Non Contrast CT Head for the EM Physician

Written by: Philip Jackson, MD (NUEM ‘20) Edited by: Logan Weygandt, MD, MPH NUEM ‘17) Expert Commentary by: Katie Colton, MD

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Relying on in-house radiology reads of imaging is a habit that EM trainees are encouraged to avoid, but one that can be appealing when practicing in a busy, large academic facility with 24-hour radiologist staffing. By reading one’s own images, not only do EM physicians gain skills in diagnostic radiology, which they can employ when an attending radiology read is not readily available but more importantly, the EM physician can correlate history and physical with imaging and help detect subtle pathology. Recent studies have shown that even attending EM physicians are often deficient in reading non-contrast CT scans of the head, however, with minimal training residents have been shown to make significant improvements. [2,3]

An elderly male with a history of hypertension and Fuch’s corneal dystrophy presented to our ED the morning after developing acute on chronic worsening of the blurry vision in his R eye. He suffered from persistent blurry vision but stated that it had suddenly worsened while watching TV the previous night. He then developed a left-sided occipital headache that continued through the following morning. He also noticed that his thinking was “cloudy” and despite being a healthcare professional could not describe his own medical history or list of medications. He described blurriness especially on the right. On visual field confrontation, the patient was found to have a binocular R sided superior quadrantanopsia. The rest of his neurologic exam was unremarkable. As these findings were concerning for stroke specifically in the left temporooccipital region known as Myer’s loop, we obtained a STAT non-contrast head CT.

As the so-called green arrow-signs on the CT image indicate, there was indeed a significant amount of cerebral edema present in the L temporal lobe white matter, which  contains the anterior optic radiations carrying information from the R superior visual field and corresponds to our patient’s deficit. Upon discovering this lesion, our team immediately called our radiology colleagues who confirmed our concern for an acute ischemic infarct.

Like any other task in the ED, reading a head CT should be conducted as efficiently and accurately as possible using a standardized approach. EM residents have been found to be somewhat deficient in our ability to evaluate noncontrast head CTs; however, studies have shown that with adequate training, our skills can significantly improve. [3] Perron et al describe the simple but systematic approach “Blood Can Be Very Bad.” This mnemonic reminds residents to examine for the presence Blood, the shape and consistency of the Cisterns, the texture of the Brain parenchyma, the Ventricles, and the presence of fractures and symmetry of the Bony structures. 

• Blood:  In a non-contrast CT, blood will appear as hyperdense (bright/white) fluid.  As blood ages over weeks, it will become increasingly hypodense (darker).  Blood will present in one of the four following ways:

  • Subarachnoid hemorrhage - A dreaded complication of trauma, a ruptured aneurysm, or an arteriovenous malformation can lead to blood pooling in gravity-dependent areas correlating with the particular arterial defect. Rupture of the anterior communicating artery (ACA) will distribute blood in and around the interhemispheric fissure, suprasellar cistern, and brainstem.  Rupture of the middle cerebral artery (MCA) will distribute blood in the Sylvian and suprasellar cistern, while the posterior cerebral artery (PCA) will also distribute in the suprasellar cistern.

  • Subdural hemorrhage (SDH) – Caused by rupture of the bridging veins, SDHs will present as a crescentic lesions that often cross suture lines. SDHs can be acute, chronic, or mixed, and thus will have varying degrees of density.

  • Epidural Hemorrhage - Another serious complication of trauma, epidural hemorrhages will present as a lenticular (biconvex) areas of hyper-attenuation.     Caused by arterial laceration, with the most common being the middle meningeal artery, epidural hemorrhages can rapidly expand and cause significant and rapid mass effect.  Early identification is thus crucial to reducing mortality from these injuries.

  • Intraparenchymal/intraventricular hemorrhage - Often the result of hypertensive disease in elderly patients or as hemorrhagic strokes, intraparenchymal hemorrhage will most often be located in the basal ganglia. Amyloid angiopathy  (associated with Alzheimer’s dementia) often presents as wedge-shaped areas of hemorrhage in the outer cortex. Trauma leading to brain contusion can also present with intraparenchymal hemorrhage. All intraparenchymal hemorrhages (as well as subarachnoid hemorrhages) can potentially rupture into ventricles causing intraventricular hemorrhage and resultant hydrocephalus.

• Cisterns:  Cisterns are spaces surrounding and cushioning brain matter with cerebrospinal fluid. Each of the four major cisterns should be examined for blood or signs of mass effect: the sylvan fissure (in between temporal and parietal lobes), the circummesencephalic or peripontine cistern, the suprasellar (surrounding the circle of Willis), and the quadrigeminal (atop the midbrain).

• Brain matter: Always examine the gyri for and for distinct grey-white matter differentiation. Ischemic strokes, as in our case, will present with blurring of the grey-white differentiation and cerebral edema (areas of hypodensity).  Early strokes may not be apparent on CT, but after 6 or more hours hypodense lesions should be present with maximal edema occurring approximately 3-5 days after the event. Always examine the falx for midline shift through multiple slices.

• Ventricles:  Examining the third and fourth ventricles is crucial in determining the presence of blood hydrocephalus (dilation) or mass effect (asymmetry).

• Bone:  The bony structures of the head should all be examined for fractures, especially depressed skull fractures, which usually denote intracranial pathology. Also, examining the sphenoid, maxillary, ethmoid, and frontal sinuses for air fluid levels should raise suspicion for a skull fracture. Separate bony windows are available for close examination of these high-density structures. [1]

As our case illustrates, it is crucially important for EM physicians to interpret non-contrast CT scans in a systematic and accurate manner. Clinical correlation is a distinct advantage that we, as emergency physicians, possess and it should be exploited to allow for timely and effective patient care.

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Expert Commentary

Thanks to Drs. Jackson and Weygandt for this great primer to the emergent head CT.  One of the obvious challenges of EM is the breadth of pathology we see, and so having a strategic approach like this one will reveal most of the emergent diagnoses we are looking for.  I will never be a radiologist, but nothing is faster than looking at my own scan. A few thoughts: I start by scrolling a scan through quickly to identify obvious pathology (a bleed, midline shift, etc.) and then try to actively redirect my attention back to a systematic approach. It is easy to hone in on the obvious abnormality and miss smaller but crucial clues. Go through the same progression every time. Get comfortable with finding different windows for your imaging. If you only look in a brain window, you’ll miss critical diagnoses. Symmetry is your best friend - until it is not.  We are remarkably good at picking out asymmetry when looking at imaging, which reveals many of the emergent diagnoses, but keep some of the symmetric processes in the back of your mind.  Many of these can wait for a radiologist’s fine- tooth comb, but a few stand out.  Get used to finding the basilar artery, particularly in your unconscious patient; an acute occlusion in this midline structure is potentially devastating but quick intervention is life-saving. Similarly, acute hydrocephalus merits immediate intervention that can lead to dramatic clinical improvement. Bilateral or midline subdural hemorrhage can also be easily missed; finding these requires a level of comfort with windowing the images and identifying abnormal CSF spaces.

