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.

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.


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.





Possible precipitating events (Is)
Infection (UTI? PNA?)

Insulin (incorrect dosing/noncompliance)

Ischemia (myocardial.mesenteric)

Initial presentation of DM.


More uncommon causes
Med effect meds that affect carb
metabolism
Steroids
High-dose thiazides
Atypical antipsychotics

CVA
Pancreatitis
Cocaine use



In hospitalized pts without DKA who
present with CVA, MI, or infection and
glucose >250

Maintain high suspicion for DKA check RFP
for AG and serum/urine ketones.
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



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
DKA HHS
Mild Mod Severe
Plasma Glc >250 >250 >250 >600
Arterial pH 7.25-7.30 7.0-7.24 <7.0 >7.30
HCO3 15-18 10-<15 <10 >18
Urine
ketones
+ + + Small
Serum osm Variable Variable Variable >320
Anion Gap >10 >12 >12 Variable
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
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
5 Step Approach to ABGs without
memorizing formulas.

1. Identify alkalosis/acidosis by pH change
from 7.4. (>7.4 = alkalosis. <7.4 = acidosis).

2. 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


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. 40+7 = 47mmHg.





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



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

4. If metabolic acidosis - calculate anion
gap.
Na - (Cl+HCO3)

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.
5. If AGMA - calculate delta gap.

Change in gap divided by change in
bicarbonate.

(AG-12) / (24-HCO3)

<1 AGMA + NAGMA
1-2 - Pure AGMA
>2 AGMA + Metabolic Alkalosis
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.
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.
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




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 1
st
hour
double the IV or SQ dose.

K <3.3 is a CONTRAINDICATION to insulin.

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!
If K <3.3 hold insulin therapy and replete K
with fluids 40-60mEq/h to NS until K 3.3+
(assuming UOP 50cc/h+).
If K >5.3 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.
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 <1.

pH <6.9 Consider HCO3 gtt (though
small studies have shown minimal
benefit)

pH >7.0 No HCO3
Ketoacidosis resolved AG is normal
(<12)
Ketonemia/Ketonuria may persist >36h
without pt actually being in true
ketoacidosis.

HHS pts are mentally alert and plasma
osmolality is <315.

Pt is able to tolerate PO.

Initiate SQ insulin AT MEALTIME with a 1-
2h taper of the gtt.
Insulin Nave 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.
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?, 3%NS?

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.
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.

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 mol/L
Glucose 262 mg/dL (14.5 mmol/L)

Urine ketones Positive


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

Questions?