23 EMCJ. Jan 2016: 1 (1) Review Article Recurrent Abdominal Pain in Children: A Review Alam R 1 , Sarkar PC 2 , Saibal AA 3 Abstract: Recurrent abdominal pain (RAP) in children is a common pediatric problem encountered by primary care physicians, medical subspecialists and surgical specialists. It is usually functional that affects 10-20% of school age children. The term recurrent abdominal pain represents a description and not a diagnosis. Many diseases can cause recurrent abdominal pain, but, in clinical practice, most children presenting with this symptoms have no evidence of disease. They are said to have functional abdominal pain; however, they often require evaluation and treatment to allay fears and improve their quality of life. This review addresses some of the issues related to epidemiology, etiology, management and prognosis of recurrent abdominal pain. 1 Dr. Rumana Alam, Assistant Professor, Dept. of Pediatrics, Eastern Medical College. 2 Dr. Palash Chandra Sarkar, Registrar, Dept. of Pediatrics, Eastern Medical College. 3 Dr. Md. Arif Akbar Saibal, Associate Professor, Dept. of Internal Medicine, Eastern Medical College. Address of Correspondence: Dr. Rumana Alam, Assistant Professor, Dept. of Pediatrics, Eastern Medical College, Comilla, Bangladesh. Mobile: +8801711972747, Email: [email protected]Introduction: Recurrent abdominal pain (RAP) is defined as at least 3 separate episodes of abdominal pain that occur in a 3-months period. These episodes are often severe, and the child is not able to do his or her normal activities 1 . It is perhaps the most common painful health problem in school-aged children. J Apley, a British pediatrician, studied abdominal pain among children extensively and observed that approximately 10% of school aged children get recurrent episodes of abdominal pain. Affected children and their families experience distress and anxiety that can interfere with their ability to perform regular activities. Epidemiology: In general, population-based studies suggest that RAP is experienced by 10-15% of school-age children 2 . Epidemiological studies in Asia have reported similar prevalence. Boey and his colleagues studied RAP among school children in Malaysia and found a prevalence of 10.2% (urban 8.2-9.6%, rural 12.4%) 3,4 . Similarly, Rasul and Khan reported RAP in11.5% of Bangladesh school children 5 . Cohort studies from India and Pakistan suggest that RAP is most likely to have an organic cause (up to 82% of cases), with giardiasis being the most common underlying condition 14,15 , while in Sri Lanka, commonest organic etiology is constipation 16 . However, another Indian cohort and a Sri Lankan cohort showed that non-organic RAP is more prevalent (74% and 76%, respectively) 16 . In Malaysia, both urban and rural population-based cohorts had a similar prevalence of RAP at 9.6% and 11%, respectively 3 . Etiology: The origin of abdominal pain is complex and does not lend itself to a single model of causation. In the four decades since Apley's seminal research, conceptual models of RAP have evolved and become more complex 1 . Walker (1999) identified three distinct periods in this evolution. Studies conducted before the 1980s were characterized by a dualistic view of abdominal pain. When no organic etiology was identified, abdominal pain was assumed to be psychogenic. In the 1980s, the focus of research shifted to non-organic causes of RAP, including a host of psychosocial factors. Conceptual models emerging in this decade were increasingly multivariate in nature. They recognized that the cause of RAP may not be either organic or psychogenic, but possibly a function of normal (i.e., non-pathological) biological mechanisms. In the 1990s, the research focus shifted to the identification of individual differences among children with RAP and the interact mode RAP are multivariate and acknowledge the contributions of a variety of biological, psychological, and social factors 16 . Organic Cause: Numerous organic disorders lead to abdominal pain; Possible causes that should be considered based on the history, physical examination and testing, are acid reflux, constipation, lactose intolerance, parasitic infections of the small and large intestines, Helicobacter pylori infection, inflammatory bowel diseases (IBD) such as Crohn’s disease and ulcerative colitis, celiac disease inflammation of the liver (hepatitis), gall bladder problems, an inflamed pancreas, an intestinal obstruction, appendicitis, and many more rare disorders.
Abstract: Ectopic pregnancy occurs in approximately 1.5-2% of all pregnancies. It presents a major health problem for women of child-bearing age. The morbidity and mortality associated with ectopic pregnancy has decreased dramatically, mainly because of earlier diagnosis with transvaginal ultrasound and b-hCG levels and subsequent treatment before rupture. Treatment options include surgical, medical and expectant management. Surgery, salpingectomy or salpingotomy is performed laparoscopically or by open surgery. The most commonly used drug for the medical treatment of ectopic pregnancies is methotrexate. This can be administered either systemically or locally or both. It was concluded that review data reflect a decrease in surgical treatment and not an actual decline in ectopic pregnancy occurrence so that further new avenues are needed to explore early detection of the ectopic pregnancy.
Recurrent Abdominal Pain in Children: A ReviewAlam R1, Sarkar PC2, Saibal AA3
Abstract: Recurrent abdominal pain (RAP) in children is a common pediatric problem encountered by primary care physicians, medical subspecialists and surgical specialists. It is usually functional that affects 10-20% of school age children. The term recurrent abdominal pain represents a description and not a diagnosis. Many diseases can cause recurrent abdominal pain, but, in clinical practice, most children presenting with this symptoms have no evidence of disease. They are said to have functional abdominal pain; however, they often require evaluation and treatment to allay fears and improve their quality of life. This review addresses some of the issues related to epidemiology, etiology, management and prognosis of recurrent abdominal pain.
1Dr. Rumana Alam, Assistant Professor, Dept. of Pediatrics, Eastern Medical College.2Dr. Palash Chandra Sarkar, Registrar, Dept. of Pediatrics, Eastern Medical College.3Dr. Md. Arif Akbar Saibal, Associate Professor, Dept. of Internal Medicine, Eastern Medical College.
Address of Correspondence: Dr. Rumana Alam, Assistant Professor, Dept. of Pediatrics, Eastern Medical College, Comilla, Bangladesh. Mobile: +8801711972747, Email: [email protected]
1Dr. Shabera Arzoo, Assistant Professor, Dept. of Gynaecology & Obstetrics, EMCH.2Dr. Musammat Shamima Akter, Associate Professor, Dept. of Gynaecology & Obstetrics, EMCH.3Dr. Sayeda Anwara Begum, Registrar, Dept. of Gynaecology & Obstetrics, EMCH.4Dr. Forhad Abedin, Resident Physician, CoMCH.5Dr. Saima Afroz, Associate professor, Dept. of Gynaecology & Obstetrics, EMCH.6Dr. Mahbubur Rahman Ammar, Intern Doctor, EMCH.7Dr. Shahriar Inam Khan, Intern Doctor, EMCH.
Address of Correspondence: Dr. Shabera Arzoo, Assistant Professor, Dept. of Gynaecology & Obstetrics, Eastern Medical College and Hospital. Mobile: +8801711385778, Email: [email protected]
Functional dyspepsia Functional abdominal pain or discomfort in the upper abdomen
Irritable bowel syndrome Functional abdominal pain associated with alteration in bowel movements
Abdominal migraine
Functional abdominal pain with features of migraine (paroxysmal abdominal pain associated with anorexia, nausea, vomiting, or pallor as well as a maternal history of migraine headache
Functional abdominal pain
Abdominal pain without demonstrable evidence of a pathologic condition, such as an metabolic, infectious, inflammatory, or neoplastic disorder; functional abdominal pain may present with symptoms typical of functional dyspepsia, irritable bowel syndrome, abdominal migraine, or functional abdominal pain syndrome
Functional abdominal pain syndrome Functional abdominal pain without the characteristics of dyspepsia, irritable bowel syndrome, or abdominal migraine
Discussion:The present study was undertaken to observe some aspects of thyroid function status in children with autism spectrum disorders by estimating serum FT3, FT4 and TSH levels. All the parameters were also estimated in apparently healthy age and BMI matched children to find out the baseline data and also for comparison. In this study, thyroid hormone levels in the control group were within physiological limit and almost similar to the findings observed by various investigators from different countries12,13.
Our study showed that, the mean serum FT3 levels in both the groups were within normal range and almost similar and no significant difference was observed among the groups. This finding was in agreement with other researchers of different countries14,15.
The mean serum FT4 level was also within normal limit but significantly lower in the autistic subjects in comparison to that of the healthy subjects. Similar findings were also made by other investigators7,8,9. Again, elevated serum TSH level was found in the autistic children and these observations are in accordance with other research workers6,10.
It has been suggested that nervous system growth and differentiation are closely correlated with thyroid hormones in the initial developmental stages. Deficiency of this hormone during the first two years of life may produce morphological brain changes that can have significant deleterious behavioral and cognitive effect9. In summary, our findings leads to the suggestion that impairment of mental and cognitive development found in autistic children may result from the subclinical hypothyroidism present in these special children.
Conclusion:From the result of this study, it may be concluded that thyroid hormone deficiency may be one of the non-genetic risk factors associated with autism spectrum disorders. Therefore, routine thyroid test of pregnant mother and new born may be useful for early detection of future risk of development of ASD.
Conflict of Interest: The authors have no conflict of interest to declare.
2. Tareen RS, Kamboj MK. Role of EndocrineFactors in Autistic Spectrum Disorder. Pediatr Clin NAm 2012; 159: 75-88.
3. Rossignol DA, Bradstreet JJ. Evidence ofmitochondrial dysfunction in autism and implications fortreatment. A J Biochem Biotechnol 2008; 4(2): 208-17.
4. Pardo CA, Eberhart G. The Neurobiology ofAutism. J Brain Pathol 2007; 17: 434-47.
5. Muhle R, Trentacoste SV, Rapin I. The Genetics ofAutism. J Pediatrics 2004; 113(5): 72-86.
6. Nir I, Meir D, Zilber N, Knobler H, Hadjez J,Lerner Y. Brief report: Circadian Melatonin, Thyroid-stimulating Hormone, Prolactin and Cortisol levels inserum of Young adults with Autism. J Autism DevDisord 1995; 25(6): 641-54.
7. Hoshiko S, Grether JK, Windham GC, Smith D,Fessel K. Are thyroid hormone concentrations at birthassociated with subsequent autism diagnosis? JAutism Research 2011; 4(6): 456-63.
9. Kellman R. The Autism – Thyroid connection. JDev Delay 2011; 15.
10. Gillberg IC, Gillberg C, Kopp S. Hypothyroidismand autism spectrum disorders. J Child PsycholPsychiatry 1992; 33 (3): 531-42.
11. Howdeshell KL. A model of the development ofthe brain as a construct of the thyroid system.Environ Health Perspect 2000; 110(3): 337-48.
12. Iwata K, Matsuzaki H, Miyachi T, Shimmura C,Suda S, Tsuchiya K J, Matsumoto K, Suzuki K, IwataY, Nakamura K, Tsujii M, Sugiyama T, Sato K, MoriN. Investigation of the serum levels of anteriorpituitary hormones in male children with autism. JMolecular Autism 2011; 2(16).
15. Campbell M, Small AM, Hollander CS, Korein J,Cohen IL, Kalmijn M, Ferris S. A controlledcrossover study of Triiodothyronine in AutisticChildren. J Autism and childhood Schizophrenia1978; 8(4): 371-81.
Introduction:In the developed world between 1% and 2% of all reported pregnancies are ectopic pregnancies1. It seriously compromise women’s health and future fertility. Currently ectopic pregnancy diagnosed before the patient condition has deteriorated. Currently diagnosis relies on a combination of ultrasound scanning and serial serum beta-Human chorionic gonadotrophin (b-hCG) measurements2.Timely diagnosis allows the clinician to consider the full range of treatment options. This is important for treatment success and retaining optimal fertility for those women desiring future pregnancy. The etiology of ectopic pregnancy remains uncertain although a number of risk factors have been identified. Its diagnosis can be difficult. The risk factors are maternal: pelvic inflammatory disease, Chlamydia trachomatis infection, smoking, tubal surgery, induced conception cycle and endometriosis. The annual incidence of ectopic pregnancy has increased over the past 30 year3. In the western world 4-10% of pregnancy related deaths have been observed from this issue and now it is growing problem in developing countries also4.
The treatment options are expectant management, medical treatment or surgery. In surgery laparoscopy is now the accepted approach to perform salpingostomy or salpingectomy. Concerning medical treatment, systemic administration of methotrexate (MTX) has gained acceptance in selected patients. It is given intramuscularly either in a fixed multiple dose regimen alternated with folinic acid or in a single dose regimen without folinic acid. Expectant management has been advocated based on the knowledge that the natural course of many early ectopic pregnancy is a self-limiting process, ultimately resulting in tubal abortion or re-absorption.
Types of Ectopic pregnancy:The fallopian tube is the dominant site in the majority cases of EP5. 75-80% of EPs occur in ampullary portion, 10-15% EPs occur in the isthmic portion and about 5% of EP is in the fimbrial end of the fallopian tube6. Cervical EP is rare and represents only 0.15% of all EP7. Ovarian EP is one of the rarest variants, and incidence is estimated to be 0.15-3% of all ectopic pregnancy8. Caesarean scar EP is another rarest form of EP with an incidence of 1:1800 pregnancies due to increase number of caesarean
deliveries over the last 30 years9. Abdominal EP with 1.3% of cases are diagnosed at a rate of 1:10,000 births and is an extremely rare and serious form of extrauterine gestation10. A heterotopic EP is diagnosed when women have any of the above said EP in conjunction with an intrauterine pregnancy. It is also more common (1-3%) in in vitro fertilization and fertility treatments involved super ovulatory drugs11.
Etiology:The exact etiology of EP is unknown. However, it is thought that tubal implantation occurs as a result of a combination of arrest of the embryo in the fallopian tube and changes in the tubal micro environment that allow early implantation to occur12. Inflammation within the tube, resulting from infection or smoking, may effect embryo-tubal transport by disrupting smooth muscle contractility and ciliary beat activity.
Clinical Presentation:Patients with an EP commonly present with pain and vaginal bleeding between 6 and 10 weeks of gestation13. However, these are common symptoms in early pregnancy, with one third of women experiencing some pain and/or bleeding14. Shoulder tip pain, syncope and shock occur in up to 20% of women and abdominal tenderness in more than 75%. Cervical motion tenderness has been reported in up to 67% of cases, and a palpable adnexal mass in about 50%15. In 2006-2008 Center for Maternal and Child Enquiries (CMACE) report, four of the six women who died from EP complained of diarrhea, dizziness or vomiting as early symptoms, without triggering any consideration of extrauterine pregnancy by their medical attendants16. However, it remains difficult to diagnose an EP from risk factors, history and examination alone.
Diagnosis:Initial diagnosis of first trimester hemorrhage presents an important challenge17. Recently, detection of EP is determined through serum b-hCG levels and vaginal ultrasonography technique18. A single serum measurement of the b-hCG concentration may not show the location of gestational sac. Demonstration of normal doubling of serum levels over 48 hours supports a diagnosis of fetal viability but does not rule out EP. Failing levels on raising the level of b-hCG concentration to reach 50% of confirm non-viability suggesting EP. In contrast with b-hCG concentrations, serum progesterone levels are stable for first 8-10 weeks of gestation. Investigate that sensitivity ranged of progesterone from 45-100% depending on the threshold. Both high (>22 ng/ml) and low ( 5 ng/ml) cutoff points have been assessed for their ability to correctly identify non-viable and ectopic pregnancies; serum progesterone levels 5 ng/ml could apparently be used to predict EP with 70-
90% sensitivity and 30-90% specificity19. If patient have serum progesterone measurement below 10ng/ml and b-hCG level below 1500 mIU/L are more likely to demonstrate spontaneous resolution of EP. Transvaginal ultrasound scan (TVS) is very popular from 1980, and by the mid 1990 sensitivity and specificity were calculated at 84.4 and 98.9% respectively it remains the gold standard for diagnosis of EP20.
Management:The treatment option of tubal EP involves surgical treatment by laparotomy or laparoscopy, and medical treatment is usually systemic or through local route, or by expectant treatment.
Expectant Treatment: Expectant management can be applied in a selected population of the patients with self-limiting EP. According to the most recent guideline, published by the American College of Obstetrician and Gyanecologists, there may be a role for expectant management when the b-hCG level is <200 IU/ml and which is further in decline phase. It should only be offered when TVS remains non-diagnostic and b-hCG levels continue to decline. Successful expectant management occurs in 98% of cases for bhCG <200 IU/L, in 73% for b-hCG <500 IU/L and in 25% for b -hCG <2,000 IU/L. If initial serum b-hCG<1,000IU/L then successful expectant managementmight occur in most patients (88%) with an EP sizeof <4 cm, without a fetal heart beat on transvaginalsonography; followed by haemoperitonium <50 ml. Evidence of ectopic resolution on scan is another wayto diagnosis. A decrease in EP size on day 7 had asensitivity of 84% and specificity of 100% inpredicting spontaneous resolution21.
Medical Treatment: Medical treatment of EP is quite less expensive than surgery22. Many different agent have been used to treat EP including systemic and local Methotrexate (MTX), local potassium chloride, hyperosmolar glucose, prostaglandins, danazol, etoposide and mifepristone23. Current therapies focus primarily on MTX treatments. Methotrexate (MTX) is a drug that inhibits the action of dihydrofolate reductase, thereby inhibiting DNA synthesis MTX affects actively proliferating tissues such as bone marrow, intestinal mucosa, malignant cells and trophoblastic tissue. MTX is contraindicated when embryonic cardiac motion or the presence of a gestational sac larger than 3.5 cm due to higher rate of treatment failure.
There are three different regimens for giving MTX: single dose, two-dose, and a fixed multidose protocol. The single 50 mg/m2 dose of MTX is most
commonly used, given as an intramuscular injection. βhCG levels are measured at 4 and 7 days post treatment with an expected 15% decrease from day 4 to day 7. Weekly βhCG levels are then checked until zero. If βhCG levels do not drop appropriately, a second MTX dose or surgical intervention is advised. Multidose regimen for MTX is available (MTX 1.0 mg/kg I/M daily; days 0,2,4 and 6 alternated with folinic acid 0.1 mg/kg orally on days 1,3,5,7)24. This treatment more appropriate for patient who present with a large adnexal mass and greater initial b-hCG level (5000 IU).
Surgical Treatment: Once the mainstay of therapy of EP, surgical treatment is now mainly reserved for patients with contraindication to medical management and for those with evidence of tubal rupture. Despite declining rates of surgical management, surgery remains the most definitive treatment of ectopic pregnancies. A laparoscopic approach is preferable to an open approach in a patient which haemodynamically stable. Laparoscopic procedure are associated with shorter operative times, less intraoperative blood loss, shorter hospital stays and lower analgesia requirements. Laparotomy should be reserved for patients who present with rupture and are in a state of hypovolaemic shock and compromise. Two techniques are described to remove the EP from the fallopian tube—1) Salpingectomy: The pregnancy is removed en bloc with the tube, 2) Salpingostomy: An incision is made on the fallopian tube over the swelling, the EP carefully removed with the forceps or irrigation and the incision should be either closed or let to heal by secondary intention. The success rate of salpingostomy is 92% and failure cases can be managed with MTX. Serial b-hCG measurement should be taken until undetectable to be certain that there is no persistence of trophoblastic tissue. Sometimes a prophylactic dose of MTX is given with salpingostomy25.
Literature Review:Gabbur et al. reported that on its retrospective analysis of stable women with small unruptured EP treated with single dose intramuscular MTX concluded that day 4 post treatmen b-hCG levels do not predict successful treatment or need for surgery26. Only day 7 b-hCG levels were associated with successful single dose MTX treatment26.
Barnhart et al. investigated in there meta-analysis of both regimens (single and multi-dose) and concluded that the multi dose regimen was more effective than single dose regimen, with success rate reported as 93% for multi dose regimen and 88% for the single dose regimen27.
Barnhart et al. was attempted by the challenge to develop an optimum regimen that balances efficacy and safety on the one hand and convenience on the other hand and it first described what is called the “double-dose-protocol”. In a study that included 101 patients, two doses of MTX were administered on days 0 and 4 without measuring b-hCG between doses. The authors reported a success rate of 76% after two doses and 87% after a further two doses28.
MTX treatment is very successful for small stable ectopic pregnancies. A meta-analysis of non-randomized studies showed success rate of 93% (95% CI 89-96%) for multi dose protocols and 88% (95% CI 89-96%) for single dose therapy29.
