gawat paru
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GAWAT PARU
Departemen Ilmu Penyakit ParuFakultas Kedokteran Methodist Sumatera Utara
Medan
2009
Dr. Parluhutan Siagian, SpP
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1. Asma berat (GINA) exacerbasi akut
2. PPOK berat/sangat berat (GOLD) exacerbasi akut
3. Pneumonia berat (PORT = PSI : Pneumonia SeverityIndex) 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
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11. Atelektase lobar komplet
12. Aspirasi benda asing (Pulmonary AspirationSyndrome)
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 lung19. Edema paru : cardiogenic / non-cardiogenik = akut
lung injury (ALI) / Acut Respiratory DistressSyndroma (ARDS)
20. Cidera toraks (Flail chest)
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Massive Pleural Effusion
Klinis : Sesak nafas yang semakin lama bertambah beratdengan atau tanpa demam, nyeri dada,peny mendasari PD.
Inspeksi: Gerakan dada sisi yang sakit tertinggal Palpasi: Stemfremitus lemahhilang di sisi yang sakit
Perkusi: Beda pada sisi yang sakit Auskultasi: Suara pernafasan lemahhilang
Foto toraks : Tampak perselubungan homogen di sisi yang sakit Tampak trakhea, mediastinum/jantung terdorongke sisi yang
sehat.
Penanganan :Thoracentesis
Aspirasi cairan pleura dengan abocart no. 14 Pasang WSD (Water Seal Drainage)
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Massive Atelectasis
Klinis : Sesak nafas, batuk, nyeri dada. PD.
Inspeksi: Gerakan dada sisi yang sakit tertinggal
Palpasi: Stemfremitus lemahhilang di sisi yang sakit Perkusi: Sonor memendekbeda pada sisi yang sakit Auskultasi: Suara pernafasan lemahhilang disisi yang sakit
Foto toraks : Tampak perselubungan homogen di sisi yang sakit
Tampak trakhea, mediastinum/jantung tertarikke sisi yangsakit. Tampak diafragma tertarikke atas
Penanganan :Bronkoskopi untuk diagnostik dan terapi.
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HaemoptisisDefinisi :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/24jam, 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.
Etiologi1. Infeksi( TB paru, pneumonia, abses paru, jamur paru),trauma
2. Kardiovaskular(stenosis mitralis dan aneurisma aorta).
3. Neoplasma (karsinoma) terutama karsinoma bronchus
4. Obstruksi benda asing
5. Kelainan sistem pembekuan darah
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Penanggulangan : Posisi pasien Trendelenbert Pemberian cairan intravena yang ditambahkan dengan hemostatika
dengan tetesan 2025 /menit (cairan Dext 5% atau R. Solution) Pemberian hemostatika perbolus 1 amp/46 jam Evaluasi jumlah perdarahan dan cek Hb,Ht.
Bila Hb menurun hingga 7 g% perlu dilakukan tranfusi dengan :1. Pertimbangkan asal perdarahan, bila ada gangguan kardiovascular
harap lapor/konsul segera dengan dokter kardiolog2. Pertimbangkan kondisi pasien apakah demam atau tidak3. Pemberian PRC 250 cc,darah segar 5001750 cc.
EKG pasien,menilai kelainan jantung
Hati-hati dengan pemberian salisilat karena dapat menambahperdarahan Awasi jangan terjadi asfiksia(tersering) atau hypovolemicshockpenyebab kematian
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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
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Pneumo Mediastinum dan SubcutaneousEmphysema
Subcutenuous emphysema = Adanya udara di sub cutis Pembengkakan di sub cutis
Adanya udara di mediastinum chest x-ray hammansscrunch 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 yangmengelilingi paru maka udara masuk ke mediastinumsebelum ke rongga pleura
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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, gasproducing bacterial mediastinitis, valsalva maneuver.
Klinis ; Chest pain, pernafasan tidak enak bila bergerakatau berubah posisi.
