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![• Conclusions: Use of PPIs in patients dialyzed using a dialysate [Mg] of 0.75-
1.0 mEq/l is associated with hypomagnesemia. We suggest monitoring
plasma [Mg] in patients taking PPIs, with discontinuation of the medication
if possible and/or adjustment of dialysate [Mg] to normalize plasma [Mg].](https://image.slidesharecdn.com/gitinhd-161223220001/85/GIT-in-Hemodialysis-36-320.jpg)
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GIT in Hemodialysis
1. Gastrointestinal symptoms are common among hemodialysis patients and include nausea, vomiting, abdominal pain, dyspepsia, constipation, and diarrhea. The causes are often multifactorial related to uremia, dialysis treatment, and medications. 2. Abdominal pain in dialysis patients can be caused by various gastrointestinal or non-gastrointestinal issues. Common gastrointestinal causes include diseases of the upper gastrointestinal tract, lower gastrointestinal tract, hepatobiliary system, and pancreas. Non-gastrointestinal causes include metabolic, hematologic, cardiovascular/pulmonary, endocrine, neurological, and toxic disorders. 3. Dialysis patients may be at increased risk for gastrointestinal
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GIT in Hemodialysis
- 1. GIT IN HEMODIALYSIS By:Ahmed Eldeep MD
- 2. AGENDA 1- Common gastrointestinal(GI) symptoms among HD patients. 2-Abdominal pain in Dialysis patient. 3- Are dialysis patients at an increased risk of GI bleeding? 4- Hemodialysis-associated ascites.
- 4. Common gastrointestinal (GI)symptoms
- 5. • The CVScomplications like hypotension & arrhythmia were at the top with frequency of 79.3%. The GIT complications like nausea, vomiting abdominal pain followed the CVS complication in decreasing order of frequency. The other major proportion of complications was Hematological complications
- 6. 1-Nausea and vomiting Occursin up to 10% of routine dialysis treatments. Etiology The cause is multifactorial. • Inadequate dialysis. • Hypotension • Early manifestation of disequilibrium syndrome. • Dialyzer reactions. • Fluid and electrolyte changes during the dialysis treatment. • Non-dialysis causes(outside of the dialysis setting) e.g: Hypercalcemia Cerebral causes or GI causes Prior to the initiation of dialysis, patients may complain of nausea and vomiting. These symptoms usually disappear with dialysis and removal of uremic toxins.
- 7.
- 8. 2-Dyspepsia. Persistent or recurrentabdominal discomfort centered in the upper abdomen epigastric pain or discomfort, bloating, belching, eructations, and flatulence. EITIOLOGY • True GI pathologic process, such as peptic ulcer disease, GERD, gastritis, duodenitis, or gastroparesis. • Medications as phosphate binders (e.g., calcium carbonate or aluminum salts) or iron supplements. TTT: Prokinetic agents, antacids, and histamine H2 receptor antagonists.
- 9. 3-Constipation common complaint amongdialysis patients. The causes of constipation are multifactorial. • Patients' fluid intake is limited. • Dietary restriction of high-potassium fruits and vegetables. • Medications : calcium- or aluminum-containing phosphate binders and iron supplements. • Patient inactivity and underlying medical conditions. Constipation may result in obstruction, fecal impaction, and even bowel perforation, diverticular disease, as well as hemorrhoids.
- 10. •Senna lax lab •Importalsach •Lactulose •Laxel sach •Enemax •Picolax drops
- 11. Management I. Increase thefiber content in food usually corrects constipation. II. If constipation persists, the following agents may be used: 1. Emollient: docusate sodium (egycusate) 100 mg PO qd to tid , 2. Stimulant: bisacodyl (Dulcolax) 1–3 tablets; and senna(senna lax lab –purgation). 1. Hyperosmotic: sorbitol ( importal sach )70% 30 mL PO qhs, lactulose 30 mL PO qhs. Sodium polystyrene sulfonate resin plus sorbitol (Kayexalate) has been associated with intestinal necrosis in ESRD patients, either given by enema or by the oral route ( Dardik et al, 2000).
