Bimbingan UKMPPD (UKDI) - Anestesi-Bedah

8/19/2019 Bimbingan UKMPPD (UKDI) - Anestesi-Bedah

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BIMBEL UKDI MANTAPdr. Andreas W Wicaksono

dr. Anindya K Zahradr. Arius Suwondo

dr. M. Dzulfikar Lingga Q M

dr. Marika Suwondo

Anesthesiology


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Algorhythm


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Patient Assesment

• Level of consciousness

• Spontaneous effort vs apneu

• Airway and cervical spine injury

• Chest expansion

• Sign of airway obstruction

• Signs of respiratorry distress

• Protective airway reflexes


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Airway and C – Spine control

Problem Airway

Trauma Maksilofasial

Trauma Leher

Trauma Laryngeal

Pasien Berbicara Lancar ‐>

airway baik

Look : Agitasi, penkes,

retraksi, otot bantu nafas

Listen : suara nafas abnormal

Feel : lokasi trakea

Adakah patensi jalan

nafas ?

•liquid or semisolid foreign material in the main airway ‐> SuctioningGurgling

•pharyng is partially occluded by soft palate or epiglottis.

Snoring•sound of laryngeal spasm.Crowing

•obsruction at laryngeal level or above.Inspiratory stridor

•obstruction of the lower airway.Expiratory wheeze


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Pengelolaan Jalan Nafas

Oksigenasi dan pasang pulse oxymetri

Chin– lift manuver atau jaw – trust manuver (pada

curiga C‐spine terganggu ‐> dipertahankan dengan

nasofaringeal airway atau orofaringeal airway

Bersihkan jalan nafas dari corpal, suctioning

Dapat teroksigenasi Definitif airway

surgicalNO

Assess airway anatomy ‐>

LEMON Difficult

Call assistance

or Awake

intubationIntubation – drug – assistanceCricoid pressure

unsuccesfull

Consider adjunct ‐> GEB/LMA/LTA

Definitif arway

surgical

NPA

OPA

Intubation


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Opening the Airway – Triple AirwayManeuver

• Slightly extend neck

(when cervival spine

injury not suspected)• Elevated mandible

• Open mouth

Head Position


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Oropharingeal Airway

• Digunakan untuk ventilasi sementara pada pasien yang tidaksadar sementara intubasi pasien sedang disiapkan

• Tidak boleh digunakan pada pasien yang sadar karena dapatmenyebabkan sumbatan, muntah dan aspirasi.

Nasopharingeal Airway

• Prosedur ini digunakan apabila pasien terangsang untukmuntah pada penggunaan OPA

Laryngeal Mask Airway

• Digunakan untuk pertolongan dengan airway yang sulit untukintubasi endotracheal atau bag mask gagal. Ingat LMA bukandefinitif


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Laryngeal Tube Airway

• Suatu alat airway diluar glotis untuk memberi ventilasi pasiendengan baik.

Gum Elatic Bougie

• Diikenal dengan nama Eschmann tracheal tube introducer(ETTI)

Multilumen Esophageal Airway

• Dapat dihunakan apabila airway definit belum dapatdilakukan.

• Alat ini memiliki lubang udara yang mengarah ke salurannafas . Sedangkan lubang lain mengarah ke esofagus.


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Airway definitif

Kebutuhan Untuk PERLINDUNGANAIRWAY

Kebutuhan Untuk VENTILASI

Penurunan Kesadaran (GCS < 9) Apneu :

‐Paralisis neuromuscular

‐Tidak sadar

Fraktur Maxilofacial berat Usaha Nafas tidak adekuat

‐Takipneu

‐Hipoksia

‐Hiperkarbia

‐Sianosis

Resiko Aspirasi : Perdarahan, muntah

muntah

Cedera kpala tertutup berat yang

membutuhkan hiperventilasi

Resiko Sumbatan : Hematoma leher,

cedera laring, trachea, stridor

Kehilangan darah yang masif dan

memerlukan resusitasi volume

Orotracheal Tube

Nasotracheal Tube

Airway surgical :

