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PERITONEAL DIALYSIS

Q.655. How to diagnose peritonitis in P.D. patients?


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PERITONEAL DIALYSIS

 

Q.655. How to diagnose peritonitis in P.D. patients?          

A. Multiple sources of bacterial peritonitis in PD., incl.:[touch contamination, cth. rel. infc., transvisceral migration due to intraabd. pathology (eg, bowel leak), hematogenous source & vaginal leak (v.rare)]. Peritonitis is easily Dgx. on clinical ground alone. Sm. & Sn. Incl.:[abdominal pain, cloudy abdominal fluid, fever, nausea, abd. tenderness & rebound tenderness]. Most ptn. present é cloudy abdominal fluid & abdominal pain. However, constellation of both cloudy abd. fluid & abd. pain is not always obstructed.. This’s esp. true in APD who may present without P.H. of cloudy abdominal. fluid.

Peritonitis is us due to contamination é pathogenic skin bacteria due to touch contamination or cth.-rel. infc.. 2nd ry  or enteric peritonitis cn be induced by G.I. path., including[cholecystitis, appendicitis, ruptured diverticulum, ttt of sev. constipation, endoscopic perforation]. Compared é P.D.-rel. peritonitis, 2ry peritonitis us. present é systemic Sn & Sm, incl. Hpt. Mj. Lab.: 🠝WBCs in Pr. fluid us. to > 100 cells/mm3, é > 50 % neutrophils. +ve Pr. fluid cultures should be obs. in 80 % of bacterial peritonitis. Leukocytosis:10-15,000/mm3 can be sn. Peritonitis is us. suspected é abd. pain & cloudy effluent. Ddx.: Start é history, physical exam., & G.st., culture & WBCs & differential of effluent Pr. fluid. Bld cultures shd be obtained é systemic Sm & close inspection 👁 of exit site. Dgx. is frequently based upon C.P. & effluent Pr. fluid WBCs of > 100 cells/mm3, é > 50 % 🠞neutrophils.

Presumptive Dgx can be made é relatively low WBCs in PD effluent but who have consistent clinical history & in whm other causes of abdominal path. have been excluded. However, clinical judgment is essential é Sn & Sm. of peritonitis but a low effluent cell count. Some clinicians obs. such ptn in clinic for a few h.s & repeat cell count & differential, then monitor Sn & Sm. & A.B. initiated if Sn & Sm & repeat cell count are most consistent é peritonitis. If obstruction period cannot be conducted, empiric A.B. shd be given. Presumptive Dgx is also noted é cloudy effluent. Empiric therapy should be initiated as soon as cloudy effluent is observed, without waiting for cell count confirmation fr. Lab.. Dgx. is confirmed by a +ve Dzt. culture. Additional tests may be performed é atypical findings & é suspected  peritonitis-induced abdominal disease (2ndry bacterial peritonitis). D.D. incl.: myriad causes of peritonitis: [abdominal pain,🠝Pr. fluid W.B.C.s and/or changed Dzt appearance].

Q.656. How to diagnose a case of peritonitis (see also the above Q.)? When to expect a negative culture?

 A. [5o-100 WBCs/cc. at least in culture] are needed for diagnosis of peritonitis. + Check for local manifestation (pain/tenderness) & systemic manif. (fever/lassitude). 

- Negative culture may be seen in:     👌

                                    

1)   A.B. umbrella.

2)   Early sampling.

3)   Poor lab. Technique.

N.B.: [+ve culture + No WBCs] = Contamination.

Q.657. Enumerate the various causes of hemoperitoneum  (H.P.)?

(1) Menstrual bleeding: Benign H.P. occur in >1/2 of menstruating women on P.D. due to: [ovulation, retrograde menstruation, or endometriosis]. Most commonly, H.P. will clear after 1-3 rapid flushes.

(2)Post-catheter insertion or manipulation: After insertion of P.D. catheter, bleeding into Pr. cavity occ. in < 5 % of cases, us. mild, rapidly resolve.  

(3)Catheter-related: Rarely, PD. cath.🠞enough blunt trauma🠞local laceration. Case report: cth. eroding mesenteric a., splenic lacerations🠞massive H.P. It’s much less common now é "curled tip" cth.. More commonly but still rare, PD cath.🠞mild contusion of the surface of the peritoneal cavity.

(4)RetroperitonealpathologyCyst rupture in autosomal dominant P.K.D., acquired cystic dis. & R. tumors . These patients may also have hematuria.

(5)Additional causesSclerosing peritonitis: serious esp. é long period P.D. Peritoneal calcification, splenic rupture & infarct, carcinomatosis liver, liver cyst rupture, retroPr. hematoma, iliopsoas hematoma, bleeding outer uterine wall in pregnancy. Hgic luteal cyst, ovarian cyst rupture, aneurysm

rupture.

Q.658. How to treat?    

A. ttt of the underlying cause is essential, curative management 🠞emergent evaluation & care. If the cause is idiopathic or benign 🠞Supportive therapy:

(1) Instillation of heparin (500 i.u./L) in Dzt 🠞 prevent catheter clotting.

(2) Frequent exchanges: in room ºC DX exchanges🠞 Pr. V.C.œœ &🠋bleeding.

(3) Menstruating Women, oral contraceptives🠞🠋Ovulation & control bleeding .

(4) Stopping aspirin or other anticoagulants: balanced against its indications.


Q.659. What are the causes & risk factors of fungal peritonitis (F.P.)?

