Distal nephrons develop diverticulae (3 per tubule by age 90) that may become retention cysts (benign \201 nding in older people) Other changes \200 Renal 1-hydroxylase activity decreases with age leading to decreased v itamin D production. Combined with low phosphate intake, this can mildly elevate parathyroi d hormone levels There is a loss of the circadian rhythm, owing to altered sodium handling and patterns of aldosterone secretion, so that over the age of 60 the proportion o f water, sodium, and potassium excretion occurring at night increases, causing nocturia 386 CHAPTER 13 Renal medicine Acute kidney injury Previous called acute renal failure. This is more common in older peopl e, but with a similar prognosis if occurring de novo and treated correctly. 2Do not deny tr eatment based on age alone \200\224 even anuric patients can make a full recovery Causes 80 % of cases of acute kidney injury (AKI) are caused by pre-renal failure and ATN ( acute tubular necrosis). Pre-renal causes Due to poor renal perfusion. May be caused by: \200 Dehydration (commonl y associated with sepsis) \200 Volume loss (eg bleeding, over-diuresis) \200 Volume red istribution (eg with low serum albumin) \200 Poor cardiac output (eg post-MI) \200 Aggr avated by many drugs (eg diuretics, ACE inhibitors, NSAIDs) Older patients are prone to sep sis, have less capacity to maintain circu- lating volume in the face of stress and are more likely to be on aggra- vating medications, making this a very common problem (eg urinary s epsis in a patient taking diuretics and NSAIDs can often cause pre-renal renal impairment, and responds well to antibiotics, \202 uids, and drug cessation). 2All unwell elderly pat ients should have renal function checked routinely and repeatedly. Consider stopping diuret ics and ACE inhibitors during an acute illness. Renal causes Due to direct damage to the kidney. Commonly ATN, which may be: \200 Ischaem ic (occurs when pre-renal failure is not corrected quickly, eg with sepsis, surgical proced ures, prolonged hypotension, etc.) \200 Nephrotoxic (usually medication such as aminoglyc oside antibiotics, eg gentamicin) Due to pigment deposition (eg myoglobin in rhabdomyolysis, See b \200\230Rhabdomyolysis \200\231, p.505) Not all renal failure is ATN. Other (rarer) causes include: \200 Glomerulonephritis \200 \224 diffuse in \202 ammatory change to glomeruli with resulting haematuria and red cell casts Acute interstitial nephritis \200\224 consider drug induced nephritis. May have \202 ank pain, rash, fever, eosinophilia, and urine white blood cells/casts but consider if new dru g recently even in absence of these features These less common causes are important because they are often respon- sive to speci \201 c treatment (usually steroids). The patient should be assessed by a renal physician promptly and often need a biopsy. ACUTE KIDNEY INJURY 387 Post-renal causes \200 Obstruction of the renal tract at some point, eg prostatic enlarge ment, renal stones, urethral strictures, pelvic tumors \200 Ultrasound scan shows a dilated col lecting system \200 These conditions are all more common in older people, and are very responsive to treatment if found early, often with full recovery of renal function 388 CHAPTER 13 Renal medicine Acute kidney injury: management Is this acute kidney injury? Older people are more likely t o have underlying chronic kidney disease (CKD), and this confers a worse prognosis. Check o ld notes, ask the patient, family, and GP about history, and look back at blood test result s. Generally, management does not differ signi \201 cantly from younger patients. Investigations \200 See Table 13.1 \200 Treat cause Older people respond as well to most treatments Monitor meticulously \200 Pulse and blood pressure, cardiac monitor, input (iv and oral) and output (urine, fecal matter, vomit, drains, sweat) May be best done on HDU \200 Aim for euvolaemia (assessed clinically may need to correct de \201 cit) then maintain by matching input to output on an hourly basis initially Fluid balance is likely to be harder in older people because of comorbidity (especially heart failure) 2The presence of peripheral oedema does not necessarily indicate \202 uid overload. Circu lating volume is best assessed by blood pressure, pulse, JVP, and skin turgor (see b \200 \230Challenges to volume status assessment in elderly patients \200\231, p.405) \200 May need central venous catheter and urinary