anesthesiology bs btkv bp ba mantap tutor

8/18/2019 Anesthesiology Bs Btkv Bp Ba Mantap Tutor

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BIMBEL UKDI MANTAPdr. Andreas W Wicaksono

dr. Anindya K Zahra

Anesthesiology


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Acid Base Regulation


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Gangguan asam

basa

pH PCO2 HCO3 Penyebab umum

Asidosis respiratorik jika

terkompensasi

PPOK, asma, ARDS

Alkalosis respiratorik jikaterkompensasi

Hiperventilasi,sepsis

Asidosis metabolik jika

terkompensasi

Dehidrasi berat,

DM, gagal ginjal,

starving

Alkalosis metabolik jikaterkompensasi Muntah, diuresis,hiperkalsemia

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

Gangguan Asam Basa


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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.


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Classification of Shock

Hypovolemic Cardiogenic

Obstructive Distributive


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Stages

Compensated Shock

• Early stages of shock where the body’s compensatorymechanisms are able to maintain normal perfusion

Decompensated Shock

• Advanced stage of shock that occurs when the body’scompensatory mechanisms fail to maintain normal perfusion

Irreversible Shock

• Stage of shock that has progressed to the point that thebody nor medical interventions correct the problem


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PreloadAfterloadContractility

Resistance

Stroke Volume Heart Rate

Arterial BloodPressureO2 Delivery

O2 Content Cardiac

Output

x

x x

Pathophysiology


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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)


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Pathophysiology

Shock CO SVR

Hipovolemik

(termasuk perdarahan)

(preload dan

afterload)

sebagai

kompensasiKardiogenik (kontraktilitas) sebagai

kompensasi

Distributif

(termasuk anafilaktik,septik, neurogenik/

spinal)

sebagai

kompensasi


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Characteristics of Shock

End organdysfunction:

reduced urineoutput

altered mentalstatus

poor peripheralperfusion

Metabolicdysfunction:

acidosis

altered metabolicdemands


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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


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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


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HYPOVOLEMIC SHOCK


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Perkiraan Kehilangan Darah

Kelas I Kelas II Kelas III Kelas IV

Kehilangan darah

(mL)*

2000

Kehilangan darah

(% volume 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)

>30 20-30 5-15 Tidak berarti

Status mental 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


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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 FUNGSIJANTUNG NORMAL

• NS DAPAT MENYEBABKAN ASIDOSIS HIPERCHLOREMIK


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Therapy - Hypovolemic

Solution Na+ Cl- K+ Ca++ Mg++ Buffer

NS 154 154 0 0 0 None

LR 130 109 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


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End point and Monitoring

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

Adequate end-organ perfusion is best indicated by urineoutput of > 0.5 to 1 mL/kg/h

Central Venous Pressure

• is the pressure in the superior vena cava, reflecting right ventricular end-diastolic 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


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CARDIOGENIC SHOCK


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Therapy - Cardiogenic

• Terapi Inisial Dg. Pemberian Cairan

• Bila Tak Ada Perbaikan→ memburuk → susp.

Syok Kardiogenik Inotropik


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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


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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


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DISTRIBUTIVE SHOCK

Anaphylactic – Septic – Neurogenic


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Distributive Shock

• Inflammatory mediators disruption of cellularmetabolism peripheral vasodilationdecreased PVR

•

Etiology – Anaphylaxis

– Septic

– Neurogenic

• Sign & symptoms – Febrile, tachycardia, clear lungs *, warm extremities,

flat neck veins, oliguria


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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 todegranulation of the mast cells

Sign & symptoms• itching, hives, and swelling

• circulatory collapse (vasodilatation)

• suffocation (bronchial and tracheal swelling)

Hipersensitivity reactions

http://en.wikipedia.org/wiki/Degranulationhttp://en.wikipedia.org/wiki/Shock_(circulatory)http://en.wikipedia.org/wiki/Shock_(circulatory)http://en.wikipedia.org/wiki/Degranulation


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Figure 12-2

Hipersensitivity reactions


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Management

Anaphylactic Shock

1. Administer oxygen.

2. Maintain an adequate airway.

3. Remove the allergen that caused the reaction.

4. 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).5. Initiale fluid therapy early with normal saline to maintain anMAP ≥ 70 mm Hg or a systolic blood pressure ≥ 90 mm Hg.

