abdominal mysteries

Nephrology Nursing Journal March-April 2011 Vol. 38, No. 2 173

Abdominal Mysteries: Pain, Peritonitis,Pancreatitis, Pseudocyst

Clinical Consult

Q:When a patient on perito nealdialysis (PD) presents withab dominal pain, what etiolo-gies should be considered?

A:The differential diagnosisfor the presenting symptomof abdominal pain is quitebroad for the patient on PD.

Infectious peritonitis is always suspect-ed, but it may not be the root or theonly cause of the abdominal pain.

Case Study

Patient Presentation A 28-year-old Asian female with a

history of chronic kidney disease(CKD) Stage 5 on PD presents to theemergency department at a universitymedical center with worsening

Maureen Craig Sergio Infante

Continuing NursingEducation

Maureen Craig, MSN, RN, CNN, is a ClinicalNurse Specialist – Nephrology, University ofCalifornia Davis Medical Center, Patient CareServices, Sacramento, CA, and a member of ANNA’sSacramento Valley Chapter. She may be contactedvia e-mail at [email protected]

Sergio Infante, MD, is an Assistant Professor ofMedicine, Department of Nephrology, Loma LindaUniversity Medical Center, Loma Linda, CA.

Statement of Disclosure: The authors reported noactual or potential conflict of interest in relation tothis continuing nursing education article.

This offering for 1.3 contact hours is provided by the American Nephrology Nurses’Association (ANNA).

ANNA is accredited as a provider of continuing nursing education (CNE) by the AmericanNurses Credentialing Center’s Commission on Accreditation.

ANNA is a provider approved by the California Board of Registered Nursing, provider numberCEP 00910.

Accreditation status does not imply endorsement by ANNA or ANCC of any commercial product.

This CNE article meets the Nephrology Nursing Certification Commission’s (NNCC’s) continu-ing nursing education requirements for certification and recertification.

The Clinical Consult department is designedto provide answers to questions concerning clin-ical problems and to report innovative clinicalpractices. Readers are invited to submit ques-tions to be answered by a guest consultant.Questions should provide background informa-tion and state specific information requested.Answers will be referenced. Manuscripts thataddress clinical problems or present innovativeideas are also invited. These should be between400 and 600 words and contain one to three ref-erences. Address correspondence to: CharlotteSzromba, Clinical Consult Department Editor,through the ANNA National Office; East HollyAvenue/Box 56; Pitman NJ 08071-0056; (856)256-2320. The opinions and assertions con-tained herein are the private views of the contrib-utors and do not necessarily reflect the views ofthe American Nephrology Nurses’ Association.

Copyright 2011 American Nephrology Nurses’ Association

Craig, M., & Infante, S. (2011). Abdominal mysteries: Pain, peritonitis, pancreatitis,pseudocyst. Nephrology Nursing Journal, 38(2), 173-186.

The differential etiology of abdominal pain in patients on peritoneal dialysis (PD) isbroad, and these patients may experience the same symptoms as those of the general popu-lation. This article provides an overview of the various types of abdominal pain in patientson PD, as well as their possible etiologies, symptoms, and treatment regimens.

GoalTo provide an overview of abdominal pain in patients on peritoneal dialysis.

Objectives1. Discuss the treatment of a patient on peritoneal dialysis who presents with acute

abdominal pain.2. Identify the potential etiologies of abdominal pain in patients on peritoneal dialysis.3. Explain the symptoms and considerations for the etiologies of abdominal pain in

patients on peritoneal dialysis.

abdominal pain and vomiting. Thepatient describes pain on a pain scaleas 10/10, similar to prior pancreatitisepisodes and unlike prior peritonitisepisodes. She has a history of peritoni-tis and multiple episodes of pancreati-tis. Her most recent pancreatitisepisode was managed at an outsidehospital about two weeks earlier witha peak serum lipase of 2489 U/L. Shewas discharged from the hospital 8days ago with improved but notabsent symptoms of nausea, vomiting,and abdominal pain. She reportsavoiding fatty foods during the lastweek, but her symptoms have againworsened. She had a soft stool oneday ago, and denies diarrhea, melena,and hematochezia. Her vomitus is bil-ious and nonbloody. The patient

denies any fever or chills, and her PDeffluent remains clear. The esophago -gastroduodenoscopy and colono -scopy performed at her previous hos-pitalization showed a small hiatal her-nia and normal colonoscopy. She isaway from her home now, visiting hersister in town, who is a potential kid-ney donor. They are awaiting medicalclearance prior to proceeding withkidney transplantation.

Past Patient History The patient has CKD Stage 5 and

reports some urine output. She startedon hemodialysis 10 months ago andconverted to PD after two months oftherapy. Her PD routine is fourexchanges per day, two liters perexchange, typically a mix of 1.5% and

Clinical ConsultClinical Consult Charlotte Szromba, Department Editor

Nephrology Nursing Journal March-April 2011 Vol. 38, No. 2174

Abdominal Mysteries: Pain, Peritonitis, Pancreatitis, Pseudocyst

2.5% dextrose PD solution. The etiol-ogy of her renal failure is unclear, andshe has a congenital solitary kidney.She presented with proteinuria andhypertension during her pregnancy,and her blood pressure neverreturned to baseline after delivery twoyears ago. The patient has a history ofperitonitis 2 and 7 months ago; bothresolved with 2 to 3 weeks of van-comycin treatment. She has had mul-tiple episodes of acute pancreatitis, themost recent occurring 1 week ago.Additionally, the patient had gout 1.5years ago; measles, mumps, chickenpox in the past; and a recent positivePPD for tuberculosis. Her allergiesinclude hydrocodone/acetaminophenwith a rash reaction, and latex with ahives reaction when exposed.

The patient’s family history is sig-nificant for a father who died of astroke at age 45 and her mother whois alive on dialysis at 55 years of age.The patient is married, and livingwith her husband and daughter. Shedenies tobacco, alcohol, or drug use.

Physical Examination The patient’s physical examina-

tion is noted to reveal a blood pres-sure of 180/114, mild chest tightness,blurry vision, burning of the eyes, anda headache. She is a thin female, whois tired but alert. The patient has a PDcatheter in the left lower quadrant,and the exit site is clean with no evi-dence of infection or local irritation.She has mild to moderate distentionof her abdomen, nontender to palpa-tion except at the low right inguinalarea and later in the mid-epigastricregion. She has normal bowel sounds.

Diagnostic TestsUltrasound (US) of the abdomen

showed no gall stones or gallbladderthickening, negative Murphy’s sign,no free fluid, normal liver, and absentleft kidney.

Laboratory results include a serumHct of 25.6%, white blood count(WBC) of 8.1 K/mm3, albumin 1.7g/dL, AST 13 U/L, ALT 12 U/L,bilirubin total 1 mg/dL, lipase 52 U/L,and amylase of 6 U/L. Urinalysisshowed WBCs 1 per high power field,

red blood counts (RBCs) 2 per highpower field, negative nitrate, and neg-ative leukocyte esterase.

The Hospital Course:Abdominal Saga Begins

The patient was made nothing bymouth (NPO) and given D5 normalsaline intravenously (IV) for hydra-tion. Computerized tomography (CT)(see Figure 1) of the abdomenrevealed a large 22x13x8.3 cmpseudocyst in the left abdomenextending into the pelvis, with tubu-lar-shaped fluid collection at inferioraspect, and the PD catheter tip ininferior portion of pseudocyst.

PD effluent samples were sent forcell count and culture. The patientwas empirically started on intraperi-toneal (IP) vancomycin and cef-tazidime. IP heparin was used due tofibrin in the peritoneal effluent fluid.She also initiated a course of oral flu-conazole for fungal prophylaxis. Herroutine outpatient medications werestarted.