catheter initially, but remove as soon as possible because of infection risk \200 Document daily weight and total \202 uid balance summary \200 Be prepared for polyuria in the recovery phase, and ensu re that the patient does not become \202 uid depleted Treat complications Importantly hyperkalaemia, acidosis, and pulmonary oedema. Refer early for further renal support ( \201 ltration or dialysis) a patient can remain ol iguric for some time while renal recovery is occurring, but it is sensible to make the rele vant teams aware of a potential patient. The indications for renal replacement therapy are as follows: \200 Refractory pulmonary oedema (older people are particularly prone to this after over enthusiastic initial \202 uid replacement) Persistent hyperkalaemia (K > 7 mmol/L) that cannot be controlled by insulin/glucose infusions and iv calcium Worsening acidosis (pH <7.2) \200 Uraemic pericarditis \200 Uraemic encephalopathy ACUTE KIDNEY INJURY: MANAGEMENT 389 HOW TO Perform a \202 uid challenge in AKI/anuria Many older patients are clearly dehydrated with mildly impaired renal function tests and th ese patients can be simply rehydrated orally or parenterally. If the patient presents with established AKI or is found to be anuric despite simple rehydr ation then a \202 uid challenge should be contemplated. This is an important clinical ski ll to develop and requires advanced clinical acumen and an investment of time. The key is a n accurate assessment of \202 uid status with the aim of rendering the patient euvolaemic . A urinary catheter is needed and a central venous pressure monitoring device is helpful if facilities exist. \200 Start by assessing and clearly documenting ba seline \202 uid status as this will inform your management and will be helpful when the p atient is reassessed If the patient is already \202 uid overloaded then a single bolus of iv loop diuretic and early contact with the renal specialist team is need \200 If the patient app ears to be hypovolaemic, give 500mL of normal saline (sodium bicarbonate may be considered if they are profoundly acidotic) over 30 \200 \22360min and review If the patient appears to be euvolaemic then the \202 uid challenge should be more cautious. Give 100mL bolus intravenously and review after about 15min For the review repeat and document the \202 uid status and urine output. Repeat this cycle of \202 uid prescription and do a careful review as the clinica l progression becomes clear 3 9 0 Table 13.1 Acute renal failure \200\224 investigations C H A P T E R Investigation Rationale Special points in older people Urea and creatinine Elevated in renal failure Elderly people with very little muscle mass will have lower baseline levels, so a urea of 1 0 in a small elderly woman will represent signi \201 cant renal impairment 1 3 R e n a l Urea: creatinine ratio can be useful \200\224 elevated in pre-renal and post- renal failur e, acting as a marker of dehydration or obstruction m e d i c i n e Electrolytes Potassium rises dangerously in ARF More prone to cardiac complications of electrolyte disturbance \200\224 monitor carefully Arterial blood gasses Monitor pH which falls in ARF pH can also be checked on a venous sample Check for infection Common precipitant of ARF in older people (may be occult) In \202 ammatory markers (ESR, CRP, white cell count) Urine dipstick Check for leucocytes and nitrites (infection) blood and protein (active renal lesion likely ) High rate of positive urine dipstick in older people \200\224 does not always imply infect ion Urine microscopy Looking for casts (red cell casts in glomerulonephritis, white cell casts in infection etc. ) and blood cells Always send for culture, even when the dipstick is negative Blood and urine cultures Identify microbes Ensure these are sent on all patients (who may have occult infection) prior to starting ant ibiotics Creatinine kinase Elevated in rhabdomyolysis Always check after falls (especially after a long period on the \202 oor before being fou nd). Even if there is not full blown rhabdomyolysis, an elevated CK level indicates the nee d for hydration and monitoring of renal function Particularly useful in older people where clinical assessment of \202 uid balance may be harder because of peripheral oedema etc. Urinary sodium Helps distinguish between pre-renal failure (urinary Na <20 mmol/L as kidney still function ing to preserve sodium) and ATN (urinary Na > 40 mmol/L as