Ilmu Bedah

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CLEFT PALATE
Dr. Mgs. Roni Saleh, SpB-SpBP(K)

I. Normal Anatomy
A. Hard palate
1. Primary (anterior) hard palate: Formed by fusion of the
bilateral palatine processes of the maxilla.
2. Secondary (posterior) hard palate: Formed by fusion of the
bilateral horizontal plates of the palatine bone.
3. Incisive foramen: Separates the primary from the secondary
hard palate.
4. Premaxilla: The maxilla anterior to the incisive foramen,
including the anterior hard palate and alveolus.
B. Soft palate (velum): contains the muscles involved in
velopharyngeal closure.
1. Levator veli palatini.
2. Tendon of the tensor veli palatini.
3. Palatopharyngeus.
4. Uvulate.
C. Vascular and nerve supply
1. Hard palate: The greater palatine artery and nerves, through
the greater platine foramen in the posterior lateral hard
palate.
2. Soft palate: The lesser palatine artery and nerves.

II. Cleft Anatomy
A. Clefts of the secondary palate
1. A variable degree of clefting can be seen.
a. Bifid uvula.
b. Submucous cleft palate triad.
1) Bifid uvula.
2) Hard palate notching (palpable).
3) Zona pellucida: Midline white line, due to the
anomalous insertion of the palatal musculature.
c. Cleft velum
d. Cleft of the entire secondary palate
2. Anomalous inseretion of the tensor veli palatini.
a. The normal bilateral tensor veli palatini muscles
interdigitate and insert transversely in the posterior
part of the velum

b. With clefting, the tensor veli palatini muscles course
anteriorly and insert onto the posterior edge of the
hard palate.
c. In this position, their ability to lift the soft palate is
significantly impaired
B. Clefts of the primary palate.
1. The lip, nostril sill, alveouls, and primary palate are all
considered derivatives of the primary palate.
2. Clefts of the primary palate can involve the lip alone, extend
into or through the alveolus and primary palate, or extend
through the secondary palate.
C. Kernahans striped Y serves as a shorthand for recording cleft
palate extent.

III. Facial Embryology
A. Five facial prominences (develop during week 4 of gestation)
1. Midline frontonasal prominence: Mesenchyme ventral the
forebrain, not a branchial arch.
2. Bilateral maxillary prominences: First branchial arch.
3. Bilateral mandibular prominences: First branchial arch.
B. Bilateral nasal placodes
1. Appear on the inferior frontonasal prominence, late in week
4.
2. The medial and lateral nasal prominences emerge on each
side of the nasal placodes.
C. Fusion: week 5
1. The lateral nasal prominence fuses with the maxillary
prominence, connecting the nose to the cheek.
2. The medial nasal prominence fuse.
3. The medial nasal prominence fuses with the maxillary
prominence, connecting the nose and lip. Failure of the
fusion results in a cleft lip.

IV. Palatal embryology
A. Primary palate and premaxilla
1. The medial nasal proceses fuse to form the median palatine
process in week 5.
2. The median palatine process becomes the premaxilla.
B. Secondary palate: weeks 5 to 12
1. The bilateral lateral palatine processes develop from the
medial portion of the maxillary process.
2. The lateral palatine processes hang vertically, and then lift
horizontally as the tongue drops.

3. Fusion stars at the incisive foramen and moves posteriorly,
forming the secondary palate.

V. Epidemiology
A. Racial distribution
1. Isolated cleft palate
a. Incidence of about 0.5 per 1,000 births.
b. Does not vary with race.
2. Cleft lip with or without cleft palate
a. Asians: 2 per 1,000 births.
b. Whites: 1 per 1,000 births
c. Blacks: 0.4 per 1,000 births
B. Gender distribution
1. Isolated cleft palate is more common in females.
2. Cleft lip with cleft palate is more
C. Familial distribution
1. Cleft lip with or without cleft palate and isolated cleft palate
appear to be genetically different
2. Isolated cleft palate is more common in relatives of cleft
palate patients.
3. Cleft lip/palate is more common in relatives of cleft lip /
palate patients
Table 24-1. Probability of subsequent children with isolated cleft palate
or cleft lip with / without cleft palate

Family members with Probability of subsequent Probability of subsequent
Cleft Palate Child with cleft palate (%) Child with cleft lip +/-
Cleft Palate (%)
One affected child only 2 4
One affected parent only 2-4 2-4
One affected child and a
Positive family history 7-0 7
( with normal parents )
One affected parent and
One affected child 15 14-17

VI. Etiology
A. Genetics
1. An isolated cleft palate is probabaly a single major gene
autosomal recessive trait with other minor genes contributing
2. Cleft lip/palate is probably polygenic with multiple major
and minor genes contributing

B. Environment
1. The exact role of anny environment factor is not clear
2. Alcohol has not been conclusively shown to cause isolated
cleft palate
3. Smoking : Data are not conclusive
4. Many teratogens ( including alcohol, isotretinoin and others )
are known to cause multiple congenital malformations,
which may include cleft palate as part of a series of
malformations
5. Folic acid and vitamn B6 intake during pregnancy may
reduce cleft lp / palate

VII. Surgical goals
A. Closure of the cleft
1. Closure of the cleft palate separates the oral and nasal
cavities
2. This prevents aerophagia and reflux of oral contens into the
nasal cavity
B. Speech and hearing
1. Cleft palate repair must be performed early in life to prevent
irreparable speech defects
2. However,early palate surgery is associated with impaired
facial growth
3. Because facial structures can be surgically repaired later in
life, whereas speech patterns cannot, most surgeons feel that
normal speech development is more important than normal
facial growth and therefore favor early repair.
C. Otitis and Hearing
1. Otitis media
A. Secondary to eustachian tube dysfunction
A. The levator veli palatini ( LVP) originates along
the eustachian tube
B. An abnormal LVP insertion is thought to
decrease milking action and therefore lead to
poor venting of the middle ear.
B. Occurs in almost all patients with cleft palate, and can
lead to permanently impaired hearing
2. Hearling in cleft palte patients generally improves after
myringotomy
3. The earliner the myringotomy is performed the greather the
improvement is hearing. Normal hearing is usually achieved
with early bilateral tympanostomy.

4. it is not clear whether repair of cleft palate or repair of
velopharyngeal inincompetence (VPI) reduce otitis media or
improves hearing
D. Facial growth
1. Early palate surgery can adversely affect maxillary growth
2. Repair of the primary palate and alveolus has more
significant effects on maxillary growth than repair of the
secondary palate alone
3. Facial growth is less affected if palatoplasty is delayed until
1 year of age.
4. For rhese reasons, some surgeons close the soft palate early (
around 3 months ) and the hard palate later ( ranging from 9
to 18 months )
5. Each case must be approached individually, carefully
considering facial growth and speech devetlopment.

VIII. Surgical repair
A. Hard palate clefts
1. Von langenbeck repair
a. Bilateral, bipidicled mucoperiosteal flaps.
b. Lateral relaxing incisions are made bilaterally
c. The flaps are closed at the mdline, nasal mucosa first
and oral mucosa
d. Many modifications exist
e. This repair may result in a short palate and contribute
to VPI
2. V-Y pushback ( Veau-Wardill-Kilner)
a. Bilateral mucoperiosteal flaps, unipedicled posteriorly
b. V-Y advancement posteriorly is performed
c. Anterior exposed areas are left open to granulate and
mucosalize.
d. Improves velopharyngeal closure by lengthening the
palate, may improved speech


B. Soft palate clefts
1. Straight-line repair : Separate nasal and oral mucosal flaps
are raised and approximated
2. Double Z-plasty ( Furlow )
a. Z-plasty flaps of oral and nasal mucosa ( with LVP
muscle included) are used in opposing directions.
b. Z-plasties are performed in layers, with nasal mucosal
flaps transposed and closed, followed by transposition
and closure of oral mucosal flaps
c. Lengthents the soft palate
d. Reorients the levator veli palatini muscles
e. Can be used along with hard palate closure in one
operation, or as veloplasty to be followed later by hard
palate closure ( see above )
C. Vomer flap
1. Flaps may be based inferiorly or superiorly and may be
unilateral or bilateral
2. Helps provide tissue for closure of wide clefts
3. Superiorly based flaps are used more commonly
4. Inferiorly based flaps are useful for wider clefts
5. May or may not impair maxillary growth ( controversial)
D. Alveolar repair
1. Mucoperiosteal flaps are raised and inset as advancement
flaps
2. Bone grafting is fermormed if necessary
3. Some perform grafting early ( primarilly), although most
prefer secondary bone grafting before the permanent cleft
canine emerges, during the period of early mixed dentition,
arround 8 yeasrs of age
4. For primary grafting a mucosal flap is raised in the vestibule
of the lip anterior to the cleft, and a rib graft is commonly
used
5. For secondary grafting, gingival mucoperiosteal flaps are
raised on both sides of the cleft, with the incision at the
gingival sulcus of the teeth, and cancellous bone from the
ilium is used

IX. Complications
A. Fistulae
1. Occur in up to 50% of procedures depending on the
preoperative anatomy and the repair technique
2. More common in wide or bilateral clefts
3. Most occur in the hard palate, posterior to the alveolus

4. More common with a single-layer closure
B. Midfacial growth problems
1. Multifactorial
2. Cleft palate patients have inherent facial growth impairment
3. Lip and alveolar repair significantly affect facial growth
4. The extent and timing of palate repair can affect facial
growth ( see above )
C. Airway obstruction
1. Maya occur secondary to postoperative bleeding
2. More common in operations that include pharyngeal flaps
3. Patients should be monitored closedly postoperatively

X. Velopharyngeal incompetence
A. Definition : Inappropriate incomplete closure of the velum against
the posterior pharynx during speech
B. Etiology
1. In cleft palate patients, the levator veli palatini inserts
anteriorly on to the hard palate, and loses its ability to lift the
soft palate to achieve velopharyngeal closure
2. Approximately 20% of patients acquire clinical VPI
following palate repair
3. Some cleft palate operations greatly improve palate length
and levator orientatin, whereas others do so a lesser extent.
a. The Von Langenbeck procedure tends to cause a short
palate because no length is added in the procedure
b. The V-Y pushback techniiques improve palate length
c. The Furlow double Z-plasty soft palate repair
lengthens the palate and corrects muscle insertion on
the palate.
C. Speech and velopharyngeal insufficiency
1. Air escapes from the oropharynx up through the
nasopharynx
2. This results in hypernasal speech and escape of excess air
from the nose during speech ( nasal emission ) causing
difficulty with consonants
3. The patient adjusts to these problems by developing
alternative methods for creating certain vocal sounds (
pharyngeal fricatives and glottal stops).Plosives :
/p/,/b/,/t/,/d/,/k/,/g/; fricatives : /f/,/v/,/th/,/s/,/z/,/sh/,/zh/.
D. Treatment of VPI
1. Pharyngeal flaps

a. Best for patients with adequate lateral pharyngeal wall
movement ( good medial excursion ) based on nasal
endoscopy or videofluoroscopy
b. A myomucosal flap from the posterior pharyngeal
wall is elevated
c. The flap contains mucosa and pharyngeal constrictor
muscle, exposing the prevertebral fascia
d. May be based superiorly or inferiorly
e. The flaps is then sutured to the posterior soft palate
f. This creates a tissue bridge betwwn the soft palate and
the posterior pharynx, alowing the lateral pharyngeal
walls to close in and cause velopharyngeal closure
g. This is a statis repair ( the flap does not move to cause
port closure ).
h. The diffuculty is in adjusting the port / opening size
correctly ; too wide an opening leaves the patien
hypernasal, whereas limiting air flow too much
induces a state of hyponasality
2. Pharyngoplasty ( dynamic sphincter pharyngoplasty )
a. Best for patients with inadequate lateral phartngeal wall
medial excursion
b. Superiorly based bilateral flaps that include the posterior
tonsillar pillars and the palatopharyngeus muscles are
elevated and are set in overlapping positions into a
horizontal incision in the posterior pharyngeal wall
c. This is a potentially dynamic repair. The sphincter created
may have some mevement to help achieve port closure
3. Complications
a. Airway obstruction in the acute postoperative period can be
life threatening and patients hould have apnea monintors
b. Obstructive sleep apnea is not uncommon in the early
postoperative period
c. Dehiscence, bleedingg and infection are other comlications
d. Patients with velocardifacial syndrome the risk of carotid
injury during flap elevation. Consider preoperative
angiogram and / or magnetic resonance angiogram. Palate
intraoperatively for medialized carotid pulsations.


Cleft Lip
Dr.Mgs. Roni Saleh,

I. Embryology
A. The critical developmental period of the lip and primary palate
occurs during weeks 4 to 6 of gestation.
B. Failure of complete union of the medial nasal prominence and the
maxillary prominence leads to a variable extent of clefting of the
primary palate, invoiving the upper lip, alveolus, and anterior hard
palate to the incisive foramen.
C. Cleft lip alone (CL) and cleft lip and palate (CLP) are considered to
be the same entity along a morphologic continuum. Clef palate
alone (CF), on the other hand, has different demographics.
II. Epidemiology and Genetics
A. Incidence of cleft lip and of cleft lip and palate
1. The overall incidence is 1 in 1,000 live births
2. White ancestry: 1 in 750 live births
3. Asian ancestry: 1 in 500 live births.
4. African ancestry: 1 in 2,000 lilve births.
B. Demographics
1. Male-to-female ratio of 2:!
2. The ratio of left (L) to right to bilateral (B) clefts (L:R:B):
6:3:1
3. The ratio of CLPmto CL is 2:1
4. Three percent are syndromic.
1. Risk factors
a. Medications: Phenytoin, methylprednisolone (Solo-
Medrol), steroids, phenobarbital, diazepam, and
isotretinoin.
b. Smoking
c. Parental age, especially fathers age, or both mother
and father over 30 years old.
d. Family history (see Genetics)

C. Genetics
1. The risk of having a child with CLP
a. If parents have one child with CLP: 4%
b. If one parent has CLP: 2% to 4%
c. If parents have two children with CLP:9%
d. If one child and one parent have CLP: 14% to 17%.


1. Most cases are sporadic(and multifactorial), but may be X-
linked, autosomal dominant (Van der Woudes syndrome) of
familial (see Syndromes Associatied with Cleft Lip and
Palate, later in this chapter).
III. Anatomy
A. Normal lip anatomy
1. Topographic landmarks
a. Nasal alae.
b. Columella
c. Philtral columns.
d. White roll: Well-defined mucocutaneus or vermilion-
cutaneous border.
e. Vermilion: Red portion of lip.
f. Tuberle.
g. Cupids bow
h. Wet-dry border: The vermilion-mucosa junction is the
border between keratinized and nonkeratinized
mucosa.
2. Musculature
a. Orbicularis oris
A. Fibers cross (decussate) in the midline and
create the opposite philtral columns.
B. Functions as a sphincters (deep fibers) and for
speech (superficial fibers).
b. Levator labli superioris.
A. Inserts into the dermis at the vermilion vorder
and the lower edge of the philtral columns.
B. Elevates the upper lip.
c. Nasalis or depressor septi nasi muscle: The fibers run
from the alveolar bone into the medial crural
footplates, skin of the columelia and the tip of the
nose, and into the opposite philtral columns.
3. Normal measurements.
a. Vertical length (height) of the upper lip
A. Newborn: 10 mm.
B. Age 3 months: 13 mm.
C. Adult: 17 mm
b. The distance between the peaks of Cupids bow:
Aprroximately 3 mm at 3 months
4. Arterial blood supply: The labial artery, bilaterally.
5. Sensory Innervation: the trigeminal nerve, cranial nerve
(CN) V, maxillary division (V2).

