Delayed Splenic Rupture After Trauma in a Patient With Chronic Myeloid Leukemia

Abstract

Background

Trauma ranks as the fourth leading cause of mortality among adults under 40 years old in Western countries. The spleen, given its location within the abdomen and highly vascularized parenchyma, is the intra-abdominal organ at the highest risk for injury. Delayed splenic rupture (DSR), characterized by post-traumatic hemorrhage exceeding 48 hours, has been documented since 1907, yet its pathophysiology continues to be a source of debate.

Summary

The management of splenic injuries encompasses a spectrum of nonoperative and operative techniques. This report details a case of delayed splenic rupture in a patient with newly diagnosed chronic myeloid leukemia (CML). The presentation necessitated a massive transfusion protocol (MTP) followed by emergent exploratory laparotomy and splenectomy due to hemodynamic instability.

Conclusion

While rare, delayed splenic rupture can occur in trauma patients with a negative initial CT scan for splenic injury, as evidenced by limited case reports. This underscores the importance of maintaining a high index of suspicion for DSR in high-risk trauma patients who exhibit signs of delayed hemorrhage, even in the absence of initial CT findings. Notably, patients with pre-existing splenic pathology represent a particularly vulnerable population and may benefit from follow-up splenic imaging. Early detection of a nascent splenic injury in such cases could facilitate prompt interventions like angioembolization, offering a potentially more favorable risk-benefit profile compared to traditional surgical management.

Key Words

delayed splenic rupture; trauma; chronic myeloid leukemia

Abbreviations

DSR: delayed splenic rupture
CML: chronic myeloid leukemia
MTP: massive transfusion protocol
HD: hospital day
AP: abdomen and pelvis
SAE: splenic artery embolization

Case Description

Approximately 30% of polytrauma cases involve intra-abdominal organ injuries, with the spleen being the most commonly affected solid organ due to its location near the left ribs (9th-11th) richly vascularized tissue.^1-3 Historically, splenectomy was the only treatment option for splenic injury (pre-1960s). However, contemporary literature supports nonoperative management for appropriate injuries.⁴

While cross-sectional imaging usually identifies immediate post-traumatic splenic injuries, some cases remain occult, leading to delayed rupture. This phenomenon, first described by Baudet in 1907, is defined as bleeding occurring more than 48 hours after blunt abdominal trauma.^2,5 The exact mechanism remains unclear, but theories suggest a role for splenic parenchymal pseudoaneurysm formation. Clot dissolution within these structures could degrade the aneurysmal wall and trigger delayed hemorrhage.⁵

A 52-year-old woman with a history of panic disorder, hypertension, and type 2 diabetes presented to the emergency department following a motor vehicle collision. Despite hemodynamic instability, she responded well to the MTP. Initial INR of 1.09 obviated the need for tranexamic acid during resuscitation. A trauma workup with CT scan using 3 mm cuts and 189 slices revealed extensive polytrauma, including bilateral clavicle and manubrium fractures, bilateral rib fractures (19 total), multiple Grade II hepatic lacerations in both lobes, bilateral adrenal hemorrhages, multilevel spinal fractures involving the cervical spine, pelvic fractures with associated hematoma, and a humeral head fracture. The spleen was read as unremarkable by an attending radiologist, with no signs of laceration, hematoma, or splenomegaly. She was admitted to the surgical intensive care unit for ongoing care, including appropriate DVT prophylaxis with Lovenox.

Admission labs revealed leukocytosis (153/µL), prompting hematology-oncology consultation. BCR/ABL on HD8 confirmed new-onset CML, for which treatment began. On HD11, fever and tachycardia led to a CT scan (AP/IV contrast) showing a 1.9 × 0.7 cm hypodensity in the superior medial spleen, suspected resolving laceration.

Figure 1. CT AP Showing Hypodensity in Medial Spleen. Published With Permission

A 6.1 g/dL hemoglobin level was identified on HD 13, signifying new-onset anemia. Two units of packed red blood cells (PRBCs) were transfused, raising hemoglobin to 7.5 g/dL. However, on the following morning (HD 14), her hemoglobin level dropped to 6.1g/dL. Despite an additional transfusion attempt, the patient demonstrated an inadequate response, characterized by persistent tachycardia and acute hypotension, prompting the use of vasopressors and further blood product administration.

A CT angiography of the chest, abdomen, and pelvis revealed a large volume hemoperitoneum and a predominantly subcapsular perisplenic hematoma measuring approximately 15.0 × 11.1 × 15.6 cm, causing significant compression on the spleen. Blood products were consistent with recent bleeding with active extravasation posterior to the spleen. Given these findings and her unstable hemodynamics, she underwent emergent exploratory laparotomy and splenectomy. Intraoperatively, the spleen was enlarged (505 g) and shattered, with pathology confirming splenic infiltration by her CML.

Figure 2. CT AP Showing Large Volume Hemoperitoneum and Shattered Spleen. Published With Permission

The patient’s postoperative course was prolonged by ventilator-associated pneumonia (VAP) in the SICU. This necessitated tracheostomy and gastrostomy tube placement. Her multiple orthopedic injuries achieved good healing with a combination of surgical and nonoperative interventions. Following transfer to the stepdown unit and then a surgical floor, she demonstrated continued improvement, ultimately tolerating a regular diet and achieving decannulation. She was discharged to a skilled nursing facility for ongoing rehabilitation. Imatinib and anagrelide were initiated for her CML with close hematologic/oncologic follow-up.

