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 t o acute complication form from diabetes mellitus that is hyperglycemia and hipoglykemia. !yperglycemia happened at ketoacidosis (D"#), hyperosmolar non ketotic (!$%") and laktat acidosis(1). Diabetic ketoacidosis (D"#) is trias from hyperglycemia, acidosis and ketonemia. D"# is the leading cause of morbidity and mortality in children ith type 1 diabetes mellitus (TIDM). Mortality is predominantly related to the occurrence of cerebral oedema& only a minority of deaths in D"# are attributed to other causes(1,'). There is agreement that prevention of D"# and reduction of its incidence should be a goal in managing children ith diabetes (1). Many patients ith diabetes die from diabetic ketoacidosis (D"#) every year.

D"# is caused by reduced insulin levels, decreased glucose use, and increased gluconeogenesis from elevated counter regulatory hormones, including ith type 1

catecholamines, glucagon, and cortisol. D"# primarily affects patients

diabetes, but also may occur in patients ith type ' diabetes, and is most often caused by omission of treatment, infection, or alcohol abuse. 1 (se of a standard protocol provides consistent results in treating D"# (').

Despite recent progress in the diagnosis and long)term treatment of type 1 diabetes, diabetic ketoacidosis (D"#) continues to be the most significant cause of death in childhood diabetes. *!$ says mortality rate is about 1)' + in 1,-.. #ccording to the studies reported from the (nited /tates, mortality due to D"# is bet een ..'1 and ..'0+. In Indonesia mortality rate due to D"# is about '1,, + 2ate referrals to hospitals and3 or insufficient treatment regimens are responsible for even higher mortality rates in some countries and regions (4). 5asic 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 6ediatric Departement 7/(D (lin 5an8armasin . ho is taken care in

'

CASE REPORT

I. IDENTITY 1. 6atient Identity 9 %ame /e: #ge ;hild !ospitali<ed '. 6arents Identity =ather 9 %ame >ducation 6rofession #ddress 9 Mr. ( 9 >lementary /chool 9 ?obless 9 ?l. #. @ani "m.- 6asar #had 7T.0 %o.' "ertak !anyar 5an8armasin. Moher 9 %ame >ducation 6rofession #ddress 9 %y. M 9 >lementary /chool 9 !ouse ife 9 ?l. #. @ani "m.- 6asar #had 7T.0 %o.' 9 Mr. / 9 5oy 9 14 years old 9 1 from 0 9 $ctober .1th, '..0

"ertak !anyar 5an8armasin.

II.

ANAMNESA #lloanamnesis ith patientAs father $ctober, .1th '..0 on .'... a.m. 1. ;hief complaint 9 Dyspneu '. 6resent !istory Illness 9 /ince 10 hour before hospitali<ed, child complain to cro ded. The ;ro ded undiminished ith change of position. 1 day before hospitali<ed the child its contents as as vomited - times (but not progressive),

hat the child eaten and drinked, its about 131 ) 431 aBua as smell and fast. There is no fever, and no sei<ure,

glass. The breath

defecate as usual. ;hildAs eyes seen concave. The lastest miction 0 hours before hospitali<ed, 13C aBua glass. ;hild also seen eak since last 4 day. /ince 4 eeks ago before hospitali<ed, child never getting insulin in8ection

because no maney to buy it. ;hild usually get insulin in8ection 4 : 1 I( (under the arm skin). The child also never check his blood sugar too. /ince 1 year before hospitali<ed, child often urinate, the amount of the urine about 134 ) 13' aBua glass. /ometime until 10 times a day. ;hild often feel thirsty and drinking many. ;hild also often feel hungry and often eat though only a fe . /ometime only eat ' tablespoon. 5ut childAs body becomes progressively eak and thin. 1 year ago the childAs urine checked in puskesmas and e:pressed the child suffer diabetes.

4. 6ast !istory illness The child has been hospitali<ed 4 times and as took care in I;( ith

diagnose ketoacidosis diabetic ( in $ctober and /eptember '..1, and also ?uly '..0). 1. !istory of pregnancy and delivery #ntenatal history 9 6atientAs mother al ays check her pregnancy in 6uskesmas every month. #s long as pregnancy, there is no hypertention and asthma. 5ut his mother have Diabertes Mellitus. %atal !istory 9 6atient as born by spontan at home helping by mid ife, ith body eight

'1.. grams. %eonatal !istory 9 The patient crying, active motion and reddish skin. 0. Devolopment history =ace do n ard ;ra ling /itting /tanding *alking 6resent ;ondition 9 1 9 D 9 C 9 , 9 1. month month month month month

9 The patient in >lementary school Dth grade.

D. Immunisation !istory %ame of the immunisation 5;E 6$2I$ !>6#TITI/ 5 D6T ' ;#M6#" 4 , 1 grade ) 5asic (age in day3month) ' ' 4 1 0 4 1 0 5ooster (year) ) ) ) >lementary school 1st

-. =eedding !istory ) ) 5reastfeedding until ' years, freBuently on demand. ' month)1 sachet3time. ) 1)' years, the patient bo l3times. ) ' years old until no the patient having rice ith meat or fish and having porridge) rice 4 times3day, one small year the patient started feeding /(% t ice a day, 1

vegetable, 4 times3day, 1 plate.

C. =amily !istory In the patientAs family there is no history about high blood pressure or asthma. 6atientAs mother suffers diabetes mellitus

G Man G *oman G DM G 6atient

%o 1 ' 4 1 0 D -

%ame Mr.( Mrs.M Miss 6 Mr. # Miss 7 Mr. / Mr. D

#ge 10 4. 1D 10 11 14 11

/e: M = = M = M M

/tatus !ealth !ealth !ealth !ealth !ealth Ill !ealth

,. /ocial >nvirontmental !istory The patient live ith his parent and his brother3sisters (total - persons) in small

house made from ood, there is ' rooms, ith the si<e 4:4 meters. The house has ventilation and enough lighting. The distance from the neighbourhood is about 0

meters. =or drinking they use ater from 6D#M, but for take a bath and ashing use the ater from river.

