Haemoptysis Diagnosis and Treatment

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Haemoptysis: Diagnosis and treatment
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Acute Medicine V11 N1:Acute Med 2/27/2012 7:37 PM Page 1
Acute
Medicine Official Journal of The Society for Acute Medicine (UK)
Online at: www.rila.co.uk

Editorial .................................................................................................................................................................................................. 2
Clinical Review
Magnesium and the Acute Physician..................................................................................................................................................3
R Allan & N Mara
Research, Audit and Clinical Practice

ECG dispersion mapping predicts clinical deterioration, measured by increase in the Simple Clinical Score ...................8
J Kellett, A Emmanuel & S Rasool
Improving the safety of patient transfer from AMU using a written checklist .........................................................................13
D Hindmarsh & L Lees
Where Do AMU Nurses Perceive Their Educational Needs? Results of the 20:10 project..................................................18
J Jepson, S Whitley, C P Subbe & L Grundy
Case Reports
A hot bath to calm what ails you – the Cannabis Hyperemesis Syndrome.............................................................................23
V Luther & L Yap
Endogenous endophthalmitis and liver abscesses.........................................................................................................................25

S Koay, S Jain, I Cropley, H Petrushkin & H Beynon
Picture Quiz: Question

A young patient with heart failure ....................................................................................................................................................28
H Patel, G Dhillon, A Bandali & N Patel
Trainee Section
Trainee Update......................................................................................................................................................................................29
A Daniel, K Freeman & A Miller
Journal Watch: November 2011-January 2012...............................................................................................................................30

KE Mellor & JR Neale
The patient presenting with acute hemiparesis..............................................................................................................................33

K Mahawish & O Otaiku
Haemoptysis: Diagnosis and Treatment ..........................................................................................................................................39

K Hurt & D Bilton
Viewpoint
Norovirus Outbreak on the AMU – A Lesson In Shared Clinical Leadership .........................................................................46
S Krishnamoorthy & N Murch
Correspondence................................................................................................................................................................................49
Picture Quiz: Answer
A young patient with heart failure ....................................................................................................................................................50
Information for Authors ................................................................................................................................................................52
© Rila Publications Ltd • Acute Medicine • 2012 • Volume 11 Issue 1 • 1–56

2 Acute Medicine 2012; 11(1): 2
Acute Medicine
Editorial
Editor
he snow and freezing temperatures will hopefully have passed by the time this edition reaches you;
Dr C D Roseveare
Consultant in Acute Medicine
Southampton University Hospital
T the sight of daffodils may be asignal that the relief of spring is not far off. Winter frequently
stretches AMU resources to the limit – in recent years we have had epidemics of seasonal and swine
NHS Trust
Tremona Road f lu, but this year Norovirus seems to have been the bigger challenge. Ward closures from diarrhoea
Mail Point 520
Southampton SO16 6YD UK outbreaks have traditionally been more of a ‘downstream’ problem (no pun intended), but the impact
Tel: 02380 794716 of closure of the AMU would be substantial.At the time of writing this has still, thankfully, been
Email: chris.roseveare@suht.swest.nhs.uk avoided in my own hospital; however it remains a circumstance for which we have to be prepared. This
edition’s ‘Viewpoint’ article describes how temporary closure of the AMU was managed in a London
Editorial Board hospital. The use of an empty ‘winter pressures ward’ eased the burden in this case, enabling the AMU
Prof. Derek Bell service to be maintained. Even with the luxury of this spare capacity, there was clearly significant
Professor of Acute Medicine disruption, requiring close collaboration between a variety of departments, which is well described by
Imperial College London
Email: d.bell@imperial.ac.uk the authors. Many hospitals have become highly dependent on a functioning AMU to provide timely,
safe and effective care for medical emergencies. Major incident plans are in place to deal with mass
Ms Liz Lees
Consultant Nurse, Acute Medicine
casualty incidents; we need to consider similar contingencies to deal with AMU closure if patient
Heart of England Foundation Trust safety is going to be maintained. This article is a timely reminder of the need for forward planning.
lizlees@aol.com
Dr Simon J Fletcher Maintaining patient safety is a mantra which will be familiar to acute physicians, particularly those who
Consultant and Honorary Senior Lecturer attended any of the recent SAM meetings, where this theme has been well rehearsed. An acute medical
Anaesthesia and Intensive Care
Norfolk and Norwich University NHS Trust
unit can provide significant safety benefits by concentrating resources in a single area. However, for
Email: simon.fletcher@nnuh.nhs.uk the 60% who cannot go directly home from the AMU, this model creates the need for care to be
transferred at some point. It is well recognised that transfer is a time at which patient safety can become
Dr Mark Jackson
Department of Respiratory Medicine compromised; so if safety is our mantra, acute physicians and nurses have a responsibility to manage
Brighton General Hospital this process effectively. The article by David Hindmash and Liz Lees provides an important addition
Email: mark.jackson@bsuh.nhs.uk
to the limited literature in this area. Structured checklists are becoming an increasing part of medical
Dr Mike Jones practice; this paper highlights how a checklist can be used to improve the quality of handover from
Consultant Physician AMU. The authors emphasise the need to keep the form simple, and the importance of regular re-
Edinburgh Royal Infirmery
Email: mike.jones3@nhs.net inforcement to ensure that it is used.
Dr Nikhil Patel What skills and attributes does an acute physician require? With interview season approaching it’s a
Consultant Cardiologist
Eastbourne District General Hospital question that many prospective trainees will be contemplating – remaining calm under pressure,
Email: nik.patel@esht.nhs.uk communication skills and teamworking are some of the standard responses; but what about a good
Dr Ashwin Pinto sense of smell? Most of us recognise the characteristic odour of melaena , or the whiff of infected urine.
Consultant Neurologist But the absence of body odour might be equally revealing. Luther and Yap noted their patient to be
Southampton University Hospitals ‘remarkably clean’ – unusual, perhaps, for a young male patient on the AMU; along with his persistent
NHS Trust
Email: ashwin@doctors.org.uk demands to use the showering facilities, this was a clue to the final diagnosis of Cannabis Hyperemesis
Syndrome.It’s a case worth reading and highlights the importance of lateral thinking, particularly
Dr Tom Heaps
Consultant in Acute Medicine when patients repeatedly attend – as well as having a ‘good nose’ to sniff out something unusual!
University Hospitals Coventry and
Warwickshire Dr Chris Roseveare
Email: tomheaps@hotmail. co.uk Editor, Acute Medicine
President, Society for Acute Medicine
Journal of Acute Medicine is indexed/abstracted in EMBASE/Excerpta Medica and now cited

in Medline and indexed in PubMed
Published by All rights reserved. No part of this publication may be Enquiries Subscription Rates:
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Acute Medicine 2012; 11(1): 3-7 3
Clinical Reviews
Magnesium and the Acute Physician
R Allan & N Mara
Key Learning Points

• Magnesium imbalance is common in patients admitted to the Acute Medical Unit.
• Following treatment of deficient or excess states, identification of the cause is vital.
• Magnesium has multiple functions including muscle relaxation, membrane stabilisation and NMDA receptor blockade.
• Magnesium may be used as a treatment for a variety of conditions
Abstract cell membrane, preventing calcium inflow, and on

Magnesium deficiency, and to a lesser extent magnesium receptors on the sarcoplasmic reticulum, inhibiting their
excess, is commonly encountered in patients admitted to the activation and preventing calcium outflow from the
Acute Medical Unit. It is important that acute physicians sarcoplasmic channel.2 In this way, muscle relaxation is
are able to identify those at risk of these states and initiate achieved. The effects of hyperexcitability and weakness
appropriate investigation and treatment. This article aims to of the musculoskeletal system resulting from hypo- and
provide the reader with a sound understanding of magnesium hypermagnesaemia respectively can therefore be
physiology and its effect at a cellular level. The causes, explained. In addition, it can be appreciated that
symptoms and treatment of magnesium disorders are vasodilatation and bronchodilation may result from its
discussed along with a review of evidence regarding the relaxatory action on smooth muscle.1
therapeutic use of magnesium. The final action of magnesium may convey some
anticonvulsant properties.2 In the synapse, there is an
Keywords N-Methyl-D-Aspartate (NMDA) receptor-
Magnesium, hypermagnesemia, hypomagnesemia, mediated component to epileptiform activity;
dysmagnesemia, asthma, COPD, arrhythmias, cardiac magnesium is an NMDA receptor antagonist.
arrest, myocardial infarction, subarachnoid haemorrhage,
migraine, seizures. Physiology
A serum magnesium level of 0.7-1.1 mmolL-1
What does Magnesium do? (1.4-2.2mEqL-1 or 16.8-26.4mgL-1) is considered the
Magnesium is essential for bone mineralization, ‘normal’ range. This, however, is a poor ref lection of
Russell Allan
muscular relaxation and neurotransmission. It is a total body magnesium given its intracellular ST4
necessary co-factor for the cell membrane enzyme predominance. Approximately 60% of total Dept of Acute Medicine,
Na/K ATPase, which provides energy for the magnesium is contained within bone, 20% in Crosshouse Hospital,
membrane Na/K pump. Therefore in deficient muscle and 20% in soft tissues. Of that in bones and Kilmarnock,
states, the intracellular levels of sodium rise and muscles, only one quarter is available for exchange KA2 0BE,
potassium fall, allowing cellular resting membrane into serum. Only 0.3% is in the serum; this is made Ayrshire
potential to approach threshold potential. The higher up of ionised (active) form (65%), protein bound Neil Mara
intracellular sodium level causes an increase in state (27%) and that contained within anion Consultant
intracellular calcium via the Na/Ca counter- complexes (8%). Measuring the intracellular level Dept of Acute Medicine,
transport system, allowing greater muscular achieves a better ref lection of total body magnesium Crosshouse Hospital,
contraction. Conversely, the administration of than serum measurements, although this is rarely Kilmarnock,
used in clinical practice. Where total magnesium KA2 0BE,
magnesium reduces the intracellular sodium, and
Ayrshire
thus calcium levels, therefore decreasing the resting deficiency exists but the serum magnesium level is
membrane potential. This reduces automaticity, normal, deficiency can be confirmed by Correspondence:
acting as a cell membrane stabiliser. Supra-normal demonstrating reduced urinary magnesium Russell Allan
levels of magnesium appear to augment this excretion following magnesium infusion (<50% of Dept of Acute Medicine,
Crosshouse Hospital,
physiological role, allowing us to consider the infusate, compared to normal excretion being
Kilmarnock,
magnesium as a Na/K pump agonist.1 >60%, of that infused).2 KA2 0BE,
Magnesium also regulates ion channels. It acts on To maintain magnesium levels it is recommended Ayrshire
potential-dependent L-type calcium channels on the that adults consume 10.4-14.6 mmol (250-350mg) per Email: russellallan@doctors
.org.uk

4 Acute Medicine 2012; 11(1): 3-7
day. Certain subgroups will require more, including administration, thereby preventing hypocalcaemia which
pregnant females and children. Magnesium can be found in would further exacerbate the effects of magnesium excess.
chocolate, nuts, vegetables, cereals and seafood. Of what is Haemodialysis may be required in severe cases along with
ingested approximately 50% is absorbed in the normal state. ventilatory support for respiratory depression.3 These
Absorption occurs throughout the GI tract but principally in should be considered as holding measures, as
the small intestine. Renal excretion occurs at approximately hypermagnesemia will recur if the cause is not identified
5mmol/day in the normal state. This is decreased when and managed.
deficient or where renal failure exists, but can be increased by
certain drugs (e.g. diuretics, cisplatin, gentamicin and Hypomagnesemia
cyclosporin). Incidence
Homeostasis of Magnesium is under the control of The incidence of hypomagnesemia in hospitalised patients
many hormones; the precise mechanism is unclear. is 11, 19 and 47% when classified as Magnesium levels of
Parathyroid hormone (PTH) has a major role, acting with less than 0.6, 0.62 and 0.74mmolL-1 respectively. It results
Vitamin D to increase intestinal absorption, renal in a worse prognosis following acute hospital admission
reabsorption and bone uptake. Insulin and glucagon also and has been seen to double death rate in an ITU
have a role by increasing cellular uptake and reducing renal population.2 The lower limit of normal is usually quoted as
excretion respectively.2 0.6mmolL-1, below which, symptoms and signs of
neuromuscular, neurological and cardiovascular
Hypermagnesemia hyperactivity may occur. It is important to remember that
Incidence the serum level is a specific indicator but lacks sensitivity as
Hypermagnesemia has a prevalence in hospitalised patients it represents less than 1% of the total body magnesium.4
of 9.3, 5.7 and 3.5% when defined as levels > 0.95 mmolL-1,
>0.99 and >1.07mmolL-1 respectively.2 Causes
The most common causes of hypomagnesemia are GI loss,
Causes starvation, malabsorption, diuretic drugs and alcoholism.
Hypermagnesemia is usually iatrogenic or secondary to Other causes are shown in Table 1.
renal failure, in particular where rhabdomyolysis is the
cause (due to muscle breakdown with release of free Clinical Features
magnesium). Magnesium deficiency can cause nervous system
irritability in the form of nystagmus, dyskinesia, altered
Clinical Features sensation and seizure activity. Muscle weakness, fatigue
Initially patients may describe f lushing, nausea and and confusion are also recognized.
vomiting, progressing to confusion, weakness (including Magnesium is also involved in parathyroid hormone
that leading to respiratory depression) and pre- (PTH) production, so at low magnesium levels, less PTH is
syncope/syncope related to atrioventricular block. produced and thus calcium will also be low. Hypocalcaemia
Ultimately hypermagnesaemia may cause deep coma and will not improve following calcium replacement unless the
cardiac and/or respiratory arrest.3 Examination may reveal hypomagnesaemia is also corrected. Accentuating this
reduced or absent deep tendon ref lexes. problem, hypomagnesemia also induces skeletal muscle
resistance to PTH.5 Hypokalaemia often also accompanies
ECG Changes these deficient states.This can be explained by considering
In the presence of hypermagnesemia, the ECG may the action of magnesium as a Na/K pump agonist as well as
demonstrate prolonged PR and QT intervals, peaked T by recognising that the causes of hypokalaemia and
waves and a variety of supraventricular and ventricular hypomagnesaemia are often similar.
tachy-arrhythmias.3
ECG Changes
Treatment A variety of ECG changes may be identified, including
If hypermagnesemia is severe and symptomatic, saline prolongation of the PR and QT intervals, ST segment
diuresis (0.9% saline and furosemide 1mg/kg) may be depression, flattening of P waves, T wave inversion and
effective in promoting magnesium excretion. Calcium increased QRS duration.3 Torsades de pointes (see Figure 1)
chloride should be given to protect the myocardium and is a lifethreatening ventricular arrhythmia which may result
replace the calcium lost following furosemide from hypomagnesaemia.
Figure 1. Torsades de pointes.

Acute Medicine 2012; 11(1): 3-7 5
Gastro-Intestinal Malabsorption, malnutrition, chronic diarrhoea, vomiting, intestinal fistula, primary intestinal
hypomagnesaemia
Renal Bartter syndrome, Gitelman syndrome, post-obstructive diuresis, diuresis phase of acute tubular necrosis,
Drugs (diuretics, cisplatin, aminoglycosides, ciclosporin), Primary renal magnesium wasting
Endocrine Hyperparathyroidism, hyperthyroidism, hyperaldosteronism, Syndrome of inappropriate ADH,
hypoparathyroidism, Diabetes Mellitus
Redistribution Hungry bone syndrome, pancreatitis, Insulin treatment, transfusions
Miscellaneous alcoholism
Table 1. Causes of Hypomagnesemia.2,5
Treatment not shown any beneficial effect despite the finding of low
Magnesium replacement can be oral or intravenous. The magnesium levels in many asthmatic patients; patients with
intravenous infusion rate is determined by the clinical lower magnesium levels also often have more severe
severity. For severe and symptomatic hypomagnesemia, 2g asthma symptoms.8
of magnesium sulphate (i.e. 4ml of 50% MgSO4 or
8mmols) should be administered over 15 minutes. It is Chronic Obstructive Pulmonary Disease (COPD)
vital that the cause is considered and managed Little work has been done to study the effect of
appropriately to prevent recurrence. magnesium in exacerbations of COPD and many are
sceptical of its use, particularly given the potential to
Magnesium as a treatment induce respiratory muscle weakness.6 One small study of
Even in the absence of hypomagnesemia, magnesium has 72 patients showed magnesium produced a statistically
been proposed as a treatment for a variety of conditions, as significant improvement in peak expiratory f low rate,
listed below. Dose, route and speed of administration will compared to placebo, when given 20 minutes after a β2
vary according to the indication, and should be adjusted in agonist. It also showed a trend towards reduced need for
patients with renal impairment. Doses of greater than hospitalization.10 Of note, this study excluded those with
2g/hour (8mmol/hour) are likely to result in adverse signs of infection. Further data have suggested that serum
effects; intravenous administration should be accompanied magnesium levels in the lower normal range are associated
by continuous assessment for side effects including with an increased frequency of exacerbation of COPD
f lushing, hypotension bradycardia and arrhythmias. The symptoms.11
presence of hyperkalaemia may augment side effects of
treatement.1 Atrial fibrillation (AF)
Magnesium was shown to be more effective than
Asthma amiodarone in achieving cardioversion in a study of
Magnesium features in the British Thoracic Society patients in an ITU environment. At 24 hours, 67% vs 33%
guidelines as a therapeutic option in the treatment of acute had cardioverted in the magnesium and amiodarone
severe or life threatening asthma.6 Patients with more severe groups respectively. This was significant, as were the
airway obstruction at presentation derive the greatest benefit differences in cardioversion rates at all time period from 2
from magnesium in regards to their FEV1. However, this to 24 hours. Although not all of the patients in this study
benefit does not extend to reducing the need for hospital were in AF (only 71% of Mg group and 52% of
admission in any subgroup.7 The guidelines specifically Amiodarone group), this demonstrates significant
suggest that magnesium use should always be discussed with antiarrhythmic activity for magnesium outside its
a senior clinician and that only a single dose is administered; established indication in patients with Torsade de Pointes.
theoretically, iatrogenic hypermagnesemia may lead to Furthermore, when patients with chronic arrhythmias
muscle weakness and respiratory failure, although this were excluded, cardioversion rate following magnesium
remains unproven. The suggested intravenous dosing infusion was 77.8%.12 Another study has shown
regimen is 1.2-2g over 20 minutes.6 magnesium to also be superior to diltiazem (57% vs 22%
Recent interest has focused on the use of nebulised p=0.03)13 and to verapamil (53% vs 40%: non-
magnesium sulphate.Doses of 135-1152mg, along with significant)14 in achieving cardioversion. A combination of
regular bronchodilators have been shown to be safe with a magnesium and digoxin has also shown a trend towards
non-significant trend towards benefit in all subgroups. In greater efficacy than digoxin alone in producing sinus
the subgroup with severe asthma, lung function rhythm (60% vs 38% p=NS).15 From these studies it is not
improvement was significant.8 always clear if there is an initial electrolyte deficiency
Nebulised magnesium produced no improvement in present; this is important as patients with K+/Mg2+
FEV1 or exhaled nitric oxide levels in patients with deficiencies cardiovert significantly more consistently
chronic, persistent airf low limitation.9 Use of oral when treated with magnesium with K+ and
magnesium in chronic asthma has also been studied but did insulin/dextrose (86% vs. 39% p<0.001).16

6 Acute Medicine 2012; 11(1): 3-7
The rate controlling effect of magnesium has also been treatment in shock-refactory VF has shown a non-
observed in patients with persistent AF. It was shown to significant trend towards improvement in ROSC, and
cause a significant reduction in heart rate,when compared survival to hospital discharge.
to placebo, to an extent similar to that of diltiazem and
amiodarone but significantly less than that of Subarachnoid haemorrhage
verapamil.12,13,14,17 When combined with digoxin, Elevation of serum magnesium level using an intravenous
magnesium controlled heart rate to less than 90bpm in infusion may improve outcome in the acute phase of
100% of patients at 24 hours compared to only 50% with subarachnoid haemorrhage, although evidence is
digoxin alone.15 conf licting. Conventional therapy with the calcium
These effects are again likely to be a result of antagonist, nimodipine, improves outcome by reducing
magnesium’s agonistic action on the Na/K pump altering vasospasm. Magnesium has been postulated to have a
electro-conduction. It should be noted, however that similar beneficial effect by blocking calcium f lux,
magnesium can cause hypotension (due to smooth muscle preventing vasoconstriction and therefore further
relaxation in the vessel walls) so should be used with neurological damage. Comparisons between magnesium
caution when blood pressure is low. and placebo have shown reduction in infarct, secondary
ischaemic events and mortality.25 Furthermore a meta-
Other Tachyarrhythmias analysis and a systematic review have suggested some
Two case studies have shown magnesium to be effective in improvement in functional outcome and reduction in
cardioverting ventricular tachycardia caused by digoxin delayed cerebral ischaemia where magnesium is combined
toxicity following failure of sodium bicarbonate, with nimodipine therapy, but have shown no benefit in
amiodarone, phenytoin, lignocaine and DC shock.18,19 mortality.26,27 The only double blind RCT in this area has
Digoxin acts as a Na/K pump antagonist which may failed to confirm any significant improvement by adding
explain this beneficial effect. magnesium to nimodipine.27 Currently this is not
Magnesium is well established for the treatment of recommended; however, if nimodipine is unavailable
Torsade de Pointes, but evidence for use in other acutely, use of intravenous magnesium should be
ventricular arrhythmias is less convincing.3 The dose of considered.
magnesium used in the presence of Torsade de Pointes is
2g over 1-2 minutes.3 Migraine
Theoretically, magnesium could treat migraine by
Myocardial Infarction (MI) blocking NMDA-receptors and modifying serotonin.2
Following an ischaemic event there is a significant Administration of IV magnesium during the acute phase of
outpouring of potassium from cells. Using a Na/K pump a migraine has been shown to improve outcome. In one
agonist in this circumstance would seem logical.There may small study, 86.6% of those who received magnesium
also be a secondary benefit due to lower intracellular experienced full symptom resolution compared to only
sodium levels, resulting in lower intracellular calcium 6.6% with placebo. This study also showed improvement
levels, reducing cardiac contractility and lower triggering in symptoms in the remaining 13.4%.29 A further study
activity including that of ventricular fibrillation.1 It has looked at the therapeutic effect of magnesium in migraines
been shown that when magnesium is used following MI with and without aura. It showed statistically significant
there is a reduction in mortality20 (7.8% in the magnesium improvement in those with aura when compared to
group and 10.3% in the placebo group, p=0.04) but a placebo, although this benefit was not seen in the group
reduction in VF, VT and SVT does not seem to account without aura.30
for this, as these were similar in the magnesium treatment
group to the placebo group.21 It has been suggested that Seizures
magnesium’s vasodilatory effect could be one explanation, Magnesium sulphate is standard treatment in eclampsia
either because of reduced afterload (pulmonary and where it is used at significantly higher doses than in
systemic) or coronary vasodilation.2 Further studies are other medical indications. A loading dose of 4 g over 5
required before magnesium treatment can become to 10 minutes, followed by an infusion of 1 g/hour
established practice following MI. maintained for 24 hours after the last seizure is the usual
regimen. If recurrent seizures occur these are treated
Cardiac Arrest Rhythms with either a further 2g bolus or an increase in the
Magnesium has not been shown to improve outcome infusion rate to 1.5 g or 2.0 g/hour.31 In contrast there is
following cardiac arrest and therefore has not been no evidence to suggest that magnesium use is of any
included in the most up-to-date Advance Life Support benefit in treating non-eclamptic seizures, despite the
algorithm.3 Following in-hospital cardiac arrest there was recognised antagonistic effect of magnesium on NMDA
no significant improvement in the end points of return of receptors. Alcohol withdrawal seizure often co-exists
spontaneous circulation (ROSC), survival at 24 hours with low levels of magnesium but, other than the
and survival to discharge.22,23 Similar results were found intuitive replacement of deficit, it remains uncertain if
following out-of-hospital cardiac arrest when magnesium further IV magnesium affects withdrawal symptoms or
was compared to placebo.24 More recently, magnesium seizure threshold.

