Introduction

Any patient presenting with an acute or emergency condition needs instant attention and quick thinking from his clinicians, who in turn need to be immediately aware of the principles of resuscitation, diagnostics and the prioritization of clinical interventions. Not infrequently the diagnosis will be unclear, despite best efforts, and the presenting syndrome or scenario (such as ‘shock’ or ‘breathlessness’) will need to be dealt with in a systematic and logical manner. The clinicians will need to overcome his own anxiety and perform quickly, efficiently and professionally.

The importance of clinical assessment

High-quality history taking and clinical examination, when used properly rather than just routinely, 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 performed 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 Many could try to argue that with the advancement of science, history taking and clinical examination should be superseded by simple awareness of available investigations. One could propose that the ability to book a high-resolution thoracic computed tomography (CT) scan is a more worthy skill than the ability to elicit a domestic history of pet budgerigars or identification of vocal resonance, and that the ability to detect a mid-diastolic murmur is irrelevant in the face of freely available echocardiography. However, most would agree that the latter view is short sighted, and that although modern investigations need to be embraced, their usage should be targeted with the prior aid of clinical history taking and examination of the highest standard. 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 or pleural taps without serious thought. The aim of this chapter is to aid your reasoning skills in the emergency situation in order to formulate working diagnoses, which will in turn facilitate the ordering of appropriate investigations and the formulation of targeted management plans.

It should be remembered that, in most cases, the history is crucially important to the formulation of a differential diagnosis. If the patient cannot communicate verbally, as is frequent in the emergency department, every attempt should be made to take a ‘collateral’ history from those able to comment on events preceding the episode. The latter may include the traditional examples of family or friends, and one should not forget hospital staff who may have been present during an acute episode occurring in a patient already in hospital.

Scenarios outside the emergency department

Although the conditions dealt with here are most often found in patients in the emergency department (either in the ‘resuscitation room’ or in ‘majors’), they may also frequently be encountered in general wards. Patients may present to the ‘ward team’ with acute features reflecting a recurrence of the initial presentation, or a new unrelated clinical event. Examples such as ‘shock’ and ‘coma’ are also found in intensive care, where the scenarios are often complex. Although some reference may be made to critical care interventions, this chapter will not deal in any detail with intensive care medicine.

Diagnosis versus resuscitation

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 differential diagnoses) in the majority of cases and 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.

Logic rather than lists

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, as 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.

The pyrexial and septic patient

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 therefore it is vital that they are identified and diagnosed speedily by the clinician. Although the majority of patients presenting with fever will have an infective cause which is easily elicited from the history and examination, it is also well recognized that there are many non-infective inflammatory causes. The latter are often debilitating pathologies, where prompt diagnosis helps prompt interventions (Table 8.1).

Table 8.1 Logical thinking for patients presenting with fever

The concept of ‘systemic inflammatory response syndrome’ (SIRS) is widely recognized. In this there is evidence of an acute-phase response (such as pyrexia or hypothermia, tachypnoea, tachycardia, leucopenia or leucocytosis) which is indicative of inflammation. If these features are present in the face of infection, the term ‘sepsis’ is often used. The term ‘severe sepsis’ is used if there is evidence of sepsis with additional physiological upset, such as: new or increased requirement for oxygen; hypotension; acute oliguria; delayed capillary refill or mottling; deranged laboratory values (e.g. raised serum creatinine, coagulation abnormalities, raised serum lactate, thrombocytopenia, raised bilirubin). Severe sepsis leading to shock (’septic shock’) will be discussed in the section dealing with shock.

The history will often identify the source of sepsis (cough, abdominal pain, dysuria, headache). One should enquire about recent travel history, and the country of origin (including period of residence). A meticulous drug and lifestyle history should be taken (such as recreational drug use). Any risk of immunosuppression should be uncovered, in particular the relevance of recent chemotherapy, steroid therapy, weight loss, chronic illnesses as well as HIV risk.

