Intramural Hemorrhage Research Articles

Diseases mimicking intussusception: Diagnostic dilemma

Intussusception is a common abdominal emergency in early childhood. The aim of this study was to describe the diseases mimicking intussusception and to discuss the causes and management of these conditions. Seven patients who were initially diagnosed as having intussusception on abdominal ultrasonography but who had a final diagnosis of diseases other than intussusception were reviewed retrospectively. Two patients with ileocolic intussusception underwent ultrasonography-guided reduction with a hydrostatic method but the ultrasonographic findings persisted. At surgery, only edematous ileocecal valve and mesenteric lymphadenopathy were observed. In three patients with Henoch-Schönlein purpura, initial abdominal ultrasonography showed intussusception. The patients with no sign of obstructive symptoms were managed conservatively with a diagnosis of intramural hemorrhage and on follow up the ultrasonographic findings of intussusception was resolved. One patient with the target sign on computed tomography and ultrasonography of the abdomen underwent ileocolic resection and end-to-end anastomosis due to a tumor in the cecum. There was no evidence of intussusception. One patient with a cyst in the right lower quadrant accompanying intussusception on ultrasonography of the abdomen underwent ultrasonography-guided reduction but the ultrasonographic findings persisted. On exploration, only cecal duplication cyst without intussusception was detected. Cecal resection including the cyst and end-to-end ileocolic anastomosis were performed. Ultrasonography, color Doppler ultrasonography, barium or hydrostatic enema and computed tomography are helpful in diagnosing intussusception, but patients with radiologic findings of intussusception should be evaluated on symptoms and clinical findings before surgical intervention. Also, other diseases mimicking intussusception should be kept in mind in the differential diagnosis.

Acute Aortic Dissection Diagnosed after Embalming: Macroscopic and Microscopic Findings

A 58-year-old man died suddenly in Madagascar and poisoning was suspected. The body was embalmed after death and the general state of preservation was good. We found a major aortic dissection with a large false lumen from the aortic root to the common iliac arteries and a hemopericardium with formalinized blood clot. The intimal tear was on the ascending aorta, and an intramural hemorrhage was noted at the right coronary artery, attesting to a retrograde dissection. Microscopic studies confirmed aortic dissection with extensive intramural hemorrhage and also confirmed the retrograde dissection to the right coronary artery with a reduction of 90% of the true lumen. Classically, aortic dissection occurs in individuals with hypertension and individuals with genetic disorders of collagen formation. The diagnosis is often first established at the postmortem examination. Aortic dissection is therefore dealt with largely in necropsy studies. The usual cause of death is rupture into the pericardial sac. One case of bloodless dissection has been reported but the sudden death was explained by acute myocardial ischemia secondary to dissection of the left coronary artery. In our case, we found major hemopericardium and also intramural hemorrhage at the right coronary artery. We were able to make the diagnosis of aortic dissection and exclude the suspicion of homicide 15days after death and after embalming.

Otvaranje koronarne arterije u primarnim PCI ne znači uvek i optimalni protok i najpovoljniji ishod za bolesnika - tretman 'no reflow' fenomena

Microvascular obstruction (MVO) commonly occurs following percutaneous coronary interventions (PCI), may lead to myocardial injury, and is an independent predictor of adverse outcome. Severe MVO may manifest angiographically as reduced flow in the patent upstream epicardial arteries, a situation that is termed 'no-reflow.' The no-reflow phenomenon was originally observed in experimental models of acute myocardial infarction (MI) and was described as a failure to restore normal myocardial blood flow despite removal of the coronary obstruction. Defined angiographically, no-reflow manifests as an acute reduction in coronary flow (TIMI grade 0-1) in the absence of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion. Lesser degrees of flow impairment (TIMI grade 2) are generally referred to as 'slow-flow'. However, studies of acute MI patients have reported that scintigraphic evidence for no-reflow may occur in the absence of angiographic slow-flow, suggesting that microvascular injury may be angiographically inapparent in some patients. The mechanisms and mediators responsible for noreflow remain speculative, but the end result appears to be severe microvascular dysfunction. Potential mechanisms of microvascular dysfunction include vasospasm, distal embolization of thrombus or other debris, oxygen free radical mediated endothelial injury, capillary plugging by erythrocytes and neutrophils, and intracellular/interstitial edema with intramural hemorrhage. Microvascular obstruction can be broadly categorized according to the duration of myocardial ischemia preceding PCI. In 'interventional MVO' (e.g., elective PCI), obstruction typically involves myocardium that was not exposed to acute ischemia before PCI. Conversely 'reperfusion MVO' (e.g., primary PCI for acute myocardial infarction) occurs within a myocardial territory that was ischemic before the coronary intervention. Interventional and reperfusion MVO have distinct pathophysiological mechanisms and may require individualized therapeutic approaches. Interventional MVO is triggered predominantly by downstream embolization of atherosclerotic material from the epicardial vessel wall into the distal microvasculature. Reperfusion MVO results from both distal embolization and ischemia-reperfusion injury within the subtended ischemic tissue. Randomized clinical trials have studied strategies for prevention of MVO and no-reflow; however, the efficacy of measures for reversing MVO once no-reflow has been demonstrated angiographically is unclear. New approaches for prevention and treatment of MVO will require a better understanding of intracellular cardioprotective pathways such as the blockade of the mitochondrial permeability transition pore.

