Chronic Skull Base Erosion from Temporomandibular Joint Disease Causes Generalized Seizure and Profound Lactic Acidosis

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Abstract

This report displays a rare presentation of lactic acidosis in the setting of status epilepticus (SE). The differential diagnosis of lactic acidosis is broad and typically originates from states of shock; however, this report highlights an alternative and rare etiology, SE, due to chronic skull base erosion from temporomandibular joint (TMJ) disease. Lactic acidosis is defined by a pH below 7.35 in the setting of lactate values greater than 5 mmol/L. Two broad classifications of lactic acidosis exist: a type A lactic acidosis which stems from global or localized tissue hypoxia or a type B lactic acidosis which occurs once mitochondrial oxidative capacity is unable to match glucose metabolism. SE is an example of a type A lactic acidosis in which oxygen delivery is unable to meet increased cellular energy requirements. This report is consistent with a prior case series that consists of five patients experiencing generalized tonic-clonic (GTC) seizures and lactic acidosis. These patients presented with a pH range of 6.8-7.41 and lactate range of 3.8-22.4 mmol/L. Although severe lactic acidosis following GTC has been described, this is the first report in the literature of chronic skull base erosion from TMJ disease causing SE.

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Most cited references 16

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A systematic review of the epidemiology of status epilepticus.

Eva R. Chin, B. Neville, R. Scott (2004)

Population-based data on the incidence, aetiology, and mortality associated with status epilepticus (SE) are required to develop preventative strategies for SE. Through a systematic review, we aimed to assess the methodological quality as well as similarities, and differences between available population based studies in order to arrive at conclusions on the epidemiology of SE. All population-based studies where primary outcome was incidence, aetiology or mortality of SE were identified through a systematic search and synthesized. Methodological quality of studies were independently rated by two examiners using a unique scoring system. Seven population-based projects on SE yielding nine published reports and five abstracts were reviewed. Quality scores were in the range of 19-34 with a possible maximum of 40 (kappa scores 0.67-1.0). The incidence of SE has a bimodal distribution with peaks in children aged less than a year and the elderly. Most SE were acute symptomatic. Short-term mortality was 7.6-22% and long-term mortality was 43%. Age and aetiology were the major determinants of mortality. There are few population-based studies on SE but most are of good quality. Most studies are primarily or exclusively based on adult populations. There is limited information on the association of ethnicity and socio-economic status and SE.

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Sodium bicarbonate for the treatment of lactic acidosis.

Evan S. Forsythe, Michael Schmidt (1999)

Lactic acidosis often challenges the intensivist and is associated with a strikingly high mortality. Treatment involves discerning and correcting its underlying cause, ensuring adequate oxygen delivery to tissues, reducing oxygen demand through sedation and mechanical ventilation, and (most controversially) attempting to alkalinize the blood with IV sodium bicarbonate. Here we review the literature to answer the following questions: Is a low pH bad? Can sodium bicarbonate raise the pH in vivo? Does increasing the blood pH with sodium bicarbonate have any salutary effects? Does sodium bicarbonate have negative side effects? We find that the oft-cited rationale for bicarbonate use, that it might ameliorate the hemodynamic depression of metabolic acidemia, has been disproved convincingly. Further, given the lack of evidence supporting its use, we cannot condone bicarbonate administration for patients with lactic acidosis, regardless of the degree of acidemia.

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Status epilepticus at an urban public hospital in the 1980s.

B Alldredge, Jacob H. Lowenstein (1993)

We retrospectively reviewed the clinical course of adult patients treated for generalized status epilepticus (SE) at the San Francisco General Hospital (SFGH) from 1980 to 1989. The review was designed to determine whether the etiologies of SE at our hospital have changed over the last two decades, and to investigate the relationships between etiology, response to anticonvulsant therapy, and short-term clinical outcome. Of 154 patients reviewed, the four leading etiologies for SE were anticonvulsant drug withdrawal (39), alcohol-related (39), drug toxicity (14), and CNS infection (12). This pattern was essentially unchanged from observations made at SFGH in the 1970s. Sixty percent of all patients responded to first-line drug treatment (usually phenytoin +/- diazepam), and the remainder required an additional agent (usually phenobarbital) for control of SE. The best response to anticonvulsants occurred in patients with SE related to tumor, anticonvulsant drug withdrawal, or refractory epilepsy, and the poor responders had anoxia, drug toxicity, CNS infection, or other metabolic abnormalities. Seventy-six percent of the patients had good outcomes. Of the 22 patients who died, SE was a likely cause of death in only two (ie, 1.3% of the entire study group). Metabolic abnormalities, stroke, and anoxia were associated with particularly poor outcomes compared with other etiologies. These observations show that the etiologies of SE have remained similar over two successive decades, and that the etiology of SE may help predict both the initial response to drug therapy and the short-term outcome.

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DOI:: 10.1155/2018/8795036

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