The examination should initially focus on critical issues which need immediate action. If the patient has a raised pulse or heart rate, respiratory rate, prolonged capillary refill, hypoxia or hypotension, one should urgently administer oxygen or fluids before proceeding with further examination. When 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 should prompt further history taking, to assess the risk of infective endocarditis. The abdominal examination should identify any tenderness (e.g. the right upper quadrant in cholecystitis or the loin in pyelonephritis). In the cellulitic patient, look carefully for skin bites, lacerations or tinea pedis, as a possible route of entry. If the patient volunteers headache as a symptom, always look for features of meningism. Lymphadenopathy and superficial or skin abscesses should not be missed.

Immediate investigations may include those which lend support to an inflammatory process (white cell count, C-reactive protein), severity of infection (blood cultures), consequences such as dehydration (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 CT scan). A clue as to a non-infectious cause of fever may show on initial investigation, or this can be suspected when the initial tests are negative.

The patient with hypotension or shock

There are numerous definitions for ‘shock’. As good a definition as any may be ‘a failure of blood flow, when the cardiac output and circulatory function are insufficient to provide perfusion to major organs’. Hypotension and shock are clinical emergencies, and require appropriate and immediate intervention. Hypotension may be defined as ‘abnormally low blood pressure for that given patient’ which means interpreting the documented blood pressure in context. For one patient, a ‘normal’ blood pressure may be significantly lowered when compared to previous readings. In another, a ‘low’ blood pressure may be entirely normal for that specific patient. If in doubt, a low blood pressure should always be acted upon. For the purpose of this chapter, we should accept that hypotension and shock encompass similar pathologies, and belong in the same spectrum. Severe hypotension may lead to shock. It is essential, therefore, that, irrespective of aetiology, this is seen as a medical emergency, and a joint effort is made to initiate resuscitative treatment and make a diagnosis.

It is good practice to begin administering intravenous fluids while other clinical features and vital observations are elicited. The fluids may be subsequently stopped if pulmonary oedema becomes evident. Team working is paramount. If more than one clinician is available, one may focus on taking a history while another may take responsibility for examination and institution of treatment. Examination findings, irrespective of the cause, may include a rapid pulse and heart rate, and a third heart sound. It should be noted that in otherwise fit individuals, in the face of severe hypovolaemia, there may be a prolonged period of ‘compensation’, in which the healthy heart maintains cardiac output and a normal blood pressure by increasing the heart rate. Therefore, the patient with unexplained tachycardia should be examined and investigated thoroughly, and pending shock should not be missed.

During resuscitation, one needs a quick starting point when assessing the causes of shock. One way to categorize shock is to differentiate causes with wide pulse pressure and narrow pulse pressure (‘pulse pressure’ is the difference between systolic and diastolic blood pressure) (Table 8.2). As a general rule, patients with widened pulse pressure will present with warmer peripheries, and the palpable peripheral pulse may be more ‘bounding’ in nature. Patients with narrowed pulse pressure often possess cooler peripheries, with ‘thready’ peripheral pulses. Although ‘normal’ pulse pressure is often quoted as 40 mmHg, it should be noted that during hypotension this figure should be interpreted with caution. For example, a blood pressure of 75/40 mmHg could be interpreted as having a widened pulse pressure of 35 mmHg, as this is in the context of a low systolic blood pressure.

Table 8.2 Logical thinking in shock

There may be mixed forms of shock. For example, it is not uncommon for septic shock (ordinarily presenting with widened pulse pressure) to rapidly lead to cardiogenic shock (narrow pulse pressure) in patients with coexisting heart disease. Septic shock is also often associated with hypovolaemic shock. It is also not uncommon for cardiogenic shock to improve with treatment, to be superseded by infection and septic shock. If it is not possible to categorize a pulse pressure into narrow or wide, other features described below will help identify the cause of shock.

