Emergency Radiology PDF

Emergency Radiology Neuro General notes Dxx of hemorrhagic masses ○ GBM ○ Pituitary macroadenoma ○ Hemorrhagic metastasis Melanoma RCC Thyroid cancer Choriocarcinoma Complications of the depres...

Emergency Radiology Neuro General notes Dxx of hemorrhagic masses ○ GBM ○ Pituitary macroadenoma ○ Hemorrhagic metastasis Melanoma RCC Thyroid cancer Choriocarcinoma Complications of the depressed skull fracture ○ Epidural abscess ○ Dural venous thrombosis, especially SSS Vessels thrombosis Venous thrombosis General notes Epidemiology; younger than 50, female (due to sex-specific risk factors) Etiology ○ Hematological / hypercoagulable state The most common causes; oral contraceptive use, pregnancy / puerperium collagen-vascular diseases (APS), vasculitis, dehydration, hypercoagulable state ○ Infections; sinusitis, meningitis, mastoiditis ○ Neoplasm invading the dura like falcine meningioma ○ Trauma; skull fracture Mechanism; venous thrombus → restriction of venous flow → venous congestion & elevated venous pressure → disruption of BBB with vasogenic edema. If infarction develops, cytotoxic edema ensues Location; the most common is- transverse sinus, followed by SSS Clinical symptoms ○ Venous HTN → headache, vomiting & irritability Venous infarction can be associated with both vasogenic & cytotoxic edema Natural history ○ It is often hemorrhagic ○ Venous ischemia is always reversible after recanalization, because the blood still delivers to the brain parenchyma A dural sinus measuring > 70 Hounsfield units is likely thrombosed Pitfalls 1  ○ Deoxyhemoglobin is dark on T2 and this mimics flow void on T2, therefore T1 is the most important sequence Sagittal sinus thrombosis Imaging ○ Bilateral & multifocal due to involvement of a large sinus ○ CT NECT- hyperdense sinus, cord sign, congested meninges, hemorrhagic infarction CECT- empty delta sign; enhancing dura around non-enhancing thrombus ○ MRI T1 (most important)- bright blood in the SSS with loss of flow void T1+c- empty delta sign T2- less sensitive because deoxyhemoglobin is dark on T2 and mimics flow void DWI- restricted diffusion if infarction develops (usually does) MRV- no flow Transverse sinus thrombosis The most common dural sinus undergoes thrombosis Common etiologies ○ Infection from mastoiditis, through the transosseous emissary veins, or scalp infection ○ Propagates from jugular venous thrombosis Differential consideration of small TS ○ Hypoplastic TS- is a normal variant 50% right dominant, 25% equal, 25% unilateral ○ Arachnoid granulation ○ Idiopathic intracranial hypertension Vein of Labbe ○ It is a cortical vein that drains into the TS ○ Thrombosis of the TS can leads to venous occlusion of vein of Galen → ischemia / hemorrhage of the posterior temporal lobe Deep Cerebral Vein thrombosis Compared to the dural venous thrombosis, it has high mortality Always bilateral → venous congestion / infarction of the basal ganglia & thalami Thrombus can be seen in the; thalamostriate, deep cerebral veins and straight sinus Common causes ○ Extension from dural sinus thrombosis ○ IF; ○ Hyperdense ICVs & straight sinuses ○ Bithalamic edema with effacement of the borders between the deep gray nuclei and internal capsule ○ Thalamic lacunar hemorrhage 2  Differential diagnosis ○ Neoplasm (bithalamic glioma) ○ Wernicke encephalopathy Cavernous sinus thrombosis / thrombophlebitis Clinical manifestations ○ Retro-orbital pain with edema ○ Proptosis ○ Ecchymosis Special causes ○ Sinusitis, the most common cause (by staphylococcus aureus) ○ Meningitis ○ Local skin infection Pathology ○ CS has numerous valveless communication with the vein of the orbit, face & neck, so infection can spread through these conduits Imaging ○ Best modality → T1+c fat-sat ○ CT NECT- lateral bulging of CS wall, thrombosed SOV, proptosis, “dirty” orbital fat, periorbital edema, sinusitis CECT- irregular filling defects within the expanded CS and SOVs ○ MRI Enlarged CV with convex lateral margins T1- isointense thrombus with loss of flow void T1+c fat-sat- nonenhancing filling defect within the enhancing dural wall Venous occlusion mimics / venous sinuses dynamics Intracranial hypertension ○ The venous sinuses, even though they're lined by dura, they're not as fixed and can get dilated / narrowed according to flow dynamics ○ So, intracranial hypertension the brain gets swollen and it actually squishes down (= narrowed) transverse sinus Intracranial hypotension ○ Other side of that coin, is if you have hypotension they can look very plump, but if you blood patch them, they go back down to normal so these can rise and fall depending on intracranial pressure dynamics Arterial occlusion PCA density PCA can mimic the petroclinoid ligament. Associated with PCA territory infarction. 3 ICA density with occipital hypodensity Occurs in fetal origin of the PCA. Uncommon IF; ○ Hyperdense ICA in the carotid canal denoting occlusion. ○ Hypodensity and acute infarction of the occipital region due to fetal origin of the PCA. Basilar artery density Very rare. Usually patients don't make it to the ER. IF; ○ Hyperdense basilar artery ○ Hypodense pons denoting acute infarction Pitfalls Hemorrhagic transformation of acute infarct ○ Occurs with extensive acute infarcts after attempted revascularization ○ Usually in the form of petechial hemorrhage not lobar ○ Location; basal ganglia & cerebral cortex (gyriform cortical) Pseudonormalization ○ It is a form of hemorrhagic transformation. ○ Occurs when there is bleeding in a non-salvageable compromised brain tissue → the dead tissue appears as normal brain (increased density due to blood). ○ It is a serious complication! Transient Ischemic Attack Definition- brief episode of neurologic dysfunction caused by a focal disturbance of brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour Hemorrhagic brain General notes Spreading of hemorrhage along the falx (parafalcine) or tentorium (peritentorium) → not EDH. It is either; ○ SDH → no blood in sulci ○ SAH → associated with blood in sulci Unruptured basilar tip aneurysm can be presented with non-communicating obstructive hydrocephalus, if they are large enough to exert mass effect on brainstem and aqueduct. ○ Remember, ruptured aneurysms can be complicated with obstructive hydrocephalus. (Don’t confuse the 2). ○ However, when finding an aneurysm, always keep looking for SAH. 4 Non-traumatic intracranial hemorrhage (a.k.a. spontaneous) Read again; intracranial which includes intraaxial and extraaxial The extraaxial variety of concern in this context is; SAH, because EDH and SDH occur with trauma. Remember; the most common cause of SAH is trauma Classification ○ Intraparenchyma Feature- no underlying structural abnormality The most common causes; 1. Hypertension. 2. Cerebral amyloid angiopathy. Together they constitute 85% of all causes of non-traumatic hemorrhage Other causes: 1. Anticoagulant / coagulopathy. 2. Illicit drugs (e.g. cocaine). 3. Hemorrhagic venous infarcts. 4. AVM. 5. Aneurysm. 6. Metastasis. 7. Primary brain tumors (ependymoma, glioblastoma). 8. Hemorrhagic transformation of arterial infarcts ○ Subarachnoid The “spontaneous” SAH Causes: 1. Ruptured aneurysm. 2. Nonaneurysmal perimesencephalic SAH Peripheral lobar intraparenchymal hemorrhage, think of; 1. CAA. 2. Hemorrhagic transformation of venous infarct. 3. Vascular malformation. Frontal / parietal lobar hemorrhages can occur with; 1. CAA. 2. Vein of Trolard hemorrhagic venous infarct. Stages of intraparenchymal hematoma ○ Hematomas consist of: A central core and a peripheral rim. ○ In general, Hgb degradation begins in the clot periphery and progresses centrally toward the core. Pearls ○ Intraparenchymal hemorrhage in patients with preexisting hypertension in typical locations (basal ganglia, thalamus, external capsule or posterior fossa) requires no further evaluation. ○ However, lobar or deep brain bleeds in younger patients or normotensive adults—regardless of age—almost always require further investigation ○ The presence of an intraventricular haematoma is considered a poor prognostic factor due to the obstruction to CSF with hydrocephalus and raised intracranial pressure. ○ As a rule, intraparenchymal hemorrhage can spread into subarachnoid space, and the opposite is true when an aneurysm ruptures the pressure of the jet can be so high, that the blood will be injected into the brain parenchyma Hypertensive Hemorrhage Pathogenesis- arteriosclerosis Location- central; basal ganglia, thalamus, external capsule, posterior fossa is less common Bleeding in the thalamus is typically seen in hypertension Extension into ventricular system is common (why) → because it is centrally close to the ventricles Cerebral amyloid angiopathy Epidemiology- age > 65Y Pathogenesis- deposition of B-amyloid protein in the wall of blood vessel leading to weakness Location- peripheral; lobar (frontal, parietal), subcortical white matter 5  Forms- ○ 1. Microbleeds. ○ 2. Macrobleeds ○ 3. Cortical superficial siderosis- cortical subarachnoid hemorrhages that follow the curvilinear shape of the surrounding cerebral gyri Usually it does not extend into the ventricular system (why?) → because it is peripherally located Imaging ○ MRI- to detect hemosiderin deposition resulting from microbleeds. It appears dark signal on gradient Hemorrhagic Venous Infarcts Location of hemorrhage may give a clue of venous thrombosis ○ Vein of Labbe thrombosis Inferior anastomotic vein between the Sylvian vein and transverse sinus Infarction/hemorrhage typically occur in the; temporal lobe ○ Vein of Trolard Superior anastomotic vein between the Sulvian vein and superior sagittal sinus Infarction/hemorrhage typically occur in the; frontal or parietal lobe Imaging ○ Triangular hyperdense sign ○ Cord-like hyperdense sign Arteriovenous Malformation AVM has 3 components; 1. Feeding artery. 