NURS 6061 University Of Texas Tricyclic Antidepressant Toxicity Presentation aymelea 1) Help with creation of a power point. 2) Integrate case study prov | Course Hero

NURS 6061 University Of Texas Tricyclic Antidepressant Toxicity Presentation aymelea

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4) https://images.app.goo.gl/wZo6rZXL5WuMFFpg6 integrated the principal slides tittle of this PPT with those of the ppt attached to create a complete and comprehensive ppt on the study case only. ( USED TITLES OF THE SLIDES OF THIS POWER POINTS ASSOCIATED WITH THAT PF THE ATTACHED POWER POINT)THE TITLES OF THIS POWER FIRST THEN THE TITLES OF THE ATTACHED PPT) ALL RELATED TO THE ATTACHED CASE STUDY ONLY ( THE TITLE ARE USES TO KNOW WHAT SHOULD BE INCLUDED IN THE SLIDES OF THIS PPT). TOPIC: SEE CASE STUDY ONLY

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THE CASE STUDY IS ABOUT Tricyclic Antidepressant Toxicity IN A GERIATRIC PATIENT

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PMHMP-NURS-6261
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06/30/2020
Topic Overview
Topic: Should ketamine be approved officially as effective
and durable treatment for suicide and suicidal ideation?
Rationale: Existing treatments take a long time before
alleviating the symptoms of depression and suicidal ideation.
Problem Description
• Suicide and suicide ideation are
emergencies that need urgent interventions.
• Depression is an emergency with social,
cultural, and economic impacts on society.
• There is no effective treatment approach to
manage suicide and suicide ideation.
Proposed Practice Change
• Due to the urgency presented by suicide/suicide ideation, the healthcare
department needs to approve the use of ketamine immediately to
lighten the condition’s burden on the economy and society.
• Practitioners can use ketamine to treat depression and its complications,
including suicide and suicidal ideation.
• Ketamine is an ideal treatment approach because it works immediately
and has minimal side effects.
Presentation of Evidence
• Andrade (2017) claims that ketamine and derivatives are effective for
treating MD, which can trigger suicidal behavior.
• Zanos and Gould (2018) assert that ketamine inhibits NMDA and
activates an acid receptor, which help in managing depression/suicide.
• Duman (2018) affirms that ketamine is effective in treating
depression/suicide ideation resistant to other medical approaches.
• Grunebaum et al. (2018) posits that treatment of MD/suicide using
ketamine has positive outcomes within 24 hours.
Recommendations
• The health care department should approve ketamine as a
treatment approach for preventing suicide and managing
suicide ideation because of its proven benefits and due to
the ineffectiveness of existing approaches.
• Ketamine can reduce the rate of suicide completed if
practitioners conduct efficient patient screening, public
education, and cultural support when implementing the
approach.
Implications for Practice
Approving the use of ketamine for treating suicide and
suicidal ideation will have numerous benefits including:
• Decreased burden on health care.
• Reduced health care costs.
• Improved economic development.
• Improved health care quality.
References
Andrade C. (2017). Ketamine for Depression, 2: Diagnostic and
Contextual Indications. The Journal of Clinical Psychiatry, 78(5),
Duman R. S. (2018). Ketamine and rapid-acting antidepressants: A
new era in the battle against depression and suicide.
F1000Research, 7
Grunebaum, M. F et al. (2018). Ketamine for Rapid Reduction of
Suicidal Thoughts in Major Depression: A Midazolam-Controlled
Randomized Clinical Trial. The American Journal of Psychiatry,
175(4), 327-335
References
Meisner, R. C. (2019). Ketamine for major depression: New tool, new
questions. Harvard Health Publishing. Retrieved from
https://www.health.harvard.edu/blog/ketamine-formajor-
depression-new-tool-new-questions-2019052216673
Menard, C., Hodes, G. E., & Russo, S. J. (2016). Pathogenesis of
depression: Insights from human and rodent studies. Neuroscience,
321, 138–162. https://doi.org/10.1016/j.neuroscience.2015.05.053
Zanos, P., & Gould, T. D. (2018). Mechanisms of ketamine action as
an antidepressant. Molecular Psychiatry, 23(4), 801– 811.
