Oxford Handbook of Geriatric Medicine (2 edn)
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Pressure sores
Areas of skin necrosis due to pressure-induced ischaemia found on sacrum, heels, 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 5–10% despite drives to improve education and preventative strategies. The financial and staffing 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
▸2 hrs of tissue ischaemia is sufficient 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 considerable lag between the ischaemic insult and the resulting ulcer. Grade I erythema often progress to deep ulcers over days/weeks without further ischaemic insult. Inspect sacrum and heels at least daily.
Risk factors
Include age, immobility (especially postoperative), low or high body weight, malnutrition, 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 judgement of individual patient risk.
Mechanisms
Pressure—normal capillary pressure 24–34mmHg—pressures exceeding 35mmHg compress and cause ischemia. This pressure is easily exceeded on a simple foam mattress at pressure points such as heels
Shear—where skin is pulled away from fixed axial skeleton small blood vessels can be kinked or torn. When a patient is propped up in bed or dragged (eg during a lift or transfer) there is considerable shear on the sacrum
Friction—rubbing the skin decreases its integrity especially at moving extremities, eg elbows, heels. Avoid crumbs, drip sets and debris between patient and sheets. Massage of pressure areas no longer recommended
Moisture—sweat, urine, and faeces cause maceration and decrease integrity
Management
Prevention—demands awareness—NICE guidelines suggest all patients are risk assessed within 6hr of admission (
www.nice.org.uk, clinical guideline 29 (2005)). Regular reassessment during hospital admission should occur especially if condition of patient changes
Turning and handling—there is no evidence to suggest how often immobile, high-risk patients should be turned in bed. Two-hourly turns are historically based and rarely achieved. Frequency should be judged individually. Modern mattresses decrease frequency but don't eradicate need for turns. Avoid friction and sheer by using correct manual handling devices. Consider limiting sitting out to 2hr. Encourage early mobilization, optimize pain control, minimize sedative drugs
Pressure-relieving devices—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)
High specification foam mattresses
Alternating pressure mattresses (air pockets intermittently inflate and deflate) eg Nimbus©
Air-fluidized (warm air pumped through tiny spheres to produce a fluid-like cushion) or waterbed mattresses
Promote healing environment
Nutrition—protein and calorie supplements. There is no evidence to support the use of vitamins, eg vitamin C, or mineAlternating pressure mattressesrals, 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
Correct anaemia (normochromic/normocytic anaemia common)
Debridement—dead tissue should be removed with scalpel (no anaesthetic required), maggots or occasionally topical streptokinase, or suction. Some patients benefit from surgery, eg debridement, skin grafting or myocutaneous flaps
Dressings—enormous choice with little evidence to favour one type over another. Use gels to soften, hydrofibre/gels (often seaweed based) for cavities then a secondary dressing over the top
Antibiotics—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 confirmation. Common organisms include mixed Gram-negatives (Bacteroides) Gram-positives (enterococci and staphylococci), and yeasts. If antibiotics are indicated, use wide-spectrum antibiotics including anaerobic cover. Consider osteomyelitis where bone is exposed (see 
‘Osteomyelitis’, 488). MRSA colonization is a growing problem, is very difficult to eradicate, and often leads to a patient having prolonged isolation, which is detrimental to their psychological well-being and rehabilitation
Compression mononeuropathy
Where nerves are compressed against bone they can be damaged
This is usually a demyelination injury (neuropraxia) which resolves spontaneously in 2–12 weeks
Alcohol, diabetes, and malnutrition increase susceptibility
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 Appendix, ‘Dermatomes’, 686)
Nerve conduction studies are rarely required to confirm diagnosis
Treatment is supportive—many such patients are acutely unwell—but recognition becomes more important during rehabilitation (Table 18.1)
| Nerve damaged | Site/mechanism | Motor effects | Sensory effects |
|---|---|---|---|
Radial | Upper arm—spiral groove on humerus | Wrist drop and finger extension weakness | Small area of numbness at base of thumb |
Ulnar | Elbow—cubital groove | Little and ring finger flexors and finger abduction and adduction | Little and ring finger |
Common peroneal | Knee—fibula head | Foot drop and failure of foot eversion and toe extension | Lateral calf and top of foot |
Sciatic | Buttock or thigh | Knee flexors plus common peroneal as this table, above | Posterior thigh plus common peroneal as this table, above |
| Nerve damaged | Site/mechanism | Motor effects | Sensory effects |
|---|---|---|---|
Radial | Upper arm—spiral groove on humerus | Wrist drop and finger extension weakness | Small area of numbness at base of thumb |
Ulnar | Elbow—cubital groove | Little and ring finger flexors and finger abduction and adduction | Little and ring finger |
Common peroneal | Knee—fibula head | Foot drop and failure of foot eversion and toe extension | Lateral calf and top of foot |
Sciatic | Buttock or thigh | Knee flexors plus common peroneal as this table, above | Posterior thigh plus common peroneal as this table, above |
Rhabdomyolysis
Following prolonged pressure (eg if patient cannot get up after a fall or stroke or after a period of unconsciousness) muscle necrosis can occur, which releases myoglobin. High levels are nephrotoxic, precipitating to cause tubule obstruction with acute renal failure especially as these patients are usually dehydrated.
▸Remember to check U,C+E in all patients who have been found on the floor after a ‘long lie’. Many frail elderly patients with bruises after a fall will have raised CK levels without developing renal problems but ensuring good hydration (often with 24–48hr of intravenous fluids) and repeating renal function in such patients is good practice.
Diagnosis
Suspect the full rhabdomyolysis syndrome in any patient with:
Prolonged unconsciousness
Signs of acute pressure sores of the skin
CK levels at least five times normal
Urine may be dark (‘Coca-Cola’ urine) and urinalysis is positive to haemoglobin but without red blood cells. Hyperkalaemia and hypocalcaemia can occur.
Treatment
Treat with aggressive rehydration. Monitor urine output, electrolytes, and renal function closely—if renal failure occurs consider temporary dialysis. Prognosis is good if patient survives initial few days.
