NAME ALEFIYAH SALEEM

ID - 07090124

Delirium tremens (DT) is the most severe form of ethanol withdrawal manifested by altered mental status and sympathetic overdrive, which can progress to cardiovascular collapse.

The syndrome was first described by Thomas Sutton in 1813, but the link to alcohol abstinence was not made until the 1950s with the work of Victor and Adams.

Delirium tremens is a medical emergency with a high mortality rate, making early recognition and treatment essential.

Ethanol interacts with GABA receptors enhancing activity. GABA receptors are a family of chloride ion channels that mediate

inhibitory neurotransmission. They are pentameric complexes composed of several glycoprotein subunits.

Chronic ethanol abuse seems to modify the GABA receptor via several mechanisms leading to a decrease in GABA activity. Chronic ethanol exposure has been found to alter gene expression and increase cellular internalization of certain subunits affecting the type of GABA receptors that are available at the cell surface and the synapse.

Chronic ethanol exposure has also been found to alter phosphorylation of GABA receptors, which may alter receptor function.

When ethanol is withdrawn, a functional decrease in the inhibitory neurotransmitter GABA is seen. This leads to a loss of the inhibitory control of excitatory neurotransmitters such as norepinephrine, glutamate, and dopamine.

Ethanol also acts as an N -methyl D-aspartate receptor antagonist. Withdrawal of ethanol leads to increased activity of these excitatory

neuroreceptors, resulting in the clinical manifestations of ethanol withdrawal: tremors, agitation, hallucinations, seizures, tachycardia, hyperthermia, and hypertension. Past episodes of withdrawal lead to increased frequency and severity of future episodes. This is the phenomenon known as kindling.

In United States, fewer than 50% of ethanol-dependent persons develop significant withdrawal syndrome requiring pharmacologic treatment.

Only 5% of patients with ethanol withdrawal progress to delirium tremens (DT).

Race increase incidence among whites than blacks Sex - Prevalence of alcohol abuse is approximately 7% in males

and 3% in females. Incidence of withdrawal symptoms is lower in females than in

males. Mortality/Morbidity

The mortality rate for delirium tremens may be as high as 35% if untreated but is less than 5% with treatment.

Patients at greatest risk for death are those with extreme fever, fluid and electrolyte imbalance, or intercurrent illness such as occult trauma, pneumonia, hepatitis, pancreatitis, alcoholic ketoacidosis, or Wernicke-Korsakoff syndrome.

Symptoms most commonly occur within 72 hours after the last drink, but may occur up to 7 - 10 days after the last drink. Symptoms may get worse rapidly, and can include:

Alcoholic tremulousness occurs 6-12 hours after cessation or decrease of alcohol intake and is characterized by autonomic hyperactivity; anxiety, tremors, hypertension, tachycardia, nausea, vomiting, or diarrhea.

Alcohol withdrawal seizures or "rum fits" occur at 6-48 hours after last drink, most commonly within the first 24 hours. They are usually generalized tonic clonic, self-limited, and rarely progress to status epilepticus.

Alcoholic hallucinosis (formerly known as Kraepelin's hallucinatory insanity) occurs 10-72 hours after the last drink. These hallucinations may often be visual, but they can also be auditory, tactile (formication), or olfactory. Outside of hallucinations, sensorium is intact.

Delirium tremens usually occurs 3-7 days after the last drink. It is differentiated from the less severe forms of withdrawal by altered sensorium and autonomic instability. Confusion, obtundation, and delirium are the hallmarks of delirium tremens. Other findings include severe agitation, hyperpyrexia, tachycardia, hypertension, and diaphoresis.

Symptoms of alcohol withdrawal Anxiety Depression Difficulty thinking clearly Fatigue Feeling jumpy or nervous Feeling shaky Headache, general, pulsating Insomnia (difficulty falling and staying asleep) Irritability or easily excited Loss of appetite Nausea Pale skin Palpitations (sensation of feeling the heart beat) Rapid emotional changes Sweating, especially the palms of the hands or the face Vomiting

A thorough physical examination should be performed to assess for level of consciousness, other serious illnesses, signs of trauma, and stigmata of chronic liver disease.

Physical examination findings may include the following: Tachycardia Hyperthermia Hypertension Tachypnea Diaphoresis Tremor Mydriasis Altered mental status Severe psychomotor agitation

Prior ethanol withdrawal seizures

History of delirium tremens

Concurrent illness

Daily heavy and prolonged ethanol consumption

Greater number of days since last drink

Serum chemistry including the following: Sodium Potassium Chloride Bicarbonate BUN Creatinine Glucose Magnesium Phosphate Liver function tests Creatine phosphokinase (Some patients develop rhabdomyolysis) Lipase Ketones

Serum ethanol concentration This is important because patients who exhibit withdrawal while ethanol is still present in the serum are likely to have a more severe course.

Complete blood count with differential Urinalysis Blood cultures

The goals of treatment are to:

1. Save the person's life

2. Relieve symptoms

3. Prevent complications

1. Hospitalize the patient 2. Secure airway appropriately 3. Oxygen supplementation 4. Large-bore intravenous line 5. Fluid resuscitation with crystalloid solution 6. Cardiac monitor 7. Bedside glucose testing with supplementation if needed 8. Thiamine administration (100 mg IV) to treat or

prevent Wernicke encephalopathy 9. Sedation with benzodiazepines 10. Check electrolytes, replace as needed 11. Physical restraints often needed to ensure patient and staff

safety.

Any hypoglycemia should be treated.

Sedation with benzodiazepines is suggested.

10mg of intravenous diazepam ( 2-4mg lorazepam), followed by 5 mg doses (1-2 mg of lorazepam) every 5-15 minutes until the patient become calm.

Diazepam has a rapid onset of action hence it is preferred.

Once the patient is stabilized the benzodiazepine dosage may be tapered slowly over the next 4-5 days.

Addition of barbiturates may also be necessary in those refractory to benzodiazepine treatment and may reduce the need for mechanical ventilation in very unwell patients in the intensive care unit.

Patients with delirium tremens may also have Wernickes encephalopathy and should be treated for both conditions: At least two pairs of ampoules of Pabrinex (500 mg

thiamine) should be given intravenously three times daily for three days

If signs or symptoms respond to treatment, continue with two ampoules of Pabrinex once daily for five days, or for as long as improvement continues.

Intravenous hydration also may be necessary, although most alcoholic patients are over hydrated than dehydrated.

Any electrolyte disturbance must be corrected and the patient should be examined for injuries or evidence of a physical illness.

A small dose of haloperidol 2-5mg/day or one of the second generation antipsychotic (resiperidone 2-6 mg/day) may help relieve the frightening auditory and visual hallucinations of the patient with alcoholic hallucinosis. The medication is usually discontinued once the hallucinations stop.

Heart arrhythmias, may be life threatening

Injury from falls during seizures

Injury to self or others caused by mental state (confusion/delirium)

Seizures