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GAWAT PARU

Dr. Parluhutan Siagian, SpP

Departemen Ilmu Penyakit Paru


Fakultas Kedokteran Methodist Sumatera Utara
Medan
2009

1.

Asma berat (GINA) exacerbasi akut

2.

PPOK berat/sangat berat (GOLD) exacerbasi akut

3.

Pneumonia berat (PORT = PSI : Pneumonia Severity


Index) score

4.

Cystic Fibrosis (CF)

5.

Intertitial pulmonary disease

6.

Penyakit pembuluh darah/darah: trombo-emboli paru,


infarksi, emboli lemak

7.

Efusi pleura masif

8.

Pleurodynia

9.

Pneumotoraks tension

10.

Pneumomediastihum & subcutaneus emphysema

11. Atelektase lobar komplet


12. Aspirasi

Syndrome)

benda

asing

(Pulmonary

Aspiration

13. Tenggelam di air tawar, air laut, air kotor

14. Batuk darah massif


15. Sumbatan saluran napas akut
16. Keracunan gas iritan, oxygen, inhalasi akut, toksis

17. Cardiopulmonary arrest, cardiopulmonary ressusitasi


(CPR)
18. Sindroma wet lung

19. Edema paru : cardiogenic / non-cardiogenik = akut


lung injury (ALI) / Acut Respiratory Distress
Syndroma (ARDS)
20. Cidera toraks (Flail chest)

Massive Pleural Effusion

Klinis : Sesak nafas yang semakin lama bertambah berat


dengan atau tanpa demam, nyeri dada,peny mendasari
PD.

Foto toraks :

Inspeksi: Gerakan dada sisi yang sakit tertinggal


Palpasi: Stemfremitus lemah hilang di sisi yang sakit
Perkusi: Beda pada sisi yang sakit
Auskultasi: Suara pernafasan lemah hilang

Tampak perselubungan homogen di sisi yang sakit


Tampak trakhea, mediastinum/jantung terdorong ke sisi yang
sehat.

Penanganan :

Thoracentesis

Aspirasi cairan pleura dengan abocart no. 14


Pasang WSD (Water Seal Drainage)

Massive Atelectasis

Klinis : Sesak nafas, batuk, nyeri dada.


PD.

Foto toraks :

Inspeksi: Gerakan dada sisi yang sakit tertinggal


Palpasi: Stemfremitus lemah hilang di sisi yang sakit
Perkusi: Sonor memendek beda pada sisi yang sakit
Auskultasi: Suara pernafasan lemah hilang disisi yang sakit
Tampak perselubungan homogen di sisi yang sakit
Tampak trakhea, mediastinum/jantung tertarik ke sisi yang
sakit.
Tampak diafragma tertarik ke atas

Penanganan :

Bronkoskopi untuk diagnostik dan terapi.

Tension / Ventil Pneumothorax

Klinis : Sesak nafas yang tiba-tiba dan berat, terasa berat/sakit di dada,
sianosis, takikardia, hipotensi, keringat besar-besar.
PD.
Inspeksi: Gerakan dada yang sakit bisa tertinggal
Palpasi: Stemfremitus lemah hilang pada sisi yang sakit
Perkusi: Hiper sonor - tympani
Auskultasi: Suara pernafasan hilang pada sisi yang sakit
Foto toraks :
Tampak hyperlucent dan corakan paru tidak ada
Tampak pleural line
Tampak gambaran paru kolaps
Trakhea terdorong ke sisi yang sehat
Mediastinum/jantung terdorong ke sisi yang sehat
Penanganan :
Segera diberik oksigen yang adekuat
Tusukkan abocat 14 18 di daerah sela iga 2 mid clavicularis ,lalu
hubungkan dengan infus set yang diletakkan di dalam air
Bila pasien sudah tenang (sesak berkurang) segera pasang WSD
Pada keadaan pasien yang life threatening jangan tunggu X-ray,
bila sudah dapat dipastikan ventil pneumothorax secara klinis .

