The prevalence of leg ulceration in adults, either active or healed, is 1% to 2%, and the majority have chronic venous insufficiency.1 Although CVI has received less attention than arterial insufficiency, estimates suggest it is 10 times more common. Despite the prevalence of venous ulcers, they are often neglected or managed inadequately.
Recognition
Venous leg ulcers are generally irregularly shaped partial thickness wounds with well-defined borders surrounded by erythematous
or hyperpigmented indurated skin (acute or chronic lipodermatosclerosis). A yellow-white exudate is common. Venous ulcers are usually located on the distal medial aspect of the lower leg. Varicose veins are often present and typically there are telangiectatic veins of the medial ankle, so-called corona phlebectatica. Edema of the ankle area is common.
Differential diagnoses—including arterial, metabolic, neuropathic, neoplastic, vasculitic, infectious, hematologic, and collagen vascular diseases and pyoderma gangrenosum—should be considered. However, if arterial insufficiency is ruled out and the patient has normal pinprick sensation in the presence of a typical appearing venous ulcer, then a venous etiology will be found in about 95% of cases.2
Macrocirculation
The calf muscle pump is the primary mechanism to return blood from the leg to the heart. The calf pump mechanism consists of the calf muscles (primarily the soleus and gastrocnemius); the deep venous compartment, or pump chamber; a superficial compartment con necting the superficial veins to the deep veins via perforators; and an outflow tract (popliteal vein).
In patients with chronic venous insufficiency, limbs with venous ulceration have been shown by air plethysmography to have significantly reduced ejection fractions and higher residual volume fractions than nonulcerated limbs.3 This substantiates the significant role calf pump dysfunction plays in venous ulceration.
Calf pump dysfunction may occur because of deep venous insufficiency (primary or post-thrombotic), deep venous obstruction, perforator insufficiency, superficial venous insufficiency, arteriovenous fistulas, neuromuscular dysfunction, or a combination of these. Calf pump dysfunction results in a failure to lower venous pressure in the distal veins of the leg, a condition called ambulatory venous hypertension.
Although any of the aforementioned factors may cause calf pump dysfunction, the main factor is usually venous insufficiency. A common misconception is that a venous leg ulcer is pathognomonic of a post-thrombotic syndrome. Superficial venous disease and perforator disease alone commonly cause venous ulceration.4 The common final pathway to venous ulceration is venous hypertension, whether the overload comes from superficial, perforator, deep vein, or combination disease.
An appropriate evaluation, including (but not limited to) directed history and physical exam and duplex ultrasound imaging, is essential in the evaluation of patients with leg ulcers.
History and physical
Clinicians should seek details relating to the ulcer, such as its duration and previous treatment, the presence and characteristics of exudate, the presence, description, and severity of pain, and factors that aggravate and alleviate the symptoms. A history of similar lesions and their course and management is also useful.
In addition, ask patients for their history of thromboembolic events, varicose veins, past vein treatment, tobacco use, arterial disease, diabetes, arthritis, ankle joint immobility, inflammatory bowel disease, and collagen vascular disease. Also note their occupation and social situation.
Physical examination should include a careful inspection and palpation of the legs, from the foot to the groin, for varicose veins. The suprapubic area should also be inspected for varicosities, which might represent collateral bypass of an old iliofemoral thrombosis. Percussion of veins helps trace the origin and extent of varices. Examine for signs of CVI, such as ankle flare, eczema, hyperpigmentation, induration, and atrophie blanche. Measure ankle and calf diameters for both legs and characterize edema as pitting or nonpitting.
Describe ulcer size, base, appearance, and location as well as the condition of the surrounding skin and note the presence and characteristics of exudate and signs of true tissue infection.
Acute lipodermatosclerosis, characterized by an erythematous tender area of induration, is commonly mistaken for cellulitis.5 However, lipodermatosclerosis is an inflammatory condition that results from venous insufficiency, does not cause fever, and is unresponsive to antibiotics. Note that both lipodermatosclerosis and cellulitis may be seen in the presence of venous ulcers.6
Signs of arterial insufficiency (cool skin, loss of extremity hair, shiny and atrophic skin, pallor on leg elevation) should be noted. Arterial pulses should be palpated. If there is suspicion of arterial insufficiency, measure the ankle brachial index (ABI=systolic pressure at the ankle divided by that at the brachial artery; normal ABI is >0.9).
