diabetic ketoacidosis dr salah mabrouk
TRANSCRIPT
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Diabetic Ketoacidosis
By
Salah Mabruok Khalaf
Master internal medicineMD Medical Oncology
South Egypt Cancer Institute2013
Local seminar Medical Oncology department
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Overview
• Definition • Epidemiology• Pathophysiology of DKA• Etiology• Clinical manifestation• Investigations• Differential Diagnosis• Prevention• Treatment• Pitfalls in DKA• A guide protocol
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DKA Definition
DKA = 3 letters= triad of D K A
Diabetic glucose >250 mg/dL (usually 500-800)
Keto
ketones producedketones – both in urine and in serumacetoacetate, acetone, betahydroxybutyrate fruity smell, not often encountered in real life)consider that if these criteria aren’t met, it may not be DKA
AcidosisIncreased anion gap, metabolic acidosis; HCO3- <15, pH<7.30
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Epidemiology
• Annual incidence in U.S. – 5-8 per 1000 diabetic subjects
• DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa.
• Higher incidence below 5 years• 2.8% of all diabetic admissions are due to DKA• Overall mortality rate ranges from 2-10%
– Higher is older patients
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Pathophysiology
Insulin
Counterregulatory hormones
Glucagon, Epinephrine, Cortisol, Growth hormone
Normal
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Pathophysiology
Excess counterregulatory hormones
Insulin deficiency
DKA
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Insulin Deficiency
Glucose uptakeProteolysis
Lipolysis
Amino Acids
Glycerol Free Fatty Acids
GluconeogenesisGlycogenolysisHyperglycemiaHyperglycemia KetogenesisKetogenesis
AcidosisAcidosisOsmotic diuresis
Dehydration
Excess counterregulatory hormones
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Etiology
• Insulin deficiency– Insulin missed dose
– Pancreatitis
– Heavy meal
• Excess Counterregulatory hormones
– Infection i.e. Pneumonia
– MI
– Stroke
– Trauma– Emotional– Pregnancy– Iatrogenic
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Insulin Deficiency
Glucose uptakeProteolysis
Lipolysis
Amino Acids
Glycerol Free Fatty Acids
GluconeogenesisGlycogenolysisHyperglycemiaHyperglycemia KetogenesisKetogenesis
AcidosisAcidosis
Osmotic diuresis
PolyuriaPolydipsia
Fruity breath (acetone smell)Kussmaul breathing (acidotic)Mental status changes
DehydrationDry tongue Tachycardia Hypotension Abd pain
Electrolyte imbalance
Clinical manifestations
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Clinical manifestations
Special notes
• Abdominal pain
It is more common in children than in adults
It is multifactorial
dehydration of muscle tissue
Delayed gastric emptying
Ileus from electrolyte disturbances
Metabolic acidosis;
It sometimes mimicks acute abdomen
It is classically periumbilical
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Differential Diagnosis
• DD of acidotic breathing– Renal failure– Amonia increase in HCF– Hysterical
• DD of diabetic coma– Lactic acidosis– Hyperosmolar non-ketotic coma– Hypoglycemia
• DD of coma in general• DD of acute abdomen
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DKA vs. HHS
DKA HHS
Age More in children More in elderly
DM type More in type I More in type II
Glucose > 250 > 600
Ketonuria/emia +++++ + or -
pH <7.3 >7.3
HCO3 <15 >15
S osmolarity Variable Hyperosmolarity
Sensitivity to insulin Variable Sensitive to small dose
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DKA vs. HYPOGLYCEMIA
DKA Hypoglycemia
Etiology Insulin deficiency or increased counter-reg hormones
Insulin overdose or hyperinsulinemia
Onset Gradual Acute
Symptoms and signs S of hyperglycemiaS of dehydration S of acidosis
-S of Brain glucopenia- S of sympathetic overactivity
RBS hyperglycemia hypoglycemia
Ketonuria Yes No
Ketonemia Yes No
IV glucose No effect Rapidly recover if early
Golden ruleGolden ruleAny diabetic patient with DKA versus hypoglycemia, give
glucose even before glucose measuring
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InvestigationsFor diagnosis
Triad for diagnosis
1.RBS Hyperglycemia > 300 mg/dl
2.Ketonemia and ketonuria
3.Blood gas metabolic acidosis
– pH < 7.35, anion gap (Na + K) – (Cl + Bicarb) > 10, and
Bicarbonate <15 mEq/L
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InvestigationsFor diagnosis
• Other findings– Electrolyte serum level
• Hyperkalemia (rarely Hypokalemia), Hyponatremia (rarely Hypernatremia )
– Investigation for the cause such as• Urine Analysis, AMI panel and ECG, Chest x-ray
– Hyperosmolarity• Normal = 285-295 milli-osmoles per kilogram (mOsmol/kg)
• [Glucose] and [BUN] are measured in mg/dL
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Investigations
For Monitoring• RBS
– Every 1 hour till RBS reaches 200 mg/dL or less, then every 6 hours
• Urine ketones– Every 8h
• Blood gas after fluid replacement• Electrolyte serum level every 4 hours till correction
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Treatment of DKA
• Treatment of predisposing factors• Initial hospital management
– Care of comatosed patients– Fluid and electrolytes replacement– Insulin replacement and glucose administration when needed– Treatment of complications
• Once resolved– Convert to home insulin regimen– Prevent recurrence
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Fluids and Electrolytes
• Fluid replacement– Restores perfusion of the tissues– Average fluid deficit 3-6 liters
• Initial resuscitation with saline– 1 L of normal saline over the first ½ hour then– ½ L of normal saline over ½ hour then– ½ L of normal saline over 1 hour then– ½ L of normal saline over 2 hours– Then the rate will depend on clinical judge (BP, CVP,
basal lung crepitation)
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Fluids and Electrolytes
• K+ level
– If Hyperkalemia (> 5.5 meqlL)
• initially present
• No treatment as it resolves quickly with insulin drip
– If normal level (3.5-5.5 meqlL)
• Add 26 mmol for each Liter of infused fluid
– If Hypokalemia (<3.5 meqlL)
• Add 39 mmol for each Liter of infused fluid
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Fluids and Electrolytes
• Phosphate deficit
– May want to use potassium phosphate
• Bicarbonate
– Not given unless pH <7 or bicarbonate <5 mmol/L or unresolved
acidosis after fluid replacement
– Dose (mmol of NaHco3) = -------------------------------------------
– Dose (No of ampoules of NaHco3) = ----------------------------------------
BW x Becar deficit
150
BW x Becar deficit
6
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Fluids and Electrolytes
• Na level:
– Calculate the corrected Sodium (for each 100 mg/dL
glucose above 100, add 1.6 meq/l to Na level)
• If corrected Na is High or Normal use Half NS (250-1000
ml/hr)
• If corrected Na is Low use NS, rate depends on severity of
volume depletion
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Insulin Therapy
• Initial dose
– IV bolus of 0.1-0.2 units/kg (~ 10 units) regular insulin
– Infusion insulin at 0.1 units/kg/hr (max 8 units/hr).
