CR-pendy Handoko-Diabetic Ketoacidosis With Cerebral Edema in A Child

INTRODUCTION
Diabetic ketoacidosis (DKA) is a state of emergency caused by absolute

or relative insulin deficiency and accompanied by metabolic disorders. 1
DKA considered pathognomonic in type 1 diabetes mellitus (type
1 diabetes) in children.2-3 Diagnosis DKA obtained approximately 16-80 %
in patients with newly diagnosed type 1 diabetes. In Europe and North
America the figure ranges from 15-67 %, whereas in Indonesia reported
between 33-66 %.1,4
DKA can occur at the time of diagnosis as well as in patients who
have already suffered a long diabetes. DKA repeatedly occurs when
insulin is irregular or because insulin is not given. Patients usually
experience abdominal pain, nausea, vomiting, dehydration and takhipnea.
Kussmaul breathing seen in acidosis and at pH < 6.9 can occur respiratory
depression is accompanied by loss of consciousness and convulsions,
especially in severe cases.5
Timely diagnosis, comprehensive clinical and biochemical
evaluation, and effective management is key to the successful resolution
of DKA. Critical components of the hyperglycemic crises management
include coordinating fluid resuscitation, insulin therapy, and electrolyte
replacement along with the continuous patient monitoring using available
laboratory tools to predict the resolution of the hyperglycemic crisis.
Understanding and prompt awareness of potential of special situations
such as DKA presentation in comatose state, possibility of mixed acid-
base disorders obscuring the diagnosis of DKA, and risk of cerebral
edema during the therapy are important to reduce the risks of
complications without affecting recovery from hyperglycemic crisis.
Cerebral edema is a pathological state in the accumulation of fluid
in the brain tissue, thus increasing the volume of the cerebral volume.
Cerebral edema as a complication of DKA is most serious in children ,
because it is the highest cause of death by a presentation of around 20-90
%. It is common in children with newly diagnosed type 1 diabetes and
rarely occurs in people over the age of 20 years . Children with DKA
1
should always be assessed whether there is a neurological dysfunction to
avoid the occurrence of cerebral edema although the estimated incidence
rates of about 0.5 % -1 %, but the biggest cause of morbidity and mortality
in children.6-8
The following report is a case of diabetic ketoacidosis with cerebral
edema in a child being treated at the department of endokrinology of Prof.
Dr.R.D. Kandou Hospital in Manado.
CASE REPORT
FJM, 14 years 2 months old boy, Christian, Minahasaneese, was admitted
to Prof. Dr. R.D. Kandou Hospital in Manado on April 19th, 2016, with chief
complained loss of consciousness since 6 hour before admitted
accompanied by fast and deep breathing.
PATIENT IDENTITY
Medical record : 44.88.96
Name : FJM
Date of birth : December 3rd, 2002
Place of birth : Manado
Gender : Male
Nationality : Indonesia
Tribe : Minahasanese
Religion : Christian
Address : Malalayang I Timur Lk III
PARENTS IDENTITY
FATHER MOTHER
Name JM PL
Age 38 39
Occupation - Housewife
Education Senior High School Senior High School
2
Religion Christian Christian
Tribe Minahasanese Minahasanese
History of ilness
(Alloanamnesis, provide by his parents)
Patient admitted to hospital at ERIA on April 19th 2016 23:00 pm with chief
complaint loss of consciousness since ± 6 hour before admitted to hospital
accompanied by fast and deep breathing. A history of trauma and seizure
was denied. Vomiting experienced by patient since morning before
admitted to hospital and followed by fast and deep breathing. Vomiting
frequency three times per day with a volume of approximately ¼ to ½ cup
aqua’s cup, contains the remains of food and fluids. A history of vomiting
before was denied. Patient complained headache and looked weak since
one day before admitted to hospital. Patient complained frequent urination
especially at night and drink more than ussualy was experienced by
patient since the first week before admitted to hospital. Normal bowel 1-2
days. One day before admitted to hospital, patients forgot the insulin
injection.
History of prenatal care and birth

Patient was born spontaneously by a doctor at RSUP Prof. Dr. R.D.
Kandou Manado, head presentation, aterm, birth weight was 3900 gram
and birth length was 48 cm. He immediately cried after birth. During
pregnancy the mother’s conduct antenatal care regularly as much as 10
times in RSUP Prof. DR. R.D. Kandou Manado. She got TT immunization
twice and during pregnancy she was in good health.
History of past illness

Patient had been diagnosed with type 1 diabetes since Juny 2015 and
routinely doing general check up.
He had several episodes of cough and cold before.
3
Developmental milestones
Growth and development of patients according to age.
Social smile : 4 months
Turning in prone position : 4 months
Sitting : 6 months
Crawling : 7 months
Standing : 9 months
Calling mama / papa : 7 months
Walking : 13 months
History of Feeding
Breast feeding : birth – 1 year
Formula milk : birth – 1 month
Milk porridge : 4 month -8 month
Soft rice porridge : 6 month – 9 month
Rice : 9 month - now
Immunizations
BCG : once
Polio : 4 times
DPT : 3 times
Measles : once
Hepatitis B : 3 times
Family History
His grandfather (from mother) and grandmother (from father) suffered
diabetic when already elderly
4
Pedigree
No. Name Relation with patient Sex Age

