1/10 VA report: large bowel obstruction

Today we discussed a 69 year old man who presented with abdominal pain and obstipation and was ultimately found to have a sigmoid volvulus.

Abdominal Pain
When considering causes of abdominal pain, always think about referred sources of pain
Thoracic causes
  1. Lower lobe pneumonia (get a CXR)
  2. ACS (EKG)
Pelvic Causes
  1. Ovarian/testicular torsion (careful testicular exam)
  2. Pelvic inflammatory disease (careful history and physical)
Think of surgical causes of abdominal pain early
  • Bowel
    • Perforation
    • Obstruction
      • Large bowel obstruction more likely to require surgery than small bowel disease
  • Vascular
    • Mesenteric ischemia
    • AAA rupture

If you’re concerned about perforation, start by getting an obstructive series, which consists of supine and upright KUBs as well as a left lateral decubitus film.

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Left lateral decubitus films allow air to rise over the liver, where it’s easier to see than if it were right next to the gastric bubble. Source: WikiRadiography

KUBs can detect as little as 1ml of air in the abdomen, but are still only 50-70% sensitive for intra-abdominal free air, so a CT is really the imaging test of choice.

This patient’s imaging revealed at first that he had a large bowel obstruction!

  • Large bowel obstruction
    • Causes: cancer, volvulus (sigmoid > cecal), less commonly: adhesions, diverticular strictures, IBD, intussusception, ischemic colitis strictures
    • p/w progressive abdominal pain, distention and obstipation
    • rapid onset distention/obstipation, slower onset nausea/vomiting (less common unless proximal obstruction)
  • Small bowel obstruction
    • Causes: post-op adhesions, malignancy, hernias, IBD, strictures, volvulus (less common)
    • p/w acute abdominal pain and nausea/vomiting
    • rapid onset nausea/vomiting, slower onset constipation/distention

Further testing revealed sigmoid volvulus, which is more common in African Americans and across the volvulus belt (Africa, Middle East, India, parts of Russia)

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Key differences in SBO and LBO management

  • SBO: can often be managed conservatively (NG tube, bowel rest)
  • LBO: may require GI input for endoscopic detorsion (if volvulus), and ultimately surgery given high rate of recurrence of sigmoid volvulus (70%), or if cause is malignant


Gingold et al. Management of Colonic Volvulus. 2012 Dec. Clin Colon Rectal Surg.


1/10 PPMC Report: Chylous ascites and small bowel obstruction

Today we discussed a really interesting case of a middle-aged gentleman with a longstanding history of lower extremity lymphedema and several months of chylous ascites of unclear etiology, who presented with 50 lb weight loss and was found to have a small bowel obstruction.

In working through this case, it is first important to understand: what is chylous ascites?

Chylous ascites means intra-peritoneal fluid with composition resembling lymphatic fluid. There are different criteria, but definitions generally require triglyceride level >200 mg/dL (some more conservative definitions use a level of 110 mg/dL). Presence of particles such as chylomicrons can also be suggestive of chylous fluid, as can an opalescent or white/milky appearance on gross examination (though this is not specific!).

There are a few general pathophysiologic mechanisms of chylous ascites formation:

1. Increased pressure in lymphatic system: When the pressure within the lymphatic vessels increases, the result is leakage down the pressure gradient into the peritoneal cavity. This causes chylous ascites. Persistence of this physiology can lead to deposition of collagen within the lymphatic vessels, which impairs absorption and can perpetuate the problem as well as causing a protein-losing enteropathy. This cycle can be caused by multiple conditions, including lymphatic obstruction, malignancy, retroperitoneal fibrosis, increased chyle production (can be seen in cirrhosis) and circulatory congestion.

2. Inflammation in the lymphatic system: Inflammatory mediators can cause increased permeability of lymphatic vessels, allowing for leakage of lymph into the peritoneal cavity. (This mechanism is similar to why sites of superficial inflammation appear edematous and red from leaky capillaries). Conditions leading to this outcome include certain infections, notably filiariasis, which is infection with the roundworm wucheria bancrofti. This entity causes dramatic lymphatic inflammation, which can result in a condition called elephantiasis in addition to chylous ascites.

