Appendicitis

Jeffrey Lam Shin Cheung, Tania Saha, Dr. Nasir Jaffer

Presentation

Sujata is a 24-year-old female presenting to the emergency room with a six-hour history of right-side lower quadrant abdominal pain. She notes that she is experiencing pain that originated from her umbilicus that now radiates diffusely with increasing intensity across the lower abdomen. Sujata describes her pain as sharp and colicky. She discloses feeling nauseous and vomiting prior to entering the emergency room. Her pain is slightly relieved by an over-the-counter analgesic and by leaning forward. However, she notes that it is exacerbated by extension of the right hip.

Physical Examination

On physical examination of Sujata, right lower quadrant pain is noted on palpation at the junction of the lateral third and medial two-thirds of a line drawn from the anterior superior iliac spine to the umbilicus. A positive psoas sign is noted as she experiences pain on passive extension of her right hip when she lies on her left side. She has no other significant findings on physical examination.

Imaging

An ultrasound of the abdomen is done as the first-line imaging and if there are non-benign appreciations, a CT is completed.

An ultrasound shows thick-walled appendix, appendicolith, dilated fluid-filled appendix, and be non-compressible.

A CT will show enlargement of the appendix (>6 mm in outer diameter), enhancement of the appendiceal wall, and appendicolith.

Figure 1. Ultrasound of acute appendicitis.

Variations in Presentation and Differential Diagnoses

Figure 2. Appendicitis may present with appendicolith, a type of fecalith in the appendix. In a CT scan, this will appear as a calcified mass, typically in the appendiceal lumen.

Figure 3. A mucocele of the appendix appears as a dilated, mucin-filled appendix, and may mimic the appearance of appendicitis.

Figure 4. A mucocele of the appendix may also result in pseudomyxoma pertionei, a mucinous tumour that spreads throughout the peritoneal cavity. The incidence is 1-3/1,000,000 annually.

Figure 5. Cecal diverticulitis has a similar clinical presentation as appendicitis. On CT imaging, both may demonstrate a dilated appendix with periappendiceal fat stranding. In cecal diverticulitis, however, one would expect to see diverticula (outpouchings) in the cecum/ascending colon with associated fat stranding.

Figure 6. Epiploic appendagitis has a similar clinical presentation as appendicitis. A typical finding on CT includes a hyperattenuating ring around the inflamed epiploic appendage.

Figure 7. It is imperative to rule out ectopic pregnancy in a female patient presenting with abdominal pain and vaginal bleeding. A high β-HCG (>6500 IU/l) and ultrasound showing an empty uterus (with possible decidual reaction) is suggestive of an ectopic pregnancy.

Practice Questions

Question 1. Which of the following imaging findings is most suggestive of a ruptured appendix on CT scan imaging?

1. Periappendiceal abscess
2. Small bowel diameter of 5cm
3. Thickened cecal wall
4. Thumbprinting in the ascending colon

Answer: 1

Explanation: Periappendiceal abscess and extraluminal gas are two common signs of a perforated appendix. A small bowel diameter >3cm is considered dilated and may be due to an obstruction or adynamic ileus. A thickened bowel wall is a nonspecific sign that may be caused by inflammation, infection, and ischemia among other causes. Thumbprinting in the colonic wall is suggestive of colitis.

Question 2. Which of the following features is not commonly associated with appendicitis on CT scan imaging?

1. Dilated (>6 mm), fluid-filled appendix
2. Multiple sacculations within the cecal wall
3. Thickening of the cecal apex
4. Perpendicular fat stranding surrounding the cecum

Answer: 2

Explanation: Multiple sacculations within the colonic wall in a patient presenting with acute abdominal pain is more suggestive of diverticulitis. A dilated, fluid-filled appendix is the most specific CT finding of appendicitis. Thickening of the cecal appendix may be a secondary sign of appendicitis, and fat stranding is a nonspecific finding that may be seen in appendicitis among other conditions such as inflammation, infection, and ischemia of the bowels.

Question 3. A 33-year-old man has right lower quadrant abdominal pain radiating to the right upper quadrant. A CT scan is ordered and reveals the following.

What treatment choice would you recommend?

1. Conservative management
2. Laparoscopic appendectomy
3. Piperacillin and tazobactam
4. NPO order for 24 hours

Answer: 1

Explanation: The fat density mass near the ileocecal junction, which also demonstrates the hyperattenuating ring sign, is suggestive of epiploic appendagitis. Conservative management with analgesics is often sufficient. Laparoscopic appendectomy may be considered for appendicitis, and antibiotic treatment may be appropriate for appendicitis or complicated diverticulitis. An NPO order may be considered for uncomplicated diverticulitis.

Question 4. A patient in a rural town presents to their doctor with a 3-day history of RLQ pain and nausea. Their doctor orders an x-ray that reveals the following.

This patient has an increased risk of all of the following except:

1. Acute appendicitis
2. Constipation
3. Abscess formation
4. Appendix perforation

Answer: 2

Explanation: This x-ray demonstrates a large calcified mass in the right lower quadrant, which is suspicious for an appendicolith (a type of fecalith occurring in the appendix). An appendicolith itself does not typically cause bowel obstruction or constipation, though a low-fiber diet increases the risk of fecalith formation.

Question 5. A 44-year-old female complains of abdominal pain and vaginal bleeding. An ultrasound is ordered and reveals the following.

Which of the following is the next best course of action?

1. Order an urgent CT
2. Tell the patient that no further management is needed
3. Refer the patient for a hysterectomy
4. Order lab investigations

Answer: 4

Explanation: The patient’s older age and symptoms are concerning for an ectopic pregnancy. The ultrasound shows an empty uterus with decidual reaction (thickening of the endometrium), which further supports a diagnosis of ectopic pregnancy. A β-hCG should have been ordered for this patient, and the typical expected value would be >6500 IU/l in a case of ectopic pregnancy.

References

Hardin Jr DM. Acute appendicitis: review and update. American family physician. 1999 Nov 1;60(7):2027.

Rizvi SA, Syed W, Shergill R. Approach to pseudomyxoma peritonei. World journal of gastrointestinal surgery. 2018 Aug 27;10(5):49.

Gaitini D. Imaging acute appendicitis: state of the art. Journal of clinical imaging science. 2011;1.

Pereira JM, Sirlin CB, Pinto PS, Jeffrey RB, Stella DL, Casola G. Disproportionate fat stranding: a helpful CT sign in patients with acute abdominal pain. Radiographics. 2004 May;24(3):703-15.

