Diabetes Mellitus

Manejo del Paciente Hospitalizado

Dra. Elizabeth Valinotti

El tratamiento de la diabetes en el hospital general, habitualmente se considera de importancia secundaria en comparación con la condición que origina la admisión hospitalaria.

Recientes estudios han centrado la atención sobre la posibilidad que la hiperglucemia en el hospital no es necesariamente una condición benigna y que tratamiento agresivo de la diabetes y la hiperglucemia resulta en la reducción de la mortalidad y la morbilidad. 

Umpierrez GE, Isaacs SD, Bazargan N, You X, Thaler LM, Kitabchi AE: Hyperglycemia: an independent marker of inhospital mortality in patients with undiagnosed diabetes. J Clin Endocrinol Metab 87:978–982, 2002 Van den Berghe G, Wouters P, Weekers F, VerWaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R: Intensive insulin therapy in critically ill patients. N Engl J Med 345:1359–1367, 2001

Cuál es la prevalencia de la Diabetes en pacientes

hospitalizados?

Una encuesta reciente calcula que el 22% de los pacientes hospitalizados por día son diabéticos.

American Diabetes Association. Economiccosts of diabetes in the U.S. in2007. Diabetes Care 2008;31:596–615

Umpierrez et al. informó un 26% la prevalencia de diabetes conocida en pacientes hospitalizados en un hospital docente. 

12% de los pacientes presentaron hiperglucemias durante su internación sin ser conocidos diabeticos.

Umpierrez GE, Isaacs SD, Bazargan N, You X, Thaler LM, Kitabchi AE: Hyperglycemia: an independent marker of inhospital mortality in patients with undiagnosed diabetes. J Clin Endocrinol Metab 87:978–982, 2002

Norhammar et al. (7) estudió 181 pacientes con infarto agudo de miocardio (IAM), consecutivos ingresados la unidad coronaria de dos hospitales en Suecia.  

Pacientes sin diagnóstico de diabetes, y una de glucosa en la sangre de 200 mg / dl al ingreso.

Una prueba de tolerancia a la glucosa standard se realizó al alta y otra vez 3 meses después. Los autores encontraron un 31% la prevalencia de la diabetes en el momento del alta hospitalaria y un 25% de prevalencia de diabetes 3 meses después del alta, en este grupo sin previo diagnóstico de la diabetes.

Norhammar A, Tenerz A, Nilsson G, Hamsten A, Efendic S, Ryden L, Malmberg K: Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study. Lancet 359:2140– 2144, 2002

La atención hospitalaria representa la mitad de los 174 mil millones de dólares que EE.UU. gasta en cuidados médicos para pacintes con diabetes.

American Diabetes Association. Economiccosts of diabetes in the U.S. in2007. Diabetes Care 2008;31:596–615

¿Cúal es el enlace entre la hiperglucemia y las

complicaciones hospitalarias?

Hiperglucemia y sistema inmune

El principal problema ha sido identificado como disfunción fagocitaria de los leucocitos.

Diversos estudios han informado de los defectos en la funcionalidad de los neutrófilos y monocitos en presencia de hiperglucemia, como por ejemplo, la adherencia, quimiotaxis, fagocitosis, muerte bacteriana, respiratorias y de ruptura. 

McManus L, Bloodworth R, Prihoda T, Blodgett J, Pinckard R: Agonist-dependent failure of neutrophil function in diabetes correlates with extent of hyperglycemia.J Leukocyte Biol 70:395–404, 2001

Hiperglucemia y sistema inmune

Se ha demostrado una mejora significativa en la adhesión de los granulocitos cuando la glucosa en sangre en ayunas se redujo de 293 ± 20 a 198 ± 29 mg / dl.

Bagdade JD, Stewart M, Walters E: Impaired granulocyte adherence. A reversible defect in host defense in patients with poorly controlled diabetes. Diabetes 27:677–681, 1978

Hiperglucemia y sistema inmune

Las complicaciones microvasculares clásicas de la diabetes son causadas por alteraciones en la vía de las aldosa reductasa aldose, vía de las especies reactivas de oxígeno, y la víade la proteína C quinasa (PKC).

Varias de estas vías puede contribuir a la disfunción inmune.

