MRSA reduction continues to be a political target in the UK Contamination and transmission \200 Anything coming into contact with an MRSA source can become contaminated \200\224 ie MRSA will exist for a short time on that surface \200 Transient carriage on the gloves or hands of healthcare workers is likely to represent the main mode of transmission to other patients \200 Up to 35 % of environmental surfaces in a room be ing used by an MRSA patient will culture positive (role in transmission is unclear) Decontamination involves cleaning. Good hand hygiene and the use of alcohol hand gel after patient contact reduce transmission signi \201 cantly Colonization \200 This is asymptomatic carriage of MRSA. Patients and families often need reassurance that this rarely has implications for the patient \200 Common sites are ante rior nares, perineum, hands, axillae, wounds, ulcers, sputum, throat, urine, venous access sites and catheters Duration of colonization varies from days to years \200 Transmission from a colonized per son is more likely if there is a heavy bacterial load with abnormal skin (eg ulcers, eczema), devices (eg catheters, cannula e) or sinusitis/respiratory tract infection Many healthcare workers are colonized (usually nasal) and are a potential reservoir, but usually colonization is short lived so that screening healthcare workers is only useful for investigating speci \201 c outbreaks \200 Screening for MRSA colonizatio n is now routine practice prior to elective procedures and for most hospital admissions especially inter- hospital transfers. Eradication of MRSA may follow; treatment regimens include the application of nasal mupiroc in, antimicrobial soaps and sometimes oral antibiotics (eg fusidic acid, rifampicin) Further reading Of \201 ce of National Statistics online : M www.statistics.gov.uk . 612 CHAPTER 24 Infection and immunity Disease caused by MRSA The most common sites of infection are: \200 Wounds \200\224 most common cause of postoperative wound infections \200 Intravenous lines \200\224 often le ading to bacteraemia \200 Ulcers \200\224 including pressure, diabetic, and venous ulcer s \200 Deep abscesses \200\224 infection can seed to many sites, eg lungs, kidneys, bones, liver, and spleen Bacteraemia \200\224 there is compulsory reporting 30 \200\22360 % of hospital patients co lonized with MRSA will go on to develop infection. This is more likely if there has been: \200 Recent prior hospitalization \200 Surgery or wound debridement \200 Invasive proc edures (including venepuncture and venous cannulation) Infections due to MRSA cause increas ed morbidity and mortality, longer hospital stays, and increased cost compared with a susce ptible organism. Management Infection control measures to reduce the reservoir and lower the rate of transmi ssion are crucial (see b \200\230HOW TO Control MRSA \200\231, p.613). Antibiotic treatment is necessary when there is active infection \200\224 do not use for c olonization, as this will promote drug resistance. Opposing responsibility to the patient ( use the best drug available) and the com- munity (do not promote antibiotic resistance) mus t be weighed up. The choice of drug will depend on local resistance patterns and the severi ty of the infection. Where possible, wait for sensitivities from microbiology. Options include: Glycopeptide antibiotics (eg vancomycin, teicoplanin) \200\224 must be given intravenously; resistance is emerging Co-trimoxazole \200\224 useful for susceptible skin, soft tissue and infections \200 Fus idic acid, rifampicin, and doxycycline \200\224 can be effective, usually given in combination Clindamycin \200\224 used for deeper infections, but most UK strains are resistant Fluoroquinolones \200\224 eg cipro \202 oxacin. Resistance is rapidly emerging \200 Lin ezolid \200\224 an oxazolidinone antibiotic with equivalent potency to vancomycin. Can be given orally or intravenously. Use with caution because of high cost and less certain side effect pro \201 le (bone marrow toxicity common, especially with prolonged use) DISEASE CAUSED BY MRSA 613 HOW TO Control MRSA Identify the MRSA type During an outbreak, the microbiology laboratory will be able to dete r- mine if this is a cluster of unrelated cases, or a series of infections by a single stra in \200\224 the latter indicating either high transmission rates or an ongoing reservoir. Identify the reservoir \200 Commonly a patient with a heavily colonized or infected wound \200 Healthcare workers may also act as reservoirs \200 During an epidemic, it is usua l to attempt to eradicate MRSA from likely reservoir sources (using nasal mupirocin, antimi crobial soap and oral antibiotics) Reduce transmission rates Transmission usually occurs from patient to patient via a healthc are worker. This is often when hands or gloves are transiently contaminated. \200 