Acute Medicine 2012; 11(1): 3-7 7
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Verapamil on Supraventricular arrhythmias, Clin Cardiol, 1993 May; 16(5): 29. Demirkaya S, Vural O, Dora B et al, Efficancy of intravenous Magnesium
429–34. Sulphate in the treatment of acute migraine attacks. Headache 2001; 41(2):
15. Brodsky MA, Orlov MV, Capparelli EV et al, Magnesium Therapy in 171–7.
New-Onset AF. Am J Cardiol, 1994; 73:1227–1229. 30. Bigal ME, Bordini CA, Tepper SJ et al, Intravenous Magnesium Sulphate
16. Cybulski J, Budaj A, Danielewicz H et al, A New-Onset AF: the incidence in the acute treatment of migraine without aura and migraine with aura. A
of potassium and Magnesium deficiency. The efficacy of IV randomised, double-blind, placebo-controlled study. Cephalagia, 2002
Potassium/Magnesium supplementation in cardioversion to sinus rhythm. June; 22(5): 345–53.
Kardiol Pol. 2004 Jun; 60(6): 578–81. 31. The Management of Severe Pre-eclampsia/Eclampsia, Royal College of
17. Hays JV, Gilman JK, Rubal BJ et al, Effect of Magnesium Sulphate on Obstertricians and Gynaecologists, Guideline No. 10A, 2010.
Ventricular Rate Control in Atrial Fibrillation. Annals of Emergency
Medicine. 1994 July, 24(1): 61–61.

8 Acute Medicine 2012; 11(1): 8-12
ECG dispersion mapping predicts clinical

deterioration, measured by increase in the
Simple Clinical Score
J Kellett, A Emmanuel & S Rasool
Key Points
• ECG dispersion mapping (ECG-DM) is a novel technique that analyzes low amplitude ECG micro-alternations.
• Clinical deterioration as measured by an increased Simple Clinical Score the day after admission to hospital is
associated with a high mortality.
• This study identified ECG-DM changes during left ventricular re-polarization and nursing home residence as the only
independent predictors of Simple Clinical Score increase the day after admission to hospital.
Abstract SCS and a 20 fold increase in mortality compared to

Objective: ECG dispersion mapping (ECG-DM) is those with a decreased SCS.5 Only three features
a novel technique that reports abnormal ECG micro- identified patients who increased their SCS: residence
alternations. We report the ability of ECG-DM to predict in a nursing home, the presence of heart failure and a
clinical deterioration of acutely ill medical patients, as Medical Admission Risk System (MARS) laboratory
measured by an increase in the Simple Clinical Score data score >0.10.6
(SCS) the day after admission to hospital. ECG dispersion mapping (ECG-DM) is a recently
Methods: 453 acutely ill medical patients (mean age developed technology that provides non-invasive
69.7 +/- 14.0 years) had the SCS recorded and ECG- assessment of myocardial pathology by analyzing low
DM performed immediately after admission to hospital. amplitude oscillations of conventional ECG signals.7-9
Results: 46 patients had an SCS increase 20.8 +/- The method examines not only the tiny fluctuations
7.6 hours after admission. Abnormal micro-alternations (micro-alternations) of the T-wave (T wave alternans)
during left ventricular re-polarization had the highest but also micro-alternations of the P wave and QRS
association with SCS increase (p=0.0005). Logistic complex. From the six traditional ECG leads of I, II,
John Kellett regression showed that only nursing home residence and III, aVR, aVL and aVF patented formulae can quickly
MD abnormal micro-alternations during re-polarization of the (i.e. within 30 seconds) and accurately determine
Consultant Physician, left ventricle were independent predictors of SCS increase micro-alternations not only of the T wave but of the
Nenagh Hospital, with an odds ratio of 2.84 and 3.01, respectively. entire PQRST complex. Nine groups of calculations
Nenagh, (G1-G9) are then made that score in arbitrary units the
Conclusion: ECG-DM changes during left
Ireland
ventricular re-polarization are independent predictors of extent of these micro-alternations in different areas of
Andrew Emmanuel clinical deterioration the day after hospital admission. the heart, as well as those associated with intra-
MB ChB ventricular blocks and ventricular hypertrophy – a
Senior House Officer, Keywords score of 0 indicates complete absence of abnormal
Nenagh Hospital, micro-alternations, higher scores indicate increasing
Hospital admissions, predictive scores, ECG dispersion.
Nenagh,
abnormality (Table 1). Micro-alternations ref lect
Ireland
Introduction abnormalities in the myocardium at a metabolic level,
Shahzeb Rasool Intuition suggests that seriously ill patients are more which may include ischemia and other causes. ECG-
MB BS likely to deteriorate and less likely to improve than DM, therefore, is not a diagnostic test but a non-
Cardiology Registrar, those with mild illness. This, however, may not be the specific indicator of myocardial health. The micro-
Nenagh Hospital,
case. The Simple Clinical Score (SCS) is a reliable alternations from all nine groups (G1-G9) represent
Nenagh,
Ireland instrument that objectively assesses and measures the overall myocardial micro-alternation index (MMI)
severity of illness that has been independently validated which is expressed as a percentage. If pathological
Correspondence: in several different clinical settings.1-4 Approximately micro-alternations are present throughout the entire
John Kellett 12% of patients increase their SCS 24 hours after myocardium the MMI is 100%, whereas an MMI of
Consultant Physician,
admission to hospital. We recently reported that low 0% indicates a total absence of abnormal micro-
Department of Medicine,
Nenagh Hospital, risk patients were just as likely to increase their SCS as alternations in any part of the heart. ECG-DM is
Nenagh, high risk patients, and that an increased SCS was much more sensitive than the direct “beat to beat”
County Tipperary, associated with a 5 fold increase in in-hospital measurement of ECG micro-alternations, and this
Ireland mortality compared to patients with an unchanged allows measurements to be performed at rest. ECG-
Email: jgkellett@eircom.net

Acute Medicine 2012; 11(1): 8-12 9
ECG dispersion mapping predicts clinical deterioration, measured by increase in the Simple Clinical Score
Corresponding region of heart or pathology Range of arbitrary units of Corresponding region of PQRST
micro-alternation
G1 Depolarization of the right atria 0-17 P wave
G2 Depolarization of the left atria 0-10 P wave
G3 Depolarization of the right ventricle 0-16 QRS
G4 Depolarization of the left ventricle 0-22 QRS
G5 Repolarization of the right ventricle 0-3 T wave
G6 Repolarization of the left ventricle 0-14 T wave
G7 Symmetry of ventricular depolarization 0-21 QRS
G8 Intraventricular block 0-2 QRS
G9 Ventricular hypertrophy 0-21 QRS
Table 1. Areas of myocardium and myocardial function associated with nine ECG-DM calculation groups (i.e. G1-G9).
DM only takes a few seconds to perform and requires no skill reported in a previous publication.11 The SCS can be
to interpret and was primarily developed as a rapid screening quickly performed at the bedside and requires no
test for heart disease. However, the role of this new additional information or investigation other than a 12 lead
technology in clinical medicine is still being defined. We ECG.12
recently reported on the ability of ECG-DM to predict in- Routine laboratory investigations performed at the
hospital mortality.10 In this paper we report the ability of time of admission were used to calculate the MARS
ECG-DM to predict clinical deterioration of acutely ill laboratory score on each patient. Approximately 24 hours
medical patients, as measured by an increase in the Simple after admission (20.8 +/- 7.6 hours) each patient was
Clinical Score the day after admission to hospital. reviewed by the nursing staff and the SCS re-calculated.
All data were corrected for errors and then entered into an
Methods Epi-Info version 6.0 database (Center for Disease Control and
All patients were recruited from the unselected acutely ill Prevention, USA). The ICD10 coded diagnoses recorded
medical patients admitted to Nenagh Hospital between at discharge or death were also entered into this database.
July 30th 2009 and 31st March 2010. Of the 1702 patients The continuous variables of age, MMI, G1-G9 etc
admitted during this period 453 (26.6%) were included in were converted into categorical variables by determining
the study – the only criterion for study inclusion was that the threshold levels with the highest odds ratio for
one of the authors was able to perform an ECG-DM predicting in-hospital mortality. This was done by a
within 10 to 20 minutes of hospital admission. process of trial and error. Continuous variables were
The presenting complaint and the clinical data required compared by Student’s t-test and categorical variables by
to calculate the Simple Clinical Score (SCS) were recorded Chi-square analysis that applied Yates continuity
at the time of admission by the nursing staff of the correction. All calculations were performed using Epi-Info
hospital’s medical admission unit. The nursing staff of the version 6.0 (Center for Disease Control and Prevention, USA),
hospital has been fully trained in the use of the SCS since and statistical significance was set at a p value <0.05. The
2007 – implementation of this training process has been independence of variables was tested by logistic regression
SCS not increased SCS increased p F Odds ratio Chi-square

(n 407) (n 46) statistic (CI 95%)
Age (years) 67.4 +/- 17.0 73.6 +/- 12.6 0.02 5.9 - -
Length of hospital stay (days) 6.2 +/- 6.2 10.9 +/- 11.5 0.00002 19.0 - -
Simple Clinical Score 6.4 +/- 3.9 7.3 +/- 4.0 0.13 2.3 - -
MARS laboratory score 0.11 +/- 0.19 0.19 +/- 0.24 0.02 5.6 - -
Myocardial micro-alternation index (%) 23.0 +/- 13.5 27.4 +/- 16.4 0.04 4.3 - -
Male sex 56.3% 43.5% 0.13 - 1.7 (0.9-3.3) 2.2
Nursing home residence 6.6% 17.4% 0.02 - 3.0 (1.1-7.5) 5.3
Discharge diagnosis of heart failure 18.4% 34.8% 0.02 - 2.4 (1.2-4.8) 5.9
In-hospital mortality 1.5% 21.7% 0.00001 - 18.6 (5.7-62.2) 44.0
Table 2. Comparison of patients with and without an increase in the Simple Clinical Score (SCS) within 24 hours of hospital admission.

10 Acute Medicine 2012; 11(1): 8-12
SCS the day after

25% 300
250
20%
a Increased S
200
Number of patients
15%
admiission
150
ateints with an
10%
100
oportion of pa
5%
50
0% 0
Pro
0 1 2 3 4 5 6 7 8 9 >=10
G6
SCS increased Number of patients
Figure 1. The association of an increase in the Simple Clinical Score (SCS) the day after admission to hospital with G6 values.
using Logistic Version 3.11E software (G.E. Dallal, Patients with G6 values >=5 had an odds ratio of 3.1 (CI
Andover MA).14 95% 1.6-6.0, Chi square 12.3, p 0.0005) for SCS increase
This study was performed while the services in the the day after admission. The majority of patients had a G6
hospital were undergoing reconfiguration, part of which was value of 0 or 1, and no patients had G6 values of 2,3 or 4.
the diversion after midnight of seriously ill patients directly to There are, therefore, two distinct patient populations and
Limerick Regional Hospital. This resulted in the majority of a G6 value >=5 clearly identified those patients most likely
patients being admitted between 3 and 9 pm. Patients studied to increase their SCS (Figure 1).
had the same age (68.0 +/- 16.7 vs. 66.2 +/- 19.0 years, p = Numerous logistic regression models were tested that
0.07), length of hospital stay (6.7 +/- 7.0 vs. 7.2 +/- 7.8 days, p included the discharge diagnosis of heart failure, the MARS
= 0.24) and in-hospital mortality (3.5% vs. 3.5%, p = 0.99) as laboratory score >0.10 and nursing home residence (i.e. the
the other patients admitted during the study period. three variables previously identified as independent predictors
Ethical approval of the study was obtained from the of SCS increase)5 as well as each of the ten ECG-DM
Mid-Western Regional Hospital Complex Scientific Research variables, both as continuous variables and using the cut-off
Ethics Committee. values in Table 3 (i.e. MMI >36% and G1 >=3, G2 >=5, G3
>=4, G4 >=6, G5 >=1, G6 >=5, G7 >=5, G8 >=1 andG9 >=20).
Results Only a G6 value >=5 and nursing home residence remained as
The day after admission no patients had died, 46 (10.2%) independent predictors of SCS increase (Table 4).
had increased their SCS by 2.2 +/- 1.5 points, in 209
(46.1%) the SCS was unchanged, in 162 (35.8%) it was Discussion
decreased by 2.5 +/- 1.6 points and 36 (7.9%) patients had Although there are several well validated scoring systems
already been discharged home. Patients with an increased that can predict imminent death,15,16 determining the
SCS were older and had a longer length of hospital stay. factors associated with clinical deterioration (or failure to
They also had a higher MARS laboratory score and a respond to treatment) has proved difficult. Despite
higher MMI, and were more likely to have heart failure examining numerous variables in our original study we
and to be admitted from a nursing home. There was no found only three features which identified patients who
association, however, between the SCS on admission and increased their SCS: residence in a nursing home, the
SCS increase. The in-hospital mortality of patients with an presence of heart failure and an elevated MARS laboratory
increased SCS was 21.7%, compared with 2.4% for those data score. This study found, however, that only increased
with no change in their SCS and 0.6% for those patients micro f luctuations associated with left ventricular re-
with a reduced SCS. An increase in SCS was highly polarization (i.e. G6 values >=5) and nursing home
significantly associated with increased mortality (OR 18.6, residence were independent predictors of clinical
CI 95% 5.7-62.2, p<0.001) (Table 2). deterioration as measured by SCS increase the day after
An MMI >36%, G1 >=3, G2 >=5, G5 >=1, G6 >=5 and hospital admission. Therefore, the likelihood of
G7 >=5 were associated with SCS increase (Table 3). deterioration would appear to be between two and three

Acute Medicine 2012; 11(1): 8-12 11
SCS not increased SCS increased p Odds ratio Chi-square

(n 407) (n 46) (CI 95%)
Myocardial micro-alternation 14.0% 28.3% 0.02 2.4 (1.1-5.2) 6.4
index >36%
G1 >=3 54.3% 71.7% 0.04 2.1 (1.0-4.5) 4.4
G2 >=5 31.7% 52.2% 0.001 2.4 (1.2-4.6) 6.9
G3 >=4 18.9% 30.4% 0.10 1.9 (0.9-3.9) 2.7
G4 >=6 12.3% 19.6% 0.25 1.7 (0.7-4.1) 1.3
G5 >=1 31.0% 47.8% 0.03 2.0 (1.1-4.0) 4.6
G6 >=5 28.0% 54.3% 0.0005 3.1 (1.6-6.0) 12.3
G7 >=5 21.4% 39.1% 0.01 2.4 (1.2-4.7) 6.4
G8 >=1 4.4% 6.5% 0.79 1.5 (0.3-5.8) 0.1
G9 >=20 2.2% 0.0% 0.64 0.0 (0.0-5.4) 0.2
Table 3. Comparison of ECG-DM findings of patients with and without an increase in the Simple Clinical Score (SCS) within 24 hours of
hospital admission.
times higher in a patient with abnormal micro f luctuations “sick” myocardium might be more likely to demonstrate
during left ventricular re-polarization and/or those subtle abnormalities during this phase of the cardiac cycle.
admitted from a nursing home. Changes in G6 will, therefore, ref lect left ventricular
There were 46 patients with an increased SCS (i.e. 46 health. Although increased micro-alternations during left
events) and four variables (i.e. ECG-DM measurements, ventricular re-polarization was a more powerful predictor
heart failure, nursing home residence and the MARS of clinical deterioration than heart failure, we diagnosed
laboratory score) tested for independence by logistic this clinically and not by echocardiography or BNP
regression. This is close to the minimal number of testing. It may be that these techniques would have been
acceptable events per variable that should be included in a better predictors of clinical deterioration than changes in
logistic regression model.17 It is possible, therefore, that a G6, but would not have been cheaper, quicker and easier
larger study might show other variables to be independent to perform.
predictors of SCS increase. Nevertheless, our results
suggest that nursing home residence and a G6 value >=5 Conclusion
will remain the major predictors of SCS increase. ECG-DM changes during left ventricular re-polarization
Although other ECG-DM changes also appear related and nursing home residence are independent predictors of
to SCS increase, changes in G6 were the most striking. clinical deterioration as measured by SCS increase within 24
Left ventricular re-polarization is an active energy hours of admission. ECG-DM is inexpensive, only takes a
consuming process and it is reasonable to postulate that a few seconds to perform and requires no skill to interpret.
Coefficient SE Odds ratio P
Constant -2.9842 0.2720 - 0.000
Nursing home residence 0.9419 0.4545 2.56 0.038
G6 >=5 0.9024 0.3360 2.47 0.007
Heart failure 0.4831 0.3596 1.62 0.179
MARS laboratory score >0.10 0.5111 0.3298 1.67 0.121
Constant -2.7463 0.2364 - 0.000
Nursing home residence 1.0446 0.4482 2.84 0.020
G6 >=5 1.1018 0.3183 3.01 0.001
Table 4. logistic regression models that include the three variables previously reported as independent predictors of an increase in the Simple
Clinical Score (SCS) (i.e. nursing home residence, heart failure and a Medical Admission Risk System (MARS) laboratory data score >0.10)
and ECG-DM G6 values >=5. Only nursing home residence and a G6 value >=5 are independent predictors of SCS increase.

12 Acute Medicine 2012; 11(1): 8-12
References
1. Subbe C.P., Gauntlett W., Kellett J. Collaborative audit of risk evaluation 9. Ryabykina G.V., Sula A.S., Shchedrina E.V. Experience with device
in Medical Emergency Treatment (CARE-MET 1) – an international Cardiovisor in cardiological care. Turkish Journal of Invasive Cardiology 2006;
pilot. Eur. J. Int. Med. 2010; 21: 222–225. 10: 138–145.
2. Subbe C.P., Jishi F., Hibbs R.A.B. The Simple Clinical Score: a tool for 10. Kellett J., Rasool S. The prediction of the in-hospital mortality of acutely
benchmarking of emergency admissions in acute internal medicine. ill medical patients by electrocardiogram (ECG) dispersion mapping
Clinical Medicine 2010; 10: 352–7. compared with established risk factors and predictive scores – a pilot study.
3. Ghanem-Zoubi N.O., Vardi M., Laor A., Weber G., Bitterman H. Eur J Intern Med (2011), doi:10.1016/j.ejim.2011.01.013
Assessment of disease-severity scoring systems for patients with sepsis in 11. Gleeson M., Kellett J, Cowan C., Casey M. An assessment tool for acutely
general internal medicine departments Critical Care 2011, 15:R95 ill medical patients. British Journal Nursing 2009; 18: 546–550.
doi:10.1186/cc10102. 12. Kellett J., Deane B. The Simple Clinical Score predicts mortality for days
4. Li J.Y.Z., Yong T.Y., Hackendorf P., Roberts S., O’Brien L. et al. The after admission to an acute medical unit. Q.J.Med. 2006; 99: 771–781.
Simple Clinical Score is associated with mortality and length of stay of 13. Kellett J., Deane B. The diagnoses and co-morbidity encountered in the
acute general medical admissions to an Australian hospital. Internal hospital practice of acute internal medicine. European Journal of Internal
Medicine Journal, doi:10.1111/j.1445–5994. 2011. 02498. Medicine. 2007; 18: 467–473.
5. Kellett J., Emmanel A., Deane B. Who will be sicker in the morning? 14. Dallal G.E. LOGISTIC: A Logisitic Regression Program for the IBM PC.
Changes in the Simple Clinical Score the day after admission and The American Statistician,1988; 42: 272.
subsequent outcomes of acutely ill unselected medical patients. Eur J 15. Smith G.B., Prytherch D.R., Schmidt P.E., Featherstone P.I. Review and
Intern Med (2011), doi:10.1016/j.ejim.2011.03.005 performance evaluation of aggregate weighted “track and trigger” systems.
6. Silke B, Kellett J, Rooney T, Bennett K, O'Riordan D. An improved Resuscitation 2008; 79: 11–21.
medical admissions risk system using multivariable fractional polynomial 16. Brabrand M., Folkestad L., Clausen N.G., Knudsen T., Hallas J. Risk
logistic regression modelling. QJM (2010 Jan) 103(1): 23–32. scoring systems for adults admitted to the emergency department: a
7. Cruz-Gonzalez I., Dejoseph-Gauthier D., Chia S., Raffel O.C. and Jang systematic review. Scandinavian Journal of Trauma, Resuscitation and
I-K. Non-invasive assessment of myocardial ischaemia by using low Emergency Medicine 2010;18 :8. doi:10.1186/1757-7241–18-8
amplitude oscillations of the conventional ECG signals (ECG dispersion 17. Ottenbacher K.J., Ottenbacher H.R., Tooth L. and Ostir G.V. A review of
mapping) during percutaneous intervention. Acta Cardiol 2009; 64: 11–15. two journals found that articles using multivariable logistic regression
8. Sula A., Grishin V., Kitachine Y., Reva M. US Patent 7519416B2: frequently did not report commonly recommended assumptions. J Clinical
Diagnostic method utilizing standard lead ECG signals, April 2009 Epidemiol 2004; 57: 1147–1152.

