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Seizure Lactic Acidosis

Lactic Acidosis - Cancer Therapy Advisor

Lactic Acidosis - Cancer Therapy Advisor

Hyperlactatemia, anion gap metabolic acidosis, strong ion gap metabolic acidosis Tissue hypoperfusion, ischemia, anaerobic metabolism, shock, acid-base disorders Lactic acidosis associated with critical illness is commonly a byproduct of a much larger problem. In 1976 Cohen and Woods classified lactic acidosis based on etiology. Type A is due to clinical evidence of tissue hypoperfusion. Type B occurs in the absence of clinical evidence of tissue hypoperfusion. Type B is further divided into subgroups B1 - underlying disease/physiologic state; B2 - medication or toxin; and B3 - inborn errors of metabolism. In critically ill patients, lactic acidosis is typically associated with increased lactate production (hypoperfusion, mitochondrial dysfunction), and/or decreased metabolism/clearance. Approximately 1400 mmol of lactic acid is produced daily. The kidneys metabolize up to 30% with no significant elimination. The liver is very efficient in lactate metabolism and elimination and serum lactate levels should remain in the normal range until about 75% of hepatic function is lost. The clinical features of lactic acidosis are similar to other forms of metabolic acidoses. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Other clinical features are related to the underlying cause of lactic acidosis, such as signs of hypoperfusion. Hyperventilaton (rapid shallow or Kussmaul respirations). Seizure (generalized seizures can cause a transient lactic acidosis). Signs of hypovolemia (dry mucous membranes, decreased capillary refill, skin tenting, oliguria). Abdominal pain (especially with mesenteric ischemia). There may only be subtle clinical findings, therefore one needs to have a high suspicion in clinically relevent situations (e.g. i Continue reading >>

Causes Of Lactic Acidosis

Causes Of Lactic Acidosis

INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>

Glycolysis In Energy Metabolism During Seizures Yang H, Wu J, Guo R, Peng Y, Zheng W, Liu D, Song Z - Neural Regen Res

Glycolysis In Energy Metabolism During Seizures Yang H, Wu J, Guo R, Peng Y, Zheng W, Liu D, Song Z - Neural Regen Res

Studies have shown that glycolysis increases during seizures, and that the glycolytic metabolite lactic acid can be used as an energy source. However, how lactic acid provides energy for seizures and how it can participate in the termination of seizures remains unclear. We reviewed possible mechanisms of glycolysis involved in seizure onset. Results showed that lactic acid was involved in seizure onset and provided energy at early stages. As seizures progress, lactic acid reduces the pH of tissue and induces metabolic acidosis, which terminates the seizure. The specific mechanism of lactic acid-induced acidosis involves several aspects, which include lactic acid-induced inhibition of the glycolytic enzyme 6-diphosphate kinase-1, inhibition of the N-methyl-D-aspartate receptor, activation of the acid-sensitive 1A ion channel, strengthening of the receptive mechanism of the inhibitory neurotransmitter -aminobutyric acid, and changes in the intra- and extracellular environment. (1) Glycolysis increases during seizures, and the glycolytic metabolite lactic acid is used as an energy source during seizures. (2) The abnormal synchronized discharge of a large number of neurons leads to great consumption of brain bio-energy, so the body has to accelerate the bio-energy of ATP to maintain energy consumption by seizures through aerobic metabolism and anaerobic glycolysis. (3) During seizures, the aerobic metabolism pathway is inhibited, and the glycolytic pathway enhances the energy shortage caused by insufficient aerobic metabolism. The glycolytic metabolite lactic acid may be involved in supplying energy during seizures. (4) The main mechanisms of seizure termination include energy consumption and metabolic acidosis. Lactic acid induces acidosis by several possible pathways: la Continue reading >>

Lactic Acidosis: Background, Etiology, Epidemiology

Lactic Acidosis: Background, Etiology, Epidemiology

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [ 1 , 2 ] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [ 3 ] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentationand Differe Continue reading >>

