ICM 2 WEEK 6

Poisoning
Poisoning refers to the development of dose-related adverse effects following
exposure to chemicals, drugs or xenobiotics.
Overdosis : Paparan racun yang disengaja dan sering dikaitkan dengan usaha
bunuh diri, kejahatan penyalahgunaan obat.
Efek Samping : Suatu reaksi yang tidak diharapkan dan berbahaya yang
diakibatkan oleh pengobatan.

Diagnosis
History taking
 Name and amount of drugs
 Onset
 Route
 Duration
 Circumstances (locations, surrounding event and intent)
 Symptoms
 Type of first aid provided
Physical examination
 Vital signs : Stimulated, depressed, discordant or normal
 Neurologic  Neuromuscular disorder, focal neurologic examination
 Cardiopulmonary
 Evidence of trauma
 Consider the underlying cause, identify toxidrome
Toxicology lab evaluation
Lab assessment
 Increased AGMA : Keracunan apapun yang menyebabkan hepatic, renal
dan pulmonary failure, methanol, salicylate.
 Serum lactate
 Increased Osmolal gap : Keracunan acetone, alcohol, calcium dan
magnesium, sugar (glycerol, mannitol, sorbitol)
 Ketosis : acetone, salicylate, alcohol.
 Glucose : Hypo (B blockers, ethanol, insulin), Hyper (acetone, B agonist,
caffeine, CCB)
 Kalium : Hypo (barium, B Agonist, diuretics, teophyline), Hyper (A
agonist, B blockers)
 Calcium : Hypo (oxalate, ethylene glycol)
ECG
 Bradycadia and AV block
 QRS and QT interval prolongation
 Ventricular tachyarrhytmia
Radiology
 Pulmonary oedema
 Aspiration pneumonia
Toxicology analysis
 Urine
 Blood
Response to antidote
  Stimulated : Increased vital signs and neuromuscular activity.
 Depressed : Decreased vital signs and neuromuscular acticity. Caused by
sympatholytics.
 Discordant : Mixed vital signs and neuromuscular abnormalities,
stimulation and disorder occur together or at different times during
clinical course.
 Normal : Due to nontoxic exposure, psychogenic illness or poisoning by
toxic time bombs.

Therapy
1. Resusitasi dam stabilisasi
2. Riwayat keracunan dan pemeriksaan fisik, evaluasi toksidrome spesifik
3. Dekontaminasi saluran cerna, kulit dan mata
4. Pemeriksaan lab, EKG dan radiologi
5. Pemberian antidote spesifik
6. Penggunaan teknik eliminasi
7. Observasi dan disposisi
Support vital signs, prevention of further poison absorption, enhancement of
poison elimination, administration of specific antidotes and prevention of
reexposure.
 Pretoxic : Decontamination is the highest priority.
 Toxic : Management is based on clinical and lab findings. Resuscitate and
stabilize. Elimination may shorten the duration and the severity of toxic
phase.
Establish IV access, oxygen saturation, initiate cardiac monitoring, ECG
and xray evaluation.
If seizure, administer glucose, naloxone and thiamine.
Elimination of theophylline or carbamazepine may be achieved by
multiple doses of activated charcoal. Elimination of salicylate may be
achieved by urinary alkalization. Elimination of metals by chelation
 Resolution : Supportive care and monitoring until clinical and lab
abnormalities resolved.
Supportive care goal is to maintain physiologic homeostasis until detoxification
is accomplished and to prevent and treat secondary complication.

Respiratory Care
 Endotracheal intubation for protection against the aspiration of GI
contents in patients with CNS depressions or seizure.
 Pulse oximetry or arterial BGA  the need for oxygenation and
ventilation

Cardiovascular Therapy
 Hypotensive : unresponsive to volume expansion, administer
norepinephrine, epinephrine, dopamine.
 Treat arrhythmia

CNS Therapy
 Seizure : Use benzodiazepine and barbiturate or pyridoxine.
 EEG monitoring.
 Cyproheptadine for serotonin syndrome.