2. Nidus. 3. Draining veins Non-Traumatic SAH The most common cause is; ruptured aneurysm. Other cause; non-traumatic perimesencephalic nonaneurysmal SAH Types of aneurysms ○ Saccular The most common type Arise at; bifurcation of the circle of Willis ○ Fusiform Extreme focal ectasia in atherosclerotic disease ○ Mycotic Result from septic emboli in patient with bacteremia Localization of aneurysm based on SAH distribution Aneurysm SAH distribution ICA - PCoA aneurysm Suprasellar cistern Anterior communicating artery Septum pellucidum (in frontal lobes), interhemispheric fissure 6  Middle cerebral artery Sylvian fissure (in temporal lobe) Anterior cerebral artery Sylvian fissure Basilar artery tip Interpeduncular fossa, brainstem or thalamus PICA 4th ventricle Vertebrobasilar aneurysms fourth ventricle, prepontine cistern and foramen magnum Post-aneurysmal SAH complications ○ Cerebral ischemia and vasospasm → CTA/DSA; multiple segments of vascular constriction and irregularly narrowed vessels. ○ Obstructive hydrocephalus. ○ Rebleeding Perimesencephalic nonaneurysmal SAH ○ Definition- non-aneurysmal type of SAH centered around pons & midbrain ○ The most common cause of non-traumatic non-aneurysmal SAH ○ Location- subarachnoid blood in the; interpeduncular, ambient and prepontine cisterns. Suprasellar cistern is clear ○ CTA; -ve for aneurysms. Convexal SAH ○ Definition- isolated spontaneous non-traumatic non-aneurysmal SAH over the brain vertex ○ Location- is characteristic; restricted to the hemispheric convexities, sparing the basal & perimesencephalic cistern ○ Common causes; < 60 → Reversible Cerebral Vasoconstriction Syndrome More in women Presents with frontal convexity SAH. > 60 → cerebral amyloid angiopathy All ages → vasculitis, venous occlusions SAH The traumatic and aneurysmal SAH has different patterns of distribution. The distribution of blood can hint at the expected location of the ruptured aneurysm. Look for hidden areas before concluding “there is not SAH” ○ Superior frontal sulcus. ○ Posterior part of the Sylvian fissure. ○ Base of the interhemispheric fissure. ○ Interpeduncular cistern. ○ Prepontine cistern. ○ Fluid level at the base of the occipital horn of the lateral ventricles. ○ Cervicomedullary junction. Traumatic SAH distribution 7  ○ Anterior-inferior frontal lobe. ○ Temporal sulci. ○ Perisylvian regions. ○ Hemispheric convexities. ○ Look also for; adjacent brain contusions, EDH, SDH, skull fractures, skull base gas Dxx ○ Perimesencephalic nonaneurysmal SAH The most common cause of non-traumatic non-aneurysmal SAH Location- subarachnoid blood in the; interpeduncular, ambient and prepontine cisterns. Suprasellar cistern is clear CTA; -ve for aneurysms. ○ Convexal SAH Definition- isolated spontaneous non-traumatic non-aneurysmal SAH over the brain vertex Location- is characteristic; restricted to the hemispheric convexities, sparing the basal & perimesencephalic cistern Common causes; < 60 → Reversible Cerebral Vasoconstriction Syndrome ○ More in women ○ Presents with frontal convexity SAH. > 60 → cerebral amyloid angiopathy All ages → vasculitis, venous occlusions ○ Pseudo-SAH In severe brain edema like in; meningitis, post-cardiac arrest, brain death, anoxic injury ○ Dural AV fistula It can mimic SAH in both symptoms and imaging presentation. It has both SAH and parenchymal hemorrhage. ○ AVM It may be presented as SAH. Syndromes associated with vascular aneurysms ○ ADPKD ○ FMD ○ Persistent trigeminal artery Aneurysms Unruptured BA aneurysm (= tip aneurysm) ○ Imaging Well-delineated midline mass with peripheral mural calcification Obstructive hydrocephalus (unusual presentation); if they are large and exerts mass effect on brainstem and aqueduct → non-communicating hydrocephalus No SAH Unruptured CPA aneurysm ○ Imaging Well-defined hyperdense mass on CPA 8  ○ Dxx Meningioma Schwannoma SDH Common among elderly (brain atrophy is susceptible to velocity injury) Like SAH, the most common cause; trauma Most common location; supratentorial Common associated with mass effect in the form of; subfalcine herniation Prognosis depends on ○ Hematoma thickness ○ Midline shift ○ Associated parenchymal injuries Forms ○ The classic; supratentorial crescent shape extraaxial collection ○ Parafalcine ○ Peritentorium Causes of isodense aSDH ○ Extremely anemic patient ○ Patient with anticoagulation ○ Associated CSF leak through torn arachnoid layer ○ How to detect this subtle hemorrhage? Mass effect in the form of midline shift. The hypodense white matter doesn;t reach the end (compare to other side) Effacement of the sulci adjacent to the bone ((compare to other side) Dxx ○ EDH Biconvex Vs. crescent shape in aSDH Always associated with skull fracture Vs. aSDH occurs with absent fracture Cross the dural attachment Vs. aSDH never cross falx or tentorium Never cross the sutures Vs. aSDH can cross the sutures Pearls ○ Unlike EDH, only small amount of SDH can be associated with massive effect. Thus, if the distinction between EDH / SDH is unclear, look for mass effect / midline shift, common with SDH. ○ Epidural hematoma is usually not associated with mass effect, because of contained blood. The exception is the EDH in the posterior cranial fossa. EDH Typically associated with skull fracture → look for suture diastasis It crosses the falx and tentorium and never cross sutures Forms ○ Most common type is arterial EDH. ○ Venous EDH Usually managed expectantly Can cross the midline especially if vertex venous EDH 9  Vertex EDH Linear or diastatic fracture crosses the SSS IF ○ Best seen in coronal view ○ Anterior hyperdensity across the midline ○ Displaces SSS & cortical veins inferiorly Anterior temporal EDH Injury to the sphenoparietal dural venous sinus IF; small biconvex anterior middle cranial fossa EDH On the posterior fossa overlying the transverse/sigmoid sinuses BRAIN CONTUSIONS Occur in highly predictable locations ○ Anterior inferior (orbital) surfaces of the frontal lobes (just like tSAH) ○ The temporal poles ○ Perisylvian gyri (just like tSAH) IF; ○ Focal areas of petechial hemorrhage, surrounded by hypodense areas of edema DIFFUSE AXONAL INJURY (= SHEAR INJURY) Typical locations; ○ Subcortical WM (usually in the frontal lobe) ○ Corpus callosum or septum pellucidum ○ Medial temporal cortex is always associated (Dr. Strong- vRad) IF; ○ Dense rounded lesions not associated with surrounding edema Vs. brain contusion DURET HEMORRHAGE Location; centrally located in the midbrain Associated with; transtentorial herniation → compromise of brainstem circulation → infarction & hemorrhage Vasculopathies MOYA-MOYA DISEASE Common among asians (korea/japan) IF; ○ Marked narrowing of both supraclinoid ICAs, which results in ○ Extensive BG and WM collaterals (puff of smoke sign) ○ Acute parenchymal hypertensive hemorrhage Miscellaneous RUPTURED DERMOID CYST ⏺️ IF; 10  ○ Well-defined hypodense midline mass usually in the suprasellar cistern (usually) ○ Multiple fatty “droplets” disseminated in the CSF cisterns; suprasellar, interhemispheric fissure and sulci Rupture causes symptoms of chemical meningitis with seizure, headache, coma, vasospasm or infarction COLLOID CYST WITH OBSTRUCTIVE HYDROCEPHALUS ⏺️ IF ○ A well-defined hyperdense mass wedged on the top of 3rd ventricle at the foramen of Monro. ○ Hydrocephalus SAH WITH VASOSPASM It is a complication of SAH IF ○ SAH with / without aneurysm. ○ Multiple cortical hypodensities scattered sporadically throughout the brain denoting acute infarction due to vasospasm. ○ Maybe associated with intraventricular hemorrhage and hydrocephalus Traumatology Based on (University of Washington Emergency Radiology Review 2023) course Chest wall & Pulmonary trauma Chest wall Bony injury Pleura Lung General notes The major distinction between pulmonary contusion & laceration is the presence of pneumatocele / hematocele in lacerated lung parenchyma Chest wall vascular injury The risk for chest wall trauma is damage to one the chest wall arteries, which is fatal Findings usually missed because radiologist trying to find the “pneumothorax” or “aortic injury” Sternal fracture Associated with; myocardial contusions, thoracic spine injury Imaging ○ Retrosternal hematoma ○ Anterior / posterior fracture displacement Posterior displaced fracture ○ Usually the case as the trauma pushed the sternum back (direct compression to the chest) 11  Anterior displaced fracture ○ Occurs due to clamshell mechanism or a distraction injury ○ Strongly associated with thoracic spine injuries Sternoclavicular dislocation The manubrium of the sternum should be 50% covered by clavicular heads Posterior dislocation ○ It is posterior displacement of the clavicular head relative to the