Arterial Anatomy of the Brain - Cerebral vascular anatomy

The brain's arterial supply is crucial for radiology students to understand, especially in imaging contexts. Here, we review the main components of the cerebral arterial system and the Circle of Willis.

1. Anterior and Posterior Circulation

Anterior Circulation
The brain's anterior circulation stems from the internal carotid artery (ICA), which branches into the middle cerebral artery (MCA) and anterior cerebral artery (ACA). Both ACAs are connected by the anterior communicating artery (AComA), an essential component of the Circle of Willis.

Posterior Circulation
The posterior circulation includes two vertebral arteries that join to form the basilar artery. The vertebral arteries give rise to the posterior inferior cerebellar artery (PICA), and the basilar artery further branches into the anterior inferior cerebellar artery (AICA), pontine branches, superior cerebellar artery (SCA), and ultimately the posterior cerebral arteries (PCA).

2. Circle of Willis

The Circle of Willis connects the anterior and posterior circulation, consisting of:

• Anterior communicating artery
• Anterior cerebral artery
• Internal carotid artery
• Posterior communicating artery
• Posterior cerebral artery

Imaging Relevance
In time-of-flight MR angiography, we can visualize the vertebral arteries, basilar artery, posterior cerebral arteries, posterior communicating artery, internal carotid artery, anterior cerebral artery, and the anterior communicating artery.

3. Anterior Cerebral Artery (ACA) Segments

The ACA segments are key landmarks. They have been classified by several systems:

• Fisher’s Classification (1938): Divides ACA into five segments (A1–A5).
• Roton’s Modification: Splits the ACA into proximal (A1, pre-communicating) and distal (A2–A5, post-communicating) segments.
• Osborne’s Classification: Recognizes three segments (A1–A3).

ACA Segment Overview

• A1 Segment (Horizontal or Pre-Communicating): Extends from the origin of the ACA to the anterior communicating artery. Branches include the medial lenticulostriate arteries.
• A2 Segment (Vertical or Post-Communicating): Extends from distal A1 to the genu and includes the recurrent artery of Heubner and orbital frontal artery.
• A3 Segment (Pre-Callosal): Anterior to the corpus callosum, giving rise to the callosomarginal artery.
• A4 (Supra-Callosal) and A5 (Post-Callosal) Segments: Continuing as the pericallosal artery, important for supplying the medial cerebral hemisphere.

Common ACA Variants

• Fenestrated ACA: A rare double-barrel appearance.
• Trifurcation of ACA: ACA divides into three branches.
• Single ACA or Azygous ACA: A single ACA supplies both hemispheres.
• Hypoplastic or Absent A1 Segment: An anatomical variation affecting flow dynamics.

4. Middle Cerebral Artery (MCA) Segments

The MCA is divided into:

• M1 Segment (Sphenoidal/Horizontal): Originates at the ICA and gives rise to medial and lateral lenticulostriate arteries.
• M2 Segment (Insular Segment): Typically bifurcates into superior and inferior branches after M1.
• M3 Segment (Opercular): Extends over the insular cortex.
• M4 Segment (Cortical): Extends to the cortical surfaces.

MCA Variants

• Duplicated MCA: Two MCAs originate from the ICA.
• Accessory MCA: Arises from the ACA’s A1 segment.
• Fenestrated MCA: A rare duplication in the artery’s lumen.
• Early MCA Branching: Common, with early division before M1 bifurcation.

5. Posterior Cerebral Artery (PCA) Segments

The PCA, crucial for posterior cerebral circulation, is divided into segments:

• P1 Segment (Pre-Communicating): From the PCA origin to the posterior communicating artery.
• P2 Segment (Post-Communicating): Divided into P2A (in the crural cistern) and P2B (in the ambient cistern).
• P3 Segment (Quadrigeminal): Courses through the quadrigeminal cistern.
• P4 Segment (Cortical): Extends along the occipital lobe sulci.

PCA Variants

• Fetal PCA: A larger posterior communicating artery than the ipsilateral P1 segment, supplying a larger portion of the PCA’s territory.

Conclusion

The Circle of Willis and the cerebral arteries’ anatomical variants are crucial for diagnosing cerebrovascular diseases and planning neurovascular interventions. Understanding the segmentation and typical variants enhances the ability to interpret imaging accurately.

