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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareCELL PHONES OF HEALTHCARE PROVIDERS AS FOMITES HARBOURING POTENTIAL PATHOGENIC MICROORGANISMS
English0104V. ArulmozhiEnglish Anand B. JanagondEnglish S. SavithaEnglish J. KalyaniEnglish G. SumathiEnglishBackground: Cell phones (CP) being used by healthcare providers are emerging as fomites capable of transmitting infections. Studies have shown presence of potentially pathogenic bacterial and fungal contamination of cell phones.
Aim: This study was conducted to detect microbial carriage of cellphones of healthcare providers Methodology: CPs of 50 healthcare providers (HCP), comprising doctors of various specialities, nurses and technicians working at various departments/areas of hospital were screened for possible bacterial and fungal contamination. Results: The overall rate of contamination of CPs of HCPs was 94%. Contamination with potential pathogens was found in 76% of CPs. S. aureus was the commonest (18/41) potential pathogen isolated and two CPs were contaminated with Methicillin Resistant
S. aureus (MRSA). Candida spp was isolated from 4% of CPs. Rates of contamination with potential pathogens in CPs used by doctors was 85%, nurses 71% and technicians 69%. Rate of contamination with potential pathogens was highest in the CPs used by HCPs having access to wards (89%) followed by OPDs (88%) and OT/ICU (85%).
Conclusion: CP contamination with potential human pathogens was common in HCPs working at various areas of the hospital including sensitive areas like OTs and ICUs and also irrespective of professional cadre. Rates of contamination with multi-drug resistant organisms were low in CPs. These findings stress the need for awareness of CPs as fomites, need for strict monitoring of hand hygiene and guidelines for routine decontamination of CPs in hospitals.
EnglishCell phones, Hand hygiene, Fomite, Staphylococcus aureusINTRODUCTION
Cell phones (CPs) have become an indispensable accessory of today’s society and they are being used extensively in a hospital setting to optimize patient care and client communications. However, CPs are commonly handled (irrespective of the cleanliness of hands), rarely disinfected and could harbour pathogenic bacteria (1) Studies of healthcare workers’ CPs conducted elsewhere have reported the overall contamination rate to be 40- 98% (2,3,4,5). CPs are potential sources of HAIs along with medical staff, the patients’ own flora. (1) Information regarding role of CPs in spread of HAIs is limited in tropical countries like India (6). Contamination rates of CPs can vary in different hospital settings. The present study was done to assess the burden and type of contamination of CPs of health-care providers (HCPs) in a tertiary care hospital in Chennai so that magnitude of the problem can be estimated and appropriate control and preventive methods can be suggested.
MATERIALS AND METHODS
This study was conducted in a tertiary care hospital attached to a medical college in Chennai after ethical committee approval. 50 HCPs including doctors, nurses, technicians working in outpatient departments, wards, operating rooms, ICUs etc were randomly selected for the study. No prior information about the study was given to the participants to avoid bias. After participants’ informed consent their CPs were swabbed with sterile cotton swab soaked with sterile brain heart infusion broth covering both the surfaces completely. The swabs were immediately brought to the microbiology laboratory and inoculated on to nutrient agar, blood agar, McConkey agar and Sabouraud dextrose agar (SDA) medium. All bacterial culture media were aerobically incubated at 37° C for 48 hours and SDA which was used for growing fungi was incubated at 25° C for 1 week. Colonies obtained were identified by standard microbiological procedures and antibiogram was done for potential human pathogens.
RESULTS
Cellphones of 50 HCPs working in a private tertiary care teaching hospital in Chennai were screened for bacterial and fungal contamination. Subjects comprised of 20 doctors, 17 nurses and 13 operating theater (OT) technicians. HCPs were belonging to various specialties (Medicine, paediatrics, dermatology, general surgery, orthopaedics, ENT, etc) and many were working in more than one area of the hospital; 34 were working in OTs/ Intensive care units (ICU), 27 in wards and 17 in outpatient departments (OPD). The overall rate of contamination of CPs of HCPs was 94% (47/50). Contamination with potential pathogens was found in 76% (38/50) of CPs. Swabs from three CPs did not yield any organisms. A total of 74 organisms were isolated out of which 41 isolates were potential human pathogens and 33 were non-pathogenic organisms. Swabs from 21 CPs yielded single organism, 25 CPs two organisms and one CP three organisms. Potential pathogens isolated (Table 1) included Staphylococcus aureus (18/41), Pseudomonas spp (7/41), Coagulase negative Staphylococci (6/41), Klebsiella spp (5/41), Escherichia coli (3/41) and Candida spp (2/41). Saprophytes isolated from the CPs included aerobic spore bearers (25/32) and Micrococci (7/32). S. aureus was the commonest (18/41) potential pathogen isolated and two CPs were contaminated with Methicillin Resistant S. aureus (MRSA) from a doctor and a technician both having access to OT. Contamination rates with potential pathogens of CPs used by doctors were 85% (17/20), nurses 71% (12/17) and technicians 69% (9/13) (Figure 1). Rate of contamination with potential pathogens was highest in the CPs used by HCPs having access to wards (89%, 24/27) followed by OPDs (88%, 15/17) and OT/ICU (85%, 29/34) (Figure 2).
DISCUSSION
Fomites play an important role in spread of hospital-acquired infections. A variety of surfaces, equipments and devices have been found to harbour pathogenic microorganisms, including drug resistant ones like MRSA and
VRE, in hospital settings. (2,7,8) Microbes can be transferred from person-to-person or from inanimate objects commonly used in hospitals (stethoscopes, pens, charts, fixed and mobile phones) to hands and vice versa. (3) Clean hands can become colonized after contact with contaminated surface or fomite while caring for patients and organisms can cause infection if they come in contact with susceptible hosts (3,8,9). Hand-to-mouth transfer of microbes after handling contaminated fomites during casual activities has also been documented (2). Clinically significant microorganisms like S. aureus, gram negative bacilli, Candida spp have been shown to persist on inanimate objects for weeks to months (8). High inoculums of the microbe, low temperature with relatively high humid environmrntal conditions provide best chances for long persistence of organisms (9). The longer a nosocomial pathogen persists on a surface, the longer it may be a source of transmission and thus endanger a susceptible patient or HCP (9). CPs are widely used and in close contact with the body. They are used for communication by HCPs in almost every location in a hospital including OTs and ICUs. (2,5). CPs allow for easy accessibility of the clinician so can help in providing timely patient care. The mobile phone technology not only allows for rapid communication but also enables storage of formulary data, clinical and diagnostic protocols that can be made available to a busy clinician at his finger tips (7,6). People frequently handle CPs and that too irrespective of the cleanliness of their hands (1). The use of CPs by HCPs in the ICU, burns wards and OTs may have more serious hygiene consequences, especially since they are used close to patients (3). The rates and composition of contamination of CPs in hospitals could be risky to general public in community if carried outside (2). More studies are required to estimate the burden of contamination of CPs of HCPs, spectrum of organisms so that appropriate preventive and control measures can be followed. In this study overall rate of contamination of CPs used by HCPs was 94% and that by potential human pathogens was 76%. The contamination rates were found high in our study and are comparable to findings of Bhat S et al and Padma K et al with overall contamination rates of 98% and 94% respectively (6, 5). S. aureus was the commonest pathogen found contaminating CPs (36%) and 4% CPs harboured MRSA. Majority of isolated S. aureus strains were sensitive to antibacterials tested (Fig). Though the MRSA were fonud in relatively less number of CPs both were found in CPs of HCPs having access to sensitive areas like OTs and ICU. Many previous studies also have found S. aureus as the commonest organism on HCPs’ CPs (12-56%) and MRSA was found in 1.9-18% CPs. Previous studies also have shown lesser rates of contamination with gram negative bacilli than gram positive cocci (2, 3, 6, 4, 5). Very few studies have looked for fungal contamination of CPs, in our study only 4% CPs were found to harbour fungi, both Candida spp. CPs of doctors harboured more pathogens (85%) compared to nurses (71%) and technicians (69%). Higher contamination of CPs of doctors than nurses was observed in other studies also (1,6). The reasons for the differences were not specifically studied. Contamination of CPs of HCPs was found to be high irrespective of the area of work in the hospital – wards (89%), OPDs (88%) or OTs/ICU (85%). A study comparing CPs of hospital and non-hospital settings showed spectrum of organisms isolated to be similar in both the groups but resistant organisms like MRSA were found only in the hospital setting (6). Today CPs, due to their various benefits, have become indispensable devices for HCPs and hence their complete restriction inside the hospitals is not practical. As the present study and the previous similar studies suggest, the problem of CPs as fomites carrying harmful microbes needs to be addressed. There is limited information available on CP disinfection methods that are both effective and do not damage the CPs.(1) Use of 70% isopropyl alcohol wipes, which is simple and can be routinely used, has been suggested to disinfect CPs by a few studies. (1,10) Sensitizing and training of HCPs about strict infection control procedures, hand hygiene, environmental disinfection methods are essential. (2,6) Engineering modifications such as use of hands-free mobile devices, use of surfaces that are easy to clean and disinfect, use of antimicrobial additive materials in CPs have been proposed as solutions (2,3). The Center for Disease Control (CDC) and Healthcare Infection Control Practices Advisory Committee (HICPAC) have recommendations for routine decontamination of all hospital equipments (8). Similar guidelines extending to CPs are the need of the hour. A study done by Obasi C et al showed a selfcleaning unit to decontaminate small reusable objects, including electronic equipments like wall-phones, keyboards, in a hospital to be effective in a single cycle (8). Applicability of similar techniques to decontaminate CPs needs to be studied.
CONCLUSION
In conclusion, this study highlights the high rates of contamination of CPs used by HCPs in a hospital setting. CP contamination with potential human pathogens was common in HCPs working at various areas of the hospital including sensitive areas like OTs and ICUs and also irrespective of professional cadre. Carriage rates of resistant organisms (MRSA) were low. These findings stress the need for awareness of CPs as fomites, need for strict monitoring of hand hygiene and guidelines for routine decontamination of CPs in hospitals.
ACKNOWLEDGEMENTS
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=741http://ijcrr.com/article_html.php?did=7411. Julian T, Singh A, Roussean J, Weese JS. Methicillin Resistant Staphylococcal contamination of cellular phones of personnel in a veterinary hospital. BMC Research Notes 2012;5:193-7.
2. Ulger F, Esen S, Dilek A, Gunaydin M, Leblebicioglu H. Are we aware how contaminated our mobile phones with nosocomial pathogens? Annals of Clin Micro Antimicrobiol 2009; 8:7-10.
3. Amira H, Al-Abdalall A. Isolation and identification of microbes associated with mobile phones in Dammam in eastern Saudi Arabia. J Family Community Med 2010;17:11-4
4. Data P, Rani H, Chander J. Bacterial contamination of mobile phones of health care workers. Indian J Med Microbiol 2009;3:279-81.
5. Panchal CA, Kamothi MN, Mehta SJ. Bacteriological profile of cell phones of healthcare workers at tertiary care hospital. J Evolution Med Dental Sciences 2012;1:198-202.
6. Padma S, Ezhilarasan R, Suchitra S, Anandhi L, Umamageswari S, Sangappan M, Kalyani J. Mobile phones: emerging threat for infection control. J Infection Prevention 2010;2:87-90.
7. Jeske HC, Tiefenthaler W, Hohlrieder M, Hinterberger H, Benzer A. Bacterial contamination of anaesthetists’ hands by personal mobile phones and fixed phone us in the operating theater. Anaesthesia 2007;62:904-6.
8. Obasi C, Agwu A, Akinpelu W, Hammons R, Clark C, Etienne-cummings R, et al. Contamination of equipment in emergency settings: An exploratory study with a targeted automated intervention. Annals Surgical Intervention Research 2009;3:8-16.
9. Kramer A, Schwebke I, Kampf G. How long do nososcomial pathogens persist on inanimate surfaces? BMC Infectious Diseases 2006;6:130-7.
10. Arora V, Devi P, Chadha A, Malhotra S. Cellphones a modern stayhouse for bacterial pathogens. JK Science 2009;11:127-9.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareASSESSMENT OF STRESSORS IN MEDICAL STUDENTS AND ITS RELATIONSHIP WITH THE SELF-RATED DEPRESSION: A STUDY CONDUCTED IN RURAL TERTIARY HOSPITAL AND TEACHING INSTITUTE OF CENTRAL INDIA
English0509Meenakshi KhapreEnglish Abhay MudeyEnglish Smrutiranjan NayakEnglish R. C. GoyalEnglishBackground: Medical students are more prone to stress either due to their rigid standards and high aspiration or due to demanding education. The stress developed in undergraduates continues further in post-graduation and practice resulting in burnout. In India this area is grossly under reported. Therefore the study was carried out with the objective to find out the amount of stressors and its relation to depression. Method: A cross sectional study was carried out with complete enumeration of students present in lecture. They were educated and informed of data collection tool. i.e HESI questionnaire and MDI. Data analysis was done by descriptive and inferential statistic. Result: No difference of level of stressors was found among the students of variable academic years and sexes. 40 % were found to be mildly depressed. All of the Stressors in totality or individual except insufficient feedback and low commitment show significant correlation with MDI scores. Conclusion: Every two student out of five were found to be depressed and it is positively correlated with the stressors like work for future endurance/ capacity, non-supportive climate, faculty shortcoming, workload, financial concern
EnglishStressors, Self-related depression, Medical studentsINTRODUCTION
Medical education is both long and costly. Though pursuit of higher education is expected to be stressful, medical students have more distress, anxiety and depression than any other graduates as reported by many studies (1, 2, 3). The cause of stress in medical students are mainly Long working hours, lack of peer support, competitive environment, rigid authoritative non encouraging faculty, an imbalance between professional and personal lives, lack of recreational activities, staying away from home, financial problems, residency queries, an uncertain future, emergency situations, speedy decisions, life and death issues, cultural and minority issues, mismatch between capability and expectation etc. medical students are high achiever and action oriented prior to admission. They can’t tolerate helplessness, dependency, failure. They have high aspiration but rigid standards for themselves. Therefore medical students are more prone to stress. The curriculum is vast and students are just expected to swallow without digesting or critically value it. Instead of developing the critical and intellectual relationship with medical knowledge, medical colleges just foster the students to accept the facts as said in books or lectures. Thus the road to dynamic and challenging profession is hindering overall personality development. Perceived stress is associated with increased levels of depression, alcohol and drug abuse, relationship difficulties, anxiety and suicide. (4,5) Stress is receiving increased attention because of the realization that tired, tense, anxious doc tors may not provide as high quality care as do those who do not suffer from these debilitating conditions.(6) In India medical education is provided by government and private universities. Government though provide it at nominal cost, it legally bond student for one year compulsory rural posting after completion. After completion of graduation he has to face fierce competition to establish practice, service or get post-graduation. His future is still unsecured. In India stress among medical students might be grossly underreported. To shift from distress to wellbeing we need to identify the stressors and reshape the salutary factors. Therefore to limelight the amount of stressors present in students and its relationship with the self-rated depression the above study was carried out.
OBJECTIVES
To find the extent of different stressors in medical students To assess the level of depression among the medical students To assess the relationship between the types of stressors and level of depression.
METHODOLOGY
Study Area:
The study was conducted in a Jawaharlal Nehru Medical College Study Design: A cross-sectional study design was adopted for the study.
Study Sample:
The participants of the study were the present students of medical college year 2013
Sample Selection
All the students of the college consenting to participate and were present in the class on the day of the delivering the data collection tool.
Study Tools
Higher education stress inventory (HESI)(7): 24 statements indicates presence and absence of stressful aspects like worries for future endurance /capacity, nonsupportive climate, faculty shortcoming, workload, insufficient feedback, low commitment and financial concern. Responses are rated in four point likert scale (value 1-4) does not apply at all, does not apply very well, apply fairly well and apply perfectly with reverse order for absence of stressor, so high scores are less favourable. Major depression inventory (MDI): self-rating scale to assess the depression was used. Data collection process: On a pre-decided date, after giving the general information on research, the questionnaire was administered to students present in class room. They were informed that the information retrieved would be used only for research purpose and anonymity would be maintained by giving unique ID to them. The students who were interested in knowing their scores were invited and if needed were referred to student guidance clinic in college. Analysis: only completed forms were included in final analysis report. Mean score of students for each stressor and depression was computed. The relationship between stressors and depression was analysed by Pearson moment Correlation.
RESULTS
As shown in Table 1, 48.11% were male and 51.89% were female. First year participants were 27.98 % followed by 26%, 24% and 21.6% students of second, third and fourth year respectively. Table 2 shows the mean score of HESI factor of each academic year. No significant difference was found among the academic years. 39. 9 % were found to be mildly depressed. 9.1% and 8.5% had moderate to severe depression at the time of interview as given in Table 3. Total HESI score and MDI score were strongly correlated as depicted in Table 4. Also strong correlation of MDI was seen with work for future endurance/ capacity and faculty shortcoming. Non supportive climate and workload were moderately correlated with MDI score. All of the factors in totality or individual except insufficient feedback and low commitment show significant correlation with MDI scores.
DISCUSSION
Stress in a medical school is global phenomenon. The tool used here has seven factors of which WFEC and Low commitment reflects the individual trait rather than effect of education and others like Non supportive climate, faculty shortcoming (academic), workload, insufficient feedback and financial concern reflects the environmental condition. In present study , the mean score for each stressors mentioned in questionnaire was approximately above 55% of maximum score, which depicts that this stressors are present at moderate to high level among the students. In many medical schools, the environment itself is an all prevailing pressure situation, providing an authoritarian and rigid system, one that encourages competition rather than cooperation between learners(8).
This creates the anonymity and non-supportive climate for learning. As medical students enter the clinical years, their concerns change as they find themselves unable to apply what they knew well enough for the examinations and insecurity for jobs creates worries for future. In India as per MCI teacher student ratio is 15: 1, which makes it difficult for teacher to give in dividend attention to each one of them. Many students struggle with questions about their ability to endure the demands of education. The feedback on skills and performance is crucial part in medical education to prepare the competent physician and teacher and create the interest in students but the higher score in low feedback is rather disturbing. More emphasis is given on passive learning rather than active self-directed learning. The curriculum with overload of information, and the environment presenting multiple hurdles ‘rather than opportunities for assessing progress’ are important sources of academic stress. It is not just the undergraduate study period which brings stress but it may continue during the internship, postgraduate study period, and later into physician’s practical life (9). The study done by Sidhu had shown that Indian students had increases stress score than Chinese and malaysisan in all the aspect academics, social, financial etc.(10) Present study does not show any significant difference among the level of stressors in between the academic years and sexes. These stresses are constantly present in all the academic years and equal in both sexes. Being a cross sectional study the changes through the transition from first year to final cannot be depicted. There are contradictory findings as some studies (1, 11, 12) showed increase in level of stress from progressing academic years while other showed decrease (13). The finding of No difference of level of stressors among the sexes is in line with other studies (11, 14). While some studies indicates female medical students perceive more stress (15) also as per available records the suicidal and depression rates in female students are more than males. The present study was conducted in private institution with well to do family may be the reason for study findings. 37.5 % scored more than cut off point of which 8.5 % that scored very high were in need of psychological counselling. Depression is quite common in medical students and range from 6 % (16) to 25 % (17) using different measures and definitions. Considering the Cohens guidelines for behavioral studies(18) all the stressors except insufficient feedback and low commitment showed the significant positive correlation with MDI score. Work for future capacity and faculty shortcoming was strongly correlated while Non supportive climate and workload were moderately correlated with MDI score. Strong positive correlation was found between total HESI score and MDI score. This shows that level of stress increases the chances of depression. Ability of medical students to deal with stress depends on multiple factors, including individual vulnerability, and psychological and social resources as well as stressors (19). The degree of distress depends on the balance between the stressors and the resources. It is necessary to increase the personnel resources by educating them for stress and time management techniques and coping skills in order to diminish the perceived distress. The stressor therefore has to be identified need to be address by policy maker, teachers, psychologist and family members.
CONCLUSION
Every two student out of five were found to be depressed and it is found to be positively correlated with the stressors like work for future endurance/ capacity, non-supportive climate, faculty shortcoming, workload, financial concern. Thus this stressors need to be address to reduce the distress in medical graduate.
RECOMMENDATION
It is time to make Medical education interesting by innovative active learning methods, restore enthusiasm in the students and to project a more realistic, humane image of the profession. The student guidance clinic should be functional by regular screening and assisting the student with psychological problems. The orientation programmes and counselling services should be started from the entry level. The students must be made aware of the stress and its self-management. It is imperative that future Physicians are healthy themselves before they Treat others.
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=742http://ijcrr.com/article_html.php?did=7421. Helmers , K.F, Danoff , D, Steinert ,Y Leyton, M and Young, S.N (1997) Stress and depressed mood in medical students, law students, and graduate students at Mc Gill University Academic medicine , 72, 708-14.
2. Rautio, A, Sunnari , V, Nuutinen ,M and Laitala , M (2005) Mistreatment of university students most common during medical studies BMC Medical education[online], 5(36)available from : http//:www.biomedcentral.com/1472- 6920/5/36
3. Frank, E. Carrera, J.S, Stratton, T, Buckle, J and Nora. L.M (2006) experience of belittlement and harassment and their correlates among medical students in the United states: longitudinal survey BMJ, 333, 682.
4. Shapiro S, Shapiro D, Schwartz G. Stress management in medical education: a review of the literature. Acad Med2000;75:748–59.
5. Stecker T. Well-being in an academic environment. Med Educ2004;38:465–78
6. Firth-Cozens J. Doctors, their well-being, and their stress. BMJ2003;326:670–1
7. Marie Dahlin, Future Doctor,Mental distress during medical education: cross sectional and longitudinal studies, publish by Karolinska University press, Stockholm, Sweden 2007.