Haemoptisis
Definisi : Adalah batuk-batuk yang disertai dengan dahak
yang bercampur darah.
Klasifikasi haemoptisis (Busroh 1978):
Haemoptisis masif :

Bila perdarahan lebih dari 600 cc/24 jam

Bila perdarahan kurang dari 600 cc tetapi lebih dari 250 cc/24
jam, akan tetapi Hb kurang dari 10g%

Bila perdarahan < dari 600 cc/24 jam,>250 cc/24 jam,Hb


>10g% dalam 48 jam perdarahan tidak berhenti.

Etiologi
1.
2.
3.
4.
5.

Infeksi( TB paru, pneumonia, abses paru, jamur paru),trauma


Kardiovaskular(stenosis mitralis dan aneurisma aorta).
Neoplasma (karsinoma) terutama karsinoma bronchus
Obstruksi benda asing
Kelainan sistem pembekuan darah

Penanggulangan :

Posisi pasien Trendelenbert

Pemberian cairan intravena yang ditambahkan dengan hemostatika


dengan tetesan 20 25 /menit (cairan Dext 5% atau R. Solution)

Pemberian hemostatika perbolus 1 amp/4 6 jam

Evaluasi jumlah perdarahan dan cek Hb,Ht.

Bila Hb menurun hingga 7 g% perlu dilakukan tranfusi dengan :


1.
2.
3.

Pertimbangkan asal perdarahan, bila ada gangguan kardiovascular


harap lapor/konsul segera dengan dokter kardiolog
Pertimbangkan kondisi pasien apakah demam atau tidak
Pemberian PRC 250 cc,darah segar 500 1750 cc.

EKG pasien,menilai kelainan jantung


Hati-hati dengan pemberian salisilat karena dapat menambah
perdarahan
Awasi jangan terjadi asfiksia(tersering) atau hypovolemic shock
penyebab kematian

PENATALAKSANAAN SELANJUTNYA

Embolisasi arteri bronkialis dan pulmoner


Pembedahan,syarat :
- Diketahui jelas sumber perdarahan
- Tidak ada kontra indikasi medik
- Setelah dilakukan pembedahan sisa paru
masih mempunyai fungsi yg adekuat (faal
paru adekuat)
- Pasien bersedia dilakukan tindakan bedah

Pneumo Mediastinum dan Subcutaneous


Emphysema

Subcutenuous emphysema =

Adanya udara di sub cutis


Pembengkakan di sub cutis

Adanya udara di mediastinum chest x-ray

hammanss crunch

Sering bersamaan dengan pneumothorax


Terjadi akibat rupture alveoli atau beberapa alveoli
(bleb) ke peri bronchovascular intertitial dengan
membelah ruang belakang bronchi ke mediastinum.
Karena pleura mediastinal lebih lemah dari pleura yang
mengelilingi paru maka udara masuk ke mediastinum
sebelum ke rongga pleura

Pneumomediastinum dapat terjadi tanpa pneumotoraks,


terjadi subcutaneus emphysema melalui masuknya
udara dari wajah ke leher dan soft tissue
Dapat juga terjadi oleh karena robeknya esophagus,
iatrogenik (menchanikal ventilation, laparoscopi,
biopsy), post traumatic atau akibat asma, diving, gas
producing bacterial mediastinitis, valsalva maneuver.

Klinis ; Chest pain, pernafasan tidak enak bila bergerak


atau berubah posisi.
Diagnosis
1.
2.
3.

Terdengar mediastinal crunech Hamman sign pada saat


sistole
Chest x-ray terutama lateral
Subcutaneus emphysema diraba / ditekan daerah kulit yang
ada udara terdengar / terasa seperti gesekan rambut
(krepitasi)

Penatalaksanaan
1.

2.
3.

Tidak ada yang spesifik kecuali, pada


rupture esophageal
Penanganan pneumothorax (bila ada)
Pasien sebaiknya dirawat

PLEURODYNIA
1.
2.
3.
4.
5.

6.
7.

Sef limited viral illnes of skletal muscle


Severe pleuritic pain in ribs
Low grade fever, malaise
Penyebab grub B coxsackievirus dan
achovirus
Chest x-ray normal terkadang tampak
minimal pleural fluid atau minimal
pulmonary infiltrate
Leukosit / LED normal atau sedikit
meningkat
Terkadang menyertai pericarditis

NEAR DROWNING

DEFINITION
Near drowning adalah bila seseorang
dapat bertahan hidup setelah
mengalami tenggelam dalam waktu 24
jam setelah peristiwa itu. Hal ini
secara tidak langsung juga
menerangkan bahwa recovery telah
terjadi. Istilah yang juga dipakai
dibeberapa artikel adalah submersion
injury atau submersion incident.

