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Endocrine Emergencies M W Savage, P M Mah, a P Weetman, J Newell-Price

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Endocrine Emergencies M W Savage, P M Mah, a P Weetman, J Newell-Price 506 Postgrad Med J: first published as 10.1136/pgmj.2004.018853 on 8 September 2004. Downloaded from REVIEW Endocrine emergencies M W Savage, P M Mah, A P Weetman, J Newell-Price ............................................................................................................................... Postgrad Med J 2004;80:506–515. doi: 10.1136/pgmj.2003.013474 Diabetic and endocrine emergencies are traditionally Endocrinology: adrenal (acute adrenocortical insufficiency, phaeochromocytoma crisis); treated by the acute medical admitting team or accident hypercalcaemia; thyroid (myxoedema coma, and emergency department staff. Most will see diabetic thyroid storm); and pituitary (pituitary apo- emergencies on a regular basis, as they are common and plexy). both type 1 and type 2 disease are increasing in DIABETES prevalence. Diabetic emergencies are usually easily treated Diabetic ketoacidosis (DKA) and the patients discharged. However, it is vital not to This is a condition characterised by hyperglycae- become complacent as these disorders can lead to death. It mia, ketosis, and acidosis. Hyperglycaemia is a result of severe insulin deficiency, either absolute is particularly important to follow local guidance and to or relative, which impairs peripheral glucose involve the diabetes team both during and after each uptake and promotes fat breakdown; relative episode. Recently it has become clear that about 30% of glucagon excess promotes hepatic gluconeogen- esis. Ketosis is caused by a switch to fat patients admitted with acute coronary syndrome (including metabolism, leading to free fatty acid oxidation infarction) have either diabetes or ‘‘stress in the liver forming the ketone bodies acetoacetic hyperglycaemia’’; evidence suggests that these patients acid and 3-hydroxybutyric acid. The dissociation of the ketone bodies (weak acids) results in should be treated not only as a cardiac emergency but also acidosis. DKA may occur in patients with known as a diabetic one. Thus, every patient with acute coronary type 1 diabetes, or be the presenting complex syndrome or acute myocardial infarction needs diabetes to leading to the diagnosis. be excluded. The other endocrine emergencies are less Clinical features common, but in some ways more important simply because The clinical symptoms and signs are predictable of their rarity. A high level of suspicion is often required to from an understanding of the pathophysiology. Hyperglycaemia leads to thirst and polyuria with make a diagnosis, although some, such as myxoedema variable circulatory stress, ranging from normal coma, are usually obvious. Treatment must be started pulse rate and blood pressure through to severe before the diagnosis can be confirmed. Guidance on collapse. Other factors, such as sepsis, may also impact on the degree of shock. Ketosis leads http://pmj.bmj.com/ making the diagnosis and initiating treatment should be to a smell of acetone on the breath. Acidosis, made available on the local NHS intranet for non- with an increased anion gap, leads to compen- endocrinologists to access; and where possible expert satory respiratory alkalosis with tachypnoea. Precipitating causes increase the circulating advice made available by telephone. The basic levels of stress hormones such as epinephrine, management steps in the common diabetic and endocrine growth hormone and cortisol, and the resulting increase in insulin resistance reduces the effec- emergencies are outlined; this is not a complete list, but on September 25, 2021 by guest. Protected copyright. tiveness of any residual insulin production or rather an insight for those involved in non-selected injected insulin. Examples of precipitants are: emergency admissions. pneumonia; myocardial infarction; urinary tract ........................................................................... infections; influenza; surgical emergencies; etc. These conditions often present with their own complex of symptoms and signs. However, it iabetic emergencies are common while must not be forgotten that errors of insulin See end of article for non-diabetic endocrine emergencies are administration are often the cause, and indeed, authors’ affiliations Drarer and require a high index of suspicion patients’ manipulation of their insulin treatment ....................... for diagnosis and management especially when is not uncommon.1 Correspondence to: presenting to emergency departments. Treatment Dr Mark W Savage, of the latter must be started before diagnostic Diagnosis Diabetes Centre, North confirmation. There is limited evidence based Patients usually present with DKA in the context Manchester General assessment of