Internal Medicine

Introduction       

Urinary tract infection (UTI) is the second most common infectious complaint in geriatric clinics overall, and the most common outpatient complaint caused by bacteria.¹ The diagnosis and treatment of UTI in the elderly is not the same as treating UTI in adults. In frail elderly patients with age-associated multiple severe underlying disorders and cognitive impairment, early recognition of bacteraemic UTI and prompt, appropriate treatment are critical in reducing the mortality.²Also, the extensive and inappropriate use of antimicrobial agents has invariably resulted in the development of antibiotic resistance which, in recent years, has become a major problem worldwide.³ The diagnosis and empirical treatment of UTI in the elderly is challenging and a sound knowledge of the prevalent epidemiology of bacteria and their resistance pattern is necessary for the same. However, there is not much information on the aetiology and resistance pattern of UTI in the elderly in India. This study was done to find out the present uropathogen profile causing UTI in our centre and their antibiotic resistance patterns.

Subjects and methods

This prospective study was done at our tertiary care centre from January to December 2008. The study included all patients who were admitted or visited the outpatient departments in the hospital with symptoms of UTI during the study period and had UTI confirmed by positive urine culture reports. Only one sample from each subject was considered. Subjects with clinical symptoms of UTI but no growth on culture were excluded from final analysis. Subjects who were treated with another antimicrobial within the previous 48 hours, or within 24 hours if only a single dose and in the presence of an appropriate positive culture and ileal loops or vesicoureteral reflux were also excluded from the study. Complete data regarding demography, sex preponderance, associated symptoms, pathogenic organisms causing UTI and their antibiotic resistance were collected.

Overall, 194 subjects were included in the study (male: 116, female: 78). The mean age of the study population was 73.54±7.19 years, ranging between the ages of 65 and 96. The distribution of patients according to gender across various age groups is given in table 1. A general trend of more male subject enrolment was seen across all the age groups. 

Isolation and identification of uropathogens

A clean catch midstream specimen, or suprapubic aspirate in subjects who were unable to give the former, was collected in a sterile, wide-mouth, leak-proof container to hold approximately 50ml from these subjects. Using a calibrated loop method of loop diameter 4 mm, 10 µL of the uncentrifuged specimen was transferred onto the agar plate and streak, using the modified Mayo’s technique without flaming the loop for isolation, and incubated at 35- 37⁰C for 24 hours. A specimen was considered positive for UTI if a single organism was cultured at a concentration of >10⁵ Colony Forming Units/ml. The Gram-positive and Gram-negative organisms culture isolates were further identified by using various biochemical reactions up to genus/species level wherever applicable.

Antibiotic sensitivity testing

In the presence of any potential growth, antibiotic sensitivity testing was done by the Modified Kirby-Bauer disc diffusion method according to the Clinical and Laboratory Standards Institute (CLSI) guidelines.⁴ The antibiotics tested were Imepenem, Meropenem, Ciprofloxacin, Ofloxacin, Norfloxacin, Amikacin, Gentamicin, Nitrofurantoin and Cotrimoxazole (Pathoteq Labs, India).

Extended Spectrum Beta-Lactamase (ESBL) detection

The screening for ESBL was done using Cefpodoxime (<17mm), Ceftazidime (<22mm), Aztreonam (<27mm), Cefotaxime (<27mm) and Ceftriaxone (<25mm). If the organisms showed the zone of inhibition lower than the minimum for any antibiotic disc, ESBL positivity was suspected. The phenotypic confirmation was done by testing the strain against Ceftazidime (Ca) and Ceftazidime/Clavulanic Acid. A > 5mm diameter of the zone of inhibition for Ceftazidime/Clavulanic Acid in comparison to Ceftazidime was considered indicative of ESBL production. Escherichia coli (E. coli) ATCC 25922 was used as ESBL negative and Klebsiella pneumoniae (K. pneumoniae) 700603 was used as ESBL positive reference strain.⁴

Statistical analysis

Descriptive statistics (totals, means, percentages, and standard deviations) were conducted using the statistical software package - SPSS Version 16.0 (SPSS Inc., Chicago, USA). Age, gender, organisms causing UTI, their antibiotic sensitivity and resistance, symptomatology of these subjects, and risk factors for UTI were included in the analysis and the results presented in tables and figures.

Results

Fever (57/194 - 29.4%) and dysuria (52/194 - 26.8%) were common symptoms of most UTI patients (Fig. 1). Diabetes mellitus (DM) and recent uro-genital instrumentation were the most common risk factors associated with UTI in the present study (Table 2). The organism profile and their antibiotic resistance profile were similar in patients with or without DM.

Figure 1. Various symptomatologies seen in patients with urinary tract infection during the initial presentation

Table 2. Frequency of various risk factors in subjects with urinary tract infection.

E. coli (138/194 - 71.1%) was the most commonly isolated pathogen responsible for UTI in the present study (Figure 2). 56.2% of the total infection was caused by ESBL positive organisms. The antimicrobial potency and spectrum for nine selected antimicrobial agents (Imepenem, Meropenem, Ciprofloxacin, Norfloxacin, Ofloxacin, Gentamicin, Amikacin, Nitrofurantoin and Cotrimoxazole) against the uropathogens were studied. The highest and least antibiotic resistance was noted against fluoroquinolones (79.9%) and carbapenems (3.61%) respectively (Fig. 3).

Figure 2. Frequency and distribution pattern of urinary tract infection pathogens and percentage Extended Spectrum Beta-Lactamase (ESBL) production.

Figure 3. Resistance pattern to various antibiotics of the uropathogens

Discussion

While increased frequency and dysuria are usual symptoms of UTI, uncertainty looms around the same as these symptoms can be masked by catheterisation, or be common and chronic in the elderly even in the absence of UTI.^5-10Fever was the most common symptom of UTI in the present study as with similar studies worldwide.^11-13 Studies have found that the elderly do not lack a febrile response; that an elevated temperature was the most common initial symptom, a marker for a serious infection, and the most important clinical indicator for antibiotic treatment.^14-16 Whitelaw et al¹⁷ reported that a delay in interpreting fever as a symptom of UTI led to a high mortality rate in the elderly within 24 hours of admission.

Diabetes isconsidered as an important risk factor for UTI with manyauthors having defined UTI in patients with DM as complicated when the UTI is symptomatic.^18-19 However, the authors did not find that DM influenced the organism profile and their antibiotic resistance in the present study. Bonadio et al²⁰ studied the influence of DM on the spectrum of uropathogens and antimicrobial resistance in elderly adult patients with asymptomatic UTI (mostly hospital-acquired). They found that DM per se did not seem to influence the isolation rate of different uropathogens and their susceptibility patterns to antimicrobials. These findings indicate that, although DM is a known immunomodulator, the role played by the same in altering the antibiotic resistance is minimal compared to recent invasive procedures.

Although the uropathogen profile of the present study resembles similar studies worldwide, the antibiotic resistance of these organisms was unusually high.^{2, 21} Cotrimoxazole is the recommended drug for treating UTI. However, more than one third of the study subjects were resistant to the first-line drug. 79.9% of the uropathogens were resistant to fluoroquinolones, which are considered as the second-line drug.  As prior fluoroquinolone use is a known risk factor for fluoroquinolone-resistantE. coli infection, it is plausible that frequent fluoroquinolone prescriptions may be contributing to the observed resistance.^22-23 Aypak et al ²⁴ found that treatment durations were statistically longer than the recommended three-day course when patients were empirically treated with fluoroquinolones due to increased resistance rates, and suggested to discourage the empirical use of fluoroquinolones in UTI.

The most troublesome finding of the present study is that ESBL-positive organisms accounted for 56.2% of the total infection. Not much information on ESBL-producing organisms causing UTI is available from India and most of these reports are from the younger population. The prevalence of ESBL-positive UTI in these studies varied between 26.6% and 48.3%.^25-26 To the best of our knowledge, this is the highest ever reported prevalence of ESBL-positive UTI in the elderly worldwide. ESBL-producing organisms are frequently resistant to many of the antimicrobial agents usually recommended for the treatment. As lesser new antibiotics are available for their management, we need to be concerned of this issue in years to come especially in tertiary care centres.  A unified antibiotic protocol is necessary to limit the morbidity and mortality associated with inappropriate and under-treatment of UTI.

The limitations of the present study were that altered mental status was not considered as one of the clinical manifestations of UTI in the elderly, which could have mitigated the total number of study subjects included in the study.  In addition, the phenotypic confirmation of ESBL-positive organisms was done using only Ceftazidime/Clavulanic Acid and not Cefotaxime/Clavulanic Acid as per the latest CLSI guidelines. As a result, there may be under-reporting of the incidence of ESBL organisms in the present study.

In conclusion, we report a significantly high resistance to common antibiotics among the uropathogens in the present study. Furthermore, the very high rate of ESBL-positive UTI is of concern, and monitoring for the same is necessary to prevent treatment failure and increased morbidity and mortality with UTI.

Case History

Introduction

Introduction

Syncope is a common condition encountered in acute medical practice. Many patients with syncope are initially labelled as having “collapse query cause”. It is defined as transient loss of consciousness (T-LOC) due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery¹. Incidence of syncope is difficult to determine accurately as many cases remain unreported. Some studies quote an overall incidence rate of a first report of syncope to be 6.2 per 100 person-years. Clearly this is age related and the incidence increases dramatically in patients over the age of 70 years². Syncope accounts for 1-6% of hospital admissions and 1% of emergency department (ED) visits per year^3-5. Hospital episode statistics from NHS hospitals in England reported a total of 119,781 episodes of collapse/syncope for the financial year 2008-09 which is about twice the number of episodes reported in the year 1999-2000. About 80% of patients were admitted and they have an average length of stay of 3 days accounting for over 269,245 bed days during that financial year⁶.

