Recomendaciones para el tratamiento farmacológico de la Hiperglicemia en DM2

Documento de Concenso

 

TEXTO COMPLETO –> http://www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=90000172&pident_usuario=0&pcontactid=&pident_revista=40&ty=136&accion=L&origen=elsevier&web=www.elsevier.es&lan=es&fichero=40v37n02a90000172pdf001.pdf

La diabetes tipo 2 es una enfermedad caracterizada por una hiperglucemia crónica secundaria a un doble mecanismo patogénico: resistencia a la acción de la insulina asociada a un fallo progresivo en la secreción pancreática de insulina. La resistencia insulínica suele mantenerse a lo largo de la evolución de la enfermedad, pero puede mejorar con modificaciones en el estilo de vida (terapia  nutricional y ejercicio), con la consecución de unas características antropométricas más favorables y con algunos fármacos. El fallo progresivo de la secreción de insulina pancreática aconseja adoptar una actitud precoz y activa, con un incremento progresivo de la dosis y el número de fármacos para mantener los objetivos de control.

Fiebre en el Anciano : Emergency Medicine Practice

Fever In The Elderly: How To Surmount The Unique Diagnostic And Therapeutic Challenges

JUST as “children are not little adults,” the elderly cannot be considered  superannuated specimens. Physiologic and behavioral differences demand that emergency physicians manage illness in the elderly differently than we do in younger adults. In  fact, two central medical principles used  for children can be applied to the elderly: Patients are more vulnerable, and symptoms are much less specific. This issue of Emergency Medicine Practice  will address the unique issues involved in assessment and treatment of the febrile senior. Special attention is given to differences in presentation between the infected elderly and  younger adults. We also emphasize changes in management due to comorbid disease. The specific recommendations for disposition and antibiotic therapy are tailored to the ED setting.

 

https://www.ebmedicine.net/topics.php?paction=showTopicSeg&topic_id=105&seg_id=2005

EN PDF TEXTO COMPLETO Fever_In_The_Elderly_How_To_Surmount_The_Unique_Diagnostic_And_Therapeutic_Challenges[1]

 

 

 

 

 

 

Diagnosticando Hipertrofia Ventricular Izquierda

Left ventricular hypertrophy (LVH) is the abnormal enlargement of the left ventricle in response to increased peripheral vascular resistance, most commonly resulting from long-standing hypertension. The ventricle is forced to work against the increased pressure, causing the muscle to hypertrophy in an effort to keep up with the demand.

Symptoms LVH by itself has no individual symptoms. However, LVH often results in a drop in ejection fraction, which leads to such symptoms as dyspnea on exertion, orthopnea, and chest pain.

Etiology While the most common etiology of LVH is long-standing hypertension, there are other, less common causes. These include hypertrophic cardiomyopathy, athletic training, and aortic stenosis.

ECG findings As discussed in a previous installment of this department on axis deviation, left axis deviation can suggest the presence of LVH. The reason for this is that all cells in the heart muscle depolarize, generating electrical activity. More cells (eg, hypertrophy) create more electricity. This can cause a shift in the axis toward the hypertrophied chamber—in this case, the left ventricle.

Other ECG findings can also indicate LVH. Increased voltages generated by hypertrophied heart muscle are best observed in the R and S waves (Figure 1) of various leads overlying the left ventricle, specifically V₁, aVL, V₅, and V₆. The R wave is the first upward deflection of the QRS complex and is measured from Q to R on the ECG. The S wave is the downward portion of the QRS complex after the R wave (R to S on the ECG).

Left ventricular hypertrophy (LVH) is the abnormal enlargement of the left ventricle in response to increased peripheral vascular resistance, most commonly resulting from long-standing hypertension. The ventricle is forced to work against the increased pressure, causing the muscle to hypertrophy in an effort to keep up with the demand.

Symptoms LVH by itself has no individual symptoms. However, LVH often results in a drop in ejection fraction, which leads to such symptoms as dyspnea on exertion, orthopnea, and chest pain.

Etiology While the most common etiology of LVH is long-standing hypertension, there are other, less common causes. These include hypertrophic cardiomyopathy, athletic training, and aortic stenosis.

ECG findings As discussed in a previous installment of this department on axis deviation, left axis deviation can suggest the presence of LVH. The reason for this is that all cells in the heart muscle depolarize, generating electrical activity. More cells (eg, hypertrophy) create more electricity. This can cause a shift in the axis toward the hypertrophied chamber—in this case, the left ventricle.

