Emergency Pediatri
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FK UNISMA
EMERGENCY PEDIATRI
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HERNIAS AND ABDOMINAL WALL
DEFECT
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Congenital/ Posterolateral Diaphragmatic HerniaCDH)
1. One of most severe conditions of neonate2. Defect in diaphragm during early fetal development3. Left side most commonly affected4. Content of the hernia:
- small bowel- colon
- spleen- stomach- liver, kidney, tail of pancreatic
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http://images.google.co.id/imgres?imgurl=http://services.epnet.com/getimage.aspx?imageiid=6883&imgrefurl=http://www.doctorsofusc.com/condition/document/222855&usg=___Es6sjY6zxBZREiMDxVpWdxABdE=&h=398&w=370&sz=105&hl=id&start=17&tbnid=uHD8lQfd6d2r5M:&tbnh=124&tbnw=115&prev=/images?q=pediatric+Diaphragmatic+Hernias&gbv=2&hl=id -
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mbryology
Week8 9division of coelomic cavity into the pleuraland peritoneal cavity by the diaphragm; a
triangular area in the posterolateral site was leftopen.
Week10 12
herniation occur through this opening into thepleural cavity at the return of midgut
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1 Hypoplasia of the lung
Pulmonary weight (ipsilateral+contralateral) Alveoli number H ypertrophy of the media of pulmonary arteriole
R esistance of the vessels
Pathophysiology
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2.Pulmonary hypertension Abdominal viscera into the thoracic cavity compression of the lungPaO2 , PaCO2 acidosis, hypoxemia
PH
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Clinical manifestations
1. Severe respiratory distress cyanosis, vomit2. Breath sounds: diminished on the side of hernia
3. Heart sounds: deviated to the contralateralchest4. Scaphoid abdomen
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Diagnosis
Prenatal diagnosis
Ultrasound : abdominal organ the fetal visibelin chest.
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After birth
X-ray film :
Typical air-filled stomach and bowels in the chest,which continues into the abdominal cavity.
Diaphram can not be seen at the affected side. Absence or scarcity of intestine in the abdominal cavity
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Treatment Before delivery: cortisone could induce the
maturation of pulmonary tissue
Preoperative preparation:
1 mechanical ventilation with pure oxygen2 nasogastric tube to decompress
stomach and intestine
3 semi-supine and inclined tothe ipsilateral side keep warm
4 i.v. fuild, correction of acidosis
(5
surgical repair
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CONGENITAL DEFECTS OFABDOMINAL WALL( Omphalocele & Gastroschizis )
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HISTORY
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A.C. Celsus ( First Century AD ) : First Report ofnewborns with Abdominal Wall Defects.Ambroise Pare ( 16 th Century ) : First descriptionof Omphalocele.Lycosthenes ( 16 th Century ) : First description ofGastrochizis.Taruffi ( 1894 ) : Introducing the termGastrochizis. Massabau & Guibal, Moore & Stokes, Bernstein
: Described specific clinical entity toAbdominal Wall defects.
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HISTORY
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Hey ( 1802 ) : First successful repair of Omphalocele.Visick ( 1873 ) : First successful repair of Gastrochizis.Ahfeld ( 1899 ) : Described painting an Omphalocelesac with Alcohol .Max Grob ( ? ) : The use of Mercurochrome.Ein & Shandling ( ? ) : The use of Semi permeableArtificial Membrane.Olhausen & Gross ( 1887 ) : The use of Skin flap after
membrane removal.Schuster ( 1967 ) : Introducing reduction of largeOmphaloceles with prosthetic material.
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ABDOMINAL WALL DEFECTS SPECTRUM
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Omphalocele ( Lateral Fold )Cephalic Fold Omphalocele( Pentalogy of Cantrell )Caudal Fold Omphalocele ( CloacalExtrophy, Vesicointestinal Fissure )GastroschizisEctopia Cordis ThoracisUmbilical Cord Hernia
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NORMAL EMBRYOLOGY
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3 Weeks gestation : the flat cellular disk ofembryo develops four folds enclose thebody cavities.Two lateral folds form the pleuroperitoneal ( PP) canal meet anteriorly in the midline. The cephalic fold will takes its place withinanterior chest wall, and also carries the SeptumTransversum continues posteriorly dividesthe PP canal into pleural and peritonealcavities.
