Alcohol, drugs, toxins and post-mortem toxicology
Helen Whitwell, Christopher Milroy, Daniel du Plessis in Forensic Neuropathology, 2021
The neuropathological features associated with thiamine deficiency are most commonly seen in people with alcohol problems but may be seen in other rare causes of extreme malnutrition (Ihara et al. 1999). Thiamine deficiency underlies Wernicke-Korsakoff syndrome and cerebellar degeneration. Clinically, Wernicke's encephalopathy typically presents with ophthalmoplegia, ataxia and alterations in mental status, which may progress to coma and death in acute cases. Chronic cases may progress to Korsakoff's psychosis, a rare irreversible psychiatric condition seen in chronic alcoholism. Cerebellar degeneration typically results in an ataxic gait and clumsiness, particularly of the lower limbs. It must be remembered that chronic alcoholism is frequently associated with recurrent falls caused by intoxication and that the clinical symptoms associated with Wernicke's syndrome and chronic cerebellar degeneration are likely to compound the problem. Evidence of both recent and old head injury is common in chronic alcoholism.
B-Group Vitamin-Producing Lactic Acid Bacteria
Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani in Lactic Acid Bacteria, 2020
Thiamine deficiency is currently an installed condition in different populations and may result from inadequate thiamine intake, increased requirements, excessive loss of the vitamin from the body, consumption of anti-thiamine factors in food, or a combination of these causes. A reduction in thiamine levels can interfere with numerous cellular functions, which is why this vitamin is implicated in several human diseases including Alzheimer’s, diabetes, dementia, depression and Beriberi disease. Chronic alcohol consumption, the main cause of thiamine deficiency in industrialized countries, acts by causing inadequate nutritional thiamine intake, decreased absorption in the gastrointestinal tract, and impairs its utilization in the cells (Martin et al. 2003) that can lead to serious brain disorders, including Wernicke-Korsakoff syndrome, which is found predominantly in alcoholics.
Dementia Associated with Medical Conditions
Marc E. Agronin in Alzheimer's Disease and Other Dementias, 2014
The best studied dementia associated with alcohol abuse is Wernicke–Korsakoff's syndrome, which is characterized by two stages: first, the acute onset of confusion, gaze palsy, nystagmus, and ataxia, collectively referred to as Wernicke's encephalopathy; second, progression to a permanent dementia syndrome involving severe retrograde and anterograde amnesia and confabulation, termed Korsakoff's syndrome (Biglan, 2008). Wernicke – Korsakoff's syndrome is attributed to thiamine deficiency and the consequent damage to the cerebral mammillary bodies and adjacent thalamic nuclei (although Korsakoff's syndrome, as a separate entity, can have other causes). Rapid treatment with thiamine supplementation may reverse the symptoms to varying degrees, but a delay in intervention frequently leads to permanent dementia in 80% of individuals (Biglan, 2008).
Thiamine deficiency disorders in women and children
Published in Paediatrics and International Child Health, 2023
Elizabeth M. Keating, Casey R. Johnson, Kristin E. Cardiel Nunez, Philip R. Fischer
However, in the absence of testing, a healthcare provider might presume a diagnosis of TDD based on the clinical setting. Symptoms suggestive of thiamine deficiency include difficulty in breathing, altered mental status, loss of voice, severe fatigue, weakness, dysesthesia, abnormal eye movements, altered cognition, abdominal discomfort, vomiting, nausea and loss of appetite [6]. Signs possibly indicative of TDD on examination are tachypnoea, tachycardia, crackles (rales) on lung examination, hepatomegaly, aphonia, hoarse voice, altered mental status, weakness, abnormal eye movements, hypertonicity and ataxia. More chronic symptoms may include developmental delay in infants and young children and difficulty in walking in older children and adults [6]. Helpful tests that suggest possible TDD include increased pulmonary markings on chest radiograph, pulmonary hypertension, and reduced ventricular function in echocardiography, and hyperdense abnormalities of the basal ganglia during cranial ultrasound or brain MRI [6].
Thiamine administration to all patients with alcohol use disorder: why not?
Published in The American Journal of Drug and Alcohol Abuse, 2021
Roberta Agabio, Lorenzo Leggio
There are no scientific or clinical reasons why patients with AUD seen in an ED should not receive thiamine supplementation, yet it appears that this often the exception rather than the norm. For patients with thiamine deficiency, thiamine supplementation is the logical state-of-the-art treatment that these patients should receive. Although there is presently not sufficient evidence to provide recommendations on the optimal route of thiamine administration (15), from a practical standpoint, if the clinical status of the patient does not prevent the safe placement of an intravenous line, the intravenous route may be a pharmacologically better choice while the patient is in the ED or hospitalized. This should be followed by oral thiamine supplementation after discharge. Failure to administer thiamine involves severe and irreversible consequences. It represents the gold-standard treatment for patients with thiamine deficiency, just like insulin is for patients with Type I diabetes mellitus. Thiamine administration has virtually no side effects and is a hydrophilic vitamin, therefore there is no risk of overdosing because it does not accumulate in the body. The only risks are nonspecific to thiamine and related to the site of injection, when given intravenously; these risks are, however, rare (16–18).
Low rates of thiamine prescribing in adult patients with alcohol-related diagnoses in the emergency department
Published in The American Journal of Drug and Alcohol Abuse, 2021
Nathan M. Peck, Theodore C. Bania, Jason Chu
Alcohol use disorder (AUD) is a pervasive issue in the United States with recent estimates at a 13.9% twelve-month prevalence for the entire population aged 18 or older (1). AUD is defined by the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) as an alcohol consumption pattern that produces significant impairment or distress and is diagnosed by identifying specific complications of alcohol use or manifestations of alcohol dependence in a given patient (2). Wernicke encephalopathy and Korsakoff’s psychosis are neurologic disorders that most frequently develop in the setting of AUD and are due to thiamine deficiency (3). Given the common etiology of thiamine deficiency for both Wernicke encephalopathy and Korsakoff’s psychosis, and because patients with Wernicke encephalopathy often progress to Korsakoff’s psychosis, these two conditions are often referenced together as Wernicke-Korsakoff Syndrome (WKS). The prevalence of WKS, based on autopsy, is estimated between 0.8% and 2.8% for the entire population and 12.5% among individuals with AUD (4–6).
Related Knowledge Centers
- Alcoholism
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- Shortness of Breath
- Tachycardia
- Thiamine
- Circulatory System
- Lactic Acidosis
- Peripheral Neuropathy
- Shortness of Breath