manubrium ○ Results from; posterior blow to the shoulder or blow to the medial clavicle ○ Less common (10 - 20%), but more dangerous ○ The risk is; impingement on or injury to the aorta, great vessels, trachea or esophagus Pseudoaneurysm to brachiocephalic artery Intimal tear to base of the carotid artery ○ Imaging Anterior mediastinal hematoma / fat stranding toward the site of dislocated clavicle Asymmetry in the proximal clavicular physis Anterior dislocation ○ More common (80 - 90%) but less dangerous ○ Results from anterior blow to the shoulder Rib fracture Could be displaced or non-displaced May result in lung herniation or flail chest Pearl ○ When you see lower rib fractures → suspect upper abdominal visceral injuries (spleen or liver) Flail chest Definition- 3 or more ribs broken in 2 or more places Associated with; lung contusion, hemo/pneumothorax or lung herniation Importance- early operative fixation of these injuries is associated with a substantial decrease in both mortality and the need for tracheostomy Lung herniation Is a consequence of a flail chest Herniation occurs through a defect created by rib or costochondral fracture It means, not the ribs are only fractured, but there is disruption of the chest wall → allow lung parenchyma to herniate through and extends outside the expected contour Pneumothorax When you see a pneumothorax, especially on supine CXR, it is big! Direct sings ○ Deep sulcus ○ Sharp aortic / cardiac / diaphragmatic contour ○ Basilar lucency Indirect signs 12  ○ Subcutaneous air ○ Rib fractures Hidden areas to look for subtle pneumothorax Tension pneumothorax Imaging ○ The same signs of pneumothorax above + ○ Contralateral mediastinal shift ○ Inferior displacement of the ipsilateral hemidiaphragm ○ Spreading-out of the ribs Hemothorax It is arterial bleeding into the chest Imaging ○ Uniform high attenuation opacity throughout the chest Lung contusion It is the simplest form of lung parenchymal injury Definition- focal alveolar hemorrhage and interstitial edema Appears; 24 hours after the insult. Clear; 72 hours after the insult It is characterized by architectural preservation Vs. lung laceration Imaging ○ CXR- patchy areas of consolidation ○ Ill-defined opacities beneath the site of injury in a non-segmental distribution (not confined to a particular lobe) ○ Associated with surrounding halo ○ Usually there is 1 - 2 mm subpleural sparing Vs. pneumonia Pulmonary laceration Localized tear in the parenchyma, spherical shape that is filled with air (pneumatocele), blood (hematocele) or both Round, because lung is an elastic structure, so even linear tear will produce rounded structure It is characterized by architectural distortion Vs. lung contusion Usually surrounded by lung contusion Healing result in residual lung scarring resemble lung nodule (pseudonodule) Pseudotumor It is organized pulmonary laceration into pulmonary nodule Comparison with previous scan at the time of insult is important to avoid miscalling it as nodule Pulmonary infarct The lung is torn-off from its pedicle There is loss of 13 Diaphragmatic & Mediastinal trauma General notes Causes of pneumomediastinum ○ Tracheobronchial injury ○ Complication of dyspnea ○ Aggressive mechanical ventilation ○ Esophageal rupture Diaphragmatic injury Etiology- penetrating injuries > blunt > iatrogenic Mechanism of injury ○ High energy force to the lateral lower chest / upper abdomen → rise in the abdominal pressure → significant impact on the weakest points in the diaphragm called; lumbocostal & sternacostal triangles ○ The tear usually happens in the radial fashion Left > right by 3:1 Right diaphragmatic injury is very difficult to diagnose (problematic!) Imaging ○ Discontinuity of the diaphragm ○ Visceral herniation +/- collor or dependent viscera signs ○ Elevation of the abdominal organs ○ Dangling of the diaphragm ○ NGT above the right hemidiaphragm ○ Dependent viscera sign; the stomach is sitting on the posterior ribs and abutting the left ventricle & pericardium. It is when the herniated viscera lie against the posterior thoracic wall in a dependent position, as they are no longer supported by the diaphragm ○ Callor sign; herniation of the abdominal viscera into the lower chest with focal constriction (or indentation). On the right where liver herniates, it is called cottage loaf sign ○ Thickening & stranding of the diaphragm at the site of injury Pitfalls ○ Diaphragmatic eventration Abnormal contour of the diaphragmatic dome, due to diaphragmatic thinning, with no disruption to the diaphragmatic continuity It has uniform thickness of the diaphragm Tracheobronchial injury Technique ○ MIP protocol improves the visualization of the the bronchial laceration Forms ○ Cervical (upper airway) ⅔ of TBI Etiology- 70 - 80% penetrating (GSW > stab) Imaging Since the cause is penetrative, the presentation is not only airway disruption, rather there will be extensive emphysema and soft tissue swelling 14  ○ Intrathoracic (lower airway) Higher detection rate Vs. cervical Etiology- most commonly; blunt trauma The most common location (80%) is; 2 - 3 cm above the carina. Trachea > rMB > lMB Imaging Disruption of the posterior wall of the trachea (the most common wall) Outpouching from the wall filled with air ○ Iatrogenic injury Most common location is; upper intrathoracic portion of the airways Presented with; longitudinal tear ○ TBI with esophageal involvement Involvement occur in the form of; fistula between the trachea & esophagus Imaging Continuous tract between the posterior wall of the trachea & esophageous Thickening of the esophageal wall at the site of the fistula Other 2ry sings; pneumomediastinum, subcutaneous emphysema, lung injury Imaging ○ Goals of MDCT Location of defect Size of defect Signs of mediastinitis Fistulization ○ Tracheal / proximal lMB Pneumomediastinum and cervical emphysema WITHOUT pneumothorax ○ Bronchial injury “Fallen lung” sign It reflects complete bronchial transection Occurs when the lung collapses against the lateral chest wall or diaphragm, rather than toward the hilum, which is the usual situation Traumatic esophageal injury Etiology- Iatrogenic > non-iatrogenic, commonly after endoscopy procedures The most common location of non-iatrogenic; cervical > thoracic > abdominal > combined The most common location of iatrogenic; thoracic > cervical Pathogenesis- increase in intraluminal pressure against a closed glottis results in a tear at the weakest point of the esophageal wall Imaging ○ Neck & Chest Subcutaneous emphysema ○ Pleura Pleural findings usually occur with lower esophageal involvement Left > right Effusion +/- air ○ Mediastinum (almost always seen) Pneumomediastinum Fluid and air collection around the esophagus and visceral compartment 15  Contrast extravasation into mediastinum or pleural space by esophagogram Abnormal contour of the esophagus Pneumopericardium (if middle esophagus is involved) Esophageal rupture from Mallory-Weiss syndrome (= Boerhaave’s syndrome) Rupture occurs due to; forceful vomiting → transmural esophageal tear Findings ○ Left sided pleural effusion, as the site of injury in Boerhaave syndrome is classically localized to the left posterolateral aspect of the esophagus at the lower third of the esophagus Dxx ○ Traumatic esophageal rupture; pneumomediastinum is LESS extensive Abdominal trauma For protocols, review here Mechanism of trauma ○ Right side trauma → injury to the liver, hemidiaphragm, right kidney, right adrenal, lung ○ Left side trauma → injury to the spleen, hemidiaphragm, left kidney, left adrenal, lung ○ Midline trauma → left liver lobe, duodenum, pancreas, aorta, spine Due to hemorrhage, victims may demonstrate “shock bowel” features ○ Flattened IVC ○ “Shock bowel” pattern Useful attenuation values ○ Free fluid; (0 - 15 HU) ○ Free (unclotted) blood; (20 - 40 HU) ○ Clotted blood or hematoma; (40 - 70 HU) Easily (but important) missed injuries ○ Bowel & mesentry ○ Pancreas ○ Diaphram ○ Major vessels: arteries, veins Abdominal contrast extravasation Vascular ○ Active extravasation (arterial, venous) of high density contrast external to vessel Within parenchyma Subcapsular “Free” intraperitoneal or extraperitoneal ○ Pseudoaneurysm ○ Arteriovenous fistula Urinary ○ Kidney ○ Ureter ○ Bladder 16  Bowel- small or large if oral / rectal contrast is administered Pseudoaneurysms ○ Definition- it is a defect of the arterial wall with disruption of intima & media, it is a contained vascular injury. Contained because, there is holding back of hematoma by; adventitia layer, clot or surrounding parenchyma ○ Shape They display well-defined edges, because they are contained Acute angles ○ Because they are connected with the artery, they enhances and become isodense to aorta in delayed phases Arteriovenous fistula ○ Definition- arterial to venous shunt due to injury to adjacent artery and vein ○ Easier to identify on selective angio → draining vein opacifies early (before other veins) due to fistula ○ Since most trauma cases are done using PV phase, it is a challenging task to detect AVF due to Non-selective opacification of arteries Absence of real time imaging Hard to see early filling of draining vein Active extravasation ○ Active extravasation (arterial, venous) of high density contrast external to vessel. 