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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2935_Библиотеки_им_академика_М_И_Перельмана
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Fungal Diseases of the Lung216
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Figure 13.6 Chest CT of patient with PCP; the CT shows septal thickening and ground
glass changes.
7. DIFFERENTIAL DIAGNOSIS
ere are many respiratory diseases with similar presentations to PCP:
•
• Infectious:
– Bacterial pneumonia
– Viral pneumonia
– Influenza
– Pulmonary TB
– Mycobacterium avium complex (MAC)
– Cytomegalovirus (CMV)
– Coccidioidomycosis
– Histoplasmosis
– Cryptococcus
– Blastomycosis
– Penicillinosis.
• Non-infectious:
Respiratory Medicine
– Acute respiratory distress syndrome (ARDS)
– Lymphocytic interstitial pneumonia
13.6 Pneumocystis Pneumonia (PCP/PJP)
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– Sarcoidosis
– Kaposi sarcoma
– Interstitial lung disease.
8. MANAGEMENT
e first-line treatment for PCP is co-trimoxazole 15- 20mg / kg /day
•
(trimethoprim/sulfamethoxazole).
• Treatment course is typically for 3 weeks.
In severe PCP infection the patient may need:
•
• Mechanical ventilation.
• Prednisolone 40 mg PO BD (with a reducing regime after 5 days of
therapy).
9. COMPLICATIONS
Complications that occur with PCP may be due to the disease itself or drugs
•
used to treat it:
• Respiratory failure.
• ARDS.
• Pneumothorax.
• Immune-reconstitution inflammatory syndrome (IRIS).
– In AIDS patients due to restoration of immune function on highly
active antiretroviral therapy (HAART).
• Drug adverse reactions including kidney injury.
• Death.
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10. PROGNOSIS
Mortality for PCP is around 11% the following factors increase the chance of
•
a poor prognosis:
• Increasing patient age
• Medical co-morbidities
• Previous PCP episodes
• Pulmonary Kaposi sarcoma
• AIDS diagnosis (CD4 count < 200 )
• Being HIV negative
• Illicit drug use.
Clinical indicators of a poor prognosis:
•
• Increased respiratory rate.
• Decreased partial pressure of O
• Hypoalbuminaemia.
• ↑ White cell count.
• ↓ Haemoglobin on admission.
• Neurological signs and symptoms.
• Patient requiring mechanical ventilation.
on room air.
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Respiratory Medicine
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Sleep Disordered
Breathing
14.1 OBSTRUCTIVE SLEEP APNOEA/
HYPOPNOEA SYNDROME (OSAHS)
1. DEFINITION
OSAHS is a sleep disordered breathing syndrome characterised by episodes
•
of partial or complete upper airway collapse during sleep causing significant
daytime sleepiness.
An apnoea is a 10-second or greater pause in breathing.
•
Hypopnoea is a 10-second or greater reduction in airflow by at least 30%
•
with oxygen desaturation of 3%.
Apnoea/hypopnoea index (AHI): number of apnoeic and hypopnoeic events
•
per hour.
2. EPIDEMIOLOGY
OSAHS is a common and under-diagnosed condition with a prevalence of
•
4% in men and 2% in women.
Prevalence is related to levels of obesity.
•
3. AETIOLOGY
Structural causes:
•
• Craniofacial abnormalities.
• Mandibular hypoplasia or retroposition.
• Nasal obstruction from causes such as polyps and septal deviation.
• Macroglossia.
• Adenotonsillar hypertrophy.
• Pharyngeal fat deposition.
Non-structural risk factors:
•
• Male sex.
• Obesity.
• Increasing age.
• Use of sedatives or alcohol.
DOI: 10.1201/9781315113937-15
14.1 Obstructive Sleep Apnoea/Hypopnoea Syndrome (OSAHS)
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• Smoking.
• Family history.
4. PATHOPHYSIOLOGY
Airway collapse secondary to pharyngeal dilator muscles inability to maintain
•
patency due to muscle relaxation/weakness and/or small pharyngeal size.
e patient may undergo apnoea or hypopnoea associated with hypoxia and
•
possibly hypercapnia resulting in arousal.
• e patient is not aware of this, but it is detectable on EEG (electroen-
cephalogram) and results in fragmented sleep and daytime somnolence.
Arousal is associated with increased blood pressure, up to an increase of
•
50 mmHg.
• Effective treatment of OSAHS with CPAP (continuous positive airway
pressure) reduces daytime blood pressure by 3 mmHg.
• e rise in blood pressure is also associated with a rise in pulse.
Hypoxia causes oxidative stress, which along with the cardiovascular disrup-
•
tion of OSAHS is thought to contribute to:
• Atherosclerosis
• Myocardial ischaemia
• Left ventricular hypertrophy
• Left ventricular failure
• Cardiac arrhythmias
• Cerebrovascular disease
• Metabolic syndrome
• Insulin resistance.
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MICRO-facts
Taking a sleep history:
Quality of sleep.
•
• Quantity of sleep.
• Shift work.
• Use of sedatives.
