Duodenal hematoma in pediatric age: a rare case report

Abstract

In pediatric age, duodenal hematoma is rare and generally occurs following a closed abdominal trauma due to the crushing of the duodenum against the rigid plane of the spine; it rarely follows anticoagulant therapy, pancreatitis, bleeding disorders, vasculitis, tumors or upper digestive endoscopy. Duodenal hematoma is a rare cause of obstruction of the upper gastrointestinal tract and acute pancreatitis, and the diagnosis is sometimes difficult and late. On the other hand, the identification of the pathology in its initial stages allows the young patients to be subjected to a conservative treatment that resolves the issue most of the time, thus avoiding surgery. In this article we describe an unusual case of duodenal hematoma, following esophagus-gastro-duodenoscopy, in a 12-year-old boy with Di George syndrome.

Introduction

Duodenal hematoma is a rare condition in children, and most of the cases described in the literature concern young adults under the age of 30 [1, 2]. In 2–5% of cases, it occurs following a closed abdominal trauma due to the compression of the duodenum against the spine. Even less frequently, it is linked to other causes such as anticoagulant therapy, pancreatitis, bleeding disorders, vasculitis, tumors or upper digestive endoscopy [1–4]. Duodenal hematoma is a rare cause of obstruction of the upper gastrointestinal tract that can be associated with acute pancreatitis and cholestasis; therefore, a timely diagnosis is essential for the prevention of serious complications, such as heart attack and intestinal perforation, pancreatic necrosis, cholangitis, diffuse peritonitis, sepsis, and shock [1–5]. Early recognition of the little patient with duodenal hematoma allows for a conservative treatment, almost always decisive, avoiding surgery [1, 3–6]. In this article, we report the case of a 12-year-old boy with Di George syndrome who presented with an abdominal mass caused by an iatrogenic duodenal hematoma associated with upper gastrointestinal obstruction and acute pancreatitis.

Case report

In June 2020, a 12-year-old boy arrived in the emergency room for epigastric pain, nausea and vomiting that had occurred for about 24 h. The history revealed that the child had Di George syndrome and suffered from gastroesophageal reflux disease (GERD); the day before the onset of symptoms, he went to another hospital to undergo an upper gastrointestinal endoscopy, and was discharged in apparent good health. The physical examination of the abdomen of the little patient revealed no signs of peritonitis, but showed a palpable mass in the epigastric region. The child was subjected to laboratory and instrumental investigations. Blood tests showed low hemoglobin (10 g/dl), leucocytosis with neutrophilia and increased C-reactive protein, pancreatic amylase and lipase; in addition, there was a minimal increase in direct bilirubin (0.36 mg/dl). The child had no personal or family history of bleeding disorders, and tests performed in our laboratory, such as platelet count, prothrombin time and activated partial thromboplastin time, were normal. Chest X-ray examination was negative. The ultrasound of the abdomen revealed in the right hypochondrium, between the pancreas head and the hepatic hilum, a voluminous expansive formation of elongated morphology, which, going beyond the midline, in front of the large vessels, extended into the left hypochondrium; the mass presented inhomogeneous mixed echostructure, without vascular signal to color Doppler; the pancreas showed dimensions and echostructure within the limits, and the gallbladder appeared distended and with inhomogeneous contents due to the presence of biliary sludge (Fig. 1). In addition, ultrasound showed gastrectasis with abundant fluid stagnation and free corpuscle fluid in all peritoneal recesses. After the introduction of the nasogastric tube (SNG) and the intravenous infusion of liquids, the child was subjected to direct radiographic examination of the abdomen, which showed gas over distension of the loops of the small intestine with low colonic meteorism and hydro-aereal levels in the left hypochondrium-flank, as well as an absence of free air (Fig. 2). The next day, the little patient underwent CT of the abdomen and pelvis without and with contrast medium. CT showed a gross collection in the upper abdomen with morphology comparable to duodenal C. The collection showed super-fluid densitometry coefficients in the basal acquisitions without significant post-contrast enhancement. Therefore, the interpretation of CT images with multiplanar reconstructions (MPR) and the anamnesis of the small patient identified a voluminous intramural hematoma of the entire posterior wall of the duodenum, resulting from esophagus-gastro-duodenoscopy (EGDS); the duodenal lumen appeared partially collapsed, without signs of stasis upstream, due to the presence of a suction tube in the gastric area. In addition, the CT showed an edematous appearance of the body-tail of the pancreas with fluid imbibition of the peripancreatic adipose tissue and free corpuscle fluid in all quadrants of the abdomen (Fig. 3). The following day, the child repeated the blood tests, which showed the resolution of the neutrophilic leucocytosis, the reduction of pancreatic amylase and the normalization of lipase. Three days after the CT examination, the child underwent MRI of the upper and lower abdomen without and with contrast medium. MRI confirmed the presence of the voluminous duodenal hematoma which, due to the different phases of hemoglobin degradation and colliquation phenomena, presented a remarkably inhomogeneous signal both in T1 and T2 weighted images, without significant enhancement in the dynamic T1 sequences after administration of contrast medium. MRI also confirmed distention of the gallbladder with endoluminal biliary sludge and the presence of free intra-peritoneal fluid (Fig. 4). Finally, the pancreas showed no significant signal changes, and the Wirsung duct and the intra- and extra-hepatic biliary tracts did not appear dilated. The little patient continued the conservative treatment with nasogastric aspiration and parenteral nutrition (PN) and underwent control ultrasound examinations. 3 weeks after diagnosis, MRI showed complete resorption of the duodenal hematoma, and the child was declared clinically cured.

