Does Ethanol Explain the Acidosis Commonly Seen in Ethanol-Intoxicated Patients?

Zehtabchi, Shahriar; Sinert, Richard; Baron, Bonny J.; Paladino, Lorenzo; Yadav, Kabir

doi:10.1081/clt-53083

Cited by 26 publications

(8 citation statements)

References 36 publications

(30 reference statements)

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“…In humans, ethanol consumption results in a mixed respiratory and metabolic acidosis and the blood pH is directly proportional to the blood ethanol concentration (Lamminpaa and Vilska, 1990, 1991; Zehtabchi et al, 2005). In this study, ethanol resulted in a mixed acidosis, a finding consistent with human clinical studies and previous reports from this laboratory where we have shown that with each bout of ethanol, the mother and the fetus were subjected to transient acidemia, irrespective of the period of gestation (Cudd et al, 2001b; Ramadoss et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…Perturbation in pH was hypothesized to be a mechanism underlying the teratogenic effects of ethanol even before FAS was described by Jones and colleagues (Horiguchi et al, 1971; Jones et al, 1973). Clinically, in humans, ethanol ingestion results in a mixed respiratory and metabolic acidosis and the blood ethanol concentration is directly proportional to the blood pH (Lamminpaa and Vilska, 1990, 1991; Sahn et al, 1975; Zehtabchi et al, 2005). In animal models of FASD, the mother and the fetus experience transient increases in arterial partial pressure of carbon dioxide (P a CO 2 ), resulting in a reduction in arterial pH (pH a ) with every bout of ethanol consumption (Cudd et al, 2001b; Ramadoss et al, 2006b; Ramadoss et al, 2007; West et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Chronic binge ethanol-mediated acidemia reduces availability of glutamine and related amino acids in maternal plasma of pregnant sheep

Ramadoss

Cudd

2008

Alcohol

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Heavy drinking during pregnancy can result in Fetal Alcohol Syndrome (FAS), of which, fetal and postnatal growth retardation and central nervous system deficits are cardinal features. While a number of mechanisms have been proposed, none fully account for these deficiencies. We have previously reported that maternal ethanol exposure (1.75 g/kg) results in transient acidemia in the mother and fetus. Alterations in pH are known to regulate glutamine homeostasis. Therefore, we hypothesized that chronic binge ethanol mediated acidosis reduces glutamine concentrations in maternal plasma that result in decreases in the circulating levels of amino acids related to glutamine metabolism. Pregnant ewes were divided into three groups: ethanol (1.75 g/kg), saline control, and acidemia (inspired fractional CO 2 was manipulated to mimic the maternal arterial pH pattern created by ethanol). The experiment was conducted on three consecutive days followed by four days without treatment beginning on day 109 of gestation, continuing to day 132. Plasma samples were analyzed for nutrients and metabolites using HPLC and spectrophotometric methods. Maternal plasma concentrations of glutamate increased (58%), while those of glutamine and related amino acids decreased (between 14 and 53%) in response to an acute challenge following the chronic exposure in ethanol treated ewes. No differences in these amino acid concentrations were noted between the ethanol and acidemic group subjects. Maternal plasma lactate increased by ~100% in response to ethanol while glucose and urea did not change in any group. We conclude that maternal chronic binge ethanol consumption results in acidosis mediated reductions in circulating levels of glutamine and related amino acids that could be responsible for neuronal deficits, altered fetal growth, development, and programming. We also speculate that the consequent increase in fetal glutamate during critical periods of brain development may contribute to the pathogenesis of FAS.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chronic binge ethanol-mediated acidemia reduces availability of glutamine and related amino acids in maternal plasma of pregnant sheep

Ramadoss

Cudd

2008

Alcohol

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“…Other investigators have reported relationships between alcohol [16, 14, 12, 13] and cocaine intoxication [16, 17] and elevated initial lactate levels. Although these findings were not replicated in the current study, we did find a very strong relationship between THC use and elevated lactate levels with 15/16 (OR 15 95%CI 1.56– 693.14) patients who screened positive for THC having an elevated initial lactate level.…”

Section: Discussionmentioning

confidence: 99%

“…These reference ranges were determined by the manufacturer of this assay system and subsequently validated by independent in-house testing. Because of the reported association between common intoxicants such as alcohol[12–15] and cocaine [16, 17] and elevated lactate levels we also explored the association between common intoxicants (ethanol, cocaine, amphetamine, barbiturates, opiates, phenylcyclidine, benzodiazepines, and tetrahyrdocannabinol) and lactate levels using the results of serum ethanol levels and urine toxicology reports in the subset of patients for whom they were available.…”

Section: Methodsmentioning

confidence: 99%

Initial venous lactate levels in patients with isolated penetrating extremity trauma: a retrospective cohort study

