Alcohol Withdrawal Seizures

SEIZURES
A seizure (from the Latin sacire, to take possession of ) is a paroxysmal event due to abnormal, excessive, hypersynchronous discharges from an aggregate of central nervous system (CNS) neurons. Depending on the distribution of discharges, this abnormal CNS activity can have various manifestations, ranging from dramatic convulsive activity to experiential phenomena not readily discernible by an observer. Although a variety of factors influence the incidence and prevalence of seizures, ~510% of the population will have at least one seizure, with the highest incidence occurring in early childhood and late adulthood.

Causes of Seizures
Seizures are a result of a shift in the normal balance of excitation and inhibition within the CNS. Three clinical observations emphasize how a variety of factors determine why certain conditions may cause seizures or epilepsy in a given patient.

1.The normal brain is capable of having a seizure under the appropriate circumstances, and there are differences between individuals in the susceptibility or threshold for seizures.
2. There are a variety of conditions that have an extremely high likelihood of resulting in a chronic seizure disorder. 3. Seizures are episodic.

BASIS
Past Medical History - alcohol withdrawal siezures - currently takes Phenytoin for seizure prophylaxis Family and Social History - alcohol abuse - enrolled in Alcoholics Anonymous - has not had a drink for > 1 year

Treatment Objectives
The major objective of drug therapy in the alcohol withdrawal period is prevention of seizures, delirium and arrhythmias. Therapy for a patient with a seizure disorder is almost always multimodal.
Includes treatment of underlying conditions that cause or contribute to the seizures Avoidance of precipitating factors Suppression of recurrent seizures by prophylactic therapy with antiepileptic medications

 The first step is to perform a thorough physical examination in all alcoholics who are considering stopping drinking, including a search for evidence of liver failure, gastrointestinal bleeding, cardiac arrhythmia,infection, and glucose or electrolyte imbalance. The second step is to offer reassurance that the acute withdrawal is short lived and to offer adequate nutrition and rest. All patients should be given oral multiple B vitamins, including 50100 mg of thiamine daily for a week or more. The third step in treatment is to recognize that most withdrawal symptoms are caused by the rapid removal of a CNS depressant, in this case, alcohol. With our case, drugs used for the treatment of seizures.

Non-Pharmacologic Therapy
The core of treatment begins with helping patients recognize the need to change, while working with them to alter their behaviors to enhance compliance.
The first step is to help the alcoholic achieve and maintain a high level of motivation toward abstinence.

The second step is to help the patient readjust to life without alcohol and to reestablish a functional lifestyle through counseling, vocational rehabilitation, and self-help groups such as Alcoholics Anonymous (AA). The third component, called relapse prevention

Pharmacologic Therapy
CYCLIC UREIDES
EFFICACY

TRICYCLICS BENZODIAZEPINES

GABA DERAVATIVES

SAFETY

SUITABILITY

COST

PHENOBARBITAL

PHENYTOIN

PRIMIDONE

EFFICACY

SAFETY

SUITABILITY

COST

DOC: PHENYTOIN
Phenytoin is a diphenyl-substituted hydantoin. It has much lower sedative properties than compounds with alkyl substituents at the 5 position. MECHANISM OF ACTION: Phenytoin has major effects on several physiologic systems. It alters sodium, potassium and calcium conductance, membrane potentials and the concentrations of amino acids and the neurotransmitters norepinephrine, acetylcholine and GABA. It blocks sustained high-frequency repetitive firing of action potentials

CLINICAL USE: Phenytoin is effective against partial seizures and generalized tonic-clonic seizures. In the latter, it appears to be effective against attacks that are either primary or secondary to another seizure type.
CONTRAINDICATIONS: History of hypersensitivity to hydrantoins DRUG INTERACTION: Plasma concentrations increased by some antibiotics and other anticonvulsants, simetidine, coumarin, anticoagulant, disulfiram, INH, some phenothiazines, phenylbutazone, sulfinpyrazone; decreased by carbamazepine, sucralfate

