RESPIRATORY CONTENTS 1. ASTHMA 2. COPD 3. GUIDELINES ON OXYGEN ADMINISTRATION IN NON-INTUBATED PATIENTS 4. GUIDELINES FOR NON-INVASIVE VENTILATORY SUPPORT (NIV) IN ACUTE HYPERCAPNIC RESPIRATORY FAILURE 5. GUIDELINES FOR ADMINISTRATION OF SEDATION IN RESPIRATORY PATIENTS 6. PNEUMOTHORAX 7. COMMUNITY ACQUIRED PNEUMONIA 8. PULMONARY EMBOLISM 9. CXR LESIONS SUGGESTIVE OF CARCINOMA 10. MASSIVE HAEMOPTYSIS 11. PLEURAL EFFUSIONS AND THORACOCENTESIS 12. ARTERIAL BLOOD GAS SAMPLING PROTOCOL ASTHMA There is no foolproof way to assess the severity of asthma, and any asthmatic can die in any attack. Although the clinical evaluation of such patients can provide a reasonable indication of the severity of the disease process, objective measurements are invaluable in assessing the initial severity of the attack and the response to treatment, and should be attempted in all patients. Management of Acute Asthma Attacks in Adults and Adolescents Classification of Severity The following criteria enable adults and older children with an attack of asthma to be classified into one of three groups. * Any of these features invariably indicates that the episode is severe. The absence of any feature does not exclude a severe attack. ** Patient may rarely be incapable of performing test Cyanosis and paradoxical pulse may be absent, even in severe obstruction, but when present indicate severe obstruction. Objective measurements (PEFR, FEV1 and blood gases) MUST be performed as quickly as possible following presentation. This will depend upon the severity and more importantly the response to initial therapy.
Transcript
RESPIRATORY CONTENTS 1. ASTHMA 2. COPD 3. GUIDELINES ON OXYGEN ADMINISTRATION IN NON-INTUBATED PATIENTS
4. GUIDELINES FOR NON-INVASIVE VENTILATORY SUPPORT (NIV) IN ACUTE HYPERCAPNIC RESPIRATORY FAILURE
5. GUIDELINES FOR ADMINISTRATION OF SEDATION IN RESPIRATORY PATIENTS
6. PNEUMOTHORAX 7. COMMUNITY ACQUIRED PNEUMONIA 8. PULMONARY EMBOLISM 9. CXR LESIONS SUGGESTIVE OF CARCINOMA 10. MASSIVE HAEMOPTYSIS 11. PLEURAL EFFUSIONS AND THORACOCENTESIS 12. ARTERIAL BLOOD GAS SAMPLING PROTOCOL
ASTHMA
There is no foolproof way to assess the severity of asthma, and any asthmatic can die in any attack. Although the clinical evaluation of such patients can provide a reasonable indication of the severity of the disease process, objective measurements are invaluable in assessing the initial severity of the attack and the response to treatment, and should be attempted in all patients. Management of Acute Asthma Attacks in Adults and Adolescents
Classification of Severity
The following criteria enable adults and older children with an attack of asthma to be classified into one of three groups. * Any of these features invariably indicates that the episode is severe. The absence of any feature does not exclude a severe attack. ** Patient may rarely be incapable of performing test Cyanosis and paradoxical pulse may be absent, even in severe obstruction, but when present indicate severe obstruction. Objective measurements (PEFR, FEV1 and blood gases) MUST be performed as quickly as possible following presentation. This will depend upon the severity and more importantly the response to initial therapy.
Mild
Moderate
*Severe & life threatening
Altered consciousness
No
No
Yes
Physical Exhaustion
No
No
Yes, may have paradoxical chest wall movement
Pulse rate
< 100/min
100-120/min
> 120/min
Central cyanosis
Absent
May be present
Likely to be present
Wheeze intensity
Variable
Moderate - loud
Often quiet
Peak expiratory flow (% predicted)
>75%
50-75%
** <Less than 50% or < 100 litres per min
FEV1 (% predicted)
>75%
50-75%
** < 50% or < 1 litre
Arterial pO2
Test not needed
> 60 mm Hg
< 60 mm Hg
Arterial pCO2
Test not needed
Normal or < 40
> 40 mm Hg
SpO2 on presentation
>95%
92-95%
<92%
Initial Treatment
Start treatment immediately. Treatment is determined by severity of attack. Check Pulse Oximetry. If SpO2 < 92% on air, perform an Arterial Blood Gas (ABG). Patients should only be given oxygen if hypoxaemic. In absence of hypercapnia, the target oxygen saturation is 92-96%. If hypercapnia present, target oxygen saturation 88-92%. Continuous oximetry monitoring. Measure ABGS frequently in patients with severe attacks or if not responding. Mild Disease
Salbutamol MDI via Spacer: 4 puffs (1 puff at a time via Spacer) or Nebulised Salbutamol: 5mg Nebulised Ipratropium: not needed Corticosteroids: Prednisolone orally 50mg daily CXR: not needed unless focal signs on examination Observations: regular Admission: probably not Other tests: not needed
Moderate Disease
Nebulised Salbutamol: 5-10mg 1-4 hourly Nebulised Ipratropium: usually not needed Corticosteroids: Prednisolone orally 50mg daily CXR: yes Observations: continuous Admission: yes Other tests: may not be needed Severe Disease
Nebulised Salbutamol: 10mg every 15-30 mins Intravenous Salbutamol: may be needed when nebulised treatment cannot be
given reliably or if patients not responding to nebulised treatment
Nebulised Ipratropium: 0.5mg 2 hourly until FEV1 improved by >30%, then stop Corticosteroids: Prednisolone orally 50mg daily. Intravenous
hydrocortisone (200mg 6-hourly if patients cannot swallow or retain oral medication)
CXR: yes Observations: continuous Admission: yes – consider ICU/high dependency Other tests: check for low K+ Other treatments
Theophylline: benefits unclear if patient on maximal beta-agonist therapy. Discuss with consultant or registrar first.
Adrenaline: No evidence of benefit over maximal beta-agonist therapy. Discuss with consultant or registrar first.
Antibiotics: Not indicated unless CXR shows pneumonia. Discoloured sputum is seen in simple asthma without infection.
NIV: No clear benefit. May cause further hyperinflation and gas trapping resulting in later deterioration. Must consult ICU and/ or Respiratory Failure before NIV initiated.
Subsequent Treatment
Mild Disease
FEV1 or PEF > 75% predicted: Discharge on:
regular inhaled bronchodilators (3 to 4 hourly) 1-2 week course of oral steroids (Prednisolone 50 mg daily) regular inhaled preventive therapy (inhaled corticosteroid +/- long acting beta-
agonist) Instruct patient to return if there is any symptomatic or peak flow deterioration or failure to obtain 3 hours of relief from their usual bronchodilator dose. Arrange appropriate medical review (GP or respiratory physician) within 7-14 days. Patients who present twice with the same attack should be admitted.
Moderate Disease
Those who do not respond substantially (see mild disease) will require hospital admission. Regular monitoring is essential (PEF, FEV1, SpO2). Treatment:
nebulised salbutamol 5 mg every 1 to 4 hours. oral steroids in high doses (e.g. prednisolone 50 mg daily) inhaled steroids should be started just prior to discharge from hospital and before
prednisolone is withdrawn. Arrange medical review by a physician within 7-14 days of hospital discharge. Severe Group
The respiratory or medical registrar should be notified immediately to direct management of the patient. Patients in this group should be admitted to a monitored bed. Treatment:
continuous pulse oximetry monitoring, and supplemental oxygen to target of 92-96% (if not hypercapnic).
frequent high dose aerosol bronchodilators ie salbutamol 10 mg 15-mins (continuous nebulization) then to 1-2 hourly plus
ipratropium 0.5 mg every 1-2 hours consider intravenous beta-agonist (e.g. salbutamol 100-300 mcg followed by 10
mcg/kg/hour) in the absence of a response to inhaled treatment oral prednisolone at 50mg daily. Consider intravenous steroids if patient cannot
swallow or retain oral medication Continuous close observation with objective measurements (PEF, FEV1, ABGs) is essential. Oximetry monitoring is mandatory. ABGs must be repeated if the PCO2 is normal or high, if patient’s oxygen requirement increases to > FiO2 40%, or there is a change in the patient’s conscious state. Intubation and artificial ventilation are indicated only when significant deterioration occurs despite aggressive therapy. This can often be picked from the end of the bed. Indications include:
significant deterioration in conscious state, a significantly increasing arterial pCO2 associated with alteration in conscious
state a decreasing pO2 despite high inspired oxygen concentrations.
Where arterial blood gas analysis cannot be performed, rapid shallow respiration, a quiet chest, and a decreasing paradoxical pulse (i.e. failing effort) would indicate impending respiratory arrest. Increasing drowsiness and restlessness are invariably present in this situation. In this situation, an ALS call should be initiated. Patients should not be discharged from hospital until there is spirometric evidence of stability; the FEV1 should be at least 75% of predicted or of known recent highest values. Patients who present with a severe life threatening attack have a high risk of death in subsequent attacks as well as significant morbidity. At the time of discharge from hospital you must arrange review by a respiratory physician within 7 days.
Other Aspects of Treatment
Any drug which may depress ventilatory drive is contraindicated (e.g. sedatives, anti-depressants, narcotics).
