SEMINAR ON MANAGEMENT

OF DKA

Presenters
1. Endegena Tadesse……..C2
2. Endeshaw Simeneh……..C2
3. Eyuoel Kassahun………...C2
MODERATOR Dr ABDI(PEDIATRICIAN)
11/10/2024 1
 OUTLINE
o INTRODUCTION
o CLASSIFICATION
o DEFINITION AND PATHOPHYSIOLOGY
o PRECIPITATING FACTOR
o PATIENT APPROACH
o INVESTIGATIONS
o MANAGEMENT

11/10/2024 2
 INTRODUCTION
o Diabetes mellitus (DM) is a common, chronic, metabolic disease
characterized
by hyperglycemia as a cardinal biochemical feature.
o DM is not a single entity but rather a heterogeneous group of
disorders in
which there are distinct genetic patterns as well as other
etiologic and
pathophysiologic mechanisms that lead to impairment of
glucose tolerance
through deficient insulin production or action. 11/10/2024 3
 CONT.

o The American diabetes association has proposed a diabetes

classification system that includes 4 categories: type 1 diabetes,
type 2 diabetes, other specific types, and gestational
diabetes.

11/10/2024 4
 TYPE 1 DM
o T1 DM accounts for approximately 10% of all cases of diabetes
in all ages peaks of presentation occur in 2 age groups: at 5-7 yr
of age and at the time of puberty.
o While T1 DM accounts for most cases of diabetes in childhood,
it is not limited to this age group; new cases continue to present
in adult life and between 25 and 50% of individuals with T1 DM
present as adults.

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PATHOPHYSIOLOGY

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 TYPE 2 DM
o T2DM is a heterogeneous disorder, characterized by peripheral insulin
resistance
and failure of the β-cell to keep up with increasing insulin demand.
o Patients with T2 DM have relative rather than absolute insulin deficiency.
Generally, they are not ketosis prone, but ketoacidosis is the initial
presentation in 5–10% of affected subjects.
o The search for diabetes in youth (search) study found that the
prevalence of
T2 DM in the 10-19 yr old age group in the united states was 0.24/1000 in
2009
11/10/2024 7
11/10/2024 8
11/10/2024 9
 DEFINITION OF DKA
o Diabetic ketoacidosis (DKA) is a condition in which there is a
severe deficiency of insulin resulting in very high blood glucose
which nonetheless is unavailable to the body tissues as a source
of energy.
o A clinical condition characterized by a triad of hyperglycemia,
metabolic acidosis and ketonemia in dm patient.
o DKA may be the initial symptom complex that leads to a
diagnosis of type 1 DM, but more frequently it occurs in
individuals with established diabetes.
11/10/2024 10
 CONT.
o These abnormalities are accompanied by hyper ketosis and
hyperosmolality. The clinical manifestations of DKA are related
to the degree of hyperosmolality, volume depletion, and
acidosis.
o Hyperosmolar hyperglycemic state is a hyperglycemia
emergency which is distinguished from classic DKA by marked
hyperglycemia (plasma glucose >600 mg/dl), serum Hco2
>15 mmol/l, absent to mild ketonuria, and effective serum
osmolality >320 mosm/l. HHS occurs most commonly in adults
with poorly controlled type 2 diabetes. 11/10/2024 11
 PATHIOPHYSIOLOGY
o Two hormonal abnormalities are largely responsible for the
development of hyperglycemia and ketoacidosis in patients with
uncontrolled diabetes
1. Insulin deficiency and/or resistance
2. Glucagon excess, which may result from removal of the normal
suppressive effect of insulin

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 CONT.
o Insulin acts to restore normoglycemia by diminishing hepatic
glucose production, via reductions in both glycogenolysis and
gluconeogenesis, and by increasing glucose uptake by skeletal
muscle and adipose tissue.
o Insulin-induced inhibition of glucagon secretion contributes to
the decline in hepatic glucose production; this effect is mediated
by direct inhibition of glucagon secretion and of the glucagon
gene in the pancreatic alpha cells.

