A 47-year-old woman with a prior medical history of SLE and chronic arterial hypertension developed a post-anoxic coma after a prolonged cardiac arrest. She also presented a convulsive status epilepticus.At admission contrast enhanced CT brain (not illustrated) showed minimal loss of gray-white differentiation in the left sylvian region.Due to detoriation of the patient a follow-up CT scan was performed two weeks later. This examination showed hyperdensity in a laminar way, following the cortical gyri, mostly in the temporoparieto-occipital region (Fig. A and B). In the left peri-rolandic region this is associated with low-attenuation sub-cortical edema (Fig. B). Low density of the lentiform nuclei was also observed.Further examination by MRI showed in the same areas thin cortical hyperintensity on sagital T1-and hypo-intense on axial T2-weighted imaging (white arrow in Fig. C). A hyperintense signal in the putamen is seen on T1 weighted imaging (black arrow in Fig. C). T2-and FLAIR-weighted sequence displayed increased signal in the white matter and throughout the subcortical layer, most accentuated in the temporoparietooccipital region (arrow in Fig. D).Diagnosis of advanced cortical laminar necrosis with bilateral deep gray nuclei involvement and encephalomalacia as typical manifestation of anoxic-ischemic brain damage was made. Shortly afterwards the patient passed away. CommentSeveral signs of advanced anoxic-ischemic brain damage were observed in our case. The most striking finding is the imaging manifestation of the so called 'cortical laminar necrosis'.Histological studies demonstrate much more vulnerability of grey matter than white matter to ischaemic necrosis due to hypoperfusion. The third layer of the gray matter is the most vulnerable and the damage is usually greater in the depths and sides of the sulci than over the crest of the gyri.Cortical laminar necrosis is a specific type of cortical infarction, which usually develops as a result of generalized hypoxia rather than a local vascular abnormality. Depletion of oxygen or glucose as in anoxia, hypoglycemia, status epilepticus, ischemic stroke and less common in immunosuppressive therapy and polychemotherapy has been attributed as an underlying cause of cortical laminar necrosis. A hypoxic insult leads to death of neurons, glia and blood vessels along with degradation of proteins.When cortical laminar necrosis is seen on CT imaging, it presents as gyriform linear hyperdensity in the superficial cortex, most frequently located in the medial occipital lobes and perirolandic regions. Mostly this is a subtle finding, but the image can be more spectacular in more severe cases. These areas are often associated with cortical hypoattenuation as presentation of oedema.Cortical enhancement is first seen after 2 weeks, peaks after 1 to 2 months, and is usually resolved after 6 months. Contrast enhancement is present due to disruption of the blood-brain barrier, where loss of neurons and vascular proliferation occur.Initially thought to be caused by hemorrhag...
A 54-year old man was admitted to the emergency department for chronic dysphagia for solid as well for liquids of several years duration, with increasing severity for two weeks.The patient also had shortness of breath grade III for two weeks. The medical history of the patient was uneventful, except for surgery on the oesophagus 26 years previously, probably for achalasia. No follow-up was performed. At the time of admission, the patient doesn't take any medication. He doesn't smoke and consumes one or two alcohol units a day.Clinical examination fails to reveal any specific findings. Blood analysis showed a decrease of the hemoglobin level (10.4 g/dL), a slightly elevated leukocytosis (10400/µL) and elevated C-reactive protein level (127 mg/L), as well as hyponatriemia and hypochloremia.Chest X-ray shows cardiomegaly and a dilated proximal oesophagus with a marked decrease in the diameter distally.Fibroscopy shows an ulcerated tumoral lesion of 6 cm at 40 cm, biopsies showing an infiltrating epidermoid carcinoma.Bronchoscopy was negative. PET-scan confirms the presence of a large, irregular, hypermetabolic mass in the lower oesophagus and enlarged hypermetabolic mediastinal lymph nodes.Barium X-ray confirms the predominantly enlarged upper oesophagus (4 cm) with stasis of liquids and absence of peristalsis. The distal part of the oesophagus is narrowed showing a pattern compatible with treated achalasia (Fg. A). On the right posterior border of the distal one third of the oesophagus the large ulcerated lesion of approximately 8 cm with