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 Many could try to argue that with the advancement of science, history taking and clinical examination should be superseded by simple awareness of available investigations.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

Mechanism	Common or important examples
Infection	Viral (upper respiratory, lower respiratory, 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
Malignancy and granulomatous disease	Solid tumours; lymphoma; leukaemia; amyloidosis; sarcoidosis
Drugs	Prescription; recreational (e.g. Ecstasy)

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

Mechanism	Common or important examples
Narrow pulse pressure	Hypovolaemic shock (haemorrhage, fluid losses from enteral tract, fluid losses from renal tract, fluid losses from skin (burns)); cardiogenic shock from myocardial failure (coronary ischaemia, acute myocarditis)
Widened pulse pressure	Septic shock; anaphylactic shock; neurogenic 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

Primary cranial diffuse or multifocal disease, where structural lesions will be obvious on imaging	Primary cranial diffuse disease where no structural lesions will be obvious on imaging
Vascular Infection Inflammation Tumours Trauma

Secondary cranial disease: systemic Secondary cranial disease: metabolic

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

Unilateral pathological dilatation (mydriasis)	Unilateral pathological constriction (miosis)	Mid-point pupil
Pupillary fibres close to the origin of the third cranial nerve are especially susceptible when uncal herniation or a posterior communicating aneurysm compresses the nerve This mydriasis is usually accompanied with sparing of oculomotor function When pupillary fibres more distal in the third cranial nerve are affected, the mydriasis usually occurs together with oculomotor dysfunction	Hypothalamic damage may lead to ipsilateral Horner’s syndrome Pontine damage may lead to bilateral miosis Lateral medullary and ventrolateral cervical cord lesions may lead to ipsilateral Horner’s syndrome	Mid-brain damage: the mid-point pupil shows no reaction to light

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

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

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

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 may be very silent)	Severe asthma Anaphylaxis Acute bronchitis Pulmonary oedema

Diffuse features Significant asymmetry of findings in a whole lung on percussion and/or auscultation Focal features of consolidation No obvious abnormality

While awaiting the urgently requested chest X-ray, one may be in a position to identify additional features to clinch the diagnosis and initiate treatment (Table 8.10). The radiographic features will not be dealt with in this chapter. If stridor as opposed to wheeze is considered, the cause may be evident from the history (airway cancer, foreign body exposure or anaphylaxis). The examiner’s ear should be placed carefully close to the mouth of the patient, to try to establish the source of airflow limitation. Acute stridor is an airway emergency, and the teams of intensive care and ear, nose and throat should be mobilized as quickly as possible.

Table 8.10 Logical thinking for conditions causing breathlessness, including the emergency conditions

Clinical assessment	Classification	Condition
Stridor	Large airways disease	Partial obstruction of trachea or major airway
Bilateral or diffuse wheeze	Small airways disease	Asthma Acute bronchitis (including bronchitic component to chronic obstructive pulmonary disease) Anaphylaxis Pulmonary oedema (presenting as bronchial oedema) Obesity hypoventilation syndrome (though often the wheeze from obesity-related airflow limitation is not heard)
Asymmetric features in whole lung field (tracheal deviation, hyperresonance 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 airways 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

This table is not intended to be an exhaustive list. It is aimed at assisting logical thought, particularly with regard to clinical features.

It may be impossible to differentiate between the wheeze of severe asthma, anaphylaxis and acute bronchitis. One should try to establish a history of asthma or exposure to potential allergens. There may be historical features of infection. Examination may identify other features of anaphylaxis, such as swollen facial tissue (orbital areas, lips, tongue). The wheeze of pulmonary oedema occurs when there is compression of the major bronchi by oedematous parenchyma (when diffuse features are heard in addition to wheeze) or when there is predominant bronchial oedema (when the diffuse auscultatory features may not be heard). The patient with pulmonary oedema manifesting as wheeze may share other clinical features seen in ‘classical’ pulmonary oedema.

Widespread bilateral unchanging fine crepitations are most often associated with acute pulmonary oedema. One should specifically enquire about chest pain, and confirm the rapidity of onset of breathlessness. The patient is often strikingly cold and sweaty as well as hypertensive, as a consequence of peripheral vasoconstriction. A cardiac dysrhythmia may be evident, which needs immediate treatment. Otherwise rapid treatment with intravenous nitrates and diuretics should be followed by ECG and echocardiogram assessments. Acute coronary pathology should be treated. The crepitations of acute pulmonary oedema may be very similar to those heard in pneumonitis, but with the latter there is no consistent association with peripheral vasoconstriction, which is found in pulmonary oedema. The presumed cause should be treated, and it should be recognized that many patients with pneumonitis deteriorate despite support, and require artificial ventilation in intensive care. Widespread bilateral fine crepitations should not be confused with widespread bilateral bronchial breathing. These auscultatory features are of widespread consolidation, and are consistent with multilobar or bronchopneumonia. Immediate treatment with antibiotics should be accompanied by an awareness that these patients also may have a tendency to deteriorate despite treatment.

Clinical examination of the breathless patient may reveal significant asymmetry in chest expansion, percussion and/or auscultation. A good rule to follow is that the side that moves less has the pathology within it. The deviated trachea will be ipsilateral to a non-tension pneumothorax or lung collapse, and be contralateral to a tension pneumothorax or massive pleural effusion. Percussion of the affected lung will be hyperresonant with pneumothorax, dull with lung collapse and ‘stony’ dull with massive pleural effusion. Breath sounds may be absent or poorly heard in the affected lung in all of these conditions. The pneumothorax in the acutely breathless patient requires emergency decompression with a chest drain. Lung collapse may lead to urgent bronchoscopy, where malignancy or foreign bodies will be specifically looked for. The massive pleural effusion will require therapeutic drainage, with cytological and microbiological laboratory analysis of the pleural fluid, and caution so as not to drain too much fluid immediately and risk unilateral pulmonary oedema.

Some diminished chest expansion on one side may be accompanied by focal features. There may be increased tactile fremitus, dullness to percussion and auscultatory features of increased vocal resonance and bronchial breathing. These focal features of consolidation may be subsequent to lobar pneumonia or lobar collapse (from tumour, foreign body or mucus plug) requiring intravenous antibiotics or an urgent bronchoscopy, respectively.

When there is no obvious abnormality on examination of the acutely breathless patient, one should revisit the history. Chest pain and risk factors should raise suspicion of PE, and there may be evidence of hypoxia from the observation of oxygen saturations and arterial blood gases. If there are no clear contraindications, treatment with anticoagulation should be empirically commenced, and investigations urgently requested. In the absence of chest pain, risk factors and hypoxia, one should consider the possibility of respiratory compensation to metabolic acidosis (tachypnoea and deep breathing, ‘Kussmaul’s respiration’). Once the arterial blood gases have confirmed the metabolic acidosis, the cause should be identified and treated.

Most acute and life-threatening conditions evolve rapidly over minutes or hours, whereas the timeframe associated with subacute and more chronic conditions may be more in the order of days to weeks. It is common for there to be a demonstrable acute history superimposed on a subacute or chronic one.

Most conditions causing breathlessness are exacerbated by lying flat and relieved by sitting up, though this ‘orthopnoea’ is most obvious with pulmonary oedema and respiratory muscle weakness. Breathlessness relieved by lying flat (platypnoea) is relatively rare, and is most often associated with PE; in this case, the supine posture improves pulmonary perfusion and provides relief.

