The spleen

Abstract

Key points•The spleen plays a vital immunological role, and attempts should be made to preserve its function.•Overwhelming post-splenectomy sepsis is an often fast and catastrophic complication of splenectomy with mortality rates of 40–70%.•For patients presenting for splenectomy, a multidisciplinary team is essential for the best perioperative outcome.•Anaesthetists play a key role in the management and coordination of the splenic trauma patient, and should have knowledge of all treatment modalities and organizational availability and capability.•Splenic artery aneurysm is a rare, but important differential diagnosis in the shocked pregnant patient with abdominal pain. •The spleen plays a vital immunological role, and attempts should be made to preserve its function.•Overwhelming post-splenectomy sepsis is an often fast and catastrophic complication of splenectomy with mortality rates of 40–70%.•For patients presenting for splenectomy, a multidisciplinary team is essential for the best perioperative outcome.•Anaesthetists play a key role in the management and coordination of the splenic trauma patient, and should have knowledge of all treatment modalities and organizational availability and capability.•Splenic artery aneurysm is a rare, but important differential diagnosis in the shocked pregnant patient with abdominal pain. Patients present for a splenectomy for a variety of reasons. Anaesthetists need to be aware of the associated implications of concurrent disease in planning appropriate perioperative care. This article will summarize the basic science and perioperative considerations for splenectomy. The adult spleen weighs ∼100–150 g, the size of a cupped hand. This encapsulated organ is situated in the left upper quadrant of the abdomen. The diaphragm separates the spleen from the pleura and ribs 9–11 posteriorly. The stomach lies anteriorly, the left kidney medially, and the splenic flexure of the colon inferiorly. The tail of the pancreas attaches to the splenorenal ligament and extends to the splenic hilum, making the pancreas vulnerable to injury during a splenectomy.1Ellis H Mahadevan V. Clinical Anatomy. Wiley-Blackwell, Chichester2010: 111-112Google Scholar The arterial supply to the spleen is via the tortuous splenic artery (one of the three branches of the coeliac axis) and the short gastric arteries (branches of the left gastroepiploic artery) supplying the upper pole of the spleen. The splenic artery divides at the hilum, providing a segmental blood supply. Posterior to the neck of the pancreas, the splenic vein joins the superior mesenteric vein to form the portal vein.2Gosling JA Harris PF Whitmore I Willan PLT Human Anatomy. Color Atlas and Text. Mosby, 2002: 148-149Google Scholar The spleen has two main functions: as a secondary lymphoid organ of the immune system and a housekeeping role destroying senescent erythrocytes and the phagocytosis of particulate material in the blood.3Kirkineska L Perifanis V Vasiliadis T. Functional hyposplenism.Hippokratia. 2014; 18: 7-11PubMed Google Scholar The bone marrow and the thymus are the primary lymphoid organs, controlling the production and maturation of lymphocytes. The spleen ‘… processes and presents antigens, ultimately leading to successful elimination of pathogens and induction of adaptive immunity…’.4Borges da Silva H Fonseca R Pereira RM Cassado Ados A Alvarez JM D'Imperio Lima MR Splenic macrophage subsets and their function during blood-borne infections.Front Immunol. 2015; 6: 480Crossref PubMed Scopus (112) Google Scholar Histologically, the spleen can be seen to consist of white pulp and, the more predominant, red pulp. The lymphoid activity occurs in the white pulp, with phagocytic activity occurring in the red pulp. Other functions are summarized in Table 1.Table 1Functions of the spleen4Borges da Silva H Fonseca R Pereira RM Cassado Ados A Alvarez JM D'Imperio Lima MR Splenic macrophage subsets and their function during blood-borne infections.Front Immunol. 