kidney not functioning, so losin g Na) Not helpful if the patient has taken diuretics (increase sodium excretion) More prone to pulmonary oedema \200\224 extra caution with \202 uid replacement if there is cardiomegaly, even where there is no history of cardiac failure CXR Looking for evidence of cardiac disease, source of infection, pulmonary oedema or pulmonary in \201 ltrates (vasculitis) A C U T E ECG Looking for evidence of cardiac disease Again alerts to occult cardiac disease if ECG is abnormal K D N E Y and monitoring for hyperkalaemia I Renal ultrasound Assess renal size and look for evidence of hydronephrosis Very useful in older people to help establish if renal failure is truly acute (small kidney s with chronic failure). Also checks for treatable obstructive causes \200\224 common in t his age group I N U R Y J Other tests All should have FBC and LFTs : M A N A G E M E N T Usually also send autoantibodies (ANA, antineutrophilic cytoplasmic antibodies (ANCA)), imm unoglobulins, complement and electrophoresis of blood and urine 3 9 1 392 CHAPTER 13 Renal medicine Chronic kidney disease CKD is a substantial, irreversible, longstanding, and usually progre ssive loss in renal function. CKD is more common in older people (incidence in the over 75s is 10 times higher than in the under 40s). Half of all renal replacement therapy is now st arted for patients > 65 years and this under- estimates the burden of renal impairment, as the majority will die with, and not of, renal failure, many never encountering a renal phys ician. Much renal impairment is discovered incidentally by \201 nding elevated urea and creatini ne levels. Many labs now quote an estimated glomerular \201 ltration rate (eGFR), which i s highlighting the prevalence of early stage renal impairment. There are adaptive mechanism s that maintain reasonable health with failing renal function until severe damage has occur red (GFR of 10 \200\22315 mL/min). Causes Common causes include hypertension, diabetes, obstruction (usually due to prostatic enlargement), glomerulonephritis, and renovascular disease. A signi \201 cant proportion p resenting late remains idiopathic. Management When abnormal renal function is discovered, \201 rstly consider the cir- cumst ances is the patient acutely unwell? Are they being over-diuresed? Correct all of remediabl e factors, and recheck renal function in a stable clinical state. If it remains deranged, t hen: \200 Estimate the GFR (see b \200\230HOW TO Estimate the glomerular \201 ltration rate \200\231, p.393). Consider checking GFR even when creatinine is within normal range for older patient with a low body weight Identify and treat any modi \201 able factors (eg diabetes, hypertension, and obstructive uropathy) Delay disease progression by controlling diabetes and hypertension and by using an ACE inhi bitor (or an ARB). Low-protein diets, lipid lowering, and correcting anemia may also help Avoid exacerbating factors such as volume depletion, intravenous contrast, urinary obstruction and nephrotoxic drugs Review drug treatment, some are better stopped (eg metformin) and others need dose adjusting (eg digoxin) Identify and treat complications as they arise (see b \200\230Chronic kidney disease: complications \200\231, p.394) Try to establish the rate of decline, using previous creatinine measurements. Deterioration tends to be steady and so it is often possible to estimate when interventions are likely to be needed Prepare for the end-stage. A frail old person with limited life expectancy and moderate impairment is likely to die of other causes before complex renal is sues become a problem. Most other patients bene \201 t from early renal specialist review (ie when impairment is moderate to severe) to clarify diagnosis, optimize management and di scuss renal replacement therapy. Late referral for dialysis is associated with a poor outco me Further reading Kidney Disease Outcomes Quality Initiative online: M www.kidney.org/profess ionals/kdoqi . CHRONIC KIDNEY DISEASE 393 HOW TO Estimate the glomerular \201 ltration rate Although elevated urea and creatinine levels often alert the clinician to renal impairment, they give a poor estimate of extent, as the levels are determined by many factors as well as GFR, eg creatinine is directly related to muscle mass, which tends to fall with age mean ing that: \200 A small rise in urea and creatinine in an elderly person is signi \201 ca nt, and should