1. MTM Sister F 16 years
Social, Economic and Evironmental Conditions

He is the youngest children in the family, has 1 sister. His father
died Oktober 2015 at 38 years old, while his mother is 39 years old,
graduate from senior high school, a housewife.
They comes from middle social economic class, live in a semi
permanent house, consisted of 2 bedroom, occupied by 2 adults and 2
children. Bathroom is located inside the house. They had electrical source
from the governmental electric company and water supply from well water.
Garbage management by burned. The patient use of government 2nd class
social health insurance.
5
Physical Examination (April 19th, 2016)
General conditions : looked severely ill, GCS E2V2M4
Body weight : 44 kg
Body height : 160 cm
CDC 2000 weight for height
BW/age = 44/52 x 100 % = 84,61 % (normal body weight)
BH/age = 160/164 x 100 % = 97,5 % (normal body height)
BW/BH = 44/48 x 100 % = 91,67 % (good nutrition)
Vital signs : Blood pressure : 100/60 mmHg

Pulse rate : 150 times/minutes
Respiratory rate : 40 times/minutes, Kusmaull
Temperature : 36,6 ° C
Head : Normocephaly, thin black hair, not easily pulled out
Eyes : Conjuntiva was not anemic and sclera was no icteric,
pupil was round, isochors, 3-3 mm, light reflex was
normal, sunken eyes (+)
Ears : Clear meatus acusticus externus, normal ear drums,
No secrets
Nose : There was no secrets, no flare
Mouth : There was no cyanosis, dry mouth mucosa, tonsils
T1/T1
Without inflammatory sign, pharynx without
inflammatory sign
Neck : There was no lymph node enlargement
Chest : Symmetrical respiratory movements,
Subcostal retraction (+)
Heart :
- Inspection : no visualization of ictus cordis
- Palpation : ictus cordis was palpable
- Percussion : left margin : linea midclavicularis sinistra
right margin : linea parasternalis dextra
6
upper margin : 2nd – 3th intercostals
spaces (ICS)
- Auscultation : heart rate 140 times/minutes, regularly, no
murmur
Lungs :
- Inspection : symmetrical respiration movement on the both
side hemithorax, subcostal retractions
- Palpation : vocal fremitus right = left
- Percussion : sonor percussion right = left
- Auscultation : bronchovesicular breath sound, rales -/-,
wheezing -/-
Abdomen : flat, soft, with normal bowel sound, liver and
spleen were not palpable, a decrease in skin turgor,
tympanic percussion
Extremities : warm, no cyanotic, capillary refill time less than 2”,
normal muscle tone, physiological
reflexes normal, no pathological reflexes.
Genitalia : male, no abnormality
Skin : no petechiae, no cyanosis
Laboratory findings
Hb : 18,5 g/dl Sodium : 138 mEq/L
Ht : 48,7% Potassium : 5,2 mEq/L
Leukocyte : 13,600/mm3 Chloride : 99 mEq/L
Thrombocyte : 148.000/mm3 Calcium : 9,49 mg/dl
Ureum : 39 mg/dl Blood glucose : 403 mg/dl
Creatinin : 0,7 mg/dl
AST : 23 U/L
ALT : 23 U/L
7
BGA
pH : 7,156
pCO2 : 14,2
pO2 : 117,8
HCO3 : 5,1
BEb : -23,9
Urinalysis
pH :5
Specific gravity : 1.025
Nitrite :-
Protein : ++
Glucose : ++++
Keton : ++++
Urobilinogen :-
Leukocyte :-
Erythrocyte ` : ++
Working Diagnosis
Diabetic ketoacidosis (E10.11)
Cerebral edema (G93.6)
Treatment
- O2 6 liter/minute by mask
- IVFD NaCl 0,9% 500 ml + 20 mEq KCl (total for 48 hours +
correction for dehydration 9%) = 186-187 ml/hour
- After 2 hours rehydration :
Line I : IVFD NaCl 0,9% 500 ml + 20 mEq KCl (total for 48 hours +
correction for dehydration 9% - insulin) = 134-135 ml/hour
Line II : IVFD NaCl 0,9% 500 ml + insulin 50 IU = 0,1 U/kg/minute =
52 ml/hour
- Ceftriaxone injection 2 x 1 g IV
- Ranitidine injection 2 x 25 mg IV
- Oral stop
- Blood Glucose, vital sign and diuresis / hour
8
- Balance diuresis / 6 hour and 24 hour
- BGA periodically
- Urinalisis / day
- Consult ophthalmology department
- Pro : IVFD Manitol 3 x 110 ml
Nutritional care :
Based on patient’s condition at this moment:
- Oral stop momentarily
Nursing treatment
1. Bed rest, head elevation 30°
2. Vital sign, GCS, blood glucose, and diuresis monitoring
3. Urinalisis / day
4. BGA periodically
5. Patient hygiene
6. Mental support to the patient and family
FOLLOW UP
April 20th, 2016 (2nd day care)
Complaint : loss of consciousness (+), fast and deep breathing
(+)
General conditions : Looked severely ill, GCS E2V2M4
9
Vital sign : Blood pressure : 100/60 mmHg
Pulse : 160 times/minutes
Respiratory rate : 36 times/minutes
Temperature : 36.6 0C
Physical examination
normal, sunken eyes (-)
No secrets
Mouth : There was no cyanosis, dry mouth mucosa (-),
tonsils T1/T1
inflammatory sign
Subcostal retraction (+)
Heart :
spaces (ICS)

