DKA-1

Manshiet Al- Bakry Hospital
Pediatrics Departement
Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA)
The biochemical criteria for the diagnosis of diabetic ketoacidosis (DKA) are:
• Hyperglycemia [blood glucose (BG) >11 mmol/L (≈200 mg/dL)]
•Acidosis, Venous pH < 7.3 or bicarbonate <15 mmol/L
• Ketonemia and ketonuria.
The severity of DKA is categorized into:

• Mild: venous pH<7.3 or bicarbonate <15 mmol/L
• Moderate: pH<7.2, bicarbonate <10 mmol/L
• Severe: pH<7.1, bicarbonate <5 mmol/L.
The clinical signs of DKA include:

1
• Tachypnea ,deep (Kussmaul) respiration; breath has the smell of acetone
• Nausea, vomiting (which may be mistaken for gastroenteritis)
• Abdominal pain that may mimic an acute abdominal condition
• Confusion, drowsiness, progressive reduction in level of consciousness and, eventually, loss of

consciousness.
• Dehydration (which may be difficult to detect)
• Tachycardia
Management:
No treatment strategy can be definitively recommended as being superior to another , Goals
of therapy are to correct dehydration, correct acidosis and reverse ketosis, slowly correct
hyperosmolality and restore BG to near normal, monitor for complications of DKA and its
treatment, and identify and treat any precipitating event.
 In case of disturbed conscious, secure the airway and empty the stomach by continuous
nasogastric suction to prevent pulmonary aspiration
 A cardiac monitor should be used for continuous electrocardiographic monitoring to
assess T waves for evidence of hyper- or hypokalemia
 Insert 2 IV lines one for sampling and later on for insulin and the other for fluid
replacement
 Laboratory investigations include :
1. Serum or plasma glucose

2. ABG
3. Perform a urinalysis for ketones.
4. Electrolytes (including bicarbonate)
5. Blood urea nitrogen, creatinine
6. Complete blood picture.
7. Serum osmolality which determines duration of treatment 36-48 hrs.
8. Albumin, calcium, phosphorus, magnesium concentrations (if possible).
9. Obtain appropriate specimens for culture (blood, urine, and throat), only if there is
evidence of infection (e.g., fever).
10. Anion gap which will be used in monitoring efficacy if treatment, in case that
BHBA is not available. Anion gap = Na − (Cl + HCO3): normal is 12 ± 2
mmol/L. In DKA, the anion gap is typically 20–30 mmol/L; an anion gap >35
2
mmol/L suggests concomitant lactic acidosis. The acidifying effect of chloride in

admintered fluids can mask recognition of resolution of ketoacidosis.
N.B:
In DKA, serum sodium may be lower than the true value because of the
shift of water into the extracellular space (sodium decreases 1.6 mEq/L per
each 100 mg/dL rise in glucose over 100 mg/dL) so Corrected sodium = measured
sodium +1.6 X [(measured glucose – 100)/100]
While there is usually a total body potassium deficit, the initial serum
potassium concentration may be normal or elevated because of insulin
deficiency, and the shifting of potassium into the extracellular space
secondary to the hyperosmolality and metabolic acidosis. The measured
potassium rises 0.6 mEq/L for every 0.1 drop in the Ph. . Finally, in the
absence of infection, the WBC count may be elevated (18,000–20,000/mm3)
in a patient with DKA, secondary to the increase in circulating
catecholamines
 There should be documentation on a flow chart of hour-by-hour clinical observations, IV

and oral medications, fluids, and laboratory results. vital signs (heart rate, respiratory
rate, blood pressure).
 Give antibiotics to febrile patients after obtaining appropriate cultures of body fluids
 Neurological observations (GCS) for warning signs and symptoms of cerebral edema:
Headache, bradycardia, change in neurological status (restlessness, irritability, increased

drowsiness, incontinence), specific neurological signs (e.g., cranial nerve palsies), rising
blood pressure and decreased oxygen saturation.
Treatment of cerebral edema
• Initiate treatment as soon as the condition is suspected.
• Reduce the rate of fluid administration by one-third.
• Give mannitol, 0.5–1 g/kg IV over 10–15 min, and repeat if there is no initial response in 2 h
• Hypertonic saline (3%), suggested dose 2.5–5 mL/kg over 10–15 min, may be used as an
alternative to mannitol, especially if there is no initial response to mannitol.
I- Fluid replacement:
3
1-Rate of fluids:
Duration of therapy depends on serum osmolarity = 2x Na+glucose/18+BUN/2.8= 300 normally
If s.osmolarity >340 treat over 48 hrs, if < 340 treat over 36 hrs.
{D+ ( M ×duration by days )−shock }

Total fluid amount is distributed evenly among duration i.e:
duration∈hours
2-Amount of fluids:
a- Shock therapy:
Fluid replacement should begin before starting insulin therapy. In a child with severe acidosis
or compromised circulation, an initial resuscitation of 10-20 mL/kg of isotonic sodium chloride
solution (0.9%) can be administered over 1 hr , it is preffered to start with 10 ml/kg over 30
minutes, then this can be repeated once more.
Remember to subtract any initial resuscitation fluid boluses given from the total calculated
deficit.
b- Deficit:
40-100 ml/kg average 70ml/kg
c- Maintenance:
100 ml/kg for 1st 10 kg

