Vertebral osteomyelitis and infective discitis should be considered in those with fever and raised in \202 ammatory markers especially if they are immunosuppress ed (eg rheumatoid arthritis on steroids) 2Not all back pain comes from the spine. Differential diagnoses that should not be missed i nclude pancreatitis or pancreatic cancer, biliary colic, duodenal ulcer, aortic aneurysm, r enal pain, retroperitoneal pathology, pulmonary embolism, Guillain \200\223Barr syndrome or MI. Investigations \200 FBC, ESR (myeloma screen if raised), CRP, ALP, calcium, PSA (in men) \200 MRI is good at identifying serious pathology, eg cancer, infection, compression syndromes CT can be done if unable to have MRI but is less good \200 Bone scan is useful especially if there are multiple sites of pain \200 Plain X-rays may reveal diagnosis but \200\230 wear and tear \200\231 changes are very common and correlate poorly with pain. May miss ser ious pathology Treatment First, make a diagnosis to guide therapy. Speci \201 c therapies include: Bisphosphonates or calcitonin for osteoporotic collapse \200 Radiotherapy is very effecti ve for metastatic deposits \200 Urgent surgery or radiotherapy should be considered for c ord compression, with high-dose iv steroids in the meantime THE PAINFUL BACK 497 General therapies for most diagnoses include: \200 Standard analgesia ladder (see b \200 \230Analgesia \200\231, p.140) \200 Physiotherapy is often helpful in improving pain and function or at least preventing deconditioning Exercise and weight loss (if obese) are dif \201 cult to achieve but will help \200 TENS can help some and is without side effects \200 Antispasmodics, eg diazepam 2mg if muscul ar spasm is prominent \200 Consider referral to pain specialist for local injections, eg facet joints or epidurals Once serious pathology has been excluded a chiropractor/osteopath can sometimes help 498 CHAPTER 17 Musculoskeletal system The painful shoulder The shoulder joint has little bony articulation (and hence little arth ritis) but lots of muscle and tendon which is prone to damage. Many condi- tions become chr onic and examining elderly people will reveal a high prevalence of pain and restricted move ment. Patients compensate (eg by avoiding clothes that need to be pulled over head) and may not report symptoms. Before diagnosing one of the conditions that follow, exclude systemic problems such as poly myalgia rheumatica and rheumatoid arthritis. Remember that neck problems, diaphragmatic pat hology, apical lung cancer, and angina can also produce shoulder pain. Frozen shoulder/adhesive capsulitis \200 Usually idiopathic but sometimes follow trauma a nd stroke \200 More common in people with diabetes \200 Loss of rotation (internal and external) and abduction \200 Painful for weeks to months then stiff (frozen) for further 4 \200\22312 months \200 Mainstay of treatment is physiotherapy/exercise \200\224 avoid rest \200 Intra-articular steroids may help pain and improve tolerance to early mobilization Bicipital tendonitis \200 Pain in speci \201 c area (anterior/lateral humeral head) aggr avated by supination on the forearm while elbow held \202 exed against body \200 Treatm ent is rest and corticosteroid injection followed by gentle biceps stretching exercises Rotator cuff tendonitis \200 Dull ache radiating to upper arm with \200\230painful arc \200\231 (pain between 60 and 120 when abducting arm) Rest, occasionally with immobilization in a sling, and corticosteroid injection Physiotherapy and exercises may help \200 Arthroscopic decompression can sometimes reliev e pain Rotator cuff tear \200 May occur following trauma \200 Reduced range of active and pass ive movements of shoulder \200 Ultrasound and MRI diagnostic \200 Treat with rest and c orticosteroid injection \200 Physiotherapy and exercises may help \200 Surgical repair possible in some cases Shoulder dislocation \200 May occur after a fall (usually anterior) or seizure (may be po sterior) \200 Shoulder is painful, appears deformed, and X-rays will con \201 rm \200 Check for neurovascular damage; arrange pain relief and joint reduction by manipulation THE PAINFUL SHOULDER 499 Glenohumeral OA \200 Uncommon site for arthritis \200\224 there is usually previous trau ma \200 Presentation and examination similar to frozen shoulder \200 Classic examinatio n \201 ndings are of: Local glenohumeral joint line tenderness and swelling anteriorly \200 Loss of range of mo tion of external rotation and abduction \200 Crepitation \200 X-rays will con \201 rm \200 Initial treatment is with analgesia and mobilization \200 Joint injection with ste roids can be useful \200 Failure to respond to conservative measures should prompt consideration of surgical referral for joint replacement \200\224 this is highly successfu l in appropriate patients This page intentionally left