Syncope is also associated with significant mortality and morbidity if left untreated. Literature reports a 6-month mortality of 10%, which can go up to 30% if cardiac syncope is untreated⁷. Non-cardiac syncope is associated with a survival rate comparable to people with no syncope². Syncope is also a risk factor for fractures related to falls especially in elderly and can cause significant morbidity in this group⁸. In addition, there are significant health care related costs associated with management of syncope. Cost per diagnosis can vary from over £611 in the UK to €1700 in Italy. Hospitalisation alone accounted for 75% of cost in some studies^9,10. Diagnosis of this condition can be difficult especially if there is a lack of structured approach. Over the last few years this topic has attracted enormous interest and several studies have been published, aiming at improving the approach to this condition. Standardised syncope pathways improve diagnostic yield and reduced hospital admissions, resource consumption and over all costs¹⁰. Recently the task force for the diagnosis and management of syncope of  the European Society of Cardiology published guidelines for the diagnosis and management of syncope¹. However, in spite of the available evidence very few hospitals have standardised syncope pathways for the management of this complex condition. Only 18% of EDs have specific guidelines and access to a specialist syncope clinic¹¹. This article focuses on evidence based structured evaluation of syncope. Current practice in the management of syncope Due to the difficulty in diagnosis and mortality associated with this condition, a cautious approach may be taken by physicians resulting in hospitalisation of majority of patients presenting with syncope. We recently audited the practice of syncope in our hospital, which is a tertiary centre in the north of Scotland. 58 patients admitted with this condition over a period of a month were included in the audit. It showed an average length of stay (LOS) of 4.76 days in these patients. Due to a lack of methodical approach and standardised pathway for management of this condition many patients were subjected to several inappropriate inpatient investigations significantly prolonging the LOS and increasing the cost. Only 7 (12%) cardiac events were observed in this group and in retrospect a good methodical approach would have predicted these events. It should be noted that even in the geriatric population, reflex syncope that carries a benign prognosis is more common than cardiac syncope². A systematic approach to the management of syncope (Figures 1 and 2).   The causes of syncope can be broadly divided in to cardiac causes and non-cardiac causes (Table 1). Initial evaluation leads to a diagnosis in less than 50% patients in most instances^4,12-14. If there is uncertainty about diagnosis then the patient is risk stratified. High-risk patients are hospitalised, evaluated and treated whereas early discharge could be considered in low risk patients. Aetiology of Syncope⁴¹

 Initial evaluation (Table 2)

 History Many patients with syncope are initially labelled as having “collapse query cause”. Loss of postural tone is termed “collapse”. Indeed, the term “collapse query cause” does not give any useful information regarding the underlying condition. A clear history from the patient and the bystander or witness (if available) is the key to the diagnosis. Firstly, determine if the collapse was associated with loss of consciousness (LOC). LOC can be transient (T-LOC) or prolonged. Categorising “collapse” is important at this stage as the aetiology and approach to each category is different (Figure 1). Secondly, establish if the collapse was syncopal. The LOC should be transient (e.g. did the patient regain consciousness in the ambulance, before or on arrival to hospital?), of rapid onset and associated with a spontaneous complete recovery. Also the mechanism should be due to transient global hypoperfusion. T-LOC secondary to other mechanisms such as trauma and brief seizures should be excluded. On occasions syncope could be associated with brief jerking movements mimicking seizures¹⁵. Also note that a transient ischemic attack (TIA), commonly listed as a differential diagnosis of syncope by physicians, is not a cause of syncope as this is not associated with global cerebral hypoperfusion. The absence of a coherent history because patient had no recollection of events and there was no witness account available can make this distinction difficult. This is also particularly difficult in the elderly with cognitive impairment. Other useful information includes whether the syncope was associated with postural change. Orthostatic hypotension occurs after standing. If present it will be useful to check drug history (new vasodepressive drugs). Features suggestive of Parkinson’s disease or amyloidosis may raise the possibility of autonomic neuropathy. A strong family history of sudden cardiac death may be of relevance. Table 3 summarises the features of neurally mediated and cardiac syncope. Table 3 Features suggesting neurally mediated and cardiac syncope⁴²

Physical examination The next step is a thorough physical examination. This should include an ABC approach if the patient is very ill and particular attention should be given to exclude immediate life threatening conditions such as pulmonary embolism, acute myocardial infarction, life threatening arrhythmias, acute aortic dissection, seizures etc… Recording the vital signs is important as it may give a clue to diagnosis (e.g., acute hypoxia may indicate massive pulmonary embolism). Recording postural blood pressure when lying and during active standing for 3 minutes is useful to exclude orthostatic hypotension¹. Recording a deficit in blood pressure in both arms may be a useful clinical finding especially if acute aortic dissection is suspected. Thorough cardio respiratory examination may reveal an obvious condition such as cardiac failure or aortic stenosis. Patients should also be examined for potential injuries as a result of syncope. Standard ECG A 12 lead ECG should be performed in all patients admitted with syncope. The abnormalities in table 4 would suggest a cardiac aetiology. The QT interval should always be measured, as it is a commonly overlooked abnormality. Blood tests Blood tests are usually unhelpful in establishing a diagnosis but can detect metabolic abnormalities such as hypoglycaemia, electrolyte abnormalities and other causes to explain LOC especially when witness account is not available. An acute drop in haemoglobin suggests blood loss. One recent study claims the usefulness of brain natriuretic peptide (BNP) for predicting adverse outcomes in syncope but it is not externally validated yet and it is too early to recommend for routine clinical practice¹⁶. Pacemaker check It is not uncommon to see a patient with a pacemaker implanted, admitted to hospital with syncope. In these circumstances, it is essential to rule out a device malfunction although this is not a common cause of syncope. A preliminary and easy test will be interrogating the pacemaker if available. This should pick up any problems with the pacemaker in most instances. With the above information establishing a diagnosis will be possible in a significant proportion of patients. Further investigations and management should be guided by the underlying diagnosis¹. However in over half of patients the diagnosis may still be uncertain^12,13,17. The following section explains the management of unexplained syncope. Risk stratification in patients with unexplained syncope (Tables 4 and 5) Table 4   ECG changes in ‘high-risk’ Syncope⁴¹

 Table 5 – Clinical features of high-risk syncope^1,18-23

 When the cause of syncope is uncertain it is essential to risk stratify patients to enable appropriate treatment and further investigation. Risk stratification tools There are several scoring systems for risk stratification of syncope.  Syncope Evaluation in the Emergency Department Study (SEEDS), Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL score), Evaluation of Guidelines in SYncope Study (EGSYS score), San Francisco Syncope Rule (SFSR), The Risk stratification Of Syncope in the Emergency department (ROSE) and American College of Emergency Physicians clinical policy are the popular ones and each has its own advantages and disadvantages^1,16,18-23. Discussing each scoring system is beyond the scope of this article and we shall restrict the discussion to the summary of these risk stratification tools (Table 5). It will be too early to include all the factors mentioned in the ROSE study, as it is not externally validated yet. It could be argued that taking all the risk factors described may increase admission rates but this approach may at least not miss the high-risk patient. This is a developing field and more evidence is likely to be published soon. High-risk vs. low-risk syncope: A high-risk syncope patient is the one where a cardiac cause is likely and where the short-term mortality is high due to major cardiovascular events and sudden cardiac death. High-risk syncope is said to be present if any of the features in the table 4 or 5 are present. Management of low-risk syncope Patients with a single or very infrequent syncope are usually reassured and discharged, as the short-term mortality is low^1,2. Tilt table test is not usually required where a single or rare episode of neurally mediated syncope is diagnosed clinically. One exceptional circumstance where single rare episodes are investigated further with a tilt table test is when there could be an occupational implication (e.g. aircraft pilot) or if there is a potential risk of physical injury. Patients with recurrent unexplained syncope need to be further investigated (see below). Management of high-risk syncope / suspected cardiac syncope High-risk patients usually require hospitalisation and inpatient evaluation. Other high-risk patients who may be considered for admission are vulnerable patients susceptible to serious injuries, for example, elderly patient or a patient with multiple co-morbidities. Further investigations (Table 6)

