8. Haemoptysis Flashcards
Haematemesis
Brownish red blood that is vomited from the GIT
Epistaxis (nosebleed)
Particularly a posterior nosebleed
Bleeding gums
Combined with a cough this may be confused with true haemoptysis
TACE questions to detect alcohol dependance
Does it TAKE more than 3 drinks to make you feel high? (+VE=2 pts)
Have you ever been ANNOYED by people’s criticism of your drinking? (+VE=1 pt)
Are you trying to CUT down on drinking? (+VE=1 pt)
Have you ever used alcohol as an EYE-OPENER in the morning? (+VE=1 pt)
[Alcohol dependance = Total score of 2+ pts]
2 reasons why Haemoptysis is a red flag
- It may be the presenting symptom for life threatening lung disease
- Massive haemoptysis, variably defined as anything from >100mL to >1000mL over 24 hrs, may be life threatening itself, usu through asphyxiation but potentially also shock
Diagnoses to be concerned about- surgical sieve: INVITED MD - most COMMON CAUSES are infective
Infective Neoplastic Vascular Inflammatory Traumatic Endocrine Degenerative Metabolic Drugs
Diagnoses to be concerned about- INVITED MD
Infective: pulmonary TB, bronchitis, pneumonia, lung abscess, mycetoma
Neoplastic: primary lung cancer, metastatic lung cancer
Vascular: PE, left ventricular failure, bleeding diathesis (ie a bleeding tendency eg coagulopathy, severe thrombocytopenia), AVM, , vascular bronchial fistula
Inflammatory: granulomatosis with polyangiitis (Wegener’s granulomatosis), Goodpasture’s syndrome. SLE, hereditary haemorrhagic telangiectasia (Osler- Weber- Rendu syndrome), polyarteritis nodosa, microscopic polyangiitis
Traumatic: iatrogenic (post lung biopsy or intubation), wounds (rib fracture, stab injury)
Endocrine: (none)
Degenerative: bronchiectasis
Metabolic: (none)
Drugs: warfarin (bleeding diathesis), crack cocaine
Associated symptoms- What are you coughing up?
- Frank blood = vascular problem eg erosion of a bl vessel, ruptured AVM, vascular bronchial fistula
- Blood streaked sputum = any infection of lungs, in large volumes it’s bronchiectasis
- Frothy sputum = PO (2’ to LVF or severe mitral stenosis), can be bl stained so appear pink but rare
Associated symptoms-How much are you coughing up?
Quantify - teaspoon, tablespoon, egg cup or more
Associated symptoms-How suddenly did it start, and has it got worse progressively?
Sudden onset = PE, or erosion of cancer into pulmonary blood vessel
Gradual onset = Progressive cond eg bronchiectasis
Associated symptoms-Cough productive of sputum?
Indicates LRTI (pneumonia, bronchitis, TB) or bronchiectasis
Associated symptoms-Fever?
More commonly associated with LRTI. Night sweats may indicate TB.
Associated symptoms-Weight loss?
Associated with lung cancer and TB. Significant WL in short time is rarely result of diet and exercise so Ix.
Associated symptoms-Pleuritic CP?
Arise after PE or pneumonia that has spread to the pleura
Associated symptoms-SOB?
Quantify in terms of exercise tolerance; how far before SOB? stairs?
Sudden onset = PE
Gradual onset = HF
Associated symptoms- Haematuria +/or oliguria?
Some RARE conditions affect both lungs and kidneys (pulmonary-renal syndrome), the main causes =
- Goodpasture’s syndrome= AI condition where autoantibodies attack lungs + glomeruli in the kidneys. Imp to identify early since pt progresses rapidly to irreversible renal failure
- Vasculitides eg granulomatosis with polyangiitis - (+ve pANCA and nANCA) (Wegener’s syndrome), microscopic polyangiitis (+ve pANCA antibodies (more specific) as well as +ve nANCA), polyarteritis nodosa
- SLE (+ANA ABs)
PMHx- Smoking history?
Smoking = RF for Lung cancer. Calculate pack yrs (20 cigs = 1 pack)
PMHx- Exposure to asbestos or other inhaled industrial substances?