JENIS CAIRAN TERASPIRASI

Air laut (asin)


Air tawar
Bahan kontaminasi seperti lumpur,
pasir, air limbah, lumut, ganggang,
bakteri .
Aspirasi dari isi lambung dan debris
yang mengandung air limbah, pasir,
lumpur, ganggang menyebabkan cidera
paru dengan pneumonitis kimia.

REAKSI SEGERA DARI ASPIRASI

Edema paru
Meningkatnya shunt
Toksisitas langsung dari cairan teraspirasi
Inaktivasi surfactan
Hanyutnya surfaktan
Cidera pada membran alveolar

PENATALAKSANAAN

Airway Maneuvers
Hipoksia, ventilasi,bantuan nafas mouth-to-mouth
Resusitasi Kardiopulmoner (A,B,C)
Oksigen 100%, intubasi, suction, posisi miring ke
lateral.

Penatalaksanaan Pasca Resusitasi


high flow dengan non rebreathing face mask, I V
line, dihangatkan. Pemantauan rutin tanda vital.

Penanganan Hipoksia

PROGNOSIS

Sulit untuk diperkirakan


Resusitasi dalam 30 menit pertama prognosisnya
akan baik
Beberapa faktor berpengaruh terhadap prognosis
tenggelam adalah :
Lamanya berada didalam air
lama dan derajat hipoterimia
umur penderita
tipe kontaminan pada air
lamanya henti napas
lamanya henti jantung
cepatnya dan efektivitasnya pertolongan

1.
2.
3.
4.

5.

6.

Pulmonary Aspiration Syndrome

High risk patient with drug or alkohol/intoxication,


seizures or swallowing disorders, obtunded patients
Immediate respiratory difficullty due to chemical burn,
hypoxemia, rales, wheezing (often unilateral)
Chest x-ray can be negative initially
Mendelson syndrome : Acute aspiration of gastric
contens lung injury by acid corrosion,
bronchial/obstruction with food particles (atelectase),
chemical pneumonitis complicated by bacterial
pneumonia.
Aspiration of gastric acid (PH < 2) pulmonary injury
ARDS
Aspiration of oropharyngeal secretion, poor dental
higyene and large amounts of dental plague
bakterial pneumonia (aspiration pneumonia lung
abscess)

7. Pulmonary aspiration during


anesthesia, cardiopulmonary resusciation
8. After aspiration cough, dyspnea,
fever, leukocytosis, consolidation (x-ray),
pulmonary rales, dullness chest x-ray
(pulmonary infiltrate) ringht lower
lobe or more commonly involved
Management

O2
Intubation/mechanical ventilation
Bronchoscopy

FLAIL CHEST

Post traumatic flail chest painful paradoxical


motion of the rib cage or sternum (inhalation and
exhalation) crepitation /subcutaneus emphysema
decreased breath sounds
Management

Continuously monitor pulse oximetry


Oxygen
Intubation/positive pressure ventilation if saturation <95%
or hypoventilation
Morphine 1 4 mg IV
carefully fo signs of
Fentatnyl 25 50 g IV
respiratory depression

Do not use analgesia if respiratory failure is imminent

Acute upper airway obstruction

Foreign body

With total upper airway obstruction, perform


heimlich maneuver (stand behind patient,
grip wrists across the patients upper
abdomen and tug sharply to raise
intrathoracic pressure and expel foreign
body). Otherwise perform chest X-ray, liaise
with respiratory/ENT/cardiothoracic teams for
retrieval under direct vision.

Epiglottitis
Usually hemophilus influenzae type b, also
strep. pneumoniae. Treat with 3rd
generation cephalosporin, e.g. cefotaxime
2 g tds (adults). Children more likely to
require intubation, but if any concens over
airway then patient (adult or child) should
be monitored on ITU after anaesthetic
assessment.

