BIMBEL UKDI MANTAP

dr. Andreas W Wicaksono

dr. Anindya K Zahra
dr. Arius Suwondo
dr. M. Dzulfikar Lingga Q M
dr. Marika Suwondo
dr. Alexey Fernanda N
dr. Denise Utami Putri
dr. Aditya Wicaksana
dr. Renaldo Faisal H

Batch Februari 2020

 Content
Emergency
Airway Assessment
Foreign body obstruction
Breathing

Basic Life Support

Shock
Hypovolemic shock
Cardiogenic shock
Distributive shock
Obstructive shock

Triage

Acid Base Balance

Poisoning
Trauma, Primary Survey
 Airway and C Spine control
Trauma Maksilofasial
Pasien Berbicara Lancar -> airway baik
Curiga cedera cervical bila pasien tidak
sadar, high-velocity and high impact injury,
defisit neurologis, C spine tenderness

Problem Airway Adakah patensi jalan

Trauma Leher
nafas ?

Look : Agitasi, penkes,

Trauma Laryngeal retraksi, otot bantu nafas
Listen : suara nafas abnormal
Feel : lokasi trakea

Gurgling liquid or semisolid foreign material in the main airway -> Suctioning

Snoring pharyng is partially occluded by soft palate or epiglottis.

Crowing sound of laryngeal spasm.

Inspiratory stridor obsruction at laryngeal level or above.

Expiratory wheeze obstruction of the lower airway.

Oropharingeal Airway
Digunakan untuk ventilasi sementara pada pasien yang tidak
sadar sementara intubasi pasien sedang disiapkan
Tidak boleh digunakan pada pasien yang sadar karena dapat
menyebabkan sumbatan, muntah dan aspirasi.

Nasopharingeal Airway
Prosedur ini digunakan apabila pasien terangsang untuk
muntah pada penggunaan OPA
Tidak boleh digunakan pada kecurigaan fraktur basis cranii

Laryngeal Mask Airway

Digunakan untuk pertolongan dengan airway yang sulit untuk
intubasi endotracheal atau bag mask gagal. Ingat LMA bukan
definitif
Laryngeal Tube Airway
Suatu alat airway diluar glotis untuk memberi ventilasi pasien
dengan baik.

Gum Elastic Bougie

Diikenal dengan nama Eschmann tracheal tube introducer
(ETTI)
Digunakan pada keadaan sulit intubasi

Multilumen Esophageal Airway (Combitube)

Dapat digunakan apabila airway definit belum dapat
dilakukan.
Alat ini memiliki lubang udara yang mengarah ke saluran
nafas, lubang lain mengarah ke esofagus.
 Airway definitif Orotracheal Tube
Nasotracheal Tube
Airway surgical :
Adalah tabung yang terpasang di dalam trakea, dengan balon
Krikotiroidotomi
yang dikembangkan di bawah pita suara. Tabung
dihubungkan ke sumber oksigen melalui alat bantu ventilasi Trakheostomi

Kebutuhan Untuk PERLINDUNGAN Kebutuhan Untuk VENTILASI

AIRWAY
Penurunan 8) Apneu :
-Paralisis neuromuscular
-Tidak sadar
Fraktur Maxilofacial berat Usaha Nafas tidak adekuat
-Takipneu
-Hipoksia
-Hiperkarbia
-Sianosis
Resiko Aspirasi : Perdarahan, muntah Cedera kepala tertutup berat yang
muntah membutuhkan hiperventilasi
Resiko Sumbatan : Hematoma leher, Kehilangan darah yang masif dan
cedera laring, trachea, stridor memerlukan resusitasi volume
 NPA
Pengelolaan Jalan Nafas
Oksigenasi dan pasang pulse oxymetri
Open mouth dengan crossed-finger, bersihkan jalan nafas OPA
dari corpal, suctioning

Chin lift manuver atau jaw thrust manuver (pada

curiga C-spine terganggu)-> dipertahankan dengan
nasofaringeal airway atau orofaringeal airway

Dapat teroksigenasi? Definitif airway/ Intubation

NO Surgical airway
Assess airway anatomy -> Call assistance
LEMON Difficult or Awake
Intubation drug assistance intubation
Cricoid pressure

unsuccesfull
Consider adjunct -> GEB/LMA/LTA

Definitif airway/
Surgical airway
 Nasotracheal intubation

Cricothyroidotomy Tracheostomy
Memegang leher adalah tanda
universal bahwa korban
sedang tersedak
AHA Choking Algorithm
without backblow
UPPER

