Portal Venous Hypertension & Imaging - 2017 PDF

Portal venous hypertension 1. Wedge pressure more then 8 mm Hg. 2. Splenomegaly – nor always, only in advanced case. 3. Portal vein size more them 15 mm. 4. Portosystemic collaterals support the diagnosis (spleno-gastric, gastroesophageal, splenorenal, recanalized paraumbilical veins). Treatment: systemic shunt creation. TIPS. US: peak velocity flow less them 10 mm. Reversal flow hepatofugal flow. Module 4: Advanced Imaging with Computed Tomography (CT) 1.Advantages of CT: Explain how CT offers higher sensitivity for detecting subtle changes and differentia ting oedema from other lung diseases. 2.CT Findings in Pulmonary Oedema: 1. Early Changes: Describe subtle findings like increased lung attenuation and vascular dilatati on. 2. Progressive Changes: Discuss the appearance of septal lines, groundglass opacification, and consolidation as oedema worsens. Refer to Figure 11.16 3. Ancillary Findings: Explain the significance of mediastinal lymph node enlargement in hear t failure. Module 5: Putting it All Together 1.Summary of Key Points: Briefly recap the essential information about pulmonary oedema, its causes, and radiographic features. 2.Clinical Correlation: Emphasize the importance of combining imaging findings with patient history, ph ysical examination, and other investigations for accurate diagnosis and management. Portal venous hypertension leads to reverse hepatofugal flow due to the increased pressure within the portal venous system. Normally, blood flows towards the liver (hepatopetal flow) through the portal vein. However, in conditions like cirrhosis, the liver becomes scarred and resistant to blood flow. This resistance increases the pressure within the portal vein, a condition known as portal hypertension. When the pressure in the portal vein becomes too high, it can reverse the direction of blood flow from hepatopetal (towards the liver) to hepatofugal (away from the liver). This reverse flow is sometimes referred to as "retrograde" flow. The blood, instead of flowing towards the liver, flows away from it, typically towards collateral veins that enlarge to accommodate the redirected blood. This can lead to complications such as varices and ascites. The phenomenon of hepatofugal flow is a sign of advanced portal hypertension and indicates significant liver function impairment Liver parenchyma injures Increase resistance High pressure Change flow to hepatogugal Portal Vein Thrombosis 1. causes: idiopathic, hepatic cirrhosis. Infection, inflammation (pancreatitis, necrosing colitis), tumor (HCC. Pancreatic carcinoma), trauma, coagulopathy, liver transplantation. 2. US: avascular thrombus occluding and expending portal vein. 3. Later : the portal vein small, calcified thrombus, cavernous transformation. 4. Is enlarged and increase in size – suspicion for tumor. Malignant Portal Vein Thrombosis. Tumour thrombus is visible on ultrasound (A) as an expansile mass of mixed echogenicity within the right portal vein exhibiting colour Doppler flow (arrow). (B) Arterial phase CT of this patient shows the same thrombus in its entirety extending into the bifurcation to the left portal vein (arrow) as a complication of diffuse hepatocellular carcinoma (arrowheads) originating in the right lobe of this cirrhotic liver. Note the similarity of enhancement pattern of tumour thrombus and diffuse parenchymal tumour. Large bowel adenoma In 30% of people over 50 years More in men, 1st degree relative 50% in rectosigmoid Right-sided in older patients Predictor is size - 3.5cm Pedunculated polyps Severe dysplasia but cured once removed due to stalk Adenomas polyps – extension of this neoplasia beyond the muscularis mucosae into the submucosa. 2/3 CRC via adenomatous precursor. High risk if adenoma is more then 1 cm. Mor common in men. 50% rectosigmoid, 25% descending, 10% transverse. Pedunculated polyps Severe dysplasia but cured once removed due to stalk Flat is higher risk of malignancy. Non-adenomatous polyps were once felt of lesser clinical importance due to a lower risk of malignancy, T2 weighted MRI in this patient with FAP shows abnormal infiltrative low signal (arrows) invading the smallbowel mesentery in keeping with desmoid disease FAP Familial adenomatous polyposis Chromosome 5q21 1% of CRC Dominant >100 polyps for diagnosis. All patients develop CRC Preventive proctocolectomy Also extracolonic disease Gastric adenomas and gastric hamartomas Duodenal adenoma: 5% risk of periampullary duodenal carcinoma. Extraintestinal Multiple osteomas of skull, mandible Epidermal cysts - facial Desmoid tumors – low signal, locally invasive in abdominal wall, SB mesentery, retroperitoneum Mesenteric infiltration, SB tethering then mass – can be huge HNPCC Hereditary non-polyposis colorectal cancer – Lynch syndrome Risk of CRC in HNPCC is 70% to 85% Polyposis Syndromes Tumors occur earlier mean 45 years, also tumors of Peutz-Jeghers syndrome Clinical criteria – ‘3-2-1 rule’: Intestinal hamartomas, mucocutaneous pigmentation “Peutz-Jeghers – hamartomas, pigmentation” (1) three or more relatives with a HNPCC-associated cancer; Hamartoma is a non-neoplastic, hyperplastic lesion (3) one or more tumours diagnosed before the age of 50 years; Extraintestinal: Ovary (2) two or more successive generations affected; (4) one should be a first-degree relative of the other two. Cancers occur at an earlier age in HNPCC (mean 45 years); about 70% are in the proximal colon, and multiple tumors are common: Cervix - Endometrium Thyroid - SB Pancreas - TCC breast - Breast Chronic pancreatitis Atrophy with fibrosis or enlargmant of the gland. Mimics pancreatic cancer, needs multiple imaging and biopsies On imaging and ERCP: Calcification – in 20% but characteristic of chronic alcohol-related pancreatitis MPD side-branches dilations and stenoses Intraductal filling defects due to protein plugs Narrowing of distal CBD On US: variable Dilation of side branches and MPD Wirsung in absence of obstructing mass – key feature Abrupt change of main duct – MRI with enhancement and DWI help to exclude pancreatic tumor On CT pathogmonic: parenchymal calcifications, intraductal calcification, parenchymal atrophy and cystic lesions When duct dilation is alongside focal enlargement it mimics pancreatic carcinoma Long-standing chronic pancreatitis increases risk of pancreatic carcinoma 16x In 20% presents as focal mass again mimicking ductal adenocarcinoma On MRI: low T1, variable T2 – again looks like carcinoma Vascular complications common Splenic thrombosis SMV Ultrasound: increased echogenicity of parenchyma with small calcifications (arrows) and ductal dilatation. CT shows segmental calcification in the pancreatic body and severe atrophy of the tail (suggestive of stricture or intraductal calculus). (E) CT (in another patient) shows duct-obstructive calculus with massive ductal dilatation upstream. Not uncommonly, thrombosis of the splenic vein is seen, with extensive collaterals (small arrows). (F) Magnetic resonance cholangiopancreatography shows stricture in the body (arrow) with dilatation of main duct and side branches upstream. It is important to rule out tumour at the site of stricture. Multidetector computed tomography shows a low-density mass (arrows) with some calcifications between the pancreatic head and duodenum The groove-predominant type includes a plate-like hypoattenuating poorly enhancing lesion located between the pancreatic head and the descending part of the duodenum. Axial T2 weighted TSE image shows multiple small typical cysts in the groove between head and duodenum as well as in the head. Magnetic resonance cholangiopancreatography shows the typical cysts quite clearly (arrow). Magnetic resonance cholangiopancreatography shows the typical cysts quite clearly Autoimmune Pancreatitis Type 1 autoimmune pancreatitis: pancreatic manifestation of an IgG4-related systemic disease. Watch out for extrapancreatic manifestations (bile ducts, kidneys, lymph nodes, etc.). Type 2: confined to the pancreas. Three different morphological forms: focal (most common; not to be confused with cancer), multifocal and diffuse. Prognosis of AIP is fundamentally different from CP, as steroid therapy will lead to significant improvement or even resolution of symptoms. without a history of alcohol abuse or biliary stone disease. AIP lesions usually display isoenhancement in the arterial phase and a hyperenhancement in late phase. Mesenteric panniculitis Definition Chronic non-specific inflammation involving the small bowel mesenteric adipose tissue a rare, slowly progressive condition of unknown origin Retractile or fibrosing mesenteritis: a dominant fibrotic component is present CT (mesenteric panniculitis) A well-delineated, inhomogeneous fatty mass located at the mesenteric root there is an absence of adjacent bowel loop involvement (or bowel displacement) there is mesenteric vascular envelopment (with a low attenuation halo surrounding the vessels) MRI (mesenteric panniculitis) T2WI: hypointense capsule + contrast enhancement CT (retractile mesenteritis) An infiltrative soft tissue mass with associated radiating linear strands of soft tissue attenuation (which may mimic a desmoid or carcinoid tumour) calcification may be present within the necrotic central portion of the mass MRI (retractile mesenteritis) T1WI/T2WI: low SI Mesenteric Oedema. 1. Mesenteric oedema: a. hypoalbuminaemia b. portal hypertension c. cirrhosis d. nephrotic syndrome Contrast-enhanced computed tomography e. heart failure, shows extensive haziness in the affected small-bowel mesentery (white arrow) f. portal vein and superior mesenteric vein (SMV) thrombosis following the mesenteric vessels in a patient g. trauma with portal hypertension. create a chart with pictures that illustrates the differential h. neoplasm diagnosis of delayed contrast enhancement at cardiac MR i. surgery imaging by location. 2. Lymphoedema: a. Inflammation, neoplasm, surgery, radiation therapy, congenital abnormality 3. Inflammation: a. pancreatitis, appendicitis, diverticulitis, inflammatory bowel disease (IBD), tuberculosis, amyloidosis, mesenteric panniculitis 4. Haemorrhage a. trauma, bowel ischaemia, coagulopathy 5. Neoplasms a. Non-Hodgkin lymphoma, mesothelioma, carcinoid, colon, pancreatic, ovarian, breast cancer, melanoma, gastrointestinal stromal tumour Arrhythmogenic Right Ventricular Dysplasia: Fibrofatty replacement appears as DE in t he right ventricle free wall. Muscular Dystrophy: Midwall enhancement in a dilated cardiomyopathy setting suggests muscular dystrophy. Limitations: DE-MRI findings are not always specific, and clinical history is essential for accurate interpretation. Some conditions have overlapping appearances, requiring careful analysis and potentially additional investig ations. CT is important for differentiating pyelonephritis from tumour or infarction. Acute pyelonephritis If nor response during first 72 hours – US: low sensitivity: 75–80% - Renal enlargement (edema) - Edema of renal fat. - Hydronephrosis, either as a cause for infection or secondary to pyelonephritis. - Doppler US can help demonstrate areas of parenchymal hypoperfusion due to arteriolar vasoconstriction and interstitial oedema - Bacteriuria, pyrexia and flank pain due to an ascending infection in 85% (usually E. coli), or haematogenous seeding in 15% (S. aureus) - Risk factors: diabetes,long-term catheterisation, faecal soiling in chronically ill patients or vesicoureteric reflux (VUR) - MRI with intravenous gadolinium helps to depict areas of renal parenchymal involvement. - With MRI, APN demonstrates heterogeneous low signal on T1 weighted sequences and high-signal intensity on T2 weighted sequences. - MRI helping to differentiate APN from renal scar, and detection of the extrarenal extension at least as well as CT. hypoattenuating wedge-shaped area in the right kidney with perinephric fat stranding Nephrographic-phase computed tomography (images A and B) shows a striated pattern of enhancement in the left kidney and perinephric fat stranding. GU CTU is recommended as the initial imaging test for patients presenting with haematuria who are at high risk of urothelial cancer, and specifically for imaging adult patients over 50 years of age presenting with visible haematuria, once