Delirium tremens

Delirium tremens (DTs) refers to the rapid onset of confusion usually caused by withdrawal from alcohol.


One form  of visual hallucination is delirium tremens. 


DTs associated with agitation and confusion, especially in the later stages of this disease. 


Insight is reduced with DTs.


Sleep is disturbed with DTs.


It often occurs three days into the withdrawal symptoms and lasts for two to three days.


Symptoms may appear suddenly, but typically develop two to three days after the stopping of heavy drinking, being worst on the fourth or fifth day.


Physical effects include:  shaking, shivering, irregular heart rate, and sweating.


The main symptoms:  nightmares, agitation, global confusion, disorientation, visual and auditory hallucinations, tactile hallucinations, fever, high blood pressure, sweating, and autonomic hyperactivity with tachycardia  and hypertension.


Some patients with DTs experience hallucinations. 


Occasionally high body temperature or seizures may result in death.


Alcohol is a dangerous drug from which to withdraw.


Differential diagnosis of DTs.


Benzodiazepine withdrawal syndrome


Barbiturate withdrawal


Risk of death ~2% with treatment and 25% without no treatment.


Occurs in about 4% of those withdrawing from alcohol.


Usually only occurs in people with a high intake of alcohol for more than a month.


With DTs  it is important to rule out associated problems such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.


Treatment requires a sedate intensive care unit with sufficient light.


 Benzodiazepines are the medication of choice-diazepam, lorazepam, chlordiazepoxide, and oxazepam.


The antipsychotic haloperidol may be beneficial.


Thiamine is recommended.


About half of people with alcoholism will develop withdrawal symptoms upon reducing their use, but only three to five percent develop DTs or have seizures.


DT symptoms are characteristically worse at night, and is the most severe manifestation of alcohol withdrawal and occurs 3–10 days following the last drink.


Common symptoms include perceptual disturbances, hallucinations or illusions- such as visions of insects, snakes, or rats. 


Delirium tremens usually includes 


feelings of impending doom.


Severe anxiety and feelings of imminent death are common.


DTs sometimes be associated with severe tremors of the extremities with anxiety, panic attacks and paranoia. 


It has extreme autonomic hyperactivity, tachycardias, elevated blood pressure, increased rate of breathing, and 35-60% of patients have a fever. 


Some patients experience seizures.


Withdrawal of  alcohol  leads to a biochemical regulation cascade. 


Delirium tremens may occur with abrupt stopping of tranquilizer drugs of the barbiturate or benzodiazepine classes in a patients with a relatively strong addiction to them.


Ethanol and tranquilizers such as barbiturates and benzodiazepines function as positive allosteric modulators at GABAA receptors.


The brain triggers the abrupt stopping of the production of endogenous GABA. 


This decrease GABA becomes more and more marked as the addiction becomes stronger and as higher doses are needed to cause intoxication. 


GABA has  sedative properties, and  is an  important regulatory neurotransmitter that controls the heart rate, blood pressure, and seizure threshold among myriad other important autonomic nervous subsystems.


It is most common in people who have a history of alcohol withdrawal.


It occurs especially in those who drink the equivalent of 7 to 8 US pints of beer or 1 US pint of distilled beverage daily. 


It commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years.


Alcohol positively allosterically modulates the binding of GABA.


Alcohol enhances GABA its effect and resulting in inhibition of neurons projecting into the nucleus accumbens, as well as inhibiting NMDA receptors. 


When alcohol use ceases, the unregulated mechanisms result in hyperexcitability of neurons as natural GABAergic systems are down-regulated and excitatory glutamatergic systems are unregulated. 


The above combined with increased noradrenergic activity results in the symptoms of DTs.


Diagnosis is based on symptoms. 


It is important to rule out other associated problems such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.


Usually treated with benzodiazepines, at high dose.


Patients are kept sedated with benzodiazepines; diazepam, lorazepam, chlordiazepoxide, or oxazepam.


In some cases antipsychotics (haloperidol) may also be used. 


Providinga well lit room is helpful people as patients often have hallucinations.


High doses of thiamine often by the intravenous route is also recommended.


Leave a Reply

Your email address will not be published. Required fields are marked *