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      SOCIETY FOR ENDOCRINOLOGY CLINICAL GUIDANCE: Inpatient management of cranial diabetes insipidus

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          Abstract

          Cranial diabetes insipidus (CDI) is a treatable chronic condition that can potentially develop into a life-threatening medical emergency. CDI is due to the relative or absolute lack of the posterior pituitary hormone vasopressin (AVP), also known as anti-diuretic hormone. AVP deficiency results in uncontrolled diuresis. Complete deficiency can lead to polyuria exceeding 10 L/24 h. Given a functioning thirst mechanism and free access to water, patients with CDI can normally maintain adequate fluid balance through increased drinking. Desmopressin (DDAVP, a synthetic AVP analogue) reduces uncontrolled water excretion in CDI and is commonly used in treatment. Critically, loss of thirst perception (through primary pathology or reduced consciousness) or limited access to water (through non-availability, disability or inter-current illness) in a patient with CDI can lead to life-threatening dehydration. This position can be further exacerbated through the omission of DDAVP. Recent data have highlighted serious adverse events (including deaths) in patients with CDI. These adverse outcomes and deaths have occurred through a combination of lack of knowledge and treatment failures by health professionals. Here, with our guideline, we recommend treatment pathways for patients with known CDI admitted to hospital. Following these guidelines is essential for the safe management of patients with CDI.

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          Hormonal Replacement in Hypopituitarism in Adults: An Endocrine Society Clinical Practice Guideline.

          To formulate clinical practice guidelines for hormonal replacement in hypopituitarism in adults.
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            SOCIETY FOR ENDOCRINOLOGY ENDOCRINE EMERGENCY GUIDANCE: Emergency management of acute adrenal insufficiency (adrenal crisis) in adult patients

