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lack of the normal gastrosplenic and splenorenal ligaments that hold the spleen to its usual left hypochondriac position. The increased association of WS with women of child-bearing age and multiparity have led to the suggestion that hormonal influences and poor abdominal wall tone can affect the laxity of these splenic ligaments.4 Clinical presentation can vary from an incidental abdominal mass or radiological finding in an asymptomatic patient, recurrent abdominal pain, gastrointestinal obstruction or an acute abdomen. Complications include torsion and infarction, pancreatitis, portal hypertension with gastric or mesenteric varices and abscess formation.5 Hypersplenism can occur secondary to venous outflow obstruction and sequestration seen in chronic torsion, resulting in a secondary thrombocytopenia.5 CT is the preferred study for diagnosing a WS when torsion is suspected clinically or on other imaging studies.7 Characteristic findings include an absence of the spleen in its normal position, and a soft tissue mass resembling the spleen elsewhere in the abdomen.7,8 The whirl sign of the splenic pedicle is specific for splenic torsion.7 In splenic infarction, the attenuation of the spleen is considerably lower than the liver, even on pre-contrast CT.8 Ultrasound is likely to show the characteristic comma-shaped spleen in ectopic position and lack of splenic tissue in left upper quadrant; however, bowel gas can obscure diagnosis.7 Doppler can show presence or absence of splenic arterial flow in suspected torsion. Fifty percent of patients with symptomatic WS will require splenectomy; however, up to 75% of patients with non-viable spleens will have had no previous symptoms.3 Thus, conservative management is not recommended in asymptomatic WS. Splenic preservation with splenopexy is recommended when possible, given the widely known risks of post-splenectomy sepsis.9 However, when splenic fixation is not possible, laparoscopic splenectomy has been advocated for improved patient recovery and cosmesis.10 Given the acuity of our case, with confirmed splenic torsion and infarction, the decision was made to proceed with immediate lower

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midline laparotomy and splenectomy as the safest and most efficient approach to stabilization and treatment.

References 1. Mayo WJ. A review of 500 splenectomies with special reference to mortality and end results. Ann. Surg. 1928; 88: 409–15. 2. Eraklis AJ, Filler RM. Splenectomy in childhood: a review of 1413 cases. J. Pediatr. Surg. 1972; 7: 382–8. 3. Dawson JHM, Roberts NG. Management of the wandering spleen. ANZ J. Surg. 1994; 64: 441–4. 4. Abell I. Wandering spleen with torsion of the pedicle. Ann. Surg. 1933; 98: 722–35. 5. Soleimani M, Mehrabi A, Kashfi A, Fonouni H, Büchler MW, Kraus TW. Surgical treatment of patients with wandering spleen: report of six cases with review of the literature. Surg. Today 2007; 37: 261–9. 6. Carswell JW. Wandering spleen: 11 cases from Uganda. Br. J. Surg. 1974; 61: 495–7. 7. Fujiwara T, Takehara Y, Isoda H et al. Torsion of the wandering spleen: CT and angiographic appearance. J. Comput. Assist. Tomogr. 1995; 19: 84–6. 8. Ben Ely A, Zissin R, Copel L et al. The wandering spleen: CT findings and possible pitfalls in diagnosis. Clin. Radiol. 2006; 61: 954–8. 9. Stringel G, Soucy P, Mercer S. Torsion of the wandering spleen: splenectomy or splenopexy. J. Pediatr. Surg. 1982; 17: 373–5. 10. Gurski RR, Schirmer CC, Fischer CA et al. Laparoscopic approach to wandering spleen: a case report and an update to the question. Surg. Laparosc. Endosc. 1998; 8: 363–5.

Jennie Gu, MBBS (Hons), BPharm Timothy Elston, FRACS, MBBS Angela Robson, FRACS, MBBS Department of General Surgery, Cairns Base Hospital, Cairns, Queensland, Australia doi: 10.1111/ans.12551

Oesophageal haematoma masquerading as cardiac ischaemia An 83-year-old woman was referred with a suspected, spontaneous perforation of the oesophagus. She had presented with central chest pain radiating to the back, following a severe bout of coughing that morning. There was a past medical history of ischaemic heart disease, requiring a coronary stent and 75 mg of clopidogrel daily. Physical examination and serial electrocardiographs were normal. There was a rise in serial troponins from 22 to 44 ng/mL. Treatment was instituted, with a further 75 mg of clopidogrel and 60 mg enoxaparin, in accordance with a chest pain protocol. A computed tomography (CT) aortogram was also performed due to a differential diagnosis of aortic dissection. This showed intramural haematoma in the oesophagus with fluid and stranding posteriorly. The post-contrast scan showed active contrast extravasation into the oesophageal lumen (Fig. 1). On initial viewing, this was felt to represent oesophageal rupture with mediastinitis. She was

then urgently transferred to our tertiary upper gastrointestinal (GI) unit. Further history obtained following transfer revealed odynophagia prior to presentation and a small volume of haematemesis following the CT scan. In order to clarify the differential diagnosis of oesophageal perforation, particularly as the patient’s clinical condition did not support this diagnosis, an urgent, water-soluble contrast swallow was performed. No leak from the oesophagus was demonstrated; however, contrast was shown tracking along the peripheries, around a large central haematoma (Fig. 2). The antiplatelet and anticoagulants were stopped and a diet of clear fluids was commenced. The patient made an uneventful recovery. With the gradual introduction of a normal diet she complained of persistent, mild dysphagia. Contrast swallow and endoscopy performed 2 weeks following discharge showed minor oesophageal mucosal changes and partial resolution of the haematoma. © 2014 Royal Australasian College of Surgeons

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Fig. 1. This axial computed tomography angiogram demonstrates contrast extravasation within the eccentric oesophageal lesion (arrow), and a normal appearance of the thoracic aorta (which is separate to the lesion).

