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      Society for Endocrinology endocrine emergency guidance

      editorial
      Endocrine Connections
      Bioscientifica Ltd

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          Abstract

          Endocrine emergencies are potentially life-threatening clinical problems and are compounded by a lack of recognition leading to delays in therapy. Every endocrinologist is aware of patients attending their out-patient clinic, with tales of suboptimal care in a non-endocrine clinical environment because of a failure to understand their chronic condition and its possible complications. This is particularly relevant in adrenal insufficiency and has led to potentially avoidable excess morbidity and mortality. To address this issue, the Clinical Committee of the Society for Endocrinology have launched a new initiative to introduce succinct and straightforward clinical guidance documents for use by the non-endocrinologist within an emergency setting. Five Emergency Guidance documents have been developed, often in conjunction with more comprehensive European, American or National guidelines. For the first time, all five are published together in this issue of Endocrine Connections. Each guidance document covers the most common endocrine-themed medical emergencies: Adrenal insufficiency (1): this is often under-recognised and, in particular, there is a lack of understanding of ‘sick day rules’ amongst non-endocrine health professionals. This document clearly outlines key points in the recognition and management of a new presentation of adrenal insufficiency as well as clarifying how to alter glucocorticoid therapy in the event of intercurrent illness of medical procedures. The lead author of this guideline is Professor Weibke Arlt who was also an author on the Endocrine Society Clinical Practice Guideline and the diagnosis and treatment of primary adrenal insufficiency published in 2016 (2). Severe symptomatic hyponatraemia (3): this has been principally authored by Professor Stephen Ball who was also an author of the Clinical Practice guideline on hyponatraemia developed by the European Society for Endocrinology in 2014 (4). The particular strength of this guidance is that it emphasises the importance of assessing the severity of acute hyponatraemia and treating accordingly in the first instance. Evaluation of volume status and confirming the exact cause of hyponatraemia, whilst important, are often done poorly by non-specialist clinicians and delay the appropriate treatment of this common and potentially life-threatening condition. Acute hypocalcaemia (5) and hypercalcaemia (6): disorders of calcium regulation are the second most common electrolyte disorder requiring endocrine input. In these documents, Professor Jeremy Turner, Dr Jennifer Walsh and colleagues provide a concise summary of the key causes of hypocalcaemia and hypercalcaemia and their immediate management based upon biochemical severity and underlying cause: in the case of hypercalcaemia, the first step is rehydration with normal saline, and intravenous zoledronic acid is now the bisphosphonate of choice. Pituitary apoplexy (7): in this condition, recognition and prompt treatment with intravenous hydrocortisone may be life-saving and prevent long-term visual complications. In this guidance, Dr Stephanie Baldeweg and colleagues emphasise that this condition must be considered in patients with acute severe headache, visual defects and/or impairment of consciousness. Authors of this Emergency Guidance were also authors on the Society for Endocrinology’s UK Guidelines for the management of pituitary apoplexy, published in 2011 and reviewed with no necessary changes in 2014 (8). Each guidance document has been principally written by authors with extensive experience and expertise in the relevant condition with consideration of the most up to date evidence available and has been peer-reviewed by the Society for Endocrinology Clinical Committee. The Society wishes to distribute these important documents as widely as possible to a non-endocrine audience, most notably Emergency Departments and acute general medical and surgical wards. Publication of all documents in Endocrine Connections and subsequent availability on the Society for Endocrinology website will allow endocrinologists to provide a single point of reference to non-specialist colleagues to guide the management of these extremely common and important conditions. Declaration of interest The author declares that there is no conflict of interest that could be perceived as prejudicing the impartiality of this editorial. Funding This work did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit sector.

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          UK guidelines for the management of pituitary apoplexy.

          Classical pituitary apoplexy is a medical emergency and rapid replacement with hydrocortisone maybe life saving. It is a clinical syndrome characterized by the sudden onset of headache, vomiting, visual impairment and decreased consciousness caused by haemorrhage and/or infarction of the pituitary gland. It is associated with the sudden onset of headache accompanied or not by neurological symptoms involving the second, third, fourth and sixth cranial nerves. If diagnosed patients should be referred to a multidisciplinary team comprising, amongst others, a neurosurgeon and an endocrinologist. Apart from patients with worsening neurological symptoms in whom surgery is indicated, it is unclear currently for the majority of patients whether conservative or surgical management carries the best outcome. Post apoplexy, there needs to be careful monitoring for recurrence of tumour growth. It is suggested that further trials be carried out into the management of pituitary apoplexy to optimize treatment. © 2010 Blackwell Publishing Ltd.
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            SOCIETY FOR ENDOCRINOLOGY ENDOCRINE EMERGENCY GUIDANCE: Emergency management of acute hypercalcaemia in adult patients