Fig. 1.

Upper abdomen ultrasound. The transversal scans show an expansive formation in the center of the abdomen, with mixed, mainly iso-hyperechoic echostructure with contextual hypo-anechoic areas of fluid aspect (a, b); the mass does not show vascularity on color Doppler (b). The transverse oblique subcostal scan highlights distended gallbladder with biliary sludge (c)

Fig. 2.

Plain X-ray of the abdomen in orthostasis shows air–fluid levels in the left hypochondrium/flank

Fig. 3.

Axial abdominal CT images before (a) and after contrast agent (b) show hyperdense duodenal collection (a) without post-contrast enhancement (b). Coronal (c) and axial (d) post-contrast CT images highlight the C-shaped duodenal hematoma (c), and slight volumetric increase and nuanced hypodensity of the body/tail of the pancreas (d) with fluid imbibition of the peripancreatic fat tissue (c, d)

Fig. 4.

Axial T1-weighted FFE (a) and T2-weighted TSE (b) MR images show voluminous duodenal hematoma with markedly heterogeneous signal, largely isointense on T1-weighted image and predominantly hypointense on T2-weighted image, with contextual foci appearing hyperintense on T1- and hypointense on T2-weighted images (white arrows in a and b). Moreover, inside the hematoma are visible areas of intermediate/high signal on T2- (white arrowhead in b) and low signal on T1-weighted images, of which the largest is hyperintense with a peripheral rim (white arrowhead in a). The lumen of the gallbladder appears hyperintense on T1-weighted image due to the presence of biliary sludge (* in a)

