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



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 รฉ 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 รฉ pathogenic skin bacteria due to touch contamination or cth.-rel. infc.. 2nd ry  or enteric peritonitis can be induced by G.I. path., incl.[Cholecystitis, appendicitis, ruptured diverticulum, ttt of sev. constipation, endoscopic perforation]. Compared รฉ P.D.-rel. peritonitis, 2ry peritonitis us. present รฉ systemic Sn & Sm, incl. Hpt. Mj. Lab.: ๐Ÿ WBCs in Pr. fluid us. to >100cells/mm3, รฉ>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 รฉ abd. ominalpain & cloudy effluent. Ddx.: Start รฉ history, physical exam., & G.st., culture & WBCs & differential of effluent Pr. fluid. Bld cultures should be obtained รฉ systemic Sm & close inspection   of exit site. Dgx. is frequently based upon C.P. & effluent Pr. fluid WBCs of >100 cells/mm3, รฉ >50 % neutrophils.

Presumptive Dgx can be made รฉ 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 รฉ 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 รฉ peritonitis. If obs. period cannot be conducted, empiric A.B. shd be given. Presumptive Dgx is also noted รฉ 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 รฉ atypical findings & รฉ suspected  peritonitis-induced abd. dis. (2ndry bacterial peritonitis). D.D. include: myriad causes of peritonitis: [abd. pain, ๐Ÿ 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:     ๐Ÿ‘Œ

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.๐Ÿ ženough blunt trauma๐Ÿ žlocal laceration. Case report: cth. eroding mesenteric a., splenic lacerations๐Ÿ žmassive H.P. It’s much less common now รฉ "curled tip" cth.. More commonly but still rare, PD cath.๐Ÿ žmild contusion of the surface of the peritoneal cavity.

(4)Retroperitoneal๐Ÿ‘ฝpathologyCyst rupture in autosomal dominant P.K.D., acquired cystic disease & R. tumors . These patients may also hv hematuria.

(5)Additional causesSclerosing peritonitis: serious especiallyรฉ 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 management๐Ÿ žemergent evaluation & care. If the cause is idiopathic or benign๐Ÿ žSupportive thpy:

(1) Instillation of heparin (500 i.u./L) in Dzt๐Ÿ žprevent catheter clotting.

(2) Frequent exchanges: in room ยบC DX exchanges๐Ÿ ž Pr. V.C.œœ & ๐Ÿ ‹ bleeding.

(3) Menstruating Women, oral contraceptives๐Ÿ ž๐Ÿ ‹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.Breaksin 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. รฉ 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 รฉ same time frame. It’s difficult to determine whether A.B. exposure & peritoneal inflmm.๐Ÿ ž to F.P. or whether these f.s merely identify a high-risk group due to poor technique. Recent exposure to A.B.๐Ÿ ž 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. รฉ fungal organisms hs bn obs. in ass. รฉ Ac. or emergent PD in hospital; this may be due to severity of illness, concurrent ttt รฉ antibacterial ag., or low experienced personnel รฉ PD techniques.

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

3. Extraperitoneal fungal infection.               

4. Abdominal surgery.

5. Environmental: Candida outbreaks ass. รฉ contamination of water baths used to warm Dzt & contact รฉ pigeon guano & soil dur. gardening ๐Ÿ ž molds. F.P.

Q.660. How to treat F.P.?    R 

A. Goals of ttt๐Ÿ ž2 folds: infc. Eradication & Pr. preservation for PD. Upon Dgx., Pr.๐Ÿ ž lavaged until returning fluid is clear; this ๐Ÿ ž๐Ÿ ‹adhesions & ๐Ÿ ‹fungal burden. Antifungals (A.F.) is indication if a calcofluor white or Gram stain๐Ÿ ž 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., รฉ yeast peritonitis occ. รฉ 2 w. of initiation of PD for A.R.F., in whm A.F. alone ๐Ÿ ž in cure. If mold infc. arises, cth. removal is almost always required  for cure . Instillation of amphotericin B (Amph.B) รฉ Pr. cavity hs bn used as a sole or adjunctive thpy. This regimen is discouraged ๐Ÿ˜Œ  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 formationรฉ subseq. loss of Pr. (dialyzing membrane). 

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

Recmmended๐Ÿ‘† strategy : If Dzt is grossly turbid ๐Ÿ ž 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 ๐Ÿ ž 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 return๐Ÿ žOral fluconazole (200 mg/d.). Ptn. รฉ prior exposure to azole A.F.ร˜ i.v. Amph.B (0.6mg/kg/d.) or i.v. echinocan-din, caspofungin [70mg/d.one, รฉ subsq. doses: 50mg/d.], micafungin [100mg/d.], or anidulafungin [200mg on d. one, รฉ subsq. dosing: 100mg/d.]. After C &S, further thpy cn be tailored to sp. isolated org.. If Candida found ๐Ÿ ž fluconazole direct thpy. C. albicans, C. parapsilosis & C. tropicalis ๐Ÿ ž 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.parapsilosis๐Ÿ ž fluconazole 200 mg/d. Dur. of ttt : 2-4 w. If cultures๐Ÿ ž C. krusei or C. glabrata๐Ÿ ž i.v. Amph.B 0.6-1mg/kg/d. or i.v. echinocandin(caspofungin [70mg/d.one,รฉ subseq. Dose : 50mg/d.], micafungin [100mg/d.], or anidulafungin [200 mg on d. one, รฉ subsq. dose:100 mg/d.]. ptn. should be ttt for 4w.. If cultures: mold ๐Ÿ ži.v.Amph.B at0.6-1mg/kg/d. until spesific organism is identified & most antifungal ag. cn be given. For Aspergillus sp. ๐Ÿ ž voriconazole oral  as alternative to Amph.B./4w. & until all Sm & Sn hv resolved . Dema-tiaceous molds๐Ÿ žoral itraconazole (loading : 200mg 3times/d./3 d. foll. by 200mg/ twice/d.) or oral voriconazole (loading: 400mg twice/d.:1std. 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 รฉ sev. infusion-related reactions to deoxycholate. Experience รฉ 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