* Specialist Investigation Echocardiography Echocardiography is a relatively inexpensive and non-invasive investigation. It should be performed if there is a clinical suspicion of a significant structural abnormality of heart such as ventricular dysfunction, outflow tract obstruction, obstructive cardiac tumours or thrombus, pericardial effusion etc… The yield of this test is low in the absence of clinical suspicion of structural heart disease. However in the presence of a positive cardiac history or an abnormal ECG, one study detected LV dysfunction in 27% of patients and half of these patients had syncope secondary to an arrhythmia. In patients with suspected obstructive valvular disease 40% had significant aortic stenosis as a cause of syncope²⁴. ECG monitoring These tests have utility in identifying arrhythmogenic syncope. If a patient has syncope correlating with a significant rhythm abnormality during the monitoring period with the device, then the cause of syncope is due to the underlying rhythm abnormality. On the other hand, if no rhythm abnormality is recorded during a syncopal attack, then an underlying rhythm problem as a cause of syncope is excluded. Therefore, these tests are meaningful only if there is a symptom-rhythm correlation, which is the working principle of these devices. In the absence of syncope, during the monitoring period, these tests may pick up other abnormalities that may be relevant. For example, rapid prolonged supra-ventricular tachycardias, ventricular tachycardias, periods of high degree AV blocks (mobitz type 2 or complete heart block) or significant sinus pauses >3seconds (except during sleep, negatively chronotropic therapy and trained athletes), which will require further investigation or treatment. Telemetry  Telemetry can be used in inpatients. Although the diagnostic yield of this investigation is only 16%, given the high short-term mortality, this test is indicated in the high-risk group ¹. Usually patients are monitored for 24 to 48 hours although there is no agreed standard period for monitoring²⁵. Holter monitoring This involves connecting the patient through cutaneous patch electrodes. It records the ECG activity conventionally over 24-48 hours or at times up to 7 days. It is particularly useful only in patients who have frequent regular symptoms (≥1 per week). For this reason, the yield of this test can be as low as 1-2% in unselected population¹. Long inpatient waiting lists in some hospitals can significantly prolong the length of stay and cost. Selecting patients carefully for this test based on risk stratification will reduce costs and waiting lists. Carotid sinus massage This simple bedside test is indicated in patients over the age of 40 years with syncope of unexplained origin after initial evaluation. A ventricular pause lasting >3 s and/or a fall in systolic BP of >50mmHg defines carotid sinus hypersensitivity (CSH) syndrome. It is contraindicated in patients with recent cerebrovascular accidents (past 3 months) or with carotid bruit except when a Doppler study has excluded significant stenosis¹. Cognition test If an elderly patient had forgotten about the events, in the absence of an obvious cause, it may be useful to test cognition. If cognitive impairment is present, common problems associated with cognitive dysfunction should be considered e.g. falls, orthostatic hypotension. Other investigations In spite of the above tests if a cause is not determined, early specialist input is recommended for further investigation and treatment. The following non-invasive and invasive investigations may be appropriate in these circumstances. An external loop recorder This is a non-invasive form of electrocardiographic monitoring. The principle is same as that of Holter monitoring. External loop recorders have a loop memory that continuously records and deletes ECG. When activated by the patient, typically after a symptom has occurred, 5 – 15 min of pre-activation ECG is stored and can be retrieved for analysis. Studies have shown that they have increased diagnostic yield compared to Holter¹. They should be considered in patients who have symptoms on a monthly basis. A Tilt table test This is indicated in cases of recurrent unexplained syncope after relevant cardiac causes of syncope are excluded and a negative Carotid sinus massage performed in the absence of contraindications. It is also indicated when it is of clinical value to demonstrate patients susceptibility to reflex syncope and thereby to initiate treatment. Other less common indications are recurrent unexplained falls, differentiate jerking movements secondary to syncope and epilepsy, diagnose psychogenic pseudo syncope and differentiate orthostatic and reflex syncope. Indication of this test in the context of a single unexplained syncope is discussed above. Ambulatory blood pressure monitoring This may be useful in patients with unexplained syncope particularly in old age to check if there is an element of autonomic failure and if a single set of orthostatic blood pressure recording is not helpful. In one study, it has been shown that 25% of the elderly patients admitted with falls or syncope had postprandial hypotension especially after breakfast²⁶. It may be more readily available than a tilt table test in some centres. Exercise stress test This may be useful in a rare entity called exercise induced syncope. Outflow tract obstruction should be excluded by echocardiography before subjecting a patient to this test especially in the presence of relevant signs. However there is no evidence for supporting this test in investigating syncope in general population. Implantable loop recorders These are implanted subcutaneously. It needs to be activated either by the patient or a bystander after a syncopal attack. It is indicated in high-risk patients where a comprehensive evaluation did not establish an underlying diagnosis. In the absence of high risk factors, it is also indicated in patients with recurrent unexplained syncope especially if infrequent. Conventionally it is used as a last resort in patients with recurrent unexplained syncope as the initial costs are high. It has been shown in one study to be more cost effective than the conventional strategy and was more likely to provide a diagnosis in patients with recurrent unexplained syncope²⁷. However patients with poor LV function and those at high risk of life-threatening arrhythmias were excluded from this study. Coronary angiography or CT coronary angiography This may be helpful in suspected myocardial ischemia or ischemia related arrhythmias. Electrophysiological study may be considered in certain circumstances by cardiologists. When a standardised pathway is used, diagnosis is ascertained in 21% patients on initial evaluation and further 61% patients with early investigations. Only in 18% patients the diagnosis was still uncertain¹². Other studies have shown similar results²⁸. Although these results are from a dedicated syncope unit following a standardised pathway, these could be extrapolated to any unit following these standardised pathways. Further management is dictated by the underlying diagnosis with early specialist input for appropriate treatment. Treatments Single or rare episodes of reflex syncope do not require treatment. However, recurrent troublesome reflex syncope may warrant treatment. Treatment modalities are primarily non-pharmacological such as tilt training, physical counter pressure manoeuvres (leg crossing, hand gripping) and ensuring adequate hydration²⁹. If refractory to non-pharmacologic measures midodrine (alpha agonist) may be considered in patients with frequent hypotensive symptoms^30,31. Fludrocortisone may be used in elderly but there is no trial evidence to support this. Betablockers have been presumed to lessen symptoms but are shown to be ineffective in several studies ³². They may potentially exacerbate bradycardia in carotid sinus syncope and are not recommended in treatment of reflex syncope. Treatment with cardiac pacing in reflex syncope is controversial and may be considered in patients with predominant cardio inhibitory response on carotid sinus massage (in CSH syndrome) or on tilt test (in reflex syncope). It should be noted that cardiac pacing has no effect on the often-dominant vasodepressor component of reflex syncope.  In patients with orthostatic hypotension, non-pharmacologic measures like increased salt and water intake, head up tilt sleeping, physical counter pressure manoeuvres, abdominal binders and compression stockings may help reducing symptoms. Midodrine is an efficient alternative in these circumstances and fludrocortisone also can be used.^33,34Syncope secondary to cardiac arrhythmias needs treatment if a causal relationship is established. Potential reversible causes such as electrolyte abnormalities and drug induced causes should be excluded. Cardiac pacing is a modality of treatment in significant bradyarrhythmias secondary to sinus node or advanced AV nodal disease such as mobitz type 2 block, complete heart block or tri-fascicular block. Catheter ablation and anti-arrhythmic drug therapy are the main modalities of treatment for tachyarrhythmias. Implantable cardioverter defibrillator may be indicated in patients susceptible to malignant ventricular tachyarrhythmias. Treatment of syncope secondary to structural cardio pulmonary abnormality will need surgical intervention if possible. Driving and Syncope Doctors are poor at addressing and documenting this issue³⁵. Table 7 gives some useful information from the DVLA website (http://www.dft.gov.uk/dvla/medical/ataglance)³⁶. This information is country specific and subject to change. Table 7 – Driving and Syncope in the UK³⁶

*Absent clinical evidence of structural heart disease and normal ECG** Abnormal ECG, clinical evidence of structural heart disease, syncope causing injury, recurrent syncope Syncope unitsSyncope units aim to evaluate syncope (and related conditions) in dedicated units consisting of generalists and specialists with an interest in syncope. A sufficient number of patients are required to justify such a unit. They are well equipped with facilities for recording ECG, blood pressures, tilt table, autonomic function testing, ambulatory blood pressure monitoring, and invasive and non-invasive electrocardiographic monitoring. It has been shown to be cost effective and reduces health care delivery costs by reducing admission rates, readmission rates and event rates. Examples include the Newcastle model, Manchester model and the Italian model.^12,18,37,38 Conclusions The incidence of syncope is increasing in the UK with an aging population. There is significant cost incurred in the delivery of health care for this condition. The approach to syncope varies widely amongst practising physicians due to lack of a methodical approach. A thorough initial evaluation yields a diagnosis in less than half of the patients. When the cause of syncope remains unexplained after initial evaluation, the patients should be risk stratified. While a patient with a single episode of low risk syncope can be reassured and discharged, those with high-risk features should be hospitalised for further management. Outpatient evaluation could be offered for low risk patients if recurrent. Early specialist input should be sought in high-risk syncope and recurrent unexplained syncope. This standardised approach or pathway will reduce cost by reducing hospitalisation, inappropriate investigations and length of stay. 

 Future Interests Syncope had been known for several decades and still remains a complex condition, as the exact mechanisms are poorly understood especially in non-cardiac syncope. Mechanism of syncope in the elderly patients may be different from those of young patients and studies should focus in understanding the mechanics. Further research is needed in risk stratifying syncope. It may enable us to develop more robust care pathways for management of syncope. The role of BNP in investigating and risk stratifying syncope need to be further clarified. In spite of sophisticated tests the cause of syncope in a proportion of patients remain uncertain. Studies should focus on the long-term outcome and management of syncope in this group. The role of implantable loop recorder in the investigation of syncope should be better defined and more studies should focus on when it should be offered in the pathway of management of syncope. Studies are also required to develop effective pharmacotherapies for this condition.  

Introduction:

Both Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) are diseases characterized by a high global prevalence, complex clinical course, and limited effectiveness of currently available antiviral therapy. Approximately 2 billion people worldwide have been infected with the HBV and about 350 million live with chronic infection. An estimated 600,000 persons die each year due to the acute or chronic consequences of HBV ^{1, 2}. WHO also estimates that about 200 million people, or 3% of the world's population, are infected with HCV and 3 to 4 million persons are newly infected each year. This results in 170 million chronic carriers globally at risk of developing liver cirrhosis and/or liver cancer ^{3, 4}. Hence, HBV and HCV infections account for a substantial proportion of liver diseases worldwide.

Introduction                                                                                                                              

Myocardial ischemia from coronary artery vasospasm can lead to variety of presentation including stable angina, unstable angina, myocardial infarction and sudden death ¹. Although, pathognomic clinical scenario includes symptom of chest pain, transient ST-segment elevation on the electrocardiogram(ECG), and vasospasm on a coronary angiography, atypical presentations have also been reported ². Various known physiological factors including stress, cold, hyperventilation and pharmacological agents including cocaine, ethanol, 5-Fluouracil, and triptans can precipitate a vasospastic attack. ^3-7.We report a case of ST-segment elevation due to right coronary artery vasospasm, in patient with hypoxic respiratory failure, and successful treatment with calcium channel blockers.

Initial reports of Obesity Hypoventilation Syndrome (OHS) date back as early as 1889¹, but it was not until 1955 that Auchincloss² and colleagues described a case of obesity and hypersomnolence paired with alveolar hypoventilation.  Burwell³ coined the term Pickwickian syndrome describing the constellation of morbid obesity, plethora, oedema and hypersomnolence.  Hypercapnia, hypoxaemia and polycythemia were described on laboratory testing. Obstructive Sleep Apnea (OSA) had not been described at that time and came to be recognized for the first time in the mid 1970s. With attention shifting to upper airway obstruction, hypercapnia began to get lesser emphasis and confusion began to emerge in describing OSA and OHS.  The term ‘Pickwickian’ began to be used for OSA-related hypersomnolence in the obese patient regardless of the presence of hypercapnia.  This confusion was finally settled by the American Academy of Sleep Medicine (AASM) in its published guidelines in 1999.⁴  The AASM statement identified that awake hypercapnia may be due to a predominant upper airway obstruction (OSA) or predominant hypoventilation (Sleep Hypoventilation Syndrome) easily distinguished by nocturnal polysomnography (PSG) and response to treatment.  Both disorders are invariably associated with obesity and share a common clinical presentation profile.