Diagnosis1. Terdengar mediastinalcrunech Hamman sign pada saat
sistole2. Chest x-ray terutama lateral3. Subcutaneus emphysema diraba / ditekan daerah kulit yang
ada udara terdengar / terasa seperti gesekan rambut(krepitasi)
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Penatalaksanaan
1. Tidak ada yang spesifik kecuali, padarupture esophageal
2. Penanganan pneumothorax (bila ada)
3. Pasien sebaiknya dirawat
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PLEURODYNIA1. Seflimited viral illnes of skletal muscle
2. Severe pleuritic pain in ribs3. Lowgrade fever, malaise
4. Penyebab grub Bcoxsackievirus danachovirus
5. Chest x-ray normal terkadang tampakminimal pleural fluid atau minimalpulmonary infiltrate
6. Leukosit / LED normal atau sedikitmeningkat
7. Terkadang menyertai pericarditis
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NEAR DROWNINGDEFINITIONNear drowning adalah bila seseorangdapat bertahan hidup setelah
mengalami tenggelam dalam waktu 24jam setelah peristiwa itu. Hal inisecara tidak langsung juga
menerangkan bahwa recoverytelahterjadi. Istilah yang juga dipakaidibeberapa artikel adalah submersioninjuryatau submersion incident.
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JENIS CAIRAN TERASPIRASI
Air laut (asin) Air tawar
Bahan kontaminasi seperti lumpur,pasir, air limbah, lumut, ganggang,bakteri .
Aspirasi dari isi lambung dan debrisyang mengandung air limbah, pasir,lumpur, ganggang menyebabkan cidera
paru dengan pneumonitis kimia.
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REAKSI SEGERA DARI ASPIRASI
Edema paru
Meningkatnya shunt
Toksisitas langsung dari cairan teraspirasi Inaktivasi surfactan
Hanyutnya surfaktan
Cidera pada membran alveolar
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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 flowdengan non rebreathing face mask, I V
line, dihangatkan. Pemantauan rutin tanda vital.
Penanganan Hipoksia
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PROGNOSISSulit 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
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Pulmonary Aspiration Syndrome1. Highrisk patient with drug or alkohol/intoxication,
seizures or swallowing disorders, obtunded patients2. Immediate respiratory difficullty due to chemical burn,hypoxemia, rales, wheezing (often unilateral)
3. Chest x-ray can be negative initially4. Mendelson syndrome : Acute aspiration of gastric
contens lung injury by acid corrosion,bronchial/obstruction with food particles (atelectase),chemical pneumonitis complicated by bacterialpneumonia.
5. Aspiration of gastric acid (PH < 2) pulmonary injury
ARDS6. Aspiration of oropharyngeal secretion, poor dentalhigyene and large amounts of dental plague bakterial pneumonia (aspiration pneumonia lungabscess)
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7. Pulmonary aspiration duringanesthesia, cardiopulmonary resusciation
8. After aspiration cough, dyspnea,fever, leukocytosis, consolidation (x-ray),pulmonary rales, dullness chest x-ray
(pulmonary infiltrate) ringht lowerlobe or more commonly involved
Management O2 Intubation/mechanical ventilation
Bronchoscopy
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FLAIL CHEST
Post traumatic flail chest painful paradoxicalmotion of the rib cage or sternum (inhalation and
exhalation) crepitation /subcutaneus emphysemadecreased breath sounds
Management
Continuously monitor pulse oximetry
Oxygen Intubation/positivepressure ventilation if saturation
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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 raiseintrathoracic pressure and expel foreignbody). Otherwise perform chest X-ray, liaisewith respiratory/ENT/cardiothoracic teams forretrieval under direct vision.
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Epiglottitis
Usually hemophilus influenzae type b, alsostrep. pneumoniae. Treat with 3rdgeneration cephalosporin, e.g. cefotaxime
2 g tds (adults). Children more likely torequire intubation, but if any concens overairway then patient (adult or child) shouldbe monitored on ITU after anaesthetic
assessment.
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Diptheria Uncommon in UK. Occasionally seen in patients
returning from abroad. Toxin-mediated problemsinclude myocarditis and neuritis. Treat with diphtheriaanti-toxin + antibiotic eradication of organism(consult microbiology).
Tumour obstruction Unlikely to cause life-threatening obstruction without
warning symptoms over few days. If significantstridor present then administer 200 mghydrocortisone and there after prednisolone 40 mg odpo. If laryngeal origin liaise with ENT regardingtracheostomy. Lung cancer in trachea, or extrinsic
cancer eroding into the trachea. Will require urgentradiotherapy (or occsionally laser or cryotherapy viabronchocope)
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Cause of acute stridor
Infective : acute epiglottitis, diphtheria, tonsillitis, oradenoiditis (chilldren)
Inhalation of foreign body
Tumour of trachea of larynx
Trauma Postoperative (thyroid surgery)
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Acute Upper airway obstructionPresentation
Stridor inspiratory noise. Generated by the collapse ofthe extra-thoracic airway during inspiration
Breathlessness
Dysphagia
Inability to swallow secretions (hunched forward,drooling)
Cyanosis
Collapse
Ask colleagues to call a senior anaesthesist and ENTassistance immediately while you continue yourassessment
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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 Europediphtheria), smoker + longer history + systemicsymptoms (?carcinoma), trauma
Examination : where infective cause is suspected then
examination of oropharynx must be undertaken in areawhere patient may be immediately intubated, with ananaesthetist standing by.
