Abstract:

Every minute a woman dies during labor or delivery. Approximately 529,000 women die from pregnancy related causes annually and almost all (99%) of these maternal deaths occur in developing nations. The highest maternal mortality rates are in Africa, with a lifetime risk of 1 in 16; the lowest rates are in western nations (1:2800), with a global ratio of 400 maternal deaths per 100,000 live births. Causes of maternal mortality include postpartum hemorrhage, eclampsia, obstructed labor, sepsis, unsafe abortion, ectopic pregnancy, embolism etc. During the past years, increased recognition of these problems has led to the ‘Safe Motherhood Initiative’ by the World Health Organization in 1987, which was integrated into the goal of “Health for All in the year 2000.’’ 45% of postpartum deaths occur within the first 24 hours and 66% occur during the first week. Of the estimated 211 million pregnancies, 46 million result in induced abortions. 60% of these abortions are unsafe and cause 68,000 deaths annually. With appropriate strategy and intensive implementation programs, some countries have made remarkable progress, not including many developing countries. Many developing nations face extreme challenges in the implementation of these strategies including lack of reliable data, shortage in human and financial resources, limited political commitment, pregnant women have minimal access to skilled labor and emergency care. Basic emergency obstetric interventions such as antibiotics. Oxytocins, anticonvulsants, manual removal of placenta and instrumental vaginal delivery are vital to improve the chance of survival.

Keywords: Maternal Health, Maternal Death, Maternal Morbidity, Ante natal Care, Emergency Obstetrics Care, Push and Pull factors, Brain drain

References:

[1].     Maternity Worldwide (2015) why do Women Die in Childbirth in low-income Countries? Available at: http://www.maternityworldwide.org/the-issues/women-die-childbirth (Accessed 19 May 2018).

[2].     Population Reference Bureau (2001) Delivery Care is key for Maternal Survival: A Story of Two States in Nigeria. Available at:

http://www.prb.org/Publications/Articles/2001/DeliveryCareIsKeyforMaternalSurvivalAStoryofTwoStatesinNigeria.aspx (Accessed 19 May 2018).

[3].     United Nations Population Fund (2016) Maternal Health. Available at: http://www.unfpa.org/maternal-health (Accessed 19 May 2018).

[4].     World Health Organization (2007) Maternal Mortality in 2005. Available at: http://www.who.int/whosis/mme_2005.pdf (Accessed 21 May 2018).

[5].     World Health Organization (2009) Monitoring Emergency Obstetric Care. Available at:

https://www.unfpa.org/sites/default/files/pub-pdf/obstetric_monitoring.pdf (Accessed 19 May 2018).

[6].     World Health Organization (2015) Trends in Maternal Mortality; 1990-2015. Available at:

https://www.unfpa.org/sites/default/files/pub-pdf/9789241565141_eng.pdf (Accessed 21 May 2018).

[7].     World Health Organization (2016) Maternal and Perinatal Health. Available at:

http://who.int/maternal_child_adolescent/topics/maternal/maternal_perinatal/en (Accessed 19 May 2018).

[8].     World Health Organization (2018) Maternal Mortality. Available at: http://www.who.int/news-room/fact-sheets/detail/maternal-mortality (Accessed 21 May 2018).

Abstract:

The term 'angioedema' describes a circumscribed edema of the skin, gastrointestinal (GI) tract or respiratory tract. Classic hereditary angioedema (HAE) can be associated with quantitative (type I) or qualitative (type II) deficiency of C1 esterase inhibitor (C1-INH), which is caused by mutations in the C1-INH gene. In classic HAE, abdominal attacks are mostly characterized by pain, vomiting and diarrhea, but rarely occur in the absence of other clinical features. Here we describe a case of angioedema of the bowel, a rare presentation, occurring in an elderly with C1-INH deficiency.

A 50-year-old man presented with an 8-month history of recurrent episodic severe abdominal pain, associated with loose bowel. Each episode lasted for a couple of days and would resolve spontaneously. The patient's medical history included hypertension, transurethral resection of the prostate for benign prostatic hyperplasia, No h/s/o any allergies. On extensive evaluation, which included several EGD’s and colonoscopies over the span of 8 months, with normal endoscopic findings. Computed tomography with contrast during episode of attack shows extensive concentric colonic and small bowel thickening with trace ascites. Most of the other workup was grossly within normal limits other than Levels of C4 (< 9 mg/dL; reference range 15 to 50 mg/dL), CH50 (< 13 U/mL; reference range 29 to 45 U/ml) and C1 inhibitor (< 4 mg/dL; reference range 14 to 30 mg/dL) were all low, supporting a diagnosis of acquired angioedema (AAE) with isolated bowel involvement. Said patient's symptoms improved with antihistamine and supportive treatment, with danazol treatment planned on an outpatient basis for prophylaxis after discharge. Patient didn’t report any attack post discharge.

References:

[1].     Bork K, Staubach P, Eckardt AJ, Hardt J. Symptoms, Course, and Complications of Abdominal Attacks in Hereditary Angioedema due to C1 Inhibitor Deficiency. Am J Gastroenterol. 2006; 101:619–27.

