Presentasi Kasus Anak Akbar Fix
Transcript of Presentasi Kasus Anak Akbar Fix
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Preceptor:
dr. Ulynar Marpaung, Sp.A
Presenter:
R.M.Affandi Akbar
(1102011216)Pediatric Department
Raden Said Soekanto Hospital
Yarsi Medical University
Periode Desember 2!" # $ebr%ari 2!&
Case Presentation
Acute
Glomerulonephritis
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IdentityPatient
• Nae ! S"• #irt$ date ! %anuary 2 t$ 2011•
Age ! & years old• 'ender ! Male• Adresss ! apung Maassar • Nationality ! Indonesia• "eligion ! Mosle• *ate o+ adission ! %anuary t$ 2016
• *ate o+ e-aination! %anuary 10t$ 2016
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Parents Identity$at'er Mot'er
Nae Mr. " Mrs. N
Age / years old years old
%o Cleaning Serie 3ouse4i+e
Nationality Indonesia Indonesia
"eligion Mosle Mosle
5duation 3ig$ s$ool
(graduate)
3ig$ s$ool
(graduate)
Address %l. 'g. 3.i$an "7.080& apung
Maassar
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Ananesis
7$e ananesis 4as taen on (an%ary !t' 2!&, yalloananesis (+ro patient9s ot$er andgrandot$er).
S4ollen +ae sine & days e+ore adission to t$e $ospital.
:eer, s$ortness o+ reat$, reddis$ urine.
)'ief complain
Additional complain
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3istory o+ Present Illness
A & years old oy ae to "aden Said SuantoPolie Center 3ospital su++ering +ro s*ollen face
since five days e+ore adission to t$e $ospital.
7$is oplains also +ollo4ed y interitten +eert$at eer rea$ noral teperature sine ; days
e+ore adission, patient also +eeling s$ortness o+
reat$ sine $e roug$t to t$e $ospital.
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3istory o+ Present Illness (2)
Patient
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3istory o+ Present Illness (/)
:or t$e lood test results in eergenyroo (t$ %anuary 2016) are Hb +,- /dl,
leuoytes .00 u8l, 'ematocrit 2&0 andtrombocytes "-./%l.=n t$e days o+ $ospital adission, patient
ondition 4as opos entis, s4ollen +ae
still e-ist, and $e got s$ortness o+ reat$.
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3istory o+ Present Illness (6)
2 4ees
e+oreadission
S*allo*indiffic%lty
; days e+oreadission
1ntermittentfever
& dayse+ore
adission
Patient9sface *as
s*ollen and$is %rinet%rn reddis'
On
Admission
Swollenface,Breathless
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3istory o+ Past Illness
P'arynitis
Bronchitis -
Pneumonia - Morbili +
Pertussis -
Varicella +
Diphteria - Malaria -
Polio -
Enteritis -
3acillary dysentry 4
Amoeba dysentry -
Diarrhea +Thyphoid -
Worms -
Surery -
Brain concussion -
!racture -
Dru reaction -
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Allergi 3istory
• 7$e patient didn
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3irt' History
Mot'er5s prenancy 'istory
7$e ot$er routinely $eed $er pregnany to t$e $ospital. S$e
denied any prole noted during pregnany.
)'ild5s birt' 'istory•aor ! Cipto Mangun usuo 3ospital•#irt$ attendants ! *otor •Mode o+ deliery ! Peragina•'estation ! > 4ee•In+ant state ! 3ealt$y
•#irt$ 4eig$t ! 200 gras•#ody lengt$ ! /0
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Development History
:irst dentition ! 6 ont$s
Psycomotor development
? 3ead up ! 1 ont$ old? Sile ! 1 ont$? aug$ing ! 1@2 ont$ old? Slant ! 2,& ont$ old? Spee$ initiation ! & ont$ old
? Prone podition ! & ont$ old
? Prone position ! & ont$old? Sitting ! 6 ont$ old? Cra4ling ! > ont$ old? Standing ! 1 years old
? aling ! 1 years old
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$amily History
7$ere are no signi+iantillness or $roni illness
in t$e +aily delared.
History of Disease
in
t'er $amilyMember
7$ere is no one liingaround t$eir $oe no4n
+or $aing sae
ondition as t$e patient.
