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14 Vernix Caseosa Peritonitis
development of peritonitis is unknown.
Meconium (contains anucleate squamous cells
and lanugo hair derived from VC) and keratinized squamous cells can induce an inammatory
response. Meconium causes neonatal meconium
peritonitis secondary to intestinal perforation
[15].
The onset of VCP after uncomplicated CS has
been attributed to incomplete peritoneal lavage of
spilled amniotic uid [13]. Keratinized squamous
cells can induce an active inammatory response
by mechanical [18] or chemical irritation [19]. A
similar presentation is found following the rupture of an ovarian mature cystic teratoma (dermoid cyst), keratinized cysts, and keratinizing
neoplasms [20]. The keratin and sebum may provoke an extensive and prominent foreign body
reaction that mimics peritoneal carcinomatosis
[21], rst described by Abitbol etal. in 1959in a
nonpregnant population [22]. Some consider that
a higher concentration of VC in amniotic uid,
observed in difcult labors with partial loss of
amniotic uid, or oligohydramnios, may have
pathogenic signicance [4]. Nevertheless, VC is
present in around half (43%) of newborns [23].
On the other hand, a hypersensitivity reaction
may occur from sensitization from previous pregnancy and delivery. However, most cases of VCP
develop in primiparous women suggesting that a
hypersensitivity reaction is less likely [16].
With premature rupture of membranes, the
placenta should be examined for acute cho-
rioamnionitis and funisitis [17].
fetal distress and anoxia during a breech delivery,
the anal sphincter may relax because of oxygen
deprivation, and the fetal intestines will empty.
During CS, meconium may spill into the abdominal cavity [24].
14.5 Clinical Presentation
Typically, a low parity patient presents 3–35days
following CS [3, 25–28], most after hospital discharge. Pyrexia is common, and nausea and vomiting could be present [29]. The abdominal pain is
localized or diffuse [29]. Dyspnea [16] or shoulder tip pain [30] represent diaphragmatic peritoneal irritation. Patient after vaginal delivery
presented 3 hours post-delivery [2]. Physical
examination reveals diffuse or lower quadrant
abdominal tenderness and often positive
Blumberg’s sign [3]. The vaginal examination
does not reveal pathology (almost all patients
delivered by CS). The severity of clinical presentation depends on the quantity and dissemination
of VC material [3, 25, 26, 30].
Probably some patients go unrecognized with
the subclinical presentation. Some patients report
discomfort, mild abdominal pain, or low-grade
fever as the only symptom. These symptoms are
present in numerous, more common postpartum
processes, and subclinical or mild VCP is not
even suspected [14].
The third type of presentation is a chronic
form with sinuses or granulomas, mainly in a CS
scar (Fig. 14.6a) or even after exploration and
extensive peritoneal lavage of all focuses of VC
(see Sect. 14.9.1).
14.4.2 Intraperitoneal Meconium
Peritonitis/Granuloma
Intraperitoneal meconium granulomas result
from amniotic uid swallowed during intrauterine
life. The ingested uid is absorbed in the intestine, leaving nondigestible elements such as
lanugo and cornied epithelium. This detritus
and secretions from the gastrointestinal tract,
liver, and pancreas constitute meconium. With
14.6 Dierential Diagnosis
The differential diagnosis depends on clinical
examination results or diagnostic imaging methods used. Clinical examination results in two
groups of differential diagnoses, whether the presentation involves peritonitis or peritoneal granulomas. Peritonitis mainly presents with maximal
pain and tenderness in the young female population in the lower right quadrant [17, 31].
14.7 Diagnosis
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Table 14.1 Differential diagnoses of vernix caseosa
peritonitis [3, 15, 16, 28, 32, 33]
Peritonitis Granuloma
Acute appendicitis Scar endometrioma
Acute cholecystitis Suture granuloma
Ruptured ovarian cyst Starch glove granuloma
Hollow organ
perforation
Bowel injury Carcinomatosis
Endometritis Disseminated peritoneal
Pelvic inammatory
disease
Starch glove
peritonitis
Meconium granulomatous peritonitis
Abdominal tuberculosis
leiomyomatosis
Therefore, acute appendicitis is the most common preoperative diagnosis (Table 14.1).
