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Spleen

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289

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5 Obsolete 5 Has been replaced by FAST and CT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

– Classication according to American

Association for the Surgery of Trauma Splenic Injury Scale (. Table11.2)

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

inuenzae, Neisseria meningitis,

Salmonella species

Prophylactic Therapy inAsplenia Patients

5 Vaccination (. Table11.3):

– Three to four weeks preoperatively

before elective splenectomy

– Threeweeks postoperatively after non-

elective splenectomy

– Pneumococcal, Haemophilus inuen-

zae type b, meningococcal and inuenza vaccinations

– Connection to asplenia outpatient

clinic

5 Antibiotics: Currently no data on antibi-

otic prophylaxis in splenectomized patients; however, recommended in children <5, 2years 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)

290

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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)

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 <1cm depth

Capsule injury Capsule injury Capsule injury

10–50% of the surface; intraparenchymal hematoma <5cm

Parenchymal laceration 1–3cm

>50% of the surface; ruptured subcapsular or intraparenchymal hematoma ≥5cm

Parenchymal laceration >3cm 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 <1cm depth

Subcapsular hematoma 10–50% of the surface; intraparenchymal hematoma <5cm

Parenchyma laceration 1–3cm

Subcapsular hematoma >50% of the surface or progressive in size; ruptured subcapsular or intraparenchymal hematoma ≥5cm

Parenchymal laceration >3cm 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 <1cm depth

Subcapsular hematoma 10–50% of the surface; intraparenchymal hematoma <5cm

Parenchymal laceration 1–3cm

Subcapsular hematoma >50% of the surface; ruptured subcapsular or intraparenchymal hematoma ≥5cm

Parenchymal laceration >3cm in depth

Parenchymal laceration with involvement of segmental or hilar splenic vessels with >25% devascularization

Hilar vascular injury with splenic devascularization

Vascular injury dened 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 dened 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

Grade classication based on highest classication by imaging, surgery or pathology. For multiple injury:

Grade+1 to Grade III

AIS abbreviated injury scale

Spleen

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. Table 11.3 Recommended vaccinations for asplenia patients

291

Vaccination

Pneumococcal vaccination

Haemophilus inuenzae type b vaccination

Meningococcal vaccinations

Inuenza vaccination

Before elective splenectomy

– Sequential vaccination with conjugate vaccine (PCV13 Prevenar 13®) followed by PPSV23 (Pneumovax 23®) 8weeks later (children <24months should be vaccinated with PCV13 only) – Repeat vaccination (PPSV23) and booster every 6years

– Single vaccination with single vaccine Act-Hib® or Hiberix – No repetition/refresher

– Vaccination against meningococci of serogroups ACWY – Children >2months 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 inuenza vaccination in autumn – Children and adolescents up to 17years of age may be vaccinated with inactivated vaccine or live nasal attenuated vaccine (LAIV)

After splenectomy

– If vaccination has not yet taken place, sequential PCV13 and PPSV23 8weeks later – If vaccination with PCV13 has already taken place, then only PPSV23 at the earliest 2weeks after splenectomy (if follow-up uncertain PPSV23 before discharge) – Repeat vaccination (PPSV23) and booster every 6years

Id. as before elective splenectomy

Two doses of MenACWY with an interval of 8–12weeks between doses

Id. as before elective splenectomy

Recommendations of the Robert Koch Institute “Vaccinations in Asplenia”

If possible, the vaccinations should have taken place at least 2weeks before the operation