Katie Colton, MD

Instructor, Feinberg School of Medicine

Department of Neuro Critical Care and Department of Emergency Medicine

Northwestern Memorial Hospital

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Philip, J. Weygandt, L. (2020, Feb 10). Non Contrast CT Head for the EM Physician. [NUEM Blog. Expert Commentary by Colton, K]. Retrieved from http://www.nuemblog.com/blog/non-contrast-ct-head-for-the-em-physician

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Other Posts You May Enjoy

References

1. Adams, James, and Erik D. Barton. Emergency Medicine: Clinical Essentials. 2nd ed. N.p.: Elsevier Health Sciences, 2013;633-644.

2. Jamal K, Mandel L, Jamal L, Gilani S. 'Out of hours' adult CT head interpretation by senior emergency department staff following an intensive teaching session: a prospective blinded pilot study of 405 patients. Emergency medicine journal : EMJ. 2014;31(6):467-470.

3. Perron AD, Huff JS, Ullrich CG, Heafner MD, Kline JA. A multicenter study to improve emergency medicine residents' recognition of intracranial emergencies on computed tomography. Annals of emergency medicine. 1998;32(5):554-562.

4. Mayfield Brain & Spine. "Visual field test." Visual Field Test | Mayfield Brain & Spine. N.p., n.d. Web. 19 Dec. 2016.

Emergency Guide to Stroke Neuroimaging

Written by: Justin Seltzer, MD (PGY-3) Edited by: Luke Neill, MD (PGY-4) Expert commentary by: Babak Jahromi, MD, PhD

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According to the CDC, an ischemic stroke occurs approximately every 40 seconds in the US, with nearly 800,000 documented cases annually.[1] This, combined with an effective national stroke symptom public education program, has resulted in a large number of patients presenting to emergency departments for evaluation of stroke or stroke-like symptoms. Essential to this initial evaluation is neuroimaging, which in the emergency department is mainly CT based. 

However, despite frequent use, many emergency physicians are not familiar enough with stroke imaging to interpret images on their own. A prior post addressed the basics of reading a complete head CT, which you can find here. The goal of this article is to discuss the indications and limitations as well as to provide a basic guide to interpretation of noncontrast CT imaging of the brain (NCCT), CT angiography (CTA) of the head and neck, and CT perfusion (CTP) imaging in acute stroke evaluation.

Acute stroke imaging is obtained in the emergency department for two purposes. 

1. To evaluate rapidly for thrombolysis contraindications like hemorrhage and certain pathology such as vascular malformations and aneurysms. Thrombolysis has a high therapeutic benefit in stroke patients, with a number needed to treat of 10 within 3 hours of symptom onset and less than 20 if administered within 4.5 hours.[2,3] In addition, door to needle time of less than one hour is an established benchmark and quality measure.[3]

2. To identify a causative vascular lesion, which may or may not be amenable or contraindicatory to thrombolysis

Non-Contrast Head CT

NCCT is usually the first imaging modality obtained in the acute evaluation for stroke. Within the thrombolysis window (<4.5 hours), however, this scan is far more likely to detect hemorrhage than infarction. Chalela, et al., reviewed 356 patients evaluated for stroke symptoms at a single center over 18 months. They showed a sensitivity of 89% for detection of acute intracranial hemorrhage; conversely, the sensitivity for ischemic strokes less than 3 hours old was 12%, 16% for those older than 12 hours, and an overall sensitivity of 16%.[4] These findings are consistent with other studies and highlights the limitations of NCCT in acute stroke imaging. 

Despite the poor sensitivity for acute infarction, there are a few ways to improve detection. Windowing adjustments can enhance grey-white matter differentiation, as loss of this in an area anatomically associated with the presenting deficit is suggestive of acute infarction. A window width and center of approximately 50 each achieves adequate grey-white differentiation (Figure 1). Additionally, asymmetric, hyperdense section of cerebral vasculature, known as the “dense vessel” sign, is also highly suggestive of middle cerebral artery (MCA) occlusion.[5] As a side note, IV contrast should not be used outside of angiography to “enhance” the image as it may extravasate into the ischemic parenchyma mimicking hemorrhage.[6] 

Figure 1. NCCT of the brain in an acute right M1 occlusion with a last known well time was approximately 13 hours before. Windowing set at C50/W50 for improved grey-white differentiation. Official read: “A diffuse asymmetric hypodensity and subtle loss of gray-white matter differentiation in the right frontal and parietal region is highly concerning for an acute right MCA stroke.”

CT Angiography of the Head and Neck

The role of CTA in acute stroke evaluation is to identify the culprit vascular lesion and is an excellent addition to the emergent evaluation of acute ischemic stroke. A 2014 pooled analysis of 21 studies from 1993 to 2013 showed CTA has a sensitivity of 83.2% and specificity of 95% with a 97.1% negative predictive value for greater than 50% cerebral vascular stenosis;[7] a 2017 pooled analysis of 7 studies from 2003 to 2012 broadly reported a sensitivity of 93% and specificity of 100% for acute ischemic stroke.[8] CTA of the neck is also obtained to evaluate the contributing cervical vasculature. Since interpretation of angiography is dependent on knowledge of the relevant anatomy, the key structures are reviewed below. If a more detailed review is desired or necessary, several neuroanatomy texts may be found in the references. 

The major cerebral vasculature is supplied by the bilateral internal carotid arteries (ICA; “anterior circulation”) and the paired vertebral arteries (VA) that merge to form the basilar artery (BA; “posterior circulation”). The anterior circulation dominates perfusion of the cerebral hemispheres apart from the occipital lobe. The posterior circulation feeds the remaining structures, mainly the occipital lobe, cerebellum, and brain stem. 

Figure 2. CTA of the neck showing bilateral patent CCAs and VAs.

Anterior circulation

The anterior circulation starts with the ICA, which branches from the common carotid artery (CCA) in the upper neck at around the level of the fourth cervical vertebra. (Figures 2, 3). The ICA has four parts with seven defined segments; in general, segments assist with lesion localization and are provided in parenthesis. The cervical part (cervical segment, C1) is first and enters the skull at the carotid foramen (Figure 5). It is distinguished from its companion external carotid artery by a lack of extracranial branching. Once in the skull, the petrous part (petrous segment, C2) traverses the carotid canal within the petrous portion of the temporal bone (Figure 5). Moving out of the temporal bone, the ICA then crosses into the cavernous sinus, where it is known as the cavernous part (lacerum segment, C3, cavernous segment, C4, clinoid segment, C5). Navigating the bony turns in this area results in a characteristic curvature known as the “carotid siphon” (Figure 6). From here, the vessel passes through the dura, where it becomes the cerebral or supraclinoid part (ophthalmic segment, C6, communicating segment, C7) and gives off the ophthalmic, posterior communicating, and anterior choroidal arteries; these posterior communicating arteries (PCommA) run to the ipsilateral posterior cerebral arteries (PCA), thus connecting the anterior and posterior circulations and forming part of the circle of Willis (Figure 7). At the terminus, the internal carotid arteries bifurcate into the bilateral anterior cerebral arteries (ACA) and MCAs. Acute ICA lesions can cause dramatic symptoms due to restricted blood flow to the ipsilateral ACA and MCA and are large vessel occlusions.[9-12]

Figure 3. CTA of the neck showing the bilateral carotid bifurcations. Artifact from metal in the patient’s teeth.