[2].     Bowen T. et al. Hereditary angiodema: a current state-of-the-art review, VII: Canadian Hungarian 2007 International Consensus Algorithm for the Diagnosis, Therapy, and Management of Hereditary Angioedema. Ann Allergy Asthma Immunol. 2008;100(Suppl): S30–S40.

[3].     Cicardi M, Zingale L. Clinical manifestations of HAE. In: Hereditary and acquired angioedema: Problems and progress. Proceedings of the third C1 esterase inhibitor deficiency workshop and beyond. J Allergy Clin Immunol. 2004; 114: S55–58.

[4].     Caldwell JR, Ruddy S, Schur PH, Austen KF. Acquired C1 inhibitor deficiency in lymphosarcoma. Clin Immunol Immunopathol. 1972; 1:39–52.

[5].     Donaldson VH, Evans RR. A biochemical abnormality in hereditary angioneurotic edema: absence of serum inhibitor of C1-esterase. Am J Med. 1963; 35:37–44

[6].     Landerman NS. Hereditary angioneurotic edema. I. Case reports and review of the literature. J Allergy. 1962; 33:316–29.

[7].     Osler W. Hereditary angioneurotic edema. Am J Med Sci. 1888; 95:362–367.

[8].     Quincke H. Concerning the acute localized oedema of the skin. Monatsh Prakt Derm. 1882; 1:129–131.

[9].     Rosen FS, Davis AE Jr. Deficiencies of C1 inhibitor. Best Pract Res Clin Gastroenterol. 2005; 19:251–261.

Abstract:

Background: Studies have shown that there were documented evidences of abnormal vital signs, without appropriate clinicians and nurses responses. We thus investigate the knowledge, and how nurses intend to respond to different combinations of vital signs values.

Methods: This study was carried out in Ladoke Akintola University of Technology Teaching Hospital Ogbomoso. Questionnaires were sent out to nurses to obtain relevant data regarding interpretation of vital sign values.

Results: Eighty questionnaires were analysed. The mean age of the respondents was 36.4 (±5.27) years. Nineteen (23.75%) respondents got correctly the normal range for all the vital signs and oxygen saturation. Seven (8.75%) respondents knew that pulse rate is the earliest vital sign to change in most deteriorating patients. Fifty-nine (73.75%) respondents considered oxygen saturation as reliable indicator of respiratory functions. Most respondents (78.73%) would not consider oxygen support until saturation fall below 90%. Seventy-five (93.75%) respondents could not identify correctly patients at risk of deterioration based on different combinations of set of vital sign values, SpO₂ and level of consciousness. Sixty-seven (83.75%) rated themselves to have good to excellent knowledge on vital signs and its interpretation, however, only 9 (11.25%) respondents have good comprehensive knowledge on interpretation of vital signs.

Conclusion: Majority of the respondents could not interpret vital sign values correctly. We suggest need for continuous nursing education to bridge this gap.

Keywords: Vital signs, interpretation, nurses, and responses.

References:

[1].     Chua WL, Liaw SY, Mackey S et al. Front-line nurses’ experiences with deteriorating ward patients: a qualitative study. Int Nurs Rev 2013; 60:501-9.

[2].     Cretikos MA, Bellomo R, Hillman K et al. Respiratory rate: the neglected vital sign. Med J Aust. 2008; 188:657-9.

[3].     Fagan K, Sable A, Mehler PS et al. Vital sign abnormalities, rapid response, and adverse outcomes in hospital patients. Am J Med Qual. 2012; 27:480-486.

[4].     Goldhill DR. The critically ill: following your MEWS. Quarterly Journal of Medicine. 2001; 94: 507-10.

[5].     Goldhill DR, McNarry AF. Physiological abnormalities in early warning scores are related to mortality in adult inpatients. Br J Anaesth. 2004;92: 882-884.

[6].     Hands C, Reid E, Meredith P et al. The prevalence of recording of the signs of critical conditions and emergency responses in hospital wards- the SOCCER study. Resuscitation. 2005; 65:149-157.

[7].     Hillman KM et al. Antecedents to hospital deaths. Internal Medicine Journal. 2009; 31:6,343-348.

[8].     Hodget TJ, Kenward G, Vlachonikolis IG et al. The identification of risk factors for cardiac arrest and formulation of activation criteria to alert a medical emergency team. Resuscitation. 2002; 54:125-31.

[9].     ISQua Wenqi Mok, Wenru Wang, Simon Cooper, Emily Neo Kim Ang and Sok Ying Liaw. Attitudes towards vital signs monitoring in the detection of clinical deterioration: scale development and survey of ward nurses. International journal for Quality in Health Care. 2015;27(3):207-213.

[10]. Lee A, Bishop G, Hillman KM, Daffurn K. The Medical Emergency Team. Anaesthesia and Intensive Care. 1995; 23:183-6.