In one randomized controlled trial of laparoscopic surgery, prophylactic MTX lower the rate of persistent ectopic pregnancy 14.5-1.9%. The major benefit was in the shorter duration of post-operative monitoring30.
Several studies done to see the subsequent pregnancies after ectopic pregnancy. Studies suggest that around 60% of women affected by an EP go on to have a viable IUP. This figure includes those who do not plant to have another pregnancy and so the proportion will be higher if further pregnancy is planned. There is thought to be a 5-20% risk of a recurrence of EP with one previous EP and a risk of 32% or more following more than one previous ectopic. However the risk is reduced after each subsequent IUP.
Recent Advance:Previously ectopic pregnancy was diagnosed on clinical symptom, TVS and by measuring b-hCG, but now-a-days some new advancement arrived for diagnostic purpose.
VEGF is a potent angiogenic factor that acts as a vascular growth, remodeling and permeability in the endomertium, decidua and trophoblast. Daponte et al. described higher serum VEGF concentrations in women with EP (medium 227.2 pg/ml) than with abnormal intrauterine pregnancy (median 107.2 pg/ml) (p<0.001) and it concluded that VEGF serum concentrations might be a useful marker for- EP and suggested 174 pg/ml as the cut-off value for EP diagnosis31.
Existing evidence suggests elevated creatine kinase (CK) as a tool for diagnosis of EP. The trophoblast usually invades the muscular layer and maternal blood vessels are eroded, allowing muscle cell products such a CK to enter the circulation; therefore, increased serum CK levels are normal during EP32.
Conclusion:EP in developing countries is a serious threat, just because of poor medical facilities so that a significant morbidity rate and the potential for maternal death generally are seen. Management is dictated by the clinical presentation, serum b-hCG levels and TVS findings. Expert consultation with radiologists and gynecologists are recommended whenever EP is suspected. The use of MTX for treatment of early unruptured EP reported to be safe and effective. Surgical treatment is appropriate for women who are haemodynamically unstable or unlikely to be complained with post treatment monitoring and those who do not have immediate access to medical care. The preferred method of surgical treatment of EP today is diagnostic laparoscopy with salpingostomy and tubal conservation followed by prophylactic dose of MTX. Existing evidence suggests elevated vascular endothelial growth factor (VEGF) and creatine kinase (CK) as a tool for diagnosis of EP. Further new avenues are needed to explore less side effects of medication of EP.
Reference:1. Goldner TE, Lawson HW, Xia Z, et al.Surveillance for ectopic pregnancy - United States,1970-1989. MMWR CDC Surveill Summ 1993;42(6): 73–85.
2. Horne AW, Duncan WC, Critchley HO. The needfor serum biomarker development for diagnosing andexcluding tubal ectopic pregnancy. Acta ObstetGynecol Scand 2010; 89: 299–301.
3. Gamzu R, Almog B, Levin Y, Avni A, Jaffa A,Lessing J. Ef cacy of methotrexate treatment inextrauterine pregnancies de ned by stable orincreasing human chorionic gonadotropinconcentrations. Fertil Steril 2002; 77: 761–5.
10. Yildizhan R, Kurdoglu M, Kolusari A, Erten R.Primary omental pregnancy. Saudi Med J 2008; 9:606–9.11. Condous G, Okaro E, Bourne T. The conservativeman-agement of early pregnancy complications: areview of the lit-erature. Ultrasound Obstet Gynecol2003; 22: 420–30.
12. Shaw JL, Dey SK, Critchley HO, et al. Currentknowledge of the aetiology of human tubal ectopicpregnancy. Hum Reprod Update 2010; 16: 432–44.
14. Chez RA, Moore JG. Diagnostic errors in themanagement of ectopic pregnancy. Surg GynecolObstet. 1963; 117: 589–96.
15. Tay JI, Moore J, Walker JJ. Ectopic pregnancy.BMJ 2000; 320: 916–9.
16. Robson SJ, O’Shea RT. Undiagnosed ectopicpregnancy: a retrospective analysis of 31 ‘missed’ ectopic pregnancies at a teaching hospital. Aust N Z JObstet Gynaecol 1996; 36:182–5.
17. Daponte A, Pournaras S, Zintzaras E, KallitsarisA, Lialios G, Maniatis AN. The value of a singlecombined measure-ment of VEGF, glycodelin,progesterone, PAPP-A, HPL and LIF fordifferentiating between ectopic and abnormal intra-uterine pregnancy. Hum Reprod 2005; 20: 3163–6.
18. Felemban A, Sammour A, Tulandi T. Serumvascular endothelial growth factor as a possiblemarker for early ectopicpregnancy. Hum Reprod2002; 17: 490–2.
19. Dart R, Ramanujam P, Dart L. Progesterone as apredictor of ectopic pregnancy when the ultrasound isindeterminate. AmJ Emerg Med 2002; 20: 575–9.
20. Condous G. Ectopic pregnancy—risk factors anddiag-nosis. Aust Fam Physician 2006; 35: 854–7.
21. Rajesh V, Lawrence M. Evidence-basedmanagement ofectopic pregnancy. Curr ObstetGynaecol 2002; 12: 191–9.
22. Rodrigues SP, de Burlet KJ, Hiemstra E,Twijnstra AR, vanZwet EW, Trimbos-Kemper TC,Jansen FW. Ectopicpregnancy: when is expectantmanagement safe? Gynecol Surg 2012; 9: 421–6.
23. van Mello NM, Mol F, Mol BW, Hajenius PJ.Conser-vative management of tubal ectopicpregnancy. Best Pract Res 2009; 23: 509–518.
24. Condous G, Okaro E, Khalid A, Lu C, Van HS,Timmerman D. A prospective valuation of a single-visit strategy tomanage pregnancies of unknownlocation. Hum Reprod 2005; 20: 1398–1403.
25. Seeber BE, Barnhart KT. Suspected ectopicpregnancy. Obstet Gynecol 2006; 107: 399–413.
26. Gabbur N, Sherer DM, Hellmann M. Do serumbeta-human chorionic gonadotropin levels on day 4following methotrexate treatment of patients withectopic pregnancy pre-dict successful single-dosetherapy? Am J Perinatol 2006; 23:193–6.
28. Barnhart K, Hummel AC, Sammel MD, Menon S,Jain J, Cha-khtoura N. Use of ‘‘2-dose’’ regimen ofmethotrexate totreat ectopic pregnancy. Fertil Steril2007; 87: 250–6.
29. Horne AW, van den Driesche S, King AE, et al.Endometrial inhibin/activin beta-B subunitexpression is related to decidualization and is reducedin tubal ectopic pregnancy. J Clin Endocrinol Metab2008; 93: 2375–82.
30. Graczykowski JW, Mishell DR. Methotrexateprophy-laxis for persistent ectopic pregnancy afterconservative treat-ment by salpingostomy. ObstetGynecol 1997; 89: 118–22.
31. Daponte A, Pournaras S, Zintzaras E, KallitsarisA, Lialios G, Maniatis AN. The value of a singlecombined measure-ment of VEGF, glycodelin,progesterone, PAPP-A, HPL and LIF fordifferentiating between ectopic and abnormal intra-uterine pregnancy. Hum Reprod 2005; 20: 3163–6.
32. Chandra L, Jain A. Maternal serum creatinekinase as a biochemical marker of tubal pregnancy.Int J Gynaecol Obstet 1995; 49: 21–3.�
Introduction:Recurrent abdominal pain (RAP) is defined as at least 3 separate episodes of abdominal pain that occur in a 3-months period. These episodes are often severe,and the child is not able to do his or her normalactivities1. It is perhaps the most common painfulhealth problem in school-aged children. J Apley, aBritish pediatrician, studied abdominal pain amongchildren extensively and observed that approximately10% of school aged children get recurrent episodes ofabdominal pain. Affected children and their familiesexperience distress and anxiety that can interfere withtheir ability to perform regular activities.
Epidemiology: In general, population-based studies suggest that RAP is experienced by 10-15% of school-age children2. Epidemiological studies in Asia have reported similar prevalence. Boey and his colleagues studied RAP among school children in Malaysia and found a prevalence of 10.2% (urban 8.2-9.6%, rural 12.4%) 3,4. Similarly, Rasul and Khan reported RAP in11.5% of Bangladesh school children5. Cohort studies from India and Pakistan suggest that RAP is most likely to have an organic cause (up to 82% of cases), with giardiasis being the most common underlying condition14,15, while in Sri Lanka, commonest organic etiology is constipation16. However, another Indian cohort and a Sri Lankan cohort showed that non-organic RAP is more prevalent (74% and 76%, respectively)16. In Malaysia, both urban and rural population-based cohorts had a similar prevalence of RAP at 9.6% and 11%, respectively3.
Etiology: The origin of abdominal pain is complex and does not lend itself to a single model of causation. In the four decades since Apley's seminal research, conceptual models of RAP have evolved and become more complex1. Walker (1999) identified three distinct periods in this evolution. Studies conducted before the 1980s were characterized by a dualistic view of abdominal pain. When no organic etiology was identified, abdominal pain was assumed to be psychogenic. In the 1980s, the focus of research shifted to non-organic causes of RAP, including a host of psychosocial factors. Conceptual models emerging in this decade were increasingly multivariate in nature. They recognized that the cause of RAP may not be either organic or psychogenic, but possibly a function of normal (i.e., non-pathological) biological mechanisms. In the 1990s, the research focus shifted to the identification of individual differences among children with RAP and the interact mode RAP are multivariate and acknowledge the contributions of a variety of biological, psychological, and social factors16.
Organic Cause: Numerous organic disorders lead to abdominal pain; Possible causes that should be considered based on the history, physical examination and testing, are acid reflux, constipation, lactose intolerance, parasitic infections of the small and large intestines, Helicobacter pylori infection, inflammatory bowel diseases (IBD) such as Crohn’s disease and ulcerative colitis, celiac disease inflammation of the liver (hepatitis), gall bladder problems, an inflamed pancreas, an intestinal obstruction, appendicitis, and many more rare disorders.
Functional Gastrointestinal Disorders: Until a decade ago ‘functional gastrointestinal disorder’ was a label used for the conditions with uncertain etiology, and was a diagnosis of exclusion. In 1999 the pediatric Rome II criteria (Table I) introduced the term abdominal pain related-functional gastrointestinal disorders (AP-FGIDs); which include functional dyspepsia (FD), irritable bowel syndrome (IBS), abdominal migraine (AM), functional abdominal pain (FAP) and functional abdominal pain syndrome (FAPS). According to Caplan, et al. validation of pediatric Rome II criteria was done6. They found that more than half the patients classified as having functional problems met at least one pediatric Rome II criteria for FGID. Children with AP-FGIDs report significantly lower quality of life scores compared to healthy peers and AP-FGIDs are ranked as second in causing school absence. In 29.1% of patients with recurrent abdominal pain, pain persists even for more than 5 years, despite frequent medical attention.
The pathogenesis underlying AP-FGIDs remains unclear. It is thought to involve abnormalities in the enteric nervous system (ENS), a rich and complex nervous system that envelops the entire gastrointestinal tract. A dysregulation of this brain-gut communication plays an important role in the pathogenesis of functional abdominal pain. It is now believed that adults and children with functional bowel disorders, rather than having a baseline motility disturbance, may have an abnormal bowel reactivity to physiologic stimuli (meal, gut distension, hormonal changes), noxious stressful stimuli (inflammatory processes), or psychological stressful stimuli (parental separation, anxiety)16.
Additionally, adult patients with functional bowel disorders attending gastrointestinal clinics were often found to have psychological disturbances regardless of the final diagnosis. It was concluded that psychological factors may have been more important in determining health-seeking behavior than the cause of the symptom17. There is growing evidence to suggest that functional abdominal pain disorders may be associated with visceral hyperalgesia, a decreased threshold for pain in response to changes in intraluminal pressure18,19. Mucosal inflammatory processes attributable to infections, allergies, or primary inflammatory diseases may cause sensitization of afferent nerves and have been associated with the onset of visceral hyperalgesia20.
Moreover, studies conducted in the United States and Europe reported that psychological symptoms, low socio-economic status, parental gastrointestinal complaints and single parent- and immigrant-households are associated with chronic abdominal pain in children. To overcome drawbacks in Rome II criteria, they were revised and modified in 2006, and Rome III criteria were developed. Table II summarizes the Rome III criteria for pediatric FGID. Using Rome III criteria, a recent study in Sri Lanka has reported FGID in 93% of patients with non-organic RAP. Of them, 45.2% had functional abdominal pain12. Therefore, it is important to consider FGID in the differential diagnosis of RAP early in the evaluation.
Emotional/ Behavioral Stress: There is evidence suggesting that the presence of anxiety, depression or behavior problems is not useful in distinguishing between functional abdominal pain and abdominal pain of other causes. There is
Abstract: Ectopic pregnancy occurs in approximately 1.5-2% of all pregnancies. It presents a major health problem for women of child-bearing age. The morbidity and mortality associated with ectopic pregnancy has decreased dramatically, mainly because of earlier diagnosis with transvaginal ultrasound and b-hCG levels and subsequent treatment before rupture. Treatment options include surgical, medical and expectant management. Surgery, salpingectomy or salpingotomy is performed laparoscopically or by open surgery. The most commonly used drug for the medical treatment of ectopic pregnancies is methotrexate. This can be administered either systemically or locally or both. It was concluded that review data reflect a decrease in surgical treatment and not an actual decline in ectopic pregnancy occurrence so that further new avenues are needed to explore early detection of the ectopic pregnancy.
Recurrent Abdominal Pain in Children: A ReviewAlam R1, Sarkar PC2, Saibal AA3
Abstract: Recurrent abdominal pain (RAP) in children is a common pediatric problem encountered by primary care physicians, medical subspecialists and surgical specialists. It is usually functional that affects 10-20% of school age children. The term recurrent abdominal pain represents a description and not a diagnosis. Many diseases can cause recurrent abdominal pain, but, in clinical practice, most children presenting with this symptoms have no evidence of disease. They are said to have functional abdominal pain; however, they often require evaluation and treatment to allay fears and improve their quality of life. This review addresses some of the issues related to epidemiology, etiology, management and prognosis of recurrent abdominal pain.
1Dr. Rumana Alam, Assistant Professor, Dept. of Pediatrics, Eastern Medical College.2Dr. Palash Chandra Sarkar, Registrar, Dept. of Pediatrics, Eastern Medical College.3Dr. Md. Arif Akbar Saibal, Associate Professor, Dept. of Internal Medicine, Eastern Medical College.
Address of Correspondence: Dr. Rumana Alam, Assistant Professor, Dept. of Pediatrics, Eastern Medical College, Comilla, Bangladesh. Mobile: +8801711972747, Email: [email protected]
1Dr. Shabera Arzoo, Assistant Professor, Dept. of Gynaecology & Obstetrics, EMCH.2Dr. Musammat Shamima Akter, Associate Professor, Dept. of Gynaecology & Obstetrics, EMCH.3Dr. Sayeda Anwara Begum, Registrar, Dept. of Gynaecology & Obstetrics, EMCH.4Dr. Forhad Abedin, Resident Physician, CoMCH.5Dr. Saima Afroz, Associate professor, Dept. of Gynaecology & Obstetrics, EMCH.6Dr. Mahbubur Rahman Ammar, Intern Doctor, EMCH.7Dr. Shahriar Inam Khan, Intern Doctor, EMCH.
Address of Correspondence: Dr. Shabera Arzoo, Assistant Professor, Dept. of Gynaecology & Obstetrics, Eastern Medical College and Hospital. Mobile: +8801711385778, Email: [email protected]
Functional dyspepsia Functional abdominal pain or discomfort in the upper abdomen
Irritable bowel syndrome Functional abdominal pain associated with alteration in bowel movements
Abdominal migraine
Functional abdominal pain with features of migraine (paroxysmal abdominal pain associated with anorexia, nausea, vomiting, or pallor as well as a maternal history of migraine headache
Functional abdominal pain
Abdominal pain without demonstrable evidence of a pathologic condition, such as an metabolic, infectious, inflammatory, or neoplastic disorder; functional abdominal pain may present with symptoms typical of functional dyspepsia, irritable bowel syndrome, abdominal migraine, or functional abdominal pain syndrome
Functional abdominal pain syndrome Functional abdominal pain without the characteristics of dyspepsia, irritable bowel syndrome, or abdominal migraine
Discussion:The present study was undertaken to observe some aspects of thyroid function status in children with autism spectrum disorders by estimating serum FT3, FT4 and TSH levels. All the parameters were also estimated in apparently healthy age and BMI matched children to find out the baseline data and also for comparison. In this study, thyroid hormone levels in the control group were within physiological limit and almost similar to the findings observed by various investigators from different countries12,13.
Our study showed that, the mean serum FT3 levels in both the groups were within normal range and almost similar and no significant difference was observed among the groups. This finding was in agreement with other researchers of different countries14,15.
The mean serum FT4 level was also within normal limit but significantly lower in the autistic subjects in comparison to that of the healthy subjects. Similar findings were also made by other investigators7,8,9. Again, elevated serum TSH level was found in the autistic children and these observations are in accordance with other research workers6,10.
It has been suggested that nervous system growth and differentiation are closely correlated with thyroid hormones in the initial developmental stages. Deficiency of this hormone during the first two years of life may produce morphological brain changes that can have significant deleterious behavioral and cognitive effect9. In summary, our findings leads to the suggestion that impairment of mental and cognitive development found in autistic children may result from the subclinical hypothyroidism present in these special children.
Conclusion:From the result of this study, it may be concluded that thyroid hormone deficiency may be one of the non-genetic risk factors associated with autism spectrum disorders. Therefore, routine thyroid test of pregnant mother and new born may be useful for early detection of future risk of development of ASD.
Conflict of Interest: The authors have no conflict of interest to declare.
2. Tareen RS, Kamboj MK. Role of EndocrineFactors in Autistic Spectrum Disorder. Pediatr Clin NAm 2012; 159: 75-88.
3. Rossignol DA, Bradstreet JJ. Evidence ofmitochondrial dysfunction in autism and implications fortreatment. A J Biochem Biotechnol 2008; 4(2): 208-17.
4. Pardo CA, Eberhart G. The Neurobiology ofAutism. J Brain Pathol 2007; 17: 434-47.
5. Muhle R, Trentacoste SV, Rapin I. The Genetics ofAutism. J Pediatrics 2004; 113(5): 72-86.
6. Nir I, Meir D, Zilber N, Knobler H, Hadjez J,Lerner Y. Brief report: Circadian Melatonin, Thyroid-stimulating Hormone, Prolactin and Cortisol levels inserum of Young adults with Autism. J Autism DevDisord 1995; 25(6): 641-54.
7. Hoshiko S, Grether JK, Windham GC, Smith D,Fessel K. Are thyroid hormone concentrations at birthassociated with subsequent autism diagnosis? JAutism Research 2011; 4(6): 456-63.
9. Kellman R. The Autism – Thyroid connection. JDev Delay 2011; 15.
10. Gillberg IC, Gillberg C, Kopp S. Hypothyroidismand autism spectrum disorders. J Child PsycholPsychiatry 1992; 33 (3): 531-42.
11. Howdeshell KL. A model of the development ofthe brain as a construct of the thyroid system.Environ Health Perspect 2000; 110(3): 337-48.
12. Iwata K, Matsuzaki H, Miyachi T, Shimmura C,Suda S, Tsuchiya K J, Matsumoto K, Suzuki K, IwataY, Nakamura K, Tsujii M, Sugiyama T, Sato K, MoriN. Investigation of the serum levels of anteriorpituitary hormones in male children with autism. JMolecular Autism 2011; 2(16).
15. Campbell M, Small AM, Hollander CS, Korein J,Cohen IL, Kalmijn M, Ferris S. A controlledcrossover study of Triiodothyronine in AutisticChildren. J Autism and childhood Schizophrenia1978; 8(4): 371-81.
