DKA

1
DKA

• Crystal Lantz PGY3

2
Pathogenesis 1

• Lack of insulin production prevents glucose
  uptake by muscle and allows unrestrained hepatic
  glucose production.
• Lack of suppression of lipolysis leads to excess
  circulating FFAs which are converted into
  ketoacids (B-OH-butyrate and acetoacetate) by the
  liver.

3
Pathogenesis 2

• This leads to acidemia which may impair vascular
  tone and cardiac function.
• Marked hyperglycemia and ketonemia cause osmotic
  diuresis with loss of water and electrolytes.

4
History 1

• Nausea, emesis
• Abdominal pain (2/2 delayed gastric
  emptying/ileus 2/2 acidosis and lyte
  abnormalities and may correlate with degree of
  acidosis)
• Polyuria/Polydipsia
• Lethargy
• Headache
• Anorexia
• Usually develop over 24h or less in DKA over
  multiple days more insidiously in HHS.

5
History 2

• Possible precipitating events (Is)
• Infection (UTI? PNA?)
• Insulin (incorrect dosing/noncompliance)
• Ischemia (myocardial.mesenteric)
• Initial presentation of DM.

6
History 3

• More uncommon causes
• Med effect meds that affect carb metabolism
• Steroids
• High-dose thiazides
• Atypical antipsychotics
• CVA
• Pancreatitis
• Cocaine use

7
DKA can develop after admission for something
else

• In hospitalized pts without DKA who present with
  CVA, MI, or infection and glucose gt250
• Maintain high suspicion for DKA check RFP for
  AG and serum/urine ketones.

8
Physical 1

• ABCs
• Mental status
• Evidence of intercurrent illness (infection, MI,
  CVA, pancreatitis)
• Abdominal exam TTP, hypoactive BS
• Volume status
• Skin turgor
• Mucosa
• Flat neck veins
• Orthostatic hypotension

9
Labs/Imaging

• RFP for lytes, glc, CALCULATE AG
• CBC
• UA/ketones
• Plasma osmolality
• Serum ketones if urine ketones are present
  (B-OH-Butyrate, Acetone, Acetaoacetate)
• ABG if serum HCO3 reduced
• ECG
• Consider infectious w/u(blood, urine, sputum,
  CXR)
• HbA1C may be useful

10
Diagnosis
DKA DKA DKA HHS
Mild Mod Severe HHS
Plasma Glc gt250 gt250 gt250 gt600
Arterial pH 7.25-7.30 7.0-7.24 lt7.0 gt7.30
HCO3 15-18 10-lt15 lt10 gt18
Urine ketones Small
Serum osm Variable Variable Variable gt320
Anion Gap gt10 gt12 gt12 Variable
11
(No Transcript)
12
DKA Lactic Acidosis Uremia ETOH Keto- acidosis ASA Intox MeOH/ Ethy Glycol Intox
pH Low Low Mild Low ? ? Low
Plasma Glc High Normal Normal Low/Nl Nl/Low Nl
Glycosuria High Negative Neg Neg Neg Neg
Plasma Ketones High Normal Normal Sm-Mod Normal Normal
Anion Gap High High Sl High High High High
Osmolality High Normal High Normal Normal High
Uric Acid High Normal Normal High Normal Normal
13

• B-OH-Butyrate ? Acetone Acetoacetate
• Direct measurement of B-OH-Butyrate is preferable
  for monitoring degree of ketonemia and is
  available at UHCMC (not VA)
• Standard ketones may become increasingly positive
  as conversion from B-OH-Butyrate to
  acetone/acetoacetate occurs

14
Switching gears to an Acid-Base talk

• 5 Step Approach to ABGs without memorizing
  formulas.

15

• Identify alkalosis/acidosis by pH change from
  7.4. (gt7.4 alkalosis. lt7.4 acidosis).
• Determine if primary disorder is respiratory or
  metabolic based on direction of change of PCO2.
• If pH and PCO2 change in same direction -
  metabolic
• If pH and PCO2 change in opposite direction -
  respiratory

16

• 3. Check compensation to identify other primary
  disorders.
• Metabolic Acidosis - Check Resp Compensation.
• PCO2 (1.5 HCO3-) 8 2
• Simplified For every 1 mEq decrease in HCO3,
  PCO2 should decrease by 1.2 mmHg.
• Example If HCO3 is 9...24-9 15. PCO2
  reduction should be 15x1.2 18. 40-18
  22mmHg.
• Metabolic Alkalosis Check Resp
  Compensation.
• PCO2 rises 0.7mmHg for each 1.0 mEq rise in
  HCO3.
• Example If HCO3 is 34...34-24 10. 10 x 0.7
  7. 407 47mmHg.

17

• Acute Respiratory Acidosis
• Every 10 mmHg rise in PCO2 1 meq rise in HCO3
• Chronic Respiratory Acidosis
• For every 10 mmHg rise in PCO2 3.5 mEq rise
  in HCO3

18

• Acute Respiratory Alkalosis
• Every 10 mmHg drop in PCO2 2 meq drop in HCO3
• Chronic Respiratory Alkalosis
• For every 10 mmHg drop in PCO2 5 mEq drop
  in HCO3

19

• 4. If metabolic acidosis - calculate anion gap.
• Na - (ClHCO3)
• Normal gap 12 or less.
• For each gram of albumin drop less than 4 add
  2.5 to calculated gap to get actual gap.
• Example Calculated gap 9. Albumin 2. Add 5 to
  gap 14.

