Check for peripheral oedema \200\224 remember that in a bedbound patient this may collect in the sacral region. It is possible to have peripheral oedema with intravascular depletion (eg in hypoalbuminaemia) so this is not a reliable indicator of \202 uid state Check the JVP, which is elevated in cardiac failure and also in tricuspid regurgitation Investigations \200 Urine speci \201 c gravity may be high in dehydration, and also in h eart failure, and is less helpful when diuretics have been used Elevated U,C + E often indicate dehydration \200\224 check for the patient \200\231s basel ine if possible. CKD will also elevate urea and creatinine, but is likely to be chronic. Re member that frail older people will have a lower creatinine (perhaps even in the normal ran ge) because of low muscle bulk, but this may still represent a marked abnormality for them \200 Elevated Hb may occur in dehydration and in chronic hypoxia 406 CHAPTER 14 Homeostasis Dehydration: management \200 Treat the underlying cause(s) \200 Suspend diuretic and AC E inhibitors \200 Continually reassess clinically, assisted by urinalysis/U,C + E. Measur e and document intake, output, BP, and weight If mild: oral rehydration may suf \201 ce. A \200\230homemade \200\231 oral rehydration mixture can be made by adding a level teaspoon of salt and eight level teaspoons of sugar t o a liter of water with a touch of fruit juice. Old frail people need time, encouragement, and physical assistance with drinking. Enlist relatives and friends to help More severe dehydration, or mild dehydration not responding to conservative measures, will require other measures \200\224 usually parenteral treatment, either s/c (see b \200\230HOW TO Administer subcutaneous fluid \200\231, p.406) or i v The speed of parenteral \202 uid administration should be tailored to the individual pati ent, based on volume of \202 uid de \201 cit, degree of physiological compromise and per ceived risks of \202 uid overload. For example, a hypotensive patient who is clinically v olume depleted with evidence of end-organ failure should be \202 uid resuscitated briskly , even if there is a history of heart failure. In the absence of end-organ dysfunction, reh ydration may proceed more cautiously, but continual reassessment is essential, to con \201 rm that the clinical situation remains benign, and that progress (input > output) is being made HOW TO Administer subcutaneous \202 uid This method (hypodermoclysis) was widely used in the 1950s, but fell into disrepute followi ng reports of adverse effects associated with very hypo/hypertonic \202 uid. Fluids that are close to isotonic delivered by competent staff are a safe and effective substitute for iv therapy. \200 A simple, widely accessible method for parenteral \202 uid/electrolyte s \200 Fluid is administered via a standard giving set and \201 ne (21 \200\22323G) butter \202 y needle into s/c tissue, then draining centrally via lymphatics and veins S/c \202 uid administration should be considered when insertion or maintenance of iv acce ss presents problems, eg dif \201 cult venous access, persistent extravasation, or lack of staff skills Iv access is preferred if rapid \202 uid administration is needed (eg gastrointestinal bl eed), or if precise control of \202 uid volume is essential Sites of administration Preferred sites: abdomen, chest (avoid breast), thigh, and scapula. In agitated patients who can tear out iv (or s/c) lines, sites close to the scapulae may f oil their attempts. Continued DEHYDRATION: MANAGEMENT 407 Fluid type Any crystalloid solution that is approximately isotonic can be used, including n ormal (0.9 % ) saline, 5 % glucose and any isotonic combination of dextrose \200\223saline. Potassium chloride can be added to the infusion, in concentrations of 20 \200\22340mM/L. I f local irritation occurs, change site and/ or reduce the concentration of added potassium. Infusion rate Typical \202 ow (and absorption) rate: 1mL/min or 1.5L/day. Infusion pumps may be used. If \202 ow or absorption is slow (leading to lumpy, oedematous areas): \200 Change site \200 Use hyaluronidase (a \200\230digester \200\231 of connective tissue). Add 150 \200\223300 units to each liter \202 uid and/or pre-treat site with 150 units Use two separate infusion sites at the same time \200 Using these techniques, up to 3L of \202 uid daily may be given. For smaller volumes, consider an overnight \200\230top-up \200\231 of 500 \200\2231000mL, or two daily boluses of 500mL each (run in over 2 \200\2233 hr) leaving the patient free of infusion lines during the daily rehabilitation/activity. So me patients need only 1L/alternate nights to maintain hydration Monitoring Patients should be monitored clinically (hydration state, input/output, weight) and biochemically as they would if they were receiving iv \202 uid. 2 Be responsive and c reative in your prescriptions of \202 uid and electrolytes. One size does not \201 t al l. Potential complications Rare and usually mild. They include local infection, and local adve rse reactions to hypertonic \202 uid (eg with added potassium) or to hyaluronidase. Contraindications \200 Exercise caution in thrombocytopenia or coagulopathy \200 S/c in fusion is not appropriate in patients who need rapid volume repletion Further reading Barua P , Bhowmick BK . ( 2005 ). Hypodermoclysis \200\224 a victim of his torical prejudice . Age Ageing 34 : 215 \200\223 17 . 