Internal Medicine

Seroprevalence of Co-infection of Hepatitis B and Hepatitis C Genotypes among Adult Female Population of Karachi, Pakistan

Shazia Tabassum Hakim, Samina Noorali, Meaghen Ashby, Anisah Bagasra, Shahana U. Kazmi and Omar Bagasra

Cite this article as: BJMP 2010;3(3):a335
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Abstract

Background: Both Hepatitis B virus (HBV) and Hepatitis C virus (HCV) are  aetiological agents of acute and chronic liver disease existing throughout the world. The high genetic variability of HBV and HCV genome is reflected by eight genotypes (A to H) and six genotypes (1 to 6), respectively. Each genotype has a characteristic geographical distribution, which is important epidemiologically. Previous studies from the province of Sindh, Pakistan have reported that genotypes D and A as well as D and B are prevalent HBV genotypes, and for HCV genotypes 3a and 3b to be dominant. The aim of this study was to investigate the prevalence of co-infection of both HBV and HCV genotypes in physically healthy females at two universities in Karachi, Sindh, Pakistan and HBV diagnosed patients41,42,56-59.

Methodology: Blood was collected from a total of 4000 healthy female volunteer students and 28 HBV diagnosed patients. Serum samples obtained were screened for Hepatitis B surface antigen (HBsAg), anti-HBs antibodies and anti-HCV antibodies by immunochromatography and ELISA. Genotyping was carried out for 6 HBV genotypes (A through F) and 6 HCV genotypes (1 through 6). Genotyping data of HBV and HCV positive individuals are described.

Results: Out of 4028 volunteers, 172 (4.3%) tested positive for HBsAg. All 172 serum samples were genotyped by PCR for both HBV and HCV. Out of 172 HBsAg positive samples, 89 (51.7%) showed a single HBV genotype D infection, followed by genotypes A (6.4%), F (4.6%), B (3.5%), E (1.7%), and C (1.7%). Out of 43 positive for HCV by PCR from the two universities and Anklesaria Hospital, 65.1% showed infection with 3a, followed by genotypes 5a (11.6%), 6a (11.6%), 3b (9.3%) and 2a (2.3%). Hence, the co-infection rate of both these viruses is 25% (43/172) among HBs Ag positive individuals.

Conclusion: Genotype D for HBV and genotype 3a for HCV appears to be the dominant genotype prevalent in Karachi’s population and co-infection of both these viruses does exist in HBsAg positive individuals.

Keywords:  Hepatitis B virus, Hepatitis C virus, type-specific primer-based genotyping

Introduction:

Both Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) are diseases characterized by a high global prevalence, complex clinical course, and limited effectiveness of currently available antiviral therapy. Approximately 2 billion people worldwide have been infected with the HBV and about 350 million live with chronic infection. An estimated 600,000 persons die each year due to the acute or chronic consequences of HBV 1, 2. WHO also estimates that about 200 million people, or 3% of the world's population, are infected with HCV and 3 to 4 million persons are newly infected each year. This results in 170 million chronic carriers globally at risk of developing liver cirrhosis and/or liver cancer 3, 4. Hence, HBV and HCV infections account for a substantial proportion of liver diseases worldwide.

These viruses have some differences, like HBV belongs to the Hepadnaviridae family and HCV belongs to the Flaviviridae family. HBV has a circular, partially double-stranded DNA genome of approximately 3.2 kb, whereas HCV has a single RNA strand genome of approximately 9.6 kb. HBV and HCV show some common biological features. Both HBV and HCV show a large heterogenicity of their viral genomes producing various genotypes. Based on genomic nucleotide sequence divergence of greater than 8%, HBV has been classified into eight genotypes labeled A through H 5,6,7,8. Different isolates of HCV show substantial nucleotide sequence variation distributed throughout the genome. Regions encoding the envelope proteins are the most variable, whereas the 5’ non-coding region (NCR) is the most conserved 9. Because it is the most conserved with minor heterogeneity, several researchers have considered the 5’ NCR the region of choice for virus detection by reverse transcription (RT)-PCR. Sequence analysis performed on isolates from different geographical areas around the world has revealed the presence of different genotypes, genotypes 1 to 6 10. A typing scheme using restriction fragment length polymorphism analysis of the 5’ NCR was able to differentiate the six major genotypes 11. Hence both HBV and HCV genotypes display significant differences in their global distribution and prevalence, making genotyping a useful method for determining the source of HBV and HCV transmission in an infected localized population 12 - 27.
 
Many studies have been conducted to study the prevalence of HBV and HCV co-infection among HIV-infected individuals and intravenous drug users globally 28 -3 4.There are only a few studies relevant to the epidemiology of these types of infection in the normal healthy population 35,36,37. The objective in this study was to determine the seroprevalence of HBV and HCV, co-infection of both these viruses and their genotypes, among an apparently healthy female population as well as from known HBV patients in Karachi, a major city in the province of Sindh, Pakistan. This study is also aimed at providing the baseline data on HBV/HCV co-infection, in order to gain a better understanding of the public health issues in Pakistan. We evaluated the antigen, antibody and genotypes of both HBV and HCV in 144 otherwise healthy female individuals and 28 diagnosed HBV patients.
 
Materials and Methods:
                                                                                                                
Study duration:From March 2002 to October 2006 & April 2009
Study participants: Total 4000blood serum samples were collected from healthy female student volunteers and 28 serum samples (April 2009) from already diagnosed Hepatitis B positive patients, aged 16 to 65 years from two Karachi universities and one Karachi hospital. University samples were obtained through the Department of Microbiology, University of Karachi and the Department of Microbiology, Jinnah University for Women. Hospital samples were obtained through the Pathological Laboratory of Burgor Anklesaria Nursing Home and Hospital.
Ethical Consent: Signed informed consent forms were collected from all volunteers following Institutional Review Board policies of the respective institutes.
Pre study screening:All 4028 volunteers had health checkups by a medical doctor before collection of specimens, they were asked about their history of jaundice, blood transfusion, sexual contacts, and exposure to needles, and if they had undergone any surgical and dental procedures.
Biochemical & Hematological screening:On completion of the medical checkups, volunteers were asked to give 5mL of blood for different haematological [(complete blood picture (CP), haemoglobin percentage (Hb%) and erythrocyte sedimentation rate (ESR)] and 10mL for different biochemical tests [(direct bilirubin, indirect bilirubin, total bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP)]. Serological analysis:Samples were also subjected to serological analysis for hepatitis B surface Antigen (HBsAg), HBs antibodies and HCV antibodiesusing rapid immunochromatography kits (ICT, Australia and Abbott, USA). Confirmatory test for HBsAg was done by using ELISA (IMX, Abbott, USA).
All the above mentioned preliminary tests were conducted at the respective institutes in Karachi. Out of 4000 female volunteer from the two universities, 144 otherwise healthy females tested positive for HBsAg. 2 out of the 144 HBsAg positive females were also found to be positive for anti-HCV antibodies. The other 28 positive HBV patients from Anklesaria Hospital were only tested for HBsAg and all 28 were positive for HBsAg. Hence, a total of 172 HBV positive samples (144 + 28 = 172) including the 39 HCV positive serum samples obtained from Karachi were used for genotypic evaluation at Claflin University, South Carolina, USA. Specific ethnicity was not determined but we assume these study participants represent a collection of different ethnic groups in Pakistan.
DNA/RNA extraction and amplification of 172 HBV positive samples: DNA was extracted for HBV, and RNA was extracted for HCV analysis from 200μL of all 172 positive HBV serum samples using PureLink™ Viral RNA/DNA Mini Kit according to manufacturer’s instructions (Invitrogen, CA). Amplification was carried out using puReTaq Ready –To-Go PCR Beads (Amersham Biosciences, UK).
Determination of HBV and HCV genotypes by nested PCR: The primer sets for first-round PCR and second-round PCR, PCR amplification protocol, and primers for both HBV and HCV genomes and genotyping amplification for all 172 samples followed previously reported methods [45, 46]. First round amplification targeted 1063bp for the HBV genome and 470bp for the HCV genome. These respective PCR products for both HBV and HCV were used as a template for genotyping different HBV genotypes A to F and HCV genotypes from 1 to 6. HBV A through HBV F genotypes and HCV 1 through 6 genotypes for each sample were determined by separating the genotype-specific DNA bands on 2% agarose gels, stained with ethidium bromide. The sizes of PCR products were estimated according to the migration pattern of a 50bp DNA ladder (Promega, WI).
 
Results:
 
Before screening for HBV status, all 4000 healthy female volunteers from the Department of Microbiology, University of Karachi, and the Department of Microbiology, Jinnah University for Women were subjected to routine physical checkups for exclusion criteria i.e., either they were apparently unhealthy or malnourished (23 volunteers were excluded). All 4000 serum samples were screened by immunochromatography for the presence of HBsAg, anti HBs antibodies and anti-HCV antibodies. Positive results were confirmed by ELISA. Out of 4000 subjects 144 (3.6%) tested positive for HB surface antigen (HBsAg), 2 (0.05%) were positive for anti-HCV antibodies, and 3856 (96.4%) were negative for HBsAg and 3998 (99.95%) were negative for HCV antibodies by both immunochromatography and ELISA. Out of these 144 individuals who tested positive for HBsAg, 20 (13.8%) were positive for anti-HB surface antibodies and 2 (1.4%) tested positive for anti-HCV antibodies. The rest of the 28 serum samples obtained from already diagnosed HBV positive samples from Anklesaria Hospital were only tested for HBsAg and were all positive for HBsAg.
 
The haematological parameters: WBC count, RBC count, hematocrit and platelet count of the 172 HBsAg positive individuals were within the normal recommended range of values, while mean Hb% was 9.8±1.6 g/dL. Direct bilirubin (0 to 0.3 mg/dL), indirect bilirubin (0.1 - 1.0 mg/dL), total serum bilirubin (0.3 to 1.9 mg/dL), ALT (0 - 36 U/L), AST (0 - 31 U/L) and alkaline phosphatase (20 - 125 U/L) were also within the normal range for 129 HBsAg positive individuals, except for the raised ALT (>36 U/L) and AST (>31 U/L) levels in 38 participants with a previous history of jaundice who were also positive for HBsAg.
 
All 172 samples that were positive for HBsAg were confirmed for the presence of different HBV genotypes as well as for different HCV genotypes by PCR to see the co-infection of both these viruses. Genotyping was carried out at the South Carolina Center for Biotechology, Department of Biology, Claflin University, Orangeburg, SC, U.S.A. For HBV: Mix A primers were targeted to amplify genotypes A, B and C, and primers for Mix B were targeted to amplify genotypes D, E and F. For HCV: primers for Mix A were targeted to amplify genotypes 1a, 1b, 1c, 3a, 3c and 4. Primers of Mix B for HCV were targeted to amplify genotypes 2a, 2b, 2c, 3b, 5a, and 6a.
 
Table 1. Prevalence of both single and co-infection of HBV genotypes among the apparently healthy female student sample and known HBV positive patients from Anklesaria hospital in Karachi.
2 Universities Samples Percentage
Total HBV 144  
Genotype D 70 48.6%
Genotype A 8 5.5%
Genotype F 7 4.9%
Genotype B 5 3.5%
Genotype E 3 2.1%
Genotype C 2 1.4%
Co-infections of HBV Genotypes 49/144 34%
Genotype B/D 30/144 20.8%
Genotype A/D 11/144 7.6%
Genotype A/D 4/144 2.8%
Genotype B/C 4/144 2.8%
Anklesaria Hospital Samples Percentage
Total HBV 28  
Genotype D 19 67.9%
Genotype A 3 10.7%
Genotype B 1 3.6%
Genotype C 1 3.6%
Genotype F 1 3.6%
Co-infections of HBV Genotypes    
Genotype B/A 3/28 10.7%
 
Figure 1: Electrophoresis patterns of PCR products from different HBV genotypes as determined by PCR genotyping system. Genotype A: 68bp, genotype B: 281bp, genotype C: 122bp, genotype D: 119bp, genotype E: 167bp and genotype F: 97bp. 
 
Table 1 illustrates the prevalence of both single and co-infection of HBV genotypes from both the universities in Karachi and Anklesaria hospital. Representative 10 samples in Fig. 1 show single and co-infections for HBV.
Besides looking at the HBV genotypic status of these 172 patients by PCR, we also looked at the HCV genotypic status of the positive HBV patients by PCR so as to see if there was existence of co-infection of the two viruses i.e. HBV and HCV in the same individuals as only 2 samples tested positive for anti-HCV antibodies by rapid immunochromatography. Table 2 shows the prevalence of HCV genotypes among the apparently healthy female student population from the 2 universities in Karachi and known HBV individuals samples obtained from Anklesaria hospital. Fig. 2 shows different HCV genotype infection in the 10 representative samples shown in Fig. 1 showing HBV infection with different genotypes.
 
Table 2. Prevalence of HCV genotypes among the apparently healthy female student sample, and known HBV individuals from Anklesaria hospital in Karachi.
2 Universities Samples Percentage
Total HCV/Total HBV 39/144 27.1%
Genotype 3a 26/39 66.6%
Genotype 6a 5/39 12.8%
Genotype 3b 4/39 10.3%
Genotype 5a 4/39 10.3%
Anklesaria Hospital Samples Percentage
Total HCV/HBV 4/28 14.3%
Genotype 3a 2/28 7.14%
Genotype 2a 1/28 3.6%
Genotype 5a 1/28 3.6%
 
Figure 2: The sizes of the genotype-specific bands for HCV amplified by PCR genotyping method are as follows: genotype 2a, 190 bp; genotype 3a, 258 bp; genotype 3b, 232 bp; genotype 5a, 417 bp; and genotype 6a, 300 bp. 
 
To summarize the results it was found that out of 172 HBsAg positive samples from the two universities (144 HBV samples) and Anklesaria Hospital (28 HBV samples), 89 (51.7%) were genotype D, 11 were genotype A (6.4%), 8 were genotype F (4.6%), 6 were genotype B (3.5%), 3 were genotype E (1.7%), and 3 were genotype C (1.7%). Out of 43 positive for HCV by PCR from the two universities (39/144 HBV samples) and Anklesaria Hospital (4/28 HBV samples), 65.1% (28/43) showed infection with 3a, followed by genotypes 5a (5/43 = 11.6%), 6a (5/43 = 11.6%), 3b (4/43 = 9.3%) and 2a (1/43 = 2.3%).
 
Discussion:
 
Viral hepatitis due to HBV and HCV has significant morbidity and mortality worldwide. The global prevalence of HCV is 3% 38 and the carrier rate of HBsAg varies from 0.1% to 0.2% in Britain and the USA, to 3% in Greece and southern Italy and up to 15% in Africa and the Asia 39. Pakistan is highly endemic with HBV. Studies are too limited to give a clear picture of the prevalence of HBV at the national level, especially among apparently healthy individuals. Most previous studies targeted different small groups of individuals with some clinical indications, so they do not accurately reflect the overall prevalence in Pakistan40. Our previous study was conducted on a first group of 4000 healthy female students from the two universities i.e., Department of Microbiology, University of Karachi and Department of Microbiology, Jinnah University for Women for the prevalence of HBV. We have reported earlier that genotype D appears to be the dominant genotype prevalent in Karachi, Pakistan’s apparently healthy female population, and genotype B appears to be the next most prevalent genotype 41, 42. In this study we checked the prevalence of both HBV and HCV in a second group of 4000 healthy female students from the same two universities in Karachi mentioned above, as well as the already 28 diagnosed HBV patients from Anklesaria Hospital in Karachi, Pakistan.
 
Both HBV and HCV are present in the Pakistani population and there are varying reports of disease prevalence. HCV is one of the silent killer infections spreading undetected in Pakistan because there are often no clinical symptoms and, when HCV is diagnosed, considerable damage has already been done to the patient. In Pakistan alone, the prevalence of HBsAg has been reported to be from 0.99% to 10% in different groups of individuals 43 - 52 and 2.2% to 14% for HCV antibodies 53 - 56. A recent study conducted in Pakistan showed that out of 5707 young men tested, 95 (1.70%) were positive for anti-HCV and 167 (2.93%) for HBsAg 57. Our previous study showed the prevalence of HBsAg among young otherwise healthy women to be 4.5% 41,42. Our present study shows that the prevalence of HBsAg in otherwise young healthy women to be 3.6%, with 0.98% testing positive for anti-HCV antibodies. On the basis of other studies conducted in different provinces of Pakistan, we can say that there is a variation in the prevalence of HBsAg and HCV antibodies in the Pakistani population as the population sample selected is limited to a particular area or segment of the provinces. 
 
HBV and HCV genotyping is important to track the route and pathogenesis of the virus. In particular, the variants may differ in their patterns of serologic reactivity, pathogenecity, virulence, and response to therapy. Both HBV and HCV has genetic variations which correspond to the geographic distribution and has been classified into 8 genotypes (A to H) on the basis of whole genome sequence diversity of greater than 8% and 6 genotypes (1 to 6) using restriction fragment length polymorphism analysis of the 5’ non-coding region (NCR), respectively .
 
In this study genotyping was carried out for 6 HBV genotypes (A through F) and 6 HCV genotypes (1 through 6). This study suggests that the HBV D genotype is the most prevalent (114/144 = 79.2%) among otherwise healthy females alone or in co-infection with other HBV genotypes in Karachi, Sindh, Pakistan. In our previous study HBV D genotype was found to be ubiquitous (100%) among otherwise healthy females alone or in co-infection with other HBV genotypes in Karachi followed by genotype B 41,42. The earlier two studies conducted for prevalence of HBV genotypes in known hepatitis B positive patients in Pakistan report the prevalence of genotypes HBV A (68%) and HBV D (100%) in the province of Sindh 58,59. Interestingly, in this study we also found the HBV D genotype to be the prevalent genotype but it was followed by genotypes HBV A (5.5%) and HBV F (4.9%). The prevalence of genotype HBV B in this study was found to be 3.5% as our earlier study has shown the prevalence of genotype B in otherwise healthy females to be 16.1% 60. These findings respectively contradict and corroborate the previous studies for HBV genotype distributions reported here as the subjects in this study were also asymptomatic but comprised of second group of female volunteer students at the two universities. Out of 144 subjects positive for HBsAg, 10 reported a previous history of jaundice and the rest were not aware of their HBV status. In the nearby north Indian population, HBV D was reported as the predominant genotype (75%) in patients diagnosed with chronic liver disease (CLDB) 60. In this study we also found other HBV genotypes existed in the study population such as HBV genotype F (4.9%) followed by genotype E (2.1%), and genotype C (1.4%). We also saw mixed HBV infections of genotypes B and D, A and D, C and D as well as B and C (20.8%, 7.6%, 2.8% and 2.8%) among these otherwise healthy females. 
 