Hand hy giene is the single most important factor in infection control. Good hand washing technique and bedside alcohol-based hand gels should be used by staff, visitors, patients, therapist s, volunteers, and service personnel after touching a patient Known MRSA patients should be isolated where possible \200 Gloves should be worn on enter ing and removed before leaving the room Gowns/aprons should be used if contact with the patient or environment is anticipated, or if the wound is open Masks may reduce nasal acquisition by healthcare workers \200 Patients should be moved ab out the hospital as little as possible. Radiological investigations should be done at the e nd of a list to allow cleaning after the test Minimize the use of foreign devices (eg catheters, NG tubes) \200 Use dedicated equipment (eg stethoscopes, blood pressure cuffs, thermometers), or clean carefully after use Active surveillance for MRSA colonization allows these procedures to be put in place earlier 2By following these guidelines, it is estimated that 70 % of transmission can be prevented Problems in geriatric care \200 Isolation can cause problems with depression and lack of social stimulation Patients and carers may feel stigmatized or scared by the diagnosis \200 Rehabilitation m ay be restricted (eg if the patient is con \201 ned to a side room and cannot visit the ph ysiotherapy gym or practice mobilizing about the ward) It may be dif \201 cult to enforce isolation in patients with dementia \200 Moving to nu rsing homes or community facilities may be delayed (eg while waiting for a side room) 614 CHAPTER 24 Infection and immunity Clostridium dif \201 cile -associated diarrhea C. dif \201 cile is a Gram-positive, spore forming, anaerobic bacillus. It was rarely described before the late 1970s but is now a ma jor hospital acquired infection. CDAD causes a huge burden of morbidity, mortality and cost , but incidence has diminished in response to more focused antimicrobial therapy and effect ive infection control measures (annual death rate from CDAD in UK fell from around 6000/yea r to 4000/year between 2008 and 2009). Pathogenesis \200 Asymptomatic C. dif \201 cile carriage occurs in less than 5 % of popu lation \200 Spores persist for months to years in the environment and are resistant to ma ny traditional cleaning \202 uids. Vegetative forms and spores can be transmitted from pa tient to patient Gastrointestinal carriage is increased in the hospital population, with advancing age, othe r bowel disease, cytotoxic drug use and debility (eg recent surgery, chronic kidney impairm ent, cancer) Most antibiotics reduce the colonization resistance of the colon to C. dif \201 cile . CDAD occurs when toxins (A and B) elaborated by C. dif \201 cile bind to the colonic mucosa, causing in \202 ammation Outbreaks in hospital can occur from cross-infection and can affect patients never exposed to antibiotics Features There is a wide range of manifestations from asymptomatic carriage to fulminant co litis. Most commonly presents with: \200 Foul-smelling watery diarrhea (mucus common but rarely blood) \200 Abdominal pain and distension \200 Fever In severe cases can mimic a n \200\230acute abdomen \200\231. Occasionally causes chronic diarrhea. 2 Beware that an a cute decline in a patient \200\231s condition (eg fever, delirium or metabolic disturbance) can precede prominent diarrhea; have a low threshold of suspicion in patients with multipl e risk factors. Investigations \200 Raised white cell count and in \202 ammatory markers (following trea tment of another infection, differential diagnosis includes relapse of the original infection) C. dif \201 cile toxin detection by enzyme-linked immunosorbent assay (ELISA) is both sens itive and speci \201 c for CDAD colitis. The test can remain positive for weeks after reso lution, so is not useful in diagnosing recurrence AXR or CT may show distended, thick-walled large bowel \200 Sigmoidoscopy is often normal in mild disease or where colitis affects proximal bowel. In more severe cases, a character istic colitis with pseudomembrane formation is seen (also known as pseudomembranous colitis ) CLOSTRIDIUM DIFFICILE-ASSOCIATED diarrhea 615 Complications Rarely occur, and include toxic megacolon, paralytic ileus, perforation, and bacteraemia. Older patients requiring surgery have at least 50 % mortality. Relapse De \201 ned as a second event within 2 months. Occurs in around 20 % . Only rarely due to antibiotic resistance, but can be dif \201 cult to treat. Patients with recurrence are then more prone to further repeated infection. For repeated infection and recalcitrant CDAD, options include: \200 Further oral antibiotics, eg metronidazole, vancomycin, baci tracin \200 Adjuvant therapy with colestyramine \200 There is very limited evidence tha t probiotics such as yeast or