Presentation on theme: "Diabetic Emergencies Andjela Drincic M.D.. Diabetic Emergencies Case Presentation Pt is a 32yo female with a hx of type 1 DM who presents with a cc."— Presentation transcript:
Diabetic Emergencies Andjela Drincic M.D.
Diabetic Emergencies Case Presentation Pt is a 32yo female with a hx of type 1 DM who presents with a cc of N/V, and diffuse abdominal pain for 24 hours What other questions would you like to ask
Diabetic Emergencies Case Presentation Pt denies F/C, URI symptoms, urinary symptoms except for frequency Pt also states that she has been using her insulin correctly, but she had not taken any insulin for the last 24 hours because she wasn’t able to eat anything
Diabetic Emergencies Case Presentation PMHx: Diagnosed with DM after episode of DKA approx 7 years ago. Meds: Insulin 70/30 28UqAM, 16UqPM NKMA SHx: Single, no children, (+) Tob 1ppd for 12 years, occ EtOH use, no recreational drugs FHx: (+) HTN What are pertinent findings on physical exam?
Diabetic Emergencies Physical Exam Gen: Mild distress but A&O x , 120, 34, 132/88 HEENT: WNL Heart: RRLungs: CTA-B Abd: (+) BS, diffuse tenderness, no rebound Ext: WNLNeuro: WNL What Lab Data would you like to obtain?
Diabetic Emergencies Case Presentation Lab Data WBC 15.7, H/H 15/45 Plt 229 NA 132, K 5.2, CL 96, HCO 11, BUN 10, Cr 1.0 Glucose 612, Ca 12.1, Phos 6.6, Mg 2.1
Diabetic Emergencies Case Presentation Lab Data Analysis NA 132, K 5.2, CL 96, HCO 11, BUN 10, Cr 1.0 Glucose 612, Ca 12.1, Phos 6.6, Mg 2.1 What is the anion gap? What is the actual serum sodium? What is the differential diagnosis for wide anion gap metabolic acidosis?
Formulas you may need sOsm = 2 (Na + K ) + Glu/18 + BUN/2.8 + ETOH/4.6 AG = Na - ( Cl + HCO3) Na = Na x (Glu - 100)/100
Diabetic Emergencies Case Presentation Lab Data (Continued) UA: Protein 3+, Large ketones Serum ketones were 1:16 Serum osmolarity was 323mOsm/kg
Diabetic Ketoacidosis (DKA) Life-threatening emergency Gross insulin deficiency is the predominant problem of DKA Most common in patients with type 1 diabetes Can occur in patients with type 2 diabetes due to progressive loss of β-cell reserve Mortality is ~5%–10% Fishsbein H, Palumbo PJ. Acute metabolic complications in diabetes. In: National Diabetes Data Group. Diabetes in America. Bethesda (MD): National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases: 1995:
Signs, Symptoms, and Treatment of Diabetic Ketoacidosis Symptoms Blurred vision Increased thirst Increased urination Nausea/vomiting Confusion Loss of consciousness Signs Deep respirations Fruity breath Dehydration Hyperglycemia Ketosis Acidosis Treatment Give insulin in a sufficient amount Attention to the potassium level is also important Hydration
Type 1 DM hormonal pathophysiology - Insuln deficiency: decreased glucose utilization - Elevations in counterregulatory hormones: increased lipolysis in adipose tissue increased proteolysis in muscle increased glycogenolysis increased gluconeogenesis hepatic ketogenesis Leading to DKA
Hyperosmolar Hyperglycemic State (HHS) Life-threatening emergency Occurs in patients with type 2 diabetes Characterized by very high blood glucose levels without ketones insulin secretion is maintained to prevent peripheral lipolysis, liver able to metabolize FFA in a nonketogenic manner relative insulin deficiency : decreased peripheral uptake and increased hepatic gluconeogenesis hyperglycemia, hyperosmolality osmotic diuresis and volume and electrolyte depletion
DKA/HHS not mutually exclusive ! Criteria for DKA hyperglycemia ( glu>250 mg/dl) ketosis acidemia ( pH <7.3)
Pathophysiology of DKA/HHS Insulin Deficiency Increased LipolysisHyperglycemia Increased ketogenesisOsmotic Diuresis KetoacidosisHyperosmolality Pure Diabetic Ketoacidosis Pure Hyperosmolar State