infection is excluded. Ultrasound as the initial imaging investigation of choice in patients with low risk of urothelial malignancy, with CTU recommended for those at high risk. Tumors metastatic to the kidney. Usually: Hematogenous, although a few occur by direct invasion or from lymphatic spread. The commonest: bronchial, colorectal, breast, Testicular, gynecological malignancies, malignant melanoma. Haematogenous metastases are usually small (8 – pathological Vascular complications: Transplant thrombosis can occur in 1% to 5% of renal transplants, usually in the early postoperative period. In renal vein thrombosis, absence of renal vein Doppler flow may be evident. Renal artery stenosis, when present, is usually a late complication of renal transplantation. Computed tomography or magnetic resonance angiography can help to further investigate and plan for intervention in cases of renal artery stenosis. Arteriovenous malformations and pseudoaneurysms are often the result of previous interventions such as biopsy or nephrostomy. Renal transplantation Acute Rejection: RIs exceeding 0.8 in the kidney transplant allograft have been defined as abnormal; Acute Rejection: 1 week after transplantation. deteriorating renal function. swelling of the medullary pyramids, reduced cortical echotexture and loss of normal corticomedullary differentiation; percutaneous biopsy still remains the gold standard for the diagnosis Chronic rejection - deteriorating graft function, typically 3 months to several years following transplantation. US examination at this stage demonstrates a small echobright kidney with parenchymal thinning and loss of corticomedullary differentiation. US: echobright kidney with parenchymal thinning and loss of corticomedullary differentiation. CT: thick cortical progressing to thinning of the cortex. Acute Tubular Necrosis Most common after cadaveric transplantation (PROLONG ISCHEMIC CHANGES in cadaveric grafts). Clinical differentiation of ATN from acute rejection occurring in the first 10 days can be difficult. histological confirmation remains the standard and biopsy. Chronic rejection is an insidious process involving deteriorating graft function, typically 3 months to several years following transplantation. US examination at this stage demonstrates a small echobright kidney with parenchymal thinning and loss of corticomedullary differentiation. Renal vein thrombosis Poor color flow in the inter-lobular arteries. Reversal diastolic flow in the vein Renal vein thrombosis with collateral venous outflow. A, Coronal view of the left kidney shows thrombosis of the main renal vein (asterisks). B, Magnified coronal color Doppler view of the left upper pole shows venous outflow through a collateral channel (arrows). C, Pulsed Doppler waveform from an intrarenal artery shows a nearly normal resistive index (0.71) and detectable venous flow below thebaseline. Tardus parvus waveform. Vascular Complications: Intermediate to Late Renal Artery Stenosis 1. Anastomosis between donor and recipient artery. 2. HPT, Renal dysfunction. 3. Velocity >200, gradient 2:1 stenotic and pre-stenotic. 4. Tr-t: angioplasty ot stent. Arteriovenous malformations (AVMs) and pseudoaneurysms 1. After percutaneous interventions such as biopsy or nephrostomy. 2. Pseudoaneurysm may appear as an intra-renal cyst on US with CDI demonstrating an associated vascular relationship. Post-Transplant False Aneurysm. (A) Computed tomography (short arrow) and (B) angiogram (arrowhead) demonstrate an incidentally discovered large false aneurysm arising from the left common iliac artery following a previous failed and resected renal graft. Urological Complications Urinoma - urine leak from a ureteric anastomosis. Lymphocele is the commonest posttransplant pelvic collection, which occurs as a result of disrupted lymphatics/leakage caused at the time of surgery. Ureteric obstruction can occur as a result of strictures secondary to ischemia or extrinsic compression from adjacent collections. Ureteric kinking can also occur. Renal calculi can be seen in both native and transplant kidneys following transplantation. Renal transplant patients are at an increased risk of infections secondary to immunosuppression. Postoperative Ureteric Leak. 1 month posttransplant demonstrates a urinoma (arrow) related to a transplant-to-native ureter anastomosis. Lymphocele is the commonest pelvic collection encountered after transplantation anechoic collection on the medial aspect of the transplant kidney. Internal septations can be present. Treatment is performed by either US-guided drainage with or without sclerosant or surgical (open or laparoscopic) marsupialisation. Simple aspiration is usually not efficacious. Ureteric strictures occur 2% - 5% of renal transplants and are usually due to ischemia of the distal ureter Post-Transplantation Ureteric Stricture. A nephrostogram performed in a patient presenting with hydronephrosis of the transplant kidney demonstrates a characteristic ischaemic stricture of the distal ureter (arrowhead) just above the bladder. Infection and Renal Transplantation 1. UTI 2. CMV, PCP Transplant Pyelonephritis. -> right lower lobe of the lung in a patient with a cough and fever 6 months following renal transplantation. Cancer and Transplant Malignancy of the skin is the commonest encountered malignancy following transplantation PTLD (related to the degree of immunosuppression) RCC – in native kidneys. TCC -> Papillary tumor Renal trauma 90% -blunt force. Children > adult, kidneys more mobile, less fat. Grade Injury Location Definition I Parenchyma Subcapsular haematoma and/or contusion Collecting system No injury II Parenchyma Laceration 1?cm in depth and into medulla, haematoma contained within Gerota fascia Collecting system No injury IV Parenchyma Laceration through the parenchyma into the urinary collecting system Collecting system Laceration, one or more into the collecting system with urinary extravasation Renal pelvis laceration and/or complete ureteral pelvic disruption Vascular - Segmental vein or artery injury Main renal artery or vein injury with contained haemorrhage V Parenchyma Completely shattered kidney Vascular Avulsion of renal hilum, which devascularises the kidney Grade 1 Contusion Subcapsular hematoma PAGE KIDNEY 1. On an unenhanced CT, an acute hematoma appears hyperdense in comparison to renal parenchyma and becomes hypodense as it ages. 2. CT +, contained hematomas similar attenuation patterns to the aorta, with enhancement during arterial phase imaging and ‘wash out’ on delayed imaging. 3. Acute or delayed hypertension develops from renal parenchymal compression resulting in activation of the renin-angiotensin–aldosterone system, the so-called ‘Page kidney’. Grade II Renal Injury - perinephric haematoma+ 1 cm laceration. No follow up Grade III Renal Injury, laceration.1 cm, no collecting systen involvment, hematoma – fascia Gerota grade III laceration of the left kidney (arrow), which abuts but does not extend into the collecting system. Delayed imaging is essential in excluding injury to the collecting system. Management: Conservative management without the need for routine follow-up imaging. IV Renal Injury Urine extravasation Artery or vein injury, contained hemorrhage. Renal artery thrombosis (arrow) with a devascularised intact left kidney consistent with a grade IV injury. Left renal artery (arrow), small amount of perivascular haemorrhage and decreased perfusion to left kidney. (B) placement of stent with patchy perfusion of the kidney MDCT cystography up to 400?mL of 4% contrast material. extraperitoneal tissues, creating a streaky, flameshaped or ‘molar-tooth’ appearance. Blunt trauma most common. Haematuria typically present. Most patients will have concurrent pelvic fractures. May be extraperitoneal rupture (most common), intraperitoneal rupture or mixed. Computed tomography cystography required for accurate diagnosis. Most EBRs managed conservatively (suprapubic or transurethral catheter)—90% healed in 10 days. IBRs usually require surgery. The bulbous urethra may be injured when crushed between the impacting object and the inferior surface of the symphysis pubis. AAST grade V injuries include a severely lacerated or ‘shattered’ kidney and avulsion of the renal hilum. Neuropathic foot Diabetic foot Soft tissue swollen Lisfranc joint dislocation. Calcification ( vascular), The second metatarsal migrates laterally. Articular involvement (in osteomyelitis – diffuse bone involvement). In case of neuropathic fracture – edema of the bone. in case of superimposed infection on CT: bone lysis, periostitis, joint errosions. MRI – involvement od subcutaneous fat, skin, sign of tract –osteomyelitis. Most bone metastases have a moth-eaten or geographic Metastatic disease of bone pattern with an ill-defined or wide zone of transition, no sclerotic margin, and often little periosteal reaction or soft Osseous metastasis occurs in 20–35% of malignancies. tissue mass Occasionally a metastasis may present as a geographic, Over age 50, an aggressive bone lesion has a high bubbly, expansile mass. likelihood of representing a metastasis or multiple Expansile solitary metastases are often caused by highly myeloma. vascular lesions such as renal cell or thyroid carcinoma. About 80% of bone metastases : Purely lytic metastases: lung origin but are also seen with Lung kidney, breast, thyroid, gastrointestinal, and neuroblastoma. breast Blastic metastases: prostate, breast, bladder, Prostate gastrointestinal (adenocarcinoma and carcinoid), lung kidney. Other common primary lesions metastasizing to bone (usually small cell), and medulloblastoma. include gastrointestinal, thyroid, and small round cell Mixed lytic and blastic metastases can be seen in breast lung, prostate, bladder, and neuroblastoma metastases. malignancies. lesser trochanter avulsion fracture in an adult pathologic Bone scan is highly sensitive blastic metastases, lower until proven otherwise Second, in patients with known breast cancer, a solitary for lytic metastases such as lung. Overall specificity of sternal lesion is rare but, if present, has an 80% probability of bone scan in screening for metastases is poor.. PET-CT is very useful for detection of recurrent disease in being caused by metastatic disease. transverse fracture in a long bone, especially without FDG-avid tumors after treatment. significant prior trauma, should alert the radiologist to the A lytic metastasis with bone pain warrants special possibility of a pathologic fracture. attention because of risk for pathologic fracture. Lytic metastasis. expansile lytic renal cell carcinoma metastasis in the right ischium. Renal cell and thyroid metastases are often highly vascular and may bleed significantly after biopsy. When presented with a lytic lesion and a request for percutaneous biopsy, chest radiography, and abdomen CT before biopsy. Because this patient had a renal mass at CT (not shown), a smaller biopsy needle would be used to reduce the risk for hemorrhage. Metastases Purely lytic: Lung most frequent, followed by kidney, breast, thyroid, gastrointestinal (GI), neuroblastoma. Blastic: Prostate, breast, bladder, GI (adenocarcinoma and carcinoid), lung (usually small cell), medulloblastoma. Mixed lytic and blastic: Breast, lung, prostate, bladder, and neuroblastoma. Therapy or radiation necrosis can change the lesion density (e.g., lytic metastases heal to more normal density). Most metastases occur where red bone marrow is found, therefore 80% of metastases are located in the axial skeleton (ribs, pelvis, vertebrae, and skull) and proximal humerus and femur. Epiphyses are rarely involved. Lesions distal to the elbows or knees are usually caused by primary lung cancers that have accessed the pulmonary venous system. Although most metastases are central medullary lesions, occasionally a cortically-based metastasis can occur, most often of lung or breast origin Metastases are frequently found in the spine, where they may appear as nonspecific compression fractures caused by vertebral body destruction. Bone or PET-CT scan and MRI are the preferred modalities for detection of vertebral metastases. MRI also provides assessment of spinal cord compression. Ewing Sarcoma Most common primary malignant bone neoplasm in thefirst