11/10/2024 13
 CONT.

o There are major pathophysiologic results associated with

insulin deficiency combined with counterregulatory hormone
excess in DKA:

 hyperglycemia

 Ketosis and

 Metabolic acidosis

11/10/2024 14
 CONT.
A. Hyperglycemia

• The increased levels of glucagon and catecholamines in the

face of low insulin levels promote glycogenolysis

• Insulin deficiency also reduces levels of the GLUT4 glucose

transporter, which impairs glucose uptake into skeletal muscle
and fat and reduces intracellular glucose metabolism

11/10/2024 15
 CONT.
B. Ketosis and acidosis

o ketosis results from a marked increase in free fatty acid release

from adipocytes, with a resulting shift toward ketone body
synthesis in the liver.

o Reduced insulin levels, in combination with elevations in

catecholamines and growth hormone, increase lipolysis and the
release of free fatty acids.
11/10/2024 16
 CONT.
o Normally, these free fatty acids are converted to triglycerides or
VLDL in the liver. However, in DKA, hyperglucagonemia alters
hepatic metabolism to favor ketone body formation.

o At physiologic pH, ketone bodies exist as ketoacids, which are

neutralized by bicarbonate.

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 CONT.
o As bicarbonate stores are depleted, metabolic acidosis ensues.
Increased lactic acid production also contributes to the acidosis.

o The increased free fatty acids increase triglyceride and VLDL

production. VLDL clearance is also reduced because the activity of
insulin-sensitive lipoprotein lipase in muscle and fat is decreased

o Hypertriglyceridemia may be severe enough to cause pancreatitis.

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 CONT.
C. Osmotic diuresis

• Hyperglycemia produces an osmotic diuresis (glycosuria) when

the renal threshold is exceeded (180 mg/dl; 10 mmol/L).

• The kidneys excrete ketone bodies (ketonuria) contributes to

osmotic diuresis.

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 CONT.
D. Electrolyte imbalance

• Glucosuria causes obligatory losses of water and electrolytes

such as sodium, potassium, magnesium, calcium and
phosphate.

• Potassium loss is caused by a shift of potassium from the

intracellular to the extracellular space in an exchange with
hydrogen ions that accumulate extracellularly in acidosis.

• High serum osmolarity also drives water from intracellular

11/10/2024 to
20

extracellular space, causing dilutional hyponatremia

 CONT.
E. Fluid deficit in DKA
o Include:
 Osmotic diuresis due to hyperglycemia
Vomiting
Inability to take due to emesis & impaired consciousness

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PRECIPITATING FACTORS

11/10/2024 22
 CONT.
o Initial presentation of type 1 diabetes
mellitus — children who are young (<6 years of age) or from a
low socioeconomic background are at increased risk for DKA at
initial presentation
o In established type 1 diabetes mellitus — the incidence of
DKA in children who are known to have type 1 diabetes mellitus
was 8 episodes per 100 person years risk factors for recurrent
DKA included:
• Higher A1C values and higher reported insulin requirements
• Highest risk in female adolescents over 13 years of age
11/10/2024 23

• Children over 13 years of age who are underinsured and/or have

 DIAGNOSTIC EVALUATION
o The clinical diagnosis of diabetes in a previously healthy child requires
a high index of suspicion. Signs and symptoms of DKA are related to
the degree of hyperosmolality, volume depletion, and acidosis.
1. Signs and symptoms — the earliest symptoms are related to
hyperglycemia. Older children and adolescents typically present with
polyuria, polydipsia, and fatigue.
o Other findings include weight loss, nocturia (with or without secondary
enuresis), daytime enuresis, and vaginal or cutaneous moniliasis.
Hypovolemia may be severe if the urinary losses are not replaced.

11/10/2024 24
 CONT.
o In infants, the diagnosis is more difficult because the patients
are not toilet trained and they cannot express thirst. However,
decreased energy and activity, irritability, weight loss, and
physical signs of dehydration are common findings.
o In addition, severe candida diaper rash or otherwise
unexplained metabolic acidosis or hypovolemia should heighten
the suspicion for diabetes.