III. Physical Examination 1. Eeneral condition # areness E;/ '. Measurement Iital sign 9 5lood 6ressure 6ulse Temperature 7espirations rate 5ody *eight 5ody 2ength 4. /kin 9 ;olor ;yanosis !emangyoma Turgor Dampness 6ale 1. !ead 9 /hape 9 ,.3D. mm!g 9 1.C :3minutes (rapid, small and eak) 9 40,- J; 9 4D :3minute 9 looks cro ded 9 delirium 9 4H1HD

9 '' "g 9 104 cm 9 bro n 9 none 9 none 9 late ( ' seconds) 9 less 9 none 9 mesosefali

=ontanela Mayor =ontanela Minor ) !air 9 ;olor Thicknes Distribution #lopesia ) >yes 9 6alpebra >yebro ;on8ungtiva /clera Tears

9 closed 9 closed 9 black 9 thick 9 spread throughout the head 9 none 9 edem )3), concave 9 hard to e:traction 9 anemic ()3)), hyperemia ()) 9 icteric ()3)) 9 less 9 4 mm3 4mm 9 isokor 9 K3K 9 clear 9 simetric 9 none 9 minimal 9 none 2ocation 9 )

6upil 9 Diameter /ymmetric 2ight refleks ;ornea ) >ars 9 /hape /ecret ;erumen 6ain ) %ose 9 /hap %otril 7espiration >pistacsis

9 simmetric 9 (K) 9 none

/ecret ) Mouth 9 /hape 2ips Eum Teeth ) Tongue 9 /hape

9 minimal 9 normal 9 lips mucosa is dry, pink 9 bleeding ()) 9 dental complete 9 simmetric

6ale ()), tremor ()), coated tongue ()) ;olor ) =aring 9 !iperemi >dem 9 pink 9 none 9 none

Membran3pseudomembran 9 none ) Tonsil 9 ;olor 9 pink

>nlargement 9 none #bcess 9 none

Membran3pseudomembran 9 none

1. %eck 9 ) ?ugularis Iein 9 6ulsation 6ressure ) %eck gland enlargement ) %eck rigidity 9 visible 9 normal 9 none 9 none

1.

) Mass ) Tortikolis 0. Thora: 9 a. ;hest all3lung Inspection ) /hape ) 7etraction ) Dyspneau ) 7espiration 6alpation 9 =remitus fokal 6ercution 9 /onor

9 none 9 none

9 symmetric 9 (K) 9 (K) 9 fast, deep and keton smell 9 symmetric 2ocation 9 subcostal

#uscultation 9 5asic 5reath /ound #dditional 5reath sound b. ;or 9 Inspection 9 Ictus 6alpation 9 #peks Thrill K 3 ) 6ercution 9 7ight margin 2eft margin 9 none

9 vesiculer 9 ronkhy ()3)), he<<ing ()3))

9 untouchable 9 ) 9 I;/ II 26/ right 9 I;/ I 2M" left

(pper margin 9 I;/ II 26/ right #uscultation 9 =reBuency 5asic sound 9 1.C :3minutes, 7hytym 9 7eguler 9 /1/' pure, murmur ())

#dditional /ound 9 none

11

D. #bdomen 9 Inspection 9 /hape 6alpation 9 2iver 2ien "idney Massa ) /i<e ) 2ocation ) /urface ) ;onsistention ) 6ain 6ercution 9 Tympani3Dull #scites #uscultion 9 flat 9 untouchable 9 untouchable 9 untouchable 9 untouchable 9 ) 9 ) 9 ) 9 ) 9 ) 9 Dull 9 ) 9 6eristaltic sound positive normal

-. >kstremity 9 ) Eeneral 9 (pper 2imb 9 cold, rapid, small and eakly

artery pulsation, pale ()), edema ()3)), parese none.

1'

9 2o er 2imb 9 cold, pale ()), rapid, small and eakly artery pulsation, edema ()3)), parese none. ) %eurological #rm 7ight 2eft #ctive #ctive %ormal %ormal >utrofi >utrofi ) ) 567 K K T67 K K !offman ) ) ) Trommer ) K K ) ) 2eg 7ight #ctive %ormal >utrofi ) "67 K #67 K 5abinsky ) ;haddock ) K ) 2eft #ctive %ormal >utrofi ) K K ) ) K )

Movement Tonus Trofi ;lonus 6hysiologic 7efleks 6atologic 7efleks

/ensibility Meningeal signs C. %ervous /ystem ,. Eenitalia 1.. #nus 11. 2ain)lain

9 nervus craniales I H LII normal 9 boy, normal 9 normal 9 )

IV.LABORATORY E AMINATION 6emeriksaan *5; 75; !b .1)1.)'..0 .1.4C am 5lood >:amination 11,-0 : 1.43ul 0,CC : 1. D3ul 1D,1 g3dl .1)1.)'..0 1..41 am 10,'C : 1.43ul 0,D. : 1. D3ul 10 g3dl

14

!;T M;I M;! M;!; 62T 7D*)/D 7D*);I 6D* M6I 6)2;7 6;T %eutrophyl 2hympocite Monocite >osinophile 5asofile Microcytosis Elucotest

1D.. + -C,' fl '-,1 pg 40,., g3dl '1C : 1. 43ul 4C,' fl 14,D + 1',0 fl 1.,4 fl 'D,1 + .,'4 + -,C4 : 1.4ul (DD,-+ ) 4,.0 : 1.43ul('D+)

