Acute Respiratory Day 21st March 2007.

Pre-course material

1. Acute exacerbation of COPD

Exacerbations may be associated with:
Increased dyspnoea
Increased sputum purulence
Increased sputum volume

Indications for hospitalisation:
The presence of high risk co-morbid conditions including pneumonia, cardiac arrhythmia, congestive heart failure, uncontrolled diabetes mellitus, renal or liver failure
Inadequate response of symptoms to outpatient management
Inability to eat or sleep due to symptoms
Worsening hypoxaemia
Worsening hypercapnia
Change in mental status
Inability of the patient to care for her/himself (lack of home support)
Uncertain diagnosis

Investigations:
§ Routine biochemistry and haematology
§ Arterial blood gases on air if SaO2 on air< 92%
§ CXR to exclude other diagnoses (e.g. pneumonia, heart failure, pneumothorax)
§ Sputum culture
§ ECG if cardiac arrhythmia or ischaemia suspected

Principles of in-patient management:
§ Bronchodilators: regular nebulised salbutamol 2.5-5mg up to 2 hourly and ipratropium 500 mcg qds
§ Prednisolone: 40 mg orally for 7 days then stop if not on maintenance prednisolone
§ Antibiotics if two of:
§ increased breathlessness
§ increased sputum volume
§ sputum purulence
o Amoxicillin
o Fluoroquinolones, macrolide or augmentin if recent treatment with amoxycillin
§ DVT prophylaxis
§ Controlled oxygen therapy
o Primary aim to maintain oxygen saturation >90%
o See flow diagram
§ Remember that respiratory failure may be chronic
§ Nicotine replacement therapy for smokers



If not improving consider:
§ Alternative diagnosis
§ Adding IV aminophylline or salbutamol
(if patient is on oral theophylline already, omit aminophylline loading dose)
§ NIV or IV doxapram if respiratory acidosis develops
ITU referral

When to discharge:
Remember Early Supported Discharge programmes
Haemodynamic stablility
Oxygenation returned to baseline
Off parenteral therapy for 12-24 hrs
Inhaled β2-agonist therapy required less frequently
Symptoms returned to baseline
Mobility returned to pre-morbid state
Follow-up and home care arrangements completed (e.g. visiting nurse, oxygen delivery, home nebuliser if indicated, meal provisions etc)



Review medications prior to discharge:
Check inhaler technique
If FEV1 <50% predicted and 2 or more exacerbations per year consider
addition of ICS
Consider tiotropium
Consider carbocysteine to aid sputum clearance
Smoking cessation advice
Follow-up in respiratory clinic and PFT in 6-8 weeks if new diagnosis
of COPD or no lung function testing has been performed previously


Follow-up after exacerbation of COPD:
Review PFT findings and diagnosis
Evaluate improvement in symptoms and adjust the treatment regime
Re-assess blood gas profile if patient may require supplemental home oxygen
Refer pulmonary rehabilitation if suitable
Reinforce smoking cessation


2. Community Acquired Pneumonia

Aetiology:
Causes are only identified in 10-25% of cases, so treatment is usually empirical.

Streptococcus pneumoniae
§ the most common pathogen (40%) and all empirical antibiotic regimes must cover this organism
§ typically causes pleuritc chest pain

H. influenzae
§ the second most common pathogen (10%)

Mycoplasma pneumoniae
§ occurs in epidemics every four years

Legionella pneumophila
§ water distribution systems, foreign travel, especially to the Mediterranean, person-to person transmission rare
§ causes more severe pneumonia
§ associated with confusion, GI symptoms especially diarrhoea, hyponatraemia and abnormal LFTs

Staphylococcus aureus
§ causes more severe pneumonia
§ complicates influenza infection

Gram negative bacilli, Chlamydia psittaci/pneumoniae and Coxiella burnetii are uncommon causes of CAP.