Sheetz M, King G: Molecular understandingof hyperglycemia’s adverse effectsfor diabetic complications. JAMA288:2579–2588, 2002

Hiperglucemia y sistema cardiovascular La Hiperglucemia aguda tiene numerosos 

efectos sobre el sistema cardiovascular.

Hiperglucemia perjudica una precondición isquémica. 

El tamaño del infarto de miocardio aumenta en presencia de hiperglucemia. 

El flujo de las colaterales coronarias disminuye en presencia de hiperglucemia grave.

La hiperglucemia aguda puede inducir apoptosis miocitos

cardiacos. 

Kersten J, Toller W, Tessmer J, Pagel P,Warltier D: Hyperglycemia reduces coronarycollarteral blood flow through anitric oxide-mediated mechanism. Am JPhysiol 281:H2097–H2104, 2001

Ceriello A, Quagliaro L, D’Amico M, DiFilippo C, Marfella R, Nappo F, BerrinoL, Rossi F, Giugliano D: Acute hyperglycemiainduces nitrotyrosine formationand apoptosis in perfused heart from rat.Diabetes 51:1076–1082, 2002

Hiperglucemia y sistema cardiovascular

Otras consecuencias vasculares de la hiperglucemia aguda hospitalaria son: cambios de la presión arterial,  elevaciones de catecolaminas, las anomalías de la función plaquetaria Cambios electrolíticos

Hiperglucemia y trombosis

Estudios pacientes con diabetes tipo 2 han demostrado la hiperactividad plaquetaria que se demuestra por el aumento de la biosíntesis de tromboxano. 

Biosíntesis de tromboxano  disminuye con la reducción en la sangre glucosa.

Hiperglucemia induce elevaciones de la interleuquina (IL) -6, niveles elevados de la misma han sido vinculado a las altas concentraciones de fibrinógeno plasmático.

Davi G, Catalano I, Averna M, NotarbartoloA, Strano A, Ciabattoni G, PatronoC: Thromboxane biosynthesis and plateletfunction in type II diabetes mellitus.N Engl J Med 322:1769–1774, 1990

Morohoshi M, Fujisawa K, Uchimura I,Numano F: Glucose-dependent interleukin6 and tumor necrosis factor productionby human peripheral bloodmonocytes in vitro. Diabetes 45:954–959, 1996

Hiperglucemia y trombosis

La Hiperglucemia también causa: aumento de las concentraciones plasmáticas del

factor y el antígeno de von Willebrand 11 -- dehidro-tromboxano B2 (una medida de 

la producción de tromboxano A2).

Estos los cambios no fueron vistos en el estado euglucemico.

Hiperglucemia e Inflamación

En humanos, la elevación moderada de la glucosa a 270 mg/dl (15 mmol/l) ha sido asociada con un incremento marcado de IL-6, IL-18, and TNF.

Esposito K, Nappo F, Marfella R, GiuglianoG, Giugliano F, Ciotola M, QuagliaroL, Ceriello A, Giugliano D: Inflammatorycytokine concentrations areacutely increased by hyperglycemia inhumans: role of oxidative stress. Circulation106:2067–2072, 2002

Hiperglucemia e Inflamación En humanos, los niveles de TNF están elevados en

el IAM y se correlacionan con la disfunción cardiaca.

TNF tambien está relacionado con el daño que ocurre en la isquemia renal y en la insuficiencia carcdiaca congestiva.

IL-18 ha sida propuesta como un desestabilizador de las placas ateroscleroticas, llevando a los sindromes isquemicos agudos.

Meldrum DR, Dinarello CA, Shames BD,Cleveland JC, Jr., Cain BS, Banerjee A,Meng X, Harken AH: Ischemic preconditioningdecreases postischemic myocardialtumor necrosis factor-alphaproduction: potential ultimate effectormechanism of preconditioning. Circulation98:II214–II218; discussion II218–II219, 1998

Hiperglucemia y disfunción endotelial

En un estado saludable, el endotelio vascular mantiene a la vasculatera en un estado quiescente, relajado, antitrombótico, antioxidante y antiadhesivo.