Figure 4. CTA of the neck showing patent bilateral ICAs as well the the bilateral VAs entering the foramen magnum

The ACAs run between the frontal hemispheres in the longitudinal fissure and supply a large portion of the medial cerebral structures such as the medial frontal and parietal lobes as well as the basal ganglia and parts of the internal capsule. They are smaller than the MCAs and their course is recurrent frontal-occipital and inferior-superior, which can make visualization in the axial plane difficult to appreciate. The paired arteries are connected by the anterior communicating artery (ACommA) early in their course which is the final connection completing the circle of Willis (Figure 7). Lesions within the A1 segment, which runs from the carotid terminus to the ACommA are considered large vessel occlusions though may be better tolerated due to collateral flow through the anterior communicating artery.[9,10,12] 

Figure 5. CTA of the head showing the ICAs as they enter the skull and traverse the petrous portion of the temporal bone.

Figure 6. CTA of the head showing the ICA as it traverses the cavernous sinus; the carotid siphon is well visualized on the left.

The MCAs provide circulation to the remaining frontal and parietal lobes, basal ganglia, and internal capsules, as well as portions of the temporal lobes. They are larger and therefore more easily visualized than the ACAs (Figure 7). A lesion of the M1 segment, which runs from the carotid terminus to the bifurcation into the M2 segments, is considered a large vessel occlusion (Figures 8, 9).[9,10,12] 

Figure 7. CTA of the head showing an intact circle of Willis

Figure 8. CTA of the head showing an acute right M1 occlusion in the axial plane

Figure 9. Coronal MIPS of the same vascular occlusion noted in Figure 8 with clear deficit on the right compared with the left.

Posterior circulation

The posterior circulation starts with the VAs, which are subclavian branches that traverse the cervical spine via transverse foramina (Figures 2, 3). Prior to joining, each vertebral artery gives off an ipsilateral posterior inferior cerebellar arteries (PICA) as well as the contributing vessels that form the anterior and posterior spinal arteries. Upon entering the skull via the foramen magnum, the bilateral vertebral arteries join to form the basilar artery at about the level of the medullo-pontine junction (Figures 4, 5, 6). As the basilar artery moves superiorly it gives off the bilateral anterior inferior cerebellar arteries (AICA), multiple bilateral small perforating pontine arteries, the bilateral superior cerebellar arteries, and then finally terminates with a bifurcation into the bilateral posterior cerebral arteries (PCA). As noted prior, these PCAs connect with the ipsilateral posterior communicating arteries from the anterior circulation (Figure 7). Vertebral, basilar, and early posterior cerebral artery occlusions are considered large vessel occlusions but there is, as of now, limited data on mechanical thrombectomy in these territories.[9,10,12,13]

Application

Reading the scan itself is fairly straightforward based on the vascular anatomy. We recommend starting caudally (usually the aortic arch) in the axial plane and tracing all four cervical vessels cranially until they form the circle of Willis and from there extend out into the major branches. The coronal plane is particularly useful for evaluation of the anterior cervical vessels and the MCAs. Significant asymmetry or loss of contrast opacification in vascular beds anatomically consistent with the presenting symptoms should be considered strokes until proven otherwise. Make note of vascular abnormalities such as significant carotid stenosis, aneurysms, and malformations. 

Additional 2-D and 3-D post-processing images may also be provided. The most common is maximum intensity projection (MIP), which highlights high density structures over low density; this allows for improved visualization of the contrast enhanced vasculature at the expense of the surrounding brain tissue. However, MIP images can be falsely negative and should not be used alone for primary vascular evaluation.[14]

CT Perfusion

Though less common than CTA, CTP may also be acquired in the emergency setting to evaluate for territorial changes in cerebral blood flow suggestive of stroke. It is particularly valuable for identifying core infarct and salvageable ischemic penumbra and is becoming an important part of interventional decision making. It has a similar sensitivity and specificity for acute ischemic stroke as CTA, its use has been validated in multiple interventional stroke studies, and it has been shown to predict core infarct size accurately compared to the gold standard MRI.[7,8,15]

Basic concepts

While the specifics of CTP are complex and beyond the scope of this article, there are a few important concepts. CTP operates under the “central volume principle,” which is represented by the equation CBF = CBV/MTT and defines the relationship between cerebral blood volume (CBV; volume of flowing blood in a set volume of brain tissue), blood flow (CBF; per time unit rate of flowing blood in a set volume of brain tissue), and mean transit time (MTT;  average time for blood to transit a set volume of brain tissue). To illustrate this concept, imagine an acute arterial occlusion. The obstruction causes an immediate increase in MTT due to slowed arterial flow through the affected tissue. To maintain CBF a local compensatory vasodilation occurs, increasing CBV. However, this vasodilation may not be able to compensate for rising MTT, causing a progressively inadequate CBF that may result in infarction.[5,16]

Algorithms translate detected changes in MTT, CBV, and CBF into images that can be used in clinical decision-making. MTT is obtained by measuring the movement of contrast through the affected tissue; this also gives a value known as Tmax, which is the time to achieve peak contrast density. CBV and CBF are calculated relative values (rCBF, rCBV) and based off of the surrounding normal tissue. Composite metrics, such as mismatch ratio, the ratio of penumbra to the core infarct volumes, and mismatch volume, the penumbra volume minus the core infarct volume, are also generated.[11] Though there is no set rule, there is evidence that thrombolysis benefit is maximized and hemorrhage risk minimized with a mismatch ratio of 1.8 or greater, a mismatch volume of 15ml or greater, and a core infarct volume less than 70ml.[17]

Figure 10. Illustrative CTP report for the same acute right M1 occlusion from Figures 8 and 9 showing the core infarct (purple) and associated penumbra (green). Note the large mismatch volume and ratio, indicating a relatively small core infarct relative to the threatened penumbra.

Application

These values are then made into “parametric maps” superimposed onto axial CT slices, allowing for visual identification (Figures 10, 11). Different software may present the values and parametric maps differently; note that our institution uses RAPID (iSchemaView, Menlo Park, CA) and our example figures were generated by this software. Using Figure 10 as an example, we see purple and green areas as well as different volumes and ratios. The purple area corresponds to the volume of tissue with a rCBF less than 30% of the unaffected, healthy tissue and is considered the core infarct area. The green area corresponds to the volume of tissue with a Tmax longer than six seconds and is considered the ischemic penumbra. Though these threshold values were used and validated by the SWIFT PRIME and EXTEND-IA trials, they are not definitive or universal.[15,18] Familiarization with an institution’s software and threshold values is vital to interpreting CTP properly.

Importantly, CTP can be abnormal in other situations such as with chronic infarcts, vasospasm from subarachnoid hemorrhage, microvascular ischemia, and cerebral changes associated with seizure and feeding vessel stenosis.[16] Always interpret CTP in the context of the other imaging findings and anatomic consistency. 

Figure 11. Illustrative CTP report for the same acute right M1 occlusion from Figured 8, 9, and 10 showing territorially increased MTT with subtle reduction in CBF and a small area of asymmetrically elevated CBV in the area corresponding to infarction in Figure 10. This figure visually highlights the relationships between rCBV, cCBF, MTT, and Tmax.

