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.
• 

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.
   • 

3. Coronal Sections:

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

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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INTERSTITIAL LUNG DISEASES: Radiological Appearances and Pathological correlation

 

Interstitial lung diseases (ILDs) are a diverse group of disorders characterized by inflammation and fibrosis of the lung interstitium. This article will explore the radiological appearances of ILDs, primarily using high-resolution computed tomography (HRCT), and will also examine the associated pathology.

Anatomy of the Secondary Pulmonary Lobule

The secondary pulmonary lobule is the smallest unit visible on HRCT imaging, measuring approximately one centimeter in size. It is supplied by the lobular bronchus and lobular artery, which divide into terminal bronchioles and respiratory bronchioles. Each bronchiole is accompanied by an associated acinar artery. 

The interlobular septa, which are thin connective tissue structures about 0.1 millimeters thick, contain pulmonary veins, lymphatics, and connective tissue, forming the lung's interstitium.

Patterns of ILD on Imaging

Interstitial lung diseases can present with various radiological patterns, which can be categorized into lesions with increased and decreased lung attenuation:

1. Increased Lung Attenuation:

• Ground Glass Opacities (GGOs): These allow for the visualization of vascular markings beneath the opacities.
• Consolidations: Characterized by obscured vascular markings, indicating more dense lung involvement.

1. Decreased Lung Attenuation:

• Honeycombing: Appears as peripheral multi-layered cystic changes.
• Bronchiectasis: Represents dilated bronchioles and bronchi.
• Emphysematous Changes and Pneumatoceles: Indicate areas of lung destruction.

Additionally, ILDs may present with nodules or linear/reticular opacities due to interlobular septal thickening.

Classification of Interstitial Lung Diseases

Interstitial lung diseases can be classified into idiopathic and known causes.

Idiopathic Interstitial Lung Diseases (IIDs)

Usual Interstitial Pneumonia (UIP): Characterized by an apical-basal gradient, more prominent in the basal regions, often presenting with honeycombing, traction bronchiectasis, and reticular opacities.

Non-Specific Interstitial Pneumonia (NSIP): Features a central sparing pattern with peripheral opacities. Commonly shows ground glass opacities, reticular opacities, and micro-nodules. A distinctive feature is the sparing of immediate subpleural regions.

Respiratory Bronchiolitis and Desquamative Interstitial Pneumonia (DIP): Associated with smoking, presenting with pigmented macrophage deposition.

Cryptogenic Organizing Pneumonia (COP): Commonly occurs in non-smokers, showing peripheral and peri-bronchial opacities with migrating patterns and no response to antibiotics.

Acute Interstitial Pneumonia (AIP): Presents with diffuse alveolar damage, often showing bilateral symmetrical opacities and progressing to consolidation.

Known Causes of Interstitial Lung Diseases

1. Sarcoidosis
2. Connective Tissue Disorders (e.g., rheumatoid arthritis, systemic sclerosis, systemic lupus erythematosus)
3. Hypersensitivity Pneumonitis
4. Silicosis
5. Lymphangioliomyomatosis and Langerhans Cell Histiocytosis
6. Pulmonary Alveolar Proteinosis

Miscellaneous Causes

• Infective: Viral pneumonias, Pneumocystis jirovecii pneumonia, Mycoplasma pneumonia.
• Non-infective: Eosinophilic pneumonia, Acute Respiratory Distress Syndrome (ARDS), Lipoid pneumonia, Diffuse Alveolar Hemorrhage.

Treatment Approaches

The treatment for ILDs varies based on the specific disease. For UIP, corticosteroids and immunosuppressive agents (like cyclosporine) are often employed to provide symptomatic relief and slow disease progression. In NSIP, corticosteroids or cytotoxic drugs can be effective, particularly in the cellular subtype.

Key Points for Reporting ILDs on HRCT

• Rule out known causes before diagnosing idiopathic interstitial lung diseases.
• Classification of ILDs is based on histological findings rather than imaging alone.
• Follow-up scans are necessary due to the dynamic nature of ILDs.
• Surgical lung biopsy may be required to confirm the diagnosis and should involve multiple lobes.