Krikotiroidotomi

Trakheostomi


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Nasotracheal intubation

Cricothyroidotomy Tracheostomy


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Bronchus Primarius


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• Apply face mask – Oro/naso‐pharyngeal

airway adjuncts

– Mouth opening – Hand positioning

• Elevate mandible and chin

• Resuscitation bagcompression – volume andfrequency

• Apply face mask – Oro/naso‐pharyngeal

airway adjuncts

– Mouth opening – Hand positioning

• Elevate mandible and chin

• Resuscitation bagcompression – volume andfrequency

Manual Assisted Ventilation


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Single‐Hand Method of FacemaskApplication

• Base of mask placedover chin and mouthopened

• Apex of mask overnose

• Mandible elevated,

neck hyperextend (nocervical injury), anddownward pressure bymask hand


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Two‐Hand Method of FacemaskApplication


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Inadequate Mask‐to‐Face SealInadequate Mask‐to‐Face Seal

• Identify leak• Reposition face mask

• Improve seal along

cheeks• Slightly increase

downward pressure over

face or neck extension ifno cervical injury

• Use two hand technique


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TemporoMandibular Joint Dislocation

(Locked Jaw)

Type :

• Anterior• Posterior

• Superior

Unilateral /

Bilateral


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The patient is unable to close the mouth and may have garbled speech,

drooling and in pain .

A depression may be noted in the preauricular area. Palpation of the TMJ

reveals one or both of the condyles trapped in front of the articular eminence

and spasm of the muscles of mastication.

In addition, the coronoid process of the mandible becomes prominent and

palpable just below the maxilla

Treatment depends on

patient status and varies

from simple reduction to

surgical intervention.


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Manual closed Reduction (Classic)


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Barton bandage

• Application of a Barton bandage

after reduction.

• Apply warm compresses to the TMJ

area for 24 hours• Avoid extreme opening of the jaw

for three weeks. In some patients,

placement of a padded rigid cervical

collar.

• Support the lower jaw when

yawning.

• Maintain a soft diet for one week.

• Take nonsteroidal anti‐inflammatory

agents (eg ibuprofen 10 mg/kg orally

every six hours as needed, maximum

single dose : 800 mg) as needed for

pain and swelling.


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Brain Death


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Shock – DefinitionA physiological state characterized by a

significant, systemic reduction in tissueperfusion, resulting in decreased tissue oxygen

delivery and insufficient removal of cellular

metabolic products, resulting in tissue injury.


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Classification of Shock

HypovolemicHypovolemic CardiogenicCardiogenic

ObstructiveObstructive DistributiveDistributive


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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

kompensasi

Kardiogenik (kontraktilitas) sebagai

kompensasi

Distributif

(termasuk anafilaktik,

septik, neurogenik/

spinal)

sebagai

kompensasi


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Characteristics of Shock

End organdysfunction:

reduced urine

output

altered mentalstatus

poor peripheralperfusion

Metabolicdysfunction:

acidosis

altered metabolicdemands


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HYPOVOLEMIC SHOCK


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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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Estimated Blood Volume (EBV)• Laki –laki = 75 cc/kgBB (70‐75 cc/KgBB)

• Perempuan = 65 cc/kgBB

• Infant = 80 cc/kgBB

• Neonatus = 85 cc/kgBB• Premature neonatus = 96 cc/kgBB


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Therapy ‐ HypovolemicPRINSIP TERAPI : CAIRAN

TUJUAN• 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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IV fluidsCrystalloid solutions (isotonic)

• Both 0.9% saline and RL are equally effective

• RL may be preferred in hemorrhagic shock because itsomewhat minimizes acidosis and will not causehyperchloremia.

• For patients with acute brain injury, 0.9% saline is preferred.

Colloid solutions (eg, HES, albumin, dextrans)

• also effective for volume replacement during major

hemorrhage.• offer NO major advantage over crystalloid solutions, and

albumin has been associated with poorer outcomes in patientswith traumatic brain injury.