Take Away Points

CT is the primary source of neuroimaging in the emergency department evaluation of stroke patients. NCCT is poor at detecting early acute infarcts directly, however it is excellent for hemorrhage detection. Use of CTA can demonstrate causative vascular lesions and addition of CTP can further delineate ischemia and determine how amenable it might be to intervention. Not all lesions identified by CTA and CTP will be amenable to thrombolysis or thrombectomy, but these are usually the only time effective ways available to emergency physicians to identify those that might be. Educating emergency physicians about these imaging modalities can both improve patient care through more rapid diagnosis in suspected stroke cases as well as help to streamline communication and treatment planning with consulting neurologists and neurointerventionalists. 

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Expert Commentary

This is a well-written synopsis of modern neuroimaging used today’s ED for workup and emergent treatment of acute stroke. The reader should keep in mind that the primary thrust of this blog segment is on acute ischemic stroke - while advanced CT imaging (i.e. CTA) also has a crucial role in hemorrhagic stroke, this is more thoroughly addressed elsewhere.

Practically speaking, today’s CT/CTP/CTA is to suspected stroke what an EKG is to chest pain in the ED. While confirmatory tests (MRI for stroke, troponin for MI) take more time, all actionable data depends on the initial CT/CTP/CTA in acute stroke. I would also categorize the purpose of acute stroke imaging in the ED into two categories, but with perhaps broader brush-strokes:

1. Determine if stroke is ischemic or hemorrhagic (“blood or no blood on CT”), and

2. Determine the next course of action:

   1. If ischemic, do temporal and anatomic criteria mandate IV tPA, endovascular thrombectomy, both, or neither, 

   2. If hemorrhagic, is there mass effect and/or an underlying vascular lesion (arterial or venous) that mandates urgent intervention beyond best medical care.

While NCCT is sufficient to determine whether to proceed with IV tPA in the 0-4.5 hour time-window (with an NNT of 10-20), CTP/CTA are key to determining whether the patient requires emergent endovascular thrombectomy in the 0-24 hour time-window (with an NNT of 2.6-4). As these two time-windows overlap, the most practical approach is increasingly to obtain multi-modality imaging up-front / as rapidly as possible in the ED. It is important to remember that as of 2015, both IV tPA and endovascular thrombectomy are considered standard-of-care, and any patient presenting with acute ischemic stroke must undergo full workup and consideration of both treatments based upon national society / consensus guidelines.

An added note on NCCT versus CTP: while NCCT is the oldest modality in the ED, it continues to have tremendous value in acute stroke imaging. Presence or absence of early stroke changes on NCCT (quantified by the ASPECT score) can at times trump CTP in the 0-6 hr time-window, and CTP within any time-window must be interpreted in context of NCCT findings. For example, CTP may show no abnormality (or even luxury perfusion) in an area of established stroke on NCCT in cases of spontaneous recanalization. On the other hand, CTP can be very helpful in detecting small areas of ischemia not well seen on CT/CTA (even when reading NCCT using optimized 35/35 or 40/40 “stroke windows”), and CTP has higher sensitivity for small/distal branch occlusions than either CT/CTA.

The approach to cerebrovascular arterial anatomy is nicely reviewed. A few additional comments:

1. ICA: acute ICA occlusions are most dramatic when reaching the terminus (thereby blocking the MCA/ACA), but those not reaching the supraclinoid ICA may at times be well-tolerated due to collaterals across the Circle of Willis,

2. VA: the course/anatomy of the VA is rather variable, with one VA (typically the right) being less dominant as we age; similarly, PICA can have a variable origin and territory of supply, and

3. BA: while randomized trials of endovascular thrombectomy for basilar occlusion have not been published, the natural history of BA occlusion is typically devastating/fatal, and a large body of non-randomized data (case series/cohorts) shows marked improvement over this natural history following endovascular thrombectomy for BA stroke in selected patients.

Vice Chair of Regional Neurosurgery

Professor of Neurological Surgery

Department of Neurological Surgery

Feinberg School of Medicine

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How to Cite this Post

[Peer-Reviewed, Web Publication] Seltzer J, Neill L. (2020, Jan 6). Emergency Guide to Stroke Neuroimaging. [NUEM Blog. Expert Commentary by Jahromi B]. Retrieved from http://www.nuemblog.com/blog/2018/4/20/stroke-neuroimaging

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References

1. National Center for Chronic Disease Prevention and Health Promotion , Division for Heart Disease and Stroke Prevention. “Stroke Fact Sheet.” Last Update: September 1, 2017. Accessed from https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_stroke.htm

2. Emberson J, Lees KR, Lyden P, et al., for the Stroke Thrombolysis Trialists’ Collaborative Group. Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. Lancet. 2014 Nov 29;384(9958):1929-35.

3. Filho JO, Samuels OB. Approach to reperfusion therapy for acute ischemic stroke. UpToDate. Last Update: September 14, 2018. Accessed from https://www.uptodate.com/contents/approach-to-reperfusion-therapy-for-acute-ischemic-stroke

4. Chaela JA, Kidwell CS, Nentwich LM, et al.. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet. 2007 Jan 27; 369(9558): 293–298.

5. Nadgir R, Yousef DM. “Vascular Diseases of the Brain.” In Neuroradiology: The requisites. 4th Ed. (2017). Philadelphia, PA: Mosby/Elsevier

6. Yoon W, Seo JJ, Kim JK, Cho KH, Park JG, Kang HK. Contrast enhancement and contrast extravasation on computed tomography after intra-arterial thrombolysis in patients with acute ischemic stroke. Stroke. 2004 Apr;35(4):876-81.

7. Sabarudin A, Subramaniam C, Sun Z. Cerebral CT angiography and CT perfusion in acute stroke detection: a systematic review of diagnostic value. Quant Imaging Med Surg. 2014 Aug;4(4):282-90.

8. Shen J, Li X, Li Y, Wu B. Comparative accuracy of CT perfusion in diagnosing acute ischemic stroke: A systematic review of 27 trials. PLoS One. 2017 May 17;12(5):e0176622. 

9. Mancall EL. “Vascular Supply of the Brain and Spinal Cord” In Gray's clinical neuroanatomy: The anatomic basis for clinical neuroscience. 1st Ed. (2011). Philadelphia, PA: Elsevier/Saunders.

10. Mtui E, Gruener G, Dockery P. “Blood Supply of the Brain.” In Fitzgerald’s Clinical Neuroanatomy and Neuroscience. 7th Ed. (2016). Edinburgh: Elsevier Saunders.

11. Bouthillier A, van Loveren HR, Keller JT. Segments of the internal carotid artery: a new classification. Neurosurgery. 1996 Mar;38(3):425-32.

12. The Joint Commission. Specifications Manual for Joint Commission National Quality Measures (v2018B). Last Updated: 2018. Accessed from https://manual.jointcommission.org/releases/TJC2018B/DataElem0771.html

13. Filho JO, Samuels OB. Mechanical thrombectomy for acute ischemic stroke. UpToDate. Last Update: March 22 2019. Accessed from https://www.uptodate.com/contents/mechanical-thrombectomy-for-acute-ischemic-stroke

14. Prokop M1, Shin HO, Schanz A, Schaefer-Prokop CM. Use of maximum intensity projections in CT angiography: a basic review. Radiographics. 1997 Mar-Apr;17(2):433-51. 

