Effexor withdrawal. Effexor withdrawal side effects, Effexor withdrawal solutions.

If you have already started Effexor withdrawal, you now know the Effexor withdrawal side effects can be crippling.

Effexor withdrawal side effects usually include; anxiety, insomnia, head spinning, electrical brain “zaps,” extreme weight gain, pain in joints, nausea, and for some people an extreme fatigue. We have included a complete list of Effexor side effects and Effexor withdrawal side effects lower on this page.

What are your options to eliminate Effexor withdrawal? Ideally you have not started Effexor withdrawal yet, but if you have there are still solutions.

The options you have available to combat Effexor withdrawal are limited. What you decide to do next may ease the Effexor withdrawal or make you continue down the spiral. It is understandable you may want to try anything to overcome how you currently feel from the Effexor, but now is the time to research, investigate, and make an informed decision.

Option 1 - The most effective Effexor withdrawal program found, is based on the book, How to Get Off Psychiatric Drugs Safely. This book includes a step-by-step guideline how to reduce Effexor, how to overcome the Effexor withdrawal side effects and feel good once again before you even reduce the Effexor and importantly, if you have already started to reduce your Effexor and are suffering, what you can do to overcome those side effects.

If you are taking Effexor and along with other medication, this book details exactly what to do with the benzodiazepine or antipsychotic medication, including which medication to reduce first.

Included in book; how to locate health care professionals that use this method, telephone and or e-mail support during the process. This list includes medical doctors, psychiatrists, naturopathic doctors, pharmacists and chiropractors.

"When I first found your site I could hardly read the print. I had tried to come off Effexor before without success. Every time I got down to the 37 mg dosage the side effects were to severe to continue so I had to go back up again to 75. This time I made it. Whew. I am sleeping again at night, anxiety is gone, that gnawing agitation feeling left and I am back. My children have a mother again and my husband has a wife that can once again show affection.

I went a little faster than your book says to go but you worked with me in such a way that allowed me to get off fast."

The book, How to Get Off Psychiatric Drugs Safely is also available, in its entirety, for Free, at The Road Back site. Click here, all chapter titles and links to each chapter are located on the left side of The Road Back site. Or you can purchase the book from Amazon.com. Link to the book at Amazon.com provided below.

How to Get Off Psychiatric Drugs Safely is the #1 seller on Amazon.com for information about antidepressants.

Review
This book is one of the most important self-help books of this century. The reason is because it provides a safe and rational way for people to withdraw from these dangerous drugs. This can be done with the help of a physician and can end some of the horrors created by both the side effects and the withdrawal effects of the drug.

As a doctor on the staff of a detox clinic, I have seen firsthand what damage this class of drugs can do. Not only do they harm people while taking them, they also can wreak havoc when a person tries to stop. Many of the people we have seen at the Institute have been disabled by them.

This is why I believe this work is so important. Patients are held hostage by their Psych meds and can have difficulty getting free. Physicians may not have the experience to successfully withdraw these drugs. Often patients are told they must remain on the drugs because terrible symptoms can develop when trying to get off.

The author provides a workable way to taper off on a comfortable gradient. He also recommends simple but powerful nutritional solutions to help the withdrawal process. These solutions are helpful and inexpensive.

I recommend this book for everyone that is on Psychiatric medications and desires to safely get off of them. I also recommend it for doctors, nurses and pharmacists.

Dr. Lance Carlton Durrett DC FASA FIAMA --Dr Lance Durrett

Review
This information can alleviate the unnecessary deep suffering caused by the appalling lack of mainstream knowledge about safe psychiatric drug tapering. I have personally witnessed the desperate psychological trauma and myriad mysterious, life-threatening symptoms caused by the abrupt discontinuation of antidepressants and anti-anxiety agents.

Physicians and other health professionals owe it to themselves and their patients to become familiar with this book. Through Jim Harper's generosity, because this information is available online for free, patients can empower themselves to discuss new options with their doctor. There really is hope!

Diane Tew, Rehabilitation Nurse --Diane Tew

Option 2 - The Antidepressant Solution: A Step-by-Step Guide to Safely Overcoming Antidepressant Withdrawal, Dependence, and "Addiction."