be taken seriously A creatinine within the normal range may represent renal failure in a small old patient GFR is a better measure of renal function, but requires a 24-hr urine collection which can be tricky in older people. Creatinine clearance approximates GFR and can be estimated using various equations. The Cockcroft-Gault formula is the best known: Creatinine clearance = [(140 \200\223 age in years) \227 weight in kil o grams] plasma creatinine ( mol/L) x 0.82 This \201 gure needs to be reduced slightly for women. It can be seen that a patient of 80, weighing 50kg with a creatinine of 140 will have an es timated GFR of 26 (ie severe failure). Another patient of 30, weighing 70kg with a creatini ne of 140, however, will have an estimated GFR of 67 (ie mild failure). eGFR should be used in calculating dose adjustments for certain drugs, eg gentamicin, low molecular weight heparin. Using this derived \201 gure, renal impairment has been classi \201 ed by the Kidney Dis ease Outcomes Quality Initiative (K/DOQI) and this acts as a guide for management (Table 13 .2 ). Table 13.2 Kidney Disease Outcomes Quality Initiative GFR (mL/min) Average creatinine for patient of 30 years weighing 70kg Average creatinine for patient of 80 years weighing 50kg Degree of renal failure 60 \200\22389 125 50 Mild failure 30 \200\22359 220 85 Moderate failure 15 \200\22329 420 165 Severe failure <15 > 1500 > 700 End-stage renal failure 394 CHAPTER 13 Renal medicine Chronic kidney disease: complications Hypertension \200 Can occur at any point in the dis ease and is a cause and a consequence of CKD Monitor blood pressure regularly in all patients \200 Treat with an ACE inhibitor (preser ves renal function) Hyperlipidaemia \200 May contribute to renal damage \200 Treat with a statin Atherosclerosis \200 Accelerated atheroma occurs with renal impairment \200 Ensure that all vascular risk factors are addressed Salt and water retention \200 Onset with moderate impairment \200 Consider loop diureti cs for oedema (eg furosemide high doses may be required, but start low and increase as needed) Restrict dietary salt intake (ideally <2g/day) \200 Fluid restriction may be necessary wi th more severe renal impairment Secondary hyperparathyroidism \200 Onset usually with moderate impairment \200 Low calc ium, high phosphate, low vitamin D and appropriately high parathyroid hormone (PTH) Ensure calcium, phosphate, and PTH are checked \200 Consider dietary phosphate restrictio n (milk, cheese, eggs, etc.), phosphate binders (eg calcium carbonate), calcium supplements, and vitamin D analogs (eg al facalcidol) if there is a problem Risk of renal bone disease (renal osteodystrophy) Anemia \200 Onset usually with moderate impairment \200 Check for alternative causes of anemia (iron de \201 ciency, chronic disease, etc.) If none found, consider erythropoietin injections to keep Hb > 11g/dL (usually initiated by renal physician) Nervous system \200 Onset with severe impairment \200 Includes peripheral neuropathy, a utonomic neuropathy and encephalopathy Acidosis and hyperkalaemia \200 Onset with moderate or severe impairment \200 Indicate need for renal replacement therapy, or plans for terminal care Further reading Kidney Disease Outcomes Quality Initiative online: M www.kidney.org/profess ionals/kdoqi . This page intentionally left blank 396 CHAPTER 13 Renal medicine Renal replacement therapy: dialysis This includes haemodialysis (usually done at a dialysis center and accounting for around 80 % of dialysis in the older age group) and peritoneal d ialysis (mainly managed at home). Survival Older patients have a shorter survival on dialysis than younger patients, probably because of an increase in complications (see b \200\230Complications \200\231, p.396) yet still can expect a 20 \200\22340 % \201 ve year survival (mean life expect- ancy 3 \200 \2235 years). Those aged over 80 on dialysis have a median survival of 26 months, irrespective of the age at onset of treatment. Effectiveness \200 Some older patients may mistakenly be under-dialysed (low muscle mass leads to lower urea and creatinine levels that do not re \202 ect the need for dialys is). In addition, dialysis sessions are more commonly stopped early because of hypotension This adversely affects outcome. Using other means to calculate dialysis frequency and optim izing health with nutritional support, erythropoietin (to keep Hb > 12g/dL) and appropriate buffer selection