Marfella R, Quagliaro L, Nappo F, CerielloA, Giugliano D: Acute hyperglycemiainduces an oxidative stress inhealthy subjects. J Clin Invest 108:635–636, 2001

Hiperglucemia y disfunción endotelial

En estudios in vivo en Humanos utilizando estos parametros confirman que la hiperglucemia aguda en niveles comumente observados en los hospitales (142–300 mg/dl) causan disfunción endotelial.

Beckman J, Goldfine A, Gordon M,Creager M: Ascorbate restores endothelium-dependent vasodilation impairedby acute hyperglycemia in humans. Circulation103:1618–1623, 2001

Hiperglucemia y disfunción endotelial

La hiperglucemia puede afectar directamente la función celular endotelial mediante la inactivación química del óxido nítrico.

Otros mecanismos incluyen la activación de la producción de especias reactivas de oxigeno (ROS).

Brodsky SV, Morrishow AM, Dharia N,Gross SS, Goligorsky MS: Glucose scavengingof nitric oxide. Am J Physiol RenalPhysiol 280:F480–F486, 2001

Hiperglucemia y cerebro

En Humanos, Parsons et al. ha demostrado que la relación lactato colina (ratio) determinada por RM por espectroscopia de protones tiene valor prediciendo los resultados clínicos y el tamaño final de un infato agudo (stroke).

Tambien se ha demostrado que existe correlación positiva entre la elevación de la glucemia y la producción de lactato. A traves de este mecanismo parece que la hiperglucemia cause un riesgo de hipoperfusión en el tejido y una progresión del infarto.

Parsons MW, Li T, Barber PA, Yang Q,Darby DG, Desmond PM, Gerraty RP,Tress BM, Davis SM: Combined (1)H MRspectroscopy and diffusion-weightedMRI improves the prediction of strokeoutcome. Neurology 55:498–505, 2000

Parsons M, Barber P, Desmond P, BairdT, Darby D, Byrnes G, Tress B, Davis S:Acute hyperglycemia adversely affectsstroke outcome: a magnetic resonanceimaging and spectroscopy study. AnnNeurol 52:20–28, 2002

Potential relationships between metabolic stress, hyperglycemia, hypoinsulinemia, and poor hospital outcomes

RECOMMENDATIONS

SSI

A topic that deserves particular attention is the persistent overuse of what has been branded as sliding scale insulin (SSI) for management of hyperglycemia.

The term “correction insulin,” which refers to the use of additional short- or rapidactinginsulin in conjunction with scheduled insulin doses to treat BG levels above desired targets, is preferred .

Prolonged therapy with SSI as the sole regimen is ineffective in the majority of patients (and potentially dangerous in those with type 1 diabetes).

Umpierrez GE, Smiley D, Zisman A, etal. Randomized study of basal-bolus insulintherapy in the inpatient managementof patients with type 2 diabetes(RABBIT 2 trial). Diabetes Care 2007;30:2181–2186

Umpierrez GE, Palacio A, Smiley D.Sliding scale insulin use: myth or insanity?Am J Med 2007;120:563–567

Critically ill patients

Insulin therapy should be initiated for treatment of persistent hyperglycemia, starting at a threshold of no greater than180 mg/dl.

Once insulin therapy has been started,a glucose range of 140 –180 mg/dl is recommended for the majority of critically ill patients.

Critically ill patients

Intravenous insulin infusions are thepreferred method for achieving and maintaining glycemic control in critically ill patients.

Validated insulin infusion protocols with demonstrated safety and efficacy, and with low rates of occurrence of hypoglycemia, are recommended.

With IV insulin therapy, frequent glucose monitoring is essential to minimize the occurrence of hypoglycemia and to achieve optimal glucose control.

Noncritically ill patients

For the majority of noncritically ill patients treated with insulin, the premeal BG target should generally be 140 mg/dl in conjunction with random BG values 180 mg/dl, provided these targets can be safely achieved.

More stringent targets may be appropriate in stable patients with previous tight glycemic control.

Less stringent targets may be appropriate in terminally ill patients or in patients with severe comorbidities.

Scheduled subcutaneous administration of insulin, with basal, nutritional, and correction components, is the preferred method for achieving and maintaining glucos control.

Prolonged therapy with SSI as the sole regimen is discouraged.

Noninsulin antihyperglycemic agents are not appropriate in most hospitalized patients who require therapy for hyperglycemia.

