Dr.Ahmed Eldeep,MD

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 CVS complications 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
Occurs in 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. Dyspepsia.

8. 2-Dyspepsia.
Persistent or recurrent abdominal 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 among dialysis 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
•Importal sach
•Lactulose
•Laxel sach
•Enemax
•Picolax drops

11. Management
I. Increase the fiber 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 in the 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
•Importal sach
•Lactulose
•Laxel sach
•Enemax
•Picolax drops

14. 4-Diarrhea
 An episode of 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 in Dialysis patient

17. Case
81-year-old female on hemodialysis
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 abdominal pain 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 and cholelithiasis 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 in patients 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:
• Metabolic disorder, 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 on hemodialysis
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
pelvis without
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. Ultrasound of
abdomen
revealing
subcutaneous
nodule.

27. Both these findings in 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 patients at an increased risk of
GI bleeding?

30. Upper GI bleeding
Etiology
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%).
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 of this 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 for UGI 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.
As nonuremic 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: 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].

37. Serum magnesium levels are lower in PPI use. In the inflammatory state
low serum magnesium level is a significant predictor of mortality in
hemodialysis patients.

38. Antacids containing aluminum and 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. Angiodysplasia.

41. Hemodialysis-associated ascites

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 fluid was 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 the best 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 DIALYSIS ASCITES
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.
Diagnostic criteria 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 to control 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. THANK
YOU