Originally Posted - November 21, 2005


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Dropping The Ball
By Karen Ward, RN

There is much difficulty putting Terri Schiavo to rest with the barrage of news reports detailing other peoples' circumstances in the United States in similar situations; put to death daily, either by state sanctioned euthanasia, hospital sanctioned euthanasia, or family sanctioned euthanasia.

Add the constant reports of Michael Schiavo speaking tours, awards, and endorsing political candidates, along with judicial activism awards, and we cannot forget. We are constantly reminded of Terri Schiavo's brutal death. Maybe we are not supposed to forget, but instead, dig deeper into what actually happened with Terri, in order to prevent the same thing from happening to disabled, elderly, and brain injured people in this country, before it becomes the norm.

If you read the news and follow laws rapidly changing in other countries of the world, we know euthanasia is advancing in this country. We even have a form of euthanasia, Physician Assisted Suicide (PAS), in Oregon. The constant reports of personal stories in the news and circulating through cyberspace, multiply daily.

One thing the media did not report, and which many were unaware, was that Michael Schiavo was on several antidepressants. This information is contained in court documents and depositions, and available to the public. Many people take antidepressants, and even more have a form of depression or other mental illness which goes untreated. Michael Schiavo's mental health and history wouldn't be an issue, except for a couple things.

There was outright nonchalance about Michael's mental health and history of antidepressant use, some completely ignored the issue, and neither the media, nor the courts, nor law enforcement provided answers. Further, they refused to acknowledge the facts existed, and totally ignored those trying to keep Terri alive.

How long Michael was on antidepressants, whether he is still on them, and whether he took any of the drugs simultaneously, is unknown. Read the 1993 deposition and you will understand why. Michael could not answer the same question phrased differently with a consistent answer. Poor recall, confusion, or not remembering specifics is not an acceptable defense. Yet he got away with it. Nary a soul challenged him.

Out of all the controversy in this case, absence of a police investigation, and the refusal of any law enforcement official to involve themselves or make any coherent statement about the lack of an investigation, the fact that Michael had a depressive disorder to the extent he was taking prescribed psychotropic agents, should have prompted the police to check his background and history for domestic violence and rule it out, at the very least.

Medications Michael took are alluded to in the 1990 police report, but not mentioned in that report. There is no mention of follow up from law enforcement with the "unusual situation" comment contained in that report, no background check of Michael Schiavo to rule out domestic violence, or in tying those circumstances, the possibility of domestic violence, with a history of antidepressant use, together.

Since Michael Schiavo was on antidepressants, we know he had mental illness in the form of depression, at the very least. According to his own sworn testimony in a 1993 testimony, he also had suicidal ideation at times.

Depressive states have been classified as endogenous psychotic depressions and reactive depressions.

Endogenous psychotic depressions are characterized by an absence of external causes for the depression, such as death of a loved one, loss of employment, or debilitating disease, and the grief and depression are of psychopathologic origin.

Reactive depressions are abnormal depressive responses to environmental factors, and are associated with emotional tension and instability.

Most antidepressants work by slowing the removal of certain chemicals from the brain. These chemicals are called neurotransmitters (such as serotonin and norepinephrine). These neurotransmitters are needed for normal brain function, and are involved in the control of mood, and other responses and functions, such as eating, sleeping, thinking, and pain.

Valrelease (Valproic Acid) is a mood stabilizer. Valrelease has also been classified as an anticonvulsant. Other brand names are Depakene and Valproate. These drugs are used in the treatment of bipolar disorder. Valrelease is also prescribed for anxiety, nervousness, and tension associated with anxiety disorders.

Besides anxiety, Valrelease may also be used to treat symptoms of acute alcohol withdrawal, to help control epilepsy, or to relieve muscle spasms. Anxiety or tension associated with the stress of everyday life usually does not require treatment with this drug.