14,0 + --,- fl 'D,C pg 41,0 g3dl ',0 : 1. 43ul 4-,, fl 14,D + 1.,' fl ,,. fl 1C,, + .,'- + ,,,1 : 1.4ul (D0 +) 4,1D : 1.43ul ('',D+) .,-C : 1.43ul 1,C4 : 1.43ul (D,D+) (1' +) .,.1 : 1.43ul .,.1 : 1.43ul (.,4+) (.,1+) .,.0 : 1.43ul (.,4 .,.1 : 1.43ul +) (.,4 +) K K 1.4 mg3 dl

Bloo! "l#cos$ la%o&ato&y 'm"(!l) * +,(-+(+. 3l#cot$st BSS +/.++ am ,+0 +,(-+(+. +/.++ am ,.0 +,(-+(+. -+.0, am 01/ 4+1 ./. +.(-+(+. +1(-+(+. +2(-+(+.

11

BSN V. RES5ME Name Sex Age Body weight Body Lenght Chief complaint Resume ) ) )

4/

9 Mr. / 9 5oy 9 14 years 9 '' "gs 9 104 cm 9 dyspneu 9

#bout 10 hours before hospitali<ed, the child as cro ded "usmaull respiration and keton smell 1 day before hospitali<ed the kid as vomited - times, concave eyes (K), the lastest miction 0 hours before hospitali<ed, 13C aBua glass

) )

/ince 4 days before hospitali<e malaise (K) /ince 4 eeks ago before hospitali<ed, child never getting insulin

in8ection and never check his blood sugar ) 1 year before hospitali<ed the kid has polydipsia, polyphagia and polyuria, the body become eaks and thin. 6uskesmas suffer diabetes. 6hysical >:amination Eeneral state # arness 9 looks cro ded 9 delirium E;/ 9 4 ) 1 H D

10

5lood 6ressure 6ulsation 7espiration Temperature /kin

9 ,.3D. mm!g 9 1.C :3minutes (rapid, small and eak) 9 4D :3minutes 9 40,- J; 9 turgor late to normally ( ' seconds) ,dampness less

!ead >yes >ar Mouth Thora:3lung

9 normal 9 concave (K), tears (M3M) 9 normal 9 lips mucosa is dry, shape is normal 9 simetric, nostril respiration dyspneu (K3K) (K),

,retraction(K),

subcostal,

"usmaull respiration (K) and keton smell voice fremitus simetric, percution sonor, ronkhy ()3)), hee<ing ()3)) ;or #bdomen >kstremity 9 normal, thrill ()), murmur ()) 9 normal 9 cold, rapid, small and eakly artery pulsation, edema ()3)), parese ()3)) %erve /ystem Eenitalia 9 normal 9 normal

1D

#nal

9 normal

VI. Dia"nos$ Differential Diagnose 9 ) ) ) Diabetic "etoacidosis !yperosmolar %on "etotic (!$%") #cidosis 2actate

*orking Diagnosa 9 Diabetic "etoacidosis

%utrition /tatus 9 5ody eight3age 9 ('')10)3-,4 G )4,10 (poor nutrition) 5ody lenght3age 9 (104)10D)3C,4 G .,1' (normal) VII. T&$atm$nt $' ' liters3minutes (if needed) II=D 72 1 liters in ' hours then 114.cc30,cc311 drops3minutes (macro) D0131 %/ 11 drops3minutes Insulin in8ection 1 I(3D hours (s.c) ;efota:ime in8ection 4 : 0.. mg (i.v) DM feeding

1-

VIII. Examination S#""$stion 5lood 7outine >:amination 5lood chemistry e:amination (5/%, 5//) (rinalisa e:amination 5lood gas analysis >lectrolyte e:amination

I . P&o"nosis Nuo ad vitam Nuo ad functionam Nuo ad sanationam 9 Dubia ad bonam 9 Dubia ad bonam 9 Dubia ad bonam

1C

DISC5SSION

D$6inition Diabetic ketoacidosis (D"#) is caused by a decrease in effective circulating insulin asso)ciated ith increases in counter regulatory hormones including glucagon, catecholamines, cortisol, and gro th hormone. This leads to increased glucose production by the liver and kidney and impaired peripheral glucose utilisation resultant hyperglycaemia, and hyper)osmolality. Increased lipolysis, ith

ith ketone

body (beta)hydro:ybutyrate, acetoacetate) production causes ketonaemia and metabolic acidosis. !yperglycaemia and acidosis result in osmotic diuresis, dehydration, and obligate loss of elec)trolytes. The biochemical criteria for the diag) nosis of D"# include hyperglycaemia (blood glucoseO11 mmol3l (O'.. mg3dl) ith

a venous p!M-.4 and3or bicarbonateM10 mmol3l. There is associated glycosuria, ketonuria, and ketonaemia. 7arely, young or partially treated children as pregnant adolescents may present ell as

ith near normal glucose values (PPeuglycaemic

ketoacidosisAA).D"# is generally categorised by the severity of the acidosis& varying from mild (venous p!M-.4., bicarbonate concentrationM10 mmol3l), to moderate (p! M -.', bicarbonate M1.), to severe (p!M-.1, bicarbonateM0). (1,1) D"# has 4 main component 9 hyperglycemia, ketonemia and acidosis. In this patient has all of the component.

