Acute Respiratory 486/12

Question 1

1. COPD precipitations

Answer 1

Common precipitants of exacerbations of COPD include: • infection (60–80% of exacerbations) – common bacterial causes include Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis. Common viral causes include influenza, parainfluenza, coronaviruses and rhinoviruses • non-infectious causes (20–40%) are due to heart failure, pulmonary embolism, pneumothorax and non-pulmonary infections • precipitating and environmental factors such as cold air, air pollution, allergens, ongoing smoking and non-adherence to prescribed medication.

Question 2

1. COPD investigations

Answer 2

Inx COPD - spirometry - ECG - CXR (looking for potential complications; pneumothorax, pneumonia or heart failure) - Inx may not be needed if clinical history and examination suggests infective cause

Question 3

1. COPD Initial Rx infective exacerbation-

Answer 3

• short-acting bronchodilators (inhaled beta 2 agonists such as salbutamol or terbutaline) - oral corticosteroids; the recommended dose of prednisolone is 30–50 mg daily for 7–14 days (without tapering) - oral antibiotics; five days of therapy with either doxycycline 100 mg twice daily or amoxycillin 500 mg 8 hourly is recommended.2 Macrolide antibiotics are often ineffective, and are likely interact with warfarin leading to a significantly elevated international normalised ratio (INR).

Question 4

1. COPD Rx Severe exacerbation at home, then in hospital

Answer 4

• ambulance - continue bronchodilators inhaled or nebuliser until ambulance arrives –> IV steroids –> O2 via nasal prongs most effective –> blood gases, ECG, CXR –> spirometry not in acute setting –> admission Specific therapy in the emergency department would include titrated oxygen therapy (aiming for oxygen saturations (SaO2) of 90–92%, inhaled bronchodilators, corticosteroids and antibiotics. The dose and route of administration of these medications are guided by the severity of illness. Non-invasive ventilation is useful in the setting of acute respiratory acidosis, and has been shown to reduce mortality and the need for intubation. It often leads to rapid clinical improvement. Occasionally, intubation and ventilation may be required if non-invasive ventilation is ineffective or contraindicated.

Question 5

2. PE

Answer 5

Symptoms - pleuritic chest pain - SOB - syncope Ddx - cardiac causes (acute ischaemia, arrhythmia, pulmonary oedema and pericarditis) and - respiratory causes (pleural effusion, pneumonia and pneumothorax).

Question 6

2. PE INx

Answer 6

• CXR - ECG - Bloods; FBC, EUC (creatine for contrast) - D -dimer if low pretest probability - ventilation/ perfusion (VQ) scan or a CT pulmonary angiogram (CTPA). A VQ scan uses lower doses of radiation (approximately 1.3 mSv), and is therefore preferred in younger patients. However, there is a significant possibility of a non-diagnostic scan, which would necessitate further testing, particularly in patients with a history of COPD or an abnormal initial CXR. A CTPA is more sensitive and cost-effective than VQ scanning, however, risks include contrast reactions, renal impairment and a much higher radiation exposure (estimated to be 8–10 mSv). The latter is an important consideration in young women, where breast tissues receive a significant radiation dose.

Question 7

2. PE pre test probability

Answer 7

The simplified Wells score (Table 1) is recommended in the draft National Institute of Clinical Effectiveness (NICE) guidelines

Question 8

2. PE Rx

Answer 8

Hospital admission and treatment with subcutaneous low molecular weight heparin (LMWH).

Warfarin is likely to be commenced, and the LMWH continued until her INR is in the target range of 2–3

Recently, alternative oral anticoagulants such as rivaroxaban and dabigatran have been trialled in patients with PE with promising results.

At this stage, neither drug is listed on the pharmaceutical benefits scheme for this indication.

Other trials are aiming to identify a group of patients with PE who may be safely treated as outpatients.

Question 9

2. PE and pregnancy

Answer 9

Plasma D-dimer is more likely to be elevated in pregnancy than in the non-pregnant state. However, a negative D-dimer is still useful
in a patient with low pre-test probability for PE, as further testing
is not necessary. An elevated D-dimer should prompt lower limb ultrasonography, which may demonstrate a reason for anticoagulation without the use of ionising radiation.

