Summary We report a rare case of posterior reversible encephalopathy syndrome (PRES), precipitated by ectopic Cushing’s syndrome, in a patient with a metastatic pancreatic neuroendocrine tumour. A 55-year-old female presented as a hypertensive emergency with seizures and severe biochemical disturbance, including alkalosis, hypokalaemia and hyperglycaemia. MRI showed vasogenic oedema in the parieto-occipital region, consistent with a diagnosis of PRES. She had a significantly raised serum cortisol (>6000 nmol/L) which did not suppress with dexamethasone. Plasma adrenocorticotropic hormone (ACTH) concentrations were neither suppressed nor raised but were consistently within the normal reference range. The unexpected finding of a normal ACTH may be explained by either tumour secretion of unmeasured ACTH-related peptides, immunoassay antibody interference or episodic ACTH secretion. PRES is usually reversible with prompt and appropriate treatment. Hypercortisolism associated PRES is rare and may be associated with a worse outcome. Learning points PRES secondary to ectopic Cushing’s syndrome is very rare. PRES in this context may indicate a worse prognosis. In ectopic Cushing’s syndrome, if the serum ACTH level is normal, consider testing for ACTH-related peptides or interfering antibodies. Further research is required to establish the best treatment approach and to improve patients’ outcomes.
NHS accident and emergency departments see 0.5 million patients presenting with a cardiac condition each year. The accurate assessment of chest pain and subsequent diagnosis or exclusion of myocardial infarction (MI) represent a significant challenge, with important consequences on patient outcome and healthcare resources. We conducted a cross-sectional analysis of patients admitted with cardiac chest pain to a busy district general hospital in London. The criteria used by physicians to admit patients for further cardiac investigations were measured against national guidance on chest pain assessment and diagnosis of MI. We found that poor adherence to guidance, unsuitable patient pathways and inappropriate diagnostic tools at the point of presentation led to unnecessary inpatient admissions to the hospital. Quality improvement methods were used with the aim to reduce avoidable admissions to hospital in patients presenting with chest pain. We describe a system to implement new high-sensitivity troponin testing into legacy chest pain pathways. This was achieved through local education of National Institute for Health and Care Excellence (NICE) guidance, the use of patient pro formas and the creation of two new chest pain pathway arms to enable physicians to streamline patients for appropriate inpatient or outpatient care. As a result of these changes, we reduced non-compliance with NICE guidance by 83% and achieved a 42% reduction in avoidable chest pain admissions. Overall, the improvements made by this project were sustained over 2 years and saved £21 000 per month in avoidable admissions.
Pancreatic neuroendocrine tumours can have varied and complex presentations. Whilst hormone hypersecretion often induces characteristic clinical syndromes, non-specific symptoms may arise due to localized tumour effects. Malignant invasion of local vasculature is an increasingly recognized complication of these neoplasms and can be associated with significant morbidity. Herein, we present the case of a 47-year-old male with a recurrence of a pancreatic neuroendocrine tumour who presented with unusual upper gastrointestinal bleeding. The tumour had recurred within the superior mesenteric vein, replacing the vessel and invading its branches. This resulted in porto-mesenteric hypertension and the formation of bleeding mesenteric varices. The patient subsequently developed progressive metabolic disturbances and was diagnosed with ectopic Cushing’s syndrome, despite his primary tumour having been non-functional. This case demonstrates not only a rare pattern of tumour recurrence but also the potential for pancreatic neuroendocrine tumours to de-differentiate and change from non-functional to hormone secreting, a phenomenon which may complicate diagnosis and management.
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