Physiotherapy to aid sputum clearance often aggravates the airway obstruction and should not be prescribed routinely. Relaxation techniques may be helpful.
Cease any ß-blockers (including eye drops) or aspirin, and stop NSAIDs. Inhaler technique should be checked during stay, and patient reinstructed or given
advice about spacer devices. Don't discharge the patient until you are certain that they are capable of using their medication device appropriately.
All patients admitted to hospital with asthma should have their long term management and crisis plan (action plan) carefully reviewed. The revised plan should be re-written.
Adequate follow-up should be ensured following recovery from an acute attack. Consultation with a respiratory physician is recommended for patients who are admitted to hospital.
Protocol for Salbutamol Infusion
Limited indications for use: discuss with registrar first! Presentation
Ampoules: 5mg/5ml 500 mcg/ml Administration
Stat dose of 100 - 300 mcg/ml salbutamol IV bolus over 1 minute Dilute salbutamol 5mg in 100 ml Sodium Chloride 0.9% (giving concentration of ~50 mcg/ml), administer as a continuous intravenous infusion at 5 – 20 mcg/min (6-24 ml/hr) Start at 5 mcg/min (6 ml/hr) and adjust according to patient response A new solution should be prepared every 24 hours Do not run any other drugs/infusions with salbutamol as there is no research available regarding the stability/compatibility Wean 1 ml/hr Continuous cardiac monitoring Hourly heart rate and respiratory rate Monitor serum potassium (may fall) Dosage Calculation
5 mg/105ml* = 5,000 mcg/105ml = 47.62 mcg/ml *100 mls N/Saline + 5 ml Salbutamol = 105 ml of fluid
Infusion Dosage (5 mg Salbutamol in 100 ml 0.9%/NaCl)
Definitions COPD is a preventable and treatable disease of the lungs, often due to inhalation of cigarette smoke or other noxious gas. COPD often has significant extrapulmonary effects that may contribute to the severity of the overall syndrome. Its pulmonary component is characterised by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases. An exacerbation of COPD is an event in the natural course of the disease characterised by a change in the patient’s baseline dyspnoea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD. Aetiology COPD almost always arises from a gene-environment interaction. The risk of COPD is related to the total burden of inhaled particles Cigarette smoking is the most important aetiological factor in the development of COPD, accounting for about 80 – 85% of the risk of developing COPD in Australia. Other particle exposures include occupational exposures (organic and inorganic dusts, chemical agents and fumes) and air pollution (occupational or urban). Other factors influencing the development of COPD include infections (especially childhood illnesses), deficiency of alpha1-protease inhibitor and other unidentified factors.
Presentation Presentation to hospital is usually due to acute exacerbations of COPD (infective and non-infective). Symptoms include:
Increased breathlessness Increased cough Change in sputum production (change in colour and/or increased amount) Patients may also display increased (or new) ankle oedema, poor sleep, and
decreased appetite Causes
The most common cause of COPD exacerbations is infection, often a viral infection of the respiratory tract. Bacterial infection may have either a primary or a secondary role in about 50% of exacerbations of COPD. Bacterial infection of the lower respiratory tract is common, and changes in the bacterial flora or the immune response to these organisms may be important factors in acute exacerbations.
Chronic bacterial contamination of the airway is common in COPD and may be an important part of the pathogenic process even when the disease is stable. Non-infective causes, such as air pollution and ambient temperature variation, may also cause acute exacerbations.
The cause of about 1/3 of severe COPD exacerbations cannot be identified. The severity of presenting symptoms often correlates poorly with spirometry and blood gases. Left ventricular failure (LVF), Right Ventricular Failure (RVF) and/or ischaemic heart disease (present in at least 50% of patients with COPD) should be considered. LVF may be difficult to detect clinically and radiologically, so a high index of suspicion is required. Investigations
Spirometry is mandatory for diagnosis. o Do not assume that every smoker with SOB has COPD. o Unless confused or comatose, even the sickest of patients can perform a
FEV1 manoeuvre. o FEV1 indicates the severity of COPD and helps to predict important
complications such as hypercapnia during oxygen therapy AND risk of life-threatening exacerbations.
o An FEV1 < 1.0L (or 40% predicted) is usually indicative of a severe exacerbation in patients with moderate COPD.
ABGs should always be performed (preferably breathing air) to evaluate respiratory failure. Venous blood gases (VBG) should not be used to assess PaCO2 or PaO2 in acutely unwell patients in order to make clinical decisions (see below). Inspired O2 concentration should ALWAYS be noted.
o For patients with severe COPD, the most important signs of a severe exacerbation will be worsening hypoxaemia, acute respiratory acidosis, or both.
o A recent systematic review has found that peripheral venous blood gas (VBG) analysis does not compare well with ABG analysis for the PaCO2 or PaO2, and that these differences are sufficiently large to be of clinical significance.
CXR to detect alternative diagnoses/complications e.g. consolidation, pneumothorax.
Sputum microscopy and culture if producing purulent sputum Full blood count for polycythaemia and neutrophilia ECG to help identify cardiac disease Theophylline level (if prescribed) Influenza rapid specific tests, such as nucleic acid amplification tests (NAAT),
performed on nose or throat swab specimens if influenza is clinically suspected Management Patients should receive treatment with the following: Bronchodilators
1. Inhaled β2-agonist (e.g. salbutamol 400-800mcg; terbutaline 500-1000mcg) and antimuscarinic agent (ipratropium 80mcg) via metered dose inhaler and spacer (preferred) OR
2. Inhaled beta-agonist (e.g. salbutamol 2.5-5.0 mg) and antimuscarinic agent (ipratropium 500mcg) via nebuliser. Medical air (and not oxygen) must be used to drive the nebuliser in hypercapnic patients (see Delivery of Oxygen Therapy below)
The dose interval for inhaled beta-agonist is titrated to the clinical response and can range from every hour to six-hourly. The dose interval for inhaled antimuscarinic agent should not be less than 4 hourly. Remember to cease inhaled long acting beta-agonist and long acting antimuscarinic bronchodilators during the period when nebulised bronchodilators are administered. Systemic Corticosteroids
3. Oral prednisolone 40-50 mg daily for up to 2 weeks OR
4. Intravenous hydrocortisone 100-200 mg 6-hourly (if unable to tolerate orally or NBM)
Blood sugar levels should always be monitored for patients on systemic corticosteroids. Please note: Mucolytic or expectorant drugs are of minimal value Antibiotics
Antibiotics are only indicated in COPD exacerbations where there is an increase in sputum volume, sputum purulence ± increased breathlessness. Empirical antibiotics are indicated in patients with severe exacerbations of COPD who require mechanical ventilatory support (invasive or non-invasive) Antibiotics for COPD patients should NOT be commenced before discussion with the Respiratory Physician. Intravenous antibiotic therapy is only required if the patient has an impaired mental state, is unable to swallow safely, or has a chest X-ray confirming pneumonia - as outlined in community acquired pneumonia guidelines.
The aim of treatment with antibiotics in acute exacerbations of chronic bronchitis is to reduce the volume and purulence of sputum. Elimination of colonising organisms is not required.
The most common bacterial pathogens of an Infective Exacerbation of COPD are: - Haemophilus influenzae - Streptococcus pneumoniae - Moraxella catarrhalis Of these three organisms, sputum specimens within WSLHD between 2013 and 2014 have demonstrated approximately 30% resistance to amoxycillin alone. Based on this local bacterial resistance pattern, the antibiotics of first choice for COPD patients being admitted with acute infective exacerbation to a hospital within the WSLHD are:
5. Oral amoxycillin-clavulanate 500 mg/125 mg (Augmentin Duo) 8-hourly or 875 mg/125 mg (Augmentin Duo Forte) bd for 5 days OR
6. Oral doxycycline 100 mg 12-hourly for 5 days Note: In patients who do not have a severe exacerbation requiring admission to hospital (i.e. being sent home from ED) and who have not failed a prior course of antibiotics, amoxycillin should be considered as per Therapeutic Guidelines:
7. Oral amoxycillin 500 mg 8-hourly for 5 days If the patient is known to have sputum colonisation with Ps. aeruginosa, discuss antibiotic choice with Respiratory Physician (in general, 2 antibiotics would be used. e.g. ceftazidime and tobramycin).
Macrolide antibiotics are much less likely than other antibiotics to suppress H. influenzae and are more likely to result in early relapse. They are therefore not recommended unless H. influenzae infection has been excluded.
Antiviral Therapy Treatment for influenza viral infection may be indicated in COPD patients with a severe exacerbation who are at high risk of respiratory complications and poor outcomes. Treatment with a neuraminidase inhibitor reduces duration of symptoms of influenza by only 1 day, on average, when treatment is started within 48 hours of the onset of symptoms (though the earlier that treatment is given, the greater the benefit). If treatment is indicated, use:
8. Oral oseltamivir 75 mg 12-hourly for 5 days The influenza virus is spread through droplets and contact with fomites (virus-contaminated objects), so infection control precautions (e.g. hand hygiene, patient isolation, use of personal protective equipment) are essential, particularly for hospitalised patients. Nebulised therapy should be avoided if possible due to increased risk of aerosol spread of viral particles. Oxygen Therapy Oxygen is a treatment for hypoxaemia, not breathlessness. Oxygen should be prescribed on the drug chart using a target saturation range. In most emergency situations, oxygen may be given to patients immediately without a formal prescription; however subsequent record should be made of oxygen given, similar to recording of all other emergency treatment.