Clinical features:
§ symptoms and signs consistent with acute LRTI
§ new radiographic shadowing for which there is no other explanation
§ elderly patients are more likely to present with non-specific symptoms and are less likely to have a fever


Assessment of severity:
CURB-65 score predicts mortality or need for ITU admission

One point for each of
C confusion
U urea >7 mmol/L
R RR ≥30/min
B Systolic BP <90mmHg or diastolic BP ≤60 mmHg
65 age ≥ 65


Score
Mortality or need for ITU admission
Management
0
0.7%
out-patient treatment
1
3.2%

2
13%
Short stay in hospital or hospital supervised treatment
3
17%
Severe pneumonia requiring hospital
4
41.5%
admission
5
57%



Investigations:
§ CXR
§ Routine biochemistry, haematology & inflammatory markers
§ ABGs ~ to assess acidosis and need for oxygen therapy

Microbiology (routine)
§ blood cultures
§ sputum for C+S
§ acute serum sample for storage
§ pleural fluid for C+S

Microbiology (severe CAP)
§ consider urgent Gram stain of sputum
§ Pneumococcal antigen (urine)
§ Legionella antigen (urine, only detects L. pneumophila serogroup 1), culture (sputum and bronchial aspirate, needs to be requested specifically) and serology (acute and convalescent samples)
§ Atypical serology
§ Nose and throat swabs for respiratory viruses

Management:
§ Give oxygen therapy as required to maintain SaO2>92%
§ IV fluids to rehydrate unless contraindicated
§ Antibiotics
o Non-severe CAP (for those admitted to hospital for clinical reasons)
First-line oral amoxicillin and clarithromycin; second-line moxifloxacin or levofloxacin

o Severe CAP – IV ceftriaxone (or augmentin) and oral clarithromycin; second-line IV benzylpenicillin and levofloxacin/moxifloxacin
§ Analgesia
§ DVT prophylaxis
§ Nutritional support or NG feeding if malnourished or prolonged illness



Consider ITU referral if there is inability to maintain PaO2>8 kPa
and H+>45 nmol/L, decreasing conscious level or exhaustion,
progressive CO2 retention or shock.



Monitoring progress:
§ Monitor HR, RR, BP, mental status, temperature and SaO2 at least twice a day until improving


Follow-up:
§ CXR in 6 weeks to assess resolution
§ Consider bronchoscopy+/- CT chest and abdomen if incomplete radiographic clearing at follow-up
§ Take serum sample for convalescent serology (initial sample will only be analysed if follow-up sample is sent)








3. Pneumothorax

Definition:
Pneumothorax may be spontaneous or traumatic/iatrogenic. Spontaneous pneumothorax may be primary (usually in otherwise healthy patients) or secondary (in patients with chronic lung disease). It may be small ie <> 2cm rim of air.


Investigation:
Expiratory chest radiographs are not recommended for routine diagnosis. A lateral or lateral decubitus chest radiograph should be performed if the clinical suspicion of pneumothorax is high, but a PA radiograph is normal.

CT scanning is recommended when differentiating a pneumothorax from complex bullous lung disease is difficult, when aberrant tube placement is suspected, and when the plain chest radiograph is obscured by surgical emphysema.


Management:

Observation only:

Patients with small (<2cm) primary pneumothoraces and have minimal symptoms do not require intervention. They can be discharged safely with out-patient review in 1-2 weeks and advice to return if worsening breathlessness develops. Observation alone is appropriate in patients with secondary pneumothoraces only if they have minimal symptoms and the pneumothorax is very small (<1cm). These patients should be admitted for 24 hours.


Simple aspiration:

Simple aspiration is recommended as the first line treatment for all primary pneumothoraces requiring intervention and is only recommended as an initial treatment in small (<2cm) secondary pneumothoraces in minimally breathless patients under the age of 50 years.
Patients with secondary pneumothoraces treated successfully with simple aspiration should be admitted to hospital and observed for at least 24 hours before discharge.
Repeated aspiration is reasonable for primary pneumothoraces when the first aspiration has been unsuccessful (i.e. patient still symptomatic) and a volume of <2.5 L is aspirated in the first attempt.