A cough acutely productive of purulent sputum may confirm the working diagnosis of pneumonia. Longer standing cough may be associated with non-purulent sputum production (asthma, chronic obstructive pulmonary disease and bronchiectasis) or non-production (interstitial lung disease and lung cancer). An absent or weak cough may suggest respiratory muscle disease. Acute, frothy sputum (occasionally tinged with blood) may be seen in pulmonary oedema. Frank haemoptysis may occur in PE, lung cancer, pulmonary vasculitis, pneumonia and acute bronchitis.

The patient with palpitations

The term ‘palpitations’ may mean different things to different patients, though one reliable definition is an ‘abnormality of the heart beat which leads to its awareness’. This symptom should be given due respect by clinicians whether the patient has palpitations present during assessment or not. The aim should be to uncover any cardiac dysrhythmia and implement prompt treatment. There will, however, be no cause found in many patients with a history of palpitations.

The patient in need of resuscitation needs to be identified. Symptoms of chest pain or breathlessness and examination findings consistent with tachycardia, bradycardia or pulmonary oedema should prompt immediate ‘ABC’ assessment and monitoring. Any hypotension should be noted and treated. Plans should be made to prepare for the emergency treatment of cardiac dysrhythmia. The monitored (3-lead) and 12-lead ECG may show any dysrhythmia. Decompensation features such as chest pain and pulmonary oedema occurring secondary to dysrhythmia often resolve on prompt treatment of the underlying dysrhythmia. In contrast, primary coronary ischaemia may lead to secondary dysrhythmia.

Bradydysrhythmias (dysrhythmias with slow heart rate) more often present with syncope than palpitations. Rhythm abnormalities may include complete heart block or sinus bradycardia. If the episode is a life-threatening one, emergency temporary pacing (cutaneous or transvenous) should be considered; otherwise, the patient should be transferred to a specialist cardiology centre where the issue of pacing is reassessed.

The decompensated patient with palpitations will more often have tachydysrhythmias (dysrhythmias with fast heart rate). Possibilities include atrial fibrillation with fast ventricular rate, supraventricular tachycardia and ventricular tachycardia. Emergency electrical cardioversion should be considered.

It is not uncommon for patients to present with a recent history of palpitations, which have resolved by the time of presentation. If palpitations are still present, and the patient is not in need of immediate resuscitation, one should embark upon ECG monitoring and 12-lead ECG analysis while the history and examination are taking place.

The history should elicit confirmation of the speed and regularity of the palpitations, with the patient reproducing the heart beat on the back of the examiner’s hand. The historical period (hours, days, weeks, months or years), duration (seconds, minutes or hours) and frequency of palpitations should be established, together with decompensating features of chest pain, syncope or breathlessness. These latter features should heighten the urgency of investigations. A past history of heart disease, accompanying features of thyroid disease, recent drug prescription, evidence of substance misuse, pregnancy and anaemia should be sought.

Examination of the pulse will reveal ‘irregular irregularity’ in atrial fibrillation. One may identify ‘cannon waves’ on examination of the jugular venous pulse which are characteristic of atrioventricular dissociation. They may be seen intermittently with ventricular extrasystoles, or persistently with ventricular tachycardia. Examination of the precordium may reveal heart murmurs consistent with valvular or structural heart disease. The thyroid gland and thyroid status should be assessed, as thyroid dysfunction may be a contributory cause.

Investigations should pursue common conditions which may cause or contribute to dysrhythmias: full blood count (for anaemia), electrolytes (particularly for plasma potassium), thyroid function tests, chest X-ray, echocardiogram and 24-hour ECG monitoring. One should also consider performing urine toxicology for the detection of recreational drug usage.

If the palpitations were associated with decompensating features and the cause has not been found, investigations should continue as an inpatient.

The syncopal patient

Syncope is a frequent cause of presentation to hospital and the emergency department. It may be defined as brief, temporary loss of consciousness with rapid onset and self-termination. The implication is that there is temporary, global hypoperfusion to the brain. The brevity of the event is mostly limited to a few minutes. Although the causes of syncope are often not sinister, the consequences may be catastrophic if, for instance, the onset occurs while driving. The condition should therefore be taken seriously (Table 8.11).

Table 8.11 Logical thinking for conditions causing syncope

Mechanism	Common or important examples
Cardiac structural disease	Valvular heart disease Obstructive cardiomyopathy Atrial myxoma Severe systolic dysfunction

Cardiac dysrhythmia Any dysrhythmia Pulmonary hypertension (poor left atrial filling) ‘Steal’ syndromes Subclavian ‘steal’ Nervous system mediated Hypovolaemia

It is likely from the above definition that the patient will present to the clinician with fully preserved brain function, and a history (or collateral history from witnesses) of recent syncope. This would exclude patients with ongoing brain dysfunction and altered conscious level; the assessment of the poorly conscious patient has been dealt with elsewhere in this chapter.

When the duration of the period of loss of consciousness is unknown or thought to be prolonged, one should consider the possibility of seizures. This impression may be reinforced by the presence of tongue biting, urinary incontinence, preceding aura or unusual behaviour, ongoing drowsiness, confusion or headache, or collateral history of involuntary movements during the episode. The assessment of the patient with seizures will be described elsewhere in this chapter.

The history of the event itself will not be complete from the patient, though the events preceding and following the syncopal event may be recounted. It is important, therefore, that any witnesses of the event are available to give a collateral history. Dramatic sequelae such as motor vehicle accidents or personal injury will prompt urgent investigations. The history should investigate any relationship between syncope and exertion, chest pain, palpitations, dyspnoea, posture changes, body fluid losses and overt bleeding. A careful drug and alcohol history should be taken and a past history of heart and lung disease or diabetes should be noted. A family history of sudden death should be taken very seriously.

One should examine for an implanted cardiac device (such as a pacemaker), irregular or rapid heart rate and for heart murmurs. Measurement of lying and standing blood pressure is mandatory unless there is a clear alternative cause. Investigations could initially include full blood count, ECG, echocardiography and 24-hour ECG monitoring. Formal autonomic function testing may be needed.

The patient with seizures

One definition of ‘seizure’ is the ‘uncontrolled electrical activity in the brain, which may produce a physical convulsion, minor physical signs, thought disturbances or a combination of symptoms’. ‘Epilepsy’ is a pattern of repeated seizures. The occurrence of a seizure or ‘fit’ is a common mode of presentation to the emergency department. In many or most cases, the diagnosis will not be epilepsy.

If the patient is actively seizing, the ‘ABC’ of resuscitation should be meticulously followed. Intravenous anticonvulsant agents should be administered as rapidly as possible, within the constraints of formulary guidelines. Benzodiazepines (e.g. lorazepam), phenytoin and levetiracetam are commonly used agents. The aim should be to suppress the seizure as quickly as possible. If there is no success with standard anticonvulsants, the administration of a general anaesthetic (together with intubation, ventilation and admission to intensive care) should be considered. The definition of ‘status epilepticus’ is under continuous scrutiny (Table 8.12).