            Introduction Under physiological conditions, serum calcium concentration is tightly regulated. Abnormalities of parathyroid function, bone resorption, renal calcium reabsorption or dihydroxylation of vitamin D may cause regulatory mechanisms to fail and serum calcium to rise. Serum calcium is bound to albumin, and measurements should be adjusted for serum albumin. This guideline aims to take the non-specialist through the initial phase of assessment and management. Severity of hypercalcaemia 3.5 mmol/L: requires urgent correction due to the risk of dysrhythmia and coma Clinical features of hypercalcaemia Polyuria and thirst Anorexia, nausea and constipation Mood disturbance, cognitive dysfunction, confusion and coma Renal impairment Shortened QT interval and dysrhythmias Nephrolithiasis, nephrocalcinosis Pancreatitis Peptic ulceration Hypertension, cardiomyopathy Muscle weakness Band keratopathy Causes Ninety percent of hypercalcaemia is due to primary hyperparathyroidism or malignancy Less common causes include Thiazide diuretics Familial hypocalciuric hypercalcaemia Non-malignant granulomatous disease Thyrotoxicosis Tertiary hyperparathyroidism Hypervitaminosis D Rhabdomyolysis Lithium Immobilisation Adrenal insufficiency Milk-alkali syndrome Hypervitaminosis A Theophylline toxicity Phaeochromocytoma Investigation History Symptoms of hypercalcaemia and duration Symptoms of underlying causes, e.g. weight loss, night sweats, cough Family history Drugs including supplements and over-the-counter preparations Examination Assess for cognitive impairment Fluid balance status For underlying causes, including neck, respiratory, abdomen, breasts, lymph nodes ECG Look for shortened QT interval or other conduction abnormalities Bloods Calcium adjusted for albumin Phosphate PTH Urea and electrolytes High calcium and high PTH = primary or tertiary hyperparathyroidism* High calcium and low PTH = malignancy or other less common causes (*Familial hypocalciuric hypercalcaemia may be misdiagnosed as primary hyperparathyroidism due to hypercalcaemia with inappropriately normal or raised PTH. However, the hypercalcaemia is not usually severe and it is less likely to present as an emergency) Management Rehydration Intravenous 0.9% saline 4–6 L in 24 h Monitor for fluid overload if renal impairment or elderly Loop diuretics rarely used and only if fluid overload develops; not effective for reducing serum calcium May need to consider dialysis if severe renal failure If further treatment required after intravenous saline, consider intravenous bisphosphonates Zoledronic acid 4 mg over 15 min OR Pamidronate 30–90 mg (depending on severity of hypercalcaemia) at 20 mg/h OR Ibandronic acid 2–4 mg Give more slowly and consider dose reduction in renal impairment Monitor serum calcium response: will reach nadir at 2–4 days Can cause hypocalcaemia if vitamin D deficiency or suppressed PTH Second-line treatments Glucocorticoids (inhibit 1,25OHD production) In lymphoma, other granulomatous diseases or 25OHD poisoning Prednisolone 40 mg daily Usually effective in 2–4 days Calcimimetics, denosumab, calcitonin Under specialist supervision Can be considered if poor response to other measures Parathyroidectomy Can be considered in acute presentation of primary hyperparathyroidism if severe hypercalcaemia and poor response to other measures
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              SOCIETY FOR ENDOCRINOLOGY ENDOCRINE EMERGENCY GUIDANCE: Emergency management of acute hypocalcaemia in adult patients

