Manag bencana & P3K.ppt

7/25/2019 Manag bencana & P3K.ppt

1/60

& P3K

pada kecelakaankegawatdaruratan

sehari2

dr. Moch Junaidy Heriyanto, p!,

"#$%


2/60

'arth(uakes

)ar

'*plosions

#ndustrial accidents such as those

occurring in mining

+oad trac accidents


3/60

--%/ %+'

Pencegahan -rauma

Pra0 +umah akit ewaktu di 1

ewaktu di kamar bedah

ewaktu perawatan


4/60

Pra0+umah akit

+esponse time

Pemilihan cairan resusitasi

electi4e hypotensi4e

resuscitation

Mencegah hipothermi


5/60

i +umah akit

-riase & response time

Penanganan segera koagulopati, hipotermia &

asidosis

-rans5usi komponen darah berdasar indikasi

amage control surgery

amage control resuscitation 6Hematologic

resuscitation7

non0operati4e management cedera organ solid

6$M7

perawatan #1


6/60

M'$%P% -+%1M%P'$-#$ %$ H%+1

#-%$%$# '!%#KM1$K#$


7/60

-+%1M%08

Penyebab kematian nomor satu di % untuk

golongan usia 8099 tahun

elama periode 8::: s;d 2


8/60

-+%1M%02

Pada trauma, penyebab kematian segera

6early death7 adalah syok hipo4olemik atau

cedera otak berat

Pada trauma berat, timbul iskemiadi seluruh

tubuh, dan kemudian setelah resusitasi

dapat ter@adi cedera reper5usi, berupa reaksi

inAamasi berlebihan diluar kendali badan


9/60

K'M%-#%$ '-'/%H

#+%)%- 1mumnya disebabkan in5eksinosokomial, sepsis dan M;M"

Penyebab kematian lain adalah cedera

otak sekunder karena hipoksia serebri

6hipotensi berlarut, sepsis intra

abdominal7


10/60

-+#%"

'%-H

Moore EE Am J Surg,1996, 172;405


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15/60

#dentiBkasi

+iwayat Per@alanan Penyakit

Presentasi Klinis

+iwayat penyakit dahulu

Pola presentasi penyakitAnamnesis

Survei Primer

Survei Sekunder +Pencitraan


16/60

ur4ei Primer

% C %irway

! C !reathing

C irculation

C isability

Cepat Mengancam Jiwa


17/60

ur4ei ekunder

etelah ur4ei Primer selesai

Ka@ian cepat D -ingkat kesadaran,

5ungsi sara5 kranial, 5ungsi motorik,

5ungsi sensorik, reAeks.

defisit neurologis fokal ???


18/60

Pengambilan Keputusan

urgery atau Konser4ati5 E

ito atau 'lekti5 E

ur4ei Primer F ekunder F Pencitraan


19/60

Call For Help

AKTIFKAN SISTEM EMS

(Emergency Medical Service)

Atau bantuan tenaga medi lain


20/60

6 %cute are F -raumatology F #ntensi4e are7-hree peaks o5 trauma related deaths

4week

s

4week

s

2weeks

2weeks

1 hour 3 hours1 hour 3 hours

First peak

Laceration of brain

brainstem

aorta

spinal cord

heartSecond peak

Extradural

Subdural

Hemopneumothorax

Pelvic fractures

Long bone fractures

Abdominal injuries

Third peak

Sepsis

Multi organ failure

Secondar !rain "njur

#EATHS


21/60

/aki laki, 2? thn, datang ke #+ keluhan

nyeri perut akibat terkena benturan

sepeda motor.

9 @am M+ saat penderita mengendarai

motor mengalami tabrakan dengan

pengendara motor lain, roda depanmotor penabrak membentur perut

penderita.


22/60


23/60

ur4ey Primer D% D baik

! D ++ D 29*;menit

D $ D 82< *;mnt - D G


24/60

Initialmanagement ??