Table 8.12 Simple terminology for seizures

Term	Description
Generalized seizure	Involvement of the whole cerebral cortex and therefore abnormalities (e.g. convulsions) may be seen in the whole of the body
	Consciousness is always impaired
Focal (partial) seizure	Involvement of a focus in the cerebral cortex and therefore abnormalities (e.g. convulsions) may be seen in one part of the body
	Consciousness may be retained (simple partial seizure) or impaired (complex partial seizure)
	There may be secondary generalization (i.e. a focal seizure leading on to a generalized seizure)
Convulsive seizure	For example tonic–clonic, tonic and clonic
Non-convulsive seizure	The term ‘absence seizure’ should generally be avoided unless a specific syndromic diagnosis is being made by a clinician experienced in epilepsy
Status epilepticus	Historically, one definition has been ‘prolonged seizures for more than 30 minutes’, though, in modern times, it is more sensible to accept that ‘any prolonged seizure’ may be classified as status epilepticus

In the non-seizing patient, the challenge may be to identify whether the episode preceding admission was a seizure or not. It should be remembered that a diagnosis of seizures may lead to social and employment consequences (including the ability to drive). It is vital, therefore, to establish a credible collateral history together with a detailed history from the patient. Tongue biting and post-event drowsiness, headache or confusion may help lend support to a diagnosis of seizures. Although urinary and faecal incontinence is often quoted, it is not a strong differentiating feature between seizures and non-seizures.

The diagnosis of non-convulsive status epilepticus may be missed unless specifically thought of. The patient may present with non-specific features, such as prolonged confusion or drowsiness. On occasions there may be clinical features to arouse suspicion such as nystagmoid eye movements or repetitive (often stereotypic for the patient) movements of the tongue, jaw or limbs.

Some conditions are commonly misdiagnosed as seizures. Severe exacerbation of extrapyramidal disease may mimic myoclonus. Vasovagal episodes may, on occasions, be followed by jerking of the limbs. Pseudoseizures (seizures simulated by patients for psychological and other complex reasons) are often difficult to differentiate from genuine seizures, even for many experienced neurologists (Table 8.13).

Table 8.13 Awareness of conditions commonly misdiagnosed as seizures

Condition	Awareness
Pseudoseizure	The reasons for patients presenting with contrived movements mimicking seizures are complex. They often occur in known epileptics. The risk of death is significantly higher in epileptics with pseudoseizures, and so the latter needs to be taken seriously and not merely dismissed as a non-organic event. Many experts in epilepsy maintain that with increasing clinical experience, there is increased awareness of the difficulty in the differentiation of seizures from pseudoseizures. There are, however, some features which may lend support to the diagnosis of pseudoseizures: resistance to attempted eye opening by the clinician; limb thrashing and pelvic thrusting; full alertness immediately after the event (i.e. lack of postictal drowsiness) and down-going plantar responses during attack
Vasovagal episode	Prolonged vasovagal episodes may lead to cerebral hypoperfusion and brief, self-limiting convulsive-type movements
Cranial trauma	This is particularly seen in sports events, where cranial trauma may lead to brief, self-limiting convulsive-type movements, similar to those seen in vasovagal episodes
Extrapyramidal disease	Patients may present with worsening or poorly controlled Parkinson’s disease, manifested as severe coarse tremor which, to the untrained eye, may resemble myoclonus

In history taking, there is considerable overlap with the principles described for the patient with syncope. It is essential that witnesses are available to give a collateral history, as the seizure itself will not be recollected by the patient. However, on recovery, the events preceding and following the seizure may be recounted by the patient. As in syncope, dramatic sequelae such as motor vehicle accidents or personal injury should be taken seriously. It should be established whether there is a known history of epilepsy. In known epileptics, a history should be taken for compliance, anticonvulsant changes, concurrent illnesses, alcohol intake and lifestyle issues. In other cases, specifically ask about alcohol intake, recreational drug usage, diabetes, head injury, foreign travel and pregnancy.

General examination will include the assessment of features of infection. One should be aware that brief fever is a common phenomenon after seizures from muscle contractions. Persistent fever together with, for instance, tachycardia and raised respiratory rate, would suggest the presence of an infection. If there is genuine doubt as to whether the fever is related to the seizure or an infection, one should look vigorously for a source of infection (including performing a lumbar puncture) and consider administering empirical intravenous antibiotics while awaiting investigations. One should examine for evidence of cranial trauma, alcoholic foetor and severe hypertension.

In the drowsy postictal patient, some aspects of neurological examination such as visual fields, voluntary eye movements, cerebellar function, power and sensory deficits will be difficult or impossible. However, the following should be performed to a high standard: fundoscopy; pupillary, corneal and gag reflexes; limb tone; limb reflexes; and spontaneous limb movement. Any asymmetry should be noted, and may prompt urgent investigations.

Blood sugar should be performed urgently, as hypoglycaemia may be quickly reversed and brain injury prevented. Plasma biochemistry and liver function tests will identify reversible electrolyte deficiencies and features of liver disease. Possible infections should be identified with the help of white cell count, blood culture and urinalysis. Toxicology tests may include blood alcohol and urine drug analysis. Women of childbearing age should have a pregnancy test. Patients with unexplained seizures and a history of travel abroad should have parasite analysis. If the patient has no known identity and therefore no known past history, plasma anticonvulsant analysis may lend support to recent ingestion and therefore the possibility of previously diagnosed epilepsy.

A cranial CT scan will be required if: the seizure is unexplained; there are features of cranial trauma; there are focal or lateralizing features; there are fundoscopic features of raised intracranial pressure; there are features of infection. The gross features uncovered by a cranial CT may include intracranial haemorrhage or space-occupying lesions. There may be subtle features of inflammation of the meninges, though these and other cerebral inflammatory features are best picked up by cranial magnetic resonance (MR) scans which may be performed at a later time. Although it is a misconception that a CT scan is always required prior to lumbar puncture, it is overwhelmingly recognized that lumbar puncture for the investigation of meningitis in the patient with seizures should always be preceded by a cranial CT. The cerebrospinal fluid from the lumbar puncture should be analysed for meningitis and for subarachnoid haemorrhage. An EEG may be performed acutely to lend support to the diagnosis of a postictal state, and occasionally to identify features of herpes encephalitis. If the acute findings are not contributory, there is the scope for repeating the EEG as an outpatient.

Once a seizure is diagnosed, the clinician should advise the patient of his duty to contact the driving licensing authority, who in turn will issue guidelines for cessation of driving for a defined period. The diagnosis of epilepsy should be made by an expert in epilepsy, as this diagnosis will have social and drug-therapy implications. The epilepsy expert will also decide, together with the patient, on the clinical value of prescription of anticonvulsants after a first seizure.

The patient with dizziness

The term ‘dizziness’ (as in the word ‘collapse’), although used frequently by patients and lay people, has no clear precise meaning, and as such always requires medical clarification by the history taker. Any sense of imbalance may be described as dizziness. Balance relies on properly functioning circulation, vestibular apparatus and general sensory function, and it follows that disturbance of these functions may lead to imbalance. It is the duty of the clinician to elicit from the patient whether the features are consistent with presyncope, disequilibrium or true vertigo (Table 8.14). It is important to appreciate the anatomical structures which are relevant; the disruption of any of these will lead to dizziness (Fig. 8.1).

Table 8.14 Logical thinking for conditions associated with dizziness

Terminology	Examples
Presyncope (brief, temporary episode of near loss of consciousness with rapid onset and self-termination) This is often described as light-headedness

Refer to the causes of syncope already described Functional impairment of vision or peripheral nerve or dorsal column True vertigo (false perception of movement in relation to environment):

Vertigo may be further characterized into ‘peripheral’ and ‘central’. Peripheral vertigo arises from pathology of the vestibular system or vestibular division of the eighth cranial nerve. Central vertigo arises from pathology of the vestibular nuclei in the brainstem or any of its sensory projections. It is also important to note that yawing vertigo may be peripheral or central, while pitching, rolling and complex vertigo almost always are central in origin.