Other ECG findings can also indicate LVH. Increased voltages generated by hypertrophied heart muscle are best observed in the R and S waves (Figure 1) of various leads overlying the left ventricle, specifically V₁, aVL, V₅, and V₆. The R wave is the first upward deflection of the QRS complex and is measured from Q to R on the ECG. The S wave is the downward portion of the QRS complex after the R wave (R to S on the ECG).

Diagnosing LVH Many ECG criteria for LVH have been published over the years. All are quite specific (greater than 90%) but not very sensitive (6.9%).^1-3 This means that patients whose ECG demonstrates findings that fulfill the criteria for LVH are likely to have clinical LVH; however, patients lacking the ECG criteria may still have clinical LVH. Sensitivity does improve with the combination of multiple sets of criteria.³ We chose to combine the Sokolow and Lyon criteria¹ with the Cornell criteria.²

Sokolow and Lyon offer two criteria: First, the S wave measurement in lead V₁ added to the R wave measurement in lead V₅ or V₆ (whichever is larger) must equal more than 35 mm. Second, the R wave in aVL must be greater than or equal to 11 mm. Cornell diagnoses LVH if the sum of the S wave in V₃ and the R wave in aVL is greater than 28 mm in men or greater than 20 mm in women.

EKG challenge

A 70-year-old white man with a history of hypertension presented with complaints of fatigue and lower-extremity edema. At this visit, his BP was 148/92 mm Hg. He takes oral hydrochlorothiazide 20 mg each day and oral lisinopril 40 mg day.

 

Using the stepwise approach to analyze the patient’s ECG (Figure 2), consider the following:

1.     Is the ECG regular? Yes. The QRS complexes march out.

2.     What is the heart rate? Find a QRS complex on or near a dark line.

Method A: Counting the large boxes, we see that there are slightly more than four large boxes before the next QRS complex. Four boxes would put the heart rate at 75 beats per minute, or we could estimate the rate to be slightly less than that at 70 beats per minute.

Method B: There are about seven QRS complexes in 6 seconds (30 large boxes), which estimates the heart rate at 7 x 10 or 70 beats per minute.

Method C: Dividing 300 by 4 (the number of large boxes between QRS complexes) gives us a heart rate of 75 beats per minute.

3.     There is a P wave for each QRS complex, and all the P waves look the same.

4.      The PR interval is about five small boxes, which is 0.2 seconds. This is borderline for a first-degree atrioventricular block (the subject of a future segment of this department).

5.     The QRS complex spans fewer than two small boxes, which is normal.

6.     In leads V₅ and V₆, the ST segment is depressed, which could suggest the presence of ischemia or injury to the lateral wall (to be discussed in a future segment).

7.     The T waves in leads V₄-V₆ are inverted. This is a nonspecific finding that could suggest underlying ischemia and should be investigated if not done previously.

8.     There are no U waves.

In order to assess this ECG for LVH criteria, we need to look at leads V₁, aVL, V₅, and V₆. Evaluating the Sokolow and Lyon criteria, we see that the S wave in lead V₁ is approximately 30 mm and the R wave in lead V₅ is approximately 21 mm; the sum of those two values is 51 mm, which is greater than 35 mm and meets one of the criteria for LVH. In addition, the R wave in lead aVL is approximately 26 mm, which is more than 11 mm and meets the second Sokolow and Lyon criterion. Finally, the S wave in V₃ is approximately 33 mm and the R wave in aVL is approximately 26 mm for a total of 59 mm, fulfilling the Cornell criterion of greater than 28 mm in a man. Because this ECG meets all three of the criteria for a diagnosis of LVH, there is a high likelihood that this patient has clinical LVH.

REFERENCES

1. Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J. 1949;37(2):161-186.

2. Casale PN, Devereux RB, Alonso DR, et al. Improved sex-specific criteria of left ventricular hypertrophy for clinical and computer interpretation of electrocardiograms: validation with autopsy findings. Circulation. 1987;75(3):565-572.

3. Levy D, Labib SB, Anderson KM, et al. Determinants of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy. Circulation. 1990;81(3):815-820

Lectura de Radiografia pediatrica

Predecir arritmia cardiaca en pacientes con palpitaciones

Does This Patient With Palpitations Have a Cardiac Arrhythmia?