Wesley Brown, a 63-year-old businessman, was “found down” in the road by police and brought to
the emergency room (ER) of a large university-affiliated hospital. The psychiatry service was
consulted for management of “psychotic behavior” in the ER. The patient’s family reported that the
patient had exhibited an approximately 2-week history of “strange behavior.” According to his
sister, Mr. Brown had been running around the kitchen with knives, sending paranoid e-mails about
the justice system to his friends, showing his guns to the neighbors, seeing people in the walls,
having paranoid thoughts that his wife was having an affair, and not sleeping. The patient’s wife had
reported him missing 3 days prior to admission. Notably, his car was found a few blocks away with
a large box in its trunk containing numerous medications and the patient’s extensive gun collection.
Mr. Brown’s vital signs were within normal limits. His medical records revealed a history of
coronary artery disease and a coronary artery bypass graft 5 years prior to admission, as well as
chronic back pain and several spinal surgeries, with an associated history of daily opiate use. He
had no prior psychiatric history, including any history of depression or antidepressant medications.
His outpatient medications included metoprolol, cyclobenzaprine, and morphine (in the form of
MS-Contin).
His physical examination was notable for heavy sedation, mydriasis, hypoactive bowel sounds,
urinary retention, epistaxis, and depressed reflexes. A computed tomography (CT) scan of the head
was negative, and CT of the cervical spine showed degeneration. His blood alcohol screen was
negative, and complete blood count and comprehensive metabolic panel results were within
normal limits, as were an electrocardiogram and cerebrospinal fluid from a lumbar puncture. His
urine toxicology screen was positive for “benzodiazepines and tricyclics.”
Mr. Brown’s mental status examination revealed waxing and waning alertness, an unkempt
appearance, lack of cooperation with nursing and medical personnel, somewhat slurred speech, and
signs of psychomotor retardation. His affect alternated between subdued/somnolent and
restless/agitated. He denied suicidal or homicidal ideation but reported significant paranoid
ideation that focused on his wife’s suspected affair. His thought process was notably tangential. He
denied both auditory and visual hallucinations. His judgment and insight were impaired. During his
initial evaluation, the patient was noted to have a Mini-Mental State Examination score of 16 of 30
possible points. He lost 7 of 10 points for orientation, 3 for attention and calculation, 2 for recall,
and 1 each for sentence writing and copying design.
Tricyclic Antidepressant Toxicity
Muhammad M. Khalid; Muhammad Waseem.
Author Information
Last Update: July 5, 2020.
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Introduction
Tricyclic antidepressants (TCAs) were introduced in the late 1950s for the treatment of
depression. However, with the advent of selective serotonin reuptake inhibitors (SSRIs) and
other new antidepressants, the use of TCAs has become limited, although it is still used to
treat depression that has not responded to treatment with less toxic agents. In adults, TCAs
are also used in migraine headache prophylaxis, treatment of neuralgic pain, including the
pain associated with Ciguatera poisoning, and obsessive-compulsive disorder. In children,
TCAs have been used to treat nocturnal enuresis. Despite the current limited use of TCAs,
the curve for TCA-overdose associated hospitalization and fatality is on the rise.[1][2][3][4]
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Etiology
Since TCAs are mostly used for treating patients with chronic pain and neuropsychiatric
disorders, toxicity and overdoses are mostly seen in these patients, who are taking them for
these debilitating diseases. These drugs are commonly prescribed for these diseases, and
therefore are readily available to these patients.
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Epidemiology
According to the database, TCA overdose accounted for 1.12 exposures per 10,000
population in 1992. Recently, the trend for antidepressant overdose has shifted more towards
SSRIs. However, the rate of hospitalization is higher in cases of TCA overdose compared to
SSRI, because of the narrower therapeutic index with TCAs.
