Diabetic ketoacidosis/es: Difference between revisions
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====Gasometría==== | |||
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''No es necesario realizar una gasometría arterial. La gasometría venosa es suficiente<ref>Ma OJ, Rush MD, Godfrey MM, Gaddis G. Arterial blood gas results rarely influence emergency physician management of patients</ref>'' | |||
''No | *La diferencia en el pH entre la gasometría venosa (VBG) y la gasometría arterial (ABG) será de ±0,02 unidades de pH<ref>Kelly AM et al. Review Article – Can Venous Blood Gas Analysis Replace Arterial in Emergency Medical Care. Emery Med Australas 2010; 22: 493 – 498.</ref><ref>Ma OJ et al. Arterial Blood Gas Results Rarely Influence Emergency Physician Management of Patients with Suspected Diabetic Ketoacidosis. Acad Emerg Med Aug 2003; 10(8): 836 – 41. </ref> <ref name="British DKA">Savage MW, Datary KK, Culvert A, Ryman G, Rees JA, Courtney CH, Hilton L, Dyer PH, Hamersley MS; Joint British Diabetes Societies. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med. 2011 May;28(5):508-15.</ref><ref>Gokel Y, et al. Comparison of Blood Gas and Acid-Base Measurements in Arterial and Venous Blood Samples in Patients with Uremic Acidosis and Diabetic Ketoacidosis in the Emergency Room. American Journal of Nephrology 2000; 20:319-323.</ref> | ||
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Revision as of 21:08, 15 January 2026
This page is for adult patients. For pediatric patients, see: diabetic ketoacidosis (peds)
Antecedentes
- Los pacientes con Cetoacidosis Diabética (DKA) casi siempre tienen depleción de K+ a pesar de tener inicialmente un K+ bastante normal.
- Esto se debe al desplazamiento extracelular de K+ debido a la acidosis, así como a la infusión de insulina, que aumenta la absorción de K+ de forma intracelular.
Epidemiología
- Tasa de mortalidad aproximadamente 2-5%[1]
Fisiopatología
Las características definitorias incluyen hiperglucemia (glucosa > 200mg/dl), acidosis (pH < 7.3), y cetonemia
Hiperoglucemia
- Conduce a diuresis osmótica y depleción de electrolitos, incluyendo sodio, potasio, magnesio, calcio y fósforo.
- La deshidratación adicional altera la tasa de filtración glomerular (TFG) y contribuye a la insuficiencia renal aguda
- La hipocalemia puede inhibir la liberación de insulina
Acidosis
- Debido a la deficiencia de insulina -> lipólisis / acumulación de cetoácidos (representada por un aumento en el espacio aniónico)
- Alcalosis respiratoria compensatoria (es decir, taquipnea e hiperventilación - respiración de Kussmaul)
- La descomposición de la grasa adiposa crea primero acetoacetato, que conduce a la conversión a beta-hidroxibutirato
Deshidratación
- Causa la activación del SASRA además de la diuresis osmótica
- Los valores iniciales del suero para electrolitos como K+ pueden ser más altos que las reservas corporales reales
- La pérdida de cationes (a cambio de cloruro) empeora la acidosis metabólica
Características Clínicas
- May be the initial presenting of an unrecognized T1DM patient
- OR symptoms/signs of inciting precipitant (e.g. history of med/dietary nonadherence, signs/symptoms of infection)
- Presenting features may include:
- Polydipsia, polyuria (initially) or decreased urine output (as volume depleted)
- Signs of dehydration (dry mouth, dry mucosa, etc.), hypotension
- +/- Weight loss
- Abdominal pain, nausea/vomiting
- Tachypnea (Kussmaul's breathing)
- Acetone or fruity smell on breath
- Generally ill-appearance
