Biography - Eamonn Brady MPSI is the owner of Whelehans Pharmacy in Mullingar. He graduated from the Robert Gordon University in Aberdeen in 2000 with a Masters in Pharmacy. He worked for Boots in the UK before moving back to Ireland in 2002. He bought Whelehans Pharmacy in Mullingar in 2005. He undertakes clinical training for nurses in the midlands.

CPD 14: PRESSURE SORES

Pressure Sores

Sponsored by Pfizer

Pressure ulcers are lesions caused by unrelieved pressure that results in damage to the underlying tissue. Generally, these are the result of soft tissue compression between a bony prominence and an external surface for a prolonged period of time. Pressure ulcers are among the most common conditions encountered in patients in hospital or requiring long-term institutional care.

American studies have shown that pressure ulcers also are common among patients admitted to nursing homes, with reported rates ranging from 10 to 35 percent1

60 Second SummaryPressure ulcers are lesions caused by unrelieved pressure that results in damage to the underlying tissue. They generally arise as a result of soft tissue compression between a bony prominence and an external surface for a prolonged period of time. Pressure ulcers most commonly occur in patients in hospital or in those requiring long-term institutional care.

Pressure ulcers are usually easily identified by their appearance and location overlying a bony prominence. It is important to distinguish pressure ulcers from ulcers that result from diabetic neuropathy or arterial or venous insufficiency. Superficial moisture-induced lesions, such as maceration (softening and whitening of skin) over a bony prominence, should not be labelled as pressure ulcers.

There are various factors that can contribute to pressure ulcers. The four main external factors that lead to the development of pressure ulcers are pressure, shearing forces, friction, and moisture. Patient specific causes that may contribute to pressure ulcer development include immobility, incontinence, nutritional status, circulatory factors, and neurological disease.

In order to prevent the development of ulcers:

1. Skin injury due to friction and shear forces should be minimised through correct positioning, transferring and repositioning techniques.

2. Eliminate any source of excess moisture due to incontinence, perspiration or wound drainage.

3. Reduce underlying risk factors such as poor nutrition.

4. Education and training, e.g. mobility, positioning, skin care, use of equipment, for patients and their carers.

Learning, Evaluation, Accredited, Readers, Network | www.learninpharmacy.ie

Clinical Manifestations & Diagnosis

Pressure ulcers are usually easy to identify by their appearance and location overlying a bony prominence. It is important to distinguish pressure ulcers from ulcers that result from diabetic neuropathy or arterial or venous insufficiency2. They also may be confused with other conditions that cause redness of skin such as cellulitis. Superficial moisture-induced lesions, such as maceration (softening and whitening of skin) over a bony prominence, should not be labeled as pressure ulcers. Characteristics of lesions that need to be distinguished from pressure ulcers are:

• Diabetic neuropathic ulcers are seen in patients with diabetes who have peripheral neuropathy. The diabetic ulcer characteristically occurs on the foot, usually on the ball of the foot just behind big toes or on the top of toes.

• Venous insufficiency ulcers are usually found on the inner part of the lower leg usually just above the ankle. Approximately 70 per cent of all leg ulcers are venous ulcers. They can occur either on one or both legs and each leg may have more than one ulcer. They can range from painless to extremely painful. These types of ulcers are common in people who have a history of leg and feet swelling. The ulcer usually presents itself as an open sore in an area that already typically exhibits a red to brown discoloration that has probably been present for some

time. The area will also be swollen. Prior to the formation of the ulceration the skin may have also been somewhat flaky and itchy as well. So long as there is no arterial disease, venous leg ulcers will benefit from elevation and compression dressings.

• Arterial ulcers occur as the result of arterial occlusive disease. Approximately 10 per cent of all leg ulcers are arterial ulcers. Feet and legs often feel cold and may have a whitish or bluish, shiny appearance. Arterial leg ulcers can be painful. Pain often increases when your legs are at rest and elevated.

Classification system

European Pressure Ulcer Advisory Panel grading system5:

• Grade 1: redness that does not whiten on touch. Discolouration of the skin, warmth, oedema and hardness may also be used as indicators, particularly on individuals with darker skin - in whom it may appear blue or purple. Grade 1 may be more difficult to detect in those with dark skin tones.