Steroid-induced Gastritis

Gastritis
The term gastritis should be reserved for histologically documented inflammation of the gastric mucosa. Gastritis is not the mucosal ery- thema seen during endoscopy and is not interchangeable with dys- pepsia. The etiologic factors leading to gastritis are broad and heterogeneous. Gastritis has been classified based on time course (acute vs. chronic), histologic features, and anatomical distribution or proposed pathogenic mechanism. The correlation between the histologic findings of gastritis, the clinical picture of abdominal pain or dyspepsia, and endoscopic findings noted on gross inspection of the gastric mucosa is poor. Therefore, there is no typical clinical manifestation of gastritis.

CAUSES OF GASTRITIS
There are numerous causes for gastritis and these are listed below:
1) Medications like ASA and other non-steroidal anti-inflammatory drugs (NSAIDS) and steroids- this type of gastritis develops slowly, in otherwise healthy people, presenting with bleeding or ulcers. Alcohol, caffeine, nicotine can also cause gastritis. 2) Stress due to severe illness- this is the most severe type of gastritis. This may occur e.g. after a severe burn and injuries. 3) Bacterial infection- commonly results from an infection by Helicobacter pylori ( bacteria that grow in the mucus secreting cells of the stomach lining). No other bacteria are known to grow in the normally acidic stomach, but many types of bacteria may grow if the stomach does not produce acid. 4) 4) Viral or fungal infections- may develop in people with a prolonged illness or impaired immune system.

5) Atrophic gastritis- results when antibodies attack the stomach lining, causing it to become very thin and also causes destruction of cells that produce acid and enzymes. This condition usually affects the elderly and those who have had partial gastrectomy ( a procedure in which part of the stomach is removed). Atrophic gastritis may cause pernicious anemia because it interferes with the absorption of vitamin B12 from food.
6) Radiation- causes damage to the stomach lining and allowing bacteria to invade the stomach wall, causing a sudden, severe and extremely painful form of gastritis. 7) Unknown causes- Plasma cell gastritis and Menetriere's disease

BASIS
Gastric pain Prednisone (Corticosteroid): an immunosuppressive drug alters the normal protective mechanism of the mucosa of stomach Alcoholism Laboratory (+) Guaiac Test, positive upper gastrointestinal bleeding

Treatment Objectives
Goals of treatment are to relieve the symptoms and eliminate the gastric irritant or other cause. To stop or change other kinds of steroids

Hospitalization may be required if excessive bleeding occurs.

Non-pharmacologic Therapy
Don't eat solid food on the first day of the attack. Drink liquids frequently, preferably milk or water. Resume a normal diet slowly, but avoid hot and spicy foods until symptoms disappear.

Avoid caffeine
Resume normal activities as soon as symptoms improve.

PHARMACOLOGIC THERAPY
Proton Pump H2Inhibitor Receptor Antagonist Efficacy +++ ++ Antacid Prostaglandin

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Safety

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Suitability

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Cost

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LANSOPRAZOLE

OMEPRAZOLE

PANTOPRAZOLE

EFFICACY

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SAFETY

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SUITABILITY

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COST

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DOC: Omeprazole
It works by decreasing the amount of acid your stomach makes. It relieves symptoms such as heartburn, difficulty swallowing, and persistent cough. This medication helps heal acid damage to the stomach and esophagus, helps prevent ulcers, and may help prevent cancer of the esophagus. Omeprazole belongs to a class of drugs known as proton pump inhibitors (PPIs). It shuts down the acid "pumps" within acid-secreting stomach cells, to limit stomach acid production.

CLINICAL USE: Omeprazole is used to treat certain stomach and esophagus problems (such as acid reflux, ulcers). DRUG INTERACTION: Diazepam, phenytoin, warfarin and other Vitamin K antagonists. Reduce plasma levels of atazanavir. Increase concentration of tacrolimus and claritomycin.