Introduction:In the developed world between 1% and 2% of all reported pregnancies are ectopic pregnancies1. It seriously compromise women’s health and future fertility. Currently ectopic pregnancy diagnosed before the patient condition has deteriorated. Currently diagnosis relies on a combination of ultrasound scanning and serial serum beta-Human chorionic gonadotrophin (b-hCG) measurements2.Timely diagnosis allows the clinician to consider the full range of treatment options. This is important for treatment success and retaining optimal fertility for those women desiring future pregnancy. The etiology of ectopic pregnancy remains uncertain although a number of risk factors have been identified. Its diagnosis can be difficult. The risk factors are maternal: pelvic inflammatory disease, Chlamydia trachomatis infection, smoking, tubal surgery, induced conception cycle and endometriosis. The annual incidence of ectopic pregnancy has increased over the past 30 year3. In the western world 4-10% of pregnancy related deaths have been observed from this issue and now it is growing problem in developing countries also4.
The treatment options are expectant management, medical treatment or surgery. In surgery laparoscopy is now the accepted approach to perform salpingostomy or salpingectomy. Concerning medical treatment, systemic administration of methotrexate (MTX) has gained acceptance in selected patients. It is given intramuscularly either in a fixed multiple dose regimen alternated with folinic acid or in a single dose regimen without folinic acid. Expectant management has been advocated based on the knowledge that the natural course of many early ectopic pregnancy is a self-limiting process, ultimately resulting in tubal abortion or re-absorption.
Types of Ectopic pregnancy:The fallopian tube is the dominant site in the majority cases of EP5. 75-80% of EPs occur in ampullary portion, 10-15% EPs occur in the isthmic portion and about 5% of EP is in the fimbrial end of the fallopian tube6. Cervical EP is rare and represents only 0.15% of all EP7. Ovarian EP is one of the rarest variants, and incidence is estimated to be 0.15-3% of all ectopic pregnancy8. Caesarean scar EP is another rarest form of EP with an incidence of 1:1800 pregnancies due to increase number of caesarean
deliveries over the last 30 years9. Abdominal EP with 1.3% of cases are diagnosed at a rate of 1:10,000 births and is an extremely rare and serious form of extrauterine gestation10. A heterotopic EP is diagnosed when women have any of the above said EP in conjunction with an intrauterine pregnancy. It is also more common (1-3%) in in vitro fertilization and fertility treatments involved super ovulatory drugs11.
Etiology:The exact etiology of EP is unknown. However, it is thought that tubal implantation occurs as a result of a combination of arrest of the embryo in the fallopian tube and changes in the tubal micro environment that allow early implantation to occur12. Inflammation within the tube, resulting from infection or smoking, may effect embryo-tubal transport by disrupting smooth muscle contractility and ciliary beat activity.
Clinical Presentation:Patients with an EP commonly present with pain and vaginal bleeding between 6 and 10 weeks of gestation13. However, these are common symptoms in early pregnancy, with one third of women experiencing some pain and/or bleeding14. Shoulder tip pain, syncope and shock occur in up to 20% of women and abdominal tenderness in more than 75%. Cervical motion tenderness has been reported in up to 67% of cases, and a palpable adnexal mass in about 50%15. In 2006-2008 Center for Maternal and Child Enquiries (CMACE) report, four of the six women who died from EP complained of diarrhea, dizziness or vomiting as early symptoms, without triggering any consideration of extrauterine pregnancy by their medical attendants16. However, it remains difficult to diagnose an EP from risk factors, history and examination alone.
Diagnosis:Initial diagnosis of first trimester hemorrhage presents an important challenge17. Recently, detection of EP is determined through serum b-hCG levels and vaginal ultrasonography technique18. A single serum measurement of the b-hCG concentration may not show the location of gestational sac. Demonstration of normal doubling of serum levels over 48 hours supports a diagnosis of fetal viability but does not rule out EP. Failing levels on raising the level of b-hCG concentration to reach 50% of confirm non-viability suggesting EP. In contrast with b-hCG concentrations, serum progesterone levels are stable for first 8-10 weeks of gestation. Investigate that sensitivity ranged of progesterone from 45-100% depending on the threshold. Both high (>22 ng/ml) and low ( 5 ng/ml) cutoff points have been assessed for their ability to correctly identify non-viable and ectopic pregnancies; serum progesterone levels 5 ng/ml could apparently be used to predict EP with 70-
90% sensitivity and 30-90% specificity19. If patient have serum progesterone measurement below 10ng/ml and b-hCG level below 1500 mIU/L are more likely to demonstrate spontaneous resolution of EP. Transvaginal ultrasound scan (TVS) is very popular from 1980, and by the mid 1990 sensitivity and specificity were calculated at 84.4 and 98.9% respectively it remains the gold standard for diagnosis of EP20.
Management:The treatment option of tubal EP involves surgical treatment by laparotomy or laparoscopy, and medical treatment is usually systemic or through local route, or by expectant treatment.
Expectant Treatment: Expectant management can be applied in a selected population of the patients with self-limiting EP. According to the most recent guideline, published by the American College of Obstetrician and Gyanecologists, there may be a role for expectant management when the b-hCG level is <200 IU/ml and which is further in decline phase. It should only be offered when TVS remains non-diagnostic and b-hCG levels continue to decline. Successful expectant management occurs in 98% of cases for bhCG <200 IU/L, in 73% for b-hCG <500 IU/L and in 25% for b -hCG <2,000 IU/L. If initial serum b-hCG<1,000IU/L then successful expectant managementmight occur in most patients (88%) with an EP sizeof <4 cm, without a fetal heart beat on transvaginalsonography; followed by haemoperitonium <50 ml. Evidence of ectopic resolution on scan is another wayto diagnosis. A decrease in EP size on day 7 had asensitivity of 84% and specificity of 100% inpredicting spontaneous resolution21.
Medical Treatment: Medical treatment of EP is quite less expensive than surgery22. Many different agent have been used to treat EP including systemic and local Methotrexate (MTX), local potassium chloride, hyperosmolar glucose, prostaglandins, danazol, etoposide and mifepristone23. Current therapies focus primarily on MTX treatments. Methotrexate (MTX) is a drug that inhibits the action of dihydrofolate reductase, thereby inhibiting DNA synthesis MTX affects actively proliferating tissues such as bone marrow, intestinal mucosa, malignant cells and trophoblastic tissue. MTX is contraindicated when embryonic cardiac motion or the presence of a gestational sac larger than 3.5 cm due to higher rate of treatment failure.
There are three different regimens for giving MTX: single dose, two-dose, and a fixed multidose protocol. The single 50 mg/m2 dose of MTX is most
commonly used, given as an intramuscular injection. βhCG levels are measured at 4 and 7 days post treatment with an expected 15% decrease from day 4 to day 7. Weekly βhCG levels are then checked until zero. If βhCG levels do not drop appropriately, a second MTX dose or surgical intervention is advised. Multidose regimen for MTX is available (MTX 1.0 mg/kg I/M daily; days 0,2,4 and 6 alternated with folinic acid 0.1 mg/kg orally on days 1,3,5,7)24. This treatment more appropriate for patient who present with a large adnexal mass and greater initial b-hCG level (5000 IU).
Surgical Treatment: Once the mainstay of therapy of EP, surgical treatment is now mainly reserved for patients with contraindication to medical management and for those with evidence of tubal rupture. Despite declining rates of surgical management, surgery remains the most definitive treatment of ectopic pregnancies. A laparoscopic approach is preferable to an open approach in a patient which haemodynamically stable. Laparoscopic procedure are associated with shorter operative times, less intraoperative blood loss, shorter hospital stays and lower analgesia requirements. Laparotomy should be reserved for patients who present with rupture and are in a state of hypovolaemic shock and compromise. Two techniques are described to remove the EP from the fallopian tube—1) Salpingectomy: The pregnancy is removed en bloc with the tube, 2) Salpingostomy: An incision is made on the fallopian tube over the swelling, the EP carefully removed with the forceps or irrigation and the incision should be either closed or let to heal by secondary intention. The success rate of salpingostomy is 92% and failure cases can be managed with MTX. Serial b-hCG measurement should be taken until undetectable to be certain that there is no persistence of trophoblastic tissue. Sometimes a prophylactic dose of MTX is given with salpingostomy25.
Literature Review:Gabbur et al. reported that on its retrospective analysis of stable women with small unruptured EP treated with single dose intramuscular MTX concluded that day 4 post treatmen b-hCG levels do not predict successful treatment or need for surgery26. Only day 7 b-hCG levels were associated with successful single dose MTX treatment26.
Barnhart et al. investigated in there meta-analysis of both regimens (single and multi-dose) and concluded that the multi dose regimen was more effective than single dose regimen, with success rate reported as 93% for multi dose regimen and 88% for the single dose regimen27.
Barnhart et al. was attempted by the challenge to develop an optimum regimen that balances efficacy and safety on the one hand and convenience on the other hand and it first described what is called the “double-dose-protocol”. In a study that included 101 patients, two doses of MTX were administered on days 0 and 4 without measuring b-hCG between doses. The authors reported a success rate of 76% after two doses and 87% after a further two doses28.
MTX treatment is very successful for small stable ectopic pregnancies. A meta-analysis of non-randomized studies showed success rate of 93% (95% CI 89-96%) for multi dose protocols and 88% (95% CI 89-96%) for single dose therapy29.
In one randomized controlled trial of laparoscopic surgery, prophylactic MTX lower the rate of persistent ectopic pregnancy 14.5-1.9%. The major benefit was in the shorter duration of post-operative monitoring30.
Several studies done to see the subsequent pregnancies after ectopic pregnancy. Studies suggest that around 60% of women affected by an EP go on to have a viable IUP. This figure includes those who do not plant to have another pregnancy and so the proportion will be higher if further pregnancy is planned. There is thought to be a 5-20% risk of a recurrence of EP with one previous EP and a risk of 32% or more following more than one previous ectopic. However the risk is reduced after each subsequent IUP.
Recent Advance:Previously ectopic pregnancy was diagnosed on clinical symptom, TVS and by measuring b-hCG, but now-a-days some new advancement arrived for diagnostic purpose.
VEGF is a potent angiogenic factor that acts as a vascular growth, remodeling and permeability in the endomertium, decidua and trophoblast. Daponte et al. described higher serum VEGF concentrations in women with EP (medium 227.2 pg/ml) than with abnormal intrauterine pregnancy (median 107.2 pg/ml) (p<0.001) and it concluded that VEGF serum concentrations might be a useful marker for- EP and suggested 174 pg/ml as the cut-off value for EP diagnosis31.
Existing evidence suggests elevated creatine kinase (CK) as a tool for diagnosis of EP. The trophoblast usually invades the muscular layer and maternal blood vessels are eroded, allowing muscle cell products such a CK to enter the circulation; therefore, increased serum CK levels are normal during EP32.
Conclusion:EP in developing countries is a serious threat, just because of poor medical facilities so that a significant morbidity rate and the potential for maternal death generally are seen. Management is dictated by the clinical presentation, serum b-hCG levels and TVS findings. Expert consultation with radiologists and gynecologists are recommended whenever EP is suspected. The use of MTX for treatment of early unruptured EP reported to be safe and effective. Surgical treatment is appropriate for women who are haemodynamically unstable or unlikely to be complained with post treatment monitoring and those who do not have immediate access to medical care. The preferred method of surgical treatment of EP today is diagnostic laparoscopy with salpingostomy and tubal conservation followed by prophylactic dose of MTX. Existing evidence suggests elevated vascular endothelial growth factor (VEGF) and creatine kinase (CK) as a tool for diagnosis of EP. Further new avenues are needed to explore less side effects of medication of EP.
Reference:1. Goldner TE, Lawson HW, Xia Z, et al.Surveillance for ectopic pregnancy - United States,1970-1989. MMWR CDC Surveill Summ 1993;42(6): 73–85.
2. Horne AW, Duncan WC, Critchley HO. The needfor serum biomarker development for diagnosing andexcluding tubal ectopic pregnancy. Acta ObstetGynecol Scand 2010; 89: 299–301.
3. Gamzu R, Almog B, Levin Y, Avni A, Jaffa A,Lessing J. Ef cacy of methotrexate treatment inextrauterine pregnancies de ned by stable orincreasing human chorionic gonadotropinconcentrations. Fertil Steril 2002; 77: 761–5.
10. Yildizhan R, Kurdoglu M, Kolusari A, Erten R.Primary omental pregnancy. Saudi Med J 2008; 9:606–9.11. Condous G, Okaro E, Bourne T. The conservativeman-agement of early pregnancy complications: areview of the lit-erature. Ultrasound Obstet Gynecol2003; 22: 420–30.
12. Shaw JL, Dey SK, Critchley HO, et al. Currentknowledge of the aetiology of human tubal ectopicpregnancy. Hum Reprod Update 2010; 16: 432–44.
14. Chez RA, Moore JG. Diagnostic errors in themanagement of ectopic pregnancy. Surg GynecolObstet. 1963; 117: 589–96.
15. Tay JI, Moore J, Walker JJ. Ectopic pregnancy.BMJ 2000; 320: 916–9.
16. Robson SJ, O’Shea RT. Undiagnosed ectopicpregnancy: a retrospective analysis of 31 ‘missed’ ectopic pregnancies at a teaching hospital. Aust N Z JObstet Gynaecol 1996; 36:182–5.
17. Daponte A, Pournaras S, Zintzaras E, KallitsarisA, Lialios G, Maniatis AN. The value of a singlecombined measure-ment of VEGF, glycodelin,progesterone, PAPP-A, HPL and LIF fordifferentiating between ectopic and abnormal intra-uterine pregnancy. Hum Reprod 2005; 20: 3163–6.
18. Felemban A, Sammour A, Tulandi T. Serumvascular endothelial growth factor as a possiblemarker for early ectopicpregnancy. Hum Reprod2002; 17: 490–2.
19. Dart R, Ramanujam P, Dart L. Progesterone as apredictor of ectopic pregnancy when the ultrasound isindeterminate. AmJ Emerg Med 2002; 20: 575–9.
20. Condous G. Ectopic pregnancy—risk factors anddiag-nosis. Aust Fam Physician 2006; 35: 854–7.
21. Rajesh V, Lawrence M. Evidence-basedmanagement ofectopic pregnancy. Curr ObstetGynaecol 2002; 12: 191–9.
22. Rodrigues SP, de Burlet KJ, Hiemstra E,Twijnstra AR, vanZwet EW, Trimbos-Kemper TC,Jansen FW. Ectopicpregnancy: when is expectantmanagement safe? Gynecol Surg 2012; 9: 421–6.
23. van Mello NM, Mol F, Mol BW, Hajenius PJ.Conser-vative management of tubal ectopicpregnancy. Best Pract Res 2009; 23: 509–518.
24. Condous G, Okaro E, Khalid A, Lu C, Van HS,Timmerman D. A prospective valuation of a single-visit strategy tomanage pregnancies of unknownlocation. Hum Reprod 2005; 20: 1398–1403.
25. Seeber BE, Barnhart KT. Suspected ectopicpregnancy. Obstet Gynecol 2006; 107: 399–413.
26. Gabbur N, Sherer DM, Hellmann M. Do serumbeta-human chorionic gonadotropin levels on day 4following methotrexate treatment of patients withectopic pregnancy pre-dict successful single-dosetherapy? Am J Perinatol 2006; 23:193–6.
28. Barnhart K, Hummel AC, Sammel MD, Menon S,Jain J, Cha-khtoura N. Use of ‘‘2-dose’’ regimen ofmethotrexate totreat ectopic pregnancy. Fertil Steril2007; 87: 250–6.
29. Horne AW, van den Driesche S, King AE, et al.Endometrial inhibin/activin beta-B subunitexpression is related to decidualization and is reducedin tubal ectopic pregnancy. J Clin Endocrinol Metab2008; 93: 2375–82.
30. Graczykowski JW, Mishell DR. Methotrexateprophy-laxis for persistent ectopic pregnancy afterconservative treat-ment by salpingostomy. ObstetGynecol 1997; 89: 118–22.
31. Daponte A, Pournaras S, Zintzaras E, KallitsarisA, Lialios G, Maniatis AN. The value of a singlecombined measure-ment of VEGF, glycodelin,progesterone, PAPP-A, HPL and LIF fordifferentiating between ectopic and abnormal intra-uterine pregnancy. Hum Reprod 2005; 20: 3163–6.
32. Chandra L, Jain A. Maternal serum creatinekinase as a biochemical marker of tubal pregnancy.Int J Gynaecol Obstet 1995; 49: 21–3.�
Introduction:Recurrent abdominal pain (RAP) is defined as at least 3 separate episodes of abdominal pain that occur in a 3-months period. These episodes are often severe,and the child is not able to do his or her normalactivities1. It is perhaps the most common painfulhealth problem in school-aged children. J Apley, aBritish pediatrician, studied abdominal pain amongchildren extensively and observed that approximately10% of school aged children get recurrent episodes ofabdominal pain. Affected children and their familiesexperience distress and anxiety that can interfere withtheir ability to perform regular activities.
Epidemiology: In general, population-based studies suggest that RAP is experienced by 10-15% of school-age children2. Epidemiological studies in Asia have reported similar prevalence. Boey and his colleagues studied RAP among school children in Malaysia and found a prevalence of 10.2% (urban 8.2-9.6%, rural 12.4%) 3,4. Similarly, Rasul and Khan reported RAP in11.5% of Bangladesh school children5. Cohort studies from India and Pakistan suggest that RAP is most likely to have an organic cause (up to 82% of cases), with giardiasis being the most common underlying condition14,15, while in Sri Lanka, commonest organic etiology is constipation16. However, another Indian cohort and a Sri Lankan cohort showed that non-organic RAP is more prevalent (74% and 76%, respectively)16. In Malaysia, both urban and rural population-based cohorts had a similar prevalence of RAP at 9.6% and 11%, respectively3.
Etiology: The origin of abdominal pain is complex and does not lend itself to a single model of causation. In the four decades since Apley's seminal research, conceptual models of RAP have evolved and become more complex1. Walker (1999) identified three distinct periods in this evolution. Studies conducted before the 1980s were characterized by a dualistic view of abdominal pain. When no organic etiology was identified, abdominal pain was assumed to be psychogenic. In the 1980s, the focus of research shifted to non-organic causes of RAP, including a host of psychosocial factors. Conceptual models emerging in this decade were increasingly multivariate in nature. They recognized that the cause of RAP may not be either organic or psychogenic, but possibly a function of normal (i.e., non-pathological) biological mechanisms. In the 1990s, the research focus shifted to the identification of individual differences among children with RAP and the interact mode RAP are multivariate and acknowledge the contributions of a variety of biological, psychological, and social factors16.
Organic Cause: Numerous organic disorders lead to abdominal pain; Possible causes that should be considered based on the history, physical examination and testing, are acid reflux, constipation, lactose intolerance, parasitic infections of the small and large intestines, Helicobacter pylori infection, inflammatory bowel diseases (IBD) such as Crohn’s disease and ulcerative colitis, celiac disease inflammation of the liver (hepatitis), gall bladder problems, an inflamed pancreas, an intestinal obstruction, appendicitis, and many more rare disorders.
Functional Gastrointestinal Disorders: Until a decade ago ‘functional gastrointestinal disorder’ was a label used for the conditions with uncertain etiology, and was a diagnosis of exclusion. In 1999 the pediatric Rome II criteria (Table I) introduced the term abdominal pain related-functional gastrointestinal disorders (AP-FGIDs); which include functional dyspepsia (FD), irritable bowel syndrome (IBS), abdominal migraine (AM), functional abdominal pain (FAP) and functional abdominal pain syndrome (FAPS). According to Caplan, et al. validation of pediatric Rome II criteria was done6. They found that more than half the patients classified as having functional problems met at least one pediatric Rome II criteria for FGID. Children with AP-FGIDs report significantly lower quality of life scores compared to healthy peers and AP-FGIDs are ranked as second in causing school absence. In 29.1% of patients with recurrent abdominal pain, pain persists even for more than 5 years, despite frequent medical attention.
The pathogenesis underlying AP-FGIDs remains unclear. It is thought to involve abnormalities in the enteric nervous system (ENS), a rich and complex nervous system that envelops the entire gastrointestinal tract. A dysregulation of this brain-gut communication plays an important role in the pathogenesis of functional abdominal pain. It is now believed that adults and children with functional bowel disorders, rather than having a baseline motility disturbance, may have an abnormal bowel reactivity to physiologic stimuli (meal, gut distension, hormonal changes), noxious stressful stimuli (inflammatory processes), or psychological stressful stimuli (parental separation, anxiety)16.