decade of life Highly aggressive: Permeative pattern, large softtissue mass, aggressive periosteal reaction. Occasional host bone sclerosis and sunburst periosteal reaction may suggest osteosarcoma. Tubular bones more frequently involved in the younger age group; flat bones and axial skeleton more frequently involved in adolescents and young adults Central and diaphyseal or metadiaphyseal Systemic symptoms are frequent and may be confused clinically with osteomyelitis. Bone and lung metastases are common. PET is used to restage and assess response. The fat pad sign Effusion gives posterior fat pad sign. Anterior fat pad may be normal finding. The anterior fat pad sign is more sensitive but less specific for the presence of elbow joint distention than the posterior fat pad sign. In the setting of acute trauma, a posterior fat pad sign in an adult nearly always indicates that a fracture is present. This finding is less specific in children because softtissue injuries may cause an effusion. The absence of a fat pad sign does not exclude a significant injury, because a distal humeral fracture may be extraarticular, and a severe injury can lacerate the joint capsule and allow decompression of effusion. Elbow Fractures in Children Fat pad sign is usually present, but is less sensitive and specific for fracture than in adults SUPRACONDYLAR (65%) Fall on an outstretched hand causes elbow hyperextension Abnormal anterior humeral line. A – anterior and posterior fat pads. posterior displacement of the capitellar growth center relative to the anterior humeral line. B - AP view shows the lateral aspect of the fracture line. MEDIAL EPICONDYLAR AVULSION (10%) Fall on an outstretched hand causes valgus stress Possible entrapment—don’t miss it! Little Leaguer’s elbow is chronic avulsive injury t medial epicondyle physis. LATERAL CONDYLAR (15%) Lateral fall with arm at side causes varus stress across elbow May be incomplete, involving only part of the physis Most involve lateral metaphysis (at least SalterHarris II fracture) Often occurs in younger children with unossified epiphyseal cartilage; rare Salter-Harris IV variant may therefore be underestimated on radiographs; ultrasound or magnetic resonance imaging can show fractures through unossified cartilage and assist in determining whether fracture extends to the articular surface A. Salter-Harris IV. Fracture distal lateral diaphysis. B. Complete displeased fracture. C. Complete fracture. Adult radial head fractures – Most common in adults Linear fracture across the radial head (arrow). B, Subtly impacted radial head fracture (arrow) with intact articular surface. These fractures are treated conservatively. C, Displaced head fracture (arrows). This fracture may be treated with internal fixation or resection of the displaced anterior head fragment. Monteggia fracture-dislocation Anterior dislocation of the radial head (elbow). Fracture of the proximal ulna. Galeazzi fracture-dislocation Radius shaft fracture. Distal ulna dislocation. Ulnar styloid fracture. Ulnar nerve injury Medial epicondyle. T, Trochlea; U, proximal ulna. Biceps tendon insertion and tear. Normal distal biceps tendon: Distal tendon (long arrows) inserting onto the radius. Most biceps tendon tears occur at the insertion. The short arrow marks the location of the cubital bursa, Inflammation of this bursa causes local fluid accumulation and can clinically simulate a distal biceps tear or tendinitis. The arrowhead marks the ulnar artery. R, Radius; U, ulna. Gout 1. Sodium urate crystal–induced arthropathy 2. Middle-aged to older adult men 3. Normal bone density, ddc RA (osteopenia) 4. Cartilage often intact even late in the disease 5. Sharply marginates erosions «rat bite» due to chronic recurrent deposicion ->erosions and articular narrowing), Overhanging margins due to newly formed bone). First metatarsophalangeal MTP, distal interphalangeal - DIP, and proximal interphalangeal joints -PIP and patella most frequent joints Gouty tophus radiographs: May show amorphous calcification (calcium urate) Gouty tophus magnetic resonance imaging: Low signal intensity on T1-weighted, variably high or low signal on T2-weighted, enhances with gadolinium Olecrenon bursitis. Avulsion of tibial insertion of anterior cruciate ligament. A, Frontal radiograph demonstrates fracture at medial tibial intercondylar eminence (arrow). B, Sagittal fat-suppressed T2-weighted MR image shows the slightly elevated, edematous avulsion fracture fragment (arrowheads) with adjacent marrow edema. The intact anterior cruciate ligament (arrows) inserts onto the fragment Segond fracture Segond fracture. Detail of AP radiograph at the lateral joint line shows small avulsion from the lateral tibia (arrow). This fracture is nearly 100% associated with acute anterior cruciate ligament tear. Avulsion fracture of lateral tibial plateau. ACL tear and IT band tear. KNEE DISLOCATION - Posttraumatic popliteal artery injuries 30% - arterial injury (intimal arterial disruption/pseudoaneurysm). CTA recommended for all knee injury. A, Sagittal inversion recovery MR image shows large pseudoaneurysm (arrowheads). Note concentric rings of clot (arrows). B, AP angiogram in a different patient with comminuted tibial fracture and knee dislocation (after reduction) shows popliteal artery intimal injury with in situ thrombosis (short arrow) and occlusion at popliteal trifurcation (long arrow). Distal runoff is limited to the peroneal artery (arrowhead). ACL tear ACL injury associated with MCL tear and meniscal tear – O'Donoghue triad. Posterior corner knee injury(. Coronal shows avulsion of the lateral collateral ligament insertion (arrow). Note increased signal at location where the ACL is expected (arrowhead). Failure of recognition and repair of posterolateral corner injury will result in persistent rotational instability of the knee and failure of ACL repair. G, Popliteus tendon strain. Note high signal throughout musculotendinous junction (arrows). Posterolateral corner injury such as this has a high association with ACL tear.) Bone contusion in the lateral femoral condyle and posterior lateral tibial plateu, kissing lesions during subluxation-> ACL tear. Buckling of PCL -> sign of ACL tear. Hyperparathyroidism PA radiograph of the hand demonstrates the tapering of the soft tissue of the distal fingers of digits 2 and 3, with acroosteolysis seen at digit 2 (arrow). Soft-tissue calcification is seen both at the thumb and digit 3 HYPERPARATHYROIDISM A. Diffuse demineralization, trabeculation of the bones, resorption of bone at distal phalangs. B. Skull – salt and pepper appearance. C. Subperiosteal, subcortical resorptions. D. metaphyseal subperiosteal resorption. E. resorption in the lateral clavicula. Radiographic features of hyperparathyroidism, pelvis AP radiographs in a patient with primary hyperparathyroidism at the time of diagnosis (A) and 6 months later (B). progression of bone resorption at the symphysis pubis (long arrow), iliac bones at the sacroiliac (SI) joints (short arrows), and ischial tuberosities at the hamstring tendon origins (arrowheads). C and D, CT images in different patients show bilateral subchondral bone resorption (arrows in C). In these cases the resorption involves the fibrous portions of the SI joints, in contrast with inflammatory arthropathy. Brown tumors of hyperparathyroidism A. femur – intracortical lytic lesion. B. Multiple leasions C. Brown tumors in fourth metacarpal bone (black arrow). Typical features of hyperparathyroidism: diffuse bone demineralization, subperiosteal bone resorption, marginal subchondral bone resorption E shows bright T2-weighted signal in the brown tumors (arrows). The MR appearance of brown tumors varies with relative amounts of hemorrhage, cystic change, and fibrous tissue in the tumor Patellar Dislocation Lateral patellar dislocation is almost always transient and is a commonly overlooked injury. Impaction occurs between the medial pole of the patella and the anterolateral margin of the lateral femoral condyle. Bone bruises (osseous contusions) or fractures occur at the sites of impaction at the medial patella and the lateral femoral condyle. The medial retinaculum and MPFL should be assessed for tear. Chondral and osteochondral injuries CHONDROBLASTOMA - geographic lytic lesion in the epiphysis with a narrow zone of transition and sclerotic (type 1A) margin (arrowheads), a typical appearance of chondroblastoma with the open physis 1. Epiphyseal location, skeletally immature patients 2. Proximal humerus most common location 3. Chondroid matrix present in 50% of cases May contain fluid levels, usually related to secondary aneurysmal bone cyst May elicit prominent periosteal reaction in the metaphysis Differential diagnosis: Langerhans cell histiocytosis, infection Other common lesions in children 1. Osteoid osteoma – osteoblastic lesion with surrounding reactive sclerosis. 2. Diaphysis of the long bones (femur or tibia), 20% spine. 3. Bone scan positive - double density sign. Focal cortical thickening of the posterior diaphysis of the tibia. dense cortical thickening adjacent to the osteoid osteoma nidus Vertebral posterior elements of L1, small, round lucent lesion with dense surrounding sclerosis. Osteoid osteoma occurs in the posterior elements of the spine Bone cyst First and second decades of life Central metaphyseal or metadiaphyseal proximal humeral location most common Expansile, geographic, nonaggressive “Fallen fragment” sign if fracture Often does not have the appearance of “simple” cyst Treated with curettage or serial steroid injections High recurrence rate following curettage Adult simple bone cyst (SBC). Sagittal fat-suppressed, postcontrast, T1-weighted (A) and axial fat-suppressed, T2-weighted (B) MR images show the typical features of a cyst, with uniform high T2 signal and fluid-fluid level in B (arrowhead), and intermediate-low T1 signal and enhancement only of the rim of the tumor i Not lobular margin NOF – fibrous cortical defect Radiolucent lesion in long bone (leg). Geographic metaphyseal lesion that has a welldefined sclerotic rim. Giant cell tumor – GCTs arise in the metaphysis and may only reach the subchondral bone when they are moderately large. Eccentric lucent lesion, lateral tibial epiphysis and diaphysis, extent to articular surface. Narrow zone of transition, but no sclerotic margin 20-40 years. Aneurysmal Bone Cyst 1. Expansile lesion in the distal third metatarsal meta diaphysis. There is no matrix or cortical breakthrough. Expansile (often extremely), lytic, narrow zone of transition, eccentric, metaphyseal in long bones. Thin, intact shell of expanded overlying bone. 2. eccentrically located metaphyseal expansile lesion. 