Online Submission
IJCP Group of Publications
Volume 23, Number 3, August 2012
Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor Dr Deepak Chopra Chief Editorial Advisor
Dr KK Aggarwal CMD, Publisher, Group Editor-in-Chief
from the desk of group editor-in-chief 125 Food Choice may Affect Ability to Keep
Weight-off
Dr Veena Aggarwal MD, Group Executive Editor Anand Gopal Bhatnagar Editorial Anchor
IJCP Editorial Board Obstetrics and Gynaecology Dr Alka Kriplani Dr Thankam Verma, Dr Kamala Selvaraj Cardiology Dr Praveen Chandra Dr M Paul Anand, Dr SK Parashar Paediatrics Dr Swati Y Bhave Dr Balraj Singh Yadav Dr Vishesh Kumar Diabetology Dr Vijay Viswanathan Dr CR Anand Moses, Dr Sidhartha Das Dr A Ramachandran, Dr Samith A Shetty
KK Aggarwal
review article 126 Probiotics: The Friendly Microbes
Manoj Goyal, Monika Bansal, Shailesh Yadav, Kriti Malhotra
131 Corrosive Poisoning
R Raghu Ramulu Naik, M Vadivelan
Clinical study 137 Efficacy and Safety of Herbal Health Drink
(HiOwna-Jr) vs Regular Diet, in Growth, Health and/or Cognition of Children
Balamma Sujatha, P Kennedy Kumar
ENT Dr Jasveer Singh Dentistry Dr KMK Masthan Dr Rajesh Chandna Gastroenterology Dr Ajay Kumar
clinical practice 145 An Overview of Burning Mouth Syndrome
Dermatology Dr Hasmukh J Shroff Nephrology Dr Georgi Abraham
Anuradha Sunil, Archana Mukunda, Merwyn Nitin Gonsalves, Ashik Bin Basheer, Deepthi K
155 Diagnosis and Treatment of Acute Low Back Pain
Brian A. Casazza
Neurology Dr V Nagarajan Journal of Applied Medicine & Surgery Dr SM Rajendran Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions
case report 162 Recurrent Urovaginal Fistula: A Sequel of
Missed Ureteral Involvement
N Rajamaheswari, Archana Bharti Chhikara, K Seethalakshmi
case report
Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Publications Ltd. and Published at E - 219, Greater Kailash, Part - 1 New Delhi - 110 048 E-mail: editorial@ijcp.com
166 Scorpion Bite causing Acute Severe Myocarditis:
A Rare Complication
Printed at IG Printers Pvt. Ltd., New Delhi E-mail: igprinter@rediffmail.com, printer_ig@yahoo.com
Tarachand Saini, Shailendar Gupta, Maniram Kumhar
169 Autologous Bone Marrow-derived
Mononuclear Cell Transplantation in Duchenne Muscular Dystrophy
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173 Large, Dark Lesion on the Arm Present
Since Birth
Medilaw 176 Illegal MTP
MC Gupta
lighter reading 176 Lighter Side of Medicine
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Food Choice may Affect Ability to Keep Weight-off
T
he mix of carbohydrate, fat and protein in your diet may be a critical factor in maintaining weight loss, a new study reports. The finding suggests that, to the body, not all calories are created equal. Many people have difficulty keeping weight off once they’ve lost it. Only 1 in six overweight people will maintain at least 10% of their weight loss. Weight regain is often caused by reduced motivation or commitment to diet and exercise. In addition, weight loss slows the body’s metabolism, making it more difficult to burn calories. A research team, led by Drs Cara Ebbeling and David Ludwig at Boston Children’s Hospital, explored the effects of different diets on the ability to burn calories after weight loss. Their 4-year study was funded in part by NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and National Center for Research Resources (NCRR). The team recruited 21 adults, ages 18-40 and placed them on an initial diet to lose 10-15% of their body weight. All participants began the study with a body mass index (BMI) (a ratio of weight to height) of 27 or higher, classifying them as overweight or obese. After their weight loss, the participants followed three different diets in random order, each for four weeks at a time. The diets had the same number of calories, but varied in their levels of carbohydrate, fat and protein. One diet was low-fat, with 60% of calories from carbohydrate, 20% from fat and 20% from protein. The second was a lowglycemic index diet (designed to prevent spikes in blood sugar), with 40% of calories from carbohydrate, 40% from fat and 20% from protein. The third was a very-low carbohydrate (‘Atkins’) diet, with 10% of daily calories from carbohydrate, 60% from fat and 30% from protein. The study was published on June 27, 2012, in the Journal of the American Medical Association. The scientists measured the participants’ energy expenditure and other aspects of metabolism. They found that the number of calories burned daily differed among the three diets. On average, the very-low carbohydrate diet resulted in 3,137 daily calories burned. That was 200 more daily calories burned than the low-glycemic diet (2,937) and 325 more than the low-fat diet (2,812). Hormone levels and other metabolic measures also varied by diet. Although the very-low carbohydrate diet produced the most improvement in metabolism, the participants had higher levels of known risk factors for diabetes and heart disease, most notably the stress hormone cortisol. The low-glycemic index diet appeared to have benefits similar to the very-low carbohydrate diet with fewer negative effects. The researchers suggest that eating low-glycemic foods like less-processed grains, vegetables and legumes may be the best choice for lasting weight loss and heart disease prevention. “In addition to the benefits noted in this study, we believe that low-glycemic index diets are easier to stick to on a day-to-day basis compared to low-carb and low-fat diets, which many people find limiting,” Ebbeling says. “Unlike low-fat and very-low carbohydrate diets, a low-glycemic index diet doesn’t eliminate entire classes of food, likely making it easier to follow and more sustainable.” (Source: NIH)
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review article
Probiotics: The Friendly Microbes Manoj Goyal*, Monika Bansal**, Shailesh Yadav†, kriti Malhotra‡
Abstract We tend to think of bacteria as harmful ‘germs’, but, many bacteria actually help the body functions work properly. These bacteria are known as probiotics. The scientific evidence of beneficial effects of probiotics in health and disease is growing. This article highlights various such beneficial and potentially beneficial effects of probiotics.
Keywords: Bacteria, beneficial effects, Lactobacillus, Bifidobacterium
A
lthough we tend to think of bacteria as harmful ‘germs’, many bacteria actually help the body functions work properly. The belief that the bacteria can influence health, has increased the demand for new knowledge in the art and science of medicine. One such novel strategy, which gained interest over recent years is ‘probiotics’. Probiotics are live microorganisms (e.g. bacteria) that are either the same as or similar to microorganisms found naturally in the human body and may be beneficial to health.1 The term was first used by Lilly and Stillwell in 1965 to describe “substances secreted by one microorganism, which stimulates the growth of another” and thus was contrasted with the term antibiotic.2 The first recorded probiotic was ‘fermented milk’ and its role in human diet was known even in Vedic times. But, the scientific interest in this area boosted after the publication of the book entitled ‘The Prolongation of Life’ by Elie Metchnikoff in 1908. He suggested that people should consume fermented milk containing lactobacilli to prolong their lives. Accelerated aging is because of autointoxication (chronic toxemia), which is due to the toxins produced by gut microflora. Bulgarian peasants who were subjected to experiments on longevity had consumed large quantities of sour milk. The pathological reaction might be removed and life expectancy could *Associate Professor, Dept. of Pharmacology **Assistant Profesor, Dept. of Physiology †Professor ‡Junior Resident Dept. of Pharmacology Maharishi Markandeshwar Institute of Medical Sciences and Research Mullana, Ambala, Haryana Address for correspondence Dr Manoj Goyal E-mail: dr_manojgoyal@yahoo.co.in
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be enhanced by implanting lactic acid bacteria from Bulgarian yogurt. Since then, researchers started investigations relating to the role of lactic acid bacteria in human and animal health and the term ‘probiotics’ - meaning ‘for life’; eventually came into use.3 After 1965, the definition of probiotics was revised, in the year 2001, by the Food and Agriculture Organization (FAO) and the World Health Organization (WHO), as “live microorganisms which when administered in adequate amounts confer health benefits on the host”. Gradually, as the body of evidence of probiotic effectiveness accumulated, new features to the definition were appended broadening their implications. Probiotics can be bacteria, moulds or yeast. But most probiotics are bacteria.4 Commonly, most of the species ascribed as having probiotic properties belong to the genera Lactobacillus and Bifidobacterium. Among bacteria, lactic acid bacteria are more popular. Lactobacillus acidophilus, L. casei, L. lactis, L. helveticus, L. salivarius, L. plantarum, L. bulgaricus, L. rhamnosus, L. johnsonii, L. reuteri, L. fermentum, L. delbrueckii, Streptococcus thermophilus, Enterococcus faecium, E. faecalis, Bifidobacterium bifidum, B. breve, B. longum are commonly used bacterial probiotics. Saccharomyces boulardii is a yeast that was isolated from litchi fruit in Indonesia, which too had probiotic properties.5 These bacteria are ‘generally regarded as safe’ (GRAS) because they can reside in the human body causing no harm. On the other hand, they are key microorganisms in milk fermentation and food preservation and are used as dietary supplements and in yogurts from the dawn of mankind.4 Recently, there has been an explosion of consumer interest in the active role of functional food such as ‘probiotics’ - food considered in the well-being
review article and life prolongation, as well as in the prevention of initiation, promotion and development of nontransmissible chronic diseases. Nowadays other than just in food supplements, probiotics are also available to consumers as other products such as ‘probiotic suppositories and creams’.6 Criteria for microorganisms to be included in the probiotic group are:
Survival on passing through gastrointestinal tract at low pH and in contact with bile
Adhesion to intestinal epithelial cells
Stabilization of the intestinal microflora
Nonpathogenicity
Survival in foodstuff and possibly for production of lyophilized preparations Fast multiplication, with either permanent or temporary colonization of the gastrointestinal tract Generic specificity of probiotics.5
Just because it says ‘probiotic’, doesn’t mean it is a probiotic. Probiotics are measured in ‘CFU’. CFU stands for colony forming unit, which is the measure of live microbes in a probiotic. CFU amount should be the same as that shown to be effective in clinical studies. More CFUs does not necessarily mean better. Different probiotics have been shown to be effective at different levels. It is not possible to provide one count for all ‘probiotics’. Scientific literature has documented health benefits for products ranging from 50 millions to >1 trillion CFU/day.7 Mechanisms of probiotic action Several mechanisms have been suggested to contribute to the probiotic action. Probiotics improve colonization resistance to gut pathogens by reinforcing the mucosal barrier and restoring normal gut microecology after diarrhea. If the intestinal microflora is deficient, antigen transport is increased. Probiotics have been shown to normalize an increased permeability. Binding is considered to be the first step in pathogenesis, and binding of bacteria to the intestinal mucosa or mucus may allow the colonization. Probiotics compete with pathogens for binding sites and available substrates. However, adhesion to the intestinal mucosa is considered important for the beneficial health effect. Probiotics also seem to diminish the rate of progression from inflammation through dysplasia to colon cancer in experimental animals.8
Prebiotic Another term prebiotic was introduced by Gibson and Roberfroid who exchanged ‘pro’ for ‘pre’, which means ‘before’ or ‘for’. They defined prebiotics as “a nondigestible food ingredient that beneficially affects the host by selectively stimulating the growth and/or activity of one or a limited number of bacteria in the colon”.2 When prebiotics are found to be effective, the purpose they serve is that of a catalyst to promote the growth of the host’s indigenous colonies of helpful bacteria. A simple way to remember this is, that a prebiotic prepares the way for a probiotic. Prebiotics do not act in isolation, they do not introduce new bacteria, and they typically do not contain an entire culture of bacteria. For a food ingredient to be classified as a prebiotic, it must:
Neither be hydrolyzed nor absorbed in the upper part of the gastrointestinal tract Be a selective substrate for one or a limited number of potentially beneficial commensal bacteria in the colon, thus stimulating the bacteria to grow, become metabolically activated or both Be able as a consequence to alter the colonic microflora toward a healthier composition.9
Modification by prebiotics of the composition of the colonic microflora leads to the predominance of a few of the potentially health-promoting bacteria, especially, but not exclusively, lactobacilli and bifidobacteria. The only prebiotics for which sufficient data have been generated to allow an evaluation of their possible classification as functional food ingredients are the inulin-type fructans, which include native inulin, enzymatically hydrolyzed inulin or oligofructose and synthetic fructooligosaccharides. Inulin-type fructans are used as sugar substitutes, as fat replacers (inulin only), and as a means of providing texture, stabilizing foam or improving mouth feel in miscellaneous products such as fermented dairy products; desserts such as jellies and ice creams; bakery products such as cookies, breads and pastries; spreads and infant formulas. In a recent consensus paper, inulin-type fructans were classified as nondigestible oligosaccharides.10 Fructooligosaccharides are the only products presently recognized and used as food ingredients that meet these criteria to be said as a prebiotic. Experimental evidence suggests that certain other carbohydrate based components such as transgalactosylated disaccharides and soybean oligosaccharides may also fit in mentioned
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review article classification. At present, most searches for prebiotics are directed towards the growth of lactic acid producing microorganisms.9 Prebiotics are predominantly a type of dietary fiber that help probiotics to grow and thrive in the digestive tract. Onions, garlic, spinach, apples, banana, berries, beans, oats are a few of the examples that provide prebiotics.11 Synbiotic The term synbiotic is used when a product contains both probiotics and prebiotics. Because the word alludes to synergism, this term should be reserved for products in which the prebiotic compound selectively favors the probiotic compound. In this strict sense, a product containing oligofructose and probiotic bifidobacteria would fulfil the definition, whereas a product containing oligofructose and a probiotic L. casei strain would not. However, one might argue that synergism is attained in vivo by ingestion of lactobacilli on the one hand and promotion of indigenous bifidobacteria on the other hand.2 Evidence of Probiotic Effectiveness The comprehensive review of the literature by the expert panel of FAO and WHO demonstrated a number of areas in which probiotics have proven their antidisease effects. Following are the various examples.12
Oral Health The interest in oral probiotics has been growing during the last decades. Some of the probiotic bacteria used in various probiotic products may colonize the oral cavity during the time they are in use; thus, the effects of probiotic bacteria in the oral cavity are important to understand.13 Molecular analyses of the oral microbiota in preschool children have shown that Streptococcus mutans is significantly associated with early childhood dental caries. Several studies suggest that consumption of products containing probiotic lactobacilli or bifidobacteria could reduce the number of Mutans Streptococci in saliva responsible for dental caries. Mutans streptococci are gram-positive bacteria commonly found in the oral cavity of humans and are the most cariogenic for the tooth enamel. It promotes the sticking of bacteria to tooth enamel forming a plaque biofilm and contributes to cariogenicity. The beneficial effects of use of these ‘live organisms’ cannot be limited to caries but may be extended to in the use of periodontal diseases, oral candidiasis and in halitosis
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as well. Potential mechanism by which probiotic bacteria affects oral health is by competing for adhesion sites and enhancing clearance of the pathogenic bacteria. They also produce antimicrobial compounds including acids and check the growth of offending organisms. They also have an influence on the local and systemic immune responses by enhancing the production of salivary immunoglobulin (IgA), defensins and proinflammatory cytokines. All these actions play an antagonistic role against pathogenic bacteria and finally reduce inflammation and tissue destruction.14
Diarrhea There is a recent resurgence of interest in probiotics due to consumer demand for better therapies and problems like drug resistance and opportunistic infections due to inadvertent use of antimicrobial therapy. Diarrhea is a common gastrointestinal problem especially in the developing world. Decrease in shortchain fatty acid important for absorption of water and electrolytes, loss of carbohydrate digesting gut bacteria leading to osmotic diarrhea or use of drugs such as erythromycin (motilin agonist), which is a direct stimulator of gut motility, are all responsible for the pathogenesis of preventable diarrhea. The problem of infectious diarrheas can be best addressed by improving sanitation and nutrition, but an inexpensive and effective probiotic are shown to reduce the incidence of diarrheal episodes when used as adjunct to oral rehydration therapy.15 The pathogen, Helicobacter pylori is responsible for type B gastritis and peptic ulcers. There is some in vitro and animal data to indicate that lactic acid bacteria can inhibit the pathogen’s growth and decrease the urease enzyme activity necessary for it to survive in the acidic environment of the stomach. In humans, there is also evidence that probiotic strains can suppress infection and lower the risk of recurrences. Similar benefits of probiotics are seen to be associated with inflammatory disease and bowel syndromes (Crohn’s disease and ulcerative colitis, polyps, diverticulosis, diverticulitis, etc.) Diarrheas in newborn and children Intestinal infections in newborn children are common, and in developing countries diarrhea is a prime cause of morbidity and mortality. Necrotizing enterocolitis is a devastating intestinal disorder, which is characterized by an inflammatory cascade with septic shock and intestinal necrosis. Bacterial colonization or infection of the intestine by pathogens such as Clostridium, Escherichia, Klebsiella, Salmonella, Shigella, Campylobacter, Pseudomonas,
review article Streptococcus, Enterococcus, Staphylococcus aureus and coagulase-negative staphylococci increases the risk of necrotizing enterocolitis. If nonpathogens, such as lactobacilli and bifidobacteria, colonize the intestine or if breast milk rather than formula is used, the incidence of necrotizing enterocolitis has been reported to decrease. Several potential mechanisms have been proposed for how lactobacilli reduce the duration of rotavirus diarrhea. One is competitive blockage of receptor sites in which lactobacilli bind to receptors, thereby preventing adhesion and invasion of the virus. The second potential mechanism may be the enhanced immune response by lactobacilli, by inducing local IgA antibodies against the virus. Alternatively, stimulation of T cells to produce ginterferon, leading to potential inhibition of chloride secretion, might also inhibit diarrhea. A final theory is that lactobacilli produce substances that inactivate the viral particles. This has been shown in vitro. Whether or not the viral killing activity can inhibit diarrhea remains to be determined.12 The mechanism of action of these probiotics as antidiarrheal more or less remains the same in all types of diarrheas on a broad aspect.
