A typical presentation of Diabetic Ketoacidosis, its pathophysiology, management and treatment.

1. Case Presentation
Uzair Ahmed

2. Chief Complaints
20 years old female, known case of Type I
Diabetes Mellitus, came to OPD on 06-06-14
with complaints of
• Abdominal pain for 1 day
• Nausea and Vomiting 1 day
• Productive Cough for 1 week
• No history of fever

3. History of Presenting Complaints
• According to attendant, the patient was alright 1 day back
when she suddenly developed abdominal pain, nausea and
vomiting.
• She also complained of cough with sputum which was yellow
in color. Sputum did not contain any blood and it was not foul
smelling. Cough was mild in intensity, no specific time of
occurrence, no aggravating or relieving factors. It was not
associated with chest pain, shortness of breath or fever.

4. Systemic Review
• Respiratory System: hx of productive cough with small amount of
yellow sputum.
• CVS: no breathlessness, palpitation or chest pain.
• GIT: Nausea and vomiting. Abdominal pain.
No heart burn, diarrhea, constipation, hematemesis or melena
present .
• CNS: Drowsiness.
• GENITO-URINARY: Polyuria but no hx of burning micturition or
incontinence was present.
• MUSCULO-SKELETAL: Normal

5. PAST MEDICAL HISTORY: She was diagnosed as Type I DM at age of 9
years. Since then she had been on a regimen of Regular and NPH insulin.
She had history of multiple hospital admission with very similar complaints.
Past Surgical History : Nothing significant
Drug History: Insulin R+N
8+6 in Morning
6+4 in Evening
PERSONAL HISTORY: decreased appetite, decreased sleep, normal bowel
habits. No addiction. Increased Micturition.
FAMILY HISTORY: Nothing significant
SOCIO-ECONOMIC HISTORY: Poor.

7. Examination
• Young healthy female of average built and height lying
comfortably on bed, oriented to time place and person.
• Vitals
GCS 15/15
B.P. 90/60
Pulse 100bpm
Temp A/F
R/R 24
• On Examination there was no evidence of anemia, jaundice ,
clubbing or edema.
• Mild to moderate dehydration was present.
• No Palpable lymph nodes.

8. Systemic Examination
• Abdominal Exam :
Mild Tenderness at Epigastric and Left Hypochondriac
region. No visceromegaly.
• CNS Examination : Intact
• Respiratory System:
Chest was clear with NVB.
R/R was increased.
• CVS: S1+S2+0

9. Case Summary
• 20 years old female, k/c of Type I DM, compliant to
insulin, comes to Emergency with complaints of nausea,
vomiting and abdominal pain for 1 day. She has
decreased appetite, increased thirst and polyuria. Her
vitals shows that she has hypotension along with
tachycardia and increased Respiratory Rate.
• O/E she is dehdyrated, and there is tenderness in
epigastric and left hypochondriac region. Rest of the
examination is unremarkable.
• There is also prior hx of hospital admissions with
similar complaints.

10. Differential Diagnosis?
• Diabetic Ketoacidosis
• Acute Pancreatitis
• Acute Appendicitis
• Lactic Acidosis
• Metabolic Acidosis
• Myocardial Infarction

11. Investigations (06-06-14)
• RBS: 465 mg/dl
• Serum Ketones: +++
ABGs:
• pH: 7.2
• HCO3: 4
• PaCO2: 11
• PaO2: 140
• SaO2: 99
LFTs:
• SGPT: 31
• Al.Phos: 194
• BUN: 16
• Cre: 1.0
• Na:132
• K:4.9
• Cl: 94
Anion gap
• [Na+K]-[HCo3+Cl]
• [132+4.9]-[4+94]
• 38.9
CBC:
• Hb: 13.1
• TLC: 13600
• MCV: 82.1
• HCt: 37.8
• Platelets: 270000

12. Investigations(contd.)
Urine D/R:
• Amorphous urates : +
• Ketone bodies: ++
• Pus cells: 4-6
• pH: 6.0
• Spec. Gravity: 1.010
• Glucose: ++
• Yeast cells: +++
• Urobilin: -ve

13. Investigations(contd.)
• CXR PA view was done which was found to be
normal.
• ECG was performed, which was also normal.
• U/S whole abdomen was done which showed
hypoechoic liver while the rest of abdomen was
normal.