• Maintenance dose (Check BG Q1hour, goal is 50-80
mg/dl/hr)
– If falling too rapidly, decrease the rate
– If falling too slowly increase the rate by 50-100%
• Continue IV insulin until urine is free of ketones and
RBS reaches 250-300 mg/dl
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Insulin Therapy
• When RBS reaches 250-300 mg/dl
– Decrease the rate of insulin inf to 0.05-0.1 IU/kg/hr (goal
is to keep RBS in this range until the gap closes (normal
gap 7-8 mEq/l) then start home maintenance SC insulin
under umbrella of infused insulin for 2 hours, then
continue on SC insulin only .
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Glucose Administration
• Supplemental glucose
– Hypoglycemia occurs
• Insulin has restored glucose uptake
• Suppressed glucagon
– Prevents rapid decline in plasma osmolality
• Rapid decrease in insulin could lead to cerebral edema
• Glucose decreases before ketone levels decrease
• Start glucose when plasma glucose < 300 mg/dl
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Insulin-Glucose Infusion for DKA
Blood glucose Insulin Infusion D5W Infusion
<70 0.5 units/hr 150 ml/hr
70-100 1.0 125
101-150 2.0 100
151-200 3.0 100
201-250 4.0 75
251-300 6.0 50
301-350 8.0 0
351-400 10.0 0
401-450 12.0 0
451-500 15.0 0
>500 20.0 0
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Complications of DKA
• Infection
– Precipitates DKA
– Leukocytosis can be secondary
to acidosis
• Shock
– If not improving with fluids r/o
MI
• Vascular thrombosis
– Severe dehydration
– Cerebral vessels
– Occurs hours to days after DKA
• Pulmonary Edema
– Result of aggressive fluid
resuscitation
• Cerebral Edema
– First 24 hours due to aggressive
correction of hypoglycemia or
administration of hypotonic
solution
– c/p: Mental status changes
– Tx: Mannitol
– May require intubation with
hyperventilation
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Causes of Cerebral Edema
Mechanism:
• The brain adapts by producing intracellular osmoles
(idiogenic osmoles) which stabilize the brain cells from
shrinking while the DKA was developing.
• When the hyperosmolarity is rapidly corrected, the
extracellular fluids is corrected faster than brain cells
– The brain becomes more hypertonic than the extracellular fluids
water flows into the cells cerebral edema
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Causes of Cerebral Edema
The many factors have been implicated:
Rapid and/or sharp decline in serum osmolality with
treatment.
High initial corrected serum Na concentration.
High initial serum glucose concentration.
Failure of serum Na to raise as serum glucose falls during
treatment. OsmolalityNa
Glucose
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Presentations of Cerebral Edema
Cerebral Edema Presentations include:
Deterioration of level of consciousness.
Headache and blurring of vision
Vomiting
Convulsion.
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Treatment of Cerebral Edema
• Reduce IV fluids• Raise foot of Bed• IV Mannitol • Elective Ventilation• Dialysis if associated with fluid overload or renal
failure.• Use of IV dexamethasone is not recommended.
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Prevention of DKA
• Never omit insulin
– Cut long acting in half
• Prevent dehydration and hypoglycemia
• Monitor blood sugars frequently
• Monitor for ketosis
• Provide supplemental fast acting insulin
• Treat underlying triggers
• Maintain contact with medical team
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Pitfalls in DKA
• Plasma glucose is usually high but not always– DKA can be present with RBS < 300 due to
• Impaired gluconeogenesis– Liver disease
– Acute alcohol ingestion
– Prolonged fasting
– Insulin-independent glucose is high (pregnancy)
• Chronic poor control but taking insulin
• Ketone in urine may be –ve in DKA, but always +ve in blood– Due to measurement of acetoacetic acid in urine not,
betahydroxybuteric acid– Acetone in blood should be done in this case
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Pitfalls in DKA
• High WBC may be present without infection
• Infection may be present without fever
• High Creatinine may be present without true renal function: it
may cross react with ketone bodies.
• Blood urea may be elevated with prerenal azotemia
secondary to dehydration.
• Serum amylase is often raised even in the absence of
pancreatitis
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Email: [email protected] [email protected]: Dr salah mabroukYouTube channel: salahmab1
Mobil: (202) 01004081234
Email: [email protected] [email protected]: Dr salah mabroukYouTube channel: salahmab1
Mobil: (202) 01004081234