Balance bene \201 ts against risks of immobility and complications (thrombosis, deconditioning) \200\224 usually only used for very resistant ulcers when adm ission to hospital may be required Elevating the foot of the bed mattress at night is helpful (easiest with electronic hospita l beds, otherwise use a wedge under the mattress) \200 During the day, sitting with the f eet on a stool is better than nothing, although it fails to raise the legs high enough Elevation should not be used when peripheral arterial disease predominates \200\224 \201 rst check pedal pulses and ABPI (see b \200\230HOW TO Measure ABPI \200\231, p.305) Ulcer care \200 Clean the ulcer by irrigation with saline \200 Debridement of dead tiss ue may improve healing (no trial evidence): Scalpel (local anesthetic cream may make this less uncomfortable) \200 Maggots (consume o nly dead tissue, leaving behind the healthy) \200 Facilitating the body \200\231s own sys tem by creating a moist environment \200 Chemical agents are not recommended (as they als o harm healing tissue) No single wound dressing has been shown to improve healing \200 An ideal dressing keeps t he wound moist with exudate, but not macerated, at an ideal temperature and pH for healing without irritants, excessive slough, or infection Simple, low-adherent, and low-cost dressings are the mainstay \200 Impregnated dressings (eg with antiseptic, antibiotic, debriding enzymes, growth factors or silver sulfadiazine) can cause contact allergic or irritant derm atitis (up to 85 % of patients), worsening the ulcer, so avoid in routine use Occlusive or semi occlusive dressings can aid with pain relief \200 Gel and hydrocolloid dressings can be useful to remove exudates \200 Metronidazole or charcoal dressings can b e used for odor control MANAGEMENT OF VENOUS LEG ULCERS 595 Compression bandaging \200 Mainstay of treatment for venous ulcers \200\224 when correct ly applied, leads to healing for 70 % in 3 months Ensure that the ABPI is > 0.8 (see b \200\230HOW TO Measure ABPI \200\231, p.305) When mixed etiology ulcers are present, some compression is often required, but this has to be carefully moderated to compensate for the arterial insuf \201 ciency Provides an active counter-pressure to venous blood pressure, and enhances the function of the muscle pump Graduated four-layer compression from the ankle to the knee (wool bandage, crepe bandage, elasticated bandage and \201 nally a self-adhesive elasticated ba ndage Should be comfortable, allow the patient to continue with daily life (eg wear shoes as usua l) and last a week (unless highly exudative) Should be applied by an experienced practitioner, as incorrect bandaging can cause more harm than good Intermittent pneumatic compression therapy may be useful for patients for whom standard com pression stockings may be ineffective or not tolerated (eg morbid obesity, severe oedema) Oral agents \200 Aspirin . May improve ulcer healing time \200 Diuretics . Short course s may reduce oedema \200 Antibiotics . Most ulcers are permanently colonized (commonly staphylococci, streptococci, E. coli , Proteus , and Pseudomonas ) and routine use of oral antibiotics will only promote resistance. Wound swabs will only grow these colonizing organ isms and are not indicated. Treat with systemic antibiotics only if there is evidence of sp reading infection (rapidly increasing size, increased pain, surrounding erythema, tracking up lymphatics system, or systemic upset) Other agents . eg pentoxifylline. May have a role in ulcer management but evidence is not robust Surgery \200 Skin grafts may be helpful. Pinch or punch skin grafts may stimulate healing Surgical correction of deep vein incompetence is considered where bandaging has failed. Involves ligation of super \201 cial veins and valvuloplasty Further reading Royal College of Nursing guidelines (in conjunction with NICE) . Online: M www.rcn.org.uk . Simon DA , Freak L ,; Kinsella A , et al . ( 2004 ). Clinical review: Mana gement of venous leg ulcers . BMJ 328 : 1358 \200\223 62 . 