Sumber: Merck Manuals


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IV Fluids Composition


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n point n onitoring

M

The actual end point of fluid therapy in shock is normalization

of 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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zdvnk


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DISTRIBUTIVE SHOCK

Anaphylactic – Septic – Neurogenic


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Distributive Shock• Inflammatory mediators disruption of cellular

metabolism peripheral vasodilationdecreased PVR

• Etiology

– Anaphylaxis

– Septic

– Neurogenic

• Sign & symptoms

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


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Anaphylactic ShockAnaphylactic 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


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Figure 12‐2


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Neurogenic Shock

Neurogenic shock is the rarest form of shock.

It is caused bytrauma 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

Gambar 4. Patofisiologi spinal shock


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Septic Shock Tx• O2

• Antibiotics• Fluids

• Vasopressor

– Indication: persistent hypotension* once

adequate intravascular volume expansion has

been achieved

– DOC: NOREPINEPHRINE

*systolic blood pressure


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OBSTRUCTIVE SHOCK


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Obstructive ShockCO↓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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START


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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


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RPMrespirasi, perfusi, mental

‐ Semua proses evaluasi

dalam START harus

dilakukan dalam waktu

kurang dari 60 detik.


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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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Gangguan asam

basa

pH PCO2 HCO3 Penyebab umum

Asidosis respiratorik jikaterkompensasi

PPOK, asma, ARDS

Alkalosis respiratorik jika

terkompensasi

Hiperventilasi,

sepsis

Asidosis metabolik

jikaterkompensasi

Dehidrasi berat,

DM, gagal ginjal,

starving, Diare

Alkalosis metabolik jika

terkompensasi

Muntah

Gangguan Asam Basa


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Tanda

Terkompensasi(sebagian/sepe

nuhnya)

ditandai dgn

ARAH panah

yang SAMAAntara PaCO2

dengan HCO3

CO Poisoning


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Cyanide Poisoning


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y g

• 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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Clinical Effects of Cyanide• Headache • Hypertension,


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• Dizziness

• Seizures

• Coma

CNS

yp ,

bradycardia

• Hypotension, later incourse

• 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

Treatment


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• 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


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• 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

Djengkolic Acid Poisoning


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• Urine analysis erythrocytes, epithelialcells, protein, and the needle‐like crystals ofdjenkolic acid.

Supporting examination

• Hydration to increase urine flow• Alkalinization of urine by sodium

bicarbonate.

Treatment

Organophosphate Poisoning


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• Insecticides, herbicides

Sources

• Inhibit acethylcholinesterase• ACh accumulates throughout the nervous system

• Overstimulation of muscarinic and nicotinic receptors

Mechanism

• SLUD + GEM

Characteristics

Organophosphate Poisoning


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Atropine


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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 menitsampai 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 noresponse 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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Management


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• Airway Management

• Gastrointestinal decontamination : activatedcharcoal and gastric lavage

• Psychomotor agitation : lorazepam 2 mg IV or

Diazepam 2 mg IV• Hyperthermia : ice packs and evaporative cooling

• Hypertension : Anti HT such as nitroprusside

• Seizure : diazepam IV

Arsenic Toxicity


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Management


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• Decontamination

– Skin Decontamination

– Gastrointestinal decontamination : nasogastricsuction, and administer activated charcoal

• Fluids – Administer intravenous fluids to maintain

adequate urine flow.• Monitoring – Patients should have continuous

cardiac monitoring. Additionally, fluid and

electrolyte balance should be monitored.• Chelation – Dimercaprol and DMSA


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Therapy


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Therapy


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• Hemodialysis can easily remove methanol and

formic acid.

Mercury Poisoning


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• 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


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Congenital Minamata Disease:

CP, MR, seizure

Management


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• Chelating agent – Penicillamine is given at doses of 500 mg PO every six

hours for five days, often in combination withpyridoxine (vitamin B6) in doses of 10 to 25 mg/day.