Decontamination
Efficacy of all decontamination procedures decrease with time. Most patient will
recover from poisoning uneventfully with good supportive care alone, but
complication of GI decontamination (aspiration) can orolong this process. Lebih
baik kalau < 1 jam.
 Activated charcoal paling bagus, kontraindikasi sedikit, lebih tidak
invasive disbanding ipecac dan gastric lavafe. Given orally via cup, straw
or small bore NGT. Dosage 1g/kg bidy weight. Charcoal adsorbs ingested
poison within the gut lumen, allowing charcoal toxin complex to be
evacuated with stool.
 Gastric lavage hanya kalau decontamination lain ga bisa. Performed by
sequentially administering and aspirating 5 mL fluid per KgBW through
orogastric tube. Patient should be placed in Trendelenburg and LLD
position to prevent aspiration.
 Ipecac syrup sekarang udah ga dipakai karena menyebabkan electrolyte
and fluid abnormalities, cardiac toxic and myopathy.
 Whole-bowel irrigation administering bowel cleansing solution
containing electrolyte and polyethy;ene glycol orally or by gastric tube
until rectal effluent is clear, patient must be in sitting position.
 Cathartics are salts or saccharides given with activated charcoal to
promote rectal evacuation of GI contents.
 Dilution drinking 5 mL/kg BW of water, only recommended after
ingestion of acids and alkali.
 Endoscopic removal useful in ingestion of toxic foreign body that fails to
transit GI tract, such as heavy metal or bezoar.
 Saline is preffered for eye irrigation.
 Water, soap, water may be best for dermal decontamination.
 Fresh air or oxygen for inhalational exposure.
 Irrigation for liquid removal from body cavities such as vagina/.
  Solid stuffs should be removed manually.

Enhancement of poison elimination

 Multiple dose activated charcoal : Enhance the elimination of previousy
absorbed substances by binding them within the gut as they are excreted
in the bile, Secreted by GI cells or passively diffuse into gut lumen. Dosage
0,5-1 g/kg every 2-4 h. Only for theophylline, phenobarbital,
carbamazepine, dapsone, quinine poisoning.
 Urinary alkalinization : Ion trapping via alteration of urine pH may
prevent renal reabsorption of poison that undergo excretion by
glomerular filtration and active tubular secretion. Producing urine pH>7,5
and UO 3-6 mL/kg/ hour by adding sodium bicarbonate to an IV solution
enhance ecretion of chlorophenoxyacetic acid, herbocides,
chlorpropamide, MTX, phenobarbitalm sulfonamide.
 Extracoporeal removal : Hemodialysis, hemofiltration, plasmapheresis
are capable of removing any toxin from blood streams. Biasa untuk pasien
dengan severe toxicity who deteriorate despite aggressive supportive
therapy, prolonged, irreversible or fatal toxicity, dangerous blood levels
of toxins, ga bisa self-detox karena liver or renal failure.
 Chelation untuk heavy metal. Hyperbaric oxygenation untuk CO.
Toxidrome
Insecticide
Organophosphate
Fisiologi
Ach merupakan neurotransmitter. Ach bekerja di parasimpatetis dan simpatis,
Ach memiliki 2 receptor utama :
 Nicotinic
 Muscranic
Ach akan diihibisi oleh Ach esterase.

Patofisiologi
Inhibisi Ach esterase  Ach tidak terdegradasi  Akumulasi dan prolonged
effects of Ach  Hyper activity of cholinergic
Manifestasi

Komplikasi
 Bronchorrhea dan bronchospasm
 Seizure
Diagnosis
 Decreased Plasma cholinesterase, kembali pada minggu 4-6
 Decreased RBC cholinesterase, kembali pada minggu 6-12
 Pada keracunan kronis yang menurun hanya RBC cholinesterase,
sedangkan plasma normal.
 Respiratory, cardio, renal function
 Fluid and electrolyte balance
 ABG  Acidosis (metabolic/ mixed)

