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Radiology Teaching
19/11/12 – 23/11/12
Approaching a CXR
• Name and date• Determine which side is LEFT and which is RIGHT• If it is supine, AP or PA etc• In situs invertus look for the gastric bubble on the right, high density liver on left• Rotation: spinous process equidistant from either clavicle• Inspiration: should be able to see the anterior 6 ribs, clear and separate from the
diaphragm• Penetration: vertebrae visible through the heart• 3 densities visible:
– 1) AIR– 2) soft tissues– 3) bone
• Key patterns to know: – Patterns of lobar collapse/consolidation– Features of Pulmonary embolism– Heart failure– Pneumothorax– Interstitial lung disease
Silhouette Sign
• 2 tissues of different densities beside each other should be easy to differentiatate. If there is loss of the intersection this is known as a silhouette sign.
• Loss of normal borders between thoracic structures, it is difficult to make out the borders of a particular structure - because it is next to another dense structure (both white)
• Silhouette sign / Felsons sign• E.g. consolidation in pneumonia• Cant see diaphragm: LLL/RLL• Cant see heart border: lingula/RML• Cant see mediastinum: RUL/LUL
Sail Sign
• Suggestive of LLL collapse
GOLDEN S SIGN
• Abnormality in RUL• GOLDEN S SIGN SYNONYMOUS WITH RUL collapse most
commonly due to bronchus tumour• Loss of volume in RUL = horizontal fissure rises +/- tracheal
deviation
RUL Consolidation
• Known abnormality as mediastinal border unclear• Fissure present but unchanged position so not
collapse, no tracheal deviation so not collapse
Multiple abnormalities
• More than one border blunted/undefined• E.g.: RIGHT hemidiaphragm – RLL and mediastinal in
RUL
VEIL’S SIGN• LEFT UPPER LOBE collapse abnormality: loss of mediastinal
border• There is still air visible on CXR in apex of lung but that is due
to the anatomy of the left lung which means the lower lobe provides air in the apex
• Left lung is “whiter” than the right
Pulmonary Embolism
• Investigations: – V/Q scan: able to tell if PE without deep contrast so reduced risk of
nephrotoxicity, especially if DM.
– CTPA scan: form of CT that shows pulmonary vasculature, white is good, BLACK IS BAD!!! NB look for saddle embolus
– CXR: WESTERMARK’S SIGN – hyperlucent area (darker) due to reduced vascular markings. Infrequently seen and not reliable
V/Q Scan
CTPA - PE
Cardiac Failure
• Cardiomegaly• Upper lobe blood diversion, pulmonary venous congestion• Perihilar haziness• Interstitial oedema – Kerley B sign• Pulmonary Oedema – BATs WING SIGN
Notes on cardiac failure
• Heart >50% thoracic border• ULBD: lines in upper lobe due to congestion,
increased markings• PH: pressure is much higher so plasma
extravasates from pulmonary arteries into the interstitial tissues
• IO: interstitial lines, shouldn’t see any lines 2cm from peripheries and out. Any horizontal lines here indicate the presence of fluid in the interstitial space. About 1-2cm long, horizontal lines!!!
