Cetoacidosis diabetica
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Transcript of Cetoacidosis diabetica
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Dr. Ivan Francisco De Paz MPostgrado Emergencia
CETOACIDOSIS DIABETICA
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BIBLIOGRAFIA
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BIBLIOGRAFIA
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BIBLIOGRAFIA
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HISTORIA
• Aretaeus de Capadocia• "...For fluids do not remain
in the body, but use the body only as a channel through which they may flow out. Life lasts only for a time, but not very long. For they urinate with pain and painful is the emaciation. For no essential part of the drink is absorbed by the body while great masses of the flesh are liquefied into urine."
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HISTORIA• En 1675 Thomas Willis• En 1918 Frederick Grant Banting• El descubrimiento de la insulina Michael Bliss
• Enero de 1922 Leonard Thompson recibe la
primera inyeccion de insulina en el hospital General de Toronto
• En 1923 se generaliza el uso de insulina• En 1938 Roberth Hinsworth describe 2 tipos
de diabetes• En 1969 se crea el primer Glucometro con
precio de 650 dolares
The patient would then fall into semi-consciousness and the lungs would heave desperately to expel the by-product of ketosis – carbonic acid in the form of carbon dioxide, with the victim taking great gasps of air known at the time as “air hunger” or “internal suffocation”. The gasping and sighing and sweet smell lingered on as the unconsciousness became a deep diabetic coma. At that point the family could make its arrangements with the undertaker, for within a few hours death would end the suffering."
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CETOACIDOSIS DIABETICA
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DEFINICION
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GENERALIDADES
• Corresponde del 8-29% de ingresos con Dx primario de DM
• 6 episodios por cada 10,000 diabeticos• Se presenta mas frecuentemente en DM1• Incidencia aun elevada• Mortalidad menor al 5% (100% preinsulina)• La mortalidad como consecuencia propia de
DKA es de un 30% siendo el resto el resultado de comorbilidades como sepsis, enf pulmonar o cardiovascular
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FACTORES DESENCADENANTES
Jarra Albarran texto de endocrinologia
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AGENTE?
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H
Jarra Albarran texto de endocrinologia
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FISIOPATOLOGIA
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FISIOPATOLOGIA
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H
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HISTORIA CLINICA
• Tiempo de evolucion• Poliuria• Perdida de peso • Dolor abdominal
• Polidipsia• Vómitos• Debilidad• Cambios en el estado
mental
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EXAMEN FISICO
• Llenado capilar deficiente
• Deshidratacion • Taquicardia• Hipotension• Choque• Coma
• Kussmaul• Hematemesis• Hipotermia• Aliento a frutas• Alteracion del estado de
conciencia• Buscar causa
desencadenante
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Kitabchi AE ,Ebenezer A . et al. Hyperglycemic crisis in diabetes. Diabetes Care. Endocrinology clinics of North America 2006
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Standard Laboratory Assessment for Patients with Diabetic Ketoacidosis
Plasma glucose
Electrolytes with calculated anion gap and effective osmolality
Phosphorous
Blood urea nitrogen and creatinine, Amylase, Lipase.
Beta-hydroxybutyrate or serum ketones if not available
Complete urinalysis with urine ketones by dipstick
Arterial blood gas or venous pH level if not available
Complete blood count with differential
Electrocardiography
As indicatedBacterial cultures of urine, blood, throat, or other sites of suspected infection
Chest radiography if pneumonia or cardiopulmonary disease is suspected
Magnesium if patient has signs of hypomagnesemia such as cardiac arrhythmias, is alcoholic, or is taking diuretics
Kitabchi AE ,Ebenezer A . et al. Hyperglycemic crisis in diabetes. Diabetes Care. Endocrinology clinics of North America 2006
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DIAGNOSTICO DIFERENCIAL
• Hipoglucemia• Coma hiperosmolar no cetósico• Cetoacidosis alcohólica• Acidosis láctica.• Acidosis hipercloremica.
• Inanición.• Ingestión de drogas como el salicilato, metanol, el
etilenglicol, paraldehyde, metformina.
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TRATAMIENTO
Objetivos principalesCorregir alteraciones metabolicas
- administracion de dosis eficaces de insulina
- aporte adecuado de liquidos y electrolitos
- uso de bicarbonato para corregir acidosis
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INSULINA• Via de administracion• Bolus Intravenoso de 10 U• Infusion de 0.1 U/Kg/Hr (5-10 u/hr)• La meta es una ↓ gradual de la glucosa
de 50-100 mg/dl/hr• Cuando la glucemia ↓ a 250 mg/dl la
infusion debe reducirse a 4U/hr (0.05-0.1 u/kg/hr) y sustituir el suero fisiologico por un dextrosado
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INSULINAGMT BIC INSULINA MANTENIMIENTO UNIDAD SUGERIDO
0-60 APAGADO DW30% 0 0
61-125 APAGADO DW10% 0 0
126-150 1 CC/HR DW5% 1 = 200 mg/dl
151-200 2 CC/HR MIXTO 2 = 200 mg/dl
201-250 4 CC/HR MIXTO 4 3.5
251-300 6 CC/HR SALINO 6 7
301-350 8 CC/HR SALINO 8 7
351-400 10 CC/HR SALINO 10 7
≥ 400 12 CC/HR SALINO 12 7
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INSULINA ESQUEMA LARGO
GMT INSULINA SUGERIDO
0-60 DW30% 0
61-150 0 0
151- 200 2 U
201-250 4 U 3.5-7
251-300 6 U 7-14
301-350 8 U 7-14
351-400 10 U 7-14
≥ 400 12 U 7-14
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FLUIDOTERAPIA• Elemento esencial del Tx• ↓de hiperglucemia y hormonas
contrarreguladoras• Reanimar con salino isotonico excepto
en casos de NaC superior a 150 meq/l (15-20 ml/kg/ primera hora)
• 0.45% Nacl 4-14 ml/kg (280-980cc/hr) • El deficit total de liquidos debe ser
restituido en 12-24 hrs.
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POTASIO• Niveles de K al momento de Dx• Deficit Total calculado en 200-500 meq• El mantenimiento de niveles normales
de K es otro pilar fundamental del Tx• Debe existir diuresis adecuada• Signos de Hiperkalemia en ecg• Concentracion serica menor a 6 meq/lt• Iniciar reposicion a 20 meq/hr
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POTASIO
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BICARBONATO• Controversial• Con pH mayor a 7 el uso de insulina
resuelve cetoacidosis• Riesgo de hipokalemia, edema
cerebral, hipernatremia, sobrecarga V• pH 6.9-7 - 50 mmol en 200 ml de agua
esteril mas 10 meq de kcl durante 1 hr• pH menor 6.9- 100 mmol en 400 ml de
agua esteril + 20 meq de Kcl para 2h
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FOSFATO• Hipofosfatemia severa puede
manifestarse como– Hipercalciuria– ICC– Rabdomiolisis– miopatia
• Reponer si fosfato serico ≤ a 1 mg/dl• 2 mg/kg peso cada 6 horas (93 mg/ml)
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COMPLICACIONES
• Hipoglucemia• Hipocaliemia• Hipofosfatemia• ARDS• Edema cerebral
• Acidosis metabolica refractaria• Choque hipovolemico• Trombosis vascular• Infecciones nosocomiales
J OLIVAR-ROLDÁN. Neumomediastino. ¿Una complicación frecuente en la cetoacidosis diabética? Volumen 53, número 02 de "Endocrinología" Ediciones Doyma, Febrero 2006 .
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GRACIAS