Although there are many general causes of widened pulse pressure (including aortic regurgitation, thyrotoxicosis, fever, anaemia, pregnancy, patent ductus arteriosus, aortic dissection, raised intracranial pressure, vasodilating drugs, Beriberi heart disease and old age), wide pulse pressure with shock is almost always a consequence of profound vasodilatation, usually with warm limb peripheries. The commonest cause is infection (sepsis, ‘septic shock’), and less common causes include anaphylaxis (‘anaphylactic shock’) and loss of neurogenic vasomotor tone (‘neurogenic shock’).

Septic shock may come with a history suggesting the source of infection. Examination findings may include a fever and evidence of a source (e.g. auscultatory features of lung consolidation, or abdominal features of peritonitis). Empirical though targeted antibiotic therapy would be appropriate if the infective source is suspected, and investigations would include tests to confirm the suspicion of infection (white cell count, C-reactive protein) and those to confirm the source (chest X-ray, any other imaging, culture of blood and/or any relevant body fluid). Definitive treatment, in addition to antibiotics, may on occasions include laparotomy for repair of perforated viscus, or other invasive interventions such as drainage of infected pleural fluid, or guided drainage of a deep-seated abscess. Vigorous intravenous fluids are always administered, often with intravenous vasopressors such as noradrenaline (norepinephrine) to constrict the dilated blood vessels. The latter will always be prescribed and administered by intensive care clinicians or other individuals experienced in treating septic shock.

Anaphylactic shock is usually apparent, but there may not be a history of allergy or hypersensitivity. Knowing the common causes of the allergy and the ability to recognize urticaria are improtant. Examination findings may include visible evidence of respiratory distress, agitation, an urticarial rash, skin tissue swelling, including the face, mouth and orbits, tongue swelling and wheeze. Immediate resuscitation is required with intramuscular adrenaline (epinephrine), together with other interventions, according to documented guidelines.

True neurogenic shock is relatively rare, and there may be a history of spinal cord injury or recent administration of epidural anaesthesia or autonomic blocking agents. Treatment is based on timely awareness of the nature of the shock, supportive treatment in the form of intravenous fluids and, in the case of spinal injury, speedy definitive specialist centre assessment and treatment.

Narrow pulse pressure associated with shock is almost always a consequence of shock secondary to cardiac failure (‘cardiogenic shock’) or hypovolaemia (‘hypovolaemic shock’). Examination findings, in addition to specific features described below, may include cold and pale limb peripheries.

Cardiogenic shock may be associated with a preceding history of chest pain, palpitations or breathlessness (in particular orthopnoea). There are frequently auscultatory features of pulmonary oedema. Mixed causes should be remembered such as a cardiac complication to septic shock, leading to cardiogenic shock. Patients with brittle cardiac function may present with cardiogenic shock irrespective of the initial trigger. Treatment will largely depend on the cause. Intravenous fluids should be prescribed with caution as, although their administration can be life-saving, on other occasions they will exacerbate coexisting pulmonary oedema. Intravenous inotropes such as dobutamine and adrenaline (epinephrine) are often required, but should only be prescribed and administered by clinicians experienced in their usage. Inotrope treatment is not straightforward (an improvement in cardiogenic shock may be accompanied by increased cardiac oxygen consumption, and worsen cardiac ischaemia and eventually worsen shock). Occasionally in cardiogenic shock, significant interventions such as the intra-aortic balloon pump are needed. This machine is traditionally inserted in the femoral artery, and helps preserve cardiac output until definitive treatment is provided.

Hypovolaemic shock will usually be obvious. Haemorrhage will usually be associated with a history or visual evidence of blood loss. This may be immediate and obvious in the emergency room, but may not become apparent for some while (such as in gastrointestinal bleeding or ruptured aortic aneurysm). In the initial period following a haemorrhage, it should be remembered that the blood haemoglobin may be preserved. There may be signs of intense dehydration leading to hypovolaemia after severe losses of body fluids, inadequate oral hydration (or intravenous hydration if in hospital) or a mixture of these two scenarios. Hypovolaemic shock may coexist with other causes of shock such as septic shock.

