Gawat Paru

8/10/2019 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


bawah

Sulfur dioksida hasil pembakaran batubara,

oli, bahan bakar memasak


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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Gawat Paru

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