6. Motor Innervation: the facial nerve, CN VII, zygomatic and
buccal branches.
B. Cleft lip anatomy
1. Alterations in the orbicularis oris, levator labii, and nasalis
result in disruption of continuity, orientation, and quality of
the muscless.
a. Fibers are disoriented and run parallel to the cleft
margin.
b. Fibers insert into the alar base on the cleft (lateral)
segment and into the columella in the non cleft
(medial)segment, as well as intradermally.
c. Incomplete clefts.
A. Simonarts band consist of a skin bridge across
the nasal sill. It does not usually contain any
significant muscle mass.
B. Some fibers may cross the cleft, if the cleft is
less than two-thirds of lip height.
d. Bilateral complete clefts: No muscle tissue is present
in the pro-labium.
2. Vertical lip length is decreased: Cupids bow and the lip are
rotated cephalad on both the lateral, cleft side as well as the
medial side.
3. Disrupted Cupids bow.
4. The alveolus and nostril floor are open in a complete cleft
lip.
5. The premaxilla is rotated and protruding, especially in
bilateral cleft lip, often with collapase of the lateral segment
of the cleft side(s).
6. Associated cleft lip nasal abnormalities
a. Hypoplastic, flattened alar dome on the affected side.
b. Lack of upper lateral cartilage overlap of lower lateral
cartilage.
c. Subluxed lower lateral cartilage with alar base
displaced cephalad and posteriorly.
d. Hypoplastic bony foundation (maxilla).
e. The caudal septum is pulled toward the noncleft side.
f. Flattening of the nasal bones.
g. Shortened columella, especially in bilateral cases.
IV. Classification
A. Extent of the cleft: Complete versus incomplete
1. Complete cleft lip
a. Complete disruption of the soft tissues
to the nasar floor.

b. Tends to be wider than incomplete celfts,
with greater nasal deformities.
2. Incomplete cleft lilp
a. Disruption of the soft tissues to varying degrees.
b. The alveolus is usually intact, with less of a tendency
for the premaxilla to protrude.
c. Forme fruste: A very mild cleft.
1) May be difficult to detect
2) May appear as vermilion notching or a scarlike
line or depression
B. Location of the cleft: Unilateral versus bilateral
1. Unilateral cleft lip
2. Bilateral cleft lip
a. May have complete or incomplete cleft on both
sides,or a combination
b. More likely to be complete clefts and are often wide
c. The premaxillary segment may include tooth buds.
d. In bilateral complete clefts, the prolabium lacks
muscle tissue, and therefore lacks philtral columns.
C. Alveolar segments
2. Narrow versus wide cleft
3. Collapse versus no collapse

Syndromes associated with cleft lip and palate
A. Van der Woudes syndrome
1. Autosomal dominant, with variable penetrance.
2. Associated with CLP or CP (40%-50% penetrance).
3. Associated with lip pits (accessory salivary glands, 70%-
80% penetrance).
4. May also have absent second molar, syndactyly, abnormal
genitalia, and popliteal pterygia.
B. Waardenburgs syndrome
1. A group of anomalies arising from abnormal development
and migration of neural crest cells.
2. Features may include cleft lip, cleft plate.
C. Down syndrome (trysomy 21)
D. Trisome 13
E. Sticklers syndrome
1. A group of anomalies caused by connective tissue dysplasia.
2. Typical features: Cleft palate, progressive joint degeneration,
and various ocular abnormalities that may lead to blindness.
3. Autosomal dominant inheritance.

4. Other anomalies: Cardiac, sensorineural, and learning
disorders or mental retardation.
F. Pierre Robin sequence (Note: A sequence is a group of anomalies
that result from a single disrupted event)
1. Micrognathia or retrognathia prevents normal descent of the
tongue. The tongue then interferes with fusionof the palatal
shelves. As a result, typical features include micrognathia or
retrognathia, glossoptosis (tongue falls back into the
pharynx, causing airway obstruction), and a U-shaped cleft
palate.
2. May be a part of multiple different syndromes or may be an
isolated finding.
3. Treatment.
A. Prone positioning to help move the tongue out of the
aierway, the most conservative approach.
B. Supplemental oxygen.
C. Tongue-lip adhesion.
D. Mandibular distraction osteogeneisi
E. Intubation/tracheostomy
4. Patients may show catch-up mandibular growth, depending
on their syndromic association.
5. Palysomnogram: Necessary to evaluate for desaturations as
well as apneic events
G. Velocardiofacial syndrome
1. Autosomal dominant inheritance: Fluorescent in situ
hybridization (FISH) may show an abnormality in
chromosome 22.
2. Characteristic feature include the following.
A. Cleft palate.
B. Congenital heart disease.
C. Broad nasal dorsum and elongated face.
D. Narrow, down-slanting palpebral fissures.
E. Velopharyngeal insufficiency is common, even with a
submucous cleft palate.
F. The carotid arteries may be displaced medially,
placing them at high risk of injury during pharyngeal
flap surgery or dynamic sphincter pharyngoplasty.
Always palpate the posterior pharynx prior to making
an incision; consider obtaining a preoperative
angiogram.
H. Median cleft lip
1. Rare

2. A different entity from the typical cleft lip; more accureately
considered a median craniofacial cleft (Tessier type zero).
3. Associated with a group of syndromes (median cerebral
facial dysgenesis) that involve more severe deformities of
midline CNS and facial structures.
4. Further workup is needed, including a formal CNS
evaluation.
5. May be associated with holoprosencephaly, pituitary
problems, and a limited lifespan.

VI. Staging of intervention
A. Initial evaluation
1. Reassure the parents and family that they are not to blame.
2. Explain the stages and operations that should be expected
throughout the childs lifetime
3. Evaluate for associated anomalies.
4. Consultations
a. Genetics, for evaluation and possible counseling
b. Social works
c. Feeding/nutrition
1) The child may need special nipples or bottles
(e.g., cross-cut nipple)
2) Monitor for appropriate weight gain
d. Otolaryngology: Children with cleft lip and palate
have a high incidence of eustachian tube dysfunction,
and therefore otitis media, requiring close follow-up.
1) The child may need myringotomy tubes.
2) If unreated, repeat otitis may affect hearing and
speech development.
B. Wide clefts (>1 cm)
1. Goal : Bring the segments closer together to facilitate a
tension-free repair.
a. Has not been shown to chanbe skeletal development in
the anteroposterior direction.
b. Does not seem to prevent future crossbite.
2. Passive: Preoperative taping
a. Steri-Strip tapes applied across both segments of the
lip.
b. Requires reliable parents who can reapply the tape and
keep it on at all times
3. Passive: Lip adhesion operation
a. Suturing the edges of the cleft together is performed
under anesthesia.

b. The definitive lip repair is performed once the
segments have moved closer together.
c. Variable success.
4. Active: Latham-type device
a. An orthodontic appliance that must be placed onto the
palatal segments under anesthesia.
b. Parents turn a screw daily, which slowly brings the
palatal segments into better alignment.
c. Removed at the time of definitive lip repair.
2. Repair
1. Timing (controversia)
a. Repair at 3 months is generally accepted.
b. Some argue for earlier repair in order to produce better
scars.
2. Rule of tens: For increased anesthetic safety, an infant
should
a. Be 10 weeks old
b. Weigh 10 pounds.
c. Have a hemoglobin level of at least 10 mg/dL.
3. Cleft palate repair and secondary alveolar frafting
4. May also choose to address the cleft, nasal deformity at time
of lip repair.

VII. Intraoperative considerations
A. Landmarks
1. Tattooed with methylene blue, using a hypodermic needle or
a quill pen.
a. Alar bases.
b. Columella.
c. Philtral columns.
d. D. Peak of Cupids bow midline on the medial
segment. Measure the anticipated distance for the new
Cupids bow (approximately 3-4 mm).
e. Peak of Cupids bow on the lateral segment.
2. Account for distortion from the uncountered pull of the
orbicularis on the medial segment. The philtral columns are
usually slightly C-shaped.
B. Mark lines for expected repair type.
C. Only after marks are completed, infiltrate tissue with local
anesthetic to avoid distortion of anatomy and measurements.
D. Goals of repair
1. Reconstitute Cupids bow
2. Minimize scarring

3. Produce a slight pout of the tubercle.
4. Produce functional continuity of the muscles
5. Recreate symmetry.

VIII. Types or repair
A. Straight-line repair
1. Historically, the first cleft lip repairs relied on freshening the
edges of the cleft and suturing them together. These have
been largely replace by various Z-plasty-base techniques.
2. Rose-Thompson repair
a. Modified straight-line repair that can be used for
minor clefts with lip length nearly equal on both sides
of cleft (e.g. forme fruste)
b. Fusiform excision with straight-line closure.
B. Quadrangular flap
1. Proposed by LeMesurier and Hagedorn.
2. Cupids bow is derived from the lateral lip.
3. 90-degree Z-plasty.
4. Violates Cupids bow and the philtral dimple.
5. May also have problem with a long lip.
C. Triangular flap
1. Proposed by Tennison and Randall
a. The Z-plasty is place at the vermilion border.
b. Produces an natural appearing Cupids bow
c. May be used for clefts of all widths.
d. Violates Cupids bow and the philtral dimple.
e. Has a tendency to produce a long lip.
2. Skoog repair
a. Consists of two Z-plasties
b. Violates Cupids bow and the philtral dimple.
D. Rotation advancement
1. Popularized by Millard
a. Likely the most commonly used repair. Often described as the cut-
as-you-go technique.
b. The medial lip is rotated downward to fill the cleft
defet.
c. A small pennant-shaped C-flap can either be rotated to
create the nasal sill or used to lengthen the columella.
d. Does not violate Cupids bow or the philtral
dimple____
e. Difficult for wider clefts.
f. Common fitfall is inadequate flaprotation leading to
nothing and in-adequate vertical lip length.

1) Repeat advancement or a small Z-plasty at the
vermilion border can be performed.
2) Better results are obtained if adequate rotation
is permormed at the time of the original
operation.
2. Poople repair
b. Preserves the integrity
of the aesthetic unit at
the columellar-labial
junction.
c. Allows lengthening of
the lip woithout
extending the
advancement flap up on
the ala or encroaching
on horizontal lip length.
c. Bilateral cleft lip repair
1. The premaxillary segment is often a greater problem than in
a unilateral cleft lip.
2. Consider taping, lip adhesion, or presurgical orthodontics
3. Most common techniques
b. Dissect the prolabium to maintain a central skin flap
to resemble the philtrum.
c. Deepithelialize the remainder of the prolabium
d. Use the prolabial vermilion to create a labial sulcus,
not for the final lip the lateral lip segments, not from
the prolabium.
e. Columellar lengthening may be performed at the time
of lip repair or as a secondary procedure.
IX. Postoperative care
A. Orders
1. Arm restraints (no-nos) for 3 weeks to prevent disruption
of repair.
2. Specialized nipple/bottle to decrease sucking effort when
bottle-feeding.
B. Leave Steri-Strips in place over the incision for reinforcement.
C. Follow up in 1 week for suture removal if nonabsorbable skin
sutures were used.
Pearls
Preoperative
1. Practice lip markings and cuts on foam first
2. Do not forget to assess for an adequate bony platform and the need
for orthogmatic surgery when assessing cleft nasal deformities.

Intraoperative
1. Mark several times, cut once.
2. Beaver scalpel blades are helpful.
3. Line up the white roll first, placing a stitch above and below the
white roll, then reapproximate the wet dry border.
4. Bilateral cleft: Do not use the vermilion of the premaxillary
segment in the final vermilion. It tends to look like an abnormal,
dry patch postoperatively.
Postoperative
1. Instruct the parents to hold off feeding prior to the clinic
appointment. In the clinic, the baby will stay quet during feeding
usually just long enough for suture removal.
2. Keep a Steri-Srip tape in place for 1 to 2 weeks for support.


GRAFT & FLAP
Dr. Mgs. Roni Saleh, SpBP
Departemen Bedah
RSMH Palembang

GRAFT & FLAP
Kulit melindungi tubuh dari invasi luar dan mencegah kehilangan
cairan, elektrolit, protein dll. Kehilangan kulit harus diganti baik
dengan epitelisasi spontan atau graft maupun flap

I. Skin Graft
Satu segmen kulit yang diambil secara komplit dari suatu daerah (donor
site) dan ditransplantasikan ke daerah lain (recipient site)
Klasifikasi
1. Berdasarkan species
a. Autograft :
graft dari satu tempat ke tempat lain pada individu yang sama
b. Allograft (homograft)
graft dari satu individu ke individu lain yang satu species
c. Xenograft (heterograft)
graft dari satu individu ke lain species

2. Berdasarkan ketebalan
a. Split Thickness

1. Seluruh epidermis dan sebagian dermis
2. Sebagian dermal skin appendiges (glandula sebacea, glandula
sudorifera,follicle rambut) masih ada didonor site dan akan sembuh
dg epitelisasi
3. Ketebalan
a. makin tipis kemungkinan take lebih besar
b. makin tipis graft makin besar akan terjadinya engkerutan
4. Pemakaian
a. Penutupan suatu daerah yang kehilangan kulit yang luas
b. Penutupan jaringan granulasi
5. Metode
a. Free hand (dengan pisau khusus atau dengan pisau lain)
b. Dermatome (drum atau dengan power driven hair clipper
type machine)
6. Donor Site
a. Sembuh dengan epitelisasi tepi luka dan skin appendige
b. Diperlukan perawatan untuk mencegah infeksi

b. Full Thickness

1. Seluruh ketebalan epidermis &
dermis
2. Sebagai penutup luka yang lokal
tetapi tidak semudah STSG
takenya karena vascularisasi
yang lambat
3. Daerah donor harus ditutup primer
atau STSG
4. Pemakaian
a. untuk wajah color match
b. jari jari tdk terjadi kontraktur
c. dimana saja diharapkan kontraksi dari graft minimal

B. Seleksi Donor Site

1. Ditentukan berapa
banyak kulit diperlukan
2. Diambil dari daerah
yang tersembunyi mis.
lateral utk STSG atau
lipat paha untuk FTSG
3. Color match penting
terutama untuk
graft di wajah.
Donor site :
Supra clavicular
Palpebra superior

C. Graft Survival

1. Graft mendapat inhibisi dari cairan pada bed
2. Dalam minggu berikutnya pembuluh darah pada bed tumbuh ke
dalam graft terjadi neovaskularisasi
3. STSG dan FTSG harus di daerah yang perdarahannya baik dengan
jumlah bakteri sedikit untuk menjamin take
4. Graft harus diimobilisasi cegah pergeseran graft dengan bed,
hematom mengganggu neovaskularisasi
5. Kontra Indikasi
- daerah yang miskin vaskularisasi seperti :
- tendo yaitu telanjang

- cortex tulang tanpa periostium
- daerah yang mendapat radiasi yang masif
- luka yang terinfeksi, dll
II. Skin Flap