If an ultrasound of the lower limbs reveals no thrombus and a PE still needs to be excluded, then definitive imaging (VQ or CTPA) should occur. The estimated radiation absorbed by the fetus depends on the modality chosen and gestational age

Appropriate initial chest imaging should be either a CTPA or perfusion-only lung scanning.

If a PE is confirmed, then LMWH is recommended in the pregnant patient. Warfarin is not recommended during the first or third trimesters, and caution should be used if given in the second trimester. Anticoagulation should be continued for 3 months after delivery, and warfarin is safe in breastfeeding.

Question 10

3. CAP Assessing severity

Answer 10

It is important to assess the severity of pneumonia in order to
make a decision on appropriate treatment and the need for hospital admission. Consider the patient’s age, comorbidities, vital signs and the presence of clinical manifestations of organ system failure.

Various scoring systems can also be used to assess the severity of pneumonia and include the Pneumonia Severity Index (PSI)16 (this uses information such as the patient’s age, comorbidities, vital signs and blood tests), CURB-65 (this uses information such as presence of confusion, urea level, respiratory rate, blood pressure and

age >65 years), CRB-65 (this uses similar information to CURB with the exception of urea),17 and SMART-COP18

Question 11

3. CAP severity

Answer 11

It is important to assess the severity of pneumonia in order to
make a decision on appropriate treatment and the need for hospital admission. Consider the patient’s age, comorbidities, vital signs and the presence of clinical manifestations of organ system failure.

There is no evidence supporting one scoring system over another. None can replace clinical assessment. Care must be taken when using scoring systems with younger patients. Severely ill patients requiring ICU care do not need scoring systems. Patients classified in a higher risk group are those with comorbidities and who are more likely to have an atypical presentation and worse outcomes.19

Question 12

3. CAP Inx

Answer 12

• A CXR should be performed in all patients with presumed pneumonia.
• Oxygen saturation and
• investigations for the causal pathogen should also be done. This may include sputum gram stain and culture, and blood cultures in patients who require hospital admission. - - Arterial blood gases should be done on severely ill patients.

Other investigations may be appropriate depending on the clinical circumstances. These include

• sputum for mycobacterium tuberculosis,
• urine antigen testing for pneumococcus,
• upper respiratory tract samples for polymerasechain reaction for respiratory tract viruses,and
• serological tests can be performed for Legionella spp. or mycoplasma pneumoniae if epidemiological reasons exist. Haematology and electrolytes may also be appropriate.

Question 13

3. CAP Guidelines for treatment

Answer 13

You could use Therapeutic Guidelines: Antibiotic.

The British Thoracic Society (BTS), American Thoracic Society and the Infectious Diseases Society also publish guidelines (see Resources).

Hospitals will also have local protocols depending on local epidemiological conditions.

Question 14

3. CAP Symp Rx

Answer 14

• A patient with CAP should be advised to rest and drink plenty of fluids.
• Oral analgesia, such as paracetamol or NSAIDS, can be used for chest pain. Smoking cessation advice should also be offered to all patients who smoke.
• Review a patient with CAP at 24–48 hours in order to detect patients who are deteriorating despite treatment.

Question 15

3. CAP causative organisms

Answer 15

Streptococcus pneumoniae, mycoplasma pneumoniae and respiratory viruses are the most common aetiological agents for CAP in Australia.

Atypical pneumonia (about one in five cases of CAP) is caused by organisms such as mycoplasma pneumoniae, chlamydia pneumoniae and Legionella spp. In one study, over 30% of culture positive CAP had co-infection with either a virus or atypical pathogen. The real figure is likely to be higher.

Question 16

3. CAP ABx choice

Answer 16

There are several antibiotic guidelines for CAP. For patients managed as an outpatient, Therapeutic Guidelines: Antibiotic recommends the following:

amoxycillin 1 gm 8 hourly for 5–7 days OR

doxycycline 200 mg for the first dose then 100 mg doxycycline daily for a further 5 days OR

clarithromycin 250 mg 12 hourly for 5–7 days.

Antibiotics should be given as soon as the diagnosis is confirmed.

