KEGAWATAN PENYAKIT DALAM

Sudarto
Divisi Paru Bagian Ilmu Penyakit Dalam
FK Unsri / RS M Hoesin Palembang

Topik pembicaraan
Kegawatan paru
Pneumotoraks
Hemoptisis
Status asthmaticus

Kegawatan jantung
Acute Coronary syndrome
Cardiogenic Shock
Acute Pulmonary Edema
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PNEUMOTORAKS

Definition
The accumulation of
air in the pleural
space with secondary
collapse of the
surrounding lung.

RONGGA PLEURA

A. Normal
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B. Efusi Pleura

Classification
Spontaneous pneumothorax
Primary spontaneous pneumothorax
Occurs without a precipitating event in a person
with no clinical evidence of lung disease

Secondary spontaneous pneumothorax

Occurs as a complication of underlying lung
disease (most often COPD)

Traumatic pneumothorax

Iatrogenic pneumothorax

Etiology of Secondary Spontaneous

Pneumothorax
Obstructive lung disease (COPD, Asthma)
Interstitial lung disease (Non-specific interstitial
pneumonitis, eosinophillic granuloma, sarcoidosis, etc)
Infection (pneumonia, tuberculosis)
Malignancy (lung cancer, pulmonary metastasis,
complications of chemotherapy)
Other (Catamenial, pulmonary infarction, PAP, etc)

Tension pneumothorax
A tension pneumothorax is a medical emergency
air accumulates in the pleural space with each breath.
The increase in intrathorasic pressure compressing
intrathorasic vessels
Severe tachycardia (Heart rate >140 beats/ mnt)
Hypotension
Cyanosis,
Tracheal deviation
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Tension pneumothorax

Each time we
inhale,
the lung collapses
further. There
is no place for the
air to
escape..

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10

Each time we
inhale,
the lung collapses
further. There is
no place for the
air to
escape..

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11

Heart is
being
compress
d

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Clinical signs
May be asymptomatic
Chest pain
Acute, localized to the side of the pneumothorax, and
typically pleuritic
Dyspnea/orthopnea (lung and cor problem)
Cough
Hemoptysis
Cyanosis
Subcutaneous emphysema
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Physical exam
I. S. Cembung sisi sakit
D. Tertinggal
P. Fremitus turun sampai
hilang
P. Hipersonor
A. Suara napas lemah
sampai hilang
Pada small pneumothorax PD dapat normal
Sukar dibedakan dengan PPOK

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Physiological consequences
Decrease of vital capacity
Decrease of PaO2
Decrease of total lung capacity
Decrease of functional residual capacity
Reduce of diffusing capacity

Coma, Death
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Radiology

Spontaneous pneumothorax.
The visceral pleural line is clearly
seen with the absence of vascular
workings beyond the pleural line.

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Estimation of the size of pneumothorax

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Treatment
The basic tenets of therapy :
evacuate the space
achieve closure of the leak
prevent or reduce this risk
The choice of treatment
Observation
Asymptomatic patient; Small unilateral pneumothorax
Asses for further progression
Simple aspiration
Tube thoracostomy/WSD (Simple; Continuous suction)
Pleurodesis
Thoracoscopy
Surgical

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Needle
Decompression

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Tube thoracostomy/WSD

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3 bottle chest tube drainage system

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Status asthmaticus

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Definition
An acute, severe asthma attack that doesn't
respond to usual use of inhaled bronchodilators and
is associated with symptoms of potential respiratory
failure

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Mechanisms Underlying the

Definition of Asthma
Risk Factors
(for development of asthma)

INFLAMMATION
Airway
Hyperresponsiveness

Risk Factors
(for exacerbations)

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Airflow Obstruction

Symptoms

Klasifikasi asthma akut

Astma ringan

Asthma sedang Asthma berat

Sesak napas

Waktu berjalan
Bisa berbaring

Waktu berbicara Saat istirahat

Lebih suka duduk Duduk membungkuk

Berbicara

Kalimat

Kata-kata

Kata demi kata

Kesadaran

Mungkin agitasi

Biasanya agitasi

Biasanya agitasi

RR

< 20 x

20 30 x

> 30 x / menit

Nadi

< 100 kali/menit

100-120 x/menit

> 120 kali/menit

Pulsus
paradoksus

Tidak ada

Mungkin ada

Biasanya ada

Otot bantu
napas

Biasanya tidak

Biasanya ada

Biasanya ada

Mengi

Akhir ekspirasi

Akhir ekspirasi

Sepanjang ekspirasi

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Klasifikasi asthma akut

Astma ringan Asthma
sedang

Asthma berat

APE %
terhadap
standard

> 70-80%

50 - 70%

< 50%

PO2

Normal

> 60 mmHg

< 60 mmHg
(mungkin sianosis)