8. Styles WM. Stress in undergraduate medical education: ‘the mask of relaxed brilliance’. Br J Gen Pract 1993;43:46-7.
9. Tyssen R, Vaglum P, Gronvold NT, Ekeberg O. The relative importance of individual and organizational factors for the prevention of job stress during internship: a nationwide and prospective study. Med Teach 2005;27:726-31
10. Jagmohni Kaur Sidhu, Effect of Stress on Medical Students, IeJSME 2007: 1 (1): 52-53
11. Niemi PM, Vainiomaki PT. Medical students’ distress—quality, continuity and gender differences during a sixyear medical programme. Med Teach2006;28:136-41.
12. Dyrbye L, Thomas MR, Shanafelt TD. Medical student distress: causes, consequences, and proposed solutions. Mayo Clin Proc2005;80:1613-22.
13. Guthire E, Black D, Bagalkote H, Shaw C, Campbell M, Creed F. Psychological stress burnout in medical students: a five-year prospective longitudinal study. J R Soc Med1998;91:237-43
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15. Amr, M., EL Gilany, A.H. and EL-Hawary, A. (2008) Does gender predict medical students stress in Mansura, Egypt Medical Education Online, 13:12, available at http/www. med.edonline.org
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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareVARIATIONS IN THE BRANCHING PATTERN OF POPLITEAL ARTERY AND IT'S CLINICAL IMPLICATIONS : A CADAVERIC STUDY
English1013Ankit KhandelwalEnglish Pooja RaniEnglish Mahindra NagarEnglishBackground: Due to the increasing number of surgical techniques used nowadays on the knee joint, the importance of the knowledge of the branching pattern of the vessels neighboring the joint becomes very significant. Anomalies of vascular patterns near the knee joint particularly the popliteal vessels, are therefore noteworthy in understanding the atypical clinical findings encountered while dealing with knee joint procedures. Popliteal artery, a continuation of femoral artery at the level of adductor hiatus, normally divides into anterior and posterior tibial arteries at the level of lower border of popliteus muscle. Aim: This study attempts to analyze the level of division and as well as the branching pattern of the popliteal artery. Methodology: A study on forty lower limbs of twenty embalmed human cadavers (twelve male and eight female cadavers/ twenty four male and sixteen female limbs) was carried out to find out the variations in the branching pattern of popliteal artery. Results: We observed the high division of the popliteal artery proximal to the popliteus muscle along with the variations in the branches of the artery in two of the limbs (5%). The photographs of the variations were taken for proper documentation and ready reference. There were no other variations found in these specimens.
Conclusion: Variations in the branching pattern of the popliteal artery may increase the risk of complications during surgeries of the knee joint. The awareness of these variations is important during radiological examinations as they may affect the therapeutic approach by the surgeons and the interventionists.
EnglishAxial artery, Peroneotibial trunk, Vascular surgery, Popliteus muscle, High divisionINTRODUCTION
The popliteal artery, about twenty cm in length is the continuation of the femoral artery and it descends laterally from the opening in adductor magnus to the femoral intercondylar fossa, inclining obliquely to the distal border of popliteus, where it divides into the anterior and posterior tibial arteries. This division usually occurs at the proximal end of the asymmetrical crural interosseous space between the wide tibial metaphysis and the slender fibular metaphysis at the level of lower border of popliteus1 . Posterior tibial artery is the larger of the two terminal branches and enters the posterior compartment of leg under cover of tendinous arch of origin of soleus. This artery gives a large branch, the peroneal artery nearly 2.7 cm distal to its origin. The popliteal artery besides its two terminal branches gives off cutaneous, muscular and genicular branches and ends beneath the flexor retinaculum by dividing into medial and lateral plantar arteries. The other terminal branch, the anterior tibial artery passes between the two heads of tibialis posterior and enters the anterior compartment of leg through an oval gap above the interosseous membrane. It then continues as dorsalis pedis artery between the medial and lateral malleoli. The popliteal artery may divide proximal to the inferior border of popliteus muscle then being termed as high division of the popliteal artery and may trifurcate into anterior tibial, posterior tibial and peroneal artery. The popliteal artery acts as a common site for above or below-knee bypass grafts. It is also frequently affected by penetrating and blunt trauma involving the lower extremity. Exposure of this artery is therefore, frequently required in both emergent and elective vascular procedures2 . Knowledge of the anatomical variation in this re gion may have clinical implications regarding vascular grafting, direct surgical repair, embolectomy, transluminal angioplasty, or the diagnosis of arterial injury3 . Also, knowledge of the variant patterns of branching of the popliteal artery is important since damage to its branches can be limb or life threatening4 . Thus the present study is an attempt to add to the existing knowledge of the popliteal artery branching pattern variations.
MATERIALS AND METHODS
Over a span of two years (2012-14) a study was conducted on popliteal regions of forty formalin fixed cadaveric limbs (twenty four males, sixteen females) in the dissection hall of Anatomy Department of University College of Medical Sciences, Dilshad Garden, Delhi, India. Medical history and cause of the death of these cadavers was known. Dissection instruments were used to dissect the popliteal regions according to the dissection steps given in Cunningham’s manual of practical anatomy5 . The popliteal artery was exposed in the popliteal fossa and the prevailing pattern of the popliteal artery, its branches and variations were observed, noted and photographed. The data were compiled, and the observations were compared with previous standard observations. Any deviation from the normal was noted and discussed.
RESULTS
Out of the forty cadaveric limbs dissected and examined, no abnormality was detected in thirty eight limbs i.e. which showed normal pattern of division of popliteal artery. But there were two limbs which showed abnormalities in the branching pattern of popliteal artery (5%). The first abnormality was observed in a fifty five years old female cadaver on the right side, where the popliteal artery continued as the posterior tibial artery and gave off a common trunk named as anterior peroneotibial trunk slightly above the proximal border of popliteus muscle (Fig. 1). The length of the popliteal artery when measured was 10.5 cm in contrast to normal value of approximately twenty cm. The diameter of the anterior peroneotibial trunk appeared larger as it traversed the posterior surface of popliteus muscle for about 8.5 cm and then gave off the peroneal artery just before the anterior tibial artery passed through the oval gap in the interosseous membrane to come on the anterior surface of interosseous membrane. The further course of anterior tibial, posterior tibial and peroneal arteries was found to be normal which divided into anterior tibial and peroneal artery. Another variation was observed in a sixty years old female cadaver on the left side where the popliteal artery divided into anterior and posterior peroneotibial trunks proximal to popliteus muscle (Fig. 2). In this limb the length of the popliteal artery was twelve cm in contrast to normal value of approximately twenty cm. The anterior tibial artery crossed posterior to the popliteus muscle and entered the extensor compartment of leg. Posterior peroneotibial trunk was long, measuring about 8.6 cm before it gave off the peroneal artery which normally arises after 2.7 cm. The further course of anterior tibial, posterior tibial and peroneal arteries was found to be normal.
DISCUSSION
Variations in the branching of the popliteal artery are mainly targeted around the high division of the artery and the resulting differences in the arrangement of the terminal branches, posterior tibial, anterior tibial and peroneal arteries6 . According to Adachi7 any terminal division of the popliteal artery which takes place at a level above the middle of the posterior surface of the popliteus muscle must be considered as a “high division” and reported high division in 2.8% specimens. In our study the popliteal artery branched at or slightly above the proximal border of the popliteus muscle in two cases (5%) this is in consonance with Keen observations, whereas percentages of high division of popliteal artery are considerably higher in American and European data. Thane (1892)8 has cited a case in which the popliteal artery extended to the middle of the back of the leg before dividing. The high level termination of the popliteal artery in relation to the upper border of the popliteus muscle was grouped into three types by Adachi. In type I the popliteal artery descended on the posterior surface of the popliteus muscle and divided into the posterior peroneotibial trunk and the anterior tibial artery. The posterior peroneotibial trunk further divided into the peroneal artery and the posterior tibial artery. The diameter of the anterior tibial artery was equal to the popliteal artery or smaller than the posterior peroneotibial trunk. In type II the popliteal artery descended on the posterior surface of the popliteus muscle and divided into the posterior tibial artery and the anterior peroneotibial trunk. The diameter of the anterior peroneotibial trunk was observed to be larger and it divided into the peroneal artery and anterior tibial artery at the lower border of the popliteus muscle. In type III the popliteal artery terminated at the upper border of the popliteus muscle by dividing into the anterior tibial artery and posterior peroneotibial trunk. The anterior tibial artery ran downward in between the anterior surface of the popliteus muscle and the posterior surface of the tibia. The posterior peroneotibial trunk ran on the posterior surface of the popliteus muscle. The posterior peroneotibial trunk divided into the peroneal artery and posterior tibial artery distal to the tendinous arch of soleus muscle. In the present study in one case the diameter of the anterior peroneotibial trunk appeared larger than normal. The average length of the popliteal artery was 11.2 cm in contrast to normal length of twenty cm. The anterior peroneotibial trunk was 8.5 cm long and traversed the posterior surface of popliteus muscle before it divided into anterior tibial artery and peroneal artery. The peroneal artery was given off just before the anterior tibial artery pierced the interosseous membrane to come onto the anterior surface of interosseous membrane. This is in accordance with Adachi’s type II, popliteal artery. In the second case the popliteal artery divided into anterior and posterior peroneotibial trunk proximal to popliteus muscle which is in accordance with the Type I of Adachi’s classification of popliteal artery. The anterior tibial artery crossed posteriorly to the popliteus muscle and entered the extensor compartment of leg. The high origin of anterior tibial artery at or above the level of the articular surface of the tibial plateau is documented in literature. Another radiological study of the femoral angiograms on 495 lower extremities was performed to view the tibial arterial anatomy, and found that 7.8% of the cases revealed variations. Normally the diameter of the posterior tibial artery is more than the diameter of the peroneal artery, but in the present case the diameter of the peroneal artery appeared more than the diameter of the posterior tibial artery which is similar to the study of Ozgur et al9 . It was reported in literature that the course of anterior tibial artery may either be from the anterior or posterior surface of the popliteus muscle. In the present cases the course of posterior tibial artery was on the posterior surface of the popliteus muscle. Another variation of the popliteal artery is trifurcation, where all the three terminal branches arise together at the level of the lower boundary of the popliteus muscle. Trifurcation of the popliteal artery into anterior tibial, posterior tibial and peroneal branches was observed in 0.8% specimens (Adachi, 1928) and in 4.3% in Keen’s study (1961), but it is not observed in the present study. He also reported an instance in which the popliteal artery divided into two branches which reunited after a course of 5 cm. Absence of the peroneal artery has also been recorded by him, but such a case was not encountered by the present researchers. A true trifurcation of the popliteal artery is unusual, occurring in 0.4% of instances, although variations of a splitting of the popliteal into three branches in close proximity are more common, occurring in about 3% of specimens10. Agenesis of the popliteal artery, although obviously extremely rare, has been reported11. Clinicians and radiologists have defined a different terminology of the popliteal artery and its main branches in popliteal surgery. The anterior tibial artery was defined as the tibial-fibular trunk as soon as it branched from the popliteal artery. The tibial arteries were referred to as anterior or posterior peroneotibial trunk depending upon the origin of the peroneal artery. In the present study in one of the cases the peroneal artery was given off from the anterior tibial artery and hence the anterior tibial artery may be defined as the tibial – fibular trunk.
EMBRYOLOGICAL BASIS
The axis artery of the lower limb is the arteria ischiadica in the embryo before the 14 mm stage. At the knee-joint level the axis artery becomes the popliteal, which at this stage runs in front of the popliteus (deep popliteal artery), and then continues as the anterior tibial. At the 14 mm stage, the arteria ischiadica is being supplemented by the femoral artery. Two longitudinal arteries which traverse the leg in the embryo, the future posterior tibial and peroneal arteries, arise from the axial vessel at the upper border of the popliteus muscles. A gradual proximodistal union of the posterior tibial and peroneal arteries occurs and is well advanced in embryos of 20 mm. This union forms the part of the definitive popliteal artery that lies behind the popliteus muscle. A communicating branch from the lower border of the popliteus enlarges to become the definitive anterior tibial, while the deep popliteal artery gradually disappears. However, it can be easily understood that, if the proximodistal fusion of the posterior tibial and peroneal vessels is abbreviated, the peroneal artery can consequently arise from the anterior tibial rather than from the posterior tibial 12. The knowledge of branching pattern of the popliteal artery is important for surgical interventions in the popliteal region in order to minimize the unwanted hemorrhage and surgical complications due to anatomical variations. These anatomical variations should be kept in mind by orthopaedicians doing knee joint surgery and total knee arthroplasty, by surgeons operating on aneurysms of popliteal artery and by radiologists performing angiographic study. These variations are compared with the earlier data and it is concluded that variations in branching pattern of the popliteal artery are frequent rather than exceptions. The possibility that these results may depend on racial or regional differences cannot be ruled out, and will need further study, with greater number of cases involving different races and regions.
CONCLUSIONS
Variations in the branching pattern of the popliteal artery may increase the risk of complications during surgeries of the knee joint. The awareness of these variations is important during radiological examinations as they may affect the therapeutic approach by the surgeons and the interventionists. Thus the present study is an attempt to add to the existing knowledge of the popliteal artery branching pattern variations.
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=743http://ijcrr.com/article_html.php?did=7431. Standring S. Gray’s anatomy. The Anatomical basis of clinical practice. In: Mahadevan V. Knee. 40th ed. Elsevier. Churchill livingstone; 2008. p. 1393-1410.
2. Colborn G L, Lumsden A B, Taylor B S, Skandalakis J E. The surgical anatomy of the popliteal artery, The American Surgeon. 1994; 60: 238-246.
3. Mauro M A, Jaques P F, Moore M. The popliteal artery and its branches: embryologic basis of normal and variant anatomy. Am J Radiol. 1988; 150: 435-437.
4. Tindall J, Shetty A A, James K D, Middleton A, Fernado K W K. Prevalence and surgical significance of high-origin anterior tibial artery. J Orthop Surg. 2006; 14: 13- 16.
5. Romanes G J. Cunningham’s manual of practical anatomy. In: popliteal fossa Vol. 1. 15th ed. Oxford, Oxford Medical Publications; p. 160-165.
6. Keen J A. A study of the arterial variations in the limbs with special reference to symmetry of vascular patterns. Am J Anat. 1961; 108: 245-261.
7. Adachi B. Das Arteriensystem der Japaner, Vol. II. Maruzen, Kyoto, 1928 pp 137-269.
8. Thane G D. Arthrology Myology Angiology. In: Schafer E A, Thane G D (editors). Quain’s Elements of Anatomy. 10th ed. Longmans, Green and Co., London, 1892, pp 495
9. Ozgur Z, Ucerler H, Aktan I Z A. Branching patterns of the popliteal artery and its clinical importance. Surg Radiol Anat. 2009; 31: 357–362.
10. Lippert H, Pabst R. Arterial variations in man: Classification and frequency. Bergmann Verlag, Munich. 1985; 60-64.
11. Senior H D. The development of the arteries of the human lower extremity. Am J Anat. 1919; 25: 55-95.
12. Neville R F, Franco C D, Anderson R J. Popliteal artery agenesis: A new anatomic variant. J Vasc Surg. 1990; 12: 573-576.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareCHANGING PATTERNS OF AETIOLOGY OF ACUTE SPORADIC VIRAL HEPATITIS IN INDIA - NEWER INSIGHTS FROM NORTH-EAST INDIA
English1420Anup Kumar DasEnglish Sakir AhmedEnglish Subhash MedhiEnglish Premashish KarEnglishBackground: Most common aetiology of viral hepatitis globally is Hepatitis A except in developing countries where Hepatitis E predominates. Geographical variation is present between the west and the east. However, in many developing countries including India, a change in aetiology is being increasingly reported in the past two decades.
Materials & Methods: 591 patients with acute viral hepatitis were prospectively screened to ascertain their aetiology (by appropriate viral markers) in a tertiary care centre from North-East India. Results were double-checked in another tertiary institute in Delhi, including Polymerase Chain Reaction for virus detection. Clinical outcomes, mortality and other relevant findings were recorded. Results: Hepatitis A was the dominant aetiology for both acute and fulminant viral hepatitis that is in contrast to other Indian reports that implicate hepatitis E virus, suggesting our region has certain differences. Overall, 16% developed complications with a 9% mortality. Those with hepatitis B had the poorest outcome. Hepatitis C virus was not detected. 2% had mixed infection. Non-A,B,C,E cases were high. History of herbal/unknown folk medicine intake was present in a large number of patients. Conclusion: North-east India, although relatively underdeveloped, is showing a shift of hepatitis A viral sero-epidemiology. Adults are affected as equally by hepatitis E. The reasons may be multi-factorial. Non-viral acute hepatitis is common here. The consumption of unidentified non-allopathic medications may influence outcome, and requires further evaluation.
EnglishAcute viral hepatitis, Northeast India, Changing aetiology, Herbal medication induced liver damageINTRODUCTION
Outbreaks of hepatitis have been recognized for centuries, but the first description of epidemic jaundice due to hepatitis is attributed to Hippocrates [1]. Acute Viral Hepatitis (AVH) is mainly caused by hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis E virus (HEV). They can be identified by serological tests only. Hepatitis A is the most common cause of acute viral hepatitis (AVH) worldwide. Viral hepatitis is a major public health problem in India too, which is hyperendemic for both HAV and HEV. [2] Most reports from India implicate HEV as the major cause, ranging from 12.6-78.6% in both sporadic and epidemic hepatitis from different parts the country [3,4,5,6,7,8] However, HAV AVH is the most common cause of acute viral hepatitis globally having a worldwide distribution. [9,10] Major geographical differences in endemicity of HAV exist and are closely related to hygiene and sanitary conditions and the level of socioeconomic development. In less developed regions and in several developing countries, HAV infection is still very common in the early years of life and its seroprevalence rates approach 100%.[11] In many other Asian countries too, HAV infection remains highly endemic. Studies from Pakistan in the 1980s, 1990s and 2000s show that >50% of children acquire anti-HAV immunity by their preschool years and nearly all adolescents and adults are immune. Between the 1980s and 1990s in Nepal, nearly all adolescents were immune by age 15. In Bangladesh, >50% of 5 year olds and almost all adolescents and adults are immune.[12]
It is believed that in our country, being in a hyperendemic zone, most of the population acquires HAV infection during childhood, which is mostly asymptomatic and then achieve lifelong immunity. But with increasing age of acquisition, both symptomatic diseases and serious complications like acute liver failure (ALF) increase. In addition, it is well known that superimposed acute HAV infection can worsen the prognosis in pre-existing chronic liver disease. However, some workers in India have recently reported that more adults are now at risk of developing HAV infections in different metropolitan cities of the country [13], and India may be in a transition in respect to seroprevalence of anti-HAV IgG that is similar to European countries. [14] Therefore, there are some conflicting reports from different regions within India, suggesting a geographical difference as regards the aetiology of AVH. Both HEV and HAV are enterically transmitted with similar risk factors, but the clinical course of hepatitis E is usually more severe than hepatitis A, frequently complicated by coagulopathy and cholestasis. Hepatitis E is mostly self-limiting but may develop into fulminant hepatitis, especially in pregnant females. Comprehensive data from the Northeastern part of India on the aetiology of AVH is lacking. Therefore, this observational, prospective study was undertaken to study the aetiology of acute viral hepatitis from this region.
MATERIALS AND METHODS
The study population included patients of suspected Acute Viral Hepatitis attending the Assam Medical College Hospital, Dibrugarh, Assam, India (a tertiary care teaching hospital), in the Medicine OPD and indoor wards from September 2005 to December 2013. Institutional Ethics Committee approval was obtained before the study. A total of 591 patients (aged 14 to 55 years) were included after written informed consent. Patients with acute onset signs and symptoms consisting of jaundice ( serum bilirubin > 3 mg/dL), ALT and AST > 3 times upper normal, malaise, fatigue, fever, nausea, anorexia, abdominal pain, vomiting, high coloured urine, altered sensorium, or encephalopathy were included in the study. The development of acute liver failure during the observation period and outcome of the illness was noted. Chronic liver disease patients were excluded by clinical, biochemical and radiological investigations, as well as past medical history/records when available. Other metabolic causes/infections/collagen diseases for disturbed sensorium were ruled out by laboratory and biochemical tests. CSF examination was done when indicated for excluding viral/bacterial/tubercular meningo-encephalitis. Those on anti-tubercular drugs were excluded. Detailed history regarding family contacts, travel, blood transfusion, occupation, source of drinking water, tattooing, herbal medication intake, food habits, alcohol intake (where appropriate with duration, type and amount), residence in urban/rural area and income were obtained. Pre-referral medical prescriptions, if any, were scrutinized for hepatotoxic drugs. Serum samples were collected and tested for the major hepatotropic Viral Markers in our college. All sera were tested for antibodies to hepatotropic virus; the serological tests included IgM anti-HAV (General Biologicals Corp., Taiwan), HBsAg (General Biologicals Corp., Taiwan), IgM anti-HBc (Radim Diagnostics, Rome, Italy), anti-HCV antibody using a third-generation enzyme immunoassay (EIA) kit (Ortho Diagnostics Inc., NJ, USA) according to the manufacturer’s instructions and, IgM anti-HEV (Immunovision, USA) using third-generation EIA Kits. Serum alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were determined from the serum aliquots using commercial kits (Boehringer Mannheim, Germany) as per the manufacturer’s instructions. The results were re-validated in the Virology Laboratory in the Maulana Azad Medical College, Delhi. The sera were sent in small aliquots in dry ice-packs. Positive samples were re-tested in duplicate at the PCR laboratory of the Dept of Gastroenterology, Maulana Azad Medical College, Delhi. All seronegative sera were tested for amplification of HBV DNA and HCV RNA by real time PCR. Only HBV and HCV PCR negative cases were included in Non-B & C group of cases. Anti-HCV positive sera were tested further for HCV-RNA, which was detected based on the 5’ UTR-core region and whenever positive, were labeled as HVC.
