Rounds

Eosinophilic Peritonitis A Clinical Decision

Bensson Samuel, MD,1* James Dylewski, DO,1 Astha Agarwal, MD,1 Gloria Fioravanti, FACP, DO,2
Ziad Dimachkie, BS,3 Christine Velasquez, BS3

ABSTRACT

A 35-year-old female was admitted to our hospital with

complaints of abdominal pain, chest pain, and shortness
of breath. The patient had a history of type 1 diabetes
mellitus since childhood. The patient also had associated
diabetic neuropathy, gastroparesis, retinopathy, and endstage renal disease on peritoneal dialysis from diabetic
nephropathy. Other chronic medical problems included
hypertension, hyperlipidemia, anxiety, asthma, chronic
pain, and peripheral vascular disease that resulted in a left
hallux amputation from ischemic disease.
The patient had been in her usual state of health until 3
days prior to admission, when she noted lower extremity
edema accompanied by poor appetite and high blood
glucose despite compliance with her medication. She was
seen at her dialysis center upon the onset of symptoms
where changes were made in her peritoneal dialysate,
with no improvement. She then began to feel feverish with
chills shortly thereafter, but had no recorded temperatures
at home. The patient also began to experience sharp

DOI: 10.1309/LMB9N5IF8MNPFLIZ

Abbreviations
WBC, white blood cell; PD, peritoneal dialysis; ISPD, International
Society of Peritoneal Dialysis
1
St. Lukes Internal Medicine Residency Program, 2St. Lukes Internal
Medicine Residency Program Director, 3Temple School of Medicine,
St. Lukes Campus, Bethlehem, PA

*To whom correspondence should be addressed.

E-mail: Bensson123@yahoo.com

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Keywords: Dialysis, peritonitis, eosinophilic peritonitis, kidney failure,

infection

non-radiating abdominal pain in the lower left quadrant

which increased in intensity over the next 2 days prior
to admission, with no associated nausea, vomiting,
loose stools, or urinary symptoms. The pain had no
association with food, and had no specific palliative or
aggravating factors. On the day of admission she also
began to have pressure-like chest pain localized to her
retrosternal region, as well as shortness of breath around
4 PM in the afternoon with no associated orthopnea or
heart palpitations. After 2 hours of these symptoms, she
presented in the emergency department. At the time of
admission, she denied headache, photophobia, or rash.
Her home medications included insulin, glargine,
lispro, amlodipine, labetalol, pravastatin, lorazepam,
ferrous sulfate, hydromorphone, metoclopramide (for
gastroparesis), and calcium acetate hypophosphatemia.
She reported allergies to promethazine, diphenhydramine,
acetaminophen, and hydrocodone, which all caused throat
swelling. The patient, who was married, was disabled and
denied current or prior history of alcohol, tobacco, or illicit
drug use. Her mother, maternal grandmother, and 2 of her
sisters also had diabetes and her father had a non-fatal
heart attack in his mid-50s.
On examination, the patients blood pressure was
199/85, pulse was 94 beats per minute, respiratory
rate was 18, and oral temperature was 98.6. She had
normal oxygenation saturation. The patient appeared
mildly distressed from her abdominal pain but otherwise
appeared well. There was bilateral periorbital edema noted
with an otherwise normal ocular exam. The patients heart

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Peritonitis is a commonly seen complication in patients with end-stage

renal disease being treated with peritoneal dialysis. Peritonitis is a
major cause of morbidity and mortality in this group of patients. In
this instance, an appropriate clinical decision should be made to start
empiric treatment with broad-spectrum antibiotics until peritoneal fluid
cultures are obtained. Prompt treatment is necessary as peritonitis

is associated with increased mortality rate, membrane damage

requiring a transfer to hemodialysis, and loss of the catheter. However,
eosinophilic peritonitis presents a challenge to the clinician in that it
may be caused by something other than an infection.