PCO2
SO2

< 45 mmHg

< 45 mmHg

> 45 mmHg

> 95%

91-95%

< 90%

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Asthma mengancam jiwa

Tidak begitu sadar
Pemakaian otot bantu napas
Pergerakan torako abdominal yang
paradoksal
Tidak ada mengi
Bradikardi
Tidak ada pulsus paradoksus (otot napas
sudah lelah)

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Clinical Danger Signs

Use of accessory muscles of respiration
Brief, fragmented speech
Inability to lie supine
Profound diaphoresis
Agitation
Severe symptoms that fail to improve with initial
emergency department treatment
Life-threatening airway obstruction can STILL OCCUR
when these signs are not present
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Diagnosis
Hx: most powerful predictor that this may be life-threatening
is a prior intubation for an asthma attack
PEX: alteration in consciousness, fatigue, upright posture,
diaphoresis, accessory muscle breathing.
Tachycardia, tachypnea, pulsus paradoxus
IMPORTANT: look in the mouth as obstruction might be
in the upper airway (epiglottitis, angioedema)
Peak Flow (PEFR): if pt is not too dyspneic. Best measure
of severity
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Diagnosis
ABG: Look at PaCO2. Resp drive almost always increased
in acute asthma hyperventilation decreased PaCO2.
Thus, an elevated or normal PaCO2 indicates airway
narrowing is so severe that the ventilatory demands
cannot be met. Failure is imminent
CXR: usually not helpful

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Obtain if diagnosis is in doubt, patient is high-risk

(IVDU, immunosuppressed, chronic pulmonary
disease), or if complications are suspected
(pneumothorax)

Resiko tinggi asthma berat

Sedang / baru saja lepas dari pemakaian steroid

sistemik

Mempunyai riwayat rawat inap dlm waktu 12

bulan terakhir

Riwayat intubasi karena asma

Mempunyai masalah psikososial atau psikiatri

Ketidaktaatan pengobatan asma

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Pengelolaan Serangan Asma di Rumah Sakit Menurut GINA

Penilaian Pertama : Tentukan berat ringannya serangan asma (lihat tabel 1)
Penanganan Permulaan :
- Inhalasi short acting -2 agonist dengan nebulisasi, 1 dosis selama 20 dlm 1 jam.
- Oksigen untuk mencapai saturasi oksigen 90% (95% pada anak-anak)
- Kortikosteroid sistemik, jika tidak ada respons segera atau jika ada pasien baru
mendapat steroid per oral, atau jika serangan asmanya berat
- Sedasi merupakan kontra indikasi pada penanganan serangan akut / eksaserbasi

Ulangi Penilaian

Serangan Asma Sedang :

- APE 50%70% dari nilai yg diperkirakan
nilai terbaik
- Pemeriksaan fisik Asma sedang, otot
bantu
- Inhalasi Agonis - 2 setiap 60
- Pertimbangkan kortikosteroid
- Ulangi pengobatan 1 3 jam

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Serangan Asma Berat :

- APE < 50% nilai terbaik
- Pemeriksaan fisik sama berat saat istirahat
- Riwayat pasien resiko tinggi
- Inhalasi Agonis -2 tiap jam atau
kontinue inhalasi anti kolinergik
- Oksigen
- Kortikosteroid sistemik
- Pertimbangan Agonis - 2 Sc, IM atau IV

Respon Baik
- Respon selama 60 sesudah
terapi terakhir
- Pemeriksaan fisik normal,
APE > 70%
- Tidak ada distress
-Saturasi O2 > 90% (anak 95%)

Respon tdk baik dlm 1-2 jam

- Riwayat pasien risiko
tinggi
- Pem.fisik : gejala ringan /
sedang
- APE > 50%, tapi < 70 %
- Saturasi O2 tidak membaik

Respon Buruk dlm 1 jam

- Riwayat : risiko tinggi
- Pemeriksaan fisik :
Asma berat, mengantuk
- APE < 30%
- PCO2 > 45 mmHg
- PO2 < 60 mmHg

