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.^[3]

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? WSES guidance is explicit that management must be based on the physiology of the patient, the anatomy of the injury, and the associated lesions — stable and clean goes to CT and non-operative management; unstable or peritonitic goes straight to theatre.^[3]

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. Increasing availability of diagnostic CT and therapeutic splenic artery embolisation now underpins the high success rate of spleen-conserving management, and regular use of embolisation has become the current standard of treatment.^[2]

The spleen links innate and adaptive immunity and protects against infection; 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, with high mortality and refractoriness to common treatment.^[7]

Where the spleen hides — anatomy you can be examined on

Surface and topography

Sonographic series, not textbook rib-level teaching, set the size numbers on this page. One adult series (n=300) reported mean spleen length 10.68 cm (SD 1.28) and mean volume 174.4 mL, with larger dimensions in males; a separate community series reported mean length 10.24 cm and volume 109.34 cm3. A palpable spleen is not by itself proof of enlargement, because a normal spleen may be palpable. Poulin: the pancreatic tail touches the spleen in 30 percent of cases and lies within 1 cm in 73 percent — that is the hilar neighbourhood that bleeds and fistulates.^[14][15][27]

^{[14] [15]}

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

The spleen hangs by its peritoneal ligaments, and the trainee who does not know what runs inside each one bleeds in theatre. Ostermann's cadaver series named four principal ligaments: gastrosplenic, colicosplenic, phrenocolic, and phrenosplenic (splenorenal). Small branches of the short gastric and left gastro-omental vessels run through the gastrosplenic ligament; the colicosplenic ligament receives small branches from the left gastro-omental vessels and the lower-pole vessels. Splenic capsular tears are a recognised complication of upper abdominal surgery, because traction during gastric and colon surgery aligns with the collagen-fibre direction in the ligaments.^[26]

^{[26] [27]}

Segmental anatomy — the partial-splenectomy trick

Poulin: the anatomy of the splenic blood supply is extremely variable. Two principal patterns — distributed and magistral — include the majority of variations. They differ in the length of the splenic trunk, the number of arterial branches, and the proportion of the medial surface of the spleen occupied by the branches as they enter the organ. That branching anatomy is why partial splenectomy is anatomically possible, but conservative surgery still does not fully protect against overwhelming infection.^[27][8]

Blood supply and venous drainage

The suspensory ligaments of the spleen, including the sustentaculum lienis, are usually avascular except for the gastrocolic and lienorenal ligaments on the medial side (Poulin). Short gastric and left gastro-omental branches therefore live in the gastrosplenic/colicosplenic ligaments (Ostermann), which is why they must be taken deliberately rather than avulsed.^[27][26]

Splanchnic (portal and splenic) vein thrombosis is a recognised post-splenectomy complication — quantified after splenectomy for cirrhosis; see the complications section for pooled rates.^[12]

^{[27] [12] [13]}

The tail of pancreas — the hidden risk at the hilum

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

Blunt mechanisms dominate splenic injury, and motor vehicle collision is the classic cause; falls, bicycle handlebar compression, direct blows and assault, and iatrogenic injury at surgery complete the list. Splenic injury is commonly encountered in severe blunt abdominal trauma, with a strong male predominance mirroring trauma demographics in young adults.^[2]

^{[5] [6]}

Associated lesions matter as much as the splenic injury itself. WSES guidance makes the associated injuries one of the three pillars of decision-making, alongside patient physiology and injury anatomy — left kidney, pancreatic tail, stomach, left hepatic lobe and lower rib injuries must all be actively excluded.^[3]

The AAST grade ladder — I to V, 2018 revision

The American Association for the Surgery of Trauma (AAST) splenic injury scale is the grading system examiners want, verbatim. First published decades ago and revised in 2018, it stratifies injury severity and guides management; the AAST Organ Injury Scale is commonly used by radiologists and clinicians alike.^[1][2]

Enlarge

Parenchymal cuts below are the AAST spleen scale as reprinted by WSES (the Kozar 2018 paper itself has no PubMed abstract, so grade wording is taken from WSES Table 1). Typical management is physiology-first, not grade-first — EAST supports NOM in stable patients irrespective of grade.^[3][16][24]