2015; 6: 480Crossref PubMed Scopus (112) Google ScholarFunctionExamplesImmuneAntigen presentationStores lymphocytes and macrophages and exposes them to the circulationFiltration and metabolismRemoves old and damaged erythrocytes and particulate matterThe splenic macrophages thus release haem from haemoglobinStorage240 ml of red cells can be stored and mobilized via splenic contraction in time of hypoxia (free diving and diving mammals) or hypovolaemia30% of plateletsIronProductionOpsonins, such as properdin (complement activation) and tuftsin (immunostimulatory peptide)HaematopoiesisAfter the fifth gestational month, haematopoiesis continues in the bone marrow, except in some pathological disorders of bone marrow disruption (e.g. myelofibrosis) Open table in a new tab Accessory spleens are relatively common, occurring in ∼10% of the population.1Ellis H Mahadevan V. Clinical Anatomy. Wiley-Blackwell, Chichester2010: 111-112Google Scholar They are rounded, encapsulated structures which may occur anywhere in the abdomen, but are usually situated near the splenic hilum. If they remain after splenectomy, they may result in persistence of symptoms. Splenic artery aneurysms (SAAs) are defined by a pathological dilatation of the splenic artery to >1 cm in diameter. SAAs are the third most common abdominal aneurysm after aortic and iliac artery aneurysms.5Lakin RO Bena JF Sarac TP et al.The contemporary management of splenic artery aneurysms.J Vasc Surg. 2011; 53: 958-964Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar The prevalence in the general population is thought to be low at ∼0.1–0.2%, although an autopsy study in patients over 60 years of age, looking specifically at the spleen, found a prevalence as high as 10.4%. The true prevalence remains unknown because 95% of individuals remain asymptomatic. Generally, SAAs manifest in one of three ways: (i) as an incidental finding at angiography, laparotomy, or postmortem, (ii) abdominal pain, and (iii) after rupture with hypotension and a sudden collapse (2–10% of patients). There is a strong association between pregnancy and SAA formation, especially in the multiparous woman; and ∼95% of SAA ruptures occur during pregnancy, most commonly during the third trimester. Though the rupture of an SAA during pregnancy is a rare event, it carries a high risk of maternal and fetal mortality. The mortality of SAA rupture in the general population is 25%. In a pregnant woman, this mortality rate increases to 75% with a fetal mortality rate of 95%.5Lakin RO Bena JF Sarac TP et al.The contemporary management of splenic artery aneurysms.J Vasc Surg. 2011; 53: 958-964Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar If a woman has an existing SAA, the risk of it rupturing during pregnancy is 20–50%. Although SAA rupture is rare, it is an important differential diagnosis to consider, especially in the context of abdominal pain or shock in pregnancy or labour, particularly as SAA rupture in pregnancy is difficult to diagnose because its symptoms mimic other obstetric and surgical emergencies. Approximately 70% of cases of SAA rupture during pregnancy are misdiagnosed as uterine rupture, placental abruption, amniotic fluid embolism, or perforated peptic ulcer. With the increasing use of high-resolution imaging, the number of incidentally detected SAAs will inevitably rise. In the non-pregnant population, SAAs that are larger in size, commonly > 2 cm, or grow during the interval observation period are appropriate for treatment. However, it has been recently shown that up to half of splenic artery aneurysms that rupture during pregnancy are <2 cm in diameter. Owing to the high fetal and maternal mortality associated with rupture during pregnancy, some experts recommend that all SAAs, regardless of size, should be treated during pregnancy. Evidence suggests that endovascular ablation is a safe and effective treatment of non-ruptured SAAs.5Lakin RO Bena JF Sarac TP et al.The contemporary management of splenic artery aneurysms.J Vasc Surg. 2011; 53: 958-964Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar However, a ruptured SAA remains a life-threatening entity, and emergency laparotomy by general and or vascular consultants is recommended. If splenomegaly is accompanied by functional disturbance (pancytopenia) then this is termed hypersplenism; each may be found separately and not necessarily coexist. There is no agreement on categorizing the degrees of