Macrolides have been proven to markedly reduce mortality in CAP and hospital acquired pneumonia. They are anti-inflammatory, cause less cell lysis and are active against mycoplasma and even some viruses. There is evidence that narrow spectrum therapy with a penicillin and macrolide or doxycycline is as effective as broader spectrum regimens such as cephalosporins and fluoroquinolones, even in severe pneumonia.

Patients should be reviewed at 24–48 hours and if there is no improvement, combination therapy with amoxycillin plus either doxycycline or clarithromycin may be appropriate.

Broad spectrum antibiotics and antibiotics not conforming with current guidelines risk Clostridium difficile associated diarrhoea and methicillin resistant Staphylococcus aureus (MRSA). They also have significantly higher rates of treatment failure and mortality.

Studies on the aetiology of CAP in Australia show that less than 5% of identifiable pathogens are resistant to standard therapy.

It is recommended that antibiotic therapy should be continued for 5–7 days, and extended depending on response and clinical judgement.

Duration of treatment depends on response.

Question 17

3. CAP immunocompriomised patients

Answer 17

In immunocompromised patients, organisms may be atypical such as Klebsiella pneumoniae, Haemophilus influenzae or Morexella catarrhalis, or typical organisms can present atypically. For example, pneumonia due to Streptococcus pneumoniae may rapidly progress to septic shock, organ dysfunction and death

Pneumonia is 3–4 times more common in patients with diabetes.

Streptococcus pneumoniae and Legionella pneumophillia are associated with much higher mortality and morbidity and Staphylococcus aureus, gram negative Bacilli Mucor and mycobacterium tuberculosis are more commonly isolated.

Question 18

3. CAP prognosis

Answer 18

In large case control trials, patients with CAP regardless of age, comorbidities and treatment setting, have 2.5 times the 1-year mortality rate following their pneumonia.

The evidence suggests this is primarily due to an increased incidence of cardiovascular events such as those related to ischaemic heart disease and cardiac failure. Jeremy will need to be counselled and his cardiac risk factors will need to be carefully monitored.

A repeat CXR should be performed after 6 weeks if symptoms or signs are not resolving esp those at high risk of secondary carcinomas of the lung with history of Ca etc.

Question 19

3. CAP vacinnations

Answer 19

Influenza vaccination prevents hospitalisation for influenza and pneumonia. It also prevents deaths from influenza-related conditions among the elderly.

Pneumococcal immunisation of at-risk individuals and children has reduced morbidity and mortality. However, there has been an increase in non-vaccine strains, recombinants and increased antibiotic resistance.

Question 20

4. Asthma severity in children

Answer 20

Guidelines from The Royal Children’s Hospital Melbourne categorise acute asthma as mild, moderate, severe or critical.

In the assessment of severity of acute childhood asthma it is important to note the following primary features:

• general appearance/mental state
• work of breathing (accessory muscle use, intercostal recession, tracheal tug).

The following secondary features should also be noted:

• initial SaO2 in room air
• heart rate (tachycardia can be a sign of severity, but is also a side effect of beta 2 agonists)
• ability to speak.

Change in mental status is viewed as heralding an impending catastrophe. Initial SaO2 in room air, heart rate and ability to speak are helpful but less reliable features.

Pulsus paradoxus and peak expiratory flow rate are not reliable indicators of severity. Wheeze is also not a good marker of severity. In critical asthma where a patient may present with a silent chest due to poor air entry, wheeze may be absent. A quiet chest in a dyspnoeic or obtunded patient with asthma is a serious event.

Question 21

4. Asthma risk of ICU admission

Answer 21

Patients at risk of requiring ICU management for asthma include those who have a history of:

• ICU admissions, mechanical ventilation, or rapidly progressive and sudden respiratory deterioration
• seizures or syncope during an asthma exacerbation
• exacerbations precipitated by food
• use of more than two beta-agonist metered dose inhaler (MDI) canisters per month
• insufficient preventer therapy or poor adherence to preventer therapy
• inability to recognise the severity of illness
• associated depression or other psychiatric disorder.

Question 22

4. Asthma Inx of severely ill kids

Answer 22

A CXR is not routinely indicated in the unintubated asthmatic child, as unexpected radiographic abnormalities are very rare. Exceptions are situations in which the clinical examination suggests the possibility of barotrauma or pneumonia.

