sábado, 13 de octubre de 2012
jueves, 11 de octubre de 2012
Más noticias del CDC 11 oct. 137 infectados. 12 muertos
Esto habla por sí solo de la cantidad astronómica de inyecciones peridurales de esteroides que se aplican en el mundo. Solo de estos lotes y de este laboratorio se supone se utilizaron 13000 ampollas en 4 meses. En contraste, me llama la atención que la evidencia que soporta el uso de inyecciones peridurales de esteroides sea pobre, debido principalmente a la falta de estudios.
martes, 9 de octubre de 2012
Hoy ya son 119. Que susto !!!
Siga la noticia en la página del CDC
El medicamento contaminado fue fabricado por la farmacéutica New England Compounding Center (NECC), con sede en Massachusetts, y las estimaciones más pesimistas señalan que podría haber 30 mil personas en riesgo. Hasta 13.000 personas podrían haber recibido potencialmente las inyecciones contaminadas entre el 21 de mayo y el 24 de septiembre, indicó a la AFP Curtis Allen, un portavoz del CDC, señalando "que sólo un pequeño número debería enfermarse".
Las autoridades sanitarias estadounidenses anunciaron la semana pasada haber descubierto el origen de la infección, un hongo parasitario encontrado en una muestra de esteroides fabricada por la empresa New England Compounding Center, con sede en Massachusetts. La compañía ha retirado todos sus productos del mercado y cerrado sus operaciones mientras se realizan más pruebas para determinar el origen del problema.
http://es-us.noticias.yahoo.com/video/idnews-26345325/cdc-steroid-related-meningitis-cases-rise-30814944.html
lunes, 8 de octubre de 2012
Meningitis asociadas a esteroides peridurales
CDC is aware that New England Compounding Center has voluntarily expanded its recall to include all products currently in circulation that were compounded at and distributed from its facility in Framingham, Massachusetts.
CDC's guidance to patients has not changed as a result of this voluntary recall. Patients who feel ill and are concerned about whether they received a medication from NECC should contact their physicians.
Clinicians should actively contact patients who have received medicines associated with three lots of preservative-free methylprednisolone acetate (80mg/ml) recalled on September 26. The potentially contaminated injections were given starting May 21, 2012. Symptoms that should prompt diagnostic evaluation include: fever, new or worsening headache, neck stiffness, sensitivity to light, new weakness or numbness, increasing pain, redness or swelling of the injection site.
Product Recall
On September 25, 2012, the New England Compounding Center located in Framingham, MA voluntarily recalled the following lots of methylprednisolone acetate (PF) 80mg/ml:
Methylprednisolone Acetate (PF) 80 mg/ml Injection, Lot #05212012@68, BUD 11/17/2012
Methylprednisolone Acetate (PF) 80 mg/ml Injection, Lot #06292012@26, BUD 12/26/2012
Methylprednisolone Acetate (PF) 80 mg/ml Injection, Lot #08102012@51, BUD 2/6/2013
All infections detected as of October 8 have occurred after injections with methylprednisolone acetate products from one of these lots. At this time, there is no evidence of infection related to other NECC products.
The FDA investigation into the NECC facility is ongoing. On October 5, FDA reported observing “fungal contamination by direct microscopic examination of foreign matter taken from a sealed vial of methylprednisolone acetate collected from the New England Compounding Center.” Further analysis is ongoing. On October 6, NECC expanded its previous recalls to include all products currently in circulation that were compounded at and distributed from its facility in Framingham, Mass. More information about this recall is available at the FDA website.
Recommendations
Physicians should contact (by phone or in person) any patient who had an injection (e.g., spinal, joint) after May 21, 2012, using any of the following three recalled lots of preservative-free methylprednisolone acetate (80mg/ml) produced by NECC, to determine if they are having symptoms:
Methylprednisolone Acetate (PF) 80mg/ml Injection, Lot# 05212012@68, BUD 11/17/2012
Methylprednisolone Acetate (PF) 80mg/ml Injection, Lot#06292012@26, BUD 12/26/2012
Methylprednisolone Acetate (PF) 80mg/ml Injection, Lot# 08102012@51, BUD 2/6/2013
Symptoms that should prompt diagnostic evaluation include: fever, new or worsening headache, neck stiffness, sensitivity to light, new weakness or numbness, increasing pain, redness or swelling at injection site. Some of the symptoms of patients who have ultimately been diagnosed with meningitis have been mild and not classic for meningitis (e.g., new or worsening headache without fever or neck stiffness).
