f La DM es un sndrome que se caracteriza por

hiperglicemia que resulta de defectos en la secrecin, en la accin de la insulina, o ambos y que provoca complicaciones agudas (cetoacidosis diabtica, estado hiperosmolar no cetsico) y crnicas (microangiopatia y macroangiopatia, neuropatia, retinopatia, etc), que redundan en la morbilidad y en el deterioro de la calidad de vida del individuo.

Pediatric Diabetes 2009: 10( Suppl. 12) : 312 doi: 10.1111/j.1399-5448.2009.00568.x All rights reserved

2009 John Wiley & Sons A/S

Pediatric Diabetes

DIABETES TIPO 1

ISPAD Clinical Practice ConsensusGuidelines2009 Compendium

D enition, epidemiology and classication of diabetes in children and adolescents

Craig M E, Hattersley A , Donaghue K C. Denition, epidemiology and classication of diabetes in children and adolescents. Pediatric Diabetes 2009: 10 (Suppl. 12): 312.
Westmead NSW 2145 Australia Tel: 02 9113 3637; fax: 02 9113 3810; e-mail: m.craig@ unsw.edu.au

f Es la forma ms comun de diabetes en los nios y adolescentes f Se caracteriza por la destruccin de las clulas beta del pncreas
Maria E. Craig a , Andrew Hattersleyb and Kim C. Donaghue c
a

Acknowledgments: Denis Daneman, Zvi Laron, Shin Amemiya, Shigetaka Sugihara, Tatsuhiko Urakami, Gun Forsander. Conicts of interest: The authors have declared no conicts of interest. Editors of the ISPAD Clinical Practice Consensus Guidelines 2009 Compendium: Ragnar Hanas, Kim Donaghue, Georgeanna Klingensmith, and Peter Swift.
This article is a chapter in the ISPAD Clinical Practice Consensus Guidelines 2009 Compendium. The complete set of guidelines can be found at www.ispad.org. The evidence grading system used in the ISPAD Guidelines is the same as that used by the American Diabetes Association. See page 2 (the Introduction in Pediatric Diabetes 2009; 10 (Suppl. 12): 1 2).

que producen insulina

University of NSW, University of Sydney, The Childrens Hospital at Westmead, Australia; b Institute of Biomedical and Clinical Sciences, Peninsula Medical School, Exeter, UK; c University of Sydney, The Childrens Hospital at Westmead, NSW, Australia Corresponding author: Assoc. Prof. Maria Craig Institute of Endocrinology and Diabetes The Childrens Hospital at Westmead Locked Bag 4001

f La destruccin de las clulas B del pncreas se debe a un

Denition
Diabetes mellitus is a group of metabolic diseases characterised by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The abnormalities in carbohydrate, fat, and protein metabolism that are found in diabetes are due to decient action of insulin on target tissues. I f ketones are present in blood or urine, treatment is urgent, because ketoacidosis can evolve rapidly.

trastorno inmunolgico (autoinmunitario), es decir, los mecanismos de defensa del organismo actan contra infecciones por virus, bacterias y el organismo desconoce a las clulas B del pncreas, las confunden como extraas y en consecuencia las destruyen.
Diagnostic criteria for diabetes in childhood and adolescence
Diagnostic criteria for diabetes are based on blood glucose measurements and the presence or absence of symptoms (E) (4; 86). Three ways to diagnose diabetes are possible and each, in the absence of unequivocal hyperglycemia, must be conrmed, on a subsequent day, by any one of the three methods given in Table 1. Diabetes in children usually presents with characteristic symptoms such as polyuria, polydipsia, blurring of vision, and weight loss, in association with glycosuria and ketonuria.

I n its most severe form, ketoacidosis or rarely a non-ketotic hyperosmolar state may develop and lead to stupor, coma and in absence of effective treatment, death. The diagnosis is usually conrmed quickly by measurement of a marked elevation of the blood glucoselevel. I n thissituation if ketonesarepresent in blood or urine, treatment is urgent. Waiting another day to conrm the hyperglycemia may be dangerous in allowing ketoacidosis to evolve rapidly. I n theabsence of symptoms or presence of mild symptomsof diabetes, hyperglycemia detected incidentally or under conditionsof acuteinfective, traumatic, circulatory or other stress may be transitory and should not in itself be regarded as diagnostic of diabetes. The diagnosis of diabetes should not be based on a single plasma glucose concentration. Diagnosis may require continued observation with fasting and/or 2 hour post-prandial blood glucose levels and/or an oral glucose tolerance test (OGTT). An OGTT should not be performed if diabetes can be diagnosed using fasting, random or post-prandial criteria as excessive hyperglycemia can result. I t is

Update of guidelines previously published in Pediatric Diabetes 2006; 7: 343351.

