PREFACE

Diabetes Mellitus is a metabolit disease causing trouble at carbohydrate

metabolism, protein and fat as effect of lacking of insulin. Diabetes Mellitus can

attack all age. In indonesia in this time diabetes mellitus disease not yet occupied

especial priority scale of health service(1).

There are two acute complication form from diabetes mellitus that is

hyperglycemia and hipoglykemia. Hyperglycemia happened at ketoacidosis (DKA),

hyperosmolar non ketotic (HONK) and laktat acidosis(1).

Diabetic ketoacidosis (DKA) is trias from hyperglycemia, acidosis and

ketonemia. DKA is the leading cause of morbidity and mortality in children with type

1 diabetes mellitus (TIDM). Mortality is predominantly related to the occurrence of

cerebral oedema; only a minority of deaths in DKA are attributed to other causes(1,2).

There is agreement that prevention of DKA and reduction of its incidence

should be a goal in managing children with diabetes (1).

Many patients with diabetes die from diabetic ketoacidosis (DKA) every year.

DKA is caused by reduced insulin levels, decreased glucose use, and increased

gluconeogenesis from elevated counter regulatory hormones, including

catecholamines, glucagon, and cortisol. DKA primarily affects patients with type 1

diabetes, but also may occur in patients with type 2 diabetes, and is most often caused

by omission of treatment, infection, or alcohol abuse.1 Use of a standard protocol

provides consistent results in treating DKA (2).

1

Despite recent progress in the diagnosis and long-term treatment of type 1

diabetes, diabetic ketoacidosis (DKA) continues to be the most significant cause of

death in childhood diabetes. WHO says mortality rate is about 1-2 % in 1970.

According to the studies reported from the United States, mortality due to DKA is

between 0.21 and 0.25%. In Indonesia mortality rate due to DKA is about 24,9 %

Late referrals to hospitals and/ or insufficient treatment regimens are responsible for

even higher mortality rates in some countries and regions (3).

Basic principle of treatments are fast rehidration, giving of insulin improve

electrolyte trouble and over come the predisposition factors.

This is a case report about ketoacidosis case in child who is taken care in

Pediatric Departement RSUD Ulin Banjarmasin .

2

CASE REPORT

I. IDENTITY

1. Patient Identity :

Name : Mr. S

Sex : Boy

Age : 13 years old

Child : 4 from 5

Hospitalized : October 04th, 2005

2. Parents Identity

Father : Name : Mr. U

Education : Elementary School

Profession : Jobless

Address : Jl. A. Yani Km.7 Pasar Ahad RT.5 No.2

Kertak Hanyar Banjarmasin.

Moher : Name : Ny. M

Education : Elementary School

Profession : House wife

Address : Jl. A. Yani Km.7 Pasar Ahad RT.5 No.2

Kertak Hanyar Banjarmasin.

3

II. ANAMNESA

Alloanamnesis with patient’s father October, 04th 2005 on 02.00 a.m.

1. Chief complaint : Dyspneu

2. Present History Illness :

Since 15 hour before hospitalized, child complain to crowded. The Crowded

undiminished with change of position.

1 day before hospitalized the child was vomited 7 times (but not progressive),

its contents was what the child eaten and drinked, its about 1/4 - 3/4 aqua

glass. The breath was smell and fast. There is no fever, and no seizure,

defecate as usual. Child’s eyes seen concave. The lastest miction 5 hours

before hospitalized, 1/8 aqua glass. Child also seen weak since last 3 day.

Since 3 weeks ago before hospitalized, child never getting insulin injection

because no maney to buy it. Child usually get insulin injection 3 x 4 IU

(under the arm skin). The child also never check his blood sugar too.

Since 1 year before hospitalized, child often urinate, the amount of the urine

about 1/3 - 1/2 aqua glass. Sometime until 15 times a day. Child often feel

thirsty and drinking many. Child also often feel hungry and often eat though

only a few. Sometime only eat 2 tablespoon. But child’s body becomes

progressively weak and thin.

1 year ago the child’s urine checked in puskesmas and expressed the child

suffer diabetes.

3. Past History illness

4

The child has been hospitalized 3 times and was took care in ICU with

diagnose ketoacidosis diabetic ( in October and September 2004, and also

July 2005).

4. History of pregnancy and delivery

Antenatal history :

Patient’s mother always check her pregnancy in Puskesmas every month. As

long as pregnancy, there is no hypertention and asthma. But his mother have

Diabertes Mellitus.

Natal History :

Patient was born by spontan at home helping by midwife, with body weight

2400 grams.

Neonatal History :

The patient crying, active motion and reddish skin.

5. Devolopment history

Face downward : 4 month

Crawling : 6 month

Sitting : 8 month

Standing : 9 month

Walking : 10 month

Present Condition : The patient in Elementary school 6th grade.

6. Immunisation History

5

Name of the

immunisation

Basic

(age in day/month)

Booster

(year)

BCG 2 -

POLIO 2 3 4 5 -

HEPATITIS B 3 4 5 -

DPT2 3 4

Elementary school 1st

grade

CAMPAK 9 -

7. Feedding History

- Breastfeedding until 2 years, frequently on demand.

- 2 month-1 year the patient started feeding SUN twice a day, 1

sachet/time.

- 1-2 years, the patient having porridge- rice 3 times/day, one small

bowl/times.

- 2 years old until now the patient having rice with meat or fish and

vegetable, 3 times/day, 1 plate.

8. Family History

6

In the patient’s family there is no history about high blood pressure or asthma.

