1. 2. DIABETIC KETOACIDOSIS (DKA) 3. DR. EMAD AHMED, MD Ass.
Professor of Anesthesia and Intensive Care Suez Canal University 4.
Diabetic Ketoacidosis (DKA) It is a life threatening but reversible
complication of type 1 diabetes due to absolute insulin deficiency.
Ketoacidosis: High anion gap metabolic acidosis due to excessive
blood concentration of ketone bodies (Ketoanion). 5. Pathogenesis
of DKA A-The basic underlying mechanisms are: -Absolute deficiency
of circulating insulin. -secretion of insulin counterregulatory
hormones; glucagon, adrenaline, cortisol and growth hormone. 6.
B-This leads to disturbances in the following physiological
processes: -glucose utilization (hyperglycemia). - proteolysis (
amino acids, glutamine and alanine). - lipolysis ( glycerol and
FFAs). - glycogenolysis (breakdown of muscle glycogen lactate). -
gluconeogensis (glutamine & alanine & glycerol &
lactate are the precursors). 7. C-This results in the following
metabolic abnormalities: 1-Hyperglycemia. 2-Hyperketonemia: 2 main
mechanisms: a- Production of ketone bodies (ketogenesis): -Increase
FFAs hepatic uptake FFAs enter the mitochondria oxidation to form
acetoacetic acid. -Large part of acetoacetic acid reduced to
-hydroxy butyric acid ( -HBA). -Small part of acetoacetic acid is
decarboxylated to acetone. The 3 ketone bodies are released to the
blood in a ratio between acetoacetic acid to -HBA of 8 : 1 . b-
Utilization of ketone bodies. 8. D-The consequences of these
metabolic abnormalities are: a-Hyperglycemia: -Osmotic diuresis.
-Excessive urinary losses of H2O & Na, K. -Dehydration and
hypotension. b-Hyperketonemia: -Ketonuria. - Blood acidity
(acetoacetic acid and -HBA are strong acids). -Obligate losses of
sodium and potassium due to urinary excretion of ketone bodies
(salt) alkaline reserve. -Acetone is a CNS anaesthetic. 9.
E-Electrolytes and acid base disturbances during DKA: a-Serum K:
Usually high (hyperkalemia) secondary to: 1-Shift of K from
intracellular to extracellular compartment due to: -Insulin
deficiency and hyperglycemia. -Extracellular hyperosmolarity.
-Acidosis. - Catabolism and breakdown of cellular protein.
2-Impaired cellular uptake of K. 10. b-Serum sodium: Usually low
secondary to: -Hyperglycemia leads to osmotic flux of H2O from
intracellular to extracellular space. -Obligate sodium loss with
ketonuria. c-Metabolic acidosis: Secondary to: - Production and
utilization of strong acids; acetoacetic acid and -HBA. - Alkaline
reserve (sodium and K losses). 11. Clinical features of DKA
A-Symptoms of DKA: 1-Classic symptoms of hyperglycemia: short
period of time: Polyuria, polydipsia, wt loss and thirst. 2-Other
symptoms: - General weakness, malaise and lethargy. -Nausea,
vomiting and abdominal pain. - Perspiration. - Disturbed
consciousness and confusion. 3-Symptoms of underlying infections or
other conditions; fever, abdominal pain, dysuria, chest painetc.
12. B- Physical signs of DKA: a-General signs: Ill appearance and
disturbed consciousness. b-Signs of dehydration: -Skin: Dry, hot,
flushed, and loss of skin turgor. -Tongue: Dry (sometimes woody
tongue). -Eyes: Sunken eyes and dark circles under the eyes.
c-Vital signs: -Tachycardia, hypotension and tachypnea. d-Specific
signs: -Ketotic breath: A strong, fruity breath odour (similar to
nail polish remover or acetone). -Acidotic breath (Kussmaul's
respiration): deep and rapid. -Abdominal tenderness. 13. Diagnostic
criteria of mild to moderate DKA: Blood glucose > 300 mg/dl.
Mild to moderate dehydration. Ketonuria: mild (+) to moderate (++).