- Altered mental status, drowsiness with decreased reflexes
- Cerebral edema increases mortality significantly, especially in children
Diagnóstico Diferencial
Causas de la Cetoacidosis Diabética
- Insulina o no cumplimiento de la medicación hipoglucémica oral (o falla de la bomba de insulina)
- Infección
- Isquemia cardíaca
- Infecciones intraabdominales
- Esteroides
- Abuso de ETOH
- Exposición toxicológica
- Embarazo
- Hiperthyroidismo
- Hemorragia gastrointestinal
- Accidente cerebrovascular
- Embolia pulmonar
- Pancreatitis
- Insuficiencia renal
- Hemorragia gastrointestinal
- Cetoacidosis alcohólica
- Inhibidores de SGLT-2 (cetoacidosis diabética euglicémica)
Hyperglycemia
- Physiologic stress response (rarely causes glucose >200 mg/dL)
- Diabetes mellitus (main)
- Hemochromatosis
- Iron toxicity
- Sepsis
Evaluación
Evaluación
Estudio para confirmar el diagnóstico y buscar posibles causas desencadenantes (por ejemplo, infección, ACS)
- Hematocrito completo (CBC)
- Bioquímica metabólica básica (BMP)
- Glucosa en sangre
- Cetonas en suero (por ejemplo, beta-hidroxibutirato y/o acetona)
- Magnesio (Mag)
- Fósforo (Phos)
- Gasometría venosa (VBG)/Gasometría arterial (ABG)
- Considerar ECG, análisis de orina, radiografía de tórax, cultivos de sangre
Prónostico
El diagnóstico se realiza en base a la presencia de acidosis (por ejemplo, pH venoso < 7,3 o HCO3 <18) y cetonemia (por ejemplo, >3mmol/L BOH o cetonuria) en el contexto de diabetes (por ejemplo, glucosa >200mg/dl) [2]
Hallazgos de Laboratorio Básicos
- Glucosa en sangre
- Azúcar en sangre capilar >200mg/dL
- La glucosa en sangre puede no estar muy elevada si hay una gluconeogénesis deteriorada (por ejemplo, insuficiencia hepática, alcoholismo severo) o el paciente está tomando un Inhibidor de SGLT-2 [3]
- Intervalo aniónico elevado
- El bicarbonato puede ser normal debido a la alcalosis compensatoria y de contracción, por lo que el intervalo aniónico elevado o la cetonuria pueden ser las únicas pistas para la CDA
- Cetonas en suero
- El beta-hidroxibutirato estará elevado
Gasometría
No es necesario realizar una gasometría arterial. La gasometría venosa es suficiente[4]
- La diferencia en el pH entre la gasometría venosa (VBG) y la gasometría arterial (ABG) será de ±0,02 unidades de pH[5][6] [7][8]
Urinary analysis (ketonuria)
- Urinalysis may be a useful screening test early in DKA, if serum ketones not available
- However, may give a false negative for ketones later in DKA, as acetoacetate is converted to beta-hydroxybutyrate the urinary ketones may turn negative[9]
End Tidal CO2
Strongly consider capnography for respiratory distress[10]
- ETCO2 can be used for bedside assessment of DKA in pts with glucose>550[11]
- An ETCO2 of ≥35 is 100% sensitive to rule out DKA
- An ETCO2 of ≤21 is 100% specific to diagnosis DKA
Management
- If the patient has an insulin pump, make sure it is shut off or disconnected
Volume Repletion
- Administer 20-30cc/kg lactated ringers bolus during the first hour
- Most important step in treatment since osmotic diuresis is the major driving force[7]
- Most adult patients are 3-6L depleted
- Increased systemic perfusion may transport insulin to previously unreached receptor sites, inhibiting ketogenesis
- Increased renal perfusion promotes renal hydrogen ion loss
- Use of LRs is preferred over NS [12],[13]
- When blood sugar(BS) < 250-300 add a D10 infusion at an equal rate to the LR using a single IV line [14]
- Patients can eat and drink if mental status is intact [15]
- Potassium (most important!)[16]
- <3.5mEq/L:
- Start potassium repleation: 20-30 mEq KCl to IVF/hr
