Nontraumatic haemarthrosis secondary to anticoagulant therapy is a recognized clinical problem. The involved joints are usually large weight-bearing joints, particularly the knee. We describe a case of spontaneous haemarthrosis in a 53-year-old female patient, who had been started on anticoagulant drugs after a pulmonary embolism in the past (international normalized ratio on admission: 2.4). The patient presented with acute onset of severe shoulder pain with no history of trauma. Her shoulder showed radiological signs of anterior dislocation. Attempts to relocate her shoulder under intravenous sedation with midazolam were unsuccessful. The patient subsequently underwent aspiration of the shoulder joint and made full recovery after a course of physiotherapy. The case is unusual because it occurred in a previously healthy shoulder joint and because the bleeding caused the shoulder to appear clinically and radiologically anteriorly dislocated. No history of trauma was reported before presentation; the apparent dislocation was caused solely by spontaneous haemarthrosis. This case emphasizes that it is important to consider spontaneous haemarthrosis as a possible diagnosis in patients with no history of trauma, particularly in those on anticoagulant drugs, who present with what appears to be an anterior shoulder dislocation.

Thunderclap headache is frequently associated with serious intracranial vascular disorders and a usual reason for emergency department admissions. Association of thunderclap headaches with autoimmune disorders, such as steroid-responsive encephalopathy with autoimmune thyroiditis (SREAT), is highly unusual. Here, we report a patient who presented with high-intensity headache of abrupt onset. Cerebrospinal fluid (CSF) analysis revealed moderate lymphocytic pleocytosis without evidence of infectious, neoplastic, or metabolic causes. Brain magnetic resonance imaging showed no specific pathologies, and examinations for neuronal antibodies in serum and CSF were negative. The medical history revealed that seven years before, an episode of an aseptic meningoencephalitis with remarkable response to steroids was present. Finally, increased levels of serum anti-TPO antibodies were identified, and against the background of a previous steroid-responsive aseptic meningoencephalitis, diagnosis of SREAT was highly probable. Methylprednisolone therapy was initiated, and the patient recovered completely. In particular, because most SREAT patients respond very well to steroids, this case underlines the importance of taking SREAT into consideration during the assessment of a high-intensity headache of abrupt onset.