Abdominal Apoplexy: A Case Report and Review

Abdominal Apoplexy: A Case Report and Review

The Journal of Emergency Medicine, Vol. 40, No. 3, pp. e49 – e52, 2011 Copyright © 2011 Elsevier Inc. Printed in the USA. All rights reserved 0736-467...

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The Journal of Emergency Medicine, Vol. 40, No. 3, pp. e49 – e52, 2011 Copyright © 2011 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$–see front matter

doi:10.1016/j.jemermed.2007.11.080

Clinical Communications: Adults

ABDOMINAL APOPLEXY: A CASE REPORT AND REVIEW John C. Cawyer,

MD

and C. Keith Stone,

MD, FACEP

Department of Emergency Medicine, Texas A&M University Health Science Center, College of Medicine, Scott & White Clinic, Temple, Texas Reprint Address: C. Keith Stone, MD, Department of Emergency Medicine, Texas A&M University Health Science Center, College of Medicine, Scott & White Clinic, 2401 South 31st St., Temple, TX 76508

e Abstract—Abdominal apoplexy, or the newer term, idiopathic spontaneous intraperitoneal hemorrhage (ISIH), represents a rare cause of non-traumatic intra-abdominal bleeding. As with any acute blood loss, this problem often presents to the Emergency Department (ED) for initial evaluation and resuscitation. The case of a 52-year-old man with abdominal pain and distention due to spontaneous intraperitoneal hemorrhage is presented. This patient developed impending cardiovascular compromise in the ED and was subsequently diagnosed by computed tomography scan as having an intra-abdominal hematoma. Emergent exploratory laparotomy was performed and the patient was found to have spontaneous bleeding from a branch of the middle colic artery that was ligated without complication. The patient recovered well with no recurrent bleeding. The pathophysiology, diagnostic approach, and treatment of ISIH are reviewed. © 2011 Elsevier Inc.

sidered with any patient with atypical abdominal pain, history of cardiovascular disease, and indication of hemodynamic instability or shock. A case of a middle-aged man presenting with abdominal pain resulting from ISIH is presented and the pathophysiology, diagnostic approach, and treatment are reviewed. CASE REPORT A 52-year-old man presented to the Emergency Department (ED) with approximately 12–18 h of abdominal pain and weakness with near-syncope on the morning of presentation. He had experienced a brief period of substernal chest pressure with associated palpitation and shortness of breath earlier in the morning that was limited in severity and duration with spontaneous resolution. He had progression of his pain through to the back and subjective sensation of abdominal distention. His past medical history was remarkable for multiple medical problems to include hypertension, hyperlipidemia, gout, seasonal allergies, and hypothyroidism. He denied use of tobacco; his family history was significant for early myocardial infarction. He had no other antecedent history and denied recent medication changes. Review of systems was generally unremarkable; he specifically denied nausea or vomiting, stool changes, or other associations. He denied any trauma. Vital signs were remarkable for a blood pressure of 119/77 mm Hg with a heart rate of 72 beats/min in triage

e Keywords—abdominal apoplexy; hemoperitoneum; middle colic artery aneurysm; visceral artery aneurysm

INTRODUCTION Abdominal apoplexy, the historical term for idiopathic spontaneous intraperitoneal hemorrhage (ISIH), was coined as a comparison to the cerebral counterpart (1). As an acute event, the patient with occult spontaneous hemorrhage is most likely to present for initial evaluation and resuscitation by the Emergency Physician. Although rare in occurrence, this disease process should be con-

RECEIVED: 30 May 2007; FINAL ACCEPTED: 9 November 2007

SUBMISSION RECEIVED:

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and 152 beats/min at the time of examination. The examination was additionally remarkable for an irregularly irregular heart rhythm without murmur. He had diffuse abdominal tenderness, worse within the lower quadrants. Pulses were all symmetric. Electrocardiogram showed atrial fibrillation with rapid ventricular response. He was treated with intravenous diltiazem with rapid rate control and subsequent spontaneous conversion to a normal sinus rhythm. His blood pressure remained stable throughout his ED stay. Hemoglobin was 13.0 g/dL with a hematocrit of 38.5%. Chemistry studies were essentially normal; creatine kinase profile was normal with troponin equivocal at 0.57 (normal ⬍ 0.4 ng/mL; possible angina or evolving myocardial infarction 0.4 –1.2 ng/mL). Ddimer was elevated at 0.75 (normal ⬍ 0.50 ␮g/mL). Coagulation studies were all within the normal range, with a prothrombin time of 13.6, international normalized ratio of 1.1, and a partial thromboplastin time of 26.4. With the history of abdominal pain with radiation to the back and the cardiovascular risk factors, the patient underwent a bedside abdominal ultrasound by the Radiology Department’s ultrasonographer to evaluate for aortic aneurysm. Due to the patient’s body habitus and bowel gas, the aorta could not be imaged by sonography. Only limited images of the right upper quadrant were obtained and the gallbladder, as visualized on these limited images, had a normal appearance. Because the patient remained hemodynamically stable, he was sent for an abdominal computed tomography (CT) scan with i.v. contrast. The CT scan was negative for abdominal aneurysm, but showed an ill-defined mass within the abdomen. Radiology recommended a repeat CT scan enhanced with oral contrast. The results of this scan showed two fluid densities around the spleen with an increased density and stranding noted at the upper abdomen around the body of the stomach and transverse colon (Figure 1). In addition, some involvement of the small bowel was noted, with the bulk of the increased density in the mesentery. There was no free air. All solid organs had a normal appearance. The fluid densities were felt to represent a hematoma. General surgery was consulted for emergent evaluation, given concern for an intra-abdominal hematoma with unknown source or mechanism for bleeding. The patient was taken for exploratory laparotomy, where a large intra-abdominal hematoma was found. The hematoma was seen extending into both upper quadrants, with the liver and spleen appearing normal. Additional hematoma was identified and removed from the lesser curvature, exposing significant bleeding from a branch of the middle colic artery that was ligated. Further exploration identified no additional bleeding after large volume irrigation. Blood loss was estimated at 2 L. The patient had an otherwise uneventful operative course.