Additionally, adult patients with functional bowel disorders attending gastrointestinal clinics were often found to have psychological disturbances regardless of the final diagnosis. It was concluded that psychological factors may have been more important in determining health-seeking behavior than the cause of the symptom17. There is growing evidence to suggest that functional abdominal pain disorders may be associated with visceral hyperalgesia, a decreased threshold for pain in response to changes in intraluminal pressure18,19. Mucosal inflammatory processes attributable to infections, allergies, or primary inflammatory diseases may cause sensitization of afferent nerves and have been associated with the onset of visceral hyperalgesia20.
Moreover, studies conducted in the United States and Europe reported that psychological symptoms, low socio-economic status, parental gastrointestinal complaints and single parent- and immigrant-households are associated with chronic abdominal pain in children. To overcome drawbacks in Rome II criteria, they were revised and modified in 2006, and Rome III criteria were developed. Table II summarizes the Rome III criteria for pediatric FGID. Using Rome III criteria, a recent study in Sri Lanka has reported FGID in 93% of patients with non-organic RAP. Of them, 45.2% had functional abdominal pain12. Therefore, it is important to consider FGID in the differential diagnosis of RAP early in the evaluation.
Emotional/ Behavioral Stress: There is evidence suggesting that the presence of anxiety, depression or behavior problems is not useful in distinguishing between functional abdominal pain and abdominal pain of other causes. There is
Traumatic Rupture of Duodenum: A Case ReportRahman MA1, Imam HM2
Abstract:Isolated duodenal rupture after blunt abdominal trauma is infrequent, liable to be missed and is associated with high morbidity and significant mortality. Diagnostic delay is a part of clinical picture in most of these cases, considering its anatomical location & lack of peritoneal sign. Among different modalities, use of CT scan for diagnosis is widely appreciated. Majority of duodenal injury can be managed by simple repair of injured site. But delayed presentation, lack of optimal diagnostic approach & delayed surgical intervention have results in many post-operative complication & hamper the possible outcome. The case of young traumatized patient with isolated duodenal rupture is presented to highlight these issues.
1Professor Md. Ataur Rahman, Department of Surgery, Eastern Medical College. 2Dr. HM Hasan Imam, Assistant Registrar, Department of Surgery, Eastern Medical College.
Address of Correspondence: Professor Md. Ataur Rahman, Professor & Head, Department of Surgery, Eastern Medical College, Comilla. Mobile: +8801711721098, Email: [email protected]
H2a. Diagnostic criteria* for functional dyspepsia Must include all of the following: 1. Persistent of recurrent pain or discomfort centered in the upper abdomen (above the umbilicus).2. Not relieved by defecation or associated with the onset of a change in stool frequency or stool form(i.e., not irritable bowel syndrome).3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’s symptoms.
H2b. Diagnostic criteria* for irritable bowel syndrome Must include all of the following: 1. Abdominal discomfort (an uncomfortable sensation not described as pain) or pain associated with 2 or more of the following at least 25% of the time:(a) Improved with defecation(b) Onset associated with a change in frequency of stool; and (c) Onset associated with a change in from (appearance) of stool.2. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms.H2c. Diagnostic criteria† for abdominal migraine Must include all of the following: 1. Paroxysmal episodes of intense acute periumbilical pain that lasts for 1 hours or more.2. Intervening periods of usual health lasting weeks to months.3. The pain interferes with normal activities.4. The pain is associated with 2 or more of the following: anorexia, nausea, vomiting, headache,photophobia, pallor.5. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms. H2d. Diagnostic criteria* for childhood functional abdominal pain Must include all of the following: 1. Episodic or continuous abdominal pain.2. Insufficient criteria for other functional gastrointestinal disorders.3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms.H2d1. Diagnostic criteria*for childhood functional abdominal pain syndrome Must include childhood functional abdominal pain at least 25% of the time and 1 or more of the following: 1. Some loss of daily functioning2. Additional somatic symptoms such as headache, limb pain, or difficulty in sleeping H1c. Diagnostic criteria* for aerophagia Must include at least 2 of the following: 1. Air swallowing.2. Abdominal distension due to intraluminal air.3. Repetitive belching and/or increased flatus.
Table II: Rome III Diagnostic Criteria for Pediatric Functional Bowel Disorders.
History: Red Flags Weight loss Persistent right upper or right lower quadrant pain Unexplained fevers Pain radiating to the back Unexplained rashes Arthritis Persistent vomiting Recurrent oral ulcers Dysphagia/odynophagia Anal/perianal ulcers Hematemesis Nocturnal symptoms (waking with diarrhea and/or vomiting) Bilious emesis Delayed puberty Chronic diarrhea (> 2 weeks) Deceleration of linear growth velocity Hematochezia/melena Physical Exam: Red Flags Decline in weight/height parameters Abdominal mass Pallor or anemia Localized tenderness Abdominal distension Perianal fissures or ulcers Organomegaly (hepatosplenomegaly) Positive hemoccult stool test
Table III: “Red Flags” In History and Examination of Recurrent Abdominal Pain.
Figure 1, 2: Huge bile, blood & food mixed fluid & material revealed after opening the abdomen by upper midline incision
Figure 3: Large perforation found in the 2nd part of duodenum
evidence that patients with recurrent abdominal pain have more symptoms of anxiety and depression (internalizing emotional symptoms) than do healthy community controls. In contrast, there is evidence that children with recurrent abdominal pain do not
have higher levels of conduct disorder and oppositional behavior (externalizing emotional symptoms) compared with healthy community controls. There are no data on whether emotional/behavioral symptoms predict symptom severity, course or response to treatment. There is evidence suggesting that children with recurrent abdominal pain are at risk of later emotional symptoms and psychiatric disorder.
Clinical Features: The primary feature of FAPS is abdominal pain. Usually, the pain is located around the umbilicus, however the pattern or location of abdominal pain is not always predictable. The pain may occur suddenly
or slowly increase in severity. The pain may be constant or may increase and decrease in severity. Some children with functional abdominal pain may experience dyspepsia, or upper abdominal pain associated with nausea, vomiting, and/or a feeling of fullness after just a few bites (early satiety). Others may experience abdominal pain with bowel movements. Pain that is usually relieved by bowel movements, or associated with changes in bowel
movement habits (mainly constipation, diarrhea, or constipation alternating with diarrhea) is the classic irritable bowel syndrome (IBS) (Table II). However, many diseases can cause chronic abdominal pain.
Therefore, any structural, organic, or chemical disease should be excluded. Patients with RAP often have pain-related behaviors. First, they often deny a role for psychosocial stressors. However, pain may diminish when patients are engaged in distracting activities but increase when they are discussing a psychologically distressing issue. Second, they express pain through verbal and nonverbal methods. They urgently report intense symptoms disproportionate to the available clinical and laboratory data. Third, they seek health care frequently. They often visit the emergency room and request analgesics. Fourth, they request diagnostic studies or even exploratory surgery to determine the organic origin of their condition. Fifth, they focus attention on complete relief of pain rather than on adapting to having a disease. Sixth, they take on limited personal responsibility for self-management. In addition to these features, distinct psychopathologies are usually found in patients with FAPS, including depressive disorders, anxiety disorders, and somatoform disorder.
History and Physical Exam: A complete history should be taken including social and dietary history and look for red flag symptoms and signs (Table III), Conduct a thorough physical exam, including rectal exam with stool hemoccult OR perianal exam with hemoccult of stool brought in by patient/family and review of the child’s growth. Children with recurrent abdominal pain are more likely than children without recurrent abdominal pain to have headache, joint pain, anorexia, vomiting, nausea, excessive gas and altered bowel symptoms. The presence of alarm symptoms or signs suggests a
higher pretest probability or prevalence of organic disease and may justify the performance of diagnostic tests. Alarm symptoms or signs include, but are not limited to, involuntary weight loss, deceleration of linear growth, gastrointestinal blood loss, significant vomiting, chronic severe diarrhea, persistent right upper or right lower quadrant pain, unexplained fever and family history of inflammatory bowel disease. The ‘red flag’ signs have long been used by clinicians to guide themselves to identify children who need further investigations and the salient ones on history and examination are noted in Table III 7,8.� Investigations: Investigations may be required to exclude particular conditions suggested by the history and examination. It is useful to pursue further diagnostic testing only in the presence of alarm symptoms9. Laboratory studies may be unnecessary if the history and physical examination clearly lead to a diagnosis of functional abdominal pain. However, a complete blood cell count, sedimentation rate, stool test for parasites (especially Giardia), and urinalysis are reasonable screening studies. If inflammatory bowel disease is suspected the sedimentation rate is often elevated. The finding of an abnormal sedimentation rate would make one look
further for an inflammatory, infectious, or neoplastic disorder. If indicated, an ultrasound examination of the abdomen can give information about kidneys, gallbladder, and pancreas; with lower abdominal pain, a pelvic ultrasonogram may be indicated.
An upper gastrointestinal tract x-ray series is indicated if one suspects a disorder of the stomach or small intestine. Helicobacter pylori infection does not seem to be associated with RAP. In patients with symptoms suggestive of gastritis or ulcer an H. pylori test (serum or fecal) may be performed to document the infection.
Esophagogastroduodenoscopy is indicated with symptoms suggestive of persistent upper gastrointestinal pathology. In the absence of this suspicion, esophagogastroduodenoscopy is unlikely to identify an abnormality and is usually not necessary.
Management: The family and the child with functional RAP may worry about the inability to identify an organic cause and may be resistant to a diagnosis of nonorganic disease. After a thorough history and physical examination the most important component of the treatment is reassurance of the children and family members10. Specifically, they need to be reassured that no evidence of a serious underlying disorder is present. Acknowledgment that the child's pain is real but not life-threatening is essential. When understood and accepted, this reassurance concludes the child and family's search for a physical cause and allows them to move into the next stage of learning to cope.
Dietary management: Data on dietary intervention are scarce and deal mainly with fiber supplementation and lactose exclusion. Whereas dietary fibre supplementation is a recognized strategy for management for childhood constipation, its value in recurrent abdominal pain is uncertain. The two randomized trials comparing fiber treatment with placebo have yielded conflicting results22,23. The data on lactose-free diets are likewise inconclusive, and a Cochrane review calls for ‘well-designed trials of all recommended dietary interventions’24.
A sensible course, despite lack of published evidence, is to recommend healthy eating including plenty of fruit and vegetables, regular sensible meals and plenty of fluids. This should be coupled with a daily routine with plenty of physical activity.
Symptom-based pharmacological therapies: In some cases, symptom-based pharmacological therapies are helpful. Medications for functional abdominal pain are best prescribed judiciously as part of a multifaceted, individualized approach to relieve symptoms and disability. It is reasonable to consider the time-limited use of medications that might help to decrease the frequency or severity of symptoms. Treatment might include acid reduction therapy for pain associated with dyspepsia; antispasmodic agents, smooth muscle relaxants, or low doses of psychotropic agents for pain or nonstimulating laxatives or antidiarrheals for pain associated with altered bowel pattern.
Cognitive–behavioural therapy: In many instances, all that is needed from the doctor is acknowledgment of the symptoms and reassurance that there is no serious underlying organic disease.
Sanders et al., compared this approach (standard paediatric care) with cognitive–behavioural therapy and found that both groups improved, though the response was somewhat better in the cognitive–behavioural therapy group21. They suggested that psychological intervention may have a role in difficult cases.
Family Functioning: Education of the family is an important part of treatment of the child with functional abdominal pain. It is often helpful to summarize the child’s symptoms and explain in simple language that although the pain is real, there is most likely no underlying serious or chronic disease. It may be helpful to explain that recurrent abdominal pain is a common symptom in children and adolescents, yet few have a disease. Functional abdominal pain can be likened to a headache, a functional disorder experienced at some time by most adults, which very rarely is associated with serious disease.
It is important to provide clear and age-appropriate examples of conditions associated with hyperalgesia, such as a healing scar, and manifestations of the interaction between brain and gut, such as the diarrhea or vomiting children may experience during stressful situations is recommended that reasonable treatment goals be established, with the main aim being the return to normal function rather than the complete disappearance of pain. Return to school can be encouraged by identifying and addressing obstacles to school attendance.
Prognosis: Many of the studies on prognosis relate to hospital practice not primary care10. It is generally more likely that children with recurrent abdominal pain will develop chronic abdominal symptoms in adulthood and as many as 30% may continue thus. Many will continue to suffer from IBS11,12. There is evidence that children with recurrent abdominal pain are more likely to have emotional and psychiatric disorders later in life. Generally speaking, however, follow-up studies show that parental factors rather than the psychological characteristics of the child are more important when predicting persistence of abdominal pain.
Conclusion:Recurrent abdominal pain (long-standing intermittent or constant abdominal pain) is common in children and adolescents. In most children, recurrent abdominal pain is functional—that is, without objective evidence of an underlying organic disorder. Yet an important part of the physician’s job is to determine which children have an organic disorder. A review of the current evidence, however, indicates
that there are no studies showing that pain frequency, severity, location or effects on lifestyle help to discriminate between functional and organic disorders. There have been few studies of the treatment of recurrent abdominal pain in children. There is inconclusive evidence that a lactose-free diet decreases symptoms or that a fiber supplement decreases the frequency of pain attacks. There is inconclusive evidence of the benefit of acid suppression with H2-receptor antagonists to treat children with dyspepsia. There is also evidence that cognitive/behavioral therapy may be useful in improving pain and disability outcome in the short term.
References:
1. Apley J. The child with recurrent abdominal pain.Pediatr Clin North Am 1967; 14: 63–72.
2. Huang RC, Plamer LJ, Forbes DA. Prevalence andpattern of childhood abdominal pain in an Australiangeneral practice. J Paediatr Child Health 2000; 36:349-353.
3. Boey CC, Yap S, Goh KL. The prevalence ofrecurrent abdominal pain in 11- to 16-year-oldMalaysian schoolchildren. J Paediatr Child Health2000; 36: 114-116.
4. Boey CC, Goh KL. Predictors of recurrentabdominal pain among 9 to 15-year-old urban school-children in Malaysia. Acta Paediatr 2001; 90: 353-5.
5. Rasul CH, Khan MAD. Recurrent abdominal painin school children in Bangladesh. J Ceylon Coll Phys 2000; 33: 110-14.
6. Caplan A, Walker L, Rasquin A. Validation of thePediatric Rome II criteria for functionalgastrointestinal disorders using the questionnaire onpediatric gastrointestinal symptoms. J PediatrGastroenterol Nutr 2005; 41: 305-16.
7. Pearl RH, Irish MS, Caty MG, Glick PL. Theapproach to common abdominal diagnosis in infantsand children. Part II. Pediatr Clin North Am 1998;45: 1287-1326.
10. Huertas-Ceballos A, Logan S, Bennett C, et al.Psychosocial interventions for recurrent abdominalpain (RAP) and irritable bowel syndrome (IBS) inchildhood. Cochrane Database Syst Rev 2008; (1):CD003014.
11. El-Matary W, Spray C, Sandhu B. Irritable bowelsyndrome: the commonest cause of recurrent abdominalpain in children. Eur J Pediatr 2004; 163(10): 584-8.
12. Nygaard EA, Stordal K, Bentsen BS. Recurrentabdominal pain in children revisited: irritable bowelsyndrome and psychosomatic aspects. A prospectivestudy. Scand J Gastroenterol 2004; 39(10): 938-40.
13. Balani B, Patwari AK, Bajaj P, Diwan N, AnandVK. Recurrent abdominal pain - a reappraisal. IndianPediatr 2000; 37: 876-81.
14. Buch NA, Ahmad SM, Ahmad SZ, Ali SW, CharooBA, Hussan MU. Recurrent abdominal pain in children.Indian Pediatr 2002; 39: 830-4.
15. Stordal K, Nygaard EA, Bentsen B. Organicabnormalities in recurrent abdominal pain in children.Acta Paediatr 2001; 90: 1-5.
16. Drossman DA, Camilleri M, Mayer EA, WhiteheadWE. AGA technical review on irritable bowelsyndrome. Gastroenterology 2002; 123: 2108–31.
17. Whitehead WE, Bosmajian L, Zonderman AB,Costa PT Jr, Schuster MM. Symptoms of psychologicdistress associated with irritable bowel syndrome.Comparison of community and medical clinic samples.Gastroenterology 1988; 95: 709–14.
18. Van Ginkel R, Voskuijl WP, Benninga MA, TaminiauJA, Boeckxstaens GE. Alterations in rectal sensitivityand motility in childhood irritable bowel syndrome.Gastroenterology 2001; 120: 31–8.
19. Di Lorenzo C, Youssef NN, Sigurdsson L, ScharffL, Griffiths J, Wald A. Visceral hyperalgesia in children with functional abdominal pain. J Pediatr 2001; 139: 838–43.
20. Talley NJ, Spiller R. Irritable bowel syndrome: alittle understood organic bowel disease. Lancet 2002;360: 555–64.
21. Sanders MR, Shepherd RW, Cleighorn G, WoolfordH. The treatment of recurrent abdominal pain inchildren: a controlled comparison ofcognitive–behavioural family intervention and standardpediatric care. J Cons Clin Psychol 1994; 62: 306-14.
23. Feldman W, McGrath P, Hodgson C, Ritter H,Shipman RT. The use of dietary fiber in themanagement of simple, childhood, idiopathic, recurrent,abdominal pain. Am J Dis Child 1985; 139: 1216-18.
24. Huertas-Ceballos A, Macarthur C, Logan S.Dietary interventions for recurrent abdominal pain(RAP) in childhood (Cochrane Review). In: TheCochrane Library. Issue 1, 2004.
Introduction:Injuries, especially as a result of blunt trauma, now constitutes one of the major causes of death in our country. The frequency of trauma to the abdomen may be increasing in almost geometric proportion as the number & speed of highway vehicles, civil unrest & terrorist attack rises.
Abdominal Trauma is a common clinical entity occurring in an emergency surgical unit and Blunt abdominal injury causing hollow viscous rupture is a common squeal. According to East multi-institutional trial of trauma indicate that after blunt abdominal trauma the incidence of small bowel injury and small bowel perforation (SBP) 1.1% and 0.3%, respectively1.
Case report:This is a story of a 20 years old boy. He had a history of road traffic accident 3 days back where he encountered by tin at supra umbilical region on right side. He was treated by local physician. On next morning he developed increasing abdominal pain, vomiting, respiratory distress & his conditions were deteriorating. On examination (OE) his abdomen was very tender & rigid, Blood Pressure (BP) - 100/60 mm Hg, Respiratory rate (RR) - 24/min, Pulse rate (PR) - 110/min. X-ray abdomen in erect posture including both dome of diaphragm revealed free gas shadow under both dome of diaphragm. Then other necessary investigations for assessing fitness for anaesthesia were done & Patient was prepared for exploratory laparotomy.
Abdomen was opened by upper midline incision revealing peritoneal cavity (Fig. 1, 2) with huge bile mixed food material & blood mixed fluid. Then content was sucked & peritoneal toileting was done. On query, large perforation was found in the 2nd part of duodenum (Fig. 3) about 10 cm distal to Gastro-Duodenal (G-D) junction & there was no other injury. Primary repair was done & two drain tube were kept in situ.
On 5th post-operative day (POD) patient was allowed to take liquid diet & sips of water orally. At the mean time observing for drain collection, abdominal pain, fever, vomiting & any discharge from wound.
On 7th POD patient was allowed to semi solid diet. Finally the drain tubes were removed on 9th POD. The recovery was uneventful. The patient left hospital giving thanks to all.
Discussion:Blunt abdominal trauma (BAT) may be from direct compression of the abdomen against a fixed object with resulting tears or subcapsular haematoma involving the solid organ associated viscera2. Hollow organs (typically small intestine) may rupture due to compression against a fixed point, usually the vertebral column. This compression causes rapid increase in intraluminal pressure leading to perforation of bowel wall at the anti-mesenteric border, where bowel is usually weaker2. Isolated duodenal injuries following a blunt abdominal trauma is uncommon. Complete transaction of duodenum is very rare presentation2. The
most common cause of blunt abdominal trauma (BAT) is motor vehicle accident (MVA).
Patients with multiple lower rib fractures are notorious for having severe intra-abdominal injuries without significant abdominal pain. The severe pain from the rib fractures becomes a distracting injury for the less noticeable abdominal pain. As a result, the patient may have a poor outcome as abdominal injuries are not recognized.