• Use of alcohol.
• Unusual behaviour during sleep.
• Signs of restless leg syndrome.
Signs of depression.
•
5. CLINICAL FEATURES
e most common presentation is excessive daytime somnolence and unre-
•
freshing sleep.
A collateral history may identify snoring or apnoeic episodes unknown to the
•
patient.
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Sleep Disordered Breathing220
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Figure 14.1 Pathophysiology of nocturia in OSAHS.
Patient may report waking up choking.
•
Irritability, change in personality or poor concentration.
•
Morning headache reflects significant nocturnal hypoventilation.
•
Decreased libido/impotence.
•
Nocturia (see Figure 14.1).
•
Occupation: daytime somnolence may impact upon driving.
•
• Occupation may be relevant, e.g. HGV drivers may be unsafe to con-
tinue with driving if OSAHS is untreated.
ere are many causes of disturbed sleep and sleepiness so a full sleep history
•
must be obtained (see MICRO-Facts box).
6. EXAMINATION
Record weight and BMI.
•
Neck circumference more than 17 inches is associated with OSAHS.
•
Inspect mandibular size, teeth and oropharynx for crowding, enlarged tonsils
•
and macroglossia.
Assess nasal patency.
•
In addition, examine for signs or respiratory or cardiovascular disease.
•
7. INVESTIGATIONS
Epworth Sleepiness Scale (ESS), available at https://epworthsleepinessscale.
•
com:
• A subjective measure of how likely a patient is to fall asleep in a given
circumstance.
• A score of more than 10 is considered clinically relevant.
• is can be completed both by the patient, and by relative or partner, as
the patient may underestimate their symptoms.
• ESS of more than 10 with symptoms of OSAHS, or sleepiness in
dangerous conditions with normal ESS but in presence of symptoms of
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•
OSAHS should prompt referral for investigation.
Overnight oximetry
• Pulse oximetry can be used as a first line screening tool for OSAHS.
14.1 Obstructive Sleep Apnoea/Hypopnoea Syndrome (OSAHS)
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• A finger or earlobe pulse oximeter records heart rate and oxygen satura-
tions overnight. Oxygen desaturation index (ODI) reflects the number
of desaturation episodes >4% per hour.
• Interpretation of oximetry by an experienced practitioner can diagnose
OSAHS, but a normal tracing does not exclude the diagnosis.
Limited sleep studies
•
• A limited sleep study may measure pulse oximetry, thoraco-abdominal
movement, nasal airflow snoring, heart rate, and body movement.
• Limited sleep studies can be performed at home after instruction from a
sleep technician.
• Limited sleep studies are adequate for diagnosis of OSAHS in the
majority of patients.
Polysomnography (PSG):
•
• To perform PSG the patient must attend a sleep centre for overnight
monitoring with EEG, electromyogram (EMG), electro-oculogram,
oronasal flow monitors, thoraco-abdominal movement and oximetry
tracing.
• Although PSG has been considered the gold standard for diagnosing
OSAHS, it is expensive and time-consuming.
• Overnight hospital PSG is appropriate for a small number of patients
who cannot be investigated at home, or whose home study does not fit
with the clinical picture.
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MICRO-facts
Assessment of severity of OSAHS:
Mild: AHI 5–14/hr.
•
Moderate: AHI 15 – 30/hr.
•
Severe: >30/hr.
•
8. MANAGEMENT
Conservative management:
•
• Weight loss should be encouraged with or without CPAP.
• Patients should avoid alcohol in the evening, and minimise the use of
sedatives or sleeping tablets.
• e patient should avoid sleeping on their back if non-sleepy snorers.
Continuous positive airway pressure (CPAP):
•
• Splints the upper airway preventing collapse, and therefore sleep
fragmentation.
• Indicated in symptomatic moderate and severe OSAHS. ere is no
evidence for use in mild OSAHS.
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Sleep Disordered Breathing222
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• CPAP improves objective and subjective sleepiness, cognitive function,
mood, blood pressure and quality of life.
• Requires an adjustment period with input from a sleep technician to
maximise compliance and time on machine.
• Common side effects include rhinitis, pressure sores from mask, dis-
comfort, claustrophobia, abdominal bloating and noise, but intensive
input from a sleep technician can minimise these.
Mandibular advancement device (MAD):
•
• MADs work by producing anterior displacement of the mandible
increasing upper airway diameter.
• Fits to the upper and lower teeth, and allows the lower jaw to be dis-
placed forward by 51- 0mm .
• MADs are suitable in mild OSAHS and excessive snoring, and can be
tried in patients unable to tolerate CPAP.
Surgical management:
•
• ere is no evidence supporting the use of surgical techniques such as
uvulopalatopharyngoplasty or mandibular advancement osteotomy for
the treatment of snoring or OSAHS.
MICRO-print
Driving Advice
All patients should be advised not to drive when sleepy and advised
•
that falling asleep at the wheel is a criminal offence.
When diagnosed, patients should be told to inform the DVLA of the
•
diagnosis. They will also need to inform their insurance company.