RESULTS
Out of 591 cases, 448 belonged to rural or semi-urban area. On an average, all patients presented to us in the second week of their illness. On enquiry, 243 (41%) used to consume unsafe drinking water. Of the study group, 69% were male (405 of 591). The average age of males in our study was ~ 31 years, and that of females ~ 5 years less. 382 (65%) patients were positive for hepatotropic viruses, while 200 (34%) had non-ABCE hepatitis (Table 1). 9 (2%) patients had combined viral infections.HAV was most common (33%) in AVH out of which 4% developed ALF. Summarizing the total outcome, 93 (16%) of 591 cases developed ALF and 9% expired. The highest mortality was in the Hepatitis A group (17 cases, 9% of total 195 Hepatitis A). But the highest proportionate mortality was seen in the Hepatitis B group (10 of 22 cases, or 36%). In the Hepatitis E group (n:121), a mortality of 9% seen. The non- ABCE hepatitis group (n:200) had 19 ALF (5% of all cases) cases with a mortality of 7% (Fig 1). Some demographic and biochemical parameters of patients in different aetiology are shown in Table 2. 50% of all patients had a history of intake of various herbal medications before coming to hospital, but could not specify the type or content of the herbal medications. Of all ALF cases, 84% had a history of ingestion of herbal medications. 60% of non-ABCE hepatitis had taken herbal medications. Paracetamol was consumed in 30% of all cases before presenting to our institute. The leading cause of AVH in Pregnancy was Hepatitis A (9 of 15) without any Hepatitis E. (Table 3).
DISCUSSION
The subjects affected by AVH in our series were young, active and of productive age, thus, leading to significant loss of DALYs. They mostly belonged to rural areas. Table3 shows the comparison of various Indian studies on the aetiology of AVH [15,16,17,18,19,20,21,22,23] with our study. Except in children from Chandigarh and Lucknow, all other studies have found Hepatitis E as the commonest cause of acute viral hepatitis. In our country Hepatitis E reportedly occurs as mostly sporadic hepatitis with periodic resurgence and is responsible for 30-70% cases of acute sporadic hepatitis,[24] primarily affecting young adults between 15-40 yr of age in an endemic region [25]and is the major cause of ALF [26]. Indian seroprevalence studies also reveal that 90%- 100% of the population acquires anti-HAV antibody and becomes immune by adolescence [2] and hence HEV is found to be the most common cause of acute sporadic hepatitis. [27] Nevertheless, our study highlights Hepatitis A as the commonest cause for both AVH and ALF. Notably, significantly more ALF occurred in the non-viral group. A third of the all ALF cases were due to Hepatitis A (Table 1), but the highest proportion of deaths due to ALF occurred in HBV group compared to HAV or HEV. It appears that HBV is not a common cause for ALF in our region (Table 4), compared to other Indian studies [15,20,22,25,26,28]. The rest of India shows Hepatitis E as the leading cause of ALF in most studies. However, the proportion of cases of fulminant hepatitis A who survived was greater compared to the proportions of survival for Hepatitis B or Hepatitis E. This series shows that acute hepatitis B has a poor outcome in our setting, and acute Hepatitis C is rare in ALF in our region. We found that ALF in both viral AVH and non-ABCE group had an almost similar mortality. HAV expectedly showed a slightly higher mortality compared to HEV as it is established that in adults AVH due to HAV produces a more severe disease. There is a paradox in the rise of liver enzymes seen in various groups (Table 2). The lowest average levels of liver enzymes were for Hepatitis B, while the highest was for hepatitis A and can be explained by more hepatocyte injury in the HBV group. Hepatitis C group showed the minimum rise of bilirubin with Hepatitis A showing the maximum rise. The rise of liver enzymes may correlate inversely with mortality, but this remains to be validated. There is no difference in the clinical course of patients with non-ABCE hepatitis compared to those positive for the major hepatotropic virus. In India, non-viral AVH is not uncommon [29] and our findings confirm this. In our series, overall mortality in ALF in the viral group was higher than in non-ABCE group. We had 34% cases without any positive viral serology. In a study involving 165 south-east Asian adult patients with AVH (from India, Nepal, Pakistan), a specific etiologic diagnosis was made in 122 (74%) patients where acute hepatitis E occurred in 40%, HAV in 18.7%, HBV in 11.5%, HCV 1.2%, and combined infection in 4.2%. No viral aetiology could be confirmed in the rest 43 (26%) cases. [30] Another Indian report found that in children Englishhttp://ijcrr.com/abstract.php?article_id=744http://ijcrr.com/article_html.php?did=7441. Krugman S. The Gordon Wilson Lecture. The ABC’s of viral hepatitis. Trans Am Clin Climatol Assoc 1992; 103: 145- 156.
2. Acharya SK, Madan K, Dattagupta S, Panda SK.Viral hepatitis in India.Natl Med J India. 2006 Jul-Aug;19(4):203-17.
3. Kumar S, Ratho RK, Chawla YK, Chakraborti A. The incidence of sporadic viral hepatitis in North India: a preliminary study. Hepatobiliary Pancreat Dis Int. 2007;6:596–9.
4. Chadha MS, Walimbe AM, Chobe LP, Arankalle VA. Comparison of aetiology of sporadic acute and fulminant viral hepatitis in hospitalized patients in Pune, India during 1978- 81 and 1994-97. Indian J Gastroenterol. 2003;22:11–5.
5. Das K, Agarwal A, Andrew R, Frösner GG, Kar P. Role of hepatitis E and other hepatotropic virus in aetiology of sporadic acute viral hepatitis: a hospital based study from urban Delhi. Eur J Epidemiol.2000;16:937–40.
6. Jain A, Kar P, Madan K, Das UP, Budhiraja S, Gopalkrishna V, et al. Hepatitis C virus infection in sporadic fulminant viral hepatitis in North India: cause or co-factor. Eur J Gastroenterol Hepatol.1999;11:1231–7.
7. Bansal J, He J, Yarbough PO, Sen S, Constantine NT, Sen D. Hepatitis E virus infection in eastern India. Am J Trop Med Hyg. 1998;59:258–60.
8. Sarguna P, Rao A, Sudha Ramana KN. Outbreak of acute viral hepatitis due to hepatitis E virus in Hyderabad. Indian J Med Microbiol. 2007;25:378–82.
9. Kamath SR, Sathiyasekaran M, Raja TE, Sudha L. Profile of viral hepatitis A in Chennai. Indian Pediatr. Jul 2009;46(7):642-3.
10. Fischer GE, Thompson N, Chaves SS, Bower W, Goldstein S, Armstrong G, et al. The epidemiology of hepatitis A virus infections in four Pacific Island nations, 1995-2008. Trans R Soc Trop Med Hyg. Sep 2009;103(9):906-10.
11. Franco E, Meleleo C, Serino L, Sorbara D, Zaratti L.Hepatitis A: Epidemiology and prevention in developing countries. World J Hepatol. 2012 Mar 27;4(3):68-73.
12. WHO. The Global Prevalence of Hepatitis A Virus Infection and Susceptibility: A Systematic Review. Available from: whqlibdoc.who.int/hq/2010/WHO_IVB_10.01_eng.pdf.
13. Hussain Z, Das BC, Husain SA, Murthy NS, Kar P. Increasing trend of acute hepatitis A in north India: need for identification of high-risk population for vaccination. J Gastroenterol Hepatol. 2006 Apr;21(4):689-93.
14. Das K, Jain A, Gupta S, Kapoor S, Gupta RK, Chakravorty A, Kar P. The changing epidemiological pattern of hepatitis A in an urban population of India: emergence of a trend similar to the European countries. Eur J Epidemiol. 2000 Jun;16(6):507-10
15. Tandon BN, Gandhi BM, Joshi YK. Etiological spectrum of viral hepatitis and prevalence of markers of hepatitis A and B virus infection in north India. Bull World Health Organ 1984;62:67-73.
16. Radhakrishnan S, Raghuraman S, Abraham P, Kurian G, Chandy G, Sridharan G. Prevalence of Enterically transmitted hepatitis viruses in pateints attending a tertiary case hospital in South India. Indian J Pathol Microbiol. 43(4): 433-6; 2000.
17. Kaur R, Gur R, Berry N, Kar P. Aetiology of endemic viral hepatitis in urban North India. Southeast Asian J Trop Med Public Health 2002;33:845-8.
18. Poddar U, Thapa BR, Prasad A, Singh K. Changing spectrum of sporadic acute viral hepatitis in Indian children. J Trop Pediatr 2002;48:210-3.
19. Hussain Z, Das BC, Husain SA, Murthy NS, Kar P. Increasing trend of acute hepatitis A in north India: Need for identification of high-risk population for vaccination. J Gastroenterol Hepatol 2006;21:689-93
20. Kumar S, Rathod RK, Chawla YK, Chakraborti A. The incidence of sporadic viral hepatitis in North India: A preliminary study. Hepatobiliary Pancreat Dis Int 2007;6:596-9
21. Irshad M, Singh S, Ansari MA, Joshi YK. Viral hepatitis in India: A Report from Delhi. Glob J Health Sci 2010;2:96- 103.
22. Jain P, Prakash S, Gupta S, Singh K P, Shrivastava S, Singh D D, Singh J, Jain A. Prevalence of hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D virus and hepatitis E virus as causes of acute viral hepatitis in North India: A hospital based study. Indian J Med Microbiol 2013;31:261- 5
23. Chandra NS, Sharma A, Rai RR, Malhotra B. Contribution of hepatitis E virus in acute sporadic hepatitis in north western India. Indian J Med Res. 2012 September; 136(3): 477–482.
24. Panda SK, Thakral D, Rehman S. Hepatitis E virus. Rev Med Virol. 2007;17:151–80.
25. Arankalle VA, Tsarev SA, Chadha MS, Alling DW, Emerson SU, Banerjee K, et al. Age-specific prevalence of antibodies to hepatitis A and E viruses in Pune, India, 1982 and 1992. J Infect Dis.1995;171:447–50.
26. Acharya SK, Panda SK, Saxena A, Gupta SD. Acute hepatic failure in India: a perspective from the East. J Gastroenterol Hepatol. 2000;15:473–9.
27. Abraham P. Viral hepatitis in India. Clin Lab Med. 2012 Jun;32(2):159-74.
28. Khuroo MS, Kamili S. Aetiology and prognostic factors in acute liver failure in India. J Viral Hepatol. 2003;May10(3): 224-31.
29. Hussain Z, Das BC, Husain SA, Asim M, Chattopadhyay S, Malik A, Poovorawan Y,Theamboonlers A, Kar P. Hepatitis A viral genotypes and clinical relevance: Clinical and molecular characterization of hepatitis A virus isolates from northernIndia. Hepatol Res. 2005 May;32(1):16-24.
30. Abro AH, Abdou AM, Saleh AA, Ustadi AM, Hussaini HS. Hepatitis E: a common cause of acute viral hepatitis. J Pak Med Assoc. 2009 Feb;59(2):92-4.
31. Samanta T, Ganguly SAetiology, clinical profile and prognostic indicators for children withacute liver failure admitted in a teaching hospital in Kolkata. Trop Gastroenterol. 2007 JulSep;28(3):135-9.
32. Uchida T, Shimojima M, Gotoh K, Shikata T, Tanaka E, Kiyosawa K.”Silent” hepatitis B virus mutants are responsible for non-A, non-B, non-C, non-D, non-Ehepatitis. Microbiol Immunol. 1994;38(4):281-5.
33. Ferraz ML, Silva AE, Macdonald GA, Tsarev SA, Di Biscelgie AM, Lucey MR. Fulminant hepatitis in patients undergoing liver transplantation: evidence for a non-A, non-B,nonC, non-D, and non-E syndrome. Liver Transpl Surg. 1996 Jan;2(1):60-6.
34. Arora NK, Nanda SK, Gulati S, Ansari IH, Chawla MK, Gupta SD, Panda SK. Acute viral hepatitis types E, A, and B singly and in combination inacute liver failure in children in north India. J Med Virol. 1996 Mar;48(3):215-21.
35. Kumar A, Yachha SK, Poddar U, Singh U, Aggarwal R. Does co-infection with multiple viruses adversely influence the course and outcome of sporadic acute viral hepatitis in children J Gastroenterol Hepatol. 2006 Oct;21(10):1533-7.
36. Hussain Z, Husain SA, Pasha ST, Anand R, Chand A, Polipalli SK, Rehman S, Kar P. Does mutation of hepatitis A virus exist in North India? Dig Dis Sci. 2008 Feb;53(2):506-10. Epub 2007 Jun 28.
37. Chitambar S, Joshi M, Lole K, Walimbe A, Vaidya S. Cocirculation of and coinfections with hepatitis A virus subgenotypes IIIA and IB in patients from Pune, western India. Hepatol Res. 2007 Feb;37(2):85-93.
38. Hussain Z, Das BC, Husain SA, Polipalli SK, Ahmed T, Begum N, Medhi S, Verghese A, Raish M,Theamboonlers A, Poovorawan Y, Kar P. Virological course of hepatitis A virus as determined by real time RT-PCR: Correlation with biochemical, immunological and genotypic profiles. World J Gastroenterol. 2006 Aug 7;12(29):4683-8.
39. Alatoom A, Ansari MQ, Cuthbert J. Multiple factors contribute to positive results for hepatitis A virus immunoglobulin M antibody Arch Pathol Lab Med. 2013 Jan;137(1):90-5.
40. Ki Tae Suk, Dong Joon Kim Drug-induced liver injury: present and future Clin Mol Hepatol. 2012 September; 18(3): 249–257.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareCOEXISTENCE OF NON-HODGKIN LYMPHOMA AND EXTRAMEDULLARY HAEMATOPOIESIS IN
A LYMPH NODE: A UNIQUE CASE DIAGNOSED BY FINE NEEDLE ASPIRATION CYTOLOGY
English2123Arindam KarmakarEnglish Tanushree GhosalEnglish Gopinath BaruiEnglish Ranjana BandyopadhyayEnglish Subhalakshmi MukhopadhyayEnglishAim: Non-Hepatosplenic extramedullary haematopoiesis is an uncommon finding and Extramedullary haematopoiesis (EMH) in lymph nodes is further rarity. This effort aims at highlighting an extremely rare coexistence of the two in the same lymph node. Case report: We report an old man with co-existent Non-Hodgkin lymphoma and EMH in the same lymph node diagnosed by FNAC. Discussion: It is rare to find extramedullary haematopoiesis in enlarged lymph nodes subjected to FNAC. To the best of our knowledge no case of co-existent Non-Hodgkin lymphoma and EMH has been reported previously. Conclusion: This case emphasizes the possibility of Extramedullary haematopoiesis (EMH) in an enlarged lymph node with or without other pathological processes. It also underscores the significance of proper correlation of information for the diagnosis of the ailment which in this case could be done with very simple investigation protocol.
EnglishCoexistence, Extramedullary hematopoiesis, Lymph node, Non-hodgkin lymphomaINTRODUCTION
Extramedullary haematopoiesis (EMH) occurs when bone marrow is destroyed due to some disease process like myelofibrosis or the marrow is replaced by malignant cells or storage cells. Lymph node may be the site of extramedullary haematopoiesis in case of myelofibrosis, haematolymphoid malignancy etc. but coexistence of Non-Hodgkin lymphoma and extramedullary haematopoiesis in the same lymph node is a very unusual finding. Here we report a case of a 63 year old male patient having extramedullary haematopoiesis coexisting with Non-Hodgkin lymphoma in the right supraclavicular lymph node which was diagnosed by FNAC.
Case Report
A 63year old male patient presented with multiple swellings in neck; weakness, abdominal discomfort for the last 6 months. On clinical examination severe anaemia, bilateral cervical lymphadenopathy (1-2 cm size) and mild hepatosplenomegaly were found. CT scan of neck revealed multiple enlarged lymph nodes at right lower jugular, bilateral supraclavicular, bilateral paratracheal (right>left), pretracheal, precarinal, aorto pulmonary, subcarinal and bilateral hilar regions. Routine haematological investigation revealed Hb -6.0 g%, TLC 24000/cmm , Platelets- 60000/cmm, NRBC – 16/100 WBC. Leukoerythroblastic blood picture was seen on examination of the peripheral smear. FNAC of the right supraclavicular lymph node was requested which was done using 23G needle. MGG stained smears revealed high cellularity comprising predominantly mixed population of atypical lymphoid cells. Along with lymphoid population some immature cells of myeloid and erythroid lineage were seen. Megakaryocytes, identified by the presence of large multilobated nuclei and abundant granular eosinophilic cytoplasm, were seen consistently scattered along the smears. A diagnosis of Non-Hodgkin Lymphoma along with extramedullary haematopoiesis was made based on cytomorphology.
Discussion
Extramedullary haematopoiesis occurs in various sites including liver and spleen. Occasionally it involves other organs. It is rare to find extramedullary haematopoiesis in enlarged lymph nodes subjected to FNAC. While reviewing literature we found cases depicting coexistence of leukaemic infiltration and extramedullary haematopoiesis in the same lymph node [1] but we are yet to encounter any past record of coexistence of Non-Hodgkin Lymphoma and extramedullary haematopoiesis in the same lymph node. Without the relevant haematological investigations, differential diagnosis on FNAC smears is that of myeloid sarcoma; inflammatory disorders; lymphoma and metastatic carcinoma with multinucleated giant cells. Morphological findings aided by clinical and haematological findings are sufficient enough to distinguish extramedullary haematopoiesis from others [2,3]. Although Non-Hepatosplenic Extramedullary Hematopoiesis (NHS-EMH) is often associated with myelofibrosis with myeloid metaplasia (MMM) or thalassemia, it can also accompany other disorders, including hereditary spherocytosis, sickle cell anaemia, congenital dyserythropoietic anaemia, immune thrombocytopenic purpura, chronic myeloid leukaemia, polycythaemia vera, myelodysplastic syndrome, Paget disease, osteopetrosis, and Gaucher disease and treatment with myeloid growth factors. Occasionally, an associated disease is not identified [4]. Clinically, NHS-EMH may present as an incidental finding or with a symptomatic disease or condition, including pleural effusion, ascites, neurologic deficit, cardiac tamponade, chronic renal failure, acute respiratory failure, orbital proptosis, and subglottic stenosis [4]. In a retrospective review of cases of non-hepatosplenic extramedullary haematopoiesis by Koch C.Y. et al, 27 cases were found of which most (26%) were around vertebra as well as in lymph nodes (inguinal, para-aortic, para-tracheal and cervical) , retroperitoneum, lung, pleura, genitourinary tract, skin etc. 18 cases were diagnosed as myelofibrosis with myeloid metaplasia (MMM) of which 12 were diagnosed as agnogenic myeloid metaplasia and 6 were diagnosed as post-polycythemic myeloid metaplasia. Of the 9 cases in the non-MMM group, 3 patients had congenital anaemia; 2 cases had chronic lymphocytic leukemia; 3 cases having chronic myeloid leukemia, pachydermoperiostosis and cerebrovascular malformation respectively. One case had no detectable underlying disorder. Cases involving lymph nodes were associated with agnogenic myeloid metaplasia and postpolycythaemic myeloid metaplasia [4]. Mass-forming foci of NHS-EMH, sometimes mimicking tumor were also reported [2,3,5]. Our case depicts a very rare instance having features of non-hodgkin lymphoma and extramedullary haematopoiesis in the same lymph node diagnosed by FNAC with guidance from the relevant clinical, haematological and radiological findings.
Conclusion
Non-Hepatosplenic extramedullary haematopoiesis is an uncommon finding and EMH in lymph nodes is further rarity. This case emphasizes the possibility of EMH in an enlarged lymph node with or without other pathological processes. It also underscores the significance of proper correlation of information for the diagnosis of the ailment which in this case could be done with very simple investigation protocol.
Abbreviations
EMH = Extramedullary haematopoiesis
FNAC = Fine Needle Aspiration Cytology
NHL = Non-Hodgkin lymphoma
NHS-EMH = Non-hepatosplenic extramedullary haematopoiesis
Hb=Haemoglobin
TLC = Total Leukocyte count
NRBC = Nucleated red blood cells
Acknowledgement
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors/ editors/ publishers of all those articles, journals and books from where the literature of this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=745http://ijcrr.com/article_html.php?did=7451. Singhal N, Tahlan A, Bansal C, Handa U, D’Cruz S. Coexistence of leukemic infiltration and extramedullary hemato-poeisis in a lymph node: A cytological diagnosis. J Cytol. 2011 Jul-Sep; 28(3):138-140.
2. Policarpio-Nicolas M, Bregman S, Ihsan M, Atkins K. Massforming extramedullary hematopoiesis diagnosed by fineneedle aspiration cytology. Diagn Cytopathol. 2006 December; 34(12):807-11.
3. Jan Y, Chen J, Chang M, Ho W. Fine-needle aspiration cytology of retroperitoneal extramedullary hematopoiesis: a case report. Kaohsiung J Med Sci. 1998 October; 14(10): 659-63.
4. Koch CA, Li CY, Mesa RA, Tefferi A. Nonhepatosplenic Extramedullary Hematopoiesis: Associated Diseases, Pathology, Clinical Course, and Treatment. Mayo Clin Proc. 2003; 78:1223-33.
5. Ahuja S, Grover G, Jha A, Sodhi K, Bansal D, Dey P. Extramedullary hematopoiesis presented as solitary renal mass: a case report with review of literature. Diagn Cytopathol. 2011 June; 39(6):435-7.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareMENTAL TAI CHI-BASED EXERCISE PROGRAMME VS TAI-CHI FOR INDIAN MULTIPLE SCLEROSIS PATIENTS: A PILOT STUDY
English2430Darshpreet KaurEnglish Kirandeep KaurEnglish Nidhi BilloreEnglish Gunjan KumarEnglish Ajay Kumar SinghEnglishBackground: Tai Chi postures have recently been shown in a number of randomized controlled trials to improve balance and posture in a variety of patient groups. Balance and mobility are problems commonly encountered by people with Multiple Sclerosis (MS). This pilot study examines the effect of Tai-Chi ± Mental practise on balance, gait and mobility in people with MS. Objective: To determine the efficacy of both protocols in inducing balance and mobility improvements.