 
Salient features of OHS consist of obesity as defined by a BMI > 30kg/m², sleep disordered breathing, and chronic daytime alveolar hypoventilation (PaCO2 ≥ 45 mmHg and PaO2 < 70 mmHg). ⁴  Sleep disordered breathing, as characterized by polysomnography in OHS, reveals OSA (Apnea-hypopnea index [AHI]>5) in up to 90% of patients and sleep hypoventilation (AHI<5) in up to 10%.⁵  Daytime hypercapnia and hypoxaemia are the hallmark signs of OHS and distinguish obesity hypoventilation from OSA.  Severe obstructive or restrictive lung disease, chest wall deformities and hypoventilation from severe hypothyroidism, and neuromuscular disease need to be excluded before a diagnosis of OHS is established.  As obesity is becoming more prevalent in western society, this disorder has gained more recognition in recent years.  However, patients with this syndrome may still go undetected and untreated.  No population-based prevalence studies of OHS exist till date but, at present, can be estimated from the relatively well known prevalence of OHS among patients with OSA.  Recent meta-analysis with the largest cohort of patients (n=4250) reported a 19% prevalence of OHS among the OSA population, confirming an overall prevalence of about 3 per 1000.⁶
 
Whilst transient rectifiable nocturnal hypercapnia is common in patients with OSA, awake hypercapnia in OHS appears to be a final expression of multiple factors.  There has been a debate about BMI and AHI not being the most important independent predictors of hypercapnia in obese patients with OSA.  More definitive evidence for the role of OSA, however, is suggested by resolution of hypercapnia in the majority of patients with hypercapnic OSA or OHS with treatment, with either PAP or tracheostomy, without any significant changes in body weight or respiratory system mechanics. Yet some recent studies have shown that nocturnal hypoxaemia and diurnal hypercapnia, persist in about 50% of such individuals even after complete resolution of OSA with CPAP or tracheostomy.  This raises questions such as how good is AHI as a measure of severity of OSA?
 
It is intuitive to argue that obesity may exert its effect through mass loading of CO₂ due to (increased production via) higher basal metabolic rate or reduced functional residual capacity on lung function.  But why do only some severely obese patients with OSA go onto develop OHS?  Is the pathophysiology driven by the severity of BMI?  Whilst weight loss, particularly surgically-induced, clearly shows resolution of both OSA and hypercapnia⁷, the role of BMI as an independent factor for hypercapnia has been challenged by the fact that only a small fraction of severely obese patients do in fact develop chronic diurnal hypercapnia.  More importantly, not only can PaCO₂ be normalized in a majority of patients without weight loss and with positive airway pressure therapy (PAP), but awake hypercapnia can develop even at lower BMIs among the Asian population.  Some investigators have tried to explain the incremental role of BMI as follows.  In situations where AHI is not a presumed independent predictor of nocturnal hypercapnia, potential pathophysiologic contributors can include pre-event (apnea or hypopnea) amplitude in relation to the post-event amplitude.⁸  Such inciting events for nocturnal hypercapnia may then be perpetuated in the daytime by factors such as AHI, functional vital capacity (FVC), FVC/FEV₁, or BMI as shown in the largest pooled data to date.⁶  It has been shown that, for a given apnea/interapnea duration ratio, a greater degree of obesity is associated with higher values of PaCO₂.⁹ However the same group of investigators, in another study, did not find any of these factors to be related to the post-event ventilatory response.⁸
 
Looking further at the breath by breath cycle, the post-event ventilatory response in chronic hypercapnia may relate to eventual adaptation of chemoreceptors perhaps in consequence to elevated serum bicarbonate known to blunt the ventilatory drive.¹⁰ Or it may relate to whole body CO₂ storage capacity which is known to exceed the capacity for storing O₂.¹¹ With definite evolution in our understanding of hypercapnia among obese patients, these questions continue to dominate. Some of the more pressing ones include: are the predictors of daytime hypercapnia different from those of nocturnal hypercapnia in obese patients with OSA?  An understanding of these facts can help us with the more important understanding of the associated morbidity and mortality from OHS and its correct management.  In addition, what is the true effect of untreated OHS on mortality independent of the co-morbidities related to obesity and OSA?  Can morbidities like cor pulmonale and pulmonary hypertension be reversed with treatment of OHS?  How do we treat patients with OHS who fail CPAP/ BiPAP short of tracheostomy?
 

Clinical Presentation

Bisphosphonates, which have been on the market for roughly a decade, have raised safety concerns in the past. Several case series and multiple individual case reports suggest that some subtrochanteric and femoral shaft fractures may occur in patients who have been treated with long-term bisphosphonates. Several unique clinical and radiographic features are emerging. Recent media spotlight in the United States (US), implying that long-term use of alendronate could cause spontaneous femur fractures in some women, has reignited the debate about the safety of bisphosphonates. The question posed: is the risk of bisphosphonate-associated fractures so great that treatment should be stopped?
 
Postmenopausal women with osteoporosis are commonly treated with the bisphosphonate class of medications, one of the most frequently prescribed medications in the US. While alendronate therapy has been shown to decrease the risk of vertebral and femoral neck fractures in postmenopausal osteoporotic patients, recent reports have associated long-term alendronate therapy with low-energy subtrochanteric and diaphyseal femoral fractures in a number of patients. In the past four years reports have been published implying that long-term bisphosphonate therapy could be linked to atraumatic femoral diaphyseal fractures.^{1, 2} According to two studies reported recently at the American Association of Orthopedic Surgeons 2010 Annual Meeting, an unusual type of bone fracture has been reported in women who have taken bisphosphonates for osteopenia and osteoporosis for more than four years.^{3, 4} The first report was published in 2005. Odvina et al⁵ reported on nine patients who sustained atypical fractures, including some with delayed healing, while receiving alendronate therapy. These authors raised the concern that long-term bisphosphonate therapy may lead to over-suppression of bone remodelling, an impaired ability to repair skeletal microfractures, and increased skeletal fragility. There have been other reports of "peculiar" fractures - i.e. low-energy femur fractures that are typically transverse or slightly oblique, diaphyseal, or subtrochanteric, with thickened cortices and a unicortical beak - in patients who have been on long-term bisphosphonate treatment.^{1-4, 6}
 
In a small prospective study, Lane et al³ obtained bone biopsies from the lateral femurs of 21 postmenopausal women with femoral fractures. Twelve of the women had been on bisphosphonate therapy for an average duration of 8.5 years, and nine had no history of bisphosphonate use. They found that the heterogeneities of the mineral/matrix ratio were significantly reduced in the bisphosphonate group by 28%, and the crystallinity of the bone was significantly reduced by 33% (p < 0.05). The authors concluded that this suggested suppression of bone turnover, resulting in a loss of heterogeneity of the tissue properties, which may be a contributing factor to the risk of atypical fractures that we are starting to see. It is believed that long-term alendronate administration may inhibit normal repair of microdamage arising from severe suppression of bone turnover (SSBT), which, in turn, results in accumulation of microdamage. This process would lead to brittle bone and the occurrence of unexpected stress fractures, characteristically at the subtrochanter of femur. The typical presentation of these fractures consist of prodromal pain in the affected leg and/or a discrete cortical thickening on the lateral side of the femur in conventional radiological examination or the presentation with a spontaneous transverse subtrochanteric femur with typical features. The morbidity of atypical femoral fractures, particularly when bilateral, is high. Surgical intervention is generally required and healing may not be achieved for several years. Despite the lack of conclusive evidence of a causal relationship with bisphosphonate therapy, the current consensus is that treatment should be discontinued in patients who develop these fractures. In view of the high frequency of bilateral involvement, imaging of the contralateral femoral shaft with X-rays, MRI, or an isotope bone scan should be performed. MRI and bone scanning havegreater sensitivity than radiography for an incipient stressfracture. If lateral cortical thickening and/or an incipient stress fracture is seen, prophylactic surgical fixation should be considered. Suppressed bone formation in these patients provides a possible rationale for the use of anabolic skeletal agents, such as parathyroid hormone peptides, but at the present time the efficacy of this approach remains to be established. Parathyroid hormone not only has activated bone-formation markersin trials in humans but has also enhanced the healing of fracturesin studies in animals.  
                                                                                                                                                     
The question of whether these fractures are causally linked to bisphosphonate therapy is widely debated but as yet unresolved. Consequences of long-term suppression of bone turnover include increased mineralization of bone, alterations in the composition of its mineral/matrix composite and increased micro damage, all of which may reduce bone strength. Whilst these lend biological plausibility to a causal association, however, they do not constitute direct evidence. The bilateral fractures seen in many patients corroborate the suspicion that patients with bisphosphonate-associated stress fractures carry some other risk factor in addition to taking the drug. Microfractures,inadequate mineralization, and outdated collagen are some of the candidate causes. However, until further studies can provide definitive evidenceof bisphosphonate-associated fractures, it is premature to attributeatypical fractures to over-suppression of bone turnover alone,while disregarding secondary and patient-related factors. Many experts believe that prolonged suppression of bone remodelling with alendronate may be associated with a new form of insufficiency fracture of the femur. Studies have not shown if the entire class of medications produce a similar result, but patients who have been treated with any bisphosphonate for an extended period of time should be considered at risk.
 