Conclusion

Understanding the radiological appearances and classifications of interstitial lung diseases is crucial for accurate diagnosis and management. For further educational content, consider following platforms dedicated to radiological education.

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TRIPLE RULE OUT CT ANGIOGRAPHY

Overview

This guide discusses Triple Rule Out CT Angiography, focusing on its protocol for patients with acute chest pain in emergency settings. We will cover indications, patient selection, contraindications, necessary CT hardware, radiation considerations, preparation steps, and image interpretation.

Understanding Acute Chest Pain

Acute chest pain can arise from various conditions, with acute coronary syndrome (ACS) accounting for only 25% of cases. Other possible causes include:

• Pulmonary Embolism
• Aortic Dissection
• Other conditions like pneumonia, pneumothorax, rib fractures, or pericardial effusion.

Use of Triple Rule Out CT Angiography

When all three conditions (ACS, pulmonary embolism, aortic dissection) are suspected, Triple Rule Out CT Angiography serves as a comprehensive diagnostic tool.

Protocol for Acute Chest Pain

Initial Assessment

1. Serial ECGs: Monitor heart activity.
2. Troponin Levels: Check for myocardial injury.
3. Stress Test: May or may not be performed.

Indications for Triple Rule Out

• Patients presenting with complex symptoms of acute chest pain, shortness of breath, or pain radiating to the neck or left arm.
• Negative troponin tests and no ECG changes.

Patient Selection Criteria

• Ideal Candidates: Young adults with low risk of ACS, negative biomarkers, and no ECG changes.
• Other Requirements: Acceptable cardiac rhythm, adequate renal function, ability to hold breath during the scan.

Contraindications

• Renal Insufficiency: Risk of contrast-induced nephropathy.
• Contrast Allergy: Previous adverse reactions to contrast agents.
• Beta Blockers: Can interfere with heart rate control.

CT Hardware Requirements

• Minimum: 64-slice CT scanner capable of scanning 20 cm in 15 seconds.
• Settings: 120 kVp, 60 mAs (modulated to 8.75 mAs during the scan).
• Radiation Reduction: Use of tube current modulation and ECG gating can significantly reduce patient radiation exposure.

Patient Preparation

1. Caffeine and Stimulants: Patients should avoid these before the study.
2. IV Access: Place an 18-gauge IV catheter.
3. ECG Leads: Attach to monitor heart activity.
4. Beta Blockers: Administer as needed (2.5 to 30 mg) to achieve bradycardia.
5. Nitroglycerin: Give sublingually just before the scan.

CT Protocol

• Contrast Administration: Use a biphasic injection method:
  • Phase 1: 70 mL of 350 mg iodine/mL contrast.
  • Phase 2: 25 mL of contrast mixed with 25 mL of saline.
• Injection Speed: 5 mL/sec to opacify the left and right heart.

Scanning Technique

• Scan from 1 to 2 cm above the aortic arch to the lower chest, ensuring coverage of the heart's base.
• Initiate acquisition 5 seconds after achieving a threshold of 100 HU in the left atrium.

Image Interpretation

• Use axial slices of 3 to 5 mm for the aorta and pulmonary arteries.
• Thin sections (6 to 8 mm) are ideal for assessing coronary arteries.
• Key Findings:
• Stenosis: Indicates coronary artery disease.
• Aortic Dissection: Visualized with thrombus.
• Pulmonary Embolism: Confirmed through typical scan patterns.

Conclusion

Triple Rule Out CT Angiography is an effective triage method in emergency settings for patients with acute chest pain. Proper patient selection, preparation, and adherence to CT protocols are critical for accurate diagnosis. For more educational content, follow our channels on Instagram and YouTube!

APPROACH TO SKELETAL DYSPLASIA: A Comprehensive Overview

                             

 An introductory guide on approaching skeletal dysplasia cases through skeletal surveys. It discusses the distinction between dysplasia and disostosis, outlines necessary X-rays, and evaluates anatomical locations and bone involvement. The classification of dysplasias into groups based on X-ray features is also explained, providing insights into various conditions and their characteristics.

