DIABETIC KETOACIDOSIS IN CHILDREN AND ADOLESCENTS
What is DKA as per ISPAD?
The biochemical
criteria for the diagnosis of diabetic ketoacidosis (DKA) are:
• Hyperglycemia
(blood glucose:11 mmol/L [≈200 mg/dL])
• Venous pH;7.3 or serum bicarbonate :15 mmol/L
• Ketonemia
(blood ß-hydroxybuyrate ≥3 mmol/L) or moderate or large ketonuria
What is DKA as per BSPED?
Diagnose DKA in
children and young people who have Acidosis (indicated by blood pH below 7.3 or
plasma bicarbonate below 15 mmol/litre) and ketonaemia (indicated by blood
beta-hydroxybutyrate above 3 mmol/litre).
What are mild, moderate & severe DKA?
When is insulin started in DKA management?
1 hour after
starting fluid resuscitation
What is the most common cause of DKA in new case of DM?
Delay in
diagnosis
Low socioeconomic
status
Residence in
a country with a low prevalence of type 1 (T1DM).
What is hyperglycemic hyperosmolar state?
• Plasma glucose
concentration 33.3 mmol/L (600 mg/dL)
• Venous pH:
7.25; arterial pH: 7.30
• Serum
bicarbonate 15 mmol/L
• Small
ketonuria, absent to mild ketonemia
• Effective serum
osmolality:320 mOsm/kg
• Altered
consciousness (eg, obtundation, combativeness) or seizures (in approximately
50%)
When is insulin started in HHS?
In HHS, begin
insulin administration at a dose of 0.025 to 0.05 U/kg/h once plasma glucose is
decreasing less than 3 mmol/L (50 mg/dL) per hour with fluid alone
What is renal threshold for glucose?
180 mg/dl
(10mmol/L)
What is the BP like in DKA patients?
Despite their
dehydration, patients generally continue to maintain normal blood pressure or
even have high blood pressure, possibly due to elevated plasma catecholamine
concentrations, increased release antidiuretic hormone (ADH) in response to
hyperosmolality (which increases blood pressure via V2 receptors), increased
osmotic pressure from marked hyperglycemia, or other factors
Why in some patients there is rise in plasma glucose after onset of therapy despite ongoing loss of glucose in the urine?
Rapid emptying of stomach contents containing an abundant quantity of sugar, which occurs as gastroparesis is relieved with therapy, accounts for the rise in plasma glucose concentration observed in some patients after onset of therapy despite ongoing large loss of glucose in the urine
Pathophysiology of DKA?
What is the average loss of fluid and electrolytes in DKA ?
When is hyperketonemia in DKA?
Level ≥3 mmol/L
is indicative of DKA.
Urine ketones are
typically ≥2+ “moderate or large” positive.
How should we treat a child with DKA are alert, not clinically dehydrated, not nauseated or vomiting, but with high ketone levels?
Children who are
alert, not clinically dehydrated, not nauseated or vomiting, do not always
require IV fluids, even if their ketone levels are high. They usually tolerate
oral rehydration and SC insulin but do require monitoring regularly to ensure
that they are improving and their ketone levels are falling.
What is euglycemic ketoacidosis?
Partially treated
children and children who have consumed little or no carbohydrate may, rarely,
have only modestly elevated blood glucose concentrations, referred to as
“euglycemic ketoacidosis”.
This can be
caused by starvation (anorexia or religious fasting), a low carbohydrate high
fat diet, or the off-label use of SGLT2-inhibitors.VpH and HCO can used for
diagnosis.
HHS can occur in
T2 DM(more common)
T1 DM
6q24-related
transient neonatal diabetes mellitus
In children in which age group is DKA common?
Young (mainly
below 2 years of age)
What increases the risk of DKA in established DM cases?
• 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, include those with eating disorders
• Children with
difficult or unstable family circumstances (eg, parental abuse)
• Peripubertal
and adolescent girls
• Binge alcohol
consumption
• Children with
limited access to medical services
What is the most useful sign for predicting 5% dehydration in children aged 1 month to 5 years?