– DMPS is administered according to the followingregimen: 250 mg intramuscular (IM) or intravenous

(IV) every four hours on day 1, 250 mg IM or IV everysix hours on day 2, and 250 mg IM or IV every six toeight hours for days 3 to 5. DMPS is not approved foruse in the United States.

– DMSA is given at a dose of 10 mg/kg PO every eighthours for five days.


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Botulinum Toxin


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Alcohol Withdrawal Syndrome


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Management

Benzodiazepines IV are used to control psychomotor agitation, seizure , DT and


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prevent progression to more severe withdrawal.

(DOC : Diazepam, lorazepam, or chlordiazepoxide)

Volume deficits replacement, isotonic intravenous fluid can be infused rapidly untilpatients are clinically euvolemic

Deficiencies of glucose, potassium, magnesium, and phosphate should becorrected as needed.

Patients being treated for moderate or severe alcohol withdrawal must be closelymonitored (vital signs, pulse oximetry, fluid status, and neurological function) andmay require admission to an intensive care unit (ICU).


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SurgeryBEDAH

BIMBEL UKDI MANTAP

NEURO SURGERY


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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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Epidural Hemorrhage

Signs and Symptoms :


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g y p

• Most patients are unconscious

when first seen. A “lucidinterval” of several minutes to

hours before coma supervenes

is most characteristic of

epidural hemorrhage• Deterioration of consciousness

• Unilateral dilated pupil on side

of injury

• Hemiparesis or hemiplegia onside of body opposite injury

Biconvex / lenticular


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Subarachnoid hemorrhage


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Aneurisma, AVM

Thunderclap headache, Muntah, stiff neck, meningeal

irritation, confusion / penkes

Intracerebral hemorrhage


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Parenkim otak

Brain trauma atau spontan pada hemorrhagic stroke.

CT‐Scan


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MRI

Specific for


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Soft Tissue


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Brain Herniation

Supratentorial herniation


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Supratentorial herniation• Subfalcine (Cingulate) herniation

• Central herniation

• Transtentorial lateral (Uncal) herniation

• Transcalvarial herniation

Infratentorial herniation

• Upward cerebellar herniation

• Downward cerebellar (Tonsillar) herniation

Uncal herniation

• Herniation of the medial temporal lobe inferiorly throughthe tentorial notch


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Clinical triad associated with uncal herniation : – Dilated pupil ipsilateral

– Hemiplegia contralateral

– Coma

• compressed ipsilateral to herniation: hemiplegia will be onthe contralateral side of the body (axons decussate atpyramidal decussation)compressed contralateral to herniation: If the herniation is

very severe, the contralateral cerebral peduncle may becompressed by the opposite side of the tentorial notchleading to an ipsilateral (to the herniation) hemiplegia(Kernohan's phenomenon).

Glasgow Comma Score


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• Motor response 2

• Motor response 3

CEDERA KEPALA

ATLS


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Klasifikasi klinis cedera kepala

berdasarkan GCS :

• Cedera Kepala Ringan (CKR)

GCS 13-15

• Cedera Kepala Sedang (CKS)GCS 9-12

• Cedera Kepala Berat (CKB)

GCS 3-8

Basis Cranii


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CLASSIFICATION


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• Posterior frontal sinus, roof of ethmoid,cribriform, and orbital roof, sphenoidbone

• Posterior frontal sinus, roof of ethmoid,cribriform, and orbital roof, sphenoidbone

Anterior Skull

Base Fracture

• Temporal bone• Temporal boneMiddle Skull

Base Fracture

• Clivus occipital, condylar occipital• Clivus occipital, condylar occipitalPosterior Skull

Base Fracture

Clinical sign :

• Presentation with anterior cranial fossa fractures is with CSF rhinorrhea

and bruising around the eyes "raccoon eyes."

f f l b h


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• Patients with fractures of the petrous temporal bone present with CSF

otorrhea and bruising over the mastoids “Battle sign. “

• Longitudinal temporal bone fractures result in ossicular chain disruption

and conductive deafness of greater than 30 dB that lasts longer than 6‐7

weeks.

