GR2011-08 DKA 2011 - Dr Rose

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Diabetic Ketoacidosis:

Diabetic Ketoacidosis (with comments about its cousins: HHS, HONC, & HHNS) Theodore Rose, M.D.,FACP

Goals of session ::

Goals of session : To assist you in recognizing DKA To review the nuances of the exam and lab work in DKA To gain an awareness of the complications of DKA and its treatment

Slide 3:

53 yo female found down on sidewalk. Diabetes for >2 years, treated with unknown insulin dose Recent bizarre behavior, with increase in thirst and urination; somnolent over past few days. PMH: DKA ’99, Pancreatitis EMT-Responds only to pain, no response to Narcan PE: BP 108/54 P101 R 24,deep Temp 88r Obtunded female Chest-clear Heart- 1/6 SEJM Abd-Pos Bowel sounds, sl tender all over, no rebound Rectal-stool heme neg Ext-Cool, clammy, no edema or ulcers Neuro- Nonfocal, moves all 4, reflexes symmetric

Diabetes in History:

Diabetes in History Ancient Chinese recognized the 3 polys 1600- Willis- “mellitic urine” -> diet 1859- Bernard- elevated blood sugar as cause 1869-Langerhans- described islets 1920-Banting and Best 1939-Hagedorn- long-acting insulin 1972-”Low dose” IV insulin for DKA

Criteria for Diagnosis ::

Criteria for Diagnosis : Blood glucose greater than 250 mg/dl Anion gap acidosis >10 B-Hydroxybutyrate greater than 3.8

Epidemiology::

Epidemiology: 8 episodes per 1000 diabetics each year 140,000 hospitalizations per year at a cost of $18,000 per episode= $2.4 billion/year. 35% increase in admits for DKA 1996-2006 Of DKA admits, 30% are new diabetics Mortality <1%, but up to 40% if comatose on admission In <24 yo, half the deaths due to DM are DKA

Precipitating factors ::

Precipitating factors : Infection, Infection, Infection Reduction or Omission of insulin New-Onset DM, esp at ACMC Acute vascular crisis : MI, CVA Drugs: Cocaine, Psych meds, steroids Psych disorders- eating disorders Unknown----30%

“Type 1.5” Diabetes:

“Type 1.5” Diabetes Winters et al, NEJM, 1987 Ketosis-Prone Type II DM >50% of new DKA in minority groups Most can come off insulin after acute episode After 10 years, 40% still off insulin

Slide 14:

Umpierrez G E et al. Ann Intern Med 2006;144:350-357

Slide 15:

Umpierrez G E et al. Ann Intern Med 2006;144:350-357

Slide 16:

53 yo female found down on sidewalk. Diabetes for >2 years, treated with unknown insulin dose Recent bizarre behavior, with increase in thirst and urination; somnolent over past few days. PMH: DKA ’99, Pancreatitis EMT-Responds only to pain, no response to Narcan PE: BP 108/54 P101 R 24,deep Temp 88r Obtunded female Chest-clear Heart- 1/6 SEJM Abd-Pos Bowel sounds, sl tender all over, no rebound Rectal-stool heme neg Ext-Cool, clammy, no edema or ulcers Neuro- Nonfocal, moves all 4, reflexes symmetric

Physical Exam Pearls in DKA:

Physical Exam Pearls in DKA A NORMAL temperature is ABNORMAL ! Note Kussmaul respirations = ph<7.2 ALL DKA patients have abdominal pain Hypotension + tachycardia= Mortality risk Mental status changes are due to hyperosmolality (coma>330) Look for signs of precipitating cause : infection, chf, ivdu, pancreatitis, etc.

Lab work ::

Na 134 K 4.6 CI 95 HCO “<5” … Anion Gap 39 GLUCOSE 1165 Ketones + @ 1:64 ABG: ph 6.69 pCO2 23 pO2 499 on 100%FiO2 Creat 1.7 BUN 37 PO4 0.6 Amylase 753 Lactic acid 3.1 Lipase 5632 WBC 18,400 with Left Shift Hb 15.0 Pits 200,000 Lab work :

Lab Pearls ::

Lab Pearls : Height of WBC related to acidosis, thus useless as indicator of infection Vomiting will “autocompensate” for acidosis Ketone assay only measures acetoacetate and underestimates actual ketoacid levels because BohButyrate/acetoacetate ratio 3:1 Amylase can go up to >400 in DKA, Lipase more specific, but can still go up in DKA alone Are ABG’s needed at all ? No