Subramaniam R. Acute appendagitis: emergency presentation and computed tomographic appearances. Emergency Medicine Journal. 2006 Oct 1;23(10):e53-.

Kaya B, Eris C. Different clinical presentation of appendicolithiasis. The report of three cases and review of the literature. Clin Med Insights Pathol. 2011;4:1-4. Published 2011 Mar 30. doi:10.4137/CPath.S6757

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Ruptured Posterior Communicating Artery Aneurysm

Tiffany Ni, Raza Syed, Dr. Kieran Murphy

Introduction

Cerebral aneurysms result from an abnormal focal dilation of an artery wall in the brain and can vary in size from 0.5 mm to greater than 25 mm(1,2). While most cerebral aneurysms are silent and may be incidentally identified on imaging, aneurysmal rupture is commonly associated with subarachnoid hemorrhage (SAH), leading to a high morbidity and mortality rate(1,2).

Despite the current uncertainties surrounding the precise mechanisms by which cerebral aneurysms develop, grow, and rupture, several factors have been associated with the formation of cerebral aneurysms(3,4). Some include hypertension, age over 40, smoking, trauma to the blood vessels, and a family history of aneurysms(3).

Posterior communicating artery (PCOM) aneurysms are the second most common aneurysms overall, accounting for 25% of all aneurysms and representing 50% of all internal carotid artery (ICA) aneurysms(5). We report a patient with a ruptured left PCOM aneurysm presenting with a left subarachnoid hemorrhage.

Patient presentation

A 52-year-old woman was presented with a sudden onset of severe headache, vomiting, nuchal rigidity, and decreased conscious level. She was transported to our hospital for management of subarachnoid haemorrhage (SAH). On admission, the patient was semi-comatose with anisocoric pupils, and a Glasgow Coma Scale (GCS) score of 5. She had no past medical history of trauma, hypertension, diabetes or other diseases.

Investigations & Diagnoses

Based on the patient’s clinical presentation, the following would be included in the list of differential diagnoses(1):

• Arteriovenous malformations
• Cavernous sinus syndromes
• Carotid/vertebral artery dissection
• Cerebral venous thrombosis
• Fibromuscular dysplasia
• Migraine and cluster headaches
• Moyamoya disease
• Pituitary apoplexy
• Stroke - ischemic or hemorrhagic
• Vein of Galen malformation

The first-line diagnostic investigations to be ordered included(6):

• conventional catheter-based angiogram (digital subtraction angiography)
• CT angiography
• magnetic resonance angiography

The repeat computerized tomography (CT) scan demonstrated diffuse subarachnoid hemorrhage (Figure 1). Digital subtraction angiography (DSA) confirmed the presence of a saccular aneurysm localizable to the PCOM on the left side (Figure 2).

Figure 1. Computed tomographic scan showing diffuse subarachnoid bleeding secondary to rupturing of the PCOM aneurysm

Figure 2. Digital subtraction angiography was performed which showcases an aneurysm originating from the PCOM

Procedure

Endovascular detachable coil embolization was performed under intravenous anesthesia. The microcatheter was navigated from the femoral artery to the left PCOM aneurysm and a microcatheter tip was positioned in the aneurysm under fluoroscopic guidance. Coil position within the aneurysm and the patency of the parent vessel were confirmed angiographically prior to every coil detachment. The left PCOM aneurysm was successfully occluded (Figure 3).

Figure 3. Digital subtraction angiography was performed following endovascular coiling of the PCOM aneurysm showing complete occlusion of the aneurysm and exclusion from circulation as well as good patency of the PCOM

One week later, follow-up CT and DSA examination was performed and revealed no abnormality in the brain parenchyma and good patency of the PCOM. The patient’s postoperative course was uneventful, and she was discharged home on the 14th postoperative day. The patient was neurologically intact at discharge.

Case Questions

What if the patient in this case was 35 years old instead? How would your treatment strategy change?

1. endovascular coiling
2. anti-platelet medications only
3. surgical clipping
4. endovascular thrombectomy

Answer: 3) surgical clipping (instead of endovascular coiling)

In endovascular coiling, a micro-catheter is inserted into the femoral artery via an initial catheter(7,8). A platinum coil is attached to the microcatheter tip. When the microcatheter reaches the lumen of the aneurysm, an electrical current is used to separate the coil from the catheter. The coil induces thrombosis of the aneurysm and is left permanently in the aneurysm.

Surgical clipping is done under general anesthesia and requires open surgery(7). The brain is gently retracted to visualize the aneurysm. A small clip is placed across the neck of the aneurysm to block the blood flow into it. Clips are made of titanium and remain on the artery permanently.

In this situation, the preferred method of treatment would be surgical clipping(9). The less invasive nature of coiling is likely to be favored in patients who are older, are in poor health, have serious medical conditions, or have aneurysms in certain locations. In patients younger than 40 years of age, the difference in the safety between coiling versus clipping is small. Therefore, the better long-term protection from bleeding may give patients with clipped aneurysms an advantage in life expectancy.

What imaging technique should be used to assess any possible residual perfusion of the aneurysm?

1. non-contrast enhanced CT scan
2. magnetic resonance angiography (MRA)
3. CT angiography
4. digital subtraction catheter angiography

Answer: 4) Digital subtraction catheter angiography

Digital subtraction catheter angiography remains the gold standard for diagnosis and characterization of vascular abnormalities and in many centers, even if the causative lesion is identified on MRA or CTA and it is thought to require surgical management, a catheter study is carried out(10).

The benefit of DSA over MRA or CTA is two-fold:

• Higher spatial resolution: better able to delineate small vessels and characterize vascular morphology (e.g. aneurysm neck and incorporation of adjacent vessels)
• Temporal resolution: contrast can be seen to wash into and out of vascular malformations, giving important information in regard to the feeding vessels (e.g. arteriovenous malformations or dural arteriovenous fistulas)

A non-contrast enhanced CT scan is commonly used as the first-line imaging modality for evaluating subarachnoid hemorrhage as it is rapid, inexpensive, and widely available.

What are the characteristics of aneurysmal subarachnoid hemorrhage (SAH)?

1. Headaches, nausea, and vomiting is always present
2. Loss of consciousness is always present
3. Patients tend to present as asymptomatic
4. Varies, specific syndromes have been associated with particular aneurysmal locations

Answer: 4) Varies, specific syndromes have been associated with particular aneurysmal locations.

