Acute Med

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 H Patel, G Dhillon, A Bandali & N Patel

Information for Authors ................................................................................................................................................................52

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


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Acute Medicine 2012; 11(1): 2

Acute Medicine Editor Dr C D Roseveare Consultant in Acute Medicine Southampton University Hospital NHS Trust Tremona Road Mail Point 520 Southampton SO16 6YD UK Tel: 02380 794716 Email: [email protected]

Editorial Board Prof. Derek Bell Professor of Acute Medicine Imperial College London Email: [email protected] Ms Liz Lees Consultant Nurse, Acute Medicine Heart of England Foundation Trust [email protected] Dr Simon J Fletcher Consultant and Honorary Senior Lecturer Anaesthesia and Intensive Care Norfolk and Norwich University NHS Trust Email: [email protected] Dr Mark Jackson Department of Respiratory Medicine Brighton General Hospital Email: [email protected] Dr Mike Jones Consultant Physician Edinburgh Royal Infirmery Email: [email protected] Dr Nikhil Patel Consultant Cardiologist Eastbourne District General Hospital Email: [email protected] Dr Ashwin Pinto Consultant Neurologist Southampton University Hospitals NHS Trust Email: [email protected] Dr Tom Heaps Consultant in Acute Medicine University Hospitals Coventry and Warwickshire Email: tomheaps@hotmail. co.uk

Editorial he snow and freezing temperatures will hopefully have passed by the time this edition reaches you; 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 f lu, but this year Norovirus seems to have been the bigger challenge. Ward closures from diarrhoea outbreaks have traditionally been more of a ‘downstream’ problem (no pun intended), but the impact of closure of the AMU would be substantial.At the time of writing this has still, thankfully, been 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 hospital. The use of an empty ‘winter pressures ward’ eased the burden in this case, enabling the AMU service to be maintained. Even with the luxury of this spare capacity, there was clearly significant disruption, requiring close collaboration between a variety of departments, which is well described by 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 casualty incidents; we need to consider similar contingencies to deal with AMU closure if patient safety is going to be maintained. This article is a timely reminder of the need for forward planning.

T

Maintaining patient safety is a mantra which will be familiar to acute physicians, particularly those who attended any of the recent SAM meetings, where this theme has been well rehearsed. An acute medical unit can provide significant safety benefits by concentrating resources in a single area. However, for 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 compromised; so if safety is our mantra, acute physicians and nurses have a responsibility to manage this process effectively. The article by David Hindmash and Liz Lees provides an important addition to the limited literature in this area. Structured checklists are becoming an increasing part of medical practice; this paper highlights how a checklist can be used to improve the quality of handover from AMU. The authors emphasise the need to keep the form simple, and the importance of regular reinforcement to ensure that it is used. What skills and attributes does an acute physician require? With interview season approaching it’s a question that many prospective trainees will be contemplating – remaining calm under pressure, communication skills and teamworking are some of the standard responses; but what about a good sense of smell? Most of us recognise the characteristic odour of melaena , or the whiff of infected urine. But the absence of body odour might be equally revealing. Luther and Yap noted their patient to be ‘remarkably clean’ – unusual, perhaps, for a young male patient on the AMU; along with his persistent 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 when patients repeatedly attend – as well as having a ‘good nose’ to sniff out something unusual! Dr Chris Roseveare 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 Rila Publications Ltd. 73, Newman Street, London W1A 4PG, UK Tel: +44(0)20 7631 1299 Fax: +44(0)20 7580 7166 Website: www.rila.co.uk Design & Production Rinald Mamachev

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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 Magnesium deficiency, and to a lesser extent magnesium excess, is commonly encountered in patients admitted to the Acute Medical Unit. It is important that acute physicians are able to identify those at risk of these states and initiate appropriate investigation and treatment. This article aims to provide the reader with a sound understanding of magnesium physiology and its effect at a cellular level. The causes, symptoms and treatment of magnesium disorders are discussed along with a review of evidence regarding the therapeutic use of magnesium.

Keywords Magnesium, hypermagnesemia, hypomagnesemia, dysmagnesemia, asthma, COPD, arrhythmias, cardiac arrest, myocardial infarction, subarachnoid haemorrhage, migraine, seizures.

What does Magnesium do? Magnesium is essential for bone mineralization, muscular relaxation and neurotransmission. It is a necessary co-factor for the cell membrane enzyme Na/K ATPase, which provides energy for the membrane Na/K pump. Therefore in deficient states, the intracellular levels of sodium rise and potassium fall, allowing cellular resting membrane potential to approach threshold potential. The higher intracellular sodium level causes an increase in intracellular calcium via the Na/Ca countertransport system, allowing greater muscular contraction. Conversely, the administration of magnesium reduces the intracellular sodium, and thus calcium levels, therefore decreasing the resting membrane potential. This reduces automaticity, acting as a cell membrane stabiliser. Supra-normal levels of magnesium appear to augment this physiological role, allowing us to consider magnesium as a Na/K pump agonist.1 Magnesium also regulates ion channels. It acts on potential-dependent L-type calcium channels on the


cell membrane, preventing calcium inflow, and on receptors on the sarcoplasmic reticulum, inhibiting their activation and preventing calcium outflow from the sarcoplasmic channel.2 In this way, muscle relaxation is achieved. The effects of hyperexcitability and weakness of the musculoskeletal system resulting from hypo- and hypermagnesaemia respectively can therefore be explained. In addition, it can be appreciated that vasodilatation and bronchodilation may result from its relaxatory action on smooth muscle.1 The final action of magnesium may convey some anticonvulsant properties.2 In the synapse, there is an N-Methyl-D-Aspartate (NMDA) receptormediated component to epileptiform activity; magnesium is an NMDA receptor antagonist.

Physiology A serum magnesium level of 0.7-1.1 mmolL-1 (1.4-2.2mEqL-1 or 16.8-26.4mgL-1) is considered the ‘normal’ range. This, however, is a poor ref lection of total body magnesium given its intracellular predominance. Approximately 60% of total magnesium is contained within bone, 20% in muscle and 20% in soft tissues. Of that in bones and muscles, only one quarter is available for exchange into serum. Only 0.3% is in the serum; this is made up of ionised (active) form (65%), protein bound state (27%) and that contained within anion complexes (8%). Measuring the intracellular level achieves a better ref lection of total body magnesium than serum measurements, although this is rarely used in clinical practice. Where total magnesium deficiency exists but the serum magnesium level is normal, deficiency can be confirmed by demonstrating reduced urinary magnesium excretion following magnesium infusion (60%, of that infused).2 To maintain magnesium levels it is recommended that adults consume 10.4-14.6 mmol (250-350mg) per

Russell Allan ST4 Dept of Acute Medicine, Crosshouse Hospital, Kilmarnock, KA2 0BE, Ayrshire Neil Mara Consultant Dept of Acute Medicine, Crosshouse Hospital, Kilmarnock, KA2 0BE, Ayrshire Correspondence: Russell Allan Dept of Acute Medicine, Crosshouse Hospital, Kilmarnock, KA2 0BE, Ayrshire Email: russellallan@doctors .org.uk


4



day. Certain subgroups will require more, including pregnant females and children. Magnesium can be found in chocolate, nuts, vegetables, cereals and seafood. Of what is ingested approximately 50% is absorbed in the normal state. Absorption occurs throughout the GI tract but principally in the small intestine. Renal excretion occurs at approximately 5mmol/day in the normal state. This is decreased when deficient or where renal failure exists, but can be increased by certain drugs (e.g. diuretics, cisplatin, gentamicin and cyclosporin). Homeostasis of Magnesium is under the control of many hormones; the precise mechanism is unclear. Parathyroid hormone (PTH) has a major role, acting with Vitamin D to increase intestinal absorption, renal reabsorption and bone uptake. Insulin and glucagon also have a role by increasing cellular uptake and reducing renal excretion respectively.2

Hypermagnesemia Incidence Hypermagnesemia has a prevalence in hospitalised patients 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 Hypermagnesemia is usually iatrogenic or secondary to renal failure, in particular where rhabdomyolysis is the cause (due to muscle breakdown with release of free magnesium).

Clinical Features Initially patients may describe f lushing, nausea and vomiting, progressing to confusion, weakness (including that leading to respiratory depression) and presyncope/syncope related to atrioventricular block. Ultimately hypermagnesaemia may cause deep coma and cardiac and/or respiratory arrest.3 Examination may reveal reduced or absent deep tendon ref lexes.

ECG Changes In the presence of hypermagnesemia, the ECG may demonstrate prolonged PR and QT intervals, peaked T waves and a variety of supraventricular and ventricular tachy-arrhythmias.3

administration, thereby preventing hypocalcaemia which would further exacerbate the effects of magnesium excess. Haemodialysis may be required in severe cases along with ventilatory support for respiratory depression.3 These should be considered as holding measures, as hypermagnesemia will recur if the cause is not identified and managed.

Hypomagnesemia Incidence The incidence of hypomagnesemia in hospitalised patients is 11, 19 and 47% when classified as Magnesium levels of less than 0.6, 0.62 and 0.74mmolL-1 respectively. It results in a worse prognosis following acute hospital admission and has been seen to double death rate in an ITU population.2 The lower limit of normal is usually quoted as 0.6mmolL-1, below which, symptoms and signs of neuromuscular, neurological and cardiovascular hyperactivity may occur. It is important to remember that the serum level is a specific indicator but lacks sensitivity as it represents less than 1% of the total body magnesium.4

Causes The most common causes of hypomagnesemia are GI loss, starvation, malabsorption, diuretic drugs and alcoholism. Other causes are shown in Table 1.

Clinical Features Magnesium deficiency can cause nervous system irritability in the form of nystagmus, dyskinesia, altered sensation and seizure activity. Muscle weakness, fatigue and confusion are also recognized. Magnesium is also involved in parathyroid hormone (PTH) production, so at low magnesium levels, less PTH is produced and thus calcium will also be low. Hypocalcaemia will not improve following calcium replacement unless the hypomagnesaemia is also corrected. Accentuating this problem, hypomagnesemia also induces skeletal muscle resistance to PTH.5 Hypokalaemia often also accompanies these deficient states.This can be explained by considering the action of magnesium as a Na/K pump agonist as well as by recognising that the causes of hypokalaemia and hypomagnesaemia are often similar.

ECG Changes Treatment If hypermagnesemia is severe and symptomatic, saline diuresis (0.9% saline and furosemide 1mg/kg) may be effective in promoting magnesium excretion. Calcium chloride should be given to protect the myocardium and replace the calcium lost following furosemide

A variety of ECG changes may be identified, including prolongation of the PR and QT intervals, ST segment depression, flattening of P waves, T wave inversion and increased QRS duration.3 Torsades de pointes (see Figure 1) is a lifethreatening ventricular arrhythmia which may result from hypomagnesaemia.

Figure 1. Torsades de pointes.




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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 Magnesium replacement can be oral or intravenous. The intravenous infusion rate is determined by the clinical severity. For severe and symptomatic hypomagnesemia, 2g of magnesium sulphate (i.e. 4ml of 50% MgSO4 or 8mmols) should be administered over 15 minutes. It is vital that the cause is considered and managed appropriately to prevent recurrence.

Magnesium as a treatment Even in the absence of hypomagnesemia, magnesium has been proposed as a treatment for a variety of conditions, as listed below. Dose, route and speed of administration will vary according to the indication, and should be adjusted in patients with renal impairment. Doses of greater than 2g/hour (8mmol/hour) are likely to result in adverse effects; intravenous administration should be accompanied by continuous assessment for side effects including f lushing, hypotension bradycardia and arrhythmias. The presence of hyperkalaemia may augment side effects of treatement.1

Asthma Magnesium features in the British Thoracic Society guidelines as a therapeutic option in the treatment of acute severe or life threatening asthma.6 Patients with more severe airway obstruction at presentation derive the greatest benefit from magnesium in regards to their FEV1. However, this benefit does not extend to reducing the need for hospital admission in any subgroup.7 The guidelines specifically suggest that magnesium use should always be discussed with a senior clinician and that only a single dose is administered; theoretically, iatrogenic hypermagnesemia may lead to muscle weakness and respiratory failure, although this remains unproven. The suggested intravenous dosing regimen is 1.2-2g over 20 minutes.6 Recent interest has focused on the use of nebulised magnesium sulphate.Doses of 135-1152mg, along with regular bronchodilators have been shown to be safe with a non-significant trend towards benefit in all subgroups. In the subgroup with severe asthma, lung function improvement was significant.8 Nebulised magnesium produced no improvement in FEV1 or exhaled nitric oxide levels in patients with chronic, persistent airf low limitation.9 Use of oral magnesium in chronic asthma has also been studied but did


not shown any beneficial effect despite the finding of low magnesium levels in many asthmatic patients; patients with lower magnesium levels also often have more severe asthma symptoms.8

Chronic Obstructive Pulmonary Disease (COPD) Little work has been done to study the effect of magnesium in exacerbations of COPD and many are sceptical of its use, particularly given the potential to induce respiratory muscle weakness.6 One small study of 72 patients showed magnesium produced a statistically significant improvement in peak expiratory f low rate, compared to placebo, when given 20 minutes after a β2 agonist. It also showed a trend towards reduced need for hospitalization.10 Of note, this study excluded those with signs of infection. Further data have suggested that serum magnesium levels in the lower normal range are associated with an increased frequency of exacerbation of COPD symptoms.11

Atrial fibrillation (AF) Magnesium was shown to be more effective than amiodarone in achieving cardioversion in a study of patients in an ITU environment. At 24 hours, 67% vs 33% had cardioverted in the magnesium and amiodarone groups respectively. This was significant, as were the differences in cardioversion rates at all time period from 2 to 24 hours. Although not all of the patients in this study were in AF (only 71% of Mg group and 52% of Amiodarone group), this demonstrates significant antiarrhythmic activity for magnesium outside its established indication in patients with Torsade de Pointes. Furthermore, when patients with chronic arrhythmias were excluded, cardioversion rate following magnesium infusion was 77.8%.12 Another study has shown magnesium to also be superior to diltiazem (57% vs 22% p=0.03)13 and to verapamil (53% vs 40%: nonsignificant)14 in achieving cardioversion. A combination of magnesium and digoxin has also shown a trend towards greater efficacy than digoxin alone in producing sinus rhythm (60% vs 38% p=NS).15 From these studies it is not always clear if there is an initial electrolyte deficiency present; this is important as patients with K+/Mg2+ deficiencies cardiovert significantly more consistently when treated with magnesium with K+ and insulin/dextrose (86% vs. 39% p0.10.6 ECG dispersion mapping (ECG-DM) is a recently developed technology that provides non-invasive assessment of myocardial pathology by analyzing low amplitude oscillations of conventional ECG signals.7-9 The method examines not only the tiny fluctuations (micro-alternations) of the T-wave (T wave alternans) but also micro-alternations of the P wave and QRS complex. From the six traditional ECG leads of I, II, III, aVR, aVL and aVF patented formulae can quickly (i.e. within 30 seconds) and accurately determine micro-alternations not only of the T wave but of the entire PQRST complex. Nine groups of calculations (G1-G9) are then made that score in arbitrary units the extent of these micro-alternations in different areas of the heart, as well as those associated with intraventricular blocks and ventricular hypertrophy – a score of 0 indicates complete absence of abnormal micro-alternations, higher scores indicate increasing abnormality (Table 1). Micro-alternations ref lect abnormalities in the myocardium at a metabolic level, which may include ischemia and other causes. ECGDM, therefore, is not a diagnostic test but a nonspecific indicator of myocardial health. The microalternations from all nine groups (G1-G9) represent the overall myocardial micro-alternation index (MMI) which is expressed as a percentage. If pathological micro-alternations are present throughout the entire myocardium the MMI is 100%, whereas an MMI of 0% indicates a total absence of abnormal microalternations in any part of the heart. ECG-DM is much more sensitive than the direct “beat to beat” measurement of ECG micro-alternations, and this allows measurements to be performed at rest. ECG-




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 micro-alternation

Corresponding region of PQRST

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 to interpret and was primarily developed as a rapid screening test for heart disease. However, the role of this new technology in clinical medicine is still being defined. We recently reported on the ability of ECG-DM to predict inhospital mortality.10 In this paper we report the ability of ECG-DM to predict clinical deterioration of acutely ill medical patients, as measured by an increase in the Simple Clinical Score the day after admission to hospital.