Oxygen (O2) is a drug used to treat hypoxemia but O2 therapy can produce severe (even fatal) complications in some patients if therapy is uncontrolled. Therapy should be initiated under the direction of a medical officer. Medical officers prescribing O2 for patients should be familiar with the different methods of administration, and should specify the O2 flow rates to be used in each case on the drug chart or in the patient notes. Changes in O2 therapy require the same considerations as any other modifications of patient treatment. All oxygen therapy for Respiratory Patients must be documented on the Medication chart or on the Respiratory Pressure Support Therapy Chart (as appropriate for patients on NIV or CPAP). Oxygen prescriptions must be reviewed and updated on a daily basis as appropriate. Changes in therapy should be documented on the appropriate chart and in the patient’s medical record. When prescribing oxygen therapy, always clearly document:
aims of treatment with oxygen therapy, ie target PaO2 from ABGs or target SpO2 from oximetry
level of oxygen supplementation method of oxygen delivery monitoring required
NOTE: Any patient requiring high inspired O2 concentrations ( 40% FiO2) to maintain oxygenation is critically unwell and requires senior medical review (registrar / SRMO) and transfer to a high-dependency ward. If a patient needs high flow nasal prongs, a respiratory consultant or advanced trainee must approve this, and the patient must be in a monitored unit. A patient acute requiring 50% FiO2 requires an ALS call and ICU consult/ referral. Group A - All patients with conditions where PaCO2 may be elevated, either at
baseline or in response to uncontrolled oxygen therapy. Target Oxygen Saturation
disease, known bilateral diaphragmatic paralysis) Severe kyphoscoliosis or other severe chest wall abnormality Severe obesity and / or severe OSA (sleep apnoea) Any patient with known elevated PaCO2 Head injury
Delivery of Oxygen Therapy:
Rebreathing masks should NEVER be used. Initially Venturi masks permitting a known O2 concentration (e.g. 24% and 28%)
should be selected. Exact inspired oxygen concentration used will depend on blood gas measurements and clinical state, but, in general, there is no need to raise the PaO2 to > 60 mmHg or SpO2 > 88-90%.
Prior to blood gases, a 24-28% Venturi mask aiming for oxygen saturation of 88-
92% is appropriate for patients with risk factors for hypercapnia but no prior history of respiratory acidosis.
Occasionally, patients with normal PaCO2 , and no history or risk of hypercapnia,
can initially elevate PaCO2 when given oxygen, though rarely to a significant extent. Small rises in PaCO2 (less than 5 mmHg) are NOT a cause for concern. If PaCO2 does rise to a major extent after oxygen is given, removal of the oxygen in the setting of concurrent hypoxaemia, may be lethal. Consultation with Respiratory CMO, respiratory registrar or senior medical officer is mandatory. Consider: reducing FIO2 and aim for target SpO2 88-92 % and monitoring PaCO2 and pH
with ABGs non-invasive ventilation intubation and ventilation
Discuss with CMO or registrar if uncertain. All patients with a PaCO2 > 60 mmHg
must be urgently discussed with Respiratory CMO or registrar. Intermittent oxygen is worse than no oxygen as it leads to worsening hypoxia and
hypercapnia, which is difficult to rectify without mechanical ventilation. Patients with high PaCO2 and normal pH values (ie chronic hypercapnic
respiratory failure) do not require immediate intubation. Controlled O2 therapy should be trialled first if these patients are hypoxic.
In patients with increased PaCO2 on 24% O2, repeat ABGs in one hour. If PaCO2
has risen less than 5 mmHg and the patient is still significantly hypoxaemic, 28% O2 via Venturi mask may be given and ABGs repeated in one hour. If PaCO2 rises more than 5 mmHg when 24% O2 is given, the oxygen therapy must not be removed; the patient must be monitored closely with medical staff checking oxygen flow rates and PaCO2 at frequent intervals. Non-invasive ventilation may be indicated (see later)
If PaCO2 is very high on admission, or becomes very high, notify CMO and
medical registrar. Non-invasive ventilation or intubation and ventilation may be necessary. It is desirable for indications for intubation and ventilation of each patient to be clearly decided before the patient is moribund, or has a ventilatory arrest.
Following the initial acute period of assessment and monitoring, nasal cannulae (at
1-2 L/min O2 flow) are the preferred method of administering long-term O2 for FIO2 concentrations < 30%. Although less exact, this approach is more practical due to better tolerance by the patient. The dangers of intermittent therapy are therefore more likely to be avoided. The cannulae can be kept on during meals and are less likely to slip off accidentally. Last but not least, they are cheap!
ABGs may need to be repeated when the patient is changed to this delivery method.
Patients with hypercapnia who require nebulised bronchodilators should use
medical air (not oxygen) to drive the nebuliser. While using the nebuliser, supplemental oxygen can continue to be provided by nasal cannulae at a flow rate of 1-2 L/min.
Uncommonly, inspired O2 concentrations >30% will be found necessary. For
these occasions, a fixed concentration mask (Venturi) with an appropriate flow rate should be used.
Group B - All patients with conditions in which PaCO2 is not usually elevated. If
the PaCO2 is not elevated, Target Oxygen Saturation should be 92-96%.
In this group of patients short periods of high concentration O2 therapy are not harmful, whereas hypoxia is dangerous. Therefore, for this group, give enough oxygen to reach a target SpO2 range of 92-96%.
Low inspired O2 concentrations (<30%) are most practically achieved with nasal cannulae for reasons given above.
High inspired O2 concentrations (>50%) may be provided by a non-rebreathing mask, or High Flow Nasal Cannulae (HFNC-see below). For a non-rebreathing mask, flow rates must be >8 L/min to ensure that the reservoir bag does not collapse completely on inspiration which may lead to rebreathing and elevation of PaCO2.
Intermediate O2 concentrations (30-50%) should be administered by means of a fixed concentration mask with appropriate O2 flow rates.
Continuous monitoring with oximetry is mandatory if the SaO2 is less than 90% on room air.
High Flow Nasal Cannulae (HFNC) Humidified High Flow Nasal Cannulae (HFNC) should be reserved for use in the ICU/HDU setting. HFNC should be initiated and prescribed by ICU or treating Respiratory team. The continued management of the patient on HFNC should be overseen by the ICU or Respiratory team, and any weaning in flow rate or FiO2 should be done under the supervision of the ICU or Respiratory team. HFNC is an alternative to low flow mask or nasal cannulae for oxygen delivery. There are no current established evidence-based guidelines to guide appropriate clinical use in adults. Indications for using HFNC:
Patients with moderate levels of arterial hypoxaemia and respiratory distress in whom the oxygen requirement is greater than that supplied by low flow oxygen delivery devices (i.e. low flow nasal cannulae, Hudson masks).
May be an alternative delivery interface in the following conditions: o Pulmonary oedema (in patients who are not critically unwell and who do
not require CPAP therapy) o Acute lung injury/chest trauma o Pneumonia o COPD exacerbation: Not appropriate in the setting of hypercapnoeic
hypoxaemic respiratory failure with PaCO2 > 45 mmHg) o Asthma (use with caution in unstable/ severe asthma)
Contraindications to using HFNP: epistaxis, base of skull fracture, maxillo-facial and upper aerodigestive tract surgery, nasal obstruction, suspected pneumothorax, and hypercapnoeic respiratory failure. Non-invasive Ventilation
NIV has a role in certain patients with acute hypercapnic respiratory failure. Discuss indications with Physician or respiratory failure registrar. There is no role for CPAP in acute exacerbations.
4. Guidelines Forfor Non-Invasive Ventilatory Support (NIV) In Acute Hypercapnic Respiratory Failure
For these guidelines, non-invasive ventilation (NIV) refers to the delivery of ventilatory support through the patient’s upper airway, using a full face or nasal mask, with bilevel positive pressure machines (eg. BiPAP or VPAP machines), rather than by endotracheal intubation (invasive ventilation). NIV has a number of advantages and disadvantages in the setting of acute hypercapnic or acute-on-chronic hypercapnic respiratory failure. NIV can be provided by different types of ventilators but bilevel positive pressure ventilators are simplest to use, cheaper and more flexible than others: they have been used in the majority of trials of NIV. CPAP refers to continuous positive airway pressure and is NOT considered to be true ventilatory support. Its indications are more limited than NIV. All patients who require NIV should be discussed with the Respiratory Failure Registrar on call (Pager 09229 or via Switchboard), or the Respiratory Consultant on call. Indications for CPAP
Cardiogenic pulmonary oedema where patients remain hypoxic despite maximal medical therapy
Obstructive Sleep Apnoea Severe pneumonia where patients remain hypoxic despite maximal medical
therapy. In this setting, treatment MUST be discussed with CMO or senior medical registrar and be instituted in ICU or high dependency area as urgent intubation and invasive ventilation may be necessary.
