2. OBJECTIVES
At the end of this session we will be able to:-
Define and clssify dm
Define DKA
Explain the basic classification, Precipitating
factors, pathogenesis and clinical manifestation of
DKA.
List the various investigative modalities and
treatment protocol of DKA
Complications with there management
2
3. OUTLINE OF THE SESSION
Introduction
Pathogenesis
Classification of DKA
Clinical feature
Precipitating factors
Approach
Investigation
Treatment protocol
complications
3
4. DIABETES MILLITUS
4
Diabetes Mellitus is a group of common
metabolic disorders that share the phenotype of
hyperglycemia.
It is a complex, chronic illness requiring
continuous medical care with multifactorial risk-
reduction beyond glycemic control.
caused by a complex interaction of genetics and
environmental factors
5. CLASSIFIFCATION
1. Type 1(Immune mediated & Idiopathic)
2. Type 2
3. GDM
4. Other specific types of diabetes
a. Genetic defects of beta cell function characterized by
mutations in: MODY1-6
b. Genetic defects in insulin action:
c. Diseases of the exocrine pancreas:
d. Endocrinopathies:
6
6. DIAGNOSTIC CRITERIA
Repeated on different day before making a definitive diagnosis unless
acute metabolic derangements or a markedly elevated plasma glucose are
present
7. PATHOGENESIS OF TYPE I DM
Environment ?
Viral infe..??
Genetic
HLA-DR3/DR4
Severe Insulin deficiency
ß cell Destruction
Type I DM
Autoimmune Insulitis
12. DEFINITION
DKA : is acute life treating metabolic complication of
diabetic mellitus characterized by
insulin defeicincy and
Hyperglycemia
Ketone bodies
Metabolic acidosis
12
13. PATHOPHYSIOLOGY
DKA results from relative or absolute
insulin deficiency combined with
counterregulatory hormones:
• glucagon
• Catecholamines
• Cortisol and
• growth hormone
13
EXCESS
14. The decreased ratio of insulin to glucagon promote
gluconeogenesis,
glycogenolysis and ketone body formation in the liver, as well
as
increased mobilization of substrates from fat and muscle (free
fatty acids, amino acids) to the liver
14
15. CONT,,,
Due to counter-regulatory hormones ,and peripheral
insulin resistance lead to profound
hyperglycemia,
dehydration,
ketosis, and
electrolyte imbalance.
15
16.
17.
18. APPROCH TO PT
Clinical hx Clinical sign Biochemical test
Polyuria,
polyphagia,
polydipsia
wt loss
abdominal pain or
vomiting
Varying degree of
dehydration
Kussmaul respiration
fruity (acetone) smell
altered sensorium
RBS
>11mmol/L(>250MG/dl)
)
Venous Blood Gas (pH
<7.3mmHg,
Serum HCO3 level
frequently <18mmol/L
<18mmol/L
18,
21. MANAGEMENT OF DKA
Emergency Management:
Airway:
If comatose, insert airways & NG tube
Breathing:
Give oxygen via face mask (even if O2 Sat > 95% in RA)
Circulation:
Insert IV cannula + IA line & take blood samples Cardiac
monitor (ECG for hypo/hyperkalemia) + IDC If in shock, give
10ml/kg normal saline bolus ½-1hr, maximum of 30mls/kg to
restore circulation. (N.B. Discuss with the Consultant if the
patient has received 30mls/kg)
21
21
22. MANAGEMENT DKA
1. Confirm diagnosis
(↑ plasma glucose, positive serum ketones, metabolic
acidosis).
2. Admit to hospital; intensive care setting
may be necessary for frequent monitoring or if pH
<7 or unconscious
3. Assess:
Serum electrolytes (K + , Na + , Mg 2+ , Cl – ,
bicarbonate, phosphate)
Acid-base status—pH, HCO3 – , PCO2 , β-
hydroxybutyrate
Renal function (creatinine, urine output)
22
22
23. 4. Replace fluids:
The goal is to replace the total volume loss within 24–36
hours with
50% of resuscitation fluid being administered during the
first 8–12 hours.
2–3 L of 0.9% saline over first 1–3 h (10–20 mL/kg per
hour);
subsequently, 0.45% saline at 250–500 mL/h
change to 5% glucose and 0.45% saline at 150–250 mL/h
when plasma glucose reaches 250 mg/dL (13.9 mmol/L).
23
24. The goal of the first hour of treatment
fluid resuscitation/volume expansion.
Always prepare Minnitol at bedside; 1g/kg IV push for CE
The goals of the second and succeeding hours
Correction of hyperglycemia,
metabolic acidosis and ketosis
continued volume replacement
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25. Tonicity of subsequent solution is dependent upon
hydration status,
electrolyte balance, and
urine output
Following the initial hydration, fluids can be
administered at a decreased rate of 4–14 mL/kg/h
with 0.45% NS
25
26. Hydration Helps
Restoring intravascular volume
Decreasing blood concentrations of counter regulatory
hormones
Improving insulin sensitivity of the tissues
26
27. 5. Control of hyperglycemia
IV (0.1 units/kg) bolus, then 0.1 units/kg per hour by continuous IV
infusion
increase two- to three fold if no response by 2–4 h
If plasma glucose does not fall by at least 10%, add 0.1 U/kg bolus while
continuing insulin infusion
When plasma glucose reaches 200–250 mg/dL, the insulin rate can
be decreased by 50% or to the rate of 0.02–0.05 U/kg/h
If the initial serum potassium is <3.3mml/l(3.3 meq/l) don’t
administer insulin until serum potassium is corrected
27
28. Administer short-acting insulin:
Regular Insulin 10units IV and 10 units IM, stat, then 0.1 units/kg
per hour by continuous IV infusion OR 5 units, I.V boluses every
hour.
