This document defines diabetic ketoacidosis (DKA) and describes its signs, symptoms, causes, treatment, and complications. DKA is characterized by hyperglycemia, metabolic acidosis, and ketosis. It most commonly occurs in patients with newly diagnosed type 1 diabetes or with poor blood glucose control. Treatment involves fluid resuscitation, insulin therapy, and monitoring for complications like cerebral edema. Electrolyte imbalances are also common and require careful monitoring during treatment.

1. DKA
-Defined by the following biochemical criteria
- Hyperglycemia,
- blood glucose of >200 mg/dL (11 mmol/L)
-Metabolic acidosis,
-defined as a venous pH <7.3 and/or
-plasma bicarbonate <15 mEq/L (15 mmol/L).
- The severity of DKA can be categorized according
to the degree of acidosis as
mild, moderate, or severe, (pH 7.2-7.3, pH 7.1-7.2,
or pH <7.1, respectively)

2. -hyperketosis
concentration of total ketone bodies >5 mmol/L)
- hyperosmolality.
serum osmolality >320 mOsm/L
- hyperglycemia
plasma glucose >600 mg/Dl
- severe dehydration and hypotension
EPIDEMIOLOGY — DKA is frequently the initial
presentation of children with new onset type 1
diabetes mellitus

3. -Recurrent episodes of DKA with established type 1
diabetes mellitus.
- the result of underlying poor metabolic control
and frequently missed insulin injections.
- Omission of insulin injections is particularly
common among adolescents.
-Stress is also an important precipitating factor.
Stress increases the secretion of catecholamines,
cortisol, and glucagon, which promote both glucose
and ketoacid production.
-As an example, infection can precede an episode of DKA

4. History
-Classic symptoms
-Often insidious
-Fatigue and malaise
-Nausea/vomiting
-Abdominal pain
-Polydipsia
-Polyuria
-Polyphagia
-Weight loss
-Fever

5. Physical
-Altered mental status without evidence of head
trauma
-Tachycardia
-Tachypnea or hyperventilation (Kussmaul
respirations)
-Normal or low blood pressure
-Increased capillary refill time
- Poor perfusion
-Lethargy and weakness
-Fever
-Acetone odor of the breath reflecting metabolic
acidosis

6. Laboratory Studies
-blood glucose level
-blood PH
-electrolytes
-urine-ketone,glucose
-serum osmolaryty
-Blood urea nitnogen and creatinine

7. -Assessment of severity — At presentation, the
following clinical and laboratory findings may be
used to estimate the severity of DKA:
-Acid-base status — The venous pH and serum
bicarbonate concentration directly reflect the
severity of the acidosis
-The respiratory rate also may be helpful, since the
magnitude of the respiratory compensation is
directly related to the severity of the acidosis.

8. -Ketosis — The magnitude of the anion gap is
another measure of the severity of the ketosis and
can be a helpful estimate of acidosis.
-Neurologic status — Severe neurologic compromise
at presentation is a poor prognostic indicator, in part
because such patients are at increased risk for
developing cerebral edema during therapy.
-Volume status — Estimated fluid deficit, (generally
5-10% fluid deficit).

9. -Duration of symptoms — A long duration of
symptoms, as well as depressed level of
consciousness or compromised circulation, is
evidence of severe DKA and should prompt close
monitoring for potential complications of DKA, such
as cerebral edema .
- Symptoms of cerebral edema typically occur several
hours after the initiation of treatment for DKA.
-The presence of such symptoms at presentation
indicates a poor neurologic prognosis.

10. -Based upon the severity of presentation, the
clinician can ascertain the appropriate clinical
setting in which to treat the child.
-As an example, mild DKA without vomiting may be
safely managed in an ambulatory setting under
close supervision and with appropriate monitoring
by an experienced diabetes team.
-On the other hand, a patient with severe DKA
should be managed in a pediatric intensive care
unit .

11. Complications of DKA
-Ketoacidosis
-DHN
-Cerebral edema
-Electrolyte inbalance

12. Cerebral edema- is an uncommon but potentially
devastating consequence of diabetic ketoacidosis
(DKA)
- It is far more common among children with
DKA than among adults.
-Young children and those with newly diagnosed
diabetes are at highest risk.
-Symptoms typically emerge during treatment for
DKA, but may be present prior to initiation of
therapy.

13. INCIDENCE — Clinically significant cerebral edema
occurs in approximately 1 percent of episodes of
diabetic ketoacidosis in children and has a mortality
rate of 20 to 90 percent .
PATHOPHYSIOLOGY — The cause of cerebral edema
in DKA is not fully understood, and the only definite
way to prevent it is to avoid DKA .

14. -Cerebral edema may be present before treatment
has begun, but more commonly occurs 4 to 12
hours after the initiation of therapy
-Numerous factors have been implicated in the
pathophysiology of DKA-related cerebral edema,
but none has been proven. Ischemic, vasogenic,
osmotic, or cytotoxic processes have been
proposed .