^[3]

The 2018 CT vascular modifiers — the blush that changes management

The 2018 update takes splenic vascular injuries into consideration: active bleed, pseudoaneurysm and traumatic arteriovenous fistula, the presence of which indicates at least a Grade IV (high-grade) injury. Morell-Hofert reprints the 2018 wording: Grade IV also includes any injury with a splenic vascular injury or active bleeding confined within the capsule; Grade V includes active bleeding extending beyond the spleen into the peritoneum. This reflects the paradigm shift towards spleen conservation, with regular use of splenic artery embolisation as the current standard of treatment.^[2][24]

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:^[3]

• Left upper quadrant pain — the commonest symptom; may radiate to the left flank.
• Left shoulder-tip pain (Kehr's sign) — pain referred to the left shoulder; with peritoneal irritation and haemodynamic instability it mandates urgent imaging or theatre.^[25]
• Diffuse abdominal pain with peritonism — suspect a coexisting hollow viscus injury.
• Signs of haemorrhagic shock — dizziness, syncope, thirst, confusion, oliguria as blood loss mounts.^[3]

^[3]

Kehr's sign is sourced; Balance's and Saegesser's signs are conventional eponyms not named in the cited papers:^[25]

• Kehr's sign — hypochondrial pain associated with pain referred to the left shoulder, peritoneal irritation and haemodynamic instability.^[25]
• Balance's sign — conventional teaching: fixed dullness in the left flank (coagulated perisplenic blood) with shifting dullness elsewhere.
• Saegesser's sign — conventional teaching: tenderness on palpation of the left sternocleidomastoid.

Enlarge

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. WSES guidance is explicit: the optimal treatment strategy must take into consideration the haemodynamic status, the anatomic derangement and the associated injuries — so an unstable patient is resuscitated and moved to bleeding control (including massive transfusion support), while the stable patient goes to CT.^[3]

^{[3] [2]}

Imaging and bloods — what to order, and why

CT with IV contrast is the diagnostic mainstay in the stable patient; FAST is a triage tool, not a definitive test. Match the modality to the question you are asking:^[2]

^{[2] [6]}

The blood tests matter as much as the scans — and the first haemoglobin is the trap.^[3]

• FBC — serial haemoglobin. The initial Hb may be normal in acute haemorrhage because equilibration takes hours; a falling trend beats any single value.
• Crossmatch — blood must be ready; activate massive transfusion support if the patient is unstable.
• Coagulation — PT/INR, APTT; correct any trauma-induced coagulopathy.
• Serum amylase or lipase — a rising trend suggests associated pancreatic injury.
• ABG or VBG — lactate and base deficit as markers of shock and resuscitation adequacy.^[3]

Save the spleen — non-operative management and its criteria

Non-operative management (NOM) is now the standard approach for the haemodynamically stable patient with a splenic injury. In a pooled meta-analysis, over two-thirds of more than 10,000 adults were managed non-operatively, with an overall NOM failure rate of about 8 percent; the vast majority of paediatric patients with blunt splenic trauma can also be managed non-operatively.^[5][3]

Enlarge

The criteria for NOM — learn them as a checklist

NOM is a privilege earned by meeting criteria, not a default you drift into. Recent trauma guidelines recommend non-operative management for Grade III splenic injury without contrast extravasation on CT, and WSES consensus work has mapped the factors that sway the decision. Tick each box before you commit:^[4]

1. Haemodynamically stable — EAST: NOM is the treatment of choice in stable patients irrespective of grade, age, or associated injuries.
2. No peritonitis — instability and peritonitis still warrant emergent operative intervention.
3. An environment that can monitor, re-examine, and open an operating room urgently — otherwise NOM is not appropriate.
4. A blush is not an automatic laparotomy — SAE is first-line in the stable patient with arterial blush, irrespective of grade.
5. WSES adult instability includes admission SBP under 90 mmHg (with vasoconstriction or altered consciousness) or a transfusion requirement of at least 4–6 units of packed red cells in the first 24 hours — not an unsourced "under 2 units" cutoff.^{[16][19][3][4]}