Methods All patients were recruited from the unselected acutely ill medical patients admitted to Nenagh Hospital between July 30th 2009 and 31st March 2010. Of the 1702 patients admitted during this period 453 (26.6%) were included in the study – the only criterion for study inclusion was that one of the authors was able to perform an ECG-DM within 10 to 20 minutes of hospital admission. The presenting complaint and the clinical data required to calculate the Simple Clinical Score (SCS) were recorded at the time of admission by the nursing staff of the hospital’s medical admission unit. The nursing staff of the hospital has been fully trained in the use of the SCS since 2007 – implementation of this training process has been

reported in a previous publication.11 The SCS can be quickly performed at the bedside and requires no additional information or investigation other than a 12 lead ECG.12 Routine laboratory investigations performed at the time of admission were used to calculate the MARS laboratory score on each patient. Approximately 24 hours after admission (20.8 +/- 7.6 hours) each patient was reviewed by the nursing staff and the SCS re-calculated. All data were corrected for errors and then entered into an Epi-Info version 6.0 database (Center for Disease Control and Prevention, USA). The ICD10 coded diagnoses recorded at discharge or death were also entered into this database. The continuous variables of age, MMI, G1-G9 etc were converted into categorical variables by determining the threshold levels with the highest odds ratio for predicting in-hospital mortality. This was done by a process of trial and error. Continuous variables were compared by Student’s t-test and categorical variables by Chi-square analysis that applied Yates continuity correction. All calculations were performed using Epi-Info version 6.0 (Center for Disease Control and Prevention, USA), and statistical significance was set at a p value =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, Andover MA).14 This study was performed while the services in the hospital were undergoing reconfiguration, part of which was the diversion after midnight of seriously ill patients directly to Limerick Regional Hospital. This resulted in the majority of patients being admitted between 3 and 9 pm. Patients studied had the same age (68.0 +/- 16.7 vs. 66.2 +/- 19.0 years, p = 0.07), length of hospital stay (6.7 +/- 7.0 vs. 7.2 +/- 7.8 days, p = 0.24) and in-hospital mortality (3.5% vs. 3.5%, p = 0.99) as the other patients admitted during the study period. Ethical approval of the study was obtained from the Mid-Western Regional Hospital Complex Scientific Research Ethics Committee.

Results The day after admission no patients had died, 46 (10.2%) had increased their SCS by 2.2 +/- 1.5 points, in 209 (46.1%) the SCS was unchanged, in 162 (35.8%) it was decreased by 2.5 +/- 1.6 points and 36 (7.9%) patients had already been discharged home. Patients with an increased SCS were older and had a longer length of hospital stay. They also had a higher MARS laboratory score and a higher MMI, and were more likely to have heart failure and to be admitted from a nursing home. There was no association, however, between the SCS on admission and SCS increase. The in-hospital mortality of patients with an increased SCS was 21.7%, compared with 2.4% for those with no change in their SCS and 0.6% for those patients with a reduced SCS. An increase in SCS was highly significantly associated with increased mortality (OR 18.6, CI 95% 5.7-62.2, p36%, G1 >=3, G2 >=5, G5 >=1, G6 >=5 and G7 >=5 were associated with SCS increase (Table 3).

Patients with G6 values >=5 had an odds ratio of 3.1 (CI 95% 1.6-6.0, Chi square 12.3, p 0.0005) for SCS increase the day after admission. The majority of patients had a G6 value of 0 or 1, and no patients had G6 values of 2,3 or 4. There are, therefore, two distinct patient populations and a G6 value >=5 clearly identified those patients most likely to increase their SCS (Figure 1). Numerous logistic regression models were tested that included the discharge diagnosis of heart failure, the MARS laboratory score >0.10 and nursing home residence (i.e. the three variables previously identified as independent predictors of SCS increase)5 as well as each of the ten ECG-DM variables, both as continuous variables and using the cut-off 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). Only a G6 value >=5 and nursing home residence remained as independent predictors of SCS increase (Table 4).

Discussion Although there are several well validated scoring systems that can predict imminent death,15,16 determining the factors associated with clinical deterioration (or failure to respond to treatment) has proved difficult. Despite examining numerous variables in our original study we found only three features which identified patients who increased their SCS: residence in a nursing home, the presence of heart failure and an elevated MARS laboratory data score. This study found, however, that only increased micro f luctuations associated with left ventricular repolarization (i.e. G6 values >=5) and nursing home residence were independent predictors of clinical deterioration as measured by SCS increase the day after hospital admission. Therefore, the likelihood of deterioration would appear to be between two and three




11


SCS not increased (n 407)

SCS increased (n 46)

Myocardial micro-alternation index >36%

14.0%

28.3%

G1 >=3

54.3%

71.7%

G2 >=5

31.7%

52.2%

G3 >=4

18.9%

30.4%

G4 >=6

12.3%

G5 >=1

31.0%

G6 >=5

p

Odds ratio (CI 95%)

0.02

Chi-square

2.4 (1.1-5.2)

6.4

0.04

2.1 (1.0-4.5)

4.4

0.001

2.4 (1.2-4.6)

6.9

0.10

1.9 (0.9-3.9)

2.7

19.6%

0.25

1.7 (0.7-4.1)

1.3

47.8%

0.03

2.0 (1.1-4.0)

4.6

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 during left ventricular re-polarization and/or those admitted from a nursing home. There were 46 patients with an increased SCS (i.e. 46 events) and four variables (i.e. ECG-DM measurements, heart failure, nursing home residence and the MARS laboratory score) tested for independence by logistic regression. This is close to the minimal number of acceptable events per variable that should be included in a logistic regression model.17 It is possible, therefore, that a larger study might show other variables to be independent predictors of SCS increase. Nevertheless, our results suggest that nursing home residence and a G6 value >=5 will remain the major predictors of SCS increase. Although other ECG-DM changes also appear related to SCS increase, changes in G6 were the most striking. Left ventricular re-polarization is an active energy consuming process and it is reasonable to postulate that a

“sick” myocardium might be more likely to demonstrate subtle abnormalities during this phase of the cardiac cycle. Changes in G6 will, therefore, ref lect left ventricular health. Although increased micro-alternations during left ventricular re-polarization was a more powerful predictor of clinical deterioration than heart failure, we diagnosed this clinically and not by echocardiography or BNP testing. It may be that these techniques would have been better predictors of clinical deterioration than changes in G6, but would not have been cheaper, quicker and easier to perform.

Conclusion ECG-DM changes during left ventricular re-polarization and nursing home residence are independent predictors of clinical deterioration as measured by SCS increase within 24 hours of admission. ECG-DM is inexpensive, only takes 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



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ill medical patients by electrocardiogram (ECG) dispersion mapping

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compared with established risk factors and predictive scores – a pilot study.

3. Ghanem-Zoubi N.O., Vardi M., Laor A., Weber G., Bitterman H. Assessment of disease-severity scoring systems for patients with sepsis in general internal medicine departments Critical Care 2011, 15:R95 doi:10.1186/cc10102. 4. Li J.Y.Z., Yong T.Y., Hackendorf P., Roberts S., O’Brien L. et al. The Simple Clinical Score is associated with mortality and length of stay of

Eur J Intern Med (2011), doi:10.1016/j.ejim.2011.01.013 11. Gleeson M., Kellett J, Cowan C., Casey M. An assessment tool for acutely ill medical patients. British Journal Nursing 2009; 18: 546–550. 12. Kellett J., Deane B. The Simple Clinical Score predicts mortality for days after admission to an acute medical unit. Q.J.Med. 2006; 99: 771–781. 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? Changes in the Simple Clinical Score the day after admission and subsequent outcomes of acutely ill unselected medical patients. Eur J Intern Med (2011), doi:10.1016/j.ejim.2011.03.005 6. Silke B, Kellett J, Rooney T, Bennett K, O'Riordan D. An improved medical admissions risk system using multivariable fractional polynomial logistic regression modelling. QJM (2010 Jan) 103(1): 23–32. 7. Cruz-Gonzalez I., Dejoseph-Gauthier D., Chia S., Raffel O.C. and Jang I-K. Non-invasive assessment of myocardial ischaemia by using low

14. Dallal G.E. LOGISTIC: A Logisitic Regression Program for the IBM PC. The American Statistician,1988; 42: 272. 15. Smith G.B., Prytherch D.R., Schmidt P.E., Featherstone P.I. Review and performance evaluation of aggregate weighted “track and trigger” systems. Resuscitation 2008; 79: 11–21. 16. Brabrand M., Folkestad L., Clausen N.G., Knudsen T., Hallas J. Risk scoring systems for adults admitted to the emergency department: a systematic review. Scandinavian Journal of Trauma, Resuscitation and 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.



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Research, Audit and Clinical Practice

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 Unsafe patient transfers are one of the top reasons for incident reporting in hospitals. Criteria guiding safe transfer have been issued by the NHS Litigation Authority. To meet this standard, a “transfer check list” was redesigned for all patients leaving the Acute Medical Unit (AMU) in the Heartlands Hospital. Following the introduction of the checklist two full audit cycles were conducted. The first cycle highlighted an extremely poor uptake of the checklist. After interventions to educate nursing staff and raise awareness of the issues at the regular staff meetings, re-audit demonstrated significant improvement in completion rate. Subsequent monitoring indicates continued improvement, with compliance up to 95% for completion of the transfer checklist on AMU. Incident reporting relating to transfer has also decreased significantly.

is not new. The need to assure patient safety during, and after transfer, has re-energised focus on the use of a transfer checklist. In order to achieve safe patient transfers in this context, both transfers in and out of an AMU must be considered.

Care pathways into AMU The patient f low into the AMU at Heartlands comprises patient transfers from the Emergency Department (ED) and patients referred directly via their GP. Following GP referral, patients are either brought to the AMU by ambulance, in which case the crew always complete a transfer checklist, leaving a copy of the form for staff. If patients transport themselves to AMU following GP referral they will bring a GP letter.

Keywords

Care pathways out of AMU

Acute medical unit, Patient Transfer, Transfer checklist/tool, Patient safety, Communication, Handover.

Following assessment and stabilisation, patients are either transferred from the AMU to other wards or are discharged and transferred directly from the AMU.

Introduction Patient transfers represent a huge part of the workload on an Acute Medical Unit (AMU). Unsafe patient admission, discharge and transfers are one of the top twelve topic areas for incident reporting to the National Reporting and Learning System (NRLS) department of the National Patient Safety Association (NPSA). Issues regarding patient transfer have been recognised by the NHS Litigation Authority, which provides the NHS with specific criteria for patient transfer, which are then interpreted locally to provide for different groups of patients requiring both internal and external transfer.1 The Heartlands Hospital is one of three hospitals, which form part of the Heart of England NHS Foundation Trust. The AMU at the Heartlands hospital has used a checklist for documenting patient transfers since 2001. To this end, the concept of using a checklist for patient transfers from the AMU


Redesign process for the transfer checklist During 2010 the staff working on the AMU re-designed our original 2001 transfer checklist. The changes were led by the consultant nurse, in close collaboration with the corporate nursing team. Each AMU had previously designed transfer documentation, necessitating negotiation for each element of the form revised. Moreover, the ED did not previously use a transfer checklist, relying upon a verbal handover. A form used by AMU for documenting telephone referrals was therefore also redesigned during this process. This ensured that the details of all patients transferred were documented using the same format. The terms ‘handover’ and ‘transfer’ became synonymous. It was decided to disseminate the checklist across each AMU,thereby standardising practice on the 3

David Hindmarsh Foundation Year 1 Doctor MBChB Heart of England NHS Foundation Trust Bordesley Green Birmingham, B9 5SS Liz Lees Consultant Nurse (Acute Medicine) and Clinical Dean RGN, DipN., BSc (hons), Dip HSM, MSc Acute Medical Unit (Ward 20) Heart of England NHS Foundation Trust Bordesley Green Birmingham B9 5SS Correspondence: Liz Lees Consultant Nurse (acute medicine) and Clinical Dean RGN, DipN., BSc (hons), Dip HSM, MSc Acute Medical Unit (Ward 20) Heart of England NHS Foundation Trust Bordesley Green Birmingham B9 5SS Email: liz.lees@heartofen gland.nhs.uk


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Improving the safety of patient transfer from AMU using a written checklist

Level 1 – 1.4.5 As a minimum, the approved documentation (policy) must include a description of the: a. Duties b. Definition of all patient groups c. Transfer requirements specific to each group d. Documentation to accompany the patient when being transferred e. Process for out of hours f. Process for monitoring compliance with all of the above Box 1. NHS Litigation Authority: Standard 4 – Criterion 5: Transfer of patients.5

a.

b. c. d. e. f. g.