Click this link The Antidepressant Solution: A Step-by-Step Guide to Safely Overcoming Antidepressant Withdrawal, Dependence, and "Addiction" to purchase the book from Amazon.com.

Review

This is a well-written book that concentrates on how to discontinue the new antidepressants {SSRIs} safely. The book also includes guidelines for discontinuing the older antidepressants. There is a step by step guide for the correct method of discontinuing these drugs. Dr. Glenmullen also has Charts which explain the difference between "withdrawal" symptoms and the actual return of depression/anxiety, etc.

This is a must read for everyone who has wished they could get off their antidepressant but has been stymied in their attempt.

Option 3 - Your Drug May Be Your Problem: How and Why to Stop Taking Psychiatric Drugs.

From Publishers Weekly
In his previous books (Toxic Psychiatry, Talking Back to Prozac), psychiatrist Breggin laid the groundwork for his battle against what he sees as American psychiatry's harmful overdependence on prescribing medication. This time out, he reiterates his primary tenets and, having teamed up with David Cohen, a professor of social work at the University of Montreal, provides practical advice for those who are considering stopping medication. According to the authors, psychiatric drugs have replaced religion, spirituality, human relationships and introspection as the solution of first resort for the suffering endemic to a full human life. Because scientists know very little about the brain, Breggin and Cohen argue, the much-touted theory that depression and mental illness arise from chemical imbalances is "sheer speculation" and the propagandistic cornerstone of a massive public relations campaign by drug companies. In a well-researched argument that suffers from a somewhat dogmatic tone, they contend that, rather than improve the brain's functioning, these drugs actually create such imbalances, causing immediate and sometimes irreversible damage. In place of medication, Breggin and Cohen recommend therapy, as well as a commitment to religious, spiritual or philosophic ideas, and offer a step-by-step approach to ending dependence on medication, to be undertaken only with medical guidance. Although the authors warn readers against feeling pressured to forgo medication, they never explore the alternatives.

If you are suffering from weight gain, Effexor may have very well have been the cause. The Road Back has information and offers solutions for Effexor weight gain as well. Click here to go directly to that page within their site.

Below is a list of Effexor withdrawal side effects. These Effexor side effects can occur while taking the Effexor before withdrawal or may become apparent once Effexor withdrawal begins. It is imperative you use a Effexor withdrawal plan designed to eliminate or reduce Effexor withdrawal side effects. Once Effexor withdrawal side effects begin, they are more difficult to get rid of.

8. Effexor withdrawal - Bundle Branch Block Right – These are specialized cells in the upper right heart chamber and are the heart’s pacemaker. They send electrical signals to the heart that keeps it beating or contracting regularly. Normally the signal goes to the lower heart chambers at the same time through the bundle of His (hiss) on both the left and right sides of the heart, so the lower chambers contract at the same time. When the bundle is damaged on the right side, the signal does not fire at the same time as the left, which changes the pace of blood flow. This can lead to a person fainting.

Triglycerides are three fatty acids bound together in one molecule stored by the body and available to create high levels of energy when used.

Pharmacology

Effexor is a phenethylamine bicyclic derivative, chemically unrelated to tricyclic, tetracyclic or other available antidepressant agents.

The mechanism of Effexor antidepressant action in humans is believed to be associated with its potentiation of neurotransmitter activity in the CNS. Preclinical studies have shown that venlafaxine and its major metabolite, O-desmethylvenlafaxine (ODV), are potent inhibitors of neuronal serotonin and norepinephrine reuptake and weak inhibitors of dopamine reuptake.

Effexor and ODV have no significant affinity for muscarinic, histaminergic, or alpha1-adrenergic receptors in vitro. Pharmacologic activity at these receptors is hypothesized to be associated with the various anticholinergic, sedative, and cardiovascular effects seen with other psychotropic drugs. Venlafaxine and ODV do not possess monoamine oxidase (MAO) inhibitory activity.