Serum bicarbonate < 15 m Eq/L. pH is acidic (Metabolic
acidosis): Arterial < 7.3. Or Venous < 7.25. 14. Diagnostic
criteria of severe DKA: Blood glucose > 300 mg/dl. Heavy
ketonuria +++ Severe dehydration. pH is acidic: Arterial < 7. Or
Venous < 6.95. Serum bicarbonate < 10 mEq/l. Anion gap >
12 mEq/l (normal gap 7-8 mEq/l) AG = (Na+ ) (Cl- + HCO3) 15. Urine
testing during DKA 1- Urine glucose conc. Is poorly correlated with
BG levels. 2- Renal threshold for glucose and ketones are increased
in DKA & HHS. 3- Most of the available laboratory urine tests
(nitroprusside test) detect only acetoacetate & acetone but not
betaHB. 4- Beta-HB is the predominant ketones in severe untreated
DKA cannot be measured or recognized by the standard nitroprussid
test . 16. 5- When the clinical condition improves with treatment ,
the urine test results become positive due to the returning
predominance of acetoacetate . 6- So, during follow up of patients
with DKA urine test for ketones is better avoided. 7- Now blood
ketone measurements are available and detect beta-HB. 17.
Complications of DKA 1-Complications of associated illnesses e.g.
sepsis or MI. 2-Adult respiratory distress syndrome.
3-Thromboembolism (elderly). 4-Complications of treatment:
a-Hypokalemia: Which may lead to: -Cardiac arrhythmias. -Cardiac
arrest. -Respiratory muscle weakness. 18. b-Hypoglycemia.
c-Overhydration and acute pulmonary edema: particularly in:
-Treating children with DKA. -Adults with compromised renal or
cardiac function. -Elderly with incipient CHF. 19. d-Neurological
complications: Cerebral Edema. -It occurs only in children with
DKA. -Very dangerous and increases mortality. -The risk is related
to the severity, duration and rapid correction of DKA. 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 brain becomes hypertonic towards the extracellular fluids water
flows into the cells cerebral edema 20. Management of DKA The main
lines of management include: A-Primary assessment: -Volume status
and degree of dehydration. -Blood pressure and cardiac condition.
-Degree of consciousness. -Degree of acidosis. -Precipitating
disease 21. B-Ongoing monitoring: -Blood glucose (using
glucometers) every hour. -Electrolytes and pH every 4 hours. -Urine
for glucose and ketones every 4 hours 22. C-Initiation of
treatment: 1-General measures: -Airway and O2 inhalation if needed.
-IV line. -Urinary Foley's catheter (if in shock). -NGT
(Nasogastric Tube): to avoid gastric dilatation and protection from
aspiration . -Thrombosis prophylaxis: 5000 units of heparin SC/12
hours. -Empiric use of 3rd generation cephalosporin antibiotics.
23. 2-Specific measures: Successful therapy of hyperglycemic crises
requires the administration of: a-Fluids: 1- Correct volume deficit
and hypotension. 2- Improve tissue perfusion. 3-Improve insulin
sensitivity (insulin counterregulatory hormones). 4-Improve
glomerular filtration rate: i- excretion of large amount of glucose
in urine. ii-Clears hyperketonemia. 5- Correct metabolic acidosis.
24. b-Insulin: Reversal of metabolic abnormalities : i-Corrects
hyperglycemia. ii-Inhibits ketogenesis. c-Potassium: Prevents
complications associated with hypokalemia. 25. Fluid Therapy The
expected volume deficits calculated as: 5-10% of body wt in DKA
(3-6 liters). 15 % of body wt in NKHH (9 liters). Replacement
therapy should be given within 24 hours after admission: 50% of the
deficit in the first 4 hours. 50% of the deficit in the next time
for up to 24 hours, guided by ongoing clinical evaluation. For
children and adolescents (less than 20 years): Fluids are given as
10-20 ml/kg/hour in the first four hours. Then given guided by
clinical evaluation 26. Type of fluid 1-Normal saline (0.9% sodium
chloride). Advantages: -Available all the time. -Rapid expansion of
extracellular compartment. -Slow decline of extracellular
osmolarity. -Slow rate of cerebral edema evolution. Disadvantages:
May accentuate hypernatrimia if present. Indications: -All cases of
DKA. -Initial (1st 2 liters) in NKHH state. 27. 2-Half strength
saline (0.45% sodium chloride): Used only if serum corrected sodium
is high >145 mEq/L. Corrected sodium level = measured sodium +
corrected value. Corrected value: For every 100 mg/dl BG above the
normal baseline of BG 100 mg/dl, Add 1.6 mEq/l Na to the measured
serum sodium. Example: Measured Na = 134 mEq/L, BG= 400mg/dl.