Indications for NIV
Acute or acute-on-chronic hypercapnic respiratory failure (pH < 7.35 AND PaCO2 >50mmHg) due to:
Acute exacerbation of COPD, including bronchiectasis and cystic fibrosis Obesity-Hypoventilation syndrome, including severe Obstructive Sleep Apnoea Neuromuscular diseases such as Duchenne’s muscular dystrophy, motor neurone
disease, known bilateral diaphragmatic paralysis Chest wall diseases such as severe kyphoscoliosis Cardiogenic Pulmonary Oedema with acute hypercapnic respiratory failure, where
acute myocardial ischaemia is excluded Other control of breathing abnormalities
Contraindications to CPAP and NIV
Cardiac Arrest, Respiratory Arrest and Coma (Absolute Contraindications) Medically unstable
Facial abnormalities such as trauma, burns, recent head & neck surgery, CSF leak Anatomical abnormalities precluding use of full-face or nasal mask Unable to protect airway (impaired cough or swallowing mechanism) Combative or uncooperative patient Recent upper gastrointestinal surgery
Undrained pneumothorax These contraindications may be considered “relative” if NIV is to be the “ceiling” of treatment. Consider Intubation if Failure of NIV
Failure of NIV may be indicated by Reduction in neurological or conscious status (not sleep) Inability to maintain oxygenation Excessive secretions with aspiration risk Failure of pH / PaCO2 to improve with adequate therapy
Procedure to Start NIV
The following is a guide only. There are a number of other considerations in instituting NIV, including inspiratory times, rise times, mask choice etc and NIV should ONLY be instituted by experienced staff members. Contact respiratory registrars or respiratory failure physiotherapist. If required, supplemental oxygen therapy can be used in conjunction with CPAP or NIV, and should be titrated on an individual basis, with arterial blood gas monitoring. IPAP refers to inspiratory positive airway pressure, EPAP to expiratory positive airway pressure. Patients MUST be closely monitored during initiation of NIV to ensure optimal settings. Interface
In the initial acute situation, full face mask is preferred to nasal mask as distressed patients mouth breathe
High dependency or 1:1 nursing is required in the initial stages Optimal tension of headgear is a balance between leak and comfort. Paradoxical
increase in leak can occur if strapping is too tight The main reason for failure of NIV is failure of interface (ie mask or mouth leak) Always ensure an expiratory valve is in the NIV circuit
CPAP
Begin CPAP at approximately 1cm H20 per 10kg body weight, up to maximum starting pressure of 10cm H20
If oxygen saturation fails to improve and/or respiratory rate fails to decrease, increase CPAP by 1 to 2 cm H2O increments as tolerated
Usual settings are between 7 and 15cm of H2O If hypercapnia develops, consider NIV
NIV
Begin IPAP at 10cm H2O, EPAP at 4cm H2O if patient < 60 kg Begin IPAP at 12cm H2O, EPAP at 6cm H2O if patient > 60 kg If required, add supplemental oxygen to maintain average oxygen saturation >
88% If PaCO2 remains > 50 mmHg, increase IPAP by 2cm H2O increments to a
maximum of 20cm H2O Usual settings are IPAP 12 to 20cm H20, EPAP 4 to 10cm H2O If there is pulmonary oedema, obesity, intrinsic PEEP, or variable upper airway
obstruction, a higher EPAP may be required. Increase EPAP at 1cmH2O
increments as needed. Intrinsic PEEP can be identified by patient ventilator asynchrony with failure of the machine to trigger on attempted breaths
A back up rate (spontaneous-timed mode) is only required if the patient fails to trigger the machine (eg. during sleep or in patients with severe muscle weakness)
Nebulised medications can be delivered in-line, to stop disruption of the interface Humidification
Humidification (28°C or between 2-5 on dial) can be added when available if there are thick tenacious secretions or if NIV is being used for prolonged periods
Humidification (38°C) is required if CPAP/NIPPV is being delivered via tracheostomy
Patient Transport
Most CPAP, BiPAP and VPAP machines do NOT have an internal battery. If the patient is to be transported on ventilatory support, portable power packs will be required.
Otherwise, two devices which have an internal battery supply, and can be used for the purposes of patient transport are the Philips Respironics V60 and the Philips Respironics Trilogy ventilator. The use of these two devices for should be under the strict supervision of either the Respiratory Failure Team or ICU.
All patients transported on NIV MUST have a nursing and medical escort. Patient Monitoring
Initial therapy MUST only occur in the Emergency Department, medical HDU or ICU setting, with trained staff. If NIV is required on the ward in an ALS situation, it will be supervised by the ALS Team and ICU registrar prior to transport to HDU/ ICU.
Pulse Oximetry should be monitored continuously Observations, including respiratory rate, oxygen saturation, heart rate and blood
pressure, should be recorded 15 minutely until stabilised Arterial Blood Gases should be taken at baseline, and within one hour of
commencement of therapy. Further gases should be performed as dictated by the treating medical officer, who must review all gas results. Repeat gases will be required following significant changes in therapy (oxygen flow rates, ventilator settings etc.)
5 Guidelines For Administration Of Sedation In Respiratory Patients
Patient distress is common among critically ill respiratory patients. This may manifest as agitation with excessive motor activity. Anxiety, pain, delirium and worsening dyspnoea are all common causes of agitation. Deteriorating respiratory status is also a common cause of worsening agitation, and must be considered in all respiratory patients prior to therapeutic intervention. All commonly prescribed sedation, anxiolytic / analgesic medication have the side effect of respiratory depression, including benzodiazepines, opioid analgesics and neuroleptics. Reversible causes of patient discomfort and distress must be identified and corrected as a first step prior to the prescription of sedative medications.
Investigations
The following should be performed (at a minimum) prior to initiation of therapy:
ABGs are mandatory to evaluate respiratory failure and to evaluate oxygen therapy.
Spirometry should always be performed. CXR to detect complications eg consolidation, pneumothorax. Clinical evaluation and review of current medication.
Management
RMOs must not initiate sedative therapy in respiratory patients without first consulting the patient’s CMO or the respiratory or medical registrar on call.
If short term sedation is required, then a Benzodiazepine would be the most
appropriate agent. Lorazepam (0.25 – 0.5 mg sublingually) has a short duration of action and is useful for anxiety. Temazepam 10 mg is another short acting hypnotic that could be trialled. The use of Oxazepam and Diazepam must be discussed first with the patient’s CMO in view of the long duration of action.
The patient should be clinically reviewed prior to repeat dose administration (for
evidence of over-sedation or respiratory depression). In cases of over sedation or respiratory depression, Flumazenil (0.3 – 0.6 mg)
should be available on the ward and administered promptly. Repeat doses may be required. Consider monitoring in Medical High Dependency.
6 Pneumothorax
Spontaneous
Presents with pleuritic chest pain, and/or dyspnoea or CXR finding (eg post procedure).
Physical signs may be subtle or absent. "Auscultatory silence with normal percussion note".
Do not order routine expiratory films in addition to standard inspiratory films: if the inspiratory film is diagnostic, an expiratory film adds nothing.
Whatever the extent of collapse DO NOT insert intercostal catheter unless the patient is breathless. Intercostal catheters usually do not relieve pain. Intercostal catheters should not be inserted without first discussing the indications with the Respiratory CMO or registrar, except in cases of dire emergency.
All management decisions should be discussed with CMO or respiratory registrar. The decision to drain a pneumothorax depends on patient symptoms (ie breathlessness) and underlying lung disease.
Pneumothorax in a patient with asthma or chronic obstructive pulmonary disease (COPD) may appear trivial and not warranting treatment. Discuss with CMO - often warrants intercostal drain. These patients nearly always need admission.
Where drainage of the pneumothorax is considered necessary AND the patient has no underlying lung disease, simple aspiration rather than intercostal catheter should be the initial step
Tension Pneumothorax
Tension pneumothorax is rare and over diagnosed. The pressure in the pleural space is above atmospheric throughout the respiratory
cycle. The patient is ALWAYS obviously and extremely ill: blue and shocked. CXR is not useful as there are NO reliable X-Ray signs of tension pneumothorax,
and if tension pneumothorax is present, the patient will die before a CXR can be done.
If suspected clinically, careful insertion of a large-bore (e.g. 14 gauge) intravenous catheter via the intercostal space will give immediate relief.
