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4 Chest medicine
Avian (pandemic) influenza
https://t.me/med1917
Avian influenza A viruses rarely infect humans and most follow direct or close
contact with infected poultry. The issue remains a public health priority because of the ability of the virus to mutate. Symptoms range from conjunctivitis
to influenza- like illness (low pathogenic forms) to severe respiratory illness and
multi- organ failure (highly pathogenic forms).
sible for most human illnesses worldwide. Highly pathogenic avian
viruses are endemic among bird and poultry populations in Eurasia.
avian flu if fever (>
38
°C), chest signs or consolidation on
infection, and contact with poultry or others with similar symptoms.
dominal pain, pleuritic pain, and bleeding from the nose and gums are reported to
be an early feature in some patients.
21
Diagnosis Viral culture ± reverse transcription
mers of respiratory specimens.
p
393
, in the UK, via your consultant in communicable disease control.23 Ventilatory
support + O
oseltamivir, peramivir, and zanamivir. Nebulizers and high- air flow O
and antivirals may be needed. Most viruses are susceptible to
2
implicated in nosocomial spread.
22 Management Get help. Contain the outbreak,
21,24
Antigenic diversity and uncertainty of the
H7N9
PCR
and
with
H5N1
CXR
have been respon-
H5N1
influenza
Suspect
, or life- threatening
20
NB:
D&V
H5-
& N1- specific pri-
masks are
2
, ab-
next pandemic virus subtype render vaccine preparedness dicult.
Precautions for close contacts of infected patients
Hand hygiene, avoid shared utensils and face- to- face contact, wear high- eciency
masks and eye protection. Start empirical antiviral treatment (oseltamivir within
48
h of exposure and zanamivir within 36h). Monitor for fever, cough, shortness of
breath, diarrhoea, or other systemic symptoms developing.
171
Coronaviruses:
Coronavirus disease
COVID- 19, SARS
2019
Severe acute respiratory syndrome (
onavirus. Major features are persistent fever (>
cough, headache, diarrhoea, and dyspnoea— with an abnormal
Respiratory failure is a complicating feature: ~
distress syndrome requiring invasive ventilation.
on age, but no cases since
cases should raise suspicion. The mechanism of transmission of
human– human.
Management: seek expert help. Largely supportive with good in-
fection control measures.
Middle East respiratory syndrome (
by novel coronavirus (
Symptoms include fever, cough, shortness of breath, and gastrointestinal upset.
Incubation period
most cases, but camels play a pivotal host role in animal- to- human transmission.
days. Human- to- human transmission has been reported in
Large outbreaks linked to healthcare facilities have been reported in the Middle
East and South Korea. The
, and
MERS
(
COVID- 19
) See p
172
.
SARS
25
) Caused by
20
2004
. Close contacts, or travel to an area with known
MERS
MERS CoV
WHO
has reported mortality up to 36%.
) A viral respiratory disease caused
) and first identified in
SARS- CoV
38
°C), chills, rigors, myalgia, dry
% progress to acute respiratory
26
Mortality is 1– 50%, depending
2012
virus— a cor-
CXR
and
WCC
SARS- CoV
is
in Saudi Arabia.
23
.
4 Chest medicine
COVID- 19
https://t.me/med1917
172
Coronavirus disease
SARS- CoV- 2
virus. The first outbreak of
China, and quickly spread globally to become a pandemic that aected >
lion people. Several variants of
continue to generate some concern because of their potential for increased transmissibility, more breakthrough infections in vaccinated individuals, and reinfection
risk in those previously infected with other variants. Fortunately, these variants
have been associated with less severe illness.
Natural history Varies from mild or asymptomatic infection to critical, life-
threatening illness with
pregnancy, and immunosuppression are all associated with more severe illness.
Severe disease aects ~
COVID- 19
for
to symptom onset.
may extend to
28
Mode of transmission Direct person- to- person transmission via respiratory
droplet secretion (eg coughing, sneezing, talking) is the main means of transmission.
