Advanced Practice Provider Academy

Transcription

1 (+)Corey M. Slovis, MD, FACEP Professor, Emergency Medicine and Medicine; Chairman, Department of Emergency Medicine, Vanderbilt University Medical Center, Nashville, Tennessee; Medical Director, Metro Nashville Fire Department and Nashville International Airport Advanced Practice Provider Academy April San Diego, CA Diabetes and Blood Glucose Emergencies: How Sweet It Is! Diabetes and derangements of blood glucose metabolism represents a significant number of true emergencies as well as has an impact on a vast number of patients who present to the emergency department. Hyperglycemic and hypoglycemic states are not only life threatening but can mimic other critical pathologic conditions and need to be identified and managed quickly. This course will introduce approaches to the identification and management of patients with blood glucose emergencies, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS) and the controversy that surrounds the management of these diseases. The extreme opposite of the above processes and the causes and management of hypoglycemic states also will be discussed. Objectives: Identify patients who have blood glucose derangements and review some common conditions that they mimic. Describe the common presentation, laboratory abnormalities, treatment and admission criteria for patients with diabetic emergencies. Discuss current differences between the approach to adults and pediatric patients with hypoglycemia. Date: 4/14/2014 Time: 2:45 PM 3:15PM Course Number: MO 12 (+) No significant financial relationships to disclose

2 DKA, HONK, Hypoglycemia Corey M. Slovis, M.D. Vanderbilt University Medical Center Metro Nashville Fire Department Nashville International Airport Nashville, TN DKA Mastering Emergency Medicine A 21 year old grad student Presents in DKA. How many causes of DKA are there? Secure the ABC s Consider or give NGT Five Causes Five Steps Five Reasons for almost everything Infection 5 Causes of DKA DKA Insulin Lack 5 Actions of Insulin Drive Glucose into cell Glu Infarction Infant Indiscretion Insulin lack Drive K into cell Anabolic Block Fat breakdown Block protein breakdown K Catabolic FFA Acids Keto Acids 1

3 How Sick in DKA? Mental Status BP/Pulse Respiratory Rate Finger Stick Glucose Venous ph Current State of the Art Standard of Care Consensus Statement of ADA Diabetes Care 2009;32: Three Levels of DKA ph in DKA Mild Moderate Severe ph below 7.0 Which is better, an ABG with arterial ph or just a venous ph? HCO below 10 MS Alert Alert + Stupor or Coma Acad Emerg Med 2003;10:8 Routinely Use VpH in DKA. 200 ABGs and VpHs in DKA Patients ABG po 2 and pco 2 changed Rx in 2/200 Very high correlation between Art ph vs. V ph (0.95) 2

4 Five Therapies to Consider in DKA How many therapies should you consider in DKA? Volume v Insulin Potassium... Bicarbonate Phosphate Therapy and Rationales in DKA Volume Enough to re-hydrate But don t wash out ketones Insulin Saturate receptors And keep saturated Potassium Avoid hyperkalemia early But avoid hypokalemia later Therapy and Rationales in DKA - 2 Bicarbonate Rarely needed Use for decompensation Phosphate Only cachectic adult patients Common in children Use for values below VOLUME in DKA Deficits: 3-5 liters is usual deficit in mild-moderate DKA What is the best IV flow rate in DKA for the first 3 to 4 hours? 5-6 liters is usual fluid deficit in severe DKA 3

5 JAMA 1989;262: Don t wash out all the Keto Acids. Let the Patient Metabolize Them Volume Therapy in DKA Begin Therapy: Bolus healthy patients with at least 1,000 cc of NSS (20 cc/kg) rapidly Stable Patients: NSS at 500 cc/hr x 4 hours Switch to NSS at 250 cc/hour Profound Dehydration: NSS wide open until well perfused For Mild DKA You Can Just Begin Therapy at 250cc/hr with Smaller or no Bolus. NSS vs. ½ NS NSS is the standard Use initially to volume load Consider ½ NS if corrected serum sodium is elevated 4

