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Kidney Transplantation

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279

. Table 10.6 Banff classication of acute and chronic renal rejection

Grade Denition

Acute kidney rejection

Borderline damage Focal mild tubulitis (1–2 mononuclear cells per cross-section) without intimal

arteritis

IA Signicant interstitial inltration (>25% of parenchyma affected) and focal,

moderate tubulitis (>4 mononuclear cells per tubular cross-section or 10 tubular cells)

IB Signicant interstitial inltration (>25% of parenchyma affected) and focal, severe

tubulitis (>10 mononuclear cells per tubular cross-section)

IIA Signicant interstitial inltration with mild to moderate intimal arteritis

IIB Signicant interstitial inltration with moderate intimal arteritis (>25% of vessel

lumen)

III Transmural arteritis or brinoid changes and necrosis of the smooth muscle cells of

the media

Chronic kidney rejection

I Signs of minor chronic ischemia with mild graft glomerulopathy, minor interstitial

brosis, and tubular atrophy (<25% of cortical surface area)

II Signs of moderate chronic ischemia with moderate graft glomerulopathy, moderate

interstitial brosis and tubular atrophy (26–50% of cortical surface area)

III Signs of severe chronic ischemia with severe graft glomerulopathy, extensive

interstitial brosis, and tubular atrophy (>50% of cortical surface area)

cross-match and HLA typing (e.g. in the case of living donation from child’s father to mother)

5 Clinical presentation: Slow, continuous

deterioration of renal function.

5 Therapy:

– Increasing immunosuppression – For donor-specic antibodies mostly

frustrating

10.6.4 Infections

5 Increased risk due to immunosuppression

Bacterial Infections

5 Mostly urinary tract infections or pulmo-

nary infections

5 Atypical germs must be included in differ-

ential diagnosis

5 Early resistance-appropriate antibiotic

therapy

Opportunistic Infections

5 Mostly in the rst year after transplanta-

tion (higher immunosuppression)

5 Mostly viral infections (CMV, BKV) 5 Common pathogens:

– CMV – Aspergillosis – Candida – Clostridium difcile

10.6.5 Aftercare

5 After discharge from hospital:

– Initially 2–3 times weekly in coopera-

tion with a nephrologic centre

– In the course increase of the interval

5 One visit per year to the transplant centre 5 Main focus: creatinine progression, immu-

nosuppression

280

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B. Jänigen et al.

10.7 Results

5 Survival rates . Table10.7

. Table 10.7 1- and 5-year survival rates of the transplant and the recipient comparing post-mortem

organ donation vs. living donation

Graft

1year

Post-mortem donation 91% 69% 96% 84%

Living donation 95% 80% 98% 91%

5years 1year

Recipient

5years

Spleen

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ThereziaBokor-Billmann andFranckBillmann

Contents

11.1 Spleen: Generalities – 282

11.1.1 Embryology andDevelopmental Disorders – 282

11.1.2 Anatomy – 282

11.1.3 Physiology – 284

11.2 Spleen Diseases – 284

11.2.1 Benign Haematological Diseases – 284

11.2.2 Other Benign Diseases – 287

11.2.3 Malignant Diseases – 288

11.2.4 Spleen Trauma – 288

11.2.5 Post-splenectomy Morbidity – 289

281

References – 291

https://doi.org/10.1007/978-3-662-66735-4_11

282

Superior End

Splenic branches of the splenic plexus

Inferior End

rosplenic Ligament

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T. Bokor-Billmann and F. Billmann

11.1 Spleen: Generalities

Key Points

5 Coffee bean shaped organ; vol-

ume=160mL

5 Intraperitoneal position, left hypo-

chondriacal region

5 Vascularization through splenic artery

and vein (variations)

5 Organ of ltering/degradation of

erythrocytes and thrombocytes + Organ of lymphatic defence

11.1.1 Embryology

andDevelopmental Disorders

Embryology

5 Development in the dorsal mesogastrium 5 Colonization of the spleen by vascular

plexus

5 Colonization by reticulum cells + lympho-

cytes (formation of splenic pulp)

