DKA Flashcards

1
Q

Diabetic ketoacidosis

A

• (ISPAD) defined the following biochemical criteria for the
diagnosis of diabetic ketoacidosis (DKA): • Hyperglycemia [blood glucose (BG) >11mmol/L (≈200 mg/dL)] • Venous pH<7.3 or bicarbonate<15mmol/L . • Ketonemia and ketonuria. Blood beta-hydroxy-butyrate (BOHB)
concentration ≥3mmol/L, or Urine ketones are typically ≥2+ .

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2
Q

Severity

A

Severity
• Mild: venous pH < 7.3 or bicarbonate <
15mmol/L.
• Moderate: pH < 7.2, bicarbonate < 10mmol/L.
• Severe: pH < 7.1, bicarbonate < 5mmol/L.

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3
Q

Pathophysiology

A

Pathophysiology
• DKA (hyperglycemia + ketones + Acidosis)
• Glucose homeostasis : the blood sugar kept
under tight control and that because of very
precise and efficient secretion of insulin and
the counter-regulatory hormone
Diabetic ketoacidosis (DKA) results from
deficiency of circulating insulin and increased
levels of the counterregulatory hormones :
catecholamines, glucagon, cortisol and growth
hormone.

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4
Q

The risk factors of DKA

A

Children who omit insulin. • Children with poor metabolic control or previous
episodes of DKA. • Gastroenteritis with persistent vomiting and inability
to maintain hydration. • Children with psychiatric disorders.

• Children with difficult family circumstances .
• Children with limited access to medical
services.
• Insulin pump therapy

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5
Q

Clinical presentation

A

Clinical presentation
• Classical diabetes presentation ( 86%) • Vomiting but no diarrhea ( gastroenritis) • Abdominal pain (Acute abdomen) • Respiratory distress (chest infection) • Dehydration

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6
Q

Main Goals of therapy are

A

Main Goals of therapy are
1. Emergency assessment (PALS). 2. Correct dehydration (fluid therapy , electrolyte). 3. Correct acidosis and reverse ketosis ( insulin therapy). 4. Slowly correct hyperglycemia and restore BG to near normal, ( adjusting
the insulin and fluid). 5. Monitor for complications of DKA and its treatment. ( clinical and
biochemical monitoring). 6. Identify and treat any complications. (cerebral edema).
Wolfsdorf et al. 2018

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7
Q

Emergency assessment (PALS).

A
1- Emergency assessment (PALS).
• Emergency assessment should  follow the general guidelines for  Pediatric Advanced
Life Support  (PALS) and includes:  Air-way, Breathing and Circulation assessment.  Immediate measurement of BG, Blood or urine ketones, Serum electrolytes.  Blood gases and full blood count.  Assessment of severity of dehydration.  Assessment of level of consciousness .  A second peripheral IV catheter should be inserted .
 Wolfsdorf et al. 2018
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8
Q

Assessment of severity

A

Assessment of severity
• Assess The severity of DKA by determining the degree of acidosis : • Mild: venous pH < 7.3 or bicarbonate < 15mmol/L.
5% dehydration
• Moderate: pH < 7.2, bicarbonate < 10mmol/L.
7% dehydration
• Severe: pH < 7.1, bicarbonate < 5mmol/L.
10% dehydration

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9
Q

2- Correct Dehydration (fluid therapy , electrolyte).

A

• The data from the available studies are
consistent with the following average losses in
severe DKA: • Water — 100 to 125 mL/kg • Sodium — 5 to 13 meq/kg • Potassium — 6 to 7 meq/kg

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10
Q

fluid therapy

A

ISPAD recommended that initial fluid
management of children with DKA be based upon
the assumption that patients present with a 7 to
10 percent fluid deficit. • Treatment should be initiated with a maximal
volume of 10 mL/kg of isotonic solution over one
hour, unless the patient is hypotensive. • Hypovolemic shock is a rare occurrence in DKA.
• The rate of fluid deficit administration should
be calculated to fully replete the patient over
48 hours.
• The rate over the first 24 hours should not
exceed 1.5 to 2 times the maintenance fluid.