DKA Absolute insulin deficiency and counter- regulatory hormones promote lipolysis shift in hepatic lipid metabolism of incoming fatty acids due to high ratio of glucagon to insulin in portal flow - fall in malonyl co A levels and disinhibition of CPT CPT catalizes beta oxidative pathway- fatty acids are oxidized to form ketone bodies rather than re-esterified into TG
Physiology of DKA Triglyceride Free Fatty Acids Fatty Acyl Co A Acetyl Co A HMA Co A Acetoaceteate Acetone 3 hydroxybutyrate Adipocyte Serum Hepatocyte Mitochondria Hormone Sensitive Lipase Carnitine palmitoyl transferase 1 Malonyl Co A Glucagon Insulin glucagon
Evaluation of patient history of DM, medications and symptoms history of complications utilization of medications social history ( including alcohol) vomiting precipitating factor - pregnancy, infection, omission of insulin, MI, CVA asses hemodynamic status examine for infection
Laboratory Evaluation BMP CBC serum ketones calculate serum osmolality and AG measure serum osmolality if ingestion of osmotically active substance other than glucose suspected UA and culture consider blood culture CXR consider HCG ABG if indicated clinically HbA1c
“Euglycemic ketoacidosis “ Glu < 300 mg/dl HCO3 < 10 mEq/l Usually in pump pts ( no “back-up insulin)
Other expected labs in DKA Hyponatermia unless pt is dehydrated Hyperkalemia due to cellular shift Leukocytosis in the absonce of infection Elevation of amylase and lipase in the absence of pancreatitis
“Serum Ketone Negative DKA” Alcoholic ketoacidosis Hypoxia Beta hydroxybutirate is the dominant ketone Not detected by nitroprusside reaction
Gudelines ofr therpay of DKA/HHS addapted from Joslin’s Diabetes Mellitus 14th edtion, 2005
Suggested Fluid Replacement in DKA/HHS Administer NS as indicated to maintain hemodynamic status than follow general guidelines: NS for first 4 hours consider 1/2 NS thereafter Change to D5 1/2 NS when BG < 259 mg/dl may need to adjust type and rate of fluid administration in the elderly and in patients with CHF and CRF
Suggested fluid replacement in DKA /HHS 1st hour : 1 l 2nd hour : 1 l 3rd hour : 500 ml - 1 l 4th hour: 500 ml - 1 l 5th hour : 500 ml - 1 l Total 1st - 5th hour l 6th - 12th hour : ml/hr
Guidelines for Insulin Management in DKA/ HHS regular insulin 10U I.v. stat ( for adults) or 0.15 U/kg I.v. stat start regular insulin infusion 0.1 u /kg per hour or 5 U per hour Increase insulin by 1 U per hour every 1-2 hours if less than 10 % decrease in glucose or no improvement in acid - base status decrease insulin by 1-2 U/hr when BG 75 mg/dl /hr do not decrease insulin infusion to < 1 u /hr maintain BG mg/dl if BG < 80 mg/dl, stop insulin infusion for no more than 1 hour and restart the infusion if BG drops consistently to <100 mg/dl, change I.V. fluids to D 10 to maintain BG mg/dl
Insulin Infusion Algorithm 1. Discontinue all subcutaneous insulin use 2. Measure blood glucose every hour measure urine ketones after each void every 4 hours 3. Give D5%W iv via insulin infusion pump 4. Make insulin solution using regular insulin to a concentration of 0.5 U/ml
Insulin Infusion Algorithm Newton et al:Arch Intern Med 164,sept 27, 2004
Guidelines for K replacement in DKA/HHS Do not administer K if serum K > 5.5 mEq/l or if patient is anuric Use KCl but alternate with KPO4 if there is severe phosphorus depletion and patient is unable to take phosphorus by mouth Add I.V. KCl to each liter of fluid administered unless contraindicated
Guidelines for K replacement in DKA/HHS serum K ( mEq/L) Additional K required < mEq/L mEq/L mEq/L > 5.5 Stop K infusion
