Anesthesiology

BIMBEL UKDI MANTAP

dr. Andreas W Wicaksono
dr. Anindya K Zahra

Acid Base Regulation

Keterangan: angka normal analisis gas darah (arteri): pH: 7,35-7,45 ; PCO2: 35-45 mmHg ; HCO3: 22-26 mmol/L.

Gangguan Asam Basa

Gangguan asam
basa
Asidosis respiratorik

pH

PCO2

HCO3
jika

Penyebab umum
PPOK, asma, ARDS

terkompensasi

Alkalosis respiratorik

jika
terkompensasi

Asidosis metabolik

jika

terkompensasi

Alkalosis metabolik

jika
terkompensasi

Hiperventilasi,
sepsis
Dehidrasi berat,
DM, gagal ginjal,
starving
Muntah, diuresis,
hiperkalsemia

Shock Definition
A physiological state characterized by a
significant, systemic reduction in tissue
perfusion, resulting in decreased tissue
oxygen delivery and insufficient removal of
cellular metabolic products, resulting in tissue
injury.

Classification of Shock

Hypovolemic

Cardiogenic

Obstructive

Distributive

Stages
Compensated Shock
Early stages of shock where the bodys compensatory
mechanisms are able to maintain normal perfusion

Decompensated Shock
Advanced stage of shock that occurs when the bodys
compensatory mechanisms fail to maintain normal perfusion

Irreversible Shock
Stage of shock that has progressed to the point that the
body nor medical interventions correct the problem

Pathophysiology
Preload
Afterload
Contractility

Stroke Volume x Heart Rate

O2 Content

x
O2 Delivery

Cardiac
Output

Resistance

Arterial Blood
Pressure

Pathophysiology
BP = CO x R
CO = SV x HR
SV components = Preload, Afterload,
Contractility
DO2 = CO x CaO2
CaO2= (Hb x sat x 1.34) + (PaO2 x 0.003)

Pathophysiology
Shock

CO

Hipovolemik
(preload dan
(termasuk perdarahan) afterload)
Kardiogenik
(kontraktilitas)
Distributif
(termasuk anafilaktik,
septik, neurogenik/
spinal)

sebagai
kompensasi

SVR
sebagai
kompensasi
sebagai
kompensasi

Characteristics of Shock
End organ
dysfunction:

Metabolic
dysfunction:

reduced urine
output

acidosis

altered mental
status
poor peripheral
perfusion

altered metabolic
demands

Therapy
Goal : meningkatnya pengangkutan o2 & me kebutuhan o2
Cara : O2, cairan, kontrol suhu,antibiotik,koreksi kelainan
metab., Inotropik

Airway : intubasi & kontrol ventilasi

Breathing :
Awal : O2 100 %, monitor saturasi

Sirkulasi
Akses iv scr cepat 60 90 dtk
Intra osseus : 4 6 th

Kateter vena sentral

Therapy contd
Gunakan cairan isotonik : NS, RL, atau albumin 5%
Kecuali pada gagal jantung : 10 20 cc/kg 2-10 mnt
40-60 cc/kgbb reassess
Amati respon terapi cairan : lab; CVP
Pada kehilangan darah : berikan PRBC atau bila setelah
pemberian kristaloid 60 cc/kg belum stabil
Untuk anak 20cc/kgBB per X

HYPOVOLEMIC SHOCK

Perkiraan Kehilangan Darah

Kelas I

Kelas II

Kelas III

Kelas IV

Kehilangan darah <750

(mL)*
Kehilangan darah <15%
(% volume darah)

750-1500

1500-2000

>2000

15-30%

30-40%

>40%

Nadi

<100

>100

>120

>140

Tekanan darah

Normal

Normal

Menurun

Menurun

Tekanan nadi

Normal atau naik

Menurun

Menurun

Menurun

Frekuensi nafas

14-20

20-30

30-40

>35

Produksi urin
(ml/jam)
Status mental

>30

20-30

5-15

Tidak berarti

Sedikit cemas

Agak cemas

Cemas, bingung

Bingung, letargis

Penggantian
cairan

Kristaloid

Kristaloid

Kristaloid dan
darah

Kristaloid dan
darah

*) untuk laki-laki dengan berat badan 70kg

Therapy - Hypovolemic
PRINSIP TERAPI : CAIRAN
GOAL
VOL. INTRAVASKULER TERCUKUPI
KOREKSI ASIDOSIS METABOLIK
OBATI PENYEBAB

