blok emergency uisu 2014-2.ppt

8/12/2019 BLOK EMERGENCY UISU 2014-2.ppt

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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



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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.


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