Transmission most likely occurs during the early stage of infection (even prior to
symptom onset) and in enclosed, poorly ventilated spaces.
Clinical features Symptoms Most symptomatic infections are mild. Major fea-
tures are cough, breathlessness, fever, myalgia, headache, and anosmia/ ageusia.
Signs Pyrexia, hypoxia. The degree of hypoxia can be out of keeping with clinical
signs and symptoms.
Complications Respiratory failure, secondary bacterial infections (20%),
arrythmias, heart failure,
GBS), AKI
. The frequency and pathophysiology of 'long
(
viral/ critical illness symptoms such as fatigue, cough, anxiety, poor memory &
concentration) is unclear.
Tests Diagnosis is via nasopharyngeal and oropharyngeal swabs (reverse transcrip-
RT)- PCR
tion (
) with serology more useful to confirm past infection. Antigen testing
(lateral flow tests) is faster and may be an acceptable alternative in some settings
but it is less sensitive than
D
- dimer,
LFTS. CXR/ CT
eral, peripheral, and lower lung zone distributions (
Management High- flow nasal cannula (
for all hypoxic patients as it mortality ± tocilizumab or baricitinib if high O
quirements.
29
There is some evidence that remdesivir may reduce time to recovery
and risk of mechanical ventilation in patients with risk factors for severe illness but
no mortality benefit.
cases, mechanical ventilation ±
Prevention Physical distancing, and isolation have some role. The eectiveness of
FFP3
routine non-
mask wearing in public is less clear. In clinical areas
respirators appear eective in reducing transmission and general infection control
measured in should be strictly adhered to. Isolation for
also helps reduce nosocomial infection.
Vaccines & immunity Following infection, individuals will have a protective im-
mune response for at least
severe illness and essential for all. Several are now available including
cines (Pfizer & Moderna;
(AstraZeneca & Johnson & Johnson;
GBS
possibly
). Due to the possibility of waning immunity over time and the risk of
immune escape by new variants, a booster dose is recommended
completion of the primary series to further reduce the risk of symptomatic or severe infection. Additional doses may be needed in immunocompromised individuals,
eg those receiving chemotherapy and those who are dialysis dependent to maximize
immune response.
2019
(
COVID- 19
) was caused by a novel coronavirus, designated
COVID- 19
acute respiratory illness occurred in
700
SARS- CoV- 2
have since emerged, eg Omicron, that
ARDS
. Male sex, hypertension,
15– 20
% of unvaccinated individuals. The incubation period
CVD, DM
, chronic lung disease,
days, with a median time of 4– 5 days from exposure
VTE
(10– 40%), encephalopathy, Guillain– Barré syndrome
RT- PCR
. Blood tests: lymphocytes,
COVID
' (persistent post-
CRP,
fibrinogen,
thorax Consolidation and ground- glass opacities, with bilat-
fig
4.12
HFNC
) oxygen or
VTE
prophylaxis. Prone positioning may be helpful. In severe
ECMO.
Infection control measures.
6– 8
months. Vaccination is highly eective against
SE
: rarely myocarditis) and 2 adenoviral vector vaccines
SE
: vaccine- induced
).
NIV.
Dexamethasone (6mg)
COVID
+ ve patients and sta
ITP (VITT—
see p
2– 3
months after
FFP3
2
m
masks/
RNA
343
mil-
re-
2
vac-
) and
27
4 Chest medicine
https://t.me/med1917
Fig 4.
12
CXR:
and mid to lower lung zone distribution consistent with pneumonitis. Note also the presence of
chronic pleural plaques.
bilateral patchy and/ or confluent, bandlike ground- glass consolidation in a peripheral
The Valley of the Shadow of Death
173
Fig 4.