Acute Medicine 2012; 11(1): 13-17 13
Improving the safety of patient transfer

from AMU using a written checklist
D Hindmarsh & L Lees
Key Points
1. Unsafe patient transfer is a significant reason for incident reporting in hospitals.
2. Effective verbal and written communication can be aided by the use of a transfer checklist.
3. Compliance with transfer documentation can be improved by a programme of education and regular re-inforcement.
Abstract is not new. The need to assure patient safety during,

Unsafe patient transfers are one of the top reasons for incident and after transfer, has re-energised focus on the use
reporting in hospitals. Criteria guiding safe transfer have of a transfer checklist. In order to achieve safe patient
been issued by the NHS Litigation Authority. To meet this transfers in this context, both transfers in and out of
standard, a “transfer check list” was redesigned for all an AMU must be considered.
patients leaving the Acute Medical Unit (AMU) in the
Heartlands Hospital. Following the introduction of the Care pathways into AMU
checklist two full audit cycles were conducted. The first cycle The patient f low into the AMU at Heartlands
highlighted an extremely poor uptake of the checklist. After comprises patient transfers from the Emergency
interventions to educate nursing staff and raise awareness of Department (ED) and patients referred directly via David Hindmarsh
the issues at the regular staff meetings, re-audit demonstrated their GP. Following GP referral, patients are either Foundation Year 1 Doctor
significant improvement in completion rate. Subsequent brought to the AMU by ambulance, in which case MBChB
monitoring indicates continued improvement, with the crew always complete a transfer checklist, leaving Heart of England NHS
compliance up to 95% for completion of the transfer checklist a copy of the form for staff. If patients transport Foundation Trust
themselves to AMU following GP referral they will Bordesley Green
on AMU. Incident reporting relating to transfer has also
Birmingham,
decreased significantly. bring a GP letter.
B9 5SS
Keywords Care pathways out of AMU Liz Lees

Acute medical unit, Patient Transfer, Transfer checklist/tool, Following assessment and stabilisation, patients are Consultant Nurse
either transferred from the AMU to other wards or (Acute Medicine) and
Patient safety, Communication, Handover.
Clinical Dean
are discharged and transferred directly from the
RGN, DipN., BSc (hons),
Introduction AMU. Dip HSM, MSc
Patient transfers represent a huge part of the Acute Medical Unit
workload on an Acute Medical Unit (AMU). Redesign process for the transfer (Ward 20)
Unsafe patient admission, discharge and transfers checklist Heart of England NHS
are one of the top twelve topic areas for incident During 2010 the staff working on the AMU Foundation Trust
re-designed our original 2001 transfer checklist. The Bordesley Green
reporting to the National Reporting and Learning
Birmingham B9 5SS
System (NRLS) department of the National Patient changes were led by the consultant nurse, in close
Safety Association (NPSA). Issues regarding patient collaboration with the corporate nursing team. Each Correspondence:
transfer have been recognised by the NHS AMU had previously designed transfer Liz Lees
Litigation Authority, which provides the NHS with documentation, necessitating negotiation for each Consultant Nurse
specific criteria for patient transfer, which are then element of the form revised. Moreover, the ED did (acute medicine) and
interpreted locally to provide for different groups of not previously use a transfer checklist, relying upon a Clinical Dean
RGN, DipN., BSc (hons),
patients requiring both internal and external verbal handover. A form used by AMU for
Dip HSM, MSc
transfer.1 documenting telephone referrals was therefore also Acute Medical Unit
The Heartlands Hospital is one of three hospitals, redesigned during this process. This ensured that (Ward 20)
which form part of the Heart of England NHS the details of all patients transferred were Heart of England NHS
Foundation Trust. The AMU at the Heartlands documented using the same format. The terms Foundation Trust
hospital has used a checklist for documenting patient ‘handover’ and ‘transfer’ became synonymous. Bordesley Green
It was decided to disseminate the checklist across Birmingham B9 5SS
transfers since 2001. To this end, the concept of
Email: liz.lees@heartofen
using a checklist for patient transfers from the AMU each AMU,thereby standardising practice on the 3
gland.nhs.uk

14 Acute Medicine 2012; 11(1): 13-17
Improving the safety of patient transfer from AMU using a written checklist
Level 1 – 1.4.5 a. Assessment: All patients must be assessed by a registered

As a minimum, the approved documentation (policy) must nurse prior to transfer, using ABCDE method of assessment
include a description of the: and documentation
a. Duties b. Communication: Discuss the transfer with the patient next
b. Definition of all patient groups of kin or carer & document on the transfer form
c. Transfer requirements specific to each group c. Transport: Identify & request appropriate mode of transfer
d. Documentation to accompany the patient when being d. Monitoring & Equipment: Infusions, oxygen saturation
transferred monitor
e. Process for out of hours e. Escort: Registered nurse escort if MEWS above 4
f. Process for monitoring compliance with all of the above f. Documentation: SBAR transfer sheet
g. Anything else: Property
Box 1. NHS Litigation Authority: Standard 4 – Criterion 5:
Transfer of patients.5 Box 2. Summary of Heart of England NHS Foundation Trust
standard operating procedure for patient transfer.
AMU Transfer Checklist

Situation
DATE: _________________CONSULTANT:___________________DNAR order Yes  or No 
MRSA screen: No  Yes   Rapid  Culture  Positive  Negative 
Background
From A&E  GP  Self ref  Ward 19  Internal transfer ________
Diagnosis:....................................................................PMH:........................................................................................
Diarrhoea within 48 hrs  Vomiting within 48 hrs  Docs the patient require isolation Yes/No
Assessment
MEWS Score:..............................If MEWS > 4 please note parameters
Airway: No  Yes   Sats____________%on__________L/%..............................
Breathing: No  Yes   RR____.......................................................................................
Circulation: No  Yes   HR_____BP_________/_____Urine O/P________mls/hr
Disability: No  Yes   A V P U (Circle)
Environment: No  Yes   Temp_________
Action
Critical Care Outreach contacted..........YES/NO Time contacted.......................... Wrist Band
Relative Aware
A. Oxygen in progress/Prescribed: YES/NO Time given..................................
Phone Numbers
B. X Rays  Sats Probe*  Valuables Yes/No
C. Cannula  IV Fluids  Pump needed*  SAD Score
Catheter  ECG  Cardiac Monitor*  Waterlow Score
Falls Assessment
D. Analgesia given  Sliding Scale 
NBM
E. IV ABx  Bloods taken  Notes Scanned
Recommendation
Tranfer to: Ward_______Placement: Bay____Bed____High Visibility 
Additional equipment required (not*): No  Yes  __________
Any patient own drugs: No  Yes  __________ Drugs trolley checked by ........................
Transport: Bed  Chair  Tranfer by: Reg Nurse if MEWS > 4  Healthcare  Porter
Signature of transferring nurse..................................................................................... Time.......................
Signature of accepting nurse........................................................................................ Time.......................
Figure 1. AMU transfer Checklist.

Acute Medicine 2012; 11(1): 13-17 15
hospital sites, and to incorporate the Situation, Data Number (n)

Background, Assessment and Recommendation (SBAR)2
telephone communication model, which was mandatory Patients 30
in the Trust for telephone handovers. This involved Completed Check list 1
reconstructing the format of the information on the
original transfer checklist into new sections related to Time documented in notes 6
SBAR and reconsidering the nature of the information MEWs documented in notes 0
required on the revised transfer checklist.3
Patients with one move 9
The strategy focussed on the information that was
pertinent to safety ‘during transfer’. Poor transfers are Patients with two moves 21
frequently characterised by an incomplete transfer of
Table 1. Data on the 1st Audit Cycle.
information, resulting from long and incomplete transfer
checklists.4 A key element of our redesign process was to
incorporate the NHS Litigation Authority (NHSLA) Audit Standard
guidance on patient transfers, (Text box 1). Adherence to this “Each patient must have a transfer checklist to accompany their
standard enables the Trust to give quality assurance on the transfer – with 100% completion of the SBAR elements”.
process of transfer and patient safety.1
Secondly, the hospital transfer policy has been updated Audit Cycle 1 Results
during 2010/2011 and from this several standard operating 36 patient notes were identified during the audit period. 6
procedures (SOPs) were devised for specialist groups of were excluded as the patients were not being transferred to
patients. The AMU devised a SOP applicable for each of AMU-2, leaving 30 records for analysis. The results of
the 3 acute medical units within the Trust (text box 2). these can be seen in Table 1.
Core information indicated from this was integrated into Out of the patient notes only one checklist had been
the revised transfer checklist. completed. In an attempt to establish where patient transfers
The policy and the SOP were analysed together to had been documented, the patient notes were also analysed.
enable development of the revised transfer checklist. This This was originally not part of the design – but in the absence
was incorporated into the AMU clerking document, of the checklist we searched for basic information regarding
which was automatically printed at the back of the Modified Early Warning Score (MEWs) and time of transfer.
document, negating the need to write a separate checklist Twenty one of the patients had originally been transferred
(Figure 1). into AMU from the ED. In this case, supplementary
information in the form of ambulance transfer sheets and
Incident reporting telephone handover forms to the AMU were present in the
Prior to the audit we requested all Incident Report forms notes. However, the standardised, NHSLA compliant
(IR-1) relating to transfer, generated by wards receiving checklist was not present in 29 out of the 30 cases.
patients from AMU. Detailed thematic analysis of the
forms revealed 23 incidents reports directly related to Interventions following audit cycle 1
transfer issues over a 2 month period. The following core A team meeting was organised to highlight the gravity of the
themes were identified: situation to Band 7 Sisters. The Sisters engaged with their
1. Inadequate clinical history prior to transfer, junior Sister colleagues in the reinforcement of the
leading to patients being reported as being importance of the checklist. A concerted effort was made to
transferred to a ward where the staff felt the raise the staff awareness on each shift over several weeks.
patient’s needs were unable to be accommodated. This was monitored through the collation of data on the
2. Inadequate verbal handover prior to transfer, AMU, with feedback at each weekly team meeting. Finally
leading to inadequate preparation for the patient’s a lunch time audit presentation using scenarios from the
arrival, such as availability of pressure relieving care, IR1 reporting database was given to a multi-professional
acquisition of electronic pump devices and the need staff audience who work on the AMU. The regular
for one-to-one nursing care. reporting continued until the start of the second audit cycle.
3. Inaccurate calculation of the modified early
warning score leading to an apparent change in Audit cycle 2 Results
the condition of the patient by comparison to the 48 case notes were analysed; two were excluded because
verbal hand over. the time and date of transfer could not be identified. The
degree of completion of the transfer checklists was
Audit Methodology analysed for the remaining 46.
Two complete retrospective audit cycles were completed 23 of the transfer checklists were, at least partially,
in November 2010 and February 2011, with the purpose completed (50%). For those not completed, 21 were left
of analysing the compliance, completion and blank and the other two patients had been clerked using a
improvements needed in practice. generic clerking document that was not generated in the
Each audit cycle included all patients transferred from AMU. Approximately twice as many transfers happened
AMU (Ward 20) to its sister unit AMU-2 (Ward 8). during the night than during the day, and 2.5 times as

16 Acute Medicine 2012; 11(1): 13-17
Completion status: Total Parts completed n
Yes/ Partially Not attempted 5 4
Total (n = 46) 23 23 4 5
3 5
Shift: 2 5
Day shift (n = 17) 6 11 1 2
Night shift (n = 29) 17 12 0 2
Total 23
Weekend/ Weekday:
Table 4. Number of parts analysed that were completed.
Weekday shift: (n = 33) 18 15
Weekend shift: (n = 13) 5 8 many transfers happened during the week than during the
Table 2. Break down of transfer check list. weekend.The differences in checklist completion rates for
night vs day and weekend vs weekdays did not reach
statistical significance by Chi-squared analysis.
Assessment: Completion Only 4 documents were deemed to have been fully
Yes No N/A
completed (17%). Fourteen documents had a signature and a
name identifying that a nurse had completed it. Monitored
Fully Completed 4 19 equipment documentation was the area least likely to be
Assessed by Registered Nurse 14 9 0
completed. The two forms which had no analysed parts were
still clearly attempted by the nursing staff, although none of
Monitoring equipment 7 12 4 – Not needed the components were fully completed.
MEWS recorded 17 6 0 Although a reduction in incidents reported was not one
of the planned outcome measures, analysis of the IR1
Escort needed 0 4 19 – Either database revealed only 4 incidents relating to patient transfer
MEWS < 4 or
stated ‘Not
in the two month period following the second audit cycle.
required’
Property 12 0 11 – Box not
Continual Monitoring
ticked Since the original AMU audit, the corporate team has
conducted intermittent audits of the transfer checklist
Table 3. Transfer checklist analysis of 23 partially / fully completed forms. across the Trust. At September 2011, the compliance
Figure 2. Continual monitoring of the transfer checklist.

Acute Medicine 2012; 11(1): 13-17 17
within the AMU was an average of 85% increasing to 95% significant improvement in use of our transfer checklist
at peak times, as illustrated in Figure 2. following the interventions involving education and
raising awareness amongst the nursing staff. This
Discussion improvement still fell short of our 100% target and further
The importance of checklists in the handover process has intervention is required. However continued monitoring
been previously documented.4,6,7,8 However our literature has shown ongoing improvements in completion rates.
search failed to identify any previous studies specifically Ongoing education is important in improving
looking at this area in relation to transfers in and out of the compliance with the checklist. New members of staff and
Acute Medical Unit. This is surprising given that patient constantly changing shift patterns means that some nursing
transfer represents a significant proportion of the AMU staff may have been unaware of the transfer checklist’s
workload; this study therefore reflects an important addition existence. The documentation is now introduced with the
to the literature in this area. With any transfer of patient care clerking document during nurse induction to the unit.
there is a significant risk for this to be sub-optimal, mainly The current checklist may also be too detailed for all
due to ineffective communication between health care patients, discouraging completion. Some aspects of the
professionals.3 This is reflected in the high level of incident checklist are not relevant to all patients. The advent of
reporting concerning patient transfers prior to the electronic patient records in the future may allow for
introduction of our checklist. bespoke completion of specific aspects; certain items i.e.
Checklists have been shown to reduce “errors of cardiac monitoring, oxygen, intra-venous f luids could be
ineptitude”, where staff fail to make use of knowledge that automatically removed from the document when not
they possess.9 An important feature of a checklist which relevant.4
improves the likelihood of accurate completion is ‘user-
friendliness’; checklists should ideally comprise between 8 Conclusion
to 10 points.10 Maintaining this simplicity and user Our audit has demonstrated that improved compliance
friendliness was a key aspect of our redesign process, and with the use of checklists relating to patient transfer in and
created some tension within the design group. The need out of AMU can be achieved by an educational
to align to a hospital wide process required the programme and ongoing work to increase staff awareness
involvement of many different staff groups, many of whom of its importance. This is ref lected in improved checklist
requested inclusion of information which they felt, completion rates and a reduction in the numbers of
subjectively was ‘required’ in their area . incident reports relating to patient transfer. Although there
Checklists are of no use if not completed. Our initial remains room for improvement we would encourage other
audit demonstrated very poor compliance with this units to adopt a similar process to optimise patient safety
documentation. However, we were able to achieve a during transfer.
References
1. HEFT (2010) The Heart of England NHS Foundation Trust, Patient 6. Ong, MS., and Coiera, E. (2011) A systematic review of failures in handoff
transfer policy: version. www.heartofengland.nhs.uk communication during intra hospital transfers. Joint commission Journal on
2. NHS Institute SBAR, Quality and service improvement tools: quality and patient safety, 37(6), pp 274–84.
http://www.institute.nhs.uk/quality_and_service_improvement_tools/ 7. Catchpole K, Sellers R, Goldman A, McCulloch P, Hignett S. Patient
quality_and_service_improvement_tools/sbar_-_situation_-_background_-_ handovers within the hospital: translating knowledge from motor racing to
assessment_-_recommendation.html Accessed 21/9/2011. healthcare. Qual Safety in Health Care. 2010; 19(4): 318–22.
3. Lertzman, R. (2006). No more hinting and hoping: An interview with 8. Park W. (1967) Patient Transfer Form. The American Journal of Nursing.
Frances Griffin. www.saferhealthcare.org 67(8): 1665–8.
4. Nagpal, K., Abboudi, M., Fischler, L. et al Evaluation of postoperative 9. Gawande A. (2009) The Checklist manifesto: How to get things right:
handover using a tool to assess information transfer and teamwork. Ann Metropolitan Books; 2009.
surg 2011: 253(4); 831–7. 10. Terrell KM., Miller DK., (2010) strategies to improve care transitions
5. NHSLA. Standard 4 – Criterion 5: Transfer of patients 2010 [cited between nursing homes and emergency departments, Journal of American
11/06/11]; Available from: http://www.nhsla.com/home.htm Directors Association, Epub ahead of publication in November 2010.

18 Acute Medicine 2012; 11(1): 18-22
Where Do AMU Nurses Perceive

Their Educational Needs?
Results of the 20:10 project
J Jepson, S Whitley, C P Subbe & L Grundy
Key Messages
1. There is no accepted curriculum for nurses working in Acute Medicine.
Jacqueline Jepson 2. Nurses felt that education needed to centre around frequently presenting symptoms.
Lead Advanced Nurse 3. Skills identified, overlapped with those traditionally performed by junior doctors, thus supporting the concept of
Practitioner for Acute interprofessional education.
Medicine, Glan Clywd 4. Formal educational support is needed to address these needs and secure future recruitment.
Hospital,
Rhyl,
Abstract admissions and may have integrated ambulatory care
Denbighshire,
LL18 5UJ, Our aim was to identify the perceived educational needs of units. Most AMUs have monitored beds and in
UK nurses working in acute medicine to enable development of a many hospitals the capability to look after patients
training curriculum specifically for this staff group. with increased monitoring needs or the need for
Stella Whitley Methods: Post-graduate nurses from North Wales were basic single organ support (level I and level II
Senior Lecturer in Nursing
invited to list 20 conditions and 10 skills for which they felt patients). Service provision can include patients with
& Clinical Simulation,
Glyndwr University, under prepared for their work in acute medicine. A workshop acute coronary disease requiring continuous cardiac
Mold Road, was then organized, attended by acute medicine nurses, monitoring, patients requiring Non-Invasive
Wrexham, medical colleagues and educationalists from two local Ventilation and patients requiring haemodynamic
LL11 2AW, universities to discuss initial data. support via central venous cannulae. Staff therefore
UK Results: Nurses identified particular needs for education need significant skills in the assessment and
around presenting symptoms with perceived deficits in management of acute illness.2
Christian P Subbe
DM, MRCP (London), knowledge or training. We found a heavy emphasis on
Senior Clinical Lecturer, respiratory and cardiac conditions. There was considerable Background - Education and Skills Development
School of Medical Sciences, overlap with frequent diagnostic categories from non-surgical In addition to offering a multifunctional service, nurses
Bangor University, hospital discharges and with priorities for training of junior working in AMUs need to be specialists in safe
Brigantia Building / Adeilad doctors. Skills were often those traditionally associated with discharge planning.3 The high turnover of patients and
Brigantia, fast pace of work is a significant risk factor for burn out
medical staff or care of patients with critical illnesses.
Bangor,
LL57 2AS, Conclusion: The 20:10 project represents the first of staff4 and can also compromise patient safety.5
UK attempt to map educational needs of nursing staff on the Recruitment into specialties is often improved by
Acute Medical Units of a large University Health Board coherent educational support6 and career progression.7
Lynne Grundy using self-reported needs. The identified needs will support Nurse education, both pre and post registration,
Head of Nursing, needs to be provided in the context of a changing
professional development, create incentives for recruitment
Professional Nursing and
and guide University postgraduate developments and healthcare landscape. Education and skills
Education,
Bwrdd Iechyd Prifysgol, commissioning. development for AMU nurses should be geared
Betsi Cadwaladr University towards the specific requirements of the AMU
Health Board, Keywords environment.
LL18 5UJ, Acute medicine, nursing, education, curriculum, professional The aim of this study was to explore the self
UK development. reported educational needs of nurses working in
Correspondence: AMUs in order to allow educational providers to
Jacqueline Jepson Introduction create a curriculum for a modular postgraduate
Lead Advanced Nurse Background - Acute Medical Unit Development qualification in acute medical nursing.
Practitioner for Acute Acute Medical Units (AMUs) were introduced in
Medicine, Glan Clywd the 1990’s to bring together the resources required to Methods
Hospital, Setting
look after acutely ill medical admissions in a more
Rhyl,
Denbighshire, effective way.1 Three District General Hospitals (DGHs, Wrexham
LL18 5UJ, This model has been adopted by the majority of Maelor Hospital, Ysbyty Glan Clywd, Rhyl and
UK UK hospitals. AMUs receive the unselected medical Ysbyty Gwynedd, Bangor) in North Wales that form
Email: Jacqueline.Jepson@
wales.nhs.uk

Acute Medicine 2012; 11(1): 18-22 19
Where Do AMU Nurses Perceive Their Educational Needs? Results of the 20:10 project
part of the same University Health Board, each covering a Project design
population of around 250,000 and a mix of rural and urban The participants were asked to list 20 conditions for which
areas. All three AMUs admit between 25 and 35 patients they felt under-prepared following qualification and
per day, have dedicated Acute Physicians, and access to employment as a registered nurse. The teams were also
level III facilities on site but no provision of level II beds asked to list which skills they felt required further training.
within either of the AMUs. There is provision of A single list was then compiled by each of the participating
Ambulatory Care in two of the hospitals. AMUs by consensus.
Newly registered nurses are largely recruited from two A workshop was organized in July 2010. It was open to
local Universities (Glyndwr University, Wrexham and all team members from the three units, and there was
Bangor University) with some additional recruitment from representation of a senior nurse from each of the units. The
Cheshire and Merseyside. More experienced nurses are participants included two educationalists. The workshop
recruited internally from other areas of the hospital, and served as a focus group for the development of the
occasionally national recruitment is carried out to meet needs. curriculum and encouraged participant collaboration. The
focus group collated the data from the three AMUs by
Participants consensus providing a core list of conditions and skills that
Staff nurses working in the three AMUs, regardless of their require further nurse education and development. The list
banding or duration of contract were invited to participate in was not ranked. Conditions and skills were listed
this study. Junior nurses, team leaders, professional alphabetically.
development leads and nurse managers were all represented Comparisons were made with conditions generated
in the group. from non-surgical emergency admissions in England for
20:10 conditions chosen by ‘Top 20’ conditions from 2009 curriculum Top conditions from HRG statistics
nursing team for GIM / AIM training 2007/2008* in order of frequency
Asthma Abdominal pain Nonspecific chest pain
Cardiac and non-cardiac chest pain Acute back pain Pneumonia (except that caused by tuberculosis
or STD)
Congestive cardiac failure Blackout Urinary tract infections
Cellulitis Breathlessness Chronic obstructive pulmonary disease and

bronchiectasis
Chronic obstructive pulmonary disease Chest pain Acute bronchitis
Dyspnoea diagnosis Confusion Cardiac dysrhythmias
Headaches Cough Coronary atherosclerosis and other heart

disease
Hyperglycaemia Diarrhoea Skin and subcutaneous tissue infections
Iron deficiency Anaemia Falls Epilepsy, convulsions
Lower respiratory tract infection Fever Acute cerebrovascular disease
Neurological Deficit in alert patients Fits Syncope
New onset atrial fibrillation and atrial Haematemesis Other connective tissue disease
flutter without ACS
Palpitations Headache Noninfectious gastroenteritis
Pleural effusion Jaundice Poisoning by other medications and drugs
Pneumothorax Limb pain Other upper respiratory infections
Pulmonary Embolism Palpitation Acute myocardial infarction
Stroke Poisoning Asthma
Transient ischemic attack Rash Other upper respiratory disease
Upper respiratory tract infection Vomiting
Urinary tract infection Paralysis

*
From Subbe CP et al. Eur J Intern Med. 2011; 22: 339-43. quoted with permission of the authors
STD: Sexually transmitted disease, ACS: Acute Coronary Syndrome; AIM – acute internal medicine; GIM – General (Internal) Medicine
Table 1. Comparisons of top 20 conditions chosen from 20:10 workshop, top 20’ conditions from 2009 GIM/AIM curriculum and the top
conditions from HRG statistics from NHS England 2007/2008.
20 Acute Medicine 2012; 11(1): 18-22
Arterial blood gas analysis

