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

 

PERITONEAL DIALYSIS

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

A.Multiple sources of bacterial peritonitis in PD., include:[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, abdominal tenderness & rebound tenderness]. Most ptn. present é cloudy abd. Fluid & abd. pain. However, constellation of both cloudy abdominal fluid & abd. pain is not always obs.. This’s esp. true in APD who may present without P.H. of cloudy abdminal. fluid.

Peritonitis is us due to contamination é pathogenic skin bacteria due to touch contamination or cth.-rel. infc.. 2^nd ry  or enteric peritonitis can be induced by G.I. path., incl.[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 >100cells/mm3, é>50 % neutrophils. +ve Pr. fluid cultures shd be obs. in 80 % of bacterial peritonitis. Leukocytosis:10-15,000/mm3cn be sn. Peritonitis is us. suspected é abd. ominalpain & cloudy effluent. Ddx.: Start é history, physical exam., & G.st., culture & WBCs & differential of effluent Pr. fluid. Bld cultures should 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 hv consistent clinical history & in whm other causes of abd. path. hv bn excluded. However, clinical judgment is essential é Sn & Sm. of peritonitis but a low effluent cellcount. 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 obs. period cannot be conducted, empiric A.B. shd be given. Presumptive Dgx is also noted é cloudy effluent. Empiric thpy shd be initiated as soon as cloudy effluent is observed, without waiting for cell count confirmation from Lab.. Dgx. is confirmed by a +ve Dzt. culture. Additional tests may be performed é atypical findings & é suspected  peritonitis-induced abd. dis. (2^ndry bacterial peritonitis). D.D. include: myriad causes of peritonitis: [abd. 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.[50-100 WBCs/cc. at least in culture] are needed for diagnosis of peritonitis. + Check for local mnf. (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. occ. in >1/2of menstruating women on P.D. due to: [ovulation, retrograde menstruation, or endometriosis]. Most commonly, H.P. will clear after 1-3rapid flushes.

(2)Post-catheter insertion or manipulation: After insertion of P.D. catheter, bleeding into Pr. cavity occur 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)Retroperitoneal…👽pathology:  Cyst rupture in autosomal dominant P.K.D., acquired cystic disease & R. tumors . These patients may also hv hematuria.

(5)Additional causes: Sclerosing peritonitis: serious especiallyé long period P.D. Peritoneal calcification, splenic rupture & infarct, carcinomatosis liver, liver cyst rupture, retro-Pr. hematoma, iliopsoas hematoma, bleeding outer uterine wall in pregnancy. Hgic luteal cyst, ovarian cyst rupture, aneurysm rupture.

Q.658. How to treat?   R 

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

(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 & transmigr-ation of fungi across bowel wall into peritoneum. = Mj. Causes. Published series: F.P. ass. é P.H. of both recent A.B. use& episodes of bacterial peritonitis. 65% of ptn hd bn 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 dur. cth. manipulation.….   Other risk f.s incl.:

1. Use of emergency P.D.: A trend towards infec. 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. Goals of 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 indication 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 abdominal pain upon instillation.  

3)   It leads to adhesion formationé subseq. loss of Pr. (dialyzing membrane). 

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

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 return🠞Oral fluconazole (200 mg/d.). Ptn. é prior exposure to azole A.F.Ø i.v. Amph.B (0.6mg/kg/d.) or i.v. echinocan-din, caspofungin [70mg/d.one, é subsq. doses: 50mg/d.], micafungin [100mg/d.], or anidulafungin [200mg on d. one, é subsq. dosing: 100mg/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.parapsilosis🠞 fluconazole 200 mg/d. Dur. of ttt : 2-4 w. If cultures🠞 C. krusei or C. glabrata🠞 i.v. Amph.B 0.6-1mg/kg/d. or i.v. echinocandin(caspofungin [70mg/d.one,é subseq. Dose : 50mg/d.], micafungin [100mg/d.], or anidulafungin [200 mg on d. one, é subsq. dose:100 mg/d.]. ptn. should be ttt for 4w.. If cultures: mold 🠞i.v.Amph.B at0.6-1mg/kg/d. until spesific organism is identified & most antifungal ag. cn be given. For Aspergillus sp. 🠞 voriconazole oral  as alternative to Amph.B./4w. & until all Sm & Sn hv resolved . Dema-tiaceous molds🠞oral itraconazole (loading : 200mg 3times/d./3 d. foll. by 200mg/ twice/d.) or oral voriconazole (loading: 400mg twice/d.:1^std. foll. by 200mg 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 ag. only used é sev. infusion-related reactions to deoxycholate. Experience é echinocandins in CAPD-ass. F.P. is only anecdotal. However, all 3echinocandins were effective for ttt of candidemia . Ptn. shd be on HDX. dur. ttt. After cth. removal, wait 4-6 w.  prior to new cth. placement