DIABETES TIPO 2
fHay un incremento en la presentacin

peditrica, en nios y adolescentes obesos y sedentarios fHay predisposicin familiar y 2 defectos:

f RESISTENCIA A LA INSULINA f DISMINUCION EN LA SECRECION DE INSULINA POR EL

PANCREAS (PARCIAL).

RESISTENCIA A LA INSULINA
f Se define como la disminucin en la capacidad de la insulina para

llevar a cabo sus acciones fisiolgicas

f La resistencia a la insulina por lo general por lo general precede

varios aos antes de la diabetes

f Durante este perodo la resistencia se compensa con un

incremento en la secrecin de insulina por el pncreas, creando un estado de hiperinsulinemia, es decir, concentraciones de insulina superiores a lo normal, que permiten mantener cifras normales de glucosa sanguinea.

DISMINUCION DE LA SECRECION DE INSULINA POR EL PANCREAS

f La deficiencia de insulina es precedida por un exceso en la

secrecion pancretica de insulina

f El estado de hiperinsulinemia evoluciona a un estado de

hipoinsulinemia por prdida progresiva de la capacidad del pncreas para producir y secretar insulina
f Entonces se establece la combinacin de resistencia a la insulina

y disminucin en la secrecin de insulina que origina la diabetes.

Pediatric Diabetes 2009: 10( Suppl. 12) : 312 doi: 10.1111/j.1399-5448.2009.00568.x All rights reserved

2009 John Wiley & Sons A/S

Pediatric Diabetes

ISPAD Cli ical Practice C

se s s

i eli es2009 C m e i m

D enition, epidemiology and classication of diabetes in children and adolescents

1. Symptoms of diabetes plus casual plasma glucose concentration 11.1 mmol/L (200 mg/dl) . Casual is dened as any time of day without regard to time since last meal. or 2. Fasting plasma glucose 7.0 mmol/l ( 126 mg/dl). Fasting is dened as no caloric intake for at least 8 h. or 3. 2-hour postload glucose 11.1 mmol/l ( 200 mg/dl) during an OGTT. The test should be performed as described by WHO (86), using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water or 1.75 g/kg of body weight to a maximum of 75 g (65).
De iti stic criteria f r ia etes i c il Dia a a lesce ce

Corresponding values (mmol/L) are 10.0 for venous whole blood and 11.1 for capillary whole blood and 6.3 for both venous and capillary whole blood
Update of guidelines previously published in Pediatric Diabetes 2006; 7: 343351.

rarely indicated in making the diagnosis of type 1 diabetesin childhood and adolescence(E) (86). If doubt remains, periodicre-testingshould beunder-

Thecorresponding categories when theOGTT is used areasfollows:

'& 

Diabetes in children usually presents with characteristic symptoms such as polyuria, polydipsia, blurring of vision, and weight loss, in association with glycosuria and ketonuria.

'& 

Diagnostic criteria for diabetes are based on blood glucose measurements a the presence or absence of symptoms (E) (4; 86). hree ways to diagnose diabetes are possible and each, in the absence of unequivocal hyperglycemia, must be conrmed, on a subsequent day, by any one of the three methods given in able 1.

Diabetes mellitus is a group of metabolic diseases characterised by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both. he abnormalities in carbohydrate, fat, and protein metabolism that are found in diabetes are due to decient action of insulin on target tissues. I f ketones are present in blood or urine, treatment is urgent, because ketoacidosis can evolve rapidly.

I n its most severe form, ketoacidosis or rarely a non-ketotic hyperosmolar state may develop and lead to stupor, coma and in absence of effective treatment, death. he diagnosis is usually conrmed quickly by measurement of a marked elevation of the blood glucoselevel. I n thissituation if ketonesarepresent in blood or urine, treatment is urgent. Waiting another day to conrm the hyperglycemia may be dangerous in allowing ketoacidosis to evolve rapidly. I n theabsence of symptoms or presence of mild symptomsof diabetes, hyperglycemia detected incidentally or under conditionsof acuteinfective, traumatic, circulatory or other stress may be transitory and should not in itself be regarded as diagnostic of diabetes. he diagnosis of diabetes should not be based on a single plasma glucose concentration. Diagnosis may require continued observation with fasting and/or 2 hour post-prandial blood glucose levels and/or an ). oral glucose tolerance test ( should not be performed if diabetes can An be diagnosed using fasting, random or post-prandial criteria as excessive hyperglycemia can result. I t is

Corresponding author: Assoc. Prof. Maria Craig Institute of Endocrinology and Diabetes he Childrens Hospital at Westmead Locked Bag 4001

his article is a chapter in the ISPAD Clinical Practice Consensus uidelines 2009 Compendium. he complete set of guidelines can be found at www.ispad.org. he evidence grading system used in the ISPAD uidelines is the same as that used by the American Diabetes Association. See page 2 (the Introduction in Pediatric Diabetes 2009; 10 (Suppl. 12): 1 2).