The top 20 presentations in the GIM / AIM curricula
are entirely symptom based, which is appropriate given
Cannulation that initial assessment of patients by junior doctors involves
Care of long lines the determination of differential diagnosis from a patient’s
ECG Interpretation narrative. However this approach has limitations, since
some conditions such as acute hyperglycaemic
External Pacing
emergencies do not present with a clearly defined set of
Management and priority of care symptoms; competencies for management of these
Non-Invasive Ventilation situations are therefore ref lected elsewhere in the
curriculum. By comparison the nursing list describes a
Phlebotomy
mixture of diagnoses and problems. There is reference to a
Triage number of specific causes of breathlessness (pleural
Use of a stethoscope for chest auscultation effusion, pulmonary embolism, congestive cardiac failure,
and pneumothorax) in addition to the generic ‘problem’ of
Table 2. Top 10 skills from 20:10 workshop.
dyspnoea. Iron deficiency anaemia and hyperglycaemia as
well as urinary tract and upper respiratory tract infection
2007/20088 and the top 20 conditions in the 2009 are also specifically listed. It is interesting to note that there
GIM/AIM curriculum.9 Nurse educationalists indicated was considerable overlap between the list generated by
that pre-registration nurse education does not use a disease nurses and the HRG coding for admissions in our hospital
model and whilst this meant that similar tables of in 2008-2009 (see Table 1).
conditions covered in nurse education were not available,
many of the conditions are introduced in pre-registration Discussion
nurse education. Our findings
Tables 1 and 2 illustrate the 20:10 project’s attempt to
Results describe the self – perceived educational needs of nurses
The results of the focus group discussions are compiled in working within today’s North Wales AMUs. For regional
Tables 1 and 2. educational providers it is now possible to start the
foundations of a postgraduate curriculum in Acute
List of conditions Medicine nursing incorporating the identified conditions
The list of conditions contained clinical diagnoses and skills. Current specialist modules delivered by local
(Chronic Obstructive Pulmonary Disease) as well as educational institutions (accident and emergency,
symptoms (“breathlessness”). The bulk of conditions coronary care, intensive care and high dependency care
(14/20) were from the areas of cardio-vascular and nursing) are able to deliver many if not all of the skills
respiratory medicine. highlighted. However this provision is fragmented in the
context of Acute Medicine nursing and only partly
List of skills addressed in undergraduate level teaching.10 The
The skills fell into three groups: skills largely restricted to comprehensive assessment of medical and functional
the care of critically ill patients (non-invasive ventilation, dimensions of patient presenting to AMU is not currently
central venous catheter care etc), skills traditionally covered by any of the educational programs on offer in this
covered by medical students, doctors and other health care area. Given that the AMU sits at the interface between
professions (phlebotomy, cannulation, interpretation of an primary and secondary care, it is surprising that skills
Electrocardiogram (ECG), interpretation of blood gases, associated with working in the social environment of the
use of a stethoscope) and organizational skills that are more patient in the community were not listed. Equally, in the
relevant in areas of high turn over (triage, management and face of an aging population, the fact that very few
prioritization of care). conditions specific to older patients (falls, acute confusion,
dementia) were mentioned is worthy of note. This
Comparison to Hospital Episodes and Acute Internal emphazises the limitations of the project in trying to
Medicine Curriculum define a curriculum based solely on the perceived needs of
The predominance of cardiovascular and respiratory the staff. A combined approach utilizing HRG data may be
conditions (14/20) corresponds to 12/20 diagnostic groups more appropriate.
in the analysis of hospital episodes in England in 2007/2008
that were attributable to ischemic heart disease or acute Interprofessional Education
respiratory illness, and to 5/20 potentially cardiac or The large overlap between the diagnostic categories, the
respiratory presenting symptoms (black-out, breathlessness, curriculum for Acute Medicine and the self-assessed
chest pain, cough, palpitations) in the “Top 20” Common learning needs of nurses working in the AMU would
Medical Presentations, as defined in the the 2009 training strongly support a move to a more interprofessional
curriculum for General Internal Medicine (GIM) and Acute approach to education.11 The benefits of interprofessional
Internal Medicine (AIM). The nursing conditions also education (IPE) are well recognised by the Department of
included specific reference to stroke and transient ischemic Health,12 General Medical Council13 and Nursing
attack. Midwifery Council14 and the UK consensus conference on

Acute Medicine 2012; 11(1): 18-22 21
Acute Medicine.15 Despite this, robust and reproducible from community to critical care nursing. The broad range
templates for IPE have not been adopted. A systematic of professional profiles means that more specialized
review undertaken by Cooper16 examined the evidence for training will be required upon qualifying, especially within
interdisciplinary learning and concluded that there are acute medical nursing. It is possible that objective
benefits relating to change in knowledge, attitude, skills educational needs of staff were different from those
and beliefs. Without the advantages of designated collated from self-assessments. This might be a fruitful area
infrastructure, facilities and staff, finding an appropriate for future work. We believe that in order to get buy-in
environment to maximise IPE can be demanding. from staff it is crucial for an educational program to start
with areas of interest to staff and develop a program from
Expanding roles there.
The information from the workshop reflects in part the Simulation might be used as an adjunct to expose the
changing professional roles and shifting boundaries nursing student to scenarios of critical illness,18,19 and
influenced by such things as European Working Time could be usefully applied to training in most of the 20
Directive and reduction in junior doctors’ hours. With conditions and 10 skills. Pre-registration nurse education
professionalization of nursing, the expanded as well as at Glyndwr University aims to provide up to 300 hours of
advanced nurse role requires the practitioner to be skilled in simulated practice, which will continue in future nurse
many areas previously undertaken by medical colleagues for curriculum development.7 Simulation training provides
example, prescribing, medical interventions and treatment, nursing students with skills which otherwise may not
clinical assessment and diagnosis.17 Healthcare workers, become developed until qualifying due to the differing
especially in acute medicine, are taking on more specialised standards and expectations of hospitals, wards or specialist
roles, including the “medical” admission and discharge area.
process, leading to a blurring of traditional professional A proportion of qualified nurses continue their
boundaries. Healthcare education should ref lect these professional educational and training at postgraduate level.
changes across the range of roles and responsibilities. Short courses which focus on skill acquisition rather than
academic achievements maybe the way forward to achieve
Limitations training that is “fit for purpose”.11 The foundation courses
Nursing staff from the three units were invited to participate may also be mapped against junior doctor training for
in generating the content of a future curriculum. However, Acute Medicine therefore promoting standardization of
there was no mechanism in place to ensure a representative practice and facilitating the principle that “those who
sample. It is possible that the suggested content for the work together, should train together”.5 Additionally the
development of a postgraduate curriculum in acute medical AMU provides a unique environment for experiential
nursing would not cater for the needs of new-comers to learning given the breath and depth of pathology as well as
AMU or senior team leaders. Additionally the focus of our the near continuous opportunity for supervision by senior
paper was perceived as opposed to objective needs; this is likely medical and nursing staff.
to be driven by the case-mix that staff experience in our local The results of our workshop give local educational
units. For example management of Deep Vein Thrombosis providers and NHS health care providers the opportunity
(DVT) in North Wales is largely done in an outpatient to develop a foundation postgraduate curriculum for acute
setting, and one of the units admits all patients with upper medical nursing by merging existing curricula. We are
gastro-intestinal bleeding through the surgical department. currently engaging all stakeholders to take this work
Similarly, patients presenting with suspected stroke in forward as we now have the opportunity, within a larger
North Wales are only admitted to a stroke unit after initial organization, to ensure such programmes are viable in a
review in the AMU. rural environment. E-learning might have to play a
Advanced nurse practitioners (ANP) and Nurse significant part in the delivery.20
Consultants in Acute Medicine have specific educational
needs which may differ from those identified in this study. Conclusion
Their roles straddle professional boundaries, involving Appropriate postgraduate education and training for
admission of patients alongside medical practitioners, nursing staff working in the demanding environment of
ordering first line investigations, prescribing medication Acute Medicine is essential to attract and retain staff, and
and managing services for defined patient groups support quality of care, efficiency of service and patient
(pulmonary emboli, asthma, cellulitis). safety. The 20:10 project identifies perceived gaps in
education and suggests a set of core conditions and skills
Implications for delivery of local education that are being shared with doctors training in Acute
Current nurse pre-registration training attempts to prepare Medicine. This highlights the opportunity for a more
students for a broad range of professional options, ranging interprofessional approach to health care education.

22 Acute Medicine 2012; 11(1): 18-22
References
1. Acute medical care: The right person, in the right setting – first time. 10. McGaughey J. Acute care teaching in the undergraduate nursing
Report of the Acute Medicine Task Force Royal College of Physicians, curriculum. Nurs Crit Care. 2009; 14: 11–6.
London 2007. 11. Lewis R. Learning the 'SMART' way... results from a pilot study evaluating
2. Lees L, Hughes T. Implementing a patient assessment framework in acute an interprofessional acute care study day. Nurse Educ Today 2011; 31: 88–93.
care. Nurs Stand. 2009; 24: 35–43. 12. Department of Health. 150 years of the annual report of the chief medical
3. Sturgess I. Planning for predictable f lows of patients into unscheduled care officer: safer medical practice, machines, manikins and polo mints. Crown.
pathways beyond the Emergency Department: Meeting Demand and London 2009.
Delivering Quality. IMAS 2010. 13. General Medical Council. Tomorrows Doctors. London 2009.
4. Gillespie M, Melby V. Burnout among nursing staff in accident and 14. Nursing & Midwifery Council. Standards for Pre-registration Nursing
emergency and acute medicine: a comparative study. J Clin Nurs. 2003 Education. London 2010.
Nov; 12(6): 842–51. 15. Jones MC, Lees L. How is multi-professional training optimized in the
5. West MA, Borril CS, Dawson JF, et al. The link between the management acute environment? Br J Hosp Med 2009; 70: S19–25.
of employees and patient mortality in acute hospitals. International Journal of 16. Copper H, Carlisle C, Gibbs T, Watkins C . Developing an evidence base
Human Resource Management 2002; 13:1299–1310. for interdisciplinary learning: a systematic review. Journal of Advanced
6. Rambur B, McIntosh B, Palumbo MV, Reinier K. Education as a Nursing 2001; 35: 228–237
determinant of career retention and job satisfaction among registered 17. Royal College of Nursing. Advanced Nurse practitioners. London 2010.
nurses. J Nurs Scholarsh. 2005; 37: 185–92. 18. Borneuf AA. The who and where of clinical skills teaching: a review from
7. Lees L, Myers L. A profile of Nurses working in acute medicine units: the UK perspective. Nurse Education Today 2008: 197–201.
What is the future? Acute Med. 2010; 9: 91–6. 19. Akhtar-Danesh BP. Nurse faculty perceptions of simulation use in nursing
8. Subbe CP, Bottle RA, Bell D. Acute Medicine: Triage, timing and education. Western Journal of Nursing Research 2009: 1–67.
teaching in the context of medical emergency admissions. Eur J Intern Med. 20. http://www.e-lfh.org.uk/projects/acumen/index.html
2011; 22: 339–43.
9. Specialty Training Curriculum for Acute Internal Medicine. Joint Royal
Colleges of Physicians Training Board. London 2009.

Acute Medicine 2012; 11(1): 23-24 23
Case Reports
A hot bath to calm what ails you – the

Cannabis Hyperemesis Syndrome
V Luther & L Yap
Teaching Points
1. Recurrent episodes of vomiting, a history of cannabis excess and symptom relief with a hot bath describes the
Cannabis Hyperemesis Syndrome (CHS).
2. A history of cannabis use should be enquired about in patients presenting with unexplained recurrent or cyclical
vomiting.
3. The only effective treatment for CHS is cannabis cessation.
4. As cannabis use is common, it is likely that CHS will become increasingly recognised as awareness of this syndrome
grows.
5. It is important that clinicians are aware of this condition in order to minimise unnecessary investigations and to
encourage patients to stop smoking cannabis.
Abstract On examination, the patient looked remarkably

The Cannabis Hyperemesis Syndrome (CHS) defines a clean with his hair wet and neatly combed
recently described paradoxical association between recurrent backwards. He was afebrile, all vital signs were
vomiting episodes, daily cannabis excess and symptomatic within normal limits and he was clinically
relief with a hot bath or shower. Importantly, symptom euvolaemic. He was tender in his epigastrium
resolution only occurs with cessation of cannabis use. We without any signs of peritonism.
describe a case of CHS which had resulted in repeated Due to the ongoing severity of his symptoms, the
hospital admissions. As cannabis use is common, it is patient was admitted under the acute medical team
important for both patients and Acute Physicians to be aware for symptom control with antiemetic therapy and
of this increasingly recognised condition. further assessment. His blood tests, including liver
function, amylase, calcium and lactate were within
Keywords normal limits. Urine analysis, chest and abdominal
Cyclical Vomiting Syndrome, Cannabis, Cannabis radiography were normal.
Hyperemesis Syndrome. That this was the patient’s eighth identical
presentation to this hospital in 3 years. He had been
Case report admitted twice, and self discharged on each occasion.
A 21 year old british caucasian male presented to the At each presentation, blood tests and radiology had
local hospital emergency department with a 12 hour always been negative. The patient had been seen in the
history of severe nausea and vomiting. He had gastroenterology clinic one year earlier. An endoscopy Vishal Luther
vomited greater than ten times since the onset earlier had revealed a normal upper gastrointestinal tract; MBBS BSc MRCP,
Core Medical Trainee Year 2,
in the day, bringing up clear liquid mixed with some urease breath test was negative for Helicobacter pulori;
Whittington Hospital,
undigested food products. He was uncooperative duodenal biopsy showed no features of Coeliac disease. London
during the assessment and oddly, he persistently An earlier abdominal ultrasound revealed a normal
demanded to use our showering facilities. liver and pancreaticobiliary system and no evidence of Lok Yap
The patient admitted that he had experienced gallstones. MBBS MCRP
This patient was demonstrating recurrent short Consultant Acute Physician
these symptoms in the past and was told it was due to
Whittington Hospital,
gastritis. He had no other significant previous lived stereotypical episodes of nausea and vomiting
London
medical history or relevant significant family history. with no clear cause. He was diagnosed as suffering
He took no regular or over the counter medications from Cyclical Vomiting Syndrome. Correspondence:
(including non-steroidal anti-inf lammatory The anti-emetic effect of cannabis is well known Vishal Luther
and it was initially postulated that he was trying to 14 Spencer Road,
medications) and drank on average about 10 units of
Wembley,
alcohol per week. control his symptoms using this illicit medication. He
Middlesex,
He did admit to using cannabis heavily, smoking continued to demand to use the showering facilities, HA0 3SF
at times up to 4 joints per day for the preceding four and oddly seemed more settled after bathing. Once Email: vluther@doct
years. again, the patient soon self discharged. ors.org.uk,

24 Acute Medicine 2012; 11(1): 23-24
A hot bath to calm what ails you – the Cannabis Hyperemesis Syndrome
Discussion satiety, thirst, digestive and thermoregulatory systems of

Cyclical Vomiting Syndrome (CVS) is a condition the hippocampus-hypothalamus-pituitary axis which have
whereby patients experience short lived episodes of been associated with chronic cannabis use.6 More
vomiting at least three times each year with a clear absence importantly, it appears that the only way of treating CHS
of symptoms between episodes.1 The exact aetiology of is cessation of cannabis use, with relapses in symptoms
this condition is unknown, and it is often attributed to a occurring on resumption.5,6
migrainous phenomenon. Cannabis is the most widely used illicit drug.8 As a
The active ingredient in cannabis, result, the prevalence of CHS may be much higher than
tetrahydrocannabinol (THC), is used synthetically as an reported. Since the realisation of this syndrome by the
antiemetic (e.g. nabilone). THC acts on endogenous author’s acute medical team in 2010, a further 4 cases have
cannabinoid receptors (CB1) present in the brain and been recognised. Wallace et al (2011) reported that since
enteric nervous system to suppress emetogenic stimuli the discovery of this condition in their organisation in
communicating between these two nervous systems.2 2010, they too have since identified a further 5 cases.8
This patient presented with an episode his presumed The economic impact of individual emergency
CVS, which seemed to improve after a hot bath. A handful department visits and acute admissions to hospitals for CHS
of case reports have revealed how chronic cannabis abuse is likely to be high. Patients with CHS may remain
appears to have a causal association with CVS.3,4 undiagnosed for several years, presenting to hospital on
Characteristically, the symptoms are improved by a hot multiple occasions and receiving a variety of expensive
bath or shower. This has been called the Cannabis (or investigations whilst they continue to smoke cannabis. It is
cannabinoid) Hyperemesis Syndrome (CHS). A case series thus very important for clinicians to be aware of this
published in February 2010 explored 8 patients who condition. Equally important is educating patients
required on average 5 baths per day, with a mean total themselves that the cause of their recurrent presentation is
bathing time of 5 hours per day to control their symptoms secondary to their excessive cannabis usage, and that their
during an episode.5 Sufferers have also scalded themselves symptoms may only cease by stopping.
in an attempt to run the bath or shower water as hot as Our 21 year old male patient was diagnosed with
possible.6 Cannabis Hyperemesis Syndrome. Despite efforts to
CHS seems to occur after several years of moderate to encourage the patient to attend a drug rehabilitation clinic,
heavy use of cannabis in susceptible individuals. The effect he failed to engage, continued to smoke, and represented
may arise from dysregulation of endo-cannabinoid once further to the emergency department. He even
receptors with chronic cannabis use or through episodic admitted on this occasion that he had only come to
gastroparesis (THC is known to delay gastric emptying).7 hospital because his showering facilities had broken at
The compulsion to take hot baths or showers (which home. As he was clinically euvolaemic, he was not
provide transient relief from symptoms) may arise from admitted, educated about the condition, and strongly
temporary improvements in autonomic dysfunction in the advised to quit smoking cannabis.
References
1. Talley NJ (2007) Functional nausea and vomiting. Aust Fam Physician Pain, and Compulsive Bathing Associated with Chronic Marijuana Use: A
36(9): 694–7. Report of Eight Cases in the United States. Dig Dis Sci 55(11): 3113–9.
2. Izzo AA, Sharkey KA (2010) Cannabinoids and the gut: new developments 6. Allen JH, De Moore GM, Heddle R, Twartz JC. (2004) Cannabinoid
and emerging concepts. Pharmacol Ther 126(1): 21–38. hyperemesis in association with chronic cannabis abuse. Gut. 53:
3. Price SL, Fisher C, Kumar R, Hilgerson A (2011) Cannabinoid 1566–1570.
hyperemesis syndrome as the underlying cause of intractable nausea and 7. Budhraja V, Narang T, Azeez S. (2008) Cannabinoid hyperemesis
vomiting. J Am Osteopath Assoc. 111(3): 166–9. syndrome: cyclic vomiting, chronic cannabis use, and compulsive bathing.
4. Schmid SM, Lapaire O, Huang DJ, Jürgens FE, Güth U (2011) Pract Gastroenterol. 32(9): 79–80.
Cannabinoid hyperemesis syndrome: an underreported entity causing 8. Wallace EA, Andrews SE, Garmany CL, Jelley MJ (2011) Cannabinoid
nausea and vomiting of pregnancy. Arch Gynecol Obstet. 284(5): 1095–7. hyperemesis syndrome: literature review and proposed diagnosis and
5. Soriano-Co M, Batke M, Cappell MS (2010) The Cannabis Hyperemesis treatment algorithm. South Med J. 104(9): 659c64.
Syndrome Characterized by Persistent Nausea and Vomiting, Abdominal

Acute Medicine 2012; 11(1): 25-27 25
Case Reports
Endogenous endophthalmitis and liver

abscesses
S Koay, S Jain, I Cropley, H Petrushkin & H Beynon
Key Learning Points

• Endogenous endophthalmitis is a serious intraocular infection resulting from haematogenous spread of bacteria from a
distant primary source.
• It is often associated with patients with an underlying medical condition, or those with risk factors for
immunosuppression.
• Prompt diagnosis and administration of antibiotics is important to optimise visual outcomes.
• Acute medical teams should be aware of this potentially blinding condition, and include it in the differential diagnosis
for painless loss of vision.
Abstract seen in the superior temporal quadrant of the left

We present a case of endogenous endophthalmitis secondary retina(Figure 1). There were also two cotton wool spots
to liver abscesses, in a patient with no previous medical seen in the right retina. Blood tests showed a white cell
comorbidities or risk factors for immunosuppression. The count of 20.57 x 109/L (neutrophils 17.3) and
patient presented with acute painless loss of vision and feeling C-reactive protein of 245mg/L. Renal and liver S Koay
generally unwell. Investigations revealed Streptococcus function tests were normal, and a HIV test was negative. MBBS
anginosus-constellatus bacteraemia, and evidence of Blood cultures were performed, following which FY2 Acute Medicine,
Royal Free Hospital,
diverticular disease that likely predisposed to the liver intravenous amoxicillin and gentamicin,
London
abscesses. Due to prompt diagnosis and administration of cyclopentolate 0.5%, and dexamethasone eye drops
antibiotics, the patient had a good visual outcome. This case were commenced for suspected endogenous S Jain
highlights the importance of being aware of endogenous endophthalmitis. FRCOphth
endophthalmitis, as early diagnosis and prompt Blood cultures and a subsequent anterior Consultant
Ophthalmologist,
administration of antibiotics will optimise visual outcomes. chamber sample grew Streptococcus anginosus-
constellatus, which was sensitive to penicillin. London
Keywords CT scanning demonstrated lesions in the liver
Endogenous endophthalmitis, liver abscesses, diverticular compatible with liver abscesses(Figure 2). A I Cropley
disease, loss of vision. subsequent colonoscopy showed evidence of FCRP
diverticular disease, which was thought to have Consultant in Infectious
Diseases,
Case Report predisposed to the liver abscesses.
Case History The patient was discharged after completing a London
A 52 year old man presented to the Acute Medical three week course of intravenous amoxicillin and
Unit with a one day history of sudden onset painless gentamicin, and continued to take a further three H Petrushkin
left sided loss of vision. He reported feeling unwell in week course of oral amoxicillin at home. Upon MBBS
Specialist Registrar in
preceding two weeks, with anorexia and sweats. He discharge, his visual acuity had improved from CF to
Ophthalmology,
also mentioned a single episode of minimal rectal 6/18 in the left eye. Royal Free Hospital,
bleeding two days prior. He was otherwise fit and London
well, with no risk factors for immunosuppresion, no Discussion
recent surgery, dental work, or foreign travel. Endogenous endophthalmitis is a rare but potentially H Beynon
blinding intraocular infection that results from FRCP
On examination, he was pyrexial at 39˚C but
Consultant Physician,
remained haemodynamically stable. Clinical haematogenous spread of bacteria from a distant
examination was normal, apart from a red left eye with primary source. London
visual acuity limited to counting fingers (CF) in that It is often associated with an underlying medical
eye. Of note there were no murmurs or signs of condition (which causes a relative Correspondence:
immunosuppression), recent surgery, or dental S Koay
infective endocarditis. Slit lamp examination by the
ophthalmology team showed cells+++, keratic manipulation.1 Recognised associations include
Pond Street,
precipitates+++ and a 1mm hypopyon in the left diabetes mellitus, malignancy, HIV infection, cardiac London NW3 2QG
anterior chamber. A yellow haemorrhagic lesion was disease, and intravenous drug usage. Email: s.koay@nhs.net

26 Acute Medicine 2012; 11(1): 25-27
Endogenous endophthalmitis and liver abscesses
Figure 1. Fundal photograph of patient’s left eye, showing a yellow haemorrhagic lesion in the superior temporal quadrant of the left retina.
Patients may present with visual loss or blurring of Streptococcus milleri group (which include Streptococcus
vision, ocular pain, discharge or a red eye. They may also anginosus-constellatus) are commensals found in the
report systemic symptoms such as lethargy, fever, anorexia mouth, oropharynx, gastrointestinal tract, and
and weight loss. It is important to note that our patient genitourinary tract.2 They are one of the commonest
presented with painless loss of vision, which is more causes of liver abscesses in the United Kingdom,3 and
commonly due to central retinal artery or vein occlusion, can be associated with suppurative metastatic
vitreous haemorrhage, retinal detachment, and non- complications.4 However, they are a rare cause of
arteritic anterior ischaemic optic neuropathy. bacterial endogenous endophthalmitis, which is most
Figure 2. CT scan demonstrating several low attenuating poorly defined areas in the liver, in keeping with liver abscesses.