Pulmonary Interstitial Fibrosis
• Thick interstitial lines• Cysts• Scar formation – causes traction bronchiectasis• Honeycombing• END STAGE: all features, shrunken lungs
Pneumothorax
• 1) simple pneumothorax/iatrogenic• 2) tension pneumothorax• 3) pneumomediastinum• 4) surgical emphysema
• 1) eg if needle introduced for biopsy• No lung markings at peripheries• free air• History of chest pain and trauma
Pneumothorax
• 2) Tension: breathing is very difficult, reduced venous return to heart to BP falls drastically, life-threatening– CXR: Hyperlucency, line indicating border of lung, tracheal and
mediastinal shift
Pneumothorax
• Hydropneumothorax: fluid and air in lung space• Pneumopericardium: air in pericardial sac. Must be released ASAP• Pneumomediastinum: see margins of mediastinum very clearly
due to the black outline caused by free air
Other Chest Pathology• Aortic injury: widening of mediastinum, may see line through
the aortic arch indicating AORTIC DISSECTION. Side with acute angles is false lumen, obtuse angles TRUE lumen
Other Chest Pathology
• Pneumoperitoneum: – RIGLERs SIGN: ability to see bowel wall clearly due to free air– FALCIFORM LIGAMENT SIGN: falciform ligament separates RIGHT lobe from
LEFT lobe, air on both sides of it so FL visible• Rupture of diaphragm:
– All organs come up through
Chest Pathology
• Position of NG tube: correct/not• Foreign bodies: e.g. coins
Cases
• 1 – upper RL mass• 2 – left hilar mass• 3 – RU zone, mets visible on CT only• 4 – Left hilar mass, huge mass seen on CT• 5 – right hilar mass: LOOK AT DENSITIES• 6 – left hilar mass• Look at– Apices– Hila– Behind the heart– Peripheries
PET CT
• Generates images to give a better idea of abnormalities, increases sensitivity and specificity of diagnostic imaging and gives you a much more confident diagnosis
• Cancer cells need/use a lot of glucose very inefficiently and this high uptake of glucose is seen on PET scan.
• Organs take lots of glucose up normally: brain, heart, vocal cords, muscles etc then it is renally excreted so can be seen in kidneys and bladder
• Abnormal to be found in the – Lung– Upper mediastinum: oesophagus– Nasopharyngeal area– If only one kidney lighting up suspect previous RCC
• FDG + tumours: lung, lymphoma, GO – oesophageal, head and neck, melanoma (CRC, Breast, hepatobiliary and panc)
PET CT
• Assessment of single pulmonary nodule if <3cm, round and surrounded by normal lung. If no uptake there is no cancer, just follow up and check
• Uptake doesn’t necessarily mean tumour: metabolically active pulmonary sarcoidosis!! Or fungal infection
• Lesion <7mm: not picked up by PET – Fasle –ves • Uses:
– Accurate staging and diagnosis– Influences management options– Follow up and response to therapy– Radiotherapy planning to clearly identify borders
Artefact (not exam)
• X-ray orbits before MRI• 4th density – metallic• 5th: fat• Cant remove previous pacing leads because fibrosis occurs• BACLOFEN pump – for stiffness in MS. Implanted• Subclavian line – under 1st rib, tip should be in SVC• Oesophageal stents, position of NG tube, pacing leads, VP shunt in
hydrocephalus (xray head, chest and abd to follow)• Bronchial stent in bronchomalacia• Pulmonary vessel shunt, coronary artery stents, SMA stent..• IVC filter, intrauterine devices• Dialysis line much thicker than normal central line, in SVC• Endotracheal tube, intra-aortic balloon pump to maintain pressure in the
aorta if AI• PICC lines in chemo patients, swan ganz catheter to measure RA pressure
in ICU
Vascular Disease
PAD• Critical limb ischaemia:
– rest pain– tissue loss/threatened– Rutherford-Becker 4-6– ABPI <0.4– ankle pressure 50-70mmHg – upper limb BP not reliable
• RFs: smoking, DM, renal failure, HTN etc
Vascular Disease
• Buerger’s Disease: used to be only Azkenazi jews and older people but due to smoking its rising in younger, white people
• Dx:– Ultrasound – realtime, dynamic information/velocity acceleration, wave
form. Operator dependent and limited image production– MRangiography: gandolium can cause NEPHROGENIC SYSTEMIC FIBROSIS
(like scleroderma)– Non-contrast TOF, INHANCE: if vessel down to trickle flow, can’t see it– CTAngiography: contrast induced nephropathy/radiation dose
Severity of Symptoms
• Stenotic disease: – single level compensation/collateralisation: can lead to claudication– Multi level: claudication CLI
• Occlusive disease:– Single: claudication– Multi: claudication CLI
• Interventions: stents, angioplasty• Claud Vs CLI
– Severe: 25% die within a year, 30% need amputations, 45% alive with limbs. With intervention its 25, 16, 59.