Developmental Disabilities

5 Aplasia (= agenesis=asplenia)

– Complete absence of the spleen – Cause = Absence of the vasa splenica

(developmental disorder 2nd–5th

embryonic week) – Often associated with cardiac malfor-

mation/situs inversus

5 Congenital hypoplasia

– Primary growth inhibition of the spleen – Very rarely cardiac malformation/situs

inversus

Splenic hypoplasia: Usually=secondary (atrophy)

11.1.2 Anatomy

Structure

Denition (. Fig.11.1)

5 Upper splenic pole=Extremitas superior 5 Lower splenic pole=Extremitas inferior 5 Posterior margin=Margo posterior 5 Anterior margin=Margo anterior 5 Surfaces:

Phrenicosplenic Ligament

Superior Polar Artery and Vein

Splenic recess of the lesser sac

Splenic Artery and Vein

Splenic Lymph node

Phrenicosplenic Ligament

Artery and Vein of the pancreas tail

. Fig. 11.1 View of the spleen from ventromedial. (From von Lanz and Wachsmuth 2004)

Tail of the Pancreas

Anterior Margin

Gastric Surface

Short Gastric arteries

Gast

Left gastroepiploic Artery and Vein

Spleen

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283

– Diaphragmatic surface (Facies dia-

phragmatica): relationship to the diaphragm

– Visceral surface (Facies visceralis): divided

into two facets: Facies gastrica (for the stomach)+Facies renalis (for the left kidney); between the two: splenic hilus.

Form

5 Similar to a coffee bean 5 Variations: possible 5 Parenchymal depression: at the anterior

border of the spleen

Variations

5 Double spleen: two separate, equally sized

and adjacent partial spleens (rare)

5 Multiple spleens: up to 10 spleens of

unequal size; supplied by splenic artery

5 Adjacent spleen: common (6–10% of pop-

ulation); very small roundish spleen adjacent to a regular spleen: CT hypervascular; DD: primitive neuroectodermal tumor

Measurements

5 Depending on the blood supply of the

organ/eventual pathology

5 Expansion capacity of the spleen = 2–3

times the basal volume

5 Decrease in height/weight from age 40

onwards

Measurements forAdults

5 Length=12.2cm 5 Width=7.8cm 5 Thickness=2.9cm 5 Weight (median):

– Men=162g – Women=155g

5 Volume (median)=160cm

Location

5 Intraperitoneal, left hypochondriacal

region

5 Spleen longitudinal axis=course of 10th

rib

5 Position dependent on movements of the

diaphragm (breathing)

– Between lower margin 8th rib and

upper margin 12th rib

– Held in position by peritoneal liga-

ments = phrenicosplenic ligament + splenorenal ligament + gastrosplenic ligament

Vessels andInnervation

Vessels

5 Splenic artery (A. splenica)=main vessel;

one of the 3 branch vessels of the truncus coeliacus

5 Polar arteries=variations:

– In number: 1–5 splenic polar arteries – In origin: mostly from splenic artery;

from left gastroepiploic (A. gastroomentalis sinistra), aorta, left gastric artery (A. gastrica sinistra), inferior pancreatic artery (A. pancreatica inferior), superior mesenteric artery (A. mesenterica superior)

5 Splenic vein (V. splenica) to portal vein (V.

portae hepatis)

5 Blood circulation=100–300mL/min

Innervation

5 Almost exclusively sympathetic postgan-

glionic rr. splenici

5 Few parasympathetic cholinergic bers 5 Spleen pain: Visceral pain, radiating from

the front into the back

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T. Bokor-Billmann and F. Billmann

11.1.3 Physiology

Filter Function

Filter/Degradation Organ oftheAltered Erythrocytes

5 Filtering of pathologically altered red

blood cells

5 Storage of hemoglobin (destruction of the

altered erythrocytes)

