Multiple Hemorrhagic Infarcts Research Articles

Atypical cerebrovascular complications of COVID-19

Many neurologic complications were recognized with COVID-19. Cerebrovascular disorders were one of these complications. In our case report we describe two cases presented with atypical cerebrovascular presentations associated with COVID-19. The first case presented with right cavernous sinus thrombosis, right cavernous portion of the internal carotid artery partial thrombosis with bilateral basal ganglia microbleeds. The second case presented with multiple hemorrhagic infarctions as a first presentation.

Successful preemptive therapy for cerebral multiple hemorrhagic infarctions due to septic embolism by Bacillus cereus after allogeneic hematopoietic stem cell transplantation for acute myelogenous leukemia

Successful preemptive therapy for cerebral multiple hemorrhagic infarctions due to septic embolism by Bacillus cereus after allogeneic hematopoietic stem cell transplantation for acute myelogenous leukemia

Primary central nervous system lymphoma with cortical laminar hemorrhage

Here we report a case of primary central nervous system (CNS) lymphoma with cortical laminar hemorrhage. The present case showed an acute onset of focal neurologic signs and bilateral cortical lesions surrounded by peripheral white matter edema on magnetic resonance imaging. A part of the left frontal cortical lesion was hyperintense on T1-weighted images and hypointense on T2-weighted and T2⁎-weighted gradient-echo images, suggesting subacute laminar hemorrhage. The patient was initially diagnosed with multiple hemorrhagic infarctions, but a biopsy specimen revealed diffuse large B-cell lymphoma with hemosiderin deposits. Immunohistochemical studies revealed that the tumor cell cytoplasm and membrane stained positively for anti-vascular endothelial growth factor antibody. The present case reconfirms the danger of making a specific lymphoma diagnosis based on magnetic resonance imaging findings alone and that histopathologic examination following brain biopsy is necessary for a correct diagnosis. Vascular endothelial growth factor expression might be associated with the intratumoral hemorrhage.

Baccharis Pteronioides Toxicity in Livestock and Hamsters

Baccharis pteronioides DC has been intermittently associated with livestock poisoning in the southwestern United States. In 2004, nearly 100 cows were reported poisoned by B. pteronioides in southern New Mexico. Initial field studies and postmortem examinations found drought conditions, evidence of B. pteronioides consumption, and a reported mortality of nearly 40%. Because postmortem materials were unsuitable for further examination, plant samples were collected for feeding trials and chemical evaluation. Forty-eight Syrian hamsters (8 weeks old) were randomly divided into 4 groups and dosed with 0, 50, 100, and 200 mg of B. pteronioides for 10 days. After dosing, the hamsters were necropsied; sera were analyzed biochemically; and tissues were collected and evaluated histologically. The hamsters treated with 200 mg and several of the 100-mg animals developed anorexia and diarrhea. These animals developed multiple hemorrhagic infarcts in the liver and kidney, with severe hemorrhagic enteritis. Histologically, the higher-dosed animals had severe necrotizing vasculitis with vascular thrombosis of hepatic and renal vessels. Many glomerular capillaries contained fibrin thrombi. The superficial intestinal and colonic mucosa was necrotic, with extensive hemorrhage and proliferation of luminal bacteria. Lower-dosed animals had mild hepatocellular swelling, with proliferation of intestinal and gastric bacteria and yeast. The findings indicate that at high doses, B. pteronioides is toxic to hamsters and produces lesions that are very similar to bacterial endotoxin-produced vasculitis and infarction. Research to purify and identify the toxin, the toxic dose, and mechanism of toxicity are ongoing.

Hypoalbuminaemia and colonic polyps: a case of protein-losing enteropathy with cap polyposis?

