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Gi presentations of non gi disorders how to avoid pitfalls
- 1. Title Speaker GI presentations ofnon GI disorders - how to avoid pitfalls. Dr Mark Fernandes B.Sc(Hons), MBChB(Hons), MRCP(UK), FAMS(Gastro) Gastroenterologist
- 2. Learning Objectives At theconclusion of this CME activity, the learner should be better able to: • Have greater knowledge of the GI presentations of systemic diseases. • Be able to discuss differential diagnoses for the cases presented • Be able to list appropriate investigations • Be able to outline a plan of management
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- 4. CASE A 45yr chineseman presented to A&E in March 2020 with a 1 day history of abdominal pain, vomiting 2x and diarrhoea<6x/day. PMHX: Hypertension on Amlodipine 5mg om. He was treated with symptomatic relief (Buscopan, Maxolon and loperamide) and told to return if symptoms did not improve. He returned to A&E 2 days later because his abdominal pain had gotten worse and diarrhoea had not resolved. He was admitted for acute GE. On the ward he developed a fever of 38.5 degrees. Patient was transferred to an isolation ward. On further questioning he revealed he did have dry cough.
- 5. On Examination Dehydrated. HR 90bpm,O2 Sats 96% RA, BP 110/80 H:S1 S2 L: few creps bibasally A: SNT BS+
- 6. Laboratory Investigations • TWC3.2 ths/uL, • Hb 15.2 g/dL, • Plt 130 (x109/ml) • Na 124 mmol/L, • K = 3.2mmol/L, • U= 7.9 umol/L, • Cr=95 umol/L • Bil 20 g/dL, • ALT 80 U/L, • AST 90 U/L, • ALP 95 U/L, • GGT 90 U/L • Summary: • 1. Bicytopenic • 2. Hyponatraemic • 3. Transaminitis
- 7. Differential Diagnosis 1. Norovirus enteritis 2.Mycoplasma pneumoniae 3. Dengue fever 4. COVID-19
- 8. Additional labs • MycoplasmaIgM non reactive • Stool sent for GI Panel PCR – NAD • Dengue antigen negative and Dengue IgM non reactive • SARS-COV2 PCR swab sent • Radiologic imaging done –CXR and CT abdomen
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- 11. Management Patient was transferredto NCID and COVID swab was positive. Started on IV Antibiotics IV hydration, Supplemental O2
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- 13. COVID-19 Symptoms • Most Common –Fever (83-89%) – Respiratory (62%), SOB (19-31%) – Neurologic: Anosmia/dysgeusia (approx. 50%), Confusion, ischaemic/haemorrhagic stroke – CVS: endothelial involvement, myocardial injury
- 14. GI Manifestations • Beforerespiratory manifestations, many patients had diarrhoea, nausea, vomiting and abdominal discomfort. • The range reported in various studies =2-40% • In Singapore, GI Manifestations have been reported at 17%
- 15. GI Symptoms Mao Ret al. Manifestations and prognosis of gastrointestinal and liver involvement in patients with COVID- 19: a systematic review and meta-analysis add text. Lancet Gastroenterol Hepatol 2020; 5: 667–78
- 16. Outcomes GI symptoms maybe associated with poor clinical outcomes including: • Higher risk of mortality. • More severe disease • Longer hospital stay • Use of drugs in hospital including antibiotics Pan L, Mu M, Ren HG, et al. Clinical characteristics of COVID-19 patients with digestive symptoms in Hubei, China: a descriptive, cross- sectional multicenter study. Am J Gastroenterol 2020 March 18 Epub
- 17. Potential mechanisms ofCOVID-19 in the GI • Uses Angiotensin converting enzyme-2 (ACE2) as a viral receptor to enter host cells • These are present throughout the GI tract and also on cholangiocytes • An intriguing finding was a higher expression of ACE2 in absorptive enterocytes from the ileum and colon than the lung Gu J, et al. Gastroenterology. 2020;doi:10.1053/j.gastro.2020.02.054. Xiao F, et al. Gastroenterology. 2020;doi:10.1053/j.gastro.2020.02.055.
