blok emergency uisu 2014-2.ppt
TRANSCRIPT
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BLOK EMERGENCY2 :NEUROGENIC SHOCK
TRAUMATIC BRAIN INJURYSTATUS EPILEPTIKUS
BAGIAN NEUROLOGIFK-UISU 2014
BOK EMERGENCY UISU 2014
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Neurogenic Shock : Defenisi
Interruption padapenghubung CNSdengan bagian perifer(spinal cord injury).
Bentuk dari shockdistributiv
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Neurogenic Shock : Penyebab
Spinal cord injury
Spinal anesthesia
Kerusakan sistem saraf Trauma, obat-obatan,
anestesi dan beberapa
stress berat
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Neurogenic Shock :
Gejala Klinis
Tekanan Darah rendah
Bradycardia
Oliguria, dyspnea, etc.
Gejala khas dari shok neurogenik adalahtekanan darah yang sangat rendah
Bradikardi adalah gejala yang serinmgterlihat di bagian awal
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Pengiriman oksigen yang inadekuat akanmengganggu metabolisme
Hasilnya adalah hipoperfusi jaringan danasidosis metabolik
Shock bisa terjadi dengan tekanan darahnormal dan hipotensi bisa terjadi tanpashock
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Diagnosis
Pemeriksaan fisik (Vital Sign, mentalstatus, warna kulit, temperature, pulses,etc)
Sumber Infeksi Labs:
CBC Chemistries
Lactate Coagulation studies CulturesABG
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Assessment, Diagnosis and Management of
Neurogenic Shock
PATIENT ASSESSMENT
Hypotension
Bradycardia
Hypothermia Warm, dry skin
RAP(right atrial pressure) PAWP (pulmonary capillary wedge
pressure ) CO
Flaccid paralysis below level of
the spinal lesion
MEDICAL MANAGEMENT
Tujuan dari terapiadalah untukmengobati ataumenghilangkanpenyebab dan menceghainstabilita kardivaskulardan mengoptimalkanperfusi jaringan
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Immediate Management
Pertahankan suhu tubuh dalam batas normal
Pada banyak kasus, elevasi kaki dan tungkai
lebih tinggi dari jantung Exceptions include:
Cedera leher imobilisasi posisi
Cedera kepala elevasi kepala dan bahu
Leg fracture splint and elevate
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Secondary Management
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Secondary Management
Vital Signs
Pulse
Respiration Blood pressure
Temperature
Skin color
Pupils
Level of consciousness Movement
Abnormal nerveresponse
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MANAGEMENT OF NEUROGENIC SHOCK
Hypovolemia- tx with careful fluid replacement for
BP
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MANAGEMENT OF NEUROGENIC SHOCK
Observasi Bradycardia-major dysrhythmia
Observasi untuk DVT- venous pooling inextremities make patients high-risk>> of PE
Use prevention modalities [TEDS, ROM,Sequential stockings, anticoagulation]
Fluid Volume Deficit r/t relative loss
Decreased CO r/t sympathetic blockade Anxiety r/t biologic, psychologic or social
integrity
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Management of Neurogenic Shock
Alpha agonist to augment tone jika perfusi
masih inadekuat
dopamine at alpha doses (> 10 mcg/kg
per min) ephedrine (12.5-25 mg IV every 3-4
hour)
Obati bradycardia dengan atropine 0.5-1
mg doses to maximum 3 mg
Bisa transcutane atau transvenous
pacing temporarily
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A,B,Cs Remember c-spine precautions
Resusitasi cairan Pertahankan MAP pada 85-90 mm Hg untuk 7 hari
pertama Thought to minimize secondary cord injury If crystalloid is insufficient use vasopressors
Cari penyebab hipotensi Untuk bradycardia
Atropine Pacemaker
Neurogenic Shock : Pengobatan
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Methylprednisolone
Gunakan hanya untuk cedera spinal cord
Terapi dosis tinggi untuk 23 jam
Harus dimulai antara 8 jam
Controversi resiko infeksi, perdarahan
saluran cerna
Neurogenic Shock : Pengobatan
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TRAUMATIC BRAIN INJURY
(TBI)
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Traumatic Brain Injury (TBI) cedera otak yangdisebabkan oleh benturan fisik dari luar
Acquired Brain Injury (ABI) adalah cedera pada
otak yang terjadi setelah lahir (termasuk: TBI,stroke, near suffocation, infeksi pada otak, etc.)
