emd166 slide pulmonary emergency medicine

8/12/2019 Emd166 Slide Pulmonary Emergency Medicine

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PULMONARY EMERGENCYMEDICINE

Parluhutan Siagian

Department of Pulmonology University of Sumatera UtaraHaji Adam Malik Hospital MedanIndonesia


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Acute Respiratory Failure A sudden fall in the PaO2 value < 50 mmHg with

a concomitant rise PaCO2 >50 mmHg.

RF I = PaO2 < 50 mmHg

= a < mm g + a > mm g A true pulmonary emergency

Without correction,this state can lead to severetissue hypoxia, hypercarbia with coma, death

The patients survival depends to a geat extents


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Type (I) respiratory failureOxygenation failure

Characterized by hypoxia with normo-orhypocapnea

Hypoxic or non hypercapnic respiratory failure

Causes Pulmonary infarction Pulmonary collapse Pulmonary oedema Pulmonary embolism Pneumonia viral or bacterial Acute respiratory lung fibrosis- Aspiration pneumonitis


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Type (II) respiratory failureVentilatory failure

Characterized by hypoxia with hypercapneaHypercapnic respiratory failure

Causes

- u monary seases- Acute and chronic obstructive lung diseases- Interstitial lung fibrosis and cystic fibrosis- sleep apnea syndrome

- Chest wall lesions : kyphoscoliosis and ankylosingspondylitis- Neuromuscular lesions : polyneuropathy and myopathy- Spinal cord lesions : poliomyelitis and spinal injury- Brain lesions: fracture base of skull and brain stemtumour


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SYMPTOM / SIGN /MANIFESTATIONACUTE HYPOXIA

Early manifestations- Central cyanosis, tachycardia and tachypnea- Systemic hypertension and arrhythmia

,Late manifestations- Mycocardial depression- Hypotension and bradycardia- Heart failure and shock- Impairment of consciousness level- Convulsion, coma and may be death


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DIAGNOSTIC APPROACH1. Arterial blood analysis :

Arterial blood gases PO 2, PCO2

For diagnosis of the type of respiratory failure, followup of the patients Arterial blood PH, HCO 3

For dia nosis of metabolic alkalosis due to increase Na

HCO3 in acidosis2. Respiratory function test3. Investigation of the causes as

Pulmonary oedema and pneumonia in type (I)respiratory failure- Chronic obstructive lung diseases in type (II)

respiratory failure


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MANAGEMENT TREATMENT 1. SUPPORTIVE AND SYMPTOMATIC TREATMENT Hospitalization Preferable in respiratory ICU Maintainance of patent airways elimination of retained secretions Encourage coughing

Expectorant as Potassium Iodide Mucolytics Respiratory exercise ( chest physiotrerapy )

2. SUCTION OF SECRETIONS THROUGH- Catheter and endotracheal tube- Bronchoscopy and tracheostomy

3. RESPIRATORY STIMULANT As doxapram


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4. OXYGEN INHALATION Type (I) RF may be given a high concentration of

inspired oxygen as CO 2 retension is not a risk Type (II) RF it depends on the cause, in COPD, the

patients is given a continuous and low concentration ofthe inspired oxygen5. ARTIFICIAL VENTILATION

MECHANICALVENTILATION = ventilator Intermittent positive pressure ventilation (IPPV) Bilevel positive airway pressure (Bipap) Continuous positive airway pressure (CPAP) Positive and expiratory pressure (PEEP) It is used in ARDS The ventilators delivers next tidal volume at the end of expiration and before

the pressure reaches the zero level It prevents alveolar collapse occuring at the end of expiration in cases of ARDS

due to destruction of surfactant


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6. TREATMENT OF THE CAUSES7. TREATMENT OF PRECIPITATING FACTORS

Bronchospasm : bronchodilator and cortisone

Pulmonary infection : antibiotics Heart failure : diuretics, digitalis,vasodilators COPD and pneumonia

8. TREATMENT OF COMPLICATIONS Asidosis and acid-base disturbance


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ENSION PNEUMOTHORA


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TENSION PNEUMOTHORAX:

Chest x ray. Do needle aspiration in an emergency

. Use flutter or heimlich valve. WSD. Open thoracotomy if not relieve the

condition.


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TRAUMATIC PNEUMOTHORAX :

Establish an airway.

,surgical correction.

Use tube postoperatively.


