient who developed acute renal failure because of rhabdomyolysis after extensive red fire ant bites. This case illustrates a serious systemic reaction that may occur from fire ant bites. Consistent with the clinical presentation in rhabdomyolysis associated with non-traumatic causes, hyperkalemia, hypophosphatemia, hypocalcemia, and high anion gap acidosis were not observed in this patient. While local allergic reactions to fire ant bites are described in the literature, serious systemic complications with rhabdomyolysis and renal failure have not been previously reported. It is our effort to alert the medical community of the possibility of such a complication that can occur in the victims of fire ant bites.