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Pathophysiology
Tricyclic antidepressants impose their therapeutic effects by inhibiting presynaptic reuptake
of norepinephrine and serotonin in the central nervous system (CNS). This effect in the CNS
can cause seizures. TCAs are weakly basic, and an acidic environment facilitates the
formation of the ionized form and potentiates this effect. In cases of toxicity, TCAs block a
number of receptors, including peripheral alpha-adrenergic, histaminic, muscarinic, and
central serotonin receptors. Blockade of alpha-adrenergic receptors can cause hypotension.
Blockade of muscarinic receptors can cause signs of anticholinergic toxicity, such as
tachycardia, fever, dry mouth and skin, decreased bowel sounds, and altered mental status.
Blockade of histamine receptors can also cause altered mental status. TCAs can cause
cardiac toxicity. Blockade of fast sodium channels in myocardial cells slows the action
potential and provides a membrane stabilizing effect. The characteristic QRS prolongation
seen in TCA overdose occurs secondary to prolongation of phase “0” of the myocardial
action potential. This effect can lead to heart block and bradycardia. QT prolongation seen in
cases of TCA overdose occurs due to potassium channel blockade that may potentially cause
torsades de pointes. TCAs can also exert a quinidine-like toxic effect on the myocardium that
can cause decreased cardiac contractility and hypotension.[5][6][7]
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Toxicokinetics
TCAs are rapidly absorbed in the gastrointestinal tract. However, following an overdose,
owing to the inherent anticholinergic effects, TCAs may decrease the gastrointestinal
motility and cause delayed absorption and toxicity. Coingestion of other anticholinergic
medications may cause more erratic absorption. TCAs have a long elimination half-life as
these drugs are largely bound to the plasma protein and highly lipid-soluble. Renal excretion
occurs after significant first-pass hepatic metabolism. TCAs are primarily metabolized by
CYP2D6, and the enzyme inducers and inhibitors of this pathway may alter their
metabolism. Toxicity may occur because of the primary compound or its metabolite.
Respiratory or metabolic acidosis may increase the unbound fraction of TCA and may
potentiate the harmful effects. Signs of toxicity usually appear within 2 hours’ post-ingestion.
If 6 hours post-ingestion, there are no signs of toxicity seen both clinically and on the
electrocardiogram, and the patient has normal bowel sounds, then most likely, the patient has
not taken a significant overdose and can be medically cleared for psychiatric evaluation if
needed. Once significant toxicity occurs, it usually lasts for 24-48 hours. However, there are
case reports of significant toxicity due to Amitriptyline that lasted up to 5 days postingestion.
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History and Physical
All patients with suspected TCA overdose should be immediately evaluated, and a 12 lead
EKG should be obtained. The therapeutic index of TCAs is narrow, and therefore, the
ingestion of 10 to 20 mg/kg is potentially life-threatening. Symptoms usually start in 30 to 40
minutes, and signs of toxicity are usually clinically apparent within 2 hours, but delayed
toxicity may occur. History of co-ingestion or access to other medications, including
acetaminophen and aspirin, is essential. Close attention to the patient’s vital signs and
repeated physical examination for evidence of an anticholinergic toxidrome, cardiac toxicity,
and neurologic toxicity should be done and will help guide proper management.
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Evaluation
Cardiovascular, anticholinergic, and neurologic manifestations are common. Vital signs may
be abnormal. The patient may not be able to protect his or her airway. Respiratory depression
may occur. Sinus tachycardia is commonly present due to anticholinergic toxicity, but more
dangerous tachydysrhythmias and even bradycardia with or without heart block can occur.
Hypotension can occur due to dehydration, cardiac toxicity, and alpha-adrenergic blockade.
