Download Problem 56 - Shortness of Breath

Shortness of Breath
Endless causes of Dyspnoea but remember the emergency presentations!
Wheezing?
ASTHMA, COPD, HF, ANAPHYLAXIS
Stridor? (upper airway obs)?
Foreign body/tumour, ACUTE EPIGLOTTITIS, ANAPHYLAXIS, TRAUMA
Crepitations?
HF, PNEUOMONIAE, BRONCHIECTASIS, FIBROSIS
Clear chest on examination?
PE, METABOLIC ACIDOSIS, ANAEMIA, DRUGS, SHOCK, CNS
Also remember
PNEUMOTHORAX (pain, inc. resonance, tracheal deviation)
PLEURAL EFFUSION (stony dullness)
Emergency situation
Airway –
Inability to talk, stridor or gesticulating to neck – consider upper airway obstruction.
Compromised airway call 2222 or fast bleep anaesthetist.
If patient is in a really bad way – needle cricothyroidotomy to buy time if your a
mega hero.
Breathing
1. Assess Respiratory rate and work of breathing.
2. Monitor SpO2 and check ABG
3. High flow O2 via non rebreathing mask (caution if COPD but HYPOXIA KILLS BEFORE
HYPERCAPNIA)
4. Nebulised bronchodilators – Salbutamol 5mg. Check response and repeat.
5. If evidence of tension pneumothorax – needle decompression.
6. Beware of failing respiratory effort – decompensating asthma. – Fall in RR can be falsely
re-assuring
7. If you get drop in Sats, GCS or a rise in PaCO2 call for SENIOUR HELP
Circulation
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4.
Establish IV access.
Assess heart rate and rhythm – Arrhythmias can present as SOB.
Pop them on a cardiac monitor.
Check BP and CRT – Taychpnoae response to shock?
Give fluids if haemodynamically unstable.
Evidence of Acute Heart Failure?
5. DEFG – Don’t ever forget glucose. Check the BM because DKA presents with Kussmaul’s
respiration.
Investigations
CXR
ECG
Spirometry
Haemaglobin
Also depending on case; Blood gases, Lung fuction tests, VQ scan for PE (or now CT pulmonary
angiograms as they show emphysema aswell) Cardiac ultrasonography, BNP (heart failure), Exercise
ECG, Cardiac catherisation
SEVERE PULMONARY OEDEMA
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Caused by left ventricular failure, ARDS, trauma, fluid overload, head injury?
Symptoms; dyspnoea, orthopnoea, pink frothy sputum.
Signs; distressed, pale, weak, pink frothy sputum, gallop rhythm, raised JVP, lung
crackles, wheeze.
Ix; CXR cardiomegaly, kerley b lines, shadowing, shadowing in costophrenic angles, fluid
in lung fissures. ECG, U&E, ECHO.
Monitor bp heart rate resp rate and urine
Mx; Oxygen 100%, Diamorphine 2-5mg slowly, Furosemide 40-80mg IV slowly, GTN 2
puffs, then iv nitrates
ACUTE SEVERE ASTHMA
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Take hx of previous attacks and any ITU admissions, check PEF, blood gases, ability to
talk? CXR( infection and pneumothorax)
Severe attack, unable to talk, resps >25, pulse>110, PEF<50
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Life threatening; PEF<33%, silent chest, unable to breathe, low sats, bradycardic,
confusion, coma...dead
Rx; 5mg salbutamol nebs with O2. Prednisolone 40-50 mg/24 PO initially. Then
hydrocortisone 100mg iv, ipratropium 0.5mg every 4-6h. THEN repeat salbutamol
discuss with ITU, MgSO4 2g IV over 20 min then consider aminophylline
Ipratropium, magnesium sulphate 1.2-2g iv over 20min, then aminophylline
(bronchodilator)
Mx; monitor closely checking sats, PEF, blood gases.
ACUTE EXACERBATION OF COPD
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Past 3B exam questions
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What is the initial dose of salbutamol that can be given nebulised?
What is the dosage of prednisolone?
Name two other drugs that can be used in the Rx of asthma?
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Exacerbated by winter and viral infection
Presentation; SOB, wheeze, cough, reduced exercise capacity.
Ix; FBC, sputum cultures, X ray, UEs, Blood cultures, Blood gases, ECG?