• SIA = subintimal angioplasty• Diabetics: generally no disease above the knee.• Ulcerated tissue is ulcerated because of poor blood supply• If you can reconnect/perfuse plantar arch, very likely to keep foot• DIABETICS DON’T FORM SMALL VESSEL COLLATERALS!!!!
Non-atheromatous Disease
• Inflammatory– Takayasu’s arteritis– Buerger’s disease– Polyarteritis nodosa– ((Wishett alderons syndrome))
• Connective Tissue– Marfans– Ehler Danlos type 4 (spontaneous colonic rupture, aneurysms,
dissections, kidney infarcts). 1/1,000,000• AAA
– M6:1F, females more likely to die from it– Elective repair or EVAR– CT unless grossly hypotensive or unconscious for idea of where renal
vessels are• Veins: DVTs
NeuroRadiology
• NR imaging techniques: CT, MRI, (X-ray and US)• X-ray only shows bone so no good for brain• MRI good for soft tissue• CT has a rim of white around the brain due to the skull• Examining the brain: 1) Hx and examination then 2) CT because
its quick but not as reliable 3) MRI – brilliant due to no signal or artefact from bone
• Neurones in white matter are white because they are surrounded by fat
• DDx unconscious pt: drunk, drugs, epilepsy…nothing visible on CT so H&E very important
• CT when: GCS <13, <15 2hours after injury, suspected fracture, vomiting in adults/children, post-traumatic seizure, coagulopathy & LOC/amnesia, focal neurological deficit
Blood in NR
• Subdural: crosses sutures, concave - banana
• Extradural: can’t cross sutures, convex
Extradural Subdural
Vessel Mid. Meningeal A Dural veins
Shape Lens (convex) Banana (crescent)
Crosses sutures NO YES
Crosses midline YES NO
Associated # YES NO
Neuroradiology
• Subarachnoid: blood (white) fills the ventricles and around the outside of the brain
• Intraparenchymal/contusions:
Neuroradiology
• Intraventricular:
• Coup and contre-coup
• EXTRA or INTRA-AXIAL
Midline Shift
• If bleeding, pressure is rising and brain matter gets pushed away, across the midline.
• This increased pressure causes brain swelling, which increases ICP which causes more swelling…
• If severe patient can die within hours.
• Mass Effect: loss of grey-white matter differentiation, effacement sulci. By tumours or blood, take up space and cause other things to move
Ischaemic Stroke
• Most commonly middle cerebral artery
• ACA
• tumours
Brain METs
• Commonly from lung and breast
Hepatobiliary System
• Jaundice– Serum bilirubin <30-60 mmol/L– Can be pre-hepatic, hepatocellular or obstructive (cholestatic)– Frequently HC and Obs occur together– A) haemolytic conditions: spherocytosis, thalassaemia, sickle cell– B) congenital hyperbilirubinaemia: Gilberts, 2-5% pop – C) cholestatic (liver parenchyma +/- large duct obstruction)– INTRA-HEPATIC: viral hepatitis, drugs, alcohol, cirrhosis– EXTRA-HEPATIC: CBD stones, Cancer of head of pancrease/ampulla/BD,
biliary stricture, pancreatitis, pseudocyst, sclerosing cholangitis• There are 8segments of the liver, 4 left and 4 right.• Pancreaticobuiliary junction = PD + CBD• Imaging techniques: US, CT, MRI, Endoscopic US, MRCP
Imaging Modalities
• Ultrasound– 1) differentiates normal from abnormal CBD. N=3/4mm– 2) Identifies solid focal liver lesions (METs)– 3) assesses for gallstones in GB– 4) can tell if there is a mass in the pancreas– 1st step in imaging
• CT– Can show multiple low density liver lesions (METs) which would cause
intrehepatic jaundice• MRI
– IV contrast given, pool in any large single masses
Liver
• Benign liver lesions– CYSTS– HAEMANGIOMAS– Focal nodular hyperplasia: common in young women
• Malignant– HCC– Hepatomas – most common 1o tumour– METS!!!!!! Most common
• Extra-hepatic lesions:– Distal to bile canaliculi– Gallstones in CBD: SQUARE shape– MRCP: T2 concentrates on fluid of biliary system, can pick up small
stones
Gallstones in CBD
• Complications– 1) biliary colic– 2) jaundice– 3) pancreatitis– 4) ascending cholangitis
• NB normal bile duct on US doesn’t necessarily mean there are no stones• If you want to MRI gallbladder but its contraindicated, do endoscopic US• Gallstones on US are echogenic and have acoustic shadowing
Cancers causing obstruction
• Ampulla of vater: adenocarcinoma – PD obstructs and CBD obstructs at ampulla (pancreaticobiliary junction)
• Head of pancreas: obstructs PD and CBD before ampulla.• BOTH HAVE DOUBLE DUCT SIGN• Cholangiocarcinoma: obstructs bile duct but not PD, which
reached the duodenum. Can see normal CBD beyond the tumour.