This systematic review by the  Rational Clinical Examination found that an arrhythmia was more likely (LR > 2) if that patient has:

• A history of cardiac disease (likelihood ratio [LR], 2.03; 95% CI, 1.33-3.11)
• Palpitations affected by sleeping (LR, 2.29; 95% CI, 1.33-3.94)
• Palpitations while at work (LR, 2.17; 95% CI, 1.19-3.96)

A arrhythmia was less likely (LR < 0.5) if that patient has:

• A known history of panic disorder (LR, 0.26; 95% CI, 0.07-1.01)
• Palpitations lasting less than 5 minutes (LR, 0.38; 95% CI, 0.22-0.63)

Additional findings that need further discussion are:

• Description by the patient of an irregular heart rate was an independent predictor of a cardiac arrhythmia(PMID: 8629647). The authors of the systematic review did not conclude this finding was helpful because the likelihood ratio, while significant, was within 0.5 to 2.0.
• An increased number of symptoms suggested psychiatric causes in the univarate, but not multivariate  analysis of Weber  (PMID: 8629647). This finding is part of a theme in general that the more symptoms are present the more likely there is an underlying psychiatric diagnosis in the evaluation of syncope (PMID: 17397948) and symptoms in general in primary care (PMID: 7987511).

Citation:

Thavendiranathan, P., Bagai, A., Khoo, C., Dorian, P., & Choudhry, N. (2009). Does This Patient With Palpitations Have a Cardiac Arrhythmia? JAMA: The Journal of the American Medical Association, 302 (19), 2135-2143 DOI: 10.1001/jama.2009.1673 – PMID 19920238

DIAGNOSTICANDO GOTA

Clinical Diagnosis of Gout    CLINDX

Even if using the prediction rule developed in this study, physicians should consider aspirating most all joints with monoarthritis as value even in joints suggestive of gout had a one in 20 chance of an alternative diagnosis. Also, the label of gout may affect future decision making and life-long medications.

In a study of 381 patients recruited by family physicians because of monoarthritis, 57% had positive crystals and one patient had a bacterial infection.

The family physicians had an accuracy of:

• Sensitivity 97%
• Specificity 28%

The authors then created a prediction rule for the 328 patients that the family physicians suspected had gout:

Male sex 2.0 points
Previous patient-reported arthritis attack 2.0 points
Onset within 1 d 0.5 points
Joint redness 1.0 points
MIP involvement  2.5 points
Hypertension or and cardiovascular diseases 1.5 points
Serum uric acid level >5.88 m9/dL  3.5 points

The prediction rule had an accuracy of:

• 8 or more points
  • Sensitivity 92% (193/209)
  • Specificity 88% (77/88)
• 4 or less points
  • Sensitivity 99% (208/209)
  • Specificity 50% (44/88)

If 4 or less points, the NPV is 98%.

If 8 or more points, the PPV=95%.

References:

1. Janssens HJ, Fransen J, van de Lisdonk EH, van Riel PL, van Weel C, & Janssen M (2010). A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis. Archives of Internal Medicine, 170 (13), 1120-6 PMID: 20625017

El Antigeno Prostatico Especifico no puede detectar el Cancer de Prostata

EACH year some 30 million American men undergo testing for prostate-specific antigen, an enzyme made by the prostate. Approved by the Food and Drug Administration in 1994, the P.S.A. test is the most commonly used tool for detecting prostate cancer.

The test’s popularity has led to a hugely expensive public health disaster. It’s an issue I am painfully familiar with — I discovered P.S.A. in 1970. As Congress searches for ways to cut costs in our health care system, a significant savings could come from changing the way the antigen is used to screen for prostate cancer.

Americans spend an enormous amount testing for prostate cancer. The annual bill for P.S.A. screening is at least $3 billion, with much of it paid for by Medicare and the Veterans Administration.

Prostate cancer may get a lot of press, but consider the numbers: American men have a 16 percent lifetime chance of receiving a diagnosis of prostate cancer, but only a 3 percent chance of dying from it. That’s because the majority of prostate cancers grow slowly. In other words, men lucky enough to reach old age are much more likely to die with prostate cancer than to die of it.

Even then, the test is hardly more effective than a coin toss. As I’ve been trying to make clear for many years now, P.S.A. testing can’t detect prostate cancer and, more important, it can’t distinguish between the two types of prostate cancer — the one that will kill you and the one that won’t.