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MR Safety: Essential Guidelines for Radiology Practice

Magnetic Resonance Imaging (MRI) is a powerful diagnostic tool; however, its operation is associated with safety risks that both patients and healthcare staff must understand. This article outlines critical safety considerations that every radiology professional should be aware of.

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Overview of MRI Hardware Components

MRI systems rely on four essential components:

1. Main Magnet: Generates a strong static magnetic field, usually maintained at low temperatures by superconducting technology. Standard clinical MRI scanners range from 0.2 to 3.0 Tesla (T), with some higher-field systems reaching 7T or beyond.
2. Gradient Coils: Used to spatially encode the MR signal. Rapid switching of these coils creates peripheral nerve stimulation.
3. Radiofrequency (RF) Coils: Stimulate tissues to emit MR signals. Surface coils are used for specific body parts, while volume coils cover larger areas.
4. Cooling Systems: Use liquid helium to maintain superconducting magnet coils. Any rise in temperature may disrupt magnet function, leading to system failure.

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Magnetic Fields and Related Safety Risks

MRI systems generate static and time-varying magnetic fields, each associated with specific risks.

1. Static Magnetic Fields

   • Fields above 1.5T may induce sensory effects, such as nausea, vertigo, and flashing lights.
   • Projectile Risks: Ferromagnetic objects can become dangerous projectiles, causing severe injury or equipment damage. All metallic items must be strictly screened to prevent such accidents.

2. Time-Varying Gradient Fields

   • Can cause peripheral nerve stimulation and cardiac effects, including ventricular fibrillation.
   • Visual flashes (magnetophosphenes) may occur due to induced retinal currents.

3. RF Energy and Specific Absorption Rate (SAR)

   • RF energy heats tissues, with risks of burns from conductive materials (e.g., tattoos or metal leads).
   • SAR limits ensure safe RF exposure:
     • 4 W/kg for the whole body over 15 minutes
     • 3 W/kg for the head over 10 minutes
     • 12 W/kg for extremities over 5 minutes

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Zone Safety System

The American College of Radiology (ACR) defines four safety zones to restrict access to MRI environments.

• Zone 1: General public access (waiting areas, hallways).
• Zone 2: Transition area where patients are screened.
• Zone 3: Restricted access; only trained personnel can enter.
• Zone 4: The MRI scanner room itself, with high magnetic fields and strict access control.

These zones help ensure that only appropriately screened individuals enter high-risk areas, reducing accidents.

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Emergency Procedures and Quenching

A quench refers to the rapid release of helium from the MRI system, usually during emergencies, to stop the magnet. It can cause oxygen depletion in the room, leading to asphyxiation risks. Quenches are only performed if:

1. A fire is present that cannot be controlled without emergency services.
2. A person is trapped by a large ferromagnetic object.

In both cases, evacuation procedures must be followed immediately.

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Patient and Staff Screening

Comprehensive screening is essential to prevent injuries. Key considerations include:

1. Metallic Objects: All jewelry, hairpins, piercings, and devices must be removed before entering the MRI room.
2. Implantable Devices: Some devices (e.g., pacemakers, neurostimulators) are contraindicated unless MR-conditional.
3. Pregnancy: MRI during pregnancy is safe if necessary, though gadolinium-based contrast agents should be avoided unless absolutely required.

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Handling Cryogens Safely

MRI machines use liquid helium to maintain superconducting magnets. Handling cryogens requires specific safety measures:

• Protective Clothing: Use gloves, goggles, and overalls to avoid frostbite.
• Ventilation: Ensure the quench pipe is functioning to prevent helium from venting into the room.
• Training: Only authorized personnel should handle cryogen systems.

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Dealing with Implants and Foreign Objects

Implants and devices must be classified based on MR safety labeling:

• MR Safe: Items that pose no risks (non-metallic and non-conductive).
• MR Conditional: Devices that can be safely used under specific conditions.
• MR Unsafe: Items that are hazardous in the MR environment (e.g., pacemakers without MR compatibility).

Additional considerations include:

• Aneurysm Clips: MRI can only be performed if documented as MR-compatible.
• Pacemakers: Generally contraindicated unless specifically designed for MRI.
• Shrapnel and Bullets: Embedded metal fragments pose risks of heating and movement, especially near vital structures.