Guidelines for Bicarbonate Therapy in DKA PRO: severe acidosis is associated with adverese effects:hypotension, decreased cardiac output decreased peripheral vascular resistance, increased pulmonary arterterial resistance, bardycardia, arrhytimas, renal and mesenteric ischemia, cerebral vasodilatation CONS: no studies have shown any benefit of bicarbonate if pH is SIDE EFF : overshoot alkalosis, paradoxical CSF acidosis, hypokalemia, volume overload, overproduction of ketoacids
Guidelines for Bicarbonate Therapy in DKA Use clinical judgement in deciding if bicarbonate therapy is indicated if pH is < 7.0 consider 100 ml HCO3 over 45 min ( mix 100 ml NaHCO3 with 400 ml sterile water and administer at rate of 200 ml/hr) check ABG 30 min later
Phosphate replacement Phos depletion is common: renal loss, intracellular uptake during insulin Rx problem: low cardiac output, respiratory muscle weakness, rhabdomyolisis, CNS deppression, seizures, coma, renal failure CAVE : iv Phos leads to hypocalcemia no benefit in routine replacement reserve replacement Rx if phos < 1.5 mg/dl AND in whom Ca is normal use of small amount of Kphos and KCL iv is safe and effective but oral replacement preferred to I.V.
Monitoring of RX BG hourly electrolytes and acid base status every 2- 4 hours ok to check venous pH if you can’t get art line ( 0.03 unit less than arterial ) frequent measurement of ketones may be misleading ( hydroxybutirate is converted to acetoacetate) consider using bedside measurement of ß hydroxybutirate repeat CXR after 4 l fluids administered
Complications of RX hypoglycemia hypokalemia hypophosphatemia hyperchloremia and hyperchloremic acidosis - chloride losses are less severe than sodium losses but replacement solutions have equal par tof Na and Cl hypoalcemia cerebral edema - children DVT/PE ( dehydration as a risk factor)
DKA - is it always type 1 DM? Arch Int Med : epidemiology of pts admitted for DKA : type 1 DM in 80 % of whites 53% of African Americans 34 % of Hispanics no difference in electrolytes,glu, pH, AG, pOsm or level of ketosis majority of pts with type 2, no preciptating event !
A” Real Life “ case 55 y/o AAF no previous h/o DM comes with polyuria,, polydipsia, fatigue Vitals: 96.9, 130, 24, 122/63 Labs: WBC 19, BS 502, K 6.0, Na 128, CO2 5
Orders Dx DKA IVF NS 3l bolus than 200 cc/hour 2 amps HCO3 blood cultures, sputum cultures,accucheck q 1hour diabetic education in am cbc, bmp in am bmp q 2hours x 4, UA Mg, PO4 levels
Orders - cont 4 hours later - K 3.0, BS 347 order : 40 mEq KCl now change IVF to D5 NS with 40 KCl at 200 cc/hour 6 hours later: phos 1.2 order : 40 mEq K phos IV soft diet for pt 24 hours later, BS 350
Diabetic Emergencies Hypoglycemia Whipple Triad Consistent signs and symptoms Low blood glucose Relief with supplemental glucose Two categories of hypoglycemia Reactive Nonreactive
Diabetic Emergencies Hypoglycemia Reactive Hypoglycemia Develops in response to a nutrient challenge Seen in pts with type 2 DM (???) and post GI surgery pts Idiopathic form Nonreactive Hypoglycemia Iatrogenic Fasting/Factious
Diabetic Emergencies Hypoglycemia Fasting/Factious Hypoglycemia 3 main causes Factitious taking of oral hypoglycemics/insulin Autoimmune etiology Insulinoma from an islet cell tumor Heavy EtOH can also cause hypoglycemia Three tests for workup of nonreactive hypoglycemia Serum insulin C-peptide Urinary sulfonylurea test
Diabetic Emergencies Hypoglycemia C-peptide Elevated indicates endogenous insulin secretion and is low if there is factitious insulin injection High levels seen in autoimmune hypoglycemia, insulinoma, and sulfonylurea ingestion Urinary sulfonylurea test will rule in or out oral hypoglycemic use Insulin levels < 100 suggest insulinoma > 100 suggest autoimmune