Therapy
 Dekontaminasi
 o Flushing of exposed skin
o Kalau dekontaminasi GI seperti pemberian charcoal katanya tidak
terlalu berguna.
 Supportive
o Airway management dengan suction dan oxygenation (ventilator
support/ intubation)
o Cardiovascular : Apabula pasien tachycardia tidak perlu diberikan
B blocker nanti makin parah
 Antidote
o Atropin untuk counteract efek muscarinic saja. Dosis 1-2 mg IV/
IM, doubling tiap 5 menit. Pada 1 jam pertama biasanya pasien
membutuhkan 200-500 mg, kemudian dilanjutkan 5-100 mg/jam.
Diberikan hingga terjadi atropinisasi ditandai dengan menurunnya
efek muscarinic (kebalikan SLUDGE). Indikasi berhenti drying
respiratory secretion, easing of respiration, MAP >60 mmHg.
o Diphenhydramine bisa menjadi alternative atropin
o Pralidoxime dapat mengcounteract muscarinic dan nicotinic. Dosis
1-2 g IV bolus during 30-60 minutes every 4-8 hours.
o Apabila disertai kejang bisa diberikan juga benzodiazepine
(diazepam).

Carbamates
Intinya sama aja dengan organophosphate namun lebih short duration. Terapi
tidak membutuhkan golongan oxime.

Alcohol
Methanol

Yang bahaya itu formic acidnya karena super toxic retina

Manifestasi
 Altered mental status
 Optic neuropathy : Misty vision, yellow spots
 Putaminal necrosis : Parkinsonism
 GIT : Vomit and abdominal pain
  Metabolic acidosis ditandai dengan compensatory tachypnea
 Bahaya kalau sudah hypotension dan bradycardia

Diagnosis
 Osmolal gap >10mOsm/kg
 Electrolyte : Hypomagnesemia, hypokalemia and hypophosphatemia
 CT, MRI

Therapy
 Resuscitation and stabilization
o NGT suction
o Intubation
 Correction of metabolic acidosis : Bicarbonate 1-2 mEq/kg IV bolus.
Target serum pH 7.45-7.5
 ADH blockade apabila symptomatic, mencegah pemebentukan toxic
metabolite.
o Fomepizole : 15 mg/kg, followed by 10 mg/kg every 12 hours for
four dose.
o Ethanol
 Hemodialysis apabila
o Metabolic acidosis
o Renal insufficiency
o Electrolyte disturbance
o Visual disturbance
o Deterioration despite intensive care
 Pencegahan pembentukan CO2 dan H2O dengan leuvocorin 50 mg IV
every 4 hours.

Ethylene Glycol

Oxalic acid ini kalau bertemu dengan calcium akan membentuk Kristal Ca
Oxalate dan akan menumpuk di ginjal dan otak.
Manifestasi
 Stage I Acute neurologic : Muncul 30 menit-12 jam setelah konsumsi,
terdapat CNS depression, nystagmus, ataxia dan vomiting.
 Stage II Cardiopulmonary : Muncul 12 jam-48 jam, terdapat mild
hypertension, tachycardia, ARDS, hypocalcemia dan circulatory collapse.
 Stage III Renal stage : Muncul 24 jam-72 jam, terdapat flank pain,
hematuria, proteinuria.
 Stage IV Delayed neurologic : Muncul 6-12 hari, terdapat cranial
neuropathy.
Diagnosis
 Electrolyte  Glycol level
 Cr BUN  ECG
 ABG  Urinalysis
 Serum osmolarity  Brain imaging
 Serum glucose  CBC :
 Blood ethanol Leukocytosis

Therapy
 Resuscitation and stabilization
o Pyridoxine 50 mg every 6 hours and thiamine 100 mg every 6
hours.
o NGT suction
o Intubation
 Correction of metabolic acidosis : Bicarbonate 1-2 mEq/kg IV bolus.
Target serum pH 7.45-7.5
 ADH blockade apabila symptomatic, mencegah pemebentukan toxic
metabolite.
o Fomepizole : 15 mg/kg, followed by 10 mg/kg every 12 hours for
four dose.
 Hemodialysis apabila
o Metabolic acidosis
o Renal insufficiency
o Electrolyte disturbance
o Visual disturbance
o Deterioration despite intensive care
 Pencegahan pembentukan CO2 dan H2O dengan leuvocorin 50 mg IV
every 4 hours.
 Kalau hypocalcemia boleh kasi calcium IV
Ethanol

