S4: The Ageing GI Tract and Skin Flashcards

1
Q

Describe ageing skin functions: barrier

A
  • Decreased sebum production.
  • Epidermal thinning: Flattening of the dermo-epidermal junction and less elasticity and thinner appearance in skin.
    Both these changes:
  • Increase risk of infection as cracking of skin breaches barrier and elderly are relatively immunocompromised already.
  • Treatment: Review dehydrating medications and improve barriers with creams/lotions.
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2
Q

Describe ageing skin functions: thermoregulation

A
  • Dermal thinning → reduced ability to thermoregulate so cant control temperature very well.
  • Reduced moisture retention so dehydration can occur during vasodilation and reduced ability to vasodilate in the capillary bed ➔ prone to heat retention.
  • Compounded by hypothalamic dysregulation of osmolality and temperature. The elderly don’t recognise they are not thirsty until at higher osmolarity and switch off thirst sensation at higher osmolarity as well
  • All these issues = Risk of dehydration.
  • Risk of hypothermia.
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3
Q

Describe ageing skin functions: protection

A
  • Accumulation of UV damage to skin as people age.
  • Cellular aging via loss of telomere ends which removes damaged DNA.
  • Nail growth reduces 50% but thicker nails with age.
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4
Q

Describe ageing skin functions: communication

A

Affects communication through visual appearance:

  • Wrinkling and sagging of skin.
  • Decrease in melanocytes in the epidermis and Hair E.g. Grey hair (Achromotrichia).
  • Rockwood’s Frailty Index (FI) accumulation of deficits related to age. Have to be deficit to be included in FI e.g. grey hair is part of normal ageing but not a deficit.
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5
Q

Describe ageing skin functions: pain

A

Pain receptor:
- Dermal thinning → reduction in nerve endings ➔ decreased sensation.
- Neuropathic pain increases which can be disabling.
Associated issues:
- Compounded by diabetes and micronutrient deficiencies.
- Neuropathic pain medications often deliriogenic (increases delirium).
- Increased risk of peripheral ulcers if they have reduced feeling in feet leading to further pain.

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6
Q

Describe Continence, Pressure Injuries and Falls –> Big clinical problem

A
  • Continence and falls are interlinked: backwards and forwards.
  • Those with pressure areas may have limitations on their mobility.
  • Cycle of deconditioning.
  • ‘Functional incontinence’ subsequently gets worse
  • Catheters may be part of management of healing wound (healing pressure wounds) e.g. Convenes alternative, Flip Flow Valve for the ambulant = Both reduce drive to need to walk and this is part of healing process.
  • National status needs to be looked at in order to heal.
  • Pressure Injuries should always raise a safeguarding alert as shows that an individuals care has not been met appropriately.
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7
Q

How does pressure injury occur?

A
  • Pressure ulcers usually occur over a bony prominence, such as the sacrum, ischial tuberosity and heels (due to lots of pressure of dense bone against another hard surface e,g. a chair).
  • However, they can appear anywhere that tissue becomes compressed, such as under a plaster cast, splint, arm sling, crutches – or under glasses / nasal cannulae.
  • This occurs when the soft tissue of the body is compressed between a bony prominence and a hard surface. This occludes the blood supply, leading to ischaemia and tissue death.
  • A cone-shaped ulcer is created, with the widest part of the cone close to the bone, and the narrowest on the body surface (the widest part may not be seen as it is deeper so pressure injury may not look severe but it is).
  • The forces of pressure are further exacerbated by moisture, and factors relating to the individual’s physical condition, such as altered mobility, poor nutritional status, medication, and underlying medical conditions.
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8
Q

Pressure Injury Grading (Pressure Ulcers)

A

Grade 1 = non-blanchable erythema (redness). Superficial.
Grade 2 = Presence of blister or abrasion. Top epidermal layer starts to break down.
Grade 3 = Necrosis but not through fascia underlying hypodermis. Breakdown of subcutaneous tissue.
Grade 4 = Damage to muscle, bone and supporting structures.