The NOM protocol — active management, not passive neglect

NOM is graded by injury severity: higher grades earn closer watching, low grades sit on a monitored ward.^[3]

• Setting and length of stay — Podda panel: admit about 1 day for low-grade (AAST I–II) and about 3 days for high-grade (AAST III–V), with high-grade injuries in a monitored setting.
• Serial haemoglobin — mobilisation is considered when three successive haemoglobins 8 hours apart after the first are within 10 percent of each other (and clinical parameters remain stable).
• Serial abdominal examinations — a new sign of peritonism mandates reassessment and often laparotomy.
• Repeat imaging — against routine imaging in WSES Class I (AAST I–II); CEUS/CT at 48–72 hours for AAST III or higher to detect delayed vascular complications. EAST: repeat imaging is guided by clinical status.
• VTE prophylaxis — in the absence of specific contraindications, start LMWH within 48–72 hours of admission.^[19][16]

When NOM fails

Pooled NOM failure is about 8 percent (95% CI 6.7–10.2), and the failure rate of observation alone climbs steeply with grade — from under 5 percent in Grade I to over 80 percent in Grade V — whereas the failure rate of SAE (about 16 percent overall) does not change significantly across grades. Failure is defined by the need for surgery: haemodynamic deterioration despite resuscitation, ongoing transfusion, or new peritonitis.^[5]

Return to activity is graded by severity, and follow-up imaging is used to detect delayed vascular complications — the rationale for repeat CT and the activity-restriction timeline.^[5][2]

Angioembolisation — the procedural bridge that extended NOM

Angioembolisation is the adjunct that let NOM reach into high-grade injuries. Regular use of splenic artery embolisation (SAE) is the current standard of treatment and reflects the paradigm shift towards spleen conservation.^[2]

Indications: a contrast blush on CT in a stable or transient-responding patient; a pseudoaneurysm (a delayed-rupture time bomb); an arteriovenous fistula; high-grade injuries in stable patients — meta-analysis shows SAE is associated with significantly higher splenic salvage rates in Grade IV and V injuries than observation alone.^[2][5]

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

Two techniques, two philosophies, chosen by where the bleeding sits — and the meta-analysis data are surprisingly clear.^[6]

• Proximal (main splenic artery) embolisation — the pooled data indicate proximal embolisation is the best option, with fewer life-threatening complications and fewer complications requiring surgical management.
• Distal (superselective) embolisation — embolisation of the specific segmental or polar branch feeding the injury; preserves maximal parenchyma.
• Embolic material matters — coil is superior to gelfoam for fewer life-threatening complications and less need for further surgical management. The primary success rate is about 90 percent, and very few embolised patients (about 6 percent) ultimately require surgical intervention.^[6]

The complications of angioembolisation are predictable: in the pooled analysis the incidence of life-threatening complications was about 20 percent, with proximal embolisation reducing severe complications compared with distal techniques — the trade-off that guides technique selection.^[6]

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. WSES guidance bases the decision on the patient's physiology, the anatomy of the injury and the associated lesions. The absolute triggers:^[3]

• Haemodynamic instability despite resuscitation — the absolute indication.
• Peritonitis — suggesting hollow viscus injury or contamination.
• Failed NOM — haemodynamic deterioration or ongoing transfusion requirement.
• Associated hollow viscus injury requiring laparotomy.
• Other intra-abdominal injuries mandating exploration.^[3]

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.^[3]

Splenorrhaphy — saving the injured spleen

Surgeons have adopted techniques to save as much splenic tissue as possible, from topical haemostatics to suture repair and mesh wrapping — because preserving splenic tissue preserves at least some splenic function.^[8]

• Topical haemostatics — oxidised cellulose, gelatin-thrombin matrix, fibrin glue — for surface ooze and small capsular tears.
• Argon beam coagulation — non-contact surface coagulation for diffuse capsular bleeding.
• Capsular suture repair — absorbable suture on a tapered needle, placed over an omental buttress.
• Mesh splenorrhaphy — an absorbable mesh bag providing tamponade for multiple lacerations; now largely supplanted by angioembolisation.^[8]

