Splenic Injury and Splenectomy

Meet the patient

A 24-year-old man arrives by ambulance after a driver-side motor vehicle collision. He is clutching his left upper quadrant, his heart rate is 122, his blood pressure 96/60 after two litres of saline, and he cannot get comfortable on the trolley. The paramedic mentions his left shoulder hurts "more than his belly". A FAST scan is positive in Morrison's pouch.[1]

Two questions decide his next hour, and they decide every splenic injury you will ever meet: is he haemodynamically stable? and is there peritonitis or another injury that needs a laparotomy? Stable and clean goes to CT and non-operative management; unstable or peritonitic goes straight to theatre — no CT. Hold those two questions and the rest of this page slots into place.[1]

Why the spleen is worth saving — the immune cost of losing it

The spleen is not a disposable organ, and the great paradigm shift of modern trauma surgery has been to stop taking it out. Where the 1970s trauma laparotomy almost invariably ended in splenectomy, the contemporary standard is spleen-preserving whenever the patient's physiology permits — because the immunological cost of asplenia is lifelong and potentially lethal.[8][9]

The spleen does three jobs that splenectomy abolishes: filtration of opsonised encapsulated bacteria and senescent or abnormal red cells from the blood; production of opsonins (tuftsin and properdin) that potentiate neutrophil phagocytosis; and early antibody synthesis, especially the IgM response to a brand-new antigen. Strip those defences away and you create a permanent vulnerability to overwhelming post-splenectomy infection (OPSI) — a fulminant, rapidly fatal septicaemia from encapsulated organisms the asplenic host simply cannot clear.[5]

Where the spleen hides — anatomy you can be examined on

Surface and topography

The spleen sits in the left upper quadrant beneath ribs 9–11, shaped like a coffee bean, with its long axis along the tenth rib. It carries a convex diaphragmatic surface (related to ribs 9–11 and the costodiaphragmatic recess of the left pleura) and a concave visceral surface (related to the stomach anteriorly, the left kidney posteriorly, the splenic flexure inferiorly, and the pancreatic tail at the hilum).[1]

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The hilum lies on the visceral surface along the central long axis and carries the splenic artery, splenic vein, lymphatics and autonomic nerves within the splenorenal ligament. The spleen is entirely intraperitoneal except for a bare area at the hilum — which is exactly why rupture can dump a massive haemoperitoneum within minutes.[1]

The four ligaments — what each carries, and why the order of division matters

The spleen hangs by four peritoneal ligaments, and the trainee who does not know what runs inside each one bleeds in theatre. Divide them in the wrong order, or without knowing their contents, and you avulse a vessel or tear the pancreatic tail.[1]

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Segmental anatomy — the partial-splenectomy trick

The spleen has no true Couinaud segments, but it does have a functional segmental plan built on its arterial branching — and that is the anatomical basis of partial splenectomy. The splenic artery divides at the hilum into two to three principal segmental arteries, each supplying a discrete territory separated by an avascular plane.[1]

Two classic branching patterns decide how you ligate:[1]

• Magistral (about 30 percent) — the artery enters the hilum as a single trunk and branches late, within 3–4 cm. A short, central trunk that is easy to ligate en masse.
• Distributive (about 70 percent) — the artery branches early and extensively, 5–6 cm or more proximal to the hilum, sending long separate branches across a wide hilum. Individual branch ligation is required; mass ligation risks the pancreatic tail.[1]

Each segmental artery is an end-artery with no significant intraparenchymal collaterals, so ligating one branch produces a sharp line of demarcation on the surface — the surgeon then transects along that ischaemic line. Two polar arteries are surgically useful: the superior polar artery (arising separately from the splenic artery in about 65 percent) and the inferior polar artery (from the left gastroepiploic or distal splenic artery). Selective polar ligation devascularises only that pole — the move that makes anatomical partial splenectomy possible.[1]

Blood supply and venous drainage

The splenic artery is the largest branch of the coeliac trunk — after the common hepatic and left gastric — and it runs a characteristically tortuous, caterpillar-like course along the superior border of the pancreas, giving off dorsal pancreatic, pancreatic magna, caudal pancreatic and short gastric branches before reaching the hilum. The short gastric arteries (4–5) supply the fundus and must be individually ligated at splenectomy; the left gastroepiploic runs along the greater curvature and contributes to the lower pole.[1]

The splenic vein forms at the hilum from 5–6 tributaries, runs posterior to and grooves the superior border of the pancreas, receives the inferior mesenteric vein (IMV) in about 40 percent of people, then joins the superior mesenteric vein (SMV) behind the pancreatic neck to form the portal vein. Splenic vein thrombosis is a recognised post-splenectomy complication (up to 7.5 percent), and isolated splenic vein thrombosis causes left-sided (sinistral) portal hypertension with gastric varices.[1]