Arterial blood gases are not usually required. They are distressing and can cause a child with respiratory compromise to deteriorate further.

Typical findings during the early phase of severe asthma are hypoxaemia and hypocapnia. With increasing airflow obstruction, hypercapnia will develop and indicate impending respiratory failure. However, the decision to intubate an asthmatic child should not depend on blood gas determination, but should be made on clinical grounds.

The intubated patient, however, requires frequent blood gas determination, ideally from an indwelling arterial line, to assess adequacy of ventilatory support and progression of illness.

Question 23

4. Asthma; management severely ill child

Answer 23

Your initial management of Ruby is to:

• transfer to resuscitation cubicle
• aim for minimal handling and allow her to adopt the most comfortable position
• ask for help from other medical staff within the hospital or in close proximity
• administer oxygen to maintain SaO2 >92%
• administer continuous nebulised salbutamol (0.5% undiluted)
• administer nebulised ipratropium (3 doses x 250 mcg, 20 minutes apart, added to salbutamol)
• obtain intravenous access – use comfort techniques such as dermal anaesthetic cream or patch, or distract her
• take blood for full blood examination (FBE), urea, electrolytes and creatinine (UEC), lactate and venous blood gases as needed. Arterial blood gases are usually not needed unless intubated
• administer methylprednisolone 1 mg/kg intravenously (IV) 6 hourly or hydrocortisone 2–4 mg/kg IV 4–6 hourly.

If not responding to initial treatment or deteriorating further, contact the nearest tertiary paediatric hospital or paediatric retrieval service to arrange retrieval and transfer to a paediatric ICU facility and commence drug infusions as shown below.

Aminophylline

Loading dose: 10 mg/kg IV (maximum dose 500 mg) over 60 minutes. If taking oral theophylline, do not give IV aminophylline – obtain a serum level. Administer a continuous infusion unless marked improvement has occurred following a loading dose.

magnesium sulphate

Dose: 50% magnesium sulphate – 0.1 ml/kg (50 mg/kg) over 20 minutes, then 0.06 ml/kg/hr (30 mg/kg/hour) by infusion. Aim to keep serum magnesium between 1.5 and 2.5 mmol/L.

iv salbutamol

IV salbutamol may also be considered. However, there is limited evidence that it is beneficial.25 It does not appear to provide any benefits over nebulised salbutamol even in severe cases.26

Loading dose: 5 mcg/kg/min for 1 hour. This should be followed by an infusion in a dose of 1–2 mcg/kg/min.25

Salbutamol may cause tachycardia, tachypnoea, a metabolic acidosis, a rise in lactate and/or hypokalaemia. Consider stopping or reducing salbutamol as a trial if you think it may be causing a problem.

Question 24

4. Asthma Rx when worsening severe

Answer 24

If there is no improvement despite pharmacological treatment, further treatment options include:

non-invasive positive pressure ventilation (nppv)

It is important to select appropriate patients for trials of NPPV in acute severe asthma. NPPV should be applied early in the course of respiratory failure and before severe acidosis occurs to reduce the likelihood of endotracheal intubation, treatment failure or mortality.

Patients who receive NPPV must be awake and cooperative, have a patent airway and have spontaneous respirations.

In children with acute severe asthma exacerbations, NPPV may be useful as a temporary measure while awaiting the maximal therapeutic benefit of pharmacotherapy, or may avoid the need for intubation by easing the work of breathing in patients who are progressing toward respiratory muscle fatigue.

Patients who are likely to benefit most are those with:

• a pH between 7.25 and 7.30
• normal mentation levels at the beginning of NPPV
• improvements in pH, PaCO2 and level of mentation after 1–4 hours of NPPV
• hypoxaemia despite high flow oxygen and/or those with documented hypercapnia
• significant respiratory distress while awaiting maximal therapeutic effects of corticosteroids and bronchodilators
• impending respiratory muscle fatigue.

intubation

The decision to intubate should be based on the bedside assessment of the degree of respiratory distress, rather than on any absolute PaCO2 or respiratory rate.