13
Crimean War: ambulancemen carrying the wounded in the Valley of the Shadow of
Death. Coloured lithograph by J. Needham,
Wellcome Collection. Public Domain Mark. https:// wel lcom ecol lect ion.org/ works/ ynmyg sd2
Most of the time we are unaware of our place in this world. It takes a pandemic or war
fig
4.13
) to remind us that we have a responsibility or role that extends far beyond the
(
reaches of a job description. As doctors, we may sometimes feel like gatekeepers in
this endless cycle of life and death but more often than we would care for, we are helpless bystanders with just a closer view than most. To bear witness to so much tragedy
and grief takes a very personal toll, not least in the midst of a pandemic, but within
this pain, there remains a great privilege that we can oer support and comfort during
these dark hours. Let us find solace in the words of the poet Seamus Heaney that ‘Hope
is not optimism, which expects things to turn out well, but something rooted in the
conviction that there is good worth working for.’
1855
, after W. Simpson.
4 Chest medicine
Fungi and the lung
ABPA
https://t.me/med1917
174
Aspergillus This group of fungi aects the lung in five ways:
1
Asthma Type I hypersensitivity reaction to fungal spores (p
2
Allergic bronchopulmonary aspergillosis (
sensitivity reactions to Aspergillus fumigatus. Aects
CF
patients.30 Initially bronchoconstriction, then permanent damage occurs causing
bronchiectasis (
taining fungal hyphae, see
fig
4.14
). Symptoms: wheeze, cough, sputum (plugs of mucus con-
p
404
in a predisposed patient, Aspergillus- specific
positive Aspergillus skin test, and serum
) Results from type I and
), dyspnoea, and ‘recurrent pneumonia’). Diagnosis:
IgE RAST
IgE
. Other criteria: positive serum precipi-
160
1– 5
% of asthmatics, 2– 25% of
(radioallergosorbent test),
tins, typical radiological findings (eg transient segmental collapse or consolidation,
central proximal bronchiectasis), and eosinophilia. Tr ea tm en t: mainstay is oral corticosteroids with a tapering course. Antifungal therapy, eg voriconazole added for
steroid weaning. Bronchodilators for asthma.
3
Aspergilloma (mycetoma) A fungus ball within a pre- existing cavity (often caused by
TB
or sarcoidosis). It is usually asymptomatic but may cause cough, haemoptysis (may
be torrential), lethargy ± weight loss. Investigations:
cavity, usually apical); sputum culture; strongly positive serum precipitins; Aspergillus
30
skin test (
and consider surgical resection if this fails. Use antifungal therapy adjunctively post-
% + ve). Tr ea tm e nt antifungal therapy if symptomatic or growing in size
CXR/ CT
(round opacity within a
resecti on and in those with progressive radiological findings/ symptoms who are unable to undergo surgery. If massive haemoptysis, may need to consider embolization.
4
Invasive aspergillosis Risk factors: 31 immunocompromise, eg
ANCA
burns,
vasculitis (p
700
), and
SLE
, or after broad- spectrum antibiotic therapy.
However, also increasingly recognized in immunocompetent, critically ill patients.
Investigations: serum biomarkers including galactomannan (an Aspergillus anti-
gen) and -
for fungal staining and culture;
BAL
to
progressive disease. Prognosis:
5
Hypersensitivity pneumonitis (extrinsic allergic alveolitis) See p
D
- glucan (non- specific; a cell wall component of many fungi), sputum
, transbronchial, CT- guided or
IV
amphotericin. 32 Consider adding echinocandin for first 1– 2 weeks if severe or
CXR/ CT
(consolidation, abscess); broncho scopy with
VATS
biopsy. Trea tm en t : voriconazole is superior
30
% mortality.
Other fungal infections Candida and Cryptococcus may cause pneumonia in the
p
404
immunosuppressed (
).
).
HIV
, leukaemia,
193
III
hyper-
.
Fig 4.
14
Aspergillosis.
4 Chest medicine
Complications of pneumonia
https://t.me/med1917
Respiratory failure (See p
common. Treatment is with high- flow (
hypoxia does not improve with O
in
COPD
patients; check
O
2
or worsening acidosis. Aim to keep SaO2 at 94– 98%, PaO2 ≥8kPa.