• Grade 2: partial thickness skin loss involving epidermis, dermis, or both. The ulcer is superficial and presents clinically as an abrasion or blister. Surrounding skin may be red or purple. If bruising is visible at this stage it can indicate deep tissue injury.

• Grade 3: full thickness skin loss involving damage to or necrosis of subcutaneous tissue. Subcutaneous fat may be visible but

CPD 14: PRESSURE SORES

tendon, muscle or bone is not exposed. Slough may be present.

• Grade 4: extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures with or without full thickness skin loss. Extremely difficult to heal and can lead to fatal infection.

Unstageable - Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed.

Eschar often covers deep ulcers, making it difficult to determine whether lesions are stage 3 or 4. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined.

Causes

External Causes

There are external factors that contribute to pressure ulcers. The four main external factors that lead to the development of pressure ulcers are pressure, shearing forces, friction, and moisture.

• Pressure - Pressure applied to the skin in excess of the arteriolar pressure (32 mmHg) prevents the delivery of oxygen and nutrients to tissues, resulting in tissue hypoxia, the accumulation of metabolic waste products, and free radical generation.7 Pressures are greatest over bony prominences where weight-bearing points come in contact with external surfaces. Extensive deep tissue damage may occur with little or no evidence of superficial tissue injury. A deep necrotic wound may be the first evidence of pressure-induced injury, rather than a gradual progression of an ulcer from stages 1 through 4.

• Shearing forces - Shearing forces occur when patients are placed on an incline.

Deeper tissues, including muscle and subcutaneous fat, are pulled

downwards by gravity, while the superficial epidermis and dermis

remain fixed through contact with the external surface

• Friction - Friction occurs when patients are dragged across an external surface. This results in an abrasion with damage to the most superficial layer of skin. It is less likely to cause stage 3 and 4 ulcers than pressure.

• Moisture - Exposure to moisture in the form of

perspiration, feces, or urine may lead to skin maceration and

predispose to superficial ulceration. There is little evidence regarding the

magnitude of the contribution of moisture to pressure ulcer development.9

Patient specific causes

Patient factors that may contribute to pressure ulcer development include immobility, incontinence, nutritional status, circulatory factors, and neurological disease.

• Immobility - Immobility is the most important patient factor that contributes to pressure ulcer development.

• Incontinence - Urinary incontinence is frequently cited as a predisposing factor for pressure ulcers. Some studies suggest that incontinent patients have up to a five-fold higher risk for pressure ulcer development10.

• Nutritional status - Among patients in hospital and care home settings, body mass index below 25 kg/m2 is associated with greater risk of pressure ulcer development11.

• Circulatory factors - The precise role of circulatory factors in pressure ulcer development must be further studied, although it appears likely that they will have a major role. Factors which can exacerbate or cause circulation issues include hypotension, dehydration, vasomotor failure, vasoconstriction secondary to shock, heart failure, or medications.

• Neurological diseases - Neurological diseases such as dementia, delirium, spinal cord injury, and neuropathy are important contributors to pressure ulcer development. This may be related to immobility, spasticity, and muscle contractions that are common in these conditions. Sensory loss is also common, suggesting that patients may not perceive pain or discomfort arising from prolonged pressure. Peripheral neuropathy due to diabetes is an example where pressure sores can occur due to sensory loss.

Prevention

The European Pressure Ulcer Advisory Panel made the following four points in relation to prevention of ulcers6.

1. Skin injury due to friction and shear forces should be minimised through correct positioning, transferring and repositioning techniques.

2. Eliminate any source of excess moisture due to incontinence, perspiration or wound drainage.

3. Reduce underlying risk factors such as poor nutrition.

4. Education and training, e.g. mobility, positioning, skin care, use of equipment, for patients and their carers.

PRESSURE RELIEF

Patient positioning

Proper positioning of bed-bound individuals is recommended, including a regular turning and repositioning schedule, with particular attention to vulnerable tissue covering bony prominences such as the sacrum13. Typically, a two-hour interval is recommended

In addition to regular turning, the position of bed-bound patients is likely to be important. It is recommended that:

• Patients should be placed at a 30 degree angle when lying on their side to avoid direct pressure over the hip bone or other bony prominences.