- 18. Transmission • Human-to-human transmissionoccurs through – Respiratory secretions droplets – Aerosols – Faeces – Contaminated surfaces • Transmission through symptomatic and asymptomatic patients • Virus viable up to 3 hrs after aerosolisation • Risk of infection - healthcare workers account for 29% of all patients in Wuhan
- 19. Faecal Oral Transmission? • Inabout 50% of COVID-19 cases, the presence of SARS-CoV-2 in faecal samples and detection of SARS-CoV-2 in intestinal mucosa of infected patients suggest that enteric symptoms could be caused by invasion of ACE2 expressing enterocytes and the GI tract may be an alternative route of infection. • In >50% of patients, faecal samples remained positive for SARS-CoV2 RNA for a mean of 11 days after clearance of respiratory tract samples • A recent study further confirmed that 8 of 10 infected children had persistently positive viral rectal swabs after nasopharyngeal testing was negative. • Importantly, live SARS-CoV-2 was detected on electron microscopy in stool samples from two patients who did not have diarrhoea, highlighting the potential of faecal-oral transmission
- 20. Detectable Faecal Virus CheungKS et al. Gastrointestinal Manifestations of SARS-CoV-2 Infection and Virus Load in Fecal Samples from the Hong Kong Cohort and Systematic Review and Meta-analysis. Gastroenterology. 2020 Apr 3
- 21. Liver Manifestations Guan W-J,Ni Z-Y, Hu Y, et al. Clinical characteristics of 2019 novel coronavirus infection in China. N Engl J Med 2020; published online Feb 28. Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020; 395: 497–506. Chen N, Zhou M, Dong X, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet 2020; 395: 507–13. Wang D, Hu B, Hu C, et al. Clinical characteristics of 138 hospitalised patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA 2020; published online Feb 7. DOI:10.1001/jama.2020.1585. Shi H, Han X, Jiang N, et al. Radiological findings from 81 patients with COVID-19 pneumonia in Wuhan, China: a descriptive study. Lancet Infect Dis 2020; published online Feb 24. DOI:10.1016/S1473-3099(20)30086-4. 9 Xu X-W, Wu X-X, Jiang X-G, et al. Clinical findings in a group of patients infected with the 2019 novel coronavirus (SARS-Cov-2) outside of Wuhan, China: retrospective case series. BMJ 2020; published online Feb 19. 10 Yang X, Yu Y, Xu J, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med 2020; published online Feb 24. DOI:10.1016/S2213-2600(20)30079-5.
- 22. Liver Manifestations • Liver impairmenthas been reported in up to 60% of patients with SARS and also in patients infected with MERS-CoV. • Current data indicate that 2–11% of patients with COVID-19 had liver comorbidities and 14–53% cases reported abnormal levels of alanine aminotransferase and aspartate aminotransferase (AST) during disease progression.
- 23. COVID-19 and LFTabnormalities The aetiology of abnormal liver function tests were due to either COVID-19 related hepatitis or drug induced liver injury Most of the patients had abnormal liver test results within 1-2 ULN at admission and only a few (<4%) had abnormal liver test results higher than 2 ULN. Patients also tended to have underlying liver diseases, including NAFLD, alcoholic liver disease, and chronic Hepatitis B (P<0.001)
- 24. Management SUPPORTIVE TREATMENT TREATMENTOF UNDERLYING DISEASE ROLE OF ANTI-VIRAL THERAPIES AND VACCINES REMAIN UNCERTAIN AND RCTS ARE ONGOING
- 25. • Be awareof asymptomatic carriers and transmission. • Be aware of atypical presentations, especially in the elderly – Eg: GI manifestations, confusion, functional decline, falls, prothrombotic events. • Current SASH workflows do not specifically tackle patients with atypical presentations • Be aware that Nasal Swab PCR testing has a sensitivity of only about 70% Learning Points about COVID-19
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- 27. CASE • 21 yearold women, shop assistant • No past history of note • Presented to ED with acute D+V and was admitted for severe GE and discharged 5 days later • Readmitted 1 week later with persistent D+V and palpitations • Found to be in SVT in ED, converted with adenosine
- 28. O/E afebrile, BP 140/80,HR 130, SpO2 96% RA - alert, dehydrated - no rash or lymphadenopathy - heart S1S2 no murmurs - lungs clear - abdo soft, generalised tenderness BS sluggish ++ bladder palpable - no focal neuro deficits
- 29. Labs FBC, U+E, LFT NORMAL(!) UFEME WBC 25, RBC 20 EC 0, PROTEIN 2+ UPCR 0.98 CXR – BILATERAL PLEURAL EFFUSIONS CTPA – PULMONARY EMBOLISM IN LEFT PULMONARY ARTERY CT ABDOMEN
- 30. Could you pleasehelp us see this patient?
