Contents
Contributors
Preface
1 Unconsciousness and Coma
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
2 Calf Pain
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Outcome
Further reading
3 Chest Pain – Cardiac
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
4 High Fever
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
5 Vaginal Bleeding
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
6 Transient Weakness
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Outcome
Further reading
7 Abdominal Pain – Epigastric
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history, examination findings and investigations what is your principal working diagnosis?
Management
Outcome
Further reading
8 Acute Headache
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
9 Acutely Painful Joint
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
10 Chest Pain – Pleuritic
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
11 Dizziness
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Note
Further reading
12 The Intoxicated Patient
Question: What differential diagnosis would you consider from the history?
Case history revisited
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
13 The Shocked Patient
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
14 Palpitations
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
15 Low Back Pain
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principle working diagnosis?
Outcome
Further reading
16 Acute Confusion
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
17 Shortness of Breath
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Given the history and examination findings what is your principle working diagnosis?
Management
Outcome
Further reading
18 Collapse of Unknown Cause
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Question: Can this man be allowed to drive?
Further reading
19 Abdominal Pain
Question: What differential diagnosis would you consider from the history?
Case history revisited
Examination
Question: Given the history and examination findings what is your principal working diagnosis?
Management
Outcome
Further reading
Index
This edition first published 2009, © 2009 by Blackwell Publishing Ltd
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Library of Congress Cataloging-in-Publication Data
ABC of emergency differential diagnosis / edited by Francis Morris, Alan Fletcher.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4051-7063-5
1. Diagnosis, Differential--Case studies. 2. Medical emergencies--Diagnosis--Case studies. I. Morris, Francis.
II. Fletcher, Alan, 1968-III. Title: Emergency differential diagnosis.
[DNLM: 1. Diagnosis, Differential--Case Reports. 2. Emergency Treatment--Case Reports. WB 141.5 A137 2009]
RC71.5.A23 2009
616.07′5--dc22
2009004444
ISBN: 978-1-4051-7063-5
A catalogue record for this book is available from the British Library.
Contributors
Arun Chaudhuri
Consultant Acute Physician, Ninewells Hospital and Medical School, Dundee, UK
Sue Croft
SpR in Emergency Medicine and Acute Medicine, Medical Assessment Unit, Northern General Hospital, Sheffield, UK
Roger Dalton
SpR in Emergency Medicine, Emergency Department, Northern General Hospital, Sheffield, UK
Scott Davison
General Practitioner, Crystal Peaks Medical Centre, Peaks Mount, Sheffield, UK
Nicki Doddridge
Consultant in Acute Medicine, Emergency Department, Northern General Hospital, Sheffield, UK
Duncan Drury
SpR in General Surgery, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK
Alan Fletcher
Consultant in Acute Medicine and Emergency Medicine, Emergency Department, Northern General Hospital, Sheffield, UK
Rachel Foster
SpR in Infectious Diseases, Royal Hallamshire Hospital, Sheffield, UK
Claire Gardner
SpR in Acute Medicine, Emergency Department, Northern General Hospital, Sheffield, UK
Carole Gavin
Consultant in Emergency Medicine, Salford Hospital, Salford, UK
Steve Goodacre
Professor in Emergency Medicine, Emergency Department, Northern General Hospital, Sheffield, UK
Charles Heatley
General Practitioner, Birley Health Centre, Sheffield, UK
Sian Ireland
Consultant in Emergency Medicine, Royal Cornwall Hospital, Truro, Cornwall, UK
Kevin Jones
Consultant Physician, Acute Medical Receiving Unit, Royal Bolton Hospital, Bolton, UK
Richard Kendall
Consultant in Emergency Medicine, Addenbrookes Hospital, Cambridge, UK
Peter Lawson
Consultant Physician and Geriatrician, Northern General Hospital, Sheffield, UK
Tom Locker
Consultant in Emergency Medicine, Barnsley District General Hospital, Barnsley, UK
Suzanne Mason
Reader in Emergency Medicine, Northern General Hospital, Sheffield, UK
Francis Morris
Consultant in Emergency Medicine, Emergency Department, Northern General Hospital, Sheffield, UK
Alastair Pickering
Academic Clinical Lecturer and SpR in Emergency Medicine, Hull Royal Infirmary, Hull, UK
Karen Selby
Consultant in Obstetrics and Gynaecology, Jessop Hospital for Women, Sheffield, UK
Rachel Tattersall
Consultant Rheumatologist, Royal Hallamshire Hospital, Sheffield, UK
Preface
What makes a good doctor? One of many essential attributes is the ability to take a good history, appropriately examine, and apply sound clinical judgement to reach the correct diagnosis.
