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A medical emergency requires swift recognition and prompt action. Recognition of urgency does not necessarily require a precise diagnosis; the fact that the patient is dangerously unwell is usually obvious owing to an abnormality revealed by the internationally recognized assessment system for critically ill people of Airway, Breathing, Circulation, Disability and Exposure of the patient (ABCD and E). When an abnormality is found it should be acted upon and followed by a reassessment to establish if the intervention was useful. The clinician simultaneously needs to decide during this time as to whether and when summon help if available.
High-quality history taking and clinical examination will usually identify a diagnosis in a timely fashion and enable the initiation of appropriate investigation and management plans. In modern medicine, much has been made of the awareness of ‘vital observations’ or ‘vital signs’, which are often recorded by nursing staff and are usually available prior to a doctor’s clinical assessment. It should be remembered that observations support clinical diagnosis and management and do not replace them.
The relationship between good history taking, sound examination skills and the ordering of appropriate investigations is as important in an emergency situation as in any other clinical setting. Many could try to argue that with the advancement of science, history taking and clinical examination should be superseded by simple awareness of available investigations. A poorly taken and rushed history, followed by numerous irrelevant investigations, is poor-quality medicine. Such an approach often leads to a wrong or missed diagnosis and some abnormal results of uncertain significance. Investigations are not always risk free, and patients should not be exposed unnecessarily to interventions, such as ionizing radiation, without serious thought.
This chapter deals with conditions requiring assessment and management within the first hour and focuses on the presenting complaint. Recognizing the nature of an emergency presentation begins with how the patient comes to medical attention. This may be from information provided by the patient himself or witnesses such as paramedical (e.g. ambulance) staff, friends, family or concerned members of the public. The clinician will make an initial assessment by simply observing the patient; no apparent signs of life should initiate a life support response. If the patient is alive, then the general impression of how sick a patient appears is a reasonably accurate judgement of urgency. The experienced clinician will make these decisions in seconds. A particular clue will be in the respiratory rate and effort. An increased respiratory rate and work of breathing are the first physiological parameters to be altered in the shocked state and are often the subtle clues that alert a clinician to an unwell patient even from the end of the bed. Observing and recording this parameter for all patients is a fundamental part of developing a sound clinical method in emergency situations.
Urgency of response depends on the patient’s responses when you are using the ABCD and E system of assessment. A talking patient has a patent airway, can maintain sufficient respiratory effort to make the vocal cords vibrate and move enough air to allow gas exchange. Similarly, if the patient is talking he must be perfusing his brain with sufficient oxygen to undertake the processes of speech as well as being responsive enough to do so. The clinician therefore has a degree of time with which to make further assessments and management decisions in this situation.
It should be stressed that the aim of this chapter is to help the reader develop a logical method for the clinical assessment of the acutely presenting patient. Although the topics covered here relate to common acute presentations, greater detail relevant to these presentations has not been provided, because much of this will be dealt with elsewhere in this book. It is also hoped that the reader will not look on this chapter as an amalgamation of lists, but rather as an approach to logical thinking.
Sometimes, the severity of illness dictates that life-saving resuscitative treatment should begin before any diagnosis is reached, especially in acutely ill patients with problems such as shock or breathlessness. However, it should be possible to make an underlying diagnosis (or a differential diagnosis) in the majority of cases; an acutely ill patient may not clinically improve until the treatment based on the correct diagnosis is provided. Acute resuscitation and the formulation of diagnoses will often be performed successfully in tandem.
Patients frequently present to emergency departments with signs and symptoms of infection, as do existing inpatients, irrespective of the cause for initial hospital admission. Severe infections have the potential for significant morbidity and mortality, and it is vital that they are identified and diagnosed promptly. Although the majority of patients presenting with fever will have an infective cause that can be easily elicited from the history and examination, it is also well recognized that there are many non-infective inflammatory causes ( Table 9.1 ).
Mechanism | Common or important examples |
---|---|
Infection | Viral (upper respiratory, lower respiratory (Covid-19), infectious mononucleosis, hepatitis A); bacterial (less-common causes include infective endocarditis, meningitis, tuberculosis, spontaneous bacterial peritonitis, pleural empyema, cholangitis); parasitic (malaria, schistosomiasis); fungal |
Systemic inflammation | Rheumatoid arthritis; systemic lupus erythematosus (SLE); polymyalgia rheumatica; Wegener’s granulomatosis; inflammatory bowel disease; malignant neuroleptic syndrome; blood transfusion reaction |
Malignancy and granulomatous disease | Solid tumours; lymphoma; leukaemia; amyloidosis; sarcoidosis |
Drugs | Prescription; recreational (e.g. ecstasy) |
Infection with evidence of life-threatening organ dysfunction is now defined as sepsis. Patients with suspected sepsis who do not respond to immediate resuscitative measures are considered to be in septic shock. Delays in initiating treatment for sepsis, in particular the correct antibiotics, have consistently been shown to lead to a worse prognosis. Screening for evidence of organ dysfunction initially revolves around physiological parameters and historical details, such as reduced urine output and, most important, episodes of confusion or drowsiness. The brain is the organ most sensitive to metabolic derangements and any evidence of impairment from baseline should be taken seriously. Sepsis can be further broken down into amber and red flag sepsis owing to risk factors (immunosuppression), recent historical events (recent surgery), physiological changes and the need for additional oxygen.