For example, aneurysms at the anterior communicating artery, the most common site of aneurysmal SAH (34%), have the following characteristics(11):

• These aneurysms are usually silent until they rupture
• Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism, amnestic syndromes, or hypothalamic dysfunction
• Neurologic deficits in aneurysmal rupture may reflect intraventricular hemorrhage (79%), intraparenchymal hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe strokes (20%)

What is the progression of aneurysmal rupture?

1. Aneurysmal rupture is typically self-limiting
2. Aneurysmal rupture results in vasodilation
3. Aneurysmal rupture typically results in SAH
4. Aneurysmal rupture results in hypernatremia

Answer: 3) Aneurysmal rupture typically results in SAH.

What typically accompanies the SAH is diffuse or focal forms of vasospasm that may lead to ischemia and infarction¹¹.

Recent animal data suggest therapeutic benefit of nitrite infusions to enhance cerebral perfusion in the setting of aneurysmal SAH¹¹. This delayed complication of vasospasm is of unclear pathogenesis but most likely is due to the presence of blood and the formation of multiple substances in the subarachnoid space. Spontaneous thrombosis of an aneurysm and subsequent recurrence have been reported in a few cases.

What are possible complications of ruptured cerebral aneurysms in general?

1. Seizures
2. Hyponatremia
3. Gastrointestinal bleeding
4. All of the above

Answer: 4) All of the above.

Some of the other complications of ruptured cerebral aneurysms include¹¹:

• Vasospasm
• Recurrent hemorrhage
• Hydrocephalus
• Cardiac arrhythmia, myocardial infarction, or congestive heart failure
• Neurogenic pulmonary edema, pneumonia, or atelectasis
• Anemia
• Venous thromboembolism

References

1. Jersey AM, Foster DM. Cerebral Aneurysm. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 [cited 2021 Jun 24]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK507902/
2. Cianfoni A, Pravatà E, Blasi RD, Tschuor CS, Bonaldi G. Clinical presentation of cerebral aneurysms. Eur J Radiol. 2013 Oct 1;82(10):1618–22.
3. Inagawa T. Risk factors for the formation and rupture of intracranial saccular aneurysms in Shimane, Japan. World Neurosurg. 2010 Mar 1;73(3):155–64.
4. Etminan N, Buchholz BA, Dreier R, Bruckner P, Torner JC, Steiger H-J, et al. Cerebral aneurysms: Formation, progression and developmental chronology. Transl Stroke Res. 2014 Apr;5(2):167–73.
5. July J. Surgery of Posterior Communicating Artery Aneurysm. In: July J, Wahjoepramono EJ, editors. Neurovascular Surgery : Surgical Approaches for Neurovascular Diseases [Internet]. Singapore: Springer; 2019 [cited 2021 Jun 24]. p. 87–92. Available from: https://doi.org/10.1007/978-981-10-8950-3_11
6. Cerebral aneurysm - Symptoms, diagnosis and treatment | BMJ Best Practice US [Internet]. [cited 2021 Jun 24]. Available from: https://bestpractice.bmj.com/topics/en-us/490
7. Kim K-H, Cha K-C, Kim J-S, Hong S-C. Endovascular coiling of middle cerebral artery aneurysms as an alternative to surgical clipping. J Clin Neurosci. 2013 Apr 1;20(4):520–2.
8. Kim YJ, Song KY. Endovascular Coiling of Multiple (More than Four) Intracranial Aneurysms. Interv Neuroradiol. 2004 Mar;10(1):75–81.
9. Molyneux A, Kerr R, Stratton I, Sandercock P, Clarke M, Shrimpton J, et al. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. Lancet Lond Engl. 2002 Oct 26;360(9342):1267–74.
10. Chen SH, Sur S, Sedighim S, Kassi A, Yavagal D, Peterson EC, et al. Utility of diagnostic cerebral angiography in the management of suspected central nervous system vasculitis. J Clin Neurosci Off J Neurosurg Soc Australas. 2019 Jun;64:98–100.
11. Chen J, Li M, Zhu X, Chen Y, Zhang C, Shi W, et al. Anterior Communicating Artery Aneurysms: Anatomical Considerations and Microsurgical Strategies. Front Neurol. 2020;11:1020.

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Congestive Heart Failure

Ashraf Altesha, Sandra Sabongui, Muhammad Uzair Khalid, Dr. Ciara O’Brien

A 67-year-old female presented to the emergency department with worsening shortness of breath (SOB) and a persistent cough. She first noticed the SOB while climbing one flight of stairs approximately one month ago. Her symptoms have become progressively worse since, with SOB upon taking 15-20 steps on a flat surface and performing household tasks such as sweeping the floor. She takes breaks often to catch her breath, and has to sleep in a recliner due to SOB while lying flat. She also reports recent weight gain, fatigue, swelling in her feet and ankles, and a progressive dry cough for one month. She denies sick contacts, fever, chills, wheezing, hemoptysis, chest pain, abdominal pain, nausea, vomiting, or diarrhea. The patient’s past medical history is significant for hypertension, type 2 diabetes mellitus, and obesity (BMI 32).  Medications include Metformin 1000 mg BID, Sitagliptin 100 mg OD, and Amlodipine 10 mg OD. She does not smoke, consume alcohol or use any recreational drugs. Her family history is unremarkable.

On physical examination, she was alert with a Glasgow Coma Scale of 15. She was tachypneic in tripod position with a respiratory rate of 24 and SpO2 of 91% on room air. HR was 110 bpm and regular, BP 154/92, and she was afebrile at 36.6°C. Her cardiac examination revealed distant heart sounds with a 3/6 holosystolic murmur best appreciated in the mitral region. Bilateral inspiratory crackles were present on auscultation, with reduced air sounds at the lung bases and dullness to percussion. Lower extremities had 2+ pitting bilaterally to the mid shins with palpable pulses. JVP was 6 cm above the sternal angle with a positive hepatojugular reflux.

Initial investigations included CBC, electrolytes, LFTs, creatinine, BNP, Troponins, ECG, and CXR. Pertinent findings included hyponatremia with Na of 132, an AKI with creatinine of 110 (baseline low 80s), and BNP of 520. ECG showed sinus tachycardia (114 BPM), and CXR findings included bilateral pleural effusions, cardiomegaly and features of interstitial and alveolar pulmonary edema including air space opacification, vascular redistribution, peribronchial cuffing, and Kerley B lines. An echocardiogram was obtained and showed moderate mitral regurgitation with EF of 44%. A diagnosis of CHF exacerbation was made. Patient was placed on 2L oxygen via nasal prongs, given 40 mg of IV furosemide and 60 mg of nitroglycerin over 24h via transdermal patch. Furosemide was continued BID for 2 more days until resolution of hyponatremia, AKI, and clinical improvement with euvolemia. Patient was then discharged on a standing dose of Furosemide 20mg BID, in addition to medications for chronic management of CHF including Ramipril 1.25mg OD, and Metoprolol 25mg OD and advised to follow up with primary care provider for titration of medications to achieve target blood pressure control.