Storage/Degradation Organ ofPlatelets (and Clotting Products)

5 Storage: up to 30% of circulating platelets 5 Filtering of coagulation products in serum

(parallel)

Lymphatic Defense Organ

5 Formation of new B-lymphocytes 5 Presentation of antigens to lymphocytes 5 Spleen = most important organ of lym-

phocyte recirculation

11.2.1 Benign Haematological

Diseases

Idiopathic Thrombocytopenic Purpura (ITP)

Denition

5 Thrombocytopenia: platelet count

<150,000/mm

5 Normal bone marrow function 5 Exclusion of another cause of thrombocy-

topenia

Mechanism

5 Increased platelet destruction 5 By autoantibodies against platelet mem-

brane antigens

5 Phagocytosis of platelets in the reticuloen-

dothelial system (spleen)

Epidemiology

5 Young women > Men 5 72% patients >10years old 5 70% young women >40years old

11.2 Spleen Diseases

Key Points

5 Benign diseases: Especially of hemato-

logical origin

5 Malignancies: Lymphomas vs. leuke-

mias vs. metastases

5 Splenic trauma: Mostly blunt abdomi-

nal trauma; conservative vs. surgical approach.

5 Post-splenectomy morbidity: vaccina-

tion (possible pre- or postoperatively)

Clinical Examination

5 Purpura 5 Epistaxis 5 Bleeding gums 5 Less common: GI (gastrointestinal) bleed-

ing, hematuria, cerebral hemorrhage.

Diagnosis

5 Laboratory diagnosis: thrombocytopenia 5 Exclusion of other causes of thrombocy-

topenia (. Table11.1)

5 Diagnosis follows this exclusion strategy

Spleen

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285

. Table 11.1 Differential diagnoses of immune

thrombocytopenic purpura

False-low platelets

Common causes of thrombocytopenia

Other causes of thrombocytopenia

Secondary thrombocytopenias

EDTA ethylenediaminetetraacetic acid, HIV human immunodeciency virus, CLL chronic lymphocytic leukemia

– EDTA-induced invitro

platelet clumping or cold agglutinins

– Giant platelets

–

Pregnancy (pregnancy

thrombocytopenia, preeclampsia)

– Drug/drug-induced

thrombocytopenia (heparin, quinidine, quinine, sulfonamides)

– Viral infections (HIV,

infectious mononucleosis, etc.)

– Hypersplenism (chronic

liver failure)

–

Myelodysplasia

– Congenital thrombocytope-

nias

– Thrombotic thrombocyto-

penic—purpura/hemolytic uremic syndrome

– Chronic disseminated

intravascular coagulation

–

Autoimmune diseases

(e.g.lupus)

– Lymphoproliferative diseases

(CLL, non-Hodgkin lymphoma)

Therapy

5 Depending on the severity of thrombocy-

topenia

Strategy

5 Platelets >50,000/mm3 + asymptomatic:

monitoring

5 30,000>Platelets >50,000/mm3+asymp-

tomatic

– Monitoring without therapy – Glucocorticoids: prednisone (1 mg/kg

BW/day)

5 Platelets >20,000/mm3 + few symptoms:

Glucocorticoids (see above)

5 Platelets <20,000/mm3 + bleeding: Inpa-

tient treatment

– Platelet transfusion only if there is seri-

ous bleeding.

– I. v. immunoglobulins in case of bleed-

ing and preoperatively (1g/kg BW/day for 2days)

Splenectomy

5 Indications:

– Refractory severe ITP – Patients requiring very high or toxic

doses of glucocorticoids – Thrombocytopenia recurrence – Incomplete response after drug therapy – Pregnant women after drug therapy

with a risk of bleeding

5 Modality:

– Open splenectomy – Laparoscopic splenectomy (see below)

5 Result: Immediate response (within

10days postoperatively)=71–95%

Surgical Procedure

Laparoscopic Splenectomy

5 Preoperative skin marking, pressure-

free right lateral positioning, slight angulation of the operation table to increase the distance between the costal arch and the spina iliaca