If at all possible, mechanical ventilation should be avoided as this may cause pneumothorax, barotrauma and hypotension. However, absolute indications for intubation include:

cardiac arrest

respiratory arrest

severe hypoxia

rapid deterioration of the child’s mental state.

Progressive exhaustion despite maximal treatment is a relative indication.

Question 25

4. Asthma when severe; transfer

Answer 25

**NETS retrieval** Despite whether patient requires intubation, they should be retrieved and transferred to a paediatric ICU by a paediatric retrieval service. Transfer should be considered in children with: - severe or critical asthma requiring intravenous therapy or respiratory support - escalating oxygen requirement - poor response to salbutamol or inability to wean salbutamol - a requirement for care above the level of that provided by the local hospital.

Question 26

5. Pneumothorax History and Symptoms

Answer 26

- dyspnoea - pleuritis chest pain - smoker - underlying lung disease – known bullae, asthma, tuberculosis, cystic fibrosis? - drugs such as marijuana or cocaine? - previous spontaneous pneumothorax?

Question 27

5. Pneumothorax Examination

Answer 27

Findings on physical examination consistent with a diagnosis of pneumothorax include: - reduced or absent breath sounds on the affected side - hyperresonance to percussion of the affected side. Less common findings include: - subcutaneous emphysema - unilateral chest enlargement - reduced excursion of the hemithorax with the respiratory cycle. Signs of a tension pneumothorax include distended neck veins, hypotension and cyanosis. Examination may be normal. A normnal examination does not exclude pneumothorax.

Question 28

5. Pneumothorax Classification

Answer 28

Pneumothoraces can be classified as spontaneous or traumatic. **Spontaneous pneumothoraces** are further divided into primary and secondary pneumothoraces. **Primary spontaneous pneumothoraces** affect patients who do not have clinically apparent underlying lung disease. **Secondary spontaneous pneumothoraces** occur in the setting of underlying pulmonary disease, most often chronic obstructive pulmonary disease, but also in conditions such as asthma, bullous lung disease, tuberculosis and cystic fibrosis.

Question 29

5. Pneumothorax Inx

Answer 29

- erect CXR --\>signs of radiological tension – the mediastinum pushed aside. - fractured ribs and - subcutaneous emphysema The lung fields are clear, suggesting no obvious underlying lung pathology. ? fluid in the pleural space (?meniscus visible costophrenic junction), suggesting haemorrhage associated with a pleural injury that may have produced the pneumothorax

Question 30

5. Pneumothorax size assessment

Answer 30

A number of formulae exist to estimate the size of a pneumothorax. Many are inaccurate as the volume of an irregular three-dimensional space – such as a hemithorax – is difficult to estimate on a two dimensional X-ray. Pneumothorax size is often underestimated. The British Thoracic Society defines a ‘small’ pneumothorax as having a visible rim of air between the lung margin and chest wall of less than 2 cm. A ‘large’ pneumothorax has a visible rim of pleural air greater than 2 cm. A 2 cm pneumothorax distance seen on CXR corresponds to a 50% pneumothorax by volume. If using the formula: volume = the third power of the radius divided by two for a hemisphere (the three dimensional object that one lung most closely represents), a decrease in the lung radius from hilum to pleura from 10 cm to 8 cm corresponds to a loss of volume of around 50%.

Question 31

5. Pneumothorax Management

Answer 31

Should be referred to the emergency department for aspiration of the pneumothorax. High flow oxygen should be administered via Hudson mask as early as possible. Large pneumothoraces in clinically stable patients should be aspirated. There are a number of options to achieve this aim, including needle aspiration or catheter aspiration. Catheters maybe ‘small bore’ catheters or larger intercostal catheters. Small bore catheters are catheters that can be inserted using the Seldinger technique (where the catheter is inserted over the introducing needle and guide wire). Larger intercostal catheters are inserted through a surgically created tract, either through the fifth intercostal space in the anterior axillary line, or through the second intercostal space in the mid-clavicular line. Larger intercostal catheters have the advantage of being more rigid, less likely to block and can have suction more successfully applied to them to assist the re-expansion of the lung. This is particularly useful in patients with underlying lung disease where the lung may be less able to spontaneously re-expand, or in cases where a persistent air leak through the pleural injury prevents spontaneous lung re-expansion without suction. Clinically unstable patients, regardless of the size of the pneumothorax, require insertion of an intercostal catheter. Asymptomatic patients with small pneumothoraces (less than 2 cm rim of pleural air seen on a CXR) are generally observed in the emergency department, and discharged in 3–6 hours if a repeat CXR confirms no progression of the pneumothorax. A repeat CXR as an outpatient should be performed in 2 weeks.