J. C. Cawyer and C. K. Stone

Figure 1. Abdominal computed tomography scan with contrast demonstrating densities around the spleen (white arrowhead), increased density and stranding involving the body of the stomach (black arrowhead) and the transverse colon (gray arrowhead).

Pathology specimens of the middle colic artery demonstrated focal disruption of the elastic lamina with blood and fibrin within the wall of the blood vessel, and associated aneurysmal dilatation. Post-operatively, the patient recovered well and was discharged on postoperative day 4. Subsequent complication included a superficial thrombophlebitis of the left leg. He had a normal follow-up dobutamine stress echocardiogram and colonoscopy.

DISCUSSION ISIH was first reported by Barber in 1909; it was later termed “abdominal apoplexy” by Green and Powers in 1931 (1). Intra-abdominal hemorrhage may be secondary to blunt trauma, aneurysmal rupture (central or visceral), solid organ malignancy (hepatic or renal), or inflammatory erosive processes (pancreatitis or pseudocyst); it may be idiopathic as well (2). Bleeding may be intraperitoneal or retroperitoneal, and is frequently found in conjunction with hypertension (33–50%) and atherosclerosis (80 – 87%) (1–5). As described initially, rupture with subsequent hemorrhage in the absence of abdominal trauma is exceedingly rare (3,5,6). Such rupture is most often at the site of an aneurysm, as seen in this case, but around 30% of cases historically have no identifiable source (3,6). There is a 2–3:1 male predominance, with the majority of cases

Abdominal Apoplexy

presenting in the fifth and sixth decades of life. The literature cites approximately 3000 cases of aneurysmal rupture recorded to date (4,5,7,8). Predictably, aneurysms occur in classic locations. They are typically located at secondary or tertiary branch points from the aorta; 60% involve the splenic artery, 22% renal, and 10 –20% hepatic, with common celiac and mesenteric arteries less common (1,2,4,7). Historically, the aneurysms have been mycotic, syphilitic, or traumatic in origin, but now are more likely related to essential or portal hypertension (2). There is an additional association with rheumatologic disorders and alpha-1-antitrypsin deficiency (9). The previous enigmatic 20 –30% of apoplexy with no identifiable source is now thought to be related to common vascular disease, with arteriosclerosis and hypertension felt to represent risk factors (2). The exact mechanism is unknown, but likely represents weakness of the tunica media, predisposing rupture in the face of abrupt increases in pressure. Pathology specimens regularly exhibit disruption of elastic lamellae (1,3,10). Less frequently, spontaneous hemorrhage is seen with inflammatory erosive processes in the absence of aneurysm (2). This may explain the association with necrotizing arteritis seen with polyarteritis nodosa and rheumatoid arthritis (1). Solid organ pathology represents yet another possible source of intra-abdominal hemorrhage. This is seen with bleeding from renal, hepatic, ovarian, and endometrial malignancy as well as bowel tumors. Similar to traumatic injury rupture of pseudocysts, ectopic pregnancy, the gravid uterus, or ovarian cysts; these should not be misinterpreted as idiopathic spontaneous bleeding (2,6). The presentation and clinical progression of abdominal apoplexy frequently follows a rather predictable course. Before rupture, there may be a history of vague abdominal pain, possibly with symptoms of local compression of the portal vein, biliary system, or pancreas (3,7). Physical examination before or soon after rupture is likely to be relatively normal. Although no one finding is pathognomonic, there may be icterus, a bruit, or a mass, depending on location (3,4). Symptoms may consist of diffuse abdominal pain, nausea or vomiting, and disturbance of bowel habit (1–7). A latent period of up to several hours may be exhibited, followed by a terminal phase with rapid progression of symptoms (1). The pain is felt to relate to rapidity and volume of extravasation rather than peritoneal irritation by blood (8). During this late phase, manifestations of peritonitis, hypovolemia, worsening pain, and eventually shock may become apparent without rapid intervention (1,8). This case as described illustrates an abatement of initial symptoms with subsequent latency. Given the development of dysrhythmia and tachycardia, elevation of cardiac bio-