A wealth of information from well-designed clinical trials clearly shows that, as a class, bisphosphonates are highly effective at limiting the loss of bone mass, deterioration of bone micro architecture, and increased fracture risk that occur with aging. The benefit/risk ratio of bisphosphonate therapy in patients at high risk of fracture remains overwhelmingly positive because of the very low incidence of atypical femoral fractures. Current estimates suggest that alendronate prevents 200 clinical fractures if 4000 women are treated over three years and will cause one femur fracture over the same course of time.⁷ A study by Schilcher et al⁸ found that the incidence density of a stress fracture for a patient on bisphosphonate was 1/1000 per year (95% CI: 0.3-2), which is acceptable considering that bisphosphonate treatment is likely to reduce the incidence density of any fracture by 15/1000.⁹ Nevertheless, limitation of treatment duration to five years in the first instance, with evaluation of the need to continue therapy thereafter, may be appropriate in clinical practice. The Fracture Intervention Trial Long-term Extension (FLEX), in which postmenopausal women who had received alendronate therapy for five years were randomised to continue receiving alendronate for five additional years or switched to placebo, provided clinical evidence that the effect of bisphosphonate therapy was maintained after discontinuation of therapy.^{7, 10} Women who are being treated with bisphosphonates should take a drug holiday if they have been on them for five years. Patients in whom bisphosphonate therapy is discontinued should typically follow up with bone mineral density measurements at 1- to 2-year intervals, with some experts advocating periodic measurement of biochemical markers of bone turnover to detect loss of the antiresorptive effect. Additional research is necessary to determine the exact correlation between the use of bisphosphonates and spontaneous or low-energy trauma fractures.

 

A restraint is any device or medication used to restrict a patient’s movement. Complications of restraints can be serious including death resulting from both medications and devices. Use of restraints should be reserved for documented indications, should be time limited, and there should be frequent re-evaluation of their indications, effectiveness, and side effects in each patient. Analysis of environmental and patient specific root causes of potentially self-injurious behavior can lead to reduction in the use of restraints. Education of the patients, families, and the health care team can increase the use of less restrictive alternatives. 

Background

Malnutrition is defined as state of nutrition in which there is a deficiency or excess of energy, protein and other nutrients causing measurable adverse effects on tissue/body form, function and clinical outcome. (1) It is recognised that 30% of in-hospital patients are malnourished (undernourished) on admission and the majority of these will lose further weight while in hospital. (2) In this review article the term undernutrition will be used instead of the generalised term malnutrition. Undernutrition develops due to increased losses (vomiting, diarrhoea, malabsorption), decreased intake (anorexia, vomiting, nausea, dysphagia), increased requirements (catabolic state) or a combination of all these processes.

 
Is undernutrition important?
 
Consequences of undernutrition include reduced muscle mass, impaired immune function, poor tissue viability, poor clinical outcome and psychosocial effects. (3) Reduced muscle mass decreases cardio-pulmonary function, lean muscle mass and muscle weakness. Impaired immune function increases infection and sepsis risk. Poor tissue viability can cause pressure sores and poor wound healing. Undernutrition can amplify the length of hospital stay. Psychosocial effects include altered mood and poor quality of life. (4)  It is therefore essential that undernutrition is properly treated to diminish patient morbidity and mortality.
 
How to recognise undernutrition:
 
1. Malnutrition screening tools
 
Screening tools should be performed easily with low-level staff training. Hospital patients at risk of undernutrition are identified by screening methods such as MUST (Malnutrition Universal Screening Tool) (5), SGA (Subjective Global Assessment) (6) or MNA (Mini Nutritional Assessment – validated for > 65 years) (7). These screening methods usually consider current body mass index (BMI), recent weight loss and possible future weight loss.   MUST is currently well advertised as a nutritional screening tool within UK hospitals. The British Association of Parenteral and Enteral Nutrition have endorsed this 5 step-screening tool. The MUST score (low, moderate, high risk) has been shown to correlate with mortality (low risk group 8% vs. high risk group 32%, p 0.01) and length of hospital stay (low risk group 15 days vs. high risk group 28 days, p 0.02) (8).   See Table 1.

 
Table 1

2. Assessment of nutritional status:

 
If a patient is found to be at risk of undernutrition, following screening, then a formal nutritional assessment ensues. This assessment involves anthropometrics, biochemical testing, clinical methods and dietary history.
a) Anthropometrical data: appropriately trained staff can perform weight, height, waist circumference, mid-upper arm circumference and skinfold thickness measurements. Indices can subsequently be calculated. These include percentage weight loss, BMI and waist-hip ratio.
b) Biochemical data: information acquired from blood testing includes renal function as a marker of hydration. Also sepsis markers including CRP, ESR and WBC’s are valuable surrogate markers for stress response.  Albumin is a poor marker of nutritional status. (9)
c) Clinical: medical history including past and present is valuable. It is essential to obtain plans regarding fasting for investigations. Knowledge of current treatment that may cause decreased intake or increased losses is essential.    
d) Dietary History: there are assorted techniques of obtaining dietary history. Mostly recall, record diary and food frequency questionnaires methods are utilised.
The overall nutritional assessment entails considering all the information obtained from these different methods. Subsequently a clinical decision is reached regarding the overall nutritional status. 
 
How to assess nutritional requirements:
 
In-patient energy requirements are calculated using a combination of: 
a) basal metabolic rate equations such as Schofield, Harris Benedict and Ireton Jones
b) stress factors or weight gain/loss
c) combined factor for activity level and diet induced thermogenesis. 
The basal metabolic rate is typically calculated using the Schofield equation (10). Schofield estimates basal metabolic rate of a healthy individual. An adjustment is then made for stress or weight gain/loss. Stress factors have been published for various clinical conditions including brain injury, infection, pancreatitis and surgery. Finally a combined factor (activity and diet-induced thermogenesis) is added to calculate total energy requirements. This combined factor is adjusted depending on patient mobility.   Community patient’s energy requirements are calculated using a separate method. Occupational and non-occupational activity is estimated to determine a physical activity level which is multiplied by basal metabolic rate to achieve overall energy requirements.   
Nitrogen/protein requirements are estimated using current patient clinical state i.e.   hypermetabolic, depleted or normal state. Normal state nitrogen requirements are 0.14-0.20 g/kg/day. Depleted state patients nitrogen requirements are 0.20-0.40 g/kg/day. (1g nitrogen = 6.25g protein)
 
Methods of treating undernutrition
 
Following identification of undernutrition a patient’s treatment can be instituted. Undernutrition is typically treated using a graded stepwise approach and subsequently monitoring response. If however it appears clinically obvious that the first steps would not be advantageous then treatment can be commenced at a more aggressive phase. Improving energy intake using the following methods can treat undernutrition:
Step 1. Increase frequency and quantity of food intake. Consider nutrient dense foods. Encourage foods that are energy and nutrient dense such as meat, fish, cheese, eggs, dairy produce and snack foods.   
Step 2. Increase nourishing drinks including milk based drinks, soups, fruit juices and sugary drinks. Nourishing drinks are simple to make and can provide high calories in a small quantity. 
Step 3. Food fortification. This essentially increases the energy density of foods by adding high-energy components such as addition of cheese, milk powder, cream, jam and butter to other foods.
Step 4. Supplements. These can be milk, yoghurt or juice based. They contain varying calories (1-2kcal/ml) and protein (4-6g protein/100ml). Supplements are very useful at boosting energy intake. Most are nutritionally complete but others contain calories only. Examples include Ensure Plus, Fortisip, Calogen and Calshake. 
Step 5. Enteral feeding. Enteral feeding is used to provide either supplementary or complete nutrition to patients that are unable to maintain adequate nutrition by oral route. It is only likely to benefit malnourished patients or those at risk of malnutrition. This includes patients that have had a failed trial of diet modification or supplementary feeds or patients at pulmonary aspiration risk from oral nutrition.
Step 6. Parenteral nutrition. The development of parenteral nutrition in the 1960’s meant that feeding was possible even in patients that did not have a functioning gastrointestinal tract. Although it is mentioned in this article as a final step in nutritional support it may also be appropriate to use early depending on clinical scenario. 
 
Enteral versus Parenteral feeding
 
Enteral feeding produces gastro-intestinal luminal contents that can decrease the possibility of gut atrophy. Maintaining a normal intestinal mucosa reduces the hazard of bacteria and toxins crossing the gastro-intestinal wall and therefore can decrease proinflammatory mediator levels. Compared with parenteral nutrition, enteral feeding attenuates the acute phase response and improves disease severity in acute pancreatitis. (11) Hernandez et al have shown that enteral feeds decrease gut mucosal atrophy in critically ill patients. (12) A meta-analysis has shown that in acute pancreatitis use of EN was associated with a significant reduction in infectious morbidity, hospital length of stay, and a trend toward reduced organ failure when compared with use of parenteral nutrition. (13) However it is important to note that many of the studies involving parenteral nutrition had full dose daily calorie intake whereas enteral feeding studies were less likely to reach estimated energy requirements. This is significant since ill stressed patients should not be given full calorie energy requirements in the first 24-48 hours of commencing feeding. Therefore the parenteral feeding groups were disadvantaged in that the patients were overfed initially and received excess energy calorie intake.   National Institute of Clinical Excellence states that parenteral nutrition is only to be used in patients with “inadequate or unsafe oral and/or enteral nutritional intake and a non-functional, inaccessible or perforated (leaking) gastrointestinal tract.”  (14) Enteral nutrition can be provided by a number of methods including nasogastic tubes, nasojejunal tubes, gastrostomy tunes (including PEG tubes) and jejunostomy tubes (including PEG-J and D-PEJ). Parenteral nutrition can be given peripherally for approximately 14 days but central access should be used if greater than 14 days. 
 
Refeeding syndrome
 
Refeeding syndrome is a potentially lethal condition with severe electrolyte and fluid shifts with resulting metabolic disturbances in malnourished patients. (15) It is caused by refeeding in malnourished patients with resulting insulin release and intracellular movement of potassium, phosphate and magnesium and increased thiamine uptake. It is essential that patients are correctly identified (See Table 2) and electrolytes corrected and intravenous Vitamin B and C is given. Feeding should be initiated slowly. Fluid balance and electrolytes should be monitored closely.

 
Table 2

Cardiovascular disease and nutrition

 
Research has confirmed link between cardiovascular disease and serum cholesterol.  The NHANES II data has shown that patients who died form myocardial infarction had increased cholesterol. (16) Hooper et al confirmed that dietary fat is linked to cardiovascular risk. (17) This group demonstrated that decreasing total dietary fat over 6 month period reduced cardiac events by 16%. The Seven Countries Study illustrated that cardiovascular mortality was linked to saturated fat intake. (18)
There has been recent interest in the role of the Mediterranean diet in the prevention of cardiovascular disease. (See Table 3)  
 

Table 3

Patients were previously educated regarding low fat diet benefits but Mediterranean diet appears to have enhanced beneficial effects. There is however some complexity with definition of a Mediterranean diet. The diet is based on dietary patterns of Greece, Crete and Southern Italy in 1960’s. This diet was abundant in plant foods, fresh fruit, olive oil as principal fat source (monounsaturated fatty acid), low red meat intake, fish (polyunsaturated fatty acid) and red wine in low to moderate amounts. In respect to dietary fats the Mediterranean diet is low in saturated fat but high in monounsaturated fatty acid and polyunsaturated fatty acid. 
 
