More Related Content
Similar to CASE PRESENTATION.pptx
Similar to CASE PRESENTATION.pptx (20)
Recently uploaded
Recently uploaded (20)
CASE PRESENTATION.pptx
- 3. Patient S.J.C.A. 28 years old Female
- 5. 3 weeks history of: (+) on and off abdominal pain (+) febrile episodes (+) loose bowel movement (+) anorexia (+) gradual abdominal distention (+) History of Gastrointestinal TB – treatment completed RR= 22 cpm Pertinent PE findings: Temp= 37 deg Celsius Distended abdomen, tympanitic, BP= 110/60 mmHg (-) masses palpated O2 sat= 98% HR= 103 bpm
- 6. Course in the wards (+) transient facial flushing Blood culture (+) growth Stenotrophomnas maltophilia organisms CBC Hgb 116, WBC 16.98, RBC 3.98, Hct 35.8, Seg 61, Stabs 27, Lymph 10, Mono 1, Eo 1, Plt 238 C3 42.2 mg/dL ANA 46.5 IU/mL Fecalysis Loose, brown, Pus 0-3, Bacteria +++, No ova or parasite seen
- 8. INFECTIOUS PSEUDOMEMBRANOUS COLITIS ENTERIC FEVER AMOEBIC COLITIS FEVER ABDOMINAL PAIN DIARRHEA ANOREXIA NAUSEA ✗ RELATIVE BRADYCARDIA ✗ LEUKOPENIA ✗ BLOOD CULTURE FEVER ABDOMINAL PAIN DIARRHEA ANOREXIA NAUSEA ✗ TENESMUS ✗ BLOOD STREAKED STOOLS FEVER ABDOMINAL PAIN DIARRHEA ANOREXIA NAUSEA ✗ HISTORY OF ANTIBIOTIC USE Wiener, C., Fauci, A., Hauser, S., Longo, D., Jameson, L. J., Kasper, D., & Loscalzo, J. (2021). Harrison’s Principles of Internal Medicine Self- Assessment and Board Review, 20th Edition (20th ed.). McGraw Hill / Medical.
- 9. NON INFECTIOUS INFLAMMATORY NON INFLAMMATORY NEOPLASM CT SCAN Moderate amount of hypodense fluid collection is present. Diffuse symmetric bowel wall thickening (stratified pattern, alternate hyper and hypodensities) is seen representing hyperemia and edema of the bowel wall. No bowel dilatation. No obstructive process identified. No skip lesions/ transition zone. Mesenteric vessels appear prominent. Stomach is normal. Large bowel loops are unremarkable with no wall thickening and dilatation. No free air in the abdomen. Vasculature is well opacified with no filling defect. No abdominal aortic aneurysm. No lymphadenopathies. No evidence of necrosis. Normal hepatic configuration and enhancement. No mass lesions. Normal caliber of intrahepatic and common bile ducts. Thin dependent layer of hyperdensity noted. The pancreas, spleen, adrenals, kidneys, reproductive organs, and musculoskeletal look normal. COLONOSCOPY The scope was inserted up to the cecum and appendiceal opening and ileocecal valve were identified. The colon had good distensibility on air insufflation. Patchy erosions were noted at the descending and sigmoid. The rest of the colonic mucosa appeared slightly edematous and pinkish with no mass, ulcer nor polyp seen. The hemorrhoidal vessels were not engorged.
- 10. NON INFECTIOUS INFLAMMATORY NON INFLAMMATORY NEOPLASM INFLAMMATORY BOWEL DISEASE ULCERATIVE COLITIS CROHN’S DISEASE SYSTEMIC LUPUS ERYTHEMATOSUS LUPUS ENTERITIS Wiener, C., Fauci, A., Hauser, S., Longo, D., Jameson, L. J., Kasper, D., & Loscalzo, J. (2021). Harrison’s Principles of Internal Medicine Self-Assessment and Board Review, 20th Edition (20th ed.). McGraw Hill / Medical.
