The Lethality of Alcohol Detoxification


The topic being addressed in this research paper is the lethality of alcohol detoxification. Detoxing from alcohol is one of the most dangerous things to withdrawal from. This topic corresponds with neurobiology in many different ways. The brain needs a very specific chemical balance to keep everything working correctly and alcohol dependency and alcohol withdrawal alters different types of neurotransmitter chemicals, which overall alters the neurobiological function of the entire body.  Although, after awhile of alcohol dependency, the brain starts to adapt to the chemical changes so the brain can perform normally in the presence of alcohol.

Consuming alcohol in large amounts for a long period of time will give someone a high tolerance to drinking, compared to someone that drinks in moderation or on occasion which will have a low tolerance when consumed. For an individual that has a high tolerance, detoxing can be much harder and they can experience symptoms of withdrawal much worse than someone who does not. Neurobiological changes when withdrawing from alcohol can happen in as little as 5 hours after the last drink somebody consumes. The brain starts to crave the alcohol and sweating, racing heartbeat, and anxiety usually begin the process of the body trying to detox. Within twenty four to forty eight hours after the last drink, tremors start to take over caused by changes to the neurotransmitters and changing the chemical balances in the brain. Delirium tremens starts to kick in and at this point, if the individual is not taken into emergency medical care there is a chance of death.

The reason why this topic interests me is because I have witnessed this medical emergency numerous times. I am currently employed at Cheshire Medical, but before working there I worked in the ICU at Berkshire Medical Center in my hometown. Working in the ICU, I have seen many medical emergencies and certainly a number of detoxing and withdrawing patients. Patients coming off opioids and amphetamines are certainly a medical emergency, but when we have patients that are withdrawing from alcohol, there are many interventions the whole medical team has to take. When these patients are admitted, they sometimes come intoxicated because of injury and they start the detoxification process in the safe environment of the hospital, or they come in already detoxing with tremors and delirium. My role when interacting with these patients was mainly safety. Sometimes it was sitting with the patients making sure they do not try and hurt themselves or somebody else, and checking vital signs and making sure they are constantly stable. I have seen individual’s start having seizures and the interventions the medical team has to take to make sure they make it through and do not code. The patients are put in almost a coma with medication for a couple days to get them through all the symptoms of withdrawal that the body has to go through. I think the whole process is so interesting from the beginning through days of treatment and recovery and all the changes that happens neurologically.

In order for somebody to have an alcohol dependency, there needs to be something that triggers them to start drinking. Many triggers are anxiety, depression, PTSD, and high levels of stress.  Drinking alcohol releases a euphoric feeling that can mask anxiety and depression. Drinking makes these individuals feel somewhat better, not treating the symptoms of these mental disorders but masking them and overall increasing them. [4] Individuals that experience PTSD have a “fight or flight” response that occurs naturally in their nervous system and respond to dangerous situations. Because they have gone through particular events that affected them mentally, their symptoms day to day can be unbearable and drinking mask’s their symptoms and they feel the euphoric feeling that alcohol provides. [3]

There are many factors that go into diagnosing a patient with alcohol addiction. If the individual consumes alcohol on a daily basis, poor nutrition and personal neglect, mood swings, sweating, tachycardia, blackouts, and not being able to get through the day without a drink. There are three different types of alcoholics, binge drinkers, casual drinkers, and chronic drinkers. Casual drinkers have 1-2 drinks per day, binge drinkers are individuals that have the intention to become heavily intoxicated over a short period of time, and chronic drinkers consume 5 or more drinks in a single day for a long period of time.  Detoxing from alcohol greatly affects the chronic drinkers, due to their body adjusting to the alcohol and craving it everyday.

Alcohol is a Central Nervous System depressant that slows down the brain function. Bing a depressant, alcohol blocks messages that are trying to get to the brain, which can cause altered speech, hazy thinking, foggy memory, impaired vision, and slow reaction time. Alcohol is able to penetrate the brain and cross the blood-brain barrier. This can result in neuron damage and even the death of neurons.

There are long-term and short-term effects of alcohol dependency. The short-term effects are impaired judgment, vomiting, distorted vision and orientation, headaches and impulsive acts. The short-term effects can lead to worse long-term effects that are much more serious. Long-term effects include high blood pressure, stroke, heart related disease, organ failure, nerve damage and cancer. These long-term effects are often neglected by alcoholics and never addressed until something drastic such as a heart attack occurs. There are also social effects from drinking such as failure to keep a job, family/relationship problems, injuries and violence. [1]


Detoxification is eliminating existing toxins and avoiding new toxins in order to start the healing process due to a particular substance. Individuals detox from different substances such as opioids, amphetamines, and other substances. Detoxing from alcohol though is far more high risk. The brain of somebody that is a chronic drinker has adapted to the alcohol being in their system and the neurotransmitters have found a way to balance the chemicals in the brain to perform proper functions of the body. When somebody stops drinking their body starts to withdraw from is and the neurons cannot fire and the chemicals become imbalanced. Withdrawing can lead to hallucinations, convulsions, and even a heart seizure that can lead to death.