Note that the ABI is unreliable in assessing arterial insufficiency in patients with diabetes or other conditions in which there may be arterial calcification.7 In such cases metatarsal or toe pressures are more reliable. Evaluate ankle mobility and gait and check peripheral sensation.
Compression
There is wide agreement on the importance of compression in treating venous ulcers.8,9 Compression therapy may be done in the context of complex (or complete) decongestive therapy (CDT), which, in addition to compression therapy, consists of patient instruction in meticulous skin care, manual lymphatic drainage, and exercise.10
There are two compression phases to CDT, an initial decongestive phase followed by a maintenance phase.10-11 Generally, the adage that compression bandaging obtains a result and compression stockings maintain the result is true. However, several multilayer compression stocking options have been designed specifically to heal venous ulcers. If those options are not available, compression bandaging during the decongestive phase is done with inelastic short-stretch bandages.
Expertise in applying a short-stretch bandage is required. In the presence of concomitant arterial insufficiency, one must exercise considerable caution; it is imperative that any compression exert a low resting pressure (inelastic compression) in order not to compromise arterial flow.12 If arterial insufficiency is severe, compression of any type may be contraindicated.
Physical limitations notwithstanding, prescription compression stockings should be used in the maintenance phase of treatment. Generally a calf-length stocking with 30 mm Hg to 40 mm Hg is used, but another option is to superimpose two 20 mm Hg to 30 mm Hg stockings (yielding 40-plus mm Hg).13 Velcro-based bandages can also be useful in patients with arthritis who have a difficult time donning stockings.
Compression leads to increased venous flow, decreased pathological reflux while walking, and increased ejection volume with activation of the calf pump.14-18 Tissue pressure is increased, which favors resorption of edema fluid. Proinflammatory cytokine protein levels are elevated in ulcer tissue, and compression therapy significantly reduces these levels.19 Noncompliance with stocking use is an independent risk factor for progression of chronic venous disease.20
Ablate superficial venous disease
If a patient has hemodynamically significant superficial venous disease, either isolated or in combination with perforator or deep vein disease, important hemodynamic improvement will be obtained by treating the varicose veins. A randomized controlled trial found that treatment of underlying reflux in combination with compression therapy reduced recurrence rate compared to compression alone.21 Minimally invasive endovenous ablation modalities, such as endovenous laser, radiofrequency ablation, and foam sclerotherapy, are largely replacing stripping in the treatment of saphenous incompetence.
The hemodynamic significance of perforators in CVI remains controversial.22 Deep venous reconstruction should only be done as a last resort and probably only as part of an appropriately designed clinical study.
Ancillary measures
A detailed review of wound care is beyond the scope of this article. Note that local wound care is a matter of clinical judgment, and even optimal wound care is no substitute for compression and other measures that address the underlying pathophysiology.
Patients should be instructed to maintain a normal weight and avoid smoking and educated about physical therapy, which can improve ankle joint mobility.23 Encourage patients to take regular brisk walks. It’s helpful to have a patient periodically elevate his or her leg above heart level and to raise the foot of their bed with 6-inch blocks.
Manual lymphatic drainage performed by trained therapists can reduce edema associated with CVI. Research has shown that pentoxifylline, a drug that improves blood flow, facilitates venous leg ulcer healing when used as an adjunct to compression and may also be effective on its own.24
If a patient doesn’t respond to appropriate therapy within two to three months, the practitioner should review the adequacy of compression as well as patient compliance. The diagnosis also needs to be reconsidered.25 In particular, one should consider obtaining a biopsy of the ulcer edge to rule out malignancy.26
Conclusion
Newer methods of investigation have led to an improvement in our understanding of the pathophysiology and management of venous disease. Compression should serve as the cornerstone of treatment in patients with venous ulcers. However, one must define the basic underlying abnormality of the venous system and any associated diseases to establish a rational, individualized management plan for patients with venous ulceration.