6 The easiest way to correct for Na in DKA is meq Na for every 100mg/dl glucose Real Formula 1.6 Na/100 mg/dl glucose to Na/100 mg/dl > 400 Once Serum Glucose approaches 250 mg%: Switch to Glucose containing fluids (D 5 1/2 NS at cc/hr) Cerebral Edema and DKA Seen in children Increased morbidity and mortality Leading cause of death in pediatric DKA Lower ph and pco 2 increases incidence Aggressive fluids also implicated NEJM 2001;344: The only therapeutic variable associated with cerebral edema in children with DKA was the administration of Bicarbonate. Low ph, low pco 2 levels and amount of dehydration also important Fluids in DKA Bolus: adults routinely, children rarely Correct hypoperfusion ASAP Less, not more, once euvolemic Under-resuscitation is to be avoided Children are at Real Risk for Cerebral Edema. Be Careful! Acidosis and Dehydration are your enemies 5

7 You must: Insulin Provide a loading dose, and then Keep all receptor sites saturated Each unit of insulin moves about 4-5 grams of glucose into cell. Insulin Dosing Loading Dose 0.1 units/kg IV Push Maintenance Dose 0.1 units/kg per hour In general load adults, not children J Emerg Med 2010;38: J Emerg Med 2010;38: ADA recommends insulin loading in adults Loading dose saturates receptors Loading may cause hypoglycemia in children Loading not recommended in Peds DKA Conclusions IV insulin bolus not of proven benefit May cause more hypoglycemia Potassium in DKA If glucose fall is not at 100 mg/dl per hour, rebolus, double infusion rate and look again for infection, infarction and infant. The average K deficit in DKA is 3-5 meq/kg IBW The ECG does not accurately predict hypokalemia 6

8 Potassium Dosing in DKA A patient in DKA presents with K=5.1, ph =7.0, good urine output. How much KCl should be given in the first 4 hours? In general 10 meq/hr But KCL Replacement in First Hours of DKA Be sure K is in the DKA range of WNL Hyperkalemia (above 5.3) DKA Kalemia ( ) Hypokalemia ( ) Severe HypoK (below 3.5) Hold K for 1 hr, recheck K KCL 10 meq/hr KCL 20 meq/hr Hold Insulin KCL meq/hr/constant ECG Unexpected Death in DKA First hour or two when sick: Hyperkalemia Later while stabilizing : A patient is treated for DKA and his glucose falls appropriately. His bicarbonate however, does not rise. First thoughts? Hypokalemia 7

9 Refractory Acidosis in DKA Bicarbonate Use Potential Benefits Potential Risks Reverses Acidosis Intracellular Acidosis Dead Gut Sepsis Abscess Improves Cardiac Output Increases Fibrillatory Threshold Improves Insulin Sensitivity Decreased Work of Breathing Decreased Length of Coma Increased Ca, H+, K fluxes Hypokalemia, Tissue Hypoxia Hyperosmolarity, Hypernatremia Increased CO2 Generation, Respiratory Acidosis Paradoxical CSF Acidosis Recommendations on Bicarbonate It is generally agreed that: ph above 7.0 requires NO bicarbonate ph between may require bicarbonate ph below 6.9 probably requires bicarbonate HCO 3 PCO 2 ph If you give HCO 3 rapidly IV: Rapid IV administration of bicarbonate in DKA can cause a respiratory acidosis in the brain Serum HCO 3 will rise Thus serum ph will rise If ph rises, less hyperventilation Serum pco 2 will rise on venous side Causing pco 2 to rise on CSF side too 8

10 Is Bicarbonate Really Hyperosmolar? N Engl J Med 2001;344:264-9 Osmolarity = 2 x Na + Glu/18 + BUN/2.8 Na is in meq/l Na HCO 3 = 1 meq/ml or 1000 meq/l Osm Na HCO 3 = 2 x 1000 = 2000 mosm! Push Bicarb ONLY For: Hyperkalemic emergency Impending cardiopulmonary arrest Phosphate Therapy in DKA Phosphate Therapy in DKA No proven benefit Rarely used in adults Up to ½ of K requirements given as K 2 PO 4 in pediatric patients. NKHC, HONK Check with your pediatrician 9