lactobacillus help induce and maintain remission Intravenous immunoglobulins and steroids have been used in severe recalcitrant colitis 616 CHAPTER 24 Infection and immunity HOW TO Manage C. dif \201 cile infection Prevention Use antibiotics wisely (see b \200\230Antibiotic use in older patients \200\231, p.610): \200 Only when good evidence o f infection. Always try to obtain a microbiological diagnosis and only treat where you have diagnosed infection or if the patie nt is gravely ill and conservative management is judged unsafe Use the smallest number of antibiotics with the narrowest-spectrum possible. Some antibiotics are less likely to cause CDAD Use the shortest course possible: 3 days for a simple urinary UTI, 5 days for bronchitis, 10 days or longer for septicaemia, abscess, etc Treatment 2 Have a high index of suspicion \200\224 if the patient is ill commence treat- ment without waiting for con \201 rmatory tests \200 Stop antibiotics unless there is ve ry good evidence they need a longer course Suspend concomitant PPIs, iron, and laxatives \200 Aggressive rehydration \200\224 patie nts can become very hypovolaemic even before they start to get diarrhea Start antimicrobials according to local policy, eg metronidazole 400mg tds po or vancomycin 125micrograms qds po. Both drugs must be enteral to obtain high intraluminal levels. If un able to swallow consider NG tube or metronidazole PR 1g bd; iv therapy may be added if sept icaemia is suspected \200 Continue 7 \200\22310 days or until a formed stool \200 Stool chart will indicate if diarrhea frequency is improving \200 Use of loperamide (2mg with each loose stool) is controversial \200\224 it may mask response to treatment and increase chances of complications. However, proponents s uggest if the diagnosis is secure and treatment initiated it can reduce debilitating sympto ms and speed recovery Surgical complications may require colectomy Infection control \200 Nurse in side room wh ere possible \200 Alcohol gels do not kill spores \200 Use gloves and aprons for all co ntact. Wash hands well with soap and water Clean the environment thoroughly, especially after bed moves \200 Patients are much less infectious once diarrhea has resolved \200 Where possible avoid moving infected patients between wards This page intentionally left blank 618 CHAPTER 24 Infection and immunity Near-patient urine tests UTI is a common problem in older people, but there is an even high er prevalence of asymptomatic bacteriuria and positive urinalysis without infection. In gen eral, UTI is overdiagnosed. 2It is important to know how to diagnose a UTI correctly, and w hen to initiate treatment appropriately. Near patient urine tests (dipsticks) Quick, cheap test that is commonly performed. Should o nly be done on urine that is collected as described in b \200\230HOW TO Sample urine for dipstick, microscopy, and culture \200\231, p.619. Urinary nitrite \200 Positive result has a high predictive value for UTI \200 Many bact eria causing UTI convert urinary nitrate to nitrite, which is detected on dipstick False negatives occur with dilute urine \200 Certain bacteria (eg Pseudomonas, Staphyloco ccus, Enterococcus ) may not convert urinary nitrate, so the dipstick will be negative Leucocyte esterase \200 Positive result has a high predictive value for UTI \200 Lysed white cells release esterase, which is detected on dipstick \200 Corresponds to signi \201 cant pyuria \200\224 may not detect low levels \200 False-negative results also occ ur when there is glucose, albumin, ketones, or antibiotic in the urine False positives ( \200\230sterile pyuria \200\231) occur with vaginal contamination, chroni c interstitial nephritis, nephrolithiasis, and uroepithelial tumors. \200\230Sterile \200 \231 pyuria can indicate renal tuberculosis and STD (eg Chlamydia ) \200\224 consider test ing if history suggestive \200\230Blood \200\231 \200 Positive result for blood has a low predictive value for inf ection \200 Dipstick does not distinguish red cells from hemoglobin or myoglobin \200 D etects red blood cells (blood in the renal tract), hemoglobin (after haemolysis) and myoglobin (rhabdomyolysis) Causes of a positive \200\230blood \200\231 dipstick are varied and may be pre-renal (eg haemolysis), renal (eg tumors, glomerulonephritis), ureteric (eg stones), bla dder (eg tumors, occasionally infection), urethral (eg trauma) or contamination (eg bleedin g from the vaginal vault) Always repeat to ensure the haematuria has resolved with treatment \200 Management of per sistent isolated dipstick haematuria without apparent cause is dif \201 cult. In a \201 tter patient, referral for renal tract invest igation by a urologist may be appropriate NEAR-PATIENT URINE TESTS 619 Protein \200 Positive result has a low predictive value for infection \200 Commercial d ipsticks generally only