Figures:

Figure 1: Kerley B lines (Shown by the red arrows) are thickened interlobular septa that are 1-2 cm long and 1 mm thick caused by interstitial fluid infiltration. They can be found at the lung bases or periphery, perpendicular to the pleural surface. Kerley B lines can be seen in pulmonary edema, pneumonia, interstitial pulmonary fibrosis, sarcoidosis, and lymphangitis carcinomatosa.

Figure 2: Peribronchial cuffing or “doughnut sign” (shown by the red arrow) is used to describe the increased density around a bronchus or large bronchiole caused by increased fluid or mucus buildup. This sign can be observed in plain films or head-on in CT scan. The differential for peribronchial cuffing is broad, and can include acute bronchitis, asthma, bronchiolitis, congestive heart failure, cystic fibrosis, diffuse parenchymal lung disease, Kawasaki disease, lung cancer, pneumonia, pulmonary edema, and smoke inhalation.

Figure 3: Pleural effusion (red arrows) is the accumulation of excess fluid in the pleural space surrounding the lung. This occurs when the influx rate of fluid into the pleural space exceeds the efflux rate, and may be caused by changes in Starling forces favouring fluid extravasation (eg. congestive heart failure and liver failure), obstruction of lymphatics (eg. malignancy), or leakage of fluid from elsewhere (eg. hemothorax, chylothorax, or urinothorax). The differential for a transudative effusion includes congestive heart failure, nephrotic syndrome, and liver failure. An exudative effusion results from disruption to the pleura and the commonest causes are cancers, and infection.

Figure 4: Cardiomegaly is defined as a transverse diameter of the cardiac silhouette that is greater than or equal to 50% of the chest transverse diameter (cardiothoracic ratio ≥ 0.5) on a posteroanterior chest X-ray or CT scan. This is caused by dilatation and hypertrophy of the heart muscle, which may be due to long-standing hypertension, coronary artery disease, valvular disease, infection, or cardiomyopathy. The differential diagnosis for cardiomegaly includes pericardial effusion, an anterior mediastinal mass, a prominent epicardial fat pad, and mediastinal widening secondary to a pulmonary or aortic pathology.

Multiple Choice:

1. Which one of the following signs on CXR refers to the finding of a well-rounded left ventricle and dilated aorta indicative of left ventricular hypertrophy?

1. Fleischner sign
2. Hampton hump
3. Shmoo sign
4. Water Bottle sign

Answer: 3

1. On a chest x-ray, findings indicative of right ventricular hypertrophy include:
   1. Rounded left heart border
   2. Uplifted cardiac apex
   3. Rotation of the heart posteriorly
   4. All of the above

Answer: 4

1. Which one of the following signs refers to bilateral perihilar airspace opacities on CXR which can be found in pulmonary edema?

1. Stag’s antler sign
2. Hampton hump
3. Bat wing sign
4. Comet tail sign

Answer: 3

1. On x-ray, a mediastinal mass consistent with malignancy was found with unilateral pleural effusion. The effusion was tapped under ultrasound guidance by an interventional radiologist. What do you expect to find?
   1. Transudate; Pleural to serum protein ratio should be greater than 0.2.
   2. Transudate; Pleural to serum protein ratio should be greater than 0.5.
   3. Exudate; Pleural to serum protein ratio should be greater than 0.2.
   4. Exudate; Pleural to serum protein ratio should be greater than 0.5

Answer: 4

1. What if the patient was an ex-smoker and a diagnosis of COPD exacerbation was made, what are some signs you may see on physical exam and CXR?
   1. Barrel chest, hyperinflation, diaphragmatic flattening, and air bronchograms
   2. Pectus carinatum, Kerley B lines, vertical and narrow heart, and hyperinflation.
   3. Barrel chest, vertical and narrow heart, diaphragmatic flattening, and hyperinflation.
   4. Barrel chest, bullae, meniscus sign, and hyperinflation.

Answer: 1

References

1. Gluecker T, Capasso P, Schnyder P, Gudinchet F, Schaller M, Revelly J et al. Clinical and Radiologic Features of Pulmonary Edema. RadioGraphics. 1999;19(6):1507-1531.
2. Bramson R, Griscom N, Cleveland R. Interpretation of Chest Radiographs in Infants with Cough and Fever. Radiology. 2005;236(1):22-29.
3. Reed J. Chest radiology. Philadelphia: Mosby; 2003.
4. Karkhanis V, Joshi J. Pleural effusion: diagnosis, treatment, and management. Open Access Emergency Medicine. 2012;:31.
5. Dähnert W. Radiology review manual. Philadelphia: Wolters Kluwer Health/Lippincott Williams Wilkins; 2011.

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Glioblastoma

Marc Anthony Manzo, Nykan Mirchi, Dr. Kieran Murphy

Introduction
Glioblastoma (GBM) is the most common neoplasm found within adult brains, originating from glial cells. GBMs are often sporadic and carry a poor prognosis (median survival 12-18 months) as they are typically aggressive in nature and treatment-resistant. Incidence of GBM peaks between the ages of 65 and 75, with a slightly higher prevalence in males (3:2=M:F).

Patient presentation is often dictated by the location of the GBM in the brain as different brain functions may be affected depending on the brain region. For example, a tumour in the central sulcus may cause weakness while one in the parieto-occipital sulcus may impair vision. Survival is also strongly dependent on location as superficial tumours in the cerebrum may be more easily surgically removed. Less surgically-accessible tumours on the other hand may only be partially removed or not at all, thereby leading to a much lower survival rate.

GBMs tend to be large in size by the time a patient presents to clinic. Histopathology and molecular testing are essential for accurate diagnosis and prognostication, and can be done at the time of surgery or through a separate biopsy. Standard treatment may involve several modalities including surgery, chemo/radiotherapy, and immunotherapy.