14. Requirement to
confirm DKA Our Findings
•Hyperglycemia
(RBS=465 mg/dl)
•Blood pH=7.2
•Serum Bicarbonate = 4
•Serum Ketones +++
DKA Confirmed!

15. Treatment given:
• Inf. N/S to replace the ECF fluid loss.
• Inf. 5% dextrose to replace ICF fluid loss.
• Insulin was administered continuously through infusion
pump initially @5units/ hour and then at 3units/hour .
• Potassium was replaced.
• Injection Ceftriaxone was given to cover up infection if
there were any.
• Inj. Gravinate was given to treat nausea and vomiting.
• RBS , BP & TPR was recorded hourly along with strict
I/O charting.
• Patient clinically improved with the given treatment and
was discharged on her 6th day of admission.

16. Hospital Course
At time of Admission At time of Discharge
ABGs
• pH: 7.2
• HCO3: 4
• PaCO2: 11
• PaO2: 140
• SaO2: 99
UCE • BUN: 16
• Cre: 1.0
• Na:132
• K:4.9
• Cl: 94
Anion Gap 38.9
Serum
Ketones
+++
Urinary
Ketones
+++
ABGs
• pH: 7.44
• HCO3: 23.9
• PaCO2: 32
• PaO2: 171
• SaO2: 99.6
UCE • BUN: 3
• Cre: 0.4
• Na:137
• K:3.9
• Cl: 105
Anion Gap 12
Serum
-
Ketones
Urinay
Ketones
-

17. Topic Discussion

18. Diabetic Ketoacidosis
• Definition
• Etiology and Epidemiology
• Pathogenesis
• Diagnosis
-clinical assessment
- lab investigations
-Essentials for diagnosis
• Treatment

19. Definition:
• Diabetic ketoacidosis (DKA) is an acute, major, life-threatening
complication of diabetes. DKA mainly occurs
in patients with type 1 diabetes, but it is also not
uncommon in some patients with type 2 diabetes.
• Also It can be the very initial presentation of the
previously undiagnosed patients with Type I DM.
• This condition is a complex disordered metabolic state
characterized by hyperglycemia, ketoacidosis, and
ketonuria.

20. Etiology
• The most common scenarios for diabetic ketoacidosis (DKA) are
underlying or concomitant infection (40%), missed insulin
treatments (25%), and newly diagnosed, previously unknown
diabetes (15%). Other associated causes make up roughly 20% in the
various scenarios.

21. Causes of DKA
• in type 1 diabetes mellitus
• In 25% of patients, DKA is
present at diagnosis of type 1
diabetes due to acute insulin
deficiency.
• Poor compliance with insulin
• Bacterial infection and
intercurrent illness (eg,
urinary tract infection [UTI],
vomiting)
• Medical, surgical, or emotional
stress
• Idiopathic
• In type II diabetes mellitus
• Intercurrent illness (eg,
myocardial infarction,
pneumonia, prostatitis, UTI)
• Medication (eg, corticosteroids,
pentamidine, clozapine)

22. Epidemiology
• DKA accounts for 50% of diabetes-related admissions in
young persons and 1-2% of all primary diabetes-related
admissions.
• The incidence of DKA is higher in whites because of the higher
incidence of type 1 diabetes in this racial group.
• The incidence of diabetic ketoacidosis (DKA) is slightly
greater in females than in males for reasons that are unclear.
• Recurrent DKA frequently is seen in young women with type
1 diabetes and is caused mostly by the omission of insulin
treatment.
• Among persons with type 1 diabetes, DKA is much more
common in young children and adolescents than it is in
adults. DKA tends to occur in individuals younger than 19
years, but it may occur in patients with diabetes at any age.

23. Pathophysiology
Insulin is a peptide hormone, produced by beta cells in thepancreas, and is central
to regulating carbohydrate and fat metabolism in the body.
Some of its physiological effects are
- Decreases blood glucose concentration by
1. increasing its uptake in the tissues
2. increasing glycogenesis
3. inhibiting gluconeogenesis and glycogenolysis
- Increases uptake of aminoacid from blood into the cells and increases protein
syntesis.
- Decreases blood fatty acid and ketoacid formation by stimulating fats deposition
in adipose tissue and inhibiting lipolysis.
- Decreases blood K+ concentration by shifting then from ECF to ICF.
Or in a nut shell, Insulin decreases concentration of glucose,
FFAs, AAs and K+ levels in blood.