Patient’s mother suffers diabetes mellitus

† † † †

= Man

= Woman

= DM

= Patient

No Name Age Sex Status1 Mr.U 45 M Health2 Mrs.M 30 F Health3 Miss P 16 F Health4 Mr. A 15 M Health5 Miss R 14 F Health6 Mr. S 13 M Ill7 Mr. D 11 M Health

9. Social Environtmental History

7

The patient live with his parent and his brother/sisters (total 7 persons) in small

house made from wood, there is 2 rooms,with the size 3x3 meters. The house has

ventilation and enough lighting. The distance from the neighbourhood is about 5

meters. For drinking they use water from PDAM, but for take a bath and washing

use the water from river.

III. Physical Examination

1. General condition : looks crowded

Awareness : delirium

GCS : 3 – 4 – 6

2. Measurement

Vital sign : Blood Pressure : 90/60 mmHg

Pulse : 108 x/minutes (rapid, small and weak)

Temperature : 35,7 °C

Respirations rate : 36 x/minute

Body Weight : 22 Kg

Body Length : 153 cm

3. Skin : Color : brown

Cyanosis : none

Hemangyoma : none

Turgor : late ( 2 seconds)

Dampness : less

8

Pale : none

4. Head : Shape : mesosefali

Fontanela Mayor : closed

Fontanela Minor : closed

- Hair : Color : black

Thicknes : thick

Distribution : spread throughout the head

Alopesia : none

- Eyes : Palpebra : edem -/-, concave

Eyebrow : hard to extraction

Conjungtiva : anemic (-/-), hyperemia (-)

Sclera : icteric (-/-)

Tears : less

Pupil : Diameter : 3 mm/ 3mm

Symmetric : isokor

Light refleks : +/+

Cornea : clear

- Ears : Shape : simetric

Secret : none

Cerumen : minimal

Pain : none Location : -

- Nose : Shap : simmetric

9

Notril Respiration : (+)

Epistacsis : none

Secret : minimal

- Mouth : Shape : normal

Lips : lips mucosa is dry, pink

Gum : bleeding (-)

Teeth : dental complete

- Tongue : Shape : simmetric

Pale (-), tremor (-), coated tongue (-)

Color : pink

- Faring : Hiperemi : none

Edem : none

Membran/pseudomembran : none

- Tonsil : Color : pink

Enlargement : none

Abcess : none

Membran/pseudomembran : none

4. Neck :

- Jugularis Vein : Pulsation : visible

Pressure : normal

10

- Neck gland enlargement : none

- Neck rigidity : none

- Mass : none

- Tortikolis : none

5. Thorax :

a. Chest wall/lung

Inspection - Shape : symmetric

- Retraction : (+) Location : subcostal

- Dyspneau : (+)

- Respiration : fast, deep and keton smell

Palpation : Fremitus fokal : symmetric

Percution : Sonor

Auscultation : Basic Breath Sound : vesiculer

Additional Breath sound : ronkhy (-/-), whezzing (-/-)

b. Cor :

Inspection : Ictus : none

Palpation : Apeks : untouchable

Thrill + / - : -

Percution : Right margin : ICS IV LPS right

Left margin : ICS V LMK left

Upper margin : ICS II LPS right

Auscultation : Frequency : 108 x/minutes, Rhytym : Reguler

11

Basic sound : S1S2 pure, murmur (-)

Additional Sound : none

6. Abdomen :

Inspection : Shape : flat

Palpation : Liver : untouchable

Lien : untouchable

Kidney : untouchable

Massa : untouchable

- Size : -

- Location : -

- Surface : -

- Consistention : -

- Pain : -

Percution : Tympani/Dull : Dull

Ascites : -

Auscultion : Peristaltic sound positive normal

7. Ekstremity :

12

- General : Upper Limb : cold, rapid, small and weakly

artery pulsation, pale (-), edema (-/-), parese

none.

: Lower Limb : cold, pale (-), rapid, small and

weakly artery pulsation, edema (-/-), parese

none.

- Neurological

Arm LegRight Left Right Left

Movement Active Active Active ActiveTonus Normal Normal Normal NormalTrofi Eutrofi Eutrofi Eutrofi EutrofiClonus - - - - Physiologic Refleks BPR +

TPR +++

KPR +APR +

++

Patologic Refleks Hoffman -

Trommer -

--

Babinsky -Chaddock -

--

Sensibility + + + +Meningeal signs - - - -

8. Nervous System : nervus craniales I – XII normal

9. Genitalia : boy, normal

10. Anus : normal

11. Lain-lain : -

IV.LABORATORY EXAMINATION

13

Pemeriksaan 04-10-200501.38 am

04-10-200510.34 am

Blood ExaminationWBC 11,75 x 103/ul 15,28 x 103/ulRBC 5,88 x 10 6/ul 5,60 x 10 6/ulHb 16,1 g/dl 15 g/dlHCT 46.0 % 43,5 %MCV 78,2 fl 77,7 flMCH 27,4 pg 26,8 pgMCHC 35,09 g/dl 34,5 g/dlPLT 218 x 10 3/ul 295 x 10 3/ulRDW-SD 38,2 fl 37,9 flRDW-CV 13,6 % 13,6 %PDW 12,5 fl 10,2 flMPV 10,3 fl 9,0 flP-LCR 26,1 % 18,9 %PCT 0,23 % 0,27 %Neutrophyl 7,83 x 103ul

(66,7% )9,94 x 103ul (65 % )

Lhympocite 3,05 x 103/ul(26%) 3,46 x 103/ul (22,6%)

Monocite 0,78 x 103/ul (6,6%)