Dipulangkan :
-Lanjutkan pengobatan & Agonis
- 2 inhalasi
- Pertimbangkan kortikosteroid
oral (pd kebanyakan pasien)
- Pendidikan pasien
- Minum obat secara benar
- Tinjau lagi rencana kerja
(action plan)
- Tindak lanjut pengobatan yg
ketat

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Dirawat di RS (ruang biasa)

- Inhalasi agonis - 2
inhalasi antikolinergik
- Kortikosteroid
- Oksigen
- Pertimbangan Aminofilin IV
- Pantau APE, saturasi O2,
nadi, teofilin

Rawat di ICU :
- Inhalasi Agonis - 2
antikolinergik
- Kortikosteroid IV
- Pertimbangkan Agonis
-2 Sc, IM dan IV
- Intubasi dan ventilasi
mekanik

Perbaikan

Tidak ada perbaikan

Dipulangkan

Masuk ICU

Jika APE 50% dan terus menerus

dalam pengobatan peroral / inhalasi

Jika tidak ada perbaikan dalam

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6 12 jam

HEMOPTYSIS

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Definition
The spitting of blood derived from the lungs
or bronchial tubes as a result of pulmonary or
bronchial hemorrhage

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 Based on the volume of blood loss:

Massive and non massive
Only 5% of hemoptysis is massive but mortality is
80%.
Massive
Blood lose > 600 ml / day
Blood lose < 600 ml / day, but > 250 ml, Hb < 10 g
% and hemoptysis still continue
Blood lose < 600 ml / day, but > 250 ml, Hb > 10 g
% and hemoptysis still continue in 48 hours
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Differentiating Features of
Hemoptysis and hematemesis

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Etiology
Infection (bronchitis, pneumonia, lung tuberculosis,
HIV)
Lung cancer (include metastatic lesions)
Old tuberculosis
Pulmonary venous hypertension (LV heart failure, MS,
Pulmonary emboli)
Idiopathic

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Etiology: Classification by site

Tracheobronchial source
Bronchitis
Bronchiactasis
Neoplasm
Broncholithiasis
Airway trauma
Foreign body

Pulmonary Vascular source

Pulmonary embolism
Arteriovenous malformations
Pulmonary arterial hypertension
Pulmonary venous hypertension
(Mitral stenosis)

Pulmonary artery rupture

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Pulmonary Parenchymal
Source
Lung abscess
Pneumonia
TB
Mycetoma (Fungus Ball)
Goodpastures Syndrome
Idiopathic pulmonary hemosederosis
Wegeners Granulomatosis
Lupus pneumonitis
Lung contusion

Miscellaneous/rare causes
Pulmonary endometriosis
Systemic coagulopathy
Use of anticoagulants or thrombolytics

Physical Examination
Vital signs
Constitutional signs (cachexia, level of distress)
Skin and mucous membranes
Lymph node
Cardiovascular examination
Lung examination
Abdominal examination
Extremities
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Physical Examination
Telangiectasias (hereditary hemorrhagic telangiectasia)
Skin rash (vasculitis, SLE, fat embolism, infective
endocarditis)
Splinter hemorrhages (endocarditis, vasculitis)
Clubbing (chronic lung diseases)
Chest bruit or murmur that increases with inspiration
(large pulmonary AV malformations)
Cardiac murmurs (congenital heart disease,
endocarditis with septic emboli, mitral stenosis)
Legs (Deep venous thrombi)
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Komplikasi
Asfiksia
Kegagalan kardiosirkulasi ( hipovolemi )
Setiap batuk darah sebaiknya dirawat kecuali blood
streak
Perlu evaluasi :
Banyaknya perdarahan
Pemeriksaan fisik
Pemeriksaan foto toraks
Pemeriksaan laboratorium ( segera )

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PENATALAKSANAAN
Tujuan
1.Mencegah asfiksia
2.Melokalisasi asal perdarahan
3.Menghentikan perdarahan
4.Mendiagnosis dan menatalaksana
penyakit dasar
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TAHAP I. Pembebasan jalan napas dan stabilisai

penderita

Menenangkan dan mengistirahatkan penderita

Penderita diberitahu agar tidak takut
membatukkan darah
Menjaga agar jalan napas tetap terbuka, bila perlu
dilakukan penghisapan (dapat dg bronkoskop)
Resusitasi cairan

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 Penderita dg refleks batuk baik posisi duduk

dan diinstruksikan cara membatukkan darah dg
benar
Penderita dg KU berat dan refleks batuk tidak
adekuat posisis trendelenberg ringan dan
miring ke sisi yang sakit
Bila batuk darah terus berlanjut pasang ETT
Bila terjadi gagal napas pasang ventilasi
mekanik