Diabetes and nutrition
 
The diabetic diet is essentially a healthy diet. The total fat intake should be less than 35% with saturated fat less than 10%. Total monounsaturated fatty acid 10-20% and polyunsaturated fatty acid less than 10% which corresponds to oily fish 1-2 per week. Interestingly polyunsaturated fatty acid supplements should be avoided in this group as they have been shown to increase LDL-cholesterol. Diabetic patients should also be encouraged to eat regular starchy carbohydrate, avoid sugar, increase fibre, eat regular meals and snacks and avoid diabetic foods.
 
Cancer and nutrition
 
Is there a link between diet and cancer?
 
The World Cancer Research Fund states that 30% of all cancers could be prevented by a change in diet, increased physical activity and healthy weight. Animal studies and metabolic studies have been performed that reveal evidence linking diet and cancer. An ecological study linking diet and cancer compared risk of cancer against intakes of fat, cereals and vegetables in 39 countries (19). The ATBC was a clinical trial that related Vitamin A and E to increased lung cancer rates. (20) 2 large cohort studies have been performed in relation to colorectal cancer and dietary fibre. (21, 22). EPIC showed a significant benefit of dietary fibre against colorectal cancer. The EPIC data showed a 40% difference in colorectal cancer rates between the lowest and highest quintile dietary fibre groups. NIH-AARP however showed no benefit when adjusted for multivariate analysis. The American Gastroenterology Association suggest that available evidence form animal, epidemiological and interventional studies does not unequivocally support protective role of fibre against development of CRC. However the whole body of evidence is analysed overall the overall conclusion is that there is an inverse relationship between dietary fibre and CRC.
 
Cancer cachexia
 
Cancer cachexia is defined as anorexia, weight loss and muscle wasting, fatigue and weakness in a cancer patient. Cancer instigates an inflammatory response and production of tumour products. This triggers metabolic abnormalities that produce lipolysis, protein loss and anorexia. As with all disease processes the dietary management of cancer cachexia is initiated by a nutritional assessment. Any symptoms including vomiting and nausea should be treated. There has also been some research regarding fish oils and cancer cachexia. One available product contains docosahexaenoic acid, eicosapentaenoic acid and antioxidants. However a Cochrane review has shown no benefit in relation to beneficial effects of fish oils and cancer cachexia. (23)
 
Critical care
 
Injury and sepsis cause major disturbance to clinical state. There is rapid weight loss, increased metabolic rate, protein losses and sodium retention. There are also changes in hormone levels including increased insulin, catecholamines, growth hormone, glucagons and cortisol. The energy requirements in critical care can vary greatly.   The Ireton-Jones equation is often used to calculate energy requirements in the critical care setting (See Table 4).
 

Table 4

 
The specific immune modulating aspects of nutrients have been widely researched in the critical care setting. This field of immunonutrition has shown disparaging results.
 
Arginine has been investigated as an immune modulating nutrient. Arginine levels can increase or decrease in relation to clinical state. It produces nitric oxide that can lower blood pressure and has been revealed to have detrimental effects in critically ill patients. (24) Glutamine is another possible immune modulating nutrient. It has lots of metabolic functions. It enhances heat shock protein that protect against sepsis. It is thought to be useful in septic shock. Omega-3 fatty acids (alpha-linolenic acid, docosahexaenoic acid, eicosapentaenoic acid) have also been investigated as an immune modulating nutrient. Omega-3 fatty acids produce less proinflammatory eicosanoids than omega-6 fatty acids. There is some evidence that omega-3 fatty acids decrease duration of hospital stay (25) Antioxidants have also been researched as an immunomodulator.   Antioxidant levels are lower in critically ill patients. Vitamins A,C,E and Selenium have been studied. A recent meta-analysis has suggested overall mortality benefit but no septic complications benefit in anti-oxidant trials. (26)
 
Gastrointestinal disease and nutrition
 
Liver disease
 
The energy requirements in chronic liver disease are dependent on clinical state i.e. compensated or decompensated. Nutritional requirements for compensated liver disease are 25-35 kcal per kg (dry body weight) day and protein 1.2g per day. Nutritional requirements for decompensated liver disease are energy 35-45 kcal per kg (dry body weight) day and protein 1.5grams per day.
 
Porto-systemic encephalopathy
 
This disease process is multifactorial and comprises increased ammonia levels, increased aromatic amino acids, decreased branched chain amino acids and alterations of brain neurotransmitters. There is a widely held belief among doctors that protein intake should be restricted but this is mistaken.   Protein requirements are approximately 1g/kg/day and should be divided throughout day.
 
Ascites
 
Low salt intake (<6g per day) is an essential component of ascites treatment. Advice should include no salt in cooking, no added salt, avoid processed foods, and avoid foods rich in salt.  
 
Inflammatory Bowel Disease
 
Inflammatory bowel disease patients are often undernourished due to meagre intake (anorexia, vomiting), amplified losses (diarrhoea and malabsorption) and increased demands (catabolic state). Protein requirements are also increased due to nitrogen losses and catabolic state. It is therefore important that nutritional measures are instituted to improve calorie and protein intake. Interestingly nutrition has been investigated as a treatment for active Crohn’s Disease. Elemental diet is used in active paediatric Crohn’s Disease more than adult Crohn’s Disease to achieve remission. (27). Often this has to be given via naso-gastric tube due to unpalatability. After 4-6 weeks if the patient is in remission foods are introduced slowly over a 3-week period. 
 
Coeliac Disease
 
Coeliac disease is genetically determined chronic inflammatory disease secondary to gluten (glaidin is the alcohol-soluble fraction) that is a component of wheat. In addition the allergy involves similar proteins found in barley, rye and possibly oats. Coeliac patients consequently exclude these dietary sources. Oats can be reintroduced later depending on response. Dietary sources can be obvious or hidden as gluten can be found in numerous manufactured foods. Coeliac patients can however eat natural gluten-free foods or gluten-free proprietary foods (e.g. Schar, Juvela, Dietary Specials, Glutafin).
 
Irritable Bowel Syndrome
 
Simple healthy eating advice is suggested. Diet is tailored to either constipation or diarrhoea symptoms. Typically increasing dietary fibre gradually ameliorates constipation symptoms. Soluble fibre appears to offer benefit more than non-soluble fibre. Decreasing dietary fibre intake treats diarrhoea symptoms. There is not enough evidence regarding exclusion diets although some centres do offer exclusion diets. 
 
Renal disease
 
Acute renal failure and nutrition is divided into non-catabolic and catabolic patients. Non-catabolic patients do not usually have increased energy requirements. Catabolic patients have high protein requirements but no benefit of >0.2 g nitrogen per kg per day. Their energy requirements should be no greater than >20% above resting energy expenditure. 
 
Chronic kidney disease patients have estimated energy requirements of 35 kcal/kg/IBW/day. (IBW = Ideal Body Weight which in the UK this approximates to BMI 23kg/m2). There has been much research regarding protein restriction and possibility of slowing progression of chronic kidney disease. The Northern Italian Co-op study (protein <0.6grams/day) did show possible slower progression of CKD. However it is known that low protein diets have poor compliance and can increase risk of malnutrition. The Renal Association Standards suggest protein intake 0.75g/kg/IBW/day. 
 
Discussing the dietary management of end-stage renal disease, nephrotic syndrome and renal stones is beyond the scope of this article.
 
Conclusion
 
This review article has highlighted the importance of undernutrition in patients under our care. There are numerous methods of screening and assessing patients for undernutrition. There is also a stepwise approach to improving calorie intake: improving oral intake by various methods to enteral and parenteral nutrition. Nutrition is an important aspect of treatment of different disease processes that include cardiovascular disease, diabetes, gastrointestinal disease, renal disease, critical care and cancer.  This review article will hopefully provide the medical practitioner with improved knowledge that can be translated into improved awareness and treatment of undernutrition.
 

