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Preface
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Clinical medicine involves the intertwining of
the lives of our patients with the health conditions that affect them. e course of an illness
may change in a matter of seconds or hours, but
many conditions progress and impact on the life
of the patient for several months or even years.
With an increasing reliance on shi work,
handovers and specialist referrals, seeing patients
longitudinally throughout their illness is less
common than it used to be. is has had a significant effect on our education and understanding
of disease progression.
In the past, clinical case books have all too
oen provided a snapshot in time, looking at what
happens to patients during a single episode. A
short vignette leads directly to questions focused
on identifying the diagnosis and the immediate
treatment required. However, we feel that this
ignores the way in which the process of disease
affects both our patients and our care for them.
We feel the need for a new paradigm that looks
at a longer time period, acknowledging the existence of developing clinical presentations and
complications which may present over the course
of several chronological episodes.
erefore, we have developed a new style of clinical ca ses, presenting the cases with a timepoint structure, taking you step-by-step through key moments
where new information becomes available, where
investigations require action, or other moments
where there is an important learning point.
We have created a series of clinical cases which
cover a range of important medical conditions,
constituting around five cases for each of the
major internal medical specialities: cardiology,
respiratory, gastroenterology, endocrinology,
rheumatology and neurology. Other important
areas such as oncology, infectious disease, toxicology, haematology, renal medicine and geriatrics
are also covered to make up a total of 40 cases.
is book is designed to complement the
learning of senior medical students and doctors
early in their training. e scope includes scenarios based within hospital medicine but, importantly, also includes timepoints based in primary
care and other community settings, as these are
also places where junior doctors are expected to
practice semi-autonomously.
We are deeply grateful for the help and support
provided by a wide range of people in the development of this book. First and foremost, we would like
to thank Dr Priti Dutta, a remarkable radiologist,
who has contributed all of the outstanding radiology images included in this book. We thank those
who have contributed partial clinical cases: Dr Tara
Belcher, Dr Sophie Anne Elands, Dr Martin Glasser
and Dr Rachel Tresman. We are also grateful to a
number of people who have reviewed and edited
content, including Dr Rebecca Bamford, Dr Katya
Christodoulou, Dr Asma Fikree, Dr David Fisher,
Louise Greenberg, Dr Catriona Hayes, Dr Rammya
Mathew and Dr Yael Santhouse. Finally, we would
like to thank our exceptional publishing team at
CRC Press, Jo Koster and Julia Molloy, without
whom this book would not have been possible.
Please inform us of any errors or anything
else that you feel is worthy of comment for future
editions.
Enjoy!
From the co-author team,
Andrew Solomon, Julia Anstey and Liora Wittner
xi
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Case 1
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TIMEPOINT 1
Mr Marsh, a 35-year-old teacher, has presented
to the emergency department with a 2-day history of feeling weak in his legs and increasing difficulty walking. He is normally very active and
plays football in his spare time; however, he is
now finding it difficult to stand for more than a
few minutes. Over the last day, he has started to
suffer from pins and needles in his arms and feet
and has pain in the rear of his neck. His bowels
are functioning normally, but he has found that
he is urinating more frequently than usual.
Prior to this, Mr Marsh has been generally
well, apart from having ‘food poisoning’ 3 weeks
ago. He has no significant past medical history,
is currently on no medications and has no drug
allergies. He does not smoke and drinks alcohol
socially twice a week.
His observations are:
Respiratory rate: 14/min
Oxygen saturations: 99% on room air
Temperature: 36.8°C
Blood pressure: 112/74 mmHg
Heart rate: 72 bpm
On examination, Mr Marsh looks generally well.
Cardiorespiratory and abdominal examinations
are normal. A neurological examination of the
upper limbs revealed asymmetric and variable
power in the biceps, triceps and other muscle
groups with altered sensation in an indistinct
distribution across both arms. Examination of
the lower limbs revealed increased tone, generalised reduced power (MRC 4+) amongst all
muscle groups, normal to brisk reflexes, positive
Babinski sign and generally impaired coordination. Rectal exam showed normal tone.
What investigations should be
arranged?
Urinalysis
Bladder scan
Bloods – FBC, U&Es, ESR, CRP, serum B12
and folate
Lumbar puncture (preceded by CT head)
MRI spinal cord
MRI brain
Urinalysis was normal. A bladder scan showed
an empty bladder.
Initial blood tests showed the following:
Venous blood results
Haemoglobin 140 g/L
9
White cell count 6.0 × 10
Platelets 253 × 10
Sodium 139 mmol/L
Potassium 4.4 mmol/L
Urea 6.1 mmol/L
Creatinine 90 μmol/L
A lumbar puncture was performed, which
showed the following:
Lumbar puncture results
CSF fluid Clear
CSF protein 1.2 g/L
CSF glucose 4.1 mmol/L
CSF cell count High
Plasma glucose 4.8 mmol/L
Gram stain No organisms
/L
9
/L
DOI: 10.1201/9781351257725-1
1
2 Clinical Cases
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e MRI spine is shown in Figure 1.1.