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NORMAL EMBRYOLOGY
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The Caudal Fold brings with it thedeveloping Bladder or Allantois startedoff distal to the anus.
During the fold process, the gut tube hasformed along the length of the embryo.5 Weeks Gestation : the gut tube begin toelongate and develop within the umbilicalcoelom.10 Weeks Gestation : the gut returns from theumbilical coelom to peritoneal cavity undergoes rotation and fixation.
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NORMAL EMBRYOLOGYCEPHALO CAUDAL FOLD
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NORMAL EMBRYOLOGYCEPHALO CAUDAL FOLD
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NORMAL EMBRYOLOGYLATERAL FOLD
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OMPHALOCELE EMBRYOLOGY
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Failure of the mostly lateral body foldsto complete the journey, and defectare always at the umbilicus ( midline )
Failure of return of the gut from theumbilical coelom to peritoneal cavity.Stopped at Extra coelomic EviscerationStage
Occurs early in embryogenesis affect other organ system associated anomalies frequently.
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GASTROCHIZIS EMBRYOLOGY
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Abnormal dissolution of abdominal wallvascularization Failure of the umbilicalcoelom to develop The elongating intestinehas no space to expand, and ruptures out the
body wall.Occurs just the right side of the umbilicus Because the right side is relatively unsupported,as a result of complete abnormal dissolution of
the right umbilical vein ( at 4 weeks gestation ).
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GENETICS CONSIDERATION
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Rare reports of Abdominal wall defects, mainlyomphalocele, occuring in families and even intwins.No specific genes have been identified.
More likely to be associated withChromosomal Anomaly ( Trisomy 13, 18, or 21 ) Usually do occur as part of syndromes (Beckwith - Wiedemann, Gershoni - Baruch,Donnai Barrow, or Fryns Syndrome )
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CLINICAL FEATURES : OMPHALOCELE
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Omphalocele = Exomphalos = Amniocele =CoelosmiaThe second most common of the abdominalwall defects.Incidence : 1 2.5 / 5000 live birth.Male preponderanceUsually happened in full term baby .
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CLINICAL FEATURES : OMPHALOCELE
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Centrally Abdominal Wall defect, larger than 4cm in diameter , and always covered by atranslucent membrane from which theumbilical cord extends .
The outer membrane layer is formed byamnion, the inner layer by peritoneum, withmesenchymal tissue, called Wharton jellyamong them.
Variation in defects size. Smaller defect, betterin outcome .
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CLINICAL FEATURES : OMPHALOCELE
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Normal muscles of abdominal wall, and thesac usually contains the liver, midgut, andfrequently other organ such as spleen, orgonad .Associated with anomalies condition, such asBeckwith - Wiedemann, Prune Belly, Gershoni- Baruch, Donnai Barrow, Down, or FrynsSyndrome.
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DIFFERENT DIAGNOSIS : OMPHALOCELE
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Umbilical Hernia( The defect is covered by normal skin not amembrane. Rarely present at birth, butusually becoming apparent in the first week
or months of life )Persistent Vitelline / Omphalomesenteric Duct( There are no umbilical cord in this defect )
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CLINICAL FEATURES : GASTROCHIZIS
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Gastroschizis ( Greek ) = Belly CleftThe most common of the abdominal walldefects .Incidence : 2 5 / 10000 live birth.Male preponderanceUsually happened in premature baby, Low BirthWeight, or baby with respiratory problems. It isassociated with Intrauterine Distress, andyounger mother .
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CLINICAL FEATURES : GASTROCHIZIS
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Periumbilical ( right ) Abdominal Wall defect,less than 4 cm in diameter , with a skin bridgemay be present between umbilical cord andthe defect .
Normal muscles of abdominal walls, with nosac or remnant of a sac.Herniation of midgut, stomach, andoccasionally gonad. Liver is very rare.