Fever, drooling, stridor, bull neck, lymphadenopathy.Pseudomembrane over oropharynx (diphtheria). Swollenthroat + epiglottis on direct/indirect laryngoscopy(epiglottis)
Investigation: do not delay treatment if the patient isin distress. If the patient is relatively stavle, perform achest x-ray (foreign body). Lateral neck x-ray(swallowen epiglottis). FBC, U&Es, blood gases.
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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. Stabilize the patient ensure adequate airway2. Identify cause of obstruction3. Specific treatment measures.
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PE is preceded by DVT, the factorpredisposing to two conditions are the
same and broadly fit Virchows triadofvenous stasis, injury to the vein wall andcoagulability of the blood .
PULMONARY EMBOLISM
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Pulmonary thromboembolism seringmerupakan komplikasi fatal daripenyakit trombosis vena
Normal, mikrotrombi (agregasi kecil seldarah, platelet dan fibrin) dibentuk dandilisis sistem sirkulasi vena.
Patologis, mikrotrombi keluar darisistem fibrinolisis dan berkembangPE timbul ketika propagating clotterlepas dan beremboli membendung
saluran darah paru.
PULMONARY EMBOLISM
TROMBOSIS VENA:
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TROMBOSIS VENA:PEMBENTUKAN BEKUAN DI LUMEN VENA
Aliran turbulensi yang
perlahan pada vena
menginduksi stasis dan
menyebabkan terjadinya
koagulasi
1.
Polimerisasi fibrin
menstabilkan bekuan
2. Bekuan terbentuk3.
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TROMBOSIS VENA
Deep vein thrombosis
Trombus terus berkembangsepanjang vena
Pulmonary embolism
Prandoni P, et al.Haematologica 1997; 82:423428.
Emboli
VTE risk factors:
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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 concentration1Hyperhomocysteinemia 1
Age1
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.
Lack of identification of thepatients overall risk profile
may lead to unexpectedevents.2,7
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
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DEEP VENOUS THROMBOSIS
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VTE: Often undetected until
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VTE: Often undetected untiltoo late
Approximately 80% of DVTsare clinically silent2,3
Over 70% of fatal PEare detected post
mortem1,3
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.
P LM N R EMB L ME
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PULMONARY EMBOLISME
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PATIENTS WITH SERIOUS MEDICAL ILLNESS, WHO
SHOULD BE CONSIDERED FOR DVT PROPHYLAXIS Severe Respiratory failure
- Acute exacerbations of Chronic Obstructive Pulmonary- Adult Respiratory Distress Syndrome- Community Acquired Pneumonia- Non cardiogenic pulmonary edema- Pulmonary malignancy- Interstitial Lung Disease
Class III IV Congestive Heart Failure
- Ischemis Cardiomyopathy- Non-ischemic cardiomyopathy- CHF Secondary to valvular Disease- Chronic idiopathic cardiomyopathy- CHF Secondary to arrythmias
Serious Infections- Pneumonia
- Urinary Tract Infection- Abdominal Infection
Elderly PatientsAll hospitalized elderly patients who are immobilized for 3 days or more and who haveserious underlying medical conditions known to be risk factor for DVT should beconsidered 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
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PASIEN BEDAH DIANGGAP MEMILIKI RESIKOTERBESAR UNTUK DVT DAN PE.