            Wiebke Arlt, (2016)
            Introduction Acute adrenal insufficiency, also termed adrenal crisis, is a life-threatening endocrine emergency brought about by a lack of production of the adrenal hormone cortisol, the major glucocorticoid. Identifying patients at risk and prompt management can save lives. This guideline aims to take the non-specialist through the initial phase of assessment and management. Underlying conditions Primary adrenal insufficiency is caused by loss of function of the adrenal gland itself, for example due to autoimmune-mediated destruction of adrenocortical tissue or surgical removal of the adrenal glands or due to inborn disruption of adrenal cortisol production in congenital adrenal hyperplasia. Secondary adrenal insufficiency is caused if the regulation of adrenal cortisol production by the pituitary is compromised, this can be the consequence of tumours in the hypothalamic–pituitary area. However, pituitary regulation of cortisol production is also switched off in patients who receive chronic exogenous glucocorticoid treatment with doses ≥5 mg prednisolone equivalent for more than 4 weeks. This may also be caused by long-lasting glucocorticoid injections into joints or chronic application of glucocorticoid cream or inhalers. In primary adrenal insufficiency cortisol deficiency is aggravated by a lack of adrenal aldosterone production, a hormone important for blood pressure and electrolyte regulation. This puts primary adrenal insufficiency patients at a somewhat higher risk of adrenal crisis. Clinical presentation Clinical signs and symptoms: Fatigue, lack of energy, weight loss Low blood pressure, postural dizziness and hypotension (≥20 mmHg drop in BP from supine to standing position), dizziness, collapse, in severe cases hypovolaemic shock Abdominal pain, tenderness and guarding, nausea, vomiting (in particular in primary adrenal insufficiency), history of weight loss Fever Confusion, somnolence, in severe cases delirium or coma Back and leg cramps/spasms are commonly reported and can be distracting if not recognised for what they are (electrolyte derangement in large muscles?) In primary adrenal insufficiency: generalised skin hyperpigmentation, in particular in areas exposed to mechanical shear stress (palmar creases, nipples, scars, inside of oral mucosa) In secondary adrenal insufficiency: alabaster-like, pale skin; dependent on underlying conditions also signs and symptoms of other pituitary axis deficiencies Lab findings: Hyponatraemia (in primary and secondary adrenal insufficiency) Hyperkalaemia (in primary adrenal insufficiency) Pre-renal failure (increased serum creatinine due to hypovolaemia) Normochromic anaemia, sometimes also lymphocytosis and eosinophilia Hypoglycaemia (primarily in affected children; can cause long-term neurological deficits, if not promptly treated) Investigations for suspected adrenal crisis in patients not already known to have adrenal failure Adrenal insufficiency should be ruled out in any acutely ill patient with signs or symptoms potentially suggestive of acute adrenal insufficiency Assess blood pressure and fluid balance status; if clinically feasible, measure blood pressure from supine to standing to check for postural drop Take drug history (glucocorticoids?) Bloods: Sodium, potassium, urea, creatinine Full blood counts TSH, fT4 (hyperthyroidism can trigger adrenal crisis; acute adrenal insufficiency can increase TSH due to loss of inhibitory control of TRH release, do not replace with thyroxine if TSH ≤ 10 mU/L) Paired serum cortisol and plasma ACTH Diagnostic measures should never delay prompt treatment of a suspected adrenal crisis! There are no adverse consequences of initiating life-saving hydrocortisone treatment and diagnosis can be safely and formally established once the patient has clinically recovered If the patient is haemodynamically stable, consider performing a short Synacthen test (serum cortisol at baseline and 30 min after i.v. injection of 250 micrograms ACTH1–24); however, if the patient is severely ill, confirmation of diagnosis can be safely left until after clinical recovery following implementation of emergency dose hydrocortisone treatment Serum/plasma aldosterone and plasma renin (aldo­sterone will be low and renin high in primary adrenal insufficiency; observe special sample collection and transport conditions; can be left to confirmation of diagnosis after clinical recovery) Management of adrenal crisis Hydrocortisone (immediate bolus injection of 100 mg hydrocortisone i.v. or i.m. followed by continuous intravenous infusion of 200 mg hydrocortisone per 24 h (alternatively 50 mg hydrocortisone per i.v. or i.m. Injection every 6 h) Rehydration with rapid intravenous infusion of 1000 mL of isotonic saline infusion within the first hour, followed by further intravenous rehydration as required (usually 4–6 L in 24 h; monitor for fluid overload in case of renal impairment and in elderly patients) Contact an endocrinologist for urgent review of the patient, advice on further tapering of hydrocortisone, investigation of the underlying cause of disease including diagnosis of primary vs secondary adrenal insufficiency Tapering of hydrocortisone can be started after clinical recovery guided by an endocrinologist. In patients with primary adrenal insufficiency, mineralocorticoid replacement needs to be initiated (starting dose 100 micrograms fludrocortisone once daily) as soon as the daily glucocorticoid dose is below 50 mg hydrocortisone/24 h Precipitating factors In more than half of patients with adrenal insufficiency the diagnosis of adrenal failure is only established after presentation with an acute adrenal crisis However, patients with established adrenal insufficiency and those receiving chronic exogenous supraphysiological glucocorticoid treatment (e.g. for asthma or autoimmune disease) are at permanent risk of adrenal crisis. Most frequent causes are: Chronic glucocorticoid intake is suddenly stopped Failure to observe Sick Day Rule 1: the need to double daily oral glucocorticoid dose during intercurrent illness with fever that requires bed rest and/or antibiotics Failure to observe Sick Day Rule 2: the need to administer glucocorticoids per i.v. or i.m. injection or iv infusion during prolonged vomiting or diarrhoea, during preparation for colonoscopy or in case of acute trauma or surgery requiring general anaesthesia After emergency care: how to prevent an adrenal crisis Regular review of the patient by an endocrinologist, initially monthly, in the long-term every 6–12 months Education of patients and partner/parents regarding symptom awareness and the correct adjustment of glucocorticoid replacement dose: Sick Day Rule 1: the need to double daily oral glucocorticoid dose during illness with fever that requires bed rest and/or antibiotics Ensure they have an additional supply of hydrocortisone tablets so that they can double their dose for at least 7 days Sick Day Rule 2: the need to administer glucocorticoids per i.v. or i.m. injection during prolonged vomiting or diarrhoea, during preparation for colonoscopy or in case of acute trauma or surgery Teach the patient and partner/parents how to self-administer and inject hydrocortisone and provide them with a Hydrocortisone Emergency Injection kit (100 mg hydrocortisone sodium succinate for injection; hyperlink to ADSHG and Pit foundation where there are picture tutorials on using this); check regularly that their kit is up to date Provide the patient with a Steroid Emergency Card www.endocrinology.org/adrenal-crisis and encourage them to wear medical alert bracelets, in addition to keeping the steroid emergency card with them at all times and showing it to any health care professional they are dealing with Provide them with emergency phone numbers and contact details for the patient self-help groups Further information For further information and to request a steroid card, please go to the Society for Endocrinology’s website www.endocrinology.org/adrenal-crisis.
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              SOCIETY FOR ENDOCRINOLOGY ENDOCRINE EMERGENCY GUIDANCE: Emergency management of severe symptomatic hyponatraemia in adult patients

