Category Archives: Gastroenterology and Hepatology

Moffitt Pearls – 8.11.17 – Saddle Nose Deformity, Upper GI Bleeding &Munchausen Syndrome

Thank you to HH and Neil for both presenting today! HH first presented a mini case of a patient who came in for a gout flare that was found to have a saddle nose deformity.

Neil then presented the interesting case of a young woman with a hx of gastric ulcers presented with epigastric pain and hematemesis who after extensive work-up including CT and EGD was found to have Munchausen syndrome!************************************************************************************

Key Pearls

  1. The differential diagnosis for saddle nose deformity falls into the classic triad of infectious, inflammatory and malignancy per table below.
  2. 80% of upper GU bleeds are due to four causes: peptic ulcer disease (35%), esophagogastric varices (30%), esophagitis (10%) and Mallory-Weiss tears (~5%).
  3. The management strategy for a pt. w/ munchausen syndrome is VERY difficult, but should include a single provider (w/ help from psychiatry) and goal to limit interventions + discuss diagnosis with patient in a supportive manner.


Differential Diagnosis for Saddle Nose Deformities

Infectious Inflammatory Malignancy Other
Syphilis GCA (formerly Wegner’s) NK T-cell Lymphoma Trauma
Leprosy Sarcoidosis Locally invasive tumor (BCC) Cocaine
TB Relapsing polychondritis Lymphomatoid Granulomatosis Surgery
Cutaneous Leishmaniosis      
Septal abscess      

 Differential Diagnosis for Hematemesis AND Fever

  • Mallory-Weiss Tear
  • Peptic ulcer bleeds c/b perforation
  • Hemosuccus pancreaticus (pseudoaneurysm/aneurysm)
  • Upper GI Malignancy – hemobilia, widespread esophageal/gastric malignancy

Munchausen Syndrome or Factitious d/o Imposed on Self

  • Definition: Falsified general medical or psychiatric symptoms
  • Risk Factors: Females, Unmarried, Healthcare professional
  • Diagnostic Criteria (DSM-5):
  1. Falsification of physical or psychological signs or symptoms, or induction of injury or disease, associated with identified deception
  2. The individual presents himself or herself to others as ill, impaired, or injured
  3. The deceptive behavior is evident even in the absence of obvious external rewards
  4. The behavior is not better explained by another mental disorder, such as delusional disorder or another psychotic disorderPrognosis: Very poor even as multiple studies have shown limited benefit even with psychotherapy
  • Management: One provider should oversee pt with help of psychiatry w/ goal to limit interventions. One should be sure to exclude all possible medical conditions and then discuss diagnosis w/ pt in supportive manner


Moffitt Pearls 7.5.17 – Wilson’s Disease & Hemolytic Anemia

Thank you to Vincent for presenting a challenging case of a young woman with anxiety and depression presenting with unexplained jaundice and cirrhosis, later representing with a severe, hemolytic anemia. Although similar to a prior case presented last month then this was a second presentation of possible Wilson’s disease

 Top Pearls:

  1. Acute alcoholic hepatitis is a chronic disease (despite the name!). Presentation is based on predominantly cumulative burden – a single binge in a patient with otherwise minimal alcohol intake is unlikely to cause severe alcoholic hepatitis.
  2. In a young patient (< 35 yo) with new diagnosis of cirrhosis, consider genetic causes including Wilson’s, hemochromatosis, alpha-1 antitrypsin disease, autoimmune hepatitis, PBC, PSC. Vascular disease and infectious hepatitis should also be considered.
  3. The combination of liver disease and hemolysis raises concern for Wilsonian Crisis, which can herald impending acute liver failure.

