DIABETIC KETOACIDOSIS

INCREASE KETONE BODIES IN BLOOD ACIDOSIS (metabolic) DIABETES

By CHELLY MAY TAN CIPRIANO
 Etiology
 Pathogenesis
 Hallmark Signs
 Physiology
 Clinical Manifestation
 Management
 ETIOLOGY: DKA
[ THE 5 I’s ]
INTERCURRENT
INFECTION INFARCTIO ILLNESSES

INTOXICATIO INAPPROPRIATE
N USE OF INSULIN
 PATHOGENESIS OF DKA
PANCREAS/ BLOOD BLOOD HYPOTHALAMUS
THIRST CENTER
DM TYPE I/ TYPE II

o Ø INSULIN o GLUCOSE IN BLOOD

(HYPERGLYCEMIA) o POLYDIPSIA
o IMBALANCE
RATIO GLUCOSE:
INSULIN

LIVER KIDNEYS

o GLYCOGENOLYSIS o GLUCOSURIA
o GLUCONEOGENESIS o POLYURIA
o GLYCOLYSIS
PATHOGENESIS OF
DKA
** BREAKDOWN OF FATS
 STRESS needs for ENERGY
e.g. infection

** LIPOLYSIS
 BREAKDOWN OF FATS IN ADIPOSE TISSUES
 “CATABOLIC PHASE” HUNGER POLYPHAGIA

** RELEASE OF FATTY ACIDS

 FREE FATTY ACIDS IN BLOODSTREAM
 GOES TO LIVER
CONVERTED TO KETOGENESIS

** KETONE BODIES
 KETONEMIA
 KETONURIA
 5 HALLMARK SIGNS
HYPERGLYCEMIA
01

KETOSIS
02

ACIDOSIS
03

DEHYDRATION
04

ELECTROLYTES
05

IMBALANCE
 KETONES
**KETONES ARE ACIDIC IN NATURE
• ACID – SUBSTANCE THAT REALESES H+ IN A SOLUTION
• BASE – SOLUTION THAT ACCEPTS H+ IONS

• PRESENT IN THE • CANNOT BE USED • CREATED IN THE LIVER

BLOOD AT THE FOR ENERGY FROM BREAKDOWN OF
HIGHEST LEVEL PRODUCTION FATTY ACIDS “KETO
WHEN PRODUCED • REMOVED FROM ACID”
NATURALLY • CONVERTED INTO BHB
THE BODY AS A FOR TRANSPORT IN
• BETTER FOR CELL
PRODUCTION
WASTE PRODUCT THE BLOOD
ENERGY THROUGH THE • CAN BE TAKEN UP INTO
URINE OR BREATH CELLS OR BROKEN
• “REDUCED DOWN TO PRODUCE
KETONES” ACETONE

KETOSIS
KETOACIDOSIS
• METABOLIC STATE IN WHICH FAT/
KETONES PROVIDES ENERGY FOR THE • KETO ACID BUILD-UP
BODY • ACIDITY OF BLOOD
• PART OF NORMAL METABOLISM • pH IN BLOOD AND URINE
**BRAIN CAN USE LARGE AMOUNT OFKETONES INSTEAD OF
GLUCOSE FOR ENERGY (STARVATION/ KETO DIET)
** pH measures of H+ ion concentrations
free H+ = ACIDOSIS
free H+ = ALKALOSIS
 ACID-BASE FACTS 101
!!!PROBLEM: NORMAL METABOLISM IS ASSOCIATED
WITH CONTINUOUS PRODUCTION OF H+ & CO₂ pH

01 ACID 02 BASE
o SUBSTANCE THAT RELEASES H+ IN A SOLUTION o SOLUTION THAT ACCEPTS H+ IONS
o STRONG ACIDS: e.g. HCO₃- + H+ -> H₂CO₃
** dissociate easily,
** Highly Concentrated (1 H+ only!)

