Muhammad aizat

308

C O M P LIC ATIO N S O F
D IA B ETES & D IA B ETIC
K ETO A C ID O S IS (D K A )

CO N TEN TS
Complications of diabetes
Definition of DKA
Pathophysiology
Clinical features
Lab evaluation/criteria
Management
Cerebral edema

CO M PLICATIO N S O F D IABETES
Acute complications
Diabetic ketoacidosis
Hypoglycemia
Blood sugar <60mg/dl
Usually occurs when children unusually active & insulin not

adjusted for increase activity

Increase in counter-reguralatory hormones (adrenaline,
glucagon, cortisol)
Tremors, pallor, tachycardia, sweating
If untreated leads to neuroglycopenia seizures, fainting,
coma
Treatment follows rule of 15, 15g of free sugar
followed by recheck of blood sugar in 15 minutes
If unconscious give glucagon IM (<25kg, 0.3mg. >25kg 1mg)
If no glucagon, IV dextrose given

Intermediate
Lipoatrophy
Limited joint mobility typically in the hands
Growth failure
Mauriac syndrome in patient with poor diabetic

control (hepatomegaly, pale skin, short stature)

Delay in sexual maturation

Hypoglycemic unawareness
Frequent hypoglycemia associated with tight

metabolic control
Due to impaired counter regulatory response

Chronic
Retinopathy
Peripheral neuropathy
Unusual in children and adolescents

Nephropathy
Albuminuria preceded by microalbuminuria
Patient with elevated microalbumin to creatinine ratio

should receive ACE inhibitors to delay progression

Dyslipidemia
Check LDL (if <100mg/dl), recheck in 5 years
Initial therapy decrease saturated fat in diet
Pharmacoogy agent added if LDL>160, risk of CVS disease

Celiac disease
Testing serum IgA, antigliadin antibodies and

transglutaminase antibodies

FO LLO W U P
Assessment of growth, weight and puberty
Physical exam (focus on thyroid, injection

sites, fundus, foot, neuro)

Assessment of blood sugar records (premeals and bedtime)
Educate the patient
Eye exam, fasting serum lipids, TFT , LDL
annually
HbA1c at 3 months interval
Urine microalbumin

D IABETIC KETO ACID O SIS

State
of hyperglycemic, dehydration
(D KA)

and ketotic acidemia

Characterized by hyperglycemia,
acidosis and ketosis

STAG ES
MILD
Blood sugar typically over 250mg/dl
Ketonemia present (ketones +ve at greater than

1:2 dilution)
Serum pH <7.3
Serum bicarbonate <15mEq/l

MODERATE
pH <7.2
Bicarbonate <10mEq/l

SEVERE
pH <7.1
Bicarbonate <5mEq/l

D KA
Can occur as initial presentation of

type 1 DM; 15-70% newly diagnosed

children present with DKA
Overall rate among pediatric patient
25%
Prevalence 36% in children <5yo
16% in patient >14yo
Mortality rate 0.15-0.3%
60-90% due to cerebral edema

 DKA most commonly occur in patient

who are non compliant to insulin

therapy
Seen in patient pump malfunction
Young patient with type 1 DM,
psychological problems complicated by
eating disorders ->20%
Infection can be a precipitating factor

PATH O PH YSIO LO GY
Basic underlying mechanism
1. Insulin deficiency
2. Increase in counter-regulatory hormones
(glucagon, growth hormone, cortisol)
. Will increase glucose production from

glycogenolysis and gluconeogenesis while

limiting glucose utilization
. Results in hyperglycemia & lipolysis
increased FFA production

 Fatty acid oxidation in liver generate

b-hydroxybutyrate & ketone acidosis &

ketosis
Hyperglycemia osmotic diuresis
dehydration & hypovolaemia shock
Dehydration also causes lactic acidosis
increase acidosis
Ketosis & acidosis electrolyte imbalance
Fruity odour & rapid respiration (Kussmaul
breathing)
Acidosis shift of intracellular ions (K&P)
lost in urine

CLIN ICAL FEATU RES

Symptoms
Abdominal pain
Nausea & vomiting
Polyuria
Shortness of breath
Polydipsia