Methods: About 25 volunteer MS patients were screened with Movement Imagery Questionnaire—Revised second version (MIQ-RS), Modified clinical test of sensory organisation and balance (mCTSIB) and Expanded Disability Status Scale (EDSS) before being included in this study. 16 people satisfying the inclusion criteria with Relapsing Remitting MS (RRMS) were randomly assigned to either a Tai Chi group or to Tai chi with mental practise group. The first group participated in 20 sessions of total 60 minutes duration (20 minutes mental practise followed by 40 minutes tai-Chi), for 10-12 weeks The second group participated in 20 sessions which were 40 minutes long for 10-12 weeks. Out of all the known forms of Tai-Chi forms, six wereselected an d practised during these sessions. Results: There was no significant difference between group 1and group 2 for age, gender, MS duration, MIQ score, mCTISB and EDSS. Both the groups showed significant improvement (pEnglishMental Practise, Tai-chi, Multiple Sclerosis, Physical rehabilitationINTRODUCTION
Multiple Sclerosis is a chronic neurological autoimmune disease which is characterized by problems in balance and coordination, motor impairment, fatigue and cognitive dysfunction. 1-4 As a consequence of multiple sclerosis, complications in walking and mobility are often debilitating and carry significant social as well as economic burden. 5 Imbalance also poses serious risk of falls which are often injurious. 6 Patients of Multiple Sclerosis therefore rely heavily on rehabilitation techniques such physical and occupational therapy. Tai Chi is a low impact, slow motion mind-body exercise which originated in China as a martial art. Over the years, Tai Chi has been repeatedly shown to improve balance, strength and gait in the elderly, the frail and patients of Parkinson’s disease. A sustained Tai Chi program (12 month duration) is reported to have long term positive effects by decreasing the number of falls as well as mental and emotional stress in various test groups.7-9 A previous study suggested the efficacy of Tai-Chi in improving balance and depression in patients of Multiple Sclerosis.10However; these results were not conclusive since they were mainly deduced from self-reported improvements in response to a subjective questionnaire. Therefore, the primary aim of this study was to test the hypothesis about the beneficial effects of Tai-Chi on balance and mobility in patients of Relapsing Remitting Multiple Sclerosis (n=16) using standardized, non-biased measuring scales. Also, rehabilitation therapies are often narrowly focused on improving a selected body function. Till date, there exists little research which links the effects of cognitive rehabilitation to balance and mobility. On the other hand, previous studies have repeatedly shown that mobility in MS is not an isolated problem and is interspersed with various other factors, of which cognitive impairment is one.11-12 One particular study demonstrated a decrease in walking ability when patients were simultaneously asked to perform a mental task.13 It is not known to what extent are symptoms of cognitive dysfunction in MS (typically-impairment in visuospatial functions, information processing, executive function, decrease in attention and concentration) responsible for motility problems. 14-16 Thus, there stands a need for an integrated approach to rehabilitation. For this purpose, an alternative regime of mental practice tailored specifically for impaired domains was administered in addition to 20-minute Tai Chi practice in the second part of this experiment. The additional effect of mental practice on mobility scores was observed.
SUBJECTS AND METHODS
Patients and controls
The inclusion criteria for recruiting the patients were: 1) A definite diagnosis of MS lasting >3 months as defined by Revised McDonalds 2010 criteria and 2)No visual impairment 3) No or minimal upper limb disability 4) Ability to walk independently. The exclusion criteria were 1) Presence of coexisting medical conditions potentially affecting cognition (e.g., vitamin B12 deficiency, hypothyroidism, chronic alcoholism, and active psychiatric disorders); 2) other conditions that might affect testing (e.g., hearing impairment), and 3) patients with significant depression or other psychiatric disorders assessed by the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders were excluded from the study. 4) Patients using any kind of assistive devise.5) Subjects who had already received the planned treatment regime were excluded. All subjects were of Indian ethnicity. The study was approved by the institutional ethical committee.
Test and study procedures
About 25 volunteer MS patients were assessed through convenient sampling. After an informed consent was obtained, subjects completed a questionnaire providing information about their age, the onset of pathology. They were screened with Movement Imagery Questionnaire-Revised second version (MIQ-RS), modified clinical test of sensory organisation and balance (mCTISB) and Expanded Disability Status Scale (EDSS) before being assigned into various groups. Four subjects dropped out because they had plans to travel out of city during study duration and two subjects dropped out for unknown reasons. All subjects were tested while they wearing their regular footwear and the assessments were carried out in one session. The assessment protocol consisted of two tests of static balance and two dynamic balance as primary outcome measures and a self-administered scales on balance confidence. Movement Imagery Questionnaire—Revised second version (MIQ-RS) Imagery training is more effective in individuals who are able to engage in imagery practice. The MIQ-RS requires movements of both the upper and lower limbs, thus assessing the ability to imagine one’s gross motor movements17. It consists of fourteen tasks. It has high test-retest reliability with a visual score of 0.83 and kinesthetic score 0.73. Modified clinical test of sensory organisation and balance (mCTISB) This test assesses patient’s balance under a variety of conditions to find out the source of instability. Time for which patient was able to maintain the starting position (maximum of 30 seconds) is recorded (in seconds). It also has good test-retest reliability (r = 0.99) for young adults18.
Dynamic Gait Index
This scale measures the mobility function and the dynamic balance of an individual. The performance is rated on a 4-point scale. The total score ranges from 0 to 24.DGI has high sensitivity (87%) in identifying fallers from non-fallers with a cut-off score ≤19 in multiple sclerosis patients19. Functional Reach (FR)- Lateral and Forward This test was developed as a clinically feasible measure of limits of stability in adults. The forward reach was chosen as the test task because it is not only a common functional movement, but it also mimics the leaning movements used to measure the excursion of the centre of pressure. It has a good intrarater reliability for Forward and Lateral reach, as measured with a yardstick (ICC3,1 = .98 and .96 respectively)20. Timed up and Go (TUG)
This test is used for measuring gait speed for a shorter distance. The TUG also provides information regarding everyday physical mobility like getting up, sitting down and turning.21In testing people with MS, the TUG had an intra-class correlation coefficient (ICC) of 0.982 Activities-specific Balance Confidence This is a scale in which the subject rates his or her perceived level of confidence while performing 16 daily living activities. Scores range from 0 to 100, where 100 means high level of confidence in balance skills. The validity and reliability of the scale has been found to be good for people with multiple sclerosis22.
Intervention
Following evaluation of balance disorders and group allocation, each subject received intensive practice with a Tai- Chi exercise programme (see Appendix). Sixteen people satisfying the inclusion criteria with RRMS were randomly assigned to either a Tai Chi with mental practise group or to Tai chi group. The first group participated in 20 sessions of total 60 minutes duration (20 minutes mental practise followed by 40 minutes tai-Chi), for 10-12 weeks .The second group participated in 20, 40 minutes long training sessions for 10-12 weeks .Out of all the known forms of Tai-Chi, six were practised during these sessions. Because of the high variability of symptoms a tailored rehabilitation programme was developed based on each group’s specific protocol. During the treatment sessions we stressed the function and quality of performance of Tai-Chi forms. The difficulty of the forms was based on the subject’s performance and followed their level of recovery. Specific and uniform guidelines for the intervention were developed and discussed with the physio therapists. Each subject, irrespective of group assignment, had a total of 20 sessions spread over ten-twelve weeks, each session lasting 60 minutes.
Statistical analysis
Data analyses included all 16 subjects who matched the inclusion criterion and completed the duration of this study. Statistical analysis was performed using the software Stata IC/13. Both the groups were compared for differences in baseline measures (EDSS, MIQ, mCTISB, MS duration, age and gender). The distribution of the data sets was tested for normality using Skewness-Kurtosis and Shapiro-Wilk test. Those which did not follow normal distribution were analysed using non- parametric tests (Wilcoxon signed-ranks test ). Normally distributed parameters were investigated for significance using paired t-test. Box-plots were constructed to estimate differences in median and percentiles of baseline parameters. The gain/ change scores were recorded in both the groups post intervention. The first step was to determine if the decided treatments have any significant effect on gait and balance of the subjects. This was done by performing t-test / Wilcoxon signed-ranks test on the pre and post test scores. The level of statistical significance was uniformly set at pEnglishhttp://ijcrr.com/abstract.php?article_id=746http://ijcrr.com/article_html.php?did=7461. Geoffrey L. Sheean, Nicholas M. F. Murray, John C. Rothwell, David H. Miller, Alan J. Thompson,An electrophysiological study of the mechanism of fatigue in multiple sclerosis Brain (1997), 120, 299–315.
2. Benedetti MG, Piperno R, Simoncini L, Bonato P, Tonini A, Giannini S. Gait abnormalities in minimally impaired multiple sclerosis patients., MultScler October 1999 vol. 5 no. 5 363-368.
3. Rao SM, Leo GJ, Bernardin L, UnverzagtF.Cognitive dysfunction in multiple sclerosis. I. Frequency, patterns, and prediction.Neurology. 1991 May;41(5):685-91.
4. Frzovic D, Morris ME, Vowels L.Clinical tests of standing balance: performance of persons with multiple sclerosis. ArchPhys Med Rehabil. 2000 Feb;81(2):215-21.
5. Pike J, Jones E, Rajagopalan K, Piercy J, Anderson P.Social and economic burden of walking and mobility problems in multiple sclerosis.BMC Neurol. 2012 Sep 18;12:94.
6. Matsuda PN, Shumway-Cook A, Bamer AM, Johnson SL, Amtmann D, Kraft GH.Falls in multiple sclerosis.PM R. 2011 Jul;3(7):624-32.
7. Wolfson L, Whipple R, Derby C, Judge J, King M, Amerman P, et.al.Balance and strength training in older adults: intervention gains and Tai Chi maintenance.J Am Geriatr Soc. 1996 May;44(5):498-506.
8. Lan C, Lai JS, Chen SY, Wong MK.12-month Tai Chi training in the elderly: its effect on health fitness.MedSci Sports Exerc. 1998 Mar;30(3):345-51.
9. Jin P.Efficacy of Tai Chi, brisk walking, meditation, and reading in reducing mental and emotional stress.JPsychosom Res. 1992 May;36(4):361-70.
10. Mills N, Allen J, Morgan SC. (2000). Does Tai Chi/Qi Gong help patients with multiple sclerosis? Journal of Bodywork and Movement Therapies2000; 4(1):39-48.
11. Fischer JS,FoleyFW,Aikens JE .What do we really know about cognitive dysfunction,affectivedisorders,and stress in multiple sclerosis A practitioner’s guide.JNeuroRehabl. 1994;8(3):151–164.
12. Chan A, Heck C. Mobility in multiple sclerosis: more than just a physical problem. Int J MS Care. 2000; 3: 35–40.
13. Motl RW, McAuley E, Sandroff BM.Longitudinal change in physical activity and its correlates in relapsing-remitting multiple sclerosis.PhysTher. 2013 Aug;93(8):1037-48.
14. Amato MP, Ponziani G, Pracucci G, Bracco L, Siracusa G, AmaducciL.Cognitive impairment in early-onset multiple sclerosis. Pattern, predictors, and impact on everyday life in a 4-year follow-up.Arch Neurol. 1995 Feb;52(2):168-72.
15. Bagert B, Camplair P, BourdetteD.Cognitive dysfunction in multiple sclerosis: natural history, pathophysiology and management.CNS Drugs. 2002;16(7):445-55.
16. Piras MR, Magnano I, Canu ED, Achene A, Solinas G, Aiello I.Longitudinal study of cognitive dysfunction in multiple sclerosis: neuropsychological, neuroradiological, and neurophysiological findings.J Neurol Neurosurg Psychiatry. 2003 Jul;74(7):878-85.
17. Gregg M., Hall C, Butler A.The MIQ-RS: A Suitable Option for Examining Movement Imagery Ability.Evid Based Complement Alternat Med. 2010 Jun;7(2):249-57.
18. Cohen H, Blatchly CA, Gombash LL.A study of the clinical test of sensory interaction and balance.PhysTher. 1993 Jun;73(6):346-51.
19. Forsberg A, Andreasson M, NilsagårdYE.Validity of the Dynamic Gait Index in People With Multiple Sclerosis.Physical Therapy October 2013 vol. 93 no. 10 1369-1376.
20. Thompson M, Medley A.Forward and lateral sitting functional reach in younger, middle-aged, and older adults. JGeriatrPhysTher. 2007;30(2):43-8.
21. Nilsagard Y, Lundholm C , Gunnarsson LG , Dcnison E. Clinical relevance using timed walk tests and ‘timed up and go’ testing in persons with multiple sclerosis. Physiother Res Int. 2007; 12: 105–114.
22. Nilsagård Y, Carling A, Forsberg A.Activities-specific balance confidence in people with multiple sclerosis.MultScler Int. 2012;2012:613925.
23. Maria G., Susan C., Neasa H, Aidan L, Jean S.Getting the Balance Right: A randomised controlled trial of physiotherapy and Exercise Interventions for ambulatory people with multiple sclerosis.BMC Neurology 2009, 9:34
24. Mass M.,Oken B.S., Kishiyama S.,Zajdel D.,Bourdette D.,CarlsenJ.et.al.Randomized controlled trial of yoga and exercise in multiple sclerosis.Neurology. 2004 Jun 8;62(11):2058-64.
APPENDIX
The rehabilitation protocol ensured that each exercise group had a consistent intervention schedule on key training parameters which included the duration (60 minutes per session), frequency (2 times per week for 10 weeks), and training structure (i.e., a 5- to 10-minute warm-up, core activities, and a 5-minutecool-down). Participants in all three conditions were instructed not to engage in any additional home practice.
Group1: Received balance rehabilitation to improve motor, sensory and cognitive strategies.
Group2: Received balance rehabilitation to improve motor and sensory strategies. For improving motor strategies, 6 forms of Tai-Chi were selected. Training of Gait patterns was also borne in mind while designing Tai-Chi programme for both the groups. These tasks required stepping in different directions, while challenging subject’s postural stability and balance control. The somatosensory information was encouraged by large and coordinated movements in order to move the center of mass with speed, safety and balance.Emphasis was laid on improving vestibular and somatosensory information by a reduction of visual input. For this purpose certain forms of Tai-Chi were performed in different perceptual contexts. The patients were encouraged to exercise in eyes-closed condition. Group 1 also engaged in mental imagery of the desired tasks, while Group 2, underwent relaxation during that duration. For this purpose episodic memory of the patients in group 1 was targeted. Anterograde component of their memory was put into action by providing visual stimulation of the Tai-Chi form, which they will be performing on that day. Lapses in working memory were challenged by intermittently questioning about their perception of visual inputs. To insure proper execution of Tai-Chi forms patients were asked about the relevance of particular form to them and potential benefits they seem to obtain from it. Throughout 40 min Tai-Chi session it was ensured that both the groups perform symmetrical and coordinated movements such as trunk rotation and weight shifting from one foot to another foot, Controlled and coordinated displacement of the body’s center of mass over the base of support, Ankle sway toward and around the perimeter of the base of support, dynamic eye and head movements and anterior-posterior and medial-lateral stepping with rhythmical weight shifting for each form.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareHEMODYNAMIC MIMICRY OF HYPERTROPHIC OBSTRUCTIVE CARDIO MYOPATHY : A CASE REPORT
English3133B. P. ChattopadhyayEnglish Hamid AliEnglish Kapildev MandalEnglish Madhab Kumar MondalEnglish Anupam MondalEnglish Pranab Kumar MaityEnglishA 64 year diabetic and hypertensive male suffering from ischaemic heart disease developed two episodes of syncopal attacks in quick succession followed by coffee-brown vomiting. He was in a state of shock following upper G.I. bleeding induced hypotension for which he was resuscitated with blood transfusion, volume repletion and inotropic support. Echo-doppler study during inotropic therapy showed hypercontractile LV with LVOT obstruction and gradient of 100 mm Hg across the LVOT. After the volume repletion echo-doppler study was repeated; the LVOT obstruction and the gradient across it was absent in repeat Echodoppler study. So echo-doppler study during inotropic treatment of shock in pre-existing hypertensive background (LVH) may temporarily mimic the haemodynamic findings of HOCM which disappears after stabilization of the shock state.
EnglishHOCM (Hypertrophic Obstructive Cardio Myopathy), LVOT (Left Ventricular Outflow Tract) Obstruction Haemodynamic mimicryINTRODUCTION
Hypertrophic Obstructive Cardio Myopathy(HOCM) is a common cardiac problem and the echo-doppler findings of HOCM can be mimicked by several other conditions. The differential diagnosis is very important because the line of management is different in different disease states. One such clinical condition is treatment of shock state with inotropic drugs in a patient who is having established hypertensive heart disease (LVH).
Clinical Summary
A 64 year old diabetic, hypertensive male presented with two episodes of syncopal attacks in quick succession which mandated admission in a city hospital outside our institute was known to be suffering from chronic stable angina and hypothyroidism since 1999. On 10.01.06 the patient had. On admission the patient had bouts of vomiting and the vomitus was coffee–brown in colour to start with, followed by frank haematemesis; it was accompanied by hypotension for which intravenous fluid and inotropes were started. Interrogation of past medication revealed that he was receiving aspirin, oral nitrates, Oral Hypoglycaemic Agents, ACE Inhibitors. On general examination the patient was observed to have pallor,tachycardia,B.P.80/60 mm of Hg and cold clammy extremities. On systemic examination there was tenderness in the epigastric region and there was a systolic murmur in the mitral area. Examination of the other systems including central nervous system was non-contributory.
Investigation summary
ECG revealed sinus tachycardia, LVH and 2 mm ST elevation in I,aVL,V5and V6; Trop-T was negative Capillary blood glucose was 223 mg/dl, Haemogram displayed Hb 6.6 g/dl with peripheral smear suggestive of hypochromic microcytic anaemia. UGI Endoscopy revealed 8 mm size active ulcer in the antrum with presence of altered blood in the stomach. Stool for occult blood test was positive (apart from G.I.
Bleeding induced true positivity, aspirin consumption may also lead to false positivity) CT Scan of brain revealed only age related cerebral atrophy. Carotid Doppler study revealed significant intimal thickening of both common carotid arteries without any significant stenosis. 24 hour Holter monitoring revealed no significant arrhythmia. Bedside Echo-doppler study (while the patient was on I/V fluid and inotropes) revealed IVS thickness 15mm,Posterior Wall thickness 12 mm. There was no typical asymmetric septal hypertrophy (septum to posterior wall ratio greater than 1.5) but there was systolic anterior motion of the anterior mitral leaflet causing dynamic LVOT Obstruction. The resting gradient of 100 mm of Hg across the LVOT(fig.1a and fig 1b) and LVH was noted.Pulse Wave Doppler revealed diastolic dysfunction .It was labeled as Hypertrophic Obstructive Cardio Myopathy outside. Inotropes were stopped and volume and blood replacement were emphasized.
Repeat Echodoppler study revealed thickness of IVS and PW to be 14.7 mm and 11.5mm respectively; there was no significant resting gradient across the LVOT. The LVOT gradient on Valsalva strain was found to be only 20 mm Hg. There was reduced diastolic compliance. There was no finding suggestive of HOCM. Another echo-doppler report (done in 1999) revealed concentric left ventricular hypertrophy and diastolic dysfunction. There was no suggestion of HOCM at that time as well.
Discussion
The purpose of the present case reporting is to draw attention to the differences in the three echo-doppler study findings. Echo on admission was done in the setting of intravenous inotropic therapy for treatment of hypotension following the G.I.Bleed. Noteworthy is the fact that the patient was hypertensive for more than 15 yrs. It has been described in the literature that the LVOT gradient mimicking HOCM can be encountered in the intensive care unit setting in the patients of hypotension following intravascular volume depletion especially while on concurrent inotropic agents 1. Often there is a history of underlying hypertension and the relatively low intravascular volume with augmented contractility result in hyperdynamic motion of the ventricle - an acquired form of dynamic LVOT obstruction2 .
Conclusion
Echodoppler suggestion of possibility of HOCM in patients of intravenous inotropic therapy for treatment of hypotension specially in the background of hypertensive heart disease should be critically reviewed after cessation of inotropic therapy and correction of shock and hypotension.High index of suspicion of such haemodynamic mimicry of HOCM helps establish actual diagnosis and management. Denial of opportunity of treating with Diuretics and many other drugs can be avoided by differentiation from HOCM.
Acknowledgements
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=747http://ijcrr.com/article_html.php?did=7471. Dynamic left ventricular outflow tract obstruction in acute myocardial infarction with shock, Anand Chockalingam, Lokesh Tejwani et al, Circulation 2007:116e:110e-113.
2. Dobutamine mediated left ventricular outflow tract dynamic obstruction associated with hypovolaemic shock. M.Basalus, S.A.M. Said, P. Danse et al, The open Cardiovascular imaging journal,2010,Volume-2,page 14-1.7.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareEFFECT OF THYROID HORMONES IN MALES WITH INFERTILITY - A CROSS SECTIONAL STUDY
English3437G. RekhaEnglish V. RajithaEnglish K. Y. ManjunathEnglishBackground: Various authors have studied the effect of thyroid hormones to estimate the male factor in infertility. Some have concluded that thyroid hormones have a role to play in determining the quality of sperms and some state that the hormones do not have any effect on spermatogenesis. This study was done to observe the effect of thyroid hormones in the affected males. Materials and Methods: The male partners of 71 infertile couples participated in the study. Semen analysis was done in the affected males after an abstinence of three days. Thyroid hormones estimation and semen analysis was done on the same day. The males were grouped as Oligospermic, severe Oligospermic and Azoospermic after semen analysis. Normospermic males were used as a control group. Result: The age range of the affected males was 24 – 53 years. The mean years of marital duration were 7.7 years. The thyroid hormonal level was within normal limits in all the 71 males investigated. In semen analysis, 17 males were Normospermic. 22 males were Oligospermic, 22 were severe Oligospermic and 10 were Azoospermic. The mean sperm count was 9.18 million/ ml in Oligospermic, 3.3 million/ml in severely Oligospermic, Nil in Azoospermic and 123.86 million/ml in Normospermic males. Conclusion: Thyroid hormones do not have any effect on spermatogenesis in males.
