Emergency #41

38-year-old-male:
– Presented with cough
– Previous history of asthma
– The patient was noted to have elevated IgE levels and a mildly raised eosinophil count
– Expectorated sputum demonstrated fungal hyphae on microscopy

What do you see?

What do you see?

Allergic Bronchopulmonary Aspergillosis (ABPA)

Finger in glove sign can be seen.

Cardiac #4

Clinical Data: A 53-year-old patient with myocardial infarction (STEMI) and cardiac decompensation (Pulmonary-to-systemic flow ratio Qp:Qs of 3.9)

What is the most likely diagnosis?

What is the most diagnosis?

Post-myocardial infarction ventricular septal defect/rupture (VSD/VSR).

Explanation

Ventricular septal defect/rupture is a rare but life-threatening complication after myocardial infarction. Generally, patients with VSR present with a transmural infarction. The defect results in left-to-right shunting and right ventricular pressure and volume overload. The rupture site can expand abruptly, resulting in sudden hemodynamic collapse in previously stable patients. Surgical closure is the definitive treatment for post-infarction VSD; however, the optimal timing of surgery remains controversial. Percutaneous closure devices have also been applied with success.

References

– Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000;101:27-32.
– Menon V, Webb JG, Hillis LD, et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol 2000;36:1110-6.
– O’Gara PT, Kushner FG, Ascheim DD, Casey DE Jr, Chung MK, de Lemos JA, Ettinger SM, Fang JC, Fesmire FM, Franklin BA,
Granger CB, Krumholz HM, Linderbaum JA, Morrow DA, Newby LK, Ornato JP, Ou N, Radford MJ, Tamis-Holland JE, Tommaso CL, Tracy CM, Woo YJ, Zhao DX. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013 Jan 29;61(4):e78-e140. doi: 10.1016/j.jacc.2012.11.019. Epub 2012 Dec 17. PMID: 23256914.

Cardiac #2

Clinical Data: Young adult with chest pain.

What do you see?

What do you see?

Intra-arterial course of the right coronary artery (RCA). RCA arises from left coronary sinus (not depicted) and passes between aorta and pulmonary trunk.

List at least three other potentially life-threatening congenital coronary artery defects.

List at least three other potentially life-threatening congenital coronary artery defects.

-Anomalous aortic origin of coronary artery (AAOCA)
-Anomalous origin of the left coronary artery originating from the pulmonary artery (ALCAPA)
-Anomalous origin of the right coronary artery originating from the pulmonary artery (ARCAPA)
-Single coronary artery
-Hypoplastic right coronary artery
-Congenital coronary artery ostial stenosis or atresia
-Anomalous circumflex coronary artery arising from the right pulmonary artery (ACARPA)

Discussion:

Congenital coronary artery anomalies (CAAs) are often incidental findings. They can be classified as CAAs of origin, course, and of termination. Although they are rare and most of them are benign variants, some are associated with an increased risk of myocardial ischemia, so recognizing and reporting them is substantial.

References and further reading:

1. Gentile F, Castiglione V, De Caterina R. Coronary Artery Anomalies. Circulation. 2021 Sep 21;144(12):983-996. doi: 10.1161/CIRCULATIONAHA.121.055347. Epub 2021 Sep 20. PMID: 34543069.
2. Waterbury TM, Tarantini G, Vogel B, Mehran R, Gersh BJ, Gulati R. Non-atherosclerotic causes of acute coronary syndromes. Nat Rev Cardiol. 2020 Apr;17(4):229-241. doi: 10.1038/s41569-019-0273-3. Epub 2019 Oct 3. PMID: 31582839.

Cardiac #1

Clinical Data: Chest pain

Coronary CT angiography was performed.

Describe salient abnormalities.

Salient abnormalities:

9 mm aneurysm arising from left anterior descending (LAD) artery. Contrast blush within pulmonary trunk near abnormal, torturous LAD branch

What is the final diagnosis?

What is the final diagnosis?

Coronary artery-to-pulmonary artery fistula with left-to-right shunt. Left coronary artery aneurysm.

Discussion:

Coronary artery-to-pulmonary artery fistula (CPAF) is a type of coronary arteriovenous fistula (CAVF), where there is an abnormal connection (fistula) between a coronary artery and either pulmonary trunk or main pulmonary artery. This condition is associated with coronary artery aneurysms (CAA), pulmonary atresia, and ventricular septal defect (VSD). Patients are usually asymptomatic; the most common clinical manifestation is chest pain and dyspnea, especially on exertion.

References and further reading:

1. Hang K, Zhao G, Su W, Bao G, Zhao Q, Jiao Z, Tian Z, Zhang H, Nie L, Luo R, Li L, Huang M, Shi L, Li S. Coronary artery-to-pulmonary artery fistula in adults: evaluation with 320-row detector computed tomography coronary angiography. Ann Transl Med. 2021 Sep;9(18):1434. doi: 10.21037/atm-21-4404. PMID: 34733986; PMCID: PMC8506747.
2. Kim H, Beck KS, Choe YH, Jung JI. Coronary-to-Pulmonary Artery Fistula in Adults: Natural History and Management Strategies. Korean J Radiol. 2019 Nov;20(11):1491-1497. doi: 10.3348/kjr.2019.0331. PMID: 31606954; PMCID: PMC6791815.

Head and Neck #15

What do you see in the following images?