Lactic Acidosis During And After Seizures

Lactic Acidosis During And After Seizures

You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Lactic Acidosis During and After Seizures The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. ClinicalTrials.gov Identifier: NCT01833247 Information provided by (Responsible Party): Robert S. Fisher, M.D., Ph.D., Stanford University Study Description Study Design Groups and Cohorts Outcome Measures Eligibility Criteria Contacts and Locations More Information This project looks at the time course of lactic acid rise (if any) after seizures. Salivary and capillary lactic acid are tested. This type of measurement may be useful in signalling the occurrence or recent history of a seizure. Lactic acid is released from cells during seizures and elevates lactic acid levels in blood and saliva. The time course of this rise is unknown. If lactic acid rises within a few minutes of a seizure, than it might be feasible to develop lactic acid sensors to provide notification of a recent seizure. This could lead to better safety monitoring for people with epilepsy. This study was designed to utilize a commercially available lactic acid sensor (investigators have no connection with the sensor manufacturer and purchased the device at list price) to measure salivary lactic acid levels after a seizure during inpatient video-EEG epilepsy monitoring. Lactic Acidosis During and After Seizures Patients with epilepsy recorded in an inpatient video-EEG monitoring unit after a seizure. Salivary Lactic Acid Levels With Seizures [TimeFrame:Within 10 minutes of end of the seizure] The investigators will assess the Continue reading >>

Metabolic Acidosis? - Usmle Forum

Metabolic Acidosis? - Usmle Forum

A 42-year-old male is brought to ER immediately after a seizure episode. Family gives a history suggestive of grand mal seizures. Jim was on phenytoin for the past 10 years for his seizure disorder until he stopped it, six months ago. He had no seizures for the past nine years. On examination, patient is confused and lethargic. His vitals are, BP: 136/88 mm Hg, RR: 18/min, PR: 96/min. Which of the following is the most appropriate treatment for his metabolic D. Observe and repeat the labs after 2 hours. this pt. had and epileptic sz ...post seizure increased anion gap m.acidosis suggestive of lactic acidosis.. this caused by accelerated production of lactic acid in muscle and reduced hepatic lactate uptake however this post ictal lactic acidosis is transeint and resloves without treatment within 60 to 90 min so best intervention is to observe with 60 to 90 min. and repeat ABG after 2 hr. to see if acidosis resolved This patient has an acidic pH with a decrease in his bicarbonate concentration suggestive of metabolic acidosis. His AG is 140-(102+12) = 26. The patient had an epileptic seizure due to non-compliance with the medication. A post-seizure increased anion gap metabolic acidosis is suggestive of lactic acidosis. This is caused by accelerated production of lactic acid in muscle and reduced hepatic lactate uptake. However, this post-ictal lactic acidosis is transient and resolves without treatment within 60 to 90 minutes. Therefore, the best intervention in this patient is to observe him and repeat his ABG after 2 hours to see if the acidosis has resolved. If it does not resolve, then look for other potential Choice A, B and C: Use of bicarbonate in the treatment of lactic acidosis is very controversial and is recommended only in severe acute acidosis with pH < 7. Continue reading >>

Postictal State - Wikipedia

Postictal State - Wikipedia

The postictal state is the altered state of consciousness after an epileptic seizure . It usually lasts between 5 and 30 minutes, but sometimes longer in the case of larger or more severe seizures, and is characterized by drowsiness , confusion , nausea , hypertension , headache or migraine , and other disorienting symptoms. Additionally, emergence from this period is often accompanied by amnesia or other memory defects. It is during this period that the brain recovers from the trauma of the seizure. While the postictal period is considered to be the period shortly after a seizure where the brain is still recovering from the seizure, the ictal period is considered to be the seizure itself, and the interictal period to be the period between seizures, when brain activity is more normal and the preictal period that time before a seizure. Jerome Engel defines the postictal state as "manifestations of seizure -induced reversible alterations in neuronal function but not structure." [1] Commonly after a seizure, a person feels mentally and physically exhausted for up to one or two days. The most common complaint is an inability to think clearly, specifically "poor attention and concentration , poor short term memory , decreased verbal and interactive skills, and a variety of cognitive defects specific to individuals." [2] This collection of symptoms is known as the postictal state, the word postictal meaning after the seizure. Postictal migraine headaches are a major complaint among persons with epilepsy , and can have a variety of etiologies. One possible cause of these migraines is high intracranial pressure resulting from postictal cerebral edema . At times, a person may be unaware of having had a seizure, and the characteristic migraine is their only clue. [2] Feeling dep Continue reading >>

