Downloaded from http://jramc.bmj.com/ on September 7, 2015 - Published by group.bmj.com
Case report
An unusual cause of peritonitis in a deployed environment Adrian Proffitt,1 R Faulconer,2 P Kreishman,3 S Graybill,4 D Craig5 1
ST3 Acute Internal Medicine, Department of Medicine, University Hospital of North Staffordshire, Stoke-on-Trent, Staffordshire, UK 2 ST5 General and Vascular Surgery, Department of Surgery, Russells Hall Hospital, Dudley, West Midlands, UK 3 Department of Surgery, Womack Military Medical Centre, Fort Bragg, North Carolina, USA 4 Department of Internal Medicine, San Antonio Military Medical Centre, Fort Sam Houston, Texas, USA 5 Department of Gastroenterology, The James Cook University Hospital, Middlesbrough, North Yorkshire, UK Correspondence to Surg Lt Cdr Adrian Proffitt RN, Department of Medicine, University Hospital of North Staffordshire, Stoke-on-Trent, ST4 6QG, UK; adrianproffi[email protected] Received 2 October 2013 Revised 17 October 2013 Accepted 19 October 2013 Published Online First 19 November 2013
To cite: Proffitt A, Faulconer R, Kreishman P, et al. J R Army Med Corps 2015;161:69–70.
ABSTRACT Acute abdominal pain is a common presenting complaint to both primary and secondary care, and is a frequent cause of hospital admission among deployed personnel. Identification of generalised peritonism on abdominal examination is a classical indicator of intra-abdominal pathology that may warrant exploratory laparotomy. Negative findings at laparotomy should serve as a diagnostic prompt to consider other non-surgical mimics of an acute abdomen.
Key messages ▸ Medical conditions can mimic an acute surgical abdomen. ▸ Exploratory laparotomy with no specific findings can be a significant aid to diagnosis. ▸ The multinational population seen on deployment may present with inherited and metabolic causes of morbidity not frequently seen in the UK.
CASE REPORT A 29-year-old Jordanian man presented to the emergency department of the Role 3 Hospital in Camp Bastion, Southern Afghanistan, with a 24-h history of right iliac fossa pain which became generalised, radiating to his suprapubic region and scrotum. This was associated with two episodes of diarrhoea and vomiting. The patient had suffered multiple similar episodes in the past 12 months, but markedly less severe in nature. Initial observations revealed a pyrexia of 37.7°C, a resting heart rate of 94 beats/min, blood pressure of 116/74 mm Hg, RR of 14 breaths/min and SpO2 of 96% on air. Initial surgical assessment demonstrated generalised abdominal peritonism, most pronounced in the right lower quadrant. Admission laboratory tests revealed a C reactive protein (CRP) of 182 mg/L (normal range 0–10 mg/L) with an isolated hyperbilirubinaemia of 73 μmol/L (normal range 2– 23 μmol/L). All other admission blood tests, including urea and electrolytes, full blood count, capillary glucose and serum amylase, were within normal limits. An erect chest radiograph showed no evidence of pneumoperitoneum, and CT of the abdomen and pelvis with intravenous and oral contrast revealed only mild prominence of small bowel loops and swirling of mesenteric vessels with loops of decompressed, unopacified small bowel. Given the significant peritonism, an emergency exploratory laparotomy was undertaken. Operative findings were remarkable for hyperaemia of the small bowel and colonic serosa and a small amount of mucoid material on the bowel wall. There was no evidence of small or large bowel perforation, volvulus or haemorrhage. The appendix was slightly firm but without evidence of perforation, but was removed intra-operatively and sent to the UK for histology, the result of which is awaited. Post-operatively, the patient was commenced empirically on intravenous co-amoxiclav 1.2 g three times a day, prophylactic enoxaparin and patientcontrolled analgesia. On post-operative day zero, the patient’s pyrexia resolved but due to worsening abdominal pain a