CDC's guidance to patients has not changed as a result of this voluntary recall. Patients who feel ill and are concerned about whether they received a medication from NECC should contact their physicians.
Clinicians should actively contact patients who have received medicines associated with three lots of preservative-free methylprednisolone acetate (80mg/ml) recalled on September 26. The potentially contaminated injections were given starting May 21, 2012. Symptoms that should prompt diagnostic evaluation include: fever, new or worsening headache, neck stiffness, sensitivity to light, new weakness or numbness, increasing pain, redness or swelling of the injection site.
Product Recall
On September 25, 2012, the New England Compounding Center located in Framingham, MA voluntarily recalled the following lots of methylprednisolone acetate (PF) 80mg/ml:
Methylprednisolone Acetate (PF) 80 mg/ml Injection, Lot #05212012@68, BUD 11/17/2012
Methylprednisolone Acetate (PF) 80 mg/ml Injection, Lot #06292012@26, BUD 12/26/2012
Methylprednisolone Acetate (PF) 80 mg/ml Injection, Lot #08102012@51, BUD 2/6/2013
All infections detected as of October 8 have occurred after injections with methylprednisolone acetate products from one of these lots. At this time, there is no evidence of infection related to other NECC products.
The FDA investigation into the NECC facility is ongoing. On October 5, FDA reported observing “fungal contamination by direct microscopic examination of foreign matter taken from a sealed vial of methylprednisolone acetate collected from the New England Compounding Center.” Further analysis is ongoing. On October 6, NECC expanded its previous recalls to include all products currently in circulation that were compounded at and distributed from its facility in Framingham, Mass. More information about this recall is available at the FDA website.
Recommendations
Physicians should contact (by phone or in person) any patient who had an injection (e.g., spinal, joint) after May 21, 2012, using any of the following three recalled lots of preservative-free methylprednisolone acetate (80mg/ml) produced by NECC, to determine if they are having symptoms:
Methylprednisolone Acetate (PF) 80mg/ml Injection, Lot# 05212012@68, BUD 11/17/2012
Methylprednisolone Acetate (PF) 80mg/ml Injection, Lot#06292012@26, BUD 12/26/2012
Methylprednisolone Acetate (PF) 80mg/ml Injection, Lot# 08102012@51, BUD 2/6/2013
Symptoms that should prompt diagnostic evaluation include: fever, new or worsening headache, neck stiffness, sensitivity to light, new weakness or numbness, increasing pain, redness or swelling at injection site. Some of the symptoms of patients who have ultimately been diagnosed with meningitis have been mild and not classic for meningitis (e.g., new or worsening headache without fever or neck stiffness).
sábado, 6 de octubre de 2012
martes 9 de octubre
Continuaremos discutiendo las técnicas analgésicas para los reemplazos totales de rodillas.
Que técnicas regionales pueden ser aplicadas en este tipo de cirugía ?
Que aspectos técnicos se deben tener en cuenta ?
Como se maneja los catéteres ?
Técnica, dosis, volumen, tipo de anestésico ...
Que técnicas regionales pueden ser aplicadas en este tipo de cirugía ?
Que aspectos técnicos se deben tener en cuenta ?
Como se maneja los catéteres ?
Técnica, dosis, volumen, tipo de anestésico ...
viernes, 28 de septiembre de 2012
martes 2 de Octubre 2012
Vamos a continuar el desarrollo del manejo analgésico de los reemplazos articulares de rodilla.
Hay varios puntos que ya hemos desarrollado:
1. No se debe manejar con infusiones peridurales. Por la limitación en el movimiento, los riesgos del procedimiento, el manejos e catéteres peridurales en paciente Anticouagulado, incremento del riesgo de caídas.
2. Hay suficiente evidencia para continuar colocando catéteres femorales en todos los pacientes, así como la administración de opioides fuertes por PCA.
3. El uso de AINES en paciente Anticoagulado permitiría como opción solo COX2 selectivos, pero a expensas de un mayor riesgo cardiovascular.
Discutiremos basados en la literatura disponible la utilidad de bloqueos y o catéteres del nervio ciático, obturador y femorocutáneo.
El impacto de intervenciones psicológicas en el preoperatorio.
El uso de anticonvulsivantes en el perioperatorio.
Nos vemos.
Hay varios puntos que ya hemos desarrollado:
1. No se debe manejar con infusiones peridurales. Por la limitación en el movimiento, los riesgos del procedimiento, el manejos e catéteres peridurales en paciente Anticouagulado, incremento del riesgo de caídas.