1,83 x 103/ul (12 %)

Eosinophile 0,04 x 103/ul (0,3%)

0,01 x 103/ul (0,1%)

Basofile 0,05 x 103/ul (0,3 %)

0,04 x 103/ul (0,3 %)

Microcytosis + +Glucotest 403 mg/ dl

Blood glucose laboratory (mg/dl) :

14

04/10/05

02.00 am

04/10/05

02.00 am

04/10/05

10.34 am

05/10/05 07/10/05 08/10/05

Glucotest 403

BSS 453 372 607 525

BSN 62

V. RESUME

Name : Mr. S

Sex : Boy

Age : 13 years

Body weight : 22 Kgs

Body Lenght : 153 cm

Chief complaint : dyspneu

Resume :

- About 15 hours before hospitalized, the child was crowded

- Kusmaull respiration and keton smell

- 1 day before hospitalized the kid was vomited 7 times, concave eyes

(+), the lastest miction 5 hours before hospitalized, 1/8 aqua glass

- Since 3 days before hospitalize malaise (+)

- Since 3 weeks ago before hospitalized, child never getting insulin

injection and never check his blood sugar

15

- 1 year before hospitalized the kid has polydipsia, polyphagia and polyuria,

the body become weaks and thin. Puskesmas suffer diabetes.

Physical Examination

General state : looks crowded

Awarness : delirium GCS : 3 - 4 – 6

Blood Pressure : 90/60 mmHg

Pulsation : 108 x/minutes (rapid, small and weak)

Respiration : 36 x/minutes

Temperature : 35,7 °C

Skin : turgor late to normally ( 2

seconds) ,dampness less

Head : normal

Eyes : concave (+), tears (</<)

Ear : normal

Mouth : lips mucosa is dry, shape is normal

Thorax/lung : simetric, nostril respiration

(+/+) ,retraction(+), subcostal, dyspneu

(+), Kusmaull respiration (+) and keton

smell

voice fremitus simetric, percution sonor,

ronkhy (-/-), wheezing (-/-)

Cor : normal, thrill (-), murmur (-)

16

Abdomen : normal

Ekstremity : cold, rapid, small and weakly artery pulsation,

edema (-/-), parese (-/-)

Nerve System : normal

Genitalia : normal

Anal : normal

VI. Diagnose

Differential Diagnose :

- Diabetic Ketoacidosis

- Hyperosmolar Non Ketotic (HONK)

- Acidosis Lactate

Working Diagnosa : Diabetic Ketoacidosis

Nutrition Status :

Body weight/age : (22-45)/7,3 = -3,15 (poor nutrition)

Body lenght/age : (153-156)/8,3 = 0,42 (normal)

VII. Treatment

O2 2 liters/minutes (if needed)

IVFD RL 1 liters in 2 hours then 1430cc/59cc/14 drops/minutes (macro)

D51/4 NS 14 drops/minutes

17

Insulin injection 4 IU/6 hours (s.c)

Cefotaxime injection 3 x 500 mg (i.v)

DM feeding

VIII. Examination Suggestion

Blood Routine Examination

Blood chemistry examination (BSN, BSS)

Urinalisa examination

Blood gas analysis

Electrolyte examination

IX. Prognosis

Quo ad vitam : Dubia ad bonam

Quo ad functionam : Dubia ad bonam

Quo ad sanationam : Dubia ad bonam

18

DISCUSSION

Definition

Diabetic ketoacidosis (DKA) is caused by a decrease in effective circulating

insulin asso-ciated with increases in counter regulatory hormones including glucagon,

catecholamines, cortisol, and growth hormone. This leads to increased glucose

production by the liver and kidney and impaired peripheral glucose utilisation with

resultant hyperglycaemia, and hyper-osmolality. Increased lipolysis, with ketone

body (beta-hydroxybutyrate, acetoacetate) production causes ketonaemia and

metabolic acidosis. Hyperglycaemia and acidosis result in osmotic diuresis,

dehydration, and obligate loss of elec-trolytes. The biochemical criteria for the diag-

nosis of DKA include hyperglycaemia (blood glucose>11 mmol/l (>200 mg/dl) with

a venous pH<7.3 and/or bicarbonate<15 mmol/l. There is associated glycosuria,

ketonuria, and ketonaemia. Rarely, young or partially treated children as well as

pregnant adolescents may present with near normal glucose values (‘‘euglycaemic

ketoacidosis’’).DKA is generally categorised by the severity of the acidosis; varying

from mild (venous pH<7.30, bicarbonate concentration<15 mmol/l), to moderate (pH

< 7.2, bicarbonate <10), to severe (pH<7.1, bicarbonate<5). (1,4)

DKA has 3 main component : hyperglycemia, ketonemia and acidosis. In this

patient has all of the component.

19

Frequency

The incidence of type 1 diabetes mellitus varies from 0.1 to 36.8 per 100 000

worldwide. Diabetic ketoacidosis (DKA)is a well-recognized complication of insulin

deficiency in children and adolescents and results in hospital admission in about 10

per 100 000 children in Canada.(5)

The incidence of DKA at diagnosis in children with type 1 diabetes mellitus

(T1DM) in Europe is approximately 1 per 10,000 children. DKA is more commonly

found at diagnosis of T1DM in children aged <4 years old, children from families

with low socioeconomic standing and children with no first degree relative with

T1DM. In children with established T1DM the risk of an episode of DKA is in the

region of 1-10% per child per year and many of these will occur as a result of poor

adherence to a therapeutic regime.(6) The patient is DKA with type 1 diabetes mellitus

(T1DM).