Safety issues Overtreatment and undertreatment of hyperglycemia represent

major safety concerns. Education of hospital personnel is essential in engaging the

support of those involved in the care of inpatients with hyperglycemia.

Caution is required in interpreting results of POC glucose meters in patients with anemia, polycythemia, hypoperfusion, or use of some medications.

Buy-in and financial support from hospital administration are required for promoting a rational systems approach to inpatient glycemic management

Discharge planning

Preparation for transition to the outpatient setting should begin at the time of hospital admission.

Discharge planning, patient education, and clear communication with outpatient providers are critical for ensuring a safe and successful transition to outpatient`glycemic management.

The importance of glycemic control onoutco me is not limited to patients in critical care areas but also applies to patients admitted to general surgical and medical wards. In such patients, the presence of hyperglycemia has been associated with prolonged hospital stay, infection, disability after hospital discharge, and death

In general surgery patients, the relative risk for serious postoperative infections (sepsis, pneumonia, and wound infection) increased 5.7-fold when any postoperative day 1 blood glucose was 220 mg/dl

Goldberg PA, Siegel MD, Sherwin RS,Halickman JI, Lee M, Bailey VA, Lee SL,Dziura JD, Inzucchi SE: Implementationof a safe and effective insulin infusion protocol in a medical intensive care unit. Diabetes Care 27:461– 467, 2004

OBJECTIVE

Study the optimal management of hyperglycemia in non– intensive care unit patients with type 2 diabetes, as few studies thus far have focused on the subject.

RESEARCH DESIGN AND METHODS

a prospective, multicenter, randomized trial to compare the efficacy and safety of a basal-bolus insulin regimen with that of sliding-scale regular insulin (SSI) in patients with type 2 diabetes.

RESEARCH DESIGN AND METHODS

RESEARCH DESIGN AND METHODS

RESEARCH DESIGN AND METHODS

RESEARCH DESIGN AND METHODS

The primary end point was to determine differences in glycemic control between treatment groups as measured by the mean daily blood glucose concentration.

Secondary outcomes include differences between treatment groups in number of hypoglycemic events, number of episodes of severe hyperglycemia, length of hospital stay, and mortality rate.

Results

Results

The most common admitting illnesses included a variety of cardiovascular (40%), infectious (20%), pulmonary (18%), renal (4%), and gastrointestinal (12%) disorders.

Results

The mean hospital length of stay was 5.3 ± 6 days in patients treated with basal-bolus and 5.1± 4 days in the SSItreated group (P NS)

Results

Only one death was reported in a patient in the basalbolus treatment group who was admitted with shortness of breath and later developed respiratory failure secondary to a pulmonary embolism.

Results

Results

The mean admission blood glucose for study patients was 227 ± 65 mg/dl and the mean A1C 8.8 ± 2%.

Results

The percentage of patients within the mean glucose target (140 mg/dl) was 66% in patients treated with glargine and glulisine versus 38% in those treated with SSI

Results

Nine (14%) patients treated with SSI remained with blood glucose 240 mg/dl despite increasing the SSI dose to the maximal or insulin-resistant scale.

Glycemic control rapidly improved in all of the SSI failure subjects after they were switched to the basal-bolus insulin regimen.

Results

The meandaily dose of insulin glargine was

22 ±2units, and the daily dose of insulin glulisine was 20± 1 units.

A total of 26 patients had the lantus dose adjusted, and 44 patients required supplemental glulisine insulin during the hospital stay.

Patients treated with SSI received a mean daily dose of 12.5 2 units regular insulin/ day, with approximately one-half of patients receiving 10 units/day.

Results

Hypoglycemia (defined as blood glucose 60 mg/dl) occurred in two patients in each treatment group.

Conclusions

We observed that treatment with insulin glargine and glulisine results in a significant improvement in glycemic control compared with that resulting from the sole use of SSI.

The mean daily glucose difference between groups ranged from 23 to 58 mg/dl during days 2–6 of therapy.