15. Mokin M, Levy EI, Saver JL, Siddiqui AH, Goyal M, Bonafé A, Cognard C, Jahan R, Albers GW; SWIFT PRIME Investigators. Predictive Value of RAPID Assessed Perfusion Thresholds on Final Infarct Volume in SWIFT PRIME (Solitaire With the Intention for Thrombectomy as Primary Endovascular Treatment). Stroke. 2017 Apr;48(4):932-938.

16. Lui YW, Tang ER, Allmendinger AM, Spektor V. Evaluation of CT perfusion in the setting of cerebral ischemia: patterns and pitfalls. AJNR Am J Neuroradiol. 2010 Oct;31(9):1552-63.

17. Bivard A, Levi C, Krishnamurthy V, McElduff P, Miteff F, Spratt NJ, Bateman G, et al.. Perfusion computed tomography to assist decision making for stroke thrombolysis. Brain. 2015 Jul;138(Pt 7):1919-31. 

18. Campbell BC, Mitchell PJ, Kleinig TJ, Dewey HM, Churilov L, Yassi N, Yan B,et al.; EXTEND-IA Investigators. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med. 2015 Mar 12;372(11):1009-18.

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The ED Guide to Neuroimaging: Part 2

Written by: Justin Seltzer, MD (NUEM PGY-3) Edited by: Priyanka Sista, MD, (NUEM PGY-4) Expert commentary by:  Peter Pruitt, MD, MS

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Make sure to check out The ED Guide to Neuroimaging: Part 1

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Part two of this series examines the literature regarding the appropriate use of the head CT in blunt head trauma, a common clinical grey zone in emergency medicine.

The Canadian Head CT Rule (Canadian), New Orleans Criteria (New Orleans), NEXUS II Head CT Rule (NEXUS), and PECARN Pediatric Head Injury Algorithm (PECARN) are four major decision rules designed to assist clinicians with this often difficult decision. This article is dedicated to comparing these rules and providing a reasonable guide for maximizing their individual utility. The provided infographics detail the specifics of each rule for quick reference. 

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To start, there are many shared characteristics between the rules. All apply to blunt head trauma only and, except for NEXUS, specifically to those presenting within 24 hours of injury. They utilize criteria to characterize high risk populations for which emergent head CT is appropriate as well as those low risk enough to forego it. Each boasts near perfect sensitivity and negative predictive values for clinically significant acute intracranial processes. Finally, all were prospective cohort studies and, aside from New Orleans, multi-center. 

However, there are differences between each rule that can impact their applicability to certain situations and populations. 

• Study population: The single center New Orleans Criteria had the smallest study population, with 1429 total patients, while the largest, PECARN, had over 42,000 patients. All aside from NEXUS had some age restrictions. Canadian included adults and pediatric patients older than 16 years and New Orleans included adults and pediatric patients older than 3 years. PECARN was exclusively pediatric and excluded anyone over 18 years old. 

• Inclusion and exclusion criteria: There was significant heterogeneity between the studies on what qualified for inclusion. New Orleans only included patients with known loss of consciousness or post-injury amnesia with a normal neurologic exam. Similarly, Canadian involved patients with GCS ≥13 and witnessed alteration or loss of consciousness. PECARN, on the other hand, was most concerned with mechanism and excluded patients with trivial mechanisms or injuries, such as ground level falls, walking into objects, and isolated scalp involvement. These are further contrasted with NEXUS, which included “all patients with blunt trauma with minor head injury (Glasgow Coma Scale [GCS] score of 15) who present to participating study center.”[1] 

• Decision rule criteria: Certain criteria, such as evidence of skull fracture, persistent vomiting, older age (>60-65 years), were nearly universally present. However, beyond these there is little consensus. NEXUS, likely because it applies to all ages, includes criteria such as alertness, behavior changes, and scalp hematoma similar to PECARN. Only New Orleans included clinical intoxication, while NEXUS was the only rule to include coagulopathy. Mechanism-based criteria were only considered by Canadian and PECARN. 

• Primary outcome: There is significant similarity in terms of primary outcome. NEXUS criteria sought “clinically important intracranial injury,” New Orleans any acute abnormality on CT, and PECARN “clinically important traumatic brain injury.” The definitions varied somewhat but were generally similar. Only Canadian stratified differently, with a set of criteria geared towards identifying the need for neurosurgical intervention specifically and another set for the more familiar “clinically important brain injury.” 

• Methods of Application: NEXUS, Canadian, and New Orleans are all or nothing; meeting even one element results in a head CT and not meeting any means a head CT is likely unnecessary. PECARN is unique in that if the major criteria are not met, minor criteria defer to observation or head CT based in part on non-standardized elements such as physician experience and parental preference. Only in the absence of major and minor criteria can a child be cleared immediately. 

Finally, it is important to understand the level of external validation and comparison to which each of these studies has been subjected. Boudia and colleagues performed an external validation study of both Canadian and New Orleans involving 1582 patients 10 years and older over a 3-year period. They noted some key differences between reported performance and performance between the two metrics. Canadian had 100% sensitivity for need for neurosurgical intervention, while New Orleans was 82% sensitive. Canadian was 95% sensitive for clinically significant head CT findings, compared with 86% sensitivity for New Orleans. Negative predictive values were 100% and 99% for Canadian and New Orleans, respectively.[5] Mower, Gupta, Rodriguez, and Hendey recently published a nearly 10 year validation of NEXUS involving 11,770 patients from four centers, which showed improved sensitivity (99% versus 98.3%), specificity (25.6% versus 13.7%), and negative predictive value (99.7% versus 99.1%) compared with the original study for clinically significant intracranial injury. This study also compared NEXUS and Canadian performance within the same study population for those who met Canadian criteria. NEXUS was found to have superior sensitivity (100% versus 97.3%) but worse specificity (32.6% versus 58.8%) for neurosurgical intervention while having worse sensitivity and specificity (97.7%/12.3% versus 98.4%/33.3%) compared with Canadian medium risk criteria for identification of significant brain injury.[6] Schachar and colleagues compared New Orleans, Canadian, and NEXUS in 2,101 pediatric patients over nearly seven years at a non-trauma center; all showed negative predictive values over 97% however Canadian and NEXUS both showed dramatically lower (65.2% and 78.3%, respectively) sensitivities in this population.[7] Smits and colleagues concluded from a Dutch cohort of 3,181 adult patients that Canadian had a lower sensitivity than New Orleans for traumatic intracranial findings but still identified all neurosurgical cases and had a much higher specificity, resulting in a greater number of avoided unnecessary scans.[8] In contrast, PECARN has been externally validated multiple times, all with near perfect sensitivity and negative predictive value;[9-13] of note, in one study two physically abused children with clinically important traumatic brain injury were misclassified as low risk, highlighting a gap in its criteria.[11]

In summary, the four major head CT decision rules all boast impressive sensitivity and negative predictive value for significant traumatic intracranial injury, though external validation and comparison studies have shown that some rules perform better than others under less controlled conditions. When properly applied to the intended patient populations, we can conclude that these are all useful clinical decision making tools, in particular to identify low risk patients and avoid unnecessary radiation exposure, costs, and resource utilization.