• Prolonged
capillary refill time (normal capillary refill is ≤1.5-2 seconds)
• Abnormal skin
turgor (“tenting” or inelastic skin)
What signs suggest 10% dehydration?
Poorly palpable
pulses
Hypotension
Oliguria
What should be done if a DKA patient arrives?
ECG
IV - 2lines Art line
Avoid Central
line unless needed as there is a high risk of thrombosis
Weigh the
child
Management of DKA
Where should a child be treated in DKA?
"As per
BSPED 2020
What should be done if a child needs central venous line?
Remove as soon as
possible.
Mechanical and pharmacologic prophylaxis (low
molecular weight heparin) should be considered especially in children >12
years
Can insulin be given through central line?
Insulin should
preferably not be given through a central line unless it is the only available
option because its infusion may be interrupted when other fluids are given
through the same line
Is antibiotic indicated in DKA?
Give antibiotics
to febrile patients after obtaining appropriate cultures of body fluids. ---
ISPAD
Is bladder catheteization required?
Bladder
catheterization usually is not necessary, but if the child is unconscious or
unable to void on demand (eg, infants and very ill young children) the bladder
should be catheterized.
How often should we monitor a case of DKA?
Hourly vitals
monitoring
Hourly
neurological status monitoring
Capillary Blood
glucose -bedside hourly (cross check with lab)
Lab electrolytes,
BUN, glucose, Mg, Potassium, Ca,
Phosphate, Hct,blood gases every 2 to 4 hourly
Blood BOHB
concentrations, if available, every 2 to 4 hours. • Near-patient (also referred to as
point-of-care) BOHB measurements correlate well with a reference method up to 3
mmol/L, but are not accurate above 5 mmol/L
What is anion gap in DKA?
Anion gap = Na −
(Cl + HCO3): normal is 12 + 2
mmol/L
In DKA the anion
gap is typically 20 to 30 mmol/L;
an anion gap >35
mmol/L suggests concomitant lactic acidosis
What is corrected Na?
Corrected sodium
= measured Na + 2([plasma glucose − 5.6]/5.6) mmol/L or measured Na + 2([plasma
glucose − 100]/100) mg/Dl
What is effective osmolality?
Effective
osmolality (mOsm/kg) = 2 × (plasma Na) + plasma glucose mmol/L; normal range is
275 to 295 mOsm/kg
What are goals of DKA treatment?
How to estimate dehydration in DKA?
Patients with DKA
have a deficit in ECF volume that usually is in the range 5% to 10% of body
weight. Shock with hemodynamic compromise is rare in pediatric DKA. Clinical
estimates of volume deficit are subjective & inaccurate; therefore, in
moderate DKA assume 5% to 7% in severe DKA 7% to 10% dehydration.
Why sodium is low in DKA?
Dilutional
hyponatremia
Pseudohyponatremia d/t high serum liquids
What happens to Na after treatment with insulin starts?
Ideally, it
should rise but it fails to rise or
continues falling it is thought to be a potentially ominous sign of impending
cerebral edema. Also rapid rise Na
is dangerous
How is the fluid given in the first hour?
ISPAD 2018
For patients who
are volume depleted but not in shock, volume expansion (resuscitation) should
begin immediately with 0.9% saline to restore the peripheral circulation. The
volume administered typically is 10 mL/kg infused over 30 to 60 minutes;
however, if tissue perfusion is poor the initial fluid bolus is given more
rapidly (eg, over 15-30 minutes) and a second fluid bolus may be needed to
ensure adequate tissue perfusion
BSPED All
children and young people with mild, moderate or severe DKA who are not shocked
and are felt to require IV fluids should receive a 10 ml/kg 0.9% sodium
chloride bolus over 60 minutes. (PlasmaLyte 148 is used by some teams in the UK
for initial resuscitation in place of 0.9% sodium chloride and either are
suitable)
What is used crystalloid or colloid?
Crystalloid
How to give resuscitation fluids in patients presenting with shock in DKA?
ISPAD-
In the rare
patient with DKA in shock, rapidly restore circulatory volume with isotonic
saline in 20 mL/kg boluses infused as quickly as possible through a large bore
cannula with reassessment of circulatory status after each bolus
BSPED Patients with shock require appropriate restoration of their circulation and circulatory volume. Shocked patients should receive a 20 ml/kg bolus of 0.9% saline over 15 minutes.
