Clinical features and management of Diabetic ketoacidosis

1. PRESENTED BY:
DR. ANAM MEHMOOD

2. Case
▪ A 24 year old female with past medical history of diabetes
mellitus I is brought to the ER by her mother with complaints of
fatigue and increased thirst and urination. Of note patient states
she ran out of her insulin last week. She also has had a runny nose
and cough for the past week. She noticed her glucose levels have
been running “very high” and got concerned.
▪ On Exam:
▪ BP 101/72; heart rate: 113; respirations: 32; Temperature: 36.8 °C; pulse oximetry:
100% on room air.
▪ HEENT: dry mucous membranes
▪ CV: tachycardic, normal s1, s2. No murmurs
▪ Lung: NVB+0
▪ Abdomen: +bs, non distended, slight tenderness to deep palpation, no rebound or
guarding
▪ no cyanosis, clubbing or edema

3. Case (contin…)
▪ LAB RESULTS
▪ EKG sinus tachycardia
▪ Biochemistry
Na: 124, K: 5.0, Cl: 95
BUN: 38, Cr: 1.8
Glucose 450
AST:40, ALT:41, Alk phos:67
▪ Arterial blood gas: pH 6.9, CO2 9, bicarb 10
▪ WBC 13K, Hb14.4 mg/dL, and Hct 43.5%.
▪ 75% neutrophils

4. ▪ UA +glucose, +protein, -leuko esterase, -nitrite NO KETONES
▪ Serum ketones test ordered is positive for beta-hydroxybutyrate

5. Likely
Diagnosis!!!!!
▪Dibetic ketoacidosis

6. Dibetic Ketoacidosis
DKA is a serious acute complications of Diabetes Mellitus. It
carries significant risk of death and/or morbidity especially with
delayed treatment.
The prognosis of DKA is worse in the extremes of age, with a
mortality rates of 5-10%.

7. Dibetic Ketoacidosis: Definition
▪ A state of absolute or relative insulin deficiency
aggravated by ensuing hyperglycemia, dehydration, and
acidosis-producing derangements in intermediary
metabolism, including production of serum acetone.
▪ Can occur in both Type I Diabetes and Type II Diabetes
▪ In type II diabetics with insulin deficiency/dependence
▪ The presenting symptom for ~ 25% of Type I Diabetics

8. Precipitating Factors:
▪ New onset of type 1 DM: 25%
▪ Infections (the most common cause): 40%
▪ Drugs: e.g. Steroids, Thiazides, Dobutamine &
turbutaline.
▪ Omission of Insulin: 20%. This is due to:
Non-availability (poor countries)
fear of hypoglycemia
 rebellion of authority
fear of weight gain
stress of chronic disease

9. Assessment:
▪ History:
▪ Symptoms of hyperglycemia, precipitating factors
▪ diet and insulin dose.
▪ Examination:
▪ Look for signs of dehydration, acidosis, and electrolytes imbalance,
including shock, hypotension, acidotic breathing, CNS status…etc.
▪ Look for signs of hidden infections (Fever strongly suggests infection)
and If possible, obtain accurate weight before starting treatment.

10. Management:
The management steps of DKA includes:
▪ Assessment of causes & sequele of DKA by taking a short history &
performing a brief examination.
▪ Quick diagnosis of DKA at the ER.
▪ Baseline investigations.
▪ Treatment, Monitoring & avoiding complications.
▪ Transition to outpatient management.

11. Diagnosis:
▪ You should suspect DKA if a diabetic patient presents with:
Dehydration.
Acidotic (Kussmaul’s) breathing, with a fruity smell (acetone).
Abdominal pain &or distension.
Vomiting.
An altered mental status ranging from disorientation to coma.

12. Diagnosis:
To diagnose DKA, the following criteria must be
fulfilled :
1. Hyperglycemia: of > 300 mg/dl & glucosuria
2. Ketonemia and ketonuria
3. Metabolic acidosis: pH < 7.25, serum bicarbonate < 15
mmol/l. Anion gap >10.
Anion gap= [Na]+[K] – [Cl]+[HCO3].
This is usually accompanied with severe
dehydration and electrolyte imbalance.

13. Diagnostic Criteria for DKA:
Mild DKA Moderate DKA Severe DKA
Plasma glucose
(mg/dL)
> 250 > 250 > 250
Arterial pH 7.25-7.30 7.00-7.24 < 7.00
Sodium
Bicarbonate
(mEq/L)
15 – 18 10 - <15 < 10
Urine Ketones Positive Positive Positive
Serum Ketones Positive Positive Positive
Serum Osmolality
(mOsm/kg)
Variable Variable Variable
Anion Gap > 10 > 12 > 12
Mental Status Alert Alert/Drowsy Stupor/Coma