Lactose Intolerance Probiotic strains are also beneficial in the lactose intolerance, a physiological state in human beings where they lack the ability to produce an enzyme named lactase or β-glycosidase, which is essential to assimilate the disaccharide present in milk and needs to be split into glucose and galactose. Individuals lacking lactase will not be able to digest milk and it often poses a problem in newborn infants. The resident bacteria in the colon ferment undigested lactose, producing acid and gas, causing symptoms such as abdominal pain, bloating and diarrhea. Yogurt contains less lactose than milk and delays gastric emptying, which partly explains why lactose-intolerant individuals tolerate yogurt. However, yogurt tolerance is mainly due to the supply of lactase activity from the lactic acid bacteria present in the yogurt itself. Evidence shows that bacteria must be live and present in sufficient quantity to be of benefit. Yogurts containing 108 bacteria/ml are required to produce beneficial effects. Another problem associated with lactose intolerance is calcium deficiency. A person consuming non-milk diet will naturally develop calcium deficiency, leading to osteoporosis. Birge et al confirmed that lactose deficiency leads to calcium malabsorption and thereby to osteoporosis. Calcium absorption is better and more in acidic conditions; hence, if lactose is converted to lactic acid, pH of the
gut decreases, i.e. it becomes acidic favoring enhanced absorption of calcium. So, if probiotics are fed to lactose intolerance patients, then milk lactose is hydrolyzed by probiotic strains and lactose is assimilated and calcium absorption is also favored.3
Cholesterol Assimilation Probiotic strains, especially lactic acid bacteria have a major role to play in the cholesterol lowering mechanism. The cholesterol levels can be brought down using probiotics. The mechanisms can be direct or indirect. Direct mechanism is by either inhibiting the de novo synthesis or decreasing the intestinal absorption of dietary cholesterol. The dietary cholesterol absorption is reduced by three ways - assimilation, binding or by degradation. Probiotic strains assimilate the cholesterol for their own metabolism. Probiotic strains can bind to the cholesterol molecule, and they are capable of degrading cholesterol to its catabolic products. The cholesterol level can be reduced indirectly by deconjugating the cholesterol to bile acids, thereby reducing the total body pool. Deconjugation by different lactic acid bacterial cultures was also tried using two forms of bile salts, viz. taurocholates and glycocholates. Though, the results were nonsignificant, there was a drastic reduction in serum cholesterol of fermented milk-fed rats, indicating that cholesterol levels in serum can be reduced by consumption of probiotics.5
Allergy A change in the proper functioning of the immune system can present itself as an allergy. Large-scale studies have indicated an alteration in the composition of the gut microflora, such as decrease in the numbers of lactobacilli, preceding the development of an allergy. Probiotics have also been shown to reduce the incidence of childhood eczema. A follow-up study demonstrated a two-fold increase in transforming growth factor β2, an anti-inflammatory cytokine, in the breast milk of mothers receiving probiotics compared to placebo. Probiotics may exert a beneficial effect on allergic reaction by improving mucosal barrier function. In addition, probiotics consumption by young children may beneficially affect immune system development. Probiotics such as Lactobacillus GG may be helpful in alleviating some of the symptoms of food allergies such as those associated with milk protein. Probiotics consumption may thus be a means for primary prevention of allergy in susceptible individuals.
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review article This could play a key role in minimizing allergy at a time when the prevalence of allergic disease in Western societies has increased dramatically over the past 40 years.
Anticancer Effects The anticancer benefits of fermented foods were regarded as folklore, with no scientific backing. But, now there is a strong attestation to the importance of Lactobacilli in human nutrition and health, as well as the inter-relationship between many dietary factors and cancer. Diets high in animal protein and fat appear to increase the susceptibility to colon cancer, apparently through conversion of pro-carcinogens to carcinogens by the intestinal microflora. Fats and fried foods also have been implicated in cancers of breast, prostate and pancreas. There is some evidence that probiotics can interfere at various stages of the cancer process. The changes in gut bacterial enzymes that generate carcinogens and tumor promoters such as ammonia (NH3) and secondary bile acids, stimulation of immune surveillance, suppression of inflammatory processes, binding of carcinogens in the gut will have various levels of scientific support.3
Other Effects It is believed that most probiotics do not permanently adhere in the intestine, but exert their effects as they metabolize and grow during their passage through the intestine (colonization). Thus, daily consumption of these bacteria is probably the best way to maintain their effectiveness. Other beneficial effects which these wonder live microorganisms produce are reduction of blood pressure in hypertensives, synthesize nutrients (folic acid, niacin, riboflavin, vitamins B6 and B12). Increase nutrient bioavailability, improve urogenital health and optimize effects of vaccines (e.g. rotavirus vaccine, typhoid fever vaccine).16 Future Implications Modern consumers are increasingly interested in their personal health, and expect the food that they eat to be healthy or even capable of preventing illness. Producers and marketers of cultured milks are making every effort to keep them growing through product development and packaging innovations while delivering a ‘good for you’ flavorful products suited for all occasions of gastronomic indulgence. Over the past century, voluminous scientific knowledge has been well-established regarding the technological aspects of fermented milks, including the physiology of starter cultures and related probiotic microflora.
There is considerable potential for the benefits of probiotics consumption over a wide range of clinical conditions. Ongoing research will continue to identify and characterize existing strains of probiotics, identify strain-specific outcomes and determine optimal doses needed for certain results. Conclusion Probiotics seem to have quite a number of beneficial effects in the different organ systems of the body. The full potential of probiotics can only be realized when their benefits can be established scientifically. It is highly likely that benefits from current and future probiotics have gone undetected and, therefore, full utilization of these organisms has not been achieved. At best, the intestinal health is greatly improved and the immune system is strengthened. At worst, there are no adverse effects and you get some nutrients in the bargain. With the current focus on disease prevention and the quest for optimal health at all ages, the probiotic market potential is enormous. Health professionals are in an ideal position to help guide their clients toward appropriate prophylactic and therapeutic uses of probiotics that deliver the desired beneficial health effects. References 1.
Oral probiotics: An introduction. Get the facts. National Centre for Complementary and Alternative Medicine. Retrieved from http://nccam.nih.gov/health/probiotics/ introduction.htm.
2.
Schrezenmeir J, de Vrese M. Probiotics, prebiotics, and synbiotics - approaching a definition. Am J Clin Nutr 2001;73(2 Suppl):361S-364S.
3.
Suvarna VC, Boby VU. Probiotics in human health: a current assessment. Curr Sci 2005;88(11):1744-8.
4.
Stamatova I, Meurman JH. Probiotics: health benefits in the mouth. Am J Dent 2009;22(6):329-38.
5.
Tomasik PJ, Tomasik P. Probiotics and prebiotics - review. 2003;80(2):113-7.
6.
Granato D, Branco GF, Nazzaro F, Cruz AG, Faria JA. Functional foods and nondairy probiotic food development: trends, concepts, and products. Comprehensive Reviews in Food Science and Food Safety 2010;9:292-302.
7.
Probiotics: A Consumer Guide for Making Smart Choices. Developed by the International Scientific Association for Probiotics and Prebiotics. March 11, 2009. Retrieved from (www.isapp.net).
8.
Meurman JH. Probiotics: do they have a role in oral medicine and dentistry? Eur J Oral Sci 2005;113(3):188-96. Cont’d on page 152...
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review article
Corrosive Poisoning R Raghu Ramulu Naik*, M Vadivelan**
Abstract Corrosive poisoning is a common emergency as corrosive agents are easily available for household use. Emetics and neutralizing agents should be avoided in treatment. Management of corrosive poisoning includes parenteral hydration and nutrition, H2-receptor antagonists or proton pump inhibitors. Upper gastrointestinal (GI) endoscopy should be done once the patient is hemodynamically stable and there are no signs of perforation. Urgent surgery is required in the event of perforation. Patients with Grade 0-1 injuries do not need hospitalization, while patients with Grade 2 and 3 injuries require intensive care unit (ICU) management.1
Keywords: Corrosive agents, proton pump inhibitors, perforation
C
orrosives are a group of chemicals that have the capacity to cause tissue injury on contact by a chemical reaction. They most commonly affect the gastrointestinal tract (GIT), respiratory system and eyes. Corrosives and caustics are synonyms, both mean ‘something that eats away’. Acids and alkalis are the two primary types of agents most often responsible for caustic exposures.2 Exposure to corrosive agents continues to be a leading toxicological source of injury for children and adults. An average home contains a dozen different cleaning products. These account for a large number of accidental and intentional poisonings. The estimated prevalence of corrosive poisoning is 2.5-5% while the morbidity is above 50% and the mortality is 13%. Eighty percent of corrosive poisoning occurs in children below five years. But, adult exposure has more morbidity and mortality due to significant volume of exposure and possible co-ingestion. COMMON CAUSTIC AGENTS The common caustic agents include:
Dehydrating agents
Halogens and organic halides
Phenol Acids
Car battery fluid (sulfuric acid)
Descalers (hydrochloric acid)
Metal cleaners (nitric acid)
Rust removers (hydrogen fluoride)
Alkalis
Bleach (hypochlorite)
Sodium hydroxide (liquid lye)
Uses of Common Caustic Agents3
Hydrochloric acid-metal/toilet bowl cleaner
Sulfuric acid-automobile batteries
Sodium hydroxide-paint remover/drain cleaner
Phenol-antiseptic
Factors Determining Corrosiveness
Strong acids and alkalis
Concentrated weak acids and alkalis
Oxidizers (with neutral pH)
Physical form: Solid/liquid
Alkylating agents
Duration of contact with tissue
Concentration of agent
Quantity of agent
pH of agent: pH <2 and >11 are more corrosive
Food: Presence or absence of food in stomach
*Junior Resident **Assistant Professor Dept. of Medicine Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry Address for correspondence Dr M Vadivelan No. E-2, JIPMER Quarters, JIPMER Campus, Dhanvantari Nagar Pondicherry - 605 006 E-mail: mevadivelan@hotmail.com
Factors that determine corrosiveness include:3
Titratable acid or alkali reserve (TAR): This quantifies the amount of neutralizing substance required to bring the pH of a caustic agent to physiological pH of the tissue.2
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review article Mechanism of Action of Corrosive Agents
Alkali ingestion: Causes liquefaction necrosis. This process includes protein dissolution, collagen destruction, fat saponification, cell membrane emulsification, submucosal vascular thrombosis and cell death.3 Acid ingestion: Causes coagulation necrosis. In this process, hydrogen (H+) ions desiccate epithelial cells producing an eschar. This process leads to edema, erythema, mucosal sloughing, ulceration and necrosis of tissues.3
Both acids and alkalis cause fibrosis and cicatrization (stricture formation).
Investigations
Laboratory Tests
Necrosis: Occurs within seconds of exposure to caustic agent
Blood grouping and cross-matching
Renal function tests
Liver function tests
Coagulation profile
Fibrosis: Occurs within 14-21 days of exposure
Stricture: Occurs after weeks to years of exposure
Carcinoma formation: Occurs after decades of alkali exposure.
Clinical Presentation in Corrosive Poisoning GIT
132
abdomen Excessive salivation Dysphagia and odynophagia Epigastric pain and hematemesis Symptoms and signs of GI perforation
Chest X-ray: The radiographic signs of early mediastinal leaks are usually subtle. However, chest X-ray helps in detection of pneumothorax, pneumomediastinum and pleural effusion. Air under the diaphragm is suggestive of visceral perforation. A lateral view is more sensitive than PA view for detecting intraperitoneal air.5 Abdominal X-ray: Can help in the detection of pneumoperitoneum. Contrast studies: Barium studies have low sensitivity in detecting perforation and high-risk of aspiration and inflammation. CT scan: CT scan of neck/chest/abdomen should be considered if there is a high-risk of suspicion for perforation despite negative plain X-rays. Contrastenhanced CT (CECT) is used to assess esophageal wall thickness, which can be used to predict the response to dilatation of stricture and the number of sessions required to achieve adequate dilatation. CT studies done with water-soluble contrast will allow localization of leak of air.
Cough
Endoscopy
Dyspnea Bronchoconstriction Pulmonary edema Chemical pneumonitis
Endoscopy has been called ‘sine qua non’ for evaluating patients with corrosive poisoning. Direct evaluation by endoscopy is useful in grading severity of tissue injury, planning for nutritional support and long-term management of strictures.6
Eyes and skin
Severe pain of lips, mouth, throat, chest and
Respiratory system
Arterial blood gas analysis: Arterial blood pH and base deficit correlate with severity and adverse outcomes.
Radiology
Ulceration and perforation: Occurs within 24-72 hours of exposure
Serum electrolytes: Hypocalcemia can occur with hydrogen fluoride poisoning.
Consequences of Caustic Injury Caustic injury may cause the following:4
Hemogram: WBC count >20,000/mm³ is an independent predictor of mortality in corrosive poisoning.
Pain at the site of exposure
Burns at the site of exposure Erythema and vesicle formation
Indian Journal of Clinical Practice, Vol. 23, No. 3, August 2012
Indications for upper GI endoscopy
Corrosive ingestion by small children
Symptomatic older children and adults
Patients with altered mental status
review article
Patients with intentional ingestion
Late Admission
Patients with ingestion of large volumes
Patients with ingestion of concentrated products.
More than three weeks of ingestion: Requires endoscopy and dilatation of stricture. If the procedure is successful, then follow-up endoscopy should be done at one month. If the procedure is unsuccessful, then surgical gastrostomy is performed, which is followed by retrograde dilatation of stricture after 10 days of operation.
Contraindications for upper GI endoscopy
Hemodynamic compromise
Peritonitis and mediastinitis
Mild ingestion (asymptomatic patients with normal oral/upper airway examination).
Endoscopy done very early (<6 hours) may not reveal the full extent of injury. The commonest practice is to perform endoscopy on Day 1-2.6 The findings on upper GI endoscopy are based on Zargar’s modified endoscopic classification of burns due to corrosive ingestion.6 They are graded as below: Grade
Description
0
Normal mucosa
1
Erythema/Hyperemia
2a
Superficial ulcer/erosion/friability/hemorrhage/ exudates
2b
Findings in 2a + deep discrete/circumferential ulcers
3a
Scattered necrosis (black/grey discoloration)
3b
Extensive/circumferential necrosis of mucosa
Clinical Approach in Management of Corrosive Poisoning Approach to the management of corrosive poisoning is based on the clinical features of the patient with caustic ingestion. 1. Asymptomatic patient: If there is history of minimal corrosive ingestion and no oropharyngeal burns on examination, then the patient requires only observation in the Emergency Room. 2. Symptomatic patient: If there is history of ingestion of large volume of corrosive along with signs like stridor, hoarseness of voice and respiratory distress, then the patient requires admission in intensive care unit (ICU) and management as detailed below.
Management Management is based on the presenting clinical features on admission to the hospital. This can be divided into emergency management, management of stable patient and long-term management.
Early Admission Within 48-72 hours of corrosive ingestion: Upper GI endoscopy should be performed on Day 1-2. (ideally between 12-24 hours of ingestion). If endoscopy reveals only mild lesions, then the patient can be discharged and clinical follow-up should be done at one month. If severe lesions are found on endoscopy, then surgical gastrostomy is indicated, which should be followed by repeat endoscopy and dilatation after three weeks.
Delayed Admission Within 72 hours to three weeks of corrosive ingestion: No endoscopy is indicated. Gastrostomy should be done if there is severe dysphagia. Endoscopy and dilatation of stricture (if present) should be done three weeks after ingestion.
Protection of airway: In the presence of respiratory distress and airway edema, urgent endotracheal intubation should be done as airway edema may rapidly progress over minutes to hours. Supraglottic edema leads to acute upper airway obstruction and cricothyrotomy or tracheostomy is needed in such a situation. Delay in prophylactic airway protection may make subsequent attempts at intubation or bag mask ventilation difficult or impossible. There is no clear role for systemic steroids in decreasing airway edema and of intravenous adrenaline or nebulization in reducing the need for endotracheal intubation. Hemodynamic status: Acute circulatory compromise usually occurs due to hypovolemia. The reasons for hypovolemia are hemorrhage, vomiting and third-space sequestration. Hemodynamic correction can be done by replacement with crystalloid fluids. Invasive hemodynamic monitoring is indicated in unstable patients. Decontamination: Any attempt at gastric emptying or dilution of compound is contraindicated in corrosive poisoning. Emetics should not be given as they increase the risk of mucosal injury and subsequent perforation. Nasogastric tube should not be inserted since it may cause esophageal perforation and increase the risk of aspiration. Exceptions to general rules of decontamination are zinc chloride and mercury chloride poisoning because both cause systemic toxicity.
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review article Dilution and neutralization: Dilution and neutralization of corrosive by nasogastric tube lavage generates heat and increases the risk of aspiration. Both have no proven benefit and hence are contraindicated. 3. Stabilized patient: Initial evaluation of a stabilized patient aims to identify the acute complications of corrosive ingestion and stratify the risk for acute and long-term complications mainly by endoscopic grading of corrosive lesions.
Corticosteroids: While there is no role of systemic steroids in the management of caustic ingestion, intralesional steroids can be given.7 Antibiotics: Tissue destruction from caustic injury increases the risk of infection by enteric organisms. Antibiotics are not recommended prophylactically in corrosive poisoning. They are recommended in GI perforation.8 Proton pump inhibitors (PPIs) and H2-blockers: Gastroenterologists routinely recommend PPIs and H2-blockers in caustic ingestion.8
Nutrition: Endoscopic grade of lesions needs to be assessed for planning nutritional support in patients with caustic ingestion. Patients with Grade 1/2a lesions on endoscopy can tolerate oral feeds, while those with Grade 2b/3a lesions will need nasoenteral feeding. Patients with Grade 3b lesions require gastrostomy for enteral feeding and rarely need total parenteral nutrition (TPN).
Complications
Acute: Airway compromise; shock (due to hemorrhage, vomiting or third-space sequestration); GI perforation (can cause esophageal leak/rupture and mediastinitis or gastric leak/bleed leading to peritonitis). Late: Stricture; obstruction Remote: Carcinoma of esophagus.9 Patients who develop esopahageal strictures after alkali consumption have high-risk (1,000 times more risk than the general population) for the development of squamous cell carcinoma of esophagus. The mean latency period is 40 years after ingestion and in 84% of the patients, the malignancy is located in the area of the bifurcation of trachea.
Management of Complications
Persistent hypotension
Respiratory distress
Ascites or pleural effusion
pH < 7.2 on arterial blood gas (ABG) analysis
Laparotomy permits tissue visualization, resection and repair of perforation. Stricture management Stricture formation begins weeks to months after injury and is the most important consequence of corrosive poisoning. Procedures used for prevention and treatment of strictures are:
Endoscopic or radiologic evidence of perforation
Severe abdominal rigidity
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Surgery: Esophageal strictures resistant to dilatation therapy may require surgery that includes resection of stricture surgically and esophageal bypass surgery.
REFERENCES 1.
Lahoti D. Corrosive injury to upper gastrointestinal tract. In: Manual of medical emergencies, 3rd edition.
2.
In: Critical Care Toxicology: Diagnosis and Management of the Critically Poisoned Patient. 1st edition, Brent, Wallace, Burkhart, Phillips, Donovan (Eds.) 2005:p. 1035-44.
3.
Caustics. In: Goldfrank’s Toxicologic Emergencies. 8th edition.
4.
Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 8th edition, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt (Eds.) 2006:p.406-9.
5.
Woodring JH, Heiser MJ. Detection of pneumoperitoneum on chest radiographs: comparison of upright lateral and posteroanterior projections. AJR Am J Roentgenol 1995;165(1):45-7.
6.
Zargar SA, Kochhar R, Mehta S, Mehta SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc 1991;37(2):165-9.
7.
Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med 1990;323(10):637-40.
8.
Acids and alkalis. The Poisoning and Toxicology Handbook. 4th edition, Jerrold B. Leikin, Frank P. Paloucek Informa Healthcare, USA 2007:p.713-9.
9.
Alkali injury. In: Clinical Management of Poisoning and Drug Overdose. 3rd edition, Lester M. Haddad, Michael W. Shannon, and James F. Winchester (Eds.) 1998: p.817-20.
Laparotomy Laparotomy is indicated in patients with:
Dilatation therapy: This is done 3-6 weeks after injury, progressively larger bougies are passed over endoscopically placed guide wires for dilatation. But, the risk of perforation, aspiration and dysphagia is high.