Kulit & jaringan subkutan,kadang-kadang dapat dengan otot dan tulang
yang ditransfer dari satu tempat ke tempat lain dengan mempertahankan
vascularisasinya.
Pedicle adalah dimana pembuluh darah dipertahankan.
A. Klasifikasi
1. Dg Vascular Pedicle
a. Flap dg pedicle yg intact
1. Cutaneous (random flap)
Perdarahan dari pleksus dermal dan subdermal
2. Arterial (axial flap)
Perdarahan dari direct cutaneous arteri
2.1. Peninsular kulit danpembuluh darah intact
2.2. Island hanya pembuluh darah intact
2.3. Musculocutaneus flap
a. Kulit, subcutan dan otot otot sekitarnya
b. perdarahan kulit dari pembuluh darah yang
menembus otot dibawahnya dan berasal dari arteri
segmentalis, pembuluh darah longitudinal dari dalam otot
c. dapat peninsular atau island
b. Free Flap
Suatu arterial flap
dimana pembuluh
darahnya dipotong,
kemudian flap
dipindahkan ke lokasi
lain dan pembuluh
darah direanastomosis
dengan tehnik micro
surgery dengan
pembuluh darah dari
recipient site


B. Penggunaan
1. Menggantikan jaringan yang hilang akibat trauma atau
akibat operasi
2. Dapat sebagai penutup kulit segera setelah operasi
3. Sebagai bantalan jaringan diatas tulang yang menonjol
4. Memberikan pendarahan yang baik pada bed yang
pendarahannya buruk
5. Meningkatkan sensasi pada suatu area (nerve pada flap skin
intact)
6. Dapat memakai jaringan lain seperti tulang untuk
rekonstruksi

III. Graft Lain

A. Tendon
1. Dipakai pada penggantian tendo yang hilang
2. Donor site : palmaris dan plantaris
B. Tulang
1. Dipakai pada defek yang rigid
seperti tulang wajah, tengkorak, tulang panjang
2. Donor site : os iliaca, costa
C. Kartilago
1. Untuk pembentukan daun telinga, hidung, dagu
2. Donor site : kartilago costa, telinga, septum nasi
D. Fascia
1. Dipakai pada dermal defek dan sling pd paralise n.fasialis
2. Donor site : fascia lata, fascia temporalis
E. Dermis
1. Untuk restorasi contour spt parut yang cekung
2. J aringan fat dg dermis dipakai sebagai pengisi
3. Donor site : dimana kulit yang tebal: bokong
F. Otot
Biasanya free graft dari otot-otot juga mempertahankan perdarahan,
graft gracillis atau gastrocnemous muscle graft
G. Syaraf
Dipakai bila ada nerve gap, terutama pada
1. N. medianus, n. ulnaris, digital & facial nerve
2. Donor site : n. suralis & n. cutaneus humeri & ante brachi

H. Pembuluh darah
1. Bila ada, vascular gap
2. Banyak dipakai pada replantasi pada free graft transfer
3. Donor site : vena lengan atas & vena saphena

HYPOSPADIAS
Dr. Mgs. Roni Saleh, SpB-SpBP(K)
Bagian Bedah FK. UNSRI/ RSMH
Palembang

I. Biology and development
A. The urethra normally coalesces at the raphe in the midline, from
proximal to distal ( from perineum to glans ). Hypospadias result
form failure of the urethral folds to fuse completely. This leaves
themeatus located along the ventral aspect of thepenis.
B. Testosterone influences the development of the genitals by
induction of virilization of indifferent external genetalia.
C. Potential causes of hypospadias.
1. Abnormal androgen production
2. Varying degrees of androgen receptor sensitivity in partinent
tissues (e.g.,the genital tubercle )
3. Environment estrogens ( controversial )
II. Characterization
A. Incidence ; 1 in 300 live births
B. Common triad : Hypospadias, chordee, and a dorsal hood.
1.Chordee
a. Ventral curvature of the penis
b. Historically was thought to be due to a band of fibrous tissue
along the course of the urethral plate, the dorsal half of the
hypoplastic urethra.
c. The true etiology is currently unclear
d. The artificial erection test ( see Pertinent Principles
in Hypospadias Repairs) is useful to gauge the severity of the
curvature and to measure the adequacy of correction.
2. Dorsal hood : in the presence of hypospadias, the dorsal
foreskin is termed the dorsal hood, and is often quite noticeable
due to the relative absence of ventral tissue.
C. Associated congenital anomalies
1. Other urinary tract anomalies are not typically associated
with isolated hypospadias. Therefore, reserve urinary tract
imaging for those patients with other congenital anomalies (
e.g. imperforate anus )
2. Enlarged prostatic utricle ( Mullerian remnant ) : Present in
10% to 15% of hypospadias patients ; can lead to difficult
urethral catheterization.
3. Cryptorchidism : Present in 9%; may be associated with
intersex ( ambiguous genitalia ).

4. Intersex conditions ; More likely to be associated with
proximal (e.g. perineal ) hypospadias or cryptorchidism.
a. Reserve intensive evaluation (e.g.,karyotyping )
for such patients
b. Mixed gonadal dysgenesis is the most common
intersex variant in thin population.
D. Location of meatus
1. Determines the type of repair to some degree ; may be
related to degree and timing of the androgen insult
2. Incidence according to the location after the correction of
chordee
a. Anterior hypospadias ( 50% ) : Granular,
coronal and subcoronal
b. Middle hypospadias ( 30 % ) : Distal penile,
midshaft, and proximal Penile
c. Posterior hypospadias ( 20 % ) :
Penoscrotal. Scorotal and perineal
III. Surgical repair
A. Best performed between 6 and 18 months of age.
1. Minimizes anesthetic risk ( after 3 months of age )
2. Limits psychological impact of surgery
3. Avoids feeling of being different (e.g. sitting to urinate )
4. Limits the potential impact on toilet training
B. Goals of repair
1. Create a functionnally straight phallus : Verified by the
artificial erection test
2. Establish a functional urethra : Allows for a directed stream
and mixturation while standing ; can be objectively followed
by uroflowmetry.
3. Pri\ovide a normal apperance : critical goal. One-third of
adult patients are dissatisfield with their cosmetic result due
to scarring, redudant skin ( from preserving skin for possible
secondary procedures ) and reduced penile lenght ( a
consequence of dorsal plication )
C. Pertinent principles in hypospadias repair
1. Optical magnification ( 2,5 x to 3,5 x operating loupes )
2. Subcutaneous injection of epinephrine along planned
incision lines facilitates hemostasis.
3. Correct the chordee first. Use the artificial erection test :
Insert a smallgauge butterfly needle into the corpora through
the glans ( to avoid penetrating Bucks fascia ) and inject
saline while having a tourniquet ( e.g.,a. Rubber drain)
around the base of the penis to prevent outflow

D. Types of repair
1. Chordee correction
a. Excision of the urethral plate
b. Dorsal plication of the corpora
1. Plication stiches are placed laterally to avoid the
neurovascular bundles in the dorsal midline
2. It is unclear if early repair predisposes to
recurrence during puberty, the period of
ciorporal growth.
3. Potential exists for penile shortening
c. Elevation of the urethral plate
d. Recurrence rates are variable ( up to 40 % )
2. Meatal advancement and glansplasty ( MAGPI )
a. Initially described in 1981
b. Indicated for glanular and coronal variants only; result
are largely dependent on patient selection
c. Meatal regression, the most troublesome
complication, may be minimized by careful
approximation of the glans ventrally
d. Urinary diversion with a ctheter is not necessary
e. Complication rate : 1 %
3. Parameatal based flap ( e.g., Mathieu )
a. For slightly more proximal variants
b. Flap cannot contain hair bearing skin
c. Complications : 6 %
4. Onlay island flap
a. Flap from the inner preputial skin of the dorsal hood
b. Useful for midshaft variants
c. Onlay on to the urethral plate ; must tailor to the
appropriate size to prevent formation of a urethral
diverticulum
d. Complications : 6%
5. Tubularized flap ( e.g., transverse preputial island flap )
a. Same flap as an only island flap, except completely
tubularized
b. Intended for longer gaps; can use event if the urethral
plate has been excised
c. There is potential for stricture formation at the
proximal anastomosis
d. Complications : 10% to 15%

6. Tubularized incised plate ( e.g.,Snodgrass repair )
a. Useful for most variants

b. Has essentially supplanted other techniques as the
procedure of choice for middle hypospadias variants
and possibly others
c. Direct incision and subsequent tubularization of the
urethral plate.
7. Grafts ( e.g.,buccal mucosa, bladdermucosa ) can be performed as
onlay or tubular grafts

E. Staged repairs
1. Generally reserved for more proximal ( osterior ) variants or
very small phallused ( to allow for growth )
2. Second stage is usually performed 6 to 12 months after the
initial procedur

IV. Outcomes
A. The more proximal the meatus, the more likely are complications
B. Potential complications of hypospadias reconstruction
1. Urethrocutaneous fistula : Occurs in 5 % to 10 % of one
stage repairs. Excision and closure of the fistula can be
performed at 6 months, provided nodistal obstruction is
present
2. Other complications include meatal stenosis ( which may
lead to urethrocutaneous fistula ), urethral stricture,
inadvertent tranfes of hair bearing skin, recurrent chordee,
and urethral diverticula.
Pearls
1. Correct the chordee first. Once the penis is adequately straight, the
best technique for hypospadias repair can be detrmined
2. Do not rush to fix fistula. Wait at least 6 months and make surethat
there is no distal urethral obstruction
3. Proximal/posterior hypospadias and any variant associated with
undescended testes warrant an interesex evaluation.
4. Never use skin that will eventually be hair-bearing
5. Most successful repairs have multilayer flap coverage.


Anatomi Traktus Genito Urinarius
Dr. Arizal Agoes, Sp.B, Sp.U

Ginjal

Pembuluh darah ginjal

Pembuluh vena ginjal


Pembuluh limfe ginjal

Nephron


Calyx dan pelvis renalis

Ureter

Ureter, pembuluh darah, saraf dan lymphatik


Kandung kemih

Kandung kemih, pembuluh darah, saraf dan lymphatik

Urethra pada pria


Prostat

Vesicula seminalis


Penis

Penis, pembuluh darah, saraf dan lymphatik


Scrotum dan testis

Epididimis dan Vas deferen

Urethra pada wanita


Pemeriksaan ginjal

Pemeriksaan kandung kemih
Pemeriksaan Rectal Toucher


UROLOGI
Dr. Arizal Agoes, SpB, SpU
Dept. Bedah RSMH Palembang

WHAT IS UROLOGY
The science of diseases of the urogenital organs, except for the female
genital tract

PENYAKIT ORGAN UROGENITAL?
Menguasai anatomi & fisiologi T.U.G
Memahami patofisiologi dari problem urologi

PROBLEM2 UROLOGI, APA SAJA ?
I. Problem gangguan kontrol B.A.K
II. Problem gangguan volding (pancaran)
III. Benjolan atau nyeri pinggang atau perut
IV. Pembengkakan scrotum
V. Urethral Discharge
VI. Disfungsi seksual/impotensi
VII. Intertility

I. GANGGUAN KONTROL
1. Kencing normal tapi pakaian dalam kadang-kadang basah
* Urgensi
- sistitis
- hipertrofi otot detrussor
- neurogenic bladdar (UMN)
- anxious woman
* Stress Incontinence
Peningkatan tek Intra abd & intra vesical yang mendadak seperti
batuk, bersin, naik tangga. Urin dalam jumlah kecil akan keluar
Penyebab :
Kelemahan Sphincter ext Prolaps
Genitalia
* Overflow Incontinence
Buli tidak pernah kosong
=Residual urine ??
Akibat frekwensi dan voiding volume sedikit
Patologi : Dekompensasi otot detrussor
(BPH lanjut)
Flaccio Bladder/Neurogenic Bladder
Tipe L.M.N

* Enuresis =Bed wetting
=ngompol
Normal usia <4 th
>5 th 50-80% (-)
2. Bak normal tapi pakaian dalam selalu
basah
- Wanita dengan ectopic ureter
- Kerusakan sphincter
operasi prostatectomy
- Uretero vaginal fistula cedera ureter saat operasi histerektomi
3. Bak sedikit/tidak sama sekali
Pakaian dalam selalu basah =True Incontinence
Patologi kerusakan total sphincter
mis : tur prostat
malignancy (wanita)
radioterapi (wanita)
* Fistula vesicavaginal
Partus kasep
Operasi vagina
Radiasi

II. Problem Voiding Urine
1. Nyeri saat kencing =dysuria
nyeri dapat dirasakan buli2, urethra atau perineum
nyeri timbul sebelum, saat atau sesudah kencing
2. Pancaran Abnormal
- lemah =weak stream (Q max >20 cc/dt
Q ave 8 -10 cc/dt)
- menetes
- hesitansi
- intermittent
- tidak lampias
- bercabang / kecil
3. Frequency
- interval/jarak antara kencing makin pendek
- voiding volume =sedikit
- Dibedakan dengan polyuria kencing sering
& voiding volume banyak
Penyakit : DM, DI, Peny. Ginjal chronis, atau banyak
minum/cuaca dingin
- day time frequency nervous origin
Psikogenik


- night time frequency nocturnal
frekwensi
* obat diuretika
* peny. J antung Kongestif
Frequency
Sehari-hari sering dijumpai
Keadaan patologi buli-buli
Inflamasi
Tumor buli
B a t u
Prostat hipertrofi (BPH)
Iritasi mukosa (pH sangat asam/alkali)
Kapasitas buli kecil (normal 300-450 ml)
mis.
TBC buli, radiasi buli
Partial sistektomi
Sistitis Intersitialis
Patologi diluar buli
Tumor Gynecologis
Fibrosis Peri Vesical
Gravid (normal)

4. Hematuria (microscopic atau gross)
Terdapat darah (erithrosit) dalam urine
dd/ urin berwarna merah
Anthocyanin (bats)
Phenolpthaline (obat pencahar)
Urate
Porphyria
Seratia marcestens (infeksi pada bayi)
Hematuria disertai nyeri =pain hematuria
Colic renal
Colic ureter batu
Sakit daerah supra pubic
Tumor buli
Inflamasi
T r a u m a
Hematuria tanpa nyeri =painless hematuria
Initial : asal urethra
Durante/selama kencing : asal ginjal sampai buli
Terminal bladder tumor


III. BENJOLAN PADA PINGGANG/ABDOMEN DISERTAI
NYERI

Disertai nyeri
Hydronefrosis/pyonefrosis
Retro peritonial hematoma
Tumor ginjal (malignancy)
Tanpa nyeri
Hydronefrosis
Tumor ginjal jinak

Nyeri pinggang/abdomen (antero lateral)

Nyeri renal
Lokasi =CVA ipsilateral
Akibat regangan kapsul ginjal
mis =- destruksi pyelum/ureter
- inflamasi parenchym ginjal
Refered pain ke anterior, ABD atas dan umbilicus
Nyeri inflamasi menetap
Nyeri obstruksi intensitas berfluktuasi
kdg2 disertai symtoms git
Dd/ =asal intra peritonial
Pancreatitis
Perforasi ulcus duodenum
=neurogen
nyeri radiculer T10-12 (iritasi N. intercostalis)

Nyeri ureter =ureter colic
Sifat nyeri
Akut, kolik
Spasme dan interperistaltic otot ureter
Ada fluktuasi / bergelombang
Penyebab
Sumbatan ureter - b a t u
- bekuan darah
Obstruksi atas =nyeri regio cva
Obstruksi tengah =nyeri abdomen bawah -sampai scrotum/labia majora
Obstruksi bawah =iritasi buli-buli
- frekwensi
- urgensi
nyeri supra pubis