- Do not administer insulin (to avoid worsening of hypokalemia)
- >3.5mEq/L and <5.5 mEq/L:
- Start potassium repleation: 20-30 mEq KCl to IVF/hr
- May start insulin (see below)
- >5.5 mEq/L:
- Hold potassium repletion and recheck electroltyes after initiaton of insulin (see below)
- <3.5mEq/L:
- Sodium
- Hyponatremia
- Correct for hyperglycemia
- Na+ decreases by 1.6mEq/L for every 100mg/dL increase in glucose (ie pseudohyponatremia)
- If truly hyponatraemic, start NS 250-500ml/hr
- Correct for hyperglycemia
- Hypernatremia
- Consider Lactated Ringers
- Hyponatremia
- Hypophosphatemia
- <1.0 mEq/L, start repletion:
- IV K2PO4 at 1mL/hour (contains 4.4meqK+ & 93mg phos)
- Severe hypophosphatemia can cause cardiac and respiratory dysfunction
- <1.0 mEq/L, start repletion:
- Hypomagnesemia
- Mg<2.0mg/DL, start repletion:
- 2g MgSO4 IV over 1h
- Mg<2.0mg/DL, start repletion:
Insulin Overview
- Check potassium prior to insulin treatment (see above)! Do not administer insulin until potassium supplementation is underway.[17]
- A bolus dose is unnecessary and may contribute to increased hypoglycemic episodes[18]
- If the patient comes in wearing an insulin pump, turn off the pump and remove the subcutaneous catheter.
- Expect BS to fall by 50-100mg/dL per hr if you administer 0.1units/kg/hr of insulin
- Refractory hyperglycemia may be due to an associated infectious process contributing to the DKA
Long-Acting (Basal) Insulin
- Two main practices exist: 1) Close the anion gap, then start basal insulin 2-3 hours before stopping insulin infusion, 2) Early basal insulin
- Potential benefits of early basal insulin (glargine or detemir) include protecting against erroneously stopping insulin infusion prematurely and eliminating the 2-3 hour waiting period of starting basal insulin while on IV infusion
- Early basal insulin:[19]
Short-Acting Insulin
Intravenous Regimen (Short-Acting)
Do not stop insulin infusion until AG normalized AND bicarb normalized, despite resolution of blood sugar. Aim of insulin regime is to correct the acidosis, not merely the hyperglycemia.
- Initial infusion 0.1 to 0.14 units/kg/hr of insulin (or 0.05units/kg/hr per local protocol)
- Maintain BS between 150 and 200mg/dL until resolution of acidosis
- May require IV fluids to be switched to Dextrose 10% when BS <150mg/dL
- Continue IV infusion for 2 hrs after subcutaneous insulin is begun
- Subcutaneous route (appropriate only for mild DKA and if able to eat and void urine; poor perfusion may hamper its absorption)
Subcutaneous Regimen (Short-Acting)
A subcutaneous (SC) regimen must use short acting insulin and follow either a 1hr or 2hr dosing protocol. Regular insulin is not effective.[25] For patients who are euglycemic (glucose <250 mg/dl) at presentation (e.g. with mild gap), using standard insulin sliding scale instead of this regimen.[26] [27]
1hr Protocol
- Initial dose SC short acting insulin (e.g. Aspart): 0.3 units/kg ideal body weight, followed by
- 0.1 units/kg SC every hour
- When blood glucose <250mg/dl (13.8 mmol/l), change IV fluids to D5<sub 0.45%NS and reduce SC aspart insulin to 0.05 units/kg/hr
- Keep glucose at 150mg/dl (11 mmol/l) until resolution of DKA.
2hr Protocol
- Initial dose SC short acting insulin (e.g. Aspart): 0.3 units/kg ideal body weight, followed by
- 0.2 units/kg SC 1 hour later followed by Q2hr dosing
- When blood glucose <250mg/dl (13.8 mmol/l), change IV fluids to D5 0.45% saline and reduce SC insulin to 0.1 units/kg/ 2hr
- Keep glucose at 150mg/dl (11 mmol/l) until resolution of DKA.