Acute Mx; oxygen start at 24% adjust according to the PaO2. Give nebulised salbutamol
5mg/4h and ipratropium 500micrograms/6h. 200mg of IV hydrocortisone and 3040mg of oral pred. Then give abx if necessary and then give PAP ventilation(expert
opinion)
Long term, discuss with the gp about lowering steroids. Prescribe a suitable short acting
beta2 agonist and ipratropium. IF severe at home give steroids as trial for improvement
and home oxygen if required.
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MASSIVE PULMONARY EMBOLUS
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Symptoms; pleuritic chest pain, haemoptysis, chest pain, palpitations, tachypnoea,
sob,syncope,
Signs; tachycardia, tachypnoea, gallop rhythm, increased JVP, loud p2, cyanosis
Ix; U&E, FBC, LFT, clotting, d-dimer, ecg; (tachycardia, s1, q3, t3. Deep s waves in 1, q
waves in 3 and inverted t waves in 3)
CXR; wedged shape area of infarction
ABG low O2 and low CO2, high pH
CTPA
Treat with low molecular weight heparin and warfarin in combination and then follow
protocol dependent on risk factors. if acute cause, six weeks treatment on warfarin
normally ok
PNEUMONIA
What are the common organisms that cause pneumonia?
Name four symptoms of pneumonia?
Name four signs of pneumonia?
What does CURB-65 stand for?
What antibiotics could you give for pneumonia?
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Common causes staph aureus, h influenza, strep pneumoniae, viral causes
Symptoms; fever, rigours, cough, wheeze, sob, dyspnoea, haemoptysis, pleuritic chest
pain.
Signs; tachycardia, tachypnoea, increased vocal resonance, creps, fever, signs of
consolidation) dull to percussion, reduced expansion, bronchial breathing)
Ix; FBC, CXR, Sputum culture, blood cultures, blood gases, u+e, LFT, CRP
Severity; CURB 65 Confusion (mini mental <8), Urea >7mmol/l, Resps >30, BP >90
systolic and over 65. If scoring above 2 needs IV abx and hospital.
ABX; amoxicillin 500mg-1g/ 8h, erythromycin 500mg/6h, if IV co-amoxiclav
HEART FAILURE
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Def- cardiac output is inadequate for the body’s requirements.
25-50% of patients die within 5years of diagnosis
Prev- 1-3% of general population and around 10% of elderly population
Different types of failure
o SYSTOLIC V DIASTOLIC FAILURE
 Systolic failure- inability of ventricle to contract normally, resulting in 
cardiac output. Ejection fraction is <40%
 Causes- IHD, MI, cardiomyopathy
 Diastolic failure- inability of ventricle to relax and fill normally causing
increased filling pressures. EF >50%.
 Causes- constrictive pericarditis, tamponade, restrictive
cardiomyopathy, hypertension.
 Both rarely occur together
o LEFT V RIGHT FAILURE
 May occur as left or right or both combined as congestive cardiac failure
 Left ventricular failure:
 Symptoms
o Dyspnoea
o Poor exercise tolerance
o Fatigue
o Orthopnoea
o PND
o Nocturnal cough
o Wheeze- cardiac asthma
o Nocturia
o Cold peripheries
o Weight loss
o Muscle wasting
 Right ventricular failure
 Causes
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o LVF
o Pulmonary stenosis
o Lung disease
 Symptoms
o Peripheral oedema
o Ascites
o Nausea
o Anorexia
o Facial engorgement
o Pulsation in neck and face (tricuspid regurgitation)
o ACUTE V CHRONIC FAILURE
 Acute- means new onset heart failure or decompensation of chronic heart
failure characterised by pulmonary and or peripheral oedema with or
without signs of peripheral hypoperfusion.
 Chronic- develops or progresses slowly. Venous congestion is common but
arterial pressure is well maintained.
o LOW-OUTPUT V HIGH-OUTPUT FAILURE
 Low cardiac output. When cardiac output is low and fails to rise normally
with exertion.
 Causes
 Pump failure- systolic and or diastolic HF, HR, negatively inotropic
drugs (anti-arrhythmics)
 Excessive preload- mitral regurgitation or fluid overload.
 Chronic excessive afterload- in aortic stenosis and hypertension
 High cardiac output. Rare. Output is increased in the face of excessive needs.
Failure occurs when CO fails to meet these needs.
 Causes
 Anaemia
 Pregnancy
 Hyperthyroidism
 Paget’s disease
 Arteriovenous malformation
 Beri beri
 Consequences- initially features of RVF then LVF becomes apparent.