1,

F&$7#$ncy The incidence of type 1 diabetes mellitus varies from ..1 to 4D.C per 1.. ... orld ide. Diabetic ketoacidosis (D"#)is a ell)recogni<ed complication of insulin deficiency in children and adolescents and results in hospital admission in about 1. per 1.. ... children in ;anada.(0) The incidence of D"# at diagnosis in children ith type 1 diabetes mellitus

(T1DM) in >urope is appro:imately 1 per 1.,... children. D"# is more commonly found at diagnosis of T1DM in children aged M1 years old, children from families ith lo socioeconomic standing and children ith no first degree relative ith

T1DM. In children

ith established T1DM the risk of an episode of D"# is in the ill occur as a result of poor

region of 1)1.+ per child per year and many of these

adherence to a therapeutic regime.(D) The patient is D"# ith type 1 diabetes mellitus (T1DM). At !is$as$ ons$t There is ide geographic variation in the freBuency of D"# at diabetes onset ith regional incidence of TIDM. 7eported freBuencies

and rates correlate inversely

range bet een 10+ and D-+ in >urope and %orth #merica and may be more common in developing countries. In ;anada and >urope, hospitalisation rates for D"# in established and ne patients ith TIDM have remained stable at about 1.

per 1.. ... children over the past '. years, but severity may be decreasing D"# at onset of TIDM is more common in younger children (...1 years of age), children

'.

ithout a first degree relative economic status. (1)

ith TIDM, and those from families of lo er socio)

!igh dose glucocorticoids, atypical antipsychotics, dia<o:ide, and some immunosuppressive drugs have been reported to precipitate D"# in individuals not previously diagnosed ith TIDM(1). The patient as diagnosed diabetes mellitus in 1' years old. In chil!&$n 8ith $sta%lish$! TIDM The risk of D"# in established TIDM is 1H1.+ per patient per year 1'H10. 7isk is increased in children ith poor metabolic control or previous episodes of

D"#& peripubertal and adolescent girls& children ith psychiatric disorders, including those ith eating disorders& and those ith difficult family circumstances, including

lo er socioeconomic status and lack of appropriate health insurance. Inappropriate interruption of insulin pump therapy also leads to D"#. ;hildren hose insulin is

administered by a responsible adult rarely have episodes of D"# and -0+ of episodes of D"# beyond diagnosis are probably associated ith insulin omission or

treatment error. The remainder are due to inadeBuate insulin therapy during intercurrent illness(1). The patient have risk factor 9 have poor metabolic control, lo er socioeconomic status. Mo&%i!ity an! Mo&tality in chil!&$n 7eported mortality rates from D"# in national population based studies are reasonably constant9 ..10+ at (/# ,..1C+ (;anada), ..'0+ (;anada),and ..41+

'1

((").In places

ith less developed medical facilities, the risk of dying from D"# is

greater, and children may die before receiving treatment(1). ;erebral oedema accounts for 0-HC-+ of all D"# deaths. The incidence of cerebral oedema has been fairly consistent bet een national population based studies 9 ..1D+ (;anada), ..DC+ ((") and ..C-+ ((/#). /ingle centre studies often report higher freBuencies because of ascertainment bias arising from secondary referral patterns9 1.1+ ((/#) to 1.D+ ((/#). 7eported mortality rates from cerebral oedema, in population based studies are '1+, '0+ and '1+. /ignificant morbidity is evident in 1.+, '1+ and 'D+ of survivors. !o ever, some individual centres have reported markedly lo er mortality and serious morbidity follo ing D"# and cerebral oedema ((/#) (1). $ther possible causes of mortality and morbidity include hypokalaemia, hyperkalaemia, hypoglycaemia, other ;%/ complications& haematoma thrombosis sepsis, and infections (including rhinocerebral mucormycosis) aspiration pneumonia, pulmonary oedema adult respiratory distress syndrome (#7D/) pneumomedias) tinum and subcutaneous emphysema, and rhabdomyolysis. 2ate seBuelae relate to cerebral oedema and other ;%/ complications& these include hypothalamopituitary insufficiency, isolated gro th hormone deficiency,and combined E! and T/! deficiency (1). The patient as hospitali<ed 4 times ith same diagnose.

''

Ca#s$ D"# is al ays caused by insulin deficiency, either relative or absolute. Many previously undiagnosed patients have been seen in physiciansA offices or emergency rooms here an adeBuate history and laboratory study could have made the diagnosis

before they became critically ill. # high inde: of suspicion is particularly important for infants and young children. #n interesting phenomenon is the occasional marked delay in diagnosis seen in medical families and in the siblings or offspring of people ith diabetes, reflecting denial. # 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, D"# results from9 (8)

=ailing to take insulin, the most common cause of recurrent D"#, particularly in adolescents .

#cute stress,

hich can be trauma, febrile illness, or psychological turmoil,

ith elevated counterregulatory hormones (glucagon, epinephrine, cortisol, gro th hormone).

6oor 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. !ome testing of urine for ketones ith test strips may be misleading

and result in delayed institution of sick)day management& the strips can

'4

deteriorate and give false)negative readings. %itroprusside tablets are less convenient but very stable and reliable. The cause of D"# in this patient because the patient stopped use insulin in8ection until 4 eeks before hospitali<ed. Patho9hysiolo"y !yperglycemia results from impaired glucose uptake because of insulin deficiency and e:cess glucagon ith resultant gluconeogenesis and glycogenolysis. ith the formation of ketoacids. "etone

Elucagon e:cess also increases lipolysis

bodies provide alternative usable energy sources in the absence of intracellular glucose. The ketoacids (acetoacetate, beta)hydro:ybutyrate, acetone) are products of proteolysis and lipolysis (-). !yperglycemia causes an osmotic diuresis that leads to e:cessive loss of free ater and electrolytes. 7esultant hypovolemia leads to tissue hypoperfusion and lactic acidosis (-). "etosis and lactic acidosis produce a metabolic acidosis& ho ever, supplemental bicarbonate is not recommended. #cidosis usually resolves ith isotonic fluid

volume replenishment and insulin therapy. # recent pediatric trial of bicarbonate in severe metabolic acidosis during D"# (p! M-.10) sho ed no benefit hen compared to placebo. Indeed, multiple studies suggest that bicarbonate therapy may cause