• Pillows or foam wedges should be placed between the ankles and knees to avoid pressure at these sites when patients have no mobility at these areas.

• The heels require particular attention; pillows may be placed under the lower legs to elevate the heels, or special heel protectors can be used.

• The head of the bed should not be elevated more that 30 degrees to prevent sliding and friction injury.

Chair-bound patients may generate considerable pressures over the hip joints; they should be repositioned at least every hour with wheelchair pushups or with tilting of the seat to reduce contact between the patient's buttocks and the seat14. Patients who are cognitively intact and are able to use their upper extremities can be trained to shift weight even more frequently, using monitoring devices as a reminder.

Support surfaces (mattresses) - these products can classified as either non-powered, overlays, or powered.

Non-powered support surfaces (previously known as static) do not require electricity and consist of mattresses that are made of gel, foam, air, or water, or a combination of these. They work by distributing pressure over a wider body surface area.

Sponsored by PfizerLearning, Evaluation, Accredited, Readers, Network | www.learninpharmacy.ie

Sponsored by PfizerLearning, Evaluation, Accredited, Readers, Network | www.learninpharmacy.ie

CPD 14: PRESSURE SORES

Overlays are support surfaces designed to be placed on top of another support surface. Foam, air, or water overlays may be used for patients who can assume a variety of positions without bearing weight on the ulcer.

Powered or dynamic support surfaces require electricity to alternate air currents in order to regulate or redistribute pressure against the body. Examples include alternating pressure mattresses, low air loss beds, and air fluidized mattresses.

For chair bound patients, appropriate wheelchair cushions are recommended. Donut cushions should not be used as they increase oedema and venous congestion and concentrate the pressure to surrounding tissue15. The three main types of seat cushions include gel and foam seat cushions, non-powered adjustable cushions and powered adjustable seat cushions.

Minimise immobility

Encouraging patient mobility is key to the prevention of pressure ulcers. Several approaches may be helpful to minimize immobility, including:

• Immobilised patients may benefit from physiotherapy.

• Severe spasticity may be relieved by muscle relaxant drugs (eg) Lioresal® or nerve block.

• Medications contributing to immobility, such as sedatives should be stopped.

Skin care

Skin condition should be inspected and documented daily.

• Skin assessment should include skin temperature, colour, moisture status, and integrity16. Any changes should be recorded as soon as they are observed17.

• Keeping the skin clean and dry, while avoiding excess dryness and scaling is the primary goal.

• Skin cleansing should be done with mild cleansing agents that minimise irritation.

• Hot water should be avoided.

• Vigorous massage over bony prominences should be avoided.

• Cleansings should be done at regular intervals to minimize exposure to excess moisture due to incontinence, perspiration, or wound drainage17-18.

Management1

• Repositioning of the patient.

• Treatment of concurrent conditions which may delay healing. (eg) poor circulation

• Pressure relieving support surfaces such as beds, mattresses, overlays or cushions.

• Local wound management using modern or advanced wound dressings and other technologies.

• Patients with identified grade 1 pressure ulcers are at a significant risk of developing more severe ulcers and should receive interventions to prevent deterioration.

Pain relief:

• Pain is often significant and disabling for those with pressure ulcers.

• Paracetamol may be sufficient, but patients often require stronger analgesia.

• Non-steroidal anti-inflammatory drugs may increase peripheral oedema and are inappropriate for patients with pressure ulcers. (eg) Ibuprofen, Diclofenac

• Opioid analgesics may be needed for moderate to severe pain.

• Topical local anesthetics such as lidocaine can provide numbness for a short period of time and can be useful for a specific procedure, but should not be used as the only method of pain relief.

• Wound cleansing and dressing techniques may need to be reconsidered if they are causing severe pain. In particular, adequate pain control should be provided for dressing changes and debridement.

• Patients may require referral to a pain clinic.