Assessment: All patients must be assessed by a registered nurse prior to transfer, using ABCDE method of assessment and documentation Communication: Discuss the transfer with the patient next of kin or carer & document on the transfer form Transport: Identify & request appropriate mode of transfer Monitoring & Equipment: Infusions, oxygen saturation monitor Escort: Registered nurse escort if MEWS above 4 Documentation: SBAR transfer sheet Anything else: Property

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

Airway: Breathing: Circulation: Disability: Environment:

No  No  No  No  No 

Yes  Yes  Yes  Yes  Yes 

MEWS Score:..............................If MEWS > 4 please note parameters  Sats____________%on__________L/%..............................  RR____.......................................................................................  HR_____BP_________/_____Urine O/P________mls/hr  A V P U (Circle)  Temp_________

Action Critical Care Outreach contacted..........YES/NO A. Oxygen in progress/Prescribed: YES/NO B. X Rays  C. Cannula  IV Fluids  Catheter  ECG  D. Analgesia given  Sliding Scale  E. IV ABx  Bloods taken 

Time contacted.......................... Time given.................................. Sats Probe*  Pump needed*  Cardiac Monitor* 

Wrist Band Relative Aware Phone Numbers Valuables Yes/No SAD Score Waterlow Score Falls Assessment NBM 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.



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15


hospital sites, and to incorporate the Situation, Background, Assessment and Recommendation (SBAR)2 telephone communication model, which was mandatory in the Trust for telephone handovers. This involved reconstructing the format of the information on the original transfer checklist into new sections related to SBAR and reconsidering the nature of the information required on the revised transfer checklist.3 The strategy focussed on the information that was pertinent to safety ‘during transfer’. Poor transfers are frequently characterised by an incomplete transfer of information, resulting from long and incomplete transfer checklists.4 A key element of our redesign process was to incorporate the NHS Litigation Authority (NHSLA) guidance on patient transfers, (Text box 1). Adherence to this standard enables the Trust to give quality assurance on the process of transfer and patient safety.1 Secondly, the hospital transfer policy has been updated during 2010/2011 and from this several standard operating procedures (SOPs) were devised for specialist groups of patients. The AMU devised a SOP applicable for each of the 3 acute medical units within the Trust (text box 2). Core information indicated from this was integrated into the revised transfer checklist. The policy and the SOP were analysed together to enable development of the revised transfer checklist. This was incorporated into the AMU clerking document, which was automatically printed at the back of the document, negating the need to write a separate checklist (Figure 1).

Incident reporting Prior to the audit we requested all Incident Report forms (IR-1) relating to transfer, generated by wards receiving patients from AMU. Detailed thematic analysis of the forms revealed 23 incidents reports directly related to transfer issues over a 2 month period. The following core themes were identified: 1. Inadequate clinical history prior to transfer, leading to patients being reported as being transferred to a ward where the staff felt the patient’s needs were unable to be accommodated. 2. Inadequate verbal handover prior to transfer, leading to inadequate preparation for the patient’s arrival, such as availability of pressure relieving care, acquisition of electronic pump devices and the need for one-to-one nursing care. 3. Inaccurate calculation of the modified early warning score leading to an apparent change in the condition of the patient by comparison to the verbal hand over.

Audit Methodology Two complete retrospective audit cycles were completed in November 2010 and February 2011, with the purpose of analysing the compliance, completion and improvements needed in practice. Each audit cycle included all patients transferred from AMU (Ward 20) to its sister unit AMU-2 (Ward 8).


Data

Number (n)

Patients

30

Completed Check list

1

Time documented in notes

6

MEWs documented in notes

0

Patients with one move

9

Patients with two moves

21

Table 1. Data on the 1st Audit Cycle.

Audit Standard “Each patient must have a transfer checklist to accompany their transfer – with 100% completion of the SBAR elements”.

Audit Cycle 1 Results 36 patient notes were identified during the audit period. 6 were excluded as the patients were not being transferred to AMU-2, leaving 30 records for analysis. The results of these can be seen in Table 1. Out of the patient notes only one checklist had been completed. In an attempt to establish where patient transfers had been documented, the patient notes were also analysed. This was originally not part of the design – but in the absence of the checklist we searched for basic information regarding Modified Early Warning Score (MEWs) and time of transfer. Twenty one of the patients had originally been transferred into AMU from the ED. In this case, supplementary information in the form of ambulance transfer sheets and telephone handover forms to the AMU were present in the notes. However, the standardised, NHSLA compliant checklist was not present in 29 out of the 30 cases.

Interventions following audit cycle 1 A team meeting was organised to highlight the gravity of the situation to Band 7 Sisters. The Sisters engaged with their junior Sister colleagues in the reinforcement of the importance of the checklist. A concerted effort was made to raise the staff awareness on each shift over several weeks. This was monitored through the collation of data on the AMU, with feedback at each weekly team meeting. Finally a lunch time audit presentation using scenarios from the IR1 reporting database was given to a multi-professional staff audience who work on the AMU. The regular reporting continued until the start of the second audit cycle.

Audit cycle 2 Results 48 case notes were analysed; two were excluded because the time and date of transfer could not be identified. The degree of completion of the transfer checklists was analysed for the remaining 46. 23 of the transfer checklists were, at least partially, completed (50%). For those not completed, 21 were left blank and the other two patients had been clerked using a generic clerking document that was not generated in the AMU. Approximately twice as many transfers happened during the night than during the day, and 2.5 times as


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Acute Medicine 2012; 11(1): 13-17


Completion status:

Total Parts completed

n

Yes/ Partially

Not attempted

5

4

23

23

4

5

3

5

2

5

Total (n = 46)

Shift: Day shift (n = 17)

6

11

1

2

Night shift (n = 29)

17

12

0

2 Total

Weekend/ Weekday:

23

Table 4. Number of parts analysed that were completed.

Weekday shift: (n = 33)

18

15

Weekend shift: (n = 13)

5

8

Table 2. Break down of transfer check list.

Assessment:

Completion Yes

No

N/A

Fully Completed

4

19

Assessed by Registered Nurse

14

9

0

Monitoring equipment

7

12

4 – Not needed

MEWS recorded

17

6

0

Escort needed

0

4

19 – Either MEWS < 4 or stated ‘Not required’

Property

12

0

11 – Box not ticked

Table 3. Transfer checklist analysis of 23 partially / fully completed forms.

many transfers happened during the week than during the weekend.The differences in checklist completion rates for night vs day and weekend vs weekdays did not reach statistical significance by Chi-squared analysis. Only 4 documents were deemed to have been fully completed (17%). Fourteen documents had a signature and a name identifying that a nurse had completed it. Monitored equipment documentation was the area least likely to be completed. The two forms which had no analysed parts were still clearly attempted by the nursing staff, although none of the components were fully completed. Although a reduction in incidents reported was not one of the planned outcome measures, analysis of the IR1 database revealed only 4 incidents relating to patient transfer in the two month period following the second audit cycle.

Continual Monitoring Since the original AMU audit, the corporate team has conducted intermittent audits of the transfer checklist across the Trust. At September 2011, the compliance

Figure 2. Continual monitoring of the transfer checklist.



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17


within the AMU was an average of 85% increasing to 95% at peak times, as illustrated in Figure 2.

Discussion The importance of checklists in the handover process has been previously documented.4,6,7,8 However our literature search failed to identify any previous studies specifically looking at this area in relation to transfers in and out of the Acute Medical Unit. This is surprising given that patient transfer represents a significant proportion of the AMU workload; this study therefore reflects an important addition to the literature in this area. With any transfer of patient care there is a significant risk for this to be sub-optimal, mainly due to ineffective communication between health care professionals.3 This is reflected in the high level of incident reporting concerning patient transfers prior to the introduction of our checklist. Checklists have been shown to reduce “errors of ineptitude”, where staff fail to make use of knowledge that they possess.9 An important feature of a checklist which improves the likelihood of accurate completion is ‘userfriendliness’; checklists should ideally comprise between 8 to 10 points.10 Maintaining this simplicity and user friendliness was a key aspect of our redesign process, and created some tension within the design group. The need to align to a hospital wide process required the involvement of many different staff groups, many of whom requested inclusion of information which they felt, subjectively was ‘required’ in their area . Checklists are of no use if not completed. Our initial audit demonstrated very poor compliance with this documentation. However, we were able to achieve a

significant improvement in use of our transfer checklist following the interventions involving education and raising awareness amongst the nursing staff. This improvement still fell short of our 100% target and further intervention is required. However continued monitoring has shown ongoing improvements in completion rates. Ongoing education is important in improving compliance with the checklist. New members of staff and constantly changing shift patterns means that some nursing staff may have been unaware of the transfer checklist’s existence. The documentation is now introduced with the clerking document during nurse induction to the unit. The current checklist may also be too detailed for all patients, discouraging completion. Some aspects of the checklist are not relevant to all patients. The advent of electronic patient records in the future may allow for bespoke completion of specific aspects; certain items i.e. cardiac monitoring, oxygen, intra-venous f luids could be automatically removed from the document when not relevant.4

Conclusion Our audit has demonstrated that improved compliance with the use of checklists relating to patient transfer in and out of AMU can be achieved by an educational programme and ongoing work to increase staff awareness of its importance. This is ref lected in improved checklist completion rates and a reduction in the numbers of incident reports relating to patient transfer. Although there remains room for improvement we would encourage other units to adopt a similar process to optimise patient safety during transfer.

References 1. HEFT (2010) The Heart of England NHS Foundation Trust, Patient transfer policy: version. www.heartofengland.nhs.uk

6. Ong, MS., and Coiera, E. (2011) A systematic review of failures in handoff 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 Frances Griffin. www.saferhealthcare.org

67(8): 1665–8.

4. Nagpal, K., Abboudi, M., Fischler, L. et al Evaluation of postoperative handover using a tool to assess information transfer and teamwork. Ann surg 2011: 253(4); 831–7. 5. NHSLA. Standard 4 – Criterion 5: Transfer of patients 2010 11/06/11]; Available from: http://www.nhsla.com/home.htm


8. Park W. (1967) Patient Transfer Form. The American Journal of Nursing. 9. Gawande A. (2009) The Checklist manifesto: How to get things right: Metropolitan Books; 2009. 10. Terrell KM., Miller DK., (2010) strategies to improve care transitions

[cited

between nursing homes and emergency departments, Journal of American Directors Association, Epub ahead of publication in November 2010.


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Research, Audit and Clinical Practice

Where Do AMU Nurses Perceive Their Educational Needs? Results of the 20:10 project J Jepson, S Whitley, C P Subbe & L Grundy

Jacqueline Jepson Lead Advanced Nurse Practitioner for Acute Medicine, Glan Clywd Hospital, Rhyl, Denbighshire, LL18 5UJ, UK Stella Whitley Senior Lecturer in Nursing & Clinical Simulation, Glyndwr University, Mold Road, Wrexham, LL11 2AW, UK Christian P Subbe DM, MRCP (London), Senior Clinical Lecturer, School of Medical Sciences, Bangor University, Brigantia Building / Adeilad Brigantia, Bangor, LL57 2AS, UK Lynne Grundy Head of Nursing, Professional Nursing and Education, Bwrdd Iechyd Prifysgol, Betsi Cadwaladr University Health Board, LL18 5UJ, UK Correspondence: Jacqueline Jepson Lead Advanced Nurse Practitioner for Acute Medicine, Glan Clywd Hospital, Rhyl, Denbighshire, LL18 5UJ, UK Email: Jacqueline.Jepson@ wales.nhs.uk

Key Messages 1. There is no accepted curriculum for nurses working in Acute Medicine. 2. Nurses felt that education needed to centre around frequently presenting symptoms. 3. Skills identified, overlapped with those traditionally performed by junior doctors, thus supporting the concept of interprofessional education. 4. Formal educational support is needed to address these needs and secure future recruitment.

Abstract Our aim was to identify the perceived educational needs of nurses working in acute medicine to enable development of a training curriculum specifically for this staff group. Methods: Post-graduate nurses from North Wales were invited to list 20 conditions and 10 skills for which they felt under prepared for their work in acute medicine. A workshop was then organized, attended by acute medicine nurses, medical colleagues and educationalists from two local universities to discuss initial data. Results: Nurses identified particular needs for education around presenting symptoms with perceived deficits in knowledge or training. We found a heavy emphasis on respiratory and cardiac conditions. There was considerable overlap with frequent diagnostic categories from non-surgical hospital discharges and with priorities for training of junior doctors. Skills were often those traditionally associated with medical staff or care of patients with critical illnesses. Conclusion: The 20:10 project represents the first attempt to map educational needs of nursing staff on the Acute Medical Units of a large University Health Board using self-reported needs. The identified needs will support professional development, create incentives for recruitment and guide University postgraduate developments and commissioning.

Keywords Acute medicine, nursing, education, curriculum, professional development.

Introduction Background - Acute Medical Unit Development Acute Medical Units (AMUs) were introduced in the 1990’s to bring together the resources required to look after acutely ill medical admissions in a more effective way.1 This model has been adopted by the majority of UK hospitals. AMUs receive the unselected medical

admissions and may have integrated ambulatory care units. Most AMUs have monitored beds and in many hospitals the capability to look after patients with increased monitoring needs or the need for basic single organ support (level I and level II patients). Service provision can include patients with acute coronary disease requiring continuous cardiac monitoring, patients requiring Non-Invasive Ventilation and patients requiring haemodynamic support via central venous cannulae. Staff therefore need significant skills in the assessment and management of acute illness.2

Background - Education and Skills Development In addition to offering a multifunctional service, nurses working in AMUs need to be specialists in safe discharge planning.3 The high turnover of patients and fast pace of work is a significant risk factor for burn out of staff4 and can also compromise patient safety.5 Recruitment into specialties is often improved by coherent educational support6 and career progression.7 Nurse education, both pre and post registration, needs to be provided in the context of a changing healthcare landscape. Education and skills development for AMU nurses should be geared towards the specific requirements of the AMU environment. The aim of this study was to explore the self reported educational needs of nurses working in AMUs in order to allow educational providers to create a curriculum for a modular postgraduate qualification in acute medical nursing.

Methods Setting Three District General Hospitals (DGHs, Wrexham Maelor Hospital, Ysbyty Glan Clywd, Rhyl and Ysbyty Gwynedd, Bangor) in North Wales that form



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 population of around 250,000 and a mix of rural and urban areas. All three AMUs admit between 25 and 35 patients per day, have dedicated Acute Physicians, and access to level III facilities on site but no provision of level II beds within either of the AMUs. There is provision of Ambulatory Care in two of the hospitals. Newly registered nurses are largely recruited from two local Universities (Glyndwr University, Wrexham and Bangor University) with some additional recruitment from Cheshire and Merseyside. More experienced nurses are recruited internally from other areas of the hospital, and occasionally national recruitment is carried out to meet needs.

Participants Staff nurses working in the three AMUs, regardless of their banding or duration of contract were invited to participate in this study. Junior nurses, team leaders, professional development leads and nurse managers were all represented in the group.