Manifestasi
 CNS depression

 Metabolic : Ketoacidosis hypoglycemia, hyperlactaemia

 Cardiovascular : Myocardial depression at high doses, systemic vasodilate
 Renal : Diuresis
 GI : Gastritis, hepatitis, acute pancreatitis
 Respi : aspiration
 MSK rhabdomyolysis
 Trauma
Diagnosis
 ECG
 Blood sugar
 Ketones
 Ethanol level
 High osmolar gap
 LFT, Lipase (kalau curiga pancreatitis)
 Paracetamol level karena sama-sama liver toxic
 Electrolyte
 CT kepala
Terapi
 Resusitasi
o Airway patency, suction
o Intubation
o Ventilatory support if respiratory depression or aspiration
o IV NS
o Treat hypoglycemia
o Coexistent life-threats (hemorrhage, trauma)
 Supportive
o Thiamine 300 mg IV
o Adequate hydration
o Replace electrolyte and vitamins

Isopropyl Alcohol

Manifestasi
 Potent CNS depression
 Cardiovascular : Vasodilates and myocardial depression
 GI tracts : Nausea and vomiting
 Dermal burns, corneal deepithelization
 Pulmonary congestion
Diagnosis
 BUN, Cr
 Electrolyte
 Serum osmolarities
 Ketones
 ABG
Therapy
 Intubation
 Gastric lavage
 Kalau hipotensi bisa diberikan cairan, kalau tidak membaik bisa
mempertimbangkan dialysis
Obat untuk Alcohol dependance
 Disulfiram : initial dose 500 mg/ day 14 days. Maintenance 125-250 mg/
day.

Opioid
Reseptornya terdistribusi di CNS, respiratory, nociceptive, euphoria, GI,
cardiovascular, immunologic. Receptornya ada 3 mu, kappa, delta.

Manifestasi
Intoksikasi
 CNS : CNS depression, seizure, hypertonic, myoclonic, parkinsonism,
spongiform, leukoencephalopathy, serotonin syndrome
 Respiratory : Low RR and tidal volume due to depression of medulla
oblongata
 Ophthalmo : Edinger westphal overstimulation  Miosis
 Otologic : SNHL
 Cardiovascular : Mild hypotension and relative bradicardia, arrhytmia
 GI : Nausea, vomiting, constipation, colic pain
 Urologic : Urinary retention, glomerulosclerosis
 Dermato : Pruritus, flushing, urticaria
 Metabolic : Hypoglycemia, hypothermia
Withdrawal
 CNS excitation
 Tachypnea
 Mydiasis
 Increased pulse and BP
 Nausea, vomiting and diarrhea

Diagnosis
 Blood glucose level : hypoglycemia
 CO2 and O2 saturation
 Chest radiography
  ECG
 Urine test
 HBsAg, anti HCV, HIV

Therapy
 GI decontamination
 Supportive
o Airway and breathing : Positive airway, PEEP
o Circulatory : Crystalloid infusion
 Naloxone 0.4-2 mg IV apabila CNS depression
 Nalmefene sebagai alternative naloxone
 Withdrawal :
o Methadone 20 mg oral, 10 mg IM in 30-60 minutes
o Clonidine 0,1 mg oral, repeated every 30-60 mins
o Buspirone apabila serotonin syndrome

Wernicke-Korsakoff Syndrome
Karena B1 deficiency biasa terjadi karena alcohol use disorder, sehingga tidak
bisa menyerap makanan dengan baik. Selain karena alcoholic, dapat juga
disebabkan oleh bariatric surgery.
Diagnosis
PF
o Abnormal eye movement
o Decreased or abnormal reflexes
o Fast pulse
o Low BP
o Low body temp
o Muscle weakness and atrophy
o Gait and coordination problems