Nutrition

If oral intake is not adequate to ensure

sufficient calories, protein, vitamins, and minerals, nutritional supplementation with enteral and parenteral nutrition (PEG feed) is recommended to correct deficiencies.19-20 Increased dietary protein intake promotes the healing of pressure ulcers. The protein target is usually 1.5 g/kg/day. Cubitan® is an example of a high energy, high protein oral nutritional supplement (ONS) with wound specific nutrients (arginine, vitamin C, zinc, vitamin E). It increases healing times of pressures sore in under nourished patients. However, it is important that oral nutritional supplements are reviewed regularly by a dietitian. While high protein ONS such as Cubitan® have an important role in helping heal ulcers and other wounds, they should be discontinued promptly once the wound has healed. Food is the best vehicle for appropriate nutrient consumption.22 According to the National Medicines Information Centre in St James Hospital, Dublin; no studies have yet determined the optimum usage of ONS in terms of the most appropriate patients, the optimum dose and duration of use23. Despite lack of evidence, ONS has a role in many circumstances; therefore it is important to liaise with nutrition specialists such as dieticians before ONS can be recommended. For the added reason of the high cost of ONS to the state, the HSE also recommend that ONS is only commenced after the patient is assessed by a dietician.

Sponsored by PfizerLearning, Evaluation, Accredited, Readers, Network | www.learninpharmacy.ie

CPD 14: PRESSURE SORES

Dressings

There is no conclusive research evidence to guide health care professional decision making about which dressings are most effective in pressure ulcer management.

However professional consensus recommends that modern dressings (e.g. hydrocolloids, hydrogels, foams, films, alginates, soft silicones) should be used in preference to basic dressing types, (eg) gauze, paraffin gauze and simple dressing pads.4

Grade 1 ulcers may be dressed with transparent films for protection. (eg) Tegaderm®, Opsite®. Grade 2 pressure ulcers usually require an occlusive or semi permeable dressing that will maintain a moist wound environment. (eg) Comfeel Plus®, Granuflex®

Ulcers with heavy exudate require an absorptive dressing to avoid build up of chronic wound fluid that can lead to wound maceration and inhibit healing. An appropriate wound dressing can remove excess wound exudate while maintaining a moist environment to accelerate wound healing21. Dressings with absorptive qualities include alginates (eg) Kaltostat®, foams (eg) Allevyn®, Biatain®, and hydrocolloids (eg) Aquacel®, Comfeel®, Granuflex®.

Desiccated ulcers are dry ulcers that lack wound fluids which help promote heeling. Thus, pressure ulcer healing is promoted by dressings that maintain a moist wound environment while keeping the surrounding intact skin dry. Choices for a dry wound include hydrogels (eg) Granugel®, Intrasite Gel® and hydrocolloids (eg) Aquacel®, Comfeel®, Granuflex®.

Debridement

Necrotic tissue promotes bacterial growth and impairs wound healing. Wound debridement may involve any of five approaches: use of sharp dissection (take care when doing this on heels), mechanical debridement (wet-to-dry dressings), application of proteolytic enzymes, autolytic debridement under occlusive dressings (hydrocolloids or hydrogels), or biosurgery with sterilized maggots.

Infection control:

• Reduce risk of infection and enhance wound healing by hand washing, wound cleansing and debridement. Protect from external sources of contamination, e.g. faeces.3

• If purulent material or foul odour is present, more frequent cleansing and possibly debridement are required.

• When there are clinical signs of infection which do not respond to treatment, x-rays should be undertaken to exclude osteomyelitis and joint infection.3

• Systemic antibiotics are required for

patients with bacteraemia, sepsis, advancing cellulitis or osteomyelitis.3

References

1. Pressure ulcers in America: prevalence, incidence, and implications for the future: an executive summary of the national pressure ulcer advisory panel monograph. Adv Skin Wound Care 2001; 14:208.