Among the 28 diagnosed HBV patients from Anklesaria Hospital, 67.9% showed HBV genotype D infection followed by genotype A infection (10.7%). In this group of 28 HBV positive patients we also saw infections with genotypes B (3.6%), C (3.6%) and F (3.6%). This group exhibited 10.7% co-infection with genotypes B and A.
As far as the HCV status of these 144 otherwise healthy females who were HBV positive is concerned only 2 (1.4%) tested positive for HCV antibodies by rapid immunochromatography. But the PCR results showed 39 (27.15%) of these 144 otherwise healthy females that were HBV positive for different genotypes were also positive for HCV including the 2 otherwise healthy females that tested positive for HCV antibodies by rapid immunochromatography. Of the 39 HCV positive otherwise healthy females, we found the predominant HCV genotype to be 3a (66.6%) followed by genotypes 6a (12.8%), 3b (10.3%), and 5a (10.3%) infections. The earlier study conducted with samples from women at the two universities in Pakistan had shown that among the HCV positive apparently healthy females 51.44% were genotype 3a, 24.03% exhibited a mix of genotype 3a and 3b, 15.86% were genotype 3b, and 4.80% were genotype 1b 42. Interestingly, among the group of 28 diagnosed HBV patients, the prevalence of HCV 3a genotype infection was dominant but was 7.1% much lower than that found in the otherwise healthy females, followed by infections with genotypes 2a (3.6%) and 5a (3.6%). Hence we see there is 25% co-infection of both these viruses i.e., HBV and HCV among the HBsAg positive individuals. The sample of 28 HBV positive patients was from a hospital located in the center of the metropolis that represents an area of Karachi where sanitation, malnourishment, illiteracy, and lack of awareness is very common. Prostitution can also be considered as one factor in some of the localities of Karachi in the spread of both HBV and HCV.
 
Conclusion:
 
In conclusion, genotype D appears to be the dominant HBV genotype and genotype 3a for HCV appears to be prevalent in Sindh, Pakistan’s otherwise healthy young female population as well as in HBV diagnosed individuals. Co-infection of both the viruses i.e., HBV and HCV exists among HBsAg positive individuals. The young female participants were advised to seek appropriate medical care for both their own benefit and public health benefit.
 

Acknowledgements
This work was partially supported from the grants: P2RR16461 (EXPORT): NIH, INBRE and EPS-044760: NSF EPSCoR.
Competing Interests
None declared
Author Details
SHAZIA TABASSUM HAKIM, SAMINA NOORALI, MEAGHEN ASHBY, OMAR BAGASRA: South Carolina Center for Biotechnology, Department of Biology, Claflin University, 400 Magnolia Street, Orangeburg, South Carolina 29115, U.S.A. ANISAH BAGASRA, Department of History and sociology, Claflin University, 400 Magnolia Street, Orangeburg, South Carolina 29115, U.S.A. SHAHANA U KAZMI, I.I.D.R.Lab., Department of Microbiology, University of Karachi, Karachi-75270, Pakistan
CORRESSPONDENCE: Dr. Shazia Tabassum Hakim, Associate Professor & Chairperson, Virology & Tissue Culture Laboratory, Department of Microbiology, Jinnah University for Women, Nazimabad, Karachi-74600, Pakistan
Email: Shaz2971@yahoo.com

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Elevated pancreatic enzymes within the content of liver abscess in a patient with a history of chronic pancreatitis.

Muhammad Z Bawany and Thomas Sodeman

Cite this article as: BJMP 2010;3(3):a331
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INTRODUCTION:

Liver abscess accounts for 48% of visceral abscesses 1 and presents with significant morbidity and mortality. The overall incidence of pyogenic liver abscess is 3.6 per 100,000 populations, 2 however; elevated pancreatic enzymes within the content of a liver abscess have never been reported in the literature.

CASE REPORT:
 
A 36-year-old African American male with a history of chronic pancreatitis presented to the emergency department for abdominal pain in the epigastric area along with nausea, vomiting, diarrhoea, fever. His symptoms began 3-4 days before presentation. The abdominal pain was dull in nature and 6/10 in intensity, non-radiating. His past medical history was significant for HTN, diabetes mellitus and chronic diarrhoea secondary to chronic pancreatitis.
On admission the patient was alert and oriented, blood pressure was 97/44 mm Hg, heart rate 16 beats per minute, respiration 16 per minute, oxygen saturation 94% on room air and temperature 102*F. Abdominal examination revealed hyperactive bowel sounds and tenderness in the epigastrium & RUQ. Liver span was 14 cm. The rest of the examination was unremarkable.
Laboratory work revealed: Haemoglobin 9.8 g/dl, WBC 22.1 Thou/mm3 with segmented neutrophils of 81% and 9% bands, BUN 54 mg/dl, Cr 4.7 mg/dl, total protein 10.4 g/dl, albumin 1.8 g/dl, total bilirubin 1.1 mg/dl, direct bilirubin 0.3 mg/dl, AST 98 IU/L, ALT 38 IU/L, alkaline phosphatase 250 IU/L, amylase 81 units/L, lipase 10 units/L, lactate 2.3 mmol/L and INR 1.39.
 
The patient was started on fluids and meropenem for broad spectrum coverage. However his condition worsened and he developed acute respiratory distress syndrome secondary to sepsis necessitating intubation. Due to his abdominal pain he underwent a computer tomography (CT) scan of the abdomen, which revealed pancreatic calcifications and multiple liver abscesses; the largest measuring 7.5cm in the right lobe of the liver (Figure 1). 
 
Figure 1
 
As the patient’s condition did not improve, he underwent liver abscess drainage. Fluid analysis showed ph 4.0, LDH 39 units/L, glucose 81 mg/dl, protein 1.6 g/dl, lipase of 16 units/L and amylase 68 units/L. The presence of amylase and lipase in the liver abscess without any evidence of a fistula between liver and pancreas on CT scan was unexpected, therefore it was decided to leave the catheter in situ for continuous drainage. 3 Even though his blood and fluid cultures remained negative during the hospital stay he was continued on antibiotics, which may have meant that the initial antibiotic therapy rendered the blood cultures negative. The success of management was assessed with a hepatic CT 10 days post drainage and was demonstrated by the observation of improvement in the patient’s general condition, as indicated by normal temperature, decreased draining catheter output and the resolution of deranged laboratory values. The catheter was then removed and the patient was discharged.
 
DISCUSSION:
 
Liver abscesses develop via seeding through portal circulation, directly via spread from biliary infections or from surgical or penetrating wounds and also from systemic organs via haematogenous spread. In our case the most reasonable explanation was through the involvement of portal circulation due to recurrent pancreatitis.
The morbidity and mortality rate for liver abscesses ranges from 2 – 12 % depending on the severity of underlying co-morbidities. 2 The clinical manifestations, as in our case, are characterized by abdominal pain (50-75%), 4, 5 fever (90%), nausea and vomiting. Other symptoms may include weight loss, malaise and diarrhoea. On physical exam RUQ tenderness, guarding, rebound tenderness, hepatomegaly and occasional jaundice can be appreciated. The diagnosis of a liver abscess can be made by radiographic imaging followed by aspiration and culture of the abscess material. Liver abscesses can be either polymicrobial or monomicrobial, unlike in the case with our patient, whose abscess was sterile. Depending on the microbial results additional sources of infection should be evaluated. Drainage of abscesses can be percutaneous 6 or open surgical. Percutaneous drainage with coverage of antibiotics was successful in our patient. 
 
CONCLUSION:
 
In summary, we present a case of pancreato-liver abscess in a patient with a history of chronic calcified pancreatitis. It was treated with antibiotics and percutaneous drainage, with satisfactory resolution. To our knowledge this has never been reported in the literature and more work needs to be done to understand the pathophysiology of elevated pancreatic enzymes in the context of a liver abscess in a patient with a history of chronic pancreatitis.

Competing Interests
None declared
Author Details
MUHAMMAD Z BAWANY M.D. Department of Internal Medicine University of Toledo Medical Center Ohio USA THOMAS SODEMAN M.D. FACP, Department of Internal Medicine University of Toledo Medical Center Ohio USA
CORRESSPONDENCE: Muhammad Z Bawany M.D. 3000 Arlington Ave, Mail Stop 1150, Toledo OH USA 43614
Email: Muhammad.Bawany@utoledo.edu

References

1. Altemeier WA, Culbertson WR, Fullen WD, et al Intra-abdominal abscesses. Am J Surg 1973;125:70-79. 
2. Meddings L, Myers RP, Hubbard J, et al. A population-based study of pyogenic liver abscesses in the United States: incidence, mortality, and temporal trends. Am J Gastroenterol;105:117-124.
3. Rajak CL, Gupta S, Jain S, et al. Percutaneous treatment of liver abscesses: needle aspiration versus catheter drainage. AJR Am J Roentgenol 1998;170:1035-1039
4. Rahimian J, Wilson T, Oram V, et al. Pyogenic liver abscess: recent trends in etiology and mortality. Clin Infect Dis 2004;39:1654-1659.
5. Mohsen AH, Green ST, Read RC, et al. Liver abscess in adults: ten years experience in a UK centre. QJM 2002;95:797-02.
6. Zerem E, Hadzic A. Sonographically guided percutaneous catheter drainage versus needle aspiration in the management of pyogenic liver abscess. AJR Am J Roentgenol 2007;189:W138-142.

 


Coronary vasospasm in a patient with respiratory failure: A case report and a brief review.

Mujeeb Sheikh, Satjit Adlakha, Steven Bruhl and Shaffi Kanjwal

Cite this article as: BJMP 2010;3(3):a330
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Abstract

Coronary vasospasm is an episodic, augmented, contractile response of coronary smooth muscles to variety of stimuli in the setting of established endothelial dysfunction. Various physiological including cold, stress and pathological factors like smoking, and ethanol have been well known to precipitate vasospasm. Despite these omnipresent factors, coronary vasospasm has become infrequent, in particular due to judicious use of medication including calcium channel blockers, statins and aspirin. We present a case of severe coronary vasospasm resulting in haemodynamic instability, in a patient with hypoxic respiratory failure. Recurrent symptomatic episodes required coronary angiography for the diagnosis and patient was successfully treated with calcium channel blockers.

Keywords:  Myocardial infarction; respiratory failure; coronary vasospasm; Diltiazem

Introduction                                                                                                                              

Myocardial ischemia from coronary artery vasospasm can lead to variety of presentation including stable angina, unstable angina, myocardial infarction and sudden death 1. Although, pathognomic clinical scenario includes symptom of chest pain, transient ST-segment elevation on the electrocardiogram(ECG), and vasospasm on a coronary angiography, atypical presentations have also been reported 2. Various known physiological factors including stress, cold, hyperventilation and pharmacological agents including cocaine, ethanol, 5-Fluouracil, and triptans can precipitate a vasospastic attack. 3-7.We report a case of ST-segment elevation due to right coronary artery vasospasm, in patient with hypoxic respiratory failure, and successful treatment with calcium channel blockers.

 
Case description
 
A 56 year old man was admitted for the repair of a large ventral incisional hernia. The patient had a prior history of morbid obesity, chronic obstructive pulmonary disease (COPD), hypertension and cigarette smoking. The postoperative course was complicated by bilateral pneumonia leading to respiratory failure requiring mechanical ventilation. An electrocardiogram at the time of intubation was essentially normal. Aside from bilateral rhonchi and crackles on lung auscultation, the rest of the physical examination findings were unremarkable. Arterial blood gases at the time of intubation demonstrated PH 7.33, PO2 58 mmHg, PCO2 65 mmHg, HCO3ˉ 20 mmol/L, suggestive of hypoxia and concomitant respiratory acidosis. Baseline laboratory studies including cardiac enzymes were within normal limits. The patient was treated with intravenous vancomycin for methicillin-resistant staphylococcus pneumonia. On postoperative day 4, the patient had recurrent episodes of transient ST-elevation on a bedside monitor (Fig.1).
Figure 1
 
These episodes lasted for 3-5 minutes and were associated with significant bradycardia and hypotension. In view of recurrent episodes, haemodynamic instability, and underlying risk factors of coronary artery disease, cardiac catheterization was performed. Coronary angiography revealed a 90% stenosis with haziness of the mid-right coronary artery without any other significant epicardial disease. An intravascular ultrasound (IVUS) was performed and was followed by administration of 100 mcg of intracoronary nitroglycerin; the lesion was reduced to almost 20%. (Fig.2).
Figure 2
 
The diagnosis of prinzmetals angina was made, based on clinical course and angiographic results and prompt therapy with diltiazem (120 mg per day) was initiated. The patient had no further recurrences of similar episodes during the hospitalization and on follow up at 3 months.
 
Discussion
 
The prevalence of vasospasm has been reported to be higher in Japanese and Korean population as compared to the western population. A recent multi-institute survey in Japan documented spasm in 921 (40.9%) of the 2251 consecutive patients who underwent angiography for angina pectoris 8. In contrast to the traditional risk factors for atherosclerotic coronary artery disease, the incidence of smoking, age and dyslipdaemia has been reported higher in patients with coronary vasospasm 9. Endothelial dysfunction is now considered to the major inciting factor in the pathogenesis of the vasospasm 10. Vasospastic angina (VA) with normal coronary arteries on the angiography, impaired endothelial-dependent and endothelial-independent vasodilatation has been frequently observed in these patients. Vascular tone is normally regulated by production of vasodilator factors like nitrous oxide (NO), prostacyclin and vasoconstricting agents like endthelin-1. In the presence of dysfunctional endothelium the agents that normally cause vasodilatation lead to paradoxical vasoconstriction, due to direct muscle stimulation, like acetylcholine.
Stress, whether physical or mental stress has been shown to induce coronary vasospasm and myocardial ischemia. In a study by Kim et al, coronary spastic angina was diagnosed in 292 patients out of 672 coronary spasm provocation tests. Among 292 patients, 21 (7.2%) had myocardial infarction and 14 out of these 21 had experienced severe emotional stress before the event 11. Recently, animal studies have also shown that high circulatory level of stress hormones (cortisol) exaggerate coronary vasoconstriction through Rho-Kinase activation 12. Hypoxia has been seen in animal models to predispose to vasospasm through superoxide formation, which leads to loss of vasodilator function of NO.(13)
 
The ECG changes that occur during attack include ST-segment elevation, and or peaking of T wave from total or subtotal coronary occlusion 1. In some cases spasm can involve more than one artery leading to ST-segment elevation in multiple leads, which may predispose to ventricular tachycardia or fibrillation 14. Coronary spasm is diagnosed by angiography, and spasm can occur at the site of atherosclerotic plaque or in normal segment of the coronary artery. In patients with equivocal diagnosis, provocative tests including administration of acetylcholine, hyperventilation to induce spasm may be required for the diagnosis.
 
Current first line therapy involves used of calcium channel blockers (CCB) alone or in combination with long acting nitrates. In a study comparing the effect of long acting nitrates (Isosorbide dinitrate 40mg/day) versus calcium channel blockers (amlodipine 5mg/day or long acting nifedipine 20mg/day) on coronary endothelium and vasoconstriction between patients with normal or minimally diseased coronary artery, treatment with long acting nitrates was associated with less favourable effects on coronary endothelial functions 15. Sudden withdrawal of CCB in patients with known vasospasm can lead to rebound of symptoms and may prove dangerous. In patients with refractory symptoms alpha-blockers, nicorandil have been used. Although beta blockers are believed to enhance vasospasm, Betaxalol, a selective beta-1 blocker, has been found to be effective in the treatment of variant angina due to its vasorelaxing effects 16. In addition, elimination of or control of all other risk factors or precipitants is very important for successful treatment. In drug refractory cases the percutaneous coronary intervention or coronary artery bypass graft has been performed for the ischemia relief 17.
 
Our patient had multiple precipitating factors for vasospasm. Endothelial dysfunction from severe physical illness and sepsis could have precipitated the VA. Furthermore, hypoxia from respiratory failure could have also been an inciting agent and cannot be ruled out. It is worth mentioning that intensive care unit patients frequently have coexistence of both the underlying risk factors and the precipitating factors for vasospasm, yet VA as a clinical syndrome is uncommonly seen or reported.
 
Conclusion:
 
The clinician needs to be aware of coronary artery vasospasm as it can pose a serious medical threat. Early diagnosis and treatment may result in improved outcomes from vasospastic angina.

Competing Interests
None Declared
Author Details
MUJEEB SHEIKH MD Assistant Professor, Department of Internal Medicine, 3000, Arlington Avenue, University of Toledo Medical Center, Toledo, Ohio SATJIT ADLAKHA, D.O Cardiology fellow 3000, Arlington Avenue, University of Toledo Medical Center, Ohio, USA STEVEN BRUHL M.D Cardiology fellow 3000, Arlington Avenue, University of Toledo Medical Center, Ohio, USA SHAFFI KANJWAL M.D, 3000, Arlington Avenue Department of Pulmonary and Critical Care, University of Toledo Medical Center, Toledo, Ohio, USA
CORRESSPONDENCE: Mujeeb Sheikh, Assistant Professor, Department of Internal Medicine 3000, Arlington Avenue, University of Toledo Medical Center, Toledo, Ohio.
Email: skmujiba@yahoo.co.in

References

1. Nakamura M, Takeshita A, Nose Y. Clinical characteristics associated with myocardial infarction, arrhythmias, and sudden death in patients with vasospastic angina. Circulation. 1987 Jun;75(6):1110-6.

2. Xiang DC, He JX, Hong CJ, Qiu J, Ma J, Gong ZH, et al. [Clinical features of patients with atypical coronary artery spasm]. Zhonghua Xin Xue Guan Bing Za Zhi. 2006 Mar;34(3):227-30.

