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Chapter9
Respiratory
2Breathlessness and low sats emergency 284
Breathlessness and low sats 285
2Stridor in a conscious adult patient 298
Cough 299
283
284 CHAPTER9 Respiratory
2Breathlessness and low sats emergency
2 Airway
2 Breathing
2 Circulation
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort—
If no palpable pulse—
CALL ARREST TEAM
CALL ARREST TEAM
3Call for senior help early if patient is deteriorating. Use emergency
call bell to summon help quickly— don’t leave the patient.
•
Sit patientup
• 5L/ min O2 in all patients if acutelyunwell
•
Monitor pulse oximeter, BP, debrillator ECG leads ifunwell
• Obtain a full set of
• Take a brief
•
Examine patient:condensed RS, CVS, GCS ±abdoexam
observations includingtemp
history if possible/ check notes/ ask wardsta
• Establish likely causes and rule out seriouscauses
• Focused bedside heart and lung US if competent and available
• Initiate
•
•
further treatment, seeEpp. 285–6
Venous access, take bloods:
•
FBC, U+E, LFT, CRP, blood cultures, D- dimer, BNP, troponin
Arterial blood gas, but don’t leave the patientalone
• ECG to exclude arrhythmias and acuteMI
• Request urgent CXR, portable if toounwell
• Call for
seniorhelp
• Reassess, starting with A, B, C…
2Life- threateningcauses
• Asthma/ COPD
• Pulmonary oedema(LVF)
• (Tension) pneumothorax
• Myocardial infarction
• Arrhythmia
Oxygen saturation targets
• Pneumonia
• Pulmonary embolism(PE)
• Pleural eusion
• Anaphylaxis
• Airway obstruction.
Oxygen saturation targets are a frequent query on the wards, and you will be called about desaturating patients who you do not know. In an emergency scenario, treat hypoxaemia,
aiming for 94–98% saturations, unless the patient has an established alternative target. A lower target (88–92%) is recommended for those at risk
of type 2 respiratory failure (T2RF; COPD, bronchiectasis, morbid obesity,
chest wall deformity, neuromuscular deformity). Use ABG analysis to
guide therapy. If at risk of T2RF, but pCO
previous T2RF failure. Evidence shows that liberal or excessive oxygen-
is normal, aim 94–98%, unless
2
ation increases patient mortality, therefore controlled therapy targeting
predened oxygen saturations should be the priority.
Mhttps://www.brit-thoracic.org.uk/quality-improvement/guidelines/emergency-oxygen/
Breathlessness and lowsats
2Worrying features RR >30, sats <92%, systolic BP <00mmHg,
chest pain, confusion, inability to complete sentences, exhaustion,
tachy/ bradycardia, silentchest, tracheal deviation.
Think about 2Life- threatening causes of respiratory failure See Table 9.;
Most likely COPD/ asthma, pneumonia, pulmonary oedema (LVF), PE, MI;
Others Pneumothorax, pleural eusion, arrhythmia, ARDS, sepsis,
metabolic acidosis, anaemia, pain, panic, foreign body/ aspiration;
ChronicCOPD, lung cancer, bronchiectasis, interstitial lung disease,TB.
Ask about Speed of onset, cough, change in sputum (quantity, colour),
haemoptysis, wheeze, chest pain (related to movement, pleuritic), trauma,
palpitations, dizziness, diculty lying at, recent travel, weightloss, calf pain;
PMH Cardiac or respiratory problems, malignancy, old or exposureto TB;
DH Inhalers, home nebulizers, home O
SH Smoking (pack- years), pets, exercise tolerance, previous/ current occupa-
tion (asbestos exposure).
PE risk factors Recent surgery/ immobility/ fracture/ travel/ hospitaliza-
tion, oestrogen (pregnancy, HRT, the pill), malignancy, previous PE/
DVT, thrombophilia, varicose veins, obesity, centrallines.
Obs Temp, RR (– 20 is normal), BP, HR, sats,
(improving or worsening?).
Look for Ability to speak full sentences, confusion, cyanosis, CO
tremor, clubbing, rashes, itching, swollen lips/ eyes, raised JVP, tracheal
shift and tug, use of accessory muscles, abnormal percussion, unequal air
entry, crackles, stridor, wheeze, bronchial breathing, swollen/ red/ hot/
tender legs, swelling of ankles, cold peripheries.
Investigations PEFRIf asthma suspected (may be tooill); bldsFBC, U+E,
LFT, CRP, D- dimer (if PE suspected and Wells score <4 E p. 292), cardiac
markers, blood cultures;
Sputum(May need physio or saline nebs to help.)
