Paediatric Bronchogenic Cyst Complicated By Atypical Mycobacterium Infection

Stacy A Frye and James M. DeCou
Article Citation and PDF Link
BJMP 2009:2(4) 54-56


Bronchogenic cysts are lesions of congenital origin derived from the primitive foregut. They form due to ectopic budding of the foregut during the first trimester. Epithelial cells of the developing trachea and lung are pinched off and grow separately from the airways. Bronchogenic cysts are most commonly mediastinal, unilocular and contain clear fluid. Clinically, most cysts are symptomatic and occur in infancy or early childhood. Respiratory distress is the most common presentation in paediatric patients, manifested by recurring episodes of cough, stridor, and wheezing.  Patient Description: A 13-year-old female presented with a two month history of right-sided back pain and five days of intermittent fever. The pain was worse on inspiration and made sleeping difficult. She denied wheezing, chest pain, or cough. She continued daily participation in competitive sports. Previous trials of antibiotics and an inhaled bronchodilator for presumed exercise-induced asthma were unsuccessful. Chest x-ray (CXR) showed a large cyst (10x10x8 cm3) in the posterior right lung. (Image 1).  Image 1: Initial chest x-ray revealing bronchogenic cyst in the posterior right middle lobe (10x10x8 cm3) Computerized tomography (CT) scan showed a large cystic lesion arising entirely within the right lower lobe and extending the width of the hemithorax. (Image 2)   Image 2: Chest CT shows bronchogenic cyst extending the entire width of the right hemithorax and approximately 50% full of fluid. There was an air-fluid level occupying ~50% of the cavity. She was diagnosed with a multilocular bronchogenic cyst. She was briefly hospitalized and discharged on azithromycin with plans to resect the cyst in one month.  Severe cough, fever, and chills prompted readmission after 3 weeks of antibiotic therapy. CXR and CT showed cyst enlargement (16x9x11 cm3) with over 95% fluid. (Images 3 and 4)   Image 3: Substantial bronchogenic cyst (16x9x11 cm3), over 95% full of fluid.   Image 4: Lateral chest x-ray revealed opacification along superior margin of cyst. She was started on ampicillin/sulbactam. Percutaneous drain placement yielded a large volume of turbid fluid. Aerobe, anaerobe and fungal studies of the fluid were negative. Resection was postponed due to significant inflammation surrounding the cyst cavity. She was discharged on a seven day course of amoxicillin/clavulanate. Following six weeks of cyst drainage, a thoracoscopic right lower lobectomy was performed. Extensive inflammation and induration made dissection of the lower lobe and pulmonary vessels challenging. Fibrinoid adhesions extended to the pleural surface. Operative time was 418 minutes.  Surgical pathology showed diffuse necrotizing granulomatous inflammation with acid-fast bacilli and multiple nodules up to 3.3 cm in diameter. Ninety-five percent of the pleural surface had nodular involvement. (Image 5) Areas of non-indurated lung also showed small nodules with a miliary appearance. Inflammation was present at the bronchovascular margins, hilar nodes, and distal lung.   Image 5: Gross specimen of right lower lobe: Approximately half of the lobe was indurated and 95% of surfaces showed nodular involvement. Sectioning through indurated region revealed diffuse nodules up to 3.3 cm. Nonindurated lung showed small nodules with miliary appearance. The patient had no history of tuberculosis exposure, foreign travel or immunodeficiency. There was no family history of tuberculosis or respiratory disease. Based on the acid-fast bacilli identified on pathology stain, fluid drained from her chest tube was sent for acid-fast bacilli culture and smear. Mycobacterium was not isolated. It was determined that the source of the atypical mycobacterial infection was likely colonizing mycobacteria from her oropharynx that became entrapped in the cyst. A six-week course of clarithromycin, rifampin, and ethambutol was prescribed to treat any remaining organisms.  At two-month follow-up, she had minimal pulmonary symptoms and inflammatory markers were improved. Erythrocyte sedimentation rate (normal: 0-15) and C-reactive protein level (normal: 0-10) decreased from 88 and 173 during her hospitalization, to 10 and 3.6, respectively. At four-month follow-up, she had resumed competitive sports and had no evidence of ongoing infection.  Discussion: This case highlights a unique presentation of infected bronchogenic cyst after substantial cyst growth. Unusual aspects include the late onset of symptoms, multilocular intraparenchymal cyst appearance, turbid drainage, extensive nodularity, necrotizing granulomatous inflammation, and atypical Mycobacterium infection. Although comorbid infection is not uncommon, causative organisms are typically Haemophilus influenzae1,2 and Streptococcus pneumoniae.3 Cases of Streptococcus pyogenes,4 Escherichia coli,5and Salmonella enteritidis6have been reported. However, only four cases of bronchogenic cyst with Mycobacterium infection have been documented.7,8,9 Three of the Mycobacterium-infected cases are adult patients. Lin et. al reported a 39-year-old female with bronchogenic cyst complicated by Mycobacterium avium infection.7 The organism was identified by genetic sequencing of biopsied lung tissue. Sputum acid-fast stain and mycobacterial cultures were negative. Liman et al. reported two adult cases: a 20 year-old male with Mycobacterium identified in a right lower lobe specimen but with negative sputum culture, and a 32 year-old female with Mycobacterium isolated in a sputum culture but a negative microscopic exam and cyst fluid culture.8  The only documented paediatric case, a 9 year-old female with a 6 cm right lower lobe bronchogenic cyst, was reported by Houser et al.9 She underwent lobectomy; Kinyoun stain of the cyst specimen showed Mycobacterium. Sputum culture and acid-fast bacilli stain were negative. Tuberculin skin test was positive. Comorbid infection with Mycobacterium tuberculosis was suggested, but they were unable to isolate an organism. Treatment consisted of four months of rifampin and two years of isoniazid with pyridoxine.  This is the first documented paediatric case of bronchogenic cyst infected with atypical Mycobacterium. Her presentation is noteworthy, given the substantially greater size of the cyst (16x9x11 cm), extensive pathologic findings, and success with a different antibiotic regimen. 

Bronchogenic cyst should be included in the differential diagnosis of a child with cough, dyspnoea, and fever. Although rare, we stress the importance of keeping mycobacterial infection in mind in cases of an infected cyst. Acid-fast culture should be done on sputum and cyst contents. Due to the frequency of negative cultures, stains should also be performed on resected cyst specimens. Antibiotic therapy should be considered and administered based on the extent of infection. All symptomatic or enlarging cysts warrant surgical excision. Prophylactic removal of asymptomatic cysts is recommended due to higher rates of perioperative complications once cysts become symptomatic.10 We raise the question of whether earlier CXR is indicated to rule out bronchogenic cyst, particularly when patients do not improve after trials of watchful waiting, antibiotics, and bronchodilators for other possible respiratory diagnoses.


Acknowledgements / Conflicts / Author Details
Details of Authors: 
STACY A FRYE, MD, Paediatrics Resident Physician, Grand Rapids Medical Education and Research Center/Michigan State University Paediatric Residency Program, Helen DeVos Children's Hospital, Grand Rapids, MI,USA JAMES M. DECOU, MD, Board-certified Paediatric Surgeon, Paediatric Surgeons of West Michigan, Grand Rapids, MI, USA
Corresponding Author Details: 
STACY A FRYE, MD, Paediatrics Resident Physician, 2470 Orchard View Drive NE, Grand Rapids, Michigan 49505 Tel: (616) 322-7047
Corresponding Author Email: 
[email protected]

1.Klapper JH, Sherman JM. Nontypable Hemophilus influenzae infection of a congenital bronchogenic cyst. J Fla Med Assoc 1986;73(6):454-5.

2.Rivero HJ, Young LW. Radiological Case of the Month. Bronchogenic cyst infected with Haemophilus influenzae. Am J Dis Child 1988;142(5):547-8 3.Fukasawa C, Ohkusu K, Sanayama Y, et al. A mixed bacterial infection of a bronchogenic lung cyst diagnosed by PCR. J Med Microbiol 2006;55(6):791-4.4.Vaos G, Zavras N, Antypas G. Bronchogenic cyst of the lung mimicking a pulmonary hydatid cyst in a child. Pediatr Surg Int 2005;21:383-5.5.Ribet ME, Copin MC, Gosselin B. Bronchogenic cysts of the mediastinum. J Thorac Cardiovasc Surg 1995;109:1003-10.6.Kostopoulos G, Efstathiou A, Skordalaki A, et al. Bronchogenic cyst infected by Salmonella enteritidis followed gastroenteritis. Eur J Cardiothorac Surg 2002;21(5):935-7. 7.Lin SH, Lee LN, Chang YC, et al. Infected bronchogenic cyst due to mycobacterium avium in an immunocompetent patient. J Infect 2005;51:131-3.8.Liman ST, Dogan Y, Topcu S, et al. Mycobacterial infection of intraparenchymal bronchogenic cysts. Respiratory Medicine 2006;100:2060-2.9.Houser WC, Dorff GJ, Rosenzweig DY, et al. Mycobacterial infection of a congenital bronchogenic cyst. Thorax 1980;35:312-3.10. Mampilly T, Kurian R, Shenai A. Bronchogenic Cyst – Cause of Refractory Wheezing in Infancy. Indian J Pediatr 2005;72(4):363-4.


Hospital at night, a survey of the junior orthopaedic doctor’s perspective

U Butt, R Wharton and G C Bannister
Article Citation and PDF Link
BJMP 2009:2(4) 49-50

Introduction: The aim of the NHS Modernisation Agency’s Hospital at night project is to “Redefine how medical cover is provided in hospitals during the out of hours period.”(1) The project “requires a move from cover requirements defined by  professional demarcation and grade, to cover defined by competency in order to release significant amounts of medical staff time and support the compliance with WTD (Working Time Directive) while enhancing clinical practice and training.”(1) Chairman of the BMA’s Junior Doctors Committee and also medical advisor to the Hospital at Night Project undertook a survey of  junior doctors’ activity in the evening, night, and weekends. They noted that the evenings were very busy and the nights quieter, that general physicians work harder at night than those in other specialties or orthopaedic surgeons. In summary their survey showed that a huge amount of doctors’ time was wasted on tasks which did not require their level of skills. Such tasks included phlebotomy, searching for notes, and x-rays.(1)  An evaluation report into the implementation and impact of the hospital at night pilot project, August 2005, identified key elements to minimize medical workload at night. These included working within a multidisciplinary, competency-based team, with extended skills ward staff to minimize reliance on the night team, reduce duplication, take away inappropriate tasks, bleep-filtering and better use of new technologies such as digital imaging and e-prescribing (2). Our aim was to assess the experience of a typical junior orthopaedic doctor’s experience during his on-call to assess their perspective of the implementation of hospital at nightand to establish whether the recommendations of the evaluation report were being implemented. Methods: A prospective review was conducted of the night duties of all junior doctors working or cross-covering trauma and orthopaedics across Frenchay and Southmead hospital sites of the North Bristol NHS Trust between December 2007 and January 2008.A questionnaire included nature of activity and level of experience, closed questions relating to the hand-over experience. Details of calls received and the nature of tasks undertaken during on-call period with times. Data were then stored and analysed using excel-office 2002. Results: Total of 51 questionnaires were completed by the junior orthopaedic doctors during their respective on-call duties. A total of 109 calls were received or tasks requested. The average time spent during hand-over was 14.1 minutes (range 5-20 minutes).  Discussion: Our data indicates busiest times occurred between 21:00 – 23:00 (Fig 1)  Figure 1, illustrates a distribution of the peak work-load period which occurred between 9pm-11pm and 1am-3am. This finding contradicts previous surveys done prior to the implementation of the hospital at night where it was noted that the nights were quieter and sub-specialist such as orthopaedic surgeons were not working as hard as general medics (1)Figure 2, shows the overall experience of the hand-over as judged by the orthopaedic juniors. There was an eighty-five percent (43/51) attendance by the on-call orthopaedic juniors of which seventy-two percent (32/44) thought that it was a useful experience Figure 3 illustrates a distribution of the calls received. As illustrated, 37/109 calls were viewed as inappropriate The majority of the orthopaedic juniors surveyed framed hospital-at-night hand-over was useful but thirty-four percent (37/109) of the calls they received were viewed as inappropriate (Fig 2,3). The most frequent of the inappropriate ward calls were ‘requests to rewrite drug-charts’ (Fig 4,5). Figure 4 describes the frequencies of these calls. As illustrated the most frequently inappropriate ward-call was to ‘rewrite drug-charts’. There were twenty-three (23/37) inappropriate ward-calls Figure 5 shows the reasons given by the on-call doctors for the inappropriate tasks. The most frequently given reason was that ‘the request should have been done during the day’. The second most frequently given reason for inappropriate calls was the fact that ‘it was a duplicated request’ Our survey also highlighted that the most frequently given reason for inappropriate tasks was firstly that the request should have been done during the day and secondly that it was a duplicated request. These findings seem to defeat the key purpose of the hospital-at-night project for an orthopaedic SHO on-call.  Conclusion: Hospital at night cannot function in isolation. There are fewer doctors available then normally and the system has to use their time effectively. 30% of inappropriate calls to wards were to rewrite drug charts and to prescribe warfarin. This should have been identified and performed by the day staff. 10% of calls were to review X-rays.  Much of the inappropriate activity could be pre-empted if both day and night staff attended the handover and the tasks outstanding from the day identified. The doctor on the night could then perform an hourly ward round completing these tasks without interrupting at the beginning of the night.

Acknowledgements / Conflicts / Author Details
Details of Authors: 
U BUTT, StR, Avon orthopaedic centre Southmead Hospital, Bristol, UK R WHARTON, StR, Avon orthopaedic centre Southmead Hospital, Bristol, UK G C BANNISTER, Consultant orthopaedic surgeon, Avon Orthopaedic Centre, Southmead Hospital, Bristol, UK
Corresponding Author Details: 
U BUTT, Bunglow 3, Frenchay Hospital , Bristol, UK. BS16 1LE.
Corresponding Author Email: 
[email protected]
  1.  News Feature. The Hospital at Night. “Rhoda MacDonald asks Simon Eccles, chairman of the BMA’s Junior Doctors Committee and medical advisor on this project, what it is all about.” BMJ Career Focus 2004;328:19;doi;10.1136/bmj.328.7431.s19.
  2. “The implementation and impact of Hospital at Night pilot projects. An evaluation report”. August 2005; DOH.

Impact and healthcare-seeking behaviour of premenstrual symptoms and dysmenorrhoea

Nabia Tariq, M Jawad Hashim, Tara Jaffery, Sumaira Ijaz, Sara Ajaz Sami, Sana Badar and Zainab Ara
Article Citation and PDF Link
BJMP 2009:2(4) 40-43
Abstract / Summary

Objective: Determine the impact and healthcare-seeking behaviour of women with dysmenorrhoea.
Design: Cross-sectional survey.
Setting: Medical college, nursing college, hospital (staff and patient attendants), schools and suburbs of Islamabad.
Population: 1236 women aged 16–50. Exclusion criteria: pregnancy; gynaecological or medical condition.
Methods: Structured-questionnaire interviews.
Main outcome measures: Impact, healthcare-seeking behaviour, and response to treatment.
Results: Prevalence of premenstrual symptoms was: low back pain 879 (72%), depressed mood 484 (40%), headache 268 (22%), premenstrual fluid retention (body swelling) 218 (18%), and nausea 218 (18%). Predictors of pain score (linear regression coefficients) were: low back pain (0.39), headache (0.25), depressed mood (0.17) and nausea (0.17). Premenstrual symptoms affected household chores in 441 women (37%), household income 129 (11%) and social obligations 395 (33%). Students and self-employed women, 282 (63%) and 38 (63%) respectively, reported one or more days missed from school/work. Treatments sought were: conventional medicine by 496 women (56%); household remedies, 285 (32%); herbal 90 (10%); and homeopathic 125 (14%). Self-reported effectiveness of treatments was: conventional medicine (OR 13, 95% CI 8.7–21); household remedies (OR 6.5, 95% CI 4.1–11); herbal (OR 4.1, 95% CI 2.2–7.7). Homeopathic treatment was not felt to be effective (OR 1.5, 95% CI 0.89–2.6).
Conclusions: Low back pain and headache contributed the most to severity of dysmenorrhoea.  Headache and body swelling (fluid retention) were predictive of days unable to work. Conventional medicine was used by more educated women and was perceived to be effective more often than other modalities.

