MANAGEMENENT OF

DIABETIC KETO ACIDOSIS

MUHAMMED YESUF(M D)
University of Gondar
Presentation outline
Overview
History
Epidemiology
Pathophysiolgy
Clinical presentation
Dx and DDX
Rx
Monitoring
DKA Resolution
Complications
Sick day rule
Overview
One of the common and life threatening acute
complication of DM
Results from absolute insulin deficiency and its
resultant metabolic alterations
Accounts for 16% of DM related deaths
History
First full description
Jullius Dreschfeld 1886
Universally fatal till 1920’s
By 1930 MR 29%
By 1950 MR <10% invention of insulin
Cerebral edema in DKA
Dr’s from Philadelphia
Contributing universities-researches
University of Tennesse
Emory university
KPD 1987
 Epidemiology
In type I
In young (<65)
More in women
MR <5% (1-2%)
Commonly from the precipitating factors
Pathophysiology
Insulin deficiency
Increased counter regulatory hormones (Glucagon,
cathecolamins, cortisol, GH)
Hyperglycemia
Impaired glucose utilization
 Decreased insulin - decreased GLUT 4
Increased glucose production
 Gluconogenesis
 Glyconogynolysis

Hyperglycemia
Draws water from cells Volume depletion
Induces glucosuria with osmotic diuresis
Volume depletion/ DHN depends on
Duration of hyperglycemia
Level of renal function
Pt fluid intake
Ketoacidosis
keton bodies from increase lipolysis
Decreased insulin

Lipolysis

Glycerol FFA
Maloyl CoA

Gluconogenesis TG, VLDL KB

Electrolyte disturbance
Na
balance of water shift from ICF to ECF Vs Osmotic
diuresis
hyperglycemia causes a sodium drop of 1meq of Na
for every 62mg/dl rise of glucose
corrected serum Na = measured Na + (∆SG(mg/dl) /42)
or
= measured Na + (∆SG (mmol/L) /2.3)
Generally loss of Na is 7-10 meq/kg
Normal Na level is equal to severe volume depletion
corrected serum Na > 140 meq/L – severe fluid
depletion
Renal failure – hyponatremia
K
Measured K can be high, low, normal. Generally there is
3-5 mg/Kg loss
urinary loss
GI loss
Loss from cells
Serum K is increase b/c of decreased insulin and
hyperosmolarity. Acidosis plays less role
Phosphate
Negative P balance
decreased intake
phoshaturia
Serum level can be normal or increased b/c of
decreased insulin
acidosis
Bicarbonate
Always low
Table : Total body deficits of water and electrolytes in DKA
DKA
Total water(l) 6
Water(ml/kg) 100
Na(meq/kg) 7-10
Cl(meq/kg) 3-5
K(meq/kg) 3-5
Po4(mmol/kg) 5-7
Mg(meq/kg) 1-2
Ca(meq/kg) 1-2
Clinical presentation
Sx
Early – poly Sx
Wt loss
Later – neurologic Sx (lethargy, focal signs, obtundation,
Coma)
Because of increased plasma osmolality. It occurs
when the effective plasma osmolality is 320 – 330. And it
can be calculated as
Effective Posm= [2*Na (meq/L)] + [glucose (mg/dl)/18]
Or
= [2*Na (mmol/L)] + [glucose (mmol/L)]

Effective Posm= [measured Posm]-[BUN (mg/dl) /2.8]

Or
= [measured Posm]-[BUN (mmol/L)]
Abdominal pain, nausea and vomiting
Abd pain associated with the degree of acidosis and could
be due to delayed gastric emptying or illus
Symptoms of precipitating factors
TABLE
Factors Most Often Associated with the Development of Diabetic Ketoacidosis
Factor
Approximate frequency (%)
Infection
35
Omission of insulin or inadequate insulin
30
Initial presentation of diabetes mellitus
20
Medical illness
10
Unknown
5
Signs
Signs of volume depletion
 Tachycardia, hypotension
 Dry mucusmembrane, reduced skin turgor

Tachypnea, kussmauls respiration

Acetone breath
Abdominal tendernes
Altered mental status
Lab abnormality
Serum glucose
 Elevated usually < 600 mg/dl. Could be >900mg/dl in
comatose pt. why?
 Could be normal – euglycemic DKA
 Starvation

 Pregnancy

 Liver disease

 Prior Rx with insulin

Serum electrolytes
 Na
K variable
P
 Bicarbonate-low

Not the total body amount reflected

BUN,Cr
 Could be elevated b/c of volume depletion
 Acetoacetate falsely elevates Cr

CBC
 Leucocytosis-b/c of increased cortisol and cathecolamines
 Can indicate infection
U/A
 Urine ketone
 UTI
 Diabetic nephropathy

Plasma osmolality
 Calculated as described before
 Usu in DKA 300-320

Serum ketones
 Nitropruside isnot a good method
 False negative b/c B-OHB is not detected by nitroprusside

 False positive with drugs like captopril,pencillamine,mesna

ABG
ECG
PH and bicarbonate
 Bicarbonate<15 meq/l
 PH 6.8-7.3

Anion gap>12
Additional lab studies
 Urine culture
 Sputum culture

 Blood culture

 CXR

 A1C

 Amylase lipase
DDX
Alcoholic ketoacidosis
Starvation ketosis
Anion gap acidosises
such as
 Lactic acidosis
 Salicylate intoxication