LOWER
Bronchoscopy

is an endoscopic technique
of visualizing the inside of
the airways for diagnostic
and therapeutic purposes.
 Manual Assisted Ventilation
Apply face mask
Oro/naso-pharyngeal airway
adjuncts
Mouth opening
Hand positioning
Elevate mandible and chin
Resuscitation bag compression
volume and frequency
Frequency = 10-12 x/minute (apneu
without cardiac arrest), 8-10
x/minute (apneu with cardiac arrest)
Ensure adequate chest wall
expansion everytime ventilation
given
Supplementary Oxygen
 Shock Definition
A physiological state characterized by a
significant, systemic reduction in tissue
perfusion, resulting in decreased tissue oxygen
delivery and insufficient removal of cellular
metabolic products, resulting in tissue injury.
Classification of Shock

Hypovolemic Cardiogenic

Obstructive Distributive
 Pathophysiology of Shock
Preload
Afterload Stroke Volume x Heart Rate
Contractility

O2 Content Cardiac
Resistance
Output
x x

O2 Delivery Arterial Blood

Pressure
 Pathophysiology
Shock CO SVR

Hipovolemik (preload dan sebagai

(termasuk perdarahan) afterload) kompensasi
Kardiogenik (kontraktilitas) sebagai
kompensasi
Distributif sebagai
(termasuk anafilaktik, kompensasi
septik, neurogenik/
spinal)
Hipotensi jika:

TDS Dewasa : < 90

TDS Geriatri : < 110
TDS Pediatri : < [70 + (2 x Usia)]
Hipotensi jika:

TDS Dewasa : < 90

TDS Geriatri : < 110
TDS Pediatri : < [70 + (2 x Usia)]
Hipotensi jika:

TDS Dewasa : < 90

TDS Geriatri : < 110
TDS Pediatri : < [70 + (2 x Usia)]
Hipotensi jika:

TDS Dewasa : < 90

TDS Geriatri : < 110
TDS Pediatri : < [70 + (2 x Usia)]
Hipotensi jika:
Hipotensi jika:

TDS Dewasa
Dewasa : < 90
TDS Geriatri
Geriatri : < 110
TDS Pediatri
Pediatri : < [70 + (2 x Age)]
Usia)]
 Characteristics of Shock

End organ Metabolic

dysfunction: dysfunction:
reduced urine
output acidosis
altered mental
status
altered metabolic
poor peripheral demands
perfusion
 Management

Goal : pengangkutan O2 & O2

Cara : O2, cairan, kontrol suhu, antibiotik, koreksi kelainan metabolik, Inotropik

Airway : intubasi & kontrol ventilasi

Breathing :
Awal : O2 100 %, monitor saturasi

Sirkulasi
Akses IV scr cepat.
Intra osseus: anak 4 6 th
Kateter vena sentral
HYPOVOLEMIC SHOCK
 Perkiraan Kehilangan Darah
Kelas I Kelas II Kelas III Kelas IV
Kehilangan darah <750 750-1500 1500-2000 >2000
(mL)*
Kehilangan darah <15% 15-30% 30-40% >40%
(% volume darah)
Nadi <100 >100 >120 >140
Tekanan darah Normal Normal Menurun Menurun
Tekanan nadi Normal atau naik Menurun Menurun Menurun
Frekuensi nafas 14-20 20-30 30-40 >35
Produksi urin >30 20-30 5-15 Tidak berarti
(ml/jam)
Status mental Sedikit cemas Agak cemas Cemas, bingung Bingung, letargis
Penggantian Kristaloid (3 for 1 Kristaloid (3 for 1 Kristaloid (3 for 1 Kristaloid (3 for 1
cairan rule) rule) rule)dan darah (1 rule)dan darah (1
for 1 rule) for 1 rule)

*) untuk laki-laki dengan berat badan 70kg

 Estimated Blood Volume (EBV)

Laki laki = 75 cc/kgBB

Perempuan = 65 cc/kgBB

Infant = 80 cc/kgBB

Neonatus = 85 cc/kgBB

Premature neonatus = 96 cc/kgBB

 Therapy - Hypovolemic
PRINSIP TERAPI : CAIRAN

TUJUAN
VOL. INTRAVASKULER TERCUKUPI
KOREKSI ASIDOSIS METABOLIK
OBATI PENYEBAB

REASSES PERFUSI, UO, TANDA VITAL

PILIHAN :
KRISTALOID ISOTONIK : 1-2 LITER ATAU 20 CC/KG (ANAK) SECARA BOLUS CEPAT BILA FUNGSI
JANTUNG NORMAL
NS DAPAT MENYEBABKAN ASIDOSIS HIPERCHLOREMIK