Rounds

Table 1. CBC With Differential

Result Name

Results

Units

Table 2. Serum Chemistries

Reference Range

Results

Units

Reference Range

Sodium
Potassium
Chloride
Carbon dioxide
Anion gap
Bilirubin, total
Protein, total
ALK phosphatase
ALT (SGPT)
AST (SGOT)
Glucose, random
Albumin
BUN
Calcium
Creatinine
Magnesium
Phosphorus
Amylase
Lipase

131 (L)
mmol/L
136-145
4.3
mmol/L 3.5-5.3
92 (L)
mmol/L
100-108
30
mmol/L
23-33
9
mmol/L
8-16
0.32
mg/dL
0.20-1.00
7.3
g/dL
6.4-8.2
118
U/L
50-136
37
U/L
0-65
21
U/L
0-45
321 (H)
mg/dL
65-140
3.1 (L)
g/dL
3.5-5.0
66 (H)
mg/dL
5-25
8.8
mg/dL 8.3-10.1
8.57 (H)
mg/dL
0.60-1.30
2.6
mg/dL 1.6-2.6
7.5 (H)
mg/dL
2.7-4.5
400 (H)
U/L
0-120
167 U/L 73-393

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WBC count
13.75 (H)
103/L 4.17-10.16
Hemoglobin
9.9 (L)
g/dL
11.3-14.8
Hematocrit
29.9 (L)
%
34.7-44.5
MCV
89 fL 81-97
MCH
29.3 pg 26.8-34.3
MCHC
33.1 g/dL 31.4-37.4
RDW
15.0 % 11.6-15.1
Platelet count
322
103/L 150-350
Segs 60 % 45-77
Lymphocytes 19
%
14-44
Monocytes 5
% 4-12
15 (H)
%
0-6
Eosinophils
Basophils 1 % 0-1
Absolute neutro
8.25 (H)
103/uL 1.88-7.82
Absolute lymph
2.61
103/uL 0.58-4.47
Absolute mono
0.69
103/uL 0.17-1.22
Absolute eos
2.06 (H)
103/uL 0.00-0.61
Absolute baso
0.14 (H)
103/uL 0.00-0.10

Result Name

Image 1
Computed tomography of abdomen and pelvis without contrast. A
small amount of abdominal pelvic free fluid may represent dialysate
fluid, although its nonspecific. There is no evidence of free air,
bowel obstruction, or discernible appendicitis. The white arrow
indicates the PD catheter seen coming from the peritoneum.

rate was mildly tachycardic with normal heart sounds. Her

abdomen was soft and non-distended with tenderness
present in her upper left and lower left quadrants. There
was no rigidity or rebound tenderness, but some voluntary
guarding. A peritoneal catheter was present with a clean
appearing insertion site, without erythema or discharge
noted. There was bilateral pitting edema that was greater
in the lower right extremity compared to the left one. The
remainder of the exam was normal.
Initial laboratory data demonstrated a new leukocytosis
as well as chronic normocytic anemia (Table 1). Serum

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chemistries (Table 2) demonstrated hyperglycemia,

mild hyponatremia, elevated blood urea nitrogen and
creatinine, and elevated phosphorus and elevated
amylase, all of which could be findings consistent with
end-stage renal disease. Computed tomography of the
abdomen and pelvis (Image 1) noted the presence of her
peritoneal dialysis catheter and some ascites, possibly
from her dialysate. Peritoneal fluid was obtained (Table
3), demonstrating an elevated white blood cell (WBC)
count of 404 with eosinophils accounting for 36% of the
WBCs present (Images 2 and 3). Urinalysis (Table 4) was
not suggestive of a urinary cause for her abdominal pain.

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Image 2
Eosinophilic cells in the peritoneal fluid (Wright-Giemsa). The
magnification is 400. (Image courtesy of David W. Anderson,
MD, chief of pathology, St. Lukes University Teaching Hospital)

Table 3. Peritoneal Fluid

Result Name

Results

No. of WBC counted 100

Basophils 3
Body fluid WBC
404 (H)
Eosinophils 36
Lymphocytes 3
Monocytes 58
Fluid culture
No growth after 5 days

Units Reference Range

/mm3 <8
%
/L
0-200
%
%
%

Discussion
Peritonitis is a commonly seen complication in patients
with end-stage renal disease being treated with peritoneal
dialysis. Estimated incidence may vary from 1 in 18 patient
treatment months to 1 in 60 patient treatment months
depending on the center, peritoneal dialysis (PD) modality

