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American Journal of Forensic Medicine & Pathology:
doi: 10.1097/PAF.0b013e3181c03caf
Case Report

Death Due to Hemorrhagic Shock After Delayed Rupture of Spleen: A Rare Phenomenon

Kodikara, Sarathchandra MBBS, MD, DLM

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From the Department of Forensic Medicine, Faculty of Medicine, University of Peradeniya, Sri Lanka.

Manuscript received February 21, 2007; accepted September 14, 2007.

Reprints: Sarathchandra Kodikara, MBBS, MD, DLM, Department of Forensic Medicine, Faculty of Medicine, University of Peradeniya, Sri Lanka. E-mail: kaskodikara@yahoo.com.

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Abstract

Delayed splenic rupture after blunt trauma is rare and contributes to a significant mortality rate. As this is accompanied by a period of clinical quiescence, a close clinical vigilance is required for early diagnosis and surgical intervention. A case report on death because of delayed rupture of healthy spleen after blunt trauma is presented. The pathophysiology of delayed rupture and importance of early detection are discussed. The case presented is the first known case of death due to delayed splenic rupture in Sri Lanka.

Delayed splenic rupture is a rare but well-recognized clinical entity, after blunt trauma to left lower chest or abdomen. This contributes to a significant mortality rate (5%-15%) compared with that associated with acute splenic rupture (1%).1,2 The mechanism of this serious and possible life-threatening complication is still not fully understood but several theories predominate.

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CASE REPORT

A 45-year-old man fell accidentally, hitting his left side chest and abdomen on a chair. He was symptomatically treated by a general practitioner. The following day he was admitted to hospital as he complained of pain on the left side of his chest. He was not suffering from any bleeding disorder.

Initial examination revealed slight tenderness over the left lateral chest with no visible bruising. There were no signs of circulatory shock. His pulse rate was 74 beats per minute, blood pressure was 130/80 mm Hg, and capillary refill time was 2 seconds (normal capillary refill time is less than 3 seconds). Tenderness, guarding, or rigidity was not elicited on abdominal palpation. Bowel sounds were present. Initial x-rays of the abdomen and chest and ultrasound scans were unremarkable. Routine blood tests revealed a hemoglobin level of 13.8 g/dL.

On the third day after the incident, the abdomen was noted to be soft and nontender. Hemodynamically, he was stable. Second abdominal ultrasound scan was also reported as normal.

Eight hours after the last ultrasound scan, the patient experienced an unbearable abdominal pain, difficulty in breathing, and left shoulder tip pain. He became pale with a hemoglobin level of 6.5 g/dL. Early signs of circulatory shock were evident with a pulse of 110 beats per minute and a blood pressure of 90/60 mm Hg. He displayed a marked tenderness with rebound and guarding on abdominal palpation. Bowel sounds were attenuated.

Emergency laparotomy revealed a ruptured spleen with a subcapsular hematoma and a hemoperitoneum with 2 L of blood. Splenectomy was done and 5 pints of blood were transfused. He was pronounced dead, 1 hour after surgery.

At autopsy, generalized pallor was noted. There were no rib fractures. The lienorenal and gastrosplenic ligaments had been ligated.

The spleen size was within the normal range. A hematoma was seen in the inferior pole dissociating parenchyma with associated capsular rupture. The histologic analysis revealed the presence of tear with hemorrhage and surrounding inflammation within the substance. Natural splenic pathologies were excluded.

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DISCUSSION

Spleen is the most commonly injured organ after abdominal trauma.3 However traumatic rupture of a healthy spleen is rare. This may be, in part, due to its well-protected position in the left upper quadrant of the abdomen.4 Intraperitoneal hemorrhage from a splenic laceration is often profuse due to its vascular nature. Most of the patients present with signs and symptoms of acute intraperitoneal hemorrhage such as abdominal pain and/or tenderness or hypotension.5

Delayed rupture of spleen is uncommon. This was first described by Baudet in 19026 and he stated that the time period from the injury to the splenic rupture was 48 hours or more and is accompanied by a period of clinical quiescence. This is referred as “the latent period of Baudet.”1

The pathophysiology behind delayed splenic rupture is not clearly understood. Baudet suggested that the force transmitted to the spleen is sufficient to lacerate the splenic parenchyma but not to injure the capsule. When intrasplenic bleeding continues, a subcapsular hematoma is formed and with progressive increase in the intrasplenic pressure, rupture of the capsule occurs with resultant intraperitoneal hemorrhage which may be delayed by days.1 This is the most widely accepted theory. Simpson and Ajuwon postulated that a capsular tear and perisplenic hematoma is formed at the time of injury and is tamponaded by surrounding organs delaying its rupture at a later date.7 Rupture of a pseudoaneurysm of intraparenchymal splenic artery branches is also a potential mechanism for delayed rupture of spleen.8

Additionally, initial bleeding from splenic laceration would be stopped by a perisplenic hematoma but begins later when hematoma is dislodged. Rupture of asymptomatic splenic pseudocyst, which occurred after blunt trauma is another possible mechanism in this context. Such pseudocysts are rare and occur after organization of an intrasplenic hematoma.