Clinical study
Efficacy and Safety of Herbal Health Drink (HiOwna-Jr) vs Regular Diet, in Growth, Health and/or Cognition of Children Balamma Sujatha*, P Kennedy Kumar**
Abstract Micronutrient malnutrition causes various physiological impairments leading to low resistance to infections, metabolic disorders, and diminished physical, and psychomotor development. Aim: To evaluate the clinical efficacy and safety of a polyherbal health drink in maintaining general growth, health and cognition in children. Study design: Open, comparative clinical trial. Material and methods: Fifty-one children including both male and female, aged between 2-10 years were included in the trial. A detailed medical history and simple physical and systemic examination was done. The selected cases were randomized into one of two groups: Subjects in Group A (n = 30) aged 2-10 years were instructed to take HiOwna-Jr at a dose of 12.5 g and those aged 7-10 years were instructed to take 25 g of HiOwna-Jr orally twice-daily for the period of eight weeks. Whereas, subjects in Group B (n = 21) were instructed to take regular diet for a period of eight weeks. Subjects were assessed at entry, Week 4 and Week 8. At each visit the subjects were evaluated for general health and growth, frequency of respiratory tract infection (RTI) and appetite. Cognition was also evaluated in children aged between 5-10 years taking into consideration attention, memory and concentration. Results: HiOwna-Jr showed a trend towards improvement in the growth as determined by height, weight and body mass index (BMI), general health as determined by decrease in the frequency of RTI and improving appetite in children between 2-10 years of age. Cognition parameters of attention, memory and concentration in children aged 5-10 years also showed beneficial results. All the children liked the formulation and completed the study. Overall compliance to the study was good. No adverse effects were either reported or observed during the clinical study. Conclusion: HiOwna-Jr in addition to regular diet is effective in children in progressively maintaining the normal natural linear growth, general health including resistance to infections and cognition in school-going children.
Keywords: HiOwna-Jr, growth, cognition
N
utrition is related to five of the 10 leading risks as causes of disease burden measured in DALYs (disability-adjusted life years) in developed countries i.e. blood pressure, cholesterol, overweight (obesity), low fruit and vegetable intake, and iron deficiency as per World Health Organization (WHO), 2002. The above measurements of health indicate the biological relationship between nutritional intake or diet and physical health outcomes. These risks are precursors to disease and illness that impact upon morbidity and mortality.1,2 However, the timing, frequency, content and quantity of food eaten are additionally related to developmental, cognitive and behavioral outcomes that influence quality-of-life. Despite the *Consultant Pediatrician **Consultant Sankreswari Clinic, Bharathiyar Nagar, Pattabiram, Chennai Address for correspondence Dr Balamma Sujatha Sankreswari Clinic 9/4 IAF Road, Bharathiyar Nagar, Pattabiram, Chennai
economic growth observed in developing countries, malnutrition and particularly undernutrition is still highly prevalent.3 There is a complex interrelationship between nutrition, health, education as well as social and economic factors. Food preferences are affected by social and family factors such as the behavior of parents and peers, advertising and marketing and practices related to food production and consumption. While the constraints of low income create practical barriers to healthy eating, additional socioenvironmental factors, such as culture and lack of literacy and education reinforce the effects of deprivation. Unfortunately, today, too many children have unhealthy eating patterns which affect their well-being now and for the future. Nutrition surveys in Canada4-6 show that children are filling up on junk foods and beverages with poor nutritional value, eating too many calories from high-fat, unhealthy fat, salty and/or sugary foods, not meeting the minimum number of recommended
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clinical study servings of the basic four food groups, especially for vegetables, fruit and milk. Poor nutrition keeps children from doing well at school along with absenteeism, behavioral and emotional problems, frequent infections due to lack of immunity, poor concentration and inability to solve problems and remember information they have lower test scores and are more irritable.7,8 Micronutrient deficiencies compromise health and development of many children worldwide. Micronutrient interventions might benefit the health and development of children; multiple micronutrients might be more effective than single micronutrients. Food fortification is a practical way to provide extra micronutrients to children. Many children around the world suffer from nutritional deficiencies, which can negatively affect their physical and mental development and increase susceptibility to infections.9-11 During early childhood, characterized by rapid growth, children should be provided with an adequate amount of energy. The macronutrients that can provide children with energy are fats, carbohydrates and proteins. Undernutrition, growth failure, overweight, micronutrient deficiencies and osteopenia are nutritional comorbidities that affect the neurologically impaired child. Studies have reviewed the epidemiology, pathogenesis, assessment and treatment of these disorders in neurologically impaired children.12 In addition, school-age children may develop a more independent eating pattern;13 this can include more outof-home food consumption without supervision, which is likely to result in increased intake of foods of low nutritional value, such as soft drinks and salty snacks in place of micronutrient-rich foods.14 A correct process of growth and development tied to a healthy diet provides the basis for maintaining good health following the growth years. Respiratory diseases are a major cause of morbidity and mortality in developing countries. Data suggest that children could suffer from 7 to 8 upper respiratory tract infections (URTIs) per year until they are five years of age, when their immune status reaches adult level.15 Acute URTIs are common in young children and contribute to ~20% of mortality in children younger than five years of age. It represents the most frequent problem in general pediatric practice and account for more than a third of school absence.16 Children with a history of recurrent infections present a diagnostic challenge due to the expectations of the parents for an explanation regarding the increase in the frequency of infections.17
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Nutrition education is important, though not sufficient to empower individuals to improve their diet. The Food and Health Action Plan identified six key targets to improve the nationâ&#x20AC;&#x2122;s diet, which include reduction of salt, sugar and saturated fat consumption, and increased fiber and fruit and vegetable intake.18 Various health drinks are available in various flavors and other requirements meeting the changing consumer preferences and good enough to attract children. HiOwna-Jr is a natural polyingredient formulation known to provide balanced nutrition and help in promoting overall health of children by their nutritive, energy boosting, digestive, memory enhancing and immunomodulatory properties. The herbs are designed to promote general health, natural appetite and wellbeing of children and to support the optimum natural linear growth and development of children between 2-10 years of age, enhance immunity and to maintain adequate natural cognitive function. Aim To compare the clinical safety and efficacy of a polyherbal formulation HiOwna-Jr with regular diet in maintaining growth, immunity in respiratory tract infections (RTIs), appetite and cognition in children. Material and methods
Study Design This was an open comparative clinical trial conducted at Sankreswari Clinic, 9/4 IAF Road, Bharathiyar Nagar, Pattabiram, Chennai after approval from an Independent Ethics Committee, National Ethics Committee at Chennai. The parents of those children, who were selected for treatment, were informed of voluntary nature of trial and written consent was obtained from the parent or guardian. They were informed that they were free to withdraw from the study. Subject selection criteria: Fifty-one children aged between 2-10 years of both sex and whose parent or guardian had given the consent to participate in the clinical study were selected. Children suffering from any cardiac, hepatic or renal failure, or concurrently taking medicines for any illness, any congenital anomaly like cleft lip, etc., which hampers food intake, history of food or drug allergy of any kind and unwilling to give consent or abide by the study requirements were excluded. Informed consent process: All parents who were willing for their children to participate in the study
clinical study were given detailed description about the investigational product, nature and duration of the study. Also, subject’s responsibilities after entering the study were explained. Subjects were prescreened by the investigators for the criteria indicated in the subject selection section. A written informed consent by the parent or guardian was obtained from each study subject. The investigator provided information about the study verbally as well as using a patient information sheet, in a language that is nontechnical and is understandable by the study subject’s parent or guardian. The investigator gave adequate time for the subject’s parents to read it before the informed consent is signed. The subject’s consent was obtained in writing using an ‘informed consent form’. The investigator retained the original copy of the signed informed consent and the subject received a copy of the signed informed consent.
Study Procedure Both male and female children (n = 51) aged between 2-10 years and suffering from recurrent RTI were included. The clinical diagnosis was made on careful physical examination. At entry, a detailed medical history was obtained from all study subjects. Subsequently, all children underwent a simple physical and systemic examination. All children were advised to follow the respective treatment as defined by the protocol as follows: As per the randomization, the selected cases would be included into one of the two groups.
Group A (n = 30): Children aged 2-10 years were instructed to take HiOwna-Jr at a dose of 12.5 g; children aged 7-10 years were instructed to take 25 g of HiOwna-Jr along with the regular diet, orally twice-daily for the period of eight weeks. Group B (n = 21): Subjects were instructed to continue with regular diet as advised by the investigator regarding a regular diet for a period of eight weeks.
Subjects were assessed at entry, Week 4 and Week 8. At each visit the subjects were evaluated for general health and growth, frequency of RTI and appetite. In addition, cognition was evaluated in children aged between 5-10 years, taking into consideration attention, memory and concentration. Ten objects commonly seen by the children were kept in an order and the children were asked to observe the objects and recollect and tell the name of the object without seeing them. This test was done differently for the different ages ranging from 5 to 10 years and accordingly scored from 0 to 3, where:
0: Not able to recollect even a single object
1: Able to recollect 1-3 of the objects
2: Able to recollect 4-7 objects
3: Able to recollect >7 of the objects.
At every follow-up visit, the children were examined clinically. The investigator recorded any information about intercurrent illness, therapeutic interventions and concomitant medications. Primary endpoints: Improvement in symptoms of maintaining health, growth, RTI, appetite and cognition in children. Secondary endpoints: To find out incidence of adverse events (AEs) during the study period, and overall compliance to the drug treatment.
Adverse Effects The incidence and type of AEs reported by various studies were also tabulated separately. All AEs, either reported or observed by patients, were recorded with information about severity, duration and action taken regarding the study drug. Relation of AEs to study medication was predefined as ‘Unrelated’ (a reaction that does not follow a reasonable temporal sequence from the administration of the drug), ‘Possible’ (follows a known response pattern to the suspected drug, but could have been produced by the patient’s clinical state or other modes of therapy administered to the patient), ‘Probable’ (follows a known response pattern to the suspected drug that could not be reasonably explained by the known characteristics of the patient’s clinical state), and ‘Certain’ (the AEs must have definitive relationship to the study drug, which cannot be explained by concurrent disease or any other agent).
Statistical Analysis All values are expressed as compared to ‘at entry’ as mean ± SD. Statistical analysis was performed using repeated measures of ANOVA followed by Tukey’s multiple comparison test for parameters like height, weight and body mass index (BMI). Growth parameters were evaluated by unpaired t-test using between the group analysis for Week 4 and Week 8, respectively. Statistical analysis for frequency of RTI was performed using repeated measures of ANOVA followed by Tukey’s multiple comparison test. Cognition parameters were evaluated using repeated measures of ANOVA using Friedman test and appetite function was analyzed using Fisher’s exact test. The minimum level of significance was fixed at p < 0.001.
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clinical study Statistical analysis was performed using Graphpad Prism Software Version 4.00 for Windows, San Diego, California, USA. Results The demographic details of the subjects are given in Table 1, which show that both the groups are comparable at entry. Within the group analysis was performed to compare the effect of HiOwna-Jr and regular diet in maintaining growth, health and cognition in children. The effect of HiOwna-Jr and regular diet on parameters of height, weight and BMI are shown in Table 2. The mean height (cm), which was 101.7 ± 13.28 at entry in Group A subjects who were on HiOwna-Jr, improved to 102.0 ± 13.31 by Week 4 (p < 0.05) and it further improved to 102.3 ± 13.36 at Week 8 (p < 0.001 as compared to initial and Week 4 Table 1. Demographic Details (n = 51) at Entry Details
HiOwna-Jr (n = 30) Regular diet (n = 21)
Age (years) mean ± SD
5.07 ± 1.83
5.05 ± 1.43
Males
9
13
Females
21
8
Diet (veg:non veg)
4:26
3:18
Height (cm)
101.7 ± 13.28
107.6 ± 10.71
Weight (kg)
14.75 ± 3.81
17.05 ± 4.24
(kg/m2)
14.16 ± 1.55
14.60 ± 2.20
BMI
Both the groups are comparable
values. Mean weight (kg), which was 14.75 ± 3.81 at entry improved to 15.02 ± 3.83 at Week 4 and further improved to 15.35 ± 3.99 at 8 weeks. Similarly, BMI (kg/m2) also improved from 14.16 ± 1.55 at entry to 14.37 ± 1.57 at four weeks and further to 14.62 ± 1.97 at eight weeks following HiOwna-Jr drink. In Group B subjects who were on regular diet, the mean height (cm), which was 107.6 ± 10.71 at entry, improved to 107.7 ± 10.77 at Week 4 and further improved to 108.0 ± 10.88 at eight weeks with a significance of p < 0.01 as compared to initial values. Mean weight (kg), which was 17.05 ± 4.24 at entry improved to 17.10 ± 4.32 at Week 4 which further improved to 17.40 ± 4.46 at eight weeks. Similarly, BMI (kg/m2), which was 14.60 ± 2.20 at entry improved to 14.62 ± 2.30 at four weeks and further to 14.71 ± 2.40 at 8 weeks following regular diet. Between the group analysis conducted to compare the effects of HiOwna-Jr and regular diet on various growth parameters are shown in Table 3. The increase in height (cm) on Week 4 was 0.25 ± 0.43, which improved to 0.60 ± 0.50 at Week 8 after HiOwna-Jr administration in Group A. Whereas, in Group B, the increase in height (cm) was found to be 0.10 ± 0.30 at Week 4 and in Week 8, it improved to 0.33 ± 0.58 with regular diet. Statistical analysis performed between the group shows that at eight weeks, there is statistically significant (p < 0.08) improvement in height in children treated with HiOwna-Jr, as compared to the group only on
Table 2. Effect of the Investigational Product on Various Parameters Using within the Group Analysis Parameter Height (cm)
HiOwna-Jr
Regular diet
Initial
Week 4
Week 8
Initial
Week 4
Week 8
101.7 ± 13.28
102.0 ± 13.31 ap < 0.05
102.3 ± 13.36 ap < 0.001, bp < 0.001
107.6 ± 10.71
107.7 ± 10.77
108.0 ± 10.88 ap
< 0.001
Weight (kg)
14.75 ± 3.81
15.02 ± 3.83
15.35 ± 3.99
17.05 ± 4.24
17.10 ± 4.32
17.40 ± 4.46
BMI (kg/m2)
14.16 ± 1.55
14.37 ± 1.57
14.62 ± 1.74
14.60 ± 2.20
14.62 ± 2.30
14.71 ± 2.40
Table 3. Effect of the Investigational Product on Various Growth Parameters Using between the Group Analysis Parameter Increase in height (cm) Increase in weight (kg) Increase in BMI (kg/m2)
140
Duration
HiOwna-Jr
Regular diet
Significance
Week 4
0.25 ± 0.43
0.10 ± 0.30
NS
Week 8
0.60 ± 0.50
0.33 ± 0.58
NS (p < 0.008)
Week 4
0.300 ± 0.39
0.048 ± 0.38
p < 0.025
Week 8
0.667 ± 0.48
0.357 ± 0.57
p < 0.042
Week 4
0.210 ± 0.39
0.019 ± 0.34
NS (p < 0.008)
Week 8
0.470 ± 0.44
0.124 ± 0.42
p < 0.007
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clinical study Table 4. Effect of the Investigational Product on the Frequency of RTI in Children
Table 6. Effect of the Investigational Products in Children with Decreased Appetite
Particulars
Initial
Week 4
Week 8
Particulars
HiOwna-Jr
1.94 ± 0.95
0.60 ± 0.65 p < 0.001
0.32 ± 0.56 p < 0.001
Regular diet
1.09 ± 0.49
0.38 ± 0.62 p < 0.01
0.22 ± 0.48 p < 0.01
No. of children with normal appetite Initial
Final
Significance
HiOwna-Jr
19/29
6/29
p < 0.0012
Regular diet
7/21
5/21
NS
Table 5. Effect of the Investigational Product on Cognition Parameter
HiOwna-Jr
Regular diet
Initial
Week 4
Week 8
Initial
Week 4
Week 8
Attention
2.31 ± 0.87
2.44 ± 0.73
2.44 ± 0.73
2.67 ± 0.50
2.67 ± 0.50
2.67 ± 0.50
Concentration
2.31 ± 0.95
2.44 ± 0.73
2.44 ± 0.73
2.78 ± 0.44
2.78 ± 0.44
2.78 ± 0.44
Memory
2.31 ± 0.95
2.44 ± 0.73
2.44 ± 0.73
2.31 ± 0.87
2.44 ± 0.73
2.31 ± 0.95
3.5
*P < 0.001 as compared to initial and Week 4 values in HiOwna-Jr #P < 0.01 as compared to initial and Week 4 values in regular diet
Frequency of RTI
3 2.5
HiOwna-Jr Regular diet
2 1.5
*
1
#
*
#
0.5 0
Initial
Week 4
Week 8
Figure 1. Effect of the investigational product on the frequency of RTI in children.
regular diet. Similarly, increase in weight (kg) at Week 4 was found to be 0.300 ± 0.39, which improved to 0.667 ± 0.48 at Week 8 in Group A. Whereas, in Group B, the increase in weight (kg) was found to be 0.048 ± 0.38 at Week 4 to 0.357 ± 0.57 at Week 8. The level of significance was found to be p < 0.025 at Week 4 and p < 0.042 at Week 8 in Group A as compared to Group B. BMI was increased from 0.210 ± 0.39 at Week 4 in Group A to 0.470 ± 0.44 at Week 8 and in Group B, the increase in BMI was 0.019 ± 0.34 at Week 4 to 0.124 ± 0.42 at Week 8. Statistical analysis performed between the groups at four and 8 weeks has shown that there is statistically significant (p < 0.008 and p < 0.007) improvement at four and 8 weeks in Group A as compared to Group B.
Within the group analysis conducted in Groups A and B for the evaluation of frequency of RTI is shown in Table 4 and Figure 1. The frequency of RTI, which was 1.94 ± 0.95 at entry reduced to 0.60 ± 0.65 at four weeks and further reduced to 0.32 ± 0.56 at Week 8 with p < 0.001 as compared to the initial and Week 4 values and in Group A. Whereas, in Group B, the frequency of RTI reduced from 1.09 ± 0.49 to 0.38 ± 0.62 at four weeks and 0.22 ± 0.48 at 8 weeks with a significance of p < 0.01 as compared to initial and Week 4 values. The effect of HiOwna-Jr and regular diet on cognitive parameters like attention, concentration and memory in children of age group 5-10 years are shown in Table 5. Attention score at entry was 2.31 ± 0.87. It improved to 2.44 ± 0.73 at Week 8 with HiOwna-Jr administration. Similarly, concentration, which was 2.31 ± 0.95 at entry improved to 2.44 ± 0.73 at the end of eight weeks after HiOwna-Jr administration. Memory also improved from 2.31 ± 0.95 to 2.44 ± 0.73 at eight weeks following administration of HiOwna-Jr. In Group B, no change in cognitive parameter scores were observed after regular diet at eight weeks. None of the parameters were significant as the baseline values in both the groups for various parameters were normal except for very few children in each study group. The effect of health drink HiOwna-Jr and regular diet on general health functional parameters like decreased appetite is shown in Table 6. Nineteen out of 29 had loss of appetite at entry in Group A, which improved with only six out of 29 after eight weeks of administration with HiOwna-Jr with a significance of p < 0.0012. In Group B, the number of children with decreased appetite improved from 7 to 5 out of 21 after regular diet administration for eight weeks.
