Acute respiratory medicine Acute respiratory medicine for the returning registrarfor the returning registrar

Dr Sarah ElkinConsultant in respiratory and general medicine,

Imperial College NHS Trust

• Pleural disease

• Respiratory failure

• Acute asthma

• COPD

• PE

• Haemoptysis

Outline: whistle stop tour of…

?symptomatic?breathless

?symptomatic?breathless

Pneumothorax

Seldinger drain, usually 12F, 4mm diameter

There’s never any medical emergency indication for a surgical drain

The kit

Measurement of needles

Drains should ALWAYS “swing”• If not:

– OUT OF PLEURAL SPACE• Check CXR / Wound / CT

– BLOCKED• 3-way tap turned off• Check not kinked by stitch / gauze / dressing

– Flush . . . UNDER ASEPTIC TECHNIQUE

– ON SUCTION (for pneumothoraces)• Disconnect briefly to assess

– Or the lung is up . . . And the drain is squashed

Drains only “BUBBLE” if air leak• So only if pneumothorax• Continuous bubbling implies a broncho-pleural

fistula . . . Consider an air leak after 48 hours • If stopped bubbling BUT IS swinging –?resolved

– Check CXR – Remove drain or ??suction

• If not bubbling OR swinging– BLOCKED – not resolved!

• (until proven otherwise)

Be sure it is a pneumothorax . . .

2014

Drain inserted by medical registrar . . .

But . . . Here’s the imaging from 2012 . . . Always look at old x-rays/CTs . . . If in doubt, do a CT

We drain effusions for 2 purposes:

• Symptom relief:– Around 500mls should be enough for this (diaphragm)

• Diagnostic purposes

• So it is RARELY an emergency

1.5L of fluid at a time . . . Risk of RPO

Often all that is necessary is a therapeutic tap to remove 500mls and relieve dyspnoea . . . Leave fluid in the patient

. . . then send home for O/P Ix

To test for a haemothorax (vs. a bloody tap): check the fluid haematocrit . . . If it’s a haemothorax get the surgeons and a large bore tube . . .

Unless it is an emergency ensure INR is <1.5, plts >50

Empyema

Respiratory failureRespiratory failure

Type I

• HYPOXAEMIC respiratory failureCauses:

– V/Q mismatch: Consolidation, pulmonary oedema and atelectasis all increase shunt

– Impairment of diffusion at level of alveolar-capillary membrane (pulmonary oedema, ILD, emphysema and pulmonary vascular diseases)

Type II

• VENTILATORY respiratory failure

i.e. reduced minute volume(RR x tidal volume)

• pH depends on duration of hypercapnoea (depends on level of HCO3, renal response occurs over days)

• Reduced ventilatory driveSedation (opiates / benzodiazepines)Brainstem eventReduced hypoxic drive (COPD)

• Reduced tidal volumeHyperinflation (COPD)Restrictive defect e.g. Obesity, Fibrosis, NM diseaseRespiratory muscle fatigue

Ventilatory Failure in Acute Exacerbations of COPD

BronchospasmIncreased airway mucus

Airway inflammation

RawAir trapping

Diaphragm flattening PEEPi

Increased elastic recoil

Increased work of breathing

VT PaCO2Respiratory muscle failure

Goals of Respiratory Support

• Treatment of hypoxia (and its cause)• To decrease the work of breathing

Treatment includes:

• Improvement of Oxygen Delivery• Removal of secretions• Ventilatory support

CPAPContinuous Positive Airway Pressure

• Continuous application of pressure throughout the ventilatory cycle during spontaneous breathing

• Improves alveolar recruitment & increases functional residual capacity, therefore used to improve oxygenation i.e. in Type I Respiratory Failure

Indications for CPAP

• AcutePulmonary OedemaDiffuse pneumonia

• ChronicObstructive Sleep Apnoea

Remember

• By increasing PEEP, intrathoracic pressure is increased• Reduced venous return (due to reduced pressure gradient)• Reduced cardiac output

Therefore, monitor haemodynamics

And don’t forget . . .

• CPAP is not a cure for T1RF

• Treat the underlying cause–Clear secretions–Offload

BiPAP Bi level positive airway pressure

-Provision of ventilatory support through the patients upper airway through a mask or similar device, thereby avoiding intubation

-Used to provide ventilatory support i.e. Type II Respiratory Failure

People admitted to hospital with an exacerbation of COPD and with persistent acidotic ventilatory failure are promptly assessed for, and receive, non-invasive ventilation delivered by appropriately trained staff in a dedicated setting.