The patient may often demonstrate anticholinergic toxicity, such as fever, dilated pupils, dry
mouth, dry, warm skin, decreased bowel sounds, and altered mental status. The patient may
be agitated or seizing, or the patient may have decreased mental status, and may even
become comatose. An EKG should be obtained early in the management of these patients,
and any evidence of sodium and/or potassium channel blockade should be promptly
addressed. Prolongation of QRS, due to sodium channel blockade of more than 100
milliseconds, is predictive of seizures while QRS > 160 milliseconds is predictive of
arrhythmia. An R/S ratio in AVR of 0.7 or more and an R wave in the AVR lead more than 3
mm is strongly predictive of seizures and arrhythmias. In addition to basic lab investigations,
including levels of possible co-investments, such as acetaminophen and aspirin, a CT scan of
the head to rule out other causes of altered mental status should be done if clinically
indicated. It should be noted that TCA levels do not correlate with toxicity, but may be
helpful in diagnosing an unknown overdose when the clinical symptoms and signs point to a
possible TCA ingestion. Any sign of toxicity warrants admission in an intensive care setting
for at least 24 hours. Asymptomatic patients should be continuously monitored for signs of
toxicity, changes in vital signs, and EKG for at least 6 hours.[8][9][10][11]
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Treatment / Management
Proper management of airway, breathing, and circulation is critical in cases of TCA
poisoning. Gastrointestinal decontamination by activated charcoal should be done only if
conditions are appropriate and the airway is protected. Charcoal decontamination may be
effective up to 2 hours’ post-ingestion, especially if the bowel sounds are diminished. Every
effort should be made to minimize the formation of acidosis, as acidosis may increase
cardiac and neurologic toxicity. Seizures usually respond to benzodiazepines, but in cases of
refractory seizures, prompt administration of anticonvulsants, such as phenobarbital or
propofol, or even general anesthesia, should be considered. Sodium bicarbonate should be
given to hemodynamically unstable patients, patients with seizures, and patients with QRS
prolongation of more than 100 msec. Sodium bicarbonate is given as a bolus of 1 meq/kg,
followed by an intravenous infusion containing sodium bicarbonate. The aim of this therapy
is to narrow the QRS and to keep the serum pH between 7.5 and 7.55. Hypotensive patients
should be treated with IV fluids and sodium bicarbonate, and if their hypotension does not
respond to this, alpha-adrenergic agents, such as norepinephrine, should be used. Sodium
bicarbonate should be used to treat dysrhythmias associated with QRS widening. Temporary
pacemakers have been used to treat refractory symptomatic bradycardias not responsive to
sodium bicarbonate. Physostigmine, Type 1A, Type 1C, and Type 3 Anti-dysrhythmic agents
should be strictly avoided, as should Flumazenil. Intralipid emulsion treatment should be
considered in hemodynamically unstable patients with overdoses of lipophilic TCAs. Since
TCA are highly protein bound with an extensive volume of distribution, enhanced
elimination with dialysis and hemoperfusion is not effective.
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Enhancing Healthcare Team Outcomes
Tricyclic antidepressant toxicity can be life-threatening and is best managed by an
interprofessional team that consists of an emergency department physician, nurse
practitioner, poison control specialist, cardiologist, neurologist, and an emergency or critical
care nurse. As with all cases of poisoning, proper management of airway, breathing, and
circulation is critical in cases of TCA poisoning. Gastrointestinal decontamination by
activated charcoal should be done only if conditions are appropriate and the airway is
protected. Sodium bicarbonate should be given to hemodynamically unstable patients,
patients with seizures, and patients with QRS prolongation of more than 100 msec. Some
patients may even require temporary pacing for bradycardia. Hydration and close monitoring
in an ICU setting are recommended. It is vital to make sure that the patient has no other coingestants in the systemic circulation. For patients managed promptly, the outcomes are
good. However, if treatment is delayed or the patient has ingested multiple other agents, the
prognosis is guarded. Before discharge, if attempted suicide is suspected, the patient should
be referred to a mental health counselor. Parents should be urged to keep all medications in a
locked cabinet away from the reach of children.[12][13][Level 5]
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Questions
To access free multiple choice questions on this topic, click here.