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Social and 6conomic History
• Patient lied at $ouse 4it$ siBe 20 - 10 toget$er 4it$
parents and a rot$er
• 7$ere 1 door at t$e +ront side,1 toilet near t$e it$en and
edroos, t$ere are / 4indo4s. 7$e 4indo4s are oasionally
opened during t$e day
• 3ygiene
✓ 7$e patient9s ot$er $anges $is lot$es eeryday 4it$ leanlot$es.
✓ #ed s$eets $anged eery t4o 4ees.
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PHYS1)A; 6 (A=UARY !t' 2!&?
@eneral stat%s• 'eneral ondition ! Mild ill
• A4areness ! Copos entis• Pulse ! 112 -8in, regular, +ull,
strong
• #reat$ing rate ! 0 -8in
• 7eperature ! 6,6 0C
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Antropometry Stat%seig$t ! 1; g
3eig$t ! 10&
=%tritional stat%s based =)HS
2
>=ational )enter for Healt'
Statistic? year 2
:A (eig$t +or Age)
1;81> - 100 D /
3:A (3eig$t +or Age)
10&8110 -100 D &
Conclusion: The patient has good
nutritional status.
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Head 9oe 6amination
• HeadNoroep$aly, $air (la, noral distriution, noteasily reoed) sign o+ traua (@)
• 6yes
Iteri slera @8@, pale onEutia @8@, lariation @8@,s4ollen eyes F8F, pupils 8 isoor, diretand indiret lig$t response FF8FF.
• 6ars
Noral s$ape, no 4ound, no leeding, seretion orseruen @8@
• =oseNoral s$ape, idline septu, seretion @8@
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Mo%t'
• ips ! Moist
• Muous ! Moist
• 7ongue ! Not dirty• 7onsils ! 71871, no $ypereia
• P$aryn- ! No $ypereia
=eck
• yp$ node enlargeent (@), sro+ulodera (@).
Head 9oe 6amination >2?
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9'ora
• Inspetion ! syetri 4$en reat$ing, retration (F),
itus ordis is not isile.
• Palpation ! ass (@), tatile +reitus F8F
• Perussion ! sonor on ot$ lungs
• Ausultation
Cor ! regular S1@S2, urur (@), gallop (@)Pulo ! esiular F8F, 4$eeBing @8@, rony F8F
Head 9oe 6amination >B?
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Abdomen
• Inspetion ! Cone-, epigastri retration (@), t$ere is
no 4idening o+ t$e eins, no spider nei.• Palpation! supple, lier and spleen not palpale, +luid
4ae (@), adoinal ass (@)
• Perussion! 7$e entire +ield o+ typani adoen,
s$i+ting dullness (@)
• Ausultation! noral o4el sound, ruit (@)
Head 9oe 6amination >C?
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•ertebra
7$ere does not appear soliosis, yp$osis, and lordosis,
do not loo any ass along t$e line o+ t$e erteral•6tremities
ar,apillary re+ill tie G 2 seonds, edea(F)
•Skin
Noral turgor
Head 9oe 6amination >"?
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=e%roloical 6amination
Meningeal sign
Nu$al rigidity @
ernig sign @
asegue sign @
#rudBinsi 1 @
#rudinsi 2 @
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Motori 5-aination
Po4er
3and
:eet
& & & &8 & & & &
& & & &8 & & & &
7onus
3and
:eet
Norotonus 8 Norotonus
Norotonus 8 Norotonus
7rop$y
3and
:eet
Norotrop$y 8 Norotrop$y
Norotrop$y 8 Norotrop$y
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P$ysiologi "e+le-
Upper e-triities
#ieps
7rieps
o4er e-triities
Patella
A$illes
F 8 F
F 8 F
F 8 F
F 8 F
Motoric 6amination >2?
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Pat$ologi "e+le-
Upper e-triities
3o++an
7roer
o4er e-triities
#ainsy
C$addo
=ppen$ei
'ordon
S$ae++er
@ 8 @
@ 8 @
@ 8 @
@ 8 @
@ 8 @
@ 8 @
@ 8 @
Motori 5-aination ()
Clonus
Patella
A$illes
@ 8 @
@ 8 @
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*e+eation
Urination S4eating
Noral ( 1@2 ties daily)
Noral ( /@& ties daily ) Noral
A%tonom 6amination
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Laboratory Investigation
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oring *iagnosis
• Suspet Aute 'loerulonep$ritis
*d8 Nep$roti syndroe
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Manageent
•=2 1,& 8
• IH:* " ;dp
• InE. Ce+ota-ie 2 - ;&0 g i..