Dysmenorrhoea, developing countries, impact

Introduction Dysmenorrhoea and other premenstrual symptoms are common among women of reproductive age and lead to suffering and impact on home, school, and work performance. Earlier studies have focused on the prevalence and risk factors of dysmenorrhoea 1, 2, 3. Surveys in Pakistan have found the prevalence of premenstrual symptoms varying from 53% to 67% in college girls 4, 5, 6. About 57% of students in one study reported that dysmenorrhoea affected their work5. Although these surveys document the prevalence and severity of symptoms they do not correlate it with the impact of specific symptoms on daily activities or with healthcare seeking behaviour. A population-based survey of 2262 women from Goa, India, revealed a linear association between pain severity and treatment seeking and time off from work 3. However the impact of specific symptoms of premenstrual syndrome on treatment seeking and rest was not reported. Aims Primary objective: The authors carried out a cross-sectional study to explore the impact of dysmenorrhoea and other premenstrual symptoms among women of reproductive age.Secondary objective: The authors intended to find out the predictors of healthcare-seeking behaviour including self-treatment for premenstrual symptoms. Methodology A cross-sectional survey study design was chosen. A 13-item questionnaire was administered to women, aged 16 to 50, who were not pregnant and had no known gynaecological, medical, musculoskeletal or neurological diagnosis. Participants were recruited from multiple sites using convenience sampling within urban areas of Islamabad and Rawalpindi in Pakistan. Trained interviewers (physicians, medical students, nursing staff, and high school students) filled out questionnaires interviewing female students at a medical college, a nursing college, and at city schools; as well as housekeeping staff and patients’ attendants at a tertiary care teaching hospital in Islamabad. A proportion of women completed the questionnaire themselves. Ethical approval was obtained from the Shifa International Hospital Ethics committee. No personally identifiable data such as the respondents’ names were recorded. Results Study population characteristics A total of 1236 women from multiple locations within Islamabad and Rawalpindi, Pakistan, participated in the survey. Most of the women were in the younger age groups: 402 women (33%) were 16–20 years old and 622 (50%) were 21–35 years old. Fewer women were in the older age groups: 147 women (12%) were 36–45 years old and 63 (5%) were more than 45 years old. About 55% were unmarried and 61% had no children. The distribution of educational achievement was weighted towards the more educated: 16% were able to read a religious book (basic literacy); 49% had some school education (up to 12th grade); and 34% had professional level education. About 27% of the respondents were homemakers (among women with professional level education, 10% reported staying at home). Age at menarche was less than 12 years old for 16%; between 12 and 14 years for 62%; and more than 14 years old for 23% of the respondents. Severity of dysmenorrhoea and its correlation with premenstrual symptoms On the 10-point visual pain scale, 465 women (38%, 95% CI 35–41) reported mild dysmenorrhoea severity from 0 to 3; 517 women (42%, 95% CI 39–45) reported moderate severity from 4 to 7; and 248 women (20%, 95% CI 18–23) reported severe pain rated from 8 to 10. The linear regression coefficient between dysmenorrhoea severity score and the number of days unable to work in a month was 0.59 (standard error: 0.031). Table 1: Prevalence of premenstrual symptoms and their contribution to pain severity and days lost from work

  Women reporting symptoms, n (%, 95% CI) a Contribution to pain score b Contribution to days out of work c
Low back pain 879 (72, 69–74) 0.39 * 0.05
Depressed mood 484 (40, 37–43) 0.17 * -0.05
Headache 268 (22, 20–24) 0.25 * 0.22 *
Swelling 218 (18, 16–20) 0.03 0.12
Nausea 218 (18, 16–20) 0.17 * 0.01

* Statistically significant values (P < 0.005)a Respondents were allowed to select more than one option. Total respondents: 1236.b Linear regression coefficients for a 10-point visual pain score categorized into three levels.c Linear regression coefficients for self-reported days unable to work in a month. Table 1 shows the prevalence of primary symptoms of preceding menstruation and their contribution to a 10-point visual pain scale and to self-reported days unable to work in a month. Low back pain and headache contributed most to the pain score while headache and swelling correlated with days out of work. Impact of dysmenorrhoea Among the working women (366 professionals and housekeeping staff) 49% (95% CI 44–54) reported one or more days out of work in a month due to pain. Similarly, among the 452 students surveyed, 53% (95% CI 48–58) reported dysmenorrhoea affecting school performance (Table 2).

Table 2: Impact of premenstrual symptoms and dysmenorrhoea on household, school and work performance

  All respondents, n (%) Students, n (%) Maids and housekeeping staff, n (%) Self-employed, n (%) Professionals, n (%)
Affected domain          
Household chores 441 (37) 124 (28) 59 (40) 31 (52) 75 (35)
Household income 129 (11) 24 (5.3) 33 (22) 12 (20) 18 (8.5)
Performance in school 313 (25) 239 (53) N/A N/A N/A
Social obligations 395 (33) 130 (29) 58 (39) 31 (52) 85 (40)
Unable to work for one or more days in a month 643 (53) 282 (63) 75 (51) 38 (63) 103 (50)

Percentages do not add up to 100% as respondents were allowed to select more than one affected domain.Values for 50% or more respondents acknowledging an impact in a domain are given in bold.


Treatment taken for dysmenorrhoea relief 

Table 3 outlines the remedies sought for the relief of dysmenorrhoea symptoms and the reported effectiveness of each type of remedy. All treatments except homeopathic were felt to be effective. Logistic regression analysis showed that the use of any treatment type was related to low back pain (odds ratio 2.2, 95% confidence interval 1.6–2.9), pain severity (OR 2.0, 95% CI 1.6–2.5), headache (OR 1.7, 95% CI 1.2–2.4), depressed mood (OR 1.7, 95% CI 1.3–2.2), increasing education (OR 1.1, 95% CI 1.0–1.2) and not being unmarried (OR 0.52, 95% CI 0.34–0.79).

Table 3: Remedies sought for dysmenorrhoea relief and their patient-reported effectiveness

  Women reporting use of treatment, n (%, 95% CI)a Odds ratio for self-reported effectiveness, (95% CI)b
Conventional medicine 496 (56, 53–59) 13 (8.7 to 21)
Household remedies 285 (32, 29–35) 6.5 (4.1 to 11)
Herbal 90 (10, 8–12) 4.1 (2.2 to 7.7)
Homeopathic 125 (14, 12–17) 1.5 (0.89 to 2.6)

a Respondents were allowed to select more than one option. Total respondents: 1236.
b Unconditional logistic regression (converged, 6 iterations, 878 cases included, using Epi Info 3.4.3). All odds ratios with P < 0.005, except homeopathic, P = 0.12.[CI, confidence interval]

Conventional medicine was sought by women with higher pain scores (OR 2.2, 95% CI 1.8–2.8) and greater years of education (OR 1.2, 95% CI 1.1–1.3); other factors such as age and specific symptoms were not statistically related. Women with a greater number of days unable to work were more likely to use herbal treatment (OR 1.4, 95% CI 1.1–1.9) while household remedies like hot water bottles and warm drinks were more commonly taken by women with headache (OR 1.66, 95% CI 1.2–2.4), depressed mood (OR 1.6, 95% CI 1.2–2.3) and lesser years of education (OR 0.88, 95% CI 0.78–0.99). Discussion This paper is the first, to the best of our knowledge, to show an association between specific premenstrual symptoms and dysmenorrhoea severity and healthcare-seeking behaviour. We found that certain symptoms, namely low back pain and headache, contributed more to the perceived severity than other complaints. This finding may be of importance to clinicians treating women with menstrual complaints especially when the treatment is symptom-oriented. In women working outside their homes clinicians may wish to target headache and swelling as these symptoms correlated with days unable to work. Prevalence of premenstrual symptoms in the present study was higher than a Japanese survey7 that reported back pain in 6.9% of women and headache in 11% of women (compared with our results of 72% and 22% respectively). This difference may be due to cultural differences in perception and reporting of symptoms, overall better health, and being strong and hardworking. It may simply be the perception difference in underdeveloped or developed country i.e. lack of resources, poor diet, and poor health. Menstrual symptoms caused a heavy impact on social, school, and work responsibilities in women, a finding we share with previous studies. A cross-sectional survey from India found that 17% of adolescent girls reported missing school classes due to dysmenorrhoea while 60% reported disruption of their daily activities8. In an Australian study, 53% of high school girls reported that dysmenorrhoea limited daily routines and 37% stated that it affected schoolwork9. A study from New York found 46% of students missing one or more days of school due to dysmenorrhoea10. Corresponding figures from the present study were: 62% students reported missing at least one day of school and 53% reported an impact on school performance. The authors would like to reiterate the need for screening for and treating menstrual symptoms because of the impact on daily activities and the potential to reduce avoidable suffering. Women seek a variety of sources for relief of menstrual symptoms. A survey of 2411 high school girls in Malaysia showed that 11% sought medical care although the majority (80%) obtained advice from their mothers regarding premenstrual symptoms11. A study of adolescent girls in Haryana, India, found that 5.3% consulted a physician for menstrual symptoms and 22% self-treated with over-the-counter medicines12. 52% reported self-treatment and 7.7% used complementary medicines in a Japanese study13. In the present study, although conventional medicine was felt to be most effective, it was used by only half of the women. This indicates poor access or awareness of available effective treatments. Even household and herbal remedies were infrequently used possibly due to their limited effectiveness. As menstruation and its associated symptoms are often thought to be a ‘normal’ part of women’s lives these issues may remain untreated in the community. Women who were more educated tended to seek more effective treatments, as did those who had more severe symptoms. Clinicians and public health professionals need to proactively reach women from less privileged background to reduce suffering from menstrual symptoms. Educational campaigns to improve awareness of safe and effective conventional medicine, such as non-steroidal anti-inflammatory drugs, could reach women not aware of these options. These public health campaigns may be addressed toward high-school girls, homemakers, and professionally employed women through separate targeted channels. The present study was limited by non-random (convenience) sampling yielding a study sample skewed towards more educated women. This may be due to sampling in urban areas only. The questionnaire was designed using closed-ended questions, to reduce subjectivity in data recording, limiting exploration of unanticipated variables. Psychosocial issues, such as socio-economic disadvantage and mental health, play an important role in the perception and reporting of menstrual symptoms3 but these factors were not explored in this study. Further research in this area should focus on awareness, access to care, and quality of life outcomes with different treatment options. Conclusion Low back pain and headache contribute the most to severity of dysmenorrhoea while headache and body swelling (fluid retention) were predictive of days unable to work. Conventional medicine is commonly used by more educated women, as well as those with more severe symptoms, and was perceived to be effective more often than other treatment modalities. Effective treatments for the relief of menstrual symptoms remain underutilized causing avoidable suffering.

Acknowledgements / Conflicts / Author Details
Competing Interests: 
None Declared
Details of Authors: 
NABIA TARIQ, Principal Investigator, Professor, Obstetrics and Gynaecology, Shifa College of Medicine, Pitras Bukhari Road, H-8/4, Islamabad, Pakistan M JAWAD HASHIM, MBBS FAAFP, Assistant Professor, Family Medicine, Shifa College of Medicine, Islamabad, Pakistan TARA JAFFERY, MD, DABIM, Associate Professor, Internal Medicine, Shifa College of Medicine, Islamabad, Pakistan SUMAIRA IJAZ, Medical Officer, Shifa International Hospital, Islamabad, Pakistan SARA AJAZ SAMI, Medical Student, Class of 2008, Shifa College of Medicine, Islamabad SANA BADAR, Medical Student, Class of 2008, Shifa College of Medicine, Islamabad Zainab Ara, Medical Student, Class of 2008, Shifa College of Medicine, Islamabad
Corresponding Author Details: 
NABIA TARIQ, Principal Investigator, Professor, Obstetrics and Gynaecology, Shifa College of Medicine, Pitras Bukhari Road, H-8/4, Islamabad, Pakistan
Corresponding Author Email: 
[email protected]

1.Harlow SD and Park M. A longitudinal study of risk factors for the occurrence, duration and severity of menstrual cramps in a cohort of college women. British Journal of Obstetrics and Gynaecology. 1996 Nov; 103(11): 1134-42.
2.Pullon S, Reinken J and Sparrow M. Prevalence of dysmenorrhoea in Wellington women. N. Z. Med. J. 1988 Feb 10; 101(839): 52-4.
3.Patel V, Tanksale V, Sahasrabhojanee M, Gupte S and Nevrekar P. The burden and determinants of dysmenorrhoea: a population-based survey of 2262 women in Goa, India. BJOG: An International Journal of Obstetrics and Gynaecology. 2006 Apr; 113(4): 453-63.
4.Akmal N, Akhtar N, Attique R and Raana G. Prevalence of pre-menstrual syndrome in young girls. Ann King Edward Med Coll. 2006 Jun; 12(2): 237-8.
5.Tabassum S, Afridi B, Aman Z, Tabassum W and Durrani R. Premenstrual syndrome: frequency and severity in young college girls. JPMA. The Journal of the Pakistan Medical Association. 2005 Dec; 55(12): 546-9.
6.Khakwani M, Zaidi HI and Tariq N. Adolescent age group; normal menstrual cycle and menstrual disorders. Professional Med J. 2006 Dec; 13(4): 543-9.
7.Hinohara S, Fukui T. Dysmenorrhea among Japanese women. Int J GynaecolObstet. 2008 Jan;100(1):13-7. .
8.Sharma P, Malhotra C, Taneja DK and Saha R. Problems related to menstruation amongst adolescent girls. Indian Journal of Pediatrics. 2008 Feb; 75(2): 125-9.
9.Hillen TI, Grbavac SL, Johnston PJ, Straton JA and Keogh JM. Primary dysmenorrhea in young Western Australian women: prevalence, impact, and knowledge of treatment. The Journal of Adolescent Health: Official Publication of the Society for Adolescent Medicine. 1999 Jul; 25(1): 40-5.
10.O'Connell K, Davis AR, Westhoff C. Self-treatment patterns among adolescent girls with dysmenorrhea. Journal of Pediatric and Adolescent Gynecology. 2006 Aug; 19(4): 285-9.
11.Lee LK, Chen PCY, Lee KK and Kaur J. Menstruation among adolescent girls in Malaysia: a cross-sectional school survey. Singapore Medical Journal. 2006 Oct; 47(10): 869-74.
12.Singh MM, Devi R and Gupta SS. Awareness and health seeking behaviour of rural adolescent school girls on menstrual and reproductive health problems. Indian Journal of Medical Sciences. 1999 Oct; 53(10): 439-43.
13.Ohde S, Tokuda Y, Takahashi O, Yanai H, Hinohara S and Fukui T. Dysmenorrhea among Japanese women. International Journal of Gynecology & Obstetrics. 2008 Jan; 100(1): 13-17

Predicting falls risk in patients – the value of cardiovascular variability assessment

Simon Freilich and Robert Barker
Article Citation and PDF Link
BJMP 2009:2(4) 44-48
Abstract / Summary

Objective: To test the hypothesis that an individual’s falls risk is a continuum and that physiological variation in the routine nursing observations in the lead up to the fall can be used to predict its occurrence when compared to the general hospital population.

Methods: This study was a retrospective case-control study.13 Fallers were randomly selected and compared to 47 Controls matched for age, sex and equivalent length of stay. Routine nursing observations such as heart rate, systolic blood pressure, respiratory rate, temperature and patient at risk (PAR) scores were recorded and compared over the 12 hours preceding the fall. Data was compared using a Student Unpaired T-Test with Power calculated as > 80%. Variability was quantified by the range and standard deviation of the values for each parameter.Results: The average (±SD) age of fallers in years (79 ± 16) was higher than of general medical admissions (67 ± 20) p<0.003. There was a predisposition to men falling (63%, p<0.001) compared to women. 70% were taking over 4 medications and most of the injuries were minor. The overall PAR score, temperature and respiratory rates were not predictive of falls and neither was their variability. There were no significant differences between the recorded heart rates or blood pressures between fallers and controls; however, there was much greater variation in both. The range of heart rate variation was 15 ± 10 bpm in fallers, and 7 ± 7 bpm in controls p<0.001. The range of systolic blood pressure variation was 26 ± 12 mmHg in fallers and 11 ± 7 mmHg in controls p<0.001. Orthostatic hypotension was recorded in 2 patients prior to their falls.Conclusions: Cardiovascular variation as measured by increasing range is an acute predictor of falls risk despite relatively normal absolute values. This implies that falls risk should be regarded as a continuum, above and beyond recognised basal risk factors. We therefore recommend that falls risk should become an integral part of patients’ daily assessments and incorporate the patients’ physiology together with pre-existent pathology

Falls, Heart Rate, Blood Pressure, Cardiovascular, Variability

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

  Fallers N = 13Mean ± SDRange (x-x) Controls N = 47Mean ± SDRange (x-x)
PAR Score 1.2 ± 0.6(1 – 3)  
PAR Score Variability 0.4 ± 0.6(0 – 2)  
Temperature (Celsius) 37.1 ± 0.5(36.4 - 38.1)  
Temperature Variability (Celsius) 0.6 ± 0.5(0 – 1.3)  
Respiratory Rate (Breaths/Minute) 18.5 ± 1.9(16 – 22)  
Respiratory Rate Variability (Breaths/Minute) 1.1 ± 1.5(0 – 4)  
Highest Heart Rate (Beats/Minute) 86 ± 13(70 - 110) 86 ± 14(60 -112)
Lowest Heart Rate(Beats/Minute) 71 ± 16(50 -101) 79 ± 14(55 – 110)
*Heart Rate Variability (Beats/Minute) 15 ± 10(0 – 39) 7 ± 7(0 – 27)
Highest Systolic BP (mmHg) 142 ± 22(102 – 180) 140 ± 24(99 – 218)
Lowest Systolic BP(mmHg) 116 ± 19(71 – 150) 129 ± 24(86 – 199)
*Systolic Variability (mmHg) 26 ± 12(2 – 40) 11 ± 7(0 – 26)

  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.