7 Community Acquired Pneumonia Guidelines for Initial Management of Community Acquired Pneumonia (CAP) This summary is limited to the immuno-competent patient with community-acquired pneumonia (CAP) and DOES NOT deal with the approach to immunocompromised or HIV patients. Acute bronchitis generally requires NO antibiotics. Exacerbations of chronic bronchitis (cough, sputum, dyspnoea) & AECOPD do NOT need the same level of antibiotic cover as pneumonia, and are dealt with in the COPD guideline. The important features to assess are: (1) severity of the pneumonic illness (2) co-existing cardiopulmonary disease (3) modifying factors - risk of gram negative infection / Pseudomonas (4) current viral infections (eg influenza) in the community Clinical / Xray findings are non-specific in identifying a likely causative pathogen, and diagnostic testing has limitations. Clinical syndromes of "typical" or "atypical" pneumonia cannot be used to limit therapy. Thus, initial therapy is empiric. Common organisms found in patients hospitalised with CAP include:
1. Chest X-ray - PA and lateral 2. Sputum collection - Gram’s stain and culture. 3. Blood cultures if febrile
4. Diagnostic aspiration of pleural fluid if present 5. Blood count, electrolytes, urea / creatinine, liver function tests, oxygen saturation
/ blood gases 6. Urinary Legionella and pneumococcal antigen may be useful in certain cases 7. Acute and convalescent serology (mycoplasma, chlamydia, legionella etc) should
be considered 8. Consider nose/throat swab into viral transport media for influenza/resp viruses-
direct IF / viral culture Decision to hospitalise depends on: Severity of pneumonia Co-existent disease Social / personal background. The decision to hospitalise or discharge remains a clinical decision. Markers of severe pneumonia: Septic shock, need for mechanical ventilation or inotropic support or development of acute renal failure are “major” markers of severe pneumonia. The CURB 65 score was developed to give an indication of 30 day mortality for an episode of community acquired pneumonia, but is sometimes used as a surrogate for severity of pneumonia. The CURB 65 score is calculated as one point for each of: Confusion Urea >7 mmol/l Respiratory rate >30/min BP - systolic <90 mm Hg or diastolic <60 mm Hg age > 65 years Score 0 or 1 = non-severe Score 2 = severe Score 3-5 = very severe – consider High Dependency or ICU admission If non-severe, consider discharge home from Emergency Dept or from ward (if admitted) on oral therapy with PACC service or early follow up by Respiratory CCC or GP taking into consideration comorbid disease / social factors Switching from intravenous to oral therapy once admitted If CURB 65 score 0 or 1 then consider switch to oral therapy on first ward round and consider same-day discharge with PACC service +/- follow up in Respiratory CCC (discuss with consultant). If CURB 65 score 2 or higher then switch to oral therapy when: Temperature < 38° C for ≥ 16 hours, and Clinically improving (eg. symptoms, respiratory rate, SpO2, etc), and Able to tolerate oral therapy (no dysphagia or malabsorption) Guideline for Early Discharge Switched to oral therapy Normal oxygenation (SaO2 ≥ 90%) on room air for 30 mins Stable co-morbid conditions Social needs attended
The decision for early discharge should be discussed by telephone with the patient’s Consultant if prior to any formal ward round review, and early follow-up should be arranged in Consultant’s rooms or Respiratory CCC. Consider discharge with PACC service on day of switch to oral antibiotics. The PACC service provides ongoing monitoring in the home facilitating earlier discharge. There is no need to delay discharge to ensure “patient is stable on oral therapy”. Initial treatment of hospitalised patients with CAP General Supportive Measures 1. Ensure adequate fluid intake. Most patients are initially dry. 2. Remember paracetamol for fever and pleuritic pain. If narcotics required for pleurisy,
then should be managed in medical high dependency ward with oximetry. 3. Ensure adequate oxygenation (with known FiO2) to maintain PaO2 above 60 mm Hg.
Patients requiring FiO2 of 0.50 or greater to maintain SaO2>90% or patients with an acute respiratory acidosis should be in medical high dependency ward.
4. Chest physiotherapy is not routinely required Initial antibiotic therapy is generally broader spectrum than ultimately required. When sputum culture & sensitivity become available, appropriate modifications can be made.
I. Moderate CAP Roxithromycin 300 mg orally daily plus Benzyl Penicillin 1.2 g iv q4h / q6h OR Ceftriaxone 1g iv daily
II. Severe CAP (B5B or ICU) Ceftriaxone 1gm IV daily plus Azithromycin 500mg IV daily In patients intolerant of beta-lactams and/or macrolides Moxifloxacin 400 mg iv once daily always requires ID approval In ICU patients, consider Timentin 3.1g q6h in place of Ceftriaxone If strongly suspect Pseudomonas: Timentin 3.1g iv q6h plus Gentamicin/ Tobramycin 5-7 mg / kg /day (or Ceftazidime 1g iv q8h) dependent on renal function If strongly suspect Staphylococcus: Consider addition of flucloxacillin 1g iv q6h (plus above) If strongly suspect anaerobic organisms: Consider addition of Metronidazole 500 mg iv q12h (plus penicillin or timentin) If strongly suspect Legionella: Consider use of Moxifloxacin 400 mg daily – will need ID approval Assessment of Response Most patients with CAP will start to improve within 2-3 days. Those patients with continued deterioration or no improvement by day 3 should be reviewed for empyema,
other site of infection, or resistant organisms. Switch to oral therapy can be tailored to any pathogens grown, or will generally be: Roxithromycin 300 mg orally / day and / or Augmentin Duo Forte 875mg bd Total duration of treatment depends on :on: Severity of illness / bacteraemia, presence of co-existing illness, subsequent progress. In general, bacterial infections should be treated for 7 to 10 days, with longer periods chosen for those with more severe episodes of pneumonia or significant intercurrent disease.
8 Pulmonary Embolism
Risk factors include:
pregnancy, postpartum period or caesarean section left and right ventricular failure fractures and injuries of legs chronic deep venous insufficiency, or previous DVT prolonged bed rest, sitting or immobilization (air travel > 4 hours duration) carcinoma obesity blood coagulation abnormalities post-operative (5-7 days) contraceptive pill (oestrogen containing) / HRT / tamoxifen trauma
Clinical presentations include
sudden onset unexplained dyspnoea pleuritic chest pain and haemoptysis (if infarction) syncope or faintness
Guidelines for the diagnosis/exclusion of Pulmonary Embolism
D-Dimer Testing A rapid quantitative ELISA test for D dimer (VIDAS D-Dimer) is now available to help exclude the diagnosis of pulmonary embolism. This test has a high sensitivity and negative predictive value, but only when considered following assessment of clinical probability. In patients with a pre-test probability of low to moderate, this D dimer test could be used to “rule out” PE. The test does not have a high specificity and therefore cannot be used to “rule in” PE. It may be falsely positive in patients >80 years, pregnancy, malignancy, etc. Pre-test Clinical Probability for Pulmonary Embolism The Departments of Emergency Medicine and Respiratory Medicine have adopted a formalised scoring system, the Wells Criteria, for assessing the clinical probability of pulmonary embolism in appropriate patients. This is combined with the VIDAS D-Dimer test to decide on the need for definitive imaging. Applicability of Guideline All patients being investigated for PE should be assessed according to this guideline. Physician override of the scoring system by either the ED Staff Specialist or Registrar is possible if the override decision places the patient in a higher probability than the score
indicates. Patients who are pregnant or post partum or have had recent long distance travel may be higher risk than calculated by the Wells Criteria. Patient Group Patients presenting to ED with suspicion of pulmonary embolism with symptoms for less than 30 days, and experiencing acute onset of new or worsening shortness of breath or chest pain. Diagnostic Pathway Procedure Step 1: Assess Pre-test Probability Using Wells Criteria Wells Criteria: Score: 1. Clinical signs and symptoms of DVT 3.0 (minimum: leg swelling and pain on palpation of deep veins) 2. An alternative diagnosis is less likely than PE 3.0 (patient should have had CXR, ECG, ABG) 3. Heart rate >100/min 1.5 4. Immobilisation/surgery in the previous 4 weeks 1.5 (immobilisation = bed rest except to toilet for ≥ 3 days) (surgery = major abdominal, pelvic or orthopaedic) 5. Previous DVT/PE 1.5 6. Haemoptysis 1.0 7. Malignancy 1.0 (on treatment, or treated in last 6 months or palliative) Low probability for PE = score <2 Moderate probability for PE = score 2-6 High probability for PE = score >6 Step 2: Confirm pre test probability with staff specialist or registrar (they may override score). Step 3: Determine need for D-Dimer Test If the patient has a low or moderate probability of PE, do an ELISA D-dimer test (the test available will be the Vidas exclusion test and the request form should specifically ask for the Vidas test) If the patient has a high probability of PE, proceed directly to definitive diagnostic imaging. Step 4: Interpretation of D-Dimer Test If D-Dimer is negative no further testing needs to be done to exclude PE. If D-Dimer is positive further testing is required. (A positive test does not confirm the diagnosis of PE in these patients) Step 5: Indications for Definitive Diagnostic Imaging If the patient has: (a) a high pre-test probability (Wells Score >6), or
(b) a positive D-dimer with a low or moderate pre-test probability,
definitive diagnostic imaging is required (see below).
Patients with high pre-test probability should be commenced on treatment if there are no contra-indications. Consideration should be given to treating low and moderate risk patients with positive D-Dimer and no contra-indications.
Step 6: Definitive Diagnostic Imaging
CTPA (CT Pulmonary Angiogram)
For patients > 40 years: CTPA is the preferred first line test
In addition to imaging the pulmonary vasculature, CTPA also provides detailed information about the lungs, pleural space and mediastinum that often provide an alternative diagnosis for the patient’s presentation. Patients with good quality negative CTPA do not require further investigation or treatment for PE Be aware of risks of contrast in patients with renal insufficiency. The following measures may be needed:
IV pre-hydration and adequate hydration afterwards (may need fluid status assessment and additional administration of diuretics)
Administration of N-acetylcysteine 600mg BD x4 doses ( 2 prior to scan and 2 afterwards)
V/Q scan (Ventilation/Perfusion Nuclear Medicine Isotope Scan) This test is reported as
Normal
High probability of PE
Low probability of PE
Intermediate probability of PE
Indeterminate
The only diagnostic results from V/Q scans are normal or high probability. The other results are essentially non-diagnostic. Therefore, PE has not been either confirmed or excluded by this result and further tests are always required. Patients with abnormal CXR or cardiorespiratory disease (eg. COPD) are more likely to have a non-diagnostic or indeterminate result on V/Q scanning For patients < 40 years with a normal CXR, V/Q scan is the preferred first line test within hours of availability. Please note V/Q scans are not available outside 08:30-17:00 hours Monday-Friday Pregnancy
Imaging investigations in pregnancy MUST be discussed with ED or Respiratory Consultant or Imaging Consultant (Radiologist or Nuclear Medicine Physician) The risks and benefits of investigations need to be clearly explained to patient and documented Lower limb Ultrasound is only available 08:30 – 17:00 hours, Monday-Friday, and remains the first test of choice. Radiation Exposure
The average human receives about 3mSv of “background” radiation per year. In general, the comparative radiation dose to a patient with CTPA is 12 mSv whilst it is 2.3mSv with V/Q scan.