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DIFFERENT DIAGNOSIS :GASTROSCHIZIS
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Rupture of Omphalocele sac( The umbilical cord is on the tip of thedefect, with is covered by rupturedmembrane )
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DEFECTS PREVIEW
Components Omphalocele GastrochizisLocation Umbilical cord Lateral ( Right ) tocord / Paraumbilical
Defect Size Large ( 2 10 cm ) Small ( 2 4 cm )
Cord Inserts in sac Normal insertion ( toleft of defect )
Abdominal Cavity Small Normal
Bowel Normal Matted, inflamed
Malrotation Present Present
GastrointestinalFunction
Normal Prolonged ileus
Associated Anomalies Common( 30 70 % )
Unusual
Outcome Good Good
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DIAGNOSTICS :ANTENATAL INTERVENTION
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Prenatal Ultrasound DetectionIrregular Bowel Contour, or Dilated bowel freein amniotic fluid adjacent to the umbilical
insertionAmniotic Fluid and Serum TestElevated AFP ( Both Maternal serum andAmniotic Fluid ), and Elevated Amniotic FluidAcH Esterase have been correlated with thisdefects ( when there is no Myelomeningocele)
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MANAGEMENT OF OMPHALOCELECONSERVATIVE / INITIAL CARE
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Maintenance of body temperature.Naso-gastric Tube insertion to keep theintestines decompressed.Ventilator support and supplementaloxygen.Intravenous fluid are provided atmaintenance rateProphylactic Antibiotics
Keep the Omphalocele sac intact, wet, andsterileCardiologic evaluation andEchocardiography are in order.
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MANAGEMENT OF OMPHALOCELESURGICAL DEFECT CLOSURE
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Primary ClosureShould be performed for small / moderatesized defect.Reduction of Abdominal contents, Incision ofOmphalocele sac, Abdominal Inspection,Mal rotation correction, and Skin Closure.
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MANAGEMENT OF OMPHALOCELESURGICAL DEFECT CLOSURE
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Delayed Primary ClosureEspecially for giant Omphalocele, with largedefect that need staged reduction of theintestinal contents by performing Silastic silo
sheeting( Extraabdominal Pouch ), with Antibiotics orSilver Sulfadiazine is applied around theedges as a dressing.
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MANAGEMENT OF GASTROSCHIZISCONSERVATIVE / INITIAL CARE
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Maintenance of body temperature.Naso-gastric Tube insertion to keep theintestines decompressed.Ventilator support and supplementaloxygen.Intravenous fluid are provided atmaintenance rate, or rehydrating rate if itsneeded.
Prophylactic Broad Spectrum AntibioticsIntestinal contents closure with Saran Wrap,Handi Wrap, or Bogotas Bag.
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COMPLICATION POSSIBILITIES
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OmphaloceleRelated with associated anomalies, Ruptureof Omphalocele sac.GastroschizisRelated with prematurity, or gastrointestinaltract anomalies, Dehydration, Hypothermia,and Sepsis
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The direct hernia protrudes through the posteriorwall of the inguinal canal, i.e., medial to deep inferiorepigastric vessels, destroying or stretching thetransversalis fascia..
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The Embryology
The indirect inguinal hernia is as follows the duct descending to the testicle is a smalloffshoot of the great peritoneal sac in thelower abdomen.During the third month of gestation, theprocessus vaginalis extends down toward thescrotum and follows the chorda gubernaculumto the scrotum.
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During the seventh month, testicle descend intothe scrotum, processus vaginalis forms acovering for the testicle and the serous sac inwhich it resides.
At about the time of birth, the portion of theprocessus vaginalis between the testicle and theabdominal cavity obliterates, leaving a peritonealcavity separate from the tunica vaginalis that
surrounds the testicle
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Incidence
Approximately 1-3% of children.
Premature babies (9-11%) is higher than full-
term (3-5%), with a dramatic risk ofincarceration (30%).
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Diagnosis
Typical patient intermittent lump or bulge inthe groin, scrotum, or labia noted at times ofincreased intra-abdominal pressure.If a loop of bowel entrapped (incarcerated),
develops pain followed by signs of intestinalobstruction.If not reduced, compromised blood supply(strangulation) leads to perforation andperitonitis.Most incarcerated hernias in children can bereduced
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Treatment
Simple high ligation of the sac
Elective herniorrhaphy is treatment of choice.
Risk of incarceration, repair should be undertakenshortly after diagnosis.
Pediatric patients are allowed to return to full activityimmediately after hernia repair .
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Patients presenting with incarceration should havean attempt at reduction (possible in greater than 98%with experience), and then admission for repairduring that hospitalization.
Bilateral exploration is done routinely by mostexperienced pediatric surgeons.
Recently the use of groin laparoscopy through thehernial sac permits visualization of the contralateral
side.
H d l
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Hydroceles
A hydrocele is a collection of fluid in the spacesurrounding the testicle between the layers of the
tunica vaginalis.