Following the initial 20 ml/kg bolus shocked patients should be reassessed and further boluses of 10 ml/kg may be given if required to restore adequate circulation up to a total of 40 ml/kg at which stage inotropes should be considered
What fluids are used for maintenance and deficit?
NS
RL
Hartmann
How do we give fluid
therapy?
Over 24-48 hours
== ISPAD AND BSPED
Over 24 hr =
Milwaukee
Requirement =
Deficit + Maintenance
How to calculate fluid deficit?
What should we do regarding resuscitation fluid?
Resuscitation fluid – The volume of any fluid boluses given for resuscitation in children with shock should NOT be subtracted from the estimated fluid deficit.
The initial 10ml/kg bolus given to all non-shocked patients requiring IV fluids SHOULD be subtracted from total calculated fluid deficit. The deficit should be replaced over 48 hours along side appropriate maintenance fluids
How is maintenance fluid calculated?
Maintenance fluid
volumes should be calculated using the Holliday – Segar formula
How is total fluid calculated?
Calculate the
fluid deficit (either 5%, 7% or 10% dehydration depending on whether the
patient has mild, moderate or severe DKA), subtract the initial 10ml/kg bolus
then divide this over 48 hours and add to the hourly rate of maintenance fluid
volume , giving the total volume evenly over the next 48 hours. i.e.
Hourly rate = ({Deficit – initial bolus} /
48hr) + Maintenance per hour
What weight should be considered for calculation?
Wherever possible the patient’s actual weight on admission should be used rather than an estimated weight or approximation. Maintenance fluids should be based on the actual weight not an estimate of the likely weight following rehydration.
To avoid excessive amounts of fluid in overweight and obese children it is recommended that consideration be given to using a maximum weight of 80kg or 97th centile weight for age (whichever is lower) when calculating both deficit and maintenance requirements.
Whilst
clinical judgement should be used regarding the height and size of the patient,
in a 80kg patient with severe DKA the recommendations would suggest a fluid
volume over 24 hours in excess of 6.5 litres. This is approaching the fluid
volumes recommended for the treatment of adults with DKA so it is suggested
that unless the clinical situation indicates otherwise that a maximum weight of
80kg is used in the majority of cases
Examples of fluid calculation
At what rate should serum sodium level fall in DKA?
Sodium should
rise by 0.5 mmol/L for each 1 mmol/L decrease in glucose concentration
What is hyperchloremic metabolic acidosis?
The use of large amounts of chloride-rich fluids (combined with preferential renal excretion of ketones over chloride) may be associated with the rapid development of hyperchloremia (defined as a ratio of chloride:sodium [Cl− :Na+ ] ; 0.79) and hyperchloremic metabolic acidosis.
The acidifying effect of chloride can mask recognition of resolution of ketoacidosis when total base deficit is used to monitor biochemical improvement.
When
hyperchloremia develops, a persisting base deficit or low bicarbonate
concentration can be erroneously interpreted as being due to ongoing ketosis.
To avoid this misinterpretation, measurement of bedside BOHB levels will prevent any confusion and can demonstrate that ketoacidosis has resolved. Hyperchloremic acidosis resolves spontaneously.
How can reduce this hyperchloremic Met acidosis?
The chloride load
can be reduced by not giving potassium as potassium chloride (use potassium
acetate instead) and by using fluids such Ringer's lactate or Plasmalyte in
which a portion of the chloride is replaced by lactate or acetate, respectively.
What dose, route and when insulin be given in DKA?
Why after 1 hour of initial bolus fluid?
May increase risk
of cerebral edema
Hypokalemia Shock
d/t rapid fall in osmotic pressure
When should we decrease dose of insulin?
When pH and
bicarb returns to normal Or if hypoglycemia persists eve after adding Iv
dextrose
When should we add glucose to IV fluid in mx of DKA?