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TAHAP II. Lokalisasi sumber dan mencari

penyebab perdarahan

Tahap kedua ini dapat dilakukan dengan

pemeriksaan radiologi (foto toraks, CT scan,
angiografi)
Pemeriksaan bronkoskopi menggunakan
bronkoskop fleksibel atau rigid

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TAHAP III. Pemberian terapi spesifik

Terapi spesifik ditujukan untuk menghentikan dan

mencegah berulangnya perdarahan :
1.Terapi dengan bronkoskop
2.Terapi medikamentosa
3.Embolisasi arteri pulmonalis / bronkialis
4.Bedah

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 Management with Bronchoscopy

Lavage with iced saline and application of topical epinephrine
(1:20,000), vasopressin, thrombin, or a fibrinogen-thrombin
combination.

Arterial embolization
85% of the time the bleeding stops after embolization
10-20% of patients re-bleed in the following 6-12 months

Surgery
Lower mortality
Highest risk patients were not considered to be surgical
candidates and were managed medically (active TB, cystic
fibrosis, diffuse alveolar hemorrhage)

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Acute coronary syndrome

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Acute coronary syndrome

Keadaan gawat darurat
Perasaan tidak enak di dada / gejala lain
akibat iskemia miokard.
SKA mencakup :
- ST elevation myocardial infarct (STEMI)
- Non STEMI
- Unstable angina Pectoris
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Diagnosis
1. Gejala klinis
Nyeri dada
Lokasi, sifat nyeri, penjalaran, perbaikan dengan istirahat /
nitrat, faktor pencetus dan gejala penyerta

2. Gambaran EKG
STEMI : Elevasi segmen pada 2 atau lebih sadapan
NSTEMI : Depresi segmen ST, Inversi gel T dalam
UAP
: Depresi segmen ST

3. Petanda biokimia
CK MB, CK NAC, Troponin T > 2x nilai normal

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Inferior myocardial infarction

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Anteroseptal myocardial infarction

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Complications
Recurrent unstable angina pectoris
Arrhythmia
Left ventricular failure
Cardiogenic shock
Cardiac arrest
Sudden death
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Management
Bed rest
Oxygen
EKG monitor
Intravenous access
Nitrogliserin sublingual ( if systolic >90 mmHg without
bradycardia )
Analgesic adequately (Morphine)
Aspirin
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Trombolytic (with indication)

SYOK KARDIOGENIK

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Definition
Cardiogenic shock is a state of inadequate
tissue perfusion due to cardiac dysfunction,
usually acute myocardial infarction

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 The most common cause of death in hospitalized

patients with acute myocardial infarction
Most extreme form of pump failure occurs in about
15% of acute MI patients
Usually occurs when 40% or more of the left
ventricular muscle mass infarcts
Mortality is 85% or more with treatment
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Signs/Symptoms
Poor tissue perfusion, including :
Oliguria
clouded sensorium, confusion, restlessness, anxiety,
stupor, coma
Cool, clammy skin
Pallor
Weak or absent extremity pulses
Tachycardia
Slow or absent capillary refill
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 BP < 90 systolic or > 30mmHg below normal

BP is NOT the same as perfusion
Shock can be present with a normal BP
Evaluate signs of peripheral perfusion in addition to
BP

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Management
Treatment Priorities

Rate
Rhythm
BP (Volume, Pump/Vascular tone)

Correct major disorders of rate, rhythm before directly

treating BP
Improve oxygenation and peripheral perfusion
Avoid increasing cardiac workload
Identify source of problem

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Acute pulmonary edema

Volume problem
Pump problem
Rate problem

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Acute pulmonary edema

IV/O2/ECG Monitor
If BP > 90-100 mm Hg

furosemide 0.5 1.0 mg/kg slow IV (or twice

patients single daily dose up to 120 mg)
Morphine 2 10 mg slow IV
Nitroglycerin 0.4 mg SL

If BP < 90 mm Hg

Vasopressors based on SBP

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Pump problem
IV/O2/ECG Monitor
SBP <70 mmHg:
norepinephrine 0.5 30 mcg/min IV inf

SBP 70 100 mm Hg & shock

dopamine 5 15 mcg/kg/min IV inf

SBP > 100 mm Hg w/o shock

dobutamine 2 20 mcg/kg/min IV inf

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TERIMA KASIH

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