Sclerosing cholangitis
• Inflammation and fibrosis of BDs causing multiple areas of narrowing in the biliary tree.
• 50% associated with IBD, raised AlkPhos• symptoms – itch, jaundice, pain• Can cause portal hypertension• MRCP/ERCP: multiple strictures of INTRA&EXTRAhepatic –
beaded appearance• Liver biopsy diagnostic
Pancreatitis
• Causes: gallstones, alcohol, trauma, ERCP, viral inf, drugs• MILD panc: inflammatory changes in fat around pancreas, fluid
in the fat. Contrast given to see if tissue viable or dead. If takes up contrast – lighter – viable
• Severe pancreatitis: necrosis
Pancreatitis
• Necrotic pancreatitis no viable tissue. Full of digestive enzymes so digests itself and becomes fluid collection.
• After 3 weeks is known as a pseudocyst• If air bubbles develop in the pseudocyst abscess. Requires emergency
treatment
Chronic pancreatitis
• CT multiple pancreatic calcifications• MR abnormal dilated pancreatic duct
Pancreatic carcinoma
• Almost always ductal adenocarcinomas, can get cystic adenocarcinomas and malignant neuroendocrine tumours
• >10% of all GI cancers, M>F, 55-70yo, head affected most• 90% mortality after 1year• US – hypopigmented mass• CT – uncinate process more white than the rest anyway. Dark mass seen
Abdominal X-ray
• Pt details, date, side marker etc• Look for large bowel: faces and gas, circumfrential• Kidneys: mass or calculi• Liver: follows costal margin, if larger – hepatomegaly• Psoas muscles: if not identifiable there is abnormal pathology• Gallbladder: wont see stones• Bones• Shouldn’t see small bowel• Look for hernias at the orifaces!!! Femoral etc
SB obstruction– Causes: adhesions, CD, hernia, volvulus, intussusception, cancer, bezoar etc– Normally <3cm– Valvulae conniventes run the full diameter of the loops– Central in the abdomen
Abdominal X-ray
• Large bowel obstruction– Causes: neoplasm, IBD, diverticular disease, constipation, volvulus, hernia
• Complications: strangulation and bowel necrosis/perf
Crohns disease
• Risk of small bowel obstruction – inflammatory strictures or adhesions
• MRI/CT show dilated small loops• Commonly affects terminal ileum• Ulceration of mucosal lining
Ulcerative Colitis
• Featureless large bowel, continuous, grainy appearance, inflammatory pseudopolyps
Barium studies
• Barium swallow looks at oesophagus and stomach
• Barium enema looks at large bowel• Small bowel series looks at small bowel
Diverticular disease
• Outpouching of mucosa in large bowel• Most commonly sigmoid colon due to high pressure and less
muscular wall• Complications: perforation, abscess, strictures• Due to reduced dietary fibre
Perforation of bowel/ulcer
• Causes of perforation: – Peptic ulcer– Appendicitis– Diverticulitis– Colitis – IBD/infection– Ischaemic bowel– Trauma– Ingestion of corrosives
• X-ray:– PNEUMOPERITONEUM– RIGLERS SIGN– FALCIFORM LIGAMENT SIGN