The Donut Sign: A New Angiographic Sign for Partially Thrombosed Aneurysms with Flow-Induced Intraluminal Thrombus

Three patients are described with unruptured large partially thrombosed aneurysms with a peculiar donut-shaped remaining lumen. Observations suggest that the flow geometry of the aneurysm and parent vessels induces a preferential circular laminar flow inside the aneurysm followed by partial intraluminal thrombosis leaving a donut-shaped lumen to accommodate the circular flow. This flow mechanism of thrombus formation inside aneurysms is different from the more common repeated intramural dissections and hemorrhages that cause growth in most large and giant partially thrombosed aneurysms.

Myocardial Rupture following Carbon Monoxide Poisoning.

We present the first case of severe cardiotoxicity of carbon monoxide leading to myocardial rupture and fatal outcome. 83-year-old woman was hospitalized 4 hours after the fire in her house with no respiratory or cardiac symptoms. After two days, she has suffered sudden collapse leading to cardiac arrest. Postmortem examination revealed intramural haemorrhage with myocardial rupture at the apex of the left ventricle. Minimal stenosis was noted in the proximal coronary arteries with no evidence of distal occlusion or any other long-standing heart disease. This case supports recommendations for targeted cardiovascular investigations in cases of CO poisoning.

Mutation Analysis and Clinical Sprectrum Of Patients With Glanzmann's Thrombasthenia and Bernard Soulier Syndrome

Introduction and Aim Glanzmann’s thrombasthenia (GT) is an inherited disorder of platelet aggregation, resulting from defective glycoprotein IIb/IIIa on platelet surface. Bernard Soulier Syndrome (BSS) is also an inherited disorder of platelet adhesion and associated with defective glycoprotein Ib-V-IX on platelet surface. Both of these disorders usually present with mucocutaneous bleedings. We aimed to evaluate the clinical and genetic characteristics of the patients diagnosed as BSS and GT in department of pediatric hematology of Meram Faculty of Medicine, retrospectively. Method Seven patients diagnosed with BSS and 20 patients diagnosed with GT were enrolled to the study. Medical records of patients were reviewed retrospectively. Glycoprotein IIb gen rearrangement was investigated in genetic department of Ankara University Medical School, Turkey. Mutational analysis for BSS was performed in Medicina Interna ed Oncologia Medica, Italy. The correlation between clinical outcome and genotyping was investigated. Results Of 20 patients of GT, 8 were male and 12 were female. Of 7 patients of BSS, all of them were female. Glycoprotein IIB gene rearrangement was detected in 7 patient of GT. 5 of 7 were newly described mutations in published literature. Mutations in GpIBB and GpIBA gene were detected in 7 patients with BSS. No correlation was observed among the clinical and genotype characteristics of patients both with GT and BSS. The most common patterns of bleeding were epistaxis and gum bleeding. Life threatening bleeding was seen in 5 of GT patients (4 gastrointestinal bleeding, 1 mediastinal hematoma) and 2 of BSS patients (1 splenic rupture and 1 gastrointestinal bleeding). No patients had died due to major bleedings. One patient with GT experienced spontaneous duodenal intramural bleeding resulting duodenal obstruction. One patient with BSS experienced spontaneous mediastinal hematoma. Although the BSS, it is interesting that the patient was able to control of mediastinal hematoma. Further investigations revealed the patient has prothrombotic mutation (heterozygous FV Leiden). Conclusion The most common bleeding pattern in patients with thrombocyte dysfunction is mucocutaneous bleeding. Some patients may suffer from life-threatening bleedings. Our study contributes to the literature because of five newly described mutations in GT patients. It may be hypothesed that the presence of prothrombotic mutation in patients with thrombocyte dysfunction may reduce the severity of bleedings. Disclosures: No relevant conflicts of interest to declare.