PD fluid analysis confirmed peri-tonitis with a rising WBC count, andby the third day, a 3+ acid fast bacilli(AFB) was found, but final speciationand sensitivities of the organismremained unanswered. Because ofher history of a Bacille Calmette-Guérin (BCG) inoculation as a childand having several positive PPD

screens, one recently, a peritonealMycobacterium tuberculosis infectionwas in the differential diagnosis.

The peritoneal effluent WBC wasinitially 890/mm3 and rose while onIP antibiotics to a peak of 3050/mm3

over 6 days. The peritoneal effluentWBC subsequently fell but neverwent below 100/mm3. The lowresponsiveness to IP antibiotics sug-gested that the cavity she was usingfor dialysis was perhaps loculatedaway from much of her viscera. Shewas switched to IV antibiotics andthen back to IP, since there was betterreduction in the WBC count in theperitoneal effluent. Clinicians enter-tained the idea of the presence of anabscess in the pseudocyst or that thepseudocyst might need to be endo-scopically or surgically drained orbiopsied via peritoneoscopy. Thepatient continued to report feelingbetter on the IP antibiotics, but con-tinued to complain about nausea,vomiting, and abdominal pain in thelower quadrants with no rebound ten-derness or guarding. She receivedpain medication for pain manage-ment.

Consultation with InfectiousDisease

During the hospital stay, theDepartment of Infectious Diseaseswas consulted and concluded in the

Figure 1Tenckhoff Catheter within a Pancreatic Pseudocyst that Extended

into the Pelvis

Note: Patient's estimated peritoneal surface area was 1560 cm2. Pseudocyst estimatedsurface area = 1153 cm2.


differential that the patient was deal-ing with a resistant peritoneal organ-ism, or the load of the organism wastoo high for standard IP antibiotictreatment. The consult from theDepartment of Infectious Diseasessuggested to rest the peritoneum,switch to hemodialysis, send peri-toneal effluent for reculture, andentertain a medication cause of pan-creatitis. A tagged WBC scan wasnegative for active focus of infectionor inflammation.

In light of the acid-fast bacilli(AFB) in the peritoneal fluid, thepatient was started on moxifloxacin,pyrazinamide, rifampin, ethambutol,and continued on fluconazole. Earlyresults from microbiology confirmeda rapidly growing AFB, so the patientwas started on clarithromycin perconsult recommendation from theDepartment of Infectious Diseases.Clinicians from the Department ofInfectious Diseases later recommend-ed an adjustment in antibiotics toinclude azithromycin. The patientwas eventually stabilized on moxi-floxacin, rifampin, and azithromycin,which continued through the hospi-talization and was expected to contin-ue for 6 to 12 months.

AFB rapidly growing in the peri-toneal fluid would indicate it was notMycobacterium tuberculosis. However,considering her recent and remotehistory of positive PPD, the Depart -ment of Infectious Diseases continuedto recommend rifampin. The patientnoted that she had previously beenstarted on isoniazid (INH) at an out-side hospital but had an allergic reac-tion, resulting in pancreatitis; hence,this drug was not restarted.

Clinical SequelaeDue to the low responsiveness of

the PD fluid WBC to the IP antibiotics,the patient was converted to hemodial-ysis 16 days after admission, and thePD catheter was removed shortly after-ward. This was consistent with evi-dence indicating a PD fluid WBC non-responsive to antibiotic therapy by daythree is predictive of treatment failuredefined as PD catheter loss or patientdeath (Chow et al., 2006).

ComplicationsThe following day after the PD

catheter was removed, the patientdeveloped a hematoma/seroma on thelower left abdominal wall. This wasvery painful for the patient. Heparinfor deep vein thrombosis (DVT) pro-phylaxis was stopped. She was takenback to surgery, and the hematomawas evacuated and closed with a drainleft in place. The patient had a reaccu-mulation of the hematoma/seromaand again went to the operating roomfor evacuation. The patient’s hemat-ocrit dropped, and she received twounits of packed red blood cells. Herabdomen remained painful, and shehad ongoing nausea and vomitingcontrolled with IV fentanyl andantiemetics around the clock. CTscan revealed a fluid collection in theleft lower abdomen over the adnexaand a bowel full of stool consistentwith the constipation the patient wasexperiencing and possibly related toopioid medication used for pain con-trol. Serial CT scans demonstratedthe fluid collection in the abdomenreducing in size over time. Review ofthe CT did not determine suspicionsthat the abdominal hematoma had acommunication with the originalabdominal fluid collection thought tobe secondary to retained peritonealdialysate.

The patient was stabilized on oralmoxifloxacin, rifampin, azithromy -cin, antihypertensive medications,and antiemetic and pain medicationsas needed. She was subsequently dis-charged.

Pain Management Can Be a Pain

The patient continued to havepain throughout her hospital stay.Abdominal pain was at times in theepigastric region and occasionally inthe lower abdominal area. Pain wasthought to be secondary to peritonitis,post-operative pain from PD catheterremoval, hematoma/seroma develop-ment, and constipation/ileus. Consti -pation was visualized on abdominalCT scan throughout the colon andextending into the small bowel, com-

plicating the picture of abdominalpain, tenderness, and ongoing nau-sea. She had an allergy tohydrocodone. The nephrologist wasconcerned about the accumulation ofmorphine in the presence of CKDStage 5. The patient was placed onoxycodone/acetaminophen, fentanyl,and ketamine for pain management.Anxiety and depression about hermedical condition and the status ofher kidney transplant were possiblycontributing to her overall pain med-ication needs.

Nausea and Vomiting Leads To Readmission

The patient returned to the ER fora second and third visit presentingwith nausea and vomiting, and unableto keep her antibiotic or pain medica-tions down. The second admissionoccurred two days after discharge, andthe patient was diagnosed withclostridium difficile colitis. An abdom-inal CT showed pancolitis, a minimaldecrease of a pelvic abscess, andenlargement of a subcutaneous hema -toma. The second of two stool cultureswas positive for Clostridium difficile.The patient was stabilized, andmetronidazole (Flagyl®) was started totreat the C. difficile colitis. Upon dis-charge, the patient was instructed totake antiemetics around the clock andnot as needed, as previously pre-scribed. On the third consecutiveadmission three days after the priordischarge, the patient presented withnausea, vomiting, diarrhea, abdomi-nal pain, and facial swelling, againunable to keep her medications down.

Gastrointestinal symptoms resolv -ed with management of her nauseawith metoclopramide (Reglan®) andpromethazine (Phenergan®), andresuming the Flagyl in a liquid form toease swallowing to continue the treat-ment of C. difficile. Facial swelling wasthe result of a nonocclusive thrombusformed around her hemodialysiscatheter that repeat scanning deter-mined was not progressing. Facialswelling resolved during the hospitalstay. The patient was again dischargedon oral medications.



Hypertensive CrisisComplication

The patient presented on the firsthospitalization with BP 180/114mmHg and a two-year history ofhypertension. She continued to haveepisodes of hypertension potentiallyexacerbated by her pain. The patientwas stable toward the end of her firsthospitalization with metoprolol, dilti-azem, and clonidine. She had elevat-ed blood pressure during each subse-quent admission. Five days after dis-charge from her third hospitalization,she was en route to the ER with com-plaints of abdominal pain with nauseaand vomiting preventing medicationintake when she experienced a tonic-clonic seizure. She had two moreseizures witnessed in the ER and hada blood pressure of 200/130 mm Hg.An MRI of the brain was consistentwith seizures secondary to posteriorreversible encephalopathy syndromesecondary to hypertensive emer-gency. She was placed on phenytoin(Dilantin®), and a repeat MRIshowed the condition resolving.Antibiotics were held in anticipationthat they may have lowered theseizure threshold. When the Dilantinlevel was therapeutic, the antibioticswere restarted. The main concernwith the patient’s hypertensive emer-gency was due to her not taking cloni-dine (Catapres®) due to her nauseaand vomiting, and thus, causing arebound hypertension. She wasplaced on a clonidine patch prior todischarge.