Advantages of BiPAP

• Avoids intubation & assoc. problems• Shorter hospital stay• Avoids sedation• Patient able to interact• Patient able to take breaks for meals• Able to administer in non-ICU setting

Contraindications to NIV• Unconscious patient, inability to maintain own airway *• Confusion/agitation *• Vomiting• High risk of aspiration• Facial trauma/burns• Recent facial/upper airway/upper GI surgery*• Fixed upper airway obstruction• Bronchial +/- pleural fistula• Haemodynamic instability *• Copious secretions *• Suspected/confirmed undrained pneumothorax *• Bowel obstruction *• Life-threatening hypoxamia *• Severe co-morbidity *

Indications for NIV• Acute

– Acidotic exacerbations of COPD– Pulmonary oedema unresponsive to CPAP– Acute-on-chronic hypercapnic respiratory failure in chest wall / NM disease / OSA– Weaning from ventilation

MAXIMISE MEDICAL TREATMENT FIRST

• Chronic– Neuromuscular & chest wall diseases, COPD, OHS

Ceiling of Treatment?

• Holding measure• Therapeutic trial with a view to intubation• Ceiling of treatment

MAKE A PLAN!!

NIV should NEVER be used instead of intubation if the latter is more appropriate

Machines

• Either pressure-controlled or volume controlled, but most centres tend to use pressure-controlled machines for NIV . . .

– IPAP – increases tidal volume– EPAP – maintains positive end expiratory pressure

Modes

Spontaneous Patient initiates all breaths. These breaths are detected by the machine trigger and supported with supplemental pressure.

Spontaneous/timed Patients can still initiate breaths, which are then supported, but a back-up rate of machine-delivered breaths is also set. For example, the back-up rate may be set to 5 breaths per minute less than the patient’s spontaneous rate. This is the most appropriate setting for NIV.

Timed This fully ventilates the patient in patients making no respiratory effort and is therefore generally an inappropriate mode for NIV.

Setting up NIV

• Decide management plan if NIV fails• Decide setting (ICU / HDU / ward)• Explain NIV to patient• Select mask (full face mask)• Set up ventilator• Entrain oxygen if indicated• Pulse oximetry• Commence NIV initially holding mask in place• Secure mask• Assess & adjust settings after few minutes if necessary• Show patient how to remove mask & how to summon help

Initial Settings

• IPAP 10 – 12 cm H2O

• EPAP 4 cm H20

• Breaths per minute 12

• Entrained O2 - sufficient to maintain SaO2 88-92% (can entrain up to 10L/min)

Frequency of assessment

• Baseline• Response to maximal medical therapy• At initiation of NIV• One hour• Frequency then depends on response

• ABG at 1 hour, then at 4-6hrs if stable• If settings are changed, ABG 30-60 minutes after change is

implemented• CXR in event of any acute deterioration

Treatment failure

• Deterioration in patients condition• Failure to improve ABGs• Complications: pneumothorax, facial bridge erosion,

sputum retention• Intolerance• Failure to alleviate symptoms• Deteriorating conscious level• Patient / carer wish to withdraw treatment

Acute asthmaAcute asthma

• Health care professionals must be aware that patients with severe asthma and one or more adverse psychosocial factors are at risk of death.

• Keep patients who have had near fatal asthma or brittle asthma under specialist supervision indefinitely

• ƒ A respiratory specialist should follow up patients admitted with severe asthma for at least one year

• Oxygen• In acute asthma B agonists should be given and the nebulised route (oxygen-

driven) is recommended.• Consider giving a single dose of IV magnesium sulphate (1.2-2 g IV infusion

over 20 minutes) for patients with:ƒ acute severe asthma who have not had a good initial response to inhaled bronchodilator therapy and life threatening asthma.

• Give steroids ASAP and continue prednisolone 40-50 mg daily for at least five days or until recovery

Treatment plan:

Pulmonary emboliPulmonary emboli

Why do people die?

• Anatomical obstruction leads to increased RV afterload, increased tension in the RV wall and possible dilatation, dysfunction and ischaemia of the RV

• Death results from RV failure

• Diastolic LV dysfunction also occurs

• In addition, release of vasoactive and bronchoactive agents from serotonin from platelets may contribute to V/Q mismatch

Clinical symptoms & signs

• Leg pain/warmth/swelling• SOB (73%)• Pleuritc chest pain (66%)• Haemoptysis (10%)• Cough (37%)• Palpitations/dizziness

• Tachycardia (30%)• Tachypnoea (70%)• Crackles (51%)• Elevated neck veins/loud

P2/R sided gallop/RV heave

• But . . .