Table 1. Criteria for the diagnosis of diabetes mellitus (4; 86) (E)

  

University of NSW, University of Sydney, he Childrens Hospital at Westmead, Australia; b Institute of Biomedical and Clinical Sciences, Peninsula Medical School, Exeter, UK; c University of Sydney, he Childrens Hospital at Westmead, NSW, Australia

Conicts of interest: of interest.

he authors have declared no conicts

Editors of the ISPAD Clinical Practice Consensus uidelines 2009 Compendium: Ragnar Hanas, Kim Donaghue, eorgeanna Klingensmith, and Peter Swift.

 

# #  ! !

"

!  %$ 

Maria E. Crai a , A re Hattersley a Kim C. D a ec

Acknowledgments: Denis Daneman, vi Laron, Shin Amemiya, Shigetaka Sugihara, atsuhiko Urakami, un orsander.

Craiget al.

Craig M E, Hattersley A , Donaghue K C. Denition, epidemiology and classication of diabetes in children and adolescents. Pediatric Diabetes 2009: 10 (Suppl. 12): 312.

Westmead NSW 2145 Australia el: 02 9113 3637; fax: 02 9113 3810; e-mail: m.craig@ unsw.edu.au

 

! ! 

MANIFESTACIONES CLNICAS
f La falta de produccin o accin de insulina causan diversos trastornos: f La

glucosa proveniente de la digestin de alimentos (azucares, almidones) pasa a travs de la pared intestinal a la circulacin sangunea que la lleva a todas las clulas del organismo glucosa sangunea penetre al interior de las clulas del tejido muscular y adiposo en donde se requiere para producir energa

f La falta de insulina o disminucin en su efecto no permiten que la

f La falta de insulina hace que el hgado produzca una gran cantidad de

glucosa que pasa a la circulacin sangunea que junto con la glucosa que no puede penetrar a las clulas incremente las concentraciones en sangre.

MANIFESTACIONES CLINICAS
f La falta de insulina no permite la formacin de

protenas, que son el constituyente bsico del tejido muscular, por el contrario, la falta de insulina activa la prdida de protenas musculares f El exceso de glucosa se filtra por los riones y se elimina por la orina con una gran cantidad de agua y electrolitos f La prdida de agua por la orina deshidrata al paciente f Se generan los siguientes sntomas:

SINTOMAS
f POLIURIA f POLIDIPSIA f POLIFAGIA f ANOREXIA f PERDIDA DE PESO f ASTENIA f INFECCIONES EN PIEL f ADINAMIA f PARESTESIAS EN EXTREMIDADES f DESCOMPENSACION HIPERGLUCEMICA CETOACIDOTICA:

ANOREXIA, NAUSEAS, ESTUPOR, COMA.

VOMITO,

DOLOR

ABDOMINAL,

Pediatric Diabetes2009: 10( Suppl. 12) : 312 doi: 10.1111/j.1399-5448.2009.00568.x All rights reserved

2009 John Wiley & Sons A/S

Pediatric D iabetes

I SPAD Clinical Practice ConsensusGuidelines2009 Compendium

MANEJO INICIAL

Denition, epidemiology and classication of diabetes in children and adolescents

Craig M E, Hattersley A, Donaghue K C. Denition, epidemiology and classication of diabetes in children and adolescents. Pediatric Diabetes2009: 10 (Suppl. 12): 312.
Westmead NSW 2145 Australia Tel: 02 9113 3637; fax: 02 9113 3810; e-mail: m.craig@unsw.edu.au

f Todos los nios con DM deben ingresar al hospital para inicio del

tratamiento medico por un endocrinlogo pediatra

a

Maria E. Craiga , Andrew Hattersley b and Kim C. Donaghue c

Acknowledgments: Denis Daneman, Zvi Laron, Shin Amemiya, Shigetaka Sugihara, Tatsuhiko Urakami, Gun Forsander. Conicts of interest: The authors have declared no conicts of interest. Editors of the ISPAD Clinical Practice Consensus Guidelines 2009 Compendium: Ragnar Hanas, Kim Donaghue, Georgeanna Klingensmith, and Peter Swift.

f Equipo multidisciplinario f Historia clnica completa f Identificar factores de riesgo f Examen fisico integral