murmur
Lungs :
side hemithorax, subcostal retractions
10
wheezing -/-
spleen were not palpable, skin turgor normal,
tympanic percussion
Blood glucose and diuresis

06.00-12.00 = 408 – 251 mg/dl, diuresis 0,5 – 1,13 ml/kgBW/hour
Laboratory findings
Ht : 44,2% Potassium : 6 mEq/L
Leukocyte : 25.600/mm3 Chloride : 100,9 mEq/L
Thrombocyte : 379.000/mm3 Calcium : 8,58 mg/dl
Blood glucose : 385 mg/dl
CRP :<6 HbA1C : 13,4 %
BGA
pH : 7,142 pH : 7,265
pCO2 : 15,1 pCO2 : 14,4
pO2 : 182,2 pO2 : 232,7
HCO3 : 5,2 HCO3 : 6,6
11
BEb : -21,0 BEb : -17,2
Urinalysis
pH :5
Nitrite :-
Protein : +++
Glucose : ++++
Keton : ++++
Urobilinogen :-
Leukocyte :-
Erythrocyte ` :+
Patient refused to consult ophthalmology department
Diagnosis
Treatment
- O2 6 liter/minute by mask
- Line I : IVFD NaCl 0,9% 500 ml + 20 mEq KCl (total for 48 hours +
correction for dehydration 9% - insulin) = 134-135 ml/hour (GDS >
250 mg/dl)
If GDS < 250 mg/dl : fluid changed to NaCl 0,9% 250 ml + D5% 250
ml + 20 mEq KCl
If GDS < 150 mg/dl : fluid changed to NaCl 0,9% 250 ml + D10%
250 ml + 20 mEq KCl
- Line II : IVFD NaCl 0,9% 500 ml + insulin 50 IU = 0,1 U/kg/minute =
52 ml/hour
- IVFD Manitol 3 x 110 ml (1)
- Ceftriaxone injection 2 x 1 g IV (1)
- Ranitidine injection 2 x 25 mg IV (1)
- Nutritional care : Oral stop momentarily
- Blood Glucose, vital sign and diuresis / hour
12
- BGA periodically
- Urinalisis / day
April 21st, 2016 (3rd day care)

Complaint : loss of consciousness (+), fast and deep breathing
(-)
General conditions : Looked severely ill, GCS E3V3M5
Temperature : 36.8 0C
No secrets
tonsils T1/T1
inflammatory sign
Subcostal retraction (-)
Heart :
13
spaces (ICS)
murmur
Lungs :
side hemithorax, subcostal retractions (-)
wheezing -/-
tympanic percussion
Blood glucose and diuresis

06.00-12.00 = 160 – 260 mg/dl, diuresis 1 – 1,13 ml/kgBW/hour
Laboratory findings
Ht : 46,9% Potassium : 4,05 mEq/L
Leukocyte : 10.300/mm3 Chloride : 113,1 mEq/L
Thrombocyte : 268.000/mm3 Blood glucose : 198 mg/dl
Ureum : 67 mg/dl
14
Creatinin : 1,0 mg/dl
BGA
pH : 7,366 pH : 7,416
pCO2 : 20,6 pCO2 : 21,9
pO2 : 119,6 pO2 : 118,0
HCO3 : 12,0 HCO3 : 14,3
BEb : -9,9 BEb : -7,8
Urinalysis
pH :5
Nitrite :-
Protein : +++
Glucose : ++++
Keton : ++++
Urobilinogen :-
Leukocyte :-
Erythrocyte ` :-
Diagnosis
Treatment
- O2 2 liter/minute by nasal canule
- Line I : IVFD NaCl 0,9% 500 ml + 20 mEq KCl (total for 48 hours +
correction for dehydration 9% - insulin) = 160-161 ml/hour (GDS >
250 mg/dl)
15
If GDS < 250 mg/dl : fluid changed to NaCl 0,9% 250 ml + D5% 250
ml + 20 mEq KCl
If GDS < 150 mg/dl : fluid changed to NaCl 0,9% 250 ml + D10%
250 ml + 20 mEq KCl
- Line II : IVFD NaCl 0,9% 500 ml + insulin 50 IU = 0,05 U/kg/minute
= 26 ml/hour
- IVFD Manitol 3 x 110 ml (2)
- Ceftriaxone injection 2 x 1 g IV (2)
- Ranitidine injection 2 x 25 mg IV (2)
- Nutritional care : Oral stop momentarily
- Blood glucose, vital sign and diuresis / hour
- BGA periodically
- Urinalisis / day
April 22nd, 2016 (4th day care)