'1

parado:ical intracellular acidosis, cerebral edema (-).

orsening tissue perfusion and hypokalemia, and

#s acidosis corrects, acetoacetate and acetone levels increase in proportion to beta)hydro:ybutyrate. #s it orsens, the reverse occurs. 7outine laboratory testing

for ketones measures only the presence of acetoacetate and acetone, not beta) hydro:ybutyrate. Therefore, ketosis may appear to be absent in early D"# and to orsen as severe D"# resolves (-). >lectrolyte imbalances are the conseBuences of hyperglycemia,

hyperosmolality, and acidosis. Despite

hat may be severe total body potassium ith D"# prior

depletion, apparent serum hyperkalemia often is observed in patients

to volume resuscitation. /erum hyperkalemia occurs as potassium ions shift from the intracellular to e:tracellular space because of acidosis from insulin deficiency and decreased renal tubular secretion. /imilar decreases in serum phosphate and magnesium concentrations are the result of ion shifts (-). !yponatremia results from a dilutional effect as free ater shifts e:tracellularly

because of high serum osmolarity. True serum sodium values can be calculated by ad8usting measured sodium levels up ard 1.D m>B32 for every 1.. mg3d2 increase in serum glucose concentration (-). #s serum osmolarity increases from hyperglycemia, intracellular osmolality in the brain also increases. $verly rapid correction of serum hyperglycemia and osmolarity may create a large gradient bet een intracerebral and serum osmolarity. =ree ater then shifts into the brain and may cause cerebral edema ith herniation.

'0

Therefore, fluid resuscitation and correction of hyperglycemia should be gradual and closely monitored (-). Dia"nos$ '/) Dia"nostic C&it$&ia 6o& Dia%$tic :$toaci!osis Mild D"# Moderate D"# /evere D"# 6lasma glucose (mg per d2 Qmmol per O '0. O '0. O '0. 2R) (14.,) #rterial p! -.'0 to -.4. -... to -.'1 M -... /erum bicarbonate (m>B per 2) 10 to 1C 1. to M 10 M 1. (rine ketones 6ositive 6ositive 6ositive /erum ketones 6ositive 6ositive 6ositive 5eta)hydro:ybutyrate !igh !igh !igh >ffective serum osmolality (m$sm per Iariable Iariable Iariable kg)S #nion gapF O 1. O 1' O 1' #lteration in sensoria or mental #lert #lert3dro sy /tupor3coma obtundation D"# G diabetic ketoacidosis& !!/ G hyperosmolar hyperglycemic state. S)>ffective serum osmolality G ' 4 measured %a (m>B per 2) K (glucose Qmg per d2R T 1C). F)#nion gap G %aK ) (;l) K !;$4) Qm>B per 2R).

P&$s$ntation ;hildren ith D"# may present ith any or all of the follo ing common features of the condition9

2ethargy ;onfusion

'D

6olyuria U polydypsia Dehydration *eight loss #bdominal pain U vomiting 7apid respiratory rate ("ussmaul respirations) "etotic breath ) fruity, pear drops smell. /hock ;oma

La%o&ato&y Fin!in" (', -, C)

Hyperglycemia: Insulin deficiency results in decreased glucose uptake

ith

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: 7esults 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 e:amination.

'-

Acidosis: Due to ketonemia from overproduction of ketones,

hich cannot be

metaboli<ed in the absence of insulin, and lactic acidosis from tissue hypoperfusion.

Rapid deep respiration !ussmaul": ;ompensatory response to the metabolic acidosis, contributing to dehydration.

Coma: 7esults from hyperosmolality, not acidosis& calculated osmolality greater than 4'. mosm32 is associated ith coma (C).

Hyperosmolality: 2argely due to hyperglycemia& calculated as

%a (mmol32) : ' K glucose 3 1C (mg3d2) K 5(% 3 '.C (mg3d2) or %a (mmol32) : ' K glucose (mmol32) K urea (mmol32)

Hyperlipidemia: Due to counter)regulatory)hormone) stimulated lipolysis and hypoinsulinemia.

#lectrolyte distur$ances: /puriously lo

%a level due to osmolar dilution by

glucose and sodium)free lipid fraction. ;orrected %a (i.e., for normal glucose level) can be estimated as measured %a K (glucose in mmol32)0.D) 3 '

'C

%a deficit is estimated at 1. mmol3kg body

eight. 6otassium may be spuriously

normal because of acidosis)related e:udation from tissues and obligatory urinary losses& estimate total " deficit at 0 mmol3kg. 6otassium deficits in ne ly diagnosed patients may be greater than in established patients because of the longer duration of polyuria before admission. Oth$& Fin!in"s '/;1;2)

5(%9 elevated as a result of dehydration. ;reatinine9 may be falsely elevated due to interference in the autoanaly<er methodology from ketones.

/erum

ketones9

dilutions

for

nitroprusside

testing

of

no

value&

betahydro:ybutyrate

ill be most abundant and is not measured by

nitroprusside, but betahydro:ybutyrate assay is available in many laboratories.

>levated *5;

ith shift to the left is a stress response that is not helpful for

diagnosing intercurrent infection.

>levated serum amylase level is salivary, not pancreatic& acute pancreatitis may occasionally be seen also be increased. ith D"#, in hich case serum lipase level ill

#bdominal pain and tenderness, improve

ith ileus, are usually nonspecific and

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

evaluated as ith any other acute abdominal problem).