11/10/2024 25
 CONT.
o A number of other clinical findings may be seen:
 Polyphagia usually occurs early in the course of the illness.
However, once insulin deficiency becomes more severe and
ketoacidosis develops, appetite is suppressed.
 Hyperventilation and deep (kussmaul) respirations represent
the respiratory compensation for metabolic acidosis.
 Neurologic findings, ranging from drowsiness, lethargy, and
obtundation to coma, are related to the severity of
hyperosmolality and/or to the degree of acidosis.
11/10/2024 26
 CONT.
o Physical examination

o General signs of diabetic ketoacidosis (DKA) may include the

following:

• Ill appearance

• Dry skin, Dry mucous membranes, Decreased skin turgor

• Labored respiration

• Decreased reflexes
11/10/2024 27

• Characteristic acetone breath odor

 CONT.
o Effects on vital signs that are related to DKA may include the
following:

• Tachycardia

• Hypotension

• Tachypnea

• Hypothermia

• Fever, if infection is present

11/10/2024 28
 CONT.
o It is difficult to assess clinically the degree of dehydration in
children presenting with DKA as these children are less likely to
show the classic signs of hypovolemia.
o Children with DKA generally present with a 5 to 10 percent fluid
deficit.
o The most useful signs for predicting 5% dehydration in young
children aged 1 month to 5 years are:
• prolonged capillary refill time (normal capillary refill is ≤1.5-2
seconds)
• abnormal skin turgor (“tenting” or inelastic skin) 11/10/2024 29
11/10/2024 30
 DIAGNOSIS
o Laboratory findings — initial laboratory testing should
include serum testing for glucose, electrolytes, creatinine and
urea nitrogen, blood gases, and hematocrit.
o The diagnosis of DKA is confirmed by the findings of
hyperglycemia, a high anion gap acidosis, ketonuria, and
ketonemia

11/10/2024 31
 CONT.
 Serum glucose — the serum glucose is, by definition, greater
than 200 mg/dl (11 mmol/L). this degree of hyperglycemia
exceeds the renal tubular threshold for glucose reabsorption,
resulting in an osmotic diuresis with polyuria and subsequent
volume depletion.
o Glucosuria also predisposes to candida infections in diapered
children and adolescent girls.

11/10/2024 32
 CONT.
 Acid-base status — the second criterion for the diagnosis of
DKA is a serum bicarbonate <15 meq/L or a venous pH <7.3.
o Insulin deficiency and increased plasma concentrations of
glucagon, cortisol and epinephrine increase glucose production,
lipolysis and ketogenesis which collectively contribute to the
development of both the hyperglycemia and the ketoacidosis.

11/10/2024 33
 CONT.
 The severity of metabolic acidosis is dependent upon the ff
factors:
o The rate of ketoacid production
o The duration of increased ketoacid production; the acidosis will
be less severe in patients who present early
o The rate of acid excretion in the urine. Patients with relatively
normal renal function can markedly increase acid excretion
o The adequacy of the compensatory respiratory alkalosis

11/10/2024 34
 CONT.
o COMMON LAB FINDINGS
Hyperglycemia- > ↑Anion Gap ↑WBC -
250mg/dl Ketosis/Infection
Hyperketonemia- > Potassium → ↑ ↓ BUN and serum Creatinine
3mmol/l ↑

↓Serum HCO3 - frequently Sodium, chloride, Hgb A1C ↑

<10meq/l magnesium, phosphorus →
↓

Low Blood pH - 6.8-7.3 ↑Serum Osmolality Pa CO2 - low

Ketonuria >= +2 hypertriglyceridemia, and Glycosuria

hyperlipoproteinemia

11/10/2024 35
 DIFFERENTIAL DIAGNOSIS OF DKA
o Starvation ketosis

o Alcoholic ketoacidosis (bicarbonate usually > 15 meq/L)

o Other increased anion gap acidosis: ingestion of aspirin,

advanced chronic kidney disease

o Acute pancreatitis

o Non-ketotic hyperosmolar coma

11/10/2024 36
 PRINCIPLES OF MANAGEMENT OF DKA
o Maintain ABC of life
o Fluid management & electrolyte therapy
o Insulin therapy
o Monitoring
o Treatment of the precipitating
o Treatment of the complication
o Patient education
11/10/2024 37
 MAINTENANCE OF ABC OF LIFE
o Assess air way, breathing and circulation.

