British Journal of Radiology (2009) 82, e11-e14
© 2009 British Institute of Radiology
doi: 10.1259/bjr/92246530
British Journal of Radiology 82 (2009),e11-e14 ©2009 The British Institute of Radiology
Acute necrotizing pancreatitis following inadvertent extensive splenic artery embolisation for trauma
R L HAMERS, MD
1
F G VAN DEN BERG, MD
2 and
A B J GROENEVELD, MD, PhD, FCCP, FCCM
1
Departments of 1 Intensive Care and 2 Radiology, VU University Medical Center (VUMC), Amsterdam, The Netherlands
Correspondence: ABJ Groeneveld, Department of Intensive Care, VUMC, PO Box 7057, 1007 MB Amsterdam, The Netherlands. E-mail: johan.groeneveld{at}vumc.nl
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Abstract
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We present a case of splenic artery embolisation (SAE) after traumatic splenic injury that was complicated by acute necrotizing pancreatitis, caused by inadvertently extensive embolisation of the splenic artery. Although SAE is increasingly used for splenic preservation in trauma, there is insufficient knowledge on its efficacy and pitfalls. This report aims to draw attention to a rare but potentially serious complication of SAE.
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Introduction
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Splenic artery embolisation (SAE) is increasingly used as an adjunct to the non-operative management of traumatic splenic injuries, with the aim of increasing splenic preservation rates [1–4]. Although SAE is described as an effective and safe procedure, complications are common, in particular rebleeding, splenic infarction and splenic abscess [1, 3, 5]. Moreover, the formal evidence for efficacy and safety is limited, being derived mainly from non-comparative retrospective studies [1–6]. We present a case of SAE that was complicated by acute necrotizing pancreatitis, in order to draw attention to this rare but potentially life-threatening complication.
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Case report
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A previously healthy 48-year-old man presented at our emergency department after a car accident. His only symptom at presentation was pain in the left side. A seat belt sign was present. During the first few hours of observation, his haemodynamics were stable, and 2000 ml of crystalloid solution was administered. Abdominal ultrasonography at presentation revealed a splenic injury and a small amount of free fluid in the paracolic and lower abdominal regions, with intact liver and kidneys. A left lateral rib fracture was diagnosed on chest radiography. Subsequent CT showed multiple small splenic lesions, including a small subcapsular injury and a capsular rupture caudally (
Figures 1 and 2). In addition, a small amount of free fluid was visible in the rectovesical pouch and bordering the liver. This finding together with a slight decrease (1 g dl–1) in haemoglobin concentration in the first 3 h after presentation was considered suggestive for an active splenic haemorrhage. As the haemodynamic status of the patient did not demand immediate surgery, the patient was referred for SAE. During the procedure by the interventional radiologist, there was some difficulty in introducing the radiological catheter (C2 and SIM2; Cook, Bloomington, IN), and ultimately the catheter position was rather unstable, via brachial access. Because distal selective embolisation proved to be difficult, it was decided to perform embolisation of the proximal main artery instead, using 035' Tornado Embolisation Coils (Cook). During placement of the second coil in the proximal main artery, the first coil, which was largest in size (5–10 mm), was inadvertently taken with the bloodstream, displacing it to the splenic hilum. As a result, a relatively long stretch of the SA, i.e. from the mid-point to the splenic hilum, was occluded (Figure 3). After the procedure, the patient had stable haemodynamics and haemoglobin concentration, but abdominal pain developed. From day 2, a rise in serum amylase and lipase levels was observed, which reached a peak at day 3 (1340 IU l–1 and 750 IU l–1, respectively). Abdominal CT scans performed during the following days showed large segmental splenic infarctions and rapidly evolving necrosis of the tail of the pancreas, with extensive infiltration of the peripancreatic fat; the head and neck of the pancreas were unaffected (Figures 4 and 5). Clinically, the patient developed a paralytic ileus and, consequently, atelectasis in the lower lung areas, requiring non-invasive ventilation with positive end-expiratory pressure for several days. From day 14, the patient improved clinically, and showed normalized serum pancreas enzymes and restored bowel function. No further splenic bleeding occurred during follow-up. On day 24, the patient was discharged from the hospital in a good clinical condition.
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Figure 1. Transverse abdominal CT scan performed pre-intervention shows active intraparenchymatous bleeding (arrow).
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Figure 2. Transverse abdominal CT scan performed pre-intervention shows subcapsular contrast-enhanced blood in the spleen and some subcapsular fluid along the edge of segment 6 of the liver (after administration of contrast).
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Figure 3. Splenic arteriogram obtained during splenic artery embolisation(SAE) shows the localization of the coils in the tortuous SA after intended proximal embolisation and inadvertent distal embolisation (arrows).
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Figure 4. Transverse abdominal CT scan performed post-intervention shows the coils and peripancreatic infiltration and necrosis of the tail of the pancreas (arrows).