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11
Q

Serum sodium

A

Hyperglycemia has a variable effect on the serum sodium concentration:
• By raising the plasma osmolality, hyperglycemia
results in osmotic water movement out of the
cells, thereby lowering the serum sodium
concentration by dilution. • This direct effect of hyperglycemia is often
counteracted by the glucosuria-induced osmotic
diuresis. • Sodium loss — 5 to 13 meq/kg

Normally, during dropping of blood sugar due to
insulin therapy, the serum sodium level will rise. • A failure of measured serum sodium levels to rise
or a further decline in serum sodium levels with
therapy is thought to be a potentially ominous
sign of impending cerebral edema . Glaser et al 2001 • The corrected serum sodium should be carefully
monitored and be plotted on a nomogram.

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12
Q

Potassium

A

Potassium
• Serum potassium — Both renal and
gastrointestinal losses can contribute to an often-
marked degree of potassium depletio n in DKA. • On the other hand, the combination of insulin
deficiency, and hyperosmolality, tend to raise the
serum potassium. • Total body Potassium loss — 6 to 7 meq/kg
• Potassium replacement will almost always be
required within one to two hours of the
initiation of fluid and insulin therapy in
children with DKA who do not have renal
failure.

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13
Q

Potassium

A

• If the patient is hypokalemic, potassium replacement needs to start
immediately, using a potassium concentration of 60 meq/L as insulin will
further reduce the serum potassium.
• For the same reason, if the patient is normokalemic, potassium
replacement should be given with the start of insulin therapy (eg, adding
40 meq/L of potassium to the saline solution ).
• If the patient is hyperkalemic, potassium replacement should be initiated
when the serum potassium falls to normal.
• The maximum recommended rate of IV potassium replacement is usually
0.5 mmol/kg/h.
Make sure good UOP =rule of thumb

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14
Q

Insulin therapy

A

Insulin therapy
• Insulin therapy as infusion: begin with 0.05–0.1 U/kg/h 1–2 h AFTER starting
fluid replacement therapy. • The lower dose should be used initially in younger
children who are more sensitive to insulin. • The insulin infusion should continue until the
venous pH is >7.3 and/or the serum HCO3 is >15
meq/L.
An Insulin IV bolus should not be used at the start
of therapy; it may increase the risk of cerebral
edema. • It can precipitate shock by rapidly decreasing
osmotic pressure and can exacerbate
hypokalemia.
• In a study of 635 episodes of DKA the mean
time to correction of DKA and complete
restoration of the circulation was 11.6±6.2
hours.
• At this point, patients were started oral intake and transitioned to subcutaneous insulin .
Fiordalisi et al 2007

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15
Q

Bicarbonate administration

A

• Bicarbonate therapy may cause paradoxical CNS
acidosis. Assal et al. 1974 • Bicarbonate administration is not recommended
except for treatment of life-threatening
hyperkalemia.

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16
Q

Transition to subcutaneous insulin

A

Transition to subcutaneous insulin
• Normalization of the anion gap is an indication for stopping the
insulin infusion and changing to subcutaneous insulin. • The patient is usually switched to subcutaneous insulin when :
 Clinically improving and fully conscious.  The serum HCO3 is greater than 16 meq/L.  The venous pH is greater than 7.30.  The anion gap is less than 16 meq/L.
• Stop IV insulin at least 30 min after S/C insulin or 60 min after long-acting insulin or restarting the pump
• Discontinue IV fluid once eating and drinking
• Educate for sick day management/ DKA
prevention

17
Q

Monitoring

A

• Hourly vital signs(heart rate, respiratory rate, blood pressure). • Hourly neurological observations, warning signs and symptoms of
cerebral edema and GCS. • Hourly accurate fluid input and output. • Capillary blood glucose concentration should be measured
hourly. • Laboratory tests: serum electrolytes, glucose, blood gases, urea
nitrogen, calcium, magnesium, phosphorus, hematocrit, and
should be repeated 2–4 h.
There should be documentation on a flow
chart of laboratory values and clinical
parameters .
• To allow better visualization and evaluation of
the clinical picture.