EnglishThyroid, Hormone, Infertility, Oligospermia, AzoospermiaINTRODUCTION
Infertility affects a significant number of married couples and the desire to beget a child in the affected population is of utmost importance in their lives. Out of every affected 100 affected couples, the male and the female factors are almost on par and the latter being marginally higher1 . In some cases, the cause is unknown and infertility can also occur with both the partners being affected. For investigation of the male factor in the affected couples, semen analysis is of prime importance. The quality and quantity of semen determines a positive conception when the affected factor is male. In a significant percentage the affected partner in infertility is usually a male2 . In affected male partners of infertile couples, the quality and quantity of semen differs. A recognizable decline in the semen quality been also observed in the south Indian population3 . Sex hormones play an important role in spermatogenesis which maintains the sperm quality and quantity. Many studies have elaborated the influence and importance of sex hormones in spermatogenesis and sperm count. Thyroid hormones play a significant role in the metabolism of the human body and also in the reproductive cycle in females. However not many studies exist which elucidate the effect of thyroid hormones in spermatogenesis. Many studies highlight the effect of thyroid hormone in female reproduction hence this study aims to probe the influence of thyroid hormones in spermatogenesis, sperm quality and quantity in affected males. In many studies on animal models like rats and goats demonstrate the presence of thyroid receptors in the testis especially in the sertoli cells. This regulation of thyroid hormone in animal models has been brought upon by the hypothalamo hypophyseal testicular axis which governs the sperm production. In humans the presence of thyroid receptors in the sertoli cells are disputed. In specific T3 does not inhibit receptors in the testis and the role of thyroid regulating hormone on the testis is indeterminate4 .
The presence of thyroid receptors in the sertoli cells in animal models influence germ cell production and maturation. The presence of Sertoli cells to the germ cells in humans is 1:11 when compared to the animal model. In humans thyroid hormones do not seem to influence spermatogenesis according to standard texts.
Materials and Methods
71 male partners of infertile couples attending the infertility clinic in a tertiary care hospital volunteered to participate in the study. After sexual abstinence of three days, the volunteers were made to collect semen in a sterile container which was analyzed using automated sperm analyzer. Prior to semen analysis, blood sample was collected in a sterile container and estimation of thyroid hormones was done.
Parameters of semen Analysis were determined based on WHO guidelines 20107 .
- Age - Marital status
- Volume of semen
- Ph - Sperm concentration
- WBC concentration
- Liquefaction duration
Thyroid hormone estimation was done to find the serum levels of
- T3
- T4
- TSH
Based on the sperm count the volunteers (n=71) were classified into four groups
Group -1 = Oligospermic males (22)
Group -2 = Severe Oligospermia (22)
Group -3 = Azoospermia (10)
Group -4 = Normospermic males (Used as a control group) (17)
Statistical Analysis
The observations and the numerical quotients obtained from the study were statistically analyzed using SPSS software version 16 to ascertain the statistical significance of the study.
Results
The age range of all the volunteers was from 24 - 53years with a mean of 35 years. The duration of married life in the affected couples was 2-15 years with a mean of 7.7years; Group wise distribution is depicted in Table -1. The parameters of semen analysis are depicted in Table -2. The thyroid hormone level estimation in the group wise was within normal limits in all the 71 males investigated. Group wise distribution of thyroid hormones T3, T4 and TSH estimation is depicted in Table -3. Analysis of variables for thyroid hormones is depicted in Table -3. In semen analysis, 17 males were Normospermic. 22 males were Oligospermic, 22 males were severe Oligospermic and 10 males were Azoospermic. The mean sperm count was 9.18 million/ml in Oligospermic males, 3.3 million/ ml in severely Oligospermic males, Nil in Azoospermic males and 123.86 million/ml in Normospermic males. Analysis of variables for the sperm count is depicted in Table -2.
Discussion
Thyroid hormones have effect on spermatogenesis in animal models, as receptors are present in the testis and influence the quality of sperms. Some authors have studied the effect of thyroid hormones on the quality of sperms but a direct and conclusive evidence still eludes5 . These studies elaborate the effect of sertoli cells rather than on the germ cells. Since such studies have been done on smaller sample size, the actual cause and effect in the case of thyroid hormones cannot be definitely established. However some studies have indicated that there is deterioration in the quality of sperms due to defective spermatogenesis arising primarily out of morphological abnormalities of sertoli cells6 . Few authors have suggested that hormonal therapy should be considered for treating hormonal insufficiency and a reproductive endocrinologist should be included to perform a hormonal assessment which should be made a part of investigations for male infertility8 . Semen analysis is the sole and reliable test to estimate the male factor in infertility. Since a majority of male factor in infertility is due to deficient sperm count and abnormal sperm parameters which is due to a error in the control mechanism of pre and post testicular reasons9 . LH and FSH have more significant role to play in spermatogenesis as they stimulate gametogenesis than thyroid hormones. Although other endocrine hormone receptors are found in the parts of the male reproductive system, it is highly unlikely that hormones other than LH and FSH influence the outcome of spermatogenesis in cases of male infertility10. Studies performed in males with infertility to find out the relationship between hypothyroidism and spermatogenesis have also primarily state that the effect of FSH and LH on the testis and sertoli cells in particular conclude that the influence of the above mentioned hormones are not direct11. Most of the studies which establish a link between hypothyroidism, hyperthyroidism and spermatogenesis have been performed in western subjects and not many studies exist on Indian test subjects and the one such study done does not find any significant effect of thyroid hormones in male infertility12.
Conclusion
To conclude this study does not establish any direct link between thyroid hormones and spermatogenesis in male infertility. However since the sample size of this study is relatively modest, extending the study with a larger sample size might validate the present findings. Also widening the parameters and methodology with repeated blood samples and semen analysis might establish a direct effect on thyroid hormones on spermatogenesis in males with infertility.
ACKNOWLEDGEMENTS
The authors sincerely wish to thank the management, administrators and the Professors and Head of the department of Anatomy of Vinayaka Missions Kirupananda Variyar Medical College, Salem for their whole hearted support and permissions to utilize their resources and conduct this study. The authors acknowledge the great help received from the scholars whose articles cited and included in references of this manuscript. The authors are also grateful to authors/editors/publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Authors are grateful to IJCRR editorial board Members and IJCRR team of reviewers who have helped to bring quality to this manuscript.
Englishhttp://ijcrr.com/abstract.php?article_id=748http://ijcrr.com/article_html.php?did=7481. K Poppe, D Glinoer, H Tournaye, Is systematic screening for thyroid disorders indicated in sub fertile men? European Journal of Endocrinology 2006:154 363–366.
2. S.Bhasin, D.M.DE Kretser, H.W.G.Baker , Clinical Review 64 Path physiology and natural History of Male Infertility. Journal of clinical Endocrinology and metabolism; vol.79, No.6.
3. Adiga SK, Jayaraman V, Kalthur G, Upadhya D, Kumar P. Declining Semen quality among South Indian infertile men : A retrospective study. J Hum Reprod Sci Issue 1 Jan –Jun 2008.15-18
4. Francis. S. Greenspan, Gordon J. Strewler Control of Thyroid function, Basic and Clinical Endocrinology, 5th Edition, 207- 217.
5. Rajender singh, Alaa J Hamada and Agarwal. Thyroid Hormones in Male Reproduction and Fertility; Central Drug Research Institute; Lucknow. The open Reproductive Science Journal, 2011:3; 98-104.
6. Sharpe RM. Declining sperm counts in men: is there an endocrine cause? J Endocrinol 1993; 136:357-60.
7. World Health Organization 2010 .WHO laboratory manual for the examination and processing of human semen - 5th edition, pg-225.
8. M.A.Emokpae,P.O Uadia,A.Z.Mohammed and A. Omale-Itodo. Hormonal abnormalities in Azoospermic men in kano, northern Nigeria. Indian J Med Res 124, September 2006, 299-304.
9. Teruaki I wamoto, Shiari Nozawa and Miki Yoshiike. Semen quality of Asian men; Reprod Med Biol 2007; 6:185- 93.
10. Muhammad Shoaib Khan, Irshad Ali et al: Determination of Serum Gonadotropin and Testosterone Levels in Male Infertility. JPMI 2007 Vol.21No.02:86-91.
11. Elzbieta Krajewaka –Kulak and Pallav Sengupta. Thyroid function in male infertility. Frontiers in Endocrinology. November 2013, Volume 4, Article 174/1.
12. Manoj Kumar Sharma, Deepak Parchwani et al; Relationship between thyroid profile and Semen Quality, National Journal of Community Medicine Vol 3 Issue 1 Jan –March 2012:20-24.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareEFFICACY OF DISTRACTION TECHNIQUE IN REDUCING PAIN AMONG CHILDREN RECEIVING VACCINATION
English4246Richa TalwarEnglish Anita YadavEnglish Rupinder DeolEnglish Jasbir KaurEnglishBackground: Vaccination is the process whereby a person is made immune or resistant to an infection. Routine vaccination is a universal phenomenon which is administered repeatedly throughout infancy, childhood and adolescence. It is the common source of iatrogenic pain in childhood. Pain from injection is a source of distress for children, their parents and vaccinators, and if not addressed, can lead to pre-procedural anxiety in future, medical fears and healthcare avoidance behaviours. So, there is a great need to study the methods of alleviation of vaccination related pain in children. Objectives: The study was undertaken with the objective to assess the efficacy of distraction technique in reducing level of pain among healthy children during vaccination. Methods: A quasi experimental study design was used to evaluate the efficacy of distraction technique in reducing level of pain among healthy children receiving vaccination at well baby clinic in selected hospital, Ludhiana. Sample size of 200 healthy children using convenience sampling (100 in each group) was used. The standardised FLACC (face, leg, activity, cry, consolability) - Behavioral Pain Assessment scale was used to observe level of pain among the healthy children during vaccination. A sound and light producing movable toy was used as distraction technique in experimental group during vaccination. Video recording of the children receiving vaccination was done and the pain score was calculated. Results: Findings revealed that 7% of the children in experimental group as compared to only 1% in control group experienced no pain during vaccination. The mean pain score among experimental and control group were 4.02±1.694 and 4.89±1.503 respectively (pEnglishDistraction technique, Pain, Vaccination, Children, FLACC (face, Leg, Activity, Cry, consolability) Behavioral Pain Assessment scaleINTRODUCTION
Immunity is a biological term that describes a state of having sufficient biological defences to avoid infection.1 Children have immature immune response against diseases unlike adults. To develop the immune response and to impart the immunity, there is a need of vaccination.2 Parents want their child to be safe from diseases. So, they choose vaccination as a preventive measure.3 Routine vaccination is a universal experience which is painful and children show behavioural distress to pain.4 Despite the benefit of vaccination5 the pain associated with vaccination is a source of great anxiety and distress for many children.5-6 Reports from children, parents and nurses consistently indicate that many children do indeed fear the “shot”4 which is often manifested by the child’s distress behaviour such as crying, temper tantrums, untoward behaviour and refusal to cooperate, which is upsetting not only for the child but also for both parents and professionals that makes it difficult to complete the needed procedure.4,7 Many mothers withhold scheduled vaccines out of concern for the excessive pain from vaccination.8 Unfortunately, despite an increased focus on pain assessment and management, vaccination related pain remains largely untreated.9 Many children are so preoccupied with the possibility of pain from vaccination that this worry dominates the entire visit. Every nurse or physician who works with children, find a cowering child whose first question is, “Am I going to get a shot?” The needle is a powerful negative symbol for many children, is a phobia for some, and unfortunately has become an icon of medical/nursing care.10-11To ensure adequate pain relief, to make pain more tolerable and to give the children a sense of control over the situation, non-pharmacological methods are widely accepted that may be used independently or in addition to medication. Distraction, electro-analgesia, imagery, relaxation technique, hypnosis and cutaneous stimulation are common non-pharmacological techniques used to alleviate pain.12 Distraction is a non-pharmacological intervention that diverts attention from a noxious stimulus by passively redirecting the child’s attention or by actively involving the child in the performance of diversion task.13 Distracters that can be commonly used for children include sound and light producing movable attractive toys, picture books, talking with the child and music etc.14 Related to the quality of the distraction, Mac Laren and Cohen found that, more the children engage in distraction, the lower is the pain experienced by them regardless of the type of distraction stimuli.15It was observed by the researcher that because of this, sometimes parents do not get their child vaccinated or postpone the vaccination. Hence the need to assess the efficacy of distraction during painful procedure was felt as Infant procedural distress is largely understudied in child health nursing literature. The purpose of the study was to assess the efficacy of distraction technique in reducing level of pain among healthy children receiving vaccination. In future, this distraction technique may allow the parents to stick with the immunisation schedule and decrease the fear of shot in children. Material and Methods: A quasi experimental (post test only) research design was used to assess the efficacy of distraction technique in reducing level of pain among healthy children receiving vaccination at well baby clinic in selected hospital Ludhiana. The distraction technique (sound and light producing movable toy) was introduced to the experimental group during vaccination and withheld in the control group. The target population included all the healthy children up to the age of 3 years. The sample size of 200 healthy children were selected by convenience sampling technique. To assess level of pain during vaccination, FLACC (face, leg, activity, cry, consolability) - Behavioral Pain Assessment Scale was used. This is a standardised scale which includes the observation of five parameters i.e. face, leg, activity, cry and consolability, which indicate behavioral pain responses of the child. The video was recorded starting from the time when child lied down on vaccination table till 1-5 minutes after vaccination and videos were graded for pain accordingly. The maximum pain score of the tool was ten and minimum was zero. Informed written consent was taken from the parents. In intervention phase, sound and light producing movable toy was shown as a method of distraction to healthy children of experimental group during vaccination. Standard needle size of twenty six gauge and thigh as a site of vaccine was used for all the children. Simultaneously, video recording of the whole procedure was done by a trained person. Videos were encoded by another person with research background. An intervention was involved in the study, so it was conducted after approval from the ethical committee of DMC and Hospital, Ludhiana. Analysis of data was done in accordance with the objectives of the study. Null hypotheses (H0 ) of the study was that there will be no significant reduction in level of pain among experimental group at 0.05 level of significance.
Statistical Methods
Both descriptive and inferential statistics were Statistical Methodsused; calculations were carried out manually, with the help of calculator, Microsoft excel and SPSS version16. Descriptive statistics such as percentage, mean, standard deviation and inferential statistics like ANOVA, ‘t’ test and chi square were used for analysing the collected data. The level of significance was set at 0.05.
RESULTS
Out of total 200 subjects, the percentage of male children in experimental and control group were 57% and 60% respectively. Three-fourth of children (75%) in control group and nearly two-third (67%) in experimental group were first born children in the family. More than half of the children (56%) in control group and 58% in experimental group weighed between 6.1-12 kg. More than half of the children (56%) in the experimental group and slightly less than half (44%) in the control group belonged to the age group of 0-6 months. Regarding the vaccination related data, most of the children (90%) in control group and majority of the children (80%) in experimental group had their mother as a primary caregiver. Mothers of more than one-third of children (44%) in control group and 40% in experimental group were present during vaccination. More than half of the children (54%) in control group and less than half (45%) in the experimental group received more than one vaccine. Majority of the children (82%) in control group and 83% in experimental group received vaccination by intramuscular route whereas only 12% in control group and 9% in experimental group received vaccine by both intramuscular and subcutaneous route. Regarding the level of pain during vaccination, only 1% of children in control group showed no pain whereas 7% of children in experimental group demonstrated no pain. Findings revealed that 16% of children in control group and 26% children in experimental group experienced mild pain. More than two-third (68%) of children in control group and less than two-third (60%) of children in experimental group experienced moderate pain during vaccination. Further findings reveals that 15% of the children in control group demonstrated severe pain, whereas only 7% of the children in experimental group demonstrated severe pain. There was statistically significant difference in the level of pain among experimental and control group (pEnglishhttp://ijcrr.com/abstract.php?article_id=749http://ijcrr.com/article_html.php?did=7491. OP, Gupta P and Paul VK.Ghai. Essential Pediatrics. 6th ed. New Delhi: CBS Publishers, 2008.p.181.
2. FDA/NIH/WHO Workshop. Immune response in children to influenza vaccination;[cited 2011 July 28].Available from: http://www.fda.gov/downloads/BiologicsBloodVaccines/NewsEvents/WorkshopsMeetingsConferences/ ucm090464 pdf.
3. Abbot K and Fowler-Kery S. The use of a topical refrigerant anaesthetic to reduce injection pain in children. Journal of Pain and Symptom Management 1995; 10: 584-90.
4. Agras S, Sylvester D andOliveau D. The epidemiology of common fear and phobias. Comprehensive Psychiatry; 1969:1511-56.
5. American Academy of Pediatrics Committee on Infectious Diseases. Recommended childhood and adolescent immunization schedule-United States, 2003.Pediatrics 2003;111: 212-16.
6. Schechter NL, Zempsky WT, Cohen LL, McGrath PJ, McMurtry CM, Bright NS. Pain reduction during paediatric immunisations: evidence-based review and recommendations. Paediatrics 2007 May; 119(5):1184-98.
7. Schecter NL, Altman A and Wiseman SJ. An introduction: American Academy of Paediatrics report of the subcommittee on management of pain associated with procedures in children with cancer. Paediatrics 1990; 86:813.
8. Help. Eliminate pain in kids. Clinical practice guidelines for pain management during childhood vaccination, Technical report, http://www.cdha.nshealth.ca/default retrieved on 25-03-2011.
9. Anand KJS, Thrivikraman KV, Engelmann M, Su Y andPlotsky PM. Adult rat behaviour and stress responses following pain in the neonatal period. Pediatr Res 1995; 37:57A.
10. Fassler D. The fear of needles in children. Am J Orthopsychiatry 1985; 55:371–77.
11. Hamilton JG. Needle phobia: a neglected diagnosis. J FamPract 1995; 41:169-75.
12. Ball JW andBindler RC. Clinical handbook for pediatric nursing. 2nd ed. St. Louis: Mosby Publication; 1998.
13. Fernandez E. A classification system of cognitive coping strategies for pain; 1986; 26,141,151.
14. McCarthy MA andKliebre C. A conceptual model of factors influencing children’s response to a painful procedure when parents are coaches. Journal of Paediatric Nursing 2006; 21.
15. MacLaren JE and Cohen LL. A comparison of distraction strategies for venipuncture distress in children. JPediatrPsychol 2005; 30:387–96.
16. French MG, Painter CE and Larry LD. Blowing away shot pain: a technique for pain management during immunisation. Paediatrics 1994 Jun; 6:210-7.
17. Bellieni CV, Cordelli DM, Raffaelli M, Ricci B, Morgese G andBuonocore G. Analgesic effect of watching TV during venipuncture. Arch Dis child. 2006 December; 91(12):1015- 1017.
18. Allen KD, White DD andWalburn JN. Sucrose as an analgesic for infants during immunisation injections. Arch PediatrAdolesc Med 1996 Mar; 150
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareIS CD38 EXPRESSION STILL RELEVANT PROGNOSTIC FACTOR IN CHRONIC LYMPHOCYTIC LEUKEMIA?
English4753Trajkova S.English Cevreska L.English Ivanovski M.English Simjanovska-Popova M.English Pivkova-Veljanovska AEnglish Dukovski D.English Panovska-Stavridis I.EnglishIntroduction: There is a decade of investigations into the role of CD38 in B cell chronic lymphocytic leukemia (B-CLL). Significant percentage of CLL patients expressed transmembrane glycoprotein- CD38 on the surface of leukemic cells. Several published studies suggested that CD38 is accepted as a dependable marker of unfavorable prognosis and as an indicator of activation and proliferation of CLL cells. The aims of the present study were to establish the predictive value of the CD38 expression and to examine the relationship between CD38 positivity and other established prognostic markers in Macedonian CLL patients. Material and methods: Peripheral blood samples from 100 consecutive treatment naïve CLL patients were analyzed by flow cytometry for CD38 expression on CD5/19 leukemic cells. Various patients established prognostic characteristics and molecular markers were studied in correlation to time to treatment (TTT). The Kaplan-Meier method was used to construct survival curves, and the log-rank statistic was used to compare these curves.Results: CD38 was expressed in 61 % of the patients. Patients with high CD38 expression (30% or more) with high value of B2M and advance disease according to Binet had significantly shorter survival times (p= 0 .00001) and (p=0.00033) respectively. Multivariate analyses showed that CD38 expression is an important prognostic factor for shorter TTT associated high B2M level (P .000002), age(P.00000), gender(P.00000), lower hemoglobin level (P.00008 ),hepatomegaly (P.00086). Conclusion: CD38 expression identified a group of patients with aggressive disease that was considered by traditional staging to be early-stage disease (Rai stages 0-II or Binet A). Patients with CD38 samples have significantly aggressive disease regardless of their clinical stage. But today in era of molecular and genetics markers when CD38 is loosing it prognostic value in CLL patients prognosis, we propose serial analyses of the percentage of CD38+cells to be done, resembling indicators of leukemic cell proliferation and may signal clone evolution to a more aggressive state.
