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Effect of intraperitoneal administration of sterile hu man cerebrospinal fluid
in rats
Article    in  Romanian journal of morpholog y and embr yolog y = R evue r oumaine de morphologie e t embr yologie · Januar y 2013
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Valentin Tit us Grig orean
Carol Davila Univ ersity of Medicine and Pharmac y
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Emer gency Clinic al Hospit al Bag dasar -Arseni
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Carol Davila Univ ersity of Medicine and Pharmac y
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Rom J Morphol Embryol 2013, 54(4):1045–1051
ISSN (print) 1220–0522 ISSN (on-line) 2066–8279 OORRIIGGIINNAALL PPAAPPEERR
Effect of intraperitoneal administration of
sterile human cerebrospinal fluid in rats
V. T. GRIGOREAN1), AURELIA MIHAELA SANDU2), RUXANDRA DIANA SINESCU3),
M. L. RIZA4), I. E. PLEȘEA5), C. D. LUPAȘCU6), M. POPESCU7)
1)Department of General Surgery,
“Bagdasar–Arseni” Emergency Clinical Hospital, Bucharest
“Carol Davila” University of Me dicine and Pharmacy, Bucharest
2)Department of Neurosurgery,
“Bagdasar–Arseni” Emergency Clinical Hospital, Bucharest
3)“Carol Davila” University of Me dicine and Pharmacy, Bucharest
4)Department of Urology
5)Department of Pathology
University of Medicine and Pharmacy of Craiova
6)Department of General Surgery, “St. Spiridon” University Hospital, Iassy
“Grigore T. Popa” University of Medicine and Pharmacy, Iassy
7)Department of Neurosurgery,
Emergency County Hospital, Pitesti
University of Pitesti
Abstract
Introduction : Distal ventriculoperitoneal shunt failure can be attributed to unabsorbed cerebrospinal fluid (CSF) from peritoneum. The
objective of the experiment was to determine peritoneal reaction in rats after intraperitoneal administration of human CSF and evolution of
local inflammatory response. Materials and Methods : Wistar rats were used divided into four groups: three groups in which intraperitoneal
injection of 3 mL, 2 mL and 0.5 mL of sterile human CSF was done and a control group. After sacrificing the animals, at 24, 48 or 72 hours,
macro- and microscopic examination of the peritoneal cavity and peritoneal fluid analysis were performed. The experiment was do ne in
compliance with legislation regarding animal research. Results : Administration of high dose CSF (3 mL) led to death of all specimens. The
dose of 0.5 mL of sterile CSF intraperitoneally administered was compatible with survival. Peritoneal response varied from necr otic-purulent
reaction, with maximum intensity in group 1, and milder in group 2, to minimum inflammation in small foci and polymorphic cells in group 3.
Inflammation only partially resolved in some specimens from group 3 after 72 hours, which incriminates the role of unabsorbed p eritoneal
CSF in pathogenesis of abdominal complications of ventriculoperitoneal shunts. Conclusions : Intraperitoneal administration of sterile human
CSF caused inflammatory response of varying degrees and with multiple locations. High doses of CSF led to death of specimens. A t 24 hours,
the peritoneal response ranging from congestion to purulent reaction was acute, intense and diffuse but after 72 hours, the inf lammatory
response was mild, focal and limited.
Keywords : cerebrospinal fluid, hydrocephalus, peritoneum.
 Introduction
Hydrocephalus is due to the impairment in production,
flow, or absorption of cerebrospinal fluid (CSF). An
abnormal increase in CSF volu me and, usually, pressure
within cerebral ventricles occur. Hydrocephalus is a health
problem worldwide. It has an estimated prevalence of
1–1.5% [1].
Hydrocephalus requires prompt treatment, because
otherwise it leads to increased intracranial pressure and
death. Treatment is challenging, because until now no infallible therapy was found. Over the years, many surgical techniques were proposed for treatment of hydrocephalus, such as medical therapy, rep eated lumbar taps, external
ventricular drainage, ventriculoperitoneal shunt, lombo-
peritoneal shunt, ventriculoatrial shunt, ventriculosinusal shunt, ventriculopleural shunt, ventriculo–gall bladder shunt, ventriculouretheral shunt, lombouretheral shunt, ventriculomastoidian shunt, ventriculo–subarachnoid–subgaleal shunt and endoscopic third ventriculostomy
(ventriculocisternostomy) [2–5]. Despite advances in neuro-
endoscopic surgery, the treatment of choice in hydro-cephalus remains ventriculoperitoneal shunt. Kausch W performed the first ventriculoperitoneal shunt in 1908 [6], but the procedure become widely used only 50 years later, and since 1960 the surgical technique has not changed
much.
Abdominal complications cause distal shunt failure
and acute hydrocephalus. Ventri culoperitoneal shunt-related
consequences are encountered in 24–47% of cases [7].
Distal shunt complications are shunt infection, shunt
disconnection with distal catheter migration, CSF pseudo-
cysts, CSF ascites, visceral perforations, bowel obstructions, inguinal hernia with or without hydrocele, mesenteric
pseudotumor, incisional hernia, subfrenic abscess and
peritoneal metastases from primary central nervous system tumors [4, 8, 9].
R J M E
Romanian Journal of
Morphology & Embryology
http://www .rjme.ro/