How to differentiate spontaneous intramural intestinal hemorrhage from acute mesenteric ischemia

ObjectsThe purpose of our study was to assess the diagnostic values of laboratory tests to differentiate spontaneous intramural intestinal hemorrhage (SIIH) from acute mesenteric ischemia (AMI) after abdominal computed tomography (CT) survey in the emergency department (ED). MethodWe retrospectively included 76 patients diagnosed SIIH or AMI after abdominal CT. ResultsThe mean ages of 28 SIIH patients and 48 AMI patients were 75.9 ± 13.7 years and 75.8 ± 11.6 years, respectively. Patients with SIIH had significantly higher rate of Coumadin use (P < .001) and localized tenderness (P < .05). In laboratory findings, SIIH patients had prolonged prothrombin time (PT) (83.6 ± 30.0 vs. 13.4 ± 3.2, P < .001), lower blood urea nitrogen (P < .05), lower creatinine (P < .05), and lower creatine kinase (P < .05). Prolonged PT showed good discriminative value to differentiate acute abdomen patients with SIIH from AMI after abdominal CT, with an area under the receiver operating characteristic curve of 0.980 (95% confidence interval, 0.918-0.998; P < .0001). Prolonged PT cut-off value of ≧22.5 seconds had a sensitivity of 92.9% and a specificity of 100%. Logistic regression analysis identified prolonged PT as an independent predictor of SIIH (odds ratio, OR, 22.2; P = .007). ConclusionAbdominal pain patients with either SIIH or AMI are rare in the ED, but abdominal CT sometimes cannot help to differentiate them due to similar CT findings. Prolonged PT might help emergency physicians and surgeons differentiate SIIH from AMI in such cases.

Reply to “Dural venous sinus thrombosis following head trauma: Possible causes and safe imaging techniques”

Dear Editor, We appreciate the critical review by colleagues from Turkey and their valuable contribution for the discussion of the subject. In response to their letter, wewould like to point out some aspects of the article “Dural sinus and internal jugular vein thrombosis complicating a blunt head injury in a pediatric patient” [1]. Regarding the figures of the article, the noncontrast computed tomography (CT) showing hypodensity on the right cerebral hemisphere consistent with edema and hyperdensity area at the sigmoid sinus suggestive of dural venous sinus thrombosis was not represented, so the reference on “Figure 1” is misplaced. On “Figure 2”, the thrombus is visible on transverse/sigmoid sinus junction on the axial image. For optimal visualization of transverse, sigmoid, and internal jugular vein thrombosis, it would require multiple images on the coronal, sagittal, and axial planes. Although not ideal, the three-dimensional volume image was an attempt to represent the extension of the thrombosis. The CT images on this letter may elucidate their doubts and understanding of the case (Fig. 1). The colleagues also questioned our hypothesis on the formation of the thrombus. We agree that their hypothesis proposed for the case reported is plausible; however, we are faced with a “chicken-egg” dilemma where the triggering factor will remain uncertain and of little relevance. In our opinion, the prevailing situation in the generation of the thrombus is the multifactorial setting (release of thromboplastin, sinus compression by intracranial edema or bleeding, intramural hemorrhages, extension of injured emissary veins, and trauma to the endothelial lining), independent of the precipitating factor. Finally, there is no doubt on the value of CT and magnetic resonance venography as a diagnostic study in cerebral venous sinus thrombosis. We are aware that the CT scan has its limitations in evaluating parenchymal brain injury and bears the potential risks of the ionizing radiation in the pediatric population. However, we should not ignore the fact that a well-justified CT scan may exceed its risk and have a favorable impact. In the trauma setting or when dealing with severely compromised patients where time may dictate the outcomes, the CT scan provides fast and sufficient information to guide the patient management [2].