Acknowledgements / Conflicts / Author Details
Competing Interests: 
None declared
Details of Authors: 
SIMON FREILICH, MBBS (Dist) BSc (Hons), Clinical Decision Unit, Barnet General Hospital, Barnet and Chase Farm NHS Trust, Enfield, UK ROBERT BARKER, MBBS MSc FRCP, Consultant Orthogeriatician, Clinical Decisions Unit, Barnet General Hospital, Barnet and Chase Farm NHS Trust, Enfield, UK
Corresponding Author Details: 
SIMON FREILICH, Clinical Decision Unit, Barnet General Hospital, Wellhouse Lane, Enfield, UK. EN5 3DJ Tel: 07730650918
Corresponding Author Email: 
[email protected]

1. Droller H. Falls among elderly people living at home. Geriatrics1955 May;10(5):239-44.
2. Healey F, Scobie S, Oliver D et al. Falls in English and Welsh hospitals: a national analysis of 12 months of patient safety incident observational study based on retrospective reports. Safety Health Care 2008;17;424-430.
3. Schwendimann R, Joos F, De Geest S et al. Are patient falls in the hospital associated with lunar cycles? A retrospective observational study. BMC Nursing 2005, 4:5 doi:10.1186/1472-6955-4-5
4. Oliver D, Britton M, Seed P et al. Development and evaluation of evidence based risk assessment tool (STRATIFY) to predict which elderly inpatients will fall: case-control and cohort studies BMJ 1997;315:1049-1053.
5. The third report from the Patient Safety Observatory. Slips, trips and falls in hospital.
6. Murray GR, Cameron ID, and Cumming RG. The Consequences of Falls in Acute and Subacute Hospitals in Australia That Cause Proximal Femoral Fractures. JAGS 55:577–582, 2007.
7. Corsinovi L, Bo M, Aimonino NR et al. Predictors of falls and hospitalization outcomes in elderly patients admitted to an acute geriatric unit. Arch Gerontol Geriatr (2008), doi:10.1016/j.archger.2008.06.004.
8. Vassallo M, Poynter L, Sharma JC et al. Fall risk-assessment tools compared with clinical judgment: an evaluation in a rehabilitation ward. Age and Ageing 2008; 37: 277–281.
9. Downton JH. Falls in the Elderly. London, UK: Edward Arnold; 1993:64-80, 128-130
10. Healey F, Monro A, Cockram A et al. Using targeted risk factor reduction to prevent falls in older in-patients: a randomised controlled trial. Age and Ageing 2004; 33: 390–395.
11. Heskestad B, Baardsen R, Helseth E et al. Incidence of hospital referred head injuries in Norway: A population based survey from the Stavanger region. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2009, 17:6.
12. van Hensbroek PB, van Dijk N, van Breda GF et al.on behalf of the Combined Amsterdam and Rotterdam Evaluation of FALLs (CAREFALL) study group. The CAREFALL Triage instrument identifying risk factors for recurrent falls in elderly patients. The American Journal of Emergency Medicine Volume 27, Issue 1, January 2009, Pages 23-36.
13. Ganz DA, Bao Y, Shekelle PG et al. Will my patient fall?  J Fam Pract. 2007 Apr;56(4):276.
14. Costello E, Edelstein JE. Update on falls prevention for community-dwelling older adults: Review of single and multifactorial intervention programs. J Rehabil Res Dev. 2008;45(8):1135-52.
15. Hanlon JT, Boudreau RM, Roumani YF et al for the Health ABC study. Number and Dosage of Central Nervous System Medications on Recurrent Falls in Community Elders: The Health, Aging and Body Composition Study. J Gerontol A Biol Sci Med Sci. 2009 Feb 4.
16. Redon J, Lurbe E. Nocturnal Blood Pressure Versus Nondipping Pattern What Do They Mean? Hypertension. 2008;51:41.
17. Marshall TP. Blood Pressure Variability: The Challenge of Variation
American Journal of Hypertension (2008) 21 3–4.
18. Verdecchia P, Schillaci G, Guerrieri M et al. Circadian blood pressure changes and left ventricular hypertrophy in essential hypertension. Circulation 1990;81;528-536
19. Roghmann MC, Warner J, Mackowiak PA. The relationship between age and fever magnitude. Am J Med Sci. 2001 Aug;322(2):68-70.
20. Norman DC. Fever in the elderly. Clin Infect Dis. 2000 Jul;31(1):148-51
21. Lovett PB, Buchwald JM, Stürmann K et al. The vexatious vital: Neither clinical measurements by nurses nor an electronic monitor provides accurate measurements of respiratory rate in triage. Annals of Emergency Medicine Volume 45, Issue 1, January 2005, Pages 68-76.

Current Management of Barrett’s Oesophagus

Sharif A Anwar, Senthooran Kathirgama Kanthan and Amjid Ali Riaz
Article Citation and PDF Link
BJMP 2009:2(4) 8-14
Abstract / Summary
BO – Barrett’s Oesophagus, GORD - Gastro-Oesophageal Reflux Disease, LSBO - Long Segment Barrett’s Oesophagus, HGD - High Grade Dysplasia, EMR – Endoscopic Mucosal Resection, 5-ALA - 5-AminoLevulinic Acid, PDT - PhotoDynamic Therapy
Barrett’s Oesophagus (BO) describes a histological abnormality of the lower oesophagus widely accepted to be associated with gastro-oesophageal reflux disease (GORD). The nature of this disease has been a subject of debate since its description by Tileston in 1906 as peptic ulceration of the oesophagus. Barrett himself initially theorised that the abnormal oesophagus was in fact stomach that had been pulled into the chest by a congenitally short oesophagus (1). This idea was ultimately challenged as the area in question lacked a peritoneal covering, contained submucosal glands and muscularis propria characteristic of the oesophagus (2). In 1976, Paull et al described a distinctive type of intestinal metaplasia the investigators called "specialised columnar epithelium”. Specialised intestinal metaplasia is now widely accepted to be the hallmark of BO with its presence predisposing to dysplasia and cancer regardless of its location within the oesophagus (3). 
Barrett’s Oesophagus, its identification and treatment continues to be an area of debate and interest. Although not sinister in itself, it is a known precursor to malignant disease and strongly associated with GORD. Barrett’s oesophagus is the most frequent predisposing risk factor for the progression to adenocarcinoma in the oesophagus. Sufferers have a 40 fold increased risk when compared to the general population (4).
The progression of GORD to BO appears to be related to exposure of oesophageal tissue to the acidic contents of the stomach. It is therefore seen in hiatus hernia, lower oesophageal dysfunction, delayed oesophageal acid clearance and duodenogastric reflux. Furthermore, it is the duration and not frequency of exposure to acidity that dictates erosive damage to the oesophagus. Levels of acidity also contribute. The damage to cells incurred leads to inflammatory infiltration and cell necrosis with replacement of oesophageal epithelium by metaplastic columnar cells.
Assessing severity of BO relies partly on endoscopic visualisation techniques and length of oesophagus involved. Long segment Barrett’s oesophagus (LSBO) indicated a >3cm segment of involvement with short segment disease involving <3cm. LSBO carries a higher risk of progression to adenocarcinoma. Its development is associated with long term symptoms, severe combined patterns of reflux (both erect and supine) on 24 hour pH monitoring and reduced lower oesophageal sphincter pressures. Patients are less sensitive to direct acid exposure than those with short segment disease. The latter group also tend to have shorter duration of symptoms, normal sphincter pressures and only upright reflux on 24 hour pH monitoring (3). 
The Prague C and M criteria is a recently developed classification system utilising the circumferential and maximal extent of oesophageal columnar tissue to assess disease severity endoscopically (5). Its accuracy is yet to be assessed clinically, however, it is believed to largely improve the overall assessment of Barrett’s (6). The further classification of disease severity is based on the degree of dysplasia, with high grade dysplasia carrying a higher risk of progression to malignancy. 
Barrett’s oesophagus is predominantly seen in the age group 55-65, with males being affected twice as frequently as females. The disease is more prevalent in the white population. Obesity, smoking and alcohol intake being further risk factors. H.pylori may be protective against Barrett’s oesophagus with two mechanisms postulated. Namely, the induction of atrophic gastritis, which results in decreased acid production and the production of neutralising ammonia independent of gastric atrophy (7). The duration of symptoms of GORD but not necessarily symptom severity is also associated with increased risk of progression to BO. The exact pathogenesis is not clearly understood and is believed to be a culmination of both hereditary and environmental factors. For example, some studies report a greater incidence of BO amongst first degree relatives in comparison to their unrelated counterparts (8). Other reports associate environmental factors such as a high body mass index, with an increasing risk of GORD and progression to BO (9). Underlying mechanisms include the proposition that central obesity predisposes to hiatus hernia formation (10) and subsequent gastric acid reflux. However further research is required to unlock the key processes that lead to the formation of BO; as these pathways may hold novel therapeutic targets.      
Prevalence of BO is difficult to ascertain due to the lack of population based studies. Studies from the United States involving patients aged over 40 years undergoing gastroscopy reported a prevalence of 6.8% in all patients (11). A Swedish study involving 1000 volunteers is the only available true population based study and found a prevalence of 1.6% (12). 
Endoscopic surveillance
The most appropriate method for both diagnosis and surveillance of Barrett’s Oesophagus is endoscopy. Its sensitivity is higher than other comparative techniques, such as barium based studies or CT/MRI. Endoscopic screening programmes can be beneficial in both highlighting patients with BO from those with chronic GORD, as well as monitoring patients with established disease who are at risk of progressing to adenocarcinoma of the oesophagus. The American College of Gastroenterologists identify older patients with chronic GORD symptoms as the most likely to benefit from endoscopic surveillance techniques. Studies have also shown that five year survival rates are generally greater for patients who have had their adenocarcinoma identified by surveillance in comparison to those who have not (13). Importance also lies in the method of surveillance, for example shorter endoscopic interval analysis for surveillance in low grade dysplasia, are associated with higher rates of detection of adeonacarcinoma (14).   
Although screening for Barrett’s oesophagus relies largely on established endoscopic techniques, it remains an area of contention for several reasons. These include low prevalence and the invasiveness of endoscopy, as well as a lack of an easily identifiable demographic group. Alternative methods include the use of capsule endoscopy which offers increased acceptability of screening, is less invasive and carries an increased uptake rate in comparison (15). However a study involving 96 patients demonstrated only 67% sensitivity and 84% specificity for identifying the condition using this technique (16). A recent meta-analysis of nine studies comprising 618 patients offers the most up to date evaluation of this technique. The pooled sensitivity and specificity for diagnosing BO using this method was found to be 77% and 86% respectively. Studies using OGD as reference demonstrated sensitivity 78% and specificity 90%. With intestinal metaplasia as the reference standard, sensitivity 78% and specificity 73% was discovered although the latter figure was particularly affected by one study with very low values for this (17). Capsule endoscopy offers benefits in patient tolerance and morbidity as well as cost as the capsule can be swallowed in an office, potentially under nursing supervision. Despite this latter point, cost-benefit analysis of this technique have proved equivocal. There are also several drawbacks. Views achieved are no longer under operator control and anatomical landmarks are more difficult and potentially impossible to identify. Oesophageal transition time has been demonstrated to be as short as 1 second and biopsy is not possible regardless of this. This greatly limits the use of capsule endoscopy in BO surveillance which relies on biopsy. Ultimately, the use of capsule endoscopy in diagnosis or screening of BO is unsupported at this current time and is an area for future research.    
Other methods include small calibre trans-nasal endoscopy, which involves inserting a small-calibre endoscope through the nose and oesophageal sphincter to visualise the oespophagus, stomach and duodenum. It has the advantage of not requiring any sedation only topical anesthesia, having a lower complication rate, requiring less nursing staff and being more cost effective in comparison to its more frequently performed counterpart. Capsule endoscopy, as described earlier, also has the advantage of lacking sedation, being less invasive and yielding lower complication rates. Other alternatives include narrow band imaging, which involves scanning large areas of mucosa for possible neoplasia and autoflourescence imaging in which dysplastic lesions are visualised by differences in colour. The usefulness of visualisation techniques including high-resolution magnification endoscopy and tissue staining with agents such as methylene blue or indigo carmine are still an area of debate. These techniques have been evaluated when used in combination and alone. Pit patterns identified using acetic acid chemoendoscopy were described in 2001 by Guelrud et al (18) and Sharma et al described differing mucosal patterns in BO (19). Numerous other agents and classification systems have been described. Currently the use of these techniques for diagnostic purposes has not been shown to offer superior results than the current gold standard of four quadrant biopsies. Comparison of biopsies taken with methylene blue directed biopsy versus conventional biopsy showed no significant benefit (20). The ability to identify areas of BO (particularly high-grade dysplasia) are not in question. However, low grade dysplasia may be missed and operator experience and skill must be greatly superior to utilise the benefits of these techniques. Staining techniques offer the additional complications and additional expense of carrying out the procedure. Methylene blue has been shown to induce cellular DNA damage in vitro via the generation of singlet oxygen when photoexcited by light (21) thereby potentially being carcinogenic in itself. Evidence to support non-biopsy detection of BO is currently not sufficient to replace the current gold standard but is another area of current and future research.   
The low prevalence of BO in the general population makes screening, with upper GI endoscopy, less viable on both a financial and logistic level. The general consensus is those individuals who suffer from chronic GORD are most susceptible to BO and would therefore benefit the most from upper GI endoscopy (22). However the factors involved in the progression of BO to dysplasia and subsequent adenocarcinoma remain unclear, and hence the value of endoscopic surveillance remains a point of discussion.  
Treatment options
The treatment options for BO must also be taken into consideration when addressing surveillance and burden of the disease. The treatment options can broadly be divided into three groups, which include conservative management with surveillance endoscopy, endoscopic therapy and surgical oesophagectomy. The pathways of treatment are governed by patient-specific factors as well as the degree of oesophageal dysplasia. Surveillance endoscopy forms an integral part of the management of BO, and this is largely due to studies which have demonstrated a greater five year survival and an earlier stage of detection of oesophageal carcinomas detected by surveillance endoscopy (13, 23). Current recommendations target individuals at high risk of BO, for example those with chronic GORD symptoms. If no dysplasia is found on biopsies from two endoscopies, surveillance intervals of 3 years are recommended. However, patients with low-grade dysplasia on biopsy should have an immediate repeat endocopy to confirm the diagnosis, and then yearly surveillance endoscopies until no dysplasia is observed. The management of patients with high-grade dysplasia is contentious and varies between centres. Recommendations include a repeat endoscopy to evaluate for cancerous progression, with some centres instituting regular three month surveillance with biopsies every 1-2cm of effected mucosa (6). Other centres, depending on the multi-focal extent of dysplasia recommend surgical intervention with oesophagectomy or endoscopic therapy; which includes mucosal resection, photodynamic therapy, argon plasma coagulation and endoscopic ablative techniques.     
Oesophagectomy is normally reserved for the management of high grade dysplasia with the potential for malignant transformation. The percentage of high grade dysplasia which progress to adenocarcinoma vary throughout the literature from 5% to 59% up to seven years from initial diagnosis (7). Although oesophagectomy provides potential for complete resolution, it also carries increased number of adverse effects which include strictures, infections and anastomotic leaks. Mortality rates may also exceed 18% in centres which perform smaller amounts of the procedure on average every year (24) in comparison to high volume centres where the mortality rates can be lower than 5% (25); making the procedure very operator-dependent.    As a result less invasive therapeutic modalities are preferred in the management of lower grade oesophageal dysplasia.          
Endoscopic Therapy
Endoscopic treatment of Barrett’s oesophagus is currently an area of great interest. Endoscopic resection alone, or in combination with other treatments, have been investigated thoroughly in the past; however studies including large populations based and long term standardised protocol are lacking. The interpretation of these results is therefore very difficult. 
Endoscopic mucosal resection (EMR) for high grade dysplasia in BO was first reported in 2000 (26). The procedure involved initial identification of macroscopically visible or chemoendoscopically identifiable Barrett’s lesions. If the lesion showed no evidence of penetration into deeper tissue or metastasis, confirmed by ultrasound guidance, it would be open to resection (27). Ideal lesions include those easily identifiable by macroscopic techniques, limited in size and restricted to the mucosa. However, almost all reports realised the risk of incomplete treatment with recurrence of disease. Some authors advocated the use of circumferential endoscopic resection in order to minimise this risk (28). Endoscopic ultrasound has also been used, prior to treatment, to optimise therapy and has a degree of use in staging of oesophageal cancers (29). Post EMR data showed a low rate of complications with high rate of complete eradication of Barrett’s tissue in the short term. Larghi et al (30) investigated the long-term follow-up of patients undergoing EMR and complete Barrett’s eradication (CBE-EMR). This study involved 24 patients over a 3 year period. Histological eradication of Barrett’s oesophagus was achieved in 87.5% of patients. 3 patients suffered strictures which were endoscopically resolved. Other studies have shown similarly successful eradication with similar complications of bleeding and stricture formation (31, 32). Comparison with previous studies also demonstrated the need for long follow-up to identify potential disease recurrence. In order to minimise stricture formation, a maximum cirmcumference of 50% could be resected during each therapy. A median of 2 sessions was required for complete eradication. 13 patients also received argon plasma photocoagulation in order to ablate isolated islands of a few centimetres of BO. These studies highlight the use of mucosal resection either alone or in conjunction with other treatment modalities, such as argon plasma coagulation, in the treatment of BO. Other options are discussed below.
Argon Plasma Coagulation
This procedure involves the use of a high voltage current to ionise a jet of argon gas and treat the effected tissue. It is also used to treat bleeding lesions endoscopically hence the term coagulation. This procedure has been suggested to be of use in the treatment of BO (33, 34) and several studies have evaluated its efficacy (35-37). Conclusions have been mixed with some studies showing high rates of Barrett’s recurrence and others also suggesting poor rates of initial lesion ablation (37). Generally, rates of complete reversal of BO range in the region of 61-70% (38-42). Other studies have shown more successful results with complete ablation in 87-100% of patients (43-46). A later study evaluated these results as well as performing a further long-term follow-up of 66 patients with high-grade dysplasia undergoing APC with anti-reflux treatment. Histologically confirmed Barrett’s oesophagus was found in 12.1% of patients during further endoscopic surveillance. Patients were treated with anti-reflux therapy (both medical and surgical) and one repeat session of APC. No intraepithelial neoplasia or oesophageal adenocarcinoma was detected during the entire follow-up period of 51 months median (range 9-85) (35). 
The available evidence in relation to APC still remains slightly difficult to interpret. Even the larger trials do not involve extensive samples of patients. Furthermore there is a variance between studies with regard to patient selection and exclusion criteria, anti-reflux strategies and the procedure itself. Other pitfalls include the difficulty in assessing the precise depth of the lesion and whether the penetration during treatment was successful enough to ablate the entire lesion. There is also no histological confirmation to help correct insufficient ablation and for this reason some studies have reported an increased risk of progression to cancer and metastasis if invasion past the muscularis occurs (47). Low rates of recurrence seem to be related to the use of higher power settings for ablation, up to 90W as demonstrated by Madisch et al (35). This group also demonstrated the potential role for high dose proton pump inhibitor therapy using a total of 120mg daily in three divided doses to suppress acid for the duration of treatment. Surgical anti-reflux procedures were also found to be associated with reduced recurrence rates. As mentioned above, this procedure may in itself provide a form of treatment for BO and further progression. 
Although rare, complications of APC can be severe. Oesophageal perforation has been reported with 2 patient deaths as a consequence (40, 42). Mild oesophageal strictures amenable to endoscopic dilatation have been widely reported. Pleural effusions and bleeding ulcers have also been reported. Despite this, APC can be useful as an adjunct and also effective in the treatment of distinct groups of Barrett’s sufferers with amenable lesions.      
Photodynamic therapy
Photodynamic therapy (PDT) involves the systemic administration of a photosensitising drug, followed by irradiation with a controlled light source via an endoscope. The light, in the presence of oxygen, activates the photosensitiser causing photochemically induced tissue destruction (48). Although technically this sounds a difficult procedure, in practice it is actually one of the simplest to perform. However, as with surgical oesophagectomy, it is operator dependent with complication rates increasing within the community in comparison to specialist centres. 
The component parts of the photosensitisation process have also evolved with time.   
Several photosensitisers have undergone trial with varying results. Trials with Hematoporphyrin derivative as the photosensitising agent showed high rates of stenosis as well as prolonged sensitivity of the skin to light (49). More recently, 5-aminolevulinic acid (5-ALA) has shown promise with good therapeutic results and reduced side-effects in the short term (50-51). 5-ALA also has a reduced period of cutaneous photosensitivity of around one week, in comparison to previous photosensitisers such as sodium porfimer, in which patients would need to take precautions for thirty to ninety days (27). Several studies have demonstrated the effectiveness of photodynamic therapy in BO. The first randomised clinical trial looked at 485 patients with BO and high grade dysplasia (HGD) (52). 208 patients were accepted into the to-treat population, and received photodynamic therapy and omeprazole (PDT+OM); whilst 202 patients formed the control group and received omeprazole alone (OM). The study demonstrated a significant difference with 77% of the PDT+OM group, compared with 39% of the OM group, receiving complete ablation of HGD. The progression from HGD to adenocarcinoma was also significantly lower in the PDT+OM group (13% vs 28%). This study highlighted the effectiveness of photodynamic therapy in conjunction with medical antacid therapy, in ablating high grade dysplasia and reducing the incidence of oesophageal adenocarinoma.      
Pitfalls of PDT include the suggestion that lesions greater than 2mm in depth cannot be effectively removed (53), although the photosensitising agent used can influence this. For example, some studies have shown sodium porfimer to have an increased treatment depth of 3-4mm in comparison to other agents (54-55). However limited depth of penetration overall can compromise the ability of PDT to effectively treat high-grade dysplasia. Other common complications post PDT include stricture formation with some studies reporting rates as high as 30% overall and 50% in patients undergoing more than one procedure (56). Although high, long term complications related to this are not reported and most cases are relieved with endoscopic dilatation. Similarly other endoscopic techniques, photodynamic therapy may be inadequate at eliminating dysplastic tissue that is not visible on endoscopy. The issue of buried glands is an area of great interest due to the implication that a treated patient with macroscopically normal tissue may have dysplastic or even malignant tissue beneath. This highlights the importance of regular follow-up endoscopies with a thorough biopsy protocol. An additional complication with photodynamic therapy is the lack of histological samples post therapy, which might be used to assess the completeness of resection as in EMR.
Despite its limitations, photodynamic therapy has been proven an effective treatment for BO in numerous trials and case reports. Future directions include steps to improve photosensitiser agents, dosimetry, and light parameters which should help minimise the associated complication rate.    
Radiofrequency Ablation
Radiofrequency ablation is one of the newer endoscopic treatment modalities to show promise in preventing the progression of Barrett’s oesophagus and eliminating the lesion completely. The technique utilises a balloon, 3cm long and consisting of a 60 electrode rings spaced narrowly together every 500micrometres in a bipolar fashion (HALO360 system, Barrx Co, Sunnyvale, CA, USA). A sizing balloon is used to ascertain the circumference of the area to be treated before the ablation balloon is introduced. The system then delivers radiofrequency energy to the tissue circumferentially for 300milliseconds. A dose of 12J/cm2 has been shown to be effective in achieving depth penetration accurately above the muscularis mucosae thus limiting the complications involved with damaging deeper tissues (57). The close spacing of electrodes allows uniform penetration of the entire treated circumference and thus this technique can be used circumferentially with reports of stricture formation being minimal (58). This ability to control the depth of ablative penetration means that many other adverse side effects seen with alternative endoscopic techniques are greatly reduced. These include lower rates of chest pain, odynophagia, perforation and pneumothorax in comparison with laser and thermal ablation techniques. 
One recent paper reviewed the progress of 142 patients with endoscopically identifiable Barrett’s oesophagus and high-grade dysplasia managed at 16 separate academic and community centres. These patients underwent a total of 229 radiofrequency ablations and were followed up with repeat endoscopy and systematic biopsy for a median length of 12 months. The only adverse event of note was a stricture noticed on endoscopy in an asymptomatic patient. At follow-up, biopsy specimens were negative for high-grade dysplasia in 90% of patients. 80% of patients had no dysplasia on biopsy and 54% of patients were negative for intestinal metaplasia (59). These results are very encouraging, particularly as high-grade dysplasia carries the greatest risk of malignant progression.
Other benefits include minimal post-procedure discomfort with patients able to go home within hours of the procedure. Regarding the issue of buried glands, a study following 102 patients post circumferential ablation showed no evidence of buried glands in 4306 biopsy samples taken over a year follow-up (60). This once again highlights the advantages of RFA in comparison to other endoscopic techniques.   