The patient with diminished consciousness

The definition of ‘consciousness’ may be the (waking) state of awareness of one’s self and environment. The absence of awareness, therefore, even when one is stimulated, may implicate diffuse or multifocal brain dysfunction, and may be defined as ‘coma’ or ‘diminished consciousness’. Although the last two terms may be seen as synonymous, the term ‘coma’ may have widespread and conflicting implications. In these situations, ambiguity should be avoided, and the patient should be described as having ‘diminished consciousness’.

Consciousness is controlled by the brainstem through a system of nerve cells and fibres known as the ‘reticular activating system’ or the ‘ascending arousal system’. The cerebrum helps maintain consciousness and alertness and at least one hemisphere, as well as the reticular activating system, must be functioning normally to maintain consciousness. The brain’s ability to adjust its activity and consciousness levels can therefore be impaired in several ways, particularly when both cerebral hemispheres are suddenly and severely damaged, when the reticular activating system malfunctions, when blood flow or the amount of nutrients (such as oxygen or sugar) supplying the brain decrease or when toxic substances impair brain function.

There are several ways to objectively describe the conscious state, though perhaps the two best known ‘scores’ are the Glasgow Coma Scale (GCS) and the ‘AVPU’ score (Tables 8.3 and 8.4). The GCS attributes a score, ranging from 3 to 15. It was originally devised to assess the level of consciousness after head injury, though now is used for almost all acutely presenting patients. When faced with a poorly conscious patient, the usual pairing of resuscitation and diagnostics should be followed. Severe neurological conditions may affect upper airway tone, respiratory drive (e.g. Cheyne–Stokes respiration), vasomotor tone and cardiac rhythm. Also, if the cause of the brain dysfunction is systemic (Table 8.5), this will need to be dealt with. Therefore, it is paramount that the ‘airway, breathing, circulation’ (ABC) algorithm is given due respect. The airway should be supported appropriately (if necessary with endotracheal intubation), the ‘recovery’ lateral position may be required in the unintubated patient to prevent aspiration, hypotension may require vigorous intravenous fluids and monitoring will be required for hypertension and cardiac dysrhythmias.

Table 8.5 Logical thinking in the poorly conscious patient

After resuscitation, one should focus on rapidly identifying the cause of brain dysfunction (Table 8.5). If there is an obvious systemic cause, this should already have been dealt with. A brief history from witnesses may reveal preceding hemiparesis, headache, trauma, fit, recreational drug or alcohol intake, or a history of cancer, diabetes, liver or renal disease. Examination should include a full body inspection for features of trauma, fundoscopy, cranial nerves and motor function (including power, tone and reflexes). The power, sensory, cerebellar and visual assessments may not be possible, due to lack of cooperation. One should attempt to examine for meningism by assessing nuchal rigidity (diminished neck flexion with otherwise retained neck movements) and knee extension with the patient supine, with the hip and knee preflexed (pain on knee extension is Kernig’s sign).

A very brief description may be made here of common pathologies leading to changes in conscious level:

Pupillary examination deserves special mention. As pupillary pathways are resistant to metabolic insult, the identification of absent pupillary reflexes usually implies structural pathology. The brainstem areas governing conscious level are anatomically close to the areas controlling the pupils and so pupillary changes help to identify brainstem pathology causing altered conscious level (Table 8.6).