The history will often suggest the source of infection (cough, abdominal pain, dysuria, headache). Other important features include details of any recent travel (country and duration of residence), a drug and lifestyle history (including any recreational drug use), weight loss, chronic illness and any risk factors for immunosuppression, such as recent chemotherapy, steroid therapy and the possibility of human immunodeficiency virus (HIV) infection.
Initially, the examination should focus on critical issues that need immediate action. If the patient has a raised pulse, heart rate or respiratory rate, prolonged capillary refill, hypoxia or hypotension, then oxygen, intravenous fluids and appropriate antibiotics should be administered urgently before embarking on a detailed examination (if possible and time allows, take blood cultures before administering antibiotics, because this may be the only opportunity for some time during what may be a long and severe illness to obtain cultures that are completely free of antibiotics). In searching for a source, look for exudate or pus at the back of the throat. Lung auscultation may reveal features of acute bronchitis (wheeze) or consolidation. Heart murmurs in the presence of fever may indicate infective endocarditis. The abdominal examination should identify any tenderness (e.g. right upper quadrant in cholecystitis, loin in pyelonephritis). If the patient complains of headache, look for features of meningism. Lymphadenopathy and superficial or skin abscesses should be noted as part of a thorough ‘top-to-toe’ examination. Less obvious sites should not be missed, especially cavities (e.g. a retained vaginal tampon leading to toxic shock), skin folds and the perineum.
Immediate investigations may include those which lend support to an inflammatory process (white cell count, C-reactive protein), severity of infection (blood lactate), consequences such as volume depletion (urea and electrolytes), underlying predisposition (blood sugar) and source (urinalysis, urine culture, blood culture, chest X-ray). In response to the history and examination, one may proceed to throat swab, blood films for malaria, faeces analysis (toxin or culture), lumbar puncture, transthoracic echocardiogram or abdominal imaging (ultrasound or computed tomography (CT) scan).
Although most patients who present with chest pain will not have clinically significant coronary artery disease, it is this potential diagnosis that often dominates the initial thoughts of the assessing doctor. This is why patients presenting with chest pain who appear unwell or in need of immediate resuscitation should have an electrocardiogram (ECG) recorded before the initial history and examination are complete. The outcome from attempts to open an occluded coronary artery depends on the speed with which arrangements can be made for either thrombolysis or angioplasty, so little is to be gained (and much to be lost) from a prolonged assessment. However, in some patients with critical coronary artery disease the initial ECG recording may be normal, so it is essential that a careful history and examination are performed on all patients with chest pain not obviously in immediate need of resuscitation or intervention. Patients with chest pain are, understandably, often anxious about the possibility of underlying serious heart disease and an important part of the doctor’s role is to project calm reassurance.
Chest pain that has a life-threatening cause ( Table 9.2 ) is usually central and of sudden/rapid onset. Certain features may be diagnostically helpful; these include radiation of the pain to the left arm and/or jaw (myocardial ischaemia) or the interscapular area (aortic dissection); accompanying breathlessness (massive pulmonary embolus or pneumothorax); or a clear temporal association with prolonged vomiting (oesophageal rupture). In pericarditis, the pain may be ‘classic’ (central pain relieved by sitting forward) or pleuritic. The features of chest infections and viral infections should be obvious. Pneumonias not infrequently are associated with headache. Important examination features to note during the initial, rapid assessment of an ill patient with chest pain include the fine crepitations of pulmonary oedema, the hyper-resonant percussion and tracheal deviation of pneumothorax or the asymmetric blood pressure readings consistent with thoracic aortic dissection.