3. Keller KB, Lemberg L. The cocaine-abused heart. Am J Crit Care. 2003 Nov;12(6):562-6.
4. Ando H, Abe H, Hisanou R. Ethanol-induced myocardial ischemia: close relation between blood acetaldehyde level and myocardial ischemia. Clin Cardiol. 1993 May;16(5):443-6.
5. Bathina JD, Yusuf SW. 5-Fluorouracil-induced coronary vasospasm. J Cardiovasc Med (Hagerstown). 2009 Jun 25.
6. Shimizu M, Hata K, Takaoka H, Kanazawa K, Shinke T, Matsumoto H, et al. Sumatriptan provokes coronary artery spasm in patients with variant angina: possible involvement of serotonin 1B receptor. Int J Cardiol. 2007 Jan 8;114(2):188-94.
7. Teragawa H, Kato M, Yamagata T, Matsuura H, Kajiyama G. The preventive effect of magnesium on coronary spasm in patients with vasospastic angina. Chest. 2000 Dec;118(6):1690-5.
8. Yasue H, Sasayama S, kikuchi K, Okumura K, Matsubara T, Miwa K. The study on the role of coronary spasm in ischemic heart disease. Osaka:National Cardiovascular Center; 2000; Osaka:National Cardiovascular Center. Osaka: Annual report of the research on cardiovascular diseases; 2000. p. 96-7.
9. Sugiishi M, Takatsu F. Cigarette smoking is a major risk factor for coronary spasm. Circulation. 1993 Jan;87(1):76-9.
10. Yasue H, Nakagawa H, Itoh T, Harada E, Mizuno Y. Coronary artery spasm--clinical features, diagnosis, pathogenesis, and treatment. J Cardiol. 2008 Feb;51(1):2-17.
11. Kim PJ, Seung KB, Kim DB, Her SH, Shin DI, Jang SW, et al. Clinical and angiographic characteristics of acute myocardial infarction caused by vasospastic angina without organic coronary heart disease. Circ J. 2007 Sep;71(9):1383-6.
12. Hizume T, Morikawa K, Takaki A, Abe K, Sunagawa K, Amano M, et al. Sustained elevation of serum cortisol level causes sensitization of coronary vasoconstricting responses in pigs in vivo: a possible link between stress and coronary vasospasm. Circ Res. 2006 Sep 29;99(7):767-75.
13. Zou MH, Bachschmid M. Hypoxia-reoxygenation triggers coronary vasospasm in isolated bovine coronary arteries via tyrosine nitration of prostacyclin synthase. J Exp Med. 1999 Jul 5;190(1):135-9.
14. Nishizaki M, Arita M, Sakurada H, Suzuki M, Ashikaga T, Yamawake N, et al. Polymorphic ventricular tachycardia in patients with vasospastic angina--clinical and electrocardiographic characteristics and long-term outcome. Jpn Circ J. 2001 Jun;65(6):519-25.
15. Ninomiya Y, Hamasaki S, Saihara K, Ishida S, Kataoka T, Ogawa M, et al. Comparison of effect between nitrates and calcium channel antagonist on vascular function in patients with normal or mildly diseased coronary arteries. Heart Vessels. 2008 Mar;23(2):83-90.
16. Suzuki J, Watanabe K, Tsuruoka T, Sueda S, Funada J, Kitakaze M, et al. Beneficial effects of betaxolol, a selective antagonist of beta-1 adrenoceptors, on exercise-induced myocardial ischemia in patients with coronary vasospasm. Int J Cardiol. 2003 Oct;91(2-3):227-32.
17. Sugimoto A, Morino Y, Ikari Y. Stent implantation for diffuse and multiple coronary spasm in a patient with variant angina refractory to optimal medical therapy. J Invasive Cardiol. 2007 Nov;19(11):E320-3.


Coronary Artery Disease in Africa: Community based study of Risk Factors

R.K.Pal and Ali Grera

Cite this article as: BJMP 2010;3(2):326
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Abstract

According to estimates of the World Health Organization (WHO), in 2005, out of 58 million total deaths in the world due to different causes 30 percent (17.4 million) were due to cardio vascular diseases, mainly heart disease and stroke. 53 percent of global deaths due to coronary heart disease occurred in males and 47 percent in women. The common modifiable risk factors identified were unhealthy diet, physical inactivity and tobacco use, leading to raised blood pressure and blood glucose, abnormal blood lipids and becoming overweight.1 The WHO MONICA Project - an international collaboration of researchers from 21 countries, studied more than 30 populations, mainly from Europe, over a period of ten years, from the mid-1980s to the mid 1990s. More than seven million men and women aged between 35 and 64 years of age were monitored to examine if and how certain coronary risk factors and new treatments for heart disease contribute to the decline or increase of heart disease rates in these communities. 2

Hence it has been observed that there have been number of studies on risk factors in patients of Coronary Artery Disease (CAD) but comparatively few studies are available on risk factors in healthy community members in Africa and still fewer on comparison of risk factors for CAD in the patients and community members from the same population. The present study was conducted on 528 community members in Tripoli the capital of Libya including 70 individuals having a history of suffering from Myocardial infarction (MI). The comparison of both the groups of same community revealed that hypertension followed by smoking, diabetes and increased body mass index were more prevalent in the community members with history of MI. It was alarming to note that these risk factors earlier thought to be more frequent after the age of 50 years are now present in higher numbers in the younger age groups of 35 to 54 and 15 to 34 years as well. As most of the risk factors stated above are modifiable there seems to be urgent need of initiating a National Health Programme on prevention and control of these risk factors. The priorities and strategy of such a National Programme has also been suggested in brief for consideration of the national decision makers. 

Keywords:  Coronary Artery Disease, Coronary Heart Disease, Risk factors

Introduction

As highlighted in the World Health Report 2002, just a few Non Communicable Disease (NCD) risk factors, account for the majority of non communicable disease burden. These risk factors; tobacco use, alcohol consumption, raised blood pressure, raised lipid levels, increased BMI, low fruit/vegetable intake, physical inactivity, and diabetes, are the focus of the STEPs approach to NCD risk factor surveillance. 3

 A tool for surveillance of risk factors, WHO STEPS, has been developed to help low and middle income countries get started. It is based on collection ofstandardised data from representative populations of specified sample size to ensure comparability over time and across locations. Step one gathers information on risk factors that can be obtained from the general population by questionnaire. This includes information on socio-demographic features, tobacco use, alcohol consumption, physical inactivity, and fruit/vegetable intake. Step two includes objective data by simple physical measurements needed to examine risk factors that are physiologic attributes of the human body. These are height, weight, and waist circumference (for obesity) and blood pressure. Step three carries the objective measurements of physiologic attributes one step further with the inclusion of blood samples for measuring lipid and glucose levels.4 The risk factors studied by MONICA project of the World Health Organization (WHO), included cigarette smoking, blood pressure, blood cholesterol and body weight.5In many resource-poor settings, laboratory access can be difficultand expensive.  A screening algorithm that includesgender, age, cardiovascular disease history, blood pressure,weight and height, and a urine dipstick test for glucose andprotein is likely to be more practical and may well providemuch of the predictive value of more complex blood-based assessments.6In addition, such algorithms should, wherever possible, useregional data on morbidity and mortality, because backgroundrates vary considerably between regions.WHO/ISH (World Health Organization/International Society of hypertension) risk prediction charts provide approximate estimates of cardiovascular disease (CVD) risk in people who do not have established coronary heart disease, stroke or other atherosclerotic disease. They are useful as tools to help identify those at high cardio vascular risk, and to motivate patients, particularly to change behavior and, when appropriate, to take antihypertensive, lipid-lowering drugs and aspirin.8  After reviewing the above information about standardised methods available for identifying the risk factors for CAD, the present study was undertaken to assess the prevalence of risk factors in the community in Tripoli, the capital of Libya. The aim of this paper also includes suggesting priorities and strategy to deal with the risk factors that were found most important. Appropriate statistical tests were applied using the software SPSS 17 for determining the relative importance of different risk factors. The specific statistical tests have been stated below. Material and Methods
528 individuals were selected from general community for the study by random sampling from different geographical areas of Tripoli. They were interviewed about risk factors for CAD and where possible, facts stated by them were validated from medical records available with them. Their body weight, height and blood pressure were also recorded. The intern doctors posted with community medicine department were briefed and trained by faculty members for the above observations and recording the body measurement and blood pressure using the uniform technique. The WHO/ISH risk prediction colourcharts for Eastern Mediterranean Region B (which includes Libya) were used as questionnaire for the study. The option of charts available for settings where blood cholesterol can’t be measured was selected as it was found difficult to convince the individuals not suffering from disease to provide blood samples.  The following criteria were used for defining Blood Pressure, BMI, Diabetes & MI : According to the WHO definition, individuals with systolic blood pressure ≥ 140 mmHg or those with diastolic blood pressure ≥ 90 mmHg were considered hypertensive. 21.  Known cases of diabetes were termed as individuals for whom the diagnosis of diabetes had been established by a physician in the past, or those who were under treatment with anti diabetic drugs. 22  Body mass index (BMI) is calculated as weight divided by height squared (kg/m2). Overweight is defined as BMI 25–29.9 kg/m2, and obesity as BMI ≥ 30 kg/m2 for all subjects.19 Known cases of Myocardial Infarction (MI) were termed as individuals for whom the diagnosis of MI had been established by a physician in the past. Observations The comparison of population characteristics of people with and without having a MI stated in the table below reveals that: distribution of males and females was similar in both the groups. 88% of individuals with a MI were from age group 35 and above. Whereas 11.43%  of people with MI were from age group 15 to 34 years which shows the need of starting screening as well as control of risk factors from teenage.  Using SPSS software, independent sample t test was applied on age distribution of individuals with and without history of MI. The result revealed that the mean age of individuals with a positive history of MI was 54. It was 43.74 for subjects with negative history of MI. The difference of age between the above 2 groups was found highly significant (P>0.001). In the same manner using SPSS software, Chi square test was applied on sex distribution of individuals with and without history of MI. The result revealed that the difference in sex distribution in the two groups was not significant (P = 0.522)  Table 1 : Age & Sex wise distribution of persons with and without MI: 

Characteristics Individuals with MI in percentage, (N= 70) Individuals without MI in percentage, (N = 458)
Sex;     Male 68.57 (48) 68.78 (315)
            Female 31.43 (22) 31.22 (143)
Age 15-34 years 11.43(8) 34.93 (160)
35-54 years 30.00 (21) 37.55 (172)
55 & above 58.57 (41) 27.51 (126)

  Independent risk factors As presented in Fig.1, in males with MI in terms of percentage the most prevalent risk factor was found to be hypertension (11.05% higher than non MI group), followed by diabetes (higher by 10.78%), smoking (higher by 8.12%) and BMI 25 & above (higher by 5.13%). As presented in Fig.2, in females with MI in terms of percentage the most prevalent risk factor was found to be hypertension (20.55% higher than non MI group), followed by BMI 25 & above (higher by 8.77%) and diabetes (higher by 6.85%). There were no smokers in the female group with MI and only one smoker was found in the females without MI.  Using SPSS software, under general linear model, multivariate analysis was performed after splitting the cases under male and female. History of MI was kept as fixed factor and age, history of hypertension, diabetes and stroke, smoking, systolic blood pressure and BMI were kept as dependent variables. The results reveal that in the males with positive history of MI, value of P was less than 0.001(highly significant) for age, History of hypertension & diabetes and systolic BP of140 and greater, followed by history of stroke (P>0.002) suggesting that prevalence of these variables were significantly higher in males with history of MI. The prevalence of BMI 25 & above (P>0.616) and smoking (P>0.882) in males with history of MI was found insignificant. In case of females with positive history of MI, the only variable having significant prevalence was f history of hypertension (P>0.008). An important reason for inability to assess significance for other variables in females may be the smaller number of females of only 22 with history of MI.  Among the community members with MI, 94.38% males and 78.57% females had one or the other risk factor which have been stated above. Hence with focused attention to health education and screening for risk factors, identifying most of the individuals at risk of MI, should be possible.  
(Fig.1) Distribution of Risk Factors in Males with and without MI  (The total number of responses are more than number of respondents because of more than one risk factor being present in many respondents)   (Fig.2) Distribution of Risk Factors in Females with and without MI  (The total number of responses are more than number of respondents because of more than one risk factor being present in many respondents)  Combination of risk factors Out of 48 males with MI, 22 (45.83%) had both diabetes and hypertension and half of them (22.92%) were also smokers. The next group among males having multiple risk factors were that of smokers 14 (29.17%), out of which half (14.58%) also had hypertension. Out of 22 females with MI, 13 (59.09%) had hypertension and 27.27 % out of them were also diabetic. The next group was that of diabetics 3 (13.64%). Hence looking at the combination of risk factors in both males and females with MI the most common risk factor in terms of prevalence was found to be hypertension followed by smoking in men and diabetes in women. As Hypertension and BMI in age group of 35 to 54 years were found to be significant and commonly present risk factors, the data was further explored.  Systolic BP 140 and above: The percentage of persons with MI having a systolic BP of 140 and above in the age group 35 to 54 years was more than double in comparison to the percentage expected by number of persons present in this age group that is 66.67% as stated in Fig.3, against 30% as stated above in Table1. Hence in this age group there appears to be considerable opportunity of detecting and treating cases of hypertension in the general community before they reach to the advanced stage  of coronary artery disease and MI.  (Fig.3) Age wise distribution of blood pressure (both sexes) Body Mass Index: As presented below in Fig.4, the percentage of overweight and obese individuals were found to be 5 to 9 percent higher in those with MI than those without MI. The percentage of obese people increased by 2 times in both the groups that is with and without MI as age advanced to 35-54 years from 15-34 years. The percentage of overweight individuals was 1.48 times in those without MI and 1.77 times in those with MI in age group 35-54 years in comparison to the age group of 15-34 years.  (Fig. 4) Age wise distribution of weight (both sexes) 
Discussion:  Comparison with other relevant studies: In our study the most common risk factors observed in community members without  MI were hypertension (total 24.35%, males 23.78 & females 25.88), followed by diabetes (total 21.13%, males 19.56 & females 25.29) and smoking (Total 27.26%, males 37.33 & females 0.59) as stated above in Fig.1 & 2. In similar studies performed in countries of Mediterranean region14-18 26% of study population were found to be suffering from hypertension, 40% males and 13% females were smokers and 14.5% were suffering from diabetes. 13   The percentage of diabetics was 10.6 in study population aged 30 years and above in Iran11.  The percentage of diabetics were 11% in males and 7% in females in United Arab Emirates (UAE)10 and the figures were the similar in Saudi Arabia in subjects aged 30 years and above were 17.3% and 12.18% respectively.9. All the above studies were performed in the period from year 2000 to 2004 except the study in UAE which was performed in 1995. It can be seen from our study in Libya that in comparison to mean percentage for the same risk factors in other countries of Mediterranean Region, the percentage of hypertension was lower by about 2%.  In Libya the percentage of total diabetics in the general community was greater by 6.6%,  while the percentage of smokers were less by about 13% in males and 12.5% in females.  The percentage of total overweight and obese individuals in all age groups and both sexes were 66.6 % in the general community without MI in our present study (Fig,4). The percentage for those overweight and obese in individuals above 19 years of age was 26.2%  in study from Iran12 and 27 % in UAE10 in the age group of 30 to 64 years. The study of 12 countries of the Eastern Mediterranean Region(EMR) by  the WHO conducted in  2004, reveals that regional adjusted mean for these countries was 43 % for overweight and obese individuals in all age groups and both sexes20. Hence in comparison to developing countries of the region having similar religious, social and dietary situation among the risk factors for CAD, diabetes and obesity can be seen as emerging major risk factors in Libya followed by hypertension and smoking. Smokers among females were found to be uncommon in Libya.        Conclusion  The findings of this study reveal that in comparison to those without MI the prevalence of following risk factors was higher in individuals with MI. In males aged 35 to 54, the percentage of those with a systolic BP of 140 and greater was more than double and in females 1.6 times greater.  Those with diabetes were greater by 10.78% in males and 6.85% in females, while smokers were higher by 8.12% in males.  The percentage of diabetes in individuals without MI was 21.13%.  The prevalence of smokers was found to be 37.33% in males without MI which suggests urgent need for prevention and control measures. Considering multiple risk factors out of 48 males with MI, 22 (45.83%) had both diabetes and hypertension and half of them (22.92%) were also smokers. Out of 22 females with MI, 13 (59.09%) had hypertension and 27.27 % out of them were also diabetic. In view of large number of individuals having risk factors of CAD in Tripoli, we would like to recommend that health education for preventing overweight and obesity, hypertension, smoking and diabetes may be started with school children and their parents as early as primary school. The screening for above risk factors needs to be implemented in the age group of 34 years and above for detecting individuals at risk as close to 34 years as possible. This step needs to be followed by relevant health education and treatment as soon as possible. More studies on a larger population sample are required from different geographical areas of Libya to refine our focus on the target population identified. At the same time waiting for action, till these additional studies are completed, is not recommended. To make the comparison of risk factors more fruitful among different countries and in the same country over time, we need to agree on uniform criteria such as using WHO/ISH risk prediction charts.  Limitations of present study It is a cross sectional study based on the questions stated in WHO/ISH prediction charts for situations where collecting blood samples is not feasible. Due to the small sample size we can only say that the prevalence of MI is indicative of the pattern observed. These figures may get refined as we cover a larger number of the population over time. Due care has been taken in selecting sample size to represent different geographical divisions of Tripoli and to ensure that this is a random sample, but it is a systematic random sample and not the stratified random sample. Hence within each geographical division all the socio economic strata of community may not have been proportionately represented.   AppendixThe questionnaire used for the study is stated below. It is based on the questionnaire recommended on page 21 of WHO/ ISH risk prediction charts for Eastern Mediterranean Region B of W.H.O. in which Libya is included.QuestionnairePrecautions: Do not interview persons below the age of 14 years. You should take height, weight and Blood Pressure of the person yourself, before recording it in the form below 

S.N. Question Subject
    1 2 3 4 5
1 Name of Person:          
2 Address in Libya          
4 Age          
5 Sex: M / F          
6 Do you smoke: Yes / No          
8 Do you have History of suffering from Diabetes:   Yes / No          
9 Hist. of suffering from: Mayo cardial Infarction: Yes/ No          
10 History of suffering from Stroke: Yes /   No          
12 History of suffering from Hypertension: Yes /   No          
13 Height in Cms:          
14 Weight in Kg:          
15 Systolic Blood Pressure ( in mm of Hg):          


 

Competing Interests
None Declared
Author Details
R.K.PAL, Department of Community Medicine, Al Fateh University of Medical Sciences, Tripoli, Libya. ALI GRERA, Department of Community Medicine, Al Fateh University of Medical Sciences, Tripoli, Libya.
CORRESSPONDENCE: R.K.PAL, Department of Community Medicine, Al Fateh University of Medical Sciences, Tripoli, Libya.
Email: palrk2002@gmail.com

References

1. Preventing chronic diseases – a vital investment, World Health Organization, www.who.int/chp.
2. WHO Study on Heart Disease, Press Release WHO/10, 28 February 2000. (http://www.who.int/inf-pr-2000/en/pr2000-10.html).
3. The World Health Report 2002: reducing risks, promoting healthy life. Geneva, World Health Organization, 2002:57– 61, 162.
4. Summary, Surveillance of risk factors for non communicable diseases, The WHO STEP wise approach, WHO/NMH/CCS/01.01 Rev.1, 2003.
5. Wilson PW, D’Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. Prediction of coronary heart disease using risk factor categories. Circulation. 1998; 97: 1837–1847.
6. Mendis S, Lindholm LH, Mancia G, Whitworth J, Alderman M, Lim S, Heagerty T. World Health Organization (WHO) and International Society of Hypertension (ISH) risk prediction charts: assessment of cardiovascular risk for prevention and control of cardiovascular disease in low and middle-income countries. J Hypertens. 2007; 25: 1578–1582.
7. Barzi F, Patel A, Gu D, Sritara P, Lam TH, Rodgers A, Woodward M. Cardiovascular risk prediction tools for populations in Asia. J Epidemiol Community Health. 2007; 61: 115–121.
8. CVD Risk reduction guide, questions and answers, page 9, W.H.O.,September 2007.
9. Risk factors of coronary artery disease in different regions of Saudi Arabia, A.K. Osman and M.M. Al-Nozha, Vol. 6, Issue 2/3, 2000, page 465-474.
10. El-Mugamer IT et al. Diabetes, obesity and hypertension in urban and rural people of Bedouin origin in United Arab Emirates. Journal of tropical medicine and hygiene, 1995, 98(6):407-15.
11. Azizi F., Modifying life style for the prevention of non-communicable disease, Iranian journal of endocrinology and metabolism, 2002, 4(2):81–4.
12. Clustering of coronary artery disease risk factors in patients with type 2 diabetes and impaired glucose tolerance, F. Sajjadi, N. Mohammadifard, R. Kelishadi, N. Ghaderian, H. Alikhasi and M. Maghrun, 1088 La Revue de Santé de la Méditerranée orientale, Vol. 14, No 5, 2008.
13. Al-Nozha MM et al. Coronary artery disease, in Saudi Arabia, Saudi medical journal, 2004, 25(9):1165–71.
14. National survey on the major non communicable diseases, Lebanon. Final Report,2003. Cairo, WHO Regional Office for the Eastern Mediterranean.
15. Diabetes atlas, 2nd ed. Brussels, International Diabetes Federation, 2003.
16. Mokhtar N et al. Diet, culture and obesity in northern Africa. Journal of nutrition, 2001, 131(3):887–92s.
17. Mokdad AH et al. Prevalence of obesity, diabetes, and obesity-related health factors.Journal of the American MedicalAssociation, 2003, 289(1):76–9.
18. National Health Survey of Pakistan1990–1994. Islamabad, Pakistan Medical Research Council, 1998.
19. North American Association for the Study of Obesity,The practical guide. Identification,evaluation and treatment of overweight and obesity in adults. Bethesda, Maryland, National Institutes of Health, 2000 (NIH Publication No. 00–4084).
20. O. Khatib, Noncommunicable diseases, risk factors and regional strategies for prevention and care, Eastern Mediterranean Health Journal, Vol. 10, No. 6, 2004.
21. Azizi F et al. Determinates of serum HDLC level in a Tehran urban population: the Tehran Lipid and Glucose study. Nutrition, metabolism and cardiovascular diseases, 2002, 12:80–9.
22. The Expert Committee of the Diagnosis and Classification of Diabetes Mellitus. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes, 2000, 25:S5–20.