Partial splenectomy — the polar-injury move

For polar injuries where the damaged segment can be sacrificed and the rest kept, partial splenectomy exploits the avascular intersegmental plane.^[8]

1. Mobilise the spleen to the midline.
2. Selectively ligate the segmental or polar artery feeding the injured segment.
3. Watch for the line of demarcation — the segment goes dusky within minutes.
4. Transect along the line, compressing the parenchyma between fingers or with a stapler.
5. Oversew the cut edge with continuous absorbable suture over an omental buttress.
6. Preserve as much perfused parenchyma as possible — partial splenectomy has preserved some splenic functions (such as pitting of red cells), but conservative surgery has not provided total protection against overwhelming infection.^[8]

Total splenectomy — when salvage is not an option

Total splenectomy is for high-grade injuries unsuitable for NOM or embolisation, hilar vascular injury with total devascularisation, the damage-control setting, or failed splenic salvage. The underlying condition leading to splenectomy itself influences the later sepsis risk — in increasing order of risk: incidental splenectomy, ITP, trauma, transplantation, hereditary spherocytosis, Hodgkin staging, portal hypertension with hypersplenism, and thalassaemia.^[8]

The intra-operative points that matter:^[8]

• Avoid mass ligation of the hilum — it risks the pancreatic tail and post-operative fistula; individual vessel ligation is safer.
• Search for accessory spleens before closure — reported in 10–30% of people; in elective haematological splenectomy a missed accessory spleen causes recurrence, and in trauma, retained accessory tissue does not reliably prevent OPSI; pathology series stress documenting and weighing all splenic tissue, including accessory spleens and splenosis.^[21][8]

Laparoscopic splenectomy is elective only, reserved for normal or modestly enlarged spleens in haematological indications. It is contraindicated in the unstable trauma patient, where open control is faster and allows packing.^[3]

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. These infections are caused by encapsulated bacteria, run a fulminant course, are refractory to common treatment, and carry high mortality — prevention through vaccination and antibiotic prophylaxis is the basis of managing patients who have had splenectomy.^[7]

^{[3] [18]}

The organisms — encapsulated bacteria above all

The encapsulated bacteria dominate, and Streptococcus pneumoniae is king of them.^[8]

• Streptococcus pneumoniae — the classic dominant pathogen of asplenic sepsis.^[8]
• Haemophilus influenzae type b — the second classic encapsulated organism.
• Neisseria meningitidis — meningococcaemia.
• Any bacterial agent — the classic pathology series stresses that any organism may cause the rapid onset of septicaemia, meningitis, pneumonia and shock characteristic of the asplenic condition.^[8]
• Capnocytophaga canimorsus — a Gram-negative rod in the oral flora of dogs and cats; it can cause catastrophic OPSI. After animal bites, WSES recommends amoxycillin/clavulanic acid for 5 days. OPSI mortality is estimated up to 70% in one ED review.^[22][3]

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

The spleen links innate and adaptive immunity and protects against infection; when splenic function is lost, encapsulated organisms — which resist non-specific clearance and need opsonisation — proliferate unchecked. Immunisation and antibiotic prophylaxis are the only standing defences, and even these measures have not eliminated the risk. The endgame is fulminant septicaemia with refractory shock.^[7][8]

The clinical course — prodrome to disaster

OPSI declares itself as a rapid cascade, and the prodrome is the window you must not miss.^[8]

• Prodromal phase — 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 — the characteristic rapid onset of septicaemia, meningitis, pneumonia and shock; any bacterial agent may be responsible, and the course is refractory to common treatment.^[8]

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. Prevention through vaccination and antibiotic prophylaxis is the basis of management after splenectomy. Davidson lists conservation, immunisation, prophylactic antibiotics, stand-by antibiotics, information sheets and a medical-alert bracelet.^[7][18]

Vaccination — conjugate first, then polysaccharide

ACIP 2012 recommended routine PCV13 for asplenic adults, in addition to PPSV23. Prime with conjugate then broaden with polysaccharide; immunise at least 2 weeks before elective splenectomy where possible; after emergency splenectomy start no sooner than 14 days, or before discharge if that risk is high.^[17][3]