detect albumin, and a positive result implies proteinuric renal disease False positives occur in very concentrated or contaminated urine 2The combination of nitrit es and leucocyte esterases on urine dipstick has the highest positive predictive value for infection. If these are negative and clinical suspicion is high, proceed to urinary microsc opy and culture. HOW TO Sample urine for dipstick, microscopy, and culture Do not sample \200 Stale urine \200 Urine that has been contaminated with feces \200 Urine from a catheter bag MSU sample \200 Ideal sampling method, but may be dif \201 cul t in confused or immobile patients The external genitalia should be cleaned, a small amount of urine voided, then the middle portion caught cleanly in a sterile container Analysis should be performed while the urine is fresh In-out catheter sample \200 Carries a small risk of introducing infection (around 1 % ) \200 Often well tolerated by older p atients \200 Discard the \201 rst urine, and sample the middle portion drained Suprapub ic aspiration of urine \200 Rarely done, but will provide a clean specimen \200 Clean t he skin, and percuss to identify the bladder \200 Aspirate with a green needle and 10mL s yringe in the midline Samples from catheterized patients \200 These should be sent only i f the patient is symptomatic, as the prevalence of positive dipstick is almost universal, a nd bacterial colonization of urine is common Clamp the catheter for a period, then collect an MSU sample directly from the draining tube sampling port Do not use stale urine that has collected in the bag 620 CHAPTER 24 Infection and immunity Asymptomatic bacteriuria De \201 ned as a positive urine culture in the absence of symptom s of urinary tract disease. \200 It becomes more common with increasing age (5 % of commu nity- dwelling females under the age of 60, rising to 30 % over the age of 80) It is less common in men but again increases with age (<1 % of those under 60, rising to 10 % over the age of 80) Up to 50 % of frail institutionalized patients and almost all catheterized patients will ha ve bacteria in their urine (see b \200\230Catheters \200\231, p.538) \200 Other risk fac tors are as for UTI (see b \200\230Urinary tract infection \200\231, p.621) Associated diseases include renal stones, diabetes, and chronic prostatitis in men What does it mean? \200 Probably represents urinary colonization rather than infection \200 No increase in mortality directly associated with asymptomatic bacteriuria Seems to be transient in most \200\224 only 6 % will grow the same organism over three seq uential cultures, however, it is estimated that around 16 % will go on to develop symptomat ic UTI Treatment No treatment is required for isolated bacteriuria. The use of antibiotics: \200 Does not impact on morbidity and mortality \200 Does not improve continence \200 Promo tes antibiotic resistance In addition, recurrence after antibiotic treatment is common. 2 A void treating patients unless they have symptoms. URINARY TRACT INFECTION 621 Urinary tract infection Major cause of morbidity and mortality in the older population. UTI s account for a fourth of infections in healthy older patients, and are the most common hos pital acquired infection. They are the most frequent cause of bacteraemia in older patients . The annual incidence is up to 10 % for older adults (but many are recurrent). Risk factors \200 Advancing age \200 Female sex (although the gap narrows with age) \200 Atrophic vaginitis and urethritis in women \200 Incomplete emptying (eg urethral st rictures, prostatic hypertrophy or carcinoma, neuropathy) Abnormalities of the renal tract (eg tumors, \201 stulae, surgery) \200 Foreign bodies (eg catheter, stones) \200 Chronic infection (eg renal abscess, prostatitis) Organisms \200 Escherichia coli is the most common, as in younger adults \200 Older patients are m ore prone to UTI caused by other pathogens, including other Gram-negative organisms (eg Pro teus , Pseudomonas ) and some Gram-positive organisms (eg group B Streptococcus , MRSA) Catheter-related UTI is often polymicrobial and antibiotic resistant Presentation The prese nce of symptoms is essential to make the diagnosis. Urinary frequency, dysuria (stinging or burning sensation on urinating), and new urinary incontinence are clear indications of uri nary infection, but symp- toms may be vague or atypical, and include: \200 Fever and gene ral malaise \200 Nausea and vomiting \200 Confusion or delirium \200 Deterioration in physical or functional ability Infection may be: \200 Uncomplicated UTI (normal renal tr act and function) \200 Complicated UTI (abnormal renal tract, patient debility, virulent organism, development of complications such as impaired renal function, bacteraemia, pyelon ephritis, and perinephric or prostatic abscess) \200 Recurrent UTI (see