CT Pathology

   

Hypodense – darker structure than surrounding tissue  

  • Ventricles hypodense compared to other brain tissue   

Isodense – same density as surrounding tissue  

  • Brain stem isodense to brain parenchyma  

Hyperdense – brighter structure than surrounding tissue  

  • Acute bleed is hyperdense  

Midline shift - displacement of brain tissue across centre line of the brain  

  • Structures encroaching into other hemisphere due to increased intracranial pressure  

Filling defect – disruption of normal opacification of a cavity or lumen  

  • Prevents full opacification of blood vessels, caused by an embolism  

Homogenous – uniform structure or composition throughout  

  • Not mottled or permeable, looks smooth/normal, usually positive appearance  

Heterogenous – consisting of different, distinguishable parts or elements  

  • Mottled, permeable, (in arterial phase of abdomen only spleen looks heterogenous but in venous phase it looks homogenous – this is normal) 

 

 

  1. Hypodensity – ischemic stroke, occlusion of an artery of circle of Willis usually middle cerebral artery, brain parenchyma has died  

  1. Hyperdensity – fresh, acute thrombus, acute ischemic stroke in middle cerebral artery, if not treated will end up with an area of hypodensity  

  1. Midline shift – falx cerebri being disrupted, hypoxia (not enough oxygen), no sulci or gyri on left side of brain (appears homogenous), raised intercranial pressure crushing other hemisphere  

  1. Heterogenous – slight difference in liver, not smooth throughout, likely metastatic disease, liver common place for secondary metastases because liver detoxifies, if contrast used there would be enhancement  

  1. Homogenous 

 

 

Key Head Pathologies 

  • Extradural haemorrhage 

  • Subdural haemorrhage 

  • Subarachnoid haemorrhage 

  • Intracranial haemorrhage 

  • Ischemic CVA 

  • TIA 

  • Abscess 

 

Extradural Haemorrhage – injury to an intracranial artery (mostly middle meningeal artery), blood collects and strips dura mater away from inner skull 

Post traumatic event in temporoparietal region (switch to bony window to assess skull fractures) 

Arterial bleed – bleed a lot and quickly due to increase pressure 

Forms lens shaped collection, pushes into brain – dura stuck strongly at sutures 

Symptoms 

  • Depends which lobe affected and how much bleeding  

  • Decreased GCS  

  • Degree of confusion – might not know what happened/who they are 

  • Can be unconscious 

  • As time increases and bleeding continues, level of conciousness and cooperation and wellness decrease  

  • Headache/pain 

  • vomitting 

 

 

Subdural Haemorrhage – venous bleed, rupture to a bridging vein 

Not limited by attachment points of dura to bone – blood between dura and arachnoid 

Slow bleed but will increase over time 

Forms crescent shaped collection  

  • Arachnoid remains intact and doesn’t cross into other hemisphere but will cause mass effect and midline shift 

Acute – bright white/hyperdense 

Acute on chronic – old bleed filled with CSF rebleeding, hypodense 

Symptoms 

  • Presents similarly to extradural 

  • Patient will not be as sick 

  • Stroke like symptoms  

  • Poor balance 

  • Weakness 

  • Numbness 

  • Pins and needles in fingertips 

Mechanisms: trumatic event (e.g., fight) 

 

 

Subarachnoid Haemorrhage – type of haemorrhagic stroke, normally associated with trauma or spontaneous bleeding from intracranial aneurysm 

Can be from spontaneous bleed from arteriovenous malformation or saccular aneurysm rupturing 

Small foramina connect subarachnoid space with fourth ventricle – haemorrhage allows blood to pass into any part of the CSF spaces (sulci/fissures/basal cisterns/ventricles/spinal cord) 

Bleed starts in circle of Willis and mixes with CSF within meningeal layers that connect to brain and spinal cord  

  • Patients can have acute subarachnoid haemorrhage that is not present on CT (won’t get hyperdensity if there is not enough blood mixing into CSF – if bleed is still small) 

Lumbar Puncture required if SAH still suspected by CT is negative 

Every patient with SAH symptoms must undergo a lumbar puncture – needle into spine 3-4th spinal vertebrae, collects CSF to see if there are blood particles 

 

Symptoms  

  • Sudden onset severe headache, reaching maximum intensity within seconds (thunderclap headache) – pain 10/10, cannot bare it  

  • Nausea and vomiting  

  • Photophobia – light sensitivity   

  

 

 

Intracerebral/Cerebral haemorrhage – type of haemorrhagic stroke, bleeding within brain due to a ruptured vessel (intraparenchymal or intraventricular) 