596 CHAPTER 23 Skin Pruritus Intense itching. Common condition in older patients, often causing consid- erable distress. Threshold for itch affected by neurological and psycholog- ical factors \200\224 exacerbated by social isolation, sensory impairment (blind, deaf) and depression. Often ig nored, yet simple measures can make a big difference. Causes Often associated with dry skin (xerosis), common with ageing, and fre- quently worst on lower legs, forearms and hands. Skin is dry, scaly, and may develop in \202 amed \201 ssures when severe (asteatotic dermatitis). Contact dermatitis may show few skin changes if mild, yet cause trouble- some itching. Limi ted to areas exposed to allergen (eg under clothing if due to washing power). Systemic disease causes up to half of pruritus in the elderly, including: Liver failure (may be mild jaundice \200\224 itch caused by bile salts) \200 Chronic ren al failure \200 Iron de \201 ciency \200\224 even before anemic \200 Hematological di sorders (lymphoma, polycythaemia \200\224 itch may be exacerbated by water) Infections (including fungal infection, scabies and lice infestations, gastrointestinal parasite infections) Metabolic disorders including: thyroid disease (affects 10 % of hyperthyroid patients, and many hypothyroid patients because of dry skin); diabetes mellitu s Malignancy Many drugs can cause a pruritic rash as an adverse drug reaction (usually allerg ic) but some cause itch without a rash (eg morphine, allopurinol and benzodiazepines) or be cause of cholestasis. Assessment \200 History should include full systems enquiry looking for underlying diseas e, drug history and speci \201 c enquiries about possible irritants (eg biological washing powder, new bath products). Ask if anyone else is itching Examination should include inspection of all skin and thorough general examination (looking for eg burrows or other signs of scabies, lymphadenopathy, hep atosplenomegaly, thyroid enlargement, etc.) \200 Investigations should include: FBC, iron and ferritin, ESR, U,C + E, LFTs, TFTs, and blood glucose. May include other tests, guided by history, eg stool examination for ova, cysts, and parasites, abdominal ultrasound if or ganomegaly felt, etc. PRURITUS 597 Treatment \200 Treat the underlying cause wherever possible \200 Iron supplements if st ores low (even if FBC normal) \200 Stop any drugs that may be causing or exacerbating the condition \200 Apply emollients \200\224 light preparations such as aqueous cream can h elp itch even if the skin does not appear dry, and may be mixed with 0.5 % menthol, which h as a cooling and antiseptic action. Greasier preparations, eg 50:50 liquid paraf \201 n, w hite soft paraf \201 n are useful when the dryness is more severe Urea-containing emollients are used where the skin is scaly, and are often useful in the el derly (eg Balneum plus, E45 itch relief cream, etc.) Avoid excessive bathing \200\224 no more than daily; avoid hot water and prolonged soaking Use preparations such as aqueous cream or emulsifying ointments instead of soap. Emollient bath additives can be added to the water. Brand names such as Oilatum and E45 are sol d as both ointments and bath oils, and there are many others available Avoid exacerbating factors, such as heat (especially hot baths), alcohol, hot drinks and vasodilating drugs Wear loose, cotton clothing \200 Keep nails short to limit skin damage from scratching \200 Consider short-term bandaging where excoriation severe to allow healing Antihistamines may be useful \200\224 sedating preparations such as hydroxyzine hydrochloride, 25mg at night can help sleep. Non-sedating agents can be used du ring the day (eg chlorphenamine, cetirizine, loratadine) Colestyramine is used to decrease itch in biliary obstruction and primary biliary cirrhosis Light therapy (phototherapy) may help \200\224 normal sunlight, or a course of UVB therapy can be arranged 598 CHAPTER 23 Skin Pruritic conditions Lichen simplex \200 Local patch of pruritus, which when scratched lea ds to skin damage with thickening, discolouration, and excoriation Worse in times of emotional stress \200 Treat with steroids (topical or intralesional) an d avoidance of scratching (bandaging may help). Capsaicin cream may alleviate itching by decreasing substa nce P levels in the skin Pruritus ani \200 Common complaint \200 Occasionally due to infection (streptococci, ca ndidiasis, threadworms) \200 Exclude allergic contact dermatitis, seborrhoeic dermatitis, lichen sclerosus (see b \200\230Vulval disorders \200\231, p.526) or psoriasis Usually due to soiling of the perianal skin, which is worse with loose stool and dif \201 culty in wiping effectively (eg with arthritis) Mainstay of treatment is improving hygiene