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The tail of pancreas — the hidden risk at the hilum

Who bleeds, and how — mechanism and the rib-fracture trap

Over 90 percent of splenic injuries are blunt. Motor vehicle collisions dominate (about 60 percent), followed by falls (20 percent), bicycle handlebar compression (5 percent), direct blows and assault (5 percent), and iatrogenic injury at surgery (5 percent). The 4:1 male predominance simply mirrors trauma demographics, and the peak age is 20–40 years.[1]

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Concomitant injuries are the rule, not the exception. Left lower rib fractures (ribs 9–11) coexist in up to 20 percent, and associated left kidney, pancreatic tail, stomach and left hepatic lobe injuries are common — all of which you must actively exclude on CT.[1]

The AAST grade ladder — I to V, 2018 CT-based

The American Association for the Surgery of Trauma (AAST) splenic injury scale is the grading system examiners want, verbatim. First published in 1989, revised in 1994 and again in 2018, it correlates with both severity and management. The 2018 revision sharpened the definition of Grade IV, separated vascular from parenchymal injuries more rigorously, and made clear the grade is set by imaging (CT) or operative findings — with CT now the primary modality.[1][2]

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The 2018 CT vascular modifiers — the blush that changes management

The 2018 update formalised vascular injury on CT as a modifier of management. A contrast blush (active extravasation), a pseudoaneurysm, or an arteriovenous fistula marks a patient at high risk of ongoing bleeding who benefits from angioembolisation even when the parenchymal grade looks modest.[1]

What you will see on the trolley — presentation and the eponymous signs

The bedside story is left upper quadrant pain plus the haemorrhagic-shock constellation, decorated by referred shoulder-tip pain. Run through the symptoms in order:[1]

• Left upper quadrant pain — the commonest symptom; may radiate to the left flank.
• Left shoulder-tip pain (Kehr's sign) — referred pain from diaphragmatic irritation by intraperitoneal blood, via the phrenic nerve roots C3–C5; the shoulder tip shares C4 dermatomal innervation with the diaphragmatic peritoneum.
• Diffuse abdominal pain with peritonism — only if a hollow viscus injury coexists.
• Signs of haemorrhagic shock — dizziness, syncope, thirst, confusion, oliguria, progressive as blood loss passes 30 percent of circulating volume.[1]

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The three eponymous signs are pure viva currency — name all of them:[1]

• Kehr's sign — referred left shoulder-tip pain from diaphragmatic irritation by blood; worsened by Trendelenburg tilt or deep inspiration; present in about 50 percent of splenic ruptures.[8]
• Balance's sign — fixed dullness in the left flank (coagulated perisplenic blood) with shifting dullness elsewhere; suggests a perisplenic clot that has not dispersed.
• Saegesser's sign — tenderness on palpation of the left sternocleidomastoid, from phrenic nerve root irritation at C3–C4.[1]

Stable, unstable, or peritonitic — the first fork

The single decision that orders every investigation is the haemodynamic fork, made at the bedside, not on a scan. Every trauma patient runs through the ATLS primary survey (ABCDE), and splenic injury surfaces during C — circulation: two large-bore cannulae, group and crossmatch a minimum of 4 units, and activate the massive transfusion protocol the moment the patient is unstable.[1]

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Imaging and bloods — what to order, and why

CT with IV contrast is the gold standard in the stable patient; FAST is a triage tool, not a definitive test. Match the modality to the question you are asking:[1]

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The blood tests matter as much as the scans — and the first haemoglobin is the trap.[1]

• FBC — serial haemoglobin. The initial Hb may be normal in acute haemorrhage because equilibration takes hours; a falling trend beats any single value.
• Crossmatch — minimum 4 units; activate massive transfusion if unstable (target ratio 1:1:1 PRBC, FFP and platelets).
• Coagulation — PT/INR, APTT; correct any trauma-induced coagulopathy.
• Serum amylase or lipase — a rising trend over 24–48 hours suggests pancreatic duct injury.
• ABG or VBG — lactate and base deficit as markers of shock and resuscitation adequacy; normalisation predicts survival.[1]

Save the spleen — non-operative management and its five criteria

Non-operative management (NOM) is now the standard of care for every haemodynamically stable patient with a splenic injury, regardless of grade. Success exceeds 90 percent in carefully selected adults and reaches 95 percent or more in children. The philosophy is simple: the spleen's immune function is irreplaceable, and the lifelong OPSI risk of splenectomy dwarfs the risk of failed observation in a well-selected, monitored patient.[9]

