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Spleen
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289
11
Ultrasound Examination
5 FAST (Focussed Assessment with Sonog-
raphy in Trauma)
5 Non-invasive, quickly available, cost-
effective
5 Quickly leads to the diagnosis and treat-
ment strategy
Diagnostic peritoneal lavage
5 Obsolete
5 Has been replaced by FAST and CT
5 CT abdomen:
– If patient is hemodynamically stable
– Excellent morphological representation
of the injury
– Classication according to American
Association for the Surgery of Trauma
Splenic Injury Scale (. Table11.2)
Therapy
5 Medical/conservative vs. surgical therapy
5 Surgical therapy: spleen- preserving sur-
gery vs. splenectomy
5 Indication for surgical exploration:
– Hemodynamic instability
– Progressive intra-abdominal blood loss
(in ultrasound, CT)
– Large hemoperitoneum
– Relative: Pseudoaneurysm in trauma-
tized splenic area
11.2.5 Post-splenectomy Morbidity
Asplenia: Pathophysiology
5 Thromboembolic consequences:
– Due to thrombocytosis (= increase in
platelet concentration in the blood)
– Increased risk of deep vein thrombosis
+ pulmonary embolism
– Lifetime pulmonary embolism
risk=35.6% vs. 9.7% (in control group)
5 Immunological consequences:
– Due to the absence of splenic function
– OPSI (Overwhelming Post- Splenectomy
Infection)
– Rare, but high mortality=50–70%
– Often prodromes (malaise, myalgias,
vomiting)
– Pneumonia
– Rapid progression of the disease
– Multi-organ failure: hypotension →
disseminated intravascular coagula-
tion → respiratory failure → coma →
death within hours of onset.
– Pathogen: Mostly S. pneumoniae;
other pathogens: Haemophilus
inuenzae, Neisseria meningitis,
Salmonella species
Prophylactic Therapy inAsplenia
Patients
5 Vaccination (. Table11.3):
– Three to four weeks preoperatively
before elective splenectomy
– Threeweeks postoperatively after non-
elective splenectomy
– Pneumococcal, Haemophilus inuen-
zae type b, meningococcal and inuenza vaccinations
– Connection to asplenia outpatient
clinic
5 Antibiotics: Currently no data on antibi-
otic prophylaxis in splenectomized
patients; however, recommended in children <5, 2years after splenectomy in children of all ages, and adults after
postsplenectomy sepsis.
5 From 1 million platelets/mm3: prophylac-
tic ASS (acetylsalicylic acid) administration (thrombosis prophylaxis)
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T. Bokor-Billmann and F. Billmann
. Table 11.2 American Association for the Surgery of Trauma Spleen Injury Scale (2018 revision)
11
GradeaAISb
severity
I 2 Subcapsular hematoma
II 2 Subcapsular hematoma
III 3 Subcapsular hematoma
IV 4 Any injury with lesion of the
V 5 Any injury with lesion of the
Imaging criteria (CT) Surgical criteria Pathological criteria
<10% of the surface
Parenchyma lazeration
<1cm depth
Capsule injury Capsule injury Capsule injury
10–50% of the surface;
intraparenchymal hematoma
<5cm
Parenchymal laceration
1–3cm
>50% of the surface;
ruptured subcapsular or
intraparenchymal hematoma
≥5cm
Parenchymal laceration
>3cm in depth
splenic vessels or active
intracapsular splenic
hemorrhage
Parenchymal laceration with
involvement of segmental or
hilar splenic vessels with
>25% devascularization
splenic vessels and active
bleeding into the peritoneal
space; injury of spleenadjacent structures
Destroyed spleen Destroyed spleen Destroyed spleen
Subcapsular hematoma
<10% of the surface