NB. Often the extent of symptoms depends on the thromboembolic burden, BUT even very large thrombi in the periphery may evolve silently & then present as symptomatic or even fatal PE, & smaller emboli may be assoc. with major symptoms particularly if cardiovascular reserve is already poor.

ABG

• ABGs and sats have a limited role in diagnosing PE (do not send home if suspicion high)

• ABGs usually reveal hypoxemia, hypocapnia, and respiratory alkalosis

• Patients with room air pulse oximetry readings <95% at the time of diagnosis are at increased risk of in-hospital complications, including respiratory failure, cardiogenic shock, and death

• Hypoxemia can be minimal or absent. A PaO2 between 11.3 and 14 kPa exists in approximately 18% of patients with PE; up to 6% may have a normal Aa gradient

Lower limb US

• DVT demonstrated in 13-15% patients suspected of having a PE, and 40% of proven PEs

• High sensitivity & specificity for symptomatic DVTs

• So only consider US as initial test if there are clinical signs of DVT

Echo

• Only 30-40% pts with PE have echo abnormalities suggestive of acute PE

– Increased right ventricular (RV) size– Decreased RV function– Tricuspid regurgitation

• Sensitivity is only ~60-70% so it a normal echo cannot exclude a PE & conversely: RV dysfunction can occur in alternative respiratory/cardiac conditions - thus NOT recommended for diagnostic purposes in haemodynamically stable patients

• In massive PE, these abnormalities are more likely and echo may be useful if a rapid presumptive diagnosis is required to justify the use of thrombolytic therapy

• The absence of RV overload/dysfunction on echo in a shocked patient rules out PE as the cause of haemodynamic instability

Imaging to prove a PE

• Involve radiation, do pregnancy test first

– CTPA (5mSv i.e. 250 CXRs)

– V/Q (1.4mSv i.e. 70 CXRs) - if CXR is normal

V/Q

• High probability– 2 perfusion defects– PPV >90%

• Intermediate probability– Solitary perfusion defect– Defect not reaching periphery

• Low– Matched defect– <5% of patients will have a PE

• BUT . . . Often only available once/week depending on your Trust

CTPA

• Multidetector CT – better image quality due to improved spatial & temporal resolution, & decreased motion artefact - visualisation to a sub-segmental level

• Sensitivity 83-100%; specificity 89-97%

• Can provide an alternative diagnosis

• Can provide prognostic information– RV:LV should be <1– ?septal bowing– ?reflux into hepatic veins

Putting all this into practice . . .

Wells scoreSymptoms of DVT (3 points)No alternative diagnosis better explains the illness (3 points)Tachycardia with pulse > 100 (1.5 points)Immobilization (>= 3 days) or surgery in the previous four weeks (1.5 points)Prior history of DVT or pulmonary embolism (1.5 points)Presence of hemoptysis (1 point)Presence of malignancy (1 point)

PE unlikely 0-4

D-Dimer Start LMWH

& get CXRPOSITIVE

NEGATIVE Normal CXR Abnormal CXR

V/Q

LOW

STOP

INTERMED.HIGH

CTPA

WARFARIN

Main/lobar PE

No PE

STOP

Segmental PE

Further Ix?

Clinical suspicion of haemodynamically stable PE? Do a Wells Score:

Hx, CXR, ECG, Wells . . .

Clinical suspicion of haemodynamically stable PE? Do a Wells Score:

PE likely >4

Start LMWH

& get CXR

Normal CXR Abnormal CXR

V/Q

HIGHINTERMEDIATE*

LOW* CTPA

WARFARIN

PE NO PE

Further Ix?

Hx, CXR, ECG, Wells . . .

PE in haemodynamically unstable patients . . .

* CT is not immediately available if the pt is too unstable for a CT

** If no contraindications; if so, consider embolectomy

CT immediately available *

No, echo Yes, CT

?RV overload

No

Look for other causes

Yes

If no other tests available, THROMBOLYSE WITH ALTEPLASE **

PE No PE

Look for other causes

• Possible indications for thrombolysis:– Persistent hypotension (SBP <90 mmHg/drop in SBP of ≥40

mmHg from baseline)

– Severe hypoxaemia

– Large perfusion defect on V/Q scans

– Extensive embolic burden on CTPA

– RV dysfunction

– Free-floating R atrial or ventricular thrombus

– Patent foramen ovale

• Case by case basis• Lack of evidence does not = lack of efficacy

Thrombolysis

• Contraindications to thrombolysis:– Absolute:

• Hx of haemorrhagic stroke

• Active or recent (<2 months) intracranial surgery or trauma

• Active or recent (< 6 months) bleeding

– Relative:• Bleeding diathesis

• Uncontrolled severe hypertension (SBP >200 mmHg or DBP >100 mmHg)

• Non-haemorrhagic stroke within the last 10 days

• Thrombocytopenia

– Consider alternatives such as surgical embolectomy/catheter-directed therapy depending on where you are based

The practicalities . . .