In acute alcohol withdrawal, it is used to relieve acute agitation, tremor, delirium tremens and hallucinosis. It is also used to relieve skeletal muscle spasm such as inflammation of the muscles or joints, or secondary to trauma); spasticity caused by diseases such as cerebral palsy and paraplegia); athetosis; stiff-man syndrome, and tetanus.

Maybe Michael did and does have a back ailment, a seizure disorder, or other, which required Valrelease use. However, since he was on several other antidepressants, and some of those are major antidepressants, we can conclude he has a history of depression as well. These are undisputable facts and again, should have been a point of investigation to rule out, by law enforcement, predicated on the "unusual situation" comment contained in the police report.

Valrelease is habit forming with physical and psychological dependence on the medication. It can increase the sedative effects of other drugs that cause drowsiness, including antidepressants, alcohol, antihistamines, (Seldane is an example, and Michael took this drug by his own admission), sedatives (used to treat insomnia), pain relievers, anxiety medicines, seizure medicines, and muscle relaxants.

If combined with other psychotropic agents, careful consideration should be given to the pharmacology of the agents to be employed which may potentiate or enhance the effect of the action of this drug, such as phenothiazines, narcotics, barbiturates, MAO inhibitors and other antidepressants. Since Michael was on antidepressants and Valrelease, there clearly was a valid reason the law should have done an investigation. We know they did no investigation.

Psychotropic drugs comprise tranquilizers and antidepressants. Psychotropic drugs exert an effect upon the mind. The use of these drugs alleviates symptoms and allows the mentally ill to participate in other forms of treatment. The drugs modify behavior, while psychotherapy shapes behavior and produces a change. A thorough evaluation of causative factors is warranted to treat depression. The Schindlers may, or may not know, whether Michael was ever in treatment and for how long. They were in a position to assess Michael's mood changes, any symptoms present, and attitude.

While antidepressant drugs help people feel better, they cannot solve problems in people's lives. Some mental health professionals worry that people who could benefit from psychotherapy rely instead on antidepressant drugs for a "quick fix." Others point out that the drugs work gradually and do not produce instant happiness. The best approach is often a combination of counseling and medicine, but the correct treatment for a specific patient depends on many factors. The decision of how to treat depression or other conditions that may respond to antidepressant drugs should be made carefully and will be different for different people.

Side effects most commonly reported with Valrelease are drowsiness and fatigue. Infrequently encountered are confusion, constipation, depression, headache, hypotension, incontinence, jaundice, and changes in libido, nausea, changes in salivation, skin rash, slurred speech, tremor, urinary retention, vertigo and blurred vision. Paradoxical reactions such as acute hyper excited states, anxiety, hallucinations, increased muscle spasticity, insomnia, rage; sleep disturbances and stimulation have been reported.

Michael Schiavo stated in court documents that he stopped taking these antidepressants due to a sick stomach and clouded thoughts. What is his definition of a sick stomach? That was never questioned. While nausea is a side effect, it is not an adverse reaction. He could have taken an antiemetic to alleviate the nausea, and not quit his psychotropic medications or keep changing them.

Of all the side effects listed above, nausea was Michael's chief complaint. Did his sick stomach include vomiting? Not rage or slurred speech or skin rash, but nausea, prompted him to quit taking his medication.

Tricyclic antidepressants are another class of psychotropic drugs listed in court documents. These drugs have been used to treat depression for a long time. They act on serotonin and another neurotransmitter, norepinephrine, and may also interact with other chemicals throughout the body. They include Elavil (amitriptyline), Norpramin (desipramine), Tofranil (imipramine), Aventyl, and Pamelor (nortriptyline). Common side effects caused by these medicines include dry mouth, blurred vision, constipation, difficulty urinating, worsening of glaucoma, impaired thinking and tiredness. These antidepressants can also affect a person's blood pressure and heart rate.

Elavil (Amitriptyline HCl) is a tricyclic antidepressant, and is used in depressive illness of psychotic or endogenous nature and in some with neurotic depression. Elavil has a sedative action, and is also of value in alleviating the anxiety component of depression.

