Pemicu 4 Blok KGD

Darren Christopher
405140071
ARDS
 ARDS
• Acute respiratory distress syndrome (ARDS) occurs when fluid
builds up in alveoli. More fluid in your alveoli means less oxygen can
reach your bloodstream. This deprives your organs of the oxygen
they need to function.

• The signs and symptoms of ARDS can vary in intensity, depending

on its cause and severity, as well as the presence of underlying
heart or lung disease. They include:

1. Severe shortness of breath

2. Labored and unusually rapid breathing
3. Low blood pressure
4. Confusion and extreme tiredness
 Diagnosa
• Imaging:
1. Chest X-ray(reveal either ARDS cause by cardiogenic or non-
cardiogenic, reveal how much fluid in your lung)
2. CT-scan.

• Lab tests
1. Arterial Blood Gas(ABG) -> reveal oxygen saturation to Hb
2. Sputum culture -> if suspect of infection

• Heart test
1. Electrocardiogram. -> diagnostic right side-heart hypertrophy
2. Echocardiogram -> reveal heart structure abnormalities
 Management
• Supplemental oxygen -> milder symptoms or as a
temporary measure. Delivered through non-rebreathing
mask.

• Mechanical ventilation -> last choice if supplemental

oxygen not adequate

• Fluid -> preventing shock. Carefully managing the amount,

too much -> lung edema.

• Antibiotic -> if ARDS cause by infection.

• Analgesic or sedation -> for pain reliever
Respiratory Failure
 Respiratory Failure
• A syndrome that respiratory fail either in gas exchange function or
ventilation function

• Classification:

1. Hypoxemic(Type I – Pulmonary fail) : most common. Mostly because of

collapse or filling in alveolar units. In this type, both PO2 and PCO2
decrease.
2. Hypercapnic(Type II – Ventilatory fail) : Mostly because of drug
overdose, chest wall abnormalities(barrel chest), or severe airway
disorders(asthma, COPD). In this type, PCO2 elevated >50mmHg.
3. Acute : develops over minutes – hours. Life-threatening because
derangement in arterial blood gases and acid-base status. Usually pH
<7.3
4. Chronic: develops over several days or longer. Usually pH is normal
Respiratory Failure
Asthma
 Asthma
• Exacerbations of Clinical Features
asthma  feared by • Chest tightness
patients  life- • Wheezing
threatening
• Dyspnea
• Controller therapy : • Cyanotic
prevent exacerbations
 ICS* and
combination inhalers
(very effective)
 Physical Examination
• ↑ ventilation
• Hyperinflation
• Tachycardia
• Pulsus paradoxus(rare)
• ABG :
– Hypoxia
– PaCO2 low (hyperventilation)
– A normal or rising PaCO2 : impending respiratory failure 
requires immediate monitoring and therapy.
• Chest roentgenogram : not usually informative, but
may show pneumonia or pneumothorax.
 Acute Severe Asthma (Status
Asthmatics)
• A severe asthma state and can’t be manage by normal agonist β-2
• Etiology: non-adequate asthma treatment
• Clinical manifest:

1. Potential life-threatening:
• Can’t complete 1 full sentence in single breathe
• Not able to stand from sitting position
• Tachypnea, RR > 25x/minutes
• HR > 110 bpm

2. Life-threatening:
• Silent chest sound on auscultation
• Cyanosis
• Unconsciousness
• Bradhycardia
• Malaise
 Management (for children)
• A child with a first episode of wheezing and no
respiratory distress can usually be managed with
supportive care.
• If the child is in respiratory distress (acute severe
asthma) or has recurrent wheezing, give salbutamol
• Reassess the child after 15 min to determine
subsequent treatment :
• Respiratory distress resolved  home care with
prescribed ihaled salbutamol
• If persists  treat with oxygen, rapid-acting
bronchodilators, and other drugs*
 Management
1. Oxygen : keep oxygen saturation >95%
2. Rapid acting bronchodilators :nebulized (2.5 mg salbutamol add
with 2-4 ml sterile saline) and with a spacer device
3. Subcutaneous adrenaline : 0.01 ml/kg of 1:1000 solution (up to
max of 0,3 ml)
4. Steroids : if a child has a severe or life-threatening acute attack of
wheezing  oral prednisolone 1 mg/kg, for 3-5 days max or 20
mg for children aged 2-5 yrs.
5. Magnesium sulfate :
– additional benefit in children with severe asthma treated with
bronchodilators and steroids!
– Better safety profile than aminophylline
– MgSO4 50% as a bolus of 0,1 ml/kg Iv over 20 min
 Management
• Supportive care : ensure the child receives daily
maintenance fluids appropriate for his or her age
• Monitoring : a hospitalized child should be
assessed every 3h or every 6h as the child shows
improvement