Steven E. Zimmet, MD, is in private practice in Austin, Texas. His practice focus is phlebology and procedural dermatology.
References
1. Callam MJ, Ruckley CV, Harper DR, Dale JJ. Chronic ulceration of the leg: extent of the problem and provision of care. Br Med J 1985;290(6485):1855-1856.
2. Burton C. Most leg ulcers stem from venous disease. Skin and Allergy News 1999;30:35.
3. Araki CT, Back TL, Padberg FT, et al. The significance of calf muscle pump function in venous ulceration. J Vasc Surg 1994;20(6):872-877.
4. Hanrahan LM, Araki CT, Rodriguez AA, et al. Distribution of valvular incompetence in patients with venous stasis ulceration. J Vasc Surg 1991;13(6):805-811.
5. Huang TM, Lee JY. Lipodermatosclerosis: a clinicopathologic study of 17 cases and differential diagnosis from erythema nodosum. J Cutan Pathol 2009;36(4):453-460.
6. Collins L, Seraj S. Diagnosis and treatment of venous ulcers. Am Fam Physician 2010;81(8):989-996.
7. Potier L, Abi Khalil C, Mohammedi K, Roussel R. Use and utility of ankle brachial index in patients with diabetes. Eur J Vasc Endovasc Surg 2011;41(1):110-116.
8. O’Meara S, Cullum NA, Nelson EA. Compression for venous leg ulcers.Cochrane Database Syst Rev 2009(1):CD000265.
9. Nelson EA, Mani R, Vowden K. Intermittent pneumatic compression for treating venous leg ulcers. Cochrane Database Syst Rev 2008(2):CD001899.
10. The diagnosis and treatment of peripheral lymphedema: Consensus document of the International Society of Lymphology. Lymphology 2003;36(2):84-91.
11. Földi M, Földi E, Strobenreuther RHK, eds. Földi’s Textbook of Lymphology: for physicians and lymphedema therapists. 2nd ed. Munich, Germany: Elsevier; 2006:272-273.
12. Hsu JTS. Leg Vein Management. In: Kaminer MS, Arndt KA, Dover JS (eds). Atlas of Cosmetic Surgery. 2nd edition. Philadelphia: W. B. Saunders; 2009:459-460.
13. Cornu-Thenard A, Boivin P, Carpentier PH, Courtet F, Ngo P. Superimposed elastic stockings: pressure measurements. Dermatol Surg 2007;33(3):269-275.
14. Labropoulos N, Giannouikas AD, Nicolaides AN, et al. The role of venous reflux and calf muscle pump function in nonthrombotic chronic venous insufficiency. Correlation with severity of signs and symptoms. Arch Surg 1996;131(4):403-406.
15. Partsch H, Clark M, Bassez S, et al. Measurement of lower leg compression in vivo: recommendations for the performance of measurements of interface pressure and stiffness: consensus statement. Dermatol Surg 2006;32(2):224-233.
16. Partsch H. Do we still need compression bandages? Haemodynamic effects of compression stockings and bandages. Phlebology 2006;21(3):132-138.
17. Igebuna V, Delis KT, Nicolaides AN, Aino O. Effect of elastic compression stockings on venous hemodynamics during walking. J Vasc Surg 2003;37(2):420-425.
18. Partsch H. Compression therapy in venous leg ulcers: How does it work? J Phlebol 2002;2:129-136.
19. Beidler SK, Douillet, CD, Berndt DF, et al. Inflammatory cytokine levels in chronic venous insufficiency ulcer tissue before and after compression therapy. J Vasc Surg 2009;49(4):1013-1020.
20. Kostas TL, Ioannou CV, Drygiannakis I, et al. Chronic venous disease progression and modification of predisposing factors. J Vasc Surg 2010;51(4):900-907.
21. Gohel M, Barwell J, Taylor M, et al. Long term results of compression therapy alone versus compression plus surgery in chronic venous ulceration (ESCHAR): randomised controlled trial. BMJ. 2007;335(7610):83.
22. O’Donnell TF. The role of perforators in chronic venous insufficiency. Phlebology 2010;25(1):3-10.
23. Robertson L, Lee A, Gallagher K, et al. Risk factors for chronic ulceration in patients with varicose veins: a case control study. J Vasc Surg 2009;49(6):1490-1498.