As with other tricyclic antidepressants, amitriptyline may precipitate hypo-manic episodes in patients with bipolar depression. These drugs are not indicated in mild depressive states and depressive reactions.

Elavil should not be given concomitantly with a MAO Inhibiting compound. Hyper-pyretic crises, severe convulsions, and deaths have occurred in patients receiving tricyclic antidepressants and MAO inhibiting drugs simultaneously. As far as we know, Michael was never on MAO Inhibitors.

When amitriptyline is used to treat the depressive component of schizophrenia, activation or aggravation of existing psychotic manifestation may occur. Likewise, in treating manic depression, hypo-manic or manic episodes and hyperactivity or agitation may become over stimulated. Paranoid delusions, with or without associated hostility, may be exaggerated.

Amitriptyline may enhance the response to alcohol and the effects of barbiturates and other CNS depressants. Therefore, alcohol consumption is a precaution. We have never heard the media discuss if Michael drank or how much.

Reported side effects include dry mouth, blurred vision, urinary retention, constipation, palpitations, tachycardia, weight loss or gain, drowsiness, nervousness, insomnia, Hypotension, dizziness, rash sweating, confusion, mania, psychosis, heart block, arrhythmias, extrapyramidal symptoms, gastric upset, changes in libido, and impotence.

Pamelor (Nortriptyline hydrochloride) is also a tricyclic anti depressant, and is used to treat depression. Side effects are the same or similar as Elavil above. Nausea is not listed as a side effect; however, Michael could have experienced nausea from the tricyclic drugs.

This medication is not to be taken along with any other antidepressant drugs. If taking Prozac, wait at least five weeks before beginning therapy with Pamelor, as a major drug interaction could result. An overdose of this type of antidepressant can be fatal.

Prozac (fluoxetine) is an antidepressant, anti obsessive, and anti bulimic agent or drug with actions that have been shown to significantly reduce the symptoms of obsessive-compulsive disorder in double-blind, placebo-controlled clinical trials. The obsessions or compulsions must be experienced as intrusive, markedly distressing, time consuming, or interfering significantly with the person's social or occupational functioning.

Prozac is an SSRI or Selective Serotonin Reuptake Inhibitor; is an Antidepressant, and is also used in the treatment of anxiety.

According to the FDA, patients with major depressive disorder (MDD), both adult and pediatric, may experience worsening of depression and/or the emergence of suicidal ideation and behavior or unusual changes in behavior, whether or not they are taking antidepressant medications, and this risk may persist until significant remission occurs. There has been a long standing concern that antidepressants may have a role in worsening depression and the emergence of suicide in certain patients. Antidepressants increased the risk of suicidal thinking and behavior in short term studies in children and adolescents with Major Depressive Disorder (MDD) and other psychiatric disorders.

Selective Serotonin Reuptake Inhibitors (SSRIs) act only on the neurotransmitter serotonin, while tricyclic antidepressants and MAO Inhibitors act on serotonin and another neurotransmitter, norepinephrine, and may also interact with other chemicals throughout the body. Selective Serotonin Reuptake Inhibitors have fewer side effects than tricyclic antidepressants and MAO Inhibitors, because Selective Serotonin Reuptake Inhibitors act only on one body chemical, serotonin.

The FDA states further that adults with MDD or co-morbid depression in the setting of other psychiatric illness being treated with antidepressants should be observed similarly for clinical worsening and suicide, especially during the initial few months of a course of drug therapy, or at times of dose changes, either increases or decreases.

The half-life of prozac after a single dose is 2 days with a range of 1 to 4 days, and after multiple dosing 4 days with a range of 2 to 7 days. Because of the long elimination half-life of prozac, changes in dose will not be fully reflected in plasma for several weeks. So, even when the drug is stopped, the active drug substance will persist in the body for weeks due to the long elimination half-lives of fluoxetine and norfluoxetine.