Potentially life-threatening conditions—all usually causing central chest pain | Other causes of central chest pain | Causes of pleuritic chest pain |
---|---|---|
Coronary artery disease (myocardial infarction or acute coronary syndrome) Massive pulmonary embolus (PE) Thoracic aortic dissection: severe, tearing in nature, radiating to interscapular area Pneumothorax (particularly tension) Oesophageal rupture |
Pericarditis Gastro-oesophageal reflux disease (GORD) Muscular or skeletal Anxiety |
Pericarditis PE (more likely to be smaller and more peripheral) Pneumothorax Pneumonia (reactive pleuritis) Empyema Viral pleuritis Malignant involvement of chest wall (including mesothelioma) Rib trauma, fracture or metastases Inflammatory pleuritis (e.g. rheumatoid arthritis, systemic lupus erythematosus) |
If ‘ABC’ interventions are not required for resuscitation, if the patient is stable and no other features are requiring immediate action (e.g. peripheral cyanosis), then a more considered assessment is appropriate. In addition to the history, the risk factors for coronary artery disease and pulmonary embolism (PE) may be factored into the diagnostic process ( Box 9.1 and Table 9.3 ). The blood pressure should be taken in both arms, particularly if the arm pulses feel unequal. Unequal blood pressure measurements in the arms raise the possibility of aortic dissection and serious consideration should be given to appropriate urgent imaging (usually thoracic CT scanning). A raised jugular venous pressure may suggest early heart failure. Precordial auscultation may reveal a pericardial rub. There may be classic signs of pneumonia. It can be difficult to differentiate between pleuritic and musculoskeletal chest pain from the history, but pain exacerbated by palpation and posture changes more than by inspiration is more likely to be musculoskeletal. Signs of deep venous thrombosis automatically raise the clinical suspicion of a PE.
Age
Blood pressure
Smoking
Cholesterol
Diabetes
Racial grouping
Family history of coronary artery disease or stroke before the age of 60
Girth (obesity)
Clinical parameter | Score |
---|---|
Clinical evidence of deep vein thrombosis (DVT) | 3 |
No alternative diagnosis likely other than PE | 3 |
Heart rate greater than 100 per minute | 1.5 |
Surgery or immobility in preceding 4 weeks | 1.5 |
Previous confirmed DVT or PE | 1.5 |
Haemoptysis | 1 |
Active malignancy | 1 |
Total score | Risk |
---|---|
> 6 | High |
2–6 | Moderate |
2 | Low |
The serious nature of many of the diagnoses of patients who present with chest pain dictates that the threshold for certain investigations is often low. In addition to being a crucial test at the moment of initial assessment, the ECG has additional value when it is repeated over a period of time, looking for any evolution in its appearance (often called ‘dynamic changes’). Detailed description and explanations of the possible ECG features of myocardial infarction and pulmonary embolism are given elsewhere. The chest X-ray may show features of pneumothorax, pneumomediastinum (from oesophageal rupture), heart failure, widened mediastinum (often seen in thoracic aortic dissection), pneumonia, rib fractures/destruction and pleural effusions. In the emergency unit, measurement of troponin in blood (a protein released when cardiac myocytes undergo ischaemic necrosis) is performed on many patients with chest pain. It is not a diagnostic test of cardiac chest pain, but ‘negative’ results (below a certain threshold) indicate that the risk of a serious acute cardiac event in the ensuing 30 days is extremely low. A negative troponin test does not obviate the need to make a detailed clinical assessment; a patient with a typical history of ‘crescendo angina’ (worsening in severity and/or frequency, occurring at rest or on minimal exertion over days to weeks) should still be treated as an emergency even if the troponin result is reassuring.
When life-threatening conditions present with breathlessness, it should be rapidly established whether immediate and resuscitative interventions are required whilst simultaneously making a clinical assessment to establish the cause ( Table 9.4 ). The patient should be placed in a safe, monitored (ECG and pulse oximetry) environment and clinicians should act quickly if there is evidence of visible distress, the usage of accessory muscles of respiration, high respiratory rate, high pulse rate, cyanosis or observable low oxygen saturations. The immediate response should be to administer high-flow oxygen to the patient with any of the above findings, unless there is good evidence that this has on this occasion, or previous occasions, caused breathing difficulties (most commonly patients with chronic obstructive pulmonary disease, COPD). In the majority of cases, arrangements for urgent ECG and chest X-ray (CXR) will be made immediately, before the initial clinical assessment is complete. There may even be certain clinical scenarios (e.g. upper airway obstruction, tension pneumothorax) in which immediate clinical intervention is necessary.