blank 501 Chapter 18 Pressure injuries Pressure sores 502 Compression mononeuropathy 504 Rhabdomyolysis 505 502 CHAPTER 18 Pressure injuries Pressure sores Areas of skin necrosis due to pressure-induced ischaemia found on sacrum, he els, over greater trochanters, shoulders, etc. Also known as decubitus ulcers or bedsores. Incidence higher in hospital (new sores form during acute illness) but prevalence higher in long-stay community settings (healing takes months/years). Average hospital prevalence 5 \200\22310 % despite drives to improve education and preventative strategies. The \201 na ncial and staf \201 ng resource burden of pressure sores is huge. Grading 0 Skin hyperaemia I Non-blanching erythema II Broken skin or blistering (epidermis 9 dermis only) III Ulcer down to subcutaneous fat IV Ulcer down to bone, joint or tendon 22 hrs of tissue ischaemia is suf \201 cient for the subsequent development of an ulcer and the causative insult often occurs just prior to or at the time of admission (on ED trolleys , intraoperative, at home). There is consid- erable lag between the ischaemic insult and th e resulting ulcer. Grade I erythema often progress to deep ulcers over days/weeks without f urther ischaemic insult. Inspect sacrum and heels at least daily. Risk factors Include age, immobility (especially postoperative), low or high body weight, m alnutrition, dehydration, incontinence, neurological damage (either neuropathy or decreased conscious level), sedative drugs, vascular impairment. Several scoring systems (eg Waterlow score) combine these factors to stratify risk. They aid/prompt clinical judgment of individual patient risk. Mechanisms \200 Pressure \200\224 normal capillary pressure 24 \200\22334mmHg \200\224 pressures exceeding 35mmHg compress and cause ischemia. This pressure is easily exceeded on a simple foam mattress at pressure points such as heels Shear \200\224 where skin is pulled away from \201 xed axial skeleton small blood vessel s can be kinked or torn. When a patient is propped up in bed or dragged (eg during a lift o r transfer) there is considerable shear on the sacrum Friction \200\224 rubbing the skin decreases its integrity especially at moving extremitie s, eg elbows, heels. Avoid crumbs, drip sets and debris between patient and sheets. Massage of pressure areas no longer recommended Moisture \200\224 sweat, urine, and feces cause maceration and decrease integrity PRESSURE SORES 503 Management \200 Prevention \200\224 demands awareness \200\224 NICE guidelines suggest all patients are risk assessed within 6hr of admission ( M www.nice.org.uk , clinical guide line 29 (2005)). Regular reassessment during hospital admission should occur especially if condition of patient changes Turning and handling \200\224 there is no evidence to suggest how often immobile, high-risk patients should be turned in bed. Two-hourly turns are historically bas ed and rarely achieved. Frequency should be judged individually. Modern mattresses decrease frequency but don \200\231t eradicate need for turns. Avoid friction and sheer by using co rrect manual handling devices. Consider limiting sitting out to 2hr. Encourage early mobili zation, optimize pain control, minimize sedative drugs Pressure-relieving devices \200\224 consider both beds and chairs. There are few RCT data to compare but most hospitals have access to (in order of increasing pressure reduction and cost) \200 High speci \201 cation foam mattresses \200 Alternating pressure mattresse s (air pockets intermittently in \202 ate and de \202 ate) eg Nimbus Air- \202 uidized (warm air pumped through tiny spheres to produce a \202 uid-like cushion) or waterbed mattresses Promote healing environment Nutrition \200\224 protein and calorie supplements. There is no evidence to support the us e of vitamins, eg vitamin C, or minerals, eg zinc, but they are unlikely to do harm Manage incontinence (one of the few times that a geriatrician might recommend a catheter) Good glycaemic control in people with diabetes \200 Correct anemia (normochromic/normocyt ic anemia common) Debridement \200\224 dead tissue should be removed with scalpel (no anesthetic required), maggots or occasionally topical streptokinase, or suction. Some patients bene \201 t from surgery, eg debridement, skin grafting or myocutaneous \202 aps Dressings \200\224 enormous choice with little evidence to favor one type over another. Us e gels to soften, hydro \201 bre/gels (often seaweed based) for cavities then a secondary dressing over the top Antibiotics \200\224 all ulcers are colonized (surface swabs positive 100 % ), only 1 % at any given time have active infection causing illness. Look for surrounding cellulitis and signs of sepsis, check blood cultures or deep tissue biopsy for con \201 rmation. Common o rganisms include mixed Gram-negatives ( Bacteroides ) Gram-positives (enterococci and staph ylococci), and yeasts. If antibiotics are indicated, use wide- spectrum antibiotics includi ng anaerobic cover. Consider osteomyelitis where bone is exposed (see b \200\230Osteomyeli tis \200\231, p.488). MRSA colonization is a growing problem, is very dif \201 cult to era dicate, and often leads to a patient having prolonged isolation, which is detrimental to th eir psychological well-being and rehabilitation 504 CHAPTER 18 Pressure injuries Compression mononeuropathy \200 Where nerves are compressed against bone they can be dama ged \200 This is usually a demyelination injury (neuropraxia) which resolves spontaneously in 2 \200\22312 weeks Alcohol, diabetes, and malnutrition increase susceptibility \200 Any patient who has had a period of immobility on a hard surface is at risk especially if they were unconscious Such injuries can be misdiagnosed as strokes but are LMN in one nerve territory only (see b Appendix, \200\230Dermatomes \200\231, p.686) Nerve conduction studies are rarely required to con \201 rm diagnosis \200 Treatment is supportive \200\224 many such patients are acutely unwell \200\224 but recognition become s more important during rehabilitation (Table 18.1 ) Table 18.1 Clinical features of common mononeuropathies Nerve damaged Site/mechanism Motor effects Sensory effects Wrist drop and \201 nger extension weakness Small area of numbness at base of thumb Radial Upper arm \200\224 spiral groove on humerus Little and ring \201 nger Ulnar Elbow \200\224 cubital groove Little and ring \201 nger \202 exors and \201 nger abduction and adduction Lateral calf and top of foot Common peroneal Knee \200\224 \201 bula head Foot drop and failure of foot eversion and toe extension Posterior thigh plus common peroneal as this table, above Sciatic Buttock or thigh Knee \202 exors plus common peroneal as this table, above RHABDOMYOLYSIS 505 Rhabdomyolysis Following prolonged pressure (eg if patient cannot get up after a fall or st roke or after a period of unconsciousness) muscle necrosis can occur, which releases myoglo bin. High levels are nephrotoxic, precipitating to cause tubule obstruction with acute rena l failure especially as these patients are usually dehydrated. 2Remember to check U,C + E i n all patients who have been found on the \202 oor after a \200\230long lie \200\231. Ma ny frail elderly patients with bruises after a fall will have raised CK levels without deve loping renal problems but ensuring good hydration (often with 24 \200\22348hr of intravenou s \202 uids) and repeating renal function in such patients is good practice. Diagnosis Suspect the full rhabdomyolysis syndrome in any patient with: \200 Prolonged un consciousness \200 Signs of acute pressure sores of the skin \200 CK levels at least \201 ve times normal Urine may be dark ( \200\230Coca-Cola \200\231 urine) and urinalysis i s positive to hae- moglobin but without red blood cells. Hyperkalaemia and hypocalcaemia ca n occur. Treatment Treat with aggressive rehydration. Monitor urine output, electrolytes, and renal function closely \200\224 if renal failure occurs consider temporary dialysis. Prognosis i s good if patient survives initial few days. Other causes of rhabdomyolysis include drugs (especially statins), compartment syndrome, ac ute myositis, severe exertion eg seizures/ rigors, heat stroke (see b \200\230Heat-related illness \200\231, p.418) and neuroleptic malignant syndrome (see b \200\230Neuroleptic ma lignant syndrome \200\231, p.169). This page intentionally left blank 507 Chapter 19 Genitourinary medicine The ageing genitourinary system 508 HOW TO Examine the older female genital system 509 Benign prostatic hyperplasia: presentation 510 Benign prostatic hyperplasia: treatment 512 Prostatic cancer: presentation 514 Prostate-speci \201 c antigen 516 Prostatic cancer: tre atment 518 Postmenopausal vaginal bleeding 520 Vaginal prolapse 522 HOW TO Care for a vaginal pessary 523 Prolapse: illustrations 524 Vulval disorders 526 Sexual function 528 HIV in older people 53 0 508 CHAPTER 19 Genitourinary medicine The ageing genitourinary system Changes in women \200 Estrogen levels fall following meno pause (usually around age 50) leading to vaginal epithelium atrophy, decreased vaginal lubrication, and acidi \201 catio n and greater vulnerability to vaginal and urinary infection The uterus and ovaries atrophy \200 The vagina becomes smaller and less elastic Hormone r eplacement therapy improves menopausal symptoms but has other serious adverse effects that severely limit its use (see b \200\230Hormone replacement therapy and the menopause \200 \231, p.448). Changes in men \200 There are gradual changes in anatomy and function, but no sudden change in fertility, and most older men remain fertile Testicular mass and sperm production fall as does semen quality \200 The prostate