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2 Emergency Medicine

2.4 Respiratory

 

 November 2007 Please Note Respiratory Centralisation guidance at Respiratory Centralisation

2.4.1 Asthma

BTS Guidelines Feb 2003

http://www.brit-thoracic.org.uk/iqs/dlcpti.55/asthma-posters.html

 

PEFR Online Calculator

On Line PEFR Calculator

 

Asthma still kills 2,000 people per year in the UK. 

 

History & Examination

It is important to establish the correct diagnoses early and differentiate life threatening and severe asthma from mild/moderate asthma

The peak flow will help do this , however some  patients may not be well enough to perform this or are unable to do this due to poor technique. Therefore it is important to look for other clues :

The presence or absence of a wheeze is not a reliable indicator of the extent of bronchial narrowing

Investigations

PEFR

ABG-if severe or life threatening asthma

CXR (should not delay treatment)

 

Treatment

Initial management

A: the patient may be obtunded leaving the airway at risk

B:This is the underlying problem

C:This may be impaired due to dehydration from overbreathing and due to affects of hypoxia and hypeercarbia on the heart

 

Bronchial narrowing is due to:

Treatment is directed at dealing with all three elements of this process. The main components are:

The BTS guidelines provide a structured approach to the treatment of the various grades of acute asthma. With severe and life threatening asthma the situation may deterirate quickly. Call for senior help early ;this may involve an anaesthetist from the start .

 

Blood gas analysis will help in quantifying the extent of the problem, but a rising CO2 with an acidosis is a late sign.

Do not wait for a blood gas result if your patient is deteriorating!!

 

It is important to continually asses and monitor the patient and their response to treatment.

Patients  presenting with severe or life threatening  asthma on presentation should not be discharged from the department no matter how good their response to treatment.

 

With mild or moderate asthma consider admission to the CDU, after stabilisation in the Emergency Department unless contraindicated, particularly if poor home circumstances and late at night.

Upon discharge all patients should have follow up arranged either with their GP or with the chest Physician

Key points

2.4.2 Management of Spontaneous Pneumothorax

Author: Rachel Johnson, Taj Hassan, Mike Henry.

Date Written: 23/01/02

Modified from BTS guidelines

1. Objective: The Management of Spontaneous Pneumothorax (PT)

2. Symptoms and Signs:

              Symptoms:         Sudden onset of pleuritic chest pain

                                          Dyspnoea

                                          Asymptomatic

              Signs:                   Classically hyperesonance on the side of the PT

                                          + Reduced expansion

                                          + Reduced breath sounds

                                          Often there are no signs

3. Definitions:

Primary PT is one that occurs in the absence of underlying lung disease

Secondary PT is one that occurs with underlying lung disease i.e. COPD whether known about before or after diagnosis.

There is no apparent precipitating event with both.

4. Diagnosis: Standard Inspiratory PA CXR (expiratory film is not necessary)

Use a Lateral decubitus CXR if high clinical suspicion and not obvious on the PA film. Consider CT chest prior to treatment of complex bullous disease orsurgical emphysema obscuring the PA film.

5. Management: Follow the new BTS Guidelines algorithm. This divides patients into a number of sub-groups:

(a) Primary S/PT:

(b) Secondary S/PT.

5. Further Management:

 

Patients at this stage have been referred to an inpatient medical team. Further advice should be sought from the Respiratory Physicians for:    

(i) If suction is needed: not in the initial treatment but is a treatment choice if there is a persistent air leak (PAL) i.e. continued air bubbling through the tube 48hrs after insertion.

N.B. suction should not be considered if the PT has been present for a few days pre-diagnosis due to Reexpansion Pulmonary Oedema (RPO) i.e. coughing and dyspnoea after chest drain insertion.

(ii) Patients with a large PT which has been present in excess of 48hrs.

 

2.4.3 Management of Suspected Pulmonary Embolus

 

Authors: Paul Jennings, Rob Halstead, Taj Hassan

January 2002

OBJECTIVE

CLINICAL CONDITION

Acute minor pulmonary embolism is the most common type caused by emboli obstructing less than 50% of the pulmonary circulation and classically presenting with dyspnoea with or without pleuritic chest pain and haemoptysis. The mortality in this group is around 1%.

Acute massive pulmonary embolism is caused by sudden obstruction of over 50% of the pulmonary circulation and presents with haemodynamic instability as well as other more “typical” PE clinical features (e.g. dyspnoea, pleuritic chest pain, haemoptysis and syncope).

Subacute massive PE is caused by repeated emboli of small or moderate size occurring over several weeks. This is the least common of the three types of PE. As the onset is over several weeks, there is time for the right ventricle to adapt and this condition may therefore present more insidiously with heart failure and decreasing exercise tolerance.

Patients in whom you are considering a diagnosis of P.E. if they are cardiovascularly stable (pulse <100 and BP>100) will usually be low or intermediate probability and should be referred to the CDU Fellow for further investigation and management on CDU.

Patients with a HIGH clinical probablity of  PE and cardiovascular instability will need URGENT investigation as per the algorithm and admission to the physicians.