Wellbutrin (bupropion) relieves certain types of major depression and can also be used for ADHD. Wellbutrin can cause agitation, insomnia, headache and nausea. Major depression involves a severely depressed mood (for 2 weeks or more) and loss of interest or pleasure in usual activities accompanied by sleep and appetite disturbances, agitation or lack of energy, feelings of guilt or worthlessness, decreased sex drive, inability to concentrate, and thoughts of suicide. Unlike tricyclic antidepressants, such as Elavil, Pamelor, Tofranil, and others, Wellbutrin tends to have a stimulating effect.

Wellbutrin should not be taken if, within the past 14 days, you have taken a Monoamine Oxidase Inhibitor (MAO Inhibitor) drug, such as the antidepressants Marplan, Nardil or Parnate. This particular drug combination could cause you to experience a sudden, dangerous rise in blood pressure.

An MAO Inhibitor affects the same neurotransmitters (serotonin and norepinephrine) that the tricyclics do, but they also affect dopamine. MAO Inhibitors are usually the antidepressant of last resort. Michael was not on MAOI's, according to court documents studied.
Factors to consider when taking any drugs are the interactions between the drugs ingested. The more drugs one ingests, the more interactions and adverse reactions may be present, not only between the drugs, but with food as well. Antidepressants can have an effect on many other medications causing serious problems.

Another risk of antidepressants is serotonin syndrome, a drug reaction resulting from the over-stimulation of serotonin receptors. This can occur when an antidepressant is taken either with another antidepressant, with certain recreational and other drugs (see below), or more rarely, even when one antidepressant is taken alone. Symptoms include hyperactivity, mental confusion, agitation, sweating, shivers, fever, seizure, diarrhea, and lack of coordination. To minimize the risk of serotonin syndrome, there must be a 'washout' period of at least two weeks when switching from one antidepressant drug to another.

Drugs that may induce serotonin syndrome when taken with antidepressants:

  • ecstasy
  • cocaine
  • lithium
  • St John's wort (Hypericum) - herbal antidepressant
  • diethylproprion - an amphetamine
  • dextromethorphan - found in many cough suppressants
  • Buspar (buspirone) - for anxiety
  • Selgene, Eldepryl (selegiline) - for Parkinson's Disease
  • anti-epileptics - Tegretol, Carbium, Teril (carbamazepine)
  • analgesics - pethidine, Fortral (pentazocine), Tramal (tramadol), fentanyl
  • anti-migraine drugs - Naramig (naratriptan), Imigran (sumatriptan), Zomig (zolmitriptan)
  • appetite suppressants - phentermine and fenfluramine
  • tryptophan - an amino acid


  • St. John's Wort is an over the counter herbal supplement that is used to treat depression. Cough suppressants and analgesics, taken in combination with other antidepressants could have posed serious effects on Michael. All he claimed in court documents was sick stomach and clouded thoughts.

    Seldane (pseudoephedrine-terfenadine) was indicated for the relief of allergy symptoms associated with seasonal allergic rhinitis; sneezing, runny nose, and nasal congestion. It was administered when both the antihistaminic properties of Seldane and the nasal decongestant activity of pseudoephedrine hydrochloride were desired. Seldane was removed from the US market in 1998, because of increased potential for QT Interval prolongation and adverse cardiac events.

    Seldane use in patients with hepatic dysfunction and in patients taking ketoconazole, itraconazole, clarithromycin, erythromycin, or troleandomycin, which are certain antibiotics and antifungal medications, is contraindicated.

    Seldane was replaced with Allegra.

    According to the Medical Malpractice document of 1992, Michael states Terri was on Seldane, but could not recall if he got some from Dr. Prawer or not.

    DRUG INTERACTIONS Most of the interactions between these medications Michael was taking have major drug-drug interactions. Many drugs have cardiac side effects. Some have libido changes. Some cause hypokalemia and other electrolyte disturbances.