Tension pneumothorax is a medical emergency & requires immediate decompression with a large bore venflon inserted into the 2nd intercostal space mid-clavicular line, followed by chest drain insertion
Insert an intravenous cannula attached to a three-way tap and a 50ml syringe in the 2nd intercostal space mid-clavicular line.

Stop if there is resistance, the patient coughs excessively, or more than 2.5 L (50x50ml syringe) is aspirated.

Repeat CXR ~ the procedure has been successful if a small or no pneumothorax remains.
Chest drain:
A chest drain is required if simple aspiration is unsuccessful or in large (>2cm) secondary pneumothoraces.

A bubbling chest tube should never be clamped. There is no evidence that large tubes (20–24F) are any better than small tubes (10–14F). It should remain in place until the lung has re-expanded and the drain has stopped bubbling for 24 hrs. It should then be removed and a repeat CXR arranged.

Senior help should be sought where:
§ The lung does not re-expand with a chest drain
§ The drain continues to bubble after 24 hours
§ The lung collapses again after removal of chest drain

Suction should be added if there is persistent air leak or if the lung fails to re-expand after 48 hrs.
Flow-chart of management of spontaneous pneumothorax

Chronic Lung Disease
Aspiration
?successful
Primary pneumothorax
Secondary pneumothorax
Rim of air>2cm on CXR
Significant dyspnoea
Rim of air>2cm
Significant dyspnoea or age>50
Discharge and follow-up in clinic
Intercostal drain
Discharge and follow-up in clinic
Consider repeat aspiration
?successful
Admit for 24 hours
Aspiration
?successful
No
Yes
Yes
No
No
No
No
Yes
Yes
Yes
No
Yes
Yes
No
Follow-up:
7-10 days in the Respiratory Clinic with repeat CXR.
§ Advise patient to return if symptoms worsen or recur
§ Advise patient not to fly until reviewed
§ Patients can fly safely 6 weeks after resolution of pneumothorax or surgery for pneumothorax
§ Diving should be avoided for life unless secure definitive surgery such as surgical pleurectomy has been performed









4. PULMONARY EMBOLISM

Pulmonary embolism is a difficult diagnosis to make. The following points should be remembered:
§ PE is easily missed in severe cardiorespiratory disease, in the elderly, and where the only symptom is breathlessness.
§ Most patients with PE are breathless and/or tachypnoeic (RR>20/min). In the absence of these, symptoms are usually due to another cause.
§ PE is rare if age<40 with no risk factors.
§ Oestrogens are only a minor risk factor.

Presentation:
Small PE – pleuritic chest pain+/- haemoptysis
Large PE – SOB, hypoxia, acute right heart strain on ECG, right heart dilatation on Echo
Massive PE – circulatory collapse

As most patients do not fit neatly into these categories, PE is both over- and under-diagnosed.


Major risk factors (relative risk 5-20 )

Surgery
§ Major abdominal, pelvic and orthopaedic surgery
§ Knee/hip replacement
§ Post-operative intensive care

Obstetrics
§ Late pregnancy
§ Puerperium
§ Caesarian section

Lower limb problems
§ Varicose veins
§ Fracture

Malignancy
§ Abdominal/pelvic
§ Advanced/metastatic

Reduced mobility
§ Hospitalisation
§ Institutional care
Previous DVT/PE


Minor risk factors (relative risk 2-4) include cardiopulmonary disease, inflammatory bowel disease, obesity, long distance travel, neurological disability, OCP, HRT and thrombotic disorders.


Assessment of clinical probability:
D-dimer should only be measured following assessment of clinical probability. It is not useful in patients with high clinical probability as false negative rates are unacceptably high in this group.

Investigations:
Most initial investigations are aimed towards excluding other diagnoses e.g. pneumonia, pneumothorax or cardiac disease.

