Podcasts about carbamazepine

La American Heart Association publicó un documento con recomendaciones específicas para el manejo del paciente en paro cardiaco por intoxicación. Este artículo repasará las principales recomendaciones. Este es el quinto episodio de una serie de episodios relacionados al manejo del paro cardiaco por envenenamientos. En este episodio discutimos el manejo de la intoxicación por digoxina. Índice terapéutico de la dioxina El índice terapéutico mide la seguridad de un medicamento. Un medicamento con un índice terapéutico reducido significa que es necesario mantener una concentración muy precisa en la sangre. De lo contrario, no es suficiente para ser efectiva, o se vuelve tóxica. Según la farmacocinética y farmacodinamia, para que un medicamento sea efectivo, el cuerpo tiene primero que absorberlo a la circulación. Una vez en la circulación, el cuerpo va a metabolizarlo hasta eliminarlo completamente. Luego de un tiempo determinado, la dosis que queda en el cuerpo ya deja de ser efectiva. Si es necesario mantener una concentración constante en la sangre, entonces es necesario seguir administrando otras dosis a intervalos definidos para asegurar que el cuerpo siga teniendo un suplido constante de la droga para reemplazar lo que se va eliminando. La digoxina tiene un índice terapéutico muy reducido. Quiere decir que es necesario administrar una cantidad precisa del medicamento y medir cuánto es el nivel en la sangre para evitar correr el riesgo de haber administrado demasiado. La digoxina se excreta a través de los riñones. Si un paciente desarrolla fallo renal agudo, pudiera tener un aumento clínicamente significativo de los niveles de digoxina. Medicamentos que alteran la fracción libre de la digoxina Disminución del efecto de la digoxina Carbamazepine, fosfenitoína y fenobarbital Rifampin Aumento del efecto de la digoxina Amiodarona, carvedilol, ranozaline, ticagrelol Verapamil, tacrolimus, cyclosporine Azitromicina, eritromicina y claritromicina Fungicidas azoles Signos y síntomas de la intoxicación por digoxina La intoxicación con digoxina puede producir una amplia gama de signos y síntomas gastrointestinales, neurológicos y cardiacos: Signos cardiacos Cambios en el segmento ST (La descripción clásica del EKG del paciente con intoxicación con digoxina es una depresión del segmento ST con una curva cóncava.) Cambios en el intervalo QTc Taquicardia atrial Taquicardia nodal Taquicardia ventricular (especialmente taquicardia ventricular bidireccional) Bradicardia y bloqueo AV (1er grado y 2ndo grado Tipo 1) Bigeminismo ventricular Fibrilación ventricular o asístole Signos gastrointestinales (intoxicación aguda) Anorexia Náusea Vómitos Diarrea Disturbios visuales (color amarillo o verde) Signos neurológicos (intoxicación crónica) Confusión Debilidad Síncope Convulsiones Hiperkalemia Nota: La hipokalemia (causada, por ejemplo, por el uso de diuréticos) puede causar toxicidad por digoxina. Si el paciente tiene hipokalemia, pudiera ser necesario suplementar con potasio si se va a usar anticuerpos antidigoxina porque estos van a bajar los niveles de potasio aún mas. Si el paciente toma digoxina, es posible que los signos y síntomas que ve sea por la digoxina. La hiperkalemia por digoxina La intoxicación por digoxina puede causar hiperkalemia, pero el mecanismo de la hiperkalemia inducida por digoxina es diferente al mecanismo de la hiperkalemia por otras causas. Por lo tanto, el manejo es diferente. Mecanismo de hiperkamia por digoxina Los glucósidos cardiacos inhiben la bomba de sodio y potasio en las células cardiacas. El movimiento de calcio hacia afuera de la célula depende del movimiento de sodio. Los glucósidos cardiacos inhiben la bomba de sodio y potasio, por lo tanto están inhibiendo el movimiento de sodio. La inhibición de la bomba de sodio y potasio produce que el potasio deje de entrar a la célula, acumulándose afuera (hiperkalemia). La bomba de sodio y potasio no produce un balance eléctrico perfecto, por lo que el cuerpo recurre al movimiento de sodio y calcio para completar la repolarización. Al dejar de funcionar la bomba de sodio y potasio, aumentan los niveles de calcio dentro de la célula. Normalmente, este aumento en la concentración de calcio produce un aumento en la fuerza de contractilidad del músculo cardiaco. En teoría, y una muy limitada evidencia, si se inyecta más calcio para tratar la hiperkalemia, se puede agravar los niveles ya elevados de calcio dentro de la célula y se puede producir una contracción continua (contracción tetánica) que lleva a paro cardiaco. Aunque esto es un riesgo teórico, no hay mucha data que apoye la teoría y tampoco hay mucha data de que el calcio apoye este tipo de hiperkalemia porque el mecanismo es diferente. Manejo de la hiperkalemia por digoxina El manejo de la hiperkalemia por inducida por digoxina consiste primariamente en la administración de anticuerpos antidigoxina. Consulte al Centro de Control de Envenenamientos En los Estados Unidos y Puerto Rico, 1-800-222-1222. Algunos pacientes con ingestas recientes (< 1 hr) pudieran beneficiarse del uso de carbón activado. Pero, en general, el manejo se centra alrededor del uso de los anticuerpos antidigoxina. Recomendaciones de la American Heart Association para paro cardiaco por intoxicación con digoxina Recomendamos la administración de anticuerpos antidigoxina para envenenamientos con digoxina o digitoxina. (Clase de recomendación: 1, Nivel de evidencia: B-NR) Es razonable administrar anticuerpos antidigoxina para envenenamiento por sapo bufo o adelfa amarilla. (Clase de recomendación: 2a, Nivel de evidencia: C-LD) Puede ser razonable administrar anticuerpos antidigoxina para tratar envenenamientos por glicósidos cardiacos que no sean digoxina, digitoxina, sapo bufo, o adelfa amarilla. (Clase de recomendación: 2b, Nivel de evidencia: C-LD) Puede ser razonable administrar atropina para bradidisritmias causadas por digoxina y otros envenenamientos por glicósidos cardiacos. (Clase de recomendación: 2b, Nivel de evidencia: C-LD) Puede ser razonable administrar un marcapasos eléctrico para tratar bradidisritmias debido a envenenamiento por digoxina y otros glicósidos cardiacos. (Clase de recomendación: 2b, Nivel de evidencia: C-LD) Puede ser razonable administrar lidocaína, fenitoína, o bretilio para tratar disritmias ventriculares causadas por digitálicos y otros glicósidos cardiacos hasta que se pueda obtener anticuerpos antidigitálicos. (Clase de recomendación: 2b, Nivel de evidencia: C-LD). No recomendamos el uso de hemodiálisis, hemofiltración, hemoperfusión, o plasmaféresis para tratar envenenamiento por digoxina. (Clase de recomendación: 3: no beneficio, Nivel de evidencia: B-NR) Referencias Lavonas EJ, Akpunonu PD, Arens AM, Babu KM, Cao D, Hoffman RS, Hoyte CO, Mazer-Amirshahi ME, Stolbach A, St-Onge M, Thompson TM, Wang GS, Hoover AV, Drennan IR; on behalf of the American Heart Association. 2023 American Heart Association focused update on the management of patients with cardiac arrest or life-threatening toxicity due to poisoning: an update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2023;148:e•••–e•••. doi: 10.1161/ CIR.0000000000001161 https://litfl.com/digoxin-toxicity-ecg-library/ https://litfl.com/digoxin-effect-ecg-library/ https://litfl.com/calcium-digoxin-toxicity-and-stone-heart-theory/#:~:text=This%20is%20based%20on%20the,by%20causing%20delayed%20after%2Ddepolarisations https://emcrit.org/ibcc/dig/#:~:text=mechanism%20of%20action%20of%20digoxin,in%20patients%20with%20digoxin%20overdose.