3. Structural abnormality in lymphatic system: The lymphatic system can have either congenital or acquired structural abnormalities that predispose to leakage and development of chylous ascites. Congenital causes are rare. Congenital lymphangiectasia is a condition in which lymphatic vessels commonly lack valves necessary to support lymphatic flow, which can result in dilation, stasis, and leakage throughout the lymphatic system. Acquired causes include damage to the thoracic duct through trauma or as a post-operative complication.

Differential for chylous ascites includes (but is not limited to!):

  • GI tumors (particularly small bowel) including lymphoma, neuroendocrine tumor, Kaposi’s sarcoma
  • lymphangiomyomatosis
  • cirrhosis
  • tuberculosis
  • MAI (usually in HIV/AIDS patients)
  • wucheria bancrofti (filiariasis)
  • Whipple’s disease
  • post-radiation fibrosis
  • pancreatitis
  • constrictive pericarditis
  • nephrotic syndrome
  • sarcoidosis
  • retroperitoneal fibrosis
  • post-operative or traumatic¬†thoracic duct injury
  • dilated cardiomyopathy or RH failure
  • congenital lymphangiectasia

Our patient’s presentation was concerning for something luminal in the small bowel. Ultimately he was evaluated with push enteroscopy and biopsy of the jejunum, which showed lymphangiectasia, lymphedema, expansion of the lamina propria and small bowel mucosa. For this patient’s constellation of symptoms – starting with unexplained chronic lymphedema, then chylous ascites and a small bowel obstruction – congenital lymphangiectasia is a highly possible diagnosis. This condition can cause SBO by dilated lymphatics becoming large enough to block transit through the bowel, and sometimes lymph can thrombose in areas of stasis. This condition is generally managed with dietary changes (diet high in medium-chain triglycerides). Our patient is awaiting a lymphangiogram for further evaluation of the structure of his lymphatic system.

HUP Report 12/19: UC-assosciated ILD after colectomy

At this conference, we reviewed the case of a 45 year old man who presented to pulmonary clinic for 2 years of productive cough and SOB.¬† His symptoms were progressive, and for the last few months he had been unable to walk a block or up a flight of stairs, which was a change from his baseline of being very fit.¬† His only medical history was having ulcerative colitis that was “cured” by colectomy many years prior.¬† His initial work-up was notable for PFTs with mixed lung disease (FEV1 40% => obstruction, FVC 65% => restriction), and a CT-scan of the chest showing diffuse bronchiectasis.¬† The salient learning points from the case were:

  1. Chronic cough is defined as lasting longer than 8 weeks.  If a patient is a non-smoker, and has a negative CXR, then the most common culprits are Meds (ACE), Upper-airway cough syndrome (aka post-nasal drip), cough-variant asthma, and GERD.  These can be diagnosed individually, or by medication trials.  This is an important differential for primary care, but our patient is already beyond this differential due to severe progressive functional restriction.
  2. Bronchiectasis is a radiographic diagnosis defined by bronchial wall thickening and dilation.  It is caused by a number of disorders that ultimately fall into one of the 4 categories in the vicious cycle shown below.  For all-comers, the most likely diagnosis is aspiration, but other common players are MAI, Immunodeficiency, ABPA, IBD, CTD, CF, and airway obstruction (ex. COPD or peanut aspiration).Capture
  3. Our patient was diagnosed (by exclusion) with IBD-associated bronchiectasis.¬† This is a rare phenomenon, but has been described since the 1970’s in various case series, and is often found after colectomy; in fact, bronchiectasis is one of the most common pulmonary manifestations of IBD (although the boards answer for most common is “necrobiotic lung nodules”).

The patient was treated with steroids and improved, although has not been able to be fully weaned.  If he cannot get off of steroids, there is a plan to treat with IBD medications even though he has no intestinal symptoms.  This would be an interesting and novel approach to care.