• Transverse temporal bone fractures involve the VIII cranial nerve and thelabyrinth, resulting in nystagmus, ataxia, and permanent neural hearing

loss.

• Occipital condylar fracture is a very rare and serious injury. Most of thepatients are in a coma and have other associated cervical spinal injuries.

These patients may also present with other lower cranial nerve injuries

and quadriplegia.


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Halo Sign

(Ring sign/Target sign)


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• Tanda CSF leak:

– Glucose (+)

– Halo sign (+) – Beta‐2‐transferrin (+) highly specific to CSF, not present

in plasma, nasal secretion, tear, saliva, or other fluid.


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THORAX AND CARDIOVASCULAR SURGERY

Trauma Algorythm


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Trauma Thorax“PRIMARY SURVEY” – Mengancam Jiwa


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• Gangguan jalan nafasAirway

• Pneumotoraks terbuka

• Pneumotoraks tension• “Flail Chest”Breathing

• Hematoraks masif • Tamponade kordis

Circulation

Hematothorax

Definition :

accumulation of blood


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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


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ataupun internal organ di thorax

– A. thoracica interna and it’s branches – A. intercostalis

– A. bronchialis

Physical Exam

• Sign : dyspneu


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• I : Jejas (+), ketingalan gerak (+)

• P : Fremitus taktil menurun

• P : Redup (+)

• A : Vesikuler turun, normal heart sound

Tube Thoracostomy / Chest Tube


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Water Sealed Drainage


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Cardiac Tamponade

• Etiology : blunt orpenetrating trauma


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penetrating trauma

in mid‐chest• Nomal breath sound

• Sign Trias Beck

1. Increase JVP2. Hypotension

3. Muffled Heartsound

• Tx :pericardiocentesis

Pericardiocentesis


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Pneumothorax


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Definition :

accumulation of air

or gas in pleuralcavity

Classification

• Spontan (primer dan sekunder) and Trauma

O d Cl d


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• Open and Closed

• Simple and Tension

Physical Exam

• Sign : Dyspneu, subcutis emfisem


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• I : Jejas (+), ketingalan gerak (+)

• P : Fremitus taktil menurun

• P : Hipersonor

• A : Vesikuler turun/hilang, normal heart sound

Open Pneumothorax

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


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( )

“Mediastinal Flutter“ “Sucking Chest Wound“

TreatmentOcclusive dressing tape in 3

sides.

• the dressing prevents atmosphericair from entering the chest wall


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gduring inspiration but allows any

intrapleural air out duringexpiration

Closed Pneumothorax

• Etiology : blunt trauma,


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gy ,

spontaneous rupture ofpleurae air leakage to

pleural cavity

• Can developed intoTension Pneumothorax

• Tx : Chest Tube

Tension Pneumothorax

• Clinical sign :• Himpitan vena cava

• Shock


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• Shock

• JVP ↑• Himpitan paru

kontra lateral• distress nafas

• deviasi trakhea

• Tx :

– Neddle

thoracostomy(decompression)

– Chest tube

Tension Pneumothorax


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• Fraktur costae segmental, multipel,berurutan

Flail Chest


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• Severe respiratory distress• Paradoxal movement

• Asymmetrical and uncoordinated chest wall

movement

• Crepitation on palpation

• Pain>>>>

Flail Chest


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• ABCDE

• Adequate ventilation, oxygenation,

Management


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analgesia

Chest X‐Ray


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Penyakit Oklusi Arteri Perifer

• Nama lain : Peripheral ArteryOcclusive Disease (PAOD),Peripheral Artery Disease


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p y

(PAD), Peripheral VascularDisease (PVD)