All 19 chapters in this book have the same format. Each starts with a patient’s history concerning a common complaint and asks you, the reader, to generate a differential diagnosis based upon the information supplied. This is then followed by the examination findings, thus helping you refine the diagnostic process so that you are able to arrive at a single principal working diagnosis. The emergency management of this condition is then discussed.
Our hope is that working through these cases will be enjoyable, and that you will refine your diagnostic skills.
Francis Morris
Alan Fletcher
CASE HISTORY
A 57-year-old man is found in an unconscious state at home. He was in bed when his wife left at 7.00 a.m. that morning to go to work. On her return home at 3.45 p.m., he was still in the same position in bed, unrousable, incontinent of urine, and the cup of tea she had left for him was untouched. He has been unwell recently, and prescribed a course of antibiotics and co-codamol from his General Practitioner for a discharging ear infection. He suffers from hypertension, type 2 diabetes mellitus and longstanding depression. His medication list shows that he has been prescribed gliclazide 80 mg twice daily, atenolol 25 mg once daily, ramipril 5 mg once daily and amitriptyline 25 mg once daily. He has no known allergies. His wife informs you that he has had bad headaches recently, but that no-one else at home has been unwell.
This man is in a coma, which is defined as ‘unrousable unresponsiveness’. Using the objective clinical assessment tool, the Glasgow Coma Score (see Table 1.1), coma is defined as a score of 8 or less. Those patients with a score between 14 and 9 are defined as having altered consciousness and those with a top score of 15 are normal, alert and orientated. When considering a differential diagnosis for the cause of a patient’s unresponsiveness it is important to consider those conditions that are easily reversible first.
The patient is a known diabetic. Hypoglycaemia or, less commonly, hyperglycaemia can result in altered consciousness and must be actively diagnosed and promptly treated. A simple bedside glucose test will identify abnormalities in blood glucose levels and will guide appropriate therapy.
It is essential that any patient with confusion, altered consciousness, coma or focal neurological signs has their blood glucose estimated as part of the initial assessment. Neurological signs resulting from hypoglycaemia usually resolve quickly with treatment, though the failure to recognise and treat hypoglycaemia promptly may lead to permanent neurological damage.
Table 1.1 The Glasgow Coma Score.
Eye opening | |
Spontaneously | 4 |
To speech | 3 |
To pain | 2 |
None | 1 |
Verbal response | |
Orientated | 5 |
Disorientated speech | 4 |
Inappropriate words | 3 |
Incomprehensible sounds | 2 |
None | 1 |
Motor response | |
Obeys commands | 6 |
Localises painful stimuli | 5 |
Withdrawal from pain | 4 |
Flexion to pain | 3 |
Extension to pain | 2 |
None | 1 |
Box 1.1 Drugs that can affect conscious level
Excess alcohol with or without other prescription or recreational drugs is the commonest cause of altered consciousness and not quickly reversible. Of all the drugs that affect a patient’s consciousness (see Box 1.1) opiates are the only group that are readily treatable. Opiate excess leads to coma, and life-threatening respiratory depression, but thankfully can be quickly and effectively treated by the antagonist naloxone. The signs of opiate poisoning are seen in Box 1.2. Naloxone should be administered to any patient with any signs compatible with opiate poisoning.
Box 1.2 Signs of opiate ingestion
Box 1.3 Signs of tricyclic anti-depressant overdose
Opiate excess should be considered in this man who has had access to the simple analgesic co-codamol, which is a combination of paracetamol and the opiate codeine.
Likewise amitriptyline overdose, a common cause of coma, should be considered in the light of his depression and access to the medication. The clinical signs of tricyclic anti-depressant overdose are found in Box 1.3.
Vascular causes of coma are common. This man is known to have hypertension, which puts him at risk of intracranial haemorrhage. The cardinal features of an intracranial haemorrhage are sudden onset of headache, altered consciousness and focal neurological signs. Spontaneous intracranial haemorrhage usually occurs either into the subarachnoid space or into the ventricles and brain substance itself giving rise to either subarachnoid haemorrhage or intra-parenchymal haemorrhage respectively (see Figure 1.1).