Immunotherapy is a rapidly developing therapeutic modality, and includes developments such as personalized tumour vaccines [7, 8]. Personalized tumour vaccines require whole-exome sequencing of an individual’s tumour and comparing it to those of normal cells to identify antigenic epitopes of the cancerous cells. The sequences of these antigenic epitopes are then used to create a vaccine. Ultimately, the vaccine triggers the production of T-cells that can recognize the antigenic epitope that was sequenced, allowing the immune system to selectively invade and destroy the patient’s GBM. A single vaccine can contain up to 20 different targeting antigens.The challenge now is to generate an immune response that is long-lasting and strong enough to have a positive effect on a patient’s overall survival.

One important approach to strengthen the antitumor immune response is through the use of checkpoint inhibitors. Tumours take advantage of checkpoints to avoid T-cell mediated death. An example of such is PD-1 signalling. PD-1 receptors are expressed by T-cells. When the PD-1 receptor binds to its ligand, T-cell mediated apoptosis is inhibited. Tumour cells express PD-1 ligands to suppress T-cell responses via this mechanism. Thus, checkpoint inhibitors, which are monoclonal antibodies, work by disrupting the interaction of the PD-1 receptor (and other similar checkpoint proteins) and its ligand, allowing the T-cell to destroy the tumour cell..

Other medications, such as dexamethasone (DEX), can be administered pre- and/or postoperatively to reduce peritumoral edema and associated cognitive impairment [4]. It is important to note that DEX administration will reduce tumour enhancement on imaging [5]. This phenomenon of reduced enhancement is also seen with Avastin (Bevacizumab). Avastin mitigates peritumoral edema and reduces tumour enhancement on imaging similar to DEX [6]. This reduction in enhancement seen with Dex and Avastin administration is troublesome because it may be falsely interpreted as tumour regression, when in fact, the tumour may be unaltered or even progressing. This phenomenon is known as the pseudoresponse, and should always be taken into account when examining images from patients receiving DEX or Avastin.

Pneumocystis pneumonia (PCP) is an opportunistic infection that may occur in patients with prolonged steroid use, including DEX, due to their immunosuppressive effects. Although there are no strict guidelines on when to begin PCP prophylaxis in these patients, the American Thoracic Society recommends considering prophylaxis when taking >20mg/day of prednisone for over 1 month. [10] Trimethoprim-sulfamethoxazole (TMP-SMX) is the recommended prophylactic agent of choice for any patient without HIV. [10]

Brain tumour patients undergoing neurosurgical interventions are in a latent hypercoagulable state and are therefore at a high risk of venous thromboembolism (VTE) and deep vein thrombosis (DVT). [11] Primary prevention is encouraged in these patients through the use of pneumatic compression stockings in addition to low molecular weight heparin (LMWH) or unfractionated subcutaneous heparin. [12] The treatments should be started pre-operatively and resumed 24-48hrs after surgery. As the risk of DVT remains high while the patient is immobile, treatments should be continued until they can ambulate.

Key radiographic features:

• CT: irregular thick margins. An irregular hypodense core signalling necrosis. Peripheral vasogenic edema and intense irregular enhancement of margins.
• MRI
  • T1: iso-to-hypointense, central heterogeneous signal.
  • T1 contrast (Gd): peripheral enhancement (irregular/nodular) around a necrotic core.
  • T2/FLAIR: Hyperintense with surrounding vasogenic edema.

Clinical case

Patient J.L. is a 58 year-old male that has been hospitalized after experiencing a generalized seizure. The patient was stabilized and treated with anti-seizure medication.  On history, patient J.L.’s spouse noted that he had been experiencing headaches and nausea for the past month. J.L. also experienced alterations in mental capacity, specifically being more forgetful during the past month.

The patient underwent an MRI scan and the following images were obtained.

Figure 1. Axial T1

Figure 2. Axial T2

Figure 3. Axial FLAIR

Figure 4. Axial T1 + Gadolinium

Figure 5. Coronal T1 + Gadolinium

Patient J.L was referred to neurosurgery for maximal resection of the tumour. Diagnosis of GBM was confirmed in surgery via histological and molecular testing. Treatment also included adjuvant radiotherapy and chemotherapy (temozolomide). Despite undergoing an intense treatment regimen, prognosis for patient J.L. remains grim. Median survival for patients diagnosed with GBM is less than 2 years.

On postoperative day 3, patient J.L. underwent contrast-enhanced MRI to determine the extent of tumour resection. No residual tumour was detected upon imaging. Patient J.L. was scheduled for follow-up imaging every 12 weeks, as GBM tends to be a highly recurrent disease with the median time to recurrence being approximately 7 months (even with standard therapeutic regimens). Recurrence of patient J.L.’s tumour was detected at 17 months post-surgery. Given his age and health, J.L. was scheduled for a second surgery to resect the tumour. Repeat surgeries have been shown to have a positive effect on overall survival [9].

Questions:

• Describe the features and anatomical location of the lesion imaged. (short answer)
  1. “Irregular shaped ill-defined intra-axial space occupying lesion involving the inferior aspect of left temporo-occipital region, exhibits heterogeneous enhancement in post contrast study and exerting a positive mass effect upon the temporal horn of left lateral ventricle. Multiple areas of intralesional necrosis are noted.”

• Given this patient’s initial presentation and imaging, what else is on your differential diagnosis? (short answer)
  1. Cerebral metastasis, primary CNS lymphoma, cerebral abscess, tumefactive demyelination, and cerebral infarction.

• What radiographic features would you expect to see on a T1 scan with contrast of a GBM?
  1. Peripheral/nodular enhancement of the tumour.
  2. Homogeneous enhancement of the tumour.
  3. Enhancement of necrotic core.
  4. Non-enhancing margins

Answer: 1

• What might the nonhomogeneous enhancement of GBM in T1 + contrast be caused by? (select all that apply)
  1. Necrosis
  2. Hemorrhage
  3. Demyelination
  4. Ischemia

Answer: 1 and 2

• List at least 3 poor prognostic factors of GBM? (short answer)
  1. Greater degree of necrosis and enhancement, older age, deeper location of the tumour, and lower pre-diagnostic functional status.

• Which of the following features may be indicative of vasogenic edema surrounding a space occupying lesion in the brain? (select all that apply)
  1. Hyperintense region on T2
  2. Hyperintense region on T1 + contrast
  3. Loss of grey/white matter differentiation
  4. Accentuation of grey-white differentiation
  5. Sulcal effacement

Answer: 1, 4, 5

• What is the recommended timeline for follow-up for this patient?
  1. 1-2 days after surgery and 1-2 months thereafter.
  2. 7-14 days after surgery and 1-2 months thereafter.
  3. 1-2 days after surgery and 6-8 months thereafter.
  4. 7-14 days after surgery and 6-8 months thereafter.