Diptheria

Uncommon in UK. Occasionally seen in patients


returning from abroad. Toxin-mediated problems
include myocarditis and neuritis. Treat with diphtheria
anti-toxin + antibiotic eradication of organism
(consult microbiology).

Tumour obstruction

Unlikely to cause life-threatening obstruction without


warning symptoms over few days. If significant
stridor present then administer 200 mg
hydrocortisone and there after prednisolone 40 mg od
po. If laryngeal origin liaise with ENT regarding
tracheostomy. Lung cancer in trachea, or extrinsic
cancer eroding into the trachea. Will require urgent
radiotherapy (or occsionally laser or cryotherapy via
bronchocope)

Cause of acute stridor

Infective : acute epiglottitis, diphtheria, tonsillitis, or


adenoiditis (chilldren)
Inhalation of foreign body
Tumour of trachea of larynx
Trauma
Post operative (thyroid surgery)

Acute Upper airway obstruction


Presentation
Stridor inspiratory noise. Generated by the collapse of
the extra-thoracic airway during inspiration
Breathlessness
Dysphagia
Inability to swallow secretions (hunched forward,
drooling)
Cyanosis
Collapse
Ask colleagues to call a senior anaesthesist and ENT
assistance immediately while you continue your
assessment

Identify the cause


History : sudden onset, something in mout or child with
unsafe toy (foreign body), fever (epiglottitis, diphtheria,
tonsillitis), hoarse voice (epiglottitis). Sore throat
(infective as listed), travel (easterm Europe
diphtheria), smoker + longer history + systemic
symptoms (?carcinoma), trauma
Examination : where infective cause is suspected then
examination of oropharynx must be undertaken in area
where patient may be immediately intubated, with an
anaesthetist standing by.
Fever, drooling, stridor, bull neck, lymphadenopathy.
Pseudomembrane over oropharynx (diphtheria). Swollen
throat + epiglottis on direct/indirect laryngoscopy
(epiglottis)
Investigation : do not delay treatment if the patient is
in distress. If the patient is relatively stavle, perform a
chest x-ray (foreign body). Lateral neck x-ray
(swallowen epiglottis). FBC, U&Es, blood gases.

Indication for ITU/surgical referral

Prior to examination of oropharynx if infective cause


suspected

Failure to maintain adquate airway or oxygenation

Inability to swallow secretion

Ventilatory failure (PaO210kPa. PaCO26kPa)

Collapse

Severe dyspnoea
Management

If severe. Fraise immediately with ITU and ENT or


general surgeons (potential for urgent tracheostomy)

Priorities are
1.
2.
3.

Stabilize the patient ensure adequate airway


Identify cause of obstruction
Specific treatment measures.

PULMONARY EMBOLISM
PE is preceded by DVT, the factor
predisposing to two conditions are the
same and broadly fit Virchows triad of
venous stasis, injury to the vein wall and
coagulability of the blood .

PULMONARY EMBOLISM

Pulmonary thromboembolism sering


merupakan komplikasi fatal dari
penyakit trombosis vena
Normal, mikrotrombi (agregasi kecil sel
darah, platelet dan fibrin) dibentuk dan
dilisis sistem sirkulasi vena.
Patologis, mikrotrombi keluar dari
sistem fibrinolisis dan berkembang
PE timbul ketika propagating clot
terlepas dan beremboli membendung
saluran darah paru.

TROMBOSIS VENA:

PEMBENTUKAN BEKUAN DI LUMEN VENA

1. Aliran turbulensi yang


perlahan pada vena
menginduksi stasis dan
menyebabkan terjadinya
koagulasi

2. Polimerisasi fibrin
menstabilkan bekuan

3. Bekuan terbentuk

TROMBOSIS VENA

Trombus terus berkembang


sepanjang vena

Emboli

Deep vein thrombosis

Pulmonary embolism

Prandoni P, et al. Haematologica 1997; 82:423428.

