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CETOACIDOSIS.pptx
- 1. DIABETES MELLITUS DR. RODRIGO COLLADO CHAGOYA ESP. MEDICINA INTERNA E INMUNOLOGIA CLINICA Y ALERGIA Servicio de Alergia e Inmunología Clínica del HGM PLÁTICA UNIVERSIDAD ANAHUAC
- 2. Emergencias Diabéticas Diabetes Mellitus Cetoacidosis Diabética -CAD Estado Hiperglucemico hiperosmolar HHS Hipoglucemia Kitabchi A et al . Hyperglucemic crises in adult pataients, a consesus statement from ADA. Diab care.2006
- 3. Epidemiología • En US ~145 K casos de cada año • 50% Causa de muerte en niños adultos jóvenes con DMT1 • La mortalidad en la CAD es de menos de <1% • La mortalidad en el EHH es del 5 a 16% • Hipoglucemia aumenta al doble o triple la mortalidad Umpierrez G.«Diabetic emergencies — ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia». NRENDO. Vol. 12, Abril 2016
- 4. Secretaria de Salud. «boletin Epidemiológico del Sistema de Vigilancia Epidemiológica hospitalaria de Diabetes tipo 2, cierre 2016. Publicación en línea
- 5. • FATALIDAD CD: <1% • EHH: 5-10% • INCIDENCIA • 8-51/1000
- 6. Fisiopatología Hormonas Contra reguladoras Catecolamidas Cortisol Gluconeogenesis Proteólisis Aminoácidos Alanina Glutamato Hiperglucemia Nyenme E., Kitabchi A. «The evolution of diabeti Ketoacidosis: An update of is etiology, pathogenesis and management». j.metabol.2015.12.007 Albumina Deshidratación K+ K+ Kaliuresis
- 7. FACTORES PRECIPITANTES INFECCIONES TRATAMIENTO INSUFICIENTE O INADECUADO 80% FENOMENOS DESCOMPENSACIÓN CRISIS HIPERGLICEMICAS
- 8. Factores precipitantes Principales Kitabchi A et al . Hyperglucemic crises in adult pataients, a consesus statement from ADA. Diab care.2023
- 9. Factores precipitantes Umpierrez G.«Diabetic emergencies — ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia». NRENDO. Vol. 12, Abril 2016 Metabolismo Corticosteroides Simpaticomiméticos Diuréticos tiazidicos Antipsicoticos atipicos Inhibidores del cotrasportador - 2 de sodio – Glucosa (5%) Biológicos (Nivolumab)
- 10. Diagnóstico: Síntomas y Signos Umpierrez G.«Diabetic emergencies — ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia». NRENDO. Vol. 12, Abril 2016 Desarrollo de horas a días Poliuria Polidipsia Pérdida de peso
- 11. Diagnóstico Glucosa HbA1c BUN Creatinina Cetonas séricas Electrolitos séricos Uroanálisis Gasometría arterial (ABG) Citometría hemática Kitabchi A et al . Hyperglucemic crises in adult pataients, a consesus statement from ADA. Diab care. 2006 Laboratorio
- 12. Mediciones adicionales • Sodio Corregido Na Medido + 1.6*(Glucosa Medida-100/100) • Brecha anicónica Na – (Cl+HCO3) • Osmolaridad efectiva 2Na + glucosa/18 • Déficit de agua WBT (Na deseado-Na real)/Na deseado • Déficit de bicarbonato (HCO3deseado + HCO3 medido )4*Peso Kitabchi A et al . Hyperglucemic crises in adult pataients, a consesus statement from ADA. Diab care. 2006
- 13. • ALGORITMO ADA: ANION GAP MAYOR 20 DIAGNÓSTICO TRÍADA DKA D: DM : GLUCOSA MAYOR 200 MG/DL O 11 MMOL (JBDS) O 250 MG(DL (AEG) K: CETONEMIA > 50 MG/DL O 3 MMOL O CETONURIA > 2++ A: ACIDOSIS HCO3 <15 Y PH <7.3
- 14. Kitabchi A et al . Hyperglucemic crises in adult pataients, a consesus statement from ADA. Diab care. 2006 Criterios Diagnósticos Triada bioquímica DKA Acidosis metabólica, hiperglucemia y cetonemia
- 17. • AUMENTO HCO3 3 • DESCENSO DE CIFRAS GLUCOSA 3 MMOL/HORA O 50 MG/HORA • MANTENER CIFRAS K ENTRE 4-5.5. • REDUCCIÓN CETONAS SANGUINEAS .5 MMOL O 10 MG /HORA METAS TRATAMIENTO
- 19. • EXPANSIÓN VOLUMEN Y ADECUADA URESIS • 15-20 ML/KG O 1-1.5 LITROS • CRISTALOIDES PREFENRENCIA SOBRE COLOIDES.