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RF Burns and Prevention Strategies

Burns occur when conductive materials come in contact with the patient's skin. To prevent this:

• Use foam insulation between cables and the patient.
• Ensure skin-to-skin contact is avoided by placing padding between body parts.
• Avoid looping cables across the patient.

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Key Takeaways

1. MRI Hardware: Critical components include the magnet, gradient coils, RF coils, and cooling systems.
2. Magnetic Field Risks: Strong magnetic fields can cause projectile injuries and peripheral nerve stimulation.
3. RF Energy and SAR: Monitoring SAR ensures tissue heating stays within safe limits.
4. Zone Safety System: Adhering to safety zones prevents unauthorized access to high-risk areas.
5. Emergency Procedures: Know when and how to perform a quench safely.
6. Patient Screening: Thorough screening identifies contraindicated devices and metallic objects.
7. Pregnancy: MRI is safe when medically necessary, but contrast agents should be used cautiously.
8. Cryogen Safety: Proper handling prevents frostbite, hypothermia, and asphyxiation.

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MRI safety is a shared responsibility, requiring vigilance from healthcare professionals to prevent accidents and ensure the well-being of both patients and staff. By following these guidelines, radiologists can ensure safe and effective imaging practices.

Renal Trauma: Diagnosis, Classification, and Management

Renal trauma refers to injury to the kidneys due to blunt or penetrating trauma, typically caused by motor vehicle accidents, falls, or violent encounters. Accurate imaging, classification of injuries, and appropriate management are critical to prevent complications and ensure optimal patient outcomes.

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Imaging Modalities for Renal Trauma

Contrast-enhanced CT (Computed Tomography) is the imaging modality of choice for evaluating renal trauma. It provides detailed visualization of renal injuries such as contusions, lacerations, infarcts, and associated complications like hematomas or urinary extravasation.

• CT Protocol: Scans are obtained at 70 seconds and 3 minutes after intravenous injection of contrast material to assess renal perfusion and detect urinary leakage.

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Classification of Renal Trauma

Renal trauma is categorized into four groups based on severity and complexity.

Category I: Minor Injuries (75%–85% of Cases)

These injuries are generally managed conservatively.

• Subcapsular Hematoma: Accumulation of blood beneath the renal capsule without significant disruption of renal function.
• Lacerations: Minor tears confined to the renal cortex.
• Subsegmental Infarcts: Localized areas of tissue ischemia, often due to small vessel injury.

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Category II: Moderate Injuries (10% of Cases)

Involves injuries extending deeper into the renal structure, potentially affecting the collecting system.

• Cortical to Medullary Lacerations: Extend from the cortex into the medulla or collecting system.
• Urinary Extravasation: Leakage of urine due to injury of the renal pelvis or ureter.

Management: These injuries are primarily treated conservatively, but surgical exploration may be necessary if the patient is hemodynamically unstable or if the injury evolves.

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Category III: Severe Injuries (5% of Cases)

These are life-threatening injuries that usually require surgical intervention, including nephrectomy.

• Multiple Renal Lacerations: Complex tears that compromise the kidney's structural integrity.
• Vascular Injuries: Injuries to the renal pedicle or thrombosis of the renal artery.
  • CT Findings: Abrupt termination of the renal artery and global renal infarction.
  • Cortical Rim Sign: A thin layer of viable renal tissue indicating partial infarction.

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Category IV: Ureteropelvic Junction Injuries (Rare)

These injuries occur due to sudden deceleration, such as in motor vehicle accidents.

• CT and Intravenous Urography: Show intact renal excretion with urinary extravasation at the ureteropelvic junction.
• Management: Often requires surgical repair to restore urinary flow and prevent long-term complications.

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Key Imaging Findings in Renal Trauma

1. Hematomas:
   • Intrarenal Hematoma: Localized within the kidney.
   • Extrarenal Hematoma: Spread into the perinephric space.
2. Urinary Extravasation: Leakage of urine, indicating a breach in the collecting system.
3. Global Renal Infarction: Complete loss of renal perfusion, often due to arterial thrombosis.
4. Cortical Rim Sign: Suggests partial infarction with preserved peripheral tissue.