Figure 1.1 (a) Sagittal T2 MRI image through
the cervical spine; (b) Sagittal T1 images
through the cervical spine; (c) The red line
demarcates a long segment of abnormal T2
increased signal within the cord. Imaging
diagnostic criteria for transverse myelitis involve
the demonstration of long segments (3 to 4
vertebral body heights or more) of spinal cord
signal change, occupying more than two-thirds
of the cross-sectional area of the cord. These
may demonstrate variable patterns of enhancement and restricted diffusion
e MRI is reported as follows: altered T2 and
gadolinium enhanced signal within the spinal cord
from the level of C3 to C7, with no suggestion of
any compressive/space-occupying lesion.
e clinical findings suggest a diagnosis of
idiopathic transverse myelitis.
What are the diagnostic criteria for
transverse myelitis?
e Transverse Myelitis Consortium Working
Group suggests the following diagnostic criteria:
Development of sensory, motor or autonomic
dysfunction attributable to the spinal cord
Bilateral signs and/or symptoms (though not
necessarily symmetric)
Clearly defined sensory level
Exclusion of extra-axial compressive
aetiology by neuroimaging (MRI or CT
myelography)
Inflammation of the spinal cord demonstrated by CSF pleocytosis, elevated IgG index
or MRI gadolinium enhancement
Progression to nadir between 4 hours and 21
days following the onset of symptoms
A significant percentage of patients presenting
with a clinical pattern resembling transverse
myelitis do not meet the inflammatory features of the criteria. It is important to note that
the absence of inflammatory markers does not
exclude transverse myelitis as the diagnosis.
How should Mr Marsh
be managed?
First line: high-dose IV glucocorticoids for 3–5
days (either methylprednisolone, 1000 mg daily,
or dexamethasone), alongside supportive care
and acute rehabilitation.
Second line: plasmapheresis with supportive care and acute rehabilitation – for CNS
demyelinating diseases that fail to respond to
glucocorticoids.
TIMEPOINT 2
Four days aer admission, Mr Marsh is seen on
the morning ward round. He says he is starting to
Case 1: Timepoint 4 3
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feel better already, and has been working with the
physiotherapists to try to get his strength back.
He has been having regular bedside capillary
blood glucose monitoring aer starting on steroids. e nurse notes that he had one value of 9.8
mmol/L yesterday evening, but all of the values
preceding this had been <7.8 mmol/L.
e medical team tested his HbA1c which
came back as 44 mmol/mol.
What does this HbA1c value mean?
Mr Marsh is pre-diabetic. Diabetes can
be diagnosed if HbA1c ≥48 mmol/mol.
Pre-diabetes is diagnosed if the value
is 42–47 mmol/mol
Continue to monitor his capillary blood
glucose
Blood glucose may return to normal once he
has finished his course of steroids
TIMEPOINT 3
ree months later, Mr Marsh is back at work,
but only standing in the classroom for brief periods and, in addition to ongoing regular physiotherapy, is doing gentle floor Pilates twice a week.
His GP plans to arrange another HbA1c test. Mr
Marsh, who has a relative with diabetes, thought
that HbA1c values were usually expressed as a
percentage. e GP explains that the standard is
now to use the mmol/mol unit. e repeat HbA1c
result is 42 mmol/mol (6%), which is reassuring.
What is the quick, simple method to
convert HbA1c mmol/mol values to
percentages?
It is the ‘Minus 2 rule’ – the exact digit percentages convert to mmol/mol, by subtracting 2 for
the larger and smaller figure; for example; 9% =
75; 8% = 64; 7% = 53; 6% = 42.
TIMEPOINT 4
A year later, Mr Marsh is referred to a neurology
outpatient clinic, as he has noticed that he gets a
tingling sensation down his back and legs when
he looks down and is worried that this might be
related to his previous symptoms.
What is the name of this
phenomenon, and what might it
indicate?
Lhermitte’s phenomenon – a tingling or ‘elec-
trical sensation’ running down the back and
into the limbs, elicited by neck flexion
It is an indicator of demyelination
is may suggest that he is developing mul-
tiple sclerosis; however, it can also be seen
in a number of other neurological disorders
including transverse myelitis, vitamin B12
deficiency (subacute combined degeneration
of spinal cord) and compression of the cervi-
cal spinal cord among others
What are the long-term implications
of transverse myelitis?
Recovery is likely to begin within 1–3 months;
however, recovery is oen only partial with
30–40% of patients retaining some degree of
disability. Recurrence is also seen in 25–33%
of patients with idiopathic transverse myelitis,
while in disease-related transverse myelitis
(connected to a wider neurological disease or
other inflammatory conditions) this figure can
rise to 70%.
ere are some features that have been recognised to increase the chance of recurrence,
which are oen markers of a wider or more severe
illness:
Multiple lesions in the spinal cord on MRI
Finding of brain lesions on MRI
Autoantibody positivity for autoantibodies
ANA, dsDNA, anti-phospholipid, c-ANCA
Oligoclonal band positivity in the cerebrospi-
nal fluid
Positive test for NMO-IgG (anti-aquaporin-4)
antibody
4 Clinical Cases
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ose with severe acute complete transverse
myelitis have the overall best prognosis as they
are less likely to present with oligoclonal bands,
less likely to suffer a relapse and have a low rate of
transition to multiple sclerosis.
