Today's case involved an elderly woman with
end-stage renal disease on intermittent hemodialysis who had presented with
chronic (2 months) diarrhea.
She had been admitted previously with a diagnosis of gastroenteritis and subsequently discharged. On presentation to the ED, she was
significantly hypovolemic and had a blood pressure in the 80’s/50’s. She was volume-resuscitated at which point
further history was obtained. She had
not had infectious symptoms, sick contacts, recent antibiotics, or changes in
her food/eating habits. She had
attempted a lactose-elimination diet to no avail. The diarrhea was non-bloody and contained
some mucous. Her initial
laboratory investigations revealed a mild lactic acidosis, a significantly elevated
plasma anion gap, and a negative C.
difficile toxin test. Initial
abdominal imaging with a plain X-ray revealed no free air or “thumbprinting”
and a CT abdomen with contrast showed some fluid in the bowels but no
significantly localizing problems. She
is currently being slated for endoscopic bowel investigation. The leading hypotheses are either microscopic
colitis or ischemic colitis.
There were multiple
learning points:
-Like everything in
medicine, there are categorizations of diarrheal illness. Acute diarrhea (many would define as less
than 2-4 weeks in duration) is generally infectious and therefore bacterial,
viral, and parasitic pathogens need to be considered and ruled out. Chronic diarrhea typically has a more
interesting differential diagnosis. One
has to consider functional causes like irritable bowel syndrome as a diagnosis
of exclusion. Inflammatory disorders
like Crohn disease and ulcerative colitis are commonly thought to occur in
people aged 15-40, but certainly can occur in a second bimodal peak in people aged 50-80.
Microscopic colitis typically
occurs in elderly and middle-aged individuals and characteristically has a
normal-appearing bowel mucosa – two types (lymphocytic and collagenous colitis)
have been identified; they are distinguished from other causes based on biopsy
results. Malabsorption of certain nutrients can also lead to diarrhea –
conditions associated include chronic pancreatitis, celiac disease, lactose
intolerance, and small-bowel intestinal overgrowth (often in association with
anatomical/surgical changes to the bowel).
Finally, chronic infections should be considered – these include Candida species, C. difficile, Giardia,
amobae, cryptosporidium, and Whipple
disease.
-Testing stool is
something that can aid in the diagnosis.
Stool can first be categorized as watery,
inflammatory, and fatty.
The fatty stool is typically associated with some type of malabsorption,
while the inflammatory diarrhea (containing strands of blood and mucous) can be
associated with an inflammatory or infectious process. Watery diarrhea is further subdivided into secretory and osmotic and the two can be distinguished based on the osmotic gap
(typically greater than 125 in secretory diarrhea). Secretory diarrheas characteristically continue despite fasting and can be
associated with certain chronic infections, as well as hormonal mediators of
secretion (Zollinger-Ellison syndrome, carcinoid syndrome, etc.). Osmotic diarrhea is typically the result of
an osmotic agent like sorbitol, so further testing is probably not necessary.
--The patient was
found to have an anion gap metabolic acidosis. We discussed the
differential diagnosis for this. While commonly-used acronyms like MUDPILES
are routinely taught in medical school, paraldehyde is so rarely used as a drug
that I don’t think it deserves its own place in limited memory-spans.
Instead, it is helpful to think of things that cause an elevated anion gap and
possible mechanisms that those could be produced:
-Lactic acid – shock, hypoperfusion, metformin
-Ketoacids (note that ketones themselves are not acidic but
betahydroxybutyrate and acetoacetic acid are) – Diabetic Ketoacidosis,
Alcoholic ketoacidosis, Starvation Ketoacidosis
-Renal failure – leads to buildup of inorganic acids like sulphates
-Toxins – salicylates, toxic alcohols (methanol, ethylene glycol), note that ethanol
does not produce an acidosis directly but can produce alcoholic ketoacidosis as
mentioned above through other hepatic mechanisms
Further Reading:
Camilleri, M. (2004).
Chronic diarrhea: a review on pathophysiology and management for the clinical
gastroenterologist. Clinical Gastroenterology and Hepatology, 2(3),
198-206.
Image Credit: https://sites.google.com/site/gracemedicalschool/2.1.3.10intestinalinflammation