408 CHAPTER 14 Homeostasis Hyponatraemia: treatment See Box 14.1 and Fig. 14.1 . \200 Combine normalization of [Na] with correction of \202 uid volume and treating underlying cause(s). The rate of correction of hyponatraemia should not be too rapid. Usually, correction to the lower limit of the normal range (7130mM) should be achieved in a few days. Maximum correction in any 24hr period should be <10mM. Full correction can reaso nably take weeks. Rapid correction risks central pontine myelinolysis (leading to quadriparesis and cranial nerve abnormalities) and is indicated only when hyponatraemia is severe and the patient critically unwell. 2By de \201 nition, hyponatraemia is a low blood sodium concentration. Therefore a low lev el may be a result of low sodium, high water, or both. Dehydration and hyponatraemia may co exist if sodium depletion exceeds water depletion. This is common \200\224 don \200\231t w orsen the dehydration by \202 uid restricting these patients. Box 14.1 Drugs and hyponatraemia \200 Most commonly diuretics (especially in high dose or combination), SSRIs, carbamazepine, NSAIDs Other drugs include opiates, other antidepressants (MAOIs, TCAs), other anticonvulsants (eg valproate), oral hypoglycaemics (sulfonylureas eg, chlorpr opamide, glipizide), PPIs, ACE inhibitors, and barbiturates Combinations of drugs (eg diuretic and SSRI) are especially likely to cause hyponatraemia If hyponatraemia is problematic and the treatment is needed, consider other drugs that are less likely to cause a low sodium (eg mirtazapine for depression) Clinical assessment of volume status Hypervolaemic Oedema, especially sacral. Pulmonary oedema. Raised JVP. No hypotension Hypovolaemic Hypotension, tachycardia, decreased skin turgor, low JVP, dry tongue, minimal or no peripheral oedema Euvolaemic No oedema. No hypotension Water and salt overload \200 Signs of overload and an underlying cause are commonly Water overload without Na retention \200 Usually less obvious signs. May be difficult to find cause. Exclude hypothroidism, Addison \200\231s. Consider SIADH. Take careful drug his tory \200 Plasma osmolality usually low; maybe normal in pseudohyponatraemia eg hyperlipi daemia (TGs >50mM) or hyperproteinaemia (TP >150g/L), or if sample taken from drip arm Saline depletion (salt > water loss) \200 Either renal or extra-renal losses, distinguish ed by spot urine [Na] \200 Cause is often obvious \200 Plasma osmolality usually low, e xcept in hypertonic hyponatraemia (e.g. hyperglycaemia or hyperglycinaemia (following TURP) ) found: often renal, liver or heart failure Plasma osmolality low \200 Decrease in circulating volume results in ADH and angiotensin release Urinary [Na] > 20mM ie renal salt/water loss Urinary [Na] > 10mM ie non-renal salt/water loss Urinary Na >20mM. Usually chronic water overload Urinary Na >20mM. Usually acute water overload Urinary Na <10mM ie renal Na retention Urinary Na >20mM CCF \200 Cirrhosis \200 Nephrotic syndrome (rarely) Acute/chronic renal failure SIADH \200 Drugs (eg thiazide) \200 Chronic renal failure \200 Hypothyroidism \200 Isolated cortisol deficiency Stress \200 Postsurgery (excess ADH, iv fluids) \200 Polydipsia (usually in addition to renal impairment) \200 Fluid depletion and hypotonic replacement (commonly iatrogenic ) Vomiting \200 Diarrhea \200 Skin loss eg burns \200 \200\230Third space \200\231 eg pancreatitis, bowel obstruction, peritonitis \200 Rectal villous adenoma, or fistula Diuretics \200 Primary adrenal failure (Addison \200\231s) \200 Osmolar diuresis, eg: h yperglycaemia \200 Salt-losing nephropathy eg: partial urinary tract obstruction, diureti c stage of ATN H Y P O N A T R A E M A Treat underlying cause. Saline repletion \200\224usually iv normal saline. May need aggress ive volume resuscitation to avert shock and organ failure. Avoid colloids or glucose soluti ons (may worsen hypo [Na]). Rarely need hypertonic saline solutions (may correct [Na] too q uickly) Treat underlying cause. Discontinue relevant medications (or infusions). If mild, and the p recipitant has passed (eg surgery), may be left to self- correct. If more severe or symptom atic, restrict water intake to a maximum of 1000mL/day; more severe restriction may be need ed in older people, whose free water losses are lower \200\224restrict to 500 \200\223800mL if necessary Treat underlying cause. Restrict water intake to <1L/day. If incomplete response, consider diuretics (furosemide). Modest hyponatraemia is often asymptomatic. In heart failure and ne phrotic syndrome, ACE inhibition helps I : T R E A T M E N T Maximum rise in [Na] = 10m/day Maximum rise in [Na] = 10m/day Maximum rise in [Na] = 10m/day Fig. 14.1 Hyponatraemia: etiology and treatment. TURP, transurethral resection of prostrate ; TG, triglyceride; TP, turgor pressure. 