- No evidence supports the use of sodium bicarb in DKA, with a pH >6.9
- However, no studies have been performed for patients with pH <6.9 and the most recent ADA guidelines recommend it for patients with pH <7.1
- Pitfalls of sodium bicarbonate therapy in DKA (outside of last ditch efforts in severe acidemia)[29]
- Paradoxical CSF acidosis
- Hypokalemia from H+ and K+ shifts
- Large sodium bolus
- Cerebral edema
- Shifts oxygen-hemoglobin dissociation curve to left, decreasing O2 delivery to tissues
Subsequent Management
Labs/Monitoring
- Glucose check Q1hr
- Chem 10 Q2r (then move to Q4hr)
- Check pH PRN based on clinical status (eval respiratory compensation)
- Check appropriateness of insulin dose Q1hr (see below)
- Corrected Electrolytes
Sliding Scale
- Insulin Sliding Scale to be started once patient's DKA has resolved and eating a full diet.
- Avoid intubation unless patient cannot generate respiratory alkalosis compensation due to extreme fatigue[30]
- Risks associated with intubation in DKA:
- During sedation/paralysis, a rise in PaCO2 can decrease pH considerably
- Severe gastroparesis in DKA creates a significant risk for aspiration
- Strong DKA patients generally can achieve greater hyperventilation than mechanical ventilated patients
- See Intubation for more information
Disposition
- Admit to higher level care (usually ICU or step-down unit initially)
- Subsequent hospital discharge requires closing on anion gap and resolution of symptoms.
- Patients with mild DKA may be treated as outpatients if reliable, close follow-up available and underlying causes not requiring admission
Complications
See Also
External Links
References
- ↑ Lebovitz HE: Diabetic ketoacidosis. Lancet 1995; 345: 767-772.
- ↑ Glaser N, Fritsch M, Priyambada L, et al. ISPAD clinical practice consensus guidelines 2022: Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes 2022; 23:835.
- ↑ Peters AL et al. Cetoacidosis diabética euglicémica: una posible complicación del tratamiento con inhibición del cotransportador de glucosa y sodio 2. Diabetes Care 2015 Sep; 38(9): 1687-1693.
- ↑ Ma OJ, Rush MD, Godfrey MM, Gaddis G. Arterial blood gas results rarely influence emergency physician management of patients
- ↑ Kelly AM et al. Review Article – Can Venous Blood Gas Analysis Replace Arterial in Emergency Medical Care. Emery Med Australas 2010; 22: 493 – 498.
- ↑ Ma OJ et al. Arterial Blood Gas Results Rarely Influence Emergency Physician Management of Patients with Suspected Diabetic Ketoacidosis. Acad Emerg Med Aug 2003; 10(8): 836 – 41.
- ↑ 7.0 7.1 Savage MW, Datary KK, Culvert A, Ryman G, Rees JA, Courtney CH, Hilton L, Dyer PH, Hamersley MS; Joint British Diabetes Societies. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med. 2011 May;28(5):508-15.
- ↑ Gokel Y, et al. Comparison of Blood Gas and Acid-Base Measurements in Arterial and Venous Blood Samples in Patients with Uremic Acidosis and Diabetic Ketoacidosis in the Emergency Room. American Journal of Nephrology 2000; 20:319-323.
- ↑ Stojanovic, V. Sherri Ihle. Role of beta-hydroxybutyric acid in diabetic ketoacidosis: A review. Can Vet J. 2011 Apr; 52(4): 426–430.
- ↑ Nagler J et al. Capnography: A valuable tool for airway management. Emerg Med Clin North Am, 26(4):881, Nov 2008.
- ↑ Chebl BR, Madden B, Belsky J, et al. Diagnostic value of end tidal capnography in patients with hyperglycemia in the emergency department. BCM Emerg Med. 2016; 16 (1).
