Refer my section in Bahasa Indonesia

Extracted by Tang Sze Mun

Case Report: A patient who was undergoing a gangrene surgery was found out by the
doctor that he suffers from alcoholism. The gangrene operation was failed and following
drugs was prescribed so that the surgery can be done well.
What is alcoholism?
According to MayoClinic (http://www.mayoclinic.org/diseasesconditions/alcoholism/basics/definition/con-20020866),:
Alcoholism is a chronic and often progressive disease that includes problems controlling
your drinking, being preoccupied with alcohol, continuing to use alcohol even when it
causes problems, having to drink more to get the same effect (physical dependence), or
having withdrawal symptoms when you rapidly decrease or stop drinking. If you have
alcoholism, you can't consistently predict how much you'll drink, how long you'll drink,
or what consequences will occur from your drinking.
According to Philip Crowley , 2015 (Long-term drug treatment of patients with alcohol
dependence ,Australian Presciber, VOLUME 38 : NUMBER 2 : APRIL 2015 ):
Alcohol dependence is typically a chronic, relapsing condition in which there is
evidence of significant change in the motivation and control systems in the brain.
Increasingly drug therapy is focused not just on the treatment of the acute withdrawal
syndrome, but on modifying these other dysregulated brain systems. It should be used in
conjunction with a comprehensive treatment plan that includes appropriate
psychological and rehabilitation strategies, with the aim of reducing alcohol craving,
compulsive use and impaired control. There is evidence that pharmacotherapy for
alcohol dependence is underused.
Many people with alcoholism hesitate to get treatment because they don't recognize they
have a problem. An intervention from loved ones can help some people recognize and
accept that they need professional help.
What are the major systems affected by chronic alcohol consumption?
http://www.frca.co.uk/article.aspx?articleid=100215
Chronic alcoholism can lead to increased requirements for volatile anesthetics and
intravenous induction drugs. Withdrawal can lead to delirium tremens or seizures. Other
findings include peripheral neuropathy, hypertension, alcoholic cardiomyopathy and its
associated symptoms of congestive heart failure and dysrrhythmias, gastrointestinal
bleeding, esophageal varices, hepatitis, pancreatitis, induction of hepatic enzymes and
increased requirement for sedatives, analgesics, and neuromuscular blockers. Thiamin,
folate and vitamin B12 deficiency may exist, as well as hypomagnesemia,

hypophosphatemia, and hypocalcemia, anemia, thrombocytopenia, and coagulation

dysfunction.
Drugs treatment for alcoholism:
According to MayoClinic (http://www.mayoclinic.org/diseasesconditions/alcoholism/basics/definition/con-20020866),:

Oral medications.
A drug called disulfiram (Antabuse) may help to prevent you from drinking,
although it won't cure alcoholism or remove the compulsion to drink. If you drink
alcohol, the drug produces a physical reaction that may include flushing, nausea,
vomiting and headaches.
Naltrexone (Revia), a drug that blocks the good feelings alcohol causes, may
prevent heavy drinking and reduce the urge to drink.
Acamprosate (Campral) may help you combat alcohol cravings. Unlike disulfiram,
naltrexone and acamprosate don't make you feel sick after taking a drink.

Injected medication. Vivitrol, a version of the drug naltrexone, is injected

once a month by a health care professional. Although similar medication can be
taken in pill alcohol dependence to use consistently.

Further discussion of drugs recommended for alcoholism

According to Philip Crowley , 2015 (Long-term drug treatment of patients with alcohol
dependence ,Australian Presciber, VOLUME 38 : NUMBER 2 : APRIL 2015 ):
Naltrexone and acamprosate have well established efficacy and are first-line treatments.
Naltrexone is recommended for patients aiming to cut down their alcohol intake who do
not have severe liver disease or an ongoing need for opioids. Acamprosate is
recommended for those who have achieved and wish to maintain abstinence. Disulfiram
is no longer considered first-line treatment due to difficulties with compliance and
toxicity. Although baclofen and topiramate have evidence of benefit, they are not
registered for alcohol dependence and should only be considered in specialist practice.