Lactate And Lactic Acidosis

Lactate And Lactic Acidosis

The integrity and function of all cells depend on an adequate supply of oxygen. Severe acute illness is frequently associated with inadequate tissue perfusion and/or reduced amount of oxygen in blood (hypoxemia) leading to tissue hypoxia. If not reversed, tissue hypoxia can rapidly progress to multiorgan failure and death. For this reason a major imperative of critical care is to monitor tissue oxygenation so that timely intervention directed at restoring an adequate supply of oxygen can be implemented. Measurement of blood lactate concentration has traditionally been used to monitor tissue oxygenation, a utility based on the wisdom gleaned over 50 years ago that cells deprived of adequate oxygen produce excessive quantities of lactate. The real-time monitoring of blood lactate concentration necessary in a critical care setting was only made possible by the development of electrode-based lactate biosensors around a decade ago. These biosensors are now incorporated into modern blood gas analyzers and other point-of-care analytical instruments, allowing lactate measurement by non-laboratory staff on a drop (100 L) of blood within a minute or two. Whilst blood lactate concentration is invariably raised in those with significant tissue hypoxia, it can also be raised in a number of conditions not associated with tissue hypoxia. Very often patients with raised blood lactate concentration (hyperlactatemia) also have a reduced blood pH (acidosis). The combination of hyperlactatemia and acidosis is called lactic acidosis. This is the most common cause of metabolic acidosis. The focus of this article is the causes and clinical significance of hyperlactatemia and lactic acidosis. The article begins with a brief overview of normal lactate metabolism. Normal lactate production and Continue reading >>

Lactic Acidosis & Seizure: Causes & Diagnoses | Symptoma.com

Lactic Acidosis & Seizure: Causes & Diagnoses | Symptoma.com

[] that result in headaches, seizures, and progressive dementia [5] . [wikigenes.org] The triad of lactic acidosis, seizures, and stroke-like episodes focus on the diagnosis. [omicsgroup.org] MELAS is the acronym for Mitochondrial Encephalopathy, Lactic Acidosis, and Stroke-like episodes. [medicinenet.com] Diabetologia (1997) [ Pubmed ] Mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes: a distinctive clinical syndrome. [wikigenes.org] This was seen in our patient with seizures, respiratory depression and severe metabolic acidosis. [omicsgroup.org] [] muscle disease with a buildup of lactic acid in the blood (lactic acidosis), temporary local paralysis (strokelike episodes), and abnormal thinking (dementia). [medicinenet.com] Oral sodium bicarbonate or sodium citrate may also be prescribed to manage lactic acidosis. [ninds.nih.gov] Lactic acidosis - a condition characterized by the accumulation of lactic acid in bodily tissues 6. [slideshare.net] The child will eventually begin to experience seizure activity as well as lactic acidosis and resulting kidney and respiratory impairments. [disabled-world.com] Researchers are currently testing dichloroacetate to establish its effectiveness in treating lactic acidosis. [ninds.nih.gov] Progressed symptoms: weakness, loss of muscle, and lactic acidosis which can later affect the kidneys and lungs. [slideshare.net] Sodium bicarbonate can also be prescribed to help manage lactic acidosis. [disabled-world.com] Aspiration pneumonitis Cardiovascular Arrythmias Tachycardia Hypotension / Hypertension Other Lactic acidosis Rhabdomyolysis Hyperglycaemia Hypoglycaemia Management Benzodiazepines [almostadoctor.co.uk] acidosis hypoxia hyperthermia rhabdomyolysis cerebral edema hypotension Please rate topic. [m Continue reading >>

Omim Entry - # 617710 - Neurodevelopmental Disorder, Mitochondrial, With Abnormal Movements And Lactic Acidosis, With Or Without Seizures; Nemmlas

Omim Entry - # 617710 - Neurodevelopmental Disorder, Mitochondrial, With Abnormal Movements And Lactic Acidosis, With Or Without Seizures; Nemmlas