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TENSION PNEUMOTHORAX Pneumothorax is the abnormal collection

of air in the pleural space Clinical : distressed,tachypnea with

c anosis rofuse sweatin tach cardiaand hypotension

Physical Examination : distended neckvein ,contralateral tracheal shift,ipsilateralhyperresonant, decreased or absentbreath sounds


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Do not wait for x-ray confirmation if thepatient is unstable

Management : Give oxygen,

Immediate Thoracentesis : 10 mlsyringe needle or venocath/abbocath no14-16 in the second intercostal space at

the midclavicular line,leave the needle inplace until the air ceases to rush out.

Insert a chest drain as soon as possible.


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SIGNS / SYMPTOMS : Usually found with 40 % or greatercollapse.

COPD uncomfortable breathing with only a 20-25 % pneumothorax.

, . Shock, cyanosis.

fremitus, trachea be shifted to the normal

side, tympany, metallic ring. Breath sound : absent or May be completelyabsent, pain.

Dyspnea, agitation.


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Diagnostic procedures :

Chest x ray. BGA

. ECG, routine blood.

INFORM CONCERNT !!


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MASSIVE PLEURAL EFFUSION Pleural effusion are an abnormal collection

of fluid between the parietal and visceralpleura.

,cough,pleuritic or non pleuritic chestpain,symptoms of malignancy or infection.


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Physical Examination : Bulging hemithorax ,

Contralateral tracheal shift,absent or decreasedtactile fremitus, dullness to percusion,absent ordecreased breath sounds.

Chest x-ray : hemithorax homogeneous andshifting the mediastinum to the contralateral.

Mana emen t : Give oxi en b mask or nasal

cannula, Thoracentesis with removal of 500-1000 ml for relief of symptom. Remove the fluidover 30-90 minutes to prevent pulmonary

edema. If the stable patient,insert a chestdrain .


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MASSIVE ATELECTASIS Atelectasis is alveolar collapse that is not

due to pneumothorax or hydrothorax (pleural effusion )

, , Physical Examination : Decrease in

chest motion on the affected side,dullness

to percussion,decreased to absent breathsounds are noted.


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Chest x ray : Increase in density of thecollapsed lung,narrowed rib interspaces,elevatedhemidiaphragm, mediastinal shift to the ipsilateral.

Treatment : Administration of oxygen is indicatedfor patients with hypoxia on pulse oximetry whilethe underlying cause is determined.

In respiratory failure give assisted ventilationin the emergency department .Hospitalization is required unless the process

known to be chronic and nonprogressive.


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NEAR DROWNINGDEFINITION

Near drowning adalah bila seseorangdapat bertahan hidup setelahmen alami ten elam dalam waktu 24

jam setelah peristiwa itu. Hal inisecara tidak langsung jugamenerangkan bahwa recovery telahterjadi. Istilah yang juga dipakaidibeberapa artikel adalah subersioninjury atau submersion incident.


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JENIS CAIRAN TERASPIRASI Air laut (asin)

Air tawar Toksisitas cairan tersebut Bahan kontaminasi se erti lum ur

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 lan sun dari cairan teras irasi 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

a era .

Penatalaksanaan Pasca Resusitasi high flow dengan non rebreathing face mask, I V

line, dihangatkan. Pemantauan rutin tanda vital. Penanganan Hipoksia


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FiO2 tinggi, analisis gas darah dan foto toraks.Tujuan O 2 ini adalah mencapai P aO2 70-100 mmHg.Intubasi bila gagal napas, positive end expiratory

pressure (PEEP), dimonitor dengan analisis gasdarah. Pemakaian PEEP akan menurunkan derajatshuntings intra pulmoner, menurunkan mismatchV/Q dan meningkatkan kapasitas residu fungsional.

Bronkodilator steroid . Bronkoskopi partikel yang teraspirasi. Metabolik Na bicarbonat. Diuretik

Antibiotik demam, infiltrat- foto toraks,bertambahnya sputum purulen.