Obesity Hypoventilation Syndrome. Where do we stand 50 years later?

Roop Kaw

Cite this article as: BJMP 2010;3(2):323
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Initial reports of Obesity Hypoventilation Syndrome (OHS) date back as early as 18891, but it was not until 1955 that Auchincloss2 and colleagues described a case of obesity and hypersomnolence paired with alveolar hypoventilation.  Burwell3 coined the term Pickwickian syndrome describing the constellation of morbid obesity, plethora, oedema and hypersomnolence.  Hypercapnia, hypoxaemia and polycythemia were described on laboratory testing. Obstructive Sleep Apnea (OSA) had not been described at that time and came to be recognized for the first time in the mid 1970s. With attention shifting to upper airway obstruction, hypercapnia began to get lesser emphasis and confusion began to emerge in describing OSA and OHS.  The term ‘Pickwickian’ began to be used for OSA-related hypersomnolence in the obese patient regardless of the presence of hypercapnia.  This confusion was finally settled by the American Academy of Sleep Medicine (AASM) in its published guidelines in 1999.4  The AASM statement identified that awake hypercapnia may be due to a predominant upper airway obstruction (OSA) or predominant hypoventilation (Sleep Hypoventilation Syndrome) easily distinguished by nocturnal polysomnography (PSG) and response to treatment.  Both disorders are invariably associated with obesity and share a common clinical presentation profile.

 
Salient features of OHS consist of obesity as defined by a BMI > 30kg/m2, sleep disordered breathing, and chronic daytime alveolar hypoventilation (PaCO2 ≥ 45 mmHg and PaO2 < 70 mmHg). 4  Sleep disordered breathing, as characterized by polysomnography in OHS, reveals OSA (Apnea-hypopnea index [AHI]>5) in up to 90% of patients and sleep hypoventilation (AHI<5) in up to 10%.5  Daytime hypercapnia and hypoxaemia are the hallmark signs of OHS and distinguish obesity hypoventilation from OSA.  Severe obstructive or restrictive lung disease, chest wall deformities and hypoventilation from severe hypothyroidism, and neuromuscular disease need to be excluded before a diagnosis of OHS is established.  As obesity is becoming more prevalent in western society, this disorder has gained more recognition in recent years.  However, patients with this syndrome may still go undetected and untreated.  No population-based prevalence studies of OHS exist till date but, at present, can be estimated from the relatively well known prevalence of OHS among patients with OSA.  Recent meta-analysis with the largest cohort of patients (n=4250) reported a 19% prevalence of OHS among the OSA population, confirming an overall prevalence of about 3 per 1000.6
 
Whilst transient rectifiable nocturnal hypercapnia is common in patients with OSA, awake hypercapnia in OHS appears to be a final expression of multiple factors.  There has been a debate about BMI and AHI not being the most important independent predictors of hypercapnia in obese patients with OSA.  More definitive evidence for the role of OSA, however, is suggested by resolution of hypercapnia in the majority of patients with hypercapnic OSA or OHS with treatment, with either PAP or tracheostomy, without any significant changes in body weight or respiratory system mechanics. Yet some recent studies have shown that nocturnal hypoxaemia and diurnal hypercapnia, persist in about 50% of such individuals even after complete resolution of OSA with CPAP or tracheostomy.  This raises questions such as how good is AHI as a measure of severity of OSA?
 
It is intuitive to argue that obesity may exert its effect through mass loading of CO2 due to (increased production via) higher basal metabolic rate or reduced functional residual capacity on lung function.  But why do only some severely obese patients with OSA go onto develop OHS?  Is the pathophysiology driven by the severity of BMI?  Whilst weight loss, particularly surgically-induced, clearly shows resolution of both OSA and hypercapnia7, the role of BMI as an independent factor for hypercapnia has been challenged by the fact that only a small fraction of severely obese patients do in fact develop chronic diurnal hypercapnia.  More importantly, not only can PaCO2 be normalized in a majority of patients without weight loss and with positive airway pressure therapy (PAP), but awake hypercapnia can develop even at lower BMIs among the Asian population.  Some investigators have tried to explain the incremental role of BMI as follows.  In situations where AHI is not a presumed independent predictor of nocturnal hypercapnia, potential pathophysiologic contributors can include pre-event (apnea or hypopnea) amplitude in relation to the post-event amplitude.8  Such inciting events for nocturnal hypercapnia may then be perpetuated in the daytime by factors such as AHI, functional vital capacity (FVC), FVC/FEV1, or BMI as shown in the largest pooled data to date.6  It has been shown that, for a given apnea/interapnea duration ratio, a greater degree of obesity is associated with higher values of PaCO2.9 However the same group of investigators, in another study, did not find any of these factors to be related to the post-event ventilatory response.8
 
Looking further at the breath by breath cycle, the post-event ventilatory response in chronic hypercapnia may relate to eventual adaptation of chemoreceptors perhaps in consequence to elevated serum bicarbonate known to blunt the ventilatory drive.10 Or it may relate to whole body CO2 storage capacity which is known to exceed the capacity for storing O2.11 With definite evolution in our understanding of hypercapnia among obese patients, these questions continue to dominate. Some of the more pressing ones include: are the predictors of daytime hypercapnia different from those of nocturnal hypercapnia in obese patients with OSA?  An understanding of these facts can help us with the more important understanding of the associated morbidity and mortality from OHS and its correct management.  In addition, what is the true effect of untreated OHS on mortality independent of the co-morbidities related to obesity and OSA?  Can morbidities like cor pulmonale and pulmonary hypertension be reversed with treatment of OHS?  How do we treat patients with OHS who fail CPAP/ BiPAP short of tracheostomy?
 

Competing Interests
None Declared
Author Details
ROOP KAW, MD, Assistant Professor of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University | Staff, Departments of Hospital Medicine and Outcomes Research (Anesthesiology Institute).
CORRESSPONDENCE: A-13, Medicine Institute I Cleveland Clinic, 9500 Euclid Ave | Cleveland, OH 44195
Email: KAWR@ccf.org

References

1. Lavie P. Who was the first to use the term Pickwickian in connection with sleepy patients? History of sleep apnoea syndrome. Sleep Med Rev 2008;12(1):5-17.
2. Auchincloss JH Jr, Cook E, Renzetti AD. Clinical and physiological aspects of obesity, polycythemia and alveolar hypoventilation. J Clin Invest 1955; 34: 1537-45.
3. Burwell CS, Robin ED, Whaley RD, Bicklemann AG. Extreme obesity associated with alveolar hypoventilation; a Pickwickian syndrome. Am J Med 1956; 21: 811-818.
4. The Report of an American Academy of Sleep Task Force. Sleep-related breathing disorders in adults: Recommendations for syndrome definition and measurement techniques in clinical research. Sleep, 1999; 22: 667-689.  
5. Mokhlesi B, Tulaimat A, Faibussowitsch I, Wang Y, Evans AT. Obesity hypoventilation syndrome: prevalence and predictors in patients with obstructive sleep apnea. Sleep Breath 2007; 11:117-124.
6. Kaw R, Hernandez AV, Walker E et al. Determinants of hypercapnia in Obese patients with hypercapnia: A systematic review and Meta-analysis of Cohort studies. Chest 2009; 136(3): 787-96.
7. Sugerman HJ, Fairman RP, Sood RK, et al. Long-term effects of gastric surgery for treating respiratory insufficiency of obesity. Am J Clin Nutr 1992; 55: 597S-601S.  
8. Berger KI, Ayappa I, Sorkin IB, Norman RG, Rapoport DM, Goldring RM. Post event ventilation as a function of CO2 loading during respiratory events in obstructive sleep apnea. J Appl Physiol 2002; 93:917-924. 
9.  Ayappa I, Berger KI, Norman RG  et al. Hypercapnia and Ventilatory periodicity in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 2002; 116: 1112-1115. 
10.  Goldring RM, Turino GM, Heinemann HO. Respiratory –renal adjustments in chronic hypercapnia in man. Extracellular bicarbonate concentration and regulation of ventilation. Am J Med 1971;51: 772-784.
11.  Nunn JF. Oxygen in: Applied Respiratory Physiology. 3rd ed. Butterworths, London 1987,p. 235

 

 


“Influenza-2009” - An Escape from Disaster.

Shailpreet Kaur Sidhu, Nidhi Singla and Jagdish Chander

Cite this article as: BJMP 2010;3(2):320
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Abstract
In April 2009, World Health Organization declared the first ever public health emergency affecting overseas countries, territories and communities of the world with a new strain of the influenza A virus causing a global pandemic. This novel strain (H1N1) of the virus appears to be of swine origin and contains a unique combination of gene segments that have not been previously identified in swine or human influenza viruses. The symptoms of the 2009 H1N1 flu virus are clinically similar to those of seasonal influenza and have ranged from mild to severe. The neuraminidase inhibitors provide valuable defences against the virus, but their massive use has lead to the development of resistance to these antiviral agents. Vaccination is the only effective way to protect people from contracting illness during epidemics and pandemics of influenza.
Keywords:  Pandemic, Influenza, H1N1, Flu, Influenza A virus

Forty one years after the last influenza pandemic, while everyone was worrying about the avian influenza A (H5N1) virus causing a pandemic, an apparent new chapter is opened with the emergence of new strain of influenza A virus. On 24th April, the World Health Organization (WHO) declared the first ever public health emergency of international concern indicating the occurrence of confirmed human cases of swine influenza in Mexico and United States.1 Subsequently the Centre for Disease Control and Prevention (CDC) confirmed that these human influenza cases were caused by a novel strain of influenza A virus to which there is little or no population immunity.2 On June 2009, the WHO rated the pandemic alert from phase 5 to 6, signalling that the first pandemic of the 21st century was underway. It was however stressed that the rise in the pandemic alert level was mainly attributed to the global spread of the virus rather than its severity. The pandemic potential of influenza A viruses has been ascribed to their genetic and antigenic instability and there ability to transform by constant genetic re-assortment or mutations, which can result in the emergence of novel progeny subtypes capable of both infecting and leading to sustained person to person transmission.3 The newly emerged strain contains a combination of gene segments that have not been previously identified in swine or human influenza viruses.4
 
Historical Perspectives
 
Influenza has been recognised for hundreds of years, but the cause was unknown for most of this time. Hippocrates had defined this disease about 2400 years ago, but lacked laboratory confirmation.5 The year 1580, marks the first instance of influenza recorded as an epidemic even though there is possibility that there were many prior influenza epidemics.6 The word influenza (meaning influence), first used in 1743 originated from the Latin word “Influenza”, named so because the disease was considered to be caused by unfavourable astrological conditions. Since 1700, there have been approximately a dozen influenza A virus pandemics and the lethal outbreak of 1918-1919 is dubbed as the greatest medical holocaust in recorded history, killing up to 50 million people worldwide.7
 
The earliest evidence of influenza A virus causing acute respiratory illness in pigs was traced to the 1930s. Swine influenza A viruses are antigenically very similar to the 1918 human influenza A virus and they may all have originated from common ancestor.8 From 1930 to 1990, classic swine influenza A was the commonest swine influenza virus circulating amongst the swine population during which the virus did not undergo much genetic change. Antigenic variants of these classical influenza viruses emerged in 1991 and the real antigenic shift occurred at the ends of last century when the classical swine influenza virus re-assorted with human influenza A virus and a North American lineage avian influenza virus. This resulted in the emergence of multiple subtypes including H1N2 and H3N2. In the past few years, sporadic cases of human infections caused by swine influenza A virus have occurred, mainly due to subtypes. Occupational exposure to swine was the most important risk factor for infection and fortunately all patients recovered without resulting in efficient, sustained human to human transmission.9
 
Origin of 2009 Strain
 
The pandemic that began in March 2009, was originally referred to as “swine flu” because laboratory testing showed that many of the genes in this new virus were very similar to influenza viruses that normally occur in pigs (swine) in North America. But further study has shown that this new strain of virus represents a quadruple re-assortment of two swine strains, one human strain and one avian strain of influenza. The largest proportion of genes come from swine influenza viruses (30.6% from North American swine influenza strains, and 17.5% from Eurasian swine influenza strains), followed by North American avian influenza strains (34.4%) and human influenza strains (17.5%).10 Analysis of the antigenic and genetic characteristics of the pandemic influenza A virus demonstrated that it’s gene segments have been circulating for many years, suggesting that lack of surveillance in swine is the reason that this strain had not been recognized previously.11 This novel strain is antigenically distinct from seasonal influenza A and possesses previously unrecognised molecular determinants that could be responsible for the rapid human to human transmission. Moreover, antigenic drift has occurred amongst different lineages of viruses, therefore, cross protection antibodies against avian, swine and human viruses are not expected to exist. Emerging scientific data support the hypothesis of a natural genesis, with domestic pigs a central role in the generation and maintenance of the virus. Protein homology analysis of more than 400 protein sequences from the new influenza virus as well as other homologous proteins from influenza viruses of the past few seasons also confirmed that this virus has a swine lineage.1 Phylogenetic analysis has suggested that initial transmission to humans occurred several months before the recognition of the outbreak and multiple genetic ancestry of this influenza A is not indicative of artificial origin.11
 
Situation Update
 
In March 2009, an outbreak of respiratory illness was first noted in Mexico, which was eventually identified as being related to influenza A.12 The outbreak spread rapidly to the United States, Canada and throughout the world as a result of airline travel.13 On 11th June 2009, the WHO raised its pandemic alert to the highest level i.e. phase 6, indicating widespread community transmission on at least two continents.14
 
Pandemic influenza was the predominant influenza virus circulating in the US, Europe, northern and eastern Africa and in Australia. Activity of the virus has initially peaked and then declined in North America and in parts of western, northern and Eastern Europe, but activity continued to increase in parts of central and southeastern Europe, as well as in central and south Asia. As of 28th  February 2010, worldwide more than 213 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza 2009, including at least 16455 deaths; a number the WHO acknowledges significantly underreported the actual number.15 Most of the deaths have been related to respiratory failure resulting from severe pneumonia and acute respiratory distress syndrome.16
In India, the number of confirmed cases till March 2010 was 29,953 and a total of 1410 deaths were reported. The rate of infection has been highest among children and young individuals of <24 years of age. To date, pandemic influenza A infections are uncommon in persons older than 65 years, possibly as a result of pre-existing immunity against antigenically similar influenza viruses that circulated prior to 1957.17 High rates of morbidity and mortality has been noted among children and young adults with underlying health problems including chronic lung disease, immunosuppressive conditions, cardiac disease, pregnancy, diabetes mellitus and obesity.18
 
Transmission and Shedding
 
Novel virus is contagious and can transmit from human to human in ways similar to other influenza viruses. The main route of transmission between humans is via inhalation of infected respiratory droplets (range in size from 0.08 µm to 0.12 µm) produced after coughing and sneezing.19 Transmission via contact with surfaces that have been contaminated with respiratory droplets or by aerosolised small-particle droplets may also occur. In addition to respiratory secretions, all other body fluids (including diarrhoeal stool) should also be considered potentially infectious.
 
The estimated incubation period is unknown and could range from 1 to 7 days, although the median incubation period in most cases appears to be approximately 2 days.20 Shedding of the virus begins the day prior to the onset of symptoms and can persist for 5-7 days in immunocompetent individuals. The amount of virus shed is greatest during the first 2-3 days of illness. Persons who continue to be ill, for a period of longer than 7 days after illness onset, should be considered potentially contagious until symptoms have resolved. Longer periods of shedding may occur in children (especially young infants), elderly adults, and patients with chronic illnesses and immunocompromised hosts who might be contagious for longer periods.
 
Clinical Manifestations
 
According to the CDC, in humans the symptoms of the 2009 “flu” virus are similar to those of influenza and of influenza-like illness in general. The illness with the virus has ranged from mild to severe and symptoms include fever, cough, sore throat, body aches, headache, chills and fatigue, which are usual features of influenza virus. The 2009 outbreak has shown an increase percentage of patients reporting diarrhoea and vomiting.16 As these symptoms are not specific to swine flu hence a differential diagnosis of probable swine flu requires not only symptoms but also a high likelihood of swine flu due to person’s recent history. The CDC advised physicians to consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness who have either been in contact with persons with confirmed swine flu or who were in states that have reported swine flu cases during the 7 days preceding their illness onset.
 