At disease onset

There is wide geographic variation in the frequency of DKA at diabetes onset

and rates correlate inversely with regional incidence of TIDM. Reported frequencies

range between 15% and 67% in Europe and North America and may be more

common in developing countries. In Canada and Europe, hospitalisation rates for

DKA in established and new patients with TIDM have remained stable at about 10

per 100 000 children over the past 20 years, but severity may be decreasing DKA at

onset of TIDM is more common in younger children (...4 years of age), children

20

without a first degree relative with TIDM, and those from families of lower socio-

economic status. (1)

High dose glucocorticoids, atypical antipsychotics, diazoxide, and some

immunosuppressive drugs have been reported to precipitate DKA in individuals not

previously diagnosed with TIDM(1). The patient was diagnosed diabetes mellitus in 12

years old.

In children with established TIDM

The risk of DKA in established TIDM is 1–10% per patient per year 12–15.

Risk is increased in children with poor metabolic control or previous episodes of

DKA; peripubertal and adolescent girls; children with psychiatric disorders, including

those with eating disorders; and those with difficult family circumstances, including

lower socioeconomic status and lack of appropriate health insurance. Inappropriate

interruption of insulin pump therapy also leads to DKA. Children whose insulin is

administered by a responsible adult rarely have episodes of DKA and 75% of

episodes of DKA beyond diagnosis are probably associated with insulin omission or

treatment error. The remainder are due to inadequate insulin therapy during

intercurrent illness(1). The patient have risk factor : have poor metabolic control, lower

socioeconomic status.

Morbidity and Mortality in children

Reported mortality rates from DKA in national population based studies are

reasonably constant: 0.15% at USA ,0.18% (Canada), 0.25% (Canada),and 0.31%

21

(UK).In places with less developed medical facilities, the risk of dying from DKA is

greater, and children may die before receiving treatment(1).

Cerebral oedema accounts for 57–87% of all DKA deaths. The incidence of

cerebral oedema has been fairly consistent between national population based

studies : 0.46% (Canada), 0.68% (UK) and 0.87% (USA). Single centre studies often

report higher frequencies because of ascertainment bias arising from secondary

referral patterns: 1.1% (USA) to 4.6% (USA). Reported mortality rates from cerebral

oedema, in population based studies are 21%, 25% and 24%. Significant morbidity is

evident in 10%, 21% and 26% of survivors. However, some individual centres have

reported markedly lower mortality and serious morbidity following DKA and

cerebral oedema (USA) (1).

Other possible causes of mortality and morbidity include hypokalaemia,

hyperkalaemia, hypoglycaemia, other CNS complications; haematoma thrombosis

sepsis, and infections (including rhinocerebral mucormycosis) aspiration pneumonia,

pulmonary oedema adult respiratory distress syndrome (ARDS) pneumomedias-

tinum and subcutaneous emphysema, and rhabdomyolysis. Late sequelae relate to

cerebral oedema and other CNS complications; these include hypothalamopituitary

insufficiency, isolated growth hormone deficiency,and combined GH and TSH

deficiency (1). The patient was hospitalized 3 times with same diagnose.

22

Cause

DKA is always caused by insulin deficiency, either relative or absolute. Many

previously undiagnosed patients have been seen in physicians’ offices or emergency

rooms where an adequate history and laboratory study could have made the diagnosis

before they became critically ill. A high index of suspicion is particularly important

for infants and young children. An interesting phenomenon is the occasional marked

delay in diagnosis seen in medical families and in the siblings or offspring of people

with diabetes, reflecting denial. A simple urine test may turn out to be lifesaving by

preventing the initial episode of ketoacidosis, particularly in the high-risk infant and

preschool child (8).

In the established patient, DKA results from: (8)

Failing to take insulin, the most common cause of recurrent DKA, particularly

in adolescents .

Acute stress, which can be trauma, febrile illness, or psychological turmoil,

with elevated counterregulatory hormones (glucagon, epinephrine, cortisol,

growth hormone).

Poor sick-day management, typically not giving insulin because the child is

not eating or failing to increase insulin for the illness, as dictated by blood glucose

monitoring. Home testing of urine for ketones with test strips may be misleading

and result in delayed institution of sick-day management; the strips can

23

deteriorate and give false-negative readings. Nitroprusside tablets are less

convenient but very stable and reliable.

The cause of DKA in this patient because the patient stopped use insulin injection

until 3 weeks before hospitalized.

Pathophysiology

Hyperglycemia results from impaired glucose uptake because of insulin

deficiency and excess glucagon with resultant gluconeogenesis and glycogenolysis.

Glucagon excess also increases lipolysis with the formation of ketoacids. Ketone

bodies provide alternative usable energy sources in the absence of intracellular

glucose. The ketoacids (acetoacetate, beta-hydroxybutyrate, acetone) are products of

proteolysis and lipolysis (7).

Hyperglycemia causes an osmotic diuresis that leads to excessive loss of free

water and electrolytes. Resultant hypovolemia leads to tissue hypoperfusion and

lactic acidosis (7).

Ketosis and lactic acidosis produce a metabolic acidosis; however, supplemental

bicarbonate is not recommended. Acidosis usually resolves with isotonic fluid

volume replenishment and insulin therapy. A recent pediatric trial of bicarbonate in

severe metabolic acidosis during DKA (pH <7.15) showed no benefit when compared

to placebo. Indeed, multiple studies suggest that bicarbonate therapy may cause

24

paradoxical intracellular acidosis, worsening tissue perfusion and hypokalemia, and

cerebral edema (7).