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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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HEMOPTISIS MASIF

Hemptisis masif : busroh 1978 Perdarahan 600 ml/24 jam 250 / 24 am hb

10 g% dalam 48 jam blm berhenti


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PANIK & PERTOLONGANMEDIS PERTOLONGAN SEGERA &

PERAWATAN MEDISPENANGANAN :1. CEGAH ASFIKSIA2. HENTIKAN PERDARAHAN

3. TERAPI ETIOLOGI4. LOKASI SUMBER PERDARAHAN


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DIAGNOSTIC SUPPORT FOTO THORAKS

SPUTUM BTA SPUTUM KULTUR DARAH LENGKAP, FAKTOR PEMBEKUAN DARAH,

GOL. DARAH EKG BRONKOSKOPY

ANGIOGRAPHY HRCT


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MANAGEMENT TREATMENT CEGAH ASFIKSIA HENTIKAN PERDARAHAN

TERAPI ETIOLOGI LOKASI SUMBER PERDARAHAN PERTOLONGAN SEGERA & PERAWATAN MEDIS MENJAGA SAL NAPAS,STABILISASI PENDERITA

LOKASI PERDARAHAN, TERAPI AKUT TERATASI,MENCEGAHBERULANG DG TERAPI YANG LBH TERARAH KE ETIOLOGI MONITOR DG KETAT DI RUANG RAWAT INTENSIF TERAPI SPESIFIK:

1. BRONKOSKOPI TERAPEUTIK, BILAS BRONKUS DG LARGARAM, OBAT TOPIKAL, TAMPONADEENDOBRONKIAL,FOTOKOAGULASI LASER

2. TERAPI NON BRONKOSKOPIK: MEDIKAMENTOSA3. EMBOLISASI ARTERI BRONKIALIS

4. BEDAH


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PROGNOSE

BAIK BILA DIATASI SEGERA DAN


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CORPUS ALIENUM Mortaliti dan morbititi di US

90 % kematian pada balita Jarum pentul, kacang-kacangan, jagung,

i i alsu tulan ikan asesori ainankancing, guli dll

Tindakan bronkoskopi banyak membantu Obstruksi total gawat napas segera

dapat pertolongan Pneumonitis supuratif kronik


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Gejala: distress pernapasan akut,rasa tercekik, sianosis, batuk berat,mengi

GAWAT NAPAS: obstruksi totalheimlich manuever, advanced cardiac

Laringoskopi Bronkoskopi Komplikasi: AB, steroid


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Synonyms and related keywords

ACUT RESPIRATORY DISTRESS SYNDROME

ARDS

adult respiratory distress syndrome = ARDS

severe acute respiratory syndrome = SARS


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Adult respiratory distress syndrome (ARDS)

is a diffuse pulmonary parenchymal injuryassociated with noncardiogenic pulmonaryedema and resulting in severe respiratory

Background

istress an ypoxemic respiratory ai ure. The pathologic hallmark is diffuse alveolardamage (DAD), but lung tissue rarely is

available for a pathologic diagnosis. Diagnosis is made on clinical grounds Estimated incidence in the US is 150,000 -

200,000 cases per year.

A di h f ll i i i f h


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According to the following criteria set forth

by the American-European ConsensusConference :

1. Acute onset2. Bilateral infiltrates3. Pulmonary artery wedge pressure less than

19 mmHg (or no clinical signs of congestiveheart failure)4. PaO2/FIO2 ratio less than 200 (ARDS) or

less than 300 (acute lung injury [ALI]): ALIis a milder clinical expression of the injuryof ARDS that may or may not progress toARDS.


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3 PHASES IN THE PATHOGENESISOF ARDS

Exudative phaseThe initial phase,injury to the endothelium andepithelium, inflammation, and fluid exudation.

Fibroproliferative phasee n ux an pro era on o ro as s an

other cellular elements.Injury may begin to resolve or become persistent.

Recover, the fibrosis phaseResolution of inflammation and development ofvarying degrees of pulmonary fibrosis.


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Mortality/Morbidity Overall risk of mortality is reported to be

40-70%. Few long-term sequelae. persistent pulmonary fibrosis with

symp oms o res r c ve ung sease. Factors that influence mortality rate

1.Age (higher rate 65 y)2.Coexisting organ failure

Age: ARDS can occur in children as well asin adults.