In this case, the patient displayed signs and symptoms of acute intraperitoneal hemorrhage, 48 hours after the incident. With rupture of the intraparenchymal hematoma and leakage of blood into the peritoneal cavity, he experienced abdominal pain and difficulty in breathing, and left shoulder tip pain due to irritation of the phrenic nerves on the diaphragm.

Fabin et al reported the sensitivity, specificity, and accuracy of computed tomography (CT) scan diagnosis after blunt abdominal trauma to be 85%, 100%, and 97%, respectively.9 The anatomy and internal architecture of the spleen are generally shown well by CT scan. Radioisotope scanning shows a defect due to hematoma, as should ultrasound, but CT usually proves diagnostic as it is able to show increased density at the site of recent hemorrhage. Therefore, it has become the procedure of choice to establish the diagnosis of splenic rupture. A CT scan provides information on the volume of hemoperitoneum, the extent of splenic laceration, and hematoma and the degree of parenchymal injury.10,11

CT scans are not always reliable in predicting delayed rupture. Evidence of expanding hematoma on CT scan may be a predictor for impending rupture. Therefore, repeated imaging during the latent period may be helpful in detecting delayed splenic rupture in the patients at risk.

Autopsy revealed an intraparenchymal hematoma with a capsular laceration. Perisplenic hematoma, pseudoaneurysms of intraparenchymal splenic artery, and pseudocysts were excluded. As a result, pathophysiology behind delayed splenic rupture is maintained more with the Baudet's theory.

Lesser trauma resulting from minor falls or fights is more likely to lead to delayed rupture.5 In the present case it was a simple fall.

The cause of death was given as hemorrhagic shock after delayed rupture of spleen due to blunt force trauma.

Although rare, the possibility of splenic rupture should always be considered in the differential diagnosis in patients with blunt chest and/or abdominal trauma, even when he is hemodynamically stable. Repeated radiologic imaging during the latent period is of great value in establishing diagnosis. However a normal ultra sound or CT scan does not exclude a delayed splenic rupture. A close clinical vigilance is required as almost invariably patient will present with signs and symptoms of acute intraperitoneal hemorrhage.

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REFERENCES

1. Kluger Y, Douglas BP, Raves JJ, et al. Delayed rupture of the spleen-myths, facts and their importance: case reports and literature reviews. J Trauma. 1994;36:568–571.

2. Webb RC. Traumatic rupture of the normal spleen with delayed haemorrhage. Lancet. 1939;59:545–547.

3. Cox EF. Blunt abdominal trauma: a 5-year analysis of 870 patients requiring celiotomy. Ann Surg. 1984;199:467–474.

4. DiMaio DJ, DiMaio VJ. Forensic Pathology. 2nd ed. Boca Raton, FL: CRC Press; 2001:135–136.

5. Farhat GA, Abdu RA, Vanek VW. Delayed splenic rupture: real or imaginary? Am Surg. 1992;58:340–345.

6. Schwartz SI, Shires GT, Spencer FC. Principles of Surgery. 5th ed. New York, NY: McGraw-Hill Book Company; 1989:271–273.

7. Simpson RA, Ajuwon R. Occult splenic injury: delayed presentation manifesting as jaundice. Emerg Med J. 2001;18:504–505.

8. Hiraide A, Yamamoto H, Yahata K, et al. Delayed rupture of the spleen caused by an intrasplenic pseudoaneurysm following blunt trauma: case report. J Trauma. 1994;36:743–744.

9. Fabin TC, Mangiante EC, White TJ, et al. A prospective study of 91 patients undergoing both computed tomography and peritoneal lavage following blunt abdominal trauma. J Trauma. 1986;26:602–607.

10. Dang C, Schlater T, Bui H, et al. Delayed rupture of the spleen. Ann Emerg Med. 1990;19:399–403.

11. Black JJ, Sinow RM, Wilson SE, et al. Subcapsular haematoma as a predictor of delayed splenic rupture. Am Surg. 1992;58:732–735.

Keywords:

blunt trauma; spleen; delayed rupture

© 2009 Lippincott Williams & Wilkins, Inc.

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