2. Hay suficiente evidencia para continuar colocando catéteres femorales en todos los pacientes, así como la administración de opioides fuertes por PCA.
3. El uso de AINES en paciente Anticoagulado permitiría como opción solo COX2 selectivos, pero a expensas de un mayor riesgo cardiovascular.
Discutiremos basados en la literatura disponible la utilidad de bloqueos y o catéteres del nervio ciático, obturador y femorocutáneo.
El impacto de intervenciones psicológicas en el preoperatorio.
El uso de anticonvulsivantes en el perioperatorio.
Nos vemos.
Medscape 2012 - El futuro. manipular CYP450
Need for High Opioid Dose Linked to CYP450
Nancy A. Melville
September 25, 2012 (Phoenix, Arizona) — Patients with chronic pain who require high doses of opioids to achieve pain relief show exceptionally high rates of defects of the cytochrome P450 (CYP450) enzyme system compared with the general population.
The CYP450 enzyme system is known to play an important role in the metabolism of opioids, and recent advances in genetic testing allow for the easy detection of defects to the enzymes.
"We\\\'ve known for years that among patients with the exact same pain conditions one may need 500 mg of morphine a day while the other may need only 50 mg, but we\\\'ve always wondered why," lead author Forest Tennant, MD, told Medscape Medical News.
"It turns out that among high-dose patients, about 85% have these defects in 1 or more of their CYP450 enzymes." In the general population, only about 20% to 30% of people have CYP450 defects, he said.
His findings were presented here at the American Academy of Pain Management (AAPM) 23rd Annual Clinical Meeting.
Emerging Frontier
To evaluate patterns among his own patients with intractable pain, Dr. Tennant tested 66 patients attending his clinic in West Covina, California, who required more than 150 mg equivalence of morphine a day for pain relief.
The patients were tested specifically for the CYP2D6, CYP2C9, and CYP2C19 enzymes. The results showed that 55 (83.3%) of the 66 patients had 1 or more CYP450 defects, 21 (31.8%) had 2 defects, and 6 (9.1%) had 3 defects.
According to chronic pain management expert Gary M. Reisfield, MD, genetic research is poised to reveal expansive new insights into the mechanisms of why some patients respond to medications whereas others don\\\'t.
"Pharmacogenomics represents the emerging frontier for understanding interindividual variability in opioid efficacy and toxicity, and in guiding safe and effective opioid pharmacotherapy," said Dr. Reisfield, an assistant professor and chief of Pain Management Services in the University of Florida College of Medicine\\\'s Divisions of Addiction Medicine and Forensic Psychiatry and Department of Psychiatry in Gainesville, Florida.
"With regard to opioid response, the mu-opioid receptor, the ATP [adenosine triphosphate]-binding cassette subfamily B, and other genes are believed to play significant roles," he explained.
With CYP450, a "superfamily" of enzymes responsible for the metabolism of most opioids, various polymorphisms and variables in activity can have clinical significance.
The enzymes, for instance, have been implicated as playing a role in the overactive metabolism of codeine. In a recent case, the US Food and Drug Administration (FDA) in fact issued a warning about the risks associated with codeine after 3 children died and a fourth child nearly died after having been administered codeine following tonsillectomy and adenoidectomy.
"Once in the body, codeine is converted to morphine in the liver by an enzyme called cytochrome P450 isoenzyme 2D6 (CYP2D6) (and) some people metabolize codeine much faster and more completely than others," the FDA wrote in a statement.
"These people, known as ultra-rapid metabolizers, are likely to have higher-than-normal levels of morphine in their blood after taking codeine. These high levels can lead to overdose and death," the agency said. "The three children who died after taking codeine exhibited evidence of being ultra-rapid metabolizers."
Conversely, some people are "poor" metabolizers of codeine, meaning that they have few, one, or no copies of the gene or CYP2D6, Dr. Reisfield added.
"Such individuals are incapable of metabolizing codeine morphine, and thus incapable of deriving analgesia from administration of the medication. Both genetic defects would be detected through CYP2D6 genotyping."
Drug Seeker or Higher Requirement?
That being said, Dr. Reisfield suggested that the new study\\\'s findings, although intriguing, leave many unanswered questions.
"The study adds to a nascent literature on pharmacogenomics in opioid therapy," Dr. Reisfield said. "Dr. Tennant demonstrates an association between CYP \\\'defects\\\' and requirements for high opioid dosages. He has not, however, established a causal association."