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patent, this will instead appear as a ‘double-barrelled’ oesophagus. In this situation, contrast tracks under the mucosa, similar to a dissection flap.5 Usual discriminating symptoms from cardiac causes of chest pain are dysphagia and small-volume haematemesis. Endoscopy has been used to confirm the diagnosis, often showing a submucosal bluish mass3,5 or organized clot,6 occasionally with a visible mucosal tear.1,7 The diagnosis may be difficult and relies on exclusion of lifethreatening causes, usually myocardial infarction8 or aortic dissection.7 Substantial morbidity may be associated with diagnostic manoeuvres. There have been case reports of haematoma mimicking malignancy, which have perforated at endoscopy,9 or resected leading to death.10 Negative thoracotomy has been performed to treat suspected aortic dissection,7 only to find intramural and paraoesophageal haematoma. In the case presented here, the patient wa anticoagulated, in misguided concern for cardiac ischaemia. This aggressive anticoagulation could have precipitated or propagated the intramural haematoma. Emergency department protocols often emphasize the early and aggressive use of anticoagulation in patients with new chest pain. This case highlights the need for careful upper GI history in these patients prior to anticoagulation. Although rare, oesophageal pathology can underlie these cases with potentially life-threatening implications as a result.

References

Fig. 2. A frontal single-contrast swallow demonstrates a smooth, sausage-like, eccentric filling defect (arrow) involving the posterior wall of the distal thoracic oesophagus in keeping with an intramural haematoma.

Intramural hematoma represents one of the outcomes from oesophageal wall trauma, which can vary considerably from relatively minor mucosal injuries to full-thickness perforation. It most commonly occurs in older women on anticoagulation.1 The precipitating incident is often a change in intrathoracic pressure such as coughing, vomiting or Valsalva.2 It can also occur secondary to trauma from ingested food (e.g. fish bones3) or instrumentation.4 The natural history is resolution with conservative treatment, in most cases. A minority of patients will have persistent dysphagia.1 The typical radiological features are an eccentric, luminal, filling defect on contrast swallow or CT. If the mucosal breach is still

© 2014 Royal Australasian College of Surgeons

1. Steadman C, Kerlin P, Crimmins F et al. Spontaneous intramural rupture of the oesophagus. Gut 1990; 31: 845–9. 2. Beumer JD, Devitt PG, Thompson SK. Intramural oesophageal dissection. ANZ J. Surg. 2010; 80: 91–5. 3. Kwan KL, Law S, Wong KH, Kwok KF. Esophageal hematoma: a masquerade of rare occurrence. Endoscopy 2006; 38 (Suppl. 2): E29. 4. Basso L, Tocchi A. Total dysphagia from intramural haematoma following sclerotherapy for oesophageal varices. Br. J. Surg. 1993; 80: 127–8. 5. Rossaak J, Wakeman C, Coulter G. Spontaneous submucosal haematoma of the oesophagus. N. Z. Med. J. 2006; 119: U2342. 6. Hong M, Warum D, Karamanian A. Spontaneous intramural esophageal hematoma (IEH) secondary to anticoagulation and/or thrombolysis therapy in the setting of a pulmonary embolism: a case report. J. Radiol. Case Rep. 2013; 7: 1–10. 7. Sen A, Lea RE. Spontaneous oesophageal haematoma: a review of the difficult diagnosis. Ann. R. Coll. Surg. Engl. 1993; 75: 293–5. 8. Tunnicliffe G, Raymond N, Nowitz M. An unexpected diagnosis after unstable angina. Lancet 2007; 369: 964. 9. Skillington PD, Matar KS, Gardner MA, Parkes RP, Cole PH. Intramural haematoma of the oesophagus complicated by perforation. Aust. N. Z. J. Surg. 1989; 59: 430–2. 10. Thompson NW, Ernst CB, Fry WJ. The spectrum of emetogenic injury to the esophagus and stomach. Am. J. Surg. 1967; 113: 13–26.

Ruelan V. Furtado,* MBBS William F. Beasley,* MBBS, FRCS Katerina Mastrocostas,† MBBS, MPH Gregory L. Falk,* MBBS, FRACS Department of *Surgery and †Radiology, Concord Repatriation General Hospital, Concord, New South Wales, Australia doi: 10.1111/ans.12562

Oesophageal haematoma masquerading as cardiac ischaemia.

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