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9
Q

Pressure Injury vs Moisture Lesion

A

Pressure Injury:
- Cause is evidence/history of pressure, shear or friction.
- Position is usually over bony prominence of compression with equipment.
- Shape is usually distinct with obvious edge and 1 or 2 wounds. Edges are distinct and may be rolled or raised in chronic stages.
- Depth can range from superficial to deep, can be down to bone.
- Necrotic tissue is frequently present as hypoxia causes necrosis.
Moisture lesion:
- Cause is moisture, history or incontinence e.g. urine.
- Position is not over bone, frequently in natal cleft and/or over buttocks.
- Shape is frequently multiple wounds with diffused edges hat are difficult to determine. Borders are often jagged.
- Always superficial unless infected.
- No necrosis.

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10
Q

What do Pressure Injuries and Moisture Lesion usually indicate about individual?

A

Implications for care needs
and indicate individual is:
- Immobility.
- Poor nutrition.
- Care needs not being met at current time (acutely or chronically).
Healing requires skilled assessment and holistic view.

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11
Q

Describe Dry Skin : Xerosis

A

Very common complaint and due to reduced moisture retention + loss of oil glands. May be worsened by:

  • Excessive air conditioning / direct heat from fire or fan heater.
  • Excessive bathing.
  • Soaps, detergents and solvents
  • Irritation from rough clothing / other abrasives.
  • Diuretics (dehydrating).
  • Medical causes: hypothyroidism, CKD, malnutrition, dermatitis/eczema.
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12
Q

Describe itchy skin

A

Common: 50% of hospitalised older adults in one study. Often associated with dryness (dry skin), rashes or underlying medical issues. ~Causes
Systemic:
- Renal: Chronic renal failure - buildup of urea and waste materials.
- Liver: Cholestatic - buildup of bilirubin.
- Endocrine/metabolic: Diabetes M; hyperthyroidism; hypoparathyroidism.
- Hematological: IDA; polycythaemia; leukaemia; lymphoma ; anaemia.
- Neurological: neuropathic pruritus.
- Oncological: can precede underlying malignancy such as lymphoma by many years before
Skin diseases:
- Psoriasis, Urticaria, Allergic contact dermatitis, Dry skin, Dermatitis herpetiformis, Scabies, Mycosis fungoides.
Exposure-related:
- Allergens/irritants - check contacts and exposures.
- Insects/infestations (i.e. bed bugs).
- Medication (i.e opioids as side effect).

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13
Q

Describe vasculitis - Inflamed blood vessels

A

Older adults are most likely to get small vessel vasculitis than large vessel vasculitis.

  • Presents with raised palpable purple areas called purpura, or occasionally ulcers. Diagnosis: Biopsy where histology shows inflamed blood vessels.
  • Reactive vasculitis E.g. Secondary to acute infection. Tends to settle in 6-8 weeks without intervention. Supportive measures includes emollients, topical steroids, light compression.
  • Vasculitis secondary to underlying inflammatory process. May be more severe and persistent. Need to manage underlying condition.
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14
Q

Describe Pemphigus and Pemphigoid

A

2 well recognised autoimmune conditions seen in older aldults.

  • Pemphigoid- dermal layer blisters. Slightly more common.
  • Pemphigus - blisters are so superficial they are hardly seen but scars left are seen due to skin coming off –.> dehydration, hypothermics.
  • Both treated with steroids.
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15
Q

What do you need to think about when prescribing steroids to elderly?

A
  • Generally steroids are tolerated well.
  • Diabetes: Can they check their own BMs? Can they administer the medication? Can they recognise hypos? How would they call for help?
  • Psychosis: Can you adjust the dose? What risks are there at home? E.g. what is their mobility…
  • Social support: Who is there to recognise / call for help if they can’t? What teams do you have locally e.g. DNs, complex care teams, hospital at home.
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16
Q

Describe cellulitis

A

Cellulitis is an infection of the skin so will be associated with features of infection such as fevers and potentially sepsis too. The onset will be rapid onset of unilateral, progressive redness. Bilateral cellulitis is very rare. Predisposing factors:
- Presence of lymphoedema (Blockage of lymphatic drainage).
- Previous cellulitis.
- Diabetes.
- Immunosuppression.
- Often caused by a pathogen on the skin gaining entry beneath: Look for and ask about skin breaks including insect bites and fungal infections. check between the toes to see if cracks present and ensure good foot care and maintaining good skin care including adequate moisture barrier maintained to prevent further infections.
Treatment: is with antibiotics. If more than two episodes in a year then can consider antibiotic prophylaxis .