b \200\230Recurr ent urinary tract infection \200\231, p.623) \200 Catheter-associated UTI (see b \200 \230HOW TO Treat catheter complications \200\231, p.540) Investigations \200 Urinalysis \200\224 collect sample and perform dipstick (see b \200 \230HOW TO Sample urine for dipstick, microscopy, and culture \200\231, p.619) and se nd for microscopy and culture 2A negative dipstick does not exclude the diagnosis if the clinical suspi- cion is high. In such cases, send urine for culture. \200 If the patient is unwell, consider checking blo od tests, including kidney function (risk of impairment), blood cultures (risk of bacteraem ia), full blood count and in \202 ammatory markers 622 CHAPTER 24 Infection and immunity Urinary tract infection: treatment Treatment involves more than just antibiotics. Consider the following: \200 Adequate hydration (oral often suf \201 cient, sicker or more confus ed patients may require iv \202 uid) Medication review (consider suspending diuretics or drugs that are potentially nephrotoxic, such as non-steroidals or ACE inhibitors) \200 Management of symptoms (eg confusion or i mmobility may necessitate increased care at home, or even admission to hospital) Assessment for complications (eg pyelonephritis, bacteraemia, abscess formation). Older pat ients are at high risk of dehydration and renal impairment. Consider admission for iv antib iotics and hydration \200 Prevention of recurrence with measures such as ensuring good \202 uid intake and avoiding catheters if possible. Topical oestrogens (vaginally) may be useful in postmenopausal women Antibiotic choice Be guided by local sensitivity patterns and local guidelines. Uncomplicated UTI can be treated empirically as follows: Trimethoprim 200mg bd (if local resistance is <20 % ) \200 or Co-amoxiclav 375mg tds \200 or Nitrofurantoin 50mg qds \200 Cipro \202 oxacin 500mg bd is effective, but there are concerns about emerging resistance and CDAD Duration of treatment \200 Younger women with uncomplicated UTI can be successfully treat ed with a short course of antibiotics (3 days, or even a single dose) \200 There is limit ed evidence for the duration required in older patients, but it is likely that a longer course (5 \200\2237 days) is needed Treatment failure: Resistant organisms \200 Review the results of the urine culture and p athogen sensitivities \200 E. coli resistant to ampicillin and sulphonamides is widesprea d, and trimethoprim resistance is increasing. Most are susceptible to nitrofurantoin and \202 uoroquinolones (eg cipro \202 oxacin) at present, although \202 uoroquinolone resis tance is increasing Pathogens are more varied in older patients and these may not be susceptible to empirical treatment MRSA UTI may occur in older patients (especially with indwelling catheters), which may require iv therapy (eg vancomycin) Candida in the frail, catheterized older patient (seen on microscopy). \200 If no culture result is available, and the diagnosis is secure, try an empirical second-line agent such as co-amoxiclav or cipro \202 oxacin Incorrect diagnosis \200 Delirium and a positive urine dipstick may be misleading. Could the patient have another pathology? RECURRENT URINARY TRACT INFECTION 623 Recurrent urinary tract infection De \201 ned as > 3 symptomatic UTIs in a year, or > 2 in 6 months. May represent either a relapse (recurrent infection caused by original infecting organism) or a reinfection (infection with different species or strain). Urinary culture i s indicated. Recurrent infection This may be due to: \200 An ongoing source of infection (eg chronic p rostatitis, renal abscess) \200 Urological abnormality (eg stones, tumor, residual volume > 50mL, cystocoele) \200 Catheterization \200 Poor hygiene (eg fecal soiling) \200 Impaired i mmunity (eg diabetes, chronic disease) \200 Genetic susceptibility Treatment of recurrent infection \200 Repeat treatment with up to a week of antibiotics \200 Remove catheter if possible (see b \200\230HOW TO Manage urinary incontinence without a catheter \200\231, p.539) General measures include increasing \202 uid intake, treating constipation \200 Arrange renal tract ultrasound to look for residual volume and any urological abnormalities (lower threshold of investigation for males) Consider blood tests (eg glucose, renal function, FBC, serum electrophoresis, PSA in men) Prevention of recurrent infection \200 In postmenopausal women, topical oestrogens (cream , pessary, estrogen-releasing vaginal ring) are effective Maintain good hydration \200 There is some evidence that cranberry juice reduces symptoma tic UTI \200 Prophylactic antibiotics are rarely indicated. Consider when there are multi ple recurrences despite general measures or signi \201 cant renal damage. Consider low dos es of trimethoprim, nitrofurantoin, or amoxicillin, dependent on local resistance