26. Diagnosis:
• Clinical Assessment:
Symptoms
•Polyuria, thirst
•Weight loss
•Weakness
•Nausea, vomiting
•Leg cramps
•Blurred vision
•Abdominal pain
Signs
• Dehydration
•Hypotension (postural or supine)
•Cold extremities/peripheral cyanosis
•Tachycardia
•Air hunger (Kussmaul breathing)
•Smell of acetone
•Hypothermia
•Confusion, drowsiness, coma (10%)

27. • Lab Findings:
i. Hyperglycemia
-Glucose ranges from 250-1000 mg/dl.
ii. Dilutional hyponatremia
-Glucose overrides sodium in controlling the osmotic
gradient. Water shifts out of the intracellular fluid
compartment into the extracellular fluid compartment and
dilutes the serum sodium.
iii. Hyperkalemia
- Transcellular shift as excess H+ions enter cells in
exchange of potassium.
iv. Increased anion gap metabolic acidosis.
-Due to ketoacidosis and lactic acidosis.
v. Prerenal azotemia
-Due to volume depletion from osmotic diuresis which
decreases cardiac output and renal blood flow.

28. •Essentials for diagnosis

29. Workup:
•The following are important but should not delay the institution of
intravenous fluid and insulin replacement:
• Venous blood: for urea and electrolytes, glucose, bicarbonate.
• Arterial blood gases to assess the severity of acidosis.
• Urinalysis for ketones.
• ECG.
• Infection screen: full blood count, blood and urine culture, C-reactive
protein, chest X-ray. Although leucocytosis invariably
occurs, this represents a stress response and does not necessarily
indicate infection.

30. Management & Treatment:
Diabetic ketoacidosis is a medical emergency
which should be treated in hospital, preferably in a
high-dependency area.The principal components of
treatment are:
• fluid replacement
• the administration of short-acting (soluble) insulin
• potassium replacement
• the administration of antibiotics if infection is
present.

31. •Fluid Replacement:
•0.9% saline (NaCl) i.v.
•1 L over 30 mins
•1 L over 1 hr
•1 L over 2 hrs
•1 L over next 2-4 hrs
•When blood glucose < 15 mmol/L (270 mg/dL)
•Switch to 5% dextrose, 1 L 8-hourly
•If still dehydrated, continue 0.9% saline and add 5%
dextrose, 1 L per 12 hrs
•Typical requirement is 6 L in first 24 hrs but fluid overload
in elderly patients should be avoided.
•Subsequent fluid requirement should be based on clinical
response including urine output

32. Insulin:
• 50 U soluble insulin in 50 mL 0.9% saline i.v. via
infusion pump
▫ 6 U/hr initially
▫ 3 U/hr when blood glucose < 15 mmol/L (270 mg/dL)
▫ 2 U/hr if blood glucose < 10 mmol/L (180 mg/dL)
• Check blood glucose hourly initially; if no reduction
in first hour, rate of insulin infusion should be
increased
• Aim for fall in blood glucose of 3-6 mmol/L
(approximately 55-110 mg/dL) per hour

33. Potassium:
• None in first L of i.v fluid unless plasma
potassium < 3.0 mmol/L
• When < 3.5 mmol/L, give 20 mmol/hr
• When plasma potassium is 3.5-5.0 mmol/L, give
10 mmol/hr

34. Additional Procedures:
• Catheterisation if no urine passed after 3 hrs
• Nasogastric tube to keep stomach empty in unconscious or
semiconscious patients, or if vomiting is protracted
• Central venous line if cardiovascular system compromised, to
allow fluid replacement to be adjusted accurately
• Plasma expander if systolic BP is < 90 mmHg or does not rise
with i.v. saline .
• Antibiotic if infection demonstrated or suspected
• ECG monitoring in severe cases .

35. Complications of DKA:
• Cerebral oedema
▫ May be caused by very rapid reduction of blood
glucose, use of hypotonic fluids and/or
bicarbonate
▫ High mortality
▫ Treat with mannitol, oxygen
• Acute respiratory distress syndrome
• Thromboembolism
• Disseminated intravascular coagulation (rare)
• Acute circulatory failure

36. Prognosis:
• The overall mortality rate from DKA ranges from
1-10% of all DKA admissions. The presence of
deep coma at the time of diagnosis,
hypothermia, and oliguria are signs of poor
prognosis.
• The prognosis of properly treated patients with
diabetic ketoacidosis is excellent, especially in
younger patients if intercurrent infections are
absent.