Pharmacokinetics:
Effexor is well absorbed, with peak plasma concentrations occurring approximately 2 hours after dosing. Effexor is extensively metabolized, with O-desmethylvenlafaxine, (ODV, the only major active metabolite) peak plasma levels occurring approximately 4 hours after dosing. Following single doses of 25 to 75 mg, mean (+/- SD) peak plasma concentrations of venlafaxine range from 34+/-14 to 96+/-43 ng/mL, respectively, and are reached in 2+/-1 hours, and mean peak ODV plasma concentrations range from 58+/-18 to 178+/-40 ng/mL and are reached in 4+/-2 hours. Approximately 87% of a single dose of venlafaxine is recovered in the urine within 48 hours as either unchanged venlafaxine (5%), unconjugated ODV (30%), conjugated ODV (26%), or other minor metabolites (27%).

Multiple-Dose Pharmacokinetic Profile:
Steady-state concentrations of both venlafaxine and ODV in plasma were attained after approximately 3 days of multiple dose therapy. The clearance of Effexor is slightly (15%) lower following multiple doses than following a single dose.

Effexor and ODV exhibited linear kinetics over the dose range of 75 to 450 mg total daily dose administered t.i.d.

The mean +/- SD steady-state plasma clearances of venlafaxine and ODV are 1.3+/-0.6 and 0.4+/-0.2 L/h/kg, respectively; elimination half-life is 5+/-2 and 11+/-2 hours, respectively.

Effexor and ODV renal clearances are 49+/-27 and 94+/-56 mL/h/kg, respectively, which correspond to 5+/-3.0% and 25+/-13% of an administered venlafaxine dose recovered in urine as venlafaxine and ODV, respectively. Similar steady-state volumes of distribution are exhibited for venlafaxine (7+/-4 L/kg) and ODV (6+/-2 L/kg).

Effexor and ODV are less than 35% bound to plasma proteins. Therefore, protein-binding-induced drug interactions with Effexor are not expected.

When equal daily doses of venlafaxine were administered either b.i.d. or t.i.d., drug exposure (AUC) and fluctuation in plasma levels were comparable.

Age and Gender:
Age and sex do not significantly affect the pharmacokinetics of Effexor. A 20% reduction in clearance was noted for ODV in subjects over 60 years old; this was possibly caused by the decrease in renal function that typically occurs with aging. Dosage adjustment based upon age or gender is generally not necessary (See Dosage).

Hepatic Disease:
In 9 patients with hepatic cirrhosis, the pharmacokinetic disposition of both venlafaxine and ODV were significantly altered. Venlafaxine elimination half-life was prolonged by about 30%, and clearance was decreased by about 50%. ODV elimination half-life was also prolonged (by about 60%) and its clearance decreased by about 30%. Three patients with more severe cirrhosis had a 90% decrease in venlafaxine clearance. Dosage adjustment is necessary in patients with liver disease (See Dosage).

Renal Disease:
In patients with moderate to severe impairment of renal function (GFR=10-70 mL/min), Effexor elimination half-life was prolonged by 50%, and clearance was deceased by about 24%. ODV elimination half-life was prolonged by about 40%, but clearance was unchanged. In dialysis patients, venlafaxine elimination half-life was prolonged by about 180% and clearance was decreased by about 56%. Dosage adjustment is necessary in patients with renal disease (See Dosage).

Indications

The effectiveness of venlafaxine in long-term use (i.e., for more than 4 to 6 weeks) has not been systematically evaluated in controlled trials. Therefore, the physician who elects to use venlafaxine for extended periods should periodically reevaluate the long-term usefulness of the drug for the individual patient.

Contraindications

Patients with known hypersensitivity to Effexor or to any of the components of the formulation.

MAO Inhibitors:
There have been reports of serious, sometimes fatal reactions in patients receiving antidepressants with pharmacological properties similar to those of venlafaxine in combination with a MAO inhibitor. Therefore, venlafaxine should not be used in combination with MAO inhibitors or within two weeks of terminating treatment with MAO inhibitor's. Treatment with MAO inhibitors should not be started until two weeks after discontinuation of Effexor therapy.

Warnings

An analysis of the blood pressure increases in patients with sustained hypertension and in the 19 patients who were discontinued from treatment because of hypertension (<1% of total venlafaxine-treated group) showed that most of the blood pressure increases were in the range of 10 to 15 mm Hg, SDBP. Since in individual patients sustained increases of this magnitude could have adverse consequences, it is recommended that patients receiving venlafaxine have their blood pressure monitored regularly.