VTE risk factors:

Numerous and common


VTE risk factors include:
Protein C deficiency1
Protein S deficiency1
Antithrombin deficiency1
Activated protein C resistance1
Prothrombin G20210A1
High factor VIII concentration1
Hyperhomocysteinemia1
Age1

Lack of identification of the


patients overall risk profile
may lead to unexpected
events.2,7
1. Rosendaal FR. Semin Hematol 1997;34(3):17187.
2. Clagett GP, et al. Chest 1998;114 Suppl 5:53160S.
3. Fraisse F, et al. Am J Respir Crit Care Med 2000;161 (4 Pt 1):110914.
4. Samama MM, et al. N Engl J Med 1999;341(11):793800.
5. Goldhaber SZ, et al. JAMA 1997;277(8):6425.
6. Cruickshank JM, et al. Lancet 1988; 2(8609):4978.
7. Hirsh J, Hoak J. Circulation 1996; 93:221245.

Surgery1
Trauma2
Malignant disease1
Acute MI3,4
Acute infection3,4
Acute heart failure2
Acute respiratory failure3,4
Antiphospholipid syndrome1
Stroke2
Congestive heart failure2
Hypertension5
Myeloproliferative disorders1
Nephrotic syndrome2
Inflammatory bowel disease2
Obesity2
Varicose veins2
Immobility1
Long-distance travel6
Pregnancy and puerperium1
Previous venous thrombosis1

DEEP VENOUS THROMBOSIS

VTE: Often undetected until


too late
Over 70% of fatal PE
are detected post
mortem1,3

Approximately 80% of DVTs


are clinically silent2,3
1. Stein PD, et al. Chest 1995;108:97881.
2. Lethen H, et al. Am J Cardiol 1997;80:10669.
3. Sandler DA, et al. J R Soc Med 1989;82:2035.

PULMONARY EMBOLISME

PATIENTS WITH SERIOUS MEDICAL ILLNESS, WHO


SHOULD BE CONSIDERED FOR DVT PROPHYLAXIS

Severe Respiratory failure

Class III IV Congestive Heart Failure

Serious Infections

Acute exacerbations of Chronic Obstructive Pulmonary


Adult Respiratory Distress Syndrome
Community Acquired Pneumonia
Non cardiogenic pulmonary edema
Pulmonary malignancy
Interstitial Lung Disease

Ischemis Cardiomyopathy
Non-ischemic cardiomyopathy
CHF Secondary to valvular Disease
Chronic idiopathic cardiomyopathy
CHF Secondary to arrythmias

Pneumonia
- Urinary Tract Infection
- Abdominal Infection
-

Elderly Patients

All hospitalized elderly patients who are immobilized for 3 days or more and who have
serious underlying medical conditions known to be risk factor for DVT should be
considered for prophylaxis with Low Molekular Weight Heparin

Reference : Bosker G. Thrombosis Prophylaxis in Seriously ill Mediccal Patients : Evidence-Based Management, Patient Risk Stratification, and
Outcome Optimizing Pharmacological Management. Internal Medicine Consensus Reports. Juni 1, 2001: 1-8

PASIEN BEDAH DIANGGAP MEMILIKI RESIKO


TERBESAR UNTUK DVT DAN PE.
PENELITIAN PROSPEKTIF MENUNJUKKAN BILA
TIDAK ADANYA PROFILAKSIS, DVT AKUT DAPAT
TERJADI PADA :
Pasien medis umum ditempat tidurkan selama
seminggu (10-13%)
Pasien pada ICU (29-33%)
Pasien penyakit paru berada di tempat tidur selam 3
hari atau lebih (20-26%)
Pasien yang dimasukkan ke Coronary Care Unit
setelah miokard infark (27-33%)
Pasien asimptomatis setelah coronary artery bypass
graft (48%)
Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM, Program Director, Associate Professor, Department of Internal Medicine, Divisions of Pulmonary and Critical Care Medicine,
University of Manitoba; Site Director of Respiratory Medicine, St Boniface General Hospital, June 2006

TANDA DAN GEJALA

Tanpa gejala
Tachypnea, rales
Suara jantung sekunder accentuated
Tachycardia (heart rate >100/min)
Fever/demam (temperature >37.8 C)
Diaphoresis (-)
S3 atau S4 gallop
Thrombophlebitis
Edema ekstrimitas bawah
Cardiac murmur
Cyanosis
Pleuritis