Conclusions

Differences in glycemic control between treatment groups can be explained by the fact that an SSI regimen treats hyperglycemia after it has already occurred instead of preventing the occurrence of hyperglycemia.

objetivo

Studies comparing the use of basal bolus with insulin analogs vs. split-mixed regimens with human insulins in hospitalized patients with type 2 diabetes are lacking.

a controlled multicenter trial, we randomized 130 nonsurgical patients with blood glucose (BG) between 140 and 400 mg/dl to receive detemir once daily and aspart before meals (n 67) or neutral protamine Hagedorn (NPH) and regular insulin twice daily (n 63).

Insulin dose was started at 0.4 U/kg d for BG between 140 and 200 mg/dl or 0.5 U/kg d for BG 201-400 mg/dl.

Insulin treatment protocols

Insulin treatment protocols

Insulin treatment protocols

The goal of insulin therapy was to maintain premeal and bedtime BG levels lower than 140 mg/dl while avoiding hypoglycemia.

The primary outcome of the study was to determine differences in glycemic control between treatment groups as measured by mean daily BG concentration during the hospital stay.

Secondary outcomes include differences between treatment groups in premeal and bedtime glucose levels, number of hypoglycemic events, length of hospital stay, and mortality rate.

Results

A total of 130 subjects with type 2 diabetes were recruited. After

randomization, 67 patients received insulin detemir once daily and insulin aspart before meals, and 63 patients received splitmixed regimen with NPH and regular insulin twice daily.

Results

Results

Admitting illnesses included a variety of cardiovascular (35%), infectious (15%), pulmonary (12%), and gastrointestinal (14%) conditions.

The mean hospital length of stay was 6.5 7 d in patients treated with detemir plus aspart and 7.1 7 d in the NPHplus regular group Pnot significant (NS). There was no mortality reported in this trial.

Results

The mean admission glucose levels in the detemir/aspart and NPH/regular insulin treatment groups were 230±102 and 231±145 mg/dl, respectively (P: NS).

Results

Results

Nineteen patients (28.4%) in the detemir/aspart group had a BGbetween 40 and 59 mg/dl, and three patients (4.5%) had a BG below 40 mg/dl.

Fifteen patients in the NPH/regular group (23.8%) had a BG of 40–59 mg/dl, and one patient (1.6%) hada BG below 40 mg/dl (P0.20 vs. detemir/aspart group).

Discussion BG target below 140 mg/dl before meals was

achieved in less than half of patients in both treatment regimens, and approximately 30% of patients experienced one or more episodes of hypoglycemia during the hospital stay.

These results indicate that the basal/bolus regimen with detemir once daily and aspart before meals results in equivalent glycemic control with no significant differences in the frequency of hypoglycemia compared with a twice daily split-mixed human insulin regimen with NPH and regular insulin in patients with type 2 diabetes.

Discussion

The American Diabetes Association recently recommended a level below 70 mg/dl to define hypoglycemia.Using this definition, we observed that 24 patients (38%) in the NPH/regular insulin group and 29 patients (43%) in the detemir/aspart group had at least one episode of hypoglycemia (P 0.67) during the hospital stay.

Discussion

A BGtarget below 140 mg/dl was achieved in 66%of patients in the glargine plus glulisine group and 38% in the sliding-scale group. Only two patients (3%) in the glargine/glulisine group and in the sliding-scale regimen developed a BG below 60 mg/dl, and no patients had a BG below 40 mg/dl during the hospital stay.

Discussion

In this study, the frequency of hypoglycemiawith detemir/aspart and NPH/regular insulin was higher than that reported with the use of glargineandglulisine in the Rabbit-2 trial.

Discussion

In this study, less than half of patients in either treatment group achieved a target BG below 140 mg/dl before meals.

Discussion

The relatively low rate of BG readings within target could be the result of a relatively high rate of hypoglycemic events, or in the case of detemir because the algorithm did not include an option for twice daily dosing of insulin detemir. Based on the reported pharmacodynamic profile of detemir (about 16-h duration, and a peak from 4–8 h), the use of detemir twice daily may have facilitated a more rapid insulin dose titration resulting in further improvements in glycemic control.

