Interpreting Head CT in Acute Settings: A Practical Guide

 

Interpreting Head CT in Acute Settings: A Practical Guide for the Internist

Dr Neeraj Manikath , claude.ai

Abstract

Head computed tomography (CT) remains the cornerstone imaging modality for evaluating acute neurological emergencies. While radiological interpretation is ultimately the domain of specialists, internists and emergency physicians must develop competency in recognizing life-threatening pathology that demands immediate intervention. This review provides a systematic approach to head CT interpretation, highlighting critical findings, common pitfalls, and practical pearls for clinical decision-making in acute care settings.

Introduction

The head CT scan has revolutionized acute neurological care since its introduction in the 1970s. With scan times now under 30 seconds and near-universal availability in developed healthcare systems, non-contrast head CT (NCCT) serves as the initial imaging study for stroke, trauma, altered mental status, and acute headache presentations. For the internist, developing a systematic approach to head CT interpretation is essential—not to replace formal radiology reads, but to recognize immediately actionable findings that cannot await specialist review.

Systematic Approach to Head CT Interpretation

The "ABCDEFGH" Framework

A structured approach prevents satisfaction of search errors and ensures comprehensive evaluation:

  • Asymmetry: Compare both hemispheres
  • Blood: Identify hemorrhage (hyperdense unless coagulopathic)
  • Cisterns: Assess basal cisterns and sulci
  • Density: Gray-white matter differentiation
  • Extra-axial collections: Subdural, epidural, subarachnoid spaces
  • Fractures: Bone windows are essential
  • Gray-white differentiation: Early stroke signs
  • Hydrocephalus: Ventricular size and symmetry

Pearl: Always review images systematically from outside-in: scalp → skull → extra-axial spaces → brain parenchyma → ventricles → posterior fossa. This prevents missing scalp hematomas or skull fractures.

Understanding CT Density

The foundation of CT interpretation rests on understanding Hounsfield units (HU):

  • Bone: +1000 HU (bright white)
  • Acute blood: +50 to +90 HU (hyperdense/bright)
  • Brain parenchyma: +20 to +40 HU (gray)
  • CSF: +0 to +15 HU (dark gray to black)
  • Fat: -50 to -100 HU (black)
  • Air: -1000 HU (black)

Hack: Acute blood appears "whiter than brain" on CT. If it's not brighter than normal brain parenchyma, it's likely not acute hemorrhage. Subacute blood (3-14 days) becomes isodense to brain, making it invisible on CT—the "invisible hematoma" phenomenon.

Critical Pathologies Every Internist Must Recognize

1. Acute Intracranial Hemorrhage

Intracerebral Hemorrhage (ICH)

ICH appears as a well-defined hyperdense mass within brain parenchyma. Hypertensive hemorrhages classically occur in:

  • Basal ganglia/putamen (40%)
  • Thalamus (15%)
  • Pons (10%)
  • Cerebellum (10%)
  • Subcortical white matter (20%)

Pearl: The "swirl sign" (heterogeneous density within hematoma) suggests active bleeding and predicts hematoma expansion. The "island sign" (satellite foci of hemorrhage separate from main hematoma) also indicates expansion risk and poor prognosis.

Clinical correlation: ICH volume can be rapidly estimated using the ABC/2 method (A = largest diameter, B = perpendicular diameter, C = number of slices × slice thickness). Volumes >30 mL have significantly worse outcomes; >60 mL is often fatal.

2. Subarachnoid Hemorrhage (SAH)

SAH appears as hyperdensity within the subarachnoid spaces, particularly:

  • Basal cisterns (interpeduncular, suprasellar, ambient)
  • Sylvian fissures
  • Interhemispheric fissure

Oyster: CT sensitivity for SAH decreases with time: 98% on day 0, 93% at 24 hours, 85% at day 3, and <50% after one week. If clinical suspicion remains high with negative CT, lumbar puncture is mandatory—preferably after 6-12 hours for xanthochromia detection.

Pearl: In aneurysmal SAH, blood distribution can suggest aneurysm location: anterior interhemispheric suggests anterior communicating artery; Sylvian fissure suggests middle cerebral artery; interpeduncular cistern suggests posterior circulation.

3. Subdural Hematoma (SDH)

SDH appears as a crescentic extra-axial collection that crosses suture lines but not dural attachments (falx, tentorium). Acute SDH is hyperdense; subacute (1-3 weeks) becomes isodense; chronic (>3 weeks) becomes hypodense.