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Figure 5. Transverse abdominal CT scan performed post-intervention shows the necrotizing pancreatitis at a more caudal position (arrow).
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Discussion
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In patients with traumatic splenic injury, surgical interventions, including splenectomy and splenorraphy, are usually performed in case of an unstable haemodynamic status, whereas patients with stable haemodynamics are preferably treated conservatively with bed rest and observation. The objective of SAE is to improve the outcome of this non-operative management. Although poor success rates have been reported for non-operative management alone [7, 8], small studies evaluating SAE have reported high splenic preservation rates (>90%) in patients with angiographic evidence of splenic vascular injury [1, 9] and in patients with splenic lacerations of American Association for the Surgery of Trauma Organ Injury Grade III or higher [10] and/or evidence of extravasation on CT scans and a stable haemodynamic status [6]. Splenic salvage rates seem to be similar for the different embolisation techniques that are in use [3], i.e. superselective embolisation of a small distal arterial branch in the injured segment and proximal embolisation of the main artery to reduce pressure on the splenic parenchyma [1].
The most widely accepted indication for SAE in trauma patients is evidence of arterial injury on CT scans [11]. However, local management protocols vary, and conditions such as significant haemoperitoneum, severe splenic injury, decreasing haematocrit (not explained by other injuries) and persistent tachycardia have also been proposed as indications for SAE [2]. In our patient, the reasons for attempting SAE were the diffuse splenic injury and the suspected (but non-massive) active haemorrhage, at otherwise stable haemodynamics; obviously, one can doubt, in retrospect, the compelling reason for performing SAE in our patient.
Few studies have specifically addressed the complications of SAE in trauma. A Western Trauma Association multicentre study reported a major complication rate of 20% and a minor complication rate of 23% [3]. Post-procedural bleeding, splenic infarction and splenic abscesses were the most frequent complications in their series. Other complications reported include contrast-induced renal insufficiency, pleural effusions, paralytic ileus and distal coil migration [5, 11]. Complication rates appear to be similar for the different embolisation techniques, with the exception of splenic infarction and abscess, which are reported to be higher for combined main artery and superselective embolisation [3–5]. Acute pancreatitis has been acknowledged as a complication following embolisation of the primary vessels supplying the pancreas [4, 5, 11, 12], but the risk has been poorly quantified and it is unknown whether this risk may differ between the various embolisation techniques. In addition, to our knowledge, pancreatitis after SAE for trauma has not been reported previously.
The pancreas has been shown to be highly susceptible to ischaemic damage both in experimental and in clinical settings, including cardiopulmonary bypass [13], haemorrhagic shock [14] and transplantation [15]. Ischaemia–reperfusion injury is increasingly recognized as an important mechanism in the pathogenesis of acute pancreatitis and especially in the progression from the mild oedematous to the severe necrotizing form [16]. In animal studies, injection of microspheres in the pancreatic artery caused pancreatitis resulting from infarction, apparently caused by occlusion of end arteries [17]. Clinical evidence, such as microthrombi and atheromatous emboli in the pancreatic artery in patients with pancreatitis, further supports pancreatic infarction as a potential aetiologic factor [18, 19]. We hypothesize that, in our patient, the occlusion of a long stretch of the SA and some of its branches resulted in ischaemia and infarction in the most distal pancreas.
Moreover, patterns of vascularization of the distal pancreas have been reported to vary greatly between individuals [20–23] and include rarities such as the presence of a single pancreatic SA branch [24] and the absence of any anastomosis between the body and tail [22]. Throughout its course, the SA gives rise to many branches that supply the pancreatic body and tail, including the dorsal pancreatic artery, the short pancreatic arteries, the greater pancreatic artery, the arteries to the tail of the pancreas, and the short gastric arteries [21]. We speculate that the tail is particularly susceptible to ischaemia owing to prevailing end arteries, especially in the absence of sufficient collateral blood supply.
Trauma could be surmised as the cause of pancreatitis in our patient, as pancreatic injury may occur in 1–3% of patients sustaining abdominal trauma. Contusions, lacerations or transections are most frequently encountered between the body and the tail [16]. As the pancreas was radiographically normal on admission and the pancreatitis was located in the tail region, a traumatic aetiology seems unlikely.
In conclusion, we present a patient with inadvertently extensive embolisation of the SA following splenic trauma. Owing to subsequent ischaemia in the most distal pancreas, acute necrotizing pancreatitis developed. As the use of splenic arterial interventions is increasing in a wide range of pathological entities, such as splenic trauma, hypersplenism, portal hypertension and splenic neoplasia [11], additional investigations to further quantify their efficacy and their risks are warranted. This report aimed to draw attention to a rare but potentially serious complication of SAE. Before undertaking SAE, a thorough knowledge of the potential of the common techniques and their limitations is required.
Received for publication April 2, 2007.
Revision received September 22, 2007.
Accepted for publication November 30, 2007.
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Abstract
Introduction