PENELITIAN PROSPEKTIF MENUNJUKKAN BILATIDAK ADANYA PROFILAKSIS, DVT AKUT DAPATTERJADI PADA:Pasien medis umum ditempat tidurkan selama
seminggu (10-13%)Pasien pada ICU (29-33%)Pasien penyakit paru berada di tempat tidur selam 3hari atau lebih (20-26%)
Pasien yang dimasukkan ke Coronary Care Unitsetelah miokard infark (27-33%)Pasien asimptomatis setelah coronary artery bypassgraft (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
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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
TANDA DAN GEJALA
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 RespiratoryMedicine, St Boniface General Hospital, June 2006
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DIAGNOSTIC SUPPORT
Clinical sign and Symptom CXR D-dimer Venous Ultrasonography
Echocardiography Spiral CT Ventilation Perfution Scan
Pulmonary Arteriography
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Penatalaksanaan
I. Penanganan pada fase akut- bed rest & elevasi kaki- mobilisasi dini
II. Terapi PEa. Antikoagulan:
- Heparin pemantauan aPTT 1,5-2,5 kalinilai normal
- LMWH
- Dilanjutkan dengan antikoagulan oral (warfarin)
b. Thrombolityc Therapyc. Inferior Vena Cava Interuptiond. Pulmonary Embolectomye. Supportive Care
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CLASSIFICATION OF ASTHMASEVERITY
INTERMITTENT
- Symptoms less than once a week
- Brief exacerbations
- Nocturnal symptoms not more than twicea month
- FEV1 or PEF > 80% predicted
- PEF or FEV1 variability < 20%
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MILD PERSISTENT
- Symptoms more than once a week butless than once a day
- Exacerbations may affect activity andsleep
- Nocturnal symptoms more than twice amonth
- FEV1 or PEF > 80% predicted
- PEF or FEV1 variability < 20-30%
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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%
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SEVERE PERSISTENT
- Symptoms daily
- Frequent exacerbations
- Frequent nocturnal asthma symptoms
- Limitation of physical activities
- FEV1 or PEF < 60% predicted
- PEF or FEV1 variability > 30%
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SEVERE OR LIFE-THREATENINGASTHMA
Severe airway obstruction
Feeble respiratory effort
Soft breath sounds or silent chest PEF < 30 % predicted
Increased work of breathing and haemodynamicstress
Exhaustion Hypotension (systolic < 100 mmHg)
Bradycardia or arrhythmia
l f h
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Ventilation-Perfusion mismatch
Cyanosis
HypoxiaVentilatory 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
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Managemen
Initial treatment
Sit the patient up in bed
Oxygen 15L/min (least 60 % )
Nebulized bronchodilator : Salbutamol 5mg or terbutalin 10 mg every 15-30
minutes
Add ipratropium bromida 0,5 mg 4-6hourly if response to B2-agonists is poor
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Start Steroid : 200 mg of hydrocortisonintravenously.Continue either hydrocortison 100 mgqds 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
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Indication to ICU
Hypoxia ( PaO2 < 60 mmHg,FiO2 60% )
Rising PaCO2
Exhaustion,drowsiness or coma
Respiratory arrest
Failure to improve despite adequatetherapy
ACUTE EXACERBATION f CHRONIC
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ACUTE EXACERBATION of CHRONICOBSTRUCTION PULMONARY DISEASE
(COPD)PRESENTATION
- Breathlessness,cough and wheeze
- Wheeze unrelieved or partially relieved byinhalers
- Increased production of purulent sputum
- Confusion/impaired consciousness
(exhaustion,CO2 retention)- Positive smoking history
- Respiratory failure (PaO2
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CAUSES Infective exacerbation (no new CXRchanges):Typically H.influenzae,
S.pneumoniae,Moraxella catarrhalis. Commonlyviral
Community acquired pneumonia (new CXRchanges)
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
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MANAGEMENT
TREAT HYPOXIA AND RESPIRATORY
FAILURE- Oxygen therapy
- Arterial blood gases
- NIV (non invasive ventilation)
- Mechanical ventilation
- Respiratory stimulants (doxapram)
TREAT BRONCHOSPASM AND
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TREAT BRONCHOSPASM ANDOBSTRUCTION
- Nebulized -agonist (salbutamol 5 mgor terbutalin 10 mg q4h)
- Aminophyline iv or iv -agonist
- Nebulized ipatropium bromide 500g 6hourly)
- Give steroid:200mg hydrocortison iv or30-40 mg prednison po
- Physiotherapy (clearing bronchialsecretions)
TREAT CAUSE f EXACERBATION
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TREAT CAUSE of EXACERBATION
Infection
Pneumothorax Pulmonary oedema
Pulmonary embolism
Myocardial ischaemia
Atelectasis
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SEPTIC SHOCK SIRS (Systemic Inflammatory Response
Syndrome) represents an organisms response toinflammation that may or may not be due toinfection ( trauma,burns, pancreatitis ,infection )
Criteria SIRS : ( 2 or 4 )
- Fever (38C) or Hypothermia (20/min orPaCO290/min)
- WBC (>10.000/mm3or
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Acute organ system dysfunction occurs(one required) such as altered mentation,hypoxemia, elevated plasma lactate level,oliguria, in SEPSIS,is termed severesepsis.