Spontaneous perforation of an hollow viscus may be the result of a range of pathological processes, where diagnosis is relatively easy for surgeon. But isolated duodenal perforation after blunt abdominal trauma is still a diagnostic challenge to surgeon.
One third of our patient did not present to the hospital until after an average of three days with advanced peritonitis. Reasons put forward to explain such delay include: 1. Relatively less initial peritoneal irritation
induced by the nearly neutral intestinal content particularly those with perforation between the duodeno-jejunal flexure and the ileo-caecal junction; 2. In small gut perforations the mucosa may prolapse through the hole and partly seal it making early sign of misleading; 3. The entity of a delayed perforation caused by an evolving injury. These patient have an initial contused bowel wall at the time of trauma that ultimately gives way after a variable period with resultant peritonitis. For this reason, physical examination during the initial evaluation is reliable for an early diagnosis in only 30% of blunt trauma injuries, in those patients who exhibit clear peritoneal signs3.
Abdominal pain, the usual symptom indicating abdominal injury is not severe & therefore the patient did not seek hospital care soon after injury most probably due to the above reasons.
Initial approach to the blunt abdominal trauma (BAT) patient is done according to fundamental principles of
advanced trauma life support (ATLS) system, which compromise primary survey & resuscitation [ABCDE (Airway, Breathing, Circulation, Disability, Exposure) of trauma care, steps of resuscitation, re-evaluation of ABC, monitoring the vital sign, introduction of gastric tube or Foley’s catheter] and secondary survey (careful abdominal examination & to identify all other injuries).
Several diagnostic modalities are being used for the identification of isolated bowel perforation. These are X-ray abdomen in erect posture including both domeof diaphragm, Serum amylase, WBC count, focusedassessment with sonography for trauma (FAST),diagnostic peritoneal lavage (DPL), Abdominal CT.Free sub-diaphragmatic gas, a radiologic signindicative of hollow viscus perforation easilydetected in plain abdominal radiographs, could leadto an early diagnosis in only 7-8% of the cases4,5.Elevated white blood cell (WBC) count and serumamylase levels could be suggestive of an intra-abdominal process and aid diagnosis in conjunctionwith history and physical findings. Althoughabnormal serum amylase can be noted in such cases,no clear cut-off value that could help differentiatepatients with SBP could be determined4. Focusedassessment with sonography for trauma (FAST) playan important roles to detect the free intra-peritonealfluid and haemo-pericardium in the assessment ofacutely traumatized patient, with the sensitivity of91-100%6. Diagnostic peritoneal lavage (DPL) canidentify Small bowel perforations (SBP) with greatsensitivity (up to 100%) but relatively lowspecificity7,8. CT has proved to be the gold-standardexamination, contributing toward a significantreduction of morbidity and mortality in traumavictims9,10. Postoperative complications like woundinfection, would dehiscence, intra-abdominal abscess,acute respiratory distress syndrome and sepsis, alloccur at two to three times higher incidence inpatients who undergo surgical repair of Small bowelperforations with extended delay11,12. The keyindividual in the development of a system of traumacare is the general surgeon.
Treatment:Urgent hospitalization of patient preferably in ICU with initial resuscitation, side by side preparation of the patient for laparotomy. After laparotomy, thorough surgical toileting, identification of injury, repair, re-toileting then drain were given. Associated injury were also looked for & treated. Abdomen was closed in layer. A meticulous follow up of the patient is needed for good outcome.
Conclusion:We present a case of successful repair of 3 days old traumatic duodenal perforation. Isolated duodenal perforation in blunt abdominal trauma victim is hard to diagnosis. Early diagnosis & appropriate operative management which are imperative to prevent morbidity in many cases. The rarity of duodenal perforation, the patient's good general condition following road traffic accident & treatment by local physician delayed the diagnosis. Cornerstone to successful management is combination of detailed history including the mechanism of injury, thorough clinical examination & Investigation under close supervision, surgical procedures to identify the perforation & repair.
References:1. Watts DD, Fakhry SM. Incidence of hollow viscusinjury in blunt trauma: an analysis from 275,557trauma admissions from the East multi-institutionaltrial. J Trauma 2003; 54(2): 289-94.
2. AH Dauterive, L Flancbaum, EF Cox. Bluntintestinal trauma. A modern-day review. Ann Surg1985; 201(2): 198-203.
3. Guarino J, Hassett JM Jr, Luchette FA. Smallbowel injuries: mechanisms, patterns, and outcome. JTrauma 1995; 39(6): 1076-80.
4. Fang JF, Chen RJ, Lin BC, Hsu YB, Kao JL, KaoYC, Chen MF. Small bowel perforation: is urgentsurgery necessary? J Trauma 1999; 47(3): 515-20.
5. Mathonnet M, Peyrou P, Gainant A, Bouvier S,Cubertafond P. Role of laparoscopy in bluntperforations of the small bowel. Surg Endosc 2003;l7(4): 641-5.
6. Fakhry SM, Watts DD, Luchette FA; EAST Multi-Institutional Hollow Viscus Injury Research Group.Current diagnostic approaches lack sensitivity in thediagnosis of perforated blunt small bowel injury:analysis from 275,557 trauma admissions from theEAST multi-institutional HVI trial. J Trauma 2003;54(2): 295-306.
7. Neugerbauer H, Wallenboeck E, Hungerfort M.Seventy cases of injuries of the small intestine causedby blunt abdominal trauma: a retrospective studyfrom 1970 to 1994. J Trauma 1999; 46(1): 116-21.
8. Fabian TC, Mangiante EC, White TJ, PattersonCR, Boldreghini S, Britt LG. A prospective study of91 patients undergoing both computed tomographyand peritoneal lavage following blunt abdominaltrauma. J Trauma 1986; 26(7): 602-8.
9. Gay SB, Sistrom CL. Computed tomographicevaluation of blunt abdominal trauma. Radiol ClinNorth Am 1992; 30(2): 367-88.
10. Fakhry SM, Brownstein M, Watts DD, Baker CC,Oller D. Relatively short diagnostic delays (<8 hours)produce morbidity and mortality in blunt small bowelinjury: an analysis of time to operative intervention in198 patients from a multicenter experience. J Trauma2000; 48(3): 408-14.
11. Mirvis SE, Gens DR, Shanmuganathan K.Rupture of the bowel after blunt abdominal trauma:diagnosis with CT. Am J Roentgenol 1992; 159(6):1217-21.
12. Ma OJ, Kefer MP, Stevison KF, Mateer JR.Operative versus nonoperative management of bluntabdominal trauma: role of ultrasound-measuredintraperitoneal fluid levels. Am J Emergency Med2001; 19(4): 284-6.�
* Criteria fulfilled at least once per week for at least 2 months before diagnosis.† Criteria fulfilled 2 or more times in the preceding 12 months.
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Case Report
Traumatic Rupture of Duodenum: A Case ReportRahman MA1, Imam HM2
Abstract:Isolated duodenal rupture after blunt abdominal trauma is infrequent, liable to be missed and is associated with high morbidity and significant mortality. Diagnostic delay is a part of clinical picture in most of these cases, considering its anatomical location & lack of peritoneal sign. Among different modalities, use of CT scan for diagnosis is widely appreciated. Majority of duodenal injury can be managed by simple repair of injured site. But delayed presentation, lack of optimal diagnostic approach & delayed surgical intervention have results in many post-operative complication & hamper the possible outcome. The case of young traumatized patient with isolated duodenal rupture is presented to highlight these issues.
1Professor Md. Ataur Rahman, Department of Surgery, Eastern Medical College. 2Dr. HM Hasan Imam, Assistant Registrar, Department of Surgery, Eastern Medical College.
Address of Correspondence: Professor Md. Ataur Rahman, Professor & Head, Department of Surgery, Eastern Medical College, Comilla. Mobile: +8801711721098, Email: [email protected]
H2a. Diagnostic criteria* for functional dyspepsia Must include all of the following: 1. Persistent of recurrent pain or discomfort centered in the upper abdomen (above the umbilicus).2. Not relieved by defecation or associated with the onset of a change in stool frequency or stool form(i.e., not irritable bowel syndrome).3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’s symptoms.
H2b. Diagnostic criteria* for irritable bowel syndrome Must include all of the following: 1. Abdominal discomfort (an uncomfortable sensation not described as pain) or pain associated with 2 or more of the following at least 25% of the time:(a) Improved with defecation(b) Onset associated with a change in frequency of stool; and (c) Onset associated with a change in from (appearance) of stool.2. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms.H2c. Diagnostic criteria† for abdominal migraine Must include all of the following: 1. Paroxysmal episodes of intense acute periumbilical pain that lasts for 1 hours or more.2. Intervening periods of usual health lasting weeks to months.3. The pain interferes with normal activities.4. The pain is associated with 2 or more of the following: anorexia, nausea, vomiting, headache,photophobia, pallor.5. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms. H2d. Diagnostic criteria* for childhood functional abdominal pain Must include all of the following: 1. Episodic or continuous abdominal pain.2. Insufficient criteria for other functional gastrointestinal disorders.3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms.H2d1. Diagnostic criteria*for childhood functional abdominal pain syndrome Must include childhood functional abdominal pain at least 25% of the time and 1 or more of the following: 1. Some loss of daily functioning2. Additional somatic symptoms such as headache, limb pain, or difficulty in sleeping H1c. Diagnostic criteria* for aerophagia Must include at least 2 of the following: 1. Air swallowing.2. Abdominal distension due to intraluminal air.3. Repetitive belching and/or increased flatus.
Table II: Rome III Diagnostic Criteria for Pediatric Functional Bowel Disorders.
History: Red Flags Weight loss Persistent right upper or right lower quadrant pain Unexplained fevers Pain radiating to the back Unexplained rashes Arthritis Persistent vomiting Recurrent oral ulcers Dysphagia/odynophagia Anal/perianal ulcers Hematemesis Nocturnal symptoms (waking with diarrhea and/or vomiting) Bilious emesis Delayed puberty Chronic diarrhea (> 2 weeks) Deceleration of linear growth velocity Hematochezia/melena Physical Exam: Red Flags Decline in weight/height parameters Abdominal mass Pallor or anemia Localized tenderness Abdominal distension Perianal fissures or ulcers Organomegaly (hepatosplenomegaly) Positive hemoccult stool test
Table III: “Red Flags” In History and Examination of Recurrent Abdominal Pain.
Figure 1, 2: Huge bile, blood & food mixed fluid & material revealed after opening the abdomen by upper midline incision
Figure 3: Large perforation found in the 2nd part of duodenum
evidence that patients with recurrent abdominal pain have more symptoms of anxiety and depression (internalizing emotional symptoms) than do healthy community controls. In contrast, there is evidence that children with recurrent abdominal pain do not
have higher levels of conduct disorder and oppositional behavior (externalizing emotional symptoms) compared with healthy community controls. There are no data on whether emotional/behavioral symptoms predict symptom severity, course or response to treatment. There is evidence suggesting that children with recurrent abdominal pain are at risk of later emotional symptoms and psychiatric disorder.
Clinical Features: The primary feature of FAPS is abdominal pain. Usually, the pain is located around the umbilicus, however the pattern or location of abdominal pain is not always predictable. The pain may occur suddenly
or slowly increase in severity. The pain may be constant or may increase and decrease in severity. Some children with functional abdominal pain may experience dyspepsia, or upper abdominal pain associated with nausea, vomiting, and/or a feeling of fullness after just a few bites (early satiety). Others may experience abdominal pain with bowel movements. Pain that is usually relieved by bowel movements, or associated with changes in bowel
movement habits (mainly constipation, diarrhea, or constipation alternating with diarrhea) is the classic irritable bowel syndrome (IBS) (Table II). However, many diseases can cause chronic abdominal pain.
Therefore, any structural, organic, or chemical disease should be excluded. Patients with RAP often have pain-related behaviors. First, they often deny a role for psychosocial stressors. However, pain may diminish when patients are engaged in distracting activities but increase when they are discussing a psychologically distressing issue. Second, they express pain through verbal and nonverbal methods. They urgently report intense symptoms disproportionate to the available clinical and laboratory data. Third, they seek health care frequently. They often visit the emergency room and request analgesics. Fourth, they request diagnostic studies or even exploratory surgery to determine the organic origin of their condition. Fifth, they focus attention on complete relief of pain rather than on adapting to having a disease. Sixth, they take on limited personal responsibility for self-management. In addition to these features, distinct psychopathologies are usually found in patients with FAPS, including depressive disorders, anxiety disorders, and somatoform disorder.
History and Physical Exam: A complete history should be taken including social and dietary history and look for red flag symptoms and signs (Table III), Conduct a thorough physical exam, including rectal exam with stool hemoccult OR perianal exam with hemoccult of stool brought in by patient/family and review of the child’s growth. Children with recurrent abdominal pain are more likely than children without recurrent abdominal pain to have headache, joint pain, anorexia, vomiting, nausea, excessive gas and altered bowel symptoms. The presence of alarm symptoms or signs suggests a
higher pretest probability or prevalence of organic disease and may justify the performance of diagnostic tests. Alarm symptoms or signs include, but are not limited to, involuntary weight loss, deceleration of linear growth, gastrointestinal blood loss, significant vomiting, chronic severe diarrhea, persistent right upper or right lower quadrant pain, unexplained fever and family history of inflammatory bowel disease. The ‘red flag’ signs have long been used by clinicians to guide themselves to identify children who need further investigations and the salient ones on history and examination are noted in Table III 7,8.� Investigations: Investigations may be required to exclude particular conditions suggested by the history and examination. It is useful to pursue further diagnostic testing only in the presence of alarm symptoms9. Laboratory studies may be unnecessary if the history and physical examination clearly lead to a diagnosis of functional abdominal pain. However, a complete blood cell count, sedimentation rate, stool test for parasites (especially Giardia), and urinalysis are reasonable screening studies. If inflammatory bowel disease is suspected the sedimentation rate is often elevated. The finding of an abnormal sedimentation rate would make one look
further for an inflammatory, infectious, or neoplastic disorder. If indicated, an ultrasound examination of the abdomen can give information about kidneys, gallbladder, and pancreas; with lower abdominal pain, a pelvic ultrasonogram may be indicated.
An upper gastrointestinal tract x-ray series is indicated if one suspects a disorder of the stomach or small intestine. Helicobacter pylori infection does not seem to be associated with RAP. In patients with symptoms suggestive of gastritis or ulcer an H. pylori test (serum or fecal) may be performed to document the infection.
Esophagogastroduodenoscopy is indicated with symptoms suggestive of persistent upper gastrointestinal pathology. In the absence of this suspicion, esophagogastroduodenoscopy is unlikely to identify an abnormality and is usually not necessary.
Management: The family and the child with functional RAP may worry about the inability to identify an organic cause and may be resistant to a diagnosis of nonorganic disease. After a thorough history and physical examination the most important component of the treatment is reassurance of the children and family members10. Specifically, they need to be reassured that no evidence of a serious underlying disorder is present. Acknowledgment that the child's pain is real but not life-threatening is essential. When understood and accepted, this reassurance concludes the child and family's search for a physical cause and allows them to move into the next stage of learning to cope.
Dietary management: Data on dietary intervention are scarce and deal mainly with fiber supplementation and lactose exclusion. Whereas dietary fibre supplementation is a recognized strategy for management for childhood constipation, its value in recurrent abdominal pain is uncertain. The two randomized trials comparing fiber treatment with placebo have yielded conflicting results22,23. The data on lactose-free diets are likewise inconclusive, and a Cochrane review calls for ‘well-designed trials of all recommended dietary interventions’24.
A sensible course, despite lack of published evidence, is to recommend healthy eating including plenty of fruit and vegetables, regular sensible meals and plenty of fluids. This should be coupled with a daily routine with plenty of physical activity.
Symptom-based pharmacological therapies: In some cases, symptom-based pharmacological therapies are helpful. Medications for functional abdominal pain are best prescribed judiciously as part of a multifaceted, individualized approach to relieve symptoms and disability. It is reasonable to consider the time-limited use of medications that might help to decrease the frequency or severity of symptoms. Treatment might include acid reduction therapy for pain associated with dyspepsia; antispasmodic agents, smooth muscle relaxants, or low doses of psychotropic agents for pain or nonstimulating laxatives or antidiarrheals for pain associated with altered bowel pattern.
Cognitive–behavioural therapy: In many instances, all that is needed from the doctor is acknowledgment of the symptoms and reassurance that there is no serious underlying organic disease.
Sanders et al., compared this approach (standard paediatric care) with cognitive–behavioural therapy and found that both groups improved, though the response was somewhat better in the cognitive–behavioural therapy group21. They suggested that psychological intervention may have a role in difficult cases.
Family Functioning: Education of the family is an important part of treatment of the child with functional abdominal pain. It is often helpful to summarize the child’s symptoms and explain in simple language that although the pain is real, there is most likely no underlying serious or chronic disease. It may be helpful to explain that recurrent abdominal pain is a common symptom in children and adolescents, yet few have a disease. Functional abdominal pain can be likened to a headache, a functional disorder experienced at some time by most adults, which very rarely is associated with serious disease.
It is important to provide clear and age-appropriate examples of conditions associated with hyperalgesia, such as a healing scar, and manifestations of the interaction between brain and gut, such as the diarrhea or vomiting children may experience during stressful situations is recommended that reasonable treatment goals be established, with the main aim being the return to normal function rather than the complete disappearance of pain. Return to school can be encouraged by identifying and addressing obstacles to school attendance.
Prognosis: Many of the studies on prognosis relate to hospital practice not primary care10. It is generally more likely that children with recurrent abdominal pain will develop chronic abdominal symptoms in adulthood and as many as 30% may continue thus. Many will continue to suffer from IBS11,12. There is evidence that children with recurrent abdominal pain are more likely to have emotional and psychiatric disorders later in life. Generally speaking, however, follow-up studies show that parental factors rather than the psychological characteristics of the child are more important when predicting persistence of abdominal pain.
Conclusion:Recurrent abdominal pain (long-standing intermittent or constant abdominal pain) is common in children and adolescents. In most children, recurrent abdominal pain is functional—that is, without objective evidence of an underlying organic disorder. Yet an important part of the physician’s job is to determine which children have an organic disorder. A review of the current evidence, however, indicates
that there are no studies showing that pain frequency, severity, location or effects on lifestyle help to discriminate between functional and organic disorders. There have been few studies of the treatment of recurrent abdominal pain in children. There is inconclusive evidence that a lactose-free diet decreases symptoms or that a fiber supplement decreases the frequency of pain attacks. There is inconclusive evidence of the benefit of acid suppression with H2-receptor antagonists to treat children with dyspepsia. There is also evidence that cognitive/behavioral therapy may be useful in improving pain and disability outcome in the short term.
References:
1. Apley J. The child with recurrent abdominal pain.Pediatr Clin North Am 1967; 14: 63–72.
2. Huang RC, Plamer LJ, Forbes DA. Prevalence andpattern of childhood abdominal pain in an Australiangeneral practice. J Paediatr Child Health 2000; 36:349-353.
3. Boey CC, Yap S, Goh KL. The prevalence ofrecurrent abdominal pain in 11- to 16-year-oldMalaysian schoolchildren. J Paediatr Child Health2000; 36: 114-116.
4. Boey CC, Goh KL. Predictors of recurrentabdominal pain among 9 to 15-year-old urban school-children in Malaysia. Acta Paediatr 2001; 90: 353-5.
5. Rasul CH, Khan MAD. Recurrent abdominal painin school children in Bangladesh. J Ceylon Coll Phys 2000; 33: 110-14.
6. Caplan A, Walker L, Rasquin A. Validation of thePediatric Rome II criteria for functionalgastrointestinal disorders using the questionnaire onpediatric gastrointestinal symptoms. J PediatrGastroenterol Nutr 2005; 41: 305-16.
7. Pearl RH, Irish MS, Caty MG, Glick PL. Theapproach to common abdominal diagnosis in infantsand children. Part II. Pediatr Clin North Am 1998;45: 1287-1326.
10. Huertas-Ceballos A, Logan S, Bennett C, et al.Psychosocial interventions for recurrent abdominalpain (RAP) and irritable bowel syndrome (IBS) inchildhood. Cochrane Database Syst Rev 2008; (1):CD003014.