Laboratory Diagnosis of Tumor Lysis Syndrome

Alcoholic Hepatitis

The clinical syndrome of acute alcoholic hepatitis includes the following compilation of laboratory and clinical features:

  • Moderately elevated transaminases in a 2:1 ratio of AST/ALT
  • Typically less than 300, rarely greater than 500
  • Elevated bilirubin and Jaundice
  • Jaundice generally develops within 3 months prior to presentation
  • Fever & Neutrophilic Leukocytosis
  • Both should only be ascribed to alcoholic hepatitis after ruling out infection!
  • Right upper quadrant pain – can often palpate tender hepatomegaly
  • Clinical history of chronic drinking with or without recent bing
  • It’s not uncommon that patients have actually decreased their drinking in the weeks-months preceding acute alc hep due to the onset of symptoms with alcohol intake.

See this RCT from NEJM regarding pentoxifylline vs. prednisolone for the treatment of alcoholic hepatitis. Bottom line:  Acute alcoholic hepatitis is a profoundly morbid disease with very high mortality (30-40% in 6 months).  Prednisolone was associated with a reduction in 28-day mortality, but did not reach significance and there were no improvements in 90-day or 1 year mortality.

Autoantibodies Associated with Causes of Cirrhosis


Autoimmune hepatitis

IgG, ANA, antismooth muscle Ab, anti-liver-kidney microsome-1 Ab, anti-liver cytosol Ab-1

Primary biliary cirrhosis

ANA, anti-mitochondrial Ab

Primary sclerosing cholangitis

IgM (40-50%), p-ANCA (30-80%)

Wilson Disease (WD) & Hemolytic Anemia

  • Wilson’s disease (WD) is an inherent disease, caused by mutations in the ATP7B gene leading to decreased excretion of copper into the bile
  • Copper accumulation results in injury to the liver and the central nervous system (thank you Muazzum for you amazing neuro ROS)
  • WD presents in a fulminant form with hepatocellular dysfunction, hemolysis and various multiorgan failures (Wilson’s crises)
  • Wilson disease can cause a Coombs-negative hemolytic anemia WITHOUT schistocytes reported in the literature
  • The exact mechanism of the haemolytic process has yet to be defined. copper inhibits sodium potassium ATPase in the erythrocyte leading to haemolysis (and likely without schistocytes as in this case).
  • Medical treatment includes chelating agents and/or zinc, but these have not proved effective in fulminant liver failure, where only liver transplantation (LTx) is regarded as lifesaving.
  • Some limited data for plasmapheresis for rapid copper removal
  • Portends very poor prognosis, often leading to acute liver failure

 (see attached an article on a review of Wilson’s and Hemolytic anemia compliments of HH!!)

Blast from the past!!! Approach to Hemolytic Anemia (thank you Katie!!)

ZSFG Morning Report 6/9/2017: Hematochezia, Massive Transfusion Protocols and Narcan

Thank you to Malia Honda and Brad Hunter for presenting a case from 5R of a middle aged man, who presented after PEA arrest and then had massive hematochezia requiring massive transfusion protocol.

Top Learning Pearls

  1. Narcan (naloxone), is the opioid antagonist used in opioid overdose. Rarely it can cause pulmonary edema through both cardiogenic and noncardiogenic mechanisms.
  2. BUN/Cr ratio can help determine location of GI bleed, if >20 is more likely to be upper GI source.
  3. Activate massive transfusion protocol when you need blood quickly for hemodynamically unstable patient. MTP will provide blood products in appropriate ratio (pRBC:FFP:plts). Rule of thumb to call for MTP if >4 u of prbc in one hour.



-Narcan can be delivered in many routes and doses (intranasal, IV, IM, subQ, inhalation).

  • Intranasal narcan prescribed to outpatients usually contains 2 or 4 mg.
  • IV/IM/SubQ: Initial 0.4mg to 2mg, and can be repeated
  • For reversal of respiratory depression with therapeutic opioid dose, more in the realm of 0.02 to 0.2mg IV to prevent severe withdrawal

-Incidence of Naloxone-Related Pulmonary Edema is overall low, thought to be between 0.2 – 3.6% of pts who receive narcan for overdose. The mechanisms of for pulmonary edema are thought to be both cardiogenic and noncardiogenic pulmonary edema, d/t the effect on cardiovascular tone from a resultant catecholamine surge, as well as increased pulmonary capillary leak.