§ ABG
§ CXR
§ ECG
§ PEFR
§ D-Dimer

The D-dimer assay (Vidas) has a high negative predictive power for PE in patients where the pre-test probability is low or intermediate, therefore a negative D-dimer reliably excludes PE in these groups. If the pre-test probability is high, D-dimer is not sufficiently sensitive to detect PE. Further lung imaging is required even if D-dimer is negative, therefore there is no value in checking D-dimer in this group. D-dimer can be positive (>500 u/l) in many other acute medical conditions.

A truly normal V/Q scan reliably excludes any significant PE and a high probability scan indicates about 80% probability of PE depending on the pre-test probability. Unfortunately most scans fall into the ‘intermediate’ classification due to other coexisting cardiopulmonary disease. It should only be performed if it is available on site, if CXR is normal and there is no significant underlying cardiopulmonary disease.

CT pulmonary angiogram (CTPA) has taken over from pulmonary angiogram as the ‘gold standard’. It is the first line investigation if CXR is abnormal or if V/Q scanning is not available on site. It should ideally be performed within 24 hours of presentation. It may provide other diagnoses if PE is excluded.

Echocardiogram may be useful in patients with PE large enough to cause cardiovascular collapse. It can detect right ventricular dilatation /raised pulmonary artery pressure or intracardiac thrombus.

DVT confirmed on ultrasound scan of leg veins can be used as a surrogate marker for PE. A negative scan does not exclude PE.

Thrombophilia screen should be performed in patients < 50 years of age with recurrent PE or a strong family history of proven DVT/PE.


Management:
LMWH should be given until PE is proven or excluded. Once PE is confirmed, patient should be started on warfarin and treatment should last for

– 3 months if it is a consequence of a clear precipitating event with no continuing risk factors
– 6 months for first idiopathic episode
– life-long for recurrent episodes or continuing major risk factors

Some patients are treated with LMWH instead of warfarin due to consideration of potential drug interactions e.g. patients with underlying malignancy undergoing chemotherapy.

Thrombolysis is indicated in massive PE with circulatory collapse. It may be life-saving in peri-arrest situations. A 50mg bolus of alteplase followed by 100mg over 2 hours is given.








































5. Acute severe asthma

Assess severity
Acute severe asthma Life threatening asthma Near Fatal asthma
· PEF: 33-50% best/predicted h PEF <33% best/predicted hRaised paCO2
· Can’t complete sentences h SpO2 <92%
· Respiration >25 breaths/min h Silent chest/cyanosis/
· Pulse >110 beats/min poor respiratory effort
h Exhaustion/confusion/coma
h Measure arterial blood gases
0 High H+
0 PaO2 <8KPa [irrespective of oxygen treatment]
0 Normal PaCO2

Immediate treatment
· Oxygen: High flow (40-60%) ~ aim for SpO2 >92

· Nebulised salbutamol 5 mg + Nebulised ipratropium bromide 0.5 mg via oxygen-driven nebuliser, continue 4-6 hourly
· Prednisolone: 50 mg daily for at least 5 days or until recovery or IV hydrocortisone 100 mg 6 hourly if oral route not possible



If patient not improving within 15-30 min or Life threatening or Near fatal attack

· Discuss with middle grade/senior clinician

· Nebulised salbutamol: give every 15 minutes or continuously 10 mg hourly [Sidestream nebuliser]

· Add IV magnesium: 1.2-2g infusion over 20 minutes

· Other treatments: Middle grade/senior clinician may consider: IV salbutamol or IV aminophylline; alerting on-call anaesthetist
Discharge planning
· Check inhaler technique & assess adherence with therapy h Stop nebulised therapy 24 hrs before discharge
· Review chronic drug treatment h Written asthma action plan
· Smoking cessation advice h Respiratory clinic appointment in 4-6 wks
Monitoring/investigations
· Oximetry: maintain O2 >92%
· Repeat blood gases if :
- Initial paO2 <8>92%
- PCO2 normal or raised
· PEF
· Chest-ray: to exclude pneumothorax or pneumonia















































6. ARDS – Acute Respiratory Distress Syndrome

ARDS is a disorder first described in 1967. It causes acute onset of respiratory distress, with severe breathlessness and hypoxia, often not improved by additional oxygen. Patients often become very sick very quickly and the majority of them will require to be ventilated in the intensive care unit.

