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 <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 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, <11=eutiroid
dranindya
GRAVE’S 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 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