Folkert

Sims

Pascual

et al. 2014

Eur J Trauma Emerg Surg

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INTRODUCTION Elevated initial lactate levels have been shown to be associated with severe injury in trauma patients, but some patients who do not appear to be in shock also present with elevated lactate levels. We hypothesized that in hemodynamically stable patients with isolated penetrating extremity trauma, initial lactate level does not predict clinically significant bleeding. METHODS A 5-year institutional database review was performed. Hemodynamically stable patients (HR<101, SBP>90) with isolated penetrating extremity trauma with an initial lactate sent were included. The exposure of interest was captured as a dichotomous variable by initial lactate level Normal (N≤2.2 mEq/l), Elevated (E >2.2. mEq/l). The primary outcome measurement was clinically significant bleeding, defined by need for intervention (operation, angioembolization, or transfusion) or laboratory evidence of bleeding (presenting Hg<7g/dL, or Hg decrease by >2g/dL/24hours). Chi-squared and Mann-Whitney tests were used to compare variables. RESULTS A total of 132 patients were identified. There were no differences in demographics or mechanism of injury between the N (n=43, 7%) and E (n=89, 14%) groups. Median lactate levels were 1.6 (IQR 1.2–1.9) mEq/dL vs. 3.8 (IQR 2.8–5.2) in the N and E groups, p<0.001. Lactate was elevated in 89 (67%) patients but was not associated with clinically significant bleeding (37% elevated vs. 39% not elevated p=0.82). CONCLUSIONS In hemodynamically stable patients with isolated penetrating trauma to the extremity, elevated initial venous lactate levels (>2.2mEq/l) are not associated with bleeding or need for interventions. Clinical judgment remains the gold standard for evaluation and management of these patients.

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“…We also wished to address the role of acidemia in alcohol-induced altered fetal cortical bone development, as alcohol exposure in human clinical cases is known to result in mixed respiratory and metabolic acidosis (Lamminpää and Vilska, 1990; 1991; Sahn et al, 1975; Zehtabchi et al, 2005). In animal models, acidemia has been described as a candidate mechanism for alcohol-induced developmental neuronal injury and altered amino acid homeostasis (Cudd et al, 2001; Horiguchi et al, 1971; Ramadoss et al, 2007; 2008b).…”

Section: Introductionmentioning

confidence: 99%

The Role of Acidemia in Maternal Binge Alcohol-Induced Alterations in Fetal Bone Functional Properties

Sawant

Ramadoss

Hogan

et al. 2013

Alcohol Clin Exp Res

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Background Heavy alcohol consumption during pregnancy negatively impacts the physical growth of the fetus. Though the deleterious effects of alcohol exposure during late gestation on fetal brain development are well documented, little is known about the effect on fetal bone mechanical properties or the underlying mechanisms. The purpose of this study was to investigate the effects of late gestational chronic binge alcohol consumption and alcohol-induced acidemia, a critical regulator of bone health, on functional properties of the fetal skeletal system. Methods Suffolk ewes were mated and received intravenous infusions of saline or alcohol (1.75 g/kg) over 1 hour on 3 consecutive days per week followed by 4 days without treatment beginning on gestational day (GD) 109 and concluding on GD 132 (term= 147 days). The acidemia group was exposed to increased inspired fractional concentrations of CO2 to closely mimic the alcohol-induced decreases in maternal arterial pH seen in the alcohol group. Results Fetal femurs and tibias from the alcohol and acidemia groups were ~3-7% shorter in length compared to the control groups (P<0.05). Three point bending procedure demonstrated that fetal femoral ultimate strength (MPa) for the alcohol group was decreased (P<0.05) by ~24% and ~29% while the acidemia group exhibited a similar decrease (P<0.05) of ~32% and 37% compared to the normal control and saline control groups, respectively. Bone extrinsic and intrinsic mechanical properties including maximum breaking force (N) and normalized breaking force (N/kg) of fetal bones from the alcohol and acidemia groups were significantly decreased (P<0.05) compared to both control groups. Conclusions We conclude that late gestational chronic binge alcohol exposure reduces growth and impairs functional properties of the fetal skeletal system and that the repeated episodes of alcohol-induced maternal acidemia may be at least partially responsible for these effects.

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Does Ethanol Explain the Acidosis Commonly Seen in Ethanol-Intoxicated Patients?

Abstract: Ethanol intoxication is associated with acidosis, which does not correlate with BD or LAC. The complexity of pathogenesis of acidosis in ethanol intoxication justifies further diagnostic evaluation of these patients in order to rule out other causes of acidosis.

Cited by 26 publications

References 36 publications

Chronic binge ethanol-mediated acidemia reduces availability of glutamine and related amino acids in maternal plasma of pregnant sheep

Chronic binge ethanol-mediated acidemia reduces availability of glutamine and related amino acids in maternal plasma of pregnant sheep

Initial venous lactate levels in patients with isolated penetrating extremity trauma: a retrospective cohort study

The Role of Acidemia in Maternal Binge Alcohol-Induced Alterations in Fetal Bone Functional Properties

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