Contributor: Aaron Lessen MD Educational Pearls: What is Carbamazepine (Tegretol)? Carbamazepine is an anti-epileptic drug with mood-stabilizing properties that is used to treat bipolar disorder, epilepsy, and neuropathic pain. It functions primarily by blocking sodium channels which can prevent repetitive action potential firing. What are the symptoms of an overdose? Common initial signs include diminished conscious state, nystagmus, ataxia, hyperreflexia, CNS depression, dystonia, and tachycardia Severe toxicity can cause seizures, respiratory depression, decreased myocardial contractility, pulmonary edema, hypotension, and dysrhythmias. How is an overdose treated? An overdose is treated with large doses of activated charcoal and correction of electrolyte disturbances. Be ready to intubate given the potential for respiratory depression. Carbamazepine is moderately dialyzable and dialysis is recommended in severe overdoses. Additional educational pearl: Individuals in correctional facilities can occasionally self-administer medications which means that medication overdose should still be on the differential for any of these individuals. References Epilepsies in children, Young People and adults: NICE guideline [NG217]. National Institute for Health and Care Excellence. (2022, April 27). https://www.nice.org.uk/guidance/ng217  Ghannoum M, Yates C, Galvao TF, Sowinski KM, Vo TH, Coogan A, Gosselin S, Lavergne V, Nolin TD, Hoffman RS; EXTRIP workgroup. Extracorporeal treatment for carbamazepine poisoning: systematic review and recommendations from the EXTRIP workgroup. Clin Toxicol (Phila). 2014 Dec;52(10):993-1004. doi: 10.3109/15563650.2014.973572. Epub 2014 Oct 30. PMID: 25355482; PMCID: PMC4782683. Seymour JF. Carbamazepine overdose. Features of 33 cases. Drug Saf. 1993 Jan;8(1):81-8. doi: 10.2165/00002018-199308010-00010. PMID: 8471190. Spiller HA. Management of carbamazepine overdose. Pediatr Emerg Care. 2001 Dec;17(6):452-6. doi: 10.1097/00006565-200112000-00015. PMID: 11753195. Tran NT, Pralong D, Secrétan AD, Renaud A, Mary G, Nicholas A, Mouton E, Rubio C, Dubost C, Meach F, Bréchet-Bachmann AC, Wolff H. Access to treatment in prison: an inventory of medication preparation and distribution approaches. F1000Res. 2020 May 13;9:357. doi: 10.12688/f1000research.23640.3. PMID: 33123347; PMCID: PMC7570324. Summarized by Jeffrey Olson, MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII  

This is the 29th podcast episode for the Psychiatric Medication Podcast Series. This episode concludes the second season of Continuing Medical Education Topics from East Carolina University. Series Description: Current literature indicates that podcasts can be an effective educational format to reach health professionals across the continuum of medical education, addressing a myriad of topics pertinent to providers. This final episode of the season serves as an overview of Carbamazepine/Tegretol & Oxcarbazepine/Trileptal. This podcast season is the second released by East Carolina University's Office of Continuing Medical Education and may be beneficial for physicians, residents, fellows, nurse practitioners, physician assistants, and nurses. This podcast season is comprised of 29 episodes, each focusing on different psychiatric medications for the non-psychiatric provider. Those tuning into the podcast's second season will receive a primer on the "bread and butter" behavioral health medications for primary care: antidepressants, antipsychotics, and mood stabilizers. Episodes will be released weekly on Wednesdays.Irene Pastis, MD & Daniel Majarwitz, MD

Below is the patient case information: 63-year-old white male. Problem List Bipolar II disorder Insomnia Epilepsy (tonic-clonic seizures) Dyslipidemia/hypertriglyceridemia Hypertension Recent weight gain History of hyponatremia  Diabetes type 2(controlled) Medications Clonazepam 2 mg QHS Risperdal 2 mg twice daily Carbamazepine 200 mg twice daily Divalproex DR 500 mg three times daily Levetiracetam 1000 mg twice daily Losartan 100 mg daily HCTZ 25 mg daily Atorvastatin 40 mg daily Fenofibrate 48 mg daily Metformin ER 500 mg twice daily Vitals: Blood pressure is currently 144/86 mmHg Lipids: LDL-C: 98 Triglycerides: 245 (down from 423 4 months ago) CMP: Na+: 133 K+: 4.1 eGFR: 95 All others WNL as well CBC: Hgb: 10:1 g/dL MCV: 73 Ferritin: 17 A1c: 6.9% Current Appointment The patient has seen multiple neuro and psych providers over the last year.  The R­­isperdal and divalproex were for the bipolar II disorder. The patient is experiencing depression symptoms. His family notes that he has also been uncharacteristically aggressive lately and becomes agitated over minor issues. His family has recently noticed that while talking with him, his face is grimacing, his tongue will randomly protrude from his lips, as well as other facial movements. The clonazepam for insomnia. It helped with insomnia symptoms for a few weeks, but the symptoms are back to pre-treatment baseline. He was taking clonazepam 1 mg 2 hours prior to bed and zopidem 5 mg 30 minutes prior to bedtime. He didn't feel like the zolpidem was working. The clonazepam was increased to 2 mg and the zolpidem was DC'd. He is also complaining of daytime fatigue He was recently hospitalized due to hyponatremia. The carbamazepine and levetiracetam were for seizure control. However, the patient has experienced multiple seizures per month for at least the last 3 months. Needs better blood pressure and triglyceride control Thanks for listening! We want to give a big thanks to our main sponsor Pyrls. Try out their drug information app today. Visit the website below for a free trial: www.pyrls.com/corconsultrx If you want to support the podcast, check out our Patreon account. Subscribers will have access to all previous and new pharmacotherapy lectures as well as downloadable PowerPoint slides for each lecture. You can find our account at the website below:  www.patreon.com/corconsultrx If you have any questions for Cole or me, reach out to us on any of the following: Text - 415-943-6116 Mike - mcorvino@corconsultrx.com Cole - cswanson@corconsultrx.com Instagram and other social media platforms - @corconsultrx This podcast reviews current evidence-based medicine and pharmacy treatment options. This podcast is intended to be used for educational purposes only and is intended for healthcare professionals and students. This podcast is not for patients and not intended as advice or treatment.