The natural background dose for a foetus during pregnancy is 1.1-2.5mGy. The foetal dose of radiation from CTPA is 0.37mGy, whilst it is 0.4mGy from a V/Q scan in early pregnancy and 0.75mGy at 6 months. Risk of childhood cancer in offspring is slightly higher risk with V/Q scan than with CTPA (1 in 280,000 for V/Q and <1 in 1,000,000 for CTPA)
In suspected PE in pregnancy, if compression ultrasonography of the legs is normal and a CXR has not further aided the diagnostic process, the decision then needed is whether to investigate further with CTPA or V/Q or treat empirically. The pro and cons need to be discussed with the patient. Step 7: Interpretation of Diagnostic Imaging If the CTPA or V/Q scan is normal PE is excluded. If the V/Q scan is high probability or CTPA confirms a PE, continue treatment as PE and admit under the care of the respiratory physician. Consideration maybe given to discharging from ED on full dose anticoagulation with PACC in consultation with the on-call Respiratory Physician, with early follow up in the Respiratory Comprehensive Care Centre, if there are no adverse risk factors (see guidelines for referrals to Respiratory Comprehensive Care Centre) If the V/Q scan result is intermediate, the patient may need further imaging (including Lower Limb Doppler, and/or CTPA) and/or continuing treatment (discuss result with the respiratory or ED physician). If the CTPA is performed after hours and is reported as negative for PE by the radiology registrar, the patient should still be discussed with the respiratory physician on-call and admitted overnight till the films have been reviewed and a formal report is available the next day.
Patient Presenting with a Possible PE (Non Pregnant) Using Wells criteria
Low / moderate probability
Vidas D-dimer
-ve
PE excluded
+ve
CTPA or V/Q (renal failure/contrast allergy)
Normal
High probability
CTPA or V/Q (renal failure/contrast allergy)
CTPA +ve or
V/Q-high
Rx as PE
V/Q- Intermediate or Low probability
Discuss with ED or respiratory physician
Normal
PE excluded
V/Q-Intermediate or Low probability
Discuss with ED or respiratory physician
Commence Rx if no contraindication
Commence Rx if no contraindication
Patient Presenting with a Possible PE (Pregnant or Suspected to be Pregnant) Abbreviations:
Baseline coagulation studies before heparin (as some of these will be altered by anticoagulant therapy). Should include APTT, INR. Other tests, including proteins S and C, lupus anticoagulant, anticardiolipin antibody, antithrombin III, homocysteine, prothrombin gene mutation (G20210A), Factor V Leiden mutation, may be required in some (but not all) cases of PE and should be discussed with the on-call Respiratory Physician.
Anti-coagulation should not await diagnostic confirmation if there is strong suspicion of embolism based on clinical findings and tests.
Treat pain with adequate analgesia
Drug Therapy: Low-Molecular Weight Heparin (LMWH) Low molecular weight heparin is the treatment of choice for most patients with established DVT or PE. There is currently insufficient evidence for the routine use of oral direct thrombin inhibitors such as Rivaroxaban or Dabigatran in the treatment of acute pulmonary venous thromboembolic disease. The utilisation of these newer oral anticoagulation agents should be made on an individual case basis by the consultant responsible. Doses: Dalteparin (either 200 units/kg/day OR 100 units/kg/12hrs as a twice daily dose). Maximum dose of 25,000 units once daily or 12,500 units twice daily OR Enoxaparin (1.5 mg/kg/day as a daily dose or 1 mg/kg/12hrs as a twice daily dose). Maximum of 180mg daily or 120mg twice daily Every patient > 50 years must have a creatinine clearance (CrCl) calculated before LMWH is commenced. If Cr Clearance 10-30mL/min, dose adjustment needs to be made: Dalteparin 100 units/kg/ as a daily dose OR Enoxaparin 1 mg/kg as a daily dose). Both subcutaneously until warfarin is therapeutic. No need for routine monitoring of activity. Choice of therapy should be as per respiratory CMO or registrar. Contraindications: Dose modification is required in patients with significant renal impairment (increased risk of accumulation of LMWH). LMWH is contraindicated for CrCl <10mL/min and unfractionated heparin should be used. Dose modification may also be required in morbid obesity. Heparin Initial heparin bolus of 5000 units Initial infusion rate is calculated at 18 units/kg/hour up to a maximum of 1900 units/hour
Check APTT at 6 hrs to keep APTT at 1.5 to 2.5 times control, to keep APTT at 60-100s. Adjust heparin infusion rate according to published hospital protocol (Guidelines for Anticoagulation Version 9.12 dated 21st January 2014). Check APTT daily when APTT in therapeutic range. Check platelet count second daily to monitor for Heparin Induced Thrombocytopenia. Do not start Warfarin until the APTT is in the therapeutic range. If patients develop Heparin Induced Thrombocytopenia with LMWH or unfractionated heparin, cease heparin/LMWH. Administer bivalirudin or fondaparinux, together with a consultation with haematology. Drug Therapy During Pregnancy
Warfarin crosses the placenta. Warfarin therapy during early pregnancy may be teratogenic (warfarin embryopathy affects 5% of foetuses exposed between 6-9 weeks of gestation). Use of warfarin in the 2nd and early 3rd trimester is associated with foetal intracranial haemorrhage and schizencephaly. These complications may be minimised by the usage of unfractionated heparin or LMWH, which do not cross the placenta. LMWH is safe for use in pregnant women and recommended during pregnancy and into the puerperium but should be discussed with the O&G team. Note that there is increased renal clearance of LMWH during pregnancy and hence the half life of LMWH heparin is decreased during pregnancy. The use of twice daily weight based regimen is recommenced (as opposed to the once daily dosing). Monitoring of anti-Xa levels is generally not recommended. Thrombolysis Below is the Westmead Hospital Algorithm for Thrombolysis. Please refer to the document “Westmead Consensus Guidelines on Thrombolysis in Pulmonary Embolism” for more details.
Surgical Thrombectomy For patients with arterial hypotension or shock, in whom thrombolysis has failed or is absolutely contraindicated, emergency surgical embolectomy may be an option. Additional indications for surgical thrombectomy may include patients who have free-floating thrombi in the RA or RV or those with impending paradoxical embolus through a PFO. This should be discussed with the CMO and the cardiothoracic team. IVC Filter
The indications for IVC filters are controversial and the decision to insert a filter requires consultant input. Indications include:
Contraindication to anticoagulation (bleeding complications of anticoagulation, known recent bleeding, recent major trauma or surgery, haemorrhagic stroke)
Chronically thrombosed IVC No access route to IVC to place filter
IVC filter insertion needs consultation with vascular team and interventional radiologist (98456522 during hours or on-call interventional radiologist if after hours). IVC filters may be temporary or permanent. If temporary, optimal timing of removal by interventional radiologist should be determined early on. The longer the IVC filter is left in situ, the harder it is to remove!
9 CXR Lesions Suggestive Of Carcinoma
Discuss with Respiratory CMO or registrar concerning appropriate management plan and follow up. Consider admission if:
haemoptysis is present and massive (greater than 100 ml in 24 hours) symptoms warranting admission (e.g. pain, intractable vomiting, leg weakness) SOB associated with stridor and orthopnoea, suggesting large airways
obstruction, which is an emergency. Other lesions without symptoms may be investigated as an outpatient.
10 Massive Haemoptysis
This is a medical emergency as patients can die from asphyxiation. Patients who are actively bleeding or who have bled 100 mls in 24 hours should be admitted. Consult urgently with CMO re need for bronchoscopy or angiographic embolisation (interventional radiology). In general, bronchoscopy is not the investigation/intervention of choice for controlling bleeding in massive haemoptysis.
11 Pleural Effusions and Thoracocentesis
Nearly always require pleural aspiration (sometimes with pleural biopsy) to determine the cause of the effusion. This should be performed following discussion with the Respiratory CMO or registrar. If an effusion is difficult to tap, do a lateral decubitus CXR: the pleural opacity may not be fluid. Ultrasound may help to localise the fluid. Always send fluid for culture (including for TB), cell count, cell differential and cell block (cytology) and biochemistry (protein, LDH, glucose, albumin, amylase), together with serum for protein, glucose, albumin, amylase and LDH. Send pleural fluid pH on ice as for a blood gas analysis, in cases where infection is being considered. Consult CMO regarding the necessity for admission. Recommended Reading: British Thoracic Society 2010 Pleural Diseases Guidelines Time-Out Before All Pleural Procedures Before any pleural procedure is performed, the relevant radiology should be available and reviewed. The proceduralist and a senior nurse should together perform a “Time-Out” to check: correct patient, correct procedure, correct side, allergies, anti-coagulation status, availability of all required equipment and written consent obtained. A bed-side ultrasound, if available, should be performed prior to any pleural procedure involving aspiration of pleural fluid. Non-urgent pleural procedures should not take place out of working hours. A senior doctor or specialist nurse should be a designated “stop-person” who prevents an inexperienced operator from attempting or continuing to perform a pleural procedure. Thoracocentesis Introduction Pleural effusions complicate a variety of thoracic and systemic diseases. Thoracentesis is an important diagnostic procedure and is often used therapeutically to relieve dyspnoea caused by large effusions. Indications for Thoracentesis
Diagnostic Thoracentesis:
Indicated for any undiagnosed pleural effusion, to help establish the probable cause. In instances where the aetiology of an effusion can be reasonably deduced from clinical circumstances (e.g. congestive heart failure), the procedure may be deferred and the response to therapy observed. Repeat thoracentesis and/or pleural biopsy may be required to establish a diagnosis when initial studies fail to do so. Therapeutic thoracentesis
May be indicated for relief of symptoms due to large pleural effusions. When frequent or repeated thoracentesis is required for effusions that reaccumulate (e.g. malignancy), early consideration should be given to tube drainage and pleurodesis.