medical consultation was requested. Further history revealed that the patient had suffered from recurrent attacks of abdominal pain and fever over the past year; these attacks normally lasted between 1 and 3 days and resolved spontaneously, but had worsened in intensity in the weeks preceding deployment. There had been no change in urine colour, skin rashes, or changes in diet or medication, including herbal remedies, prior to these attacks. There was no family history of recurrent abdominal pain. In addition to generalised abdominal discomfort, the patient described dyspnoea and pleuritic chest pain at rest. Chest examination demonstrated widespread expiratory rhonchi with reduced breath sounds bibasally and saturations of 88% on room air on resting pulse oximetry. There was generalised abdominal tenderness without guarding. Repeat laboratory tests showed a rising CRP level of 281 mg/L and a persistent isolated hyperbilirubinaemia of 84 mmol/L; other routine laboratory tests remained within normal limits. Rapid antigen testing for malaria was negative. A repeat chest radiograph revealed bibasal atelectasis. Resting ECG showed normal sinus rhythm, with non-specific flattening of the lateral T-waves. A number of medical pathologies, including typhoid, mesenteric ischaemia, Addison’s disease, C1 esterase inhibitor deficiency and acute intermittent porphyria, were considered, but none were consistent with the overall clinical picture. Given the patient’s ethnic origin, history of recurrent abdominal pain, pyrexia and isolated hyperbilirubinaemia, a presumptive diagnosis of familial Mediterranean fever (FMF) was made. The patient was treated with a reducing course of colchicine, leading to a rapid clinical improvement over the next 48 h, with an associated fall in the CRP level to 53 mg/L. The National Amyloid Centre in London was contacted to discuss the possibility of testing for the common mutations found in FMF; unfortunately, as the patient was not NHS-entitled this was not feasible. A clinical recommendation was made for aeromedical evacuation from theatre
Proffitt A, et al. J R Army Med Corps 2015;161:69–70. doi:10.1136/jramc-2013-000185
69
Downloaded from http://jramc.bmj.com/ on September 7, 2015 - Published by group.bmj.com
Case report for further convalescence from his surgery and formal genetic testing for FMF in Jordan. The patient was discharged on regular colchicine 0.5 mg twice daily.
DISCUSSION FMF is an inherited autosomal recessive disease, most prevalent in those of Sephardic Jewish, Armenian, Turkish and Arab descent.1 The condition is caused by a number of mutations in the gene MEFV, located on the short arm of chromosome 16. MEFV codes for pyrin, a protein involved in regulation of the innate immune system and the inflammatory response.2 The prevalence of FMF in Jordanian children has been estimated at 1:2600, with a carrier rate for MEFV defects of 1:50 in the Jordanian population.3 FMF typically manifests as a recurrent serositis and fever, affecting the pleura, pericardium and peritoneum as well as synovial surfaces. Specific triggers precipitating an acute attack have not been identified, but emotional stress has been implicated.4 Pathophysiologically, the systemic and local manifestations of FMF result from increased secretion of interleukin (IL)-1 β, the archetypal pro-inflammatory cytokine, due to ineffective suppression of caspase-1 activity by the defective pyrin protein.5 Caspase-1 is essential in converting IL-1β from its inactive precursor to its mature form which can then be secreted. Clinical diagnostic criteria for FMF have been developed (Table 1), and the presence of one or more major criteria, or two or more minor criteria, allow the diagnosis of FMF to be made with a sensitivity of over 95% and specificity of 98%.6 Genetic testing is available in some centres, and although the sensitivity and specificity of the various MEFV assays range from 99% to 100%,7 the variable penetrance of some alleles may reduce the predictive value of these tests.8 We can be confident of the diagnosis of FMF in this case due to the presence of two major criteria (a typical abdominal attack and pleural involvement) along with a favourable response to colchicine. The mainstay of therapy for FMF is with colchicine, which acts by binding to tubulin thereby preventing microtubule polymerisation. Acute attacks of pain due to FMF can be difficult to control, but colchicine at a dose of 1–3 mg per day has been shown to reduce both the frequency and severity of attacks, and is effective secondary prophylaxis in up to 75% of patients. Colchicine therapy also reduces the progression of AA amyloid deposition,
which is significant since renal failure due to amyloidosis is the major cause of mortality in FMF.9 The recognition of the pivotal pathophysiological role of IL-1β in FMF has led to the effective use of anakinra, a biologic IL-1β receptor antagonist, in selected FMF cases intolerant of, or unresponsive to, colchicine.