Parenchyma lazeration
<1cm depth
Subcapsular hematoma
10–50% of the surface;
intraparenchymal
hematoma <5cm
Parenchyma laceration
1–3cm
Subcapsular hematoma
>50% of the surface or
progressive in size;
ruptured subcapsular or
intraparenchymal
hematoma ≥5cm
Parenchymal laceration
>3cm in depth
Parenchymal laceration
with involvement of
segmental or hilar splenic
vessels with >25%
devascularization
Hilar vascular injury with
splenic devascularization
Subcapsular hematoma
<10% of surface
Parenchyma lazeration
<1cm depth
Subcapsular hematoma
10–50% of the surface;
intraparenchymal
hematoma <5cm
Parenchymal laceration
1–3cm
Subcapsular hematoma
>50% of the surface;
ruptured subcapsular
or intraparenchymal
hematoma ≥5cm
Parenchymal laceration
>3cm in depth
Parenchymal laceration
with involvement of
segmental or hilar
splenic vessels with
>25% devascularization
Hilar vascular injury
with splenic devascularization
Vascular injury dened by pseudoaneurysm or arteriovenous stula; presents as focal collection of contrast
from a vessel with decrease in intensity on delayed imaging. Active bleeding from a vascular lesion dened as
contrast leakage from a vessel, focal or diffuse, with increase in size or decrease in intensity on delayed imaging. Vascular thrombosis can lead to infarction of the organ
a
Grade classication based on highest classication by imaging, surgery or pathology. For multiple injury:
Grade+1 to Grade III
b
AIS abbreviated injury scale
Spleen
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. Table 11.3 Recommended vaccinations for asplenia patients
291
11
Vaccination
Pneumococcal vaccination
Haemophilus
inuenzae
type b
vaccination
Meningococcal vaccinations
Inuenza
vaccination
a
Before elective splenectomy
– Sequential vaccination with conjugate
vaccine (PCV13 Prevenar 13®) followed by
PPSV23 (Pneumovax 23®) 8weeks later
(children <24months should be vaccinated
with PCV13 only)
– Repeat vaccination (PPSV23) and booster
every 6years
– Single vaccination with single vaccine
Act-Hib® or Hiberix
– No repetition/refresher
– Vaccination against meningococci of
serogroups ACWY
– Children >2months and adults: single dose
of a 4-valent conjugate vaccine MenACWY
(Menveo®, Nimenrix®)
– Currently no refresher recommended
– Vaccination against meningococci of
serogroup B
– Since 2015 STIKO recommendation for
vaccination using Bexsero® or Trumenba® (risk
assessment by the treating physician)
– Currently no refresher recommended
– Annual inuenza vaccination in autumn
– Children and adolescents up to 17years of
age may be vaccinated with inactivated vaccine
or live nasal attenuated vaccine (LAIV)
b
®
After splenectomy
– If vaccination has not yet taken place,
sequential PCV13 and PPSV23 8weeks
later
– If vaccination with PCV13 has already
taken place, then only PPSV23 at the
earliest 2weeks after splenectomy (if
follow-up uncertain PPSV23 before
discharge)
– Repeat vaccination (PPSV23) and
booster every 6years
Id. as before elective splenectomy
Two doses of MenACWY with an
interval of 8–12weeks between doses
Id. as before elective splenectomy
Id. as before elective splenectomy
c
a
Recommendations of the Robert Koch Institute “Vaccinations in Asplenia”
b
If possible, the vaccinations should have taken place at least 2weeks before the operation
c
After splenectomy, vaccination can be given as soon as the patient is in a stable general condition
References
von Lanz T, Wachsmuth W (2004) Praktische anatomie.