14. Diagnostic Studies in DKA
▪ Chemistry
▪  Glucose
▪  Bicarbonate
▪ Anion gap = (Na+) – (Cl- + HCO3
-)
▪ Frequently seen:
▪  BUN/creatinine (dehydration)
▪  potassium
▪  sodium
Pseudohyponatremia: to correct, add 1.6 mEq of sodium to every 100mg/dL
of glucose above normal
▪ Serum acetones
▪ Positive in DKA

15. Diagnostic Studies in DKA (continued..)
▪ Urinalysis
▪ Ketones (for DKA); leukocyte esterase, WBC (for UTI)
▪ CBC
▪ Leukocytosis (possible infection)
▪ Amylase/Lipase
▪ To evaluate for pancreatitis
▪ BUT, DKA by itself can also increase them!
▪ EKG
▪ Evaluate for possible MI

16. MANAGEMENT

17. MANAGEMENT:
▪ Correction of fluid loss with intravenous fluids
▪ Correction of hyperglycemia with insulin
▪ Correction of electrolyte disturbances, particularly potassium loss
▪ Correction of acid-base balance
▪ Treatment of concurrent infection, if present

18. Correction of Fluid Loss:
Determine hydration status:
Hypovolemic shock:
Administer 0.9% saline, Ringer’s lactate or a plasma
expander as a bolus dose of 20-30 ml/kg. This can
be repeated if the state of shock persists.
Patient needs to be catheterized to measure the urine output to
forsee Acute kidney injury.

19. Correction of Fluid Loss:
B- Dehydration without shock:
Initially correction is by isotonic saline,
recommended schedule is:
▪ Administer 1-3 L during the first hour.
▪ Administer 1 L during the second hour.
▪ Administer 1 L during the following 2 hours
▪ Administer 1 L every 4 hours, depending on the degree of
dehydration and central venous pressure readings
BSL<180mg/dl …. Switch to 5-10% dextrose with half isotonic
saline.

20. Insulin Therapy:
▪ Short acting insulin i.e regular Insulin is the best choice.
▪ The initial insulin dose is a continuous IV insulin infusion using an
infusion pump, if available, at a rate of 0.1 U/kg/h. A mix of 24
units of regular insulin in 60 mL of isotonic sodium chloride
solution usually is infused at a rate of 15 mL/h (6 U/h) until the
blood glucose level drops to less than 180 mg/dL; the rate of
infusion then decreases to 5-7.5 mL/h (2-3 U/h) until the
ketoacidotic state abates.
▪ The optimal rate of glucose decline is 100 mg/dL/h.
▪ If insulin pump is not available, IV insulin can be givenly hourly i.e
Loading dose of 10U followed by 6U/hr, adjusted according
to Bsl.

21. Electrolyte Correction:
▪ Potassium replacement:
If K >6mEq/L no replacement
If K 4.5-6mEq/L administer 10mEq/L
If K 3-4.5mEq/L administer 20mEq/L
Usually rule of thumb: 20mEq/L in alternate drip
▪ Correction of Acid base balance:
IV sodium bicarbonate only in case of decompensated acidosis.

22. Metabolic Acidosis:
Acidosis
K correction
If K<3.3mmol/l
start correcting K before
correcting insulin
If K >3.3mmol/l
give IV short acting insuin
0.1U/kg/h
If pH <7.0
NaHCO3
one ampoule per
hour until pH>7.0

23. Treatment of Concurrent Infection
▪ In the presence of infection, the administration of proper
antibiotics is guided by the results of culture and sensitivity
studies. Starting empiric antibiotics on suspicion of infection until
culture results are available may be advisable.

24. Monitoring
A flow chart must be used to monitor fluid
Balance, urine output & Lab measures.
 serum glucose must be measured hourly.
 electrolytes also 2-3 hourly.
ABGs and urine ketones atleast 4 hourly
 Ca, Mg, & phosphate must be measured initially & at least once
during therapy.
 Neurological & mental state must examined frequently,
& any complaints of headache or deterioration of mental
status should prompt rapid evaluation for possible cerebral edema.

25. When to shift to S/C Insulin
▪ When urinary ketones are negative
(Atleast 2 consecutive sets)
▪ Anion gap closes
▪ Patient becomes conscious and starts tolerating orally
▪ Acidosis settles

26. Treatment complications:
▪ Cerebral edema
▪ Rare, but life threatening
▪ Usually in pediatric, adolescent patients
▪ Symptoms: Headache, altered mental status
▪ Treat with mannitol, hyperventilation
▪ Myocardial infarction, DVT/PE, cardiac dysrhythmias
▪ AKI (acute tubular necrosis, hypovolemia)
▪ Hypoglycemia, Hypokalemia
▪ Hypophosphatemia
▪ Occurs after aggressive hydration/treatment
▪ Monitor phosphorus and replete as needed to keep > 1

27. PREVENTION of DKA:
▪ Type 1 diabetes
▪ Education around sick day management
▪ Continuation of insulin even when not eating
▪ Frequent monitoring when ill
▪ Type 2 diabetes
▪ Education around sick day management
▪ Frequent monitoring when ill

28. Thank you

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