A number sign (#) is used with this entry because of evidence that mitochondrial neurodevelopmental disorder with abnormal movements and lactic acidosis and with or without seizures (NEMMLAS) is caused by homozygous or compound heterozygous mutation in the WARS2 gene ( 604733 ) on chromosome 1p12. NEMMLAS is an autosomal recessive multisystemic disorder characterized by delayed psychomotor development, intellectual disability, and abnormal motor function, including hypotonia, dystonia, ataxia, and spasticity. Patient tissues may show deficiencies in one or more of the mitochondrial oxidative phosphorylation (OXPHOS) enzymes, but this is not a constant finding (summary by Wortmann et al., 2017 ). Musante et al. (2017) reported 2 teenaged sisters, born of consanguineous Iranian parents (family 2), with delayed psychomotor development, moderate intellectual disability (IQ range, 41-46), speech impairment, and aggressive behavior. The sisters also had movement abnormalities, including muscle weakness, ataxia that became apparent in childhood, and athetosis. Brain imaging and laboratory studies were apparently not performed. They had an affected brother who died of an infectious disease. Theisen et al. (2017) reported a 24-year-old man, born of unrelated parents of European ancestry, with infantile-onset leukoencephalopathy. He showed hypoglycemia and transient thrombocytopenia at birth, followed by delayed development with profound intellectual disability, absent speech, and inability to achieve crawling, standing, or walking. Additional neurologic findings included axial hypotonia, spastic quadriplegia with diffuse muscle atrophy, dysmetria, hyperreflexia, tremor, nystagmus, exotropia, and amblyopia with difficulty tracking. At age 6 months, he developed multifocal seizur Continue reading >>

Isoniazid Toxicity Litfl Life In The Fast Lane Medical Blog

Isoniazid Toxicity Litfl Life In The Fast Lane Medical Blog

isoniazid toxicity, like other hydrazines, primarily cause life-threatening seizures and lactic acidosis through depletion of vitamin B6 hydrazines like isoniazid decreased pyridoxal 5-phosphate levels (by inhibiting formation, binding and inactivating free P5P and increasing rate of P5P elimination) P5P is a cofactor in >100 enzyme reactions, including conversion of glutamate to GABA thus hydrazines cause GABA depletion resulting CNS excitation and seizures lactic acidosis results from seizures and from impaired conversion of lactate to pyruvate hepatic metabolism via acetylation or cytochrome P450 mediated hydrolysis half life varies from 1-4 hours depending on whether the patient is a fast or slow acetylator Toxicity is rapid (30 min to 2 hours) and predictable >3g (40mg/kg) seizures, metabolic acidosis, coma >10g (130 mg/kg) always lethal without treatment isoniazid levels are rarely available, and only have a potential role in retrospectively confirming the diagnosis treat seizures with benzodiazepines (high doses may be needed), escalate to barbiturates and give pyridoxine as soon as available (See below) prepare for and perform intubation in the event of prolonged seizures only give activated charcoal after securing the airway by intubation hemodialysis is not indicated even though it removes isoniazid because it is too slow pyridoxine is indicated for isoniazid-induced seizures give 1g pyridoxine for each gram of isonizid ingested up to a maximum of 5g (70mg/kg in children) give 5g IV if isonizid dose is unknown give as slow infusion of 0.5g/min until seizures stop also used for toxicity from other hydrazines e.g. Gyromitra mushrooms, rocket fuel (give 25mg/kg slow IV bolus initially); and as an adjunct in ethylene glycol toxicity (give 50mg IV q6h) 50% oral bi Continue reading >>

Lactate As A Diagnostic Marker In Transient Loss Of Consciousness

Lactate As A Diagnostic Marker In Transient Loss Of Consciousness

Lactate as a diagnostic marker in transient loss of consciousness Determining the etiology of transient loss of consciousness is often challenging. Generalized tonic-clonic seizures lead to increased serum lactate levels. After syncopes and psychogenic non-epileptic seizures, lactate levels are normal. Lactate levels help to distinguish between epileptic and non-epileptic seizures. The diagnostic classification of disorders of consciousness is often challenging, particularly the distinction between epileptic and non-epileptic seizures. The aim of the study was to examine serum lactate as a diagnostic marker of transient loss of consciousness. Serum lactate levels in blood samples drawn within 2h of the event were compared retrospectively between patients with generalized tonic-clonic seizures (n=195) and patients with other seizures (syncopes [n=52], psychogenic non-epileptic seizures [n=17], and complex focal seizures [n=37]), respectively. Serum lactate in patients with generalized tonic-clonic seizures was significantly (p<0.001, MannWhitney-U test) increased in comparison to other forms of seizure incidences. The area under the ROC-curve was 0.94 (95% CI 0.910.96). For a cut-off concentration of 2.45mmol/l, the sensitivity was 0.88 and the specificity 0.87. Serum lactate levels in the acute diagnosis were an excellent biomarker for the discrimination of generalized seizures from psychogenic non-epileptic and syncopal events, corroborating its importance for the standard work-up of acute disturbances of consciousness. Continue reading >>