3 forms Within parenchyma (called intraparenchymal hematoma) Subcapsular “Free” intraperitoneal or extraperitoneal ○ Features of high density contrast outside the expected location in the vessels Rule- characterization of active bleed is done by comparing the PVP and the delayed phase “Contrast blush” (80 - 370 HU), more dense than surrounding hematoma Not contained collection (irregular margins) Change in size & morphology over time, as it continues to spread due to continuous leaking Attenuation is likely > aorta on delayed images ○ Density often within 10-15 HU of adjacent arteries. This is essential to differentiate IV contrast from the rectal one for example ○ Bleeding rate “brisk” ○ Remember, observation is unacceptable How to differentiate pseudoaneurysm / AVF from active extravasation? ○ Contained collection (better defined margins) ○ PSA / AVF have similar attenuation to arteries on all phases ○ On delayed phase, doesn’t meet the criteria for active extravasation Contrast “washes out” rather than accumulating 17  No change in morphology or size on delayed Splenic trauma Protocol ○ PV phase! ○ However, 10-15% of splenic pseudoaneurysms are not The most frequently injured intra abdominal organ Usually by penetrating injury from broken ribs → so, lower rib fractures may indicate upper abdominal visceral injuries In splenic injury, try to detect if it is multifocal or focal as the management differs! Grading ○ I- < 1 cm deep ○ I- ~ 2 cm deep ○ III- > 3 cm deep ○ IV- Vascular bleeding is confined. ¼ laceration ○ V- Vascular bleeding is beyond the capsule. Shuttered kidney Forms ○ Laceration Most conspicuous on PV phase Linear, irregular or branching areas of decreased attenuation ○ Fracture “Thru-and-thru laceration” = shuttered spleen No definable splenic tissue is present in the LUQ ○ Hematomas Imaging of intraparenchymal hematoma 40 - 70 HU, lower than PV perfused spleen Round / oval Vs. laceration (linear) or infarction (peripheral wedge) Subcapsular hematomas exert mass effect on underlying parenchyma ○ Pseudoaneurysm They fade on the delayed images Vs. active bleed (expand) ○ Active bleeding Extraparenchymal (capsular) = jet-like as blood “escapes the capsule” Intraparenchyma = patchy / globy Both show expanded areas of contrast on delayed images Pearls ○ Any focus of hyperdensity within the spleen after trauma is either activa extravasation or pseudoaneurysm. Differentiate between them in delayed images Active extravasation → expands Pseudoaneurysm → fades away ○ Differentiation between active extravasation & pseudoaneurysm / AVF is important, especially in splenic trauma since the management is different → pseudoaneurysms / AVF: embolization; active extravasation: may be splenectomy 18  ○ Severe injuries can affect the hilar vascular structures, leading to total or subtotal organ devascularization Pitfalls ○ Over / Under call During the arterial phase, marked heterogeneity of the spleen can mimic / obscure lacerations (due to zebra pattern) → need PV phase ○ Under call Delayed phases → decreased enhancement → decreased conspicuity of lacerations & hematomas. Always PV ○ Preserved islands of parenchyma In severe injuries, it might be confusing to differentiate between remaining parenchymal islands Vs. active extravasation → compare with delayed images ○ Over call Splenic clefts, beam hardening artifact, respiratory motion, pre-existing splenic lesion Pancreatic trauma Protocol ○ Pancreatic protocol (early arterial) Rare, but if missed, pancreatic duct leak could be lethal due to complications of fistula, hemorrhage, sepsis and eventual death 90% is associated with other injuries ○ Left lobe of the liver ○ Spleen ○ Duodenum ○ Stomach Location- neck of the pancreas Complications ○ Cause of early death: acute hemorrhage ○ Delayed complications: fistula, abscess, hemorrhage, sepsis Imaging ○ Direct signs Laceration Transection Focal enlargement ○ Indirect signs Peripancreatic fluid Fluid between the splenic vein & the gland Fat stranding Hemorrhage ○ Pancreatic duct disruption Evaluation of the MPD is important for 2 reasons Injury to the duct causes the leak and then the complications (abscess > fistula) The management differs if pancreatic injury is associated with duct disruption 19  Can be evaluated by: MDCT, MRCP, ERCP MDCT ○ Disruption is predicted by depth of laceration (50% of AP diameter) ○ Can demonstrate the duct directly Renal trauma Renal injuries after trauma ○ Renal contusion ○ Renal laceration ○ Renal fracture (a severe subtype of of renal laceration) ○ Shattered kidney (subtype of renal fracture) ○ Renal infarct (due to thromboembolic event following arterial -usually aortic- injury, spleen might also affected, or renal vascular pedicle injury) ○ Renal hematoma ○ Renal vascular pedicle injury ○ Ruptured UPJ Grading ○ I- ○ II- ○ III- ○ IV- urine leak, segmental infarct, ○ V- devascularized kidney, main vascular injury, Renal contusion ○ Definition- parenchymal injuries that produce interstitial edema and hemorrhage ○ Self-limiting disease ○ IF; Well-defined wedge area of reduced enhancement Hypofunctioning, manifested as delayed enhancement relative to non-contused areas Delayed images shows persistent nephrogram with delayed contrast excretion No perinephric hematoma (to differentiate it from renal fracture) ○ Pitfalls (other Dxx of this pattern; renal artery injury -vasospasm- or associated big artery -aorta- injury) → repeat CT after 1 week Renal laceration ○ Definition- ○ IF; Linear defect of low hypodensity in the renal parenchyma associated with perinephric hematoma ○ Dxx; Renal infarction- wedge shaped hypodensity Vs. linear hypodensity, no perinephric hematoma Vs. with perinephric hematoma Renal fracture 20  ○ Severe form of renal laceration in which the renal laceration extends through a full thickness of renal parenchyma → divides the kidney into 2-3 separate segments ○ Patients usually hemodynamically unstable ○ IF; Marked renal injury extending into the renal hilum & dividing the kidney into multiple segments Extensive perirenal hematoma with contrast extravasation Collecting system laceration ○ Protocol- delayed imaging ○ IF; The kidney is surrounded by fluid density (perinephric urinoma) in the perinephric space Delayed scans show extravasation of contrast into this fluid A linear “cut” of the pelvis is noted in delayed scans with no traces of contrast distally No kidney deformity. Homogenous enhancement Dxx; Subcapsular hematoma ○ High density fluid in one side of the kidney (not surrounding it) ○ It displaces / deforms the kidney Collecting system hemorrhage ○ It is arterial hemorrhage into the collecting system ○ IF; Hyperdense focus within the collecting system during the corticomedullary phase Extravasation of contrast Renal AV fistula Renal cyst rupture Horseshoe kidney with laceration Prune belly with laceration Congenital UPJO with laceration Bowel trauma It is rare (1-2%) but challenging diagnosis Increased risk with ○ “Seat belt sign” ○ Chance fracture Importance ○ Needs to be diagnosed early, because no specific clinical sign to make the diagnosis of bowel injury in patient with abdominal trauma 21  ○ Delay is diagnosis (~8-h) is an important cause of mortality & morbidity CT findings ○ Extraluminal air ○ Intramural hematoma / intraluminal bleeding ○ Bowel wall thickening (>4 mm) ○ Bowel wall hypoenhancement ○ Pneumatosis Extraluminal air ○ Intra- or retroperitoneal (pneumoperitoneum) ○ Appropriate window setting: lung or bone ○ Pitfalls Pseudopneumoperitoneum Definition- linear air foci trapped between abdominal wall & peritoneum Associated with ○ Extraperitoneal rectal injuries ○ Rib fractures ○ Pneumothorax ○ Pneumomediastinum How to differentiate it from true (+ve) pneumoperitoneum? ○ Gas collection deeper in abdomen and adjacent to ruptured viscus ○ Decubitus series → look for any change with gravity, which would imply a likelihood of pneumoperitoneum Bowel wall thickening (>4 mm) ○ Patterns of bowel thickening in the context of trauma Focal: contusion, hematoma, ischemia (sign of bowel injury) Diffuse: shock bowel (due to hypovolemia) ○ Focal pattern is what matters regardless of the cause, because the entire segment will undergo laparotomy & resection ○ Associated findings Mesenteric hemorrhage Hemoperitoneum ○ Pitfalls Transient peristalsis Delayed series help differentiating transient peristalsis from true bowel wall thickening, as the latter tends to be stable during the subsequent exams Bowel wall hypoenhancement ○ It caused by vascular injury to the associated mesentery (remember, mesentery carries blood supply to small bowel) ○ This will leads to ischemic bowel Abdominal major vascular injuries Mechanism of injury: rapid deceleration, direct crush injury, flexion-extension Findings ○ Active extravasation 22  ○ Pseudoaneurysms ○ Dissections ○ Intimal flaps ○ Thrombosis ○ AVF Pelvic trauma General notes Protocol Essential lines to be evaluated ○ Shenton line- a curvilinear line along the under surface of the femoral neck to the inferior margin of the superior pubic ramus ○ Iliopectineal line- begins at the sciatic notch and extends downward to the pubic tubercle (break of this line= anterior column fracture) ○ Ilioischial line- begins at the sciatic notch and extends vertically