Click here to see the answer

Scalp haemangioma
Right parietal subcutaneous well-defined soft tissue oval lesion. It demonstrates low signal on T1W image, Intermediate signal on T2W image with prominent vascular flow voids, and avid enhancement on the post contrast image. No adjacent osseous or soft tissue abnormality. No intracranial extension.

More information

Infantile hemangiomas are benign vascular tumours, most of these tumours arise in the craniofacial region. Most of them are not present at birth but they increase in size during the first year of life, with a subsequent progressive involution during early childhood.

Differential diagnosis includes: epidermoid cyst, lymphatic malformation,  and sinus pericranii.

Abdominal #22

45-year-old female patient:

* Generally unwell with abdominal pain and palpable cervical lymph nodes

Clinical information:

– Newly diagnosed HIV infection with a very low CD4 count of 30 cells/uL
– Generally unwell
– Presents at the emergency department with abdominal pain and palpable cervical lymph nodes

What do you see?

Diagnosis:

Most likely pulmonary and extrapulmonary tuberculosis in an immunocompromised patient with miliary pulmonary lesions, tuberculous colitis and ileitis, and necrotic extrapulmonary adenopathy (cervical and abdominal adenitis)
Microbiological analysis of an excised abdominal node confirmed the presence of Mycobacterium tuberculosis

Treatment:

Ileocaecal resection, tuberculostatic medication, and HAART

Teaching points:

– Be aware of TB in immunocompromised patients
– Cervical nodes are the #1 site of extrapulmonary TB adenopathy and the most common cause of adenopathy worldwide
– Intestinal tuberculosis can mimic inflammatory bowel disease

Neuroradiology #36

Clinical Information

A young adult male presents with progressive limb numbness and gait disturbances. Medical history was unremarkable.
MRI brain was performed and showed no intracranial abnormalities.
The neurologist ordered an MRI scan of the cervical spinal cord.

Showing MRI images:

What do you see?

A long segment T2-hyperintense lesion in the posterior part of the cervical myelum, specifically in the dorsal columns (‘inverted V-sign’). There is no perilesional oedema, mass effect, or enhancement.

What is the differential diagnosis based on the MRI findings?

Subacute Combined Degeneration due to Vitamin B12 deficiency or inactivation
Intrathecal MTX-induced myelopathy
Vitamin E deficiency
Copper deficiency
Tabes dorsalis (neurosyphilis)
HIV vacuolar myelopathy

More information
The laboratory values of Vitamine B12 were normal, as well as Copper and Vitamin E values.
HIV and Syphilis screening were negative.

The patient finally confirmed recreational (ab)use of nitrous oxide.

What is the most likely diagnosis?

Subacute Combined Degeneration due to nitrous oxide-induced Vitamin B12 inactivation.

Subacute Combined Degeneration

SCD is a neurological complication of vitamin B12 deficiency or inactivation. Several drugs can inactivate vitamin B12 such as metformin and nitrous oxide. Abuse of nitrous oxide inactivates vitamin B12 by oxidizing Cobalt-ion. In case of nitrous oxide abuse, vitamin B12 serum levels can appear normal.
Clinical symptoms include loss of vibration and proprioception in hands and feet and sensory gait ataxia. In severe cases, muscle weakness especially in the distal extremities can be seen.
MRI shows bilateral T2 high signal in the dorsal columns (inverted V sign) which explain the sensory deficits (paraesthesia, propriocepsis, and fine touch). In severe or untreated cases, the lateral columns may be involved leading to motor deficits such as limb weakness, spasticity, and paraplegia. The lesions typically involve a long segment in the cervical and higher thoracic spinal cord and show no enhancement or cord expansion.
It is crucial to promptly identify this disease and treat the vitamin B12 deficiency and/or discontinue the inactivating drug to prevent serious complications.

Abdominal #21

86-year-old patient:

– With sudden collapse

Clinical information:

– Patient known with infrarenal aortic aneurysm
– Sudden collapse at home
– Transfer to the hospital with ambulance

Axial and coronal slices of an abdominal CT in 2019 show a tortuous abdominal aorta with aneurysmal dilatations and eccentric thrombus. There is a thrombosed saccular component at the level of the aortic bifurcation (arrow)

CT at presentation:

What is the diagnosis?

Diagnosis:

Ruptured aortic aneurysm
* known infrarenal aortic aneurysm
* massive retroperitoneal hematoma extending into the posterior pararenal and perirenal compartments
* active contrast extravasation
Point of weakness: saccular aneurysmal component

Teaching points:

This case did not show a classic sign of pending rupture; however, a clear point of weakness was retrospectively identified (the saccular aneurysmal component at the aortic bifurcation)
Radiological signs of pending rupture:
* !! High attenuating crescent (= acute haematoma within the mural thrombus or aneurysmal wall)
* Focal discontinuity of intimal calcification and ‘tangential calcium sign’
* ‘Draped aorta sign’, present when
* The posterior aortic wall is unidentifiable as a distinct line
* The posterior aorta follows the contour of the spine on one or both sides
Reference: CT signs of pending aortic aneurysm rupture, J.P. Heiken, radiologyassistant.nl
https://radiologyassistant.nl/abdomen/aorta/aneurysm-rupture

Abdominal #20

61-year-old female:
– With elevated ALT, AST, and bilirubin

What do you see?

What do you see?

Wall thickening and enhancement of the gallbladder wall
Mild common bile and intrahepatic duct dilatation
Filling defect within the distal common bile duct

Diagnosis:

Choledocholithiasis