24. Jull A, Arroll B, Parag V, Waters J. Pentoxifylline for treating venous leg ulcers. Cochrane Database Syst Rev 2007(3):CD001733.
25. Cornu-Thenard A, Lehodey Y, Meninge T. Leg ulcers of venous origin. Rate of basic healing. Practical consequences. Phlebologie 1984;37(3):347-354.
26. Olewiler SD. Marjolin’s ulcer due to venous stasis. Cutis 1995;56(3):168-170.
Showing posts with label venous ulcers. Show all posts
Showing posts with label venous ulcers. Show all posts
Monday, August 29, 2011
Thursday, February 3, 2011
Exploring The Potential Of Procedures That Address Venous Ulcer Etiology
The complexity of venous ulcerations leads to prolonged healing and doubt. Clinicians have traditionally treated venous wounds with debridement, multi-layer compression dressings and skin grafts.
Most of the literature focuses on various topical ointments, the use of allogenic grafting, compression therapies, etc. Unfortunately, there is little research on addressing the etiology of venous wounds. Understanding and treating the etiology in all aspects of medicine is imperative in order to achieve a successful result.
Venous insufficiency is a condition in which veins do not adequately return blood back to the central system. In the lower extremity, both the superficial and deep vein systems of the legs utilize valves to ensure cephalad flow. The deep vein system also uses muscular contraction to assist in pumping the blood upward. A perforating vein is a vein that penetrates a fascial plane and may connect the superficial venous system to the deep vein system or connect greater saphenous veins to small saphenous veins.
Over time, various risks factors such as heredity, hormones, pregnancy and prolonged standing cause the smooth muscle in the vein’s wall to relax. When this occurs, there is an inability of the vein valves to approximate. In the legs, the normal flow opposes gravity. However, with insufficiency, the blood refluxes and backflow occurs to the ankles. In severe cases, blood pooling leads to edema, hyperpigmentation, loss of skin turgor and ulceration. An ulcer can also occur after a varicose vein opens and causes bleeding.
Consider a patient who presents with a venous ulceration. In most cases, these patients receive wound care and compression therapy. One does not usually perform an ultrasound. Ultrasound is crucial in finding out where the insufficiency lies and which veins lead to the ulceration. It is imperative that the physician or registered vascular technician evaluates both the deep vein and superficial vein systems for reflux. Just scanning the deep vein system for a thrombus would be incomplete and will not identify the pathology involved.
Direct attention to the lower extremities while the patient is standing. Evaluate the deep vein system, including the femoral, popliteal, tibial and peroneal veins, and look for the presence of a thrombus and reflux. In the superficial system, test the greater and small saphenous veins as well as anterior and posterior circumflex and perforating veins.
In general, one should utilize the following guidelines to identify insufficiency in the superficial system: a greater saphenous vein larger than 0.4 cm in diameter, longer than 0.5 seconds of reflux and a small saphenous or perforating vein larger than 0.3 cm in diameter and 0.5 seconds of reflux. If varicosities are present, one can follow the varicosities towards their tributary. This is called vein mapping.
With the presence of a venous ulcer, the ultrasonographer will be able to scan over the ulcer and trace it back to the insufficient vein. The ulcer is usually a direct extension from a superficial varicosity. However, the underlying etiology is a result of insufficiency of the superficial, deep or perforating vein system. By addressing the insufficient vein either through ultrasound guided chemical ablation or endovenous ablation, venous ulcerations heal on an average of four weeks barring that no infection is present.
Key Insights On Ultrasound Guided Chemical Ablation
Ultrasound guided chemical ablation is a treatment in which one injects a sclerosant into the refluxing vein. The two most common sclerosants are sodium tetradecyl sulfate (Sotradecol, Angiodynamics), which recently received FDA approval, and polidocanol (Asclera, Merz). Traditional saline injections are not strong enough to treat large veins and should be reserved for cosmetic spider and reticular veins only.