Intramural dissecting hemorrhage of the myocardium

A 59-year-old man suffering anterior myocardial infraction 3 months ago with persistent dyspnea. Echocardiography revealed marked hypokinesia of the anterior and septal left ventricular walls with reduced ejection fraction (30%.) as well as turbulent flow at the apical region was noted with suspected apical thrombus formation. Coronary artery angiogram images show total occlusion of the LAD at its proximal and mid segment, tight long 90% stenosis of the first obtuse marginal artery as well as 99% mid segment stenosis of the RCA. Cardiac MRI was done and steady state free precession (SSFP) cine images revealed localized myocardial tearing and a flap appeared at the LV apex with a small tear at the flap containing fresh blood. Delayed-enhancement magnetic resonance imaging (intravenous dosage of 0.2 mmol/kg of Gad-DTPA; inversion recovery delay 260 ms; delayed time 10 min) revealed that the flap was enhanced and deviated toward the LV cavity and scarred enhanced myocardium deviated toward the epicardial border denoting the diagnosis of an intramural dissecting hemorrhage of the myocardium at the LV apical region. This entity accounts for fewer than 10% of cardiac ruptures and may occur after myocardial infarction, chest trauma, or surgery, or even spontaneously. Preoperative diagnosis is difficult, with differential diagnosis including pseudoaneurysm and intracavitary thrombus. Considering the poor prognosis of patients treated medically (less than 10% survival), corrective surgery is usually the treatment of choice.

Sudden death due to a dissecting intramural hematoma of the esophagus (DIHE) in a woman with severe neurofibromatosis-related scoliosis

Dissecting intramural hematoma of the esophagus (DIHE) is a rare condition in which intramural hemorrhage can lead to submucosal dissection of the esophageal wall. DIHE is generally considered a benign disease, and the only mortality associated with DIHE has been due to operative intervention or to the presence of another underlying, life-threatening condition. We report, however, a case of sudden death due to the spontaneous rupture of a DIHE that occurred in a 32-year-old woman, affected by neurofibromatosis type1. She was admitted to the local emergency room, presenting a 24-hour history of sudden onset, severe central chest and interscapular pain associated with dysphagia, odynophagia and vomiting. Her condition worsened and proved fatal within a 6-hour period. A complete autopsy was then conducted, showing a complete dissecting intramural hematoma with laceration of the third superior of the esophagus. We can hypothesize that abnormal variations of gastro-esophageal pressure during ingurgitation and during bolus movement could be predisposing factors in the pathogenesis of the dissection. On the other hand angular kyphoscoliosis deformity may have had play a role as precipitating factor while vomiting in the subject's medical history can then be interpreted as the likely activation phenomenon.

Small bowel intramural hematoma secondary to abdominal massage

Oral anticoagulant therapy with warfarin is commonly used to prevent thromboembolic event in patients at risk with atrial fibrillation [1]. Spontaneous intramural hematoma of small intestine is rare complication of anticoagulant therapy and occurs in patient who receives excessive warfarin that may result in potentially serious complications. Small bowel intramural hematoma secondary to warfarin therapy is a recognized complication [2]. In the present report, we report an unusual case of small bowel intramural hemorrhage secondary to anticoagulant therapy after abdominal massage. The emergency physicians should be aware that the potential spontaneous small bowel intramural hemorrhage in the patients has a high index of suspicion because most patients are treated nonoperatively with a good outcome.

Post-traumatic myocardial infarction with hemorrhage and microvascular damage in a child with myocardial bridge: is coronary anatomy actor or bystander?

We present the case of a 13 year old patient with myocardial bridge in left anterior descending coronary artery, who develops a myocardial infarction after a cardiothoracic trauma.&nbsp;About 24 hours after admission for trauma, an Electrocardiogram (ECG) showed an ST-segment elevation on anterior-lateral leads and QS complex referable to anterior-septal infarction, and an increase in troponin T serum levels was noted. An impaired left ventricular ejection fraction with diffuse regional wall motion abnormalities involving the left ventricular apex and interventricular septum were seen at transthoracic echocardiography. Contrast enhanced cardiac magnetic resonan-ce showed a widespread myocardial edema and necrosis at the level of left ventricular apex and interventricular septum. Intramural hemorrhage and signs of microvascular damage were found mainly at the mid-ventricular level of the antero-septal and anterior segments of myocardium. The coronary angiography revealed normal coronary arteries except for a myocardial bridge on distal part of left anterior descending coronary artery. A myocardial infarction with hemorrhage and microvascular damage was diagnosed, but the absence of a correspondence between site of the most severe myocardial injury and distal location of myocardial bridge was noted. Whether myocardial infarction and microvascular damage have been caused only by traumatic hit, or also by the contribution of myocardial bridge, is unknown. An intense constriction of left anterior descending coronary artery at the level of myocardial bridge could have determined thrombus formation with subsequent septal and distal embolization and myocardial infarction.&nbsp;

Lack of haptoglobin results in unbalanced VEGFα/angiopoietin-1 expression, intramural hemorrhage and impaired wound healing after myocardial infarction