18
Q

Management

A

• Airway: patent • Breathing: kussmauls resps. , O2 sat 100% on O2
mask • Circulation HR 130 BP 125/60, cold peripheries
cap. Refill 3 sec • D alert oriented, obeys command , pupils reactive
and equal with normal eye movement • What are your next steps? • Shock ?
• Recurrent vomiting insert NGT • Give 100% O2 • 10ml/kg normal saline over one hour • If shock give 20 ml/kg normal saline over 15 min to max 40
ml/kg • If ongoing shock /hypotension —- inotropes • GCS if decreases , PICU , Anesthetic review

19
Q

How do you calculate insulin dose

A

How do you calculate insulin dose
• Start insulin infusion 1-2 hours after initial fluid • 0.05- 0.1 units/kg/hr • 50 U in 50 ml NS • Continue until resolving acidosis • If glucose fall below 14 mmols/l add glucose to fluid • Close monitoring • If DKA resolved stop insulin infusion one hour after giving basal insulin or
starting insulin pump

If acidosis not corrected
• Inadequate Insulin dose • Inadequate fluid resuscitation • Fluid calculation error • IV site infiltration • Sepsis • Hyperchloremic acidosis • Other causes of acidosis

20
Q

Identify and treat any complications.

A

6- Identify and treat any complications.
• Cerebral edema.
• Venous thrombosis — Children with DKA appear to be at increased risk for deep
venous thrombosis, particularly in association with femoral central venous
catheter placement.
• Aspiration — Children with DKA who present with an altered state of
consciousness and vomiting are at increased risk for aspiration.
• Cardiac arrhythmia — Cardiac arrhythmias may be seen with either hypokalemia
or hyperkalemia.

21
Q

Cerebral edema

A

headache is usually the earliest Warning signs and symptoms of cerebral edema include:
• Headache (variable severity). • Slowing of heart rate . • Change in neurological status (restlessness, irritability,
increased drowsiness, incontinence). • Specific neurological deficits(e.g., cranial nerve palsies). • Rising blood pressure and decreased oxygen saturation .
• Risk Factors that have been associated with an
increased risk of cerebral edema include: I. Younger age. II. New onset diabetes. III. Longer duration of symptoms. IV. Severe acidosis and dehydration at
presentation. V. Elevated serum urea nitrogen concentration,
severe hypocapnia
Rosenbloom et al 1990

patients with multiple risk factors for
cerebral edema (elevated serum urea
nitrogen concentration, severe acidosis,
severe hypocapnia), have mannitol or
hypertonic saline at the bedside and the dose
calculated.

22
Q

Diagnosis of cerebral edama

A
Diagnosis
• One Diagnostic criterion.
• Two major criteria.
• One major and two minor criteria
• have a  sensitivity of 92% and a false positive
rate of only 4%.
23
Q

Tt cerebral edema

A

Treatment
• Initiate treatment as soon as the condition is suspected in ICU setting and starting with ABC
assessment. • Exclude hypoglycemia • 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 30 min to
2 h. • Hypertonic saline (3%), suggested dose 2.5–5 mL/kg over 10–15 min, may be used as an
alternative to mannitol. • Elevate the head of the bed to 30◦. • CT brain if patient is stable • Intubation may be necessary for the patient with impending respiratory failure.

24
Q

To prevent hyperglycemia and ketoacidosis

A

To prevent hyperglycemia and ketoacidosis
• DO NOT STOP INSULIN! (Insulin dose may need to be increased or
decreased, based on blood glucose (BG) level and food intake) • Do frequent blood sugar and urine or blood ketones every 2-4
hours. • If ELEVATED BG more than 250 mg /dl WITH ABSENCE OR SMALL
KETONES give correction dose 0.05 u per kg of short or rapid
acting insulin . • If ELEVATED BG more than 250 mg /dl WITH positive KETONES
give correction dose 0.1 u per kg of short or rapid acting insulin

25
Q

To prevent hypoglycemia

A

To prevent hypoglycemia
• Monitor blood sugar every 2-4 hours • How to address hypoglycemia symptoms (tremor
,tachycardia,drowseness, LOC). • If BG less than 70 mg/dl give 10-15 gram of CHO (glucose tab,
juices) then check BG every 15 min till stabilization. • If there is altered mental status give Glucagon 0.5-1 mg IM
injection and seek medical advice • At hospital give 2-4 ml of 10% dextrose bolus and recheck the BG