o Patients with GCS < 8 may need intubation to secure air way
and prevent aspiration.
o Gastric decompression (NG tube) to reduce risk of aspiration.

o Administer oxygen if patient is in shock or low oxygen saturation

11/10/2024 38
11/10/2024 39
 Fluid management & electrolyte therapy
o Consensus recommended that initial fluid management of
children with moderate or severe DKA be based upon the
assumption that patients present with a 7 to 10 percent fluid
deficit.
o Urinary losses from the glucose osmotic diuresis (due to
osmotic action of glucose and ketones in the urine) and
gastrointestinal losses from vomiting and/or diarrhea, if present,
result in extracellular volume depletion.

11/10/2024 40
 CONT.
 Fluid repletion — the goals of initial volume expansion are:
o To restore the effective circulating volume by replacing sodium
and water loss
o To restore glomerular filtration rate to enhance clearance of
ketones and glucose from the blood.
o Increase sensitivity of cells to insulin.

11/10/2024 41
 CONT.
 Initial volume expansion — the volume and rate of
administration depend upon the effective circulating volume.
o Fluid repletion in moderate to severe DKA is usually begun with
an infusion of 10 ml/kg over one hour. If and only if the effective
circulating volume is still compromised, an additional infusion of
10 ml/kg can be given over the next hour.
o We generally do not give more than 20 ml/kg in total boluses
unless the patient's cardiovascular status is compromised.

11/10/2024 42
 CONT.
o Subsequent fluid administration — once the child is
hemodynamically stable, subsequent volume expansion should be
given more slowly. The rate of fluid administration should not exceed
1.5 to 2 times the maintenance rate and should not include urinary
losses.
o The solution used for this ongoing volume repletion should initially
consist of isotonic saline (NS or RL) for approximately four to six
hours.
o For most patients, 40 meq/L of potassium salts should be added to
the solution to correct the total body potassium deficit.
11/10/2024 43
 CONT.
o When hemodynamic stability and adequate urine output are
achieved, IV fluids should be switched to 0.45% saline
depending on the calculated volume deficit

11/10/2024 44
 INSULIN THERAPY
o After the initial fluid bolus is complete, an insulin infusion is
begun at a rate of 0.05 to 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)
o An IV bolus should not be used at the start of therapy; it is
unnecessary, may increase the risk of cerebral edema, can
precipitate shock by rapidly decreasing
osmotic pressure, and can exacerbate hypokalemia.

11/10/2024 45
 CONT.
o The insulin can be mixed in one-half isotonic saline and
administered in a syringe infusion pump to control the rate of
insulin administration.
o Within 60 minutes, steady state serum insulin levels are
achieved (100 to 200 microU/ml), which offset insulin resistance,
suppress glucose and ketone production, and stimulate
peripheral glucose and ketone metabolism.

11/10/2024 46
 CONT.
o In most patients, the hyperglycemia corrects before the
ketoacidosis. Normalization of the serum glucose concentration
may not always be accompanied with an improvement in the
metabolic acidosis.
o If the ketoacidosis persists, the patient should be reassessed.
Possible explanations are severe insulin resistance due to
infection, incorrect preparation of the insulin infusion, and
decreased insulin delivery due to adhesion of insulin to tubing.