The Sodium Story:

The Sodium Story Dogma: Serum Na drops 1.6 mEq for every 100 mg/dl increase in CHO Add to measured sodium “1.6” times every “100” of glucose above normal. RBS 1100,Na 135 : 1.6 x 10=16 ; 135+16=151

:

BUT, studies (in med student volunteers) show a factor of 4.0 more accurate if RBS >400 4.0 x 10=40 135+40=175 !!! ? Compromise by using 2.4 in all cases

Slide 23:

Lesson: Many DKA patients are severely hypernatremic despite normal serum sodium !

Osmolality:

Osmolality For our case: Osm(ser )calc-336 [Osm meas- 373]

If the osmolarity is near normal, look for other causes of coma….:

If the osmolarity is near normal, look for other causes of coma….

Useful formulas ::

Useful formulas :

Goals of therapy ::

Goals of therapy : Replace fluid losses Correct hyperglycemia and acidosis Replace electrolyte losses Detect and treat precipitating cause Convert to SQ insulin and then to an outpatient treatment regimen Prevent recurrence

1. REPLACE FLUID DEFICIT:

1. REPLACE FLUID DEFICIT To Correct volume deficit : Run in 1-2 L of Normal saline stat, if hypotensive will need more. NEVER add potassium to first liter, unless you have the electrolyte report in your hand. To correct water deficit : change to half-normal saline after BP stabilizes. Goal: replace 50% of TBW deficit in first 8 hrs

Fluid deficit continued……:

Fluid deficit continued…… Rehydrate before insulin Add dextrose when RBS <250 If RBS drops below 150 mg/dl, may need to go to D10 or even D20. DO NOT reduce the insulin until ketones have cleared and anion gap has closed. Never interrupt the insulin infusion. Can reduce IV fluids when patient able to take drink oral fluids.

Normal Saline is not “Normal”:

Normal Saline is not “Normal” 154 meq Na + 154 meq CL = 308 mOsm/L Too much Cl, no K, no Ca, no Mg Soooo, let’s add 20 meq KCl: 154 meq Na + 174 meq Cl + 20 meq K= 348 mOsm/L

2. Correct hyperglycemia:

2. Correct hyperglycemia Insulin infusion, 0.1 u/Kg/hr , avg 6-10 u/hr If RBS does not fall by 50-100 in first hour, double the infusion rate. If RBS falls by >100 mg/dl/hr, halve the rate Continue the drip until gap has closed, and patient appears improved and stable. You may then give SQ insulin as per the inpatient protocol. Allow an hour overlap. A shorter overlap might be OK if Lyspro used. A 2009 study showed less hypoglycemia (15% vs 41%) with glargine/glulisine vs NPH/Reg in recovery from DKA

Do you have to use IV regular insulin ?:

Do you have to use IV regular insulin ? Why not SQ Lyspro ? Am J Med, Sept 1,2004: Study at Emory, 20 patients randomized to standard IV insulin or Hourly SQ Lyspro. Conclusion: No difference in outcome; SQ route is “safe and cost-effective” Diabetes Care,July,2009: “Insulin Analogs vs Human insulin in DKA”- Glulisine vs reg IV,34 pts, no difference

Treatment effect::

Treatment effect:

3. Replace Electrolyte losses ::

3. Replace Electrolyte losses : Potassium - Avg 100-200 mEq needed in first 24 hrs. If initial K normal or even low, will need aggressive K replacement. Phosphate - 60-80 mM deficient, can use KPhos po. No need to replete aggressively.

Should everyone get bicarbonate?::

Should everyone get bicarbonate?: No proven value down to pH of 6.9 No randomized studies at lower ph levels Potential side-effects of hypokalemia, hypernatremia, and unfavorable CNS ph shifts. Animal studies suggest bicarb prolongs ketonemia My opinion- useless . May consider using if pH<6.9 and pt in shock

4. Detect and treat cause ::

4. Detect and treat cause : Always OK to treat for sepsis initially Culture urine, sputum, etc Carefully examine feet, perirectal area, any skin lesions Look out for “silent” MI, ischemic bowel, and CVA