Trade: Tegretol Class:  Anticonvulsant MOA: Binds preferably to voltage gated Sodium channels in their inactive conformation, which prevents repetitive and sustained firing of an action potential.Indications: Partial and generalized tonic – clonic seizures Contraindications: AV Block, bundle branch block, agranulocytosis, bone marrow supression, monoamine oxidase inhibitor therapySide effects: Dizziness, drowsiness, ataxia, N/V, blurred vision, confusion, headache, transient diplopia, visual hallucinations, life threatening rashes.Dosing:Adult:200mg POPediatric:6-12 years old: 100mg PO        Less then 6: 10mg/kg PO

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.28.509973v1?rss=1 Authors: Dogra, D., Meza-Santoscoy, P. L., Rehak, R., de la Hoz, C. L. R., Gavrilovici, C., Ibhazehiebo, K., Rho, J. M., Kurrasch, D. M. Abstract: Objective: KCNA1 mutations are associated with a rare neurological movement disorder known as episodic ataxia type 1 (EA1), with epilepsy as a common comorbidity. Current medications only provide partial relief to ataxia and/or seizures, making new drugs needed. Here, we investigate the utility of zebrafish kcna1a-/- as a model of EA1 with epilepsy by characterizing its phenotype and comparing the efficacy of the first-line therapy carbamazepine in kcna1a-/- zebrafish to Kcna1-/- rodents. Methods: We used CRISPR/Cas9 mutagenesis to introduce a mutation in the sixth segment of the zebrafish Kcna1 protein. Behavioral and electrophysiological assays were performed on kcna1a-/- larvae to assess ataxia- and epilepsy-related phenotypes. We also carried out real-time qPCRs to measure the transcript levels of brain hyperexcitability markers and bioenergetic profiling of kcna1a-/- larvae to evaluate their metabolic health. Carbamazepine efficacy was tested using behavioral assessments in kcna1a-/- zebrafish and seizure frequency in Kcna1-/- mice. Results: kcna1a-/- zebrafish showed uncoordinated movements and locomotor deficits. The mutants also exhibited impaired startle responses when exposed to light-dark flashes and acoustic stimulation. Extracellular field recordings and upregulated fosab transcript levels showed hyperexcitability of the kcna1a-/- brain. Further, vglut2a and gad1b transcript levels were altered, indicative of neuronal excitatory/inhibitory imbalance in the kcna1a-/- brain. Metabolic health was also compromised in kcna1a-/- as seen by a significant reduction in measures of cellular respiration. Notably, carbamazepine reduced the impaired startle response in kcna1a-/- zebrafish but had no effect on the seizure frequency in Kcna1-/- mice, suggesting that this EA1 zebrafish model might better translate to human efficacy compared to rodents. Significance: We conclude that zebrafish kcna1a-/- larvae show ataxia and epilepsy-related phenotypes and that they are responsive to carbamazepine treatment, consistent with EA1 patients. This study supports the notion that these zebrafish disease models can be useful for drug screening as well as studying the underlying disease biology. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

Thank you Chase Zaremba, OMS III and Brandon Brown, OMS III for developing this podcast. This podcast identifies medications (Duloxetine, Carbamazepine, Amitriptyline, Pregabalin, Milnacipran and Gabapentin) and a therapy (CBT) that often are associated with psychiatry and the indications for use in treatment of pain. There is a surprising amount of moderate yield information spread throughout. We enjoyed our discussion and hope you find it as interesting as we did! Thank you Jordan Turner for creating the perfect bumper music!

This is Episode 4 of CLOT Conversations from Thrombosis Canada. In this episode Dr Jameel Abdulrehman and David Airdrie are joined by Dr Vinai Bhagirath and Dr Sam Schulman, two of the authors of a recently published paper entitled Carbamazepine, phenytoin, and oral anticoagulants: Drug-drug interaction and clinical events in a retrospective cohort. The paper was published in Research and Practice in Thrombosis and Haemostasis (Res Pract Thromb Haemost. 2022;6:e12650. https://doi.org/10.1002/rth2.12650)The authors discuss the results of the retrospective cohort of patients taking carbamazepine or phenytoin with warfarin or DOACs. In particular, they explore whether there is a relationship between anticoagulant levels and thromboembolic events. Dr Schulman and Dr Bhagirath discuss their perspectives on the issues relevant to each type of anticoagulant when used in patients on anti-seizure medications and what their study added to the understanding of drug-drug interactions.Dr Sam Schulman graduated from Karolinska Institutet, Stockholm, Sweden in 1977 and has worked with coagulation disorders since 1984. Research activities have been clinical studies in venous thromboembolism, in hemophilia and bleeding. He has been a member of the Executive Committee of the World Federation of Hemophilia, was President for the XXV ISTH Congress, Toronto, 2015, is member of the ISTH Council and Treasurer. In 2017 he received Harold R. Roberts medal of the ISTH SSC. He is Director of the Thrombosis Service at Hamilton General Hospital and professor in Medicine at McMaster University, Hamilton, Canada, and at Department of Obstetrics and Gynaecology, The First I.M. Sechenov Moscow State Medical University, Moscow, Russia.Dr Vinai Bhagirath, is a Thrombosis physician at Hamilton Health Sciences and Assistant Professor of Medicine at McMaster University. His research interests include bleeding risk with anticoagulants and clinical measurement of DOAC drug levels. His quality improvement interests include optimization of medical therapy in peripheral artery disease and standardization of periprocedural management of antithrombotic medications. His educational activities include Directorship of Thrombosis Fellowship programs at McMaster, and he is co-chair of the upcoming 2022 THSNA Summit and chair of Thrombosis Canada's Continuing Professional Development committee.Thrombosis Canada Tools related to the content:DOAC Drug Interaction tool: https://thrombosiscanada.ca/wp-uploads/uploads/2021/09/DDI-Tool-Final-English.pdfThrombosis Canada Clinical Guides: https://thrombosiscanada.ca/clinicalguides/Follow us on Twitter: Thrombosis Canada: @ThrombosisCan Sam Schulman: @SamSchulman6Reference: Candeloro, M., Eikelboom, J. W., Chan, N., Bhagirath, V., Douketis, J. D., & Schulman, S. (2022). Carbamazepine, phenytoin, and oral anticoagulants: Drug‐drug interaction and clinical events in a retrospective cohort. Research and Practice in Thrombosis and Haemostasis, 6(2), e12650.Support the showhttps://thrombosiscanada.caTake a look at our healthcare professional and patient resources, videos and publications on thrombosis from the expert members of Thrombosis Canada

