Early anion gap metabolic acidosis in acetaminophen overdose

Zein, Joe; Wallace, David J.; Kinasewitz, Gary T.; Toubia, Nagib; Kakoulas, Christine

doi:10.1016/j.ajem.2009.04.005

Cited by 19 publications

(11 citation statements)

References 10 publications

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“…Resolution of pyroglutamic acidosis occurred after discontinuation of APAP. Lactic acidosis, another organic acid causing metabolic acidosis, has been reported at the early stage of or prior to APAP-induced liver injury in patients overdosed with APAP (Shah et al 2011 ; Vichot and Rastegar 2014 ; Zein et al 2010 ).…”

Section: Metabolomics For Evaluation Of Apap Injury Biomarkersmentioning

confidence: 99%

Translational biomarkers of acetaminophen-induced acute liver injury

et al. 2015

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Acetaminophen (APAP) is a commonly used analgesic drug that can cause liver injury, liver necrosis and liver failure. APAP-induced liver injury is associated with glutathione depletion, the formation of APAP protein adducts, the generation of reactive oxygen and nitrogen species and mitochondrial injury. The systems biology omics technologies (transcriptomics, proteomics and metabolomics) have been used to discover potential translational biomarkers of liver injury. The following review provides a summary of the systems biology discovery process, analytical validation of biomarkers and translation of omics biomarkers from the nonclinical to clinical setting in APAP-induced liver injury.

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Section: Metabolomics For Evaluation Of Apap Injury Biomarkersmentioning

confidence: 99%

Translational biomarkers of acetaminophen-induced acute liver injury

et al. 2015

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“…The criteria were intended for use in a transplant centre and not early after presentation in the emergency room where intravenous fl uid resuscitation has not been undertaken and the eff ect of high blood levels of paracetamol might contribute to a reversible lactic acidosis. 10,11 The criteria perform less accurately in accidental or intentional staggered overdoses of the drug than after single timepoint deliberate ingestions, and are diffi cult to interpret because their component variables might be confounded by alteration by medical interventions. 12 Since the criteria provide a binary outcome prediction rather than a continuum of risk, their application can also be diffi cult, and they do not address a key clinical question in wait listed patients who show signs of improvement-is it better to remove them from the list or to proceed with transplantation?…”

Section: Introductionmentioning

confidence: 99%

Development and validation of a dynamic outcome prediction model for paracetamol-induced acute liver failure: a cohort study

Bernal

Wang

Maggs

et al. 2016

The Lancet Gastroenterology & Hepatology

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“…Although the elevated acetaminophen concentration surprised us, we were familiar with cases of massive acetaminophen overdoses presenting with coma and severe lactic acidosis in the absence of hepatic dysfunction [101][102][103][104][105][106][107][108][109][110][111][112][113][114][115][116]. Analysis of the previously reported cases revealed that hyperglycemia and hypothermia have also been described [103, 105-107, 111, 112, 116].…”

Section: Does An Isolated Massive Acetaminophen Overdose Explain the mentioning

confidence: 99%

Case Files from the University of California San Diego Health System Fellowship Coma and Severe Acidosis: Remember to Consider Acetaminophen

Villano

O'Connell

et al. 2015

J. Med. Toxicol.

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A 28-year-old man was brought to the Emergency Department (ED) for evaluation of a depressed level of consciousness that developed while in jail. Sixteen hours previously, he had been arrested on charges of murder. The patient's mental status was reported as normal at the time of arrest, and it had remained so during several hours of interrogation and during the booking process at jail. Following interrogation, the patient was placed into a cell with no other inmates. During the jail intake process, the patient had not reported any history of medical problems nor was he prescribed with any medications. Paramedics arrived to find him unresponsive, but maintaining airway reflexes and hemodynamically stable. They measured a blood glucose of 300 mg/dL and noted one episode of blood-tinged emesis during transport to the ED. No seizure activity was witnessed.On arrival to the ED, vital signs were: heart rate 132/min, blood pressure 129/74 mmHg, temperature 35.3°C (95.5°F), respiratory rate 24/min, and 100 % oxygen saturation on 15 l/ min of oxygen delivered by non-rebreather face mask.Physical examination was notable for a depressed level of consciousness. His eyes remained closed to pain, he withdrew all extremities equally to pain, and he was non-verbal. He had no signs of trauma, and his pupils were normal in size and reactive. Rapid sequence tracheal intubation was performed for airway protection. An electrocardiogram was normal except for sinus tachycardia at a rate of 111/min. An initial peripherally drawn arterial blood gas obtained immediately after intubation revealed: pH 6.97, pCO 2 40 mmHg, pO 2 215 mmHg. A computed tomography scan of the brain was normal. Initial blood chemistry panel was significant for a serum bicarbonate of 7 mEq/L, glucose of 362 mg/dL, and a normal potassium, blood urea nitrogen (BUN), creatinine, and calcium. The initial serum anion gap was 34 mEq/L. Measured serum osmolality was 320 mOsm/kg, yielding an osmol gap of 9 mOsm/kg (using formula of [2(Na)+BUN/2.8+glu-cose/18] for calculated serum osmolarity). Initial lactate was 156.5 mg/dL (normal reference range 4.5-19.8 mg/dL) and beta-hydroxybutyrate (βHB) 2.9 mg/dL (normal reference range 0.0-2.8 mg/dL). Initial liver panel included an aspartate aminotransferase (AST) of 64 U/L, alanine aminotransferase (ALT) of 27 U/L, and bilirubin of 0.4 mg/dL. Prothrombin time was 13.1 s (reference range 9.7-12.5), and lipase was normal at 25 U/L. Initial creatinine phosphokinase (CK) was slightly elevated at 373 U/L (0-175). Urinalysis was positive for small ketones and crystals were not present. Measurements of acetone and acetoacetate were not performed. Serum ethanol and salicylate levels were undetectable, and a urine drug of abuse panel by immunoassay was negative for amphetamines as a class, barbiturates as a class, benzodiazepines as a class, benzoylecgonine (cocaine metabolite), methadone, opiates as class, oxycodone, phencyclidine, and tetrahydrocannabinoids. Iron concentration was normal at 87 mcg/dL.Over the first hour of management,...

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Early anion gap metabolic acidosis in acetaminophen overdose

Cited by 19 publications

References 10 publications

Translational biomarkers of acetaminophen-induced acute liver injury

Translational biomarkers of acetaminophen-induced acute liver injury

Development and validation of a dynamic outcome prediction model for paracetamol-induced acute liver failure: a cohort study

Case Files from the University of California San Diego Health System Fellowship Coma and Severe Acidosis: Remember to Consider Acetaminophen

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