The surveillance and treatment of Barrett’s Oesphagus remains an area of interest and controversy. This is heightened by the inability to discriminate those patients with BO which are most likely to progress to high grade dysplasia and then to adenocarcinoma of the oesophagus. This places greater emphasis on the endoscopic surveillance programme to identify this potentially pre-malignant state at an early stage. Future advances, particularly in endoscopic techniques, will help to increase efficacy of treatment and minimise complication rates. Further developments include progress in identification of genetic biomarkers which may help elucidate those patients at greatest risk. The management of Barrrett’s Oesophagus is becoming increasingly more important, particularly with the rise in incidence of oesophageal carcinomas in the Western world. The issues to address therefore include the identification and screening of at-risk groups and the further management from diagnosis of BO. Patients with chronic GORD symptoms are most in need of screening. Currently this should include the gold-standard four quadrant biopsy technique. This may include techniques to enhance visualisation as described above. In the authors opinion, non-biopsy screening does not carry enough evidence to support its use in replacement of biopsy as of yet. Medical treatment with PPI (if necessary in high-dose) as well as surgical treatment of GORD are essential considerations in the prevention and treatment of BO. Their use in combination with endoscopic therapy has proven benefits as outlined. Of the endoscopic therapies, the lack of complications combined with excellent post-procedure rates of disease elimination seen with RFA are most encouraging. Oesophagectomy should be reserved for those patients with disease not amenable to conservative or endoscopic therapy.  Continual research is required to help us gain more understanding into the pathogenesis of this condition, enabling us to effectively target and manage BO appropriately.   

Acknowledgements / Conflicts / Author Details
Competing Interests: 
None declared
Details of Authors: 
SHARIF A ANWAR, Watford General Hospital, Watford, UK SENTHOORAN KATHIRGAMA KANTHAN, Watford General Hospital, Watford, UK AMJID ALI RIAZ, Watford General Hospital, Watford, UK
Corresponding Author Details: 
AMJID ALI RIAZ, BSc(Hons) MBBS FRCS(Eng) FRCS(I) FRCS(Gen) PhD. Hunterian Professor RCS(Eng) & Consultant Upper GI, Laparoscopic and General Surgeon, Watford General Hospital, Watford, Hertfordshire, UK<br> Tel: 01923-244366 ext 7692<br> Fax: 01923-217962
Corresponding Author Email: 
[email protected]
1. Barrett NR. Chronic peptic ulcer of the oesophagus and 'oesophagitis'. Br J Surg. Oct 1950;38(150):175-82.
2. Allison PR, Johnstone AS. The oesophagus lined with gastric mucous membrane. Thorax. Jun 1953;8(2):87-101.
3. Johnston MH, Eaststone JA, Barrett esophagus and barrett ulcer. http://emedicine.medscape.com/article/171002-overview.
4. Gamliel Z. Incidence, epidemiology and etiology of esophageal cancer. Chest Surg Clin North Am 2000; 10:441-450.
5. Sharma P, Dent J, Armstrong D, Bergmann JJGHM, Gossner L, Hoshihara Y, et al. The development and validation of an endoscopic grading system for barrett’s oesophagus: The Prague C & M criteria. Gastroenterology 2006; 131: 1392-1399.
6. Odze. Update on the diagnosis and treatment of Barrett esophagus and related neoplastic precursor lesions. Arch pathol lab med Vol 132.
7. Wood RK, Yang Y. Barrett’s Esophagus in 2008: an update; Keio J Med 2008; 57(3): 132-138.
8. Chak A, Lee T, Kinnard MF et al. Familial aggregation of Barrett’s oesophagus, oesophageal adenocarcinoma, and oesophagogastric junctional adenocarcinoma in Caucasian adults. Gut 2002; 51:323-328. 
9. Hampel H, Abraham NS, El-Serag HB. Meta-analysis:obesity and the risk for gastroesophageal reflux disease and its complications. Ann Intern Med 2005; 143:199-211.
10. Wilson LJ, Ma W, Hirschowitz BI. Association of obesity with hiatal hernia and oesophagitis. Am J Gastroenterol 1999;94: 2840-44.
11. Rex DK, Cummings OW, Shaw M, Cumings MD, Wong RKH, Vasudeva RS et al. Screening for barrett’s oesophagus in colonoscopy patients with and without heartburn. Gastroenterology 2003;125:1670-1677.
12. Ronkainen J, Aro P, Storkrubb T, Johansson S, Lind T, Bolling-Sternevald E, et al. Prevalence of barrett’s oesophagus in the general population: An endoscopic study. Gastroenterology 2005; 129: 1825-1831.
13. Corley DA, Levin TR, Habel LA, Weiss NS, Buffer PA. Surveillance and survival in Barrett’s adenocarcinoma: a population-based study. Gastroenterology 2002; 122:633-640.
14. Ramus JR, Gatenby PA, Caygill CP, Winslet MC, Watson A. Surveillance of Barrett’s columnar-lined oesophagus in the UK: endoscopic intervals and frequency of detection of dysplasia. Eur J Gastroenterol Hepatol. 2009; 21(6):636-41.
15. Swain P. The future of wirelss capsule endoscopy. World J Gastroenterology 2008: 14(26): 4142-4145.
16. Lin OS, Schrembre DB, Mergener K, Spaulding W, Lomah N, Ayub K, et al. Blinded comparison of esophageal capsule endoscopy for a diagnosis of barrett’s esophagus in patients with chronic gastroesophageal reflux. Gastrointestinal Endoscopy 2007; 65: 577-583.
17.A Meta-Analysis of the Diagnostic Accuracy of Esophageal Capsule Endoscopy for Barrett’s Esophagus in Patients with Gastroesophageal relux Disease; Am J Gastroent Apr 2009; 104:1533-1539
18. Guelrud M, Herrera I, Essenfeld H, Castro J.Enhanced magnification endoscopy: a new technique to identify specialized intestinal metaplasia in Barrett's esophagus; Gastrointest Endosc 2001 May;53(6):559-65
19. Sharma P, Weston AP, Topalovski M, et al. Magnification chromoendoscopy for the detection of intestinal metaplasia and dysplasia in Barrett's oesophagus;Gut. 2003 Jan;52(1):24-7
20. Wo JM, Ray MB, Mayfield-Stokes S, et al. Comparison of methylene blue-directed biopsies and conventional biopsises in the detection of intestinal metaplasia and dysplasia in Barrett’s esophagus: a preliminary study. Gastrointest Endosc 2001; 54:294-301
21. Boiteux S, Gajewski E, Laval J, et al. Substrate specificity of the Escherichia Coli FBG protein (formamidopyrimidine-DNA glycosylase): excison of purine lesions in DNA produced by ionising radiation of photosensitisation. Biochemistry 1992; 31:106-10
22. Sampliner RE. Practice Parameters Committee of the American College of gastroenterology: Updated guidelines for the diagnosis, surveillance, and therapy of barrett’s esophagus. Am J Gastroenterol 2002; 97:1888-1895.
23. Peters JH, Clark GWB, Ireland AP, Chandrasoma P, Smyrk TC, DeMeester TR. Outcome of adenocarcinoma arising in Barrett’s oesophagus in endoscopically surveyed and nonsurveyed patients. J Thorac Cardiovasc Surg. 1994; 108:813-822.
24. Birkmeyer JD, Stukel TA, Siewer AE, et al. Surgeon volume and operative mortality in the United States. N Engl J Med 2003:349;2117-2117.
25. Williams VA, Watson TJ, Herbella FA et al. Esophagectomy for high grade dysplasia is safe, curative, and results in good alimentary outcome. J Gastrointest Surg 2007; 11:1589-97.
26. Ell C, May A, Gossner L, Pech O et al. Endoscopic mucosal resection of early cancer and high grade dysplasia in Barrett’s esophagus. Gastroenterology 2000; 118: 670-667.
27. Wang KK. Current strategies in the Management of Barrett’s Esophagus. Curr Gastroenterol Rep. 2005 June; 7(3):196-201.
28. Seewald S, Akaraviputh T, Seitz U et al. Circumferential EMR and complete removal of Barrett’s epithelium; a new approach to management of Barrett’s esophagus containing high-grade intraepithelial neoplasia and intramucosal carcinoma. Gastrointest endosc 2003; 57: 854-859.
29. Familiari P, Marchese M, Larghi A, Spada C, Costamagna G. Staging of esophageal carcinoma: endoscopic ultrasonography rays. 2005 Oct-Dec; 30(4) 357-62.
30. Larghi A, Lightdale CJ, Ross AS et al. Long-term follow-up of complete Barrett’s eradication endoscopic mucosal resection (CBE-EMR) for the treatment of high grade dysplasia and intramucosal carcinoma. Endoscopy 2007; 39(12):1086-91.
31. Seewald A, Giovannini M, Bories E, Pesenti C et al. Circumferential endoscopic mucosal resection in Barrett’s esophagus with high-grade intraepithelial neoplasia or mucosal cancer. Preliminary results in 21 patients. Endoscopy 2004; 36; 782-787.   
32. Peters FP, Kara MA, Rosmolen WD et al. Stepwise radical endoscopic resection is effective for complete removal of Barrett’s esophagus with early neoplasia; A prospective study. Am J Gastroenterol 2006; 101:1449-1457.
33.   Dumoulin FL, Terjung B, Neubrand M, Schuerlan C, Fischer HP, Sauerbruch T. Treatment of Barrett’s esophagus by endoscopic argon plasma coagulation. Endoscopy 1997; 29:751-753. 
34. Deviere J. Argon plasma coagulation therapy of Barrett’s oesophagus. Gut 2002; 51: 763-764.
35. Madisch A, Miehlke S, Bayerdoerffer E et al. Long-term follow-up after complete ablation of Barrett’s esophagus with argon plasma coagulation. World J Gastroenterol 2005; 11(8): 1182-1186. 
36. Attwood S, Lewis C, Caplin S et al. Argon beam plasma coagulation as therapy for high-grade dysplasia in Barrett’s esophagus.  Clin Gastroenterol and Hepatology 2003; 1:258-263.
37.   Mork H, Al-Taie O, Berlin F et al. High recurrence rate of Barrett’s epithelium during long-term follow-up after argon plasma coagulation. Scand J of Gastroenterol 2007; 42: 23-27.
38. Kahaleh M, Van Laethem JL, Nagy N, Cremer M, Deviere J. Long-term follow-up and factors predictive of recurrence in Barrett’s esophagus treated by argon plasma coagulation and acid suppression. Endoscopy 2002; 34: 950-955.
39. Basu KK, Pick B, Bale R, West KP, de Caestecker JS. Efficacy and one year follow up of argon plasma coagulation therapy for ablation of Barrett’s esophagus: factors determining persistence and recurrence of Barrett’s epithelium. Gut 2002; 51: 776-780.
40.   Morris CD, Byrne JP, Armstrong GR, Attwood SE. Prevention of the neoplastic progression of Barrett’s esophagus by endoscopic argon beamer plasma ablation. Br J Surgery 2001; 88: 1357-1362.
41. Van Laethem JL, Cremer M, peny MO, Delhaye M, Deviere J. Eradication of Barrett’s mucosa with argon plasma coagulation and acid suppression: Immediate and mid term results. Gut 1998; 43: 747-751.
42. Byrne JP, Armstrong GR, Attwood SE. Restoration of the normal squamous lining in Barrett’s esophagus by argon beamer plasma coagulation. Am J gastroenterol 1998; 93: 1810-1815.
43. Pereira-Lima JC, Busnello JV, Saul C, Toneloto EB, Lopes CV, Rynkowski CB, Blaya C. High power setting argon plasma coagulation for the eradication of Barrett’s esophagus. Am J Gastroenterol 2000; 95: 1661-1668.
44. Schulz H, Miehlke S, Antos D, Schentke KU, Vieth M, Stolte M, Bayerdorffer E. Ablation of Barrett’s epithelium by endoscopic argon plasma coagulation in combination with high dose omeprazole. Gastrointest Endosc 2000; 51: 659-663.
45. Mork H, Barth T, Kreipe HH, Kraus M, Al-Taie O, Jakob F, Scheurlen M. reconstitution of squamous epithelium in barrett’s esophagus with endoscopic argon plasma coagulation; A prospective study. Scand J Gastroenterol 1998; 33: 1130-1134. 
46. Tigges H, Fuchs KH, Maroske J, fein M, freys SM, Muller J, Thiede. A combination of endoscopic argon plasma coagulation and antireflux surgery for treatment of Barrett’s esophagus. J Gastrointest Surg 2001; 5: 251-259.
47. May A, Gossner L, Pech O, et al. Local endoscopic therapy for intraepithelial high-grade neoplasia and early adeno-carcinoma in Barrett’s oesophagus:acute-phase and intermediate results of a new treatment approach. Eur J Gastroenterol Hepatol 2002;14:1085-1091.
48. Wang KK, Kim JY. Photodynamic therapy in Barrett’s esophagus. Gastrointest Endosc Clin N Am 2003;58:483-9.
49. Pech O, Gossner L, May A, Rabenstein T et al. Long-term results of photodynamic therapy with 5-aminolevulinic acid for superficial Barrett’s cancer and high grade intraepithelial neoplasia. Gastrointest Endosc 2005. 62;1 24-30.
50. Gondrie JJ, Pouw RE, Sondermeijer CM et al. Stepwise circumferential and focal ablation of Barrett's esophagus with high-grade dysplasia: results of the first prospective series of 11 patients. Endoscopy 2008; 40(5):359-69.
51.   Sharma VK, Jae Kim H, Das A, Wells CD, Nguyen CC, Fleischer DE. Circumferential and focal ablation of Barrett's esophagus containing dysplasia. Gastroenterol. 2009;104(2):310-7.              
52. Overholt BF, Lightdale CJ, Wang KK et al. Photodynamic therapy with porfimer sodium for ablation of high-grade dysplasia in Barrett’s esophagus: internationally, partially blinded, randomized phase III trial. Gastrointest Endosc 2005;62:488-498.
53. Gossner L, Stolte M, Sroka R, Rick K, May A, Hahn EG et al. Photodynamic ablation of high-grade dysplasia and early cancer in Barrett’s esophagus by means of 5-aminlevulinic acid. Gastroenterology 1998; 114:448-455.
54. Tang S-J, Marcon NE. Photodynamic therapy in the esophagus. Photdiagn Photodyn Ther 2004; 1:65-74. 
55. Kelty CJ, Marcus SL, Ackroyd R. Photodynamic therapy for Barrett’s esophagus: a review. Dis Esophagus 2002; 15:137-44.
56. Overholt BF, Panjehpour M, Haydek JM. Photodynamic therapy for Barrett’s esophagus; Follow-up in 100 patients. Gastrointestinal Endosc 1999; 49:1-7
57. Dunkin BJ, Martinez J, Bejarano PA et al. Thin layer ablation of human esophageal epithelium using bipolar radiofrequency balloon device. Surg Endosc 2006; 20:125-30.
58. Eldaif SM, Lin E, Singh KA, Force SD, Miller DL. Radiofrequency ablation of Barrett’s esophagus: Short-term results. Ann Thorac Surg 2009; 87:405-11.
59. Ganz RA, Overholt BF, Sharma VK et al. Circumferential ablation of Barrett’s esophagus that cntains high-grade dysplasia: a U.S. multicenter registry. Gastrointest Endosc 2008; 68:35-40. 
60. Sharma VK, Wang KK, Overholt BF et al. Balloon based circumferential, endoscopic radiofrequency ablation of Barrett’s esophagus: 1-year follow-up of 100 patients. Gastrointest Endosc 2007; 65: 185-202.

