Diabetes Mellitus and

diabetic ketoacidosis
Dr. Abdulfetah (MD)
November,2023

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 Introduction
Incidence
Classification
Risk factor
Pathogenesis
u t
Clinical features
O ne
L i and Dx
lx
Management
Complication
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Diabetes mellitus (DM) is a common, chronic,
metabolic disease characterized by
hyperglycemia as a cardinal biochemical
feature.

 The major forms of diabetes are differentiated

by insulin deficiency vs insulin resistance

Type 1 diabetes mellitus (T1DM) results from

deficiency of insulin secretion because of
pancreatic β-cell damage.
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Type 2 diabetes mellitus (T2DM) is a consequence
of insulin resistance occurring at the level of
skeletal muscle, liver, and adipose tissue, with
various degrees of β-cell impairment.

T1DM is the most common endocrine-

metabolic disorder of childhood and
adolescence, with important consequences for
physical and emotional development.

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 Diagnostic
criterias:
Diabetes Mellitus
 Symptoms of DM plus random plasma glucose
≥200mg/dL (11.1mmol/L) Or

 Fasting plasma glucose ≥126mg/dL (7.0mmol/L)

 2-hr plasma glucose during the OGTT ≥200mg/dL

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 Complication of DM
EARLY COMPLICATIONS
Diabetic Ketoacidosis
Hyperosmolar diabetic coma

LONG -TERM COMPLICATIONS:-divided into 3 major categories:

Microvascular complications, specifically, retinopathy and nephropathy;
 Macrovascular complications, particularly accelerated coronary artery
disease, cerebrovascular disease, and peripheral vascular disease; and
 Neuropathies, both peripheral and autonomic, affecting a variety of
organs and systems.

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 DKA
DKA is an acute complication of Diabetes mellitus due to insulin
deficiency or ineffectiveness. The diagnosis is clinical and
biochemical.
Classification of DKA: is classified based on the clinical
presentation, PH and bicarbonate
Clinically it is classified as
Mild:- alert but fatigued and no Kussmaul respirations
Moderate :-oriented but sleepy and has Kussmaul respirations
Severe :- has Kussmaul breathing or depressed respiration with
coma
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Biochemical criteria to diagnose DKA are:
Blood glucose >200mg/dl
Urine ketone.

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 Incidence
• DKA occurs in 20-40% of children as initial presentation of
new-onset diabetes.
• It can also occur in children with known diabetes who omit
insulin doses or who do not successfully manage an
intercurrent illness
• DKA and its complications are the most common cause of
hospitalization, mortality, and morbidity in children with
established type 1 diabetes mellitus.

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Classification…

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 Risk factor
Factors associated with increased risk for having DKA
at presentation are
younger age (<5 years)
Lower income and parental education
Infections
Acute stress
lower body mass index, and delayed
treatment.

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Clinical features and
diagnosis of DKA in
children

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• The clinical manifestations of DKA are related to the degree of
hyperosmolality, volume depletion, and acidosis.
Symptoms
• Nausea/vomiting
• Thirst / polyuria ( worsening poly symptoms )
• Abdominal pain
• Shortness of breath
Physical Findings
• Tachycardia
• Dehydration/hypotension
• Acetone( "fruity") odor
• Tachypnea/Kussmaul respirations/respiratory distress
• Abdominal tenderness (may resemble acute pancreatitis or
surgical abdomen)
• Lethargy/obtundation/cerebral edema/possibly coma
The biochemical criteria for the diagnosis of
DKA are
Hyperglycemia, blood glucose >11 mmol/L
(200mg/dL)
Metabolic acidosis, defined as Venous pH <7.3
or bicarbonate <15 mmol/L
Ketonemia and ketonuria
These abnormalities are accompanied by
hyperketosis (concentration of total ketone bodies
>5 mmol/L) and hyperosmolality

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 Investigatio
n for glucose
Serum testing
blood gases and hematocrit
Creatinine
blood urea nitrogen
Serum electrolytes:- Sodium, Potassium, Calcium,
Phosphorus and Chloride
Direct measurement of beta-hydroxybutyrate
in the blood should also be performed if possible

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Management of
DKA

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Principles of management of DKA: include as follows
1.Resuscitation ( ABCD ),
2.Potassium replacement therapy,
3.Insulin therapy,
4.Monitoring, Treatment of precipitating factors and
5.Treatment of complications (eg cerebral edema).
6. Check for shock and if the child is in shock give 20ml/kg as
fast as possible

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 Resuscitation
 Patients with DKA have a deficit in extracellular fluid
volume that usually is in the range 5–10%
 Clinical estimates of the volume deficit are subjective
and inaccurate therefore, in moderate DKA use 5–7%
and in severe DKA 7–10% dehydration

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 Initial volume expansion

 Volume expansion in moderate to severe DKA is

usually begun with an infusion of 10 -
20 mL/kg over one hour and may be repeated if
clinical improvement is not quickly seen.