gland e nlarges and \201 broses \200\224 benign prostatic hypertrophy (BPH) \200\224 but the volume of ejaculate remains similar \200 Erection bec omes less sustained, less \201 rm, and the refractory period between erections lengthens. However, severe erectile dysfunction, ie inability to sustain an erection suf \201 cient to have sexual intercourse, is usually the result of pathology or drug treatment rather tha n ageing itself Testosterone levels remain stable or decrease slightly. In a minority, more severe falls are seen and hypogonadism may become symptomatic, manifesting as fatigue, weakness, osteoporosis, muscle atrophy, declining sexual function, and impaired cognition Testosterone replacement may be considered in those with low hormone levels and symptoms. T his may have symptomatic bene \201 t, but risks serious side effects (eg rising haematocri t, prostatic hypertrophy). Low doses (delivered by patches or injection) may reduce this ri sk, but monitoring is probably needed. There are no good-quality long-term trials of replac e- ment therapy. Changes in both sexes Cross-sectional studies show much reduced frequency of sexual behavio r of all kinds in older people. However, longitudinal studies show much smaller changes, su ggesting that many changes are due to cohort effects, eg changes in the prevailing social e nvironment during early adulthood. Other factors include physical and psychological illness (eg arthritis, depression), reduce d potency, social changes (eg lack of a partner due to bereavement). Most of these factors are modi \201 able. Further reading Read J . ( 2004 ). Sexual problems associated with infertility, pregnancy, and ageing . BMJ 329 : 559 \200\223 61 . THE AGEING GENITOURINARY SYSTEM 509 HOW TO Examine the older female genital system This is an important part of the asses sment for symptoms such as post- menopausal bleeding, urinary incontinence and symptoms of prolapse. Approach tactfully \200\224 many older women will not be keen on pelvic examinat ion. Proceed as follows: Reassure the patient and position for examination \200\224 the standard position with the patient on her back and the legs spread may not be possible with hip dise ase; consider rolling the patient onto her side, drawing up the knees and inspecting from t his position Inspect the external genitalia, looking for atrophy, erythema, infection, and abrasions. Se vere prolapse may be immediately apparent Ask the patient to bear down, which may reveal smaller degrees of prolapse Perform a vaginal examination, remembering to use plenty of lubrication. Begin with a single digit if the vaginal opening is tight \200 Some rectocoe les are only detected by bimanual examination of the vagina and rectum Use a speculum if available and tolerated 510 CHAPTER 19 Genitourinary medicine Benign prostatic hyperplasia: presentation BPH is characterized by non-malignant enlargemen t of the prostate gland and an increase in prostatic smooth muscle tone. The resulting blad der outlet obstruction leads to lower urinary tract symptoms (LUTS; \200\230prostatism \200\231). Prostatism affects 25 \200\22350 % of men over 65 years, although the histological changes of BPH are even more common \200\224 almost universal in those > 70. The natural history i s variable \200\224 some deteriorate, some stay the same, and some improve, even without t reatment. Assessment Symptoms LUTS are variable, and may be mostly either: \200 Obstructive . Weak stream, straining, hesitancy, nocturia, acute retention, or chronic retention with over \202 ow incontinence \200 Irritative . Frequency, dysuria, urgency, and urge incontinence Other presentations include haematuria (the prostate is hypervascular), UTI, and renal fai lure secondary to hydronephrosis. Obstructive symptoms may be worsened by drugs, eg sedatin g antihistamines. Tricyclic antidepres- sants may improve irritative symptoms, but worsen o bstruction. Scoring systems (see Box 19.1 ) can help determine symptom severity, track progression, and response to treatment. Examination Include the genitals (phimosis or meatal stenosis), abdomen (palpable bladder), neurological system, and digital rectal examination (DRE). In BPH, the prostate is usually smooth, \201 rm, and enlarged. An irregular prostate can occur in BPH, calculi, infarction, or cancer. Investigations Tests may help con \201 rm the diagnosis, exclude other pathology, and iden tify complications: \200 Urinary \202 ow rate con \201 rms obstruction, but is rarely needed \200 Blood glucose to exclude diabetes, a common cause of urinary symptoms U,C + E (renal failure) \200 Urinalysis (infection, haematuria) \200 USS renal tract (h ydronephrosis, high residual volume (see Box 20.1) \200 PSA . Consider this, especially i f the prostate is irregular. However, testing is not mandatory, and in general should be gu ided by