Patient who develop hypotension is calledSeptic Shock
Immediate Measures :
- Maintain airway and Ventilation
- Establish Adequacy of Circulation
- Obtain Complete Vital Signs
R l t d Bl d P
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- 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 patientsin septic shock and for those seriously illwith infection.
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SEVERE PULMONARY EDEMA
Clinical : Extremely dyspneic especially inthe supine position,cough up frothy,pink
sputum.In cardiogenic pulmonary edema :chestpain, tachycardia,distended neck veins or
hepatojugular reflux,peripheral edema,cardiomegaly,gallop.Wheezing may alsobe present (so-called cardiac asthma)
N di P l Ed h
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Noncardiac Pulmonary Edema has many causes.Drug overdose (heroin and other narcotis),septicshock,pulmonary contusion,pancreatitis and fatembolism.
Treatment
- Give oxygen 10-15 L/min,by nonrebrether mask
- Diuresis (furosemide) 40-80 mg iv orbumetanide 1-2 mg
- Morphine 2-10 mg iv
- Nitrates sublingual (0,4 mg)- Cutaneously (1-2 inches of nitroglycerinointment) or by intravenous infusion (5-10g/min)
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- NIPPV (noninvasive positif pressureventilation) via continuous positive airway
pressure (CPAP) or bilevel positive airwaypressure (BiPAP)
INHALASI ZAT TOKSIK
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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, refleksbronkokontriksi,asfiksia Gas, debu, uap, asap Cedera paru, ARDS
INHALASI ZAT TOKSIK
BAHAN PENYEBAB
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Tipe Inhalan Sumber Mekanisme
Gas iritan
Amonia Pabrik pupuk, pendingin,
pabrik pewarna, plastik, nilon
Kerusakan epitel saluran napas
atas
Klorin Bahan pemutih, limbah dan
disinfektan air, produk-
produk pembersih
Kerusakan epitel saluran napas
bawah
Sulfur dioksida hasil pembakaran batubara,
oli, bahan bakar memasak
Kerusakan epitel saluran napas
atas
Nitrogen dioksida Hasil pembakaran diesel,pengelasan, pabrik pewarna,
wall paper
Kerusakan saluran napasdistal/terminal
Penyebab asfiksia
Karbon monoksida* Hasil pembakaran rumput-
ruput, batubara, gas,
pemanas
Menduduki tempat oksigen
berikatan dengan hemoglobin,
mioglobin, protein intrasel yang
mengandung heme
Tabel Beberapa inhalan toksik dan mekanismekerjanya
BAHAN PENYEBAB
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Hidrogen
sianida
Pembakaran polyurethane,
nitrocellulose (sik, nilon, wool)
Asfiksia jaringan dengan menghambat
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
Toksin sistemik
Hidrokarbon Penyalahgunaan inhalan(toluene, benzena, freon),
aerosol, lem, bahan bakar
kendaraan, pembersih
pewarna kuku, bensin, cairan
pembersih
Narkotik system saraf pusat (SSP), statusanastesi, 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,
perak magnesium, pembuat
permata
Gejala seperti flu (Flu-like symptoms(,
demam, mialgia, lemah
PATOGENESIS CEDERA SALURAN NAPAS
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PATOGENESIS CEDERA SALURAN NAPAS
Partikel 5 um:bronkiolus terminal,Alveoliritan inflamasi
Termal epithel,subepithel regio alveolar
Asam koagulasi
Alkali perlunakan mukosa,jaringan
Reactive oxygen species (ROS)lipid peroksida respon inflamasi
asfiksia dan toksik sistemik
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Endothelial injury
Disturbed capillary
Blood flow
Microvaskular permeabilityMacrophages
MediatorsNeutrophyls
Intertitial and alveolarPulmonary
microcirculation
Injury to alveolarcapillary membrane ARDS
Damage, Edema
Gejala Klinis dan Diagnosis
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Gejala Klinis dan Diagnosis
Rasa terbakar di saluran napas atas danbawah
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
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DIAGNOSTIC SUPPORT
Anamnesis yang cermat
Laringoskopi Bronkoskopi, BAL
Foto toraks
Laboratorium
Toksikologi gas, Radioisotop
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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
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KHUSUS
Monitor 4-12 jam
Kembali ke RS, bila perburukan setelah24-48jam
Progresivitas gawat napas intubasi
ventilator Bronkial toilet
Kasus akut : steroid, bronkodilator
Atasi infeksi sekunder segera Antidotum
Oksigenisasi adekuat
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