Question 32

5. Pneumothorax and flying

Answer 32

Luke should avoid air travel for 6 weeks following a CXR that confirms resolution of the pneumothorax. Commercial airlines arbitrarily advise a 6-week interval between the diagnosis of a pneumothorax and flying. Scuba diving should be discouraged permanently unless a definitive prevention strategy – such as a surgical pleurectomy – has been performed. All divers who wish to continue diving should be referred to a thoracic surgeon for ongoing management and advice, regardless of the type or size of the pneumothorax.

Question 33

5. Pneumothorax tension treatment

Answer 33

Requires immediate decompression of tension pneumothorax; - The largest intravenous catheter available should be inserted in the left second intercostal space in the mid-clavicular line to release the air under tension. - The catheter should be left in situ until a functioning intercostal catheter can be inserted.

Question 34

5. Pneumothorax recurrance

Answer 34

According to one study, the risk of recurrence of primary pneumothorax is 54% in the next 4 years.

Question 35

6. Acute Pulmonary Oedema Causes

Answer 35

acute pulmonary oedema, common precipitating causes of acute pulmonary oedema include: * infection * myocardial ischaemia * uncontrolled hypertension * significant valvular disease (both stenosis and regurgitation) • arrhythmias * anaemia * thyroid disease * pulmonary embolism * changes in medication (including non-compliance) * excessive alcohol and salt intake.

Question 36

6. Acute pulmonary oedema Inx

Answer 36

An ECG and CXR should be performed immediately in all patients with suspected acute congestive heart failure (CHF).37,38 **ECG** ECG findings are commonly related to the underlying pathologies. These findings may include: presence of Q waves ST-T changes left ventricular hypertrophy (LVH) left bundle branch block atrial fibrillation. **CXR** CXRs may show cardiac enlargement (cardiothoracic ratio \>50%); however, there is poor correlation between the cardiothoracic ratio (CTR) and presence of heart failure. This is because the heart size may be normal in patients with diastolic dysfunction, acute valvular regurgitation as part of infective endocarditis, or acute myocardial infarction. An enlarged CTR may also be seen in the absence of heart failure such as where a pericardial effusion or LVH is present. Evaluation of the lung fields in the presence of pulmonary oedema shows signs of pulmonary congestion, initially in the upper zones, then in the horizontal fissures followed by pulmonary oedema and pleural effusion(s). Other useful investigations are listed below. **Cardiac enzymes** More than 50% of patients with cardiogenic pulmonary oedema (but without evidence of MI) have elevated troponin T levels. Elevated troponin levels in patients with acute CHF may reflect subendocardial ischaemia due to elevated left ventricular end diastolic pressure. **Bloods** full blood examination (fbE), urea, electrolytes and creatinine (uEC) and estimated glomerular filtration rate (egfr) Anaemia may be a precipitating factor, as might a chest infection. The choice of medication may depend on the patient’s renal status, hence knowing the patient's eGFR will provide important information. **b-natriuretic peptide (bnp)** Measurement of serum BNP level in patients with symptoms of heart failure is sometimes carried out in larger centres for monitoring patients, and in some instances for guiding acute management of CHF. B-Natriuretic peptide or N-terminal pro-brain natriuretic peptide (NT-proBNP) levels have been shown in some studies to: increase the accuracy of diagnosis and effectiveness of acute management assist in differentiating a cardiac from a non-cardiac cause of respiratory distress predict in-hospital mortality in patients with acute decompensated heart failure, however, an elevated BNP level should only be taken in the context of the clinical picture as it may be increased in a variety of other conditions such as atrial fibrillation, pulmonary embolism, or sepsis. **other blood tests** In a first-time presentation thyroid function and other metabolic tests may be performed to look for endocrine causes of heart failure.