To prevent an
unduly rapid decrease in plasma glucose concentration and hypoglycemia, 5%
glucose, initially, should be added to the IV fluid when the plasma glucose
falls to approximately 14 to 17 mmol/L (250-300 mg/dL), or sooner if the rate
of fall is precipitous
If BG falls very rapidly (>5 mmol/L/h) after initial fluid expansion, consider adding glucose even before plasma glucose has decreased to 17 mmol/L (300 mg/dL).
Is it possible to give SC insulin instead of IV insulin in DKA?
In circumstances
where continuous IV administration is not possible and in patients with
uncomplicated DKA, hourly or 2-hourly SC rapid-acting insulin analog (insulin
lispro or insulin aspart) is safe and may be as effective as IV regular insulin
infusion,153–158 but, ideally, should not be used in patients whose peripheral
circulation is impaired.
Subcutaneous administration of short-acting insulin (regular) every 4 hours is also a safe and effective alternative to IV insulin infusion in children with pH ≥7.0.
What are the causes of low serum potassium in DKA?
Osmotic
diuresis
Hyperosmolarity
Vomiting
During treatment
due to transcellular shift caused by insulin
How shall we supplement K+?
If the patient is
hypokalemic, start potassium replacement at the time of initial volume
expansion and before starting insulin therapy. Otherwise, start replacing
potassium after initial volume expansion and concurrent with starting insulin
therapy. If the patient is hyperkalemic, defer potassium replacement therapy
until urine output is documented
If immediate serum potassium measurements are unavailable, an ECG may help to determine whether the child has hyper- or hypokalemia.
What is the dose of K+?
The starting
potassium concentration in the infusate should be 40 mmol/L. Subsequent
potassium replacement therapy should be based on serum potassium measurements.
If potassium is given with the initial rapid volume expansion, a concentration of 20 mmol/L should be used
What formulations of K+ are used?
Potassium
phosphate may be used together with potassium chloride or acetate; for example,
20 mmol/L potassium chloride and 20 mmol/L potassium phosphate or 20 mmol/L
potassium phosphate and 20 mmol/L potassium acetate .
Administration of
potassium entirely as potassium chloride contributes to the risk of
hyperchloremic metabolic acidosis whereas administration entirely as potassium
phosphate can result in hypocalcemia.
How long should IV correction k continue?
Potassium
replacement should continue throughout IV fluid therapy. • The maximum recommended rate of IV
potassium replacement is usually 0.5 mmol/kg/h.
If hypokalemia
persists despite a maximum rate of potassium replacement, then the rate of
insulin infusion can be reduced.
Profound
hypokalemia (<2.5 mmol/L) in untreated DKA is rare and necessitates vigorous
potassium replacement while delaying the start of insulin therapy until serum
potassium levels are>2.5 mmol/L to reduce the risk of cardiopulmonary and
neuromuscular compromise.
Why hypophosphatemia occurs?
osmotic
diuresis
Insulin
treatment
Mx -- Phosphate
supplementation and K phosphate administration.
When is bicarb given?
Bicarbonate
administration may be beneficial in the rare patient with life-threatening
hyperkalemia or unusually severe acidosis (vpH <6.9) that has
compromised cardiac contractility
Bicarbonate
therapy may cause paradoxical CNS acidosis & rapid correction of acidosis
with bicarbonate causes hypokalemia
At what rate is bicarbonate given?
If bicarbonate is
considered necessary, cautiously give 1 to 2 mmol/kg over 60 minutes
What are the Complications of DKA treatment?
When should we introduce oral fluids?
Oral fluids
should be introduced only when substantial clinical improvement has occurred
(mild acidosis/ketosis may still be present
Can we use ketonuria as an end-point for determining resolution of DKA?
No
When is IV insulin changed to oral?
When ketoacidosis
has resolved, oral intake is tolerated, and the change to SC insulin is
planned, a dose of basal (long- or intermediate-acting) insulin should be
administered in addition to rapid- or short-acting insulin
The most
convenient time to change to SC insulin is just before a mealtime
BSPED -- Once ketones below 1.0 mmol/l, consider
switching from intravenous to subcutaneous insulin
When should we give SC while stopping IV infusion of insulin?
To prevent rebound hyperglycemia the first SC injection should be given 15 to 30 minutes (with rapid-acting insulin) or 1 to 2 hours (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 administration gradually decreased.