University of NSW, University of Sydney, The Childrens Hospital at Westmead, Australia; b Institute of Biomedical and Clinical Sciences, Peninsula Medical School, Exeter, UK; c University of Sydney, The Childrens Hospital at Westmead, NSW, Australia Corresponding author: Assoc. Prof. Maria Craig Institute of Endocrinology and Diabetes The Childrens Hospital at Westmead Locked Bag 4001

This article is a chapter in the ISPAD Clinical Practice Consensus Guidelines 2009 Compendium. The complete set of guidelines can be found at www.ispad.org. The evidence grading system used in the ISPAD Guidelines is the same as that used by the American Diabetes Association. See page 2 (the Introduction in Pediatric Diabetes 2009; 10 (Suppl. 12): 12).

Denition
Diabetes mellitus is a group of metabolic diseases characterised by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The abnormalities in carbohydrate, fat, and protein metabolism that are found in diabetes are due to decient action of insulin on target tissues. I f ketones are present in blood or urine, treatment is urgent, becauseketoacidosis can evolverapidly.

f Percentil de peso y talla, IMC, Peso ideal para la talla, clculo de

la dieta e insulina
f IDEA

Diagnostic criteria for diabetes in childhood and adolescence

(INSULINA, AUTOVIGILANCIA).

DIETA,

EDUACION,

Diagnostic criteria for diabetes are based on blood glucose measurements and the presence or absence of symptoms (E) (4; 86). Three ways to diagnosediabetes are possible and each, in the absence of unequivocal hyperglycemia, must be conrmed, on a subsequent day, by any one of thethree methods given in Table1. Diabetes in children usually presents with characteristic symptoms such aspolyuria, polydipsia, blurring of vision, and weight loss, in association with glycosuria and ketonuria.

EJERCICIO

I n its most severe form, ketoacidosis or rarely a non-ketotic hyperosmolar state may develop and lead to stupor, coma and in absence of effective treatment, death. The diagnosis is usually conrmed quickly by measurement of a marked elevation of the blood glucoselevel. I n thissituation if ketonesarepresent in blood or urine, treatment is urgent. Waiting another day to conrm the hyperglycemia may bedangerous in allowing ketoacidosis to evolverapidly. I ntheabsenceof symptomsor presenceof mild symptomsof diabetes, hyperglycemiadetected incidentally or under conditionsof acuteinfective, traumatic, circulatory or other stress may betransitory and should not in itself be regarded as diagnostic of diabetes. The diagnosis of diabetes should not be based on a singleplasma glucoseconcentration. Diagnosis may require continued observation with fasting and/or 2 hour post-prandial blood glucose levels and/or an oral glucosetolerance test (OGTT). An OGTT should not be performed if diabetes can bediagnosed using fasting, random or post-prandial criteria as excessive hyperglycemia can result. I t is

Update of guidelines previously published in Pediatric Diabetes 2006; 7: 343351.

EDUCACION
f Explicacin sobre que es la diabetes f Objetivos del control de esta enfermedad f Vigilancia, interpretacin y valores de glucemia f Hipoglucemias y complicaciones f Planificacin de las comidad y la dieta f Ejercicio f Cuidados de pies f Interaccin con los miembros del equipo de atencion al paciente con

diabetes
f Consideraciones psicolgicas f Como mantenerse saludable, que hacer cuando est enfermo y cuando

consultar a su mdico
f Viajes

INSULINA

DOSIS
EDAD LACTANTES Y PREESCOLARES 5 A 14 AOS DESARROLLO PUBERAL TANNER II A III PUBERTAD TANNER IV DESPUES DE LA PUBERTAD ADULTOS EMBARAZO REQUERIMIENTOS 0.1 A 0.4 U/KGPIT/DIA 0.5 A 0.8 0.9 A 1.5 HASTA 2 U/KGPIT/DIA 0.5 A 1 0.5 A 1 0.1 A 0.7

ESQUEMAS

DIETA

CALORIAS
CALORIAS KCAL/DIA 1 AO 1000 + 100 KCAL POR AO 12 AOS DE EDAD 1500 A 2000 + 100 A 200 KCAL POR AO 15 AOS DE EDAD 30 A 40 KCAL/KG DE PESO IDEAL PARA LA TALLA 20 AOS DE EDAD 22 A 40 KCAL/KG DE PESO IDEAL PARA LA TALLA

EJERCICIO
f 60 MIN 3 VECES POR SEMANA

AUTOVIGILANCIA
f 2 A 4 DIARIAMENTE f PREPRANDIALES f ANTES DE LA COMIDA DONDE APLIQUE INSULINA

MANEJO

HIPOGLUCEMIANTES ORALES