A 43-year-old man with type 2 diabetes and hypertension presented to the emergency department with fever, cough, abdominal pain, nausea and vomiting for 2 days. His medical history and lab results were consistent with diabetic ketoacidosis. He was treated with IV fluids, insulin infusion to lower his blood glucose and correct the acidosis, potassium supplementation, and monitoring for complications of treatment. The goal of treatment was to safely rehydrate the patient and reduce ketones and hyperglycemia while avoiding hypoglycemia.

2. A 43-year-old man with a long history of type 2 diabetes (> 6years)
and hypertension presented to the emergency department with a
history of fever, cough , diffuse abdominal pain, nausea and
vomiting. Fever and cough started 2 days ago.
He was on gliclazide and metformin since diagnosis. Long acting
insulin (30 ) units was started 1 year ago because of poor glycemic
control .
Case …..

3.  The patient is Drowsy and he had dry mucous membranes, poor skin
turgor.
 Lungs is clear
 Heart sounds normal.
 In the abdomen , he has mild epigastric tenderness to deep
palpation; no rebound tenderness or guarding.

4. BPO saturationRRPRTemperature
96/60 mmHg98%4013638.9
HCOpCO2pH
9 mEq/L17 mmHg7.06
 Patient blood gases:
 Patient vital signs :

5. CreatinineUreaChloridePotassiumSodiumglucose
1.4 mg/dl60 mg/dl101 mmol/L5.3 mEq/L142 mEq/L417 mg/dl
 Chemistry and Renal profile:
HbRBCWBC
14 g/d5.510^12/ μ l18,000/ μ l
 CBC:
Urine analysis :
• Glucose +4
• ketones +3
• nitrite and leucocyte negative
Anion gap = 29.4 mmol/L
([Na+] + [K+]) − ([Cl-] + [HCO3−])

6. Diabetic
ketoacidosis
what’s your professional diagnosis?

7. Diabetic ketoacidosis (DKA) is an acute, major, life-
threatening complication of diabetes. DKA mainly occurs in
patients with type 1 diabetes, but it is not uncommon in
some patients with type 2 diabetes.

8. DKA defined :
 Clinically as an acute state of sever uncontrolled diabetes the
require emergency treatment with insulin and IV fluid .
 Biochemically as an increase blood glucose > 250 mg/dl ,
increase ketones in the serm > 5 mEq / L or urine ketone ≥ +2
and ( PH< 7.30 , HCO3< 18 mEq/L) .

9. Causes
poor compliance with
hypoglycemic treatment
Infection:
• Pneumonia
• UTI
• Virus
New presentation
Unknown 5%
Medications:
• Steroids
Infraction :
• MI
Others :
• Emotional stress
• Trauma
• Surgery

10. Decrease in blood PH
No insulin
No glucose uptake
by cells
No glucose
metabolism
Increase counter –
regulatory hormones
+KetogenesisGluconeogenesis Liver
So , no energy for body
Osmotic diuresis
Hyperglycemia
Dehydration and
electrolyte loss
Peripheral tissue
decrease glucose
uptake
Ketoacidosis and release energy for body
Metabolic acidosis
Adipose tissue
increase FFA
Decrease in urine PH
Insulin :
• Breaks down glucose
• Uptake by muscle and liver
+

11. • Increase UOP (polyuria)
• Electrolyte disturbance
• Acidosis
• General symptoms :
•
Weakness , anorexia , polydipsia and weight loss
Tachycardia, hypotension , hypothermia.
ECG changes, N&V.
Fruity breath (acetone), Kussmaul
breathing , confusion, coma

12. 1- priority is rehydrate the patient to increase tissue perfusion
and prevent renal failure
Give 20ml/kg/hr 0.9% NaCl
• 1L over 1 hr
• 1L over 2 hrs
But once plasma glucose <200 mg /dl ; switch to 5% dextrose 0.45 NS
2- priority is correct Hyperglycemia and inhibit ketogenesis by giving
Regular Insulin 0.1unit/kg/hr rate of infusion ( 6unit /hr)
Continue until acidosis clears ( PH > 7.30 , HCO3 > 18 mEq/L)
Decrease to 0.05 U/ kg/ hr until SC insulin replacement initiated

13. Add potosaum
• If K+ > 5.5 no added
• If K+ 3.3 -5.5 give 20 mEq/L of IV
• If K+ < 3.3 give 40 mEq/L until >3.3
Aims of treatment:
• Rate of fall of ketones of at least 0.5 mmol/L/hr.
• Biaroate rise 3 mmol/L/hr.
• Blood gluose fall 3 mmol/L/hr
• Maintenance potassium in normal range
• Avoid hypoglycaemia
• Assess for complications of treatment e.g. fluid overload, cerebral oedema