The history should establish whether the ‘dizziness’ is in actual fact light-headedness, gait disturbance or perception disturbance consistent with vertigo. The latter may include visual or balance disturbance. Complex vertigo may be described on occasions as ‘tilting’ or ‘swaying’. Benign positional paroxysmal vertigo (BPPV) is associated with episodic, rapid-onset brief-duration (seconds or minutes) vertigo related to specific head positions. Ménière’s disease may also be recurrent (each vertiginous episode lasting hours or days). In this condition, with each event, the vertigo may become less intense while being replaced by increasing deafness. Acute labyrinthitis is of more insidious onset, and the vertigo may be present for days or weeks. It may be recurrent (though not as clearly episodic as BPPV) and posture related (as significant as BPPV). Hearing loss and tinnitus may be present. Brainstem conditions tend to cause non-episodic non-posture-related vertigo and may be associated with features such as diplopia or dysarthria.

General examination should include a check of peripheral pulses, erect and supine blood pressure and features of anaemia. The precordium should be auscultated, and one should listen carefully for heart murmurs. Visual and hearing disturbance should be identified, as should any sensory disturbance or ataxia.

Neurological examination will include cranial nerve assessment; any deficit may point towards brainstem pathology. Papilloedema should be looked for on fundoscopy.

One should specifically look for nystagmus. The latter may be seen on forward gaze in any vestibular pathology, or lateral gaze in cerebellar disease. Non-specific horizontal nystagmus may be seen in either vestibular or cerebellar disease. Vertical nystagmus is most commonly seen in upper brainstem disease, while down-beat nystagmus is seen in conditions affecting the cervicomedullary junction. One may, on occasions, perform a specific provocation test, called the Dix-Hallpike manoeuvre, to elicit nystagmus. This involves laying the patient supine, with the head beyond the end of the couch. The neck is slightly extended and the head rotated. Any nystagmus is noted, with rotation to the right and the left (the nystagmus is provoked by rotation to the affected side). Subsequently, sitting the patient up should lead to the disappearance of the nystagmus. A positive test (the presence of nystagmus) usually points to the diagnosis of BPPV.

The patient with acute confusion

This is a common problem in any clinical setting involving patients being seen as emergencies. Often, the patient will have pre-existing cognitive dysfunction, which may have been prevalent for weeks, months or years. It is important in this scenario to investigate both the acute confusion and the pre-existing pathology. One should recognize that those with longer-standing cognitive dysfunction (e.g. subsequent to cerebrovascular pathology) will be more susceptible to episodes of acute confusion when affected by minor pathology such as infection and metabolic derangement. Particularly in elderly patients, systemic problems such as infections or cardiac disease may not lead to any symptoms other than acute confusion.

The causes and mechanisms of confusion should be logically arranged in the mind of the clinician (Table 8.15). Toxaemia from infections, inflammation and drugs will lead to varying degrees of cerebral dysfunction, as will metabolic derangements. Any episode of acute pain or anxiety affects intellectual function. Poor cerebral oxygenation will occur with episodes of hypoxia and diminished cerebral perfusion from circulatory impairment. Any brain pathology may cause cerebral dysfunction; one should be aware that in these cases, confusion may progress to diminished conscious level. The possibility of underlying psychiatric disorder must never be ignored, particularly in the younger patient.

Table 8.15 Logical thinking for conditions causing acute confusion

Mechanism	Common or important examples
Infection	Urine, chest
Inflammatory	Acute pancreatitis, vasculitis, ischaemic bowel, myocardial ischaemia
Drugs and external toxins	Prescription drugs, recreational drug usage, alcohol (toxicity or withdrawal)
	The most severe form of alcohol withdrawal is ‘delirium tremens’, a condition which traditionally starts up to 3 days after cessation of heavy alcohol consumption
Metabolic derangement	Hypoglycaemia, hyperglycaemia, hyponatraemia, hypernatraemia, hypercalcaemia, liver dysfunction (synthetic or cholestasis), uraemia, thyroid dysfunction, nutritional deficiency (particularly vitamin B12, thiamine and niacin)
Acute pain or anxiety	Urinary retention, severe constipation
Psychiatric issues	Depression, schizophrenia
Hypoxaemia	Chest infection, pulmonary oedema, pulmonary embolism
Circulatory impairment	Cardiac disease (dysrhythmia, systolic dysfunction), sepsis, haemorrhage, prolonged vagal episode
Brain pathology	Haemorrhage, ischaemia, seizure disorder, infection (encephalitis and meningoencephalitis), head injury, cerebral vasculitis

The history, as in cases of altered conscious level, syncope and seizures, will often not be meaningful from the patient. The collateral history from relatives and other sources is therefore paramount. One should establish the presence of any longstanding cognitive issues. Specific, directed questioning should deal with the presence of head injury, pain (including chest pain), breathlessness, light-headedness, headache and features of infection. A meticulous history should be taken for drugs and alcohol. One should confirm the nutritional history and the presence of established chronic diseases such as diabetes, seizure disorders, liver, kidney or thyroid disease. One should also enquire about psychiatric illness and longstanding mood changes.

The examination should be targeted, as the patient will most likely not be able to comply with complicated directions which are required in neurological and other assessments. One should commence with the ‘vital’ observations, namely oxygen saturations, respiratory rate, blood pressure (erect and supine) and heart rate. Pyrexia, features of head injury, smell of alcohol, cachexia and features of jaundice or uraemia should be looked for. There may be obvious features of a thyroid disorder. The presence of pain on palpation and abnormalities on chest examination should be identified. Neurological examination will elicit any gross focal or lateralizing features, and also features of meningism. One may conclude with an abbreviated mental test (see Ch. 7). The latter will make the confusion objective, and help track any progress.

Unless the diagnosis is absolutely clear, investigations may commence with full blood count, C-reactive protein, standard electrolytes, liver function, thyroid function, vitamin B₁₂, urinalysis, urine culture, blood culture (if there is pyrexia), chest X-ray, plasma drug level (if toxicity is suspected and the assay may be practically measured), blood alcohol (to help differentiate alcohol withdrawal from toxicity), urine toxicology (if toxicity is suspected), ECG and arterial blood gases (if low oxygen saturation is identified). If there is evidence of focal or lateralizing features, meningism, altered conscious level or unexplained headache, a cranial CT scan should be considered. A lumbar puncture should be performed if meningitis remains a consideration.

The patient with acute headache

Many patients present to the emergency department with severe acute headache. This will either be a ‘worst ever’ exacerbation in the context of chronic, long-term headache, or a first presentation of headache.

On initial presentation, it should be established whether there have been any additional features which may suggest sinister pathology. One should specifically enquire about: severity (is this the ‘worst ever’?); rapidity of onset (implying vascular pathology such as subarachnoid haemorrhage); recent head injury; loss of consciousness; altered intellect; features of sepsis; features of meningism (photophobia and neck stiffness); features of raised intracranial pressure (headache exacerbated by straining, coughing and lying flat); asymmetry (consistent with temporal arteritis and glaucoma, as well as migraine and sinusitis); and blurred visual disturbance (consistent with raised intracranial pressure, glaucoma and temporal arteritis).