5 Inferior dissection of the spleen, possi-

ble partial mobilization of the left colonic exure

5 Transection of the splenogastric ligament

and the gastricae-breves vessels (ligasure)

5 Visualization of the splenic hilus and

vessels

5 Minimal skeletonization of the splenic

artery and clipping by means of laparoscopic clips/vascular clips + transection

5 Initial clipping of the artery: reduction

of the spleen volume

5 Dissection of the lateral and retroperi-

toneal splenic ligaments

5 Identication of the pancreas tail and

mobilization of the pancreas without injury

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286

T. Bokor-Billmann and F. Billmann

5 Visualization of the splenic vein, skele-

tonization, clipping by means of laparoscopic clips/vascular clips and transection

5 Transection the splenodiaphragmatic

ligament

5 Extraction of the spleen using of a lap-

aroscopic extraction bag

5 Irrigation and closure, drainage if nec-

essary

Hereditary Spherocytosis

Denition

5 Hereditary autosomal dominant disease 5 Genetic defect: Alteration of the proteins

of the ankyrin complex (= erythrocyte cytoskeleton protein) (e.g. ankyrin, α- and β-spectrin protein)

Mechanism

5 Ankyrin/spectrin alteration/de-

cit = erythrocyte cell membrane decit = erythrocytes smaller, rounder, non-deformable

5 Consequence=increased osmotic fragility 5 In the spleen: spherocytes increasingly

trapped = erythrocytopenia (= haemolysis)

Therapy

5 Splenectomy 5 Mechanism: Reduction of hemolysis by

abolishing destruction in the spleen; no inuence on spherocytosis

Hemolytic Anemia DuetoErythrocyte Enzyme Defect

Denition

5 Two enzymatic defects:

– Glucose-6-phosphate dehydrogenase

(G6PD): X-linked inheritance

– Pyruvate kinase: autosomal inheritance

5 Mechanism: defect = abnormal glucose

metabolism = abnormal erythrocyte deformability=hemolysis in the spleen

Clinical Examination

5 Glucose-6-phosphate dehydrogenase de-

cit: anemia following drug, medication, or chemical exposure

5 Pyruvate kinase decit: anemia + spleno-

megaly

Therapy

5 Glucose-6-phosphate dehydrogenase de-

cit: splenectomy rarely indicated

5 Pyruvate kinase decit: splenectomy

Clinical Examination

5 Variable: asymptomatic carrier to severe

hemolysis

5 Anemia 5 Possibly jaundice 5 Splenomegaly

Diagnosis

5 Spherocytes 5 Increased reticulocyte count 5 Increased osmotic fragility of erythrocytes 5 Negative Coombs test

Haemoglobinopathies

Denition

5 Two entities:

– Sickle cell anemia: Autosomal recessive

disease

– Thalassemia: Autosomal dominant dis-

ease

5 Mechanism:

– Sickle cell anaemia: deformation of

erythrocytes in haemoglobin S homozygous patients=destruction of erythrocytes in spleen = anaemia; in

Spleen

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287

heterozygous patients deformation in certain reduced PaO2-situations

– Thalassemia: defect in hemoglobin syn-

thesis=hemolytic anemia

Clinical Examination

5 Sickle cell anaemia: haemolytic anaemia +

thrombosis=microinfarctions (especially in the spleen)+hypersplenism

5 Thalassemia: Hemolytic anemia + spleno-

megaly + splenomegaly + hypersplenism

Hypersplenism + splenic sequestration

5 For sickle cell disease and thalassaemia 5 Consequence: Acute splenomegaly = severe pain +

need for transfusion

Therapy

5 Medical/conservative therapy: transfu-

sions, painkillers, etc.