Definition
Slide 2
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Tipe dari cedera otak
Closed brain injury
Open brain injury
Cedera otak bisa terjadi bahkan jika pasien
tidak kehilangan kesadaran
Brain injury is unpredictable in its consequences
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Closed Head Injury
Bisa karena jatuh, kecelakaan motor, dll
Kerusakan fokal dan kerusakan difus pada
axon
Tidak ada penetrasi ke tulamng tengkorak
Effects tend to be broad (diffuse)
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Open Head Injury
Results from bullet wounds, etc.
Kerusakan fokal lebih luas
Penetrasi ke tulang tengkorak
Efek yang lebih serius
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TBI: A biologicalevent within the brain
Kerusakan jaringan
Perdarahan
bengkak
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Cedera ringan0-20 menit hilang kesadaran GCS = 13-15
PTA < 24 hours
Cedera sedang
20 minutes to 6 hours LOC GCS = 9-12
Cedera berat
> 6 hours LOC GCS = 3-8
CLASSIFICATION
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75% dari cedera otak adalah ringan.
A mild brain injury --> sadar
Brief (less than 15 minutes) or NO loss ofconsciousness
A dazed, vacant stareright after the injury
A normal neurological exam
Deficits may be invisible
Cedera Otak Ringan
Optional Slide 20
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penurunan respon terhadap pertanyaan danperintah
Disorientasi ingatan
Sakit kepala, nausea dan pusing
Gangguan tidur
Biasanya tidak ada komplikasi
Slurred speech
Cedera Otak Ringan
Optional Slide 21
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gejala tidak segera terlihat
Post concussive syndrome:
sakit kepala sementara,pusing,gangguan mental
dan fatique
Gejala dari cedera otak ringan biasanya sembuh
selama 1-3 bulans
There are some individuals who will experience an
extended and sometimes incomplete recovery
Cedera Otak Ringan
Optional Slide 24
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Cedera Otak Sedang
Defenisi :Trauma kepala berhubungan dengan
Glasgow Coma Score of 9-12
Cedera otak sedang adalah salah satu hasil dari
hilangnya kesadaran bisa beberapa menit atau sampaibeberapa jam yang diikuti oleh variasi level dari
kesadaran
Optional Slide 27
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Cedera Otak Berat
Defenisi : traum akepala berhubungan denganGlasgow Coma Score of 8
Severe brain injury is life threatening and frequentlyresults in prolonged unconsciousness or coma lasting
days, weeks or even longer
Optional Slide 28
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TBI - Patofisiologi
TBI merupakan suatu peroses,bukan kejadian !
Cedera sekunder bisa lebih merusak daripada
cedera primerMechanisms of Brain Injury :
1. Brain Contusion
2. Increased intracranial pressure3. Diffuse Axonal Injury
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1. Brain Contusion
A brain contusiondidefenisikan sebagaikematian sel yang diikuti olehperdarahan(leakage of blood)
The soft brain tissue isvulnerable to contusion inhead trauma
The contusion often occurs ata site distant from the pointof impact
Gross brain image from http://neuropathology.neoucom.edu/chapter4/chapter4bContusions_dai_sbs.html#contusion
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2. Increased ICP
Intracranial Contents:
80% jaringan otak 10% darah
10% cerebrospinal fluid
Peningkatan pada volume di bagian intrakranial
ini dapat menyebabkan peningkatan intrakranial
Penyebab :
1. Otak bisa membengkak(edema)
2. Kelebihan darah yang bisa berakumulasi menjadi
hemorrhage
3. CSF can accumulate due to blockage of outflow
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Key Concept #2 : There is only one way out of the
intracranial vault --> the opening at the base ofthe skull known as theforamen magnum
3D CT Angiogram from
www.auntminnie.com/.../
65000/66000/66173.asp
Skull base image from www.octc.kctcs.edu
2. Increased ICP
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Key Concept #3:
When the brain issqueezed through the
foramen magnum(herniation), thebrainstem iscompressed, the patientstops breathing, and the
patient dies
Herniation schematic from Robbins and Cotran. Pathologic Basis of Disease. 7th ed. Philadelphia: Elselvier; 2005.
2. Increased ICP
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Causes of ICP: Epidural Hematomas
Figure 7-15 Examples (A, B-arrows) of epidural hematomas in CT scans on the patient's right side. The
smaller lesion in A is obviously of traumatic origin; this patient has soft tissue damage, a fractured skull,
blood in the substance of the brain, and blood in the anterior horn of the lateral ventricle and in the third
ventricle. The cause of the larger lesion (B) is not obvious.