Nyeri asal testis
Akut
Torsio testis keadaan emergensi, nyeri awal regio abd
bawah ipsilateral
T r a u m a
Epididymitis akut
Kronis
Hidrocele
Varicocele

IV. PEMBENGKAKAN DAERAH SCROTUM
Cancer Inf Hernia Hydrocel Torsio Varicocel
Onset
akut
- + - - + -
Nyeri ? - + - - ++ -
Trauma ? - + - - - -
Hub. Sex - + - - - -
Discharge - -/+ - - - -
Perubahan
(size)
- - ++ +/- - +

V. URETHRAL DISCHARGE
Kekentalan =encer =clamydia/NGU
Warna discharge, purulent =GO
Hub sex =veneral disease
Trauma =blood

VI. DISFUNGSI SEXUAL
Male sexual dysfunction
Klasifikasi
Disorders of desire
Hyperactivity
Hypoactivity =adrogen menurun
Sexual aversion
Disorders of erection
Erectile dysfunction
Prolonged erection (priapism)
Erectile deformity

Disorders of ejaculation
Premature E emotional disorders
Delayed E
An E Denervasi simpatis
Retrograde E prostatectomy
Disorders of orgasm
An O psyciatric disorders
Delayed O
Disorder of sensation
Hyposensitivity
Hypersensitivity
Sexual pain disorders
CLINICAL DIAGNOSIS
Clinical diagnosis dibuat berdasarkan :
I. History of the presenting illness
II. Physical examinations
III. Performance of special tests

I. History =riwayat
=anamnesa

dimulai dengan keluhan/problems yang menjadi alasan pasien mencari
pertolongan, keluhan dicatat secara kronologis
Contoh :
Laki-laki, 64 tahun datang dengan keluhan pancaran kencing
melemah
Sejak 2 tahun yang lalu
Pancaran mulai melemah
Hesistensi, mengedan
Terminal dribling
Frekwensi siang 1-2 jam
Nocturia 4 x
Sejak 6 bulan
Urgensi
Pakaian dalam sering basah
Sering ke toilet
Malam tidur terganggu
Perut bagian bawah terasa penuh

Anamnesa diatas mengarahkan ke suatu keadaan retensio chronis
Tanya hal yang berhub dengan fungsi ginjal mis : anoreksia,
nausea, vomitting
Tanya hal yang mungkin berhubungan dengan obstruksi

Infeksi =dysuria, frekwensi, urgensi
Hematuria =BPH
malignancy
Veneral disease =stricture urethra

Hasil anamnesa operasi ?
Perlu ditanya keadaan
Kardiorespiratori
Perokok, batuk kronis
MCI
Gangguan pembekuan darah
Obat-obat yang dikonsumsi
Allergy ???
Anamnesa oleh dokter yang berpengalaman
Masalah mudah diketahui
Terarah / tidak bertele-tele
Mengurangi/menghindari test-test yang tidak perlu
Dapat menilai apakah diperlukan tindakan emergensi (tampak
sesak, sianosis)
A. KEADAAN UMUM =STATUS GENERALIS
KESAN UMUM :
Status Gizi : - Cachexia
- Obesity
Edema
Gynecomastia
limfadenopati
Kulit : - Pucat
- Icterus
- Dehidrasi
B. STATUS UROLOGI
1. Ginjal
pemeriksaan : Inspeksi, palpasi, perkusi,
auskultasi, transilluminasi
Daerah sudut costovertebra, abdomen quadran atas
kanan/kiri
2. Vesica urinaria=buli-buli=bladder
Normal :
Volume <150 cc palpasi (-)
Volume 500 cc distensi terlihat/inspeksi (+)
Perkusi lebih informatif dibanding palpasi
3. PENIS
Inspeksi :
Sirkumsisi/tidak

Kulit ditarik kebelakang :
Inflamasi =balanoposthitis
Tumor
Meatus Urethra : - posisi : -hipospadia
-epispadia
Kulit Penis : - Ulkus
- Condyloma/warts
Palpasi :
Corpus cavernosa fibrotik
Nyeri +/-
4.SCROTUM +TESTIS
Abnormalitas kulit scrotum : - Infeksi
- Kista sebasea
Palpasi testis : - ukuran
- bagian yang keras/tumor
- UDT +/-
Transiluminasi
Palpasi : - epididymis
- vas deferens
5. COLOK DUBUR =RT =DRE
Rutin untuk laki laki >40 th
TSA
Prostat
Buli
Faeces - darah?
KEADAAN ABNORMAL YG SERING DITEMUKAN
PADA SAAT PEMERIKSAAN FISIK
O Ginjal
Tumor =kistik : hydronefrosis
poli - multi
=Malignancy :
+ Wilms tumor
+ Neuroblastoma
+ Grawitz tumor
O Scrotum dan Isinya :
+ torsio
+ hydrocele
+ varicocele
O Penis :
+ phimosis
+ paraphimosis
+ peyronies
+ Priapismus

+ Hypospadia
+ Epispadia
+ Carsinoma
O Prostat :
+ prostatitis
+ BPH
+ prostat cancer
III. PEMERIKSAAN PENUNJ ANG =TEST KHUSUS
1. URINALISA
Pada wanita : midstream
Pada laki-laki : void I urethra
void II Bladder
void III prostat washing
- Mikroskopik sedimen :
- eritrosit : normal (-) atau <3 /LPB
- lekosit : normal <5 /LPB pada wanita
<2 /LPB pada laki-laki
- cast : - hyalin
- granular
- lekosit
- eritrosit
- kristal : Calcium Oxalat
Calcium Phosphat
Calcium amonium magnesium phosphat
Uric acid
Cystinuria
Kultur Urin
Cytology

2. TEST FUNGSI GINJ AL : - Ureum
- Creatinin
- C.C.T.
3. URORADIOLOGI
BNO-IVP - Arteriografi
Urethrografi - Limfografi
Cystografi - CT Scan
Tomografi - MRI
RPG - Caversonografi
APG


Pemeriksaan Dasar UROLOGI
URO + LOGOS
UROLOGI: TRAKTUS URINARIUS PRIA & WANITA DAN TRAKTUS
REPRODUKSI PRIA
(UROLOGI & ANDROLOGI)

General Urology
Pediatric Urology
Endourology
Oncologic Urology
Female Urology
Neuro Urology
Andrology
Male Infertility
Pemeriksaan dasar Urologi
Anamnesa / Keluhan (symptoms)
Pemeriksaan fisik
Laboratorik
Radiologik

keluhan utama
riwayat penyakit dahulu
riwayat penyakit keluarga
keluhan utama
harap diingat oleh dokter
durasi, beratnya, akut/kronik, periodik, derajat gangguan dan
hal2 penting (demam, BB turun, lemah)
apa yang mengganggu saat ini
Symptoms GU tracts
Systemic manifestations
Fever & weight loss
Unexplained attacks of fever
General malaise
Local & referred pain
LOCAL : Involved organ:
kidney (T10-12, L1)
testicle
REFERRED :
From diseased organ:
ureteral colic ^ipsilateral testicle (T11-12)

I.Ureter 1/3 proximal
2
\
II.Ureter 1/3 tengah
III.Ureter 1/3 distal
Urologic organ ^(common nerve supply)
GI
Gynec.

KELUHAN (Symptoms)
Nyeri
Hematuria
LUTS (lower urinary tract
symptoms)
Disfungsi seksual
Hematospermia
Pneumaturia
Discharge urethra
Demam & menggigil

Nyeri
nyeri ginjal (renal pain)
nyeri ureter (ureteral pain)
nyeri vesika (vesical pain)
nyeri prostat (prostatic pain
nyeri penis (penile pain)
nyeri testis (testicular pain)
nyeri ginjal (renal pain)
tumpul & menetap (dull pain) keradangan
kolik (colicky pain) obstruksi
DD: pseudorenal pain (radikulitis)
--lokal
--dari tempat lain (referred pain)
nyeri ureter (ureteral pain)
akut, kolik, (obstruksi)
referred pain (=lokasi)
ureter distal: frekuensi, urgensi
DD: divertikulitis (kiri) adnexitis (ki/ka)
appendisitis (kanan) kolik tr.digestivus


Nyeri
nyeri vesikal (vesical pain)
Menetap / konstan: retensi urin
Intermiten : inflamasi (suprapubic discomfort)
mis: sististis bakterial atau sistitis interstisialis
nyeri prostat (prostatic pain)
sekunder o.k. inflamasi dan distensi kapsul prostat
nyeri penis (penile pain)
kausa: priapismus, Peyronies, parafimosis, inflamasi
buli2 & uretra (BBB)
nyeri testis (testicular pain)
dari testis: orko-epididimitis, torsio testis, torsio
apendiks testis
kemeng: hidrokel, varikokel
referred: dari ginjal, ureter
Hematuria
makros (gross) / mikros ? Sedimen: eri >3 hpf
inisal / terminal / total
nyeri / tidak
bekuan (clots) & bentuk
selalu curiga keganasan sampai terbukti sebaliknya
LUTS (lower urinary tract symptoms)
keluhan iritatif:
keluhan obstruktif
inkontinensia
enuresis
keluhan iritatif (STORAGE):
frekuensi / nokturia / urgensi / disuria
keluhan obstruktif (VOIDING):
pancaran melemah
hesitansi
intermitensi
menetes
retensi urin
Inkontinensia
continue (true)
stress
overflow
urge
Enuresis
diurnal
nocturnal

Disfungsi seksual
libido menurun
impotensi
gagal ejakulasi
anorgasmus
ejakulasi prematur
Hematospermia
sering sembuh sendiri
jarang ada patologi
o.k.inflamasi non spesifik uretra prostat, ves.seminalis
Pneumaturia
Discharge urethra
Demam & menggigil

Riwayat penyakit dahulu
penyakit dahulu dg sequelae urologik : keluar batu, DM,
neurologik, dll
obat-obatan
pembedahan y.l.
merokok dan alkohol
alergi
Riwayat penyakit keluarga
kanker
BSK
Pemeriksaan fisik
kesan umum:
cachexia
striae
jaundice
hiperpigmentasi
ginekomastia
edema
uremic frost
anemia
septic
Pemeriksaan fisik
Inspeksi
Palpasi
Auskultasi


Pemeriksaan fisik
ginjal
buli-buli
penis
skrotum & isi
rektal & pem. prostat (laki2)
pem. pelvis (perempuan)

ginjal
dewasa: sulit teraba (bimanual)
palpasi bimanual
Bila teraba : permukaan, konsistensi, nyeri tekan
K.p. : perkusi, transilluminasi
buli-buli
teraba bila terisi 150 ml
palpasi (bimanual)
perkusi
mobilitas
penis
bila tdk circ., tarik preputium
kulit
meatus urethrae
palpasi indurasi, batu
fimosis
Peyronies disease
priapismus
Hipospadia (+chordee)
karsinoma
skrotum & isi
kulit
testis (ganas)
epididimis, vas (jinak)
transiluminasi
kanalis inguinalis (HIL)
pem. rektal & prostat pd. pria (CD/RT/DRE)
semua pria dg . keluhan urologik
semua pria diatas 40 th


pem. pelvis pd. perempuan
pemeriksa pria didampingi dr./prw. perempuan
inspeksi teliti dlm posisi litotomi
VT atau RT (+ palpasi bimanual)

Pemeriksaan fisik ----- abnormal:

skrotum dan isi
tumor testis (hampir selalu ganas)
tumor para testikular (hampir selalu jinak)
hidrokel, spermatokel, kista epididimis,
varikokel
torsio testis
epididimitis
orkitis / orko-epididimitis
prostat
prostatitis akuta
benign prostate hyperplasia (BPH)
karsinoma prostat

Laboratorik
urinalisis
pd semua pend urologi
UL: kimiawi & mikroskopik
cara koleksi:
pria: arus tengah (midstream)
perempuan: bersihkan & arus tengah atau urin dg
kateter
neonatus dan bayi: spp (supra pubic puncture /
aspiration)
pem. fisik urin: warna, kekeruhan, BJ , pH
pem. kimiawi:
urine dipsticks: darah, protein, glukosa, keton,
urobilinogen & bilirubin, leukosit
hematuria & DD
proteinuria
glukosa & keton
bilirubin & urobilinogen
test nitirit
pem. mikroskopik: sel, silinder (cast), kristal, bakteria, ragi,
parasit
biakan dan test kepekaan AB


sekresi prostat (expressed prostatic secretion)
darah:
DL: Hb, leuko, diff, PCV, LED
faal ginjal: BUN, kreatinin serum, as.urat
k/p: elektrolit
Radiologik
USG
foto polos abdomen (BOF, BNO,KUB)
IVP / IVU (intravenous pyelo/uro-graphy)
Diagnosis
Primer
Sekunder
Komplikasi
DD (differential diagnosis=diagnosis banding)
Diagnosis kerja
Diagnosis klinik
Diagnosis patologik


UROLITHIASIS
defenisi
UROLITHIASIS or urinary calculi or urinary stone disease (USD) or
batu saluran kemih (Indonesia) is the accurence of stones WITHIN the
urinary tract
Human suffered urolithiasis since the beginning of recorded history. It
was found by archeologist in the egyptian mummys that estimated to be
over 7000 years old.
Over the last decade the incidence has significantly increased.
EPIDEMIOLIGY
Incidence : 2 4 % of population
The average lifetime risk of stone formation range from 5 10 %
In the USA stone diseases hospitalization account for more than
400.000 annually
The peak incidence : 3rd 5th decades of life
Males are affected 3 times as female
Recurrence rates : 15 % in 3 years
30 50 % in 15 years
In the developing countries the incidence has significantly
increased over the last decades

The development of USD is a complex, still
poorly understood and multifactorial
process
The theories of stone formation :
1
I. CRYSTA LLIZA TI ON TH EORY

SUPERSA TURA TED SOLUTION

CRYSTA L N I D US

CRYSTA LGRO WTH
( A GGREGA TION )

STON E
Solute
pH
temperature

-
Inhibitors :
Magnesium
Citrate
Pyrophoshate
Peptides
Heavy Metals

Prerenal
Exogenous :
Dietary
Immobilization
Medication : vit D over dosage
vit C more 4 g/day
Endogenous :
Hyperpara thyroidism
Uric acid diasthesis
Malabsorbsi
Renal
Glomerular
Tubular : RTA
Idiopathic hypercalciuria
Post renal
Epithelial lesion
Obstruction
infection

II. COLLOID/ MA TRIX TH EORY :

Ki d ney excr et e or ga ni c com p ou nd

Mu co Pr ot ei n
( MA TRIX)

STON E

Crystal deposition

I. GENETICS/heredity :
Cystinuria
Renal tubular acidosis
Medullarry sponge kidney
II. GEOGRAPHY :
High temperature
High humidity
III. DIET :
Increase intake of
Calcium
Oxalat
IV. OCCUPATION
Scdentary job

Composition Freq
(%)
Effect of pH
On solubility
R
density
Calcium :
oxalat
phosphate
oxalat &
phosphate
80
35
10
35

Little effect

0,50
1,0
Struvit 10 ' At pH <5,5 0,2
Uric acid 8 ' At pH >6,8 0,05
Cystine 1 ' At pH >7,5 0,15
Other 1 0,05


Type of stone Etiologic Factors
Calcium oxalate
Calcium phosphate
Calcium carbonate

Uric acid

Cystine

Struvit

Matrix
Supersaturation of urine with
calcium from :
a. Renal leak
b. Intestinal absorption
c. Bone resorption hyperoxaluria