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Management of Renal Trauma

Management strategies vary based on the injury category and patient stability.

Conservative Management

• Preferred for Category I and some Category II injuries.
• Includes monitoring with serial imaging and supportive care (hydration, analgesia).

Surgical Intervention

• Required for Category III and some complicated Category II injuries.
• Nephrectomy may be necessary for catastrophic injuries or extensive vascular involvement.
• Ureteropelvic Junction Repair: Surgery is needed to re-establish urinary flow in cases of significant junction disruption.

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Complications of Renal Trauma

1. Renal Artery Thrombosis:
   • Can lead to global renal infarction, often requiring urgent intervention.
2. Urinary Fistulas: Persistent urinary leakage can form fistulas.
3. Infections and Abscess Formation: Due to hematomas or urinary extravasation.
4. Hypertension: Chronic kidney damage may result in renovascular hypertension.

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Conclusion

Renal trauma is a serious consequence of abdominal trauma, with outcomes dependent on the severity of injury and prompt intervention. Contrast-enhanced CT remains the gold standard for diagnosis, enabling clinicians to identify and classify injuries effectively. While most renal injuries can be managed conservatively, severe cases often require surgical intervention. Understanding the categories of renal trauma and appropriate management strategies is essential for ensuring optimal patient care.

Encapsulating peritoneal sclerosis

We will discuss a case of encapsulating peritoneal sclerosis, including imaging findings with differential diagnosis. 

28-year-old man presented with pain abdomen associated with vomiting for 1 month. He is having abdominal distension with non passage of faeces and flatus for 1 week. On clinical examination, the abdomen was distended with soft non tender mass palpable in central part of the abdomen. 

X-ray abdomen erect supine was done which shows (a) essentially a normal study. 

USG abdomen was performed which shows (b) central clumping of small bowel loops with a narrow base resembling a cauliflower and shows the characteristic US trilaminar appearance: from superficial to deep formed by a (1) superficial hyperechoic membrane, (2) middle hypoechoic layer of the bowel wall, and a (3) deep hyperechoic layer of bowel gas and/or bowel contents. (c) US image shows septated ascites. 

Subsequently, CECT abdomen was performed which shows (d) clumping of small bowel loops including jejunum and ileal loops in central abdomen which appears mildly prominent and shows enhancing circumferential wall thickening. The clumped bowel loops are encapsulated by a thick enhancing membrane. The sac contains free fluid. There is associated smooth enhancing peritoneal thickening, mesenteric fat heterogeneity and omental nodularity. There is kinking of proximal jejunum at the junction with membrane with resultant upstream dilatation of duodenum measuring 3.5mm in maximal calibre s/o obstruction (e). Mild ascites and bilateral pleural effusion were also present. 

In view of patient history and imaging findings a diagnosis of encapsulating peritoneal sclerosis (EPS) with small bowel obstruction likely secondary to tuberculosis was given. 

EPS is characterised by fibrocollagenous cocoon like encapsulation of the bowel. Causes of this condition are divided into primary (idiopathic) and secondary causes. Secondary causes include peritoneal dialysis, ventriculoperitoneal shunt, tuberculosis, drugs such as beta blockers & methotrexate, autoimmune diseases such as sarcoidosis, SLE and GI malignancies. 

Clinically the patient can present with features of intestinal obstruction with or without a palpable abdominal mass. 

The imaging differential includes:

1)  Congenital peritoneal encapsulation (CEP): it is a benign condition characterised by a thin membrane around small bowel and is usually asymptomatic.

2)   Peritoneal carcinomatosis: it is characterised by nodular peritoneal thickening with nodular deposits in omentum, pouch of Douglas and surface of bowel. 

3)   Internal hernias: they occur in fixed anatomic locations and complication such as bowel ischemia are more common in them. 

Telangiectatic osteosarcoma

 

We will discuss a case of telangiectatic osteosarcoma, including imaging findings with differential diagnosis.

16-year-old man presented with complaints of left upper arm swelling for 1 year.

Xray left shoulder was performed which shows ill-defined lesion with osteoid matrix (orange arrow) causing geographic lytic destruction of proximal meta-diaphysis of left humerus with a wide zone of transition, spiculated or sunburst (blue arrow) and Codman type of periosteal reactions in its inferior aspect (yellow arrow).