CONCLUSIONS Diagnostic uncertainty usually arises from atypical presentations of common conditions or misleading presentations. This is a particular problem during multinational deployed operations due to the dual problems of endemic local diseases of which the physician may have limited experience and also imported pathology from the multinational population at risk. This substantially widens the differential diagnosis of most presentations from those considered in the UK. Besides increased awareness of infectious diseases endemic in theatre, it is also important for clinicians to consider inherited and metabolic conditions relevant to the patient’s country of origin. Given the patient’s clinical presentation with generalised peritonism, it could be argued that exploratory laparotomy to exclude intra-abdominal pathology was justified despite no specific findings on CT, as the sensitivity and specificity of cross-sectional imaging for acute abdominal conditions such as appendicitis are not 100%.10 The positive value of a ‘negative’ laparotomy in such cases should not be overlooked in aiding the clinician in making a definitive diagnosis, though given our patient’s previous history of similar symptoms a medical consultation may have been indicated prior to surgery. This could have led to a trial of medical therapy and obviated the need for surgery. Contributors AP and DC identified the case report, and AP drafted the manuscript while DC provided revision. The manuscript was then reviewed by RF and PK who clarified the surgical findings and added to the manuscript appropriately. Further revision was then enacted by AP, DC and SG. Following remarks from the reviewers and editors, AP, DC and PK amended the manuscript with review and agreement from SG and RF. Competing interests None. Patient consent Obtained. Provenance and peer review Not commissioned; externally peer reviewed.
REFERENCES 1 2
Table 1 Diagnostic clinical criteria for familial Mediterranean fever
3
Major criteria
Minor criteria
4
One or more of: Typical* attacks affecting the: 1. peritoneum 2. pleura or pericardium 3. monoarthritis (hip, knee or ankle) 4. fever alone 5. incomplete† abdominal attacks
Any two of: An incomplete† attack involving 1. the chest 2. a joint (not hip, knee or ankle) 3. exertional leg pain 4. a favourable response to colchicine
5
*The definition of typical applies to the first four major criteria and involves recurrence of symptoms (>3 of the same site) and pyrexia (rectal temperature >38°C). †Incomplete attacks differ from typical attacks in that they may lack peritonitis in abdominal attacks, lack rectal temperature >38°C and/or are longer/shorter than 1–3 days.
70
6 7 8 9 10
Yepiskoposyan L, Harutyunyan A. Population genetics of familial Mediterranean fever: a review. Eur J Hum Genet 2007;15:911–16. Stehlik C, Reed J. The PYRIN Connection: novel Players in Innate Immunity and Inflammation. J Exp Med 2004;200:551–8. Rawashdeh M, Majeed H. Familial Mediterranean fever in Arab children: the high prevalence and gene frequency. Eur J Pediatr 1996;155:540–44. Yenokyan G, Armenian HK. Triggers for attacks in familial Mediterranean fever: application of the case-crossover design. Am J Epidemiol 2012;175:1054–61. Guz G, Kanbay M, Ozturk M. Current perspectives on familial Mediterranean fever. Curr Opin Infect Dis 2009;22:309–15. Livneh A, Langevitz P, Zemer D, et al. Criteria for the diagnosis of familial Mediterranean fever. Arthritis Rheum 1997;40:1879–85. http://www.ncbi.nlm.nih.gov/gtr/tests/?term=MEFV%5Bgene%5D (accessed 22 Sep 2013). Gershoni-Baruch R, Shinawi M, Leah K, et al. Familial Mediterranean fever: prevalence, penetrance and genetic drift. Eur J Hum Genet 2001;9:634–7. Akar S, Yuksel F, Tunca M, et al. Familial Mediterranean fever: risk factors, causes of death, and prognosis in the colchicine era. Medicine 2012;91:131–6. Cuschieri J, Florence M, Flum D, et al. Negative appendectomy and imaging accuracy in the Washington State Surgical Care and Outcomes Assessment Program. Ann Surg 2008;248:557–63.
Proffitt A, et al. J R Army Med Corps 2015;161:69–70. doi:10.1136/jramc-2013-000185
Downloaded from http://jramc.bmj.com/ on September 7, 2015 - Published by group.bmj.com
An unusual cause of peritonitis in a deployed environment Adrian Proffitt, R Faulconer, P Kreishman, S Graybill and D Craig J R Army Med Corps 2015 161: 69-70 originally published online November 19, 2013
doi: 10.1136/jramc-2013-000185 Updated information and services can be found at: http://jramc.bmj.com/content/161/1/69
These include:
References Email alerting service
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This article cites 9 articles, 2 of which you can access for free at: http://jramc.bmj.com/content/161/1/69#BIBL Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.
