Subcutaneous fat necrosis causing neonatal hypercalcaemia.

Hypercalcaemia in neonates is rare and often asymptomatic, but can have significant morbidity. If severe, it can cause symptoms including irritability, vomiting and seizures. We present the case of a baby girl, born at term after a traumatic delivery, who developed severe hypercalcaemia with nephrocalcinosis. She had several large areas of subcutaneous fat necrosis following delivery, with prolonged low-level elevation of C reactive protein. Subcutaneous fat necrosis of the newborn is a rare and underdiagnosed condition, often accompanied by high plasma calcium. Although self-limiting, it is important to recognise and treat this condition to minimise kidney damage, and to avoid unnecessary investigations or treatment with long courses of antibiotics. The infant recovered well, although a degree of nephrocalcinosis remains.

A not so simple analgesic.

Many of the common causes of a high anion gap metabolic acidosis, like salicylate toxicity or diabetic ketoacidosis, are well recognized and promptly treated. Pyroglutamic acidosis (or 5-oxoproline acidosis) is a less common cause and is likely substantially underdiagnosed for two reasons: firstly, urine or serum measurements of pyroglutamic acid are performed only in specialist laboratories, and secondly, because awareness of the condition is still low, despite widespread reports in the medical and biochemical literature. The condition is often precipitated by the chronic use of paracetamol. Paracetamol is increasingly being widely prescribed as an alternative to NSAIDs often in maximal doses, given its innocuous reputation, and we anticipate more similar presentations. We present a case of a young pregnant woman who developed a severe metabolic acidosis secondary to raised pyroglutamate. Her treatment necessitated an emergency Caesarean section, ventilation and haemodiafiltration, despite normal renal function. We provide a reminder of other risk factors associated with the diagnosis.

Deep corneal calcification associated with preservative-free eyedrops and persistent epithelial defects.

PURPOSE: To describe the formation of deep calcareous degeneration of the cornea associated with the use of preservative-free eyedrops in patients with a persistent epithelial defect and active ocular surface inflammation. METHODS: A case series of 6 patients with persistent epithelial defects (1 with diabetes, 3 with penetrating keratoplasty, and 2 with herpes zoster) treated with preservative-free medications was reviewed over 18 months. Each patient subsequently developed deep calcareous corneal degeneration. Data regarding underlying etiology, diagnosis, clinical findings, and medications used were recorded. Each medication used was analyzed for phosphate levels by using a Roche 917 analyzer. RESULTS: All 6 cases of calcareous degeneration of the cornea had persistent epithelial defects, treated with preservative-free medications (timolol, dexamethasone, and prednisolone), in the presence of active inflammation on the ocular surface. The mean levels of phosphate were 130, 42.9, and 22.9 mM in timolol, dexamethasone, and prednisolone, respectively. All 6 patients had some degree of corneal opacification and reduced visual acuity. CONCLUSIONS: A contributory factor in our case series seems to be the use of preservative-free medications in persistent epithelial defects. The preservative-free medications we measured had high levels of phosphate, which may not be common knowledge.

Commentary on the British Thoracic Society guidelines for the investigation of unilateral pleural effusion in adults.

The publication of guidelines for the investigation of unilateral pleural effusion in adults by the British Thoracic Society has focused attention on this subject which, although comprising only a small proportion of laboratory workload, is a fairly common clinical problem. We critically reviewed the guidance applicable to clinical biochemistry laboratories and found a number of deficiencies. In particular, the need for anaerobic sample collection for pH measurement and preservation of samples for glucose assay is not mentioned and health and safety issues related to the handling of potentially infected fluids are also not considered. There are discrepancies between recommendations in the text and in the accompanying diagnostic algorithm, which require clarification. Measurement of total protein is an essential first step in the analysis of pleural fluid and will usually distinguish transudates from exudates. Measurement of lactate dehydrogenase activity is only required when total protein results are equivocal. There are practical difficulties with measurement of fluid pH as recommended in the guidelines and there is little evidence that such measurements are valuable. Similarly, there is little evidence to support the recommendation for measurement of complement in suspected rheumatoid effusions, and the recommendation for amylase isoenzyme studies if acute pancreatitis is a possibility is not practical. The different nature of pleural fluid demands a good understanding of the handling of these samples, the limitations of the analytical methods and the subsequent result interpretation by laboratory staff. We propose a modified diagnostic algorithm reflecting our criticisms of the original. Dialogue between the laboratory and local clinicians, possibly with the production of local guidelines, informed by these recommendations, should help optimize diagnostic management of patients with pleural effusion.