RF for Lung cancer = silica (stonecutter’s dust), coal, radon, arsenic, haloethers, polycyclic aromatic HCs
Asbestos = RF for mesothelioma
PMHx - prior lung disease?
Indicates chronic condition eg TB or bronchiectasis, or a vulnerability to repeated infections eg pneumonias
PMHx- Did he grow up abroad or travel recently?
If yes which country?
Vaccinated for TB? TB is endemic in many countries, particularly in the Asian subcontinent and southern African states and has reappeared in many eastern European countries since collapse of Soviet union.
Pts with TB can be relatively asymptomatic for extended periods of time
PMHx- Does he have RF for DVT/PE?
Includes prolonged STASIS (bed rest or long haul flight), BL VESSEL DAMAGE from recent trauma or surgery, MALIGNANCY causing hypercoagulable blood, other CLOTTING abnormalities, or a hx of previous venous thromboembolism
Also ask about a painful swollen limb, particularly leg, which could be a DVT leading to a PE
PMHx- Is he on anticoagulant meds or does he have a known bleeding diathesis?
Increases risk +/or magnitude of internal haemorrhage
Signs O/E - General inspection
Hoarse voice:?invasion of recurrent laryngeal n by cancer
Cachexia
Purpuric rash or petechiae:?vasculitis affecting lungs
Signs O/E - Hands
Clubbing:?Lung cancer, lung abscesses, bronchiectasis
Tar stains:?smoker
Wasting of the dorsal interossei:?invasion of T1 nerve root by apical lung cancer (Pancoast tumour)
Signs O/E - Arms
Hypotonic, hyporeflexive, weak arms:?hypercalcaemia due to bone mets from lung cancer
Signs O/E - Face
Swollen face:?obstruction of SVC by tumour
Bleeding from oral or nasal mucosa:?source of blood ie not true haemoptysis
Saddle nose:?granulomatosis with polyangiitis (Wegener’s)
Horner’s syndrome (miosis, ptosis and anhydrosis ie ipsilateral constricted pupil, droopy eyelid, and lack of facial sweating):?invasion of the sympathetic supply to the face by apical lung cancer
Jaundice: ?liver cancer which has spread to lungs or vice versa
Focal neurology: ?brain mets from lung cancer
Signs O/E - Neck
Cervical lymphadenopathy, non- tender: ?TB, bronchial carcinoma
Left supraclavicular lymphadenopathy (Virchow’s node): ?GI malignancy which may have metastasised to the lungs
Tracheal deviation: ?Pleural effusion due to cancer? lung collapse secondary to a large mass such as a tumour or abscess
Signs O/E - Chest
Asymmetrical lung expansion: ?lung pathology in side of reduced expansion
Dullness to percussion:?pneumonia, lung abscess, malignant pleural effusion
Stridor: ?tumour or foreign body obstructing bronchus
Crackles: ?pneumonia, left ventricular failure, bronchiectasis
Pleural rub:?mesothelioma, pleuritis from pneumonia
Signs O/E - Abdomen
Hepatomegaly:?liver malignancy which may spread to the lungs and vice versa
Signs O/E - Legs
Unilateral signs of DVT: a DVT may have caused a PE. Look for unilaterally inflamed leg, unilateral pitting oedema, tenderness over the deep veins or distended, non varicose superficial veins
If haemoptysis, weight loss and hepatomegal, refer urgently to respiratory clinic. Perform Ix=
1.02 sats - form part of the vital obs + shows severity of the underlying pulmonary disease
2.Bloods-
FBC- anaemia =reflects magnitude and duration of bleeding may be manifestation of underlying malignancy. High WCC = infection
CRP- High in infection, inflammation + sometimes malignancy
Clotting screen -for bleeding disoreders
U&Es - for renal involvement eg Goodpasture’s + Wegener’s (P- R Syndrome)
Calcium, phosphate, and ALP - for bone mets from primary lung cancer
Liver enzymes - for liver involvement of cancer
3. Urine test- urinalysis looking for haematuria (P-R-Syndrome)
4.Imaging - chest radiography
Signs on chest radiograph (CXR)
Mass lesion/Nodule(s)/ COIN lesion Diffuse alveolar infiltrates Hilar lymphadenopathy Lobar or segmental infiltrates Patchy alveolar infiltrates Lobar collapse
CXR: Mass lesion/nodule(s)/ COIN lesion
Carcinoma, TB, abscess, vasculitides, eg granulomatosis wtih polyangiitis (Wegener’s)
CXR: Diffuse alveolar infiltrates
Pulmonary oedema
CXR: Hilar lymphadenopathy