after bowel movement (assist with wiping if phys ically dif \201 cult; consider wiping with a damp cloth, etc) Use aqueous cream as a soap substitute \200 Once developed, the itch may be self-perpetua ting \200\224 break the cycle with steroids topical antifungals or antiseptics Patch test to exclude allergy PRURITIC CONDITIONS 599 HOW TO Recognize and manage scabies 2 Thinking of this diagnosis is the \201 rst st ep. \200 Caused by Sarcoptes scabiei mite \200 Spread by skin-to-skin contact \200 Ou tbreaks can occur within institutions (eg nursing homes, hospital wards) Occasionally serious, even fatal Symptoms and signs \200 Intense itch (worse at night) \200 Widespread excoriation \200 Examine the patient carefully for burrows and/or erythematous papules that are found: \200 Between \201 ngers and toes \200 On the wrist \202 exo r surface \200 Around the nipples and umbilicus \200 In the axillae and groin Treatment \200 Isolate the patient in a side room \200 Barrier nurse (gloves, aprons) \200 Apply topical pesticidal lotions or creams, eg permethrin, malathion \200 Apply to the whole body including the scalp, neck, and face. Ensure the interdigital webs are well covered Treat all household members (or all others in close contact in an institution) simultaneous ly, including asymptomatic contacts Wash clothes and bedding \200 Repeat treatment after a week \200 Prescribe 30 \200\2236 0g of cream and 100mL of lotion for each application \200 Applying after a hot bath is no longer recommended \200 Antibiotics may be needed for secondary infection \200 Itch ma y persist for weeks after treatment has eradicated the mite, but should slowly diminish. To pical steroids and sedating antihistamines to aid sleep can be helpful \200 Persistent it ch may indicate treatment failure Norwegian scabies occurs in immunosuppressed and frail ol der patients. A heavy load of mites produces hyperkeratotic lesions. Highly contagious. May require additional oral treatment (eg ivermectin \200\224 not licensed). 600 CHAPTER 23 Skin Blistering diseases There are many disorders causing skin blistering in older people \200 \224 see Table 23.2 for a differential. Common causes include blistering secondary to cellu litis or rapid onset oedema. Bullous pemphigoid is signi \201 cant in that it occurs almos t exclusively in the elderly population. Bullous pemphigoid Chronic autoimmune bullous eruption. Clinical features \200 Patient is systemically well \200 Skin becomes erythematous and itchy \200 Large, tense blisters then appear, usually on the limbs, trunk, and \202 exures (rarely mucous membranes) Blisters then heal without scarring \200 May appear in normal looking skin, or at the sit e of previous skin damage (eg ulcer, trauma) Chronic and recurrent condition Diagnosis \200 Con \201 rmed by skin biopsy, that shows linear IgG deposited at the basement membrane Circulating autoantibody (anti-BPAg1 and anti-BPAg2) is found in the serum of up to half of patients Treatment \200 Should be managed by a dermatologist \200 Responds well to steroids \200 Mild, local disease can be treated with strong topical steroids \200 More widesprea d disease requires oral prednisolone (40 \200\22360mg daily initially, reducing fairly rapidly to 10mg within a few weeks) \200 Topical or intralesio nal steroids are used for resistant lesions \200 Remember to monitor for and protect agai nst steroid side effects \200 Consider steroid-sparing agents for longer treatment course s (eg azathioprine) Prognosis \200 50 % have self-limiting disease \200 The majority will be off medication within 2 years BLISTERING DISEASES 601 Causes of blistered skin (Table 23.2 ) Table 23.2 Overview of blistering disorders Blistering disorder Clinical features Features of cellulitis present (see b \200\230Cellulitis \200\231, p.589) Blisters secondary to cellulitis Occurs when onset is rapid, eg heart failure Blisters secondary to oedema Traumatic blisters Due to friction, pressure, or knocks to skin Localized to site of insult, eg heel blister with ill- \201 tting shoes Pressure blisters Due to prolonged pressure that causes skin ischaemia Can occur after 2hr of immobility Risk factors include advancing age, immobility, dehydration, extremes of body size May prog ress to pressure sore (see b \200\230Pressure sores \200\231, p.502) Fixed drug eruption Itch, erythema, and blistering that appears and