P
aCO2
Hypotension and septic shock May be due to a combination of volume depletion
and vasodilation due to sepsis. If systolic
500
mL crystalloid over 15min. If systolic BP remains <90mmHg despite adequate
of
fluid resuscitation (ie
request urgent
ITU
Atrial fibrillation (See p
ment of the pneumonia but the patients may still require long- term anticoagulation
depending on
required to slow the ventricular response rate in the short term.
CHA2DS
(Parapneumonic) pleural eusion Inflammation of the pleura by adjacent pneu-
monia may cause fluid exudation into the pleural space. If this accumulates faster
than it is reabsorbed, a pleural eusion develops. If small, it may be of no consequence. If larger and patient symptomatic, or infected (empyema), drainage is re-
p
176
, p
quired (
750
Empyema Pus in the pleural space. It should be suspected if a patient with a re-
solving pneumonia develops a recurrent fever. Clinical features:
pleural eusion. The aspirated pleural fluid is typically yellow and turbid with a pH
7.2
, glucose, and
<
serted under radiological guidance. Adhesions and loculation can make this dicult.
Lung abscess A cavitating area of localized, suppurative infection within the lung.
Causes •Most commonly, aspiration (eg alcoholism, oesophageal obstruction,
bulbar palsy).
foreign body).
endocarditis,
•Inadequately treated pneumonia. •Bronchial obstruction (tumour,
•Pulmonary infarction. •Septic emboli (septicaemia, right heart
IV
drug use). •Subphrenic or hepatic abscess.
Clinical features Swinging fever; cough; purulent, foul- smelling sputum; pleuritic
chest pain; haemoptysis; malaise; weight loss. Look for: finger clubbing; anaemia;
crepitations. Empyema develops in
Tests Blood:
copy, culture, and cytology.
CT
scan to exclude obstruction, and bronchoscopy to obtain diagnostic specimens.
FBC
(anaemia, neutrophilia),
Treatment Antibiotics as indicated by sensitivities; empiric regimens should target
both strict anaerobes and facultatively anaerobic species (ie streptococci); continue until healed (
stillation, or surgical excision may be required.
Septicaemia May occur as a result of bacterial spread from the lung parenchyma
into the bloodstream. This may cause metastatic secondary infection, eg infective
endocarditis, meningitis. Treat with
Pericarditis and myocarditis May also complicate pneumonia.
Jaundice This is usually cholestatic, and may be due to sepsis or secondary to anti-
biotic therapy (particularly flucloxacillin and co- amoxiclav).
158
.) Type I respiratory failure (PaO2 <8kPa) is relatively
60
%) oxygen. Transfer the patient to
therapy or PaCO2 rises to >6kPa. Be careful with
2
ABG
S frequently, and consider elective ventilation if rising
BP
is <90mmHg, give an IV fluid challenge
30
mL/ kg over 3h period), this may indicate septic shock—
assessment for vasopressor support.
126
.) Common in the elderly. It usually resolves with treat-
-
VAS
c score and other risk factors. - blocker or digoxin may be
2
).
CXR
LDH
. The empyema should be drained using a chest drain, in-
20– 30
%.
ESR, CRP
CXR:
walled cavity, often with a fluid level. Consider
4– 6
wks). Postural drainage. Repeated aspiration, antibiotic in-
IV
antibiotic according to sensitivities.
, blood cultures. Sputum micros-
ITU
indicates a
175
if
4 Chest medicine
Pleural eusion
https://t.me/med1917
176
Definitions A pleural eusion is fluid in the pleural space. Eusions can be divided
by their protein concentration into transudates (<
table
4.7
see
. Blood in the pleural space is a haemothorax, pus in the pleural space is
an empyema, and chyle (lymph with fat) is a chylothorax. Both blood and air in the
pleural space is called a haemopneumothorax.