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17
Q

Describe Lipodermatosclerosis

A

Inflammatory condition of the lower legs usually due to venous insufficiency.
Usually a deep red colour, compared to the bright pink of a cellulitis.
Acute flares can happen (top):
- Red.
- Painful.
- Scaly.
- Usually bilateral, which cellulitis rarely is.
Chronic Lipodermatosclerosis:
- Increased swelling in the leg.
- Moderate redness.
- Increased pigmentation
- Atrophe blanche (small white areas).
Does not have an acute progression so no effect systemically. No antibiotics needed.

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18
Q

List causes of swollen leg

A
  • Fluid Overload
  • Dependent oedema
  • Low protein states
  • Drugs (Iatrogenic)
  • Lymphoedema
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19
Q

Describe Swollen leg: Fluid Overload

A
  • Fluid overload is commonly seen as a consequence of heart failure.
  • If this happens quite quickly it can often appear red and may blister (red due to stretching of skin and inflammation rather than infection of skin so no raised inflammatory markers present).
  • Usually though it will just be a swelling of the skin with subcutaenous fluid. It will be bilateral and pitting and when pushing down on skin there will be a dent left.
  • The history will usually help to differentiate this. Start at ankles and moves its way up the legs and even to abdomen.
  • Treatment of the underlying cause, so in this case, through diuresis to remove the excess fluid as well as good wound care of any breaks to prevent deterioration.
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20
Q

Describe Swollen leg: Dependent Oedema

A
  • Looks similar to fluid overload.
    Clues to differentiate:
  • No evidence of heart failure.
  • Reduces with elevation (e.g. overnight or feet up).
  • Follows gravity.
  • Tends to not get above knees.
    The mainstay of advice is usually to elevate the legs closer to the level of the heart to help the fluid to be cleared from the legs.
21
Q

Describe Swollen leg: Low protein states

A

Includes critical illness, nephrotic states, severe protein malnutrition.
Low protein states cause:
- oedema in all extremities.
- including the upper limbs.
- worse in dependent areas.
Other causes are not usually seen in the upper limbs e.g. Heart failure.
Nephrotic syndrome:
- Kidneys release excess protein leading to a whole body depletion of stores.
- Urine dipstick for protein will be highly positive.
- Oedema will often include the arms and sometimes the face.

22
Q

Describe Swollen leg: Drugs

A
  • Drugs causing fluid retention. Mechanism often interruption of lymphatic drainage, so doesn’t respond to diuretics e.g. amplodipine antihypertensive drug.
  • Often diuretics used: prescribing cascade (amlodipine and furosemide are commonly together (high BP and heart failure). Trial off medication for treatment in this case.
23
Q

Describe Swollen leg: Lymphoedema

A
  • Lymphoedema is a condition affecting the lymphatic system of the body, a network of channels and glands which help fight infection and remove excess fluid.
  • Primary = problem in the development of the lymphatic system.
  • Secondary = due to damage to the lymphatic system.
  • Following lymph node surgery or radiotherapy treatment of cancers
  • Severe cellulitis can cause scarring of the lymphatic system.
  • Inflammatory conditions such as RA or eczema for same reason;
  • Venous disease (including DVT and varicose veins) - abnormal or damaged veins causes overflow of fluid from veins into tissue spaces which overwhelms and eventually exhausts the lymphatic system involved.
  • In its early stages, lymphoedema can be pitting and resemble fluid overload. In the latter stages skin becomes hardened and tight resulting in deep, chronic lines. In particular ‘squaring of the toes’ can be an early sign of this.
24
Q

Role of gut

A
  • GI tract is from mouth to anus.
  • Normal stool output is about 200 g daily.
  • Activity in the proximal colon determines the consistency and volume of delivery of contents to the rectum.
  • The rectum is a reservoir.
  • An intact internal anal sphincter (IAS) ensures continence.
25
Q