Articles on similar topics can be found in the following collections Op HERRICK (94)
Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
Case report
An unusual cause of peritonitis in a deployed environment Adrian Proffitt,1 R Faulconer,2 P Kreishman,3 S Graybill,4 D Craig5 1
ST3 Acute Internal Medicine, Department of Medicine, University Hospital of North Staffordshire, Stoke-on-Trent, Staffordshire, UK 2 ST5 General and Vascular Surgery, Department of Surgery, Russells Hall Hospital, Dudley, West Midlands, UK 3 Department of Surgery, Womack Military Medical Centre, Fort Bragg, North Carolina, USA 4 Department of Internal Medicine, San Antonio Military Medical Centre, Fort Sam Houston, Texas, USA 5 Department of Gastroenterology, The James Cook University Hospital, Middlesbrough, North Yorkshire, UK Correspondence to Surg Lt Cdr Adrian Proffitt RN, Department of Medicine, University Hospital of North Staffordshire, Stoke-on-Trent, ST4 6QG, UK; adrianproffi[email protected] Received 2 October 2013 Revised 17 October 2013 Accepted 19 October 2013 Published Online First 19 November 2013
To cite: Proffitt A, Faulconer R, Kreishman P, et al. J R Army Med Corps 2015;161:69–70.
ABSTRACT Acute abdominal pain is a common presenting complaint to both primary and secondary care, and is a frequent cause of hospital admission among deployed personnel. Identification of generalised peritonism on abdominal examination is a classical indicator of intra-abdominal pathology that may warrant exploratory laparotomy. Negative findings at laparotomy should serve as a diagnostic prompt to consider other non-surgical mimics of an acute abdomen.
Key messages ▸ Medical conditions can mimic an acute surgical abdomen. ▸ Exploratory laparotomy with no specific findings can be a significant aid to diagnosis. ▸ The multinational population seen on deployment may present with inherited and metabolic causes of morbidity not frequently seen in the UK.
CASE REPORT A 29-year-old Jordanian man presented to the emergency department of the Role 3 Hospital in Camp Bastion, Southern Afghanistan, with a 24-h history of right iliac fossa pain which became generalised, radiating to his suprapubic region and scrotum. This was associated with two episodes of diarrhoea and vomiting. The patient had suffered multiple similar episodes in the past 12 months, but markedly less severe in nature. Initial observations revealed a pyrexia of 37.7°C, a resting heart rate of 94 beats/min, blood pressure of 116/74 mm Hg, RR of 14 breaths/min and SpO2 of 96% on air. Initial surgical assessment demonstrated generalised abdominal peritonism, most pronounced in the right lower quadrant. Admission laboratory tests revealed a C reactive protein (CRP) of 182 mg/L (normal range 0–10 mg/L) with an isolated hyperbilirubinaemia of 73 μmol/L (normal range 2– 23 μmol/L). All other admission blood tests, including urea and electrolytes, full blood count, capillary glucose and serum amylase, were within normal limits. An erect chest radiograph showed no evidence of pneumoperitoneum, and CT of the abdomen and pelvis with intravenous and oral contrast revealed only mild prominence of small bowel loops and swirling of mesenteric vessels with loops of decompressed, unopacified small bowel. Given the significant peritonism, an emergency exploratory laparotomy was undertaken. Operative findings were remarkable for hyperaemia of the small bowel and colonic serosa and a small amount of mucoid material on the bowel wall. There was no evidence of small or large bowel perforation, volvulus or haemorrhage. The appendix was slightly firm but without evidence of perforation, but was removed intra-operatively and sent to the UK for histology, the result of which is awaited. Post-operatively, the patient was commenced empirically on intravenous co-amoxiclav 1.2 g three times a day, prophylactic enoxaparin and patientcontrolled analgesia. On post-operative day zero, the patient’s pyrexia resolved but due to worsening abdominal pain a