Inspect and send for M,C+S; AFBs if TBrisk;
O
if acutelySOB; ECG(Epp. 600–2); CXR(E pp. 510–11); portable if
2
unwell, though image quality may bepoor;
the patient has been stabilized to help conrm the diagnosis (Ep. 614).
TreatmentSit all patients up and give oxygen (Ep. 284).
•
Stridor— call an anaesthetist (Ep. 298)
•
Wheeze— give nebulizer (E p. 287), eg salbutamol 5mg ±ipratropium
500micrograms STAT (drive by oxygen or air as appropriate)
•
Unilateral resonance, reduced air entry ±tracheal deviation and shock—
consider tension pneumothorax and treat urgently (Ep. 293)
•
Asymmetrical coarse crackles, dair entry, bronchial breathing— consider
pneumonia (Ep. 290)
•
Symmetrical ne crackles, dair entry, iJVP— consider LVF (Ep. 296)
•
Normal exam— consider PE, asthma, cardiac, and systemic causes.
•
Oxygen escalation— if low sats despite 5L/min oxygen, consider high-
ow oxygen, critical care outreach team, and/or HDU referral.
, cardiac medication, allergies;
2
O2 requirements
ap,
2
ABG(E pp. 512–13), keep on
SpirometryShould be done once
285BREATHLESSNESS AND LOWSATS
286 CHAPTER9 Respiratory
Table9. Common causes ofbreathlessness
History Examination Investigations
COPD Usually smoker,
Asthma Known asthma,
Pneumonia Productive cough,
Pulmonary
embolism
Pulmonary
oedema
Pneumo-
thorax
Pleural
eusion
ARDS Concurrent
Anaemia/
MI/
arrhythmias
3
Anaphylaxis
change in
productive
cough, worsening
wheeze
recent exposure to
cold air, allergens or
drugs (NSAIDs, β-
blockers), viruses
green sputum,
feels unwell
±pleuritic pain
PE risk factors, leg
pain, ±pleuritic
chest pain and
haemoptysis
Known cardiac
problems,
orthopnoea,
swollen legs
Sudden-onset
pleuritic chest
pain ±trauma.
Underlying lung
disease and
previous episodes
or tall, slim, male
Gradual onset
breathlessness,
±pleuritic chest
pain
severe illness
Chest pain,
palpitations,
dizziness, tiredness
Sudden onset,
itching, swelling,
urticarial rash,
new drugs/ food
±wheeze/ crackles,
±cyanosed/ pursedlip breathing, look
for infection and
pneumothorax
Wheeze ±crackles,
look for signs
of infection or
pneumothorax
Febrile, asymmetrical
air entry, crackles,
bronchial breath
sounds ±dpercussion
iJVP, iHR (may be
only sign); may have
evidence of DVT; can
be severely shocked
iJVP, symmetrical
ne inspiratory
crackles, pink frothy
sputum, dependent
oedema, cold
peripheries
Unequal air entry
and expansion,
hyper- resonant
±displaced trachea
(late)
Reduced expansion,
stony dull base
Hypoxic, very unwell New bilateral
Irregular or fast
pulse, shocked, pale
Stridor, ±wheeze,
shock, swollen lips
and eyes, blanching
rash
CXR hyperexpanded,
at diaphragms;
exclude pneumonia
and pneumothorax
ABG; sputum
dPEFR; CXR;
exclude pneumonia
and pneumothorax
ABG; eosinophil
count
iWCC/ NØ/ CRP,
consolidation or
blun ted angles on
CXR (E pp. 610–
11); sputum M,C+S
dPaCO
±hypoxia
2
on ABGs, iDdimer, ECG, CXR
often normal, CTPA
Cardiomegaly + uid
overload on CXR
(E pp. 610–11),
ECG may show
ischaemia or previous
MI, US heart/lung
Needle
decompression
of tension
pneumothorax;
CXR shows pleura
separated from ribs
Eusion on CXR
or portable heart/
lung US
inltrates on CXR
Abnormal ECG
(E pp. 600–2),
dHb, icardiac
markers
IM adrenaline,
IV steroids
(E pp. 474–5);
acute and
convalescent serum
tryptase
Asthma
K A common chronic disease characterized by variable airow obstruction,
inammation, and hyper- responsiveness that results in wheeze, chest tightness, dyspnoea, andcough.
