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![Investigation
FBC, renal profile, electrolyte (Ca, Mg, Phos)
Blood glucose
Urinalysis
ECG
VBG
Calculate anion gap [Na – (Cl + HCO3)]
Blood C&S as per indicated](https://image.slidesharecdn.com/dkahhs-220627010927-46ab2c2f/75/Diabetic-Emergencies-16-2048.jpg)
![Should We Bolus Insulin Before Starting
the Infusion?
Is there any benefit to an initial insulin bolus in Diabetic Ketoacidosis?
Goyal et al. Utility of Initial Bolus Insulin in the Treatment of Diabetic Ketoacidosis. J
Emerg Med 2010; 38(4): 422 – 7.
Prospective, Observational Study of 157 patients with DKA:
Insulin bolus at the start of an insulin infusion IS EQUIVALENT to no insulin bolus at the start
of an insulin infusion in several endpoints including:
Decrease normalization of glucose
Affect the rate of change of anion gap
Reduce ED or hospital length of stay
Insulin bolus at the start of an insulin infusion DOES:
Increase hypoglycemic events by 6 fold (6% vs 1%) [NOT Statistically Significant]](https://image.slidesharecdn.com/dkahhs-220627010927-46ab2c2f/75/Diabetic-Emergencies-56-2048.jpg)
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Diabetic Emergencies
- 1. Diabetic Emergencies DR ADIBMURSYIDI IM EMERGENCY AND TRAUMA DEPARTMENT, HCTM
- 2.
- 3. Introduction and Epidemiology Acute, life threatening complication of DM in predominant in Type 1 Overall mortality is <1%, but a mortality rate >5% in the elderly has been reported Mortality in patients with DKA is frequently related to the underlying etiological precipitant rather than the metabolic sequelae of hyperglycaemia or ketoacidosis
- 4. Precipitating Factors Common- infection (often pneumonia or urinary tract infection) & discontinuation of or inadequate insulin therapy Acute major illnesses such as myocardial infarction, cerebrovascular accident, sepsis, or pancreatitis. New-onset type 1 diabetes, in which DKA is a common presentation. Poor compliance with the insulin regimen.
- 5.
- 6. Insulin Ingested glucoseis primary stimulant of insulin release from B-cells of pancreas Insulin main action : Liver, adipose tissue and skeletal muscle
- 7. Deficiency ininsulin secretion due to loss of islet cell mass in type 1 DM Initial stage secretory failure of B cells impairs fuel storage Evident during glucose tolerance test Later stage as level of insulin decrease, fuel stores are mobilized during fasting resulting hyperglycemia As disease progression increase blood glucose level can no longer trigger insulin activity lead to cell starvation
- 8. Pathogenesis Complex relationshipbetween insulin and counterregulatory hormones DKA is a response to cellular starvation due to insulin deficiency Relative absence insulin and excess counterregulatory hormones result in hyperglycemia Insulin Glucagon Cortisol Catecholamines GH
- 9.
- 10. Ketone Body Formation Lipolysis B-oxidation splits fatty acids into Acetyl- CoA Acetyl-CoA either: Enter Kreb’s cycle to produce ATP Enters Ketogenic pathway to produce acetoacetic acids (ketones body)
- 11. Ketones bodies Acetoacetic acid (20%) urine ketone strip B-hydroxybutyric acid (78%) blood ketone strip Acetone (2%) lungs
- 12. Clinical Presentation Diabeticketoacidosis (DKA) usually evolves rapidly - over a 24-hour period. In contrast, symptoms of HHS develop more insidiously, often persisting for several days before hospital admission. Clinical manifestation of DKA related directly to Hyperglycemia Volume depletion Acidosis Osmotic diuresis gradually led to volume loss, in addition to renal losses of Na, Cl, K, Phos, Ca, Mg
- 13. Clinical Features Alterationof consciousness seems to correlate better with elevated serum osmolality (>320mmol/kg) than with severity of metabolic acidosis Kussmaul respiration (increase rate and depth of breathing) Acetone produce fruity odor breathing Abdominal pain and tender in DKA correlate with level of acidosis Pain can be due to gastric dilatation, ileus or pancreatitis
- 14. Diagnosis Blood glucose>13.9 mmol/L Anion gap >10 mmol/L Bicarbonate <15 mmol/L pH <7.3
- 15. Differential Diagnosis Alcoholicketoacidosis Starvation ketoacidosis Renal failure Lactic acidosis Ingestion Salicylates Ethylene glycol Methanol
- 16. Investigation FBC, renalprofile, electrolyte (Ca, Mg, Phos) Blood glucose Urinalysis ECG VBG Calculate anion gap [Na – (Cl + HCO3)] Blood C&S as per indicated
- 17. Principles of Management 1.Volume repletion 2. Reversal of metabolic consequences of insulin insufficiency 3. Correction of electrolyte and acid-base balance 4. Recognition and treatment of precipitating cause 5. Avoidance complications
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- 22. Complications Related to acutedisease In general, the greater initial Serum osmolality BUN Blood glucose Serum HCO3 (<10 mEq/L) Infection and myocardial infarction main contributors for mortality Greater mortality
- 23. Complications - Relatedto therapy
- 24.