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References
1.
Avau B, Borra V, Vanhove AC, Vandekerckhove P, De Paepe P, De Buck E. First
aid interventions by laypeople for acute oral poisoning. Cochrane Database Syst
Rev. 2018 Dec 19;12:CD013230. [PMC free article] [PubMed]
2.
Kassim T, Mahfood Haddad T, Rakhra A, Kabach A, Qurie A, Selim M, Nayfeh
AS, Aly A, Holmberg MJ. A Case of Amitriptyline-induced
Myocarditis. Cureus. 2018 Jun 19;10(6):e2840. [PMC free article] [PubMed]
3.
Methling M, Krumbiegel F, Hartwig S, Parr MK, Tsokos M. Toxicological
findings in suicides – frequency of antidepressant and antipsychotic
substances. Forensic Sci Med Pathol. 2019 Mar;15(1):23-30. [PubMed]
4.
Guan Y, Li X, Umetani M, Boini KM, Li PL, Zhang Y. Tricyclic antidepressant
amitriptyline inhibits autophagic flux and prevents tube formation in vascular
endothelial cells. Basic Clin. Pharmacol. Toxicol. 2019 Apr;124(4):370384. [PMC free article] [PubMed]
5.
Giwa A, Oey E. The return of an old nemesis: Survival after severe tricyclic
antidepressant toxicity, a case report. Toxicol Rep. 2018;5:357-362. [PMC free
article] [PubMed]
6.
Lubna NJ, Wada T, Nakamura Y, Chiba K, Cao X, Izumi-Nakaseko H, Ando K,
Naito AT, Satoh Y, Sugiyama A. Amitriptyline May Have Possibility to Induce
Brugada Syndrome Rather than Long QT Syndrome. Cardiovasc. Toxicol. 2018
Feb;18(1):91-98. [PubMed]
7.
Dempsey SK, Poklis JL, Sweat K, Cumpston K, Wolf CE. Acute Toxicity From
Intravenous Use of the Tricyclic Antidepressant Tianeptine. J Anal Toxicol. 2017
Jul 01;41(6):547-550. [PMC free article] [PubMed]
8.
Carr MJ, Ashcroft DM, Kontopantelis E, While D, Awenat Y, Cooper J, ChewGraham C, Kapur N, Webb RT. Clinical management following self-harm in a
UK-wide primary care cohort. J Affect Disord. 2016 Jun;197:182-8. [PMC free
article] [PubMed]
9.
Bergen H, Murphy E, Cooper J, Kapur N, Stalker C, Waters K, Hawton K. A
comparative study of non-fatal self-poisoning with antidepressants relative to
prescribing in three centres in England. J Affect Disord. 2010 Jun;123(1-3):95101. [PubMed]
10.
Bek K, Ozkaya O, Mutlu B, Da?demir A, Sungur M, Açikgöz Y, I?lek I, Baysal K.
Charcoal haemoperfusion in amitriptyline poisoning: experience in 20
children. Nephrology (Carlton). 2008 Jun;13(3):193-7. [PubMed]
11.
Gillman PK. Tricyclic antidepressant pharmacology and therapeutic drug
interactions updated. Br. J. Pharmacol. 2007 Jul;151(6):737-48. [PMC free article]
[PubMed]
12.
Cao D, Heard K, Foran M, Koyfman A. Intravenous lipid emulsion in the
emergency department: a systematic review of recent literature. J Emerg
Med. 2015 Mar;48(3):387-97. [PubMed]
13.
Güloglu C, Orak M, Ustündag M, Altunci YA. Analysis of amitriptyline overdose
in emergency medicine. Emerg Med J. 2011 Apr;28(4):296-9. [PubMed]
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Introduction
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Etiology
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