Hyperuricosuria
Constantly low urine pH

Cystinuria

Alkaline urine caused by ure
splitting organism

As above (idem dito)

I. UPPER TRACT USD :
Renal Calculi : Asymtomatic until :
Causes obstruction or Infection
Obstruction :
Acute
Colicky pain, may be radiate to :
Groin
Testis
Tip of the penis
Hematuria, negative in 15 %
Nausea, vomiting
Chronic : asymtomatic
Infection : Fever and chills
Pain in the costovertebral angle


Blood examination : WBC
creatinine
Urine analysis and culture
Plain abdominal film (KUB)
USG if available
Spiral / helical CT Scan
IVU : recently is infrequenly used
I. Acute Treatment
A. Ureteric Colic _ adequate pain relief
Parenteral narcotics :
Morphine sulfat
Pethidine HCL
Nonsteroid anti inflamatory drugs (NSAID)
Ketonoloc tromethamine
Acetaminophen
Ibuprofen : 600 8 mg/8 hours
Nifedipine XR : 30 mg/once/day
Cox-2 inhibitor : Parecoxib : i.v. 40 mg
Anti emetic drugs
B. Immediate intervention
The form of intervention :
Ureteral stenting
Percutaneous/open nephrostomy tube
Indications :
A solitary functioning kidney
Elevated creatinine
Pre existing renal insufficiency
Fever of unclear etiology/suspected UTI
Intractable pain/colick
Pyonephrosis
II. Definitive treatment of upper tract USD
1. Expectant treatment/non surgical treatment
Indications :
a. Small opaque stone ( <5 mm )
b. Minimal hidronephrosis
c. No UTI
d. Stone in the lower third ureter
e. asymptomatic

Methods :
a. Oral hydration _ drink copious quantities of
water
b. Drugs : Kalkurenal, enatin, o 1 blocker
c. J ump around
d. Save for analysis any stone passaged out
e. Weekly plain abdominal film
f. Expectative time : 4 6 weeks
Result :
a. 90% of s 4 mm stone pass spontaneously
b. 20% of stone >6 mm pass spontaneously
2. ESWL
Indications :
a. Renal stone with size of 1,5 cm 2 cm
b. Ureter proximal stone <8 mm or after pushed
up and stenting
c. Distal ureteral stone

3. Endoscopic Treatment :
A. Ureteroscopic :
Rigid /semirigid ureteroscope
Flexible ureteroscope

Usage of ureteroscope :
Stone extruction :
Grasped forcep
Stone basket
Stone fragmentation (lithotripsy) using :
Ultrasound
Electrohydraulic
Pneumatic
Laser (Holmium-YAG)

Pushing stone upward
Succes rate : up to 95%
B. Percutaneous Nephrolithotripsy
(PCNL) :
Indications :
Stone size >2 cm
Staghorn calculi
(multistage treatment)
Succes rate : up to 85%
4. Laparoscopic Surgery :
Indication : proximal large ( >2 cm )
ureteral stone
5. Open Surgery :
Pyelolithotomy
Nephrolithotomy
Bivalve/anatrophic
Ureterolithotomy
I. Bladder Stone :
A. Predisposing factors :
Bladder outlet obstruction
Foreign bodies
Passing of ureteral stone _ nidus in the bladder
Hyperuricosuria
Diverticle
B. Clinical Presentation
Pain :
Hypogastrium area
Referred pain to the penis
Hematuria
Dysuria
Intermittent stream
Recurrent UTI
C. Diagnosis :
KUB photo
USG
cystoscopy
D. Treatment :
1. Lithotripsy :
Mechanical
Electrohydraulic

Laser
ESWL
Pneumatic
2. Vesicolithotomy

Most of the small bladder stones will pass spontaneously
A small amounts of urethral stone entrappe and impacted in the
urethra i.e in the verumontanum and in the fossa naviculare

Gently posterior lubrication
Dorsal meatolithotomy
Pushing endoscopycally into the bladder and lithotripsy
USD :
90% of patients USD accosiated with metabolic,
environmental and life style etiology
Up to 80% will recure after first episode of USD
Prevention of recurrent USD is utmost important

Normal value of substances in 24 hr urine
Substance Male (mg) Female (mg)
Calcium
Uric acid
Oxalate
Citrate
<300
<800
<50
450 - 600
<250
<750
<50
650 - 800

Baseline evaluation for USD
Determination of :
Serum Ca, phosphorus, and uric acid
24 hour excretion in the urine of :
Ca, P, uric acid, oxalate and creatinine
If any abnormality found should a more extensive evaluation
performed


Causes :
Hyperparathyroidsm
_ Bone resorption
Renal leak
Hyperabsorption from g i tract
Metabolic evaluation :
1. Baseline studies :
Regular diet
Collect 24 hours urine for :
Creatinine
Calcium
P
Uric acid
Oxalat
Citrate
Metabolic evaluation :
2. Dietary Restriction :
Diet limited to 400 mg Ca
100 m Eq Na/day _ 1 week
Urine 24 hours examination as foremention

1. Calcium loading :
Overnight fasting
First voided urine discarded
2 hours urine collection _ examination
Receive 1 g Ca gluconate _ 4 hours urine collection
and examination
Classification Hypercalciuria
Type Serum Ca
Urine Calsium
Fasting After Loading
Resorptive
Absorptive
Renal Leak
Up
N
N

Up
N
Up

Up
Up
Up


ETIOLOGY :
1. Hyperparathyroidsm
2. Bone metastatic Cancer
3. Multiple myeloma
4. Immobilization
5. Cushings syndrome
6. Hyperthyroidism
Treatment :
Treat the etiology
Found in >50% of patients USD
After loading test positive
Hyperabsorption of ingested Ca
Treatment :
1. Diet and hydration
Restructed Calcium to 400 mg Ca/day and Na 100 m
Eq/day
Drink 3 4 L water daily
2. Cellulose phosphate 3 x 5 g/day
need : Magnesium supplement and lowering oxalate diet
3. Orthophosphate 3 6 g daily

Accounts for appreoxmately 10% patients with hypercalciuria
Pathogenese : innability of the tubulus to resorb calcium
Treatment :
1. Thiazide diuretics :
Increase resorption in the tubulus
Dosis : 2 x 50 mg a day
Pottasium supplement is necessary
2. Orthophosphates

Pure uric acid stones : 10% of USD
Uric acid insoluble in pH <5,8
Etiology : - gout disease in 25%
- others unknown
Risk factors : - constantly
- low urine output
Treatment :
1. Hydration : >3 L/day

2. Alkalinization of urine : sodium bicarbonate orally 650 mg
(2tablets) every six hours
3. Low purine diet
Low protein diet, 90 g/day
4. Allupurinol : 200 600 mg daily

Oxalic acid :
Extremely insoluble
End product of metabolism (mostly)
10% is absorbed from g.l. tract
Hyperoxaluria divided in :
1. Primary
2. Enteric
3. Exogenous

1. Primary Hyperoxaluria :
An autosomal recessive disorder
Urinary oxalate >100 mg/day
Early onset of nephrocalcmiosis
R/ - pyridoxine 100 400 mg daily
- hydration
- low oxalate diet
2. Enteric hyperoxaluria :
Malabsorption (increase) of oxalat
due : inflamatory bowel disease small bowel by pass
R/ - low oxalate/fat diet
- calcium supplement
- cholestyramine
3. Exogenous hyperoxaluria
Ascorbic acid >5 g/day
methoxyflurane

Found in up to 50% pts with Ca stones
_ check rutinly urinary citrate
R/ Potassium citrate


Are composed of : magnesium ammonium
phosphate and carbonate apatite
=triple-phosphte strued
Need : - markedly elevated urine pH
- high concentration in the urine of : ammonia, bicarbonate
and carbonate
- produce by urea splitting organisms
The urea splitter : Protein ( >75% )
Klebsiella
Pseudomonas
Providenced
Staphylococcus
Ureaplasma urealyficum
Female 2 x male
Occurred in 10% of praplegic pts

Urinary infection with high urine pH
Relative radiolucent big stone in the PCS

Treatment :
1. Anatrophic nephrolithotomy
2. P N L
3. P N L & ESWL (sandwich technique)
4. Chemolysis :
10% Hemiacidrin salution (Renacidin) (pH =4,0) is dilevered via
nephrostomy tube or ureteral catheter


Benign Prostatic Hyperplasia (BPH)

Anatomi prostat:
Kel.prostat: kel.seks
asesorius pria
Normal sebesar buah kenari
dikelilingi
kapsul fibrous dan
mengelilingi uretra
Pada waktu ejakulasi
memproduksi cairan prostat
yang bersama dengan
produk dari testis,
ves.seminalis &
kel.bulbouretral membentuk
semen
Prostat & buli2 normal
Letak anatomik prostat
Perubahan patologik pada prostat juga berakibat pada buli2
Perubahan pada buli2 bisa berakibat perubahan pada traktus
urinarius bagian atas (ureter dan ginjal)

Pembesran prostat jinak
Lobus medius menonjol ke dasar buli2
Uretra pars prostatika menyempit
Terjadi trabekulasi dari dinding buli2
Akibat dari BPH
o Penebalan dinding buli2
o Hematuria berulang
o Terbentuk divertikel buli2
o Infeksi saluran kemih
o Terbentuk batu buli2
o Dilatasi bgaian atas

Diketahui sejak 1500 S.M.
1000 tahun kemudian
didiskusikan oleh Hippocrates
Insidensi: 50% (klinis) pria 60-
69 tahun, k.l. 100% pada umur
80 tahun (mikroskopik sejak
umur 35 tahun)

BPH - DMS 2002 3
Anatomi
kelenjar prostat
Uretra pars
prostatika
Prostat
Muara dukt us
ejakul atorius
Sfingter uretra
ekster na

Patogenesis BPH
Syarat terjadinya BPH :
* Testis yg memproduksi
androgen
* Ketuaan ( ? )

BPH 2000 - DMS
Cinical prevalence in the Baltimore Longitudinal Study of Ageing (based on history and
Physical examination, n =1,057)
Clinical prevalence in the Baltimore Longitudinal Study of Ageing (based on rectal
examination, n=1,057)
27
51
69
80
9
42
57
27
0 20 40 60 80 100
40-49
50-59
60-69
70-79
A
g
e

(
y
e
a
r
s
)
Prevalence (%)
0 20 40 60 80 100
Age-specific prevalence of BPH

13
Theory
Dihydrotestosteron
hypothesis
Oestrogen-testosteron
imbalance
Stromal-epithelial
interactions
Reduced cell death
Stem cell theory
Theories for the cause of BPH
Cause
| 5-o reductase and
androgen receptors
| Oestrogens
+ Testosteron
| Epidermal growth
factor/fibroblast
growth factor
+ Transforming growth
factor |
| Oestrogens
| Stem cells
Effect
Epithelial and stromal
hyperplasia
Stromal hyperplasia
Epithelial and stromal
hyperplasia
| Longevity of stroma
and epithelium
Proliferation of transit
cells

Simptomagenesis
Prostatisme
Sindroma Prostatisme
LUTS
(lower urinary tract symptoms)

Fungsi unit Vesiko Urethral
1. Penyimpanan (STORAGE)
2. Mengeluarkan urin periodik (VOIDING)
BPH
LUTS keluhan obstruktif:
1. Hesitansi
2. Pancaran lemah
3. Mengejan
4. Kencing lama
5. Terasa tak habis
6. Retensi urin
7. Overflow Incontinence (ischuria paradoxa)
BPH
LUTS keluhan iritatif
-1.Urgensi Urge incontinence
-2.Frekuensi (pollakisuria)
-3.Nokturia


International Prostate Symptom Score (I-PSS)

Dalam 1 bulan terakhir:
1. Terasa sisa kencing 0 1 2 3 4 5
2. Sering kencing 0 1 2 3 4 5
3. Terputus-putus 0 1 2 3 4 5
4. Tidak bisa menunda 0 1 2 3 4 5
5. Pancaran lemah 0 1 2 3 4 5
6. Mengejan 0 1 2 3 4 5
7. Kencing malam 0 1 2 3 4 5
Total .
Total IPSS score: 0-7: ringan, 8-18 : sedang, 19-35 : berat

Provokator Retensi Urine Akuta
1. Minum alkohol
+
Stimulan simpatetik
+
Tonus Prostat &
otot polos bladder outlet
2. Bepergian jauh
3. Masukan cairan banyak
4. Konstipasi
5. Agen anti cholinergik
DRE (digital rectal examination) = RT = CD
Ukuran
Konsistensi: padatkenyal/keras/nodul
Mobilitas
Batas2 anatomik: atas, lateral, sulkus
PSA interpretation
Kadar PSA
0.5 - 4 ng/ml
4 - 10 ng/ml
> 10 ng/ml

kenaikan >20% / tahun

Uroflowmetri
Max.flow rate (ml/sec)
>15 ml/sec
10 - 15 ml/sec
Interpretasi
Normal
20% kemungkinan Ca
50% kemungkinan Ca

Perlu biopsi
Interpretation
Normal
Mild obstructed
Obstructed

<10 ml/sec
TRUS (Transrectal ultrasound)
Accurate measurement of the prostate
Hypoechoic focus
Prostatic biopsy (if indicated)
Diagnosa BPH
Anamnesa:
- I-PSS
Pem.fisik:
- buli-buli
- CD / RT
Pem.tambahan:
- lab: UL,DL,RFT,PSA
- pencitraan: USG/BOF/TRUS/IVP
Terapi BPH
Konservatif: observasi (watchful waiting) 0 - 7
Medikamentosa (Tx medik) 8 - 18
Pembedahan: 19 - 35
- terbuka
- endoskopik: TURP, TUIP
Invasif minimal:
- balloon dilatation
- stent
- microwave (thermotherapy)
- radiofrequency
- laser ablation
Kontra-indikasi Tx medik BPH
Retensi urin (akut atau kronik)
Insufisiensi renal
Dilatasi traktus atas
Hematuria berulang
ISK berulang
Batu buli-buli / divertikel
Terapi medik BPH
Alpha blocker
- terazosin
- prazosin
- tamsulosin, dll
Supresi Androgen
- 5 alfa-reduktase inhibitor
Fitoterapi
Morfometri BPH
Rasio of epithelium terhadap stroma:

Efikasi vs. risiko terapi BPH
efikasi
risiko
OPEN
PROSTATECTOMY
OPEN
PROSTATECTOMY
TURP
TURP
TUNA
TUNA
THERMOTHERAPY
THERMOTHERAPY
ALPHA BLOCKERS
ALPHA BLOCKERS
5-ALPHA
REDUCTASE
INHIBITORS
5-ALPHA
REDUCTASE
INHIBITORS
PHYTOTHERAPY
PHYTOTHERAPY
epith : stroma =21.6 - 50 % : 60 - 78 %
BPH simtomatik: proporsi stroma lebih tinggi
Respons terhadap Tx:
predominan otot polos : alpha blocker
predominan epithel : supresi androgen
predominan fibrosis : bedah
Rasional penggunaan alpha blocker
Kontraksi otot polos prostat dimediasi oleh : stimulasi simpatis
reseptor alpha
Kontraksi otot polos (kapsul, adenoma, leher buli) : merupakan
40% dari penyebab obstruksi saluran keluar
Alpha blocker :
- relaksasi otot polos prostat
- mengurangi simtom
- memperbaiki pancaran kencing
Agen fitoterapi untuk BPH
Pygeum africanum (African plum)
Urtica spp. (stinging nettle)
Sabal serrulatum (Dwarf palm)
Serenoa repens B (American dwarf palm)
Cucurbita pepo (Pumpkin seed)
Populus tremula (Aspen)
Echinaceapurpurea (Purple coneflower)
Secale cerelea (Rye)
Intervensi urologis di Surabaya
Balloon
dilatation
Prostatic stent
Thermotherapy
TUIP
(transurethral
incision of the
prostate)
TURP
(transurethral
resection of the
p.)
Laser TURP
Open
prostatectomy