Postpartum fever, with or without peritoneal
signs, is usually attributed to “endometritis.”
Without apparent clinical signs, VCP may go
unrecognized and undocumented. Peritoneal
deposits on imaging mimic peritoneal carcinomatosis or tuberculosis. Disseminated peritoneal
leiomyomatosis probably develops after laparoscopic myomectomy, in addition to the role of
estrogen. Fragments from the morcellation of
myoma left in the peritoneum would be capable
of inducing metaplasia of the peritoneal mesenchymal cells, and particularly vulnerable women
could develop it.
14.7.1 Laboratory Findings
Leukocytosis and neutrophilia are always present
[3]. Vaginal, urinary, hematological, serum, and
tissue microbiological specimens are negative [1,
16, 25, 34]. There are cases with elevated CA-125
[30].
14.7.2 Diagnostic Imaging
Diagnostic imaging methods commonly show
nonspecic changes or normal ndings, especially during the rst few days of the disease.
14.7.2.1 Plain X-Rays
A plain abdominal X-ray is not diagnostic and
primarily denes the consequences of peritonitis or partial bowel obstruction—air–liquid
levels [1, 27]. Due to pleuritic pain, dyspnea,
or shoulder tip pain, patients undergo chest
X-rays or thoracic CT, which is always normal
[30].
14.7.2.2 Transabdominal Ultrasound
This is the rst diagnostic modality of choice, but
it is nonspecic. In some cases, free uid is present in an amount larger than normal. In rare cases,
larger deposits can be revealed (Fig.14.2), but
14.7 Diagnosis
Clinical presentation with additional diagnostic
workup may raise a suspicion of VCP and potentially prevent unnecessary removal of healthy
organs at laparotomy.
Cultures are negative, and antibiotics do
not affect the fever or white blood cell
count [5].
Fig. 14.2 An echogenic oval lesion indenting the hepatic
capsule lies between the liver parenchyma and abdominal
wall. (Reproduced with permission from [30])
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14 Vernix Caseosa Peritonitis
without the possibility of accurate diagnosis.
Some gastrointestinal causes can be ruled out,
such as acute cholecystitis.
14.7.2.3 Abdominal CT
The CT appearance of VCP has not been welldened or well-reported. Also, <50% of patients
underwent abdominal CT [5]. Abdominal CT of
proven VCP shows normal ndings in 16%,
while most remaining cases described nonspecic ndings [5]. Possibly, the CTs were performed too early to demonstrate peritoneal
nodules [5].
Contrast-enhanced abdominal CT reveals
multiple oval rim-enhancing peritoneal lesions
misinterpreted as peripheral hepatic metastases,
peritoneal carcinomatosis (which can be excluded
with a high level of certainty due to normal intraperitoneal status during recent CS), or abdominal
tuberculosis [35]. Abdominal CT made during
the rst several days commonly shows a small
amount of free uid (Fig.14.3a) because neutrophils are predominant soon after delivery. After
several days, an acute and foreign body inammatory reaction starts, forming multiple oval
rim-enhancing peritoneal lesions (Fig. 14.3b).
These lesions progress in number and size [5,
30]. Subsequent abdominal CT made for persis-
tent symptoms shows an increase in the number
and size of such lesions (Fig.14.3c).
a
b
c
14.7.2.4 Abdominal PET-CT
In complicated medical, gynecological, or surgical history, even PET-CT is made with high glucose uptake suggesting malignancy (Fig. 14.4)
primarily due to the mass irregularity. High glucose uptake is due to the inammatory origin of
VCP (ow cytometry demonstrated that
M1-polarized glut+ macrophages were the most
dominant cell subsets) [36].
14.7.2.5 Abdominal MRI
MRI can dene peritoneal nodules (Fig. 14.5),
but there are no VC pathognomonic MR ndings.