For IV insulin infusion insulin mixed with what fluid?
0.9% NS
For children who are already on long-acting insulin, should we continue it while giving IV insulin infusion?
You may wish to
continue this at the usual dose and time throughout the DKA treatment, in
addition to the IV insulin infusion, in order to shorten length of stay after
recovery from DKA.ISPAD guidelines suggest that starting an appropriate dose of
long acting background insulin alongside the intravenous infusion should be
considered.
BSPED supports ISPAD guideline
How can corrected Na help in adjusting fluid rate?
If the rise in
Na(corr) is more than 5mmol/L in 4-8 hrs it suggests too much fluid loss or
insufficient replacement. Consider increasing the fluid rate
If there is a
fall in Na(corr) by more than 5mmol/L in 4-8 hrs it suggests too much fluid gain
or too rapid replacement. Consider reducing the fluid rate
If there is persisting acidosis despite insulin therapy what can be the causes?
Insufficient
insulin to switch off ketones (including incorrectly made insulin
infusion)
Inadequate
resuscitation
Fluid calculation
error
Sepsis
Hyperchloremic
acidosis
Salicylate or
other prescription or recreational drugs
What is the mortality rate of DKA?
0.15 to 0.3%
What is the most common cause of death in DKA?
Cerebral injury
is the major cause of mortality and morbidity and cerebral edema accounts for
60% to 90% of all DKA deaths. From 10% to 25% of survivors of cerebral edema
have significant residual morbidity
What is the cause of Cerebral Edema in DKA?
Factors intrinsic
to DKA may be the cause of brain injury, which could be worsened during
treatment. It is noteworthy that the degree of cerebral edema that develops
during DKA correlates with the degree of dehydration and hyperventilation at
presentation, but not with initial osmolality or osmotic changes during
treatment.
What are the risk factors of CE?
Younger age
New onset
diabetes
longer duration
of symptoms
When do clinically significant cerebral edema usually develop?
Clinically
significant cerebral edema usually develops within the first 12 hours after
treatment has started but can occur before treatment has begun or, rarely, may
develop as late as 24 to 48 hours after the start of treatment.
What are the diagnostic criteria for CE in DKA?
• Abnormal motor
or verbal response to pain
• Decorticate or
decerebrate posture
• Cranial nerve
palsy (especially III, IV, and VI)
• Abnormal
neurogenic respiratory pattern (eg, grunting, tachypnea, Cheyne-Stokes respiration, apneusis)
When DI like picture is seen in DKA mx what should be suspected?
The appearance of
diabetes insipidus, manifested by increased urine output with a concomitant
marked increase in the serum sodium concentration, reflecting loss of free
water in the urine, is a sign of cerebral herniation causing interruption of
blood flow to the pituitary gland
How do we treat CE?
Same as other
causes of CE
Give mannitol, 0.5 to 1 g/kg IV over 10 to 15 minutes.
The effect of
mannitol should be apparent after ~15 minutes, and is expected to last about
120 minutes. If necessary, the dose can be repeated after 30 minutes.
Hypertonic saline (3%), suggested dose 2.5 to 5 mL/kg over 10 to 15 minutes, may be used as an alternative to mannitol, or in addition to mannitol if there has been no response to mannitol within 15 to 30 minutes
Hypertonic saline (3%) 2.5 mL/kg is equimolar to mannitol 0.5 g/kg.
Acute ingestion of alcohol causes?
Acute ingestion
of alcohol can cause hypoglycemia (rather than DKA) by decreasing hepatic
gluconeogenesis. But case reports are there for DKA caused by alcohol
consumption.
Which is better urine ketones or blood Beta-hydroxybutyrate?
Clinical testing with
urine strips can be used to determine the presence of ketosis but is inaccurate
for assessment of the degree of ketosis. In addition, this test may give a
false impression of persistent ketoacidosis during recovery from DKA.
This is because
the nitroprusside test strip reacts with acetoacetate and acetone but not BOHB,
which makes up 75 percent of circulating ketones. During recovery from DKA,
BOHB is converted to acetoacetate and acetone, which are excreted in urine for
several hours after the serum BOHB concentration has returned to normal.
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