• InE. asi- 2 - ;,& g i..
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• uo ad ita ! duia ad ona
•uo ad +untiona ! duia ad ona
• uo ad sanationa ! duia ad ona
Pronosis
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$;;E UP
(A=UARY !9H
2!& #(A=UARY !"9H 2!&
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$;;E UP >!4!4!&?
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$;;E UP >!!4!4!&?
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$;;E UP >!B4!4!&?
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$;;E UP >!C4!4!&?
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$;;E UP >!"4!4!&?
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Acute Glomerulonephritis
iterature "eie4
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*e+inition
Aute gloerulonep$ritis ('N) oprises a
spei+i set o+ renal diseases in 4$i$ an
iunologi e$anis triggers in+laation
and proli+eration o+ gloerular tissue t$at an
result in daage to t$e aseent erane,
esangiu, or apillary endot$eliu.
Aute poststreptooal gloerulonep$ritis
(PS'N) is t$e ar$etype o+ aute 'N.
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5pideiology
In deeloping ountries APS'N, usually ours in c'ildren,
predoinately males and o+ten as epideis. Sporadi APS'N
follo*in %pper respiratory tract infection, p'arynitis, and
tonsillitis is ore oon in 4inter and spring in teperateareas, 4$ereas sin in+etions are oonly +ound to preede
APS'N in t$e ore tropial and sutropial areas, 4it$ a pea
inidene during suer and autun. Postin+etious 'N an
our at any age ut usually deelops in $ildren. Most ases
our in patients aged &@1& yearsJ only 10 our in patients older
t$an /0 years.
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5tiology•
In+etious
Streptococcus speies (ie, group A, eta@$eolyti).
Usually deelops 1@ 4ees a+ter in+etion. 74o types
$ae een desried, inoling di++erent serotypes!? Serotype 12 @ due to an upper respiratory in+etion
? Serotype / @ due to a sin in+etion7$e inidene o+ 'N is appro-iately &@10 in persons 4it$
p$aryngitis and 2& in t$ose 4it$ sin in+etions
Nonstreptooal postin+etious 'N ay also result +ro
in+etion y ot$er ateria, iruses, parasites, or +ungi.
? Non@in+etious
Mig$t e primary renal diseases or systemic diseases
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PA73='5N5SIS
• Glomerular injury may be result of : genetic, immunologic ,
perfusion, or coagulation disorder.
• Immunologic injury to the glomerulus results in
glomerulonephritis .• Evidence that glomerulonephritis is caused by immunologic
injury includes morphologic and immunopathologic
similarities to experimental immunemediated
glomerulonephritis! the demonstration of immune reactants"immunoglobulin, complement# in glomeruli! abnormalities in
serum complement! and the $nding of autoantibodies in
some of these diseases .
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Clinial Mani+estation
5dea
3ypertension
3eaturia
%. &ematuria: the classicdescription of tea or colacolored urine occurs inapproximately '()*+ ofpatients
'. Edema: Edema usuallyappears abruptly and $rstinvolves the periorbital area,but it may be generali-ed
. &ypertension : &ypertension
occurs in approximately /+)0+ of cases . 1erebralcomplications of hypertensionincluding headaches, sei-ures,mental status changes, and
visual changes occur in +)
RIAD OF POST-STREPTOCOCCAL GN
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*iagnosis
1. Ananesis2. P$ysial e-aination
. aoratory +indings
?. Urinalysis ! "#C asts, proteinuria, PMN leuoytes
?. ':" is o+ten dereased during aute p$ase o+ t$e
disease
?. Serologial arers ! AS= titer and depression o+
leel.?. "enal iopsy
*i++erential *iagnosis
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*i++erential *iagnosis
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7reatent
? 2reatment remains largely supportive and usually
addresses the most urgen problem hypertension.
? 2he importance of supportive therapies in acute
glomerulonephritis can not be over emphasised. 2ight
blood pressure control, appropriate use of diuretics, and
control hyper3alemia, uraemia, and 4uid overload, if
necessary by dialysis, are 5uite literally life saving.
? In most cases of poststreptococcal glomerulonephritis6here in4ammation does resolve spontaneously,
supportive therapies alone 6ill be su7cient 6ith
improved renal function being seen bet6een four and
%8 days after the initial acute failure in 0( of patient.