splenomegaly. Splenic size has been characterized in terms of length or weight and has consequences for the surgical management of disease. Normal spleens are <12 cm in longest craniocaudal length, moderately enlarged spleens are 12–20 cm, and severely enlarged spleens are >20 cm.6Poulin EC Mamazza J. Laparoscopic splenectomy: lessons from the learning curve.Can J Surg. 1998; 41: 28-36PubMed Google Scholar In terms of weight, spleens weighing 500–1000 g are splenomegalic and >1000 g are ‘massive’. There are numerous causes of splenomegaly, which may also result in hypersplenism (see Table 2). In the developed world, infectious mononucleosis remains the commonest cause of splenomegaly, followed by infiltration from haematological malignancy, and portal hypertension secondary to liver disease.Table 2Causes of splenomegalyCauseExamplesInfectionMononucleosis; malaria; HIV; chronic hepatitis; splenic abscess; tuberculosis; typhoid fever; brucellosis; leptospirosis; leishmaniasis (kala-azar)Neoplasia (benign and malignant)Leukaemias; lymphomas; myeloproliferative disease; metastatic tumours; splenic cysts; hamartomas; eosinophilic granulomaCongestion (persistent elevation of splenic venous pressure)Pre-hepatic: portal or splenic vein thrombosisHepatic: cirrhosisPost-hepatic: Budd Chiari, decompensated right heart failure, pulmonary or tricuspid valve diseaseIncreased function (removal of defective erythrocytes)Hereditary haemolytic anaemias; early sickle cell anaemia (preceeding multiple splenic infarcts, which cause reduction in size and function); acquired haemolytic anaemias (infections, toxin, drugs); autoimmune haemolytic anaemiasImmune disordersRheumatoid disease (Felty's syndrome); idiopathic thrombocytopenia purpura; systemic lupus erythematosus; sarcoidosisStorage disordersGaucher's disease; Niemann–Pick disease; mucopolysaccharidoses (e.g. Hurler syndrome); amyloidosis Open table in a new tab ‘Functional hyposplenism’ was a term first used by Pearson and colleagues in 1969,7Pearson HA Spencer RP Cornelius EA Functional asplenia in sickle-cell anemia.N Engl J Med. 1969; 281: 923-926Crossref PubMed Scopus (302) Google Scholar who noticed that children with sickle cell disease had the same clinical findings as splenectomized patients. Conditions associated with functional hyposplenism include alcoholic liver disease, sickle-cell anaemia, bone marrow transplantation, coeliac disease, and inflammatory bowel disease.3Kirkineska L Perifanis V Vasiliadis T. Functional hyposplenism.Hippokratia. 2014; 18: 7-11PubMed Google Scholar Removal of senescent erythrocytes is defective in hyposplenism, causing pathological erythrocyte appearances on a blood film: acanthocytes (spikey appearance), target cells (central staining resembling a ‘bullseye’ target), surface pitting (‘poked’), and Howell–Jolly bodies (spots of basophilic nuclear remnants). As there is no reliable way of assessing splenic function, the presence of these abnormal erythrocytes is taken as a surrogate marker of hyposplenism; however, their absence does not exclude it. Functional hyposplenism is characterized by an increased susceptibility to infection by encapsulated microorganisms, with potentially rapid progression similar to that seen in the syndrome of life-threatening overwhelming post-splenectomy infection (OPSI). OPSI remains a rare condition (estimated incidence of 0.23–0.42% per year, with a lifetime risk of 5%);8Davidson RN Wall RA Prevention and management of infections in patients without a spleen.Clin Microbiol Infect. 2001; 7: 657-660Abstract Full Text Full Text PDF PubMed Scopus (222) Google Scholar the highest risk is among those who have had a splenectomy for haematological malignancy and children (particularly those under two). It carries a high mortality, with risk highest in the first 3 yr after splenectomy, declining thereafter, although lifelong risk remains. It is owing to the recognition of this syndrome that we attempt to preserve the spleen if at all possible. OPSI has a catastrophically rapid onset; it is characterized by the following findings: •Massive bacteraemia; blood cultures can show the number of bacterial colonies up to 10 000 times higher than the colony count in common septicaemia.8Davidson RN Wall RA Prevention and management of infections in patients without a spleen.Clin Microbiol Infect. 