Acute Medicine 2012; 11(1): 25-27 27
Endogenous endophthalmitis and liver abscesses
commonly caused by Gram negative organisms the case described above, the decision was made to not
(particularly Klebsiella spp.).5 administer intravitreal antibiotics, as the patient was
Prompt administration of antibiotics is important in responding well to intravenous antibiotics, evidenced by
endogenous endophthalmitis, as it helps to optimize visual his improving visual acuity.
outcomes. In most cases, the diagnosis is based on history Visual prognosis is often poor, with 26%-44% of patients
and examination findings, and treatement is initiated being left blind.5,9 Poor prognostic factors include delay in
empirically whilst awaiting results of intraocular and blood diagnosis;9 use of inappropriate antibiotics;10 diffuse infection
cultures.1 There is no clear consensus or guidelines of the vitreous and retina, or panophthalmitis;9 infection
regarding the optimal route of administration of with virulent organisms;7 and gram negative infection.5,7,9
antibiotics. As many topical, subconjunctival and systemic There is also an appreciable mortality rate of 5%, as a direct
antibiotics do not reach therapeutic levels within the result of extraocular infection.5
vitreous,6 it has been suggested that intravitreal injection of The importance of a prompt diagnosis in ensuring a
antibiotics will deliver rapid therapeutic levels of favourable visual prognosis emphasises the need for acute
intraocular antibiotic.5 However, administration of physicians to be aware of this condition; the possibility of
intravitreal antibiotics does not necessarily significantly endogenous endophthalmitis should be included in the
improve visual prognosis.5,7 It has also been suggested that differential diagnoses for any patient presenting with
intravenous antibiotics may be all that is necessary to treat systemic upset and painless loss of vision. Early referral to
the intraocular infection, if a specific organism is cultured the ophthalmology team and discussion with microbiology
from blood.8 Intraocular antibiotics and steroids can then regarding appropriate choice of antibiotics is essential if
be considered if the inf lammatory response worsens.8 In this condition is suspected.
References
1. Connell PP, O’Neill EC, Fabinyi D, et al. Endogenous endophthalmitis: 6. Barza M, Kane A, Baum J. Intraocular penetration of gentamicin after
10-year experience at a tertiary referral centre. Eye 2011; 25: 66–72. subconjunctival and retrobulbar injection. Am J Ophthalmol 1978; 85:
2. Piscitelli SC, Shwed J, Schreckenberger P, et al. Streptococcus milleri 541–7.
group: renewed interest in an elusive pathogen. Eur J Clin Microbiol Infect 7. Wong JS, Chan TK, Lee HM, et al. Endogenous bacterial endophthalmitis:
Dis 1992; 11: 491–8. an East Asian experience and a reappraisal of a severe ocular aff liction.
3. Mohsen AH, Green ST, Read RD, et al. Liver abscess in adults: ten years Ophthalmology 2000; 107(8): 1483–91.
experience in a UK centre. QJM 2002; 95(12): 797–802. 8. Brod RD, Flynn HW Jr. Endophthalmitis: current approaches to
4. Gossling J. Occurrence and pathogenicity of the Streptococcus milleri diagnosis and therapy. Curr Opin Infect Dis 1993; 6: 628–37.
group. Clin Infect Dis. 1988; 10(2): 257–85. 9. Greenwald MJ, Wohl LG, Sell CH. Metastatic bacterial endophthalmitis:
5. Jackson TL, Eykyn SJ, Graham EM, et al. Endogenous bacterial a contemporary reappraisal. Surv Ophthalmol 1986; 31(2): 81–101.
endophthalmitis: 17-year prospective series and review of 267 reported 10. Wang LS, Lee FY, Cheng DL, et al. Klebsiella pneumoniae bacteremia:
cases. Surg Ophthalmol 2003; 48(4): 403–23. analysis of 100 episodes. J Formos Med Assoc 1990; 89(9): 756–63.

28 Acute Medicine 2012; 11(1): 28
Picture Quiz Questions
A young patient with heart failure
Case report was a mottled appearance to his skin on his upper and
A 28 year old gentleman presented after an episode lower limbs.
of collapse with loss of consciousness. Chest radiograph was unremarkable. ECG is as
He gave a history of non-specific malaise and shown (Figure 1).
myalgia over the previous 7 days, with fever, a Blood tests revealed normal full blood count and
generalised rash and a non productive cough. He urea and electrolytes, CRP 26 mg/L, troponin T
H Patel developed progressive shortness of breath with 0.17 µg/L (normal 0-0.1).
MRCP sharp, pleuritic chest pain that was unresponsive to An echocardiogram showed severely impaired
Cardiology registrar
antibiotics in the community. left ventricular (LV) systolic function with an
Department of Cardiology
Eastbourne District General There was no past medical history. He was taking ejection fraction (EF) of 30%. There was a moderate
Hospital amoxicillin and paracetamol. sized pericardial effusion.
Eastbourne He smoked 30 cigarettes a week and had smoked
BN22 2UD cannabis recently. He drank 14 units of alcohol a Questions
week. He worked as a painter. 1. What does the ECG show?
G Dhillon
MRCP On examination, his blood pressure was 110/72, 2. What is the diagnosis?
Cardiology trainee heart rate 110 beats per minute and saturations of 99%, 3. What are the possible aetiologies?
Department of Cardiology breathing room air. He was short of breath at rest. 4. What features suggest an adverse prognosis in this
Eastbourne District General Cardiovascular, respiratory and abdominal condition?
Hospital examinations were otherwise unremarkable. There 5. How would you manage this patient?
Eastbourne
BN22 2UD
A Bandali
MBBS
Cardiology trainee
Eastbourne District General
Hospital
Eastbourne
BN22 2UD
N Patel
FRCP
Cardiology Consultant
Hospital
Eastbourne
BN22 2UD
Correspondence: Figure 1. ECG recorded on admission.

H Patel
MRCP
Cardiology registrar C/O Dr
NR Patel
Hospital
Eastbourne
BN22 2UD
Email: dochiteshpatel
@hotmail.com

Acute Medicine 2012; 11(1): 29 29
Trainee Section
Trainee Update
A Daniel, K Freeman & A Miller
Acute Medicine Awareness Day Of course, if you have a question which falls
As trainees in Acute Medicine, you will almost outside these topic areas, we would be happy to help,
certainly have had to explain the concept of your and there should be time at the end of the forum to
specialty at some point – both to members of the discuss any additional issues.
public and to NHS staff, who may still be unfamiliar You can register for the conference, and submit
with the purpose of the Acute Medical Unit and the an abstract, through the SAM website as usual.
role of the Acute Physician.
The Society for Acute Medicine feels that Acute Changes to AIM and GIM decisions aids
Medicine needs to be more effectively promoted to At the last Acute Medicine specialty advisory
both patients and to staff, and in order to achieve committee (SAC) meeting in January 2012, the
this, SAM has launched Acute Medicine Awareness committee finalised some revisions to the AIM and
Day. This will take place on 20th June 2012. We GIM decisions aids – the documents setting out
need as many AMUs as possible to take part in targets for trainees in each year of their higher
raising awareness of the specialty both locally and specialty training. As we mentioned last time, the
nationally, and we would encourage trainees to take total number of workplace-based assessments
a central role in helping to organize their own units’ (WBAs) required each year is going to fall, and there
activities on Awareness Day. Have a look at the SAM will no longer be such a rigid structure in terms of
website for more details about how to get involved the number of each type of assessment required. We
( h t t p : / / w w w. a c u t e m e d i c i n e . o r g . u k / have been told that these changes will come into
index.php?option=com_content&view= operation in August 2012. The new decision aids
a r t i c l e & i d = 16 5 : a w a r e n e s s - d a y - 2 0 - j u n e - should be visible on the JRCPTB website by then.
2012&catid= 2:news&Itemid=10). All those trainees on the 2009 AIM or GIM
curricula should follow these new guidelines once
SAM Dublin they have been released, since they will be used to
The Spring conference this year is being held in monitor your progress at your ARCP.
Dublin, at the Radisson Blu Hotel, on May 3rd and The long-awaited streamlining of the ePortfolio
4th. The programme has a variety of clinical, (to remove irrelevant curricula and make the whole
political and practical topics – hopefully something process more efficient) is still in the pipeline. We
for everyone! See http://www.acutemedicine. know how frustrated many of you are by the
org.uk/images/stories/samdublin/samdublin%20 ePortfolio in its current incarnation, but we are
programme%2025th%20jan.pdf for more details. hoping that some of the promised changes will be
As you’ll know from our last update, the trainee made by August 2012.
session will take the form of a forum this time, to
give you a chance to discuss any burning issues you Increase in JRCPTB enrollment fees
have about your training. In order to give the session The JRCPTB has recently announced an increase in
some structure, we have decided to focus on three enrollment fees, which will come into effect from 1st
main areas: April 2012. This will not affect those of you who
paid the upfront fee at the start of your training, but
1. specialist skills training; it will affect you if you pay in yearly installments.
2. how to market yourself as an Acute There is more information about this on the
Physician; and JRCPTB website (http://www.jrcptb.org.uk/
3. SAM’s role in developing successful and enrolment/Pages/Enrolment- Fees.aspx). If you are
Amy Daniel
satisfied trainees in Acute Medicine. just about to start your Acute Medicine training, it is
Email: amy_dan@hotmail.
well worth thinking about paying the upfront fee in com
If you have a specific question you would like to order to protect yourself from any future fee rises
ask, we would be grateful if you could email us (especially if you plan to extend your training in any Kirk Freeman
way). Email: k.freeman@doctors.
before the conference so that we can plan the session
org.uk
to help as many of you as possible. We will send out That’s all for now. We are looking forward to
an email nearer the time to remind you to submit seeing many of you in Dublin (remember to email Alice Miller
your queries, if you have them. us if you have any questions for the forum). Email: alice.miller1@nhs.net

30 Acute Medicine 2012; 11(1): 30-32
Trainee Section
Journal Watch: November 2011-January 2012
K E Mellor & J R Neale
Serum Potassium Levels and Mortality unlikely, given the high cost of such trials and the
in Acute Myocardial Infarction regulatory processes involved.
This study was limited to in-hospital mortality in
Goyal A et al. JAMA. 2012; B157-164 patients following AMI. The mortality rates seen
were not limited to arrhythmias. This raises the
The importance of potassium homeostasis in the question whether potassium levels may have a similar
post-infarction period has become a cornerstone in predictive value for mortality in acute medical
modern clinical practice. Several studies have shown admissions of different aetiology. For example,
that potassium levels of less than 3.5 led to a higher studies have suggested that patients with cardiac
risk of arrhythmia induction. This study investigated failure may have higher rates of mortality with
what the optimal target potassium level should be, potassium levels of <4.0.
given the lower rates of serious arrhythmias
following interventions such as beta-blockade and Low-Molecular-Weight Heparin and
reperfusion therapy. Mortality in Acutely Ill Medical Patients
This large retrospective observational study
looked at 38689 patients admitted to American Kakkar A.K et al. N Engl J Med 2011; 365: 2463
hospitals with ICD-10 coded Acute Myocardial – 2472 December 29, 2011
Infarction and appropriate positive biochemical
markers. They documented admission serum The routine use of pharmacological agents in
potassium and then a mean potassium level based on prevention of hospital induced venous
the average of all post-admission potassium levels. thromboembolism (VTE) has been one of the
Their results show a U-shaped relationship between notable intervention success stories of acute
in-hospital mortality and mean potassium levels, medicine. Use of subcutaneous heparin is now
suggesting an increase in all cause mortality with almost universal in patients considered high risk and
potassium levels of less than 3.5 and higher than 5.0. it has identified as a key quality performance
In the group potassium 4.5 to 5.0 mortality was indicator. Whilst its use in prevention of VTE is
10%(95% CI, 9.1%-10.9%) compared to mortality widely accepted to reduce morbidity from acute
rates of 4.8% and 5.0% in the groups of 3.5 to 4.0 venous thromboembolism, subsequent
and 4.0 to 4.5 respectively (95% CI, 4.4%-5.2% and improvement in all cause mortality has not been
4.7%-5.3%). This suggests a twofold increase in definitively demonstrated.
mortality if the potassium level is above 4.5. This is This interesting multi-national study appears to
contrary to current practice which targets levels demonstrate no additional mortality benefit in
between 4.5 and 5.5. The strength of this study is medical patients. Two studies from over thirty years
that it utilised all cause mortality as its primary end ago showed the reduction of fatal pulmonary
point rather than focusing on fatal arrhythmia embolism and all cause mortality in post surgical
induction as in previous studies. patients treated with subcutaneous heparin, this has
The problem with observational studies is that an not been replicated in medical patients. A meta-
K E Mellor
observed relationship between two variables does analysis of five studies assessing the reduction in fatal
ST5 Acute Medicine
Royal Bournemouth NHS not confirm causality. ‘Normal’ potassium levels are PE following pharmacological VTE prophylaxis
Trust considered to be 3-5-4.5; patients with levels outside appeared to conclude there was benefit, but other
Email: katherinemellor@ this may be more unwell and failing to maintain authors have called the findings into question as the
doctors.org.uk homeostasis. This may result in higher mortality diagnosis of fatal PE was not uniform across the
rather than the potassium level itself per se. To fully studies included.
J R Neale
ST6 Gastroenterology and answer the question posed a randomized trial with This was a randomised, double-blinded, placebo
General Internal Medicine patients allocated to target potassium levels would be controlled trial. They recruited 8323 patients from
Hampshire Hospitals NHS required. The authors themselves admit this is 193 centres across India, South America and the Far
trust

Acute Medicine 2012; 11(1): 30-32 31
East. They were randomized to treatment with 40mg administration of placebo. CDT involves venous puncture
subcutaneous enoxaparin versus placebo injection with of the popliteal vein followed by localised administration of
0.9% saline. Both groups received compression stockings. a thrombolytic agent, in this case alteplase, via an
The primary end point was all cause mortality at 30 days. indwelling venous catheter. The mean duration of
Secondary end points included 14 and 90 day all cause thrombolysis therapy was 2.4 days. They assessed
mortality, mortality from PE and bleeding. incidence of PTS using a validated score (The Villalta
They found no difference in all cause mortality at 14, score) at 6 and 24 months.
30 or 90 days. 4.8 % of patients in the placebo group died They report a 14% risk reduction of post thrombotic
at 30 days compared with 4.9% in the enoxaparin group. syndrome in the CDT group. The recorded occurrence
Only one patient in each group died from pulmonary was 41.1% compared to 55.6% in the group treated with
embolism at 30 days. However 28 patients in each group anticoagulation alone. While this represents a statistically
are classified as having died from ‘sudden death’, the significant reduction, the risk of PTS remains high
authors do not comment on whether there was more regardless of intervention. Other groups studying PTS
information available post mortem on these patients. found lower rates post CDT. Possible reasons for this could
This is a robust and well-designed study demonstrating be that they had a higher incidence of pelvic thrombosis
mortality outcomes which go against expectations. This (indicating more extensive DVT) in the CDT group than
doesn’t take away from the importance of VTE the anticoagulation group alone (46% vs 36%). Pelvic
prophylaxis in preventing the health care burden associated thrombosis is a strong predictor of subsequent PTS.
with symptomatic VTE. A note of caution must be An additional important factor was that venous
exercised in applying data from a different patient group to stenting, which is common practice in Americaperi-
that of the UK. Patients in the Far East have been reported thrombolysis, was left to individual investigators
to have a lower incidence of PE. This may have to do with discretion.Only 15 patients received venous stenting in
factors such as lower obesity rates and genetic this trial. Previous studieshave shown that 80% of patients
predisposition. with ileo-femoral DVThave an underlying venous stenosis
proximally, whichhas to be treated to restore good venous
Long-term outcome after additional outf low afterthrombolysis. This low incidence of stenting
catheter-directed thrombolysis versus may have reduced the overall impact of CDT.
standard treatment for acute iliofemoral An incidence of significant post procedure bleeding of
deep vein thrombosis (the CaVenT study): 9% was reported, which is compatible with previous
a randomised controlled trial studies. No patients had intracranial or fatal haemorrhage.
Most of the bleeding complications were related to the
Enden T CaVenT Study Group. Lancet. 2012 Jan 7; puncture site due to multiple attempts to gain venous
379(9810): 31-8. Epub 2011 Dec 13. access, highlighting the need for operator experience with
this technique.
Current UK practice in the management of extensive A larger multicentre study in America is currently
DVT is to offer standard anticoagulation. This leaves recruiting with the aim to assess catheter directed
patients with a significant risk of post thrombotic thrombolysis in nearly 700 patients (ATTRACT); the
syndrome (PTS). Whilst not life threatening PTS does results are expected in 2015. If this study confirms that
constitute a major burden in terms of ongoing morbidity CDT is a safe approach to the treatment of massive DVT it
and is reported in over fifty percent of patients with is possible the UK will need to develop interventional
extensive DVT. Common symptoms include pain and radiology services to meet this need.
swelling of the affected leg resulting in reduced mobility.
NICE guidelines on the treatment of confirmed DVT are Host and Pathogen Factors for Clostridium
currently in development. The SIGN guidance suggests difficile Infection and Colonization
that catheter directed thrombolysis should be considered
on an individual patient basis when the DVT is massive Loo V.G. et al. N Engl J Med 2011; 365: 1693 – 1703
and limb threatening or there is incipient venous November 3, 2011
gangrene.
The aim of this Norwegian study was to assess whether Clostridium difficile has a huge impact on our approach to
catheter directed thrombolysis (CDT) was effective at healthcare associated infections; it is the leading cause of
preventing PTS without inducing unacceptable bleeding healthcare associated infectious diarrhoea. Pressure from
risk. Previous studies looking at systemic thrombolysis the Department of Health to reduce infection rates has
concluded that although it was effective at reducing seen a radical shift in the way antibiotics are prescribed.
thrombosis load, the incidence of bleeding was Stringent infection control policies and mandatory
unacceptably high. reporting of cases has brought this subject to the forefront
200 patients were randomised into conventional of healthcare policy.
anticoagulation or conventional anticoagulation plus This study from Canada was carried out in 2006, a
CDT. The study was not blinded as it was felt unethical to time at which there was already heightened awareness in
put patients through an invasive procedure for the UK. A total of 4143 patients were included in the

32 Acute Medicine 2012; 11(1): 30-32
study; 117 (2.8%) had symptomatic C.difficile (CD) Effect of intravenous β-2 agonist treatment
infection consistent with previously published infection on clinical outcomes in acute respiratory
prevalence. It was a large well designed study attempting distress syndrome (BALTI-2): a multicentre,
to tease out relative impact of host and pathogen factors on randomised controlled trial
risk of CD colonisation and infection in an unselected
population. Gao Smith F et al BALTI-2 study investigators Lancet.
This study provides information about absolute risk 2012 Jan 21; 379(9812): 229-35.
increases for factors implicated in CD infection that had
been identified in previous studies. Advancing age (odds Acute respiratory distress syndrome (ARDS) is a condition
ratio OR 1.02 per increase of one year), use of antibiotics with a high mortality rate (40-60%) for which effective
(OR 5.25) and proton pump inhibitors (PPIs) (OR2.64) interventions are constantly being sought. This study is the
were all independent risk factors for developing CD follow up from the earlier promising BALTI study which
infection. Interestingly 26.7% of CD infections occurring showed that intravenous Beta-2 agonist showed
within 72 hours of admission had no history of hospital improvement in ARDS severity markers such as plateau
care within the past 12 months suggesting true community pressure and extravascular lung waterin ventilated patients.
acquired infections. The initial BALTI trial was a single centre study of 40
Hospitalisation in the past 2 months, PPIs and H2 patients and hence was not powered to look at mortality
blockers, chemotherapy and serum antibodies were data. Following on from this a larger multi-centre study
associated with a higher prevalence of CD colonisation, aiming to recruit over 300 patients was initiated. The study
defined as a positive stool culture for CD in the absence of was stopped early as interim analysis from 273 patients
diarrhoea. These agents disrupt gut microbiota and may showed convincing evidence that the 28 day mortality in
predispose to CD colonisation. Approximately half the the salbutamol arm exceeded that in the placebo and that
patients were colonised on admission to hospital whilst the the two mortality curves appeared to be continuing to
other half developed colonisation after more than 72 hours diverge. Intravenous salbutamol resulted in a 10⋅9%(95%
in hospital. There is some limited evidence that CI 1⋅0–20⋅4) absolute increase in 28-day mortality.
colonisation with CD regardless of strain offers protection
against the development of symptomatic infection. This was an unexpected finding. On further analysis
In terms of pathogen factors; the study confirmed that the risk of tachycardia, new arrhythmia and significant
the NAP1 strain (associated with epidemic outbreaks of lactic acidosis was markedly higher in the treatment group
CD) was more prevalent in infected patients. Other strains compared with placebo. The dose of salbutamol they used
were more prevalent in colonised patients. It is postulated was 15µg/kg after an earlier dose-ranging study showed this
that NAP1 is more virulent due to genetic deletions to be the maximum dose in critically unwell patients
resulting in increased toxin production. without a significant increase in arrhythmias. The authors
One of the limits of the study was the relatively low accept that this is at the higher end of the manufacturer’s
participation rate (57%) and the fact that large numbers of recommended dosing regimen; hence the beneficial
patients could not be included due to incomplete effects might have been outweighed by the increase in
laboratory studies; therefore when the data was analysed adverse incidents seen. The exact mechanism by which
the number in each subgroup is relatively small. This study salbutamol causes harm is not clear, stimulation of
highlights the relative importance of different risk factors adrenergic drive causing cardiovascular effects such as
for CD infection. tachyarrhythmias may well be important.
A cautionary tale highlighting the need to use data
from properly conducted randomized control trials before
leaping on a treatment that seems promising from small
studies which are often not powered to detect significant
adverse effects.