reappears at the same site after ingestion of a drug (eg furosemide) Reaction usually within 6hr Eczema Blisters may occur in eczema, especially if there is secondary infection (eg eczema herpeti cum, staphylococcal infection) Infections Herpes simplex \200\224 usually cause blisters on the face or genitals Herpes zoster \200 \224 shingles is common in older patients (see b \200\230Varicella zoster infection \200 \231, p.624) Staphylococci and streptococci may cause primary infections (eg impetigo \200\224 facial b listers that rupture to leave a yellow crust; erysipelas \200\224 well-de \201 ned area o f redness and swelling that later blisters, usually on face or lower leg) or secondary infe ction of, eg, a leg ulcer or wound. Either may result in blistering See b \200\230Bullous pemphigoid \200\231, p.600 Bullous pemphigoid Pemphigus vulgaris Serious autoimmune blistering disease Rare disorder, mainly affecting young or middle aged patients Widespread \202 accid, super \201 cial blisters that rupture early Patients are systemically unwell Dermatitis herpetiformis Symmetrical extensor surface tense blisters, associated with coeliac disease Rare, with peak incidence in the fourth decade 602 CHAPTER 23 Skin Skin cancers and pre-cancers All increase in frequency with increasing age and sun exposure . They are most common on sun-exposed areas, especially the head and neck and are diagnosed by biopsy. Any suspicious skin lesion should be referred to a dermatologist for considerat ion of this after discussion with the patient. Actinic keratoses \200 Rough, scaly patches \200 Vary from skin colored to red, brown, yellow, and black (often patchy) Pre-malignant, with a small risk of becoming squamous cell carcinoma over years. Some resol ve spontaneously. Treat established lesions \200 Removal with cryotherapy, topical 5- \202 uorouracil (5-FU \200\224 applied bd for 4 \200\2236 weeks, causes erythema, burning, ulceration, and then healing) or topical diclofenac (treat for 60 \200\22390 days; therape utic effect may occur up to 30 days after stopping) Bowen \200\231s disease \200 Intraepidermal carcinoma, with small risk of transformation into squamous cell carcinoma Typically occurs on the lower leg of elderly women \200 Caused by sun exposure, arsenic e xposure, or human papilloma virus infection Pink or reddish scaly plaques with well-de \201 ned edges \200 Histology should be con \201 rmed \200 Watchful waiting may be appropriate, but most lesions are removed by cryotherapy, topical 5-FU, curettage, or excision Lentigo maligna \200 Irregular pigmented macules that can be brown, black, red, or white \200 Usually over 1cm in size, they occur in areas of sun exposure \200 1 \200\2232 % b ecome invasive with time \200 Excision is required, although watchful waiting may be appr opriate if the patient is frail Basal cell carcinoma \200 Commonest, accounting for 75 % of all skin cancers \200 Other risk factors include irradiation, arsenic ingestion, or chronic scarring Slow growing and usually only locally invasive (metastasis virtually unknown), but facial t umors left untreated can cause erosion of cartilage and bone with signi \201 cant dis \201 gurement Begins as a pearly papule, that then ulcerates, characteristically with a rolled everted ed ge and surface telangiectasia (so called rodent ulcer) Most lesions need excision with a 5mm margin; Moh \200\231s microsurgical method involves i nspecting histology during the procedure to limit tissue loss; radiotherapy can be used whe re surgery is not an option, or in cases of recurrence. Intralesional interferon or photody namic therapies are newer options Recurrence in 5 % at 5 years, so follow-up is required SKIN CANCERS AND PRE-CANCERS 603 Squamous cell carcinoma \200 Second most common skin cancer \200 Other risk factors inc lude irradiation, chronic ulceration or scarring, smoking, or exposure to industrial carcinogens 5 \200\22310 % will metastasize, usually to local lymph nodes initially \200 Begins as an erythematous, indurated area that becomes hyperkeratotic and scaly, and may then ulcerate Removal is by surgical excision with 5mm margins. Radiotherapy can be used for recurrence, or in older patients if excision would be hard (eg on the face) 2May develop in the edge of a leg ulcer. Malignant melanoma \200 Most lethal of skin tumors, readily metastasizing \200 Differen t subtypes include