4 0 9 410 CHAPTER 14 Homeostasis Syndrome of inappropriate antidiuretic hormone secretion (SIADH) De \201 nition Less than maximally dilute (ie inappropriately concentrated) urine in the presence of subclinical exc ess body water. 2SIADH is massively over-diagnosed, especially in older people, leading to inappropriate \202 uid restriction. Consider it a diagnosis of exclusion \200\224 drugs or organ impairment cause a similar clinical syndrome. Diagnosis Essential features include: \200 Hypotonic hyponatraemia ([Na]<125mM and plasma osmolarity <260mOsm/L) Normal volume status, ie euvolaemia \200\224 there is slight water overload, but not clinically identi \201 able Normal renal, thyroid, hepatic, cardiac, and adrenal function \200 Inappropriately concen trated, salty urine: osmolarity > 200mOsm/L and [Na] > 20mM) No diuretics, or ADH-modulating drugs (opiates, anticonvulsants, antidepressants, NSAIDs, b arbiturates, and oral hypoglycaemics). Drug effects may take days or weeks to diminish Causes Common causes include: \200 Surgical stress \200 Neoplasms (especially bronchoge nic, pancreatic) \200 CNS disease (especially trauma, subdural haematoma, stroke, meningoencephalitis) Lung disease (TB, pneumonia, bronchiectasis) \200 Some drugs cause low Na by an SIADH-lik e effect, but this is not the true syndrome Treatment \200 Treat underlying cause \200 If mild, and the precipitant has passed (eg surgery), may be left to self-correct If more severe and/or symptomatic, restrict water intake to a maximum of 1000mL/day; more severe restriction may be needed in older people, whose free wa ter losses are lower \200\224 restrict to 500 to 800mL if necessary Drug treatments are generally reserved for refractory cases, or where the \202 uid restri ction is not tolerated. Demeclocycline acts by blocking the renal tubular effect of ADH and is \201 rst line. Urea and vasopressin receptor antagonists can also be used SIADH 411 HOW TO Perform a short ACTH stimulation test (short Synacthen test) The diagnosis of adrenocortical insuf \201 ciency is made when the adrenal cortex is found not to synthe size cortisol despite adequate stimulation. Within 30min of ACTH stimulation, the normal ad renal releases several times its basal cortisol output. Performing the test \200 The test can be done at any time of day \200 Take blood for ba seline cortisol. Label tube with patient identi \201 ers and time taken Give 250micrograms Synacthen (synthetic ACTH, 1 \200\22324 amino acid sequence). Give intravenously if iv access is present; otherwise intramuscularly 30min after injection, take more blood for cortisol. Label tube with patient identi \201 ers and time taken Interpreting the test A normal response meets three criteria: \200 Baseline cortisol leve l > 150nmol/L \200 30min cortisol > 500nmol/L \200 30min cortisol greater than baseline cortisol by 200nmol/L or more The absolute 30min cortisol carries more signi \201 cance t han the baseline \200\22330min increment, especially in patients who are stressed (ill) an d at maximal adrenal output. A normal Synacthen test excludes Addison \200\231s disease. If the test is not normal: \200 Consider further tests, such as the prolonged ACTH stimulation test, usually after specialist advice, eg: \200 ACTH level (elevated in primary, and low in sec ondary hypoadrenalism) The prolonged ACTH stimulation test If the patient is very unwell, give hydrocortisone 100mg iv pending con \201 rmation of hypoadrenalism 412 CHAPTER 14 Homeostasis Hypernatraemia Causes \200 Usually due to true \200\230dehydration \200\231 ie water los s > sodium loss \200 Not enough water in, or too much water out, or a combination, eg poo r oral intake, diarrhea, vomiting, diuretics, uncontrolled diabetes mellitus Rarely due to salt excess \200\224 iatrogenic (iv or po), psychogenic or malicious (poisoning) Very rarely due to diabetes insipidus (urine osmolarity low) or mineralocorticoid excess (Conn \200\231s) Commonly seen in septic older people: increased losses (sweating), reduced oral intake and reduced renal concentrating (water-conserving) mechanism. Clinical features \200 Hypotension (supine and/or orthostatic) \200 Sunken features \200 Urine scanty and concentrated \200 Lethargy, confusion, coma, and \201 ts Tests Urea and