Psychiatry in decline

Francis J Dunne
Article Citation and PDF Link
BJMP 2009:2(4) 59-61

What is Psychiatry?                                                                     

“The mind is its own place, and in itself can make a heaven of hell, a hell of  heaven” John Milton                                                                                                                                                                                                                                                                                    
The word 'psychiatry' is derived from the Greek for "doctor of the soul" and was first coined in the early 19th century by the German physician and anatomist, Johann Reil (1759-1813), although the treatment of mental disturbances dates back hundreds of years prior to this. The specialty of Psychiatry is regarded as dealing with the prevention, assessment, diagnosis, treatment, and rehabilitation of ‘mind’ illnesses or mental disorders. Diseases of the brain itself, for example encephalitis, tumours, and so forth, fall within the realm of neurology, generally. There are, of course, many overlapping disorders which cause neurological symptoms (paresis, slurred speech, ataxia, to cite a few) and ‘mind’ symptoms (depression, anxiety, psychosis). Disorders which affect several organ systems, for example, the autoimmune diseases, often cause multiple, bewildering neurological and mental symptoms. The primary goal of the psychiatrist is relief of suffering associated with ‘psychiatric’ disorders which include inappropriate anxiety, clinical depression, and psychotic disorders. Attempts have also been made to categorize and ‘treat’ different types of personality disorder. The latter is a contentious issue (perhaps with the exception of antisocial and borderline types) sometimes based on value judgments rather than clear scientific evidence. Treatment for mental health problems nowadays is usually community-orientated for less severe conditions and often hospital-based for more intractable disorders. The vast majority of patients are treated on a voluntary basis, whether in hospital or the community.
Medical, biological, social or psychological?                                                            
“ I think we ought always to entertain our opinions with some measure of doubt. I shouldn’t wish people to dogmatically believe any philosophy, not even mine.” Bertrand Russell
Psychiatry is sometimes criticized for adopting a ‘too’ medical or biological approach, despite the fact that many physical conditions masquerade initially with ‘mental’ symptoms. It would seem strange, if not irresponsible, were a psychiatrist, who is after all, a qualified medical doctor, not to enquire about a patient’s physical history. What is conveniently overlooked is that in everyday practice psychiatry uses a holistic approach to the patient, taking social and cultural backgrounds into account, as well as the general medical status. Treatment may thus involve medication, various forms of psychotherapy, or both, in addition to practical measures such as help with family problems, debts, housing, residential placements and so forth. In recent years, particularly in the UK, there has been a much greater emphasis on psychological treatments and social interventions. The ‘medical’ approach has taken a definitive back seat. Psychotropic drugs are frowned upon because of their side-effects, or perceived as a form of control used by psychiatrists towards their patients. Sweeping statements are made about their lack of efficacy and selective abstraction of the research is used to support such statements. Psychiatrists are denigrated for being in the grip of Big Pharma and are further demoralized by the being perceived as ‘drug pushers’. They are perceived by mostly non-medical ‘therapists’ as not being in touch with the psychological and sociological issues which are cited as underlying and perpetuating psychiatric disorders. Electroconvulsive therapy is considered barbaric; it is banned in some states in the USA. Complementary or ‘alternative’ therapies, regardless of whether or not they stand up to scientific scrutiny, are proliferating, and prescribed drugs are being replaced by ‘natural’ herbal products, despite the inherent dangers of the latter (1). Psychiatry is in decline and is becoming obsolete, a victim of its own psychobabble and increasingly mind-numbing research, understandable to the elite few. The profession is in danger of being ‘psychologised’ in order to appear acceptable and user-friendly, advocating therapies which in themselves do not stand up to scientific scrutiny. Outcome studies are quoted as favourable, when the very tenet of their foundations is very shaky, to say the least.
Perhaps there is not much reason for surprise when one considers not very long ago psychiatry advocated behaviour therapy for the treatment of homosexuality, orgone energy accumulators for neuroses, and insulin coma for schizophrenia. In hindsight such practices were totally unsound, unacceptable, and in the case of insulin coma therapy, dangerous; fortunately, they are now obsolete. Yet the history medicine is replete with such ‘cures’: mercury was once used to treat syphilis, and in surgery trepanation was widely used in ancient times for the treatment of seizures. In retrospect these procedures could be also be considered outrageous and barbaric, though with the development of scientific knowledge it is easy now to understand, reflect, and accept, that no other effective treatments were available at the time. Not so the case for psychiatry. Psychiatrists and other mental health professionals, who by and large genuinely have empathy and sympathy for their patients and want them to get better quickly, discharge them from hospital or outpatient clinics, and reunite them with their families whenever possible, are still unjustly accused of wanting to exert social control. There is no doubt that abuse of psychiatric practice does occur in some institutions and that political regimes throughout the world have used and still use powerful neurotropic drugs to subdue and control individuals who challenge the authority of the State. It is common knowledge that psychiatry was used by some totalitarian regimes as part of a system to enforce political control, for example in Nazi Germany, the Soviet Union, and the apartheid system in South Africa. Whether such abusive practices, which no doubt still exist, will ever be abolished will depend on the will of Governments and pressure from Human Rights campaigners such as Amnesty International. 
What is madness?
“ Madness is rare in individuals - but in groups, parties, nations, and ages it is the rule” Friedrich Nietzche
It is not possible to delineate the boundary between sanity and insanity. Broad definitions of mental disorder have been attempted and an individual might be said to be ‘mentally disordered’, or as formerly described, ‘of unsound mind’, when there is a more than temporary impairment of cognitive functions such as memory, orientation and comprehension, an alteration of mood leading to a delusional appraisal of one’s situation, abnormal perceptions and disordered thinking. However, this concept is criticised for being overinclusive and precise definitions of mental illness remain elusive. It is probably easier to envisage mental health problems as being on a continuum from normal to abnormal for example, from a relative sense of well-being and contentment to a state of distress and unhappiness. Further exacerbations or stressors lead to a disintegration of oneself and that sense of oneness with the environment. Loss of reality ensues with further anxiety and perplexity, disordered and confused thinking or delusions, and perceptual disturbances (usually auditory hallucinations), in some cases. The same symptoms can be caused by drugs such as cocaine or amphetamines. It is known that these drugs alter the effects of dopamine, serotonin, noradrenaline, and perhaps other transmitters, leading to the assumption that anxiety, depression and psychoses are biologically driven, the often cited chemical imbalance approach. In the case of dopamine, implicating this neurotransmitter as a sole trigger factor in psychoses is simplistic and naïve. Likewise, depression and anxiety may have other biological causes such as hormone irregularities or fluctuating glucose levels. The dopamine hypothesis alone has largely been discredited in the aetiology of psychoses. Dopamine as an causative factor is only one small part of a much wider as yet unknown picture: for example, psychosis occurs in Parkinson’s disease where dopamine is actually deficient.
The ‘psychologised’ individual                                                           
 ‘Common sense is not so common’   Voltaire
One major criticism of psychiatry concerns the endless diagnostic categories or disorders which set out to describe and define the whole range of normal human expression, from the histrionic to the shy. No wonder then that psychiatry and allied specialties, for example, psychology and sociology, are accused of a sweeping disregard for the extraordinary complexity and richness of human behaviour. Whole subsets of psychiatric specialties have mushroomed over the last 30 or more years, to include substance misuse, forensic issues, autistic spectrum disorders and many others(2). Many disorders have variants, for example schizoaffective or schizomanic subtypes for schizophrenia, without any real scientific basis for such assertions. The eccentric individual becomes ‘schizotypal’; the individual who is detached from others and prefers his/her own company, is labelled ‘schizoid personality disorder’. Some would question whether many psychiatric descriptions are indeed ‘disorders’. There are very few ‘mental’ conditions which really could be regarded as disorders, save for example, severe clinical depression, bipolar disorder, obsessive compulsive states, and the psychoses, the latter often drug-induced. The diagnostic categories become bewildering and meaningless when subtypes are used, for example schizoaffective, bipolar I and bipolar II, depression with or without psychotic symptoms, and so forth; all have their supporters and detractors. Objectively, the symptoms are merely variations on a theme and cannot be accurately rated scientifically, unlike the gradings of say, Hodgkins or non-Hodgkins lymphoma. The distinction between normal and abnormal is blurred and varies among cultures. This is particularly pertinent when describing or defining personality disorder. For example, when does narcissistic behaviour become an illness? Why should it be seen as a disorder?  Indeed, high self-esteem is encouraged in today’s’ climate and we are told to ‘love themselves more’. The usual response to the questioning of such behaviour is that it is ‘inappropriate’ or ‘out of proportion’ to the individual’s circumstances, or that ‘the patient is suffering’. Yet the entire media business, arts and entertainment, modelling and fashion industry is engaged in a narcissistic mind set, and the public love it! In other scenarios words are used interchangeably such that a psychopath, say, is perceived as a cold-blooded killer without conscience or feeling for his victim, or considered a creative genius, or indeed admired as a successful politician. The list of descriptions in the psychiatric disorders classification is wearisome and meaningless in many respects.
Much research in psychiatric journals nowadays is organic-based with ever intensive searches for newer receptors or transmitters, with increasing emphasis on the neurological basis for psychiatric conditions. In the past, emphasis was placed on the positive outcomes of drug trials, though this, fortunately, is now changing and reputable medical journals are now prepared to publish the results of negative findings. On the other hand, other researchers attempt to prove one type of psychotherapy is more effective than drug therapy, or that both together are better than either alone. Psychiatry has become polarized, with the ‘organic camp’ advocating a neurobiological basis and reductionist paradigm for psychiatric disorders, while the ‘psychotherapy model’ emphasizes the individual’s part in his/her illness with the development of strategies to defeat and overcome irrational beliefs and counterproductive emotions. There are problems with both approaches.  A great deal of criticism is now being targeted against the psychology industry with its claims of treating serious illnesses through talking cures, and using labels to categorize almost every aspect of human behaviour (3). For example, how does one account for biological symptoms which are pervasive in severe depression without considering the role of neurotransmitters and regulatory hormones? How does one measure the complexity of suffering in any one individual and translate that into a rating scale for myriads of others whose problems have different origins? Are two people with severe depression really the same if they score identical marks on a depression scale? Whole books are written on the use of rating scales for research into psychological/psychiatric disorders. Yet there are over 250 different psychotherapy treatment approaches, which inevitably leads one to question the overall value of psychotherapy (4). In Epstein’s view, the whole field of psychotherapy is ‘pseudoscientific, an elaborate mysticism only differentiated from religion by a seemingly modern orientation and the cant of science (5). Research in psychotherapy is in any event notoriously difficult because of sample sizes, control groups, placebo effects and the nature of the therapeutic intervention itself (cognitive therapy, family therapy, psychoanalytic therapy). Besides, even when some patients show a moderate improvement, nonspecific factors are always operating in the period between therapy sessions and follow-up. Patients may have had a better social adjustment because of a new job, an increase in salary, or a change in a relationship and so forth, while others may have had a general decrease in life stresses, for example, through improved physical health (recovery from surgery, better control of diabetes). Some patients will deteriorate, despite ‘cognitive restructuring’, because of redundancy from a job, or ending of a relationship and so forth.
What next?                                                   
“Just trust yourself and you’ll learn the art of living”  Goethe      
Although many of the psychological treatments available nowadays were initially propounded by psychiatrists, psychotherapy and behavioural management are now more often carried out by psychologists, nurse practitioners and counsellors. Psychiatrists tend to deal with more severely affected individuals, ironically, those deemed to need psychotropic medication or where ‘counselling’ has failed. It could be argued that talking to a stranger for a fixed number of sessions (ranging from 10–12 one-hour slots) actually impedes the normal process of recovery and that a patient would benefit more from using his/her own social networks including family, friends, general practitioner and others, who are better placed to view the patient’s problems in context. Research claiming that depressed people are most likely to benefit from cognitive therapy, or that the majority of people suffering from panic attacks will recover with anxiety management, is deceptive and naively optimistic. Too many nonspecific factors are at play. The notion that a psychologist/counsellor/psychiatrist could turn a patient’s life around in 10 hours or so (10 sessions) is difficult to sustain when such problems have accumulated over that person’s lifetime, no matter how long or short-lived. The human mind is too complex and the human condition too intricate to be hoodwinked into such quick-fix solutions. Perhaps the best way forward is, ironically, to revert to an holistic approach with better education and training of both psychiatrists and psychologists. The former need further training in neurology (they already receive extensive training in psychology) and time spent in GP surgeries, the latter should be required to gain more experience of patients with severe types of psychiatric disorders (many hospital-affiliated psychologists already do), and general exposure to medicine via an acute emergency department or at a GP surgery (say, one year in total), preferably both, in order to broaden their horizons. The author appreciates the inherent, perhaps, unfortunately, insurmountable difficulties in setting up such a system involving the various disciplines. All ‘therapists’ should have a grounding in philosophy and sociology. It needs to be made clear that many patients simply feel better by talking to someone, though this ‘feeling better’ is not often sustained, and that knowing the cause of one’s problems does not equate with ‘cure’. Many patients have intractable conditions which are not amenable to ‘talking therapies’, and such individuals do not fit the category of the ‘worried well’, the usual ‘clients’ of counsellors and other therapists.