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Expert Commentary

I applaud Dr. Seltzer for his interesting and informative summary of decision instruments for patients with blunt head trauma. It is important to have a clear strategy for managing patients with this complaint, since traumatic brain injury is one of the most common ED complaints, accounting for an estimated 2.8 million annual visits in 2013, and the number of visits are steadily increasing.[1] Using a well validated decision instrument, such as the Canadian CT Head Rule in adults or the PECARN rule in children, reduces the frequency of unnecessary imaging and decreases length of stay while increasing the diagnostic yield (frequency of positive tests) amongst those patients that are imaged.[2,3] With this in mind, integration of these rules into clinical practice is a key component of appropriate resource utilization, and is recommended by multiple clinical practice guidelines.[4–6] However, the use of decision instruments cannot completely replace clinical gestalt, defined as the impression of the patient derived from the clinical evaluation. Unfortunately, studies comparing decision instruments to gestalt are extremely limited.[7] One study compared the PECARN decision instrument to clinician gestalt and found gestalt to be much more specific with similar sensitivity, although clinicians were asked about the criteria used in the decision instruments prior to making their “gestalt” decision.[8] There are no studies comparing the decision instruments used in adults to gestalt, so their relative performance is still open to assessment. Clinical instinct is still a valuable tool, and decision instruments only function to support this core skill. It is also important to consider what constitutes a positive outcome in these studies. Most notably, the Canadian CT Head Rule in its simplest form does not attempt to identify individuals who will have no hemorrhage at all.[9] Instead, the authors pre-defined defines a “clinically important injury”, which allowed patients to have small subdural hematomas or trace subarachnoid hemorrhage while still being considered low risk by the rule. Because these lesions rarely require intervention, the clinical significance of identifying them is minimal.

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Peter Pruitt, MD, MS

Assistant Professor

Department of Emergency Medicine

Northwestern University

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 How to cite this post

[Peer-Reviewed, Web Publication]  Seltzer J,   Sista P, (2019, December 15 ). The ED Guide to Neuroimaging: Part 2.  [NUEM Blog. Expert Commentary by Pruitt P ]. Retrieved from http://www.nuemblog.com/blog/emergency-neuroimaging-pt2.

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References

1. Mower WR, Hoffman JR, Herbert M, Wolfson AB, Pollack CV Jr, Zucker MI; NEXUS II Investigators. Developing a decision instrument to guide computed tomographic imaging of blunt head injury patients. J Trauma. 2005 Oct;59(4):954-9.

2. Kuppermann N, Holmes JF, Dayan PS, Hoyle JD Jr, Atabaki SM, Holubkov R, Nadel FM, Monroe D, Stanley RM, Borgialli DA, Badawy MK, Schunk JE, Quayle KS, Mahajan P, Lichenstein R, Lillis KA, Tunik MG, Jacobs ES, Callahan JM, Gorelick MH, Glass TF, Lee LK, Bachman MC, Cooper A, Powell EC, Gerardi MJ, Melville KA, Muizelaar JP, Wisner DH, Zuspan SJ, Dean JM, Wootton-Gorges SL; Pediatric Emergency Care Applied Research Network (PECARN). Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009 Oct 3;374(9696):1160-70.

3. Haydel MJ, Preston CA, Mills TJ, Luber S, Blaudeau E, DeBlieux PM. Indications for computed tomography in patients with minor head injury. N Engl J Med. 2000 Jul 13;343(2):100-5.

4. Stiell IG, Wells GA, Vandemheen K, Clement C, Lesiuk H, Laupacis A, McKnight RD, Verbeek R, Brison R, Cass D, Eisenhauer ME, Greenberg G, Worthington J. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001 May 5;357(9266):1391-6.

5. Bouida W, Marghli S, Souissi S, Ksibi H, Methammem M, Haguiga H, Khedher S, Boubaker H, Beltaief K, Grissa MH, Trimech MN, Kerkeni W, Chebili N, Halila I, Rejeb I, Boukef R, Rekik N, Bouhaja B, Letaief M, Nouira S. Prediction value of the Canadian CT head rule and New Orleans for positive head CT scan and acute neurosurgical procedures in minor head trauma: a multicenter external validation study. Ann Emerg Med. 2013 May;61(5):521-7.

6. Mower WR, Gupta M, Rodriguez R, Hendey GW. Validation of the sensitivity of the National Emergency X-Radiography Utilization Study (NEXUS) Head computed tomographic (CT) decision instrument for selective imaging of blunt head injury patients: An observational study. PLoS Med. 2017 Jul 11;14(7):e1002313.

7. Schachar JL, Zampolin RL, Miller TS, Farinhas JM, Freeman K, Taragin BH. External validation of New Orleans (NOC), the Canadian CT Head Rule (CCHR) and the National Emergency X-Radiography Utilization Study II (NEXUS II) for CT scanning in pediatric patients with minor head injury in a non-trauma center. Pediatr Radiol. 2011 Aug;41(8):971-9.

8. Smits M, Dippel DW, de Haan GG, Dekker HM, Vos PE, Kool DR, Nederkoorn PJ, Hofman PA, Twijnstra A, Tanghe HL, Hunink MG. External validation of the Canadian CT Head Rule and New Orleans for CT scanning in patients with minor head injury. JAMA. 2005 Sep 28;294(12):1519-25.

9. Schonfeld D, Bressan S, Da Dalt L, Henien MN, Winnett JA, Nigrovic LE. Pediatric Emergency Care Applied Research Network head injury clinical prediction rules are reliable in practice. Arch Dis Child. 2014 May;99(5):427-31.

10. Lorton F, Poullaouec C, Legallais E, Simon-Pimmel J, Chêne MA, Leroy H, Roy M, Launay E, Gras-Le Guen C. Validation of the PECARN clinical decision rule for children with minor head trauma: a French multicenter prospective study. Scand J Trauma Resusc Emerg Med. 2016 Aug 4;24:98.

11. Ide K, Uematsu S, Tetsuhara K, Yoshimura S, Kato T, Kobayashi T. External Validation of the PECARN Head Trauma Prediction Rules in Japan. Acad Emerg Med. 2017 Mar;24(3):308-314.

12. Babl FE, Borland ML, Phillips N, Kochar A, Dalton S, McCaskill M, Cheek JA, Gilhotra Y, Furyk J, Neutze J, Lyttle MD, Bressan S, Donath S, Molesworth C, Jachno K, Ward B, Williams A, Baylis A, Crowe L, Oakley E, Dalziel SR; Paediatric Research in Emergency Departments International Collaborative (PREDICT). Accuracy of PECARN, CATCH, and CHALICE head injury decision rules in children: a prospective cohort study. Lancet. 2017 Jun 17;389(10087):2393-2402.

13. Nakhjavan-Shahraki B, Yousefifard M, Hajighanbari MJ, Oraii A, Safari S, Hosseini M. Pediatric Emergency Care Applied Research Network (PECARN) prediction rules in identifying high risk children with mild traumatic brain injury. Eur J Trauma Emerg Surg. 2017 Dec;43(6):755-762.