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clinical study For all the parameters, the results indicate marked improvement in most subjects on HiOwna-Jr administration for a period of eight weeks. Two children in Group A reported loose stools of mildto-moderate intensity. One was given medication for treatment and withdrawn from the study as the same adverse drug reaction was again observed after resumption of health drink. The other child did not require any medication and was continued with the health drink till the end of the study. Discussion Undernutrition continues to be a primary cause of ill health and mortality among children in developing countries. Besides poverty, there are other factors that directly or indirectly affect the nutritional status of children. In this study, HiOwna-Jr was evaluated versus regular diet in general health, growth of the children. The principal herbal ingredients of HiOwna-Jr include Nartaka (Eleusine coracana), Piper nigrum, Amalaki (Emblica officinalis), Mandukaparni (Centella asiatica) and other nutrients like sucrose, Peeyusha (colostrum) skimmed milk powder, corn solids, pea protein powder, whey protein concentrate, minerals (calcium, phosphorous, iron, magnesium, zinc, chromium, selenium, molybdenum, iodine), colostrum, red beet juice powder, nature identical flavoring substance, vitamins (vitamin A, vitamin C, vitamin D, vitamin E, vitamin K, vitamin B1, vitamin B2, vitamin B6, vitamin B12, niacin, biotin, folic acid, pantothenic acid). The ingredients of HiOwna-Jr provide balanced nutrition and help in promoting overall health of children by their nutritive, energy boosting, digestive, memory-enhancing and immunomodulatory properties. E. coracana is a good source of nutrients. P. nigrum improves digestion and enhances absorption of nutrients from the gastrointestinal tract. E. officinalis has potential immunomodulatory activity and protects from repeated infections which are common in children. C. asiatica has memory-enhancing activity and improves cognitive ability. Bovine colostrum is an excellent source of nutrition and being a rich source of immunoglobulins helps in enhancing immunity. In addition to the unique botanicals, Hiowna-Jr contains various essential macro- and micronutrients, which meet the nutritional demands of children at various stages of development and are also required for optimal health. Proteins, carbohydrates and fats provide energy, promote growth and development and
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regulate body functions. Vitamins and minerals lead to beneficial effect on linear growth, health and cognitive development in school children. The beneficial effects of the health drink are discussed as follows. Nutritive and health-promoting: E. coracana is known for its nutritive and strength-enhancing properties.19,20 It is rich in protein, iron, calcium, phosphorus, fiber and vitamin content. The calcium content is higher than all cereals. Ragi has the best quality protein along with the presence of essential amino acids, vitamin A, vitamin B and phosphorus. Thus, it is a good source of diet for growing children. Ragi provides highest level of calcium, antioxidants, phytochemicals, which makes it easily and slowly digestible. Malting of finger millet improves its digestibility, sensory and nutritional quality as well as pronounced effect in the lowering the antinutrients.21 Bovine colostrum has been regarded as an excellent source of nutrition which helps in promoting body growth.22 Proteins, carbohydrates and fat are required for growth, maintenance and highly specialized functions of the body. These macronutrients are also used as the energy source.23 Vitamins and minerals are known for their health-promoting functions in the body.24 Enhancement of nutrient absorption and gastroprotective effects: P. nigrum, which is a rich source of piperine increased bile secretion in experimental studies.25 This suggests that P. nigrum aids the digestion and absorption of dietary fats. It protects against the gastric damage caused by gastric irritant agents, which might be related to the inhibition of gastric motor activity and the stimulation of prostaglandin synthesis.26 Dietary piperine, by favorably stimulating the digestive enzymes of pancreas, enhanced the digestive capacity and significantly reduced the gastrointestinal food transit time, enhanced the bioavailability of a number of phytochemicals by inhibitory influence on enzymatic drug biotransforming reactions in the liver. Piperineâ&#x20AC;&#x2122;s bioavailability enhancing property is also partly attributed to increased absorption as a result of its effect on the ultrastructure of intestinal brush border.27 Immunomodulatory activity: An experimental study showed that the presence of Amla (E. officinalis) was effective against the cytotoxic effects of chromiuminduced oxidative damage of murine macrophages and resulted in an enhanced cell survival, decreased free radical production and higher antioxidant levels similar to that of control cells. Further, chromium (VI) treatment resulted in decreased phagocytosis and g-interferon (g-IFN) production, while E. officinalis inhibited chromium-induced immunosuppression and
clinical study restored both phagocytosis and g-IFN production, by macrophages significantly.28 These findings suggest the cytoprotective and immunomodulatory potential of E. officinalis fruit. In another in vitro study, E. officinalis relieved the immunosuppressive effects of chromium on lymphocyte proliferation and even restored the interleukin-2 (IL-2) and g-IFN production considerably.29
All the children liked the taste and flavor. Overall compliance to the study was good. Therefore, it can be concluded that HiOwna-Jr helps to maintain adequate natural linear growth, enhances immunity against recurrent RTI and favorably modifies cognition in children when given along with regular diet.
An experimental study conducted on mice demonstrated that the aqueous extract of E. officinalis was very effective in reducing cyclophophamideinduced suppression of humoral immunity.30 All the above studies indicate the immunomodulatory potential of E. officinalis. A clinical study proved that bovine colostrum had the ability to increase IgA, indicating its potential to enhance human special immune response.31
1.
Must A, Strauss RS. Risk and consequences of childhood and adolescent obesity. Int J Obes Relat Metab Disord 1999;23 Suppl 2:S2-11.
2.
Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D, Khoury PR, Zeitler P. Increased incidence of non-insulindependent diabetes mellitus among adolescents. J Pediatr 1996;128(5 Pt 1):608-15.
3.
M端ller O, Krawinkel M. Malnutrition and health in developing countries. CMAJ 2005;173(3):279-86.
4.
Pate RR, Ross JG. Factors associated with health-related fitness. J Physical Educ Recreation Dance 1987;58(9):93-5.
5.
Breakfast for Learning-Canadian Living Foundation. 2006. Report Card on Nutrition for School Children. Accessed at: www.breakfastforlearning. ca/English resources/ index_report_card.html
6.
King AJC, Boyce WF, King MA. 1999. Trends in the Health of Canadian Youth. Ottawa. Health Canada.
7.
Evers S, Taylor J, Manske S, Midgett C. Eating and smoking behaviours of school children in southwestern Ontario and Charlottetown, PEI. Can J Public Health 2001;92(6):433-6.
8.
Pollitt E, Cueto S, Jacoby ER. Fasting and cognition in well- and undernourished school children: a review of three experimental studies. Am J Clin Nutr 1998;67(4): 779S-784S.
9.
World Health Organization. Physical status: the use and interpretation of anthropometry. Report of a WHO Expert Committee. Technical Report Series No. 854. Geneva, World Health Organization, 1995.
Promoting mental health: A double-blind clinical trial on C. asiatica showed a significant increase in the general mental ability of mentally retarded children after three months and 6 months of drug administration. Significant improvement was found in the overall general adjustment, attention and concentration after six months.32 In an experimental study, it was concluded that C. asiatica leaf extract had a neuronal dendritic growth stimulating property; hence, the extract could be used for enhancing neuronal dendrites in stress and neurodegenerative and memory disorders.33 These studies indicate that C. asiatica improves memory and learning ability. Multiple micronutrients such as vitamins and minerals when delivered through either supplements or fortified foods were found to have a positive effect on reasoning ability and academic performance in school children.34 Conclusion This clinical study clearly demonstrates that HiOwna-Jr, a polyherbal natural health drink supplement when given along with regular diet, showed a beneficial improvement as compared with regular diet in the growth as determined by height, weight and BMI including improving immunity as determined by reduction of the frequency of RTI and improving appetite in children aged 2-10 years. The improvement in the growth corresponded to the normal natural growth in the children, which implies that HiOwna-Jr helps in the natural normal linear growth of children. Cognition parameters like attention, memory and concentration evaluated in school-going children aged 5-10 years also showed beneficial results and are comparable to the children with regular diet.
References
10. De Benoist B, McLean E, Egli I, Cogswell M. Worldwide Prevalence of Anaemia 1993-2005: WHO Global Database on Anemia. Geneva: World Health Organization and Centers for Disease Control and Prevention, 2008. 11. Allen L, de Benoist B, Dary O, et al. Guidelines on Food Fortification with Micronutrients. Geneva: World Health Organization and Food and Agricultural Organization of the United Nations, 2006. 12. Motil KJ. Enteral nutrition in the neurologically impaired child. In: Pediatric Enteral Nutrition. Baker SB, Baker RD Jr, Davis A (Eds.), Chapman & Hall: New York 1994: p.217-37. 13. Poskitt EME, Morgan B. Infancy, childhood and adolescence. In: Human Nutrition. Geissler C, Powers H (Eds.), 11th edition, Elsevier Churchill Livingstone: New York, NY 2005:p.257-98.
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clinical study 14. Schmidt M, Affenito SG, Striegel-Moore R, Khoury PR, Barton B, Crawford P, et al. Fast-food intake and diet quality in black and white girls: the National Heart, Lung, and Blood Institute Growth and Health Study. Arch Pediatr Adolesc Med 2005;159(7):626-31. 15. Paramesh H. Practical approach to recurrent respiratory infections. Indian J Pediatr 1996;63(2):181-7. 16. Wasik M, Kaczorowska M, Demkow U. Altered expression of immune surface markers in children with recurrent infections of respiratory tract. J Physiol Pharmacol 2005;56 Suppl 4:237-43. 17. Gunseli Bozdogan, Ismail Reisli, Figen Dogu, Aydan Ikinciogullari, Emel Babacan. Evaluation of the children with recurrent respiratory tract infections. J Med Sci 2003;3(5-6):411-7. 18. Zaninotto P, Wardle H, Stamatakis E. Forecasting Obesity to 2010. Report prepared for UK Department of Health 2006. Available at: http://www.dh.gov.uk/en/ Publicationsandstatistics/Publications/PublicationsStatistics/ DH_4138630. 19. Golokavasi Lala Shaligramji Vaishya. Brihannighanturatnakara. Khemraj Shrikrishnadas Prakashan, Mumbai, 7-8 Vol, p. 639. 20. Sastri BN. The Wealth of India, CSIR, Vol III, New Delhi, 1952:p.165. 21. Desai AD, Kulkarni SS, Sahoo AK, Ranveer RC, Dandge PB. Effect of supplementation of malted ragi flour on the nutritional and sensorial quality characteristics of cake. Adv J Food Sci Technol 2010;2(1):67-71. 22. Kaviraj Ambikadattashastri. Sushruta Samhita. Part I. 11th edition, Chaukambha Sanskrit Sansthan, Varanasi, 1997:p.176. 23. Joshi SA. Nutrition and Dietetics. Tata McGraw-Hill Publishing Company Limited. 1992:p.46-69. 24. Best C, Neufingerl N, Del Rosso JM, Transler C, van den Briel T, Osendarp S. Can multi-micronutrient food fortification improve the micronutrient status, growth, health, and cognition of schoolchildren? A systematic review. Nutr Rev 2011;69(4):186-204. 25. Ganesh Bhat B, Chandrasekhara N. Effect of black pepper
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and piperine on bile secretion and composition in rats. Nahrung 1987;31(9):913-6. 26. Al-Moflehi A, Alhaider AA, Mossa JS, Al-Sohaibani MO, Rafatullah S, Qureshi S. Inhibition of gastric mucosal damage by Piper nigrum (Black pepper) pretreatment in Wistar albino rats. Pharmacogny Mag 2005;1(2):64-8. 27. Srinivasan K. Black pepper and its pungent principlepiperine: a review of diverse physiological effects. Crit Rev Food Sci Nutr 2007;47(8):735-48. 28. Sai Ram M, Neetu D, Deepti P, Vandana M, Ilavazhagan G, Kumar D, et al. Cytoprotective activity of Amla (Emblica officinalis) against chromium (VI) induced oxidative injury in murine macrophages. Phytother Res 2003;17(4):430-3. 29. Sai Ram M, Neetu D, Yogesh B, Anju B, Dipti P, Pauline T, et al. Cytoprotective and immunomodulating properties of Amla (Emblica officinalis) on lymphocytes: an in-vitro study. J Ethnopharmacol 2002;81(1):5-10. 30. Haque R, Bin-Hafeez B, Ahmad I, Parvez S, Pandey S, Raisuddin S. Protective effects of Emblica officinalis Gaertn. in cyclophosphamide-treated mice. Hum Exp Toxicol 2001;20(12):643-50. 31. He F, Tuomola E, Arvilommi H, Salminen S. Modulation of human humoral immune response through orally administered bovine colostrums. FEMS Immunol Med Microbiol 2001;31(2):93-6. 32. Appa Rao VR, Srinivasan K, Koteswara Rao T. The effect of Centella asiatica on the general mental ability of mentally retarded children. Indian J Psychiat 1977;19(4):54-9. 33. Mohandas Rao KG, Muddanna Rao S, Gurumadhva Rao S. Centella asiatica (L.) leaf extract treatment during the growth spurt period enhances hippocampal ca3 neuronal dendritic arborization in rats. Evid Based Complement Alternat Med 2006;3(3):349-57. 34. Eilander A, Gera T, Sachdev HS, Transler C, van der Knaap HC, Kok FJ, et al. Multiple micronutrient supplementation for improving cognitive performance in children: systematic review of randomized controlled trials. Am J Clin Nutr 2010;91(1):115-30.
clinical practice
An Overview of Burning Mouth Syndrome Anuradha Sunil*, Archana Mukunda**, Merwyn Nitin Gonsalves†, Ashik Bin Basheer‡, Deepthi K‡
Abstract Burning mouth syndrome (BMS) is an idiopathic condition characterized by a chronic continuous burning sensation of intraoral soft tissues, typically involving the tongue, with or without extension to the lips and oral mucosa. It is classically accompanied by gustatory disturbances like dysgeusia and parageusia and subjective xerostomia. This syndrome commonly affects people all over the world without racial or socioeconomic predilection. Some patients may develop a single episode of burning sensation while some may show recurrent episodes that last for months or years. It commonly affects perimenopausal and postmenopausal women. The etiology remains obscure and multifactorial, hence the treatment is complicated with multiple approaches involving drugs, psychotherapy along with latest techniques like acupuncture and low level laser therapy being used to treat BMS effectively.
Keywords: Orofacial pain, stomatodynia, glossodynia, neuropathic pain, glossopyrosis, scalded mouth syndrome
B
urning mouth syndrome (BMS) refers to chronic orofacial pain without any visible mucosal changes or lesions and laboratory findings. It is also known by various terminologies such as orofacial pain, stomatodynia, glossodynia, neuropathic pain, glossopyrosis and scalded mouth syndrome. It is characterized by an intense burning or stinging sensation, preferably on the tongue or in other areas of the oral mucosa.1 The etiology has remained unclear and numerous local, systemic and psychological factors have been implicated in the etiology and current knowledge throws light on the underlying neurological disorder. The International Association for the Study of Pain and International Headache Society defines it as a “distinctive nosological entity, including ‘all forms of burning sensation in the mouth with stinging sensation or pain, in association with
an oral mucosa that appears clinically normal in the absence of local or systemic diseases or alterations.’’2 BMS is seen more commonly in postmenopausal females.3 There is no single accepted treatment for BMS and hence there are a variety of therapeutic approaches available. This present article focuses on updated knowledge on etiology, classification of BMS and also adds a note on latest treatment modalities, home remedies and techniques to cope with BMS successfully. CLASSIFICATION BMS is classified as follows:
Based on etiology as
Primary, where etiology is unknown
Secondary, where the etiology is known3,4
Based on symptoms as
*Professor and Head **Reader Dept. of Oral and Maxillofacial Pathology Royal Dental College (KUHS), Chalissery, Kerala †Reader Dept. of Oral and Maxillofacial Pathology AJ Institute of Dental Science, Mangalore ‡Senior Lecturer Dept. of Oral and Maxillofacial Pathology, Royal Dental College (KUHS) Chalissery, Kerala Address for correspondence Dr Anuradha Sunil Professor and Head Dept. of Oral and Maxillofacial Pathology, Royal Dental College (KUHS) Chalissery, Kerala E-mail: anuradhasunil@hotmail.com
Type 1 BMS: Patients have no symptoms upon waking but symptoms progress throughout the day reaching its peak intensity by evening. Night-time symptoms are variable. It is linked to systemic disorders like nutritional deficiency and diabetes. Type 2 BMS: Patients have continuous symptoms throughout the day and are symptomatic at night resulting in sleepless nights. This type is associated with chronic anxiety due to altered sleep pattern and is related to use of antidepressant drugs, which cause xerostomia.
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Type 3 BMS: Patients have intermittent symptoms throughout the day with symptomfree periods. Usually seen due to anxiety or allergic reactions especially to food allergens.3
Etiologies Different factors have been proposed for secondary BMS as follows:
implicated. Food allergens include peanuts, chestnuts, cinnamon, nicotinic acid and sorbic acid.8
Psychological Factors Patients with BMS show increase in salivary cortisol level indicating higher levels of stress.9 However, anxiety and depression are considered as exacerbating factors rather than the cause of BMS as the symptoms disappear following their remission.
Local factors
Systemic factors
Iatrogenic Factors
Nutritional factors
Allergic or immunological factors
Psychological factors
Iatrogenic factors
Infections
Hormonal imbalances
Neurological disturbances3,5,6
Drug-associated BMS have been observed with use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs).10 The product of inflammatory reaction generates increased bradykinin. The mechanism is clearly not understood but kallikrein, a molecule active in the kinin pathway, is increased in the saliva of BMS patients, resulting in increased inflammation. Other drugs like antiretrovirals nevirapine and efavirenz may also result in BMS. However, the mechanism is not clearly understood.