can vastly improve effectiveness in older people Complications In older people: \200 Nausea, vomiting, and hypotension during dialysis are more common (due to autonomic dysfunction and decreased cardiac reserve) Malnutrition occurs in up to 20 % \200 There is increased risk of infection (ageing immun e system and malnutrition), depression, and gastrointestinal bleeds (from uraemic gastritis, diverticulo sis, and angiodysplasia) Quality of life Many older patients on dialysis enjoy a high quality of life. They resent t he intrusion of visits to a dialysis center less than younger patients and can \201 nd it offers positive social interaction. Many of this highly selected cohort (frailer elderly p atients with renal impairment are not appropriate for this service) retain their independen ce with over 90 % maintaining good com- munity social contacts, and over 80 % regularly goi ng outdoors. Around 40 % rate their health positively. However, for some it becomes tiring and burdensome, especially if relying on hospital transportation for attendance. RENAL REPLACEMENT THERAPY: DIALYSIS 397 Who should be offered dialysis? Dialysis is expensive, and the number of elderly people wit h end-stage renal failure is large. Many elderly patients with end-stage renal failure elec t to have dialysis if offered, but offering it to all is not sensible or feasible. It should not be offered to simply delay dying, rather used if the renal failure is the mai n threat to continued survival. Severe dementia, advanced malignancy (except possibly multi ple myeloma), or advanced liver disease generally makes dialysis inadvisable. Caution shoul d be exercised before offering dialysis to patients with severe heart or lung disease, or f rail patients with multiple comorbidities. What next? Many patients need to swap dialysis modalities for some reason. 40 % would like to proceed to transplant if an organ was available. The rate of voluntary withdrawal (overa ll about 5 % ) increases with age and is usually because of general dissatisfaction with li fe or the development of signi \201 cant comorbidity (often cancer). Guidelines suggest th at patients approaching the end of their life should have input into an individual palliati ve care plan, often in conjunction with palliative care services. Further reading National Service Framework for Renal Services online: M www.dh.gov.uk . 398 CHAPTER 13 Renal medicine Renal replacement therapy: transplantation This is the gold standard of renal replacement t herapy for end-stage renal failure, as it improves survival and quality of life when compar ed with dialysis, as well as releasing the patient from the burden of regular dial- ysis se ssions. It is also cost-effective, being cheaper than dialysis after the \201 rst year. Transplant recipients are getting older (10 % of transplants in 2002 were performed for pat ients over 65, compared with only 5 % a decade earlier) however, as the majority of end-sta ge failures occur in the elderly population, this still represents an imbalance. Donated ca daver kidneys are in short supply, and tend to be given to those who will get the most use out of them namely younger patients with a longer natural life expectancy. The most common cause of graft failure in older people is death of the host with a functioning graft. This is due to a number of factors: \200 The most common c ause of death after transplantation is cardiovascular disease Older people have altered immune responses \200\224 this makes it less likely that they will reject a donated kidney, and allows for modi \201 ed immunosuppressi ve medication. However, it also increases the risk of serious infection Older people have increased side effects to immunosuppressive medication particularly steroids Other common conditions make the transplant procedure more complicated, eg peripheral vascu lar disease (technical surgical problems), diverticular disease (predisposes to post-transp lant perforation) and cholelithiasis (predisposes to biliary sepsis) There are limited outcome data for older patients, but: \200 Patients > 60 have a 70 % 5- year survival post-transplantation compared with > 90 % for younger patients although graft survival is equivalent \200 Transplant carries a greater chance of survival than dialysi s, in older as in younger patients (around 10 years compared with six on dialysis for those aged 60 \200\22374) Each individual must be considered separately, taking