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marker, and abdominal tenderness on examination, the patient was likely entering the more severe terminal phase of the process upon presentation to the ED. Diagnostic evaluation specific to abdominal apoplexy is largely dependent on imaging techniques. Some 60 years ago there were no diagnoses made before surgical intervention (3). Today, rarity of the process and lack of suspicion continue to represent diagnostic delay (11). In the hemodynamically unstable patient, FAST (focused assessment by sonography in trauma) examination may be useful to detect intra-abdominal hemorrhage. However, CT scan represents the most important imaging technique, with peritoneal lavage (DPL), endoscopy, ultrasound, traditional angiography, and magnetic resonance imaging (MRI) held as complementary. The use of both oral and i.v. contrast is currently recommended if the patient is stable enough for the delay associated with administering oral contrast. CT angiography of vessels has proven useful as a screening tool, using small amounts of contrast to elucidate sites of active bleeding (4,8). Before advancements in helical CT scanning, imaging of lesions smaller than 7 mm was limited (5). Predictably, radiographic appearance depends on the location, age, and extent of bleeding (8). DPL is noted to be the most sensitive test to identify ISIH, but is likewise most invasive (6). Ultrasound is the modality of choice for pelvic hemorrhage, given the high sensitivity for detecting intrapelvic fluid (8). Selective visceral angiography has proven accurate for detecting splanchnic artery aneurysms that would otherwise be undetectable before onset of symptoms (7). MRI has not yet proven practical. Double-contrast CT imaging provided adequate initial localization for the case described; his rupture was further localized intraoperatively, with definitive treatment in the form of arterial ligation. Treatment of spontaneous intraperitoneal bleeding, as with other bleeding phenomena, revolves around resuscitation and correction of the underlying problem. This has traditionally been via surgical correction. For the Emergency Physician, simultaneous restoration of circulating volume and rapid diagnosis are key in determining patient outcome. For aneurysmal rupture, the patient may then undergo definitive treatment in the form of ligation, aneurysmectomy, gastrectomy, or embolization (2,5). Trans-arterial embolization has recently been described as the treatment of choice. Intervention is determined by location, type, and size of the aneurysm, as well as age and condition of the patient (5). Outcomes, paralleling advancement in diagnosis and treatment, have improved drastically over several decades. Risk of rupture of the described aneurysms varies with the vessel involved and ranges from 70% to 90% (4,5). Non-surgical mortality has historically approached 100%. Reported mortality with non-therapeutic explor-

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atory laparotomy varies from 40% to 66% (2). Surgical ligation represents the most well studied definitive treatment, reducing mortality to 8.6% (1). After ligation there are no reported recurrences (3). CONCLUSION Abdominal apoplexy represents a rare but life-threatening process presenting initially for evaluation in the ED. Alongside trauma, solid organ rupture, and erosive processes, this uncommon entity represents a true emergency. Over the past half-century, significant advancements in diagnostic imaging and options for definitive care have allowed for further improvement in evaluation and treatment. Early recognition, diagnosis, and rapid treatment initiated by the Emergency Physician remain central to a successful outcome. REFERENCES 1. Carmeci C, Munfakh N, Brooks JW. Abdominal apoplexy. South Med J 1998;91:273– 4.

2. Carr SR, Dinsmore RC, Wilkinson NW. Idiopathic spontaneous intraperitoneal hemorrhage: a clinical update on abdominal apoplexy in the year 2001. Am Surg 2001;67:374 – 6. 3. Berk JE, Rothschild NS, Doane JC. Intraabdominal apoplexy. Ann Surg 1941;113:513–20. 4. Rohatgi AA, Cherian TT. Spontaneous supture of a left gastroepiploic artery aneurysm. J Postgrad Med 2002;48:288 –9. 5. Matsuo S, Yamaguchi S, Miyamoto S, et al. Ruptured aneurysm of the visceral artery: report of two cases. Surg Today 2001;31: 660 – 4. 6. Suber WJ Jr, Cunningham PL, Bloch RS. Massive spontaneous hemoperitoneum of unknown etiology: a case report. Am Surg 1998;64:1177– 8. 7. Borioni R, Garofalo M, Innocenti P, et al. Hemoperitoneum due to spontaneous rupture of an aneurysm of the left gastroepiploic artery. J Cardiovasc Surg (Torino) 1999;40:63– 4. 8. Mortele KJ, Cantisani V, Brown DL, Ros PR. Spontaneous intraperitoneal hemorrhage: imaging features. Radiol Clin North Am 2003;41:1183–201. 9. Chino O, Kijima H, Shibuya M, et al. A case report: spontaneous rupture of dissecting aneurysm of the middle colic artery. Tokai J Exp Clin Med 2004;29:155– 8. 10. Nissman SA, Mann BD, Vitvitsky EV, Fyfe BS. Spontaneous nontraumatic hemoperitoneum due to a bleeding arteriovenous malformation on the serosal surface of the transverse colon: a case report. Am Surg 2002;68:911–2. 11. Schattner A, Kozack N, Friedman J. Idiopathic spontaneous hemoperitoneum. Arch Intern Med 2001;161:1009 –10.