Sat Sharma, MD, FRCPC, FACP, FCCP, DABSM, Program Director, Associate Professor, Department of Internal
Medicine, Divisions of Pulmonary and Critical Care Medicine, University of Manitoba; Site Director of Respiratory
Medicine, St Boniface General Hospital, June 2006

DIAGNOSTIC SUPPORT
Clinical sign and Symptom
CXR
D-dimer
Venous Ultrasonography
Echocardiography
Spiral CT
Ventilation Perfution Scan
Pulmonary Arteriography

Penatalaksanaan
I. Penanganan pada fase akut
- bed rest & elevasi kaki
- mobilisasi dini
II. Terapi PE
a. Antikoagulan:
- Heparin pemantauan aPTT 1,5-2,5 kali
nilai normal
- LMWH
- Dilanjutkan dengan antikoagulan oral (warfarin)
b. Thrombolityc Therapy
c. Inferior Vena Cava Interuption
d. Pulmonary Embolectomy
e. Supportive Care

CLASSIFICATION OF ASTHMA
SEVERITY

INTERMITTENT
Symptoms less than once a week
Brief exacerbations
Nocturnal symptoms not more than twice
a month
FEV1 or PEF > 80% predicted
PEF or FEV1 variability < 20%

MILD PERSISTENT
-

Symptoms more than once a week but


less than once a day
Exacerbations may affect activity and
sleep
Nocturnal symptoms more than twice a
month
FEV1 or PEF > 80% predicted
PEF or FEV1 variability < 20-30%

MODERATE PERSISTENT
-

Symptoms daily
Exacerbations may affect activity and sleep
Nocturnal symptoms more than once a week
Daily use of inhaled short acting B2-agonist
FEV1 or PEF 60-80% predicted
PEF or FEV1 variability >30%

SEVERE PERSISTENT
-

Symptoms daily
Frequent exacerbations
Frequent nocturnal asthma symptoms
Limitation of physical activities
FEV1 or PEF < 60% predicted
PEF or FEV1 variability > 30%

SEVERE OR LIFE-THREATENING
ASTHMA
Severe airway obstruction

Feeble respiratory effort

Soft breath sounds or silent chest

PEF < 30 % predicted


Increased work of breathing and haemodynamic
stress

Exhaustion

Hypotension (systolic < 100 mmHg)

Bradycardia or arrhythmia

Ventilation-Perfusion mismatch
Cyanosis
Hypoxia
Ventilatory failure
Rising Pa Co2
Confusion or coma
Acute severe asthma
Inability to complete sentences in one breath
Respiratory rate > 25x/min
Tachycardia (HR > 100/min
PEF 30-50 % predicted

Managemen
Initial treatment
Sit the patient up in bed
Oxygen 15L/min (least 60 % )
Nebulized bronchodilator : Salbutamol 5
mg or terbutalin 10 mg every 15-30
minutes
Add ipratropium bromida 0,5 mg 4-6
hourly if response to B2-agonists is poor

Start Steroid : 200 mg of hydrocortison


intravenously.Continue either hydrocortison 100 mg
qds iv or prednisolon 30-50 mg od po
Antibiotics should be given if any infection
Adequate hydration
Monitoring progress
Pre and post nebulizer peak flows
Repeated arterial blood gases ( 1- 2 hourly )
If response not brisk
Continue nebulized B2-agonist every 15 min
Magnesium sulphate iv
Aminophyline infusion
Salbutamol infusion
Summon anaesthetic help

Indication to ICU
Hypoxia ( PaO2 < 60 mmHg,FiO2 60% )
Rising PaCO2
Exhaustion,drowsiness or coma
Respiratory arrest
Failure to improve despite adequate
therapy

ACUTE EXACERBATION of CHRONIC


OBSTRUCTION PULMONARY DISEASE
(COPD)
PRESENTATION
- Breathlessness,cough and wheeze
- Wheeze unrelieved or partially relieved by
inhalers
- Increased production of purulent sputum
- Confusion/impaired consciousness
(exhaustion,CO2 retention)
- Positive smoking history
- Respiratory failure (PaO2<60mmHg,normal
PaCO2 or PaO2<60mmHG,high PaCO2)