  To view this teaching video click on the link below

                          https://youtu.be/pUgm-drP7xQ?si=lfd72jmyNoucZsu0

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Skeletal dysplasia refers to a group of disorders characterized by abnormal growth and development of bones and cartilage, often due to genetic mutations. Understanding how to evaluate skeletal dysplasia requires a systematic approach, particularly when analyzing skeletal surveys.

Understanding Skeletal Dysplasia vs. Dysostosis

• Dysplasia: Genetic mutations lead to ongoing changes throughout life.
• Dysostosis: Static defects resulting from one-time damage during embryonic development, such as in conditions like cleidocranial dysostosis.

X-Ray Protocol for Skeletal Survey

A skeletal survey typically includes:

1. Skull: Anteroposterior (AP) and lateral views.
2. Thoracolumbar Spine: AP and lateral views.
3. Chest: AP view.
4. Pelvis: AP view, including bilateral hips.
5. Upper and Lower Limbs: One of each, or both limbs if epiphyseal dysplasias are suspected.

Evaluation Framework: ABCs of Evaluation

A: Anatomical Location

1. Axial vs. Appendicular Skeleton:

   • Axial Skeleton: Includes the skull, spine, and ribs.
   
   
   • Appendicular Skeleton: Comprises limbs and pelvis.
   • 

2. Specific Bone Locations:

• Epiphyseal: Conditions like chondrodysplasia punctata.
• Metaphyseal: Notable in achondroplasia.
• Diaphyseal: Seen in Progressive Diaphyseal Dysplasia (Angelman’s disease).

3. Complications: Monitor for scoliosis, osteoarthritis, and pathological fractures.

B: Bone Locations and Their Implication

Axial Skeleton Involvement:

• Skull: Conditions like achondroplasia and cleidocranial dysplasia.
• Mandible: Involvement in conditions like pignodysostosis.
• Clavicle: Seen in cleidocranial dysplasia.
• Spine: Look for beaking or platyspondyly in conditions like spondyloepiphyseal dysplasia

Appendicular Skeleton:

• Proximal Limb Segments (Humerus/Femur): Shortened—rhizomelia (e.g., achondroplasia).
• Middle Limb Segments (Radius/Ulna, Tibia/Fibula): Shortened—mesomelia (e.g., mesomelic dysplasia).
• Distal Segments (Hand/Foot): Shortened—acromelia (e.g., acrodisostosis).

C: Classification of Dysplasias

Based on the 2010 revision by the International Skeletal Dysplasia Society, dysplasias can be categorized into four groups:

1. Group 1: Epiphyseal dysplasia (with/without spine involvement).
2. Group 2: Metaphyseal dysplasia (with/without limb shortening).
3. Group 3: Dysplasias with altered bone densities.
4. Group 4: Miscellaneous disorders.

Detailed Breakdown of Groups

Group 1: Epiphyseal Dysplasia

• Normal vertebral body height: Possible chondrodysplasia punctata.
• Flattened vertebral bodies: Look for platyspodyly—conditions include pseudoachondroplasia and mucopolysaccharidosis

Group 2: Metaphyseal Dysplasia

• Abnormal limb length; types include:
• Rhizomelic: (e.g., achondroplasia).
• Mesomelic: (e.g., chondroectodermal dysplasia).

Group 3: Altered Bone Density

• Osteopenia: Seen in osteogenesis imperfecta.
• Osteosclerosis: Conditions like osteopetrosis

Group 4: Miscellaneous

• Includes conditions like cleidocranial dysplasia.

Summary of the Evaluation Process

1. Evaluate the Spine:

   • Check for platyspondyly.
   • Assess extremities for epiphyseal or metaphyseal involvement.

2. Analyze the Skull:

   • Look for abnormal bone density (e.g., thick skull in osteopetrosis).

Flowcharts for Quick Reference

Spine Flowchart:

• If platyspondyly is present, evaluate extremities for epiphyseal/metaphyseal conditions.

Skull Flowchart:

• If abnormal findings are noted, differentiate between cleidocranial dysplasia and pignodysostosis.

Conclusion

Understanding skeletal dysplasia requires familiarity with various conditions and their radiographic features. This structured approach can aid in accurate diagnosis and management. For a deeper dive into specific conditions, please comment below, and I’ll create focused content for those topics.

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