Symptoms Episodic breathlessness, wheeze, and chest tightness; family or
personal Hx of atopy (hayfever, eczema, asthma).
Signs Wheeze, tachypnoea, silent chest, hyperinated chest, atopic.
Investigations PEFR Reduced in acute setting compared with best or pre dicted
based upon age/ height, or diurnal variation on self- monitoring as out-
patient; ABGNormal or dPaO
3Beware normal/ rising CO
clude pneumonia and pneumothorax;
Acute exacerbation Sit up and give 5L/ min O
±ipratropium 500micrograms NEB and prednisolone 40mg PO (or
hydrocortisone 200mg IV). Drive the nebulizer mask from O
air. Repeat salbutamol 2.5mg NEB every 0– 5min and reassess PEFR
with a dPaCO2 due to hyperventilation.
2
?Patient tiring; CXR Hyperexpanded, ex-
2
Spirometry dFEV
, dFEV:FVCratio.
. Salbutamol 5mg NEB
2
supply, not
2
and sats frequently. Antibiotics if evidence of infection.
3Severe Incomplete sentences, PEFR <50% of best, HR ≥0, RR≥25.
3
Life- threatening PEFR <33% of best, silent chest, sats <92%, PaO
<8kPa, normal PaCO
altered GCS, arrhythmia. 2CallICU.
3
Near- fatal CO
2Beware those with previous ICU admissions.
, poor respiratory eort, exhaustion, cyanosis,
2
retention. 2CallICU.
2
2
No improvementCall for senior help. Consider:
•
Early ICU input/ assessment
•
Aminophylline 0.5– 0.7mg/ kg/ h, stop oral theophylline; monitor levels
•
Magnesium sulfate 2g (8mmol) IV over20min.
Improving Admit those in whom PEFR <75% predicted after h therapy;
gradually reduce supplemental O
several days; always check inhaler technique, ensure patient books
and step from nebs to inhalers over
2
follow- up with GP 48h post discharge and discuss with asthma nurse.
Chronic treatment (E OHCM1 p. 64.) See Table 9.2, aiming for
minimum treatment resulting in symptom control; monitor PEFR; always
check inhaler technique before escalation; ensure allergen avoidance,
smoking cessation, and comorbidities (GORD, nasal polyposis, OSA,
breathing pattern disorder) identied and controlled.
Table9.2 Simplied stepwise management ofasthma(209)
Step 2 3* 4* 5
Salbutamol
Low- dose inhaled corticosteroid (ICS)
Low- dose ICS and LABA (combination)
Medium- dose ICS and LABA (combination) or add
leukotriene receptor antagonist
Refer for specialist care (e.g. to consider steroids or MABs)
* If no response to LABA, stop LABA and use medium- dose ICS alone. BTS guidelines include tables to predict PEFR where unknown. Source:data from Mhttps://www.sign.ac.uk/
sign-58-british-guideline-on-the-management-of-asthma
✓ ✓ ✓ ✓ ✓
✓
✓
✓ ✓
✓
287BREATHLESSNESS AND LOWSATS
288 CHAPTER9 Respiratory
COPD(E OHAM4 p. 92.)
2
K Predominantly xed airow obstruction due to loss of elastic recoil in alveoli
(emphysema) and narrowing of airways with excess secretions (bronchitis).
2
Worrying signs dGCS, risingpCO
Symptoms Breathlessness, cough, isputum, tight chest, confusion,
.
2
dexercise tolerance. NB iindex of suspicion in (ex- )smoker.
Signs Wheeze, cyanosis, barrel- chested, poor expansion, tachypnoea.
Investigations ABG
previous samples and pay close attention to FiO
ill patients; CXR Hyperexpanded, at diaphragm (look for evidence of infection,
pneumothorax, or bullae);
Acute exacerbation Sit the patient up. Give the minimum amount of O
maintain target sats (E p. 284). Give salbutamol 2.5mg ±ipratropium
500micrograms NEB (drive by air, leaving nasal O
if necessary) and prednisolone 30mg PO (or hydrocortisone 200mg IV).
Often deranged in COPD, with T2RF common. Compare with
; repeat after 30min in seriously
2
Spirometry
(E p. 614) dFEV, dFEV:FVC ratio (<70%).
cannulae on under mask
2
2
to
Sputum for M,C+S. Get a CXR (portable if unwell). Use ABG and clinical
observations to guide further management including sats target.
• Normal ABG (for them) Continue current O
• Worsening hypoxaemia iFiO
which should prompt a repeat ABG sooner; considerNIV
• iCO
retention or dGCS Request senior help 2urgently; consider:
2
•
ICU
input/ assessment.