REASSES PERFUSI, UO,TANDA VITAL

PILIHAN :
KRISTALOID ISOTONIK : 20 CC/KG SCR CEPAT BILA FUNGSI
JANTUNG NORMAL
NS DAPAT MENYEBABKAN ASIDOSIS HIPERCHLOREMIK

Therapy - Hypovolemic
Solution
NS
LR

Na+
154
130

Cl154
109

K+ Ca++ Mg++ Buffer

0
0
0
None
4
3
0
Lactate

Inotropic and vasoactive drugs are not a substitute for

fluid, however...

Can have various combinations of hypovolemic

and septic and cardiogenic shock
May need to treat poor vascular tone and/or poor
cardiac function

End point and Monitoring

The actual end point of fluid therapy in shock is normalization
of DO2

Adequate end-organ perfusion is best indicated by urine

output of > 0.5 to 1 mL/kg/h
Central Venous Pressure
is the pressure in the superior vena cava, reflecting right ventricular enddiastolic pressure or preload.
Normal CVP: 2 to 7 mm Hg (3 to 9 cm H2O)
CVP > 12 to 15 mm Hg : fluid administration risks fluid overload

CARDIOGENIC SHOCK

Therapy - Cardiogenic
Terapi Inisial Dg. Pemberian Cairan
Bila Tak Ada Perbaikan memburuk susp.
Syok Kardiogenik Inotropik

Vasoactive/Cardiotonic Agents
Dopamine

1-5 mcg/kg/min: dopaminergic

5-15 mcg/kg/min: more beta-1
10-20 mcg/kg/min: more alpha-1
may be useful in distributive shock

Dobutamine
2.5-15 mcg/kg/min: mostly beta-1, some beta-2
may be useful in cardiogenic shock

Epinephrine
0.05-0.1 mcg/kg/min: mostly beta-1, some beta-2
> 0.1 to 0.2 mcg/kg/min: alpha-1

Vasoactive/Cardiotonic Agents
Norepinephrine
0.05-0.2mcg/kg/min: only alpha and beta-1
Use up to 1mcg/kg/min

Milrinone
50mcg/kg load then 0.375-0.75mcg/kg/min: phosphodiesterase
inhibitor; results in increased inotropy and peripheral vasodilation
(greater effect on pulmonary vasculature)

Phenylephrine
0.1-0.5mcg/kg/min: pure alpha

Anaphylactic Septic Neurogenic

DISTRIBUTIVE SHOCK

Distributive Shock
Inflammatory mediators disruption of cellular
metabolism peripheral vasodilation
decreased PVR
Etiology
Anaphylaxis
Septic
Neurogenic

Sign & symptoms

Febrile, tachycardia, clear lungs *, warm extremities,
flat neck veins, oliguria

Anaphylactic Shock
Anaphylactic shock
a type of distributive shock, which involves the immune system
(Hurst, 2008)

Type 1 hypersensitivity
antigen binds to IgE antibodies on mast cells, which leads to
degranulation of the mast cells

Sign & symptoms

itching, hives, and swelling
circulatory collapse (vasodilatation)
suffocation (bronchial and tracheal swelling)

Hipersensitivity reactions

Figure 12-2

Management
Anaphylactic Shock
1.
2.
3.
4.
5.
6.
7.
8.
9.

Administer oxygen.
Maintain an adequate airway.
Remove the allergen that caused the reaction.
Administer epinephrine (0.3 to 0.5 mL of a 1:1.000 solution
IM/SC or 0.3 to 0.5 mL of a 1:10.000 solution IV).
Initiale fluid therapy early with normal saline to maintain an
MAP 70 mm Hg or a systolic blood pressure 90 mm Hg.
Administer vasopressor agents if crystalloid therapy is
inadequate for maintaining CO.
Consider other pharmacologic treatments: antihistamines,
bronchodilators, and corticosteroids are other options.
Perform cardiac monitoring.
Observe for a possible second-phase reaction.

Keterangan:
Penatalaksanaan Syok Anafilaktik

1. Posisi trendeleburg atau berbaring dengan kedua tungkai diangkat

(diganjal dengan kursi) akan membantu menaikkan venous return
sehingga tekanan darah ikut meningkat.