How bad are valproic acid effects in the newborn? Is there a role for carbamazepine and oxcarbazepine? How to prescribe lamotrigine during pregnancy? Faculty: Wendy Marsh, M.D. Hosts: Jessica Diaz, M.D; Flavio Guzman, M.D. Prescribing Antiepileptic Drugs for Bipolar Disorder During Pregnancy: Valproate, Carbamazepine, and Lamotrigine Earn 1 CME: Clinical Management of Bipolar Disorder in Pregnancy Learn more about Premium Membership here

This episode covers carbamazepine!

WARFARIN. Introduction , mechanism of action , Side Effects :- BLEEDING , RETROPERITONEAL HEMORRHAGE ,PURPLE TOE SYNDROME , OSETEOPOROSIS RELATED BONE FRACTURE .. CLINICAL CONSIDERATIONS:- FIRST TRIMESTER - FETAL WARFARIN STNDROME - Nasal hypoplasia , narrowed Nasal bridge , other limbic and cardio abornmalities , SECOND & THIRD TRIMESTER : CNS abornmalities , ocular defects , seizures , low birth weight. ... ANTIDOTE : PHYTOMENADIONE (VIT k) CYP P450 INHIBITORS: macrolides, Flucanazole , Protease inhibitors. CYP 450 INDUCERS : Phenytoin , Carbamazepine, Rifampin .. insta id : Srinath Kalepu .. LINKEDIN : Kalepu Srinath

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.11.245951v1?rss=1 Authors: Crisp, D., Parent, R., Nakatani, M., Murphy, G. G., Stacey, W. C. Abstract: Optimizing antiepileptic drug therapy is very challenging due to the absence of a reliable method to assess how brain activity changes between seizures. This work uses the Taxonomy of Seizure Dynamics (Saggio et al., 2020) to investigate how anticonvulsants influence seizure onset dynamotypes. The no Mg2+/high K+ mouse brain-slice seizure model (N = 92) was used to generate consistent epileptiform onsets. We compared the onset bifurcations of controls with slices treated with either GABA or carbamazepine. Each anticonvulsant uniquely changed the types of bifurcations in the slices. This experiment provides proof-of-concept evidence that brain states exist on a "map" of seizure dynamics, and that antiepileptic drugs with different mechanisms can change the positioning of the brain states on the map. Copy rights belong to original authors. Visit the link for more info

Reference https://en.wikipedia.org/wiki/Carbamazepine https://en.wikipedia.org/wiki/Stevens%E2%80%93Johnson_syndrome https://en.wikipedia.org/wiki/Prenatal_perception#Prenatal_pain

Reference https://en.wikipedia.org/wiki/Carbamazepine https://en.wikipedia.org/wiki/Stevens%E2%80%93Johnson_syndrome https://en.wikipedia.org/wiki/Prenatal_perception#Prenatal_pain

  Reference https://en.wikipedia.org/wiki/Carbamazepine https://en.wikipedia.org/wiki/Stevens%E2%80%93Johnson_syndrome https://en.wikipedia.org/wiki/Prenatal_perception#Prenatal_pain

Dolutegravir is an integrase inhibitor that is used in the management of HIV infection/ Carbamazepine along with other enzyme inducers can substantially lower the concentrations of dolutegravir. Dolutegravir can potentially increase blood sugars, this should be closely monitored in our patients with diabetes. CNS adverse effects like insomnia and dizziness can happen with dolutegravir.

On this episode, I discuss carbamazepine pharmacology. This drug is most commonly used for seizures, bipolar disorder, or trigeminal neuralgia. Carbamazepine is an autoinducer and can reduce the concentrations of numerous drugs. Some examples include apixaban, warfarin, rivaroxaban, diltiazem, verapamil, and many more! Carbamazepine has the potential to cause Steven Johnson's Syndrome. This has a much greater chance of happening in patients with certain genetics. Carbamazepine can contribute to SIADH and cause significant hyponatremia. Carbamazepine has boxed warning for numerous potential events like aplastic anemia, agranulocytosis, and the above-mentioned SJS.

Up to 70 million people worldwide have epilepsy and there are many Cochrane Reviews of ways to treat it. These include reviews that work with the original researchers to gather data on everyone who was in their studies, to perform individual participant data meta-analyses. In June 2018, Sarah Nevitt and colleagues from the University of Liverpool in the UK updated one of these reviews, comparing two commonly used drugs, lamotrigine and carbamazepine.

Up to 70 million people worldwide have epilepsy and there are many Cochrane Reviews of ways to treat it. These include reviews that work with the original researchers to gather data on everyone who was in their studies, to perform individual participant data meta-analyses. In June 2018, Sarah Nevitt and colleagues from the University of Liverpool in the UK updated one of these reviews, comparing two commonly used drugs, lamotrigine and carbamazepine.

Up to 70 million people worldwide have epilepsy and there are many Cochrane Reviews of ways to treat it. These include reviews that work with the original researchers to gather data on everyone who was in their studies, to perform individual participant data meta-analyses. In June 2018, Sarah Nevitt and colleagues from the University of Liverpool in the UK updated one of these reviews, comparing two commonly used drugs, lamotrigine and carbamazepine.

Conventional approaches to drug testing rely on a primary screening step followed by a secondary confirmation.  Best practice dictates that the secondary confirmation step utilize a separate methodology than the initial screening step and have improved sensitivity and specificity.  This approach is widely utilized in clinical, pre-employment, and forensic settings.  Despite the standard adoption of this approach, issues can occur that impact the accuracy of results. “False Positive Carbamazepine Results by Gas-Chromatography Mass Spectrometry and VITROS 5600 Following a Massive Oxcarbazepine Ingestion” was published in the July 2018 issue of The Journal of Applied Laboratory Medicine.  The case study highlights unique circumstances that affected both screening and confirmatory methods for urine drug testing.