Check out these two sources for some more information on narcan-related pulmonary edema


GI Bleeds in patient with cirrhosis

We are familiar with esophageal variceal bleeding, but Dr. Cello reminded us there are many sites where varices/collaterals occur at splanchic-systemic junctions, which all have a theoretical risk of bleeding, including

  • gastric vein + esophageal veins –> gastric varices
  • superior rectal vein + inferior rectal veins –> rectal varices
  • duodenal varices
  • jejunoileal varices
  • colonic and rectal varices
  • Paraumbilical veins + subcutaneous veins in anterior abdominal wall –> caput medusa

LABS to pay attention to in a GI Bleed:

  • -BUN/Cr ratio: if greater than 20 suggests UGIB, as blood is readily absorbed pre-jejunum, and broken down. As opposed to Lower GI bleed where the BUN/Cr ratio is normal
  • -Hemoglobin/hematocrit: Remember that acute blood loss is not reflected in hemoglobin/hematocrit! Take a GI bleed seriously even when H/H are normal, and pay attention to vitals and the clinical picture. Hemoglobin represents a concentration, so starts going down when we give IVF or when the body increases its intravascular plasma concentration.

Dr. Cello also made the good point that in a middle aged patient with LGIB, it is critical to do an anorectal exam to investigate for any anorectal masses. Remember to include malignancy on your differential for bleeding sources!


VA Intern Report Pearls 6.8.17: Behcet’s and the Silk Road

Case summary

Thanks to Colin Purmal for presenting the case of a 26F presenting with diffuse abdominal pain, bloody diarrhea and oral ulcers, who was diagnosed with Behcet’s disease.

Top pearls

1. Oral ulcers have a fascinating differential, including infection, autoimmune disease, malignancy, medication-induced, and vitamin deficiencies. But the most common cause is the aphthous ulcer!

2. Consider treating severe infectious bloody diarrhea (e.g. systemically ill, immunocompromised or elderly) with ciprofloxacin. The benefits outweigh the risks except in cases with high concern for EHEC or Salmonella typhi.

3. Behcet’s disease is a key “Crohn’s disease mimicker.”

Oral ulcers

  • Pocket reference Ddx:

Infection– primary HSV, HIV,TB, CMV, EBV, coxsackie, GC/CT, syphilis, fungal

Autoimmune– Behcet’s, SLE, Crohn’s, blistering skin disease (Pemphigus)

Malignant– SCC, lymphoma



Vit Deficiencies

Antibiotics in infectious bloody diarrhea

  • Most acute infectious diarrhea does not require antibiotic therapy.
  • 2001 IDSA guidelines for dysentery (to use the Oregon Trail-approved terminology) recommend obtaining stool cultures and treating empirically for 3 days in 3 cases: 1) toxic-appearing, 2) elderly, 3) immunocompromise.
  • The main benefit of antibiotic therapy is reduced duration of symptoms.
  • Ciprofloxacin is first-line, but Azithromycin can be used in pregnancy or if high suspicion for resistant Campylobacter (e.g. recent SE Asia travel).
  • Contraindications: 1) high concern for enterohemorrhagic E. coli (concern for precipitating HUS), 2) high concern for Salmonella typhi (concern for promoting carrier state and relapse)

IDSA Guidelines:

Crohn’s disease mimickers

  • Thinking about Crohn’s disease?
  • Consider Behcet’s disease in…patients from eastern Asia or the Middle East (the Silk Road!) with oral ulcerations (more frequent and more severe); genital ulcerations (more specific but less sensitive); systemic symptoms, including ocular symptoms, rashes, pan-vasculitis, weird clots (Budd-Chiari or cerebral venous thrombosis), pathergy (a 20G needle prick causes a papule or pustule within 48 hours).
  • International Study Group for Behcet’s Disease Diagnostic Criteria:
Recurrent oral ulceration: Aphthous (idiopathic) ulceration, observed by physician or patient, with at least three episodes in any 12-month period
Plus any 2 of the following:  
Recurrent genital ulceration Aphthous ulceration or scarring, observed by physician or patient
Eye lesions Anterior or posterior uveitis cells in vitreous in slit-lamp examination; or retinal vasculitis documented by ophthalmologist
Skin lesions Erythema nodosum-like lesions observed by physician or patient; papulopustular skin lesions or pseudofolliculitis with characteristic acnelform nodules observed by physician
Pathergy test Interpreted at 24 to 48 hours by physician