Carcinoma, infection (if accompanying infiltrates), TB
CXR: Lobar or segmental infiltrates
Pneumonia, infarction due to PE, TB, adenocarcinoma causing malignant consolidation (if tumour is in the airway)
CXR: Patchy alveolar infiltrates
Bleeding disorders, Goodpasture’s syndrome, idiopathic pulmonary haemosiderosis
CXR: Lobar collapse
Obstructing carcinoma
Suspected Lung Cancer Ix to confirm diagnosis pathologically
- Cytology of sputum and bronchoscopic washings
- Tissue biopsy via CT -guided percutaneous fine needle biopsy (if it’s peripheral) or bronchoscopy (if it’s more central, either endobronchial or transbronchial biopsy depending on whether it protrudes into the airway lumen)
- CT scan to stage cancer- looking for local spread and LN involvement
- Bone scan - bone mets
Mx of lung cancer short + long term
- Resus ABC
- If hemoptysis v serious, priority = stopping haemorrhage (with help of interventional radiologist to identify + embolise the bleeding pt)
- Once dx confirmed and tumour staged, refer to MDT for mx ; depends on histology (grade), stage (spread) of tumour
Wells criteria
Criteria Points Clinical signs and symptoms of DVT = 3 PE is the most likely diagnosis = 3 HR >100bpm =1.5 Immobilisation >3d or surgery in last 4 weeks = 1.5 Previously diagnosed DVT or PE =1.5 Haemoptysis = 1 Malignancy diagnosed in the last 6 mths = 1
Wells criteria analysis
Score of > or equal to 4 = CTPA (or perfusion scan) to Ix as approx 30% risk of PE
Score of <4 only justifies a D-dimer test to exclude a PE, but negative D dimer is not 100% specific to rule out a PE, so if risk is high, need a better test to rule out PE
Pulmonary TB symptoms + signs
Grew up in India
Chronic cough (absence of smoking)
Haemoptysis
Night sweats
Weight loss
O/E: tachycardia, raised WCC, raised CRP, consolidation (reduced expansion, dullness to percussion, reduced breath sounds, crackles, increased vocal resonance), mild anaemia (suggest chronic disease process)
Reactivation of TB typically affects the upper lobes as Mycobacterium TB is a highly aerobic bacterium and the apices are the most oxygenated part of the lungs
Pulmonary TB general Mx plan
1.Review need for resuscitation ABC
2. Ensure microbiology look for acid fast bacilli (using a Ziehl-Nielson or silver stain), M.TB is a slow growing bacteria so may take weeks to obtain a +ve result on culture
3.TB is a notifiable disease, may screen contacts for latent or active TB + treat as appropriate
4.Place pt in isolation to prevent further spread
5.Test for HIV, as although most likely acquired TB in childhood she may have acquired it more recently secondary to HIV infection which affects prognosis and Mx
6.Look for signs of spread to other organs. Check for meningeal irritation, bone or joint pain particularly in weight bearing joints eg Pott’s fracture in spinal column, dysuria, or pelvic pain (genitourinary infection) or abdo pain
7.If dx is confirmed, refer pt to the TB service, which offers specialised care for such pts
(NB. Skin sensitivity tests = Heaf and Mantoux, and newer interferon gamma release assays (IGRAs) are only useful to determine latent TB not active disease activity, so instead do SPUTUM OR BIOPSY CULTURE for active disease IX)
Pulmonary TB medical Mx
First line tx depends on likelihood of drug resistant strain and longer term results of culture and sensitivites
Initial approach = tx with long term regimen of 4 ABx: rifampicin and isoniazid (for first 4 mths) , pyrazinamide and ethambutol (for first 2 mths)
Rifampicin - turns urine rich orange, and makes OCP less effective so consider other contraception
Long term tx leads to poor compliance, leading to multidrug resistant TB
Bronchiectasis symptoms and signs
Hx of recurrent cough Productive green sputum Occasional haemoptysis CXR: dilated bronchi Associated conditions: otitis media (glue ear), sinusitis - both suggest inability to clear mucus
Bronchiectasis pathophysiology
Bronchi are clinically inflamed as the lungs struggle to clear irritant mucus for any of a variety of reasons eg obstruction, thickened mucus, poor ciliary function of the epithelia.