Local Factors
Oral conditions: Lichen planus, geographic tongue
Infections
Oral habits: Tongue thrusting, bruxism
Few microbes like Candida, Enterobacter, Fusospirochetes, Helicobacter pylori and Klebsiella are prevalent in patients with BMS without visible mucosal lesions.3,11
Excessive mouth irritation: Overbrushing, overuse of mouth washes, overingestion of acidic drinks.3,5,6
Systemic Factors
Xerostomia caused by various health problems like Sjogren’s syndrome and radiation therapy. Gastroesophageal reflux disease (GRED)3,5,6
Nutritional Factors Deficiencies of B vitamins 1, 2, 6 and 12, as well as zinc, folate and iron, have been suggested as causes of secondary BMS, occurring from direct neurologic damage or in relation to anemia.3,5,6
Allergic or Immunological Factors Elevated erythrocyte sedimentation rate (ESR) and salivary IgA levels is seen in BMS patients suggestive of immunologic or allergic phenomenon. Allergies are seen in type 3 BMS as intermittent symptoms, associated with signs of mucosal irritation. Suggested irritants include dental materials such as mercury (present in amalgam), methyl methacrylate, cobalt chloride, zinc and benzoyl peroxide.7 Components of lotions such as petrolatum cadmium sulfate, octyl gallate, benzoic acid and propylene glycol have been
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Endocrine Disorders Menopause, whether surgical or physiological, is associated with higher prevalence of BMS. The mechanism is unclear but hormonal alterations may possibly affect the oral mucosa. Estrogen has documented effects on oral mucosa, and deprivation may lead to atrophic changes thereby altering stimulation of the nerve endings within the epithelium. Alternatively, atrophic epithelia may be more prone to inflammation.12 Thyroid hormones are involved in maturation and specialization of taste buds and recent studies have shown that thyroid hypofunction may be responsible for hypogeusia, for bitter taste and for the release of inhibitions for sensitive trigeminal sensation.13
Neurological Disorders Sensory testing has revealed taste deficits and heat/pain intolerance among BMS patients due to an abnormal interplay between the sensory function of chorda tympani and lingual nerve either in the peripheral or central nervous systems resulting in BMS.
clinical practice PATHOPHYSIOLOGY
BMS was originally described as a psychogenic illness, however, a neuropathic mechanism is currently favored. This is based on objectively measured abnormalities of physiologic responses of the trigeminal nerve in BMS patients.14 Taste to the anterior twothird of the tongue is by the chorda tympani branch of facial nerve and somatosensory is supplied by lingual nerve branch of trigeminal nerve. Chorda tympani hypofunction results in lingual nerve hyperfunction by disrupting the centrally-mediated equilibrium between the two.15 Individuals with high density of fungiform papillae present on the anterior aspect of the tongue are known as supertasters and are more at risk for developing BMS. Supertasters are mainly females who are able to perceive the bitter taste of a substance called PROP (6-n-propylthiouracil) and also experience a more intense burning sensation in the oral cavity, especially when stimulated with chili peppers. Unilateral anesthesia of the chorda tympani nerve intensifies the perception of burning pain on the contralateral anterior portion of the tongue, suggesting the presence of central inhibitory interactions between taste and oral pain.5 Damage to the chorda tympani or any alteration in the gustative papillae releases this inhibition, and may lead to an intensification of normal trigeminal sensations leading to spontaneous pain, altered sensations of touch, subjective sensations, of oral dryness and taste alterations (dysgeusia and phantom tastes). Xerostomia seen in BMS is more due to neuropathy than glandular dysfunction. It is noted that salivary content shows differences but there is no change in salivary quantity or flow.16 Clinical Features
Symptoms may vary from mild-to-severe but moderate pain is seen frequently. Symptoms may appear early in the morning or develop later in the day. Altered taste sensation such as bitter or metallic taste Oral mucosa appears apparently normal without any visible changes.
Xerostomia
Geographic and fissured tongue
Painful teeth, jaw and temporomadibular joint
Loss of a comfortable jaw position and uncontrollable jaw tightness
Headache, neck and shoulder pain
Increased parafunctional activity
Difficulty in speaking, nausea, gagging and dysphagia
Usually bilateral but can be unilateral as well
Multiple mood and emotional disturbances1,3,5,17,18
Investigations
Blood tests: Complete blood cell count, glucose level, thyroid function, nutritional factors and immune function Oral cultures: For bacterial, viral and fungal infections Imaging: Magnetic resonance imaging (MRI), computed tomography (CT) scan or other imaging test to check for other health problems. Patch tests: To check allergy to certain foods, additives or even denture materials. Sialometric analysis to measure and check salivary flow.
Occurs most commonly, but not exclusively in females though occurs in men as well.
Seen in women
Gastric reflux tests: To determine GERD.
Biopsy of tongue or oral mucosa.
perimenopausal
or
postmenopausal
Unexplained, usually persistent burning sensation or pain of the oral soft tissues. The diagnostic criteria for BMS are that pain episodes must occur continuously for at least 4-6 months. They may last for 12 years or more with an average duration of 3.4 years.3 Commonly affects the tongue presenting as glossodynia (painful tongue) and glossopyrosis (burning tongue).
Psychological questionnaires: To check symptoms of depression, anxiety, etc.
Treatment and Management The goal of treating BMS is to first identify the underlying etiology, then to try to reduce or eliminate the etiology thoroughly. Attempting combinations of therapies may be appropriate as there is no definitive cure. The treatment can thus comprise of medical management, home remedies and self help measures.
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clinical practice antidepressants may act as analgesics thereby decreasing chronic pain.24
Medical Management Primary BMS
Topical therapy:
Clonazepam, a benzodiazepine, when applied as 0.5-1 mg 2-3 times daily, acts by locally disrupting the neuropathologic mechanism that underlies stomatodynia. But it decreases the density and/or ligand affinity of peripheral benzodiazepine receptors. This, in turn, could cause spontaneous pain from the tissues concerned.19,20 Low doses of clonazepam dissolvable wafers available commercially are better than tablets.21
Chlordiazepoxide, a benzodiazepine, works by slowing down the movement of chemicals in the brain. This results in a reduction in nervous tension (anxiety) and muscle spasm, and also causes sedation. These effects are unlikely as maximum effect of benzodiazepine is not observed at lower dosage.19 Capsaicin induces desensitization to thermal, chemical and mechanical stimuli by inducing selective and reversible desensitization of the afferent sensory C fiber endings. It is used as mouth rinse one teaspoon of a 1:2 dilution or higher of hot pepper and water. The strength of capsaicin can be increased if it can be tolerated by the patient to a maximum of 1:1 dilution. But the restrictions are limited effect over time and magnitude of improvement. Moreover, the use of capsaicin rinse itself produces burning sensation thus limiting the use among patients.22,23
Chlordiazepoxide, a benzodiazepine, is advised 10-30 mg/day, to start with 5 mg at bedtime and increase the dose to 5 mg every 4-7 days until oral burning is relieved. Medication is taken in divided doses as side effects increase as the dosage is increased.20 Gabapentin, an anticonvulsant drug, is advised 300-1,600 mg/day; 100 mg at bedtime. The dosage is increased by 100 mg every 4-7 days until oral burning is relieved or side effects occur. As the dosage increases, the medication should be taken in three divided doses.25 Alpha lipoic acid is a mitochondrial coenzyme, trometamol salt of thioctic acid. It has antioxidant effect that eliminates the toxic free radicals produced in stress. It has neuroprotective property; hence, used to manage these patients.26 Usually administered in doses of 400 mg twice-daily for a month. Acupuncture appears to be the current valid therapeutic choice as it influences oral microcirculation, resulting in a significant variation of the vascular pattern associated with significant reduction of the burning sensation as long as 18 months.27 Low level laser therapy may be an alternative treatment for the relief of oral burning in patients with BMS.28
Secondary BMS Secondary BMS is treated depending on the perceived etiological factor
Oral thrush: Topical and oral antifungal are used
Nutritional deficiency: Oral supplements
Xerostomia: High fluid intake, sialagogues
Clonazepam, a benzodiazepines, exert its effect by acting as a sedative hypnotic 0.25-2 mg dosage/day, 0.25 mg at bedtime, increase dosage by 0.25 every 4-7 days until oral burning is relieved or side effects occur. As the dosage is increased, medication is taken in three divided doses.19
Menopause: Hormone replacement therapy
Amitriptyline, a tricyclic antidepressant, is given in doses of 10-150 mg/day, to start with 10 mg at bedtime and increase the dose by 10 mg until oral burning is relieved or side effects occur. It is noted that in low doses
Oral lidocaine has also been used topically for relieving the burning sensation.
Systemic therapy:
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Behavioral interventions: Cognitive behavioral therapy by a clinical psychologist.
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Cranial nerve injury: Central pain control with benzodiazepines, tricyclic antidepressants, gabapentin, topical capsaicin
Drug allergy: Change the medication
Specific oral rinses and mouth washes
Oral lidocaine and topical steroids can be used
BMS can be managed with medical approaches and variety of drugs. In addition, self help measures and simple home remedies may also be of great help to the patients.
clinical practice Many patients with BMS show reduction or disappearance of symptoms during meals or when chewing gum or confectionary is used. So the following measures may be taken
Sip water frequently
Chew sugarless gum
Symptoms of BMS can be reduced and also prevented from becoming worse by
Avoidance of tobacco products
Avoidance of products with cinnamon or mint
Avoidance of spicy and hot foods
Avoidance of acidic foods and liquids
Using different brands of toothpastes
Take steps to reduce excessive stress
Some of these adjunct techniques may help patients in coping up with BMS.
Practice of relaxation exercise such as yoga
Joining a pain support group
Engaging in pleasurable activities such as exercise and hobbies. Making an effort to stay socially active by connecting with understanding family members and friends.
Conclusion BMS is a difficult and challenging problem for the dental practitioner. It is a clinical diagnosis made via the exclusion of all other causes. No universally accepted diagnostic criteria, laboratory tests, imaging studies or other modalities definitively diagnose or exclude BMS. The key to successful management is a good diagnostic work-up and coordination between the dental practitioners and appropriate physicians and psychologists. References
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17. Grushka M. Clinical features of burning mouth syndrome. Oral Surg Oral Med Oral Pathol 1987;63(1):30-6. 18. Grushka M, Epstein JB, Gorsky M. Burning mouth syndrome. Am Fam Physician 2002;65(4):615-20.
Scala A, Checchi L, Montevecchi M, Marini I, Giamberardino MA. Update on burning mouth syndrome: overview and patient management. Crit Rev Oral Biol Med 2003;14(4):275-91.
19. Woda A, Navez ML, Picard P, Gremeau C, Pichard-Leandri E. A possible therapeutic solution for stomatodynia (burning mouth syndrome). J Orofac Pain 998;12(4): 272-8.
3.
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clinical practice 20. Gorsky M, Silverman S Jr, Chinn H. Clinical characteristics and management outcome in the burning mouth syndrome. An open study of 130 patients. Oral Surg Oral Med Oral Pathol 1991;72(2):192-5. 21. Patton LL, Siegel MA, Benoliel R, De Laat A. Management of burning mouth syndrome: systematic review and management recommendations. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;103 Suppl:S39.e1-13. 22. Silvestre FJ, Silvestre-Rangil J, Tamarit-Santafé C, Bautista D. Application of a capsaicin rinse in the treatment of burning mouth syndrome. Med Oral Patol Oral Cir Bucal 2012;17(1):e1-4. 23. Epstein JB, Marcoe JH. Topical application of capsaicin for treatment of oral neuropathic pain and trigeminal neuralgia. Oral Surg Oral Med Oral Pathol 1994;77(2): 135-40.
24. Sharav Y, Singer E, Schmidt E, Dionne RA, Dubner R. The analgesic effect of amitriptyline on chronic facial pain. Pain 1987;31(2):199-209. 25. Grushka M, Bartoshuk LM. Burning mouth syndrome and oral dysesthesia: taste injury is a piece of the puzzle. Can J Diagn 2000;17:99-109. 26. Femiano F. Burning mouth syndrome (BMS): an open trial of comparative efficacy of alpha-lipoic acid (thioctic acid) with other therapies. Minerva Stomatol 2002;51(9):405-9. 27. Scardina GA, Ruggieri A, Provenzano F, Messina P. Burning mouth syndrome: is acupuncture a therapeutic possibility? Br Dent J 2010;209(1):E2. 28. Kato IT, Pellegrini VD, Prates RA, Ribeiro MS, Wetter NU, Sugaya NN. Low-level laser therapy in burning mouth syndrome patients: a pilot study. Photomed Laser Surg 2010;28(6):835-9.
...Cont’d from page 130 9.
Khurana HK, Kanawjia SK. Recent trends in development of fermented milks. Curr Nutr Food Sci 2007;3(1):91-108.
13. Haukioja A. Probiotics and oral health. Eur J Dent 2010;4(3):348-55.
10. Roberfroid MB. Prebiotics and probiotics: are they functional foods? Am J Clin Nutr 2000;71(6 Suppl): 1682S-7S; discussion 1688S-90S.
14. Hasslöf P, Hedberg M, Twetman S, Stecksén-Blicks C. Growth inhibition of oral mutans streptococci and candida by commercial probiotic lactobacilli - a in vitro study. BMC Oral Health 2010;10:18.
11. The Excell Express. Saturday Nov. 26, 2011. Jammu. Empower your palate with probiotics. Health and Entertainment. Pg.4. (col. 3). 12. Reid G, Jass J, Sebulsky MT, McCormick JK. Potential uses of probiotics in clinical practice. Clin Microbiol Rev 2003;16(4):658-72.
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15. Sharma AK, Mohan P, Nayak BB. Probiotics: making a comeback. Indian J Pharmacol 2005;37(8):358-65. 16. Probiotics – Friendly bacteria with a host of benefits. Dairy Council of California. 2000. Available from: www. dairycouncilofca.org.
clinical practice
Diagnosis and Treatment of Acute Low Back Pain BRIAN A. CASAZZA
Abstract Acute low back pain is one of the most common reasons for adults to see a family physician. Although most patients recover quickly with minimal treatment, proper evaluation is imperative to identify rare cases of serious underlying pathology. Certain red flags should prompt aggressive treatment or referral to a spine specialist, whereas others are less concerning. Serious red flags include significant trauma related to age (i.e., injury related to a fall from a height or motor vehicle crash in a young patient, or from a minor fall or heavy lifting in a patient with osteoporosis or possible osteoporosis), major or progressive motor or sensory deficit, new-onset bowel or bladder incontinence or urinary retention, loss of anal sphincter tone, saddle anesthesia, history of cancer metastatic to bone, and suspected spinal infection. Without clinical signs of serious pathology, diagnostic imaging and laboratory testing often are not required. Although there are numerous treatments for nonspecific acute low back pain, most have little evidence of benefit. Patient education and medications such as nonsteroidal anti-inflammatory drugs, acetaminophen, and muscle relaxants are beneficial. Bed rest should be avoided if possible. Exercises directed by a physical therapist, such as the McKenzie method and spine stabilization exercises, may decrease recurrent pain and need for health care services. Spinal manipulation and chiropractic techniques are no more effective than established medical treatments, and adding them to established treatments does not improve outcomes. No substantial benefit has been shown with oral steroids, acupuncture, massage, traction, lumbar supports, or regular exercise programs.
Keywords: Acute low back pain, red flag, osteoporosis, cancer
M
ost persons will experience acute low back pain during their lifetime. The first episode usually occurs between 20 and 40 years of age. For many, acute low back pain is the first reason to seek medical care as an adult. Pain can be moderate to severe and debilitating, causing anxiety. Many cases are self-limited and resolve with little intervention. However, 31 percent of persons with low back pain will not fully recover within six months,1 although most will improve. Recurrent back pain occurs in 25 to 62 percent of patients within one to two years, with up to 33 percent having moderate pain and 15 percent having severe pain.2-4 Acute low back pain can be defined as six to 12 weeks of pain between the costal angles and gluteal folds that may radiate down one or both legs (sciatica). Acute low back pain is often nonspecific and therefore cannot be attributed to a definite cause. However, possible causes of acute low back pain (e.g., infection, tumor, osteoporosis, fracture, inflammatory arthritis) need
BRIAN A. CASAZZA, MD, is medical director of the University of North Carolinaâ&#x20AC;&#x2122;s Spine Center in Chapel Hill. He is also a clinical associate professor in the Department of Physical Medicine and Rehabilitation at the University of North Carolina School of Medicine. Source: Adapted from Am Fam Physician. 2012;85(4):343-350.
to be considered based on the patientâ&#x20AC;&#x2122;s history and physical examination. Table 1 presents the differential diagnosis of acute low back pain.5,6 The goals of treatment for acute low back pain are to relieve pain, improve function, reduce time away from work, and develop coping strategies through education. Optimizing treatment may minimize the development of chronic pain, which accounts for most of the health care costs related to low back pain.7 History and Physical Examination An accurate history and physical examination are essential for evaluating acute low back pain. Often, patients awaken with morning pain or develop pain after minor forward bending, twisting, or lifting. It is also important to note whether it is a first episode or a recurrent episode. Recurrent episodes usually are more painful with increased symptoms. Red flags are often used to distinguish a common, benign episode from a more significant problem that requires urgent workup and treatment (Table 2).5,6,8 A recent study shows that some red flags are more important than others, and that red flags overall are poor at ruling in more serious causes of low back pain.8 Patients with back pain in the primary care setting (80 percent) tend
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clinical practice Table 1. Differential Diagnosis of Acute Low Back Pain Diagnosis
Key clinical clues
Intrinsic spine Compression fracture
History of trauma (unless osteoporotic), point tenderness at spine level, pain worsens with flexion, and while pulling up from a supine to sitting position and from a sitting to standing position
Herniated nucleus pulposus
Leg pain is greater than back pain and worsens when sitting; pain from L1-L3 nerve roots radiates to hip and/or anterior thigh, pain from L4-S1 nerve roots radiates to below the knee
Lumbar strain/sprain
Diffuse back pain with or without buttock pain, pain worsens with movement and improves with rest
Spinal stenosis
Leg pain is greater than back pain; pain worsens with standing and walking, and improves with rest or when the spine is flexed; pain may be unilateral (foraminal stenosis) or bilateral (central or bilateral foraminal stenosis)
Spondylolisthesis
Leg pain is greater than back pain; pain worsens with standing and walking, and improves with rest or when the spine is flexed; pain may be unilateral or bilateral
Spondylolysis
Can cause back pain in adolescents, although it is unclear whether it causes back pain in adults; pain worsens with spine extension and activity
Spondylosis (degenerative disk or facet joint arthropathy)
Similar to lumbar strain; disk pain often worsens with flexion activity or sitting, facet pain often worsens with extension activity, standing, or walking
Systemic Connective tissue disease
Multiple joint arthralgias, fever, weight loss, fatigue, spinous process tenderness, other joint tenderness
Inflammatory spondyloarthropathy
Intermittent pain at night, morning pain and stiffness, inability to reverse from lumbar lordosis to lumbar flexion
Malignancy
Pain worsens in prone position, spinous process tenderness, recent weight loss, fatigue
Vertebral diskitis/osteomyelitis
Constant pain, spinous process tenderness, often no fever, normal complete blood count, elevated erythrocyte sedimentation rate and/or C-reactive protein level
Referred Abdominal aortic aneurysm
Abdominal discomfort, pulsatile abdominal mass
Gastrointestinal conditions: pancreatitis, Abdominal discomfort, nausea/vomiting, symptoms often associated with eating peptic ulcer disease, cholecystitis Herpes zoster
Unilateral dermatomal pain, often allodynia, vesicular rash
Pelvic conditions: endometriosis, pelvic inflammatory disease, prostatitis
Discomfort in lower abdomen, pelvis, or hip
Retroperitoneal conditions: renal colic, pyelonephritis
Costovertebral angle pain, abnormal urinalysis results, possible fever
Information from references 5 and 6.
to have one or more red flags, but rarely have a serious condition.8 However, physicians should be aware of the signs and symptoms of cauda equina syndrome, major intra-abdominal pathology, infections, malignancy, and fractures (Tables 15,6 and 25,6,8). Cauda equina syndrome and infections require immediate referral. Family physicians should rely on a comprehensive clinical approach rather than solely on a checklist of red flags. Pain from spine structures, such as musculature, ligaments, facet joints, and disks, can refer to the thigh region, but rarely to areas below the knee. Pain related
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to the sacroiliac joint often refers to the thigh, but can also radiate below the knee. Irritation, impingement, or compression of the lumbar root often results in more leg pain than back pain. Pain from the L1-L3 nerve roots will radiate to the hip and/or thigh, whereas pain from the L4-S1 nerve roots will radiate below the knee. Neurologic examination of the lower extremities includes strength, sensation, and reflex testing (Table 3), even in the absence of significant sciatica. A straight leg raise test is positive for L4-S1 nerve root pain if it radiates below the knee. A reverse straight leg raise test (extending hip and flexing knee while in the
clinical practice Table 2. Red Flags for Serious Etiologies of Acute Low Back Pain Possible etiology
History findings
Physical examination findings
Cancer
Strong: Cancer metastatic to bone Intermediate: Unexplained weight loss
Weak: Vertebral tenderness, limited spine range of motion
Weak: Cancer, pain increased or unrelieved by rest Cauda equina Strong: Bladder or bowel incontinence, urinary retention, syndrome progressive motor or sensory loss
Strong: Major motor weakness or sensory deficit, loss of anal sphincter tone, saddle anesthesia Weak: Limited spine range of motion
Fracture
Strong: Significant trauma related to age*
Weak: Vertebral tenderness, limited spine range of motion
Intermediate: Prolonged use of steroids Weak: Age older than 70 years, history of osteoporosis Infection
Strong: Severe pain and lumbar spine surgery within the past year
Strong: Fever, urinary tract infection, wound in spine region
Intermediate: Intravenous drug use, immunosuppression, Weak: Vertebral tenderness, limited spine range of severe pain and distant lumbar spine surgery motion Weak: Pain increased or unrelieved by rest Note: Presence of one or two weak or intermediate red flags may warrant observation because few patients will be significantly harmed if diagnosis of a serious cause is delayed for four to six weeks. Presence of any strong red flag warrants more urgent workup and probable referral to a spine subspecialist. *Fall from a height or motor vehicle crash in a young patient, minor fall or heavy lifting in a patient with osteoporosis or possible osteoporosis. Information from references 5, 6, and 8.
