Diabetic Emergencies in Pregnancy Brian A. Mason, MS, MD
Objectives Recognize the three major risks of major morbidity in the diabetic gravida. Treat these 3 risks promptly and effectively.
Diabetic Emergencies Severe Hypoglycemia Diabetic Ketoacidosis (DKA) Hyperosmolar Hyperglycemia State (HHS)
Does This Matter? >2,000,000 reproductive-age women with DM 1 in 3 is unaware Most common metabolic disease in pregnancy 14% of all pregnancies 2011: >280,000 ER visits hypoglycemia 2010: 2,400 deaths from hyperglycemia conditions (fetuses not included)
Why Do We Care? 1 in 20 gravidas with DM are pre-gestational Incidence of DKA in diabetic gravidas: 3% Nearly 1 in 10 fetuses die during DKA 80% DKA 2 nd, 3 rd trimester
Causes of Hypoglycemia Mismatch of Glucose: Intake Uptake Metabolic Consumption
Causes of Hypoglycemia Fasting NPO Medications: Hypoglycemics Accelerated metabolism Exercise, stress
Hypoglycemia Symptoms Confusion/dizziness Tremor/anxiety Headache Irritability Tachycardia/PVCs Weakness Diaphoresis Syncope/seizure/coma
Treatment of Hypoglycemia (Rule of 15) Mild: BG 50-70 mg/dl Hold insulin D5 IV @ 200 ml per hour Check BG every 15 minutes When BG >= 70 mg/dl, resume lower dose insulin Or, if tolerating PO: 15 grams CHO, wait 15 minutes Check BG, repeat until BG >= 70
HHS vs. DKA HHS Medical emergency DKA Medical emergency
HHS vs. DKA HHS Medical emergency Slower onset DKA Medical emergency Fast onset
HHS vs. DKA HHS Medical emergency Slower onset Severe hyperglycemia DKA Medical emergency Fast onset Moderate hyperglycemia
HHS vs. DKA HHS Medical emergency Slower onset Severe hyperglycemia No Ketoacidosis DKA Medical emergency Fast onset Moderate hyperglycemia Ketoacidosis
HHS vs. DKA HHS Medical emergency Slower onset Severe hyperglycemia No Ketoacidosis More neurologic change DKA Medical emergency Fast onset Moderate hyperglycemia Ketoacidosis Less neurologic change
HHS vs. DKA HHS Medical emergency Slower onset Severe hyperglycemia No Ketoacidosis More neurologic change Rarely abdominal pain DKA Medical emergency Fast onset Moderate hyperglycemia Ketoacidosis Less neurologic change Often N+V and abdominal pain
HHS vs. DKA HHS Medical emergency Slower onset Severe hyperglycemia No Ketoacidosis More neurologic change Rarely abdominal pain No ketone breath DKA Medical emergency Fast onset Moderate hyperglycemia Ketoacidosis Less neurologic change Often N+V and abdominal pain Ketone breath
HHS vs. DKA HHS Medical emergency Slower onset Severe hyperglycemia No Ketoacidosis More neurologic change Rarely abdominal pain No ketone breath No Kussmaul breathing DKA Medical emergency Fast onset Moderate hyperglycemia Ketoacidosis Less neurologic change Often N+V and abdominal pain Ketone breath Kussmaul breathing
Clinical Presentation DKA Tachypnea (Kussmaul) Abdominal pain Mild neurologic signs/symptoms Signs of dehydration/hypovolemia Fruity acetone odor Nausea/Vomiting
Clinical Presentation HHS Profound neurologic signs/symptoms Signs of dehydration/hypovolemia
This is Your Body
This is Your Body with Pre- Diabetes
This is Your Body with DKA/HHS
Pathophysiology DKA Switch from CHO->fat catabolism
Pathophysiology DKA Switch from CHO->fat catabolism FFA production
Pathophysiology DKA Switch from CHO->fat catabolism FFA production Break down to ketoacids
Pathophysiology DKA Switch from CHO->fat catabolism FFA production Break down to ketoacids Anaerobic production of lactate
Pathophysiology DKA Switch from CHO->fat catabolism FFA production Break down to ketoacids Anaerobic production of lactate Overwhelms Buffer system