11 5 Actions of Insulin Drive Glucose into cell Glu Drive K into cell K Anabolic Catabolic Nonketotic Hyperosmolar Coma (NKHC, HONK) Not enough insulin to move glucose Enough insulin to drive K into cell Enough insulin to block catabolic state Block Fat breakdown Block protein breakdown FFA Keto Acids Enough to not breakdown fat & protein Extreme glucose elevations Nonketotic Hyperosmolar Coma (NKHC) DKA NKHC Insulin levels very low may be normal Ketoacidosis profound minimal Glucose 600 1,000 HCO OSM Age young old Onset acute chronic Associated diseases rare common Seizures very rare common Coma rare common Mortality approaches % NKHC AMS in most patients Up to 50% present in deep coma Seizures in up to 1/4 of patients Often focal (20-85% of reported cases) Patients usually lethargic or comatose 10% present without AMS NKHC/HONK Volume resuscitate NSS Slow fluids to cc/hr Use NSS if corrected Na < 135 Use ½ NSS if Na corrects > 135 Insulin in NKHC ADA guidelines recommend bolus and maintenance like in DKA 0.1 units/kg bolus and 0.1 units/kg per hour My bias, go slower KCI at about 10meq/hr 10

12 It takes hours to 1-2 days to develop DKA Treat aggressively It takes many days to weeks to develop NKHC Do not treat aggressively Treating NKHC Twice the volume deficit, but Treat ½ as aggressively as DKA Tease with insulin, no drip DKA pts should never die, NKHC often do Hypoglycemia Why does every hypoglycemic patient s low blood glucose have to be ReExplained? Hypoglycemia ReExPLAIND Hypoglycemia (Renal) Re Ex P L A I N D Renal Exogenous Insulin/antihyperglycemics Pituitary Insufficiency Liver Alcohol, Addison s, Aspirin Infection, Insulinoma Neoplasm Drugs Decreased insulinase Decreased excretion Decreased caloric intake Increased number of infection 11

13 Hypoglycemia (Drugs) Beta Blockers Alcohol Aspirin Pentamidine Valproic Acid One amp of D 50 should raise serum glucose by about 200 mg/dl for up to 30 minutes. If it doesn t look for complicating factors like sepsis, insulin OD, oral agent OD, or ASA OD One Amp of D 50 50% Dextrose in Water 50 cc of 50% = 25 grams 100 calories Dextrose does not last too long reliably, But in first 5-10 minutes will raise glucose by about 200 mg% Lasts 5-30 minutes reliably After 30 minutes: feed or D 5 W D 50 Mistakes Glucose Dosing Not needed Repeated too quickly No secure IV line Pushed too quickly Given in too young a patient Adult Child Neonate D 50 1 cc/kg D 25 2 cc/kg D cc/kg 12

14 Hypoglycemic But No IV Ann Emerg Med 1991;20: Oral Glucose Gel Glucagon IM Glucagon stimulates camp and block insulin Can be given IM if no IV available 1.0 mg IM will elevate glucose about 100 mg% Onset of action is 5-15 minutes Effective 50-98% of the time Ann Emerg Med 2000;36: Decreased Hypoglycemic episodes by a factor of 27 D 50 rarely required post octreotide Stabilization was immediate The signs and symptoms of hypoglycemia are variable and are dependent on both: Low Glucose Levels Rate of Fall of Glucose Always Check Glucose Nobody dies of hyperglycemia They do from Hypoglycemia AMS Seizures Post-ictal CVA Weak, Dizzy 13

15 Therapy and Rationales in DKA Summary Volume Enough to re-hydrate But don t wash out ketones Insulin Saturate receptors And keep saturated Potassium Avoid hyperkalemia early But avoid hypokalemia later Therapy and Rationales in DKA - 2 Bicarbonate Rarely needed Use for decompensation Phosphate Only cachectic patients Use for values below Volume Therapy in DKA Begin Therapy: Bolus healthy patients with at least 1,000 cc of NSS (20 cc/kg) rapidly Stable Patients: NSS at 500 cc/hr x 4 hours Switch to NSS at 250 cc/hour Profound Dehydration: NSS wide open until well perfused Refractory Acidosis in DKA Dead Gut Sepsis Abscess NKHC/HONK Volume resuscitate NSS Slow fluids to cc/hr Use NSS if corrected Na < 135 Use ½ NSS if Na corrects > 135 KCI at about 10meq/hr 14

16 Re Ex P L A I N D Hypoglycemia ReExPLAIND Renal Exogenous Insulin/antihyperglycemics Pituitary Insufficiency Liver Alcohol, Addison s, Aspirin Infection, Insulinoma Neoplasm Drugs Summary DKA - fluid bolus - NSS, insulin, K Beware Hypokalemia in DKA Go slow in HONK Re-explained all hypoglycemia Check glucose 15