3. Axial T2-weighted MR image of the left shoulder shows an ABC in the proximal humerus of a 35-year-old woman, with the typical bone expansion and multiple fluid levels. DDX between chondrosarcoma $ enchondroma Chondrosarcoma Enchondroma Enchondroma: Location in hands or feet Common, usually incidental benign cartilage-forming neoplasm Small lesion, stable over time Central, metaphyseal location No endosteal cortical scalloping Chondroid matrix, but may be entirely lytic (especially in the hand or foot) Asymptomatic Geographic, although often without a sclerotic margin Favors chondrosarcoma: Magnetic resonance imaging shows lobulated bright signal on T2-weighted images, with low–signal-intensity calcifications. Proximal location Large size Enlarging Pain without mechanical cause Destruction of previously present matrix Endosteal cortical scalloping greater than two thirds of cortical thickness Cortical breakthrough. Chondrosarcomas may be histologically heterogeneous, so biopsy is not reliable Fifty percent of cases occur in tubular bones of hands and feet. May present with bone expansion, pathologic fracture. Small risk for malignant transformation in axial skeleton and proximal extremity enchondromas Exostosis (Osteochondroma Exostosis (Osteochondroma) Metaphyseal: Exostosis usually points away from adjacent joint; the cartilage cap is so small as to not be visible Sjogren Sialadenitis. Ultrasound of the left parotid gland. Multiple hypoechoic foci scattered throughout a shrunken gland, appearances are typical of Sjogren siladenitis. Salivary glands tumors US is first-line Sialadenitis Globally enlarged, diffusely hypoechoic with globa hypervascularity Most salivary gland tumors are benign because: Most cancers are from the parotid, and most parotid gland lesions are benign Abscess also hypoechoic – warthin tumor, pleomorphic salivary adenoma Focal sclerosing sialadenitis / Kuttner’s tumor Focal lesion Half of submandibular gland lesions are malignant Parotid tumors can displace parapharyngeal space - most sublingual gland lesions are malignant Warthin tumors In parotid gland – albeit name of duct is of submandibular gland Multifocal, bilateral Cystic Seen in smokers Need FNA or core biopsy Pleomorphic salivary adenoma / pleomorphic mixed tumor Sjogren’s disease Diffuse lymphocytic infiltration results in dry mouth On US: Hypoechoic shrunken salivary tissue Multiple hypoechoic foci Increased risk of MALT lymphoma Pleomorphic salivary adenoma / pleomorphic mixed tumor Around 80% most of salivary tumours Typically arise in the superficial portion of the parotid gland, being most common in middle-aged women These appear uniform or mildly loculated hypoechoic lesions on US and characteristically give a low T1 signal and high T2 If untreated becomes malignant Salivary mucoepidermoid and adenoid cystic carcinomas, acinic cell carcinoma, adenocarcinoma The commonest malignant epithelial salivary tumours Secondary Brain Injury Most common forms of brain herniation are subfalcine and transtentorial. both forms of herniation can lead to parenchymal ischaemia caused by compression of the anterior cerebral and posterior cerebral arteries, respectively. If this compression is not reduced, then infarcts in the distal anterior cerebral and posterior cerebral artery territories Diffuse Axonal Injury Diffuse axonal injury (DAI; thin arrows) left cerebrum in addition to more superficial haemorrhagic contusions (thick arrow). Susceptibility weighted images (SWI) (upper row) and T2 weighted images (lower row) are shown. The SWI demonstrates haemorrhagic hypointense foci in the right frontal parasagittal white matter (A), corpus callosum (B), left thalamus (C) and brainstem (D) (arrows) consistent with grade I to III diffuse axonal injury. Only some of the lesions are evident on the T2 weighted sequence. Diffuse Axonal Injury https://epos.myesr.org/poster/esr/ecr2015/C-1160 Grade 1 - subcortical and deep white matter of the cerebrum Grade 2 - corpus callosum Grade 3 - the brainstem Idiopathic Intracranial Hypertension 1. young, obese women. 2. No intra-cranial disorder. 3. Tortuosity and ectasia optic nerve. 4. Flat posterior globe. 5. Papilledema 6. Empty sella 7. Narrowing venous sinuses. Pathologies of the Posterior Visual Pathway (Lateral Geniculate Nucleus, Optic Radiation and Visual Cortex) 1. Posterior cerebral artery (PCA) infarction is a common central cause for acute-onset visual impairment. 2. If involving the entire primary visual cortex, bilateral PCA infarction may lead to ‘cortical blindness’ or Anton–Babinski syndrome. 3. MRI diffusion-weighted imaging, is the most sensitive method, particularly for the detection of small infarcts. Optic Pathway Compressive Tumours (A) and post-contrast sagittal T1 (B) of an enhancing calcific meningioma of the planum sphenoidale, compressing the optic chiasm. Sagittal (C) and coronal (D) T1 of a pituitary macroadenoma compressing the optic chiasm. Note the optic chiasm draped over the suprasellar component of the tumour (white arrowheads). Coronal T2 (E) and post-contrast T1 weighted (F) MRI of a craniopharyngioma causing similar compression. Axial T2 (B) and post-contrast T1 weighted (C) MRI of enhancing primary CNS lymphoma in a periventricular distribution T2 (D) and post-contrast T1 weighted (E) MRI of enhancing metastases from a lung primary. F), post-contrast T1 (G) and diffusion-weighted (H) MRI of a right occipital lobe abscess. AVM Diffuse Idiopathic Skeletal Hyperostosis Preservation of disk height. Ossification of the ALL of 4 vertebra. No facet joint ankylosis. No sacroiliac joint erosions or fusions. Dense ossification of anterior longitudinal ligament (versus fine calcification of the annulus fibrosis in ankylosing spondylitis) Ossification of superior portion of sacroiliac joint, pelvic ligaments, posterior longitudinal ligament DURAL AV FISTULA 1. 2. 3. 4. 5. 80% from all the AVM. Spinal dural mater. Near the nerve root. Thoraco-lumbar region – most common. Supply – one or two branches of radiculomeningeal artery to radicular vein -> high spinal venous pressure, chronic venous congestion, cord edema, ischemia > progressive myelopathy. heavily T2 weighted sequences (constructive interference in steady state (CISS), fast imaging employing steady-state acquisition (FIESTA) or 3D turbo spin-echo (3D TSE)) SMALL VESSEL VASCULAR DEMENTIA extensive white matter lesions—confluent hyperintensities involving >25% of white matter; multiple lacunes—at least two lacunes in basal ganglia and centrum semiovale each; and bilateral thalamic lesions—small infarcts in both medial thalami. (FLAIR) is best suited for detecting smallvessel disease and is able to differentiate (hyperintense) white matter lesions from (hypointense) lacunes. VaD involve most of the deep white matter of the frontal and parietal lobes but tend to spare the U-fibres (in contrast to multiple sclerosis) and the temporal lobes (in contrast to multiple sclerosis Basilar Tip Syndrome. The basilar artery supplies the posterior cerebral arteries (PCAs) unless the posterior communicating artery(s) is/are large, in which case emboli from the carotid circulation may enter their territory. Brainstem infarcts commonly result from occlusion of short perforating vessels. A combination of infratentorial, thalamic and occipital infarcts suggests an occlusion of distal basilar artery, or ‘top of the basilar’ syndrome Borderzone Infarction 1. Watershed ischemia between the leptomeningeal collaterals of the MCA and ACA, which also extend into the corona radiata deep to the superior frontal sulcus, and those of the MCA and PCA. 2. In the deep white matter of the inferior corona radiata and external capsules lies the deep border zone between the cortical branches and deep M1 perforators of the MCA ASPECTS Infarct Two NECT axial slices are examined a, level of basal ganglia and internal capsule; b, upper margin of the bodies of the lateral ventricles) Ten regions are identified (four deep and six cortical) Starting with a score of 10, 1 point is deducted for each of these areas that is involved If the score is less than 7, the infarct is considered greater than 1/3 of an MCA territory. C, Caudate nucleus; L, lentiform nucleus; IC, internal capsule; M1, M2 and M3, middle cerebral artery (MCA) territory at the level of the ganglionic nuclei. (B) M4, M5 and M6, MCA territory at the level above the ganglionic nuclei: 1 point is deducted for each area involved. A normal computed tomography scan will have an ASPECT of 10. Perfusion imaging. CT (CTP) and perfusion weighted MRI (PWI) – ACUTE STROKE IMAGING. Tmax > 6 sec - marker of penumbra. ‘Restricted diffusion’ in acute infarcts returns high signal on DWI and appears dark on the ADC map - almost always areas of irreversible ischaemia. Brain anatomy https://radiologykey.com/introduction-tobrain-imaging/ https://radiologykey.com/introduction-tobrain-imaging/ Wernicke Encephalopathy FLAIR/T2WI periaqueductal grey matter (*), hypothalamic, mamillary bodies, colliculi (arrows), and mid-thalamic regions (arrowheads) hyperintensities, but without restricted diffusivity. Triad of: nystagmus, ataxia, confusion – only in 30% ► T1WI: mamillary body haemorrhage is a bad prognostic sign ► T1WI + Gad: marked mamillary body enhancemen Hepatic encephalopathy Most cases associated with cirrhosis and portal hypertension or portal-systemic shunts T1WI: high SI in the globus pallidum T2WI: bilateral symmetric high SI abnormalities involving cortical grey matter – involvement of subcortical white matter hyperintense lesions involving bilaterally the temporal, frontal and insular cortical grey matter (arrows), the thalami (arrowheads) and dorsal brainstem (*). The lesions show restricted diffusivity. Osmotic demyelination Hyponatremia too quickly corrected “Sodium from low to high, pons will die” Destroyed BBB, hypertonic flid accumulation extracellularly and non-inflammatory demyelination Affects the pontine fibers – central pontine demyelination Rarely other regions On MRI: - High T2 in central pons, sparing periphery and corticospinal tracts - Low T1 - Rarely enhances - Restricted diffusion - If survives, there is a cavitated pontine lesion - If extrapontine, in the cerebellum and lateral geniculate body A-DWI, (B) ADC, axial T2-FLAIR- (C), T1- (D and E) -weighted pontine lesion (*), hyperintense on diffusion and T2-FLAIR, and hypointense on T1 without contrast enhancement. The ADC is increased and the corticospinal tracts are spared (arrows). FLAIR, Fluid-attenuation inversion recovery. Cerebral hypoglycemia Diffuse gyral swelling including cerebellum, high T2 in hippocampus, parietal and occipital cortex, basal ganglia Restricted diffusion Sparing of thalami – DDx unlike in severe anoxia DWI(a-C) high signal. D-E ADC map – low. F- FLAIR - hyperintense lesions involving the cortical grey matter (arrowheads), the deep cerebral nuclei (*) and both hippocampi (arrows). Methanol poisoning Counterfeit beverages or accidental ingestion of solvents and coolants Toxic due to formic acid – metabolic acidosis More susceptible are putamen, pallidum, caudate, hemispheric white matter “Putamen - Methanol” Putamen necrosis hypodense on CT and high T2 MRI Putamen ecchymosis hemorrhage – high T1 Carbon monoxide poisoning Carbon monoxide poisoning bilateral globus pallidus Medulloblastoma Medulloblastoma With Extensive Nodularity. (A) Sagittal T1 weighted image and (B and C) sagittal and axial T2 weighted. Large, cerebellar mass predominantly involving the vermis, composed of a macronodular conglomerate. There is marked supratentorial hydrocephalus. Medulloblastoma Postcontrast T1 weighted images show enhancement of the macronodules, as well as secondary lesions in the cerebral aqueduct and right cerebellopontine cistern (arrows). Note the mass is superficially located in the cerebellar vermis and abuts the pial surface posteriorly, whereas the fourth ventricle is compressed DWI restricted diffusion consistent with hypercellularity. (H) spectroscopy (PRESS), elevated choline, reduced creatine and N-acetylaspartate, and an abnormal lipid peak, consistent with a high-grade lesion. Medulloblastoma CT - hyperdense midline vermian mass abutting the roof of the fourth ventricle, with perilesional oedema, variable patchy enhancement and hydrocephalus. The brainstem is usually displaced anteriorly rather than directly invaded. Cystic change, haemorrhage and calcification are frequently seen. On MRI, the mass is hypointense or isointense compared with grey matter. Medulloblastoma 1. Intracranial, intraspinal dissemination: irregular, nodular leptomeningeal enhancement. 2. Imaging > sensitive then CSF. 3. Sulcal and cisternal effacement, communicating hydrocephalus. 4. Surgical resection >radiotherapy if more then 3, chemotherapy. Pilocytic astrocytoma Second most common in children. Ass with NF -1. CT, MRI: The solid component is hypointense to isodense on CT, hyperintense on T2 weighted FSE and hypointense on T1 weighted sequences, reflecting the hypocellular and loosely arranged tumoural architecture. The solid component is highly vascular with a deficient blood–brain barrier and therefore enhances avidly and homogeneously. Rare - diffuse nodular enhancement of the leptomeninges, indicating intracranial or intraspinal pial dissemination Ependymoma MRI: a solid and microcystic fourth ventricular tumour extending out through the foramina of Luschka, Magendie and the foramen magnum (arrows). 10% of paediatric posterior fossa tumours, and the posterior fossa is the most common site for ependymomas in children. Children with von Hippel–Lindau disease may occasionally present with cerebellar haemangioblastoma (WHO grade I), usually a tumour of adults. - rich capillary network with vacuolated stromal cells. - On imaging, haemangioblastomas may mimic a CLGA with an intensely enhancing mural nodule and a cystic component. - The tumour abuts the pial surface, but unlike the CLGA, it may be associated with prominent vascular flow voids. - Haemorrhage and frank necrosis may occur but are less common. MIDGUT VOLVULUS 1. Upper GI - Position of the duodenojejunal flexure (DJF). 