Pathophysiology DKA Switch from CHO->fat catabolism FFA production Break down to ketoacids Anaerobic production of lactate Overwhelms Buffer system Metabolic Acidosis
More Bad News Intracellular hypoglycemia
More Bad News Intracellular hypoglycemia Releases glucagon
More Bad News Intracellular hypoglycemia Releases glucagon Inhibits glycolysis, increases gluconeogenesis
More Bad News Intracellular hypoglycemia Releases glucagon Inhibits glycolysis, increases gluconeogenesis Increased glucose + ketone bodies = hyperosmolarity
More Bad News Intracellular hypoglycemia Releases glucagon Inhibits glycolysis, increases gluconeogenesis Increased glucose + ketone bodies = hyperosmolarity Osmotic diuresis/intracellular desiccation
The Hits Keep Rollin Osmotic Diuresis/Intracellular Desiccation
The Hits Keep Rollin Osmotic Diuresis/Intracellular Desiccation Circulatory collapse
The Hits Keep Rollin Osmotic Diuresis/Intracellular Desiccation Circulatory collapse Decreased C.O., peripheral hypo-perfusion
The Hits Keep Rollin Osmotic Diuresis/Intracellular Desiccation Circulatory collapse Decreased C.O., peripheral hypoperfusion More lactic acid secondary to anaerobic metabolism
The Hits Keep Rollin Osmotic Diuresis/Intracellular Desiccation Circulatory collapse Decreased C.O., peripheral hypoperfusion More lactic acid secondary to anaerobic metabolism H + K + ion exchange
The Hits Keep Rollin Osmotic Diuresis/Intracellular Desiccation Circulatory collapse Decreased C.O., peripheral hypoperfusion More lactic acid secondary to anaerobic metabolism H + K + ion exchange Intracellular hypokalemia
When You Thought It Couldn t Get Any Worse Na + excreted to maintain osmolarity
When You Thought It Couldn t Get Any Worse Na + excreted to maintain osmolarity Na +, K +, other ions excreted
When You Thought It Couldn t Get Any Worse Na + excreted to maintain osmolarity K +, other ions, glucose excreted Diuresis up to 150 ml/kg body weight
DKA More Likely and Worse for Pregnant Women Normal increase minute ventilation
DKA More Likely and Worse for Pregnant Women Normal increase minute ventilation Respiratory alkalosis
DKA More Likely and Worse for Pregnant Women Normal increase minute ventilation Respiratory alkalosis Renal HCO 3 - excretion
DKA More Likely and Worse for Pregnant Women Normal increase minute ventilation Respiratory alkalosis Renal HCO 3 - excretion Lower Buffering Capacity
Other Pregnancy DKA Factors Normal emesis/anorexia Accelerated Starvation Physiologic decreased insulin sensitivity Dehydration Increased FFA, increased hydroxybuterate HPL, cortisol, HGH 14 hour fast
DKA Effects on Fetus Decreased uterine perfusion secondary to CV collapse
DKA Effects on Fetus Decreased uterine perfusion secondary to CV collapse Glucose/ketones freely diffuse per placenta Decreased maternal and fetal placental perfusion
DKA Effects on Fetus Decreased uterine perfusion secondary to CV collapse Glucose/ketones freely diffuse per placenta Decreased maternal and fetal placental perfusion H + ions decrease fetal ph
DKA Effects on Fetus Decreased uterine perfusion secondary to CV collapse Glucose/ketones freely diffuse per placenta Decreased maternal and fetal placental perfusion H + ions decrease fetal ph Hypokalemia, hyponatremia
Suspect DKA/HHS in Any Diabetic Hyperglycemia or Ketoacidosis or Neurologic changes or N+V or Abdominal pain or Ketone breath or Kussmaul breathing or Signs of dehydration Gravida With:
In Published Series 90% of Pregnant DKA Pts had N/V 46% had profound abdominal pain 1 in 3 had BGs LESS than 200 mg/dl!