If serum glucose does not fall by 50 to 70 mg/dL from the initial
value in the 2-3 hours, the insulin infusion rate should be doubled
every hour until a steady decline in serum glucose is achieved
28
29. Hyperglycemia usually improves at a rate of 4.2–5.6 mmol/L
(75–100 mg/dL) per hour as a result of insulin-mediated
glucose disposal, reduced hepatic glucose release, and
rehydration.
The latter reduces catecholamines, increases urinary
glucose loss, and expands the intravascular volume.
28
30. Continue above until patient is stable, glucose goal is 150–
200 mg/dL, and acidosis is resolved.
Insulin infusion may be decreased to 0.02–0.1 units/kg per
hour.
Administer long-acting insulin as soon as patient is
eating.
Allow for a 2–4 hour overlap in insulin infusion and SC
long-acting insulin injection
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31. Two ways of administration
1. With a Perfusor: 0.1U/kg/hr
the preferred method
2. Intermittently: 0.5 U/kg every 4-6 hours half
IV & half SC.
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32. Do not correct glucose too rapidly:
Aim for decr of 100mg/dl or 5 mmol/l per hour.
Switch to BID SC insulin when
acidosis resolved How do we know?
V/S are stable and
the Pt able to take PO fluid
Combine Lente ⅔ and ⅓ Regular Insulin
Divide the dose in to ⅓ in the evening and ⅔ in the
morning
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33. Ketoacidosis begins to resolve as Insulin
reduces lipolysis,
increases peripheral ketone body use,
suppresses hepatic ketone body formation, and
promotes bicarbonate regeneration
33
34.
35. 6. Assess patient
What precipitated the episode (noncompliance, infection,
trauma, pregnancy, infarction, cocaine)
Initiate appropriate workup for precipitating event (cultures,
CXR, ECG).
7. Follow up:
Measure capillary glucose every 1–2 h
measure electrolytes (especially K + , bicarbonate, phosphate)
and anion gap every 4 h for first 24 h.
35
36. 8. Replace K + :
10 meq/h when plasma K +<5- 5.2 mmol/L or(or 20–30
meq/L of infusion fluid)
ECG normal,& normal urine out put creatinine
administer 40–80 meq/h when plasma K +<3.5 meq/l
If initial serum potassium is >5.2 mmol/L (5.2 meq/L), do not
supplement K +
36
37. Potassium stores are depleted in DKA (estimated deficit
3–5 mmol/kg [3–5 meq/kg]).
Factors for development of hypokalemia
insulin-mediated potassium transport into cells,
resolution of the acidosis (which also promotes potassium
entry into cells),
urinary loss of potassium salts of organic acids.
Thus, potassium repletion should commence as soon
as adequate urine output and a normal serum
potassium are documented
37
39. Potassium
All patients with DKA have potassium depletion irrespective
of the serum K+ level
If the initial serum K+ is 5.3 mmol/L, do not supplement K+
until the level reaches < 5.3
If K+ determination is not possible delay intiation of K+
replacement until there is a reasonable urine put(>50 ml/hr)
The serum potassium should be maintained between 4.0
and 5.0 meq/l
Add 40–60 meq/l of IV fluid when serum K+ < 3.7 meq/L
Add 20-40meq/l of IV fluid when serum K+ < 3.8-5.2 meq/l
39
40. INFECTION MANAGEMENT
If infection is suspected, treat with broad-spectrum
antibiotics you may have
Since it can precipitate DKA
WBC is often elevated because of stress
40
41. SUPPORTIVE CARE
Give oxygen
low molecular weight heparin .. Venous
thromboembolism
NG tube to prevent aspiration, if the patient is
excessively vomiting or low GCS.
Urinary catheterization if incontinent, difficulty
in monitoring urine output (mini uop not be <
0.5 ml/kg/hr), or if the patient is anuric (i.e., not
passed urine by 60 minutes).
Education(compliance, exercise, feeding habit,
home 40%glucose
41
45. CEREBRAL EDEMA
Keep NBM, give 100% O2, and elevate the
head of the bed by 30º Reduce the rate of IVF to
2/3 of the calculated IVF
Give mannitol 0.5-1g/kg IV over 20 mins, may
repeat if no initial response in 30 mins to 2hrs.
Hypertonic saline (2.7-3%) 5-10 ml/kg over
30mins may be an alternative or a second line of
therapy if no initial response to mannitol
Intubation and mechanical ventilation for
impending repiratory failure, avoid aggressive
hyperventilation (keep PCO2 at 30-35 mmHg 45