Table 3. Neurologic Examination Findings in Patients with Acute Low Back Pain Affected nerve root
Motor deficit
Sensory deficit
Reflex
Disk herniation Central
Paracentral
Lateral
L3
Hip flexion
Anterior/medial thigh
Patella
Above L2-L3
L2-L3
L3-L4
L4
Knee extension
Anterior leg/medial foot
Patella
Above L3-L4
L3-L4
L4-L5
L5
Dorsiflexion/great toe
Lateral leg/dorsal foot
Medial hamstring
Above L4-L5
L4-L5
L5-S1
S1
Plantar flexion
Posterior leg/lateral foot
Achilles tendon
Above L5-S1
L5-S1
None
prone position) is positive for L3 nerve root pain if it radiates into the anterior thigh. A central, paracentral, or lateral disk herniation may affect different nerve roots at the same level. Examination of the lumbosacral, pelvic, and abdominal regions may provide clues to underlying abnormalities relating to back pain (Table 15,6 and 25,6,8). Diagnostic Workup Imaging is not warranted for most patients with acute low back pain. Without signs and symptoms indicating a serious underlying condition, imaging does not improve clinical outcomes in these patients.9-11 Even with a few weaker red flags, four to six weeks of treatment is appropriate before consideration of imaging studies.8-10 If a serious condition is suspected, magnetic resonance imaging (MRI) is usually most
appropriate. Computed tomography is an alternative if MRI is contraindicated or unavailable.10 Clinical correlation of MRI or computed tomography findings is essential because the likelihood of false-positive results increases with age.12-14 Radiography may be helpful to screen for serious conditions, but usually has little diagnostic value because of its low sensitivity and specificity.10 Laboratory tests such as complete blood count with differential, erythrocyte sedimentation rate, and C-reactive protein level may be beneficial if infection or bone marrow neoplasm is suspected. These tests may be most sensitive in cases of spinal infection because lack of fever and a normal complete blood count are common in patients with spinal infection.15 Because laboratory testing lacks specificity, MRI with and without contrast media and, in many cases, biopsy are essential for accurate diagnosis.15
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clinical practice Table 4. Approach to the Treatment of Nonspecific Acute Low Back Pain First visit Patient education Reassure the patient that the prognosis is often good, with most cases resolving with little intervention Advise the patient to stay active, avoiding bed rest as much as possible, and to return to normal activities as soon as possible Advise the patient to avoid twisting and bending Initiate trial of a nonsteroidal anti-inflammatory drug or acetaminophen Consider a muscle relaxant based on pain severity Consider a short course of opioid therapy if pain is severe Consider referral for physical therapy (McKenzie method and/ or spine stabilization) if it is not the first episode Second visit* Consider changing to a different nonsteroidal anti-inflammatory drug Consider referral for physical therapy (McKenzie method and/or spine stabilization) if not done at initial visit Consider referral to a spine subspecialist if pain is severe or limits function *Two to four weeks after the initial visit, if the patient has not significantly improved.
Treatment of Nonspecific Pain Many treatments are available for acute low back pain, but strong evidence for their benefit is lacking. Based on the evidence, a reasonable approach to treatment is described in Table 4.
Recommended Medications. Nonsteroidal anti-inflammatory drugs (NSAIDs) are often first-line therapy for low back pain. Low-quality evidence suggests that they are effective for short-term symptom relief, compared with placebo.16 No patient characteristics at baseline can predict the success of NSAID therapy.17 Moderate evidence suggests that no one NSAID is superior, and switching to a different NSAID may be considered if the first is ineffective. Whether NSAIDs are more effective than acetaminophen is unknown, but the addition of an NSAID to acetaminophen therapy is no more beneficial than acetaminophen alone.16,18 Moderate-quality evidence shows that nonbenzodiazepine muscle relaxants (e.g., cyclobenzaprine, tizanidine, metaxalone) are beneficial in the treatment of acute low back pain. Most pain reduction from these medications occurs in the first seven to 14 days,
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but the benefit may continue for up to four weeks.19,20 However, nonbenzodiazepine muscle relaxants do not affect disability status.19,20 Very low-quality evidence shows that a short course (up to five days) of oral diazepam may also be beneficial for pain relief.19 Because all muscle relaxants have adverse effects, such as drowsiness, dizziness, and nausea, they should be used cautiously. Diazepam and carisoprodol use should be brief to decrease the risk of abuse and dependence. There is also moderate-quality evidence that muscle relaxants combined with NSAIDs may have additive benefit for reducing pain.19 Opioids are commonly prescribed for patients with severe acute low back pain; however, there is little evidence of benefit. Three studies showed no difference in pain relief or time to return to work between oral opioids and NSAIDs or acetaminophen, and there is risk of harmful dose escalation over time with opioids, especially with purer formulations.16,21 Although epidural steroid injections are not beneficial for isolated acute low back pain, they may be helpful for radicular pain that does not respond to two to six weeks of noninvasive treatment. Transforaminal injections appear to have more favorable short- and long-term benefit than traditional interlaminar injections.22 Patient Education. Patient education involves a discussion of the often benign nature of acute back pain and reassurance that most patients need little intervention for significant improvement. Patients should be advised to stay as active as possible, within pain limits; to avoid twisting and bending, particularly when lifting; and to return to normal activities as soon as possible. The goal is to reduce worry about back pain and to teach ways to avoid worsening of pain or pain recurrence. High-quality evidence shows that individual patient education of greater than two hours is more effective than no education or less-intense education for pain that persists for four weeks or more.23 Moderate-quality evidence shows that less-intense individual education and advice to stay active have small benefits and are at least as effective as other back pain interventions.23,24 It is unclear whether patient education and advice for patients with acute low back pain are cost-effective.25
Acceptable Physical Therapy. Physical therapists often recommend the McKenzie method or spine stabilization exercises for the treatment of low back pain. The McKenzie method is described at http://www.mckenziemdt.org/ approach.cfm, and a video demonstration is available
clinical practice at http://www.youtube.com/watch?v=wBOp-ugJbTQ. The McKenzie method has been shown to be slightly more effective than other common low back pain treatments; however, the difference is not clinically significant,26,27 and evidence on its effect on disability is conflicting.26,27 There also do not appear to be good long-term benefits with the McKenzie method, other than decreased need for health care services.27 Spine stabilization exercises have been shown to decrease pain, disability, and risk of recurrence after a first episode of back pain.28 According to moderate-quality evidence, physical therapist窶電irected home exercise programs for acute back pain can reduce the rate of recurrence, increase the time between episodes of back pain, and decrease the need for health care services. Therefore, most of these exercise programs are cost-effective treatments for acute low back pain.29-31 Application of Ice or Heat. Low-quality evidence shows that in the first five days of acute low back pain, the use of heat treatments may be more effective for reducing pain and disability than nonheat wraps, NSAIDs, or acetaminophen, but shows no difference between heat application and McKenzie therapy at seven days.32 A low-quality study found that heat therapy in conjunction with education or NSAIDs is more effective than education or NSAIDs alone at 14 days.33 Ice and heat therapy have similar analgesic effects.32
Unsupported Oral Steroids. A short course of oral corticosteroids has questionable benefit for patients with acute radicular leg pain.34 However, there are no studies to support the use of oral steroids for isolated acute low back pain. Acupuncture. Several low-quality trials show that acupuncture has minimal or no benefit over sham treatment, naproxen, or the Chinese herbal therapy moxibustion.35,36 Although evidence to support its effectiveness is limited, acupuncture may be costeffective in patients with pain lasting longer than four weeks.25 Exercise. Aerobic conditioning, strengthening exercises, flexibility exercises, or a combination of these exercises is no more effective than other treatments in patients with acute low back pain.37-39 Lumbar Support. It is unclear whether lumbar support is more effective than no intervention or other treatments for acute low back pain.40 Massage. There is insufficient evidence to recommend for or against massage therapy for acute low
back pain.41,26 It is unlikely to be cost-effective.25 Spinal Manipulation and Chiropractic Techniques. Lowquality evidence shows that spinal manipulation may be more effective than sham treatments in the shortterm reduction of pain (less than six weeks), but no more effective in reducing disability.18,20,42,43 There is little evidence that manipulation is cost-effective for treating acute low back pain.25 Although chiropractic techniques are considered safe if performed by a well-trained chiropractor, a systematic review found that these techniques (e.g., manipulation, temperature modalities, exercises, mechanical devices, patient education) provide no clinically relevant improvement in pain or disability compared with other treatments.44 Traction. High-quality trials show no evidence of benefit with traction, as a single treatment or in combination with other treatments, in patients with acute or chronic back pain.45 There are no studies on acute low back pain alone.
Inadvisable Bed Rest. Bed rest should not be recommended for patients with nonspecific acute low back pain. Moderatequality evidence suggests that bed rest is less effective at reducing pain and improving function at three to 12 weeks than advice to stay active.46 Prolonged bed rest can also cause adverse effects such as joint stiffness, muscle wasting, loss of bone mineral density, pressure ulcers, and venous thromboembolism.37 REFERENCES 1.
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19. van Tulder MW, Touray T, Furlan AD, Solway S, Bouter LM. Muscle relaxants for non-specific low back pain. Cochrane Database Syst Rev. 2003;(2):CD004252. 20. Hoiriis KT, Pfleger B, McDuffie FC, et al. A randomized clinical trial comparing chiropractic adjustments to muscle relaxants for subacute low back pain. J Manipulative Physiol Ther. 2004;27(6):388-398. 21. Cifuentes M, Webster B, Genevay S, Pransky G. The course of opioid prescribing for a new episode of disabling low back pain: opioid features and dose escalation. Pain. 2010;151(1):22-29. 22. Roberts ST, Willick SE, Rho ME, Rittenberg JD. Efficacy of lumbosacral transforaminal epidural steroid injections: a systematic review. PM R. 2009;1(7): 657-668. 23. Engers A, Jellema P, Wensing M, van der Windt DA, Grol R, van Tulder MW. Individual patient education for low back pain. Cochrane Database Syst Rev. 2008;(1):CD004057. 24. Dahm KT, Brurberg KG, Jamtvedt G, Hagen KB. Advice to rest in bed versus advice to stay active for acute lowback pain and sciatica. Cochrane Database Syst Rev. 2010;(6):CD007612. 25. Lin CW, Haas M, Maher CG, Machado LA, van Tulder MW. Cost-effectiveness of guideline-endorsed treatments for low back pain: a systematic review. Eur Spine J. 2011;20(7):1024-1038. 26. Machado LA, de Souza MS, Ferreira PH, Ferreira ML. The McKenzie method for low back pain: a systematic review of the literature with a meta-analysis approach. Spine (Phila Pa 1976). 2006;31(9):E254-E262. 27. Machado LA, Maher CG, Herbert RD, Clare H, McAuley JH. The effectiveness of the McKenzie method in addition to first-line care for acute low back pain: a randomized controlled trial. BMC Med. 2010;8:10. 28. Hides JA, Jull GA, Richardson CA. Long-term effects of specific stabilizing exercises for first-episode low back pain. Spine (Phila Pa 1976). 2001;26(11):E243â&#x20AC;&#x201C;E248. 29. Choi BK, Verbeek JH, Tam WW, Jiang JY. Exercises for prevention of recurrences of low-back pain. Cochrane Database Syst Rev. 2010;(1):CD006555. 30. Gellhorn AC, Chan L, Martin B, Friedly J. Management patterns in acute low back pain: the role of physical therapy [published ahead of print November 19, 2010]. Spine (Phila Pa 1976). http://journals.lww.com/ spinejournal/Abstract/publishahead/Management_ Patterns_in_Acute_Low_Back_Pain__The.99251.aspx (subscription required). Accessed May 2, 2011. 31. Fritz JM, Cleland JA, Speckman M, Brennan GP, Hunter SJ. Physical therapy for acute low back pain: associations with subsequent healthcare costs. Spine (Phila Pa 1976). 2008;33(16):1800-1805. 32. French SD, Cameron M, Walker BF, Reggars JW, Esterman AJ. Superficial heat or cold for low back pain. Cochrane Database Syst Rev. 2006;(1):CD004750.
clinical practice 33. Tao XG, Bernacki EJ. A randomized clinical trial of continuous low-level heat therapy for acute muscular low back pain in the workplace. J Occup Environ Med. 2005;47(12):1298-1306. 34. Holve RL, Barkan H. Oral steroids in initial treatment of acute sciatica. J Am Board Fam Med. 2008;21(5): 469-474. 35. Furlan AD, van Tulder MW, Cherkin DC, et al. Acupuncture and dry-needling for low back pain. Cochrane Database Syst Rev. 2005;(1):CD001351. 36. Kennedy S, Baxter GD, Kerr DP, Bradbury I, Park J, McDonough SM. Acupuncture for acute non-specific low back pain: a pilot randomised non-penetrating sham controlled trial. Complement Ther Med. 2008;16(3):139-146. 37. Casazza BA, Young JL, Herring SA. The role of exercise in the prevention and management of acute low back pain. Occup Med. 1998;13(1):47-60. 38. Hayden JA, van Tulder MW, Malmivaara A, Koes BW. Exercise therapy for treatment of non-specific low back pain. Cochrane Database Syst Rev. 2005;(3):CD000335. 39. Lau PM, Chow DH, Pope MH. Early physiotherapy intervention in an accident and emergency department reduces pain and improves satisfaction for patients with acute low back pain: a randomised trial. Aust J Physiother. 2008;54(4):243-249.
40. van Duijvenbode IC, Jellema P, van Poppel MN, van Tulder MW. Lumbar supports for prevention and treatment of low back pain. Cochrane Database Syst Rev. 2008;(2):CD001823. 41. Furlan AD, Imamura M, Dryden T, Irvin E. Massage for low back pain: an updated systematic review within the framework of the Cochrane Back Review Group. Spine (Phila Pa 1976). 2009;34(16):1669-1684. 42. Assendelft WJ, Morton SC, Yu EI, Suttorp MJ, Shekelle PG. Spinal manipulative therapy for low back pain. Cochrane Database Syst Rev. 2004;(1):CD000447. 43. J端ni P, Battaglia M, N端esch E, et al. A randomised controlled trial of spinal manipulative therapy in acute low back pain. Ann Rheum Dis. 2009;68(9):1420-1427. 44. Walker BF, French SD, Grant W, Green S. A Cochrane review of combined chiropractic interventions for low-back pain. Spine (Phila Pa 1976). 2011;36(3): 230-242. 45. Clarke JA, van Tulder MW, Blomberg SE, et al. Traction for low-back pain with or without sciatica. Cochrane Database Syst Rev. 2007;(2):CD003010. 46. Hagen KB, Hilde G, Jamtvedt G, Winnem M. Bed rest for acute low-back pain and sciatica. Cochrane Database Syst Rev. 2004;(4):CD001254.
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Recurrent Urovaginal Fistula: A Sequel of Missed Ureteral Involvement N Rajamaheswari*, Archana Bharti Chhikara**, K Seethalakshmiâ&#x20AC;
Abstract A 44-year-old multipara presented with continuous urinary leakage per vagina of 15 months duration despite abdominal vesicovaginal fistula repair. Intravenous urography revealed normal upper urinary tract. Methylene blue test was positive but no fistula was detected on cystoscopy. Failure to cystoscopically visualize the catheter, which was easily introduced through the vaginal end of fistulous tract warranted a fistulogram that simulated retrograde ureteropyelogram and showed contrast in the bladder confirming ureterovesicovaginal fistula. Patient underwent transvesical ureteroneocystostomy with closure of bladder communication and remains continent at six months follow-up. Recurrence of urovaginal fistulae after vesicovaginal fistula repair may be attributable to undiagnosed ureteral involvement despite normal upper tract imaging. Simple procedures like cystoscopic visualization of catheter along with fistulogram can clinch the diagnosis in such cases.
Keywords: Fistulogram, ureterovesicovaginal fistula, urovaginal fistula
I
solated vesicovaginal fistula or ureterovaginal fistula can be easily diagnosed but there is a tendency to overlook one or the other components of communication in cases of complex fistulas. Though diagnosis of ureterovesicovaginal fistula poses challenges, a high-degree of clinical suspicion and methodical evaluation can clinch the diagnosis which will avoid inadequate surgical repair and persistence of urinary leakage. Case Report A 44-year-old multipara developed continuous urinary leakage per vagina following total abdominal hysterectomy for abnormal uterine bleeding. Urinary leakage per vagina started from the 9th postoperative day, which was managed conservatively with indwelling urethral catheter for two months. As urinary leakage persisted, she underwent abdominal vesicovaginal fistula repair at her home town three months after the index surgery.