2. US – dilated stomach and duodenum. SMV/SMA abnormal in 2/3. not sensitive not specific for malrotation. 3. the ‘whirlpool sign’; colour Doppler studies show the SMV spiralling clockwise around the SMA. –diagnostic. Idiopathic respiratory distress syndrome (IRDS) Premature inadequate gas exchange, leads to prolonged ventilation, hazy lung opacification 28 days of supplemental oxygen requirement from birth. Hyperinflation and hazy and streaky opacification, similar to the changes seen in bronchopulmonary dysplasia. Salyer-Harris Salter-Harris I fracture involves only the physis, with displacement of the epiphysis relative to the metaphysis. Salter-Harris II. This is the most frequent pattern 85% of physeal fractures. fracture also extends through a portion of the metaphysis. Salter-Harris III fractures involve the physis and epiphysis. Salter-Harris IV fracture extends through the epiphysis, physis, and metaphysis. Salter-Harris V fracture is a compression injury of the physis, which may be missed or confused with a Salter-Harris I Asymmetric Lung Densities Ideal Positions of Tubes and Lines ET tube – tip above the carina (consider chin position) UAC – T6-T9 (high position) or below L3 (low position), not in between UVC – junction between IVC and right atrium Temperature probe – within the thoracic oesophagus NG tube – within the stomach NJ tube – side hole at the duodenojejunal flexure (noting that the side hole is often proximal to a long weighted section of tubing). The tip of the umbilical arterial catheter is at T7 level (long arrow). The tip of the umbilical venous catheter is in the inferior vena cava (IVC) (short arrow) and should ideally be placed more distally in the IVC, close to the right atrium. Congenital Lobar Overinflation 1. Left upper lobe – most common ->RML. 2. Immediate post natal – full of fluid -> radiopaque. 3. Mediastinal shift. 4. CT I to exclude other causes of hyperinflation. Specificity of Skeletal Injuries in Child Abuse; Highest Specificity Applies in Infants Revised Hepatoblastoma Hepatoblastoma Suggest diagnosis when increased AFP and thrombocytosis Uncommon in first few months and after 3 years Associated with - Beckwith-Wiedemann syndrome - Biliary atresia Neuroblastoma 1. Most common extracranial neoplasm. 2. May in newborn or antenatal period. 3. Adrenal glands (48%), extra-adrenal retroperitoneum (25%), chest (16%), neck (3%) and pelvis (3%). About 50% of patients have metastatic disease at diagnosis. 4. High catecholamines. Wilms tumor - nephroblastoma Around 3 year old. Asymptomatic abdominal mass, hematuria, HPT. 10% of Wilms tumors are bilateral. 15%, including cryptorchidism and horseshoe kidney. may invade the renal vein and IVC with tumour thrombus extending superiorly, often into the right atrium. Metastases to local para-aortic lymph nodes and haematogenous spread to the lungs and liver are seen. US is the best way to assess renal vein and IVC tumour invasion/thrombus. CT or MRI for further delineation of tumor extent. MRI is the imaging of choice Wilms tumor - nephroblastomaWilms tumor nephroblastoma Stage I (43%)—tumour confined to the kidney without capsular or vascular invasion. Stage II (23%)—tumour extends beyond the renal capsule, vessel infiltration, biopsy performed before resection or intraoperative tumour rupture. Stage III (23%)—positive abdominopelvic lymph nodes, peritoneal invasion or residual tumour at surgical margins/unresectable elements. Stage IV (10%)—haematogenous spread (typically lung, liver, bone or brain) or metastatic disease outside the abdomen or pelvis. Stage V (5%)—bilateral tumours at original diagnosis. Tuberous sclerosis 1.Introduction 1. Hamartomas, cortical tubers, giant cell astrocytomas (GCA) 2. Commonly affect various organs: skin, brain, retina, lungs, heart, skeleton, kidneys 3. Autosomal dominant inheritance pattern 4. Majority of cases (70%) are sporadic 2.Triad of Presentation 1. Intellectual impairment 2. Epilepsy 3. Adenoma sebaceum 3.Tuberous Sclerosis Radiological Criteria 1. Calcified subependymal nodules 2. Noncalcified subependymal nodules 3. Cortical tubers 4. Renal angiomyolipomas (AML) 5. Cardiac rhabdomyoma 6. Retinal hamartomas near optic disc, often bilateral and multiple 4.Intracranial Manifestations of Tuberous Sclerosis 1. Subependymal hamartomas or subependymal nodules (SEN) 1. Most common manifestation (90%) 2. Project into ventricles, may calcify with age 3. Histologically identical to giant cell astrocytomas (GCA) but have different location 4. Can enhance on imaging 2. Subependymal giant cell astrocytomas (GCA) 1. Located adjacent to foramen of Monro in caudothalamic groove 2. Can grow and cause hydrocephalus 3. Radially oriented linear bands observed 4. May enhance on imaging 3. Cortical tubers Intracranial Manifestations of Tuberous Sclerosis. (A) Multiple tubers involving the cortex and subcortical white matter. (B) Bilateral lesions are seen at the foramina of Monro, in keeping with giant cell astrocytoma's (arrows). (C) Subependymal nodules project into the ventricles, some of which are markedly hypointense, in keeping with calcification (arrowhead). Nephrostomy In the majority of patients, the anterior calyces in the right kidney are situated medially and the posterior calyces are situated laterally. The opposite is true in the left kidney. Intravenous Sedoanalgesia Procedure with Fentanyl and Midazolam: Physiologic Narrowing in the Ureter: Physiologic Narrowing in the Ureter: 1. UPJ (Ureteropelvic Junction) 2. The common iliac artery 1. Patient positioning: Prone on the fluoroscopy table. 2. Preprocedural antibiotics: Administered if suspicion of pronephroses or an infected collecting system. 3. Ureterovesical junction Bladder Access: Posterior and lateral supply makes anterior access safe. Avoiding Inferior Epigastric Vessels: The inferior epigastric vessels run down the anterior abdominal wall alongside the rectus muscles. To avoid them, select an entry site close to the midline. Complications: 1. Sepsis 2. Hemorrhage Complications in Nephrolithotomy Case: Hemorrhage and sepsis Possible pneumothorax or hemothorax. Major Branches of the Abdominal Aorta Celiac T12-L1 Superior mesenteric L1-L2 Renal L2 Inferior mesenteric L3-L4 Common iliac L4-L5 CBD AND LIVER STENT - DUE TO PANCREATIC HEAD CANCER Low CBD obstruction. Palliative stent placement. Metal stent for palliative patient. if the patient is not fit for surgery, a duodenal stent can be placed or a long-term internal/external drainage catheter can be placed with its tip placed in the proximal jejunum. Metal stent placement Metal stent placement in a patient with pancreatic cancer who had a failed endoscopic retrograde cholangiopancreatography. A. Biliary drainage was performed and the stricture (curved arrows) was traversed with a hockey-stick catheter and hydrophilic guidewire. Note the normal duodenum without evidence of encasement. C. The patient returned for a tube injection 3 days later. The stent was in good position and there was good flow of contrast into the duodenum. The safety catheter was removed. Endpoints for Catheter Removal Improvement in clinical well-being and resumption of appetite Defervescence and normalization of white cell count Catheter drainage (10-15 mL daily) Disappearance or reduction in size of collection on repeatimaging. Complication of Crohn: Fluid collections with air (arrow) can be seen in the psoas muscle. Abscess also extends into the iliacus muscle (arrow). Abscesses associated with Crohn disease, diverticulitis, and appendicitis fall in this group Abscess drainage generally allows elective one-stage surgery Computed tomography best for abscess localization and access route planning Good bowel opacification is mandatory Pancreatic Pseudocyst ndications for Pseudocyst Drainage Size > 5 cm Enlargement over time Pain Suspected infection Biliary/gastrointestinal obstruction If there is communication with the pancreatic duct, the duration of drainage is prolonged for often up to 6-8 weeks. Splenic artery aneurysms Splenic artery aneurysms occur in approximately 0.8% of the population and 8%-10% of patients with portal hypertension. Splenic artery pseudoaneurysms due to pancreatitis can rupture into a pancreatic pseudocyst. Endovascular treatment options include placement of a stent-graft in the splenic artery or embolization. Angiogram in a patient with a multiple splenic artery aneurysms, one of which has ruptured into the splenic vein (arrow RENAL VEIN VARICES/NUTCRACKER SYNDROME “Nutcracker syndrome” in a 25-year-old woman with chronic left flank pain and intermittent hematuria with a noВ rmal urologic workup. A, Computed tomography scan with contrast showing compression of the left renal vein (arrow) between the aorta and superior mesenteric artery. B, Selective left renal venogram showing varices (solid arrow, catheter from inferior vena cava [IVC]). The kidney drains entirely via retroperitoneal collatera veins including paralumbar, the left ovariaВ n (arrowhead), and the hemiazygous (open arrow) veins. The pressure gradient between the IVC and the renal hilum was 7 mm Hg. Digital subtraction venogram after embolization of the left ovarian vein for chronic pelvic pain. The coils extended to the renal vein. Indications for Ovarian Vein Embolization Pelvic varicosities with: Chronic pelvic pain and otherwise negative work-up Dyspareunia and otherwise negative work-up Severe labial and perineal varicosities Type 1- always treatment. Inadequate seal between the device and the aortic wall Type 2 –retrograde flow – embolization of the sac. Most common is Type II leak Type 3 – always treatment. Disconnection of endograft components or tears in the endograft. Type 4 –sac expansion. No treatment. Type 5 – device migration. tratment EVAR “Treat, No treat, Treat, No treat, Treat for endoleak types from 1-5” Device migration can result in limb kinking and occlusion, thrombus formation, distal embolization Seen in Type I and Type III endoleaks Treated by additional stent-graft insertion If this fails, then surgical repair Device kinking and device dislocation can happen without migration due to changes in vessel Most common is Type II leak Pulmonary embolism The CXR is of limited value, either being normal or revealing non-specific atelectasis. peripheral area of more or less wedge-shaped consolidation may indicate associated infarction (the so-called ‘Hampton's hump’). Regional oligaema with sharp cut-off of pulmonary arteries may be seen (the Westermark sign). MRA is comparable to CTPA for central and segmental pulmonary arteries, but still limited for PE in the peripheral pulmonary vessels. pulmonary angiograpy is still considered the gold standard for the diagnosis of distal chronic PE, but as with acute PE, V/Q scintigraphy is the imaging method of choice to rule out suspected CTEPH, as a normal perfusion scintigram confidently excludes the disease whereas multiple, bilateral segmental perfusion defects are suggestive but not specific for chronic PE. Renal Artery Stenosis Causes of Renal Artery Stenosis: Atherosclerosis Fibromuscular dysplasia Indications for Intervention in Renal Artery Stenosis Severe hypertension* with: Unilateral or bilateral renal artery stenosis. Dissection Atherosclerosis, fibromuscular dysplasia, Takayasu disease, dissection Vasculitis Renal failure with: Neurofibromatosis No other explanation for severe azotemia Developmental (abdominal aortic coarctation) Bilateral stenosis† Compression of kidney by mass or hematoma Atherosclerosis, dissection Iatrogenic Etiologies of Renal Artery Aneurysms Fibromuscular dysplasia Degenerative Idiopathic Vasculitis Polyarteritis nodosa (small arteries) Behзet disease (large arteries) Neoplasm (angiomyolipoma) Trauma Mycotic Ehlers-Danlos syndrome Iatrogenic (i.e., after biopsy, angioplasty) Paget Disease AP radiograph shows a sharp linear transition between pagetic and normal bone (arrow). This finding is highly uncharacteristic of neoplasm. Moderate bone expansion, increased cortical thickness, and trabecular bone thickening assure the diagnosis of Paget disease. Hyperparathyroidism Brown tumors Paget Cirrhosis Atrophy: posterior segments 6,7 – right lobe Hypertrophy – 1, 2,3 – left lobe. Ct is not sensitive in the initial diagnosis. Multicystic Dysplastic Kidney Congenital renal dysplasia - cysts with intervening dysplastic, usually non-functioning, renal tissue unilateral, with the contralateral compensatory hypertrophy. MCDK is commonly diagnosed on antenatal US, which shows large peripheral cystic areas with no discernible renal parenchyma. Autosomal Recessive Polycystic Kidney Disease. EAnlarged kidneys bilaterally Congenital megaureter Ultrasound, VCUG and diuretic renography are used to diagnose, ADPKD Coexisting aneurysms of the circle of Willis are seen in 10%–16% of patients in autopsy series and as many as 41% of patients undergoing cerebral angiography. US demonstrates cysts in the adolescent or young adult, who is usually not yet clinically symptomatic. CT and MRI are more sensitive and frequently show more cysts than US. Adults presenting with adult polycystic kidney disease usually have enlarged kidneys with numerous cysts of varying sizes. Hepatic adenoma hemorrhage Bosniak classification 1. Simple cyst - Fluid density. No septa, calcification or solid components, No enhancement. 