[11]. Ludikhuize J, Smorenburg SM, de Rooij SE, de Jonge E. Identification of deteriorating patients on general wards; measurement of vital parameters and potential effectiveness of the Modified Early Warning Score 2012 [updated Aug; cited 27 4]. 2012/02/22: [424 e7–13].

[12]. McGloin H, Adams SK, Singer M. Unexpected deaths and referral to intensive care of patients on general wards: are some potentially avoidable? J R Coll Physicians Lond. 1999; 33:255-9.

[13]. Olusola O. Akanbi, David A. Onilede, Moses L. Adeoti1, Olawale A. Olakulehin, Najeem A. Idowu and Olusegun O. Olanipekun. Improving Clinicians’ and Nurses’ Response to Abnormal Vital Signs in Hospital: The Roles of Modified Early Warning Scoring System and Rapid Response System. British Journal of Medicine & Medical Research 2017; 21(6): 1-11,

[14]. Rose L, Clarke SP, Vital signs. AJN. 2010; 110:11.

[15]. Royal College of Physicians. National Early Warning Score (NEWS): Standardising the assessment of acute-illness severity in the NHS. Report of a working party. London: RCP, 2012

[16]. Sax FL, Charlson ME. Medical patients at high risk for catastrophic deterioration. Critical Care Medicine. 1994;22: 244-7.

[17]. Society of Critical Care Medicine. Recognition and Assessment of the Seriously Ill Patient. In Fundamental Critical Care Support. 4^th edition. Society of Critical Care Medicine. 2007. Pg 1-10.

[18]. Soong JTY, Soni N. Circulatory shock. Mrdicine 2013; 41:64-69.

[19]. Van LCH, Mitchell I. Missed opportunities. An observational study of vital signs measurement. Crit-care Resusc. 2008; 10:111-115.

Abstract:

Sclerosing mesenteritis is a rare, benign, and chronic fibrosing inflammatory disease with unknown etiology that affects the mesentery. On rare occasions, it may involve the mesocolon, peripancreatic region, omentum, retroperitoneum, or pelvis. Our patient 57-year-old male presented with chronic abdominal pain for about 6 months and intra-abdominal mass for about 2 months. The abdominal pain, mainly located around navel, was intermittent and mild. The mass, located in the right lower quadrant, was mobile, smooth, rigid and about the size of a fist. The laboratory profile of routine blood test, renal and hepatic function tests were normal. Abdominal CT scan demonstrated a solid soft-tissue mass with calcification in the right lower abdomen, which correlated with small bowel and mesentery. The patient was subjected to exploratory laparotomy because of radiologist apprehension of the mass being celiac teratoma, the intraoperative frozen section indicated that it was an inflammatory mass. The mass and adhered intestines were removed. The biopsy of pathological specimens with paraffin section showed fat necrosis, sclerosing fibrosis, clusters of inflammatory cells and lipid-laden macrophages in mesentery mass; and the inflammatory stopped abruptly at the edge of bowel wall So this case was diagnosed with sclerosing mesenteritis in the end. The patient recovered well after surgery without any digestive discomfort. No recurrence of the sclerosing mesenteritis was observed during follow-up.

References:

[1].     Azzam I, Croitoru S, Naschitz JE. Sclerosing mesenteritis: a diagnostic challenge. Isr Med Assoc J. 2004;6(9):567–568.

[2].     Emory TS, Monihan JM, Carr NJ, Sobin LH. Sclerosing mesenteritis, mesenteric panniculitis and mesenteric lipodystrophy: a single entity? Am J Surg Pathol. 1997;21(4):392–398. doi: 10.1097/00000478-199704000-00004.]

[3].     Goh J, Otridge B, Brady H, Breatnach E, Dervan P, MacMathuna P. Aggressive multiple myeloma presenting as mesenteric panniculitis. Am J Gastroenterol. 2001;96(1):238–241. doi: 10.1111/j.1572-0241.2001.03384.x.

[4].     Grieser C, Denecke T, Langrehr J, Hamm B, Hanninen EL. Sclerosing Mesenteritis as a Rare Cause of Upper Abdominal Pain and Digestive Disorders. Acta Radiol. 2008; 23:1–3.

[5].     Ginsburg PM, Ehrenpreis ED. A pilot study of thalidomide for patients with symptomatic mesenteric panniculitis. Aliment Pharmacol Ther. 2002;16(12):2115–2122. doi: 10.1046/j.1365-2036.2002.01383.x.

[6].     Hammoud D, Khoury N, Rouhana G, Abou Sleiman C, Haddad M. Intraabdominal panniculitis. Report of three cases and review of the literature. J Med Liban. 1999;47(5):321–325.

[7].     Horton KM, Lawler LP, Fishman EK. CT findings in sclerosing mesenteritis (panniculitis): spectrum of disease. Radiographics. 2003;23(6):1561–1567. doi: 10.1148/rg.1103035010.

[8].     Kishimoto K, Hokama A, Irei S, Aoyama H, Tomiyama R, Hirata T, Kinjo F, Fujita J, Sakiyama M. Chronic diarrhoea with thickening of the colonic wall. Gut. 2007;56(1):94–114. doi: 10.1136/gut.2006.093096.