2. Pemberian Oksigen 35 ltr/menit harus dilakukan, pada keadaan yang

amat ekstrim tindakan trakeostomi atau krikotiroidektomi perlu
dipertimbangkan.

3. Pemasangan infus, Cairan plasma expander (Dextran) merupakan

pilihan utama guna dapat mengisi volume intravaskuler secepatnya. Jika
cairan tersebut tak tersedia, Ringer Laktat atau NaCl fisiologis dapat
dipakai sebagai cairan pengganti. Pemberian cairan infus sebaiknya
dipertahankan sampai tekanan darah kembali optimal dan stabil.

4. Adrenalin 0,3 0,5 ml dari larutan 1 : 1000 IM yang dapat diulangi 5

10 menit. Dosis ulangan umumnya diperlukan, mengingat lama kerja
adrenalin cukup singkat. Jika respon pemberian secara intramuskuler
kurang efektif, dapat diberi secara intravenous setelah 0,1 0,2 ml
adrenalin dilarutkan dalam spuit 10 ml dengan NaCl fisiologis, diberikan
perlahan-lahan. Pemberian subkutan, sebaiknya dihindari pada syok
anafilaktik karena efeknya lambat bahkan mungkin tidak ada akibat
vasokonstriksi pada kulit, sehingga absorbsi obat tidak terjadi.

5. Aminofilin, dapat diberikan dengan sangat hati-hati apabila

bronkospasme belum hilang dengan pemberian adrenalin. 250 mg
aminofilin diberikan perlahan-lahan selama 10 menit intravena. Dapat
dilanjutkan 250 mg lagi melalui drips infus bila dianggap perlu.

6. Antihistamin dan kortikosteroid merupakan pilihan kedua setelah

adrenalin. Kedua obat tersebut kurang manfaatnya pada tingkat syok
anafilaktik, dapat diberikan setelah gejala klinik mulai membaik guna
mencegah komplikasi selanjutnya berupa serum sickness atau prolonged
effect. Antihistamin yang biasa digunakan adalah difenhidramin HCl 5 20
mg IV dan untuk golongan kortikosteroid dapat digunakan deksametason
5 10 mg IV atau hidrokortison 100 250 mg IV.

7. Resusitasi Kardio Pulmoner (RKP), seandainya terjadi henti jantung

(cardiac arrest) maka prosedur resusitasi kardiopulmoner segera harus
dilakukan sesuai dengan falsafah ABC dan seterusnya. Mengingat
kemungkinan terjadinya henti jantung pada suatu syok anafilaktik selalu
ada, maka sewajarnya ditiap ruang praktek seorang dokter tersedia selain
obat-obat emergency, perangkat infus dan cairannya juga perangkat
resusitasi (Resuscitation kit) untuk memudahkan tindakan secepatnya

Neurogenic Shock
Neurogenic shock is the rarest form of shock.

It is caused by trauma to the spinal cord sudden loss

of autonomic and motor reflexes below the injury level
Stimulation by sympathetic nervous system (-) the vessel
walls relax uncontrollably sudden decrease in peripheral
vascular resistance vasodilation and hypotension

Gambar 4. Patofisiologi spinal shock

OBSTRUCTIVE SHOCK

Obstructive Shock
COakibat OBSTRUKSI FISIK terhadap ALIRAN DARAH

KOMPENSASI SVR
PENYEBAB :

TAMPONADE PERIKARD
TENSION PNEUMOTHORAX
CRITICAL COARCTASIO AORTA
STENOSIS AORTA

TERAPI
CAIRAN
ATASI PENYEBAB

THYROID
STORM
3 Sistem:
CNS
CVS
GIT

Skor Burch Wartofsky

TRH

Waynes Index

Skor >19 = toksisk, 1-19 = equivokal, <11=eutiroid

dranindya

GRAVES
DISEASE
1. Hyperthyroidism
with diffuse
goiter
2. Opthalmopathy
3. Dermopathy
Acropachy

The most common form of

hyperthyroidism (60-70%)

Stress, infection, trauma, drugs

Epinephrine in Anaphylactic

START
Simple Triage and Rapid Treatment

TRIASE
proses pemilihan pasien berdasarkan beratnya kondisi
pasien

Terdiri dari 4 prioritas penanganan:

Merah immediate care/life-threatening

Kuning urgent care/can delay up to 1 hour
Hijau delayed care/can delay up to 3 hours
Hitam dead/no care required

Response
Respirasi
Ada

Walking wounded
(HIJAU)

Tidak Ada

>30x/<10x/menit 10-30x/menit

Periksa Ulang

(MERAH)

Perfusi
>2 detik

Tidak Ada
(HITAM)

<2 detik

RPM

(MERAH)

Status Mental
Tidak Mengikuti Perintah
(MERAH)

Mengikuti Perintah
(KUNING)

respirasi, perfusi, mental

- Semua proses evaluasi
dalam START harus
dilakukan dalam waktu
kurang dari 60 detik.

Algorhythm

Brain Death

Recognition of Airway Obstruction

Systematic method of detecting airway
obstruction :
Look, listen and feel
Look for chest and abdominal movement
Listen and feel for airflow at the mouth and nose.

Recognition of Airway Obstruction

Gurgling

liquid or semisolid foreign material in the main

airway.

Snoring

pharyng is partially occluded by soft palate or

epiglottis.

Crowing

sound of laryngeal spasm.

Inspiratory stridor

obsruction at laryngeal level or above.

Expiratory wheeze

obstruction of the lower airway.

Locked Jaw

Locked Jaw

Barton bandage

Patient Assessment
Level of consciousness
Spontaneous efforts vs. apnea
Airway and cervical spine
injury
Chest expansion
Signs of airway obstruction
Signs of respiratory distress
Protective airway reflexes

Opening the Airway the Triple Airway

Maneuver

Slightly extend neck

(when cervical spine
injury not suspected)
Elevate mandible
Open mouth

Hand Positioning the Triple Airway

Maneuver

Bronchus Primarius

Bronchoscopy

Oro Pharyngeal Airway

Reassess Spontaneous Breathing

(Ventilation) When Airway Open
Adequate
oxygen supplementation

Inadequate
manual assisted ventilation

Manual Assisted Ventilation

Apply face mask
Oro-/nasopharyngeal
airway adjuncts
Mouth opening
Hand positioning
Elevate mandible and chin
Resuscitation bag
compression volume and
frequency

Single-Hand Method
of Facemask Application
Base of mask placed
over chin and mouth
opened
Apex of mask over nose
Mandible elevated,
neck
hyperextended (no
cervical spine injury),
and downward pressure
by mask hand

Two-Hand Method of
Facemask Application

Indications
Demonstration

Inadequate Mask-to-Face Seal

Identify leak
Reposition face mask
Improve seal along cheek(s)
Slightly increase downward
pressure over face or neck
extension (if no cervical spine
injury)
Use two-hand technique

Perkiraan Kehilangan Darah

Kelas I

Kelas II

Kelas III

Kelas IV

Kehilangan darah <750

(mL)*
Kehilangan darah <15%
(% volume darah)

750-1500

1500-2000

>2000

15-30%

30-40%

>40%

Nadi

<100

>100

>120

>140

Tekanan darah

Normal

Normal

Menurun

Menurun

Tekanan nadi

Normal atau naik

Menurun

Menurun

Menurun

Frekuensi nafas

14-20

20-30

30-40

>35

Produksi urin
(ml/jam)
Status mental

>30

20-30

5-15

Tidak berarti

Sedikit cemas

Agak cemas

Cemas, bingung

Bingung, letargis

Penggantian
cairan

Kristaloid

Kristaloid

Kristaloid dan
darah

Kristaloid dan
darah

*) untuk laki-laki dengan berat badan 70kg

CO Poisoning

Cyanide Poisoning
Sources
Naturally in foods (some fruits, lima beans, SINGKONG)
Cyanide salts used in industry
Produced in smoke of burning plastics/synthetics, electroplating,
metal polishing
Mechanism
Inhibits cellular respiration
Tissue cannot utilize O2
Arterialization of venous blood
Characteristics
Smells like almonds

Cyanide inhibit cellular respiration

Clinical Effects of Cyanide

Headache
Dizziness
Seizures
Coma

Hypertension,
bradycardia
Hypotension, later in
course
Cardiovascular
collapse

CNS

Cardiovascular

Dyspnea
Tachypnea
Pulmonary edema
Apnea

Nausea, vomiting
Caustic effects

Pulmonary

Gastrointestinal

Cyanide Diagnosis
Clinical picture : sweet almond breath
Lactic acidosis
ABG:
metabolic acidosis