20:10 conditions chosen by nursing team

Project design The participants were asked to list 20 conditions for which they felt under-prepared following qualification and employment as a registered nurse. The teams were also asked to list which skills they felt required further training. A single list was then compiled by each of the participating AMUs by consensus. A workshop was organized in July 2010. It was open to all team members from the three units, and there was representation of a senior nurse from each of the units. The participants included two educationalists. The workshop served as a focus group for the development of the curriculum and encouraged participant collaboration. The focus group collated the data from the three AMUs by consensus providing a core list of conditions and skills that require further nurse education and development. The list was not ranked. Conditions and skills were listed alphabetically. Comparisons were made with conditions generated from non-surgical emergency admissions in England for

‘Top 20’ conditions from 2009 curriculum for GIM / AIM training

Top conditions from HRG statistics 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 flutter without ACS

Haematemesis

Other connective tissue disease

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.



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Arterial blood gas analysis Cannulation Care of long lines ECG Interpretation External Pacing Management and priority of care Non-Invasive Ventilation Phlebotomy Triage Use of a stethoscope for chest auscultation Table 2. Top 10 skills from 20:10 workshop.

2007/20088 and the top 20 conditions in the 2009 GIM/AIM curriculum.9 Nurse educationalists indicated that pre-registration nurse education does not use a disease model and whilst this meant that similar tables of conditions covered in nurse education were not available, many of the conditions are introduced in pre-registration nurse education.

Results The results of the focus group discussions are compiled in Tables 1 and 2.

List of conditions The list of conditions contained clinical diagnoses (Chronic Obstructive Pulmonary Disease) as well as symptoms (“breathlessness”). The bulk of conditions (14/20) were from the areas of cardio-vascular and respiratory medicine.

List of skills The skills fell into three groups: skills largely restricted to the care of critically ill patients (non-invasive ventilation, central venous catheter care etc), skills traditionally covered by medical students, doctors and other health care professions (phlebotomy, cannulation, interpretation of an Electrocardiogram (ECG), interpretation of blood gases, use of a stethoscope) and organizational skills that are more relevant in areas of high turn over (triage, management and prioritization of care).

Comparison to Hospital Episodes and Acute Internal Medicine Curriculum The predominance of cardiovascular and respiratory conditions (14/20) corresponds to 12/20 diagnostic groups in the analysis of hospital episodes in England in 2007/2008 that were attributable to ischemic heart disease or acute respiratory illness, and to 5/20 potentially cardiac or respiratory presenting symptoms (black-out, breathlessness, chest pain, cough, palpitations) in the “Top 20” Common Medical Presentations, as defined in the the 2009 training curriculum for General Internal Medicine (GIM) and Acute Internal Medicine (AIM). The nursing conditions also included specific reference to stroke and transient ischemic attack.

The top 20 presentations in the GIM / AIM curricula are entirely symptom based, which is appropriate given that initial assessment of patients by junior doctors involves the determination of differential diagnosis from a patient’s narrative. However this approach has limitations, since some conditions such as acute hyperglycaemic emergencies do not present with a clearly defined set of symptoms; competencies for management of these situations are therefore ref lected elsewhere in the curriculum. By comparison the nursing list describes a mixture of diagnoses and problems. There is reference to a number of specific causes of breathlessness (pleural effusion, pulmonary embolism, congestive cardiac failure, and pneumothorax) in addition to the generic ‘problem’ of dyspnoea. Iron deficiency anaemia and hyperglycaemia as well as urinary tract and upper respiratory tract infection are also specifically listed. It is interesting to note that there was considerable overlap between the list generated by nurses and the HRG coding for admissions in our hospital in 2008-2009 (see Table 1).

Discussion Our findings Tables 1 and 2 illustrate the 20:10 project’s attempt to describe the self – perceived educational needs of nurses working within today’s North Wales AMUs. For regional educational providers it is now possible to start the foundations of a postgraduate curriculum in Acute Medicine nursing incorporating the identified conditions and skills. Current specialist modules delivered by local educational institutions (accident and emergency, coronary care, intensive care and high dependency care nursing) are able to deliver many if not all of the skills highlighted. However this provision is fragmented in the context of Acute Medicine nursing and only partly addressed in undergraduate level teaching.10 The comprehensive assessment of medical and functional dimensions of patient presenting to AMU is not currently covered by any of the educational programs on offer in this area. Given that the AMU sits at the interface between primary and secondary care, it is surprising that skills associated with working in the social environment of the patient in the community were not listed. Equally, in the face of an aging population, the fact that very few conditions specific to older patients (falls, acute confusion, dementia) were mentioned is worthy of note. This emphazises the limitations of the project in trying to define a curriculum based solely on the perceived needs of the staff. A combined approach utilizing HRG data may be more appropriate.

Interprofessional Education The large overlap between the diagnostic categories, the curriculum for Acute Medicine and the self-assessed learning needs of nurses working in the AMU would strongly support a move to a more interprofessional approach to education.11 The benefits of interprofessional education (IPE) are well recognised by the Department of Health,12 General Medical Council13 and Nursing Midwifery Council14 and the UK consensus conference on



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21


Acute Medicine.15 Despite this, robust and reproducible templates for IPE have not been adopted. A systematic review undertaken by Cooper16 examined the evidence for interdisciplinary learning and concluded that there are benefits relating to change in knowledge, attitude, skills and beliefs. Without the advantages of designated infrastructure, facilities and staff, finding an appropriate environment to maximise IPE can be demanding.

Expanding roles The information from the workshop reflects in part the changing professional roles and shifting boundaries influenced by such things as European Working Time Directive and reduction in junior doctors’ hours. With professionalization of nursing, the expanded as well as advanced nurse role requires the practitioner to be skilled in many areas previously undertaken by medical colleagues for example, prescribing, medical interventions and treatment, clinical assessment and diagnosis.17 Healthcare workers, especially in acute medicine, are taking on more specialised roles, including the “medical” admission and discharge process, leading to a blurring of traditional professional boundaries. Healthcare education should ref lect these changes across the range of roles and responsibilities.

Limitations Nursing staff from the three units were invited to participate in generating the content of a future curriculum. However, there was no mechanism in place to ensure a representative sample. It is possible that the suggested content for the development of a postgraduate curriculum in acute medical nursing would not cater for the needs of new-comers to AMU or senior team leaders. Additionally the focus of our paper was perceived as opposed to objective needs; this is likely to be driven by the case-mix that staff experience in our local units. For example management of Deep Vein Thrombosis (DVT) in North Wales is largely done in an outpatient setting, and one of the units admits all patients with upper gastro-intestinal bleeding through the surgical department. Similarly, patients presenting with suspected stroke in North Wales are only admitted to a stroke unit after initial review in the AMU. Advanced nurse practitioners (ANP) and Nurse Consultants in Acute Medicine have specific educational needs which may differ from those identified in this study. Their roles straddle professional boundaries, involving admission of patients alongside medical practitioners, ordering first line investigations, prescribing medication and managing services for defined patient groups (pulmonary emboli, asthma, cellulitis).

Implications for delivery of local education Current nurse pre-registration training attempts to prepare students for a broad range of professional options, ranging


from community to critical care nursing. The broad range of professional profiles means that more specialized training will be required upon qualifying, especially within acute medical nursing. It is possible that objective educational needs of staff were different from those collated from self-assessments. This might be a fruitful area for future work. We believe that in order to get buy-in from staff it is crucial for an educational program to start with areas of interest to staff and develop a program from there. Simulation might be used as an adjunct to expose the nursing student to scenarios of critical illness,18,19 and could be usefully applied to training in most of the 20 conditions and 10 skills. Pre-registration nurse education at Glyndwr University aims to provide up to 300 hours of simulated practice, which will continue in future nurse curriculum development.7 Simulation training provides nursing students with skills which otherwise may not become developed until qualifying due to the differing standards and expectations of hospitals, wards or specialist area. A proportion of qualified nurses continue their professional educational and training at postgraduate level. Short courses which focus on skill acquisition rather than academic achievements maybe the way forward to achieve training that is “fit for purpose”.11 The foundation courses may also be mapped against junior doctor training for Acute Medicine therefore promoting standardization of practice and facilitating the principle that “those who work together, should train together”.5 Additionally the AMU provides a unique environment for experiential learning given the breath and depth of pathology as well as the near continuous opportunity for supervision by senior medical and nursing staff. The results of our workshop give local educational providers and NHS health care providers the opportunity to develop a foundation postgraduate curriculum for acute medical nursing by merging existing curricula. We are currently engaging all stakeholders to take this work forward as we now have the opportunity, within a larger organization, to ensure such programmes are viable in a rural environment. E-learning might have to play a significant part in the delivery.20

Conclusion Appropriate postgraduate education and training for nursing staff working in the demanding environment of Acute Medicine is essential to attract and retain staff, and support quality of care, efficiency of service and patient safety. The 20:10 project identifies perceived gaps in education and suggests a set of core conditions and skills that are being shared with doctors training in Acute Medicine. This highlights the opportunity for a more interprofessional approach to health care education.


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References 1. Acute medical care: The right person, in the right setting – first time. Report of the Acute Medicine Task Force Royal College of Physicians, London 2007. 2. Lees L, Hughes T. Implementing a patient assessment framework in acute care. Nurs Stand. 2009; 24: 35–43. 3. Sturgess I. Planning for predictable f lows of patients into unscheduled care pathways beyond the Emergency Department: Meeting Demand and Delivering Quality. IMAS 2010. 4. Gillespie M, Melby V. Burnout among nursing staff in accident and emergency and acute medicine: a comparative study. J Clin Nurs. 2003 Nov; 12(6): 842–51. 5. West MA, Borril CS, Dawson JF, et al. The link between the management of employees and patient mortality in acute hospitals. International Journal of Human Resource Management 2002; 13:1299–1310. 6. Rambur B, McIntosh B, Palumbo MV, Reinier K. Education as a

10. McGaughey J. Acute care teaching in the undergraduate nursing curriculum. Nurs Crit Care. 2009; 14: 11–6. 11. Lewis R. Learning the 'SMART' way... results from a pilot study evaluating an interprofessional acute care study day. Nurse Educ Today 2011; 31: 88–93. 12. Department of Health. 150 years of the annual report of the chief medical officer: safer medical practice, machines, manikins and polo mints. Crown. London 2009. 13. General Medical Council. Tomorrows Doctors. London 2009. 14. Nursing & Midwifery Council. Standards for Pre-registration Nursing Education. London 2010. 15. Jones MC, Lees L. How is multi-professional training optimized in the acute environment? Br J Hosp Med 2009; 70: S19–25. 16. Copper H, Carlisle C, Gibbs T, Watkins C . Developing an evidence base for interdisciplinary learning: a systematic review. Journal of Advanced 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: What is the future? Acute Med. 2010; 9: 91–6. 8. Subbe CP, Bottle RA, Bell D. Acute Medicine: Triage, timing and teaching in the context of medical emergency admissions. Eur J Intern Med.

the UK perspective. Nurse Education Today 2008: 197–201. 19. Akhtar-Danesh BP. Nurse faculty perceptions of simulation use in nursing education. Western Journal of Nursing Research 2009: 1–67. 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 The Cannabis Hyperemesis Syndrome (CHS) defines a recently described paradoxical association between recurrent vomiting episodes, daily cannabis excess and symptomatic relief with a hot bath or shower. Importantly, symptom resolution only occurs with cessation of cannabis use. We describe a case of CHS which had resulted in repeated hospital admissions. As cannabis use is common, it is important for both patients and Acute Physicians to be aware of this increasingly recognised condition.

Keywords Cyclical Vomiting Syndrome, Cannabis, Cannabis Hyperemesis Syndrome.

Case report A 21 year old british caucasian male presented to the local hospital emergency department with a 12 hour history of severe nausea and vomiting. He had vomited greater than ten times since the onset earlier in the day, bringing up clear liquid mixed with some undigested food products. He was uncooperative during the assessment and oddly, he persistently demanded to use our showering facilities. The patient admitted that he had experienced these symptoms in the past and was told it was due to gastritis. He had no other significant previous medical history or relevant significant family history. He took no regular or over the counter medications (including non-steroidal anti-inf lammatory medications) and drank on average about 10 units of alcohol per week. He did admit to using cannabis heavily, smoking at times up to 4 joints per day for the preceding four years.


On examination, the patient looked remarkably clean with his hair wet and neatly combed backwards. He was afebrile, all vital signs were within normal limits and he was clinically euvolaemic. He was tender in his epigastrium without any signs of peritonism. Due to the ongoing severity of his symptoms, the patient was admitted under the acute medical team for symptom control with antiemetic therapy and further assessment. His blood tests, including liver function, amylase, calcium and lactate were within normal limits. Urine analysis, chest and abdominal radiography were normal. That this was the patient’s eighth identical presentation to this hospital in 3 years. He had been admitted twice, and self discharged on each occasion. At each presentation, blood tests and radiology had always been negative. The patient had been seen in the gastroenterology clinic one year earlier. An endoscopy had revealed a normal upper gastrointestinal tract; urease breath test was negative for Helicobacter pulori; duodenal biopsy showed no features of Coeliac disease. An earlier abdominal ultrasound revealed a normal liver and pancreaticobiliary system and no evidence of gallstones. This patient was demonstrating recurrent short lived stereotypical episodes of nausea and vomiting with no clear cause. He was diagnosed as suffering from Cyclical Vomiting Syndrome. The anti-emetic effect of cannabis is well known and it was initially postulated that he was trying to control his symptoms using this illicit medication. He continued to demand to use the showering facilities, and oddly seemed more settled after bathing. Once again, the patient soon self discharged.