pattern Pre-emptive treatment can be useful in cognitively intact patients. A short course of antibiotics is held in reserve by the patient, to be taken when symptomat ic 624 CHAPTER 24 Infection and immunity Varicella zoster infection Initial exposure usually occurs in childhood, causing chickenpox . The virus lies dormant in the sensory dorsal root ganglia of the spinal cord and can be r eactivated later in life to cause shingles. Shingles is a painful, self-limiting, unilateral eruption of vesicles in a dermatomal distr ibution. It occurs in 20 % of the population at some time but is most common in older peopl e (probably due to a decline in cell- mediated immunity with age). Clinical presentation \200 Prodrome of fever, malaise, headache, and sensory symptoms (pa in, tenderness, or paraesthesia) in the dermatome to be affected \200 Rash follows after a fe w days, initially with a cluster of vesicles that spread across the dermatome and then become pustular 50 % affect thoracic dermatomes (T5 \200\223T12), 16 % lumbosacral, and 15 \200\22320 % cranial nerve distribution Usually affects single dermatome, but may involve several adjacent ones Can rarely affect motor nerves, with focal weakness \200 Acute herpetic pain is often a f eature \200\224 may precede the rash by days, and often described as sharp Crusting occurs after about a week, then the patient is no longer infectious (prior to this, susceptible individuals may catch chickenpox). Healing generally occurs within a month, but may leave scars \200 Recurrence in around 5 % Treatment \200 General measures include adequate oral \202 uid intake, simple analgesia (eg paracetamol) and topical agents such as calamine lotion Antiviral therapy (eg aciclovir 800mg 5 times a day, famciclovir 250mg tds, valaciclovir 1g tds) should be given within 72hr of rash onset to all patients over 50 years old, for a we ek. It reduces attack severity, promotes rash healing and reduces incidence of postherpetic neuralgia Prednisolone (eg 40mg tailing down over a week) can be given with antiviral therapy to redu ce the severity of the attack, but has limited value and possible drawbacks (eg increasing bacterial superinfection, causing signi \201 cant side effects) and should only be used wh ere the infection is severe Analgesia for neuralgia should be given early where indicated Ophthalmic shingles \200 More common in older patients \200 Occurs when the ophthalmic division of the trigeminal nerve is involved, resulting in a rash on the forehead and aroun d the eye \200 Ocular involvement commonly occurs, causing a red painful eye. In \202 ammation of the iris and cornea can cause vision loss, and topical steroid eye dro ps are used to limit the in \202 ammatory response Prompt use of antivirals may limit the disease VARICELLA ZOSTER INFECTION 625 Ramsay \200\223Hunt syndrome \200 Shingles of several adjacent cranial nerves cause vesic les in the ear canal, ear pain, and an LMN facial droop May also cause vertigo, deafness, and disturbance of taste + lacrimation 2Always look in th e ears for vesicles when a patient present with a facial palsy. \200 Facial paralysis is less likely to fully recover than in Bell \200\231s palsy \200 Treat with antivirals Post-herpetic neuralgia \200 Distressing sensory symptoms that persist months beyond rash onset \200 Occurs in up to 10 % of cases \200 More common in older patients (up to a t hird of those > 60) who have sensory symptoms at prodrome and a more severe initial infecti on \200 Subsides in the majority by a year; may become chronic and disabling \200 Usual ly a deep steady burning sensation, sometimes exacerbated by movement or touch. Occasionally paroxysmal and stabbing Can cause signi \201 cant psychological symptoms (low mood, poor sleep, loss of appetite, etc.) Treatment is with tricyclic antidepressants (eg amitriptyline 10 \200\223150mg nocte), opio ids, or anticonvulsants (eg gabapentin, carbamazepine, phenytoin) Topical treatments with lidocaine or capsaicin are also effective \200 Other options are used in specialist pain clinics, such as iv lidocaine, intrathecal steroids, or local nerve blocks Other complications All the following are more common in older patients: \200 Bacterial s uperinfection (around 2 % , can delay rash healing. Treat with topical antiseptic or antibi otic initially \200\224 more severe cases require systemic treatment) Motor neuropathy (occurs when virus spreads to the anterior horn; symptoms depend on segment affected, eg C5/6 may cause diaphragmatic paralysis. Major ity will recover spontaneously) Meningeal irritation (causes headache; occurs in up to 40 % ; the CSF shows reactive change s \200\224 lymphocytosis and elevated protein) \200 Meningitis and encephalitis (rare; d iagnosis enhanced by MRI imaging and CSF PCR. Usually occur with the rash, but may be up to 6 months