, repeat ABG <30min, watch for confusion
2
Aminophylline
oral theophylline and monitor levels (under senior guidance).
and give regularnebs
2
0.5– 0.7mg/ kg/ h, discontinue any
NIV
(Box9.).
AntibioticsConsider prescribing antibiotics (eg PO doxycycline or amoxi-
cillin) if the patient has iSOB, fevers, worsening cough, purulent sputum,
or focal changes onCXR.
Chronic treatment(E OHCM1 p. 66.) Smoking cessation is paramount.
Stepwise therapy with inhalers can reduce symptoms, frequency, and severity
of exacerbations, and improve health status and exercise tolerance (Tables9.3
and 9.4). If breathless despite maximal inhaler therapy, give home nebulizers.
If PaO
consistently ≤7.3kPa (or ≤8kPa with additional risk factors), LTOT for
2
≥5h/ d confers survival advantage. Annual inuenza vaccines decrease incidence
3
of LRTI.
Consider rescue packs (abx/ steroids) for patients for acute (infective)
exacerbation. Pulm rehab (Box9.2). Consider theophylline, prophylactic abx,
bronchoscopic intervention, and surgery in select refractory cases.
Complications Exacerbations, infection, cor pulmonale, pneumothorax,
respiratory failure, lung cancer (beware haemoptysis and weightloss).
K Box 9. Non- invasive ventilation(NIV)
Machines assist ventilation through a tightly tting mask. Bi- level positive airway
pressure (BiPAP) used in COPD patients with a pH ≤7.35 and CO
who have failed to respond to initial medical therapy reduces mortality and
≥6.0kPa
2
length of admission. Patients who need NIV usually stay on the respiratory
ward, HDU, or ICU. Continuous positive airway pressure (CPAP) is technically not NIV since it does not help with mechanics of ventilation (Ep. 296).
2
NICE guidelines available at Mguidance.nice.org.uk/ NG5
3
Global Initiative for Chronic Obstructive Lung Disease. 202 report. Mhttps://goldcopd.org/
wp-content/uploads/2020//GOLD-202-POCKET-GUIDE-v.0-7Nov20_WMV.pdf
Table9.3 Simplied COPD severity assessment and treatment
GOLD
Yearly
group
exacerbations
A or less Breathless only on
B or less Has to stop on
C 2 or more
(or hospital
admission)
D 2 or more
(or hospital
admission)
Source:data from Global Initiative for Chronic Obstructive Lung Disease, 202 report, Mhttps://
goldcopd.org/wp-content/uploads/2020//GOLD-202-POCKET-GUIDE-v.0-7Nov20_WMV.pdf
Dyspnoea Initial
strenuous exercise
walking
Breathless only on
strenuous exercise
Has to stop on
walking
Treatment
SABA or
SAMA
LAMA or
LABA
LAMA 30– 49 (Severe)
LAMA or
LAMA + LABA
or
LABA + ICS
Severity (FEV
% predicted)
≥80 (Mild)
50– 79 (Moderate)
<30 (Very severe)
Table9.4 Some common inhalers forasthma andCOPD
Drug type Medication Trade name eg Colour
Short- acting
β-agonist
Salbutamol Ventolin
Terbutaline Bricanyl
Inhaled steroids Beclometasone Qvar
Budesonide Pulmicort
Fluticasone Flixotide
Ciclesonide Alvesco
Inhaled steroids
and long- acting
β-agonist
(combination)
Beclomethasone/ formoterol Fostair
Budesonide/ formoterol Symbicort
Fluticasone/ salmeterol Seretide
Fluticasone/ vilanterol Relvar
Long- acting
anticholinergic
Tiotropium Spiriva
Umeclidinium Incruse
Glycopyrronium Seebri
Aclidinium Eklira (Genuair)
Long- acting
β-agonist and
long- acting
anticholinergic
(combination)
Vilanterol and umeclidinium Anoro
Indacaterol and glycopyrronium Ultibro
Oldaterol and tiotropium Spiolto
Formoterol and aclidinium Duaklir
®
®
®
®
®
®
®
®
®
®
®
®
®
Blue
Blue
Brown
®
Brown
®
Orange
Red
Pink
®
Red
®
Purple
Yellow
Grey
Green
Orange
®
Green
Red
Yellow
Green
Orange
289BREATHLESSNESS AND LOWSATS
Box 9.2 Pulmonary rehabilitation
Patients with chronic lung disease who take part in a structured 8– 2wk pulmonary
rehabilitation programme with a graduated exercise regimen see increased exercise
tolerance and improved well- being,
4
although this does not reverse pathological
processes or improve spirometry. Diet and other lifestyle advice are also covered.