2. European Pressure Ulcer Advisory Panel; Pressure Ulcer Grading System. 2003.

3. Bergstrom N, Braden B, Kemp M, et al; Predicting pressure ulcer risk: a multisite study of the predictive validity of the Braden Scale. Nurs Res. 1998 Sep-Oct;47(5):261-9. [abstract]

4. Pressure ulcers: The management of pressure ulcers in primary and secondary care, NICE Clinical Guideline (2005)

5. Thomas DR, Goode PS, Tarquine PH, et al; Hospital-acquired pressure ulcers and risk of death. J Am Geriatric Soc. 1996 Dec;44(12):1435-40. [abstract]

6. European Pressure Ulcer Advisory Panel; Pressure Ulcer Prevention Guidelines. 2003.

7. Kosiak, M. Etiology of decubitus ulcers. Arch Phys Med Rehabil 1961; 42:19.

8. Nola, GT, Vistnes, LM. Differential response of skin and muscle in the experimental production of pressure sores. Plast Reconstr Surg 1980; 66:728.

9. Cooney, LM Jr. Pressure sores and urinary incontinence. J Am Geriatr Soc 1997; 45:1278.

10. Lowthian, PT. Underpads in the prevention of decubiti. In: Bedsore biomechanics, Kenedi, RM, Cowden, JM, Scales, JT (Eds), University Park Press, Baltimore, MD 1976. p.141.

11. Berlowitz, DR, Brandeis, GH, Morris, JN, et al. Deriving a risk-adjustment model for pressure ulcer development using the Minimum Data Set. J Am Geriatr Soc 2001; 49:866.

12. Makhsous, M, Priebe, M, Bankard, J, et al. Measuring tissue perfusion during pressure relief maneuvers: insights into preventing pressure ulcers. J Spinal Cord Med 2007; 30:497.

13. Reddy, M, Gill, SS, Rochon, PA. Preventing pressure ulcers: a systematic review. JAMA 2006; 296:974.

14. Makhsous, M, Priebe, M, Bankard, J, et al. Measuring tissue perfusion during pressure relief maneuvers: insights into preventing pressure ulcers. J Spinal Cord Med 2007; 30:497.

15. Stechmiller, JK, Cowan, L, Whitney, JD, et al. Guidelines for the prevention of pressure ulcers. Wound Repair Regen 2008; 16:151.

16. Lyder, CH, Ayello, EA. Chapter 12. Pressure ulcers: a patient safety issue. Available online at: www.ahrq.gov/qual/nurseshdbk/docs/LyderC_PUPSI.pdf - 2008-03-11 (Accessed on October 10, 2008).

17. European Pressure Ulcer Advisory Panel (EPUAP). Guidelines on treatment of pressure ulcers. EPUAP Review 1999; 1:31.

18. Pressure ulcers in adults: Prediction and prevention. Clinical Practice Guideline Number 3, AHCPR Publication no. 92-0047, May 1992.

19. Allman, RM, Walker, JM, Hart, MK, et al.

Air-fluidized beds or conventional therapy for pressure sores. A randomized trial. Ann Intern Med 1987; 107:641.

20. Breslow, RA, Hallfrisch, J, Guy, DG, et al. The importance of dietary protein in healing pressure ulcers. J Am Geriatr Soc 1993; 41:357.

21. Schultz, GS, Sibbald, RG, Falanga, V, et al. Wound bed preparation: a systematic approach to wound management. Wound Repair Regen 2003; 11 Suppl 1:S1.

22. Tripp F, The use of dietary supplements in the elderly: Current issues and recommendations J Am Diet Assoc 1997; 97(suppl 2): S181-S183.

23. National Medicines Information Centre, St James Hospital, Dublin 8. Volume 10, Number 2. The role of oral nutritional supplements in primary care. 2004.

Disclaimer: The information expressed in this CPD article is that of the author and is independent of Pfizer Healthcare Ltd. and/or IPN Communications Ltd.

Pfizer Healthcare Ireland are committed to supporting the continuous professional development of pharmacists in Ireland. We are delighted to be partnering with Irish Pharmacy News in order to succeed with this.

Throughout the year, Irish Pharmacy News will deliver 12 separate modules of continuous professional development, across a wide range of therapy areas. These topics are chosen to support the more common interactions with pharmacy patients, and to optimise the patient experience with retail pharmacy.

We began the 2011 programme with a section on the Gastrointestinal System. Other topics include Diabetes (Types I and II), the Cardiovascular System, Smoking Cessation, Infections, Parkinson’s Disease, Alzheimer’s Disease, Depression and others. We hope you will find value in all topics.