50 ml/kg for 2nd 10 kg
20 ml/kg for >20 kg
3-Type of fluid:
According to blood glucose level:
>250 mg/dl use isotonic normal saline (0.9%)
150-250 mg/dl use glucose 10%: NS 1:1
<150 mg/dl use glucose 25%: glucose 10%: NS 3:2:5
N.B:
4
1) If BG falls very rapidly (>5 mmol/L/h) after initial fluid expansion, consider adding glucose
even before plasma glucose has decreased to 12 mmol/L (200 mg/dL).
2) If BG falls below 80 mg/dL and still there is acidosis(<7.3) decrease insulin rate to 0.5 u/kg/hr
Oral fluids:
Oral fluids should be introduced only when substantial clinical improvement has occurred (mild
acidosis/ketosis may still be present). When oral fluid is tolerated, IV fluid should be reduced
accordingly so that the sum of IV and oral fluids does not exceed the calculated IV rate (i.e., not
in excess of 1.5–2 times maintenance fluid rate). This fluid restriction should be applied for 48 h
from admission (72 h if there is severe hyperosmolality at onset of treatment).
K replacement:
Make sure there is adequate urine out put
If K level 3.5-5.5à20 meq i.e :1 cm kcl for each 100 cc fluids

If K level < 3.5à40 meq i.e : 2cm kcl for each 100 cc fluids
If K level >5.5 no kcl replacement
II- Insulin therapy:
Start insulin infusion 1–2 h after starting fluid replacement therapy; i.e., after the patient has
received initial volume expansion• Dose: 0.05–0.1 unit/kg/h [e.g., one method is to dilute 50
units regular (soluble) insulin in 50 mL normal saline, 1 unit = 1 mL {solution must be flushed
through syringe pump before adminsteration to child}
When ketoacidosis has resolved, oral intake is tolerated, and the change to SC insulin is planned,
the most convenient time to change to SC insulin is just before a mealtime to prevent rebound
hyperglycemia, the first SC injection should be given 15–30 min (with rapid acting insulin) or 1–
2 h (with regular insulin) before stopping the insulin infusion to allow sufficient time for the
insulin to be absorbed. With intermediate or long-acting insulin, the overlap should be longer and
the rate of IV insulin infusion gradually lowered. For example, for patients on a basal-bolus
insulin regimen, the first dose of basal insulin may be administered in the evening and the insulin
infusion is stopped the next morning
5
Hyperosmolar hyperglycemic state (HHS)
It is a serious complication of Type II DM with a mortality rate of 10–20%. It is characterized by

hyperosmolarity, hyperglycemia, dehydration, and minimal ketoacidosis. The HHS can be the
initial presentation of Type II DM orcan occur in patients with a known history of Type II DM
during an intercurrent illness. Unlike DKA, the onset is more insidious and patients may initially
present with nonspecific flu-like symptoms. Plasma glucose levels (>600 mg/dL), as well as
serum osmolality is significantly elevated. The bicarbonate level is generally >15 mEq/L, the
venous pH >7.30, and urine and serum ketones are small or absent. Neurologic features are
prominent, including stupor and coma. Volume depletion in HHS is greater than in DKA, so that
patients require aggressive fluid resuscitation. Although many patients with HHS will respond to
fluids alone, administer IV insulin as in DKA to facilitate correction of the hyperglycemia. Do
not give insulin without adequate fluid resuscitation.

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Manshiet Al- Bakry Hospital

Diabetic ketoacidosis (DKA)

•Acidosis, Venous pH < 7.3 or bicarbonate <15 mmol/L

• Ketonemia and ketonuria.

The severity of DKA is categorized into:

• Moderate: pH<7.2, bicarbonate <10 mmol/L

• Severe: pH<7.1, bicarbonate <5 mmol/L.

The clinical signs of DKA include:

• Tachypnea ,deep (Kussmaul) respiration; breath has the smell of acetone

• Nausea, vomiting (which may be mistaken for gastroenteritis)

• Abdominal pain that may mimic an acute abdominal condition

• Confusion, drowsiness, progressive reduction in level of consciousness and, eventually, loss of

• Dehydration (which may be difficult to detect)

1. Serum or plasma glucose

mmol/L suggests concomitant lactic acidosis. The acidifying effect of chloride in

 There should be documentation on a flow chart of hour-by-hour clinical observations, IV

Headache, bradycardia, change in neurological status (restlessness, irritability, increased

Treatment of cerebral edema

• Initiate treatment as soon as the condition is suspected.

• Reduce the rate of fluid administration by one-third.

Duration of therapy depends on serum osmolarity = 2x Na+glucose/18+BUN/2.8= 300 normally

{D+ ( M ×duration by days )−shock }

100 ml/kg for 1st 10 kg

Make sure there is adequate urine out put

If K level 3.5-5.5à20 meq i.e :1 cm kcl for each 100 cc fluids

II- Insulin therapy:

Hyperosmolar hyperglycemic state (HHS)

It is a serious complication of Type II DM with a mortality rate of 10–20%. It is characterized by

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