A. Breaks in sterile technique when connecting Pr. cth. to bags of Dzt, infc. at site of cath. entry, intestinal perforation, peritoneovaginal fistulae & transmigration of fungi across bowel wall into peritoneum. = Mj. Causes. Published series: F.P. associated é P.H. of both recent A.B. use & episodes of bacterial peritonitis. 65% of ptn had been exposed to A.B. within 30 d. of onset of F.P.& 48 % hd experienced an episode of bacterial peritonitis é same time frame. It’s difficult to determine whether A.B. exposure & peritoneal inflmm.🠋to F.P. or whether these f.s merely identify a high-risk group due to poor technique. Recent exposure to A.B.🠋F.P. by shifting balance of ptn endogenous skin & bowel flora towards yeast species contamination during cth. manipulation.   ….   Other risk f.s incl.

  1. Use of emergency P.D.: A trend towards infection é fungal organisms hs bn obs. in ass. é Ac. or emergent PD in hospital; this may be due to severity of illness, concurrent ttt é antibacterial ag., or low experienced personnel é PD techniques.

2. HIV infection: HIV ptn. who receive ch. PD have a higher frequency of peritonitis é yeasts when compared to other ch. PD ptn.

3. Extraperitoneal fungal infection.               

4. Abdominal surgery.

5. Environmental: Candida outbreaks ass. é contamination of water baths used to warm Dzt & contact é pigeon guano & soil dur. gardening  molds. F.P.

Q.660. How to treat F.P.?    @    R 

A. Goalsof ttt 2 folds: infc. eradication & Pr. preservation for PD. Upon Dgx., Pr.lavaged until returning fluid is clear; this ⮞🠟adhesions &🠟fungal burden. Antifungals (A.F.) is indic. if a calcofluor white or Gram stain yeast or hyphae. Therapy is based upon culture results, suscep. of org. & ptn. response.

Guidelines: cth.: removed immediately after fungi identified by microscopy/culture & ptn placed on HDX. IDSA guidelines for ttt of candidiasis, as well as other IDSA guidelines, can be accessed thr.: Infec. Dis. Society of America's website”.

A v. small No. of ptn., é yeast peritonitis occ. é 2 w. of initiation of PD for A.R.F., in whm A.F. alone in cure. If mold infc. arises, cth. removal is almost always required  for cure . Instillation of amphotericin B(Amph.B) é Pr. cavity hs bn used as a sole or adjunctive thpy. This regimen is discouraged  😞  as:

1)   It’s not consistently successful in complete cure.  😞

2)   It’s a frequent cause of abd. pain upon instillation.  😞

3)   It leads to adhesion formation é subseq. loss of Pr. (dialyzing membrane). 😞

4)   Decisions of type of A.F. shd be based upon C.P. & sp. fungal infection.   😞

Recmmended 👆 strategy : If Dzt is grossly turbid Pr. lavage, continued until returning fluid is clear. Systemic A.F. shd be given & cth. removed as soon as possible. A.F. indicated if a calcofluor white or G-stain yeast or hyphae.

Choice of A.F.: For empiric coverage of F.P. when there’s no sugg. of identity of fungus fr. inspection of fluid & until cultures returnOral fluconazole (200 mg/d.). Ptn. é prior exposure to azole A.F. i.v. Amph.B (0.6 mg/kg/d.) or i.v. echinocandin, caspofungin [70 mg/d.one, é subsq. doses: 50 mg/d.], micafungin [100 mg/d.], or anidulafungin [200 mg on d. one, é subsq. dosing: 100 mg/d.]. After C & S, further thpy cn be tailored to sp. isolated org.. If Candida found fluconazole direct thpy. C. albicans, C. parapsilosis & C. tropicalis susceptible to fluconazole, C.krusei is resistant & C. glabrata hs variable suscep., but generally is resistant. If fluid cultures yield:C.albicans/C.tropicalis/C.parapsilosisØfluconazole 200 mg/d. Dur. of ttt :2-4 w. If cultures C.krusei or C.glabratai.v. Amph.B 0.6-1 mg/kg/d. or i.v. echinocandin(caspofungin [70 mg/d.one,é subseq. Dose : 50 mg/d.], micafungin [100 mg/d.], or anidulafungin [200 mg on d. one, é subsq. dose:100 mg/d.]. ptn. shd be ttt for 4 w.. If cultures: mold i.v.Amph.B at 0.6-1 mg/kg/d. until sp. org. is identified & most antifungal ag. cn be given. For Aspergillus sp. voriconazole oral  as alternative to Amph.B./4w. & until all Sm & Sn have resolved . Dematiaceous molds oral itraconazole (loading : 200 mg 3 times/d./3 d. followed by 200 mg/ twice/d.) or oral voriconazole (loading: 400 mg twice/d.:1std. foll. by 200 mg twice/d.), alth. some cases resp. to i.v. Amph.B/4 w. & until all Sm. & Sn. resolved. Limited experience using lipid form. of Amph.B, but they shd be as effective as deoxycholate form.. As nephrotoxicity is not an issue, these agents only used é severe infusion-related reactions to deoxycholate. Experience é echinocandins in CAPD-ass. F.P. is only anecdotal. However, all 3 echinocandins were effective for ttt of candidemia . Ptn. should be on HDX. dur. ttt. After cth. removal, wait 4-6 w.  prior to new cth. placement


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Q.655. How to diagnose peritonitis in P.D. patients?
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