• Definisi : gangguan alirandarah akibat penyempitanatau kerusakan pembuluhdarah perifer (selainpembuluh darah koroner dan

pembuluh darah otak)• Etiologi : aterosklerosis (>>>),

non‐aterosklerosis


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• Penyebab Non‐aterosklerosis

– Raynaud’s syndrome


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– Buerger’s disease (Thromboangiitis Obliterans)

– Vasculitis

• Large‐vessel vasculitis = Giant Cell Arteritis (Temporal

Arteritis), Takayasu’s Disease

• Medium‐vessel vasculitis = Polyarteritis Nodosa,

Kawasaki’s Disease, Behcet’s Disease, Cogan’s Syndrome,

• Small‐vessel vasculitis = Antineutrophil CytoplasmicAntibody‐associated Vasculitidies, Vasculitis Associated

with Connective Tissue Diseases


• Penyebab Non‐aterosklerosis (con’t)

– Heritable arteriopathies


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• Cystic Medial Necrosis• Pseudoxanthoma Elasticum

• Arteria Magna Syndrome

– Congenital Conditions Affecting the Arteries• Persistent Sciatic Artery

• Popliteal Entrapment Syndromes

• Adventitial Cystic Disease

– Peripheral Artery Aneurysms• Femoral Artery Aneurysms

• Popliteal Artery Aneursyms

Claudicatio Intermitten

• Definition : pain incalf region during


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exercise (walking)cause narrowing ofvessel due toatheroscleroticplaque (e.c PeripheralArtery Disease)



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Critical Limb Ischemia


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Tatalaksana PAD ‐ Revaskularisasi

• Prosedur endovaskular (angioplasti, stenting),

• Pembedahan (bypass, profundoplasty),


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simpatektomi

Acute Limb Ischemia

• 5 P Pain, Pallor, Pulseless,Paresthesia, Paralysis

• Chronic Limb ischemia adakolateralisasi, Acute Limb


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ischemia tidak ada / sedikitkolateralisasi, kurang bisamenolerir iskemia

• Etiologi tromboembolism

(atrial fibrilasi, valvularleaflets, riwayat bypass ataustent placement)

Acute Limb Ischemia


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Acute Limb Ischemia


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I, IIA revaskularisasi dengan trombolitik

IIB revaskularisasi dengan intervensi operatif

Thromboangitis Obliterans

• Also called as “Buerger Disease”

• Male, 20‐40 y.o


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• 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 otherconditions.


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• 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,

d ll h


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and occasionally other areas.

– Raynaud's disease ("Primary

Raynaud's phenomenon") →

idiopathic

– Raynaud's syndrome

(secondary Raynaud's), →

commonly connective tissue

disorders such as Systemiclupus erythematosus

Takayashu


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Deep Vein Thrombosis

(Trias Virchow)


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Deep Vein Thrombosis

Sign and Symptoms :

• Leg swelling

P i f th ff t d l


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• Pain of the affected leg

• Erythema or discolored skin ofthe affected leg

• Warmth of the affected leg skin

• Leg fatigue

Commonly affects leg veins –popliteal, femoral, pelvic

(Half of all DVT cases cause no symptoms)


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PLASTIC SURGERY


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Burn Injury

Etiology The Depth of

skin burn


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Size and extent of

the burn wound

Burn Injury


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prick test (+)

Superficial PartialThickness Burn (IIa)


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Deep Partial

Thickness Burn (IIb)


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Full Thickness Burn

(III)


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Total Body

Surface Area


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To estimate scattered burns: patient's

palm surface = 1% total body surface

areaParkland formula = baxter formula


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Labio‐Gnato‐Palato Schisis


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The Neonatal Period

• Surgical Repair

– Cleft Lip

• In US ‐ “the rule of tens” ‐ 10 wks, 10 lbs, Hgb 10


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• 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


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Urachal anomaliesare due to failure of complete obliteration of the lumen during gestation.

Presenting symptoms :

Umbilical drainage or a mass and/or pain due to infection. The umbilicaldrainage may be clear, serous, purulent, or bloody.