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Subsequent fluid
administration
 Once the child is hemodynamically stable,
subsequent volume expansion should be given more
slowly.
• Fluid volume = deficit + maintenance
• Deficit= 85ml/kg (8.5% loss)
• Maintenance (24 hr) = 100 mL/kg (for the first 10 kg) + 50
mL/kg (for the second 10 kg) + 25 mL/kg (for all remaining
kg)

Total fluid rate= Deficit+2(Maintenance)-Bolus

48hr 22
 Insulin therapy
• Dose:- 0.1 unit/kg/hour (If there is perfuser)
• Route of administration IV
• After the initial fluid bolus is complete, an insulin
infusion is begun at a rate of 0.1 unit/kg per hour.
• Give insulin every 6 hours (0.5 iu/kg) Subcutanously except the first dose
which should be given ½ IM and ½ IV (If there is no perfuser)
• Switch to BID SC insulin when acidosis resolved

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 Local management of insulin
• In circumstances where continuous IV administration is
not possible, SC or IM administration of a short- or
rapid-acting insulin analog is safe and may be as
effective as IV regular insulin infusion.
• Initial dose half SC & half IM:- 1IU/kg, followed by
0.5 IU/kg SC
• Every 6 hour until patient is out of DKA
• If blood glucose falls to<14 mmol/L (250 mg/dL) before
DKA has resolved, (pH still<7.30), add 5% glucose and
continue with insulin as above.
• Aim to keep blood glucose at about 11 mmol/L (200
mg/dL) until resolution of DKA.
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Electrolyte replacement

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 Potassium replacement
• Children with DKA suffer total body potassium deficits
of the order of 3 to 6 mmol/kg
• The major loss of potassium is from the intracellular
pool.
• Intracellular potassium is depleted because of
transcellular shifts of this ion caused by hypertonicity and
glycogenolysis and proteolysis secondary to insulin
deficiency cause potassium efflux from cells.
• Potassium is lost from the body from vomiting and as a
consequence of osmotic diuresis.
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• If the patient is hypokalemic, start potassium
replacement at the time of initial volume
expansion and before starting insulin therapy.
• If immediate serum potassium measurements
are unavailable, an ECG may help to determine
whether the child has hyper- or hypokalemia.
Flattening of the T wave, widening of the QT
interval, and the appearance of U waves
indicate hypokalemia.
Tall, peaked, symmetrical, T waves and
shortening of the QT interval are signs of
hyperkalemia.
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• If no ECG, Adequate URINE OUT OUP
• The starting potassium concentration in the
infusion rate should be 40 meq/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 meq/L should be
used

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Monitorin
g

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• During management of DKA, the child needs to be carefully
monitored as follows:

• Record hourly: heart rate, blood pressure, respiratory rate, level of

consciousness, RBS
• Monitor urine ketones in every sample of urine passed
• Record fluid intake, insulin therapy and urine output
• Repeat blood urea and electrolytes every 2-4 hours
• Measure blood ketones (β-hydroxybutyrate) if possible
 Example of DKA flow sheet
Date Time BP PR Temp RBS Urine Urine Neurologic Insulin Fluid Fluid
glucose ketone status (GCS) dose input out put

DKA FLOW SHEET

• Monitor for warning signs and symptoms of cerebral
edema including
• headache,
• inappropriate decrease in HR,
• recurrence of vomiting,
• changes in neurologic status,
• rising BP, and
• decreased oxygen saturation.
Complications of therapy

• Inadequate rehydration
• Hypoglycemia
• Hypokalemia
• Hyperchloremic acidosis
• Cerebral edema
Complications and
mortality of DKA
• Mortality rates for DKA are consistent in developed
countries, ranging from 0.15 to 0.51 percent in national
population studies in Canada, the United Kingdom, and
the United States.

• Cause of death in DKA

Cerebral edema (60 to 90 percent of deaths).
Aspiration pneumonia,
Multiple organ failure,
Gastric perforation, and traumatic hydrothorax.
 Cerebral edema
• Usually 4 to 12 h after initiation of therapy
• Risk of cerebral edema increased in:
Younger children
Newly diagnosed with diabetes
Initial presentation with severe acidosis or dehydration
Early bolus adminstration of insulin and high volumes
of fluid
• Signs and symptoms of cerebral edema include
• Sudden deterioration in mental status,
• Severe headache,
• Sudden drop in heart rate not attributed to rehydration,
• Hypertension,
• Cranial nerve dysfunction, and
• Incontinence.
• If cerebral edema is suspected, treatment should be
initiated immediately.
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 20 minutes
and repeat if there is no initial response in 30
minutes to 2 hours.
• Hypertonic saline (3%), 5–10 mL/kg over 30
minutes, may be an alternative to mannitol or a
second line of therapy if there is no initial response
to mannitol. 38
Treatment
• Better prevented than treated.
• Reduce the rate of fluid administration by 1/3
• Mannitol 0.25 to 1.0 g/kg IV over 20 minutes.
• 3% saline (5 to 10 mL/kg over 30 minutes).
• Intubation and mechanical ventilation.
• Head elevation.
References
 Nelson Textbook of Pediatrics – 20E
ISPAD_Guidelines_2009_DKA
UpToDate 21.2