2001; 7: 657-660Abstract Full Text Full Text PDF PubMed Scopus (222) Google Scholar•No obvious primary source of infection.•Short, vague prodromal phase (e.g. a slight upper respiratory tract infection).•Septic shock accompanied by multi-organ dysfunction and disseminated intravascular coagulation.•Waterhouse–Friedrichsen syndrome: bilateral adrenal haemorrhage. Streptococcus pneumoniae, Neisseria meningitides and Haemophilus influenza are the most common causative microorganisms.9Sheng CF Liu BY Zhang HM Zheng X. Overwhelming postsplenectomy infection.Genet Mol Res. 2015; 14: 2702-2706Crossref PubMed Scopus (4) Google Scholar Prompt recognition of patients at risk for OPSI, followed by early intensive care sepsis treatment strategies, including (for example): antibiotics, vasopressors, goal-directed i.v. fluids, steroids, heparin, red blood cells, platelets, cryoprecipitates, and fresh frozen plasma are essential to limit morbidity and mortality. However, owing to the fulminant nature of this condition, even these aggressive strategies may fail to alter the clinical course, and a high mortality rate (40–70%) still remains. Prevention has become key. Important preventative measures are patient and clinician education, vaccination schedules, and the avoidance of total splenectomy by an individualized approach to traumatic injuries and underlying pathology. There are no agreed rules regarding prophylactic antibiotics in asplenic patients. Prophylactic penicillin has been shown to confer protection against pneumococcal infection in asplenic children with sickle cell disease; however, no studies have been undertaken in splenectomized adults. Due to the lifelong risk of OPSI, lifelong prophylactic antibiotics should be offered to those at high risk of pneumococcal infection: •Aged <16 yr or >50 yr•Inadequate serological response to pneumococcal vaccine.•With a history of previous invasive pneumococcal disease, or after an episode of post-splenectomy sepsis.•Impaired immune function (malignancy) and in whom a splenectomy was carried out for haematological malignancy. Counselling regarding the risks and benefits of lifelong antibiotics should be offered to patients not at high risk of infection, and in these patients, it may be appropriate to discontinue.8Davidson RN Wall RA Prevention and management of infections in patients without a spleen.Clin Microbiol Infect. 2001; 7: 657-660Abstract Full Text Full Text PDF PubMed Scopus (222) Google Scholar10Rubin LG Schaffner W. Clinical practice. Care of the asplenic patient.N Engl J Med. 2014; 37: 349-356Crossref Scopus (155) Google Scholar11Hildebrand DR Ben-Sassi A Ross NP Macvicar R Frizelle FA Watson AJ Modern management of splenic trauma.Br Med J. 2014; 348: 1-7Crossref Scopus (32) Google Scholar Patient education is of vital importance, and asplenic patients should be given a 5-day supply of stand-by antibiotics to be stored in their household refrigerator, with advice cards on when to use them. A vaccination schedule should include cover for the commonly implicated microorganisms (pneumococcal, Hib, meningococcal, influenza; all can be given together if necessary).8Davidson RN Wall RA Prevention and management of infections in patients without a spleen.Clin Microbiol Infect. 2001; 7: 657-660Abstract Full Text Full Text PDF PubMed Scopus (222) Google Scholar Ideally, these should be administered at least 2 weeks before scheduled splenectomy as the immune response to vaccines is thought to be better with an intact spleen. In emergency splenectomy patients, a better antibody response occurs if vaccination is delayed for 14 days after surgery to minimize the immunosuppressive effects of surgery. Careful coordination with primary care is necessary upon discharge to ensure all vaccinations are given. In hyposplenic patients receiving immunosuppressive therapies (steroids or chemotherapy), it is recommended that vaccination is given at least 2 weeks before immunosuppressive therapy and/or delayed for 3 months after the therapy has been completed. Despite receiving a vaccination schedule, clinical vigilance for vaccine failures should