- 31. Radiologic Findings • asciteswith increased peritoneal enhancement • circumferential, symmetrical, multisegmented mural thickening usually of the jejunum and ileum with associated submucosal oedema (target sign)
- 32. Radiologic Findings • engorgementof mesenteric vessels with a palisade pattern or comb-like appearance • dilatation of intestinal segments mesenteric fat stranding
- 33. Radiologic Findings • Thumbprinting
- 34. Summary • Anti-Nuclear Antibody1/320 homogenous, anti-dsDNA >200 • ANCA negative • Anti-Cardiolipin Antibody IgG/M, Lupus Anti- Coag negative • SLE – Lymphopenia – Serositis – Lupus gut – Lupus cystitis – Lupus nephritis – Lupus myocarditis? – Positive serology • IV Methylprednisolone, IV cyclophosphamide
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- 36. Updated SLE Diagnostic Criteria References 1 AringerM, Costenbader K, Daikh D, et al. 2019 European League against Rheumatism/ American College of rheumatology classification criteria for systemic lupus erythematosus. Ann Rheum Dis 2019;78:1151–9.
- 37. GI Presentations • Side effectsof drugs – GERD, Dysphagia – Dyspepsia – Gastric ulcers, GI Bleed • peritoneum: ascites is found in up to 10% of patients due to serositis • gastrointestinal vasculature – vasculitis causing colitis, mucosal ulceration with haemorrhage or perforation, intestinal ischaemia, "watermelon stomach" or gastric antral vascular ectasia, oesophageal dysmotility or intestinal pseudo-obstruction4 – thrombosis of the intestinal vessels may also occur in association with antiphospholipid syndrome • mucosa – mouth ulcers in 50% of patients – protein-losing enteropathy and fat malabsorption – associated ulcerative colitis or Crohn disease • pancreas: pancreatitis • liver and biliary tract – hepatomegaly, steatosis, hepatitis, cholestasis, primary biliary cirrhosis and eventually cirrhosis may be found. – Budd-Chiari syndrome which may be associated with antiphospholipid antibodies in SLE – acalculous cholecystitis and benign biliary stricture • spleen: splenic infarction • adrenal glands – adrenal haemorrhage – hypoadrenalism G Bertsias et al. Systemic Lupus Erythematosus: Pathogenesis and Clinical Features. 2012 GI tract manifestations are reported in 25-40% of patients
- 38. Learning Points Perform athorough physical examination and be on the look out for dermatological features of SLE. Have a high index of suspicion if a patient has multi-system involvement.
- 39. Case 3: ACase of Intestinal Obstruction
- 40. CASE 82yr Chinese gentleman spendshis time between here and brunei PMHx – IHD s/p PCI Meds: Plavix 75mg om Admitted with 1 day history of severe abdominal pain and vomiting
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- 45. Management • Patient underwenta laparotomy, cause of intestinal obstruction not found. • Bowel however was still viable and no resection was performed. • He was planned for a gastroscopy and colonoscopy but delayed this for a few months
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- 48. Differential Diagnosis • Adenocarcinoma • GIST •Carcinoid Tumour • TB gut • DLBCL • Crohns Disease
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- 50. Predisposing conditions • Helicobacter pyloriinfection • Autoimmune diseases • Immunodeficiency and immunosuppression • Celiac disease • Inflammatory bowel disease • Nodular lymphoid hyperplasia
- 51. Learning Points • The twolargest studies of GI lymphoma reported the following sites of involvement in Greek and German populations • Stomach – 68 to 75 percent • Small bowel (including duodenum) – 25 percent • Ileo-cecal region – 7 percent • More than one GI site – 6 to 13 percent • Rectum – 2 percent • Diffuse colonic involvement – 1 percent • Koch P, del Valle F, Berdel WE, et al. Primary gastrointestinal non-Hodgkin's lymphoma: I. Anatomic and histologic distribution, clinical features, and survival data of 371 patients registered in the German Multicenter Study GIT NHL 01/92. J Clin Oncol 2001; 19:3861 • Papaxoinis G, Papageorgiou S, Rontogianni D, et al. Primary gastrointestinal non-Hodgkin's lymphoma: a clinicopathologic study of 128 cases in Greece. A Hellenic Cooperative Oncology Group study (HeCOG). Leuk Lymphoma 2006; 47:2140.