20

• 5. If AGMA - calculate delta gap.
• Change in gap divided by change in
  bicarbonate.
• (AG-12) / (24-HCO3)
• lt1 AGMA NAGMA
• 1-2 - Pure AGMA
• gt2 AGMA Metabolic Alkalosis

21

• In DKA, initially AGMA as treatment proceeds
  many will develop a subsequent NAGMA.
• Ketoacid anions are excreted in the urine with
  sodium which would have been used to reproduce
  HCO3 in the kidney ? loss of potential HCO3
  which is equivalent to actual bicarb loss ?
  subsequent NAGMA.

22
Serial Monitoring

• Q1H POCT Glucose until stable
• RFP/Serum osmolality q2-4h with close FU of HCO3.
  
• Consider VBG rather than frequent ABGs for pt and
  intern comfort venous pH is about 0.03 units
  lower than ABG.

23
DKATx
24
HHS Tx
25
Fluids, fluids, fluids.

• Severe Hypovolemia NS 1000cc/h
• Milder Dehydration evaluate corrected Na
  (Corrected Na Measured Na (Glc-100/100)
• Hyponatremia 250-500cc/h NS
• Normal-Hypernatremia 250-500c/h 1/2NS
• When serum glc reaches 200 (or 300 in HHS) ?
  Change to D51/2NS 150-250cc/h

26
Insulin therapy 1

• Usually IV route except in mild DKA.
• IV Regular insulin 0.1U/kg bolus then 0.1U/kg/h
  continuous infusion OR no bolus with infusion
  rate alone at 0.14U/kg/h
• SQ Lispro 0.3U/kg x1 then 0.2U/kg in 1hr then
  0.2U/kg SQ q2h.
• If serum glc doesnt fall by 50-70 mg/dL in 1st
  hour double the IV or SQ dose.
• K lt3.3 is a CONTRAINDICATION to insulin.

27
Insulin therapy 2

• When glc to 200 (in DKA) or 250-300 (in HHS)
  reduce infusion to 0.02-0.05U/kg/h IV or change
  SQ dosing to 0.1U/kg q2h with goal glc 150-200.
• Never discontinue insulin prior to closure of
  anion gap!

28
Potassium therapy

• If K lt3.3 hold insulin therapy and replete K
  with fluids 40-60mEq/h to ½NS until K 3.3
  (assuming UOP 50cc/h).
• If K gt5.3 no K supplementation but check q2h.
• 3.3-5.3 Give 20-30mEq per liter of 1/2NS goal K
  4-5 (assuming UOP 50cc/h).
• Substantial losses in almost all 2/2 urine loss
  shifts out of cells 2/2 insulin deficiency and
  hyperosmolality so K artifically elevated at
  presentation.

29
Phosphate?

• Whole body PO4 depletion is common though PO4
  will be normal or elevated initially due to
  migration out of cells.
• With treatment hypophosphatemia will develop
  usually without adverse effects in a self-ltd
  fashion.
• No benefit to repleting PO4 unless cardiac
  dysfx/hemolytic anemia/resp depression,
  concentration lt1.

30
Assess need for HCO3

• pH lt6.9 ? Consider HCO3 gtt (though small studies
  have shown minimal benefit)
• pH gt7.0 ? No HCO3

31
Resolution

• Ketoacidosis resolved AG is normal (lt12)
• Ketonemia/Ketonuria may persist gt36h without pt
  actually being in true ketoacidosis.
• HHS pts are mentally alert and plasma osmolality
  is lt315.
• Pt is able to tolerate PO.

32
What to do with the insulin gtt when gap has
closed

• Initiate SQ insulin AT MEALTIME with a 1-2h taper
  of the gtt.
• Insulin Naïve ? 0.5-0.8U/kg per day in sliding
  scale long-acting regimen
• 25 as long acting.
• 25 as scheduled meal-time insulin
• Sliding Scale
• Known DM ? start at previous insulin regimen.

33
Potential Complications 1

• Cerebral edema
• Very rare in adults but 40 mortality.
• Sxs ha, lethargy, decreased arousal ? seizures,
  incontinence, brady, resp arrest, pupul changes.
• Mortality 20-40.
• Prevented by following protocol, adding dextrose
  to fluids when appropriate.
• Tx unit, mannitol?, 3NS?

34
Potential Complications 2

• Non-cardiogenic pulmonary edema
• Hypoxemia 2/2 decreased osmotic pressure ?
  migration of fluid into lungs.
• If initial A-a gradient is widened on ABG, higher
  risk of development of pulmonary edema.

35

• A 23-year-old woman with type 1 diabetes mellitus
  is admitted to the hospital with a diagnosis of
  community-acquired pneumonia and lethargy. Before
  admission, her insulin pump therapy was
  discontinued because of confused mentation.
• On physical examination, temperature is 37.5
  C (99.5 F), blood pressure is 108/70 mm Hg,
  pulse rate is 100/min, and respiration rate is 24
  min. There are decreased breath sounds in the
  posterior right lower lung. Neurologic
  examination reveals altered consciousness.

36

• Sodium 130 meq/L (130 mmol/L)
• Potassium 5.0 meq/L (5.0 mmol/L)
• Chloride 100 meq/L (100 mmol/L)
• Bicarbonate 16 meq/L (16 mmol/L)
• Blood urea nitrogen 38 mg/dL (13.6 mmol/L)
• Creatinine 1.4 mg/dL (123.8 µmol/L
• Glucose 262 mg/dL (14.5 mmol/L)
• Urine ketones Positive

37

• Which of the following is the most appropriate
  next step in management?
• A Add insulin glargine
• B Add neutral protamine Hagedorn (NPH)
  insulin
• C Implement a sliding scale for regular
  insulin
• D Start an insulin drip

38

• Questions?