Severe metabolic acidosis after a single tonic‐clonic seizure

Baba, Riaz H; Zwaal, J

doi:10.1111/j.1365-2044.2005.04245.x

Cited by 5 publications

(11 citation statements)

References 5 publications

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“…Early relative lactate decrease is faster compared to a rate of 5% for sepsis [21]. It is however lower than the rate observed in athletes after heavy exertion [5] and after the cessation of tonic-clonic convulsions [14] (Fig. 2).…”

Section: Resultsmentioning

confidence: 72%

“…After physiological stress such as seizures or strenuous exercise, lactate levels can be higher than 15 mmol/L [5,14] due to generalized muscular contractions and strong adrenergic stimulation. Upon OHCA, the body enters a noflow or low-flow state with accompanying hyperlactatemia Fig.…”

Section: Discussionmentioning

confidence: 99%

“…2 Evolution of fraction of initial lactate in different settings in the first 8 h after event. Here we compare the changes in lactate levels in our patients after OHCA with the lactate levels after exercise [5], after a tonic-clonic seizure [14], and with the desired lactate decrease in the setting of sepsis of 5% per hour [12]. Shaded area indicates 95% confidence interval and hyperglycemia as a result of glycolytic metabolism and strong glycogenolysis, which in turn result from hypoxia and strong endogenous and (subsequent) exogenous catecholamine and cortisol surges [1,2,15].…”

Section: Discussionmentioning

confidence: 99%

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Early lactate and glucose kinetics following return to spontaneous circulation after out-of-hospital cardiac arrest

et al. 2021

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Objective Lactate has been shown to be preferentially metabolized in comparison to glucose after physiological stress, such as strenuous exercise. Derangements of lactate and glucose are common after out-of-hospital cardiac arrest (OHCA). Therefore, we hypothesized that lactate decreases faster than glucose after return-to-spontaneous-circulation (ROSC) after OHCA. Results We included 155 OHCA patients in our analysis. Within the first 8 h of presentation to the emergency department, 843 lactates and 1019 glucoses were available, respectively. Lactate decreased to 50% of its initial value within 1.5 h (95% CI [0.2–3.6 h]), while glucose halved within 5.6 h (95% CI [5.4–5.7 h]). Also, in the first 8 h after presentation lactate decreases more than glucose in relation to their initial values (lactate 72.6% vs glucose 52.1%). In patients with marked hyperlactatemia after OHCA, lactate decreased expediently while glucose recovered more slowly, whereas arterial pH recovered at a similar rapid rate as lactate. Hospital non-survivors (N = 82) had a slower recovery of lactate (P = 0.002) than survivors (N = 82). The preferential clearance of lactate underscores its role as a prime energy substrate, when available, during recovery from extreme stress.

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Section: Resultsmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Early lactate and glucose kinetics following return to spontaneous circulation after out-of-hospital cardiac arrest

et al. 2021

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“…Intra‐ and extracellular pH can significantly influence neurological function and would ideally have been included as well. However, even a single brief episode of seizure‐like activity can cause severe acidosis and hyperlactatemia and, therefore, cause and effect would have been difficult to differentiate in foals with neurological signs . Due to the retrospective nature, the volume status (hypo‐, normo‐, or hypervolemic) could not be assessed and any effect this might have on symptoms was therefore not accounted for.…”

Section: Discussionmentioning

confidence: 99%

Retrospective evaluation of the association between hyponatremia and neurological dysfunction in hospitalized foals (2012‐2016): 109 cases

Dunkel

Dodson

Chang

et al. 2019

J Vet Emergen Crit Care

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Objective: Hyponatremia and rapid correction of hyponatremia can lead to neurological abnormalities. The objective of the study was to determine whether plasma sodium concentrations (Na + ) and speed of correction of hyponatremia are significantly associated with neurological abnormalities in foals.Design: Retrospective cohort study 2012 to 2016.Setting: Equine hospital. Animals:One hundred and nine foals <6 months old with hyponatremia (Na + concentration ≤125 mmol/L).Interventions: Case records were reviewed for any foal with hyponatremia. Clinicopathological findings, presence or absence of neurological signs on the day of the lowest Na + concentration measured and the following 5 days, diagnosis and outcome were recorded, and changes in Na + concentration per hour were calculated for up to 5 subsequent days. Logistic regression was used to assess the association between presence or absence of neurological signs, Na + concentration, other known risk factors for neurological dysfunction in foals, and possible confounders. Measurements and Main Results:In the final multivariable model, only Na + (odds ratio [OR]: 0.86; 95% CI 0.79-0.95; P = 0.002) and BUN concentrations (OR: 1.04; 95% CI: 1.02-1.06; P = 0.001) were significantly associated with neurological signs. Changes in Na + concentrations per hour were not associated with neurological signs on any day after the lowest Na + concentration had been measured (P = 0.18-0.82), and development of new neurological signs following correction of hyponatremia was not reported in any foal.Conclusions: Na + concentrations were associated with the development of neurological signs in hyponatremic foals. Increased BUN concentrations might contribute to neurological dysfunction, but further studies are necessary to confirm or refute these findings. K E Y W O R D Sacid-base,

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“…7,8 Patients who suffered from a generalized tonic-clonic insult have a marked elevation of lactate and often suffer from lactate acidosis. 9 The treatment of GHB intoxications is supportive because no antidote is available. In our patient, the pH was corrected with bicarbonate infusions.…”

Section: Discussionmentioning

confidence: 99%

Gamma-hydroxybutyrate (GHB), an unusual cause of high anion gap metabolic acidosis

Carlier

Belleghem

Croes

et al. 2017

CJEM

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The causes of high anion gap metabolic acidosis (HAGMA) are well described in the literature. However, sometimes more frequent causes of HAGMA cannot explain its occurrence.In the case of HAGMA and severe neurological depression in the absence of other causes of HAGMA, clinicians should consider an intoxication with gamma-hydroxybutyrate (GHB) as a possible cause.GHB is endogenous to the mammalian central nervous system (CNS). Synthetic GHB was initially used as an anesthetic but is now only licensed for medical use in a limited number of indications such as the treatment of narcolepsy. Because of its euphoric effects, it became popular for recreational use under the street names: Liquid Ecstasy, Georgia Home Boy, and Liquid G.We describe the clinical case of a patient who suffered from severe neurological depression and HAGMA.

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Severe metabolic acidosis after a single tonic‐clonic seizure

Cited by 5 publications

References 5 publications

Early lactate and glucose kinetics following return to spontaneous circulation after out-of-hospital cardiac arrest

Early lactate and glucose kinetics following return to spontaneous circulation after out-of-hospital cardiac arrest

Retrospective evaluation of the association between hyponatremia and neurological dysfunction in hospitalized foals (2012‐2016): 109 cases

Gamma-hydroxybutyrate (GHB), an unusual cause of high anion gap metabolic acidosis

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