ARDS can be diagnosed if the patient satisfies the following criteria

NAECC Criteria – North American and European Consensus Conference Criteria
· Known predisposing cause
· Acute onset
· Bilateral infiltrates on CXR
· Pulmonary artery occlusion pressure <18mmHg or no clinical signs heart
Failure
· PaO2/FiO2<200mmHg

ARDS can be caused by a variety of stimuli, not all of them act directly on the lung. These causes can be subdivided into direct (acting on the lung) and indirect (acting elsewhere) causes.

Direct - pneumonia
Pulmonary aspiration
Lung contusion
Fat embolism
Near drowning
Inhalational injury
Reperfusion injury

Indirect - non-pulmonary sepsis
Multiple trauma
Massive transfusion
Pancreatitis
Coronary bypass

Pathophysiology

ARDS causes pulmonary oedema due to damage to the alveolar-capillary membrane (not like heart failure, where the oedema is due to increased hydrostatic pressure). There is then a leak of fluid, proteins and inflammatory infiltrate (neutrophils, cytokines, proteases) into the alveolus. This fills the alveoli and makes them stiff and they are then unable to take part in gas exchange. This process can affect a variable proportion of the lung. This is why patient with ARDS are severely hypoxic, it is almost as though they are working on 1 lung or even less depending on the severity. Because the lung is so stiff, they often have difficulty taking big breaths and breath with rapid shallow breaths – another reason why they often need ventilated. All these changes can occur within 12-36 hours of the stimulating cause.

Epidemiology
The incidence of ARDS is variable but is about 5: 100 000. 20% of all patients who require ventilation in ICU fulfil the criteria for ARDS. You may not see it much on the wards as patients will often be so sick that they go straight from A&E or theatre to ICU so it is probably commoner than you think.

Mortality rate has not changed much in the last 30-40 years and is around 30-60% depending on cause and the premorbid health and age of the patient.

Only 10-15% of patients will die of respiratory failure. The others die of non-pulmonary organ failure, either because they are critically ill in some other way or because the severe hypoxia has damaged other organs. Of the patients who survive, most of them will regain full functional ability but a fair amount will have residual mildly deranged pulmonary function tests.

Treatment
As with any critically ill patient, general supportive management is very important from the outset. This includes:-

· Good nutrition
· Thromboembolism prophylaxis
· Gastric prophylaxis
· Careful fluid balance

In addition, the way patients are ventilated is also very important. The ARDSNet group published a paper in 2000 looking at a different way of ventilating patients and showed that this can reduce mortality by 22%. The change in strategy is due to the thinking that a large proportion of the lung is unable to take part in ventilation as the alveoli are full of ‘gunk’. Therefore, if we were to ventilate a lung normally, the unaffected lung would get a much greater tidal volume than it needs, stretching it and causing damage. The aim of the ventilation strategy is to do as little damage to the normal lung as possible, while aiming to try to ‘recruit’ as much of the damaged lung as we can and allow it to take part in ventilation.

This is done by:-

· Smaller tidal volumes – to reduce the chance of overdistension of normal lung
· Limiting the maximum pressure produced in the lungs
· Adding an additional pressure – PEEP – to hold open areas of lung which would otherwise collapse down
· Trying to decrease the amount of oxygen to <60% as soon as possible
· Tolerating a higher CO2 level than normal

Other treatments are tried now and again but none have been shown to produce any increase in survival rates. These include:-

· Prone ventilation – lying patients on their face to ventilate
· Inhaled nitric oxide
· ECMO – extra corporeal membrane oxygenation
· High dose steroids in chronic cases

Summary

Ø ARDS is a disorder causing acute onset respiratory distress, breathlessness and severe hypoxia due to a number of predisposing causes.
Ø Most patients will require ventilation in ICU.
Ø Mortality continues to remain high.
Ø Care and attention to general supportive management is very important.
Ø Patients with ARDS should be ventilated in a specific manner to avoid further lung damage.