Prostatektomi terbuka
Retropubik (Millin) atau Suprapubik (Freyer)
Indikasi:
Prostat yang besar (>40-60 mg)
BPH +BBB besar
Kelainan sendi coxae (tak bisa litotomi)
RS yang tak ada alat TURP
TURP (transurethral resection of the prostate)
Memakai alat resektoskop
Dengan atau tanpa endokamera (video)
Indikasi:
- Gold standard terapi operatif BPH
- Harus dilakukan oleh dokter spesialis urologi
Paramedis harus terlatih, di OK maupun ruangan
TURP (transurethral resection of the prostate)
Penyulit intra bedah:
- Perforasi buli2
- Perforasi kapsul prostat (sinus terbuka)
- Perdarahan
- Lesi sfingter uretra eksterna
- Sindroma TUR
Penyulit pasca bedah dini:
- Sindroma TUR
- Perdarahan
- Retensi bekuan darah
- Urosepsis
- Retensi urin pasca lepas kateter
Penyulit pasca bedah lanjut:
- Hematuria berulang
- Infeksi saluran kemih
- Orko-epididimitis
- Ejakulasi retrograd
- Inkontinensia urin
- Striktura uretra
- Stenosis leher buli2


Prostat Hipertrofi

Pembesaran jinak prostat
BPH =Benign Prostate Hyperplasia
Definisi :
Suatu keadaan terjadinya pertumbuhan yang berlebihan dari
komponen stroma dan epitel gld. Prostat

Berdasarkan PA yang terjadi sebenarnya hiperplasia
kelenjar periurethral yang kemudian mendesak
jaringan prostat yang asli ke perifer menjadi kapsul
= surgical capsule

Prevalensi
Data di indonesia belum ada
Berry dkk ( 1984 )
hasil autopsi tentang hubungan usia dengan besarnya prostat :
41 50 th 23%
51 60 th 42%
61 70 th 71%
71 80 th 82%
81 - 90 th 88%
Watanabe (1984)

37% laki-laki jepang 55 tahun BPH berdasarkan skriningUSG

Glynn ( 1985 )
Angka prostatektomi per 1000 pria/tahun
40 49 thn 0,9%
50 59 thn 4,1%
60 69 thn 12,1%
70 80 thn 19,4%
Insiden di RSUP palembang
I. Batu saluran kencing
II. Prostat hipertrofi
III.Striktur
IV. Trauma
V. Keganasan
Etiologi
Belum jelas benar
Beberapa teori :
Teori stem cell
Teori reawakening
Teori hypothalamic-pituitary gonade axis = DHT
Teori groeth factors
Terdapat hubungan antara usia dengan faktor hormonal
Teori Stem Cell ( Isaac 1987, Cohey 1990 )
Normal : sel tumbuh sebanding dengan sel mati
=steady cell
BPH : pembentukan sel baru lebih banyak
dibanding sel mati
Berry, 1987 :
pengaruh estrogen memperlambat kematian sel prostat
Stem Cell proliferasi/sel baru sebanding dgn sel mati

- usia
- ggn keseimbangan hormonal
Teori Reawakening ( Mc Neal 1978 )
Proses hiperplasia prostat merupakan interaksi antara
elemen stroma dan elemen epitel
Pada kehidupan embrional elemen stroma
menginduksi pertumbuhan epitel
Pengulangan proses ini =reawakening mungkin
merupakan mekanisme pembentukan BPH
Estrogen turut mempengaruhi perkembangan stroma
dan DHT mempengaruhi komponen epitel


Teori Growth Factors
adanya interaksi antara unsur stroma dan unsur epitel ternyata
dipengaruhi oleh faktor faktor pertumbuhan seperti ;
EGF =epidermal growth factor
KGF =keratinocyte growth factor
IGF =insuline like growth factor
TGF =Transforming growth factor
Skema antara stimulasi inhibisi factor
androgen
( DHT)
- KGF
- EGF TGF
- IGF
proliferasi sel sel mati
seimbang
prostat normal

androgen
( DHT )
Agonistic antagonistic
KGF
EGF TGF
IGF
sel mati
Proliferasi sel
prostat hiperplasia


Patologi prostat hiperplasia
Lowsley : 5 lobus
Mc Neal (1972) : Zona perifer
Zona sentral
Zona transisional
Zona pre prostatik sfinkter
Zona segmen anterior
Daerah predileksi tersering terbentuknya nodule hiperplasia yaitu
zona transisi dan zona preprostatik spinkter
Gejala prostat hypertrofi
Tidak ada korelasi antara besar prostat dengan beratnya
gejala
Boyarsky ( 1977) : gejala gangguan miksi sebab pembesaran
prostat
1. gejala Obstruksi =statik
Pancaran melemah =menetes
Intermitten = terputus
Driblling terminal
Hesitansi
2. gejala iritatif =dinamik
Frekwensi, nocturia
Urgency
Dysuria
Tidak lampias =sisa kencing
Gejala Umum :
nyeri pinggang
Mual muntah ggn fungsi ginjal
somnolen disorientasi
lemah ,BB menurun azotemia

Patofisiologi Gejala
timbulnya manifestasi obstruksi di tentukan oleh :
volume kelenjar
elastisitas leher vesika, otot polos prostat dan kapsul
kekuatan kontraksi detrusor
gejala iritatif oleh karena faktor :
gangguan tonus otot buli o.k. hipertrofi detrusor
infeksi
residual urin
acut retensi
infeksi
pemberian cairan >>
obat obat anti cholinergik, sympatomimetik

hematuria
Pelebaran vena prostat ruptur
Infeksi
Batu
Keganasan
DIAGNOSTIK
Rekomendasi WHO/ICC For BPH :
I. 1. Menggunakan symptom score untuk penderita BPH
2. Menggunakan kriteria Quality of Life Assesment ( QOL )

II. Rekomendasi diagnostic Work-up terhadap laki-laki 50 th dengan
simtom LUTS dan kecurigaan B.O.O.

1. Highly Recommended Diagnostic Test
a. History =anamnesa
meliputi :
Tractus urogenital
Operasi sebelumnya
Kesehatan umum
Obat yang dikonsumsi
Kondisi ( fitness ) untuk kemungkinan tindakan operasi
b. Quantification of symptom ( penghitungan scor
simtom )
I-PSS 0 - 35
QOL 0 - 6
c. Voiding Diary
meliputi frekwensi dan volume miksi sepanjang
hari ( 24 jam )
membedakan dengan ;
DM
Penyakit J antung Kongestif
Banyak minum
Penyakit ginjal
d. Pemeriksaan fisik dan RT
difokuskan untuk mengassess :
Regio suprapubik tanda-tanda distensi buli
Tonus spinkter
Bulbo cavernosus refleks
status neurologis ekst. Inf.
R T mengevaluasi Gld. Prostat
perkiraan ukuran
konsistensi
bentuk

kecurigaan cancer prostat
e. Urinalisa
hematuria
proteinuria
pyuria
Keadaan patologis lain misal : krystal, glukosa, bilirubin,dll
f. Assesment Fungsi Ginjal
serum creatinin - ureum
g. Serum Prostate Spesific Antigen ( PSA )
terutama :
perkiraan usia >10 thn lagi =life expectancy
diagnostik Ca.prostat
PSA meningkat - setelah ejakulasi
- inflamasi =infeksi prostat
- ischemic =infark prostat
- BPH
- PIN
- Prostat Ca
PSA Menurun - pengurangan ukuran prostat
- stimulus androgen :
- LNRH Analog
- Castrasi
- Estrogen
- 5 alfa reduktase inhibitors
PSA density =nilai PSA/Vol Prostat
PSA Velocity=perubahan PSA/ml/thn
Normal ( Cut off Level ) PSA =4,0 ng/ml
2. Recommended Diagnostic Test
Bila : LUTS (+) tapi BOO tidak spesifik
a. Flow Rate
alat ; Uroflowmeter
satuan ; ml/dtk =cc/dtk
Qmax =max.urinary flow rate
Qave =average urinary flow rate
b. Residual urine
cara : - cateterisasi post void
- USG / TRUS
3. Optional
a. Pressure flow studies
b. Imaging :
TAUS atau TRUS PSA
saluran kencing atas =U U T dengan USG atau
IVP - riwayat infeksi UUT

- hematuria
- riwayat urolithiasis
- pernah operasi TUG
- renal insufisiensi
DIFFERENTIAL DIAGNOSE
O Ca. prostat
O Prostatitis
O Ca. Vesika
O Tumor ekstra Vesika
O Obstruksi leher vesika ( Fibrosis, Kontraktur )
O Obstruksi urethra ( striktur, Batu )
O NMeurogenic Bladder =spinchter dyssinergia
TERAPI BPH
1. Watchful waiting
BPH dengan simptom minimal

2. Medical therapy
a. Alfa adrenergic rec. antagonist
( Alfa Blockade )
Terazosin =Hytrin
Prazosin =minipress
b. 5 alfa reduktase inhibitor
proscar
c. Phytoterapi
epi prostat
tandenan
3. Non Surgical invasive therapy
Ballon dilatation

Urethral stents
Thermo therapy =hyperthermia

4. Surgery
TUR - P
TUI - P
Open prostatectomy
Laser prostatectomy
Electrovaporization
Prostatectomy terbuka
+ Cara : 1. Freyer : trans vesica
2. Terrence millin : retro pubic
+ Indikasi :
perkiraan berat prostat >60 gram
disertai : batu buli, divertikel
+ Kelemahan/kerugian
morbiditas tinggi 10 - 25 %
mortalitas 1 - 4 %
nyeri pasca operasi ++
ada luka sayatan di kulit
+ Keuntungan
mudah/sederhana, tanpa alat mahal
dapat dikerjakan ahli bedah umum
4 T U R - P
+ merupakan pengobatan terpilih, gold standard
pada prostat hipertrofi
+ morbiditas 8 - 10 %
+ mortalitas 0,2 - 1 %
+ Nyeri pasca bedah minimal
+ tanpa luka sayat operasi pada kulit
+ Kelemahan :
perlu alat khusus
hanya dapat dikerjakan oleh ahli urologi


ORTHOPAEDIC SURGERY
Dr. MUZAKKIE, SpB, SpOT.

NICOLAS ANDRY 1741
ORTHOS =LURUS
PAIS =PAEDOS =ANAK

Orthopaedic Definition ( Salter )
Art & Science
Investigation
Diagnosis
Treatment
Prevention

Disorder & Injury of musculoskeletal system by medical surgical &
physical study. Physiology, pathology & basic science

ORTHOPAEDIC
- TRAUMA
- DISORDERS

TRAUMA FRACTURE & DISLOCATION

DEGENERATIF SCOLIOSIS
OSTEOPOROSIS ARTHROSCOPY
RHEUMATOID TUMOR
C P

BONE : STRUKTUR
1. FRAME WORK
2. LEVERS
3. PROTECTION
ORGAN
4. HEMOPOETIC
5. STORAGE

EMBRYONIC
MESENCHYMAL MOD. CARTILAGE MOD. CO PERISOTEUM
5th WEEK 6 th WEEK 6 BLN 9 BLN


GROWTH
LENGTH :
1. ARTICULAR CARTILAGO
2. EPIPHYSEAL PLATE CARTILAGO
WIDTH : PERIOSTEUM

REMODELING WOLF LAW (J ulius Wolf 1872)
DEPOSIT STRESS (+) CONCAF
RESORBSI STRESS (-) CONVEX

PROSTHESIS PARTIAL
AUSTIN MOORE
THOMSON
TOTAL

-> Calcar Femorale

SENDI
SYNDESMOSIS IV DISC
SYNCHONDROSIS EPIPH. PLATE
SYNOSTOSIS SKULL
SYMPHYSIS SYMP. PUBIS
SYNOVIAL J OINT

MOVE
ABDUCTION ADDUCTION
FLEXI EXTENSI
INTERNAL ROTATION EXTERNAL ROTATION
PRONASI SUPINASI EVERSI INVERSI
DEVIASI : - RADIAL DEVIASI
- ULNAR DEVIASI
DEFORMITAS
CALCANEUS >< EQUINUS
CAVUS >< PLANUS
VARUS >< VALGUS
ANGULASI =BOWING DEFORMITY

PEMERIKSAAN
LOOK - INSPEKSI
FEEL - PALPASI
MOVE - ROM
SYMETRISITAS
RADIOLOGI

TEST
HIP : - THOMAS TEST
- TRENDELENBERG
- BARLOW ORTOLANI

ORTHOPAEDIC DISORDERS

VARIASI NORMAL
J OINT LAXITY - PES PLANUS
- GENU VALGUM
INTERNAL TORSION - FEMORAL TORSION
- TIBIAL
EXTERNAL TORSION - FEMORAL
- TIBIAL
GENU VARUM
KYPHOSIS
CONGENITAL
APLASIA/ HYPOPLASIA
DISPLASIA
HIPERTROPHY : LOCAL GIGANTISM
DUPLICATION :
POLYDACTYLY THUMB :
WASSEL TYPE 7 TYPE
CONGENITAL SPESIFIC
FOOT :
* METATARSUS PRIMUS VARUS
HALLUX VALGUS

* METATARSUS ADDUCTUS ( VARUS)

CTEV (congenital talipes equino varus)

CLUB FOOT
>
INSIDENS , 2
DEFORMITAS
MIDTARSAL J OINT ^ FOREFOOT ADD & SUP
SUBTALAR J OINT ^ HEEL VARUS
ANKLE JOINT ^ EQUINUS
NECK OF TALUS ANGULATION ^ FOOT DEVIATION


TH/ - SERIAL CAST
- DENIS BROWNE SPLINT
- OUT FLARE SHOES
- SURGICAL
RIGID
NEGLECTED
PES CALCANEOVALGUS
TARSAL COALITION =RIGID VALGUS FOOT
ACESSORY TARSAL NAVICULAR
(OS TIBIALE EXTERNA)

LONG BONE
PSEUDO ARTHROSIS OF TIBIA
KNEE : DISCOID MENISCUS
HIP : COXA VARA
CDH BARLOW ORTOLANI
Th/ FREJ KA PILLOW
PAVLIC HARNESS
POLYDACTYLY / MIRROR FINGER
TRIGGER THUMB
HIPOPLASIA OF RADIUS
SPINA BIFIDA
SCOLIOSIS
TORTICOLLIS
OSTEOGENESIS IMFERFECTA
ACHONDROPLASIA
ARACHNODACTYLY
MULTIPLE EXOSTOSIS
AMYOTONIA CONGENITAL =
FLOPY CHILD
AMYOPLASIA CONGENITAL =
ATHROGRYPOSIS MULTIPLEX CONGENITA.