ABG sample

Treatment
Remove from source
Oxygen
Cyanide antidote kit:
Amyl nitrite perle until IV established
Sodium Nitrite (300mg IV)
Peds: 0.33 ml/kg of 10% solution)

Sodium Thiosulfate (12.5gm IV)

Peds: 1.65 ml/kg of 25% solution

Djengkolic Acid Poisoning

Sources
JENGKOL bean
Mechanism

poor solubility under acidic conditions

the amino acid precipitates into crystals
mechanical irritation of the renal tubules and urinary tract
Characteristics
abdominal discomfort, loin pains, severe colic, nausea,
vomiting, dysuria, gross hematuria, and oliguria, occurring 2 to
6 hours after the beans were ingested.

Djengkolic Acid Poisoning

Supporting examination
Urine analysis erythrocytes, epithelial
cells, protein, and the needle-like crystals of
djenkolic acid.
Treatment

Hydration to increase urine flow

Alkalinization of urine by sodium
bicarbonate.

Organophosphate Poisoning
Sources
Insecticides, herbicides
Mechanism
Inhibit acethylcholinesterase
ACh accumulates throughout the nervous system
Overstimulation of muscarinic and nicotinic receptors
Characteristics
SLUD + GEM

Organophosphate Poisoning

Sign and Symptom

+ GEM
G : Gastrointestinal
E : Emesis
M : Miosis

Atropine
Competitive inhibitor at autonomic postganglionic cholinergic receptors (GI &
pulmonary smooth muscle, exocrine glands, heart, and eye)

Dosis awal dewasa: 2 mg IM. Dosis dapat digandakan setiap 10 menit

sampai teratropinisasi.

The main concern with OP toxicity is respiratory failure from

excessive airway secretions. The endpoint for atropinization
is dried pulmonary secretions and adequate oxygenation.
Tachycardia and mydriasis must not be used to limit or to stop
subsequent doses of atropine.

Opiates Intoxication

 Antidote for Opiate Intoxication:

NALOXONE
Dosage
Adult: As hydrochloride: 0.4-2 mg repeated if necessary at 2-3 min intervals. If there is no
response after a total of 10 mg has been given, consider the possibility of overdosage with
other drugs. Reduce dose for opioid-dependent patients: 0.1-0.2 mg. IM/SC routes may be
used (at IV doses) if IV admin is not feasible.
Child: As hydrochloride: Initially 10 mcg/kg IV followed by 100 mcg/kg IV if necessary.
Alternatively, 0.4-0.8 mg IM or SC, repeated as necessary, if IV admin is not feasible.
Parenteral

Amphetamine Intoxication

Arsenic Toxicity

Methanol Toxicity
Methanol
wood alcohol
organic solvent that, because of its toxicity, can
cause metabolic acidosis, neurologic sequelae,
and even death, when ingested

Complication
Visual loss (optic nerve damage)
Metabolic acidosis
Movement disorder (damage in putamen >>)

Therapy

Therapy
Hemodialysis can easily remove methanol and
formic acid.

Mercury Poisoning
Sensory disturbance
peripheral neuropathy paresthesia, itching,
burning

Visual field constriction

Ataxia
Cognitive decline
Bizarre behavior
excessive shyness or aggression

Tremor
Gingivitis
Acrodynia
Neuropsychiatric
emotional lability or subtle performance
decline

Death

Mercury Poisoning

Congenital Minamata Disease:

CP, MR, seizure

Botulinum Toxin

BEDAH
Surgery

BIMBEL UKDI MANTAP

Neuro Surgery

Epidural Hemorrhage

>>a. meningea media, temporo parietal,

biconvex/lenticular, lucid interval

Subdural Hemorrhage

Bridging vein, semilunar

Subarachnoid hemorrhage

Aneurisma, AVM
Thunderclap headache, Muntah, stiff neck, meningeal
irritation, confusion / penkes

Intracerebral hemorrhage

Parenkim otak
Brain trauma atau spontan pada hemorrhagic stroke.