creatinine are often high, but may be in the high normal range; the patient is still water-depleted. K is low in Conn \200\231s. Hemoglobin and albumin often high (hae moconcentration), correcting with treatment. Treatment \200 Encourage oral \202 uid \200 Usually iv \202 uid is required; rarely s/c \202 uid will be suf \201 cient \200 Fluid infusion rates should not be too cauti ous: eg 3 \200\2234L/24hr is reasonable, guided by clinical and biochemical response. Too rapid infusions risk cerebral oedema, especially in the more chronically hypernatraemic patient Ensure the patient becomes clinically euvolaemic as well as normo- natraemic: most dehydrat ed patients have a normal [Na], and will correct into the normal range before the patient i s fully hydrated \200 Many patients are Na-deplete as well as water-deplete; therefore consider alternating normal saline with 5 % glucose infusions 2Even mild hypernatraemia is usually clinically important, and needs attention. HYPONATRAEMIA: ASSESSMENT 413 Hyponatraemia: assessment A common problem. May safely be monitored rather than treated if modest in severity ([Na] > 125mM), stable and without side effects, and if there is an iden ti \201 able (often drug) cause. Clinical features \200 Subtle or absent in mild cases \200 Between [Na]=115 \200\223125 mM: lethargy, confusion, altered personality \200 At <115mM: delirium, coma, \201 ts, a nd death Causes Iatrogenic causes are most common. Acute onset, certain drugs, or recent iv \202 u ids make iatrogenesis especially likely. Important causes include: Drugs. Many are implicated (see Box 14.1 ) \200 Excess water administration \200\224 eit her NG (rarely oral) or iv (5 % glucose) Failure of heart, liver, thyroid, kidneys \200 Stress response, eg after trauma or surger y, exacerbated by iv colloid or 5 % glucose Hypoadrenalism: steroid withdrawal or Addison \200\231s disease \200 Syndrome of inapprop riate ADH secretion (SIADH) In older people, multiple causes are common, eg heart failure, diuretics, and acute diarrhea. Approach Take a careful drug history, including those stopped in the past few weeks. Examin e to determine evidence of cause and volume status (JVP, postural BP, pulmonary oedema, ank le/sacral oedema, peripheral perfusion). Investigations Clinical history and examination, urine, and blood biochemistry are usually all that are needed. Ensure that the sample wasn \200\231t delayed in transit or taken from a drip arm. If genuine hyponatraemia, take: \200 Blood for creatinine, osmolarity, TFTs, LFTs, glucose, random cortisol \200 Spot urine sample for sodium and osmolarity Consider a short adrenocorticotropic hormone (ACTH) test to exclude hypoadrenalism, particularly if the patient is volume-depleted and hyperkalaemic (see b \200\230HOW TO Perform a sh ort ACTH stimulation test (short Synacthen test) \200\231, p.411). 414 CHAPTER 14 Homeostasis Hypothermia: diagnosis A common medical emergency in older people, occurring both in and ou t of hospital. De \201 nition \200 Core temperature <35 C, but <35.5 C is probably abnormal \200 Mild: 32 \200\22335 C, moderate: 30 \200\22332 C, severe: <30 C \200 Fatality is high and correlates with severity of associated illness Causes Often multifactorial. \200 Illness (drugs, fall, pneumonia) \200 Defective homeo stasis (failure of autonomic nervous system-induced shivering and vasoconstriction; decreased muscle mass) Cold exposure (clothing, defective temperature discrimination, climate, poverty) In established hypothermia, thermoregulation is further impaired and is effectively poikilo thermic (temperature varies with environment). 2Hypothermia is a common presentation of sep sis in hospital in older people, and probably an indicator of poor prognosis. Don \200\231t ignore the temperature chart. Diagnosis Rectal temperature is the gold standard but well-taken oral or tympanic temperatu re will suf \201 ce. Ensure the thermometer range includes low temperatures (mercury-in- glass thermometer range usually 34 \200\22342 C, thereby underestimating severity in all but the mildest cases) . Presentation Often insidious and non-speci \201 c. The patient will frequently not complai n of feeling cold. Multiple systems affected. \200 Skin : May be cold to touch (paradoxic ally warm if defective vasoconstriction). Shivering is unusual (this occurs early in the cooling process). There m ay be increased muscle tone, skin oedema, erythema or bullae Nervous system : Signs can mimic stroke with falls, unsteadiness, weakness, slow speech, and ataxia. Re \202 exes may be depressed or exaggerated with abnor mal plantar response and dilated sluggish pupils. Conscious level ranges from confused/slee py to coma. Seizures and focal signs can occur \200 Cardiovascular system : Initially vasoconstriction, hypertension, and tachycardia \200 Then myocardial suppressio