Vishal Luther MBBS BSc MRCP, Core Medical Trainee Year 2, Whittington Hospital, London Lok Yap MBBS MCRP Consultant Acute Physician Whittington Hospital, London Correspondence: Vishal Luther 14 Spencer Road, Wembley, Middlesex, HA0 3SF Email: vluther@doct ors.org.uk,


24

Acute Medicine 2012; 11(1): 23-24

A hot bath to calm what ails you – the Cannabis Hyperemesis Syndrome

Discussion Cyclical Vomiting Syndrome (CVS) is a condition whereby patients experience short lived episodes of vomiting at least three times each year with a clear absence of symptoms between episodes.1 The exact aetiology of this condition is unknown, and it is often attributed to a migrainous phenomenon. The active ingredient in cannabis, tetrahydrocannabinol (THC), is used synthetically as an antiemetic (e.g. nabilone). THC acts on endogenous cannabinoid receptors (CB1) present in the brain and enteric nervous system to suppress emetogenic stimuli communicating between these two nervous systems.2 This patient presented with an episode his presumed CVS, which seemed to improve after a hot bath. A handful of case reports have revealed how chronic cannabis abuse appears to have a causal association with CVS.3,4 Characteristically, the symptoms are improved by a hot bath or shower. This has been called the Cannabis (or cannabinoid) Hyperemesis Syndrome (CHS). A case series published in February 2010 explored 8 patients who required on average 5 baths per day, with a mean total bathing time of 5 hours per day to control their symptoms during an episode.5 Sufferers have also scalded themselves in an attempt to run the bath or shower water as hot as possible.6 CHS seems to occur after several years of moderate to heavy use of cannabis in susceptible individuals. The effect may arise from dysregulation of endo-cannabinoid receptors with chronic cannabis use or through episodic gastroparesis (THC is known to delay gastric emptying).7 The compulsion to take hot baths or showers (which provide transient relief from symptoms) may arise from temporary improvements in autonomic dysfunction in the

satiety, thirst, digestive and thermoregulatory systems of the hippocampus-hypothalamus-pituitary axis which have been associated with chronic cannabis use.6 More importantly, it appears that the only way of treating CHS is cessation of cannabis use, with relapses in symptoms occurring on resumption.5,6 Cannabis is the most widely used illicit drug.8 As a result, the prevalence of CHS may be much higher than reported. Since the realisation of this syndrome by the author’s acute medical team in 2010, a further 4 cases have been recognised. Wallace et al (2011) reported that since the discovery of this condition in their organisation in 2010, they too have since identified a further 5 cases.8 The economic impact of individual emergency department visits and acute admissions to hospitals for CHS is likely to be high. Patients with CHS may remain undiagnosed for several years, presenting to hospital on multiple occasions and receiving a variety of expensive investigations whilst they continue to smoke cannabis. It is thus very important for clinicians to be aware of this condition. Equally important is educating patients themselves that the cause of their recurrent presentation is secondary to their excessive cannabis usage, and that their symptoms may only cease by stopping. Our 21 year old male patient was diagnosed with Cannabis Hyperemesis Syndrome. Despite efforts to encourage the patient to attend a drug rehabilitation clinic, he failed to engage, continued to smoke, and represented once further to the emergency department. He even admitted on this occasion that he had only come to hospital because his showering facilities had broken at home. As he was clinically euvolaemic, he was not admitted, educated about the condition, and strongly advised to quit smoking cannabis.

References 1. Talley NJ (2007) Functional nausea and vomiting. Aust Fam Physician 36(9): 694–7. 2. Izzo AA, Sharkey KA (2010) Cannabinoids and the gut: new developments and emerging concepts. Pharmacol Ther 126(1): 21–38. 3. Price SL, Fisher C, Kumar R, Hilgerson A (2011) Cannabinoid hyperemesis syndrome as the underlying cause of intractable nausea and vomiting. J Am Osteopath Assoc. 111(3): 166–9. 4. Schmid SM, Lapaire O, Huang DJ, Jürgens FE, Güth U (2011) Cannabinoid hyperemesis syndrome: an underreported entity causing nausea and vomiting of pregnancy. Arch Gynecol Obstet. 284(5): 1095–7. 5. Soriano-Co M, Batke M, Cappell MS (2010) The Cannabis Hyperemesis

Pain, and Compulsive Bathing Associated with Chronic Marijuana Use: A Report of Eight Cases in the United States. Dig Dis Sci 55(11): 3113–9. 6. Allen JH, De Moore GM, Heddle R, Twartz JC. (2004) Cannabinoid hyperemesis in association with chronic cannabis abuse. Gut. 53: 1566–1570. 7. Budhraja V, Narang T, Azeez S. (2008) Cannabinoid hyperemesis syndrome: cyclic vomiting, chronic cannabis use, and compulsive bathing. Pract Gastroenterol. 32(9): 79–80. 8. Wallace EA, Andrews SE, Garmany CL, Jelley MJ (2011) Cannabinoid hyperemesis syndrome: literature review and proposed diagnosis and 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 We present a case of endogenous endophthalmitis secondary to liver abscesses, in a patient with no previous medical comorbidities or risk factors for immunosuppression. The patient presented with acute painless loss of vision and feeling generally unwell. Investigations revealed Streptococcus anginosus-constellatus bacteraemia, and evidence of diverticular disease that likely predisposed to the liver abscesses. Due to prompt diagnosis and administration of antibiotics, the patient had a good visual outcome. This case highlights the importance of being aware of endogenous endophthalmitis, as early diagnosis and prompt administration of antibiotics will optimise visual outcomes.

Keywords Endogenous endophthalmitis, liver abscesses, diverticular disease, loss of vision.

Case Report Case History A 52 year old man presented to the Acute Medical Unit with a one day history of sudden onset painless left sided loss of vision. He reported feeling unwell in preceding two weeks, with anorexia and sweats. He also mentioned a single episode of minimal rectal bleeding two days prior. He was otherwise fit and well, with no risk factors for immunosuppresion, no recent surgery, dental work, or foreign travel. On examination, he was pyrexial at 39˚C but remained haemodynamically stable. Clinical examination was normal, apart from a red left eye with visual acuity limited to counting fingers (CF) in that eye. Of note there were no murmurs or signs of infective endocarditis. Slit lamp examination by the ophthalmology team showed cells+++, keratic precipitates+++ and a 1mm hypopyon in the left anterior chamber. A yellow haemorrhagic lesion was


seen in the superior temporal quadrant of the left retina(Figure 1). There were also two cotton wool spots seen in the right retina. Blood tests showed a white cell count of 20.57 x 109/L (neutrophils 17.3) and C-reactive protein of 245mg/L. Renal and liver function tests were normal, and a HIV test was negative. Blood cultures were performed, following which intravenous amoxicillin and gentamicin, cyclopentolate 0.5%, and dexamethasone eye drops were commenced for suspected endogenous endophthalmitis. Blood cultures and a subsequent anterior chamber sample grew Streptococcus anginosusconstellatus, which was sensitive to penicillin. CT scanning demonstrated lesions in the liver compatible with liver abscesses(Figure 2). A subsequent colonoscopy showed evidence of diverticular disease, which was thought to have predisposed to the liver abscesses. The patient was discharged after completing a three week course of intravenous amoxicillin and gentamicin, and continued to take a further three week course of oral amoxicillin at home. Upon discharge, his visual acuity had improved from CF to 6/18 in the left eye.

S Koay MBBS FY2 Acute Medicine, Royal Free Hospital, London S Jain FRCOphth Consultant Ophthalmologist, Royal Free Hospital, London I Cropley FCRP Consultant in Infectious Diseases, Royal Free Hospital, London H Petrushkin MBBS Specialist Registrar in Ophthalmology, Royal Free Hospital, London

Discussion Endogenous endophthalmitis is a rare but potentially blinding intraocular infection that results from haematogenous spread of bacteria from a distant primary source. It is often associated with an underlying medical condition (which causes a relative immunosuppression), recent surgery, or dental manipulation.1 Recognised associations include diabetes mellitus, malignancy, HIV infection, cardiac disease, and intravenous drug usage.

H Beynon FRCP Consultant Physician, Royal Free Hospital, London Correspondence: S Koay Royal Free Hospital, Pond Street, London NW3 2QG Email: [email protected]


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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 vision, ocular pain, discharge or a red eye. They may also report systemic symptoms such as lethargy, fever, anorexia and weight loss. It is important to note that our patient presented with painless loss of vision, which is more commonly due to central retinal artery or vein occlusion, vitreous haemorrhage, retinal detachment, and nonarteritic anterior ischaemic optic neuropathy.

Streptococcus milleri group (which include Streptococcus anginosus-constellatus) are commensals found in the mouth, oropharynx, gastrointestinal tract, and genitourinary tract.2 They are one of the commonest causes of liver abscesses in the United Kingdom,3 and can be associated with suppurative metastatic complications.4 However, they are a rare cause of 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 (particularly Klebsiella spp.).5 Prompt administration of antibiotics is important in endogenous endophthalmitis, as it helps to optimize visual outcomes. In most cases, the diagnosis is based on history and examination findings, and treatement is initiated empirically whilst awaiting results of intraocular and blood cultures.1 There is no clear consensus or guidelines regarding the optimal route of administration of antibiotics. As many topical, subconjunctival and systemic antibiotics do not reach therapeutic levels within the vitreous,6 it has been suggested that intravitreal injection of antibiotics will deliver rapid therapeutic levels of intraocular antibiotic.5 However, administration of intravitreal antibiotics does not necessarily significantly improve visual prognosis.5,7 It has also been suggested that intravenous antibiotics may be all that is necessary to treat the intraocular infection, if a specific organism is cultured from blood.8 Intraocular antibiotics and steroids can then be considered if the inf lammatory response worsens.8 In

the case described above, the decision was made to not administer intravitreal antibiotics, as the patient was responding well to intravenous antibiotics, evidenced by his improving visual acuity. Visual prognosis is often poor, with 26%-44% of patients being left blind.5,9 Poor prognostic factors include delay in diagnosis;9 use of inappropriate antibiotics;10 diffuse infection of the vitreous and retina, or panophthalmitis;9 infection with virulent organisms;7 and gram negative infection.5,7,9 There is also an appreciable mortality rate of 5%, as a direct result of extraocular infection.5 The importance of a prompt diagnosis in ensuring a favourable visual prognosis emphasises the need for acute physicians to be aware of this condition; the possibility of endogenous endophthalmitis should be included in the differential diagnoses for any patient presenting with systemic upset and painless loss of vision. Early referral to the ophthalmology team and discussion with microbiology regarding appropriate choice of antibiotics is essential if this condition is suspected.

References 1. Connell PP, O’Neill EC, Fabinyi D, et al. Endogenous endophthalmitis: 10-year experience at a tertiary referral centre. Eye 2011; 25: 66–72. 2. Piscitelli SC, Shwed J, Schreckenberger P, et al. Streptococcus milleri group: renewed interest in an elusive pathogen. Eur J Clin Microbiol Infect Dis 1992; 11: 491–8. 3. Mohsen AH, Green ST, Read RD, et al. Liver abscess in adults: ten years experience in a UK centre. QJM 2002; 95(12): 797–802. 4. Gossling J. Occurrence and pathogenicity of the Streptococcus milleri group. Clin Infect Dis. 1988; 10(2): 257–85. 5. Jackson TL, Eykyn SJ, Graham EM, et al. Endogenous bacterial endophthalmitis: 17-year prospective series and review of 267 reported cases. Surg Ophthalmol 2003; 48(4): 403–23.


6. Barza M, Kane A, Baum J. Intraocular penetration of gentamicin after subconjunctival and retrobulbar injection. Am J Ophthalmol 1978; 85: 541–7. 7. Wong JS, Chan TK, Lee HM, et al. Endogenous bacterial endophthalmitis: an East Asian experience and a reappraisal of a severe ocular aff liction. Ophthalmology 2000; 107(8): 1483–91. 8. Brod RD, Flynn HW Jr. Endophthalmitis: current approaches to diagnosis and therapy. Curr Opin Infect Dis 1993; 6: 628–37. 9. Greenwald MJ, Wohl LG, Sell CH. Metastatic bacterial endophthalmitis: a contemporary reappraisal. Surv Ophthalmol 1986; 31(2): 81–101. 10. Wang LS, Lee FY, Cheng DL, et al. Klebsiella pneumoniae bacteremia: analysis of 100 episodes. J Formos Med Assoc 1990; 89(9): 756–63.


28


Picture Quiz Questions

A young patient with heart failure

H Patel, G Dhillon, A Bandali & N Patel

Case report

H Patel MRCP Cardiology registrar Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD G Dhillon MRCP Cardiology trainee Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD

A 28 year old gentleman presented after an episode of collapse with loss of consciousness. He gave a history of non-specific malaise and myalgia over the previous 7 days, with fever, a generalised rash and a non productive cough. He developed progressive shortness of breath with sharp, pleuritic chest pain that was unresponsive to antibiotics in the community. There was no past medical history. He was taking amoxicillin and paracetamol. He smoked 30 cigarettes a week and had smoked cannabis recently. He drank 14 units of alcohol a week. He worked as a painter. On examination, his blood pressure was 110/72, heart rate 110 beats per minute and saturations of 99%, breathing room air. He was short of breath at rest. Cardiovascular, respiratory and abdominal examinations were otherwise unremarkable. There

was a mottled appearance to his skin on his upper and lower limbs. Chest radiograph was unremarkable. ECG is as shown (Figure 1). Blood tests revealed normal full blood count and urea and electrolytes, CRP 26 mg/L, troponin T 0.17 µg/L (normal 0-0.1). An echocardiogram showed severely impaired left ventricular (LV) systolic function with an ejection fraction (EF) of 30%. There was a moderate sized pericardial effusion.

Questions 1. What does the ECG show? 2. What is the diagnosis? 3. What are the possible aetiologies? 4. What features suggest an adverse prognosis in this condition? 5. How would you manage this patient?

A Bandali MBBS Cardiology trainee Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD N Patel FRCP Cardiology Consultant Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD Correspondence: H Patel MRCP Cardiology registrar C/O Dr NR Patel Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD Email: dochiteshpatel @hotmail.com

Figure 1. ECG recorded on admission.




29

Trainee Section

Trainee Update A Daniel, K Freeman & A Miller

Acute Medicine Awareness Day As trainees in Acute Medicine, you will almost certainly have had to explain the concept of your specialty at some point – both to members of the public and to NHS staff, who may still be unfamiliar with the purpose of the Acute Medical Unit and the role of the Acute Physician. The Society for Acute Medicine feels that Acute Medicine needs to be more effectively promoted to both patients and to staff, and in order to achieve this, SAM has launched Acute Medicine Awareness Day. This will take place on 20th June 2012. We need as many AMUs as possible to take part in raising awareness of the specialty both locally and nationally, and we would encourage trainees to take a central role in helping to organize their own units’ activities on Awareness Day. Have a look at the SAM website for more details about how to get involved ( 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 / index.php?option=com_content&view= 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 2012&catid= 2:news&Itemid=10).

SAM Dublin The Spring conference this year is being held in Dublin, at the Radisson Blu Hotel, on May 3rd and 4th. The programme has a variety of clinical, political and practical topics – hopefully something for everyone! See http://www.acutemedicine. org.uk/images/stories/samdublin/samdublin%20 programme%2025th%20jan.pdf for more details. As you’ll know from our last update, the trainee session will take the form of a forum this time, to give you a chance to discuss any burning issues you have about your training. In order to give the session some structure, we have decided to focus on three main areas: 1. specialist skills training; 2. how to market yourself as an Acute Physician; and 3. SAM’s role in developing successful and satisfied trainees in Acute Medicine. If you have a specific question you would like to ask, we would be grateful if you could email us before the conference so that we can plan the session to help as many of you as possible. We will send out an email nearer the time to remind you to submit your queries, if you have them.


Of course, if you have a question which falls outside these topic areas, we would be happy to help, and there should be time at the end of the forum to discuss any additional issues. You can register for the conference, and submit an abstract, through the SAM website as usual.