Strokes due to cerebral infarction usually present differently to intracranial haemorrhages. The most important difference is that in most strokes consciousness is not impaired. There may be difficulty communicating with the patient, due to expressive or receptive dysphasia, but conscious level itself is not often altered. In brainstem infarctions, which can produce ‘locked in syndromes’ patients are aware of their surroundings, but unable to respond or communicate, so the patient can appear to be comatose.
Infection can lead to coma, either systemic infection as in a septicaemic illness, or intracranial infection such as meningitis or encephalitis. Patients with meningitis or encephalitis may present in coma especially if there is raised intracranial pressure.
There will often be a preceding phase characterised by symptoms suggestive of meningeal irritation (stiff neck, headache, photophobia), the signs of raised intracranial pressure (irritability, altered level of consciousness, vomiting, fits) and infection (fever, lethargy). If Neisseria meningitidis is the causative organism, the characteristic petechial/purpural rash is seen in approximately 50% of patients (see Figure 1.2); other organisms can cause less well-defined rashes. Other causative organisms can be seen in Table 1.2.
Figure 1.1 Intracranial haemorrhage. CT scan of a patient with an extensive intra-parenchymal haemorrhage. Intra-ventricular blood is seen, as is dilatation of the temporal horns of the lateral ventricles suggesting hydrocephalus.
Figure 1.2 Purpuric rash.
Prompt recognition of the possibility of meningitis is vital, as if left untreated, it has a mortality rate approaching 100%.
This man has a discharging ear infection which could potentially be the source of intracranial infection.
Table 1.2 Causes of meningitis/encephalitis.
Bacterial | Neisseria meningitidis, Streptococcus pneumoniae, listeria (elderly), Haemophilus influenzae, TB |
Viral | Herpes simplex, Coxsackie, mumps, echovirus, HIV |
Fungal | Cryptococcus neoformans |
Other | Drugs (trimethoprim/NSAIDs), sarcoidosis, systemic lupus erythematosus |
Box 1.4 Atypical clinical signs in coma
Following a generalised seizure, patients can be unresponsive as part of a post-ictal state. Typically, though the patient may be in coma immediately following the fit, their conscious level quickly improves within 30–60 minutes, by which time they are usually able to provide you with a history of events. Evidence of urinary incontinence and tongue biting with bleeding in or around the mouth supports the diagnosis but is not diagnostic. The duration of this man’s unconscious state would be out of keeping with a post-ictal state.
However, on examination it would be important to look for evidence of ongoing seizure activity (e.g. hypertonicity) as status epilepticus may be a possibility.
Psychogenic coma is uncommon and accounts for less than 2% of all cases of coma and is strictly a diagnosis of exclusion. Accordingly, the patient must be assessed thoroughly to check for other causes of altered consciousness as conditions such as hydrocephalus and vertebral artery dissection have on occasions been initially labelled as psychogenic. There are a number of clinical features that may suggest that the patient is physiologically awake (see Box 1.4) but none could be said to be diagnostic.
Head injury is one of the commonest causes of coma but this man’s history is not suggestive of an intracranial injury.
Structural causes of coma are relatively rare. Intracerebral space-occupying lesions cause coma, either as a result of their mass effect on the brain, or because of the anatomical position of the lesion.
By far the most common cause of cerebral space-occupying lesions are tumours, either primary or secondary. Other causes include cerebral abscess, cysts (e.g. cysticercosis, third ventricular colloid cysts) and granulomas (e.g. sarcoidosis, TB).
Box 1.5 Metabolic causes of coma
Typically, space-occupying lesions are responsible for slowly progressive symptoms, though it is possible for acute coma to be caused by haemorrhage into a space-occupying lesion.
Carbon monoxide poisoning is a relatively uncommon cause of coma. Smoke inhalation, fumes from poorly maintained gas appliances and car exhaust fumes are all potential causes. If the poisoning is chronic, prodromal symptoms such as fatigue and headaches may provide clues as to the cause. It is common for members of the same household to be affected, and the lack of symptoms in his wife suggests that this is not the diagnosis.
Other metabolic causes not mentioned above are listed in Box 1.5.
On further questioning, the patient’s wife confirmed that he hadn’t taken any of the prescribed co-codamol or amitriptyline tablets as the bottles remained full, and that he didn’t drink alcohol.
They had a domestic carbon monoxide monitor, which had been checked recently and was in perfect working order.