DKA/HHS Immediate Response 1. ABCs (CABD) 2. Volume status 3. Laboratory evaluation 4. Mental Status 5. Seek precipitating events
ABCs (CABD) Circulation Breathing Airway Defibrillate
Volume Resuscitation Establish IV access Draw initial labs plus finger-stick BG 0.9 saline 1000 cc over 1 hour then: 0.9 saline 500-1000 cc over next hour then: Next 4-6 hours 250-500 cc/hour. 0.45 Vs. 0.9 D5 and additives based on labs
Initial Laboratory Evaluation Serum glucose and finger-stick BG Serum electrolytes with anion gap CBC with differential BUN/creatinine UA with urine ketones (dipstick) Serum ketones (if negative urine ketones) ABG if low bicarb or suspect hypoxia ECG
Insulin Bolus Based on sliding scale from finger-stick BG IV route Short-acting insulin (Regular or Humalog)
Insulin Sliding Scale Capillary BG (mg/dl) Units Insulin or ml/hour (1 unit/ml) <70 0 70-90 0.5 91-110 1 111-130 2 131-150 3 151-170 4 171-190 5 >190 Call MD, check urine ketones
Quick Neuro Assessment Level of consciousness Airway protection Metric of severity Suggests HHS Vs. DKA
Precipitating Events Severe acute illness (sepsis, pancreatitis, pneumonia, UTI) New onset Type I DM Established Type I DM with Gastroenteritis Patient self D/C s insulin Drugs altering CHO metabolism Corticosteroid, Terbutaline Cocaine use Poor insulin compliance
Serum Glucose Dx and Tx Don t be fooled! 1 in 3 gravidas with DKA had BG < 200 mg/dl! Give R or log insulin IV Bolus, then infusion per sliding scale D5 0.45 NS @ 100 cc/hour when BG <=200
Serum Electrolytes Anion Gap Our lab Na + - (Cl - +HCO 3- ) Normal=3-10 meq/l Serum K + 1 in 20 hypokalemic 1 in 3 elevated serum K + on admission
Serum Electrolytes Total body K + (deficits 300-600 meq) If K + 3-5 meq/l: put 10 meq in 1 L infusion x 2 L If K + <3 meq/l: Supplement in addition 40-60 meq/l KCl in 1000 cc NS, infuse at 150 cc/hour
Serum Electrolytes Na + : generally hyponatremic Adjust after 1 st 2 Liters 0.9 Other ions (Ca ++, Mg ++, PO 4- ) supplement PRN
CBC with Differential Assess for possible infection WBC/ Differential Leukocytosis normal in DKA WBC > 25k or > 10% bands suggests infection
BUN/Creatinine Assess renal failure Pre Intra Post Adjust fluid and electrolyte replacement
UA and Urine Ketones Urine ketones lag serum Beta hydroxybutyrate Check serum if urine ketones negative UA UTI If suggestive, send C&S
ABG Not needed in every case Suspect hypoxia Low bicarb
ECG 12 lead R/o dysrhythmia Sensitive measure of effective K + levels
Additional Testing CXR Serum amylase Glycated hemoglobin Plasma osmolality
Fetal Management Treat mom quickly and effectively Monitor fetus Baby recovers with mom Delivery ONLY if maternal/fetal indication Maternal code > 4 minutes Fetal bradycardia Prolonged non-reassuring fetal status
Case Study
Patient Presents to Triage 22 year-old G2P0010, 29 weeks EGA History of Type I diabetes, on insulin 2 day H/O abdominal pain/anorexia Held insulin secondary to decreased PO intake Knows she s not dehydrated, she s Drinking and peeing a lot.