The post Carbamazepine (Tegretol) Nursing Pharmacology Considerations appeared first on NURSING.com.

Myocardial infarction (MI) in children is uncommon, but underdiagnosed.  This is due to two main factors: the etiologies are varied; and the presenting symptoms are “atypical”. We need a mental metal detector!  Case examples Congenital Two main presentations of MI due to congenital lesions: novel and known.  The novel presentation is at risk for underdiagnosis, due to its uncommonness and vague, atypical symptoms.  There are usually some red flags with a careful H&P.  The known presentation is a child with a history of congenital heart disease, addressed by corrective or palliative surgery.  This child is at risk for expected complications, as well as overdiagnosis and iatrogenia.  Risk stratify, collaborate with specialists. The fussy, sweaty feeder: ALCAPA Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA) is an example of what can go wrong during fetal development: any abnormality in the number, origin, course, or morphology of the coronary arteries can present as a neonate with sweating during feeds (steal syndrome), an infant in CHF, or an older child with failure to thrive or poor exercise tolerance. The stable child with chest pain: myocardial bridge Normal coronary arteries run along the epicardial surface of the heart, with projections into the myocardium.  If part of the artery’s course runs within the myocardium (i.e. the artery weaves into and/or out of the myocardium), then there is a myocardial bridge of the coronary artery.  With every systolic contraction, the artery is occluded.  Although a myocardial bridge may not cause symptoms (especially at distal portions), the area it supplies is at risk. With any minor trauma or exertion, demand may outpace supply, resulting in ischemia.  Diagnosis is made on coronary angiography. The unwell child post-cardiac surgery: Fontan problems The child with single ventricle physiology may have a Norwood procedure at birth (creation of a neoaorta, atrial septectomy, and Blalock-Taussig shunt), a Bidirectional Glenn procedure at 3-6 months (shunt removed, superior vena cava connected to pulmonary arteries), and a Fontan procedure at about 2-3 years of age (inferior vena cava blood flow is shunted into the pulmonary arteries). These children depend on their preload to run blood passively into the pulmonary circuit; afterload reduction is also important to compensate for a poor left ejection fraction, as well as to avoid the development of pulmonary hypertension.  They are typically on an anticoagulant (often aspirin), a diuretic (e.g. furosemide), and an afterload reduction agent (e.g. enalapril).  Any disturbance in volume status (hyper- or hypovolemia), anticoagulation, or afterload may cause myocardial strain or infarction.  Take the child s/p Fontan seriously and involve his specialists early with any concerns. Autoimmune The body’s inflammatory-mediated reaction to a real or perceived insult can cause short- and long-term cardiac sequelae.  Find out how well the underlying disease is controlled, and what complications the child has had in the past. The red, hot, crispy, flaky child: acute Kawasaki disease Kawasaki disease (KD) is an acute systemic vasculitis, diagnosed by the presence of fever for five or more days accompanied by four or more criteria:  bilateral conjunctival injection, mucositis, cervical lymphadenopathy, polymorphous rash, and palmar or sole desquamation.  The criteria may occur (and disappear) at any time during the illness. Infants are under double jeopardy with Kawasaki Disease.  They are more likely to have incomplete KD (i.e. not fulfill strict criteria) and if they have KD, they are more likely to suffer the dangerous consequences of aneurysm formation (chiefly coronary arteries, but also brain, kidney).  Have a low threshold for investigation. Treatment includes 2 g/kg/day IVIG and high-dose aspirin (30-50 mg/kg/day) acutely, then low-dose aspirin (5 mg/kg/day) for weeks to months.  Regular and long-term follow-up with Cardiology is required. The aftermath: sequelae of Kawasaki disease The family and child with a history of KD may have psychological trauma and continuous anxiety about the child’s risk of MI.  Approximately 4.7% of children who were promptly diagnosed and correctly treated will go on to have cardiac sequelae. Children who have no detected cardiac sequelae by 8 weeks, typically continue to be asymptomatic up to 20 years later.  Smaller aneurysms tend to regress over time, especially those < 6 mm. Thrombi may calcify, or the lumen may become stenotic due to myofibroblast proliferation.  Children with any coronary artery dilatation from KD should be followed indefinitely. Giant aneurysms (≥8 mm) connote the highest risk for MI.  Parents often are concerned about recurrence, and any subsequent fever can be distressing.  There is a low rate of recurrence for KD: approximately 2%.  Infants who have coronary aneurysms are at the highest risk for recurrence. The older child with vague chest complaints and hypercoagulability: Systemic Lupus Erythematosus and Anti-Phospholipid Syndrome Up to 15% of cases of SLE begin in childhood.  Adult criteria are used, with the caveat that the diagnosis of SLE in children can be challenging; many children only manifest a few of the criteria initially before going on to develop further systemic involvement. The Systemic Lupus International Collaborating Clinics (SLICC) revised the criteria in 2012.  The patient should have ≥4/17 clinical and/or immunologic criteria.  The clinical criteria are: acute cutaneous (malar); chronic cutaneous (discoid); oral; alopecia; synovitis; serositis; renal; neurologic; hemolytic anemia; leukopenia; or thrombocytopenia.  The immunologic criteria are: ANA; anti-dsDNA; anti-Sm; antiphospholipid; low complement; and/or Direct Coombs (in absence of hemolytic anemia).  At least one criterion should be clinical, and at least one should be immunologic.  Children with antiphospholipid syndrome (APS) may occur with or without SLE.  Patients are at risk for venous and arterial thrombi formation.  APS may also cause structural damage, such as valvular thickening and valvular nodes (Libman-Sacks endocarditis).  Mitral and aortic valves are at the highest risk. Although most children with chest pain will not have MI, those with comorbidities should be investigated carefully. Trauma Direct, blunt trauma to the chest can cause myocardial stunning, dysrhythmias, or an asymptomatic rise in Troponin I.  However, some children are at risk for disproportionate harm due to a previously unknown risk factor.  Clinically significant cardiac injury occurs in up to 20% of patients with non-penetrating thoracic trauma. The motor vehicle collision: blunt myocardial injury Direct trauma (steering wheel, airbag, seatbelt), especially in fast acceleration-deceleration injury, may cause compression of the heart between the sternum and the thoracic spine. Electrocardiography (ECG) should be performed on any patient with significant blunt chest injury.  A negative ECG is highly consistent with no significant blunt myocardial injury. Any patient with a new abnormality on ECG (dysrhythmia, heart block, or signs of ischemia) should be admitted for continuous ECG monitoring. Elevation in troponin is common, but not predicted.  A solitary elevated troponin without ECG abnormality is of unclear significance.  Author’s advice: obtain troponin testing if there is an abnormal ECG, more than fleeting suspicion of BCI, and/or the child will be admitted for monitoring. Hemodynamically labile children should be resuscitated and a stat transesophageal echocardiogram obtained. The high-velocity object: coronary artery dissection or thrombus Direct trauma (e.g. MVC, baseball, high-velocity soccer ball) may cause damage to the left anterior descending artery or left circumflex artery, at the highest risk due to their proximity to the chest wall.  Thrombosis and/or dissection may result, often presenting in a focal pattern of ischemia on the ECG. Echocardiography may reveal valvular damage related to the injury, as well as effusion and ejection fraction.  Since there is often a need to investigate the coronary anatomy, percutaneous coronary intervention (PCI) is recommended. The minor trauma with disproportionate complaint: myocardial bridge As mentioned in the congenital section (above), a known variation of a coronary artery’s course involves weaving in and out of the myocardium, creating a baseline risk for ischemia.  