For patients who experience a sustained increase in blood pressure during treatment with venlafaxine, either a dose reduction or discontinuation of venlafaxine should be considered.

Precautions

General:
Suicide:
The possibility of a suicide attempt in seriously depressed patients is inherent to the illness and may persist until significant remission occurs. Close supervision of high-risk patients should accompany initial drug therapy, and consideration should be given to the need for hospitalization. In order to reduce the risk of overdose, prescriptions for venlafaxine should be written for the smallest quantity of tablets consistent with good patient management.

Seizures:
During premarketing testing, seizures were reported in 8 out of 3082 venlafaxine-treated patients (0.26%). In 5 of the 8 cases, patents were receiving doses of 150 mg/day or less. However, patients with a history of convulsive disorders were excluded from most of these studies. venlafaxine should be used cautiously in patents with a history of seizures, and should be promptly discontinued in any patient who develops seizures.

Activation of Mania/Hypomania:
During Phase II and III trials, mania or hypomania occurred in 0.5% of venlafaxine-treated patients. Activation of mania/hypomania has also been reported in a small proportion of patients with major affective disorder who were treated with other marketed antidepressants. As with all antidepressants, venlafaxine should be used cautiously in patients with a history of mania.

Patients with Concomitant Illness:
Clinical experience with venlafaxine in patients with concomitant systemic illness is limited. Caution is advised in administering venlafaxine to patients with diseases or conditions that could affect hemodynamic responses or metabolism. Patients should be questioned about any prescripton or "over the counter drugs" that they are taking, or planning to take, since there is a potential for interactions.

Cardiac Disease:
Venlafaxine has not been evaluated or used to any appreciable extent in patients with a recent history of myocardial infarction or unstable heart disease. Patients with these diagnoses were systematically excluded from many clinical studies during the product's clinical trials. Evaluation of the electrocardiograms for 769 patients who received venlafaxine in 4- to 6 week double-blind trials showed that the incidence of trial-emergent conduction abnormalities did not differ from that with placebo. The mean heart rate was increased by about 4 beats per minute during treatment. Venlafaxine treatment has been associated with sustained hypertension (see Warnings).

Hepatic and Renal Disease:
In patients with hepatic or renal disease the pharmacokinetic disposition of both venlafaxine and ODV are significantly altered. Dosage adjustment is necessary in these patients (See Dosage).

Occupational Hazards:
Any psychoactive drug may impair judgment, thinking or motor skills. Therefore, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that the drug treatment does not affect them adversely.

Pregnancy, Labor and Delivery:
There are no adequate and well controlled studies with venlafaxine in pregnant women. Therefore, venlafaxine should only be used during pregnancy if clearly needed.

Lactation:
It is not known whether venlafaxine or its metabolites are excreted in human milk. Because many drugs are excreted in human milk, lactating women should not nurse their infants while receiving venlafaxine.

Children:
Safety and efficacy in children below the age of 18 have not been established.

Geriatrics:
Of the 2,897 patients in Phase II and III trials, 357 (12%) were 65 years of age or older. No overall differences in effectiveness and safety were observed between these patients and younger patients. However, greater sensitivity of some older individuals cannot be ruled out.

Discontinuation Symptoms:
While the discontinuation effects of Effexor have not been systematically evaluated in controlled clinical trials, a retrospective survey of new events occurring during taper or following discontinuation revealed the following six events that occurred at an incidence of at least 5%, and for which the incidence for venlafaxine was at least twice the placebo incidence: asthenia, dizziness, headache, insomnia, nausea and nervousness. Therefore, it is recommended that the dosage be tapered gradually and the patient monitored (See Dosage).

Drug Interactions:
As with all drugs, the potential for interaction by a variety of mechanisms is a possibility.

Lithium:
The steady-state pharmacokinetics of venlafaxine administered as 50 mg every 8 hours was not affected when a single 600 mg oral dose of lithium was administered to 12 healthy male subjects. Venlafaxine had no effect on the pharmacokinetics of lithium. It should be noted that the venlafaxine dose was in the low end of the therapeutic dosage, as was the single lithium dose. The potential interaction of venlafaxine and lithium in clinical practice is unknown.

