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Diabetic Ketoacidosis (DKA) (LABORATORY FINDINGS (SIGN) (Elevated pulse…
Diabetic Ketoacidosis (DKA)
GOAL OF TREATMENT
To correct metabolic disturbance
To prevent more complications
To provide adequate glucose control through each 24hour period
Identify and treat precipitating events
TRIGGERS
weak and nausated
blood glocose level high
PHARMACOLOGICAL TREATMENT
CONTINUOUS INSULIN INFUSION 0.1ml/kg/hr
Restart of IV regular insulin at 0.15u/kg bolus💉
0.1u/kg/hr infusion
Start after 1 hour of initial IVF
Change SC insulin before meal when metabolic stable (glucose 8-12mmol/l, pH >7.3, HCO3 >15)
Once glucose is 200mg/dL, :fast_forward: to 5% dextrose
IV FLUID THERAPY
Initiate 0.9% NS IVF with rate 500-100 ml/hr for 1-2 hrs👩⚕️
Cardiac, renal, ECG, lab measurements of glucose, bedside measurement of blood ketones, electrolytes, venous pH, anion gap, and bicarbonate must be repeated.
Treatment at emergency department (✔Correction in 48 hrs)
0.45% NS IVF ➕ KCl 20-30mEq/L with rate of 250-500 ml/hr
Once plasma glucose level reached 200 mg/dL, the IV fluids should hold 5% to 10% of dextrose to permit insulin administration until ketonemia is improved
SYMPTOMS
lethargy
polyurea
nausea
polydipsia
blurry vision
slurred speech
slightly confused
ketone on breath
vomit
shortness of breath
NON PHARMACOLOGICAL TREATMENT
DIET
-decrease intake food rich in carbs & fat
-avoid food rich in saturated fats & cho
-consume food rich in mono & polu unsaturated fatty acids
a/oxidants, vit A,C,E, minerals, fibre
EXERCISE
check feet for blisters/sores
wear proper shoes & socks
drink plenty of fluid
warm up & cool down
have a snack handy
FOOT CARE
daily foot inspections
wash feet with lukewarm water &mild soap
dry feel well and keep skin smooth
medicated powder
x treat calluses, x barefoot, x let feet get too hot / cold
COUNSELING
constantly check the condition of the pump and also each time before injecting
PRIORITIZE-Diabetic ketoacidosis (DKA)
type 1 DM
insulin deficiency
ketone smell when breathing
Kussmaul respiration
insulin pump disconnected(missed doses)
If not treated immediately? any complications?
blood glucose continue to increase
more fats are used to convert to energy
cerebral edema
hypokalemia
cardiac arrest
kidney failure
worsen the dehydration
MONITORING
White blood cell count
normal range = 4,000 and 11,000 per microliter of blood
Vital sign
Body temperature
Pulse rate
Respiration rate (rate of breathing)
Blood pressure
Kidney function tests
ACR (Albumin to Creatinine Ratio)
GFR (glomerular filtration rate).
. Blood glucose
100-180 mg/dL
Ketone level
<0.6mmol/L
Eye examination
Fluorescein angiography
Optical coherence tomography
Comprehensive dilated eye exam
Electrolyte
PO43-, 2.5 to 4.5 mg/dL
HCO3-, 23 to 30 mEq/L
Na+, 136-145mEq/L
K+ , 3.5-5.0mEq/L
PATHOPHYSIOLOGY OF DIABETIC KETOACIDOSIS
Poor knowledge on using insulin pump leads to diabetic ketoacidosis
Patient is diagnosed with DM TYPE 1 3years ago
Immune mediated destruction of pancreatic beta cells causes deficiency of insulin
Patient is treated with insulin therapy by using insulin pump
Insulin helps to bring in glucose into the body cells to be used as a source of energy
Deficiency of insulin leads to high blood glucose level
The liver makes a huge amount of blood sugar by breaking down fats into glycerol & fatty acids and this produce ketone bodies
Ketone bodies causes blood to become acidic and prevents glucose uptake by muscle and brain cells
This causes patient to become weak and confused
LABORATORY FINDINGS (SIGN)
Elevated pulse rate
Sinus tachycardia
Low BP
Elevated glucose level
Rapid respiratory rate
Presence of ketone and glucose in urine analysis
Kussmaul respiration (hyperventilation)
Low carbon dioxide
Elevated serum creatinine
Elevated WBC level
Slightly elevated BUN level
Justification of information for DKA
Ketone +
Cell does not get enough glucose
activate hormone-sensitive lipase
breakdown of triglycerides and release of free fatty acids, taken up by the liver and converted to ketone bodies
ketone bodies
acetone ( breath smell like nail polish
B-hydroxybutyrate
acetoacetate
Kussmaul respiration
Body try to remove the acidity by exhale more CO2
Deeper breathing rate
Consequences of (MA)
Polyurea
Blood sugar level exceed ability of kidney to reabsorb
Go to urine, with water ( osmotic diuresis)
Frequent urination
Leading to Polydipsia :unlock:
High blood glucose level (479 mg/dL)
Insulin deficient, glucose cannot enter cell
Glucose stay in blood
more than 250 mg/dL :!:
low ABG pH ( 7.26)
pH < 7.3 :!:
overproduction of β-hydroxybutyric acid and acetoacetic acid
Metabolic acidosis (MA)
low serum bicarbonate 7.1 mEq/l
serum bicarbonate <15 mEq/l :!:
overproduction of β-hydroxybutyric acid and acetoacetic acid
When dissociate completely,excess H+ bind the HCO3-, resulting decreased serum bicarbonate levels
CAUSES
Ethnicity (Caucasians)
Gender (female)
Family history
Patient knowledge
PROBLEM
Metabolic acidosis
Diabetic ketoacidosis
Type 1 DM
Hypothesis
Diabetes ketoacidosis
Acute complication of diabetes
A state of emergency
Metabolic acidosis
Type 1 Diabetes Mellitus
Poor patient knowledge
Poor knowledge using the insulin pump
Blood gas analysis (BGA)
pH
Oxygen (O2)
Metabolic acidosis without additional metabolic disorders
Carbon dioxide (CO2)
