KEGAWATAN PENYAKIT DALAM

Fenny Febrianty
Internal Medicine Department
Medical Faculty, Jambi University

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Topik pembicaraan

• Kegawatan paru
– Pneumotoraks
– Hemoptisis
– Status asthmatikus

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 PNEUMOTORAKS

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Definition

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

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 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

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Etiology of Secondary Spontaneous
Pneumothorax

• Obstructive lung disease (COPD, Asthma)

• Interstitial lung disease (IPF, Non-specific interstitial
pneumonitis, eosinophillic granuloma, sarcoidosis, etc)
• Infection (pneumonia, tuberculosis)
• Malignancy (lung cancer, pulmonary metastasis,
complications of chemotherapy)
• Connective tissue disease (RA, ankylosing spondylitis,
Marfan’s syndrome, scleroderma)
• Other (Catamenial, pulmonary infarction, PAP, etc)
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Tension pneumothorax
• A tension pneumothorax is a medical emergency as air
accumulates in the pleural space with each breath. The
increase in intrathorasic pressure results in massive
shifts of the mediastinum away from the affected lung
compressing intrathorasic vessels
• Severe tachycardia (Heart rate >140 beats/ mnt)
• Hypotension
• Cyanosis,
• Tracheal deviation

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Tension pneumothorax

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Proposed mechanism of alveolar rupture
in spontaneous pneumothorax

A. Normal structures B. Overdistention of

marginal alveoli
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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
• Symptoms in secondary spontaneous pneumothorax
more severe than patients with PSP
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Pneumothorax
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 for pneumothoraces are to
evacuate the space, achieve closure of the leak, and
either 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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Tube thoracostomy/WSD

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3 bottle chest tube drainage system

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 Status asthmaticus

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 Mechanisms Underlying the
Definition of Asthma
Risk Factors
(for development of asthma)

INFLAMMATION

Airway
Hyperresponsiveness Airflow Obstruction

Risk Factors Symptoms

(for exacerbations)
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Klasifikasi asthma akut
Astma ringan Asthma sedang Asthma berat
Sesak napas Waktu berjalan Waktu berbicara Saat istirahat
Bisa berbaring 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 Tidak ada Mungkin ada Biasanya ada
paradoksus
Otot bantu Biasanya tidak Biasanya ada Biasanya ada
napas
Mengi Akhir ekspirasi Akhir ekspirasi Sepanjang ekspirasi
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Klasifikasi asthma akut

Astma ringan Asthma Asthma berat

sedang
APE % > 70-80% 50 - 70% < 50%
terhadap
standard
PO2 Normal > 60 mmHg < 60 mmHg
(mungkin sianosis)
PCO2 < 45 mmHg < 45 mmHg > 45 mmHg
SO2 > 95% 91-95% < 90%

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 Definition

Severe attack of asthma poorly responsive to

adrenergic agents and associated with signs or
symptoms of potential respiratory failure

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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
– Obtain if diagnosis is in doubt, patient is high-risk
(IVDU, immunosuppressed, chronic pulmonary
disease), or if complications are suspected
(pneumothorax)
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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 0 – 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 : Serangan Asma Berat :

- APE 5–70% 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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- 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 : Dirawat di RS (ruang biasa)

-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
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ketat
- Inhalasi agonis  - 2 
Rawat di ICU :
inhalasi antikolinergik
- Inhalasi Agonis  - 2 
- Kortikosteroid
antikolinergik
- Oksigen
- Kortikosteroid IV
- Pertimbangan Aminofilin IV
- Pertimbangkan Agonis
- Pantau APE, saturasi O2,
-2 Sc, IM dan IV
nadi, teofilin
- Intubasi dan ventilasi
mekanik
 Perbaikan Tidak ada perbaikan

Dipulangkan Masuk ICU

Jika APE 50% dan terus menerus Jika tidak ada perbaikan dalam
dalam pengobatan peroral / inhalasi 6 – 12 jam

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 Emergency therapy of the asthma exacerbation

Asthma patient with Consider causes

severe symptoms

Clinical Evaluation A. Oxygen B. Monitor C. Obtain

First-Line Therapy A. Beta-2 agonist B. IV Corticosteroid

Second-Line Therapy Subcutaneous Beta Agonist

(Epinephrine or Terbutaline)

Third-Line Therapy Methylxanthines

(Aminophylline/Theophylline)

A
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 A

Adjunctive therapy A. Ipratropium B. Antibiotics C. Magnesium

Bromide Sulfate

PROCEED FUTHER IN THE SETTING

OF PATIENT DETERIORATION DESPITE
MAXIMAL MEDICAL THERAPY

Intubation and Mechanical Intubation and Mechanical Ventilation

Ventilation Considerations

Postintubation Therapy Step 1 Therapy : Sedation

Step 2 Therapy : IV Ketamine
Step 3 Therapy : General inhalation anesthesia
(avoid halothane)
Step 4 Therapy : Extracorporeal lung assist

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 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
• 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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Diagnostic Clues in Hemoptysis: Physical History

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 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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Management (1)

Difficult
• Multitude of potential etiologies.
• Course of bleeding is unpredictable.
• It is frightening to see patients dying from asphyxiation,
even in spite of intubation.
• There is no consensus regarding the optimal
management of these patients

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 Management (2)
• Adequate airway protection, ventilation, and
cardiovascular function
• Intubate if pt. has poor gas exchange, rapid ongoing
hemoptysis, hemodynamic instability, or severe
shortness of breath
• Reverse coagulation disorders
• A major priority in the acute management in protection
of the non-bleeding lung.
• Spillage of blood into the non-bleeding lung can either
block the airway with clot or fill the alveoli and prevent
gas exchange.
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 Management (3)

Protection of non-bleeding lung

• Place bleeding lung in the dependant position
• Selectively intubate the non-bleeding lung- easiest if
you want to intubate right main stem bronchus during
a left lung bleed.
• Balloon tamponade via bronchoscopy
• Placement of a double lumen ETT specially designed
for selective intubation of the right or left main stem
bronchi

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Management (4)
• 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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TERIMAKASIH

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