[9].     Lim CS, Singh Ranger G, Tibrewal S, Jani B, Jeddy TA, Lafferty K. Sclerosing mesenteritis presenting with small bowel obstruction and subsequent retroperitoneal fibrosis. Eur J Gastroenterol Hepatol. 2006;18(12):1285–1287. doi: 10.1097/01.meg.0000243874.71702.21.

[10]. McMenamin DS, Bhuta SS. Mesenteric panniculitis versus pancreatitis: a computed tomography diagnostic dilemma. Australas Radiol. 2005;49(1):84–87. doi: 10.1111/j.1440-1673.2005.01406.x.

[11]. Pickhardt PJ, Bhalla S. Unusual nonneoplastic peritoneal and subperitoneal conditions: CT findings. Radiographics. 2005;25(3):719–730. doi: 10.1148/rg.253045145.

[12]. Vettoretto N, Diana DR, Poiatti R, Matteucci A, Chioda C, Giovanetti M. Occasional finding of mesenteric lipodystrophy during laparoscopy: A difficult diagnosis. World J Gastroenterol. 2007;13(40):5394–5396.

Abstract:

Background: Pain is an inevitable occurrence following surgery and its control is an important component of post-operative care. Many patients still suffer from poor post-operative pain control which is associated with a lot of secondary undesirable consequences.

Methods: We conducted a prospective observational study on 120 patients undergoing abdominal surgery over a 3-year period in a teaching hospital to determine adequacy and pattern of analgesic prescriptions. The patients’ case notes were retrieved from the record unit of the hospital following discharge and relevant data extracted.

Results: The mean age of the patients was 47.36 (±8.933). Twenty-four (20%) were older than 65 years. The most common abdominal surgical procedure performed was appendectomy. Non-steroidal anti-inflammatory drugs only, opiod only, opiod-NSAID combination and NSAID-NSAID combinations were prescribed for 42.5% ,30.83%, 14.16%) and 7.85% of cases respectively and no prescription in 3.3% of cases. Pentazocine was the most commonly prescribed opiod. Females tend to have more opiod prescriptions than males (OR= 3.4, p=0.0052). Other factors that favoured opiod prescription include; age <65 years (OR=4.8571, p= .0019), patient in high social class (OR= 3.6364, p=0.4182), and Yoruba ethnicity (OR=3.2406, p= 0.0149). Non-steroidal analgesics were the most commonly prescribed analgesic to patients that underwent major abdominal surgeries.

Conclusion: We thus recommend use of analgesic combinations and dose adjustment based on patients’ severity of pain in post-operative abdominal pain control.

Keywords: Pattern, Analgesic prescription, Abdominal surgery and Postoperative pain.

References:

[1].     Acute pain services revisited: Good from far, far from good? Reg Anesth Pain Med. 2002;117-121.

[2].     Agency for Health Care Policy and Research. Acute pain management: operative or medical procedures and trauma, part 1. Clin Pharm. 1992; 11:309-331.

[3].     Apfelbaum JL, Chen C, Mehta SS, Gan TJ. Postoperative pain experience: results from a national survey suggest postoperative pain continues to be under managed. Anesthy Analg. 2003; 97:534-540.

[4].     Becker DE. Pain management: Part 1: managing acute and postoperative dental pain. Anesth Prog 2010; 57:67-79.

[5].     Becker DE, Phero JC. Drug therapy in dental practice: nonopiod and opiod analgesic. Anesth Prog. 2005; 52:140-149.

[6].     Bruster S, Jarman B, Bosanquet N, Weston D, Erens R, Delbanco TL. National survey of hospital patients. Br Med J. 1994; 309: 1542-1546.

[7].     Buvanendran A, Kroin JS. Multimodal analgesia for controlling acute postoperative pain. Curr Opin Anaesthsiol. 2009; 22:588-593.

[8].     Cohen FL. Post surgical pain relief: patients’ status and nurses’ medication choices. Pain 1980; 9:265-274.

[9].     Hemmes SN, Gama de Abreu M, Pelosi P, Schultz MJ, PROVE Network Investigators for the Clinical Trial Network of the European Society of Anaesthesiology. High versus low positive end-expiratory pressure during general anaesthesia for open abdominal surgery (PROVHILO trial): a multicentre randomised controlled trial. Lancet. 2014; 384(9942):495–503.

[10]. Heyburn G. Pain management in elderly hip fracture patient. 2002. Retrieved from the World Wide Web 02 October 2003 http://www.gerimed.

[11]. International Narcotics Control Board. Report of the International Narcotics Control Boardon the availability of international controlled drugs: Ensuring adequate Access for Medical and Scientific Purpose. New York, NY: International Narcotics Control Board; 2011.

[12]. Jones JS, Johnson K, McNinch M. Age as a risk factor for inadequate emergency department analgesia. Am J Emerg Med. 1996; 14:157-160.