There are additional features which need clarification. A past history and temporal patterns of longstanding headache need to be established, as does the presence of coexisting illness. Viral infections and pneumonia are not uncommonly associated with headache. Foreign travel may be relevant, as may the drug history.

It is important to be aware of some distinctive features of the commoner causes of headache (Table 8.16). Missing a subarachnoid haemorrhage is one of the clinician’s worst fears. Distinctive historical features include a sudden-onset, ‘worst ever’ headache. There may have been an episode of loss of consciousness (this may be seen in up to half of all patients presenting with subarachnoid haemorrhage). Features of meningism and raised intracranial pressure are not uncommon. Urgent investigations (cranial CT scan, with targeted lumbar puncture) and specialist referral are paramount. Bacterial meningitis may be rapidly fatal, and treatment with intravenous antibiotics must commence as soon as the diagnosis is suspected. Viral meningitis is usually less virulent, though this is not inevitably the case. The headache of meningitis is of acute onset and severe. There are accompanying features of photophobia and neck stiffness. In severe cases, there may be features of raised intracranial pressure. Although pure encephalitis does not produce features of meningism, meningoencephalitis does. Temporal arteritis is a form of vasculitis where the temporal arteries are inflamed and tender. The headache is usually asymmetric. There may be pain in the jaw with chewing (‘jaw claudication’). Vision changes (blurred vision) should prompt urgent treatment with steroids (to prevent complete loss of vision), followed by specialist referral and confirmation of the diagnosis with a temporal artery biopsy. The migrainous headache is typically unilateral and pulsating. The acute period often lasts between 4 and 72 hours, and there may be accompanying nausea, vomiting, photophobia, phonophobia (increased sensitivity to sound) or osmophobia (sensitivity to pungent smells).

Table 8.16 Logical thinking for conditions causing acute headache

Mechanism	Common or important examples
Vascular – haemorrhage	Subarachnoid, intracerebral, subdural, extradural
Vascular – occlusive	Migraine, temporal arteritis, carotid artery dissection
Muscular	Tension-type headache
Meningeal irritation	Meningitis (bacterial, viral), subarachnoid haemorrhage
Raised intracranial pressure	Space-occupying lesion (tumour, abscess, localized haemorrhage), malignant hypertension, benign intracranial hypertension
Drugs and toxins	Oral or sublingual nitrates, carbon monoxide
Carbon dioxide retention from respiratory failure	Obstructive sleep apnoea, obesity hypoventilation syndrome
Tropical disease	Malaria, any one of the tropical endemic encephalitides
Upper respiratory tract infections	Influenza, sinusitis
Intraocular pressure	Glaucoma
Neuralgia	Trigeminal neuralgia, cluster headache

Approximately one-third of people who suffer from migraine headaches sense an aura (visual, olfactory or other sensory experiences) that may predict that the migraine will soon occur. Visual auras include not only the well-known zig-zags and flashing lights, but also temporary hemianopia or scotoma. Tension-type headache (TTH) is the commonest type of headache, and probably occurs at some point in up to half the adult population. The pain is often likened to a ‘band around the head’ or ‘squeezing’ or ‘pressure’. This will commonly either spread down the neck or travel up from the neck. The headache may last from a few hours to a few days. Confusingly, prolonged TTH may develop some mild migraine features. Contributing factors causing TTH include neck pathology such as osteoarthritis, stress and anxiety. Cluster headaches (also known as migrainous neuralgia) are excruciating asymmetrical headaches, which may last from as short as 15 minutes to 3 hours or more. The onset of an attack is rapid, and most often without the preliminary auras that are characteristic of migraine. The pathophysiology involves the dilatation of blood vessels which then impinge on the trigeminal nerve. The underlying aetiology though is unclear. Trigeminal neuralgia is often described as an ‘electric shock’ or ‘spasm’ or ‘burning sensation’ in any of the divisions of the trigeminal nerve. The pain may last a few seconds to a few minutes. The commonest cause of trigeminal neuralgia is thought to be vascular compression resulting from abnormal arterial roots near the nerve root. Occasionally this may be seen on MR scans. Other causes include malignancy, intracranial aneurysms and cranial arteritis. Headache from glaucoma tends to begin around the orbital area and spreads to develop into a general headache. The eye pain is caused by an increase in the intraocular pressure. If glaucoma is left untreated, blindness may follow.

The examination should include identification of general and specific features of sepsis, such as pyrexia, tachycardia and signs of lung consolidation. Altered conscious level should have been detected on initial encounter and immediately acted upon. Altered intellectual function and disorientation, though, may only be apparent when specifically sought. A history of neck stiffness should prompt an examination of nuchal rigidity, where there is a painful deficit of neck flexion, with relative preservation of all other neck movements. When meningism is suspected, both legs should also be examined where each leg in turn is bent at the hip and knee at 90° angles; if subsequent further extension in the knee is painful (leading to resistance), this should be described as a ‘Kernig’s positive’ sign, which in turn suggests that there is significant inflammation of the meninges. Positive features of meningism should prompt the clinician to search for a non-blanching purpuric rash, which may lend support to a diagnosis of meningococcal meningitis. A full neurological examination should identify any focal or lateralizing motor or sensory abnormalities, and also any cranial nerve or cerebellar deficits. One should look for papilloedema on fundoscopy. Additional areas of clinical examination may include: palpation of the temporal arteries or the sinuses, looking for tenderness in these areas; examination of the scalp looking for herpetic lesions; and inspection of the sclerae, looking for the acute red eye of glaucoma.

Investigations should be performed quickly when there are any sinister features as described above. In contrast, clinicians should be aware that normal neuroimaging in itself will not help the clinician or patient arrive at a diagnosis.

Cranial CT scans should, if possible, be performed with contrast if obvious haemorrhage or cerebral oedema cannot be seen in the non-contrast scan, to identify space-occupying lesions. It should be noted that in cases of suspected subarachnoid haemorrhage, a cranial CT is not diagnostic in all cases, particularly more than 24 hours after the acute event. If the diagnosis is suspected and the CT scan is normal, a lumbar puncture is mandatory to exclude the diagnosis, and is best done more than 12 hours after the onset of symptoms. If encephalitis is suspected, a magnetic resonance image (MRI) should be considered. Lumbar puncture for cerebrospinal fluid analysis should be performed when meningitis is suspected. Antibiotics should never be withheld while waiting for the lumbar puncture. Other investigations which may help identify or support a diagnosis are chest X-ray, white cell count, blood culture, parasite analysis for malaria and viral serology. In unexplained headache, particularly in the presence of drowsiness, plasma carboxyhaemoglobin may support a diagnosis of carbon-monoxide poisoning.

The acutely weak patient

The term ‘weakness’ will often be used by patients for a variety of complaints. Although the term should be reserved for the original definition of ‘reduced motor power’, many patients will confess to ‘weakness’ when in fact they are ‘fatigued’ or ‘lethargic’. It is reasonable to infer reduced motor power when weakness is present without significant tiredness. This should be contrasted with fatigue and lethargy, where the diminished power is generalized, commensurate with, and caused by significant tiredness. This should form the basis of initial questioning. (’Do you feel weak because you are tired, or do you think that you have specifically lost muscle power?’) One should realize that often, even the best clinical history taker and the best historian will not differentiate between weakness, fatigue and lethargy. It should be noted that the term ‘fatigue’, which is used here synonymously with the term ‘lethargy’, should not be confused with the neurological term ‘fatiguability’ (Table 8.17).