V. T. Grigorean et al.
1046
Opening of the peritoneal cavity in patients with
ventriculoperitoneal shunt for distal shunt revision or for
other abdominal pathology reveals, in some cases, extensive
adhesions between distal tube and viscera. Distal shunt failure can be attributed to the presence of unabsorbed
CSF in peritoneum, causing inflammatory reaction.
Aim and objective
The aim of the experiment was a better understanding
of phenomena occurring within peritoneal cavity in patients with hydrocephalus and ventriculoperitoneal
shunt. The objective was to determine the response and
most of all the peritoneal reaction in rats after intra-peritoneal administration of human CSF and the evolution
of the local inflammatory response.
 Materials and Methods
The experimental study was carried out in the Center
for Experimental Medicine of “Iuliu Ha țieganuˮ University
of Medicine and Pharmacy, Cluj-Napoca, Romania, using
Wistar female healthy rats , each weighing 180–190 g.
The experiment has been done in compliance with the
legislation regarding animal research. The rats had standard
living conditions. Euthanasia of the animals has been performed dynamically, by intra-cardiac inoculation of
Vetased in lethal dose.
The cerebrospinal fluid inoculated intraperitoneally
came from a human patient with hydrocephalus, was clear,
with negative Pandy reaction and was harvested and stored
under sterile conditions for 72 hours at 4
0C.
The experiment was designed in two steps:
▪ First step aimed to set the suitable dose of CSF to be
intraperitoneally administered without causing animals’ death within 24 hours;
▪ The second step aimed to assess the morphological
changes of abdominal cavity and abdominal organs after prolonged exposure to CSF introduced in peritoneal cavity.
Four groups of 10 animal s, each were used in each
step. The first group in each step was the control group
where each animal received a single dose of 0.5 mL of
normal saline. The other three groups of each step received
a single dose of CSF.
All subjects were kept under observation after the
intraperitoneal administration in standard life conditions,
according to the animal facility microclimate. The protocol for the first step was as follows:
▪ The animals in the cont rol group, which received
normal saline, showed no behavioral changes neither
immediately nor 24 hours after inoculation.
▪ The animals in the group A received 3 mL of CSF
each. A sudden deterioration of general state occurred
15 minutes after inoculation: subjects developed a muscular contracture, adopting a hedgehog position, suggestive for
severe abdominal cramps and had cold extremities. All
subjects were dead at 24 hours, most of them within the first hours.
▪ The animals in the group B received 2 mL of CSF
each. The symptoms occurred and the results were the
same, all subjects being dead at 24 hours.
▪ The animals in the gr oup C received 0.5 mL of
CSF each. No behavioral changes occurred during the first six hours after administration, and all subjects were
alive at 24 hours.
Thus, the dose of 0.5 mL CSF/subject was considered
suitable for the second step of the experiment.
The protocol for the second step was as follows:
▪ The animals in the control group were inoculated
with a single dose of 0.5 mL CSF and were sacrificed at
24 hours.
▪ The animals in the group 1 were inoculated with a
single dose of 0.5 mL CSF and were sacrificed at 24 hours.
▪ The animals in the group 2 were inoculated with a
single dose of 0.5 mL CSF and were sacrificed at 48 hours.
▪ The animals in the group 3 were inoculated with a
single dose of 0.5 mL CSF and were sacrificed at 72 hours.
After sacrificing the animals, peritoneal fluid analysis,
macroscopic and microscopic ex amination of the peritoneal
cavity and abdominal organs were carried out.
Cytological analysis of peritoneal fluid was carried out
on smears stained with May–Grünwald–Giemsa (MGG).
Histopathological examination of visceral and parietal
peritoneum, abdominal wall, small bowel, epiploon and uterus was carried out using formalin-fixed paraffin-
embedded samples, stained with Hematoxylin–Eosin (HE).
 Results
The main observations iden tified in each group are
described below by categories of morphological parameters
and summarized in Table 1.