If the patient is symptomatic, then they should not drive. Once their
•
symptoms are controlled and have been reviewed, they can resume
driving.
Holders of a bus, coach or lorry licence cannot resume driving until
•
they have been reviewed in a specialist clinic, have a normal ESS and
have adequate usage of their CPAP machine.
www.gov.uk/excessive-sleepiness-and-driving
•
14.2 CENTRAL SLEEP APNOEA
Central sleep apnoea is defined by reduction or absence of ventilation lasting
•
more than 10 seconds due to loss of neural output to the respiratory muscles.
Cheyne-Stokes respiration refers to periods of hyperventilation alternating
•
with central apnoea.
It is associated with heart failure, PH, stroke, neuromuscular disease, obesity,
•
Respiratory Medicine
hypoventilation syndrome and drug use.
CPAP, Adapto-Servo ventilation or BiPAP can be used to manage this condition.
•
14.4 Other Causes of Poor Sleep/Daytime Somnolence
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14.3 SLEEP-RELATED HYPOVENTILATION
Sleep-related hypoventilation is defined as an increased pCOk26 > PA
•
during sleep, or disproportionately raised nocturnal
daytime levels.
Sleep-related hypoventilation can be caused by decreased ventilatory drive, or
•
by failure of the mechanical aspect of ventilation.
Obesity hypoventilation disorder (previously called Pickwickian syndrome)
•
is the association of obesity and alveolar hypoventilation leading to hypercapnia. Respiratory failure is present in the awake daytime state. Often overlaps
with OSAHS with similar symptoms.
pCO2
compared to
14.4 OTHER CAUSES OF POOR SLEEP/
DAYTIME SOMNOLENCE
Shift work patterns
•
High caffeine intake
•
Alcohol intake
•
Drugs, e.g. benzodiazepines
•
Nocturia
•
Restless legs syndrome.
•
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Respiratory Medicine
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Occupational Lung
Disease
15.1 WORK-RELATED ASTHMA
1. DEFINITION
Work-related asthma (WRA) is subdivided into three main phenotypes:
•
• Work-aggravated asthma (WAA).
• Allergic occupational asthma due to allergic sensitisation.
• Irritant-induced asthma (IIA).
Patients with WAA either have pre-existing asthma or develop coincidental
•
adult-onset asthma and report symptoms that are made worse by non-specific
factors in the workplace such as exercise, cold air or dust.
In contrast, occupational asthma is caused by airborne exposures in the
•
working environment.
2. EPIDEMIOLOGY
Occupational asthma accounts for 1 in 6 cases of adult asthma.
•
e reported incidence of occupational asthma is between 12 and 300 cases/
•
million workers/year.
• e true incidence is likely to be higher as it is an under-diagnosed
disease.
One-third of patients diagnosed with occupational asthma are unemployed
•
up to 6 years after diagnosis.
3. AETIOLOGY
Inhaled aeroallergens can cause symptoms via immunological or non-
•
immunological means.
Immunologically mediated occupational asthma:
•
• Repeated exposure to high-molecular-weight agents and some low-
molecular-weight agents triggers an IgE response to the inhaled
substance.
– ese sensitiser-induced cases have a latency period between
exposure to the sensitiser and development of asthma symptoms.
DOI: 10.1201/9781315113937-16
15.1 Work-Related Asthma
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• In some patients with disease caused by low-molecular-weight agents,
there is often no clear IgE antigen detectable, or only detectable in
some.
– Patients in this group have symptoms consistent with allergic disease
and have reproducible symptoms to specific challenge tests.
– is subgroup of patients tend to be non-atopic non-smokers, and
have atypical or late asthmatic reactions.
Non-immunological occupational asthma:
•
• ere is no latency period between expose and symptoms.
• e symptoms are provoked by exposure to a high concentration of
irritant agent.
4. SYMPTOMS
Patients will present with the classic symptoms of asthma:
•
• Cough
• Wheeze
• Chest tightness
• Shortness of breath.
e patient may or may not link these symptoms to work, so it is impor-
•
tant that the diagnosis is considered in all causes of new or worsening adult
asthma.
Important points for history:
•
• A careful occupational history should be obtained including work
duties, possible irritants, level of exposure, use of protective devices and
any respiratory problems in colleagues.
• Patients should be asked if their symptoms improve when they are not
at work or on holiday.
• Atopy is associated with occupational asthma.
• Work-related rhinitis or conjunctivitis may be early signs of occupa-
tional asthma.
• It is important to assess the level of exposure to potential allergens as
this is a determinant of occupational asthma (See Table 15.1).
• You should be aware that the latency period between exposure and
developing symptoms can be up to several years in some cases.
Important point for examination:
•
• Expected examination findings will resemble those of asthma (see
Chapter 3: Asthma).
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Respiratory Medicine
5. INVESTIGATIONS
Presence of asthma should be confirmed (see Chapter 3: Asthma).
•
Peak expiratory flow rate (PEFR): e patient should keep a PEF diary tak-
•
ing recordings 4 times a day and noting when they are and are not at work.
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