Diabetic ketoacidosis

1. NCM 106: Acute Biologic Crisis
DIABETIC KETOACIDOSIS

2. DIABETIC KETOACIDOSIS
• caused by an absence or markedly
inadequate amount of insulin
• deficits in available insulin results in
disorders in the metabolism of carbohydrate,
protein and fat
• common in type 1 diabetes
3 main clinical features:
1. Hyperglycemia
2. Dehydration and electrolyte loss
3. Acidosis

3. Causes:
1. Decreased or missed dose of insulin
2. Illness or infection
3. Undiagnosed or untreated diabetes
4. Patient error in drawing up or injecting
insulin
5. Intentional skipping of insulin doses
6. Physical and emotional stressors
7. Drugs

4. Prevention:
1. Never eliminate insulin doses when
nausea and vomiting occur.
2. Consume frequent small portions of
carbohydrates.
3. Drinking fluids to prevent dehydration
4. Assessment of blood glucose levels and
urine ketones every 3 to 4 hours.
5. Have foods available for use on sick days.
6. Assess for underlying cause of DKA.

5. Pathophysiology:
Lack of Insulin
↓
Increased release of glucose by the liver
↓
Elevation of glucagon
↓
High glucose levels spill over into the urine with water and solutes
(sodium and potassium)
↓
osmotic diuresis
↓
Polyuria
↓
Dehydration
↓
Compensatory thirst and Polydipsia

6. Lack of Insulin
↓
Breaking down muscle, fat, and liver cells into glucose and fatty
acids
↓
Release of free fatty acids from adipose tissue (lipolysis)
Oxidation (body consumes its own muscle, fat, and liver cells for
fuel)
↓
Conversion to ketones in the liver
↓
Metabolic acidosis
↓
Increased buffering activity
↓
Hyperventilation to lower the blood carbon dioxide levels
(Kussmaul respiration)

7. Clinical Manifestations:
1. Polyuria and polydipsia
2. Blurred vision
3. Weakness
4. Headache
5. Orthostatic hypotension
6. Hypotension- with weak, rapid pulse
7. Metabolic acidosis
8. Gastrointestinal symptoms:
• Anorexia
• Nausea and vomiting

8. • Abdominal pain
• Acetone breath- with elevated ketone
levels
9. Hyperventilation, Kussmaul respirations-
deep respirations
10.Mental changes- alert, lethargic or comatose
11.Increased markers of inflammation even in
the absence of infection
12.Dehydration

9. Assessment and Diagnostic findings
1. Blood glucose levels
2. ABG
3. Kussmaul respiration
4. Accumulation of ketone bodies in the blood and
urine
5. Dehydration
6. Creatinine and BUN levels

10. Management:
I. Treatment of hyperglycemia
II. Rehydration
a. Fluid replacement
b. May need as much as 6-10 liters of IVF to
replace fluids caused by polyuria,
hyperventilation, diarrhea and vomiting
c. Initial administration of 0.9% sodium chloride
solution at a rapid rate= 0.5-1 liter/H for 2-3
hours

11. Management:
d. 0.45% NSS (half-strength)
e. D5W if the blood glucose level reaches 300 mg/dL (16.6
mmol/L) or less
f. Monitor fluid volume status:
• Frequent measurement of VS= orthostatic changes in
the BP and heart rate
• Lung assessment
• MIO
• Plasma expanders
• Monitor signs of fluid overload

12. Management:
III. Restoring electrolytes
a. Rehydration
b. Insulin administration
c. Potassium replacement
d. Frequent ECG and laboratory measurements of
potassium
IV. Reversing Acidosis
* Acidosis is reversed with insulin

13. Considerations in insulin administration in
reversing acidosis:
• Infusion is done intravenously at a slow continuous
rate.
• Hourly blood glucose level must be measured.
• Insulin must be infused continuously until
subcutaneous administration of insulin can be
resumed
• Insulin is often infused separately from the
rehydration solutions.

14. Dosage administration:
IVF with higher concentration of glucose (NSS- D5NSS,
D50.45NSS) are administered when blood glucose
reach 250 to 300 mg/dL (13.8-16.6 mmol/L to avoid a
too rapid drop in the blood glucose level during the
treatment
Regular insulin is the only type of insulin approved for
IV use= usually added to IV solutions

15. Eg.
Doctor’s order is 100 units in 500 ml of IVF
= Ratio is 1unit: 5 ml
If given at a rate of 5 units/ hour then 25
ml will be infused

16. Hyperglycemic Hyperosmolar
Nonketotic Syndrome

17. Hyperglycemic Hyperosmolar Non-
Ketotic Syndrome
 Extreme hyperglycemia occurs without ketosis
and acidosis
 Syndrome occurs most often in individuals with
type 2 DM
 The major difference between HHNS and DKA is
that ketosis do not occur (but can be minimal)
with HHNS
 Onset is usually slow and takes hours to days to
develop

18. Causative factors:
1. Old age
2. Type 2 diabetes
3. Acute illness
4. Medications that exacerbate hyperglycemia-
thiazides
5. Dialysis
6. Days to weeks of polyuria with adequate fluid
intake

19. Pathophysiology
Lack of effective insulin
↓
Persistent hyperglycemia
↓
Osmotic diuresis
↓ ↓
Glycosuria Dehydration
↓ ↓
Loss of water and electrolytes
↓
Shifting of water from the ICF space to the ECF space
↓ ↓
Hypernatremia Increased Osmolarity

20. Clinical Manifestations:
1. Profound dehydration
• Dry mucus membranes
• Poor skin turgor
2. Hypotension
3. Tachycardia
4. Variable neurologic signs
• Alteration of sensorium
• Seizures
• Hemiparesis

21. Assessment and Diagnostic Findings
• Blood glucose level- 600 to 1200 mg/dL
• Osmolality- exceeds 350 mOsm/kg
• BUN levels- elevated
• Changes in mental status, focal neurologic
deficits and hallucinations
• Postural hypotension

22. Management:
*The overall approach to the treatment of HHNS is similar
to DKA
1. Fluid replacement:
a. Close monitoring of volume and electrolyte status
b. Fluid treatment is started with 0.9% or 0.45% Normal
saline
c. Central venous or hemodynamic pressure monitoring
2. Correction of electrolyte imbalances
a. Potassium administration if with adequate urinary output

23. 3. Insulin administration
a. Insulin administration is continuous and given at a low
rate
- IV fluids with dextrose are administered after glucose
levels are decreased to 250-300 mg/dL
4. Continue in evaluating clinical and laboratory findings

24. NCM 106: Acute Biologic Crisis Lecture
Series
DIABETIC KETOACIDOSIS
Hyperglycemic Hyperosmolar Non-ketotic
Syndrome