6. Administer vasopressor agents if crystalloid therapy isinadequate for maintaining CO.

7. Consider other pharmacologic treatments: antihistamines,bronchodilators, and corticosteroids are other options.

8. Perform cardiac monitoring.

9. Observe for a possible second-phase reaction.


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Keterangan:


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Keterangan:

Penatalaksanaan Syok Anafilaktik• 1. Posisi trendeleburg atau berbaring dengan kedua tungkai diangkat

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

• 2. Pemberian Oksigen 3 –5 ltr/menit harus dilakukan, pada keadaan yangamat ekstrim tindakan trakeostomi atau krikotiroidektomi perludipertimbangkan.

• 3. Pemasangan infus, Cairan plasma expander (Dextran) merupakanpilihan utama guna dapat mengisi volume intravaskuler secepatnya. Jikacairan tersebut tak tersedia, Ringer Laktat atau NaCl fisiologis dapatdipakai sebagai cairan pengganti. Pemberian cairan infus sebaiknyadipertahankan 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 kerjaadrenalin cukup singkat. Jika respon pemberian secara intramuskulerkurang efektif, dapat diberi secara intravenous setelah 0,1 – 0,2 mladrenalin dilarutkan dalam spuit 10 ml dengan NaCl fisiologis, diberikanperlahan-lahan. Pemberian subkutan, sebaiknya dihindari pada syokanafilaktik karena efeknya lambat bahkan mungkin tidak ada akibat

vasokonstriksi pada kulit, sehingga absorbsi obat tidak terjadi.


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• 5. Aminofilin, dapat diberikan dengan sangat hati-hati apabilabronkospasme belum hilang dengan pemberian adrenalin. 250 mgaminofilin 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 setelahadrenalin. Kedua obat tersebut kurang manfaatnya pada tingkat syokanafilaktik, dapat diberikan setelah gejala klinik mulai membaik gunamencegah komplikasi selanjutnya berupa serum sickness atau prolonged

effect. Antihistamin yang biasa digunakan adalah difenhidramin HCl 5–

20mg IV dan untuk golongan kortikosteroid dapat digunakan deksametason5 – 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 harusdilakukan sesuai dengan falsafah ABC dan seterusnya. Mengingatkemungkinan terjadinya henti jantung pada suatu syok anafilaktik selaluada, maka sewajarnya ditiap ruang praktek seorang dokter tersedia selainobat-obat emergency, perangkat infus dan cairannya juga perangkatresusitasi (Resuscitation kit) untuk memudahkan tindakan secepatnya


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Neurogenic Shock

Neurogenic shock is the rarest form of shock.

It is caused by trauma to the spinal cord sudden lossof autonomic and motor reflexes below the injury level

Stimulation by sympathetic nervous system (-) the vesselwalls relax uncontrollably sudden decrease in peripheralvascular resistance vasodilation and hypotension


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Gambar 4. Patofisiologi spinal shock


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OBSTRUCTIVE SHOCK


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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


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THYROID

STORM

3 Sistem:

CNS

CVSGIT

Skor Burch Wartofsky


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w

TRH


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Wayne’s Index

• Skor >19 = toksisk, 1-19 = equivokal,


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GRAVE’S

DISEASE

1. Hyperthyroidism

with diffuse

goiter

2. Opthalmopathy3. Dermopathy

Acropachy

The most common form of

hyperthyroidism (60-70%)


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Stress, infection, trauma, drugs


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Epinephrine in Anaphylactic


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STARTSimple 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

R


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ResponseWalking wounded

(HIJAU)

Respirasi Ada

>30x/2 detik

(MERAH)


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Algorhythm


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Brain Death


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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.