• Complications : obtain a chest X-ray to look for

evidence of pneumothorax.
• Follow-up care : inhaled salbutamol should be
prescribed
COPD
Pneumonia
 Pneumonia Aspirasi
• Definisi: merupakan pneumonia yang disebabkan karena masuknya
makanan, cairan, atau muntahan ke dalam paru-paru.
• Etiologi: benda asing(cairan, saliva), bakteri(tergantung kesehatan)
• Faktor resiko: orang tua, poor gag reflex, problem with swallowing,
• Tanda dan gejala: demam, lemah, batuk berdahak dengan sputum
bewarna kehijauan atau gelap, sakit dada, swallowing problem,
dyspnea.
• Komplikasi: abses paru, shock, bacteremia, kematian
• Diagnosis: PF -> inspeksi(cyanosis -> oksigen menurun, setengah
sadar), palpasi(takikardi), auskultasi(crackling). PP -> arterial blood
gas, x-ray, pulse oxymetry, swallowing test, sputum culture,
bronchoscopy
• Tatalaksana: antibiotik, ventilator
Pneumothorax
 Pneumothorax
• Occurs when free air enters the potential
space between the visceral and parietal
pleura.
• Classification:
1. Primary pneumothorax : occur without
clinically apparent lung disease
2. Secondary pneumothorax : occur in patients
with underlying lung disease.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 Pneumothorax
• Classic symptoms: sudden onset of dyspnea
and ipsilateral, pleuritic chest pain.
– Peluritic component: resolve within 24 hours
– Sinus tachycardia  the most common physical
finding
– Clinical hallmarks of tension pneumothorax:
tracheal deviation away from the involved side,
hyper-resonance of the affected side,
hypotension, and significant dyspnea

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 Pneumothorax
• Imaging:
– Chest X-ray: demonstrates loss of lung markings in
the periphery and a pleural line that runs parallel
to the chest wall.
Critically ill patients (cannot be moved to an erect
position) look for the deep sulcus sign, a deep
lateral costophrenic angle, on the affected side.
– US  detects traumatic pneumothorax
– Chest CT  can detect other pathology such as
pulmonary blebs.
Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.
Tuberculosis
 Pulmonary Tuberculosis
• Etiology: infection Mycobacteria tuberculosis complex
(MTBC)
• Transmission via droplet nuclei & airborne
• Classification:

1. Primary Tuberculosis
– Usually asymptomatic, often detected only by a positive
screening tuberculin skin test or by abnormalities on chest
radiograph
– Common symptoms include fever, malaise, weight loss,
and chest pain
2. Reactive Tuberculosis
 Clinical Manifestation
• Cough—usually productive
• Sputum—usually mucopurulent or purulent
• Haemoptysis—not always a feature, volume variable
• Breathlessness—gradual increase rather than sudden
• Weight loss—gradual
• Anorexia—variable
• Fever—may be associated with night sweats
• Malaise—patient may realise only retrospectively,
when feeling better after treatment
• Wasting and terminal cachexia—late, ominous signs
 Diagnose
• Tuberculin test
– injecting a small amount of fluid (called tuberculin)
– return within 48 to 72 hours
– result depends on the size of the raised, hard area or
swelling
• Specimen collection
– at least three sputum samples, each 5 to 10 mL,
should be collected at least 1-hour apart.
– For those patients unable to expectorate
spontaneously, sputum induction (with nebulized
hypertonic saline) or bronchoalveolar lavage (BAL)
 Tuberculosis
• Possible complications of TB include:
– Development of a multidrug resistant strain
– TB beyond the lungs, frequently associated with
HIV
– TB-related meningitis, in children
– Pneumothorax (collapse of a lung due to a buildup
of gas between the membranes that surround the
lungs)
– Massive coughing up of blood

http://www.umm.edu/health/medical/altmed/condition/tuberculosis
Pleural Effusion
 Efusi Pleura
• Definisi: merupakan koleksi abnormal cairan pada rongga pleura akibat dari
produksi cairan berlebih atau kurang absorbsi atau bisa dua-duanya
• Etiologi: altered permeability of pleural membrane(inflammation), reduction of IV
oncotic pressure(cirosis, nephrotic syndrome), Increased capillary permeability or
vascular disruption (eg, trauma, malignancy), Increased capillary hydrostatic
pressure in the systemic and/or pulmonary circulation (congestive heart failure),
Reduction of pressure in the pleural space, preventing full lung expansion or
"trapped lung" (extensive atelectasis), Decreased lymphatic drainage or complete
blockage, including thoracic duct obstruction or rupture (malignancy, trauma),
Increased peritoneal fluid, with migration across the diaphragm via the lymphatics
or structural defect (cirrhosis), Movement of fluid from pulmonary edema across
the visceral pleura, Persistent increase in pleural fluid oncotic pressure from an
existing pleural effusion, causing further fluid accumulation
• Tanda dan gejala: dyspnea, batuk, sakit dada
• Pemeriksaan fisik: inspeksi(pengembangan dada asimetris),
palpasi(pengembangan salah satu paru tertinggal, fremnitus kurang pada salah
satu lapang paru), perkusi(dull, redup), auskultasi(pleural friction rub)
• Pemeriksaan penunjang: CXR(perselubungan)
• Tatalaksana: antibiotic(bila ada infeksi -> ampycillin, clyndamycin),
vasodilator(nitroglycerin), diuretik(furosemide), anticoagulan(heparin),
thoracentesis, thoracostomy, pleurodesis, pleural drainage,

http://emedicine.medscape.com/article/299959-overview
http://emedicine.medscape.com/article/299959-overview
thelancet.com