15. Ischemia/cytotoxic edema — Studies shows a
decrease of N-acetylaspartate (NAA), a marker of
neuronal function or viability, in children with DKA in
several areas of the brain, including the basal ganglia
and occipital and peri-aqueductal gray matter.
-These observations suggest cerebral ischemia may
play a role in the pathophysiology of DKA-related
cerebral edema
-There is a hypothesis further supported by reports of
increased lactate production in the basal ganglia in
children with DKA

16. Vasogenic edema — The term "vasogenic"
edema describes a process in which primary
damage to the cerebral vascular endothelium
results in increased blood-brain barrier
permeability or a disturbance in
autoregulation, which permits abnormal
diffusion of intravascular fluids into the
cerebral tissues.

17. Osmotic edema -as a consequence of fluid therapy
- If the extracellular compartment is at a lower
osmolarity than the intracellular compartment,
osmotic pressure promotes water movement into
the intracellular compartment.
-During DKA, the combination of insulin and fluid
repletion lowers the serum glucose and plasma
osmolality, promoting osmotic water movement into
the brain

18. Risk factors — for developing cerebral edema
-Younger children
-Children with newly diagnosed diabetes
-Failure of the serum sodium to rise as predicted
following insulin therapy  fall in plasma osmolality
-Increased blood urea nitrogen at presentation of DKA,
which may represent a greater degree of hypovolemia
-The severity of acidosis at presentation
-The use of bicarbonate therapy for correction of the
acidosis in DKA

19. SIGNS AND SYMPTOMS
-Altered mentation/fluctuating level of consciousness
-Sustained heart rate deceleration (decline more than 20
beats per minute) not attributable to improved
intravascular volume or sleep state
-Age-inappropriate incontinence
-Vomiting
-Headache
-Lethargy or not easily aroused from sleep
-Diastolic blood pressure >90 mmHg
-Age <5 years

20. -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)
TREATMENT
-The rate of fluid administration should be reduced.
-Mannitol
-Intubation and mechanical ventilation may be required.
OUTCOME — The mortality rate among children with
DKA who develop cerebral edema is
approximately 20 to 25 percent; among
survivors, approximately 15 to 35 percent
have permanent sequelae

21. Electrolyte Imbalance
-Serum sodium — The serum sodium concentration
is affected by hyperglycemia. The magnitude of this
effect is determined by two major factors.
-Hyperglycemia will increase the plasma osmolality,
resulting in osmotic water movement out of the cells
which lowers the serum sodium by dilution.
-Inadequate water intake, which may be a particular
- problemin infants and young children who cannot
independently access water, prevents partial
correction of the hyperosmolality and can even lead
to hypernatremia despite the presence of
hyperglycemia.

22. - On the other hand, consumption of large volumes
of dilute fluid, since thirst is stimulated by
hyperosmolality, can contribute to hyponatremia.
-Serum potassium — The osmotic diuresis and
increased ketoacid excretion promote urinary potassium
loss, while vomiting and diarrhea, if present, increase
gastrointestinal potassium losses.
-The potassium losses will tend to produce hypokalemia.
-However insulin deficiency impairs potassium entry into
the cells, and hyperosmolality, which pulls water and
potassium out of the cells, tends to raise the serum
potassium concentration.

23. -Because of these counteracting effects, the serum
potassium at the time of presentation can be
normal, increased, or decreased.
- Regardless of the initial level, therapy with insulin
and fluids will predictably lower the serum
potassium concentration, which needs to be
monitored carefully.

24. -Serum phosphate — Children with DKA are typically in
negative phosphate balance because of decreased
phosphate intake and phosphaturia caused by the
glucosuria-induced osmotic diuresis.
-Blood urea nitrogen — Patients with severe
hypovolemia often have elevated blood urea nitrogen
concentrations . This finding at presentation may have
predictive value since it is a risk factor for cerebral
edema during therapy.

25. Tretment of DKA
1-Tretment of DHN -10%
2-Tretment of hyperglacemia
3-Prevent complications
-Tx DHN
-1st hour 10-20ml/kg bolous Nacl
Insulin drip at 0.05-0.1u/kg/hr
-2nd hour reapeat bolus or
0.45% Nacl: plus continue Insulin drip
20mEq/L Kphos and 20mEq/L kac
-start 5% glucose if blood
suger<250mg/dl

26. IV rate = 85ml/kg+ mentenance-bolus
23hrs
Mentenance(24hrs)=100ml/kg+50ml/kg(for the 2nd
10kg+25ml/kg(for all remaining kg)
RBS(blood glucose level mg/dl Insulin regular
> 600 1 IU/kg (0.5IU/kg IV +0.5 IU/kg IM)
600-300 0.5 IU/KG(0.25 IU/kg IV+0.25 IU/kg IM)
<300 Start 5% DW , 0.2-0.4 IU/kg s/c
RBS done Q 6 hrly

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