              Introduction Hyponatraemia (serum sodium 130 mmol/L and alternative causes of neurological dysfunction should be considered in this context. Management decisions should be made on the basis of presenting clinical symptoms and signs rather than the degree of hyponatraemia (1, 2). Treatment of the patient presenting with severe or moderately severe symptomatic hyponatraemia See Fig. 1 for the recommended approach. Patients with severe symptoms require immediate treatment with hypertonic saline, irrespective of the cause of the hyponatraemia. Figure 1 Patients with hyponatraemia presenting with severe symptoms. Recommended approach to the use of hypertonic sodium chloride. The decision to treat with hypertonic fluid and the supervision of treatment with hypertonic fluid should the responsibility of a senior clinician with appropriate training and experience. The aim is to achieve a 5 mmol/L rise in serum Na+ within the first hour, reducing immediate danger from cerebral oedema while minimising the risk of over-rapid correction and osmotic demyelination. If the clinical status of the patient does not improve after a 5 mmol/L rise in serum Na+ in the first hour, we recommend taking additional steps as outlined in Fig. 2. Figure 2 Patients with hyponatraemia treated with hypertonic saline. Recommended approach if no improvement following 5 mmol/L rise in Na+ in the first hour. Managing over-correction of serum Na+ Over-correction of serum Na+ risks precipitating osmotic demyelination. The condition underlying the patient’s presentation with hyponatraemia may well change during the first 24 h with cause-specific intervention; the situation is dynamic. If the limit of 10 mmol/L in the first 24 h or 18 mmol/L in the first 48 h of treatment is exceeded, hypertonic fluid should be stopped. We recommend consulting a clinician with experience in managing over-correction who may wish to consider introducing hypotonic fluid, with or without concurrent anti-diuresis (3). Differential diagnosis of hyponatraemia following emergency treatment Measurement of urine osmolality and urine Na+ concentration are central to defining the aetiology of hyponatraemia. An algorithmic approach to establishing the cause of hyponatraemia, in-line with other recent guidance, is outlined in Fig. 3 (1, 4). Figure 3 Diagnostic algorithm for patients presenting with hyponatraemia. For use following emergency treatment.
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                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                July 2018
                08 May 2018
                : 7
                : 7
                : G8-G11
                Affiliations
                [1 ]Department of Diabetes and Endocrinology University College London NHS Foundation Trust and Univeristy College London, London, UK
                [2 ]Department of Medicine and Endocrinology Manchester University Foundation Trust & Manchester Academic Health Science Centre Manchester, Manchester, UK
                [3 ]Royal Devon and Exeter NHS Foundation Trust Exeter, UK
                [4 ]Department of Endocrinology Queen Elizabeth Hospital, Birmingham, UK
                [5 ]University of Leicester and University of Leicester Hospitals Trust Leicester, UK
                [6 ]Croydon Health Services NHS Trust Croydon, UK
                [7 ]Department of Endocrinology Oxford Centre for Diabetes, Endocrinology & Metabolism, Oxford, UK
                [8 ]The Society for Endocrinology Starling House, 1600 Bristol Parkway North, Bristol, UK
                Author notes
                Correspondence should be addressed to S E Baldeweg: stephanie.baldeweg@ 123456nhs.net
                Article
                EC180154
                10.1530/EC-18-0154
                6013691
                29930026
                50f634a4-3403-48cd-ab74-a03a41fa4b44
                © 2018 Society for Endocrinology
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                Categories
                Guidelines and Guidance

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