The liver has a very important role in the detoxification process. This organ is the primary site for alcohol metabolism. The liver oxidizes the alcohol absorbed into the bloodstream to prevent it from accumulating and destroying the body tissues. Although the liver has the capacity to regenerate cells, but can only perform this function in the early stages of liver damage.  Chronic use of alcohol can cause liver damage, which can lead to medical conditions such as fatty liver, cirrhosis and alcoholic hepatitis. Many patients that suffer from liver failure have to undergo a liver transplant.

Beginning the detoxification process usually happens two different ways. The patient willing takes themselves to a rehab facility where the medical team comes up with a care plan to keep the patient as safe as possible when detoxing. The other way an individual starts detoxing is when they stop drinking on their own and start having withdrawal symptoms. These symptoms can lead them to injuries and result in being rushed to emergency room. Also if patients are intoxicated and fall or hurt themselves, they end up waking up in the ICU not remembering how they got there.

The medical plan for these patients is an examination upon arrival, followed by maintain and stabilizing vital signs, and run IV fluids. One hundred mg of thiamine is given during the withdraw period. Treatments with pharmaceuticals lessen the chance of alcohol-induced toxicity to nerve cells (neurotoxicity). This Toxicity to the nerve cells increase the patients susceptibility to seizures following the withdraws. Benzodiazepines are often administered with duration of 1-2 days and they are a sedative to reduce anxiety, insomnia, and seizures. In the autonomic nervous system there are adrenergic receptors that are specialized proteins on the surface of nerve cells. These receptors play a key role in the regulation of the ANS and they influence occupancy and severity of some withdraw systems. Adrenergic medications alter the function of these receptors and are used to improve withdraw symptoms such as reducing blood pressure and heart rate.

Intoxication is thought to result from changes in neuronal communication taking place while alcohol is in the brain and bloodstream. Intoxicated behavior and actions are altered by synaptic transmission, which is the process by which neurons in the CNS communicate with one another. There are select neurotransmitters strongly implicate alcohol dependence and addiction. One of the neurotransmitters is GABA, which mediates the fast synaptic inhibition in the brain. The GABA neuro-inhibitor acts as a moderator for neuron activity and an excess of these inhibitors is what causes the euphoric feeling. GABAergic transmission is a target for acute and chronic effects of alcohol. Following chronic exposure of alcohol, the brains GABAergic system makes adaptations to the acute alcohol actions that potentiate GABAergic transmission. Current research that alcohol exposure can increase and decrease GABA release in different parts of the brain. When a patient is withdrawing, the body is not renewing GABA production as fast as the liver can eliminate the alcohol. By not renewing GABA, it can be responsible for activation of seizures and delirium tremens. GABA receptor site is a binding site for Benzodiazepines and many compounds bind to the site and have potent allosteric enhancing effects on the receptor. [4] [6] Neurotoxicity is produced by alcohol consumption and it involves a number of cellular and molecular adaptations that begin during alcohol exposure, and neurotransmitters can modulate these mechanisms. The predominant effect of chronic alcohol consumption makes the brain hyperexcitable during withdraw, which leads to increased anxiety and even overt seizures.

Another neurotransmitter involved is Glutamate. It is the major excitatory transmitter in the brain that has a function of fast transmission for synaptic excitation in most brain neurons. During excitatory synapse, Glutamate is released from presynaptic vesicles that cross the synapse and bind to AMPA-type glutamate receptors. This then activates the ion pore intrinsic to this protein and produces a rapid depolarization of the potassium neuron, which increases the chance that that neuron will fire an action potential. NMDA is also a receptor associated with glutamate. This receptor has a key role in producing lasting changes in synaptic function in memory and learning. Chronic consumption leads to increased NMDA receptors and is a specific change induced by the inhibitory effects of alcohol exposure. This change when detoxing can lead to hyperexcitability and alcohol induced neuronal damage. [4]