later) Transverse myelitis (rare; occurs with thoracic shingles) \200 Stroke (rare and serious; due to cerebral angiitis) This page intentionally left blank 627 Chapter 25 Malignancy Malignancy in older people 628 HOW TO Describe performance status 628 An approach to malignancy 629 Presentation of malignancy 630 HOW TO Screen for malignancy 631 Treati ng malignancy in older people 632 HOW TO Manage symptomatic hypercalcaemia 633 Cancer with an unknown primary 634 628 CHAPTER 25 Malignancy Malignancy in older people Cancer is a disease of the elderly population, being relatively rare in people under 35 years of age, and increasing in incidence with each decade. Why is there more cancer in older people? \200 As more people avoid death from infection and vascular events, so they remain alive to develop cancer Some cancers are caused by cumulative exposure to environmental agents. A good example would be sunlight and skin cancer, or smoke and lung cancer, but die tary factors and exposure to other carcinogens are also likely to contribute over time The process of cell replication may senesce, increasing the chance of malignant change Is cancer different in older people? \200 Development of metastases may appear to be slow er, the cancer overall having a more indolent course, possibly due to altered immune or hormonal responses In contrast, some cancers appear to be more aggressive in older people (eg acute myeloid le ukemia, Hodgkin \200\231s disease, ovarian carcinoma) \200 Overall, age itself has limite d in \202 uence over disease progression and prognosis \200\224 factors such as comorbidi ty and performance status (Table 25.1 ) are much more important The impact of cancer may be different in an older person. Non-cancer deaths are common in f rail elderly people with malignancy, so cancer control by non-invasive means (eg tamoxifen for breast cancer) may be a better option than cancer cure by more unpleasant treatments (e g surgery) Never underestimate the psychological impact of a cancer diagnosis, whatever the age. Heart failure carries a worse prognosis than many cancers, yet news of its diagnosis rarely has such an impact. Whatever your assessment of a person \200\231s quality of life, they may se e things very differently \200\224 you will not know until you ask. The adverse reaction t o the diagnosis is often tied up with fears about a slow and painful death (rather than dea th itself) and careful explanation about symptom control measures may allay some concerns HOW TO Describe performance status Table 25.1 Performance status scoring 0 Active, no limitations 1 Active, but unable to carry out strenuous or heavy physical work 2 Active, spending less than half the day in bed or resting 3 Spend over half the day in bed or resting, but still able to get up 4 Bedridden AN APPROACH TO MALIGNANCY 629 An approach to malignancy Make the diagnosis \200 Even if no curative treatment is possib le, a diagnosis allows targeted symptom control and gives an idea about the likely course o f the disease and the expected prognosis Many people \201 nd \200\230not knowing what is wrong \200\231 very hard, and may \201 nd a diagnosis a relief, as it allows the future to be planned Sometimes a frail patient is obviously dying, and investigations can be an additional burde n, without hope of \201 nding reversible pathology. In this case, blind palliation of sym ptoms is the best course. This should be combined with careful explanation to the patient a nd family \200 There are many shades of gray in between these two extremes. In some cases , \201 nding multiple metastases on a scan may be enough to plan management. In others, a histological diagnosis by biopsy is required to fully balance risks and bene \201 ts of t reatment. Each individual should have bene \201 ts of diagnosis weighed up against discomf ort (and cost) of investigation Once diagnosis is made, attempt to stage the disease This allows accurate prognostication a nd gives the patient better information on which to base treatment decisions. Again, there are exceptions to this (eg the very frail who are likely to die from other causes), and eac h individual should be considered separately. Assess patient factors that will in \202 uence outcome 2 Age is not one of these factors \200 Comorbidity will adversely affect both disease prognosis and tolerance to treatment Functional status is the other main predictor \200\224 is the patient active and asymptoma tic, active but with symptoms, slowed down by symptoms or incapacitated by them? Oncologist s use performance status (see Table 25.1 ) as an indicator of functional ability and a scor e of (cid:100) 3 correlates with a median survival of 3 months. Comorbid conditions and poo rer functional status will be more common in older people, but not universal, so purely age -related treatment decisions