Discussion

We presented the case of a 12-year-old boy with Di George syndrome, which is a genetic disease caused by a microdeletion of the long arm of chromosome 22 and which causes gastrointestinal complications in about 30% of cases [7]. Our patient suffered from GERD, and following an EGDS with multiple biopsies, he developed a duodenal hematoma. Hematoma after duodenal biopsy is a rare complication; it is estimated that in children, the incidence is 1 in 1250 upper digestive endoscopies [8]. In a 2006 review, Diniz-Santos et al., identified 18 published cases of post-endoscopic duodenal hematoma, and of these patients, 13 were under the age of 21 [9, 10]. Duodenal hematoma has sometimes developed in patients with impaired blood clotting or with platelet dysfunction and in children with leukemia after bone marrow transplant [11]; however, it often happens that no predisposing conditions are identifiable, and our child was one who did not have any risk factors [8–12]. The anatomical features of the duodenum, such as predominantly retroperitoneal localization, poor mobility due to close adherence to the posterior abdominal wall, and rich submucosal vascular plexus, are believed to favor the formation of post-biopsy hematoma in otherwise healthy patients [2, 8, 10–12]. The typical clinical presentation of duodenal hematoma is represented by symptoms of obstruction of the upper gastrointestinal tract, such as abdominal pain, nausea and vomiting, which generally occur a few hours after performing the biopsy and rarely after a few days or weeks; it follows that the diagnosis of iatrogenic duodenal hematoma is probable when the obstructive symptomatology arises within 48 h of the endoscopic procedure, as happened in our case [1, 2, 5, 6, 8–12]. 21–40% of patients also have acute pancreatitis, which can be caused either by the obstruction of the ampulla of the Vater or by the compression exerted by the duodenal hematoma on the pancreas; in our case, the mass effect of the blood collection had determined a mild acute pancreatitis, and had hindered the biliary outflow with stagnation of bile in the gallbladder, in the absence of dilation of the Wirsung duct and the biliary tree [1, 2, 5, 8–12]. Ultrasound is the first-choice radiological investigation in children with gastrointestinal symptoms, since it is a rapid, non-invasive, readily available diagnostic method and does not involve exposure to ionizing radiation. In addition, in pediatric age, the ultrasound study of the abdomen can be performed both with convex probes and with high-frequency linear transducers thanks to the scarce presence of subcutaneous adipose tissue and the reduced depth of the abdominal structures [5, 10–13]. Ultrasound provides immediate information on the presence and age of the hematoma with high diagnostic accuracy, and typically detects a non-vascularized mass adjacent to the head of the pancreas and with an elongated shape in transverse scans; the echostructure is initially uniform and iso-hyperechoic, becoming more and more heterogeneous during the phases of organization and resorption of the hematoma, due to the growing development of hypo-anechoic fluid areas, as demonstrated by our ultrasound examinations [1, 2, 8, 10–12]. In patients with duodenal hematoma, ultrasound is very useful for studying the structures of the upper right quadrant of the abdomen, and in particular for evaluating the liver, biliary tract, gallbladder and pancreas. In our case, the ultrasound detected with great accuracy the absence of dilation of the intra- and extra-hepatic biliary tracts and the presence of biliary sludge in the lumen of the gallbladder; the pancreas did not show echo-structural alterations, and this confirmed the low diagnostic sensitivity of the ultrasound method, which is negative in 50% of children with mild acute pancreatitis [8, 10, 13, 14]. In consideration of its safety and low cost, ultrasound is a valuable tool for controlling the resorption of duodenal hematoma in children hospitalized and undergoing conservative treatment [2, 8–12]. In spite of its numerous advantages, ultrasound is a highly operator-dependent method, and not very specific for the diagnosis of duodenal hematoma, posing problems of differential diagnosis with solid tumor and pancreatic pseudocyst. Moreover, it is an investigation with a reduced field of view and does not allow a precise assessment of the extent of the duodenal hematoma [8–10]. In our case, diagnostic completion was performed first with CT and then with MRI. As our images show, on CT examination the hematoma appears as a mass in the context of the duodenal wall, hyperdense in the basal phase and without enhancement in post-contrast acquisitions, and coronal reconstruction allows to establish its exact extension; the mass shows homogeneous density with high attenuation in the acute/subacute phase (50–90 UH) and subsequent reduction in density and size [1, 2, 5, 8, 10–12]. CT can show obstruction of the duodenum and the presence of secondary acute pancreatitis, as happened in our case, and can also show signs of a duodenal perforation such as minimal amounts of free air in the abdominal cavity and/or extraluminal spread in contrast medium administered orally; the simultaneous presence of air and free liquid in the supramesocolic spaces is highly suggestive of duodenal perforation, which must be promptly diagnosed, since a delayed surgical intervention determines a significant increase in the mortality rate [2, 8, 9, 12, 13]. CT exposes children to ionizing radiation, and, therefore, the imaging methods used in the follow-up of small patients with duodenal hematoma are ultrasound and/or MRI [2, 8, 9]. MRI is a diagnostic technique that does not use ionizing radiation and exploits the properties of magnetic fields to obtain images with high contrast resolution, acquired directly in three dimensions [2, 9, 16]. MRI allows further characterization of the duodenal hematoma for the modification of the signal induced by the different hemoglobin degradation products. In our case, the MRI, performed 7 days after the biopsy was performed, showed the marked inhomogeneity of the duodenal hematoma signal in both T1 and T2 sequences, unlike what happens in intracranial hematomas; in fact, the duodenal hematoma was mainly made up of deoxyhemoglobin (signal largely iso-hypointense in T1 and hypointense in T2) with hyperintense foci in T1 and hypointense in T2 attributable to methemoglobin [2, 3, 16]. Moreover, thanks to its high contrast resolution, MRI can identify minimal inflammation of the pancreatic parenchyma, and with cholangiography sequences, it allows for a detailed study of the intra- and extra-hepatic biliary tracts, of the cystic duct, of the gallbladder and of the duct of Wirsung[15]. MRI findings were negative for biliopancreatic disease, and the child's clinical condition was continuously and progressively improving [2, 13]. Conservative management of patients with duodenal hematoma achieves excellent results, and complete resolution of the hematoma generally occurs within 3 weeks of diagnosis, as happened in our case; surgery is necessary in hemodynamically unstable patients, in suspected or overt cases of duodenal perforation, or if no clinical improvement has been achieved within 7–14 days with conservative treatment [1, 4–6, 8–11, 16, 17].

Conclusions

Our case demonstrates the importance of considering duodenal hematoma in children presenting symptoms of upper gastrointestinal obstruction and/or acute pancreatitis following an upper digestive endoscopy with duodenal biopsy, even in the absence of coagulation disorders or other identifiable risk factors. The patient’s clinical history and ultrasound examination are already sufficient to formulate the diagnosis, which must be timely to avoid the onset of serious complications. The prognosis is good, as most children undergoing conservative treatment recover within 3 weeks of diagnosis, and ultrasound, due to the absence of ionizing radiation and the speed of execution, is extremely useful in monitoring the resorption of duodenal hematoma.

Compliance with ethical standards

Disclosures

The Authors declare that they have no conflict of interest.

Informed consent

All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, and its late amendments. Additional informed consented was obtained from all patients for which identifying information is not included in this article.

Human and animal rights

This article does not contain any studies with human or animal subjects performed by any of the Authors.