2. Cyst with some hairline thin septa, smal calcification, (3 cm,. FOLLOW UP: IF cysts every 6 months for 1 year with CT or MRI and then annually after that for at least 5 years. TREAT: 3. Thickened irregular or smooth enhancing walls or septa > 50 % risk of malignancy. 4. Thickened irregular or smooth enhancing walls or septa – 90% risk of malignancy. high signal on T1 pre-contrast (arrow) BOSNIAK 2 Bosniak Classification of Renal Cysts. Approximately 15% of IIF cysts will progress to 3,4. follow-up of IIF cysts every 6 months for 1 year with CT or MRI and then annually after that for at least 5 years. imaging follow-up, triphasic CT. unenhanced CT, corticomedullary (40 seconds) and nephrographic phases (100 seconds). True enhancement - increase in attenuation of greater than 20 HU. Changes of up to 10 HU are considered to be within the technical limits of CT and are not significant Attenuation increases of between 10 HU and 20 HU may be due to pseudoenhancement and so lesions demonstrating such increases in attenuation remain indeterminate and will likely require additional imaging with another technique or interval follow-up. Causes of Peritoneal Seeding in Radiology Causes of Peritoneal Seeding in Radiology Peritoneal seeding, often referred to as peritoneal carcinomatosis, involves the spread of cancer cells to the peritoneum, which is the lining of the abdominal cavity. This condition is typically identified through radiological imaging, particularly computed tomography (CT) scans. Primary Sources of Cancer: 1. 2. 3. Ovarian Cancer: One of the most common sources of peritoneal seeding. Cancer cells from the ovaries can detach and spread to the peritoneal surfaces. Gastric Cancer: After ovarian cancer, gastric cancer is a frequent cause of peritoneal seeding, often spreading through direct extension or via lymphatic dissemination. Colon Cancer: Cells from colon cancer can spread to the peritoneum, particularly in advanced stages of the disease (Radiopaedia). 1. Radiological Findings: 1. 2. 3. Multifocal Discrete Nodules and Infiltrative Masses: These are typical CT findings in cases of peritoneal carcinomatosis. They appear as irregular masses or nodules scattered throughout the peritoneal cavity. Omental Cake: This term describes the appearance of a thickened omentum due to tumor infiltration, commonly seen in CT scans and associated with various cancers, including ovarian and gastric (NCBI). Ascites and Peritoneal Thickening: The presence of fluid in the abdominal cavity (ascites) and thickening of the peritoneal lining are common indicators of peritoneal seeding. 2. Pathophysiology: 1. The spread of cancer cells to the peritoneum can occur through several mechanisms, including direct extension from the primary tumor, dissemination through the lymphatic system, or via hematogenous routes. The flow of peritoneal fluid also plays a crucial role in the distribution of cancer cells within the abdominal cavity. Diffuse steatosis Diffuse steatosis, or fatty liver disease, involves increased triglyceride accumulation in liver cells due to factors: alcohol abuse, obesity, diabetes mellitus, insulin resistance, cystic fibrosis, malnourishment, total parenteral nutrition, tetracyclines, steroids ileal bypass Imaging Techniques for Hepatic Steatosis: Ultrasound (US): Detects increased liver reflectivity, which may obscure portal vein margins, indicating fat accumulation. However, similar signs can appear due to fibrosis, necessitating further imaging. Computed Tomography (CT): Measures liver attenuation decrease, which correlates with triglyceride levels. However, results can be influenced by conditions like fibrosis or hemochromatosis. Magnetic Resonance Imaging (MRI): The most sensitive method, using Dixon-based chemical shift imaging to accurately diagnose and quantify liver fat. Corrosive Ingestion and its Consequences Ingestion of caustic chemicals can lead to severe injuries in the stomach, potentially causing gastric necrosis, perforation, and even death. Acids are particularly harmful to the stomach and duodenum, with acids like sodium hypochlorite (found in household bleach) posing significant risks due to their strength. Consequences of Corrosive Ingestion: The ingestion of corrosive agents follows a distinct course, starting with necrosis and sloughing of the mucosal and submucosal layers. Severe cases may progress to full-thickness necrosis of the gastric wall, leading to perforation, while less severe cases can result in fibrosis and stricture formation. Total gastrectomy may be necessary in extreme cases where the stomach is deformed, contracted, and obstructed. Radiographic Findings in Corrosive Gastritis: Radiographic findings in corrosive gastritis vary based on the severity of the chemical insult and the time elapsed since the injury. Initial signs include swelling and irregularity of the gastric mucosa, sometimes with visible blebs. As the mucosa sloughs, barium may flow beneath it, creating a radiolucent line. Fibrotic contraction of the stomach becomes evident after a week or two, with severe cases potentially leading to a significant reduction in stomach size. Exam 2017 NEuro ‫‪1‬‬ ‫‪:‬באיזה מהגידולים האינארה –קרניאליים הבאים דימום אינו נפוץ‬ ‫א‪.‬אוליגודנדרוגליומה‬ ‫ב ‪Anaplastic Astrocytoma.‬‬ ‫ג‪.‬גרורות של מלנומה‬ ‫‪. GBM‬ד‬ Oligodendroglioma (IDHmut With 1p19q Codeletion) 1. favorable prognosis with a mean survival of approximately 8 years. 2. Oligodendrogliomas: 3. Location: frontal lobes, contain calcification, subcortical white matter and cortex. 4. 90% of oligodendrogliomas contain calcification on CT, which can be central, peripheral or ribbon-lik occur, mimicking the appearance of calcification. 5. On MRI, intratumoural calcification appears typically T2 hypo- and T1 hyperintense and causes marked signal loss on T2* or SWI images. 6. Intratumoural haemorrhage, which occurs uncommonly. 7. Low-grade oligodendrogliomas show moderately elevated rCBV on perfusion MRI which can overlap with IDHwt. 8. MRS can be helpful in identifying anaplastic oligodendroglioma through the presence of lipid/lactate CT: left frontal tumour involves the cortex. solid with irregular enhancement, but there are also cysts and coarse calcification. Follow-up after 2 years with CT (B), T2 i (C) and T1+(D) more extensive cyst formation and calcification than on the first image. The calcification is much less apparent on MRI and appears as non-specific low signal areas. Posterior infiltration of the tumour is, however, best seen on MRI (C). Note that the patient had undergone a left frontal craniotomy after the first CT. Anaplastic Astrocytoma Isocitrate Dehydrogenase-Mutant Astrocytoma (IDHmut 1p19q Intact) (WHO grade II and III) are most frequent in the third decade of life. WHO grade II astrocytomas have a low mitotic activity, but most eventually progress to a higher histological grade, usually within 3 to 10 years—a progress known as ‘malignant transformation’. WHO grade II astrocytomas are commonly hyperintense on T2 weighted imaging; they less commonly enhance with gadolinium compared with oligodendrogliomas. (FLAIR) Mismatch Sign Brain MRI for tumors T1, T2 variable Sometimes FLAIR grey-white matter detail less well than T2 Blood products and calcifications are best seen on T2*/SWI as low signal – strong magnetic susceptibility Hemorrhage, atypical calcification, melanin and fat – high T1 Gadolinium uptake often non-specific Post-contrast FLAIR sequences used for leptomeningeal disease Improve visibility by tripling gadolinium dose, injecting high-relaxativity gadolinium compounds On MRS MR spectroscopy: Low NAA – neuron-specific marker Low creatinine High choline No lactate or lipids On MRI DWI: Lower ADC values (without restricted diffusion) help identify malignant gliomas Very restricted diffusion – lymphoma Isocitrate dehydrogenase wild-type glioma / astrocytoma (WHO grade II-III) 40-50 years No IDH mutation / wild-type - Multiple - Reduced diffusion - Neovascularity/high perfusion DDx IDH mutant astrocytoma are less so - Glioblastoma GBM (WHO grade IV) Some are non-enhancing Central necrosis – high T2 Most primary - Most wild-type - Avid enhancement of nodular rim enhancement Secondary from IDH- - Non-enhancing high T2/ high FLAIR signal of vasogenic edema – DDx brain metastases also - Areas of restricted diffusion, non-specific mutant astrocytoma - - Oligodendroglio ma (IDH mutant with 1p19q codeletion) Astrocytoma (IDH mutant, 1p19q intact) (WHO grade II-III) - 20-30 years (earlier than wild type) Image soon after surgery to avoid linear enhancement of surgical margins already after 48h Characteristic in frontal lobes Best prognosis, low grade Subcortical white matter and cortex - 90% are calcified – central, peripheral, ribbon-like - Rare but can have hemorrhage - On MRI: - Calcification is high T1, low T2, very low T2* - Hemorrhage is high T1, low T2, very low T2* - 20% moderate enhancement High T2 - Rarely enhance - Increased perfusion indicates increased vascularity and so anaplasia (WHO III) but DDx less than in wild-type astrocytoma - FLAIR-mismatch sign is pathognomonic, present in 50% - Very high T2 but low FLAIR signal “from the sky to the floor – astrocytoma” Anaplastic Astrocytoma Intraventricular tumors ‫ ‪..‬מה לא נכון לגבי התרומה של ‪MRI‬לאבחנה של ‪HIPPOCAMPAL SCLEROSIS (MESIAL TEMPORAL‬‬ ‫? )‪SCLEROSIS‬‬ ‫ א‪MRI.‬מאפשר לזהות שינויים מבנים בהיפוקמפוס‬ ‫ ב‪.‬מאפשר זיהוי שקיעת המוסידרין בהיפוקמפוס‪.‬‬ ‫ ג‪.‬מאפשר זיהוי אטרופיה של פורינק ) ( ‪FORNIX‬וממילרי‬ ‫ בודי ) ( ‪MAMILLARY BODY‬איפסילטרלי‪.‬‬ ‫ ד‪.‬מאפשר לזהות הרחבה של קרן טמפורלית סמוכה‬ Hippocampal Sclerosis Hippocampal sclerosis is a common pathology found in mesial temporal lobe epilepsy. It is classified into typical and atypical groups based on histological patterns of subfield neuronal loss and gliosis MRI hippocampal volume loss, T2 high, small hippocampus. Loss of the internal architecture of the hippocampus; Atrophy of the ipsilateral mamillary body and fornix; Dilatation of the adjacent temporal horn. bilaterally in up to 20%. Surgery is curative in up to 70% of patients with hippocampal sclerosis, ‫‪.5‬מה מהבאים נכון לגבי‪NMO‬‬ ‫א‪.‬נפוץ יותר בגברים‬ ‫ב‪.‬הנגעים בחוט השדרה הם לרוב קצרים )פחות מ ‪ -2‬סגמנטים( והיקפיים‪.‬‬ ‫)‪IgG MOG (myelin oligodendrocyte glycoprotein‬ג‪.‬טיטר‬ ‫גבוה בסרום לנוגדנים מסוג‬ ‫ד‪.