medical consultation was requested. Further history revealed that the patient had suffered from recurrent attacks of abdominal pain and fever over the past year; these attacks normally lasted between 1 and 3 days and resolved spontaneously, but had worsened in intensity in the weeks preceding deployment. There had been no change in urine colour, skin rashes, or changes in diet or medication, including herbal remedies, prior to these attacks. There was no family history of recurrent abdominal pain. In addition to generalised abdominal discomfort, the patient described dyspnoea and pleuritic chest pain at rest. Chest examination demonstrated widespread expiratory rhonchi with reduced breath sounds bibasally and saturations of 88% on room air on resting pulse oximetry. There was generalised abdominal tenderness without guarding. Repeat laboratory tests showed a rising CRP level of 281 mg/L and a persistent isolated hyperbilirubinaemia of 84 mmol/L; other routine laboratory tests remained within normal limits. Rapid antigen testing for malaria was negative. A repeat chest radiograph revealed bibasal atelectasis. Resting ECG showed normal sinus rhythm, with non-specific flattening of the lateral T-waves. A number of medical pathologies, including typhoid, mesenteric ischaemia, Addison’s disease, C1 esterase inhibitor deficiency and acute intermittent porphyria, were considered, but none were consistent with the overall clinical picture. Given the patient’s ethnic origin, history of recurrent abdominal pain, pyrexia and isolated hyperbilirubinaemia, a presumptive diagnosis of familial Mediterranean fever (FMF) was made. The patient was treated with a reducing course of colchicine, leading to a rapid clinical improvement over the next 48 h, with an associated fall in the CRP level to 53 mg/L. The National Amyloid Centre in London was contacted to discuss the possibility of testing for the common mutations found in FMF; unfortunately, as the patient was not NHS-entitled this was not feasible. A clinical recommendation was made for aeromedical evacuation from theatre
Proffitt A, et al. J R Army Med Corps 2015;161:69–70. doi:10.1136/jramc-2013-000185
69
Downloaded from http://jramc.bmj.com/ on September 7, 2015 - Published by group.bmj.com
Case report for further convalescence from his surgery and formal genetic testing for FMF in Jordan. The patient was discharged on regular colchicine 0.5 mg twice daily.
DISCUSSION FMF is an inherited autosomal recessive disease, most prevalent in those of Sephardic Jewish, Armenian, Turkish and Arab descent.1 The condition is caused by a number of mutations in the gene MEFV, located on the short arm of chromosome 16. MEFV codes for pyrin, a protein involved in regulation of the innate immune system and the inflammatory response.2 The prevalence of FMF in Jordanian children has been estimated at 1:2600, with a carrier rate for MEFV defects of 1:50 in the Jordanian population.3 FMF typically manifests as a recurrent serositis and fever, affecting the pleura, pericardium and peritoneum as well as synovial surfaces. Specific triggers precipitating an acute attack have not been identified, but emotional stress has been implicated.4 Pathophysiologically, the systemic and local manifestations of FMF result from increased secretion of interleukin (IL)-1 β, the archetypal pro-inflammatory cytokine, due to ineffective suppression of caspase-1 activity by the defective pyrin protein.5 Caspase-1 is essential in converting IL-1β from its inactive precursor to its mature form which can then be secreted. Clinical diagnostic criteria for FMF have been developed (Table 1), and the presence of one or more major criteria, or two or more minor criteria, allow the diagnosis of FMF to be made with a sensitivity of over 95% and specificity of 98%.6 Genetic testing is available in some centres, and although the sensitivity and specificity of the various MEFV assays range from 99% to 100%,7 the variable penetrance of some alleles may reduce the predictive value of these tests.8 We can be confident of the diagnosis of FMF in this case due to the presence of two major criteria (a typical abdominal attack and pleural involvement) along with a favourable response to colchicine. The mainstay of therapy for FMF is with colchicine, which acts by binding to tubulin thereby preventing microtubule polymerisation. Acute attacks of pain due to FMF can be difficult to control, but colchicine at a dose of 1–3 mg per day has been shown to reduce both the frequency and severity of attacks, and is effective secondary prophylaxis in up to 75% of patients. Colchicine therapy also reduces the progression of AA amyloid deposition,
which is significant since renal failure due to amyloidosis is the major cause of mortality in FMF.9 The recognition of the pivotal pathophysiological role of IL-1β in FMF has led to the effective use of anakinra, a biologic IL-1β receptor antagonist, in selected FMF cases intolerant of, or unresponsive to, colchicine.