EnglishCLL, CD38, prognosisINTRODUCTION
Chronic lymphocytic leukemia (CLL) is defined as a proliferation of B lymphocytes that express surface CD19 and CD5 with expression of CD23, and low levels of immunoglobulin (Ig), CD79b and CD22(1). Some patients with CLL die within 2 years of diagnosis, yet others have a normal lifetime. A significant number of CLL patients show an aggressive form of the disease from the early stages, characterized by refractoriness to treatment, infectious and autoimmune complications, and a relatively rapid fatal outcome. However, unlike the situation in non-Hodgkin’s lymphoma, there is no standard Prognostic Index that can be used to group patients with CLL according to likely outcome or to guide treatment. The earliest staging systems, Rai and Binet systems for CLL relied on disease burden parameters. Histology patterns of bone marrow (BM) involvement and lymphocyte doubling time (LDT) have also been used as valid prognostic indicators. However, these classifications fail to distinguish patients who will eventually progress to an aggressive form of the disease from those who have a more stable form of the disease. During the past 20 years, several soluble molecules have been used as prognostic tools in CLL, including thymi dine kinase, CD23, and B2M and genetic markers of tumor cells, such as genomic aberrations, gene abnormalities (p53, ATM), the mutation status of the variable segments of the immunoglobulin heavy chain genes (IGVH) or surrogate markers for these factors, such as CD38 and ZAP-70. However, some of these markers do help in determining predicting the outcome. Fais et al. (2) were the first to report that the presence or absence of immunoglobulin gene mutation could classify patients with B-CLL into 2 groups. Hamblin et al( 3) and Damle et al( 4) independently confirmed this observation and demonstrated that patients without the immunoglobulin gene mutation had more aggressive disease with shorter survival times, whereas patients with the immunoglobulin gene mutation had less aggressive disease and prolonged survival times. Damle et al(4) studied CD38 expression in CLL patients and reported that cells from patients with unmutated immunoglobulin genes were positive for CD38 expression and this was associated with aggressive disease. In this study, we measured the levels of CD38 expression in 100 patients with CLL and correlated these values with various clinical, molecular characteristics in ordered to investigate prognostic value of CD38 in CLL population when mutational status of IG gene plays the most important prognostic role.
Materials and methods
Patient population
One hundred consecutive treatment naïve patients with B-CLL seen at University Clinic for Hematology between September 2011 and August 2013 were included in this study. At initial evaluation, date of CLL diagnosis was recorded, and the time-to- treatment end point was defined as time from first University Clinic for Hematology visit to first CLL treatment. There was no restriction for time from diagnosis to presentation to University Clinic for Hematology. All patients had more than 1 months of treatment-free follow-up from initial University Clinic for Hematology evaluation, and physicians were to conform to 1996 NCIWG guidelines for initiating treatment. The study was conducted in accordance with the Helsinki declaration. Clinical and laboratory evaluation at first University Clinic for Hematology visit included history and physical examination, standard clinical laboratory evaluation, evaluation for CD38 by flow cytometry was performed on peripheral blood at University Clinic for Hematology. Traditional prognostic factors and clinical and laboratory variables included sex, age, Rai stage, Eastern Cooperative Oncology Group performance status, physical examination with evaluation of number of involved lymph node sites (cervical, axillary, and inguinal), measurement of liver and spleen size, white blood cells count (WBC), absolute lymphocyte count(ALC), hemoglobin level, platelet count, Beta-2 microglobulin(B-2M), lactate dehydrogenase (LDH), creatinine, albumin, and quantitative immunoglobulin (Ig) levels (IgG, IgA, and IgM)(5). Peripheral blood samples were collected at the time of presentation. The samples were taken to confirm the diagnosis by flow cytometry and characterization of CD38 expression before therapy was initiated. IGHV mutation status was characterized by direct sequencing method, and patients were categorized as unmutated (IGHV ≥98% germline homology) or mutated (< 98% homology) (6). There were 100 patients who had IGHV mutation status performed by Center for biomolecular pharmaceutical analyses, Faculty of Pharmacy, Skopje Macedonia.
Measurement of CD38 expression by flow cytometry
CD38 measurements were performed at University Clinic for Hematology, as reported (6). Peripheral blood samples were obtained at the time of presentation and diagnosis and were used for flow cytometry analysis. Samples were prepared using a 3-color staining method (4). Directly labeled monoclonal antibodies (mAbs) against the lymphoid antigens CD5-phycoerythrin (PE), CD19- allophycocyanin (APC) and CD38- fluorescein isothiocyanate (FITC; Becton Dickinson Immunocytochemistry Systems, San Jose, CA) were used. Immunophenotyping expression was measured by FACS IICalibur (Becton Dickinson) using DIVA softer program. B-CLL cells (CD5/19) were gated. The degree of CD38 expression in this gated population was expressed as percentage positivity, using a threshold at 30% expression to define positive cases.
Statistical analyses
The univariate Cox proportional hazard model was used to evaluate the possible associations between time tofirst-treatment (TFT) and each risk factor singly. Variables identified as statistically significant (P, .05) in univariate analyses were subsequently included in the stepwise multivariate Cox proportional hazards model. Survival time was measured from the test date to either the last follow-up date (censored) or to the time of death by any cause. Variables examined were age, sex, Rai and Binet stages, splenomegaly, hepatomegaly, Hgb level, B2M level in the serum, WBC)count, platelet count, lymphocyte count in the peripheral blood, number of nodal sites involved with disease, IGHV mutation status. All data were collected from reviewing the patient’s record and were entered into the leukemia database. The Kaplan-Meier method was used to construct survival curves, and results were compared using the log-rank test.
Results
Patient characteristics
Patient characteristics are summarized in Table 1. An like other published data, there was female predomination in our population, and the median age was 64, 8 years. Ninety -one percent of patients had Rai stages 0 to II disease. CD38 expression varied in patients with CLL (Figure1). Sixty-one percent of the patients had CD38 expression in 30% or more of the cells, and 39% of the patients had CD38 expression in less than 30% of the cells. Sixteen percent of the patients had CD38 expression in more than 80% of the leukemic cells. Using 30% as a cut-off point in our analysis was arbitrary, and most of the analysis was repeated using CD38 as a continuous variable. Of the 100 patients we studied, 59% were previously untreated.
Comparison of CD38+ and CD38- patient subgroups
When the percentages of CD38+ cells were plotted for the entire patient population (data not shown), the patients could be segregated into 2 groups. Patients with 30% or more B cells expressing CD38 were considered positive, and those with less than 30% were considered negative. As shown in Table 2, there was no significant difference between the 2 groups in terms of Rai or Binet staging, splenomegaly, age, or sex. In addition, there was no significant difference between the 2 groups in WBC count, number of circulating lymphocytes. CD38+ patients were predominantly associated with unmutated IGHV (U-CLL) in addition CD38- patients were predominantly associated with mutated IGHV (M-CLL).
Figure 1: Time to first treatment by CD38 expression, KaplanMeier survival curves. Kaplan-Meier survival curve comparing patients with B-CLL whose samples were positive (30% or more) or negative (less than 30%) for CD38 expression; the difference is not significant at p= 0 .67.
Statistical analyses for CD38 expression
We used the univariate Cox proportional hazard model to assess associations between Treatment free survival time and various risk factors in this group of patients with CLL (Table 3).
As expected patients with >30%CD38 expression have had shorter time to first treatment, associated with these prognostic factors: gender,platelet count, number of involved lymph node sites, increased spleen, advanced Rai and unmutated IGHVgene A multivariable model for time to first treatment was developed with 100 patients (100%), who had complete data available for the fitted covariates (table4). The following patient characteristics were independently associated with shorter time to first treatment: high b2M level (P .000002), age(P .00000), gender (P .00000 ),lower hemoglobin level (P .00008 ), hepatomegaly (P .00086 ).
Discussion
In this study, we found that patients with CLL could be divided into 2 prognostic groups one with worse prognoses had high CD38 expression on malignant cells (30% or more), and those with a better prognoses which had low CD38 expression (less than 30%). Multivariate analyze in our study did not confirmed that CD38 expression is an important prognostic factor in time when mulational status of IGHV gene plays the most important prognostic role. The prime subject behind the clinical observations is why expression of this molecule on the cell surface would correlate with a worse clinical outcome. One of the propose possibility is that CD38 expression reflects events occurring inside the cell. Indeed, the percentage of CD38+cells within a leukemic clone was originally described as one of two independent indicators along with IGHV gene mutations of clinical outcome in CLL (4). Because both indicators marked somewhat overlapping populations, a link with IGHV mutation status, signals mediated by B cell receptor (BCR), and CD38 was proposed(5). These two parameters are not obligatorily linked; there is one hypothesis that the presence of cell surface CD38 provides a more global molecular association to the setting, changing the balance between survival/proliferation and apoptosis in favor of the survival. CD38 is a transmembrane type II glycoprotein with a short amino-terminal cytoplasmic tail, a single mem-brane spanning region, and a long extracellular carboxyterminal domain with molecular weight of 45 kDa. It has ecto-enzymatic activity that serves in the conversion of nicotinamide adenine dinucleotide to cyclic adenosine diphosphate ribose, or cADP, an important regulator of intracellular Ca 2+ release. CD38 has no lineage restriction and mediates variable functions. In myeloid cells, CD38 is expressed on immature precursors and can be up-regulated using all-trans retinoic acid. Its presence has been associated with better prognosis in acute myeloid leukemia (AML), with the exception of AML-M3. CD38 has been reported to play a complex role in lymphocyte proliferation. Ligation of CD38 using an agonistic monoclonal antibody produced diverse responses manifested as growth or apoptosis. CD38 ligation on mature B cells protected against apoptosis and up-regulated the expression of the Bcl-2 proto-oncogene. In contrast, ligation of the CD38 molecule suppressed the growth of immature B cells in the bone marrow micro-environment. Recent studies divided patients with CLL into two prognostic groups based on their IgHV gene mutation status, one with mutation and good outcome and the other without mutation but with poor outcome. But they also identify two subgroups of CLL patients with different clinical outcomes according to CD38 expression. This distinction is based on the percentage of CD38+ leukemic cells within a CLL clone. In the majority of studies, the threshold is considered as +30% CD38+ clone members (7). The two patient subgroups that result from this cut-off point differ clinically in several ways, including overall survival, time to first treatment, (8) toward male gender, number of leukemic cells with atypical morphology(9), extent and level of adenopathy, lactate dehydrogenase and B2-microglobulin levels, (10) and absolute lymphocyte counts. These subgroups also differ in responsiveness to various therapies. In the past decade Damle et al (4) found that patients with B-CLL with high CD38 expression did not have IgH mutations and that this correlated with poor prognosis, whereas patients with low CD38 expression had IgH mutations that correlated with good prognosis. Based on this observation, they proposed that the B-CLL subset with high CD38 expression arises from pregerminal center B cells and that the subset with low CD38 expression arises from postgerminal center cells. Today it is accepted that more sensitive prognostic CLL marker is mutational status of IGHV, and where is the place of CD38 like prognostic CLL marker? IGHV mutation status is a more static marker, indicative of the cell of origin and the maturational events that occurred in the life of the B cell before its leukemic transformation. Antigen binding specificity correlates with outcome because it indicates the extent of antigenic epitopes that the BCR can engage, the affinity of these engagements, and therefore the likelihood that survival signals will be delivered to the CLL cell. It is for these reasons that CD38 expression, which is a reflection of the existing level of cellular activation within. leukemic clone often correlates with a lack of IGHV somatic mutations, which is more likely to lead to polyspecific binding, cell signaling, and eventual cellular proliferation. Thus, both prognostic indicators can be linked by the common thread of leukemic cell proliferation: IGHV mutations indicating the likelihood of binding multiple antigens and of cellular stimulation and CD38 expression representing the consequence of such binding and stimulation. But CD38 is dynamic marker, although CD38 expression was constant (negative or positive) over a variable period of time it increased. This increase in CD38 expression was associated with marked worsening of the patient’s clinical parameters. This was an unexpected finding and contradicted the concept that CD38 expression reflects the origin of B cells from pregerminal or postgerminal centers. Although we cannot rule out the possibility of an evolving new clone of pregerminal center origin, the fact that the patient was untreated suggests an evolution of the same disease. According to some other studies(11) this change is usually not large (10%) and more often, does not disregard the restrictions that mark “superior” or inferior” clinical outcome, it can occur. However, when it does, the suggested weakness can be actually viewed as a positive feature of this prognostic indicator as an rising trend in CD38-expressing cells may signal clone evolution to a more aggressive state (12). Therefore, we propose serial analyses of the percentage of CD38+cells to be done, like indicators of leukemic cell proliferation and prediction of worsening the clinical course of the disease. This laboratory setting can have an additional advantage of indicating a change in clone behavior. Some scoring systems are involving a multiplicity of markers: IGHV mutations, CD38 and/or ZAP-70 levels, chromosomal abnormalities, p53 mutations, and serum molecules such as B2-microglobulin, can be effective risk assessors and group stratifies. These approaches may require further prospective testing to refine and simplify the methods.
Conclusion
CD38 expression identified a group of patients with aggressive disease that was considered by traditional staging to be early-stage disease (Rai stages 0-II or Binet A). Patients with CD38 samples have significantly aggressive disease regardless of their clinical stage. But today in era of molecular and genetics markers when CD38 is loosing it prognostic value in CLL patients prognosis, we propose serial analyses of the percentage of CD38+cells to be done, resembling indicators of leukemic cell proliferation and may signal clone evolution to a more aggressive state.
Acknowledgement
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=750http://ijcrr.com/article_html.php?did=7501. Rozman C, Montserrat E. Chronic lymphocytic leukemia. N Engl J Med. 1995;333:1052-1057
2. Fais F, Ghiotto F, Hashimoto S, et al. Chronic lymphocytic leukemia B cells express restricted sets of mutated and unmutated antigen receptors. J Clin Invest. 1998; 102:1515- 1525.
3. Hamblin TJ, Davis Z, Gardiner A, Oscier DG, Stevenson FK. Unmutated Ig VH genes are associated with a more aggressive form of chronic lymphocytic leukemia. Blood. 1999;94:1848- 1854.
4. Damle RN, Wasil T, Fais F, Ghiotto F, Valetto A, Allen SL, Buchbinder A, Budman D, Dittmar K, Kolitz J, Lichtman SM, Schulman P, Vinciguerra VP, Rai KR, Ferrarini M, Chiorazzi N: Ig V gene mutation status and CD38 expression as novel prognostic indicators in chronic lymphocytic leukemia. Blood 1999, 94(6):1840-1847.
5. Wierda GW, O‘Brien S.,Xuemei Wang X., et all. Multivariable model for time to first treatment in patients with chronic lymphocytic leukemia.J Clin Oncol.2011;vol. 29 (31): 4088-4095
6. Chiorazzi N, Ferrarini M. Cellular origin(s) of chronic lymphocytic leukemia: cautionary notes and additional considerations and possibilities.Blood.2011;117(6):1781-1791.
7. Matrai Z. CD38 as a prognostic marker in CLL. Hematology. 2005;10(1):39-46.
8. Morabito F, Mangiola M, Stelitano C, Deaglio S, Callea V, Malavasi F. Peripheral blood CD38 expression predicts time to progression in B-cell chronic lymphocytic leukemia after first-line therapy with high-dose chlorambucil. Haematologica. 2002;87(2):217-218.
9. Nowakowski GS, Hoyer JD, Shanafelt TD, et al. Percentage of smudge cells on routine blood smear predicts survival in chronic lymphocytic leukemia. J Clin Oncol. 2009;27(11):1844-1849.
10. Domingo-Domenech E, Domingo-Claros A, Gonzalez-Barca E, et al. CD38 expression in B-chronic lymphocytic leukemia: association with clinical presentation and outcome in 155 patients. Haematologica. 2002;87(10):1021-1027
11. Ghia P, Guida G, Scielzo C, Geuna M, Caligaris-Cappio F. CD38 modifications in chronic lymphocytic leukemia: are they relevant? Leukemia. 2004;18(10):1733-1735.
12. Chang CC, Cleveland RP. Conversion of CD38 and/or myeloid-associated marker expression status during the course of B-CLL: association with a change to an aggressive clinical course. Blood. 2002;100(3):1106.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareESTIMATION OF SERUM LIPOPROTEIN (A), LIPID PROFILE AND HBA1C IN PATIENTS WITH TYPE 2 DIABETES MELLITUS - A CASE CONTROL STUDY
English5458Sunita PujarEnglish Kavitha HiremathEnglish L.L. PujarEnglish Shankar PrasadEnglish Mahanthesh BhuthalEnglishObjective: Diabetes is a major worldwide health problem, leading to markedly increased mortality and serious morbidity. It is characterised by chronic hyperglycemia resulting from a diversity of aetiologies and environmental and genetic factors acting together. Type 2 diabetes mellitus itself leads to dyslipidemia like elevated triglyceride levels and low HDL levels, which are known risk factors for coronary artery disease (CAD). Increased lipoprotein (a)[Lp(a)] concentrations are predictive of CAD. The study was designed to estimate serum lipoprotein (a) and glycosylated hemoglobin (HbA1c) in south Indian patients with type 2 diabetes mellitus and compare them with healthy controls. Material and Methods: The study included 50 patients of type 2 diabete mellitus and 50 age and sex matched controls. Fasting venous blood sample was analysed for fasting blood glucose(FBS), glycated hemoglobin (HbA1c), lipid profile and serum Lp(a). Statistical analysis was done using student t test. Results: The serum Lp(a) and HbA1c levels were significantly elevated in type 2 diabetics compared to healthy controls (pEnglishType 2 diabetes mellitus, Glycated hemoglobin, Lipid profile, Lipoprotein aINTRODUCTION
Diabetes mellitus (DM) is world-wide in distribution. Diabetes mellitus is a chronic metabolic disorder that is often associated with unacceptably high disease burden especially in developing countries and the cardiovascular complications of DM are highly contributory to this scenario1 . In India, diabetes is not an epidemic anymore but has turned into a pandemic, according to the International Journal of Diabetes in developing countries which labelled India the diabetes capital of the world. Mainly because India now has the highest number of diabetes patients in the world. The International Diabetes Federation estimates that the number of diabetic patients in InIJCRR Section: Healthcare dia more than doubled from 19 million in 1995 to 40.90 million in 2007. It is projected to increase to 69.9 million by 2025.Currently upto 11 percent of India’s urban population and 3 percent of rural population above the age of 15 has diabetes. The most prevalent is type 2 diabetes2 . Well studied and documented CVS risk factors in DM include components of metabolic syndrome namely dyslipidemia, central obesity and hypertension3 . Other CVS risk factors that have not been widely studied in Indian population include C-reactive protein, hyeruricemia, HbA1c and lipoprotein (a). Lipoprotein (a) [Lp(a)] consists of an LDL like particle and the specific apolipoprotein (a) [apo(a)],which is covalently bound to the apo B of the LDL like particle. The structure of Lp(a)
resembles LDL and its atherogenic properties can be explained by its binding to glycosaminoglycans and inhibition of fibrinolysis. The atherogenic properties of Lp(a) are expressed over 30 mg/dl4 . Persistent hyperglycaemia causes glycosylation of the proteins especially hemoglobin5 . Haemoglobin glycation, estimated by percentage of glycated haemoglobin (HbA1c) ,was first used clinically 30 years ago to asses the degree of chronic hyperglycaemia among diabetic patients in whom values reflect weighted mean glucose levels over the preceding 3 months period; it is useful for characterizing dysglycemia in population studies because it is simpler to perform than the oral glucose tolerance test(GTT) 6 . In Diabetics an increase in HbA1c of 1 percent was associated with a 20 % to 30% increase in mortality associated with cardiovascular events7 .
MATERIALS AND METHODS
Study Participants: The present study comprises 50 patients with Non-Insulin dependent diabetes mellitus (NIDDM) reporting to Hanagal Shree Kumareshwar Hospital and Research Centre. The criteria for the diagnosis of DM was according to the criteria of the American Diabetes Association (ADA) 2007 guidelines. 8 50 subjects of similar age, sex and socioeconomic status served as controls. The controls were free from any major aliment which could affect the parameters under study (the clinical history or investigative results showed no involvement of any organ).The exclusion criteria included type 1 DM, Gestational diabetes , other specific causes for diabetes, micro- and mcro-vascular complications frank proteinuria detected by albustix, cigarette smoking and on lipid altering drugs like oral contraceptive, diuretics, beta blockers and lipid lowering drugs. Subjects with lipid altering diseases: hepatobiliary disease, hypothyroidism, chronic kidney disease and nephrotic syndrome were also excluded. Informed written consent was obtained from all the subjects enrolled for the study. Institutional ethical committee clearance was obtained for the study (Ref No:SNMC/09-10/612).The study was conducted from June 2009 to February 2010. A detailed history was taken to know duration of the disease, treatment history and any complication of the disease. All the subjects underwent clinical examination including anthropometric measurements. The anthropometric measurements comprised of waist circumference, height, body weight and body mass index (BMI) was calculated as weight in Kg/height in m2 .The waist circumference was determined by applying a tape measure to the midpoint between the inferior margin of the last rib and the crest of the ileum. Biochemical analysis-The fasting blood sample, 2 ml in fluoride bulb for sugar estimation and 5ml in plain bulb for lipid profile estimation was collected from the cubital vein with aseptic precaution. Serum was separated by centrifugation at 3000 rpm for 10 minutes.
The following parameters were studied.
1. Fasting blood glucose –Enzymatic, GOD-POD, end point colorimetric, single reagent chemistry.( Trinder P and Teitz N W by autospan kit method).
2. Serum total cholesterol – cholesterol oxidase / peroxidase method. CPT diagnostics kit.
3. Serum HDL cholesterol – phosphotungstate / magnesium precipitate method. Ident i kit.
4. Serum Triglycerides – Glycerol phosphate oxidase / peroxidase method, Ident i kit.
5. Serum VLDL cholesterol – calculated by formula Triglyceride / 5
6. Serum LDL cholesterol – calculated by formula LDL cholesterol = TC – (HDL-C+VLDL-C)
7. TC/HDL-C Ratio All the parameters read using semi auto analyser (Erba, Transasia).
8. Glycosylated Haemoglobin (HbA1c) was determined using Biorad equipment.
9. Lp (a) levels were determined using immunoturbidimetric methods. The statistical analysis was done using student‘t’ test and p value < 0.005 was considered statistically significant.