*Professor and Head **Fellow in Urogynecology â&#x20AC; Assistant Professor Dept. of Urogynecology, Government Kasturba Gandhi Hospital and Institute of Social Obstetrics, Madras Medical College, Triplicane, Chennai Address for correspondence Dr Archana Bharti Chhikara H.No.: 1398, Sector-15, Sonepat, Haryana -131 001 E-mail: archanachhikara@gmail.com
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Unfortunately, continuous urinary leakage was recognized soon after the vesicovaginal fistula surgery. She endured leakage for a year and presented at our institute for further management. General examination was unremarkable except for the previous midline abdominal scar. Local examination revealed pooling of urine in vagina but palpation failed to reveal the fistulous defect in the vagina. Routine biochemical investigations were normal. Both ultrasound imaging and intravenous urography (Fig. 1) did not reveal dilatation of the collecting system of the upper urinary tract. Examination under anesthesia revealed the continuous leakage of urine in the vagina suggesting urovaginal fistula. With great difficulty a pinhole fistula was detected in the middle of anterior vaginal wall through which clear urine was dribbling. Positive methylene blue test reassured the existence of vesicovaginal fistula. Cystoscopy revealed no fistula in the bladder, normal right ureteric orifice with clear efflux and scarring in the supratrigonal area (due to previous repair) with no discernible left ureteric orifice. An important step of our evaluation is cystoscopic visualization of ureteric catheter passed through the vaginal end of the fistulous opening, which could be passed for a length of 10 cm without resistance. The turning point of the evaluation was failure to visualize the catheter inside the bladder which
case report
(a)
Figure 1. Intravenous urogram showing normal upper urinary tract.
(b)
(c) Figure 2. Fistulogram simulating retrograde ureteropyelogram and showing contrast in the bladder.
Figure 3. Transvesical ureteroneocystostomy and closure of bladder component of the fistula.
compelled us to resort to fistulogram (Fig. 2). The contrast study simulated a retrograde ureteropyelogram along with the presence of the contrast in the bladder confirming the ureteral and vesical components of the ureterovesicovaginal fistulous communication.
She underwent transvesical ureteroneocystostomy and closure of the bladder component of the fistula (Fig. 3 a, b, c). She was completely free of leakage following her repeat repair and she had completed six months of her follow-up.
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case report Discussion Diagnosis of vesicovaginal fistula or ureterovaginal fistula per se may not pose great difficulty. On the contrary, complex fistulous communications like ureterovesicovaginal may either go unrecognized or misinterpreted as isolated vesicovaginal fistula. Highdegree of suspicion and methodical evaluation need to be adopted to clinch the diagnosis. Unless precise diagnosis is ensured, relief from urinary leakage is unlikely. For successful management of ureterovesicovaginal fistula, both the ureterovaginal and vesicovaginal components of the communication warrant appropriate surgical correction. Unintended repair of a single component as in the current case will result in persistent urinary leakage after surgical closure.1 At times intravenous urography may fail to demonstrate hydroureteronephrosis despite ureteral involvement as in this case, which proves the inadequacy of intravenous urography as a diagnostic tool.2 However, precise diagnosis is obligatory to administer appropriate surgical treatment. The diagnosis was challenging because the radiological imaging (ultrasonography and intravenous urography) studies showed unobstructed upper urinary tract. In addition, the infant feeding tube could not be visualized cystoscopically despite positive methylene blue test. Though fistulogram (which simulated a retrograde ureteropyelogram) may primarily appear to have clinched the diagnosis, it was the failure to cystoscopically visualize the catheter which compelled us to consider the fistulogram. The role of abdominal CT with urogram in identifying the intricacies of complex fistulous communications is valuable.3 However, in centers where access to high end imaging modalities like CT is restricted,
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evaluation using simple techniques like fistulous tract catheterization along with cystoscopic visualization can establish the diagnosis. Usually, ureteral injuries are managed by minimally invasive procedures (retrograde/antegrade double J [DJ] stenting) failing which open surgical techniques are adopted. This patient underwent transvesical ureteroneocystostomy. Ureteroscopic DJ stenting and extravesical approach was intentionally omitted as she required additional closure (under vision) of the bladder component of the fistula. Patient was leakage free after surgery and remains continent at six months follow-up. Conclusion Recurrence of urinary tract fistulae after vesicovaginal fistula repair may be attributable to undiagnosed ureteral involvement despite normal upper tract imaging. The role of simple procedures like cystoscopic visualization of catheter passed through the fistulous tract in the routine evaluation of urovaginal fistula is highlighted, which along with fistulogram will enable precise diagnosis of ureterovesicovaginal fistula even in the absence of CT and permit appropriate surgical management and permanent relief from urinary leakage. References 1.
Fichtner J, Voges G, Steinbach F, Hohenfellner R. Ureterovesicovaginal fistulas. Surg Gynecol Obstet 1993;176(6):571-4.
2.
Elliott SP, McAninch JW. Ureteral injuries from external violence: the 25-year experience at San Francisco General Hospital. J Urol 2003;170(4 Pt 1):1213-6.
3.
McAninch JW, Santucci RA. Renal and ureteral trauma. In: Campbell-Walsh Urology. 9th edition, Wein AJ. (Ed.), Saunders Elsevier: Philadelphia, Pa 2007:p.1274-92.
case report
Scorpion Bite causing Acute Severe Myocarditis: A Rare Complication TARACHAND SAINI*, SHAILENDAR GUPTA**, MANIRAM KUMHAR†
Abstract Scorpion bites are common in India as well as in other countries. Usually, these bites are harmless but sometime have serious clinical sequelae, including death. We report herein a case of scorpion bite that presented with acute severe myocarditis - a rare complication.
Keywords: Scorpion bite, severe myocarditis, pulmonary edema
T
here are about 1,500 species of scorpions worldwide, out of these 50 are dangerous to human. Among 86 species in India, Mesobuthus tamulus and Palamnaeus swammerdami are of medical importance.1
and cardiovascular collapse. Cardiovascular effect are particularly prominent after stings by Indian red scorpion (M. tamulus).3
Almost all lethal scorpions except Hemiscorpius species, belong to the scorpion family called Buthidae. The lethal member of Buthidae include genera Buthus, Parabuthus, Mesobuthus, Tityus, Leiurus, Androctonus and Centruroides.
An 18-year-old girl was stung by a scorpion on the distal phalanx of the left index finger and presented with intense pain and swelling on the local site. She admitted with heart rate 140 beats/minute, and blood pressure 70/40 mmHg. Symptomatic treatment was given. But the patient’s condition continued to worsen, and she developed severe respiratory distress. Because of respiratory failure, she was immediately intubated and admitted to the intensive care unit. Bilateral basal rales were heard on auscultation, and cardiovascular examination revealed a loud S3 gallop at the apex.
Scorpions live in warm dry regions throughout India. They commonly inhabit the crevices of dwellings, underground burrows, under logs or debris, paddy husk, sugarcane fields, coconut and banana plantations. Their distribution is more in regions with abundant red soil.2 They hunt during night and hide in crevices and burrow during the day to avoid light. Scorpion stings increase dramatically in summer months and lower in winter. Scorpion stings causes a wide range of manifestation, from local skin reaction to neurological, respiratory
*2nd Year Resident **3rd Year Resident †Associate Professor Dept. of Medicine, Jawaharlal Nehru Medical College, Ajmer Address for correspondence Dr Tarachand Saini 20, Gaurav Enclave, Near City Palace, Civil Line, Ajmer, Rajasthan E-mail: drtcsaini20@gmail.com
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CASE REPORT
Laboratory results were as follows: Hemoglobin was 12.6 g/dl, white blood cell count was 24,380 cells/mm3, platelet count was 1,80,000 cells/mm3 and urine microscopy showed hematuria. Blood urea 71 mg/dl (17-43 mg/dl), serum creatinine 1.6 mg/dl (0.5-1.1 mg/ dl), aspartate transaminase 93 U/l (5-38 U/l), alanine transaminase 30 U/l (5-41 U/l), creatine kinase (CK) 743 U/l (26-190 U/l), CK-MB 52 U/l (0-24 U/l), Trop-I 0.02 ng/ml (0.00-0.04 ng/ml). An electrocardiogram (ECG) revealed sinus tachycardia and ST-T wave changes. Chest X-ray demonstrated bilateral fluffy shadows indicative of pulmonary edema (Fig. 1). Echocardiography reveal hypokinesia of the basal two-third of the interventricular septum with reduced ejection fraction (Fig. 2).
case report dependent sodium channels in the open state leading to continuous, prolonged, repetitive firing of the somatic, sympathetic, and parasympathetic neurons results in autonomic and neuromuscular overexcitation symptoms due to release of excessive neurotransmitters such as epinephrine, norepinephrine, acetylcholine glutamate and aspartate. Meanwhile, the short polypeptide neurotoxin blocks the potassium channels.
Figure 1. Chest X-ray showing bilateral fluffy shadows.
Scorpion bites usually have a good prognosis. However, occasionally potentially fatal complications such as myocarditis, pulmonary edema and shock occur.4 Among these, myocarditis and resultant pulmonary edema are important causes of death.5 Three possible mechanisms might explain cardiac dysfunction, including adrenergic myocarditis, toxics myocarditis and myocardial ischemia. a-receptor stimulation by toxins play a major role in development of tachycardia, myocardial dysfunction and pulmonary edema.6 Unopposed a-receptors stimulation lead to suppression of insulin secretion, hyerglycemia, hyperkalemia, free fatty acid and free radical accumulation that are injurious to myocardium. Bahloul et al4 examined the histopathology of two fatal myocarditis cases resulting from a scorpion bite. The pathologic conditions revealed a mixed picture of toxic myocarditis and coagulative myocytolysis, similar to catecholamine-induced cardiotoxicity.4
Figure 2. Echocardiography.
In accordance with these symptoms and findings, a diagnosis of acute heart failure with pulmonary edema was made. Dopamine, dobutamine, diuretics and steroids were given. With treatment, patientâ&#x20AC;&#x2122;s status improved. Repeat chest X-ray was clear within 24 hours of initiating this treatment. DISCUSSION Scorpion venom may contain multiple toxin-like neurotoxin, cardiotoxin, nephrotoxin and hemolytic toxin. The primary targets of scorpion venom are voltage-dependent ion channels. The long-chain polypeptide neurotoxin causes stabilization of voltage-
Myocardial ischemia is not only due to the release of catecholamines but also due to effect of cytokines and/or neuropeptide Y on coronary vessels. Cardiac damage might be enhanced by the depressive effect of cytokines upon myocardial cells. Hyperglycemia may also contribute to myocardial injury.7 Valdivia et al8 reported a series of 32 children with scorpion bites who developed cardiac complications. Among these, 50% exhibited myocarditis, 12.5% had subclinical disease, and 63% had observable ECG changes. We observed both ECG changes and myocarditis in this case. Conclusion We report here the case of an 18-year-old girl who developed life-threatening, acute toxic myocarditis and pulmonary edema, after a scorpion bite. Aggressive medical treatment with inotropic agents, diuretics and parenteral corticosteroids resulted in rapid clinical resolution.
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case report REFERENCES 1.
Erfati P. Epidemiology, symptomatology and treatment of buthinae stings. In: Arthpod Venoms. Handbook of Experimental Pharmacology. Bettini S (Ed.), SpringerVerlag: New York 1978:p.312-5.
2.
Bawaskar HS. Personal communication. 1998.
3.
Bawaskar HS, Bawaskar PH. Indian red scorpion envenoming. Indian J Pediatr 1998;65(3):383-91.
4.
Bahloul M, Kallel H, Rekik N, Ben Hamida C, Chelly H, Bouaziz M. Cardiovascular dysfunction following severe scorpion envenomation. Mechanisms and physiopathology. Presse Med 2005;34(2 Pt 1):115-20.
5.
Gueron M, Yaron R. Cardiovascular manifestations of severe scorpion sting. Clinicopathologic correlations. Chest 1970;57(2):156-62.
6.
Bawaskar HS, Bawaskar PH. Management of the cardiovascular manifestations of poisoning by the Indian red scorpion (Mesobuthus tamulus). Br Heart J 1992;68(5):478-80.
7.
Garg AK, Pimparkar AB, Abraham P, Chikhalikar AA. Myocarditis and pulmonary edema following scorpion bite. (A case report). J Postgrad Med 1983;29(1):46-8.
8.
Valdivia HH, Kirby MS, Lederer WJ, Coronado R. Scorpion toxins targeted against the sarcoplasmic reticulum Ca(2+)release channel of skeletal and cardiac muscle. Proc Natl Acad Sci U S A 1992;89(24):12185-9.
Vitiligo Management Guidelines Released The most effective management for vitiligo includes phototherapy and combination therapy, according to updated guidelines from the writing group of the Vitiligo European Task Force (VETF), which were accepted for publication and published online August 3 in the British Journal of Dermatology. The European Academy of Dermatology and Venereology and the Union Européenne des Médecins Spécialistes collaborated with the VETF in developing the new evidence- and expert-based guidelines for vitiligo. The reviewers recommend the following principles of management for segmental vitiligo or limited nonsegmental vitiligo (involving <2-3% of body surface): First-line treatment should be to avoid triggering factors and to use local agents such as corticosteroids or calcineurin inhibitors.
Second-line treatment should be localized narrow-band ultraviolet B (NB-UVB) radiation (311 nm), preferably with the excimer monochromatic lamp or laser. Third-line treatment for patients left with cosmetically unsatisfactory repigmentation on visible areas after first- or second-line therapy is to consider use of surgical techniques.
The reviewers recommend the following principles of management for nonsegmental vitiligo:
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First-line management is to avoid triggering or aggravating factors and to stabilize the patient with NB-UVB therapy for at least three months. Patients who respond to NB-UVB should continue this treatment for nine months or more. An additional consideration is to combine localized UVB therapy with systemic or topical therapies. Second-line treatment for patients with rapidly progressive disease or lack of stabilization with NB-UVB is systemic corticosteroids, 3- to 4-month minipulse therapy or immunosuppressants. Third-line treatment is to graft areas failing to respond to previous treatment, particularly those areas with high cosmetic effect. The Koebner phenomenon, or new development of vitiligo in a previously unaffected area of skin undergoing traumatic injury, may limit graft persistence, Grafts are relatively contraindicated on the dorsum of the hands and similar areas. Fourth-line treatment for widespread (covering >50% of body surface), refractory or highly visible vitiligo is depigmentation using hydroquinone monobenzylether or 4-methoxyphenol alone or in combination with Q switch ruby laser. (Source: Medscape)
case report
Autologous Bone Marrow-derived Mononuclear Cell Transplantation in Duchenne Muscular Dystrophy A Sharma* Pooja Kulkarni**, G Chopra*, N Gokulchandran*, M Lohiaâ&#x20AC; , P Badhe**
Abstract Duchenne muscular dystrophy (DMD) is the most common childhood muscular dystrophy. Presently, there is no known cure for the disorder. We report an 18-year-old boy with DMD who underwent autologous bone marrow-derived mononuclear cell transplantation intrathecally as well as intramuscularly in specific muscles. The parameters used to assess the patient pre- and postoperatively were creatine phosphokinase levels, electromyography, magnetic resonance imaging (MRI) musculoskeletal system upper and lower limbs and manual muscle testing. On follow-up at six months, he showed significant functional improvements along with improvements in his muscle strength. Clinically, his MRI also showed muscle fiber regeneration with decrease in fatty infiltration.
Keywords: Duchenne muscular dystrophy, autologous, mononuclear cells
D
uchenne muscular dystrophy (DMD) is an X-linked, neuromuscular, recessive disorder, which is caused due to mutation in the dystrophin gene located on the X-chromosome at the location Xp21.2. Hence, it occurs in male children.1,2 Defect in the dystrophin gene leads to progressive muscle degeneration and eventually loss of ambulation and death. DMD has an early onset with symptoms like difficulty in walking, frequent falls, difficulty in motor skills, muscle wasting, contractures, pseudohypertrophy, respiratory disorders and skeletal deformities in some cases.3 Diagnosis of DMD is based on a combination of clinical findings like family history and serum creatine kinase concentration. The muscle biopsy, genetic testing, electromyogram (EMG), nerve conduction velocity (NCV) confirm the diagnosis of DMD. We hereby present a case of an 18-year-old boy diagnosed with DMD, who underwent autologous bone
*Dept. of Medical Services and Clinical Research **Dept. of Research and Development â&#x20AC; Dept. of Neurorehablitation NeuroGen Brain and Spine Institute, Surana Sethia Hospital and Research Centre Sion-Trombay Road, Chembur, Mumbai Address for correspondence Ms. Pooja Kulkarni Research Scientist, NeuroGen Brain and Spine Institute, Surana Sethia Hospital and Research Centre, Sion-Trombay Road, Chembur, Mumbai - 400 071 E-mail: poojakul28@gmail.com, publications@neurogen.in
marrow-derived mononuclear cell (MNC) transplantation. He showed significant improvements functionally as well as clinically. Case Report An 18-year-old boy with a family history of DMD was diagnosed at the age of one year with increased creatine phosphokinase (CPK) levels. He showed delayed milestones. He developed bilateral lower limb weakness with difficulty in walking and could walk on toes. He had a history of frequent falls with difficulty in climbing stairs and also in getting up from the sitting position. He stopped walking at the age of 15 years. Gradually, upper extremity weakness also developed with difficulty in overhead activities. On examination, right-sided scoliosis of spine was observed. Functionally, he was dependent on his caretaker for all the activities of daily living. On Functional Independence Measure (FIM), he scored 63, while on Brooke and Vignos scale, he scored 6 and 10, respectively. Neurologically, he was hypotonic and hyporeflexic. All his sensations were intact. According to manual muscle testing, strength in muscles and force of contraction in them was assessed extensively. He had Grade 1 strength in bilateral upper limb and lower limb proximally and Grade 3 distally in all four limbs. On examination, he was cachexic with poor chest expansion and history of repeated lower respiratory tract infection. His CPK levels were 995 IU/l. Magnetic
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case report resonance imaging (MRI) of musculoskeletal system showed diffuse fatty infiltration in the muscles of upper arm, fore arm, pelvic girdle, thigh and leg. EMG showed primary muscle disease wherein proximal muscles were more affected than the distal muscles and 2D-Echo was normal with left ventricular ejection fraction (LVEF) - 60%. He was on continuous physiotherapy since he was diagnosed. He underwent autologous bone marrow-derived MNC transplantation at our center. Material and Methods Patient selection and protocol design has been based on the inclusion criterion as per the World Medical Associations, Helsinki declaration. The protocol had been reviewed and approved by the Institutional Committee for Stem Cell Research and Therapy (IC-SCRT). The patient was informed about the procedure and a duly filled informed consent was obtained from him and his family. Granulocyte colony-stimulating factor (G-CSF) (300 Âľg) injections were administered subcutaneously, 48 hours and 24 hours before the therapy. Before the therapy, he underwent extensive evaluation by a team of medical and rehabilitation experts. Detailed evaluation of muscle strength and functional ability was done. Weak group of muscles were selected and then their motor points were plotted with the help of an electrodiagnostic stimulator. Bone marrow (100 ml) was aspirated from the iliac bone under local anesthesia. The MNCs were separated and approximately 33 x 106 MNCs were immediately injected intrathecally in L4-L5 space. MNCs (diluted in cerebrospinal fluid) were also injected intramuscularly bilaterally in the glutei, quadriceps, deltoid and abdominals, which were decided prior to the therapy. Solumedrol 750 mg was given intravenously at the time of transplant. Following the transplantation, he underwent intensive neurorehabilitation, which included physiotherapy, occupational therapy as a part of the treatment program. He was put on exercise program emphasizing on strengthening individual muscles that were injected with stem cells so as to facilitate mobility and multiplication of the injected stem cells thereby giving enhanced results. Results Our case presented typical symptoms of DMD. The CPK level, EMG and MRI musculoskeletal system of upper and lower limb confirmed the diagnosis. Post-transplantation, he did not report any side effects.