Question 37

6. Acute Pulmonary oedema CXR findings

Answer 37

The key findings of acute pulmonary oedema are: **- fluid in the fissures** – thickening of the major or minor fissures **- Kerley B lines** (septal lines) – seen at the lung bases, usually no more than 1 mm thick and 1 cm long, perpendicular to the pleural surface **- pleural effusions –** usually bilateral, frequently the right side being larger than the left; if unilateral, more often on the right **- peribronchial cuffing –** visualisation of small doughnut-shaped rings representing fluid in thickened bronchial walls. **\*\*('bats' wings’ distribution of interstitial oedema)** **Collectively, the above four findings comprise pulmonary interstitial oedema.** Note that the heart may or may not be enlarged. Also, when the fluid enters the alveoli, the airspace disease is typically diffuse and there are no air bronchograms.

Question 38

6. Acute pulmonary oedema Rx

Answer 38

**Initial investigation and treatment** should start concurrently and are listed below. * Manage the patient in a sitting position (if tolerated). * Apply high flow oxygen (8–10 L via mask). * Perform an ECG on arrival to determine if a STEMI is present, or a life threatening or compromising arrhythmia is present. • Perform pulse oximetry (if available) to estimate the percentage of oxygen saturation of the blood. It will not, however, provide any information on carbon dioxide levels and it should be kept in mind that respiratory failure by definition occurs when partial pressure of oxygen (PO2) is \<50 mmHg and when partial pressure of carbon dioxide (PCO2) is \>50 mmHg. The best clinical guide to the PCO2 is the patient’s conscious state. * Obtain IV access. * Obtain a sample of blood for tests (as described in Answer 2). • Medication: – glyceryl trinitrate (sublingual or topical) as a vasodilator – if the BP systolic \>90 mmHg, administer 0.4–0.8 mg of glyceryl trinitrate sublingually or administer topical glyceryl trinitrate – diuretics – if not intravascularly deplete, administer usual daily dose frusemide or up to 1–1.5 mg/kg IV. Its beneficial effect is accelerated by pre-treatment with a vasodilator. Monitor for signs of the following adverse effects that frusemide can potentially cause: i a reduction in renal blood flow due to vasoconstriction in pulmonary oedema ii an initial increase in afterload and reduced cardiac output iii an initial increase in preload, which reduces only through diuresis iv delayed adverse effects in volume depletion v significant hypovolemia and electrolyte imbalance with pre- hospital use – morphine is no longer recommended because emerging data links its administration with increased intubation and mortality rates. No studies have ever shown benefit, and there are also concerns due to sedation and respiratory depression – nitrate 10–20 mcg/min IV, adjusting its rate of administration to response and ensuring BP is \>100 mmHg systolic, although this may not be feasible in some rural settings – an anti-arrhythmic for a haemodynamically compromising arrhythmia. **Non-invasive ventilation (NIV) with CPAP** is also useful, but has limited availability in most smaller hospitals. Other therapies that may be used in an ICU setting are: - an adrenaline infusion - vasodilators (sodium nitroprusside) - inotropes (for cardiogenic shock or hypoperfused state with systolic blood pressure \<90 mmHg) - mechanical support (eg. intra-aortic balloon pump) for cardiogenic shock.

Question 39

6. Acute Pulmonary Oedema and CPAP

Answer 39

CPAP is effective in both pre-load and afterload reduction. Its use in acute pulmonary oedema has been demonstrated to be associated with reduced intubation and mortality rates. In patients with acute cardiogenic pulmonary oedema CPAP induces a more rapid improvement in respiratory distress and metabolic disturbance than does standard oxygen therapy. Patients with the following conditions may benefit from early CPAP, listed in order of level of evidence: - acute exacerbations of COPD - acute cardiogenic pulmonary oedema - pneumonia where the benefit has been shown in patients with infection associated with COPD and in immunocompromised patients - COPD or pulmonary oedema where a decision has been made not to intubate – prevention of deterioration or improvement in acute dyspnoea may occur - COPD or pulmonary oedema where extubation has failed after a brief course of intubation for COPD or pulmonary oedema. CPAP might ease this transition, but there should always be a backup plan - CPAP is currently not recommended in asthma and little consistent benefit has been reported for its use in other causes of respiratory failure, such as acute respiratory distress syndrome. - Complications of CPAP include pain or an ulcer over the nasal bridge; mucosal dryness; eye irritation, if the mask seal is not complete, and rarely gastric insufflation or aspiration. In conclusion, in many conditions there is strong evidence for early improvement in symptoms and physiological parameters with the use of CPAP, but there is still uncertainty whether intubation or mortality rates are reduced (with the exception of its use, for example, in acute pulmonary oedema).

