PMH: DM HTN Colon cancer s/p left hemicolectomy, chemo Now with mets to liver and peritoneum. Restarted on chemo 2/4/13 oxaliplatin, cepecitabine

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2 75 y.o M with PMH of HTN, DM II with nephropathy, CKD stage III(b/l cr 1.5), colon cancer s/p hemicolectomy (8/2011) now with recurrence and mets to liver and peritoneum undergoing chemo at woodhull, recent bilateral DVT presented with abdominal pain, nausea, intermittent nb/nb vomiting, diarrhea of several weeks duration PMH: DM HTN Colon cancer s/p left hemicolectomy, chemo Now with mets to liver and peritoneum. Restarted on chemo 2/4/13 oxaliplatin, cepecitabine Home Meds: Metoprolol 50 mg qday, ferrous sulfate 325 mg bid, Acarbose 50 mg daily Sodium bicarbonate 325 mg bid, Calcium carbonate 650 mg daily Renagel 400 mg tid, Ramipiril 2.5 mg daily, Miglitol 25 mg daily Januvia 100 mg po daily, Coumadin 1 mg daily

3 Vitals: T F, BP /50-64, P 84-92, RR 18 HEENT: dry mucous membranes Lungs: Clear to ausc bilaterally CV: RRR, nl S1 and S2, no mr/g Abd: soft, non-distended, +BS, mild tenderness to palpation in epigastric area Extremities: trace pitting edema

4 BMP Na 136 K 3.6 CL 108 bicarb <10 BUN 79 Cr 3.3 Ca 8.4 VBG ph 7.22 pco po HCO Lactate 0.9 UA: negative ketones, glucose negative, protein 2+ CT abdomen: s/p partial left colectomy with evidence of metastatic disease to the transverse colon, mesenteric nodes and peritoneal implants in the RUQ. Question of local residual/recurrent tumor at the anastomotic site Left sided colitis, infectious vs ischemic Cirrhosis with left sided varices.

5 Date Na K CL CO2 BUN Cre Ca AnGap 02/23/ <10 79 m /24/ m 77 m /25/ <10 43 m /26/ <10 55 m /27/ m /28/ m /01/ m /02/ m /03/ m Date PH PCO2 PO2 HCO3 Lactate 02/ / / / /

6 Normally 7-8 L of fluid is secreted each day, and almost all these secretions, as well as any ingested fluid, are absorbed by the end of the colon Throughout the gut, fluid and electrolyte transport is driven primarily by Na/K ATPase transport activity across the basolateral membrane of the epithelial cells. Several key apical membrane electrolyte transporters, including Cl/HCO3 and Na/H ion exchanger and CFTR Cl channel, all of which are present in many segments of the gut and H/K ATPases, which are confined to stomach and colon

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9 For acid-base and electrolyte abnormalities to occur in diarrheal states, the volume of fluid lost must be sufficiently large to overcome the kidney s ability to adjust excretion to maintain acid-base equilibrium When losses are sufficiently large, the disorder that develops is determined by the specific electrolyte content of the loses

10 Cholera Caused by vibrio cholera V.cholera produces a toxin that increases camp levels by permanently activating adenyl cyclase in intestinal crypt cells, producing sustained activation of CFTR Chloride channel and thereby leading to excessive chloride secretion into the ileum and colon The increase in chloride secretion in turn stimulates the apical Cl/Hco3 exchanger, increasing stool [HCO3] Increase in anion secretion results in increased paracellular Na and water entry, resulting in high volume diarrhea that contains large amount of HCO3, as well as Na, K, Cl Clinical presentation is severe volume depletion, hypercholremic metabolic acidosis and hypokalemia.

11 Other diarrhea Enteropathic E.coli and other bacteria and viruses can cause diarrhea producing metabolic acidosis and hypokalemia Pathophysiology of these diarrhea states is less well defined, but both increased absorption and secretion seems to contribute Enterotoxin from pathogenic E.coli activates guanyl cyclase which increases cyclic GMP levels, stimulating chloride secretion in intestinal epithelial cells It has also been suggested that inflammation downregulates both the intestinal Cl/HCO3 exchanger and Na/K ATPase and also increases the gut water permeability non specifically

12 Autoimmune diarrhea Diarrheas that occur with UC, crohn and celiac diseases all are associated with T cell mediated gut inflammation Stool volume is only moderately increased, acid base and or electrolyte disorders rarely occur in these

13 Short Bowel Syndrome In patients who have jejunoileal bypass surgery for weigh reduction or shortened small intestine connected to the colon, undigested glucose delivery to the colon is increased, providing a substrate for bacteria that metabolize this sugar to lactic acid- D and L-Lactic acid. D-Lactic acid is slowly metabolized resulting in metabolic acidosis with an increased anion gap.

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16 A non gap acidosis is characterized by a serum anion gap that is unchanged from baseline, or a decrease in serum bicarb that exceeds the rise in anion gap. Nongap metabolic acidosis(hyperchloremic)refers a metabolic acidosis in which the fall in serum bicarb is matched by an equivalent increment in serum chloride Hyperchloremic acidosis is a descriptive term, and does not imply any primary role of chloride in the pathogenesis of the metabolic acidosis

17 Potential mechanisms leading to a nongap metabolic acidosis Clin J Am Soc Nephrol 7: , 2012

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