              Introduction Acute hypocalcaemia can be life threatening, necessitating urgent treatment. In severe cases, intravenous calcium forms the mainstay of initial therapy, but it is essential to ascertain the underlying cause and commence specific therapy as early as possible. This guideline aims to take the non-specialist through the initial phase of assessment and management. Clinical presentation Symptoms of hypocalcaemia typically develop when adjusted serum calcium levels fall below ~1.9 mmol/L. However, this threshold varies greatly and is dependent on the rate of fall. Symptoms and signs of hypocalcaemia include: Peri-oral and digital paraesthesiae Positive Trousseau’s and Chvostek’s signs Tetany and carpopedal spasm Laryngospasm ECG changes (prolonged QT interval) and arrhythmia Seizure Potential causes The most common cause of acute symptomatic hypocalcaemia in hospital practice is disruption of parathyroid gland function due to total thyroidectomy. Hypocalcaemia may be temporary or permanent. Other causes include: Following selective parathyroidectomy (hypocalcaemia is usually transient and mild) Severe vitamin D deficiency Mg2+ deficiency (consider PPI-associated hypo­magnesaemia) Cytotoxic drug-induced hypocalcaemia Pancreatitis, rhabdomyolysis and large volume blood transfusions Investigations Serum calcium (adjusted for albumin) Phosphate Parathyroid hormone (PTH) Urea and electrolytes Vitamin D Magnesium Management ‘Mild’ hypocalcaemia ‘Mild’ hypocalcaemia: asymptomatic; serum calcium >1.9 mmol/L. Commence oral calcium supplements such as Sandocal 1000, 2 tablets BD (Alternatives include Adcal 3 tablets BD, Cacit 4 tablets BD, or Calcichew Forte 2 tablets BD). If post-thyroidectomy and patient asymptomatic, repeat calcium 24 h later: When adjusted calcium is >2.1 mmol/L, patient may be discharged and recheck calcium within 1 week. If serum calcium remains between 1.9 and 2.1 mmol/L increase Sandocal 1000 to three BD If patient remains in mild hypocalcaemic range beyond 72 h post-operatively despite calcium supple­mentation, start alfacalcidol 0.25 micrograms/day (calcitriol may also be used) with close monitoring (see ‘Long-term follow-up’ below) If vitamin D deficiency is the cause, commence vitamin D supplementation: load with ~300,000 units of cole- or ergocalciferol over ~6–10 weeks If hypomagnesaemia-related, stop any precipitating drug and administer i.v. Mg2+, 24 mmol/24 h, made up as 6 g of MgSO4 (30 mL of 20%, 800 mmol/L, MgSO4) in 500 mL Normal saline or 5% dextrose. Monitor serum Mg2+ and aim to achieve normal serum magnesium level If other cause of hypocalcaemia, treat underlying condition. Severe hypocalcaemia Severe hypocalcaemia: serum calcium <1.9 mmol/L and/or symptomatic at any level below reference range. This is a medical emergency Administer i.v. calcium gluconate Initially, give 10–20 mL 10% calcium gluconate in 50–100 mL of 5% dextrose i.v. over 10 min with ECG monitoring. This can be repeated until the patient is asymptomatic. It should be followed up with a calcium gluconate infusion as follows: Dilute 100 mL of 10% calcium gluconate (10 vials) in 1 L of Normal saline or 5% dextrose and infuse at 50–100 mL/h. (Calcium chloride can be used as an alternative to calcium gluconate, but it is more irritant to veins and should only be given via a central line) Titrate the rate of infusion to achieve normocalcaemia and continue until treatment of the underlying cause has taken effect Treat the underlying cause; in post-operative hypo­calcaemia and other cases of hypoparathyroidism, this consists of alfacalcidol or calcitriol therapy. Starting doses should be approximately 0.25–0.5 micrograms per day 1-alpha hydroxylated vitamin D metabolites are potent causes of hypercalcaemia. Frequent blood tests are required in stabilisation phase of treatment alfacalcidol can be administered (at equivalent doses) intravenously if there are concerns about absorbtion or difficulties with oral drug administration NB: Large volume calcium infusions should not be used in patients with end stage renal failure or who are on dialysis. Guidance on management of hypocalcaemia in these patients is available in the NKF KDOQI guidelines (http://www2.kidney.org/professionals/KDOQI/guidelines_bone/Guide14.htm) Vitamin D deficiency or hypomagnesaemia should be treated as described above Hazards of i.v. calcium administration Uncommon, but include local thrombophlebitis, cardiotoxicity, hypotension, calcium taste, flushing, nausea, vomiting and sweating. Patients with cardiac arrhythmias or on digoxin therapy need continuous ECG monitoring during i.v. calcium replacement. Long-term follow-up For patients commenced on alfacalcidol or calcitriol, monitoring of adjusted serum calcium levels should initially be performed approximately one week post discharge, then if satisfactory at one, three and then six months. Follow-up by a specialist with an interest in calcium disorders is recommended.

                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                September 2016
                4 October 2016
                : 5
                : 5
                : E1-E2
                Affiliations
                [1]Queen Elizabeth University Hospital Glasgow, UK
                Author notes
                Correspondence should be addressed to M Freel; Email: Marie.Freel@ 123456glasgow.ac.uk
                Article
                EC160068
                10.1530/EC-16-0068
                5314804
                27935812
                4bb14c40-fc8f-4bfb-8f9b-d06a8984f22d
                © 2016 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License .

                History
                : 26 August 2016
                : 26 August 2016
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                Editorial

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