Physical findings
Tachycardia
Dry mucous membrane, reduced skin
turgor, hypotension
Tachypnea, Kussmaul respiration,
respiratory distress
Abdominal tenderness
Lethargy, cerebral edema, coma

LABO RATO RY EVALU ATIO N CRITERIA

Blood glucose >250mg/dl
Blood pH <7.3
Serum bicarbonate <15mmol/dL
Serum potassium normal initially but

declines with therapy

Serum sodium low
Elevated creatinine
Serum ketones positive
B-hydroxybutyrate higher than
acetoacetate

M AN AG EM EN T
Goal of treatment is slow correction

of dehydration and acidosis

To prevent cerebral edema
Principles
1. Fluids & electrolytes
2. Use of bicarbonate
3. Insulin therapy
4. Monitoring

H istory
New onset diabete; Evaluate onset

and duration
Know diabetic
Insulin dose, illness, stress, dietary
Duration
Recent home glucose level
Most recent insulin dose and timing

Physicalexam ination
Vital sign, hydration
CNS status
Sign of acidosis

Laboratory
Bedside blood glucose, urine for

glucose and ketone

HBa1c, lipid profile, insulin
autoantibodies
Blood gas and serum electrolyte 4
hourly
Calcium, magnesium, phosphate 12
hourly
Culture

Fluid and electrolytes (correct dehydration over

24-48 hours)
1. Initial fluid bolus (based on BP & CRT)

10-20ml/kg NS bolus over 1 hour

If hypovolaemic present, repeat NS for another hour

2. Calculate fluids based on 10% dehydration, not

3.
4.
5.
6.

more 4000ml/m2/day.
Infuse 0.45% saline until blood sugar
<300mg/dl.
Dextrose containing fluid (5%) added once
blood glucose fall below 250-300
10% glucose administered when glucose <180
Potassium (20-40mEq/l ) added once urine flow
established & serum K+ <5.5mEq/l

Use of bicarbonate
1. Not used routinely
2. Therapy with sodium bicarbonate considered if pH
not improve & arterial pH remains <7.0 and
bicarbonate <5-10mEq/l
3. Calculate deficit : total deficit= (expected
bicarbonate-actual bicarbicarbonate) x 0.6 x pt
weight in kg
4. Plan half correction of deficit in IV fluid over 24 hour,
by targetting total bicarbonate 25mEq/l
5. Discontinue bicarbonate in IV when >10 and pH
>7.1

Insulin therapy
1. Insulin drip 0.1units/kg/hour. If patient known diabetic &
received insulin SC, start lower dose (0.05U/kg/hr)
2. When blood glucose <300, change IV fluids to 5%
dextrose with 0.45 saline
3. Glucose <180, 10% dextrose with 0.45 saline
4. Glucose <150, reduce insulin drip in decrements of
0.02U/kg/hr
5. Rate of fall of glucose should be 80-100mg/dl/hr or
40mg/dl/hr in severe infection. If no change in 2-3hr,
increase infusion to 0.15U/kg/hr
6. When patient acidotic & ketotic, dont decrease insulin
infusion below 0.05 & dont discontinue until SC insulin
given
7. Monitor blood glucose
8. Continue insulin until pH >7.36 or bicarbonate >20mEq/l

Monitoring
1. Monitor vital signs every hour, neurological
signs every 1-2hr
2. Fluid balance: intake & output hourly
3. Blood sugar, electrolytes pH, bicarbonate:
initially 1-2 hour then every 4 hour
4. Calcium, phosphate and magnesium every 12
hr
5. Also send HbA1c, lipid profile, insulin
autoantibodies
6. Screen for infections with appropriate
cultures, xray

CEREBRAL ED EM A
Complications of DKA
Characterized by headache, bradycardia,

altered neurological status and

desaturation in an otherwise improving
child
Occurs during first 5-15hr of therapy
Rate of fluid administration should be
reduced
IV mannitol (0.25-1g/kg) over 20 min
Hypertonic saline (5-10ml/kg) over 30 min

REFEREN CES
Ghai Essential Pediatrics 8th Edition

by Vinod K Paul and Arvind Bagga