4
Summarized at Mhttps://www.brit-thoracic.org.uk/quality-improvement/quality-standards/
290 CHAPTER9 Respiratory
Pneumonia(E OHAM4 p. 172.)
5
2Worrying signs CURB- 65 score ≥3 (see ‘Severity’).
Symptoms Cough, purulent sputum, pleuritic chest pain, breathless,
haemoptysis, fever, unwell, confusion, anorexia.
Signs itemp, iRR, iHR, dsats, unequal air entry, reduced expansion, dull
percussion, bronchial breathing.
Severity The CURB- 65 criteria
6,7
are a validated set of variables that support (but do not replace) clinical judgement in community- acquired pneumonia (CAP) on whether to admit a patient. Score point for each of:
• Confusion (abbreviated mental test ≤8).
• Urea >7mmol/ L.
• Respiratory rate ≥30/ min.
• BP <90mmHg systolic and/ or 60mmHg diastolic.
• Age ≥65.
A score of 0– indicates low severity and <3% risk of death. If no
other reasons for admission, treat with PO antibiotics at home; if other
reasons for admission, treat with PO antibiotics at hospital. A score of 2
indicates moderate severity and 9% risk of death and should be treated
in hospital. A score of ≥3 indicates high severity and 5–40% risk of
death; consider ITU assessment.
In the outpatient setting, omit urea to get a CURB- 65 score; patients scoring
0 (and possibly – 2) may be suitable for home treatment.
Management Antibiotics Follow your local hospital antibiotic policy. If pneu-
monia not severe and not vomiting (CURB-65 –2) give PO antibiotic; severe
(CURB-65 >2) give IV;
IV uids (anorexia, volume depletion, shock) and VTE prophylaxis;
If pleurisy;
ITU Consider if shock, hypercapnia, or remains hypoxic; Steroids
Oxygen Keep PaO
>8.0 and/or saturation ≥94%.
2
Analgesia
Consider adjunctive steroids in signicant hypoxia (eg requiring NIV), refractory septic shock, COVID-9, or COPD;
Follow-up At 6 weeks (±CXR).
Investigations blds iWCC;ineutrophils;iCRP; bld cultures.If CURB- 65≥2;
Sputum culturesIf CURB- 65 ≥3 (or CURB- 65 = 2 and not had anti biotics);
UrineIf CURB- 65 ≥2 test for pneumococcal antigen; if CURB- 65 ≥3 or
clinical suspicion, test for legionella antigen; ABG dPaO
to hyperventilation but not if tiring or COPD); CXR May show focal
(±dPaCO2 due
2
consolidation; repeat at 6wk if ongoing symptoms or high risk for malignancy/ empyema.
Treatment Sit up and give O
local policy or E p. 77 for empirical treatment. Consider IV uids.
Most patients who require IV antibiotics can safely be switched to PO
therapy by day 3.
8
Oer a 5d course of antibiotic therapy for patients
as required. Give antibiotics according to
2
with low- severity CAP; consider a 7– 0d course of antibiotic therapy for
patients with moderate and high severity CAP. If symptoms not resolving
by day 3, repeat CRP and CXR to exclude pleural eusion/ empyema.
Complications Empyema, respiratory failure, sepsis, confusion.
5
NICE guidelines available at Mguidance.nice.org.uk/ NG38
6
Man SY, etal. Thorax 2007;62:348:Mwww.ncbi.nlm.nih.gov/ pmc/ articles/ PMC2092476
7
Lim WS, etal. Thorax 2007;62:287:Mwww.ncbi.nlm.nih.gov/pmc/articles/PMC2092475
8
Oosterheert JJ, etal. BMJ 2006;333:93 full- text a vailable free at:Mwww.ncbi.nlm.nih.gov/ pmc/
articles/ PMC693658
Hospital- acquired pneumonia
K Pneumonia developing ≥48h after admission and not felt to have been
incubating at time of admission.
Causative organisms include Gram – ve bacilli (eg Pseudomonas or
Klebsiella species, Escherichiacoli) as well as Streptococcuspneumoniae
and Staphylococcus aureus (including MRSA). Symptoms and signs can
be severe, particularly in frail patients with other comorbidities, and
lung necrosis and cavitation may develop. Empirical antibiotic selection
should be guided by local policy ±discussion with a microbiologist.