the patient \200\231s views, after a discussion of risks and bene \201 ts of furth er investigation and treatment (see b \200\230Prostatic cancer: presentation \200\231, p.5 14 and b \200\230Prostate-specific antigen \200\231, p.516) Cystoscopy and USS . If haematuria is detected, to exclude renal and bladder cancer BENIGN PROSTATIC HYPERPLASIA: PRESENTATION 511 Box 19.1 International prostate symptom score (IPSS) This is a well-validated, widely used assessment tool that can be either self-administered, or given as part of a structured assessment by a health professional. Aggregate scores fro m the seven questions to give a total score range of 0 \200\22335 (Table 19.1 ): \200 0 \200\2237 Mildly symptomatic \200 8 \200\22319 Moderately symptomatic \200 20 \200\2233 5 Severely symptomatic Table 19.1 International prostate symptom score e m e m i t e m i t e h t e h t i t f l a h s y a w l a e h t f l a h 5 f l a h n a h t n l l a n a h t i e m t s o m A t a t u o b A e r o M i t s s e L t o N 1 < l 0 1 2 3 4 5 Incomplete emptying. Over the past month, how often have you had a sensation of not emptyin g your bladder completely after you \201 nish urinating? 0 1 2 3 4 5 Frequency. Over the past month, how often have you had to urinate again<2hr after you \201 nished urinating? 0 1 2 3 4 5 Intermittency. Over the past month, how often have you found you stopped and started again several times when you urinated? Urgency. Over the past month, how dif \201 cult have you found it to postpone urination? 0 1 2 3 4 5 Weak stream. Over the past month, how often have you had a weak urinary stream? 0 1 2 3 4 5 Straining. Over the past month, how often have you had to push or strain to begin urination ? 0 1 2 3 4 5 e r o m r o s e m s e m s e m s e m e m e n o N i t i t i t i t i t 1 2 3 4 5 0 1 2 3 4 5 Nocturia. Over the past month, many times did you most typically get up to urinate, from th e time you went to bed until the time you got up in the morning? 512 CHAPTER 19 Genitourinary medicine Benign prostatic hyperplasia: treatment Treatment choice is in \202 uenced by patient pref erence, severity of symptoms, presence of complications, and \201 tness for surgery. Conservative measures \200\230Watchful waiting \200\231 is reasonable if symptoms are mild or moderate and complications absent. Reassure the patient. Reassess clinically and check renal function at 6 \200\22312 monthly intervals. Advise reduction in evening \202 uid in take; stop unnecessary diuretics. The main risk is acute urine retention (1 \200\2232 % per year). Herbal preparations These are widely used by patients, bought \200\230over the counter \200\231; always ask about non-prescription remedies. The most widely used is saw pal- mett o ( Serenoa repens ) extract, and there is some evidence that it works, especially in milde r disease, perhaps acting as a 5-A-reductase inhibitor (see b \200\230Drugs \200\231, p.51 2). PSA levels may therefore be reduced. Drugs Suitable for mild, moderate, or severe symptoms without complica- tions, especially i f patient preference is strong. Patients with more severe symptoms bene \201 t most. Two d rug classes may help: \200 A-adrenergic blockers ( \200\230 A -blockers \200\231 eg doxaz osin, terazosin, tamsulosin). They relax prostatic smooth muscle, increasing urine \202 ow rates and reducing symptoms in days. Side effects are common: the most important are hypotension, especially orthostati c hypotension, and syncope. Use cautiously, starting with low dose (eg doxazosin 1mg od, in creased in 1mg increments at 2-week intervals to 4mg). Exercise great caution if prescribed with diuretics or other vasodilators, if there is a past history of syncope, and in the fr ail. Tamsulosin may be more prostate-selective than other A -blockers and may have fewer ci rculatory side effects 5-A-reductase inhibitors (eg \201 nasteride). These inhibit prostatic testosterone metabolism, reducing prostatic size. Bene \201 t occurs slowly (months) and i s most likely if the prostate is large ( > 40mL); those with mild enlargement bene \201 t little or not at all. Side effects are uncommon but include erectile dysfunction (<5 % ), g ynaecomastia, and loss of libido. Given the absence of cardiovascular side effects, 5-A-red uctase inhibitors may be a better option in the frail older person. PSA levels fall by 750 % , so double the observed value to give an indication of prostate cancer risk Combination treatment . There is no evidence that this is more effective than monotherapy. If there is no signi \201 cant bene \201 t with one drug class, switch to another, or con sider surgery BENIGN PROSTATIC HYPERPLASIA: TREATMENT 513 A -Blockers, prostatism, and hypertension Many men have symptoms of prostatism and are also hypertensive. A -blockers can be an attractive option as the one drug may treat both. Howe ver, the evidence