11/10/2024 47
 CONT.
o When the serum glucose concentration decreases to 250 to
300 mg/dl, the intravenous fluid infusion should be changed to 5
percent dextrose in isotonic NS or LR's solution.
o This allows continued administration of insulin, which is often
necessary to correct the residual ketoacidosis.
o If the serum glucose falls below 250 mg/dl (13.9 mmol/L) before
complete resolution of the ketoacidosis, the concentration of
dextrose in the intravenous solution should be increased to up
to 10 to 12.5 percent.
11/10/2024 48
 CONT.
o Once glucose decreases below 180 mg/dl (10 mmol/L), the
osmotic diuresis
stops and rehydration accelerates without further increase in
the infusion rate.
o Insulin is still needed to control fatty acid release and ketosis
after normal glucose levels are reached. If serum glucose levels
fall below 100 mg/dl.
o Despite infusion of D10 containing IV fluids, the IV insulin rate
can then be decreased from 0.1 units/kg/hr.
11/10/2024 49
 CONT.
o In circumstances where continuous IV administration is not
possible and in patients with uncomplicated DKA, hourly or 2-
hourly SC rapid-acting insulin analog is safe and may be as
effective as IV regular insulin infusion.
o Initial dose SC: 0.3 unit/kg, followed 1 hour later by SC insulin
lispro or aspart at 0.1 unit/kg every hour, or 0.15 to 0.20
units/kg every 2 to 3 hours.
o If blood glucose falls to 250 mg/dl before DKA has resolved,
reduce SC insulin lispro or aspart to 0.05 unit/kg/h to keep BG
≈200 mg/dl until resolution of DKA. 11/10/2024 50
 CONT.
o 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.
o A suggested starting dose is 0.8 to 1 unit per kg per 24-hours;
calculated 24-hour dose is divided by 6 to provide an insulin
dose injected every 4 hours.
o Doses are increased or decreased by 10% to 20% based on the
blood glucose level before the next insulin injection. For
example, if a child weighs 45 kg: 45 × 0.8 = 36 units; starting
dose is 6 units. 11/10/2024 51
11/10/2024 52
 ELECTROLYTE THERAPY
o Both the metabolic shift to a catabolic predominance and the
acidosis move
potassium and phosphate from the cell to the serum.
o The osmotic diuresis, the kaliuretic effect of the
hyperaldosteronism, and the ketonuria then accelerate renal
losses of potassium, phosphate and Sodium.
o With prolonged illness and severe DKA, total body losses can
approach 10-13 meq/kg of sodium, 5- 6 meq/kg of potassium,
and 4-5 meq/kg of phosphate.
11/10/2024 53
11/10/2024 54
 CONT.
o Serum sodium — the initial sodium concentration will depend
on the net sodium and water losses prior to hospitalization, the
degree of hyperglycemia and the degree of lipemia
o Serum potassium — both renal and gastrointestinal losses can
contribute to an often marked degree of potassium depletion in
DKA.
o On the other hand, the combination of insulin deficiency, which
impairs potassium entry into the cells, and hyperosmolality, which
pulls water and potassium out of the cells, tend to raise the serum
potassium
11/10/2024 55
 CONT.
o Optimal therapy varies with the initial serum potassium :-
 if the patient is normokalaemia, potassium replacement should be
given with the start of insulin therapy, as insulin will reduce the serum
potassium.
 If the patient is markedly hypokalemic, potassium replacement should
be started immediately , using an initial potassium of
40 meq/l, concurrent with volume expansion.
 If the patient is hyperkalemic, potassium replacement should be
initiated when the serum potassium falls to normal and after verifying
urine production.
11/10/2024 56
 CONT.
o Metabolic acidosis — insulin and fluid repletion leads to partial
correction of the acidosis seen in DKA.
o Insulin promotes the metabolism of ketoacid anions, resulting in the
generation of bicarbonate, and stops the ongoing production of new
ketoacids.
o Improved tissue perfusion corrects any lactic acidosis that might be
present.
o Ketoacid anions have been called "potential bicarbonate," because
their metabolism following the administration of insulin results in the
generation of bicarbonate and reversal of the acidosis.
11/10/2024 57
 MONITORING
o Treatment of DKA requires close monitoring of the patient's
clinical condition including changes in vital signs, neurologic
status, fluid status, and metabolic state.
o Emphasis should be placed on the hourly evaluation of the
patient as outlined below:
 Monitor blood glucose hourly during the initial 4 to 6 hours of
therapy
 Electrolytes and venous Ph should be initially evaluated hourly
for the first three to four hours and then every two hour. The
frequency of measurement can be reduced to every four to six 58
11/10/2024

hours.
 CONT.
 Clinical parameters including heart rate, respiratory rate, blood
pressure, oxygen saturation, and neurologic status should be
monitored continuously. Monitor for warning signs and
symptoms of cerebral edema.
 Initiate electrocardiographic monitoring in patients with severe
DKA or abnormal serum potassium concentrations.
 Measure and record fluid input and output accurately.