Subsequent Follow Up During the fourth hospitalization,

CT of the abdomen showed noabnormalities, and compared to priorexaminations, there was significantimprovement in the diffuse colonicwall thickening. There was markedinterval improvement in the left later-al abdominal wall fluid collection aswell as in the mid-pelvic fluid collec-tion that was identified previously onCT scan of the abdomen. Fourmonths after the specimen was col-lected, the organism in the PD fluidwas identified at an outside laborato-ry as a scotochromogenic Mycobacter -

ium with susceptibilities to all antibac-terial agents tested. The patient com-pleted the 6-month course of moxi-floxacin, rifampin, and azithromycin.She was cleared to again pursue kid-ney transplantation. The infectiousdisease consult recommendationincluded a prophylaxis with trimetho-prim/sulfamethoxazole at the time oftransplantation.

Discussion

Some Questions to Ponder What was the etiology of this

patient’s abdominal pain? Thepatient had four consecutive hospital-izations over a 2-month period. Shereturned each time to the emergencydepartment with nausea and vomitingusually accompanied by abdominalpain. The potential etiologies of herabdominal pain included hiatal hernia,a non-tuberculosis mycobacteria(NTM) infectious peritonitis, pancre-atitis, C. difficile colitis, a post- opera-tive wound with a reoccurring sero-ma/hematoma, and constipation/ileusrelated to pain medication. Her multi-ple etiologies for abdominal painmade treatment challenging; since anetiology for the abdominal pain wasdetermined, treatment focused on res-olution for that etiology (antibiotics forinfections, drainage of the seroma/hematoma, and adjustments to med-ications to improve elimination ofbowel contents).

The original abdominal pain pres-entation was deemed by the patient tobe “pancreatitis like,” even thoughshe was found to not have pancreati-tis by enzyme level but did have peri-tonitis. This initial pain presentationmay have occurred because thepatient was dialyzing in the pancreat-ic pseudocyst that communicatedwith the pancreas, and therefore,when the fluid became infected, it wasinterpreted by the patient as ”pancre-atitis like” pain.

The WBC count in the PD fluidremaining above 100/mm3 combinedwith a prolonged time to organismidentification and antibiotic suscepti-bility complicated the patient’s man-

agement. The PD catheter materialcould have been seeded with the bac-terial organism, so PD catheterremoval was the expected choicewhen the PD fluid WBC did notrespond to the antibiotics as expect-ed.

Why did the patient becomeinfected with the strotochro-mogenic Mycobacterium? The organ-ism cultured from the patient’s PDeffluent was eventually identified as astrotochromogenic Mycobacterium.This is an environmental Mycobacter -ium in soil and tap water, and is morelikely to cause opportunistic diseasein an immunocompromised patient.Patients with CKD Stage 5 are typi-cally immunocompromised; howev-er, the exact mechanism throughwhich this patient contracted thisorganism or why this organism grewin this patient is unclear. Case reportsin the literature identify NTM peri-tonitis as an unusual complication ofPD (Li et al., 2010). NTM peritonitisshould be in the differential when abacterial peritonitis does not respondto IP antibiotics. Recovery can beexpected if appropriate antibiotics areused and the catheter removed if indi-cated (Lee, Chen, & Wu, 2008).

One report looked at 39 patientsreported in the literature on PD withan NTM infection, and reviewed thetreatment and outcomes for thesepatients (Singh & Saha, 2008). Thisstudy concluded there is growing con-sensus that treatment of NTM inpatients on PD should be consideredin the differential of exit site infectionsor peritonitis if routine cultures arerepeatedly negative or if the patientdoes not respond to first-line therapy.Antibiotics should be guided by sus-ceptibility results. Treatment durationhas not been defined, but severalmonths of antibiotics may berequired. If peritonitis develops, thecatheter should be removed (Singh &Saha, 2008).

Why did the patient have priorepisodes of pancreatitis? Studies inthe literature suggest that the inci-dence of pancreatitis may be up tothree times higher in patients usingPD compared to those on hemodialysis


(Lankisch, Weber-Dany, Maisonneuve,& Lowenfels, 2008). The basis for thisincreased incidence is not clear.Abnormalities, however, such ashypertriglyceridema, hypercalcemia,and irritation of the pancreas from theretroperitoneal diffusion of thedialysate, may play a role. Serumamylase levels may be increased, butdialysate amylase levels may be morevaluable in providing diagnosticinformation. Pancreatitis in the PDpopulation causes increased morbidi-ty and mortality, so early diagnosisand vigilant management are impor-tant to improve patient outcomes(Mehrota & Kathuria, 2008).

How could this patient havedialyzed in this pancreaticpseudocyst? Historically, this pati -ent’s PD experience was complicatedwith the PD catheter migrating intowhat was eventually determined to bea pancreatic pseudocyst, which possi-bly resulted from a previous pancre-atitis. Reviewing the PD equilibrationtest, this relatively small patient wasadequately dialyzed with a Kt/V ureaof 1.9 prior to admission. Further cal-culations showed that the surface areaof the cyst was 1153 cm2. Her estimat-ed peritoneal surface area is 1560cm2. The size of the pseudocyst waslarge enough to accomodate the vol-ume of her PD exchanges and tomaintain an adequate Kt/V urea. Thepresence of inflammation may haveenhanced solute transport (Infante,Depner, Morfin, & Pappoe, 2009).

Patients with large body surfacearea do not stay on dialysis as long assmaller patients mostly because ofinadequate clearances (Prowant,Moore, Satalowich, & Twardowski,2010). This relatively small patient (5feet, 2 inches, and whose weight was56.3 kg) was able to maintain an ade-quate Kt/V urea via her pseudocystmembrane with an estimated surfacearea of 1153 cm2.

Assessment of AbdominalPain in the Patient on PD

Acute abdominal pain is one ofthe most frequent complications for apatient undergoing PD. The differen-tial diagnosis for abdominal pain in

these patients is broad and should beapproached based on the patient’spresentation and history. Pain recep-tors in the abdomen respond tomechanical and chemical stimuli.Stretch is the principal mechanicalstimulus involved in visceral nocicep-tion, although swelling, distention,contraction, traction, compression,and torsion are also perceived.Mucosal receptors respond primarilyto chemical stimuli, in contrast toother visceral nociceptors thatrespond to chemical or mechanicalstimuli. A variety of chemical stimuliare capable of triggering these recep-tors, including substance P,bradykinin, serotonin, histamine, andprostaglandins, which are released inresponse to inflammation or oxygendeprivation caused by ischemia.Opioids are the most effective painmedication for this classification ofpain (Miranda, 2011), which feels likea deep ache with cramping. Visceralabdominal pain may radiate to otherlocations in the back and chest(Miranda, 2011).

The clinician assessing a patienton PD with abdominal pain shouldconsider the location and descriptionof the abdominal pain in addition toassociated symptoms and patient his-tory to guide assessment and to createthe treatment plan. The clinicianshould gather pertinent informationfrom the patient’s presentation andhistory, including changes in temper-ature, blood pressure, heart rate,breath sounds, bowel sounds,appetite, weight, urine, stool, or med-ications taken. Abdominal pain isoften associated with symptoms thatinclude nausea, vomiting, diarrhea,constipation, bloating, hematochezia,melena, and/or jaundice (Penner &Majumdar, 2009). The history shouldinclude a gynecological history inwomen. Physical examination shouldinclude palpation of the abdomen formasses or tenderness, inspection ofthe PD catheter exit site, palpation ofthe PD catheter tunnel, rectal exami-nation for occult blood, and pelvicexamination for women with lowerabdominal pain. Infor mation is pro-vided in Table 1 to differentiate the

etiology of the abdominal pain basedon pain location and characteristics.