As acidosis corrects, acetoacetate and acetone levels increase in proportion to

beta-hydroxybutyrate. As it worsens, the reverse occurs. Routine laboratory testing

for ketones measures only the presence of acetoacetate and acetone, not beta-

hydroxybutyrate. Therefore, ketosis may appear to be absent in early DKA and to

worsen as severe DKA resolves (7).

Electrolyte imbalances are the consequences of hyperglycemia,

hyperosmolality, and acidosis. Despite what may be severe total body potassium

depletion, apparent serum hyperkalemia often is observed in patients with DKA prior

to volume resuscitation. Serum hyperkalemia occurs as potassium ions shift from the

intracellular to extracellular space because of acidosis from insulin deficiency and

decreased renal tubular secretion. Similar decreases in serum phosphate and

magnesium concentrations are the result of ion shifts (7).

Hyponatremia results from a dilutional effect as free water shifts extracellularly

because of high serum osmolarity. True serum sodium values can be calculated by

adjusting measured sodium levels upward 1.6 mEq/L for every 100 mg/dL increase in

serum glucose concentration (7).

As serum osmolarity increases from hyperglycemia, intracellular osmolality in

the brain also increases. Overly rapid correction of serum hyperglycemia and

osmolarity may create a large gradient between intracerebral and serum osmolarity.

Free water then shifts into the brain and may cause cerebral edema with herniation.

25

Therefore, fluid resuscitation and correction of hyperglycemia should be gradual and

closely monitored (7).

Diagnose (2)

Diagnostic Criteria for Diabetic Ketoacidosis

Mild DKA Moderate DKA Severe DKA

Plasma glucose (mg per dL [mmol per L])

> 250 (13.9)

> 250 > 250

Arterial pH 7.25 to 7.30 7.00 to 7.24 < 7.00

Serum bicarbonate (mEq per L) 15 to 18 10 to < 15 < 10

Urine ketones Positive Positive Positive

Serum ketones Positive Positive Positive

Beta-hydroxybutyrate High High High

Effective serum osmolality (mOsm per kg)*

Variable Variable Variable

Anion gap† > 10 > 12 > 12

Alteration in sensoria or mental obtundation

Alert Alert/drowsy Stupor/coma

DKA = diabetic ketoacidosis; HHS = hyperosmolar hyperglycemic state.

*-Effective serum osmolality = 2 3 measured Na (mEq per L) + (glucose [mg per dL] ÷ 18).

†-Anion gap = Na+ - (Cl- + HCO3- [mEq per L]).

Presentation

Children with DKA may present with any or all of the following common features of

the condition:

Lethargy Confusion

26

Polyuria ± polydypsia

Dehydration

Weight loss

Abdominal pain ± vomiting

Rapid respiratory rate (Kussmaul respirations)

Ketotic breath - fruity, pear drops smell.

Shock

Coma

Laboratory Finding (2, 7, 8)

Hyperglycemia: Insulin deficiency results in decreased glucose uptake with

tissue starvation resulting in proteolysis and lipolysis providing amino acids and

glycerol for gluconeogenesis, enhanced by counterregulatory hormone response

to both the precipitating and tissue starvation stress; in the liver, insulin deficiency

results in glycogenolysis and enhanced gluconeogenesis, also stimulated by

counterregulatory hormones.

Dehydration and thirst: Results from osmotic diuresis due to hyperglycemia

and hyperketonemia, hyperventilation, and vomiting as part of the primary

precipitating illness or resulting from the ketosis; since dehydration is usually

hyperosmolar and mostly intracellular, dehydration may be underestimated by

clinical examination.

27

Acidosis: Due to ketonemia from overproduction of ketones, which cannot be

metabolized in the absence of insulin, and lactic acidosis from tissue

hypoperfusion.

Rapid deep respiration (Kussmaul): Compensatory response to the metabolic

acidosis, contributing to dehydration.

Coma: Results from hyperosmolality, not acidosis; calculated osmolality

greater than 320 mosm/L is associated with coma (8).

Hyperosmolality: Largely due to hyperglycemia; calculated as

Na (mmol/L) x 2 + glucose / 18 (mg/dL) + BUN / 2.8 (mg/dL)

or

Na (mmol/L) x 2 + glucose (mmol/L) + urea (mmol/L)

Hyperlipidemia: Due to counter-regulatory-hormone- stimulated lipolysis and

hypoinsulinemia.

Electrolyte disturbances: Spuriously low Na level due to osmolar dilution by

glucose and sodium-free lipid fraction. Corrected Na (i.e., for normal glucose

level) can be estimated as

measured Na + (glucose in mmol/L-5.6) / 2

28

Na deficit is estimated at 10 mmol/kg body weight. Potassium may be spuriously

normal because of acidosis-related exudation from tissues and obligatory urinary

losses; estimate total K deficit at 5 mmol/kg. Potassium deficits in newly

diagnosed patients may be greater than in established patients because of the

longer duration of polyuria before admission.

Other Findings (2,7,8)

BUN: elevated as a result of dehydration.

Creatinine: may be falsely elevated due to interference in the autoanalyzer

methodology from ketones.

Serum ketones: dilutions for nitroprusside testing of no value;

betahydroxybutyrate will be most abundant and is not measured by

nitroprusside, but betahydroxybutyrate assay is available in many laboratories.

Elevated WBC with shift to the left is a stress response that is not helpful for

diagnosing intercurrent infection.

Elevated serum amylase level is salivary, not pancreatic; acute pancreatitis

may occasionally be seen with DKA, in which case serum lipase level will

also be increased.