Instead, the test simply reveals how much of the prostate antigen a man has in his blood. Infections, over-the-counter drugs like ibuprofen, and benign swelling of the prostate can all elevate a man’s P.S.A. levels, but none of these factors signals cancer. Men with low readings might still harbor dangerous cancers, while those with high readings might be completely healthy.

In approving the procedure, the Food and Drug Administration relied heavily on a study that showed testing could detect 3.8 percent of prostate cancers, which was a better rate than the standard method, a digital rectal exam.

Still, 3.8 percent is a small number. Nevertheless, especially in the early days of screening, men with a reading over four nanograms per milliliter were sent for painful prostate biopsies. If the biopsy showed any signs of cancer, the patient was almost always pushed into surgery, intensive radiation or other damaging treatments.

The medical community is slowly turning against P.S.A. screening. Last year, The New England Journal of Medicine published results from the two largest studies of the screening procedure, one in Europe and one in the United States. The results from the American study show that over a period of 7 to 10 years, screening did not reduce the death rate in men 55 and over.

The European study showed a small decline in death rates, but also found that 48 men would need to be treated to save one life. That’s 47 men who, in all likelihood, can no longer function sexually or stay out of the bathroom for long.

Numerous early screening proponents, including Thomas Stamey, a well-known Stanford University urologist, have come out against routine testing; last month, the American Cancer Society urged more caution in using the test. The American College of Preventive Medicine also concluded that there was insufficient evidence to recommend routine screening.

So why is it still used? Because drug companies continue peddling the tests and advocacy groups push “prostate cancer awareness” by encouraging men to get screened. Shamefully, the American Urological Association still recommends screening, while the National Cancer Institute is vague on the issue, stating that the evidence is unclear.

The federal panel empowered to evaluate cancer screening tests, the Preventive Services Task Force, recently recommended against P.S.A. screening for men aged 75 or older. But the group has still not made a recommendation either way for younger men.

Prostate-specific antigen testing does have a place. After treatment for prostate cancer, for instance, a rapidly rising score indicates a return of the disease. And men with a family history of prostate cancer should probably get tested regularly. If their score starts skyrocketing, it could mean cancer.

But these uses are limited. Testing should absolutely not be deployed to screen the entire population of men over the age of 50, the outcome pushed by those who stand to profit.

I never dreamed that my discovery four decades ago would lead to such a profit-driven public health disaster. The medical community must confront reality and stop the inappropriate use of P.S.A. screening. Doing so would save billions of dollars and rescue millions of men from unnecessary, debilitating treatments.

Richard J. Ablin is a research professor of immunobiology and pathology at the University of Arizona College of Medicine and the president of the Robert Benjamin Ablin Foundation for Cancer Research.

En diabetes, la HbA1C esta afectada si el paciente presenta hemoglobina baja?

In diabetes, is the HBA1C affected if the patient has a low haemoglobin? If so, does for example, any anaemia need to be corrected & how long after before re-checking HBA1C? What conditions may affect HBA1C?

Answer:

19 May 2008 note: This question is over 2 years old and may differ to any new research.

The US National Glycohemoglobin Standization Programme (NGSP) web site contains a section on factors that interfere with HbA1c test results on which it states:

“Shortened Erythrocyte Survival: Any condition that shortens erythrocyte survival or decreases mean erythrocyte age (e.g., recovery from acute blood loss, hemolytic anemia) will falsely lower HbA1c test results regardless of the assay method used (23).  HbA1c results from patients with HbSS, HbCC, and HbSC must be interpreted with caution given the pathological processes, including anemia, increased red cell turnover, transfusion requirements, that adversely impact HbA1c as a marker of long-term glycemic control.  Alternative forms of testing such as glycated serum protein (fructosamine) should be considered for these patients.