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The steady-state pharmacokinetics of venlafaxine administered as 50 mg every 8 hours was not affected when a single 10 mg oral dose of diazepam was administered to 18 healthy male subjects. Venlafaxine had no effect on the pharmacokinetics of diazepam or its active metabolite, desmethyidiazepam. It should be noted that the venlafaxine dose was in the low end of the therapeutic dosage, as was the single diazepam dose. The potential interaction of venlafaxine and diazepam in clinical practice is unknown.

Cimetidine:
Concomitant administration of cimetidine and venlafaxine in a steady-state study for both drugs in 18 healthy male subjects resulted in inhibition of first-pass metabolism of venlafaxine. The oral clearance of venlafaxine was reduced by about 43%, and the exposure (AUC) and maximum concentration (Cmax) of the drug were increased by about 60%. However, there was no effect on the pharmacokinetics of ODV. The overall pharmacological activity of venlafaxine plus ODV is expected to rise only slightly, and no dosage adjustment should be necessary for most subjects.

However, for patients with pre-existing hypertension, for elderly patients and for patients with hepatic or renal dysfunction, the interaction associated with the concomitant use of cimetidine and venlafaxine is not known and potentially could be more pronounced. Therefore, caution is advised in these patients.

Other CNS-Active Drugs:
The risk of using venlafaxine in combination with other CNS-active drugs (including alcohol) has not been systematically evaluated. Consequently, caution is advised if the concomitant administration of venlafaxine and such drugs is required.

Electroconvulsive Therapy:
There are no clinical data on the use of electroconvulsive therapy combined with venlafaxine treatment.

Cytochrome P450 IID6:
Venlafaxine is metabolized to its active metabolite, ODV, by cytochrome P450 IID6 Therefore, the potential exists for a drug interaction between venlafaxine and drugs that inhibit cytochrome P450-IID6 metabolism. Venlafaxine is a relatively weak inhibitor of cytochrome P450 IID6, however, the clinical significance of this finding is unknown.

Drug Abuse and Dependence:
Physical and Psychological Dependence:
In vitro studies revealed that venlafaxine has virtually no affinity for opiate, benzodiazepine, phencyclidine (PCP), or N-methyl-D-aspartic acid (NMDA) receptors. It has no significant CNS stimulant activity in rodents. In primate drug discrimination studies, venlafaxine showed no significant stimulant or depressant abuse liability.

While venlafaxine has not been systematically studied in clinical trials for its potential for abuse, there was no indication of drug-seeking behaviour in the clinical trials. However, it is not possible to predict on the basis of premarketing experience the extent to which a CNS active drug will be misused, diverted, and/or abused once marketed. Consequently, physicians should carefully evaluate patients for history of drug abuse and follow such patients closely, observing them for signs of misuse or abuse of venlafaxine (e.g., development of tolerance incrementation of dose, drug-seeking behaviour).

Adverse Effects

Commonly Observed Adverse Reactions:
The most commonly observed adverse events associated with the use of venlafaxine (incidence of 5% or greater) and not seen at an equivalent incidence among placebo-treated patients (i.e., incidence for venlafaxine at least twice that for placebo), derived from the 1% incidence Table III, were asthenia, sweating, nausea, constipation, anorexia, vomiting, somnolence, dry mouth, dizziness nervousness, anxiety, tremor, blurred vision, and abnormal ejaculation/orgasm and impotence in men.

Adverse Reactions Associated with Discontinuation of Treatment:
Nineteen percent (537/2897) of venlafaxine-treated patients in Phase II and III depression studies discontinued treatment due to an adverse reaction (see Table II). The more common events (>=1%) associated with discontinuation of treatment and considered to be drug-related (i.e., those events associated with dropout at a rate approximately twice or greater for venlafaxine compared to placebo) included Table II.

Incidence in Controlled Trials:
Table III that follows enumerates adverse events that occurred at an incidence of 1% or more, and were more frequent than in the placebo group, among venlafaxine-treated patients who participated in 4- to 8-week placebo-controlled trials in which patients were administered doses in the range of 75 to 375 mg/day. Reported adverse events were classified using a standard COSTART-based Dictionary terminology.