IntroductionHospital inpatient falls have remained the subject of extensive research and intervention over the past 55 years¹. Despite risk factor identification, multiple prediction system developments and harm reducing technologies, the issue of falls remains. The incidence of falls varies between 2.2 and 14 per 1000 patient days ^2,3 and increases with age ⁴. In the UK’s National Health Service, 32% of adverse incident reports are due to falls ² . In 2007 it reported 200,000 inpatient falls to the National Patient Safety Association ⁵. Whilst most patients (96%) came to no harm or minor harm, they estimated that over 500 hip fractures and 26 deaths resulted from these falls.Inpatient falls lead to greater morbidity and mortality than equivalent fractures in the community, ⁶ and they significantly increase the length of stay in hospital⁷. Apart from physical harm, there are also psychological consequences for patients such as anxiety, loss of confidence, and fear of falling ⁴. The risk of falls leads to a conundrum in rehabilitative care. Ideally, patients’ mobility, autonomy and dignity must be encouraged and respected - yet slips, trips and falls must be pre-empted often with varying degrees of intrusion and even restraint. In order to selectively target individual patients who would benefit from closer attention, many risk stratification tools have been developed to predict potential fallers. They were developed on a background of over 400 independent risk factors identified with falls ⁸. The most prominent in the UK are STRATIFY (St Thomas's risk assessment tool in falling elderlyinpatients) and Downton with the recent addition of the Wandering Behaviour Assessment ⁸. STRATIFY ⁴ was designed to be used once per week and assesses 5 factors –falls history, patient agitation, visual impairment that limits daily function, frequent toileting, and a transfer or mobility score of 3 or 4 . Each factor scores 1 point and a score greater than 2 was found to have a 92% sensitivity and 68% specificity for a fall in the following week. In the Wandering Behaviour study the STRATIFY criteria results were not reproduced and were found to have only an 82% sensitivity and 34% specificity in their study population ⁸. Downton ⁹ also has 5 categories of assessment; falls history, medication subtypes, audio-visual-sensory deficits, mental state (using the Mini Mental State Score <24) and stability of gait. Each category scores 1 point and a score of greater than 3 is considered significant. In the Wandering Behaviour study, when applying the Downton criteria they only found an 82% sensitivity and 36% specificity ⁸. The Wandering Behaviour assessment looks for the presence of the following :checking, pottering, aimless walking, walking with inappropriate purpose, walking with appropriate purpose but inappropriate frequency, excessive activity, night-time walking, attempts to leave the hospital and being brought back to hospital. The presence of any one of these was found to have a sensitivity of 43% but specificity of 91% ⁸. Thus, both STRATIFY and Downton are limited by the multi-disciplinary assessments required, so that even when implemented, it is difficult to repeat them on a daily or weekly basis. The Wandering Score is easily repeatable on a daily basis, but lacks the sensitivity of STRATIFY and Downton ⁸. The aim of this study is to investigate whether changes in a patient’s physiology can be predictive of falls risk, and if so, can they become a useful tool for calculating risk?  The reason why we have chosen to investigate this is that many of the commonly encountered risk factors can potentially be reflected in the patient’s routine observations ¹⁰. For example, fever could indicate infection and delirium. Hypotension could result from anti-hypertensives, sedatives, or dehydration. Hypertensive states could result from stroke, stress response to infection, or even be a surrogate marker of cardiovascular disease predisposing to arrhythmias. Blood pressure variation could also be predictive since dynamic orthostatic challenges such as lying and standing blood pressure measurements are known to predict falls ¹⁰. Thus, by measuring fluctuations in the observations we hypothesised that it may be possible to make an accurate short term prediction of falls risk MethodsSubjectsWe obtained consent for this retrospective study from the hospital’s ethics committee. We based this study in the Acute Medical Unit of our hospital, as it has the largest case mix of patients recently admitted and is therefore most likely to have the largest physiological instability. We aimed to detect a mean difference of 10% in the physiological variability prior to falling with 80% power, p-value < 0.05, and a common standard deviation of  5 %. Our power calculation indicated that we needed to study 12 patients. We identified all the falls in the calendar year of 2008 by examining the records of all the incident report forms submitted by the ward. A total of 33 incident reports related to falls were logged. Two reports related to staff slips and trips and were excluded, and a third incident report failed to adequately identify either the patient’s name, date of birth or hospital number and so had to be excluded. One of the 30 patients fell twice, and this was treated as its own incident as with the STRATIFY paper. The incident report forms were also used to identify the time, nature, and outcome of the fall. Of all the case notes related to the 30 falls requested from medical records, only 13 were available for detailed review. MeasurementsHeart rate (HR), Blood Pressure (BP), Temperature and Respiratory Rates were all recorded and analysed. The PAR (Patient at Risk) Score as calculated by the nursing staff was included too. PAR Scores are validated mechanisms of identifying sick patients who may go on to develop deterioration to the point of requiring Intensive Care. Scores of >3 are associated with a high risk of deteriorating health and are calculated using the routine nursing observations set. Oxygen saturations were not included in this study, as even small deviations tend to be rapidly corrected by staff with oxygen and therefore were not thought to be a useful marker. Recordings of blood pressure and heart rate were all done with ward based equipment. It is impossible to know which machines were used on individual patients as the equipment has varied, both over the course of time, and between multiple wards. However, because the subjects were their own controls, we are confident that the same machine and cuff were used for taking all the 12 hour recordings as each individual machine is allocated to a given bay. Blood pressures were obtained using semi-automatic Dynamap equipment,   therefore the readings are in effect calculated from the Mean Arterial Pressure (MAP). We elected to study the systolic readings only, as this represents the maximum perfusion pressure to the brain and carotid sinus. Two of the thirteen patients were known to have undergone orthostatic challenges as part of their admission work up and these were included. Other parameters recorded included the time of the fall, number of medications on the drug chart, whether the fall was observed and any injuries sustained.  ControlsWe had two sets of controls. The first set was used to compare the age and gender profile of the fallers to those of the general adult admissions. We had to do this because the official hospital statistics included obstetric and paediatric admissions and comparison would have been inaccurate. We therefore took 4 random days’ of acute adult medical admissions (i.e. over the age of 18) in order to compile an age and gender profile of patients admitted with a ratio of 4:1 (n=110). In order to compare the variability in physiological parameters between fallers and non fallers we generated a second set of controls matched for age (± 5 years) and gender in a ratio of 4 to 1 from a random week’s cohort of patients in February 2009 (for practical purposes). For each matched control, recordings were made at the equivalent length of stay and the controls were not known to have previously fallen. The patients were taken from across the hospital’s medical wards (not Intensive Care or Surgical) with their diagnosis blinded from the investigators. We were able to match 47 of the 52 controls that we were aiming for. Only  BP and HR data were recorded in the controls, as we already established that temperature and respiratory rate were not sensitive markers from our faller data. StatisticsOur 13 patients allowed us to reach sufficient statistical power of 80%. Physiological parameters were tested within groups using the Students t-test (paired, two tailed) and when comparing to controls using the Students t-test (unpaired, two tailed). The null hypothesis were rejected when p<0.05. Variability in heart rate, temperature, respiratory rate and PAR (Patient At Risk Score) were calculated using the mean, range and standard deviation between maximum and minimum values. Blood pressure variability was measured by using the maximum and minimum systolic pressure and calculating the mean, range and standard deviation. We have chosen to primarily measure variability by the range as it is a simple calculation that can be done by anyone on a ward. It doesn’t require a calculator nor any detailed knowledge of mathematics. It is therefore an effective and repeatable measure which could be easily implemented as part of a scoring system. Data processing and Statistical Analyses was done in MS Excel 2002 and SPSS v.14. ResultsThe mean age of fallers was 79 years old (SD 16, n=30) and of the acute medical admission controls 67 years old (SD 20, n=110) with p=0.003. The gender distribution of males to females was 63% to 37% respectively for fallers (n=30), but 38% to 62% in general medical take controls (Fishers exact test p<0.001). 54% of fallers (n=13) were admitted from their own home with 31% from Residential Homes and 15% from Nursing Homes. 54% were known to have a preceding falls history (n=13). The timings of the falls showed that 60% of falls occurred between 08.00 and 20.00 (n=30). 77% of falls occurred within 48 hours of admission (n=13). The circumstances of the falls were consistent with the NPSA statistics with 20% falling out of bed, 17% from chair, 17% from commode / toilet, 20% when walking, 3% in the bath and 23% not documented. The significance of the falls as measured by the incident report forms (n=26, in 4 cases not recorded) was 70% under the level of 6 (i.e. low level and did not require further investigation), 13% were over the level of 6 (i.e. were serious and required further investigation) and 17% were unrecorded. Most of the injuries (n=30) were none or minor – 47%, 10% had a head injury and 43% were not recorded. 95% of the falls were not observed. 31% of the patients (n=13) were taking fewer than 4 medications, 38% were taking between 4 and 7 medications and 32% were taking over 8 medications. Comparing the demographic characteristics of our fallers to the age and gender matched controls; average age was 79 for both fallers and controls (p=0.94) and the gender distribution was 7 females : 6 males in the fallers, and 27 females: 21 males in the controls (Fisher’s Exact Test p=1.0).   The overall PAR score (n=13) was not sufficiently sensitive to predict falls risk – 77% had no change in their PAR score, 8% had a 1 point change and 15% had a 2 point change ( Table 1). Temperature variation (n=13) was minimal with 69% having less than 1 degree Celsius change and 31% having change of 1 to 1.5 degrees Celsius . Recorded respiratory rate variation was also minor (n=13) with 85% having a maximum change of up to 4 breaths per minute. Table 1. Physiological Parameter Data * denotes p<0.05

  In fallers (n=13), the mean highest heart rate was 86 bpm (SD=13) and the mean lowest heart rate was 71 bpm (SD=16). The range was 15 bpm (SD=9.6) with p<0.001. In controls (n=47) the mean highest heart rate was 86 bpm (SD=14) and the mean lowest heart rate was 79 bpm (SD=14). The range was 7 bpm (SD=7) with p<0.001. The significance test when comparing the highest average heart rate between fallers and controls shows p=0.98 showing that they were well matched. The significance test for comparing the variation of the heart rate between fallers and controls is p<0.001. In fallers (n=13), the mean highest systolic BP was 142 mmHg (SD=22) and the mean lowest systolic BP was 116 mmHg (SD=19). The average variation was 26 mmHg (SD=12) with p<0.001. In controls (n=47) the mean highest systolic BP was 140 mmHg (SD=24) and the mean lowest systolic BP was129 mmHg (SD=24). The average variation was 11 mmHg (SD=6.5) with p<0.001. The significance test when comparing the highest average systolic BP between fallers and controls shows p=0.77 showing that they were well matched. The significance test for comparing the variation of the systolic BP between fallers and controls is p<0.001. Charts 1 and 2 show the spread of measurements in the cardiovascular parameters between fallers and controls.

