ACUTE MEDICAL EMERGENCIES - PART 3 potx

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ACUTE MEDICAL EMERGENCIES - PART 3 potx

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PRIMARY ASSESSMENT AND RESUSCITATION Airway Assessment This has been described in Chapter 4 and is summarised in the box below. Treatment High flow oxygen (FiO 2 = 0·85) may relieve some of the patient’s distress. If airway obstruction is suspected, request immediate review by a specialist. If a foreign body has been inhaled attempt a Heimlich or modified Heimlich manoeuvre. Breathing Assessment This is summarised in the box. Treatment Irrespective of the underlying cause of the bronchospasm, treat patients with nebulised bronchodilators whilst clues to the underlying diagnosis are sought. Immediate management of a tension pneumothorax is needle thoracentesis followed by intravenous access and then chest drain insertion. Summary of breathing assessment ● Look colour, sweating posture respiratory – rate – effort – symmetry ● Feel tracheal position tracheal tug chest expansion ● Percuss ● Listen Summary of airway assessment ● Look – respiratory – rate – effort – symmetry ● Feel – expired air – trachea ● Listen –‘count to 10’ – breath sounds Key point It is important to remember that the breathless patient does not always have pathology affecting the respiratory or cardiovascular systems ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 84 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 84 Circulation Assessment This has been described in Chapter 6 and is summarised in the box. Treatment All patients should receive high flow oxygen, be treated in a seated position and have their oxygen saturation, pulse, blood pressure, and cardiac rhythm monitored. Intravenous access is necessary and at least one large venflon (12–14 gauge) is required in the antecubital fossa. The management of the “shocked” patient will depend on the underlying cause. Treatment options are summarised in the box. Treatment of shock Cause Treatment Acute, severe, left ventricular failure Inotropes Dysrhythmia – tachycardia Cardioversion – bradycardia Atropine Inotropes Pacing Hypovolaemia Fluid challenge Pulmonary embolus Anticoagulation Thrombolysis Fluids Sepsis Fluids Antibiotics Inotropes Anaphylaxis Adrenaline Fluids Chlerpheniramine Hydrocortisone Cardiac tamponade Fluids Pericardiocentesis Summary of circulatory assessment ● Look: pallor, sweating, venous pressure ● Feel: pulse – rate, rhythm and character capillary refill time blood pressure apex beat ● Listen: heart sounds, extra sounds TIME OUT 8.1 Take 30 seconds to mentally rehearse the key components of the assessment so far. THE PATIENT WITH BREATHING DIFFICULTIES 85 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 85 Once the patient’s condition is stabilised then further information can be obtained from the secondary assessment. Key points If the patient is still breathless and the cause remains in doubt, a rapid reevaluation of the ABC is required It is important to remember that hypovolaemia is an important cause of breathlessness ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 86 Figure 8.1 Broad complex tachycardia 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 86 Summary In the breathless patient, the immediately life threatening problems are: ● Airway obstruction ● Breathing acute severe asthma acute exacerbation of COPD pulmonary oedema tension pneumothorax ● Circulation acute severe left ventricular failure dysrhythmia hypovolaemia pulmonary embolus cardiac tamponade These conditions can be identified and differentiated clinically. All patients require oxygen and intravenous access. SECONDARY ASSESSMENT Many patients with breathlessness will be able to give a history, albeit fragmented. The conditions diagnosed in this assessment phase are shown in the box. Potentially life threatening causes of breathlessness Severe asthma Acute chronic respiratory failure Pulmonary oedema Simple pneumothorax Pneumonia Pleural effusion Pulmonary embolus Metabolic acidosis – diabetic ketoacidosis, salicylate overdose Pontine haemorrhage TIME OUT 8.2 Mentally rehearse your approach to the patient with breathing difficulties. Then list the major components of the primary assessment. Armed with this structure read the following information and then answer the associated questions. A 64 year old man with known ischaemic heart disease was admitted to the coronary care unit after becoming acutely breathless. He denied any chest pain or cough. The following physical signs were elicited: ● respiratory rate 