Background: Internal mammary artery pseudoaneurysms most commonly develop from thoracic penetrating trauma or procedures. However, other important etiologies should not be overlooked. Case Report: A 27-year-old female presented with antiphospholipid antibody syndrome, thrombotic microangiopathy, end-stage renal disease on hemodialysis, and epilepsy. On admission, the patient had pulseless electrical activity and hypertensive emergency. After the patient was successfully resuscitated, she developed status epilepticus. Laboratory workup on admission revealed a subtherapeutic international normalized ratio, elevated C-reactive protein and sedimentation rate, and acute anemia. Imaging showed a right-sided subdural hematoma with a midline shift and likely internal mammary artery pseudoaneurysm. Angiography demonstrated aneurysmal dilation, segmental narrowing, and a string of beads appearance. Because of our patient's demographics, string of beads appearance on diagnostic angiography, history of renal disease, and negative hepatitis serology, fibromuscular dysplasia was considered the etiology of the internal mammary artery pseudoaneurysm. The family opted for 2 burr holes and a subdural drain but declined further diagnostic and therapeutic interventions because of anoxic brain injury and poor prognosis. Conclusion:In this patient, the etiology of the internal mammary artery pseudoaneurysm was attributed to fibromuscular dysplasia. Although this patient's family chose comfort measures, treatment methods are available for internal mammary artery pseudoaneurysms.

Ignatzschineria spp. bacteremia associated with maggot infestation is extremely rare in humans. There are only a few cases worldwide ever reported in the literature. We described a clinical case with a male patient who presented with maggot manifestation at his lower extremity, was found with bacteremia, and subsequently identified as Ignatzschineria spp by 16S rRNA sequencing.

IgA nephropathy (IgAN) is commonly associated with psoriasis; however, psoriasis presenting with crescentic IgAN is uncommon. A 49-year-old man with erythrodermic psoriasis with arthritis and stage 2 chronic kidney disease presented to the emergency department with worsening peripheral oedema and difficulty breathing. The patient had been hospitalised previously for a psoriasis flare. He was found to have an acute kidney injury on chronic kidney disease and was diagnosed with crescentic IgA glomerulonephritis on his first hospitalisation. He was treated with corticosteroids and was discharged stable with a plan to start cyclophosphamide in the outpatient setting. On his current hospitalisation, cyclophosphamide was added to his corticosteroids. Crescentic IgAN is rare. Its management has been based largely on observational studies. Our case highlights the importance of starting combined corticosteroids and cyclophosphamide early in crescentic IgAN and that corticosteroid monotherapy is insufficient in controlling disease progression.

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We present a case of a 43-year-old man with a medical history of paroxysmal atrial fibrillation that presented with acute onset generalised vesiculobullous rash of 1-week duration. The rash was initially noticed on his groin and then spread to his hands, feet and mucosal surfaces. Laboratory tests were unremarkable, including an extensive infection aetiology work-up. Punch biopsies were obtained of a fresh lesion and were stained with H&E and sent for direct immunofluorescence. Light microscopy and immunofluorescence study demonstrated a subepidermal blister with predominant neutrophilic infiltrates and a linear band of IgA at the dermoepidermal junction, respectively. The patient was diagnosed with linear IgA bullous dermatosis and was subsequently treated with 0.5 mg/kg of prednisone daily following previous case reports. At 1-week follow-up as an outpatient, the bullae became crusted, and the rash was nearly completely regressed.