5 Splenectomy:

– Indication: recurrent acute sequestra-

tion crises; recurrent blood transfusions; massive splenomegaly; splenic abscesses

– Open vs. laparoscopic splenectomy

5 Acute symptoms due to hemorrhage of

the cyst; usually due to increase in size of the cyst

Epidemiology

5 True cysts: mostly parasitic (Ecchinococ-

cus species)

5 Non-parasitic cysts: 70–80% = pseudo-

cysts

Therapy

5 Suspicion of parasitic cysts: Preoperative

serological conrmation

5 Parasitic cysts/pseudocysts: splenectomy 5 Non-parasitic cysts: partial splenectomy 5 Pseudocysts: If <4cm: Monitoring

Splenic Abscess

5 Rare, potentially life-threatening disease 5 Incidence=0.7% 5 Mortality:

– 15–20% in previously healthy patients – Up to 80% in immunocompromised

patients

11.2.2 Other Benign Diseases

Splenic Cysts

Classication

5 True cysts (parasitic/non-parasitic) 5 Pseudocysts: Mostly secondary after trauma 5 Cystic-impressing tumors: cystic lymphan-

giomas, cavernous hemangiomas

Clinical Examination

5 Mostly asymptomatic 5 Symptoms: vague pain in the left upper

abdomen, left back or shoulder pain, pleuritic chest pain, shortness of breath

Risk Factors

5 Malignant diseases 5 polycythemia vera 5 Endocarditis 5 Haemoglobinopathies 5 I. v. drug abuse 5 AIDS (“acquired immunodeciency syn-

drome”)

5 Urinary tract infections

Clinical Examination

5 Often non-specic:

– Abdominal pain in the left upper quad-

rant – Fever – Peritonitis signs – Pleuritic chest pain

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T. Bokor-Billmann and F. Billmann

Diagnosis

5 CT abdomen with contrast medium

Therapy

5 Unilocular abscesses: CT-guided drainage

(success rate=75–90%)+antibiotics.

5 Multilocular abscesses: Splenectomy +

peritoneal drainage + antibiotics

11.2.3 Malignant Diseases

Lymphomas

5 Hodgkin lymphoma: surgical ther-

apy=staging laparoscopy

5 Non-Hodgkin lymphoma: splenectomy in

patients with isolated splenic involvement

Leukemia

5 Hairy-cell leukemia: splenectomy in

patients with splenomegaly.

5 Chronic lymphocytic leukemia: splenec-

tomy = palliative measure for symptomatic splenomegaly

5 Chronic myelocytic leukemia: splenec-

tomy=palliative measure in symptomatic splenomegaly or hypersplenism

tumors = splenectomy (diagnostic, therapeutic, palliative)

11.2.4 Spleen Trauma

5 See polytrauma; blunt abdominal trauma

Epidemiology

5 Spleen trauma=most frequent indication

for laparotomy after blunt abdominal trauma

5 Mechanisms:

– Car/truck accident most frequent – Other: Falls; pedestrian vs. car/motor-

cycle; bicycle accident; sports accidents.

Pathophysiology

5 Injury by:

– Rapid deceleration (with avulsion of

the splenic ligaments)=capsular avul-

sion – Compression – Energy transfer through the posterolat-

eral thoracic wall – Impaling through a (fractured) rib

5 Spleen perfusion = 5% of cardiac out-

put = minimal splenic trauma = severe bleeding

Non-hematological Malignant Tumors

5 Metastases:

– Mostly from cancers of the breast, lung

or melanoma – Mostly asymptomatic – Symptoms if: Splenomegaly/spleen rup-

ture – Splenectomy=effective palliative treat-

ment

5 Vascular tumors:

– Benign: Hemangiomas – Malignant: angiosarcomas, hemangio-

sarcomas; highly aggressive

Diagnosis

Anamnesis

5 Mostly orienting/typical 5 Important=accident mechanism

Clinical Examination

5 Peritoneal irritation (pain, defense) 5 External signs of direct force (deformity,

haematoma, etc.)

5 Hemodynamic status (hypotension, tachy-

cardia)

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