Acute Medicine 2012; 11(1): 33-38 33
Trainee Section
The patient presenting with acute hemiparesis
K Mahawish & O Otaiku
Abstract Stroke type Clinical features

Acute hemiparesis is a common cause of presentation to Lacunar Infarct (LACI) Pure motor/pure
hospital. In the majority of cases the cause is acute stroke, sensory/sensorimotor/ataxic
which is ischaemic in 80% of cases. This article aims to hemiparesis
provide the reader with a practical approach to the initial ≥ 2 affected out of
management of suspected stroke.The problem-based format face/arm/leg
No cortical dysfunction
highlights some of the specific questions raised in the 2009
curriculum for training in Acute Internal Medicine, with Total anterior circulation Hemianopia
reference to recent guidance from the National Institute for infarct (TACI) Cortical dysfunction e.g.
Health and Clinical Excellence (NICE). dysphasia, inattention
Limb motor and/or sensory
abnormalities
Introduction
Hemiparesis can result from a lesion at any point along Partial anterior Two of the features of TACI or
the motor system from the cerebral cortex, through the circulation infarct (PACI) Limb weakness/numbness
more restrictive than LACI
centrum semiovale, internal capsule, brainstem and
pyramids and along the cervical spinal cord. Similarly Posterior circulation Brainstem/cerebellar
sensory disturbance may arise from a lesion in peripheral infarct (POCI) dysfunction or
nerves, spinal cord, brainstem, thalamus or primary Isolated hemianopia
sensory cortex. Parietal lesions in either hemisphere may Table 1. The Oxford Community Stroke Project
give rise to visual and/or sensory inattention – the failure Classification system for stroke.
to attend to stimuli on either side of the body.1
Acute stroke is the commonest cause of
hemiparesis and is ischaemic in 80% of cases, with hour earlier. Witnesses reported that he slumped to the floor
haemorrhagic stroke accounting for the remaining after attempting to stand and he appeared to be unable to
20%. Ischaemic strokes are most commonly the move the right side of his body, although he did not lose
result of cardioembolism, large vessel atherosclerotic consciousness. His face is asymmetrical with a droop to the
disease (resulting in artery-to-artery embolism) and right side of his mouth, and he is unable to speak or move his
right arm or leg. KarimMahawish
small vessel disease. The two commonest causes of Consultant Physician
spontaneous intracerebral haemorrhage include Warrington Hospital NHS
hypertensive vasculopathy, with bleeds typically What key aspects of the history should Foundation Trust
arising within the basal ganglia; and lobar be sought? Warrington,
haemorrhages secondary to cerebral amyloid In patients with suspected stroke, the history is a key UK
angiopathy, occurring mainly in the elderly. There is part of the clinical evaluation. Onset tends to be
sudden, with loss of function the predominant OlayiwolaOtaiku
no reliable clinical method to distinguish between Consultant Physician
these two main stroke subtypes. feature rather than involuntary movements or
Elderly/Stroke Medicine
In the UK, the Oxfordshire Community Stroke visual/sensory phenomena. Timing of onset is Warrington Hospital NHS
Project (OCSP) has provided the most commonly crucial since this will determine the treatment Trust
used classification system for ischaemic stroke2 options. Obtaining a witness account of the events Warrington,
(Table 1). It is simple to use and has been shown to leading up to the presentation is also important, UK
have good inter-observer reliability. Further, it particularly if the patient is aphasic, as in this case.
Correspondence:
predicts the site and size of cerebral infarction shown Improving symptoms may suggest a transient KarimMahawish
on CT with reasonable accuracy3 and allows ischaemic attack (TIA). This is defined as an acute Consultant Physician
prediction of case fatality and functional recovery. episode of focal loss of cerebral or visual function Warrington Hospital NHS
lasting less than 24 hours and attributed to Foundation Trust
A Typical Case History inadequate blood supply. It may be unclear at the Warrington,
A 64 year old man is brought to the Emergency Department time of presentation to hospital whether the UK
Email: k.mahawish
by ambulance having collapsed at a wedding ceremony one symptoms are going to resolve within 24 hours;
@nhs.net

34 Acute Medicine 2012; 11(1): 33-38
Age ≥ 60 years 1point What is the main differential diagnosis?

Age < 60 years 0 points Important differential diagnoses include seizure,
Blood pressure >140/90 mmHg at acute 1 point hemiplegic migraine, reversible posterior
presentation leukoencephalopathy, malignancy and functional
Clinical features, score 1 of:
weakness. Hypoglycaemia may also present with focal
Speech disturbance without focal weakness 1 point neurological deficit, including hemiparesis.
Unilateral weakness 2 points Features which may be helpful in distinguishing some
Other 0 points of these conditions are listed below:
Duration of symptoms, score 1 of:
< 10 minutes 0 points • Seizures may be followed by post-ictal confusion
10-59 minutes 1 point or hemiparesis (Todd’s paresis) lasting for several
≥60 minutes 2 points hours. An eye witness description of tonic-clonic
Diabetes 1 point movements at the time of onset, or a past history
of seizure, alcohol excess, malignancy or other
Table 2. ABCD2 Score.
known structural brain disease should arouse
suspicions. It should also be remembered that
however in reality, the duration of TIA is typically much seizure may also complicate acute stroke.
shorter, with the majority of episodes resolving within an • Migraine may present with a progressive
hour. Approximately half of TIAs extending beyond one hemiparesis over several minutes, usually in
hour demonstrate ischaemic changes on neuroimaging, association with unilateral headache, nausea and
which has led to some authorities adopting a vomiting; however the motor signs can occur in
pathophysiological classification of TIA, rather than the isolation. Patients are usually younger and may
traditional chronological approach; however this has not describe a series of symptoms occurring
been adopted in the UK.4 The ABCD2 score (Table 2) is sequentially including positive visual phenomenon,
useful for risk stratification of TIA. Patients with a score ≥ word finding difficulty and limb paraesthesia. A
4 have a high risk of progression to stroke, and may require history of previous events should be sought.
admission to hospital for early investigation and treatment • Reversible posterior leukoencephalopathy
(Figure 1).5 syndrome manifests with posterior fossa symptoms
Symptoms of vertigo, dysarthia, ataxia or dysphagia in including visual disturbances (e.g. hemianopia,
isolation without other focal neurological signs rarely cortical blindness), headaches, vomiting and
point to a diagnosis of stroke. Furthermore, transient loss seizures. Cerebral autoregulatory failure and
of consciousness or syncope is rarely due to stroke or TIA endothelial dysfunction is thought to be
unless it is the result of a severely disabling stroke, a responsible.Magnetic resonance imaging
brainstem stroke (when associated with additional demonstrates white matter oedema in the posterior
brainstem signs), or seizure complicating a stroke. cerebral hemispheres.
Defining the speed of onset is may also be helpful in • Functional symptoms represent transient motor or
determining the cause of hemiparesis. A subacute process sensory symptoms not attributable to an identifiable
developing over hours or days may suggest an infectious, neurological abnormality. In one case series,
inf lammatory, malignant or metabolic pathology. functional symptoms accounted for a third of ‘stroke
mimics’ in patients under 50, which overall
Figure 1. Short term risk of stroke following TIA as predicted by ABCD2 Score.

Acute Medicine 2012; 11(1): 33-38 35
accounted for 21% of stroke department admissions sounded ‘jumbled’ for a short period; this had recovered after
in this age group.6 Functional symptoms were very around 30 minutes and he had declined her suggestion of visiting
uncommon in those aged over 50 years. his GP. He usually took ramipril 5mg and bendroflumethiazide
2.5mg once daily for high blood pressure. His father died of a
What key physical examination findings myocardial infarct, aged 75, and he had smoked 20/day since the
could help in localisation and differential age of 18.
diagnosis? Examination revealed right hemiplegia with brisk reflexes on
The purpose of the physical examination is to localise the the right and up-going plantar. There was an upper motor neurone
lesion and attempt to identify aetiological factors such as VII nerve palsy and he was looking to the left with homonymous
atrial fibrillation. However this should not delay neuro- hemianopia on the right. He had not spoken since arrival in
imaging for patients presenting acutely, as early diagnosis hospital but was able to follow simple commands.
and treatment is crucial. In some cases detailed Cardiovascular examination revealed a regular pulse of 80/min
examination may need to be deferred until after the with blood pressure 150/90; there were no carotid bruits or heart
imaging has been undertaken. murmurs. ECG confirmed sinus rhythm.
Neurological and general examination should include
assessment of speech and cognitive function. In the acute What immediate imaging should be
phase, affected limbs become hypotonic and deep tendon undertaken?
ref lexes may be hypo- or hyper-ref lexic. Limb weakness Computed tomography (CT) remains the first line
typically follows a pyramidal pattern, with extensors investigation for the early differentiation of haemorrhage
affected to a greater degree than f lexors in the upper limb from infarct, and to exclude non-stroke pathology, such as
and vice versa in the lower limb. Mild weakness may result cerebral tumours. In this case the patient has a past history
in a pronator drift (a downward drift of the arm with of hypertension, raising the possibility of intracerebral
pronation when held extended with the palm facing haemorrhage as a cause for his symptoms; however he also
upwards). Later, affected limbs become hypertonic with has risk factors for ischaemic stroke (smoking,
brisk ref lexes. Limb weakness, ataxia or sensory loss in hypertension and family history) and a possible recent left
association with cranial nerve involvement may help hemisphere TIA causing transient dysphasia. Given the
localise the lesion to the posterior circulation. importance of early intervention following acute
ischaemic stroke the patient should undergo CTscan as
What features may suggest ‘functional‘ soon as possible after arrival in hospital. An unenhanced
hemiparesis? brain scan takes approximately 10 seconds to obtain.
Inconsistent examination findings may help to distinguish Folllowing intracerebral haemorrhage, CT appearances
functional disorders from stroke; features of functional evolve with time. After 5 days, small lesions may become iso-
disturbance may include: dense with the surrounding brain, particularly following a
small bleed. By the end of the first week, lesions may become
• Equal proximal/ distal and f lexion/ extension hypo-dense. Indeed CT appearances of previous
weakness in the limbs. intracerebral haemorrhages will often mimic the appearances
• Ipsilateral sternocleidomastoid weakness. of old infarction, such as the ex-vacuo effect of ventricular and
• Intermittent voluntary effort with simultaneous sulcal enlargement near sites of previous haemorrhage.
contraction of flexion and extension muscles groups. Following ischaemic stroke, 60 % will have changes
• Ref lexes and muscle tone tend to be normal. visible on CT scan within first 24 hours rising to 70% of
• Prominent verbal grunts during examination – those scanned within 72 hours. Early CT changes found in
‘Wrestler’s sign’. acute ischaemic stroke include cortical sulcal effacement
• Raising the contralateral leg may elicit a downward and loss of the insular ribbon, a hyperdense middle
movement of the ‘paretic’ leg – ‘Hoover’s sign’. cerebral artery due to thrombus within the artery, and loss
• Finally, the patient may seem remarkably of grey-white matter differentiation within the basal
unconcerned and calm in the presence of marked ganglia. Such findings are associated with larger infarcts
weakness - ‘la belle indifference’. and worse functional outcomes.7 As with haemorrhagic
stroke, CT appearances evolve with time with lesions
With encouragement, it is often possible to elicit full becoming more demarcated and hypodense during the
power. No single clinical sign is definitive and clinical first few days. Cerebral oedema is maximal around day
judgement should always take precedence. Ultimately, a 3 – 5, gradually subsiding during the 2nd – 3rd week, such
diagnosis of functional weakness should only be made that by the 2nd week infarct may increase in density and
when other possibilities have been excluded. Further, it become isodense. Later, the infarct lesion forms sharp
should be remembered that exaggerated signs may be demarcated hypodense lesions.
elicited following stroke, mimicking the feature of Magnetic resonance imaging may provide a more detailed
functional disorders in some cases. view of anatomical and pathological changes, as well as
enabling non-invasive imaging of intracranial vessels.
Case Progression Diffusion weighted MR sequences are able to detect
The patient had been well immediately prior to this episode, ischaemia within 30 minutes of onset. Patient related factors
although two weeks earlier his wife reported that his speech had such as claustrophobia and the high level of co-operation
36 Acute Medicine 2012; 11(1): 33-38
needed for the longer period needed to obtain images may risk of symptomatic intracerebral haemorrhage in around
limit the use of this test in the acute setting, along with 1 in 14 patients. Should intrancranial haemorrhage occur,
resource factors such as expense and accessibility. treatment options are limited and it may be fatal.
Treatment also carries a risk of anaphylaxis of < 1%. The
Case Progression patient and their next of kin should be counselled carefully
The patient undergoes urgent CT scan within 30 minutes of regarding the risks and informed consent should be
arrival in the Emergency Department, which reveals evidence of obtained where possible.
acute ischaemic change in the left middle cerebral artery territory.
There is no evidence of intracerebral haemorrhage. On return from What are the other key management issues
the scanner, his condition remains unchanged with evidence of in acute hemiparesis?
persistent right hemiplegia. Patients should be kept nil-by-mouth until a formal swallow
assessment has been performed. If this is delayed, or if the
What immediate treatments should be assessment demonstrates that the patient is at risk of aspiration
considered for patients with acute ischaemic a nasogastric tube should be sited to enable initiation of
stroke? enteral feeding and the administration of medication.
Antiplatelet therapy should be commenced as soon as CT Additional management measures are aimed at
has excluded intracranial haemorrhage; aspirin 300mg is maintaining homeostasis in an attempt to rescue ischaemic
usually administered initially and can be given rectally if tissue at risk of infarction (i.e. penumbral salvage). Such
the patient is unable to swallow. NICE now recommends measures are illustrated in Table 3.
clopidogrel 75mg daily for secondary prevention of Admission to a stroke unit is strongly associated with
ischaemic stroke. A combination of aspirin with better outcomes, due to improved monitoring of
dipyridamole 200mg twice daily is recommended where physiological parameters, prevention of complications and
clopidogrel is contraindicated or not tolerated.9
In 1995 the National Institute of Neurological Hyperglycaemia Associated with worse outcome
Use insulin to maintain glucose ≤
Disorders & Stroke study10 (NINDS) demonstrated the
11mmol/l
efficacy of rt-PA intravenous thrombolysis when given
within three hours of stroke onset. Patients in the Hypoxia Use supplementary oxygen only to
maintain saturations >95%
treatment group were 30% more likely to have minimal or (use clinical judgement in those with
no disability at 3 months, at the expense of a significant significant airways disease)
rise in the incidence of symptomatic intracranial
Pyrexia Associated with worse outcomes
haemorrhage (6.4%). There was no mortality difference Identify potential sources then treat with
observed at three months. The European Co-operative antipyretics
Acute Stroke Study(ECASS III)11 demonstrated the Hypertension No evidence in favour of treating in the
efficacy of thrombolysis up to 4.5 hours, with similar acute phase
benefit in mortality and intracranial haemorrhage rates to Treat if evidence of end organ damage
the original NINDS trial. European Union approval of (NICE)8
alteplase permits its use up to 3 hours post stroke onset,
Table 3. Maintaining homeostasis following acute stroke.
however some units in the UK have extended treatment
time to 4.5 hours following ECASS III data. Improved
outcomes are strongly associated with shortened door-to- early mobilisation. National guidelines in England now
needle times, and early thrombolysis is critical. recommend that all patients are managed throughout their
In this case the patient has presented to hospital early hospital stay in a specialist stroke unit.8
and CT findings confirm that he would be candidate for
thrombolysis. What other complications may arise
Intravenous thrombolysis results in restoration of vessel following middle cerebral artery infarction?
patency (i.e. recannalisation) in 46.2% of patients treated.12 Malignant middle cerebral artery syndrome occurs in
Should thrombus be demonstrated on angiography within 10% of MCA infarcts. Findings include dense hemiplegia
an intracranial artery, intra-arterial thrombolysis may be and forced eye deviation, while CT will demonstrate a
attempted (recannalisation rates of 63.2% - 67.5%) or large area of hypodensity and midline shift. Left untreated,
mechanical clot disruption techniques (83.6%). There are it carries a mortality of 78% as a consequence of herniation
no national guidelines to guide therapy and patients should of the temporal lobe onto the brainstem.13 Decompressive
be discussed with the affiliated tertiary centre on a case by hemicraniectomy and durotomy is the surgical technique
case basis. Recannalisation is associated with favourable used to relieve the increased intracranial pressure, thus
functional outcomes and reduced mortality compared improving cerebral perfusion pressure. A pooled analysis of
with failure to recannalise, with similar rates of outcome following the procedure demonstrated greater
haemorrhagic transformation. survival (numbers needed to treat 2) and favourable
outcome at one year mRS 0-4 (75 Vs 24 percent in the
What are the risks of thrombolysis? control group).14 Referral for decompressive
The likelihood of improved outcome following hemicraniectomy is recommended for patients fulfilling
thrombolysis needs to be balanced against the increased the following criteria:8
Acute Medicine 2012; 11(1): 33-38 37
1. Age < 60 years by using the OCSP classification (Figure 2). Recovery
2. Clinical deficits suggestive of MCA territory from stroke occurs through a variety of mechanisms.
infarction, with a score on the National Institutes Penumbral salvage results in the restoration of
of Health Stroke Scale (NIHSS) of > 15. functioning neurones. Neuroplasticity refers to the
3. Decrease in the level of consciousness to give a ability of neighbouring cells to take over the lost
score of 1 or more on item 1a of the NIHSS. function. Adaptive behaviour is learned with the support
4. Signs on CT of an infarct of at least 50% of the of various members of the multi-disciplinary team,
middle cerebral artery territory, with or without including physiotherapists, occupational therapists,
additional infarction in the territory of the anterior speech therapists and neuropsychologists.The rate of
or posterior cerebral artery on the same side, or recovery is highest in first few weeks after stroke;
infarct volume greater than 145 cm3 as shown on functional improvement continues at a slower rate for
diffusion-weighted MRI. many months (occasionally up to 2 years). It remains
diff icult to predict the rate and completeness of
What other investigations should be recovery.
considered?
In anterior circulation ischaemic stroke, carotid doppler Case progression
assessment should be considered to enable imaging of The patient was transferred to the acute stroke unit and treated with
extracranial carotid vessels, particularly where there has been rt-PA within 1 hour of arrival in hospital
significant functional improvement. In ischaemic stroke in (2 hours after onset of the weakness). Following this treatment an
younger patients, tests for vasculitis and lupus should be improvement in his weakness was noted with power improving to
performed and CT or MR angiography if intracranial carotid 3/5 in his limbs and some recovery of speech. He was initially fed
or vertebral artery dissection is considered a possible cause. via a nasogastric tube after failing a swallow assessment, but this
Trans-thoracic echocardiography should also be considered improved within 72 hours enabling oral nutrition to be initiated.
to enable identification of a cardiac source of embolic stroke, Carotid doppler showed minor plaque only, and an echocardiogram
which may require treatment with long-term anticoagulant was normal. He was commenced on clopidogrel 75mg daily and
drugs. simvastatin 40mg daily and his blood pressure control was
maintained without alteration of his usual medication. The
What is the prognosis for patients presenting improvement continued over subsequent weeks with the support of
with acute hemiparesis? the multiprofessional team on the stroke unit and he was transferred
Mortality and functional recovery following stroke is to a community rehabilitation unit after an inpatient stay of 2
dependent on the stroke subtype and may be predicted weeks.
N.B PICH: primary intracerebral haemorrhage
Figure 2. Stroke prognosis based on OCSP subtype1 & primary intracerebral haemorrhage.
38 Acute Medicine 2012; 11(1): 33-38
Additional on-line training resources:

1. NIHSS certification (used in stroke thrombolysis assessment): http://nihss-english.trainingcampus.net/uas/modules/trees/windex.aspx
2. Stroke thrombolysis training: http://www.strokeadvancingmodules.org/labyrinth_thrombo/
3. Resource on functional symptoms for professionals and patients: http://www.neurosymptoms.org/
References
1. Bamford J, Sandercock P, Dennis M et al. Classification and natural history 8. NICE Clinical Guideline 68. Stroke: Diagnosis and initial management of
of clinically identifiable subtypes of cerebral infarction. Lancet 1991; 337: acute stroke and transient ischaemic attack (TIA)
1521-6. http://www.nice.org.uk/CG68
2. Meldrum D, Hardiman O, Pittocj SJ et al. The Oxfordshire community 9. NICE Technology Appraisal 210: clopidogrel and modified-release
stroke project classification: correlation with imaging, associated dipyridamole for prevention of occlusive vascular events.
complications and prediction of outcome in acute ischaemic stroke. Stroke http://guidance.nice.org.uk/TA210/
Cerebrovasc Dis 2003: 12(1): 1-7. 10. The National Institute of Neurological Disorders and Stroke rt-PA Stroke
3. Stone SP, Halligan PW, Greenwood RJ. The Incidence of Neglect study group. NEJM 1995; 333(24): 1581-7.
Phenomena and Related Disorders in Patients with an Acute Right or Left 11. Hacke W, Kaste M, Bluhmki E et al. Thrombolysis with alteplase 3 to 4.5
Hemisphere Stroke. Age Ageing 1993; 2: 46-52. hours after acute ischaemic stroke. NEJM 2008; 359(13): 1317-29.
4. American Heart Association & American Stroke Association Stroke 12. Rha JH, Saver JL. The Impact of Recanalization on Ischemic Stroke
Council. Definition and evaluation of transient ischemic attack: a scientific Outcome: A Meta-Analysis. Stroke 2007. 38: 967-973.
statement for healthcare professionals. Stroke 2009; 40(6): 2276-93. 13. Hacke W, Schwab S, Horn M et al. ‘Malignant’ middle cerebral artery
5. Johnston SC, Rothwell PM, Nguyen-Huynh MN et al. Validation and territory infarction: clinical course and prognostic signs. Arch Neurol 1996;
refinement of scores to predict very early stroke risk after transient 53(4): 309-15.
ischaemic attack. Lancet 2007; 369: 283–92. 14. Vahedi K, Hofmeijer J, Juettler E et al1. Early decompressive surgery in
6. Vroomen PCAJ, Buddingh MK, Luijckx GJ et al. The Incidence of Stroke malignant infarction of the middle cerebral artery: a pooled analysis of
Mimics Among Stroke Department Admissions in Relation to Age three randomised controlled trials. Lancet Neurol 2007; 6(3): 215-22.
Group. J Stroke Cerebrovas Dis 2008; 17(6): 418-422.
7. vonKummer R, Bourquain H, Bozzao S et al. Early prediction of
Irreversible brain damage after ischaemic stroke at CT. Radiol 2001; 219:
95-100.