Answer: 1

• Which brain region is most commonly affected by GBM?
  1. Cerebral cortex
  2. Cranial nerves
  3. Brainstem
  4. Cerebellum
  5. Deep brain nuclei

Answer: 1

Sources

1. Gaillard F. Glioblastoma: Radiology Reference Article [Internet]. Radiopaedia Blog RSS. [cited 2021Jul23]. Available from: https://radiopaedia.org/articles/glioblastoma
2. Jeffrey N Bruce MD. [Internet]. Glioblastoma Multiforme Clinical Presentation: History, Physical Examination. Medscape; 2021 [cited 2021Jul23]. Available from: https://emedicine.medscape.com/article/283252-clinical
3. Clinical presentation, diagnosis, and initial surgical management of high-grade gliomas [Internet]. UpToDate. [cited 2021Jul23]. Available from: https://www.uptodate.com/contents/clinical-presentation-diagnosis-and-initial-surgical-management-of-high-grade-gliomas
4. Cenciarini M, Valentino M, Belia S, Sforna L, Rosa P, Ronchetti S, et al. Dexamethasone in Glioblastoma Multiforme Therapy: Mechanisms and Controversies. Frontiers in Molecular Neuroscience. 2019;12.
5. Dietrich J, Rao K, Pastorino S, Kesari S. Corticosteroids in brain cancer patients: benefits and pitfalls. Expert Review of Clinical Pharmacology. 2011;4(2):233–42.
6. Gaillard F. Glioblastoma with pseudoresponse: Radiology Case [Internet]. Radiopaedia Blog RSS. [cited 2021Jul23]. Available from: https://radiopaedia.org/cases/glioblastoma-with-pseudoresponse?lang=us
7. Huang B, Li X, Li Y, Zhang J, Zong Z, Zhang H. Current Immunotherapies for Glioblastoma Multiforme. Frontiers in Immunology. 2021;11.
8. Baratta MG. Glioblastoma is ‘hot’ for personalized vaccines. Nature Reviews Cancer. 2019;19(3):129.
9. Lu VM, Jue TR, McDonald KL, Rovin RA. The Survival Effect of Repeat Surgery at Glioblastoma Recurrence and its Trend: A Systematic Review and Meta-Analysis. World Neurosurgery. 2018;115.
10. Limper AH, Knox KS, Sarosi GA, Ampel NM, Bennett JE, Catanzaro A, et al. An official American Thoracic Society Statement: Treatment of fungal infections in ADULT pulmonary and critical care patients. American Journal of Respiratory and Critical Care Medicine. 2011;183(1):96–128.
11. Collen JF, Jackson JL, Shorr AF, Moores LK. Prevention of venous thromboembolism in neurosurgery. Chest. 2008;134(2):237–49.
12. Khan NR, Patel PG, Sharpe JP, Lee SL, Sorenson J. Chemical venous thromboembolism prophylaxis in neurosurgical patients: An updated systematic review and meta-analysis. Journal of Neurosurgery. 2018;129(4):906–15.

Images: Case courtesy of Dr Ahmed Abdrabou, Radiopaedia.org, rID: 22779

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Ischemic Stroke

Kesikan Sabapathy Jayaraj, James Sanayei, Dr. Kieran Murphy

ID: Mrs. Jane Doe, 67-year-old female

Case presentation:

Mrs. Doe was found on her kitchen floor by her son at 8:00 AM this morning. He immediately called 911, and EMS arrived by 8:15 AM. They found that Mrs. Doe was conscious but unable to communicate. Her vital signs were within normal limits, though her pulse was irregular. Suspecting a possible stroke, EMS called ahead to the nearest stroke centre, and a “Code Stroke” was initiated. Mrs. Doe arrived at Toronto Western Hospital at 8:35 AM, and a team of neurologists was ready to evaluate her.

On arrival, Mrs. Doe displayed right-sided hemiparesis, facial droop, hemisensory impairment, and homonymous hemianopia, as well as global aphasia. Her gaze was deviated to the left. Her son noted that she had appeared normal when he last saw her the night before, at roughly 10:00 PM. Her NIH Stroke Score was > 20.

Differential diagnosis:

Some of the following conditions were considered: ischemic stroke, hemorrhagic stroke, seizure, head trauma, neoplasm, complex migraine, and AVM. An ECG study confirmed the presence of atrial fibrillation. Due to the clinical presentation, middle cerebral artery stroke (MCA) stroke resulting from a cardiac embolism was considered the most likely pathology. Urgent imaging studies were ordered to confirm the diagnosis and evaluate potential treatment options. Due to the acute presentation, CT imaging was selected over MRI.

Imaging:

CT head without contrast:

Brain parenchyma: No acute hemorrhage. No mass effect or herniation. Gray-white differentiation is maintained. Hyperdense MCA sign in M1 segment of left MCA.

Ventricles/extra-axial spaces: No hydrocephalus or extra-axial fluid collections. Normal bones and soft tissues. Visualized paranasal sinuses and mastoids are clear.

Other: Visualized lung apices are clear. No neck mass or suspicious lymph nodes. Bones demonstrate no significant abnormality.

Figure 1: Axial head CT image without contrast showing hyperdense MCA sign.

CTA Head:

Complete occlusion of the M1 segment of the left MCA. No aneurysm.

Figure 2: Coronal CT angiography image of the cerebral arteries showing a complete occlusion of the left MCA.

CTA Neck:

Great vessels: Visualized segments are patent.

Internal carotid arteries: Mild stenosis (<50%) bilaterally by NASCET criteria at the carotid bifurcation. Not hemodynamically significant. No dissection.

Vertebral arteries: Patent extracranial segments. No dissection.

CT Perfusion:

Total hypoperfusion: Using the threshold of Tmax >6 seconds, there is an area of hypoperfusion in the left MCA territory with a total volume of 92 ml.

Infarct core: Using the threshold of CBF <30%, there is an infarct core in the left MCA territory with a total volume of 21 ml.

Penumbra: The penumbra volume is 71 ml. The mismatch ratio is 4.38.

Figure 3: CT perfusion map showing areas of hypoperfusion in the left MCA territory as defined by different Tmax thresholds.

Impression:

Complete occlusion of the M1 segment of the left MCA. Infarct present in left MCA territory with significant tissue at risk (infarct core volume of 21 ml, penumbra volume of 71 ml).