Hals. Springer, Berlin
Further Reading
Beauchamp RD, Holzman MD, Fabian TC, Weinberg
JA (2008) The spleen. In: Townsend CM Jr,
Beauchamp RD, Evers BM, Mattox KL (eds)
Sabiston textbook of surgery. The biological basis
of modern surgical practice, 18th edn. Saunders,
Elsevier, Philadelphia
Bhangu A, Nepogodiev D, Lal N, Bowley DM (2012)
Meta-analysis of predictive factors and outcomes
for failure of non-operative management of blunt
splenic trauma. Injury 43:1337–1346
Cooper N, Ghanima W (2019) Immune thrombocytope-
nia. N Engl J Med 381:945–955
Feig BW, Ching CD (2019) The MD Anderson surgical
oncology handbook, 6th edn. Wolters Kluwer,
Philadelphia
Germer CT, Keck T, Grundmann RT (2017)
Evidenzbasierte Viszeralchirurgie benigner
Erkrankungen. Springer, Berlin
Iolascon A, Andolfo I, Russo R (2019) Advances in
understanding the pathogenesis of red cell membrane disorders. Br J Haematol 187:13–24
Keck T, Germer CT (2017) Minimal invasive
Viszeralchirurgie. Springer, Berlin
292
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T. Bokor-Billmann and F. Billmann
Leonhardt H, Tillmann B, Töndury G, Zilles K (2003)
Lehrbuch und Atlas der Anatomie des Menschen,
Innere Organe, vol 2, 3rd edn. Thieme, Stuttgart
Piel FB, Steinberg MH, Rees DC (2017) Sickle cell dis-
ease. N Engl J Med 376:1561–1573
Piel FB, Weatherall DJ (2014) The α-thalassemias. N
Engl J Med 371:1908–1916
Rauber A, Kopsch F (1948) Lehrbuch und Atlas der
Anatomie des Menschen, Eingeweide, vol 2, 17th
edn. Thieme, Leipzig
Robert Koch Institut (2019) Impfungen bei Asplenie.
https://www. rki. de/sharedDocs/FAQ/Impfen/Allg
Fr_Grunderkrankungen/FAQ01. html. Accessed on
7.6.2021
Rubin LG, Schaffner W (2014) Clinical practice. Care of
the apslenic patient. N Engl J Med 371:349–356
Standring S (2009) Gray’s anatomy. the anatomical basis
of clinical practice, 40th edn. Churchill Livingstone,
Elsevier, London
The American Association for Surgery of Trauma (2018)
Injury scoring scale. A resource for trauma care professionals. http://www. aast. org/library/traumatools/
injuryscoringscales. aspx#spleen. Accessed on 7.6.2021
Theilacker C, Ludewig K, Serr A, Schimpf J, Held J,
Bögelein M, Bahr V, Rusch S, Pohl A, Kogelmann
K, Frieseke S, Bogdanski R, Brunkhorst FM, Kern
WV (2016) Overwhelming postsplenectomy infection: a prospective multicenter cohort study. Clin
Infect Dis 62:871–878
von Lanz T, Wachsmuth W (2004) Praktische Anatomie.
Bauch. Springer, Berlin
Zilles K, Tillmann B (2010) Anatomie. Springer, Berlin
11
Peritoneum
https://t.me/medicina_free
JörgPelz
Contents
12.1 Anatomy andPhysiology ofthe
Peritoneum – 294
12.1.1 General Anatomy – 294
12.1.2 Physiology (Tasks) ofthePeritoneum – 294
12.2 Benign Diseases ofthePeritoneum – 294
12.2.1 Peritonitis – 294
12.2.2 Peritoneal Adhesions – 295
12.3 Pseudomyxoma Peritonei – 296
12.3.1 Denition – 296
12.3.2 Classication – 296
12.3.3 Aetiology – 296
12.3.4 Clinical Presentation – 296
12.3.5 Therapy – 296
12.3.6 Prognosis – 296
293
12
12.4 Malignant Diseases ofthePeritoneum – 297
12.4.1 Mesothelioma – 297
12.4.2 Peritoneal Carcinomatosis – 297
12.5 Cytoreductive Surgery (CRS) andHIPEC – 298
12.5.1 Curative CRS andHIPEC – 298