Lab
o Serum albumin
o Serum B1
o Treansketolase activity in RBC
Therapy
 Thiamine replacement therapy IV
 Alcohol abstinence
 Psychotherapy
 Intoxication
Opidoid Alcohol Organophosphate
CNS CNS depression Headache, Seizure
hallucination,
memory loss,
cerebellar
dysfunction,
slurred speech,
seizure
Eye Miosis Blurred vision Miosis, lacrimation
Respiratory Depression Respiratory Bronchorrhea and
depression bronchospasm
Cardiovascular Hypotension and Myocardial Bradycaria
bradycardia depression,
hypertension and
tachycardia
GI Nausea and Nausea and Diarrhea,
vomiting, vomiting abdominal cramps,
constipation emesis, salivasi
Urology Urinary retention Diuresis, kidney Urinary
stones incontinencea
Skin Pruritus, flushing, Diaphoresis Diaphoresis
urticaria
Others SNHL Ketoacidosis, Salivation
hypoglycemia,
rhabdomyolysis
Antidote Naloxone Fomepizole, Atropine and
hemodialysis pralidoxime
WITHDRAWAL
Opioid Alcohol
CNS CNS excitation Anxiety, insomnia,
hallucination,
seizure
Eyes Mydriasis
Respiratory Tachypneic Respiratory
acidosis 
Alkalosis
Cardiovascular Tachycardia and Tachycardia and
hypertensive hypertension
GI Dirrhaea Nausea, vomit,
abdominal pain
Skin Hot flushes, goose Diaphoresis
bumps
Antidote Naloxone Disulfiram
Burn

Patophysiology
Burn
 Burn injury  Inflammatory response  Oedema and occlusion of
dermal microcirculation and formation of thrombi  Reduced perfusion
and tissue ischemia  Cellular apoptosis  Further inflammation
 Increased permeability  Hypovolemic shock
 Derajat kedalaman luka bakar juga mempengaruhi terjadinya infeksi dan
metabolic derangement.

Pada luka bakar terdapat 3 zona

 Coagulative : Center of the burn, irreversible necrosis dan paling cepat
terbentuk.
 Ischemic : Zona yang mengelilingi zona koagulatif, terdapat reduksi pada
mikrosirkulasi dermis sehingga beresiko nekrosis apabila tidak segera
direperfusi.
 Hyperemia : Immediate and transient increase in perfusion.

Regenerasi kulit dapat terjadi melalui 2 mekanisme

 Basal layer of cells from uninjured adjacent epidermis can give rise to
reepithelization of the burn; however this is limited to 1 cm from the
wound edges.
 Scar formation mediated by dermal cell appendages (hair follicles and
sebaceous gland).

Inhalation
Direct thermal injury is generally not seen below vocal cords, but products of
incomplete combustion (CO, cyanide, aldehyde and oxides of sulfur and
nitrogen) result in significant V/Q mismatch and pulmonary edema.

 Inhalation injury  Airway edema and deepithelization of

tracheobronchial mucosa  Progressive shedding of necrotic lining of
airway and the formation of pseudomembranous casts  Airway
obstruction
 Damage to mucociliary function of the endobronchial mucosa reduces the
ability to eliminate excess mucus and secretions  Pulmonary
parenchyma becomes infiltrated with leukocyte  Release inflammatory
mediators  Bronchospasm and tissue inflammation
 Inhalation results in deactivation of pulmonary surfactant 
Microatelectasis  V/Q mismatch, pulmonary shunting and progressive
hypoxemia  ARDS

Etiology
 Thermal burn
 Electrical
 Chemical
 Radiation
  Friction
 Cold injury

Assesment
History Taking
 Associated injury (fracture, CNS, pulmonary, myocardial, abdominal
injury)
 Anoxic brain injury, loss of consciousness
 Preexisting illnesses
 Drug therapy and allergies
 Tetanus immunization
Body Surface Area
Ada juga metode palmar surface, 1 tangan pasien berarti 1%.