Signs: to diagnose there should be signs of HF and objective evidence of cardiac dysfunction
(at rest). Use Framingham criteria to diagnose heart failure.
o Diagnosis for CCF requires at least 2 major criteria or 1 major criterion in
conjunction with at least 2 minor criteria.
 Major criteria
 PND
 Crepitations
 S3 gallop
 Cardiomegaly (>50% on CXR)
 Increased central venous pressure
 Weight loss
 Neck vein distension
 Acute pulmonary oedema
 Hepatojugular reflux
 Minor criteria
 Bilateral ankle oedema
 Dyspnoea on ordinary exertion
 Tachycardia >120bpm
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 Decrease in vital capacity by 1/3 from maximum recorded
 Nocturnal cough
 Hepatomegaly
 Pleural effusion
Ix: ECG, B-type naturietic peptide are normal heart failure is unlikely. If abnormal then
proceed to echo and CXR.
o Blood tests- FBC, UEs, BNP
o CXR- cardiomegaly, prominent upper lobe veins, peribronchial cuffing, diffuse
interstitial or alveolar shadowing, classical peripheral bats wing shadowing. Fluid in
fissures, pleural effusions, Kerley B lines.
o ECG
o Echo- may indicate the cause and can confirm the presence of LV dysfunction.
HEART FAILURE MX
CHRONIC HEART FAILURE
 Treat the cause
 Treat exacerbating factors- anaemia, thyroid disease, infection, BP
 Avoid exacerbating factors- NSAIDs (fluid retention) and verapamil (-ve inotrope)
 DRUGS
o Diuretics- can reduce the risk of death and worsening with heart failure. Give loop
diuretic to relieve symptoms
 Furosemide 40mg/24h PO or butmetanide 1-2mg/24h increase dose as
necessary. (loop diuretics working on the Na-K-2CL channel)
 Caution for K+ levels and renal impairment.
 If K+ is low then they have an increased risk of arrhythmias. If pt is on
digoxin and the K+  then they are at increased risk of digoxin toxicity.
 If K+ is low then start the patient on K+ sparing diuretic eg Spironalactone
 If refractory oedema consider adding a thiazide diuretic. (act in distal
convoluted tubule and work on the Na-Cl channel)
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ACE-i- consider their use in patients with left ventricular systolic dysfunction –
LVSD. Improves symptoms and prolongs life.
 If problem with cough can start the patient on Angiotensin recptor blocker
Candesartan 4mg/24h
Beta blockers- decrease mortality in heart failure. Appear to be in addition to ACE-I
due to LV dysfunction. Initiate after diuretic and ACE-I. Use with caution and go
slow if not sure
 Bisoprolol 1.25mg/24h OD
 Carvedilol 3.125mg/12h 25-50mg/12h.
 Wait two weeks between each dose increment
Spironalactone
 25mg/24h PO mortality by 30%.
 Improves endothelial dysfunction and prevents remodelling
 Spironalactone is K+ sparing very small risk of hyperkalaemia
Digoxin- helps symptoms even in those with sinus rhythm. Should be considered for
pts with LV dysfunction who have signs/symptoms of HF whilst on standard
therapy.
 Dose 0.125-0.25mg/24h.
 Monitor use
 Maintain K+
 Caution of digoxin toxicity- fatigue, n+v, visual disturbances, diarrhoea,
confusion, nightmares, agitation.
Vasoldilators- hydralazine and isosorbide dinitrate should be used if intolerant to
ACE-I and ARBs as it reduces mortality.
NEW YORK CLASSIFICATION
 I- heart disease present but no undue dyspnoea from ordinary activity
 II- comfortable at rest: dyspnoea on ordinary activities
 III- less than ordinary activity causes dyspnoea, which is limiting.
 IV- dyspnoea present at rest: all activity causes discomfort.