Aspiration pneumonia
K Aspiration of gastric contents reuxing up the oesophagus and down
the trachea may lead to a sterile chemical pneumonitis. Alternatively,
oropharyngeal bacteria may be aspirated causing a bacterial pneumonia.
Risk factorsinclude dGCS (eg sepsis, anaesthesia, seizures), oesophageal
pathology (eg strictures, neoplasia), neurological disability (eg dementia,
MS, Parkinson’s disease, stroke), or iatrogenic interventions (eg NG
tube, OGD, bronchoscopy). At- risk patients can be identied by bedside
swallow evaluation (E p. 367). Care is supportive, with O
tation, suctioning of secretions, and attention to prevention of further
supplemen-
2
aspiration (involve SALT and chest physio). Empirical antibiotics can be
of benet if bacterial pneumonia suspected (eg persistent fever, purulent sputum)— follow local guidelines.
291BREATHLESSNESS AND LOWSATS
292 CHAPTER9 Respiratory
Pulmonary embolism(E OHAM4p. 26.)
K Disruption of the pulmonary artery or its branches by a thrombus,
usually from the deep veins of the legs. PEs vary in size with important
clinical implications. Paradoxically, larger PEs may be less obvious; smaller
peripheral PEs produce typical pleuritic chest pain whereas larger clots
may be associated with subtle haemodynamic compromise.
Symptoms Breathlessness, pleuritic chest pain, haemoptysis, dizziness, leg pain;
consider risk factors in Table9.5;
9
Signs iJVP, iRR, iHR, dBP, RV heave,
hypotension, pleural rub, ±pyrexia. Tachycardia and tachypnoea may be the
only clinicalsigns;
Investigations D- dimer Will be raised in many situations (eg in-
fection, malignancy, MI, CVA, renal dysfunction) while normal results must be
interpreted in context (Box9.3); ECGsinus tachycardia (commonest nding),
RBBB, inverted T waves V– V4 or S
CTPA Is the denitive imaging modality,though V/ Q scanmay be used, eg in
pregnancy.
Acute treatment
Sit up (unless dBP) and give 5L/ min O2. If life-
; ABG type RF (if large PE);
Q3T3
threatening (hypotension +shock) seek immediate senior support, arrange
an urgent CTPA and echo, and consider thrombolysis. Otherwise parenteral
anticoagulation (E pp. 428–30), eg enoxaparin .5mg/ kg/ 24h SC and pain
relief; IV uids if dBP.
Chronic treatment Anticoagulation (E pp. 428–30) eg
warfarin/ DOAC. Length of treatment will depend on risk factors/ context.
K Box 9.3 Clinical risk assessmentforPE
PEs are common and potentially fatal, but can present non-specically. CTPA
oers diagnostic accuracy but with exposure to radiation and nephrotoxic IV
contrast medium. The value of D- dimer testing lies in the excellent negative
predictive value when the risk of PE is low. In high-risk patients, a negative Ddimer is not suciently reassuring. Dierent scoring tools exist but the Wells
score for PE (Table9.5) is a reliable method of identifying the risk of PE, and
hence deciding on further testing.
• Score ≤4: low risk:test for D- dimers. If elevated, proceed to CTPA; if
negative, then consider alternative diagnoses
• Score >4: high risk:proceed to CTPA testing and start treatment dose
LMWH pending results.
Table9.5 Wells score forpulmonary embolism
Clinical feature Points
Signs/ symptoms of DVT (leg swelling and pain on deep vein palpation) 3
PE most likely clinical diagnosis 3
HR >00 .5
>3d immobilization or surgery in past 4wk .5
Previous DVT/ PE .5
Haemoptysis
Malignancy (current treatment or treatment in past 6mth or palliative)
Source:data from Wells etal. Thromb Haemost 2000;83:358.
9
NICE guidelines available at Mguidance.nice.org.uk/ NG58
0
3mth may suce if low risk (eg rst PE with identied risk factor now removed); if higher risk
(recurrent or unprovoked PEs, or thrombophilia) treatment may need to be longterm.
In pregnancy, D- dimer testing uninterpretable. If clinical suspicion, Doppler US of leg veins is safest initial in-
vestigation— treat if DVT. If negative, half- dose V/ Q scan provides acceptable balance of utility and radiation
exposure. Risk of CTPA not to foetus (which can be shielded) but to proliferating maternal breast tissue.
0