‬נגעים מוחיים סביב חדר שלישי ורביעי וסביב האקוודוקט‬ NMO Neuromyelitis optica (NMO) is an autoimmune disease characterized by the presence of a specific serum autoantibody called NMO-IgG that targets aquaporin-4 – NMO-IgG - highly specific and sensitive, serum marker for NMO. NMO. all ages, including children and the elderly, with a relapsing course observed in 80% of cases. More common in women. Affect: spinal cord, optic nerves, brain. MRI of acute optic neuritis: MRI findings typically include: Unilateral optic nerve swelling High T2 signal intensity Follow-up images may reveal optic nerve atrophy and residual hyperintensity. Spinal Cord Involvement: NMO Intramedullary T2 high signal extending over three vertebral segments. Up to 90% of cases show enhancement. In the cervical spinal cord, a 'shaggy ring enhancement' pattern may be present in 30% of patients. MRI Findings: Axial T2 weighted MRI shows 'bright spotty lesions' in NMO, a distinguishing feature from multiple sclerosis (MS). Follow-up MRIs may reveal defects, atrophy, and central cavities. Brain abnormalities in 40%-60% of NMO patients include various lesions in different brain regions. A) B) Brain Abnormalities: supratentorial WM lesions, diencephalic lesions, brainstem lesions, corticospinal tract lesions, and periventricular signal intensity abnormalities. Enhancement on brain MRI is less common, with 'cloud-like enhancement' being the most frequent type. Association with Autoimmune Diseases: Associated conditions: hypothyroidism, Sjögren syndrome, lupus, pernicious anemia, ulcerative colitis, rheumatoid arthritis, and others. C) D) E) FLAIR bilateral symmetrical hyperintensity of the hypothalamus. T2 weighted image of the optic nerve demonstrating a hyperintense and swollen left optic chiasm C) T2 weighted image of the cervicothoracic spine showing illdefined hyperintensity of the cord extending throughout the cervical and upper thoracic cord, with mild expansion. T1+ patchy enhancement of the lesion. T 2 e lesion occupying more than twothirds of the cord cross-section. ‫‪.6‬שאלה לגבי וונטריקוליטיס‪ ,‬מה הסיבה הסבירה ביותר‪:‬‬ ‫‪intraventricular debris‬א‪.‬ממצא לא נפוץ הוא‬ ‫שנט והתפשטות המטוגנית של ‪VP‬ב‪.‬הסיבות השכיחות הן טראומה‪ ,‬קרע של אבצס לתוך החדר‪ ,‬זיהום‬ ‫זיהום לכורואיד פלקסוס‪.‬‬ ‫ג‪.‬תהליך נפוץ יחסית‬ ‫ד‪.‬החדרים לרוב לא יהיו מורחבים עם אפנדימה בעלת אות גבוה‬ Understanding Ventriculitis and Imaging Findings: Ventriculitis is a rare condition characterized by inflammation of the ventricles in the brain. Causes: trauma, abscess rupture, shunt infections, or hematogenous spread of infections to the ependyma or choroid plexus. Intraventricular Debris: The most common imaging finding in ventriculitis is the presence of intraventricular debris. hyperattenuating on CT scans compared to cerebrospinal fluid (CSF) and shows increased signal intensity on FLAIR and DWI sequences with low signal intensity on ADC maps. Periventricular and Subependymal Changes: Less common periventricular and subependymal high signal intensities and enhancement of the ventricular margins Ventricular Dilation: Affected ventricles in ventriculitis are typically dilated. (A) CT dilated lateral ventricles that contain intermediate attenuation debris. rim of low-attenuation interstitial oedema surrounding the ventricles. (B) DWI restricted diffusion in the debris. Modic described three types of degenerative changes in the end plates and the subchondral bone Type 1 changes indicate bone marrow edema with acute or subacute inflammation. This is seen as a decreased signal intensity on T1 and an increased signal on T2 both end plates at level L5 to S1 and also in the upper-end plate at L4 to L5, indicating bone marrow oedema associated with acute or subacute inflammation. Modic 2 Replacement of the normal bone by fat. increased T1 and isointense to hyperintense on T2 Type 2 changes are the most commonly seen. Type 3 Type 3 changes are seldom seen and indicate reactive osteosclerosis, seen as a decreased signal on T1 and T2. Reactive osteosclerosis, as seen on MRI, is characterized by decreased signal intensity on both T1- and T2-weighted images. This type of change is associated with Modic type III changes, indicating reactive osteosclerosis. 1.1. Modic Type 1 MRI changes: T1 Low signal; T2 High signal. 2.2. Modic Type 2 MRI changes: T1 high signal; T2 Iso to High signal. 3.3. Modic Type 3 MRI changes: T1 Low signal; T2 Low signal. Modic changes are commonly seen on MRI Modic changes are commonly seen on MRI most commonly the anterior part. Most cases these changes transform to type 2 changes over a period of 1–2 years and can be related to a change in patients’ symptoms. Modic type 1 changes are often observed in patients with painful lumbar instability. Type 2 and 3 changes are chronic changes and remain unchanged for years. Vestibular schwannoma Vestibular schwannomas most common in the cerebellopontine angle (CPA) lead to asymmetrical sensorineural hearing loss. Location and Occurrence: centered within the internal auditory canal or at the porus acusticus. usually occur sporadically. Bilateral in NF 2. NF-2 can also be associated with meningiomas and ependymomas. No direct correlation between tumor size and the degree of hearing loss. Management Approach: The management of vestibular schwannomas a "wait and watch“. About 60-70% of vestibular schwannomas remain stable on follow-up MR imaging. For those that do require intervention, surgical options like retrosigmoid, translabyrinthine, or subtemporal middle cranial fossa approaches are available, as well as gamma-knife (radiation) treatment. Imaging: MRI is the imaging modality of choice. Vestibular schwannoma A) T2 of posterior fossa. Star, vestibular schwannoma (VS); white line shows acute angle between VS and posterior surface of petrous bone which helps differentiate between VS and posterior fossa meningioma with the latter having an obtuse angle; C, Cerebellar hemisphere; MCP, middle cerebellar peduncle; P, pons. (B) T1 + 1, intracochlear schwannoma (in distal half of basal turn); 2, right CPA schwannoma; 3, left intracanalicular schwannoma. q Cavernous Haemangioma 1. Cavernous hemangioma, angiographically silent venous malformation commonly found in the orbit. 2. Prevalence: the most common primary orbital tumor in adults, about 6% of all orbital masses. 3. Pathology: It consists of endothelial-lined vascular spaces with a fibrous pseudocapsule. 4. Intraconal compartment of the orbit, but intraosseous occurrences are rare. 5. Clinical Presentation: painless, slowly progressive proptosis (protrusion of the eyeball) and diplopia (double vision). Growth may increase during pregnancy or following trauma. 6. Imaging Characteristics: 7. On MRI, low on T1 and high on T2-weighted images, may show variable enhancement, and a characteristic feature is progressive spread of enhancement from a single point or small component of the mass on dynamic post-gadolinium MRI. 8. Management Approach: In many cases, a conservative approach with monitoring may be favored over surgical resection due to the slow-growing nature of the lesion and the potential risks associated with surgery in the delicate orbital region. Overview of Capillary Haemangioma Characteristics and Presentation Capillary hemangioma is a vascular malformation seen in the pediatric population soon after birth. It demonstrates rapid growth during the first year of life and often begins to involute around the age of 10. Association with Facial Malformations There is an association with cutaneous facial malformations, which can aid in the diagnosis of capillary hemangioma. Common Locations and Differentiations Extraconal compartment anteriorly and within the superomedial orbital quadrant. It should not be confused with cavernous hemangioma; understanding their differences is crucial for accurate diagnosis and management. Photos provided by Pexels A subdural hematoma (SDH) 1. Injury to the cortical bridging veins, which extend radially from the cortical surface to drain into the dural venous sinuses, between the inner dural layer and the arachnoid mater. 2. Configuration: 3. crescentic shape due to the absence of anatomical constraints, allowing the hemorrhage to spread freely along the subdural space over the cerebral convexity. 4. The hemorrhage may extend medially adjacent to the falx and inferiorly towards the floor of the anterior and middle cranial fossae. 5. Location: along the tentorium, 6. Associated Findings: Unlike epidural hematomas (EDHs), associated calvarial fractures may or may not be present with SDHs (SDH) on unenhanced CT scans 1. Early Imaging (Within a Few Hours): hyperdense relative to brain parenchyma. This hyper density is due to the presence of acute blood within the subdural space. 2. Areas of reduced density within the hyperdense SDH may indicate active bleeding and ongoing hematoma expansion. 3. Subacute Period (Several Days to Weeks): slightly hyperdense to isodense compared to brain parenchyma. The density decreases as the clot undergoes degradation. 4. Chronic Phase (Several Weeks and Longer, the density of the SDH decreases further. The clot continues to degrade, resulting in a reduction in density. Additionally, membranes of reactive granulation tissue may form within the subdural space. These membranes appear as septations within an iso- to hypodense hematoma on imaging. 5. Appearance of Reactive Granulation Tissue: The presence of membranes of reactive granulation tissue within the subdural space is characteristic of subacute and chronic SDHs. Nasal polyposis 1. in adults, often associated with chronic rhinosinusitis. 2. in children with cystic fibrosis 3. Location and Distribution: - middle meatus, roof of the nasal cavity, and ethmoidal regions. - multiple, bilateral, and can involve both the nasal cavity and sinuses - Appearance: soft tissue masses within the nasal cavity and paranasal sinuses. - grape-like or teardrop-shaped structures protruding into the nasal passages. Diagnostic Considerations: typically benign. Unilateral polyps require direct inspection ± biopsy to exclude neoplasia. anterior skull base is mandatory to exclude a meningocele or encephalocele or sinonasal neoplasia. – meningoencephalocoele of the right gyrus rectus defect in anterior skull base An antrochoanal polyp solitary dumbbell-shaped polypoid mass that largely fills the antrum and extends through a widened accessory sinus ostium or infundibulum into the nasal cavity and from there posteriorly through the choana into the postnasal space and even the oropharynx These polyps are most commonly seen in young adults Nasal endoscopy for unilateral sinus disease to exclude underlying more sinister lesions. Mucocoeles 90% of mucocoeles occur in the frontal and ethmoidal sinuses occasionally become infected and result in osteomyelitis and subperiosteal abscess leading to a dramatic fluctuant swelling in the glabella,. The coronal T2 MRI image of the sphenoid sinus further demonstrates the expanded and opacified sphenoid sinus filled with material showing increased T2 signal intensity. Global Hypoxic–Ischaemic Injury 1. 2. 3. 4. 5. Sever hypotension. Impaired blood oxygenation. watershed infarcts and symmetric ischemia relatively vulnerable to reduction in perfusion pressure. Watershed infarcts typically involve the cortical and subcortical regions, particularly in the border zones between the anterior cerebral artery (ACA) and middle cerebral artery (MCA), as well as between the MCA and posterior cerebral artery (PCA). 6. bilateral symmetric grey matter hypodensity involving the basal ganglia, thalami, and cerebral cortex is typical, acutely with cerebral swelling. 7. the normal grey-white matter relationship is reversed. 8. restricted diffusion is demonstrated in the affected areas on magnetic resonance imaging. 9. the frontal and parietal lobes are infarcted 10. Carbon Monoxide Poisoning: lead to unique patterns of brain injury. Carbon monoxide has a high affinity for hemoglobin, leading to reduced oxygen-carrying capacity of the blood. In carbon monoxide poisoning, infarcts often occur in sensitive regions such as the globus pallidus due to the preferential vulnerability of certain brain areas to hypoxia. Renal Trauma approximately 10% of cases of blunt. Risk factors: Children (more large and mobile) Congenital renal anomaly Renal transplant horseshoe kidney, ectopic kidney, renal cyst. renal neoplasm or hydronephrosis are especially vulnerable to injury A 29-Year-Old Man With a Horseshoe Kidney Following a Fall From Height. a mass arising from the lower pole of the right kidney (arrow) with a large perinephric hematoma (asterisk Testicular Masses risk factor is cryptorchidism -10% of primary. Mumps orchitis, testicular microlithiasis, infective orchitis and infertility. Risk contralateral malignancy. 95% of primary testicular tumours - of germ cell origin.