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Recognition of Airway Obstruction

• liquid or semisolid foreign material in the mainairway.Gurgling

• pharyng is partially occluded by soft palate orepiglottis.Snoring

• sound of laryngeal spasm.Crowing

• obsruction at laryngeal level or above.Inspiratory stridor

• obstruction of the lower airway.Expiratory wheeze

L k d J


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Locked Jaw

L k d J


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Locked Jaw


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Barton bandage


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Patient Assessment

• Level of consciousness

• Spontaneous efforts vs. apnea

•

Airway and cervical spineinjury

• Chest expansion

• Signs of airway obstruction

• Signs of respiratory distress

• Protective airway reflexes


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Opening the Airway – the Triple Airway

Maneuver

• Slightly extend neck(when cervical spineinjury not suspected)

• Elevate mandible

•

Open mouth

Hand Positioning the Triple Airway


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Hand Positioning – the Triple Airway

Maneuver


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Bronchus Primarius


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Bronchoscopy


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Oro Pharyngeal Airway


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Reassess Spontaneous Breathing

(Ventilation) When Airway Open

• Adequate –

oxygen supplementation

• Inadequate –

manual assisted ventilation


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Manual Assisted Ventilation

• Apply face mask

– Oro-/nasopharyngeal

airway adjuncts – Mouth opening

– Hand positioning

• Elevate mandible and chin

• Resuscitation bagcompression – volume andfrequency

l d h d


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Single-Hand Method

of Facemask Application

• Base of mask placedover chin and mouthopened

• Apex of mask over nose

• Mandible elevated,neckhyperextended (no

cervical spine injury),and downward pressureby mask hand

T H d M th d f


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Two-Hand Method of

Facemask Application

»Indications»Demonstration


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Inadequate Mask-to-Face Seal

• Identify leak

• Reposition face mask

• Improve seal along cheek(s)

• Slightly increase downwardpressure over face or neckextension (if no cervical spine

injury)• Use two-hand technique


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Perkiraan Kehilangan DarahKelas I Kelas II Kelas III Kelas IV

Kehilangan darah

(mL)*

2000

Kehilangan darah

(% volume 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)

>30 20-30 5-15 Tidak berarti

Status mental 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


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CO Poisoning


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g


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d


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Cyanide Poisoning

• Naturally in foods (some fruits, lima beans, SINGKONG)

• Cyanide salts used in industry

• Produced in smoke of burning plastics/synthetics, electroplating,metal polishing

Sources

• Inhibits cellular respiration

• Tissue cannot utilize O2

• “Arterialization” of venous blood

Mechanism

• Smells like “almonds”

Characteristics

Cyanide inhibit cellular respiration


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y p


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Clinical Effects of Cyanide


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• Headache

• Dizziness

• Seizures

• Coma

CNS

• Hypertension,bradycardia

• Hypotension, later in

course

• Cardiovascularcollapse

Cardiovascular

• Dyspnea

• Tachypnea

• Pulmonary edema

• Apnea

Pulmonary

• Nausea, vomiting

• Caustic effects

Gastrointestinal


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Cyanide Diagnosis• Clinical picture : sweet almond breath

• Lactic acidosis

• ABG:

– metabolic acidosis

ABG sample

T


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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

Dj k li A id P i i


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Djengkolic Acid Poisoning

• JENGKOL bean

Sources

• poor solubility under acidic conditions

• the amino acid precipitates into crystals

• mechanical irritation of the renal tubules and urinary tract

Mechanism

• abdominal discomfort, loin pains, severe colic, nausea,vomiting, dysuria, gross hematuria, and oliguria, occurring 2 to6 hours after the beans were ingested.

Characteristics

Dj k li A id P i i


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Djengkolic Acid Poisoning

• Urine analysis erythrocytes, epithelialcells, protein, and the needle-like crystals of

djenkolic acid.

Supporting examination

• Hydration to increase urine flow

• Alkalinization of urine by sodiumbicarbonate.