Table 1 – Synopsis of the morphological study
Group Fluid Outcome Necropsy Cytology Histopathology
Control Normal
saline,
0.5 mL No changes Few mature cells No changes
Group 1 Euthanasia
at 24 hoursParietal and visceral
peritoneal congestionObvious inflammatory reaction
Bacteria free and within the
phagocytic cells
↓
Elements suggestive for
acute peritonitis Necrotico-purulent inflammation of
parietal and visceral peritoneum
Areas of desquamation and necrosis
Epiploic necrosis
Inflammatory process extended to
the abdominal wall
Group 2 Euthanasia
at 48 hoursDiscrete peritoneal
and abdominal
wall congestion
Moderate wall
edema Reduction in number of free or
phagocytized bacteria
Increasing in number of macrophages
with significantly phagocytosis
↓
Acute peritonitis in remission Histopathologic examination similar
to group 1, but with less intensity
Group 3 Sterile CSF,
0.5 mL
Euthanasia
at 72 hoursAlmost total remission
of congestion and
edema Small amount of inflammatory cells Reduced inflammatory process,
in small foci, with macrophages,
neutrophils, lymphocytes, mast cells

Effect of intraperitoneal administration of sterile human cerebrospinal fluid in rats
1047

Necropsy
The necropsy revealed no changes in the peritoneum
and abdominal organs of control group animals (Figure 1).

Figure 1 – Control group. Normal aspect of the
peritoneum and abdominal organs. In group 1 of animals, a strong congestion of the
abdominal wall, peritoneum and abdominal organs was observed (Figure 2, a and b). In some animals, increased amount of turbid, yellow-white abdominal fluid was found.
In group 2, there was a slight congestion of the
peritoneum in some animals, but most of them showed
no obvious macroscopic changes of the peritoneum and abdominal organs (Figure 2c).
In group 3, complete or almost complete remission of
peritoneal and abdominal organs macroscopic changes was observed (Figure 2d).
Cytological examination of peritoneal fluid
The peritoneal fluid in the control group contained
predominantly old neutrophils, with multilobulated nuclei, eosinophils and lymphocytes (Figure 3). Other rare cells were mononuclear cells, mast cells and mesothelial cells.

Figure 2 – Different aspects of macroscopic changes of the peritoneum and th e abdominal wall in studied groups:
Group 1 – intense congestion of the abdominal wall (a) and abdominal viscera (b); Gr oup 2 – abdominal viscera
showing only slight congestion (c); Group 3 – perito neum and abdominal viscer a with normal aspect.

Figure 3 – Control group. Peritoneal fluid cytology.
MGG stain, ×400. In group 1, the peritoneal cytology revealed a large
number of young and old neutrophils and macrophages
containing phagocytized bacteria with diplo and strepto
arrangement (Figure 4, a and b), aspect which pleaded
for the diagnosis of purulent bacterial peritonitis.
The cytological examination performed in group 2
showed a few free or phagocytized bacteria, an obviously
increased number of macroph ages (some of them multi-
nucleated) who had phagocytized bacteria and dead cells,
of neutrophils and old and young eosinophils (Figure 4c).
The cytological diagnosis was purulent bacterial peritonitis,
with lower intensity than in group 1.
In group 3, the peritoneal fluid cellularity was slightly
higher than in the control group, with an increased number
of macrophages, neutrophils and young mast cells
(Figure 4d). This aspect pleaded for a milder bacterial
inflammation than in groups 1 and 2.

V. T. Grigorean et al.
1048
Histopathological changes
As expected, the control group showed no obvious
morphological changes of all studied structures (Figure 5,
a and b).
In group 1, an intense purulent necrotic inflammation
of visceral and parietal peritoneum was found. Neutrophils
and macrophages containing co cci were present on the
mesothelial surface. Mesothelia l cells containing bacteria
presented, in desquamated areas, necrosis and transfor-
mation into macrophages. The epiploon showed areas of necrosis, infiltrates of m acrophages and neutrophils
containing cocci, as well as free bacteria, on a background
of intense congestion. All abdominal organs studied
showed abundant infiltration with macrophages and granulocytes beneath the serous layer. The abdominal
wall was congested, with granulocytes and macrophages
infiltration beneath the peritoneum. Adherent peritoneal mesothelial cells b ecame cuboidal or co lumnar in shape,
with abundant cytoplasm, morphological changes defining
the so-called mesothelial ac tivation (Figure 6, a–e).