downward adjacent to the radiographic teardrop of the acetabulum (posterior column) ○ Sacral arcuate lines- ○ Greater sciatic notch- Pubic ramus is abnormal when it is > ,5 cm The pelvic bone is not a complete solid ring as it has “discontinuity” at ○ Bilateral sacroiliac joints, posteriorly ○ Symphysis pubis, anteriorly ○ So, then a ring breaks at one location, it is very common to break in at least 2 locations Complications of the pelvic bone fractures ○ Associated with vascular injury (therefore arterial phase to evaluate arteries is important) ○ Can leads to pulmonary fat embolism (causing noncardiogenic pulmonary edema) Pelvic vascular injuries Protocol ○ Pelvic CTA is done on selective basis: patients with pelvic fractures (pelvic ring disruption) on admission portable pelvic radiograph ○ Arterial phase is essential in any patient with displaced pelvic fracture, because PVP is not sensitive for detection the “source” of blood; arterial, venous, bone or combination ○ Why CTA is done? Rapid (early) detection of source of bleeding Differentiate between active arterial & active venous hemorrhage Detect other types of vascular injuries; occlusion, intimal injury, Importance- major bleeding (40%) with pelvic fractures Sources- arterial, pelvic venous plexus, major veins, osseous or in combination Q- why differentiating the source of bleed is important ? ○ Because the management is different ○ Venous or osseous bleeds respond effectively to conservative measures such as external fixation or stabilization without endovascular therapy 23  ○ Whereas, patients with arterial source of bleeding don’t respond well to the conservative measures alone, and most often require interventional therapy, usually by embolization Differentiating between arterial & venous hemorrhages ○ Arterial source- “blush” of contrast during the arterial phase ○ Classification of pelvic fractures AP compression Lateral compression Vertical shear Complex (combined) AP compression force The 1st point of failure is at; symphysis pubis Etiology- MVA with front end collision Injuries ○ Diastasis of the symphysis pubis ○ SIJ book open anteriorly ○ Iliac wing fractures 3 subtypes ○ AP-I Anterior disruption; Vertical pubic rami fractures or Symphysis diastasis < 2.5 cm No posterior ligament injuries No pelvic instability ○ AP-II (a.k.a.; open book fracture) Anterior disruption; Vertical pubic rami fractures or Symphysis diastasis > 2.5 cm Posterior disruption; Sacrospinous ligament disruption Sacrotuberous ligament disruption Anterior SI ligament disruption It causes external rotation of the iliac wing It is pelvic unstable injury ○ AP-III All features of AP-II + Posterior SI ligament disruption Hemipelvis displacement Gross instability Lateral compression force 24  Etiology- T-bone collision / side compact force Injuries ○ Pubic compression fractures ○ Sacral impaction fractures ○ SI “book open” posteriorly 3 subtypes ○ LC-I Commonest, least destructive Mechanism- lateral force to the posterior pelvis Features Transverse pubic rami fractures Sacral crush (buckle) fracture, manifested as disruption of sacral arcuate lines No significant pelvic instability ○ LC-II Mechanism- lateral force to the anterior pelvis All characterized by Anterior ○ Transverse pubic rami fractures ○ Medial displacement Posterior ○ Crush / buckle to sacrum II-A Posterior SI ligament disruption II-B Oblique iliac fracture ○ LC-III Most severe, grossly unstable Mechanism Lateral force continues across the midline and sweeps over contralateral side (“rollover”) Lateral compression on 1 side and anterior compression on the opposite side Contralateral sacrospinous, sacrotuberous and anterior SI disruption (windswept) Features Ipsilateral ○ By lateral compression force ○ Internal rotation ○ Obturator ring transverse fracture involving superior & inferior pubic rami Contralateral ○ By anterior compression force ○ External rotation ○ Vertical pubic rami fracture 25  ○ Disruption of anterior SI joint (open) Comparison between APC and LC APC LC pubic rami fractures vertical horizontal symphysis diastasis II, III III sacral fracture 4% 88% acetabular fracture posterior central Vertical shear injury It is separation of one hemipelvis completely from the rest of the ring Gross instability Injuries ○ Anterior injury Vertical pubic rami fractures Symphysis disruption (rupture) ○ Severe posterior disruption Vertical iliac or sacral fracture Sacrospinous / sacrotuberous ligament disruption Anterior and posterior sacroiliac ligament distribution Superior displacement ○ Associated (jumper) fractures Calcaneal fracture Thoracolumbar burst fractures Acetabular roof fractures Acetabular fractures Anatomical consideration ○ Detailed General notes ○ Anterior column fractures extend above the acetabular articular surface onto the iliac wing ○ Mechanism- occurs when the femoral head or neck impacted on the acetabulum ○ 4 fundamental lines Anterior wall Posterior wall Iliopectineal line Ilioischial line ○ All column fractures run through the ischiopubic ramus and obturator ring ○ Coronally oriented fractures are typical of column fractures (on axials) Classification (represent 80% of acetabular fractures, ⅔ ) ○ Elementary fractures 26  Anterior wall The least common fracture Fracture involves the anterior acetabular wall with involving the quadrilateral surface The connection of the anterior column to the sciatic buttress is intact Does not involve obturator foramen (to distinguish it from anterior column) Pitfalls ○ The anterior wall fracture liberate a bone fragment, a feature distinguishing it from superior pubic ramus fracture Posterior wall It involves the posterior acetabular surface (rim) Mechanism; trauma to the distal femur with flexed hip (dashboard) → drives the femoral head posteriorly into the posterior acetabular wall → posterior wall fracture & posterior hip dislocation Imaging ○ On axial, the fracture is obliquely oriented, impacted fragments also seen, Anterior column Involves the anterior portion of the acetabulum separating it from the sciatic buttress, iliac bone, obturator foramen (a feature distinguishing it from the anterior wall fracture) and extends into ischiopubic ramus Associated with posterior hip dislocation Posterior column It involves the posterior wall of the acetabulum separating it from the sciatic buttress The fracture runs from the greater sciatic notch through the acetabulum and greater sciatic notch to the ischiopubic ramus Unstable and associated with posterior femoral dislocation / subluxation Transverse Although it traverses both columns is not considered both columns because no fracture involving the iliac wing (anterior column) and a portion of each column is connected to the Transverse fractures of the acetabulum are predominantly transverse in the acetabular plane but are actually sagittal oblique (with the me-dial aspect superior to the lateral aspect) in the anatomic plane The fracture line extends through the quadrilateral plane The fracture separates the acetabulum into superior (ileum) and inferior (ischiopubic) ○ Associated fractures Transverse with posterior wall T-shaped Transverse fracture with inferior extension into the inferior pubic ramus or ischium Both column fractures Completely dissociates the acetabular column from the sciatic buttress Anterior column or wall with posterior hemitransverse 27  Anterior component of the fracture could be anterior wall or anterior column It differs from T-shaped fracture in which the anterior component rises anteriorly towards the anterior column, whereas the T-shaped fracture continue as a straight line Posterior column with posterior wall ○ Temporal bone fractures 2 types of petrous bone fractures ⏺️ ○ Longitudinal (=linear) fracture of the petrous part → disruption of the ossicles & tympanic membrane rupture → conductive hearing loss Might extend to the other side straight across the central skull base and causes bilateral temporal bone fractures. How to suspect? → look for sphenoid hemosinus. It is important to be aware of this as the patient might require CTA (due to potential carotid injury) ○ Transverse fracture → disruption of the otic capsule and / or damaging CN7 or CN8 → sensorineural hearing loss ○ This classification is classic and not accurate. Therefore, a new classification is developed that provide much prognostic information Temporal bone fractures- new classification 1 Otic capsule involvement / sparing ○ It is binary; involved or not Ossicles dislocation / fracture ○ Can be hard to evaluate ossicles in case of associated hemotympanum ○ IF; Loss of normal ice cream-cone arrangement Associated with longitudinal temporal bone fracture Facial nerve involvement Any skull base gas is either due to ⏺️ ○ Associated soft tissue laceration or ○ Skull fracture with communication to the PNSs including mastoid air cells. Neck Emergencies Penetrating neck trauma 1 http://uwmsk.org/temporalbone/trauma.html 28 Maxillofacial Trauma General notes Rules ○ Any bone displaced into the intracranial space, will potentially damage the dura and cause infection; meningitis, epidural abscess. Examples; blow-out fracture of the superior orbital rim, ○ Clear sinus sign; if sinuses & mastoid air cells are clear, the only facial fractures one can have are; (other bones have walls with the sinuses) Nasal bones Zygomatic arches (mandible) ○ Maxilla is very sensitive to horizontal impact ○ Mandible is very sensitive to lateral impact ○ Maxillofacial fractures Nasal bone fractures Naso-Orbital-Ethmoid fractures (NOE) Frontal sinus fractures Orbital fractures Floor ○ Blow-out, ZCM ○ NOE, Le Fort II Medial wall ○ Blow-out ○ NOE, Le Fort II / III Lateral wall ○ ZMC ○ Le Fort III Roof ○ Blow-in, blow-up ○ Skull base fractures Blow-out fractures ○ Floor / medial wall fractures ○ + / - herniation Non blow-out fractures ○ Orbital roof; blow-in , blow-up ○ Lateral wall; associated with zygoma fracture ○ Medial wall; associated with NOE, Le Fort II / III Zygomatic fractures Maxillary fractures Mandibular fractures Nasal bone fractures Forces ○ Lateral force 29  Commonest Nasal bones are displaced to one side ○ Inferior force Associated with septal injury only while the nasal bones are preserved Why is nasal septum fracture of special importance? → because treatment of nasal hematoma is important to avoid; 1. Ischemic necrosis. 