- 12. Medicinal fiber inthe form of psyllium (Regmucil sach) should be avoided. Both sodium and potassium are present in the preparation. and a large volume of liquid is required in preparation. Laxatives containing magnesium, citrate, or phosphate should be avoided (e.g., milk of magnesium, magnesium citrate, and Fleet's products containing phosphate). Magnesium is poorly handled by patients with ESRD. Hypermagnesemia can result in development of neurologic disorders. (laxel sach- Epico-eff. Sach) • Citrate, in general, should be avoided in patients with ESRD because it increases absorption of aluminum from the GI tract.(Mg citrate) • Hyperphosphatemia from phosphate intake can upset the delicate calcium/phosphorus balance and contribute to the sequela of secondary hyperparathyroidism.(Enemax- Laxel sach) • Mg sulphate االنجليزي الملح) Epsom salt- laxel sach) • Na picosulphate (picolax drops)
- 13. •Senna lax lab •Importalsach •Lactulose •Laxel sach •Enemax •Picolax drops
- 14. 4-Diarrhea An episodeof diarrhea. Diarrhea following a period of constipation. An acute episode of bloody diarrhea associated with abdominal pain, fever and signs of sepsis, and hypotension, especially during hemodialysis, may suggest ischemic bowel disorder or bowel infarction. Diarrhea associated with fever suggests an infectious cause. Persistent diarrhea requires a workup similar to that in patients without ESRD. Suspect autonomic neuropathy in patients with diabetes mellitus. Endoscopy is required to diagnose inflammatory bowel disorders.
- 16. Abdominal pain inDialysis patient
- 17. Case 81-year-old female onhemodialysis C/O: worsening of abdominal pain of 2 days’ duration. The pain started as a dull ache over the lower abdomen 2 months earlier, diffuse but especially prominent over the lower quadrant, and was unrelieved by analgesic medications. EX.: her whole abdomen was diffusely tender, but the lower quadrant was extremely tender with palpable nodular lesions. Lab: normal amylase and lipase level along with a white cell count of 13.5K/CUMM (3.5- 10.6 K/CUMM), calcium of 10.6 mg/dL (8.2-10.6 mg/dL), phosphorus of 5.9 mg/dL (2.3-5.0 mg/dL) and intact PTH 880 pg/mL (18-86 pg/mL). CT abdomen and pelvis and ultrasound of her abdomen revealed ………….
- 18. Causes of abdominalpain in dialysis patient GIT causes: Upper GI diseases. Lower GI diseases. Hepato-biliary. Pancreatic. Non-GIT causes:
- 19. Upper GI diseases:e.g., Gastritis, duodenitis, and peptic ulcer disease.
- 20. Lower GI diseases: A.Diverticulosis and diverticulitis • Constipation. • Colonic diverticula increased among pt with polycystic kidney disease. B. Spontaneous colonic perforation. diverticular disease, amyloidosis, constipation, post-transplantation immunosuppressive treatment, and infections. C. Discrete colonic ulceration. discrete, nonspecific single ulcers of the cecum or ascending colon. D. Colonic carcinoma.
- 21. Hepato-biliary. Chronic cholecystitis andcholelithiasis are common in dialysis patients. Symptomatic patients can be treated with laparoscopic cholecystectomy or traditional cholecystectomy. Asymptomatic patients usually undergo cholecystectomy if they are renal transplant candidates.
- 22. Pancreatic. - Diagnosis inpatients with renal failure is confounded by the observation that serum concentrations of pancreatic amylase and lipase are elevated in patients with ESRD in the absence of acute pancreatitis. - The highest levels of amylase and lipase are noted in hemodialysis patients. The absolute values do not exceed three times the upper limit of normal. The degree of elevation is roughly proportional to the degree of renal dysfunction.
- 23. Non-GIT causes: • Metabolicdisorder, e.g. hyperlipidemia, porphyria,calciphylaxix. • Hematologic disorder, e.g., sickle cell crisis, hemolysis, acute leukemia. • Cardio/pulm. disorder, e.g., acute MI, pulmonary embolus, pneumonia, pericarditis. • Endocrine disorder, e.g., DKA, pheo, Addison’s disease, hyperparathyroidism. • Neurologic, e.g., herpes zoster. • Toxic, e.g., Drugs, toxins, narcotic withdrawal. Also, heat stroke.