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(continuous ambulatory PD or automated PD), patient

compliance, or length of treatment.1,5 Peritonitis is a major
cause of morbidity and mortality in this group of patients,
accounting for 1 out of 6 deaths in patients undergoing
continuous peritoneal dialysis.17 An appropriate clinical
decision should be made to start empiric treatment with
antibiotics until peritoneal fluid cultures are obtained. The
2010 International Society of Peritoneal Dialysis (ISPD)
guidelines recommend that the selection of empiric
therapy must cover both gram positive and gram negative
organisms.8,9 Prompt treatment is necessary as peritonitis
is associated with increased mortality rate, membrane
damage requiring a transfer to hemodialysis, and loss of
the catheter.10,11 However, eosinophilic peritonitis presents
a challenge to the clinician in that it may be caused by
something other than an infection.
Peritonitis in a PD patient is a clinical diagnosis taking
into account the history, presentation, and laboratory
findings. The clinical picture of bacterial peritonitis may

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Image 3
Eosinophilic cells in the peritoneal fluid (Wright-Giemsa). The
magnification is 400. (Image courtesy of David W. Anderson, MD,
chief of pathology, St. Lukes University Teaching Hospital)

Rounds

range from a silent course to mild symptoms such as fever,

abdominal pain, nausea or vomiting, and cloudy effluent to
systemic manifestations of sepsis.3,4 Peritonitis is a highly
suggestive diagnosis with peritoneal fluid WBC count of
100/L with at least 50% polymorphonuclear cells. Of the
patients that develop peritonitis, almost greater than 90%
have neutrophil predominance in the peritoneal fluid cell
count.2,6,7

With a clinical presentation of nausea and vomiting,

abdominal pain, fever, and a cloudy effluent dialysate with
WBC of >100, peritonitis was suspected in this patient.
Empiric antibiotics covering both gram positive and
negative organisms were started. A microscopic view of
the dialysate specimen (Table 3) showed 36 percent of
eosinophils. Eosinophilic peritonitis is defined as 10%
eosinophils on presentation, and is seen in less than 10%
of peritonitis cases per a 2003 study.2
Eosinphilic peritonitis may result from various infections
such as bacterial, fungal, viral, or noninfectious causes
such as allergic reactions, drug effects (eg, chemical
peritonitis due to vancomycin), or using icodextrincontaining dialysate or the more commonly seen early
presentation after catheter placement due to CO2
insufflations during laparoscopy.12,13 As eosinphilic
peritonitis may often be culture negative, it may be
challenging to manage these patients as it is difficult to
differentiate between culture negative infectious peritonitis
from sterile peritonitis. In a review which compared 465
cases over a 15-year period, during which 45 cases had
eosinophilic peritonitis, 22 had a bacterial source that was
identified and 20 were culture negative.14
With a normal chest x-ray, normal urine analysis, negative
blood cultures, and a peritoneal WBC count of 404
demonstrating an eosinophillic predominance, our patient
was clinically diagnosed with eosinophillic peritonitis.
Blood cultures are typically negative in peritonitis and
hence should not be used to rule out this condition.15
Peritoneal fluid or dialysate culture is only positive

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Result Name

Results

Units

Reference Range

Color Yellow Yellow

Clarity Clear Clear
Bilirubin, urine Negative
Negative
Specific gravity 1.011
1.003-1.030
Occult blood
Small
Negative
pH
7.5 4.5-8.0
Urobilinogen 1.0
EU/dl 0.2-1.0
Nitrate Negative Negative
Leukocytes Trace Negative
Glucose
500 (1/2%)
mg/dL Negative
Ketones
Negative
mg/dL Negative
Protein
100 (2+)
mg/dL Negative
4-10
/hpf Negative
WBC
4-10
/hpf Negative
RBC
/hpf
None seen
Epithelial cells None seen
Bacteria
Occasional
/hpf
None seen
Urine culture
No growth after 3 days