11. El-Matary W, Spray C, Sandhu B. Irritable bowelsyndrome: the commonest cause of recurrent abdominalpain in children. Eur J Pediatr 2004; 163(10): 584-8.
12. Nygaard EA, Stordal K, Bentsen BS. Recurrentabdominal pain in children revisited: irritable bowelsyndrome and psychosomatic aspects. A prospectivestudy. Scand J Gastroenterol 2004; 39(10): 938-40.
13. Balani B, Patwari AK, Bajaj P, Diwan N, AnandVK. Recurrent abdominal pain - a reappraisal. IndianPediatr 2000; 37: 876-81.
14. Buch NA, Ahmad SM, Ahmad SZ, Ali SW, CharooBA, Hussan MU. Recurrent abdominal pain in children.Indian Pediatr 2002; 39: 830-4.
15. Stordal K, Nygaard EA, Bentsen B. Organicabnormalities in recurrent abdominal pain in children.Acta Paediatr 2001; 90: 1-5.
16. Drossman DA, Camilleri M, Mayer EA, WhiteheadWE. AGA technical review on irritable bowelsyndrome. Gastroenterology 2002; 123: 2108–31.
17. Whitehead WE, Bosmajian L, Zonderman AB,Costa PT Jr, Schuster MM. Symptoms of psychologicdistress associated with irritable bowel syndrome.Comparison of community and medical clinic samples.Gastroenterology 1988; 95: 709–14.
18. Van Ginkel R, Voskuijl WP, Benninga MA, TaminiauJA, Boeckxstaens GE. Alterations in rectal sensitivityand motility in childhood irritable bowel syndrome.Gastroenterology 2001; 120: 31–8.
19. Di Lorenzo C, Youssef NN, Sigurdsson L, ScharffL, Griffiths J, Wald A. Visceral hyperalgesia in children with functional abdominal pain. J Pediatr 2001; 139: 838–43.
20. Talley NJ, Spiller R. Irritable bowel syndrome: alittle understood organic bowel disease. Lancet 2002;360: 555–64.
21. Sanders MR, Shepherd RW, Cleighorn G, WoolfordH. The treatment of recurrent abdominal pain inchildren: a controlled comparison ofcognitive–behavioural family intervention and standardpediatric care. J Cons Clin Psychol 1994; 62: 306-14.
23. Feldman W, McGrath P, Hodgson C, Ritter H,Shipman RT. The use of dietary fiber in themanagement of simple, childhood, idiopathic, recurrent,abdominal pain. Am J Dis Child 1985; 139: 1216-18.
24. Huertas-Ceballos A, Macarthur C, Logan S.Dietary interventions for recurrent abdominal pain(RAP) in childhood (Cochrane Review). In: TheCochrane Library. Issue 1, 2004.
Introduction:Injuries, especially as a result of blunt trauma, now constitutes one of the major causes of death in our country. The frequency of trauma to the abdomen may be increasing in almost geometric proportion as the number & speed of highway vehicles, civil unrest & terrorist attack rises.
Abdominal Trauma is a common clinical entity occurring in an emergency surgical unit and Blunt abdominal injury causing hollow viscous rupture is a common squeal. According to East multi-institutional trial of trauma indicate that after blunt abdominal trauma the incidence of small bowel injury and small bowel perforation (SBP) 1.1% and 0.3%, respectively1.
Case report:This is a story of a 20 years old boy. He had a history of road traffic accident 3 days back where he encountered by tin at supra umbilical region on right side. He was treated by local physician. On next morning he developed increasing abdominal pain, vomiting, respiratory distress & his conditions were deteriorating. On examination (OE) his abdomen was very tender & rigid, Blood Pressure (BP) - 100/60 mm Hg, Respiratory rate (RR) - 24/min, Pulse rate (PR) - 110/min. X-ray abdomen in erect posture including both dome of diaphragm revealed free gas shadow under both dome of diaphragm. Then other necessary investigations for assessing fitness for anaesthesia were done & Patient was prepared for exploratory laparotomy.
Abdomen was opened by upper midline incision revealing peritoneal cavity (Fig. 1, 2) with huge bile mixed food material & blood mixed fluid. Then content was sucked & peritoneal toileting was done. On query, large perforation was found in the 2nd part of duodenum (Fig. 3) about 10 cm distal to Gastro-Duodenal (G-D) junction & there was no other injury. Primary repair was done & two drain tube were kept in situ.
On 5th post-operative day (POD) patient was allowed to take liquid diet & sips of water orally. At the mean time observing for drain collection, abdominal pain, fever, vomiting & any discharge from wound.
On 7th POD patient was allowed to semi solid diet. Finally the drain tubes were removed on 9th POD. The recovery was uneventful. The patient left hospital giving thanks to all.
Discussion:Blunt abdominal trauma (BAT) may be from direct compression of the abdomen against a fixed object with resulting tears or subcapsular haematoma involving the solid organ associated viscera2. Hollow organs (typically small intestine) may rupture due to compression against a fixed point, usually the vertebral column. This compression causes rapid increase in intraluminal pressure leading to perforation of bowel wall at the anti-mesenteric border, where bowel is usually weaker2. Isolated duodenal injuries following a blunt abdominal trauma is uncommon. Complete transaction of duodenum is very rare presentation2. The
most common cause of blunt abdominal trauma (BAT) is motor vehicle accident (MVA).
Patients with multiple lower rib fractures are notorious for having severe intra-abdominal injuries without significant abdominal pain. The severe pain from the rib fractures becomes a distracting injury for the less noticeable abdominal pain. As a result, the patient may have a poor outcome as abdominal injuries are not recognized.
Spontaneous perforation of an hollow viscus may be the result of a range of pathological processes, where diagnosis is relatively easy for surgeon. But isolated duodenal perforation after blunt abdominal trauma is still a diagnostic challenge to surgeon.
One third of our patient did not present to the hospital until after an average of three days with advanced peritonitis. Reasons put forward to explain such delay include: 1. Relatively less initial peritoneal irritation
induced by the nearly neutral intestinal content particularly those with perforation between the duodeno-jejunal flexure and the ileo-caecal junction; 2. In small gut perforations the mucosa may prolapse through the hole and partly seal it making early sign of misleading; 3. The entity of a delayed perforation caused by an evolving injury. These patient have an initial contused bowel wall at the time of trauma that ultimately gives way after a variable period with resultant peritonitis. For this reason, physical examination during the initial evaluation is reliable for an early diagnosis in only 30% of blunt trauma injuries, in those patients who exhibit clear peritoneal signs3.
Abdominal pain, the usual symptom indicating abdominal injury is not severe & therefore the patient did not seek hospital care soon after injury most probably due to the above reasons.
Initial approach to the blunt abdominal trauma (BAT) patient is done according to fundamental principles of
advanced trauma life support (ATLS) system, which compromise primary survey & resuscitation [ABCDE (Airway, Breathing, Circulation, Disability, Exposure) of trauma care, steps of resuscitation, re-evaluation of ABC, monitoring the vital sign, introduction of gastric tube or Foley’s catheter] and secondary survey (careful abdominal examination & to identify all other injuries).
Several diagnostic modalities are being used for the identification of isolated bowel perforation. These are X-ray abdomen in erect posture including both domeof diaphragm, Serum amylase, WBC count, focusedassessment with sonography for trauma (FAST),diagnostic peritoneal lavage (DPL), Abdominal CT.Free sub-diaphragmatic gas, a radiologic signindicative of hollow viscus perforation easilydetected in plain abdominal radiographs, could leadto an early diagnosis in only 7-8% of the cases4,5.Elevated white blood cell (WBC) count and serumamylase levels could be suggestive of an intra-abdominal process and aid diagnosis in conjunctionwith history and physical findings. Althoughabnormal serum amylase can be noted in such cases,no clear cut-off value that could help differentiatepatients with SBP could be determined4. Focusedassessment with sonography for trauma (FAST) playan important roles to detect the free intra-peritonealfluid and haemo-pericardium in the assessment ofacutely traumatized patient, with the sensitivity of91-100%6. Diagnostic peritoneal lavage (DPL) canidentify Small bowel perforations (SBP) with greatsensitivity (up to 100%) but relatively lowspecificity7,8. CT has proved to be the gold-standardexamination, contributing toward a significantreduction of morbidity and mortality in traumavictims9,10. Postoperative complications like woundinfection, would dehiscence, intra-abdominal abscess,acute respiratory distress syndrome and sepsis, alloccur at two to three times higher incidence inpatients who undergo surgical repair of Small bowelperforations with extended delay11,12. The keyindividual in the development of a system of traumacare is the general surgeon.
Treatment:Urgent hospitalization of patient preferably in ICU with initial resuscitation, side by side preparation of the patient for laparotomy. After laparotomy, thorough surgical toileting, identification of injury, repair, re-toileting then drain were given. Associated injury were also looked for & treated. Abdomen was closed in layer. A meticulous follow up of the patient is needed for good outcome.
Conclusion:We present a case of successful repair of 3 days old traumatic duodenal perforation. Isolated duodenal perforation in blunt abdominal trauma victim is hard to diagnosis. Early diagnosis & appropriate operative management which are imperative to prevent morbidity in many cases. The rarity of duodenal perforation, the patient's good general condition following road traffic accident & treatment by local physician delayed the diagnosis. Cornerstone to successful management is combination of detailed history including the mechanism of injury, thorough clinical examination & Investigation under close supervision, surgical procedures to identify the perforation & repair.
References:1. Watts DD, Fakhry SM. Incidence of hollow viscusinjury in blunt trauma: an analysis from 275,557trauma admissions from the East multi-institutionaltrial. J Trauma 2003; 54(2): 289-94.
2. AH Dauterive, L Flancbaum, EF Cox. Bluntintestinal trauma. A modern-day review. Ann Surg1985; 201(2): 198-203.
3. Guarino J, Hassett JM Jr, Luchette FA. Smallbowel injuries: mechanisms, patterns, and outcome. JTrauma 1995; 39(6): 1076-80.
4. Fang JF, Chen RJ, Lin BC, Hsu YB, Kao JL, KaoYC, Chen MF. Small bowel perforation: is urgentsurgery necessary? J Trauma 1999; 47(3): 515-20.
5. Mathonnet M, Peyrou P, Gainant A, Bouvier S,Cubertafond P. Role of laparoscopy in bluntperforations of the small bowel. Surg Endosc 2003;l7(4): 641-5.
6. Fakhry SM, Watts DD, Luchette FA; EAST Multi-Institutional Hollow Viscus Injury Research Group.Current diagnostic approaches lack sensitivity in thediagnosis of perforated blunt small bowel injury:analysis from 275,557 trauma admissions from theEAST multi-institutional HVI trial. J Trauma 2003;54(2): 295-306.
7. Neugerbauer H, Wallenboeck E, Hungerfort M.Seventy cases of injuries of the small intestine causedby blunt abdominal trauma: a retrospective studyfrom 1970 to 1994. J Trauma 1999; 46(1): 116-21.
8. Fabian TC, Mangiante EC, White TJ, PattersonCR, Boldreghini S, Britt LG. A prospective study of91 patients undergoing both computed tomographyand peritoneal lavage following blunt abdominaltrauma. J Trauma 1986; 26(7): 602-8.
9. Gay SB, Sistrom CL. Computed tomographicevaluation of blunt abdominal trauma. Radiol ClinNorth Am 1992; 30(2): 367-88.
10. Fakhry SM, Brownstein M, Watts DD, Baker CC,Oller D. Relatively short diagnostic delays (<8 hours)produce morbidity and mortality in blunt small bowelinjury: an analysis of time to operative intervention in198 patients from a multicenter experience. J Trauma2000; 48(3): 408-14.
11. Mirvis SE, Gens DR, Shanmuganathan K.Rupture of the bowel after blunt abdominal trauma:diagnosis with CT. Am J Roentgenol 1992; 159(6):1217-21.
12. Ma OJ, Kefer MP, Stevison KF, Mateer JR.Operative versus nonoperative management of bluntabdominal trauma: role of ultrasound-measuredintraperitoneal fluid levels. Am J Emergency Med2001; 19(4): 284-6.�
* Criteria fulfilled at least once per week for at least 2 months before diagnosis.† Criteria fulfilled 2 or more times in the preceding 12 months.
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31EMCJ. Jan 2016: 1 (1) 32EMCJ. Jan 2016: 1 (1)
Case Report
Traumatic Rupture of Duodenum: A Case ReportRahman MA1, Imam HM2
Abstract:Isolated duodenal rupture after blunt abdominal trauma is infrequent, liable to be missed and is associated with high morbidity and significant mortality. Diagnostic delay is a part of clinical picture in most of these cases, considering its anatomical location & lack of peritoneal sign. Among different modalities, use of CT scan for diagnosis is widely appreciated. Majority of duodenal injury can be managed by simple repair of injured site. But delayed presentation, lack of optimal diagnostic approach & delayed surgical intervention have results in many post-operative complication & hamper the possible outcome. The case of young traumatized patient with isolated duodenal rupture is presented to highlight these issues.
1Professor Md. Ataur Rahman, Department of Surgery, Eastern Medical College. 2Dr. HM Hasan Imam, Assistant Registrar, Department of Surgery, Eastern Medical College.
Address of Correspondence: Professor Md. Ataur Rahman, Professor & Head, Department of Surgery, Eastern Medical College, Comilla. Mobile: +8801711721098, Email: [email protected]
H2a. Diagnostic criteria* for functional dyspepsia Must include all of the following: 1. Persistent of recurrent pain or discomfort centered in the upper abdomen (above the umbilicus).2. Not relieved by defecation or associated with the onset of a change in stool frequency or stool form(i.e., not irritable bowel syndrome).3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’s symptoms.
H2b. Diagnostic criteria* for irritable bowel syndrome Must include all of the following: 1. Abdominal discomfort (an uncomfortable sensation not described as pain) or pain associated with 2 or more of the following at least 25% of the time:(a) Improved with defecation(b) Onset associated with a change in frequency of stool; and (c) Onset associated with a change in from (appearance) of stool.2. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms.H2c. Diagnostic criteria† for abdominal migraine Must include all of the following: 1. Paroxysmal episodes of intense acute periumbilical pain that lasts for 1 hours or more.2. Intervening periods of usual health lasting weeks to months.3. The pain interferes with normal activities.4. The pain is associated with 2 or more of the following: anorexia, nausea, vomiting, headache,photophobia, pallor.5. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms. H2d. Diagnostic criteria* for childhood functional abdominal pain Must include all of the following: 1. Episodic or continuous abdominal pain.2. Insufficient criteria for other functional gastrointestinal disorders.3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms.H2d1. Diagnostic criteria*for childhood functional abdominal pain syndrome Must include childhood functional abdominal pain at least 25% of the time and 1 or more of the following: 1. Some loss of daily functioning2. Additional somatic symptoms such as headache, limb pain, or difficulty in sleeping H1c. Diagnostic criteria* for aerophagia Must include at least 2 of the following: 1. Air swallowing.2. Abdominal distension due to intraluminal air.3. Repetitive belching and/or increased flatus.
Table II: Rome III Diagnostic Criteria for Pediatric Functional Bowel Disorders.
History: Red Flags Weight loss Persistent right upper or right lower quadrant pain Unexplained fevers Pain radiating to the back Unexplained rashes Arthritis Persistent vomiting Recurrent oral ulcers Dysphagia/odynophagia Anal/perianal ulcers Hematemesis Nocturnal symptoms (waking with diarrhea and/or vomiting) Bilious emesis Delayed puberty Chronic diarrhea (> 2 weeks) Deceleration of linear growth velocity Hematochezia/melena Physical Exam: Red Flags Decline in weight/height parameters Abdominal mass Pallor or anemia Localized tenderness Abdominal distension Perianal fissures or ulcers Organomegaly (hepatosplenomegaly) Positive hemoccult stool test
Table III: “Red Flags” In History and Examination of Recurrent Abdominal Pain.
Figure 1, 2: Huge bile, blood & food mixed fluid & material revealed after opening the abdomen by upper midline incision
Figure 3: Large perforation found in the 2nd part of duodenum
evidence that patients with recurrent abdominal pain have more symptoms of anxiety and depression (internalizing emotional symptoms) than do healthy community controls. In contrast, there is evidence that children with recurrent abdominal pain do not
have higher levels of conduct disorder and oppositional behavior (externalizing emotional symptoms) compared with healthy community controls. There are no data on whether emotional/behavioral symptoms predict symptom severity, course or response to treatment. There is evidence suggesting that children with recurrent abdominal pain are at risk of later emotional symptoms and psychiatric disorder.
Clinical Features: The primary feature of FAPS is abdominal pain. Usually, the pain is located around the umbilicus, however the pattern or location of abdominal pain is not always predictable. The pain may occur suddenly
or slowly increase in severity. The pain may be constant or may increase and decrease in severity. Some children with functional abdominal pain may experience dyspepsia, or upper abdominal pain associated with nausea, vomiting, and/or a feeling of fullness after just a few bites (early satiety). Others may experience abdominal pain with bowel movements. Pain that is usually relieved by bowel movements, or associated with changes in bowel
movement habits (mainly constipation, diarrhea, or constipation alternating with diarrhea) is the classic irritable bowel syndrome (IBS) (Table II). However, many diseases can cause chronic abdominal pain.
Therefore, any structural, organic, or chemical disease should be excluded. Patients with RAP often have pain-related behaviors. First, they often deny a role for psychosocial stressors. However, pain may diminish when patients are engaged in distracting activities but increase when they are discussing a psychologically distressing issue. Second, they express pain through verbal and nonverbal methods. They urgently report intense symptoms disproportionate to the available clinical and laboratory data. Third, they seek health care frequently. They often visit the emergency room and request analgesics. Fourth, they request diagnostic studies or even exploratory surgery to determine the organic origin of their condition. Fifth, they focus attention on complete relief of pain rather than on adapting to having a disease. Sixth, they take on limited personal responsibility for self-management. In addition to these features, distinct psychopathologies are usually found in patients with FAPS, including depressive disorders, anxiety disorders, and somatoform disorder.
History and Physical Exam: A complete history should be taken including social and dietary history and look for red flag symptoms and signs (Table III), Conduct a thorough physical exam, including rectal exam with stool hemoccult OR perianal exam with hemoccult of stool brought in by patient/family and review of the child’s growth. Children with recurrent abdominal pain are more likely than children without recurrent abdominal pain to have headache, joint pain, anorexia, vomiting, nausea, excessive gas and altered bowel symptoms. The presence of alarm symptoms or signs suggests a
higher pretest probability or prevalence of organic disease and may justify the performance of diagnostic tests. Alarm symptoms or signs include, but are not limited to, involuntary weight loss, deceleration of linear growth, gastrointestinal blood loss, significant vomiting, chronic severe diarrhea, persistent right upper or right lower quadrant pain, unexplained fever and family history of inflammatory bowel disease. The ‘red flag’ signs have long been used by clinicians to guide themselves to identify children who need further investigations and the salient ones on history and examination are noted in Table III 7,8.� Investigations: Investigations may be required to exclude particular conditions suggested by the history and examination. It is useful to pursue further diagnostic testing only in the presence of alarm symptoms9. Laboratory studies may be unnecessary if the history and physical examination clearly lead to a diagnosis of functional abdominal pain. However, a complete blood cell count, sedimentation rate, stool test for parasites (especially Giardia), and urinalysis are reasonable screening studies. If inflammatory bowel disease is suspected the sedimentation rate is often elevated. The finding of an abnormal sedimentation rate would make one look
further for an inflammatory, infectious, or neoplastic disorder. If indicated, an ultrasound examination of the abdomen can give information about kidneys, gallbladder, and pancreas; with lower abdominal pain, a pelvic ultrasonogram may be indicated.
An upper gastrointestinal tract x-ray series is indicated if one suspects a disorder of the stomach or small intestine. Helicobacter pylori infection does not seem to be associated with RAP. In patients with symptoms suggestive of gastritis or ulcer an H. pylori test (serum or fecal) may be performed to document the infection.
Esophagogastroduodenoscopy is indicated with symptoms suggestive of persistent upper gastrointestinal pathology. In the absence of this suspicion, esophagogastroduodenoscopy is unlikely to identify an abnormality and is usually not necessary.