- 25. Complications of DKA(summary) Related to Acute Disease Related to Therapy Later Complication Loss of airway Hypokalemia Recurrent anion gap metabolic acidosis Sepsis Hypophosphatemia Non-anion gap metabolic acidosis Myocardial infarction Acute respiratory distress syndrome Vascular thrombosis Hypovolemic shock Cerebral edema Mucormycosis Hypoglycemia
- 26. Disposition and followup Required hospitalization in a monitored setting (ICU) Nursing experienced with IV Insulin infusion
- 27. What to monitor?Our treatment aim? Parameters Rate Aim DXT Hourly Drop by 3 VBG (HCO3, K) 1H 4H 6H HCO3 rise by 3 K : 3-5 mmol/L Ketone 4 hourly 0.5 mmol/L/H BUSE 6 hourly Vital signs, I/O charting Hourly Aim positive balance Urine output >0.5ml/kg/H Cardiac monitor SPO2 Continuous
- 28. What else tomonitor? Clinical Monitor Possible causes A B Respiration Tachypneic Worsening acidosis C Circulation Hypotension Arrythmias Dehydration Electrolyte imbalance D GCS Drop of GCS Hypoglycemia Cerebral edema Hyponatremia
- 29. Input/output aim? ForI/O, how much of positive balance? Estimated deficit in DKA up to 100ml/kg (estimated 10% of body weight), in HHS up to 200ml/kg) Aim to replace this deficit within the next 24-48 hours Aim positive balance 2-3L within this period
- 30. If DXT <14 Once blood glucose falls below 14 mmol/L Switch to 5% dextrose at 125ml/H and reduce insulin infusion rate to 0.05 units/kg/hour; or Switch to 10% dextrose at 125ml/H with no change in insulin infusion rate If equipment is working but response to treatment inadequate, increase insulin infusion rate by 1 unit/hr increments hourly until target achieved
- 31. When to stop/overlapIVI insulin? Resolution of DKA: Patient able to eat Blood ketone <0.3 mmol/L pH. >7.3 Do not discontinue intravenous infusion until 30 minutes after S/C short acting insulin has been given
- 32. Calculating SCinsulin: Estimated dose = patient’s weight (kg) x 0.5 50% of dose as bedtime, another 50% to 3 basal bolus Example: 80 kg required approximately 80kg x 0.5 = 40 units in 24 hours Eg: short acting insulin 7u & 20 units bedtime
- 33.
- 34. Background HHS :characterized by progressive hyperglycemia and hyperosmolarity Mostly in poor controlled or undiagnosed Type 2 DM Occurred in elderly, with common risk factors being obesity
- 35. Pathophysiology Insulin resistance and/or deficiency Osmoticdiuresis followed by impaired renal excretion of glucose Inflammatory state with marked elevation in proinflammatory cytokines vs counter-regulatory stress hormones (catecholamines, GH, glucagon, cortisol)
- 36. As serum glucose concentration increases Osmoticgradient develops Shifting water from intracellular into intravascular compartment Cellular dehydration
- 38. Clinical features Historyand comorbidities Elderly, baseline cognitive impairment, multiple comorbid, referred for abnormalities in V/S Mostly evolved over days to weeks Nonspecific complaints Malaise, weakness, anorexia, fatigue, vomiting, cognitive impairment 15% may present with seizures (typically focal)
- 39. Diagnosis Severe hyperglycemia (>33.3mmol/L) Elevated plasma osmolality (>315 mmol/kg) Serum HCO3 >15 mmol/L pH >7.3 Serum ketones negative to mild positive * Important to recognize the potential for a variety of mixed acid-base patterns in patients with HHS
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- 42. Treatment Improvement oftissue perfusion is the key to effective recovery in HHS The therapeutic plan must be carefully considered and adjusted for concurrent medical illnesses such as cardiac, renal, and pulmonary disease. Overzealous resuscitation can result in significant harms and should be avoided. Treating severely ill patients likely requiring intensive care unit
- 43. Correction of hypovolemia Identifyingand treating precipitating causes Correcting electrolyte abnormalities Gradual correction of hyperglycemia and hyperosmolarity Frequent monitoring
- 44. Begin normalsaline infusion before insulin therapy is started. The average fluid deficit in HHS is in the range of 20% to 25% of total body water, or 8 to 12L. One half of the fluid deficits should be replaced over the initial 12 hours and the balance over the next 24 hours when possible. Begin fluid resuscitation with 0.9% normal saline at a rate of 15 to 20 mL/kg/h during the first hour, followed by rates from 4 to 14 mL/kg/h. Limit the rate of volume repletion during the first 4 hours to <50 mL/kg of normal saline. Once hypotension, tachycardia, serum hyponatremia, and urinary output improve, 0.45% NaCl can be used to replace the remaining free water deficit. Hourly glucose, electrolyte, and osmolality measurements should be taken to monitor progress in the critically ill.
