Acute intussusception 15 years postgastrectomy

Correspondence ACUTE INTUSSUSCEPTION 15 YEARS POSTGASTRECTOMY To the Editor:—Intussusception is a rare complication of all types of gastric resection and occurs in less than 0.1% of gastric resections.1 Early diagnosis is extremely important because delayed diagnosis could result in bowel ischemia that can be fatal. The mortality rate of this condition is as high as 50% if surgery is delayed for more than 48 hours.2 We report on a patient with acute jejunogastric intussusception that occurred 15 years after the gastric surgery. A serial workup and computed tomography (CT) confirmed the timely diagnosis. The patient was a 37-year-old woman who presented to the ED several hours after the onset of severe epigastric pain and coffeeground emesis. She had undergone a partial gastrectomy and Billroth II gastroenterostomy for gastric cancer approximately 15 years earlier. Physical examination revealed an ill-defined palpable mass in the left upper quadrant. Laboratory finding showed anemia (hemoglobin ⫽ 9.7 g/dL). Endoscopy revealed a large oozing blood clot in the afferent loop. Sonographic examination showed a mixed echogenic mass lesion with a peripheral rim in the left upper quadrant. CT showed a long segment of the jejunum with a thickened bowel wall in a markedly dilated lumen. The fat density indicated that mesentery was present in the dilated lumen (Fig 1). No definite free air or air bubble in the bowel wall was identified. These findings are consistent with intussusception. An exploratory laparotomy was performed after the CT study. In addition to the previous partial gastrectomy with Billroth II anastomosis and a Braun procedure, we found a markedly dilated afferent loop distal to the enteroanastomosis and approximately 70 cm of efferent loop retrograde invaginated into the dilated afferent

© 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2205-0003$30.00/0 doi:10.1016/j.ajem.2004.02.030

loop and remnant of the stomach through the enteroanastomosis. After reduction, the invaginated jejunum showed hemorrhagic and gangrenous change, and was then resected. No leading point was found. The patient recovered smoothly and was discharged. Jejunogastric intussusception after gastric resection can be classified into four types: type I (5.5%)—afferent limb intussusception, type II (75.5%)— efferent limb intussusception, type III (6.5%)—a combination of type I and II, and type IV (8%)— intussusception through a Braun side-to-side enteroanastomosis.3 Our case was classified as type IV. Jejunogastric intussusception usually presents with sudden epigastric pain, tenderness, vomiting, and a palpable mass (in 33-50% of cases) and the emesis becomes bloody because of compromised jejunal vascular supply. These symptoms also occur in high intestinal obstruction as a result of other causes.4,5 The diagnosis of acute intussusception after gastric resection is rarely established on clinical examination, and multiple image modalities such as endoscopy, sonography, and CT provide valuable assistance in making the diagnosis. Endoscopy is becoming the diagnostic procedure of choice for the patient with hematemesis, but could be difficult in patients with acute jejunogastric intussusception. The intussusceptum could be mistaken as an immobile clot on endoscopy like in our case.3,5 Sonography demonstrates an echogenic center surrounded by concentric echogenic rings with a peripheral rim of hypoechogenicity, described as “pseudokidney” or “doughnut” sign. Sonography is a convenient bedside diagnostic tool, but the procedure is highly technique- and experience-dependent. Gasfilled bowel loops commonly seen in patients with acute abdomen could ruin the images. CT, unaffected by bowel gas, provides a global perspective of the gut, mesenteries, omentum, peritoneum and retroperitoneum and is becoming the premier technique for patients with acute abdomen.6 CT also led to the correct diagnosis in our case. The typical CT feature of intussusception is a soft tissue mass with a “sausage” or “target” appearance. If a long

FIGURE 1. Emergency computed tomography shows mass-like, thickwalled bowel loops (arrowheads) and a markedly dilated afferent loop (arrow). Fat attenuation shows mesenteric fat (small arrow) also entrapped in the dilated lumen. The findings are consistent with intussusception.

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AMERICAN JOURNAL OF EMERGENCY MEDICINE ■ Volume 22, Number 5 ■ September 2004

segment of the jejunum is invaginated into the residual stomach or a dilated afferent or efferent loop, CT could show thick-walled bowel loops in a bag-like dilated lumen, like our case. Other CT features include entrapped mesenteric fat and mesenteric vessels. Intraluminal air, suggesting bowel infarction, can sometimes be detected. Intussusception after gastric surgery could become more frequently seen because of the increased numbers of gastric bypass surgeries for morbid obesity and improved survival after gastric cancer surgery. To reduce delays in diagnosis, we should keep in mind that intussusception is a possibility when a patient presents with hematemesis, even many years after gastric surgery. HSIU-CHEN SHIH, MD CHIH-HSING WU, MD Department of Radiology En Chu Kong Hospital Taipei, Taiwan MING-TE HUANG Department of Surgery En Chu Kong Hospital Taipei, Taiwan

References 1. Wheatley MJ: Jejunogastric intussusception diagnosis and management. J Clin Gastroenterol 1989;11:452-454 2. Hovelius L: Jejunogastric intussusception after gastric resection, a report of two cases. Acta Chir Scand 1971;137:491-494 3. Brynitz S, Rubinstein E: Hematemesis caused by jejunogastric intussusception. Endoscopy 1986;18:162-164 4. Walstad PM, Ritter JA, Arroz V: Delayed jejunogastric intussusception after gastric surgery: an ever-presented threat. Am Surg 1972;38:172-175 5. O’Dell KB, Gordon RS, Victory C: Acute jejunogastric intussusception: a rare cause of abdominal pain. Ann Emerg Med 1992; 21:565-567 6. Gore RM, Miller FH, Pereles FS, et al: Helical CT in evaluation of the acute abdomen. AJR. Am J Roentgenol 2000;174:901-911