The study\\\'s limitations include that "the most frequent defects were in CYP2C19, which plays an inconsequential role in methadone metabolism, but plays no role in the metabolism of other opioids," Dr. Reisfield said.
Meanwhile, CYP3A4, an important enzyme for the metabolism of most opioids, was not genotyped in the study, Dr. Reisfield said.
In addition, the specific opioids used were not identified, which is important because some opioids, including hydromorphone, oxymorphone, and morphine, are not metabolized by CYPs, he added.
It\\\'s not known whether subjects were receiving other medications that could have affected CYP metabolic activity.
Dr. Tennant acknowledged that the study would have benefited from more information from a control group of patients with chronic pain who did not require the high doses.
No one should be called a drug-seeker these days until you\\\'ve done the CYP450 testing.
"It is unknown just how prevalent severe intractable pain patients with CYP 450 defects who require high dose opioid therapy may be compared to the general, chronic pain population, but it is probably a small percentage," he wrote.
"This study makes it clear, however, that some severe chronic pain patients have major CYP defects that affect opioid metabolism and dosage."
At the very least, the findings suggest that CYP450 testing can represent an important starting point for evaluation when high doses of opioids are required, Dr. Tennant asserted.
"No one should be called a drug-seeker these days until you\\\'ve done the CYP450 testing to see if that patient simply needs an awful lot more medication than someone else."
Dr. Tennant and Dr. Reisfield have disclosed no relevant financial relationships.
American Academy of Pain Management (AAPM) 23rd Annual Clinical Meeting. Abstract 5. Presented September 21, 2012.
Medscape Medical News © 2012 WebMD, LLC
Send comments and news tips to news@medscape.net.
Nancy A. Melville
September 25, 2012 (Phoenix, Arizona) — Patients with chronic pain who require high doses of opioids to achieve pain relief show exceptionally high rates of defects of the cytochrome P450 (CYP450) enzyme system compared with the general population.
The CYP450 enzyme system is known to play an important role in the metabolism of opioids, and recent advances in genetic testing allow for the easy detection of defects to the enzymes.
"We\\\'ve known for years that among patients with the exact same pain conditions one may need 500 mg of morphine a day while the other may need only 50 mg, but we\\\'ve always wondered why," lead author Forest Tennant, MD, told Medscape Medical News.
"It turns out that among high-dose patients, about 85% have these defects in 1 or more of their CYP450 enzymes." In the general population, only about 20% to 30% of people have CYP450 defects, he said.
His findings were presented here at the American Academy of Pain Management (AAPM) 23rd Annual Clinical Meeting.
Emerging Frontier
To evaluate patterns among his own patients with intractable pain, Dr. Tennant tested 66 patients attending his clinic in West Covina, California, who required more than 150 mg equivalence of morphine a day for pain relief.
The patients were tested specifically for the CYP2D6, CYP2C9, and CYP2C19 enzymes. The results showed that 55 (83.3%) of the 66 patients had 1 or more CYP450 defects, 21 (31.8%) had 2 defects, and 6 (9.1%) had 3 defects.
According to chronic pain management expert Gary M. Reisfield, MD, genetic research is poised to reveal expansive new insights into the mechanisms of why some patients respond to medications whereas others don\\\'t.
"Pharmacogenomics represents the emerging frontier for understanding interindividual variability in opioid efficacy and toxicity, and in guiding safe and effective opioid pharmacotherapy," said Dr. Reisfield, an assistant professor and chief of Pain Management Services in the University of Florida College of Medicine\\\'s Divisions of Addiction Medicine and Forensic Psychiatry and Department of Psychiatry in Gainesville, Florida.
"With regard to opioid response, the mu-opioid receptor, the ATP [adenosine triphosphate]-binding cassette subfamily B, and other genes are believed to play significant roles," he explained.
With CYP450, a "superfamily" of enzymes responsible for the metabolism of most opioids, various polymorphisms and variables in activity can have clinical significance.
The enzymes, for instance, have been implicated as playing a role in the overactive metabolism of codeine. In a recent case, the US Food and Drug Administration (FDA) in fact issued a warning about the risks associated with codeine after 3 children died and a fourth child nearly died after having been administered codeine following tonsillectomy and adenoidectomy.
"Once in the body, codeine is converted to morphine in the liver by an enzyme called cytochrome P450 isoenzyme 2D6 (CYP2D6) (and) some people metabolize codeine much faster and more completely than others," the FDA wrote in a statement.
