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Diabetes & Diabetic Keto Acidosis BY RHIH, LEVEL III STUDENT NURSE
NDICUNGUYE JEAN PAUL
TABLE OF CONTENT
Definition of DKA as complication of DM
Patophysiology
Causes
Signs and symptoms
Diagnosis or investigation
INTRODUCTION
DKA (Diabetic Keto Acidosis ): is an acute, severe, life-
threatening complication of uncontrolled diabetes mellitus
with plasma glucose of ≥ 300 mg/dl, that requires emergency
treatment with insulin and intravenous fluids.
DKA mainly occurs in patients with type 1 diabetes, but it is
not common in patients with type 2 diabetes.
CAUSES OF DKA
Underlying infection and intercurrent illness
Interruption of insulin treatment
New onset of diabetes
Medication (eg. corticosteroids)
Signs and symptoms
Polyuria and polydipsia
Malaise
Nausea, vomiting with diffuse abdominal pain, decreased
appetite, and anorexia
dry mucous membranes, decreased skin turgor.
Shallow rapid breathing
Characteristic acetone (ketotic) breath odor.
Tachycardia, Hypotension
Altered consciousness or coma
DIABETIC KETOACIDOSIS PATHOPHYSIOLOGY
Diabetic KetoAcidosis pathophysiology focuses on :
Ketone production
Severe dehydration from osmotic diuresis
Electrolyte imbalance
So those are the initial of all the previous signs and symptoms
Diabetic KetoAcidosis pathophysiology
Diabetic KetoAcidosis is the complication of type 1
diabetes mellitus (insulin dificient)
Due to lack of insulin in the body , the cells are not able to
use glucose as source of energies.
even though it is over loaded in blood, the cell start
starvation mode.
The starvation mode trigger the gluconeogenesis (the
process by which the body use non carbohydrates carbon
substance like: proteins and fats, …..
Pathophysiology cont …..
..to produce glucose when glucose is low in the body) this lead
to release of glucose for starving cells and this lead to further
elevation of blood glucose as the cells are not able to use them.
The breaking of fats and proteins as source of energy increase
also free fatty acids and circulate in the blood
Then those fatty acids metabolized into strong acid :
acetoacetic acid and B-hydroxybutric acid referred as
ketones
Pathophysiology cont …..
as acetoacetic acid is being metabolized it produces acetone
which begins to accumulate in blood .
If small amount of acetone are exhaled in respiratory system
they lead to fruity breath odor.
In normal metabolism those ketones would be used by
perpheral tissue as fuel but due to the starvation they are not
using those ketones
Pathophysiology cont …..
The accumulation those ketones lead to metabolic acidosis
know as ketoacidosis as blood HP falls below 7.35
So now the body start to eliminate those ketones through
renal excretion (urine)
When blood glucose is above 180mg/dl the significant
amout of glucose are spills out into the urine and when they
reach in tubules of nephrons they create osmotic pressure
that attract large amount of water into tubules and lead to
polyuria.
Pathophysiology cont …..
So this process is called osmotic diuresis and lead to volume
depletion and dehydration
Due to the large amount of ketones in urine (acidic urine )
they must be buffered before excretion.
Sodium is typically used as the buffer, and remember that
where sodium goes water follows and lead to further volume
depletion (dehydration).
Pathophysiology cont …….
The loss of large amount of fluids is associated with loss of
electrolytes like potassium,calcium, magnesium and
phosphorous.
INVESTIGATION
Blood tests for glucose every 1 h until patient is stable, then every 6 hrs
Urine Dipstick testing (positive for glucose and ketones)
Serum electrolytes every 4-6 h while acutely ill
Blood urea (raised in DKA)
Urine and Blood Cultures
ECG
Abdominal ultrasound
DKA Management Principles
• Admission in high dependency area of Medical Ward or
ICU.
• Correction of fluid loss with intravenous fluids
• Correction of hyperglycemia with insulin
• Correction of electrolyte disturbances, particularly
hypokalemia
• Correction of acid-base balance but most of time corrected
with above mentioned measures
• Treatment of concurrent infection, if present
Correction of fluid loss
• Normal Saline or Ringer’s Lactate
→ A administer 1-3 L during the first hour
→ A administer 1 L during the second hour
→ A administer 1 L during the following 2 hours
→ A administer 1 L every 4 hours, depending on the degree
of dehydration
Correction of hyperglycemia
Insulin therapy: 0.1 UI/kg/hr
→ Only short-acting insulin is used for correction of
hyperglycemia
→ Use subcutaneous or intramuscular route if IV line not
accessible
→ Doses and route : Initial insulin dose: Continuous IV
using electric syringe at a rate of 0.1 U/kg/h
Insulin administration
Mix 24 units of regular insulin in 60 mL of isotonic sodium chloride OR
If electric syringe is not available mix 60 units of short acting insulin with 500 ml of normal saline solution
Infuse at a rate of 15 mL/h (6 U/h) until the blood glucose level drops to less than 180 mg/dL.
Adjust (usually decrease) insulin dosing as required to ensure that:
The maximum decrease rate of glucose is 100 mg/dL/h
Blood glucose should not fall below 200 mg/dl during the first 6 hours
Insulin administration cont….
If blood glucose stable and urine ketones negative, then stop
insulin infusion and start standard insulin regimen
Correction of electrolyte disturbances
If K+ level > 6 mEq/L: don’t administer K+.
If K+ level = 4.5-6 mEq/L: administer 10 mEq/h of Potassium chloride
If K+ level is 3-4.5 mEq/L: administer 20 mEq/h of Potassium chloride
Monitor serum potassium levels hourly
stop potassium infusion if the K+ level is greater than 5 mEq/L
The monitoring of serum potassium must continue even after potassium infusion is stopped to detect recurrence of hypokalaemia
Remark !!!
In severe hypokalaemia: don’t start insulin therapy unless
potassium replacement is under way; this is to avoid
potentially serious cardiac arrhythmias that may result from
hypokalaemia
Treatment of intercurrent infection
Start empiric antibiotics on suspicion of infection until
culture results are available
Complications related to DKA
Cardiovascular: Myocardial infarction, dysarthymia.
Metabolic and electrolytic: Hypoglycemia, hypokalemia,
hypophosphatemia
Respiratory: Respiratory distress, pulmonary edema.
Cerebral edema, Coma, Death
REFERENCES
Dalton al, Limmer D, Mistovich JJ, Werman HA. Advanced
medical life support: a practical approach to adult medical
emergencies , 3rd edition . Upper saddle river, NJ Hall, 2011
Guton , A.C, and J.E. Hall .Textbook of medical physiology.
10TH Edition .Philadelphoia : W.B. SAUDERS, 2013
Agnes B,Internal medicine clinical guideline : metabolic and
endocrine emergencies << Diabetic Keto-acidosis>> ,sept 2012 ,
Kigali Rwanda available at www.moh.gov.rw accessed on 03 Dec
2018