Ph i l


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PhysicalPhysical examination are not specific forARDS and can be found in pulmonary edema of

any cause. Labored breathing and tachypnea Cyanosis and moist skin

Tachycardia Hyperventilation Scattered crackles

Increased work of breathing Agitation Lethargy followed by obtundation

Causes


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CausesMany conditions have been found to precipitateARDS. In some cases a predisposing conditioncannot be identified.The most common predisposing conditions:

Infection - Pneumonia of any etiology (especiallyviral) and systemic sepsis (especially gramnegative)

-

traumatic shock Aspiration - Gastric contents, near drowning,and toxic inhalation

Trauma - Pulmonary contusion, fat embolization,and multiple trauma

Other - Systemic inflammatory responsesyndrome, pancreatitis, postcardiopulmonarybypass, massive blood transfusion, drug ingestion(eg, heroin, methadone, barbiturates,salicylates)


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DIAGNOSIS SUPPORT ABG Other laboratory the underlying or

predisposing conditions. chest radio ra h

Chest CT Echocardiography

Sputum BAL A pulmonary artery catheter

Emergency Department Care


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Emergency Department Care1.Airway and support of ventilation and oxygenation are

the initial priorities of management (ABCs life )2.Perform ET intubation for hypoxemia refractory to

supplemental oxygen or for clinical signs of respiratoryfailure.3.Monitor vital signs frequently, especially with

echanical ventilation since arked decreases in

venous return can result with subsequent impairmentof cardiovascular function.4.An intravenous (IV ) line should be available at all

times for fluid and/or medication administration.5.Avoid excessive fluid administration. Use only what is

necessary to treat signs of intravascular volumedepletion or hypotension.6.Treat the underlying etiology.


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6.Mechanical ventilation with positive end-expiratorypressure (PEEP) of 5-10 cm H2O is effective inreducing intrapulmonary shunting and improvingoxygenation. Initiate with an FIO2 of 1 and decrease only

while monitorin ulse oximetr maintainin the

Emergency Department Care

oxygen saturation at 92-94%.

Select an initial tidal volume of 8-10 mL/kg andrespiratory rate of 10/minute.

Pressure-controlled ventilation offers severaladvantages over volume-controlled modes.

Hypercapnia alone on these settings should notprompt an increase in ventilator settings unlesspH is less than 7.1 (permissive hypercapnia).


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MEDICATION As of yet , no medication has been shown to affect

the pulmonary inflammatory process of ARDSdirectly. Late cases with a persistent fibroproliferativephase may respond to steroids, but these cases

.

Antibiotics following appropriate cultures in casesof pulmonary or extrapulmonary infection leadingto ARDS.

Cardiopulmonary support and treatment/eradicationof the underlying or predisposing conditions.

Catecholamines, such as dopamine and/ordobutamine.

FOLLOW UP


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FOLLOW-UP1.Further Inpatient Care:

Admit all patients to the ICU. Patients with earlyARDS with mild pulmonary findings may deterioraterapidly.

. omp ca ons:

Multiple organ failure Death

Permanent lung disease Oxygen toxicity Barotrauma Superinfection

3 P i


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3. Prognosis:

Mortality rate averages 60%. Nonsurvivors usually die from sepsis or

multiple organ failure. Survivors usually have a good outcome with

minimal, if any, persistent pulmonarys m toms.

Survivors of severe cases may have somedegree of permanent pulmonary fibrosis andsymptoms of restrictive lung disease.

4. Patient Education

For excellent patient education resources.


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PULMONARY EMBOLISM


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Pulmonary thromboembolism seringmerupakan komplikasi fatal daripenyakit trombosis vena

Normal, mikrotrombi (agregasi kecil sel

PULMONARY EMBOLISM

,dilisis sistem sirkulasi vena.

Patologis, mikrotrombi keluar darisistem fibrinolisis dan berkembangPE timbul ketika propagating clotterlepas dan beremboli membendung

saluran darah paru.

TROMBOSIS VENATROMBOSIS VENA::


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PEMBENTUKAN BEKUAN DI LUMEN VENAPEMBENTUKAN BEKUAN DI LUMEN VENA

Aliran turbulensi yangperlahan pada venamenginduksi stasis danmenyebabkan terjadinyakoagulasi

1.