Acknowledgements / Conflicts / Author Details
Competing Interests: 
None Declared
Details of Authors: 
FRANCIS J DUNNE , FRCPsych, Consultant Psychiatrist and Honorary Senior Lecturer, University College London, North East London Foundation Trust, United Kingdom.
Corresponding Author Email: 
[email protected]

1.Dunne FJ. The ‘Natural Health Service’: natural does not mean safer. Adv Psych Treat, 2009; 15: 49-56.
2.Diagnostic and Statistical Manual of Mental Disorders. American Psychiatric Association, 1994.
3.Tana Dineen. Manufacturing Victims. What the Psychological Industry is doing to people. Constable
   London, 1999.
4.Freeman C, Tyrer P. Research Methods in Psychiatry Royal College of Psychiatrists. Gaskell, 1989.
5.Epstein WM. Psychotherapy as Religion. The Civil Divine in America. University of Nevada Press, 2006.

Chlamydia Screening in General Practice

Anita Sharma
Article Citation and PDF Link
BJMP 2009:2(4) 62-64

Chlamydia Screening In General Practice
Sexually transmitted infections are reaching epidemic proportions in Britain and Chlamydia is the commonest sexually transmitted bacterial infections.
Chlamydia is thought to be prevalent in 5-10% of 20-24 years old. About 75% of women and 50% of men are asymptomatic. The National Chlamydia Screening Programme currently finds about 8% of young people tested to be positive 1 but this may represent selective testing of higher risk individual.
National Chlamydia Screening Programme (NCSP)
This was initiated in 2003.The aims & objectives were early detection and treatment of asymptomatic infection, to reduce the onward transmission and to prevent the development of sequelae by screening all sexually active under the age of 25 years annually or with each change of sexual partner.
The positive rate for this group in 2008 was 8.7% 1.
An ideal setting to provide screening is General Practice. The nationally agreed target is for 25% of 15-25 years olds-males and females to be screened by 2009/2010 and 35% by 2010/2011.
Chlamydia is an intracellular bacteria and causes disease by chronic inflammation which is exacerbated by re-infection. It infects the female & male genital tract and is primarily sexually acquired. It can be carried in the throat, thus oral sex can transmit the bacteria.
Over 70% of women and 50% of men are asymptomatic.
Women may experience:
•  post coital or inter- menstrual bleeding
•  pelvic pain
•  dysuria
•  increased vaginal discharge
•  P.I.D with infertility (10-40% incidence)
Men may experience:                      
•   urethral discharge
•   dysuria
•   epididymo- orchitis
•   urinary frequency
Symptoms in both men and women:
•   rectal discharge
•   rectal bleed following rectal infection
•   pharyngeal infection - rare.
Early diagnosis and treatment will reduce the risk of long term complications. A detailed history of following should be taken-
1) History of discharge-Enquire about:
•   colour & consistency of the discharge
•   odour
•   is it aggravated by sexual intercourse
•   any associated itching
•   when was it first noticed
•   any past history of the discharge
•   was it diagnosed and treated earlier
•   any association of the discharge with menstrual cycle
2) Sexual history:
•   date of last sexual intercourse
•   were condoms used
•   and if so were they used consistently
•   regular partner or not
•   any other partners in the last six months
•   has she or her partner had sex with some one else of the same sex
•   any history of sex with a partner from a different country
•   any drug abuse in either the woman or her partner
3) Contraception and cytology:
•    which contraception does she use
•    any recent change of contraception 
•    whether she is up to date with cervical cytology
•    whether all previous screens have been normal
4) Menstrual history:
•    date of LMP
•    are periods regular or have they altered recently
•    any bleeding in between periods or after intercourse
5) History of sexually transmitted infection:
•    any past history of STI
•    was it treated
•    was the partner also treated
•    did they have a test of cure
6) Others symptoms:
•   ower abdominal pain
•   dysparunia
•   dysuria
•   any soreness or warts.
7) History of treatment:
•   any medication been prescribed.
•   any usage of over the counter medications
Examination of the female patient is usually normal but may show some muco -purulent discharge with contact bleeding. If pelvic inflammation is present there will be tenderness on uterine and adnexal bimanual palpation. The patient may sometimes be unwell with temperature. In suspected rectal chlamydia, Proctoscopy may be normal or may show changes of bloody/muco-purulent discharge or ulceration of mucosa.In men with epididymo-orchitis there may be epididymal and testicular tenderness with or with out systemic features.
•  The older less sensitive (EIAs) Enzyme immunoassays are replaced by Nucleic acid amplification tests (NAATs) .They are based on polymerase chain reaction technology.
•  In some areas a combined NATT is in use for diagnosis of both Chlamydia & gonorrhoea. NATTs are not licensed for rectal or pharyngeal sampling.
•  Men should have a first void urine sample tested. In symptomatic women an endocervical swab is the sample of choice. If the patient does not require a per speculum examination a blind vulvovaginal swab could be an appropriate sample. These are almost as accurate and have become the basis for self test kits, now available widely.
•  A first catch urine (FCU) sample may be taken for women (having not passed urine for at least one hour before) but this is less sensitive in women than in men2
•  Sexually transmitted infection screen should include serological testing for HIV and syphilis. Current guidelines for HIV testing can be found at www.bashh.org.
No opportunity should be lost to discuss safe sex with young people at the time of new patient check up and when prescribing contraception. It is a good practice to screen Chlamydia with informed consent when performing cervical screening in sexually active women under 25 and those over 25 with two or more partners in the last year or a change of partner in the past year.
•  It is appropriate to treat Chlamydia in a general practice setting. Treatment is with either macrolides or tetracyclines.
•  Oral Azithromycin (Zithromax) 1gm stat should be the first choice as it avoids compliance issues. Patients must be advised to avoid sex for 7 days after the treatment. An alternative is oral Doxycycline (Vibramycin) 100 mg twice daily for 7 days or oral Erythromycin (Erymax) 500 mg twice daily for 14 days.
•  Interaction with oral contraceptive pill should be discussed. In pregnant women or those at risk of pregnancy, Azithromycin is still an option.
•  Retesting to verify cure is not advocated, partly because of the high cure rate and partly the test using NAA may remain positive for up to five weeks causing confusion.
•  All at risk partners in the last six months for females and asymptomatic males or four weeks for symptomatic males should be informed. They should be invited and treated even if the test is negative 3.The discussion and treatment can take place by the GP if the patient is registered with the practice or by referral to local genitourinary clinic.
Locally Enhanced Service
Each primary care trust has a Chlamydia screening officer. This year the target from the Department of Health is to screen 25% of patients aged 16 to 25 years registered at the practice who are sexually active.
Fee Structure
On agreeing a service plan with the PCT the general practice can receive: ( this may vary from one PCT to another PCT)
•  £4.50 per test received in the laboratory for coverage of ≤ 10% of the practice population aged 15-24 years.
•  £5.00 per test received in the laboratory for coverage of 10% to ≤20% of the practice population aged 15-24 years.
•  £6.50 per test received in the laboratory for coverage of 20% to ≤25% of the practice population aged 15-24 years.
•  £8.00 per test received in the laboratory for coverage of over 25% of the practice population aged 15-24 years.
How To Achieve Targets
•  Do a computer search of all the target patients.
•  Have a practice meeting
•  Involve the whole team: practice nurses, health care assistants and receptionists
•  Delegate, delegate and delegate! Practice nurses or health care assistants can screen at risk groups
• “new patient health check” is an ideal opportunity to offer screening. Involve the receptionist to hand out leaflets, forms and urine pots
• Make sure the reception area is suitable for handing out these items otherwise use a side room to ensure privacy
• Decide who would be dealing with positive results, treatment and partner notification
• To earn the money for extra effort you and your staff has made, make sure you use the appropriate read codeand ask the practice manager to send the claims monthly
• Remember only patients tested with in the practice premises are included when calculating the percentage screened 

• Make sure you reward your staff appropriately with the money otherwise their enthusiasm may soon vanish 

Acknowledgements / Conflicts / Author Details
Competing Interests: 
None Declared
Details of Authors: 
ANITA SHARMA, General Practitioner, Chadderton South Health Centre, OL9 8RG, UK
Corresponding Author Email: 
[email protected]

1) National Chlamydia Screening Programme team.National Chlamydia Screening Programme Agency,2008.Available at www.chlamydiascreening.nhs.uk/ps/index.html.

2) British Association for Sexual Health and HIV.Management of Chlamydia trachomatis genital tract infection-2008.Available at www.bash.org/guidelines.
3) Horner P,Boag F,2006 UK National guideline for the management of genital tract infection with Chlamydia trachomatis.BASHH 2006

Healthcare Reform in the United States: Fact, Fiction and Drama

Khalid J Qazi
Article Citation and PDF Link
BJMP 2009:2(4) 5-7

Contrary to the period in 1993, when the United States (US) President Bill Clinton failed to gain any traction on his healthcare reform, the current President, Barack H Obama, has been able to embark on historic healthcare reform. This is because major stakeholders agree that US healthcare is in crisis and requires major reform. Businesses and consumer groups have joined the insurance industry, pharmaceutical industry, and physician groups in asking for this healthcare reform that would blunt the rapidly escalating costs and provide healthcare for all Americans. While the number of uninsured Americans increased from 39.8 million in 2001 to 46.3 million in 2008, the National Health Expenditure (NHE) grew from 7.2% of the gross domestic product (GDP) in 1970 to 16% in 2005 1. This growth is projected to climb further to 19.5% in 2016. To put these figures into perspective, the US is projected to spend almost $13 trillion on healthcare over the ten years from 2010 to 2019 if the current trend continues2. Add to that the number of bankruptcies filed in the US due to healthcare expenses. Himmelstein and colleagues have recently demonstrated that of all the bankruptcies filed in the US in 2007, 62.1% were due to medical reasons as opposed to 46.2% in 2001 and only 8% in 19813 .

Hence, there is no longer any debate about ‘whether there is a problem’ but rather ‘what can be done to fix this problem’. How to fix it has been, and will continue to be, a highly contentious issue that will pitch Democrats against Republicans even after the passage of the pending legislation. Some of the key elements President Obama had identified as his basic objectives in healthcare legislation, that he is expected to sign into law by the end of 2009, include:
  1. Providing universal coverage to all Americans and requiring employers to provide health insurance to their employees.
  2. Barring insurance companies from providing policies that would exclude patients with ‘pre-existing conditions’ thereby ensuring uniform health insurance premiums for all Americans irrespective of their health status.
  3. Providing a one-stop marketplace for national health insurance exchange to allow consumers to compare and shop for different insurance plans.
  4. Promoting the use of electronic medical records and the practice of evidence-based medicine.
  5. Introducing a government-run health insurance option providing low cost, affordable health insurance that would directly compete with the private insurance industry.
This last provision, often called the ‘Public Option’, has been regarded by its opponents as an indication of how the federal government would grab political power and control the lives of all Americans. Some have gone as far as to say that the Administration is trying to introduce a ‘socialist system’ and set up ‘death panels’ to decide the fate of terminally ill Americans. 
The raging debate in both Houses of Congress (House of Representatives and US Senate), since the introduction of the legislation early this year, has been highly partisan and, at times, acrimonious. The primary debate will continue to target accessibility and the ‘Public Option’ on one hand and affordability and deficit reduction on the other. Additionally, fundamental ideological issues of the rights of women to their health (read right for abortion) and accusations of ‘socialist medicine’ (read demand for free market healthcare with little or no government oversight) will continue to fuel this debate well after the legislation has been enacted into law. At the time of writing it is clear that President Obama’s deadline of this year will not be met.
On 7th November 2009, President Obama won a major battle in this war when the House of Representatives passed the ‘Affordable Healthcare for America Act’. The vote was 220-215 and essentially along party lines with the Democrats and only one Republican voting for this legislation. According to Representative John Dingle, the 83-year-old Michigan lawmaker who had introduced national health insurance in every congress since 1955, this 1990-page bill provides coverage for ‘96% of Americans and offers everyone, regardless of health or income, the peace of mind that comes from knowing that they will have access to affordable healthcare when they need it’. However, in the run-up to the final vote, conservatives from both political parties joined hands to impose tough restrictions on abortion coverage that will continue to be a divisive issue throughout the legislative process 4 .
President Obama won the second major victory on 21st November 2009 when the Democrats (with the help of two independents) in the US Senate pushed the legislation past a key hurdle, despite vocal Republican opposition, with 60-39 votes. Sixty votes are needed in the US Senate to prevent ‘filibuster’ or an indefinite discussion on any bill 5 . With this vote the bill will now be debated in the Senate. Table 1 highlights some of the important features of the two bills:
Table 1: Important features of the Senate Bill and House Bill.
  Senate Bill House Bill
Cost* $848 billion $1.02 trillion
Projected deficit savings* $127 billion $104 billion
New patients* 31 million 36 million
Protection against generic drugs** 12 years 12 years
Government sponsored program New plan to compete with private plans; government to negotiate payment rates. New public plan through insurance exchanges; government to negotiate payment rates.
Projected reduction in Medicare growth*** $400 billion $400 billion
How is it paid for? Fees on insurance companies, pharmaceutical and medical devices industries. A new payroll tax and 5% tax on elective cosmetic surgery. $460 billion over the next decade from income tax on individuals making over $500,000 and couples making over $1 million per year.
* These are the estimates for the 10-year-period (2009-2019) from the Congressional Budget Office 6 .
** Both bills would protect biological drugs (made from living organisms rather than chemical
     compounds) from competition from generic drugs.
*** The reduction in Medicare spending is non-binding and future Congress can restore these cuts.
In this national debate, two well-known medical centres in the US, the Mayo Clinic of Minnesota and the Cleveland Clinic in Ohio, have frequently been cited as examples that could perhaps be emulated to deliver quality care in an efficient and cost-effective fashion. Both centres practise a ‘medical home’ concept based on a coordinated team approach that was introduced by the American Academy of Paediatrics in 1967. This has been further refined into the ‘patient-centred medical home’ by the American College of Physicians (ACP), American Academy of Family Physicians, and the American Academy of Paediatrics in 2007. This concept is exceedingly important for the management of chronic illnesses because the cost associated with unmanaged chronic conditions is astronomically high. It is estimated that 45% of the US population has a chronic medical condition. Amongst Medicare recipients aged 65 and above, 83% have at least one chronic health problem and almost 25% have at least five co-morbidities. Whereas the current system rewards acute care, it generally does not reimburse preventative care, chronic care management or active integrated inter-specialty management 7. A medical home provides expanded primary care that is personalized, focuses on prevention, actively involves patients in making decisions about their care and helps coordinates all of their care.
One of the deficiencies of the proposed reform is the absence of any tort reform. For physicians in the US the threat of a malpractice lawsuit is real. Without legislative relief, ‘defensive medicine’ will take a significant chunk out of healthcare dollars. Estimates suggest that savings accrued from such legislation could account for 20-25% of the NHE and may be prudently used to reduce the healthcare costs. President Obama’s outright rejection to consider tort reform in his address to the American Medical Association in June is very unfortunate and runs counter to his passionate plea to help reduce medical waste. Some of the important discussions that will take place relate to the need to revamp the physician reimbursement schedules and empower the Medicare Payment Advisory Commission to enhance primary care reimbursement, establish incentives to implement health information technology (including electronic medical records), and mandate the use of evidence based medicine and established protocols to stem the tide of escalating costs with ‘pay for performance’ and other quality measurements 8.
Healthcare reform must also address the physician shortage issue. Several studies, including those from the Institute of Medicine and the American Association of Medical Colleges (AAMC), have indicated a growing physician shortage particularly in Primary Care. In order to address this rising tide of physician shortages the Balanced Budget Act of 1996, that froze the number of reimbursable training positions at the 1996 level, needs to be revisited. As a preliminary target ACP and AAMC have recommended that the availability of Medicare-funded training positions in adult primary care specialties be increased by 3000 each year for the next 15 years 9-11.
From here on I suspect a bruising legislative debate (and drama) will continue with passion and, undoubtedly, some acrimony. Since mid-term elections are coming up in 2010, both the parties are jockeying their position as best as they can. To end the ‘filibuster’ the Democrats will need, yet again, 60 votes to pass the bill in the Senate. However that is not guaranteed at this time since many Democratic senators continue to have concerns and Republicans have made it clear that they will do whatever they can to derail this initiative. Hence further deliberation, particularly in the Senate, will entail significant manoeuvring and arm-twisting, passionate appealing, horse-trading, and perhaps additional funding for select senators to achieve 60 votes. However, in the end there will be a bill from the Senate, perhaps in mid to late January 2010. Subsequently, a conference committee will hammer out the differences in the two bills that can be presented to both houses for final passage and submitted to the President for signature.  I believe the President will have the bill on his desk for signature at the end of January or early February 2010.
Acknowledgements / Conflicts / Author Details
Competing Interests: 
None Declared
Details of Authors: 
KHALID J QAZI, MD&nbsp;MACP, Clinical Professor of Medicine, University at Buffalo,&nbsp;Program Director, UB Internal Medicine (CHS-Sister&rsquo;s Hospital)&nbsp;Master, American College of Physicians
Corresponding Author Email: 
[email protected]
  1. http://www.census.gov/prod/2009pubs/p60-236.pdf
  2. USA Today; Necessary health overhaul moves step closer to success; November 23, 2009
  3. Himmelstein DU, etal; Medical bankruptcy in the United States, 2007: Results of a national study; Am. Jr. Med. 2009, 122, 741
  4. Buffalo News; Narrow win for Obama: Health care bill clears House; November 8, 2009
  5. New York Times; Healthcare reform bill passes crucial senate test; November 22, 2009
  6. http://www.cbo.gov/ftpdocs/107xx/doc10741/hr3962Revised.pdf
  7. Editorial: Home Sweet Home; Pharmacy & Therapeutics, Vol. 34, No. 9, 2009.
  8. AAIM (Alliance for Academic Internal Medicine) Healthcare Reform; November 12, 2009.
  9. AAMC Statement on the Physician Workforce: www.aamc.org/workforce
  10. Solutions to the Challenges facing the primary care medicine: www.acponline.org/advocay
  11. Will generalist physician supply meet demands of an increasing and aging population? Health Affairs: April 29, 2008

