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Itchyworms.

Delirium Tremens  mortality rate of up to 37% (-) treatment

 A rare, life-threatening condition, which is the most severe manifestation of alcohol withdrawal.
 Occurs as early as 48 to 72 hours after abrupt cessation of alcohol

Meaning or definition

It is typically in those with a history of chronic alcohol use and those who have previously experienced severe
alcohol withdrawal symptoms, and it doesn’t occur in everyone who withdraws from alcohol. It has an
anticipated mortality of up to 37% without appropriate treatment. It is crucial to identify early signs of
withdrawal because it can become fatal. This activity examines when delirium tremens should be considered
and how to properly evaluate it.

The pathophysiology of delirium tremens (DTs) is complex and not fully understood, but it is thought to involve
a combination of neurochemical, neuroadaptive, and neuroinflammatory processes. DTs typically occur in
individuals with a history of heavy and prolonged alcohol use, and the sudden cessation or significant
reduction in alcohol intake triggers this severe withdrawal syndrome.

Pathophysiology:

Here is an overview of the key factors and processes involved in the pathophysiology of DTs:

Neurochemical Imbalance:

Chronic alcohol abuse affects the balance of various neurotransmitters in the brain, including gamma-
aminobutyric acid (GABA), glutamate, and dopamine. GABA is an inhibitory neurotransmitter that is enhanced
by alcohol, leading to sedation and relaxation. When alcohol is abruptly discontinued, GABA activity decreases,
leading to a state of hyperexcitability in the central nervous system.

Glutamate Excitation:

Glutamate is an excitatory neurotransmitter in the brain. Chronic alcohol use suppresses glutamate
activity to counterbalance the sedative effects of GABA. During alcohol withdrawal, there is an excess release of
glutamate, which contributes to increased neural excitation and the development of symptoms such as anxiety,
restlessness, and seizures.

Neuroadaptive Changes:

Prolonged alcohol exposure leads to neuroadaptive changes in the brain, including upregulation of
certain receptors (e.g., N-methyl-D-aspartate or NMDA receptors) in response to chronic inhibition by alcohol.
When alcohol is abruptly removed, these adaptations result in an increased sensitivity to glutamate, further
exacerbating neural excitation.

GABA Receptor Dysfunction:

Chronic alcohol use can lead to dysfunction of GABA receptors, making them less responsive to GABA
and contributing to hyperexcitability during withdrawal.

Inflammatory Processes:

Alcohol abuse can also lead to systemic inflammation, which can affect the brain's microenvironment.
Inflammatory cytokines may contribute to the development of delirium and other neuropsychiatric symptoms
seen in DTs.

Genetic and Individual Factors:

Genetic predisposition and individual variations in neurochemistry may play a role in the susceptibility
to DTs. Some individuals are more prone to severe withdrawal symptoms than others.
 In summary, the pathophysiology of delirium tremens involves dysregulation of neurotransmitters,
particularly GABA and glutamate, as well as neuroadaptive changes in response to chronic alcohol exposure.
These factors contribute to the hyperexcitable state of the central nervous system observed during DTs. It is
important to recognize that DTs is a medical emergency, and prompt medical intervention is essential to
manage and mitigate the potentially life-threatening complications associated with this condition.

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Risk Factors

“Please Act Immediately Self-assured in Emergency”

- Past history of severe Alcohol Withdrawal Syndrome

- Above forties – determines how long you intake alcohol and also demonstrates that advanced age compared to
young-dependent alcohol receives more intensive pharmacological treatment.
- Increased number of days since last drink
- Strong alcohol cravings
- Excessive alcohol abuse over a period of years

This sums up to alcohol intoxication.

First Aid when you knew someone experiencing delirium tremens

RESCUE DT:

 Recognize the symptoms and severity.

 Emergency services (call 911 or local emergency number).
 Stay calm and reassure the person.
 Create a safe environment (remove hazards).
 Understand the importance of professional care.
 Ensure the person is not left alone.

Do not provide more alcohol.

Take note of vital signs and be prepared for CPR if necessary.

Assessment

Assessment of DT should take into account multitude of factors:

 severity of alcohol withdrawal

 severity of delirium
 assessment of other risk factors
 commonly occurring co-morbidities associated with chronic heavy use of alcohol.

Assessment and Diagnostic Findings

General Assessment

 brief history regarding the quantity, pattern, duration, and type of alcohol intake
 past history of DT or withdrawal seizure
 History regarding the use of other substances (Benzodiazepines)
 Physical examination

Instruments for the Assessment of Alcohol Withdrawal Syndrome

Clinical institute withdrawal assessment scale (CIWA-AR) - the most commonly used instrument is Clinical
Institute Withdrawal Assessment for Alcohol (CIWA-A) scale, particularly the 10 item revised version, known as CIWA-Ar.
Most of the measures in the CIWA-Ar are objective; therefore require minimum patient's cooperation. This is important
to note because patients with DT are usually agitated and less likely to cooperate

Alcohol withdrawal scale (AWS) -Alcohol Withdrawal Scale (AWS) which is an eleven item scale is based entirely on
objective physical or cognitive measures.

Instruments Commonly Used for the Assessment of Delirium

 Confusion assessment method - Confusion Assessment Methods (CAM) most commonly used screening
instruments of delirium. The instrument assesses features of acute onset, inattention, disorganized thinking and
altered level of consciousness.

 Confusion assessment method-ICU - developed for ICU or for nonverbal patients. Delirium is diagnosed
when patients demonstrate: (1) an acute change in mental status or fluctuating changes in mental status; (2)
inattention measured using either an auditory or visual test; and either (3) disorganized thinking; or (4) an
altered level of consciousness.

Assessment of Risk Factors and Co-Morbidities

Clinical:
 Looking for Wernicke Encephalopathy: clinically by eye signs, cerebellar signs, altered mental state or
memory problems, signs of dietary deficiency (any two of these four features) - One of the most common
but frequently ignored co-morbidity; WE is reported to be 1.4% (the figure is close to the occurrence of DT) in
hospitalized patients with chronic alcohol use. However, the incidence could rise to 58%, when autopsy samples
are taken from patients with severe alcohol problems.

 Persistent tachycardia and dyspnea: suggestive of cardiomyopathy; cardiac arrhythmias

Hydration, Jaundice, ascites, hematemesis, other stigmata of chronic liver disease

Laboratory:
 ECG
 Liver function test
 Serum electrolytes
 Complete blood count
 Acid-Base Balance
 Echocardiography
 Magnetic Resonance Imaging brain

REFERENCES:
Rahman, A. (2023, August 14). Delirium Tremens. StatPearls - NCBI Bookshelf.

https://www.ncbi.nlm.nih.gov/books/NBK482134/

Grover, S., & Ghosh, A. (2018). Delirium Tremens: Assessment and management. Journal of Clinical and Experimental

Hepatology, 8(4), 460–470. https://doi.org/10.1016/j.jceh.2018.04.012