Except for diagnosis, MR serves as a follow-up
after conservative therapy, estimating the
decrease in peritoneal nodule size (Fig.14.6).
Fig. 14.3 (a) Abdominal CT on postoperative day 4
shows only a small amount of ascites (arrow). (b)
Abdominal CT on postoperative day 9 at the same level
shows a new small, well-dened, peripherally enhancing
cystic nodule anterior to the liver (arrow). (c) Abdominal
CT on postoperative day 14 shows two new small, welldened, peripherally enhancing cystic perihepatic nodules
(arrows). (Reproduced with permission from [5])
14.7.3 Fine-Needle Aspiration
In the chronic course, ne-needle aspiration
reveals a mixed inammatory response and a few
anucleate and mature squamous cells,
granulation- type tissue. This conrms the diagnosis of VCP or VC granuloma [30].
14.7 Diagnosis
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363
a
b
Fig. 14.4 Preoperative PET (a–c) and CT (d) show the
irregular mass in the lower part of the rectus muscles of
the abdomen. The PET shows an area of irregular and
inhomogeneous hypercaptation in the context of the for-
c
d
mation of the anterior abdominal wall with a very high
maximum standardized uptake value (SUV max up to
12.9). (Reproduced with permission from [36] under the
CC Attribution License)
a
Fig. 14.5 (a) T2-weighted MRI shows a juxta-hepatic
lesion with an increased T2 signal. (b) Post-gadolinium
fat-saturated T1-weighted MRI shows peripheral contrast
14.7.4 Diagnostic Exploration
Diagnostic laparoscopy or laparotomy to exclude
common conditions (acute appendicitis, ruptured
viscus, bowel, or ureter injury) shows character-
b
enhancement of the juxta-hepatic lesion with central low
T1 signal. (Reproduced with permission from [30])
istic white and yellow cheese-like plaques
(Fig. 14.7) deposited on visceral and parietal
peritoneal surfaces throughout the abdominal
cavity, in the absence of inammation or perforation of viscera. A non-purulent peritoneal collec-
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a
b
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14 Vernix Caseosa Peritonitis
c
e
d
f
Fig. 14.6 Scar (a) 3 months and (b) 20 months after the
CS. (c) Pelvic MRI 3 months after the CS, axial
T1-weighted sequence contrast-enhanced with fat suppression. (d) Pelvic MRI 3months after the CS, sagittal
T2-weighted sequence. (e) Pelvic MRI 6months after the
CS, axial T1-weighted sequence contrast-enhanced with
fat suppression. (f) Pelvic MRI 6 months after the CS,
sagittal T2-weighted sequence. (g) Pelvic MRI 13months
after the CS, axial T1-weighted sequence contrastenhanced with fat suppression. (h) Pelvic MRI 13months
after the CS, sagittal T2-weighted sequence [4]
14.8 Treatment
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365
a
b
c
Fig. 14.7 (a) Vernix caseosa deposits scattered through-
out the peritoneal cavity (gray arrows) in a diagnostic
laparoscopy. (Reproduced with permission from [16]
under the CC BY 2.0). (b) Vernix caseosa plaques were
found scattered on the surface of the omentum. These
tion may be present. The cheesy exudate was
present in all patients [29]. Peritoneal or omental
biopsies and biopsies of white serosal patches are
diagnostic (see Sect. 14.3).
Another advantage of diagnostic laparoscopic
is the possibility of converting to Pfannenstiel or
midline incision, depending on the underlying
pathology. Many nonobstetrical and obstetrical
conditions, such as a ruptured uterus, cannot be
repaired by laparoscopy.
14.8 Treatment
14.8.1 Conservative Treatment
The nonoperative management is rarely initiated
because pretreatment diagnosis is challenging and
commonly attributed to other causes of acute abdomen. Some patients were treated nonoperatively
plaques were associated with loose adhesions to the anterior abdominal wall. (c) Cheesy white exudate covering
the surface of the uterus. There is no inammation of the
underlying tissue. (Reproduced with permission from
[37])
with analgesia and antibiotics, but exploration was
performed due to the worsening of symptoms [16].