Table 8.17 Logical thinking for conditions causing acute weakness

Scenario	Common or important examples
Fatigue or lethargy leading to generalized weakness	Chronic heart failure, chronic lung disease, sleep disorders, anaemia, chronic kidney disease, diabetes mellitus, chronic infection, malignancy, depression
Loss of motor power leading to generalized weakness	Myasthenia gravis (crisis), post-infectious inflammatory polyneuropathy (‘Guillain-Barré syndrome’), acute myopathy (myositis, rhabdomyolysis)
Hemiparesis or hemiplegia (weakness or total paralysis of one side of body)	Lesion in contralateral cerebral motor cortex or contralateral brainstem Lesion in ipsilateral high cervical cord (often with ipsilateral dorsal column, i.e. proprioception deficit, and contralateral spinothalamic tract deficit, i.e. pain and temperature)

Monoparesis or monoplegia (weakness or total paralysis of single limb) Paraparesis or paraplegia (weakness or total paralysis of both legs) Quadriparesis and quadriplegia (weakness or total paralysis of both arms and both legs)

When assessing the patient, it is also helpful to differentiate between lesions of the ‘upper motor neurone’ (lesions of the motor cortex or pyramidal tracts) from the ‘lower motor neurone’ (lesions of the ‘motor unit’, that is the anterior horn cell, axon, neuromuscular junction or muscle). This differentiation is important in order to help direct investigations.

Acute quadriparesis and paraparesis deserve special mention. One should assume that the cause is external cord compression until proven otherwise. As recovery from the latter depends on speedy decompression, one should urgently organize imaging and specialty assessment. Any delay in imaging should not lead to a delay in specialty assessment.

The history should establish the speed of onset and distribution of weakness. As in most cases, rapid onset of weakness over minutes suggests vascular pathology, whereas an onset over hours or days may suggest an infective or inflammatory condition. Associated pain is most often a consequence of nerve root or peripheral nerve involvement, and also occurs with acute myopathy, where there may be muscle tenderness. A careful drug history should be taken to identify agents such as chemotherapy drugs which may cause peripheral neuropathy, and a family history enquiry may uncover inherited muscle disorders. Risk factors for stroke, such as hypertension, hyperlipidaemia, diabetes mellitus, alcohol intake and smoking history should be documented.

On general inspection, one should look for gait disturbance, facial palsy, muscle wasting and fasciculation. One should test tone and reflexes before testing power, as muscle tone may be affected by pre-existing muscle contraction. Diminished tone and diminished reflexes are seen in lower motor neurone conditions. In addition to formally testing power, a quick functional test for power is to ask the patient to: stand from a sitting position, testing hip and knee extension; walk on his heels, to test ankle dorsiflexion; and walk on his toes, to test ankle plantarflexion. Coordination should be tested in the upper limbs (finger-to-nose tests) and lower limbs (heel-to-knee-to-toe), though one should be aware that weakness in itself will affect coordination. Sensory examination, testing for sensory loss, paraesthesiae, hyperaesthesiae and pain, will only be meaningful in cooperative and coherent patients. This should not prevent the clinician from attempting to establish sensory deficits consistent with nerve, nerve root or central pathology.

Timely cranial CT scans are essential in stroke, while MR scans are useful in a variety of cranial and spinal cord lesions. The spinal cord MR scan should be booked as an emergency when cord compression is suspected. Nerve conduction studies and electromyography (EMG) are useful to confirm the diagnosis of Guillain-Barré syndrome and, on occasions, will help differentiate peripheral nerve from nerve-root pathology.

The patient with abdominal pain

The differentiation of abdominal pain into ‘medical’ and ‘surgical’ causes, although occasionally useful, is often artificial. This type of arbitrary categorization may lead to the missing of ‘non-surgical’ causes including metabolic syndromes and cardiac-referred pain. Furthermore, many patients with acute abdominal pain from surgical conditions will have coexisting medical conditions. It is important, therefore, for the general physician to have a sound working knowledge of the mechanisms and common causes of abdominal pain, so as to know when urgent surgical assessment and intervention is needed (Table 8.18).

Table 8.18 Logical thinking for conditions causing acute abdominal pain

Mechanism	Common or important examples
Enteral visceral pain (usually colicky pain)	Oesophageal spasm or oesophagitis, duodenal ulcer, small bowel enteritis or ischaemia, colitis, colonic obstruction or ischaemia, complex gut perfusion deficit (diabetic ketoacidosis, sickle crisis)
Non-enteral visceral pain	Gallbladder pain from cholecystitis, pancreatic pain from pancreatitis or malignancy
Peritoneal pain (exacerbated by any changes in intra-abdominal pressure such as coughing, moving)	Perforated enteral viscus (gastric, duodenal, small bowel, appendix, large bowel), perforated non-enteral viscus (gallbladder, spleen, ruptured ectopic pregnancy), inflamed organ (pancreatitis), spontaneous bacterial peritonitis, malignant infiltration, bleeding vessel
Non-visceral pain	Aortic aneurysm, renal colic, referred pain

It is important to be familiar with some principles governing the location of pain. Oesophageal, gastric or duodenal pain may be evident over the lower chest or epigastrium (and oesophageal pain may radiate to the arms); gallbladder pain usually commences in the right upper quadrant, and often radiates around the right chest wall to the right dorsal area; pancreatic pain usually localizes over the epigastrium and radiates through to the back; pain from the small bowel is often manifested diffusely or over the periumbilical area, whereas large bowel pain is usually found over the site of the pathology or lesion (e.g. splenic flexure); pain from the distal colon may be referred to the lumbar area; any pathology affecting or irritating the diaphragm (e.g. a subphrenic abscess) may present with referred pain in the shoulder; ureteric colic usually radiates from the flank to the inguinal area on the affected side (‘loin to groin’).

In contrast, pathology in areas distant to the abdomen may present with referred or radiated pain in the abdomen. For example, pneumonia, pleuritis and pleural effusions may manifest as upper quadrant pain on the affected side, and coronary artery pain may be felt most in the epigastrium. When taking a history, establishing the abdominal location of pain will help identify the affected organ, using the principles outlined above. The speed of onset of pain is also relevant; rapid onset may be associated with vascular catastrophes and rupture. The timing of the last menstrual period and the possibility of pregnancy should be considered in the appropriate age group. There may be some association between eating and abdominal pain: exacerbation by food may indicate gastritis, intestinal obstruction or gut ischaemia, whereas rapid relief upon eating may be suggestive of peptic ulceration. The presence of diarrhoea with or without blood may be suggestive of gut infection, inflammatory bowel disease or gut ischaemia.

The examination should initially focus on general features, such as hydration and cachexia, and vital parameters including respiratory rate, peripheral pulses, heart rate and blood pressure. Peritonitis may particularly be associated with severe hypotension or shock. Abdominal distension consistent with intestinal obstruction should be noted. Initial palpation may reveal diffuse, severe tenderness consistent with peritoneal inflammation, or localized tenderness. Rectal examination should be performed as a matter of routine; rectal masses and evidence of bleeding per rectum should be identified. If there is any suspicion of pelvic pathology, a gynaecological opinion should be sought.