Leg Ulcers in Older People: A Review of Management

Adeyemi Adeyi, Sharon Muzerengi and Indrajit Gupta
Article Citation and PDF Link
BJMP 2009: 2(3) 21-28
Abstract / Summary

Leg ulcers are a common presentation in the elderly population associated with a negative impact in the quality of life. Several factors including venous and arterial insufficiency, immobility and obesity all contribute to an increased incidence in this age group. A thorough assessment including comprehensive history of ulcer development, examination of the ulcer site, size, shape, appearance and vascular assessment with Doppler ultrasound are all essential in deciding type of treatment. Various treatment modalities are available for the management of different types of leg ulcers although no clinical trials comparing the efficacy of one treatment over the other have been done. Some of them have not got strong evidence to show that they actually improve healing, still awaiting further research.

Leg ulcers are defined as discontinuity of the epidermis and dermis in the lower limb of more than 6 weeks duration 1, 2. They are a common presentation in the elderly population and are associated with a negative impact on the quality of life of patients and they also cause a substantial burden on the health budget 3. Pathogenesis of leg ulceration is heterogeneous 4. Prevention strategies, early identification and proper management are paramount in improving quality of life of patients and reducing costs on an already strained health budget. In this article we review the prevalence of leg ulcers in the elderly people, its common causes and management.

Prevalence                          The estimated prevalence of leg ulcers in the UK is between 1.5 and 3 per 1,000 population 3.A studies by Moffat et al 2004 showed a prevalence of 0.45 per 1000 which is less than the previously reported figures 5. In the same study leg ulceration was found to be more common in females than males  5. In a systematic review of prevalence studies for leg ulcer, the authors also reported an increase in prevalence of leg ulcers with age and in women 6.The overall prevalence of ulcers is not affected by social class although ulcers tend to take longer to heal in lower socio economic classes 7. Quality of life Several studies have shown that patients with leg ulcers have a poor quality of life compared to age matched controls 8, 9.A systematic review of studies measuring quality of life of patients with leg ulcers showed a negative impact on several domains of quality of life 8. In most of the studies pain was shown to be the major complaint among leg ulcer patients compared to controls, with males experiencing greater pain intensity than female patients. 10, 11 Restricted mobility and sleep disturbance due to pain was also reported in other studies.12 Leg ulcer patients often complain of itchiness, odour and leg swelling 8.  In one study, unpleasant odour was reported as causing social embarrassment leading to higher anxiety and depression scores as well as altered body image 12.Reduced mobility due to leg ulceration can restrict working capacity in younger patients13.A negative emotional impact on life with symptoms such as anger, depression, and social isolation was reported by 68% of patients in another study looking at impact of leg ulcers on quality of life 14Aetiology Several factors contribute to the development of leg ulcers. However majority of ulcers are due to venous insufficiency which accounts for about 80-85% of all cases. 15, 16. Frequency of venous ulcers increases with age as a result of several factors such as immobility and venous disease15.  Other risk factors for venous ulceration include obesity, previous deep vein thrombosis, thrombophlebitis, previous fracture, and varicose veins 17.Venous ulcers(also referred to as varicose or stasis ulcer)are commonly found between the malleoli and lower calf and are associated with a shallow base covered with granulation tissue and fibrinoid material, and have irregular margins 16,17. The mechanism of venous ulceration involves initial damage to valves as a result of thrombosis or valve incompetence in varicose veins leading to pooling of blood in lower limbs. Extravasation of red blood cells then follows which causes a local inflammatory reaction and collagen deposition. This impairs the healing process eventually resulting in tissue breakdown and hence ulceration16. Venous ulcers are also associated with symptoms such as oedema, eczema.Arterial ulcers form the second largest group of leg ulcers and account for about 20% of leg ulcers. Atherosclerosis and diabetes are the commonest causes of this group of ulcers. Thrombotic episodes secondary to vasculitis, thromboangitis, and sickle cell disease can also result in arterial ulcers17.Arterial insufficiency causes hypoxia, ischaemia, tissue necrosis and consequently ulceration 18.Arterial ulcers are usually found below the ankle especially on the toes. The ulcers are characteristically small, have steep edges and a dry base. Risk factors for arterial ulcers include conditions that predispose to peripheral vascular disease such as smoking, diabetes, hypertension, hyperlipidaemia and obesity 17. It is worth mentioning that diabetes causes foot ulcers via two mechanisms: ischemia and neuropathy. Neuropathic ulcers are usually found on the plantar surface of metatarsal heads or on the toes. They are a consequence of poor glycaemic control19. The risk of malignancy in chronic leg ulcers is generally believed to be small, but a study by Yang et al 1997 showed a rate of 4.4% in chronic leg ulcers. The diagnosis should be considered in patients with non healing ulcers despite optimum management 20.  Chronic inflammatory conditions such as rheumatoid arthritis, inflammatory bowel diseases are also associated with leg ulceration. Rare causes of leg ulceration such as ill fitting shoes have also been reported in literature. In a study looking at complications of ill fitting footwear among 65 elderly patients, foot ulceration was reported by 15% of the patients 21. Although small, this study showed that simple measures such as appropriate foot wear may be useful in preventing foot ulcers. Table 1: summarises causes of ulcers and main characteristics of leg ulcers 16, 17

Aetiology of ulcer Characteristics  
Venous Between malleoli and lower calf, shallow, irregular margins, granulation base. Oedema, eczema
Arterial Painful, below ankle distal, especially toes, small, dry baseIntermittent claudication
Vasculitis Associated with Rheumatoid arthritis, Polyarhritis Nodosa(PAN)
Malignancy Basal cell , squamaous cell carcinoma, melanoma
Neuropathic Common in diabetes, wet, deep, sharp borders on pressure points

 Management  Like all medical conditions, management of leg ulcer should include a detailed history of the onset of the problem (as well as past medical history), examination of the legs and skin, investigations and modalities of treatments. The underlying causes need to be identified as this has crucial implications for management. A medical history suggestive of venous and arterial ulcers have been mentioned above but other factors to consider while assessing leg ulcer are: general health status, cigarette smoking, nutrition, limitation to self care, pedal pulses, Ankle Brachial Pressure Index (ABPI), oedema, limb size and shape, sensation and pain (Table 2). Table 2: Assessment of lower limb ulcers 

Patient History of ulcer developmentPast and current medical problemsGeneral health statusNutritionSocial, occupationMobility problemsLimitation to self careObesityDepression 
Skin changes VenousArterialMalignantAuto immune 
Vascular assessment Pedal pulsesAnkle Brachial Pressure Index
Limb factors OedemaCircumferencesLymphoedemaOrthopaedic problemsSensation and pain 
Ulcer SiteAppearanceSize-measureWound baseExudate levelSurrounding skin

Examination of the legs and skin identifies markers of underlying pathology. Venous disease may present with some or all of the following: brawny skin, haemosiderin staining, lipodermatosclerosis, atrophie blanche (patchy areas of ischemia),and stasis eczema, while the skin of patients with arterial disease is often shiny, hairless, pale and cool; with thickened nails and changes in foot structure. The absence of venous or arterial signs and symptoms raises the possibility of less common causes of ulceration like: Sun damaged skin, Bowen disease or a history of previous skin cancer treatment is an alert to a malignant lesion.                                                                    Site & Appearance: Most venous ulcer occur in the “gaiter” area of the leg (i.e. area extending from just above the ankle to below the knee and tends to occur on both lateral and medial aspect of the leg), they are usually superficial with poorly defined margins. The base of the wound is usually red granulation tissue with moderate to high levels of exudates. Arterial ulcers can occur anywhere on the lower leg and may appear in the gaiter region, especially with coexisting venous disease. Many arterial/ischaemic ulcers occur over bony prominences and have a history of pressure related cause. They are often deeper with a punched out appearance and may involve structures such as muscles, tendon and bone in the base. They have sloughy, devitalized tissue in the wound base and low levels of wound exudates. Ulcers occurring in atypical site with an atypical appearance require further investigation to determine the cause. Ulcers with a violaceous (purple) border, inflammation, and extreme pain, may be related to vasculitis problem or underlying connective tissue disorder. Size: Dimensions of the ulcer should be taken at first presentation and fortnightly thereafter and recorded in the notes. This is important as it gives an objective assessment of the effectiveness of the current treatment plan, and modify as necessary22.There are a range of techniques available such as digital photography, ruler based vertical, horizontal and depth measurements and circumferential tracings of wound margins using acetate sheets over cling film .The system chosen needs to reflect consistency, accuracy, and reduced operator error, and also provide visual feedback to the patient. Pain: The level of pain associated with ulcer must be assessed on presentation and at each visit thereafter using a standardized pain scale (0-10). Pain may suggest infection or arterial disease, so careful assessment is required.Surrounding skin area should be observed for the presence of eczema, hyperkeratosis skin, maceration, cellulitis, signs of irritation and scratching which are signs and symptoms associated with underlying venous disease.Assessment should also include palpation of peripheral pulses, regular blood pressure measurement, weight (with reference to a Body Mass Index chart) as well as routine urinalysis (to screen for diabetes). Vascular Assessment: This is mainly carried out by the use of Doppler ultrasound to measure the Ankle Brachial Pressure Index (ABPI).This is mandatory and must be repeated every 3 months. All patients with a non healing wound on the leg of greater than 4-6weeks should have a vascular assessment to eliminate any underlying ischaemic disease22.The result of ABPI are used to determine the likelihood of arterial insufficiency and can be used to guide the management plan, especially in relation to healing potential, referral for vascular assessment and use of appropriate compression bandages. 23 The normal range for ABPI is 0.8-1.2. An ABPI of less than 0.5 or greater than 1.2 needs vascular opinion. Treating the ulcer Many dressing materials are available for the treatment of leg ulcers and there is no adequate evidence from clinical trials to recommend one dressing type over another, but we have to bear in mind few criteria in choosing a particular dressing. The dressing should be low adherent, cost effective and must also be comfortable as well as acceptable for the service user. The choice of product should be determined by   the level of exudate. Products which commonly cause skin sensitivity such as those containing lanolin and topical antibiotics should not be used on any service user22. The use of white soft paraffin has been identified as a potential fire hazard risk, hence a water based emollient should be considered as an alternative to a paraffin emollients e.g aqueous cream. Please note water based emollients are not as effective in providing sustained emollient therapy as an ointment and also contain preservatives, which are known potential irritants. Other modalities of treatments of leg ulcers are described below.  Compression Therapy The mainstay of treatment of any venous component to ulceration is the application of sustained, graduated compression at therapeutic level 24 .Graduated compression increases venous flow, decreases valvular reflux while walking and increases the effectiveness of the calf muscle pump resulting in a “thinning leg”. The most effective level of compression to overcome venous hypertension has been determined to be around 40mmHg at the ankle 25. Correct application of bandages is essential to avoid pressure ulceration over the bony high points and along the anterior border of the tibia. It is acknowledged that the application of compression bandaging is a specialized skill traditionally undertaken by nurses. The combination of compression bandages used to achieve compression of 40mmHg at the ankle will depend on ankle circumference, according to Laplace’s law, which states that the sub bandage pressure is inversely proportional to the circumference of the limb. A modified compression regimen is necessary when pain is present. This may be achieved by providing periods of relief until pain is controlled or removing the bandage at night when the leg is elevated. Patients with mixed arterial and venous disease may only tolerate up to 20mmHg compression to treat oedema. Bandage choices include short stretch, long stretch, multilayer systems and stockings. A Cochrane Review of compression regimens identified increased healing rates with compression compared to no compression26 . A high compression bandages were better than moderate compression bandages, and that multi-layered bandages were better than single layered bandages. Comparisons between various high compression bandages systems, e.g. 4 layer and short stretch bandages, were unable to find any difference in effectiveness. For venous ulcer with ABPI > 0.8, use 4 layer bandages as per ankle circumference below (Table 3) Ulcers with ABPI between 0.6-0.8: Reduced compression is achieved by omitting the outer cohesive bandage (e.g. Coban) Table 3: Multilayered bandage regime in relation to ankle circumference. 

