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