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1. *iet and atiity
• 9 lo6sodium, lo6protein diet should be prescribed
during the acute phase, 6hen edema and
hypertension are in evidence.
•imitation of 4uid and salt inta3e is recommended inthe child 6ho has either oliguria or edema.
• ;otassium inta3e should be restricted to prevent
hyper3alemia.
• imited activity is probably indicated during the early
phase of the disease, particularly if hypertension is
present.
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2. In Patient Manageent
• Severe Hypertension
Seere $ypertension, or t$at assoiated 4it$ signs o+ ereral
dys+untion, deands iediate attention. 7$ree drugs are
oonly ited as $aing a $ig$ ene+it@to@ris ratio!
1. aetalol (0.&@2 g8g8$ intraenously KIHL),
2. *iaBo-ide, and
. Adnitroprusside (0.&@2 g8g8in IH)
Seere $ypertension 4it$out enep$alopat$y
1. $ydralaBine or ni+edipin
• Mild4to4moderate 'ypertension
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yp
1. #edrest, +luid restrition.
2. 7$e use o+ loop diuretis, su$ as +uroseide (1@ g8g8d oral KP=L,
ad+linistered 1@2 ties daily), ay $asten resolution o+ t$e
$ypertension.
•. 6dema
1. "estrition o+ +luids
2. oop diuretis (+uroseide).
. I+ ongestion is ared, adinister +uroseide parenterally (2
g8g).
•. An%ria or oli%ria
#eause t$ey ay e ototo-i, aoid large doses o+ +uroseide in$ildren 4it$ syptos o+ anuria or seere and persistent oliguria. In
addition, osoti diuretis, su$ as annitol, are ontraindiated, as
t$ey ig$t inrease asular olue.
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. ong@7er Monitoring
• ong@ter +ollo4@up +or a patient +ollo4ing aute
poststreptooal gloerulonep$ritis (APS'N) priarily
onsists o+ lood pressure easureents and urine
e-ainations +or protein and lood
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Copliation
• &ypertensive encephalopathy.
• ;rolonged hypertension can lead tointracranial bleeding.
• =ther potential complications include heartfailure, hyper3alemia, hyperphosphatemia,hypocalcemia, acidosis,sei-ures, and uremia.
• 9cute renal failure
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GGG 7ae 3oe Messages
• Aute 'loerulonep$ritis is spei+i set o+ renal diseases in
4$i$ an iunologi e$anis triggers in+laation
and proli+eration o+ gloerular tissue t$at an result in
daage to t$e aseent erane, esangiu, or
apillary endot$eliu.
• 7$e ost oon in+etious ause o+ aute 'N is in+etion
y Streptococcus speies (group A, eta@$eolyti)
• 7riad o+ A'N ! 5dea, 3eaturia, and 3ypertension
• 7$e treatent is supportie. >upportive therapies alone
6ill be su7cient 6ith improved renal function being
seen bet6een 8 and %8 days after the initial acute
phase in 0( of patient.
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7$an ou
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"5:5"5NC5S
• liegan, ". and Nelson, . (200;). Nelson textbook of pediatrics. P$iladelp$ia! Saunders.
• 3all, %. and 'uyton, A. (2006). Guyton & Hall physiology review . P$iladelp$ia! 5lseier
Saunders.
• uar, H., Aas, A., :austo, N. and Aster, %. (201/). Robbins and Cotran Pathologic asis
of !isease" Professional #dition. ondon! 5lseier 3ealt$ Sienes.• 7ortora, '. and 'rao4si, S. (200). Principles of anato$y and physiology . Ne4 or!
iley.
• Han*eHoorde, ". (201&). Aute Poststreptooal 'loerulonep$ritis! 7$e Most Coon
Aute 'loerulonep$ritis. Pediatrics in Review , 6(1), pp.@1.
• 5ison, 7., Ault, #., %ones, *., C$esney, ". and yatt, ". (2010). Post@streptooal aute
gloerulonep$ritis in $ildren! linial +eatures and pat$ogenesis. Pediatric Nephrology ,
26(2), pp.16&@1>0.
• Martin, %., aul, A. and S$a$t, ". (2012). Aute Poststreptooal 'loerulonep$ritis! A
Mani+estation o+ Iune "eonstitution In+laatory Syndroe. P#!%'R%CS, 10(),
pp.e;10@e;1.
• Hinen, C. (201). Aute gloerulonep$ritis. Postgraduate (edical )ournal , ;(0), pp.206@
21.
•