n, hypotension, sinus bradycardia \200 Eventually extreme bradycardia, bradypnoea, and hy potension. May lead to false diagnosis of death, however, the protective effect of cold on vital organs means survival may be possible Dysrhythmias include AF (early), ventricular \201 brillation, and asystole (late) HYPOTHERMIA: DIAGNOSIS 415 Renal : There is early diuresis with later oliguria and acute tubular necrosis Respiratory : Respiratory depression and cough suppression occur with secondary atelectasis and pneumonia. Pulmonary oedema and ARDS occur late Gastrointestinal : Hypomotility may lead to ileus, gastric dilation and vomiting. Hepatic metabolism is reduced (including of drugs). There is a risk of pancreatit is with hypo- or hyper-glycaemia Other : Disseminated intravascular coagulation (DIC), pressure injuries, and rhabdomyolysis Investigations \200 FBC, ESR \200 U,C + E \200 Glucose \200 Amylase \200 CRP \200 LFTs \200 TFTs \200 Blood culture \200 Drug/toxin screen \200 CK and urinalys is (may show rhabdomyolysis) \200 ABG s(looking for metabolic and respiratory acidosis an d lactate. Do not correct for temperature) ECG (abnormalities include prolonged PR interval, J waves (peak between QRS and T in leads V4-6) at <30 C and dysrhythmia) \200 Serum cortisol (consider if there are features of hypoadrenalism or hypothermia is unexplained or recurrent) 2It is important to repeat key investigations during rewarming, eg U,C + E, ECG, and ABGs. 416 CHAPTER 14 Homeostasis Hypothermia: management Monitoring Regular BP, pulse, temperature, respiratory rate, oxygen saturation, glucose; continuous ECG; consider urinary catheter. Consider ITU. Treatment principles \200 Mild hypothermia should be managed with gentle warming and clos e monitoring The features of severe hypothermia may mimic those of death. Begin resuscitation whilst gat hering information that permits a decision as to whether further intervention is likely to be futile or else not in the patient \200\231s interests. Stop resuscitation according to c linical judgment; generally don \200\231t declare dead until re-warmed, or re-warming fails \200 Re-warming: rate should approximate that of onset (0.5 \200\2231 C/hr if not cri tically unwell). Caution, as re-warming may lead to hypotension. A combination of the follo wing modalities is usually suf \201 cient: \200 Passive external: surround with dry clot hes, blankets/space blankets \200 Active external: hot air blanket ( \200\230Bair Hugger TM \200\231), hot water bottle, bath Active internal: heated oxygen, \202 uid, and food System support: maintain airway, ventilate as necessary. Good iv access. Warm iv \202 uid : may need large volumes as warming causes vasodilatation. Treat organ dysfunction as appro priate. Cardiac pacing only if bradycardia is disproportionate to reduced metabolic rate \200 If severe, or multiple organ failure, consider ITU. Handle carefully \200\224 rough handling and procedures (including intubation) may precipitate VF Sudden, severe hypothermia cardiac arrest (eg due to water immersion) is uncommon in old er people. If it occurs, manage in the usual way with rapid, invasive re-warming, supported by ITU. Drug treatment Consider: \200 Empirical antibiotics (most have evidence of infection on c areful serial assessment) Adrenal insuf \201 ciency (treatment: hydrocortisone 100mg qds) \200 Hypothyroidism (tre atment: liothyronine 50micrograms then 25micrograms tds iv, always with hydrocortisone) Thiamine de \201 ciency (malnourished or alcoholic) (treatment: B vitamins oral or iv) (as Pabrinex ) Drug metabolism is reduced, and accumulation can occur. Ef \201 cacy at the site of action is also reduced. Exercise caution with s/c and intramuscular (im) drugs (including insulin ) that may accumulate and be mobilized rapidly as perfusion improves. Prevention Before discharge, establish why this episode occurred \200\224 is recurrence li kely? (Consider housing, cognition, hypoglycaemia, sepsis, etc.) Consider how further episo des may be prevented, or terminated early. HYPOTHERMIA: MANAGEMENT 417 HOW TO Monitor temperature No method is absolutely precise. \200 Traditional mercury-in-glass thermometers are now r arely used in hospital, having been replaced due to risks to patients, staff, and the publi c Digital electronic and infrared thermometers can provide reliable results when used correctly and in accordance with manufacturer \200\231s instructions Thermochromic (forehead) thermometers are imprecise, although they may be useful for screen ing or with uncooperative patients Digital electronic thermometers These may permit oral, axillary, or rectal measurement. The y typically require a small period of equilibration and patient compliance. Infrared ( \200\230tympanic \200\231) thermometers These measure the temperature of tissue within and close to