Contraindications to Thoracentesis
There are no absolute contraindications to diagnostic thoracentesis if clinical judgement dictates that the information gained from pleural fluid analysis is essential for diagnosis and/or therapy. Relative contraindications include:
1. Insufficient patient co-operation. 2. Anticoagulation or a bleeding diathesis (PT or APTT > twice normal, platelet count
< 25000 / mm3) 3. Active skin infection at the site of needle insertion
Conditions Associated with Increased Risk of Morbidity / Mortality
1. Coagulopathy (see above) 2. Inability of the patient to co-operate. 3. Chest wall infection 4. Very small effusions 5. Removal of large (>1.5 L) amounts of fluid. 6. Performance by inexperienced persons, without direct supervision 7. Unstable medical condition. Thoracentesis and pleural biopsy may be performed in
the outpatient setting, but hospitalisation may be required due to underlying illness 8. Mechanical ventilation – risk of pneumothorax is the same, however higher risk of
tension if a pneumothorax occurs Complications
1. Pneumothorax: 3 to 30%, depending upon operator skill. Approximately 20% of these require tube thoracostomy
Pneumothorax and re-expansion pulmonary oedema are more common after therapeutic thoracentesis because of the attempt to remove as much fluid as possible. A chest film should be performed after therapeutic thoracentesis in most instances. Detailed Procedure For Thoracentesis
1. Informed consent should be obtained 2. The clinical and radiological evidence of pleural effusion should be reviewed just
prior to the procedure to confirm the laterality, and assist with site selection 3. The site for pleural aspiration can be chosen according to the clinical and
radiological signs; on some occasions prior marking after ultrasound localisation is useful (especially in the case of loculated fluid). When the pleural fluid is free flowing, a site midway between the spine and posterior axillary line should be selected
4. The chosen site should be marked with indelible ink, occasionally an unmistakable
skin marking (e.g. a mole) is a useful reference point. Any sites below the 6th
interspace selected for aspiration MUST be confirmed by ultrasound if there is any doubt about the presence of fluid (NB beware of elevated hemidiaphragm). The patient should be seated comfortably for the procedure, and should lean on a bedside table and pillow
5. After the operator has washed and gloved (gowning is optional for small volume
diagnostic taps but mandatory if biopsies or large volume aspirations are being performed) the skin should be cleansed. This will usually be with Betadine. The operator should adhere strictly to sterile technique
6. If no contraindication exists to local anaesthesia, 5 to 10 mls of 1% lignocaine
should be infiltrated via a 23-gauge needle inserted at the chosen site. Firstly, inject sufficient to raise a small skin bleb. Change to a 21 gauge needle and then inject deeper, aiming ABOVE THE LINE OF A RIB (remember the neurovascular bundle is just below a rib) into the subcutaneous tissue and as far down as the pleura. When injecting deep to the skin, attempt to aspirate periodically from the tissues first, to avoid inadvertent injection of local anaesthetic directly into an intercostal (subcostal) vessel. Finally, confirm that the pleural space can be accessed at this injection site by aspirating a small volume of pleural fluid into the local anaesthetic syringe. In some circumstances, a longer needle will be required to access the pleural space
7. Once adequate surface anaesthesia has been obtained, aspiration of the pleural
space can proceed. The apparatus now used depends on the purpose of aspiration, but a small volume diagnostic tap will usually be done first even if it is intended to drain a lot of fluid (see below), or perform pleural biopsies (see separate protocol)
8. For a small-volume diagnostic tap:
Fit an 18 or a 16 gauge intravenous cannula onto a preheparinized arterial blood gas syringe (5 mls), keeping a 50 ml Luer-lock syringe handy. Advance the needle/cannula slowly through the anaesthetized skin and subcutaneous tissues (over the top of the rib), aspirating periodically until a flashback of pleural fluid is obtained. Fill the small syringe, then switch over to the 50-ml syringe and draw off about 50-ml of fluid. Then remove the syringe and needle/cannula together and place an "Airstrip", Bandaid or similar small dressing over the site from which you have aspirated
9. For a large-volume diagnostic and therapeutic tap:
This procedure is as described above, except that the 50 ml syringe should already be attached to a 3-way tap before the aspiration is commenced. After collection of the ABG syringe (pH) sample, the 3-way tap and syringe should be attached to the cannula, which has its tip in the effusion. The 3rd arm of the 3-way tap can be connected to a conventional IV giving set, which in turn can be directly connected into a urinary drainage bag. Fluid can then be withdrawn from the patient's chest into the syringe, and after turning the tap appropriately the fluid can be dispensed into the drainage bag. Often the fluid will flow freely (because of gravity) directly from the chest into the drainage bag using the 3-way tap merely as a conduit, BUT it is useful to have tap for those occasions when gravity alone does not facilitate drainage. A maximum volume of 1.5L per drainage is recommended for a single procedure, to minimise the risk of re-expansion pulmonary oedema.
A “dry tap” may result from the absence of pleural fluid (e.g. elevated hemidiaphragm rather than fluid), incorrect needle placement, or inappropriately short needle. Appropriate readjustment usually results in a successful procedure. The aspiration of air implies that the lung has been punctured, either because the needle was superior to the effusion, or was inserted too deeply. A post-procedure CXR is indicated. Laboratory Testing Of Fluid
The fluid specimen should be routinely sent for the following:
1. pH: This sample should be "treated like a blood gas", i.e. the fluid withdrawn initially into the blood gas syringe and sent off to biochemistry immediately for processing within an hour of collection. It is not necessary to send the sample in ice. Significant depressions of pleural fluid pH can be missed because of delays in fluid processing.
2. protein, albumin, glucose, LDH and amylase: This sample (about 10 mls) can go
in a sterile yellow-top jar to biochemistry, with an accompanying request form. This must be accompanied by a simultaneous (same day) determination of serum values for protein, glucose, LDH and amylase
3. differential white cell count: This small sample, in an ordinary EDTA (full blood
count) tube, should be sent to haematology with an accompanying request form. It should be noted that the differential cell count obtained from haematology is not as accurate as that obtained by cytology.
20 mls), carefully dispensed into a sterile yellow-top jar, to Bacteriology with an accompanying request form. If unusual organisms are suspected, please request them specifically (e.g. Legionella DFA). Never forget to specifically request ZN stains and culture for mycobacteria
5. cytology: The residue of the specimen, usually the largest portion, should be sent
in a yellow-top sterile container to Cytology, with an accompanying request form. A differential cell count should be specifically requested. A cell block should also be requested if suspicion of malignancy is high. Send 2-3 containers if possible.
Liaise with Registrar or CMO re other special tests that may be required. It is wisest to take these specimens personally to specimen reception especially if the procedure is performed late in the afternoons or on weekends
Intercostal Catheter Insertion
Strategies for reducing risk Intercostal catheter and pleural catheter insertions is a procedure in Respiratory medicine that carries a high risk of complications. The details of this procedure are not within the scope of the handbook. However it is important to recognise and manage the complications that can arise from pleural catheters.
Complications
Please refer to pages 26 to 28 in the ACI Pleural Drain in Adults NSW Consensus Guideline: Trouble shooting of UWSD and Tubing.
Due to Incorrect Placement
1. Subdiaphragmatic: Intra-abdominal with possible splenic, liver or stomach laceration
2. Subcutaneous: 3. Intrapulmonary: Especially in the presence of pre-existing disease such as
adhesions between visceral and parietal pleura, or underlying lung disease (bullous lung disease or “stiff lungs”). Expert advice should be sought from a radiologist, respiratory physician or registrar before placement of a chest tube in patients with bullous lung disease, or any loculated pneumothorax.
Complications may be prevented by careful consideration of the position of the ICC. The needle used to inject the local anaesthetic can be inserted into the pleural cavity and fluid or air aspirated to confirm that the position is correct. Removal of the trocar and insertion of the ICC without force after the gloved finger has been placed into the pleural space to confirm the position and to locate adhesions also reduces the risk of incorrect placement. Due to Incorrect Technique
1. Bleeding from intercostal artery: A potential problem, more so in elderly patients with tortuous intercostal vessels.
2. Re-expansion pulmonary oedema: This is generally found in those with large effusions that are drained too quickly. One to 1.5L is the maximum volume recommended for a single drainage, and the chest tube should then be clamped for 1 to 4 hours before allowing further controlled drainage to occur.