Diagnostic Assessment Laboratory assessment should

always include PD fluid for cell countwith differential, culture, and sensitiv-ity to look for peritonitis. Additionallaboratory assessment when indicatedshould include serum CBC with dif-ferential, electrolytes, glucose, amino-transferases, alkaline phosophatase,bilirubin, lipase, urinalysis (if produc-ing urine), a pregnancy test forwomen of child bearing age, andblood and urine cultures. Furtherwork-up recommendations (such asabdominal X-ray, US, or CT) basedon pain location and characteristicsare shown in Table 1.

Causes of Abdominal Pain In Patients on PD

PeritonitisThe most common cause of

abdominal pain in the patient on PDis peritonitis. Peritonitis is most com-monly caused by bacterial infectionsfrom a skin or bowel source, but mayoccur secondary to a fungal pseudo -monas or mycobacterial infection. Inaddition to abdominal pain, turbiddialysate effluent, rebound tender-ness, and occasionally fever, nausea,and vomiting may be present. Theincidence of peritonitis in recent yearshas decreased to 0.5 episodes perpatient year or about one episodeevery 24 to 26 patient months. Thisdecrease is due to improved technol-ogy and connection techniques(Ponferrada, Prowant, & Satalowich,2008). Aseptic peritonitis occurs infre-quently and can be caused by a reac-tion of the peritoneum to medicationsor intraabdominal foreign material(such as PD catheter). Turbiddialysate and a relatively low WBCcount are characteristic of this condi-tion (Ponferrada et al., 2008).

Clinical course of peritonitis.When a patient on PD presents withinfectious peritonitis, clinical im -provement and a reduced peritonealfluid WBC should occur within 72



Table 1 Abdominal Pain in the Patient on PD by Location

Potential Etiology Accompanying Symptoms and Considerations

Epigastric Region Abdominal Pain

Diabetic gastroparesisand delayed gastricemptying

Patient may present with dyspepsia, upper abdominal fullness, early satiety, bloating, nausea, andvomiting. Delayed gastric emptying of solids and liquids has been detected in 50% of both symptomaticand asymptomatic patients undergoing PD, including those patients without diabetes (Barri & Golper,2010).

A scintigraphic gastric emptying study is useful to reach diagnosis.

Gastro-esophageal refluxdisease, hiatal hernia,and/or Mallory-Weisssyndrome

The patient may present with a pain pattern synchronized with eating. Symptoms worsen with increasedpressure on the gastro esophageal sphincter and include post-prandial and/or substernal fullness,dysphagia, nausea and vomiting, and hematemesis in a Mallory-Weiss tear. Reflux symptoms may beworsened by increased intra-abdominal pressure from PD fluid, although changes are usually notmeasurable in the lower esophageal sphincter pressures (Holley & Schmidt, 2010). Patients on CAPDwho were symptomatic were observed to have a significantly higher number of reflux episodes and anincreased time in which the lower esophageal pH was less than 4 as determined by 24-hour gastric andesophageal pH monitoring (Kim, Kwon, & Lee, 1998).

Gastroscopy is useful to visualize the tissue for inflammation, trauma, and/or bleeding.

Gastritis and peptic ulcerdisease

The patient presents with burning, gnawing stomach pain. Symptoms occur 2 to 5 hours after eating andare typically worst between 11:00 p.m. and 2:00 a.m. Patients will report relief with alkali or antisecretoryagents (Fishman & Aronson, 2010). Although the incidence of peptic ulcer disease is not increased inpatients on dialysis, an enhanced frequency of underlying mucosal inflammation in the upper GI systemmay be observed (Barri & Golper, 2010).

Gastroscopy is useful to visualize the tissue for inflammation, trauma, and/or bleeding.

Myocardial ischemia orinfarction

The patient may have referred cardiac pain to the epigastric area. This pain is typically accompanied byshortness of breath. Patients with CKD Stage 5 are at increased risk for cardiovascular disease.Cardiovascular disease accounts for 50% of deaths in the CKD Stage 5 population (United States RenalData System, 2010). Presenting patient may have recurrent hypotension that prevents attaining dryweight and heart failure that is unresponsive to changes in dry weight.

An EKG, echocardiogram, and cardiac troponin-I can aid diagnosis.

Ruptured aorticaneurysm

The patient may present with a pulsatile abdominal mass, usually combined with unstable bloodpressure. Typically, patient pain is very acute and radiates to the back. This is a life-threatening condition;consider an abdominal ultrasound if the patient is hemodynamically stable; otherwise, the patient shouldgo directly to surgery (Fishman & Aronson, 2010).

Pancreatitis The patient may have a history of gallbladder disease or recent alcohol ingestion (previous 1 to 3 days).The patient may present with rapid onset (10 to 20 minutes) diffuse pain or band-like radiation of pain tothe back, with nausea, vomiting, and anorexia. Pain may last for many days. The patient may be restlessand agitated. The patient may have relief when bending forward. The most common cause of pancreatitisin the U.S. is a gallstone blocking pancreatic outflow (Go & Everhart, 1994). Patients on PD have anincreased risk for developing acute pancreatitis. Possible causative factors related to PD therapy includeexposure to PD solutions or dialysis-related irritants, the incidence of peritonitis, or the presence ofhypertriglyceridema.

Abdominal ultrasound and CT scan aid diagnosis. A serum lipase level is preferred to an amylase levelbecause elevations in amylase in patients with CKD Stage 5 are most often due to impaired renalclearance. Lipase levels may be elevated in patients on hemodialysis thought to be secondary to theheparin exposure. Icodextrin, in one study, decreased measured amylase activity by as much as 90%(Soundararajan & Golper, 2009).

GI and pancreatic cancer The patient can present with pain worsening with eating and radiating straight through to the back. Thepatient may prefer the fetal position. The patient is usually experiencing weight loss. Tumors in thepancreatic tail present with more pain. Tumors in the head of the pancreas present with steatorrhea,weight loss, and often jaundice (Fernandez-del Castillo, 2010).

Gastroscopy is useful to determine pathology and can include biopsies.

continued on next page


Table 1 (continued)Abdominal Pain in the Patient on PD by Location


Right Upper Quadrant Abdominal Pain

Pancreatitis (See above.)

Cholecystitis Cholecystitis symptoms often occur one hour after fatty food ingestion. Pain may be deep and gnawingor severe and sharp. Pain may radiate to right shoulder. Pain may last 4 to 8 hours and may beaccompanied by a fever. Pain with jaundice but without a fever may be ascending cholangitis (Fishman& Aronson, 2010). The clinical management of patients with CKD Stage 5 with cholecystitis is similar tothose without renal failure.

Ultrasound may show dilated biliary tree. Endoscopic retrograde cholangiopancreatography (ERCP)allows visualization to diagnose and sometimes to treat (removal of stones or blockage) disorders of thebile and pancreatic ducts.

Hepatitis Pain may be accompanied by malaise, nausea, vomiting, anorexia, and/or fever. Hepatitis may be viralor alcohol related. Historically, the most common cause of viral hepatitis in patients on hemodialysis wasthe hepatitis B virus (HBV). Implementation of standard precautions, screening of patients and staff,vaccinations of all susceptible patients and staff, and the use of dedicated rooms and machines has ledto the decline in spread of HBV in dialysis units. Hepatitis C virus and hepatitis G virus are both moreprevalent in patients on dialysis (Natov & Pereira, 2010).