',

Increased blood pressure and heart rate are due to constricted circulatory volume and stress state.

7etrosternal or neck pain

ith dysphonia, dyspnea, or subcutaneous

emphysema can occur from pneumomediastinum due to alveolar rupture from hyperventilation or retching. Typically, ho ever, pneumomediastinum is asymptomatic (,). =or this patient the diagnose as made from the anamnesa, physical

e:amination and laboratory e:amination. This patient had the trias that support the diagnose of diabetes (polydipsia, polyphagia and polyuria). #bout 10 hours before hospitali<ed, the child as cro ded, "usmaull respiration and keton smell. 1 day as vomited - times, concave eyes (K), the lastest

before hospitali<ed the patient

miction 0 hours before hospitali<ed, 13C aBua glass. /ince 4 days before hospitali<e malaise (K). /ince 4 eeks ago before hospitali<ed, child never getting insulin

in8ection and never check his blood sugar. 1 year before hospitali<ed the child has polydipsia, polyphagia and polyuria, the body become suffer diabetes. =rom the physical e:amination found hypotensoin, takikardi, "usmaull respiration and dyspneu, hipotermi, the signs of dehydration like dry skin, dry lips mucosa, and the concave eyes. This is as results from osmotic diuresis due to eaks and thin. 6uskesmas

hyperglycemia and hyperketonemia, hyperventilation, and vomiting as part of the primary precipitating illness or resulting from the ketosis& since dehydration is

4.

usually hyperosmolar and mostly intracellular, dehydration may be underestimated by clinical e:amination. In this patient found "ussmaull respiration. Its cause as a compensatory response to the metabolic acidosis, contributing to dehydration. In this patient is also found elevated *5; ith shift to the left is a stress response that is not helpful for diagnosing intercurrent infection.

Di66$&$ntial Dia"nos$ '<;-+;--;-/) !yperosmolar non ketotic ithout ketocis and

#t hyperosmolar coma of non ketotic happened hiperglikemia

acidosis, usually happened at type ' diabetes mellitus, because insulin still last for preventing ketosis. 6atient suffered of heavy hyperglycemia ithout a hitch

electrolyte balance and lipolisis. !igh glucose level O D.. mg 3 dl so that happened osmotik diuresis. intrasel dehydration and decreasing of plasma volume cause ide of function trouble, heavy hipotensi, stupor, comma. 2actat acidosis hen anaerob metabolism is very mounting. It is usually

2aktat acid piled up

differentiated by t o kinds of asidocis by laktat acid, first effect of tissue hypoksia by failing of circulation of blood, or systematical hipoksia. /econd because damage in renal metabolism or hepatic or because of drugs.

41

T&$atm$nt ;hildren ith ketosis and hyperglycaemia ho are not vomiting or

dehydrated may be managed as an outpatient under the supervision of the local specialist team. ;hildren ho have long duration of symptoms, any element of

confusion or a compromised circulation should be admitted to a childrenVs unit or high dependency unit here staff have considerable e:perience in treating children onset T1DM are at high risk of

ith D"#. ;hildren age less than 0 and ne

developing cerebral oedema and should be referred for consideration for treatment in an intensive care unit. The management of D"# may be considered under four headings, monitoring of condition, fluid balance, insulin therapy and electrolyte and acid3base balance (D). 5asic rules in dealing ith D"# are9 (-,1.,1') 1. #dmit patients only to a unit in hich neurologic status and vital signs can be monitored freBuently and blood glucose level measured hourly. '. 6ersonally evaluate the patient early on admission and freBuently thereafter. 4. "eep good records, including rationali<ation for decisions, and a flo sheet. 1. Develop a relationship him or her ith a pediatric diabetes specialist you trust and call hether the patient needs to be

ith any Buestions, including

transferred to a speciali<ed unit.

4'

0. The patient

ho does not have persistent vomiting,

ith a p! O-.'0, can be

treated and observed in the emergency room over a fe hours ithout hospital admission. The goals of treatment are9 (8) 7estore perfusion, hich ill increase glucose use in the periphery and reverse

1.

the progressive acidosis.

2.

/top ketogenesis by giving insulin,

hich

ill reverse proteolysis and lipolysis,

and stimulate glucose uptake and processing, normali<ing blood glucose concentration.
3. 4.

;orrect electrolyte losses. #void the complications of treatment insofar as possible, including intracerebral complications, hypoglycemia, and hypokalemia.

Fl#i! th$&a9y '/;1;2;<;-+;--) o ;an generally assume 1.+ dehydration (1.. m23kg), up to 10+ in infants.
o

6rovide '. m23kg ..,+ %a;l in first one to t o hours to restore peripheral perfusion.

In the patient as initial hydration.

ith shock or preshock give 0+ albumin, '.)'0 m23kg,

44

;alculate maintenance in usual fashion (e.g., 1,... m2 for first 1. kg K 0.. m2 for ne:t 1. kg K '. m23kg over '. kg).

;alculate remainder of replacement after the loading dose based on 1.+ dehydration, and maintenance for administration over the subseBuent '' to '4 hours.

If osmolality (calculated or measured) is O4'. mosm32, correct in 4D hours and if O41. mosm32, correct in 1C hours.

#fter initial ..,+ %a;l bolus, continue rehydration3maintenance ..10+ %a;l. /ome prefer to continue

ith

ith 7ingerAs lactate or acetate solution&

ho ever, hyperosmolar patients should be changed to ..10+ %a;l after the initial bolus of ..,+ %a;l. During rehydration the measured %a can increase to the level of the corrected %a as glycemia declines and then decline to normal levels if the corrected level as elevated.
o

6rovide " ('.)1. mmol32 or up to C. mmol32 as needed) as half ";2, half "6$1 (to replenish lo phosphate levels and to decrease the risk of hyperchloremia) or as half "6$1 and half " acetate ( hich, like lactate, is converted to bicarbonate to help correct acidosis) after serum " reported as less than D mmol32 or urine flo is established.