CT-Scan

MRI
Specific for
Soft Tissue

Brain Herniation

Glasgow Comma Score

 Motor response 2

Motor response 3

Thorax and Cardiovascular

Surgery

Trauma Algorythm

Trauma Thorax
PRIMARY SURVEY (132) Mengancam Jiwa
Airway (1)

Gangguan jalan nafas

Breathing (3)

Pneumotoraks terbuka
Pneumotoraks tension
Flail Chest

Circulation (2)

Hematoraks masif
Tamponade kordis

C. 1. Hematothorax
Definition :
accumulation of blood
in pleural cavity

Simple
Massive :
> 1.5litres blood on
chest drainage or >
200cc blood/ hour on
drainage

Etiology
Trauma : ruptur arteri di dinding thorax
ataupun internal organ di thorax
A. thoracica interna and its branches
A. intercostalis
A. bronchialis

Physical Exam
Sign : dyspneu

I : jejas (+), ketingalan gerak (+)

P : taktil fremitus turun
P : redup (+)
A : vesikuler turun, normal heart sound

Tube Thoracostomy / Chest Tube

Water Sealed Drainage

C.2. Cardiac Tamponade

Etiology : blunt or
penetrating trauma
in mid-chest
Nomal breath sound
Sign Trias Beck
1. Increase JVP
2. Hypotension
3. Muffled Heart
sound

Tx :
pericardiocentesis

Pericardiocentesis

Pneumothorax

Definition :
accumulation of air
or gas in pleural
cavity

Classification
Primary (non-trauma) and Secondary (trauma)
Open and Closed
Simple and Tension

Physical Exam
Sign : dyspneu, subcutis emfisem

I : jejas (+), ketingalan gerak (+)

P : taktil fremitus turun
P : hipersonor
A : vesikuler turun/hilang, normal heart sound

B.1. Open Pneumothorax

Etiology : Penetrating Trauma lubang dinding
dada (ukuran mendekati diameter trakea)
Mediastinal Flutter
Sucking Chest Wound

Treatment
Occlusive dressing
tape in 3 sides.

Closed Pneumothorax
Etiology : blunt trauma,
spontaneous rupture of
pleurae air leakage to
pleural cavity
Can developed into
Tension Pneumothorax
Tx : Chest Tube

B.2. Tension Pneumothorax

Clinical sign :
Himpitan vena cava
Shock
JVP

Himpitan paru
kontra lateral
distress nafas
deviasi trakhea

Tx :
Neddle
thoracostomy
(decompression)
Chest tube

Tension Pneumothorax

Needle Thoracostomy
Location :
SIC II / III Linea
Midclavicula

B.3. Flail Chest

Fraktur costae segmental, multipel,
berurutan
Severe respiratory distress
Paradoxal movement
Asymmetrical and uncoordinated chest wall
movement

Crepitation on palpation
Pain>>>>

Flail Chest

Management
ABCDE
Adequate ventilation, oxygenation,
analgesia

Chest X-Ray

Claudicatio Intermitten
Definition : pain in
calf region during
exercise (walking)
cause narrowing of
vessel due to
atherosclerotic
plaque (e.c Peripheral
Artery Disease)

Thromboangitis Obliterans
Also called as Buerger Disease
Male, 20-40 y.o
An acute inflammation and trombosis of
vessel on peripeheral region (foot and hand)
that associate with smoking.
Symptom : claudicatio intermitten

Raynaud Phenomenon
May appear as a component of other
conditions.
Causes:
connective tissue diseases (scleroderma & SLE)
arterial occlusive disorders.
carpal tunnel syndrome,
thermal or vibration injury.

Pale > Cyanosis > Redness

Aggrevated with cold

Raynauds
Phenomenon vs
Syndrome
Vasospastic disorder causing
discoloration of the fingers, toes,
and occasionally other areas.
Raynaud's disease ("Primary
Raynaud's phenomenon")
idiopathic
Raynaud's syndrome
(secondary Raynaud's),
commonly connective tissue
disorders such as Systemic
lupus erythematosus

Takayashu

Disorder

Onset

Etiology

Clinical Feat.