^{[17] [3]}

The order and intervals matter as much as the list:^[17][3]

1. PCV13 first, then PPSV23 at least 8 weeks later in pneumococcal vaccine-naive asplenic adults (ACIP 2012).
2. A second PPSV23 dose 5 years after the first for asplenia in adults aged 19–64 years.
3. WSES timing after trauma splenectomy: start vaccination programmes no sooner than 14 days after splenectomy (or total splenic vascular exclusion); if discharge is before day 15 and the miss-risk is high, vaccinate before discharge.
4. Elective splenectomy: give encapsulated-bacteria vaccines at least 2 weeks before the operation where possible.
5. Annual influenza vaccine — to cut the risk of secondary bacterial pneumonia.^[17][3]

Antibiotic prophylaxis — the daily safety net

Antibiotic prophylaxis is recommended for asplenic patients, with the heaviest emphasis on the highest-risk groups.^[7]

^{[10] [3]}

The risk is greatest in infants and young children. In sickle-cell anaemia, daily oral penicillin prophylaxis greatly reduced pneumococcal infection (Gaston OR 0.37), with strong evidence under 3 years of age and moderately strong evidence that withdrawal at 5 years did not result in serious consequences — that trial population is SCA, not trauma splenectomy. WSES notes that most severe infections occur within the first 2 years, so some authors recommend at least 2 years of prophylactic antibiotics, but duration is controversial. Adult standby supply: amoxycillin 3 g then 1 g every 8 hours (levofloxacin 500 mg daily or moxifloxacin 400 mg daily if beta-lactam allergic). After dog or other animal bites, WSES recommends amoxycillin/clavulanic acid for 5 days.^[10][3]

Patient education — what every asplenic patient leaves with

Every asplenic patient must leave hospital with the bundle documented and reinforced at each visit:^[7]

1. A medical alert card or bracelet — recording the asplenic state and infection risk.
2. Standby (rescue) antibiotics — carried at all times for self-administration at the first sign of fever, with instruction to still seek emergency care.
3. Warning-sign education — fever, rigors, lethargy, myalgia, confusion or purpura mean emergency care now, not a routine appointment.
4. Vaccination maintenance — completing and boosting the schedule against encapsulated organisms, with annual influenza.
5. A written management plan shared with the family doctor, with explicit escalation triggers.^[7][18]

Complications worth a viva question

The early and late complications of splenectomy are table material — reproduce both lists.^[3]

Early (within 30 days)

^{[6] [12]}

Late (after 30 days)

^{[8] [12]}

Special situations that change the threshold

Children — save the spleen at almost any cost

The management of adults and children must be different, and the vast majority of paediatric patients with blunt splenic trauma can be managed non-operatively. WSES guidance is explicit that children with splenic injury should always be treated in dedicated paediatric trauma centres.^[3]

• NOM is preferred for almost all grades, including most high-grade injuries in stable children.
• Angioembolisation has a smaller role than in adults — but physiology still decides.
• Children should be treated in dedicated paediatric trauma centres.
• Splenorrhaphy and partial splenectomy are preferred over total splenectomy if surgery is unavoidable.
• Lifelong vigilance is mandatory — the risk of overwhelming sepsis is greatest in infants and young children, and prophylaxis plus the full vaccine schedule apply.^[3][8]

Accessory spleens and splenosis — congenital versus acquired

Accessory spleens (splenunculi) are congenital nodules of normal splenic tissue; reported incidence is 10–30% of the population. Hansen instructs that all splenic tissue — including accessory spleens and splenic implants (splenosis) — be carefully identified and weighed.^[21][8]

Clinical significance — the two scenarios examiners test:^[8]

• In elective splenectomy for haematological disease (especially ITP), a missed accessory spleen is a recognised cause of recurrence — meticulous search and removal is mandatory.
• After traumatic splenectomy, accessory spleens and splenosis implants may give partial immune function but are insufficient to prevent OPSI — full vaccination and prophylaxis are still required.^[8]

