Anesthesiology Bs Btkv Bp Ba Mantap Tutor
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Transcript of 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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