Hydroceles can be scrotal, of the cord, abdominal, ora combination of the above.
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A hydrocele of the cord is the fluid-filled remnant ofthe processus vaginalis separated from the tunicavaginalis.
A communicating hydrocele is one thatcommunicates with the peritoneal cavity by way of anarrow opening into a hernial sac.
Some are associated with an inguinal hernia. They
are often bilateral, and like hernias, are morecommon on the right than the left.
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Hydrocele noncommunican Hydrocele communican
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Most hydroceles will resolved spontaneously by 1-2years of age.
After this time, elective repair can be performed atany time.
Operation is done through the groin and searchmade for an associated hernia.
Aspiration of a hydrocele should never beattempted.
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INVAGINASI
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INVAGINASIIntusussepsi atau Invaginasi sering terjadi
pada bayi dan anak, dimana satu segmen ususmengalami konstriksi oleh gelombangperistaltik dan tiba tiba masuk ke dalam
segmen distalnya ( Dayal dan DeLellis ,1989). Ujung usus yang masuk : intussuseptum Bagian usus yang menerima : intussussepiensIntussussepsi pertamakali dipublikasikan olehPaul Baebette pada pertengahan abad ke 17,
Salah satu sebab obstruksi usus
Tindakan pembedahan
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Invaginasi usus ini akan diikuti oleh mesenterium yang
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Invaginasi usus ini akan diikuti oleh mesenterium yangberisi pembuluh darah, kelenjar limfe, saraf sertalemak dibelakangnya.
Terjadi strangulasi pembuluh darah dan limfeEdema jaringan usus,Jaringan mukosa membengkak berisi darahdan mukus produksi sel goblet.
Red Current Yelly Stools .
Lebih lanjut darah dan mukus masuk kedalam lumen keluar bersama feses,sehingga feses merah dan berlendir
Jika keadaan ini berlanjut dapat terjadi nekrosis
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Jika keadaan ini berlanjut dapat terjadi nekrosisdan gangren usus (Ong dan Beasley, 1990 ;Spitz,1990 ).Pada Invaginasi terjadi :
cedera vasa mesenterika, pertumbuhan bakteri berlebihan,
malabsorbsi, translokasi kuman ( Spitz, 1990 ).
Semua keadaan ini perlu dipertimbangkan pada
penanganan kasus invaginasi.Keterlambatan diagnosis penatalaksanaanpenderita berbeda satu dengan yang lain disertairesiko kematian menjadi besar.
SEJARAH
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Abad ke 17, Paul Barbatte dari amsterdam menulis
tentang intussussepsi dan dapat direduksi secaraoperatif.
Tahun 1876 Hirschprung dari copenhagen telah
mempublikasikan beberapa laporan mengenaireduksi intussussepsi dengan menggunakantekanan hidrostatis. Hasilnya mempunyaikeunggulan dibanding terapi operatif selama 70tahun berikutnya.
SEJARAH
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INSIDENSI
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Laki-laki dan perempuan 3 : 2.
Kasus intussussepsi terjadi dibawah umur 1 tahun
sebesar 65 %,
Jumlah yang terbanyak ditemukan pada usia 5-9 bl( Mark, 1979 ).
INSIDENSI
I i d di k b d k
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Intussussepsi dapat ditentukan berdasarkan :
a. Atas dasar perjalanan penyakitnya:Gibson, Dockerty dan Dixonmembagi dalam 3 macam :
1. Akut : gejala-gejala terjadi kurang dari1 minggu2. Sub akut : gejala-gejala terjadi antara 1-2
minggu
3. Kronik : gejala-gejala yang sudah berlangsung lebih 2 minggu.
b A d il j l
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b. Atas dasar penampilan gejala :Sven Berghdahl at al, membagi intussussepsi menjadi2 macam :1. Intussussepsi yang typis, yakni intussussepsi
dengan gejala yang khas yang mudahdikenal antara lain muntah-muntah, nyeri perut,
massa abdomen dan perdarahan perectal.2. Intussussepsi yang atypis, golongan inimenampakkan gejala-gejala yang bervariasi darigambaran diatas, sehingga kadang kadang
terlambat didiagnosa. Golongan ini baik denganoperatif maupun dengan ba-enema mudahtereduser secara spontan, terdapat lesi spesifik,mudah rekurens dan sering menjadi kronis.
c. Klasifikasi atas dasar lokalisasi :
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Ellis menggolongkan intussussepsi dalam :1. Enteric : adalah intussussepsi usus kecil ke
usus kecil.2. Colic : adalah invaginasi colon ke colon
(colo-colic)..