- 24. Case 81-year-old female onhemodialysis C/O: worsening of abdominal pain of 2 days’ duration. The pain started as a dull ache over the lower abdomen 2 months earlier, diffuse but especially prominent over the lower quadrant, and was unrelieved by analgesic medications. EX.: her whole abdomen was diffusely tender, but the lower quadrant was extremely tender with palpable nodular lesions. Lab: normal amylase and lipase level along with a white cell count of 13.5K/CUMM (3.5- 10.6 K/CUMM), calcium of 10.6 mg/dL (8.2-10.6 mg/dL), phosphorus of 5.9 mg/dL (2.3-5.0 mg/dL) and intact PTH 880 pg/mL (18-86 pg/mL). CT abdomen and pelvis and ultrasound of her abdomen revealed ………….
- 25. CT abdomen and pelviswithout contrast showing multiple soft tissue densities in the anterior abdominal wall (A). Calcification of blood vessels within the abdomen and pelvis was also noted (B).
- 26.
- 27. Both these findingsin the setting of end stage renal disease were consistent with calciphylaxis , a rare, and often fatal, complication. Although ulceration is considered a hallmark of calciphylaxis, it can also present as non-ulcerative nodular lesions, as in our patient. (Fine et al.,2002).
- 29. Are dialysis patientsat an increased risk of GI bleeding?
- 30. Upper GI bleeding Etiology Angiodysplasiaof the stomach or duodenum (24%), Erosive gastritis (18%), Duodenal ulcer (17%), Erosive esophagitis (17%), Gastric ulcer (12%), Mallory–Weiss (8%), and Erosive duodenitis (3%). Zuckerman et al (1985),
- 31. upper GI (n=34),lower GI (n=14), and unknown (n=4). Duodenal ulcer (26%) and gastric antral vascular ectasia (26%), followed by gastric ulcer (14%). *lower GI: colorectal cancer, angiodysplasia and ischemic enteritis were identified in equal numbers (21%).
- 32. The aim ofthis study was to examine the risk of UGIB among the dialysis patients during a 6-year period following their initiation of hemodialysis (HD) therapy in Taiwan- a country with the highest incidence of ESRD in the world, using general population as an external comparison group.
- 34. Proposed mechanisms forUGI Hge. with CRF include disturbances in : •Serum gastrin, in •Gastric acid secretion, •Mucosal barrier, •Clotting process, •Use of ulcerogenic drugs(NSAIDs, and aspirin); and •Infection associated with H. pylori.
- 35. Diagnosis. Esophagogastroduodenoscopy (EGD) Management. Asnonuremic patients. ( nasogastric aspiration, transfusion, H2 blockers or pump inhibitor and antacids). H2 blockers include Cemetidine ,ranitidine , famotidine, and nizatidine . All of these drugs are partially excreted renally, and their usual dosage should be reduced by at least 50% in CRF. For nizatidine, the recommendation is to give 150 mg every other day (versus the usual 150 mg twice a day dosing in nonuremic patients). Proton pump inhibitor - Dosing is unchanged in renal insufficiency.
- 36. • Conclusions: Useof PPIs in patients dialyzed using a dialysate [Mg] of 0.75- 1.0 mEq/l is associated with hypomagnesemia. We suggest monitoring plasma [Mg] in patients taking PPIs, with discontinuation of the medication if possible and/or adjustment of dialysate [Mg] to normalize plasma [Mg].
- 37. Serum magnesium levelsare lower in PPI use. In the inflammatory state low serum magnesium level is a significant predictor of mortality in hemodialysis patients.
- 38. Antacids containing aluminumand magnesium hydroxide should be avoided in dialysis patients to avoid aluminum toxicity and hypermagnesemia. Sucralfate is a sulfated polysaccharide,, complexed with aluminum hydroxide. Sucralfate should not be used in dialysis patients because of the risk of intestinal aluminum absorption ( Robertson et al, 1989 ). Risk factors for ulcer formation (NSAIDs and aspirin ingestion, smoking, etc.) should be eliminated if possible.
- 39.
- 41.