The consequence of chronic inflammation is the laying down of scar tissue in the interstitial tissue.
Remember that scars shrink, so the airway walls are pulled back and the airways expand.
Mucus is often green due to the constant presence of neutrophils and macrophages fighting pathogens growing in the retained mucus.
As neutrophils and macrophages die, they release an enzyme called myeloperoxidase which is green (and closely related to enzymes in spicy wasabi sauce)
Primary ciliary dyskinesia (PCD)
Autosomal recessive disorder that affects the protein machinery used by epithelial cels to rhythmically beat their cilia and by spermatozoa to rhythmically beat their tails
Typical consequences of PCD
- Bronchiectasis, due to inability to clear mucus from the lungs
- Rhinitis and sinusitis, due to an inability to clear mucus from the nasal sinuses
- Otitis media (both secretory and acutely infective) due to an inability to clear mucus from the middle ear, down to the eustachian tube
- Male infertility, due to sperm immotility. F usu fertile as passage of the oocyte along the fallopian tubes is more dependant on the peristalsis of the fallopian tubes than on the mvmnt of the cilia that line these tubes
- Situs inversus. The rhythmical beating of the cilia is thought to play imp part in setting up the usual body asymmetry during embryogenesis. Many pts with PCD have their organs on the ‘other side’ eg dextrocardia
PCD triad
1.Bronchiectasis 2.Sinusitis 3.Situs inversus aka Kartagener’s syndrome
Ix of PCD
- Biopsy of nasal mucosa and examination under microscope, to look for abnormal beating of the ciliated epithelia
- Microscopy of spermatozoa of PCD males often reveals immobile spermatozoa
Mx of PCD
1.Regular physio, to help clear lungs of mucus
2.Regular or prophylactic ABx, to prevent recurrent chest infections and sinusitis
3.Mucolytics, which can help clear mucus in the lungs and sinuses more easily in some pts
NB. Many pts with PCD show improvement of symptoms by early 30s and many pts lead normal adult lives
Haemoptysis + Nephritic syndrome triad + red cell casts
1.HTN 2.Porteinuria 3.Haematuria
Suggests inflammation of her kidneys, possibly glomerulonephritis manifesting as nephritic syndrome
Presence of red cell casts (clumps of red cells that have squeezed through damaged glomeruli) is indicative of glomerular damage
Combo of haemoptysis + glomerulonephritis = PULMONARY RENAL SYNDROME
Causes of Clubbing: CV RESP GI OTHER
CV: IE (subacute bacterial endocarditis) Congenital cyanotic heart disease Atrial myxoma Axillary artery aneurysm Brachial arteriovenous fistula
RESP: Pulmonary fibrosis
Suppurative lung diseases: abscess,empyema, CF, bronchiectasis
Bronchial carcinoma, mesothelioma (although these pts do not always survive long enough to become clubbed)
TB
GI: IBD Cirrhosis Malabsorption eg coeliac disease Gastric lymphoma Liver abscess Liver or bowel cancer
OTHER:
Congenital clubbing
Thyroid acropachy
Pleural effusion: transudate vs exudate
Transudate: <25g/L of protein. Low in protein as they are the result of fluid alone being squeezed into the pleural space, either due to increase hydrostatic pressure in the lung vasculature (HF, fluid overload, constrictive pericarditis) or due to reduction in the oncotic pressure which usu keeps fluid in the vasculature (reduced serum protein due to liver failure, malabsorption/malnutrition, nephrotic syndrome)
Exudate: >35g/L of protein. Exudates are rich in protein as they are the result of cells in the pleural space: either pathogens (infection), inflammatory cells, or malignant cells