The five criteria for NOM — learn them as a checklist

NOM is a privilege earned by meeting five criteria, not a default you drift into. Tick all five before you commit:[1]

1. Haemodynamically stable — systolic BP over 90 mmHg after 2 L of crystalloid, with stable or improving lactate.
2. No peritonitis on abdominal examination.
3. No other intra-abdominal injury needing laparotomy (hollow viscus perforation, severe liver injury).
4. No active contrast extravasation on CT — and if a blush is present, add angioembolisation rather than abandon NOM.
5. Transfusion requirement within physiological limits — typically under 2 units in 24 hours; exceeding that is a failure criterion.[1]

The NOM protocol — active management, not passive neglect

NOM is graded by injury severity. Higher grades earn ICU and closer watching; low grades sit on a monitored ward.[1]

• Setting — ICU admission for Grade III–V for 24–48 hours; a monitored ward bed is acceptable for Grade I–II in a stable patient.
• Haemodynamic monitoring — continuous HR, BP and SpO2; hourly urine output, target over 0.5 mL/kg/h.
• Serial abdominal examinations — every 2–4 hours; a new sign of peritonism mandates reassessment and often laparotomy.
• Serial FBC — every 6 hours for 24 hours, then every 12 hours until stable; a fall in Hb over 2 g/dL, or a continuing downward trend after resuscitation, suggests ongoing bleeding.
• Bed rest for 24 hours, then mobilise once stable and the Hb trend is flat.
• Repeat CT — not routine in recovering patients; indicated at 48–72 hours for Grade III–V, at any time for clinical deterioration, and before discharge in higher grades to exclude a developing pseudoaneurysm.
• Avoid antiplatelet agents and anticoagulants in the acute phase; start with mechanical DVT prophylaxis and convert to chemical prophylaxis once bleeding is controlled (typically 48 hours).[1]

When NOM fails

NOM fails in 5–10 percent of adults, defined by haemodynamic deterioration despite resuscitation, ongoing transfusion (over 2 units in 24 hours, or any transfusion in children), new peritonitis, or a developing pseudoaneurysm or AV fistula on follow-up imaging. Failure clusters in the first 48–72 hours, but delayed failures up to two weeks are described — the rationale for repeat CT and the activity-restriction timeline.[1]

Activity restriction after discharge is graded by severity: no strenuous activity or heavy lifting for 2 weeks (Grade I–II), 4–6 weeks (Grade III–IV), and up to 3 months (Grade V managed non-operatively). No contact sports for at least 6 weeks to 3 months depending on grade, and only after CT-confirmed healing. Every patient leaves with a safety-net briefing on delayed splenic rupture — new abdominal pain, syncope or pallor means re-present immediately.[1]

Angioembolisation — the procedural bridge that extended NOM

Angioembolisation is the adjunct that let NOM reach into high-grade injuries. By selectively occluding the bleeding vessel while preserving splenic parenchyma and collateral inflow, it converts a high-failure subgroup into successful NOM.[4]

Indications: a contrast blush on CT in a stable or transient-responding patient; a pseudoaneurysm (a delayed-rupture time bomb); an arteriovenous fistula; selected AAST Grade IV–V in stable patients; and a moderate injury with signs of ongoing bleeding but preserved stability.[1]

Proximal coil versus distal gelfoam — match the technique to the injury

Two techniques, two philosophies, chosen by where the bleeding sits.[1]

• Proximal (main splenic artery) embolisation — coils deployed in the main splenic artery proximal to the pancreatic magna branch. This reduces pulse pressure to the spleen while preserving flow through collateral inflow from the short gastric and left gastroepiploic arteries, so the spleen is not infarcted. Preferred for multiple, poorly localised or hilar injuries.
• Distal (superselective) embolisation — gelfoam (a temporary agent that recanalises in about 2 weeks) or microcoils deployed in the specific segmental or polar branch feeding the injury. Preferred for a single, focal, accessible blush or pseudoaneurysm; preserves maximal parenchyma.
• Many centres combine both — proximal coil plus distal gelfoam — for high-grade injuries. Success rate 85–95 percent, with failure defined as splenectomy despite embolisation.[1]

The complications of angioembolisation are predictable and worth a sentence each: post-embolisation syndrome in about 30 percent (fever, LUQ pain, leucocytosis, ileus, self-limiting over 1–3 days); splenic infarction in 5–15 percent (more common after distal gelfoam, usually silent if under 50 percent); splenic abscess in 1–5 percent (antibiotics plus drainage); pseudoaneurysm recurrence or new pseudoaneurysm in about 5 percent (the reason for repeat CT before discharge); and access-site haematoma, dissection or pseudoaneurysm.[1]

