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IntroductionIntroduction
• Acute life threatening complication of DM
• DKA predominantly seen in type 1 DM
• DKA represents body’s response to cellular
starvation due to insulin deficiency & counter
regulatory hormone excess
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• Facilitate uptake
of glucose &
conversion into
glycogen
• Inhibits
glycogenolysis &
gluconeogenesis
• Increase
lipogenesis
• Inhibit
lipolysis
• Uptake of
amino acids into
muscle cell
• Prevents release
of amino acids
from muscle
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Pathophysiology
Insulin Deficiency is the primary defect in
patients with DKA
Muscle Hepatocyte Adipose
Glucose
Amino
Acids
Glucose-P
Glycogen
Pyruvate, CO2
Glucose
Free
fatty
acidsKetoacids
Normal Insulin Activity
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Clinical featuresClinical features
• Increased PGI2 and PGE2peripheral
vasodilation ,nausea, vomiting and abdominal
pain.
• Vomiting maladaptive response to counter
acidosis exacerbates the potassium losses
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Signs of DKASigns of DKA
• Dehydration
• Hyperventilation
• Ketotic breath
• Tachycardia and hypotension
• Disturbed conscious state and shock
• Alteration of consciousness correlate better with
elevated serum osmolality (>320 mOsm/L) than with
severity of metabolic acidosis
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Approach to therapyApproach to therapy
• Correcting the hyperosmolar state and
dehydration is the initial aim of therapy.
• Insulin therapy should be undertaken only
after the patient is stable hemodynamically.
Glucose and H2O
H2O lost in urine Loss of ECF, vascular collapse and death
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Fluid ResuscitationFluid Resuscitation
• Single most important step
• Fluid deficit around 100ml/kg (5-10L)
• Helps in Restore I/V volume
• Perfuse vital organs
• Increase GFR
• Decrease serum Glucose & Ketone levels
• To restore normal tonicity
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Fluid balance in diabeticFluid balance in diabetic
hyperosmolarityhyperosmolarity
ECF = 14 L ICF = 28 L
H2O
ECF ICF
H2O
Osmotic Diuresis
Osmotic Diuresis ECF hyperosmolar from ICF autotransfusion
ECF and ICF both hyperosmolar
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Fluid ResuscitationFluid Resuscitation
• 2–3 L of 0.9% saline over first 1–3 h (10–15
mL/kg per hour)
• 0.45% saline at 150–300 mL/h; change to 5%
glucose and 0.45% saline at 100–200 mL/h
when plasma glucose reaches 250 mg/dl.
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Insulin therapyInsulin therapy
• Ideal way to administer insulin by continuous
infusion of small doses of regular insulin
0.1unit/kg/hr once hypokalemia is excluded.
• I/M or S/C administration of regular insulin
should be avoided as insulin absorption may be
erratic in volume depleted & vasocostricted
patient
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Insulin therapyInsulin therapy
• Goal is to decrease Glucose by 50-75mg/dl/hr.50-75mg/dl/hr.
• Infusion should continue until anion gap normalized
• S/C insulin should bridge for atleast one hour before
discontinuation of I/V insulin
• Insulin administration should be W/H if K <3.3 mEq
till K is supplemented
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DKA: Switch to S.C. insulinDKA: Switch to S.C. insulin
Can consider switch to SC insulin when:
• AG normalized
• BS < 250 mg/dl
• Insulin IV requirements < 2U/h
• Patient able to eat
• Hemodynamically stable
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DKA: Switch to S.C. insulinDKA: Switch to S.C. insulin
• Overlap insulin IV with 1st
SC insulin by 2-4h
to avoid recurrent ketosis
• T2 DM patients with DKA:
• Don’t necessarily have to be continued on
insulin
• Once acute stress resolved, many do well on
OHA
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Goal of K ReplacementGoal of K Replacement
• To maintain a normal extracellular K+
conc during
the acute phase of therapy and to replace intra-
cellular deficits over a period of days
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K SupplementationK Supplementation
Serum Potassium < 3 mEq/L Give 60mEq/l to IVF
3-3.9 mEq/L 40mEq/l to IVF
4-5.4 mEq/L 20 mEq/L to IVF
> 5.5 mEq/L No Replacement necessary
Verify Normal kidney function &
Urine output before treatment
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ADA RecommendationADA Recommendation
If PH 6.9-7.0 50mEq of NaHCo3+200ml sterile
water+10mEq KCl over 1 hour
If Ph <6.9 100mEq of NaHCo3+400ml sterile
water+10mEq KCl over 2 hours
Repeat dose of bicarb every 2 hours till PH>7
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Theoretical AdvantagesTheoretical Advantages
• In case of severe acidosis
• Improve myocardial contractility
• Improve catecholamine tissue response
• Decrease work of breathing
• In case of Hyperkalemia
• Elevate ventricular fibrillation threshold
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Correction of acidosisCorrection of acidosis
Don’t use bicarbonate as
• It will increase chances of cerebral edema
by 4 times.
• can lead to volume overload,
hypernatremia, paradoxical cerebral
acidosis, accelerated K+
loss
Is there any role for bicarbonate in DKA?
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Indication for bicarbonateIndication for bicarbonate
• pH < 7.0
• Hemodynamically unstable
• Not responding to fluids
• Depressed cardiac contractilty
• Poor perfusion
Dose: 0.5 – 2 mEq/kg over 1-2 hrs
Stop correction once pH >7.0
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Major complication of DKAMajor complication of DKA
• Cerebral Edema: most dreaded complication
• 57-87% of all pediatric DKA-associated
deaths
• More in < 5yrs Rare in > 20 yrs.
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Reasons for Cerebral EdemaReasons for Cerebral Edema
• Over aggressive fluid correction
• Failure of Na+
to rise with fall of glucose
during treatment
• Cerebral ischemia due to severe dehydration
and hypocarbia
Onset : 6-12 hrs. after onset of therapy
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IntroductionIntroduction
• A metabolic emergency that occurs in
diabetic patient usually Type 2 Diabetes
Mellitus
• Characterised by uncontrolled hyperglycemia
that induces hyperosmolar state and
dehydration without significant ketoacidosis.
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Diagnostic featuresDiagnostic features
• Plasma glucose level of 600 mg/dL or greater
• Effective serum osmolality of 320 mOsm/kg
or greater
• Profound dehydration (8-12 L) with elevated
serum urea nitrogen (BUN)-to-creatinine ratio
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Clinical features
• Severe dehydration invariable
• May have associated lactic acidosis due to
hypoxia
• Precipitating factors similar to DKA
• Mortality rate is high
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SymptomsSymptoms
A wide variety of focal and global neurologic
changes may be present :
• Drowsiness and lethargy
• Delirium
• Coma
• Focal or generalized seizures
• Visual changes or disturbances
• Hemiparesis
• Sensory deficits