- 42. Case A 53-year-old male,ESRD secondary to type2 DM on maintenance HD for 2Y presented with ascites of six months duration. He was on twice-weekly HD with target wt of 68–70 kg, which progressively reduced since the last two months. Examination: BP: 130/80 mm Hg, he had moderate to massive ascites and no palpable abdominal organomegaly. Investigations : Hb of 8.6 g/dL, bl. urea of 84 mg/ dL, s cr. of 7.4 mg/dL, s. ca. of 8.7 mg/dL and s. phosphorus of 3.9 mg/dL. His URR on dialysis was 56%. Ascitic fluid analysis revealed an exudate with protein of 5.4 g/dL, albumin of 2.3 g/dL, LDH of 145 U/L and cell count of 250, 95% of which were lymphocytes. Serum albumin was low at 2.7 g/dL, with SAAG of <1.0.
- 43. Culture of fluidwas negative and AFB and malignant cells were negative. A complete evaluation to look for cardiac and hepatic causes was negative. He was diagnosed to have dialysis-related ascites. His dialysis treatments were intensified and his dry weight was gradually reduced by 1.0 kg/week till 66 kg. At the last follow-up of four months, there has been a minimal reduction in ascites.
- 44. What is thebest known successful treatment for Dialysis Associated Ascites? 1. Intense Hemodialysis 2. Intense Ultrafiltration 3. Kidney Transplantation 4. Angiotensin Converting Enzyme Inibitors 5. Repeated Paracentesis 6. Albumin infusion with ultrafiltration
- 45. Hemodialysis-associated ascites IDIOPATHIC DIALYSISASCITES Patients on maintenance hemodialysis may develop ascites in the absence of a clear underlying cause ( a diagnosis of exclusion). Incidence :declining due to improvement in hemodialysis technology, better control of volume overload, enhanced dialysis dose, and better nutrition. Pathogenesis — multifactorial, including: • Chronic volume overload. • Changes in peritoneal membrane permeability. • Impaired lymphatic peritoneal resorption. • Contributing factors, such as hypoalbuminemia and congestive heart failure. • Hyperparathyroidism.
- 46. Diagnosis: Exclude other causes. Diagnosticcriteria for idiopathic dialysis ascites includes: Ascetic fluid with the following characteristics: Straw-colored appearance High protein content (3 to 6 gm/dL) A leukocyte count ranging from 25 to 1600 cells/mm3 Laparoscopic examination (to eliminate various possibilities - to perform appropriate biopsies for histologic examinations and cultures).
- 47. Treatment Initial strategies tocontrol ascites : • Salt and fluid restriction, • Aggressive fluid removal by ultrafiltration, • Intermittent paracentesis, and/or • Better nutritional intake. If these initial measures fail, • Switching to CAPD • Peritoneovenous shunt (Denver or LeVeen shunt). • Renal transplantation. definitive treatment of these patients as complete resolution of ascites within six weeks. • Prognosis — The prognosis of idiopathic dialysis ascites is poor. Approximately 45 % of patients die within 15 months of diagnosis.
- 48.
Editor's Notes
- #7 Etiology. Nausea or vomiting occurs in up to 10% of routine dialysis treatments. The cause is multifactorial. Most episodes in stable patients are probably related to hypotension. Nausea or vomiting also can be an early manifestation of the so-called disequilibrium syndrome described in II.A. Both type A and type B varieties of dialyzer reactions can cause nausea and vomiting. Non-dialysis causes must always be considered when nausea and vomiting occur outside of the dialysis setting, as discussed in Chapter 34. For example, hypercalcemia may manifest as (primarily interdialytic) nausea and vomiting, and should be looked for when no other explanation is at hand. 2. Management. The first step is to treat any associated hypotension. If nausea persists, an antiemetic (see Table 6-5) can be administered. 3. Prevention. Avoidance of hypotension during dialysis is of prime importance. In some patients, reduction of the blood flow rate by 30% during the initial hour of dialysis may be of benefit. However, the treatment time must then be lengthened accordingly.