the eardrum, returning a value rapidly. Ensure that the earlobe is gent ly pulled posteriorly and superiorly, straightening the external ear canal, before insertin g the probe fairly \201 rmly. Ear wax has only a slight effect, reducing measured temperature by <0.5 C. Note that tympanic thermometers may offer a choice of displaying temperature as either \200\230true tympanic \200\231 or the derived value \200\230oral equivalent \200\231. Ensu re that you are familiar with the thermelometer in use in your hospital and what output the y give: tympanic or \200\230oral equivalent \200\231. Measurement in practice \200 Precise temperature measurement is fundamental to detecting and monitoring disease Fever may be due to infection, malignancy, in \202 ammation, connective tissue disease, or drugs A reduced or absent fever response to sepsis is seen in some elderly patients. Do not dismi ss modest fever (<37.5 C) as insigni \201 cant, or rule out infection because the patie nt is afebrile Hypothermia occurs inside and outside hospital, and may be missed unless thermometers with an appropriate range (30 \200\22340 C) are used \200 Temperature varies continuously: lowest in peripheral skin, highest in the central vessels and brain. No site is truly repre sentative of \200\230core \200\231 temperature. Typically, when compared with oral tempera ture, axillary temperatures are 1.0 C lower, and rectal and tympanic temperatures 0.5 \200\2231.0 C higher (but see notes on tympanic thermometry, also in this box) Where clinical suspicion is high, make measurements yourself, complementing monitoring by n ursing staff. Body temperature changes continuously, and a fever may manifest only after th e patient has re-warmed following a cooling ambulance journey The hand on the forehead to assess core temperature (and on the palm of the hand, to determ ine peripheral vasodilation) is of value in screening for sepsis, and can be incorporated i nto daily rounds without time penalty 418 CHAPTER 14 Homeostasis Heat-related illness An important cause of morbidity and mortality in older people, but the risk is much less appreciated than that of hypothermia. The contribution of heat stress to death is rarely mentioned on death certi \201 cates, but epi- demiological studies indica te signi \201 cant excess morbidity and mortality during extended periods of unaccustomed hot weather (eg France 2003: 15,000 excess deaths). There is an increased incidence of acut e cerebrov- ascular, respiratory and, especially, cardiovascular disease. Risk factors \200 Consider older people as being relatively poikilothermic, ie, lacking close control of body temperature in some circumstances Homeostasis is weakened due to raised sweating threshold, reduced sweat volume, altered vas omotor control and behavioral factors (lessened sensation of temperature extremes) Climate: high temperature, high radiant heat (sitting in sunshine, indoors or out), high humidity Drugs: eg diuretics, anticholinergics, psychotropics \200 Comorbidity: frailty, cerebrova scular, and cardiovascular disease A spectrum of illness The presentation is usually different in older people, typically occu rring not after extreme exertion, but during heatwaves in temperate zones. \200 Prickly h eat ( \200\230miliaria \200\231) : itchy, erythematous, papular rash. Treatment: cool, wash, antihistamines Heat oedema : peripheral oedema, usually self-limiting \200 Heat syncope : increased sync ope risk due to \202 uid depletion and vasodilation Heat exhaustion : is a potentially catastrophic illness. Dehydration and heat stress leads to non-speci \201 c presentation with collapse, immobility, weakness, vo miting, dizziness, headache, fever, and tachycardia. However, treatment should result in ra pid improvement Heat stroke occurs when untreated heat exhaustion progresses to its end stage (hyperthermic thermoregulatory failure). Core temperature is generally > 40 C, mental state is altere d (confusion l coma), circulatory and other organ failure is common, and sweating is often absent. CNS changes may be persistent and severe. Prognosis re \202 ects pre-existing como rbidity, severity, and complications, and is often poor Management \200 Individual response . Emergency inpatient treatment required. Identify and reverse precipitants. Cool rapidly until temperature 38 \200\22339 C \200\224 fan, tepid sponging, remove clothing. Close monitoring (temperature, BP, pulse saturation, urine output); consider invasive central venous pressure monitoring. Cool iv \202 uids accordi ng to assessment of \202 uid/electrolyte status Community response . Local environment modi \201 cation \200\224 fans, air conditioning, shade windows, open windows at night, seek cooler areas, avoid exercise, main tain or increase cool \202 uid intake, light/loose clothing. Education of patient and