Hack: The "isodense subdural" is easily missed. Look for:

  • Medial displacement of gray-white junction from inner skull table
  • Compression of cortical sulci
  • Ventricular shift disproportionate to visible pathology
  • Loss of sulcal definition
  • "Ribbon-like" appearance along convexity

Clinical significance: SDH volume matters less than mass effect. A 5mm SDH with 10mm midline shift is far more concerning than a 15mm SDH with no shift.

4. Epidural Hematoma (EDH)

EDH presents as a biconvex (lens-shaped) hyperdense extra-axial collection that does not cross suture lines (dural attachments to skull). Classically associated with middle meningeal artery injury and temporal bone fracture.

Pearl: The classic "lucid interval" (initial loss of consciousness, followed by recovery, then deterioration) occurs in only 20-30% of cases. Any biconvex extra-axial collection warrants urgent neurosurgical consultation.

5. Acute Ischemic Stroke

Early signs of acute ischemic stroke on NCCT are subtle but critical:

Hyperdense vessel sign: The "hyperdense MCA sign" or "dot sign" (hyperdense middle cerebral artery) indicates thrombus and predicts larger infarct size. Present in approximately 30% of acute MCA occlusions.

Loss of gray-white differentiation: The earliest parenchymal sign (within 3-6 hours), beginning in the insular ribbon and lentiform nucleus. The "insular ribbon sign" indicates M1/M2 MCA territory infarction.

Sulcal effacement: Loss of normal sulcal definition indicates cytotoxic edema.

ASPECTS Score: The Alberta Stroke Program Early CT Score systematically evaluates 10 regions in the MCA territory. Each region showing early ischemic changes subtracts 1 point from a baseline of 10. ASPECTS ≤7 predicts worse outcomes with thrombolysis and may influence thrombectomy decisions.

Oyster: The "1/3 MCA rule"—if early ischemic changes involve more than one-third of MCA territory, hemorrhage risk with thrombolysis increases significantly. This is incorporated into modern imaging protocols emphasizing CTA and perfusion imaging.

Hack: To detect subtle loss of gray-white differentiation, increase your monitor brightness and compare both hemispheres at identical anatomical levels. The affected hemisphere appears "hazy" or "dirty" compared to the normal side.

6. Hydrocephalus and Mass Effect

Hydrocephalus may be communicating or obstructive:

  • Obstructive: Enlarged ventricles proximal to obstruction with normal/small distal ventricles
  • Communicating: All ventricles enlarged with effaced sulci

Pearl: The "temporal horn sign"—enlargement of the temporal horns (normally slit-like) is an early sign of hydrocephalus. Periventricular hypodensity ("transependymal edema") indicates elevated intraventricular pressure.

Mass effect indicators:

  • Midline shift (>5mm is significant)
  • Ventricular compression/effacement
  • Cisternal effacement
  • Subfalcine herniation
  • Uncal herniation (effacement of suprasellar and perimesencephalic cisterns)

Critical pearl: Loss of basal cisterns is an ominous sign suggesting impending transtentorial herniation. Specifically, effacement of the circum-mesencephalic cisterns indicates uncal herniation—a neurosurgical emergency.

Common Pitfalls and Mimics

1. Pseudosubarachnoid Hemorrhage

Diffuse brain edema (from cardiac arrest, severe hypoxia) causes diffuse hypoattenuation of brain parenchyma, making normal vessels and dura appear relatively hyperdense—mimicking SAH. The "pseudo-SAH sign" is distinguished by:

  • Diffuse parenchymal hypodensity
  • Loss of gray-white differentiation
  • Clinical context (anoxic injury)
  • HU measurements (blood is typically >60 HU; pseudo-SAH is 40-50 HU)

2. Calcification vs. Acute Blood

Both appear hyperdense. Distinguishing features:

  • Calcification: Very high density (>100 HU), follows vascular distribution (basal ganglia, dentate nuclei), stable on serial imaging
  • Acute blood: Moderate hyperdensity (50-90 HU), mass effect, clinical correlation

3. Posterior Fossa Blind Spots

The posterior fossa is challenging due to beam-hardening artifacts from the skull base. Cerebellar hemorrhage and brainstem infarction are easily missed.

Hack: Always review posterior fossa images with wide windows (width 150-200, level 35-40) to reduce artifacts. Clinical correlation is essential—posterior fossa lesions present with ataxia, cranial nerve palsies, and rapid neurological deterioration.