12.5.2 Prophylactic/Adjuvant CRS andHIPEC – 301
12.5.3 Palliative Therapeutic Concepts forAscites – 301
12.5.4 Complications – 301
12.5.5 Results – 302
12.5.6 PIPAC (Pressurized Intraperitoneal Aerosol
Chemotherapy) – 302
12.5.7 Guidelines – 302
References – 303
© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer
Nature 2023
F. Billmann, T. Keck (eds.), Essentials of Visceral Surgery,
https://doi.org/10.1007/978-3-662-66735-4_12
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J. Pelz
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12.1 Anatomy andPhysiology
ofthePeritoneum
12.1.1 General Anatomy
Denition
5 Peritoneum=serous membrane
5 One of the largest organ in terms of area
5 Mesothelial covering of the abdominal
cavity and the organs therein (peritoneum
viscerale) (excluded: retroperitoneal and
extraperitoneal organs)
5 Total area: 1.6 and 2.0m
5 Blood ow: approx. 100–200mL/min
5 Lymphatic absorption rate
– Approx. 1–2mL/min
– Drainage via the lymphatic channels to
the thoracic duct
2
Structure (Histology)
5 Mesothelium (Tunica serosa) = serous
membrane
5 Extracellular matrix (lamina propia)
5 Connective tissue layer (Tela subserosa)
5 Thickness=90–130μm
Division
5 Visceral peritoneum (Peritoneum vis-
cerale) (80%)
– Covering of the abdominal viscera and
organs
– Innervated=pain (visceral pain)
5 Parietal peritoneum (Peritoneum pari-
etale) (20%)
– Covering of the inner side of the
abdominal wall (somatic pain)
5 Peritoneal uid (physiologically produc-
tion 50–70mL/day)
Resorption
5 Within minutes; in cranial direction trans-
diaphragmatic
5 Metabolically highly active membrane
(semi-permeable)
5 Used for peritoneal dialysis or intraperito-
neal chemoperfusion/therapy
Immunological Tasks (= Defence)
5 Especially for infections of the abdominal
cavity
5 Inammatory process (vasodilation,
phagocytic clearance)
5 Involved in macrophage activation
5 Humoral immunity by complement sys-
tem
5 Clearance limitation: Critical limit at >105
germs/mL
5 High regeneration capacity
12.2 Benign Diseases
ofthePeritoneum
Key Points
5 Peritonitis (inammation of the peri-
toneum)
– Manifestation up to a severe septic
course
– Medical/conservative vs. surgical
treatment
5 Peritoneal adhesions= most frequent
cause of small bowel obstruction
(ileus)
– Surgical therapy for ileus
12.2.1 Peritonitis
12.1.2 Physiology (Tasks)
ofthePeritoneum
Organ Mobility
5 Mobility (sliding) of the abdominal organs
5 Through liquid lm on the serosal epithe-
lium
Denition
5 Inammation of the peritoneum
5 Evolution: Up to a severe septic course
Etiology
Primary Peritonitis (Without Previous
Abdominal Disease)
5 About 1% of peritonitis
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5 By hematogenous seeding of bacteria
5 Frequent association with liver cirrhosis
Secondary Peritonitis
5 Inammations (cholecystitis, appendicitis,
etc.)
5 Perforation of an abdominal organ (gas-
tric ulcer, anastomotic insufciency, etc.)
5 Perforation of the abdomen (e.g. stab
wounds)
Spontaneous Bacterial Peritonitis
(e.g. inAscites, Liver Cirrhosis)
Special Form: Peritonitis After CAPD
Catheter Insertion
5 Frequently!
5 CAPD: “continuous ambulatory perito-
neal dialysis”.