- ↑ Carrillo et al. Balanced Crystalloid Versus Normal Saline as Resuscitative Fluid in Diabetic Ketoacidosis. https://pubmed.ncbi.nlm.nih.gov/34986659/
- ↑ Self et al. Clinical Effects of Balanced Crystalloids vs Saline in Adults With Diabetic Ketoacidosis: A Subgroup Analysis of Cluster Randomized Clinical Trials. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2772993/
- ↑ https://emcrit.org/ibcc/dka/
- ↑ Lipatov, K. et al. Early vs late oral nutrition in patients with diabetic ketoacidosis admitted to a medical intensive care unit. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6347656/
- ↑ *http://emupdates.com/2010/07/15/correction-of-critical-hypokalemia/
- ↑ Aurora S, Cheng D, Wyler B, Menchine M. Prevalence of hypokalemia in ED patients with diabetic ketoacidosis. Am J Emerg Med 2012; 30: 481-4.
- ↑ Goyal N, Miller J, Sankey S, Mossallam U. Utility of Initial Bolus insulin in the treatment of diabetic ketoacidosis. Journal of Emergency Medicine, Vol 20:10, p30.
- ↑ Rao P, et al. Evaluation of Outcomes Following Hospital-Wide Implementation of a Subcutaneous Insulin Protocol for Diabetic Ketoacidosis. JAMA Netw Open. 2022;5(4):e226417. doi:10.1001/jamanetworkopen.2022.6417
- ↑ Hsia E, Seggelke S, Gibbs J, et al. Subcutaneous administration of glargine to diabetic patients receiving insulin infusion prevents rebound hyperglycemia. J Clin Endocrinol Metab. 2012;97(9):3132-3137.
- ↑ Doshi P, Potter A, De L, Banuelos R, Darger B, Chathampally Y. Prospective randomized trial of insulin glargine in acute management of diabetic ketoacidosis in the emergency department: a pilot study. Acad Emerg Med. 2015;22(6):657-662.
- ↑ Rappaport S, Endicott J, Gilbert M, Farkas J, Clouser R, McMillian W. A Retrospective Study of Early vs Delayed Home Dose Basal Insulin in the Acute Management of Diabetic Ketoacidosis. J Endocr Soc. 2019;3(5):1079-1086.
- ↑ Paranthaman, K & Srinivasan, B. Fixed Rate Insulin Infusion (FRII) vs Variable Rate Insulin Infusion (VRII) in Management of Patients with Diabetic Ketoacidosis (DKA). https://www.gavinpublishers.com/article/view/fixed-rate-insulin-infusion-frii-vs-variable-rate-insulin-infusion-vrii-in-management-of-patients-with-diabetic-ketoacidosis-dka
- ↑ Evans, K. Diabetic ketoacidosis: update on management. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6771342/
- ↑ Umpierrez G. et al. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Diabetes Care. 2004 Aug;27(8):1873-8 [PDF http://care.diabetesjournals.org/content/27/8/1873.full.pdf]
- ↑ Rao P, et al. Evaluation of Outcomes Following Hospital-Wide Implementation of a Subcutaneous Insulin Protocol for Diabetic Ketoacidosis. JAMA Netw Open. 2022;5(4):e226417. doi:10.1001/jamanetworkopen.2022.6417
- ↑ Griffey R. et al. The SQuID protocol (subcutaneous insulin in diabetic ketoacidosis): Impacts on ED operational metrics. https://pubmed.ncbi.nlm.nih.gov/36775281/
- ↑ EBQ:Sodium Bicarbonate use in DKA
- ↑ Nickson C. Sodium Bicarbonate and Diabetic Ketoacidosis. Jan 28, 2014. http://lifeinthefastlane.com/ccc/sodium-bicarbonate-and-diabetic-ketoacidosis/.
- ↑ Four DKA Pearls. May 7, 2014. http://www.pulmcrit.org/2014/05/four-dka-pearls.html