Age changes in gut

A
Oesophagus:
- Oesophageal peristalsis decreases.
- Oesophageal sphincters lose tension.
Liver:
- Shrinkage of liver occurs with loss of hepatocytes.
- Reduced ability to detoxify substances including drugs.
- Changes in bile consitution.
Large Intestine:
- Peristalsis slows down.
- Decline in rate of cell diving and lining repair.
- Changes in microbial fauna.
- Changes in DNA of epithelial cells.
Nose and Mouth:
- Reduction in sense of smell and taste.
- Gum recession.
- Difficulty in swallowing.
Stomach:
- Reduced elasticity of stomach wall.
- Decreased bicarbonate production and gastromucosal protection.
- Delayed gastric emptying.
Pancreas:
- Decreased secretion of pancreatic protease and lipase.
Small Intestine:
- Compromised gut associated lymphoid tissue capacity.
26
Q

Describe mouth care matter in hospital

A

Mouth care less good in hospitals compared to home so at risk groups of patients
Risk of tooth decay x4 in psychiatric inpatients
At home more likely to brush teeth twice a day than in hospital

27
Q

Links to systemic disease with poor mouth hygiene

A

Poor oral health –> colonisation of mouth bacteria –> chronic inflammation in other places in body. For example:

  • Cancer
  • Dementia
  • Hospital acquired pneumonia
  • Stroke
  • CVD
  • Pregnancy outcomes
  • Diabetes
28
Q

Signs of unhealthy mouth

A
  • Dry mouth.
  • Thrush.
  • Tooth decay.
  • Bleeding and swollen gums.
  • Undiagnosed red and white patches.
  • Ulcers.
  • Denture problems.
29
Q

Xerostomia (dry mouth) management

A
  • Frequent sips of cold water
  • Sugar free chewing gum
  • Water based moisturising gels or sprays
  • Control of sugar intake
  • Daily checks for thrush
30
Q

Risk factors for oral thrush

A
  • Dry mouth as saliva contains antifungal enzymes
  • Steroids including steroid inhalers
  • Antibiotic use
  • Wearing dentures at night
  • Older age
  • Impaired immune system
  • Smoking
31
Q

Treatment of oral thrush

A
  • Keep oral cavity clean
  • Treat any dry mouth
  • Antifungal treatment , Nystatin first line
  • Leave dentures out at night
  • Clean dentures
  • Wash mouth after inhaler usage
32
Q

Describe oesophageal dysmotility in age

A

Aging is correlated to esophageal motor abnormalities termed presbyesophagus.

  • Duration of esophageal peristalsis is prolonged and amplitude decreases (60–80 years). Harder to push food down and through
  • Esophageal contraction amplitude diminishes but function remains intact (80-90 years). Harder for people to swallow as quickly and may need more time.
  • GERD has a significant impact on esophageal contraction wave amplitude, but not on peristalsis.
  • Investigations: Barium Swallow and Rx.
  • Promotility medications: Erythromycin and Metoclopramide.
33
Q

Describe age changes to NS of gut

A
  • Neurodegenerative changes in the enteric nervous system (ENS) may be key to functional changes observed with advanced age.
  • Gut transit time is not generally changed in elderly volunteers and does seem to be exquisitely sensitive to thyroid hormone status and can be considerably prolonged even in subclinical hypothyroidism.
  • In colons of people older than age 65 there is a 37% loss of enteric neurons was found when compared with younger people.
34
Q

Describe faecal continence in age

A
  • Rectum Mechanical changes (i.e. muscle) in the rectum cause most of the problems older people suffer in evacuating as well as the increasing prevalence of faecal incontinence with increasing age.
  • A reduction in rectal wall elasticity means that tonic activity of the external sphincter is lost at a smaller volume.
  • An age dependent increase in rectal pressure needed to produce an initial sensation of rectal filling has been found.
  • Maximum resting anal pressure and maximum squeeze pressure have been shown to decline with age, particularly in postmenopausal women.
35
Q

Describe nutritional support and malnourishment

A

Nutrition support should be considered in people who are malnourished, as defined by any of the following:

  • BMI of less than 18.5 kg/m2.
  • Unintentional weight loss greater than 10% within the last 3–6 months.
  • A BMI of less than 20kg/m2 and unintentional weight loss greater than 5% within the last 3–6 months. 3 million people in the UK are malnorished or at risk. Nutrition support should be considered in people at risk of malnutrition who, as defined by any of the following:
  • Have eaten little or nothing for more than 5 days and/or are likely to eat little or nothing for the next 5 days or longer.
  • Have a poor absorptive capacity, and/or have high nutrient losses and/or have increased nutritional needs from causes such as catabolism (e.g. sepsis).
36
Q

Appetite in older patients

A

The average daily intake of food decreases by up to 30% between 20 and 80 years. Healthy older people are:

  • Less hungry.
  • Fuller before meals,
  • Consume smaller meals,
  • Eat more slowly,
  • Have fewer snacks between meals.
  • Become satiated after meals more rapidly after eating a standard meal than younger people.
  • Appetite is: Associated with cognition and vision. Studies has shown that people more likly to eat more from a coloured plate,
  • Consider eating disorder.
37
Q

History taking for malnutrition

A

Hx of the weightless, how long, how much.
Was it intentional?
Screen for malnutrition - change in weight is key
HX of oral intake
HX of other things - thyroid disease etc.
“In the absence of fever or other cause for increased energy expenditure (eg, hyperthyroidism), weight loss is predominantly due to decreased food intake.”

38
Q

Examination for malnutrition

A
General physical examination.
Pay attention to the mouth!
Pay attention for lymph nodes.
Feel for liver edge.
Look for signs of occult disease.
Mental state examination.
39
Q

Causes of unintentional weight loss

A

Malignant disease (16%-36%)
Psychiatric disorder (especially depression) (9%-42%)
Unknown (10%–36%)
Gastrointestinal disease (6%-19%) - Malabsorption eg. Coeliac, IBD, colitis.
Endocrine disorder (especially hyperthyroidism) (4%-11%), Diabetes, adrenal insuffiency, hyperthyroidism, Pheo.
Cardiovascular disease (2%-9%)
Nutritional disorders or alcoholism (4%-8%)
Neurologic disorder (2%-7%)
Chronic infection (2%-5%)
Renal disease (~4%)
Connective tissue disease (2%-4%)
Respiratory disease (~6%)
Drug-induced weight loss (medication side effects) (~2%)
Infection - TB, HIV hepatitis
Chronic disease in advanced form - eg CCF, COPD, CKD

40
Q

Describe constipation in elderly

A

Constipation is not a disease entity in itself
Patients and clinicians use different definitions of constipation
- Frequency: Passing stool less than once every 3 days.
- Consistency: Hard stool.
- Difficulty: initiating evacuation despite regular bowel motions and feeling of incomplete evacuation.
- Constipation is commoner in older people than younger people. But it’s really quite subjectiive therefore a detailed history is needed. Some studies suggest that older adults perceive constipation as straining during defecation rather than decreased bowel frequency. Embarrassment factor also… may not have raised this before, or are other things more important to them (eg arthritis pain etc.).

41
Q

Common causes of constipation

A

Most constipation is ‘functional’ in nature - the rest likely to ‘pathological’ or ‘iatrogenic’ - caused by drugs.
- “Functional” is used to describe symptoms or problems that have no underlying anatomic abnormalities. However… the normal ‘function’ of an organ has changed. Functional bowel disorders, including functional constipation, are diagnosed primarily through patients’ reporting of symptoms.

42
Q

Rome IV functional constipation

A

Must have ≥2 of the following, each for >1/4 (25%) of defecations except (f):

a. Straining.
b. Lumpy or hard stools (form 1 or 2 on the Bristol Stool Form Scale - see below).
c. Sensation of incomplete evacuation.
d. Sensation of anorectal obstruction/blockage.
e. Manual maneuvers to facilitate defecation (e.g. digital evacuation, pelvic floor support).
f. <3 spontaneous bowel movements per week.
g. Loose stools rarely present without use of laxatives.