Subsequent MRI left shoulder was performed, coronal T2W images shows a large relatively well-defined lobulated heterogeneously enhancing solid cystic mass in proximal meta-diaphyseal region of left humerus causing cortical destruction of head, neck, and proximal shaft. Cystic component of the mass shows multiple locules and enhancing thick intervening septae within. On GRE MEDIC images, the locules shows blood fluid levels within.

This was a proven case of telangiectatic variety of osteosarcoma.

Telangiectatic osteosarcoma is a subtype of osteosarcoma consists of large haemorrhagic or necrotic cavities. It occurs in the medullary cavity in the metaphyseal region of long bones. Most frequently affected site for these tumors is the distal femur and proximal humerus. The classic radiographic appearance of telangiectatic osteosarcoma is a lesion with geographic bone destruction, a wide zone of transition, endosteal scalloping and osteoid type of matrix mineralisation.

Important differential of fluid-fluid levels containing bone lesions are:

·         Aneurysmal bone cyst (ABC)

·         Telangiectatic variety of osteosarcoma

·         Simple bone cyst (after fracture)

The main differential diagnosis for telangiectatic osteosarcoma is an aneurysmal bone cyst. The distinction between the two conditions is usually made with MR imaging.

·         ABCs shows thin enhancing peripheral septa (usually 2–3 mm thick) whereas in telangiectatic osteosarcoma, the periphery and septa around the haemorrhagic spaces are thickened and often nodular and enhance with contrast.

·         At CT, the presence of an osteoid matrix within nodular or septal regions (intraosseous or soft-tissue component) is a feature of telangiectatic osteosarcoma

·         Telangiectatic osteosarcomas are associated with aggressive growth features such as cortical destruction and extension into the surrounding soft tissues. In contrast, ABCs cause marked expansile remodelling of bone and cortical thinning but lack true soft-tissue involvement.

 

IMAGING IN ACUTE PANCREATITIS

 

Overview

In this session, we will explore imaging techniques used in acute pancreatitis, including diagnosis, phases of the disease, and key radiographic signs.

Causes of Acute Pancreatitis

• Common Causes:
• Alcohol intake
• Gallstone disease

• Uncommon Causes:
  • Trauma
  • Drugs
  • Post-ERCP complications
  • Tumors
  • Infections (e.g., mumps)

Diagnosis Criteria

Acute pancreatitis is diagnosed when any two of the following criteria are met:

1. Symptoms of epigastric pain radiating to the back.
2. Elevated amylase and lipase levels (more than three times the normal).
3. Typical imaging features present on ultrasound, CT, or MRI.

Phases of Acute Pancreatitis

1. Early Phase (first week):
   • Possible systemic inflammatory response syndrome (SIRS) or multi-organ failure.
2. Late Phase (after the first week):
   • May develop complications like infections or sepsis.

Severity Grading

• Mild: No organ failure or complications.
• Moderate: Transient organ failure (< 48 hours) or local/systemic complications.
• Severe: Persistent organ failure (> 48 hours), with or without complications.

Revised Atlanta Classification

• Acute Interstitial Edematous Pancreatitis:
  • Less than four weeks: peripancreatic collection.
  • More than four weeks: pseudocyst.
• Acute Necrotizing Pancreatitis:
• Less than four weeks: acute necrotic collection.
• More than four weeks: wall of necrosis.

Key Radiographic Signs

• Colon Cutoff Sign: Lack of visualization of the colon due to spasm.
• Sentinel Loop Sign: Localized ileus of a small intestinal loop, typically in the jejunum.

• Emphysematous Pancreatitis: Presence of air foci in the upper abdomen due to anaerobic infections.

• Pleural Effusion: More commonly on the left side; can lead to basal atelectasis.

Imaging Modalities

Ultrasound

• First-line modality to visualize gallstones and assess pancreatic size and echogenicity.
• Bulky, edematous pancreas appears hypoechoic.

CT Imaging

• Timing: Best performed 72 hours after onset for optimal visualization of necrosis.
• Phases:
• Arterial Phase: Visualizes vascular complications.
• Pancreatic Parenchymal Phase: Homogeneous enhancement of pancreatic parenchyma.
• Portal Venous Phase: Visualizes portal vein thrombosis.