Complaint : loss of consciousness (-), fast and deep breathing
(-), vomiting (-)
General conditions : Looked ill, GCS E4V5M6
Temperature : 36,3 0C
No secrets
tonsils T1/T1
16
inflammatory sign
Heart :
spaces (ICS)
murmur
Lungs :
wheezing -/-
tympanic percussion
Laboratory findings
17
BGA
pH : 7,419
pCO2 : 26,3
pO2 : 146,2
HCO3 : 16,8
BEb : -7,6
Urinalysis
pH :7
Nitrite :-
Protein :+
Glucose : ++++
Keton : +++
Urobilinogen :-
Leukocyte :-
Erythrocyte ` :-
Diagnosis
Post diabetic ketoacidosis (E10.11)
Treatment
- O2 1 liter/minute by nasal kanul (if needed)
- Aff IVFD  INT
- Ceftriaxone injection 2 x 1 g IV (3) / INT
- Ranitidine injection 2 x 25 mg IV (3) / INT
- Diuresis / day : 1,64 ml/kgBW/hour
- Urinalisis / day
- Insulin basal bolus
Bolus (Novorapid) Breakfast =8U
Morning snack =4U
Lunch = 12 U
Afternoon snack =4U
Dinner =8U
18
Evening snack =4U
Basal (Levemir) = 38 U
Correction if blood glucose ≥ 300 mg/dl
( Correction dose = blood glucose – 200 / 23 )
- Nutritional care :
1. Nutritional assessment : good nutritional status based on CDC 2000
growth charts
2. Nutritional requirement : based on Recommended Daily Allowance
(RDA)
Ideal body weight : 52 kg
Calorie needed : 2860 kkal/day (55 kkal/kgBW/day)
Carbohydrate needed : 1430 kkal/day (50%)
Protein needed : 572 kkal/day = 143 g (20%)
Fat needed : 858 kkal/day = 85 g (30%)
Fluid needed : 3640-4420 mL (70-85 mL/kgBW)
3. Adminitration route
Oral
4. Food
- Breakfast : 1 cup rice + ¾ piece of medium chicken + 2 pieces of
Tofu + 3 tbs sauted vegetables
- Morning snack : 3 biskuit crackers / 2 red apples / 2 slice bread
- Lunch : 1 cup rice + 1 egg + 4 pieces tempe + 4 tbs sauted
vegetables
- Afternoon snack : 3 biskuit crackers / 2 red apples / 2 slice bread
- Dinner : 2 ½ potatoes + ½ fish + 1 ½ pieces of tofu + 3 tbs sauted
vegetables
- Evening snack : 3 biskuit crackers / 2 red apples / 2 slice bread
5. Monitoring and evaluation : every 15 minutes before ating, check blood
glucose and insulin is given based on blood glucose result
19
April 23 rd – 24 th , 2016 (5 th – 6th day care)
(-), vomiting (-), intake (+)
No secrets
tonsils T1/T1
inflammatory sign
Heart :
spaces (ICS)
20
murmur
Lungs :
wheezing -/-
tympanic percussion
Laboratory findings
April, 23rd 2016 Blood glucose : 141 mg/dl
April, 24th 2016 Blood glucose : 128 mg/dl
Urinalysis
April, 23rd 2016
pH :7
Nitrite :-
Protein :+
Glucose : ++++
Keton : ++
Urobilinogen :-
Leukocyte :-
Erythrocyte ` :-
21
April, 24th 2016
pH :7
Nitrite :-
Protein :-
Glucose : ++++
Keton :-
Urobilinogen :-
Leukocyte :-
Erythrocyte ` :-
Diagnosis
Treatment
- Urinalisis / day
- Move to endokrinology unit
Morning snack =4U
Lunch = 12 U
Afternoon snack =4U
Dinner =8U
Evening snack =4U

22
Adminitration route : oral
vegetables
vegetables
Every 15 minutes before eating, check blood glucose and insulin is
given based on blood glucose result
April 25 th , 2016 (7 th day care)