RESULTS
The descriptive characteristics and the glycemic status of the control and diabetics subjects are shown in table 1. There was no statistical significant difference seen in age and height of control and diabetic patients (pEnglishhttp://ijcrr.com/abstract.php?article_id=751http://ijcrr.com/article_html.php?did=7511. Ogbera AO:Burden of diabetes mellitus in Nigeria.Trop Doct 2007;37(3):153-154.
2. Smith S and Lall AM. A Study on Lipid Profile levels of Diabetics and Non-Diabetics among Naina Region of Allahaba d,India.2008;33(4):138-141.
3. AlbertiKG,Eckel RH,Grundy SM,Zimmet,Paul Z,Cleeman,James I.Donato karen harmonizing the metabolic syndrome.Ajoint interim statement of the International Diabetes Federation Task Force on epidemiology and prevention ;National Heart,Lung and Blood Institute;American Heart Association ;World Heart Federation ;International Atherosclerosis Society; and International Association for the study of Obesity.Circulation 2009;120:1640-45
4. Chattanda SP and Mgonda YM. Diadetic dyslipidemia among diabetic patients attending specialised clinics in Darer Salaam.Tanzania Med.J 2008;23(1):08-11.
5. Romics L,Karadi I,Csaszar A,Kostner G.Physiological and Clinical Importtance of Lipoprotein(a).J Exp Clin Med 1990;15:149-154.
6. Marshall SM,Barth JH.Standardisation of HbA1c measurements -a consensus statement.Diabet Med 2000;17:-6.
7. Naomi BM, Craig SW,Grad D,Noemie T,Cunningham CW,Hornell J,Pearce N, Jeffreys M. A New Zealand Linkage Study Examining the Association Between A1c Concentration and Mortality.2008;31(6):1144-49.
8. American Diabetes Association. Standards of medical Care in Diabetes. Diabetes Care.2007; 30:4-41.
9. Gitanjali G,Sudeep G,Neerja ,Mili G,Deepak A,Priyanka S. The effect of hyperglycemia on some biochemical parameters in diabetes millitus.2019;4(5):3181-3186.
10. Hanssen KF,Bangstad HJ,Brinchmann-Hansen O et al. Blood glucose control and diabetic microvascular complications:Long -term effects of near-normoglycemia. Diabet Med .1992;9:697-705.
11. Fox CS,Coady S,Sorlie PD et al. Increasing cardiovascular disease burden due to diabetes mellitus:The Framingham Heart Study. Circulation .2007;115:1544-1550
12. International Expert Committee report on the role of the A1c assay in the diagnosis of Diabetes. Diabetes care .2009;32:1327-1334
13. Alam SM, Ali S, Khalil M, Deb K, Ahmed A, Akhter K. Serum lipid profile in hypertensive and normotensive type 2 DM patients- a comparative study. Mymensingh Med J.2003;12(1):13-6.
14. Gambir JK,Kaur H,Gambir DS,Prabhu KM.Lipoprotein (a) as an independent risk factor for coronary artery disease in patients below 40 years of age. Indian Heart J . 2000;52:411-15.
15. Solfirizzi V, Panza F, Colacicco AM, Capurso C, DIntrono A, Torres F,et al. Relation of lipoprotein(a) as coronary risk factor to type 2 DM and low density lipoprotein cholesterol in patients ≥65 years of age.Am J Cardiol 2002;89:825-9.
16. Edelberg JM, Gonzalez-gronow M, Pizzo SV.Lipoprotein(a) inhibition of plasminogen activation by tissue-type plasminogen activator. Thromb Res 1990;57:155-62.
17. Karadi I, Kostner GM, Gries A, Nimpf j, Romics L, Malle E. Lipoprotein(a) and plasminogen are immunochemically related. Biochem Biophys Acta 1988;960:91-7.
18. Miles LA, Fless GM, Levin EG, Scanu AM, Plow EF. A potential basis for the thrombotic risks associated with lipoprotein(a). Nature 1989;339:301-3.
19. Kluft C, Jie AFH, Los P, de Wit E, Havekes L. Functional analogy between lipoprotein(a) and plasminogen in the binding to the kringle 4 binding protein,tetranectin. Biochem Biophys Res commun 1989;161:427-33.
20. Wollesen F, Dahlen G, Berglund L,Berne C. Peripheral atherosclerosis and serum lipoprotein(a) in diabetes. Diabetes Care1999;22:93-8.
21. Unluhizacri K, Muhtaraglu S, Kabak S,Bayram F, Kelestimur F. Serum lipoprotien(a) levels in diabetic foot lesions. Diab Res and Clin Pract 2006;71:119-23.
22. Singla S, Kaur K, Kaur G, Kaur H, Kaur J, Jaswal S. Lipoprotein(a) in type 2 diabetes mellitus: Relation to LDL:HDL ratio and glycemic control. Int J Diab Dev Ctries. Apr-June 2009;29(2):80-4.
23. Heller FR, Jamart J, Honare P. Serum lipoprotein(a) in patients with diabetes mellitus. Diabetes Care 1993;16:819- 23.
24. Uterman G,Mazel HJ,Kraft HG,Duba HC,Kemmeler HG,Seitz C.Lp(a) glycoprotein phenotypes inheritance and relation to Lp(a) concentrations in plasma.J Clin Invest 1987;80:458-65.
25. Habib SS. Serum lipoprotein (a) and high sensitivity C reactive protein levels in Saudi patients with type 2 diabetes mellitus and their relationship with glycemic control. Turkish Journal Of Medical Sciences.2013;43:33.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareCONGENITAL DIAPHRAGMATIC HERNIA IN POST NEONATAL PERIOD
English5960Nitin PandeyEnglish Krishna Kumar YadavEnglishBackground: Late presentation of right sided congenital diaphragmatic hernia can present with recurrent cough in postneonatal period. Case characteristics: A 1 - year male child presented to outpatient with complain of recurrent cough since birth. Observation: Child was malnourished and had respiratory distress. There was no cyanosis and pallor was present. Auscultatory finding show decreased breath sound to right side and normal heart sounds. Outcome: Late presentation of right sided congenital diaphragmatic hernia. Message: CDH though, rare condition in postneonatal period could be encountered in outpatient practice with children presenting with recurrent cough and growth failure.
EnglishCongenital diaphragmatic hernia, Post- neonatal periodINTRODUCTION
Congenital diaphragmatic hernia is usually suspected during neonatal period, when newborn presents with respiratory distress. Very few case reports are available in literature for its late presentation in childhood. In developing countries with limited healthcare resources, this condition could be kept in differential diagnosis in post neonatal period.
CASE REPORT
We present a case of 1 year male child presenting with recurrent cough and fever since birth. For which he had received trials of all common antibiotics and cough relieving medicine by many doctors on outpatient basis with no relief from the basic problem permanently. On examination child was in respiratory distress (Respiratory rate- 62/ min with diaphragmatic and intercostal retractions), weight 6 Kg, length 67 cm (Malnutrition according to WHO standards). Pallor was present, cyanosis absent, icterus was absent, clubbing absent and lymphadenopathy was insignificant. Temperature was 99.4 IJCRR Section: Healthcare degree F, heart reate 112/min, Blood pressure 80/54 mmHg. On auscultation there was diminished breath sound on right chest field. Cardiovascular, neurological and per abdomen examination was within normal limit. There was no suggestive history of contacts with tuberculosis. We ordered complete blood count, chest X-Ray and Mantoux test for the patient. Complete blood count was within normal limit but surprisingly in chest X- Ray we got right sided intestinal loops shadow like bag of worms and now our diagnosis was late presentation of congenital diaphragmatic hernia. Mantoux test came to be negative. After stabilizing patient condition and ruling out pulmonary hypertension in 2-D echo, we referred the patient to tertiary care center for surgical management.
DISCUSSION
Congenital diaphragmatic hernia presents with respiratory distress in neonatal period with few differential diagnosis (Anderson KD). With advances in neonatal care and resuscitation programme, congenital diaphragmatic hernia is easily diagnosed in neonatal period and managed surgically (Buttler M ). There are also sporadic case reports showing delayed presentation of CDH (craigie rj,
vandy fc, ng cp). Literature also suggests that children with right sides CDH presents with chronic symptoms in 57.4% cases, while left sided CDH mostly presents with acute symptoms, which is also the common anatomical type of CDH ( Macei Bg). In our case CDH was right sided, which is still rare in rare late presentation of CDH. Our patient’s main complain was off and on cough, which support previous finding suggesting that symptoms of respiratory system predominate the right sided CDH, while left sided CDH mainly presents with gastrointestinal symptoms (Kitano Y). Diagnosis of CDH mainly depends on clinical suspicion and chest X-Ray, although the size of herniation and amount of gastrointestinal tract herniated may cause confusion in interpretation of chest X-Ray and may confuse the picture showing differential diagnosis of pneumonia, tumor, pneumothorax and diaphragmatic eventration (Lee HM). So a quality chest x-Ray done for some other cause may diagnose a rare condition like CDH.
CONCLUSION
Congenital diaphragmatic hernia usually presents with respiratory distress in neonatal period and differential diagnosis should be considered in neonates with respiratory distress. But this condition can be missed in some neonate where respiratory distress is not so severe or proper neonatal care facility is not available. We conclude that CDH though, rare condition in postneonatal period could be encountered in outpatient practice with children presenting with recurrent cough and failure to thrive.
ACKNOWLEDGEMENTS
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=752http://ijcrr.com/article_html.php?did=7521. Anderson KD. Congenital diaphragmatic hernia. In: WelchK.J., Randolph JG, Ravitch MM, et al (eds.). Paediatric Surgery. Chicago, Year Book Medical 1986; 589-601.
2. Bag?aj M. Late-presenting congenital diaphragmatic hernia in children: a clinical spectrum. Pediatr Surg Int. 2004 Sep;20(9):658-69.
3. Butler M, Stolar C, Altman P (1993) Contemporary management of congenital diaphragmatic hernia. World J Surg 17:350–355.
4. Craigie RJ, Mullassery D, Kenny SE. Laparoscopic repair of late presenting congenital diaphragmatic hernia. Hernia. 2007 Feb;11(1):79-82.
5. Kitano Y, Lally KP, Lally PA: Congenital Diaphragmatic Hernia study group: Late-presenting congenital diaphragmatic hernia. J Pediatr Surg 2005, 40(12):1839–1843.
6. Lee HM, Addavide KE, Prince NJ: Late presentation of a diaphragmatic hernia. Arch Dis Child 2011, 96(9):837.
7. Ng CP, Lo CB, Chung CH. Congenital diaphragmatic hernia masquerading as pneumonia. Emerg Med Australas. 2004 Apr;16(2):167-9.
8. Vandy FC, Landrum JE, Gerig NR, Prahlow JA. Death due to late-presenting congenital diaphragmatic hernia in a 2-year-old child. Am J Forensic Med Pathol. 2008 Mar;29(1):75-9.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareA RARE CASE OF GLOMANGIOPERICYTOMA OF THE NASAL CAVITY
English6165S. VijayasundaramEnglish P. KarthikeyanEnglish V. Nirmal CoumareEnglish Satvinder Singh BakshiEnglish Davis Thomas PulimoottilEnglishAim: Here we present a rare case of Glomangiopericytoma of the nasal cavity and review the recent literature. This case is presented because of its rarity. Case report: A 36-year-old woman presented to the Outpatient Department of ENT and Head and Neck Surgery in a tertiary care centre with complaints of progressive unilateral nasal obstruction and anosmia over a 6 month period. Anterior rhinoscopicex amination revealed a pinkish globular mass occupying the left nasal cavity. Computed tomography (CT) scan revealed an ill defined homogenous soft tissue density lesion involving the left nasal cavity, infiltrating the nasal septum posteriorly and extending upto the choana with a deviated nasal septum to the right side. The tumor was resected completely by endoscopic approach. Histopathologic examination with immunohistochemistry of the resected mass confirmed the diagnosis of glomangiopericytoma. Discussion: Glomangiopericytoma is a rare sinonasal neoplasm characterized by a perivascular myoid phenotype and is considered
as distinct from conventional soft tissue hemangiopericytoma. It accounts for less than 0.5% of all sinonasal tumors. It
is classified as a borderline low malignancy tumor.Conclusion: This tumour is associated with a very good prognosis following surgery and complete surgical resection with negative margins preferably via a transnasal endoscopic approach is the treatment of choice.
EnglishNasal mass, Glomangiopericytoma, Endonasal endoscopic resectionINTRODUCTION
Glomangiopericytoma belongs to a spectrum of lesions which include myofibromatosis, myofibroma, infantile haemangiopericytoma and myopericytoma.1 According to the World Health Organization 2005 Classification of Head and Neck tumors, Glomangiopericytoma is a recently proposed term describing the sinonasal tumors demonstrating a perivascular myoid differentiation.2 Glomangiopericytoma was initially reported as hemangiopericytoma,3 but this definition has been questioned.4 Otherwise known as sinonasal type hemangiopericytoma, glomangiopericytoma is a rare tumor of borderline low malignant potential, differing from conventional soft tissue hemangiopericytoma in terms of location and clinical and histopathological features.2 Glomangiopericytoma characteristically has a component of cells with glomus-type features including cuboidal cells, distinct IJCRR Section: Healthcare cell borders, clear to eosinophilic cytoplasm and central round nuclei. The etiology may involve past trauma, hypertension, pregnancy and use of corticosteroids.5
CASE REPORT:
A 36 year old female presented to the outpatient Department of ENT and Head and Neck Surgery of a tertiary care centre with 6-month history of progressive left nasal airway obstruction and ipsilateral anosmia. The patient gave a history of one episode of left sided epistaxis . The patient had a history of previous nasal surgery 10 years prior, but no records were available. Anterior rhinoscopy revealed a pinkish globular mass occupying the left nasal cavity, sensitive to touch with minimal bleeding on probing and appeared to be sessile, arising from the nasal septum. The mass appeared to have pushed the septum to the opposite side. There was no enlargement of cervical lymph nodes. Diagnostic nasal endoscopy revealed a pink globular mass occupying the left nasal cavity and extending posteriorly up to the choana. The mass appeared to be attached to the septum, pushing it to the opposite side. Computed tomography (CT) scan showed an ill defined homogenous soft tissue density lesion involving the left nasal cavity, infiltrating the nasal septum posteriorly and extending upto the choana with a deviated nasal septum to the right side, without involvement of the surrounding sinuses. Biopsy from the mass was not realized due to the risk of bleeding. An endoscopic endonasal resection of the mass was performed, during which the tumour was found to arise from the nasal septum, and following complete excision, a defect was found in the posterior bony septum. Hemostasis was attained with the use of bipolar cautery and compression with pledgets soaked in diluted adrenaline. Histopathological examination of the specimen revealed tissue fragments lined by respiratory epithelium and underlying subepithelium consisting of well delineated diffuse growth of tumor cells arranged in the form of interlacing short fascicles and whorls. The tumor cells were round to elongated with vesicular to hyperchromatic nuclei and scanty eosinophilic cytoplasm. Dilated ectatic blood vessels with hyalinization were also seen. Necrosis and cytological atypia were absent. Immunohistochemically, the tumor was positive for vimentin and smooth muscle actin, and negative to CD34, S-100 protein and cytokeratin. These histopathologic findings were consistent with a diagnosis of glomangiopericytoma. Postoperatively, the patient was followed up regularly every two months. At 12 months follow up the patient does not have recurrence.
DISCUSSION
Glomangiopericytoma is defined as a sinonasal tumor showing perivascular myoid phenotype.6 Initially reported as hemangiopericytoma in 1942,3 this tumor arising from the sinonasal tract was later described by Compagno in 1976 as ‘‘hemangiopericytoma-like’’ because of the lower rates of metastasis and mortality.7 Most tumors formerly designated as soft tissue hemangiopericytomas are fibroblast-derived and represent the cellular variant of solitary fibrous tumors. As true hemangiopericytomas are related to glomus tumors, the designation ‘‘myopericytoma’’ or ‘‘glomangiopericytoma’’ is preferred by the WHO as the diagnostic category for these soft tissue tumors.6 Clinically and histologically, sinonasal hemangiopericytomas differ from hemangiopericytoma developing elsewhere in the body and thus is considered a distinct entity.4 The pathogenesis of glomangiopericytoma is unclear and previous trauma, hypertension and prolonged steroid use have been speculated to be possible causes.5 Our patient gave a history of previous nasal surgery ten years prior to presentation. Glomangiopericytoma represents less than 0.5% of all sinonasal neoplasms and develops in the nasal cavity and/or paranasal sinuses6 with a slight female preponderance and the peak age of incidence in the seventh decade.8 The most common mode of presentation is unilateral nasal obstruction with or without recurrent epistaxis. Less common complaints include difficulty in breathing, visual disturbance and headache.9 Gross examination of the tumor usually reveals a polypoid mass, beefy red to grayish pink in colour, soft or fleshy or friable in consistency and oedematous or hemorrhagic in appearance, and which bleeds on touch. Rarely there may be regional lymph node involvement.10 Computed tomography (CT) scan demonstrates a non calcified soft-tissue mass in a nasal fossa or a paranasal sinus and may be associated with sinusitis, displacement of adjacent structures and bone erosion. Contrast enhanced imaging demonstrates the vascular nature of the tumor.10 The diagnosis of a glomangiopericytoma is based on histopathology. Microscopically, glomangiopericytomas are submucosal polypoid tumors rimmed by a border of superficially spared stroma and respiratory epithelium with pushing and/or locally infiltrative borders. These tumors are composed of short, bland spindle cells forming fascicular, storiform, or whorled patterns. Tumor nuclei are uniform and evenly spaced and tumor cells have a moderate amount of eosinophilic cytoplasm with indistinct cell membranes imparting a syncytial appearance. A characteristic feature is perivascular hyalinization and tumor cells may be seen oriented perpendicular to these hyalinized vessel walls. Generally, there is a low mitotic rate and nuclear pleomorphism is absent or minimal.4 Malignant glomangiopericytoma is uncommon and usually presents with large size, bone invasion, profound nuclear pleomorphism, increased mitotic activity and necrosis.11 Immunohistochemically, glomangiopericytomas characteristically express vimentin, smooth muscle actin (SMA), muscle specific actin (MSA), and factor XIIIa and there is usually no expression of desmin, CD34, bcl-2, factor VIII or S100 protein. D2-40 stains vascular channels within all glomangiopericytomas to a variable degree which is in contrast to conventional soft tissue hemangiopericytoma/solitary fibrous tumors which reveal no intratumoral D2-40 vascular staining.12
Glomangiopericytomas are considered to be low malignant tumors with a low propensity to metastasize, a recurrence rate of 7% to 40%, and a 5-year survival of 88% or higher. Treatment for glomangiopericytomas is local excision with negative margins. Excellent overall survival was achieved with complete surgical excision and recurrence is often due to incomplete tumor resection. Metastatic disease and disease-related mortality is extremely rare (3%). Thus, a regular follow-up postoperatively is essential.1,12,13,14
CONCLUSION
Glomangiopericytoma is a rare sinonasal tumor demonstrating a perivascular myoid phenotype. It differs from usual soft-tissue hemangiopericytoma in location, biologic behavior and histopathologic characteristics and is categorized as a borderline low malignancy tumor. Complete surgical resection with negative margins is the treatment of choice. Regular post-operative follow- up is essential in view of the risk of local recurrence.
ACKNOWLEDGEMENT
The authors would like to thanks to Prof. Dhananjay S. Kotasthane, Professor and Head, Department of Pathology, MGMCRI, Pondicherry. The authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors and editors of all those articles and journals from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=753http://ijcrr.com/article_html.php?did=7531. Sun Q, Zhang C, Chen W, He Y. The molecular mechanisms on glomangiopericytoma invasion. Orphanet J Rare Dis. 2013 Sep 29;8:152.
2. Chihani M, Aljalil A, Touati M, Zoubeir Y, Labraimi A, Ammar H, Bouaity B. Glomangiopericytoma: an uncommon sinonasal perivascular tumor with particular characteristics. EJENTAS (2011);12:167-170.
3. Stout AP, Murray MR: Hemangiopericytoma: a vascular tumor featuring Zimmermann’s pericytes. Ann Surg 1942, 116:26–33.
4. Thompson LD, Miettinen M, Wenig BM. Sinonasal-type hemangiopericytoma: a clinicopathologic and immunophenotypic analysis of 104 cases showing perivascular myoid differentiation. Am J Surg Pathol. 2003;27:737–749.
5. Angouridakis N, Zaraboukas T, Vital J, Vital V: Sinonasal hemangiopericytoma of the middle turbinate: a case report and brief review of the literature. B-ENT 2007, 3:139–143.
6. Thompson LDR, Fanburg-Smith JC, Wenig BM. Borderline and low malignant potential tumours of soft tissues. In: Barnes L, Eveson JW, Reichart P, Sidransky D, eds. World Health Organization Classification of Tumours: Pathology and Genetics of Head and Neck Tumours. Lyon: IARC Press; 2005:43–45.
7. Compagno J, Hyams VJ. Hemangiopericytoma-like intranasal tumors: a clinicopathologic study of 23 cases. Am J Clin Pathol. 1976;66:672–683.
8. Lester D, Thompson M. Sinonasal tract glomangiopericytoma (hemangiopericytoma). Ear Nose Throat J. 2004;83:807. 9. Watanabe K, Saito A, Suzuki M, Yamanobe S, Suzuki T. True hemangiopericytoma of the nasal cavity. Arch Pathol Lab Med. 2001;125:686–690.