[13]. Kehler H, Wilkison RC, Fischer HB, Camu F. Prospect working group. PROSPECT: Evidence-based, procedure-specific postoperative pain management, Best Pract Res Clin Anaesthsiol. 2007; 21:149-159.

[14]. Kehler PF. Effect of postoperative pain treatment on outcome-current status and future strategies. Lagenbecks. Arch Surg. 2004; 389:244-249.

[15]. Kuhn S, Cooker K, Collins M, Mucklow JC. Perc eption of pain rrelief after surgery. Br Med J. 1990; 300:1687-1690.

[16]. Macintyre PE, Schug SA, acute pain management. 3^rd ed. Edinburgh: Saunders Elsevier; 2007.

[17]. Mark RM, Sachar EJ. Undertreament oof medical inpatients with narcotic analgesic. Ann Intern Med. 1973; 76:173-181.

[18]. McQuay H, Moore A, Justin D. Treating acute pain in hospital. Br Med J. 1997; 314:1531-1535.

[19]. Raftery KA, Smith-Coggins R, Chen AH. Gender- associated differences in emergency department pain management. Ann Emerg Med.1995; 26:414-421.

[20]. Rawal N. Analgesiafor day case surgery. Br J Anaesth. 2001; 87:73-87.

[21]. Rowbotham D. Postoperative pain. Prescriber’s J 1993; 33:237-243.

[22]. Seiler CM, Deckert A, Diener MK, Knaebel HP, Weigand MA, Victor N, et al. Midline versus transverse incision in major abdominal surgery: a randomized, double-blind equivalence trial (POVATI: ISRCTN60734227). Ann Surg. 2009; 249(6):913–20.

[23]. Sinan Sermet, Muserref Asuman Akgun, Sukran Atamer-Simsek. Analgesic prescription pattern in the management of dental pain among dentist in Istanbul. Marmara Pharmaceutical Journal. 2012; 16:41-47. DOI:10.12991/201216419.

[24]. Todd KH, Deaton C, D’Adamo AP, et al. Ethnicity and analgesic practice [comments]. Ann Emerg Med, 2000; 35(1):11-6.

[25]. Todd KH, Samaroo N, Hoffman JR. Ethnicity as a risk factor for inadequate emergency department analgesia [comments]. JAMA, 1993. 269(12):1537-9.

[26]. Torda T. Postoperative analgesia. Aust Prescriber. 1995; 18:88-91.

[27]. White PF and Kehler H. Improving postoperative pain management: what are the unresolved issues? Anesthesiology. 2010; 112:220-225.

[28]. White PF. Pain management after ambulatory surgery- where is the disconnect? Can J Anaesth. 2008; 55:201-207.

[29]. World Health Organization. The World Health Report 2003. Geneva: WHO. 2003; Available from: http://www.who.int/whr/2003/en/overview /en.pdf.

Abstract:

Hyperuricemia, previously thought as a consequence of renal impairement, has been recently identified as an independent risk factor for the development of Chronic Kidney disease. This study was done to find out the effect of treatment of hyperuricemia in CKD patients. This observational study was conducted at Jubilee memorial hospital and Dr sm csi medical college, Trivandrum. The study population included 200 patients with CKD with hyperuricemia from the department of General medicine and department of Nephrology. Detailed history, anthropometry and clinical examination were recorded from all patients and serum uric acid levels and GFR before and 3 months after treatment were compared. Other study parameters were analysed within the CKD group. Treatment response of hyperuricemia with febuxostat among various stages of CKD was observed. Comparing prevalence hyperuricemia among different stages of CKD after 3month treatment with febuxostat, there was significant association between different stages of CKD and uric acid (p value=0.000). The present observational study suggests that febuxostat may slow the progression of mild-to-moderate CKD. Prevalence of hyperuricemia is significantly higher in chronic kidney diseases patients, especially stages 3 and 4. Uric acid level is significantly higher in overweight CKD subjects.

Keywords: Hyperuricemia, CKD, GFR.

References:

[1].Johnson, R. J., Lanaspa, M. A., & Gaucher, E. A. (2011). Uric acid: a danger signal from the RNA world that may have a role in the epidemic of obesity, metabolic syndrome, and cardiorenal disease: evolutionary considerations. Seminars in Nephrology, 31(5), 394–399.

[2].Mazzali M, Kanellis J, Han L, et al. Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure independent mechanism. Am J Physiol Renal Physiol. 2002; 282(6): F991-F997. 


[3].Omori, H., Kawada, N., Inoue, K., Ueda, Y., Yamamoto, R., Matsui, I., …Rakugi H. (2012). Use of xanthine oxidase inhibitor febuxostat inhibits renal interstitial inflammation and fibrosis in unilateral ureteral obstructive nephropathy. Clin Exp Nephrol, 16,549–556. https://doi.org/10.1007/s10157-012-0609.