General investigations which may help include full white cell count, haemoglobin, urea and electrolytes, liver function tests, amylase and pregnancy test (for the appropriate age group). Samples of diarrhoea should be sent for Clostridium difficile toxin analysis and also culture. A chest X-ray may demonstrate a perforated viscus or primary chest pathology. Erect and supine abdominal films may show features of obstruction. Abdominal ultrasound may demonstrate biliary tract dilatation or ureteric stones. Abdominal CT scans may reveal free fluid, the site of intestinal obstruction, pancreatic structure, evidence of ruptured aortic aneurysm or some detail with regard to intra-abdominal masses. Sigmoidoscopy may be useful if inflammatory bowel disease is suspected.

The patient with haematemesis or melaena

These are common causes of presentation to the emergency department. The term ‘haematemesis’ describes the vomiting of blood, which may be bright red and fresh, or altered (commonly described as ‘coffee grounds’). The presence of haematemesis usually means acute bleeding from a source above the duodenojejunal flexure. ‘Melaena’ is faeces made up of digested blood; it has a black (often described as ‘jet black’), tarry appearance, and possesses a characteristic and offensive smell. Although its presence may suggest acute bleeding from any source proximal to the ascending colon, the commonest source is in the upper-gastrointestinal tract (Table 8.19).

Table 8.19 Logical thinking for conditions causing haematemesis or melaena

Mechanism	Common or important examples
Peptic ulcer disease	Gastric or duodenal (with or without Helicobacter pylori colonization)
Inflammation of upper gastrointestinal tract	Reflux oesophagitis, gastritis, duodenitis (the latter two often occur secondary to excess alcohol intake or usage of non-steroidal anti-inflammatory drugs)
Oesophageal and/or gastric varices, or portal hypertensive gastropathy	Portal hypertension from chronic liver disease
Coagulopathy or increased bleeding tendency	Liver synthetic dysfunction, altered warfarin metabolism (infection, antibiotics), clotting factor deficiencies, thrombocytopenia, anti-platelet drug usage (aspirin, clopidogrel), recent thrombolytic therapy – note: over-anticoagulation may reveal bleeding from specific pathology previously unknown
Upper gastrointestinal malignancy or malformation	Oesophageal carcinoma, gastric carcinoma, upper gastrointestinal angiodysplasia (vascular malformation)
Mallory–Weiss tear	Tear of lower oesophagus or upper stomach from recurrent vomiting
Nose bleeds (epistaxis)	A large amount of swallowed blood may lead to melaena

The passing of fresh blood per rectum (as opposed to melaena) usually means that the source of bleeding is in the large or small bowel. However, it is possible for very rapid upper gastrointestinal bleeding to lead to fresh blood per rectum as there is insufficient time for melaena to develop. Patients who incidentally describe dark stools without the characteristic appearance and smell of melaena do not usually have gastrointestinal bleeding. Iron-stained stool is black but usually solid and formed.

One should take a detailed history, including epistaxis, alcohol intake, pre-existing liver disease and both prescription and over-the-counter drugs. One severe or several episodes of vomiting before the onset of haematemesis may suggest a Mallory-Weiss tear. Epigastric pain may suggest peptic ulcer disease, and unexplained weight loss and anorexia could be due to malignancy.

The initial examination should focus on identifying if the patient is shocked and acting accordingly (see above). Young, otherwise fit hypovolaemic individuals may compensate with raised cardiac output and remain normotensive for some considerable time, but may exhibit a fall in blood pressure on sitting or standing up. Features of malignancy (cachexia, supraclavicular lymphadenopathy, abdominal mass) and chronic liver disease (spider naevi, palmar erythema, jaundice, splenomegaly, ascites) should be identified. The clinical features of anaemia could suggest that there has been a period of occult bleeding before the acute bleed. Rectal examination is mandatory to see if there is objective evidence of melaena or fresh blood.

The initial investigations should include full blood count, clotting screen, urea, electrolytes and liver function tests. Blood should be ‘grouped and saved’, unless the patient is shocked, in which case (for example) four units of blood should be ‘cross-matched’ immediately. Blood is the best replacement fluid for a shocked patient with gastrointestinal bleeding, but should not necessarily be given immediately for the stable patient who is anaemic.

The Rockall score predicts mortality based on initial clinical parameters (Table 8.20). A score of 0 or 1 predicts a very low mortality, and the patient often does not need admission and can go for urgent outpatient investigation. A score of 8 or more predicts a mortality of >25%. There may be occasions when the patient’s history (or collateral history from a relative) of haematemesis or melaena is not substantiated by the overall assessment in the emergency department, and the Rockall score is 0 or 1. In these situations, significant gastrointestinal bleeding is excluded on clinical grounds and occult blood testing of stool or vomit (using urine dipsticks) is not helpful for decision-making.

Upper gastrointestinal endoscopy is the essential initial investigation for haematemesis or melaena. If the Rockall score predicts a patient at risk, this should be done urgently and out of hours if necessary. An endoscopy within the first 24 hours increases the diagnostic yield, and if there is no active bleeding, no endoscopic stigmata of recent bleeding and no varices, the patient can be safely discharged. Recently bled ulcers and varices can be treated endoscopically, which reduces the need for blood transfusion, the need for surgery and mortality. If the source of bleeding is thought to be in the small or large bowel, different investigations will be needed after the resolution of any shock, such as lower gastrointestinal endoscopy or angiography.

The patient with diarrhoea and vomiting

Both diarrhoea and vomiting are often non-specific symptoms. In the absence of additional clinical features, the numerous possible causes provide a substantial challenge to the clinician, and therefore history taking and direct questioning are particularly important. Many patients describe ‘diarrhoea’ in a variety of circumstances; it is reasonable to accept the term when there has been at least an increased frequency of watery faeces (Tables 8.21 and 8.22).

Table 8.21 Logical thinking for conditions causing vomiting

Mechanism	Common or important examples
Upper gastrointestinal obstruction	Malignant or benign tumours of upper gastrointestinal tract; benign stricture of upper gastrointestinal tract (e.g. pyloric stenosis)
Upper gastrointestinal inflammatory pathology or infections	Acute cholecystitis; acute pancreatitis; acute hepatitis; infective gastritis (often presents as vomiting and diarrhoea, e.g. norovirus)
Raised intra-abdominal pressure	Pregnancy
Constipation	Almost exclusively in elderly patients
Systemic effects of infection	Pneumonia; urinary tract infection
Endocrine, metabolic and toxic	Uraemia; cholestasis; hypercalcaemia; diabetic crisis (ketotic and non-ketotic); thyrotoxicosis; hypoadrenalism; drugs (recreational, antibiotics, chemotherapy, opiate analgesic drugs); alcohol
Any cause of vertigo	Peripheral rather than central pathology will more commonly lead to nauseation and vomiting (see Ch. 20)
Raised intracranial pressure	Space-occupying lesions in the brain; hydrocephalus; benign intracranial hypertension
Psychiatric	Bulimia