for A -blockers in the treatment of hypertension is inferior than that fo r several other drug classes. Assess the impact on each problem separately, and consider pr escribing the most appro- priate treatment for each individual condition. See b \200\230HO W TO Use anti-hypertensives in a patient with comorbid conditions \200\231, p.271. Surgery More effective than drugs or \200\230watchful waiting \200\231, but side effects a re more common and usually irreversible. Indicated if: \200 Symptoms are moderate or seve re (with patient preference) \200 There are complications (recurrent UTI or haematuria, r enal failure) \200 A trial of drug treatment has failed Transurethral resection of the pr ostate (TURP). The (gold-) standard procedure. Success rates are > 90 % . Adverse effects i nclude retrograde ejaculation (most), erectile dysfunction (5 \200\22310 % ), incontinence (1 % ) and death (<1 % ). 10 % need further surgery within a few years. Newer procedures . Several have been developed. They are generally less invasive and probab ly have fewer adverse effects, but long-term outcome data are less good. Local availability and expertise are limited. For example: \200 Transurethral incision. of the prostate (TU IP). Effective in those with smaller prostate glands. Low incidence of side effects Transurethral microwave thermotherapy (TUMT) and transurethral needle ablation (TUNA). These newer systems are well tolerated, and require only local anes thesia in an outpatient setting. However, some are time-consuming and dif \201 cult to lea rn, long-term results are less well known, and availability varies locally Open prostatectomy is reserved for very large glands and where other interventions are need ed, eg removal of bladder stones. It is very effective, but comorbidity is higher. Urinary catheterization Urinary catheterization is an option where: \200 Symptoms are sev ere, or signi \201 cant complications have occurred (eg retention) Surgical mortality and morbidity would be high \200 Drug treatment has not been tolerated , or is unlikely to be effective A long-term catheter may be required if the patient fails a trial (or trials) without catheter. 514 CHAPTER 19 Genitourinary medicine Prostatic cancer: presentation A very common cancer in men, much more so with age: median a ge at diagnosis is over 70. However: \200 Most die with tumor rather than because of it \200 Most are asymptomatic, or have only obstructive symptoms \200 Many tumors do not pr ogress, even without treatment This leads to dif \201 cult management decisions, especiall y in older people, where life expectancy for other reasons may be low, and expensive, unple asant or risky treatments may not be worthwhile. Assessment Predictors of an adverse disease course (symptoms, local progression, metastases and death) include more advanced stage (TNM classi \201 cation) and histological grade (e g Gleason score: see b \200\230Gleason score \200\231, p.514). Localized cancer \200\224 often detected when evaluating a man with lower tract symptoms due to BPH (by \201 nding an elevated PSA), or incidentally, eg, at TURP for BPH. Tumor remains within the gland caps ule; the tumor focus may be very small, and in no way responsible for symptoms. DRE may be normal. Prognosis is generally good, especially if grade is favorable. Cure may be possible , although for more indolent tumors, attempts at cure (surgery, radiotherapy) may be worse than the disease. Locally advanced cancer without metastases \200\224 usually detected in patients with urin ary symptoms, or at DRE performed for other reasons. A much larger group now that PSA testi ng is more common. The tumor has broken through the capsule, and prognosis is more adverse. Cure is not usually possible, but survival may be prolonged. Metastatic cancer \200\224 up to half of newly diagnosed patients have metastatic disease. Many are asymptomatic. Features (decreasing frequency) include urinary symptoms, bone pain , constitutional symptoms (eg weight loss), renal failure, pathological fracture, and anemi a due to bone marrow in \201 ltration. A minority have an indolent course, and with treatm ent may survive many years. Gleason score A histological grading system that correlates well with outcome and helps gui de treatment choice. A composite of two scores (each range 1 \200\2235), therefore range 2 \200\22310: \200 2 \200\2234: Well differentiated \200 5 \200\2237: Moderately differen tiated \200 8 \200\22310: Poorly differentiated Screening There is no good evidence that earlier detection through screening improves progn osis. This often requires careful explanation. Rectal exami- nation is insensitive: tumors detected in this way are often large and locally advanced. PSA has its own drawbacks (see b \200\230Prostate-speci \201 c antigen \200\231, p.516). PROSTATIC CANCER: PRESENTATION 