Other factors: Vitamins C and E are reported to falsely lower test results, possibly by inhibiting glycation of hemoglobin (24, 25); vitamin C may increase values with some assays (25).  Iron-deficiency anemia is reported to increase test results (26).  Hypertriglyceridemia, hyperbilirubinemia, uremia (see carbamylated Hb in Table 1), chronic alcoholism, chronic ingestion of salicylates, and opiate addiction are reported to interfere with some assay methods, falsely increasing results (3, 5, 9, 11, 12, 14, 16-18, 21-22, 27-30).” [1]

Reynolds et al writing in the ‘BMJ’ on glycated haemoglobin note:

“…A loss of red cells reduces the average age of the red cell pool. The glycation of haemoglobin to produce HbA1c occurs over the lifespan of the cells; approximately 50% occurs in days 90-120, and the remainder occurs before this.1 2 HbA1c thus represents a weighted average of the blood glucose concentration over the previous two to three months. In the presence of anaemia, blood loss results in a reduction in the average red cell lifespan and HbA1c is lower than would be expected for the degree of chronic hyperglycaemia. If blood loss is sufficient to shorten average lifespan to 90 days, the HbA1c concentration would theoretically be halved and could give the false impression that glucose control is exemplary…” [2]

In diabetic patients with anaemia (low haemoglobin level), does this need to be corrected before HbA1c is measured again? How long is it necessary to wait before rechecking HbA1c?

We searched the NLH Diabetes Specialist Library and the TRIP and Medline databases but found no guidance or studies to help answer this question. Thus, we can only recommend seeking advice from local specialist. Alternatively, you could call the Diabetes UK Careline:

By telephone
For enquiries to Careline and Careline Scotland:
Telephone: 0845 120 2960, Monday-Friday, 9am-5pm

References
1. NGSP. Factors that interfere with GHB (HbA1c) Test Results. April 2008. (http://www.ngsp.org/prog/factors.htm)
2. Reynolds TM, Smellie WS and Twomey PJ. Glycated haemoglobin (HbA1c) monitoring. BMJ. 2006 Sep 16;333(7568):586-8. (http://www.bmj.com/cgi/content/full/333/7568/586)

7° CURSO DE ACTUALIZACION EN PEDIATRIA 2010 – Asociación Española de Pediatria de Atención Primaria

Mesas redondas

Hematología e inmunología

Moderador
Ángel Hernández Merino. Pediatra, CS La Rivota. Alcorcón, Madrid

El niño con infecciones frecuentes
Jesús Ruiz Contreras. Profesor titular. Universidad Complutense. de Madrid. Sección de Lactantes e Inmunodeficiencias. Departamento de Pediatría. Hospital Universitario 12 de Octubre. Madrid.

Abordaje de la anemia microcítica, nuevas herramientas diagnósticas
Julián Sevilla Navarro. Servicio de Hematología. Hospital Infantil Universitario Niño Jesús. Madrid.

Estudio del paciente con adenopatías periféricas
Jaime García Aguado. Pediatra, CS Villablanca. Madrid.

Endocrinología

Moderador.
José Luis Montón Álvarez. Pediatra, CS Mar Báltico. Área 4, SERMAS. Madrid.

Introducción
José Luis Montón Álvarez. Pediatra, CS Mar Báltico. Área 4, SERMAS. Madrid.

Pubertad precoz y adelantada en niñas
Lourdes Ibáñez Toda. Profesor Asociado de Pediatría. Sección de Endocrinología. Hospital Sant Joan de Déu. Universidad de Barcelona.

Evidencias en el tratamiento con hormona del crecimiento. Nuevas indicaciones
Emilio García García. Unidad de Endocrinología Pediátrica. Hospital Universitario“Virgen del Rocío”. Sevilla.

Niños en movimiento: tratamiento de la obesidad infantil, una nueva forma de abordar un viejo problema
Norma Irene García Reyna. Servicio de Pediatría. Unidad de Obesidad Infantil. Hospital Materno-infantil Vall d’Hebron. Barcelona. Universidad Autónoma de Barcelona.

Cuestiones a debate:“Dividencias”

Resumen
José Cristóbal Buñuel Álvarez. Pediatra, Área Básica de Salut Girona-4. (Institut Català de la Salut).
Paz González Rodríguez. Pediatra, CS “Barrio del Pilar”. Área 5. Madrid.
Javier González de Dios. Pediatra, Departamento de Pediatría. Hospital de Torrevieja. Universidad Miguel Hernández. Alicante.

Tratamiento preventivo en el lactante con sibilancias recurrentes
José Cristóbal Buñuel Álvarez. Pediatra, Área Básica de Salut Girona-4. (Institut Català de la Salut).
Paz González Rodríguez. Pediatra, CS “Barrio del Pilar”. Área 5. Madrid.
Javier González de Dios. Pediatra, Departamento de Pediatría. Hospital de Torrevieja. Universidad Miguel Hernández. Alicante.