Even minor trauma in a child with a myocardial bridge may cause acute thrombus, or slow stenosis from resulting edema.  Unfortunately, the presence of myocardial bridging is often unknown at the time of injury.  Approximately 25% of the population may have myocardial bridging, based on autopsy studies. Take the child seriously who has disproportionate symptoms to what should be a minor injury. Hematologic Coagulopathic and thrombophilic states may predispose children to focal cardiac ischemia.  The best documented cormorbidity is sickle cell disease, although other pro-thrombotic conditions also put the child at risk. The child with sickle cell disease and chest pain: when it’s not acute chest syndrome Sickle cell disease (SCD) can affect any organ system, although the heart is traditionally considered a lower-risk target organ for direct sickling and ischemia.  The major cardiac morbidity in sickle cell is from strain, high-output failure and multiple, serial increases in myocardial demand, causing left ventricular hypertrophy and congestive heart failure. However, there is mounting evidence that acute myocardial ischemia in sickle cell disease may be underappreciated and/or attributed to other causes of chest pain. Other cardiac sequelae from SCD include pulmonary hypertension, left ventricular dysfunction, right ventricular dysfunction, and chronic iron overload. Evidence of myocardial ischemia/infarction in children with SCD has been demonstrated on single-photon emission computed tomography (SPECT) scan. The puffy faced child with chest pain: nephrotic syndrome hypercoagulability Children who suffer from nephrotic syndrome lose proteins that contribute to the coagulation cascade.  In addition, lipoprotein profiles are altered: there is a rise in the very low-density lipoproteins (LDL), contributing to accelerated atherosclerosis.  Typically nephrotic patients have normal levels of high-density lipoproteins (HDL), unless there is profuse proteinuria. Children with difficult-to-control nephrotic syndrome (typically steroid-resistant) may form accelerated plaques that rupture, causing focal MI, as early as school age. The previously well child now decompensated: undiagnosed thrombophilia Asymptomatic patent foramen ovale (PFO) is the cause of some cases of cryptogenic vascular disease, such as stroke and MI.  However, the presence of PFO alone does not connote higher risk.  When paired with an inherited or acquired thrombogenic condition, the venous thrombus may travel from the right-sided circulation to the left, causing distal ischemia.  Many of these cases are unknown until a complication arises. The chronically worried, now with a reason: hypercholesterolemia A family history of adult-onset hypercholesterolemia is not necessarily a risk factor for early complications in children, provided the child does not have the same acquired risk factors as adults (e.g. obesity, sedentary lifestyle, smoking, etc).  Parents may seek help in the ED for children with chest pain and no risk factors, but adult parents who have poor cholesterol profiles. The exception is the child with familial hypercholesterolemia, who is at risk for accelerated atherosclerosis and MI. Infectious Myocarditis has varied etiologies, including infectious, medications (chemotherapy agents), immunologic (rheumatologic, transplant rejection), toxins (arsenic, carbon monoxide, heavy metals such as iron or copper), or physical stress (electrical injury, heat illness, radiation). In children, the most common cause of myocarditis is infectious (viruses, protozoa, bacteria, fungal, parasites).  Of these, viral causes are the most common (adenovirus, enterovirus, echovirus, rubella, HHV6). The verbal child may complain of typical chest complaints, or may come in with flu-like illness and tachycardia or ill appearance out of proportion to presumed viral illness. The most common presenting features in children with myocarditis are: shortness of breath, vomiting, poor feeding, hepatomegaly, respiratory distress, and fever. The infant in shock after a ‘cold’: myocarditis Beware of the poor feeding, tachycardic, ill appearing infant who “has a cold” because everyone else around him has a ‘cold’.  That may very well be true, but any virus can be invasive with myocardial involvement.  Infants are only able to increase their cardiac output through increasing their heart rate; they cannot respond to increased demands through ionotropy.  Look for signs of acute heart failure, such as hepatomegaly, respiratory distress, and sacral edema. The child with tachycardia out of proportion to complaint: myocarditis The previously healthy child with “a bad flu” may simply be very symptomatic from influenza-like illness, or he may be developing myocarditis.  Look for chest pain and tachycardia out of proportion to presumed illness, and constant chest pain, not just associated with cough. The “pneumonia” with suspicious chest x-ray: myocarditis Acute heart failure may mimic viral pneumonia.  Look for disproportionate signs and symptoms. Toxins Younger children may get into others’ medications, be given dangerous home remedies, take drugs recreationally, have environmental exposures (heavy metals), suffer from a consequence of a comorbidity (iron or copper overload) or have adverse events from generally safe medications. The hyperactive boy with a hyperactive precordium: methylphenidate Attention deficit hyperactivity disorder (ADHD) is growing in rate of diagnosis and use of medications.  As the only medical diagnosis based on self-reported criteria, many children are given stimulants regardless of actual neurologic disorder; with a higher proportion of children exposed to stimulants, adverse effects are seen more commonly. Methylphenidate is related to amphetamine, and they both are dopaminergic drugs.  Their mechanisms of action are different, however.  Methylphenidate increases neuronal firing rate.  Methamphetamine reduces neuronal firing rate; cardiovascular sequelae such as MI and CHF are more common in chronic methamphetamine use. Although methylphenidate is typically well tolerated, risks include dysrhythmias such as ventricular tachycardia. The child with seizure disorder and chest pain: anti-epileptics Some anti-epileptic agents, such as carbamazepine, promote a poor lipid profile, leading to atherosclerosis and early MI.  Case reports include school-aged children on carbamazepine who have foamy cells in the coronary arteries, aorta, and vasa vasorum on autopsy.  It is unclear whether this is a strong association. The spice trader: synthetic cannabinoids Synthetic cannabinoids are notoriously difficult to regulate and study, as the manufacturers label them as “not for human consumption”.  Once reports surface of abuse of a certain compound, the formula is altered slightly and repackaged, often in a colorful or mysterious way that is attractive to teenagers. The misperceptions are: are a) synthetics are related to marijuana and therefore safe and b) marijuana is inherently “safe”. Both tend to steer unwitting teens to take these unknown entities.  Some suffer MI as a result. Exposure to tetrahydrocannabinol (THC) in high-potency marijuana has been linked to myocardial ischemia, ventricular tachycardia, and ventricular fibrillation.  Marijuana can increase the heart rate from 20-100%, depending on the amount ingested. K2 (“kush 2.0”) or Spice (Zohai, Genie, K3, Bliss, Nice, Black Mamba, fake weed, etc) is a mixture of plant leaves doused in synthetic chemicals, including cannabinoids and fertilizer (JWH-108), none of which are tested or safe for human consumption.  Synthetic cannabinoids have a higher affinity to cannabinoid receptors, conferring higher potency, and therefore worse adverse effects.  They are thought to be 100 to 800 times more potent as marijuana. Bath salts (Purple Wave, Zoom, Cloud Nine, etc) can be ingested, snorted, or injected.  They typically include some form of cathinone, such as mephedrone, similar to the substance found in the naturally occurring khat plant. Hallucinations, palpitations, tachycardia, MI, and dysrhythmias have been reported from their use as a recreational drug. Chest pain with marijuana, synthetic cannabinoid, or bath salt ingestion should be investigated and/or monitored. Riding that train: high on cocaine Cocaine is a well-known cause of acute MI in young people.  