12/14 PPMC Report: Wilson’s Disease

Today we discussed a really interesting case of Wilson’s disease. We all remember from medical school that Wilson’s disease is a problem with copper excretion:

Wilsons1.pngIn patient’s affected by this condition, the body’s normal mechanisms for excreting copper do not function appropriately, which leads to accumulation of free copper (and decreased ceruloplasmin), which then can get deposited in body tissues. The main sites that are affected are the liver, the cornea, and the brain. Neurologic manifestations of Wilson’s disease can include movement disorders, neuropsychiatric symptoms, and dysarthria. Corneal involvement is seen with presence of a Kayser-Fleischer ring. This disease can also be associated with a hemolytic anemia.

Degree of liver involvement can be variable, and in its most severe form can include acute liver failure. We reviewed criteria for acute liver failure:


Of note, patients with Wilson’s disease and the top two¬†criteria¬†can still be considered acute liver failure even if there is underlying cirrhosis; this has important implications for status of transplant listing.

Wilson’s disease is suggested by low ceruloplasmin and¬†elevated free copper in the blood.¬†LFT abnormalities in a pattern of AST:ALT>2 and Alk Phos:T Bili <4 is also highly specific for this¬†diagnosis. ¬†In a less acute setting, copper chelators can be used for treatment. In acute liver failure, supportive measures can be helpful, and transplant is the definitive therapy. Plasmapheresis has also been reported in such cases!

11/7 HUP Report – Acute Liver Failure due to HSV

Thanks to Dr. Khungar for joining our discussion about a very interesting case. Today we discussed a patient with a history of poorly-managed SLE who was hospitalized with concern for pleuritis/pericarditis and rapidly developed acute liver failure. In a matter of a couple days this patient’s liver function tests went from normal to peak values of AST >14000, ALT >6000, Alk Phos 144 and T. Bili 9.6.

We reviewed the clinical definition of acute liver failure:


Our patient met criteria for acute liver failure. Within the broad differential for this condition, there are not all that many pathologies that will cause transaminase elevation to the degree seen in our patient. Some things to think about include:

  • drug induced liver injury
  • acetaminophen overdose
  • ischemic liver injury
  • viral hepatitis (rarely)
  • HSV

Care for acute liver failure involves supportive measures and evaluating for liver transplantation. We also discussed some data suggesting benefit to administration of N-Acetylcysteine (NAC) even in patients who did not overdose on acetaminophen.

In a prospective, double-blind trial published in Gastroenterology, acute liver failure patients without clinical or historical evidence of acetaminophen overdose were stratified by site and coma grade and assigned randomly to groups that were given NAC or placebo (dextrose) infusion for 72 hours. The primary outcome was overall survival at 3 weeks. Secondary outcomes included transplant-free survival and rate of transplantation.

Transplant free survival was significantly better¬†in patients receiving NAC, with the most notable benefit in patients with coma grades I‚ÄďII.


Our patient received an orthotopic liver transplant, and her explanted native liver stained positive for HSV. This is a rare cause of acute liver failure but should remain on your differential, particularly in patients at risk (including pregnant women or patients with compromised cellular immunity).



Lee, WM et al. Intravenous N-acetylcysteine improves transplant-free survival in early stage non-acetaminophen acute liver failure. Gastroenterology. 2009 Sep;137(3):856-64, 864.e1. doi: 10.1053/j.gastro.2009.06.006. Epub 2009 Jun 12.



11/1 Presby report: pancreatic masses, with a helping of chronic diarrhea

Today we discussed the interesting case of a middle aged man with chronic diarrhea who was found to have a pancreatic mass, ultimately found to be a gastrinoma. We spent some time discussing pancreatic masses, as the differential doesn’t just start and end with pancreatic cancer!

Pancreatic masses are not a trivial problem: 2-20% of patients who get MRIs for other reasons will have a pancreatic cysts or other solid lesions!

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Mets to the pancreas are usually from RCC or melanoma, or occasionally ovarian cancer.