Behcet’s review:


Thanks to Ashley Stein-Merlob for presenting an yet to be solved case of a 63 yo female with worsening cognitive impairment, chronic diarrhea and weight loss undergoing a work-up for malabsorption.

The dirty scoop on STOOL STUDIES

  • Fecal fat
    • Sudan Ill Stain: Qualitative assessment, less sensitive, often used as a first pass test
    • Quantitative 72-96 hour collection. Gold standard. More sensitive but difficult to get.
  • Bacterial culture
    • Not necessary in chronic diarrhea
    • Indications in acute diarrhea: severe illness, inflammatory diarrhea, high risk hosts, symptoms lasting > 7d days, public health concerns
  • Osms and Electrolytes
    • Order if suspect surreptitious diarrhea from laxative abuse
  • Biofire PCR
    • Available at the VA, tests for 22 pathogens including C. dif, e. coli, shigella, giardia, and more. May be helpful for acute diarrhea but more costly than targeted testing

Approach to UNEXPLAINED WEIGHT LOSS in Older Adults

  • The differential is broad and includes almost every organ system.
    • Most common categories: malignancy, psychiatric, gastrointestinal disease, endocrine.
    • In the elderly consider the 9 D’s of weight loss: Dementia, Dentition, Depression, Diarrhea, Disease (acute and chronic), Drugs, Dysfunction, Dysgeusia, and D
  • First pass work-up
    • Basic labs: CBC, BMP, LFTs, TSH
    • CRP, ESR
      • ** Pearl from Meg Pearson – Although non-specific an elevated test result may prompt you to do a more thorough work-up.***
    • LDH, UA, CXR, FOBT
    • Consider: Abdominal ultrasound
    • A prospective study demonstrated that if this baseline work-up is normal none of the patients went on to have malignancy demonstrated on additional testing. Therefore if the baseline work-up is normal, no further testing is necessary but continue with close follow-up.
    • When to get colonoscopy?
      • Primarily to look for microscopic colitis, IBD, malignancy
      • Should be considered if there are persistent symptoms, inconclusive diagnosis, or failure to respond to therapy.
      • Probably best to refer to GI prior to colo to ensure biopsies are taken
    • Resource: AAFP Practice guidelines for Unexplained Weight Loss in Older Adults



ZSFG AM Report – 6.2.17 – HIV-Associated GI Pathology

Thank you Kenny for presenting a case of a patient with AIDS, abdominal pain, diarrhea, and fevers found to have a partial SBO and inflammation in the terminal ileum.

Top Pearls:

  1. Partial or complete small bowel obstruction in a patient without prior surgery is very unusual and should raise suspicion for tumors, complicated hernias, Crohn’s disease or other inflammatory processes, gallstones, volvulus, or intussusception.
  2. CT Abdomen/Pelvis is better than KUB for identifying the specific site and severity of obstruction (partial vs. complete), as well as potentially determining the etiology.
  3. Infections in HIV can localize to different parts of the bowel with small bowel etiologies including: HIV enteropathy, MAC, protozoan (Giardia and the spordia), and helminths (strongy)


More Information on HIV-Associated GI Pathology by Location in GI Track:
HIV-Associated GI Pathology (By Location):
                -CMV, HSV
                -Kaposi’s Sarcoma
                -Idiopathic ulceration
                -Neoplasia (Kaposi’s sarcoma, lymphoma)
Small Bowel:
                -HIV enteropathy
                -Protozoa (Giardia, Isospora, Cryptosporidia, Microsporidia)
                -Helminths (Stronglyoides)
                -Viral (CMV, HSV)
                -Bacterial (Clostridia, Salmonella, Shigella, Campylobacter)
                -Fungal (Cryptococcus, histoplasmosis)
                -Neoplastic (KS, lymphoma)


For more info on HIV-associated diarrhea, see this Evernote from Rachel Greenblatt:


Bhaijee F, Subramony C, Tang SJ, Pepper DJ. Human immunodeficiency virus-associated gastrointestinal disease: common endoscopic biopsy diagnoses. Patholog Res Int 2011;2011:247923.