Treatment

O h h t P i i


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Organophosphate Poisoning

• Insecticides, herbicides

Sources

• Inhibit acethylcholinesterase

• ACh accumulates throughout the nervous system

• Overstimulation of muscarinic and nicotinic receptors

Mechanism

• SLUD + GEM

Characteristics

O h h t P i i


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Organophosphate Poisoning

Si d S t


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Sign and Symptom

• + GEM

• G : Gastrointestinal

• E : Emesis

•

M : Miosis

At i


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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 fromexcessive airway secretions. The endpoint for atropinization

is dried pulmonary secretions and adequate oxygenation.Tachycardia and mydriasis must not be used to limit or to stopsubsequent doses of atropine.”

Opiates Intoxication


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• 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


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Amphetamine Intoxication

Arsenic Toxicity


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Arsenic Toxicity


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Methanol Toxicity


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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


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Therapy

Therapy


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Therapy

•Hemodialysis can easily remove methanol andformic acid.

Mercury Poisoning


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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 performancedecline

• Death


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Neuro Surgery


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Epidural Hemorrhage


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>>a. meningea media, temporo parietal,

biconvex/lenticular, lucid interval


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Subdural Hemorrhage


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Bridging vein, semilunar

Subarachnoid hemorrhage


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Aneurisma, AVM

Thunderclap headache, Muntah, stiff neck, meningeal

irritation, confusion / penkes

Subarachnoid hemorrhage

Intracerebral hemorrhage


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Parenkim otak

Brain trauma atau spontan pada hemorrhagic stroke.

Intracerebral hemorrhage

CT-Scan


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MRI


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MRI

Specific for

Soft Tissue

Brain Herniation


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Brain Herniation

Glasgow Comma Score


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• Motor response 2

• Motor response 3


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Thorax and Cardiovascular

Surgery

Trauma Algorythm


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Trauma Algorythm

Trauma Thorax“ PRIMARY SURVEY “ (132) M Ji


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“ PRIMARY SURVEY “ (132) –Mengancam Jiwa

• Gangguan jalan nafasAirway (1)

• Pneumotoraks terbuka

• Pneumotoraks tension

• “ Flail Chest “

Breathing (3)

• Hematoraks masif

• Tamponade kordisCirculation (2)

C. 1. Hematothorax


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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


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gy

• Trauma : ruptur arteri di dinding thorax

ataupun internal organ di thorax

– A. thoracica interna and it’s branches

– A. intercostalis

– A. bronchialis

Physical Exam


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y

• Sign : dyspneu

• I : jejas (+), ketingalan gerak (+)

• P : taktil fremitus turun

• P : redup (+)

• A : vesikuler turun, normal heart sound

Tube Thoracostomy / Chest Tube


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Water Sealed Drainage


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g

C.2. Cardiac Tamponade


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p

•Etiology : blunt orpenetrating traumain mid-chest

• Nomal breath sound

• Sign Trias Beck

1. Increase JVP

2. Hypotension

3. Muffled Heartsound

• Tx :pericardiocentesis

Pericardiocentesis


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Classification


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• Primary (non-trauma) and Secondary (trauma)

• Open and Closed

• Simple and Tension

Physical Exam


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y

• 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


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p

Etiology : Penetrating Trauma lubang dindingdada (ukuran mendekati diameter trakea)

“ Mediastinal Flutter “

“ Sucking Chest Wound “

Treatment


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•

Occlusive dressingtape in 3 sides.

Closed Pneumothorax


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• Etiology : blunt trauma,

spontaneous rupture of

pleurae air leakage to

pleural cavity

• Can developed into

Tension Pneumothorax

• Tx : Chest Tube


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Tension Pneumothorax


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B.3. Flail Chest


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•

Fraktur costae segmental, multipel,berurutan

• Severe respiratory distress

•

Paradoxal movement• Asymmetrical and uncoordinated chest wall

movement

• Crepitation on palpation

• Pain>>>>


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Management


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•

ABCDE• Adequate ventilation, oxygenation,

analgesia


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Claudicatio Intermitten


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• Definition : pain incalf region duringexercise (walking)cause narrowing of

vessel due toatheroscleroticplaque (e.c PeripheralArtery Disease)

Thromboangitis Obliterans


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• 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


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Raynaud Phenomenon


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•May appear as a component of otherconditions.