Discussion

Non-recognition of splenic injury is the leading cause of preventable mortality after blunt abdominal trauma. Delays in diagnosis significantly worsen outcomes, with mortality rates rising tenfold compared to immediate identification. While traditionally described as occurring within 4-8 days post-injury with a 5-15% mortality rate (compared to 1% for acute rupture),⁶ Furlan et al. reported a wider incidence range of 3-15%.⁷

Moreover, Traub and Perry observed an 80% prevalence of concomitant extra-abdominal injuries (head, chest, extremities) in blunt splenic trauma patients.⁸ Additionally, 61% exhibited associated intra-abdominal injuries, most commonly involving the liver, gastrointestinal tract, and kidneys.⁸ Despite negative CT findings for the spleen in our case, the mechanism and pattern of injury maintained a high index of suspicion for splenic involvement.

The precise pathogenesis of delayed splenic rupture remains elusive. However, several leading theories are proposed: 1) formation of a post-traumatic pseudocyst, 2) increased oncotic pressure within a subcapsular hematoma due to cell lysis, and 3) development of a pseudoaneurysm.⁹

In contrast, spontaneous splenic rupture, particularly in patients with hematologic malignancies (accounting for 25% of cases), is the leading theory attributed to rapid infiltration of the spleen by lympho- or myeloproliferative cells. The relatively inflexible splenic capsule cannot accommodate the rapid increase in volume, leading to rupture.^10,11 While the specific contribution of these processes to our patient’s splenic rupture is unclear, a combined effect is likely.

The treatment of choice for splenic injury is dictated by the hemodynamics of the patient as well as the etiology of the injury.¹¹ Over the years, treatment options for splenic injury have shifted from operative to nonoperative management. For hemodynamically stable patients, observation or splenic artery embolization (SAE) are both valid management options depending on the severity of the injury and the age of the patient.^11,12 In cases of hemodynamic instability or significant intraabdominal/retroperitoneal bleeding, treatment options include partial or total splenectomy or splenorrhaphy.¹¹

Splenectomy was historically the mainstay of treatment for delayed splenic rupture. However, this approach has fallen out of favor due to its associated surgical complications (pneumonia, subphrenic abscess, pancreatitis) and the risks of asplenia, particularly overwhelming post-splenectomy sepsis.

A shift toward a management strategy similar to blunt splenic injury is proposed based on studies by Liu et al. This approach includes close observation with adequate resuscitation and SAE. Studies suggest SAE preserves splenic function. Surgery (laparotomy) is reserved for hemodynamically unstable patients despite resuscitation or for other clear surgical indications, such as peritonitis.¹³

The utility of serial imaging for splenic trauma remains debated, with a lack of consensus on timing or preferred modality. For low-grade injuries, inpatient management includes close observation, serial abdominal exams, and serial hemoglobin checks. While some studies advocate for repeat imaging 36-72 hours post-injury, particularly for grade II or higher injuries, to detect pseudoaneurysm formation, other guidelines suggest restricting repeat scans to specific patient subsets. These include:

• Development of anemia
• High-grade injury or subcapsular hematoma
• Underlying splenic pathology or coagulopathy
• Inability for reliable clinical follow-up for delayed rupture symptoms³

A key challenge is the highly variable timeframe for delayed splenic rupture, ranging from days to weeks.¹³ Our case exemplifies this conundrum. The patient, who met the criteria for repeat imaging, did not exhibit signs of imminent rupture, highlighting the limitations of predicting delayed rupture and the need for judicious use of repeat scans.

Conclusion

Limited data suggest delayed splenic rupture in trauma patients, especially those with initially negative CT scans for splenic injury, is uncommon. However, clinicians should maintain a high index of suspicion for delayed rupture in high-risk trauma patients who develop signs of bleeding despite negative initial cross-sectional imaging. Pre-existing splenic conditions may elevate this risk. Early identification of an evolving splenic lesion with follow-up imaging could facilitate minimally invasive interventions like angioembolization, potentially offering a more favorable risk-benefit profile compared to traditional surgery.

Lessons Learned

In trauma patients with known splenic pathology who present with new-onset anemia, hypotension, or increased transfusion requirements, delayed splenic rupture should be a top differential diagnosis. Early identification facilitates minimally invasive approaches like angioembolization, potentially avoiding a total laparoscopic splenectomy.

Authors

Lombardi ME; Marulanda K; Scarlet S, Ra JH

Author Affiliation

Department of Surgery, University of North Carolina, Chapel Hill, NC 27599

Corresponding Author

Jin H. Ra, MD
Department of Surgery
4013 Burnett Womack Bldg.
Chapel Hill, NC 27599
Email: jin_ra@med.unc.edu

Disclosure Statement

The authors have no conflicts of interest to disclose.

Funding/Support

The authors have no relevant financial relationships or in-kind support to disclose.

Received: August 3, 2021
Revision received: December 12, 2021
Accepted: January 24, 2022

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