- #8 Dyspepsia. Dyspepsia is defined as persistent or recurrent abdominal discomfort centered in the upper abdomen (epigastrium). Dyspepsia and indigestion are terms that are frequently interchangeable. Symptoms may include epigastric pain or discomfort, bloating, belching, eructations, and flatulence. Dyspepsia may be due to a true GI pathologic process, such as peptic ulcer disease, gastroesophageal reflux disease, gastritis, duodenitis, or gastroparesis, as seen in diabetic patients. Alternatively, dyspepsia may be related to medications that dialysis patients are required to take, such as phosphate binders (e.g., calcium carbonate or aluminum salts) or iron supplements. Evaluation for organic lesion is warranted if the history and physical examination are suggestive of such lesions. Prokinetic agents, antacids, and histamine H2 receptor antagonists are the most widely used agents in the management of dyspepsia. Dosing of these drugs in renal failure is discussed below in Section II.A.3. (prokinetic drugs) and Section II.B.3. (H2-blockers).
- #9 Dyspepsia. Dyspepsia is defined as persistent or recurrent abdominal discomfort centered in the upper abdomen (epigastrium). Dyspepsia and indigestion are terms that are frequently interchangeable. Symptoms may include epigastric pain or discomfort, bloating, belching, eructations, and flatulence. Dyspepsia may be due to a true GI pathologic process, such as peptic ulcer disease, gastroesophageal reflux disease, gastritis, duodenitis, or gastroparesis, as seen in diabetic patients. Alternatively, dyspepsia may be related to medications that dialysis patients are required to take, such as phosphate binders (e.g., calcium carbonate or aluminum salts) or iron supplements. Evaluation for organic lesion is warranted if the history and physical examination are suggestive of such lesions. Prokinetic agents, antacids, and histamine H2 receptor antagonists are the most widely used agents in the management of dyspepsia. Dosing of these drugs in renal failure is discussed below in Section II.A.3. (prokinetic drugs) and Section II.B.3. (H2-blockers).
- #10 Constipation. Constipation is not an uncommon complaint among dialysis patients. The causes of constipation are multifactorial. Patients' fluid intake is limited. Dietary restriction of high-potassium fruits and vegetables decreases the fiber content of ingested food. Medications such as calcium- or aluminum-containing phosphate binders and iron supplements cause constipation. Patient inactivity and underlying medical conditions may contribute to constipation. Narcotics given as an analgesic, such as codeine and meperidine, can cause constipation, as well as mental status change in patients with end-stage renal disease (ESRD). Constipation may result in obstipation with obstruction, fecal impaction, and even bowel perforation. Long-term complications of constipation are thought to contribute to the etiologic process of diverticular disease, as well as hemorrhoids. In patients treated with peritoneal dialysis, decreased bowel motility can cause dialysate outflow obstruction through the peritoneal catheter.
- #12 Dietary changes to increase the fiber content in food usually corrects constipation. If constipation persists, the following agents may be used: Emollient: docusate sodium (Colace) 100 mg PO qd to tid prn, casanthranol and docusate sodium (Peri-Colace) 1–2 capsules or 1–2 tablespoons PO qhs prn; Stimulant: bisacodyl (Dulcolax) 1–3 tablets PO qd prn; and Hyperosmotic: sorbitol 70% 30 mL PO qhs, lactulose (Chronulac) 30 mL PO qhs. Sodium polystyrene sulfonate resin plus sorbitol (Kayexalate) has been associated with intestinal necrosis in ESRD patients, either given by enema or by the oral route ( Dardik et al, 2000). It is not clear if the sorbitol component alone is equally dangerous. Whereas the combination is still widely used to treat hyperkalemia, use of sorbitol to treat constipation, where there are alternatives available, may not be wise. Soap suds, mineral oil, and tap water enemas or bisacodyl or glycerin suppositories once daily may be used for more immediate results. Colyte or GoLYTELY may be used for bowel preparation for endoscopy or radiology studies despite the high electrolyte content and the large volume ingested. Medicinal fiber in the form of psyllium (Metamucil) should be avoided. Both sodium and potassium are present in the preparation, and a large volume of liquid is required in preparation. Laxatives containing magnesium, citrate, or phosphate should be avoided (e.g., milk of magnesium, magnesium citrate, and Fleet's products containing phosphate). Magnesium is poorly handled by patients with ESRD. Hypermagnesemia can result in development of neurologic disorders. Citrate, in general, should be avoided in patients with ESRD because it increases absorption of aluminum from the GI tract. Hyperphosphatemia from phosphate intake can upset the delicate calcium/phosphorus balance and contribute to the sequela of secondary hyperparathyroidism.