Polimerisasi fibrinmenstabilkan bekuan

2. Bekuan terbentuk3.

TROMBOSIS VENATROMBOSIS VENA


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TROMBOSIS VENATROMBOSIS VENA

Trombus terus berkembang

Deep vein thrombosis

sepanjang vena

Pulmonary embolism

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

VTE risk factors:VTE risk factors:


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Numerous and commonNumerous and commonVTE risk factors include:Protein C deficiency 1

Protein S deficiency 1

Antithrombin deficiency 1

Activated protein C resistance 1

Prothrombin G20210A 1

High factor VIII concentration 1

Surgery 1

Trauma 2

Malignant disease 1

Acute MI 3,4

Acute infection 3,4

Acute heart failure 2

Acute respiratory failure 3,4

1

Age 1

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 profilemay lead to unexpectedevents. 2,7

Stroke 2

Congestive heart failure 2Hypertension 5

Myeloproliferative disorders 1

Nephrotic syndrome 2

Inflammatory bowel disease 2

Obesity 2

Varicose veins2

Immobility 1

Long-distance travel 6

Pregnancy and puerperium 1

Previous venous thrombosis 1

DEEP VENOUS THROMBOSIS


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DEEP VENOUS THROMBOSIS


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VTE: Often undetected untilVTE: Often undetected until


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too latetoo lateOver 70% of fatal PE

are detected postmortem 1,3

Approximately 80% of DVTsare clinically silent 2,3

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


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PULMONARY EMBOLISME

PATIENTS WITH SERIOUS MEDICAL ILLNESS, WHO


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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

- on- sc em c car omyopat y- 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, andOutcome Optimizing Pharmacological Management. Internal Medicine Consensus Reports. Juni 1, 2001: 1-8

PASIEN BEDAH DIANGGAP MEMILIKI RESIKO


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PASIEN BEDAH DIANGGAP MEMILIKI RESIKO

TERBESAR UNTUK DVT DAN PE.PENELITIAN PROSPEKTIF MENUNJUKKAN BILATIDAK ADANYA PROFILAKSIS, DVT AKUT DAPATTERJADI PADA :Pasien medis umum ditempat tidurkan selamaseminggu (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 Unit

setelah miokard infark (27-33%)Pasien asimptomatis setelah coronary artery bypassgraft (48%)

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) - S3 atau S4 gallop Thrombophlebitis Edema ekstrimitas bawah Cardiac murmur Cyanosis Pleuritis


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DIAGNOSTIC SUPPORT Clinical sign and Symptom

CXR D-dimer

Venous Ultrasonography Echocardiography Spiral CT Ventilation Perfution Scan Pulmonary Arteriography

Penatalaksanaan


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PenatalaksanaanI. Penanganan pada fase akut

- bed rest & elevasi kaki- mobilisasi dini

II. Terapi PEa. Antikoagulan:- Heparin pemantauan aPTT 1,5-2,5 kali

- LMWH- Dilanjutkan dengan antikoagulan oral (warfarin)

b. Thrombolityc Therapyc. Inferior Vena Cava Interuptiond. Pulmonary Embolectomye. Supportive Care

INHALASI ZAT TOKSIK


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TANGKI GAS, PIPA GAS BOCOR Tangki truk amonia, klorin, asam nitrit

tumpah Ledakan pabrik kimia, pabrik kertas,

INHALASI ZAT TOKSIK

Inhalasi asap pada kebakaran Trauma panas(particulate matter) padasaluran napas,iritasi, refleks

bronkokontriksi,asfiksia Gas, debu, uap, asap Cedera paru, ARDS


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Hidrogensianida

Pembakaran polyurethane,nitrocellulose (sik nilon wool)

Asfiksia jaringan dengan menghambataktiviti cytochrome axidase intrasel


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sianida nitrocellulose (sik, nilon, wool) aktiviti cytochrome axidase intrasel,

menghamabt produksi ATP, meningkatkananoksia sel

Hidrogen sulfida Fasilitas pengolahan limbah,gas volkanik, pertambanganbatubara, sumber air panasalami

Sama seperti sianida, asfiksia jaringandengan menghambat cytochrome axidase,meningkatkan kerusakan pada rantaitransport elektron, menghasilkanmetabolisme anaerob

Hidrokarbon Penyalahgunaan inhalan Narkotik system saraf pusat (SSP), status

Toksin sistemik

(toluene, benzena, freon),

aerosol, lem, bahan bakar kendaraan, pembersihpewarna kuku, bensin, cairanpembersih

anastesi, gejala gastrointestinal difus,

neuropati perifer dengan kelemahanumum, koma, kematian mendadak,pneiumonitis kimia, abnormaliti SSP,iritasi gastrointestinal, kardiomiopati,toksisiti ginjal

Organofosfat Insektisida, gas saraf Memblokade acetylcholinesterase, krisiskolinergik dengan peningkatanacetylcholine