PENYAKIT METABOLIC ORTHOPAEDIC
RICKETS - DEF VIT D CALCIFIC MATRIX
- RACHIITIC ROSARY
OSTEOMALACIA
- DEWASA RICKETS
- PSEUDO FRAKTUR
- MILKMANS SYNDROME
SCURY - AVITAMINOSIS C
- MATRIX
- PSEUDOPARALYSIS

OSTEOPOROSIS
- OSTEOPLASTIC MATRIX ()
- OSTEOPENI
- HORMONAL IMBALANCE
- DISUSE
- POST MENOPAUSAL & SENILE

OSTEITIS FIBROSA CYSTICA =
HYPERPARATHYROIDISM
OSTEOCLASTIC RESORBSI
- OSTEOLYTIC LESION =BROWN TUMOR
- PATHOLOGIC FRACTURE

HYPERPITUITARISM =
- GIGANTISM FEMORAL EPIP SLIP
(COXA VARA)
- AEROMEGALY ( ADULT )

CUSHING SYNDROME
- HYPER ADRENOCORTICISM

HIPOPITUITARISM
HORMON - DWARFISM
- FROLIC SYNDROMW
POLYOSTOTIC FIBROUS DYSPLASIA
PATHOLOGIC FRACTURE
ALBRIGHTS SYNDROME
- , SEX PRECOC

OSTEITIS DEFORMANS
(PAGETS DISEASE)
- UMUR TUA BOWING PROGRESIF & SAKIT
TULANG PANJ ANG

SKELETAL RETICULOSIS
- NON LIPID RETICULOSIS (HISTIOCYTOSIS X)
1. LETTERES SIWES
2. HAND SCHULLER- CHRISTIAN DIS
3. EOSINOPHYLIC GRANULOMA
- LIPID RETICULOSIS :
GAUCHERSS
- LIPID KERASIN


PENYAKIT INFLAMASI ORTHOPAEDI
I. PYOGENIC BACTERIAL
II. GRANULOMATOUS BACTERIAL
III. NON SPESIFIC INFLAMATORY DISORDER

I.1. OSTEOMYELITIS AKUT
- HEMATOGENOUS METAPHYSIS
- STAPHLOCOCCUS
* FOCUS REAKSI PERIOSTEAL => UBCUTAN ABSES
- BONE NECROSIS =>SEQUESTER CLOACA
- NEW BONE FORMATION =>INVOLUCRUM
- SEPTIC ARTHRITIS
KOMPLIKASI : ACUTE : -
- ABCESS >
LATE : - CHRONIC
- FRAKTUR PATOLOGIS
- KONTRAKTUR
2. OSTEOMYELITIS KRONIK
- SEQUESTRUM
- INVOLUCRUM
* ONCE OSTEOMYLITIS FOR EVER
OSTEOMYELITIS
3. ACUTE SEPTIC ARTHRITIS
DALAM PERSENDIAN
4. OSTEOMYELITIS OF THE SPINE
- STAPHYLOCOCCUS, E.COLI
5. J ARI-J ARI
- PARONICHIA, FELON
II. GRANULOMATOUS BACTERIAL INFECTION
CAUSA : - TB
- SYPHYLIS
- FUNGI : ACTINOMYCOSIS
TUBERCULOSIS OSTEOMYELITIS OF THE SPINE
- BATSON PLEXUS
- ANTERIOR PART DARI CORPUS VERT PUS
- KIPOSIS KOMPLIKASI PARAPLEGIC

III. NON SPECIFIC
RHEUMATOID ARTHRITIS
ANKYLOSING SPONDYLITIS
HEMOPHYLIC ARTHRITIS
TB SPINE
ANTERIOR SPINAL FUSION

PENYAKIT DEGENERASI
HNP = PID
SPINAL STENOSIS
NON ARTICULAR RHEUMATISM
* CALCIFIC SUPRASPINATUS TENDINITIS
- PAINFULL ARCH SYNDROME
* ADHESIVE CAPSULITIS
- FROZEN SHOULDER
TENNIS ELBOW : EPICONDYLITIS
DE QUERVAINS : APL & EPB
TRIGGER FINGER : CAPSUL & TENDON SHEATHS OF THE
PALM
POPLITEAL CYST (BAKERS CYST)
- KNEE J OINT
(SPT GANGLION)
BURSITIS
- BUNION - MP I
- HOUSEMAIDS KNEE PREPATELLA
- WEAVERS BUTTON RADIAL
- STUDENT ELBOW - OLECRANON
NEUROMUSCULAR DISORDER
Cerebral Palsy - SPASTIC
- ATAXIC
- ATHETOID
* SCISSOR GAIT
* EQUINUS DEFORMITY
* THUMB CLUTCHED
* POLIOMYLITIS
- RESIDUAL DEFORMITY ADL
NERVE ENTRAPMENT
- CARPAL TUNNEL SYNDROME (CTS)
- ULNAR TARDY PALSY
- SCALENUS SYNDROME
* BRACHIAL PLEXUS pd THORAX OUT LET
- MORTON : METATARSALGIA
BRACHIAL PLEXUS INJ URY
( OBSTETRICAL)
UPPER ARM TYPE
* ERBS PALSY (C5-6)
LOWER ARM TYPE
* KLUMPKES PALSY (C7-8)
* MUSCLE DYSTROPY
(DMP) GOWER SIGN

ORTHOPAEDIC disorder congenital




Neglected CTEV

Matatarsus primus varus halux valgus
Genu varum Congenital constriction band

Congenital constriction bands are partial or complete annular skin
depressions seen at birth. The cause is unknown. The incidence in Malays
is estimated to be 1 in 3500 births-about 5 times that of Chinese and
Indians. In severe constriction, gangrene may occur distally.

The constriction band was
excised and the skin closed by Z-
plasty in a two-stage procedure.


Habitual patella dislocation Amyoplasia congenital

Congenital Dislocation of the Hip

The Ortolanis test to
assess hip stability is done
by abducting and flexing
the hip to reduce a
dislocated hip.

The Barlows test the
reverse of the Ortolanis.
An unstable hip is
dislocated by adducting
the hip and gently
pushing it posteriorly.
Excessive force must not
be used and the baby
should be calm.

Syndactyly polylydacty


ORTHOPAEDIC disorder Metabolic

RICKETS


Sofield osteotomy = cis kebab



Ehler Danlos Syndrome


Senile osteoporosis



Trendelenburgs test

true length apparent length


Perthes diseasae

Bryants triangle


Heberden,s nodes


Swan neck deformity

Musculo Skeletal Tumors
( MST )

FKUI / RSCM 1995 1999
Prof Dr Errol U Hutagalung
Incidence MST : 1.2 %
Malignant : 1.3 %
Benign : 1 %

Dept. of Pathology FKUI
13.160 cases of neoplasm :
8.718 cases of malignant tumor
4.442 cases of benign tumor
.154 cases of MST :
.111 cases (72%) malignant
. 43 cases (28%) benign

J anuary 1995 December 2004 (10 years periods)
FKUI .455 cases
- Malignant : 72% ( 327 cases )
- Benign : 28% ( 128 cases )

Mayo Clinic 11.087 cases
- Malignant : 77 %
- Benign : 23 %

USA : 93.000 new cases of Lung Ca /year
88.000 new cases of Breast Ca /year
Only 1.500 new cases of Bone Sa

WHO (2002) : MST only 0.2% of overall human
tumor burden
On a numeric basis,
Musculo Skeletal Tumors (MST)
are uncommon and unimportant.

However, many of bone tumor affect
young children and are associated with
radical surgery, extensive and painful
chemotherapy


It is universally accepted that the management
of patients with MST needs a
TEAM APPROACH
consisted of Orthopedic Surgeon, Pathologist
and Radiologist.

that works in close cooperation, good communication,

Orthopedic Surgeon
Pathologist
Radiologist.

These 3 specialist considered as
the THREE PILLARS of the team

the setting it is called
the Clinico Pathological Conference ( CPC ) of Musculo Skeletal
Tumor ( MST )

Diagnosis established in Clinico Pathological Conference (CPC)

Surgical Staging

Tumor detected Surgical staging studies
Information from clinical and radiological studies surgical staging
Surgical Staging SystemEnneking WF
Enneking Surgical Staging
Benign : Stage 1 : Latent
Stage 2 : Active
Stage 3 : Aggressive
Malignant : Stage I : Low grade A : Intracomp.
Stage II : High grade B : Extracomp.
Stage III : Meta (+)
Procedure
FKUI : FNAB as first procedure
Literature : accuracy in bone lesions : 70 95%
FKUI : 79.7%
accuracy in Osteosarcoma : 80 95%
FKUI : 93%
FNAB if inconclusive, discrepancy with clinical,
radiological studies open biopsy
Final diagnosis : C.P.C.

Benign Tumors

Accepted treatment methods for benign tumor
1. Curettage : w/wo bone grafting for lesion with
cavitary formation such as in GCT, enchondroma, etc.
2. Resection only : osteochondroma; Bone Tumor in expendable bones
3. Resection +reconstruction : GCT stage 2 or 3
4. Sometimes amputation is necessary : GCT stage 3 ++

Osteochondroma

Complain (+) Resection


Giant Cell Tumor

GCT of Bone :
8 years period (1990 1997) : 32 cases
Demography :

Surgical Treatment
Curettage +autograft, allograft, w/wo bone
cement
Resection in expendable bones
Resection +Reconstruction such as fibular
autograft, allograft, arthrodesis or prosthesis
replacement

O+31 YEARS

Currently : for contaminated surgery in
stage 3 post operative
adjuvant radiotherapy

Literature :
- Megavoltage range 40-70 Gy
- Follow up average 10 years :
recurrences (-), malignant deg. (-)

F FK KU UI I. . W We es st t e er r n n S Su un ng g
L Li i t t e er r a at t u ur r e e R Ra as s C Ch hi i n na a
S St t 2 2 3 31 1 % % 7 70 0- -8 80 0% % M Ma aj jo or ri it ty y

S St t 3 3 6 69 9 % % 1 10 0- -2 20 0% % 7 7% %

S Se ex x M Ma al le e F Fe em ma al le e M Ma al le e


PRIMARY MALIGNANT GCT


Demography of Demography of Osteo Osteo Sarcoma S arcoma
FKUI F KUI Literature Literature
(Mayo Clinic) (Mayo Clinic)
S ex Sex Male Male Male Male
A ge Age Mostly Mostly Mostly Mostly
second decade second decade second decade second decade
L ocalization Localization Mostly around Mostly around Mostly around Mostly around
the knee the knee the knee the knee
F requency F requency 31 % 31 % 19% 19%
S tage Stage 90 % in St I I B 90 % in S t II B ??
10 % in St I II B 10 % in S t III B
Malignant Tumor
Most common : Osteo Sarcoma
10 years period (1995 2004) : 102 cases

OSTEOSARKOMA
Procedure : Clinical, Radiological
Fine Needle Aspiration Biopsy (FNAB)
Advantage of FNAB :
- Avoid complication of open biopsy
- Immediate neoadjuvant therapy
Final diagnosis CPC
Surgical Treatment :
Limb ablation for large tumors
Limb salvage : - Arthrodesis
- Resection only
- Resection +Reconstruction
Reconstruction using :
- Autograft / Allograft
- Prosthesis /Megaprosthesis
- Composite
Autograft :
As alternative due to unavailability of allograft
or megaprosthesis
For osteoblastic tumors
Technique - Autoclaved
- Extracorporeal irradiation (ECI)

Autoclaved 1200C 20
1350C 10

ECI : - Range : 50 300 Gy
- FKUI / RSCM cases : 100-150 Gy at BATAN
(National Atomic Energy)
Problems
. Diagnostic: small number of cases ^
limited experience difficulties in tissue
diagnosisunder or over diagnosis
. Late presentationbenign : stage 3 or 3+
malignant: stage II B or II B+
. Funding / education: chemotherapy in complete
drop out or refused treatmentalternative
Diagnostic
CPC can make or break (make a new diagnosis)

Funding / Education:
chemotherapy in complete
^ drop out or refused treatment
^ alternative

THREE PILLARS
setting of the Clinico Pathological Conference ( CPC ) of MST


Spinal Cord lesions

Anatomy
Spinal cord lies within protective covering of vertebral column.
Begins just below foramen magnum of the skull.
Ends opposite 2nd lumbar vertebra.
Below L2 continue as a leash of nerve roots known as cauda
equina.
Prolongation of the pia matter forms filum terminale.

Tumors
Tumors are classified into 3 types according to their site:
-extradural ( between the meninges and spine bones)
-intradural extramedullary (within meninges)
-intramedullary ( inside the cord)

Spinal tumors
Most spinal tumors are extradural about 85%
They may be primary tumors originating in the spine, or secondary
tumors that are the result of the spread of cancer from other
locations primarily the lung, breast, prostate, kidney, or thyroid
gland.
Any type of tumor may occur in the spine, including lymphoma,
leukemic tumors, myeloma, and others. A small percentage of
spinal tumors occur within the nerves of the spinal cord itself, most
often consisting of ependymomas and other gliomas.


Symptoms of spinal tumors
Pain (in 90% of patients), numbness or sensory changes, motor
problems and loss of muscle control.
Pain can feel as if it is coming from various parts of the body.
Numbness or sensory changes can include decreased skin
sensitivity to temperature and progressive numbness or a loss of
sensation, particularly in the legs.
Motor problems and loss of muscle control can include muscle
weakness, spasticity (in which the muscles stay stiffly contracted),
and impaired bladder and/or bowel control.

17% have Multiple level involvement.
Metastatic lesion mostly found in Thoracic spine.
Myelopathy develops over days to weeks.
Acute SCC does occur if tumor enlarges very rapidly due to
hemorrhage or if a vertebral body suddenly collapses.

Extradural tumors
The most common spinal tumor 85%
mostly metastatic.
Arise from osseous element of spinal column.
Grow rapidly.
Primary ; Lung, Breast, prostate and kidney.
Compress the spinal cord by Growing in epidural space
Causing collapse of vertebrae, distortion and narrowing.
e.g. lymphoma, hemangioma and neuroblastoma.
Intradural extramedullary tumors
Inside the dura but outside the spinal cord.
e.g. Meningioma, Neurinoma.
Arise from the dural sheath around the cord or showann cell sheath
around the spinal root.
Multiple tumors in Pt. with neurofibromatosis.
Can grow extradurally into retropleural or retroperitoneal through
intervertebral foramen.
Intradural intramedullary tumors
Inside the spinal cord
O Examples: Glioma, ependymoma, astrocytoma
Arise from glial elements of spinal cord or trapped ectodermal
elements.
More common in children.
Astrocytoma of spinal cord is the most common intramedullary
tumor of childhood.

Ependymoma of spinal cord is the most common intramedullary
tumor of adulthood.
O Arise from ependyma of central canal.
O Well demarcated.
Investigations
Plain X-rays.
Myelography contrast material is injected into the thecal sac fluid
surrounding the spinal cord and nerve root within the spinal canal
CT.
MRI ( study of choice ).

Rx spinal tumors
The goal of treatment is to reduce or prevent nerve damage from
compression of the spinal cord, relieve pain and maintain the function.
- Surgical excision is the treatment for extramedullary tumors.
- Radiation therapy for intramedullary tumors.
The traditional treatment of intramedullary gliomas has been biopsy
followed by radiation therapy.
Radiotherapy is clearly of value in metastatic lesions.
- Chemotherapy can be considered in patients with progression of disease
after radiation therapy.