exist: strains may not be included in the vaccine, or there may have been a poor vaccine antibody response because of the splenectomy or underlying disease. Revaccination should occur every 5 yr. Splenic infarction may occur in the whole spleen or via occlusion of one of the segmental secondary arterial branches to the spleen, which would result in a wedge-shaped infarct. Collateral flow from the short gastric arteries often preserves some or all of the spleen. There are numerous causes of splenic infarction (Table 3). The majority are attributable to infiltrative haematological diseases congesting the splenic circulation with pathological cells, or thromboembolic conditions which obstruct larger vessels.12Nores M Phillips EH Morgenstern L Hiatt JR The clinical spectrum of splenic infarction.Am Surg. 1998; 64: 182-188PubMed Google ScholarTable 3Causes of splenic infarctionCauseExamplesMalignant haematological disordersLeukaemia; lymphoma; myelofibrosisBenign haematological disordersSickle cell diseaseHypercoagulable states (protein C or protein S deficiency); antiphospholipid syndrome; erythropoietin therapy; polycythemia vera; oral contraceptivesEmbolic disordersEndocarditis; atrial fibrillation; paradoxical emboli; left ventricular mural thrombus following myocardial infarctTraumaBlunt trauma; torsion of the vascular pedicle of a wandering spleenIatrogenic/ operativeDeliberate splenic artery embolization; pancreatectomy; oesophagectomy; gastrectomy; liver transplant; sclerotherapy of bleeding gastric varices; vasopressin infusionMiscellaneousSplenic vein thrombosis; postpartum toxic shock syndrome; pancreatitis; sarcoidosis; amyloidosis; pancreatic cancer; acute respiratory distress syndrome Open table in a new tab The clinical spectrum of splenic infarction ranges from asymptomatic infarction in approximately one-third (thus discovered incidentally on radiological studies or during surgery for another indication) to haemorrhagic shock (from subcapsular haemorrhage or rupture into the peritoneal cavity). The commonest presenting symptom, however, is left-upper-quadrant abdominal pain (∼70%), with signs resembling sepsis (fever, rigors, nausea, and vomiting), pleuritic chest pain, and left shoulder pain (Kehr sign).12Nores M Phillips EH Morgenstern L Hiatt JR The clinical spectrum of splenic infarction.Am Surg. 1998; 64: 182-188PubMed Google Scholar Computed tomography (CT) with contrast is the best diagnostic modality. Prognosis is variable, depending upon the underlying disease state. If infarction renders the individual hyposplenic, patients should be counselled as to the risk of OPSI. Splenic infarction alone is not an indication for surgery; however, conservative management will include surveillance in light of the complications of infarction: haemorrhage, rupture, abscess, or persistent pseudocyst where surgery may be indicated. Splenectomy is primarily performed for trauma and refractory haematological disease (e.g. idiopathic thrombocytopenia purpura, hereditary spherocytosis, thalassemia, Hodgkin disease, leukaemias and myeloproliferative disease, Felty syndrome). Splenectomy for haematological disease is managed predominantly by a laparoscopic technique. The commonest exception is massive splenomegaly,13Poulin EC Mamazza J Schlachta CM Splenic artery embolization before laparoscopic splenectomy. An update.Surg Endosc. 1998; 12: 870-875Crossref PubMed Scopus (95) Google Scholar for the obvious reasons of limitation in instrumentation and visualization. A basic understanding of the underlying disease state is necessary to provide an individualized perioperative management plan. In addition to routine preoperative assessment for major surgery, close liaison with a haematologist is necessary; these patients are often anaemic (spherocytosis, thalassemia, sickle cell disease) and thrombocytopenic (ITP), they may have systemic complications of previous chemotherapy, chronic disease states and malignancy, they may require irradiated or human leucocyte antigen (HLA) matched products, immunoglobulins, steroids, or preoperative splenic artery embolization (refractory thrombocytopenia in ITP). Involvement of a multidisciplinary team (haematologist, oncologist, interventional