How Alcoholism affects Anaesthesia: (perubahan pathofisiological pd tubuh caused

of alcoholism)
According to Lola ODaniel, CRNA, 1980, Anesthetic Management of the alcoholic
patient, Journal of the American Association of Nurse Anesthetics:
Alcohol can cause enzyme induction but this is quite variable among individuals (under
genetic control). Where alcohol has produced enzyme induction there is an increase in
the effectiveness of the detoxifying pathway; this can include the detoxifying of
alcohols, sedatives, tranquilizers, hypnotics or narcotics. Therefore there is a decrease in
clinical response to drugs in some alcoholics. The anaesthetist should be wary of more
than enzyme induction in the chronic alcoholic who requires surgery and anaesthesia
while he is still intoxicated. Since alcohol causes enzyme suppression, the alcoholic is
more sensitive to anaesthetics, narcotics and tranquilizers. Cross tolerance is the result of
alcohol, sedatives, tranquilizers, other abused drugs, hypnotics, and anaesthetics
following a similar metabolic pathway through the liver. Where an increased
effectiveness of the detoxifying pathway has occurred, there will be a decreased
response to these drugs.
Alkohol dapat menyebabkan induksi enzim tapi ini cukup bervariasi antara individuindividu (di bawah kontrol genetik). Dimana alkohol memiliki induksi enzim yang
dihasilkan ada peningkatan efektivitas jalur detoksifikasi; ini dapat mencakup
detoksifikasi alkohol, obat penenang, obat penenang, hipnotik atau narkotika. Oleh
karena itu ada penurunan respon klinis terhadap obat di beberapa pecandu alkohol.
Dokter anestesi harus waspada terhadap lebih dari induksi enzim dalam alkohol kronis
yang membutuhkan pembedahan dan anestesi sementara ia masih mabuk. Karena
alkohol menyebabkan penekanan enzim, alkohol lebih sensitif terhadap anestesi,
narkotika dan obat penenang. Toleransi lintas adalah hasil dari alkohol, obat penenang,
obat penenang, obat disalahgunakan lainnya, hipnotik, dan anestesi mengikuti jalur
metabolisme yang sama melalui hati. Dimana efektivitas meningkat dari jalur
detoksifikasi telah terjadi, akan ada respon menurun terhadap obat ini.
http://doctorspiller.com/Local_Anesthetics/local_anesthetics_5.htm
High alcohol intake produces a state of metabolic acidosis which affects all the tissues of
the body. Metabolic acidosis is due to lactic acidosis, ketoacidosis and acetic acidosis.
An acidic environment at the site of the injection reduces the ability of the anesthetic to
cross the cell membrane into the nerves, thus limiting its effects. A good discussion of
this is found on page 4 of this course, and I advise persons who want to know more
about the physiology of nerves and local anesthesia to read the entire page, but the
specific reference to acid/base balance is found here.
Alcohol acts as a vasodilator. In other words, it causes relaxation of the smooth muscles
that line the blood vessels, at least during the initial stages of inebriation. This causes
them to widen (dilate) and increases the volume of blood that flows through them. One
obvious sign that this is happening is the tendency of persons who are drunk to have
flushed faces. Vasodilation also occurs at deeper levels, and the increased blood flow at
the site of the injection carries away the anesthetic bolus more quickly than would
otherwise be the case. This reduces the time during which the anesthetic solution is
available to produce its effect.

Asupan alkohol yang tinggi menghasilkan keadaan asidosis metabolik yang

mempengaruhi semua jaringan tubuh. Asidosis metabolik karena asidosis laktat,
ketoasidosis dan asidosis asetat. Lingkungan asam di tempat suntikan mengurangi
kemampuan anestesi untuk menyeberangi membran sel ke dalam saraf, sehingga
membatasi dampaknya. Sebuah diskusi yang baik dari ini ditemukan pada halaman 4
dari kursus ini, dan saya menyarankan orang-orang yang ingin tahu lebih banyak tentang
fisiologi saraf dan anestesi lokal untuk membaca seluruh halaman, tetapi referensi
khusus untuk keseimbangan asam / basa ditemukan di sini.
Alkohol bertindak sebagai vasodilator. Dengan kata lain, hal itu menyebabkan relaksasi
dari otot polos yang melapisi pembuluh darah, setidaknya pada tahap awal mabuk. Hal
ini menyebabkan mereka untuk memperluas (membesar) dan meningkatkan volume
darah yang mengalir melalui mereka. Salah satu tanda yang jelas bahwa hal ini terjadi
adalah kecenderungan orang-orang yang mabuk untuk memiliki wajah memerah.
Vasodilatasi juga terjadi pada tingkat yang lebih dalam, dan aliran darah meningkat di
tempat suntikan membawa pergi bolus anestesi lebih cepat daripada yang akan terjadi.
Hal ini mengurangi waktu selama solusi anestesi tersedia untuk menghasilkan efeknya.
http://www.chem.ufl.edu/~fanucci/courses/CHM6304/pdf_papers/Review%20on
%20anesthetics%20and%20alcohol%20interactions%20with%20membranes.pdf
Effects of alcohols on membranes
The fundamental thermodynamic information about the properties of anesthetic
molecules is incomplete regarding the molecular mechanism of local anesthesia.
Alcohols that form hydrogen bonds with water molecules are generally thought to
disrupt normal membrane function by penetrating into membrane domains and
hydrophobically interacting with the membranes. Despite the controversy on membrane
fluidizing theory of anesthesia, or the questioning problem if alcohols really fluidize the
erythrocyte membrane, an enhance of the membrane fluidity with the alcoholic
concentration was observed.
Informasi termodinamika mendasar tentang sifat-sifat molekul anestesi tidak lengkap
mengenai mekanisme molekuler dari anestesi lokal. Alkohol yang membentuk ikatan
hidrogen dengan molekul air umumnya dianggap mengganggu fungsi membran yang
normal dengan menembus ke dalam domain membran dan hidrofobik berinteraksi
dengan membran. Terlepas dari kontroversi tentang membran fluidisasi teori anestesi,
atau masalah pertanyaan jika alkohol benar-benar fluidize membran eritrosit, seorang
meningkatkan dari fluiditas membran dengan konsentrasi alkohol diamati.