If pleural fluid protein is between 25-35g/L, Light’s criteria should be used to differentiate E vs T. These state that the fluid is an exudate if any of the following applies:
-Pleural fluid protein/Serum protein >0.5
-Pleural fluid LDH/serum LDH>0.6
-Pleural fluid LDH>2/3s the upper limit of normal serum LDH
Classification of lung neoplasms
- Benign (eg hamartoma) or Malignant (ie. cancerous)
- Malignant - Primary or Secondary
- Primary Lung cancers classified based on histology:
- NSCLC 80%: –>subdivided into adenocarcinoma 30-40%, squamous 20-30%, large cell carcinoma 10% and others 5%
- -> if localised, attempt to remove surgically or treat with radiotherapy
- -> otherwise responds poorly to chemotherapy and has poor prognosis if disseminated
- SCLC 20% –> responsive to chemotherapy, although rapid relapse is common, chemo given to improve symptoms not mortality
- -> early metastasis so surgery is rarely the therapy of choice
Haemoptysis and squamous cell carcinoma
Haemoptysis is more common in squamous cell carcinoma, which usu affects lung tissue closer to the hilar region and so bood has little distance to travel before being coughed up
Primary cancers most commonly metastasising to lung
- Colorectal
- Breast
- Renal
- Femal genital tract: cervix, ovary
Metastatic lung cancer and haemoptyis
Haemoptysis rarely occurs as they are spreading haematogenously and so tend to be deep in the interstitium rather than endobronchial
Extrapulmonary manifestations of lung cancer
- Bone mets causing bone pain
- Hypertrophic pulmonary osteoarthropathy (HPOA) - dull, aching, swollen wrists/ankles (rare)
- Ectopic ACTH secretion –> cushings features, muscle weakness, oedema, and skin hyperpigmentation
- Hypercalcaemia secodnary to bone mets or PTH- related peptide (PTHrP) secreting lung cancer–> confusion, polyuria, polydipsia, hypotonia, hyporeflexia and muscle weakness
- Eaton-Lambert syndrome- rare neuromuscular disorder most commonly seen in pts with SCLC, characteristic proximal muscle weakness that improves on repetition (unlike myasthenia gravis)
What ectopic endocrine secretions are associated with lung cancers
- SCLC are derived from endocrine cells in the lung, and so have the potential to synthesis and secrete hormones or hormone like substances. Subs secreted are ADH, resulting in HYPONATRAEMIA, and ACTH, resulting in CUSHING’s
- Squamous cell caricnomas may not have the cell machinery to produce cholesterol based steroids, but can produce peptides eg PTHrP, which causes HYPERCALCAEMIA
What extrapulmonary sites does TB most commonly affect? What does it cause in each?
TB can affect virtually any organ. Some of the mroe common manifestations include:
LNs (often cervical or mediastinal)
Bone: osteomyelitis, septic arthritis, Pott’s disease (in spine)
Neurological: meningitis, intracranial granulomas
Renal: granuloma
TB less commonly affects heart, skeletal muscle, pancreas, thyroid or adrenals (Addison’s dis)
Differential for a solitary coin lesion on a chest radiograph
- Parenchymal tumour: benign, 1’LC, 2’LC
- LN: lymphoma
- Granuloma: TB, sarcoidosis
- Abscess
- Hamartoma
- Foreign object
Why does warfarin use result in initial paradoxical increase in clot formation?
Warfarin works as an ANTICOAGULANT by blocking VIT K EPOXIDE REDUCTASE which activates Vit K. This means Vit K clotting factors have reduced ability to function.
BUT because depletion of protein C and S occurs faster than that of the Vitamin K dependant clotting factors.
Protein C and S are anticoagulants (anticlotting proteins) as they block coagulation proteins so there is paradoxical initial increase in clot formation
Staging v Grading
Staging = Extent of spread Grading= Abnormality of cells