CONCLUSIONS Diagnostic uncertainty usually arises from atypical presentations of common conditions or misleading presentations. This is a particular problem during multinational deployed operations due to the dual problems of endemic local diseases of which the physician may have limited experience and also imported pathology from the multinational population at risk. This substantially widens the differential diagnosis of most presentations from those considered in the UK. Besides increased awareness of infectious diseases endemic in theatre, it is also important for clinicians to consider inherited and metabolic conditions relevant to the patient’s country of origin. Given the patient’s clinical presentation with generalised peritonism, it could be argued that exploratory laparotomy to exclude intra-abdominal pathology was justified despite no specific findings on CT, as the sensitivity and specificity of cross-sectional imaging for acute abdominal conditions such as appendicitis are not 100%.10 The positive value of a ‘negative’ laparotomy in such cases should not be overlooked in aiding the clinician in making a definitive diagnosis, though given our patient’s previous history of similar symptoms a medical consultation may have been indicated prior to surgery. This could have led to a trial of medical therapy and obviated the need for surgery. Contributors AP and DC identified the case report, and AP drafted the manuscript while DC provided revision. The manuscript was then reviewed by RF and PK who clarified the surgical findings and added to the manuscript appropriately. Further revision was then enacted by AP, DC and SG. Following remarks from the reviewers and editors, AP, DC and PK amended the manuscript with review and agreement from SG and RF. Competing interests None. Patient consent Obtained. Provenance and peer review Not commissioned; externally peer reviewed.
REFERENCES 1 2
Table 1 Diagnostic clinical criteria for familial Mediterranean fever
3
Major criteria
Minor criteria
4
One or more of: Typical* attacks affecting the: 1. peritoneum 2. pleura or pericardium 3. monoarthritis (hip, knee or ankle) 4. fever alone 5. incomplete† abdominal attacks
Any two of: An incomplete† attack involving 1. the chest 2. a joint (not hip, knee or ankle) 3. exertional leg pain 4. a favourable response to colchicine
5
*The definition of typical applies to the first four major criteria and involves recurrence of symptoms (>3 of the same site) and pyrexia (rectal temperature >38°C). †Incomplete attacks differ from typical attacks in that they may lack peritonitis in abdominal attacks, lack rectal temperature >38°C and/or are longer/shorter than 1–3 days.
70
6 7 8 9 10
Yepiskoposyan L, Harutyunyan A. Population genetics of familial Mediterranean fever: a review. Eur J Hum Genet 2007;15:911–16. Stehlik C, Reed J. The PYRIN Connection: novel Players in Innate Immunity and Inflammation. J Exp Med 2004;200:551–8. Rawashdeh M, Majeed H. Familial Mediterranean fever in Arab children: the high prevalence and gene frequency. Eur J Pediatr 1996;155:540–44. Yenokyan G, Armenian HK. Triggers for attacks in familial Mediterranean fever: application of the case-crossover design. Am J Epidemiol 2012;175:1054–61. Guz G, Kanbay M, Ozturk M. Current perspectives on familial Mediterranean fever. Curr Opin Infect Dis 2009;22:309–15. Livneh A, Langevitz P, Zemer D, et al. Criteria for the diagnosis of familial Mediterranean fever. Arthritis Rheum 1997;40:1879–85. http://www.ncbi.nlm.nih.gov/gtr/tests/?term=MEFV%5Bgene%5D (accessed 22 Sep 2013). Gershoni-Baruch R, Shinawi M, Leah K, et al. Familial Mediterranean fever: prevalence, penetrance and genetic drift. Eur J Hum Genet 2001;9:634–7. Akar S, Yuksel F, Tunca M, et al. Familial Mediterranean fever: risk factors, causes of death, and prognosis in the colchicine era. Medicine 2012;91:131–6. Cuschieri J, Florence M, Flum D, et al. Negative appendectomy and imaging accuracy in the Washington State Surgical Care and Outcomes Assessment Program. Ann Surg 2008;248:557–63.
Proffitt A, et al. J R Army Med Corps 2015;161:69–70. doi:10.1136/jramc-2013-000185
Downloaded from http://jramc.bmj.com/ on September 7, 2015 - Published by group.bmj.com
An unusual cause of peritonitis in a deployed environment Adrian Proffitt, R Faulconer, P Kreishman, S Graybill and D Craig J R Army Med Corps 2015 161: 69-70 originally published online November 19, 2013
doi: 10.1136/jramc-2013-000185 Updated information and services can be found at: http://jramc.bmj.com/content/161/1/69
These include:
References Email alerting service
Topic Collections
This article cites 9 articles, 2 of which you can access for free at: http://jramc.bmj.com/content/161/1/69#BIBL Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.
Articles on similar topics can be found in the following collections Op HERRICK (94)
Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