radiologist, surgeon, anaesthetist, and intensivist) is essential. In the case of ITP, there have been numerous case reports and expert reviews on what constitutes a safe platelet count for laparoscopic splenectomy [all published data reviewed describe normal prothrombin time (PT) and activated partial thromboplastin times (APTT)] (implications for neuraxial blockade are described later); predictably, those patients undergoing laparoscopic splenectomy with very low platelet counts (<20×109 litre−1) received more blood transfusions, suffered more complications, and had a much longer hospital stay than patients with platelet counts of 20–50×109 litre− 1 or higher. The evidence agrees that the strongest predictor for transfusion, morbidity, and mortality in this group of patients is the platelet count.14Keidar A Feldman M Szold A. Analysis of outcome of laparoscopic splenectomy for idiopathic thrombocytopenic purpura by platelet count.Am J Hematol. 2005; 80: 95-100Crossref PubMed Scopus (43) Google Scholar Every effort should be made to liaise with haematologists to elevate platelet counts to >20×109 litre− 1 before surgery.14Keidar A Feldman M Szold A. Analysis of outcome of laparoscopic splenectomy for idiopathic thrombocytopenic purpura by platelet count.Am J Hematol. 2005; 80: 95-100Crossref PubMed Scopus (43) Google Scholar If it is necessary to increase the platelet count in ITP patients before surgery, i.v. immunoglobulins or steroids are used. Platelet transfusion should be avoided until after surgery (or if required during surgery) after ‘inflow’ vascular isolation has occurred15McLure HA Trenfield S Quereshi A Williams J. Post-splenectomy thrombocytopenia: implications for regional analgesia.Anaesthesia. 2003; 58: 1106-1110Crossref PubMed Scopus (7) Google Scholar to avoid sequestration in the spleen. These patients may be chronically dependent on steroids and adrenal insufficiency, and perioperative steroid supplementation should be considered. The surgical approach depends on splenic size, indication, and surgical preference. In emergency or trauma, open surgery in the supine position via an upper midline incision is preferable as it affords excellent exposure, rapid access, and evaluation of other structures. In most patients undergoing open splenectomy for haematological disorders, a left subcostal incision is used. Positioning for laparoscopic splenectomy is supine or lateral. The original approach for laparoscopic splenectomy was anterior, with the viscera retracted away from the left upper quadrant by a steep reverse Trendelenberg position. The anterior approach should also be considered when simultaneous procedures may be needed (e.g. cholecystectomy) or with larger spleens, which may require an extraction strategy (e.g. a Pfannenstiel incision). However, there are disadvantages to the anterior approach: the spleen must be lifted off its posterior attachments and as splenic size increases, this becomes more challenging, especially in obese patients. Adapting positioning from laparoscopic adrenalectomy, the lateral approach has developed, with the patient in lateral decubitus; many authors advocate this approach as the weight of the spleen acts as its own retractor, falling away from the posterior and lateral attachments.6Poulin EC Mamazza J. Laparoscopic splenectomy: lessons from the learning curve.Can J Surg. 1998; 41: 28-36PubMed Google Scholar As per standard NICE guidance, local antibiotic formulary for antibiotic prophylaxis for major abdominal surgery should be adhered to, and a vaccination schedule organized before surgery. After induction of general anaesthesia, the patient is intubated and an orogastric tube inserted to ensure deflation of the stomach. When ventilating a patient in the lateral position, a ventilation–perfusion mismatch occurs, with perfusion greatest in the dependent lung and ventilation greatest in the non-dependent lung; this is usually well tolerated, but may lead to atelectasis and hypoxia in susceptible patients aggravated by the reduction in functional residual capacity caused by the pneumoperitoneum. Vacuum beanbags aid positioning in the lateral decubitus position. The radial, saphenous, and the common peroneal nerves are susceptible