Possible contraindications could be the complications that arise from residual VC even after exploration and its removal (see Sect. 14.9.1).
Some recommend postoperative antibiotic
therapy [17, 18, 26, 28, 38]. However, uneventful
cases without perioperative antibiotics [3] are
probably due to (1) the chemical nature of the peritonitis and (2) at least 10 peptides within VC with
antibacterial properties [39, 40]. Abdominal swabs
are always negative (see Sect. 14.7.1). Even the
administration of adjuvant steroid therapy for
resistant symptoms without infection has been
proposed [38]. The notable response is observed
with steroid use for 1–2weeks, gradually tapering
off over the next 2weeks [38]. It is postulated that
steroids signicantly enhance the clinical course
by suppressing the inammatory response. This
concept is successful even in conservatively
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14 Vernix Caseosa Peritonitis
treated patients after unsuccessful antipyretic and
antibiotic therapy with objective improvement on
abdominal MR [4]. Similar therapy conrms
maternal intraperitoneal meconium peritonitis/
granulomas with the addition of nonsteroid antiinammatory drugs [15]. However, these various
treatments remain empirical and controversial.
14.8.2 Surgical Treatment
14.8.2.1 Vernix Caseosa Peritonitis
Laparotomy is performed in 88% when numerous areas of cheese-like brinous exudates are
seen on the serosal surface of the viscera [4].
Commonly appendix is covered with exudate,
and acute appendicitis is a typical intraoperative
diagnosis. Therefore, appendectomy and extensive peritoneal lavage are routinely performed
even when VCP is recognized [27]. Awareness of
the characteristics of VCP helps to avoid extensive excisional procedures (64%) [4] with suspicion of other processes, such as total hysterectomy,
salpingo-oophorectomy, cholecystectomy, or
partial colectomy, with subsequent normality in
the histopathological study of these organs [14,
28, 34]. Therefore, pathologists are essential for
correct diagnosis with intraoperative or deferred
consultation. Unnecessary, additional procedures
add to perioperative morbidity and compromise
recovery [16].
14.8.2.2 Vernix Caseosa Granuloma
With chronic presentation, the granulomatous
changes can occur as sinus tracts or palpable
abdominal wall masses (Figs. 14.4 and 14.8
Lower row). With the potential of malignancy,
radical excision is common with challenging
adequate abdominal wall closure (Fig. 14.8
Upper row).
Fig. 14.8 (Upper row) Intraoperative pictures of abdom-
inal wall vernix caseosa granuloma. The mass started
from the anterior sheath of the rectus muscle of the abdomen and extended to the fatty tissue of the subcutaneous
layer. (Lower row) Macroscopic view of the excised
abdominal wall mass weighing approximately 300g and
sized 11×10×4cm. (Reproduced with permission from
[36] under the CC Attribution License)
References
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14.9 Prognosis
14.9.1 Maternal Outcome
Even after exploration and irrigation/suction of
the entire intraperitoneal cavity, consequences of
intraperitoneal VCP could develop. These primarily present in the form of small bowel obstruction, sometimes with recurrent episodes [16],
wound discharge [16], or chronic VC sinus [16].
The sequel is common with operative and
nonoperative treatment. The sinus tract of proven
VC should be excised, together with abdominal
mass, if found on preoperative imaging [16]. The
operative intervention should eliminate recurrent
or intermittent abdominal pain due to adhesions
[16]. The location of VC granuloma determines
the type of operation. Abdominal wall granuloma
[36] should be excised, while intraperitoneal
granuloma sometimes requires bowel resection
[41]. In such cases, ne-needle aspiration reveals
a mixed inammatory response, scattered foci of
anucleate keratin/squames conrmed by a cytokeratin immunostain, a few anucleate and mature
squamous cells, and a granulation-type tissue
[30]. Also, PET-CT can dene lesions without a
denitive preoperative diagnosis [36].
14.9.2 Fetal Outcome
Almost all cases develop and present several after
CS.Therefore, the delivery and the fetus are not
compromised by the VCP.
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Part III
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Surgery
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