Evernote Link:


MOFFITT GI REPORT PEARLS 5/10/17: Ischemic Colitis!

Hey Everyone! Thanks to Meghan for presenting an interesting case from the med consult service of an elderly woman with abdominal pain, vomiting, and diarrhea, who was found to have transverse colitis on CT scan without clear signs of ischemia and a negative infectious workup. Curious! Pearls on ischemic colitis below.


Top Pearls:

  1. CT abdomen with IV contrast is the study of choice in ischemic colitis
  2. Mainstay of treatment is fluids, with antibiotics suggested in moderate/severe cases
  3. Ischemic colitis itself is NOT an indication for anticoagulation (unless embolic) or antiplatelet therapy


For those who want more info:

Check out this 2016 BMJ “Clinical Updates” article on ischemic colitis:

Box 1: Common causes of ischaemic colitis (from above BMJ article)

  • Systemic—Heart failure, systemic inflammatory response syndrome (SIRS), atherosclerosis
  • Embolic—Atrial fibrillation
  • Thrombotic—Concurrent malignancy and haematological disorders
  • Pharmacological—Chemotherapy, sex hormones, interferon therapy, pseudoephedrine, cardiac glycosides, diuretics, statins, non-steroidal anti-inflammatory drugs (NSAIDS), immunosuppressive drugs, vasopressors
  • Surgical—Abdominal aortic aneurysm repair
  • Endoscopic—Colonoscopy and bowel preparation media for colonoscopy


Workup: Urgent CT abdomen with IV contrast! Controversial whether plain films or ultrasound are helpful. Early endoscopy confirms the diagnosis by direct visualization and helps distinguish cases that merit conservative management or emergency resection.

See these prior pearls on the ddx and management of ischemic colitis including an algorithm that risk stratifies patients into mild, moderate, and severe ischemic colitis:

A little more about antibiotics for ischemic colitis:

  • There is no strong evidence for the routine use of antibiotics in colonic ischemia, but ACG suggests empiric broad spectrum antibiotics (cipro + flagyl or broader if healthcare associated risk factors) for most patients with colonic ischemia except those with mild disease. The rationale is to prevent translocation of colonic bacteria across the mucosal defense barrier. Evidence is from animal studies showing reduced inflammation and colonic damage, small heterogeneous retrospective human trials, and expert opinion.
  • Caution with empiric antibiotics if EHEC is on the differential since there is evidence that antibiotic treatment of EHEC is associated with the development of HUS!

Indications for surgical exploration:

  • Perforation
  • Generalized peritonitis
  • Severe ischemia on radiography or endoscopy (pneumatosis, portal venous gas, gangrene)
  • Ongoing hemorrhage causing instability or requiring repeated transfusions
  • Lack of improvement with conservative management
  • >3 risk factors: right-sided colitis, male sex, renal dysfunction, colonic strictures, pain without rectal bleeding, SBP<90, HR>100, WBC>15, hgb<12, Na<136, BUN>20, LDH>350

Patients requiring surgical intervention have 37-48% mortality compared to 6.2% in those treated conservatively.

*Pearl: Anticoagulation is NOT indicated unless the etiology is embolic.

*Pearl: Ischemic colitis is NOT itself an indication for antiplatelet therapy since it is not purely an atherosclerotic condition.

*Pearl: DVT prophylaxis IS recommended in ischemic colitis as long as bleeding is not severe.




Have a great day everyone!