Figure 4 – Different aspects of peritoneal fl uid cytology, MGG staining, ×400: (a and b) Group 1 – neutrophils and
macrophages containing cocci, pleadi ng for purulent inflammation; (c) Group 2 – numerous neutrophils and
macrophages characteristic for purule nt inflammation; (d) Group 3 – numer ous monocytes and four mast cells.

Figure 5 – Control group: (a) Epiploon, normal aspect, HE staining, ×200; (b) Uterin e wall, serous layer with normal
aspect, HE staining, ×400.

Effect of intraperitoneal administration of sterile human cerebrospinal fluid in rats
1049

Figure 6 – Different histopathological aspects of peritoneal cavity structures in group 1, HE staining, ×400: (a) Epiploon:
Mesothelial cells, neutrophils and ma crophages containing bacteria, purulent inflammation; (b) Abdominal wall:
Mesothelial cells, neutrophils and macr ophages containing bacteria, purulent in flammation; (c) Ovary with purulent
exudate on the surface; (d) Abdominal wa ll: Neutrophils and eosinophils infiltrated in the serous and muscular layers;
(e) Uterine wall: Activated, hypertrophic mesothelial cells.
In group 2, lesions were similar to those in group 1,
but with a lower intensity. Congestion was much weaker, the number of bacteria free or contained within the
cytoplasm of phagocytes was significantly reduced,
sometimes very difficult to be identified. The inflammation was dominated by neutrophils and macrophages (Figure 7a). In group 3, the inflammatory process was present
only as small foci of multiform cellular infiltration (macrophages, neutrophils, lymphocytes, mast cells,
eosinophils) beneath the peritoneal serous layer.
Mesothelial cells still presented a diffuse activation feature (Figure 7, b and c).

Figure 7 – Different histopathologica l aspects of peritoneal cavity structures in groups 2 and 3, HE staining, ×400:
(a) Group 2: Epiploon – infiltrates with neutrophils and ma crophages suggestive for purulent inflammation; (b) Group 3:
Epiploon – rare infiltrates with mast ce lls, lymphocytes and eosinophils, activate d mesothelium; (c) Abdominal wall: Rare
foci with neutrophils under the serous layer.