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4. Multiple intussussepsi dan retrograde
5. Appendicular ( jarang )6. Gastroduodenal.
7. Yeyunogastrik.
Insiden tertinggi intussussepsi adalah type :enterocolic/ileosekalis,
Mencapai 95 % dari kasus ( Mark, 1979 ).
A
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PENYEBAB
Pada anak-anak: Umumnya tak diketahuipenyebabnya sehingga ada yang menggolongkanidiopatik atau primer.
Orloff meneliti dari 1424 kasus pada anak:95 % kausa tak diketahui5 % divertikel Meckels, polip, duplikasi usus.
F kt b b d i l idi tik i i t
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Faktor pemyebab dari golongan idiopatik ini antaralain:
Motilitas coecum yang berlebihan,
Perkembangan usus besar yang lebih cepat dari
usus kecil selama masa kanak-kanak
Pembesaran lymphe follikel ileum distal
Lymphadenitis mesenterial
Pada orang dewasa : Kebanyakan disebabkan oleh lesi
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Pada orang dewasa : Kebanyakan disebabkan oleh lesiorganis (pada umumnya tumor), tapi tidak berartikasus idiopatik tidak ada. Donhauser dan Kellymengemukakan penyebab intussussepsi orang dewasaseperti tabel dibawah ini :
Jenis lesi Jumlah %
Neoplasma benigna 213 44 %Neoplasma maligna 123 26 %
Divertikel Meckels 53 9 %Gastroenteeeerostomy 27 6 %Ulcus usus 13 3 %Tidak diketahui 59 12 %
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Dasar : - anamnesa yang baik- pemeriksaan fisisk yang cermat- penunjang : radiologi dan USG
Anamnesis : - Anak sehat , menangis, serangan
nyeri perut (sifat kolik), gelisah
- Bayi . nyeri perut mungkin tak nyata. pendiam. muntah. pucat dan berkeringat
- Anak >2 th keluhan nyeri perut
lebih jelas
DIAGNOSIS
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Pemeriksaan fisik
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Stadium dini : fungsi vital masih baik 6-8 jam setelah serangan sakit pertama :
Bila perut makin kembung :Muntah Dehidrasi Demam Takicardi
bakteremia
Bila perut tak kembung:Palpasi dinding abdomen : Dinding abdomensupel, tidak nyeri tekan. teraba massa berbentuklonjong sosis sign
Dance sign : pada perut kanan bawah terabakosong karena sekum dan colon ascenden bergerak
keatas mengikuti proses invaginasi
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RADIOLOGI
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Plain foto abdomen : Gambaran obstruksi saluran cerna
Distribusi udara yang tidak merata
Perselubungan pada daerah perut kanan bawah,
tengah dan atas
Udara hanya menempati perut kiri atas Pada keadaan lanjut tanda obstruksi berupa
multiple air fluid level
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Barium enema
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Barium enema
Untuk diagnosis sekaligus terapiGambaran foto radiologis Gambaran obstruksi , aliran barium terhenti
pada daerah distal invaginasi
Suatu gambaran berbentuk mangkok padabarium yang terhenti ( Cupping appeareance)
Gambaran yang berbentuk lingkaran pir, daribarium yang terdifusi diantara celah invaginasi(coil spring appearance)
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Ultrasonografi
Pada potongan longitudinal tampak masaberbentuk tubulerPada potongan melintang tampak gambarantarget appearance atau doughnut appearance
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Terapi
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psebelum dilakukan tindakan definitif
1. resusitasi2. Pasang NGT3. Pasang kateter4. Periksa lab darah5. persiapan donor darah untuk transfusi6. injeksi antibiotik
Pembedahan dapat dilakukan bila :
1. Produksi urin 0,5-1 ml/kgBB/jam2. suhu tubuh < 38 o C3. nadi < 120 kali/menit4. RR < 40 kali/menit
5. kesadaran baik
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CARA PENGELOLAAN
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1. Tanpa operasi :
Reduksi dengan barium enema, untuk mengerjakatindakan ini kamar operasi harus disiapkan, bila terjadikegagalan reposisi langsung dikerjakan operasi
Indikasi: semua kasus kecuali ada kontra indikasiKontra indikasi:
1. Strangulasi2. KU jelek3. Demam tinggi4. Dehidrasi5. Perforasi
6. Intussusepsi yang rekuren
Keuntungan:
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1. terhindarnya dari stress operasi2. terhindarnya bahaya adesi dan strangulasi dikemudian
hari
Komplikasi :1. perforasi kolon2. kolon yang tereduksi mungkin tidak viable lagi