Examination of the patient showed him to have a Glasgow Coma Score (GCS) of 7 (E2, M4, V1).
The patient had a clear airway and was breathing with a respiratory rate of 18 per minute.
There was no smell of alcohol or ketones on his breath. Chest auscultation revealed no abnormality. His heart rate was 94 beats/minute and regular, blood pressure was 180/105 mmHg and his temperature was 36.2oC. His bedside blood glucose level was 6.2 mmol/l.
There were no external signs of head injury, and examination of the thorax, abdomen and limbs was unremarkable. There was no visible rash.
His pupils were equally sized and reactive to light. His limbs were generally hypotonic with brisk reflexes on his right upper and lower limbs, with an upgoing right plantar reflex.
The clinical information given allows us to discount a number of the differential diagnoses.
The patient is not hypoglycaemic and there is no suggestion of opiate or amitriptyline ingestion. He is afebrile and has no evidence of meningococcal disease. The patient’s history of hypertension and the acute nature of the onset of coma strongly suggest a vascular cause such as an intracerebral haemorrhage.
This man is in coma and requires an urgent CT scan. As his GCS is 7, his airway is vulnerable and he requires a definitive airway. Intubation and ventilation is required. No specific management is required to control his blood pressure at this time.
A CT scan of the patient’s brain showed a large intracerebral haemorrhage, with intraventricular blood and hydrocephalus. Urgent neurosurgical advice was sought but unfortunately this man died during an operation to drain his hydrocephalus.
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CASE HISTORY
A 43-year-old man presents with pain and swelling in his right calf. Three days before he was aware of discomfort and cramping in his right calf associated with some swelling. He took paracetamol but the symptoms continued. On the day of presentation he had slipped on getting out of the shower and developed a pulling sensation in the back of his leg associated with a sudden increase in the amount of pain and consequently he is now walking with a limp. In the past he suffered with ulcerative colitis which was controlled with Salazopyrin and had recently received a course of ciprofloxacin for epididymo-orchitis. He is a smoker but there is no other relevant past medical history. He denies any other symptoms.
There are a variety of causes of calf pain which can be divided into those of sudden onset, which frequently have a musculoskeletal origin, and those of an insidious onset, which include important conditions such as deep venous thrombosis (DVT).
One of the commonest problems giving rise to sudden acute pain in the calf is a tear of the medial head of the gastrocnemius muscle (Figure 2.1). This injury is commoner in men and typically occurs in those individuals who are unaccustomed to regular exercise. The injury occurs when the leg is loaded and the person is involved in activities such as running up an incline, jumping or suddenly pushing off as in running for a bus. An audible pop or tearing sensation may be felt in the upper medial aspect of the calf causing the individual to occasionally complain of being struck by a flying object or hit from behind. The patient’s calf suddenly becomes painful and full weight bearing is difficult.
Clinical examination reveals localised tenderness to the medial head of the gastrocnemius muscle which may be associated with some swelling. Bruising and discolouration tends to appear days later when it has a tendency to track down the leg to the ankle.
Figure 2.1 Anatomical drawing of the gastrocnemius and plantaris muscle.
The plantaris muscle is a vestigial structure that comprises a small muscular belly and a long tendon. Rupture of this structure will also occur suddenly and painfully but unlike the much commoner gastrocnemius injury the clinical findings are much less specific, hence this is not a diagnosis that will be obvious on clinical examination.
Injury to the plantaris muscle is the diagnosis that one is usually left with when all other common causes of sudden calf pain have been excluded.
A Baker’s cyst is an outpouching of the synovium of the knee joint which occurs in people with an inflammatory or degenerative arthritis (see Figure 2.2). Patients may be aware that they have developed a Baker’s cyst because of a fullness in the popliteal fossa behind their knee. When the fluids leaks out of the synovium into the calf muscle it excites an intense inflammatory response giving rise to the sudden onset of pain and swelling.
Figure 2.2 Diagram showing a Baker’s cyst.
In a typical case the patient will complain of recurrent pain, stiffness and swelling of the knee joint and occasionally they notice how their knee symptoms and signs improve at about the same time as the pain and swelling develops in their calf. The moment of rupture may be felt as a sharp pain behind the knee when the patient is engaged in activities that will increase the pressure within the joint, e.g. squatting, or alternatively the leak may occur more insidiously giving rise to pain and swelling in the calf which may resemble the onset of a DVT.