Changes to AIM and GIM decisions aids At the last Acute Medicine specialty advisory committee (SAC) meeting in January 2012, the committee finalised some revisions to the AIM and GIM decisions aids – the documents setting out targets for trainees in each year of their higher specialty training. As we mentioned last time, the total number of workplace-based assessments (WBAs) required each year is going to fall, and there will no longer be such a rigid structure in terms of the number of each type of assessment required. We have been told that these changes will come into operation in August 2012. The new decision aids should be visible on the JRCPTB website by then. All those trainees on the 2009 AIM or GIM curricula should follow these new guidelines once they have been released, since they will be used to monitor your progress at your ARCP. The long-awaited streamlining of the ePortfolio (to remove irrelevant curricula and make the whole process more efficient) is still in the pipeline. We know how frustrated many of you are by the ePortfolio in its current incarnation, but we are hoping that some of the promised changes will be made by August 2012.

Increase in JRCPTB enrollment fees The JRCPTB has recently announced an increase in enrollment fees, which will come into effect from 1st April 2012. This will not affect those of you who paid the upfront fee at the start of your training, but it will affect you if you pay in yearly installments. There is more information about this on the JRCPTB website (http://www.jrcptb.org.uk/ enrolment/Pages/Enrolment- Fees.aspx). If you are just about to start your Acute Medicine training, it is well worth thinking about paying the upfront fee in order to protect yourself from any future fee rises (especially if you plan to extend your training in any way). That’s all for now. We are looking forward to seeing many of you in Dublin (remember to email us if you have any questions for the forum).

Amy Daniel Email: amy_dan@hotmail. com Kirk Freeman Email: k.freeman@doctors. org.uk Alice Miller Email: [email protected]


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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 in Acute Myocardial Infarction Goyal A et al. JAMA. 2012; B157-164

K E Mellor ST5 Acute Medicine Royal Bournemouth NHS Trust Email: katherinemellor@ doctors.org.uk J R Neale ST6 Gastroenterology and General Internal Medicine Hampshire Hospitals NHS trust

The importance of potassium homeostasis in the post-infarction period has become a cornerstone in modern clinical practice. Several studies have shown that potassium levels of less than 3.5 led to a higher risk of arrhythmia induction. This study investigated what the optimal target potassium level should be, given the lower rates of serious arrhythmias following interventions such as beta-blockade and reperfusion therapy. This large retrospective observational study looked at 38689 patients admitted to American hospitals with ICD-10 coded Acute Myocardial Infarction and appropriate positive biochemical markers. They documented admission serum potassium and then a mean potassium level based on the average of all post-admission potassium levels. Their results show a U-shaped relationship between in-hospital mortality and mean potassium levels, suggesting an increase in all cause mortality with potassium levels of less than 3.5 and higher than 5.0. In the group potassium 4.5 to 5.0 mortality was 10%(95% CI, 9.1%-10.9%) compared to mortality rates of 4.8% and 5.0% in the groups of 3.5 to 4.0 and 4.0 to 4.5 respectively (95% CI, 4.4%-5.2% and 4.7%-5.3%). This suggests a twofold increase in mortality if the potassium level is above 4.5. This is contrary to current practice which targets levels between 4.5 and 5.5. The strength of this study is that it utilised all cause mortality as its primary end point rather than focusing on fatal arrhythmia induction as in previous studies. The problem with observational studies is that an observed relationship between two variables does not confirm causality. ‘Normal’ potassium levels are considered to be 3-5-4.5; patients with levels outside this may be more unwell and failing to maintain homeostasis. This may result in higher mortality rather than the potassium level itself per se. To fully answer the question posed a randomized trial with patients allocated to target potassium levels would be required. The authors themselves admit this is

unlikely, given the high cost of such trials and the regulatory processes involved. This study was limited to in-hospital mortality in patients following AMI. The mortality rates seen were not limited to arrhythmias. This raises the question whether potassium levels may have a similar predictive value for mortality in acute medical admissions of different aetiology. For example, studies have suggested that patients with cardiac failure may have higher rates of mortality with potassium levels of 140/90 mmHg at acute presentation

1 point

Clinical features, score 1 of: Speech disturbance without focal weakness Unilateral weakness Other

1 point 2 points 0 points

Duration of symptoms, score 1 of: < 10 minutes 10-59 minutes ≥60 minutes

0 points 1 point 2 points

Diabetes

1 point

Table 2. ABCD2 Score.

however in reality, the duration of TIA is typically much shorter, with the majority of episodes resolving within an hour. Approximately half of TIAs extending beyond one hour demonstrate ischaemic changes on neuroimaging, which has led to some authorities adopting a pathophysiological classification of TIA, rather than the traditional chronological approach; however this has not been adopted in the UK.4 The ABCD2 score (Table 2) is useful for risk stratification of TIA. Patients with a score ≥ 4 have a high risk of progression to stroke, and may require admission to hospital for early investigation and treatment (Figure 1).5 Symptoms of vertigo, dysarthia, ataxia or dysphagia in isolation without other focal neurological signs rarely point to a diagnosis of stroke. Furthermore, transient loss of consciousness or syncope is rarely due to stroke or TIA unless it is the result of a severely disabling stroke, a brainstem stroke (when associated with additional brainstem signs), or seizure complicating a stroke. Defining the speed of onset is may also be helpful in determining the cause of hemiparesis. A subacute process developing over hours or days may suggest an infectious, inf lammatory, malignant or metabolic pathology.

What is the main differential diagnosis? Important differential diagnoses include seizure, hemiplegic migraine, reversible posterior leukoencephalopathy, malignancy and functional weakness. Hypoglycaemia may also present with focal neurological deficit, including hemiparesis. Features which may be helpful in distinguishing some of these conditions are listed below: • Seizures may be followed by post-ictal confusion or hemiparesis (Todd’s paresis) lasting for several hours. An eye witness description of tonic-clonic movements at the time of onset, or a past history of seizure, alcohol excess, malignancy or other known structural brain disease should arouse suspicions. It should also be remembered that seizure may also complicate acute stroke. • Migraine may present with a progressive hemiparesis over several minutes, usually in association with unilateral headache, nausea and vomiting; however the motor signs can occur in isolation. Patients are usually younger and may describe a series of symptoms occurring sequentially including positive visual phenomenon, word finding difficulty and limb paraesthesia. A history of previous events should be sought. • Reversible posterior leukoencephalopathy syndrome manifests with posterior fossa symptoms including visual disturbances (e.g. hemianopia, cortical blindness), headaches, vomiting and seizures. Cerebral autoregulatory failure and endothelial dysfunction is thought to be responsible.Magnetic resonance imaging demonstrates white matter oedema in the posterior cerebral hemispheres. • Functional symptoms represent transient motor or sensory symptoms not attributable to an identifiable neurological abnormality. In one case series, 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.



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35

The patient presenting with acute hemiparesis

accounted for 21% of stroke department admissions in this age group.6 Functional symptoms were very uncommon in those aged over 50 years.

What key physical examination findings could help in localisation and differential diagnosis? The purpose of the physical examination is to localise the lesion and attempt to identify aetiological factors such as atrial fibrillation. However this should not delay neuroimaging for patients presenting acutely, as early diagnosis and treatment is crucial. In some cases detailed examination may need to be deferred until after the imaging has been undertaken. Neurological and general examination should include assessment of speech and cognitive function. In the acute phase, affected limbs become hypotonic and deep tendon ref lexes may be hypo- or hyper-ref lexic. Limb weakness typically follows a pyramidal pattern, with extensors affected to a greater degree than f lexors in the upper limb and vice versa in the lower limb. Mild weakness may result in a pronator drift (a downward drift of the arm with pronation when held extended with the palm facing upwards). Later, affected limbs become hypertonic with brisk ref lexes. Limb weakness, ataxia or sensory loss in association with cranial nerve involvement may help localise the lesion to the posterior circulation.

What features may suggest ‘functional‘ hemiparesis? Inconsistent examination findings may help to distinguish functional disorders from stroke; features of functional disturbance may include: • Equal proximal/ distal and f lexion/ extension weakness in the limbs. • Ipsilateral sternocleidomastoid weakness. • Intermittent voluntary effort with simultaneous contraction of flexion and extension muscles groups. • Ref lexes and muscle tone tend to be normal. • Prominent verbal grunts during examination – ‘Wrestler’s sign’. • Raising the contralateral leg may elicit a downward movement of the ‘paretic’ leg – ‘Hoover’s sign’. • Finally, the patient may seem remarkably unconcerned and calm in the presence of marked weakness - ‘la belle indifference’. With encouragement, it is often possible to elicit full power. No single clinical sign is definitive and clinical judgement should always take precedence. Ultimately, a diagnosis of functional weakness should only be made when other possibilities have been excluded. Further, it should be remembered that exaggerated signs may be elicited following stroke, mimicking the feature of functional disorders in some cases.

Case Progression The patient had been well immediately prior to this episode, although two weeks earlier his wife reported that his speech had


sounded ‘jumbled’ for a short period; this had recovered after around 30 minutes and he had declined her suggestion of visiting his GP. He usually took ramipril 5mg and bendroflumethiazide 2.5mg once daily for high blood pressure. His father died of a myocardial infarct, aged 75, and he had smoked 20/day since the age of 18. Examination revealed right hemiplegia with brisk reflexes on the right and up-going plantar. There was an upper motor neurone VII nerve palsy and he was looking to the left with homonymous hemianopia on the right. He had not spoken since arrival in hospital but was able to follow simple commands. Cardiovascular examination revealed a regular pulse of 80/min with blood pressure 150/90; there were no carotid bruits or heart murmurs. ECG confirmed sinus rhythm.

What immediate imaging should be undertaken? Computed tomography (CT) remains the first line investigation for the early differentiation of haemorrhage from infarct, and to exclude non-stroke pathology, such as cerebral tumours. In this case the patient has a past history of hypertension, raising the possibility of intracerebral haemorrhage as a cause for his symptoms; however he also has risk factors for ischaemic stroke (smoking, hypertension and family history) and a possible recent left hemisphere TIA causing transient dysphasia. Given the importance of early intervention following acute ischaemic stroke the patient should undergo CTscan as soon as possible after arrival in hospital. An unenhanced brain scan takes approximately 10 seconds to obtain. Folllowing intracerebral haemorrhage, CT appearances evolve with time. After 5 days, small lesions may become isodense with the surrounding brain, particularly following a small bleed. By the end of the first week, lesions may become hypo-dense. Indeed CT appearances of previous intracerebral haemorrhages will often mimic the appearances of old infarction, such as the ex-vacuo effect of ventricular and sulcal enlargement near sites of previous haemorrhage. Following ischaemic stroke, 60 % will have changes visible on CT scan within first 24 hours rising to 70% of those scanned within 72 hours. Early CT changes found in acute ischaemic stroke include cortical sulcal effacement and loss of the insular ribbon, a hyperdense middle cerebral artery due to thrombus within the artery, and loss of grey-white matter differentiation within the basal ganglia. Such findings are associated with larger infarcts and worse functional outcomes.7 As with haemorrhagic stroke, CT appearances evolve with time with lesions becoming more demarcated and hypodense during the first few days. Cerebral oedema is maximal around day 3 – 5, gradually subsiding during the 2nd – 3rd week, such that by the 2nd week infarct may increase in density and become isodense. Later, the infarct lesion forms sharp demarcated hypodense lesions. Magnetic resonance imaging may provide a more detailed view of anatomical and pathological changes, as well as enabling non-invasive imaging of intracranial vessels. Diffusion weighted MR sequences are able to detect ischaemia within 30 minutes of onset. Patient related factors such as claustrophobia and the high level of co-operation


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needed for the longer period needed to obtain images may limit the use of this test in the acute setting, along with resource factors such as expense and accessibility.

Case Progression The patient undergoes urgent CT scan within 30 minutes of arrival in the Emergency Department, which reveals evidence of acute ischaemic change in the left middle cerebral artery territory. There is no evidence of intracerebral haemorrhage. On return from the scanner, his condition remains unchanged with evidence of persistent right hemiplegia.

What immediate treatments should be considered for patients with acute ischaemic stroke? Antiplatelet therapy should be commenced as soon as CT has excluded intracranial haemorrhage; aspirin 300mg is usually administered initially and can be given rectally if the patient is unable to swallow. NICE now recommends clopidogrel 75mg daily for secondary prevention of ischaemic stroke. A combination of aspirin with dipyridamole 200mg twice daily is recommended where clopidogrel is contraindicated or not tolerated.9 In 1995 the National Institute of Neurological Disorders & Stroke study10 (NINDS) demonstrated the efficacy of rt-PA intravenous thrombolysis when given within three hours of stroke onset. Patients in the treatment group were 30% more likely to have minimal or no disability at 3 months, at the expense of a significant rise in the incidence of symptomatic intracranial haemorrhage (6.4%). There was no mortality difference observed at three months. The European Co-operative Acute Stroke Study(ECASS III)11 demonstrated the efficacy of thrombolysis up to 4.5 hours, with similar benefit in mortality and intracranial haemorrhage rates to the original NINDS trial. European Union approval of alteplase permits its use up to 3 hours post stroke onset, 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-toneedle times, and early thrombolysis is critical. In this case the patient has presented to hospital early and CT findings confirm that he would be candidate for thrombolysis. Intravenous thrombolysis results in restoration of vessel patency (i.e. recannalisation) in 46.2% of patients treated.12 Should thrombus be demonstrated on angiography within an intracranial artery, intra-arterial thrombolysis may be attempted (recannalisation rates of 63.2% - 67.5%) or mechanical clot disruption techniques (83.6%). There are no national guidelines to guide therapy and patients should be discussed with the affiliated tertiary centre on a case by case basis. Recannalisation is associated with favourable functional outcomes and reduced mortality compared with failure to recannalise, with similar rates of haemorrhagic transformation.

What are the risks of thrombolysis? The likelihood of improved outcome following thrombolysis needs to be balanced against the increased

risk of symptomatic intracerebral haemorrhage in around 1 in 14 patients. Should intrancranial haemorrhage occur, treatment options are limited and it may be fatal. Treatment also carries a risk of anaphylaxis of < 1%. The patient and their next of kin should be counselled carefully regarding the risks and informed consent should be obtained where possible.