5icarbonate is rarely indicated. There is no evidence that bicarbonate facilitates metabolic recovery. It should be given hen there is absence of hyperventilation& never give bicarbonate by push, for this can produce dangerous

41

hypokalemia. /afe administration to avoid risk of hypokalemia is to give 1)' mmol3kg body eight or C. mmol3m' body surface area over ' hours (1.). 7educe %a;l concentration in the fluids to allo for added %a ion unless %a level in the serum is subnormal. Ins#lin '/;1;2;-+) Insulin can be started immediately at the time of the initial fluid e:pansion or it can be held until the fluid e:pansion is completed for a more realistic starting glucose level.
o

The most infusion, using a pump.

idely used system is ..1 (3kg hourly as a continuous

It may be more convenient in some settings to administer ..I (3kg II and ..1 (3kg IM ith subseBuent doses of ..1 (3kg IM or /; hourly. In adults, hether insulin as administered

there did not seem to be any difference

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

o

There is no evidence that lo )dose insulin as currently used results in any less freBuency of hypoglycemia, hypokalemia, or cerebral edema than the earlier treatment ith much higher doses. The principal advantages of lo )dose

therapy given as continuous II or hourly in8ections are that there is freBuent contact ith the patient and hourly blood glucose determinations are done.

40

During initial fluid e:pansion, a high blood glucose level may drop 1.)10 mM32, even ithout insulin infusion. !igh blood glucose levels should

drop 4)C mmol323hr (but not O 1' mmol323hr), and if they do not, the dose should be increased. This is rarely necessary.
o

*hen the blood glucose level falls to 10 mmol32 or O1' mmol323hr, 0) 1.+ de:trose should be added to the intravenous fluids.

If the blood glucose level falls belo

C mmol32

ith 1.+ de:trose

solution running, the insulin dose should be reduced to ...0 (3kg3hr.

o

Do not stop insulin or reduce it belo

...0 (3kg3hr, for a continuous

supply of insulin is needed to prevent ketosis and permit continued anabolism. Monito&in" '/;1;2;-+;--;-/) o # flo sheet is essential to record the measures noted in Table 1 at hourly intervals.
o

The nursing personnel must have clear guidelines on attending physician, such as findings listed in Table '.

hen to call the

>;E monitoring should be done and hourly potassium measurements made if the initial potassium level is M4 or OD mmol32.

Mannitol in Buantities sufficient to give 1)' g3kg body

eight should

be kept at the bedside for the first 4D hours (see belo under complications).

4D

7esist the convenience of catheteri<ation for monitoring output. The occasional older patient may have bladder atony hile ketoacidotic and reBuire

initial catheteri<ation, but it is rare to need an ind elling catheter.

o

=ailure of measured serum %a level to rise

ith falling blood glucose

concentration or an actual decrease in serum %a may indicate impending cerebral edema. !ydration should continue slo ly and ith ..,+ %a;l solution.

MONITORIN3 TREATMENT OF D:A (C,1.,11,1') Clinical Iital signs ;oma score (e.g., Elasgo ) La%o&ato&y Elucose 6otassium !ourly bedside& in the laboratory ith electrolyte assay, or 1)' hourly if outside bedside monitor range !ourly if abnormal (M4 or OD mM32) Int$&=al '.)4. minutes '.)4. minutes

/odium, potassium, ;$' or !;$4, #dmission, ', D,1., '1 hrs. venous p!, osmolality (or ')1 hourly until osmolalitv normal) 5(% "etonuria ;alcium, phosphorus (optional) Fl#i!s Type and rate Intake (include oral and reduce II intake accordingly) $utput Ins#lin (D:A 3#i!$lin$s) #dmission, 1', '1 hrs. #dmission, 11 hourly #dmission, 1', '1 hrs. 5etahydro:ybutyrate (if available) #dmission, D,1', '1 hrs.

4-

The patien have treatment $:ygen because he has dispneu, 7inger lactate 1 liters (in ' hours) to rehidration, then maintenance 11 drops3minute. Eiving insulin 1 I( every D hours, antibiotic (;efota:ime) as broad spectrum antibiotic and having DM diet.

Com9lications '/;1;4;2;<; -0)

Hypoglycemia
InfreBuent ith hourly blood glucose monitoring. *ith the presence of an ith intravenous glucose.

intravenous line, severe hypoglycemia is best treated

Elucagon can produce ketosis and nausea ith vomiting, particularly in children.

%ersistent Acidosis
Defined as persistence of a bicarbonate value less than 1. mmol32 after eight to ten hours of treatment. (sual cause is inadeBuate insulin effect, indicated by persistent hyperglycemia. ;heck insulin dilution and rate of administration, consider inadeBuate absorption if insulin is being given by subcutaneous or IM in8ection or resistance due to unusually high counter regulatory hormones, as ith concomitant febrile illness. May need to s itch to II administration if patient is not receiving insulin II. If receiving II insulin, solution should be changed every si: hours. >:tremely rare causes are lactic acidosis due to an episode of hypotension or apnea or inadeBuate renal competency in the handling of hydrogen ion as a result of an episode of renal hypoperfusion.