• Resucitation +/- ventilation, PERIPHERAL access

• 100mg alteplase (rt-PA) over 2 hours if stable

• Or 0.6mg/kg over 15 minutes (maximum dose is 50mg) if peri-arrest

• Follow this with IV unfractionated heparin infusion of 80 IU/kg bolus, then maintenance infusion of 1300 IU/hr; check APTT 4-6hrs after bolus, aim APTT 1.5-2.5

Treatment

• Thrombolysis - life-saving restoration of pulmonary blood flow

• Anticoagulation - prevention of potentially fatal early recurrence

• Surgical intervention• Radiological intervention

– Catheter-directed therapy– Drilling– IVC filter placement

Anticoagulation

• LMWH should be administered for 5/7 or until INR has been >2 for 48 hrs (whichever is longer)

• FBC after 5/7 LMWH (to ensure no HIT) or the day after initiation if they have had previous exposure (in last 100 days) to heparin

• LMWH is the long-term anticoagulation of choice in patients with cancer (less risk of bleeding & improved survival)

– If on long-term (>7 weeks) LMWH consider DEXA scan (risk of osteoporosis)

• Rivaroxaban at 15 mg twice daily for the first 21 days followed by 20 mg once daily is now licensed for PE

– A reduced dosage of 15 mg twice daily for 21 days followed by 15 mg once daily should be used in people with moderate (creatinine clearance 30–49 ml/min) or severe (creatinine clearance 15–29 ml/min) renal impairment if their risk of bleeding outweighs the risk of recurrent deep vein thrombosis or pulmonary embolism.

Duration of anticoagulation

BTS ESC

Temporary risk factor: 6 weeks 3 months

1st idiopathic (non-ca): 3 months ≥ 3 months

Other: ≥6 months Long-term

You must weigh up the benefits with the risk of bleeding, & anticoagulation must be reviewed

What about pregnant women?• Try to avoid radiation

– Lower limb US

• If that’s not possible, use as little radiation as possible– V/Q (just do the perfusion bit)

• In pregnancy there is a higher % of normal scans, probably because there is a lower threshold for Ix in pregnant women

• Foetal dose of radiation is 0.2-0.3mGy (insignificant)– CTPA

• Similar foetal radiation dose as a V/Q BUT the maternal radiation dose is much higher (4-6 mSv vs 1.2 mSv for a V/Q)

• Exposure to 10mGy to the breasts of a woman aged 35yrs increases the risk of breast cancer by about 14% over the background risk for the general population

• The radiation dose administered to breast tissue during CTPA is 10-70 mGy• Breast tissue in pregnancy is particularly radiation-sensitive

– Reassuringly:• Combined foetal radiation dose of CXR + V/Q + CTPA is <background radiation dose

over a 9/12 period

Rx in pregnancy

• LMWH or unfractionated heparin (IV or S/C)• Never use warfarin (OK when breast feeding though)• Try to stop anticoagulation 24-36hrs before delivery

(minimum of a 12hr gap between stopping LMWH & inserting an epidural)

• Can restart unfractionated heparin 6hrs after a vaginal delivery or 12hrs after a C-section

• Treat for 6 months in total (BTS) / 3 months (ESC)

Pregnancy Clinical suspicion of PE LMWH

Lower limb US

DVT No DVT

CXR

Normal CXR Abnormal CXR, suggestive of alternative diagnosis

V/Q

PE CTPA

Abnormal CXR

STOP

No PE Indeterminate

Continue LMWH

PENo PE

Continue LMWH

STOP

Acute life-threatening Acute life-threatening haemoptysishaemoptysis

• “Life-threatening haemoptysis”• Any haemoptysis that:

– is >100 mL in 24 h – causes abnormal gas exchange/airway obstruction– causes haemodynamic instability

+

• TB, Bronchiectasis & Carcinoma

• Bronchiectasis (Bronchitis – bullous emphysema)• Aspergilloma• Tuberculosis• Tumour, Trauma• Lung abcess• Embolus – fat / clot / septic