Acute Medicine 2012; 11(1): 39-45 39
Trainee Section
Haemoptysis: Diagnosis and Treatment
K Hurt & D Bilton
Abstract There are no consensus guidelines available for

Haemoptysis is a common symptom in clinical practice, the management of haemoptysis and its treatment
which requires further investigation. Fortunately, massive can be challenging, even for experienced physicians.
haemoptysis only accounts for a small proportion of these
episodes. It is a medical emergency that carries a high Pathophysiology
mortality rate. There are no agreed management guidelines. The lungs have a double arterial supply. The
This review discusses proposed methods of resuscitation as pulmonary arteries carry deoxygenated blood under
well as outlining a diagnostic algorithm and discusses low pressure to the lungs for the purpose of gas
treatments including bronchial artery embolization, exchange. The bronchial arteries account for <1% of
endobronchial therapy, surgery and medical therapies. the circulation to the lungs and supply oxygenated
blood to the lung parenchyma. They are under
Keywords systemic pressure, originating from the descending
Haemoptysis, bronchoscopy, bronchial artery embolization, aorta, usually between 3rd and 8th thoracic vertebral
CT thorax, lung cancer, bronchiectasis, cystic fibrosis. level, most commonly between the 5th and 6th.6
There is a wide anatomical variation in bronchial
Introduction artery anatomy. In around 5-10% of people the
Haemoptysis can be defined as the expectoration of anterior medullary artery that supplies the anterior
blood from the lower respiratory tract. The amount spinal artery arises from the intercostal bronchial
of blood can vary widely, from streaking of the trunk. However a recent report of bronchial artery
sputum to rapidly fatal massive haemoptysis. Whilst embolizations suggests that this figure is somewhat
haemoptysis in general is a relatively common lower.7
clinical problem, massive haemoptysis remains Around 90% of haemoptysis will originate from
fortunately very rare. The exact incidence is the bronchial arteries and around 5% from the
unknown because there is no agreed definition in pulmonary arterial circulation.8
the literature as to what constitutes massive Mechanisms of bleeding are multi-factorial. In
Katharine Hurt
haemoptysis. Definitions range from a blood loss of the presence of chronic inf lammation and infection MBBS MRCP
100 mls of blood expectorated in 24 hours1 up to bronchial arteries hypertrophy and proliferate. There Clinical Research Fellow,
1000mls in 24 hours.2 Most respiratory physicians is also enlargement of the usual systemic to Royal Brompton Hospital
would use a definition somewhere between 200- pulmonary artery and pulmonary vein and Imperial College,
600mls/24 hours. It has been suggested that volume communications. These factors lead to increased London
expectorated definitions are not useful in clinical blood f low and neovascularization. The resultant Diana Bilton
practice and actually it is better to define thin walled vessels are at risk of rupturing into the FRCP MD
functionally.3,4 There are good reasons for this. airway causing haemoptysis.7,9 Consultant Respiratory
Haemoptysis is difficult to quantify, patients may Physician,
over report amounts produced and the physiological Case History Royal Brompton Hospital
A 28 year old woman with cystic fibrosis (CF) and severe and Imperial College,
effects of haemoptysis will depend on the patient’s
London
clinical status. Death from massive haemoptysis is bronchiectasis presented to her local hospital after a single
usually through a process of asphyxiation, rather than episode of haemoptysis. This was estimated, by the patient, Correspondence:
exsanguination.5 to have been around 200mls. She also described increased Katharine Hurt
Haemoptysis is a serious symptom that requires shortness of breath, right sided chest pain and dizziness. Department of Cystic
Fibrosis
further investigation as it may be a sign of underlying Her CF was complicated by diabetes, for which she
Royal Brompton Hospital
severe disease. The most common causes vary required insulin, and chronic infection with Pseudomonas Sydney Street
geographically with tuberculosis (TB) being the aeruginosa; she took a number of regular medications London
most common underlying aetiology in the including pancreatic enzymes, vitamins, prophylactic SW3 6NP
developing world and elsewhere bronchitis and lung nebulised antibiotics (colomycin) and a nebulised mucolytic. Email: k.hurt@imperial
cancer.2 She was not taking anticoagulant or anti-platelet drugs. .ac.uk

40 Acute Medicine 2012; 11(1): 39-45
Neoplastic Airway Disease History of presenting complaint

It is important to clarify that bleeding has arisen from the
Bronchogenic carcinoma Bronchiectasis
lower respiratory tract and to exclude haematemesis and
Pulmonary metastatic Bronchitis epistaxis as alternative explanations. Attempts to quantify
disease the amount of blood should also be made, although this
Kaposi’s sarcoma Cystic Fibrosis can be very difficult.
Infection Primary Vascular Disease
Associated symptoms and risk factors
Bacterial pneumonia Pulmonary AV malformations Any current or past diagnoses of respiratory disease should
TB Pulmonary embolism be elicited and a detailed respiratory history should be
taken to try and ascertain the underlying diagnosis.
Mycetoma Pulmonary hypertension
Symptoms of cough, sputum production, fever, chest pain
Non tuberculous Congestive cardiac failure and weight loss could suggest acute infection, TB, chronic
mycobacterial disease bronchitis, chronic suppurative lung disease or lung cancer
Respiratory viral infection Mitral stenosis depending on time course. Risk factors for PE should be
Parasitic disease Miscellaneous
considered as well as symptoms of heart failure and valvular
heart disease. In addition a smoking and travel history
Systemic Disease Foreign body inhalation should be taken.
Goodpasture’s syndrome Endometriosis A careful drug history, especially use of anticoagulant
should be noted, any association with menses for female
Wegener’s granulomatosis Amyloidosis
patients should be considered and risk factors for HIV
Microscopic polyarteritis Pulmonary sequestration infection should be identified. Concurrent systemic upset
Systemic lupus Iatrogenic Lung Injury and rash may suggest an underlying vasculitis.
erythematosus
Coagulopathy
Clinical examination
In addition to a detailed respiratory examination, general
Table 1. Important causes of haemoptysis. examination should involve assessment of nutritional
status. Finger nails should be checked for signs of clubbing.
What are the possible causes of her Lymph nodes should be examined in the neck,
haemoptysis? supraclavicular and axilla regions. The skin and mucous
Table 1 lists the most important causes of haemoptysis. membranes should be inspected for signs of bruising,
Lung cancer accounts for around 20-30% of cases in pallor, rash, telangiectasia and gingivitis.
recent series. Despite extensive investigation, the cause of Full cardiovascular examination should be performed,
haemoptysis remains unknown in 3-43% of patients.10-12 looking specifically for signs of congestive heart failure,
In this case the presence of known bronchiectasis pulmonary hypertension, thromboembolic disease and
makes this the most likely cause of her haemoptysis, valvular heart disease.
although other causes in the list should be considered.
How do you investigate and manage non
On arrival in the emergency department she was apyrexial, massive haemoptysis?
alert and orientated; her heart rate was 88/min with a blood Chest x-ray (CXR) is an important initial investigation.
pressure of 100/64mmHg. Her respiratory rate was 18/min and Tumours, consolidation and mycetomas may be obvious.
oxygen saturations 97% on air. Cardiovascular and abdominal Bilateral alveolar shadowing may suggest alveolar
examination was unremarkable. Respiratory examination revealed haemorrhage and bronchiectasis may be seen. However,
coarse crepitations throughout her right lung. CXR will fail to reveal the diagnosis in up to 46% of
cases.14 It is also important to remember that a normal
What are the important features of history CXR does not mean that a diagnosis of lung cancer can be
and examination when assessing a patient excluded. When investigating haemoptysis up to 24% of
with haemoptysis? patients diagnosed with lung cancer had a normal CXR at
For the purposes of management the patient needs to be the time of presentation.15 Depending on the CXR there
allocated into one of the following groups based on history are three main investigation routes.16
and clinical findings. 1. If the CXR demonstrates a mass lesion, the
patient should be referred to a respiratory specialist
1. Minor haemoptysis (which may be investigated for further investigation and treatment,17 which will
and treated as an outpatient) usually involve a staging CT scan, bronchoscopy (or
2. Major / massive haemoptysis with clinical stability. percutaneous lung biopsy) and cancer
3. Major / massive haemoptysis with clinical multidisciplinary team discussion.
instability 2. If the CXR demonstrates parenchymal
Initial assessment should use the ‘ABCDE’ approach in abnormalities referral to a respiratory specialist is
accordance with resuscitation council guidelines.13 recommended. A high resolution CT scan would

Acute Medicine 2012; 11(1): 39-45 41
be the next investigation of choice, and further mortality rates of up to 38%,10 although this is probably
more specialist investigation and treatment based on falling, with older reviews suggesting higher mortality
this result should be initiated. If the history is rates.19 Despite the high mortality associated with massive
suggestive of vasculitis, blood should be sent for haemoptysis there are no agreed consensus guidelines for
specific autoantibodies such as anti-neutrophil management and respiratory physicians will adopt varying
cytoplasmic antibodies (ANCA) or anti nuclear approaches.20
antibodies (ANA). If sputum is produced this
should be sent for microscopy, culture and acid-fast Resuscitation and airway management
bacillus smear and culture. Initial stabilisation using the ABCDE approach should
3. If the chest x-ray is normal and the focus on airway protection, appropriate oxygenation and
haemoptysis is low volume the patient should adequate volume resuscitation.13
be referred to a respiratory specialist as an The patient should be managed in a high dependency
outpatient. If the history or examination suggests area, supported by experienced physicians, nursing staff
bacterial infection, antibiotics should be given and allied healthcare professionals. If there is immediate
according to local policy.16 If the patient has risk threat to the patient’s airway or evidence of respiratory
factors for lung cancer, CT scanning and failure the patient should be intubated with a large
bronchoscopy may be arranged following endotracheal tube (>size 8) to allow for adequate
respiratory specialist review.17 This is usually suctioning followed by bronchoscopy.8
unnecessary for non-smoking patients aged less If it is known which lung the bleeding originates from,
than 40, particularly after an isolated episode.18 If the patient should be managed bleeding side down to try
the haemoptysis recurs or persists, CT scanning and prevent contralateral aspiration. The patient may be
and bronchoscopy may still be required. able to give a history of bubbling on one side. Single lung
ventilation can also be considered to protect the
Case Progression contralateral lung.21 This will require the use of a double
Initial blood test revealed a raised white cell count and normal lumen endotracheal tube inserted by an experienced
haemoglobin, platelets and clotting. Renal and liver function were operator.22 If a double lumen tube is not available the
also normal patient can undergo selective lung intubation by inserting
an endotracheal tube directly over a bronchoscope into the
Her initial CXR demonstrated severe bronchiectasis that was
left or right main bronchus. However it should be borne in
unchanged from previous films. There was no evidence of acute
mind that selectively ventilating the right lung may lead to
infection, mycetoma or any other cause for the haemoptysis
inadvertent occlusion of the right upper lobe due to its
(Figure 1).
proximal origin, leaving only the lower and middle lobe
for ventilation. In this situation a Fogarty catheter may be
How should massive haemoptysis be managed?
passed into the left main bronchus under bronchoscopic
Massive haemoptysis is a medical emergency, which carries
guidance and the balloon inf lated, occluding the bronchus
a high mortality. Recent studies have demonstrated
and allowing the trachea to be Intubated and the right lung
to be ventilated without risk of aspiration.23 Thorough
suctioning of blood and clots should take place to improve
gas exchange.
Large bore cannulae should be inserted; blood should
be taken for full blood count, clotting studies, liver and
renal function, arterial blood gases, inf lammatory markers
and cross match of at least 6 units of blood.8
The patient should be volume resuscitated with
crystalloid or blood24 and clotting abnormalities corrected.
What do you do once the patient is

stabilized?
Once the patient has been haemodynamically stabilized,
the airway is secure and the patient has adequate gas
exchange the next priority of treatment is to localise and
treat the source of bleeding (Figure 2).
Transfer to a specialist centre for definitive treatment
may be required; early consultation with a thoracic surgical
team is advised. If this is the case discussion with a senior
physician experienced in patient transfer should be
Figure 1. Admission chest X-ray demonstrating widespread consulted for the safest way to do this.
bronchiectasis; a port-a-cath is present overlying the lateral aspect of There is no consensus on further investigation. If the
the right lung field. patient has been stabilized a CT scan can be performed,

42 Acute Medicine 2012; 11(1): 39-45
Massive haemoptysis
Admit to HDU/ICU
At risk
Airway
Patent Intubate with large ET
tube. Consider single
lung ventilation
Breathing Respiratory distress
No respiratory distress
Give Oxygen
Circulation
Volume resuscitation.
Xmatch and correct clotting Crystalloid and blood
Reassess
Unstable Stable
Bronchoscopy CT scan
Bronchial Artery
Embolization
Medical Therapy
Endobronchial
treatment Failure
Surgery
Figure 2. Treatment algorithm for massive haemoptysis.
which will often identify the source of bleeding and procedures are being considered. Otherwise fibre optic
establish the cause.19 Contrast enhanced multidetector CT bronchoscopy can be used, which identifies the site of
provides angiographic studies that have recently been bleeding in up to 93% of cases.19
shown to be superior to conventional angiography25 and is
important for considering suitability and planning What are the treatments available for
bronchial artery embolizations. Bronchoscopy may be massive haemoptysis?
required after CT scanning in some circumstances.23 In the Bronchoscopic treatment for endobronchial lesions
case of bronchiectasis and CF, bronchoscopy is not There are a number of therapeutic techniques that can be
indicated as endobronchial therapy is unlikely to be performed through a bronchoscope, most of them best
beneficial and may delay time prior to bronchial artery performed through a rigid bronchoscope and usually only
embolization.26,27 in specialist centres. Instillation of epinephrine (1:20,000)
If the patient with massive haemoptysis is too unstable to an identified point of bleeding can be used. It is effective
to undergo CT scanning, bronchoscopy should be in mild to moderate haemoptysis but of doubtful efficacy
performed immediately. Rigid bronchoscopy may be in major haemoptysis.28 Cold saline lavage,29 fibrinogen
required if there is massive bleeding (to allow for rapid compounds combinations30 and tranexamic acid31 may also
suctioning) or if certain therapeutic bronchoscopic be used, although evidence is limited.

Acute Medicine 2012; 11(1): 39-45 43
Interventional bronchoscopic techniques include

endobronchial balloon tamponade. In this procedure a
Fogarty catheter can be used to tamponade using
f lexible bronchoscopic guidance.32 Stents have also been
used with success. Other methods that have been used
but are not routinely available include the endobronchial
insertion of a haemostatic mesh and endobronchial
sealing with glue.19
Laser photocoagulation using a Nd-Yag laser was first
used in 198233 and is potentially a definitive treatment,
however, the literature is mixed in reporting it’s success.
Eletrocautery, cryotherapy and brachytherapy may play a
role in palliation of haemoptysis in the context of lung
cancer but there is very little evidence available to support
their use.
Bronchial artery embolization (BAE)

BAE is now a widely used and successful technique, which
provides immediate control of bleeding in most patients
(86-99%).34 Outcomes have gradually improved since the
1970s when the procedure was first performed.35 During
Figure 3. The contrast enhanced CT aorta/thorax demonstrates
the procedure the patient undergoes a descending thoracic multiple enlarged bronchial arteries, more evident on the right.
aortogram to identify bronchial artery anatomy and
bleeding site. The most commonly used embolic material
is polyvinyl alcohol.36 resistant mycetoma. Otherwise, it is indicated only
Recurrence is common, occurring in 10-55% of following failure of BAE,8 due to high mortality rates,
patients, and outcome is dependent on underlying disease.34 particularly in the context of significant comorbidities.2
Minor temporary side effects such as chest pain and
dysphagia are common but fortunately neurological Medical treatment
complications secondary to spinal cord ischaemia are rare Treatment of the underlying cause should be initiated
(1.4-6.5%) and becoming rarer with super selective when possible.
catheterisation.34 Systemic embolization is also a risk. Treatments include antibiotics for infection,
antituberculous therapy in the case of TB and systemic
Surgery antifungals for Aspergillus lung disease.
Surgery is the treatment of choice for AV malformations, Bleeding abnormalities should be treated with the
trauma including pulmonary artery rupture and treatment appropriate blood product. In the case of alveolar
Figure 4. Bronchial artery angiography. These images demonstrate bronchial artery angiography pre and post embolization using
embolization particles.

44 Acute Medicine 2012; 11(1): 39-45
haemorrhage, management should be in conjunction with Case Outcome

renal physicians and may include immunosuppression and The patient was treated with analgesia, intravenous tranexamic
plasma exchange.37 acid, intravenous terlipressin and intravenous ceftazidime and
Although tranexamic acid is often used, the evidence colomycin. She remained haemodynamically stable, and was
for its use is limited mainly to CF.38 Intravenous subsequently transferred to a specialist centre with a view to
vasopressors have been advocated but currently their use is bronchial artery embolization.
probably best restricted to patients with CF in specialist She proceeded to undergo contrast CT of the thorax/aorta
centres.39 (Figure 3), which demonstrated multiple enlarged bronchial arteries
The treatment of pulmonary embolism and significant with two arteries identified for embolization. The CT also
haemoptysis provides an uncomfortable situation for the demonstrated severe bronchiectasis and small airway disease.
clinician and risk benefit ratios of immediate Angiography and bronchial artery embolization were undertaken
anticoagulation will have to be considered. (Figure 4). She had no further episodes of haemoptysis during that
admission but repeat embolization was required 3 months later
following a similar admission with recurrent haemoptysis.
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patients with pulmonary tuberculosis. The American review of respiratory Fam Physician. 2005; 72: 1253–1260.
disease. 1968; 97: 187–192. 17. National Institute for Health and Clinical Excellence. The Diagnosis and
2. Corey R, Hla KM. Major and Massive Hemoptysis - Reassessment of Treatment of Lung Cancer CG24. London: National Institute for Health
Conservative Management. American Journal of the Medical Sciences. 1987; and Clinical Excellence. 2005.
294: 301–309. 18. Poe RH, Kallay MC, Israel RH et al. Utility of Fiberoptic Bronchoscopy
3. Håkanson E, Konstantinov IE, Fransson SG., Svedjeholm R. Management in Patients with Hemoptysis and a Nonlocalizing Chest Roentgenogram.
of life threatening haemoptysis. British Journal of Anaesthesia. 2002; 88: Chest. 1988; 93: 70–75.
291–295. 19. Sakr L, Dutau H. Massive haemoptysis: An update on role of bronscopy
4. Ibrahim WH. Massive haemoptysis: the definition should be revised. in diagnosis and management. Respiration. 201; 80: 38–58.
European Respiratory Journal. 2008; 32: 1131–1132. 20. Haponik EF, Fein A, Chin R. Managing Life-Threatening Hemoptysis*.
5. Crocco JA, Rooney JJ, Fankushen DS, DiBenedetto RJ, Lyons HA. Chest. 2000; 118: 1431–1435.
Massive hemoptysis. Arch Intern Med. 1968; 121: 495–498. 21. Gourin A, Garzon AA. Control of hemorrhage in emergency pulmonary
6. Cauldwell EW, Siekert RG, Lininger RE, et al. The bronchial arteries: an resection for massive hemoptysis. Chest. 1975; 68: 120–121.
anatomic study of 150 human cadavers. Surg Gynecol Obstet. 1948; 86: 22. Klein U, Karzai W, Bloos F et al. Role of fiberoptic bronchoscopy in
395–412. conjunction with the use of double-lumen tubes for thoracic anesthesia -
7. Marshall TJ, Jackson JE. Vascular intervention in the thorax: bronchial A prospective study. Anesthesiology. 1998; 88: 346–350.
artery embolization for haemoptysis. European Radiology. 1997; 7: 23. Lordan JL, Gascoigne A, Corris PA. The pulmonary physician in critical
1221–1227. care. Illustrative case 7: Assessment and management of massive
8. Jean-Baptiste E. Clinical assessment and management of massive haemoptysis. Thorax. 2003; 58: 814–819.
hemoptysis. Crit Care Med. 2000; 28: 1647. 24. American College of Surgeons Committee on Trauma: Advanced Trauma
9. Mcdonald DM. Angiogenesis and Remodeling of Airway Vasculature in Life Support Course Manual. Chicago, Ill. American College of Surgeons.
Chronic Inf lammation. Am J Respir Crit Care Med. 2001; 164: S39–S45. 1997.
10. Hirshberg B, Biran I, Glazer M, Kramer MR. Hemoptysis: Etiology, 25. Remy-Jardin M, Bouaziz N, Dumont P, Brillet PY, Bruzzi J, Remy J.
evaluation, and outcome in a tertiary referral hospital. Chest. 1997; 112: Bronchial and Nonbronchial Systemic Arteries at Multi - Detector Row
440–444. CT Angiography: Comparison with Conventional Angiography1.
11. Reisz G, Stevens D, Boutwell C, Nair V. The causes of hemoptysis Radiology. 2004; 233: 741–749.
revisited. A review of the etiologies of hemoptysis between 1986 and 1995. 26. Flume PA, Mogayzel PJ, Jr., Robinson KA et al. Cystic Fibrosis Pulmonary
Mo Med. 1997; 94: 633–635. Guidelines: Pulmonary Complications: Hemoptysis and Pneumothorax.
12. Santiago S, Tobias J, Williams AJ. A Reappraisal of the Causes of Am J Respir Crit Care Med. 2010; 182: 298–306.
Hemoptysis. Arch Intern Med. 1991; 151: 2449–2451. 27. Pasteur MC, Bilton D, Hill AT. British Thoracic Society guideline for
13. The Resuscitation Guidelines 2010. The Resuscitation council (UK). non-CFbronchiectasis. Thorax. 2010; 65: i1–i58.
2010. 28. Cahill BC, Ingbar DH. Massive Hemoptysis - Assessment and
14. Marshall TJ, Flower CDR, Jackson JE. The role of radiology in the Management. Clinics in Chest Medicine. 1994;15: 147–168.
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Radiology. 1996; 51: 391–400. Rigid Bronchoscope and Cold Saline Lavage. Thorax. 1980; 35:901–904.
15. Herth F, Ernst A, Becker HD. Long-term Outcome and Lung Cancer 30. Tsukamoto T, Sasaki H, Nakamura H. Treatment of Hemoptysis Patients
Incidence in Patients With Hemoptysis of Unknown Origin*. Chest. 2001; by Thrombin and Fibrinogen-Thrombin Infusion Therapy Using A
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31. Solomonov A, Fruchter O, Zuckerman T, Brenner B, Yigla M. 36. White RI. Bronchial Artery Embolotherapy for Control of Acute
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33. Dumon JF, Reboud E, Garbe L, Aucomte F, Meric B. Treatment of 38. Wong LTK, Lillquist YP, Culham G, Dejong BP, Davidson AGF.
Tracheobronchial Lesions by Laser Photoresection. Chest. 1982; 81: Treatment of recurrent hemoptysis in a child with cystic fibrosis by
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34. Chun JY, Morgan R, Belli AM. Radiological Management of Hemoptysis: Pediatric Pulmonology. 1996; 22: 275–279.
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46 Acute Medicine 2012; 11(1): 46-48
Viewpoint
Viewpoint: Norovirus Outbreak on the AMU –

A Lesson In Shared Clinical Leadership
S Krishnamoorthy & N Murch
Introduction doctors and a discharge co-ordinator to function as

Three times a year, the first Wednesday of the month the designated dirty team. The team was to staff the
heralds a changeover of junior doctors within our AMU, and not engage in patient contact outside
hospital. This year, the first Wednesday in December the ward. It was agreed that medical registrars
provided a different kind of challenge. The voice on would staff the ‘shop f loor’, allowing the decision
the phone confirmed the words that no one wanted making process to continue whilst minimising the
to hear: “You have three confirmed cases of Norovirus footfall of junior doctors and consultants within
and you have to close to new admissions”. the AMU. All members of the dirty team were
Over the last year, there have been 1852 required to wear scrubs whilst in the ward, and
outbreaks of Norovirus (formerly known as ‘Norwalk these were to be discarded on leaving the ward,
Virus’) reported to the Health Protection Agency1 helping to minimise the exposure to other
(HPA), affecting 18,600 patients and 4900 staff. This colleagues in communal areas of the hospital
resulted in a loss of 22,800 bed days. The impact of (Doctors’ Mess, coffee shops etc).
the yearly winter outbreaks on the health services is The focus of care was to expedite discharge of
undeniable. It is estimated to cost the NHS in excess stable patients to their own homes, whilst
of £100 million per annum.2 In addition, as the above minimising disruption to care for patients who were
figures illustrate, it poses a significant risk to staff required to remain in hospital. This involved
working within the health sector. engaging the Post Acute Care Evaluation (PACE)
An outbreak of an infective viral gastroenteritis team, community physiotherapists and general
proves a unique challenge within the acute medical practitioners. Emphasis was placed on effective
setting. The functioning of acute services within a handover between the hospital and community
hospital is dependant on the rapid turnover of teams. Occupational therapists from clean wards
patients, for which the specialty of Acute Medicine provided services such as home access visits to ensure
plays a key part. There is an increasing shift in policy, the safe discharge of vulnerable patients.
Sanjay Krishnamoorthy moving from the traditional focus solely on
MBChB MRCP infection control, to a more pragmatic approach Isolation of the Assessment Area and
Specialist Registrar Acute involving maintaining acute services and minimising Ambulatory Care
Medicine disruption to patient care.3 This requires a consensus The assessment area of the AMU was geographically
The Royal Free Hospital multi-disciplinary team approach to acute care isolated from the rest of the ward by closing two large
provision, and strong clinical leadership. double doors. A clean nurse was in charge, overseeing
Nick Murch
MB.BCh FHEA PG Cert patients in this area and medical care was provided by
Med Ed MRCP, How did we deal with the outbreak? the on-call medical team. This area also provides care
Locum Consultant in Acute A meeting was immediately convened between our for ambulatory patients, which is usually overseen by
Medicine and Medical infection control team, matrons and acute medicine the AMU ward team. For the short duration of the
Education consultants. The hospital protocol deemed that outbreak however this responsibility was placed with
The Royal Free Hospital the acute medical team on-take to ensure
immediate ward closure was imperative. However
Correspondence: the impact of this would be substantial, putting uninterrupted provision of this essential service.
Sanjay Krishnamoorthy significant strain both on the AMU and the
Department of Acute Emergency Department (ED) for the admission of Maintenance of Non-Invasive Ventilation facility
Medicine new patients. It was clear that a rapid re-organisation The Acute Medical Unit in our hospital provides
8th Floor, non-invasive ventilation (NIV) services for the
of services was required to ensure the continued
The Royal Free Hospital
delivery of clinical care for acute medical patients. hospital outside the Intensive Care Unit setting.
Pond Street
London Recognising the need for potentially life-saving
NW3 2QG A multidisciplinary approach intervention, patients who needed NIV, were
Email: skmoorthy@ A multi-disciplinary team was assembled including carefully selected and were fully consented on the
doctors .net.uk nurses, physiotherapists, occupational therapists, risks of admission into an infected ward. The risks