Peni laian keberhasilan reduksi :a. terjadi pembebasan dari intussusepsib. terlihat cairan barium masuk kedalam ileum terminalc. adanya flatus bersama keluarnya cairan barium
bersama feses
d. tidak ditemukanya lagi massa di abdomen
2 D i
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2. Dengan operasi
Laparotomi Eksplorasi Irisan tranversal diatas/dibawah umbilikus Reduksi dikerjakan dengan manual, distal
intussusepsi dilakukan milking dengan udara usus
sebagai pendorong Bila terjadi reposisi nilai viabilitas usus, bila usus
nekrosis lakukan reseksi dan anatomose end to endbila kondisi memungkinkan
Bila reduksi gagal lakukan reseksi dan anastomoseend to end
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Duodenal Atresia
Incidence--1 in 5,000 to 10,000 livebirths
75% of stenoses and 40% of atresias arefound in DuodenumMultiple atresias in 15% of cases
50% pts are LBW and prematurePolyhydramnios in 75%Bilious emesis usually present
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Duodenal Atresia Cont
Associated AnomaliesDowns (30%)
MalrotationCongenital Heart DiseaseEsophageal Atresia
Urinary Tract Malformations Anorectal malformationsVACTERL
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Duodenal Atresia Diagnosis
RadiographsDouble -Bubble
Pyloric dimple sign Absence of beak sign seen in pyloricobstruction
Workup of potential associatedanomaliesECHO, abd US, possible VCUG
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Double Bubble
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Small Bowel Atresia
Jejunal is most common, about 1 per2,000 live births
Atresia due to in-utero occlusion of all orpart of the blood supply to the bowelClassification--Types I-IV
Presents w/bilious emesis, abddistension, failure to pass meconium(70%)
Intestinal Atresia Classification
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Intestinal Atresia Classification
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Small Bowel Atresia Cont
Associated Anomaliesother atresias
Hirschsprungs Biliary atresiapolysplenia syndrome (situs inversus,cardiac anomalies, atresias)CF (10%)
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Malrotation
1 per 6,000 live birthscan be asymptomatic throughout lifeUsually presents in first 6 months of life18% children w/short gut had malrotation withvolvulusEtiology
physiologic umbilical hernia--4th wk gestationReduction of hernia 10th - 12th wks of gestation
Normal Embryology
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Normal Embryology
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Malrotation Classification
Nonrotationwhen neither duodenojejunal or cecocolic
limbs undergo correct rotation Abn Rotation of Duodenojejunal limb
causes Ladds bands to form acrossduodenum
Abn rotation of Cecocolic limbcecum lies close to midline, narrowmesenteric base
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Abnormal Rotation/Fixation
l
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Malrotation Diagnosis
Varying symptoms from very mild tocatastrophic**Bilious emesis is Volvulus until provenotherwise**Bilious emesis, bloody diarrhea, abddistension, lethargy, shockUGI shows abnormal position ofDuodenum
if Volvulus, see birds beak in duodenum
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Malrotation UGI
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Malrotation--Treatment
Surgical-- Ladds Procedure Evisceration
Untwisting of volvulus (counterclockwise)Division of Ladds Bands Widening mesenteric base
Relief of Duodenal obstruction Appendectomy
Recurrence 10% after Ladds
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Common Disorders
NEC Duodenal Atresia
Small Bowel AtresiaMalrotationHirschsprungs
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Hirschsprungs Disease
Migratory failure of neural crest cellsIncidence 1 in 5,000 live births, males
affected 4:1 over females90% of pts w/Hsprungs fail to passmeconium in first 24-48 hrs
Abd distension, bilious emesis,obstructive enterocolitis
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Transition Zone on BE
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Transition Zone on BE
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Hirschsprungs Treatment
In neonates, can do primary pull-through--bringing normal colon down to
anorectal junctionIn older infants, may need divertingcolostomy first to decompress
May need prolonged dilatations andirrigations
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