Abdominal pain and tenderness, with ileus, are usually nonspecific and

improve with improvement of the metabolic state (if not, these need to be

evaluated as with any other acute abdominal problem).

29

Increased blood pressure and heart rate are due to constricted circulatory

volume and stress state.

Retrosternal or neck pain with dysphonia, dyspnea, or subcutaneous

emphysema can occur from pneumomediastinum due to alveolar rupture from

hyperventilation or retching. Typically, however, pneumomediastinum is

asymptomatic (9).

For this patient the diagnose was made from the anamnesa, physical

examination and laboratory examination. This patient had the trias that support the

diagnose of diabetes (polydipsia, polyphagia and polyuria). About 15 hours before

hospitalized, the child was crowded, Kusmaull respiration and keton smell. 1 day

before hospitalized the patient was vomited 7 times, concave eyes (+), the lastest

miction 5 hours before hospitalized, 1/8 aqua glass. Since 3 days before hospitalize

malaise (+). Since 3 weeks ago before hospitalized, child never getting insulin

injection and never check his blood sugar. 1 year before hospitalized the child has

polydipsia, polyphagia and polyuria, the body become weaks and thin. Puskesmas

suffer diabetes.

From the physical examination found hypotensoin, takikardi, Kusmaull

respiration and dyspneu, hipotermi, the signs of dehydration like dry skin, dry lips

mucosa, and the concave eyes. This is was results from osmotic diuresis due to

hyperglycemia and hyperketonemia, hyperventilation, and vomiting as part of the

primary precipitating illness or resulting from the ketosis; since dehydration is

30

usually hyperosmolar and mostly intracellular, dehydration may be underestimated by

clinical examination. In this patient found Kussmaull respiration. Its cause as a

compensatory response to the metabolic acidosis, contributing to dehydration. In this

patient is also found elevated WBC with shift to the left is a stress response that is not

helpful for diagnosing intercurrent infection.

Differential Diagnose (9,10,11,12)

Hyperosmolar non ketotic

At hyperosmolar coma of non ketotic happened hiperglikemia without ketocis and

acidosis, usually happened at type 2 diabetes mellitus, because insulin still last for

preventing ketosis. Patient suffered of heavy hyperglycemia without a hitch

electrolyte balance and lipolisis. High glucose level > 600 mg / dl so that happened

osmotik diuresis. intrasel dehydration and decreasing of plasma volume cause wide of

function trouble, heavy hipotensi, stupor, comma.

Lactat acidosis

Laktat acid piled up when anaerob metabolism is very mounting. It is usually

differentiated by two kinds of asidocis by laktat acid, first effect of tissue hypoksia by

failing of circulation of blood, or systematical hipoksia. Second because damage in

renal metabolism or hepatic or because of drugs.

31

Treatment

Children with ketosis and hyperglycaemia who are not vomiting or

dehydrated may be managed as an outpatient under the supervision of the local

specialist team. Children who have long duration of symptoms, any element of

confusion or a compromised circulation should be admitted to a children's unit or

high dependency unit where staff have considerable experience in treating children

with DKA. Children age less than 5 and new onset T1DM are at high risk of

developing cerebral oedema and should be referred for consideration for treatment in

an intensive care unit. The management of DKA may be considered under four

headings, monitoring of condition, fluid balance, insulin therapy and electrolyte and

acid/base balance (6).

Basic rules in dealing with DKA are: (7,10,12)

1. Admit patients only to a unit in which neurologic status and vital signs can be

monitored frequently and blood glucose level measured hourly.

2. Personally evaluate the patient early on admission and frequently thereafter.

3. Keep good records, including rationalization for decisions, and a flow sheet.

4. Develop a relationship with a pediatric diabetes specialist you trust and call

him or her with any questions, including whether the patient needs to be

transferred to a specialized unit.

32

5. The patient who does not have persistent vomiting, with a pH >7.25, can be

treated and observed in the emergency room over a few hours without hospital

admission.

The goals of treatment are: (8)

1. Restore perfusion, which will increase glucose use in the periphery and reverse

the progressive acidosis.

2. Stop ketogenesis by giving insulin, which will reverse proteolysis and lipolysis,

and stimulate glucose uptake and processing, normalizing blood glucose

concentration.

3. Correct electrolyte losses.

4. Avoid the complications of treatment insofar as possible, including intracerebral

complications, hypoglycemia, and hypokalemia.

Fluid therapy (2,7,8,9,10,11)

o Can generally assume 10% dehydration (100 mL/kg), up to 15% in

infants.

o Provide 20 mL/kg 0.9% NaCl in first one to two hours to restore

peripheral perfusion.

o In the patient with shock or preshock give 5% albumin, 20-25 mL/kg,

as initial hydration.

33

o Calculate maintenance in usual fashion (e.g., 1,000 mL for first 10 kg

+ 500 mL for next 10 kg + 20 mL/kg over 20 kg).

o Calculate remainder of replacement after the loading dose based on

10% dehydration, and maintenance for administration over the subsequent 22 to

23 hours.

o If osmolality (calculated or measured) is >320 mosm/L, correct in 36

hours and if >340 mosm/L, correct in 48 hours.

o After initial 0.9% NaCl bolus, continue rehydration/maintenance with

0.45% NaCl. Some prefer to continue with Ringer’s lactate or acetate solution;

however, hyperosmolar patients should be changed to 0.45% NaCl after the initial

bolus of 0.9% NaCl. During rehydration the measured Na can increase to the level

of the corrected Na as glycemia declines and then decline to normal levels if the

corrected level was elevated.

o Provide K (20-40 mmol/L or up to 80 mmol/L as needed) as half KCL,

half KPO4 (to replenish low phosphate levels and to decrease the risk of

hyperchloremia) or as half KPO4 and half K acetate (which, like lactate, is

converted to bicarbonate to help correct acidosis) after serum K reported as less

than 6 mmol/L or urine flow is established.

o Bicarbonate is rarely indicated. There is no evidence that bicarbonate

facilitates metabolic recovery. It should be given when there is absence of

hyperventilation; never give bicarbonate by push, for this can produce dangerous

34

hypokalemia. Safe administration to avoid risk of hypokalemia is to give 1-2

mmol/kg body weight or 80 mmol/m2 body surface area over 2 hours (10).