    Fluoxetine (Prozac) and pseudoephedrine-terfenadine (SELDANE)
    (major Drug-Drug Interaction)

    Theoretical concerns and one case report have suggested that co-administration of fluoxetine and terfenadine or astemizole may be associated with cardiotoxic effects, including prolongation of the QT interval. The mechanism probably is related to the inhibition of terfenadine and astemizole metabolism by fluoxetine or norfluoxetine, which is a potent inhibitor of CYP450 3A4 (an isoenzyme).

    Other selective serotonin reuptake inhibitors (SSRIs) may interact with terfenadine and astemizole in a similar manner. If terfenadine or astemizole must be used with an SSRI, caution and close observation for evidence of cardiotoxicity are recommended.

    Diazepam (Valium) and fluoxetine (Prozac)
    (moderate Drug-Drug Interaction)

    Several studies have suggested that the effects of benzodiazepines, particularly their effects on psychomotor performance, may be increased by fluoxetine. The mechanism may be related to additive CNS depressant effects and/or inhibition of CYP450 2C19 and/or 3A4 benzodiazepine metabolism by fluoxetine.

    The clinical implications are uncertain, but effects may be more pronounced in the elderly. Dose reductions may be required, and patients should be made aware of the possibility of additive CNS effects (e.g., drowsiness, dizziness, lightheadedness, confusion) and counseled to avoid activities requiring mental alertness until they know how these agents affect them. Patients should also be advised to notify their physician if they experience excessive or prolonged CNS effects that interfere with their normal activities.

    Nortriptyline (Pamelor) and Fluoxetine (Prozac)
    (major Drug-Drug Interaction)

    Administration with fluoxetine may significantly increase the plasma concentrations of some tricyclic antidepressants (TCAs). The proposed mechanism is fluoxetine inhibition of CYP450 2D6, the isoenzyme responsible for the metabolic clearance of many antidepressant and psychotropic drugs.

    Seizures and delirium have been reported, as well as a fatality attributed to fluoxetine-induced chronic amitriptyline toxicity.

    Pharmacodynamically, the combination of fluoxetine (or any other selective serotonin reuptake inhibitor) and a TCA may potentiate the risk of serotonin syndrome, which is a rare but serious and potentially fatal condition thought to result from hyper stimulation of brainstem 5HT1A receptors.

    Patients should be monitored closely for signs and symptoms of TCA toxicity (e.g., sedation, dry mouth, blurred vision, constipation, urinary retention) and/or excessive serotonergic activity (e.g., CNS irritability, altered consciousness, confusion, myoclonus, ataxia, abdominal cramping, hyperpyrexia, shivering, pupillary dilation, diaphoresis, hypertension, and tachycardia).

    Due to the long half-life of fluoxetine and its active metabolite, norfluoxetine, the risk of interaction may persist for several weeks after discontinuation of fluoxetine.

    Nortriptyline (Pamelor) and Amitriptyline (Elavil)
    (moderate Drug-Drug Interaction)

    Agents with anticholinergic properties (e.g., sedating antihistamines; antispasmodics; neuroleptics; phenothiazines; skeletal muscle relaxants; tricyclic antidepressants; class IA antiarrhythmics especially disopyramide) may have additive effects when used in combination.

    Excessive parasympatholytic effects may result in paralytic ileus, hyperthermia, heat stroke, and the anticholinergic intoxication syndrome. Peripheral symptoms of intoxication commonly include mydriasis, blurred vision, flushed face, fever, dry skin and mucous membranes, tachycardia, urinary retention, and constipation. Central symptoms may include memory loss, disorientation, incoherence, hallucinations, psychosis, and delirium; hyperactivity, twitching or jerking movements, stereotypy, and seizures.

    Central nervous system-depressant effects may also be additively or synergistically increased when these agents are combined, especially in elderly or debilitated patients. Use of neuroleptics in combination with other neuroleptics or anticholinergic agents may increase the risk of tardive dyskinesia.