Asap metal Oksidasi metal dari seng,perak magnesium, pembuatpermata

Gejala seperti flu (Flu-like symptoms(,demam, mialgia, lemah

PATOGENESIS CEDERA SALURAN NAPAS


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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


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Disturbed capillaryBlood flow

Microvaskular permeability

MacrophagesMediators

Neutrophyls

n er a an a veo arPulmonary

microcirculation

Injury to alveolarcapillary membrane ARDS

Damage, Edema


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DIAGNOSTIC SUPPORT

Anamnesis yang cermat Laringoskopi

ron os opi, A Foto toraks Laboratorium Toksikologi gas, Radioisotop


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TATA LAKSANASUPORTIF Tanda vital tetap stabil,

paparan zattoksik, eliminasi zat toksik

N aman life s savin A B C.. se era

Resusitasi, sistim respirasi,patensi salnapas, ventilasi, oksigenisasi Monitor, hemodinamik Cegah kerusakan organ lain Rawat intensif

KHUSUS


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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

SEVERE OR LIFE-THREATENING


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ASTHMASevere 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

Ventilation-Perfusion mismatch


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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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Start Steroid : 200 mg of hydrocortisonintravenously.Continue either hydrocortison 100 mg


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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


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ACUTE EXACERBATION of CHRONICOBSTRUCTION PULMONARY


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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


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Infective exacerbation (no new CXRchanges):Typically H.influenzae,S.pneumoniae,Moraxella catarrhalis. Commonlyviral

Community acquired pneumonia (new CXRchanges) Ex r kn wn ll r n

Pneumothorax Expansion of large bullae Sputum retention with lobar or segmental

collapse (atelectasis) Myocardial ischaemia,pulmonary oedema,cor

pulmonale,pulmonary embolism

MANAGEMENT


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TREAT HYPOXIA AND RESPIRATORYFAILURE

- Oxygen therapy- Arterial blood gases

-- Mechanical ventilation- Respiratory stimulants (doxapram)

TREAT BRONCHOSPASM AND


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OBSTRUCTION- Nebulized -agonist (salbutamol 5 mg orterbutalin 10 mg q4h)

- Aminophyline iv or iv -agonist- Nebulized ipatropium bromide 500g 6

our y- Give steroid:200mg hydrocortison iv or

30-40 mg prednison po- Physiotherapy (clearing bronchial

secretions)

TREAT CAUSE of EXACERBATION


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Infection Pneumothorax Pulmonary oedema Pulmonary embolism

Atelectasis

SEPTIC SHOCK


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SIRS (Systemic Inflammatory ResponseSyndrome) represents an organisms response toinflammation that may or may not be due to

infection ( trauma,burns, pancreatitis ,infection ) Criteria SIRS : ( 2 or 4 )- Fever 38 C or H othermia 20/min or

PaCO290/min)- WBC (>10.000/mm 3 or


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(one required) such as altered mentation,hypoxemia, elevated plasma lactate level,oliguria, in SEPSIS,is termed severe

sepsis. Patient who develop hypotension is called

ep c oc Immediate Measures :

- Maintain airway and Ventilation

- Establish Adequacy of Circulation- Obtain Complete Vital Signs

- Regulated Blood Pressure


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- Correct Asidosis- Correct Coagulopathy- Select Theraphy- Search for Source of Infection- Perform Dia nostic Tests

- Start Antibiotic Treatment DISPOSITIONIntensive care is required for all patients inseptic shock and for those seriously ill withinfection.

SEVERE PULMONARY EDEMA


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Clinical : Extremely dyspneic especially in

the supine position,cough up frothy,pinksputum.

pain, tachycardia,distended neck veins orhepatojugular reflux,peripheral edema,cardiomegaly,gallop.Wheezing may alsobe present (so-called cardiac asthma)

Noncardiac Pulmonary Edema has many causes.

D d (h i d h i ) i


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Drug overdose (heroin and other narcotis),septicshock,pulmonary contusion,pancreatitis and fatembolism.

Treatment- Give oxygen 10-15 L/min,by nonrebrether mask- -

bumetanide 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)

- NIPPV (noninvasive positif pressure

il i ) i i i i i


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ventilation) via continuous positive airwaypressure (CPAP) or bilevel positive airwaypressure (BiPAP)


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emd166 slide pulmonary emergency medicine

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