Pfizer’s support of this programme is the latest element in a range of activities designed to benefit retail pharmacy. Other initiatives include the Multilingual Pharmacy Tool, a tailored Medical Communications Programme, Educational Meetings and Grants, our Patient Information Pack, new pharmacy Consultation Room brochures and other patient-assist programmes including the Quit with Help programme and www.mysterypain.ie.

If you would like additional information on any of these pharmacy programmes, please contact Pfizer Healthcare Ireland on 01-4676500 and ask for the Established Products Business Unit.

MADE IN IRELAND3

40% PRICE REDUCTION1

EFFECTIVE JANUARY 1ST 2011

ZOTON* FasTab - Abbreviated Prescribing Information (Republic of Ireland)ZOTON* FasTab Presentation Oro-dispersible tablet containing 30 mg or 15 mg of lansoprazole. White to yellowish-white, circular fl at beveled-edge oro-dispersible tablet with “15” or “30 “ debossed on one side. Containing orange to dark brown microgranules. Indications Treatment of duodenal and gastric ulcer. Treatment of refl ux oesophagitis. Prophylaxis of refl ux oesophagitis. Eradication of Helicobacter pylori (H. pylori) concurrently given with with appropriate antibiotic therapy for treatment of H. pylori-associated ulcers. Treatment of NSAID-associated benign gastric and duodenal ulcers in patients requiring continued NSAID treatment. Prophylaxis of NSAID-associated gastric ulcers and duodenal ulcers in patients at risk requiring continued therapy. Symptomatic gastroesophageal refl ux disease (GORD). Zollinger-Ellison syndrome. Dosage and Administration Duodenal ulcer: 30 mg daily for 2 weeks. If not fully healed within 2 weeks, then 30 mg daily for a further 2 weeks. Gastric ulcer: 30 mg daily for 4 weeks. If not fully healed within 4 weeks, then 30 mg daily for a further 4 weeks. Refl ux oesophagitis: 30 mg daily for 4 weeks. If not fully healed within 4 weeks, then 30 mg daily for a further 4 weeks. Prophylaxis of refl ux oesophagitis: 15 mg or 30 mg daily. Eradication of H. pylori (both regimens twice daily for 7 days): 30 mg plus: clarithromycin 250 – 500 mg and amoxicillin 1 g or clarithromycin 250 mg and metronidazole 400 – 500 mg. Treatment of NSAID-associated benign gastric and duodenal ulcers: 30 mg daily for 4 weeks. If not fully healed with 4 weeks, then 30 mg for further 4 weeks. Use higher dose and/or longer duration in patients at risk or with ulcers diffi cult to heal. Prophylaxis of NSAID-associated gastric and duodenal ulcers: 15 mg daily. 30 mg daily if treatment fails. Symptomatic GORD: 15 mg or 30 mg daily for 4 weeks. Zollinger-Ellison syndrome: Initially 60 mg daily, then adjust individually. For most rapid healing and symptom relief, the morning dose of Zoton FasTab should be taken before food. The tablet can be placed on the tongue and gently sucked or, if preferred, swallowed whole with a drink of water. Zoton FasTab can also be dispersed in a small amount of water and administered via a nasogastric tube or oral syringe. No dosage adjustment is necessary in patients with impaired renal function. 50% reduction of the daily dose is recommended in patients with moderate or severe liver disease. A daily dose of 30 mg should not be exceeded in the elderly. The use of Zoton FasTab in children is not recommended due to limited clinical data. Treatment of small children below one year of age should be avoided as no clinical benefi t has been observed in the treatment of GORD. Contra-indications Hypersensitivity to any of the ingredients. Zoton FasTab should not be administered with atazanavir. Precautions Exclude the possibility of malignancy when treating a gastric ulcer. Use with caution in patients with moderate to severe hepatic dysfunction. Decreased gastric acidity increases gastric counts of endogenous bacteria. Treatment may lead to a slightly increased risk of gastrointestinal infections (e.g. Salmonella, Campylobacter). In patients with gastro-duodenal ulcers, consider the possibility of H. pylori as an etiological factor. Cases of colitis have