80%-95% of the time, leaving a distinct possibility of a

persisting infection.9,16 Therefore, laboratory investigations
should be used in conjunction with a clinically-guided
process to establish a diagnosis.
The patient in this case was treated for 3 days with
an intravenous antibiotic course of vancomycin and
ceftazidime. Blood and dialysate culture were negative
after 3 days of incubation, and with clinical improvement,
antibiotics were discontinued. In light of these findings, the
most likely cause of this patients symptoms is eosinophilic
peritonitis following a change in the dialysate fluid. The
patient was discharged and was followed up as an
outpatient for continuity of care. LM

References
1. Keane WF, Bailie GR, Boeschoten E, et al. Adult peritoneal dialysisrelated peritonitis treatment recommendations: ISPD guidelines,
2000 update.
2. Fontn MP, Rodrguez-Carmona A, Galed I, et al. Incidence and
significance of peritoneal eosinophilia during peritoneal dialysisrelated peritonitis. Perit Dial Int. 2003;23(5):460-4.
3. de Freitas DG, Gokal R. Sterile peritonitis in the peritoneal dialysis
patient. Perit Dial Int. 2005;25:146.
4. Shrestha BM, Brown P, Wilkie M. Surgical peritonitis in patients on
peritoneal dialysis. Perit Dial Int. 2008;28(4):33 1-4.
5. Kam-Tao Li P, Szeto CC, Piraino B, et al. Peritoneal dialysis-related
infections recommendations: ISPD guidelines, 2010 update.
6. Holley, HL, Piraino, BM. Complications of peritoneal dialysis:
diagnosis and management. Semin Dial 1990;3:245

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Patients with poor immune response and a short time

indwelling catheter can have a WBC of <100/L. With
a cloudy dialysate, any cell type could be found with
or without an infection. In the case of a dry tap, where
cell count doesnt reach 100/L, a proportion of 50%
polymorphonuclear cells is a strong indicator of peritonitis.5
Fungal, mycobacterial peritonitis may present with a higher
number of lymphocytes, but the majority of cases still have
neutrophil predominance.6,7

Table 4. Urinalysis With Urine C/S Reflex

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7. Cheng IK, Fang GX, Chan TM, et al. Fungal peritonitis complicating
peritoneal dialysis: report of 27 cases and review of treatment. QJM.
1989;71:407-16
8. Piraino B, Bailie GR, Bernardini J, et al. Peritoneal dialysisrelated infections recommendations: 2005 update. Perit Dial Int.
2005;25(2):107.
9. Li PK, Szeto CC, Piraino B, et al. Peritoneal dialysis-related infections
recommendations: 2010 update. Perit Dial Int. 2010;30(4):393.
10. Schreiber M, Burkart JM, Tabor T. . Peritonitis remains the leading
cause of transfer from PD to HD [abstract]. Perit Dial Int. 1996;16
(Suppl 2):S66.
11. Sipahioglu MH, Aybal A, Unal A, et al. Patient and technique survival
and factors affecting mortality on peritoneal dialysis in Turkey: 12
years experience in a single center. Perit Dial Int. 2008;28(3):238.

13. Charney DI, Gouge SF. Chemical peritonitis secondary to

intraperitoneal vancomycin. Am J Kidney Dis. 1991; 17(1):76.
14. Fontn MP, Rodrguez-Carmona A, Galed I, et al. Incidence and
significance of peritoneal eosinophilia during peritoneal dialysisrelated peritonitis. Perit Dial Int. 2003;23(5):460.
15. Szeto CC, Wong TY, Chow KM, et al. The clinical course of culturenegative peritonitis complicating peritoneal dialysis. Am J Kidney Dis.
2003;42(3):567.
16. Vas, SI. Peritonitis. In: Nolph KD, ed. Peritoneal Dialysis. 3rd ed.
Dordrecht, Netherlands: Kluwer Academic Publishers; 1989:261.
17. Prez Fontan M, Rodrguez-Carmona A, Garca-Naveiro R, et al.
Peritonitis-related mortality in patients undergoing chronic peritoneal
dialysis. Perit Dial Int. 2005;25(3):274-84.

12. Johnson CA. Intraperitoneal vancomycin administration. Perit Dial Int.

1991;11(1):9.

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