car ers. Governments should have public health measures in place to reduce the impact of heat w aves 419 Chapter 15 Endocrinology The ageing endocrine system 420 Diabetes mellitus 422 HOW TO Diagnose diabetes in older people 423 Diabetes: treatment 424 Diabetes: oral drug treatment 426 HOW TO Manage older diabetic people in care homes 427 Diabetes: insulin treatment 428 Diabetes: complications 430 Diabetic emergencies 432 HOW TO Manage diabetes in the terminally ill patient 434 HOW TO Interpret thyro id function tests 435 Hypothyroidism: diagnosis 436 Hypothyroidism: treatment 438 Hyperthyroidism: diagnosis 440 Hyperthyroidism: investigation 441 Hyperthyroidism: drug treatment 442 Hyperthyroidism: non -drug treatment 444 Primary adrenal insuf \201 ciency 446 Hormone replacement therapy and the menopause 448 420 CHAPTER 15 Endocrinology The ageing endocrine system Ageing and thyroid function Normal thyroid function is preserve d in healthy older people. Median TSH levels drift upwards very slowly with age, but remain within normal limits in the absence of disease. Lower triiodothyronine (T3) and TSH levels seen in institutionalized older people and in very advanced old age ( > 95 years) are prob ably due to illness. Sick euthyroid syndrome \200 TFTs are often abnormal in euthyroid patients who are ill wi th non \200\223thyroid systemic disease; this reverses spontaneously when the underlying illne ss improves 2Do not automatically initiate thyroid treatment changes \200 Changes depend on illness s everity, and when TFTs are checked (during acute illness or recovery) TSH secretion decreases early in the illness. Falls in levothyroxine (T4) and (especially) T3 may follow, the result of reduced TSH, lower thyroid hormone bindi ng and reduced peripheral T4 l T3 conversion Changes are more likely due to true hypothyroidism if: Free T4 levels are low \200 Changes are severe Secondary hypothyroidism (due to hypothalamo-pituitary failure) causes a similar pattern of TFTs, but is very much less common, and other features of pitui tary failure are present (eg hypogonadism) In the convalescent phase following illness, TSH may be elevated as low thyroid hormone lev els drive TSH production. For a time, TSH may be high and T4/T3 low, mimicking primary hypo thyroidism. TFTs repeated a few weeks later are usually normal. Ageing and glucose metabolism In older people: \200 Glucose-induced insulin release is de layed and reduced in size \200 Insulin-induced suppression of hepatic glucose production is delayed \200 Insulin-mediated peripheral (muscle and fat) glucose uptake is reduced In addition to reductions in physical activity and lean muscle mass, the factors listed here lead to higher frequency of impaired glucose tolerance (IGT) with age. IGT is associated wi th macrovascular disease but not with speci \201 c diabetic complications. A minority of p eople with IGT progress to diabetes. This page intentionally left blank 422 CHAPTER 15 Endocrinology Diabetes mellitus Diabetes is much more common with age: about 40 % of new diagnoses are in people over 65. Prevalence in people over 65 is 10 % in the UK, up to 50 % in some ethnic groups and obese patients. Comparing type 1 and type 2 diabetes \200 Both type 1 (insulin \200\223dependent; IDDM) a nd type 2 (non-insulin dependent; NIDDM) diabetes can occur in older people. The prevalence of type 2 is much higher In overweight older people, diabetes is mostly due to peripheral tissue insulin resistance (type 2). Glucose-induced insulin release is normal \200 Lean older people with diabetes often have impaired insulin release and may have islet cell antibodies more typical of type 1 diabetes. They respond poorly to oral hypoglycaemics There are increasing numbers of older people with type 1 diabetes who developed the disease in early or mid-life and have survived decades on insulin, sometimes with no or few compli cations Many people with type 2 diabetes progress to require insulin to achieve acceptable glycaemi c control. This group is insulin-requiring (hence IRDM) and are unlikely to develop ketoaci dosis if insulin is withdrawn When assessing a patient on insulin, determine whether they are insulin-dependent (type 1; must always have background insulin infused) or insulin-requiring (type 2; in which insulin may safely be withheld for a time, without risk of ketosis) Secondary diabetes More common in older people. Causes include: \200 Drugs. Often steroid s, sometimes high-dose thiazides, rarely other drugs Pancreatic disease, eg chronic pancreatitis \200 Other endocrine diseases, eg Cushing \200\231s, hyperthyroidism Presentation \200 Diabetes often presents atypically or late in older people \200 Up to 50 % of older people with diabetes are undiagnosed. This is at least partly due to physiological age-related changes, eg the renal threshold