No secrets
23
tonsils T1/T1
inflammatory sign
Heart :
spaces (ICS)
murmur
Lungs :
wheezing -/-
tympanic percussion
24
Laboratory findings
Urinalysis
April, 25rd 2016
pH :7
Nitrite :-
Protein :-
Glucose : ++
Keton :-
Urobilinogen :-
Leukocyte :-
Erythrocyte ` :-
Diagnosis
Treatment
- Urinalisis / day
Morning snack =4U
Lunch = 12 U
Afternoon snack =4U
Dinner =8U
Evening snack =4U
25
Adminitration route : oral
vegetables
vegetables
Every 15 minutes before eating, check blood glucose and insulin is
given based on blood glucose result
April 26 th , 2016 (8th day care)

No secrets
26
tonsils T1/T1
inflammatory sign
Heart :
spaces (ICS)
murmur
Lungs :
wheezing -/-
tympanic percussion
27
Laaboratory finding
Urinalysis
April, 26th 2016
pH :7
Nitrite :-
Protein :-
Glucose : +++
Keton :-
Urobilinogen :-
Leukocyte :-
Erythrocyte ` :-
Diagnosis
Treatment
Morning snack =4U
Lunch = 12 U
Afternoon snack =4U
Dinner =8U
Evening snack =4U
- Discharged from hospital
28
Prognosis
Ad vitam : bonam
Ad functionam : bonam
Ad sanationam : dubia ad bonam
DISCUSSION
Diabetic ketoacidosis ( DKA ) still plays a role in causing morbidity