2. Saddle deformity. 3. Abscess formation ○ Frontal impact This area is the most resistance Telescoping as driven inward → frontal processes splayed laterally → NOE Terminology to describe nasal fractures ○ Displaced / Nondisplaced ○ Unilateral / Bilateral ○ Telescoped Naso-Orbital-Ethmoid fractures (NOE) Injury to the “interorbital space”, the space between the eyes and is composed of; 1. Cribriform plate on top. 2. Lower border of the ethmoid sinus below. 3. Medial orbital walls laterally Injuries to these structures → widening of the intercanthal distance Frontal sinus fractures Essential anatomy ○ Anterior frontal sinus wall is usually with thick bone ○ Posterior frontal sinus wall is usually thin walled and it separates the sinus from the brain ○ When the frontal sinus is large, this act as protective for posterior wall ○ When the frontal sinus is small, the posterior wall is usually fractured ○ When there is posterior wall is fractured, the assumption is that there is; 1. The dural matter has been breached. 2. CSF leak should be considered Fracture of the frontal sinus requires high G-forces, so it is associated with head & hyperextension C-spine injuries Posterior wall fractures complications ○ Epidural abscess ○ Meningitis (dural tear) ○ CSF leak Orbital fracture- Blow-out It involves the weakest bones of the orbit; floor / medial walls Zygomaticomaxillary complex fractures Essential anatomy ○ Zygoma has 4 attachments to; 1. Maxillary bone. 2. Frontal bone. 3. Arch of the temporal bone. 4. Greater wing of sphenoid It is the 2nd most commonly fractured bone after the nasal bone Injury will disrupt all 4 attachments rather than fracture the body of the zygoma 30 Le Fort fractures Definition- injuries result in separation of the maxilla from the skull base They are horizontal fractures All fractures involved the pterygoid plates posteriorly 3 types ○ I- transverse ○ II- pyramidal ○ III- suprazygomatic Le Fort I Transverse fracture of the maxilla involving the; 1. Maxillary sinus. 2. Nasal septum. 3. Pterygoid plates → free floating hard palate Le Fort II Pyramidal fracture involving; 1. Zygomaticomaxillary suture. 2. Inferior orbital rim. 3. Inferior orbital wall. 4. Medial orbital wall. 5. Nasal bone / nasofrontal suture. 6. Pterygoid plates The maxilla will be separated from the rest of the face Le Fort III (craniofacial disjunction) Suprazygomatic fracture involving the; 1. Nasofrontal suture. 2. Medial orbital wall. 3. Lateral orbital wall / ZF suture. 4. Zygomatic arches. 5. Pterygoid plates posteriorly Mandibular fractures Essential anatomy ○ Mandible is considered a ring structure with some flexibility due to TMJ → therefore, 1 or fractures usually occurs (contrecoup injuries) ○ Parts; alveolar, symphysis, parasymphysis, body, ramus, coronoid, condyle When mandibular fracture is considered open? → when it extends into the tooth Patterns ○ Parasymphyseal fracture with contralateral angle / condylar (70%) ○ Symphyseal fracture with bilateral condylar fractures leading to; flail mandible, occurs when when you hit a man taller than you in front of the chin ○ Bilateral TMJs dislocations without fractures is uncommon and can occur due to symphysis trauma Associations with this fracture ○ Hematoma of the masticator space ○ Airway compromise; when there is parasymphyseal fracture allowing the symphysis to become free fragment, thus allowing the tongue to obstruct the oral cavity ○ Injury to the inferior alveolar nerve , resulting in paresthesia of the chin ○ Risk of aspiration in fractures / avulsed tooth Mustication forces & fracture 31  ○ Mastication force can act favourably or unfavorable, resulting in nondisplaced or displaced fractures ○ Favourable orientation- when pull from the masseter reduces fracture, thus very tough to detect on CT as the fracture is reduced! ○ Unfavorable fracture- pull from the masseter displaces fragments Orbital emergencies General notes Causes of emphysematous orbit ○ Fracture of the thin medial wall (lamina papyracea) ○ Inferior floor fracture in case of; blow-out fracture ○ Foreign body FOREIGN BODY Due to the low attenuation of the wooden foreign body, it can be mistaken for air. They have to be large enough to be detected by CT IF; ○ Metal density structure may be noted in the; cornea, Dxx; ○ Drussens Tiny calcification in bilateral optic disc Vs. usually unilateral and associated with traumatic injury ○ Senile calcific scleral plaques Bilateral calcification anterior to the insertion of the medial & lateral recti GLOBE RUPTURE (OPEN GLOBE INJURY) US is contraindicated as applying pressure might cause extrusion of intraorbital content IF; ○ Global contour deformity, collapse of the normal spherical shape (flat-tire sign) ○ Intraocular air ○ Acute intraocular foreign body ○ Gross asymmetry in globe size ○ Asymmetry in anterior chamber size (too shallow or too deep) ○ Extruded lens IF of hyphema (= anterior chamber hemorrhage) ○ Hyperdense fluid layering anterior to the lens (appear as 2 lenses) LENS INJURY ⏺️ It can be spontaneous as it can be seen in systemic conditions; Marfan’s syndrome, Ehler-Dahmer syndrome, homocystinuria → the presence of bilateral dislocation without the history of traumatic orbital injury, a systemic etiology should be suspected 3 forms of lens injury ○ Lens subluxation Disruption of 1 attachment (aka. Suspensory ligament) ○ Lens dislocation 32  Disruption of both attachments Typically falls to the dependent portion of the posterior segment ○ Acute cataract Pathogenesis- trauma → disruption of the lens capsule → edema within the lens Heterogeneous hypoattenuating lens RETINAL DETACHMENT (BETTER ON CORONALS) It begins peripherally either far medially or laterally Fluid accumulates between the retina & the choroid IF; ○ V-shaped fluid collection in the posterior segment, with the apex at the optic disc CHOROIDAL DETACHMENT Occurs when blood / fluid accumulates between the sclera & the choroid IF; ○ Biconvex or lentiform configuration along the medial & lateral walls of the globe, diverging posteriorly and creating an hourglass shape in the center of the globe on axial imaging ○ It spares most of the posterior portion Vs. retinal detachment RETINAL HEMORRHAGE ORBITAL NERVE AVULSION Disruption of the optic nerve at its attachment to the globe with fluid density in between BLOWOUT FRACTURE ⏺️ Mechanism; Intraorbital pressure is acutely increased and relieved by fracture of the orbital floor The most common nerve injuries; inferior orbital nerve IF; ○ Inferior orbital wall (floor) fracture ○ Orbital emphysema ○ Herniation of the intraorbital fat and muscle (IR) into the sinus → vertical diplopia ○ Ipsilateral maxillary hemosinus ○ Rarely, blow-in fracture occur; when fragments of the orbital floor “buckle” upwards Pitfalls ○ Regarding the orbital blow-out fracture, CT should be obtained when with the patient lying prone. In the supine position, fluid and debris in the maxillary antrum will layer against the orbital floor and could obscure soft tissue herniating through the fracture Carotid-cavernous fistula Patient presented with chemosis IF; ○ Thickened swollen lid Vitreous hemorrhage IF; 33  ○ Ill-defined relatively heterogeneous hyperattenuating collection within a normal hypoattenuating posterior segment of the globe ○ Layering hyperdense fluid in the posterior segment Terson syndrome ○ Originally described as vitreous hemorrhage in patients with intracranial SAH. However, now it is a broad term describing any intraocular hemorrhage in the setting of intracranial hemorrhage. The likely etiology; increased IC pressure Vascular emergencies following trauma Upper limb emergencies Elbow injuries Important lines ○ Radiocapitellar line It is drawn parallel to the shaft of the radius It should always pass through the capitellum no matter what position the elbow is in Commonly disrupted by radial head dislocation ○ Anterior humeral line Drawn on true lateral view of the elbow (the elbow is flexed 90 degrees) It is parallel to the anterior aspect of the distal humerus It should normally pass through the middle ⅓ of the capitellum. That is why true lateral view should be optimized Commonly disrupted by supracondylar fracture The elbow