43
Q

Non-pharmacological management of constipation

A

Non pharmacological:

  • Increase dietary fibre. Decrease in portion sizes and lack of dietary fibre lead to reduced motility. 18g per day of fibre recommended by the British Nutrition Foundation..
  • Ensure adequate fluid intake to maintain both bowel contents and normal transit time.
  • Maintain mobility: immobility can reduce muscle tone in the bowel and abdo walls > constipation.
  • Toileting conditions- Often a large factor in care home admission… think re timing of POC and reassessment if needed.
  • Regular toileting - making use of the Gastrocolic reflex.
44
Q

Pharmacological management of constipation

A
  • Bulk forming laxatives e.g. Fybogel. Increase the bulk of stools by enabling fluid to be retained within the faeces.Same mechanism as adding fibre to diet by increasing the mass>increases peristalsis. Must have adequate fluid hydration to prevent intestinal obstruction. Caution with frailty and not suitable for those taking opioids.
  • Osmotic laxatives e.g. Lactulose/Macrogels/Phosphate enemas. Soften the stool makes them easier to pass by increasing the amount of water in the bowels. Lactulose causes increased bloating and colic symptoms. Movicol / Laxido volume can be difficult for those to drink or those who are fluid restricted (125mls per sachet) typical dose would be 2-4 sachets. Movicol-half is available (60mls per sachet). Can affect medication absorption. Caution in pts with heart failure
  • Stimulant Bisacodyl/Senna. Stimulating nerves that control the muscles lining the digestive tract. Senna: Short term license only. Stimulate the nerves in the large bowel. This causes the muscle in the wall of the large bowel to squeeze harder than usual. This pushes the stools along and out. Their effect is usually within 8-12 hours. Stimulant laxative suppositories act more quickly (within 20-60 minutes). Need to be against the rectal wall though…Possible side-effects from stimulant laxatives include abdominal cramps, and long-term use can lead to a bowel that is less active on its own (without laxatives). This can be thought of as a ‘lazy bowel’.
  • Stool softener laxatives e.g. Docusate (stimulant activity also) ‘Surface wetting agent’. Makes the surface of the stools permeable, water can be absorbed, which increases the fluid content of hard stools. Glycerin Suppositories work mostly by hyperosmotic action, but the sodium stearate in the preparation also causes local irritation to the colon.
45
Q

Impact of constipation

A

Complications: Urinary Retention, Overflow Diarrhoea, Bowel Obstruction, Rarely Bowel Perforation and Faecal impaction.
Quality of life:
- The impact of chronic constipation on quality of life for patients is comparable with that for conditions such as COPD, diabetes and depression.
- Chronic constipation-associated GI symptoms significantly interfere with many aspects of sufferers’ daily lives, including: mood (44%), mobility (37%), normal work (42%), recreation (47%), and enjoyment of life (58%).

46
Q

Describe faecal incontinence

A

Prevalence: Depends on who and how you ask!
- around 8% for face-to-face or telephone interviews
and around 12% for postal surveys.
- Frequency of FI increases with age.
- 50% of those with ‘major’ symptoms reported it affecting their quality of life.
- Difficulties in managing continence put an additional strain on this relationship and can lead to carer breakdown.

47
Q

Causes of faecal incontinence

A
  • Structural anorectal abnormalities (e.g., sphincter trauma, rectal prolapse) including congenital abnormalities, when symptoms may recur in adult life despite surgical repair.
  • Neurological abnormalities (e.g., multiple sclerosis, stroke, pudendal neuropathy).
  • Alterations in stool consistency (e.g., infectious diarrhoea, inflammatory bowel disease).
  • Overflow (e.g., impaction).
  • Cognitive/behavioural dysfunction (e.g., dementia, learning difficulties).
  • General disability (e.g., age, acute illness).
  • Idiopathic.
48
Q

Management for faecal incontinence

A
  • Use the gastro-colic reflex and set a regular pattern of toileting.
  • Send stool sample - to exclude infection.
  • If loose stools - loperamide may help (assuming no infection). Codeine if not tolerated. Amitriptylline may reduce rectal motor activity in long term low dose. If not settling then refer to gastroenterology for sigmoidoscopy (colitis?).
  • Overflow - may need regular enemas - in addition to laxatives.
  • Pelvic floor exercises.