o WEAK ACIDS:
e.g. HCl -> H+ + Cl-

** DO NOT dissociate easily,

03 pH and BUFFERS
** Less Concentrated (2 H+) o MEASURES OF H+ ion CONCENTRATION
e.g. H₂CO₃ -> HCO₃- + H+ o BUFFERS minimize changes in pH by “mopping up” H+
o BUFFERS are a solution of WEAK ACID AND CONJUGATED BASE
e.g. blood: principle Buffer System is the WEAK ACID-> H ₂CO ₃ ,
o HCl (strong acid) **dissociate easily: HCl -> H+ + Cl-
and its CONJUGATED BASE -> HCO ₃-
HCO₃ = H₂CO₃ (weak acid)
**picked up by BUFFER to make weaker acid -> NO in FREE H+ -> NO pH
BUFFERING SYSTEM
Accumulation of ketoacids overwhelms the normal buffering capacity of blood
The pH of blood (ECF) is normally maintained within very narrow limits (7.35-7.45)
by a complex synergy of action involving the lungs, kidneys and bicarbonate buffering system in blood.
Normal metabolism is associated with continuous production of hydrogen ions (H+) which tend to reduce pH
**but bicarbonate in blood (ECF) combines with these hydrogen ions forming carbonic acid:
H+ + HCO-3 --------------------> H2CO3
(bicarbonate) (carbonic acid)
This is then converted to carbon dioxide and water:
H2CO3 ------------------------> H2O + CO2
**Carbon dioxide is eliminated from the body by the lungs in expired air and bicarbonate is regenerated in the kidneys.
- By this means, the concentration of hydrogen ions in blood, and therefore the pH, remains constant despite continuous production of
metabolic acids.
- The abnormal accumulation of ketoacids in blood that occurs in DKA overwhelms this buffering system.

Both ketoacids are strong acids and dissociate completely at physiological pH:
CH3COCH2COOH --------------------> CH3COCH2COO- + H+
(acetoacetic acid) (acetoacetate)
CH3CH(OH)CH2 COOH ----------------------> CH3CH(OH)CH2 COO- + H+
(β-hydroxybutyric acid) (β-hydroxybutyrate)

**yielding hydrogen ions. The rate at which bicarbonate can be regenerated cannot keep pace with the rate at which it is being used to
buffer this abnormal influx of hydrogen ions.
• Eventually, a point is reached when buffering fails and hydrogen ion concentration increases, and pH falls below normal.
• The patient is said to be suffering a metabolic acidosis, and blood gas analysis at this stage reveals:
reduced pH in combination with a reduced bicarbonate concentration.
ACID-BASE FACTS 101
ACID-BASE FACTS 101
01 HYPERKALEMIA
02 HYPERKALEMIA
03 HYPERKALEMIA
04 HYPERKALEMIA
 CLINICAL MANIFESTATIONS
3 0CCURANCES

A B C D
ALTERED NAUSEA & POLYURIA METABOLIC
MENTAL STATUS VOMITING COMPENSATION TO ACIDOSIS
 LETHARGIC WEAKNESS GET RID OF EXCESS
 DROWY POLYPHAGIA GLUCOSE AND  pH > 7.35
 CEREBRAL EDEMA KETONES  Kussmaul’s Respiration
POLYDYPSIA (rapid RR and fruity breath)

HYPERKALEMIA BUN/ CREATININE

Urine Analysis Reveals:
•Glycosuria
•Ketonuria
Blood Testing Reveals:
•Raised blood (plasma) glucose (hyperglycemia)
•Raised blood ketones (ketonemia)
•Metabolic acidosis
(reduced pH, bicarbonate and pCO2
•Electrolyte disturbance
(raised plasma potassium, reduced/normal plasma sodium)
•Raised urea/creatinine
(due to dehydration, reduced renal function)
•Raised plasma osmolality (reflecting dehydration)
DKA : A MEDICAL EMERGENCY
 Airway- , Breathing-
 Circulation – Establish IV Access and hydrate with IV fluids
- Usually with NS / ½ NS (depends on MD order)
- Once blood sugar is near 250mg/dL, switch to D5NS or D5½NS
**prevent rapid drop in blood sugar to prevent cerebral edema
 Electrolytes Correction
**monitor LAB values
**ECGs, Cardiac Monitor
-establish baseline for Serum K+
-ABG
**Hyperkalemia
- ION exchange resin/ potassium binders
artificial resins that exchange bound cations (Ca2+ or Na+) for potassium ions in the large intestine.
After exchange, the released cation and potassium adhering to the resin are excreted with the feces.
o Kayexalate, Calcium Resonium (oral/rectal)
**should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action
**Administer at least 3 hours before or 3 hours after other oral medications.
- Calcium Gluconate – to protect the heart (myocardium membrane stabilization )
- Beta-2 Agonist/Salbutamol activates Na+K+ pump by activating Beta-2 Adrenergic Receptors
**correct K+ if LOW
** if pH is less than 7.0 – Sodium Bicarbonate as per MD order
 Insulin Administration
**insulin drip (slow rate) (insulin+glucose)
**close monitoring of Blood Sugar
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