Suplementación con vitamina D en la infancia
José Cristóbal Buñuel Álvarez. Pediatra, Área Básica de Salut Girona-4. (Institut Català de la Salut).
Paz González Rodríguez. Pediatra, CS “Barrio del Pilar”. Área 5. Madrid.
Javier González de Dios. Pediatra, Departamento de Pediatría. Hospital de Torrevieja. Universidad Miguel Hernández. Alicante.

Pruebas de imagen en el niño con infección del tracto urinario
José Cristóbal Buñuel Álvarez. Pediatra, Área Básica de Salut Girona-4. (Institut Català de la Salut).
Paz González Rodríguez. Pediatra, CS “Barrio del Pilar”. Área 5. Madrid.
Javier González de Dios. Pediatra, Departamento de Pediatría. Hospital de Torrevieja. Universidad Miguel Hernández. Alicante.

Seminarios

Radiología pediátrica en Atencion Primaria

Moderadora:
M.ª Jesús Geijo Rincón. Pediatra, CS Las Margaritas. Área 10. Getafe, Madrid. Vocal Junta AMPap.

Ponente
Josefina Vicente Rueda. Facultativo Especialista de Área de Radiodiagnóstico.. Hospital Universitario Reina Sofía de Córdoba. Sección de Radiología Pediátrica

Trastornos oftalmológicos frecuentes

Moderadora
M.ª Luisa Serrano Gómez. Pediatra de Atención Primaria de la UGC Huerta de la Reina. Córdoba.

Ponente
Diego Puertas Bordallo. Oftalmólogo. Unidad de Estrabología. Hospital Infantil Universitario Niño Jesús. Madrid.

Atencion inicial a las emergencias pediátricas. Casos clínicos comentados

Moderadora
M.ª Julia Hernández Delgado. Pediatra, CS Ciudad San Pablo. Coslada, Madrid.

Ponente
Montserrat Nieto Moro. Servicio de Cuidados Intensivos Pediátricos. Hospital Infantil Universitario Niño Jesús. Madrid.

Cómo escuchar para curar. Introducción a la Psicoterapia Breve

Moderadora
Concepción Bonet de Luna. Pediatra, CS Segre. Madrid.

Ponentes
Concepción Bonet de Luna. Pediatra, CS Segre. Madrid.
José Luis Marín López. Psiquiatra. Director de Psicociencias.

Cómo interpretar ECGs pediátricos y no sucumbir en el intento

Moderador
Benjamín Herranz Jordán. Pediatra, CS El Abajón. Área 6. Las Rozas, Madrid.

Ponente
F. Javier Pérez-Lescure Picarzo. Cardiología infantil. Unidad de Pediatría. Hospital Universitario Fundación Alcorcón, Madrid.

Dermatología en pieles oscuras

Moderadora
Dolors Canadell i Vilaret. Pediatra, CAP Barberá del Vallés. Barcelona.

Ponente
Asunción Vicente Villa. Sección de Dermatología Pediátrica. Hospital Sant Joan de Déu de Barcelona. Universitat de Barcelona.

Vacunacomopuedas.org: un seminario interactivo

Moderador
Juan Bravo Acuña. Pediatra, CS El Greco. Getafe, Madrid.

Ponentes
Juan Bravo Acuña. Pediatra, CS El Greco. Getafe, Madrid.
Manuel Merino Moína. Pediatra, CS El Greco. Getafe, Madrid.

Promoción de la salud emocional del pediatra de Atención Primaria

Moderadora
Narcisa Palomino Urda. Pediatra, CS Las Flores. Granada.

Ponente
José Luis Bimbela Pedrola. Escuela Andaluza de Salud Pública

PAGINA DE ENLACE : http://www.aepap.org/congresos/curso2010.htm

GUIA DE PRACTICA CLINICA: MENINGITIS BACTERIANA Y SEPSIS MENINGOCOCICA (NICE)

The management of bacterial meningitis and meningococcal septicaemia in children and young people younger than 16 years in primary and secondary care

Description

This guideline offers best practice advice on the care of children and young people younger than 16 years with bacterial meningitis and meningococcal septicaemia. Bacterial meningitis is an infection of the surface of the brain (meninges) by bacteria that have usually travelled there from mucosa …

http://guidance.nice.org.uk/CG102