are unwise. Utilize a specialist multidisciplinary approach Cancer care changes rapidly, and it is hard for the generalist to keep up to date, so specialist referral is usually needed. Many diff erent specialists work together in MDTs to provide cancer management, determining the best options individually. Specialist nurses often perform a coordinating role in the patient \200\231s journey through the system, providing consistent, non-threatening support, allowi ng fears to be discussed and providing practical help (eg arranging additional help at home ). Discuss decisions carefully with the patient Some patients who have led a long and healthy life (and so would poten- tially do well from therapy) may wish simply to die without being \200\230messed about \200\231. Other patients with multiple problems and poorer outlook m ay take any chance at a prolongation of life whatever the cost. 630 CHAPTER 25 Malignancy Presentation of malignancy In a cognitively intact and physically \201 t older patient wi th a malignancy, presentation is often typical \200\224 eg a breast lump, a thyroid nodule , altered bowel habit with an iron de \201 ciency anemia. In these cases, there is little dilemma \200\224 management is as for all patients with such a complaint. In the frail elderly person, the presentation is often less clear. Cancer may be found inci dentally (eg a mass on a routine CXR) or there may be a highly suggestive clinical scenario . Judging how hard to look and to what end is a common challenge in geriatric practice. Common presenting scenarios include Weight loss without apparent cause \200 Always check a dietary history (and corroborate it with family or friend), measure thyroid function, screen for depression, and assess cognitive state If there are no localizing symptoms or signs on careful history or examination, then check screening investigations (see b \200\230HOW TO Screen for ma lignancy \200\231, p.631) If these are normal, then malignancy is relatively unlikely, and dietary support with reass essment at an interval may be appropriate (see b \200\230HOW TO Manage weight loss i n older patients \200\231, p.357) Following up hints offered in a systems enquiry (eg admits to occasional loose stool) will depend on the individual patient \200\224 whether they would tolerate bo wel investigation, whether they would be \201 t for treatment if malignancy is found and, crucially, what they wish to do Elevated in \202 ammatory markers (ESR, CRP) \200 This is a relatively common scenario \200 Begin with the screening history, examination and investigations \200 An important differential diagnosis is sepsis, and this should be actively sought with cultures and appr opriate tests such as echocardiogram \200 Consider giving the patient a thermometer and t emperature chart to \201 ll in Look at joints and bones as a possible source (gout, septic arthritis, discitis, osteomyelitis, etc.) Remember diverticular and sub-diaphragmatic abscesses \200 Have a low threshold for think ing of endocarditis (see b \200\230Overview of infection in older people \200\231, p.608) Vasculitides (especially see b \200\230Giant cell arteritis \200\231, p.474) should be con sidered and a trial of steroids may be appropriate, even if the history is not convincing, but remember to check response and rethink the diagnosis if the blood results do not normal ize A CT scan of the thorax, abdomen and pelvis (looking for lymphadenopathy) may be justi \201 ed if the patient is otherwise \201 t and has signi \201 cantly abnormal tests Chasing mildly elevated markers in the frail elderly person is often unrewarding, and can b e very distressing for the patient. If initial assessment is unhelpful, watchful waiting my be a valid approach PRESENTATION OF MALIGNANCY 631 Anemia \200 Iron de \201 ciency anemia should always raise the query of gastrointestinal malignancy, and investigation tailored to the individual situation (see b \200\230Iron de \201 ciency anemia: diagnosis \200\231, p.454) \200 A normochromic norm ocytic anemia with normal haematinics is rather more dif \201 cult \200\224 it may repres ent anything from mild myelo \201 brosis or renal failure to disseminated malignancy Screening history, examination, and tests should be performed. If normal, then a decision about suitability for bone marrow biopsy needs to be made on an ind ividual patient basis. Does the patient have a reasonable life expectancy? Would treatments (eg chemotherapy) be appropriate if hematological malignancy was con \201 rmed? HOW TO Screen for malignancy History Should include: \200 Dietary history \200 Mood assessment \200 History of fev ers and night sweats \200 Travel history \200 HIV risk factor assessment (if appropriat e) \200 Full systems enquiry (especially meticulous enquiry into gastrointestinal symptoms and postmenopausal bleeding)