[4].Sezai, A., Soma, M., Nakata, K., Hata, M., Yoshitake, I., Wakui, S., … Shiono, M. (2013). Comparison of febuxostat and allopurinol for hyperuricemia in cardiac surgery patients (NU-FLASH Trial) Circ J,77,2043–2049. https://doi.org/10.1253/circj.CJ-13-0082.

[5].    Sircar, D., Chatterjee, S., Waikhom, R., Golay, V., Raychaudhury, A., Chatterjee, S., &Pandey, R. (2015). Efficacy of febuxostat for slowing the GFR decline in patients with CKD and asymptomatic hyperuricemia: a 6-month, double-blind, randomized, placebo-controlled trial. Am J Kidney Dis,66,945–950. https://doi.org/10.1053/j.ajkd.2015.05.017.

[6].Tanaka, K., Nakayama, M., Kanno, M., Kimura, H., Watanabe, K., Tani, Y., … Watanabe, T. (2015). Reno-protective effects of febuxostat in hyperuricemic patients with chronic kidney disease: a parallel-group, randomized, controlled trial. Clin Exp Nephrol,19,1044–1053. https://doi.org/10.1007/s10157-015-1095-1.

[7].Verzola, D., Ratto, E., Villaggio, B., Parodi, E. L., Pontremoli, R., Garibotto, G., & Viazzi, F. (2014). Uric acid promotes apoptosis in human proximal tubule cells by oxidative stress and activation of NAPDH oxidase NOX 4. PloS ONE,9(12). https://doi.org/10.1371/journal.pone.0115210.

Abstract:

Background: Large numbers of stimuli are contained within the prison environment which can impact both the behaviour and attitudes of inmates within it. This inmate-environment interaction has implication for the safety and overall well-being of inmates.

Objectives: This study aimed to compare the differences between homicide and non-homicide offenders in relation to effects of prison environmental factors. The relationship between these factors and socio-demographic factors was also explored and compared between both groups of offenders.

Methods: A case-control study design was employed with 102 homicide and an equal number of non-homicide offenders. Each participant was interviewed using a questionnaire for ascertaining socio-demographic characteristics as well as the Prison Environment Inventory for inmates concerns within the prison.

Results: A significant association was found in all prison environment subscales between offender groups except safety (p = 0.060) and privacy (p = 0.084) with homicide offenders having better total overall score in the prison environment. A younger age and higher educational attainment were associated with better prison experience.

Conclusion: The study found an overall better adjustment in homicide offenders compared to their non-homicide counterparts. However, prison administrators have a role in improving specific aspects of prisoner experience for both homicide and non-homicide offenders during incarceration.

Keywords: Prison, Environment, Homicide, Nigeria, Maximum security.

References:

[1].    Akerstrom, M. (1985). Crooks and squares (2^nd ed.). New Brunswick, NJ: Transaction Publishers.

[2].    Bradford, A.R. (2006). "An Examination of the Prison Environment: An Analysis of Inmate Concerns across Eight Environmental Dimensions." Electronic Theses and Dissertations. Paper 2216. http://dc.etsu.edu/etd/.

[3].    Bruce D, and Larweh E. (2017). Self-esteem, Needs satisfaction and Psychological well-being of Inmates at James Camp Prison in Ghana. International Journal of Humanities and Social Sciences and Education 4(9), 32-39.

[4].    Cai, J., and Zeng, D. (2004). Sample size/power calculation for case-cohort studies. Biometrics, 60, 1015-24.

[5].    Cobden, J., and Stewart, G. (1984). Breaking out: A perspective on long-term imprisonment and the process of release. Canadian Journal of Criminology, 26, 500-510.

[6].    Colsher, PL, Robert BW, Paul LL, Marilyn S. (1992). Health status of older male prisoners: A comprehensive survey. American Journal of Public Health 82(6):881–884.

[7].    Crank, B.R. (2010). Adapting to incarceration: Inmate perceptions of prison life and adjustment. Thesis Georgia State University. Available at: http://scholarworks.gsu.edu/cj_thesis/10 (Accessed on 12/11/2018).

[8].    Crouch, B.M. (1993). Is incarceration really worse? Analysis of offenders’ preferences for prison over probation. Justice Quarterly, 10(1), 67-88.

[9].    Dhami, M.K., Ayton, P., and Loewenstein, G. (2007). Adaptation to imprisonment: Indigenous or imported? Criminal Justice and Behaviour, 34(8), 1085-110.

[10].Edwards, W.T., and Potter, R.H. (2004). Psychological distress, prisoner characteristics, and system experience in a prison population. Journal of Correctional Health Care, 10(2), 129 – 149.

[11].     Finn, M.A. (2008). Disciplinary incidents in prison: effects of race, economic status, urban residence, prior imprisonment. Journal of Offender Rehabilitation22(1/2): 143-156.

[12].     Fogel, C., and Sandra, M. (1992). The mental health of incarcerated women. Western Journal of Nursing Research 14(1):30–47.

[13].     Hurley, W., and Michael D. (1991). Psychological distress and psychiatric morbidity in women prisoners. Australian and New Zealand Journal of Psychiatry 35:461–470.

