BACKGROUND:Orbital myositis is an idiopathic, inflammatory, non-infectious condition, typically confined to more than one extraocular muscle and usually targeting young females in their third decade.CASE REPORT:We describe a case of orbital myositis uncommonly afflicting an adult male. He initially presented with a sensation of dizziness when turning his head and mobilising, together with right-sided orbital pain that failed to respond to the vestibular sedative cinnarizine. Failure to resolve and development of diplopia initially prompted a working diagnosis of ocular myasthenia gravis. On further investigation using HESS charting, paresis in the inferior and medial rectus and superior oblique ocular muscles of the right eye were elicited correlating with clinical examination. However, the lack of response to low dose steroids and acetylcholinesterase inhibitors, together with a negative screen for myasthenia antibodies, precluded a diagnosis of ocular myaesthenia gravis from being made. Other investigations included a high creatinine kinase and lactate dehydrogenase which indicated pathology in the extraocular muscles themselves. An MRI scan showed normal extraocular muscle thickness while excluding other orbital pathology. Exclusion of a variety of other conditions subsequently led to a diagnosis of orbital myositis.CONCLUSION:Response to high dose steroids consolidated this diagnosis with a rapid response ascertained clinically by resolution of pseudo-vertigo and pain, as well as the ophthalmoplegia with follow-up on HESS charting. We aim to raise awareness of this rare condition that carries a good response to steroids.

This case report describes an elderly lady who was maintained on a high dose of loop diuretics following resolution of her acute pulmonary oedema, which in turn led to wasting of calcium and magnesium at the nephron level. Her hypomagnesaemia further contributed to the hypocalcaemia by rendering ineffective the normal parathyroid negative feedback physiological response. This state of low calcium increased the neuromuscular excitability leading to myoclonic epilepsy which was resistant to benzodiazepines. Such hypocalcaemic tetany in this case would only be adequately addressed once the magnesium levels are repleted, as this would allow the parathyroid mechanism to function effectively and redress the calcium level as a result.

BACKGROUND:This case report intends to highlight the importance of safeguarding renal function from rhabdomyolysis in neuroleptic malignant syndrome (NMS) by concomitant administration of parenteral fluids at a high rate together with high doses of parenteral loop diuretics (we utilised 6 mg bumetanide daily) and tailed over a few days, in order to preserve glomerular/renal medullary perfusion and nephron function.CASE REPORT:This case describes an elderly lady previously diagnosed with Lewy body dementia who had been started on low dose quetiapine a few days previously and presented with an acute 24 – 48 hour onset of fever, generalised stiffness, rapidly becoming uncommunicable and with high blood pressure. Haemoglobinuria was present prompting intravenous treatment with labetalol to address the BP, whereas rapid isotonic saline fluid infusions together with intravenous high dose bumetanide were instituted to safeguard the kidneys against damage due to nephron deposition, both from haemoglobinuria as well as possibly myoglobin from rhabdomyolysis. A working diagnosis of the neuroleptic malignant syndrome with secondary malignant hypertension was made, and the quetiapine withdrawn. Blood pressure was after that subsequently controlled on amlodipine, and the haemoglobinuria quickly settled within 24 hours, with large amounts of dilute urine being passed on account of the forced diuresis. The fact that renal function and creatinine kinase remained normal is testimony to how these expedient measures averted progression to both rhabdomyolysis and renal failure in this case, thereby ameliorating prognosis.CONCLUSION:The patient was kept on infused fluids with maintenance bumetanide alone, achieving a full clinical recovery within the following 3 days.