Dose Dependency of Adverse Events:
A comparison of adverse event rates in a fixed-dose study comparing Effexor 75, 225, and 375 mg/day with placebo revealed a dose dependency for some of the more common adverse events associated with Effexor use, as shown in Table IV. The rule for including events was to enumerate those that occurred at an incidence of 5% or more for at least one of the venlafaxine groups and for which the incidence was at least twice the placebo incidence for at least one Effexor group. Tests for potential dose relationships for these events (Cochran-Armitage Test, with a criterion of exact 2-sided p-value <= 0.05) suggested a dose-dependency for several adverse events in this list, including chills, hypertension, anorexia, nausea, agitation, dizziness, somnolence, tremor, yawning, sweating, and abnormal ejaculation .

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-- Incidence less than 1%
[2] Incidence based on number of male patients.
[3] Incidence based on number of female patients.
-------------------------------------------------------------------------

Adaptation to Certain Adverse Events:
Over a 6-week period, there was evidence of adaptation to some adverse events with continued therapy (e.g., dizziness and nausea), but less to other effects (e.g., abnormal ejaculation and dry mouth).

Vital Sign Changes:
Venlafaxine treatment (averaged over all dose groups) in clinical trials was associated with a mean increase in pulse rate of approximately 3 beats per minute, compared to no change for placebo. It was associated with mean increases in diastolic blood pressure ranging from 0.7 to 2.5 mm Hg averaged over all dose groups, compared to mean decreases ranging from O.9 to 3.8 mm Hg for placebo. However, there is a dose dependency for blood pressure increase (see Warnings).

Laboratory Changes:
Of the serum chemistry and hematology parameters monitored during clinical trials with venlafaxine, a statistically significant difference with placebo was seen only for serum cholesterol, i.e., patients treated with venlafaxine had mean increases from baseline of 3 mg/dL, a change of unknown clinical significance.

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In an analysis of ECGs obtained in 769 patients treated with venlafaxine and 450 patients treated with placebo in controlled clinical trials, the only statistically significant difference observed was for heart rate, i.e., a mean increase from baseline of 4 beats per minute for venlafaxine.

Other Events Observed During the Premarketing Evaluation of Venlafaxine:
During its premarketing assessment, multiple doses of venlafaxine were administered to 2,181 patients in phase II and III studies. The conditions and duration of exposure of venlafaxine varied greatly, and included (in overlapping categories) open and double-blind studies, uncontrolled and controlled studies, inpatient and outpatient studies, fixed-dose and titration studies. Untoward events associated with this exposure were recorded by clinical investigators using terminology of their own choosing. Consequently, it is not possible to provide a meaningful estimate of the proportion of individuals experiencing adverse events without first grouping similar types of untoward events into a smaller number of standardized event categories.

In the tabulations that follow, reported adverse events were classified using a standard COSTART-based dictionary terminology . The frequencies presented, therefore, represent the proportion of the 2,181 patients exposed to multiple doses of venlafaxine who experienced an event of the type cited on at least one occasion while receiving venlafaxine. All reported events are included except those already listed in Table III and those events for which a drug cause was remote. If the COSTART term for an event was so general as to be uninformative, it was replaced with a more informative term. It is important to emphasize that, although the events reported occurred during treatment with venlafaxine, they were not necessarily caused by it.

Events are further classified by body system and listed in order of decreasing frequency according to the following definitions: frequent adverse events are those occurring on one or more occasions in at least 1/100 patients (only those not already listed in the tabulated results from placebo controlled trials appear in this listing); infrequent adverse events are those occurring in 1/100 to 1/1000 patients; rare events are those occurring in fewer than 1/1000 patients. The frequent adverse events have been provided below.

Body as a whole: accidental injury, malaise, neck pain.
Cardiovascular: migraine.
Digestive: dysphagia, eructation.
Hemic and lymphatic: ecchymosis.
Metabolic and nutritional: peripheral edema, weight gain.
Nervous: emotional lability, trismus, vertigo.
Respiratory: bronchitis, dyspnea.
Special senses: abnormal vision, ear pain.
Urogenital: anorgasmia, dysuria, hematuria, metrorrhagia*, urination impaired, vaginitis*.