Management: The family and the child with functional RAP may worry about the inability to identify an organic cause and may be resistant to a diagnosis of nonorganic disease. After a thorough history and physical examination the most important component of the treatment is reassurance of the children and family members10. Specifically, they need to be reassured that no evidence of a serious underlying disorder is present. Acknowledgment that the child's pain is real but not life-threatening is essential. When understood and accepted, this reassurance concludes the child and family's search for a physical cause and allows them to move into the next stage of learning to cope.
Dietary management: Data on dietary intervention are scarce and deal mainly with fiber supplementation and lactose exclusion. Whereas dietary fibre supplementation is a recognized strategy for management for childhood constipation, its value in recurrent abdominal pain is uncertain. The two randomized trials comparing fiber treatment with placebo have yielded conflicting results22,23. The data on lactose-free diets are likewise inconclusive, and a Cochrane review calls for ‘well-designed trials of all recommended dietary interventions’24.
A sensible course, despite lack of published evidence, is to recommend healthy eating including plenty of fruit and vegetables, regular sensible meals and plenty of fluids. This should be coupled with a daily routine with plenty of physical activity.
Symptom-based pharmacological therapies: In some cases, symptom-based pharmacological therapies are helpful. Medications for functional abdominal pain are best prescribed judiciously as part of a multifaceted, individualized approach to relieve symptoms and disability. It is reasonable to consider the time-limited use of medications that might help to decrease the frequency or severity of symptoms. Treatment might include acid reduction therapy for pain associated with dyspepsia; antispasmodic agents, smooth muscle relaxants, or low doses of psychotropic agents for pain or nonstimulating laxatives or antidiarrheals for pain associated with altered bowel pattern.
Cognitive–behavioural therapy: In many instances, all that is needed from the doctor is acknowledgment of the symptoms and reassurance that there is no serious underlying organic disease.
Sanders et al., compared this approach (standard paediatric care) with cognitive–behavioural therapy and found that both groups improved, though the response was somewhat better in the cognitive–behavioural therapy group21. They suggested that psychological intervention may have a role in difficult cases.
Family Functioning: Education of the family is an important part of treatment of the child with functional abdominal pain. It is often helpful to summarize the child’s symptoms and explain in simple language that although the pain is real, there is most likely no underlying serious or chronic disease. It may be helpful to explain that recurrent abdominal pain is a common symptom in children and adolescents, yet few have a disease. Functional abdominal pain can be likened to a headache, a functional disorder experienced at some time by most adults, which very rarely is associated with serious disease.
It is important to provide clear and age-appropriate examples of conditions associated with hyperalgesia, such as a healing scar, and manifestations of the interaction between brain and gut, such as the diarrhea or vomiting children may experience during stressful situations is recommended that reasonable treatment goals be established, with the main aim being the return to normal function rather than the complete disappearance of pain. Return to school can be encouraged by identifying and addressing obstacles to school attendance.
Prognosis: Many of the studies on prognosis relate to hospital practice not primary care10. It is generally more likely that children with recurrent abdominal pain will develop chronic abdominal symptoms in adulthood and as many as 30% may continue thus. Many will continue to suffer from IBS11,12. There is evidence that children with recurrent abdominal pain are more likely to have emotional and psychiatric disorders later in life. Generally speaking, however, follow-up studies show that parental factors rather than the psychological characteristics of the child are more important when predicting persistence of abdominal pain.
Conclusion:Recurrent abdominal pain (long-standing intermittent or constant abdominal pain) is common in children and adolescents. In most children, recurrent abdominal pain is functional—that is, without objective evidence of an underlying organic disorder. Yet an important part of the physician’s job is to determine which children have an organic disorder. A review of the current evidence, however, indicates
that there are no studies showing that pain frequency, severity, location or effects on lifestyle help to discriminate between functional and organic disorders. There have been few studies of the treatment of recurrent abdominal pain in children. There is inconclusive evidence that a lactose-free diet decreases symptoms or that a fiber supplement decreases the frequency of pain attacks. There is inconclusive evidence of the benefit of acid suppression with H2-receptor antagonists to treat children with dyspepsia. There is also evidence that cognitive/behavioral therapy may be useful in improving pain and disability outcome in the short term.
References:
1. Apley J. The child with recurrent abdominal pain.Pediatr Clin North Am 1967; 14: 63–72.
2. Huang RC, Plamer LJ, Forbes DA. Prevalence andpattern of childhood abdominal pain in an Australiangeneral practice. J Paediatr Child Health 2000; 36:349-353.
3. Boey CC, Yap S, Goh KL. The prevalence ofrecurrent abdominal pain in 11- to 16-year-oldMalaysian schoolchildren. J Paediatr Child Health2000; 36: 114-116.
4. Boey CC, Goh KL. Predictors of recurrentabdominal pain among 9 to 15-year-old urban school-children in Malaysia. Acta Paediatr 2001; 90: 353-5.
5. Rasul CH, Khan MAD. Recurrent abdominal painin school children in Bangladesh. J Ceylon Coll Phys 2000; 33: 110-14.
6. Caplan A, Walker L, Rasquin A. Validation of thePediatric Rome II criteria for functionalgastrointestinal disorders using the questionnaire onpediatric gastrointestinal symptoms. J PediatrGastroenterol Nutr 2005; 41: 305-16.
7. Pearl RH, Irish MS, Caty MG, Glick PL. Theapproach to common abdominal diagnosis in infantsand children. Part II. Pediatr Clin North Am 1998;45: 1287-1326.
10. Huertas-Ceballos A, Logan S, Bennett C, et al.Psychosocial interventions for recurrent abdominalpain (RAP) and irritable bowel syndrome (IBS) inchildhood. Cochrane Database Syst Rev 2008; (1):CD003014.
11. El-Matary W, Spray C, Sandhu B. Irritable bowelsyndrome: the commonest cause of recurrent abdominalpain in children. Eur J Pediatr 2004; 163(10): 584-8.
12. Nygaard EA, Stordal K, Bentsen BS. Recurrentabdominal pain in children revisited: irritable bowelsyndrome and psychosomatic aspects. A prospectivestudy. Scand J Gastroenterol 2004; 39(10): 938-40.
13. Balani B, Patwari AK, Bajaj P, Diwan N, AnandVK. Recurrent abdominal pain - a reappraisal. IndianPediatr 2000; 37: 876-81.
14. Buch NA, Ahmad SM, Ahmad SZ, Ali SW, CharooBA, Hussan MU. Recurrent abdominal pain in children.Indian Pediatr 2002; 39: 830-4.
15. Stordal K, Nygaard EA, Bentsen B. Organicabnormalities in recurrent abdominal pain in children.Acta Paediatr 2001; 90: 1-5.
16. Drossman DA, Camilleri M, Mayer EA, WhiteheadWE. AGA technical review on irritable bowelsyndrome. Gastroenterology 2002; 123: 2108–31.
17. Whitehead WE, Bosmajian L, Zonderman AB,Costa PT Jr, Schuster MM. Symptoms of psychologicdistress associated with irritable bowel syndrome.Comparison of community and medical clinic samples.Gastroenterology 1988; 95: 709–14.
18. Van Ginkel R, Voskuijl WP, Benninga MA, TaminiauJA, Boeckxstaens GE. Alterations in rectal sensitivityand motility in childhood irritable bowel syndrome.Gastroenterology 2001; 120: 31–8.
19. Di Lorenzo C, Youssef NN, Sigurdsson L, ScharffL, Griffiths J, Wald A. Visceral hyperalgesia in children with functional abdominal pain. J Pediatr 2001; 139: 838–43.
20. Talley NJ, Spiller R. Irritable bowel syndrome: alittle understood organic bowel disease. Lancet 2002;360: 555–64.
21. Sanders MR, Shepherd RW, Cleighorn G, WoolfordH. The treatment of recurrent abdominal pain inchildren: a controlled comparison ofcognitive–behavioural family intervention and standardpediatric care. J Cons Clin Psychol 1994; 62: 306-14.
23. Feldman W, McGrath P, Hodgson C, Ritter H,Shipman RT. The use of dietary fiber in themanagement of simple, childhood, idiopathic, recurrent,abdominal pain. Am J Dis Child 1985; 139: 1216-18.
24. Huertas-Ceballos A, Macarthur C, Logan S.Dietary interventions for recurrent abdominal pain(RAP) in childhood (Cochrane Review). In: TheCochrane Library. Issue 1, 2004.
Introduction:Injuries, especially as a result of blunt trauma, now constitutes one of the major causes of death in our country. The frequency of trauma to the abdomen may be increasing in almost geometric proportion as the number & speed of highway vehicles, civil unrest & terrorist attack rises.
Abdominal Trauma is a common clinical entity occurring in an emergency surgical unit and Blunt abdominal injury causing hollow viscous rupture is a common squeal. According to East multi-institutional trial of trauma indicate that after blunt abdominal trauma the incidence of small bowel injury and small bowel perforation (SBP) 1.1% and 0.3%, respectively1.
Case report:This is a story of a 20 years old boy. He had a history of road traffic accident 3 days back where he encountered by tin at supra umbilical region on right side. He was treated by local physician. On next morning he developed increasing abdominal pain, vomiting, respiratory distress & his conditions were deteriorating. On examination (OE) his abdomen was very tender & rigid, Blood Pressure (BP) - 100/60 mm Hg, Respiratory rate (RR) - 24/min, Pulse rate (PR) - 110/min. X-ray abdomen in erect posture including both dome of diaphragm revealed free gas shadow under both dome of diaphragm. Then other necessary investigations for assessing fitness for anaesthesia were done & Patient was prepared for exploratory laparotomy.
Abdomen was opened by upper midline incision revealing peritoneal cavity (Fig. 1, 2) with huge bile mixed food material & blood mixed fluid. Then content was sucked & peritoneal toileting was done. On query, large perforation was found in the 2nd part of duodenum (Fig. 3) about 10 cm distal to Gastro-Duodenal (G-D) junction & there was no other injury. Primary repair was done & two drain tube were kept in situ.
On 5th post-operative day (POD) patient was allowed to take liquid diet & sips of water orally. At the mean time observing for drain collection, abdominal pain, fever, vomiting & any discharge from wound.
On 7th POD patient was allowed to semi solid diet. Finally the drain tubes were removed on 9th POD. The recovery was uneventful. The patient left hospital giving thanks to all.
Discussion:Blunt abdominal trauma (BAT) may be from direct compression of the abdomen against a fixed object with resulting tears or subcapsular haematoma involving the solid organ associated viscera2. Hollow organs (typically small intestine) may rupture due to compression against a fixed point, usually the vertebral column. This compression causes rapid increase in intraluminal pressure leading to perforation of bowel wall at the anti-mesenteric border, where bowel is usually weaker2. Isolated duodenal injuries following a blunt abdominal trauma is uncommon. Complete transaction of duodenum is very rare presentation2. The
most common cause of blunt abdominal trauma (BAT) is motor vehicle accident (MVA).
Patients with multiple lower rib fractures are notorious for having severe intra-abdominal injuries without significant abdominal pain. The severe pain from the rib fractures becomes a distracting injury for the less noticeable abdominal pain. As a result, the patient may have a poor outcome as abdominal injuries are not recognized.
Spontaneous perforation of an hollow viscus may be the result of a range of pathological processes, where diagnosis is relatively easy for surgeon. But isolated duodenal perforation after blunt abdominal trauma is still a diagnostic challenge to surgeon.
One third of our patient did not present to the hospital until after an average of three days with advanced peritonitis. Reasons put forward to explain such delay include: 1. Relatively less initial peritoneal irritation
induced by the nearly neutral intestinal content particularly those with perforation between the duodeno-jejunal flexure and the ileo-caecal junction; 2. In small gut perforations the mucosa may prolapse through the hole and partly seal it making early sign of misleading; 3. The entity of a delayed perforation caused by an evolving injury. These patient have an initial contused bowel wall at the time of trauma that ultimately gives way after a variable period with resultant peritonitis. For this reason, physical examination during the initial evaluation is reliable for an early diagnosis in only 30% of blunt trauma injuries, in those patients who exhibit clear peritoneal signs3.
Abdominal pain, the usual symptom indicating abdominal injury is not severe & therefore the patient did not seek hospital care soon after injury most probably due to the above reasons.
Initial approach to the blunt abdominal trauma (BAT) patient is done according to fundamental principles of
advanced trauma life support (ATLS) system, which compromise primary survey & resuscitation [ABCDE (Airway, Breathing, Circulation, Disability, Exposure) of trauma care, steps of resuscitation, re-evaluation of ABC, monitoring the vital sign, introduction of gastric tube or Foley’s catheter] and secondary survey (careful abdominal examination & to identify all other injuries).
Several diagnostic modalities are being used for the identification of isolated bowel perforation. These are X-ray abdomen in erect posture including both domeof diaphragm, Serum amylase, WBC count, focusedassessment with sonography for trauma (FAST),diagnostic peritoneal lavage (DPL), Abdominal CT.Free sub-diaphragmatic gas, a radiologic signindicative of hollow viscus perforation easilydetected in plain abdominal radiographs, could leadto an early diagnosis in only 7-8% of the cases4,5.Elevated white blood cell (WBC) count and serumamylase levels could be suggestive of an intra-abdominal process and aid diagnosis in conjunctionwith history and physical findings. Althoughabnormal serum amylase can be noted in such cases,no clear cut-off value that could help differentiatepatients with SBP could be determined4. Focusedassessment with sonography for trauma (FAST) playan important roles to detect the free intra-peritonealfluid and haemo-pericardium in the assessment ofacutely traumatized patient, with the sensitivity of91-100%6. Diagnostic peritoneal lavage (DPL) canidentify Small bowel perforations (SBP) with greatsensitivity (up to 100%) but relatively lowspecificity7,8. CT has proved to be the gold-standardexamination, contributing toward a significantreduction of morbidity and mortality in traumavictims9,10. Postoperative complications like woundinfection, would dehiscence, intra-abdominal abscess,acute respiratory distress syndrome and sepsis, alloccur at two to three times higher incidence inpatients who undergo surgical repair of Small bowelperforations with extended delay11,12. The keyindividual in the development of a system of traumacare is the general surgeon.
Treatment:Urgent hospitalization of patient preferably in ICU with initial resuscitation, side by side preparation of the patient for laparotomy. After laparotomy, thorough surgical toileting, identification of injury, repair, re-toileting then drain were given. Associated injury were also looked for & treated. Abdomen was closed in layer. A meticulous follow up of the patient is needed for good outcome.
Conclusion:We present a case of successful repair of 3 days old traumatic duodenal perforation. Isolated duodenal perforation in blunt abdominal trauma victim is hard to diagnosis. Early diagnosis & appropriate operative management which are imperative to prevent morbidity in many cases. The rarity of duodenal perforation, the patient's good general condition following road traffic accident & treatment by local physician delayed the diagnosis. Cornerstone to successful management is combination of detailed history including the mechanism of injury, thorough clinical examination & Investigation under close supervision, surgical procedures to identify the perforation & repair.
References:1. Watts DD, Fakhry SM. Incidence of hollow viscusinjury in blunt trauma: an analysis from 275,557trauma admissions from the East multi-institutionaltrial. J Trauma 2003; 54(2): 289-94.
2. AH Dauterive, L Flancbaum, EF Cox. Bluntintestinal trauma. A modern-day review. Ann Surg1985; 201(2): 198-203.
3. Guarino J, Hassett JM Jr, Luchette FA. Smallbowel injuries: mechanisms, patterns, and outcome. JTrauma 1995; 39(6): 1076-80.
4. Fang JF, Chen RJ, Lin BC, Hsu YB, Kao JL, KaoYC, Chen MF. Small bowel perforation: is urgentsurgery necessary? J Trauma 1999; 47(3): 515-20.
5. Mathonnet M, Peyrou P, Gainant A, Bouvier S,Cubertafond P. Role of laparoscopy in bluntperforations of the small bowel. Surg Endosc 2003;l7(4): 641-5.
6. Fakhry SM, Watts DD, Luchette FA; EAST Multi-Institutional Hollow Viscus Injury Research Group.Current diagnostic approaches lack sensitivity in thediagnosis of perforated blunt small bowel injury:analysis from 275,557 trauma admissions from theEAST multi-institutional HVI trial. J Trauma 2003;54(2): 295-306.
7. Neugerbauer H, Wallenboeck E, Hungerfort M.Seventy cases of injuries of the small intestine causedby blunt abdominal trauma: a retrospective studyfrom 1970 to 1994. J Trauma 1999; 46(1): 116-21.
8. Fabian TC, Mangiante EC, White TJ, PattersonCR, Boldreghini S, Britt LG. A prospective study of91 patients undergoing both computed tomographyand peritoneal lavage following blunt abdominaltrauma. J Trauma 1986; 26(7): 602-8.
9. Gay SB, Sistrom CL. Computed tomographicevaluation of blunt abdominal trauma. Radiol ClinNorth Am 1992; 30(2): 367-88.
10. Fakhry SM, Brownstein M, Watts DD, Baker CC,Oller D. Relatively short diagnostic delays (<8 hours)produce morbidity and mortality in blunt small bowelinjury: an analysis of time to operative intervention in198 patients from a multicenter experience. J Trauma2000; 48(3): 408-14.
11. Mirvis SE, Gens DR, Shanmuganathan K.Rupture of the bowel after blunt abdominal trauma:diagnosis with CT. Am J Roentgenol 1992; 159(6):1217-21.
12. Ma OJ, Kefer MP, Stevison KF, Mateer JR.Operative versus nonoperative management of bluntabdominal trauma: role of ultrasound-measuredintraperitoneal fluid levels. Am J Emergency Med2001; 19(4): 284-6.�
* Criteria fulfilled at least once per week for at least 2 months before diagnosis.† Criteria fulfilled 2 or more times in the preceding 12 months.
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Case Report
Traumatic Rupture of Duodenum: A Case ReportRahman MA1, Imam HM2
Abstract:Isolated duodenal rupture after blunt abdominal trauma is infrequent, liable to be missed and is associated with high morbidity and significant mortality. Diagnostic delay is a part of clinical picture in most of these cases, considering its anatomical location & lack of peritoneal sign. Among different modalities, use of CT scan for diagnosis is widely appreciated. Majority of duodenal injury can be managed by simple repair of injured site. But delayed presentation, lack of optimal diagnostic approach & delayed surgical intervention have results in many post-operative complication & hamper the possible outcome. The case of young traumatized patient with isolated duodenal rupture is presented to highlight these issues.
1Professor Md. Ataur Rahman, Department of Surgery, Eastern Medical College. 2Dr. HM Hasan Imam, Assistant Registrar, Department of Surgery, Eastern Medical College.
Address of Correspondence: Professor Md. Ataur Rahman, Professor & Head, Department of Surgery, Eastern Medical College, Comilla. Mobile: +8801711721098, Email: [email protected]
H2a. Diagnostic criteria* for functional dyspepsia Must include all of the following: 1. Persistent of recurrent pain or discomfort centered in the upper abdomen (above the umbilicus).2. Not relieved by defecation or associated with the onset of a change in stool frequency or stool form(i.e., not irritable bowel syndrome).3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’s symptoms.
H2b. Diagnostic criteria* for irritable bowel syndrome Must include all of the following: 1. Abdominal discomfort (an uncomfortable sensation not described as pain) or pain associated with 2 or more of the following at least 25% of the time:(a) Improved with defecation(b) Onset associated with a change in frequency of stool; and (c) Onset associated with a change in from (appearance) of stool.2. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms.H2c. Diagnostic criteria† for abdominal migraine Must include all of the following: 1. Paroxysmal episodes of intense acute periumbilical pain that lasts for 1 hours or more.2. Intervening periods of usual health lasting weeks to months.3. The pain interferes with normal activities.4. The pain is associated with 2 or more of the following: anorexia, nausea, vomiting, headache,photophobia, pallor.5. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms. H2d. Diagnostic criteria* for childhood functional abdominal pain Must include all of the following: 1. Episodic or continuous abdominal pain.2. Insufficient criteria for other functional gastrointestinal disorders.3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’ssymptoms.H2d1. Diagnostic criteria*for childhood functional abdominal pain syndrome Must include childhood functional abdominal pain at least 25% of the time and 1 or more of the following: 1. Some loss of daily functioning2. Additional somatic symptoms such as headache, limb pain, or difficulty in sleeping H1c. Diagnostic criteria* for aerophagia Must include at least 2 of the following: 1. Air swallowing.2. Abdominal distension due to intraluminal air.3. Repetitive belching and/or increased flatus.