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

https://t.me/medicina_free

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

Peritoneum

https://t.me/medicina_free

JörgPelz

Contents

12.1 Anatomy andPhysiology ofthe Peritoneum – 294

12.1.1 General Anatomy – 294

12.1.2 Physiology (Tasks) ofthePeritoneum – 294

12.2 Benign Diseases ofthePeritoneum – 294

12.2.1 Peritonitis – 294

12.2.2 Peritoneal Adhesions – 295

12.3 Pseudomyxoma Peritonei – 296

12.3.1 Denition – 296

12.3.2 Classication – 296

12.3.3 Aetiology – 296

12.3.4 Clinical Presentation – 296

12.3.5 Therapy – 296

12.3.6 Prognosis – 296

293

12.4 Malignant Diseases ofthePeritoneum – 297

12.4.1 Mesothelioma – 297

12.4.2 Peritoneal Carcinomatosis – 297

12.5 Cytoreductive Surgery (CRS) andHIPEC – 298

12.5.1 Curative CRS andHIPEC – 298

12.5.2 Prophylactic/Adjuvant CRS andHIPEC – 301

12.5.3 Palliative Therapeutic Concepts forAscites – 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

https://doi.org/10.1007/978-3-662-66735-4_12

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J. Pelz

12.1 Anatomy andPhysiology

ofthePeritoneum

12.1.1 General Anatomy

Denition

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 2.0m 5 Blood ow: approx. 100–200mL/min 5 Lymphatic absorption rate

– Approx. 1–2mL/min – Drainage via the lymphatic channels to

the thoracic duct

Structure (Histology)

5 Mesothelium (Tunica serosa) = serous

membrane

5 Extracellular matrix (lamina propia) 5 Connective tissue layer (Tela subserosa) 5 Thickness=90–130μm

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 50–70mL/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 Inammatory 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

ofthePeritoneum

Key Points

5 Peritonitis (inammation 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)

ofthePeritoneum

Organ Mobility

5 Mobility (sliding) of the abdominal organs 5 Through liquid lm on the serosal epithe-

lium

Denition

5 Inammation 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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295

5 By hematogenous seeding of bacteria 5 Frequent association with liver cirrhosis

Secondary Peritonitis

5 Inammations (cholecystitis, appendicitis,

etc.)

5 Perforation of an abdominal organ (gas-

tric ulcer, anastomotic insufciency, etc.)

5 Perforation of the abdomen (e.g. stab

wounds)

Spontaneous Bacterial Peritonitis (e.g. inAscites, Liver Cirrhosis)

Special Form: Peritonitis After CAPD Catheter Insertion

5 Frequently! 5 CAPD: “continuous ambulatory perito-

neal dialysis”.

Classication

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 inamma-

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 inammatory 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 inammatory 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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J. Pelz

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 nonspecic, 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/nonspecic 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 inltrative 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 Denition

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 Classication

5 Three groups (1995 classication)

– “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 signicantly better

outcome

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297

12.4 Malignant Diseases

ofthePeritoneum

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:

– Signicant survival benet 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

Denition

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 signicantly worse outcome 5 Median (overall) survival of 33months 5 Better survival in epithelioid subtype and

after CC-0 resection

Therapy

5 Difcult 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 – Specicity 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 inltration 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

Therapy

5 Cytoreductive therapy alone not sufcient

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=9–12months (pallia-

tive chemotherapy)

– Median survival=up to 20months (mod-

ern combination chemotherapeutics)

– Median survival=up to 30months in

selected patients

5 Pros:

– Systemic effect (inuence also on poten-

tial distant metastases)

– Fewer complications when compared

with surgery

5 Disadvantages:

– Still limited efcacy in peritoneal carci-

nomatosis

12.5 Cytoreductive Surgery (CRS)

andHIPEC

5 Denition:

– Combination of cytoreductive sur-

gery (CRS) followed by hyperthermic intraperitoneal chemoperfusion (HIPEC)

12.5.1 Curative CRS andHIPEC

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-

intensied + timely adjuvant/additive chemotherapy with cytotoxic concentration (not possible with systemic administration)

– Schematic representation of a HIPEC

perfusion: . Fig.12.1

Temperature

40-41,5

. Fig. 12.1 Schematic representation of HIPEC according to Pelz

Cytostatic Drug

Heat exchanger

Inow

Outow

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