IDENTIFICACIÓN CLARA DE LOS PACIENTES CON DIABETES

CONTROL DE GLUCEMIA A TODOS LOS PACIENTES QUE INGRESAN AL HOSPITAL

Glucemia ≥ 140 mg/dl sin historia de Diabetes, MONITORIZAR POR 24 A 48 HS Y TRATAR SI

FUERA NECESARIO

Paciente con CORTICOIDES U OCTREOTIDE, NUTRICIÓN ENTERAL O PARENTERAL , deben ser monitorizados por 24 a 48 hs despues el inicio

del tto. Si es ≥ requiere seguir con los controles e instaurar

terapeútica

Pacientes con DM o hiperglucemia (mayor ≥

GLUCEMIA CAPILAR COMO GUÍA DEL MANEJO INDIVIDUAL DE LOS PACIENTES

GLUCOMETROS QUE SEAN CONFIABLES

CONTROLES DE GLUCEMIA CAPILAR PRE PRANDIALES Y ANTES DE DORMIR EN LOS QUE SE ALIMENTAN.

CONTROLES DE GLUCEMIA EN PCTES QUE NO SE ALIMENTEN CONTROLES DE GLUCEMIA CAPILAR CADA 4-6 HS

OBJETIVO PRE PRANDIAL: < 140 mg/dlAL AZAR: < 180 mg/dl

PACINTES NO CRÍTICOS HOSPITALIZADOS

GLUCEMIA < 200 mg/dl en Pacientes con: Enfermedad terminal

Expectativa de Vida Pequeña Riesgo de hipoglucemia

PARA EVITAR HIPOGLUCEMIAS, REEVALUAR LA TERAPIA CUANDO LAS GLUCEMIAS SEAN < 100 MG/DL

MODIFICACION NECESARIA SI LA GLUCEMIA <70 MG/DL

NECESITAMOS NUTRICIONISTAS EN LA INTERNACIÓN

Las comidas del hospital deben contener una cantidad consistente de carbohidratos en cada comida que sea util para coordinar la dosis de la

insulina de acción rápida

LA INSULINA ES LA TERAPIA PREFERIDA COMO METODO PARA

ALCANZAR LOS CONTROLES GLUCEMICOS EN PACIENTES

HOSPITALIZADOS

DISCONTINUAR LOS ANTIDIABETICOS ORALES E INICIAR INSULINA EN LOS DM2 INTERNADOS POR UNA ENFERMEDAD AGUDA

EVALUAR Y CAMBIAR LA DOSIS DE INSULINA QUE YA RECIBIA EL PACIENTE EN SU CASA A FIN DE DISMINUIR EL RIESGO DE

HIPOGLUCEMIAS

LOS QUE YA RECIBIAN INSULINA EN SU CASA DEBEN SEGUIR RECIBIENDO INSULINA SUBCUTÁNEA EN EL

HOSPITAL

NO USAR LA ESCALA MOVIL DE INSULINA COMO TERAPIA UNICA PARA ALCANZAR EL CONTROL

GLUCEMICO DURANTE LA INTERNACION EN PACIENTES CON

DIABETES

IMPLEMENTAR: INSULINA BASAL (1 O 2 VECES) +

INSULINA RÁPIDA O ULTRARRÁPIDA PRE PRANDIALES

LAS CORRECCIONES CON INSULINA DEBEN SER INCLUIDAS EN EL ESQUEMA INSULINICO

RESTITUIR EL ESQUEMA PRE INTERNACIÓN EN PACIENTES CON CONTROL ACEPTABLE EN LA

PRE ADMISIÓN SIN CONTRAINDICACIONES PARA LA CONTINUACIÓN DEL ESQUEMA

ANTERIOR

Se sugiere que la insulina se instaure al menos un día antes del alta para parmitir evaluar la eficacia y

la seguridad de esta transición

Entregar INDICACION ESCRITA Y EXPLICAR VERBALMENTE, todo lo referente al

manejo glucémico.