Clinical assessment | Potentially life-threatening conditions |
---|---|
Stridor (may be mistaken for wheeze) | Partial obstruction of trachea or major airway |
Audible wheeze (one should listen very carefully, as it may be very quiet) | Severe asthma Anaphylaxis Acute bronchitis Pulmonary oedema |
Diffuse features | Pneumonitis Widespread pneumonia Pulmonary oedema |
Significant asymmetry of findings in a whole lung on percussion and/or auscultation | Pneumothorax Massive pleural effusion Total lung collapse |
Focal features of consolidation | Lobar collapse from tumour, foreign body or mucus plug Pneumonia |
No obvious abnormality | Pulmonary embolism (hypoxia often present) Metabolic acidosis (hypoxia often absent) |
A rapid clinical assessment will establish if detailed history taking is going to be realistic. A conscious, alert patient who is able to speak in full sentences is reassuring. Features suggestive of an obstructed airway include complete absence of airway sounds (complete obstruction) or added sounds of laboured breathing where air entry is diminished (partial obstruction). Tachycardia and tachypnoea may reflect respiratory distress. Use of accessory muscles of respiration is typical in the partially obstructed airway, and signs include a tracheal tug (a slight downward movement of the trachea with each inspiratory effort), paradoxical chest and abdominal movement (‘see-sawing’—the chest wall moves inwards during inspiration and outwards in expiration and there is dyssynchrony between the rib cage and the abdomen), with supraclavicular and intercostal ‘in-drawing’. Irritability, agitation and a reduced consciousness level may reflect hypoxaemia and carbon dioxide retention. Do not rely on cyanosis as a feature in identifying an obstructed airway as this is a very late preterminal sign. Observe or ask about ‘best breathing position’. Be aware that the patient may have positioned himself for optimal airflow in the setting of airway obstruction; moving the patient into a supine position may precipitate loss of the airway altogether. Low pulse oximetry readings (SpO 2 ) reflect inadequacy of oxygenation, which is not the same as ventilation. Arterial blood gas sampling may be helpful but should not delay treatment. Respiratory acidosis, with a high carbon dioxide tension (PaCO 2 ) and reduced pH, reflects alveolar hypoventilation. When assessing patients, look carefully for these signs and symptoms and always call for help early from an anaesthetist if airway compromise is suspected. The young can compensate well initially, masking impending desaturation and hypoxaemia. Be mindful of injuries that will compromise the airway, such as facial burns, bleeding and foreign bodies obstructing the airway. Always provide high flow oxygen with a reservoir bag at 15 litres/minute, and reassess frequently, looking for signs of deterioration, which may be caused by deterioration of the underlying condition, or excess oxygen in a patient with chronic CO 2 retention.
In the emergency situation of the acutely breathless patient it is helpful to consider the potential problem in one of two ‘groupings’: upper airway obstruction and cardiopulmonary pathologies that affect ventilation and/or gas exchange ( Table 9.5 ).
Clinical assessment | Classification | Condition |
---|---|---|
Stridor | Large airway disease | Partial obstruction of trachea or major airway |
Bilateral or diffuse wheeze | Small airway disease | Asthma Acute bronchitis (including bronchitic component to chronic obstructive pulmonary disease) Anaphylaxis Pulmonary oedema (presenting as bronchial oedema) Obesity hypoventilation syndrome (although often the wheeze from obesity-related airflow limitation is not heard) |
Asymmetric features in whole lung field (tracheal deviation, hyper-resonance to percussion and diminished breath sounds) | Pleural disease | Pneumothorax |
Asymmetric features in whole lung field (tracheal deviation, stony dullness to percussion and diminished breath sounds) | Pleural disease | Massive pleural effusion |
Asymmetric features in whole lung field (tracheal deviation, dullness to percussion and diminished breath sounds) | Large airway disease | Total lung collapse (tumour, foreign body, mucus plug) |
Diffuse bilateral abnormalities (crepitations) | Diffuse parenchymal disease | Pneumonitis Pulmonary oedema Pulmonary fibrosis |
Diffuse bilateral abnormalities (bronchial breathing) | Diffuse parenchymal disease | Multilobar or bronchopneumonia |
Focal abnormality (bronchial breathing) | Focal parenchymal disease | Pneumonia Lobar collapse Bronchiectasis |
Focal abnormality (dullness to percussion and diminished breath sounds) | Pleural disease | Pleural effusion |
Bilateral, focal abnormalities (basal stony dullness and diminished breath sounds) | Pleural disease | Bilateral pleural effusions |
Bilateral, focal abnormalities (bronchial breath sounds) | Parenchymal disease | Bilateral pneumonia (e.g. bibasal pneumonia) |
Thoracic deformity | Chest wall skeletal disease | Scoliosis Thoracic surgery |
No obvious abnormality | Pulmonary vascular disease | Pulmonary embolism Pulmonary hypertension |
Respiratory muscle weakness | Diaphragm paralysis Neuromuscular disease |
|
Compensatory effort | Metabolic acidosis Anaemia |
|
Psychogenic | Psychogenic hyperventilation |
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