• Coagulopathy, Cystic fibrosis• Autoimmune disorders, AVM, Alveolar haemorrhage, Aneurysm

(Thoracic)• Mitral stenosis, Mycetoma• Pneumonia, PHT

• Remember Spurious causes – epistaxis, haematemesis

• Only 5% have significant bleeds– Mortality

• 58% if blood loss >1000ml/24h• 9% if <1000ml/24h

• 59% mortality if underlying malignancy• Death by exsanguination or asphyxiation• Independent risk factors for mortality

– IPPV– Infiltrates in ≥2 quadrants– Bleeding from PA– Cancer– Aspergillosis– ETOH excess

Fartoukh et l Respiration 2012

• ABC paradigm– Aim is to prevent further soiling

1. If bleeding site known position bleeding lung down / dependent

2. If any airway or haemodynamic compromise establish secure airway– Early anaesthetic referral

• Inform of Dx – DLT +/- paed bronch & ODP– Largest ETT possible – size 9 / 8 ETT OR– DLT

3. No optimal ventilation strategy4. Resuscitation

– Crystalloid– PRC & products as per Hb (>80) and clotting

1. Products as per any major bleed– Tranexamic acid

2. Bronchoscopy once airway secure & stability

– Flexible & Early – Diagnostic & therapeutic– Balloon tamponade– Iced saline lavage

• 50mL aliquots– Topical adrenaline (1:20,000) or topical fibrin

3. ImagingCahill et al, Clin Chest Med 1994Hunt BJ NEJM 2014

Imaging

• Chest X-ray– Underlying Parenchymal abnormality

• Computed Tomography– Localize bleeding in 63-100%– Higher sensitivity in combination with

bronchoscopy

• Digitally subtracted pulmonary angiogram and Aortogram

COPD• Hospital care : Treatment Duration in COPD Exacerbations:

Longer Isn't Necessarily Better (dressler et al JAMA 2013)

• 5 days of oral glucocorticoids suffice as good as longer

Hospital care

• NICE quality statement:

People admitted to hospital with an exacerbation of COPD are cared for by a respiratory team, and have access to a specialist early supported-discharge scheme with appropriate community support.

COPD : models of care

• People from lower socio-economic groups are at higher risk of avoidable emergency admissions.

• In primary care, higher continuity of care with a GP is associated with lower risk of admission.

• Integrating health and social care may be effective in reducing admissions.• Integrating primary and secondary care can be effective in reducing

admissions.• Structured discharge planning is effective in reducing future re-admissions.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) DISCHARGE CARE BUNDLE

Inform the COPD specialist of all COPD patients within 24 hours of arrival including patients discharged . Put patients sticker on this form and ward and fax to Hammersmith 33066 or Charing Cross 17044 or St Marys 27988

1. If patient is a smoker offer smoking cessation assistance

2. Pulmonary rehabilitation screened for suitability First point of contact, either by the CNS Nurses or Physiotherapist, who will assess and refer patient. If not done ward nurse to contact prior to discharge (fax referral form)

3. Self Management

5. Follow up arrangements made and given to patientPatient should see respiratory medical specialist and COPD respiratory nursing specialist within 1 month of discharge.

4. Satisfactory use of inhalers demonstrated and understoodPlease assess during medication rounds. Observe the patients using the device(s) and document on electronic prescribing record adequate technique demonstrated. (Refer to pharmacist or CNS if extra support is needed).

GO TOPatient

COPD Safe Discharge Checklist

CARE BUNDLE STEPSAll required documents are included in package.

Patient Sticker

Checklist Completed

Date:___/___/___

Nurse (Initials)Satisfactory

Community Appointment Requested

Non Smoker Completed Declined

Referral Made Declined N/A

Management Plan Oxygen Alert Card Breathe Easy Rescue pack Given

N/A N/A

Care bundle components are based on: NICE COPD guidelines 2004 (1-5) A Patient Experience Survey CLAHRC team April 2009 (6)Systematic Literature Review supported by CLAHRC April 2009 (1-6)Chelsea and Westminster Hospital COPD Discharge Care Bundle

n/a N/A

Outpatient Appointment Requested

Ward: _________

Referral Made

Spirometry on discharge

Given Already hasAlready has

What specialist adds: knowledge of treatments

London Respiratory teams value triangle

Value care

"Study while others are sleeping; work while others are loafing; prepare while others are playing; and dream while others are wishing."

‘Do what you love to do and give it your very best. If you don't love what you're doing, get out of it. Life is too short’

‘You will have a certificate of guilt if you work or if you don’t work…’