Clinical presentation
Symptoms vary depending on the cause of the compression, its location,
severity, extent and rate of development but can include:
- Back pain at the spinal site of compression.
- Pain or burning in other parts of the body.
- Difficulty breathing.
- Weakness in the arms, legs, or both.
- Numbness or tingling in the neck, shoulder, arms, hands, or legs.
- Loss of coordination or difficulty walking.
- Loss of fine motor skills.
- Loss of sexual function.
- Loss of bladder or bowel control.
- Paralysis.
- Cervical spine disease produce Quadriplegia.
- Thoracic spine disease produce paraplegia.

- TENDON REFLEXES
O Increase; below level of compression
O Absent; at the level of compression
O Normal; above the level of compression

- Sphincter disturbances are late feature of cervical and thoracic cord
compression.
Cauda equina syndrome;
is a serious condition caused by compression of the nerves in the lower
portion of the spinal canal .
is considered a surgical emergency because if left untreated it can lead to
permanent loss of bowel and bladder control and paralysis of the legs.

Investigation
X ray.
CT scan.
MRI.
Myelogram.
Biopsy.
Bone scan.
Blood and spinal fluid studies.


Evaluation and Management of Head
and Spinal Injuries
Welcome to Trauma!
First and ForemostABCs
airway
breathing
circulation
disability
exposure
Head Injuries:
Account for about one half of all trauma deaths
Survivors range from baseline function to severe morbidity
Even minor head injury can have severe impact
As with most trauma, broken down into blunt and penetrating
Anatomy for Head Injuries
Scalp
may result in significant bleeding
Skull
well placed fractures place vessels and nerves at risk for
injury
protective, but a rigid, fixed space
Dura
Falx separates hemispheres
Tentorium separates cerebrum
Brain
Direct (Primary)
Indirect (secondary)
Direct (Primary) Brain Injuries
Direct damage done to brain parenchyma
Damage is already done
Irreversible
Damage control (debridement)
Indirect (Secondary) Brain Injury
Damage that occurs after the initial insult
Expanding mass lesions, swelling or bleeding quickly overwhelm
buffers
End result is increased intracranial pressure (ICP) and/or herniation
Diagnosis and treatments target minimizing the effects of these
indirect insults


Intracranial Pressure (ICP)
Intracranial space essentially full of brain, blood vessels, and a
little CSF
In response to an insult, small amount of CSF can be displaced, can
decrease blood volume, then increase ICP
At higher ICP, loss of autoregulation occurs
Cerebral perfusion pressure =(MAP-ICP)
Ischemia and neuronal death
Herniation
Other possible result of insult is to displace brain parenchyma itself
Damage to brain from trauma against the dura itself as well as
producing ischemia as well
Uncal herniation classic, but may see others as well
Categories of Brain Injuries
Diffuse
Concussion (movement to TBI!)
Diffuse Axonal Injury
Focal
Laceration (blunt) and penetrating
Contusions
Intracerebral hematomas
Epidural and subdural
Subarachnoid hemorrhage
Diffuse Brain Injuries
Concussion
Mild traumatic brain injury
No significant imaging findings
Does not mean no injury
Diffuse Axonal Injury
Severe injury globally caused by sheering of axons
Often neurologically devastated
Focal Brain Injuries
Penetrating injuries often intuitively obvious
Contusions (including contrecoup)
Hematomas
Epidural
Subdural
Contusions
Focal areas of hemorrhage within the parenchyma
Contrecoup injuries occur from a whiplash effect of the brain
against the skull on the opposite side of the initial point of impact
or injury

Epidural Hematomas
Blood between inner table of the
skull and the dura
Usually a tear of the MMA
Lens shaped hematomas that do
not cross suture lines on CT
Rare in elderly

Subdural Hematomas

Blood beneath the dura, overlying
the brain and arachnoid, resulting
from tears to bridging vessels
Crescent shaped density that may
run length of skull
Very common in the elderly

Subarachnoid blood vessels ruptured
May be the most common finding on moderate to severe brain
injuries
Penetrating Brain Injury (GSW) Contusions


Prehospital Care of Head Injured Patient
Historically, most patients were hyperventilated (bad!)
ABCs
Spinal immobilization
Initial resuscitation
Rapid transport
Head Injury Management
Management overall goal is to prevent or minimize secondary
injuries to the brain
Prevent hypoxia
Prevent hypotension
Prevent hemorrhage (anemia)
Prevent or limit increasing pressure
ED Assessment of Head Injured Patient
ABCs (again)
History (think alternate sources)
Clues to brain injury (examples: Cushings reflex, raccoon eyes,
etc)
Physical exam treat prioritized life threats first
The D of the ABCs (neuro exam)
Glasgow Coma Scale (GCS)
MOTOR VERBAL EYES
6 follow commands 5 conversant +
oriented
4 open
spontaneously
5 localizes 4 conversant +
disoriented
3 open to
command
4 flexion/withdrawal 3 inappropriate words 2 open to pain
3 decorticate post 2 incomprehensible
sounds
1 doesnt open
2 decerebrate post 1 no sounds
1 no movement
GCS 13-15 Mild head injury
GCS 9-12 Moderate head injury
GCS <8 Severe head injury


Management Principles
ABCs (Get used to it)
Protect spine as well (C spine injury assumed until proved
otherwise)
Stop blood loss elsewhere
Maintain perfusion (why hyperventilation is detrimental!)
Rapid imaging for definitive diagnosis
Assumes a patient stable enough to go to CT
Early, rapid specialty care
Neurosurgeons, trauma centers
Temporizing measures
Hyperventilation
Mannitol
Burr holes
Delayed Problems in Head Injured Patients
Postconcussive Syndrome
Delayed CSF leak
Delayed Seizure
Future of Traumatic Brain Injury
Ongoing efforts at UF and elsewhere to investigate approaches to
minimize damage
Have already debunked what not long ago was good care
(hyperventilation)
Free radical scavengers
C Spine Injuries
Varied mechanisms of injury (flexion, extension, rotation,
distraction, compression, lateral flexion, combination of forces)
Mostly blunt, some penetrating
Spinal cord injury obviously feared, particularly for cervical spine
Range from unstable injuries (ruptured transverse atlantal
ligament) to stable (Clay shovelers fracture)
Evaluation of C Spine Trauma
ABCs (get it yet!)
History
Palpation
Neuro exam
GCS
Motor
Sensory
Reflexes and tone
Complete vs Incomplete Spinal Cord Injuries
Complete is the total loss of movement and sensation below the
level of injury

Incomplete spares some function
3 incomplete cord syndromes
Anterior cord syyndrome
Central cord syndrome
Brown-Sequard syndrome
C Spine Imaging
NEXUS study provided evidence to forego unnecessary x rays
Cross table lateral most useful
Run the 4 lines of the lateral film
Look for other evidence of injury
Flexion and extension views assess for ligamentous injuries
CT Scan for C spine Injuries
Data shows that x rays miss a significant number of serious injuries
CT is beginning to become the study of choice in many trauma
centers and emergency departments
ED Management of C Spine Injuries
Immobilization
Early neurosurgical of orthopaedic consultation
Steroid protocol for cord injury
Solumedrol 30 mg/kg bolus followed by infusion 5.4 mg/kg
over next 23 hours
Controversy exists
Thoracic and Lumbar Injuries
Believe it or not, not much more to add beyond C spine discussion
in terms of ED care (immobilization, neuro exam, imaging,
appropriate consultation, solumedrol protocol for neurologic
compromise
Backboard are a transport device, not definitive immobilization
devices (ie, get them off the backboards ASAP)
Neck Trauma
Numerous structures packed in tight space
Blunt vs Penetrating Injuries
Innocuous appearing injuries may quickly become dangerous or
lethal with both blunt and penetrating injuries
Death from Neck Trauma
1. Associated CNS injury
2. Hemorrhage
3. Airway compromise
Blunt Neck Trauma
Difficult to assess
Airway protection a concern for various causes:
Intrinsic bleeding
Extrinsic bleeding

Tracheal or pharyngeal injury
Aspiration
Blunt Trauma Assessment and Management
Airway protection
CT scan evaluation
Esophagram
Esophagoscopy
Trauma surgeon experience with management
Penetrating Neck Trauma
Old school
Neck divided into 3 zones
Zone 1 base of neck to cricoid
Zone 2 - cricoid to angle of mandible
Zone 3 - above angle
If zone 2 and violated platysma, take to OR for exploration;
others get CT, angiography, esophagram, etc
New school
Selective management with imaging
rather than OR with zone 2 injuries
Take home points
As always with trauma, ABCs
Early recognition of injuries, stabilization, and rapid initiation of
definitive treatment will minimize morbidity and reduce mortality
Must rapidly involve or transfer to appropriate trauma surgeons
and or neurosurgeons
Life threats dealt with first


COMPLAINTS OF HEADACHE

INTRACRANIAL NEOPLASM
Epidemiology
Risk Factors
Pathophysiology
Classification
Clinical Presentation
Syndromes

Patient concerns
How serious are brain tumors?
What can I expect?
How long do I have?

Epidemiology
Incidence:
19.1 per 100,000 persons per year
11.8/100,000 - symptomatic
7.3/100,000 asymptomatic
Central Brain Tumor Registry of the United States
annual rate: 11.5/100,000
Primary Brain Tumors:
Astrocytoma 45-50%
Most common primary intra-axial brain
tumor
Meningioma 15-20%
Pituitary Adenoma 10%
Acoustic Neuroma 8%
Secondary/Metastatic Brain Tumors: 25-30% of all intracranial
tumors
Risk Factors
Ionizing radiation
only unequivocal risk factor identified for glial and
meningeal neoplasms
Cranial Irradiation (even low doses)
| incidence of meningiomas: factor of 10
| incidence of glial tumors: factor of 3 to 7
latency period: 10 years to >20 years after exposure

No other environmental exposure or behavior has been clearly
identified as a risk factor
conflicting and unconvincing data:
cellular telephones
exposure to high-tension wires
hair dyes
head trauma
dietary exposure to N-nitrosourea compounds or other
nutritional factors
all reported to increase the risk of brain tumors

Clinical Presentation
Focal or generalized neurologic symptoms
Generalized symptoms/signs
reflect raised ICP
include:
1. headache
when the illness is severe:
2. Nausea
3. Vomiting
4. CN VI (Abducens) palsy
Focal symptoms/signs
reflect intracranial tumor location
include:
1. Hemiparesis
2. Aphasia
3. Seizures
the most common presentation of brain tumors is progressive
neurologic deficit - 68%
usually motor weakness - 45%
rapidly evolving hemiparesis is more typical of a high-grade than a
low-grade glioma
Symptom frequency and duration vary with tumor type
Symptoms of Brain Tumors


Tumor Headache
occurs in about half of all patients with brain tumors
typically diffuse
can accurately indicate the hemisphere in which the
tumor is located
occasionally unilateral and throbbing
generally more noticeable on awakening in the morning
even without treatment, dissipates within a few hours
can mimic migraine or cluster headaches
often exacerbated by coughing, straining, bending forward
associated nausea and vomiting frequently
Etiologies:
1. Increased ICP:
Tumor, hydro, edema, hemorrhage
2. Invasion or compression of pain sensitive structures
Dura, vessels, periosteum
3. Secondary to difficulty with vision
4. Extreme Hypertension
5. Psychogenic
Intracranial Pressure
Monroe Kellie Hypothesis:limited space for expansion whitin the
skull
Skull=Brain tissue+Blood+CSF
Increase in any volume IncICP
Compensation (shifting of CSF, increased CSF
absorption,decreased cerebral blood volume)
Increased ICP
Reduced cerebral blood flow^ischemia
Systemic Response: increased Blood Pressure, slowing pulse,
respiratory irregularity (+decreases consciousness^Cushing
Response)
Management of IICP
Prevent hipoxia, ischemia (ABCs), increase intrathoracal( smooth
sucktion) and abdominal pressure (NGT,Urine cathether)
Prevent high metabolic( fever, pain, seizures)
Controlled edema( steroid)
Osmotic diuresis
Seizures
occur at presentation in 15-95% of patients with brain tumors,
depending on tumor type
Typically:

Focal seizures
may become generalized and cause loss of
consciousness
Postictal hemiparesis or aphasia (Todd's phenomenon) may
indicate tumor location
Other Symptoms
Other symptoms that reflect tumor location such as:
Hemiparesis
Aphasia
(when not associated with seizures)
Typically
subacute onset
progressive
Exception: Visual-field deficit
may develop progressively
often goes unnoticed by the patient until it contributes
to an accident (frequently an automobile accident)
Diagnosis
MRI central to the workup of a brain tumor is cranial magnetic
resonance imaging
Computed tomography (CT)
can miss structural lesions
particularly in the posterior fossa, or nonenhancing
tumors such as low-grade gliomas
if a brain tumor is a diagnostic consideration, MRI with gadolinium
enhancement =test of choice
a normal contrast-enhanced MRI scan essentially rules out the
possibility of a brain tumor.
Tumors of the Nervous System - Classification
1. WHO Classification
2. Age
3. Location Supratentorial, Infratentorial
4. Cell Type/Histology
5. Primary vs. Secondary
6. Benign vs. Malignant
Neoplasms may be classified according to localization and
histological features


Histological classification can be sub-divided according to whether
the cells are:
1. Normally present within the cranial or spinal cavity
2. Derived from the skull or spine
3. Represent cells that are not normal components of the central
nervous system, usually representing embryonal components
4. Metastatic from elsewhere in the body
WHO Classification Tumors of the Nervous System
1. Tumors of Neuroepithelial Tissue
2. Tumors of Peripheral Nerves
3. Tumors of the Meninges
4. Lymphomas and Haemopoietic Neoplasms
5. Germ Cell Tumors
6. Tumors of the Sellar Region
7. Metastatic Tumors
Tumors of Neuroepithelial Tissue
WHO GRADING OF ASTROCYTOMAS
n HISTOLOGICAL CRITERIA (4)
anaplasia
increased mitoses
vascular proliferation
tumour necrosis
4 HISTOLOGIC GRADES OF MALIGNANCY
Grades I - II : BENIGN
Grades III - IV : ANAPLASTIC/MALIGNANT
Tumors of Peripheral Nerves

WHO Classification Tumors of Peripheral Nerves
Schwannoma (Neurilemmoma,Neurinoma)
Neurofibroma
Malignant peripheral nerve sheath tumour

Tumors of the Meninges

MENINGIOMAS
Benigns tumor
Meningothelial
Fibrous
Transtitional
Psammomatous
Angiomatous

Lymphomas and Haemopoietic Neoplasms
Malignant lymphomas
Plasmacytoma
Granulocytic sarcoma
Germ Cell Tumors
1. Teratoma
2. Choriocarcinoma
Tumors of the Sellar Region
1. Craniopharyngioma Adamantinomatous Papillary
2. Granular cell tumour
3. Pituitary adenoma
Metastatic Tumors
25-30% of all intracranial tumours
Lung, breast commonest primary sites

PEDIATRIC INTRACRANIAL NEOPLASM
Second most common malignancy
Epidemiology :inc 2-5/100.000
No sex predominance
Metastatic are very rare
Clinical feature
Often have different patterns of clinical presentations, often a
function of location
I.posterior fossa tumor
II.low grade hemispheric tumord
III.sellar region
Posterior fossa tumors
Signs and symptoms
Headache (morning), nausea, projectile vomiting, drowsiness and
lethargy, diplopia, ataxia, papiledema
Medulloblastoma (25-30%)
Cerebellar astrocytoma (25%)
Management
Similar to adults intracranial neoplasm


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