Assessment of probability of likelihood of PE using Wells Model

Signs and symptoms                                                                                                         Points

Haemoptysis                                                                                                                      1.0

Malignancy (treatment  ongoing, within the past 6 months, or palliative)                                       1.0

Immobilization

(bed rest, except to access the bathroom, for at least 3 consecutive days

or surgery in the previous 4 weeks)                                                                                        1.5

Previous objectively diagnosed DVT or PE                                                                                1.5

Heart Rate >100 beats per minute                                                                                          1.5

Clinical signs and symptoms of DVT

(leg swelling and pain with palpation of the deep veins)                                                              3.0

PE as likely or more likely than an alternative diagnosis*                                                             3.0

 

Total points                  Risk group                  

<2 points                         Low                  

2 to 6 points                  Moderate                     

>6 points                         High                 

 

CDU protocol for management of suspected PE

INVESTIGATIONS

ECG – most commonly shows only sinus tachycardia but recognised patterns also include right axis deviation, right bundle branch block, T inversion in V1-3, P pulmonale and the well-known but relatively infrequent SIQIIITIII. The main role of the ECG is to help to exclude acute myocardial infarction or pericarditis

 

ABG – classical findings are hypoxaemia and hypocapnia. Sensitivity and specificity for PE on ABGs is low (approx 50%)

CXR – may well be normal. However, it may show peripheral opacities (wedge infarcts or Hampton’s humps), prominent pulmonary hilar vessels or hyperlucency (due to oligaemia) of lung parenchyma (Westermark sign). However the chest X-ray is most useful in helping to rule out, or rule in, other possible diagnoses.

D-dimer – a measure of fibrin degradation products in the blood and therefore used to detect the process of clot breakdown. Due to significant numbers of false positives, this test is only really helpful in patients with low clinical probability of PE who can then be safely discharged if their D-dimer levels are low and another explanation of the clinical findings can be justified.

 

Ventilation-Perfusion (V/Q) scanning –

Spiral CT Chest –

Angiography –

Echocardiogram –

TREATMENT

Consider the following options :

Oxygen – 10-15L/min via rebreathing mask – give especially if signs of massive PE.

Fluid resuscitation – Massive PE leads to acutely increased pulmonary vascular resistance with RVF and a reduced preload for the LV. Rapid fluid resuscitation with the consideration of inotropic support is indicated.

IV Heparinisation – Heparinisation has long been established to reduce both mortality and recurrence of PE 5. In the acute setting, IV Heparin rather than subcutaneous LMWH is recommended 1. An initial loading dose of 80 units/kg (usually rounded to 5000 units) should be given, which is then followed by a continuous IVI with dosing dependent on regular aPTT levels.

 

Thrombolysis –

Key points

Evidence based joint guidelines are being developed to give better support for patients with MASSIVE P.E.. The algorithm is at this stage only a guide. Discuss with SENIORS.

REFERENCES

 

 

2.4.4 Chronic Obstructive Pulmonary Disease

Author A Mohammed, Taj Hassan Jan 2002

Chronic obstructive pulmonary disease is characterised by reduced respiratory function caused by a combination of destruction of  alveoli and obstruction of bronchioles by a chronic inflammatory process. There is often a reversible element to the latter caused by bronchospasm.

 

History and Examination

Investigations

Treatment:

Sit up right

A: Ensure adequate airway . May be at risk due to high CO2 or low O2 ,both causing a decreasing conscious level. Give additional oxygen as guided by initial ABG

B: Breath sounds may be very quiet .There may or may not be a wheeze. Ensure there is no pneumothorax , particularly before starting Non Invasive Ventilation. Start nebuliser and steroids and aminophylline as per asthma protocol.

C: This may also be affected due to hypoxic injury to the heart.

D: Refer to ARCU if requiring NIPPV.

 

2.4.5 Pneumonia

Authors : A Mohammed, Taj Hassan

Jan 2002

 

History &Examination

This is the most common  serious infection seen in patients who present in A&E and may be fatal even in patients who are previously healthy. The outcome is greatly improved  with early treatment .

 

Patients most often present with a few days history of cough and fever, although in the elderly, symptoms can range from collapse to confusion due to hypoxia. Children may present with abdominal pain. Aspiration pneumonia has a more sudden onset usually associated with a collapse.

 

Examination may show classic signs of consolidation and dehydration secondary to fever

and tachypnoea, but again may be non specific. A chest X-Ray will help  make the

diagnoses, although differentiating  broncho-pneumonia from pulmonary oedema is sometimes difficult.

 

Investigations: minimum necessary investigations are:

Treatment

High flow O2

Sit patient up

Rehydrate

Start IV antibiotics:

 

Community acquired

Hospital acquired

Aspiration

Augmentin plus

Clarithromycin

Cefotaxime +/_

Erythromycin

Cefotaxime plus Metronidazole

The following signs are indicators of severe infection:

Consider  ITU /HDU for anyone who cannot maintain pA O2 >8.0Kpa.

Pitfalls

 

 

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