 Methanol/ethylene glycol intoxication

 Rhabdomyolysis
Table :Diagnostic criteria for DKA and classifications
parameters Mild Moderate Severe
Plasma glucose(mg/dl) >250 >250 >250
Arterial PH 7.25-7.30 7.00-7.24 <7.00
Serum bicarbonate(meq/l) 15-18 10-15 <10
Urine ketone positive positive positive
Serum ketone positive positive positive
Effective serum osm variable variable variable
Anion gap >10 >12 >12
Mentation alert Alert/drowsy Stupor/coma
 TREATMENT
Initial evaluation
ABC
Mentation
altered-NG Tube
Volume status
Precipitating factors
May need emergency Rx
Goals of Rx
Improving circulatory volume and tissue perfusion
Reducing blood glucose and serum osmolality to normal
level
Clearing ketone from serum and urine at a steady state
Correcting the electrolyte imbalance
Identifying precipitating factors
Components of Rx
Fluid
Insulin
electrolytes
 FLUID MX
It will
Increase intra vascular volume
Decrease BG (30-70mg/l) trough increase insulin
 Hemodilution sensitivity
 Urinary loss

Decrease counter regulatory hormones

The fluid deficit should be corrected over 24hrs
Rate depends on Pt volume status
Generally 10-15ml/Kg NS
Roughly the fluid can be given like this
1L-30 min
1L-2hrs
1L-4hrs
1L-6hrs
Then 1L every 6 hrs
Type of fluid depends on
Glucose level
Osmolality
Electrolyte composition
So initially NS then ½ NS
when BG<200-250mg/dl D5
When 1/2NS?
Why Dextrose?
NS Vs RL?
Fluid initially then insulin Vs simultaneous??????
 INSULIN
Multiple dosing styles
1. 0.1u/kg bolus followed by 0.1u/kg continuous infusion
2. 0.14u/kg continuous infusion
3. S C administration –for mild DKA
0.3u/kg followed by 0.1u/kg till BG<250 mg/dl
then 0.05-0.1u/kg q1-2hr till resolution after that the
hrly admn will be stopped to change it to the standing
dose
This has shown equal efficacy with reduced
cost(39%)
4.??our protocol
0.3u/kg 1/2iv 1/2im/sc
Then 0.1u/kg im/sc q hr till BG is <250mg/dl
Then 0.05u/kg q hr till resolution
If no drop as expected(50-70mg/dl)
10iu iv bolus q hr
5. Im insulin
initially 20iu im then 5iu im q hr
if BG<250mg/dl-sc
After resolution
Naive Pts 0.5-0.8u/kg calculated to be given as
combination with 2/3 M and 1/3E
Known diabetics put on the previous dose
NB :regular insulin and the standing should overlap for
1-2 hr
Sliding scale
BG q 4 hr and for every 50mg/dl increase above
150mg/dl increase the insulin by 5iu up to a maximum of
20iu
For pts not feeding,in stressful condition
Standing dose with correction???
 ELECTROLYTES
Potassium
<3.3meq/l
 Avoid insulin
 40-60meq of kcl /l

3.3-5.3meq/l
 Give insulin
 20-30meq of kcl /l

>5.3meq/l
 Give insulin
 No k

So k replacement is when serum k is <5.3 and with adequate urine out put
Better be replaced as 2/3 potassium chloride and 1/3 as potassium
phosphate b/c-it prevents hyperchloremic acidosis
-it provides phosphate
Bicarbonate
Not routine
Indications
 PH<7.0

 Life threatening hyperkalemia

Administration
PH <6.9 -100meq in 400ml sterile water with monitoring of
venous PH q 2hr till PH>7.0
Fear
 Neurologic deterioration

 Slow recovery from ketosis

 Post Rx metabolic alkalosis

Phosphorous
Not routine
Indications
 Cardiac dysfunction
 Hemolytic anemia
 Resp depression
 Serum level<1.0meq/l

Administration
 20-30meq of potassium phosphate
 MONITORING
We can prepare pt data flow sheet w/h contains
Mental status
Vital sign
 T,PR,RR and depth, BP
Chemistries
 Serum glucose
 Urine ketone

 Serum e

 Serum BUN

 Effective serum osm

Insulin
 IV,IM,SC
Fluid
 NS/D5
UOP
Generally serum glucose q hr, chemistries q 2-4 hr with frequent clinical evaluation
 DKA RESOLUTON
General improvement in sx
Pt able to feed
Normal anion gap <12meq/l
Serum glucose <200mg/dl
Serum bicarbonate>18meq/l
Venous PH>7.3
 COMPLICATIONS
Hypokalemia
Hypoglycemia
ARDS
Cerebral edema
MI
DVT
Acute gastric dilatation
Erosive gastritis
Resp distress
Hypophospatemia
Infection……
Cerebral edema
Dxic criteria(murei etal)
 Abnormal response to pain
 Decorticate,decerebrate posturing
 CN palsy
 Abnormal resp pattern
 Fluctuating LOC
 Sustained bradycardya
 Incontinence
 More non specific-vomiting, headache, lethargy, elevated DBP
RX of cerebral oedema
 Mannitol 0.5-1gm/kg over 15-30 min, if no response repeat
after 20-30 min
 3%Saline 5-10mg/kg over 30min
 Hyper ventilation
 Surgical
Special considerations
pregnancy
 fetal mortality as high as 30% and increased to 60% when the
DKA is associated with coma
Children
 be alert to headache and reduced LOC
 SICK DAY RULE
Golden rule –Never stop taking your insulin,b/c when
you are sick the body sugar increases
Foods and drinks-take non sugary fluids, continue
eating
Blood glucose and urinary ketone –q2-4hr
Insulin mx
BG>7mmol/l-increase the usual insulin by 10%
UK +ve-increase insulin by 20% of the daily dose
Calculate and take a correction insulin dose
could be repeated q2-4hr
THE END
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