into account bio- logical and not chr onological age. Careful screening for comorbidity will reveal those most likely to bene \201 t, regardless of age. The use of older donors for older recipients could partially red ress the imbalance, as the grafts themselves will have a limited lifespan and so be most ap propriate for an age-matched recipient. Live organ donation is a rapidly expanding area whi ch may improve kidney availability. NEPHROTIC SYNDROME 399 Nephrotic syndrome Increased glomerular permeability to protein causes proteinuria ( > 3g/ day), hypoalbuminaemia, generalized oedema, and hyperlipidaemia. There is an increased susc eptibility to infection, thrombosis, and renal failure. More common in older people, but often missed as oedema may be attributed to cardiac failure and a low serum albumin to poor nutrition. 2Always dipstick t he urine for protein in an oedematous patient. Causes Membranous and minimal change nephropathy, glomerulonephritis, and amyloid are commo n pathologies. Look for associated conditions, including malignancy (eg carcinoma, lymphoma ), infection (eg hepatitis B), systemic disease (eg systemic lupus erythematosus, rheumatoi d arthritis, chronic infection) and diabetes. NSAID use may be the only cause. Presentation Frothy urine, anorexia, malaise, muscle wasting, oedema (mobile depending on g ravity \200\224 moves from sacrum and eyelids at night to legs during day) and effusions ( pleural, pericardial, ascites). Blood pressure varies. Patients are prone to intravascular depletion with increased total body water, especially when over-diuresed due to assumed car diac failure. Investigations \200 Routine blood screen (FBC, U,C + E, glucose, LFTs) \200 Urinalysis \200 24-hr urinary protein \200 ANA, ANCA, complement \200 Urine and serum electropho resis, immunoglobulins \200 Hepatitis serology \200 Renal ultrasound \200 Refer to re nal team for possible biopsy Treatment \200 Usually requires admission and involvement of renal physician \200 Monit or proteinuria, U + E, \202 uid balance, blood pressure \200 Fluid and salt restriction \200 Diuretics (eg furosemide 80 \200\223250mg) \200 Prophylactic heparin s/c in immob ile patient \200 Monitor closely for infection \200 Speci \201 c treatment with steroi ds/immunosuppressants after histology known (specialist advice) Control of hypertension in diabetic patients 400 CHAPTER 13 Renal medicine Glomerulonephritis \200 A diffuse in \202 ammatory process involving the glomeruli \200 Presents with renal failure, hypertension, oedema, haematuria, red cell casts and proteinuria Older people often present non-speci \201 cally (eg with nausea, malaise, arthralgia and pulmonary in \201 ltrates due to vasculitis) 2Often misdiagnosed initially, causing delay in treatment. In unwell older people, always d ipstick the urine. Think of glomerulonephritis if there is haematuria (see b \200\230Near- patient urine tests \200\231, p.618). Causes \200 Post-infectious (usually streptococcal/staphylococcal, 2 \200\2236 weeks post-exposure) Systemic disease (vasculitis, lupus, Wegener \200\231s granulomatosis, Churg \200\223 Strau ss, Goodpasture \200\231s syndrome, Henoch-Sch nlein purpura, etc.) Primary renal (eg IgA nephropathy) \200 Unknown etiology is not uncommon Investigation \200 As for nephrotic syndrome \200 Usually best supervised by a renal ph ysician \200 Biopsy required for de \201 nitive diagnosis \200 Speci \201 c investiga tions for individual causes, eg anti-glomerular basement antibodies for Goodpasture \200\231s syndrome Treatment \200 Supportive \200 20 % require dialysis \200 Steroids can be used for al l but postinfectious, so refer early to a renal team to con \201 rm diagnosis (usually by renal biopsy) Outcome \200 Worse in older people. More die, and more progress to CKD RENAL ARTERY STENOSIS 401 Renal artery stenosis More common with increasing age. Usually due to atheroma (as opposed to intimal hyperplasia pathology in younger patients) so patients often have known vascular disease in other areas. Diagnosis Think of renal artery stenosis when: \200 Renal function deteriorates after sta rting an ACE inhibitor. Stopping the drug promptly should reverse the changes Blood pressure is hard to control \200 There is unexplained hypokalaemia (due to low aldo sterone levels) \200 A renal bruit is heard on clinical examination \200 There is a uni lateral small kidney seen on imaging \200 Flash pulmonary oedema MRI or