super \201 cial spreading melanoma (most common; plaque with irregular border and uneven pigmentation), nodular melanoma (dark pigmented nodule), lentigo maligna melanoma and acral lentiginous melanoma (pigmented macule in nail beds, palms and soles) Suspect if a pigmented lesion has changed in size or color, become irregular in shape, bleeds, itches, or looks in \202 amed Early detection is key as the thicker the lesion the worse the outlook and once metastasize d, the disease is fatal \200\224 older men often ignore suspicious-looking skin lesions Removal is by surgical excision with wide margins 604 CHAPTER 23 Skin Other skin lesions Campbell de Morgan spots \200 Small bright red papules on the trunk \200 Benign capillary proliferations \200 Occur from middle age onwards, almost universa l by old age in Caucasians Skin tags \200 Pedunculated, benign \201 broepithelial polyps \200 Occur in older pat ients \200 Benign, usually multiple, cause unknown \200 Removal for cosmetic reasons by snipping the stalk with scissors, or cryotherapy (liquid nitrogen) Seborrhoeic warts \200 Also called basal cell papilloma \200 Not infectious \200 Oval papules (1 \200\2236cm diameter) occurring on the face and trunk of older patients Initially yellow, become darker and more warty in appearance \200 Seem to be \200\230stu ck-on \200\231, usually multiple \200 Removal can be done (usually for cosmetic reasons) by cryotherapy or curettage Where concerns exist about more serious pathology, excision biopsy is performed 605 Chapter 24 Infection and immunity The ageing immune system 606 Overview of infection in older people 608 HOW TO Accurately diagnose infection in an older patient 609 Antibiotic use in older patients 610 Meticillin-resistant Staphylococcus aureus 611 Disease caused by MRSA 612 HOW TO Control MRSA 613 Clostridium dif \201 cile -associated diarrhea 614 HOW TO Manage C. dif \201 cile infection 616 Near-patient urine tests 618 HOW TO Sample urine for dipstick, microscopy, and culture 619 Asymptomatic bacteriuria 620 Urinary tract infection 621 Urinary tract infection: treatment 622 Recurrent urinary tract infection 623 Varicella zoster infection 624 606 CHAPTER 24 Infection and immunity The ageing immune system The immune system ages in a complex manner: \200 Some activities increase (eg production of memory T lymphocytes, IgA, and autoantibodies) Other activities diminish (eg production of some interleukins, antibodies in response to foreign antigens, macrophage clearance of antigens, and complemen t during acute infection) Overall, immune responses become less ef \201 cient, less appropriate, and occasionally harmful with age The immune system does not wear out \200\224 it becomes dysfunctional \200 This is an in sidious process, often unnoticed until times of physiological stress (eg acute illness) It is more marked in older people with chronic disease, multiple comorbidities and signi \201 cant genetic and environmental factors This immune dysfunction alters the response to infection in older people: \200 Infectious disease is a more signi \201 cant cause of morbidity and mortality in older people (up to 10 times more likely to be the cause of death) \200 Impaired cellular immunity predispos es older people to reactivation of certain diseases eg: \200 Shingles (see b \200\230Varicella zoster infection \200\231, p .624) \200 Tuberculosis (see b \200\230Tuberculosis: presentation \200\231, p.336) \200 Altered antibody production increases fatality from pneumonia, in \202 uenza, bacterial endocarditis, and hospital-acquired infections \200 Decreased levels of lymphokines incre ase susceptibility to parasitic infections Age-related immune dysfunction probably has a negative impact of the course of AIDS in olde r patients (see b \200\230HIV in older people \200\231, p.530) 2Investigations may not sho w characteristic changes associated with infection, or these changes may develop more slowl y (eg rise in white cell count, CRP, and complement). It also has other clinical consequences: Increased autoantibody production does not lead to an increase in autoimmune disease (this peaks in middle age), but may contribute to degenerative diseases Response to vaccination may be less good \200 Falling immune surveillance may contribute to higher cancer incidence \200 T lymphocyte dysfunction may contribute to the increasing incidence of monoclonal gammopathy