Treatment:

Because of the significant time since Mrs. Doe was last seen normal, tPA was not administered. Mrs. Doe was taken to the angiography suite and underwent endovascular thrombectomy, which was successful.

Figure 4: AP cerebral angiography images showing (A) a complete blockage of the left MCA (arrow) and (B) restoration of blood flow following endovascular thrombectomy.

Outcome and follow up:

Repeat CT scan 48 hours later showed no signs of mass effect, hemorrhagic transformation, or hydrocephalus. Mrs. Doe was started on ASA (162 mg OD), then switched to dabigatran (150 mg BID) after two weeks. She was also referred to a cardiologist for ongoing assessment and treatment of her atrial fibrillation.

Follow-up Questions:

• If an acute stroke is suspected, which imaging protocol is used to identify if the patient is a candidate for IV thrombolytic therapy or endovascular thrombectomy (EVT)?
  1. CT head without contrast + CT angiography (CTA) of the neck arteries and the circle of Willis + CT perfusion scan (CTP)
  2. MRI head without contrast + MR angiography (MRA) of the neck arteries and the circle of Willis
  3. CT head with contrast and skull X-ray
  4. Carotid angiography

Answer: 1

Explanation: If an acute stroke is suspected, a rapid and informative imaging examination is required to determine whether a patient is a candidate for therapy.[1] While MRI is considered the gold standard for stroke diagnosis, CT scans can be performed more quickly than MRI scans, making them more useful in an emergency setting.[1,2] Answer A shows the standard CT protocol used in most regional stroke centres that accept “code strokes”. CT head without contrast helps to rule out hemorrhages, established infarcts, and pathologies that may mimic stroke.[1,2] CTA is used to confirm arterial occlusion, supporting the diagnosis of ischemic stroke and localizing the occlusion to evaluate the use of EVT.[2] 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.[2] 

• Which of the following is NOT a role of CT head without contrast in acute stroke?
  1. To rule out an established infarct
  2. To rule out an acute hemorrhage
  3. To rule out other mimicking pathologies that may present like a stroke
  4. To confirm an arterial occlusion

Answer: 4

Explanation: A noncontrast head CT is used to rule out an established infarct or intracerebral hemorrhage that would contraindicate interventions such as IV tPA.[2] It can also help rule out lesions that might mimic acute ischemic stroke, such as tumors.[3] Thus, only answer D is not a role of CT head without contrast in the assessment of suspected acute stroke. Although the presence of hyperdense artery sign on CT is highly specific for an occlusion, it is not very sensitive, as many occlusive thrombi are not large or dense enough to be detected.[4] One of the most accurate means of localizing an occlusive thrombus is computed tomography angiography (CTA), which is why this modality is typically included in a stroke workup. In addition to locating the occlusion, CTA can also be used to measure clot length, grade collateral blood flow, and detect arterial dissection.[4] 

• If an MRI scan was performed on a patient who suffered a stroke 1 week ago, which of the following findings might be seen?
  1. DWI – high intensity, T2 FLAIR – low intensity
  2. DWI – low intensity, T2 FLAIR – high intensity
  3. DWI – normal, T2 FLAIR – normal
  4. DWI – high intensity, T2 FLAIR – high intensity

Answer: 4

Explanation: In ischemic stroke, DWI sequences will show high signal intensity almost immediately, which usually persists for 10-14 days. After that point, the DWI signal may be variable.[5] FLAIR sequences will show high signal intensity starting from the late hyperacute stage (6-24 hours). The signal intensity usually remains high until the chronic stage (>3 weeks).[5]

• In a patient with homonymous hemianopsia, we might expect a CTA scan to show an occlusion of which of the following arteries:
  1. Contralateral ACA
  2. Contralateral PCA
  3. Ipsilateral MCA
  4. Ipsilateral basilar artery

Answer: 2

Explanation: Homonymous hemianopsia (HH) is a visual defect characterized by the loss of the same side of the visual field in both eyes.[6] It is common following a stroke, with as many as 10% of stroke patients suffering from permanent HH.[6] It results from damage to the retrochiasmal visual tract (occipital lobe or optic radiations) on the side contralateral to the visual field loss.[6,7] Therefore, in patients with HH, ischemic stroke of the contralateral MCA or PCA should be suspected.  

• Malignant MCA infarction is a term used to describe a significant infarction of the MCA causing space occupying cerebral edema and rapid neurological deterioration. Which of the following agents would be most helpful in treating this condition?
  1. Dexamethasone
  2. 9% saline
  3. Mannitol
  4. Fosphenytoin

Answer: 3

Explanation: Osmotic therapy is rapid and effective medical intervention for lowering intracranial pressure (ICP). Osmotic agents, such as mannitol or hypertonic saline, work primarily by drawing water out of the brain parenchyma and into the intravascular compartment, decreasing brain volume and ICP.[8] Mannitol also acts as a diuretic: by increasing the osmotic pressure of glomerular filtrate, it decreases reabsorption of water and electrolytes and increases urinary output.[8] Finally, it is thought to also reduce ICP by decreasing blood viscosity, which leads to a transient increase in cerebral blood flow. This increase in blood flow causes vasoconstriction, leading to reduced ICP.[8]

References

[1]         Fox AJ, Symons SP, Howard P, Yeung R, Aviv RI. Acute stroke imaging: CT with CT angiography and CT perfusion before management decisions. Am J Neuroradiol 2012;33:792–4. https://doi.org/10.3174/ajnr.A3099.

[2]         Lin MP, Liebeskind DS. Imaging of Ischemic Stroke. Contin (Minneap Minn) 2016;22:1399–423. https://doi.org/10.1212/CON.0000000000000376.

[3]         Birenbaum D, Bancroft LW, Felsberg GJ. Imaging in acute stroke. West J Emerg Med 2011;12:67–76. https://doi.org/10.1093/med/9780199582808.003.008.

[4]         Gasparian GG, Sanossian N, Shiroishi MS, Liebeskind DS. Imaging of occlusive thrombi in acute ischemic stroke. Int J Stroke 2015;10:298–305. https://doi.org/10.1111/ijs.12435.

[5]         Allen LM, Hasso AN, Handwerker J, Farid H. Sequence-specific MR imaging findings that are useful in dating ischemic stroke. Radiographics 2012;32:1285–97. https://doi.org/10.1148/rg.325115760.