Physical Exam Thin, gaunt gravida. Lethargic, but appropriate. Pt weighs 70 Kg S<D, 25 cm FH BP: 105/65, P: 113, RR: 28, Temp: 99.3 F, SpO 2 : 100% Next move?
Admit L and D FS BG: 189 mg/dl FHR tracing: Minimal variability, late decels with contractions every 3-5 minutes Next move?
Admit L and D FS BG: 189 mg/dl FHR tracing: Minimal variability, late decels with contractions every 3-5 minutes Next move? Cervix: 1 cm, long, high Next move?
Admit L and D IV access Labs 1 L NS @ 1000 cc/hour IV bolus insulin plus: D5 0.45NS @ 100 cc/hr Give insulin bolus (dose?) Start insulin infusion (rate?)
Admit L and D IV access Labs NS @ 1000 cc/hour plus D5 o.45 NS @ 100cc/hr IV bolus insulin and start insulin infusion Bolus 5 units Humalog Infusion 5 units/hour Humalog Next move?
One Hour Later Check BG on 5 units/hour Repeat BG: 154 mg/dl Next move?
One Hour Later Check BG on 5 units/hour Repeat BG: 154 mg/dl Next move? Decrease insulin, 4 units/hour IV fluids, continue NS 1000 cc/hour, D5 0.45 NS 100 cc/hour
Labs Return Serum glucose: 179 mg/dl (action?)
Labs Return Serum glucose: 179 mg/dl (action?) Continue same insulin dose Na + : 133 meq/l (action?)
Labs Return Serum glucose: 179 mg/dl (action?) Continue same insulin dose Na + : 133 meq/l (action?) Continue NS K + : 4.5 meq/l (action?)
Labs Return Serum glucose: 179 mg/dl (action?) Continue same insulin dose Na + : 133 meq/l (action?) Continue NS K + : 4.5 meq/l (action?) Add 10 meq KCl to each bag UA: Ketones 3+, Nitrates, Leukocytes, Bacteria (action?)
Labs Return Serum glucose: 179 mg/dl (action?) Continue same insulin dose Na + : 133 meq/l (action?) Continue NS K + : 4.5 meq/l (action?) Add 10 meq/l KCl to each bag UA: Ketones 3+, Nitrates, Leukocytes, Bacteria (action?) Add IV Abx Anion Gap: 21 meq/l
Fluids One Hour Later (Hour 3) 500 cc NS @ 500 cc/hour + D5 0.45 NS @ 100 cc/hour Repeat BG 138 mg/dl Action?
Fluids One Hour Later (Hour 3) 500 cc NS @ 500 cc/hour + D5 0.45 NS @ 100 cc/hour Repeat BG 138 mg/dl Action? Decrease insulin drip to 3 units/hr Repeat labs
One Hour Later (Hour 4) Adjust fluid 0.45 NS @150 cc/hr plus D5 0.45 NS @ 100 cc/hr Labs return
Labs from Hour 3 Return Na + : 138 meq/l K + : 3.1 meq/l UA: Ketones 1+ Anion Gap: 11 meq/l Action?
Labs from Hour 3 Return Na + : 138 meq/l K + : 3.1 meq/l UA: Ketones 1+ Anion Gap: 11 meq/l Action? Infuse KCL 40 meq in 1 L NS @ 150 cc/hr
One Hour Later (Hour 5) Pt c/o HUNGRY! Abdominal pain and nausea resolved Feed Pt ADA diet Give scheduled insulin Last effective regime plus sliding scale subq
When Patient tolerating PO D/C glucose and insulin infusions after 1 st scheduled insulin dose Strict I/O until fluid deficit replaced Follow up on precipitating causes
Congratulate yourselves You and your patients have just dodged a bullet because: You quickly and accurately identified the problem You acted quickly and appropriately