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Immediately after the therapy, few improvements were observed. His sitting posture was better than before. His CPK levels reduced to 460 IU/l from 955 IU/l. After four months, he was reassessed. Manual muscle charting (MMT) was carried out and as it is a standard component of the neuromusculoskeletal physical examination, intratestor error was kept at minimum. His hand grip strength had improved significantly. His neck control and movements were better than before. His upper extremity muscles were stronger than before. He could stand on balance board with push knee splints for 15-20 minutes. His trunk balance had also improved. On comparing the MRI before and after the therapy, improvements were observed in the degree of fatty infiltration with minimal possible muscle regeneration in the vastus medialis, vastus lateralis and semitendinosus muscle in the thigh. Similar improvement was also noted in the tibialis anterior, medial and lateral head of gastrocnemius muscle in the leg (Figs. 1-4). In the arm, improvements were noted in the long and lateral head of triceps muscle and biceps brachii muscle. RIGHT
LEFT
a RIGHT
LEFT
b Figure 1. Axial T1W images at the level of upper thigh. (a) Pre-stem cell therapy show marked fatty infiltration of the right vastus medials (thick arrow) and lateralis muscle (thin arrow), seen as high signal intensity. (b) Post-stem cell therapy shows reduced high signal in both the vastus medialis (thick arrow) and lateralis (thin arrow) suggestive of less fatty infiltration and regeneration of muscle fibers.
case report
RIGHT
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LEFT
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a
a RIGHT
RIGHT
LEFT
b
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b
Figure 2. Axial T1W images at the level of upper thigh. (a) Pre-stem cell therapy show marked fatty infiltration of the left semitendinosus (thin arrow) seen as high signal intensity. (b) Post-stem cell therapy shows reduced high signal in the left semitendinosus (thin arrow) suggestive of less fatty infiltration and regeneration of muscle fibers. RIGHT
LEFT
Figure 4. Axial T1W images at the level of the calf. (a) Prestem cell therapy show marked fatty infiltration of the left medial (thick arrow) and lateral gastrocnemius muscles (thin arrow) seen as high signal intensity. (b) Post-stem cell therapy shows reduced high signal in left medial (thick arrow) and lateral gastrocnemius muscles (thin arrow) suggestive of less fatty infiltration and regeneration of muscle fibers.
Histological evaluation was not done since our Ethical Committee â&#x20AC;&#x153;Institutional Committee for Stem Cell Research and Therapyâ&#x20AC;? does not permit invasive tests as biopsy in patients whose muscles are already weakened. Hence, the improvements were enumerated on the basis of MRI, CPK and clinical monitoring. Discussion
a RIGHT
LEFT
b Figure 3. Axial T1W images at the level of the calf. (a) Pre-stem cell therapy show marked fatty infiltration of the bilateral tibialis anterior muscle (thin arrows) seen as high signal intensity. (b) Post-stem cell therapy shows reduced high signal in bilateral tibialis anterior muscle (thin arrows) suggestive of less fatty infiltration and regeneration of muscle fibers.
Presently, there is no cure for the disorder. Treatments available currently are palliative. Suitable management provided to the DMD patient can prolong survival and improve the quality-of-life significantly. Use of corticosteroids, physical therapy, surgical interventions, and respiratory management are few of the symptomatic treatments practiced for DMD.4 Encouraging experiments have been carried out wherein a number of adult-derived stem cells have been isolated, characterized and transplanted in mouse models for DMD. In humans, Gussoni et al have presented the clinical case of a young DMD patient showing deletion of the exon 45 in the dystrophin gene, wherein 12 years after bone marrow transplantation, showed donor nuclei fused to 0.5% of dystrophic myofibers.5 We carried out autologous bone
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case report marrow- derived MNC transplantation for the patient since they have no immunologic reaction, no ethical issues and no uncontrollable proliferation as in the case of embryonic stem cells. These MNCs comprised of a variety of cells like hematopoietic stem cells, tissue specific progenitor cells, stromal cells and specialized blood cells in different stages of development. MNCs diluted in CSF were also injected intramuscularly at specific motor points. CSF is known to harbor growth factors which helps the growth of the cortical epithelium and promotes vascularization in the nervous system. In addition, the G-CSF and methylprednisolone administered before and during the transplantation, respectively helped in stimulation of CD34+ cells and also in survival and multiplication of the stem cells.6 The extensive neurorehabilitation provided along with MNC transplantation has shown to promote recovery and independence through neurofacilitation. Apart from their individual impact, study shows that exercise enhances the effect of stem cells by helping the mobilization of local stem cells, encouraging angiogenesis and release of cytokines and nerve growth factors.7 The present data provides clinical and radiological evidence that autologous bone marrow-derived MNC transplantation along with neurorehabilitation can result in improvements in the case of DMD with no
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side effects. However, more clinical studies will be needed to prove this definition. References 1.
Monaco AP, Bertelson CJ, Middlesworth W, Colletti CA, Aldridge J, Fischbeck KH, et al. Detection of deletions spanning the Duchenne muscular dystrophy locus using a tightly linked DNA segment. Nature 1985;316(6031): 842-5.
2.
Yoshida M, Ozawa E. Glycoprotein complex anchoring dystrophin to sarcolemma. J Biochem 1990;108(5):748-52.
3.
Emery AE. The muscular 2002;359(9307):687-95.
4.
Bushby K, Bourke J, Bullock R, Eagle M, Gibson M, Quinby J. The multidisciplinary management of Duchenne muscular dystrophy. Curr Pediatr 2005;15(4):292-300.
5.
Gussoni E, Bennett RR, Muskiewicz KR, Meyerrose T, Nolta JA, Gilgoff I, et al. Long-term persistence of donor nuclei in a Duchenne muscular dystrophy patient receiving bone marrow transplantation. Clin Invest 2002;110(6):807-14.
6.
Petit I, Szyper-Kravitz M, Nagler A, Lahav M, Peled A, Habler L, et al. G-CSF induces stem cell mobilization by decreasing bone marrow SDF-1 and up-regulating CXCR4. Nat Immunol 2002;3(7):687-94.
7.
Fabel K, Wolf SA, Ehninger D, Babu H, Leal-Galicia P, Kempermann G. Additive effects of physical exercise and environmental enrichment on adult hippocampal neurogenesis in mice. Front Neurosci 2009;3:50.
dystrophies.
Lancet
photo quiz
Large, Dark Lesion on the Arm Present Since Birth
A
n otherwise healthy 16-year-old boy presented with an asymptomatic, black to brown plaque on his right proximal forearm. The lesion was present at birth, but was flatter and lighter in color. Physical examination revealed a discrete, oval-shaped plaque that measured 7 Ă&#x2014; 3 cm. The lesion had a cobblestone pattern with prominent hair growth (see accompanying figure). Question Based on the patientâ&#x20AC;&#x2122;s history and physical examination, which one of the following is the most likely diagnosis?
C. Congenital melanocytic nevus.
A. Acquired melanocytic nevus.
D. Melanoma.
B. Becker nevus.
E. Plexiform neurofibroma. SEE THE NEXT PAGE FOR DISCUSSION.
Source: Adapted from Am Fam Physician. 2011;84(11):1287-1288.
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photo quiz Discussion The answer is C: congenital melanocytic nevus. Congenital melanocytic nevi are generally present at birth or appear within the first few months of life.1 The incidence ranges from 1 to 2 percent for any size of congenital melanocytic nevi to approximately one in 20,000 for giant nevi.2 Most congenital melanocytic nevi are intradermal or compound in nature.3 They are classified according to their expected diameter in adulthood as small (less than 1.5 cm), medium or intermediate (1.5 to 19.9 cm), and large or giant (20 cm or greater).2,4,5 Small and medium nevi are usually round or oval and symmetric. At birth, these lesions are flat or mildly palpable and tan in color, but over time they become raised and darken. They may have a verrucous or cobblestone surface.5 Hypertrichosis may become prominent. Giant congenital melanocytic nevi can have irregular color patterns and are often accompanied by multiple smaller “satellite” nevi. Although nevi are usually benign, some, particularly giant nevi, may be associated with the development of malignant melanoma.1 Congenital melanocytic nevi, especially those occurring in the posterior trunk, may rarely involve the central nervous system. The usual treatment for small and medium congenital melanocytic nevi is observation.4 The decision to remove a lesion is based on the malignant potential and its cosmetic outcome.4 Prophylactic excision is performed for giant congenital melanocytic nevi to lower the risk of melanoma. Other treatments include superficial excision, laser treatment, curettage, chemical peel, and dermabrasions with regular follow-up. A conservative approach with serial photography of the nevus and close follow-up has also been recommended.2 All patients with congenital melanocytic nevi should be instructed on sun protection.1,4 Acquired melanocytic nevi are small (less than 8 mm in diameter), well circumscribed, and round or ovoid with a homogenous surface and even pigmentation. Compared with the congenital type, acquired melanocytic nevi are smaller, are more uniform in architecture and morphology, and occur in greater numbers. Becker nevi are more common in males. They typically appear at 10 to 20 years of age as a brownish, circumscribed macule or patch that gradually enlarges in an irregular fashion, similar to a geographic configuration.6 Hypertrichosis may develop a few years after the pigmentation. The lesion is asymptomatic and unilateral with a predilection for the upper torso, often the shoulder. Melanoma is a malignant tumor that can present as an enlarging, asymmetric, variegated lesion with an irregular border. It is rare in childhood and typically
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Summary Table Condition
Characteristics
Acquired melanocytic nevus
Small, well-circumscribed, round or ovoid lesion with a homogenous surface and even pigmentation; multiple nevi present
Becker nevus
Asymptomatic, brownish, circumscribed macule or patch that gradually enlarges in an irregular fashion; usually occurs on one shoulder; hypertrichosis may be present
Congenital melanocytic nevus
Flat to mildly palpable, tan-colored lesion present at birth or soon after; tends to become raised and darken over time; hypertrichosis may be present
Melanoma
Malignant tumor that can present as an enlarging, asymmetric, variegated lesion with irregular border
Plexiform neurofibroma
Subcutaneous manifestation of type 1 neurofibromatosis; tender, firm nodules; early lesions may appear as hyperpigmentation and hypertrichosis
does not have hypertrichosis. Melanoma can be diagnosed with a biopsy. Plexiform neurofibromas are a subcutaneous manifestation of type 1 neurofibromatosis.7 They are often present at birth and result from diffuse thickening of nerve trunks.7 Although most are associated with tender, firm nodules, early lesions may appear as hyperpigmentation and hypertrichosis. REFERENCES 1.
Yan AC, Smolinski KN. Melanocytic nevi: challenging clinical situations in pediatric dermatology. Adv Dermatol. 2005;21:65-80.
2.
Kinsler V, Bulstrode N. The role of surgery in the management of congenital melanocytic naevi in children: a perspective from Great Ormond Street Hospital. J Plast Reconstr Aesthet Surg. 2009;62(5):595-601.
3.
McLaughlin MR, O’Connor NR, Ham P. Newborn skin: part II. Birthmarks. Am Fam Physician. 2008;77(1):56-60.
4.
Marghoob AA, Borrego JP, Halpern AC. Congenital melanocytic nevi: treatment modalities and management options. Semin Cutan Med Surg. 2007;26(4):231-240.
5.
Schaffer JV. Pigmented lesions in children: when to worry. Curr Opin Pediatr. 2007;19(4):430-440.
6.
Leung AK, Kong AY. What’s your diagnosis? Hairy hyperpigmented lesion on a teenager’s back. Consultant. 2010;50(9):395-396.
7.
Leung AK, Robson WL. Case in point: a young girl with café au lait spots. Consultant Pediatricians. 2006;5(4): 229-232.
Medilaw
Illegal MTP MC Gupta
Q. A lady doctor and an anesthetist were arrested in connection with an illegal MTP. I have the following questions: a.
surgeon. This was a case of illegal abortion. There is rarely an illegality if pregnancy is upto 12 weeks. One can safely presume that the lady was pregnant upto 20 or even more weeks. The anesthetist has no business giving anesthesia without PAC. PAC includes: talking to the patient, doing necessary clinical examination and, checking the medical record (there can be no medical record in such a case without the mention of LMP and the duration of pregnancy). All these three, within a minute, would have certainly made it clear to any doctor that the pregnancy is between 12 and 20 weeks (when two doctors’ opinion is required) or more than 20 weeks, when abortion is illegal. This does not call for special knowledge of anesthesia or gyne-obs or any other specialty. If he is a party to crime done by another, he cannot escape the clutches of law.
My opinion is that an anesthesiologist is never in a position to check the legality of a surgical procedure. Wherever there is pain, the anesthesiologist is justified in administering anesthesia if asked for. It is neither illegal nor unethical. Am I right?
b. Can the anesthesiologist refuse to anesthetize the patient if the surgery is illegal? c.
Is it a legal binding on the anesthesiologist to report any such incidences to authorities?
d. Do we have right to refuse any case? e.
What help can be given to the concerned anesthetist in this case?
Ans.
It is incorrect that an anesthesiologist is never in a position to check the legality of a surgical procedure. There is something called pre-anesthetic check-up where the anesthetist is required to personally examine the patient, take necessary history, look at the diagnosis and the surgery proposed to be done and any complications that may be likely to occur during the procedure. An anesthetist needs to check the basics about what is to be done by the surgeon. If the left limb is to be amputated and the anesthetist has done a PAC before the surgery and the surgeon amputates the right limb in the presence of the anesthetist and somebody sues the anesthetist for being partly responsible for the mishap, an experienced lawyer may be able to convince the court regarding this. After all, an anesthetist is not a robotic machine simply to give some injections and gases and do intubation etc. with eyes and mind closed to everything else. Even otherwise, if a healthy limb is being amputated (as is sometimes done by child lifters to maim the child and make a beggar out of him), the anesthesiologist is expected to know it is illegal. On similar lines, an anesthetist needs to check the basics about what is to be done by the gyne-obs
Advocate and Medicolegal Consultant New Delhi
There is no question of a responsible anesthetist giving anesthesia for incision and drainage of a small abscess on one’s forearm, even though it may be painful. Every doctor, including an anesthetist, has to use his professional expertise before taking a decision regarding treatment. He gives a medicine not because the patient wants it or demands it but because he needs it. Yes, the anesthesiologist can refuse to anesthetize the patient if the surgery is illegal. In general, every citizen, including an anesthesiologist, is expected to bring the occurrence of a crime to the knowledge of the authorities. Yes, any doctor has a right to take up or not take up a case. A doctor is not bound to treat each and every case that comes to him. He can refuse to give treatment/anesthesia if there are valid grounds. The best help such a person can get is from a lawyer. An expert opinion from a committee of three anesthetists will help. Let the Association of anesthetists appoint such a committee, which should examine the case of the accused who has been arrested. If they come to a conclusion that, as an anesthetist, he has not done anything wrong, then let the Association render an Expert Opinion on its letterhead stating so.
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lighter reading
What really constitutes a good person? This is one of the questions I have in my life that I long to find the answer for. Does being an upright citizen equate to being a good man? Does going to church regularly and paying your colleagues compliments that they are due make you virtuous and moral? Is it enough to do good things for other people to make you an ethical and just human being?
With all the norms that the society we live in sets for being good, sometimes, it’s just too easy to be bad. Whether that takes the form of gossiping about your co-worker, cheating on a test, changing lanes too fast or merely having malicious thoughts of others, I’ve done all sort of things that I can never be proud of, nor justify.
QUOTE
A Good Person
“In matters of style, swim with the current; in matters of principle, stand like a rock. ” —Thomas Jefferson
“Forgiveness is the sweetest revenge. ” —Isaac Friedmann
laugh a while
An Inspirational Story
Lighter Side of Medicine
Doctor: You’re in good health. You’ll live to be 80. Patient: But, doctor, I am 80 right now. Doctor: See, what did I tell you. — Dr GM Singh
ILLUSION
Sometimes, it’s just way too easy to be bad. The idea of being good is occasionally easier said than done. Doing something I already regard as greatly noble may not be good enough to the person sitting next to me. Let’s admit it, we can never please everyone, no matter how we try.
I have stopped resisting my nature, instead, tried to work my way around it. I have come to admit that I am not perfect and I do succumb to temptation sometimes. What matters is the fact that every day, I try to be a better person than I was yesterday. If I fail, I try again. Somebody once said, “I may not be a nice person, but I am a good human being”. Being good is like beauty. It is a biased, prejudiced, over-rated and subjective issue. I’ve learned not to put too much pressure on myself with all the standards that our society has. Instead, I try to simplify them by struggling not to step on anyone’s shoes. Then maybe... just maybe, I can be a good person in the process. —Ms Ritu Sinha
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Dr. Good and Dr. Bad Situation: A patient with Mediclaim wanted angiography.
Get admitted for 24 hours
You can go after six hours
©IJCP Academy
I’ve just recently stopped apologizing for my existence and started to accept and love myself. I have realized that the key to becoming a truly good person is in also accepting the parts of my personality that I am not very proud of.
Lesson: If you can justify that due to technological
advances, hospitalization is required for less than 24 hours, Mediclaim will be applicable. Dr KK Aggarwal
Information for Authors Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96: 766-767). Indian Journal of Clinical Practice strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so. The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklist should accompany each manuscript. Authors may provide on the checklist, the names and addresses of experts from Asia and from other parts of the World who, in the authors’ opinion, are best qualified to review the paper. Covering letter –
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Illustrations must be drawn neatly by an artist and photographs must be sent on glossy paper. No captions should be written directly on the photographs or illustration. Legends to all photographs and illustrations should be typed on a separate sheet of paper. All illustrations and figures must be referred to in the text and abbreviated as “Fig.”.
Please complete the following checklist and attach to the manuscript: 1. Classification (e.g. original article, review, selected
Paintal AS. Impulses in vagal afferent fibres from specific pulmonary deflation receptors. The response of those receptors to phenylguanide, potato S-hydroxytryptamine and their role in respiratory and cardiovascular reflexes. Q. J. Expt. Physiol. 1955;40:89-111.
2. Total number of pages ________________________
Books
5. Special requests _____________________________
Stansfield AG. Lymph Node Biopsy Interpretation Churchill Livingstone, New York 1985.
6. Suggestions for reviewers (name and postal address)
Articles in Books
2.____________
2._ _______________
Strong MS. Recurrent respiratory papillomatosis. In: Scott Brown’s Otolaryngology. Paediatric Otolaryngology Evans JNG (Ed.), Butterworths, London 1987;6:466-470.
3.____________
3._ _______________
4.____________
4._ _______________
Tables –
These should be typed double spaced on separate sheets with the table number (in Roman Arabic numerals) and title above the table and explanatory notes below the table.
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summary, etc.)_______________________________ 3. Number of tables ____________________________ 4. Number of figures ___________________________
Indian 1.____________Foreign 1._ _______________
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Online Submission Also e- Issue @ www.ijcpgroup.com For Editorial Correspondence
Dr KK Aggarwal
Group Editor-in-Chief Indian Journal of Clinical Practice E-219, Greater Kailash, Part-1 New Delhi - 110 048. Tel: 40587513 E-mail: editorial@ijcp.com Website: www.ijcpgroup.com