- #15 An episode of diarrhea on an occasional (bowel irritability associated with dietary intake or viral GI disorder). Diarrhea following a period of constipation may signal fecal impaction. Treatment is focused on constipation. An acute episode of bloody diarrhea associated with abdominal pain, fever and signs of sepsis, and hypotension, especially during hemodialysis, may suggest ischemic bowel disorder or bowel infarction. ( ESRD patients are prone to this disease because of their atherosclerosis-associated risk factors such as hypertension, diabetes mellitus, and Dyslipidemia). Diarrhea associated with fever suggests an infectious cause. Blood and stool specimen for culture and sensitivity are required. Clostridium difficile enteritis may occur after prolonged antimicrobial therapy. Oral vancomycin or metronidazole is used in the treatment of C. difficile enteritis. Persistent diarrhea requires a workup similar to that in patients without ESRD. Suspect autonomic neuropathy in patients with diabetes mellitus. Endoscopy is required to diagnose inflammatory bowel disorders. In noninfectious diarrhea, loperamide hydrochloride (Imodium) or diphenoxylate hydrochloride and atropine sulfate (Lomotil) may be used for temporary relief.
- #21 A. Diverticulosis and diverticulitis. Right-sided diverticular disease is more common in the dialysis population than in the general population. Constipation due to dietary restriction of fluid, fruits, and vegetables and due to the use of certain phosphate binders predisposes dialysis patients to diverticular disease. Colonic diverticula are increased among those suffering from polycystic kidney disease. These large diverticula are prone to perforate. Complications of diverticulosis include diverticulitis and colonic perforation. Diverticulitis is a relative contraindication for peritoneal dialysis. In renal transplant candidates with recurrent diverticulitis, segmental resection of the lesions prior to transplantation may prevent subsequent perforation when high-dose steroid therapy is initiated after renal transplantation. B. Spontaneous colonic perforation. Spontaneous colonic perforation may be seen in patients with increased risk, such as those with diverticular disease, amyloidosis, constipation, post-transplantation immunosuppressive treatment, and infections. Spontaneous perforation may occur in the absence of an obvious cause or risk factor. A vasculitic pathogenesis has been proposed. When a patient receiving dialysis presents with abdominal pain, consider impending or actual colonic perforation. If perforation occurs, the mortality rate is extremely high. C. Discrete colonic ulceration. A patient with ESRD who is receiving hemodialysis and who presents with symptoms similar to those of appendicitis or carcinoma of the colon, or even with rectal bleeding, may have discrete, nonspecific single ulcers of the cecum or ascending colon. The pathogenesis of such lesions is unknown. Treatment is oriented towards symptoms. D. Intestinal necrosis. Necrosis of the small and large intestines has been reported in renal failure patients receiving oral or rectal sodium polystyrene sulfonate in sorbitol. Whether the culprit is the exchange resin or sorbitol is under investigation. E. Colonic carcinoma. With regard to colonic carcinoma, vigilance should be exercised in their detection. At a minimum, the official clinical practice guidelines for their detection in the general population should also apply to ESRD patients.