A 69-year-old woman was admitted in September 2005 dehydrated and unwell. She had a 6-month history of constipation, poor appetite and weight loss, and was hypoalbuminaemic (21 g/litre). She had initially been referred for colonoscopy in March to exclude colonic malignancy. Multiple pedunculated polyps up to the splenic flexure were seen, with histology felt to be consistent with hyperplastic polyps and mild inflammation. Her symptoms persisted, and by August she had lost 3 stone in weight. She started to experience loose stools, and repeat colonoscopy was planned. However, the bowel preparation made her feel unwell. She couldn't walk, and so presented to the acute medical take. The patient looked pale and dehydrated. Her chest was clear, with a diffusely tender abdomen. Bowel sounds were present, and there were no palpable masses. Bloods showed a corrected calcium of 1.58 mmol/litre. Fluid resuscitation and calcium replacement was started. A malignant process was queried. Liver function tests showed a low albumin of 21 g/litre but were otherwise unremarkable. A computed tomography scan of the abdomen and chest were normal. A gastroscopy showed mild oesophagitis with Candida in the mid and lower oesophagus, gastritis in the antrum of the stomach with heavy Helicobacter pylori growth, and a normal duodenum. Biopsies showed no evidence of coeliac disease or giardia. The patient's albumin fell to 8 g/litre. A 24-hour urine protein collection was 0.46 g, excluding nephrotic syndrome. Nasogastric feeding was commenced. Gut hormones showed a modestly elevated chromogranin A (164 pmol/litre) and gastrin (307 pmol/ litre) but were not diagnostic of a neuroendocrine tumour. Amyloid was queried and the original colonic biopsies re-examined. This was not found, but cap polyposis was suggested. The patient failed to improve and died 15 days after admission. Post mortem found the distal large bowel to contain multiple dark sessile polyps, looking like slugs, on exaggerated mucosal folds (Figure 1). The histological findings comprised elongated, tortorous and distended crypts, with evidence of inflammation and a 'cap' of granulation tissue, confirming cap polyposis. In addition the patient had a right haemothorax. This was caused by a dissection in the pulmonary artery, with evidence of atheroma identified. The right ventricle was hypertrophic, with the lungs showing multiple haemorrhagic infarcts. These changes suggested pulmonary hypertension. Whether this was related to the cap polyposis was unclear. A reasonable explanation is that the patient had showered off pulmonary emboli from a deep vein thrombosis (DVT) for some time, secondary to immobility associated with her poor state of health. This was supported by a right calf DVT identified at post mortem. The dissection of the pulmonary artery was probably secondary to the low protein state and pulmonary artery hypertension.

CT and MR findings of brain aspergillosis

CT and MR findings of a case of brain aspergillosis with histopathologic correlation are reported. On both CT and MR images, there were multiple lesions in the corticomedullary junction (CMJ) that appeared to disrupt the cortical sulci and that were not enhanced by intravenous contrast material. In most of these lesions, there were centrally located structures that were enhanced by intravenous contrast material and that appeared to be continuous from markedly enhanced adjacent dilated cortical vessels. Histopathologic examination of the autopsy specimen showed multiple hemorrhagic infarcts in the CMJ with remaining dilated cortical vessels that had been thrombosed by aspergillus hyphae.

Disseminated Histoplasmosis Causing Reversible Gaze Palsy and Optic Neuropathy

Subacute disseminated histoplasmosis is an uncommon entity. Typical neuro-ophthalmologic manifestations are usually secondary to histoplasmomas or encephalitis. A 45-year-old man noted blurred vision while receiving empiric antituberculosis therapy for fever and diffuse granulomatous disease of unknown origin. Vertical-gaze palsy, right horizontal-gaze paresis, and mild right optic neuropathy were found on neuro-ophthalmologic examination. Further questioning revealed a history of frequent contact with fighting cocks from South America. Magnetic resonance images were consistent with multiple hemorrhagic infarcts, areas of inflammation, or both, and cerebral angiography showed changes consistent with vasculitis. A previously obtained biopsy specimen from the duodenum was restained and found to be positive for fungal elements. Serum antigen titers for Histoplasma capsulatum demonstrated evidence of active infection. This case is a rare example of a supranuclear ocular motility disturbance and optic neuropathy secondary to an occlusive vascular process in a patient with subacute disseminated histoplasmosis.