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., 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
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 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. 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
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