Up to 18cm 2 or more wool padding1 light stretch bandage(Elastocrepe)1 light elastic bandage 3a(K-plus)1 cohesive bandage 3b(Coban)
18cm-25cm 1 wool padding1 light stretch bandage(Elastocrepe)1 light elastic bandage (K-plus)1 cohesive bandage (Coban)
25cm-30cm 1 wool padding1 high elastic bandage(Tensopress)1 cohesive bandage (Coban)
Greater than 30cm 1 wool padding1 light elastic bandage (K-plus)1 high elastic bandage(Tensopress)1 cohesive bandage (Coban)

Once the ulcer site is well healed, continue with the compression bandages for at least 4 weeks and then maintain compression at a slightly lower level indefinitely as tolerated. It must be replaced annually. Other factors to consider and deal with include: Infection This requires regular cleansing, more frequent changes of dressing (especially if exudates levels are high), topical antimicrobial dressings or systemic antibiotics. Pain Ranging from simple analgesia to potent opioid (depending on severity of pain), non steroidal anti inflammatory drugs may be beneficial. For neuropathic pain, amitriptyline can be started which can be replaced by gabapentin if no improvement. The dose can be titrated upwards. Pressure: Requires pressure relief for the ulcer to heal especially over bony prominences. Larval Therapy Larval therapy has been used for debridement of wounds for many years.27 Debridement is an essential component of wound care as the presence of devitalized tissue can impede the healing process. While the exact mechanism of larval therapy remains unknown, it encompasses three processes: debridement, disinfection and promotion of healing. The beneficial effects of larval therapy were first observed during the Napoleonic war by Larrey, who noted that soldiers whose wounds had become infested with maggots had an improved prognosis 27. During the First World War, Baer documented the successful treatment of leg ulcers and osteomyelitis using larval therapy, and paved the way for further use of it by doctors of that time. However, the development of antibiotics and improvements in surgical techniques reduced larval therapy to a “treatment of last resort”, reserved for the most intractable wounds 28. The emergence of antibiotic- resistant strains of bacteria such as methicillin resistant staphylococcus aureus (MRSA) and the curiosity of researchers has prompted a resurgence of interest in larval therapy. Larval therapy has been employed effectively to treat a wide spectrum of wounds including venous and arterial leg ulcers29.Some of the benefits of larval therapy include: reduction in wound pain and odour, and promoting healing process with relatively few side effects30 .Larval therapy is also reported as being cost-effective in comparison with conventional wound dressings. The use of larval therapy often resulted in quicker healing, and a subsequent reduction of nursing time and materials30. A further advantage of larval therapy is that, as larvae are typically applied for 3 days, wounds are disturbed less frequently than conventional dressings that require changing every 1-2days.In addition to this, a further advantage is that treatment can usually be carried out in outpatient and community settings. A study   at an outpatient wound clinic on chronic wounds, of varying aetiologies reported that using larval therapy resulted in a 62% decrease in need of amputation 31. Larvae offer the benefit of eliminating bacteria from the wound through ingestion and subsequent degradation within their intestinal tract. They also act to reduce bacterial activity through the production of inhibitory secretions. The most commonly mentioned disadvantage of larval therapy is the negative perception with which it is regarded by both patients and practitioners because of the unpleasant appearance. The use of Biobags, which completely enclose the larvae within a polyvinyl alcohol membrane, has become a popular method of improving the application of this treatment, as larvae are able to feed freely through the open cell polymer. Pain has occasionally been reported by patients, the cause may be the sharp mouth hooks and spicules with which larvae anchor themselves onto tissue. A case history has suggested larval therapy to be contraindicated with fistulae, exposed wounds connecting to vital organs32  because bloodstream infections have been reported with some larvae33.Alteration of the disinfection process appeared to eliminate this problem, and with no further cases of sepsis occurring during the subsequent 12 months The risk of cross-infection by escaped larvae may be greatly reduced through careful dressing. Vacuum Assisted Closure therapy Vacuum Assisted Closure (VAC) therapy involves the application of controlled negative pressure to wounds 34. Negative pressure, as a method of management for difficult to heal wounds, was initially explored in 1970, with the first wound drainage system being introduced in 1989. The use of negative pressure to heal wounds, however, is more commonly associated with the work of Argenta and Morykwas in 1997.35 VAC therapy was designed with the aim of improving healing, decreasing morbidity, and decreasing the cost and length of hospital stay in patients with chronic, non healing wounds. VAC therapy promotes healing in several ways. Firstly, the foam dressing, in combination with adhesive tape, creates an occlusive dressing. This alone prevents dessication and increases the rate at which epithelial tissue is developed, therefore aiding healing times. Occlusive dressing prevents an increase in infection. Secondly, the suction effect and the mechanical forces generated at the interface of the foam work to decrease interstitial fluid accumulation, control wound exudates, stimulate granulation tissue formation, reverse tissue expansion, decrease bacterial colonisation and increase blood flow and dermal perfusion. In summary, VAC therapy aids wound healing by:       Maintaining a moist environment       Increasing local blood flow       Removing wound exudates       Promoting granulation tissue formation       Reducing infection       Exerting mechanical pressuresVAC therapy is suitable for the following wound types/processes 36        Acute   (trauma, burns)        Chronic (pressure sores, leg ulcers, diabetic ulcers)        Surgical (skin grafts, flap surgery, wound bed preparation)        Salvage (wound dehiscence, wound infection, post operative sternum infections) Contraindications to the use of vacuum therapy include: wounds with untreated osteomyelitis, grossly infected wounds, when necrotic tissue is present or when there is unspecified disorder of the blood. VAC therapy should also not be used in wounds with malignancy .Dressings should not be placed over any exposed vessels or organs and VAC therapy should be used with caution in patients with active bleeding, difficult wound haemostasis and in patients taking anticoagulants. Skin grafting Skin grafting is the transplanting of skin, and, occasionally, other underlying tissues to another location of the body. It is the only means of reconstructing a defect in the skin, regardless of the cause of the defect 37. Generally, skin grafting is used when, in the opinion of the reconstructive surgeon, other methods of reconstruction such as primary closure, secondary intention healing, or local skin flap are inappropriate, are unavailable or would produce a suboptimal result. Skingraft are divided into 2 major categories: full thickness skin graft (FTSGs) and split thickness skin graft ( STSGs).STSGs may be subdivided into thin (0.008-0.012mm),medium(0.012-0.018mm) and thick (0.018-0.030mm)grafts 37. STSGs are the one used in covering chronic unhealing cutaneous ulcer. Split skin grafting is technically demanding and requires hospital admission25. The discharge from the surface of venous ulcers tends to dislodge continuous sheets of split skin, leaving a choice between mesh and pinch skin grafting. Pinch skin grafting provides epithelial islands, from which epithelial growth may spread outwards as well as inwards from the ulcer margin. Pinch skin grafting has been done by district nurses in the community and has been found to be cost effective accelerating healing when used with multilayer compression bandaging.25 Some contraindications to the use of skin graft generally include: vascular tissues such as exposed bone or cartilage (as this will lead to graft necrosis), uncontrolled bleeding of the recipient because of haematoma and/or seroma formation under the graft compromises graft survival. Venous Surgery Superficial venous surgery has been shown to improve ulcer healing in patients with only superficial venous incompetence38. In patients with no deep reflux on duplex imaging, superficial venous surgery has been shown to reduce long term ulcer recurrence25 . Indications for superficial venous surgery are:

  •  Patient fit for surgery
  •  Sufficient mobility to activate calf muscle pump
  •  Prepared to attend hospital for investigation and surgery
  •  Obesity controlled (BMI <30)
  •  Superficial venous incompetence

 There are few other modalities of treatment of leg ulcers currently in use, although no strong evidence has been found to show they really improve healing. Intermittent Pneumatic Compression Intermittent pneumatic compression (IPC) is a mechanical method of delivering compression to swollen limbs that can be used to treat venous leg ulcers and limb swelling due to lymphoedema.It uses an air pump to inflate and deflate an airtight bag wrapped around the leg.39 However, review of trials found conflicting evidence about whether it is better than compression bandages. It may increase healing compared with no compression but it is unclear whether it improves healing when added to treatment with bandages. Electromagnetic Therapy  Electromagnetic therapy involves the use of electromagnetic, microwave, or infrared energy to diagnose or treat an illness by detecting and correcting imbalances in the body's energy fields. Electronic devices that emit some form of low-voltage electrical current or radio frequency are often involved. It has been used in the treatment of chronic diseases like venous leg ulcers. Cochrane wound group conducted trials on several occasions comparing electromagnetic therapy with other treatments and up till now, there is no reliable evidence of benefit of electromagnetic therapy in the healing of venous leg ulcers.40 Further research is still needed.  Oral Zinc Supplement Leg ulcers may take long time to heal despite good wound care. This may be due to poor nutrition which reduces the ability of the body to repair itself. Minerals such as zinc are necessary for good healing and so it has been thought that taking zinc sulphate tablets might aid healing of ulcers especially if patients were found to have low baseline Zinc level. Few trials were found where zinc was used to treat leg ulcers but all were too small to pick up on any benefit, if such a benefit exists. In addition, the quality of those trials was mediocre. On the basis of the evidence available so far, it appears that taking zinc tablets does not improve leg ulcer healing, however more good quality trials are needed.41 Laser Therapy Low level laser therapy (LLLT) refers to the use of red beam or near infrared laser with a wavelength between 600and 1000nm power from 5-500 milliwatts.It is also referred to as cold laser therapy, low power laser therapy (LPLT), low intensity laser and low energy laser therapy. The exact effect of its mechanism is unknown; however, hypotheses have included improved cellular repair and stimulation of the immune, lymphatic and vascular system. Several randomised controlled trials involving patients with venous ulcers failed to demonstrate any significant benefits of LLLT when compared to standard treatment methods or placebos.42 Hyperbaric Oxygen Therapy Oxygen is one of the most versatile and powerful agents available to the modern medical practitioner. The therapeutic use of oxygen under pressure is known as hyperbaric oxygen therapy (HBO2) and has been used to assist wound healing for almost 40 years. HBO2 has several specific biological actions which can enhance wound healing processes .These include: Hyper-oxygenation of tissue, vasoconstriction, down regulation of inflammatory cytokines, up-regulation of growth factors, antibacterial effects, potentiation of antibiotics, and leukocyte effects.43 Systemic oxygen can be administered via 2 basic chambers: Type A( multiplace) and Type B(monoplace). Both types can be used for routine wound care, treatment of most dive injuries, and treatment of patients who are ventilated or in critical care.HBO2 is a relatively safe non-invasive therapy. Side effects include middle ear and pulmonary barotraumas and myopia. Contraindications include poor cardiac output and severe obstructive pulmonary disease. Conclusion In this article, we have been able to show that leg ulcers are a common presentation in the elderly population and have negative impact on the quality of life of affected patients. It has been found to be more common in females. Most leg ulcers (about 80-85%) are caused by venous insufficiency, followed by arterial ulcers. A comprehensive assessment of the patient, skin, vascular status, limb and ulcer is required to determine aetiology and to formulate an appropriate management plan as described above. Several researches are still going on other modalities of treatment of leg ulcers. However, all patients should be provided with both verbal and written information to help them understand their condition and treatments they receive, as this will enable them to better understand their conditions, and will support concordance between patients and staff.


Acknowledgements / Conflicts / Author Details
Competing Interests: 
None Declared
Details of Authors: 
ADEYEMI ADEYI MBBS, Locum Specialist Registrar, Department of Medicine for Older People, Basildon and Thurrock University Hospital NHS Foundation Trust, Essex, UK. SHARON MUZERENGI MBCHB, Specialty doctor,Department of Medicine for Older People, Basildon and Thurrock University Hospital NHS Foundation Trust, Essex, UK. INDERJIT GUPTA MBBS (Hons) FRCP (Lond) FRCP (Glas), Consultant physician Department of Medicine for Older People Basildon and Thurrock University Hospital NHS Foundation Trust, Essex, UK.
Corresponding Author Details: 
ADEYEMI ADEYI MBBS, Locum Specialist Registrar, Department of Medicine for Older People, Basildon and Thurrock University Hospital NHS Foundation Trust, Essex, UK
Corresponding Author Email: 
[email protected]

1. Compression therapy for venous ulcers, effective health care 1997; 3(4) NHS centre for reviews and dissemination, University of New York.
2. Nelson E A and Jones J. Venous Leg Ulcers. Wounds.
3. Palfreyman S. Assessing the impact of venous ulceration on quality of life Nurs Times. 2008 Oct 14-20; 104(41):34-7.
4. Korber A, Schadendorf D, Dissemond J. Causes of leg ulcers: Analysis of data from a dermatologic wound care center. Hautarzt. 2009 Mar 22. [Epub ahead of print}
5. Moffat CJ, Franks PJ, Doherty DC et al. Prevalence of Leg ulcers in a London population. J Med 2004: 97; 431-437.
6. Graham ID, Harrison MB et al. Prevalence of Lower –limb ulceration: a systematic review of prevalence studies.Adv Skin Wound Care.2003; 16(6):305-16.
7. Sign 1998. http://cks.library.nhs.uk/leg_ulcer/evidence/refereence#A6658.
8. Herber OR, Schnepp W, Rieger M. A systematic review on impact of leg ulceration on patients’ quality of life. Health and quality of life outcomes of life outcomes.2007; 5:44.
9. Walter SJ, Morrel CJ, Dixon S. Measuring health related quality of life in patients with venous leg ulcers. Qual Life Res.1999; 8(4):327-36.
10. Lindholm C, Bjellerup M et al. Quality of life in chronic leg ulcers.1993: Acta Dermatology Venereal.1993:73:440-444.
11. Goncalves ML, de Gouveia Santos VL et al. Pain in chronic leg ulcers. Journal of wound, Ostomy, continence nursing 2004; 31(5):275-283.
12. Cullum NRB. Leg ulcers: Nursing Management-A research based guide. Scutari Press 1995:125-134.
13. Chase S, Melloni M, Savage A: A forever healing: the lived experience of venous ulcer disease.Journal of Vascular nursing.1997; 10(2):73-78.
14. Phillip T, Stanton B et al.A study on impact of leg ulcers on quality life: financial, social and psychological implications. Journal of the American academy of Dermatology. 1994, 31(1):49-53.
15. Simon, D.A., Dix, F.P. and McCollum, C.N. Management of venous leg ulcers. British Medical Journal.2004; 328(7452), 1358-1362.
16. John Hickey.Management of leg ulcers.http://www.theberries.ca/ARchives/2006Winter/ulcer_management.htlm.
17. Grey JE, Harding KG, Enock S. Venous and arterial ulcers. BMJ. 2006; 332(7537): 347–350.
18. Sieggreen MY, Kline RA. Arterial Insufficiency and Ulceration: Diagnosis and Treatment Options. Advances in Skin & Wound care.2004; 17:242-51.
19. Edmonds M E. Diabetic foot ulcers. BMJ. 2006; 332(7538): 407–410.
20. London NJM and Donnely R. Ulcerated Lower limb. BMJ. 2000; 320(7249): 1589–1591.
21. Burns SL, Leese GP, McMurdo M E P. Older people and ill fitting shoes. Postgrad Med J 2002; 78:344–346.
22. RCN (Royal College of Nursing) leg ulcer guidelines 2006.
23. Australian family Physician. Leg ulcers-causes and management.2006; 35(7).
24. Nelson E.compression bandaging for venous leg ulcers Wound care 1996; 5:57-9.
25. Deborah Simon, Francis P Dix, Charles N McCollum. Management of venous leg ulcers, (clinical review). BMJ 2004; 328:1358-1362.
26. Cullum N, Nelson E, Fletcher A, Sheldon T. Compression bandages and stockings for venous ulcers. The Cochrane Library 2006, issue 4.
27. A Parnes; K.M.Lagan Int J clin Pract. 2007; 61(3): 488-493.Larval Therapy in Wound Management: A review.
28. Evans H. A treatment of last resort. Nurs times 1997; 93:62-5.
29. Donald J.Grande, David S Mezebish. Skin grafting. EMedicine Dermatology, October 2008.
30. Green T. Larval therapy in the community-challenge or opportunity? Nurse to Nurse 2004; 4:51-2
31. Sherman RA, Sherman J, Gilead L et al.Maggot debridement therapy in outpatients. Arch phys Med Rehabil 2001; 82: 1226-9
32. Thomas S, Jones M. The use of sterile maggots in wound management. Wound care Soc Educ Leaflet 1999; 6
33. Nuesch R, Rahm G, Rudin W et al. Clustering of bloodstream infections during maggot debridement therapy using contaminated larvae of Protophormia terraenovae. Infection 2002; 5:306-9
34. CEP 08017: June 2008.Evidence review Vacuum Assisted Therapy.
35. Argenta, Land M.Morykwas, and vacuum assisted closure: a new method for wound control and treatment: clinical experience. Annals of plastic surgery, 1997.38: p 563-576.
36. Jones, S.M, P.E.Banwell, and P.G.Shakespeare, Advances in wound healing: topical negative pressure therapy. Postgraduate Medical Journal, 2005.81(956): p353-357.
37. Donald J.Grande, David S Mezebish. Skin grafting. eMedicine Dermatology, October 2008.
38. Bello M, Scriven M, Hartshorne T, Bell PRF, Naylor AR, London NJM. Role of superficial venous surgery in the treatment of venous ulceration.Br J surg 1999; 86:755-9. [Medline]
39. Nelson EA, Mani R, Vowden K. Intermittent pneumatic compression for treating venous leg ulcers. Cochrane Database of Systematic Reviews 2008, Issue 2.
40. Ravaghi H, Fleming K, Cullum N, Olyaee Manesh A. Electromagnetic therapy for treating venous leg ulcers. Cochrane Database of Systematic Reviews 2006, Issue 2. Art. No.: CD002933. DOI: 10.1002/14651858.CD002933.pub3.
41. Cochrane Database of systemic Reviews. Oral zinc for arterial and venous leg ulcers 2009.
42. Fleming K, Cullum N. Laser therapy for venous leg ulcers. The Cochrane Database of systematic Reviews 2007 issue 1.
43. James Wright. Hyperbaric Oxygen therapy for wound healing. World wide wound, May 2001

Syndicate content