MENINGOVASCULAR SYPHILIS AND IMPROVEMENT WITH TISSUE-PLASMINOGEN ACTIVATOR (T-PA) To the Editor:—Meningovascular syphilis is commonly sited as a common cause of stroke in young patients, but it has an unusual presentation that can commonly be misdiagnosed. Once a common disease, meningovascular syphilis has become rare since the advent of antibiotics. Now with the rise in the incidence of primary and secondary syphilis, corresponding increase in neurosyphilis may become a more common cause for stroke, especially in young adults.1 Meningovascular syphilis a form of neurosyphilis now accounts for approximately 38.5% of all cases of neurosyphilis.2 Thus, in a young patient presenting with a focal neurologic deficit, meningovascular syphilis must be added to the differential diagnosis. Furthermore, the optimal treatment for any form of neurosyphilis is uncertain, and certainly meningovascular syphilis is no exception. We report a young individual presenting with a focal neurologic deficit who was later found to have meningovascular syphilis. The patient was treated with tissue plasminogen activator (t-PA) emergently with immediate improvement in neurologic status. A 33-year-old Hispanic man from Mexico was brought to the emergency department (ED) after developing right-sided weakness, dysarthria, and right facial droop since approximately 10:00 AM. Patient was alert, awake and spoke to EMS staff and friends

© 2004 Elsevier Inc. All rights reserved. 0735-6757/04/2205-0004$30.00/0 doi:10.1016/j.ajem.2004.04.015

at home. However, by the time the patient arrived in the ED, he was obtunded and responded only to tactile stimuli. The patient’s friends stated that he had loss of appetite for the past 3 months and a severe headache for the past 3 weeks. No further history could be obtained. On examination, his blood pressure was 126/76 mm Hg; pulse, 92 beats/min; respiration, 21 breaths/min; temperature, 39.2 0 C. There was a right upper motor neuron facial palsy, dysarthria, right hemiparesis with hyperreflexia and Babinski’s sign. The remainder of the neurologic examination was normal. A computed tomographic scan of the head without contrast was normal and the patient did not have any exclusion criteria for the administration of t-PA. t-PA was given to this patient with subsequent improvement. Patient’s alertness, dysarthria, and facial palsy improved dramatically post t-PA. The initial cerebrospinal fluid (CSF) analysis showed: 295 WBC/mm3 ( 78 % poly, 2% band, 17% lymph 3% mono); protein of 1.61 g/L (161mg/dL); glucose 52 mg/dL (serum glucose 140 mg/dL). Serum white blood cell (WBC) count was 9.5 X 109 L (9500 mm3). The patient was put on empiric antibiotic therapy with vancomycin, ceftriaxone, and acyclovir. A repeat lumbar puncture was performed on hospital day 3 with CSF results as follows: 66 WBC/mm3 ( 2 % poly, 98% lymph); protein of 1.16 g/L (116mg/dL); glucose 46 mg/dL (serum glucose 108 mg/dL). Coagulation profile and immunological screening tests were unremarkable. Cardiac source of an emboli was ruled out with a transesophageal echocardiogram (TEE). Cultures for bacteria, fungi, and other microorganisms were negative. Urine toxicology screening test was also negative. On hospital day 3, a repeat computed tomographic scan of the head with contrast revealed a new focus of decreased attenuation in the left pons and thalamus suggestive of acute infarction. Subsequently, a cerebral angiography was performed on hospital day 10 which showed occlusion at the distal basilar artery. Once the CSF and blood venereal disease research laboratory (VDRL) was found to be reactive (1:1) and (1:128), respectively the patient was started on aqueous (crystalline) penicillin G 4 million units IV every 4 hours. Serum rapid plasma reagin (RPR) was also found to be reactive (1:128) as well as microhemagglutination-Treponema pallidum (MHA-TP). Neurologic signs fluctuated in severity for the next 72 hours after therapy was initiated, but improvements were observed in the patient steadily. The patient was also found to be HIV ⫹. HIV-1antibody was detected by enzyme immunoassay and confirmed by Western blot analysis. T4 (CD4) count was 46/mm3; ESR, 80 mm/h. At the end of the 6-week course of antibiotics, the patient was alert and oriented to person, place, and time. There was minimal amount of residual dysarthria and right hemiparesis. The patient was discharged on hospital day 41 and instructed to follow up with primary physician in Mexico. Tertiary syphilis consists of 3 types: neurosyphilis, cardiovascular syphilis, and late benign (ie, gummatous) syphilis. Some symptoms of neurosyphilis are as follows by decreasing frequency: (1) personality change, 33%; (2) ataxia, 28%; (3) stroke, 23%; (4) ophthalmic symptoms (ie, blurred vision, decreased color perception, impaired acuity, photophobia); (5) headache,10%.3 Some signs of neurosyphilis include in order of decreasing frequency: (1) hyporeflexia, 50%; (2) sensory impairment, 48%; (3) pupillary changes, 43%; (4) cranial neuropathy; (5) dementia, mania, or paranoia, 35%.3 In our case, the patient had exhibited a new onset headache for the past 3 weeks. Including the headache, friends of the patient stated that the patient had been complaining of malaise and decreased appetite for several months. In many previous case reports of meningovascular syphilis, a description of a prodromal clinical course of several weeks to months before a focal neurologic deficit have been also described.2,4,5,6 Our case is no exception. Tertiary syphilis lesions are caused by an obliterative endarteritis, which usually involves the vaso vasorum of the central