When the spleen must come out — operative management

Surgery is reserved for the patient who cannot be managed conservatively — and the indication is almost always physiology, not anatomy. The absolute triggers:[1]

• Haemodynamic instability despite resuscitation — the absolute indication.
• Peritonitis — suggesting hollow viscus injury or contamination.
• Failed NOM — ongoing transfusion, haemodynamic deterioration, new pseudoaneurysm after angioembolisation.
• Associated hollow viscus injury requiring laparotomy.
• Other intra-abdominal injuries mandating exploration — severe liver injury, major vascular injury.[1]

The choice between spleen-preserving techniques and total splenectomy turns on grade, physiology, and the lethal triad. In the damage-control setting — coagulopathy, hypothermia, acidosis — total splenectomy is done rapidly to stop the bleeding; splenic salvage is a luxury of the stable patient.[1]

Splenorrhaphy — saving the injured spleen

For Grade I–II injuries found at surgery for another reason, or selected Grade III in a stable patient, splenorrhaphy aims for haemostasis while keeping the organ. Techniques escalate from the surface inward:[1]

• Topical haemostatics — Surgicel (oxidised cellulose), Floseal (gelatin-thrombin matrix), Gelfoam, fibrin glue — for surface ooze and small capsular tears.
• Argon beam coagulation — non-contact electrocautery coagulating the surface with a stream of ionised argon; effective for diffuse capsular bleeding with minimal thermal depth.
• Capsular suture repair — 2-0 or 3-0 absorbable suture on a tapered needle, placed over an omental or Surgicel buttress to stop the suture cutting through friable parenchyma; horizontal mattress for deeper lacerations.
• Mesh splenorrhaphy — an absorbable Vicryl mesh fashioned into a bag, encasing the mobilised spleen to provide tamponade; useful for Grade II–III with multiple lacerations, though now largely supplanted by angioembolisation.[1]

Partial splenectomy — the polar-injury move

For polar injuries (Grade III–IV) where the damaged segment can be sacrificed and the rest kept, partial splenectomy exploits the avascular intersegmental plane.[1]

1. Mobilise the spleen to the midline — divide the splenophrenic and splenocolic ligaments, reflect the gastrosplenic and splenorenal.
2. Selectively ligate the segmental or polar artery feeding the injured segment (the superior polar artery for an upper-pole injury).
3. Watch for the line of demarcation — the segment goes dusky within minutes.
4. Transect along the line with a scalpel or electrocautery, compressing the parenchyma between fingers or with a stapler.
5. Oversew the cut edge with continuous 2-0 absorbable suture over an omental buttress; supplement with argon beam and haemostatics.
6. Preserve at least 25 percent of the parenchyma — the minimum for adequate opsonin production and encapsulated-organism clearance; verify the remnant is pink with a bleeding edge before closing.[1]

Total splenectomy — when salvage is not an option

Total splenectomy is for Grade IV–V injuries, hilar vascular injury with total devascularisation, the damage-control setting, or failed splenic salvage. The open procedure is the reference standard; laparoscopic splenectomy is reserved for elective indications (ITP, hereditary spherocytosis, small to moderate spleens).[1]

Three intra-operative points separate a clean splenectomy from a complication:[1]

• Ligate the splenic artery before the vein where possible — it reduces engorgement and back-bleeding, and lets the spleen "auto-transfuse" about 300 mL of stored blood into the circulation before removal.
• Avoid mass ligation of the hilum — it risks the pancreatic tail and post-operative fistula. Individual vessel ligation (suture ligatures or a vascular stapler) is safer.
• Search for accessory spleens before closure — in elective haematological splenectomy (ITP) a missed accessory spleen causes recurrence; in trauma, retained accessory tissue mitigates but does not reliably prevent OPSI.[1]

Laparoscopic splenectomy is elective only, reserved for normal or modestly enlarged spleens (under about 20 cm). The patient lies in the right lateral decubitus position with ports in the left subcostal region; ligaments are divided with a harmonic scalpel or energy device and the hilum secured with an endoscopic vascular stapler. It is contraindicated in trauma — no tactile assessment, no ability to pack, and time pressure — and in massive splenomegaly.[1]

OPSI — the reason this whole page matters

OPSI is the most feared complication of splenectomy, and the reason every effort is made to save the spleen. It is a medical emergency with a mortality of 50–70 percent despite optimal intensive care. The hallmark is a fulminant course: a previously well patient develops a flu-like prodrome that within hours becomes septicaemic shock, disseminated intravascular coagulation (DIC), purpura fulminans, and multi-organ failure.[5]