Overdose

Human Experience:
There were 14 reports of acute overdose with venlafaxine, either alone or in combination with other drugs and/or alcohol, among the patients included in the premarketing evaluation. The majority of the reports involved ingestions in which the total dose of venlafaxine taken was estimated to be no more than several-fold higher than the usual therapeutic dose. The 3 patients who took the highest doses were estimated to have ingested approximately 6.75 g, 2.75 g and 2.5 g. The resultant peak plasma levels of venlafaxine for the latter 2 patients were 6.24 and 2.35 mcg/mL, respectively and the peak plasma levels of O-desmethylvenlafaxine were 3.37 and 1.30 mcg/mL, respectively. Plasma venlafaxine levels were not obtained for the patient who ingested 6.75 g of venlafaxine. All 14 patients recovered without sequelae. Most patients reported no symptoms. Among the remaining patients, somnolence was the most commonly reported symptom. The patient who ingested 2.75 g of venlafaxine was observed to have 2 generalized convulsions and a prolongation of QTc to 500 msec, compared with 405 msec at baseline. Mild sinus tachycardia was reported in 2 of the other patients.

Overdosage Management:
Treatment should consist of those general measures employed in the management of overdosage with any antidepressant. Ensure an adequate airway, oxygenation, and ventilation. Monitoring of cardiac rhythm and vital signs is recommended. General supportive and symptomatic measures are also recommended. Use of activated charcoal, induction of emesis, or gastric lavage should be considered. Due to the large volume of distribution of venlafaxine hydrochloride, forced diuresis, dialysis, hemoperfusion and exchange transfusion are unlikely to be of benefit. No specific antidotes for venlafaxine are known.

In managing overdosage, consider the possibility of multiple drug involvement. The physician should consider contacting a poison control centre on the treatment of any overdose.

Dosage

Adults:
The recommended treatment dose is 75 mg per day, administered in two or three divided doses, taken with food. If the expected clinical improvement does not occur after a few weeks, a gradual dose increase to 150 mg/day may be considered. If needed, the dose may be further increased up to 225 mg/day. Increments of up to 75 mg/day should be made at intervals of no less than 4 days. In outpatient settings there was no evidence of the usefulness of doses greater than 225 mg/day for moderately depressed patients. More severely depressed inpatients have responded to higher doses, between 350 and 375 mg/day, given in 3 divided doses.

Maximum:
The maximum dose recommended is 375 mg per day (in an inpatient setting).

Patients With Hepatic Impairment:
Given the decrease in clearance and increase in elimination half-life for both venlafaxine and ODV that is observed in patients with hepatic cirrhosis compared to normal subjects (see Pharmacology), it is recommended that the total daily dose be reduced by about 50% in patients with moderate hepatic impairment. Since there was much individual variability in clearance between patients with cirrhosis, it may be necessary to reduce the dose even more than 50%, and individualization of dosing may be desirable in some patients.

Patients with Renal Impairment:
Given the decrease in clearance for venlafaxine and increase in elimination half-life for both venlafaxine and ODV that is observed in patients with renal impairment (GFR = 10 to 70 mL/min) compared to normals (see Pharmacology), it is recommended that the total daily dose be decreased by 25% in patients with mild to moderate renal impairment. It is recommended that the total daily dose be reduced by 50% and the dose be withheld until the dialysis treatment is completed (4 hrs) in patients undergoing hemodialysis. Since there was so much individual variability in clearance between patients with renal impairment, individualization of dosing may be desirable in some patients.

Geriatrics:
No dose adjustment is recommended for elderly patients on the basis of their age. As with any antidepressant, however, caution should be exercised in treating the elderly. When individualizing the dosage, extra care should be taken when increasing the dose.

Discontinuing Venlafaxine:
When venlafaxine therapy that has been administered for more than 1 week is stopped, it is generally recommended that the dose be tapered gradually to minimize the risk of discontinuation symptoms. Patients who have received venlafaxine for 6 weeks or more should have their dose tapered gradually over a 2-week period.

Common Effexor Side Effects

Effexor

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Effexor withdrawal. Effexor withdrawal side effects, withdrawal warnings, withdrawal precautions, withdrawal adverse effects, overdose, withdrawal symptoms and Effexor natural alternatives. Before you begin the spiral down with Effexor, try giving your body what it really wants.