joints fat pads ○ There are 2 fat pads; anterior & posterior ○ The posterior fat pad is normally NOT visualized because it is hidden within the olecranon fossa Diseases to be discussed ○ Posttraumatic elbow effusion ○ Proximal forearm fractures Radial head fractures- bimodal (young & elderly) Radial neck fractures- young men & elderly women Olecranon fractures- elderly men & women ○ Forearm fractures- young men ○ Distal humerus fractures- elderly women ○ Osteoporotic fractures Olecranon fractures Distal humerus fractures 2 causes of elbow effusion in acute setting 34  ○ Intra-articular fracture ○ Traumatic synovitis Order of elbow ossification (CRITOE) ○ Capitellum- 1 Y ○ Radial epiphysis- 3 Y ○ Internal (= medial) epicondyle- 5 Y ○ Trochlea- 7 Y ○ Olecranon- 9 Y ○ External (= radial) epicondyle- 11 Y Metaphysis, epiphysis and diaphysis ○ In children Diaphysis- is the long portion of the bone Metaphysis- the flared long portion Physis- the growth line Epiphysis on top ○ In adults Metaphysis- the flared portion of all bone to the end Once the physis is fused, this entire portion will become metaphysis Physis is; unossified cartilaginous bone zone, it is very slippy and thus Posttraumatic elbow effusion Imaging ○ The posterior fat pad is displaced posteriorly and the anterior fat pad is elevated (when visible?) → lateral view of flexed elbow The anterior fat pad maybe seen normally as a triangular lucency But the posterior fat pad is normally not seen. Thus, posterior fat pad sign is always abnormal Radial head fractures The most common fracture in adult elbow Mechanism- FOOSH, fall on outstretched hand When considered displaced? → when the fragments involves 30% of more of the radial head or > 2 mm displacement Types Classification Description Notes Type 1 2 mm displacement Conservative treatment if ROM preserved Displaced but not comminuted Type 3 Comminuted Surgical treatment Type 4 Associated proximal radial Surgical Treatment dislocation Olecranon fractures 2nd to radial head fractures in adults Mechanism- FOOSH or direct blow to the olecranon Why is there distraction of the fracture fragments? → due to pull of the fracture fragments proximally by triceps tendon, resulting in wide fracture gap In children, there is entity; fracture of the olecranon apophysis ○ Don’t mistake apophysis for fracture ○ Appears ~ 9, fuses at 18 ○ Fuses anterior to posterior ○ Associated with throwing ○ Look for positive fat pad sign Coronoid fractures 3rd most common elbow fractures in adults Commonly fractured with elbow dislocations (why?) → because coronoid fractures occur due to shearing mechanism caused by posterior dislocation Pearl ○ In any posterior dislocation, examine thoroughly the coronoid process for any subtle fracture Elbow dislocation Types 36  ○ Posterior dislocation- the most common type (80%) The fracture that is associated with posterior elbow dislocation is; coronoid process fracture ○ Terrible triad fracture-dislocation Elbow dislocation Radial head fracture Coronoid process fracture ○ Posterior elbow fracture-dislocation Supracondylar fractures The most common elbow fractures in children Supracondylar are the weakest points in the distal humerus, thus they are prone to injury in if cubital force applied Types ○ Medial epicondyle fractures Due to pull of the ulnar collateral ligament Caused by; throwing motion ○ Lateral epicondyle fractures Imaging ○ Positive fat pad sign ○ The anterior humeral line will pass anteriorly to the capitellum Fragments usually displaced posteriorly → so the capitellum is more posteriorly to its normal location → therefore, the anterior humeral line will either passes through the anterior ⅓ of the capitellum or misses it entirely Lateral condyle fractures The 2nd most common fracture around the elbow in the children after supracondylar fractures Mechanism- lateral blow to the forearm → stress varus & avulsion fracture Considered Salter IV Forearm ring fractures-dislocation Subtypes ○ Monteggia fracture-dislocation (MUGR) Components; 1. Proximal ulnar fracture. 2. Radial head dislocation from radioulnar and radiocapitellar joints Radial head dislocation is diagnosed by; disruption of the radiocapitellar line Pearls In the presence of an isolated ulnar shaft fracture, one must always anticipate the possibility of the injuries to the radius and vice versa ○ Galeazzi fracture-dislocation (MUGR) Components; 1. Fracture of the distal ⅓ of the radial shaft. 2. Dislocation / subluxation of the ulna at the DRUJ Signs of traumatic DRUJ disruption 37  Fracture of the ulnar styloid at its base Widens of the DRUJ space on frontal radiograph Dislocation of the radius relative to the ulna on lateral view Radial shortening ○ The Essex-Lopresti fracture The Essex-Lopresti fracture Combination of ○ Radial head & neck fracture ○ Proximal subluxation of the DRUJ Wrist Injuries Approach to distal radial fractures ○ Is the fracture line reaching the articular surface? Yes → Barton, reverse Barton, Chauffeur No → Colles, Smith ○ Is there volar or dorsal angulation? Dorsal → Colles, Barton, Volar → Smith, reverse Barton Important signs ○ Terry Thomas sign Scapholunate dissociation due to scapholunate ligament disruption ○ Pronator Quadratus sign Pronator quadratus is a thin flat muscle located in the volar aspect of the radioulnar joint It is outlines anteriorly by thin radiolucent fat stripe When a hemorrhage occurs beneath or in the muscle, the muscle bulges anteriorly and can displace/efface the fat plane → volar bulge of the thin fat stripe Fractures of the distal radius ○ Extra-articular Don’t affect the radiocarpal joint or DRUJ Colle’s, Smith ○ Intraarticular Extends into radiocarpal joint or DRUJ Barton, reverse Barton & Chauffeur fractures Chauffeur fracture Mechanism ○ FOOSH → disruption of the radial collateral ligament → avulsion fracture of the radial styloid process ○ Or direct blow to the radial styloid process 38  It is associated with ○ Scapholunate dissociation ○ Perilunate dislocation ○ Dorsal Barton fracture Colles fracture ‫ ك‍‍وليز… باك‬back Definition- is a transverse extra-articular distal radial fracture with dorsal displacement together with the bones of the wrist and hand Epidemiology- age > 40Y Everything is dorsal; dorsal displacement, dorsal angulation The carpals & metacarpals follow the course of the fracture dorsally It is associated with ○ Scapholunate dissociation ○ Ulnar styloid process fracture Deformity- dorsal Smith’s fracture ‫س‍‍ميث… س لل‍س‍‍هم الرايح لألمام‬ It is a reverse of Colles, extra-articular fracture where everything is going volar The distal radius is displaced proximally concerning for shortening Barton Definition- transverse intra-articular fracture with dorsal displacement The dorsal fragments, as well as the carpals & hands are displaced dorsally Reverse Barton ‫ريفرس… فوالر‬ Definition- transverse intra-articular fracture with volar displacement Ulnar styloid process Definition- small avulsion fractures involving the tip of the ulnar styloid process Epidemiology- up to 70% of the distal radial fractures TORUS FRACTURE ⏺️ Epidemiology; common in children (7-12 Y) Most common site; distal radius IF; ○ Outward bulging (= buckling) of the cortex of the distal radius in an immature skeleton ○ Complete fracture line is not visualized Dxx; ○ Greenstick fracture; mid diaphysis Vs. metaphysis, complete fracture line Vs. incomplete, angulation ○ Salter-Harris fracture; epiphysis Vs. metaphysis Comparison between distal radial fractures 39  Fracture Relation to the articular surface Dorsal or Volar displacement Colles Extra-articular Dorsal Smith or reverse Colles Extra-articular Volar Barton Intra-articular Dorsal Reverse Barton Intra-articular Volar Chauffeur Intra-articular - Lower limb emergencies Normal variants ○ Enthesopathy ○ ○ Foot injuries Lisfranc fracture Lisfranc injuries (= tarsometatarsal injury) Definition- traumatic subluxation at the at the base of metatarsals The tarsometatarsal joint is known as Lisfranc’s joint The most important sign for this injury; loss of alignment between tarsometatarsal joints Types ○ Type A (also called homolateral) All TMT joints disrupted and displaced on the same direction There is total incongruity ○ Type B- 1 or more MTs disrupted B1- medial displacement of the 1st MT B2- lateral displacement of the lesser MTs (2nd / 3rd). The most common ○ Type C (also called divergent) MTs displaced in opposite direction C1- (1st MT displaced medially while lesser MTs laterally) C2- (1st MT displaced medially while all 4 MTs laterally) Imaging ○ Widened Lisfranc joint > 2 mm (the space between medial cuneiform & 2nd MT base) ○ Step-off between tarsal / metatarsal bones (loss of alignment) ○ Chip bone fragment (fleck sign)- it is avulsion fracture from the base of the metatarsal ○ Lateral or medial MT subluxation / dislocation ○ Dorsal subluxation (on lateral view) SEGOND FRACTURE ⏺️ 40  Mechanism of injury; Internal rotation and varus stress at the knee Commonly associated with; ACL tear IF; ○ Avulsion fracture of the lateral tibial condyle ○ Joint effusion Proximal femur fractures Types (determined by the relation of the fracture to the joint capsule) ○ Intracapsular- have high incident of; non-union and avascular necrosis ○ Extracapsular Intracapsular ○ Extent- fracture involving the femoral head and neck proximal to trochenters Cervical spine injuries Regarding protocol ○ Patient should be on C-collar in the setting of trauma ○ No use head-holder because that flexes the neck rather than be flat on the table and completely neutral Cervical spine can be divided into ○ Upper cervical spine (= craniocervical junction) ○ Lower cervical spine Atlantoaxial General notes Sources ○ 13. Imaging Craniocervical Spine Trauma.pptx To image or not to image (clearance)? The 5 NOs of NEXUS ○ Clearance of the cervical spine on clinical grounds alone has become the standard of care in alert adult patients with no midline cervical tenderness, neurologic symptoms, or distracting injuries No midline tenderness (physical exam) No focal neurological deficits (history) Normal alertness (to make it reliable) No intoxication (to make it reliable) No distraction injury (to make it reliable) ○ What about an Obtunded patient? → MDCT ○ What about MRI? Indications; Neurological deficit Obtunded > 48 h Unstable injury Look for EDH (epidural hematoma) ○ Indications of CTA If injury extends into the vertebral artery transverse canal To assess carotid & vertebral arteries occlusions & dissections ○ Dynamic radiographs are contraindicated in acute setting. Criteria Active patient 41  30° flexion, 30° extension Must see C7/T1 on each Only performed after -ve CT Best done at 1 week post C-collar Important lines ○ C1-C3 spinolaminar line This works better among; pediatrics A line drawn through the C1-C3, spinolaminar line should intercept the C2 spinolaminar line A displacement of the C2 spinolaminar line > 1 mm, compared with a line drawn between the spinolaminar lines of C1 & C3, is abnormal ○ AOI (Atlanto-Occipital Interval) Normal < 1.4 mm, congruent ○ ADI Normal < 3 mm ○ BDI A line from the tip of the basion to the tip of the dens Normal < 9.5 mm ○ PAL (Posterior Axial Line) A line from the back of C2 Unreliable in CT Normal < 12 mm on XR Stability consent ○ Imaging assess stability indirectly by evaluating the vertebrae and their ligamentous supports ○ It depends on the integrity of; transverse ligament, tectorial membrane, alar & apical ligaments and bony attachments ○ 3 columns Anterior column- ALL, anterior vertebral body & disc Middle column- PLL, posterior vertebral body cortex & posterior disc annulus Posterior column- PLC, posterior bony arches & facets Injury to 2 columns is considered unstable with key contributing factor being failure of the middle column Fracture mimics ○ Nonfusion (= congenital fusion anomalies) Fusion anomaly can affect either anterior or posterior arches They can be in the midline Posterior is the most common Look for; smooth cortical margins ○ Os Odontoideum ○ Os Terminale ○ Schmorl’s node ○ Limbus vertebra ○ Pseudo-spread of the atlas Age- typically at 4Y 42  IF- bilateral overhang of the atlas lateral masses on the axis Atlanto-Occipital Dissociation (AOD) = Craniocervical Junction Trauma Essential anatomy ○ Tectorial membrane The superior continuation of the PLL to the clivus ○ The cruciate ligament Transverse band It fixes the dens to the anterior arch of C1 → allow rotation around the dens It attaches to the “tubercles” of the C1, underneath the lateral masses Longitudinal band; has superior & inferior parts ○ Alar ligament It moves up diagonally between the dens & the occipital condyles ○ Apical ligament It extends from the tip of the dens to the tip of the basion Definition- high-energy trauma sufficient to separate the skull base from the upper cervical spine An umbrella term to describe complete dislocation or less fatal subluxation or distracting injuries Mechanism of injury ○ High energy trauma (MVA) ○ “Curbing”; ○ Distraction with variable flexion / extension ○ Disruption of the tectorial membrane, apical membrane or alar ligament Abnormal findings ○ Prevertebral soft tissue swelling against C2 ○ BDI > 9.5 mm ○ AOI > 1.4 mm and noncongruent 3 different types of injuries; Subluxation ○ The occipital condyles are not sitting perfectly on the lateral masses of C1 ○ The head is not properly aligned with the spine, there is incongruent occipital condyles to lateral masses ○ Survivable ○ Subtle Distraction ○ There is increased distance (= elevation) of the occipital condyle to the lateral masses = longitudinal distraction of the occiput from the atlas ○ The occipital condyles are pulled apart from the lateral masses of C1 ○ Survivable ○ Might be subtle ○ Imaging Increased Basion-Dens Interval (BDI) > 12 mm 43  Increased Posterior Axial Line (PAL) > 12 mm MRI To look for ligament injury, cord or epidural hematoma Angiography Carotid & Vertebral arteries occlusion or dissection Dislocation ○ Usually fatal ○ The occiput is pulled away from the cervical spine → Increased BDI ○ Definition- anterior displacement of the occipital condyles (or= Anterior translation of the skull on the vertebral column) ○ Epidemiology- common among children due to larger head ○ Usually fatal, due to stretching of the brainstem with subsequent pulmonary arrest ○ Mechanism of injury High energy trauma (MVA) “Curbing”; the act of making a person bite the curb, then stepping on the back of their head killing them (american history X) There is disruption of whole junction between the skull base and the cervical spine with damage to the; alar ligament, apical ligament and tectorial membrane ○ Presentation Severe neurological deficits Often with multitrauma, due to high energy trauma ○ Imaging features The occipital condyles are floating anteriorly The whole cervical spine is kicked posteriorly relative to the head Atlanto-Axial Rotatory Fixation Definition- a form of atlantoaxial dissociation characterized by rotational malalignment between the C1 and C2 vertebrae May occur within physiological range of motion Mechanism of injury ○ Muscle spasm ○ Swelling and/or tearing capsular soft tissues ○ In adults, AARF is invariably traumatic in cause and is associated with cervical pain and torticollis ○ In kids Occurs with URTI → laxity of the ligaments due to spread of the infection (Grisel syndrome) Congenital predisposition of ligamentous laxity (Down, JRA) Traumatic Presentation ○ Cervical pain ○ Torticollis (“cock robin ‫)”زي شكل هذا العصفور‬ 44  Head tilted to one side Turned opposite side ○ Limited cervical ROM Diagnosis ○ Rotation / dislocation of the at C1 / C2 lateral masses → jaw & neck are pointed in different directions ○ The problem; AARF, atraumatic torticollis & head turning = have same CT appearance, therefore HISTORY is important Also turn the head into opposite direction Has 3 different types ○ Type I (the most common type) Stable The lateral masses of C1 & C2 are rotated and malaligned but still pivoting around the dens, therefore the ADI would be normal due to intact transverse ligament which prevents anterior displacement of C1 Axis of rotation: dens Indistinguishable Vs. atraumatic torticollis & head turning ○ Type II Unstable Anterior translation & rotation of C1 relative to C2 Increased ADI due to disruption of the transverse ligament Axis of rotation: lateral mass of C1 which is the new pivot point ○ Type III Unstable Anterior translation & rotation of C1 over C2 > 5 mm Disruption of the transverse ligament & alar ligament The spinal cord may be impaction due to narrow canal caused by anterior translation Occipital condyle fractures It is a marker of high energy trauma Associated injuries ○ Closed head injury ○ Facial fractures ○ Carotid & vertebral artery injuries ○ C-spine injuries (atlas fracture, atypical hangman fracture, hyperextension teardrop fx) Classification ○ Type I Axial loading- impact injury Undisplaced fracture ○ Type II Skull base Fx extending into occipital condyle ○ Type III Unstable Displaced fracture from avulsion of alar ligament 45 Jefferson fracture MOI- axial load on a straight spine: the force comes through the vertex of the skull → propagates down the occipital condyles, hits the lateral masses of the angles of C1 → drive the lateral masses out laterally and fracturing the C1 ring How to assess stability? → ○ by the rule of Spence ○ Look for any avulsion fragment of tubercle → unstable ○ ADI Associated with other injuries (dens fracture) Typical jefferson has 4 part fracture ○ 2 anterior arch fractures (double fractures) ○ 2 posterior arch fractures (double fractures) ○ MOI: symmetrical axial load ○ Decompressive injury, because the force tends to open the canal as the parts are moving apart laterally, so no injury to the spinal cord, therefore is considered stable ○ Intact transverse ligament ○ Stable due to intact transverse ligament and decompressive force Atypical Jefferson ○ Anything less than 4 type fracture ○ MOI: asymmetrical axial load ○ Unstable due to disruption of the transverse ligament Pitfalls ○ Congenital fusion anomalies C2 Hangman fracture Misnomer! It is “hanged man” fracture MOI- submental knot → forceful hyperextension. However today: MVA, falls Typical Hangman- bilateral C2 arch fractures and anterior subluxation of C2 on C3 Atypical- if the fracture involves the vertebral body Types ○ Type I MOI- hyperextension with axial load Bilateral pars interarticularis (equivalent of pedicles) fractures No significant translation Disk & ligaments intact Stable ○ Type II