and mortality in children. DKA is a state of emergency due to a lack of
insulin in absolute and relative accompanied by increased counter
-regulatory hormones.6,9,10 DKA is the result of a state of emergency and
absolute insulin deficiency or relative and metabolism disorders
accompanied protein, carbohydrate and fat that is characterized by
hyperglycemia, osmotic diuresis, dehydration hypertonic and
ketoasidosis.1
Based on research in Brazil in 2010, DKA occurred about 15-67
% in patients with type 1 diabetes especially in children aged under 5
years and caused the deaths of approximately 50 % in diabetic patients up
to the age of 24 years. The death rate reported to be less than 5 % in
developed countries but in developing countries the death rate is still high
enough that DKA 13.2 % and about 0.15 % - 5 % caused by cerebral
edema.13
In the years 2004-2006 in the Child Health Department - RSCM
Jakarta found 46 cases type 1 diabetes treated as DKA with a mortality
rate of 21.7 %, while in Manado based on epidemiological data that the
29
prevalence of diabetes mellitus in children up to the age of 15 years at 6.1
% and DKA cases estimated to be about 2-3 cases every year. 7
Hyperglycemia will cause osmotic diuresis and this can lead to
dehydration and loss of minerals and electrolytes (Na +, K+, Ca2+, Mg2+, Cl-
and PO4-). Renal threshold value on blood glucose levels (± 200 mg/dL)
and ketones will be exceeded, resulting in excretion of glucose by the
kidney, which reached 200 g/day and urine ketones which reached ± 20-
30 g/day, with a total of 2000 ± urine osmolality mOsm. Osmotic effect of
glucosuria causes disruption and H2O NaCl reabsorption in the proximal
tubule and loop of Henle.12,13
The mechanism of lipolysis in increasing the ratio of insulin
glukagon- is through the activation of "hormone-sensitive lipase" in the fat
tissue. Increased lipase activity in fat tissue caused a breakdown of
triglycerides into glycerol and free fatty acids. Glycerol is the precursor of
gluconeogenesis in the liver tissue, while the free fatty acid oxidation in the
liver after suffering through the stimulation of glucagon is converted into
ketones consisting of acetoacetate, β-hydroxybutyrate and acetone. Β-
hydroxybutyrate and acetoacetate is a strong acid that can cause acidosis
metabolik.11,14
About 20 % of patients newly identified DKA suffering from
diabetes for the first time . In patients who are known to suffer DKA before
diabetes, 80 % identifiable precipitating factors, while 20 % more unknown
factors originators.11,13
Criteria DKA are as follows: 1) hyperglycemia (blood glucose ≥
11.1 mmol/L or 200 mg/dL, 2) acidosis (venous pH <7.3 and or
bicarbonate <15 mmol/L), and 3) ketosis (find ketones in the blood, urine,
or both). DKA can be further divided into mild (7,20- 7,29 pH, bicarbonate
10-14), medium (pH 7,10- 7,19, bicarbonate 5-9), and severe (pH <7.10,
bicarbonate <5).15
DKA in this case is made from the history, physical examination
and laboratorium. DKA clinical manifestations vary from mild to severe that
can be accompanied by loss of consciousness and this would complicate
30
early diagnosis DKA. Diagnosis should be suspected when there is a
complaint of abdominal pain, vomiting or malaise. In this patient, obtained
complaints of vomiting since morning before admitted to hospital. There is
history of polidipsi, polyuria, nocturia, eneuresis, and for the new diabetes,
found weight loss in recent times. In this patient complained frequent
urination especially at night. Other symptoms are nausea, dehydration,
shortness, vomiting without diarrhea. In this patients, shortness of breath
since 6 hour before admitted to hospital. Decreased consciousness and
seizures occur in severe cases.6,16 In this patient there is a loss of
consciousness since 6 hour before admitted to hospital.
Clinically, physical examination of the DKA will find their
dehydration which can reach 10% of the body weight, Kussmaul
breathing, and progressive loss of consciousness. Kussmaul breathing
looked for their acidosis, when pH <6.9 can occur depression of breath. 17
In this patient obtained their loss of consciousness (GCS E2M4V2), a sign
of severe dehydration sunken eyes, dry mouth mucosa and decrease in
skin turgor and found a Kussmaul breathing. Results of laboratory tests
found that hyperglycemia their blood glucose level 403 mg/dL. In this
patient examination blood glucose by stick or through the venous blood.
According to the ADA recommendations, which are used for the diagnosis
of diabetes is blood glucose measured levels of venous blood. In
urinalysis obtained ketonuria (++++). Examination of blood gas analysis
obtained 7.156 pH and HCO3- 5,1, thus including in the case of medium
DKA.
Diabetes mellitus can be diagnosed if there is one of the following
criteria, fasting blood glucose levels ≥ 126 mg/dL, there is clinical
symptoms of polyuria, polydipsia, polyphagia, and weight loss and blood
glucose levels > 200 mg/dL, in patients who are asymptomatic blood
glucose levels are found 200 mg/dL or fasting blood glucose levels are
higher than normal with impaired glucose tolerance tests on more than
one examination.1 Blood glucose measurement in this patient obtained
403 mg/dL.
31
In addition to the diagnostic criteria for diabetes above, also
known as HbA1c measurement has been recommended by the American
Diabetes Association (ADA) as a diagnostic and screening tool for
diabetes. One of the advantages in the measurement of HbA1c is comfort
in the examination is not the necessity of fasting before the examination.
Levels of HbA1c> 6.5% on two different occasions diagnosed diabetes
mellitus. In this patients with HbA1c levels was obtained 13,4%.
C - peptide can help differentiate type 1 with type 2 diabetes .
Normally levels of C - peptide normal or elevated in type 2 diabetes and
found decreased in type 1 diabetes. 17 In this patient from examination
approximately 1 year ago obtained decreased levels of C- peptide is 0.60
ng/mL. According to the literature, C-peptide < 1.51 ng/mL has a positive
predicitive value ( PPV ) 96 % in diagnosing type 1. 18
DKA management is complex and must be careful. Improper in
handling DKA can result in under or overhydration, hypoglycemia,
hypokalemia, hypernatremia and cerebral edema. Interest therapies
include correcting dehydration and acidosis, eliminating ketosis, restores