• 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


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e o e o s

Syndrome• Vasospastic disorder causing

discoloration of the fingers, toes,

and occasionally other areas.

–

Raynaud's disease ("PrimaryRaynaud's phenomenon")→

idiopathic

– Raynaud's syndrome

(secondary Raynaud's),→

commonly connective tissuedisorders such as Systemic

lupus erythematosus

Takayashu


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Disorder Onset Etiology Clinical Feat.Buerger Disease chronic Segmental vascular

inflammation

Intermitten claudicatio,Smoking

Polyarteritis nodosa acute immune complex– Fever Malaise Fatigue Anorexia


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Polyarteritis nodosa

necrotizinginflammatory lesions

small and medium-

sized arteries

acute immune complex –

induced disease

Fever,Malaise,Fatigue,Anorexia,

weight loss,Myalgia,Arthralgia in large

joints,polyneuropathy, cerebralischemia, 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


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Plastic Surgery


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Superficial PartialThickness Burn (IIa)


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( )

Deep Partial

Thickness Burn (IIb)


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Thickness Burn (IIb)

Full Thickness Burn

(III)


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(III)

Total BodySurface Area


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To estimate scattered burns: patient's

palm surface = 1% total body surface

areaParkland formula = baxter formula

Labio-Gnato-Palato Schisis


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The Neonatal Period


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• 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


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Pediatric Surgery

Urachal Abnormalities


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Gastroschisis


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•Definition : defectin development of

abdominal wall

results in

protrusion of

abdominal viscera

without a visceral

sac

Omphalocele


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•Definition : defectin development of

abdominal wall

results in

protrusion of

abdominal viscera

in a visceral sac

Megacolon Congenital


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•

Sign : – Frog like abdomen

– Late meconium >

24hours

• Phyiscal exam:

Sprout fecal material

on Rectal Touche

Hirschprung Disease• Kelainan kongenital akibat kegagalan


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g g gmigrasi krista neuralis ke colon.

• Tidak terbentuk sel ganglionik pdplexus myentericus (Auerbach) danplexus submucosal (Meissner)

• 80% rectosigmoid

• Klinis : – Delayed meconium (>24h)

– Abdominal distention

– Bilous vomiting

– Severe diarrhea alternating withconstipation

• Dx : – Barium enema

– Rectal biopsy

– Anorectal manometry


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InvaginasiKEY ANAMNESIS:• Well being baby• 3- 12 months old (>> 9 mos)• TRIAS:


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– Colicky & cramping

abdominal pain – Bilious vomiting

– Mucous-red current jellystools

PHYSICAL EXAM:• Abdominal mass (sausage

appearance)

• Dance sign

RADIOLOGICAL

• USG: Doughnut sign,sandwich sign,Pseudokidney

• BARIUM ENEMA: Cupping

80% ILEOCOLIC

INTUSSUSCEPTUM (bowel PROXIMAL) yang masuk

INTUSSUSCIPIENS (DISTAL)

yang nerima

Intussusception: USG


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Doughnut signSandwich sign

Doughnut sign


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Abdominal Ultrasonography

Sandwich sign


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BARIUM ENEMA


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A

B

C

D

BARIUM ENEMA: Cupping

DiagnosticTherapeutic

Atresia Esophageal


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Hypertrophy Pyloric Stenosis

• Hipertrofi m.sphincter pylorus


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p p py

• 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


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Umbrella sign


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Atresia / Stenosis Duodeni

• Atresia: complete


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• Atresia: complete

obstruction; stenosis:partial obstruction

• Lokasi tersering diduodenum pars

horizontal

• Symptom: regurgitasi &vomit (bilous vomit)

•Dx : (double bubble) – Plain photo

– Barium meal / OMD

Double bubble sign


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• Double bubble

sign

• Withoutabdominal

distension

Atresia Jejunum


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• Triple bubble sign

• With abdominal

distension

• No gas in pelvic

cavity

Atresia Ani


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