- #23 Elevated baseline levels of serum amylase. In most dialysis patients, due to the loss of urinary excretion, serum total amylase activity is elevated up to three times the upper limit of normal, even in the absence of clinical evidence of pancreatitis. The magnitude of elevation is higher in patients with acute renal failure than in chronic dialysis patients. Serum amylase levels may be spuriously low in peritoneal dialysis patients using icodextrin-containing dialysis solutions ( Schonicke et al, 1999). Serum concentrations of the pancreas-specific P3 isoenzyme have been variably reported to be increased or normal in asymptomatic dialysis patients. In fact, P 3 values exceeding three times the upper limit of normal are seen in up to 18% of asymptomatic dialysis patients. In contrast, in the nonuremic population, the P 3 amylase fraction is consistently absent and appears only with acute pancreatitis. 2. Question of occult pancreatitis in dialysis patients. Autopsy studies of largely asymptomatic dialysis patients have revealed a high incidence of pancreatic abnormalities, including chronic pancreatitis. The extent to which persistent elevations of the serum amylase levels are due to decreased catabolism of the enzyme versus pancreatitis is not known. 3. Serum and peritoneal fluid amylase levels during pancreatitis in dialysis patients. In a dialysis patient suspected of having pancreatitis, the finding of a serum total amylase value in excess of three times the upper limit of normal suggests that pancreatitis is present. Unfortunately, very severe pancreatitis can be present in dialysis patients with only slight, and therefore nondiagnostic, elevations in the serum total amylase level. We have found elevation of the plasma P3 isoenzyme level to be a reliable indicator of pancreatitis in dialysis patients ( Vaziri et al, 1988). The peritoneal fluid amylase concentration, easily obtainable in patients receiving peritoneal dialysis, is not a sensitive indicator of pancreatitis because the peritoneal fluid amylase levels can be only slightly elevated in the presence of severe pancreatitis. Nevertheless, an effluent amylase level greater than 100 units per dL is suggestive of pancreatitis or some other intra-abdominal catastrophe ( Caruana et al, 1987; Gupta et al, 1992). B. Lipase 1. Elevated baseline serum lipase levels in dialysis patients. Serum lipase activity is elevated (as high as twice the upper limit of normal) in about 50% of dialysis patients. Serum lipase activity rises following hemodialysis due to (a) heparin-induced increase in lipolytic activity and (b) presumably, ultrafiltration-induced hemoconcentration. Therefore, predialysis samples should be used for this test. C. Serum
- #28 With the above treatment, she had significant improvement of symptoms. Our case highlights the need for emergency physicians to be cognizant of this life-threatening complication in end stage renal disease patients and of the fact that calciphylaxis has different modes of presentation, among which is acute abdominal pain.
- #31 1. Incidence and etiology. According to one study, the sources of upper GI bleeding are gastritis (38%), duodenal ulcer (24%), duodenitis (14%), gastric ulcer (9.5%), esophageal varices (9.5%), and Mallory–Weiss tear (5%). Proposed mechanisms for upper GI hemorrhage with chronic renal failure include disturbances in serum gastrin, in gastric acid secretion, in the mucosal barrier, and in the clotting process; the use of ulcerogenic drugs, such as anti-inflammatory drugs that inhibit prostaglandin synthesis (nonsteroidal anti-inflammatory drugs, or NSAIDs, and aspirin); and infection associated with H. pylori. However, in another study by Zuckerman et al (1985), angiodysplasia was the most common source of upper GI bleeding, as well as recurrent bleeding in the patients with renal failure. Causes for upper GI bleeding in patients with chronic renal failure are as follows: angiodysplasia of the stomach or duodenum (24%), erosive gastritis (18%), duodenal ulcer (17%), erosive esophagitis (17%), gastric ulcer (12%), Mallory–Weiss (8%), and erosive duodenitis (3%). It is possible that angiodysplastic lesions in both the upper and lower tract in these patients are no more common than in the general population. However, they are discovered more frequently because of their greater tendency to bleed. It has been suggested that renal failure plays a role in the pathogenesis of these lesions. One theory states that functional failure of the precapillary sphincter due to volume overload and submucosal venous obstruction leads to vascular ectasia. Another theory states that a low blood flow state during dialysis followed by reactive hyperemia results in eventual angiodysplasia. Finally, others suggest that potassium or gastrin, agents known to reduce precapillary arteriolar tone, have a causative role in the development of these lesions. Angiodysplastic lesions in patients with chronic renal failure are more likely to bleed
- #32 upper GI (n=34), lower GI (n=14), and unknown (n=4). Duodenal ulcer (26%) and gastric antral vascular ectasia (26%) were the most frequently identified causes of upper GI bleeding, followed by gastric ulcer (14%). In patients with lower GI bleeding, colorectal cancer, angiodysplasia and ischemic enteritis were identified in equal numbers (21%).
- #34 The incidence rate of UGIB (42.01 per 1000 person-year) was significantly higher in the HD cohort than in the control cohort (27.39 per 1000 person-years). After adjusting for potential confounders, the adjusted hazard ratios for UGIB during the 6-year follow-up periods for HD patients was 1.27 (95% CI=1.03-1.57) compared to patients in the comparison cohort.