blood sugar to almost normal levels, prevent complications of therapy and
identify and provide a trigger management of DKA. 19,20
Supportive treatment start to do is to free the airway, oxygen
delivery, intravenous fluids, catheters urine, especially in patients who are
not aware/severe ill and infants/young children, cardiac monitoring (ECG
continuous) to determine the existence of hyper/hypokalemia, and patients
is fasted and can be given antibiotics if discovered infection evidence. 13
This patient was administered with severe dehydration because of the loss
of consciousness, accompanied sunken eyes, dry mouth mucosa and a
decrease skin turgor. Early management is given to this patient was to free
the airway to ensure an open airway and giving oxygen mask, intravenous
fluids to overcome dehydration, urinary catheters, cardiac monitoring and
antibiotics.
The main priority in the management of DKA is fluid therapy. 19 Van
Zyl21 in his research indicates that during the first 4 hours, more than 80%
32
reduction in blood sugar levels caused by rehydration. The choice of
therapy fluid used for initial resuscitation at DKA has been widely studied,
but there are advantages and disadvantages of using each of these fluids.
But the physiological fluid (0.9% NaCl) is a choice as initial therapy for the
resuscitation fluid other than isotonic fluids such as Ringer Lactate (RL). In
DKA patients, there is shortage of total potassium in the body. Therapy to
replace potassium adjusted with potassium concentrations in serum can
be started simultaneously with the start of resuscitation fluids or after
resuscitation fluids and in conjunction with insulin therapy. Potassium is
given 20-40 mEq/L. Speed potassium administration should not exceed 40
mEq/h or 0.3 mEq/kg/hour. Although there are a total deficiency of
potassium in the body, mild to moderate hyperkalemia often happens. This
occurs due to the displacement of intracellular to extracellular potassium
due to acidosis, insulin deficiency and hypertonicity that insulin therapy,
correction of acidosis and fluid volume expansion will make serum
potassium concentrations lower. A method to calculate fluid needs in the
management of DKA is a maintenance dose of 48 hours plus a fluid deficit.
In this patient given IVFD 500 ml of 0.9% NaCl + 20 mEq KCl as initial
resuscitation fluid drops in accordance with a maintenance requirement of
48 hours plus a fluid deficit of 9%.
Besides fluids and potassium, insulin is also a major component in
the therapeutic management of DKA . The use of insulin will make levels
of the hormone glucagon lower, thereby suppressing the production of
ketone bodies in the liver, the release of free fatty acids from adipose
tissue, the release of amino acids from muscle tissue and increasing the
utilization of glucose. Method with using low-dose insulin drip is
recommended because it is easier to control the dose of insulin, lowering
blood glucose levels more slowly, the insulin effect quickly disappears, the
entry of potassium into the intracellular slower and the occurrence of
complications such as hypoglycemia and hypokalemia decrease. 5 This
patient was given insulin therapy that began 2 hours after initial
resuscitation therapy.
33
Chua et all22 conducted a systematic review to look at the
usefulness and risks of bicarbonate in the treatment of severe acidemia
emergency happens to DKA. Showed that the use of bicarbonate is not
recommended, because the gains were limited and the risks are high.
All patients DKA should get a comprehensive laboratory evaluation
included a complete blood laboratory including electrolytes and blood gas
analysis. Fluids and urine output should be monitored carefully and
recorded every hour.23,24 In this patient, complete blood count was checked
and diuresis was monitored hourly.
Increased intracranial pressure is asymptomatic during therapy
DKA has been known for more than 25 years . The reduced size of the
lateral ventricles significantly, can be found in 9 of 11 patients during
therapy DKA. However, in another study, nine children with DKA were
compared before and after treatment can be concluded that brain swelling
can usually be found on DKA even before treatment begins. Symptomatic
cerebral edema is common in pediatric patients and more frequently in
first onset diabetes.25
Cerebral edema is one of important complication associated DKA
with high mortality rates of about 20-90%. In patients who recovery from
cerebral edema around 20-40% will leave neurological deficits include
motor deficits, visual disturbances, seizures, learning disabilities, speech
disorders. In the clinic, cerebral edema occurs in about 1% of the episodes
DKA.26,27
The incidence of cerebral edema relatively constant on a number
of the countries studied: USA 0.87%, Canada 0.46%, 0.68% English.
Nevertheless, a number of the population did not experience a significant
increase in morbidity and mortality after the incident DKA and edema
serebri.26
From a population study in Canada found that the incidence of
cerebral edema ranged in 5.1 per 1000 cases of DKA (13 episodes from
1960 episode of DKA).28 Edge et all27 reported their frequency of cerebral
edema was higher in newly type 1 diabetes diagnosed (11.9 per 1,000
34
cases) compared with children who had been previously diagnosed
diabetes (3.8 per 1000 cases).
The risk factors of cerebral edema at DKA has been widely
studied, but still unclear relation to the occurrence of ketoacidosis
diabetik.27 In a study conducted by Nicole et all 25, in some hospitals in the
UK found that children with diabetic ketoacidosis has a concentration of
serum urea nitrogen were high and found to have severe hipokapnea have
a higher risk of the occurrence of cerebral edema. In this study also found
that there are several other risk factors, such as younger age, diabetes
mellitus who are newly diagnosed, and administration of fluid too fast, high
glucose levels, low levels of sodium and bicarbonate, the long duration of
symptoms, and the low partial pressure of carbon dioxide is said to be
associated with the occurrence of cerebral edema in children with DKA.
The occurrence of cerebral edema in diabetic ketoacidosis
distinguished by two mechanisms of pathogenesis or a combination of
both, 1) damage to the endothelium of blood-brain barrier which causes
cerebral edema (vasogenic edema) or 2) is derived from the swelling of