[14].Lawrence, C., and Andrews, K. (2004). Prison subculture in Poland. Crime and Delinquency, 40, 273-283.

[15].Lindquist CH. (2000). Social Integration and Mental well-being. Sociological Forum. 15:3;431-440.

[16].McGuire, J. (2000). Reducing re-offending: Putting research into practice. Presentation to a meeting of the Forensic College of the Australian Psychological Society. Adelaide, August.

[17].Ruback, R. B., Carr, T. S., and Hopper, C. H. (1986). Perceived control in prison: Its relation to reported crowding, stress, and symptoms. Journal of Applied Social Psychology, 16, 375-386.

[18].Shover, N. (1985). Aging Criminals: Beverly Hills, CA: Sage Publications.

[19].Slotboom A, Kruttschnitt C, Bijleveld K, Menting B. (2011). Psychological well-being of incarcerated women in the Netherlands: Importation or deprivation? Punishment and Society 13(2) http://doi.org/10.1177/1462474510396313.

[20].Twaddle, Andrew C. (1976). Utilization of medical services by a captive population: An analysis of sick call in a state prison. Journal of Health and Social Behaviour 17:236-248.

[21].Uzoeshi K.C. (2003). Sources of stress among Prisoners in Nigeria: Implications for Counselling. Nigerian Journal of Emotional Psychology, 5; 78-82.

[22].Williams, A., May, D.C., and Wood, P.B. (2008). The lesser evils? A qualitative study of offenders’ preferences for prison compared to alternatives. Journal of Offender Rehabilitation, 46(3), 71-90.

[23].     Wooldredge, J. (1999). Inmate Experiences and Psychological well-being. Criminal Justice and Behaviour 26(2):235-250.

[24].Wright, K.N. (1989). Race and economic marginality in explaining prison adjustment. Journal of Research in Crime and Delinquency, 26, 67-89.

[25].Zamble, E. (1992). Behaviour and adaptation in long-term prisoners. Criminal Justice and Behaviour, 19, 409-425.

Abstract:

Diabetes is a significant risk factor for ACS and adds to the overall burden of cardiovascular disease. This study was done to compare clinical and demographic features and signs and symptoms of ACS, diagnosed by history, ECG, Cardiac enzymes markers among Type 2 diabetic patients and non-diabetic patients. This cross-sectional study was conducted at jubilee memorial hospital and Dr SM CSI medical college, trivandum. The study population included 93 patients with DM and 107 subjects without DM as controls from the department of General medicine. Detailed history, anthropometry and clinical examination were recorded from all patients and Profile of ACS was compared between the two groups. Out of 93 diabetic patients, 67.7% (n63) had STEMI while compared to nondiabetic (51.4%, n55) patients and 32.2% (n30) had NSTEMI/UA compared to non-diabetic (48.6%, n52) patients. There is statistically significant association between STEMI and diabetes mellitus. (P value is 0.019). In our study smoking increased the mortality in diabetic patients (p value .013). There was no significant association between dyslipidemia and diabetes mellitus (p value .077) even though higher proportion of patients with diabetes mellitus had dyslipidemia. It was concluded that incidence of STEMI is significantly more in diabetic patients compared to non-diabetic patient in our study. High prevalence of diabetes mellitus among ACS patients were observed and this study also shown that smoking increased the mortality in diabetic patients. Dyslipidemia in diabetic patient is more when compared to non-diabetic patients even though statistically not significant in this study group.

Keywords: STEMI, NSTEMI, ACS, DM, ECG.

References:

[1].     Abildstrom, S.Z., Rasmussen, S., Rosen, M., & Madsen, M. (2003). Trends in incidence and case fatality rates of acute myocardial infarction in Denmark and Sweden. Heart,89(5),507-11.

[2].     Adler, A. I., Stratton, I.M., Neil, H.A., Yudkin, J.S., Matthews, D.R., Cull, C. A .,…. Holman, R. R. (2000). Association of systolic blood pressure with macrovascular and microvascular complications of type 2 diabetes (UKPDS 36): prospective observational study. BMJ, 321 ,412-9

[3].     Dauerman, H.L., Lessard, D., Yarzebski, J., Furman, M.I., Gore, J. M., & Goldberg, R. J. (2000). Ten- year trends in the incidence, treatment, and outcome of Q-wave myocardial infarction. Am J Cardiol ,86(7),730-5.

[4].     Fergus, S. R. F. (2004). Presentation, management, and outcomes of diabetic patients compared to non-diabetic patients admitted for acute coronary syndromes. Heart, 1501-1502

[5].     Garcia, M.J., McNamara, P.M., Gordon, T., & Kannel, W. B. (1974). Morbidity and mortality in diabetics in the Framingham population. Sixteen-year follow-up study. Diabetes, 23,105-11.

[6].     Geiss, L.S., Herman, W.M., & Smith, P. J. (1995). Mortality in non-insulin- dependent diabetes. In: National Diabetes Data Group, editor. Diabetes in America, 2nd ed. Bethesda, MD: NIH & NIDDK. National Diabetes Information Clearing House, 233- 55.