COR PULMONALE
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Right heart failure caused by chronic pulmonary arterial hypertension
V
I
T
A
•LUNG- PE, pulmonary vasculitis,
•Sickle cell disease
•LUNG- asthma, COPD, bronchiectasis, fibrosis,
•Thoracic cage abnormality- kyphosis, scoliosis, thoracoplasty
•Myasthenia gravis,
M
I
•ARDS
N
C
D
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Clinical feature
o Symptoms
 Dyspnoea
 Fatigue
 Syncope
o Signs
 Cyanosis
 Tachycardia
 Raised JVP with prominent a and v waves
 RV heave
 Loud P2
 Pansystolic murmur
 Early diagnostic Graham steel murmur
Ix
o FBC- Hb and haematocrit  (secondary polycythaemia)
o ABG- hypoxia with or w/o hypercapnia
o CXR- enlarged right atrium and ventricle, prominent pulmonary arteries.
o ECG- P pulmonale, RAD, right ventricular hypertrophy/ strain.
Mx
o Treat underlying cause
Treat respiratory failure
 In acute situation give 24% O2 if PaO2 <8kPa
 Monitor ABG and gradually increase oxygen concentration if PaCO2 is stable
o Treat cardiac failure
 Diuretics such as furosemide 40-160mg/24h PO
 Monitor U+E and give amiloride or potassium supplements if necessary. Can
also use spironalactone.
o Venesection if haematocrit is >55%
o Consider heart/lung transplant in young patients.
Prognosis- 50% die in 5 years.
o
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BRONCHIECTASIS
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Chronic infection of bronchi and bronchioles leading to widening of these vessels
Common pathogens are H. Influenza, Strep pneumoniae, Staph aureus, Pseudomonas
aeruginosa
Causes
o Congenital
 Cystic fibrosis
 Young’s syndrome
 Primary ciliary dyskinesia
o Post infection
 Measles
 Pertussis
 Bronchiolitis
 Pneumonia
 TB
 HIV
o Other
 Bronchial obstruction
 Allergic bronchopulmonary aspergillosis
 Hypogammglobulinaemia
 UC and RA
Clinical features
o Symptoms
 Persistent cough
 Copious purulent sputum
 Intermittent haemoptysis
o Signs
 Finger clubbing
 Coarse insp creps
 Wheeze
o Complications
 Pneumonia
 Pleural effusions
 Pneumothorax
 cerebral abscess
 amyloidosis
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Ix
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o
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Sputum
CXR- cystic shadows and thickened bronchial walls with tramline shadows
HRCT- to assess how widespread it is
Spirometry- shows obstructive pattern
Bronchoscopy to locate site of haemoptysis
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Postural drainage- twice daily, chest physio
Abx- according to causative organism
Bronchodilators
Corticosteroids
Surgery
Mx
PNEUMOTHORAX
V
•asthma, COPD, TB, lung abscess, pneumonia
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T
•Trauma
A
M
•spontaneous, (esp in young thin men) due to rupture of subpleural bulla.
•Iatrogenic- when inserting central lines, bronchoscopy
I
N
C
•carcinoma
•cystic fibrosis, connective tissue disorders (marfan's, Ehler-Danlos syndrome)
D
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Clinical features
o Symptoms
 May be no symptoms
 May be sudden onset of dyspnoea and/or pleuritic chest pain.
 Patients with asthma may present with sudden deterioration
 Mechanically ventilated patients may present with hypoxia or an increase in
ventilation pressures.
o Signs
 Reduced expansion
 Hyper-resonance to percussion and diminished breath sounds on affected
side
 With a tension pneumothorax the trachea will be deviated away from the
affected side.
TENSION PNEUMOTHORAX
o Requires immediate relief
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Air drawn into the pleural space with each inspiration has no route of escape during
expansion.
Clinically
 Symptoms
 Asymptomatic
 Sudden onset dyspnoea and/or pleuritic chest pain
 Sudden deterioration of asthma or COPD
 Mechanically ventilated patients may present with hypoxia or an
increase in ventilation pressures
 Signs
 Reduced expansion
 Hyper-resonance
 breath sounds
 Trachea deviated away from the affected side. (?due to an increase
in pressure on the affected side forcing the mediastinum to shift,
taking the trachea with it)
 Distended neck veins
Ix
 CXR should NOT be performed start immediate Rx.
 Check ABG
Mx
 Depends on the cause and whether it is due to anything else
 Insert a large bore needle with syringe, partially filled with 0.9%saline into
the 2nd intercostals space in the midclavicular line on suspected side.
Remove plunger to allow air to bubble through the saline as a water seal.