Acute Medicine 2012; 11(1): 46-48 47
Viewpoint: Norovirus Outbreak on the AMU – A Lesson In Shared Clinical Leadership
and benefits were clearly explained to both patients and diseases, such as the haematology wards, oncology wards
family members prior to the transfer. A designated bay for and the transplant units were required to be symptom free
the provision of NIV was identified with a dedicated nurse for forty-eight hours prior to moving on to the service.
allocated to this bay. It was recognised that cross This was essential in maintaining a sterile environment for
contamination was likely given that the same medical staff some of our most vulnerable patients. Inevitably this
were involved in the care of symptomatic patients with placed a strain on these clinical areas. Doctors who were
diarrhoea and patients on NIV. Additional precautions already working on these wards were asked to continue
were therefore taken with careful hand-washing and working there, giving their colleagues a forty-eight hour
cleaning of clinical equipment used in the bay. This proved window within which to be symptom free. A cross
successful and we provided the necessary acute speciality meeting was held between the heads of
intervention for critically unwell patients without departments to ensure adequate staffing across all the
spreading the infection. Critical in this scenario was the wards in the hospital.
careful consenting of patients needing NIV, and the risk-
benefit analysis of patients needing an acute intervention Outcome
versus the likelihood of contracting a viral gastroenteritis. The outbreak lasted on the AMU for ten days. We were
successful in limiting the spread to other wards. Even with
Radiology involvement maintenance of careful hygiene standards within the
The Radiology team were engaged into the process, wards, we were unable to prevent the sporadic spread of
ensuring that all urgent imaging was undertaken whilst virus to previously asymptomatic patients across bays. This
adhering to safety precautions to minimise the spread of once again reiterates the highly infectious nature of
infection. Urgent chest and abdominal plain films were Norovirus, and justifies the decision taken early to close the
performed using mobile equipment, which was disinfected entire ward to new admissions. The AMU was
after imaging. Computerised tomography (CT) scans were subsequently re-opened by decanting individual bays of
deferred to the end of the list whenever possible. Cleaning patients up to our seventeen bedded overf low unit and
services were expedited after scanning to ensure a terminal subsequently deep cleaning the bays. This approach was
clean prior to resuming the service. rolled out across the entire AMU.
Relatives and visitors Discussion

Hospital policy dictated that relatives and visitors were not We were largely successful in curbing the potentially
allowed on the ward whilst the it remained closed. This devastating effects a widespread Norovirus outbreak can have
proved challenging for patients who did not converse in on a hospital. The key approaches are summarized in
English and for patients who were terminally ill. A Table 1. An outbreak of Norovirus has unique implications to
pragmatic approach was adopted, ensuring that the merits the AMU. Maintaining an active AMU is central to
of each case were considered individually. By outlining the managing an intake of patients through the ED. A key
risks involved and highlighting precautions that they could component to our management of the outbreak was the use
take (wearing scrubs, diligent hand-washing), we were of the winter overflow ward. This had been identified early
able to cater to the best interests of these patients and the in the summer as focus for patient care in the eventuality of
wishes of their families. an outbreak. This allowed us to maintain our acute medical
service. It is crucial for all Acute Medical Units to identify a
Establishment of a temporary AMU potential area in their hospital which might be used in such
A ward with seventeen private rooms with ensuite showers eventualities. The assessment area within the AMU should
had previously been designated the winter overflow ward. also have the provision to be isolated from the remainder of
Resources were rapidly mobilised to staff this ward as a the unit. This enables initial stabilisation of newly admitted
temporary Acute Medical Unit. Acute physicians managed patients, who are in the most vulnerable stage of their illness,
patients on this ward, ensuring the provision of optimum before transfer to other areas of the hospital.
acute care and a continued rapid turnaround of patients.
Junior doctors on rota to work on the AMU worked with a Importance of shared leadership
consultant to effect management plans. AMU nursing staff, A key component of our success was the shared leadership
lead by a charge nurse provided critical input in managing taken by the infection control team and the acute medical
patients on the overflow ward. In order to maintain adequate consultant. The different perspectives of the two
staff levels, bank nurses were hired to assist the team. departments were immediately apparent: the infection
Furthermore, the overflow ward was provided with a duty control team was keen to close the ward, having identified
physiotherapist, occupational therapist and discharge co- culture positive patients across different bays; the AMU
ordinator to ensure uncompromising provision of service. consultant was more focussed on ensuring that the closure of
This provided the overflow ward with the capabilities of a the ward did not adversely affect patient care. Both
fully functioning AMU. perspectives have their own merits; however, recent
guidelines stress the importance of maintaining the acute
Impact on other departments medical service.3 If facilities to decant existing or new
Junior doctors moving in the change-over, to higher patients onto a clean ward are not available, we need to
dependency wards with patients susceptible to infectious consider isolating bays within the AMU in which
48 Acute Medicine 2012; 11(1): 46-48
Viewpoint: Norovirus Outbreak on the AMU – A Lesson In Shared Clinical Leadership
1. On confirming Norovirus infection in patients from separate bays, consider immediate closure of the ward. If outbreak confined to
one bay, barrier nurse patients on closed bay with dedicated dirty staff.
2. Identify multi-professional team comprising doctors, nurses, physiotherapists, occupational therapists, discharge co-ordinator and
ward clerk as a designated dirty team.
3. Middle grade doctors to be identified by consultant to staff AMU to ensure uninterrupted decision making process and safe
discharges.
4. Members of the dirty team to wear scrubs whilst on the ward, to be discarded on leaving the ward.
5. Early liaison with radiology team to identify strategies to ensure completion of urgent imaging.
6. Close ward to relatives and visitors, except in extra-ordinary circumstances (patients needing interpreters, terminally ill patients.).
The clinical needs of each patient should be judged individually.
7. Early identification of winter overflow ward to function as alternative AMU. Full complement of multi-disciplinary team required.
8. If unable to identify overflow ward, isolate bays within AMU to nurse infected patients. Early policy decisions to address
compromise in nursing patients in single sex bays.
9. Daily team meeting with infection control team, charge nurse, hospital managers and AMU consultant to review bed situation.
10. On reaching capacity in the hospital, early dialogue with neighbouring hospitals to ensure diversion of patients if appropriate.
Table 1. 10 key recommendations for managing a Norovirus outbreak on the AMU.
symptomatic patients are nursed. Bold decisions may be was maintained through team working and dialogue. A
required, including compromising on the provision of single team of health professionals, each with their individual
sex bays, to maintain the balance between infection control, areas of expertise, worked collectively towards a common
provision of clinical care and patient dignity. A goal: the safe and efficient delivery of acute care
multidisciplinary approach, ensuring involvement of patients The publishing of the Medical Leadership
and their carers in the process, is critical to this process. Competency Framework4 (MLCF) highlights the need for
all healthcare professionals to show medical leadership in
Learning points – a trainee’s perspective the delivery and transformation of services. The concept of
As a medical registrar, I was deeply entrenched in the shared clinical leadership heavily underpins these
management of patients during this outbreak. I was one of recommendations.
the designated dirty team - a tag that I initially resented. I gained valuable insight into the camaraderie that
However I subsequently found the experience hugely develops between team members when faced with a
valuable, gaining first hand experience in the importance challenging situation. The experience helped me to
of shared clinical leadership. There was a smooth understand the concepts of team building, which I now
transition in service provision to a pre-decided, well recognise are imperative in becoming an effective leader. I
thought out contingency plan. Guidelines were followed, feel, as a result, better equipped to deal with similar
and the balance between infection control and clinical care outbreaks in the future.
References
1. Hospital Norovirus Outbreak Reporting. Update September 2010. Health Infection Association; Healthcare Infection Society; Infection Prevention
Protection Agency. Society; National Concern for Healthcare Infections; NHS
2. Lopman BA, Reacher MH, Vipond IB, Hill D, Perry C, Halladay T, et al. Confederation. Website:www.hpa.org.uk/webc/HPAwebfile/HPAweb_c/
Epidemiology and cost of nosocomial gastroenteritis, Avon, England, 1317131639453.
2002-2003. Emerg Infect Dis. 2004 Oct; 10(10): 1827–34. 4. Medical Leadership Competency Framework – Enhancing Engagement in
3. Guidelines for the management of Norovirus outbreaks in acute and Medical Leadership. July 2010. Academy of Medical Royal Colleges and
community health and social care settings. Authors: HPA, British NHS institute for Innovation and Improvement.

Acute Medicine 2012; 11(1): 49 49
Correspondence Section
Dear sir,
I read with interest your article regarding the performance of lumbar puncture in your most recent issue, in particular the timing of this
procedure with regards to the administration of low molecular weight heparins.1 I feel it should also be pointed out that antiplatelet therapy
is also a relevant consideration as, whilst the risk of epidural or spinal haematoma remains low, it can result in significant, permanent
neurological deficit.2
No European specific advice regarding this issue exist; however, the American Society of Regional Anesthesia have produced
guidelines.2 Whilst not directly applicable to diagnostic lumbar puncture, it is relevant that these recommendations be highlighted. The
guidelines suggest that neuraxial blockade is safe in patients receiving aspirin or non-steroidal anti-inflammatory medications alone, but that
in patients receiving thienopyridines or GIIb/IIIa medications these should be discontinued; for clopidogrel, this requires a washout period
of seven days. It is reasonable to consider lumbar puncture a similar intervention to spinal or epidural blockade. In most cases where LP is
performed on the Acute Medical Unit the procedure cannot be delayed to enable discontinuation of medication. The potential diagnostic
benefit of the procedure should be weighed up against an increased bleeding risk and consideration of methods to normalise platelet
function. Such patients should be counseled regarding the risk of spinal cord haematoma and observed closely for this complication, in
particular the development or localised, often severe and constant back pain with or without a radicular component that may mimic disc
herniation. Associated symptoms may include weakness,numbness, and sphinchter disturbance.4 Where these occur, prompt imaging and
neurosurgical referral are required as surgical decompression remains the treatment of choice in this situation.5
Yours sincerely
Dr. Stephen Shepherd
ST4 Anaesthesia and Intensive Care
References
1. Cooper N. Lumbar Puncture. Acute Medicine 2011; 10: 188-193.
2. Joseph A, Vinen J. Acute spinal epidural haematoma. Journal of Emergency Medicine, 1993; 11: 437-441.
3. Horlocker TT, Wedel DJ, Rowlingson JC et al. Regional Anesthesia in the Patient Receiving Antithrombotic or Thrombolytic Therapy: American Society of Regional
Anesthesia and Pain Medicine Evidence-Based Guidelines (Third Edition). Regional Anesthesia and Pain Medicine 2010; 35: 64-101.
4. Wolfgang P, Klaus M. Spinal haematoma unrelated to previous surgery: analysis of 15 consecutive cases treated in a single institution within a 10-year period. Spine, 2004; 24:
555-561.
5. Rohde V, Küker W, Reinges MHT, et al. Microsurgical treatment of spontaneous and non-spontaneous spinal epidural hematomas: Neurological utcome in relation to aetiology.
Acta Nurochirchiga, 2000; 142: 787-793.

50 Acute Medicine 2012; 11(1): 50-51
Picture Quiz Answer
Key Learning Points

• Myocarditis is a clinico-histopathological diagnosis which has several subtypes.
• Poor prognostic factors such as history of syncope, ECG and echo abnormalities should be identified early
• Treatment includes supportive treatment, standard heart failure treatment and in severe cases invasive cardiac support
therapies
H Patel • Cardiac MRI and endomyocardial biopsies can be helpful
MRCP • There is a limited role for antiviral and immunosuppressive agents in management
Cardiology registrar
Eastbourne District General Answers dyspnoea, ST segment changes, an elevated
Hospital 1. Sinus tachycardia, saddle shaped ST segment troponin, a pericardial effusion and a reduced left
Eastbourne elevation in leads V2-6 and II. ventricular (LV) function, which allows narrowing of
BN22 2UD 2. Fulminant myocarditis. the differential to the first four listed in Box 1.
G Dhillon 3. Viral or secondary to cannabis. It is important to consider congenital, valvular,
MRCP 4. The history of syncope and an EF<40%. and ischaemic causes and restrictive/hypertrophic
Cardiology trainee 5. Standard heart failure management including: cardiomyopathies before attributing myocarditis as a
Department of Cardiology angiotensin converting enzyme (ACEi) inhibitors, cause of heart failure.
Eastbourne District General beta blockers, monitoring.
Hospital Classification
Eastbourne There are four main subtypes of myocarditis,1 each of
BN22 2UD Discussion
There is no ‘gold standard’ non-invasive test to which has different prognosis and potential treatments:
A Bandali diagnose myocarditis. It is a clinico-histopathological
MBBS diagnosis.1 Clinical manifestations include: heart A. Fulminant myocarditis
Cardiology trainee Presents with acute heart failure up to 2 weeks after
failure, chest pain (from either pericarditis or angina
Department of Cardiology a viral prodrome. Treatment is supportive and
Eastbourne District General from coronary artery spasm/inf lammation), sudden
cardiac death and arrhythmias (sinus tachycardia, ventricular function often recovers if the patient
Hospital
Eastbourne ectopics, ventricular tachycardia, heart blocks). survives the initial episode. This has a better
BN22 2UD Examination may reveal raised JVP, pulmonary prognosis.
crackles, a gallop rhythm or a pericardial rub.
N Patel B. Acute myocarditis
FRCP
Cardiac troponins may be elevated, which have a
high specificity but low sensitivity for myocarditis.2 Patients present with established heart failure that
Cardiology Consultant
Department of Cardiology ECG changes are variable and in our case there may progress to dilated cardiomyopathy.
Eastbourne District General was ST segment elevation, which has a wide
Hospital differential (Box 1). The patient had chest pain, C. Chronic active myocarditis
Eastbourne Patients have relapses associated with reduced
BN22 2UD ventricular function and fibrosis on histology.
ST elevation myocardial infarction
Correspondence: Acute myopericarditis
D. Chronic persistent myocarditis
H Patel Pulmonary embolism
MRCP Cardiomyopathy Patients have typical symptoms and histological
Cardiology registrar C/O Dr Ventricular aneurysm changes but with preserved ventricular function.
NR Patel Electrolyte abnormalities
Department of Cardiology Left ventricular hypertrophy Causes of Myocarditis
Eastbourne District General Left bundle branch block The aetiology of myocarditis can be grouped as shown
Hospital Paced rhythm in Box 2. Viruses account for most cases of
Eastbourne Repolarisation changes
Central nervous system pathology myocarditis.3 Our patient gave a history of fever and
BN22 2UD
myalgia which suggests a viral cause. Performing acute
Email: dochiteshpatel@hot-
mail.com Box 1. Causes of ST elevation on an ECG. and convalescent antibody titres to determine aetiology

Acute Medicine 2012; 11(1): 50-51 51
Infections Viral, bacterial, spirochetal, mycotic, has limited applications due to low sensitivity and risks.
rickettsial, protozoal, helminthic Class 1 indications include: new onset heart failure of less
Toxic Carbon monoxide, alcohol, recreational than 2 weeks with haemodynamic compromise; and new
drugs, anthracyclines, radiation onset heart failure of 2 weeks to 3 months duration with a
dilated ventricle complicated by either arrhythmias or not
Hypersensitivity Antibiotics, antipsychotics, dobutamine,
lithium, vaccines, venomous animals
responding to conventional treatment.6 Biopsy results can
guide use of antiviral agents and immunosuppression.
Systemic Disorders Vasculitis, sarcoidosis, HIV,
The general usage of antiviral agents and
hypereosinophilia, thyrotoxicosis,
inflammatory bowel disease immunosuppressive therapy is not recommended.
Myocarditis secondary to sarcoidosis,7 coeliac disease,8
Box 2. Causesof myocarditis. giant cell myocarditis9 and dilated cardiomyopathy with
evidence of viral persistence10 may benefit from specific
appears to be of limited use clinically.4 The rash might have therapies.
resulted from his reduced cardiac output but could also
indicate a toxic/hypersensitivity reaction to recent cannabis Prognosis
usage. In the acute setting, risk stratification can help to guide
outcome. The following suggest a good prognosis:
Initial Treatment and Investigation - Short history of clear symptom onset (weeks-months)
All patients with reduced LV function should be treated with - Normal left ventricular diastolic dimensions with
an angiotensin converting enzyme-inhibitor and beta increased septal thickness (myocardial oedema) on
blocker.3 Fluid overload should be managed with salt and echocardiography
water restriction and diuretics. Non-steroidal anti- The following suggest a poorer prognosis :
inflammatory drugs should be avoided as they increase - History of syncope
mortality. Cardiac monitoring is important to enable early - Q waves, bundle branch block, high degrees of AV
identification and treatment of supraventricular tachycardias, block and ventricular tachycardia on ECG
ventricular tachycardias and bradycardias. Hypoxia should be - Increased left ventricular diastolic dimensions, normal
corrected with supplemental oxygen. Aggravating septal thickness, pulmonary hypertension, ejection
substances such as alcohol, recreational drugs and prescribed fraction <40% on echocardiography
drugs should be stopped. Physical activity should be reduced.
If the patient is in cardiogenic shock, transfer to a high Patient outcome
dependency area should be undertaken to enable additional The patient was started on Ramipril 1.25mg once a day and
cardiovascular support using inotropes, an intra-aortic Bisoprolol 1.25mg once a day for heart failure. Within 6 days
balloon-pump, extra-corporeal membrane oxygenation repeat echocardiogram demonstrated that his left ventricular function
and/or a left ventricular assist device.3 had improved to normal and he was discharged home. An
Further investigations may include cardiac magnetic outpatient cardiac MRI showed normal biventricular function with
resonance imaging (MRI) and endomyocardial biopsy. no fibrosis or inflammation. On review in clinic he described light-
MRI can help diagnose myocarditis with a sensitivity of headedness and pre-syncope which were deemed likely to be related
76% and specificity of 96%.5 It helps identify the extent of to his Ramipril and Bisoprolol, which were therefore discontinued.
inf lammation, differentiate ischaemic cardiomyopathy and He has not described any further symptoms since. Repeat
identify areas amenable for biopsy. Endomyocardial biopsy echocardiogram is planned in one year.
References
1. Lieberman EB, Hutchins GM, Herskowitz A, et al. Clinicopathologic 7. Kim JS, Judson MA, Donnino R, et al. Cardiac sarcoidosis. Am Heart J
description of myocarditis. J Am Coll Cardiol 1991; 18: 1617–26. 2009; 157: 9–21.
2. Smith SC, Ladenson JH, Mason JW, et al. Elevations of cardiac troponin I 8. Frustaci A, Cuoco L, Chimenti C, et al. Celiac disease associated with
associated with myocarditis. Circulation 1997; 95: 162–8. autoimmune myocarditis. Circulation. 2002; 105: 2611–18.
3. Cooper LT. Myocarditis. NEJM 2009; 360: 1526–38. 9. Cooper LT Jr, Berry GJ, Shabetai R. Idiopathic giant-cell myocarditis-
4. Keeling PJ, Lukaszyk A, Poloniecki J, et al. A prospective case-control natural history and treatment. Multicentre Giant Cell Myocarditis Study
study of antibodies to coxsackie B virus in idiopathic dilated Group Investigators. NEJM 1997; 336: 1860–66.
cardiomyopathy. J Am Coll Cardiol 1994; 23: 593–8. 10. Kuhl U, Pauschinger M, Schwimmerbeck PL, et al. Interferon-beta
5. Abdel-Aty H, Boye P, Zagrosek A, et al. Diagnostic performance of treatment eliminates cardiotrophic viruses and improves left ventricular
cardiovascular magnetic resonance in patients with suspected acute function in patients with myocardial persistence of viral genomes and left
myocarditis: comparison of different approaches. J Am Coll Cardiol 2005; ventricular dysfunction. Circulation 2003: 107: 2793–8.
45: 1815–22. 11. Goldberg LR, Sulk J, Patton KK, et al. Predictors of adverse outcome in
6. Cooper LT, Baughman KL, Feldman AM, et al. The role of biopsy proven myocarditis (abstract) . J Am Coll Cardiol 1999; 33: A850.
endomyocardial biopsy in the management of cardiovascular disease: a 12. Cappola TP, Felker GM, Kao WH, et al. Pulmonary hypertension and risk
scientific statement from the American Heart Association, the American of death in cardiomyopathy: patients with myocarditis are at higher risk.
College of Cardiology, and the European Society of Cardiology. Circulation Circulation 2002; 105:1663–68.
2007: 116: 2216–33.

52 Acute Medicine 2012; 11(1): 52
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Research, Audit and Clinical Practice

Endogenous endophthalmitis and liver abscesses.........................................................................................................................25

Picture Quiz: Question

Journal Watch: November 2011-January 2012...............................................................................................................................30

The patient presenting with acute hemiparesis..............................................................................................................................33

Haemoptysis: Diagnosis and Treatment ..........................................................................................................................................39

© Rila Publications Ltd • Acute Medicine • 2012 • Volume 11 Issue 1 • 1–56

2 Acute Medicine 2012; 11(1): 2

Journal of Acute Medicine is indexed/abstracted in EMBASE/Excerpta Medica and now cited

© 2012 Rila Publications Ltd.

Acute Medicine 2012; 11(1): 3-7 3

Magnesium and the Acute Physician

R Allan & N Mara

Key Learning Points

Abstract cell membrane, preventing calcium inflow, and on

© 2012 Rila Publications Ltd.

4 Acute Medicine 2012; 11(1): 3-7

Magnesium and the Acute Physician

Figure 1. Torsades de pointes.

© 2012 Rila Publications Ltd.

Acute Medicine 2012; 11(1): 3-7 5

Magnesium and the Acute Physician

Table 1. Causes of Hypomagnesemia.2,5

© 2012 Rila Publications Ltd.

6 Acute Medicine 2012; 11(1): 3-7

Magnesium and the Acute Physician

© 2012 Rila Publications Ltd.

Acute Medicine 2012; 11(1): 3-7 7

Magnesium and the Acute Physician

© 2012 Rila Publications Ltd.

8 Acute Medicine 2012; 11(1): 8-12

Research, Audit and Clinical Practice

ECG dispersion mapping predicts clinical

J Kellett, A Emmanuel & S Rasool

Abstract SCS and a 20 fold increase in mortality compared to

© 2012 Rila Publications Ltd.

Acute Medicine 2012; 11(1): 8-12 9

G1 Depolarization of the right atria 0-17 P wave

G2 Depolarization of the left atria 0-10 P wave

G3 Depolarization of the right ventricle 0-16 QRS

G4 Depolarization of the left ventricle 0-22 QRS

G5 Repolarization of the right ventricle 0-3 T wave

G6 Repolarization of the left ventricle 0-14 T wave

G7 Symmetry of ventricular depolarization 0-21 QRS

G8 Intraventricular block 0-2 QRS

G9 Ventricular hypertrophy 0-21 QRS

SCS not increased SCS increased p F Odds ratio Chi-square

Male sex 56.3% 43.5% 0.13 - 1.7 (0.9-3.3) 2.2

Nursing home residence 6.6% 17.4% 0.02 - 3.0 (1.1-7.5) 5.3

In-hospital mortality 1.5% 21.7% 0.00001 - 18.6 (5.7-62.2) 44.0

© 2012 Rila Publications Ltd.

10 Acute Medicine 2012; 11(1): 8-12

SCS the day after

© 2012 Rila Publications Ltd.

Acute Medicine 2012; 11(1): 8-12 11

SCS not increased SCS increased p Odds ratio Chi-square

Coefficient SE Odds ratio P

Constant -2.9842 0.2720 - 0.000