Splenosis is the acquired counterpart — autotransplanted splenic implants on peritoneal surfaces after traumatic rupture, explicitly distinguished from congenital accessory spleens in the pathology literature. Like accessory spleens, it gives partial immune function but inadequate protection — surgical removal is only for symptomatic implants.^[8]

Iatrogenic injury — the splenectomy you did not plan

Iatrogenic injury is a recognised cause of "medical" splenectomy — the classic pathology series notes that splenectomy incidental to other operations (such as gastrectomy) carries the lowest sepsis risk of any indication, but still some 35-fold greater than the general population's risk of overwhelming infection.^[8]

• 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.
• Left nephrectomy or adrenalectomy, distal pancreatectomy, and upper abdominal vascular surgery — direct retraction or en-bloc resection.

Management: intra-operative recognition is critical — small capsular tears can be managed with topical haemostatics or splenorrhaphy. If splenectomy is required for iatrogenic injury, vaccinate before discharge (WSES: if discharge is before day 15 and miss-risk is high), document the asplenic state prominently, and deliver the full patient-education package.^[8][3]

Spontaneous rupture — the abnormal spleen that tears itself

Pathological spleens rupture with minimal or no trauma, and the underlying disease leading to splenectomy influences the later sepsis risk.^[8]

• Infectious mononucleosis (EBV) — the classic cause of spontaneous rupture in young adults.
• Malaria — acute splenomegaly.
• Haematological malignancy — acute leukaemia, lymphoma.
• Haemolytic anaemia — hereditary spherocytosis, sickle cell disease, thalassaemia.
• Splenic abscess or infarction with capsular inflammation.
• Connective tissue disease and pregnancy — rare.

Advice in infectious mononucleosis: occult rupture complicates about 0.5% of cases with about 30% mortality; patients with rupture generally undergo emergency splenectomy. There is no consensus on return to contact sport — suggested abstinence ranges from 2 weeks to 6 months; in one serial-ultrasound series 84% had normal splenic dimensions at 1 month (the rest by 2 months). Any patient with EBV who develops acute abdominal pain and signs of shock has a splenic rupture until proven otherwise.^[25][23]

Delayed rupture — the time bomb

Delayed deterioration after splenic injury is now understood to reflect vascular complications — pseudoaneurysm and arteriovenous fistula — which the 2018 AAST revision explicitly grades as high-grade vascular injuries. This is the rationale for follow-up imaging in high-grade injuries and for the activity-restriction timeline. Presentation is re-attendance with new abdominal pain and shock in a patient with a recent — often seemingly minor — splenic injury. Management is angioembolisation or surgery depending on stability.^[2]

Elective splenectomy — the non-trauma indications

Beyond trauma, splenectomy is performed for a defined set of haematological and structural indications — and the indication itself sets the later sepsis risk:^[8]

• Hereditary spherocytosis — chronic haemolysis; removing the site of destruction.
• Immune thrombocytopenic purpura (ITP) — refractory disease; recurrence from missed accessory spleens is recognised.
• Thalassaemia major — massive splenomegaly with hypersplenism (higher sepsis risk than ITP or trauma).
• Portal hypertension with hypersplenism — among the higher-risk indications.
• Staging laparotomy in Hodgkin lymphoma (historical).
• Splenic abscess, wandering spleen, splenic artery aneurysm — selective indications.^[8]

For all elective splenectomies, vaccinate at least 2 weeks before the operation — one of the few chances to optimise immune protection while the spleen is still in place.^[3]

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.^[3]

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?^[3]

Stem 1 (answer)ShowHide

Immediate management of the bleeding — unstable plus positive FAST means no CT. EAST: instability and peritonitis warrant emergent operative intervention. At laparotomy: midline incision, evacuate blood, pack, then systematically deal with the bleeding source; an unreconstructable splenic injury comes out. Post-op, the asplenic bundle starts before discharge: vaccination (no sooner than 14 days, or before discharge if that risk is high), antibiotic prophylaxis, alert card, standby amoxycillin.^[3][16]

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?^[7]