Urachal abnormalities are a frequent concern in newborns with umbilicaldrainage that persists beyond a few weeks.


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drainage that persists beyond a few weeks.

A patent urachus or urachal sinus can appear as a dimple or indentation in

the base of the umbilicus.

In general, symptomatic urachal remnants should be treated with surgicalexcision. This should include complete excision of the urachus from theumbilicus to the dome of the bladder.

If the urachal disorder presents with an infection, the infection is treatedfirst. This requires antibiotics, possible admission for intravenous antibiotics,and occasional surgical drainage of any infected cyst or poorly draining cavity.


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Sign and Symptoms

• Symptoms may recur after previouslyresolving with laxatives, or feeding

changes.

• Digital Rectal examination maydemonstrate a tight anal sphincter

d l i di h f t l d


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and explosive discharge of stool and

gas.‐ Frog‐like abdomen

‐ Darm contour

‐ Darm steifung‐ Metallic sound


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Atresia Esophageal


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• The first sign of esophageal atresia in the fetus may be polyhydramnios in

the mother.

• Prematurity has also been associated with esophageal atresia.

• Classically, presents with copious, fine, white, frothy bubbles of mucus inthe mouth and, sometimes, the nose.

• The infant may have rattling respirations and episodes of coughing, choking

and cyanosis, may be exaggerated during feeding.

Diagnosis


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• (A) Diagnosis of esophageal atresia is confirmed when a 10‐gauge(French) catheter cannot be passed beyond 10 cm from the gums.

• (B) A smaller‐caliber tube is not used because it may curl up in the upper

esophageal segment, giving a false impression of esophageal continuity.

• The normal distance to an infant's gastric cardia is approximately 17 cm


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Hypertrophy Pyloric Stenosis

• Hipertrofi m.sphincter pylorus

• Stenosis > canalis pyloricus

• Klinis :

– Muntah proyektil, bile free,bolus+gastric juice

B b l k h


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– Baby looks hungry

– Palpable mass (olive)

• Dx : – Plain photo (Single bubble sign) – Barium meal / OMD (Umbrella sign)

• Komplikasi : dehidrasi & aspirasi

• Tx : – Non surgery : resusitasi cairan

– Surgery : pyloromyotomy

HPS

• Typical presentation is onset of non‐bilious vomiting at 1‐12 weeks of age

(3‐4 weeks), becomes more predictable, occurring at nearly every feeding.

• Vomiting intensity also increases until pathognomonic projectile vomiting

ensues

• Slight hematemesis of either bright‐red flecks or a coffee‐ground

appearance is sometimes observed.

• Persistent hunger, weight loss, dehydration, lethargy, and infrequent or


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g , g , y , gy, q

absent bowel movements may be seen. Stomach wall peristalsis may be

visible.

• An enlarged pylorus, classically described as an "olive," can be palpated in

the right upper quadrant or epigastrium of the abdomen in 60‐80% of

infants

• Pre‐operative management is directed at correcting the fluid deficiencyand electrolyte imbalance.


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Atresia / Stenosis Duodeni

• Atresia: completeobstruction; stenosis:partial obstruction

• Lokasi tersering diduodenum pars


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horizontal

• Symptom: regurgitasi &vomit (bilous vomit)

• Dx : (double bubble)

– Plain photo – Barium meal / OMD

In approximately 80% of affectedneonates, the site of duodenal atresia is

postampullary, so that the patient may

present with bilious vomiting.

Double bubble Sign


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• Plain film radiograph

“Double bubble” Sign

(gas‐filled stomach and duodenum

dilatation with no distal gas)

• Without abdominal distension

Barium meal / OMD

Intestinal Obstruction(jejunoileal obstruction)

Classic signs of patients with jejunoileal atresia :

• Bilious vomit

• Abdominal distention (in distal atresia)

• Jaundice (32%) which is characteristically due to indirect


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Jaundice (32%) which is characteristically due to indirect

hyperbilirubinemia

• Failure to pass meconium in the first 24 hours (rule out Hirschsprung

disease; passage of meconium does not rule out intestinal atresia)

• Abdominal distention is most evident in cases of ileal atresias, in which it

is diffuse, as opposed to proximal jejunal atresias, in which the upper

abdomen is distended and the lower abdomen is scaphoid.