In addition to the direct stimulant causes acutely, such as hypertension, tachycardia, and impaired judgement (coingestions, risky behavior), chronic cocaine use has long-term sequelae.  Cocaine causes accelerated atherosclerosis.  That, in conjunction with arterial vasospasm and platelet activation, is a recipe for acute MI in the young. Cranky: methamphetamine Methamphetamine is a highly addictive stimulant that is relatively inexpensive and widely available.  Repeated use causes multiple psychiatric, personality, and neurologic changes.  Risky behavior, violence, and motor vehicle accidents are all linked to this drug.  Like cocaine, methamphetamine may cause fatal dysrhythmias, acute MI from demand ischemia, and long-term sequelae such as congestive heart failure. Summary Acute MI is a challenging presentation in children: Easily missed: uncommon and atypical Varied etiology Respect vague symptoms with a non-reassuring H&P Try to detect it: CATH IT! References Congenital AboulHosn JA et al. Fontan Operation and the Single Ventricle. Congenit Heart Dis. 2007; 2:2-11. Aliku TO et al. A case of anomalous origin of the left coronary artery presenting with acute myocardial infarction and cardiovascular collapse. African Health Sci. 2014; 14(1): 23-227. Andrews RE et al. Acute myocardial infarction as a cause of death in palliated hypoplastic left heart syndrome. Heart. 2004; 90:e17. Canale LS et al. Surgical treatment of anomalous coronary artery arising from the pulmonary artery. Interactive Cardiovascaulr and Thoracic Surgery. 2009; 8:67-69. Güvenç O et al. Correctable Cause of Dilated Cardiomyopathy in an Infant with Heart Failure: ALCAPA Syndrome. J Curr Pediatr. 2017; 15:47-50. Hastings RS et al. Embolic Myocardial Infarction in a Patient with a Fontan Circulation. World Journal for Pediatric Congenital Heart Surgery. 2014; 5(4)L631-634. Hoffman JIE et al. Electrocardiogram of Anomalous Left Coronary Artery From the Pulmonary Artery in Infants. Pediatr Cardiol. 2013; 34(3):489-491. Kei et al. Rare Case of Myocardial Infarction in a 19-Year-Old Caused by a Paradoxical Coronary Artery Embolism. Perm J.2015; 19(2):e107-e109. Liu Y, Miller BW. ALCAPA Presents in an Adult with Exercise Inlerance but Preserved Cardiac Function. Case Reports Cardiol. 2012; AID 471759. Möhlenkamp S et al. Update on Myocardial Bridging.Circulation. 2002;106:2616-2622. Murgan SJ et al. Acute myocardial infraction n the neonatal period. Cardiol Young. 2002; 12:411-413. Sieweke JT et al. Myocardial infarction in grown up patients with congenital heart disease: an emergening high-risk combination. International Journal of Cardiology. 2016; 203:138-140. Schwerzmann M et al. Anomalous Origin of the Left Coronary Artery From the Main Pulmonary Artery in Adults. Circulation. 2004; 110:e511-e513. Tomkewicz-Pajak L et al. Arterial stiffness in adult patients after Fontan procedure. Cardiovasculr Ultrasound. 2014; 12:15. Varghese MJ et al. The caveats in the diagnosis of anomalous origin of left coronary artery from pulmonary artery (ALCAPA). Images Paediatr Cardiol. 2010; 12(3): 3–8. Autoimmune Ayala et al. Acute Myocardial Infarction in a Child with Systemic Lupus Erythematosus and Antiphospholipid Syndrome. Turk J Rheumatol. 2009; 24:156-8. Nakano H et al. Clinical characteristics of myocardial infarction following Kawasaki disease: Report of 11 cases. J Pediatr. 1986; 108(2):198-203. Pongratz G et al. Myocardial infarction in an adult resulting from coronary aneurysms previously documented in childhood after an acute episode of Kawasaki’s disease. European Heart J. 1994. 15:1002-1004. Newburger JW et al.  Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease. A Statement for Health Professionals From the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation. 2004;110:2747-2771. Son MB et al. Kawaski Disease. Pediatr Rev. 2013; 34(4). Yuan S. Cardiac surgical procedures for the coronary sequelae of Kawasaki disease. Libyan J Med. 2012; 7:19796. Trauma Abdolrahim SA et al. Acute Myocardial Infarction Following Blunt Chest Trauma and Coronary Artery Dissection. J Clin Diagnost Res. 2016; 10(6):14-15. Galiuto L et al. Post-traumatic myocardial infarction with hemorrhage and microvascular damage in a child with myocardial bridge: is coronary anatomy actor or bystander. Signa Vitae. 2013; 8(2):61-63. Janella BL et al. Acute Myocardial Infarction related to Blunt Thoracic Trauma. Arq Bras Cardiol. 2006; 87:e168-e171. Liu X et al. Acute myocardial infarction in a child with myocardial bridge World J Emerg Med. 2011; 2(1):70-72. Long WA et al. Childhood Traumatic Infarction Causing Left Ventricular Aneurysm: Diagnosis by Two-Dimensional Echocardiography. JACC. 1985; 5(6):1478-83. Smith S. Right Bundle Branch Block after Blunt Trauma: A Tragic Case. [Blog Post] July 22, 2012. Retrievable at: http://hqmeded-ecg.blogspot.com/2012/07/right-bundle-branch-block-after-blunt.html. Hematologic Carano N et al. Acute Myocardial Infarction in a Child: Possible Pathogenic Role of Patent Foramen Ovale Associated with Heritable Thrombophilia. Pediatr. 2004; 114(2):255-258.      Chacko P et al. Myocardial Infarction in Sickle Cell Disease. J Cardiovascl Transl Res. 2013; 6(5):752-761. De Montalembert M et al. Myocardial ischaemia in children with sickle cell disease. Arch Dis Child. 2004; 89:359-362. Gladwin MT et al. Cardiovascular Abnormalities in Sickle Cell Disease. JACC. 2012; 59(13):1123-1133. Osula S et al. Acute myocardial infarction in young adults: causes and management. Postgrad Med J. 2002; 78:27-30. Silva JMP et al. Premature acute myocardial infarction in a child with nephrotic syndrome. Pediatr Nephrol. 2002; 17:169-172. Suryawanshi SP. Myocardial infarction in children: Two interesting cases. Ann Pediatr Cardiol. 2011 Jan-Jun; 4(1): 81–83. Infectious Cunningham R et al. Viral myocarditis Presenting with Seizure and Electrocardiographic Findings of Acute Myocardial Infarction in a 14-Month-Old Child. Ann Emerg Med. 2000; 35(6):618-622. De Vettten L et al. Neonatal Myocardial Infarction or Myocarditis? Pediatr Cardiol. 2011; 32:492-497. Durani Y et al. Pediatric myocarditis: presenting clinical characteristics. Am J Emerg Med. 2009; 27:942-947. Erden I et al. Acute myocarditis mimicking acute myocardial infarction associated with pandemic 2009 (H1N1) influenza virus. Cardiol J. 2011; 552-555. Hover MH et al. Acute Myocarditis Simulating Myocardial Infarction in a Child. Pediatr. 1191; 87(2):250-252. Lachant D et al. Meningococcemia Presenting as a Myocardial Infarction. Case Reports in Critical Care. 2015; AID 953826. Laissy JP et al. Differentating Myocardial Infarction from Myocarditis. Radiology. 2005; 237(1):75-82. Miranda CH et al. Evaluation of Cardiac Involvement During Dengue Viral Infection. CID. 2013; 57:812-819. Rettig JS et al. Myocarditis in Children Requiring Critical Care Transport. In:  "Diagnosis and Treatment of Myocarditis", Milei J, Ambrosio G (Eds). DOI: 10.5772/56177. Toxins De Chadarévian JP et al. Epilepsy, Atherosclerosis, Myocardial Infarction, and Carbamazepine. J Child Neurol. 2003; 18(2):150-151. McIlroy G et al. Acute myocardial infarction, associated with the use of a synthetic adamantly-canabinoid: a case report. BMC Pharmacology and Toxicology. 2016; 17:2. Mir A et al. Myocardial Infarction Associated with Use of the Synthetic Cannabinoid K2. Pediatr. 2011; 128(6):1-6 Munk K et al. Cardiac Arrest following a Myocardial Infarction in a Child Treated with Methylphenidate. Case Reports Pediatr. 2015; AID 905097. Rezkalla SH et al. Cocaine-Induced Acte Mycardial Infarction. Clin Med Res. 2007; 5(3):172-176. Schelleman H et al. Methylphenidate and risk of serious cardiovascular events in adults. Am J Psychiatry. 2012 Feb;169(2):178-85. Sheridan J et al. Injury associated with methamphetamine use: a review of the literature. Harm Reduction Journal, 2006; 3(14):1-18. Stiefel G et al. Cardiovascular effects of methylphenidate, amphetamines and atomoxetine in the treatment of attention-deficit hyperactivity disorder. Drug Saf. 2010 Oct 1;33(10):821-42.   This post and podcast are dedicated to Edwin Leap, MD for his sanity and humanity in the practice of Emergency Medicine.  Thank you, Dr Leap for all that you do.