Normal Pancreas Appearance on CT

• Positioned anterior to the portal vein.
• Size criteria:
  • Head: 23 ± 3 mm
  • Neck: 19 ± 2.5 mm
  • Body: 20 ± 3 mm
  • Tail: 15 ± 2.5 mm

MRI Appearance

• Slightly hyperintense on T1-weighted images compared to liver and spleen.

Pathologies

Acute Interstitial Pancreatitis

• Bulky, edematous pancreas with surrounding fluid collections.
• Differentiates into peripancreatic collections or pseudocysts based on time.

Acute Necrotizing Pancreatitis

• Necrotic collections appear hypodense and heterogeneous within the pancreatic parenchyma.
• After four weeks, this becomes a wall of necrosis.

Pseudocyst

• Thick-walled, homogeneously appearing cystic lesions.

Complications

• Vascular Complications: Arterial pseudoaneurysm or rupture, venous thrombosis.
• Infected Necrosis: Can occur due to collections.
• Bowel Complications: Necrosis or perforation.
• Pancreatic Ascites: Accumulation of fluid.

Conclusion

Imaging plays a crucial role in diagnosing and managing acute pancreatitis. Understanding the various stages, complications, and imaging characteristics helps guide appropriate treatment.

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Gallbladder Carcinoma

We'll discuss a case of gallbladder carcinoma, including imaging findings, clinical features, and differential diagnoses.

Imaging Findings

CT Imaging

1. Axial Sections:

• Initial views show the liver and spleen, followed by the liver in its entirety during the portal venous phase.
• An ill-defined, isodense mass replaces the gallbladder, with central necrotic areas visible on contrast-enhanced CT.
• The liver interface with the mass is poorly defined, suggesting liver involvement.
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2. Common Bile Duct (CBD):

   • The cystic duct is not separately visualized; the mass abuts the CBD, which shows dilation along its entire course.
   • Upstream, there is intrapatic biliary radical dilation (IHBRD), more pronounced centrally.
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3. Coronal Sections:

   • The ill-defined mass in the gallbladder fossa is confirmed with necrotic areas and dilated CBD.
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Clinical Features and Epidemiology

• Demographics: More common in women, particularly in regions like New Mexico, Bolivia, and Israel.

• Risk Factors:

  • Female gender and postmenopausal age.
  • Chronic infections (e.g., Salmonella typhi), smoking, and industrial exposures.
  • Cholelithiasis and congenital conditions (e.g., choledochal cyst, primary sclerosing cholangitis).

• Symptoms: Often present with advanced disease. Early symptoms are rare but may include:

  • Chronic abdominal pain
  • Anorexia and weight loss
  • Jaundice and a palpable mass
  • Incidental detection on imaging; elevated serum alpha-fetoprotein and CA levels may occur.

Radiological Features

• X-ray: First-line imaging, although not definitive.
  • Can show porcelain gallbladder or calcified gallstones.
  • Abnormal contour may indicate fistula formation.

Types of Gallbladder Carcinoma

1. Mass Replacing the Gallbladder: Most common presentation.
2. Focal or Diffuse Wall Thickening: May mimic benign processes.
3. Intra-luminal Polypoid Mass: Polyp >1 cm is a risk for malignancy.

Ultrasound Findings

• Polypoid Mass: Shows internal vascularity.
• Ill-defined Mass: Indicates invasion into liver tissue.

Cross-Sectional Imaging

• Contrast-Enhanced CT: Critical for assessing mass replacement, wall thickening, and potential metastases.

• MRI: Useful for differentiating gallbladder carcinoma from benign conditions like adenomyomatosis.

Differential Diagnosis

1. Wall Thickening Causes:

   • Inflammatory: Acute and chronic cholecystitis, abscess.
   • Non-inflammatory: Heart failure, cirrhosis, renal failure leading to ascites.

2. Xanthogranulomatous Cholecystitis: Radiologically similar to carcinoma, often with fat stranding.

3. Adenomyomatosis: Characterized by focal wall thickening with ring down artifacts.

Conclusion

Gallbladder carcinoma is a challenging diagnosis often identified at advanced stages. Imaging plays a vital role in detection and differentiation from other conditions.

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