[7].     Haffner, S. M., Lehto, S., Ronnemaa, T., Pyorala, K., & Laakso, M. (1998). Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med, 339, 229-34.

[8].     Hellermann, J.P., Reeder, G.S., Jacobsen, S.J., Weston, S.A., Killian, J. M., & Roger, V. L. (2002). Longitudinal trends in the severity of acute myocardial infarction: a population study in Olmsted County, Minnesota. Am J Epidemiol,156(3),246-53.

[9].     Hu, F.B. (2011). Globalization of Diabetes: The role of diet, lifestyle, and genes. Diabetes Care,34(6),1249-1257.

[10]. Kannel, W.B., & McGee, D.L. (1979). Diabetes and cardiovascular disease. The Framingham studies. JAMA ,241,2035-8.

[11]. Kempler, P. (2005). Learning from large cardiovascular clinical trials: classical cardiovascular risk factors. Diabetes Res Clin Pract, 68 (1), S43-7.

[12]. King, H., Aubert, R. E., & Herman, W. H. (1998). Global burden of diabetes, 1995–2025: prevalence, numerical estimates, and projections. Diabetes Care, 21, 1414–1431.

[13]. Laakso, M. (1997). Dyslipidemia, morbidity, and mortality in non- insulin-dependent diabetes mellitus. Lipoproteins and coronary heart disease in non-insulin-dependent diabetes mellitus. J Diabetes Complications, 11 ,137-41.

[14]. Lehto, S., Ronnemaa, T., Haffner, S.M., Pyorala, K., Kallio, V., &Laakso, M. (1997). Dyslipidemia and hyperglycemia predict coronary heart disease events in middle-aged patients with NIDDM. Diabetes, 46 ,1354-9.

[15]. Mak, K.H., Ma, S., Heng, D., Tan, C. E., Tai, E.S., Topol, E.J., & Chew, S. K. (2007). Impact of sex, metabolic syndrome, and diabetes mellitus on cardiovascular events. Am J Cardiol,100(2),227-233.

[16]. Mohan, V., Deepa, M., Farooq, S., Prabhakaran, D., &Reddy, K.S. (2008). Surveillance for risk factors of cardiovascular disease among an industrial population in southern India. Natl Med J India,21(1),8-13.

[17]. Mohan, V., Deepa, M., Farooq, S., Narayan, K.M., Datta, M., &Deepa, R. (2007). Anthropometric cut points for identification of cardiometabolic risk factors in an urban Asian Indian population. Metabolism,56(7),961-968.

[18]. Mohan, V., Sandeep, S., Deepa, R., Shah, B., & Varghese, C. (2007). Epidemiology of type 2 diabetes: Indian scenario. Indian J Med Res,125(3),217-230.

[19]. Mohan, V., Venkatraman, J.V., & Pradeepa R. (2010). Epidemiology of cardiovascular disease in type 2 diabetes: the Indian scenario. J Diabetes Sci Technol,4(1),158-170.

[20]. Moss, S.E., Klein, R., &Klein, B.E. (1991). Cause-specific mortality in a population-based study of diabetes. Am J Public Health, 81,1158-62.

[21]. Peto, R. (1994). Smoking and death: the past 40 years and the next 40. BMJ, 309(6959),937-939.

[22]. Prabhakaran, D., Yusuf, S., Mehta, S., & Pogue, J (2005). Two-year outcomes in patients admitted with non-ST elevation acute coronary syndrome: results of the OASIS registry 1 and 2. Indian heart journal,57(3),217-225.

[23]. Ramachandran, A., Ma, R.C., & Snehalatha, C.(2010). Diabetes in Asia. Lancet, 375(9712),408-418.

[24]. Reddy, K.S., &Gupta, P. C. (2004). Tobacco Control in India. New Delhi, India: Ministry of Health & Family Welfare, Government of India, Centers for Disease Control and Prevention, USA and World Health Organization.

[25]. Reddy, K.S., Prabhakaran, D., Chaturvedi, V., Jeemon, P., Thankappan, K. R., Ramakrishnan, L.,… Jaison, T. M. & (2006). Methods for establishing a surveillance system for cardiovascular diseases in Indian industrial populations. Bull World Health Organ,84(6),461-469.

[26]. Schroeder, S.A. (2007). Shattuck Lecture. We can do better–improving the health of the American people. N Engl J Med,357(12),1221-1228.

[27]. UKPDS 32.(1998). Ethnicity and cardiovascular disease. The incidence of myocardial infarction in white, South Asian, and Afro-Caribbean patients with type 2 diabetes (U.K. Prospective Diabetes Study 32). Diabetes Care,21(8),1271-1277.

[28]. Xavier, D., Pais, P., Devereaux, P.J., Xie, C., Prabhakaran, D., Reddy, K.S., …Yousuf, S.(2008). Treatment and outcomes of acute coronary syndromes in India (CREATE): a prospective analysis of registry data. Lancet,371(9622),1435-1442.