• Intestinal loops and their peristalsis may be seen through the thinabdominal wall of newborns.


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Anorectal

Malformations

• The resulting malformations range from

isolated imperforate anus to persistent cloaca.

• Atresia ani (imperforate anus) is a congenital abnormality characterized by

persistence of the anal membrane resulting in a thin membrane covering

the normal anal canal or is the failure of the anal membrane to break


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down (Noden and Lahunta 1985)

• If, after 24 hours, there is no meconium on the perineum, we recommendperforming a cross‐table lateral x‐ray with the baby in knee chest (prone)

position.

useful in determining the

level of atresia

Klasifikasi

• Menurut Berdon, membagi atresia ani berdasarkan tinggi rendahnya

kelainan, yakni :~ Atresia ani letak tinggi : bagian distal rectum berakhir di atas muskulus

levator ani (jarak > 1,5 cm dengan kulit luar)

~ Atresia ani letak rendah : bagian distal rectum melewati musculus

levator ani (jarak < 1,5cm dari kulit luar)

• Menurut Stephen, membagi atresia ani


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Menurut Stephen, membagi atresia ani

berdasarkan pada garis pubococcygeal :

~ Atresia ani letak tinggi : bagian distal rectumterletak di atas garis pubococcygeal.

~ Atresia ani letak rendah: bagian distal rectum

terletak di bawah garis pubococcygeal.

“high” supralevator lesions are typically associated

with fistulas


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Intussusception(Invagination)

• Invagination of a proximal portion of intestine (intussusceptum) into a

more distal portion (intussuscipiens), is one of the most common causesof bowel obstruction in infants and toddlers.

• > 80% involves the ileocecal region.

• Occur in children less than one year of age, with a peak incidenceof between 6‐10 months. (>> 9 months)


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TRIAS :

• Colicky & Cramping abdominal pain

• Bilious vomiting

• Mucous‐red “currant jelly stools”

Physical Exam :

• Palpable abdominal mass

(Sausage Appearance)

• Dance ‘s sign

Radiographic Features Intussusception

USG :• Target or doughnut sign (Transverse cross section)

• Sandwich sign, pseudokidney sign (Longitudinal

section)


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Pseudokidney sign


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Barium Enema : Cupping sign(as a diagnostic) or therapeutic (non‐operative reduction)

Volvulus

• Volvulus of the intestine, the twisting of a segment of intestine on its

mesentery, can be a primary pathology or secondary to malrotation of theintestine. Clinical presentations vary from acute abdominal emergency

requiring immediate surgical intervention to insidious history of colicky


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abdominal pain.

• Volvulus of the small intestine is commonly associated with abnormality

of intestinal rotation and fixation. This is due to failure of fixation and

narrow mesenteric base which allow volvulus to occur. Midgut volvulus

can lead to irreversible intestinal necrosis, which is potentially fatal.

• Large bowel volvulus on the other hand is rare in children; it usually

occurs as a result of redundant sigmoid colon and affects mainly adults.

• Up to 80% of patients present in the first month of life (20% of patients

present after the first year of life) and in this age group the cardinal

symptom is bile (green) vomiting due to duodenal obstruction through

midgut volvulus.

• Pain, irritability, and other non‐specific symptoms (anorexia or nausea was

noted) are more common in toddlers and older children.


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• The coffee‐bean sign (also known as bent inner tube sign) is a sign on anabdominal plain film.

• This thick 'inner wall' represents the double wall thickness of opposed

loops of bowel, with thinner outer walls due single thickness.


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TERIMA KASIH

Bimbingan UKMPPD (UKDI) - Anestesi-Bedah

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