- #38 Abstract Introduction This study aimed to evaluate the association between proton pump inhibitor (PPI) use and serum magnesium levels, and the role of hypomagnesemia and PPI use as a risk factor for mortality in hemodialysis patients. Methods An observational study, including a cross-sectional and 1-year retrospective cohort study. The study comprised 399 hemodialysis patients at a single center, and was conducted from January to September 2014. Multiple linear regression analysis was used to investigate the independent relationship between serum magnesium levels and base- line demographic and clinical variables, including PPI and histamine-2 receptor antagonist use. Cox regression model was used to identify lower serum magnesium level and PPI as a predictor of 1-year mortality. Findings Serum magnesium levels were lower with PPI use than non-PPI use (2.39 6 0.36 vs. 2.56 6 0.39 mg/dL, P < 0.001). Multiple linear regression analysis showed that PPI use, low serum albumin levels, and low serum potassium and high-sensitivity C-reactive protein (hs-CRP) levels were significantly associated with low serum magnesium levels. A total of 29 deaths occurred during the follow-up period. According to Cox regression analysis stratified by hs- CRP, only high serum hs-CRP levels (>4.04 mg/L) in association with low serum magnesium levels was an independent risk factor for 1-year mortality (hazard ratio: 2.92; 95% CI: 1.53–6.40, P < 0.001). Discussion Serum magnesium levels are lower in PPI use. In the inflammatory state, a low serum magnesium level is a significant predictor of mortality in hemodialysis patients.
- #46 Patients on maintenance hemodialysis may develop ascites in the absence of a clear underlying cause. This entity, known as idiopathic dialysis ascites, is a diagnosis of exclusion. Associated findings may include volume overload, cachexia, hypoalbuminemia, and malnutrition. The incidence of this complication is declining due to improvement in hemodialysis technology, better control of volume overload, enhanced dialysis dose, and better nutrition. Pathogenesis — The pathogenesis of idiopathic dialysis ascites is most likely multifactorial, including [80-84]: Chronic volume overload with hepatic congestion and increased hepatic vein hydrostatic pressure. Changes in the permeability of the peritoneal membrane, as some affected patients previously underwent peritoneal dialysis. Impaired lymphatic peritoneal resorption. The rate of lymphatic fluid removal, as demonstrated by lymphatic flow studies, is slower in uremic patients. Contributing factors, such as hypoalbuminemia and congestive heart failure. Hyperparathyroidism.
- #47 Diagnosis — Intensive investigations are usually required to exclude other causes. (See "Initial therapy of ascites in patients with cirrhosis".) In addition to the proper clinical setting, diagnostic criteria for idiopathic dialysis ascites includes ascitic fluid with the following characteristics: Straw-colored appearance High protein content (3 to 6 gm/dL) A leukocyte count ranging from 25 to 1600 cells/mm3 As part of the evaluation, a laparoscopic examination is usually required to eliminate various possibilities and to perform appropriate biopsies for histologic examinations and cultures.
- #48 Treatment — Initial strategies to control ascites include salt and fluid restriction, aggressive fluid removal by ultrafiltration, intermittent paracentesis, and/or better nutritional intake [85]. However, hypotension may be a limiting factor in some patients. If these initial measures fail to provide substantial benefit, switching to CAPD has been shown to reduce the severity of ascites and to improve nutritional status. In addition, in some studies, placement of a peritoneovenous shunt (Denver or LeVeen shunt) has reportedly resulted in hemodynamic stability, reduction of ascites, and improvement of nutritional status [86]. However, major complications of peritoneovenous shunt include infections and malfunction. As a result, careful follow up of these patients and monitoring is usually required. (See "Peritoneovenous shunt for ascites and hepatorenal syndrome".) Renal transplantation appears to be the definitive treatment of these patients as complete resolution of ascites has been reported to occur within six weeks of transplantation in almost all patients [87,88]. Recurrence of ascites has been observed following graft failure [86,87]. (See "Treatment of diuretic-resistant ascites in patients with cirrhosis".) Prognosis — The prognosis of idiopathic dialysis ascites is poor. Approximately 45 percent of patients die within 15 months of diagnosis [89,90].