515 Tests These should be selected advisedly, after considering the patient \200\231s wishes, t he implications of a negative or positive result, and any risks of the test. \200 PSA . S ee b \200\230Prostrate-speci \201 c antigen \200\231, p.516 \200 FBC . Evidence of marr ow in \201 ltration \200 Serum calcium, LFTs . Evidence of metastases \200 U,C + E . E vidence of post-renal renal failure \200 Transrectal ultrasound and biopsy . Provides tis sue for histological diagnosis and grading. Risks hemorrhage and infection Bone scan or X-rays . If there are symptoms, or bone biochemistry is suggestive. Metastasis to bone is common; appearance is sclerotic much more commonly than lytic CT/MRI scan . For tumor staging where surgery is contemplated 516 CHAPTER 19 Genitourinary medicine Prostate-speci \201 c antigen PSA is made in the prostate and blood levels re \202 ect pr ostatic synthesis. Using PSA It has two de \201 nite useful roles: \200 In very early detection of localize d prostate cancer when treatment may be curative In tracking tumor progression: changes in PSA usually re \202 ect changes in tumor mass Screening with PSA PSA is produced by both benign and malignant prostatic tissue, and there is no single useful cut-off point that separates those with cancer from those without: \200 Two-thirds of men with a high PSA do not have prostate cancer \200 One- \201 fth o f men with prostate cancer have a normal PSA The higher the PSA level, the more likely is c ancer. However, even at moderately high levels (>10microgram/L) the positive predictive val ue is only 65 % . Speci \201 city is even less in older people as the benign causes of ele vated PSA are more common. Combining this with the limitations of treatment, any screening program utilizing PSA yields: \200 Many people with high PSA, but no cancer is found afte r further tests \200 Many people with locally advanced prostate cancer for whom early treatment is not known to improve prognosis Non-malignant causes of increased PSA PSA increases with age and with: \200 BPH \200 Pr ostatitis \200 Urinary tract infection \200 Rectal examination (up to 7 days) \200 Pr ostatic biopsy (6 weeks) \200 Urethral catheterization \200 Urethral instrumentation, e g cystoscopy \200 Vigorous exercise (48hrs) \200 Ejaculation (48hrs) (Figures in bracke ts are approximate durations of elevation.) Age-speci \201 c PSA values The following have been suggested as cut-off points to reduce unnecessary referral and investigation of patients with benign prostate disease. \200 50 \200\22359 years: (cid:116) 3.0microgram/L \200 60 \200\22369 years: (cid:116) 4.0microgr am/L \200 (cid:116) 70 years: (cid:116) 5.0microgram/L PSA reduces with some drug treatme nt (eg 5-A-reductase inhibitors; herbal remedies such as saw palmetto ( S. repens )), and m ay therefore reduce the thresholds given for referral. This page intentionally left blank 518 CHAPTER 19 Genitourinary medicine Prostatic cancer: treatment \200 Localized cancer \200\224 there are several treatment o ptions, including \200\230watchful waiting \200\231, hormonal treatment, radiotherapy, and surgery. Cure can often be achieved \200\230 Watchful waiting \200\231 \200\224 usually reserved for those with modest life expectancy (<10 years) and lower grade (Gleason score 2 \200\2236) localized tumors, where progression is rare within 10 years. Check PSA every 4 \200\2236 months. Start treatment (u sually hormonal) if symptoms, or if PSA rises Hormone treatment \200\224 there is doubt whether early hormone treatment improves outcome compared to \200\230watchful waiting \200\231 Radiotherapy \200\224 the most usual choice for high-grade localized tumors. Probably as effective as surgery, but better tolerated. Side effects include erectile dysfu nction, irritative urinary symptoms, and radiation proctitis Surgery \200\224 radical prostatectomy is a major procedure, usually indicated only for th ose with long life expectancy, high-grade tumors, and in good health. Major side effects ar e incontinence, impotence and hemorrhage Locally advanced disease without metastases \200\224 key treatments are radiotherapy (also discussed here) and/or androgen deprivation (also discussed here). The r elative bene \201 ts are unclear. Surgery probably offers no bene \201 t, other than TURP to relieve out \202 ow symptoms \200 Metastatic disease \200\224 androgen deprivation ( \200\230hormone treatment \200\231) is the linchpin of treatment. This can be achieved by castration (bilateral orchidectomy, usua lly under local anesthesia), but is usually chemical, largely for reasons of patient prefer ence. Treatment should not be delayed, even if there are no symptoms. Luteinizing hormone r eleasing hormone (LHRH) agonists are used commonly and are usually effective for 12 \200 \22318 months. If disease progresses despite LHRH