management in the literature and Hospital, Delauneys Road, of a known diagnosis of type 1 diabetes. More Manchester M8 5RB, UK; here we outline management guidelines used in [email protected] clinical practice for the following conditions: Diabetes: diabetic ketoacidosis; hyperosmolar Abbreviations: ACTH, adrenocorticotrophic hormone; Submitted non-ketotic ‘‘coma’’ ‘‘HONK’’ (also known as DKA, diabetic ketoacidosis; ECG, electrocardiogram; 20 November 2003 HDU, high dependency unit; HONK, hyperosmolar Accepted hyperglycaemic hyperosmolar state); hypogly- non-ketotic coma; PAI, primary adrenal insufficiency; 21 February 2004 caemia; and hyperglycaemia in acute coronary PTH, parathyroid hormone; SAI, secondary adrenal ....................... syndromes/myocardial infarction. insufficiency www.postgradmedj.com Endocrine emergencies 507 Postgrad Med J: first published as 10.1136/pgmj.2004.018853 on 8 September 2004. Downloaded from hospitals). Intravenous fluids should start with 0.9% saline Box 1: Catches for the unwary in DKA solution unless there is clinical shock, in which case intravenous colloids should be considered. The saline infu- N Ketones may be apparently absent in urine during the sion should initially be relatively rapid, about 1 litre per hour early stages of DKA due to the ‘‘Ketostix’’ inability to for the first two hours, thereafter it can usually be slowed. detect 3-hydroxybutyric acid, which may initially be the Most physicians recommend erring on the side of slight main ketone body in the urine. If in doubt plasma under-replacement of the fluid deficit in the first 24 hours, ketones should be measured. The laboratory based particularly in the young adult or adolescent who is at greater tests usually only detect acetoacetone but with higher risk of cerebral oedema. It has, however, not been proven that sensitivity than urine testing. over-enthusiastic fluid replacement is responsible for the N occasional case of cerebral oedema, and risk factors for this If there is any suggestion that DKA is not the reason for include: high initial urea concentrations, low carbon dioxide the acidosis, serum salicylate and lactate should be pressure during artificial ventilation, and treatment with measured. bicarbonate.4 N Blood glucose may not be very high due to partial If the patient is confused, hypoxic or hypotensive, then treatment with insulin before admission, either by the management in the high dependency unit (HDU) is patient or primary care physician. mandatory. N Not everyone can smell acetone to the same degree, Blood glucose should be monitored hourly using capillary assess yours by comparison with colleagues’ ability to readings from an approved meter and ensuring the blood smell commercial acetone—for example, nail varnish sample is taken properly. When capillary glucose readings fall remover. to ,15 mmol/l normal saline infusions should be replaced N Pseudohyponatraemia may result from highly lipaemic with 5% dextrose. serum—if the serum sodium is low this should be checked with the laboratory. Bicarbonate Among diabetologists, it is now the majority view that N Serum potassium levels may be initially very high as intravenous bicarbonate should usually be avoided; some acidosis drives potassium into the extracellular com- even suggest that if blood gases are not measured the pH will partment and levels will fall (sometimes rapidly) as treatment continues and acidosis resolves. Box 2: Fluids and insulin in treatment of DKA and HONK rarely these days, at least in the developed world, they may be a newly presenting case. Diagnosis is confirmed by three Intravenous fluids: features. (1) There is a raised random blood glucose N Give 1 litre 0.9% saline solution during the first hour. concentration greater than 11.1 mmol/l. It is usually, but N If hypotension, give a plasma expander. not always, greater than 15 mmol/l and is generally below 44 mmol/l. (2) The presence of ketonaemia can be inferred by N Rate of fluids thereafter depends on age/fitness of the presence of large quantities of ketones in the urine patient, typically: checked with ‘‘Ketostix’’. It is important to note that significant ketonaemia leads to large amounts of ketones in – 1 litre in next 2 hours the urine, and a ‘‘trace’’ on the stick is not sufficient evidence – 1 litre in next 4 hours http://pmj.bmj.com/ of ketonaemia. (3) The presence of acidosis is best confirmed – then 1 litre 6 hourly by estimation of venous bicarbonate; a level below 15 mmol/l confirms acidosis. N Reduce rate in elderly/cardiac disease/mild DKA Modern blood glucose meters are now able to measure 3- (bicarbonate .10). hydroxybutyric acid allowing earlier confirmation of keto- N More rapid infusion increases risk of respiratory naemia.2 The use of these meters, while not yet common, is distress syndrome. increasing. Venous bicarbonate can be measured
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