Chart 1. Comparison of the heart rate variation between Fallers and Controls

Chart 2. Comparison of the systolic blood pressure variation between Fallers and Controls

 DiscussionThe average age of the fallers was significantly greater than  the average age of those admitted to the hospital in general. This is unsurprising considering both mechanical deterioration of the musculoskeletal system with advancing age and the accumulation of disease processes. It is noteworthy that despite making up the smaller percentage of admissions to the hospital, men made up the greater proportion of fallers. Other much larger studies show considerable variability in their gender proportions ^11,12, therefore this finding is unlikely to be truly significant.  Apart from age and gender, polypharmacy was also a feature of our fallers. This is consistent with other studies ^13,14,15. Additionally, our data was consistent with the overall NPSA statistics in terms of the significance and circumstances of the falls ⁵. The main and novel finding of our study was that fallers were significantly more likely to display a larger range in their cardiovascular observations than the standard hospital population. Whilst it is generally expected that subjects undergoing any routine measurement of heart rate and blood pressure will have a variation in measurements of about 10% over the course of 12 hours ^16,17, we found that our fallers had a variation in their heart rate and blood pressure of approximately 20%. This is similar to the dips experienced by the normal population over the course of the night and during orthostatic challenge. This was despite the fact that the baseline measurements of highest value were virtually the same for both populations. Furthermore, almost all the values recorded were within normal limits – and would not normally require specific remedial action to be taken. This could also explain why this risk factor has not previously been identified in other studies. Our study indicates that it is the cardiovascular lability rather than the cardiovascular measurements per se, which acts as an acute predictor of falls. In fact, the sensitivity for falls prediction with either a range of HR values > 15 beats per minute or range of BP systolic values >25 mmHg was 77%. We would therefore expect that when such patients mobilize, the superadded orthostatic challenge would be too great for cardiac output to be suitably matched and so patients are at greater risk of falling. In terms of the 12 hour prospective risk of falling this could certainly explain why a patient with known risk factors will fall during a given nursing shift.  Indeed it may also explain why a patient may fall during a hospital admission when patients were, for example, already parkinsonian and arthritic and yet had not previously fallen.  Interestingly, neither temperature, respiratory rate, nor PAR Score showed any significant lability in the lead up to the falls. This was surprising as we would have expected them to be predictive of other well known risk factors. The lack of fluctuation in temperature and respiratory rate could provide further evidence that the key short term factor responsible for falls is cardiovascular lability. More detailed analysis showed that it was more likely that these measurements were insufficiently sensitive. Only four of the fallers were admitted with infections, and those subjects showed some temperature fluctuations. However, only 2 had temperatures above 37.5 degrees Celsius, which is consistent with the blunted fever response that is well known to occur in 50% of the elderly population ^19,20 (and most fallers were elderly). The lack of value in respiratory rate recordings probably reflects the lack of due care and attention paid to this, the only manually measured parameter. It has long been recognized that respiratory rate recordings tend to be inaccurate  ²¹ . The highly limited range of measurements recorded (16-22 breaths per minute) amongst all the fallers, despite some patients having severe pneumonia, further supports this finding. Finally, the PAR score tended to be quite static. This was a result of its constituent parameters not being sensitive (temperature, respiratory rate) and the fact that most of the heart rate and blood pressure recordings were within normal limits. LimitationsDespite the fact that this study was well powered and statistically significant, ultimately it is quite limited in numbers with just 13 patients. It was disappointing that we were not able to obtain case-notes or the appropriate file in the other 17. We are also presenting calculated data from the MAP measurements, without knowing the exact algorithms being used. For this reason, we analysed the given systolic pressures as further data manipulation would have increased inaccuracies. Our data is taken from relatively acute admissions and as such may not necessarily be applicable to long stay patients, where cardiovascular lability may not play an important role.Furthermore, controls were not matched for diagnosis or for the number of medications taken. This could lead to criticism that the comparison was poor, though the baseline measurements for the two were remarkably consistent. One of our aims was to see if variability could be used to accurately model general falls risk. We therefore thought it would be more useful to study the hospital’s general physiology, in all its varying degrees of illness. ConclusionsThis study shows the value of looking closely at patients’ observations and that even ‘normal’ values have to be interpreted in context . The data supports the finding that the risk of falling at a given point in time relates not only to predisposing factors, but also to their current cardiovascular status. We therefore suggest that a one-off falls risk assessment is no longer appropriate, but should be continuously reviewed on a shift-by-shift basis by nursing staff. This has significant ramifications for modernizing current risk stratification tools so that they are able take this into account.

Spasticity is a common symptom seen as a consequence of an injury to the brain (stroke, trauma, hypoxia, infection, cerebral palsy and post surgery), spinal cord injury or multiple sclerosis. It is a complex problem, which can cause profound disability alone or in combination with other features of upper motor neuron syndromes (figure 1). The word “spasticity” is derived from the Greek word “spasticus”, which means “To pull or To Tug”. Spasticity is defined¹ as “Disordered sensori-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles”. Simply stated, spasticity is stiffness of muscles that occurs after injury to the spinal cord or brain. Awareness of the implications and associated symptoms can minimise development of long term secondary complications (table 1). The impact of spasticity can be devastating. If not managed early and appropriately it may result in progressive disability, resulting in secondary complications such as contractures and pressure sores. This significant impact has ensured that spasticity management is a prominent feature in the national management guidelines for long term neurological conditions, promoting coordination of care between primary, secondary and social care providers. Symptoms Spasticity can range from mild muscle stiffness to severe, painful and uncontrollable muscle spasms. It is associated with both positive and negative components of upper motor neuron syndromes. Positive components include muscle overactivity, flexor and extensor spasm, hyperreflexia, athetosis, spastic dystonia, clonus, and an extensor plantar response. Common negative symptoms comprise weakness/ paralysis, early hypotonia, fatigue and loss of dexterity. Spasticity can be distinguished from rigidity by its dependence on the speed of muscle stretch and characteristic distribution in antigravity muscle groups. Spasticity does not always cause harm and can occasionally assist in the rehabilitation process by enabling a patient to stand when their limb weakness would not otherwise allow it Table 1 Clinical and functional problems associated with severe Spasticity

 Figure 1 Vicious cycle of spasticity   Assessment of spasticity Before any intervention is undertaken to modulate hypertonicity, it is important to attempt to assess the severity of spasticity. Many grading scales are used to quantify spasticity. These address the degree of muscle tone, the frequency of spontaneous spasms and the extent of hyperreflexia. Goniometry, Ashworth scale, Tardieu Scales, Goal attainment scale are only a few of these scales. One of the most widely used scales is the modified Ashworth scale². Table 2 Modified Ashworth scale

  It is also important to remember that not every “tight” muscle is spastic. The clinically detectable increase in muscle tone may be due to spasticity, rigidity or a fixed muscle contracture. Management  The key to successful spasticity management is education of the patient and carers with both verbal and written information. This allows them to understand, appreciate and be fully involved in the management plan. All patients with spasticity should be followed up by a coordinated multidisciplinary team, which allows more timely intervention and close monitor of the progress. Liaison between health and social services in both primary and secondary care is essential in long term management. This helps to deliver a more consistent approach to the individual over time (figure 2). Table 3 Aims of spasticity management.

 The first step in the management of spasticity is to identify the key aims and realistic goals of therapy. Understanding the underlying pathology and possible prognosis is helpful in planning these goals (table 3). Other key points to consider are: ·          Identification and management of any trigger or aggravating factors-Initial assessment should exclude any co morbidity that may worsen spasticity such as pressure sores, chronic pain, infection (commonly urinary tract infection), constipation or in-growing toe nails.·          Instigation of an effective and realistic physical programme including attention to posture and positioning Figure 2
Approach to spasticity assessmentComprehensive assessment of spasticityRecognition of underlying provocative factorsImpact on the individualMeasurement of spasticityPotential goals- individualised and person focussed 
Initial approachEducation to patient/ and their family /carersMultidisciplinary team assessmentIdentification of clear treatment goalsEstablish mechanism for monitoring and review  Management Manage triggering factorsBalance between positioning and movementPosture and seatingPhysical therapy and active exercise programmeSplinting and use of orthoticsPharmacotherapy A)      Physical modalities·          Stretching- this intervention has the benefit of being benign and non-invasive. Maintaining muscle length through passive or active exerciseand stretching regimens including standing or splinting canbe key to managing spasticity both in the short and the longterm.·          Cooling of muscles- this inhibits mono synaptic stretch reflex and lowers the receptor’s sensitivity, different techniques such as quick icing and evaporating spray like ethyl chloride are occasionally used.·          Heat-heat may increase the elasticity of the muscles. Techniques used include ultrasound, fluidotherapy, paraffin, superficial heat and whirlpools. These techniques should be combined with stretching and exercise.·          Orthosis/equipment/ aids – an orthosis or splint is an external device designed to apply, distribute or remove forces to or from the body in a controlled manner to control body motions and /or alter the shape of body tissues. E.g. ankle foot orthosis, insoles, ankle supports, wrist/ hand/ elbow splints, knee splints, spinal brace, hip brace, neck collar. Some equipment can also aid positioning e.g. T roles, wedges, cushions and foot straps.These are usually used in combination with other modalities like botox therapy. Attention to posture and positioning, whichmay include the provision and regular review of seating systems,is paramount in managing severe spasticity·          Massage– althoughvarious techniques are in use there is no evidence to support this·          Dynamic physiotherapy technique- many schools of physiotherapy claim that particular technique has antispastic and functional benefits, particularly for the more mobile person. E.g. Bobath technique, proprioceptive neuromuscular facilitation, Brunnstrom technique. B) Electrical therapy·          Functional Electrical stimulation –Thisis an adjunct to physiotherapythat can be of benefit to selected individuals who are predominantlyaffected by upper motor neuron pathologies resulting in a foot drop. Randomised controlled trial by Burridge et al in patients following stroke found that the use of functional electrical stimulation in combination with physiotherapy was statistically superior to physiotherapy alone³·          Transcutaneous electrical nerve stimulation – this has been found to reduce spasticitythrough its nociceptive action and reduction of pain. C) PharmacologicalMedicationshould always be used as adjunct to good general management and education. Identification of treatment goals will help optimise drug therapy not only in terms of choice of agent, but also in timing and dose. Aims of medication should be to improve function or relieve troublesome symptoms rather than to simply reduce the degree of spasticity. Table 4 Useful things to remember to optimise medication effects

 Table 5 Different methods of delivery of medication

 The oral agentsAlthough different categories of drugs are available, those most commonly used to treat spasticity are baclofen,tizanidine, benzodiazepines, dantrolene, and gabapentin^{4, 5, 6}. Different agents act through different mechanisms (table 6 and 7) for e.g. GABA-like (baclofen, benzodiazepine), central alpha 2 agonists (tizanidine, clonidine) and peripheral anti-spastics (dantrolene). Antispastic drugs act in the CNS either by suppression of excitation (glutamate), enhancement of inhibition (GABA, glycine) or a combination of the two. Table 6 Mechanism of action of commonly used oral antispasticity medication