CT angiography ca n be useful in diagnosis as long as renal function allows (contrast contraindicated if eGFR <30mL/min/1.73m 2 ). Digital sub- traction angiography is the gold standard and usually pre cedes stenting. Management As there are often no symptoms, conservative management with blood pressure cont rol, optimizing vascular secondary prevention but avoiding ACE inhibitors is often appropri ate. If, however, renal function declines or blood pressure cannot be controlled, then perc utaneous angioplasty or stent insertion is well tolerated even in very old people. This page intentionally left blank 403 Chapter 14 Homeostasis Volume depletion and dehydration 404 Dehydration: management 406 HOW TO Administer subcutaneous \202 uid 406 Hyponatraemia: treatment 408 Syndrome of inappropriate antidiuretic hormone secretion (SIADH) 410 HOW TO Perform a short ACTH stimulation test (short Synacthen test) 411 Hypernatraemia 412 Hyponatraemia: assessment 413 Hypothermia: diagnosis 414 Hypothermia: ma nagement 416 HOW TO Monitor temperature 417 Heat-related illness 418 404 CHAPTER 14 Homeostasis Volume depletion and dehydration An important, common, easily missed clinical condition, es pecially in older people. Highly prevalent among acutely unwell older people admitted to ho spital due to a combination of increased \202 uid loss (fever, gastrointes- tinal loss), and decreased intake (nausea, anorexia, weakness). Causes Often multifactorial, and include: \200 Blood loss \200 Diuretics \200 Gastroi ntestinal losses (eg diarrhea, NG drainage) \200 Sequestration of \202 uid (eg ileus, b urns, peritonitis) \200 Poor oral intake \200 Fever Symptoms and signs \200 Thirst is uncommon in older people \200 Malaise, apathy, weakne ss \200 Orthostatic symptoms (lightheadedness or syncope) and/or postural hypotension Nausea, anorexia, vomiting, and oliguria in severe uraemia \200 Tachycardia, supine hypot ension (late signs, also in \202 uid overload ) \200 Decreased skin turgor, sunken faci es, absence of dependent oedema The symptoms and signs of clinically important dehydration may be subtle and confusing. It is therefore under-recognized. Continual clinical assessmen t, assisted by basic tests (urinalysis; U,C + E) is essential. Invasive monitoring or other tests are rarely needed. Older patients commonly become dehydrated because: They are \200\230run dry \200\231 on the wards, as medical (and nursing) staff fear precip itating acute pulmonary oedema through excessive iv \202 uid administration Iv infusions often run more slowly than prescribed, or cannot run for periods if iv access is lost Moderate leg oedema is very poorly speci \201 c for heart failure \200\224 don \200\231t treat this sign alone, in the absence of supporting evidence, with diuretic 2 Poor urine output on the surgical (or medical) wards is more often a sign of dehydration than of heart failure. Improving urine volume with diuretics is the wrong treatment. 2There is no sensitive biochemical marker of dehydration \200\224 urea and creatinine are common ly in the normal range, and may be abnormal when normally hydrated (eg in CKD). VOLUME DEPLETION AND DEHYDRATION 405 Challenges to volume status assessment in elderly patients This can be dif \201 cult and requires care. There is no gold standard in routine clinical examination, although a capillary wedge press ure will give a reliable estimate in ITU/HDU settings. Most symptoms and signs can occur in both \202 uid overload and dehydration \200\224 use multiple indicators to make an overall decision about volume status. Use serial assessments and if the response to treatment is not as anticipated, review your judgment. Symptoms \200 Thirst is often absent in dehydration \200 Confusion can occur in dehydra tion and \202 uid overload \200 Breathlessness may occur in \202 uid overload, but al so in, eg, chest sepsis with dehydration Signs \200 Tachycardia may occur in dehydration (may be absent if there is B -blockade) but also occurs in cardiac failure Hypotension similarly occurs both in dehydration and cardiac failure. A postural drop is mo re likely to indicate dehydration, but may also be induced by medication or autonomic dysfu nction Look at the skin turgor \200\224 choose a site away from peripheral oedema, eg the forehead. Pinch the skin gently and see how quickly it returns to normal. A sluggish response indicates dehydration 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