These may be reduced by careful adherence to the outlined technique, in particular avoiding the neurovascular bundle by dissecting over the upper edge of the rib, and slow drainage of large pleural effusions. For haemorrhagic and purulent effusions, avoid clamping for prolonged periods as it may lead to a blocked drain. Recommended actions if a patient develops haemodynamic instability or severe hypoxaemia suspected to be related to re-expansion pulmonary oedema:
Prevent further air or fluid drainage: clamp the chest tube Administer high-flow oxygen Call for help, including a MET call if necessary
Other Complications
1. Empyema 2. Subcutaneous emphysema 3. ICC dislodgement 4. Tubing disconnection 5. Tube obstruction, secondary to clotting or kinking
These may be reduced by meticulous adherence to aseptic technique, and to the insertion technique described above. In particular, ensuring the ICC is correctly positioned with all drainage holes located in the pleural space, firmly suturing the tube in place, attaching a mesentery and taping the tube connections together. Tube
obstruction may be suggested by the lack of movement in the underwater seal with respiration, and dealt with as described above (see Troubleshooting). In the event of accidental dislodgement or removal or pleural drain, do not reinsert the same tube or a new tube into the previous site. Antibiotic prophylaxis is not recommended for non-trauma patients with a pleural drain, but should be considered for trauma patients especially after penetrating trauma. Tube Removal
There are currently no data available with regards to the optimal timing of chest tube removal and the decision is usually individualised depending on the original indication for the chest tube. It is important to minimise the time the patient has a chest tube in situ and it would be unusual to need a tube in for more than 5 days. As a general guideline, when the ICC is inserted for pneumothorax, consideration should be given to chest tube removal when the air leak has ceased. In general, the air leak has ceased if the lung is fully inflated on CXR and no further bubbling occurs from the chest tube whilst patient coughs. However, simple observation may miss a small persistent air leak. Hence, prior to removal of the chest tube, a trial of clamping for 4-6 hours in duration within working hours should be undertaken. A small airleak is still present after 4-6 hours of clamping if:
1) Pneumothorax re-accumulates or increases in size on CXR 4-6 hours post clamping, or
2) Bubbling occurs as per direct observation by a respiratory registrar, when the registrar personally unclamps the tube after 4-6 hours of clamping
The 4-6 hour post clamping CXR must be reviewed by the respiratory registrar and not left to after hours staff or JMO to attend. If breathlessness, pleuritic chest pain, change in voice or subcutaneous emphysema develops at any stage whilst the tube is clamped, the tube must be immediately unclamped and the medical team informed and patient reviewed by a doctor. If the ICC is inserted for drainage of effusion, consideration should be given for chest tube removal if fluid drainage is < 150 ml in a 24 hour period. However, if the drainage is above this level for more than 2 days, discuss with senior registrar/CMO with regards to further management strategy (ie removal of ICC, definitive diagnostic or therapeutic procedure, continual drainage). When an ICC is inserted for medical pleurodesis, removal within 24 hours after pleurodesis is desirable. If drainage is substantial in 24 hours post-procedure (>500mL), consider repeat pleurodesis (medical or surgical). Prompt decision making is essential to ensure ICC is not left in situ unnecessarily – this increases the patient’s discomfort and the rate of complications. Process of Tube Removal
The doctor must document the decision for removing the chest drain in the progress notes. Prior to chest drain removal, check the coagulation profile and when anticoagulants were last given in all patients with anticoagulation therapy. The INR should be 1.5 or less when removing chest tubes. Chest tubes should only be removed by a nurse or supervised by a nurse who is experienced at the removal of pleural catheters.
The perception of the procedure will be unique for each patient. Perform a pain assessment prior to removal and offer analgesia as required. The dressings are removed and the area cleaned with antiseptic. The sutures holding the ICC in place are clipped. The patient is instructed to perform a Valsalva manoeuvre, the tube is withdrawn and the previously placed closure sutures are tied. The site is then covered with an occlusive dressing to prevent air entering the pleural space. Take care NOT to allow air to leak in whilst tube removed. Please note that pleural catheters inserted in the Radiology department may need an additional step (cutting and removing a stitch that is sutured subcutaneously to secure the tube) to uncoil the tip of the catheter prior to removal. Please do not use excessive force to remove this tube. If unable to remove this tube with gentle traction, please contact the radiology department for further guidance about removal of this tube. A chest x-ray should be performed within 24 hours. The remaining sutures are removed 3-5 days later.
12 Arterial Blood Gas Sampling Protocol
Arterial blood gas (ABG) analysis is performed to evaluate the adequacy of alveolar ventilation, oxygenation, blood oxygen-carrying capacity and acid-base status. Specifically, ABG analysis measures:
1. Presence and severity of hypoxaemia 2. Presence and severity of hypercapnia and degree of metabolic compensation 3. Acid-base status abnormalities
Indications
1. Establish diagnosis and severity of respiratory failure 2. Assess gas exchange impairment in respiratory patients 3. Direct management and determine prognosis of patients in ICU/HDU 4. Monitoring of patients during cardiopulmonary surgery, cardiopulmonary exercise
testing and sleep studies Contraindications
1. Radial artery aneurysm 2. Raynaud’s disease 3. Local infection/burns 4. Severe peripheral vascular disease
with 60IU balanced heparin – available on most wards). *Check expiry date.
3. Alcohol swabs 4. Gauze sponge 5. Gloves 6. Rolled towel to assist in wrist positioning (optional) 7. 1% lignocaine for local infiltration (25G needle/2Ml syringe). Optional 8. Identification labels and laboratory request form
Procedure
Site
Blood can be drawn from an artery either via an indwelling arterial cannula or by direct arterial puncture. The commonest artery used is the radial followed by the dorsalis pedis; rarely the brachial and the femoral vessels (as they are the principal sources of blood supply to the limbs). Samples should ideally be taken with the patient breathing air, or if the patient is significantly hypoxic, breathing a known percentage/ concentration of oxygen. Time should usually be allowed for the attainment of a steady state after alteration of ventilatory parameters or FiO2 (at least 20 minutes if the patient has obstructive lung disease). Technique
1. Explain the procedure to the patient and obtain informed consent. 2. Perform an Allen test to check ulnar artery sufficiency. 3. Prepare equipment, attach the needle to the syringe, and draw the plunger on
the syringe to the 0.5ml mark. 4. Locate the radial artery on the thumb side of the wrist, using the index finger and
middle finger. Palpate the artery to determine size, depth and direction. Never use the thumb, because it has its own pulse and can be confused with the patient’s.
5. Clean the site using alcohol swab. Allow to dry, being careful not to touch the site.
6. If local anesthetic is used, infiltrate the skin over the selected site, entering the skin with the needle at ~ 10-degrees to the surface of the skin. Pull back slightly on the plunger to check if you have punctured a vein (if a vein has been punctured, you will have to perform the procedure again). Otherwise, inject the anesthetic into the skin forming a raised weal. Wait about 1 to 2 minutes to take effect.
7. Hold arterial syringe in the dominant hand as if holding a dart. 8. Locate the artery and insert the needle (bevel up) into the skin at ~ 45-degrees,
at ~ 5-10 mm distal to the finger locating the artery. Direct needle away from the hand with the bevel facing the flow of blood.
9. As you insert the needle slowly deeper into the wrist, a flash of blood will appear in the hub of the needle. At this point, stop advancing the needle further. Hold the syringe still until the amount of blood needed has been collected. Note: Suspect venous puncture if pulsation is minimal and blood dark in colour.
10. If you missed the artery, slowly withdrawal the needle out to just below the skin and re- insert. Do not probe with the needle, as this can be very painful and can lead to a hematoma, thrombus formation and damage to the artery itself.
11. After the required amount of blood has been collected, quickly withdraw the needle and immediately place firm direct pressure on the puncture site using a dry gauze pad.
12. Examine the sample carefully and expel any air. Insert the needle in the rubber or latex square.
13. After 2-5 minutes of pressure on the puncture site, remove the needle now attached to the rubber square and replace the needle with the luer cap.
14. Rotate the filled syringe back and forth between fingers to thoroughly mix the heparin in the syringe with the arterial blood sample.
15. Label the specimen and place it in a specimen bag without ice, and take immediately to specimen collection to prevent sample clotting.
Important Technical Points
The following are problems that may cause erroneous results in ABG analysis.
1. For accurate ABG results, samples drawn in plastic syringes should be analyzed immediately. Samples should not be stored “on ice” since results for blood stored on ice may show significant errors in PaO2 and PaCO2.
2. Air bubbles. If not removed immediately, oxygen from the bubbles can diffuse into the sample and CO2 can escape, changing the results.
3. Delay in sample analysis. Blood cells continue to consume oxygen and nutrients and produce acids and carbon dioxide at room temperature. If the specimen remains at room temperature for more than 5-10 minutes, pH, blood gases, and glucose values will change. Processing the specimen as soon as possible after collection will ensure the most accurate results.
4. Venous blood mixed in ABG sample. Normal arterial blood is bright red, whereas venous blood is slightly darker in color. Sometimes it is difficult to distinguish between arterial and venous blood in patients with poor oxygen content. This will make their arterial blood appear as dark as venous blood. The best way to be certain that a specimen is arterial is if the blood pulses into the syringe. In some cases, such as with low cardiac output, a specimen may need to be aspirated. In such instances, it is hard to be certain that the specimen is arterial.