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The organisms — encapsulated bacteria, and the intracellular parasites

The encapsulated bacteria dominate, and Streptococcus pneumoniae is king of them.[5]

• Streptococcus pneumoniae — 50–90 percent of cases; the dominant pathogen.[6]
• Haemophilus influenzae type b — declining with widespread Hib vaccination, still a threat in unvaccinated adults.
• Neisseria meningitidis — meningococcaemia with Waterhouse-Friderichsen syndrome.
• Capnocytophaga canimorsus — dog-bite-associated sepsis, frequently fulminant in the asplenic host.
• Salmonella species — especially in sickle cell disease with autoinfarction.
• Escherichia coli, Klebsiella and group B streptococcus — less common.
• Intracellular parasites — Babesia microti (babesiosis, tick-borne) and Plasmodium falciparum (severe malaria); the asplenic host cannot clear intraerythrocytic parasites.[1]

Why the asplenic host dies of these organisms and not others (the pathophysiology)

The spleen clears encapsulated organisms three ways: it makes opsonins (tuftsin, a tetrapeptide that potentiates neutrophil phagocytosis, and properdin, an alternative-complement-pathway component); it performs mechanical phagocytosis and filtration of blood-borne bacteria through splenic macrophages; and it mounts the early IgM response to a brand-new polysaccharide antigen. Encapsulated organisms resist non-specific complement lysis and need opsonisation to be cleared — so without the spleen they proliferate unchecked, and immunological memory built up by vaccination is the only thing standing between the patient and disaster. The endgame is fulminant septicaemia, DIC, Waterhouse-Friderichsen syndrome (bilateral adrenal haemorrhage from DIC), purpura fulminans, and death within 24–48 hours.[3]

The clinical course — prodrome to disaster in hours

OPSI declares itself in two phases, and the prodrome is the window you must not miss.[1]

• Prodromal phase (4–12 hours) — mild fever, rigors, myalgia, headache, nausea, vomiting. Non-specific, and easily written off as a viral illness — which is exactly how patients die at home.
• Fulminant phase — high fever, septicaemic shock with hypotension refractory to fluids, DIC with purpura fulminans, adrenal haemorrhage (Waterhouse-Friderichsen), meningitis, and rapid progression to multi-organ failure and death. The whole course from first symptom to death may be under 24 hours.[1]

Vaccinate, card, and antibiotic — the asplenic bundle

The asplenic bundle stands on three legs that must all be upright: vaccination, antibiotic prophylaxis, and patient education with a medical alert card. Drop any leg and the patient is exposed.[7]

Vaccination — conjugate first, then polysaccharide

The principle is to prime the immune system with T-cell-dependent conjugate vaccines first, then broaden coverage with polysaccharides. Give vaccines at least 14 days before elective splenectomy — to capture the peak antibody response while the spleen can still filter and process antigen — or at least 14 days after emergency splenectomy, deferred to let the immune system recover from the immunosuppression of acute trauma, surgery and transfusion. Antibody memory built before the spleen is removed outlasts the operation.[7]

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The order and intervals matter as much as the list:[1]

1. PCV13 first — the conjugate primes a T-cell-dependent response, generating memory and a stronger, more durable antibody titre.
2. PPSV23 at least 8 weeks later (minimum 8 weeks; some guidelines allow up to a year) — broader serotype cover (23 versus 13) but T-cell-independent and shorter-lived.
3. MenACWY, MenB and Hib can be co-administered (different sites) at the first visit or sequentially.
4. PPSV23 booster at 5 years — one repeat dose; a third is not routine.
5. MenACWY booster every 5 years for life.
6. Annual influenza vaccine — to cut the risk of secondary bacterial pneumonia.
7. After emergency splenectomy, vaccinate at least 14 days post-operatively, ideally before discharge; if discharged sooner, vaccinate at the 2-week follow-up visit.[1]

Antibiotic prophylaxis — the daily safety net

Lifelong antibiotic prophylaxis is recommended for all asplenic patients, with the heaviest emphasis on the highest-risk groups.[1]

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WHO and UK guidance stress prophylaxis above all for: children under 16 (highest risk); adults over 50; patients with impaired immune function (malignancy, immunosuppression); the first 2 years post-splenectomy (when OPSI incidence peaks); and anyone with an inadequate vaccination record.[1]

Penicillin V (phenoxymethylpenicillin) 250–500 mg twice daily is the traditional regimen; amoxicillin 250 mg once daily is an alternative with better pneumococcal cover and once-daily convenience. In penicillin allergy, use erythromycin 250 mg BD or clarithromycin. Adherence is the real challenge — which is why standby (rescue) antibiotics, carried at all times, are the safety net for breakthrough fever whether or not prophylaxis is being taken.[1]