26/minute ● fine inspiratory crackles were heard at both bases ● pulse rate 140/minute and regular ● blood pressure 80/50 ● peripherally shut down ● no other relevant features a. What would be your immediate management? b. What investigations would you request? THE PATIENT WITH BREATHING DIFFICULTIES 87 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 87 SPECIFIC CONDITIONS Asthma Asthma is a chronic inflammatory condition resulting in reversible narrowing of the air- ways. It affects approximately 5% of the population and can occur for the first time at any age with a male predominance in childhood and females in later life. Asthma in children is usually associated with atopy, whilst in adults it is more commonly non-atopic. Both, however, have an inherited component. Although there are many potential triggers, asthma is characterised by wheezing due to widespread narrowing of the peripheral airways.There may be an associated increase in sputum volume and viscosity. Occasionally a nocturnal cough will be a prominent symptom and patients may describe tightness in the chest or a sensation of choking rather than wheezing. Furthermore, exposure to external stimuli like cold air, cigarette smoke and paint fumes may induce an acute “asthmatic” attack. This does not indicate an allergic response but demonstrates that the airways are hyperreactive and produce an exaggerated response to non-specific irritants. Pathophysiology Acute attacks of bronchospasm may be precipitated by IgE mediated mast cell degran- ulation. In contrast, when exposed to environmental factors, e.g. allergens and pollu- tants, the airways of known asthmatics are susceptible to chronic inflammation characterised by eosinophil and T lymphocyte infiltration. These cells are responsible for liberating inflammatory mediators that evoke a variety of responses (see next box) culminating in airways narrowing and hence increased airflow resistance. Since resis- tance is inversely proportional to the fourth power of the radius (Poiseulle’s law) a small increase in airways thickness will have a marked effect on airways resistance and therefore reduce airflow.The change in airway radius is usually due to bronchial muscle contraction, but in the asthmatic this is exacerbated by mucosal oedema, increased mucus production and epithelial cell damage. In addition, the chronic inflammatory response reduces elastic recoil of the airways, further exacerbating the narrowing (Figure 8.2). This disturbed and decreased airflow is manifest clinically as audible wheeze, reduced forced expiratory volume in one second (FEV 1 ) and peak expiratory flow rate (PEFR), along with increased functional residual capacity (FRC) due to air trapping, with no change in the total lung capacity (TLC). Thus, because of increased airways resistance the work of breathing is increased and the patient feels breathless. In an acute asthmatic attack some of the airways become blocked by mucus plugs resulting in hypoxia due to ventilation perfusion (V/Q) mismatch. This further increases the work of breathing, causing hyperventilation in an attempt to reverse the hypoxaemia. Inflammatory mediator induced changes in asthma: ● disrupt the functional and structural integrity of the epithelium ● stimulate mucus secretion oedema formation smooth muscle contraction ● induce collagen deposition under the basement membrane ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 88 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 88 Figure 8.2 Diagrammatic representation of the pathophysiology of asthma: (a) longitudinal section (b) cross section. Management Management is summarised in Figure 8.3, the British Thoracic Society guidelines. Key point Preventable deaths from acute asthma still occur due to treatment delay Key point Failure to sustain this increased respiratory effort, usually in a severe exacerbation, will be mani- fest by a silent chest, hypoxaemia and a rising PaCO 2 THE PATIENT WITH BREATHING DIFFICULTIES 89 mucus plug mucus plug 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 89 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 90 Figure 8.3 The British Thoracic Society guidelines for asthma treatment 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 90 Life threatening asthma Assessment This is characterised by: ● airway – normally patent but can be compromised by exhaustion ● breathing – cyanosed, exhausted, minimal respiratory effort and a silent chest ● circulation – tachycardia greater than 130 beats per minute, brachycardia, hypoten- sion. In addition the peak expiratory flow is less