Not confined by any dura 

Arterial bleed – damage to one vessel of circle of Willis 

Causes 

  • Hypertension 

  • Haemorrhagic stroke 

  • Trauma 

  • Whiplash injuries 

  • Racing/motorbike accidents – coming in with speed and crashing to an immediate stop 

  • AVM 

  • Diffusion exon injury 

  • Drug abuse – vessels shut 

  • Tumour 

  • Primary brain tumours/metastases bleeding into brain parenchyma – check patient history 

 

 

Ischemic Cerebral Vascular Accident (CVA) - blood supply to area of brain tissue reduced leading to tissue hypoperfusion 

Most common type of stroke (87%) 

Brain tissue dies off creating hypodensity 

Mechanisms 

  • Embolism 

  • Thrombosis – blood clot forms locally, directly into vessel 

  • Systemic hypoperfusion 

  • Cerebral venous sinus thrombosis 

  • Cardiac arrest 

  • Hypoxia – entire brain has ischemic attack 

 

 

Appears different according to when patient scanned 

Acute – symptoms happened in last hour 

  • Hyperdensity in cerebral vessels, fresh thrombus/clot 

Over time brain tissue becomes hyperdense – tissue not receiving oxygen and nutrients and die 

  • Eventually, will be entirely black and filled with CSF 

Patient outcome affected by when patient is scanned  

Treatment criteria very strict because treatments can be risky – time from onset critical, sooner medical intervention likely to have better outcomes 

Treatment: 

  • Thrombolysis (clot bursting) - inject medicine via cannula to dissolve clot 

  • If stroke occurred under 4 hours ago – cannot have it even if a minute over 

  • Cannot use if haemorrhagic stroke/very bad stroke/history of bleeding/if on medicine contraindicative to medicine used 

  • High percentage will have haemorrhagic stroke following 

  • Thrombectomy (mechanical clot removal) - interventional procedure to physically move clot 

  • If stroke occured six and a half hours after stroke 

  • Can only be done at a stroke centre – time constraint must account to transportation to stroke centre 

  • Enter via groin to carotid 

  • Antiplatelets and anticoagulants (blood thinning) 

  • Given if outside time limit for other treatment 

  • Antiplatelets make blood less sticky, producing less placements 

  • Aspirin 

  • Clopidogrel 

  • Dipyridamole/Persantine  

  • Anticoagulants prevent clotting 

  • Rivaroxaban 

  • Apixaban 

Thrombolysis and Thrombectomy good at preventing strokes but not many patients have it done because criteria is so strict 

 

MCA Sign in Acute Infarct 

Thrombosis whiter in occluded left middle cerebral artery on non-contrast study 

 

5-7 days after initial event, completely infarcted area has well defined geographic appearance with mass effect 

Chronic infarcts have volume loss 

Infarcts can undergo haemorrhagic conversion usually within first few days 

 

 

MCA Chronic Stroke with Volume Loss 

 

 

Haemorrhagic Stroke 

Berry aneurysm off MCA, would be clipped off in interventional 

  

 

Intracerebral haemorrhage – more common (2/3) 

Subarachnoid haemorrhage – 1 in 20 

Haemorrhagic Stroke Treatment 

  • Medication 

  • Surgery 

  • Interventional 

 

Ischemic vs Haemorrhagic Stroke 

 

Transient Ischemic Attack (TIA) - temporary disruption in blood supply to part of brain 

‘mini stroke’ - pre cursor for a larger stroke 

Causes sudden symptoms like stroke  

  • Speech/visual disturbance 

  • Numbness/weakness in face/arms/legs 

Symptoms last for 24 hours but resolve  

Doppler used after a TIA to assess plaque in blood vessels in carotid to see if it will cause a bigger stroke 

 

Abscess – focal area of necrotic tissue 

Can be life threatening 

Symptoms of raise ICP, seizures, neurological deficits 

Hyperdense ring with central low attenuation 

 

Key Chest Pathologies 

  • Pneumothorax 

  • Pulmonary Embolism 

 

Pneumothorax – abnormal collection of air in pleural space between lung and chest wall, collapsed lung 

Mechanism 

  • Trauma – broken ribs 

  • Spontaneous  

CT identifies small pneumothoraxes missed by CXR – shows more about surrounding lung tissue if cause unknown (e.g., emphysematous changes) 

  • Diagnosed on CT if unsuspected previously and CT performed to exclude other causes of chest pain 

  • CT used if had CXR but still deteriorating 

Any chest scan (depending on clinical indications) will need lung windows 

Appearance: pocket/rim of air located outside lung and adjacent to chest wall, most commonly in apices, associated lung collapse, only visible on lung window 

Treatment: reinflation with chest drain 

 

 

Pulmonary Embolism – occlusion of pulmonary vessels in lungs, usually pulmonary arteries 