Adjuvan pada Syok Hemoragik

penggunaan kristaloid (dapat mendilusi
faktor koagulasi) dan resusitasi awal dengan produk darah (RBC:FFP:PLT ~ 1:1:1)
Asam traneksamat diberikan dalam <3 jam trauma. (Dewasa 1 gram atau 10mg/kgBB/kali)
 IV fluids
Crystalloid solutions (isotonic)
Both 0.9% saline and RL are equally effective
RL may be preferred in hemorrhagic shock because it
somewhat minimizes acidosis, controls bleeding and will not
cause hyperchloremia.
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 patients
with traumatic brain injury.
Sumber: Merck Manuals
IV Fluids Composition
 Normal Saline vs Ringer Lactate
Hal yang harus dipertimbangkan pada pemberian kristaloid

Risiko untuk edema otak lebih rendah,
sehingga dipilih untuk kasus cedera
kepala dan stroke.
Kadar Klorida yang tinggi, sehingga
pemberian volume yang banyak dapat
berakibat Hiperkloremik asidosis.
SE: Hiperkloremik Asidosis SE: Hiperkalemia
Laktat akan dimetabolisme di hepar
menjadi bikarbonat (HCO3), pada
pasien sirosis hepar akan terjadi
penumpukan laktat (Alt: Ringer
asering, karena dimetabolisme di
otot)
Mengandung Kalsium sehingga
memicu koagulasi

Dextrose tidak digunakan untuk resusitasi karena risiko hiperglikemia dan

mortalitas tinggi akibat hiperglikemia akut.
 End point and Monitoring

The actual end point of fluid therapy in shock is normalization of

DO2

Adequate end-organ perfusion is best indicated by urine

output of > 0.5 to 1 mL/kg/hour (1-2 mL/kg/hour for pediatric)

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
CARDIOGENIC SHOCK
 Therapy - Cardiogenic
Terapi Inisial Dg. Pemberian Cairan

Bila Tak Ada Perbaikan memburuk susp.

Syok Kardiogenik Inotropik
Anaphylactic Septic Neurogenic - Spinal

DISTRIBUTIVE SHOCK
 Distributive Shock
Inflammatory mediators disruption of cellular metabolism
peripheral vasodilation decreased PVR

Etiology

Anaphylaxis
Septic
Neurogenic
Spinal

Sign & symptoms

Febrile, tachycardia, clear lungs *, warm extremities, flat neck veins, oliguria
 Anaphylactic Shock
Anaphylactic shock
a type of distributive shock, which involves the immune system
(Hurst, 2008)

Type 1 hypersensitivity
antigen binds to IgE antibodies on mast cells, which leads to
degranulation of the mast cells.

Sign & symptoms

itching, hives, and swelling
circulatory collapse (vasodilatation)
suffocation (bronchial and tracheal swelling)
Tatalaksana Syok Anafilaksis
 Septic Shock Tx
O2
Antibiotics
Fluids
Vasopressor
Indication: persistent hypotension* once
adequate intravascular volume expansion has
been achieved
DOC: NOREPINEPHRINE

*systolic blood pressure <90 mmHg or MAP<65 mmHg

OBSTRUCTIVE SHOCK
 Obstructive Shock
CO akibat OBSTRUKSI FISIK terhadap ALIRAN DARAH

PENYEBAB :
TAMPONADE PERIKARD
TENSION PNEUMOTHORAX
CRITICAL COARCTASIO AORTA
STENOSIS AORTA

TERAPI
CAIRAN
ATASI PENYEBAB
 START
Simple Triage and Rapid Treatment
TRIASE
proses pemilihan pasien berdasarkan beratnya kondisi pasien
Situasi
Multiple casualties (jumlah pasien/cedera >1, namun tidak melampaui
kemampuan dan fasilitas rumah sakit) pasien dengan masalah yang
mengancam jiwa dan multi trauma akan dilayani terlebih dahulu
Mass casualties (jumlah pasien dan beratnya cedera melampaui
kemampuan dan fasilitas rumah sakit pasien dengan kemungkinan
bertahan hidup yang terbesar, serta membutuhkan waktu, perlengkapan,
dan tenaga paling sedikit
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
 RPM
respirasi, perfusi, mental
- Semua proses evaluasi
dalam START harus
dilakukan dalam waktu
kurang dari 60 detik.
:
pH: 7,35-7,45
PCO2: 35-45 mmHg
HCO3: 22-26 mmol/L.