25/60


26/60

pada pasien ini dilakukan D

#n5us +/ 3


27/60

ur4ey sekunder D

+egio abdomen D

# D tampak @e@as berupa hematom di

epigastrium

PD $- 6F7, $/ 607, M607

P D -ympani

% D !1 6F7

+- D -% baik, mukosa licin, $yeri 607

sarung tanganI 5eses 6F7, darah 607


28/60


29/60


30/60

General Principles of vascular

trauma/injury Always start with ABC

Large IV pore lines

External compression to control

bleeding

Look for hard signs of arterial

injuries


31/60

+e4iew 5 irculation

ells need supply o5 nutrients and remo4al

o5 by products

#n a unicellular organism this may occur 4ia

the cell membrane into say a pond or sea

Multicellular organisms need a circulatory

system


32/60

Prolonged & se4ere skeletal muscle ischemia

releaseD

Myoglobin 6nephroto*ic7

Potassium 6arrhythmia7

Acute interruption of extremity lood flow can

lead to organ failure and deat!if not recogni"ed and treated aggressively


33/60

'/% D increase the risk o5 irre4ersible

ischemic in@ury, organ 5ailure, and death

EARL RE!"#$I%I"$ A$& %REA%ME$%

%/D reper5usion o5 the ischemic

limb within > hour or less


34/60

'ects 5 %cute

#schemia +educed blood Aow

# Pulseless, pallor, perishing cold

$er4e ischemia# Pain, paralysis, Paresthesia

Muscle ischemia

# +habdomyolysis

ompartment syndrome

#schemia reper5usion syndrome


35/60

Hard sign

Pulsatile bleeding

'*panding hematoma

Palpable thrill

%udible bruit '4idence o5 regional ischemiaD

Pallor

Paresthesia

Paralysis

Pain

Pulselessness Poikilothermia


36/60

Is this Arterial or Venous injury ?

Arterial

- Pulse examination

- Hard signs

Pulsetile ext !leeding

A!sent distal pulses

"xpanding hematoma

#istal ischemia

$hrill or !ruit


37/60

Is this Arterial or Venous injury ?

Venous

- %o& pressure dar' !lood external !leeding

- (on-expanding hematoma

- )hoc' is rare unless associated &ith arterial injury


38/60

Lascular trauma

$the clock starts ticking%

!lood loss

Progressi4e ischemia

ompartment syndrome

-issue necrosis

Irreversible damage after 6 hours

%rterial in@uries associated


39/60

%rterial in@uries associatedwith 5ractures or dislocations

*lavicle fracture su!clavian artery

)houlder fx/dislocation axillary artery

)upracondylar humerus fx !rachial artery

"l!o& dislocation !rachial artery

Pelvic fracture gluteal arteries

+emoral shaft fx femoral artery

#istal femur fracture popliteal artery

,nee dislocation popliteal artery

$i!ial shaft fx ti!ial arteries

Ph i l


40/60

Physical e*am

Ma@or hemorrhage;hypotension

%rterial bleeding

'*panding hematoma

%ltered distal pulses

Pallor

-emperature dierential between e*tremities

#n@ury to anatomically0related ner4e


41/60

%symmetric pulses warrant doppler

e*amination 6determine %!#7

%bsent pulses warrant emergent

4ascular consultation;surgical

e*ploration

# t l


42/60

#amage control

%rteries that can be ligated with 5ew

conse(uencesD

0 -he common and e*ternal carotid,

subcla4ian, a*illary , internal iliac arteries &

eliac a*is.

0 #% ligation D 8


43/60

#amage control

%lmost all 4eins including the #L canbe ligated when necessary


44/60

hock D

# % state o5 inade(uate tissue per5usion in

which the deli4ery o5 o*ygen to tissues

and cells is insucient to maintain

normal aerobic metabolism.

an imbalance between substrate

deli4ery 6supply7 and substrate

re(uirements 6demand7 at the cellular

le4el.


45/60

lassiBcation o5 shockbased on etiology D

Hypo4olemic

ardiogenic

$eurogenic

#nAammatory 6eptic7

bstructi4e

-raumatic

$ombination$ombination

is possibleis possible


46/60

-he rgans +esponses!lood loss

Micro4ascular ystem #mmune

& inAammatory organresponse

responses

cellular $euro0endocrine

metabolic ardio4ascular

response Pulmonary

+enal


47/60

Licious ycle o5

Hemorrhagic hock

&ndot!elial Activation

Microcirculatory damageCellular aggregation


48/60

%ssessment o5 the class

o5 shock 6%-/0 a < kgpatient7

lass

# ## ### #L

!lood loss 6ml7 up to ?< ?


49/60

Principles o5 Medical

are %ims D to control the source o5 bleeding assoon as possible and to replace Auid loss

Pre hospital care D# '4acuation time = 8 hour 6usually urban trauma7,

immediate e4acuation to a surgical 5acility 6a5ter airway

and breathing 6%, !7 ha4e been secured 6scoop and run7.

# '4acuation time O 8 hour, an intra4enous line is introduced

and Auid treatment is started be5ore e4acuation.


50/60

"luid replacement

strategy #n controlled hemorrhagic shock 6H7, where the source o5bleeding has been occluded, Auid replacement is aimed

toward normaliQation o5 hemodynamic parameters.

#n uncontrolled hemorrhagic shock 61H7, in which the

bleeding has temporarily stopped because o5 hypotension,

4asoconstriction, and clot 5ormation, Auid treatment is aimed

at restoration o5 radial pulse or restoration o5 sensorium or

obtaining a blood pressure o5 G< mm Hg by ali(uots o5 2?

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Manag bencana & P3K.ppt