What are the other key management issues in acute hemiparesis? Patients should be kept nil-by-mouth until a formal swallow assessment has been performed. If this is delayed, or if the assessment demonstrates that the patient is at risk of aspiration a nasogastric tube should be sited to enable initiation of enteral feeding and the administration of medication. Additional management measures are aimed at maintaining homeostasis in an attempt to rescue ischaemic tissue at risk of infarction (i.e. penumbral salvage). Such measures are illustrated in Table 3. Admission to a stroke unit is strongly associated with better outcomes, due to improved monitoring of physiological parameters, prevention of complications and Hyperglycaemia

Associated with worse outcome Use insulin to maintain glucose ≤ 11mmol/l

Hypoxia

Use supplementary oxygen only to maintain saturations >95% (use clinical judgement in those with significant airways disease)

Pyrexia

Associated with worse outcomes Identify potential sources then treat with antipyretics

Hypertension

No evidence in favour of treating in the acute phase Treat if evidence of end organ damage (NICE)8

Table 3. Maintaining homeostasis following acute stroke.

early mobilisation. National guidelines in England now recommend that all patients are managed throughout their hospital stay in a specialist stroke unit.8

What other complications may arise following middle cerebral artery infarction? Malignant middle cerebral artery syndrome occurs in 10% of MCA infarcts. Findings include dense hemiplegia and forced eye deviation, while CT will demonstrate a large area of hypodensity and midline shift. Left untreated, it carries a mortality of 78% as a consequence of herniation of the temporal lobe onto the brainstem.13 Decompressive hemicraniectomy and durotomy is the surgical technique used to relieve the increased intracranial pressure, thus improving cerebral perfusion pressure. A pooled analysis of outcome following the procedure demonstrated greater survival (numbers needed to treat 2) and favourable outcome at one year mRS 0-4 (75 Vs 24 percent in the Referral for decompressive control group).14 hemicraniectomy is recommended for patients fulfilling the following criteria:8



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37


1. Age < 60 years 2. Clinical deficits suggestive of MCA territory infarction, with a score on the National Institutes of Health Stroke Scale (NIHSS) of > 15. 3. Decrease in the level of consciousness to give a score of 1 or more on item 1a of the NIHSS. 4. Signs on CT of an infarct of at least 50% of the middle cerebral artery territory, with or without additional infarction in the territory of the anterior or posterior cerebral artery on the same side, or infarct volume greater than 145 cm3 as shown on diffusion-weighted MRI.

What other investigations should be considered? In anterior circulation ischaemic stroke, carotid doppler assessment should be considered to enable imaging of extracranial carotid vessels, particularly where there has been significant functional improvement. In ischaemic stroke in younger patients, tests for vasculitis and lupus should be performed and CT or MR angiography if intracranial carotid or vertebral artery dissection is considered a possible cause. Trans-thoracic echocardiography should also be considered to enable identification of a cardiac source of embolic stroke, which may require treatment with long-term anticoagulant drugs.

What is the prognosis for patients presenting with acute hemiparesis? Mortality and functional recovery following stroke is dependent on the stroke subtype and may be predicted

by using the OCSP classification (Figure 2). Recovery from stroke occurs through a variety of mechanisms. Penumbral salvage results in the restoration of functioning neurones. Neuroplasticity refers to the ability of neighbouring cells to take over the lost function. Adaptive behaviour is learned with the support of various members of the multi-disciplinary team, including physiotherapists, occupational therapists, speech therapists and neuropsychologists.The rate of recovery is highest in first few weeks after stroke; functional improvement continues at a slower rate for many months (occasionally up to 2 years). It remains diff icult to predict the rate and completeness of recovery.

Case progression The patient was transferred to the acute stroke unit and treated with rt-PA within 1 hour of arrival in hospital (2 hours after onset of the weakness). Following this treatment an improvement in his weakness was noted with power improving to 3/5 in his limbs and some recovery of speech. He was initially fed via a nasogastric tube after failing a swallow assessment, but this improved within 72 hours enabling oral nutrition to be initiated. Carotid doppler showed minor plaque only, and an echocardiogram was normal. He was commenced on clopidogrel 75mg daily and simvastatin 40mg daily and his blood pressure control was maintained without alteration of his usual medication. The improvement continued over subsequent weeks with the support of the multiprofessional team on the stroke unit and he was transferred to a community rehabilitation unit after an inpatient stay of 2 weeks.

N.B PICH: primary intracerebral haemorrhage

Figure 2. Stroke prognosis based on OCSP subtype1 & primary intracerebral haemorrhage.



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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

1521-6.

http://www.nice.org.uk/CG68

2. Meldrum D, Hardiman O, Pittocj SJ et al. The Oxfordshire community

stroke

and

transient

dipyridamole

complications and prediction of outcome in acute ischaemic stroke. Stroke

http://guidance.nice.org.uk/TA210/

Cerebrovasc Dis 2003: 12(1): 1-7. Phenomena and Related Disorders in Patients with an Acute Right or Left Hemisphere Stroke. Age Ageing 1993; 2: 46-52. 4. American Heart Association & American Stroke Association Stroke Council. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals. Stroke 2009; 40(6): 2276-93. 5. Johnston SC, Rothwell PM, Nguyen-Huynh MN et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet 2007; 369: 283–92. 6. Vroomen PCAJ, Buddingh MK, Luijckx GJ et al. The Incidence of Stroke Mimics Among Stroke Department Admissions in Relation to Age

attack

(TIA)

9. NICE Technology Appraisal 210: clopidogrel and modified-release

stroke project classification: correlation with imaging, associated

3. Stone SP, Halligan PW, Greenwood RJ. The Incidence of Neglect

ischaemic

for

prevention

of

occlusive

vascular

events.

10. The National Institute of Neurological Disorders and Stroke rt-PA Stroke study group. NEJM 1995; 333(24): 1581-7. 11. Hacke W, Kaste M, Bluhmki E et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischaemic stroke. NEJM 2008; 359(13): 1317-29. 12. Rha JH, Saver JL. The Impact of Recanalization on Ischemic Stroke Outcome: A Meta-Analysis. Stroke 2007. 38: 967-973. 13. Hacke W, Schwab S, Horn M et al. ‘Malignant’ middle cerebral artery territory infarction: clinical course and prognostic signs. Arch Neurol 1996; 53(4): 309-15. 14. Vahedi K, Hofmeijer J, Juettler E et al1. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of 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.



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Trainee Section

Haemoptysis: Diagnosis and Treatment

K Hurt & D Bilton

Abstract Haemoptysis is a common symptom in clinical practice, which requires further investigation. Fortunately, massive haemoptysis only accounts for a small proportion of these episodes. It is a medical emergency that carries a high mortality rate. There are no agreed management guidelines. This review discusses proposed methods of resuscitation as well as outlining a diagnostic algorithm and discusses treatments including bronchial artery embolization, endobronchial therapy, surgery and medical therapies.

Keywords Haemoptysis, bronchoscopy, bronchial artery embolization, CT thorax, lung cancer, bronchiectasis, cystic fibrosis.

Introduction Haemoptysis can be defined as the expectoration of blood from the lower respiratory tract. The amount of blood can vary widely, from streaking of the sputum to rapidly fatal massive haemoptysis. Whilst haemoptysis in general is a relatively common clinical problem, massive haemoptysis remains fortunately very rare. The exact incidence is unknown because there is no agreed definition in the literature as to what constitutes massive haemoptysis. Definitions range from a blood loss of 100 mls of blood expectorated in 24 hours1 up to 1000mls in 24 hours.2 Most respiratory physicians would use a definition somewhere between 200600mls/24 hours. It has been suggested that volume expectorated definitions are not useful in clinical practice and actually it is better to define functionally.3,4 There are good reasons for this. Haemoptysis is difficult to quantify, patients may over report amounts produced and the physiological effects of haemoptysis will depend on the patient’s clinical status. Death from massive haemoptysis is usually through a process of asphyxiation, rather than exsanguination.5 Haemoptysis is a serious symptom that requires further investigation as it may be a sign of underlying severe disease. The most common causes vary geographically with tuberculosis (TB) being the most common underlying aetiology in the developing world and elsewhere bronchitis and lung cancer.2


There are no consensus guidelines available for the management of haemoptysis and its treatment can be challenging, even for experienced physicians.

Pathophysiology The lungs have a double arterial supply. The pulmonary arteries carry deoxygenated blood under low pressure to the lungs for the purpose of gas exchange. The bronchial arteries account for size 8) to allow for adequate suctioning followed by bronchoscopy.8 If it is known which lung the bleeding originates from, the patient should be managed bleeding side down to try and prevent contralateral aspiration. The patient may be able to give a history of bubbling on one side. Single lung ventilation can also be considered to protect the contralateral lung.21 This will require the use of a double lumen endotracheal tube inserted by an experienced operator.22 If a double lumen tube is not available the patient can undergo selective lung intubation by inserting an endotracheal tube directly over a bronchoscope into the left or right main bronchus. However it should be borne in mind that selectively ventilating the right lung may lead to inadvertent occlusion of the right upper lobe due to its proximal origin, leaving only the lower and middle lobe for ventilation. In this situation a Fogarty catheter may be passed into the left main bronchus under bronchoscopic guidance and the balloon inf lated, occluding the bronchus 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?

Figure 1. Admission chest X-ray demonstrating widespread bronchiectasis; a port-a-cath is present overlying the lateral aspect of the right lung field.


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 consulted for the safest way to do this. There is no consensus on further investigation. If the patient has been stabilized a CT scan can be performed,


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Massive haemoptysis Admit to HDU/ICU At risk

Airway Intubate with large ET tube. Consider single lung ventilation

Patent

Breathing

Respiratory distress

No respiratory distress

Give Oxygen

Circulation Volume resuscitation. Crystalloid and blood

Xmatch and correct clotting

Reassess

Unstable

Stable

Bronchoscopy

CT scan

Bronchial Artery Embolization Endobronchial treatment

Medical Therapy

Failure

Surgery Figure 2. Treatment algorithm for massive haemoptysis.

which will often identify the source of bleeding and establish the cause.19 Contrast enhanced multidetector CT provides angiographic studies that have recently been shown to be superior to conventional angiography25 and is important for considering suitability and planning bronchial artery embolizations. Bronchoscopy may be required after CT scanning in some circumstances.23 In the case of bronchiectasis and CF, bronchoscopy is not indicated as endobronchial therapy is unlikely to be beneficial and may delay time prior to bronchial artery embolization.26,27 If the patient with massive haemoptysis is too unstable to undergo CT scanning, bronchoscopy should be performed immediately. Rigid bronchoscopy may be required if there is massive bleeding (to allow for rapid suctioning) or if certain therapeutic bronchoscopic

procedures are being considered. Otherwise fibre optic bronchoscopy can be used, which identifies the site of bleeding in up to 93% of cases.19

What are the treatments available for massive haemoptysis? Bronchoscopic treatment for endobronchial lesions There are a number of therapeutic techniques that can be performed through a bronchoscope, most of them best performed through a rigid bronchoscope and usually only in specialist centres. Instillation of epinephrine (1:20,000) to an identified point of bleeding can be used. It is effective in mild to moderate haemoptysis but of doubtful efficacy in major haemoptysis.28 Cold saline lavage,29 fibrinogen compounds combinations30 and tranexamic acid31 may also be used, although evidence is limited.



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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 the procedure the patient undergoes a descending thoracic aortogram to identify bronchial artery anatomy and bleeding site. The most commonly used embolic material is polyvinyl alcohol.36 Recurrence is common, occurring in 10-55% of patients, and outcome is dependent on underlying disease.34 Minor temporary side effects such as chest pain and dysphagia are common but fortunately neurological complications secondary to spinal cord ischaemia are rare (1.4-6.5%) and becoming rarer with super selective catheterisation.34 Systemic embolization is also a risk.

Surgery Surgery is the treatment of choice for AV malformations, trauma including pulmonary artery rupture and treatment

Figure 3. The contrast enhanced CT aorta/thorax demonstrates multiple enlarged bronchial arteries, more evident on the right.

resistant mycetoma. Otherwise, it is indicated only following failure of BAE,8 due to high mortality rates, particularly in the context of significant comorbidities.2

Medical treatment Treatment of the underlying cause should be initiated when possible. Treatments include antibiotics for infection, antituberculous therapy in the case of TB and systemic antifungals for Aspergillus lung disease. Bleeding abnormalities should be treated with the 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.



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haemorrhage, management should be in conjunction with renal physicians and may include immunosuppression and plasma exchange.37 Although tranexamic acid is often used, the evidence for its use is limited mainly to CF.38 Intravenous vasopressors have been advocated but currently their use is probably best restricted to patients with CF in specialist centres.39 The treatment of pulmonary embolism and significant haemoptysis provides an uncomfortable situation for the clinician and risk benefit ratios of immediate anticoagulation will have to be considered.

Case Outcome The patient was treated with analgesia, intravenous tranexamic acid, intravenous terlipressin and intravenous ceftazidime and colomycin. She remained haemodynamically stable, and was subsequently transferred to a specialist centre with a view to bronchial artery embolization. She proceeded to undergo contrast CT of the thorax/aorta (Figure 3), which demonstrated multiple enlarged bronchial arteries with two arteries identified for embolization. The CT also demonstrated severe bronchiectasis and small airway disease. Angiography and bronchial artery embolization were undertaken (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.

References 1. Amirana M. An aggressive surgical approach to significant hemoptysis in patients with pulmonary tuberculosis. The American review of respiratory disease. 1968; 97: 187–192. 2. Corey R, Hla KM. Major and Massive Hemoptysis - Reassessment of Conservative Management. American Journal of the Medical Sciences. 1987;

Fam Physician. 2005; 72: 1253–1260. 17. National Institute for Health and Clinical Excellence. The Diagnosis and Treatment of Lung Cancer CG24. London: National Institute for Health and Clinical Excellence. 2005. 18. Poe RH, Kallay MC, Israel RH et al. Utility of Fiberoptic Bronchoscopy

294: 301–309. 3. Håkanson E, Konstantinov IE, Fransson SG., Svedjeholm R. Management of life threatening haemoptysis. British Journal of Anaesthesia. 2002; 88: 291–295.

in Patients with Hemoptysis and a Nonlocalizing Chest Roentgenogram. Chest. 1988; 93: 70–75. 19. Sakr L, Dutau H. Massive haemoptysis: An update on role of bronscopy

4. Ibrahim WH. Massive haemoptysis: the definition should be revised. European Respiratory Journal. 2008; 32: 1131–1132. 5. Crocco JA, Rooney JJ, Fankushen DS, DiBenedetto RJ, Lyons HA. Massive hemoptysis. Arch Intern Med. 1968; 121: 495–498. 6. Cauldwell EW, Siekert RG, Lininger RE, et al. The bronchial arteries: an anatomic study of 150 human cadavers. Surg Gynecol Obstet. 1948; 86:

in diagnosis and management. Respiration. 201; 80: 38–58. 20. Haponik EF, Fein A, Chin R. Managing Life-Threatening Hemoptysis*. Chest. 2000; 118: 1431–1435. 21. Gourin A, Garzon AA. Control of hemorrhage in emergency pulmonary resection for massive hemoptysis. Chest. 1975; 68: 120–121. 22. Klein U, Karzai W, Bloos F et al. Role of fiberoptic bronchoscopy in conjunction with the use of double-lumen tubes for thoracic anesthesia -

395–412. 7. Marshall TJ, Jackson JE. Vascular intervention in the thorax: bronchial artery embolization for haemoptysis. European Radiology. 1997; 7:

A prospective study. Anesthesiology. 1998; 88: 346–350. 23. Lordan JL, Gascoigne A, Corris PA. The pulmonary physician in critical care. Illustrative case 7: Assessment and management of massive

1221–1227. 8. Jean-Baptiste E.