Increased Blood Lactate Indicates Hypoxia Or Circulatory Failure

Increased Blood Lactate Indicates Hypoxia Or Circulatory Failure

Lactic acidosis is seen in hypoxia associated with acute cardiac or respiratory failure, shock, and acute blood loss. Blood lactate levels rise very rapidly as oxygen delivery to the peripheral tissues decreases below a critical level.An increased blood lactate level is an earlier indicator of tissue hypoxia than pH.In patients with circulatory shock, mortality increases from 10 to 90% as lactate concentration increases from 2 to 8 meq/L. A sudden increase in oxygen requirement occurs in patients with grand mal seizures and in patients with severe asthma.The increased work of breathing results in release of lactate from the muscles of respiration. Increases in lactate synthesis in the absence of tissue hypoxia may occur when the rate of glucose metabolism exceeds mitochondrial function.Blood lactate levels often increase slowly in patients with lymphoma, leukemia, neoplasms, and sepsis.Increases are usually modest, in the range of 1 to 2 meq/L.Malignant cells have a higher rate of anaerobic glycolysis. Certain drugs and ethanol can also increase blood lactate levels.Phenformin, a biguanide, causes lactic acidosis by increasing both glucose utilization in peripheral tissues and conversion of pyruvate to lactate.Metformin, another biguanide, acts similarly to phenformin, but causes lactic acidosis much less frequently and usually only in patients with coexisting renal failure. Because lactate is normally metabolized in the liver, blood levels are highly dependent on hepatic perfusion and function. During circulatory failure, lactate clearance is slowed down, especially in the presence of liver dysfunction. Hepatic tumors or metastases impair the livers ability to clear lactate. Lactate is the most widely used marker of tissue hypoperfusion in patients with severe sepsis. Continue reading >>

Natural History Of Lactic Acidosis After Grand-mal Seizures. A Model For The Study Of An Anion-gap Acidosis Not Associated Wtih Hyperkalemia

Natural History Of Lactic Acidosis After Grand-mal Seizures. A Model For The Study Of An Anion-gap Acidosis Not Associated Wtih Hyperkalemia

Orringer, C. E. ; Eustace, J. C. ; Wunsch, C. D. ; Gardner, L. B./ Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated wtih hyperkalemia . In: New England Journal of Medicine . 1977 ; Vol. 297, No. 15. pp. 796-799 @article{deb206a3e1a24da0994ab735f04d9ad9, title = "Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated wtih hyperkalemia", abstract = "To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean ( S.E.M.) venous lactate concentration was 12.71.0 meq per liter, the mean carbon dioxide content 17.11.1 nmol per liter, and the mean arterial pH 7.140.06. Sixty minutes later their values were 6.60.7 meq per liter (P<0.005), 23.61.1 mmol per liter (p<0.005) and 7.380.04 (P<0.005) respectively. The spontaneous resolution of the acidosis was due, in large part, to the metabolism of lactate and to the concomitant removal of hydrogen ion. There was no change in the serum potassium concentration, despite the development of a severe systemic acidemia and the subsequent return to normal of the pH. We suggest that the patient with seizures may serve as a unique model of lactic acidosis.", author = "Orringer, {C. E.} and Eustace, {J. C.} and Wunsch, {C. D.} and Gardner, {L. B.}", N2 - To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean ( S.E.M.) venous lactate concentration was 12.71.0 meq per liter, the mean carbon dioxide content 17.11.1 nmol per liter, an Continue reading >>

[lactic Acidosis In The Postictal State].

[lactic Acidosis In The Postictal State].

1. Ned Tijdschr Geneeskd. 2015;159:A9068. [Lactic acidosis in the postictal state]. Epilepsy is a neurological disorder with an annual incidence in the Netherlandsof 30 per 100,000 people. We present two cases of a patient admitted to theemergency department upon experiencing a generalized seizure. In each case,severe metabolic lactic acidosis was identified through routine laboratorydiagnostics. Based on their clinical presentation, we had no reasons to suspectanother cause of this severe acidosis apart from the seizure. We repeatedarterial blood sample one to two hours later and found that both pH and lactatewere normalized. Severe lactic acidosis may occur in patients who experienceseizures but otherwise do not require treatment. Taking an arterial blood sample from these patients in the emergency setting will be of limited value, because inmost patients hyperlactatemia in the postictal state is self-limiting. In somepatients, however, a persistent hyperlactatemia may indicate a serious underlyingpathology. It is therefore advisable to repeat an arterial blood sample a fewhours later. Continue reading >>

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