Classication
5 According to aetiology (see above)
5 According to localization
– Local peritonitis
– Diffuse (generalized) peritonitis
5 According to clinical course
– Acute peritonitis
– Chronic peritonitis
– Localized peritonitis
– Generalized peritonitis
– Contrast medium image of the parietal
peritoneum
– Search of the source of peritonitis
– Peritoneocentesis as direct pathogen
detection
Therapy
Surgical Therapy
5 Eradication of the source of infectious (if
present)
5 Closed peritoneal lavage
– Irrigation of the peritoneal space
(through drains placed during the oper-
ation) after appropriate operations
– For accelerated removal of inamma-
tory secretion/pus as a consequence of
various surgical diseases of the abdomi-
nal cavity
– Caution: Often irrigation limited to
area directly adjacent to drains (not
entire peritoneal cavity)
5 Staged lavage (= programmed lavage)
– For high-grade inammatory diseases
of the abdominal cavity
– Planned relaparotomy (with irrigation)
performed at set intervals evidence-
based worse than on-demand lavage
(according to patient’s clinical condi-
tion)
Symptoms
5 Abdominal tension
5 Fever
5 Increase in inammatory signs (leukocyto-
sis, CRP, erythrocyte sedimentation rate
ESR, procalcitonin)
5 Pain (localized/generalized)
5 Fluid shift
Diagnosis
5 Anamnesis
5 Clinical examination
– Abdominal tenderness and guarding
– Abdominal rigidity
– Pain localization
5 Laboratory (leukocytosis, CRP elevation)
5 Ultrasound
5 Computer tomography CT
! Caution
In pancreatitis usually conservative
approach.
Conservative Therapy
5 Calculated antibiotic administration
5 Adequate uid management (volume and
catecholamine controlled, hemodynamic
monitoring)
5 Intensive care unit monitoring for severe
peritonitis
12.2.2 Peritoneal Adhesions
Epidemiology
5 Mostly postoperative
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12
5 Most frequent cause of small bowel
obstruction (ileus = approx. 60% of
obstructions)
5 More often in the lower abdomen:
– After gynecological surgery
– After appendectomy
– After colorectal resection
Clinical Presentation
5 Asymptomatic to full image of ileus
(7 Sect. 16.2)
5 Usually nonspecic, occasionally crampy
abdominal pain
Diagnostic Imaging
5 CT: Indirect evidence of adhesions: dilated
small bowel loops on the anterior abdominal wall; caliber change of the small bowel.
5 MRI: MRI-sellink if necessary
Therapy
5 Asymptomatic adhesions/nonspecic pain:
– Symptomatic therapy preferred
– Adhesiolysis: Only in individual cases,
due to high incidence of recurrence.
5 In case of manifest ileus: surgical therapy
(7 Sect. 16.2)
12.3 Pseudomyxoma Peritonei
Controversy: Benign disease vs malignant disease without inltrative growth.
12.3.3 Aetiology
5 Mucinous cystadenoma (= mucocele) of
the appendix vermiformis
– Second most common tumor of the
appendix (after appendiceal carcinoid)
– In case of accidental detection: indi-
cation for metachronous or synchronous right hemicolectomy (better
outcome)
– In 50% of cases further intra- abdominal
manifestation at diagnosis
5 Mucinous tumor of the ovary (= muco-
cele)
– Rare
5 Tumour cell spillage of malignant tumours
of the abdominal cavity (e.g. appendix,
ovary, colon, uterus)
12.3.4 Clinical Presentation
5 Local problems due to displacing growth,
subileus
12.3.1 Denition
5 Accumulation of mucus masses in the
abdominal cavity due to a mucus-forming
tumour. Lymph node (<5%) or distant
metastases may rarely occur.
12.3.2 Classication
5 Three groups (1995 classication)
– “Disseminated peritoneal adenomucino-
sis (DPAM): Rather benign appearance.
– “peritoneal mucinous carcinomatosis”
(PMCA): cause = disseminated carcinoma cells, malignant appearance
– Intermediate category
12.3.5 Therapy
5 7 Section 12.5: Cytoreductive surgery
(CRS) + hyperthermic intraperitoneal
chemotherapy (HIPEC)
5 Poor/no effect of systemic chemotherapy
5 Absolute indication for HIPEC therapy
(highest evidence)
5 Right hemicolectomy for R0-resected
“low-grade tumours”=not recommended
12.3.6 Prognosis
5 With CRS+HIPEC: 10-year survival rate
approx. 70%
5 Low-grade tumor with signicantly better
outcome
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12.4 Malignant Diseases
ofthePeritoneum
Key Points
5 Peritoneal carcinomatosis= most fre-
quent secondary, malignant disease of
the peritoneum
5 Therapy: Paradigm shift with cytore-
ductive surgery (CRS)+HIPEC
5 CRS+HIPEC:
– Signicant survival benet in
selected tumor entities
– Optional treatment strategy in the
current S3 guidelines for colorectal
cancer
– High morbidity between 25% and
60%
– Mortality between 2 and 10
– The impact of chemoperfusion is
unclear!