agonists, patients occasionally respond t o antiandrogens. Surgery offers no bene \201 ts LHRH agonists (eg goserelin) \200\224 given as injections or implants, these cause initial (2 weeks) stimulation and then sustained depression of testosterone release. The initial i ncrease can cause tumor growth ( \200\230 \202 are \200\231) with adverse effects, eg urin ary out \202 ow obstruction, spinal cord compression, or bone pain. If anticipated, anti-a ndrogens may help. Continuous therapy is not needed: survival appears similar if therapy is stopped when PSA levels are normal and restarted when they rise Antiandrogens (eg bicalutamide, \202 utamide) \200\224 useful in inhibiting tumor \202 are after LHRH agonist initiation, in tumor refractory to LHRH agonists, if LHRH agonists are not tolerated or accepted (eg because of erectile dysfunction) or where oral drugs are preferred. There is no evidence that combined antiandrogens and LHRH agonists are helpful Side effects of LHRH agonists and antiandrogens include hot \202 ushes, erectile dysfunct ion, and gynaecomastia. PROSTATIC CANCER: TREATMENT 519 Late-stage prostate cancer Eventually, prostate cancer may become resistant (refractory) to hormone treatment, manifesting as a rising PSA and/or worsening symptoms whilst on treatme nt. Other treatments (eg oestrogens) may be tried, but are rarely very effective. Death fol lows, often in months. Common complications, usually in more advanced disease, include: Bone pain A major cause of reduced quality of life \200 Optimize oral analgesia: combinations of pa racetamol, opiates and NSAIDs are effective Local pain is helped by radiotherapy \200 Bisphosphonates or steroids may also help Pathological bone fracture Usually requires surgical \201 xation Acute urine retention Catheterize \200 Intensify anti-tumor treatment if appropriate (eg hormone treatment, radiotherapy) Consider TURP Post-renal renal failure \200\224 determine site of obstruction by ultrasound: Prostatic obstruction: catheter, TURP, intensify anti-tumor treatment Ureteric obstruction: stenting or nephrostomy Spinal cord compression An emergency, as early decompression improves neurological outcome Con \201 rm with CT or MRI \200 Steroids, radiotherapy, or surgery help decompress the c ord 520 CHAPTER 19 Genitourinary medicine Postmenopausal vaginal bleeding De \201 ned as bleeding from the genital tract over 1 year after onset of menopausal amenorrhoea. The time criterion re \202 ects the fact that men- struation is often irregular and infrequent around menopause, and investi- gations for sin ister pathology are not then worthwhile. Most cases are secondary to benign pathology, but treatment of the few cases of cancer (lar gely endometrial) is far more effective if identi \201 ed early, so do not delay assessmen t. Malignancy is more likely if bleeding is signi \201 cant and recurrent \200\224 invest igate vigorously if no cause is apparent. Causes of post-menopausal vaginal bleeding In approximate order of frequency: Atrophic vaginitis In \202 ammation results as the thinner, less corni \201 ed epithelium is exposed to a more alkaline vaginal environment colonized by a broad microbial \202 or a Endometrial hyperplasia Secondary to: \200 Exogenous estrogen (eg HRT) \200 Unopposed e ndogenous estrogen (especially in older, obese women where peripheral conversion of steroid hormones to oestrogens by fat cells is higher) Benign tumor, eg cervical or endometrial polyps \200 Vaginal prolapse and ulceration Vagi nal infection Carcinoma \200 Endometrial \200 Cervical \200 Vulval \200 Vaginal \200 Ovarian Spurious Other relatively common causes of \200\230vaginal \200\231 bleeding are haematuria and rectal bleeding. Drugs causing endometrial disease (hyperplasia, polyps and cancer) include: \200 HRT (with cyclical replacement: investigate if bleed at unexpe cted times; for continuous estrogen and progestogen: investigate if irregular bleeding pers ists for > 12 months after treatment initiation) Tamoxifen (via a paradoxical endometrial estrogen-like effect) After hysterectomy bleeding is commonly due to atrophic vaginitis or overgrowth of post-surgical granulation tissue. POSTMENOPAUSAL VAGINAL BLEEDING 521 Assessment \200 History \200\224 assess the amount and frequency of bleeding, if necessa ry by discussing with carers. Consider other possible sources of blood, eg urinary, rectal. Take an accurate drug history. Examine \200\224 examine the genitalia, perineum, and rectum to exclude tumor, trauma, and bleeding from atrophic sites. Obesity or osteoarthritis may make examina tion dif \201 cult; the left or right lateral positions are usually more successful. Investigation \200\224 FBC to exclude severe anemia. Urine dipstick for haematuria is unlikely to be speci \201 c to blood of urinary tract origin, especially if bleeding is recurrent or ongoing.