than 33% of the predicted or the patient’s best. Immediate treatment See Figure 8.4. It is important to remember that acute breathless- ness in an asthmatic is usually due to bronchospasm. However, because of “gas trapping” there is an increase in positive end expiratory pressure. This increases the potential to develop a pneumothorax that can further embarrass the respiratory system. Always be alert to this possibility in asthmatics who either fail to respond to treatment or become acutely breathless. Regular reassessment and an urgent chest X-ray are required. Intravenous fluids should be administered as most patients have coexisting dehydra- tion. Adequate hydration also helps to render the sputum less tenacious. In addition, hypokalaemia can occur as a consequence of either asthma or coexistent with β 2 ago- nist therapy. Thus, careful monitoring and appropriate replacement therapy are required. The patient’s clinical response to treatment (as described earlier) should be monitored continuously and arterial blood gases should be performed regularly. If the patient either becomes exhausted, retains CO 2 or adequate oxygenation is not possible then intermittent positive pressure ventilation will be required (see box). Early liaison with the anaesthetist/intensivist is vital. Please also see Figure 8.4 for the assessment and management of patients with acute asthma that is not immediately life threatening. Indications for intensive care Hypoxia (PaO 2 < 8 kPa despite FiO 2 > 0·6) Hypercapnia ( PaCO 2 > 6 kPa) Exhaustion Altered conscious level (confused, drowsy, unconscious) Respiratory arrest Key point A silent chest is a life threatening sign as it means there is insufficient air being moved (in and out of the chest) to generate a wheeze THE PATIENT WITH BREATHING DIFFICULTIES 91 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 91 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 92 Figure 8.4 British Thoracic Society’s Guidelines for Asthma Treatment 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 92 Acute on chronic respiratory failure This is an important cause of breathlessness and is considered in detail in Chapter 19 on organ failure. Pulmonary oedema This is an important cause of breathlessness and is considered in detail in Chapter 19. Pneumothorax A pneumothorax results from gas entering the potential space between the visceral and parietal pleura. This may arise spontaneously from the rupture of a bulla or cyst on the lung surface or following penetrating trauma. Underlying lung disease is therefore an important predisposing factor in the development of a pneumothorax. However, there are a number of invasive procedures such as subclavian vein catheterisation that can also be responsible (see box). Pathophysiology The outward recoil of the chest and inward elastic retraction of the lung produces a negative pressure in the potential space between the visceral pleuro and parietal pleura. This pressure, with respect to atmosphere, becomes more negative during inspiration. Following a breach of the visceral pleura, air preferentially moves from the alveolus into the pleural space until these pressures equilibrate – hence the lung collapses, resulting in a simple pneumothorax. If, however, the breach in the pleura acts as a one-way valve then air will preferentially enter the pleural space during inspiration and not return during expiration. Thus the pressure in the intrapleural space rises above atmospheric pressure. The resulting hypoxaemia acts as a respiratory stimulus causing deeper inspi- ratory efforts which in turn further increase the intrapleural pressure. This produces a tension pneumothorax. If untreated, mediastinal shift occurs, causing kinking of the great vessels, impairing venous return, and compressing the opposite lung. This process Iatrogenic pneumothoraces Attempted internal jugular/subclavian vein access Pleural aspiration/biopsy Percutaneous lung/liver biopsy Transbronchial biopsy Intermittent positive pressure ventilation (IPPV) TIME OUT 8.3 Have a five minute break, then answer the following questions. a. What type of condition is asthma? b. List the major components of this response. c. What is the overall effect of this process? d. How does this affect pulmonary physiology? e. Describe how you would manage life threatening asthma f. What are the indications for ventilation? THE PATIENT WITH BREATHING DIFFICULTIES 93 08-AcuteMed-8-cpp 28/9/2000 3:58 pm Page 93 [...]