Buerger Disease

chronic

Segmental vascular
inflammation

Intermitten claudicatio,Smoking

Polyarteritis nodosa

acute

immune complex
induced disease

Fever,Malaise,Fatigue,Anorexia,
weight loss,Myalgia,Arthralgia in large
joints,polyneuropathy, cerebral
ischemia, rash, purpura, gangrene,
Abdominal pain, does not involve the
lungs

Vasculitis hypersensitif

Acute/
chronic

Circulating immune
complexesdrugs,
food,other
unknown cause

a small vessel vasculitis,usually affect

skin, but can also affect joints,
gastrointestinal tract, and the
kidneysitching, a burning
sensation, or pain, purpura

Wegener
granulomatosis

chronic

autoimmune

tissue destruction of upper

respiratory tract (sinuses, nose, ears,
and trachea *the windpipe+), the
lungs, and the kidneys

Takayasu arteritis

chronic

unknown of
inflammatory
proscess

systolic blood pressure difference

(>10 mm Hg) between arms,
pulselessness,bruit a.carotid

necrotizing
inflammatory lesions
small and mediumsized arteries

Plastic Surgery

Burn Injury

prick test (+)

Superficial Partial
Thickness Burn (IIa)

Deep Partial
Thickness Burn (IIb)

Full Thickness Burn

(III)

Total Body
Surface Area

Parkland formula = baxter formula

To estimate scattered burns: patient's

palm surface = 1% total body surface
area

Labio-Gnato-Palato Schisis

The Neonatal Period

Surgical Repair
Cleft Lip
In US - the rule of tens - 10 wks, 10 lbs, Hgb 10
Lip adhesion vs baby plates

Cleft Palate
Varies from 6-18 months - most around 10 mo
Early repair may lead to midface retrusion
Early repair improves speech

Pediatric Surgery

Urachal Abnormalities

Gastroschisis
Definition : defect
in development of
abdominal wall
results in
protrusion of
abdominal viscera
without a visceral
sac

Omphalocele
Definition : defect
in development of
abdominal wall
results in
protrusion of
abdominal viscera
in a visceral sac

Megacolon Congenital
Sign :
Frog like abdomen
Late meconium >
24hours

Phyiscal exam:
Sprout fecal material
on Rectal Touche

Hirschprung Disease
Kelainan kongenital akibat kegagalan
migrasi krista neuralis ke colon.
Tidak terbentuk sel ganglionik pd
plexus myentericus (Auerbach) dan
plexus submucosal (Meissner)
80% rectosigmoid
Klinis :

Delayed meconium (>24h)

Abdominal distention
Bilous vomiting
Severe diarrhea alternating with
constipation

Dx :
Barium enema
Rectal biopsy
Anorectal manometry

Invaginasi

KEY ANAMNESIS:
Well being baby
3- 12 months old (>> 9 mos)
TRIAS:
Colicky & cramping
abdominal pain
Bilious vomiting
Mucous-red current jelly
stools

PHYSICAL EXAM:
Abdominal mass (sausage
appearance)
Dance sign
RADIOLOGICAL
USG: Doughnut sign,
sandwich sign,
80% ILEOCOLIC
Pseudokidney
INTUSSUSCEPTUM (bowel PROXIMAL) yang masuk
BARIUM ENEMA: Cupping
INTUSSUSCIPIENS (DISTAL) yang nerima

Intussusception: USG

Sandwich sign

Doughnut sign

Doughnut sign

Abdominal Ultrasonography

Sandwich sign

BARIUM ENEMA

BARIUM ENEMA: Cupping

Diagnostic
Therapeutic

Atresia Esophageal

Hypertrophy Pyloric Stenosis

Hipertrofi m.sphincter pylorus
Stenosis > canalis pyloricus
Klinis :
Muntah proyektil, bile free,
bolus+gastric juice
Baby looks hungry
Palpable mass (olive)
Dx :
Barium meal / OMD
( single bubble)
Plain photo (umbrella sign)

Komplikasi : dehidrasi & aspirasi

Tx :
Non surgery : resusitasi cairan
Surgery : pyloromyotomy

Single Bubble sign

Umbrella sign

Atresia / Stenosis Duodeni

Atresia: complete
obstruction; stenosis:
partial obstruction
Lokasi tersering di
duodenum pars
horizontal
Symptom: regurgitasi &
vomit (bilous vomit)
Dx : (double bubble)
Plain photo
Barium meal / OMD

Double bubble sign

Double bubble
sign
Without
abdominal
distension

Atresia Jejunum
Triple bubble sign
With abdominal
distension
No gas in pelvic
cavity

Atresia Ani

TERIMA KASIH