11/10/2024 59
 CONT.
o Here is substantial evidence that bicarbonate therapy should
not be used in DKA:-
 The administration of alkali may slow the rate of recovery of
ketosis.
 The administration of bicarbonate can lead to a post-treatment
metabolic alkalosis after insulin-induced metabolism of ketones
 Bicarbonate therapy may be a risk factor for cerebral edema
 The rapid correction of acidosis with bicarbonate therapy may
result in hypokalemia
11/10/2024 60
 Additional sodium load can further increase the degree of
hyperosmolality
 DIABETIC KETOACIDOSIS PROTOCOL
o Even though DKA can be of variable severity, a common
approach to all cases simplifies the therapeutic regimen and can
be safely used for most children.
o Fluids are best calculated based on weight, not body surface
area (m2 )
o Children with milder DKA recover in 10-20 hr (and need less
total iv fluid before switching to oral intake), whereas those with
more severe DKA may require up to 36 hr with this protocol

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 CONT.
o Any child can be easily transitioned to oral intake and
subcutaneous insulin when DKA has resolved.
o The first subcutaneous injection should be given at an
appropriate interval to allow for absorption prior to stopping
insulin infusion. The onset of rapid-acting insulin (i.e.
insulin lispro ) is approximately 15 minutes, whereas that of
short-acting (regular) insulin is 30 to 60 minutes.

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 CONT.
o Borderline DKA — patients with borderline DKA (venous ph
>7.30, serum bicarbonate >16 meq/L), no neurologic
impairment, and estimated volume deficit less than 3 percent
who are not vomiting may be managed in an ambulatory setting
under the supervision of an experienced medical team.
o However, hospitalization may appropriate for young children
(<5 years of age) because of their sensitivity to insulin as
compared with older children, and because of their increased
risk for cerebral edema.

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 CONT.
o A short-acting insulin ("regular" insulin) can be given
subcutaneously and repeated at three to six hour intervals as
needed. The dose is adjusted depending upon the response.
o Close monitoring of serum electrolytes, glucose, and fluid
balance is required. The patient should be transferred to an
appropriate inpatient setting if there is an inadequate response
or the clinical condition deteriorates.

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 COMPLICATIONS AND MORTALITY
o Reported mortality rates for DKA are consistent in developed
countries, ranging from 0.15 to 0.51 percent cerebral edema
accounts for the majority of deaths
o Other causes include aspiration pneumonia, multiple organ
failure, hypokalemia, hyperkaliemia, hypoglycemia, cardiac
dysrhythmia and pulmonary edema.

11/10/2024 65
 CEREBRAL EDEMA
o 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.
o Symptoms typically emerge during treatment for dka, but may
be present prior to initiation of therapy.
o Clinically significant cerebral edema occurs in approximately 1
percent of episodes of diabetic ketoacidosis in children and has
a mortality rate of 20 to 24 percent.

11/10/2024 66
 CONT.
o PATHOPHYSIOLOGY:- the cause of cerebral edema in DKA is
not fully understood, and the only definite way to prevent it is to
avoid DKA.
o Cerebral edema may be present before treatment has begun,
but more commonly occurs 4 to 12 hours after the initiation of
therapy.
o Thus, therapy may exacerbate but not initiate the pathologic
process(es) leading to cerebral edema.