Reduce NaCl concentration in the fluids to allow for added Na ion unless Na level

in the serum is subnormal.

Insulin (2,7,8,10)

o Insulin can be started immediately at the time of the initial fluid

expansion or it can be held until the fluid expansion is completed for a more

realistic starting glucose level.

o The most widely used system is 0.1 U/kg hourly as a continuous

infusion, using a pump.

o It may be more convenient in some settings to administer 0.I U/kg IV

and 0.1 U/kg IM with subsequent doses of 0.1 U/kg IM or SC hourly. In adults,

there did not seem to be any difference whether insulin was administered

intravenously, intramuscularly, or subcutaneously after the first couple of hours of

treatment

o There is no evidence that low-dose insulin as currently used results in

any less frequency of hypoglycemia, hypokalemia, or cerebral edema than the

earlier treatment with much higher doses. The principal advantages of low-dose

therapy given as continuous IV or hourly injections are that there is frequent

contact with the patient and hourly blood glucose determinations are done.

35

o During initial fluid expansion, a high blood glucose level may drop

10-15 mM/L, even without insulin infusion. High blood glucose levels should

drop 3-8 mmol/L/hr (but not > 12 mmol/L/hr), and if they do not, the dose should

be increased. This is rarely necessary.

o When the blood glucose level falls to 15 mmol/L or >12 mmol/L/hr, 5-

10% dextrose should be added to the intravenous fluids.

o If the blood glucose level falls below 8 mmol/L with 10% dextrose

solution running, the insulin dose should be reduced to 0.05 U/kg/hr.

o Do not stop insulin or reduce it below 0.05 U/kg/hr, for a continuous

supply of insulin is needed to prevent ketosis and permit continued anabolism.

Monitoring (2,7,8,10,11,12)

o A flow sheet is essential to record the measures noted in Table 1 at

hourly intervals.

o The nursing personnel must have clear guidelines on when to call the

attending physician, such as findings listed in Table 2.

o ECG monitoring should be done and hourly potassium measurements

made if the initial potassium level is <3 or >6 mmol/L.

o Mannitol in quantities sufficient to give 1-2 g/kg body weight should

be kept at the bedside for the first 36 hours (see below under complications).

36

o Resist the convenience of catheterization for monitoring output. The

occasional older patient may have bladder atony while ketoacidotic and require

initial catheterization, but it is rare to need an indwelling catheter.

o Failure of measured

serum Na level to rise with

falling blood glucose

concentration or an actual

decrease in serum Na may

indicate impending

37

cerebral edema. Hydration

should continue slowly and

with 0.9% NaCl solution.

MONITORING TREATMENT OF DKA (8,10,11,12)

Clinical Interval

Vital signs 20-30 minutes

Coma score (e.g., Glasgow) 20-30 minutes

Laboratory

Glucose Hourly bedside; in the laboratory with electrolyte assay,or 1-2 hourly if outside bedside monitor range

Potassium Hourly if abnormal (<3 or >6 mM/L)

Sodium, potassium, CO2 or HCO3, venous pH, osmolality

Admission, 2, 6,10, 24 hrs.(or 2-4 hourly until osmolalitv normal)

BUN Admission, 12, 24 hrs.

Betahydroxybutyrate (if available) Admission, 6,12, 24 hrs.

Ketonuria Admission, 44 hourly

Calcium, phosphorus (optional) Admission, 12, 24 hrs.

Fluids

Type and rate

Intake (include oral and reduce IV intake accordingly)

38

Output

Insulin

(DKA Guidelines)

The patien have treatment Oxygen because he has dispneu, Ringer lactate 1 liters (in

2 hours) to rehidration, then maintenance 14 drops/minute. Giving insulin 4 IU every

6 hours, antibiotic (Cefotaxime) as broad spectrum antibiotic and having DM diet.

Complications (2,7,6,8,9, 13)

Hypoglycemia

Infrequent with hourly blood glucose monitoring. With the presence of an

intravenous line, severe hypoglycemia is best treated with intravenous glucose.

Glucagon can produce ketosis and nausea with vomiting, particularly in children.

Persistent Acidosis

Defined as persistence of a bicarbonate value less than 10 mmol/L after eight to

ten hours of treatment.

Usual cause is inadequate insulin effect, indicated by persistent hyperglycemia.

Check insulin dilution and rate of administration, consider inadequate absorption if

insulin is being given by subcutaneous or IM injection or resistance due to unusually

high counter regulatory hormones, as with concomitant febrile illness.

May need to switch to IV administration if patient is not receiving insulin IV. If

receiving IV insulin, solution should be changed every six hours.

39

Extremely rare causes are lactic acidosis due to an episode of hypotension or

apnea or inadequate renal competency in the handling of hydrogen ion as a result of

an episode of renal hypoperfusion.