The overall severity with this 2009 virus has been less than what was observed during the influenza pandemic of 1918-1919. Most patients appear to have uncomplicated, typical influenza-like illness and recovered without requiring any medical treatment. About 70% of people who have been hospitalised have had one or more medical conditions, which include pregnancy, diabetes, heart disease, asthma and kidney disease.21 The most common cause of death is acute respiratory distress syndrome. The other causes of death are severe pneumonia with multifocal infiltrates (leading to sepsis), high fever (leading to neurological problems), dehydration (from excessive vomiting and diarrhoea) and electrolyte imbalance. Fatalities are more likely in young children (<5 years), elderly (>65 years) and in people with underlying conditions, which include pregnancy, asthma, lung diseases, diabetes, morbid obesity, autoimmune disorders, immunosuppressive therapies, neurological disorders and cardiovascular disease.22
 
Laboratory Diagnosis
 
All diagnostic laboratory work on clinical samples from suspected cases of virus infection should be done in a Biosafety Level 2 (BSL-2) Laboratory. Suspected cases of novel infection should have respiratory specimens (nasopharyngeal, nasal or oropharyngeal swab, bronchoalveolar lavage and endotracheal aspirate) collected to test for the 2009 flu virus. Specimens should be placed into sterile viral transport media (VTM) and to be kept at 4°C. Real time reverse transcriptase polymerase chain reaction (RT-PCR) is the recommended sensitive method for the detection of virus, as well as to differentiate between pandemic 2009 and regular seasonal flu.23 The other rapid influenza diagnostic tests (RIDTs), although provide results within 30 minutes or even less, none of these tests can distinguish between influenza A virus subtypes. Moreover, RIDTs do not provide any information about antiviral drug susceptibility. Isolation of the virus in cell cultures or embryonated eggs is another method for diagnosis of infection, but may not yield timely results for clinical management and negative viral culture does not exclude the influenza A infection.
 
However, most people with flu symptoms do not need a test for pandemic 2009 flu, specifically because the test results usually do not affect the recommended course of treatment. The CDC recommends testing only for people who are hospitalised with suspected flu and persons having underlying medical conditions and those with weak immune systems.24 It is also expressed that treatment should not be delayed by waiting for laboratory confirmation of test results, but rather make diagnosis based on clinical and epidemiological backgrounds and start treatment early.
 
Treatment
 
The virus isolates in the 2009 outbreak are found to be resistant to amantidine and rimantidine. The CDC recommends the use of neuraminidase inhibitors as the drugs of choice for treatment and prevention of 2009 influenza in both children and adults.25 Tamiflu (oseltamivir phosphate) and Relenza (zanamivir) are the two FDA-approved influenza antiviral drugs and a third neuraminidase inhibitor peramivir is an experimental drug approved for hospitalised patients in cases where the other available methods of treatment are ineffective or unavailable. Antiviral drugs not only make the illness milder but also prevent serious flu complications. However, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs. Treatment is recommended for patients with confirmed or suspected 2009 influenza who have severe, complicated or progressive illness or who are hospitalised. People who are not from the at-risk group and have persistent or rapidly worsening symptoms should also be treated with antivirals. Therapy should be started as soon as possible, since evidence of benefit is strongest when treatment is started within 48 hours of illness onset.26 Treatment should not be delayed while awaiting the results of diagnostic testing nor should it be withheld in patients with indications for therapy who present >48 hours after the onset of symptoms. Beside antivirals, supportive care at home or in hospital, focuses on controlling fevers, relieving pain and maintaining fluid balance as well as identifying and treating any secondary infections or other medical problems.
 
Major Concern
 
The neuraminidase inhibitors oseltamivir and zanamivir provide valuable defences and have been used widely for treatment and chemoprophylaxis of 2009 pandemic influenza A.But the recent emergence of resistance to these antiviral drugs is a matter of immediate concern. Influenza A strain resistant to oseltamivir has been reported from a variety of geographical locales and poses a challenge for the management of severely compromised patients.27 The CDC warned that the indiscriminate use of antiviral medications to prevent and treat influenza could ease the way for drug resistant strains to emerge, which would make the fight against the pandemic much harder. Most of the patients recover spontaneously without any medical attention and use of antiviral medications should be reserved primarily for people hospitalised with pandemic flu and persons, with pre-existing or underlying medical conditions who are at higher risk for influenza-related complications. It has also been emphasised that early treatment once a patient has developed symptoms, rather than chemoprophylaxis, should reduce opportunities for the development of oseltamivir resistance.26 The degree to which these drugs will remain effective for the treatment of the novel strain of influenza in the coming months is still a question.
 
What’s next?
 
The only possible way to combat the situation is large scale immunization. Antiviral drugs are not a substitute for vaccinination and are used only as an adjunct to vaccines in the control of influenza. Vaccines are one of the most effective ways to protect people from contracting illness during epidemics and pandemics of influenza. The seasonal vaccines do not confer any protection against 2009 H1N1; new vaccines have been licensed and are available.28 The vaccines are available in both live-attenuated and inactivated formulations. Two types of vaccines are approved by the FDA for use in the prevention of 2009 pandemic influenza virus. These are TIV (“flu shot” of trivalent inactivated vaccine) and LAIV (nasal spray of live attenuated vaccine). The inactivated vaccine is contraindicated in patients with severe allergic reaction to eggs or any other component of the vaccine. The live attenuated vaccine is licensed for persons aged 2 through 49 years who are not pregnant, are not immunocompromised and have no underlying medical conditions. Children less than 5 years who have asthma and are taking long term aspirin therapy should also not receive live vaccines. Otherwise, both vaccines are safe and highly immunogenic and a single administration leads to robust immune response in 80% to 90% of adults aged 18-64 years and in 56% to 80% of adults aged 65 years and older with in about 10 days.29 Children younger than 10 years will require two administrations of the vaccine separated by at least 21 days. Adverse effects following vaccination are minor, just like those of seasonal influenza vaccine and are self limiting. Concerns regarding the risk of Guillain-Barre syndrome (GBS) after vaccination have been raised. Various studies have suggested that the risk of GBS is higher from influenza itself rather than from the vaccine and the other adverse effects.30 The CDC is now encouraging everyone including people of 65 years and above to get vaccinated against the 2009 strain of influenza.
 
The Government of India has recently approved a split virus, inactivated, non-adjuvant monovalent vaccine (Panenza by Sanofi Pasteur) to inoculate frontline health workers and those who have a high risk of getting infected.31 Groups of health care workers has also been singled out by the European council for attention and immunization.32 Infection control practices in the health care settings should be followed along with as per the guidelines.33 Patients should also be educated regarding the other preventive measures, including using tissues to cover their mouth and nose when coughing and sneezing, developing good hand washing techniques, use of alcohol based hand-rubs, avoiding contact with ill persons if possible and staying home when ill unless medical attention has been given.
 
The flu season seems to be dying down in 2010 but the war is yet not over. Lessons must be learnt from the previous influenza pandemics and it is still important to get vaccinated against the flu and be prepared, as activity as well as virulence might increase again in the coming season. The words of Margaret Chan (Director General, WHO) to be remembered that “the virus writes the rule and this one like all influenza viruses can change the rules, without rhyme or reason, at any time”.

 

Competing Interests
None declared
Author Details
Shailpreet Kaur Sidhu, MD, Demonstrator Nidhi Singla, MD, Assistant Professor Jagdish Chander, MD, MAMS, Professor & Head Department of Microbiology, Government Medical College Hospital, Sector 32, Chandigarh.
CORRESSPONDENCE: Dr Nidhi Singla Assistant Professor H.No. 1205, Sector 32-B, Chandigarh 160030 (India)
Email: nidhisingla76@gmail.com

References

1. Mathew BC, Daniel RS, Cambell IW. Swine – origin influenza A (H1N1) pandemic revisited. Libyan j Med 2009; 4: 176-9.
2. Centre for Disease Control and Prevention (CDC).Update: Swine influenza A (HINI) infections-California and Texas, April 2009. MMWR Morb Mortal Wkly Rep 2009; 58: 435-7.
3. Taubenberger JK, Morens DM. The pathology of influenza virus infections. Annu ssRev Pathol 2008; 3: 499-22.
4. Luan YC, Shin RS, Pei-Len S, et al. Novel Swine-origin influenza virus A (H1N1): The first pandemic of the 21st Century. J Formos Med Assoc 2009; 108: 526-32.
5. Martin PM, Martin-Granel E .Twenty five hundred years evolution of the term epidemic. Emerg Infect Dis 2006; 12: 976-80.
6. Sagar G, Angela C. Swine influenza A (H1N1) strikes a potential for global disaster. Journal of Emergencies Trauma and Shock 2009; 2: 99-05.
7. Johnson NP, Mueller J. Updating the accounts: Global mortality of the 1918-1920 Spanish influenza pandemic bull. Hist Med 2002; 76: 105-15.
8. Reid AH, Taubenberger JK .The origin of the 1918 pandemic influenza virus: A continuing enigma. J Gen Virol 2003; 84: 2285-92.
9. Patrick CY Woo. Swine influenza: Then and now: Hong Kong Med J 2009; 15: 166-7.
11. Cohen J. Swine flu outbreak: Out of Mexico? Scientists ponder swine flu's origins. Science 2009; 324: 700.
13. Khan K, Arino J, Hu W, et al. Spread of a novel influenza A (H1N1) virus via global airline transportation. N Engl J Med 2009; 361: 212.
14. World Health Organization. World now at the start of 2009 influenza pandemic. Available at: http:/www.who.int/mediacentre/news/statements/2009/_ pandemic phase6_20090611/en/index.html (Accessed June 11, 2009).
15. World Health Organization. Pandemic (H1N1) 2009 - update 90. Available at:http://www.who.int/csr/don//2010_01_15/en/index.html (Accessed March 5, 2010).
16. Louie JK, Acosta M, Winter K, et al. Factors associated with death or hospitalization due to pandemic 2009 influenza A (H1N1) infection in California. JAMA 2009; 302: 1896.
17. Belshe RB. Implications of the emergence of a novel influenza virus. N Engl J Med 2009; 360: 2667.
19 Clem A, Galwankar S. Avian influenza: Preparing for a pandemic. J Assoc Physicians India 2006; 54: 563-70.
20. Cao B, Li XW, Mao Y, et al. Clinical features of the initial cases of 2009 pandemic influenza A () virus infection in China. N Engl J Med 2009; 361: 2507.
21. World Health Organization. Human infection with new influenza A (H1N1) virus: Clinical observations from Mexico and other affected countries. Available at: http:/www.who.int/wer/2009/wer8421.pdf (Accessed May 28, 2009).
22. Hospitalized patients with novel influenza A infection: California, April- May, 2009. Morb Mortal Wkly Rep 2009; 58: 536.
23. Centers for Disease Control and Prevention Interim Guidance on Specimen Collection, Processing, and Testing for Patients with Suspected Novel Influenza A (H1N1) Virus Infection. Available at http://www.cdc.gov/flu/specimen collection.htm (Accessed November 23, 2009).
24. Centers for Disease Control and Prevention. Influenza Diagnostic Testing during the
2009-2010 Flu Season. Available at: http://www.cdc.gov/flu/diagnostic_testing_ public_qa.htm (Accessed November 23, 2009).
25. Centers for Disease Control and Prevention. Antiviral Drugs and Swine Influenza. Available at: http://www.cdc.gov/swineflu/antiviral_swine.htm (Accessed April 27, 2009).
26.Centers for Disease Control and Prevention. Interim recommendations for the use of antiviral medications in the treatment and prevention of influenza for the 2009-2010 season. Available at: http://www.cdc.gov/flu/recommendations.htm (Accessed December 15, 2009).
27. Pandemic (H1N1) 2009 briefing note 1: Viruses resistant to oseltamivir (Tamiflu) identified. Wkly Epidemiol Rec 2009; 84: 299-399.
28. Centers for Disease Control and Prevention. Update in influenza A (H1N1) 2009 monovalent vaccines. MMWR Morb Mortal Wkly Rep 2009; 58:1100-1101. 
29. Fauci AS. Statement by Dr. Anthony Fauci, Director, National Institute of allergy and Infectious Diseases, NIH, regarding early results from clinical trials of 2009 H1N1 influenza vaccines in healthy adults. Available at: http://www.hhs.gov/news/press/2009pres/09/2009011a (Accessed November 12, 2009).
30. Stowe J, Andrews N, Wise L, Miller E. Investigation of the temporal association of Guillain – Barre syndrome with influenza vaccine and influenza like illness using the United Kingdom General Practice Research Database. Am J Epidemiol 2009; 169:382- 88.
31. Sanofi’s H1N1 vaccine approved for use. Available at: http//epaper.livemint.com (Accessed March 16, 2010).
32. Nicoll A. A new decade, a new seasonal influenza: the council of the European union recommendation on seasonal influenza vaccination. Euro Surveill 2010, 15(1): 1-2.
33. Centers for Disease Control and Prevention. Interim Guidance for infection control for care of patients with confirmed or suspected novel influenza A (H1N1) virus infection in healthcare settings. Available at http://www.cdc.gov/h1n1flu/guidelines infection control.htm (Accessed September 18, 2009).

 


Aorto-enteric fistulas: a cause of gastrointestinal bleeding not to be missed

Louise MacDougall, John Painter, Terry Featherstone, Claus Overbeck, Shyju Paremal and Suvadip Chatterjee

Cite this article as: BJMP 2010;3(2):317
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Abstract
Aorto-enteric fistulas are a rare cause of gastrointestinal (GI) bleeding. The high mortality associated with this condition and relatively low incidence make this a diagnostic and management challenge. This case report describes a classic presentation of such a case along with a discussion on the diagnosis and treatment of this condition. We hope that this will be a clinical reminder to all physicians particularly those involved in managing GI hemorrhage in an acute medical take.

Clinical Presentation

A 87-year old man was referred to hospital with a five day history of lethargy and increased urinary frequency. He denied symptoms of gastrointestinal bleeding or abdominal pain. His past medical history included diabetes mellitus, chronic kidney disease, peripheral vascular disease and surgery for repair of ruptured aortic aneurysm 6 weeks ago. Systemic examination, including per rectal examination, was normal. Haemoglobin was 83g/L and C-reactive protein was 148 (Normal <5). Twelve hours after admission he developed pyrexia (37.8 degree) accompanied with tachycardia (103 beats per minute) and hypotension (BP 87/43). Soon afterwards, he had a small amount (<50 mls) of fresh haemetemesis. He also complained of lower back pain and clinical examination revealed tenderness in the left iliac fossa. He was cross-matched for blood and initiated on intra-venous fluids. As his Rockall score was six an urgent oesophago-gastro-duodenoscopy (OGD) was planned. Over the next few hours he complained of increasing central abdominal pain and had several episodes of melaena. In view of the history of recent aortic surgery and current GI bleed the possibility of aorto-enteric fistula (AEF) was considered. An urgent contrast CT scan of the abdomen (Figure 1) was therefore arranged prior to OGD.
 
Figure 1: Contrast CT scan demonstrating the aorta (A) with extravasation of contrast (B) and a large collection (C) around it with trapped air suggestive of infection.
 
Contrast computed tomogram (CT) scan of the abdomen revealed an inflammatory soft tissue mass anterior to the infra-renal aortic graft with pockets of gas and leakage of contrast into it. These findings were suggestive of an AEF. The patient was informed of the diagnosis of AEF and the need for emergency surgical repair to which he consented. During the operation the vascular surgeons found that the duodenum was adherent to the aortic graft with evidence of fistulisation and infection, thus confirming the diagnosis. Although operative repair appeared to be successful, the patient continued to bleed on the table due to disseminated intravascular coagulation and died twenty fours after admission.
 
Discussion 
 
AEF is defined as a communication between the aorta and the GI tract.1 The diagnosis of AEF should be considered in every patient with a GI bleed and a past history of aortic surgery.2 Our case patient had had emergency repair of a ruptured aortic aneurysm with a prosthetic graft 6 weeks prior to his current admission.
 
AEFs are a rare cause of gastro-intestinal (GI) hemorrhage. AEFs can be primary or secondary. Primary AEF (PAEF) is a communication between the native aorta and the GI tract.1 The incidence of PAEF ranges from 0.04 to 0.07%.3 PAEFs commonly arise from an abdominal aortic aneurysm of which 85% are atherosclerotic.1
 
Secondary AEFs (SAEF) are an uncommon complication of abdominal aortic reconstruction.4  The incidence of SAEF ranges from 0.6% - 4%.Generally two types of SAEFs have been described. Type 1, termed as true AEF develops between the proximal aortic suture and the bowel wall. These usually present with massive upper GI hemorrhage.4 Type 2, or the paraprosthetic–enteric fistula does not develop a communication between the bowel and the graft and accounts for 15% to 20% of SAEFs.4 In this type of fistula, bleeding occurs from the edges of the eroded bowel by mechanical pulsations of the aortic graft. Sepsis is more frequently associated with this type of AEF (75% of cases).4 The mean time interval between surgery and presentation with SAEF is about 32 months6 but the time interval can vary from 2 days to 23 years.7 AEFs can involve any segment of the GI tract but, 75% involve the third part of the duodenum and the affected part is generally proximal to the aortic graft.8
 
The pathogenesis of AEF is not fully understood but two theories exist. One theory suggests repeated mechanical trauma between the pulsating aorta and duodenum causes fistula formation and the other suggests low-grade infection as the primary event with abscess formation and subsequent erosion through the bowel wall.9 The latter theory is felt to be most likely. The majority of grafts show signs of infection at the time of bleeding and up to 85% of cases have blood cultures positive for enteric organisms.10
 
The main symptom of AEF is GI bleeding. Secondary AEFs have been traditionally said to present with a symptom triad (as in our patient) of abdominal pain, GI bleeding and sepsis; however, only 30% of patients present in this manner.11 Patients often have a “herald bleed” which is defined as a brisk bleed associated with hypotension and hematemesis that stops spontaneously followed by massive gastro-intestinal haemorrhage in 20% – 100% of patients.8 Sometimes the GI bleeding can be intermittent.
 
The commonest investigations for diagnosis of AEFs are OGD, conventional contrast CT scan and angiography.12 OGD is often the initial investigation, as in any upper GI bleed mainly because of lack of clinical suspicion of the diagnosis. The endoscopic findings vary from those of a graft protruding through the bowel wall to fresh bleeding in distal duodenum to that of an adherent clot or extrinsic compression by a pulsating mass with a suture line protruding into the duodenum.13   Less than 40% of patients have signs of active bleeding at OGD.8 Conventional CT with contrast is widely available and most commonly performed to diagnose AEFs. Perigraft extravasation of contrast is a pathognomic  sign of AEF and this may be associated with signs of graft infection i.e perigraft fluid and soft tissue thickening along with gas.12 Multi-detector CT and MRI are more sensitive diagnostic imaging tools with MRI now being used mainly in patients with renal failure to avoid the use of contrast.12
 
PAEFs can be treated with endovascular stent placement in selected cases especially in those who cannot tolerate emergency surgery.12 The treatment of choice in SAEFs is graft resection and establishment of an extra-anastomotic circulation with repair of the duodenal wall although overall survival rates vary from 30% to 70%.13
 
Conclusion
 
SAEFs are a catastrophic complication of aortic surgery. AEFs are relatively rare and need a high index of suspicion in the appropriate clinical situation in order to diagnose this condition. Left untreated they are universally fatal. Surgical repair carries a very high mortality.
 