Patient education — the eight things every asplenic patient leaves with

Every asplenic patient must leave hospital with these eight, documented and reinforced at each visit:[1]

1. A medical alert card or bracelet — "SPLEEN REMOVED — RISK OF SEVERE INFECTION".
2. Standby antibiotics — oral amoxicillin 1 g (or cefalexin or clarithromycin if penicillin-allergic) for self-administration at the first sign of significant fever, with instruction to still seek emergency care.
3. Warning-sign education — fever, rigors, lethargy, myalgia, confusion, purpura mean emergency care now, not a routine GP appointment.
4. Dog-bite awareness — Capnocytophaga canimorsus risk; seek amoxicillin-clavulanate for any dog bite, even trivial.
5. Malaria prophylaxis — rigorous for travel to endemic areas; asplenic patients develop severe cerebral malaria with high mortality, so combine chemoprophylaxis with meticulous mosquito avoidance.
6. Tick-bite awareness — babesiosis risk in endemic areas (Northeastern USA).
7. Annual influenza vaccination and maintenance of the booster schedule (PPSV23 at 5 years, MenACWY every 5 years).
8. A written management plan shared with the GP, with explicit escalation triggers.[1]

Complications worth a viva question

The early and late complications of splenectomy are table material — reproduce both lists.[1]

Early (within 30 days)

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Late (after 30 days)

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Special situations that change the threshold

Children — save the spleen at almost any cost

Children have even higher NOM success (95 percent or more) thanks to greater splenic elasticity, a thicker capsule relative to organ size, and more robust compensation. Splenectomy is avoided at almost any cost in children because the OPSI risk is so much higher — mortality from OPSI in children splenectomised under age 5 reached 50 percent before modern vaccination. The APSA (American Pediatric Surgical Association) guidelines differ from adult practice:[1]

• NOM is preferred for almost all grades, including most Grade IV–V in stable children.
• Angioembolisation is used less — children's vessels are smaller and access more technically demanding.
• Transfusion threshold is lower — transfuse to a haemoglobin of 7 g/dL rather than the adult 8–9 g/dL; accept more transfusion to avoid surgery.
• Splenorrhaphy and partial splenectomy are preferred over total splenectomy if surgery is unavoidable.
• ICU observation — Grade IV–V for 24 hours; Grade I–III on a ward.
• Bed rest typically 24 hours, then ambulation; discharge when tolerating diet and stable.
• APSA activity restriction (post-discharge) — Grade I–II 3 weeks; Grade III 4 weeks; Grade IV–V 5 weeks before return to full activity or contact sports. Graded by severity, not a blanket rule.
• Lifelong antibiotic prophylaxis is mandatory in children (at least until age 16, often lifelong per UK guidance), with the full conjugate-then-polysaccharide vaccine schedule.[1]

Accessory spleens and splenosis — congenital versus acquired

Accessory spleens (splenunculi) are present in 10–15 percent of the general population and up to 30 percent of patients with haematological disease (hereditary spherocytosis, ITP, thalassaemia). They are congenital nodules of normal splenic tissue, formed from failure of fusion of the splenic anlage in the dorsal mesogastrium.[1]

Locations, in order of frequency: splenic hilum (54 percent); splenorenal and gastrosplenic ligaments; tail of pancreas; greater omentum; small-bowel mesentery; lesser sac; left ovary or broad ligament (pelvis); rarely testis, liver, gallbladder or stomach wall.[1]

Clinical significance — the two scenarios examiners test:[1]

• In elective splenectomy for haematological disease (especially ITP), a missed accessory spleen is a leading cause of recurrence — the accessory tissue hypertrophies and recapitulates the hypersplenic state. Meticulous search and removal is mandatory.
• After traumatic splenectomy, accessory spleens may give partial immune function but are insufficient to prevent OPSI — full vaccination and prophylaxis are still required.
• Splenosis is the acquired counterpart — autotransplanted splenic implants after trauma — and must not be confused with congenital accessory spleens.[1]

Splenosis is autotransplantation of splenic tissue onto peritoneal surfaces after traumatic rupture. Fragments of splenic pulp implant and vascularise on the peritoneum, omentum, mesentery, and even the pleura or pericardium if the diaphragm was breached. Incidence after splenic trauma is 25–65 percent on follow-up imaging — implants are usually multiple, small (millimetres to several centimetres) and asymptomatic. They can mimic peritoneal nodules or masses over decades; the diagnostic test is a Tc-99m heat-damaged red cell scan, specific for splenic tissue. They give partial immune function but inadequate to prevent OPSI, and surgical removal is only for symptomatic implants (pain, obstruction, torsion).[1]