"These people, known as ultra-rapid metabolizers, are likely to have higher-than-normal levels of morphine in their blood after taking codeine. These high levels can lead to overdose and death," the agency said. "The three children who died after taking codeine exhibited evidence of being ultra-rapid metabolizers."
Conversely, some people are "poor" metabolizers of codeine, meaning that they have few, one, or no copies of the gene or CYP2D6, Dr. Reisfield added.
"Such individuals are incapable of metabolizing codeine morphine, and thus incapable of deriving analgesia from administration of the medication. Both genetic defects would be detected through CYP2D6 genotyping."
Drug Seeker or Higher Requirement?
That being said, Dr. Reisfield suggested that the new study\\\'s findings, although intriguing, leave many unanswered questions.
"The study adds to a nascent literature on pharmacogenomics in opioid therapy," Dr. Reisfield said. "Dr. Tennant demonstrates an association between CYP \\\'defects\\\' and requirements for high opioid dosages. He has not, however, established a causal association."
The study\\\'s limitations include that "the most frequent defects were in CYP2C19, which plays an inconsequential role in methadone metabolism, but plays no role in the metabolism of other opioids," Dr. Reisfield said.
Meanwhile, CYP3A4, an important enzyme for the metabolism of most opioids, was not genotyped in the study, Dr. Reisfield said.
In addition, the specific opioids used were not identified, which is important because some opioids, including hydromorphone, oxymorphone, and morphine, are not metabolized by CYPs, he added.
It\\\'s not known whether subjects were receiving other medications that could have affected CYP metabolic activity.
Dr. Tennant acknowledged that the study would have benefited from more information from a control group of patients with chronic pain who did not require the high doses.
No one should be called a drug-seeker these days until you\\\'ve done the CYP450 testing.
"It is unknown just how prevalent severe intractable pain patients with CYP 450 defects who require high dose opioid therapy may be compared to the general, chronic pain population, but it is probably a small percentage," he wrote.
"This study makes it clear, however, that some severe chronic pain patients have major CYP defects that affect opioid metabolism and dosage."
At the very least, the findings suggest that CYP450 testing can represent an important starting point for evaluation when high doses of opioids are required, Dr. Tennant asserted.
"No one should be called a drug-seeker these days until you\\\'ve done the CYP450 testing to see if that patient simply needs an awful lot more medication than someone else."
Dr. Tennant and Dr. Reisfield have disclosed no relevant financial relationships.
American Academy of Pain Management (AAPM) 23rd Annual Clinical Meeting. Abstract 5. Presented September 21, 2012.
Medscape Medical News © 2012 WebMD, LLC
Send comments and news tips to news@medscape.net.
viernes, 21 de septiembre de 2012
Martes 25 de Septiembre 2012
Andrés tiene 59 años, es hipertenso controlado con losartan, diabético tipo 2 manejado con dieta e hipoglicemiantes orales y alérgico a la penicilina. Desde hace un año Andrés tiene dolor tipo punzada y presión en la parte interna de la rodilla. Ese dolor es incidental, sin componente neuropático y para los últimos 2 meses es generalmente mayor a 6/10. Desde entonces, toma acetaminofén hidrocodona (500mg/5mg) 2 tabletas cada 6 horas. Estaba preocupado por el dolor en el postoperatorio.
Lo sometieron a un reemplazo articular de rodilla en la Fundación Santa Fe. Su anestesiólogo, decidió utilizar una técnica NEUROAXIAL periraquidea asociado una infusión continúa de dexmedetomidina. El intraoperatorios ocurre sin inconveniente.
Es llevado a recuperación con una infusión peridural de bupivacaina al 0,125% a 8 ml/ hora. Se le fórmula además dosis de rescate de hidromorfona de 0,6mg. Como parte del protocolo de anticoagulación el paciente se le fórmula dabigatrán.
Hoy es el primer día postoperatorio. El paciente refiere un vas de 0/10, no ha utilizado rescates de hidromorfona. Está muy satisfecho ya que se le había explicado antes de la cirugía que iba a estar con dolor moderado.
Andrés siente los miembros inferiores pesados y por eso solicita postponer la terapia física por un día.
Cual es el problema ? Hay algún problema ?
Este manejo alcanza las metas analgésicas propuestas ?
Cual debería ser, según su opinión, el manejo analgésico en este postoperatorio ?
Hay evidencia que soporte el inicio temprano de terapia física en este tipo de cirugía ?
Como siempre, por favor, referencia sus repuestas.
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