Dilantin treatment duration - What is Cerebellar Atrophy?

Elderly patients, debilitated persons, and patients with certain kidney or liver diseases may need lower doses. The suspension should not be given at the same time as tube feedings since tube feedings bind to phenytoin and reduce its absorption.

The recommended adult dose is mg two to four times daily. Some patients may require mg three times daily. What is Cerebellar Atrophy? A degenerative disorder with permanent effects on the brain possibly caused by Dilantin therapy.

Cerebellar atrophy is medical condition characterized by degeneration of the cerebellum, the part of the brain that is responsible for posture, balance and voluntary muscle movements. Individuals diagnosed with cerebellar atrophy typically experience symptoms like unsteady gait, trouble speaking or swallowing, and poor muscle control, which may onset slowly or rapidly, depending on the cause of the cerebellar degeneration.

In some cases, cerebellar atrophy may result in debilitating complications like weakness on one side of the body or difficulty controlling the hands for tasks requiring fine motor skills. Other possible signs of cerebellar atrophy may include: Other common manifestations include jaundice , hepatomegaly , elevated serum transaminase levels, leukocytosis , and eosinophilia. The clinical course of acute phenytoin hepatotoxicity ranges from prompt recovery to fatal outcomes.

These have included thrombocytopenia , leukopenia , granulocytopenia , agranulocytosis , and pancytopenia with or without bone marrow suppression. There have been a number of reports suggesting a relationship between phenytoin and the development of lymphadenopathy local or generalized including benign lymph node hyperplasia , pseudolymphoma, lymphoma , and Hodgkin's disease.

Although a cause and effect relationship has not been established, the occurrence of lymphadenopathy indicates the need to differentiate such a condition from other types of lymph node pathology. In all cases of lymphadenopathy, follow-up observation for an extended period is indicated and every effort should be made to achieve seizure control using alternative antiepileptic drugs. Local Toxicity Including Purple Glove Syndrome Soft tissue irritation and inflammation has occurred at the site of injection with and without extravasation of intravenous phenytoin.

Soft tissue irritation may vary from slight tenderness to extensive necrosis , and sloughing. The syndrome may not develop for several days after injection. Although resolution of symptoms may be spontaneous, skin necrosis and limb ischemia have occurred and required such interventions as fasciotomies, skin grafting, and, in rare cases, amputation.

Because of the risk of local toxicity, intravenous DILANTIN should be administered directly into a large peripheral or central vein through a large-gauge catheter.

Prior to the administration, the patency of the IV catheter should be tested with a flush of sterile saline. Each injection of parenteral DILANTIN should then be followed by a flush of sterile saline through the same catheter to avoid local venous irritation caused by the alkalinity of the solution. Renal Or Hepatic Impairment Or Hypoalbuminemia Because the fraction of unbound phenytoin is increased in patients with renal or hepatic disease, or in those with hypoalbuminemia , the monitoring of phenytoin serum levels should be based on the unbound fraction in those patients.

Exacerbation Of Porphyria In view of isolated reports associating phenytoin with exacerbation of porphyria , caution should be exercised in using this medication in patients suffering from this disease.

Prenatal exposure to phenytoin may increase the risks for congenital malformations and other adverse developmental outcomes [see Use In Specific Populations]. Increased frequencies of major malformations such as orofacial clefts and cardiac defects , and abnormalities characteristic of fetal hydantoin syndrome, including dysmorphic skull and facial features, nail and digit hypoplasia , growth abnormalities including microcephaly , and cognitive deficits, have been reported among children born to epileptic women who took phenytoin alone or in combination with other antiepileptic drugs during pregnancy.

There have been several reported cases of malignancies, including neuroblastoma. Patients with unusually low levels may be noncompliant or hypermetabolizers of phenytoin. The patient with large variations in phenytoin serum levels, despite standard doses, presents a difficult clinical problem. Serum level determinations in such patients may be particularly helpful.

As phenytoin is highly protein bound, free phenytoin levels may be altered in patients whose protein binding characteristics differ from normal. Excretion Most of the drug is excreted in the bile as inactive metabolites which are then reabsorbed from the intestinal tract and excreted in the urine.

Urinary excretion of phenytoin and its metabolites occurs partly with glomerular filtration but, more importantly, by tubular secretion. Since phenytoin clearance is decreased slightly in elderly patients, lower or less frequent dosing may be required [see Dosage and Administration 2.

Gender and race have no significant impact on phenytoin pharmacokinetics. Furthermore, over the years, they may require a second or third drug to control breakthrough episodes and finally may need surgical intervention.

Simpler, less invasive procedures are well tolerated but usually provide only short-term relief. At this point, further and perhaps more invasive operations may be required, and with these procedures the risk of the disabling adverse effect of anesthesia dolorosa increases. Thus, treatment can be subdivided into pharmacologic therapy, percutaneous procedures, surgery, and radiation therapy. Adequate pharmacologic trials should always precede the contemplation of a more invasive approach.

Transcranial magnetic stimulation appears promising, but results are still scarce. Self-adhesive bandages may also be used. Depression is often seen in patients with trigeminal neuralgia; thus, this underlying depression should be adequately treated. Tricyclic antidepressants eg, amitriptyline, nortriptyline , as well as sodium valproate or pregabalin, have not been well studied.

Amitriptyline Elavil can be tried, but the success rate is low. Since the carbamazepine studies, however, newer second- and third-generation AEDs have expanded the choice of AED in trigeminal neuralgia, having demonstrated their efficacy in a variety of neuropathic pain syndromes, including trigeminal neuralgia, as well as in painful diabetic polyneuropathy and postherpetic neuralgia.

Other anticonvulsant agents possibly useful in the treatment of this disorder include sodium valproate and clonazepam Klonopin. Clonazepam has moderate efficacy but is not recommended because of a low level of evidence and its adverse effects eg, sedation and dependence. Also see Antiepileptic Drugs. Cost Because patients with trigeminal neuralgia will be using medications for years, perhaps decades, their cost is relevant. Generic carbamazepine is the cheapest; costs vary widely for the other agents, depending on the source, but approach a 4-fold increase for generic gabapentin GBP , 8-fold for lamotrigine LTG , fold for topiramate TPM , and fold for oxcarbazepine OCB in moderate daily doses.

To justify these hugely higher costs, providers can point to the promise of improved tolerability of the new agents, often a determining factor in a person with multiple sclerosis or with advanced age. Some drugs do not affect serious idiosyncratic hepatic and hematopoietic reactions, eliminating the burden and cost of routine laboratory monitoring.

Variations within the CYP2C9 gene that result in decreased enzymatic activity have been associated with increased phenytoin concentrations, as well as reports of drug toxicities due to these increased concentrations. Phenytoin induces metabolizing enzymes in the liver. This leads to increased metabolism of vitamin D , thus decreased vitamin D levels. Vitamin D deficiency , as well as low calcium and phosphate in the blood cause decreased bone mineral density.

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