    Nortriptyline (Pamelor) and Diazepam (Valium)
    (moderate Drug-Drug Interaction)

    Central nervous system and/or respiratory depressant effects may be additively or synergistically increased in patients taking multiple drugs that cause these effects, especially in elderly or debilitated patients.

    Nortriptyline (Pamelor) and Pseudoephedrine-Terfenadine (Seldane)
    (moderate Drug-Drug)

    Theoretically, concurrent use of two or more drugs that can cause QT interval prolongation may increase the risk of ventricular arrhythmias, including ventricular tachycardia and torsade de pointes, due to additive arrhythmogenic potential related to their effects on cardiac conduction.

    The risk of an individual agent or a combination of these agents causing ventricular arrhythmia in association with QT prolongation is largely unpredictable but may be increased by certain underlying risk factors such as congenital long QT syndrome, cardiac disease, and electrolyte disturbances (e.g., hypokalemia, hypomagnesemia).

    In addition, the extent of drug induced QT prolongation is dependent on the particular drug(s) involved and dosage(s) of the drug(s). MANAGEMENT: Caution and clinical monitoring are recommended if multiple agents associated with QT interval prolongation are prescribed together. Patients should be advised to seek medical attention if they experience symptoms that could indicate the occurrence of torsade de pointes such as dizziness, palpitations, or syncope.

    Amitriptyline (Elavil) and diazepam (Valium)
    (moderate Drug-Drug Interaction)

    Central nervous system and/or respiratory-depressant effects may be additively or synergistically increased in patients taking multiple drugs that cause these effects, especially in elderly or debilitated patients. During concomitant use of these drugs, patients should be monitored for potentially excessive or prolonged CNS and respiratory depression.

    Patients should be made aware of the possibility of additive CNS effects (e.g., drowsiness, dizziness, lightheadedness, confusion) and counseled to avoid activities requiring mental alertness until they know how these agents affect them. Patients should also be advised to notify their physician if they experience excessive or prolonged CNS effects that interfere with their normal activities.

    Amitriptyline (ELAVIL) and pseudoephedrine-terfenadine (SELDANE)
    (moderate Drug-Drug Interaction)

    Theoretically, concurrent use of two or more drugs that can cause QT interval prolongation may increase the risk of ventricular arrhythmias, including ventricular tachycardia and torsade de pointes, due to additive arrhythmogenic potential related to their effects on cardiac conduction. The risk of an individual agent or a combination of these agents causing ventricular arrhythmia in association with QT prolongation is largely unpredictable but may be increased by certain underlying risk factors such as congenital long QT syndrome, cardiac disease, and electrolyte disturbances (e.g., hypokalemia, hypomagnesemia). In addition, the extent of drug-induced QT prolongation is dependent on the particular drug(s) involved and dosage(s) of the drug(s).

    Caution and clinical monitoring are recommended if multiple agents associated with QT interval prolongation are prescribed together. Patients should be advised to seek medical attention if they experience symptoms that could indicate the occurrence of torsade de pointes such as dizziness, palpitations, or syncope.

    Diazepam (Valium) and buPROPion (Wellbutrin)
    (moderate Drug-Drug Interaction)

    Excessive use or abrupt discontinuation of benzodiazepines and other sedatives after chronic ingestion may precipitate seizures in patients receiving bupropion. Conversely, bupropion may antagonize the central pharmacologic effects of sedatives. Bupropion can cause agitation, anxiety, and insomnia and has been shown to decrease the sedative effect of diazepam in healthy volunteers given single doses of the drugs.

    Although sedatives may be prescribed to treat agitation, anxiety, and insomnia associated with bupropion use, patients should be alerted to the possibility of an increased risk of seizures during excessive exposure to these drugs. Patients should not attempt to alter the dosages or discontinue the medications on their own without consulting with their physician. The use of bupropion is contraindicated in patients undergoing abrupt discontinuation of sedatives.