- 45. Any questions? NOPLEASE. PROCEED.
- 46. “ ” Blood gas: VBGor ABG?
- 47. Blood gas: VBGor ABG? Kelly AM et al. Review Article – Can Venous Blood Gas Analysis Replace Arterial in Emergency Medical Care. Emery Med Australas 2010; 22: 493 – 498 For pH, 3 studies of patients with DKA (265 patients) were reviewed showing a weighted mean difference of 0.02 pH units. Only one study, which was the largest study (200 patients) reported 95% limits of agreement of pH that were -0.009 – 0.02 pH units. For bicarbonate, 7 studies with just over 900 patients were reviewed showing a weighted mean difference of -1.41 mmol/L. Only 2 studies (246 patients and 95 patients) reported 95% limits of agreement which ranged from -5.8 to +5.3 mmol/L.
- 48. Blood gas: VBGor ABG? 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. ABG analysis changed ED physicians diagnosis in 1% (95% CI 0.3 – 3.6%) of patients ABG analysis changed ED physicians treatment in 3.5% (95% CI 0.3 – 3.6%) of patients (Change from SQ to IV insulin or vice versa) ABG analysis changed patient disposition in 2.5% (95% CI 1.1% – 5.7%) of patients Venous pH correlated well with arterial pH with difference of -0.015 +/- 0.006 pH units
- 49.
- 50. Insulin versus Electrolyte? Patients with DKA will have total body potassium depletion from osmotic diuresis and electrolyte losses. Measured levels of serum potassium may be falsely normal or elevated due to extracellular shifts of potassium from secondary acidosis. The American Diabetes Association (ADA) actually recommends obtaining a a serum potassium level before initiating insulin, but this is based on anecdotal evidence. That being said, according to Arora et al, approximately 5% of patients with DKA will have hypokalemia.
- 51. Insulin versus Electrolyte? Eg: In VBG you will see your K+ is 2.8. If you start insulin therapy before electrolyte replacement, you will worsen hypokalemia which is a very real cause of morbidity and mortality from cardiac arrhythmias and respiratory muscle weakness. Why? Don’t forget that insulin will activate your Na-K ATPase which will shift potassium intracellular and worsen your hypokalemia.
- 52. “ ” Do Sodium Bicarbonatereally benefit?
- 53. Do Sodium Bicarbonatereally benefit? Chua et al. Bicarbonate in Diabetic Ketoacidosis – A Systematic Review. Ann Intensive Care 2011; 1 (23). 44 studies of DKA patients reviewed which showed: Transient improvement in metabolic acidosis No improved glycemic control Risk of cerebral edema in pediatric patients No studies with pH <6.85
- 54. Do Sodium Bicarbonatereally benefit? Duhon et al. Intravenous Sodium Bicarbonate Therapy in Severely Acidotic Diabetic Ketoacidosis. Ann Pharmacother 2013. 47(7 – 8): 970 – 5. Retrospective study of 86 patients with DKA which showed: No difference in: Time to resolution of acidemia, time to hospital discharge, time on IV insulin, potassium requirement in 1st 24hrs Subgroup Analysis of pH < 6.9 (n = 20) showed no statistical difference in time to resolution of acidemia
- 55. “ ” Should We BolusInsulin Before Starting the Infusion?
- 56. Should We BolusInsulin Before Starting the Infusion? Is there any benefit to an initial insulin bolus in Diabetic Ketoacidosis? Goyal et al. Utility of Initial Bolus Insulin in the Treatment of Diabetic Ketoacidosis. J Emerg Med 2010; 38(4): 422 – 7. Prospective, Observational Study of 157 patients with DKA: Insulin bolus at the start of an insulin infusion IS EQUIVALENT to no insulin bolus at the start of an insulin infusion in several endpoints including: Decrease normalization of glucose Affect the rate of change of anion gap Reduce ED or hospital length of stay Insulin bolus at the start of an insulin infusion DOES: Increase hypoglycemic events by 6 fold (6% vs 1%) [NOT Statistically Significant]
- 57. References Tintinalli’s EmergencyMedicine (Chapter 225, 227, 9th Edition) Up-to-date Medscape
- 58.
Editor's Notes
- #32 To avoid potential relapse
- #36 (CRP, interleukins, TNF) increase hepatic gluconeogenesis and glycogenolysis
- #45 The actual rate of fluid administration should be individualized for each patient, based on the level of renal and cardiac impairment.
- #49 Other Reasons ABGs may not be preferred Although rare, ABGs can cause radial artery spasm, infarct, and/or aneurysms ABGs are painful to patients, even more so than IV access By the way, when is the last time you checked a Modified Allen’s Test before doing a radial ABG? Block off Radial and Ulnar Artery for 30 seconds Have pt make fist Let go of ulnar artery and should have color return in <10seconds If no color return or delayed…then pt DOES NOT have collateral blood flow (i.e. – Allen’s Test) Myth#1 Busted: VBG can be used in place of ABGs