Table 8.22 Logical thinking for conditions causing diarrhoea

Mechanism	Common or important examples
Infections (enteritis)	May present as vomiting and diarrhoea (gastroenteritis); viral; bacterial (Salmonella, Shigella, Yersinia, Campylobacter, Escherichia coli, Clostridium difficile); protozoal (particularly giardiasis); amoebae
Tumours of small or large intestine	Colonic carcinoma; small bowel lymphoma; rectal villous adenoma
Bowel inflammation	Inflammatory bowel disease (Crohn’s disease; ulcerative colitis); radiation colitis; ischaemic colitis
Endocrine, metabolic or toxic	Thyrotoxicosis; hypoadrenalism; Zollinger-Ellison syndrome; drugs (antibiotics, proton pump inhibitors, non-steroidal anti-inflammatory drugs)
Malabsorption	Coeliac disease; tropical sprue
Miscellaneous	Irritable bowel syndrome; ‘overflow’ diarrhoea in the setting of constipation (this occurs almost exclusively in elderly patients); laxative abuse

When taking a history, the relative prominence of vomiting or diarrhoea should be established, as this should help direct further questioning. When vomiting and diarrhoea are as prominent as each other in the absence of any other pointers, infective gastroenteritis is the most likely cause. A short relationship between eating and vomiting may suggest an obstructive pathology. Brown vomitus (‘faeculent vomiting’) may indicate small intestinal obstruction. One should enquire about close contacts having similar symptoms, to investigate the possibility of contaminated food or water. A meticulous travel and drug history should be taken. Recent antibiotic usage will mean the need to test for, and probably treat, Clostridium difficile. With regard to diarrhoea, there may be some historical features which may help identify the focus of pathology: frequent amounts of small volume diarrhoea may suggest a rectal lesion; in contrast, small bowel disease may lead to large volumes of diarrhoea; if this is also foul smelling, floating and pale, one should suspect small bowel malabsorption. Bloody diarrhoea indicates colonic disease, particularly inflammatory bowel disease, ischaemic colitis and infective colitis (especially Salmonella and Shigella).

As always, the examination should initially aim to identify features of hypovolaemia which have been described elsewhere. General examination should include inspection and palpation for cachexia, jaundice and lymphadenopathy. Pain on palpation, guarding and masses should be identified on abdominal examination. Features of obstruction may be seen and auscultated, namely abdominal distension, visible peristalsis and ‘tinkling’ bowel sounds. One should identify masses and blood on rectal examination.

Initial investigations should examine for blood loss, infection and dehydration, therefore full blood count, C-reactive protein, urea and electrolytes are required. Liver function and plasma calcium should be checked. If malabsorption is suspected, serum albumin is important, as well as haematinic measurements. In cases of diarrhoea, stool microscopy (looking for ova, cysts and parasites), culture and Clostridium difficile toxin assay should be performed. Supine abdominal X-rays may display features of intestinal obstruction, and this may be further investigated with abdominal CT scans, especially when malignancy is suspected. Upper gastrointestinal endoscopy may be helpful in cases of upper gastrointestinal obstruction, while lower gastrointestinal endoscopy and biopsy may clinch the diagnosis in inflammatory bowel disease or colonic cancer.

The jaundiced patient

Jaundice is both a symptom and a sign, is common and has numerous causes which include emergency, urgent and debilitating conditions. It is important, therefore, to have a logical and systematic approach to diagnosing the underlying pathology.

The traditional classification of the causes of jaundice into ‘prehepatic’, ‘hepatic’ (or ‘hepatocellular’) and ‘posthepatic’ is tried and tested. A more detailed analysis can be based on the way in which any pathology relates to the metabolism of bilirubin, but this is beyond the scope of this chapter (Table 8.23).

Table 8.23 Logical thinking for conditions causing jaundice

Mechanism	Common or important examples
Prehepatic	Haemolysis, Gilbert’s syndrome (jaundice appears when starving)
Hepatic	Acute hepatitis (alcohol, viral hepatitis, autoimmune, drugs); chronic liver disease (either advancement or acute-on-chronic)
Posthepatic (obstructive)	Intrahepatic cholestasis (drugs, pregnancy, postviral, chronic liver disease); common bile duct obstruction (gallstone, porta hepatis lymph node, pancreatic cancer, bile duct cancer)

When taking a history, it should be remembered that haemolytic jaundice is milder than the other forms. One should specifically enquire about risk factors for viral hepatitis including food exposure, travel, IV recreational drugs, body piercing, blood transfusion and sexual history. A detailed drug and alcohol history is essential, as well as questions about abdominal pain and weight loss. Pale stools and dark urine are classically present with posthepatic jaundice.

On examination, one may identify general features such as fever, tattoos and needle marks. There may be cachexia or lymphadenopathy, which may be suggestive of malignancy. There may be obvious features of chronic liver disease, for example spider naevi, palmar erythema, splenomegaly or ascites. Hepatomegaly and splenomegaly should be identified if present. If the gallbladder is palpable in posthepatic jaundice, a gallstone cause is less likely (Courvoisier’s law – a gallbladder containing stones is usually fibrotic and cannot enlarge enough to become palpable).

General investigations will include liver function tests. A raised white cell count and C-reactive protein may suggest an infective process. Clotting derangement may point to liver synthetic dysfunction or vitamin K malabsorption in posthepatic jaundice. Serum transaminases raised much more than alkaline phosphatase suggests a hepatitic cause. A full viral hepatitis screen will be needed. Most jaundiced patients need an abdominal ultrasound scan, unless acute viral hepatitis is obvious. Ultrasound makes an accurate assessment of the gallbladder but the exact nature of extrahepatic biliary obstruction is often better seen on CT (or MR) scanning.

Some special scenarios

In addition to the common clinical scenarios already described, the clinician will also face additional situations and circumstances which need a strategic approach on behalf of the patient. Three important examples are pain, aggression and general vulnerability.

The resolution of pain should be given the utmost priority. In the past, it had been presumed that the prescription and administration of analgesia would lead to loss of clinical signs, and therefore missed diagnoses. This concept has never been substantiated and is inhumane. One should be aware of the basic principles of the categorization of pain, and the agents which best deal with visceral, inflammatory and neurogenic pain. Most hospitals have pain ‘teams’, which should be utilized if appropriate. When it is apparent that there may be a functional aspect to pain, such as depression or behavioural disorders, every effort should be made to tackle the source.

Aggression, to the point of violence, may be seen in consequence to acute confusional states (see Ch. 7) and true psychiatric disorders. Irrespective of the cause, every effort must be made to keep the patient safe from harm, and also safeguard the surrounding staff. This may involve the application of humane physical restraint; the methods used should ideally be predetermined and part of the hospital protocol. The administration of sedation should be planned and prescribed by experienced individuals. Additional help may be provided by psychiatrists, and psychiatrically trained nurses, and by intensive care clinicians if high-dose intravenous sedation is considered.

Vulnerability may come in many guises. Frail and elderly patients may live in precarious circumstances, where minor changes in functional ability may lead to decompensation. In these cases, when a minor urinary tract infection may cause an acute confusional state and inability to cope in the living environment, it is vital to recognize that the medical diagnosis is often the minor issue. It is the functional support with physiotherapy and augmented nursing care which will determine outcome, as well as antibiotics. Patients in police or prison custody often need emergency department care. In these circumstances, the safety of the police and prison officers, and of the general public, will need to be carefully balanced with the basic medical and human rights of the patient, including the right to confidentiality. Patients who do not speak the same language as their medical attendants will have difficulty receiving high-quality healthcare. Advocates and interpreters are often not available throughout the day and night, or in the right language, and their lack can impede rapid and accurate diagnosis. Patients in poverty or who are homeless will not access healthcare efficiently, and will often present to the emergency department in the later stages of illness, occasionally with opportunistic infections.