Depth of Burn
 First degree burns (e.g., sunburn) are characterized by erythema, pain.
Not life threatening and generally do not require IV replacement because
the epidermis remains intact.
 Second degree partial thickness burns are characterized by a red or
mottled appearance with associated swelling and blister formation. The
surface can have a weeping, wet, appearance and is painfully
hypersensitive, even to air current,

 Third degree full thickness burns usually appear dark and leathery. Skin
also may appear translucent or waxy white. The surface is painless and
generally dry, it may be red but does not blanch with pressure. There is
little swelling of the full thickness burned tissue.
Management
Pre Hospital
 Adequacy of airway and ventilation is the priority.
o Patient with compromised airway  Orotracheal intubation.
o Suspected inhalation injury or CO or cyanide intoxication  100%
O2 NRM
Burn may cause massive edema of upper airway, therefore early
evaluation of the need for endotracheal intubation is essential. Inhalation
injury may cause more localized edema and pose a greater risk for airway
compromise.

 Stop the burning and protect the patient from additional injury
 Extinguish the flames with water or smother the flames with a blanket
and gently remove the involved clothing. Cover patients with warm, clean
and dry linens to prevent hypothermia.
 The involved body surface area should be rinsed with copious amounts of
water.
  Dry chemical powder should be brushed from the wound before rinsed
with tap water.
 Prehospital IV RL (crystalloid) is beneficial if extensive burn (>20%).
Large calibers 16 gauge, upper extremities are preferable to the lower
extremities as a site for venous access because the increased rosk of
phlebitis and septic phlebitis when saphenous veins are used for venous
access.

Hospital
Primary survey
Airway and Breathing Management
Airway
 If there is doubt regarding upper airway compromise, fibreoptic
laryngoscopy should be performed.
 Circumferential neck burns, the stiff burn eschar may compress the
airway and require escharotomies.
 Nasogastric tube to prevent gastric distention.
Breathing
 Hypoxia may be related to inhalation injury, inadequate ventilation due to
circumferential chest burns or traumatic thoracic injury.
 CO poisoning
o Headache and nausea
o Confusion
o Coma
o Death
o Cherry red skin color
Require high flow oxygen via NRM prior to intubation
All patients with moderate to severe burns or suspected inhalation injury
should receive supplemental oxygen  Maintain oxygen saturation >92%
 Endotracheal intubation guided by fibreoptic laryngoscopy or
bronchoscopy is a useful technique, and if attempts at intubation are
unsuccessful, surgical cricothyrotomy or needle cricothyrotomy may be
necessary.
 Elevation of the head and chest by 30 degrees to reduce neck and chest
wall edema.
 Obtain ABG, pulse oximeter monitoring and chest Xray
Circulation
 Measure blood pressure, hourly urinary output (urinary catheter should
be inserted). Melalui urinalysis juga bisa memantau rhabdomyolysis
 Intravenous access should be obtained in peripheral uninjured limb, if
peripheral access cannot be obtained, central venous access will be
required.
  Amount of fluid provided should be adjusted based on the urine output
target of 0.5 mL/ kg/hr, electrolyte. Adjust cairan dengan mengatur IV
rate.
 Cardiac monitorin via ECG karena bisa terjadi aritmia.

Secondary Survey
Physical Examination
 Extent and depth of the burn
 Associated injuries
  Weigh the patient

Baseline Determinations For Patients With Major Burns

 CBC
 Type and crossmatch/ screen
 ABG with HbCO
 Serum glucose
 Electrolyte
 Pregnancy test
 Chest xray repeated films as necessary
 Other xrays may be indicated for appraisal of associated injuries

Peripheral Circulation In Circumferential Extremity Burns

 Rule out compartment syndrome. Ditandai dengan increased pain with
passive motion, tightness, numbness and decreased distal pulse.
Management
o Remove all jewelry on the patients extremities
o Asses distal circulation, cyanosis, CRT, paresthesia, deep tissue
pain
o Inserting needle connected to pressure tubing into compartment
o Fasciotomy may be necessary to restore circulation for patients
with associated skeletal trauma, crush injury, high-voltage
electrical injury, burns involving tissue beneath the investing
fascia.
 Apabila compartment pressure >30 mmHg  Muscle necrosis. Require
escharotomy within the first 6 hours
 Chest and abdominal compartment syndrome may require escharotomies

Gastric Tube insertion

Untuk suction pada pasien yang nausea, vomiting, abdominal distention or if
burns involve more than 20%. Preventing possible aspiration.