Tolerance plays a key role in the risks and complication of detoxing. Tolerance is regulated in the body in two different ways. It can be due to homeostatic mechanisms that resist environment temptations and epigenetic alterations. These alterations can be phosphorylation, methylation, acetylation, MiRNA, and chromatin remodeling. In rodents tolerance is shown in the BK channel’s phosphorylation state. Phosphorylation of BK channels by PKA is needed for ethanol potentiation of the channel. Alcohol can change the phosphorylation patterns to characterize alcohol tolerant BK channels. MiRNA contributes to rapid and chronic alcohol tolerance by altering the expression of proteins. Tolerance depends on these modified protein syntheses. The slowpoke gene, slo abbreviated is the gene that gets mutated and the mutation causes tolerance or intolerance. The link between MiRNA and alcohol is that MiRNA is able to regulate expression of multiple genes and multiple genes influence alcoholism. [6]

Depending upon the intensity of the patient’s detoxification process, they can experience seizures and Delirium Tremens. During a seizure, there is electrical activity caused by chemical changes that occur in the nerve cells in the brain. The brain cells either excite or inhibit other brain cells from sending messages. The patient typically loses consciousness and rapid twitching and shaking of the limbs are common. There are three types of alcohol withdraw seizures, partial seizures, generalized tonic-clonic seizures, and status epilepticus. Like I previously said, reduced numbers of GABAergic interneurons can cause these seizures, but also increased recurrent excitatory circuitry and proliferation of neurons that are abnormal. Benzodiphenes are usually used in the treatment of seizures and as prevention. Medical professionals take precautions such as putting seizure pads on the hospital bed to reduce risk of injury and have medical staff with medication ready. Delirium Tremens is an altered mental status and sympathetic overdrive (autonomic hyperactivity). Going back to the neuroreceptor NMDA, the inhibition may lead to seizures and delirium. Some more causes of delirium are interactions with serotonin and dopamine receptors, increased GABA receptors, which result in an influx of chloride ions and activation of inhibitors in different neurotransmitters. The prognosis of delirium is oversadation, respitory depression, and cardiac arrhythmias. Delirium is a medical emergency and has a high mortality rate.[2] [3] [6]

There are significant neuronal damage from detoxing and alcoholism in the central nervous system. The frontal lobes are the most damages region of the brain resulting from alcohol. There is dark cell regeneration, inhibition of brain neural stem cell proliferation and neurogenesis that happens in the brain going through this process. Also in the brain there is increased expression of proinflammatory cytolane and microglia protein expression. These are some of the protein expressions that correlate with tolerance as well. CNS depression occurs due to acute withdraw/rebound and causes neurotransmission systems to go into a hyper-excitability state. This hyper-excitability state is what causes neurotoxicity. Patients that suffer from alcoholism have a smaller brain volume and neurodegeneracy in the corticolombic brain regions. These brain regions include the olfactory bulb, piriforno cortex, and perianal cortex and hippocampal dentate gyros.7

In conclusion, there are many risk factors when a patient is detoxing from alcohol. Depending upon the severity of their addiction, risks can increase and decrease. It is very important for the patient to be admitted into a rehab facitley and in a safe environment with trained professions to lessen the risk of lethality. Approximately 16.3 million adults suffer with this addiction and only about 1.5 million received treatments. Being in the worst-case scenario which is experiencing seizures and delirium due to alcohol consumption can be lethal and is a medical emergency. The patient’s nervous system is highly affected and most of the time brain damage is the result. Researchers have powerful screening methods such as PET scans and magnetic resonance imaging that show the damaged part of the brain from alcohol and after detoxing. Detoxing from alcohol overall is a good thing, in the hope that a patient will one day quit and not relapse, but it is also very dangerous and has high risks. Relapse can be common for heavy users, and patients trying to stay away should avoid the triggers talked about previously. 6













Works Cited






2) “ALCOHOL’S DAMAGING EFFECTS ON THE BRAIN.” U.S National Library of Medicine. U.S. National Library of Medicine, Oct. 2004. Web. 22 Nov. 2016.


3) Azuar, Julien, Frank Questel, and Eric Hispard. “Hospital Stay and Engagement in Outpatient Follow-up after Alcohol Emergency Detox: A 1-year Comparison Study.” N.p., 9 Nov. 20115. Web.


4) @braindecoder. “What Detoxing from Excessive Alcohol Use Does to Your Brain.” Braindecoder. N.p., n.d. Web. 22 Nov. 2016.


5) Cservenka, Anita. “Neurobiological Phenotypes Associated with a Family History of Alcoholism.” Niaa. N.p., 20 Aug. 2016. Web.


6) Lovinger, David. “NIAAA Publications.” U.S National Library of Medicine. U.S. National Library of Medicine, n.d. Web. 22 Nov. 2016.


7) Stephens, David N., and Theodora Duka. “Cognitive and Emotional Consequences of Binge Drinking: Role of Amygdala and Prefrontal Cortex.” Philosophical Transactions of the Royal Society B: Biological Sciences. The Royal Society, 12 Oct. 2008. Web. 22 Nov. 2016.



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