Corrected Na value: 3 x 1.6 mEq/L=4.8 mEq/L. The serum corrected Na
is: 134+4.8 = 138.8 mEq/L. 28. Insulin Therapy Standard low dose
insulin regimen: This regimen is the only effective therapy in DKA
& NKHH state: 1-Inhibits ketogenesis and gluconeogenesis. 2-
Presence of insulin resistance state secondary to: a- Stress
insulin counterregulatory hormones. b- Ketone bodies & FFAs. c-
Hemoconcentration and electrolytes imbalance. d- Hyperosmolarity.
e- Infection. 29. Type of insulin : Regular : Rapid or short acting
insulin U-40 & U-100. Regimen: Initial bolus: 0.1 U/kg body wt
given IV. Maintenance: 0.1 U/kg/body wt /hour: a- IV Infusion set:
Add 100 units of regular insulin +500 ml saline i.e. every 5 cc
fluid contains 1 unit of insulin b-IV infusion set is not
available: IM route. 30. Potassium Therapy Initially: Mild to
moderate hyperkalemia occur in patients with DKA. Later on: After
initiation of: Insulin therapy Correction of acidosis lead to
hypokalemia. Volume expansion & hydration 31. Rational of
potassium therapy In the 1st 2 liters of fluid add no potassium. If
urine output confirmed add KCl from 3rd liter on. If serum
potassium: < 3 mEq/L add 20 40 mEq KCl/liter to IV saline. 3-5
mEq/L add 10 20 mEq KCl/liter to IV saline. > 5 mEq/L add no
potassium. Patient with oliguria or renal insufficiency: K levels
must be frequently monitored with continuous ECG evaluation. The
infusion continues until the patient can tolerate oral potassium
supplement (15 CC potassium syrup/ 8 hours). 32. A Guide Protocol
33. 6-Order the rehydration program as follow (normal saline):
First 4 hours : 50% of the calculated total fluid deficit. Next
time for up to 24h: 50% of the calculated total fluid deficit. 34.
7-Order and start insulin regimen: Type of insulin: Rapid or short
acting insulin. Initial bolus = 0.1 unit X BW in Kg / direct IV.
Maintenance = 0.1 unit X BW in Kg / hour. Infusion set available:
Order: Add 100 units of regular insulin to 500 cc saline i.e. every
5 cc contains one unit of insulin, calculate the dose and give by
IV drip. Infusion set is not available IM route NB: For IM route:
it is important to use a needle that is long enough to insure that
the insulin is not given SC 35. 8-Order potassium replacement
regimen: Type of fluid: potassium chloride ( amp=10 mEq). Aim: K
level should be in the range 4-5 mEq/L. If serum potassium: < 3
mEq/L add 20 40 mEq KCl/liter to IV saline. 3-5 mEq/L add 10 20 mEq
KCl/liter to IV saline. > 5 mEq/L add no potassium. 36.
9-Monitoring: Blood glucose by glucometer every hour. Urine
analysis for glucose and ketones every 4 hours. 10-Order IV glucose
5% (second line) once blood glucose reaches: < 250 mg/ dl in
DKA. < 300 mg/ dl in NKHH state. 11-Re-evaluate parameters of
rehydration establishment: Stable blood pressure. Normal urine
output. Clinical signs of rehydration. 37. 12-Evaluate the criteria
for stopping hourly insulin regimen (resolving DKA): Acidosis
corrected clinically and by pH. Negative ketonuria. Eating. Patient
looks good and feels good. 38. 13-Initiate SC insulin therapy: Give
10 units NPH/SC one hour before stopping hourly insulin regimen
a-Patients with newly diagnosed diabetes: Initial dosage is 0.5 -
0.8 U/Kg BW/day: calculate the dose and give (2/3) before breakfast
and (1/3) before dinner in a ratio (2/3) NPH and (1/3) regular
insulin. b-Patients with known diabetes: Initial dosage is the same
as the dosage they were receiving before onset of DKA. Monitor
blood glucose before and after each meal and at bed time, and
upgrade the insulin doses accordingly. 39. Thank you