What should an anesthetist do on alcoholics during the operation?l

According to Lola ODaniel, CRNA, 1980, Anesthetic Management of the alcoholic
patient, Journal of the American Association of Nurse Anesthetics:
In approaching the anesthetic management of the acutely intoxicated, we should
consider: The rapid sequence induction versus the awake intubation: anesthetists know
the awake intubation is the prime choice in this situation. However, most anesthetists
lean toward the technique they find works best for them. The technique used depends on
the skill of the anesthetist and the patient's degree of cooperation.
IV fluids: Dextrose 5% with Ringer's lactate plus plasmanate calculated hourly per the
patient's needs will halt the fluid shifting that occurs due to the intoxication. This will
hold the fluid in the extracellular compartment where it is more manageable and usable
for our evaluation of kidney function and hourly fluid needs.
Balanced anesthesia: Here, it should be remembered that the patient has anesthetized
himself with alcohol and possibly anything else he happened upon (Valium,
barbituates, or possibly street drugs). The anesthetic needs of such patients vary widely.
Although the patient may have a cross tolerance to anesthetic agents, while he is
intoxicated, he is in enzyme suppression.
Intraoperative management. Valium or Librium r" is indicated, pre-, intra- and postoperatively to allay apprehension and prevent DTs. If DTs are as imminent as surgery is
necessary, an intravenous infusion of alcohol by continuous administration may be
indicated-administering the anesthetic agent in addition to the intravenous alcohol

According to Dental Considerations for the Alcoholic Patient

(http://www.pc.maricopa.edu/dental/ChemDepAlc/Module2/Module2_pr
int.html)

Drug Metabolism

Liver damage profoundly affects drug metabolism. Alcoholics with "normal livers" have
faster than normal drug metabolism, alcoholics with mild liver disease (fatty liver) have
normal drug metabolism, and alcoholics with severe liver disease, hepatitis or cirrhosis
have slower than normal drug metabolism. How would the clinician know this? They
probably wouldn't unless the patient offered this information. That is why consultation
with the patient's physician is critical when drugs will be administered.
If alcohol is consumed while the patient is also taking other drugs, potentially lethal
results can occur. At least half of the top 100 most-prescribed drugs contain at least one
ingredient which is known to interact adversely with alcohol - sometimes after only one
drink. Twenty percent of individuals over the age of 65 use some type of medication
which can place them at risk for developing a drug-alcohol reaction. Dental
professionals need to be aware of how the alcoholic status of their patient will affect the
use of local anesthetics, antibiotics, over-the-counter medications, and drugs that may be
prescribed to their patients pre- or post-dental treatment. When in doubt, ALWAYS
consult your Dental Drug Reference.
Any lipid-soluble drug or a drug that is metabolized in the liver should be administered
with caution to the alcoholic patient. Over-the-counter medicines that interact with
alcohol include aspirin, anti-histamines and acetaminophen. Aspirin, as well as aspirincontaining drugs and other non-steroidal anti-inflammatory drugs (NSAIDS) can create
gastritis when taken concurrently with alcohol and can also exacerbate hemostatic
abnormalities. The metabolism of acetaminophen is increased and the possibility exists
for this to lead to hepatotoxicity and hepatic injury. Patients should be cautioned to
refrain from taking more than 4 grams (or 8 extra-strength tablets) of acetaminophen per
day if they have underlying alcohol-related liver disease.
Frequent drug-alcohol interactions occur when minor tranquilizers are prescribed, as
well as morphine barbiturates, anticonvulsants, anticoagulants, antihypertensives and
antibiotics.

Local Anesthetic

Amides are primarily metabolized in liver; while esters are hydrolyzed by plasma
pseudocholinesterase. If the dental clinician doesn't know the magnitude of the patient's
liver problem, esters may be the better choice (Benzocaine) as they may lessen the risk
of an adverse drug reaction or medical complication. However, studies have shown that
the use of lidocaine (an amide), when carried out appropriately, has not been associated
with any side effects. Studies have also shown a prolonged effect to local anesthetic
agents by alcoholics, and also that long-term heavy drinkers, when sober, are more
difficult to anesthetize and have a decreased reaction to barbiturates, sedatives,
bonzodiazepines and other similar drugs. The effects are just the opposite when the

patient is inebriated, though. Other studies have shown that alcoholics in recovery are
not at an increased risk for inadequate pain control with local anesthetic agents.
Systemic complications that affect the patient's cardiovascular system make alcoholic
patients susceptible to the stress some experience when undergoing dental treatment.
Therefore, it is critical that adequate local anesthesia is used, with vasoconstrictor, to
increase the efficacy of the anesthetic and also to diminish its systemic absorption.
After reading all the information above, DRUGS that I considered to be taken as
Lidocaine 0.2% with vasoconstrictor (