Decreased haptoglobin (Hp) functionality due to allelic variations is associated with worsened outcome in patients after myocardial infarction (MI). However, mechanisms through which haptoglobin deficiency impairs cardiac repair remain to be elucidated. In the present study, we identified novel molecular alterations mediated by Hp involved in early and late cardiac repair responses after left coronary artery ligation in Hp−/− and wild-type (WT) mice. We observed a higher mortality rate in Hp−/− mice despite similar infarct size between groups. Deaths were commonly caused by cardiac rupture in Hp−/− animals. Histological analysis of 3 and 7days old non-ruptured infarcted hearts revealed more frequent and more severe intramural hemorrhage and increased leukocyte infiltration in Hp−/− mice. Analyses of non-ruptured hearts revealed increased oxidative stress, reduced PAI-1 activity and enhanced VEGFα transcription in Hp−/− mice. In line with these observations, we found increased microvascular permeability in Hp−/− hearts 3days after infarction. In vitro, haptoglobin prevented hemoglobin-induced oxidative stress and restored VEGF/Ang-1 balance in endothelial cell cultures. During long-term follow-up of the surviving animals, we observed altered matrix turnover, impaired scar formation and worsened cardiac function and geometry in Hp−/−mice. In conclusion, haptoglobin deficiency severely deteriorates tissue repair and cardiac performance after experimental MI. Haptoglobin plays a crucial role in both short- and long-term cardiac repair responses by reducing oxidative stress, maintaining microvascular integrity, myocardial architecture and proper scar formation.

Cystic Medionecrosis of the Carotid Bifurcation as an Uncommon Cause of Stroke

Cystic medionecrosis is characterized by degeneration of elastic and collagenous fibers in the media and predominantly involves the thoracic aorta. This rare disease is usually manifested clinically by a dissecting aneurysm. Cystic medionecrosis as a cause of moderate stenosis of the carotid artery in a patient having a stroke has not been reported. We report a case of a man who had a cerebral infarction caused by medium-degree stenosis of the left internal carotid artery. Duplex sonography and magnetic resonance imaging revealed no typical signs of dissection. The stenosis was caused by cystic medionecrosis that involved only the carotid bifurcation with microdissection, predominantly older intramural hemorrhage, and fresh intraluminal thrombotic deposits. Patients with cystic medionecrosis may have a stroke due to short-track stenosis of the internal carotid artery.

Histological examination and evaluation of donor bile ducts received during orthotopic liver transplantation—a morphological clue to ischemic-type biliary lesion?

Ischemic-type biliary lesions (ITBL) belong to a group of biliary disorders that are regarded as the major complication in patients with orthotopic liver transplantation (OLT). We performed histological evaluation of donor common bile ducts received during OLT to find morphological clues to the pathomechanisms of ITBL. We investigated 93 grafts of 92 patients (recipients: mean age, 56.5 years; underlying disease: hepatocellular carcinoma (n = 45), alcoholic cirrhosis (n = 16), viral hepatitis with cirrhosis (n = 9), retransplantations (n = 9), others (n = 14); donors: mean age, 53.2 years). Donor common bile ducts were received after recirculation of the hepatic artery prior to biliary end-to-end anastomosis and routinely processed. Statistical evaluation was performed by chi-square analysis and multivariate analysis using a logistic regression model. With regard to ITBL (observed in 19.4 %), the following phenomena were found to be statistically relevant: necrosis of the bile duct wall, arteriolonecrosis, vascular lesions (such as subintimal edema), and intramural bleeding (P < 0.001, P < 0.001, P = 0.029, and P = 0.031, respectively). In logistic regression analysis, arteriolonecrosis was the only parameter with significance (P = 0.001). Based on these results on the morphology of the donor common bile duct, we conclude that these phenomena of vascular damage, reflecting microangiopathy, play a major role in the pathogenesis of ITBL.

Coronary Arterial Wall Disruption and Intramural Hematoma in a Patient With Coronary Spastic Angina

Acute myocardial infarction is sometimes complicated in patients with coronary spastic angina. The mechanisms are known to be plaque rupture and thrombosis induced by spasm, and reduced coronary flow due to prolonged spasm. We describe the case of a 45-year-old woman with coronary spastic angina who had a complication of an acute myocardial infarction. A specimen obtained with thrombectomy was the disrupted coronary artery wall accompanied by massive intramural hemorrhage. The cause of the acute myocardial infarction was thought to be an embolism of the coronary arterial wall that was disrupted by spasm and intramural hemorrhage.