5. Change to SQ insulin: When:

5. Change to SQ insulin: When Glucose is below 200-250 Anion gap is <12 Patient is awake and able to eat --------------------------------------------------- Venous ph >7.3 B-Hydroxybutyrate levels normalized (data?) DON’T wait for Bicarb to come up, or urine ketones to clear

5. Change to SQ insulin: How:

5. Change to SQ insulin: How Best to simply restart them on their outpatient insulin schedule, as long as they’re eating and improving. Weight-based method : 0.6 u/Kg body wt. 0.6 u X 70 kg = 42 u/d Insulin drip method : Most recent stable drip rate x 0.666 x 24hrs. 2 u/hr x 0.666 x 24 = 31.9 u/d

OVERLAP INSULIN!!:

OVERLAP INSULIN!! Continue IV insulin infusion for 1-2 hours after giving SQ insulin Never, ever allow a DKA patient to gho without insulin “on-board”

Grading the Therapies::

Grading the Therapies: Vigorous Fluid Replacement 1A Low dose insulin IV 1B Potassium replacement 1A Bicarbonate if pH<6.9 2B Do not give phosphate 1A

4. Prevent Recurrence:

4. Prevent Recurrence Education : never omit insulin, watch for infection, etc. “Sick day” algorithms Diabetic hotline Early contact with MD Education of family members $$$ for insulin

Complications due to therapy..:

Complications due to therapy.. Hypoglycemia Hypokalemia Hyperchloremic acidosis Relapse of DKA on transfer to floor Line sepsis, thrombosis, etc. Cerebral edema ARDS Fluid overload

Complications due to the disease…..:

Complications due to the disease….. Vascular occlusion- MI, CVA, mesenteric, etc Thromboembolism Erosive gastritis Acute gastric distention, gastroparesis Acute renal failure Pancreatitis Death- 5-15% mortality in centers, can be up to 70% in elderly or those with comorbidities

Slide 47:

Casey Johnson, 1981-2011 Cause of death- DKA

Hyperglycemic Hyperosmolar Syndromes:

Hyperglycemic Hyperosmolar Syndromes Definition: Decompensated diabetes with hyperglycemia, hyperosmolality, and dehydration. Ketosis absent or mild, may have mild acidosis 20% of admissions for HHS resided in SNFs

HHS-Demographics:

HHS-Demographics HHS pts commonly have associated acute medical problems: MI,CVA,PE,ARF, ischemic bowel, etc. Common thread-> RESTRICTED ACCESS TO WATER

HHS- Causes:

HHS- Causes Infection Noncompliance 1 st presentation of DM – 15%, but goes up to 40% in those older than 65

Treatment of HHS:

Treatment of HHS Mainstay is volume repletion; average deficit is 10 liters !! Normal saline is HYPOTONIC for them. 1-2 liters NS stat, then follow DKA guidelines. VERY sensitive to insulin, start at 0.05 units /kg/hr IV (SQ not absorbed) Watch potassium levels Consider heparin, at least as prophylaxis

HHS Rx II:

HHS Rx II Don’t forget the underlying medical problem !!!

Complications of HHS:

Complications of HHS Vascular occlusive disease-venous/arterial DIC Rhabdomyolysis Cerebral edema ARDS Death – Mortality 27% ! , usually from comorbid conditions.

Hint: :

Hint: Most patient with severe decompensated diabetes that you will see here have a combination of DKA and HHS.

Slide 57:

Are there any new ways to manage diabetes that would prevent DKA?

What's New: NEJM, 7/22/10:

What's New: NEJM, 7/22/10 Effectiveness of Sensor-Augmented Insulin-Pump Therapy in Type 1 Diabetes Bergenstal et al, N Engl J Med 2010; 363:311-320 Method : Sensor-Pump vs Multiple daily injections Results : N o reduction in DKA between standard injections vs pump therapy. BUT, only 5 cases of DKA total out of 485 subjects. Overall, study showed better control (A1C 7.1 vs 8.3) with pumps without increase in hypoglycemia.

The “Artificial pancreas” is here now….:

The “Artificial pancreas” is here now…. An automatic insulin infusion device linked to an instantaneous glucose sensor-

Goals of session ::

Goals of session : To assist you in recognizing DKA To review the nuances of the exam and lab work in DKA To gain an awareness of the complications of DKA and its treatment

Standard Reference::

Standard Reference: Diabetes Care, Vol 32, Number7 July,2009 “Hyperglycemic Crises in Adult patients With Diabetes”

Questions?:

Questions?

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