for glucos e increases (glucosuria and polyuria occur later) and the thirst mechanism is impaired (pol ydipsia occurs later) \200 The diagnosis is often made by screening blood or urine tests, or during intercurrent illness Think of diabetes in many clinical circumstances, eg coma, delirium, systemic stress (eg pneumonia), oral or vaginal thrush (candida), vulval itch (subclinical candida), cellulitis (and necrotising fasciitis), weight loss, urinary incontinence, polyur ia, malaise, vascular disease or peripheral neuropathy Steroid administration may reveal a diabetic tendency \200\224 always monitor, especially when high doses are used DIABETES MELLITUS 423 HOW TO Diagnose diabetes in older people \200 Con \201 rm the diagnosis with a ran dom blood sugar or fasting sugar. Criteria are the same as for younger patients In general, the diagnosis is con \201 rmed with a second measurement, unless the diagnosis is clear (eg severe hyperglycaemia with metabolic decompensation). A s ingle high measurement in the absence of symptoms is not diagnostic In some older diabetic people, fasting sugars may be normal. This is more common in lean ol der people, who have only postprandial hyperglycaemia. If in doubt, do an oral glucose tole rance test Elevated glycosylated hemoglobin (HBA 1c ) levels are only moderately speci \201 c and sensitive to diabetes and are not suf \201 cient either to co n \201 rm or to exclude the diagnosis. HBA 1c is helpful in monitoring established disease Screen annually in those with risk factors (eg family history, obesity), at least every 3 years in those without Diagnostic criteria At least one of the following criteria must apply: \200 Symptoms + ra ndom plasma glucose > 11.1mmol \200 Fasting plasma glucose > 7.0mmol \200 2-hr plasma g lucose > 11.1mmol during oral glucose tolerance test (75g anhydrous glucose or the equivale nt volume of a proprietary glucose drink such as Lucozade) Obtaining a fasting blood sugar \200 Give the completed request card to the patient \200 The patient should make an early morning appointment with a phlebotomist or general practice nurse There must be no caloric intake for at least 8hr before the blood test Tell the patient to go for the blood test before breakfast \200 Clear \202 uids (water; tea or coffee without milk or sugar) may be taken Other beverages or food must be avoided 424 CHAPTER 15 Endocrinology Diabetes: treatment \200 In all patients, aim to avoid symptoms of hyper- and hypoglycaem ia \200 In the more robust older patient, good glycaemic control probably reduces complication rates: \200 Aim for HBA 1c levels close to normal (6.5 \200\2237.5 % ) and fasting sugar of 5 \200\2237mmol/L The frail, and the very old ( > 80 years) have not been included in most prospective treatm ent studies. There is therefore doubt whether tight glycaemic control improves long-term ou tcome. Shorter-term bene \201 ts may include improved cognition, functional status, mood, and vitality \200 Balance the potential bene \201 ts of tight control with the risk of d rug-induced symptomatic hypoglycaemia, falls, and fractures Symptoms of hypoglycaemia may go unrecognized or be considered an ageing change by carers Reasonable targets for the frail are HBA 1c 7.5 \200\2238.5 % and fasting sugar 7 \200\22310mmol/L Vulnerable older patients are probably at higher risk of hypoglycaemia (eg causing confusion and falls) than hyperglycaemia. In some circumstances (eg where gluco se levels appear very variable) it may be safest to accept very high ceiling levels (eg up to 20mmol/L) 2In general, in frail older people, the approach is to reduce symptoms, not to normalize sugars. Diet \200 Dietary change is often the only treatment needed in obese people with type 2 diabetes Wholesale changes to diet may not be accepted, but even small changes are worthwhile and on their own can result in much increased insulin sensitivity wi thin weeks Full compliance may not be possible for the functionally or cognitively impaired, but an ex perienced dietician or nurse working with the patient and family is usually effective Severe dietary restrictions are often not appropriate, especially for the very old or very frail Beware the strict diet that takes enjoyment from (the last months of) life while giving little back Education \200 Educate family, carers, and nursing home staff continually \200 Provide simple written information and instructions \200 The approach must be tailored to the ind ividual, taking note of cognitive and sensory impairments Other interventions \200 Exercise, especially endurance exercise (eg walking, cycling) im proves insulin sensitivity Weight loss. Even modest reductions are bene \201 cial \200 Reduction of other vascular risk factors, including smoking \200 Home or pendant alarm systems in case of hypoglycaem ia DIABETES: TREATMENT 425