Competing Interests
None declared
Author Details
Louise MacDougall, John Painter, Suvadip Chatterjee, Department of Gastroenterology, Sunderland Royal Hospital. United Kingdom. Terry Featherstone, Department of Radiology, Sunderland Royal Hospital. United Kingdom. Claus Overbeck, Department of Vascular Surgery, Sunderland Royal Hospital. United Kingdom. Shyju Paremal, Department of Medicine, Sunderland Royal Hospital. United Kingdom.
CORRESSPONDENCE: Dr Suvadip Chatterjee, MRCP(UK), MRCP(Ireland), MD, Specialist Registrar in Gastroenterology. Sunderland Royal Hospital. Kayll Road. Sunderland, SR4 7TP
Email: suvadip_chatterjee@yahoo.com

References

1.Ihama Y, Miyazaki T, Fuke C, Ihama Y, Matayoshi R, Kohatsu H, Kinjo F. An autopsy case of a primary aortoenteric fistula: a pitfall of the endoscopic diagnosis. World Journal of Gastroenterology 2008 August 7; 14(29):4701-4704.
2.Asfoor A M A, Nair G R. Secondary Aorto-duodenal fistulas. Bahrain Medical Bulletin Vol29, No 2,June 2007 : 1- 6.
3. Saers SJ, Scheltinga MR. Primary aortoenteric fistula.Br J Surg 2005;92:143 – 152.
4.Mohammadzade M A, Akbar H M. Secondary Aortoenteric fistula. Medscape General Medicine.2007; 9(3):25: 1-4.
5.Elliot JP, Smith RF, Sizlagyi DE. Aorto-enteric and paraprosthetic enteric fistula. Problems of diagnosis and management. Arch of Surg.1974;108:479.
6. Bastounis E, Papalambros E, MermingasV, Maltezos C, Diamantis T, Balsa P. Secondary aortoduodenal fistulae. J Cardiovasc Surg. 1997; 38: 457 – 464.
7.Shindo S, Tada Y, Sato O, et al. A case of aortoenteric fistula occurring 27 years after aorto-femoral bypass surgery, treated successfully by surgical management. Surg Today.1993;23: 993-997.
8.Busuttil SJ, Goldstone J. Diagnosis and management of aortoenteric fistulas. Semin Vasc Surg. 2001;14: 302 – 311.
9.Bussetil RW,Reese W,Baker JD,et al.Pathogenesis of aortoduodenal fistula, experimental and clinical correlates. Surgery. 1979;85:1-12.
10. Rosenthal D, Deterling Jr RA, O’Donnel Jr TF, et al. Positive blood culture as an aid in the diagnosis of secondary aortoenteric fistula. Arch Surg. 1979;114: 1041 -4.
11. Lau H, Chew DK, Gembarowicz RM, Makrauer FL, Conte M. Secondary aortoduodenal fistula. Surgery. 2001;130: 526-527.
12. Odemis B, Basar O, Ertugul I, Ibis M, Yuksel I, Ulcar E ,Arda K. Detection of an aorto-enteric fistula in a patient with intermittent bleeding. Nature Clinical Practice Gastroenterology and Hepatology.2008 (5):226 – 230.
13. Champion MC, Sullivan SN, Coles JC, Goldbach M, Watson WC. Aortoenteric fistula. Incidence, presentation, recognition and management. Ann Surg 1982(3): Vol 195; 314-317.


Sudden Death in a Patient with Left Atrial Myxoma: Report of two cases and review of literature

Kalgi Modi, Prasanna Venkatesh, Sujata Agnani, Tanya Rowland and Pratap Reddy

Cite this article as: BJMP 2010;3(2):318
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Abstract
Sudden death is known to occur in patients with primary cardiac tumours; however it is rare and is estimated to constitute 0.005% of all sudden deaths. We report here two cases of sudden death that occurred in patients with left atrial myxoma. We also present a brief review of available literature on this subject.

 

Case 1
 
A 55 year old white male with a history of hypertension, hyperlipidemia, smoking and transient ischaemic attacks was admitted to the hospital with worsening dyspneoa on exertion over a period of 6 weeks. He also reported significant weight loss, loss of appetite and fatigue over several weeks. Physical examination revealed tachycardia, and moderate respiratory distress with prominent jugular venous distention. Cardiac auscultation revealed normal S1 and loud P2. Also heard were an early diastolic heart sound ( tumour plop) and a mid-diastolic murmur at the apex. An ECG revealed evidence of left ventricular hypertrophy with repolarization abnormalities. A transthoracic echocardiogram (Figures 1 and  2) revealed a large, pedunculated, mobile left atrial mass measuring 3x4 cm, impinging on the mitral orifice with a mean gradient across the mitral valve of 15 mm Hg. Left ventricular systolic function was normal.

Figure 1: Parasternal long axis echocardiograph of the left atrial myxoma prolapsing into the mitral valve   during diastole.
 
A diagnosis of probable left atrial myxoma was made. The patient had four episodes of syncope within 24 hrs, the first at 3: 53 am after returning from the bathroom,  subsequently leading to cardiac arrest at 14:20 pm.
 
Figure 2: parasternal long axis echocardiograph showing the large left atrial myxoma during systole.
 
He was intubated and initiated on vasopressors.  An emergent Left heart catheterization was performed prior to a referral for surgical excision, which revealed triple vessel coronary artery disease. During cardiac catheterization the patient became more hypotensive requiring an intra-aortic balloon pump.  While arrangements were made for a referral for surgery, the patient’s clinical condition deteriorated rapidly and he went into pulseless electrical activity at 18:54 pm and could not be resuscitated. The patient’s death was presumably due to persistent  intracardiac obstruction.  On autopsy, the left atrial mass was identified as a haemorrhagic left atrial myxoma, 5x4x3.5cm in size attached by a stalk to an inter-atrial septum. Multiple organizsing thrombi were present in the 1tumour. Histology showed abundant ground substance with stellate myxoma cells and haemosiderin-laden macrophages (Figures 3 and 4). The cause of death was attributed to valvular “ball-valve” obstruction.
 
Figure 3:  Histopathology of left atrial myxoma showing spindle shaped myxoma cells (white arrow) in a myxoid matrix (black arrow) and blood vessels (top arrow) (H & E 40X)
 
Figure 4: Histopathology of left atrial myxoma showing vascular spaces filled with relatively fresh blood and evidence of old bleeding (hemosiderin) suggesting repeated episodes of hemorrhage within the myxoma (H & E 4X)
 
Case 2
 
A 57 year old African American female presented with recurrent syncopal episodes and dyspnea on exertion, orthopnea, leg swelling, abdominal distention, loss of appetite and fatigue for the preceding nine months. Physical examination revealed jugular venous distention, a displaced apical cardiac impulse, a parasternal heave, and a loud S2. Also detected were  a pan-systolic murmur at the lower left sternal border, an early diastolic heart sound with a mid diastolic murmur at the apex, bibasilar crackles, ascites, and oedema up to the thighs.
 
Significant laboratory values were a total bilirubin of 1.6 mg/dl, and B- Type Natriuretic Peptide of 1323 pg/ml. A chest x-ray revealed an enlarged cardiac silhouette, right lung atelectasis and effusion. An ECG revealed left atrial and right ventricular enlargement.
 
The patient was admitted with the diagnosis of new onset congestive heart failure and was treated with intravenous lasix, and fosinopril. A 2-D Echocardiogram revealed a large mass suggestive of myxoma in the left atrium measuring 4.5 x 7.5 cm, occupying the entire left atrium protruding through the mitral valve into the left ventricle (Figure 5) .
 
Figure 5: Apical four chamber echocardiograph of the left atrial myxoma prolapsing into the mitral valve   during diastole.
 
This mass was obstructing flow with a mean trans mitral gradient of 17 mm Hg, with a reduced stroke volume and severe pulmonary hypertension with an estimated Right Ventricular systolic pressure of 120 mm hg.  A presumptive diagnosis of left atrial myxoma was made and the patient was scheduled for its surgical removal the following morning. The patient was transferred to the intensive care unit for closer monitoring; and fosinopril and lasix were discontinued. At about 22:30 hours that night patient was noted to be hypotensive with systolic blood pressure of around 80mm Hg. The patient was treated with normal saline and concentrated albumin. She then developed acute respiratory distress at 23:00 hours requiring intubation and ventilator support. Intravenous dobutamine, dopamine and later norepinephrine were added for continued hypotension. The patient went into pulseless electrical activity, she was successfully coded with a return of her pulse but continued to be hypotensive. Cardiothoracic surgery decided not to take the patient for emergency surgery due to her unstable haemodynamic condition. The patient’s family was notified of the poor prognosis and the decision was made not to resuscitate her if her condition deteriorated further. The patient ultimately became bradycardic and went into asystole at 5: 30 am. An autopsy was not performed. The cause of death was attributed to large left atrial myxoma causing valvular obstruction and cardiovascular collapse.
 
Discussion
 
These two cases illustrate an uncommon, malignant course of a left atrial myxoma with rapid progression of symptoms which proved fatal.  The most common primary tumour of the heart is myxoma accounting for 40-50% of primary cardiac tumours(2,3) .Nearly 90% of myxomas occur in the left atrium(3) .In over 50% of patients,  left atrial myxoma causes symptoms of mitral stenosis or obstruction. Systemic embolic phenomena are known to occur in 30-40% of patients(3) .
 
Table 1. Summary of 17 published cases of sudden cardiac death associated with cardiac myxoma in adults (1950-2008)
Author/Reference
Year
No
Age
Gender
Symptoms
Interval Between Symptoms To Scd
Size Of Myxoma In Cm
Autopsy
Vassiliadis (8)
1997
1
17
M
Dizziness
3 months
6
yes
McAllister (10)
1978
5
40 to60
NA
NA
NA
5 to 6
yes
Cina (2)
1996
6
Below 40
NA
Embolic, syncope
16.6 months
5.7
yes
Puff (9)
1986
1
41
M
Syncope,
months
1.5
yes
Puff (9)
1986
1
19
F
Syncope
6 months
3
yes
Maruyama (7)
1999
1
20
M
Dizziness
1 day
8
None, Patient survived SCD; Myxoma resected
Turkman (6)
2007
1
73
M
DOE
months
8
yes
Ito (13)
1987
1
28
M
Syncope
7 days
NA
yes
NA: not available 

Constitutional symptoms reported in approximately 20% of patients include myalgia, muscle weakness, athralgia, fever, fatigue, and weight loss. Around 20% of cardiac  myxomas are asymptomatic (3) .Severe dizziness/syncope is experienced by approximately 20% of patients due to obstruction of the mitral valve. (4) Of all the symptoms associated with cardiac myxomas, syncope is one of the most ominous prognostic indicators.

 
Although sudden death is known to occur in patients with primary cardiac tumour it is rare and is estimated to constitute 0.01 to 0.005% of all sudden deaths (1). Association between sudden death and cardiac myxoma has been reported as early as 1953 by Madonia et al (5). A review of the literature on this subject between 1950 to2008 revealed 17 cases of sudden death attributed to cardiac myxoma in adults (1, 6, 7, 8, 9, 10, 13) (Table 1) .
 
In all patients with unexpected death syncope was a predominant presenting symptom and their age ranged from seventeen to seventy three. The majority of patients with sudden death were men even though the tumour is more common in women. The size of the tumour did not influence clinical presentation and in some reports of sudden cardiac death tumour was as small as 1.5 cm and without previous symptoms (3). Sudden death in myxoma is attributed to either severe acute disturbance in cardiac haemodynamics from cardiac obstruction (ball-valve syndrome) or to coronary embolization from the tumour. The latter is probably responsible for sudden death in patients with very small tumours. In the study of Alverez Sabin et al (11) the initial neurological manifestation was Transient Ischemic Attack (TIA), but in none of the patients’ was a diagnosis of myxoma made because of the initial neurological symptom. Even though cardiac myxomas are a rare cause of TIA and syncope, it is important to consider cardiac myxoma in the differential diagnosis of any patient with a TIA or syncope (11). The patients presented here had a TIA and recurrent syncope placing them at high risk for sudden death.
 
The timing of surgical excision of myxoma is not clear and it is not unusual for patients to die or experience a major complication while awaiting surgery (2, 12). Intraaortic balloon pump (IABP) use has been described in one case of left atrial myxoma and life-threatening cardiogenic shock with favorable outcome(14) .As illustrated by the cases presented here it is essential that surgery be performed urgently once it has been identified that a patient has a myxoma that is large enough to cause complete intracardiac obstruction.
 

Acknowledgements
David Baldwin, Marlissa Curtis, Mike Yates and Baryl Cowthran for images IRB approved
Competing Interests
None Declared
Author Details
Kalgi Modi MD, FACC, Prasanna Venkatesh MD, Sujata Agnani MD, Tanya Rowland MD, Pratap Reddy MD, FACC, Department of Medicine, Section of Cardiology, Louisiana State University Health Science Center.
CORRESSPONDENCE: Kalgi Modi MD, FACC, 1501 Kings Highway Shreveport, LA 71106
Email: kmodi@lsuhsc.edu

References

1. Cina SJ, Smialek JE,  Burke AP, et al . Primary cardiac tumors causing sudden death: a review of the literature. American Journal of Forensic Medicine & Pathology. 1996; 17(4):271-81.
2 Reynen, K, M.D. Cardiac Myxoma NEJM. 1995; 14:1610 -16176.
3. Burke A, Jeudy J, Virmani R, Cardiac Tumors: an update. Heart. 2008; 94: 117-123
4. Kapoor MC, Singh S, Sharma S, Resuscitation of a patient with giant left atrial myxoma after cardiac arrest. Journal of cardiothoracic and vascular anesthesia. 2004; 18:769-771
5. Madonia, PF, Boggiano R, Gubner, R, Ball Valve Syndrome caused by primary cardiac tumor. NY State J Med. 1953; 53:3043-3044
6. Turkmen N. Eren B. Fedakar R. Comunoglu N. An unusual cause of sudden death: cardiac myxoma. Advances in Therapy. 2007; 24(3):529-32 .
7. Maruyama T. Chino C. Kobayashi T. Ohta K. Kono T. Nakano H. A survivor of near sudden death caused by giant left atrial myxoma. Journal of Emergency Medicine. 1999; 17 (6):1003-6.
8. Vassiliadis N. Vassiliadis K. Karkavelas G. Sudden death due to cardiac myxoma. Medicine, Science & the Law. 1997; 37(1):76-8.
9. Puff M. Taff ML. Spitz WU. Eckert WG. Syncope and sudden death caused by mitravalve myxomas. American Journal of Forensic Medicine & Pathology. 1986; 7(1):84-6.
10. McAllister HA, Fenoglio JJ, Tumors of the Cardiovascular System, second series, 1978; fascicle 15: page 5-20
11 J.Alvarez Sabin, M. Lozano, J. Sastre-Garriga, J. Montoyo, M. Murtra, S. Abilleira, Transient Ischemic Attack: A Common Initial Manifestation of Cardiac Myxomas Eur Neurol 2001;45:165-170
12. Braunwald’s Heart Disease, A Textbook of Cardiovascular Medicine, 7th edition, pp    1745
13. Ito Y, Tsuda R, Hara M. An Autopsy case of sudden death from Left atrial myxoma Nihon Hoigaku Zasshi 1987; 41(4): 369-373.
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A Cross-Sectional Study of Men with Genital Piercings

LaMicha Hogan, Katherine Rinard, Cathy Young, Alden E. Roberts, Myrna L. Armstrong and Thomas Nelius

Cite this article as: BJMP 2010;3(2):315
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Abstract

Purpose: More men with genital piercings (GP) are presenting to health care facilities, yet a paucity of medical literature exists about their body modifications, health issues, and medical needs. Historically, they have turned to a piercer or the internet for medical advice which may put their health at risk by receiving inappropriate guidance or delayed treatment by an experienced, well-informed clinician. 

Methods: A comparative, descriptive cross-sectional study was conducted using an 83 item web-based survey.Demographics, risk behaviours, procedural motives, and post-piercing experiences about men with GP were examined, as well as depression, abuse, self-esteem, and need for uniqueness. Similarly published studies were also compared.
Results: 445 men from 42 states and 26 international sites reported 656 genital piercings. The average participant was 36 years of age, Caucasian, possessing some college education, married or in a monogamous, heterosexual relationships, and in excellent health. Deliberate decision-making was present: 36% chose a Frenum/Frenum Ladder GP and 56% chose a Prince Albert GP, with 25% experiencing urinary flow changes. Outcomes were related to their motives: sexual expression, uniqueness, and aesthetics, with improvement of personal and partner’s sexual pleasure.   
Conclusions: Several unsubstantiated assumptions about men with GP were challenged regarding the amount of STDs, GP complications, and overall demographics. Currently their GP care information is still obtained from a piercer or the internet. Clinician awareness of GP is important to educate and inform adequately, give professional advice, and provide a realistic picture of structural complications.
Keywords:  male genital piercings, need for uniqueness, self-esteem, depression
Abbreviations: STD= sexually transmitted disease; GP = genital piercings

 

INTRODUCTION
 
Humans have always been interested in altering their body. Whether through piercings or tattoos, for aesthetics, religious reasons, or self-expression, the practice of body modification is a well known art.1 One not as familiar or easily observed body modification type is genital piercings. Genital piercings (GP) are defined as developing a tract under the skin with a large bore needle to create an opening into the anatomical region for decorative ornaments such as jewelry.2-3 Historically, GPs are not a new procedure. 
 
Currently, this once taboo practice is on the rise and more men with GP are presenting with a variety of medical needs to clinics and hospitals.3 From the rare Pubic Piercing (a piercing through the dorsal base of the penis) to the Guiche (a piercing through the perineum), the male genitalia provides ample area to pierce. Men commonly choose from nine different types of GP and often use three major types of piercing jewellery (Figure 1).3-6
 
Figure 1 Common Types of Genital Piercings (GP) Worn by Men
Illustrations by Larry Starr, Senior Design Specialist Texas Tech University Health Sciences Center. Text modified with permission:   Urologic Nursing 2006, 26(3), 175-176.
 