CAUSES
Infective exacerbation (no new CXR
changes):Typically H.influenzae,
S.pneumoniae,Moraxella catarrhalis. Commonly
viral
Community acquired pneumonia (new CXR
changes)
Exposure to known allergen
Pneumothorax
Expansion of large bullae
Sputum retention with lobar or segmental
collapse (atelectasis)
Myocardial ischaemia,pulmonary oedema,cor
pulmonale,pulmonary embolism

MANAGEMENT
TREAT HYPOXIA AND RESPIRATORY
FAILURE
- Oxygen therapy
- Arterial blood gases
- NIV (non invasive ventilation)
- Mechanical ventilation
- Respiratory stimulants (doxapram)

TREAT BRONCHOSPASM AND


OBSTRUCTION
- Nebulized -agonist (salbutamol 5 mg
or terbutalin 10 mg q4h)
- Aminophyline iv or iv -agonist
- Nebulized ipatropium bromide 500g 6
hourly)
- Give steroid:200mg hydrocortison iv or
30-40 mg prednison po
- Physiotherapy (clearing bronchial
secretions)

TREAT CAUSE of EXACERBATION


Infection
Pneumothorax
Pulmonary oedema
Pulmonary embolism
Myocardial ischaemia
Atelectasis

SEPTIC SHOCK

SIRS (Systemic Inflammatory Response


Syndrome) represents an organisms response to
inflammation that may or may not be due to
infection ( trauma,burns, pancreatitis ,infection )
Criteria SIRS : ( 2 or 4 )
- Fever (38C) or Hypothermia (<36C)
- Tachypnea(RR>20/min or
PaCO2<32mmHg)
- Tachycardia (Pulse>90/min)
- WBC (>10.000/mm3 or <4.000/mm3)
When SIRS is caused by infection,the
condition is termed SEPSIS

Acute organ system dysfunction occurs


(one required) such as altered mentation,
hypoxemia, elevated plasma lactate level,
oliguria, in SEPSIS,is termed severe
sepsis.
Patient who develop hypotension is called
Septic Shock
Immediate Measures :
- Maintain airway and Ventilation
- Establish Adequacy of Circulation
- Obtain Complete Vital Signs

- Regulated Blood Pressure


- Correct Asidosis
- Correct Coagulopathy
- Select Theraphy
- Search for Source of Infection
- Perform Diagnostic Tests
- Start Antibiotic Treatment
DISPOSITION
Intensive care is required for all patients
in septic shock and for those seriously ill
with infection.

SEVERE PULMONARY EDEMA

Clinical : Extremely dyspneic especially in


the supine position,cough up frothy,pink
sputum.
In cardiogenic pulmonary edema :chest
pain, tachycardia,distended neck veins or
hepatojugular reflux,peripheral edema,
cardiomegaly,gallop.Wheezing may also
be present (so-called cardiac asthma)

Noncardiac Pulmonary Edema has many causes.


Drug overdose (heroin and other narcotis),septic
shock,pulmonary contusion,pancreatitis and fat
embolism.
Treatment
- Give oxygen 10-15 L/min,by nonrebrether mask
- Diuresis (furosemide) 40-80 mg iv or
bumetanide 1-2 mg
- Morphine 2-10 mg iv
- Nitrates sublingual (0,4 mg)
- Cutaneously (1-2 inches of nitroglycerin
ointment) or by intravenous infusion (5-10g/min)

- NIPPV (noninvasive positif pressure


ventilation) via continuous positive airway
pressure (CPAP) or bilevel positive airway
pressure (BiPAP)

INHALASI ZAT TOKSIK

TANGKI GAS, PIPA GAS BOCOR


Tangki truk amonia, klorin, asam nitrit
tumpah
Ledakan pabrik kimia, pabrik kertas,
tempat peluncuran senjata
Inhalasi asap pada kebakaran
Trauma panas(particulate matter) pada
saluran napas,iritasi, refleks
bronkokontriksi,asfiksia
Gas, debu, uap, asap
Cedera paru, ARDS