10. Gillman G, Pavlovich JB. Sinonasal hemangiopericytoma. Otolaryngol Head Neck Surg. 2004;131:1012–1013
11. Kowalski PJ, Paulino AF. Proliferation index as a prognostic marker in hemangiopericytoma of the head and neck. Head Neck. 2001;23:492–496.
12. Catalano PJ, Brandwein M, Shah DK, Urken ML, Lawson W, Biller HF. Sinonasal hemangiopericytomas: a clinicopathologic and immunohistochemical study of seven cases. Head Neck. 1996;18:42–53.
13. Billings KR, Fu YS, Calcaterra TC, Sercarz JA. Hemangiopericytoma of the head and neck. Am J Otolaryngol. 2000;21:238–243.
14. Castelnuovo P, Pagella F, Delu` G. Endoscopic resection of nasal haemangiopericytoma. Eur Arch Otorhinolaryngol. 2003;260: 244–247.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10HealthcareHISTOID HANSENS DISEASE - A RARE CASE REPORT
English6668Vimal Chander R.English Jayaganesh P.English Ganthimathy SekharEnglish Chitra S.EnglishIntroduction: Histoid Hansens disease is a very rare variant of lepromatous leprosy with nodules and plaques over normal appearing skin with characteristic histopathological and bacterial morphology and clinically simulating dermatofibromas, xanthomas, neurofibromas or reticulohistiocytosis. Case report: We report a case of histoid Hansens disease in a 34 year old male presenting with multiple papulovesicular nodules in the skin of lower back, arms, elbow and abdomen which on microscopy showed features of Histoid Hansens disease witha bacillary index of 6+. Conclusion: A high index of suspicion is necessary especially when patients present with unusual skin lesions and estimation of bacterial index is highly indicated as was proven in our case.
EnglishHansens disease, Histoid leprosy, Histoid, LepromatousINTRODUCTION
Histoid Hansens disease is a very rare variant of lepromatous leprosy characterized by cutaneous and/or subcutaneous nodules and plaques present over normal appearing skin, with characteristic histopathological and bacterial morphology. The term ‘histoid leprosy’ was originally coined by Wade as a histological concept of acid fast bacilli-rich leproma composed of numerous spindle shaped cells with the absence of globus formation (which is so conspicuous in classical lepromatous leprosy). It exhibits fibromatoid features in the chronic form. Since then, there have been many reports, with variable findings. We report a case of histoid leprosy in a 34 year old male, presenting with multiple papulovesicular nodules in the skin in view of the rarity of the condition.
CASE REPORT
A 34 year old male, complained of multiple nodules all over the body since one year. The nodules were seen on his lower back, arms, elbows, and abdomen. On clinical IJCRR Section: Healthcare examination, there were multiple papulovesicular nodules, nontender, firm to soft in consistency, measuring 0.5 cm to 1.5 cm in diameter. Papules were also present over the extensor surface of the arm, abdomen and lower back. There was no impairment of touch, pain or thermal sensation. There was no nerve thickening or any lymph node enlargement. A clinical diagnosis of molluscum contagiosum was made. Punch biopsy of a nodule over the elbow was taken and sent for histopathological examination. The specimen received was a linear piece of skin with underlying soft tissue measuring 1.5x0.5x0.5cm. It was bisected and both the pieces were embedded. Microscopic examination showed skin with atrophic epidermis with a subepidermal Grenz zone. [Figure 1] The dermis showed diffuse infiltrates of foamy histiocytes and lymphocytes in the superficial dermis as well as mixture of spindle cells and foamy histiocytes surrounding the dermal appendages and nerves. [Figures 2, 3 and 4] The Fite-Faraco stain showed plenty of uniformly stained acid fast bacilli arranged singly and in globi with a bacterial index of 6+. [Figure 5]
An impression of Histoid leprosy was then given. The patient was put on multibacillary multidrug therapy and is on regular follow-up. DISCUSSION Histoid leprosy is an uncommon variant of lepromatous leprosy and its incidence among leprosy patients in India is estimated to be 2.79 to 3.60%. There is a male preponderance with average age at diagnosis between 21 and 40 years. The incidence of histoid leprosy was found to be 8.7% among lepromatous leprosy cases. Clinically, histoid leprosy is characterized by cutaneous and/or subcutaneous nodules or papules, which are usually painless, discrete, firm, smooth, globular and skin colored to yellowish brown, with normal appearing skin surrounding it. The lesions are usually found in the posterior and lateral aspects of the arms, thighs, buttocks, lower part of the back, dorsum of the hands, and over the bony prominences, especially over elbows and knees. Ears may be unaffected. Histoid lesions have also been reported to be present along the course of the peripheral nerve trunks and cutaneous nerves. The histoid leproma has also been reported to occur during the early stages of lepromatous leprosy or borderline lepromatous leprosy. In such cases, the lesion is transient and disappear as the lepromatous leprosy progresses Histoid leprosy clinically simulates dermatofibromas, xanthomas, reticulohistiocytosis, neurofibroma or cutaneous metastasis. They can be differentiated from histoid leprosy on the basis of their characteristic histopathology, the absence of the acid fast lepra bacilli on slit skin smear and absence of nerve thickening. There are three histological variants of histoid leprosy, namely the pure fusocellular, fusocellular with epithelioid component and fusocellular with vacuolated cells. The last pattern is most commonly observed. Slit skin smear from the lesions in histoid leprosy show abundant acid fast bacilli in singles, clusters, or tightly packed in macrophages (globi). These bacilli tend to be longer with tapering ends when compared to the ordinary lepra bacilli. The bacillary index may be 5+ to 6+ and the morphological index may also be very high. The high bacillary index in histoid leprosy is suggested to be due to focal loss of immunity. Classical histopathological findings include epidermal atrophy as a result of dermal expansion of the underlying leproma and a grenz zone located immediately below the epidermis. The macrophage reaction is unusual in that the cells frequently become spindle shaped or fusiform and oriented in a storiform or a whorled pattern, similar to those of a fibrohistiocytoma or a dermatofibroma. These histiocytes usually resemble fibroblasts and it has been suggested that fibroblast-like macrophages may have arisen from the tissue histiocytes rather than blood monocytes. Within these histiocytes, an abundance of acid-fast bacilli can be seen. The Histoid leprosy patients are usually treated with the World Health Organisation multibacillary multidrug therapy for one year. Among 17 cases of leprosy reported in our institution over the past 5 years, there were 5 cases of borderline tuberculoid, 1 mid borderline, 3 borderline lepromatous, 3 lepromatous, 4 indeterminate leprosy and this was the first case of histoid leprosy diagnosed in our institution.
CONCLUSION
Histoid leprosy is a distinctive type of lepromatous leprosy, clinically and histopathologically simulating a dermatofibroma. Due to endemicity of leprosy in our country, there should be a high index of suspicion of this disease for all unusual skin lesions and estimation of bacterial index is highly indicated as was proven in our case. Though many studies indicate that leprosy is not prevalent as before, time and again it has been proven that we require a high index of suspicion especially when patients present with unusual skin lesions. Hence it is essential to continue the surveillance for new and relapsed cases, rather than waiting for voluntary reporting to treat and eliminate leprosy.
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=754http://ijcrr.com/article_html.php?did=7541. Murthy SV, Rao SM, Thejaswini, and Mannan K. De-novo Histoid Leprosy. J Lab Physicians 2011;3:110–2.
2. Kaur I, Dogra S, De D, Saikia UN. Histoid leprosy: a retrospective study of 40 cases from India. Br J Dermatol 2009;160:305-10.
3. Nair SP, Kumar GN. A clinical and histopathological study of histoid leprosy. Int J Dermatol 2013;52:580-6.
4. Nair SP, Moorthy KP, Suprakasan S, Jayapalan S, Mini G. Histoid leprosy - unusual presentation. Int J Dermatol 2006;45:433-4.
5. Kamath H D, Sukumar D, Shetty NJ, NandaKishore B. Giant lesions in histoid leprosy - an unusual presentation. Indian J Lepr 2004;76:355-8.
6. Bakry OA, Attia AM. Histoid leprosy: case report. Acta Dermatovenerol Croat 2012;20:256-9.
7. Annigeri SR, Metgud SC, Patil JR. Lepromatous leprosy of histoid type. Ind J Med Microbiol 2007;25:70-1.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241619EnglishN2014October10TechnologyFREE AND FORCED VIBRATION ANALYSIS OF EXTRADOSED BRIDGE
English6978M. V. SardesaiEnglish A. K. DesaiEnglishCable supported structures have distinctive dynamic behaviour. Extradosed bridge, which is intermediate to Girder Bridge and cable stayed bridge, owing to its shallow cables, the structure behaviour of Extradosed Bridge differs from that of cable stayed bridge. The shallower cables add to the prestress in the deck. While there are many articles available on the design of specific extra-dosed bridges, very little has been published on their dynamic behaviour from a general perspective. The paper highlights the free vibration and forced vibration behaviour of the extra-dosed Bridge.
EnglishEquivalent modulus, Extradosed bridge, Vibration of cables, Elastic foundation, Static behaviourINTRODUCTION
The recent research has shown that a Extradosed bridge, which is intermediate to Girder Bridge and a cable stayed bridge, adds substantial prestress to the deck because of the shallow pylon, are found to be economical for spans upto 250m. Dynamic response prediction has been the matter of research for many authors, in particular as the structural design of many structures is governed by the earthquake load cases or combinations thereof. The intrados is defined as the interior curve of an arch, or in the case of cantilever-constructed girder bridge, the soffit of the girder. Similarly, the extrados is defined as the uppermost surface of the arch. The term ‘extradosed’ was coined by Jacques Mathivat (1988) to appropriately describe an innovative cabling concept he developed for the Arrêt-Darré Viaduct , in which external tendons were placed above the deck instead of within the cross-section as would be the case in a girder bridge. To differentiate these shallow external tendons, which define the uppermost surface of the bridge, from the stay cables found in a cable-stayed bridge, Mathivat called them ‘extradosed’ prestressing. IJCRR Section: Technology Some features of extradosed bridge as given below;
• External appearance resembles cable-stayed bridge – but structural characteristics are comparable to those of conventional girder bridge • The Girder Depth are lesser than that of conventional girder bridges
• The stay cables (prestressing tendons outside the girder) need no tension adjustment necessary for cable-stayed bridges, and can be treated as usual tendons as in girder bridges
• The height of pylon is half as that of cable-stayed bridge and hence easier to construct
• With small stress fluctuation under live load the anchorage method for stay cables can be same as that of tendons inside girder and thereby achieve economy
The reduced cable inclination in an extradosed bridge leads to an increase in the axial load in the deck and a decrease in vertical component of force at the cable anchorages. Thus, the function of the extradosed cables is also to prestress the deck, not only to provide vertical support as in a cable-stayed bridge. Extradosed bridges are characterised by a low live load stress range in the stay cables.
With the rapid increase in span length, combined trend and also trend of using high strength materials have resulted in slender structures and a concern is being raised over dynamic behavior of such structures, in case of cable supported structures it is more pronounced as this further includes vibrations of cable elements also. An accurate analysis of natural frequencies is fundamental to the solution of its dynamic responses due to seismic and wind and traffic loads.
Highlights on Static Behaviour
The basic difference between cable stayed bridge and Extradosed Bridge is its tower height. For Cable stayed bridge the span to tower height ratio is generally kept at 5, whereas for Extradosed Bridge it is 10, which means Extradosed bridges have half the tower height than cable stayed bridge. The stiffer, lower towers enable the use of the full range of effective depth of cross-section. Since the short towers act as cantilevers, effectively prestressed by the dead load of the girder acting through the cables, they require relatively little reinforcement to resist bending due to live load. Neither a flexurally stiff girder nor backstays are required in order to provide adequate system stiffness to control deformations due to live load. With short towers, larger stay cables are required, but the towers are more economical than the tall towers normally found in cable-stayed bridges. The methods of providing stiffness in cable supported structures are shown in figure 2. SETRA (2001) published recommended allowable stress limits that cover the full range of external cables. In that document, external prestressing tendons are defined as being subjected to a stress range of up to 15 MPa under live load while stays for cable-stayed bridges are subjected to a stress range of around 100 MPa and above. Extradosed cables are characterised as being subjected to a live load stress range between 30 MPa and 100 MPa and are not sensitive to wind vibrations. These specifications resulted from a need for design recommendations for bridges that do not fall into distinct categories, and they propose design limits and approximations based on rational principles. This explains use of 0.6fu allowable stress in the Extradosed cables, which leads to material economy.
Governing Equations
A) Vibration of structure
When finite element is used, each stay cable is modeled as either a single truss element with an equivalent modulus or number of cable elements with the original modulus. The deck and tower are modeled as BernoulliEuler beam elements with axial forces due to prestress imparted by horizontal component of cable force due to its shallow cables. Consider a typical Extradosed bridge as shown in figure 1; let us take a small section as shown in the figure 3 below. The boundary conditions for this element can be considered as that of beam on elastic the provided by cable. Further this beam will be subjected to prestressing force due to horizontal component of cable forces, as shown in figure 3 foundation to relate effect of elastic support below;
Now, consider an element i-j of length L of a beam on an elastic foundation as shown in Figure.3 having a uniform width b and a linearly varying thickness h(x). It will be a simple matter to consider an element having a linearly varying width if the need arises. Neglecting axial deformations this beam on an elastic foundation element has two degrees of freedom per node a lateral translation and a rotation about an axis normal to the plane of the paper and thus possesses a total of four degrees of freedom. The (4x4) stiffness matrix k of the element is obtained by adding the (4x4) stiffness matrices kB, kF and kQ pertaining to the usual beam bending stiffness and foundation stiffness and stiffness due to prestressing force (Q) respectively Since, there are four end displacements or degrees of freedom a cubic variation in displacement is assumed in the form v Aa = Eq. (1) Where, A= (1 x x2 x3 ) and aT= (a1 a2 a3 a4 ) (Displacement variation within element) The four degrees of freedom corresponding to the displacements v1 , v3 and the rotations v2 v4 at the longitudinal nodes are given by
q=Ca (Nodal displacements) Eq. (2) Where qT= (v0 v1 v2 v3 ) and C is the connectivity matrix for an element ij between x=0 and x=L as given in Figure 2 From equations (Eq.1) and (Eq.2) V=AC-1q Eq. (3) If E is the Young|s modulus and I=bh(x)3 /12 is the second moment of area of the beam Cross-section about an axis normal to the plane of the paper the bending moment M in the element is given by
For Extradosed bridge, since the cable are shallower and the effect of prestressing force is more the effecting of prestress shall be taken in to account as shown in the equation above.
B) Vibration of Cables
i) With equivalent modulus In global analysis of cable stayed / Extradosed bridges, one common practice is to model each cable as a single truss element with an equivalent modulus to allow for sag. The element stiffness matrix in local coordinates for such a cable element can be written as,
Where, cl is chord length, Ac is the horizontal projection length, Ac is the cross-sectional area, Ec is the effective material modulus of elasticity, T is the weight per unit length and T is the updated cable tension of the cable. A certain cable profile has been assumed to account for the effect of cable sag. However, once the equivalent modulus has been obtained, the profile will not have a role to play in the final analysis, and hence the method cannot model transverse vibrations of the cable.
ii) With original modulus
Another approach for accounting for the transverse vibrations of cables is to model each cable by number of cables elements with the original modulus. Following the sign conventions adopted by Broughton and Ndumbara (1994), the element incremental stiffness matrix in local coordinates can be written as
C) Vibration of stay cables
To demonstrate the abilities of various methods in predicting local cable vibrations, each stay cable was analyzed as an inclined stay cable fixed/pinned at both ends to evaluate the natural frequencies of local vibrations. It is noted however that the real situation is slightly different, as the end anchorages themselves are movable. The first symmetric and anti-symmetric in-plane transverse vibration frequencies ω in radians per second can be computed, respectively, as
Free and Forced Vibration analysis
Research methodology
To study dynamic behavior of Extradosed Bridge, 3 numbers of models with variable parameters are prepared. Basic span configuration as applicable for Extradosed span is selected to be 120, 200 and 260m main span, the side span is about 0.45 of main span. The pylon height is varied from 8 to 12 to account for the effect of varying cable inclinations. The cable inclination varies from 17 to 30 degrees. The requirement of cable area and prestressing is as per preliminary design. Box beam superstructure is adopted with solid rectangular pylon designed by working stress method. For details of model refer table-1
The dynamic response of structure for free vibrations as well as forced vibration has been studied. Software SAP2000 V14 has been verified and used in the study. Deck is modelled as Euler Bernoulli Beam and the stay cables have been modelled as single truss elements in static/ dynamic analysis. Free Vibrations of Extradosed Bridge With the rapid increase in span length, combined trend and also trend of using high strength materials have resulted in slender structures and a concern is being raised over dynamic behaviour of such structures, in case of cable supported structures it is more pronounced as this further includes vibrations of cable elements also. An accurate analysis of natural frequencies is fundamental to the solution of its dynamic responses due to seismic and wind and traffic loads. The modal shapes and frequencies for above listed models are presented below
Free Vibrations of Extradosed Bridge
With the rapid increase in span length, combined trend and also trend of using high strength materials have resulted in slender structures and a concern is being raised over dynamic behaviour of such structures, in case of cable supported structures it is more pronounced as this further includes vibrations of cable elements also. An accurate analysis of natural frequencies is fundamental to the solution of its dynamic responses due to seismic and wind and traffic loads. The modal shapes and frequencies for above listed models are presented below;
By looking at the mode shapes of the stay cables, it is possible to relate these natural frequencies of the “”fixed/free end’’ cables to those obtained by analyzing the whole bridge using the finite element method. The results are shown in fig 12 and 13. Apart from those natural frequencies that are obviously outside the range under consideration, all local cable vibrations can be reflected by finite element analysis with multiple-element modelling of stay cables. In addition to those pure local vibrations of stay cables, some new frequencies are also discovered indicating strongly the existence of coupled vibration modes. Obviously, these coupled vibration modes cannot be predicted by Equations. For investigating the possibility of coupled mode of vibration the time periods for various modes of vibration are superimposed for structure and cables.
Forced Vibrations of Extradosed Bridge
Forced vibration is studied for selected earthquakes; the earthquakes selected were having different characteristics as given in table 1
The time history analysis for these was performed on selected models and force effects at various points were recorded
Non-Dimensionalizing of parameters
Forced vibration analysis for three earthquake time histories having different characteristics are undertaken. To compare the results all parameter have been non dimensionalised using equivalent factors as mentioned below;
Where, V and M are non dimensioning factors for shear force, bending moment. Where, r = Mass Density, g= Gravitational acceleration, A= Cross section area of component and L= Half span length of the component.
Span and pylon height are non-dimensionlalized by using parametric length. The results obtained from the time history analysis in terms of bending moment and shear forced in the structure are non-dimensionalised and superimposed and presented in Fig 14 to 18
Forced Vibrations of Cables
Cable excitations can be caused by rain, wind, stochastical vibration due to plying vehicles or parametric vibrations due to vibration of the deck. Due to the infinite number of damping values and angles of inclination that a cable may take, several values can be selected to represent typical cables. It is evident that zones of large-amplitude cable vibrations do tend to change with varying angles of inclination, when the geometric nonlinearity of the cable lessens, as the angle of inclination moves towards 90. Also, the onset of these regions of large-ampli-tude cable vibrations required higher amplitudes of cable end excitation as the damping of the cable increases. It was considered important that the stochastic excitation or parametric excitations, which may be occur due to various reason, but the main reason being the vehicles plying on the bridge, which was to be imposed on the cables, be representative of a prototype stochastic timehistory that might be imposed on a stay by a full-scale cable structure such as an extradosed bridge. Even though an approximation, cable structures, such as telecommunications masts and cable-stayed bridges, are subject to random wind forces, which have time-histories that are very similar to random normal distribution, for the lowfrequency bandwidth under examination. An extradosed bridge or other similar structure will act as a signal filter, by filtering wind signals (or white noise signals) through its own structural characteristics. The resulting dynamic response input will be the actual response of the structure to the wind load. This filtered signal or structural response can then be used as a stochastic time-history (stochastic support excitation) for the examination of a cable’s response to that time-history. As the wind will have varying characteristics, such as wind speed and wind direction, the force acting on the structure will also have varying characteristics. These will excite the structure at different frequencies with varying amplitudes of force.
Discussions
Free Vibrations: - An accurate analysis of natural frequencies and mode shapes of cable supported structures such as Extradosed Bridge is fundamental to the solution of its dynamic responses due to seismic, wind and traffic loads. Now days, from economic considerations, the stay cables are often closely spaced, with the cable lengths and tensions gradually varying from position to position. The natural frequencies of their self-vibrations are therefore rather closely spaced. This may cause boundaryinduced vibrations of the stay cables. This complicates the overall dynamic behavior of cable stayed structures. In addition to pure local vibrations of stay cables, some new frequencies are also present indicating strongly the existence of coupled vibration modes, these coupled vibration modes cannot be predicted by equations. The frequencies of cables with actual boundary conditions are expected to lie in-between those of with fixed and pinned ends. For investigating the possibility of coupled mode of vibration the time periods for various modes of vibration are superimposed for structure and cables. The intersection zone (intersection of stay cable vibrations and bridge vibrations) suggests the possibility of coupled vibrations. Forced Vibrations: - Forced vibration studies of deck and pylon of three types of bridges reaffirms following facts for extradosed bridge, Magnitude of bending moment / shear force is directly proportional to the magnitude of forcing function / PGA. With increase in the distance between cables supports the shear force in deck also increases. Pylon stiffness does not have any effect on the deck moments/shear. With increase in the pylon height/slenderness the shear force changes its sign in the upper part of pylon. It is observed that only for cable stayed bridge with harp shape cable arrangement the shear force reduces at the junction of deck It is observed that there is some relationship between Peak Ground Accelerations and the response of structure, relationship between these needs to be established by further study.
Acknowledgements
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
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