V. T. Grigorean et al.
1050

 Discussion
There is no clear evidence until now regarding the
pathophysiology of specific complications such as: extensive peritoneal adhesion syndrome, CSF pseudocysts, CSF ascites, viscus adhesion with secondary perforation or bowel obstruction through volvulus, occurring in the
peritoneum of patients with hydrocephalus and ventriculo-
peritoneal shunt, when the abdominal cavity is the site of shunt dysfunction [4, 8, 10]. Therefore, this study was designed to assess the local and general reactions after intraperitoneal administration of sterile CSF and the local
inflammatory process using macroscopic cytological and
histopathological criteria in order to better understand
the appearance of these phenomena.
The control group was necessary in order to follow
the outcome of subjects that received intraperitoneal
normal saline. The subjects in this group had a normal evolution after intraperitoneal administration of the fluid,
with no mortality or local cytological or histopathological
changes, confirming once again the impressive resorption power of the peritoneum.
CSF administration in large quantities led to the death
of all subjects, probably beca use of the toxic effects of
high doses. Gradually decr easing doses made subjects’
survival possible and the dose of 0.5 mL sterile CSF
intraperitoneally administered was compatible with survival, confirming the presence of th e peritoneum tolerance for
CSF.
Subjects were divided into three groups in order to
identify dynamic changes in peritoneum. Preliminary
conditions, including dose of CSF were the same, the
only distinguishing element being the time elapsed until subjects were euthanized: 24 hours, 48 hours, and 72 hours respectively.
In group 1, macroscopic examination revealed a
pronounced congestion of the parietal and visceral
peritoneum, confirming that the CSF is a chemical which can cause local reacti on with possible general
consequences.
Cytological examination of the intraperitoneal fluid
showed polymorphonuclear cells, free bacteria and mono-
nuclear phagocytic cells, suggesting a process of early
peritonitis. Bacterial seeding occurred by chance, given the sterile administration of CSF, through translocation of intestinal bacteria amid the initial chemical peritonitis.
Aforementioned elements were confirmed by histo-
pathological examination, which showed the presence
of an inflammatory process involving both parietal and
visceral peritoneum, with areas of desquamation and necrosis, dispersed throughout the peritoneal cavity.
The conclusion at this point of the experiment was
that intraperitoneal administration of foreign bodies, such as the CSF, could rapidly induce non-specific reactions
due to changes of local biochemical microenvironment,
with fatal secondary infections.
In group 2, necropsy confirmed, from the macroscopic
point of view, the peritoneal, abdominal wall and viscera inflammation, which had similar features to those found in group 1.
Peritoneal fluid cytology, although partially overlapping
the picture observed in the previous group found some
new changes, consisting in the reducing of the free or phagocytized bacteria number, and the tendency to replace
the polymorphonuclear type elements with macrophages. Given that the histopathologi cal elements also were of
lower intensity as compared to those found in the previous group, it could be concluded that the morphological picture is that of acute peritonitis in remission.
In the third group, morphologic investigation high-
lighted from microscopic point of view reduced cellularity and histopathological changes.
Data analysis in the short term, showed a very prompt
inflammation, developed within 24 hours of the experiment and associated with elements as the infection determined
by bacterial translocation fr om the bowel, meeting thus
all the criteria of an acute purulent peritonitis.
This inflammatory response was secondary to the
presence of CSF in the peritoneum.
The reduction almost complete after 72 hours of the
above-mentioned phenomena, is the result of a very active
immune response, characteristic of experimental animals.
In humans, although peritoneal opening is minimal and
no abdominal viscera are injured during distal catheter placement, patients with ventri culoperitoneal shunt have
dynamic ileus, with absent or reduced gastric and bowel movements, nausea and vomiting just after surgery. They
do not tolerate full meals in the first days after operation.
These symptoms usually disappear spontaneously over time, in the vast majority of cases. However, there were cases that developed acute persistent ileus after ventroculo-peritoneal shunt insertion, which imposed the shunt removal [11].
Corroborating data from the experiment with the
reported outcome of the patients with hydrocephalus and ventriculoperitoneal sh unt, we can suppose that
peritoneal inflammation found in many patients shortly after surgery could be largely due to the mechanisms
observed in our experiment. The consequences of the
presence of CSF in the peritoneal cavity probably have a more complex and mixed pathogenesis, in which chronic inflammatory, immunologic, allergic and vascular elements are overlapping.
The presence of adherence peritoneal syndrome, found
in patients, with no abdominal co-morbidities, may be the
result of a low, prolonged, local inflammatory response of the peritoneum to CSF aggression, which proved to be a highly irritating factor for the peritoneum.
The peritoneal inflammation causes more or less
extensive peritoneal adhesions, which can lead to various
abdominal complications, such as CSF pseudocyst, viscus
perforation, bowel obstruction, volvulus, and CSF ascites [8, 10, 12–14].
Infection, symptomatic or clinically silent peritonitis
or low-grade sepsis are also incriminated in the patho-physiology of specific abdominal complications following
ventriculoperitoneal shunt [4, 8, 15, 16]. The presence of
an inflammatory process leads to an impaired peritoneal capacity of absorption [15–17].
The limit of this experiment is the impossibility of
assessing the long-term outcome of specimens.

Conclusions
Intraperitoneal administration of sterile human CSF
caused an inflammatory response in varying degrees and

Effect of intraperitoneal administration of sterile human cerebrospinal fluid in rats
1051
with multivisceral locations. Doses greater than 2 mL of
CSF intraperitoneally injected resulted in the death of the
animals whereas the dose of 0.5 mL of CSF was consistent with animals’ survival. The peritoneal response at 24 hours,
ranging from congestion to purulent reaction, was intense
and diffuse, but after 72 hours the inflammatory response became mild, focal and limited only to small areas. The
remission of acute peritonitis started at 48 hours after
intraperitoneal CSF injection. Acute, congestive and, sometimes, purulent chemical peritonitis frequently causes
animal’s death, through cumulative toxic effect of CSF.
However, the subjects who have survived the acute moment showed remission of peritoneal and general phenomena.
Data from this experiment suggest that the peritoneal
inflammatory response to the inoculation of CSF is dose dependent, usually transitory but, if prolonged, it could
explain specific abdominal complications occurred in the
peritoneal cavity following ventriculoperitoneal shunt
insertion.
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Corresponding author
Aurelia Mihaela Sandu, MD, Department of Neurosurgery, “Bagdasar–Arseni” Emergency Clinical Hospital, 10–12
Berceni Highroad, Sector 4, 041915 Bucharest, Romania; Phone +40724–263 023, e-mail: aurasandu@gmail.com,
aurassandu@yahoo.com

Received: May 28, 2013
Accepted: December 12, 2013

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