What is the risk of multiple sclerosis
in such patients?
ere is a notable risk of developing MS following an episode of transverse myelitis. is rate
is between 5–30% over 3–5 years in patients in
whom the initial cause is unknown, depending on whether it is acute complete (5–10%) or
acute partial (10–30%). If at initial presentation of
partial transverse myelitis there are already cranial lesions typical of MS seen on MRI, this rate
goes up to 60–90% over 3–5 years.
What are the differential diagnoses
of idiopathic transverse myelitis?
See Figure 1.2.
FURTHER READING
1. Proposed diagnostic criteria and nosology
of acute transverse myelitis. Transverse
Myelitis Consortium Working Group.
Neurology 2002.27;59 (4):499–505.
SECONDARY TM
Dierentials of idiopathic transverse myelitis
INFECTION
– West Nile virus
– Herpes
– CNS Lyme disease
– Mycoplasma
– Brucella
– Intravascular lymphoma
s
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DISORDERS
ACQUIRED CNS
DEMYELINATING
DISORDERS
NON-MYELOPATHIC
– Multiple sclerosis
– Neuromyelitis optica
– Acute disseminated encephalomyeliti
– Guillain–Barré
– Acute Inflammatory
Demyelinating Polyneuropathy
(AIDP)
Further Reading 5
MYELOPATHY
– Vascular
– Anterior spinal artery infarction
– Spinal-dural arteriovenous fistula
– Fibrocartilagenous embolism
– Metabolic & Nutritional
– Vit B12 deficiency
NON-INFLAMMATORY
– Disc herniation
– Epidural masses/blood
– Vertebral body
COMPRESSION
SYSTEMIC
compression fractures
DISEASE
– SLE
– Sjögren's
RHEUMATOLOGICAL
– Vit D deficiency
– Spondylosis
– TB
syndrome
– Sarcoidosis
– Vit E deficiency
– Copper deficiency
– Nitrous oxide toxicity
– Neurolathyrism & Neurocassavism
– Neoplasms
– Intramedullary primary spinal cord tumour
– Primary CNS lymphoma
Figure 1.2 The differential diagnoses for idiopathic transverse myelitis.
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Case 2
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TIMEPOINT 1
Mr Patel, a 60-year-old businessman, collapsed
at home and was brought into the emergency
department by ambulance. At 11 am this morning he had been working from home, when his
wife heard a thud and rushed into the room to
find that he had collapsed and was unconscious.
He describes feeling light-headed for a few seconds before ‘blacking out’. His wife thinks he was
unconscious for about 30 seconds before waking up. He did not bite his tongue or make jerky
movements and was not incontinent of urine or
feces. Upon waking, he was particularly short
of breath and his lips looked blue. He has had a
cough for the past week.
His past medical history includes obesity,
hypertension and high cholesterol, for which he
takes atorvastatin, amlodipine and ramipril. He
had a previous deep-vein thrombosis 4 years ago.
He has recently been under a lot of extra family
and professional stress, making several long journeys to business meetings in the last few weeks. He
has no allergies, drinks occasionally and smokes
8 cigarettes per day. He went to see his practice
nurse for a health check 6 weeks ago, where they
discussed weight loss and smoking cessation. He
has had no recent trauma or surgery.
On examination, Mr Patel’s observations are:
Respiratory rate: 26/min
Oxygen saturations: 92% on high-flow oxygen
(79% before oxygen administered)
Temperature: 36.8°C
Blood pressure: 85/65 mmHg
Heart rate: 110 bpm
Cardiorespiratory examination reveals a raised
JVP and loud S2 heart sound. His fingertips and
lips have a blue discolouration. Lung fields are
clear on auscultation, percussion and vocal fremitus are normal and equal. He has cool peripheries. ere are no other examination findings of
note.
What investigations might be
ordered and why?
ECG – to look for a cardiac cause for collapse
or evidence of pulmonary embolism (PE)
Routine blood tests including D-dimer and
troponin – to look for MI or PE
ABG – may show reduced PaO2 and/or
PaCO
2
Chest X-ray – to look for lung pathology,
e.g. tension pneumothorax, or may show
Westermark’s Triad
Echocardiography – for structural abnormalities, e.g. aortic stenosis
CTPA – to investigate for PE
Investigations
Initial blood tests showed the following:
Venous and arterial blood results
D-Dimer 3867 ng/mL
pH 7.44
PaCO
2
PaO
2
HCO
3
Base excess 2 mmol/L
e ECG shows a dominant R wave in V1 and
sinus tachycardia.
4.8 kPa
7.7 kPa
22 mmol/L
DOI: 10.1201/9781351257725-2
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