BAHAN PENYEBAB
Tabel Beberapa inhalan toksik dan mekanisme
kerjanya
Tipe

Gas iritan

Penyebab asfiksia

Inhalan

Sumber

Mekanisme

Amonia

Pabrik pupuk, pendingin, Kerusakan epitel saluran napas


pabrik pewarna, plastik, nilon atas

Klorin

Bahan pemutih, limbah dan Kerusakan epitel saluran napas


disinfektan
air,
produk- bawah
produk pembersih

Sulfur dioksida

hasil pembakaran batubara, Kerusakan epitel saluran napas


oli, bahan bakar memasak
atas

Nitrogen dioksida

Hasil pembakaran diesel, Kerusakan


saluran
pengelasan, pabrik pewarna, distal/terminal
wall paper

Karbon monoksida*

Hasil pembakaran rumput- Menduduki


tempat
oksigen
ruput,
batubara,
gas, berikatan dengan hemoglobin,
pemanas
mioglobin, protein intrasel yang
mengandung heme

napas

Hidrogen
sianida

Pembakaran
polyurethane, Asfiksia jaringan dengan menghambat
nitrocellulose (sik, nilon, wool) aktiviti cytochrome axidase intrasel,
menghamabt produksi ATP, meningkatkan
anoksia sel

Hidrogen sulfida

Fasilitas pengolahan limbah,


gas volkanik, pertambangan
batubara, sumber air panas
alami

Sama seperti sianida, asfiksia jaringan


dengan menghambat cytochrome axidase,
meningkatkan kerusakan pada rantai
transport
elektron,
menghasilkan
metabolisme anaerob

Hidrokarbon

Penyalahgunaan
inhalan
(toluene, benzena, freon),
aerosol, lem, bahan bakar
kendaraan,
pembersih
pewarna kuku, bensin, cairan
pembersih

Narkotik system saraf pusat (SSP), status


anastesi, gejala gastrointestinal difus,
neuropati perifer dengan kelemahan
umum, koma, kematian mendadak,
pneiumonitis kimia, abnormaliti SSP,
iritasi gastrointestinal, kardiomiopati,
toksisiti ginjal

Organofosfat

Insektisida, gas saraf

Memblokade acetylcholinesterase, krisis


kolinergik
dengan
peningkatan
acetylcholine

Asap metal

Oksidasi metal dari seng, Gejala seperti flu (Flu-like symptoms(,


perak magnesium, pembuat demam, mialgia, lemah
permata

Toksin sistemik

PATOGENESIS CEDERA SALURAN NAPAS

Partikel 5 um:bronkiolus terminal,Alveol


iritan inflamasi
Termal epithel,subepithel regio alveolar
Asam koagulasi
Alkali perlunakan mukosa,jaringan
Reactive oxygen species (ROS)
lipid peroksida respon inflamasi
asfiksia dan toksik sistemik

Endothelial injury
Disturbed capillary
Blood flow
Macrophages
Neutrophyls

Pulmonary
microcirculation

Injury to alveolar
capillary membrane

Microvaskular permeability
Mediators
Intertitial and alveolar
Damage, Edema

ARDS

Gejala Klinis dan Diagnosis

Rasa terbakar di saluran napas atas dan


bawah
Batuk kering, batuk darah, mengi, sesak
Sekresi mukus, bersin, penutupan glotis,
apnea, peningkatan tonus otot sal napas
Edema, spasme, sianosis, edema paru
Sakit kepala,hiperventilasi, mual, takikardi,
kejang, penurunan kesadaran, henti jantung,
apnea dan kematian

DIAGNOSTIC SUPPORT

Anamnesis yang cermat


Laringoskopi
Bronkoskopi, BAL
Foto toraks
Laboratorium
Toksikologi gas, Radioisotop

TATA LAKSANA
SUPORTIF
Tanda vital tetap stabil, paparan zat
toksik, eliminasi zat toksik
Nyaman, lifes saving A,B,C.. segera
Resusitasi, sistim respirasi,patensi sal
napas, ventilasi, oksigenisasi
Monitor, hemodinamik
Cegah kerusakan organ lain
Rawat intensif

KHUSUS
Monitor 4-12 jam
Kembali ke RS, bila perburukan setelah
24-48jam
Progresivitas gawat napas intubasi
ventilator
Bronkial toilet
Kasus akut : steroid, bronkodilator
Atasi infeksi sekunder segera
Antidotum
Oksigenisasi adekuat