LA INDICACIÓN DEBE ESTAR ESCRITA DE MANERA ENTENDIBLE PARA LA PERSONA QUE VA

A ADMINISTRAR LA MEDICACIÓN

EN PACIENTES QUE RECIBIAN INFUSIÓN CONTINUA DE INSULINA, INICIAR EL ESQUEMA SUCRUTANEO 1 – 2 HS ANTES DE LA

DISCONTINUACIÓN DEL GOTEO

USAR UN ESQUEMA DE INSULINA SUB CUTÁNEA EN PACIENTES QUE RECIBEN INFUSIÓN CONTÍNUA DE INSULINA SIN

HISTORIA PREVIA DE DIABETES PERO QUE HAYAN REQUERIDO MÁS DE 2 UI/HORA

CONTROLES DE GLUCEMIA CAPILAR LUEGO DE LA DISCONTINUADCIÓN DE LA INFUSIÓN CONTINUA DE INSULINA

CONTROLAR LA GLUCEMIA CAPILAR EN PACIENTES QUE RECIBEN NUTRICION

PARENTERAL O ENTERAL

INICIAR INSULINA EN PACIENTES DIABETICOS CONOCIDOS Y EN AQUELLOS QUE NO SE CONOCEN PERO CON GLUCEMIAS > 140

MG/DL, QUE DEMOSTRARON UN REQUERIMIENTO PERSISTENTE (> 12 - 24 HS ) DE CORRECCIONES CON INSULINA.

TODOS LOS PACIENTES CON DM1 QUE SERÁN SOMETIDOS A UN PROCEDIMIENTO QUIRURGICO (MAYOR O MENOR) DEBEN RECIBIR INFUSIÓN O

INSULINA SC BASA CON BOLOS PARA PREVENIR LA HIPERGLUCEMIA EN EL PERIODO PERIOPERATORIO

DISCONTINUAR LA TERAPIA ANTIDIABÉTICA NO INSULINICA ANTES DE LA CIRUGIA CON

INICIO DE INSULINA EN LOS QUE DESARROLLAN HIPERGLUCEMIA DURANTE EL

PERIODO PERIOPERATORIO

CUANDO SE INSTITUYE LA TERAPIA SC CON INSULINA EN EL POST OPERATORIO.

USAR INSULINA BASAL (PARA LOS PACIENTES NPO) o BASAL BOLUS (para paciente que comen).

CONTROL DE GLUCEMIA CAPILAR EN PACIENTES QUE RECIBEN CORTICOIDES.

CON O SIN HISTORIA DE DIABETES

DISCONTINUAR EL CONTROL DE GLUCEMIA CAPILAR SI ESPUES DE 24 – 48 HS NO EXISTIERA HIPERGLUCEMIA (GLUCEMIAS MENORES A 140

MG/DL)

INICIAR INSULINA EN LOS PACIENTES CON HIPERGLUCEMIA PERSISTENTE QUE

RECIBEN TERAPIA CON GLUCOCORTICOIDES

USAR INFUSIÓN CONTÍNUA COMO ALTERNATIVA A LA INSULINA SC EN LOS PACIENTES CON GLUCEMIA CAPILAR ELEVADA A PESAR DE UN ESQUEMA

BASAL BOLUS SC

PREPARAR PROTOCOLOS CON DIRECCIONES ESPECÍFICAS PARA EVITAR Y MANEJAR LAS HIPOGLUCEMIAS EN EL HOSPITAL

IMPLEMENTAR UN PROTOCOLO QUE DEBE SER INICIADO POR ENFERMERIA INMEDIATAMENTE UNA VEZ RECONOCIDA UNA HIPOGLUCEMIA (DEFINIDA

COM GLUCEMIA POR DEBAJO DE 70 MG/DL)

INSTAURAR UN PLAN DE BUSQUEDA DE LA FRECUENCIA DE EVENTOS

HIPOGLUCEMICOS CON ANALISIS DE SUS CAUSAS Y LOS EVENTOS ASOCIADOS CON

EL DAÑO POTENCIAL AL PACIENTE

IMPLEMENTAR UN COMITE INTERDISCIPLINARIO PARA MEJORAR EL CUIDADO DE PACIENTES CON DIABETES

CADA INSTITUCIÓN DEBERÍA TENER UN METODO DE COLECCIÓN Y EVALUACIÓN DE LAS GLUCEMIAS CAPILARES Y LA INSULINA Y

UTILIZAR ESA INFORMACIÓN COMO MANERA DE MONITORIZAR LA SEGURIDAD Y EFICACIA DEL CONTROL GLUCÉMICO

LAS INSTITUCIONES DEBEN PROVEER GLUCOMETROS EFICACES Y EXACTOS

Muchas Gracias