4C

 Hypo&alemia
>:tracellular " concentrations fall as a result of treatment, ith potassium

reentering cells. If initial serum " M4 mmol32, " must be put into the initial e:pansion fluids ithout aiting 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 freBuent complications of D"# and can occur despite adherence to the guidelines above. There is no evidence for reduction in the freBuency of intracerebral complications ith the advent of lo )dose insulin use by continuous infusion or the shift to more isotonic initial fluids. #lthough the classic picture is one of metabolic and clinical improvement ith sudden deterioration, there may be up to several hours of

decreasing sensorium and change in vital signs, as noted in Table ', and some children ill be admitted in coma and not recover. #n occasional patient ill develop intracerebral complications even before treatment, raising the suspicion of cerebral thrombosis. In more than half of patients ho develop intracerebral complications, there is a sufficient arning period to permit administration of mannitol to reduce edema and,

if indicated by respiratory distress, intubation3hyperventilation to reduce intracerebral blood flo . *hen this is accomplished before respiratory arrest, there is a greater than 0.+ chance of survival in the normal state or ith disability that does not

4,

preclude independence (l). ;omputeri<ed tomographic (;T) scans should not be depended upon to determine the need for intervention& this decision should be made on clinical grounds. Initial ;T scans, even after respiratory arrest, often appear normal or sho only locali<ed basilar edema. The dose of mannitol is 1 g3kg body

eight intravenously, over 10 minutes, repeated as necessary.6articularly susceptible to intracerebral complications are previously undiagnosed patients and children under 0 years of age. In this case, the patient didnAt get complication from D"#.

1.

Concl#sion !ave been reported a Diabetic ketoacidosis case at a boy age 14 years ho as taken care in 6ediatric departement 7/(D (lin 5an8armasin. 6atient hospitali<e cro d. 5ase on anamnesa, physical e:amination and laboratory, the patient diagnose as

ith D"#. !ave been done rehydration therapy, giving of insulin,

preventive of infection and DM diet. 6atient came home ith better condition.

11

REFERENCES

1. Dunger. ESPE(L>PES Cons$ns#s Stat$m$nt on Dia%$tic :$toaci!osis in Chil!&$n an! A!ol$sc$nt. '..0. available at http:''adc($m))ournals(com'cgi'content'full'*+','-** '. Trachtenbarg,D. Dia%$tic :$toaci!osis. #merican =amily 6hysician Illinois.'..0. #vailable at http933 .aafp.org 4. !atun, /. C$&$%&al Com9lications in Dia%$tic :$toaci!osis. The Turkish ?ournal of 6ediatrics. '..0. #vailable at http933 . t8p.dergisi.org

1. Maldonado @. :$toaci!osis. Dalam9 *ahab #./ (editor penter8emah). %elson Ilmu "esehatan #nak >disi 10 Iolume '. ?akarta9 >E;, '.... h.1.DC)-1 0. Ianelli,M. E66$cti=$n$ss o6 aP&$=$ntion P&o"&am 6o& Dia%$tic :$toaci!osis in Chil!&$n. Diabetes care volume '', 8anuary 1,,,.page -), D. !o, ?. Dia%$tic :$toaci!osis an! P$!iat&ic St&o?$. ;M#?.=ebruary 1.'..0 #vailable at http933 .;M#?.org -. #nonim. Chil!hoo! :$toaci!osis. '..0. #vailable at http933 .patient.co.uk .

C. @oung, ?. P$!iat&ics Dia%$tic :$toaci!osis.'..1. #vailable at http933 emedicine. ;om ,.

!asan 7, #latas !, ed."elainan Metabolik . Dalam 9 Buku Ilmu Kesehatan Anak .ilid ,( 5agian ="(I, ?akarta9'...9 D'1)C

1.. 7osenbloom, #. Dia%$tic :$toaci!osis 'D:A) * T&$atm$nt 3#i!$lin$s . (niversity of =lorida ;ollege of Medicine,Eainesville. '..0. #vailable at http933 . ispad. org 11. Mans8oer #, dkk. "etoasidosis Diabetik. Dalam9 :a9ita S$l$?ta :$!o?t$&an. ?ilid I >disi "etiga. ?akarta9 Media #esculapius =akultas "edokteran (I, 1,,,9 D.1)D.C. 1'. 5oedisantoso # dan /ubekti I. "omplikasi #kut Diabetes Mellitus. Dalam9 /oegondo / (ed). P$natala?sanaan Dia%$t$s M$llit#s T$&9a!#. ?akarta9 5alai 6enerbit =akultas "edokteran Indonesia (niversitas Indonesia, '..'9 1D1)1D-

1'

14. 6rice /#, *ilson 2M. Pato6isiolo"i; :ons$9 :linis P&os$s@9&os$s P$nya?it. 5uku ' >disi 1. ?akarta9 >E;, 1,,0

14

Lampiran FOLLO> 5P PENDERITA TAN33AL , O?to%$& /++. sam9ai 2 O?to%$& /++. 1 0 D /(5?>;TII> ) Dyspneu K ) ) ) Iomiting ) ) ) ) =ever ) ) ) ) Defecate ) ) ) ) (rinate K K K ) >at ) K K ) Drink K K K IIT#2 /IE% 6ulse (times3minute) 1.C CC C, 5reath (times3minute) 'D 41 41 o Temperature ( ;) 40,4D 4D,0 5ody *eight (kg) '' '' '' #//>/M>%T DI#5>TI; ">T$#;ID$/I/ 62#%%I%E II=D 72 11 K ) ) drops3minute II=D D0131 %/ 11 ) K K drops 3 minutes #ctravid In8 II 1 I(3D K K K hour ;efota:ime In8 II K K K 4:0..mg DM diet K K K D#T> ) ) ) K K K K -' '0 4D '',0 ) ) ) ) K K K -4 '0 4D,'4 C

) K K ) K

) K K ) K

) Day 1 9 II=D 72 1 liters in ' hours then 114.cc30,cc311 drops3minutes (macro)

11

10