- 12. INFLAMMATORY INFLAMMATORY BOWEL DISEASE SYSTEMIC LUPUS ERYTHEMATOSUS CHRON’S DISEASE LUPUS ENTERITIS Zhu, X.-L., Xu, X.-M., Chen, S., Wang, Q.-M., & Zhang, K.-G. (2019). Lupus enteritis masquerading as crohn’s disease. BMC Gastroenterology, 19(1). https://doi.org/10.1186/s12876-019-1058-1
- 13. Typical endoscopic findings in CD include discontinuous distribution of longitudinal ulcers (defined as ≥4 to 5 cm ulcers in the Japanese criteria), cobblestone appearance, and/or small aphthous ulcerations arranged in a longitudinal fashion. Lee, J. M., & Lee, K.-M. (2016). Endoscopic diagnosis and differentiation of inflammatory bowel disease. Clinical Endoscopy, 49(4), 370–375. https://doi.org/10.5946/ce.2016.090
- 14. INFLAMMATORY INFLAMMATORY BOWEL DISEASE SYSTEMIC LUPUS ERYTHEMATOSUS CHRON’S DISEASE LUPUS ENTERITIS
- 15. FINAL DIAGNOSIS ELECTROLYTE IMBALANCE (HYPOKALEMIA) SECONDARY TO LUPUS ENTERITIS
- 16. Increase production of nucleic acids and self antigen 28/Female Autoimmune inducing activation of innate immunity, autoantibodies and T cells Immune complex formation and complement activation Deposition of autoantibodies and immune complexes Tissue Destruction Ischemia of the Digestive Tract LUPUS ENTERITIS Fever Abdominal Pain Diarrhea Nausea/ Vomting INFLAMMATORY RESPONSE CHRONIC INFLAMMATION Facial Flushing Ascites Abnormal Immune Response (+) Blood Culture ↓ C3 levels (+) ANA Hypokalemia ↑ WBC count (+) Stabs (+) Toxic Granulation Antibiotic therapy Steroids Potassium correction
- 17. THANK YOU!
- 18. REFERENCES Wiener, C., Fauci, A., Hauser, S., Longo, D., Jameson, L. J., Kasper, D., & Loscalzo, J. (2021). Harrison’s Principles of Internal Medicine Self-Assessment and Board Review, 20th Edition (20th ed.). McGraw Hill / Medical. Zhu, X.-L., Xu, X.-M., Chen, S., Wang, Q.-M., & Zhang, K.-G. (2019). Lupus enteritis masquerading as crohn’s disease. BMC Gastroenterology, 19(1). https://doi.org/10.1186/s12876-019-1058-1 García, M. J., Rodríguez-Duque, J. C., Pascual, M., Rivas, C., Castro, B., Raso, S., López-Hoyos, M., Arias-Loste, M. T., & Rivero, M. (2022). Prevalence of antinuclear antibodies in inflammatory bowel disease and seroconversion after biological therapy. Therapeutic Advances in Gastroenterology, 15, 175628482210778. https://doi.org/10.1177/17562848221077837 Lee, J. M., & Lee, K.-M. (2016). Endoscopic diagnosis and differentiation of inflammatory bowel disease. Clinical Endoscopy, 49(4), 370–375. https://doi.org/10.5946/ce.2016.090 Feldman, M. L., Friedman, L. S., Brandt, L. J., Sleisenger, M. H., & Fordtran, J. S. (2021). Sleisenger and Fordtran's gastrointestinal and liver disease: Pathophysiology, diagnosis, management. Elsevier.
- 19. Icon pack
Editor's Notes
- A place where questions far outweigh the answer; Where Most if not all interactions are directly added to the puzzles you have to solve. We may be misled by differing factors but let us take into mind that achieving the result should start with the process, not the desired outcome.
- Good Afternoon, doctors. I am Georzenn Cabanayan presening to you our Clinicopathologic case entitled… Embracing the limbo
- We are presented with 28 year old female,
- Who came in due to abdominal discomfort with the following salient features
- Who came in due to abdominal discomfort with the following salient features
- Who came in due to abdominal discomfort with the following salient features
- With the above signs and symptoms, we came up with both infectious and non infectious differential diagnosis
- For the infectious diagnosis, we considered Enteric Fever Pseudomembraous colitis Amoebic colitis Enteric (typhoid) fever is a systemic disease characterized by fever and abdominal pain and caused by dissemination of S. Typhi or S. Paratyphi. Fever is documented at presentation in >75% of cases, abdominal pain is reported in only 30–40%. The incubation period for S. Typhi averages 10–14 days but ranges from 5 to 21 days, depending on the inoculum size and the host’s health and immune status. The most prominent symptom is prolonged fever (38.8°–40.5°C; 101.8°104.9°F), which can continue for up to 4 weeks if untreated. However, we ruled this out since they usually present with relative bradycardia at the height of fever associated with leukopenia. Pseudomembranous Colitis – Diarrhea is the most common manifestation caused by C. difficile. Stools are almost never grossly bloody and range from soft and unformed to watery or mucoid in consistency, with a characteristic odor. Clinical and laboratory findings include fever in 28% of cases, abdominal pain in 22%, and leukocytosis in 50%. is usually acquired most commonly in association with antimicrobial use and the consequent disruption of the normal colonic microbiota. It is the most commonly diagnosed diarrheal illness acquired in the hospital. Amoebic Colitis usually present with gradual onset of lower abdominal pain and mild diarrhea is followed by malaise, weight loss, and diffuse lower abdominal pain however, The stools contain little fecal material and consist mainly of blood and mucus. In contrast to those with bacterial diarrheas, fecal findings suggestive of amebic colitis include a positive test for heme, a paucity of neutrophils, and amebic cysts or trophozoites. With these, we ruled out infectious cause.