 Aspiration of pneumothorax
 Insert chest drain
 Intercostal tube drainage
 Small tube (10-14F) unless blood/ pus is also present
 Never clamp a bubbling tube
 Tubes may be removed 24h after lung has re-expanded and air leak
has stopped. Done during expiration or a Valsalva manoeuvre
PLEURAL EFFUSION
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Fluid in the pleural space
Can be divided into their protein concentration (both are clear, straw coloured)
o Transudates <25g/L
o Exudates >35g/L
Blood in the pleural space is known as a haemothorax
Pus in pleural space is known as an empyema
Causes
o Transudates
 May be due to venous pressure
 Cardiac failure
 Constrictive pericarditis
 Fluid overload
 Hypoproteinaemia
 Cirrhosis
 Nephrotic syndrome
 Malabsorption
 Hypothyroidism
 Meig’s syndrome (right pleural effusion and ovarian fibroma)
o Exudates
 Are mostly due to increased leakiness of pleural capillaries secondary to
infection, inflammation, malignancy,
 Causes
 TB
 Pneumonia
 Pulmonary infarction
 RA
 Malignancy
 SLE
 Lymphoma, mesothelioma, bronchogenic carcinoma
Symptoms
o Asymptomatic or dyspnoea, pleuritic chest pain
Signs
o Decreased expansion
o Stony dull percussion note
o Diminished breath sounds on the effected side
o Above the effusion where the lung is compressed there may be bronchial breathing
o With large effusion- tracheal deviation away from the effusion
o Look for aspiration marks or signs of associated disease:
 Malignancy (cachexia, clubbing, lymphadenopathy, radiation marks,
mastectomy scar)
 Chronic liver disease
 Cardiac failure
 Hypothyroidism
 RA
 Butterfly rash of SLE
Ix
o CXR- small effusions blunt costophrenic angles, larger ones are seen as water-dense
shadows with concave upper borders. Completely horizontal upper border implies a
pneumothorax.
o US- useful in identifying pleural fluid and in guiding diagnostic or therapeutic
aspiration.
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Aspiration
 Percuss the upper border of the pleural effusion and choose a site 1-2
intercostal spaces below it.
 Infiltrate down to pleura with 5-10mL of 1% lignocaine
 Attach a 21G needle and syringe and insert along the top border of a rib to
avoid the neurovascular bundle.
 Draw off 10-30ml and send to lab for analysis
 Protein levels
 Glucose, pH, LDH, amylase
 Bacteriology (microscopy, culture, auramine stain, TB)
 Cytology adn immunology if indicated.
Pleural biopsy
 If fluid analysis is inconclusive, consider parietal pleura biopsy with Abram’s
needle.
 Thoracoscopic or CT guided pleural biopsy increases diagnostic yield.
Mx
o
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Drainage- if effusion is symptomatic, drain it. Fluid is best removed slowly
Pleurodesis with tetracycline, bleomycin, or talc may be helpful.
INTERSTITIAL LUNG DISEASE
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Generic term used to describe a number of conditions that affects the lung parenchyma in a
diffuse manner.
Characterised by chronic inflammation or progressive interstitial fibrosis and share a
number of clinical and pathological features.
Clinical features
o Dyspnoea on exertion
o Non productive paroxysmal cough
o Abnormal breath sounds
o Progressive interstitial fibrosis
Pathological features
o Fibrosis and remodelling of the interstitium
o Chronic inflammation
o Hyperplasia of type II epithelial cells or type II pneumocytes
Can be grouped into three categories
o Those with known cause
 Occupational/ environmental (asbestos, berylliosis, silicosis, cotton workers
lung)
 Drug (nitrofurantoin, bleomycin, amiodarone, sulfasalazine, busulfan)
 Hypersensitivity reactions
 Infections (TB, fungi, viral )
o Those associated with systemic disorders
 Sarcoidosis
 RA
 SLE, systemic sclerosis, mixed connective tissue disorders.
 UC, renal tubular acidosis, autoimmune thyroid disease.
o Idiopathic
 Idiopathic pulmonary fibrosis
 Cryptogenic organising pneumonia
 Lymphocytic interstitial pneumonia
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EXTRINSIC ALLERGIC ALVEOLITIS
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Widespread diffuse inflammatory reaction in the alveoli and small airways of the lung as a
response to inhaling a range of antigen
In the acute phase: the alveoli are infiltrated by acute inflammatory cells.
In the chronic phase: granuloma formation and obliterative bronchiolitis occur.