very rarely been reported in patients taking lansoprazole. Treatment for prevention of peptic ulceration of patients in need of continuous NSAID treatment should be restricted to those at high risk. Zoton FasTab contains lactose. Pregnancy and Lactation Avoid in pregnancy. Avoid during breast feeding unless essential. Interactions Medicinal products with pH dependent absorption: Lansoprazole may interfere with the absorption of drugs where gastric pH is critical to bioavailability. Lansoprazole should not be co-administered with atazanavir. The absorption of ketoconazole and itraconazole from the gastrointestinal tract is enhanced by the presence of gastric acid, this may lead to sub-therapeutic concentrations. As co-administration of lansoprazole and digoxin may lead to increased plasma levels, level monitoring is recommended. Medicinal products metabolised by P450 enzymes: Lansoprazole may increase plasma concentrations of drugs that are metabolised by CYP3A4. Caution is advised when combining lansoprazole with drugs which are metabolised by this enzyme and have a narrow therapeutic window, such as theophylline or tacrolimus. Medicinal products transported by P-glycoprotein: Lansoprazole has been observed to inhibit the transport protein P-glycoprotein (P-gp) in vitro. The clinical relevance of this is unknown. Drugs which inhibit CYP2C19: A dose reduction may be considered when combining lansoprazole with fl uvoxamine. A study shows that the plasma concentrations of lansoprazole increase up to 4-fold. Drugs which induce CYP2C19 & CYP3A4: Enzyme inducers affecting CYP2C19 and CYP3A4, such as rifampicin and St John’s wort, can markedly reduce the plasma concentrations of lansoprazole. Others: Sucralfate / antacids may decrease the bioavailability of lansoprazole. Therefore lansoprazole should be taken at least 1 hour after taking these drugs. No clinically signifi cant interactions of lansoprazole with NSAIDs have been demonstrated, although no formal interactions studies have been performed. Side Effects The most common side effects include headache, dizziness, nausea, diarrhoea, stomach ache, constipation, vomiting, fl atulence, dry mouth or throat, fatigue, urticaria, itching, rash, and increase in liver enzyme levels. Uncommon side effects include depression, thrombocytopenia, eosinophilia, leucopenia, arthralgia, myalgia, and oedema. Anaemia, insomnia, hallucinations, confusion, restlessness, vertigo, paraesthesia, somnolence, tremor, visual disturbances, glossitis, candidiasis of the oesophagus, pancreatitis, taste disturbances, hepatitis, jaundice, petechiae, purpura, hair loss, erythema multiforme, photosensitivity, interstitial nephritis, gynaecomastia, fever, hyperhidrosis, angioedema, anorexia and impotence have been reported rarely. Very rarely agranulocytosis, pancytopenia, colitis, stomatitis, Steven-Johnson syndrome, toxic epidermal necrolysis, anaphylactic shock, increase in cholesterol and triglyceride levels, and hyponatraemia have been reported. Legal Category POM. Product subject to prescription which may be renewed (B) Package Quantities 30 mg Zoton FasTab: Blister packs of 28, 14, 7 (hospitals only) and 7 (sample pack) tablets.15 mg Zoton FasTab: Blister packs of 28 tablets. Product Authorisation Numbers 30 mg Zoton FasTab: PA 0822/101/003 15 mg Zoton FasTab: PA 0822/101/002 Full Prescribing Information is available on request. Name and Address of Authorisation Holder Pfi zer Healthcare Ireland, 9 Riverwalk, National Digital Park, Citywest Business Campus, Dublin 24, Ireland *Trademark of, and under licence agreement with, Takeda Pharmaceutical Company Limited, Japan. Date of Prescribing Information: 29 June 2011 Ref: ZT 2_0 References: 1 Ex-factory prices for all community packs of Zoton FasTab have dropped by 40% with effect from 1st January 2011. 2 Table represents ex-factory prices (equivalent to MIMS prices) before and after 40% price reduction. 3 Data on fi le. Date of preparation: November 2011. ZTB/2011/011.

Old Price New Price2 REDUCTION30mg(28) 36.29 21.77 40%15mg (28) 18.26 10.96 40%