Hepatitis serologies are useful in determining a patient’s exposure to a virus; however, patients on dialysisare often immunocompromised, and serum reactivity can be challenging to interpret. Aminotransferasestend to be below normal in patients on dialysis without liver disease present. Upper limit of normal inthese patients is AST 24 IU/L, and ALT 17 IU/L (Soundararajan & Golper, 2009). Gammaglutany l -transpeptidase (GGT) increases with hepatobiliary disease. Alkaline phosphatase may be increasedrelated to renal osteodystrophy.

Pulmonary or pleuralpathology

Pain may be related to volume overload secondary to heart failure or a pleuroperitoneal leak giving riseto a pleural effusion (hydrothorax). Finding the effusion is only right-sided should prompt a search for apleuroperitoneal communication in the patient on PD (Holley & Schmidt, 2010).

Left Upper Quadrant Abdominal Pain

Splenic abscess orinfarction

A splenic abscess is usually associated with a fever and may be associated with splenic infarction.Splenic infarction may be the result of an embolic insult from atrial fibrillation (Fishman & Aronson, 2010).Patients with polycystic kidney disease can present with cysts in the spleen.

Gastritis and peptic ulcerdisease

(See above.)

Pancreatitis Pancreatitis infrequently presents on the left. (See pancreatitis above.)

Hepatobiliary disease (See cholecystitis and hepatitis above.)

Periumbilical Region Abdominal Pain

Early appendicitis (See appendicitis below.)

Diverticular disease (See below.)

Mesenteric ischemia orinfarction

Mesenteric infarction may be a life-threatening condition. Pain appears to be out of proportion to physicalfindings and may be accompanied by diarrhea. Risk factors include a personal or family history of ahypercoagulable state or venous thrombosis, congestive heart failure, recent myocardial infarction,hypotension, hypovolemia, sepsis, cardiac surgery, or a requirement for dialysis. Patients on dialysis arefrequently older, have extensive peripheral vascular disease, and may experience prolonged periods ofhypotension, thereby increasing the risk for ischemia of the mesenteric vasculature (Barri & Golper,2010).

Mesenteric angiography is the most effective diagnostic tool.






Periumbilical Region Abdominal Pain (continued)

Intestinal obstruction Pain may be accompanied by bloating following meals, vomiting, weight loss, abdominal distention tenderto palpation, and constipation. Intestinal obstruction may be partial or complete and result fromincarcerated hernias, surgical adhesions, intussusceptions, volvulus, inflammatory bowel disease,colonic carcinoma, and constipation leading to fecal impaction (Fishman & Aronson, 2010; Penner &Majumdar, 2009).

Constipation is a common complication of the patient on PD who often uses phosphate binders,analgesics, and iron. Additionally, the patient on PD may have a motility disorder and a sedentary lifestyle.Constipation causes nearly half of all cases of PD catheter outflow failure (Schmidt & Holley, 2010b).Prolonged constipation should be treated promptly because it may lead to a secondary peritonitis.

Computerized tomography (CT) has been replacing the small bowel radiographic series as the adjunctivestudy of choice since it can simultaneously provide information about the presence, level, severity, andcause of intestinal obstruction.

Ruptured aortic aneurysm (See above.)

Gastroenteritis (See below.)

Right Lower Quadrant Abdominal Pain

Appendicitis Pain and rebound tenderness may migrate from the periumbilical area to the right iliac fossa as theappendiceal inflammation involves the peritoneal surface. Pain may be accompanied by fever, anorexia,nausea, and vomiting (Fishman & Aronson, 2010).

A serum WBC and an abdominal CT with contrast are useful to confirm clinical suspicion.

Diverticulitis (See below.) In Asian countries, diverticulitis commonly presents uniquely with pain on the right side.Right-sided pain can lead to misdiagnosis of appendicitis (Fishman & Aronson, 2010).

Salphingitis (See pelvic inflammatory disease below.) Symptoms and causes are the same but may be more one-sided in the event the focus of the inflammation is on one fallopian tube.

Ectopic pregnancy Pain is accompanied by missed or late menstrual period (6 to 8 weeks) and vaginal bleeding (Fishman& Aronson, 2010). Pregnancies are uncommon in the patient on dialysis but do occur. There are nofindings to indicate an increased risk for ectopic pregnancy in the patient on PD; however, both conditionsare associated with infertility.

A transvaginal ultrasound combined with a serum or urine human chorionic gonadotropin level will aiddiagnosis (Fishman & Aronson, 2010).

Hernia Hernias present with a bulge that can become more prominent when coughing, straining, or standing up.Hernias are rarely painful, and pain is suggestive of strangulated or incarcerated bowel. Hernias occur moreoften in patients on PD secondary to the increased abdominal pressure from the PD fluid/treatment. Surgicalincisions in the abdominal wall to place the PD catheter also increase the risk for an abdominal hernia.Dialysate fluid leaks can occur from acquired or congenital defects in the abdominal and thoracic wall. Thismay demonstrate as a hydrothorax, hernia, or genital/abdominal wall edema (Ponferrada et al., 2008).

Peritoneal scintigraphy and CT peritoneography are useful tests to detect peritoneal defects.

Nephrolithiasis The colicky pain of nephrolithiasis is most often located in the back, but can present in the abdomen andmay be accompanied by nausea, vomiting, hematuria, pyuria, oliguria, and/or hydronephrosis (Fishman& Aronson, 2010). If the patient on PD has had a history of nephrolithiasis, he or she would be atincreased risk for a repeat occurrence.

A non-contrast helical CT scan can detect both stones and urinary tract obstruction, and is the goldstandard for diagnosing nephrolithiasis (Fishman & Aronson, 2010).

Inflammatory boweldisease

Crohn’s disease and ulcerative colitis are the primary examples of inflammatory bowel disease andinvolve ulcerations of the intestine from the distal ileum to the anus. Pain is accompanied by vomiting,diarrhea, rectal bleeding, and weight loss. Among current asymptomatic patients on dialysis, for example,routine colonoscopy reveals no enhanced incidence of mucosal lesions (Barri & Golper, 2010).

Diagnosis is generally achieved by colonoscopy with biopsy of pathological lesions.





Mid-Lower Region Abdominal Pain

Pelvic inflammatorydisease (PID)

Lower abdominal pain with menses, coitus, or jarring movement is the classic symptom of PID. Pain maybe accompanied by fever (50%), uterine bleeding (33%), and/or vaginal discharge (Fishman & Aronson,2010). PID is associated with sexually transmitted diseases or invasive gynecological procedures. Thereare no findings to indicate the patient on PD has increased risk for PID.

Diagnosis is aided by a urinalysis and microscopic evaluation of vaginal discharge.

Ectopic pregnancy (See above.)

Endometriosis Pain associated with endometriosis is typically worse during menses. Pain typically occurs withabnormal menstrual bleeding and infertility (Fishman & Aronson, 2010). The female patient on PD mayexperience benign hemoperitoneum secondary to ovulation, retrograde menstruation, orendometriosis; however, there are no findings to indicate an increased incidence for endometriosis inthe patient population on PD.

Laparoscopy is the preferred technique for diagnosing endometriosis.

Leiomyomas Pain may be accompanied by urinary frequency, difficulty emptying the bladder, constipation, anddyspareunia. Degeneration, torsion, or infarction of the fibroid is associated with pain, nausea, vomiting,and vaginal bleeding (Fishman & Aronson, 2010). The female patient on PD may experienceleiomyomas; however, there are no findings to indicate an increased incidence in the patient on PD.