[6]         Goodwin D. Homonymous hemianopia: Challenges and solutions. Clin Ophthalmol 2014;8:1919–27. https://doi.org/10.2147/OPTH.S59452.

[7]         Zhang X, Kedar S, Lynn MJ, Newman NJ, Biousse V. Homonymous hemianopia in stroke. J Neuro-Ophthalmology 2006;26:180–3. https://doi.org/10.1097/01.wno.0000235587.41040.39.

[8]         Hinson HE, Stein D, Sheth KN. Hypertonic saline and mannitol therapy in critical care neurology. J Intensive Care Med 2013;28:3–11. https://doi.org/10.1177/0885066611400688.

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Osteomyelitis

Kalter Hali, Brian Tsang, Dr. Angela Atinga

Introduction

A.B. is a 58-year-old male with type II diabetes presenting to the ER with swelling and pain in his right middle finger. The pain and swelling started ten days earlier, caused by an accidental injury to his right middle finger while pruning the garden. He immediately went to the ER, and the emergency doctor at that time ordered an X-ray (see X-ray at initial visit) and determined no bone fracture. His wound was cleaned and bandaged. Tetanus prophylaxis was given, and he was instructed to take Tylenol as needed for pain. Currently, A.B. tells you that his pain has been worsening over the past ten days and that he is concerned because “it's not getting any better”. You observe that his finger is visibly swollen and red. You determined that the swollen finger is warm, tender and has a significantly reduced range of motion. At this point, you decide to take his vitals and X-ray his hand.

Figure 1. X-rays at initial visit (10 days earlier)

Figure 2. X-rays at current visit

• How would you describe the X-ray images?

X-Rays at initial visit (10 days earlier)

• Slight soft tissue swelling of the right middle finger
• No fracture present

X-Rays at current visit

• Marked soft tissue swelling of right middle finger
• The distal interphalangeal joint (DIP) space of the right middle finger is narrowed and less distinct compared to adjacent DIP joints.
• Mixed lucency of the middle phalanx, cortical disruption and periosteal reaction

Review Questions

What is your working diagnosis and differential diagnosis?

• Osteomyelitis
• Septic arthritis
• Cellulitis
• Charcot joint
• Osteosarcoma
• Metastasis
• Arthritis

What additional diagnostic tests will you consider in this case?

• CBC to look for signs of infection
• Blood culture to look for any microorganisms
• MRI can be done if still unsure from the results of the x-rays and blood cultures
• Ultrasound to assess the surrounding soft tissues
• Bone biopsy

What are the option treatments for osteomyelitis?

• Surgical debridement of the area
• Targeted antibiotics

What is the most common bacteria that causes osteomyelitis?

• Staphylococcus aureus [1]

What are the four features of aggressive bone lesions?

• Cortical or bone destruction
• Periosteal reaction
• Poor zone of transition (i.e. poorly defined)
• Soft tissue mass.

Additional Images

Metastasis from squamous cell carcinoma

Lung cancer metastasis

Melanoma

Breast cancer metastasis

References

[1] Schmitt SK. Osteomyelitis. Infect Dis Clin North Am. 2017 Jun;31(2):325-338. doi: 10.1016/j.idc.2017.01.010.

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Rheumatoid Arthritis

Oliver Chow, Ananya Srivastava, Dr. Angela Atinga

A 45-year-old woman presents to the clinic with pain in her hands. She has been employed as a seamstress for over 20 years and is concerned about how this will affect her work. She says she had flu-like symptoms last month, around the same time that she noticed the pain. Since then, she has been feeling fatigued, and complains of a slight fever. She is perimenopausal and is not currently on any medications. Her blood pressure was 110/75, her temperature was 39.7°C, and her heart rate was 82bpm. You decide to take x-rays of her hands, as seen below.

=What is not a part of the differential diagnosis?

1. 1. Joint manifestation of psoriasis
   2. Gout
   3. CPPD (Calcium pyrophosphate dihydrate crystal deposition disease)
   4. Rheumatoid Arthritis

2. Which one of the following is the greatest risk factor for being diagnosed with rheumatoid arthritis?
   1. Family history of osteoarthritis
   2. Diagnosis of lupus
   3. Previous history of cancer
   4. Repeated use of hand joints at work

3. Which joints are most likely to be affected if this is a case of rheumatoid arthritis?
   1. Metacarpophalangeal joints and radiocarpal joints
   2. Metacarpophalangeal joints and proximal interphalangeal joints
   3. Metacarpophalangeal joints and distal interphalangeal joints
   4. Radiocarpal joints and distal interphalangeal joints

What would you do next?

1. 1. Secondary imaging studies
   2. Perform a joint biopsy
   3. Treat with methotrexate
   4. Watch and wait

Differentials:

PA and lateral radiographs of left and right hands presenting with rheumatoid arthritis

Rheumatoid Arthritis

Classic signs:

• Symmetrical soft tissue swelling around affected joints that is fusiform
• Subluxations of damaged joints
• Marginal erosions, frequently on the radial side of metacarpophalangeal joints
• Joint space narrowing
• Spared DIPs

-------------------------------------

PA radiograph of left and right hands presenting with psoriatic arthritis

PA and oblique radiographs of right hand presenting with psoriatic arthritis

Psoriasis (Psoriatic arthritis)

Classic signs:

• Erosive change with bone proliferation in a predominantly distal distribution
• Classic “pencil-in-cup” deformity (but is not pathognomonic)
• Bone proliferation results in irregular, “fuzzy” appearance around the affected joint
• Joint space narrowing

-------------------------------------

PA and lateral radiographs of right hand presenting with calcium pyrophosphate dihydrate crystal deposition disease (CPPD)

PA and lateral radiographs of left hand presenting with calcium pyrophosphate dihydrate crystal deposition disease (CPPD)

CPPD (Calcium pyrophosphate dihydrate crystal deposition disease)

Classic signs:

• Tend to be symmetric in their distribution pattern and involve non-weight bearing joints
• Cartilage calcification seen as punctate and linear radiodensities in articular cartilage

-------------------------------------

Lateral and AP radiographs of left ankle presenting with gout

AP and oblique radiographs of left and right feet presenting gout

Gout

Classic signs:

• Lumpy and bumpy soft tissue swelling around affected joints
• Well-defined “punched-out” erosions with sclerotic margins (rat bite erosions) in a marginal and juxta-articular distribution
• Asymmetric distribution (most common at MTP joints
• Presence of tophi (monosodium urate crystal deposits) in surrounding soft tissues (this is pathognomonic)

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