    BuPROPion (WELLBUTRIN) and fluoxetine (PROZAC)
    (moderate Drug-Drug Interaction)

    Co administration with bupropion may increase the plasma concentrations of drugs that are substrates of the CYP450 2D6 isoenzyme. The mechanism is decreased clearance due to inhibition of CYP450 2D6 activity by bupropion, which is expected to occur in patients who are CYP450 2D6 extensive metabolizers (93% or more of the general population). Caution is advised if bupropion must be used concomitantly with medications that undergo metabolism by CYP450 2D6, particularly those with a narrow therapeutic range. Concomitant medications should be initiated at a lower dosage. Clinical and laboratory monitoring may be appropriate for some drugs whenever bupropion is added to or withdrawn from therapy.

    Amitriptyline (ELAVIL) and buPROPion (WELLBUTRIN)
    (major Drug-Drug Interaction)

    Concomitant use of bupropion and tricyclic antidepressants (TCAs) may potentiate the risk of seizures. These agents are individually epileptogenic and may have additive effects on the seizure threshold. Additionally, bupropion can increase the plasma concentrations of some TCAs due to inhibition of CYP450 2D6.

    In one case report, plasma levels of imipramine and its metabolite, desipramine, increased approximately fourfold in a 64-year-old woman following the addition of bupropion 225 mg/day. Plasma levels of desipramine were increased twofold more than the imipramine levels, which is consistent with the fact that desipramine is primarily metabolized by CYP450 2D6 while imipramine is also metabolized by other CYP450 isoenzymes.

    Similarly, a 62-year-old woman with no history of seizures developed a generalized tonic-clonic seizure in association with toxic trimipramine plasma levels following the addition of bupropion. No further seizures occurred after dosage reductions of both drugs.

    The manufacturer advises extreme caution if bupropion is co-administered with TCAs. Low initial TCA dosages with gradual titration are recommended. In patients who are already stabilized on TCA therapy, plasma TCA levels and pharmacologic response should be monitored more closely whenever bupropion is added to or withdrawn from therapy, and the TCA dosage adjusted as necessary. Patients should be advised to notify their physician if they experience seizures or increased TCA adverse effects such as somnolence, dry mouth, urinary retention, orthostasis, tachycardia, or irregular heartbeats.

    Amitriptyline (ELAVIL) and fluoxetine (PROZAC)
    (major Drug-Drug Interaction)

    Co-administration with fluoxetine may significantly increase the plasma concentrations of some tricyclic antidepressants (TCAs). The proposed mechanism is fluoxetine inhibition of CYP450 2D6, the isoenzyme responsible for the metabolic clearance of many antidepressant and psychotropic drugs. Seizures and delirium have been reported, as well as a fatality attributed to fluoxetine-induced chronic amitriptyline toxicity.

    Pharmacodynamically, the combination of fluoxetine (or any other selective serotonin reuptake inhibitor) and a TCA may potentiate the risk of serotonin syndrome, which is a rare but serious and potentially fatal condition thought to result from hyper stimulation of brainstem 5HT1A receptors. In general, the use of fluoxetine (or other SSRIs) with TCAs should be avoided if possible, or otherwise approached with caution if potential benefit is deemed to outweigh the risk. Pharmacologic response and plasma TCA levels should be monitored more closely whenever fluoxetine is added to or withdrawn from therapy in patients stabilized on their existing antidepressant regimen, and the TCA dosage adjusted as necessary. Patients should be monitored closely for signs and symptoms of TCA toxicity (e.g., sedation, dry mouth, blurred vision, constipation, urinary retention) and/or excessive serotonergic activity (e.g., CNS irritability, altered consciousness, confusion, myoclonus, ataxia, abdominal cramping, hyperpyrexia, shivering, pupillary dilation, diaphoresis, hypertension, and tachycardia). Due to the long half-life of fluoxetine and its active metabolite, norfluoxetine, the risk of interaction may persist for several weeks after discontinuation of fluoxetine.