typical neo plastic pattern is demonstrated on the lateral view (Fig. B). Contrast enhanced computerized tomography of the thorax confirms the presence of the ulcerated mass and shows an enlarged lymph node in the mediastinum and the right hilus (Fig. C). Treatment consisted of radio-chemotherapy. CommentAchalasia is a primary oesphageal motility disorder affecting mainly adults of both sexes equally and predominantly presenting with dysphagia, sometimes with regurgitation.The treatment of achalasia is symptomatic and designed to improve the oesophageal emptying. The most effective treatments are pneumatic balloon dilatation and cardiomyotomy, follow-up being based on X-ray and manometry. Late complications are related to recurrent dysphagia after treatment. Perihiatal scarring, peptic stricture or obstructing tumors can all cause recurrent symptoms. The most important late complication is the occurrence of oesophageal cancer, patients having similar symptoms in recurring achalasia and in oesophageal cancer. Therefore, mostly cancers are diagnosed in an advanced stage.The relationship between achalasia and cancer was first described in 1872 by Fagge. An increased risk of developing oesophageal carcinoma in patients with long standing achalasia has been reported by several authors, with incidences varying widely from 1.7 to 20%.It has been established that the consumption of alcohol and tobacco increases the risk of developing esophageal cancers due to the content of carcinogens i...
An 18-year-old young man with no medical history presented at the emergency department with nausea, vomiting and pain in the right iliac fossa and the periumbilical region. Blood analysis was normal except for an elevated C-reactive protein (CRP) of 64 mg/L.High frequency gray-scale sonogram was performed and showed a normal presentation of the appendix. A tubular hypo-echogenic structure (length of 3 cm, width of 1 cm) with a cystlike center and an irregular thickened wall was discovered in the right periumbilical region (Fig. A). Color Doppler sonogram reveals a hypervascular wall (Fig. B) and infiltration of the surrounding mesenteric fat arrow in Fig. A and B). Diagnosis of Meckel diverticulitis was suggested, although a complicated duplication cyst could not be excluded.CT scan that followed showed a rim-enhancing tubular structure in the right peri-umbilical region with surrounding inflammatory changes (Fig. C). Surgery and pathology that followed confirmed a Meckel diverticulitis. CommentMeckel's diverticulum is the most common congenital anomaly of the gastrointestinal tract, with an incidence of 1-3% of the population, although only 4% of those affected become symptomatic. When the vitelline (omphalomesenteric) duct fails to obliterate during fetal development, several anomalies appear, Meckel's diverticulum being the most frequent. It occurs on the antimesenteric border of the ileum, 40-100 cm proximal to the ileocecal valve.Clinical symptoms arise from complications of the diverticulum, which are most common in male and in the pediatric population. Hemorrhage from peptic ulceration, small intestinal obstruction, and diverticulitis are the most frequent complications. Diverticulitis can mimic appendicitis clinically and on sonography the inflamed Meckel's diverticulum can be wrongly interpreted as an abnormal cecal appendix.Meckel's diverticulitis appears as a round or tubular, cystlike structure with a thick, irregular hyperechoic internal wall and a hypoechoic external wall (Fig. A). The outer hypoechogenic layer corresponds to the muscularis propria of the intestinal wall, and the inner hyperechogenic layer corresponds to the mucosa and submucosal layers. This mural pattern of echogenicity is called the gut signature. The inflamed diverticulum may resemble appendicitis because it may be non-compressible when pressure is applied to the abdominal wall with the ultrasound transducer; in contrast, the inflamed diverticulum may be compressible and resemble a duplication cyst. In the latter circumstance, a duplication cyst usually has a smooth internal wall, compared with the irregular internal wall and the more tubular structure of an inflamed Meckel's diverticulum. The presence of air inside the Meckel's diverticulum and its mobility during the peristaltic activity of the adjacent bowel loops can give the Meckel's diverticulum an appearance that is similar to the rest of the intestine. Color Doppler sonography can be important in revealing hypervascularization, signs of inflammation of the Meckel's dive...
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