This rapid growth trend is creating its own set of complications and questions among clinicians. The medical literature suggests the most common risks are infection and bleeding, but there are other structural considerations as well.3-4, 6-8 An example of this is with the most widely known and commonly encountered male GP, the Prince Albert; the jewellery pierces the urethral meatus, exiting through the ventral surface of the penis.  The piercing effectively creates a fistula for urine to drain, and many men report experiencing the need to sit down during urination due to the change in stream and difficulty in aiming.3,4 Other reported single case histories of more severe complications are Fournier’s gangrene, urethral tears, priapism, post-coital bleeding or lost jewellery in female partners, paraphimosis, and recurrent sexually transmitted diseases.8-20
 
Given the variety of negative issues that could arise from GP, any subject related to the health and well being of men having an intimate piercing should be directed to a well informed clinician. Currently, when questions or problems arise, men are more likely to seek assistance from the internet or a piercer rather than a health care provider.3,21-22 Considering the limited medical literature, as well as the minimal availability of clinicians knowledgeable about body piercings and modifications, men with GP are at high risk for delays in appropriate treatment of complications related to piercings as well as for overall preventive healthcare. Over concentration on the presence of GP by clinicians could delay important health care.23
 
Our purpose for this study was to elucidate information about men with GP in order to aid the clinician in providing relevant information for patients considering GP, as well as to provide further scientific evidence by examining their demographics, risk behaviours, procedural motives and post-piercing experiences. Additionally, several motives or characteristics of those with body art such as depression, abuse, self-esteem, and need for uniqueness were examined.24-29 Authors of this study have experience in urology, various aspects of piercing, and two decades of published body art research. 
 
Problems in attempting any study about those with GP is reaching a sizeable sample for a study and an acceptable data collection methodology as those with GP have a hidden variable of study, making it difficult to make contact. Networking or “snowball” sampling for data collection, as well as anonymous questionnaires, becomes one approach,30 but this also makes it difficult to validate if respondents actually have GP. In an effort to address this issue, survey questions were specifically written for individuals with GP, making it extremely difficult and time-consuming to answer if the respondents did not have applicable experiences. Previous research experience also indicates that after about 10-15 questions, interest can wane and the questionnaire will not be completed.3,7,31  
 
Only two published studies could be located to provide preliminary information about individuals with GP.21,22 In the first study21 data, collected in 2000 and actually published in 2005 had a national convenience sample of 63 women and 83 men with nipple and/or GP. Forty-eight men in the study had GP; the average man was 31 years of age, single, heterosexual, Caucasian, in good-excellent health, who sought out annual physicals, possessed some college education, and spoke of moderately strong religious faith. Almost all were employed, reporting an average annual salary of $36,000, or higher. Over half admitted and continued their belief they were risk takers; many of them also had 3 or more general body piercings. Most did not smoke or use drugs routinely and in this study, no questions about alcohol use were asked. Their average age at first sexual intercourse was 15.7 (the national male average is 16.9).32   Of those that participated (37%) in sport activities or exercise, they reported with no problems. They voiced minimal, if any, regrets to obtaining a genital piercing and would repeat the procedure. The Prince Albert was the most common male GP. Few (12%) voiced any problems with their GP, with urinary flow changes and site hypersensitivity being the most frequently mentioned. Six participants stated partners had refused sexual intercourse with them after their GP. One case of STD (Gonorrhoea) was reported post-procedurally.
 
In 2008, data were collected for a second study involving women with GP.22 This time the collection methodology took advantage of young adults highly routine usage of the world-wide internet and combined this with a successful, accessible networking sampling software entitled SurveyMonkey© (Portland, OR). The average woman with GP participant in the 2008 study (N = 240) was 32 years of age, Caucasian, heterosexual, married, in excellent health, who sought out annual physicals, participated in athletic activities, had an Undergraduate or Graduate Degree, reported few other friends with GP, and had 3 or more general body piercings. Their average age at first sexual intercourse was 15.9 (the national female average is 17.4).32 Many of the women reported themselves as risk takers and most believed they continue to have those ideas. Most did not smoke or use drugs routinely and their alcohol intake was infrequent, but when they consumed alcohol, they reported consuming 5+ consecutive drinks. They voiced minimal, if any, regrets to obtaining a genital piercing and reported that they would repeat the procedure. Only a few cited any problems, with site sensitivity as the most frequently mentioned health problem. No bleeding, rips, tears, or STDs were reported following their GP and no one had refused sexual intercourse with them.    Additionally, an adjoining survey of 60 health care providers (physicians, registered nurses, midwives) who had previously cared for women with GP were queried; their viewpoints regarding women with GP and STDs, GP complications, and general concerns produced no major deviations of data from what was previously described.22
 
METHODS
 
Design
 
As the internet survey demonstrated marked success in reaching those with GP, a similar study was undertaken to query a larger cohort of men with GP to increase clinician awareness in caring for men with GP. Thus, a cross-sectional descriptive study of men with GP was conducted so the collected information could be compared with the previously mentioned studies of those with GP.21,22   To ensure that the rights and dignity of all research participants were protected, exempt study status was obtained for this study from the university institutional review board. Notices of the study and a request for participation were posted on a number of popular body piercing sites with the assistance of an internationally-known Expert Piercer. The survey was available on the web for a total of 6 months during late 2008 and early 2009.
 
Questionnaire
 
Questionnaire items were based on a review of literature, the Armstrong Team Piercing Attitude Survey,31 previous work examining women with GP, 3,21-22, 33 and recent findings about those with body art. 24-29  The study purpose and benefits were presented on the front page of the survey. The subjects were informed that completion of the survey indicated their consent to participate in the study and that they could stop at any point during the survey if they were uncomfortable with a question (s). Ethnicity was included to note GP acquisition patterns; the ethnic categories were not defined and participants self-reported. Assurances were provided that the information would be analyzed as group data and no identifying information would be sought. Respondents were encouraged to answer questions honestly and not to be offended by any questions as some of them directly related to unsubstantiated assumptions written about GP in the medical literature. 21-22 There was no ability to tabulate how many individuals viewed the survey if they did not start the survey.
 
The survey had 4 sections: (a) Obtaining the GP (13 questions); (b) Personal experiences with the GP (32 questions); (c) General information including depression and abuse (26 questions), and (d) Sexual behaviour including forced sexual activity (12 questions). Four scales were also included: motives (14), outcomes (16), pre and post procedural self-esteem (16), and need for uniqueness (4). The previous reliabilities for the motive scale was 0.75,22 outcome scale 0.88,22 and need for uniqueness scale was 0.80;25 data was not available for the self-esteem scale.34   Various response formats were used throughout the survey such as a 5 point Likert scale (1 = strongly disagree or unlikely to 5 = strongly agree or likely), multiple choice, and short answers.
 
Data Analysis
 
The Statistical Package for the Social Sciences (16.0 Ed.) was used for data analysis to obtain frequencies, cross-tabulation, and chi-square analysis.30 Additionally, T-tests were used to compare means of similar questions from both the 2005 and 2008 studies with data from the current study. Significant differences were found in both study samples so they were judged as different groups from this current study. 
 
RESULTS
 
Study Population
 
While 545 respondents started the survey, responses were analyzed from 445 men with GP (82%) residing in 42 states and 26 international countries; they declared a total of 656 piercings. Clusters of participants were evident from CA (22), NY (17), TX (16), FL (11), Europe (43), Canada (21), and Australia (20). Ages of the men with GP at survey time ranged from 15 to 72 (Table 1). The average participant in this study was 36 years of age, Caucasian, some college education, married, in excellent health, who sought out annual physicals, reported no/few friends with GPs, and declared a salary of $45,000 or higher. Religious beliefs were grouped into either non-existent or moderately to very strong faith. There was almost equal numbers of blue collar and white collar workers: others were from health care, arts, academia or military, while some were self-employed; very few mentioned unemployment, or retirement.
 
Table 1 Self-Reported Characteristics Of Men with Genital Piercings (GPs) continued
Demographics
Current Study* N = 445
Age at time of survey
   20 or <
   21-35
   36-50
   51+
 
61/29%
77/36%
41/19%
33/16%
Ethnicity
   Caucasian
 
319/89%
Martial Status
   Single
   Living/significant other
   Married with/out children
 
96/27%
69/20
143/41%
Education
 High school Diploma
 Some college
 Bachelor’s degree
 Graduate/Doctoral degree
 
34/10%
113/32%
77/22%
88/20%
Occupations
 Technical/vocational
 Professional 
 Students
 Artists
 
90/28%
92/29%
44/14%
23/07%
Salary
 <45,000
 $45,000+
 
135/44%
169/56%
Strength/Religious Faith
 Non-existent
 Mod Strong-Strong
 
135/39%
99/28%
State of Health
 Excellent
 
310/88%
Health care visits
 Annual physicals
 Only when problems
 
150/43%
142/40%
Close friends w/GPs
 None
 1-3
 4+
 
239/68%
100/28%
14/ 4%
Feel sad/depressed
Little/Some
   Pre-piercing
   Post-piercing
 
 
248/57%
210/59%
*Numbers will not always add up to 100 because of missing data or multiple answers. 
 
Risk Behaviours
Those who reported pre-procedural risk taking tendencies continued to have significant tendencies for them post-procedurally (χ2 = 2.13) = 16; p = 0.000) (Table 2). Some risky behavior was observed; over half had body art, with an average of 2 piercings or more, as well as tattoos. Alcohol use was infrequent, but when they did, they had 5+ drinks. Other answers did not bear out the risk taker image with their monogamous, heterosexual relationships, limited tobacco, and drugs. Their average age at first intercourse was 17.05 (national male average 16.9).32 Most (391/88%) did not report STDs before their piercings, but of those that did itemize their STDs, Chlamydia was the most frequently mentioned (n =18).
 
Table 2   Self-Reported Risk Behavior From Men with Genital Piercings (GPs)
Risk Behaviour
Current Study* N = 445
Age at first intercourse
 Never had intercourse
 12 or less
 13-15
 16-18
 19+
  
12/03%
14/04%
80/25%
160/48%
74 /23%        
Sexual Orientation
 Women
 
286/82%
Risk Taker Before Piercing
222/52%
Remains Risk Taker
198/52%
Cigarettes Smoked
 None
 ½-1 pack daily
 
252/75%
75/22%
Monthly Alcohol Consumption
 1-3 times
 5+ drinks @ one setting, 1-3x
 
118/33%
191/55%
Drugs Used monthly
 None
1-15 times
 
294/87%
27/08%
Sexual Partners in 6 months
 One
 Two or more
 
211/62%
98/32%
General body piercings
 None
 1-4 piercings
 5+ piercings
 
119/27%
259/59%
108/33%
Tattoos
 None
 1-4
 5+
 
115/35%
134/38%
76/21%
STDs before piercing
54/12%

*Numbers will not always add up to 100 because of missing data or multiple answers.

 

Genital Piercing Procedure
 
A deliberate time delay between their consideration to making the decision to have a GP was present as many had waited almost 5 years before procurement (Table 3). Over half reported the Prince Albert GP, with another third choosing a Frenum/Frenum Ladder (Figure 1). While a small-moderate amount of pain and bleeding was reported procedurally, virtually no drugs or alcohol were used before their GP.  
 
Table 3   Self-Reported Procedural Information From Men with Genital Piercings (GPs)
Genital piercing procedure
Current Study* N = 445
Amt of decision time
Waited long time, then a few minutes
 A long time (over a year)
 
49/24%
143/37%
Age of GP Decisions
 Consideration
 Procurement
 
29 years
34 years
Type of Genital Piercings        
 Ampallang
 Apadavya
 Dydoe
 Foreskin
 Frenum/Frenum ladder
 Guiche
 Hafada
 Prince Albert
 Other
 
35 08%
46/10%
27/06%
27/06%
160/36%
32/07%
43/10%
248/56%
38/09%
No Drug/alcohol at piercing
364/94%
Small-mod amt of pain
292/75%
Small-mod amt of bleeding
274/71

*Numbers will not always add up to 100 because of missing data or multiple answers.

 

Motives and Outcomes
 
Table 4 illustrates participant motives and outcomes for each group in the various GP studies.21,22 For the highest motive response of “just wanted one” there was consistency over the three studies; of the top five responses, they were similar but just ranked differently. Alpha measurements for the motive response scale ranged from 0.40 to 0. 75 except for our current study, where the covariance matrix was zero or approximately zero so the statistics based on its inverse matrix could not be computed. Motives centered around wanting a GP, trying something new, have more functional sexual control, and seeking uniqueness. Measureable outcomes (Alpha range 0.88-0.89) of their GP evolved around their sexual expression, uniqueness, and aesthetics, as well as the improvement of their personal and partner’s sexual pleasure. In review, their motives for the GP were met in their stated outcomes.   
 
Table 4   A Three Study Comparison Of Self-Reported Motives and Outcomes From Those Wearing Genital Piercings.
Variable
Caliendo et al, 2005 Study:
Data Collected 2000
Men with GPs N = 48*
Young, et al, 2010 Study
Data collected 2008
Women with GPs N = 240*
Current Study
Data collected 2009
Men with GPs N = 445*
Motives for their genital piercing
34/71% “Just wanted one”
24/50% “Trying to feel sexier”
23/45% “For the heck of it”
18/38% “Wanted to be different”
18/38% “Make myself more attractive”
(alpha 0.40)
163/70% “Just wanted one”
120/51% “Trying to feel sexier”
111/48% “More control over my body”
 93/40% “Seeking uniqueness”
 91/39% “Make myself more attractive”
(alpha 0.75)
196/90% “Just wanted one”
73/60% “For the heck of it”
 67/60% “Trying to feel sexier”
 56/58% “More control over body”
 51/56% “Seeking uniqueness”
(alpha unobtainable)
Outcomes of their genital piercing
36/77% “Improved my sexual pleasure”
35/73% “Helped express myself sexually”
35/73% “Helped me feel unique”
29/62% “Improved partner’s sexual pleasure”
27/56% “Helped express myself” (alpha 0.89)
176/76% “Helped express myself sexually
173/75% “Improved my sexual pleasure
157/68% “Helped me express myself
134/58% “Helped me feel feminine”
134/58% “Helped me feel unique”
(alpha 0.88)
278/81% “Improved my sexual pleasure
234/71% “Helped express myself sexually”
218/67% “Helped me feel unique”
229/67% “Improved partners sexual pleasure
211/64% “Helped genital look better”
(alpha 0.88)

*Numbers will not always add up to 100 because of missing data or multiple answers.

 

Post-piercing Experiences

 
The men reported continued satisfaction with their GP and would repeat the procedure. While not many were engaged in exercise/sport activities, those that did, were active (Table 5). A few reported partner refusal of sexual activities when their GP was in place.   Almost half reported no piercing complications; of those that did, only 2 major problems were cited. First, with over half reporting Prince Albert piercings, it was not surprising that 25% discussed changes in their urinary flow. Site hypersensitivity was the second most reported problem (23%), otherwise there were no further trends of other severe complications. While 80 (18%) reported STDs after their GP, only 19 itemized the specific type: the most responses were Chlamydia (9). Those that had a history of STDs (Table 2 & 5) before their piercings were significantly more likely to have them post-procedurally (χ2 = 11.5) = 1; p = 0.001).   
 
Table 5 Self-Reported Post Procedural Information From Men with Genital Piercings (GPs)
Post Procedural Experiences
Current Study* N = 445
Have had partners refuse sex
38/10%
**Reported STDs since piercing
80/18%
Still like genital piercing
334/87%
Would do it again
358/93%
Sports/exercise involvement
 None
 Jog/ride bike/exercise, etc
 
366/82% 
79/18%
Complications from piercing
  No problems
   Change in urinary flow
   Site hypersensitivity
   Skin irritation
   Rips/tears at site
   Problems using condoms
   Keloids @ site
   Site infection
   Urinary tract infection
   Site hyposensitivity
   Sexual problems
   Jewellery embedded
   Erection problems
   Other, not named
 
209/47%
109/25%
101/23%
30/07%
30/07%
24/05%
16/04%
11/03%
7/02%
70/2%
401%
4/01%
4/01%
18/04%
*Numbers will not always add up to 100 because of missing data or multiple answers.
 
Depression, Abuse, Self-Esteem, and Need for Uniqueness
 
Four additional characteristics about individuals with GP were examined.24-29 Men with GP respondents reported a small amount of “sad or depressed feelings”; those that had these depressed feelings before their piercings were significantly more likely to continue these depressed feelings post-procedurally 2 = 4.1), = 16; p = 0.00). Only 5 (1%) reported being forced to participate in sexual activity against their will, while a few cited (56/12%) physical, emotional, or sexual abuse.  
 
To extract a profile of self-esteem, 8 questions were asked in the pre and post piercing survey sections; internal consistency (Cronbach alpha) of both scales was 0.75. Their responses to both the pre procedure (M = 22.3, SD = 4.51) and the post piercing time (M = 23.1, SD = 3.97) was highly correlated at 0.79 (P<0.01). Two statements triggered split, negative and positive responses with “I make demands on myself that I would make on others” and “I blame myself when things do not work the way I expected.” Lastly, their Need for Uniqueness (NU) was asked using a four item scale24,25  in the pre-piercing survey section. When all five responses of the scale were totaled (20), the mean was 11.3 documenting a more positive perspective about their GP, close to the moderate level (Cronbach alpha 0.86), for intentionally wanting to be different, distinctive, and unique. When asked if their overall feelings of NU had changed since obtaining their GPs, those that had NU before their piercings were significantly more likely to have them post-procedurally (χ2 = 11.5) = 16; p = 0.03).  
 
DISCUSSION
 
When examining this data from men with GP alongside the 2005 published study,21 the cohort almost equalled 500 participants. To our knowledge this is the largest repository of data currently available to provide further evidence of the demographics and health issues regarding men with GP. The anonymous data, obtained by networking sampling and accessible, economical web-based survey, could be viewed as a study limitation. Yet, finding similarities between this data and data collected almost ten years ago suggests that our findings tapped into a core body of knowledge about men with GP. Similar data, obtained at different times, from different respondents increases the credibility and lends the information to further generalizability to influence use in practice.30
 
The “social reality” 2 of the GP phenomenon is here. All of the men had one type of GP, and some had multiple GP, and many had other general body piercings.35 Awareness of the current types of body modification including GP will help the clinician educate and inform adequately, to give professional advice, and also provide a realistic picture of structural considerations. Respondents stated their GP were an important and satisfying part of their life, they still liked them, and would repeat the procedure; the GP improved their sexual activities, few refused sexual intercourse, those that exercised were active, and they were not troubled by the GP complications. From a medical standpoint the insertion of a GP could be considered a minor surgical procedure, and yet the data suggests that when the GP is performed by experienced hands only minimal side effects are reported. Thus, finding a knowledgeable, expert piercer is an important educational theme. However, patients need to also be aware that certain types of piercing may require some behavioral changes such as toileting and consistent body cleaning. Unfortunately virtually no health care providers, including clinicians, were mentioned in the GP decision making process or care, they usually went to the internet or returned to a piercer for information.21,22  Hopefully, as more clinicians are made aware of GPs, those who are considering GP will find their physician to be a helpful and more informative resource.
 