Causes
o Bird fancier’s and pigeon fancier’s lung (proteins in bird droppings)
o Farmer’s and mushroom worker’s lung (caused by Micropolsopora faeni)
o Malt worker’s lung (aspergillus clavatus)
o Bagassosis or sugar worker’s lung
Clinically
o 4-6h post exposure
 Fever
 Rigour
 Myalgia
 Dyspnoea
 Cough
 Crackles
o Chronic
 Increasing dyspnoea
 Weight loss
 Exertional dspnoea
 Type I resp failure
 Cor pulmonale
Ix
o Acute
 Blood
 FBC, neutrophils, ESR, ABGs, positive serum precipitins
 CXR
 Upper zone mottling/ consolidation. Hilar lymphadenopathy(rare)
 Lung function tests
 Reversible restrictive defect, reduced gas transfer during acute
attacks
o Chronic
 Blood tests
 Positive serum precipitants
 CXR
 Upper zone fibrosis and honeycomb lung
 Lung function tests
 Persistent changes
Mx
o Acute attack- remove allergen and give O2 (35-60%)
 Oral prednisolone 40mg/24h followed by reducing dose
o Chronic- avoid exposure to allergens
 Long term steroids may improve XR appearance of condition. Reducing
upper zone fibrosis and honeycombing.
IDIOPATHIC PULMONARY FIBROSIS (IPF) (CRYPTOGENIC FIBROSING
ALVEOLITIS)
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Idiopathic interstitial pneumonia
Inflammatory cells infiltrate and pulmonary fibrosis of unknown cause
Symptoms
o Dry cough
o Exertional dyspnoea
o Malaise
o weight
o Arthralgia
Signs
o Cyanosis
o Finger clubbing
o Fine end inspiratory creps
Complications
o Resp failure
o Increased risk of lung cancer
Ix:
o Blood
 ABG (PaO2; PaCO2), CRP, immunoglobulins , ANA (30% +ve), rh
factor (10% +ve)
o CXR
 Lung volume , bilateral lower zone reticulo-nodular shadows, honeycomb.
o Spirometry
 Restrictive.  transfer factor.
o Lung biopsy
Mx
o Best supportive care- O2, pulmonary rehab, opiates, palliative care input
o DO NOT USE high dose steroids
Prognosis- 50% 5 year survival.
Industrial lung disease
COAL WORKER’S PNEUMOCONIOSIS (CWP)
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Common dust disease in countries which have had underground coal mines.
Exposure of usually 15-20 years without adequate protection
Dust is ingested by macrophages, which die and release their enzymes which cause fibrosis
Clinical features
o Asymptomatic but existing bronchitis is common
o CXR- may show round opacities (1-10mm) esp in upper zone
Mx
o Avoid exposure to coal dust, treat co-existing chronic bronchitis
Progressive massive fibrosis
o Due to progression of CWP
o Causes progressive dyspnoea and fibrosis and eventually cor pulmonale.
o
SILICOSIS
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Caused by an inhalation of silicone particles which are very fibrotic.
Common in ceramic workers, sandblasters, metal mining, quarrying.
Clinical features
o Dyspnoea
o incidence of TB
o CXR- diffuse military or nodular pattern in upper and mid zones and egg shell
calcification of hilar nodes.
o Spirometry- restrictive ventilator defect
Mx; avoid exposure
ASBESTOSIS
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Caused by inhalation of asbestos fibres
Chrysotile (white asbestos) is the least fibrogenic and blue asbestos (crocidolite) the most
fibrogenic
Clinically
o Fibrosis
o Increasing dyspnoea
o Clubbing
o Fine end-inspiratory crackles
o Also cause pleural plaques
o  risk of bronchial adenocarcinoma and mesothelioma
Mx- symptomatic.
MALIGNANT MESOTHELIOMA
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Tumour of mesothelial cells that usually occur in the pleura, rarely in the peritoneum or
other organs
Exposure to asbestos. 90% report previous exposure to asbestos
May have 45year latent period
Clinical
o Chest pain
o Dyspnoea
o Weight loss
o Finger clubbing
o Pleural effusions
o Metastasis
 Lymphadenopathy
 Hepatomegaly
 Bone pain/ tenderness
 Abdominal pain/ obstruction
Ix
o CXR/CT- pleural thickening/ effusion. Bloody pleural fluid
Dx
o
Made on biopsy with an Abram’s needle.

Mx

o Pemetrexed +cisplatin chemotherapy can improve outcome
Prognosis is poor and survival short esp w/o pemetrexed.