12.4.1 Mesothelioma
Denition
5 Primary malignant disease of the perito-
neum
Epidemiology
5 Most common primary malignant disease
of the peritoneum
5 Mostly limited to the abdomen
5 Median survival = 4–12 months (due to
advanced stage at diagnosis)
5 history of asbestosis: 50–70% of patients
5 Men with signicantly worse outcome
5 Median (overall) survival of 33months
5 Better survival in epithelioid subtype and
after CC-0 resection
Therapy
5 Difcult to treat
5 Goal=complete surgical resection
5 Concept of CRS+HIPEC
12.4.2 Peritoneal Carcinomatosis
Epidemiology
5 Synchronous peritoneal carcinomatosis in
5–10% of all gastrointestinal tumors
5 Another 5–15%=metachronous
5 Mean survival time of these patients is
severely limited
Clinical Presentation
5 History of malignancy
5 Abdominal pain
5 Ascites
5 Weight loss
Diagnosis
5 Pretherapeutic staging=essential
Imaging Techniques
5 CT, MRI or PET-CT
5 Frequent understaging:
– Sensitivity between 50 and 96
– Specicity between 62 and 100
– Radiologic diagnosis of carcinomatosis
of the small intestine: in only 50% of
cases
Clinical Presentation
5 Abdominal pain
5 Ascites
5 Weight loss
Prognosis
5 Frequent inltration of the other intra-
abdominal organs (liver, intestine, bladder,
abdominal wall)
Staging Laparoscopy
5 Small tumor nodules can be detected
earlier
5 Biopsy and pathological workup possible
5 If necessary, limited tumor removal is pos-
sible laparoscopically
5 Disadvantage: Second-look operation is
usually necessary
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J. Pelz
12
Therapy
5 Cytoreductive therapy alone not sufcient
for cure
5 Systemic chemotherapy=currently pallia-
tive standard treatment procedure
5 Interdisciplinary treatment concept=cen-
tral (tumor board)
5 Development of new therapeutic strate-
gies (CRS+HIPEC; 7 Sect. 12.5)
Systemic Chemotherapy
5 Always as an interdisciplinary approach
5 Important factor in multimodal treatment
5 Results:
– Median survival=9–12months (pallia-
tive chemotherapy)
– Median survival=up to 20months (mod-
ern combination chemotherapeutics)
– Median survival=up to 30months in
selected patients
5 Pros:
– Systemic effect (inuence also on poten-
tial distant metastases)
– Fewer complications when compared
with surgery
5 Disadvantages:
– Still limited efcacy in peritoneal carci-
nomatosis
12.5 Cytoreductive Surgery (CRS)
andHIPEC
5 Denition:
– Combination of cytoreductive sur-
gery (CRS) followed by hyperthermic
intraperitoneal chemoperfusion
(HIPEC)
12.5.1 Curative CRS andHIPEC
Theoretical Approach
5 Cytoreductive surgery: goal=removal of
all visible tumor manifestations
5 HIPEC: goal = destruction of remaining
tumor cells after CRS
– Chemotherapeutic agents can be dis-
tributed throughout the abdomen
– Intraoperative application = dose-
intensied + timely adjuvant/additive
chemotherapy with cytotoxic concentration (not possible with systemic
administration)
– Schematic representation of a HIPEC
perfusion: . Fig.12.1
Temperature
º
40-41,5
C
. Fig. 12.1 Schematic representation of HIPEC according to Pelz
Cytostatic Drug
Heat exchanger
Inow
Outow
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