Pancreatic cysts vary in their malignant potential

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JAMA 2016



There are 5 questions that will help you work-up chronic diarrhea:

  1. Is it really diarrhea? Make sure it’s not fecal incontinence due to chronic constipation or stool impaction/overflow
  2. Is it medication-induced? Beware of metformin, NSAIDs, PPIs, SSRIs, antibiotics, Mg-containing meds, mycophenolate mofetil; also sorbitol- or xylitol-containing gums, and herbal teas/supplements which contain sennosides or other compounds
  3. Is it factitious? (consider if stool osm <290 or >600, female healthcare worker age ~45)
  4. How long? acute (<2 weeks) vs chronic (>4 weeks) diarrhea
  5. What’s the diarrhea like?¬†inflammatory (frequent/bloody BMs, fever) vs fatty (greasy, hard to flush, weight loss) vs watery diarrhea
Screen Shot 2017-11-01 at 9.51.58 AM.png

Mayo Clinic Proceedings 2012

The majority of people with chronic diarrhea do not need stool cultures! In patients with chronic diarrhea, the highest yield would be in immunosuppressed patients (AIDS, organ transplant, etc), as they are more likely to have prolonged infection with a pathogenic organism like Salmonella or Shigella; this type of prolonged infection just doesn’t happen in immunocompetent individuals.

Other pearls

  • CA 19-9 can be elevated in pancreatic cancer but ALSO in any cause of pancreatic inflammation; so it is very NONSPECIFIC, meaning you shouldn’t jump to order it on anyone with a pancreatic mass
  • Gastrinomas generally don’t require adjuvant chemo after resection since they’re so slow growing
  • Carcinoid tumors will only produce symptoms (flushing etc) once they’ve metastasized to the liver, even if they’re radiographically invisible by CT or MRI
  • Blastocystis hominis is a commonly seen fecal protozoan, but it’s not clear that it truly causes diarrhea; for most people, it’s probably just a bystander to some other cause of diarrhea
  • Fecal calprotectin is secreted by neutrophils, and is a sign of inflammation; it’s most commonly used in IBD, but any cause of inflammatory diarrhea would cause it to be elevated

A lot of this is pulled from Becca’s excellent post from the summer. Take a look at hers for more re: the workup of chronic diarrhea!


  1. AGA Guideline on Diagnosis/Management of Asymptomatic Neoplastic Pancreatic Cysts. 2015.
  2. Stark et al. Pancreatic cystic disease: a review. JAMA 2016.
  3. Sweester S. Evaluating the Patient with Diarrhea: A Case Based Approach. Mayo Clin Proc.June 2012;87(6):596-602.

10/23 Presby report: acute abdominal pain, terminal ileitis

Tim Day presented a great case of a young man with acute abdominal pain, and was ultimately diagnosed with epiploic appendagitis (NOT appendicitis). Along the way we waded into some of the murky waters surrounding diagnosis of acute appendicitis and reviewed some important physical exam maneuvers.

In patients in whom appendicitis is suspected, two historical features make it more likely:

  • migration of pain to RLQ (OR 3.4)
  • vomiting (OR 5.4)

The Alvarado score is a clinical decision rule that can help rule out a diagnosis of acute appendicitis.

Screen Shot 2017-10-24 at 11.00.47 AM

Higher scores predict a higher risk of appendicitis, while scores less than 4 indicate a low risk of appendicitis, such that imaging may be avoided.

Note:¬†the Alvarado score is highly sensitive but not specific, so it’s good for ruling OUT appendicitis, but not ruling it in, particularly for the purpose of deciding on surgery. It also performs best in men, and may overpredict the probability of appendicitis in women.

A brief note on the antibiotics-first strategy: several European trials have attempted to give antibiotics first in an attempt to avoid surgery. While the data is heterogenous, generally the conclusions are that:

  • Antibiotic-first strategy can be considered in those who’ve had complications of prior intraabdominal surgery (fistulas, adhesions, etc)
  • The abx-first strategy is NOT associated with a higher risk of perforations or complications, but IS associated with a high risk of recurrent appendicitis

A quick note on the differential diagnosis of terminal ileitis: it’s not always Crohn’s!

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Bojic et al, 2011

One category to add to the list above: spondyloarthropathies (AS, reactive arthritis, psoriatic arthritis, etc).


  1. Bojic D et al. Terminal ileitis is not always Crohn’s Disease. Annals of Gastroenterology 2011.
  2. Flum D. Acute Appendicitis ‚ÄĒ Appendectomy or the ‚ÄúAntibiotics First‚ÄĚ Strategy. NEJM 2015.