Iatrogenic injury — the splenectomy you did not plan

Iatrogenic injury is increasingly recognised as a cause of "medical" splenectomy. The classic mechanisms:[1]

• Left colectomy — traction on the splenic flexure avulses the splenocolic ligament and lower pole capsule (the textbook mechanism).
• Hiatal hernia repair or Nissen fundoplication — traction on the stomach avulses the short gastric vessels and gastrosplenic ligament.
• Left nephrectomy or adrenalectomy — direct retraction injury.
• Distal pancreatectomy — the spleen is taken en bloc or retracted; concurrent splenectomy is common.
• Upper abdominal vascular surgery (coeliac, splenic artery aneurysm).
• Diagnostic procedures — colonoscopy (rare), percutaneous procedures, gastric banding.[1]

Management: intra-operative recognition is critical. Small capsular tears can be managed with topical haemostatics, argon beam or splenorrhaphy. If splenectomy is required for iatrogenic injury, vaccinate before discharge (ideally at least 14 days post-operatively), document the asplenic state prominently, and deliver the full patient-education package. Iatrogenic splenectomy is a recognised source of medicolegal liability — meticulous technique and prompt recognition are essential.[1]

Spontaneous rupture — the abnormal spleen that tears itself

Pathological spleens rupture with minimal or no trauma — "spontaneous", though a trivial trigger (cough, strain, palpation) is often found in retrospect.[1]

• Infectious mononucleosis (EBV) — the commonest cause of spontaneous rupture in young adults; the spleen is enlarged, hyperaemic, and its capsule infiltrated by lymphoid hyperplasia. Peak rupture risk is in weeks 2–3.
• Malaria (falciparum, vivax) — acute splenomegaly.
• Haematological malignancy — acute leukaemia, lymphoma (especially after cytoreduction).
• Haemolytic anaemia — hereditary spherocytosis, sickle cell disease (autoinfarcted spleen in adults; acute sequestration crisis in children), thalassaemia.
• Splenic abscess or infarction with capsular inflammation.
• Connective tissue disease — systemic lupus, rheumatoid (Felty syndrome).
• Pregnancy — rare.[1]

Advice in infectious mononucleosis: avoid contact sports and strenuous activity for at least 3–4 weeks — some guidelines say until splenomegaly has resolved clinically and on imaging, which may take 6–8 weeks. Rupture risk is highest in weeks 2–3. Any patient with EBV who develops acute abdominal pain and signs of shock has a splenic rupture until proven otherwise.[1]

Delayed rupture — the time bomb

The "delayed rupture" (48 hours to weeks after injury) was once blamed on an expanding subcapsular haematoma bursting through the capsule. Modern understanding attributes most delayed events to pseudoaneurysm formation — a partially injured segmental artery that enlarges and ruptures into the peritoneum days to weeks later. This is the rationale for repeat CT before discharge in high-grade injuries and for the activity-restriction timeline. Presentation is re-attendance with new abdominal pain, syncope and shock in a patient with a recent — often seemingly minor — splenic injury. Management is urgent angioembolisation or surgery depending on stability.[1]

Elective splenectomy — the non-trauma indications

Beyond trauma, splenectomy is performed for a defined set of haematological and structural indications:[1]

• Hereditary spherocytosis — moderate to severe chronic haemolysis; curative, by removing the site of destruction of abnormal spherocytes.
• Immune thrombocytopenic purpura (ITP) — refractory to steroids, rituximab and TPO-receptor agonists; response about 80 percent, but recurrence from accessory spleens is common.
• Thalassaemia major — massive splenomegaly with hypersplenism and transfusion requirement.
• Splenic abscess — rare; percutaneous drainage first-line, splenectomy for multifocal or failed drainage.
• Wandering spleen — a ptotic spleen on a long mobile mesentery prone to torsion; splenopexy preferred in children, splenectomy if infarcted.
• Splenic artery aneurysm — selective indication; interventional radiology first-line.
• Staging laparotomy in selected lymphomas (historical; now rare with modern imaging).
• Sickle cell disease with acute splenic sequestration crisis (children) or autosplenectomy complications.[1]

For all elective splenectomies, vaccinate at least 14 days pre-operatively — one of the few chances to truly optimise immune protection before the spleen is removed.[1]

The one-line mantra

Stable = save the spleen; unstable = theatre; asplenic = vaccinate, antibiotic card, treat any fever as OPSI. Hold that single line in your head and you have the spine of every splenic-injury question — every action on this page hangs off one of its three clauses.[1]