- 20. • INSULINOTERAPIA: • SUPRESIÓN CETOGENESIS • REDUCCIÓN HIPERGLICEMIA • CORRECCIÓN ELECTROLITICA • ESQUEMA ADA CIFRAS G<250: CAMBIAR A SOLUCIÓN GLUCOSADA • ESQUEMA JBDS <250 AGREGAR DEXTROSA 10% A SOLUCION Y CAMBIAR INFUSION A .05UI/KG TRATAMIENTO
- 21. TRATAMIENTO
- 22. • BICARBONATO • NO BENEFICIO EN METANALISIS SI ES >7 • USO EN PH< 6.9 TRATAMIENTO
- 23. • CA • HCO3 > 15 • AG >12 • GLUCOSA < 200 • PH >7.3 • EHH: OSM <320 CRITERIOS RESOLUCIÓN
- 24. PERSONAJES HISTORICOS DM: TOM HANKS GEROGE LUCAS SHARON STONE SALMA HAYEK WOODY ALLEN SHARON STONE GRACIAS!!!!!!
Notas del editor
- DKA is the leading cause of mortality among children and young adults with T1DM, accounting for ~50% of all deaths in this population. The overall DKA mortality recorded in the USA is <1%, but a higher rate is reported among patients aged >60 years and individuals with concomitant life -Threatening illnesses Death occurs in 5–16% of patients with HHS4,11, a rate that is ~10fold higher than that reported for DKA4,12. Similarly, hypoglycaemia is associated with twofold to threefold increased mortality, particularly as age increases and among patients who have a history of severe hypoglycaemic episodes1
- protein catabolism with resultant potassium shifts into the extracellular space, decreased potassium re-entry into the cell secondary to insulinopenia and significant renal potassium losses as a result of osmotic diuresis and ketonuria contribute to potassium dyshomeostasis.
- Drugs that affect carbohydrate metabolism, such as corticosteroids, sympathomimetics and atypical antipsychotics, might also precipitate the development of DKA1,14,23. In addition, an association has been reported between the use of sodium–glucose cotransporter 2 (SGLT2) inhibitors (a class of oral antidiabetic agents that decrease concentrations of plasma glucose by inhibiting proximal tubular reabsorption in the kidney) and the development of DKA among patients with T1DM and T2DM Antipsicoticos atipicos: Olanzapina, quetiapina, risperidona, Clozapina Simpaticomimeticos Inhibidores del SGLT-2 :canagliflozina, dapagliflozina, and empagliflozina.
- Patients with DKA usually present within hours to days of developing polyuria, polydipsia and weight loss. Nausea, vomiting and abdominal pain are detected in 40–75% of cases32. Physical examination reveals signs of dehydration, changes in mental status, hypothermia and the scent of acetone on the patient’s breath. A deep laboured breathing pattern (Kussmaul respirations) is observed among patients with severe metabolic acidosis. DKA comprises a triad of hyperglycaemia, hyperketonaemia and metabolic acidosis. The condition can be classified as mild, moderate or severe, depending on the extent of metabolic acidosis and alterations in the sensorium or mental obtundation. The key diagnostic criterion is an elevation in the serum concentration of ketone bodies. Although the majority of patients with DKA present with plasma glucose levels >16.7 mmol/l, some patients exhibit only mild elevations in plasma glucose levels (termed ‘euglycaemic DKA’) after withholding or decreasing the dose of insulin in the context of reduced food intake or illness. Euglycaemic DKA is also observed during pregnancy, among patients with impaired gluconeogenesis owing to alcohol abuse or liver failure, and among patients treated with SGLT2 inhibitors15,25,33. Thus, plasma glucose levels do not determine the severity of DKA. Confirmation of increased ketone body production is performed using either the nitroprusside reaction or direct measurement of βhydroxybutyrate14. The nitroprusside reaction provides a semiquantitative estimation of acetoacetate and acetone levels in the plasma or urine, but does not detect the presence of βhydroxybutyrate, which is the predominant ketone body among patients with DKA34. Although more expensive than evaluation of urinary ketone bodies, direct measurement of βhydroxybutyrate — either via a laboratory service or through use of a pointofcare metre — is the preferred option to diagnose ketoacidosis (≥3 mmol/l), as well as to follow the patient’s response to treatment
- 78% de ß-Hidroxibutirato, 20% de acetoacetato, y 2 % de acetona