(Seminomas). Radiosensitive; associated with high levels of alpha-fetoprotein (AFP). Teratomas respond to chemotherapeutic agents. elevated AFP and hCG. less responsive to radiotherapy. CT to assess the retroperitoneal and mediastinal lymph nodes. Seminoma The slightly hyporeflective lesion is almost replacing the entire testis. Microcalcifications are seen in the normal and abnormal parenchyma. Teratoma of the Testis. The cystic areas (arrowed) within the lesion are characteristic. Right-sided aortocaval metastasis from right testicular tumour. Epidermoid cysts of the testis have been described as cystic, mixed and solid lesions, with a characteristic whorled appearance on US Left-sided paraaortic metastasis from left testicular tumour. Scrotal masses review Seminomas are usually hypoechoic and homogeneous. Nonseminomatous germ cell tumors are usually heterogeneous and frequently have cystic components and calcifications. The most common scrotal mass is the spermatocele. Most hydroceles, especially large ones, are idiopathic. D and E, Longitudinal views of different patients show large, lobulated, and septated spermatoceles (cursors). F, Doppler view of a spermatocele shows acoustic streaming, which is relatively common in spermatoceles and should not be confused with blood flow Varicoceles Varicoceles are very common and appear as enlarged, multiple, tortuous veins in the peritesticular region. Approximately 85% are on the left and 15% are bilateral Isolated right varicoceles are rare. The upper limit of normal for the caliber of scrotal veins is 2 mm. Epidermoid cysts typically have peripheral calcification or an onion peel appearance. Testicular Microlithiasis (TM): Associated with a minimal increased risk of germ cell tumors; annual exams recommended. Testicular Torsion: 1. Imaging Findings: Twisted cord, torsion knot, possible bell-clapper deformity. 2. Testis Appearance: Can vary from normal to heterogeneous; viability indicated by homogenously hyperechoic appearance. 3. Vascular Flow: Usually absent, occasionally decreased. The spermatic cord (C) is also surrounded by fluid indicating a bell-clapper deformity. Infections 1. Epididymitis and Orchitis: Can cause an enlarged, hypoechoic, and hypervascular epididymis and testis; 2. epididymitis is often focal, while orchitis is usually diffuse. (F) views of the epididymis (E) show epididymal enlargement and a small hypoechoic lesion (cursors) due to an epididymal abscess. Power Doppler shows intense hypervascularity of the epididymis but no detectable flow in the abscess. 1.Testicular Rupture: 1. Appearance: Distorted testis with abnormal contour; tear in the tunica albuginea sometimes visible. Urothelial Cancer of the Bladder: Characteristics: Typically a polypoid mass along the posterior wall; distinguishable from blood clots by mobility and vascularity. Blood clots after biopsy URocele Urachus cyst Calcified urothelial cell cancer. Longitudinal (A) and transverse (B) views show a solid, polypoid mass (cursors) arising from the wall of the bladder with a hyperechoic surface due to calcification Cystitis. Longitudinal gray-scale (A) and transverse power Doppler (B) views show bladder wall thickening (cursors) and hyperemia. There is also blood in the lumen Post-traumatic pseudoaneurysm and arteriovenous fistula. (A) and an adjacent vessel (B) shows arterial signals with marked discrepancy in the velocity of these vessels. The vessel supplying the lesion also has a low-resistance arterial flow. The high-velocity flow without a to-and-fro pattern is not consistent with an isolated pseudoaneurysm and indicates this is a combined pseudoaneurysm and arteriovenous fistula CRYPTORCHIDISM Undescended testes are a common condition that can occur alone or in association with other abnormalities such as prune belly syndrome, Beckwith–Wiedemann syndrome, congenital rubella, and renal agenesis. 100% of premature male infants under 900 grams. 80% are located in the inguinal region - palpable. Ultrasound (US) is effective in detecting undescended testes in the inguinal region, with a high sensitivity of 97% for palpable testes. lower for intra-abdominal testes (45% sensitivity, 75% specificity). Undescended testes is associated with subfertility and a significantly increased risk of malignancy, particularly seminoma. This risk remains elevated even after corrective surgery (orchidopexy) and affects the contralateral normal testis as well. CRYPTORCHIDISM CT and MRI studies can be used to demonstrate undescended testes not located in the inguinal region. MRI provides improved detection of undescended testes compared to CT. Testes appear as low signal on T1 weighted images and high signal on T2 weighted images in MRI. T2 fat-saturated images are particularly useful for detecting testes in an intra-abdominal location. The sensitivity of MRI enhanced by using diffusion-weighted imaging, increasing from 85% to 90%. MRI has a high specificity approaching 100% for detecting undescended testes. Xanthogranulomatous Pyelonephritis (XGP) Xanthogranulomatous Pyelonephritis (XGP) is a chronic granulomatous inflammatory. Common in middle-aged women and diabetic patients (approximately 10%). Bacterial infections by P. mirabilis and E. coli are often associated. Symptoms include loin pain, low-grade fever, chills, dysuria, and weight loss. Imaging, particularly CT scans, is essential for preoperative assessment to document extrarenal disease in XGP. CT scans include: Non-functioning enlarged kidney with a central calculus in a contracted renal pelvis. Expansion of the calyces and inflammatory changes in the perinephric fat. Hypoattenuating branching patterns due to lipid content, resembling hydronephrosis. Xanthomatous material does not enhance, and approximately 10% of cases are acalculous. Patterns of disease progression may include psoas abscess, fistula formation, and focal disease. Staghorn stones – Xray Kideney enlarged. Loss of coercion-medullary differentiation. enlarged right kidney with a staghorn calculus, multiple renal parenchymal collections and perinephric fat stranding right kidney (image A) and a fistula between the ascending colon and right kidne TB Epidemiology: Renal tuberculosis (TB) is the most common extrapulmonary manifestation of TB, occurring in 48% of patients with pulmonary TB. Pathophysiology: The disease typically spreads hematogenously to the kidneys from active or dormant pulmonary TB, affecting periglomerular or peritubular regions. TB CT Imaging: pelvicalyceal thickening, ulceration, fibrosis, and strictures. Shows infundibular strictures, phantom calyx, cavities, contour deformities, and calcifications (occurring in 40%-70% of cases). Reactivated disease hypoperfusion and a striated nephrogram at contrast medium–enhanced CT. CT can also detect papillary necrosis, which gives calyces a moth-eaten appearance, and CT examines for extrarenal spread MRI Imaging: Effective for visualizing TB cavities, sinus tracts, fistulous communications, and extrarenal spread. C) Coronal T2 weighted magnetic resonance imaging (MRI) of the left kidney shows the lesion with high signal intensity. (D) T1 weighted MRI identifies the lesion as isointense to the renal parenchyma. MRI features of renal macronodular tuberculoma include hypointensity on T1 weighted images and a thick, irregular, hypointense peripheral wall with intralesional fluid–debris level on T2 weighted images. Ultrasound (US) and Intravenous Urography (IVU): US can detect focal hyperechoic or hypoechoic masses, diffuse parenchymal hyperechogenicity from calcification, or renal abscess formation. IVU is useful for detecting early urothelial changes, parenchymal calcification, cavitary lesions, and infundibular stenosis. Renal Tract Calcifications Causes of Nephrocalcinosis: renal stones, are radio-opaque, as are struvite stones, which represent 15% of renal stones, and develop in the setting of infection and alkaline urine. Approximately 95% of patients with acute renal colic have haematuria. prevalence of nephrolithiasis in patients with microscopic and macroscopic haematuria is 7.8% and 8.8%, respectively Medullary Nephrocalcinosis: Hyperparathyroidism: Excessive parathyroid hormone leads to increased calcium levels, which can deposit in the renal medulla. Medullary Sponge Kidney: A congenital disorder where cysts form in the inner part of the kidneys, leading to calcium accumulation. Renal Tubular Acidosis: A disorder that results in acid build-up in the body, causing calcium phosphate stones and calcification in the kidneys. Hypervitaminosis D: Excessive vitamin D intake leading to increased calcium absorption and deposition in the kidneys. Primary Hyperoxaluria: A rare genetic condition causing excessive production of oxalate which combines with calcium to form calcium oxalate deposits in the kidneys. Cortical Nephrocalcinosis: Acute Cortical Necrosis: Severe injury to the renal cortex, often due to significant ischemia or toxins, leading to calcification. Chronic Glomerulonephritis: Long-standing inflammation and scarring of the glomeruli can lead to calcium deposition in the renal cortex. Primary Hyperoxaluria: Also causes cortical nephrocalcinosis as mentioned above. Conventional Radiography: sensitivity of only 60%, US-40%. Difference of greater than 20 HU between unenhanced and nephrographic phase images is strongly predictive of enhancement and therefore renal neoplasm. Adrenal Mass 1. lesions greater than 4?cm in size, adrenal resection without any other additional imaging work-up should be considered once biochemical evaluation to exclude phaeochromocytomas. Unenhanced CT should be performed to confirm a lipid-rich adenoma (HU < 10). MRI is recommended as the primary imaging technique in children and adults below 40 years old and in pregnant women. >70% adenomas - high intracellular lipid content. Adenomas enhance rapidly and a rapid washout of contrast medium—a phenomenon termed ‘contrast medium washout’. Malignant lesions and phaeochromocytomas enhance rapidly but demonstrate a slower washout of contrast medium. Non contrast, 60s, 15 min. Phaeochromocytomas low attenuation (1.8 to 42 HU) on non-contrast-enhanced CT to be mistaken for adenomas. washout similar to adenomas Phaeochromocytomas, present as incidental masses and on CT and mimic both benign adenomas and malignant masses excluded by clinical and biochemical evaluation. MRI adrenals 90% of adenomas - homogeneous or ring enhancement, 60% of malignant masses heterogeneous enhancement. Adenomas contain intracellular lipid lose SI on out-of-phase images compared to in-phase images, malignant lesions and phaeochromocytomas no intracellular lipid remain unchanged. On the out-of-phase image, both drop significant visual signal intensity; all the parameters are in keeping with typical lipid-rich adenomas. C) Chemical-shift imaging: in-phase image. (D) Chemical shift imaging: out-of-phase image. myelolipoma A large right-sided adrenal mass with multiple foci of high T1 signal intensity is present within the mass (arrows). These areas of high T1 signal lose signal on fat-saturation sequences, and on out-of-phase chemical-shift sequences, confirming the fatty tissue. Cushing's Syndrome 80% to 85% of cases, Cushing's syndrome is ACTH-dependent, secondary to a pituitary ACTHsecreting tumour. cortisol levels are high and the ACTH levels are low Phaeochromocytomas Commonest tumours of the adrenal medulla On MR imaging, most phaeochromocytomas are iso- or hypointense to the liver on SE T1 weighted imaging. High T1 weighted SI corresponding to areas of haemorrhage has been reported in up to 20% of phaeochromocytomas catecholamines or their metabolites, vanillylmandelic acid (VMA) and metanephrine. FIGO staging system for endometrial cancer, cervical cancers Stage I endometrial cancers represent tumours confined to the uterine corpus. Stage II is indicated by the presence of tumour invasion into the cervical stroma. stage III , the tumour extends outside the uterus but not beyond the true pelvis. Serosal involvement, tumour deposits along the serosa of sigmoid colon. T2 endometrial thickening (asterisk) secondary to an endometrial tumour and heterogeneous bilateral adnexal masses (M). In stage IV disease, the tumour extends beyond the true pelvis or invades the bladder or rectal mucosa, distan

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