Refer my section in Bahasa IndonesiaExtracted by Tang Sze MunCase 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/diseases-conditions/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 isunderused.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=100215Chronic 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/diseases-conditions/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 alcoholismAccording 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 individu-individu (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.htmHigh 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 onpage 4of 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 foundhere.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.pdfEffects 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?lAccording 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 post-operatively 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_print.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 yourDental 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 aspirin-containing 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 alcoholicsin recoveryare 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 (