16. Bidwell JL, Pachner RW. Hemoptysis: Diagnosis and mangement. Am

Clinical assessment and management of massive

hemoptysis. Crit Care Med. 2000; 28: 1647. 9. Mcdonald DM. Angiogenesis and Remodeling of Airway Vasculature in Chronic Inf lammation. Am J Respir Crit Care Med. 2001; 164: S39–S45.

haemoptysis. Thorax. 2003; 58: 814–819. 24. American College of Surgeons Committee on Trauma: Advanced Trauma Life Support Course Manual. Chicago, Ill. American College of Surgeons. 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 revisited. A review of the etiologies of hemoptysis between 1986 and 1995. Mo Med. 1997; 94: 633–635. 12. Santiago S, Tobias J, Williams AJ. A Reappraisal of the Causes of Hemoptysis. Arch Intern Med. 1991; 151: 2449–2451. 13. The Resuscitation Guidelines 2010. The Resuscitation council (UK). 2010. 14. Marshall TJ, Flower CDR, Jackson JE. The role of radiology in the investigation and management of patients with haemoptysis. Clinical Radiology. 1996; 51: 391–400.

Radiology. 2004; 233: 741–749. 26. Flume PA, Mogayzel PJ, Jr., Robinson KA et al. Cystic Fibrosis Pulmonary Guidelines: Pulmonary Complications: Hemoptysis and Pneumothorax. Am J Respir Crit Care Med. 2010; 182: 298–306. 27. Pasteur MC, Bilton D, Hill AT. British Thoracic Society guideline for non-CFbronchiectasis. Thorax. 2010; 65: i1–i58. 28. Cahill BC, Ingbar DH. Massive Hemoptysis - Assessment and Management. Clinics in Chest Medicine. 1994;15: 147–168. 29. Conlan AA, Hurwitz SS. Management of Massive Hemoptysis with the 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

120: 1592–1594.

Fiberoptic Bronchoscope. Chest. 1989; 96: 473–476.



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31. Solomonov A, Fruchter O, Zuckerman T, Brenner B, Yigla M. Pulmonary hemorrhage: A novel mode of therapy. Respiratory Medicine. 2009; 103: 1196–1200. 32. Hiebert CA. Balloon Catheter Control of Life-Threatening Hemoptysis. Chest. 1974; 66: 308–309.

36. White RI. Bronchial Artery Embolotherapy for Control of Acute Hemoptysis. Chest. 1999; 115: 912–915. 37. Chan A, Louie S, Leslie K, Juarez M, Albertson T. Cutting Edge Issues in Goodpasture's Disease. Clinical Reviews in Allergy and Immunology. 2011; 1–12.

33. Dumon JF, Reboud E, Garbe L, Aucomte F, Meric B. Treatment of

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Tracheobronchial Lesions by Laser Photoresection. Chest. 1982; 81:

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35. Remy J, Voisin C, DC, ea. Traitement des hémoptysies par embolisation de la circulation systémique. Ann Radiol (Paris). 1974; 17: 5–16.



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Viewpoint

Viewpoint: Norovirus Outbreak on the AMU – A Lesson In Shared Clinical Leadership S Krishnamoorthy & N Murch

Introduction

Sanjay Krishnamoorthy MBChB MRCP Specialist Registrar Acute Medicine The Royal Free Hospital Nick Murch MB.BCh FHEA PG Cert Med Ed MRCP, Locum Consultant in Acute Medicine and Medical Education The Royal Free Hospital Correspondence: Sanjay Krishnamoorthy Department of Acute Medicine 8th Floor, The Royal Free Hospital Pond Street London NW3 2QG Email: skmoorthy@ doctors .net.uk

Three times a year, the first Wednesday of the month heralds a changeover of junior doctors within our hospital. This year, the first Wednesday in December provided a different kind of challenge. The voice on the phone confirmed the words that no one wanted to hear: “You have three confirmed cases of Norovirus and you have to close to new admissions”. Over the last year, there have been 1852 outbreaks of Norovirus (formerly known as ‘Norwalk Virus’) reported to the Health Protection Agency1 (HPA), affecting 18,600 patients and 4900 staff. This resulted in a loss of 22,800 bed days. The impact of the yearly winter outbreaks on the health services is undeniable. It is estimated to cost the NHS in excess of £100 million per annum.2 In addition, as the above figures illustrate, it poses a significant risk to staff working within the health sector. An outbreak of an infective viral gastroenteritis proves a unique challenge within the acute medical setting. The functioning of acute services within a hospital is dependant on the rapid turnover of patients, for which the specialty of Acute Medicine plays a key part. There is an increasing shift in policy, moving from the traditional focus solely on infection control, to a more pragmatic approach involving maintaining acute services and minimising disruption to patient care.3 This requires a consensus multi-disciplinary team approach to acute care provision, and strong clinical leadership.

How did we deal with the outbreak? A meeting was immediately convened between our infection control team, matrons and acute medicine consultants. The hospital protocol deemed that immediate ward closure was imperative. However the impact of this would be substantial, putting significant strain both on the AMU and the Emergency Department (ED) for the admission of new patients. It was clear that a rapid re-organisation of services was required to ensure the continued delivery of clinical care for acute medical patients.

A multidisciplinary approach A multi-disciplinary team was assembled including nurses, physiotherapists, occupational therapists,

doctors and a discharge co-ordinator to function as the designated dirty team. The team was to staff the AMU, and not engage in patient contact outside the ward. It was agreed that medical registrars would staff the ‘shop f loor’, allowing the decision making process to continue whilst minimising the footfall of junior doctors and consultants within the AMU. All members of the dirty team were required to wear scrubs whilst in the ward, and these were to be discarded on leaving the ward, helping to minimise the exposure to other colleagues in communal areas of the hospital (Doctors’ Mess, coffee shops etc). The focus of care was to expedite discharge of stable patients to their own homes, whilst minimising disruption to care for patients who were required to remain in hospital. This involved engaging the Post Acute Care Evaluation (PACE) team, community physiotherapists and general practitioners. Emphasis was placed on effective handover between the hospital and community teams. Occupational therapists from clean wards provided services such as home access visits to ensure the safe discharge of vulnerable patients.

Isolation of the Assessment Area and Ambulatory Care The assessment area of the AMU was geographically isolated from the rest of the ward by closing two large double doors. A clean nurse was in charge, overseeing patients in this area and medical care was provided by the on-call medical team. This area also provides care for ambulatory patients, which is usually overseen by the AMU ward team. For the short duration of the outbreak however this responsibility was placed with the acute medical team on-take to ensure uninterrupted provision of this essential service.

Maintenance of Non-Invasive Ventilation facility The Acute Medical Unit in our hospital provides non-invasive ventilation (NIV) services for the hospital outside the Intensive Care Unit setting. Recognising the need for potentially life-saving intervention, patients who needed NIV, were carefully selected and were fully consented on the risks of admission into an infected ward. The risks



Acute Medicine 2012; 11(1): 46-48

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Viewpoint: Norovirus Outbreak on the AMU – A Lesson In Shared Clinical Leadership

and benefits were clearly explained to both patients and family members prior to the transfer. A designated bay for the provision of NIV was identified with a dedicated nurse allocated to this bay. It was recognised that cross contamination was likely given that the same medical staff were involved in the care of symptomatic patients with diarrhoea and patients on NIV. Additional precautions were therefore taken with careful hand-washing and cleaning of clinical equipment used in the bay. This proved successful and we provided the necessary acute intervention for critically unwell patients without spreading the infection. Critical in this scenario was the careful consenting of patients needing NIV, and the riskbenefit analysis of patients needing an acute intervention versus the likelihood of contracting a viral gastroenteritis.

diseases, such as the haematology wards, oncology wards and the transplant units were required to be symptom free for forty-eight hours prior to moving on to the service. This was essential in maintaining a sterile environment for some of our most vulnerable patients. Inevitably this placed a strain on these clinical areas. Doctors who were already working on these wards were asked to continue working there, giving their colleagues a forty-eight hour window within which to be symptom free. A cross speciality meeting was held between the heads of departments to ensure adequate staffing across all the wards in the hospital.

Outcome

The Radiology team were engaged into the process, ensuring that all urgent imaging was undertaken whilst adhering to safety precautions to minimise the spread of infection. Urgent chest and abdominal plain films were performed using mobile equipment, which was disinfected after imaging. Computerised tomography (CT) scans were deferred to the end of the list whenever possible. Cleaning services were expedited after scanning to ensure a terminal clean prior to resuming the service.

The outbreak lasted on the AMU for ten days. We were successful in limiting the spread to other wards. Even with maintenance of careful hygiene standards within the wards, we were unable to prevent the sporadic spread of virus to previously asymptomatic patients across bays. This once again reiterates the highly infectious nature of Norovirus, and justifies the decision taken early to close the entire ward to new admissions. The AMU was subsequently re-opened by decanting individual bays of patients up to our seventeen bedded overf low unit and subsequently deep cleaning the bays. This approach was rolled out across the entire AMU.

Relatives and visitors

Discussion

Hospital policy dictated that relatives and visitors were not allowed on the ward whilst the it remained closed. This proved challenging for patients who did not converse in English and for patients who were terminally ill. A pragmatic approach was adopted, ensuring that the merits of each case were considered individually. By outlining the risks involved and highlighting precautions that they could take (wearing scrubs, diligent hand-washing), we were able to cater to the best interests of these patients and the wishes of their families.

We were largely successful in curbing the potentially devastating effects a widespread Norovirus outbreak can have on a hospital. The key approaches are summarized in Table 1. An outbreak of Norovirus has unique implications to the AMU. Maintaining an active AMU is central to managing an intake of patients through the ED. A key component to our management of the outbreak was the use of the winter overflow ward. This had been identified early in the summer as focus for patient care in the eventuality of an outbreak. This allowed us to maintain our acute medical service. It is crucial for all Acute Medical Units to identify a potential area in their hospital which might be used in such eventualities. The assessment area within the AMU should also have the provision to be isolated from the remainder of the unit. This enables initial stabilisation of newly admitted patients, who are in the most vulnerable stage of their illness, before transfer to other areas of the hospital.

Radiology involvement

Establishment of a temporary AMU A ward with seventeen private rooms with ensuite showers had previously been designated the winter overflow ward. Resources were rapidly mobilised to staff this ward as a temporary Acute Medical Unit. Acute physicians managed patients on this ward, ensuring the provision of optimum acute care and a continued rapid turnaround of patients. Junior doctors on rota to work on the AMU worked with a consultant to effect management plans. AMU nursing staff, lead by a charge nurse provided critical input in managing patients on the overflow ward. In order to maintain adequate staff levels, bank nurses were hired to assist the team. Furthermore, the overflow ward was provided with a duty physiotherapist, occupational therapist and discharge coordinator to ensure uncompromising provision of service. This provided the overflow ward with the capabilities of a fully functioning AMU.

Impact on other departments Junior doctors moving in the change-over, to higher dependency wards with patients susceptible to infectious


Importance of shared leadership A key component of our success was the shared leadership taken by the infection control team and the acute medical consultant. The different perspectives of the two departments were immediately apparent: the infection control team was keen to close the ward, having identified culture positive patients across different bays; the AMU consultant was more focussed on ensuring that the closure of the ward did not adversely affect patient care. Both perspectives have their own merits; however, recent guidelines stress the importance of maintaining the acute medical service.3 If facilities to decant existing or new patients onto a clean ward are not available, we need to consider isolating bays within the AMU in which


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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 required, including compromising on the provision of single sex bays, to maintain the balance between infection control, provision of clinical care and patient dignity. A multidisciplinary approach, ensuring involvement of patients and their carers in the process, is critical to this process.

Learning points – a trainee’s perspective As a medical registrar, I was deeply entrenched in the management of patients during this outbreak. I was one of the designated dirty team - a tag that I initially resented. However I subsequently found the experience hugely valuable, gaining first hand experience in the importance of shared clinical leadership. There was a smooth transition in service provision to a pre-decided, well thought out contingency plan. Guidelines were followed, and the balance between infection control and clinical care

was maintained through team working and dialogue. A team of health professionals, each with their individual areas of expertise, worked collectively towards a common goal: the safe and efficient delivery of acute care The publishing of the Medical Leadership Competency Framework4 (MLCF) highlights the need for all healthcare professionals to show medical leadership in the delivery and transformation of services. The concept of shared clinical leadership heavily underpins these recommendations. I gained valuable insight into the camaraderie that develops between team members when faced with a challenging situation. The experience helped me to understand the concepts of team building, which I now recognise are imperative in becoming an effective leader. I feel, as a result, better equipped to deal with similar outbreaks in the future.

References 1. Hospital Norovirus Outbreak Reporting. Update September 2010. Health Protection Agency. 2. Lopman BA, Reacher MH, Vipond IB, Hill D, Perry C, Halladay T, et al. Epidemiology and cost of nosocomial gastroenteritis, Avon, England, 2002-2003. Emerg Infect Dis. 2004 Oct; 10(10): 1827–34. 3. Guidelines for the management of Norovirus outbreaks in acute and community health and social care settings. Authors: HPA, British

Infection Association; Healthcare Infection Society; Infection Prevention Society;

National

Concern

for

Healthcare

Infections;

NHS

Confederation. Website:www.hpa.org.uk/webc/HPAwebfile/HPAweb_c/ 1317131639453. 4. Medical Leadership Competency Framework – Enhancing Engagement in Medical Leadership. July 2010. Academy of Medical Royal Colleges and NHS institute for Innovation and Improvement.




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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.



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Picture Quiz Answer

A young patient with heart failure

H Patel, G Dhillon, A Bandali & N Patel

H Patel MRCP Cardiology registrar Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD G Dhillon MRCP Cardiology trainee Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD A Bandali MBBS Cardiology trainee Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD N Patel FRCP Cardiology Consultant Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD Correspondence: H Patel MRCP Cardiology registrar C/O Dr NR Patel Department of Cardiology Eastbourne District General Hospital Eastbourne BN22 2UD Email: [email protected]

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 • Cardiac MRI and endomyocardial biopsies can be helpful • There is a limited role for antiviral and immunosuppressive agents in management

Answers 1. Sinus tachycardia, saddle shaped ST segment elevation in leads V2-6 and II. 2. Fulminant myocarditis. 3. Viral or secondary to cannabis. 4. The history of syncope and an EF