Abdominal ultrasound will aid diagnosis.

Urinary tract infection Pain may be suprapubic and accompanied by pelvic pressure, dysuria, hematuria, diarrhea, nausea,vomiting, lethargy, incontinence, urinary frequency, foul-smelling or cloudy urine, and fever.

Diagnosis is aided by a urine culture and urinalysis.

Left Lower Quadrant Abdominal Pain

Diverticulitis Patient may present with nausea, vomiting, diarrhea, or constipation. Left lower quadrant pain is mostcommon in Western countries, while right-sided disease with right lower quadrant pain is the mostcommon finding in Asian countries (Fishman & Aronson, 2010). Diverticula may progress with theformation of an abscess, fistula, obstruction, perforation, and/or peritonitis, all of which are very seriousfindings for the patient on PD. Incidence for patients on PD is increased if patient has a diagnosis of polycystic kidney disease (Barri & Golper, 2010).

Abdominal CT scan with contrast will assist in confirming clinical suspicions.

Constipation (See above.)

Nephrolithiasis (See above.)

Salpingitis (See pelvic inflammatory disease above.) Symptoms and causes are the same but may be more one-sided in the event the focus of the inflammation is on one fallopian tube.

Ectopic pregnancy (See above.)

Hernia (See above.)

Irritable bowel syndrome Irritable bowel syndrome is a diagnosis of exclusion and presents with abdominal pain or discomfort inassociation with frequent diarrhea or constipation. No change of incidence is noted in the PD population.


(See above)

Infectious bowel disease ofdistal intestinal tract

(See gastroenteritis below.) Patients on dialysis are particularly susceptible to Clostridium difficile colitis,since they commonly receive antibiotics. Pain may be accompanied by watery diarrhea, fever, and ileus.One study noted the dismal long-term prognosis was 60 of 70 patients with C. difficlie died over a follow-up period of five years (Schmidt & Holley, 2010a).

Cytotoxin assay and endoscopic examination may be needed to support clinical suspicions.






Left Lower Quadrant Abdominal Pain (continued)

GI cancer Pain may be accompanied by blood loss and changes in bowel habits. Presentations of colonic neoplasiaare highly variable, so risk factors for colon cancer (particularly age and family history) should beconsidered in patients with lower abdominal pain. Patients on PD have a higher incidence ofnonmalignant gastrointestinal abnormalities leading to a positive stool guaiac test (Barri & Golper, 2010).For early detection of a colorectal malignancy, the patient on dialysis should receive annual screeningwith stool guaiac testing, followed by colonoscopy if indicated.

Multifocal, Global, or Diffuse Abdominal Pain

Mesenteric ischemia andinfarction

(See above.)

Pancreatitis (See above.)

Intestinal obstruction (See above.)

Irritable bowel syndrome (See above.)

Ruptured aneurysm (See above.)

Lactose intolerance Pain is accompanied by stomach cramps, nausea, bloating, acid reflux, and flatulence. Incidence is mostcommon in African and Asian populations, and is independent of the presence of PD.

The lactose breath hydrogen test is a noninvasive test that measures lactose nonabsorption.


(See above)

Gastroenteritis Pain with vomiting and diarrhea caused by a viral or bacterial ingestion. Family may present with thesame symptom history if toxin-mediated food poisoning (Penner & Majumdar, 2009).

A careful history is used to determine the etiology of symptoms. Diagnostic work-up should continue ifthe patient presents with diarrhea-associated hypovolemia, small volume stools containing blood andmucus, bloody diarrhea, temperature equal to or greater than 38.5ºC, passage of more than six unformedstools per 24 hours or a duration of illness greater than 48 hours, severe abdominal pain, recent use ofantibiotics, diarrhea in the elderly (70 years of age or older), or the patient is immunocompromised(Penner & Majumdar, 2009).

Abdominal Pain Directly Related to PD Treatments

Peritonitis Pain is characteristically diffuse with rebound tenderness. Patient will be very still to decrease pain frommovement. Patients on PD are at increased risk for peritonitis secondary to a break in aseptic techniquein appropriately performing the PD treatment itself. This typically results in a bacterial peritonitis from askin or bowel source; however, the patient on PD can also experience a fungal, pseudomonal,mycobacterial, or aseptic peritonitis (Ponferrada et al., 2008).

The PD fluid cell count should be measured and tracked over time; a WBC greater than 100/microliterwith greater than 50% polymorphonuclear cells is diagnostic of peritonitis. The PD fluid should be culturedto determine the organism and susceptibility to treatment (Ponferrada et al., 2008).

PD infusion or drain pain Pain predominately occurs at the time of PD fluid drain or fill. This complaint is thought to be caused bythe acidic pH (5.2 to 5.5) of conventional PD solution and is often improved when alternative solutionsare used that have added bicarbonate. Contributing factors may include poor catheter position, dialysissolution temperature, rapidity of the dialysis solution inflow, and the hypertonicity of the dialysis solutioncontaining an elevated glucose concentration (Holley & Schmidt, 2010).

Catheter position Severe pain in the rectum or perineum can be the result of an improperly placed catheter that is abuttingagainst sensitive abdominal structure (Ponferrada et al., 2008).





Abdominal Pain Directly Related to PD Treatments (continued)

Dialysis solution leaks Fluid may leak due to high pressure in the abdomen. The leak may occur into the abdominal wall, throughthe abdominal wall as a hernia, or into the pleural space through a diaphragmatic leak. When a leakoccurs and causes pressure in an adjacent space, the tissue can be swollen, tender, or painful (Holley &Schmidt, 2010).

(See hernia above.)

Exit site/tunnelcomplications

Pain is local to the exit site and/or tunnel. A tender exit site or tunnel should be treated and watchedcarefully because either of these conditions may lead to peritonitis if the infection tracts down the tunnelinto the peritoneal space. Culture the exit site and any fluid or pus expressed from the tunnel. If the exitsite does not appear healthy, exit site care should be performed 2 to 3 times a day.

Constipation (See intestinal obstruction section above.)

Hemoperitoneum This condition may occur painlessly. Very small amounts of blood will make the dialysis effluent appearpink tinged. Pink or bloody effluent suggests bleeding inside the abdomen. The female patient on PD mayexperience benign hemoperitoneum secondary to ovulation, retrograde menstruation, or endometriosis.Catheter manipulation can result in some bleeding and typically resolves with time. If bleeding continues,any anticoagulation therapy should be stopped, and the source should be investigated and could includeruptured cysts from polycystic kidney disease or other retroperitoneal pathology (Bleyer & Burkart, 2010).

A cell count of the dialysis effluent can help quantify the volume of blood loss. Abdominal imaging can beuseful to find the source of the bleeding.

Abdominal Pain in Special Populations

Elderly patients Elderly patients may present with little to no symptoms and underwhelming laboratory findings that donot demonstrate the etiology of the abdominal pain. A thorough history is critical in developing clinicalsuspicion. Mortality related to under-diagnosis of the acute abdomen in the elderly is high (Fishman &Aronson, 2010).

Hemophilia Patients with hemophilia presenting with abdominal pain should be screened for hematomas in the bowelwall with appendicitis-like pain (Fishman & Aronson, 2010).

Sickle cell disease Patients with sickle cell disease presenting with abdominal pain (usually right upper quadrant) should beevaluated for injury to the bowel related to ischemia (Fishman & Aronson, 2010).

hours after treatment initiation. Whenfaced with an elevated peritoneal fluidWBC and the absence of positive cul-tures, the clinician must think beyondthe most common causes of peritoni-tis. If a drop in WBC does not occurwith initial treatment, then further andaggressive work-up is indicated foralternative causes of the peritonitis,including fungal or mycobacterialsources. The clinician should keep inmind that by day three, a WBCgreater than 1090/mm3 in the PDfluid increases the mortality exponen-tially (Chow et al., 2006).