11/10/2024 67
 CONT.
o Proposed mechanisms :-
 Ischemia/cytotoxic edema
 vasogenic edema
 Osmotic edema as a consequence of fluid therapy

11/10/2024 68
 RISK FACTORS
o Younger children and children with newly diagnosed diabetes
o Failure of the serum sodium to rise as predicted
o The severity of acidosis at presentation
o The use of bicarbonate therapy for correction of the acidosis in
DKA
o Increased blood urea nitrogen at presentation of DKA
o A marked early decrease in serum effective osmolality
o Greater volumes of fluid given in the first 4 hours
o Administration of insulin in the first hour of fluid treatment
11/10/2024 69
 SIGNS AND SYMPTOMS
o The presentation of cerebral edema varies but the onset of
headache is usually the earliest symptom.
o Altered level of consciousness, sustained heart rate
deceleration, or age-inappropriate incontinence are important
early signs of impending neurologic collapse.
o Frequent monitoring at the bedside for early symptoms of
cerebral edema may identify these children sufficiently early for
intervention to prevent brain damage

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11/10/2024 71
 THERAPY
o An essential part of therapy in DKA is careful monitoring for
changes in mental or neurologic status. As soon as cerebral
edema is suspected, treatment should be initiated. Consensus
statement recommends the following :-
Elevation of the head of the bed
The rate of fluid administration should be reduced
 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 11/10/2024 72
 CONT.
o 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
o Intubation may be necessary for the patient with impending
respiratory failure due to severe neurologic compromise
o After treatment for cerebral edema has been started, cranial
imaging may be considered as with any critically ill patient with
encephalopathy or acute focal neurologic deficit
11/10/2024 73
 HYPERKALEMIA
o High serum [K+ ] and the presence of ECG changes require
vigorous treatment.
o The first action in a child with a concerning elevation of plasma
[k+ ] is to stop all sources of additional k+
o if the [k+ ] is >6.5 meq/L, an ECG should be obtained to help
assess the urgency of the situation. Peak T waves are the first
sign of hyperkalemia, followed by a prolonged PR interval, and
when most severe, prolonged QRS complex.
o Life-threatening ventricular arrhythmias may also develop
11/10/2024 74
 CONT.
o The treatment of hyperkalemia has 2 basic goals: (1) to
stabilize the heart to prevent life-threatening arrhythmias and
(2) to remove K+ from the body.
o Calcium stabilizes the cell membrane of heart cells, preventing
arrhythmias; it is given intravenously over a few minutes, and
its action is almost immediate
o Bicarbonate causes potassium to move intracellularly,
lowering the plasma [K+ ]; it is most efficacious in a patient with
a metabolic acidosis.
11/10/2024 75
 CONT.
o Insulin causes k+ to move intracellularly but must be given
with glucose to avoid hypoglycemia. The combination of insulin
and glucose works within 30 min.
o Nebulized albuterol , by stimulation of β1 - adrenergic
receptors, leads to rapid intracellular movement of k+.

11/10/2024 76
 HYPOKALEMIA
o Factors that influence the treatment of hypokalemia include the
K+ level, clinical
symptoms, renal function, the presence of transcellular shifts of
K+ , ongoing
losses, and the patient's ability to tolerate oral K+
o Supplementation is more cautious if renal function is decreased
because of the kidney's limited ability to excrete excessive K+
o The plasma potassium level does not always provide an
accurate estimation of the total body K+ deficit because there
may be shifts of K+ from the ICS to the plasma 11/10/2024 77
 CONT.
o When these problems are corrected, K+ moves into the ICS, so
more K+ supplementation is required to correct the
hypokalemia.
o Potassium chloride is the usual choice for supplementation,
although the presence of concurrent electrolyte abnormalities
may dictate other options.
o Patients with acidosis and hypokalemia can receive potassium
acetate or potassium citrate.

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 DIABETIS AND EDUCATION
o Adherence to therapy & proper dosing.
o Self injection techniques & injection site care.
o Appropriate drug storage.
o Symptoms of hypoglycemia.
o Dietary management, & regular exercise
o Need for regular follow up & hygiene (oral, foot,…)
o Self blood sugar monitoring & interpretation of results.
o Awareness & avoidance of precipitating factors of DKA

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 REFFERNCE
o HARRISON`S PRINCIPLE OF INTERNAL MEDICINE
EDITION 20TH. PAGE 2870-2872
o UPTODATE VOL 20.1
o NELSON TEXTBOOK OF PEDIATRICS, 20TH EDITION,
PAGE 11814-11851
o ISPAD CLINICAL PRACTICE CONSENSUS GUIDELINE
2018: DIABETIC KETOACIDOSIS AND HHS
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