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., 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)Retroperitoneal pathology: Cyst rupture in autosomal dominant P.K.D., acquired cystic dis. & R. tumors . These patients may also have hematuria.
(5)Additional causes: Sclerosing 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
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 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. &🠋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. 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 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 return⮞ Oral 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.glabrata⮞i.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