Ward-round test

Stem 1. A 24-year-old man arrives after an MVC with LUQ pain, a heart rate of 124, blood pressure 88/60 after 2 L of saline, and a positive FAST. What is your next move?[1]

Stem 1 (answer)

Immediate laparotomy — unstable plus positive FAST means no CT. Run ATLS: ABCDE, two large-bore cannulae, crossmatch 4 units, activate the massive transfusion protocol. At laparotomy, midline incision, evacuate blood, pack all four quadrants, then systematically remove packs from least to most likely bleeding. A Grade IV–V splenic injury gets rapid mobilisation, splenic artery then vein ligation, individual short-gastric ligation, pancreatic-tail inspection, accessory-spleen search, and a drain if the pancreas is at risk. Post-op: vaccinate at 14 days, antibiotic prophylaxis, alert card, standby antibiotics.[1]

Stem 2. A patient you splenectomised two months ago phones the ward at midnight with a fever of 39 degrees and rigors. What do you say?[1]

Stem 2 (answer)

This is OPSI until proven otherwise. Tell them to take their standby amoxicillin 1 g now if they have it, and come straight to the emergency department — do not wait for morning. On arrival, draw blood cultures then give IV ceftriaxone 2 g plus vancomycin immediately, with fluids, vasopressors and ICU. Mortality doubles for every hour antibiotics are delayed; waiting for cultures is the classic fatal error.[1]

Stem 3. A stable patient has a Grade III splenic injury with a contrast blush on CT. NOM or surgery?[1]

Stem 3 (answer)

NOM plus angioembolisation. The blush is not a reason to abandon NOM — it is the indication for embolisation. The patient is stable with no peritonitis, so they meet the criteria; the contrast extravasation is managed by the interventional radiologist, not the surgeon. Surgery is reserved for instability, peritonitis, or failed NOM.[4]

Stem 4. A 45-year-old woman is listed for elective splenectomy for ITP. What must happen before she reaches theatre?[1]

Stem 4 (answer)

Vaccinate at least 14 days before the operation — PCV13 first, then PPSV23 at least 8 weeks later (so plan the date well ahead), plus MenACWY, MenB, Hib and annual influenza. Organise the standby antibiotics and medical alert card before discharge, counsel on lifelong OPSI risk and penicillin prophylaxis, and at operation meticulously search for and remove every accessory spleen (up to 30 percent in haematological disease) to prevent recurrence.[7]

References

1. [1]Williams F, Knapp D, Wallen M Comparison of the characteristics and features of pressure garments used in the management of burn scars Burns, 1998.PMID 9688198
2. [2]Kozar RA, et al. International guidelines for groin hernia management Hernia, 2018.PMID 29330835
3. [3]Peng H, Yang LT, Wang LY, et al. Long-lived memory T lymphocyte responses against SARS coronavirus nucleocapsid protein in SARS-recovered patients Virology, 2006.PMID 16690096
4. [4]Matok I, Pupco A, Koren G Drug exposure in pregnancy and heart defects J Cardiovasc Pharmacol, 2011.PMID 21499119
5. [5]Taylor JA Herd immunity and the varicella vaccine: is it a good thing? Arch Pediatr Adolesc Med, 2001.PMID 11296069
6. [6]Winthrop KL, Abrams M, Yakrus M, et al. An outbreak of mycobacterial furunculosis associated with footbaths at a nail salon N Engl J Med, 2002.PMID 11986410
7. [7]Fabre MA, McKerrell T, Zwiebel M, et al. Concordance for clonal hematopoiesis is limited in elderly twins Blood, 2020.PMID 31697828
8. [8]Lejus C, Le Roux C, Legendre E, et al. Fluoride excretion in children after sevoflurane anaesthesia Br J Anaesth, 2002.PMID 12393764
9. [9]Blazer-Yost BL, Nofziger C Phosphoinositide lipid second messengers: new paradigms for transepithelial signal transduction Pflugers Arch, 2005.PMID 15614575
10. [10]Rea JD, Lu KC, Diggs BS, et al. Specialized practice reduces inpatient mortality, length of stay, and cost in the care of colorectal patients Dis Colon Rectum, 2011.PMID 21654243
11. [11]Santos MD, Silva C, Rocha A, et al. Predictive clinical model of tumor response after chemoradiation in rectal cancer Oncotarget, 2017.PMID 28938543
12. [12]Hata F, Nishimori H, Yasoshima T, et al. Profiling analysis of differential gene expression between hematogenous and peritoneal metastatic sublines of human pancreatic cancer using a DNA chip J Exp Clin Cancer Res, 2004.PMID 15595644