C -II Student

1. DEPARTMENT OF ENTERNAl MEDCINE
SEMINAR PRESENTATION ON
MNAGMENT OF DKA
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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
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3. OUTLINE OF THE SESSION
 Introduction
 Pathogenesis
 Classification of DKA
 Clinical feature
 Precipitating factors
 Approach
 Investigation
 Treatment protocol
 complications
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4. DIABETES MILLITUS
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 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:
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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

8. PATHOGENESIS OF TYPE II DM
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9. 9

10. COMPLICATIONS OF DIABETES MELLITUS
 Diabetic ketoacidosis “DKA”
 Hyperglycemic hyperosmolar
state “HHS”
 Hypoglycemia
 Microvascular
 Retinopathy
 Nephropathy
 Neuropathy
 Macrovascular
 Coronary heart disease
 Peripheral arterial
disease
 Cerebrovascular
disease
 Others
Acute complication Chronic complication

11. COMPLICATIONS OF DIABETES MELLITUS
 Diabetic ketoacidosis “DKA”
 Hyperglycemic hyperosmolar
state “HHS”
 Hypoglycemia
 Microvascular
 Retinopathy
 Nephropathy
 Neuropathy
 Macrovascular
 Coronary heart disease
 Peripheral arterial
disease
 Cerebrovascular
disease
 Others
Acute complication Chronic complication

12. DEFINITION
 DKA : is acute life treating metabolic complication of
diabetic mellitus characterized by
 insulin defeicincy and
 Hyperglycemia
 Ketone bodies
 Metabolic acidosis
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13. PATHOPHYSIOLOGY
DKA results from relative or absolute
insulin deficiency combined with
counterregulatory hormones:
• glucagon
• Catecholamines
• Cortisol and
• growth hormone
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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
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15. CONT,,,
 Due to counter-regulatory hormones ,and peripheral
insulin resistance lead to profound
 hyperglycemia,
 dehydration,
 ketosis, and
 electrolyte imbalance.
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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,

20. PRECIPITATING EVENTS
 Inadequate insulin
administration
 Omission of insulin
therapy
 Tissue ischemia
 Infection
 pneumonia
 UTI
 Gastroenteritis
 Sepsis
 Infarction
 cerebral,
 coronary,
 mesenteric,
 peripheral
 Drugs (cocaine)
 Pregnancy
 Alcohol intoxication or
abuse
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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)
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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)
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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).
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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
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26. Hydration Helps
Restoring intravascular volume
Decreasing blood concentrations of counter regulatory
hormones
Improving insulin sensitivity of the tissues
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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
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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
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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.
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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
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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.
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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 +
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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
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38. CORRECTION OF POTASSIUM

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
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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
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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
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42. FOLLOW UP
 Vital sign(hrly)
 Input & out put(hrly)
 Neurological status(hrly)
 Blood glucose (hrly)
 Blood betahydrobutrat(2hrly)
 Electrolyte(2hrly)
 ECG
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44. TREATMENT COMPLICATION
 Hypoglycemia
• Hypokalemia
• Aspiration pneumonia
• Cerebral oedema
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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

46. REFERENCES
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47. 47
Thank you!!