References (Expert Commentary)

1. Taylor CA, Bell JM, Breiding MJ, Xu L. Traumatic Brain Injury–Related Emergency Department Visits, Hospitalizations, and Deaths — United States, 2007 and 2013. MMWR Surveill Summ. 2017;66(9):1-16.

2. Sharp AL, Huang BZ, Tang T, et al. Implementation of the Canadian CT Head Rule and Its Association With Use of Computed Tomography Among Patients With Head Injury. Ann Emerg Med. 2017;33(0):1505-1514.

3. Stiell IG, Clement CM, Rowe BH, et al. Comparison of the Canadian CT Head Rule and the New Orleans Criteria in patients with minor head injury. JAMA. 2005;294(12):1511-1518.

4. Rosenberg A, Agiro A, Gottlieb M, et al. Early Trends Among Seven Recommendations From the Choosing Wisely Campaign. JAMA Intern Med. October 2015:1.

5. Schuur JD, Carney DP, Lyn ET, et al. A top-five list for emergency medicine a pilot project to improve the value of emergency care. JAMA Intern Med. 2014;174(4):509-515.

6. Mills AM, Raja AS, Marin JR. Optimizing Diagnostic Imaging in the Emergency Department. Acad Emerg Med. 2015:n/a-n/a.

7. Schriger DL, Elder JW, Cooper RJ. Structured Clinical Decision Aids Are Seldom Compared With Subjective Physician Judgment, and are Seldom Superior. Ann Emerg Med. 2016.

8. Babl FE, Oakley E, Dalziel SR, et al. Accuracy of Clinician Practice Compared With Three Head Injury Decision Rules in Children: A Prospective Cohort Study. Ann Emerg Med. 2018;71(6):703-710.

9. Stiell IG, Lesiuk H, Wells GA, et al. The Canadian CT head rule study for patients with minor head injury: Rationale, objectives, and methodology for phase I (derivation). Ann Emerg Med. 2001;38(2):160-169.

The ED Guide to Neuroimaging: Part 1

Written by: Justin Seltzer, MD (NUEM PGY-1) Edited by: Andrew Cunningham, MD, (NUEM PGY-3) Expert commentary by:  David Rusinak, MD

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Neuroimaging, mainly using CT, has become an indispensable part of our emergency diagnostic process, but, all too often we rely on radiologists to interpret what we ordered. The goal of this multi-part blog is as follows:

• To cover the basics of how to look at a CT brain and quickly identify life threat

• Review the literature supporting the major ED indications

• Discuss special considerations, such as when to use contrast, angiography, or MRI instead.

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Systematic Reading of a CT Brain

The first portion of this blog will focus on how to read a CT brain quickly with a focus on life threats.

The classic mnemonic, “Blood Can Be Very Bad,” is a pathology oriented, step-wise method to look for blood, cistern changes, and alterations to the brain parenchyma, ventricle appearance, and bony anatomy.  Applying this approach to each image cut individually can help reveal subtle findings that would otherwise be easily missed by quick scrolling.

Blood:

Blood can collect both intra-axially (parenchymal) and extra-axially (outside the parenchyma).

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Figure 1

• Classically, spontaneous intra-axial bleeding originates in deep structures such as the basal ganglia and thalamus (Figure 1).

  • In the setting of trauma, intra-axial bleeding is often ipsilateral or directly contralateral to the injury site (coup-contrecoup) but can be anywhere

  • Inferior frontal and anterior temporal lobes are high risk for traumatic contusions due to close proximity to bone (Figure 2)

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Figure 2

• Extra-axial bleeding is defined by location: mainly subdural, epidural, subarachnoid, and intraventricular hemorrhages. The patterns for these are well known and readily identified, however below are some key points on extra-axial bleeding.

  • Finding chronic subdural hematomas can be difficult as older blood and grey matter are similar appearing

  • Mass effect, abnormal appearing brain folds on that side, and use of coronal reconstructions can help identify

  • Subarachnoid hemorrhage becomes difficult to see within hours to days but acutely is often observed well in the cisterns (see below)

  • Be careful not to mistake choroid or pineal calcifications for hemorrhage

  • Don’t forget about scalp hematomas

Cisterns:

The cisterns are not ventricles but rather outpouchings of the subarachnoid space. When evaluating a CT brain the following, certain cisterns have clinical relevance for potential herniation syndromes, layering of subarachnoid blood, and/or the significant structures that run through them. Figures 3-5 show the locations of the major cisterns described below.

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Figure 3

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Figure 4

• Suprasellar: Located in the area of the sella turcica, forms a pentagon/star shape

  • Classic location of subarachnoid hemorrhage due to proximity to circle of Willis

  • Obliteration associated with downward transtentorial (i.e. uncal) herniation or due to severe elevated ICP

• Perimesencephalic cistern: A group of interconnected basal cisterns surrounding the midbrain (mesencephalon), important location of subarachnoid hemorrhage, may see effacement (reduction or loss) with tonsillar herniation

  • Interpeduncular: Located in the area of the cerebral peduncles

  • Quadrigeminal: Classically forms a W shape, obliteration associated with upward herniation

  • Ambient and crural: Connections between quadrigeminal and interpeduncular cisterns

• Cerebellopontine: Located between anterior cerebellum and lateral pons, synonymous with area of cerebellopontine angle

• Cisterna magna: Located between the cerebellum and medulla, receives fourth ventricular CSF outflow (Figure 4)

• Prepontine: Located at the anterior aspect of the pons

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Figure 5

Brain parenchyma:

CT allows for gross evaluation of the major structures as well as a differentiation of grey and white matter by Hounsfield units. The focus here is major parenchymal disruptions.

• Mass lesions, mass effect, midline shift: Because of the fixed nature of the skull, mass lesions of any type easily exert pressure on the surrounding tissue (mass effect) that can result in increased ICP, midline shift, and herniation.

  • Midline shift is measured in millimeters of displacement of the septum pellucidum at the level of the foramen of Monro from the midline of the skull

• Ischemic changes: depending on the size of the involved territory and duration, may be subtle or obvious density or architectural changes.

  • Early signs of infarction: reduced grey-white matter distinction and loss of insular hyperdensity

Ventricles:

The ventricular system is where CSF is produced and the route by which it travels into the subarachnoid space. The lateral ventricles drain via the foramina of Monro to the third ventricle, which then drains via the cerebral aqueduct (aqueduct of Sylvius) to the fourth ventricle and then to the cisterna magna and the rest of the subarachnoid space via the median and lateral apertures (foramina of Magendie and Lushka, respectively). Figures 3-5 also show the locations of the major ventricles.

• Interruption of ventricular CSF flow will cause proximal ventricular dilation that helps localize the level of obstruction

• If unsure between hydrocephalus and atrophy, dilation of temporal horns of the lateral ventricles can be helpful as it occurs in hydrocephalus involving the lateral ventricles but not with hydrocephalus ex vacuo

Bones:

Intimate knowledge of bony anatomy is not essential fracture evaluation. However, it is crucial that the bony anatomy be viewed with a dedicated bone window. Skull and facial fractures can be subtle and the presence of blood, especially an epidural hematoma, may help localize them. As noted above, soft tissue findings such as scalp hematomas are important to rule out as well.