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- 54. Case Study 4: ChronicDiarrhoea
- 55. CASE • 44yr oldIndian Expat from Bombay living in Sg for >5years, Investmant banker • referred by GP • PMHX UC dx 1999 in India goes for scopes every 3 years colonoscopy in 2000 - polyp - leiomyoma capsule endoscopy normal HP negative iGG4 normal Hep Bs Ag neg • FHX Father/Grandfather - pancreatitis Mother ulcerative colitis
- 56. Colonoscopy Findings Endoscopic evidenceof inflammation noted with skip lesions affecting the sigmoid colon and terminal ileum These findings were consistent with histology Acute on chronic inflammation Cryptitis Crypt distortion Crypt abscesses No granulomas seen AFB smear negative
- 57. Differential Diagnosis • UC orCrohns? • Parasitic infection such as amoeba, giardia, crytococcocus • TB • Malignancy/Lymphoma
- 58. Investigations • Amoebic antibodynegative • Stool FEME and culture – Neg • Stool GI Panel PCR - NAD • Biopsies sent for histological examination • Sent for AFB smear, TB PCR, AFB culture • TB PCR Positive
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- 60. Management • Patient wasreferred to ID and treated for TB
- 61. Learning Points: Abdominal tuberculosis is a greatmimicker • Extrapulmonary tuberculosis occurs in about 20% of tuberculosis. • GI tuberculosis constitutes about 10% of extra- pulmonary tuberculosis. • GI tuberculosis (TB) can present with involvement of any site. Symptoms and signs may include fever, weight loss, abdominal pain and/or distension, ascites, hepatomegaly, diarrhea, abdominal mass, and abnormal liver function tests. • Risk factors include (history of prior TB infection or disease, known or possible TB exposure, and/or past or present residence in or travel to an area where TB is endemic). • Spread through ingestion of infected sputum or milk, (2) through hematogenous or lymphatic spread and finally (3) through direct spread into the peritoneum from the fallopian tubes
- 62. Learning Points • The diagnosisof abdominal TB may be definitively established by demonstration of Mycobacterium tuberculosis in peritoneal fluid or a biopsy specimen of an involved site. • AFB smear, AFB culture, Nucleic Acid Amplification Test (TB-PCR) are recommended • Interferon-gamma response assays may be helpful but cannot differentiate between latent and active TB (TB Quantiferon Gold or T- Spot tests) Lewinsohn DM et al. Official American Thoracic Society/Infectious Diseases Society of America/Centers for Disease Control and Prevention Clinical Practice Guidelines: Diagnosis of Tuberculosis in Adults and Children. Diagnosis of TB in Adults and Children • CID 2017:64 (15 January)
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- 64. Case • 29yr oldchinese lady admitted with 4days of abdominal pain. • She had already been to EMD once but cont to have persistent pain and was admitted.
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- 67. Progress • On the4th day of admission around I saw her in the morning and she was clinically well. • At 7pm I was notified that the patient was extremely breathless.
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- 71. Management • Diagnosis: DiabeticKetoacidosis • Transferred to MICU • Started on IV Insulin • IV Bicarbonate • Aggressive fluid rehydration • Correction of electrolytes • Patient discharged and currently on insulin
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- 75. THANK YOU Thank youfor your participation. Email: drmarkfernandes@gmail.com