These study participants with GP were older, well-educated men, often in a stable relationship, different than what is usually thought about people with body piercings.7, 22,26-27,29,31 This scientific evidence about their overall demographics pose challenges to the current medical literature. Sample demographics from this study and the other two cited GP studies 21,22 do not reflect individuals from stereotypical low performing social and economical backgrounds.   Demographically, the people with GP were in their early thirties, Caucasian, heterosexual, well educated, employed, in good health, with some religious beliefs, but not ethnically diverse. In contrast to literature describing men with GP as antisocial miscreants or mostly homosexual, 2,4,18 our data support that these men are more part of the mainstream culture. The avoidance of “rushing to judgment”28 is an important aspect, especially in the way they are often perceived. 
 
Men with GP did not deny their propensity to be risk takers, but being a risk taker was not synonymous with being deviant, but more with achieving individualization.21,28,31 Threads about stable relationships were provided throughout their information, including sexual orientation, marital status, GP complications, and even their lack of many risk behaviours. Their first time for sexual intercourse was close to the male national average. While procurement of any type of body art is thought to be impulsive 7,21-23, their time for GP decision-making was deliberate, as well as their practice of on-going, conscientious care of their piercings.21,22 Absence of alcohol and/or drug consumption before the GP procedure has been a frequent finding in other body art studies.7,21-22,31 Reputable piercing artists advocate for no use of alcohol and drugs as they want their customers to be making realistic procedural decisions about their GP and listening carefully to post GP care instructions.
 
The unsubstantiated assumptions in the literature about GP complications such as male infertility, scrotal infections, reduction of erotic stimulation, and frequent infections with bicycle rides were also challenged.6,21,36-40 Overall, only two problems of urinary flow changes and site hypersensitivity were reported with their GP. They took their sexual concerns seriously, as part of their internal influences of self esteem and their need for uniqueness. Their documented motives reflected sexual enhancement, aesthetics, as well as uniqueness. Their stated outcomes of the GPs reflected an ability to better express themselves sexually and create a sense of uniqueness; these elements obviously took precedence over the two problems of urinary flow changes and hypersensitivity. Both these motives and outcomes were similar when compared with the other two studies.21,22 Further procedural research is suggested to obtain more information about the reasons some with Prince Albert GP have urinary flow changes, while others do not, to eliminate this as a possible side-effect.  
 
Negative bias continues with the assumption that individuals with GP frequently have STDs.18-20, 36-40 Historically, concern for those who have “exotic adornments” such as body piercings have led some health facilities to require STD screening, no matter what the nature of the presenting complaint.22,35 Yet, in this study and the other two related GP studies,21,22 respondents reported only a few STDs. Their reporting incidence of STD was low compared to the national Guttmacher Institute report of one in three sexually active people will have contracted a STD by age 24.32   As in this study, Chlamydia remains the most highly reported STD in the US.32  While it is important to always conduct a thorough sexual history, 20 perhaps the conscientious care related to the deliberate decision for the GP,  and the mostly monogamous relationships reported may account for the limited reporting of STDs. One STD clinic study found that neither socioeconomic status, method of contraception, multiple partners, or the presence of genital infections correlated with GP.38   Further longitudinal research is suggested to examine the long-term effects of GPs, as well as further GP complications and STD prevalence.19    
 
Men, like women, with GP21 reported depressed feelings26,27,29 both pre and post procedure, but gender differences were present with abuse and forced sexual activity. The men with GP reported few incidents of abuse (emotional, physical, or sexual) or forced sexual activity against their will whereas over a third of the women with GP22 reported this.   Although women frequently spoke of their use of GPs to take more control in reclaiming their body to “free them from the bonds of molestation and give them strong feelings of empowerment,” 22   men verbalized their use of GPs to give them more sexual control. 
 
STUDY LIMITATIONS
 
As with any study, several limitations to generalizability of data must be considered and one of methodology has been previously discussed. This was a non experimental, descriptive study design and the respondents self-selected to complete a web-based survey. Bias, inaccurate recall, and/or inflation can result from self-reporting.30 Respondents had to use their personal judgment to interpret questions with the use of an anonymous survey so socially desirable responses could have been entered. Participants with strong negative or positive feelings may have been more likely to complete the survey. Yet, as random sampling is almost impossible in a population with hidden variables, and in spite of these limitations, the respondents did contribute further quantitative data.21,22  
 
CONCLUSIONS
 
The trend of those obtaining GP continues to increase and is not limited by age, gender, socio-economical backgrounds, or sexual preferences. Many in this study still reported seeking advice of a piercer or the internet. As an identified population at risk for quality health care, further evidence of demographics, piercings and jewellery, motivations, outcomes, and health issues were presented about men with GP so clinicians can provide clinically competent and applicable approaches for care. The collective data examined here, along with some collected almost ten years ago, begins to dispel some of the negative assumptions about this segment of the body modification population regarding their overall demographics, GP complications, and STD prevalence.

 

Acknowledgements
The authors acknowledge the support and manuscript reviews of Bernhard T. Mittemeyer, Elayne Angel, Jerome Koch, Joanna Guenther and Scott De Boer.
Competing Interests
Funding in part by the Texas Tech University Anita Thigpen Perry School of Nursing Research & Practice Committee.
Author Details
LAMICHA HOGAN MSN, RN, FNP-BC Clinical Instructor/Family Nurse Practitioner, Anita Thigpen Perry School of Nursing Texas Tech University Health Sciences Center 3601 4th Street, Lubbock, TX 79430 KATHERINE RINARD MD Department of Urology, School of Medicine, Texas Tech University Health Sciences Center 2601 4th, 3B163 Lubbock, TX 79430-7 CATHY YOUNG, DNSc, APRN, BC Family Nurse Practitioner, University of Texas, Arlington Student Services, Arlington TX ALDEN E ROBERTS Ph.D., Professor Department of Sociology, Anthropology, and Social Work Texas Tech University Lubbock, TX 79409 MYRNA L ARMSTRONG Ed.D., RN, FAAN Professor and Regional Dean, Anita Thigpen Perry School of Nursing Texas Tech University Health Sciences Center @ Highland Lakes 806 Steven Hawkins Parkway, Marble Falls, TX 78654 THOMAS NELIUS MD, Ph.D, Assistant Professor Department of Urology, School of Medicine Texas Tech University Health Sciences Center 2601 4th, 3B163 Lubbock, TX 79430
CORRESSPONDENCE: MYRNA L. ARMSTRONG Ed.D., RN, FAAN Professor and Regional Dean, Anita Thigpen Perry School of Nursing Texas Tech University Health Sciences Center, Highland Lakes, 806 Steven Hawkins Parkway, Marble Falls, TX 78654 tel. 830 798-9548; fax 830 798-8598 Cell 512 699-9150 THOMAS NELIUS MD, Ph.D, Assistant Professor Department of Urology, School of Medicine Texas Tech University Health Sciences Center 2601 4th, 3B163 Lubbock, TX 79430. Cell: 806 445-4999 fax 806 743-1335
Email: Myrna.armstrong@ttuhsc.edu, Thomas.nelius@ttuhsc.edu

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Dysphagia Lusoria presenting with Pill-induced Oesophagitis - A case report with review of literature

Malhotra A, Kottam RD and Spira RS

Cite this article as: BJMP 2010;3(2):312
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Abstract

Extrinsic oesophageal compression from vascular structures usually remains asymptomatic. Occurrence of dysphagia is an uncommon problem. We present a rare case of dysphagia lusoria from right sided aortic arch presenting as pill-induced oesophagitis caused by a testosterone pill. A thorough literature review on both the conditions is then presented to address pathogenesis, diagnosis, and management.

Keywords:  Dysphagia Lusoria, Pill-induced oesophagitis, drug-induced oesophagitis

Introduction

Oesophageal compression by a vascular structure resulting in dysphagia is uncommon. There have been multiple reports in the medical literature of almost every major vascular structure in the chest causing some degree of oesophageal compression and subsequent dysphagia(1, 2). In 1794, David Bayford, described a case of a 62 year-old lady having dysphagia due to an aberrant right subclavian artery. He coined the term “dysphagia lusus naturae”, which means “Freak of nature” (3).

Pill-induced esophagitis is associated with the ingestion of many pills and presents an uncommon cause of erosive oesophagitis (4). Multiple different classes of drugs have been described to be hazardous to the oesophageal mucosa and cause pill-induced oesophagitis (5, 6). Although uncommon in itself, dysphagia lusoria has not been described in literature to present as pill-induced oesophagitis. We present the first case of dysphagia lusoria causing pill-induced oesophagi's by testosterone pills in a young healthy man. Pubmed review of the English medical literature has been conducted to discuss the epidemiology, pathogenesis and management of this uncommon disorder.

Case Presentation:

A 26 year-old man with no significant past medical history presented with 5 days of dysphagia (for both solids and liquids), odynophagia and retrosternal chest discomfort. He admitted to having occasional difficulty swallowing for past 2-3 months for solids only. He denied any heartburn, cough, regurgitation, loss of appetite, weight loss, fever, chills, haematemesis or melaena. He denied tobacco or alcohol use. 2 weeks prior to presentation he had started taking testosterone pills for body-building. Physical examination was completely unremarkable.

A barium oesophagram showed extrinsic oblique compression of the oesophagus at the level of the carina as it passes through the aorta. CT scan and MRI of the chest revealed a right-sided aortic arch crossing posteriorly to the oesophagus with proximal oesophageal dilatation consistent with Dysphagia Lusoria. Endoscopy noted erosive oesophagitis/distinct ulceration extending from 18cm into a pulsatile area of narrowing at 20 cm with normal mucosa visualized distally.

Biopsies revealed oesophageal squamous mucosa with marked acute inflammation, reactive changes and no evidence of viral inclusions. Surgical management was discussed with the patient, but given the short duration of symptoms and the patient's stable weight, providing symptomatic relief with lifestyle changes, together with a trial of medications such as proton pump inhibitors were considered. At 2 weeks follow-up whilst taking proton pump inhibitors and having discontinued the testosterone pills, the patient experienced complete resolution of symptoms.

Epidemiology:

Dysphagia Lusoria: Moltz et al, found that lusorian artery has a prevalence of about 0.7% in the general population, based on the post-mortem findings(7). Also, out of 1629 patients who underwent endoscopy for various reasons, 0.4% had a finding of a lusorian artery in a report from Fockens et al(8). It has also been concluded based on the autopsy results and retrospective analysis of patients’ symptoms during life that about 60-70% of these patients remain asymptomatic (7). Coughing, dysphagia, thoracic pain, syncope and Horner's syndrome may develop, but usually present in old-age(9).

Pill-Induced Oesophagitis: The data on pill-induced oesophagitis is rather limited. A Swedish study found an incidence of 4 cases per 100,000 population/year(10). Wright found the incidence of drug-induced oesophageal injury to be 3.9/100,000(11). This may be underestimated and does not include subclinical or misdiagnosed cases. Also, cases are reported selectively, due to clustering of cases, newly implicated pills or rare complications. The incidence today is probably much higher due to increased use of prescription medications, widespread use of endoscopy and an ageing population. All these factors limit our ability to correctly assess the true epidemiology of this iatrogenic disorder. 

Pathogenesis

Dysphagia Lusoria: During embryological development, the aortic sac gives rise to six aortic arches and with further development the arterial pattern is modified and the fourth arch persists on both sides and some vessels regress. In right arch anomaly, the left arch atrophies and disappears whereas the right arch persists. If both arches persist, they form a double arch or a vascular ring encircling the trachea and oesophagus (12).

Pill-induced oesophagitis: Several lines of evidence confirm that oesophageal mucosal injury is caused by prolonged contact with the drug contents(13, 14) .On clinical grounds, patients frequently report a sensation of a pill stuck in the oesophagus before the development of symptoms and the frequent occurrence of symptoms after improper pill ingestion. Endoscopically, the evidence includes occasional observation of pill fragments at the site of injury, sharp demarcation of the injury site from the normal tissue and the frequent localization of the injury to the areas of oesophageal hypomotility or anatomic narrowing(4, 15). Therefore factors predisposing to the drug-induced oesophageal injury can be divided into two main categories: patient or oesophageal factors (16, 17, 18,19,20,21) and drug or pharmaceutical factors as shown in tables 1 and 2 (13,14,22,23,24).

 

Table 1: Patient/Esophageal facors for pill-induced esophagitis
Old Age
Decreased Salivation
Pill intake in recumbent position
Lack of adequate fluid intake with the drug
Structural abnormalities of esophagus
Hypomobility of the esophagus
 
Table 2: Drug related factors for pill-induced esophagitis
Chemical structure(sustained release pills, gelatinous surface)
Formal structure (capsule increases risk over the tablet)
Solubility
Simultaneous administration of multiple medications
It is important to note that most patients who experience pill-induced damage have no antecedent oesophageal disorder, neither obstructive nor neuromuscular (25). It is the combination of anatomic narrowing coupled with the caustic effects of the implicated drug that caused the oesophageal injury in our case. Although testosterone pills have never been reported to cause pill-induced oesophagitis, 6 cases of corticosteroid-induced oesophagitis have been described in the literature(26) .

Clinical Presentation

Dysphagia Lusoria: As previously mentioned the disorder remains asymptomatic in majority of the patients. Symptomatic adults usually present with dysphagia for solids, (91%), chest pain (20% or less). Less commonly, patients may have cough, thoracic pain or Horner’s syndrome (27,28). In infants, respiratory symptoms are the most predominant mode of clinical presentation. This is believed to be due to absence of tracheal rigidity, allowing for its compression with resulting stridor, wheezing, cyanosis etc (9) . Richter et al. reported average age of presentation to be 48 years (27). Various mechanisms to explain this delayed presentation have been proposed such as increased rigidity of the oesophagus, rigidity of the vessel wall due to atherosclerosis, aneurysm formation (especially Kommerell’s diverticulum), elongation of the aorta etc (9, 29,30) .

Pill-induced oesophagitis: Patients with pill-induced injury usually present with odynophagia, dysphagia and/or retrosternal chest pain(4) . Symptoms can occur after several days after starting a drug, but frequently occur after the first dose. (13) .Fever and haematemesis signifying a possible mediastinal extension can occur without chest pain(32,33). Pharyngitis due to the pill lodged in the hypopharynx has been reported(34).

Our case presents a typical example of asymptomatic Dysphagia Lusoria, who developed acute dysphagia, odynophagia and retrosternal chest discomfort immediately after the initiation of the offending agent; which is very typical of pill-induced oesophageal injury.

Diagnostic approach

Dysphagia Lusoria: The best method to diagnose an aberrant right subclavian artery presenting with difficulty swallowing is initially with a barium oesophagram followed by a CT or MRI scan. (27) .Angiography although considered gold standard for the diagnosis of vascular abnormalities is now largely supplanted by newer less invasive techniques such as CT or MR angiography. Upper endoscopy may reveal a pulsating compression of the posterior wall of the oesophagus as in our case(9, 27). Endoscopic ultrasound, especially with Doppler technology may be helpful to confirm the vascular nature of the abnormality(27). Oesophageal manometry usually shows non-specific findings. High peristaltic pressures have been reported in the proximal oesophagus above the level of the compression (9, 35).

Pill-induced oesophagitis: Barium studies can be normal, and slowing of barium column may be the only abnormality seen(31). Double contrast studies may however, increase the yield of a positive result(36). Kikendall et al. reported that endoscopy revealed the evidence of injury in all the patients (5) . Endoscopy most commonly reveals one or more discrete well demarcated ulcers with normal surrounding mucosa. Ulcers may range from pin-point to several centimetres in diameter(5). Biopsies, if performed, help to distinguish the condition from infection and neoplasia.

Our case shows a distinct oblique compression in the posterior wall of oesophagus on the barium study (fig 1) and classic findings on MR/CT with contrast which also excluded any other thoracic vascular abnormalities (fig 2-5). Endoscopic images of a shallow ulcer are shown in fig 6,7.

Figure 1- Barium esophagram depicting the extrinsic indentation of the esophagus as it crosses the aorta.

 

Figure 2- CT scan of the thorax demonstrating esophageal compression from a posteriorly placed aorta.

 

Figure 3- Magnetic resonance image showing esophageal compression with proximally dilated esophagus.

 

Figure 4- CT image showing the right sided origin of the aortic arch.

 

Figure 5- Three Dimensional image of the heart and the right sided approach of the arch.

 

Figure 6- Endoscopic view of esophageal inflammation at the site of compression.

 

Figure 7- Endoscopic image of the esophageal injury using narrow band imaging.

Treatment

Dysphagia Lusoria: The treatment of patients with DL primarily depends upon the severity of symptoms. Mild to moderate cases are managed by lifestyle and dietary changes such as eating slower, chewing well, sipping liquids, weight reduction and reassurance as in our case.(9,27) Janssen et al also reported in a series of 6 patients that 3/6 improved with proton-pump inhibitor alone or in combination with the prokinetic drug cisapride (9) .Severe symptoms and failure of medical therapy may need surgical evaluation and treatment. Richter et al. reported 14/24 patients who underwent surgical repair of the aberrant vessel for DL(27) . Bogliolo et al proposed endoscopic dilation as a temporary alternative to relieve symptoms in patients who are poor surgical candidates (37) .

Pill-induced oesophagitis: Most uncomplicated cases of pill-induced oesophagitis may heal spontaneously, with resolution of symptoms in a few days to a few weeks. Withdrawal of the offending drug and avoidance of topically irritating foods such as citrus fruits, alcohol is imperative to aid healing (4, 13). Sucralfate, topical anaesthetics, and acid suppression are often used to aid in relief of pain(4, 15). Rarely, in severe cases, parenteral nutrition or endoscopic dilation of chronic strictures may be required. (15, 25)

Conclusion

Our case demonstrates a typical case of DL presenting with pill-induced oesophagitis who responded to conservative and acid suppressive therapy. Identifying the risk factors and adequate patient education is the key to prevention.

 

Competing Interests
None Declared
Author Details
MALHOTRA A, Division of Gastroenterology, Seton Hall University of Health and Medical Sciences, South Orange, NJ KOTTAM RD, Division of Gastroenterology, Seton Hall University of Health and Medical Sciences, South Orange, NJ SPIRA RS, Division of Gastroenterology, Seton Hall University of Health and Medical Sciences, South Orange, NJ and Department of Medicine, Clinical Assistant Professor of Medicine, UMDNJ, Newark, NJ
CORRESSPONDENCE: RAGHU D KOTTAM, MD, Dept. of Gastroenterology, St.Michael’s Medical Center, 111 Central Avenue, Newark, NJ, 07102
Email: raghudk@yahoo.com

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