Table 8.6 Relationship of pupillary changes to site of anatomical damage

Investigations, as always, should be targeted to the index of suspicion from clinical assessment. Those pertaining to resuscitation, including chest X-ray, electrocardiogram (ECG) and blood sugar, should be performed on initial encounter. Cranial imaging (usually a cranial CT scan) will be indicated if there is a significant possibility of structural lesions. It should be remembered, however, that the displacement of the patient to the radiology department may carry major risk, particularly if the patient requires general anaesthesia for intubation. Therefore, the advantages of performing neuroradiology should always be measured against risk. A lumbar puncture may be required; contraindications according to existing national and local guidelines should be referred to and, if present, the procedure should be deferred. An electroencephalogram (EEG) may reveal abnormalities consistent with a seizure disorder. Plasma alcohol may easily be measured, and may lend support to a clinical diagnosis of alcohol toxicity. Some, though not all, hospitals are able to perform urine toxicology analyses for recreational and other drugs. Plasma levels for paracetamol, salicylates and anticonvulsant medications are also easily available. These may be relevant in cases of deliberate or inadvertent self-harm. Some plasma levels for drugs are only available in specialist ‘poisons’ units. It is therefore often good practice to have a saved sample of serum, which may subsequently be transported if required. Tests of renal function and liver function (including blood clotting) should be included in the context of altered conscious level.

The patient with chest pain

The pathologies causing chest pain may range from life-threatening coronary artery disease to benign muscular pain. Not surprisingly, the patient is often very anxious, thinking he has serious heart disease.

It should be remembered that, with pericarditis, the pain may be ‘classic’ (central pain relieved by sitting forward) or central pleuritic. The features more associated with ischaemic cardiac chest pain are: feeling ill, radiation down the left arm (or occasionally both arms), nausea, sweating and preceding temporal relationship with exercise. Insidious, intractable chest wall pain should prompt an enquiry about malignancy and asbestos exposure. The features of chest infections and viral infections should be obvious. Pneumonias are not infrequently associated with headache.

In addition to the history, the risk factors for coronary artery disease and pulmonary embolism (PE) may be factored into the diagnostic process (Box 8.1 and Table 8.8).

Table 8.8 Modified Wells criteria for assessing the risk of pulmonary embolism (PE) in a patient with symptoms consistent with pulmonary embolism

If ‘ABC’ interventions are not required for resuscitation, if the patient is stable and there are no other features requiring immediate action (e.g. peripheral cyanosis), a fuller examination is required. The blood pressure should be taken in both arms, particularly if the arm pulses are unequal. Blood pressure inequalities should prompt rapid action in the form of thoracic CT scanning and cardiothoracic referral. A raised jugular venous pressure may suggest early heart failure. Precordial auscultation may reveal a pericardial rub. There may be classical signs of pneumonia. It may 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.

The ECG should be inspected to look for evidence of coronary artery disease, with a low threshold for repeating and looking for dynamic changes. Myocardial infarctions will be treated with primary angioplasty or thrombolysis. It should be remembered that the changes on the ECG with PE are usually non-specific. The ‘S1Q3T3’ changes, indicating right heart strain, are not pathognomonic of PE and their absence in the ECG should never be instrumental in excluding the diagnosis of PE. One should look for global ST changes consistent with acute pericarditis. The chest X-ray should be inspected, and one should look for features of pneumothorax, pneumomediastinum (from oesophageal rupture), heart failure, widened mediastinum (which would prompt a contrast-enhanced CT scan looking for thoracic aorta dissection), pneumonia, rib fractures or destruction and pleural effusions. Cardiac troponin levels should be performed in cases of central chest pain where acute coronary artery pathology is suspected. If PE is suspected, a CT pulmonary angiogram (CTPA) or ventilation/perfusion (V/Q) scan should be performed. In the shocked patient with suspected pulmonary embolus, an echocardiogram is the immediate investigation of choice, looking for right ventricular and pulmonary artery dilatation.

The breathless patient

The method of dealing with the breathless patient is similar to that of chest pain. It should be established as rapidly as possible whether immediate and resuscitating interventions are required, and both ECG and chest X-ray performed early.

When life-threatening conditions present with breathlessness, one should as ever simultaneously resuscitate and use immediate clinical assessment to establish the cause (Table 8.9). The patient should be placed in a safe, monitored 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. Unless there is good evidence that high-flow oxygen has on this occasion, or previous occasions, caused breathing difficulties, the latter should be administered. The clinical assessment will be of life-saving value to direct subsequent therapy, especially if the chest X-ray is not suggestive of one specific pathology.

Table 8.9 Potentially life-threatening conditions presenting as breathlessness