In neurology, paroxysmal syndromes are well-known, eg, as manifestations of multiple sclerosis. We report a patient with meningeal carcinomatosis, who presented with therapyrefractory nausea and vomiting. The clinical suspicion of a paroxysmal syndrome prompted a trial of carbamazepine, which resulted in complete cessation of the symptoms. In cancer patients with central nervous system (CNS) involvement and therapy-refractory symptoms with sudden onset, carbamazepine treatment should be considered.

In a randomized clinical trial with an observation period of 2.5 years, the differential efficacy of lithium versus carbamazepine was compared in 171 bipolar patients (DSM-IV). In order to investigate the efficacy of the two drugs in clearly defined subsamples, a series of subgroup analyses was carried out. First, patients with a bipolar I disorder (n = 114) were analyzed separately. In these patients, lithium was superior to carbamazepine. In contrast, carbamazepine was at least equally as efficacious as lithium in the subsample of patients with bipolar II disorder or bipolar disorder not otherwise specified (n = 57). In a second analysis on differential efficacy, the whole sample was subdivided into a classical subgroup (bipolar I patients without mood-incongruent delusions and without comorbidity; n = 67) and a nonclassical subgroup including all other patients (n = 104). Classical bipolar patients had a significantly lower hospitalization rate under lithium than under carbamazepine prophylaxis (26 vs. 62%, p = 0.012). For the nonclassical group, a tendency in favor of carbamazepine was found. In a third step, we analyzed the impact of episode sequence on differential efficacy. In a global view, the episode sequence prior to the index episode was not correlated to differential efficacy. Our results might, however, indicate that patients with an episode sequence of mania-depression-free interval responded better to lithium. Besides differential efficacy, suicidal behavior and patients' satisfaction with treatment were investigated. Regarding suicidal behavior, a trend in favor of lithium was found. The data on patients' satisfaction were significantly in favor of carbamazepine. In conclusion, lithium appears to be superior to carbamazepine in classical bipolar cases and might have additional impact on proneness to suicide. The distinctly larger group of patients with nonclassical features might profit more from carbamazepine which seems to be well accepted by the patients. Hence, treatment alternatives to lithium a re desirable for the majority of bipolar patients. Copyright (C) 2000 S. Karger AG, Basel.