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Key Learning Points and Conclusions

• A systematic approach is essential to avoid missing significant findings, especially with complex neuroimaging—remember “Blood Can Be Very Bad”

• Immediately look for: blood anywhere (don’t forget the scalp!), effacement of major cisterns, mass effect/midline shift, enlarged ventricles (temporal horns), skull fractures

• Older blood, such as a chronic subdural hematoma, can be hard to find and may require different cuts or inference from mass effect or effaced sulci

• Signs of infarction may be subtle (more on this later)

In the next installation, we will discuss the major indications for CT brain and the utility of CT for these indications.

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Expert Commentary

Overall, this is a very nice approach to head CT interpretation.  The classic mnemonic, “Blood Can Be Very Bad,” is not something I’ve heard of before, but it works.  Let’s take each search item in turn.

Blood

A helpful way to think about intracranial hemorrhage is to consider the causes of hemorrhage and the most common location for each pathology.  Common causes include trauma, stroke (hypertensive or hemorrhagic conversion of a venous or arterial infarct), neoplasm (primary or secondary), vascular (aneurysm, AVM, dural AV fistula), and spontaneous (anticoagulation, amyloid angiopathy, vasculitis).  If you consider the location of each of these pathologies, the hemorrhage will typically be primarily in this location.  A tumor, for example, will cause a parenchymal bleed, a ruptured aneurysm will cause subarachnoid hemorrhage, an AVM will result in a parenchymal bleed, etc.  Often with parenchymal bleeds additional imaging, vascular and MRI, as well as follow up imaging will be necessary to determine the underlying cause.

A correction is that subacute hemorrhage, not chronic, has a density similar to gray matter.  Chronic subdural hemorrhages are usually very hypodense and easy to detect on CT. So, from a practical perspective, a patient experiencing headaches from subarachnoid hemorrhage that is greater than 3 or 4 days old may be occult by CT.  This underscores the role of lumbar puncture and vascular imaging in working up patients with headaches.

Another important concept to keep in mind is window and level when interpreting CTs. Different substances (air, metal, bone, blood, fat, etc) have different and defined densities.  The pathologies associated with each of these substances (fractures, edema in the setting of stroke, etc) can be better seen by adjusting the window and level settings.  This can be done manually or, typically, PACS viewers have preset brain, bone, lung and soft tissue windows that can be displayed by pressing different numbers on the keypad.  Subtle subdural hemorrhages are often only seen with the appropriate window and level that allows distinction of the hemorrhage from the overlying calvarium.

Cisterns

The blood vessels course through the cisterns, so these must be scrutinized for the presence of hemorrhage secondary to a ruptured aneurysm in a patient presenting with an atraumatic headache.  The cisterns are also effaced in the setting of mass effect. Mass effect may be from a space occupying lesion; such as a tumor, abscess, or hemorrhage; or from diffuse cerebral edema with generalized brain swelling.  Often the absence of something (i.e. patent basal cisterns) can be harder to detect than the presence of something, like hemorrhage.  It is, therefore, important to examine the basal cisterns on each case to get comfortable with their normal variation of appearance so that their absence, such as in diffuse cerebral edema, is not missed.

Brain parenchyma

Subtle changes in parenchymal density can be difficult to detect.  It is important to get acquainted with ideal window and level settings to uncover subtle parenchymal changes.  Also comparison with prior imaging, if available, is necessary to determine the chronicity of parenchymal findings.  Understanding where a physical exam finding localizes intracranially can also be very useful- aphasia or left upper extremity weakness localize to very different locations, for example.  Lastly, always look at the vessels in the subarachnoid space to identify hyperdense thrombus in the setting of a suspected stroke.

Ventricles

Distinguishing volume loss from ventricular dilatation takes experience to understand the variation of normal across the entire age spectrum.  If hydrocephalus is suspected, determining if it is obstructive or communicating can help to understand the underlying cause. The temporal horns are the most elastic portion of the ventricles and dilate first in the setting of hydrocephalus. 

Bones

Depressed skull fractures and easy to see on routine bone windows.  Things get complicated when subtle non-displaced fractures mimic normal sutures or if the fracture involves the skull base/temporal bones.  It is probably not within the normal ED physician’s scope of practice to have a detailed knowledge of skull base anatomy, but if a skull base fracture is suspected (loss of hearing, hemorrhage in the external auditory canal, facial nerve paralysis, etc) it is important or order the proper test for further evaluation, like a temporal bone CT.  A helpful tip is to look for subtle foci of intracranial air and soft tissue swelling which may direct you to a subtle fracture.    

David Rusinak, MD

Assistant Professor of Radiology, Northwestern Medicine

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 How to cite this post

[Peer-Reviewed, Web Publication]  Whipple T,   Gappmeier V (2018, April 23 ). Demystifying the Hand Exam.  [NUEM Blog. Expert Commentary by Rusinak D ]. Retrieved from http://www.nuemblog.com/blog/neuroimaging

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References

1. Shaw AS, Prokop M. Computed Tomography. In Grainger & Allison's Diagnostic Radiology, 6th Edition (2016).

2. McKetty MH. The AAPM/RSNA physics tutorial for residents. X-ray attenuation. RadioGraphics, 1998; 18(1):151-163

3. Cadogan M. CT Head Scan. Life in the Fast Lane. Retrieved from https://lifeinthefastlane.com/investigations/ct-head-scan/.

4. Nadgir R, Yousem DM. Approach and Pitfalls in Neuroimaging. In Neuroradiology: The Requisites, 4th Edition (2017).

5. Mehta A, Jones BP. Neurovascular Diseases. In Grainger & Allison's Diagnostic Radiology, 6th Edition (2016). Chapter 62, 1456-1496.

6. Jones J. Subarachnoid Cisterns. Radiopaedia. Retrieved from https://radiopaedia.org/articles/subarachnoid-cisterns.

7. Nadgir R, Yousem DM. Cranial Anatomy. In Neuroradiology: The Requisites, 4th Edition (2017).

8. Skalski M, Dawes L. Cerebral herniation. Radiopaedia. Retrieved from  https://radiopaedia.org/articles/cerebral-herniation.

9. Baron EM, Jallo JI. TBI: Pathology, Pathophysiology, Acute Care and Surgical Management, Critical Care Principles, and Outcomes. In Brain Injury Medicine: Principles and Practice, 2nd Edition (2012). Chapter 18: 265-282.

10. Nadgir R, Yousem DM. Head Trauma. In Neuroradiology: The Requisites, 4th Edition (2017).

11. Waxman SG. Ventricles and Coverings of the Brain. In Clinical Neuroanatomy, 28th Edition (2013).

12. Nadgir R, Yousem DM. Neurodegenerative Diseases and Hydrocephalus. In Neuroradiology: The Requisites, 4th Edition (2017).

13. Galliard F, Jones J. Intraventricular haemorrhage. Radiopaedia. Retrieved from https://radiopaedia.org/articles/intraventricular-haemorrhage