Stem 2 (answer)ShowHide

This is OPSI until proven otherwise. Tell them to take their standby oral antibiotic now if they have it, and come straight to the emergency department — do not wait for morning. On arrival, draw blood cultures and give immediate empirical broad-spectrum IV antibiotics covering encapsulated organisms including penicillin-resistant pneumococcus, with fluids, vasopressors and ICU as needed. These infections carry high mortality and are refractory to common treatment — waiting is the classic fatal error.^[7][8]

Stem 3. A stable patient has a Grade III splenic injury with a contrast blush on CT. NOM or surgery?^[4]

Stem 3 (answer)ShowHide

NOM plus angioembolisation. Guidelines support non-operative management for Grade III injury without contrast extravasation, and where vascular injury is present the answer is embolisation, not abandonment of NOM — vascular injury marks a high-grade lesion and SAE is the standard adjunct, with significantly higher salvage in high grades than observation alone. Surgery is reserved for instability, peritonitis, or failed NOM.^[4][5]

Stem 4. A 45-year-old woman is listed for elective splenectomy for ITP. What must happen before she reaches theatre?^[9]

Stem 4 (answer)ShowHide

Vaccinate at least 2 weeks before the operation — PCV13 first, then PPSV23 at least 8 weeks later, plus meningococcal/Hib cover and annual influenza. Organise standby amoxycillin and a medical alert bracelet, counsel on lifelong OPSI risk, and at operation meticulously search for and remove every accessory spleen (reported in 10–30%) — a missed accessory spleen is a recognised cause of ITP recurrence.^{[17][3][8][21]}

References27ShowHide

1. [1]Kozar RA, et al. Organ injury scaling 2018 update: Spleen, liver, and kidney. J Trauma Acute Care Surg, 2018.PMID 30462622
2. [2]Shi H, et al. CT of blunt splenic injuries: what the trauma team wants to know from the radiologist. Clin Radiol, 2019.PMID 31471062
3. [3]Coccolini F, et al. Splenic trauma: WSES classification and guidelines for adult and pediatric patients. World J Emerg Surg, 2017.PMID 28828034
4. [4]Amico F, et al. Grade III blunt splenic injury without contrast extravasation - World Society of Emergency Surgery Nijmegen consensus practice. World J Emerg Surg, 2020.PMID 32746885
5. [5]Requarth JA, et al. Nonoperative management of adult blunt splenic injury with and without splenic artery embolotherapy: a meta-analysis. J Trauma, 2011.PMID 21986737
6. [6]Rong JJ, et al. The impacts of different embolization techniques on splenic artery embolization for blunt splenic injury: a systematic review and meta-analysis. Mil Med Res, 2017.PMID 28573044
7. [7]Di Sabatino A, et al. Post-splenectomy and hyposplenic states. Lancet, 2011.PMID 21474172
8. [8]Hansen K, Singer DB Asplenic-hyposplenic overwhelming sepsis: postsplenectomy sepsis revisited. Pediatr Dev Pathol, 2001.PMID 11178626
9. [9]Rubin LG, et al. 2013 IDSA clinical practice guideline for vaccination of the immunocompromised host. Clin Infect Dis, 2014.PMID 24311479
10. [10]Gwaram HA, et al. A systematic review of effectiveness of daily oral penicillin v prophylaxis in the prevention of pneumococcal infection in children with sickle cell anaemia. Niger J Med, 2014.PMID 24956685
11. [11]Davies JM, et al. Review of guidelines for the prevention and treatment of infection in patients with an absent or dysfunctional spleen: prepared on behalf of the British Committee for Standards in Haematology by a working party of the Haemato-Oncology task force. Br J Haematol, 2011.PMID 21988145
12. [12]Wu Y, et al. Splanchnic Vein Thrombosis in Liver Cirrhosis After Splenectomy or Splenic Artery Embolization: A Systematic Review and Meta-Analysis. Adv Ther, 2021.PMID 33687650
13. [13]Liao Z, et al. Long term prophylactic anticoagulation for portal vein thrombosis after splenectomy: A systematic review and meta-analysis. PLoS One, 2023.PMID 37582105
14. [14]Fateh SM, et al. Sonographic measurement of splenic size and its correlation with body parameters. Medicine (Baltimore), 2023.PMID 36742195
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