Causes Tr an su da tes may be due to venous pressure (cardiac failure, constrictive
pericarditis, fluid overload), or hypoproteinaemia (cirrhosis, nephrotic syndrome,
malabsorption). Also occur in hypothyroidism and Meigs’ syndrome (right pleural
eusion and ovarian fibroma).
pleural capillaries secondary to infection, inflammation, or malignancy. Causes: pneu-
TB
; pulmonary infarction; rheumatoid arthritis;
monia;
malignant metastases; lymphoma; mesothelioma; lymphangitic carcinomatosis.
Symptoms Asymptomatic— or dyspnoea, pleuritic chest pain.
Signs Decreased expansion; stony dull percussion note; diminished breath sounds
occur on the aected side. Tactile vocal fremitus and vocal resonance are (inconstant and unreliable). Above the eusion, where lung is compressed, there may
be bronchial breathing. With large eusions there may be tracheal deviation away
from the eusion. Look for aspiration marks and signs of associated disease: malignancy (cachexia, clubbing, lymphadenopathy, radiation marks, mastectomy scar);
stigmata of chronic liver disease; cardiac failure; hypothyroidism; rheumatoid arthritis; butterfly rash of
Tests
CXR
Small eusions blunt the costophrenic angles, larger ones are seen as
water- dense shadows with concave upper borders (
zontal upper border implies that there is also a pneumothorax.
Ultrasound Useful in identifying the presence of pleural fluid and in guiding diag-
nostic or therapeutic aspiration. Detects pleural fluid septations with greater sensitivity than
CT
scanning.
Diagnostic aspiration
guided to improve success rate, reduce complications (including pneumothorax),
and reduce the risk of organ puncture. Infiltrate down to the pleura with
1
% lidocaine. Attach a
of
border of an appropriate rib (avoids neurovascular bundle). Draw o
pleural fluid and send it to the lab for clinical chemistry (protein, glucose, pH,
amylase), bacteriology (microscopy & culture, auramine stain,
(malignant eusions can be diagnosed based on pleural fluid cytology results in
60
% of cases), and, if indicated, immunology (rheumatoid factor,
ment). Send adenosine deaminase if a
should be used to distinguish between a pleural fluid exudate and transudate. In
order to apply Light’s criteria, the total protein and
in both blood and pleural fluid. See
CT thorax With pleural phase contrast enhancement should be considered in all
patients with an undiagnosed exudative pleural eusion. Useful in distinguishing
malignant from benign pleural thickening.
Pleural biopsy If pleural fluid analysis is inconclusive, consider parietal pleural
biopsy. Thoracoscopic or
enabling direct visualization of the pleural cavity and biopsy of suspicious areas).
Management is of the underlying cause.
• Drainage: if the eusion is symptomatic or if empyema is present (pH <7.2), drain
it, repeatedly if necessary. Fluid is best removed slowly (
aspirated in the same way as a diagnostic tap, or using an intercostal drain (
• Pleurodesis with talc may be helpful for recurrent eusions. Thoracoscopic mech-
anical pleurodesis is most eective for malignant eusions. Empyemas (
best drained using a chest drain, inserted under ultrasound or
• Intra- pleural alteplase and dornase alfa may help with empyema.
• Surgery: persistent collections and increasing pleural thickness requires surgery.
25
g/ L) and exudates (>35g/ L),
Exudates are mostly due to increased leakiness of
SLE
; bronchogenic carcinoma;
SLE
.
fig
4.15
). A completely flat hori-
33
BTS
recommend that all aspirates should be ultrasound-
21G
needle to a syringe and insert it just above the upper
TB
culture), cytology
TB
eusion is suspected. Light’s criteria
LDH
table
4.7
.
CT
- guided pleural biopsy increases diagnostic yield (by
values should be measured
0.5– 1.5
ANA
L/ 24h). It may be
CT
guidance.
5– 10
10– 30
, comple-
p
175
mL
mL of
LDH
p
750
) are
,
).
34
4 Chest medicine
Table 4.