astrocytes as a result of the changing balance of intracellular osmotic or
dysfunction cellular membrane (cytotoxic edema).27-30
1. Vasogenic edema
- Hypoxia-induced breakdown of the blood brain barrier. Acidosis and
dehydration causing decreased perfusion CNS and induce hypoxia will
eventually cause damage to the blood brain barrier. With the background
of the minor damage to the blood brain barrier, then immediately after
rehydration and plasma osmolarity decreases, will occur transfer of water
from the low plasma osmolarity to high plasma osmolarity in interstitial
fluid in the brain, which ultimately will continue on increasing the
intracranial pressure.
- Saline bolus during initial treatment will increase in hydrostatic pressures
in capillary and forces the water in and outinto interstitial faster.
2. Cytotoxic edema
35
- Osmolaritas formaation in brain cells. During periods of prolonged
hyperglycemia, before being given treatment for diaabetes mellitus and
DKA, plasma osmolarity and instertisial will increase. The osmolarity of the
cells will continue to increase and will form idiogenic osmoles currently
known as molecules, such as taurine and myoinositol. When therapy
intravenous fluids is started, hypotonic saline will be compared with the
patient's plasma osmolarity. Plasma osmolarity sudden decrease, while
because of the slow movement of the molecules so the intracellular
osmolality will increase, which will force water to move from a lower
osmolarity (plasma) to a place with high osmolarity (astrocytes).
- Activation of Na+ - H- exchange in the brain caused by insulin.
Movement of Na+ entry into the cell and H+ moved out of the cell, which is
normally in the brain in an inactive form and movement of the ions
depends directly on the concentration of each. However, a bolus of insulin
can activate the movement of ions. During acidosis intracellular
concentration of high H+ ions will cause the movement of H+ ions out from
the cell and Na+ entry into the cell. H+ ions which initially binds to protein
and does not contribute, enter the cell. The converse of Na+ ions moving
into the cell and increase the osmolarity. This will result in increased
intracellular osmotic pressure that causes cell swelling.
The diagnosis of cerebral edema can use clinical findings and
neurologic status as follows :
Diagnostic criteria :
- motor and verbal response abnormally to pain stimuli
- dekortisasi and decerebrate posture
- cranial nerve weakness (especially III, IV, V)
- abnormal breathing pattern (grunting, takipnea, Cheyne-Stokes,
apnea)
Major criteria :
- decreased or altered consciousness
36
- deceleration of the heart rhythm (less than 20 beats per minute)
that does not increase with the improvement of intravascular
volume or state of consciousness
- incontinence that is not in accordance with age
Minor criteria
- vomiting
- headache
- lethargy or not easily awakened
- diastole pressure > 90 mmHg
- age < 5 years old
One diagnostic criteria or two major criteria or one major criteria and two
minor criteria has sensitivity 92 % and false positive value 4 %. 1,28 In this
patient, edema cerebri was diagnosed from one diagnostic criteria
(abnormal breathing pattern) or one major criteria (decreased or altered
consciousness) and three minor criteria (vomiting, headache and
lethargy).
Therapy was given to children with cerebral edema in diabetic
ketoacidosis : 1,28,30,31
1. Lowering the speed of fluid administration (reduced one-third
2. Given mannitol intravenously at a dose of 1-2 g/kgBW for 20 minutes
3. Given hypertonic saline (3 %) of 5-10 ml/kgBW for 30 minutes as an
alternative when there is no mannitol
4. Adjust the position of the bed so that the head is higher
5. Brain CT scan if posibble
In this patient we gave mannitol intravenously 3 x 110 ml.
In this patient discovered severe dehydration with cerebral
edema, but without neurological deficit. In this patient also discovered
moderate acidosis, normal electrolyte levels and found no systolic
hypotension. So the prognosis ad vitam and ad functionam of this patient
is bonam. Prognosis ad sanationam patient also depends on the
compliance of patient using insulin and a healthy way of life of the patient
37
to avoid infection. So the prognosis ad sanationam of patient is dubia ad
bonam.
Education to patient and his familiy play an important role. Patient
education should include information about how to adjust your insulin
dosage during illness and how to monitor blood glucose levels and
ketones, as well as information about the importance of adherence to
therapy. Measurement of blood glucose levels portable can be done by
patient hisself at home or school. It is known as self-monitoring of blood
glucose (SMBG). The ADA recommend SMBG ≥ 3 times per day for all
patients with diabetes mellitus with multiple insulin injections. 32 In this
patient also applied SMBG. During his stay in hospital the patient was
doing SMBG with physician monitoring. Patient has been educated to
keep doing SMBG at home after outpatient.
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ATTACHMENTS
Patient’s Photo
41
42
43
Nutritional Status
FJM
BW/age = 44/52 x 100 % = 84,61 %
BH/age = 160/164 x 100 % = 97,5 %
BW/BH = 44/48 x 100 % = 91,67 %
Good nutrition
44

CR-pendy Handoko-Diabetic Ketoacidosis With Cerebral Edema in A Child

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CR-pendy Handoko-Diabetic Ketoacidosis With Cerebral Edema in A Child

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INTRODUCTION

Diabetic ketoacidosis (DKA) is a state of emergency caused by absolute

History of prenatal care and birth

History of past illness

No. Name Relation with patient Sex Age

Social, Economic and Evironmental Conditions

Vital signs : Blood pressure : 100/60 mmHg

- Auscultation : heart rate 160 times/minutes, regularly, no

Blood glucose and diuresis

Patient refused to consult ophthalmology department

April 21st, 2016 (3rd day care)

Blood glucose and diuresis

April 22nd, 2016 (4th day care)

Correction if blood glucose ≥ 300 mg/dl

April 25 th , 2016 (7 th day care)

April 26 th , 2016 (8th day care)

Diabetic ketoacidosis ( DKA ) still plays a role in causing morbidity

1. Rustama DS, Subardja D, Oentario MC, Yati NP, Satriono,

BW/age = 44/52 x 100 % = 84,61 %

BH/age = 160/164 x 100 % = 97,5 %

BW/BH = 44/48 x 100 % = 91,67 %

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