4. Chronic Subdural Mimics

Bilateral chronic subdurals may appear symmetric and be mistaken for normal findings or brain atrophy. Clues include:

  • Disproportionate sulcal effacement for patient age
  • History of falls or anticoagulation
  • Smooth inner membrane (SDH membrane) distinct from brain surface

Advanced Considerations

Contrast Administration

While most acute presentations require only NCCT, contrast-enhanced CT (CECT) is valuable for:

  • Suspected mass lesions or metastases
  • Cerebral venous sinus thrombosis
  • Infection/abscess
  • Vascular malformations

Pearl: In suspected venous sinus thrombosis, the "empty delta sign" on CECT (hypodense thrombus within contrast-enhanced sinus) is specific but insensitive. CT venography is the preferred modality.

CT Angiography (CTA)

CTA has become standard in acute stroke protocols, identifying:

  • Large vessel occlusions amenable to thrombectomy
  • Aneurysms in SAH
  • Vascular dissections
  • Collateral circulation status

When to Order MRI Instead

MRI supersedes CT for:

  • Acute stroke <6 hours (diffusion-weighted imaging is far more sensitive)
  • Posterior fossa pathology
  • Suspected mass lesions requiring characterization
  • Chronic subdural discrimination
  • Venous sinus thrombosis
  • Suspected prion disease or encephalitis

However, CT remains first-line in hyperacute settings due to speed and availability.

Clinical Integration: Putting It All Together

Case-Based Pearl: A 67-year-old on warfarin presents with headache and confusion after a fall. CT shows a thin, isodense extra-axial collection with 8mm midline shift. Despite the seemingly modest collection, significant mass effect demands urgent neurosurgical evaluation and coagulopathy reversal. The "isodense" appearance suggests subacute SDH (1-3 weeks)—correlate with history for missed earlier trauma.

Oyster: In hypertensive ICH, the presence of intraventricular hemorrhage (IVH) dramatically worsens prognosis, increasing mortality from 30% to >50%. IVH also increases hydrocephalus risk, potentially requiring external ventricular drainage.

Practical Recommendations

  1. Establish a systematic review protocol and follow it for every CT
  2. Communicate immediately with neurosurgery for any extra-axial collection with mass effect, large ICH, or herniation signs
  3. Document clearly: Note specific findings, measurements (hematoma size, midline shift), and ASPECTS score when applicable
  4. Understand limitations: CT sensitivity decreases over time for SAH and in posterior fossa; when clinical suspicion remains high, pursue additional imaging
  5. Correlate clinically: Imaging without clinical context leads to errors; always integrate examination findings

Conclusion

Competency in head CT interpretation is an essential skill for internists managing acute neurological presentations. While definitive interpretation belongs to radiologists, recognizing immediately life-threatening pathology—acute hemorrhage, herniation, large vessel occlusion—enables rapid decision-making that saves lives and brain tissue. The systematic approach outlined here, combined with pattern recognition of critical findings and awareness of common pitfalls, provides the foundation for confident preliminary assessment. Remember: every minute counts in neurological emergencies, and your initial CT review may be the most important intervention you provide.

Key Takeaway Pearls

  • Blood is bright; if it's not brighter than brain, it's not acute blood
  • Empty cisterns = impending herniation = neurosurgical emergency
  • Isodense subdurals are the most commonly missed pathology
  • ASPECTS ≤7 changes stroke management decisions
  • When CT is negative but suspicion high (especially SAH), pursue further evaluation
  • Posterior fossa requires dedicated attention and wide windows
  • Clinical correlation trumps imaging findings alone

References

  1. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines. Stroke. 2019;50(12):e344-e418.

  2. Hemphill JC 3rd, Greenberg SM, Anderson CS, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2015;46(7):2032-2060.

  3. Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage. Stroke. 2012;43(6):1711-1737.

  4. Birenbaum D, Bancroft LW, Felsberg GJ. Imaging in acute stroke. West J Emerg Med. 2011;12(1):67-76.

  5. Lee KE, Kim EJ, Kim YS, et al. Significance of hyperacute change on CT in intracerebral hemorrhage. J Korean Neurosurg Soc. 2016;59(2):129-135.

  6. Barber PA, Demchuk AM, Zhang J, Buchan AM. Validity and reliability of a quantitative computed tomography score in predicting outcome of hyperacute stroke before thrombolytic therapy. Lancet. 2000;355(9216):1670-1674.

  7. Novelline RA, Rhea JT, Rao PM, Stuk JL. Helical CT in emergency radiology. Radiology. 1999;213(2):321-339.

  8. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med. 2000;342(1):29-36.

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