Hemorrhagic Bowel Syndrome in A Holstein Cow - Case Report

Summary In this report, hemorrhagic bowel syndrome (HBS) was defined pathologically for the first time in Turkey in a Holstein dairy cow. It was reported that a 4-year-old cow died suddenly with symptoms of loss of appetite, decreased milk yield, dehydration, and abdominal bloating in a dairy farm. Grossly, serosa of jejunum was observed with dark red color and its lumen was completely filled with blood clots. Some parts of jejunum lumen were narrowed due to submucosal and intramural bleeding. Microscopically, necro-hemorrhagic enteritis, and eosinophilic granulocyte and mononuclear cell infiltrations with extensive submucosal hemorrhages were observed. In addition, Gram-positive, rod-shaped and endospore-forming bacteria were seen intensively around of bleeding areas in the lamina propria. The death was concluded to be associated with HBS by macroscopic and microscopic findings, characteristic for the syndrome and in accordance with the literature evaluating this case. HBS causes significant losses in dairy cattle in many countries of the world. This report aimed to point out the importance of the topic, which is the first case report of HBS in Turkey, where dairy cow enterprises are growing rapidly.

Is There a Difference between Endoscopic Finding andHelicobacter pyloriInfection in Patients with Chronic Gastritis?

Background/Aims: This study verifies whether endoscopic findings differ according to the infection of Helicobacter pylori in patients with chronic gastritis. Materials and Methods: The study surveyed upper gastrointestinal symptoms of 382 patients with chronic gastritis and conducted esophagogastroduodenoscopy. The endoscopic findings were classified according to the Sydney classification, as edema, erythema, friability, exudates, flat erosion, raised erosion, rugal hyperplasia, atrophy, visibility of vascular pattern, intramural bleeding spot, nodularity, respectively in antrum, body, fundus. Results: 1) The average age of 382 patients was 52.3 years and there were 176 males and 206 females. 2) Among 382 patients, 167 (43.7%) had epigastric pain syndrome and 215 (56.3%) had postprandial distress syndrome. 3) Among 167 patients with epigastric pain syndrome, 85 (51.1%) patients were infected with H. pylori, while 82 (48.9%) patients were uninfected. Among 215 patients with postprandial distress syndrome, patients infected with H. pylori were 102 (47.6%), while those uninfected with H. pylori were 113 (52.4%). This shows no difference between patients with and without H. pylori infection (P＞0.05). 4) Compared to patients uninfected with H. pylori, those infected with H. pylori had more erythema (70.2% vs. 66.4%, P＞0.05) in antrum, (48.5% vs. 45.2%, P＞0.05) in body, and (36.4% vs. 32.7%, P＞0.05) in fundus, which shows no difference (P＞0.05). Conclusions: Patients infected with H. pylori tend to show more erythema, while those uninfected with H. pylori showed more atrophy. However, such difference between two groups was statistically insignificant, leading to a conclusion that endoscopic findings do not differ according to H. pylori infection. (Korean J Helicobacter Up Gastrointest Res 2012;12:178-182)

Small bowel obstruction caused by intramural hematoma secondary to warfarin therapy: A report of two cases

Spontaneous intestinal hematoma is a rare complication of anticoagulant therapy, and small bowel obstruction caused by intramural hematoma secondary to anticoagulant therapy is even rarer. The first symptom is usually abdominal pain, frequently accompanied by nausea and vomiting. A history of anticoagulant use with prolonged international normalized ratios in patients presenting with abdominal pain should alert physicians to search for this entity. Typical findings on abdominal computed tomography yield the diagnosis. Early diagnosis is crucial because most patients are treated non-operatively with a good outcome. Herein, we present the non-enhanced and enhanced computed tomography findings of two cases who were admitted to the emergency clinic with acute abdominal pain and diagnosed as spontaneous intramural ileal hematomas and partial small bowel obstruction secondary to intramural ileal hemorrhage.

Bowel wall hemorrhage after death by hanging

We describe and discuss autopsy findings of bowel wall hemorrhage in a study population comprising cases of suicidal death by hanging. Intramural hemorrhages were seen in approximately 12% of the cases examined; no preexisting bowel diseases were found. In hanging deaths with a longer agonal phase, we opine that abdominal congestion during the hanging process provides a viable pathophysiological explanation for bowel wall hemorrhage. Though we are not dealing here with obligatory autopsy findings, the detection of bowel wall hemorrhage might be used as another sign of vital hanging after considering differential diagnostic aspects.