Pain Management
Terdapat 3 jenis pain
 Background pain : underlying pain that results directly from the injury,
continuous sensation of burning or throbbing when patient is immobile.
  Breakthrough : Experience sudden increase in the pain intensity, as the
analgesic level decreases with time.
 Procedural pain : When the burn wound is manipulated or debrided.
Narcotics, analgesic and sedative should be administered in small, frequent dose
by IV only. (kata ATLS)

Minor pain
 Oral acetaminophen 1g in adults every 4-6 hours
 Ibuprofen 400-800 mg

Moderate-severe
 Opioid IV 0.05-0.1 mg
 Frntanyl 0.5 – 1.0 μg/kg untuk breakthrough and procedural pain
 Benzodiazepin tapi bisa bikin hypoventilation and hypotension.
Lorazeoan 1 mg IV or oral, midazolam 1 mg IV or intranassaly.

Wound Care
 Covering the burn with clean sheets will relieve pain and deflects air
current.
 Do not break blisters or apply antiseptic agent.

Graft
 Split thickness : Epidermis hingga dermis, untuk luka >5 cm
 Full thickness : Lebih tebal
Ambilnya dari paha anterolateral dan bokong

Gagal apabila
 Graft kotor
 Regio sendi
 Teknik salah

Graft tidak dapat dilakukan pada daerah avascular seperti tendon, tulang.

Antibiotics
Pemberian antibiotic tidak diperlukan pada fase akut, karena meningkatkan
resiko infeksi jamur.

Tetanus Immunization

Electrical Burn
Occurs when a source of electrical power makes contact with patient body. Bisa
relatively normal overlying skin to coexist with muscle necrosis. Current travels
inside the blood vessels and nerves  Local thrombosis and nerve injury

Management
 Hentikan sumber listrik
 ABCDE, establishment of IV line
 ECG monitoring and placement of indwelling bladder catheter
 Examine associated musculoskeletal damage, spinal injuries,
rhabdomyolysis. Kalau rhabdomyolysis UO harus 100 mL/hr.

Chemical Burn
Exposure to acids, alkalies, petroleum. Yang paling bahaya alkali karena bersifat
prenetratif. Cuci bagian yang kena dengan air mengalir 20-30 menit dengan
shower, Alkali lebih lama dan sembuhnya lamam jadi dibersihkan lebih lama.
Kalau menggunakan neutralizer malah semakin mebuat daerah itu panas,

Cold Injury
Frostnip
Paling ringan. Gejala pain, pallor, numbness of the affecred body part. Reversible
with rewarming, Kalau berulang baru menyebabkan fat pad loss or atrophy.

Frostbite
 Freezing of tissue with intracellular ice crystak formation, microvascular
occlusion, subsequent tissue anoxia,
 First degree : Hyperemia and edema
 Second degree : Large clear vesicle, hyperemia and edema with partial
thickness skin necrosis.
 Third degree : Ful thickness and subcutaneous tissue necrosis,
 Fourth degree : Skin necrosis and muscle and bone with grangrene,
Manajemen
 Preserve damaged tissue
 Prevent infection
 Avoid opening of blister
 Affected tissue should be protected
 Tetanus prophylaxis
 Keep the wound clean for 7-10 days
 Weight bearing is prohibited until edema is resolved
 Thrombolytic agents and LMW dextran shown some promise.

Non freezing injury

Karena microvascular, endothelial damage, stasis, vascular occlusion. Contoh
trench foot pada marinir.
Manajement
 Rewarming : Mandikan pasien dengan air 400C (20-30 menit), biasa
diperlukan analgesic bahkan narcotics.
 Cardiac monitoring,

Hypothermia
Apabila suhu dibawah 36, namun dikatakan severe apabila dibawah 32.
Membutuhkan IV fluid dan blood products untuk warm environment.
Hypothermia dapat menyebabkan koagulopati dan asidosis.

Kriteria Rujukan