)(
https://t.me/med1917
7
Pleural fluid analysis
Gross appearance Cause
Clear, straw- coloured Transudate, exudate
Turbid, yellow Empyema, parapneumonic eusion
Haemorrhagic Trauma, malignancy, pulmonary infarction
Cytology
Neutrophils + +
Lymphocytes + +
Parapneumonic eusion,
Malignancy,
TB, RA, SLE
PE
, sarcoidosis
Mesothelial cells + + Pulmonary infarction
Abnormal mesothelial cells Mesothelioma
Multinucleated giant cells
Lupus erythematosus cells
RA
SLE
Malignant cells Malignancy
Clinical chemistry
*Protein<25g/ L
>
35
g/ L
25– 35
g/ L
Glucose <
3.3
pH <7.
*
mmol/ L Empyema, malignancy,
2
LDH
(pleural:serum >0.6) Empyema, malignancy,
Transudate
Exudate
Use Light's criteria: if pleural fluid protein/ serum protein
0.5
or ple ural
LDH
/ serum
LDH
>
Empyema, malignancy,
>0.6, eusion is an exudate
TB, RA, SLE
TB, RA, SLE
TB, RA, SLE
Amylase Pancreatitis, carcinoma, bacterial pneumonia, oesopha-
geal rupture
Immunology
Rheumatoid factor
Antinuclear antibody
Complement levels
* Light’s criteria for defining an exudate: eusion protein/ serum protein >0.5; eusion
eusion
LDH
>⅔ upper reference ran ge for seru m
RA
SLE
RA, SLE
, malignancy, infection
LDH
. 98% sensitive and 83% specific.
LDH
/ serum
LDH
177
>0.6;
(a
(c) (d)
b)
Fig 4.
15
CXR
rance s of a freeflowing left pleural
eusion imaged erect
(a); a massive right
pleural eusion with
mediastinal shift (b);
and a pleural eusion
radiographed supine
(c) and erect (d) in the
same patient.
appea-
Reproduced from
Firth J et al., Oxford
Textbook of Medicine
2020
, with permission
from Oxford
University Press.
4 Chest medicine
Acute respiratory distress syndrome (
ARDS
https://t.me/med1917
178
ARDS
is a type of respiratory failure characterized by the acute onset of bilateral
alveolar infiltrates and hypoxaemia. Lung injury causes increased capillary permeability resulting in excess fluid in both the interstitium and alveoli. This leads to
impaired gas exchange, decreased compliance, increased pulmonary arterial pressure, and non- cardiogenic pulmonary oedema, often accompanied by multiorgan
failure. The myriad of causes are listed below and on
which are pneumonia, sepsis, and aspiration.
Causes Pulmonary Pneumonia; gastric aspiration; inhalation injury; vasculitis
p
554
); contusion. Other Shock; sepsis; haemorrhage; multiple transfusions;
(
p
350
); pancreatitis; acute liver failure; trauma; head injury; malaria; fat embolism;
(
burns; obstetric events (eclampsia; amniotic fluid embolus); drugs/ toxins (aspirin,
heroin, paraquat).
Clinical features Cyanosis; tachypnoea; tachycardia; peripheral vasodilation; bilat-
eral fine inspiratory crackles.
blood cultures, troponin,
culture, respiratory BioFire®
with dependent atelectasis. There are usually widespread patchy and/ or coalescent airspace opacities, particularly in the dependent lung zones on
be helpful if uncertainty whether cardiogenic vs non- cardiogenic pulmonary oedema. Occasionally, pulmonary artery catheter was used in the past to measure
pulmonary capillary wedge pressure (
tions/ mortality so is no longer routinely indicated.
Dierential diagnoses Cardiogenic pulmonary oedema, bilateral pneumonia, dif-
fuse alveolar haemorrhage, vasculitis, cryptogenic organizing pneumonia.