... with systemic lupus erythematosus but to a much lesser extent in those who have rheumatoid disease Haemothorax As an acute medical emergency this is rare because most cases occur in association with penetrating or non-penetrating trauma However, it can occur after: 1 03 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH ● attempts at central venous access due to disruption of associated arteries or veins... think in equations, it is also possible to link these factors as follows Delivery of oxygen to tissues = cardiac output × arterial oxygen content = cardiac output × [(Hb × 1 34 × oxygen saturation) + (0·0 03 × PaO2)] 1 13 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH Under normal circumstances using previously defined values the delivery of oxygen to the tissues approximately equals: 5000 ml/min × 19·8... excluded SUMMARY ● Breathlessness is a common medical emergency ● The structured approach will ensure that the immediately life threatening causes are identified and treated ● Immediately life threatening causes of breathlessness are: airway obstruction breathing acute severe asthma acute exacerbation of COPD acute pulmonary oedema tension pneumothorax circulation acute severe left ventricular failure dysrhythmia... partial lung collapse (and no deterioration for 24 hours) at approximately 1·25% of the volume of the hemithorax per day Occasionally pain relief is required in the form of non-steroidal antiinflammatory analgesics Do not forget to reassure the patient! Guidelines for the management of a confirmed and treated pneumothorax are shown in Figure 8.5 Figure 8.5 Management of chest drain 95 ACUTE MEDICAL EMERGENCIES: ... structural integrity Transdiaphragmatic passage of fluid 101 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH ? Chest infection Seek other diagnosis No Abnormal Normal ? COPD Yes No No antibiotics Is patient in hospital or discharged 38 °C Purulent sputum WBC Yes No ? Pneumonia CXR No No... findings ● Echocardiography This will show right ventricular abnormalities in 40% of patients 109 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH ● Pulmonary angiography This remains the gold standard ● Spiral CT and MRI scans are increasing in popularity, but are not yet routinely available Specific treatment for acute pulmonary embolism Irrespective of the results of investigations, if the clinical suspicion... Organisms causing community acquired pneumonia Streptococcus pneumoniae Haemophilus influenzae Staphylococcus aureus Influenza virus Mycoplasma pneumoniae Chlamydia psittaci/Q fever Legionella species 97 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH Streptococcus pneumoniae (pneumococcal pneumonia) is the major pathogen involved, whilst influenza is the commonest viral infection It is important to realise... PULMONARY EMBOLISM Pulmonary embolism is an important condition because it is potentially fatal, often preventable, and sometimes treatable The majority of pulmonary emboli originate in the 105 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH deep veins of the legs and pelvis Occasionally, however the right side of the heart can be the source of emboli, e.g atrial fibrillation, right ventricular infarction... that warrant mention here in the context of acute breathlessness, hypotension, central chest pain, and unconsciousness are acute ventricular failure, myocardial infarction, and cardiac tamponade All of the major features are related to diminished cardiac output and hence hypoxia and relative hypovolaemia.The differential diagnosis of these conditions, in the acutely ill patient, can be difficult but there... help (Table 8.1) As with all shocked patients high flow oxygen (FiO2 = 0·85) is required More comprehensive details regarding the management of the shocked patient are provided in Chapter 9 107 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH (a) (b) (c) Figure 8.7 108 The different sites of pulmonary emboli: (a) main trunk (b) third division vessel (c) multiple peripheral THE PATIENT WITH BREATHING . DIFFICULTIES 91 08-AcuteMed-8-cpp 28/9/2000 3: 58 pm Page 91 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 92 Figure 8.4 British Thoracic Society’s Guidelines for Asthma Treatment 08-AcuteMed-8-cpp 28/9/2000. be mani- fest by a silent chest, hypoxaemia and a rising PaCO 2 THE PATIENT WITH BREATHING DIFFICULTIES 89 mucus plug mucus plug 08-AcuteMed-8-cpp 28/9/2000 3: 58 pm Page 89 ACUTE MEDICAL EMERGENCIES: . diagnosis. Needle thoracocentesis is the immediate manage- ment ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 94 08-AcuteMed-8-cpp 28/9/2000 3: 58 pm Page 94 Management Simple pneumothorax Spontaneous

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