Slides from Haines:Fundamental Neuroscience for Basic and Clinical Applications 3e -www.studentconsult.com
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Slide from Haines:Fundamental Neuroscience for Basic and Clinical Applications 3e -www.studentconsult.com
Figure 7-16 An example of a subdural hematoma (arrows) in CT scan on the patient's left side. This lesion
is long and thin and extends for considerable distance over the surface of the hemisphere: note the shift
in the midline.
Causes of ICP: Subdural Hematomas
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Causes of ICP: Swelling
Head CT from rad.usuhs.mil/rad/ home/peds/ihsdarrow.jpg
Observe swelling (darker tissue) on brain CT scan of a 7-month-old victim of
child abuse. What other injuries are present?
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3. Cedera Axon Difus
Terjadi lebih dari dari trauma cedera otak
Bentuk difus dari cedera, artinya kerusakan terjadipada area yang lebih luas daripada cedera otak
fokal
Involves the shearing of axons in the white
matter tracts
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Basic Principles of Clinical Management
Monitor ICP (invasively) and intervene to lowerICP when necessary
Elevate head of bed
Medications to decrease swelling
Decrease brain activity to reduce blooddelivery and swelling --> medically inducedcoma
Hypothermia
Surgical Decompression when risk forherniation is high
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Seizure prophylaxis
Seizures occur in up to 20% of severe TBIpatients, with ~50% occurring within first 24hours1
Other priorities
Adequate nutrition, correction of electrolyteabnormalities, strict control of blood sugar,
strict temperature regulation
Basic Principles of Clinical Management
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Definition
Single seizure > 30 minutes
Series of seizures > 30 minutes withoutfull recovery
Status Epilepticus
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Status epilepticus
Prolonged seizures
Duration of seizure
Life
threatening
systemicchanges
DeathTemporarysystemicchanges
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Manifestasi Klinis
Biasanya kejang tanpa adanya respon\
Seizure with subtle motor manifestationsin critically ill patients
Electrographic status epilepticus: noobservable, repetitive motor activity, andthe detection of ongoing seizuresrequires EEGstill at risk of CNS injury
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Etiology
Meningitis / encephalitis
Subdural hematoma / traumatic braininjury
Ischemic or hemorrhagic infraction
Cerebral anoxia / hypoxic damage
Metabolic disorder
Drug toxicity
Renal failure / uremic encephalopathy
Sepsis
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Etiology
Abrupt cessation of anticonvulsants
Brain tumor / space- occupyinglesion
Pre-existing epilepsy
Chronic alcoholism
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Pathophysiology - SE
numerous mechanisms - poorlyunderstood
failure of mechanisms that usu abort isolated
sz Kelebihan eksitasi atau inefektif inhibis
there are excitatory and inhibitory receptorsin the brain - activity is usually in balance
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PENANGANAN STATUS EPILEPTIKUS
PROSEDUR PENANGANAN :
1. Perbaiki jalan nafas dan sirkulasi.
2. Beri oksigen.
3. Monitor : EKG, pernafasan & suhu tubuh.
4. Anamnese dan pemeriksaan neurologis.
5. Periksa : elektrolit, BUN, glukosa, toksikologi,
kadar OAE dan gas darah.
6. Infus NaCl 0,9% dengan tetesan lambat.7. Berikan glukosa 40 % 50ml IV.
KMI 46
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8. Berikan tiamin 100 mg im/iv.9. Lakukan rekaman EEG bila ada.
10. Berikan diazepam 0,3mg/kgbb/iv (kecepatan
5mg/menit) max 20mg. Bila masih kejang diulangisetelah 5 menit.
11. Bila kejang teratasi beri fenitoin 18mg/kgbb
dengan kecepatan 50mg/menit.
12. Bila kejang belum teratasi beri fenitoin 15-
20mg/kgbb/iv, dengan kecepatan 150mg/menit.
KMI 47
PENANGANAN STATUS EPILEPTIKUS
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13. Bila setelah 20-30 menit kejang menetap :intubasi, kateter, EKG, suhu tubuh.
Beri fenobarbital dengan dosis rumat 20 mg/kgbb/ivdengan kecepatan 100 mg/menit.
14. Bila setelah 40-60 menit kejang masih menetap :beri pentobarbital dengan dosis awal 5 mg/kgbb/iv.
Ditambah terus sampai kejang berhenti. Dilanjutkan
dengan dosis 1 mg/kgbb/jam dengan infus lambat
setiap 4-6jam.15. Bila masih kejang > 60 menit anastesi dgn
Pentobarbital, intubasi dan ventilator.
PENANGANAN STATUS EPILEPTIKUS