Tanda
Terkompensasi
(sebagian/sepe
nuhnya)
ditandai dgn
ARAH panah
yang SAMA
Antara PaCO2
dengan HCO3
Step 1 Step 3 Lihat
kompensasi
(uncompensate
Step 2 d arah tanda
Lihat Lihat kausa
panah PaCO2
dan HCO3 tidak
pH (respiratorik
PaCO2;
searah; partially
compensated
(<7,35 atau PaCO2 dan
HCO3 searah
metabolik
= asam HCO3), naik.turun, pH
masih abnormal,
Gunakan
atau ROME
fully PaCO2
dan HCO3
>7,45 = searah
naik.turun, pH
basa) sudah normal)
Anion gap
Fisiologi manusia adalah isoelektrik, sehingga:

Jumlah anion = Jumlah kation

Anion terukur + Anion tak terukur =

Kation terukur+ Kation tak terukur

Anion tak terukur - Kation tak terukur =

Kation terukur - Anion terukur

Anion gap = Kation terukur - Anion terukur

atau
AG= [Na+ - (Cl- + HCO3 -)]
Anion gap = Anion tak terukur Kation tak terukur Nilai Normal = 8-12 mEq/L

Anion Gap akan meningkat saat terjadi kondisi peningkatan asam yang tidak
terukur: Laktat, Keton (Ketoasidosis), Alkohol, Aspirin, Parasetamol, Sulfate, dsb.
POISONING

dosis facit
The dose makes the poison

-Theophrastus von Hohenheim, Father of Toxicology-

 Organophosphate Poisoning
Sources

Insecticides, herbicides

Mechanism

Inhibit acethylcholinesterase
ACh accumulates throughout the nervous system
Overstimulation of muscarinic and nicotinic receptors

Characteristics

DUMBBELS
Organophosphate Poisoning
ORGANOPHOSPOSPHATE POISONING
SIGN AND SYMPTOM
 Atropine
Competitive inhibitor at autonomic postganglionic cholinergic receptors (GI &
pulmonary smooth muscle, exocrine glands, heart, and eye)

Dosis awal dewasa: 2 mg IM. Dosis dapat digandakan setiap 10 menit

sampai teratropinisasi.

The main concern with OP toxicity is respiratory failure from

excessive airway secretions. The endpoint for atropinization
is dried pulmonary secretions and adequate oxygenation.
Tachycardia and mydriasis must not be used to limit or to stop
subsequent doses of atropine.
CO Poisoning
 In CO intoxication, SpO2 are normal.
Standard pulse oximetry (SpO2) is unable to
distinguish between oxyhemoglobin and COHb.

Tx : O2 (Oxygen)

Half-life of COHb in a patient breathing:

Room air (FiO2 21%) : 250-320 minutes
NRM (FiO2 100%) : 90 minutes
Hyperbaric Oxygen : 30 minutes
 Djengkolic Acid Poisoning
Sources

JENGKOL bean

Mechanism

poor solubility under acidic conditions

the amino acid precipitates into crystals
mechanical irritation of the renal tubules and urinary tract

Characteristics

abdominal discomfort, loin pains, severe colic, nausea,

vomiting, dysuria, gross hematuria, and oliguria, occurring 2 to
6 hours after the beans were ingested.
 Djengkolic Acid Poisoning
Supporting examination

Urine analysis erythrocytes, epithelial

cells, protein, and the needle-like crystals of
djenkolic acid.

Treatment

Hydration to increase urine flow

Alkalinization of urine by sodium
bicarbonate.
 Cyanide Poisoning
Sources

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

Cyanide salts used in industry
Produced in smoke of burning plastics/synthetics, electroplating,
metal polishing

Mechanism

Inhibits cellular respiration

Tissue cannot utilize O2

Characteristics
Cyanide inhibit cellular respiration
Clinical Effects of Cyanide
Headache Hypertension,
Dizziness bradycardia
Seizures Hypotension, later in
Coma course
Cardiovascular
collapse

CNS Cardiovascular

Dyspnea Nausea, vomiting

Tachypnea Caustic effects
Pulmonary edema
Apnea

Pulmonary Gastrointestinal
 Cyanide Diagnosis
Clinical picture : sweet almond breath
Lactic acidosis
ABG:
metabolic acidosis
 Treatment
Remove from source
Oxygen
Cyanide antidote kit:
Amyl nitrite perle (inhalation)
until IV established
Sodium Nitrite (300mg IV)
Peds: 0.33 ml/kg of 10% solution)
Sodium Thiosulfate (12.5g IV)
Peds: 1.65 ml/kg of 25% solution
Hydroxocobalamine (5 g)
Peds: 70 mg/mg (max 5 g)
Treatment with amyl nitrite or sodium nitrite is contraindicated in cases of
concurrent carbon monoxide toxicity, because of methemoglobin production
 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 >>)
Parkinsonian motor impairment
Therapy
 Therapy
Hemodialysis can easily remove methanol and
formic acid.
Descending Paralysis
(Craniocaudal)
Botulinum Toxin
 Treatment
Monitoring
Pulse oximetry
Spirometry
ABG
Ventilation, perfusion, upper airway integrity

Antitoxin
Equine serum heptavalen botulism antitoxin children >1 year old and adult
Human-derived botulism immune globin
Antibiotics
Penicillin G (3 million units IV every four hours in adult)
Metronidazole (500 mg IV every eight hours) is a possible alternative for penicillin-allergic patients
Other treatments
Laxatives, enemas