Diagnostic criteria Are as follows: 1 Respiratory symptoms must have begun within
1
week of a known clinical i nsult. 2
failure n ot fully explained by cardiac failure o r fluid overload.
impairment of oxygenation must be present, as defined by the ratio of arterial oxygen
tension to fraction of inspired oxygen (P
40
kPa) for
ARDS
(or <
and is cla ssified as seve re if ≤
Management Admit to
• Respiratory support In early
face mask or high- flow nasal cannulae (
CPAP
) with 40– 60% oxygen may be adequate to maintain oxygenation. But
sure (
most patients need mechanical ventilation. The large tidal volumes (
produced by conventional ventilation plus reduced lung compliance in
lead to high peak airway pressures leading to barotrauma ± pneumothorax. Lung
protective ventilation with a tidal- volume of
proach, with either low or moderate high positive end- expiratory pressure (
improves outcome.
the majority), neuromuscular blockade or
tentially reversible acute respiratory failure—
• Circulatory support Invasive haemodynamic monitoring with an arterial line and
central venous catheter. A conservative fluid management approach improves outcome. Maintain cardiac output and O
transfusion. Consider using nitric oxide, a pulmonary vasodilator that improves oxygenation due to better
• Sepsis Identify organism(s) and treat. If septic, but no organisms cultured, use
empirical broad- spectrum antibiotics (
60
% of severe
• Other Nutritional support: enteral is best: p
formulations. Steroids may have a mortality benefit in moderate– severe refractory
ARDS
ARDS
to standard therap ies.38
Prognosis Mortality has declined over time but remains at least 25– 40%. However,
prognosis varies with age of patient, cause, and number of organs involved.
)
p
179
, the most common of
Investigations
BNP, D
- dimer, lactate,
PCR
±
BAL. CXR
FBC, U&E, LFT
ABG. COVID
, amylase, clotting,
/influenza swab. Sputum
shows bilateral diuse alveolar opacities
CT. TTE
PCWP
) but this is associated with complica-
may
35
CXR
or CT: bilateral infiltrates (fig
/ FiO2). The PaO2: FiO2 is typic all y ≤
aO2
100
ITU
; give supportive therapy; treat the underlying cause.
ARDS,
high- flow oxygen can be provided through a
37
Consider proning (>16h per day— improves oxygenation in
delivery with inotropes, vasodilators, and blood
2
V/ Q
matching a nd helps ameliora te pulm onary hypert ensio n.
patients.
DVT
p
and GI ble eding prop hylaxis. Gluc ose contro l.
mmHg (<14kPa).
HFNC
). Continuous positive airway pres-
6– 8
mL/ kg
ECMO
(for patients with severe but po-
p
784
).
169
). Nosocomial pneumonia develops in
584
& p
585
4.16
). 3 Respiratory
4
A moderate to severe
300
mmHg
36
10– 15
mL/ kg)
ARDS
may
IBW
, pressure- limited ap-
PEEP
, with high- fat, antioxidant
39,40
DIC
CRP
,
),
4 Chest medicine
Fig 4.
https://t.me/med1917
16
Supine chest radiograph showing air- space shadowing in a perihilar distribution
spreading into the peripheries. This appearance can also be seen with infection and cardiogenic
pulmonary oedema, but clues from the history, the heart size, and lack of pleural eusions can
ARDS
suggest
lying flat with the
larged and pleural eusions to level out on the posterior chest wall so they will not obscure the
costophrenic angles unless very large.
over the latter. Remember though that this is a supine projection— the patient is
X
- ray beam anteroposterior— causing the cardiac shadow to be artificially en-
Image courtesy of Nottingham University Hospitals
NHS
Trust Radiology Department.