Hypokalemia

Extracellular K concentrations fall as a result of treatment, with potassium

reentering cells. If initial serum K <3 mmol/L, K must be put into the initial

expansion fluids without waiting for demonstration of renal function and insulin

should be delayed or stopped until after the initial bolus fluids are infused.

Intracerebral complications

Intracerebral complications comprise the most serious and frequent

complications of DKA and can occur despite adherence to the guidelines above.

There is no evidence for reduction in the frequency of intracerebral complications

with the advent of low-dose insulin use by continuous infusion or the shift to more

isotonic initial fluids. Although the classic picture is one of metabolic and clinical

improvement with sudden deterioration, there may be up to several hours of

decreasing sensorium and change in vital signs, as noted in Table 2, and some

children will be admitted in coma and not recover. An occasional patient will develop

intracerebral complications even before treatment, raising the suspicion of cerebral

thrombosis.

In more than half of patients who develop intracerebral complications, there is a

sufficient warning period to permit administration of mannitol to reduce edema and,

if indicated by respiratory distress, intubation/hyperventilation to reduce intracerebral

40

blood flow. When this is accomplished before respiratory arrest, there is a greater

than 50% chance of survival in the normal state or with disability that does not

preclude independence (l). Computerized tomographic (CT) scans should not be

depended upon to determine the need for intervention; this decision should be made

on clinical grounds. Initial CT scans, even after respiratory arrest, often appear

normal or show only localized basilar edema. The dose of mannitol is 1 g/kg body

weight intravenously, over 15 minutes, repeated as necessary.Particularly susceptible

to intracerebral complications are previously undiagnosed patients and children under

5 years of age. In this case, the patient didn’t get complication from DKA.

41

Conclusion

Have been reported a Diabetic ketoacidosis case at a boy age 13 years who was

taken care in Pediatric departement RSUD Ulin Banjarmasin. Patient hospitalize

crowd. Base on anamnesa, physical examination and laboratory, the patient was

diagnose with DKA. Have been done rehydration therapy, giving of insulin,

preventive of infection and DM diet. Patient came home with better condition.

42

REFERENCES

1. Dunger. ESPE/LWPES Consensus Statement on Diabetic Ketoacidosis in Children and Adolescent. 2005. available at http://adc.bmjjournals.com/cgi/content/full/89/2/188

2. Trachtenbarg,D. Diabetic Ketoacidosis. American Family Physician Illinois.2005. Available at http://www.aafp.org

3. Hatun, S. Cerebral Complications in Diabetic Ketoacidosis. The Turkish Journal of Pediatrics. 2005. Available at http://www. tjp.dergisi.org

4. Maldonado Y. Ketoacidosis. Dalam: Wahab A.S (editor penterjemah). Nelson Ilmu Kesehatan Anak Edisi 15 Volume 2. Jakarta: EGC, 2000. h.1068-71

5. Vanelli,M. Effectiveness of aPrevention Program for Diabetic Ketoacidosis in Children. Diabetes care volume 22, january 1999.page 7-9

6. Ho, J. Diabetic Ketoacidosis and Pediatric Stroke. CMAJ.February 1.2005 Available at http://www.CMAJ.org

7. Anonim. Childhood Ketoacidosis. 2005. Available at http://www.patient.co.uk

8. Young, J. Pediatrics Diabetic Ketoacidosis.2004. Available at http://www. emedicine. Com

9. Hasan R, Alatas H, ed.Kelainan Metabolik . Dalam : Buku Ilmu Kesehatan Anak Jilid 2. Bagian FKUI, Jakarta:2000: 624-8

10. Rosenbloom, A. Diabetic Ketoacidosis (DKA) : Treatment Guidelines. University of Florida College of Medicine,Gainesville. 2005. Available at http://www. ispad. org

11. Mansjoer A, dkk. Ketoasidosis Diabetik. Dalam: Kapita Selekta Kedokteran. Jilid I Edisi Ketiga. Jakarta: Media Aesculapius Fakultas Kedokteran UI, 1999: 604-608.

12. Boedisantoso A dan Subekti I. Komplikasi Akut Diabetes Mellitus. Dalam: Soegondo S (ed). Penatalaksanaan Diabetes Mellitus Terpadu. Jakarta: Balai Penerbit Fakultas Kedokteran Indonesia Universitas Indonesia, 2002: 161-167

43

13. Price SA, Wilson LM. Patofisiologi, Konsep Klinis Proses-proses Penyakit. Buku 2 Edisi 4. Jakarta: EGC, 1995

44

Lampiran

FOLLOW UP PENDERITA TANGGAL 4 Oktober 2005 sampai 8 Oktober 2005

DATE 4 5 6 7 8SUBJECTIVE

- Dyspneu + - - - -- Vomiting - - - - -- Fever - - - - -- Defecate - - - + -- Urinate + + + + +- Eat - + + + +- Drink + + + + +

VITAL SIGNPulse (times/minute) 108 88 89 72 73Breath (times/minute) 26 34 31 25 25Temperature (oC) 35,7 36 36,5 36 36,7Body Weight (kg) 22 22 22 22,5 23

ASSESMENTDIABETIC KETOACIDOSIS

PLANNINGIVFD RL 14 drops/minute

+ - - - -

IVFD D51/4 NS 14 drops / minutes

- + + + +

Actravid Inj IV 4 IU/6 hour

+ + + + +

Cefotaxime Inj IV 3x500mg

+ + + - -

DM diet + + + + +

- Day 1 : IVFD RL 1 liters in 2 hours then 1430cc/59cc/14 drops/minutes (macro)

45

46