to injury in this position. The forearm can be supported with specially designed rests or the upper arm can hug a pillow; meticulous attention should be given to pressure points, with pillows between the legs and arms. This position is associated with the greatest number of ocular complications, so confirm the eyes are taped shut and that pressure is not being applied to the globe. Ensure the ear has not folded during positioning. In the case of elective splenectomy, one of the first steps is transection of the ligamentous attachments, which contain numerous blood vessels. Pathological spleens often have more attachments, and may contain aberrant vessels that could cause further blood loss. Then the splenic artery and veins are identified, dissected, and ligated. To avoid injury to the pancreas, this dissection is carried out at the hilum in close proximity to the spleen. There is potential for massive blood loss (aggravated by associated disease and disease-related coagulopathies), and blood loss can be highly variable. Predictably, the data show that splenomegaly is the main determinant for operative blood loss, and blood loss is the main factor correlating with morbidity and mortality. Pneumoperitoneum and the reverse Trendelenburg position may exacerbate haemodynamic instability, with deleterious effects on preload and cardiac output. Therefore, we advocate a minimum of one large-bore peripheral cannula and a low threshold for insertion of invasive and cardiac output monitoring, allowing earlier detection and management of fluctuations in haemodynamic status. Appropriate fluid management is particularly important in sickle cell anaemia and spherocytosis, where avoidance of crises through appropriate filling, prevention of hypoxia and acidosis, and temperature regulation are paramount. Haematological issues (pre-, peri- and postoperative) may preclude central neuraxial block owing to the risk of epidural haematoma. In haemato-oncology patients, there are insufficient data on a safe platelet number to guide neuraxial catheter placement or removal (as we use number as a surrogate of function); however, evidence agrees that the cut-off be set at counts >100×109 litre−1.15McLure HA Trenfield S Quereshi A Williams J. Post-splenectomy thrombocytopenia: implications for regional analgesia.Anaesthesia. 2003; 58: 1106-1110Crossref PubMed Scopus (7) Google Scholar There is huge variability in preoperative platelet counts and postoperative platelet profiles, meaning that attempts to predict postoperative platelet behaviour are impossible (with authors reporting both postoperative thrombocytopenia and thrombocytosis).15McLure HA Trenfield S Quereshi A Williams J. Post-splenectomy thrombocytopenia: implications for regional analgesia.Anaesthesia. 2003; 58: 1106-1110Crossref PubMed Scopus (7) Google Scholar In the thrombocytopenic parturient, high circulating levels of fibrinogen and clotting factors, reduced fibrinolysis, and largely normal platelet function allow neuraxial block at lower platelet thresholds; this is of course not seen in haemato-oncology patients, who have intrinsic platelet defects with no compensatory increase in clotting factors, explaining the more conservative cut-off of 100×109 litre−1.15McLure HA Trenfield S Quereshi A Williams J. Post-splenectomy thrombocytopenia: implications for regional analgesia.Anaesthesia. 2003; 58: 1106-1110Crossref PubMed Scopus (7) Google Scholar Patients having splenectomies for myeloproliferative disorders deserve special mention here, as the incidence of postoperative portal vein thrombosis is high (40%), especially in those with massive splenomegaly. Therefore, in this cohort of patients, the risk of needing postoperative anticoagulation or emergency thrombolysis may further preclude the placement of an epidural catheter. If postoperative emergency thrombolysis is required in a patient with an epidural catheter in situ, it should be done under close monitoring, weighing the risks and benefits. The maximal nadir of fibrinogen and plasminogen after thrombolytic therapy is at 5 h, and they are still depressed at 27 h.16Horlocker TT Wedel DJ Benzon HT Regional anaesthesia in the anticoagulated patient: defining the risks (The second ASR