- For the non infectious cause, non inflammatory causes primarily due to neoplasms where ruled in. imaging studies was done including: CT Scan of the Whole Abdomen which revealed the following findings: presence of diffuse symmetric bowel thickening with stratified pattern which may signify inflammatory causes. No obstructive process and mass lesions were identified. Colonoscopy was also done which showed patchy erosions and absence of mass, ulcer or polyp. With these findings, we immediately ruled out neoplasm.
- As previously presented through imaging studies, the presence of bowel thickening with stratified patterns are usually present in inflammatory bowel disease which is an immune-mediated chronic intestinal condition. The two major types of IBD include Crohn's Disease and Ulcerative Colitis. In this case, UC was ruled out since they usually present with gross blood and mucus in stools compared to Chron's disease. Another differential diagnosis under inflammatory cause include SLE. Under the SLICC criteria, the patient presented with the 2 clinical symptoms: Acute cutaneous manisfestation as evidenced by the presence of facial flushing which may be transient (in which our patient presented) or progressive The presence of abdominal distention can be due to ascites which is a form of a peritoneal serositis in patients with LUPUS 2 immunologic findings includes (+) ANA and decreased levels of C3 fulfilling the criteria in diagnosis SLE. Since the patient presented with GI symptoms associated with imaging findings of diffuse bowel wall thickening with mesenteric edema and prominent vessels hence Lupus Enteritis was considered.
- Thus we are now left, with 2 entities, IBD specifically CD that could show similar signs and symptoms for SLE patients with GIO involve =ment.
- Thus we are now left, with 2 entities, IBD specifically CD that could show similar signs and symptoms for SLE patients with GIO involve =ment. In a journal by Zhu et al, entitled lupus enteritis masquerading as Crohns disease they presented a table which shows the difference between CD and Lupus Enteritis by Clinical Presentations and Imaging studies. Although, both entities presented with non specific GI manifestations and CT scan findings of combs sign described as engorgement of mesenteric vessels with an increased number of visible vessels.
- Comb sign is the engorgement of the mesenteric vessels with vascular dilatation, tortuosity with spacing of the vasa recta, and prominence of surrounding mesenteric fat resembling a comb and is associated with Crohn’s disease and Lupus enteritis. Zhu, X.-L., Xu, X.-M., Chen, S., Wang, Q.-M., & Zhang, K.-G. (2019). Lupus enteritis masquerading as crohn’s disease. BMC Gastroenterology, 19(1). https://doi.org/10.1186/s12876-019-1058-1
- García, M. J., Rodríguez-Duque, J. C., Pascual, M., Rivas, C., Castro, B., Raso, S., López-Hoyos, M., Arias-Loste, M. T., & Rivero, M. (2022). Prevalence of antinuclear antibodies in inflammatory bowel disease and seroconversion after biological therapy. Therapeutic Advances in Gastroenterology, 15, 175628482210778. https://doi.org/10.1177/17562848221077837
- In a journal by Lee et al, entitled Endoscopic findings and differentiation of Inflammatory Bowel Disease. Typical endoscopic findings in CD includes cobblestone appearance and presence of ulcers arranged in a longitudinal fashion which was not seen on the imaging of our patient thus leaving us with the primary consideration of LUPUS ENTERITIS.
- With the final diagnosis of ELECTROLYTE IMBALANCE (HYPOKALEMIA) SECONDARY TO LUPUS ENTERITIS
- As a recap, we are presented with a case of a 28 year old female who came in with the following constitutional signs and symptoms of fever, abdominal pain, nausea and vomiting and diarrhea. The abnormal immune responses underlying SLE may be summarized as leading to production of increased quantities and immunogenic forms of nucleic acids, their accompanying proteins, and other self-antigen leading to the activation of innate immunity, autoantibodies and T cells. These activation can lead to aberrant formation of immune complexes and complement activation promoting deposition leading to ischemia of the GI tract causing LUPUS ENTERITIS resulting to the following symptoms. The deposition of these complexes can lead to tissue destruction exacerbating further activation of inflammatpry response leading to chronic inflammation which can result to symptoms of acute cutaneous rash as evidence by the transient facial flushing and inflammation of the peritoneum leading to increase permeability and accumulation of exudative peritoneal fluid as evidenced by the ascites. the uncontrolled activation of the immune system can lead to further abnormal immune response leaving the patient in an immunocompromised state as evidenced by the presence of positive growth on blood cultures, decreased levels of c3 and positive antinuclear antibodies. furthermore, patient presented with leukocystosius with presence of stabs and toxic graniulation which may suggest a systemic inflammation. The persistence of diarrhea can lead to electrolyte imbalance particularly hypokalemia. Patient was started with antibiotics and hypokalemia was corrected. Ideally, for patients with autoimmune disease such as in this case, Aggressive immunosuppressive therapy with high-dose glucocorticoids is recommended for short-term control; evidence of recurrence is an indication for additional therapies. As the Noble laureate Albert Szent-Gyorgyi (last name pronounced as /sen yuryi/) exclaimed, ”Discovery consists of looking at the same thing as everyone else and thinking something different”.