Anesthesiology Bs Btkv Bp Ba Mantap Tutor

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 body’s compensatory mechanisms are able to maintain normal perfusion

Decompensated Shock • Advanced stage of shock that occurs when the body’s 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

x

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 –cont’d  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 40%

Nadi

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 3–5 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 CO↓akibat 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

w

TRH

Wayne’s Index

• Skor >19 = toksisk, 1-19 = equivokal, 30x/2 detik

Tidak Ada (HITAM)

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 it’s 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

Raynaud’s 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 complexes→drugs, food,other unknown cause

a small vessel vasculitis,usually affect skin, but can also affect joints, gastrointestinal tract, and the kidneys→itching, 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

A

B

C

BARIUM ENEMA: Cupping Diagnostic Therapeutic

D

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