When the patient has relapsing orrefractory peritonitis, the clinicianshould drain the peritoneum, removethe PD catheter, and focus on preserv-

ing the peritoneum rather than savingthe peritoneal catheter (Li et al., 2010).

Diagnosing peritonitis causedby Mycobacterium. Difficulties inidentifying and determining suscepti-bilities of Mycobacterium in a timelymanner lead to delays in targetedtreatment. One case report describesusing real-time polymerase chainreaction (PCR) methods to identifythe M. tuberculosis DNA instead ofwaiting for a traditional positive AFBsmear (Dervisoglu, Sayan, Sengul, &Yilmaz, 2006). This approach can leadto isolating the Mycobacterium morequickly, allowing the clinician to initi-ate appropriate treatment.

Currently, there are 71 recognizedspecies of Mycobacterium. The relative

virulence of mycobacteria encoun-tered in clinical situations varies fromthe pathogenic species, such as M.tuberculosis, to the typically nonpatho-genic species of Mycobacterium(Shinnick & Good, 1994).

Mycobacteria thought to be non-pathogenic may still present in theimmunocompromised patient. A casereport for a peritonitis caused byMycobacterium simiae in a patient withhuman immunodeficiency virus (HIV)on PD demonstrated the difficulty ofdiagnosing and treating peritonitis withan NTM. Peritonitis caused bymycobacteria should be considered inall patients with recurrent peritonitisthat fails to resolve with conventionaltherapy. Additionally, NTM isolated in



the PD fluid should be confirmed onmore than one specimen, given thepossibility of an environmental con-tamination (Keenan, Jeyaratnam, &Sheerin, 2005).

Treatment of peritonitis. Whentreating a patient with peritonitis sec-ondary to mycobacteria, the peri-toneal fluid concentration of theantibiotics must reach a therapeuticlevel. When measured, the peritonealfluid concentrations of standard-dosed, orally administered isoniazidand pyrazinamide were maintainedabove the minimum inhibitory con-centrations (MICs); however, peri-toneal fluid concentration of rifampinwas below the therapeutic range mostof the time. Orally administeredrifampin did not reach MICs forMycobacterium tuberculosis in the peri-toneal fluid (Ahn et al., 2003).

Treatment for NTM, dependingon the organism and its susceptibilitypattern, generally requires prolonged(6 to 12 months) multi-drug antimi-crobial therapy and PD catheterremoval. The mycobacterial agentsrequire dosing adjustments for clear-ance and careful monitoring for toxi-city (Rho, Bia, & Brewster, 2007).

Although NTM is not a commoncause of peritonitis in the patient onPD, its presence is an indication toremove the PD catheter and to trans-fer the patient to hemodialysis. AJapanese study looked at risk factorsand causes for removal of the PDcatheter and found 47% of thecatheters were removed secondary toinfections including Staphylococcus,Candida, Pseudomonas, and NTM(Nodaira et al., 2008).

The patient on PD with peritonitissecondary to an NTM needs to beadequately treated to resolve the peri-tonitis. This includes culturing the PDfluid, often more than one time; treat-ing the infection with antibiotics towhich the organism is susceptible(although susceptibility informationmay take a long time to result, mean-ing the clinician will use the clinicalresponse of the patient in combina-tion with treating the organism withbroad antibiotic coverage); usuallyremoving the PD catheter; and sup-

porting the patient through the rigorsof a prolonged course of antibiotics(Keenan et al., 2005; Lee et al., 2008;Rho et al., 2007; Singh & Saha, 2008).

PancreatitisThe most common cause of acute

pancreatitis in the U.S. is gallstonesblocking pancreatic flow. Patients canalso experience acute pancreatitisafter alcohol ingestion (1 to 3 days).Patients on dialysis, especially PD,have an increased risk for developingacute pancreatitis. Acute pancreatitisin patients undergoing PD is morefrequent and seems to be more severethan in those receiving hemodialysistreatments. Some causative factorsrelated to PD therapy include PDsolutions or dialysis-related irritants,the incidence of peritonitis, or hyper-triglyceridema (Lankisch et al., 2008).

Pseudocyst Pancreatic pseudocysts develop

after an acute attack of pancreatitis inapproximately 10% of cases(Cameron, 1983; O Malley, Cannon,& Postier, 1985). Pseudocysts arelined by fibrous tissue and granula-tion tissue. The lack of an epitheliallining distinguishes pseudocysts fromtrue cystic lesions of the pancreas.The pseudocyst can be filled withnecrotic material and fluid, and maycommunicate with the pancreaticductal system and contain high con-centrations of digestive enzymes(Khalid & McGrath, 2010).

When assessing an encapsulated,fluid-filled peripancreatic lesion in apatient with acute pancreatitis, diag-nosis of a pancreatic pseudocystshould occur cautiously since there isno single test that can definitively ruleout a pancreatic cystic neoplasm.Ideally, there is a baseline abdominalimaging study that demonstrates the

absence of the lesion, chronologicallyfollowed by a clinical history that doc-uments pancreatitis, again followedchronologically by abdominal CTdemonstrating the presence of thepancreatic lesion and associatedinflammatory changes. Managementof the pancreatic pseudocyst canoccur conservatively by watching thelesion for resolution, or with drainageaccomplished surgically with or with-out percutaneious catheter or endo-scopically with or without stenting(Howell, Shah, & Lawrence, 2009).

Nursing Implications When a patient undergoing PD

presents with abdominal pain, the dif-ferential etiology is broad. Patients onPD may experience similar types ofabdominal pain as the general popula-tion. The clinician, however, shouldalways check the PD fluid for cellcount and culture, and sensitivity.Abdominal pain may be PD-relatedperitonitis, or it could be multi-factori-al, as was the case in this scenario pre-sented. Patients on PD have anincreased risk for some abdominalpathologies, and additionally, areimmunocompromised because ofCKD Stage 5. Careful assessment ofthe patient upon presentation willguide the work-up for abdominal painand lead the clinician to the causativefactor(s) and appropriate interventions.

ReferencesAhn, C., Oh, K.H., Kim, K., Lee, K.Y.,

Lee, J.G., Oh, M.D., ... Shin, S.G.(2003). Effect of peritoneal dialysison plasma and peritoneal fluid con-centrations of isoniazid, pyrazi-namide and rifampin. PeritonealDialysis International, 23 ,362-367.

Nephrology Nursing Journal Editorial Board Statements of Disclosure

In accordance with ANCC-COA governing rules Nephrology Nursing Journal Editorial Board statements of disclo-sure are published with each CNE offering. The statements of disclosure for this offering are published below.

Paula Dutka, MSN, RN, CNN, disclosed that she is a consultant and research coordinator, is on the speaker’sbureau, and has sat on the advisory board for Genentech.

Patricia B. McCarley, MSN, RN, NP, disclosed that she is on the Consultant Presenter Bureau for Amgen,Genzyme, and OrthoBiotech. She is also on the Advisory Board for Amgen, Genzyme, and Roche and is therecipient of unrestricted educational grants from OrthoBiotech and Roche.


Barri, Y., & Golper, T. (2010). Gastro -intestinal disease in dialysis patients.Retrieved from http://www.uptodate.com/contents/gastrointestinal-disease-in-dialysis-patients

Bleyer, A., & Burkart, J. (2010). Bloody peri-toneal dialysate (hemoperitoneum).Retrieved from http://www.upto-date.com/contents/bloody-peri-toneal-dialysate-hemoperitoneum

Cameron, J. (1983). Acute pancreatitis. InR. Shackelford & G. Zuideme (Eds),Surgery of the alimentary tract (2nd edi-tion) (p. 31), Philadelphia: WBSaunders.