Table II: Rome III Diagnostic Criteria for Pediatric Functional Bowel Disorders.
History: Red Flags Weight loss Persistent right upper or right lower quadrant pain Unexplained fevers Pain radiating to the back Unexplained rashes Arthritis Persistent vomiting Recurrent oral ulcers Dysphagia/odynophagia Anal/perianal ulcers Hematemesis Nocturnal symptoms (waking with diarrhea and/or vomiting) Bilious emesis Delayed puberty Chronic diarrhea (> 2 weeks) Deceleration of linear growth velocity Hematochezia/melena Physical Exam: Red Flags Decline in weight/height parameters Abdominal mass Pallor or anemia Localized tenderness Abdominal distension Perianal fissures or ulcers Organomegaly (hepatosplenomegaly) Positive hemoccult stool test
Table III: “Red Flags” In History and Examination of Recurrent Abdominal Pain.
Figure 1, 2: Huge bile, blood & food mixed fluid & material revealed after opening the abdomen by upper midline incision
Figure 3: Large perforation found in the 2nd part of duodenum
evidence that patients with recurrent abdominal pain have more symptoms of anxiety and depression (internalizing emotional symptoms) than do healthy community controls. In contrast, there is evidence that children with recurrent abdominal pain do not
have higher levels of conduct disorder and oppositional behavior (externalizing emotional symptoms) compared with healthy community controls. There are no data on whether emotional/behavioral symptoms predict symptom severity, course or response to treatment. There is evidence suggesting that children with recurrent abdominal pain are at risk of later emotional symptoms and psychiatric disorder.
Clinical Features: The primary feature of FAPS is abdominal pain. Usually, the pain is located around the umbilicus, however the pattern or location of abdominal pain is not always predictable. The pain may occur suddenly
or slowly increase in severity. The pain may be constant or may increase and decrease in severity. Some children with functional abdominal pain may experience dyspepsia, or upper abdominal pain associated with nausea, vomiting, and/or a feeling of fullness after just a few bites (early satiety). Others may experience abdominal pain with bowel movements. Pain that is usually relieved by bowel movements, or associated with changes in bowel
movement habits (mainly constipation, diarrhea, or constipation alternating with diarrhea) is the classic irritable bowel syndrome (IBS) (Table II). However, many diseases can cause chronic abdominal pain.
Therefore, any structural, organic, or chemical disease should be excluded. Patients with RAP often have pain-related behaviors. First, they often deny a role for psychosocial stressors. However, pain may diminish when patients are engaged in distracting activities but increase when they are discussing a psychologically distressing issue. Second, they express pain through verbal and nonverbal methods. They urgently report intense symptoms disproportionate to the available clinical and laboratory data. Third, they seek health care frequently. They often visit the emergency room and request analgesics. Fourth, they request diagnostic studies or even exploratory surgery to determine the organic origin of their condition. Fifth, they focus attention on complete relief of pain rather than on adapting to having a disease. Sixth, they take on limited personal responsibility for self-management. In addition to these features, distinct psychopathologies are usually found in patients with FAPS, including depressive disorders, anxiety disorders, and somatoform disorder.
History and Physical Exam: A complete history should be taken including social and dietary history and look for red flag symptoms and signs (Table III), Conduct a thorough physical exam, including rectal exam with stool hemoccult OR perianal exam with hemoccult of stool brought in by patient/family and review of the child’s growth. Children with recurrent abdominal pain are more likely than children without recurrent abdominal pain to have headache, joint pain, anorexia, vomiting, nausea, excessive gas and altered bowel symptoms. The presence of alarm symptoms or signs suggests a
higher pretest probability or prevalence of organic disease and may justify the performance of diagnostic tests. Alarm symptoms or signs include, but are not limited to, involuntary weight loss, deceleration of linear growth, gastrointestinal blood loss, significant vomiting, chronic severe diarrhea, persistent right upper or right lower quadrant pain, unexplained fever and family history of inflammatory bowel disease. The ‘red flag’ signs have long been used by clinicians to guide themselves to identify children who need further investigations and the salient ones on history and examination are noted in Table III 7,8.� Investigations: Investigations may be required to exclude particular conditions suggested by the history and examination. It is useful to pursue further diagnostic testing only in the presence of alarm symptoms9. Laboratory studies may be unnecessary if the history and physical examination clearly lead to a diagnosis of functional abdominal pain. However, a complete blood cell count, sedimentation rate, stool test for parasites (especially Giardia), and urinalysis are reasonable screening studies. If inflammatory bowel disease is suspected the sedimentation rate is often elevated. The finding of an abnormal sedimentation rate would make one look
further for an inflammatory, infectious, or neoplastic disorder. If indicated, an ultrasound examination of the abdomen can give information about kidneys, gallbladder, and pancreas; with lower abdominal pain, a pelvic ultrasonogram may be indicated.
An upper gastrointestinal tract x-ray series is indicated if one suspects a disorder of the stomach or small intestine. Helicobacter pylori infection does not seem to be associated with RAP. In patients with symptoms suggestive of gastritis or ulcer an H. pylori test (serum or fecal) may be performed to document the infection.
Esophagogastroduodenoscopy is indicated with symptoms suggestive of persistent upper gastrointestinal pathology. In the absence of this suspicion, esophagogastroduodenoscopy is unlikely to identify an abnormality and is usually not necessary.
Management: The family and the child with functional RAP may worry about the inability to identify an organic cause and may be resistant to a diagnosis of nonorganic disease. After a thorough history and physical examination the most important component of the treatment is reassurance of the children and family members10. Specifically, they need to be reassured that no evidence of a serious underlying disorder is present. Acknowledgment that the child's pain is real but not life-threatening is essential. When understood and accepted, this reassurance concludes the child and family's search for a physical cause and allows them to move into the next stage of learning to cope.
Dietary management: Data on dietary intervention are scarce and deal mainly with fiber supplementation and lactose exclusion. Whereas dietary fibre supplementation is a recognized strategy for management for childhood constipation, its value in recurrent abdominal pain is uncertain. The two randomized trials comparing fiber treatment with placebo have yielded conflicting results22,23. The data on lactose-free diets are likewise inconclusive, and a Cochrane review calls for ‘well-designed trials of all recommended dietary interventions’24.
A sensible course, despite lack of published evidence, is to recommend healthy eating including plenty of fruit and vegetables, regular sensible meals and plenty of fluids. This should be coupled with a daily routine with plenty of physical activity.
Symptom-based pharmacological therapies: In some cases, symptom-based pharmacological therapies are helpful. Medications for functional abdominal pain are best prescribed judiciously as part of a multifaceted, individualized approach to relieve symptoms and disability. It is reasonable to consider the time-limited use of medications that might help to decrease the frequency or severity of symptoms. Treatment might include acid reduction therapy for pain associated with dyspepsia; antispasmodic agents, smooth muscle relaxants, or low doses of psychotropic agents for pain or nonstimulating laxatives or antidiarrheals for pain associated with altered bowel pattern.
Cognitive–behavioural therapy: In many instances, all that is needed from the doctor is acknowledgment of the symptoms and reassurance that there is no serious underlying organic disease.
Sanders et al., compared this approach (standard paediatric care) with cognitive–behavioural therapy and found that both groups improved, though the response was somewhat better in the cognitive–behavioural therapy group21. They suggested that psychological intervention may have a role in difficult cases.
Family Functioning: Education of the family is an important part of treatment of the child with functional abdominal pain. It is often helpful to summarize the child’s symptoms and explain in simple language that although the pain is real, there is most likely no underlying serious or chronic disease. It may be helpful to explain that recurrent abdominal pain is a common symptom in children and adolescents, yet few have a disease. Functional abdominal pain can be likened to a headache, a functional disorder experienced at some time by most adults, which very rarely is associated with serious disease.
It is important to provide clear and age-appropriate examples of conditions associated with hyperalgesia, such as a healing scar, and manifestations of the interaction between brain and gut, such as the diarrhea or vomiting children may experience during stressful situations is recommended that reasonable treatment goals be established, with the main aim being the return to normal function rather than the complete disappearance of pain. Return to school can be encouraged by identifying and addressing obstacles to school attendance.
Prognosis: Many of the studies on prognosis relate to hospital practice not primary care10. It is generally more likely that children with recurrent abdominal pain will develop chronic abdominal symptoms in adulthood and as many as 30% may continue thus. Many will continue to suffer from IBS11,12. There is evidence that children with recurrent abdominal pain are more likely to have emotional and psychiatric disorders later in life. Generally speaking, however, follow-up studies show that parental factors rather than the psychological characteristics of the child are more important when predicting persistence of abdominal pain.
Conclusion:Recurrent abdominal pain (long-standing intermittent or constant abdominal pain) is common in children and adolescents. In most children, recurrent abdominal pain is functional—that is, without objective evidence of an underlying organic disorder. Yet an important part of the physician’s job is to determine which children have an organic disorder. A review of the current evidence, however, indicates
that there are no studies showing that pain frequency, severity, location or effects on lifestyle help to discriminate between functional and organic disorders. There have been few studies of the treatment of recurrent abdominal pain in children. There is inconclusive evidence that a lactose-free diet decreases symptoms or that a fiber supplement decreases the frequency of pain attacks. There is inconclusive evidence of the benefit of acid suppression with H2-receptor antagonists to treat children with dyspepsia. There is also evidence that cognitive/behavioral therapy may be useful in improving pain and disability outcome in the short term.
References:
1. Apley J. The child with recurrent abdominal pain.Pediatr Clin North Am 1967; 14: 63–72.
2. Huang RC, Plamer LJ, Forbes DA. Prevalence andpattern of childhood abdominal pain in an Australiangeneral practice. J Paediatr Child Health 2000; 36:349-353.
3. Boey CC, Yap S, Goh KL. The prevalence ofrecurrent abdominal pain in 11- to 16-year-oldMalaysian schoolchildren. J Paediatr Child Health2000; 36: 114-116.
4. Boey CC, Goh KL. Predictors of recurrentabdominal pain among 9 to 15-year-old urban school-children in Malaysia. Acta Paediatr 2001; 90: 353-5.
5. Rasul CH, Khan MAD. Recurrent abdominal painin school children in Bangladesh. J Ceylon Coll Phys 2000; 33: 110-14.
6. Caplan A, Walker L, Rasquin A. Validation of thePediatric Rome II criteria for functionalgastrointestinal disorders using the questionnaire onpediatric gastrointestinal symptoms. J PediatrGastroenterol Nutr 2005; 41: 305-16.
7. Pearl RH, Irish MS, Caty MG, Glick PL. Theapproach to common abdominal diagnosis in infantsand children. Part II. Pediatr Clin North Am 1998;45: 1287-1326.
10. Huertas-Ceballos A, Logan S, Bennett C, et al.Psychosocial interventions for recurrent abdominalpain (RAP) and irritable bowel syndrome (IBS) inchildhood. Cochrane Database Syst Rev 2008; (1):CD003014.
11. El-Matary W, Spray C, Sandhu B. Irritable bowelsyndrome: the commonest cause of recurrent abdominalpain in children. Eur J Pediatr 2004; 163(10): 584-8.
12. Nygaard EA, Stordal K, Bentsen BS. Recurrentabdominal pain in children revisited: irritable bowelsyndrome and psychosomatic aspects. A prospectivestudy. Scand J Gastroenterol 2004; 39(10): 938-40.
13. Balani B, Patwari AK, Bajaj P, Diwan N, AnandVK. Recurrent abdominal pain - a reappraisal. IndianPediatr 2000; 37: 876-81.
14. Buch NA, Ahmad SM, Ahmad SZ, Ali SW, CharooBA, Hussan MU. Recurrent abdominal pain in children.Indian Pediatr 2002; 39: 830-4.
15. Stordal K, Nygaard EA, Bentsen B. Organicabnormalities in recurrent abdominal pain in children.Acta Paediatr 2001; 90: 1-5.
16. Drossman DA, Camilleri M, Mayer EA, WhiteheadWE. AGA technical review on irritable bowelsyndrome. Gastroenterology 2002; 123: 2108–31.
17. Whitehead WE, Bosmajian L, Zonderman AB,Costa PT Jr, Schuster MM. Symptoms of psychologicdistress associated with irritable bowel syndrome.Comparison of community and medical clinic samples.Gastroenterology 1988; 95: 709–14.
18. Van Ginkel R, Voskuijl WP, Benninga MA, TaminiauJA, Boeckxstaens GE. Alterations in rectal sensitivityand motility in childhood irritable bowel syndrome.Gastroenterology 2001; 120: 31–8.
19. Di Lorenzo C, Youssef NN, Sigurdsson L, ScharffL, Griffiths J, Wald A. Visceral hyperalgesia in children with functional abdominal pain. J Pediatr 2001; 139: 838–43.
20. Talley NJ, Spiller R. Irritable bowel syndrome: alittle understood organic bowel disease. Lancet 2002;360: 555–64.
21. Sanders MR, Shepherd RW, Cleighorn G, WoolfordH. The treatment of recurrent abdominal pain inchildren: a controlled comparison ofcognitive–behavioural family intervention and standardpediatric care. J Cons Clin Psychol 1994; 62: 306-14.
23. Feldman W, McGrath P, Hodgson C, Ritter H,Shipman RT. The use of dietary fiber in themanagement of simple, childhood, idiopathic, recurrent,abdominal pain. Am J Dis Child 1985; 139: 1216-18.
24. Huertas-Ceballos A, Macarthur C, Logan S.Dietary interventions for recurrent abdominal pain(RAP) in childhood (Cochrane Review). In: TheCochrane Library. Issue 1, 2004.
Introduction:Injuries, especially as a result of blunt trauma, now constitutes one of the major causes of death in our country. The frequency of trauma to the abdomen may be increasing in almost geometric proportion as the number & speed of highway vehicles, civil unrest & terrorist attack rises.
Abdominal Trauma is a common clinical entity occurring in an emergency surgical unit and Blunt abdominal injury causing hollow viscous rupture is a common squeal. According to East multi-institutional trial of trauma indicate that after blunt abdominal trauma the incidence of small bowel injury and small bowel perforation (SBP) 1.1% and 0.3%, respectively1.
Case report:This is a story of a 20 years old boy. He had a history of road traffic accident 3 days back where he encountered by tin at supra umbilical region on right side. He was treated by local physician. On next morning he developed increasing abdominal pain, vomiting, respiratory distress & his conditions were deteriorating. On examination (OE) his abdomen was very tender & rigid, Blood Pressure (BP) - 100/60 mm Hg, Respiratory rate (RR) - 24/min, Pulse rate (PR) - 110/min. X-ray abdomen in erect posture including both dome of diaphragm revealed free gas shadow under both dome of diaphragm. Then other necessary investigations for assessing fitness for anaesthesia were done & Patient was prepared for exploratory laparotomy.
Abdomen was opened by upper midline incision revealing peritoneal cavity (Fig. 1, 2) with huge bile mixed food material & blood mixed fluid. Then content was sucked & peritoneal toileting was done. On query, large perforation was found in the 2nd part of duodenum (Fig. 3) about 10 cm distal to Gastro-Duodenal (G-D) junction & there was no other injury. Primary repair was done & two drain tube were kept in situ.
On 5th post-operative day (POD) patient was allowed to take liquid diet & sips of water orally. At the mean time observing for drain collection, abdominal pain, fever, vomiting & any discharge from wound.
On 7th POD patient was allowed to semi solid diet. Finally the drain tubes were removed on 9th POD. The recovery was uneventful. The patient left hospital giving thanks to all.
Discussion:Blunt abdominal trauma (BAT) may be from direct compression of the abdomen against a fixed object with resulting tears or subcapsular haematoma involving the solid organ associated viscera2. Hollow organs (typically small intestine) may rupture due to compression against a fixed point, usually the vertebral column. This compression causes rapid increase in intraluminal pressure leading to perforation of bowel wall at the anti-mesenteric border, where bowel is usually weaker2. Isolated duodenal injuries following a blunt abdominal trauma is uncommon. Complete transaction of duodenum is very rare presentation2. The
most common cause of blunt abdominal trauma (BAT) is motor vehicle accident (MVA).
Patients with multiple lower rib fractures are notorious for having severe intra-abdominal injuries without significant abdominal pain. The severe pain from the rib fractures becomes a distracting injury for the less noticeable abdominal pain. As a result, the patient may have a poor outcome as abdominal injuries are not recognized.
Spontaneous perforation of an hollow viscus may be the result of a range of pathological processes, where diagnosis is relatively easy for surgeon. But isolated duodenal perforation after blunt abdominal trauma is still a diagnostic challenge to surgeon.
One third of our patient did not present to the hospital until after an average of three days with advanced peritonitis. Reasons put forward to explain such delay include: 1. Relatively less initial peritoneal irritation
induced by the nearly neutral intestinal content particularly those with perforation between the duodeno-jejunal flexure and the ileo-caecal junction; 2. In small gut perforations the mucosa may prolapse through the hole and partly seal it making early sign of misleading; 3. The entity of a delayed perforation caused by an evolving injury. These patient have an initial contused bowel wall at the time of trauma that ultimately gives way after a variable period with resultant peritonitis. For this reason, physical examination during the initial evaluation is reliable for an early diagnosis in only 30% of blunt trauma injuries, in those patients who exhibit clear peritoneal signs3.
Abdominal pain, the usual symptom indicating abdominal injury is not severe & therefore the patient did not seek hospital care soon after injury most probably due to the above reasons.
Initial approach to the blunt abdominal trauma (BAT) patient is done according to fundamental principles of
advanced trauma life support (ATLS) system, which compromise primary survey & resuscitation [ABCDE (Airway, Breathing, Circulation, Disability, Exposure) of trauma care, steps of resuscitation, re-evaluation of ABC, monitoring the vital sign, introduction of gastric tube or Foley’s catheter] and secondary survey (careful abdominal examination & to identify all other injuries).
Several diagnostic modalities are being used for the identification of isolated bowel perforation. These are X-ray abdomen in erect posture including both domeof diaphragm, Serum amylase, WBC count, focusedassessment with sonography for trauma (FAST),diagnostic peritoneal lavage (DPL), Abdominal CT.Free sub-diaphragmatic gas, a radiologic signindicative of hollow viscus perforation easilydetected in plain abdominal radiographs, could leadto an early diagnosis in only 7-8% of the cases4,5.Elevated white blood cell (WBC) count and serumamylase levels could be suggestive of an intra-abdominal process and aid diagnosis in conjunctionwith history and physical findings. Althoughabnormal serum amylase can be noted in such cases,no clear cut-off value that could help differentiatepatients with SBP could be determined4. Focusedassessment with sonography for trauma (FAST) playan important roles to detect the free intra-peritonealfluid and haemo-pericardium in the assessment ofacutely traumatized patient, with the sensitivity of91-100%6. Diagnostic peritoneal lavage (DPL) canidentify Small bowel perforations (SBP) with greatsensitivity (up to 100%) but relatively lowspecificity7,8. CT has proved to be the gold-standardexamination, contributing toward a significantreduction of morbidity and mortality in traumavictims9,10. Postoperative complications like woundinfection, would dehiscence, intra-abdominal abscess,acute respiratory distress syndrome and sepsis, alloccur at two to three times higher incidence inpatients who undergo surgical repair of Small bowelperforations with extended delay11,12. The keyindividual in the development of a system of traumacare is the general surgeon.
Treatment:Urgent hospitalization of patient preferably in ICU with initial resuscitation, side by side preparation of the patient for laparotomy. After laparotomy, thorough surgical toileting, identification of injury, repair, re-toileting then drain were given. Associated injury were also looked for & treated. Abdomen was closed in layer. A meticulous follow up of the patient is needed for good outcome.
Conclusion:We present a case of successful repair of 3 days old traumatic duodenal perforation. Isolated duodenal perforation in blunt abdominal trauma victim is hard to diagnosis. Early diagnosis & appropriate operative management which are imperative to prevent morbidity in many cases. The rarity of duodenal perforation, the patient's good general condition following road traffic accident & treatment by local physician delayed the diagnosis. Cornerstone to successful management is combination of detailed history including the mechanism of injury, thorough clinical examination & Investigation under close supervision, surgical procedures to identify the perforation & repair.
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* Criteria fulfilled at least once per week for at least 2 months before diagnosis.† Criteria fulfilled 2 or more times in the preceding 12 months.