with age (see b \200\230Paraproteinaemias \200\231, p. 459) IgE-mediated hypersensitivity reactions are less frequent, so allergic symptoms tend to improve with age This page intentionally left blank 608 CHAPTER 24 Infection and immunity Overview of infection in older people Susceptibility to infection is increased by: \200 I mmune senescence (see b \200\230The ageing immune system \200\231, p.606) \200 Altered s kin and mucosal barriers \200 Acute and chronic illnesses (cause relative immunosuppressi on) Blunted response to infection may occur in those with: \200 Decreased cardiac adaptat ion to stress \200 Comorbid conditions and frailty \200 Decreased lean body mass or mal nutrition \200 Multiple previous hospital admissions or residence in a long-term care facility Presentation \200 Frequently atypical eg global deterioration, non-speci \201 c function al decline, delirium, falls, incontinence May initially give no clue to the site of sepsis, eg chest infections may present with falls, rather than cough Fever is often absent, reduced, or delayed (due to senescent hypothalamic and other responses) Often indolent with a slow deterioration over several days 2By the time sepsis is obvious, the patient may be very unwell. Investigation Obtaining samples can be dif \201 cult, eg delirious uncooperative patient, urinary or fecal incontinence, inability to expectorate sputum, etc. Misleading results are common: Positive urine dipstick often does not indicate symptomatic infection (see b \200\230Near-patient urine tests \200\231, p.618) Urine samples from a catheterized patient will usually be heavily colonized; dipstick tests will be positive and culture results dif \201 cult to interpret Ulcers will usually be colonized and swab results should be interpreted with caution (see b \200\230Leg ulcers \200\231, p.593) Abdominal ultrasound scan will often reveal gallstones in older patients \200\224 these are usually asymptomatic and do not necessarily imply biliary seps is Classical markers of infection (leucocytosis, elevated CRP, increased complement) may be ab sent or delayed in older patients. Repeating them after 24hr improves sensitivity Treatment Because of the dif \201 culties in making an accurate diagnosis: \200 Therapy is often empirical \200 Antibiotic failures are more common \200 Antibiotic resistance frequently develops In addition, treatment may be dif \201 cult to administer in delirious patients. OVERVIEW OF INFECTION IN OLDER PEOPLE 609 HOW TO Accurately diagnose infection in an older patient Making an accurate diagnosis with evidence to support it is important to allow tailored ant ibiotic therapy. Have a low threshold for considering sepsis as a cause for decline of any sort, but conversely do not assume that all problems stem from infection. Investigations \200 Full blood count \200\224 white cell count may be elevated, suppress ed (poor prognostic indicator) or be unchanged ESR, CRP \200\224 often become elevated early on in infection, but this is very non-speci \201 c and they may take 24 \200\22348hr to rise or remain normal. Serial measurements adv ised U,C + E \200\224 septic older patients are prone to renal impairment \200 Blood and urin e cultures \200\224 send before antibiotics are started and even in the absence of fever CXR \200\224 a patch of consolidation on an X-ray may be the \201 rst indicator that a g lobal deterioration is due to pneumonia Consider stool analyzes (if diarrhea) If the source remains unclear, repeat basic tests, th en consider: \200 Skin \200\224 check carefully for cellulitis and/or ulceration (see b \200\230Cellulitis \200\231, p.589) Bones \200\224 osteomyelitis (particularly vertebral, after joint replacement or where there is chronic deep ulceration of skin) may present indolently. Check for bony t enderness and consider X-rays, bone scans, or MRI (see b \200\230Osteomyelitis \200\231, p .488) Heart valves \200\224 bacterial endocarditis can be very hard to diagnose. Consider in all with a murmur, and actively exclude in those with prosthetic heart valves Biliary tree \200\224 asymptomatic gallstones are common in older patients, but if an ultrasound also shows dilatation of the gall bladder or biliary system with a thickened, oedematous wall, then infection is likely. There is usually (but not alwa ys) abdominal pain. Send blood cultures. ERCP may be needed to remove any