Question 40

7. Influenza

Answer 40

Combination of respiratory symptoms with the **systemic symptoms** of - fever, - myalgia and - headache supports a clinical diagnosis of an influenza-like illness. The **differential diagnosis** includes a - common cold, - pneumonia, - invasive meningococcal disease and - meningitis due to other causes.

Question 41

7. Influenza causes

Answer 41

Seasonal influenza is caused by **influenza A or B viruses.** Between 2009 and 2010 there was an outbreak of influenza caused by an H1N1 influenza A virus (swine flu). During the H1N1 epidemic the rate of infection was highest in those aged 18–24 years (\>50% of cases). Infection in people over 65 years was uncommon because of pre-existing immunity from previous exposure to anti-genically similar viruses.

Question 42

7. Influenza and anti-virals

Answer 42

Studies have demonstrated an average reduction in symptom duration between 12–72 hours if treatment with antiviral medication (neuraminidase inhibitors) is initiated within 24 hours of onset of symptoms. Therapeutic Guidelines: Antibiotic recommends that antiviral medications can be prescribed within 48 hours of onset of symptoms where clinically indicated, and for patients at higher risk for complications of influenza, more than 48 hours from onset of symptoms. In general, the decision to treat a patient with suspected influenza depends on the likelihood of influenza, the time since onset of symptoms, the likely benefits of treatment based on age and comorbities and the potential for transmission to others. Antivirals are not necessarily indicated in the relatively young, usually healthy and if it is more than 48 hours since the onset of symptoms. Indications for treatment with antiviral medication include illness requiring hospitalisation, progressive severe disease, at-risk individuals,45 healthcare workers and Indigenous Australians. There are a number of groups of patients at higher risk for complications of influenza. These groups include children \<2 years of age; adults \>65 years of age; pregnant women and people with chronic medical conditions including active malignancy, chronic liver, renal, pulmonary and cardiac disease, diabetes mellitus and any form of immunosuppression. Pregnancy predisposes women to a higher mortality for both seasonal and pandemic influenza than the general population. There are also concerns regarding the effect of influenza on the fetus. Some studies have suggested there is an increased rate of congenital abnormalities. Fever is an independent risk factor for birth defects and should be treated with simple antipyretics during pregnancy. In general, obtaining the appropriate sample for rapid diagnostic testing for influenza is recommended prior to commencing antiviral medication except during influenza epidemics.

Question 43

7. Influenza spread

Answer 43

Transmission is via respiratory droplets and potentially with contaminated fomites. Immunocompetent adults shed the virus for an average of 5 days, which includes 1–2 days during the 1–4 day incubation period. The duration of shedding may be increased up to 10 days in immunocompromised patents. Should avoid visiting immunocomprimised people until 24 hours after her fever has subsided, and at least 7 days have elapsed since her respiratory symptoms commenced. In general, prophylaxis with antiviral medication can be considered for close contacts of proven cases, particularly for those at higher risk of complications of influenza.

Question 44

7. Complications of Influenza

Answer 44

In most adults, influenza is an acutely debilitating, but self-limiting, infection. Pneumonia is the most common complicationand can be either primary viral pneumonia or secondary bacterial pneumonia. Bacterial pneumonia accounts for approximately 25%of all influenza deaths. The most common organisms for secondary pneumonia are Streptococcus pneumoniae, Staphylococcous aureus and Haemophilus influenzae. Neurological complications include encephalitis, transverse myelitis, aseptic meningitis and Guillian Barre syndrome. Myocarditis and pericarditis have also been reported. Rhabdomyolysis and myositis are most commonly seen in children.