    The drugs Valrelease, elavil, pamelor, prozac, wellbutrin and seldane are noted in court documents, and by Michael Schiavo's own account, as drugs he had once taken. All the drugs listed above can cause serious problems if the directions are not read are not followed.

    We know Michael has a history of depression. We know he was taking medications for other forms of mental illness than simply depression. We also know he had been treated for depression and other mental illnesses. We know he was on psychotropic agents for depression.

    We know Michael had suicidal ideation. According to the 1993 deposition, Michael admittedly agreed he had been treated by a psychiatrist. He stated that he saw this psychiatrist for treatment due to Terri's collapse, and that it was for a temporary period of time; "couple years, on, off."

    Michael Schiavo was treated for endogenous psychotic depression. The fact that he was on Elavil and Valrelease is very telling. He could have had a reactive depression over the injury to Terri which compounded his depressive state. However, treatment with psychotropic medications for Bipolar Disorder does not indicate a reactive depression.

    We do not know if Michael had tapered off his medications per physician orders, or if he stopped taking them abruptly. His testimony is simply unclear, contradictory, and was never challenged. He stated he used to fight with the doctors all the time. One has to presume the fights were because he was noncompliant with his medication regimen or treatment. His statements reflect the facts that the doctors prescribed the antidepressants when he became "real down." Building a therapeutic level over the course of a few months was not accomplished with the frequent changes of his medications.

    The doctors changed the medications, according to Michael's testimony. How frequently is unknown. However, he does say that he would call the doctor up and tell him he wasn't feeling well on the pills. "And he says let's try this." While Michael was playing musical meds, the physicians involved were all too obliging, and Terri suffered as a result.

    We do not know how long Michael has had a history of depression. We do not know how long he had been on psychotropic drugs for depression. We do not know how many physicians he saw for the depression.

    We know by Michael's own accounting in the 1993 document, he was prescribed medication; he picked it up, but never took it. He then goes on to say "not all at the same time", in reference to taking Wellbutrin, Pamelor, Elavil, and Prozac. Yet he reiterates he never took the meds. He further states there were "spans between each one". He should have said not any at the same time, but he said he never took them. Or, maybe he did, but does not remember due to his mental state.

    When asked about another medication change, Michael's reply was that a lot of the pills made him sick to his stomach. A question then follows asking him whether he took some of the medications mentioned. Michael affirms he did. That sets the record straight as far as taking the medications. However, nary a soul went back to challenge the inconsistencies and confusion in his testimony.

    We do not know the degree Michael continued to suffer from depression, manic-depressive states, bipolar disorder, or anxiety during the years he was responsible for Terri's care. There is no guarantee he acted in Terri's best interests with his history, and failure to take the medications for his health problems. There is no guarantee he made sound judgments regarding Terri's care.

    The St. Pete police department to Bernie McCabe's office on down know nothing either, as they never investigated. Who truly knows Michael's state of mind prior to the night Terri collapsed and directly afterwards? What mental and emotional condition was he in when he decided to pull her feeding tube? What mental state was he in every time he took an emotional swipe at Terri's parents?

    In the interests of all fairness, there is a possibility Terri could have inadvertently ingested one or more of Michael's psychotropic agents, thereby causing an adverse reaction. An overdose that involves other drugs in combination with Wellbutrin may also cause breathing difficulties, coma, fever, rigid muscles, and stupor. And some medications do cause electrolyte disturbances. Regardless, a toxicology screen was never performed in the hospital for traces of any drugs other than alcohol and substances of abuse.

    Also at issue is whether Terri and Michael shared the Seldane like an over the counter aspirin. This is a frequent occurrence, and can cause severe side effects and adverse reactions.

    If ever there was a missed opportunity to rule out or confirm anything, the ineptness from the law was it. Law enforcement dropped the ball by not investigating the "unusual situation", and the hospital dropped the ball by not following up and ruling out the "unusual situation." 11-20-05

    © 2005 North Country Gazette


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