obstruction Abdomen \200\224 diverticulosis is common, and abscesses may present atypically. Examine for masses and consider abdominal ultrasound or CT if there is a histor y of diverticulae or abdominal pain Brain \200\224 meningitis, brain abscess, and encephalitis may present indolently in older patients, and the usual warning signs (confusion, drowsiness) may be mi sinterpreted. Headache and photophobia may be late or absent, and neck stiffness dif \201 cult to interpret. Consider CT head followed by CSF analysis if a septic patient has focal neurology, headache, photophobia, or bizarre behavioral change \200 TB \200\224 may reac tivate in older people and cause chronic infection. If there is known previous TB (clinical or CXR evidence) then look very carefully for reactivation. Consider early morning urines, sputum culture (induced if necessary), bronchoscopy, or biopsy of any abnormal tissue (eg enlarged lymph nodes) 2Remember that fever and raised in \202 ammatory markers can also be due to non-infectious conditions (eg malignancy, vasculitis, etc.) 610 CHAPTER 24 Infection and immunity Antibiotic use in older patients Antibiotics are among the most frequently prescribed drugs , and their widespread use is promoting increasing antibiotic resistance. This is a particular problem in older patients where infections are more common, yet accurate diagnosis can be more dif \201 cult. Antibiotic resistance Resistance is encouraged by: \200 \200\230Blind \200\231 antibioti c therapy (where likely microbe and sensitivities are not known) Inappropriate antibiotic therapy (eg for viral respiratory infections) \200 Inadequate tr eatment courses \200 Poor concordance with therapy \200 Transmission of resistant strai ns within healthcare settings Sensible antibiotic prescribing Helps to limit the problem. Applies to all ages, but may be more of a chal- lenge in older patients: \200 Make a diagnosis \200\224 identify the so urce of sepsis (and so possible pathogens), which will guide therapy before microbiological con \201 rmation is obtained Avoid antibiotics for infections that are likely to be viral, eg pharyngitis, upper respiratory tract infection Where practicable, send samples for culture and sensitivity before initiating antibiotics Local variations (eg diagnostic mix, local sensitivities) should be considered. Use local antimicrobial guidelines Choose the dose based on the patient (allergies, age, weight, kidney function, etc.) and th e severity of the infection. Inadequate doses promote resistance Choose the route \200\224 aim for oral wherever possible, and convert iv therapy to oral a s soon as feasible; im antibiotic therapy is uncomfortable but can be useful (eg cognitivel y impaired patients who refuse oral medication) Choose the duration based on the type of infection, eg simple UTI can be adequately treated in 3 days, whereas bacterial endocarditis can require many weeks of therapy. Unnecessarily long treatment courses will promote resistance, increase the risk of side effects, complic ations (eg CDAD) and increase cost Change empirical broad-spectrum antibiotics to narrow-spectrum alternatives as soon as sensitivities are known Further reading British National Formulary (BNF) Section 5.1 Antibacterial drugs . METICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS 611 Meticillin-resistant Staphylococcus aureus Meticillin was introduced in the 1960s to treat staphylococcal infections. It was used wide ly (including spraying solutions into the air on wards) and initially successfully. Meticil lin has now been discontinued and replaced by \202 ucloxacillin but the term MRSA persist s. Resistance to meticillin gradually emerged \200\224 \201 rstly small numbers within hosp itals, but the problem slowly increased and spread into the commu- nity, until globaly disp ersed epidemic strains emerged. All staphylococci are easily transmissible, virulent (capacity to cause disease) and have capacity to develop further antibiotic resistance. The problem today \200 Varies enormously eg > 25 % of invasive Staph. aureus isolates are resistant in UK, Spain, and Italy, compared with <1 % in Scandinavia \200 However, rates peaked in 2005/6 and are now reducing \200\224 deaths where MRSA was mentioned on death certi \201 cates have decreased from > 1600/year to <800/year between 2005 and 2009 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