Chow, K., Szeto, C., Cheung, K., Leung. C.,Wong, S., & Li, P. (2006). Predictivevalue of dialysate cell counts in peritoni-tis complicating peritoneal dialysis.Clinical Journal of American Society ofNephrology, 1, 768-773.

Dervisoglu, E., Sayan, M., Sengul, E., &Yilmaz, A. (2006). Rapid diagnosis ofMycobacterium tuberculous peritoni-tis with real-time PCR in a peritonealdialysis patient. APMIS, 114, 656-658.

Fernandez-del Castillo, C. (2010). Clinicalmanifestations, diagnosis, and surgicalstaging of exocrine pancreatic cancer.Retrieved from http://www.upto-date.com/contents/clinical-manifesta-tions-diagnosis-and-surgical-staging-of-exocrine-panc reatic-cancer

Fishman, M., & Aronson, M. (2010).Differential diagnosis of abdominal pain inadults. Retrieved from http://www.uptodate.com/contents/differential-diagnosis-of-abdominal-pain-in-adults

Go, L., & Everhart, J. (1994). Pancreatitis. InDigestive diseases in the United States:Epidemiology and impact (p. 693).Washington, D.C.: U.S. Department ofHealth and Human Services, PublicHealth Service, National Institutes ofHealth, National Institute of Diabetesand Digestive Kidney Diseases. U.S.Government Printing Office NIHPublication no 94-1447.

Holley, J., & Schmidt, R. (2010).Noninfectious complications of continuousperitoneal dialysis. Retrieved fromhttp://www.uptodate.com/contents/noninfectious-complications-of-contin-uous-peritoneal-dialysis

Howell, D. Shah, R., Lawrence, C. (2009).Diagnosis and management of pseudocystsof the pancreas. Retrieved fromhttp://www.uptodate.com/contents/diagnosis-and-management-of-pseudo-cysts-of-the-pancreas

Infante, S., Depner, T., Morfin, J., & Pappoe,A. (2009). Inadvertent but adequate “peri-toneal” dialysis via pancreatic pseudocyst.

Paper presented at the Meeting of theAmerican Nephrology Society (ASN),November 2009, San Diego, CA.

Keenan, N., Jeyaratnam, D., & Sheerin,N.S. (2005). Mycobacterium simiae:A previously undescribed pathogen in peritoneal dialysis peritonitis.American Journal of Kidney Diseases,45(5), e75-e78.

Khalid, A., & McGrath, K. (2010).Classification of pancreatic cysts. Re -trieved from http://www.uptodate.com/contents/classification-of-pancreatic-cysts

Kim, M., Kwon, K., & Lee, S. (1998).Gastroesophageal reflux disease inCAPD patients. Advances in PeritonealDialysis, 14, 98-101.

Lankisch, P., Weber-Dany, B., Maisonneuve,B., & Lowenfels, A. (2008). Frequen cyand severity of acute pancreatitis inchronic dialysis patients. Nephrol ogy,Dialysis transplantation, 23, 1401-1405.

Lee, K.F., Chen, H.H., & Wu, C.J. (2008).Mycobacterium chelonae peritonitisin a patient on peritoneal dialysis.Renal Failure, 30(3), 335-338.

Li, P.K., Szeto, C.C., Piraino, B.,Bernardini, J., Figueiredo, A.E.,Gupta, A., ... Struijk, D.G. (2010).ISPD peritoneal dialysis-related infec-tions recommendations: 2010 update.Peritoneal Dialysis Inter national, 30,393-423.

Mehrota, R., & Kathuria, P. (2008).Abdominal catastrophes, peritonealeosinophillia and other unusualevents in peritoneal dialysis. In A.R.Nissenson & R.N. Fine (Eds) Hand -book of dialysis therapy (pp. 645-654),Philadelphia: Saunders/Elsevier.

Miranda, K. (2011). Somatic pain vs. visceralpain. Retrieved from eHow.com athttp://www.ehow.com/about_5393798_somatic-pain-vs-visceral-pain.html

Natov, S., & Pereira, B. (2010). Hepatitis Cvirus infection in patients on maintenancehemodialysis. Retrieved from http://www.uptodate .com/contents/hepatitis-c-virus-infection-in-patients-on-maintenance-dialysis

Nodaira, Y., Ikeda, N., Kobayashi, K.,Watanabe, Y., Inoue, T., Gen, S., ...Suzuki H. (2008). Risk factors and causeof removal of peritoneal dialysiscatheter in patients on continuousambulatory peritoneal dialysis. Advancesin Peritoneal Dialysis, 24, 65-68.

O’Malley, V., Cannon, J.,& Postier, R.(1985). Pancreatic pseudocysts:Cause, therapy and results. AmericanJournal of Surgery, 150, 680-682.

Penner, R., & Majumdar, S. (2009).Diagnostic approach to abdominal pain inadults. Retrieved from http://www.uptodate.com/contents/diagnostic-approach-to-abdominal-pain-in-adults

Ponferrada, L., Prowant, B., & Satalowich,R. (2008). Peritoneal dialysis compli-cations. In C. Counts (Ed.) Core cur-riculum for nephrology nursing (pp. 824-851). Pitman, NJ: AmericanNephrology Nurses’ Association.

Prowant, B., Moore, H., Satalowich, R., &Twardowski, Z. (2010). Peritoneal dial-ysis survival in relation to patientbody size and peritoneal transportcharacteristics. Nephrology NursingJournal, 37(6), 641-647.

Rho, M., Bia, M., & Brewster, U. (2007).Nontuberculous mycobacterial peri-tonitis in peritoneal dialysis patients.Seminars in Dialysis, 20, 271-276.

Schmidt, R., & Holley, J. (2010a). Non-accessrelated infections in chronic dialysispatients. Retrieved from http://www.uptodate.com/contents/non-access-related-infections-in-chronic-dialysis-patients

Schmidt, R., & Holley, J. (2010b). Non-infectious complications of peritonealdialysis catheters. Retrieved fromhttp://www.uptodate.com/contents/noninfectious-complications-of-peritoneal-dialysis-catheters

Shinnick, T., & Good, R. (1994). Myco -bacterial taxonomy. European Journalof Clinical Microbiology and InfectiousDiseases, 13(11), 884-901.

Singh, H., & Saha, T. (2008). Exit-site infec-tion due to nontubercular Myco -bacteria in an immune-compromisedperitoneal dialysis patient. NephrologyDialysis Transplantation, 37(10), 401-409.

Soundararajan, R., & Golper, T. (2009).Serum enzymes in patients with renal fail-ure. Retrieved from http://www.uptodate.com/contents/serum-enzymes-in-patients-with-renal-failure

United States Renal Data System. (2010).USRDS 2009 annual data report. U.S.Department of Health and HumanServices. The National Institutes ofHealth, National Institute of Diabetesand Digestive and Kidney Diseases.Baltimore: Author.

Additional ReadingHolley, J. (2010). Cancer screening in patients

with end stage renal disease. Retrievedfrom http://www.uptodate.com/con-tents/cancer-screening-in-patients-with-end-stage-renal-disease


Abdominal Mysteries: Pain, Peritonitis, Pancreatitis, Pseudocyst ANNJ1112

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ANSWER/EVALUATION FORMAbdominal Mysteries: Pain, Peritonitis, Pancreatitis, Pseudocyst

Maureen Craig, MSN, RN, CNN; Sergio Infante, MD

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