Usually caused by blood clots that dislodge and travel to lungs – usually arise from deep vein thrombosis in legs  

  • Patient immobile 

  • Recent surgery 

  • Long haul flight 

Other causes: fat, gas 

Symptoms: 

  • Depends on how big embolism is and what it’s occluding 

  • Chest pain in walking, otherwise healthy-looking patient 

  • Patient can be collapsed and very unwell 

  • SOB 

  • Coughing/coughing up blood 

  • Dizziness  

Lung infarct occurs if embolism blocks off lung tissue 

Potentially life-threatening medical emergency 

CXR rules out infection or other causes (lung cancer, pneumothorax) 

CTPA used to image – 75ml @ 4.5-5ml/s followed by saline chaser, time delay or bolus tracking (over pulmonary trunk) 

  • Fast flow requires large cannula 

Appearance: clots seen as ‘filling defects’, contrast cannot fill areas occupied by clots, contrast (bright) surround clots (darker) 

  • Really good opacification in pulmonary arteries 

  • No contrast in descending aorta 

  • Some contrast left in ascending  

Wells score assigns various clinical features to features to a number – predicts clinical probability of a DVT/PE 

  • More than 4 likely PE 

D-dimer can help predict positive scans – protein made when a blood clot dissolves 

Pregnant women need RNI not CTPA where possible 

  • PE common in pregnant women 

  • Higher contrast flow required (6-7ml/s) - pregnant women heart beats faster 

 

Saddle PE – affects both lungs 

 

Key Abdominal/Pelvic Pathologies 

  • Liver metastasis 

  • Abdominal Aortic Aneurysm (AAA) 

  • Renal stones 

  • Hydronephrosis 

CT imaging or choice prior to interventional 

 

Liver Metastasis – cancerous tumour cells that has spread to liver from cancer in another place in body, secondary liver cancer 

Cancer cells found in metastatic liver tumour not liver cells but cells from part of body where primary cancer is (cancerous breast, colon, lung cells) 

  • Many primary cancers metastasise to liver (colorectal/pancreatic/breast/lung/ovarian etc.) 

Portal Venous Contrast Phase 

  • 70 second delay 

  • Contrast @ 3ml/s 

Need IV contrast where possible – give ?staging cancer contrast to see metastases 

Appearance: 

  • Non contrast – multiple low attenuation density lesions 

  • Contrast enhancement – multiple low attenuation metastases, more obvious, enhancement typically peripheral but can be central filling 

  • Stomach lining hypodense 

  • Descending aorta hyperdense 

  • Hepatic vessels highlighted slightly 

  • Liver enhances normally by metastases appear hypodense 

 

 

 

Abdominal Aortic Aneurysm (AAA) - localised enlargement of abdominal aorta, diameter greater than 3cm or more than 50% larger than usual 

Symptoms:  

  • Back pain 

  • Pulsating abdominal mass  

  • Acutely unwell patient, unstable vital signs 

AAA rupture can lead to severe internal bleeding, hypovolemic shock, low BP and unconsciousness 

High mortality rate up to 90% 

 

CT aortogram usually pre and post clavicles to groin  

  • 75ml @ 4.5-5ml/s 

  • Contrast will leak into surrounding visceral area 

  • Time delayed or bolus tracked 

  • Arrested respiration 

  • Image past groin to visualise femoral artery 

Screening available to all men over 65 years – ultrasound used  

Treatment – can only be decided after CT taken 

  • Open surgical repair 

  • Anastomoses – sewing aorta back together 

  • EVAR – Endovascular Aortic Repair 

  • Looking for leaks or if graph infected 

Treatment followed up with outpatient CT scans 

 

Urolithiasis – renal stones, presence of calculi anywhere along course of urinary tract 

Renal cholic presentation 

  • Flank pain 

  • Vomiting  

  • Haematuria – large stone scrapes against walls of small vessel 

  • High temperature/fever 

Non contrast CT KUB Prone/Supine 

 

 

Hydronephrosis – complication of renal stones, cancers, prostatic hypertrophy, pregnancy, congenital, large blood clot 

Ultrasound commonly used first 

CTPV abdomen may be used to rule out cause being pelvic malignancy  

CT Urogram – 150ml @ 3ml/s with saline chaser, 7-11 minute delay 

PV Abdomen – 75ml @ 3ml/s with saline chaser at a 78 second delay 

 

 

Gynaecology and Reproductive System CT Imaging 

CT isn’t first choice 

CT used in cancer staging of these cancers to look for metastatic spread 

TNM Score – Tumour Node Metastatic spread 

 

Gynaecological cancers 

 

Left: thickening of omentum – thicken bowel lining, omentum heterogenous 

Right: Ascites