Diarrhea…Cha, Cha, Cha

Every year during baseball season, certain things just return to my consciousness.

Lucky you, this year I’ve turned this childhood favorite into a blog post!  It’s time to talk about chronic diarrhea (I know you are excited).  Much credit to Dr. Erin Contratto who prepared this topic for AMR last month, and from whom I’ve stolen a lot of this information. Here’s a case to get us started.

65 year old female who complains of 6 months of intermittent diarrhea. She has periods of up to 10-15 loose, watery stools a day, other times she has more like 2-3 stools.  She frequently wakes up at night with crampy abdominal pain and diarrhea.  She has tried to eliminate lactose and gluten for short periods during this time, but it didn’t really make a difference.  She has not seen any blood, has not had fevers, has not lost any weight.  She doesn’t have stools that are greasy or hard to flush. No one else at home has similar sx.  She lives in the city, doesn’t camp, and hasn’t traveled in this time.

She has diabetes that is currently diet controlled with an HbA1c around 6.5%, hypertension, and GERD. She has not had medicine changes.

Step 1 is to classify the diarrhea as Fatty, Inflammatory, or Watery.  Fatty diarrhea will be hard to flush, and patients may describe a greasy sheen on the water in the toilet.  Malabsorption is the most common diagnosis in this category. Inflammatory diarrhea is characterized by blood, fever, and abdominal pain, and may get you thinking about infection, ischemia, or inflammatory bowel disease (the i’s have it?).  Watery diarrhea is more common than either of the other types, and is just what it sounds like, voluminous watery stools- without blood or fat.

Step 2- Is the watery diarrhea osmotic or secretory?  I try to reason these out based on the wording.  Osmotic diarrhea refers to “something” in the colon that attracts/keeps water there- leading to more water in the stool/diarrhea.  Polyethylene glycol is an osmotic laxative so would cause an osmotic diarrhea.  The pathologic etiologies of osmotic diarrhea include factitious ingestion of these kinds of laxatives, as well as carbohydrate malabsorption.  Osmotic diarrhea often occurs after meals (after the ingestion), and thus doesn’t wake patients up at night.

Secretory diarrhea on the other hand, refers to something secreted into the colon that then leads to the diarrhea. This can occur any and all times of the day, and often wakes patients up from sleep.  Included in this category are: post-cholecystectomy syndrome (from bile salts), certain toxins, and, neuroendocrine tumors, and vasculitis.  Also here is colitis, particularly microscopic colitis, disordered motility (IBS, hyperthyroidism), and cancer. Based on history, our patient has secretory diarrhea.

You could also calculate a stool osmotic gap to figure out secretory vs osmotic. The formula is           290 – 2 ({Na+} + {K+}), and a gap >125mOsms suggests osmotic diarrhea, while a gap <50mOsms suggests secretory.

Step 3: Once you figure out the big category, you can run down a differential diagnosis and decide what testing to order.  Commonly done: hemoccult, stool WBC, c.diff toxin, serum and stool electrolytes, qualitative fecal fat, laxative testing.  Certainly you wouldn’t do everything on every patient, but use your history and physical as a guide.

Step 4: What about endoscopy?  Many patients with chronic diarrhea will end up getting either a colonoscopy or flex sig.  Certainly if there is weight loss, fever, bleeding/iron deficiency, or unclear diagnosis, you would consider. Patients with typical IBS signs and no red flags may not require endoscopy.  Flex sig may be fine for an initial test, but consider getting the full colonoscopy if you are concerned for Crohn’s disease (to look at terminal ileum), malignancy, or bleeding.

From here, you’ll treat the disorder that you uncover.  And that is a post for another day…

 

 

Chronic Pancreatitis

Guest Poster:  Chronic pancreatitis  by Dr. Josh Stripling

 Definition: Irreversible destruction of the pancreatic parenchyma causing varying degrees of endocrine and exocrine dysfunction

  •  most patients typically present with persistent abdominal pain and steatorrhea
  • exocrine dysfunction – chronic diarrhea and weight loss
  • approx 20% present with maldigestion without pain

Causes:

  • The most common cause of chronic pancreatitis is alcohol use (usually more than 10y and more than 50g/day)
  • TIGAR-O (Toxic-metabolic, Idiopathic, Genetic, Autoimmune, Recurrent and severe acute pancreatitis, Obstructive)
  • tobacco also increase the risk of developing chronic pancreatitis

Diagnosis:  there are two specific entities: large- duct and small-duct (minimal change)

  • no consensus on gold standard for diagnosis: difficult testing and not always available
  • typical diagnosis is clinical based on symptoms and imaging
  • available testing includes: Secretin and CCK stimulation tests, fecal elastase, serum tripsinogen, stool sudan stain
  • most patients should undergo MRCP (not ERCP) or EUS to evaluate pancreatic ducts
  • patients can progress to development of pancreatic cancer

Plain film or CT can highlight pancreatic calcification to support the diagnosis

Management

  • avoidance of cause: EtOH cessation, pancreatic duct stenting, etc.
  • enteric coated pancreatic enzyme supplementation (40,000 units of lipase recommended) plus acid suppressant
  • fat-soluble vitamin replacement
  • monitor for endocrine dysfunction
  • pain management is difficult and theoretical improvement in pain with enzyme supplementation may occur
  • total pancreatectomy with islet cell transplantation is becoming more frequent

Resources: MKSAP 16, Harrison’s, “Chronic Pancreatitis” AFP 2007

Images: Medscape, http://www.meddean.luc.edu, healthcentral.com, drug3K.com