179
Risk factors for
ARDS
• Sepsis
• Hypovolaemic shock
• Tra um a
• Pneumonia
• Diabetic ketoacidosis
• Gastric aspiration
• Pregnancy
• Eclampsia
• Amniotic fluid embolus
• Drugs/ toxins
• Paraq uat, heroi n, aspi rin
• Pulmo nary contusion
• Massive transfusion
• Burns (p
828
• Smoke inhalation
• Near drowning
• Acute pancreatitis
•
DIC
• Head injury
•
• Fat em bo lu s
• Heart/ lung bypass
• Tu mo ur ly si s sy nd ro me ( p
• Malaria
)
(p
350
)
ICP
525
)
4 Chest medicine
Bronchiectasis
HRCT
https://t.me/med1917
180
Pathology Chronic inflammation of the bronchi and bronchioles leading to per-
manent dilatation and thinning of these airways. The induction of bronchiectasis
requires an infectious insult plus impairment of drainage, airway obstruction, and/
or a defect in host defence. Exacerbations are caused by acute bacterial infections,
typically H. influenzae; Strep. pneumoniae; Staph. aureus; Pseudomonas aeruginosa.
Causes Congenital Cystic fibrosis (CF); Young’s syndrome; primary ciliary dyskin-
OHCS
p
850
esia; Kartagener’s syndrome (
chiolitis; pneumonia;
TB; HIV
. Other Bronchial obstruction (tumour, foreign body);
allergic bronchopulmonary aspergillosis (
). Post- infection Measles; pertussis; bron-
ABPA,
p
174
); hypogammaglobulinaemia;
rheumatoid arthritis; ulcerative colitis; idiopathic.
Clinical features Symptoms Persistent cough; copious purulent sputum; intermit-
tent haemoptysis.
(asthma,
Signs Finger clubbing; coarse inspiratory crepitations; wheeze
COPD, ABPA
). Complications Pneumonia, pleural eusion; pneumothorax;
haemoptysis; cerebral abscess; amyloidosis.
Tests Sputum culture.
and ring shadows); see
sess extent and distribution of disease. Typical findings include airway dilatation,
lack of airway tapering, bronchial thickening, and cysts.
an obstructive pattern; reversibility should be assessed.
obstruction and obtain samples for culture.
gate site of bleeding/ embolizable target if significant haemoptysis. Serum immuno-
CF
globulins;
saccharin, nasal brushings, nasal
and total
sweat test or
IGE
.
CXR
: cystic shadows, thickened bronchial walls (tramline
fig
4.17
.
chest (p
156
) is required to diagnose and to as-
Spirometry often shows
Bronchoscopy to exclude
Other tests CT angiogram to investi-
CFTR
genotyping; test for primary ciliary dyskinesia, eg
NO
; Aspergillus precipitins or skin- prick test
Management • Treat the underlying disease where possible, eg certain im-
munodeficiencies,
mucolytics:
sputum expectoration and mucus drainage.
cording to bacterial sensitivities but azithromycin is frequently used prophylactically. Pseudomonas will require either oral ciprofloxacin or suitable
If ≥
3
exacerbations a year consider long- term antibiotics (may be nebulized).
CF
, recurrent aspiration. • Airway clearance techniques and
chest physiotherapy and devices such as a flutter valve may aid
• Antibiotics should be prescribed ac-
• Bronchodilators (eg nebulized salbutamol) may be useful in patients with asthma,
COPD, CF, ABPA
(p
174
). • Corticosteroids (eg prednisolone) and itraconazole for
• Surgery may be indicated in localized disease or to control severe haemoptysis.
Bronchial artery embolization may be needed for patients with brisk haemoptysis.
• Other: immunizations,
with moderate- to- severe airflow limitation on
PPI
if
GORD
present, pulmonary rehabilitation for patients
PFTS.
IV
antibiotics.
RAST
ABPA
.
Fig 4.
17
Poste roanter ior (PA) chest
radio graph showing marked abnormal
dilatation of the airways throughout the
right upper lobe, subtle similar changes
throughout the rest of the lung (particularly periphery of the left upper zone).
The fine background reticular pattern in
the lungs suggests that there may also
be some interstitial lung disease present.
Image courtesy of Nottingham University
Hospitals
NHS
Trust Radiology Department.
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