With ultrasound guidance, inject liquid sclerosant or foam sclerosant (sclerosant mixed with air or CO2) into the insufficient vein. Foam has become widely accepted for its advantages. Foam solution makes more contact with the vein wall due to increased surface area properties, disperses quicker and stays in the vein longer than liquid. Furthermore, one can easily visualize and follow the solution on ultrasound during treatment. With sclerotherapy treatment, the chemical damages the vessel wall. The vein hardens and the body breaks it down. Larger and deeper veins will harden, thicken and shrink but may not disappear altogether.
One does not directly inject the ulceration but rather the insufficient vein along its course. If one performs ultrasound chemical ablation alone, it will take a few treatments before treatment addresses the veins at the ulceration site. Accordingly, this method usually occurs after an ablative procedure. Only perform this treatment on the superficial and perforating vein systems. Do not inject the deep venous system.
A Closer Look At Endovenous Laser Ablation
Endovenous laser or radiofrequency ablation is a procedure that closes the long segment of the insufficient vein. First access the insufficient vein under the guidance of ultrasound. Through the access needle, insert a guide wire. Remove the needle and place a dilator and sheath over the wire and into the vessel. Remove the wire and the dilator, and leave the sheath in the vein. Proceed to instill a fiber optic laser or catheter for radiofrequency. Confirm the placement of the fiber or cathode exiting the end of the sheath. Be sure to avoid superficial/deep vein junctions by at least 1.5 inches.
Then deliver anesthetic agents mixed with saline, creating what is known as a sea of tumescence. After administering adequate anesthetic, remove the sheath along with the laser and/or catheter while delivering laser energy or radiofrequency. One must apply enough laser energy or radiofrequency to the vein in order to create appropriate closure and stop the flow through the insufficient portion. After the procedure, the patient wears compression stockings and bandages over the ulceration for approximately one week.
Follow-up with the patient includes the use of post-procedure ultrasound to confirm the success of the procedure (namely ensuring there is no deep thrombus) and mapping the vein to the ulcerated site.
Perform traditional debridement and have the patient wear compression dressings for two weeks. After the two-week period, if the ulceration has not already healed, ultrasound guided chemical ablation may close any remaining branches of veins that have reflux flow. Do not inject sclerosant directly through the ulceration. It is imperative to treat any and all vessels leading to the ulceration but it is not necessary to treat all superficial vein structures if insufficiency is not present.
Over the course of therapy, the ulceration will decrease in size and the vessels will become hardened. Perform injections every three to four weeks. Four to six sessions may be needed to complete the course of therapy. On ultrasound, these vessels will not be able to compress and there is no filling on color flow Doppler.
Final Thoughts
It is important to note that once an individual has venous insufficiency, it does not go away and may in fact affect other veins. Other veins may become insufficient due to increased load and hypertension, and new vessels can develop. This process is called neovascularization. It is necessary to perform maintenance and follow-up care to ensure a new ulceration does not develop.
Performing procedures to improve and control the chronic venous insufficiency should be the focus of venous ulcer healing. Depending on the size and healing potential of the patient, the wound healing time is significantly shorter. This positively affects all aspects of patient care including increased patient adherence, decreased risk of infection, decreased healthcare costs and more efficient medical care.
Most of the literature focuses on various topical ointments, the use of allogenic grafting, compression therapies, etc. Unfortunately, there is little research on addressing the etiology of venous wounds. Understanding and treating the etiology in all aspects of medicine is imperative in order to achieve a successful result.
Venous insufficiency is a condition in which veins do not adequately return blood back to the central system. In the lower extremity, both the superficial and deep vein systems of the legs utilize valves to ensure cephalad flow. The deep vein system also uses muscular contraction to assist in pumping the blood upward. A perforating vein is a vein that penetrates a fascial plane and may connect the superficial venous system to the deep vein system or connect greater saphenous veins to small saphenous veins.
Over time, various risks factors such as heredity, hormones, pregnancy and prolonged standing cause the smooth muscle in the vein’s wall to relax. When this occurs, there is an inability of the vein valves to approximate. In the legs, the normal flow opposes gravity. However, with insufficiency, the blood refluxes and backflow occurs to the ankles. In severe cases, blood pooling leads to edema, hyperpigmentation, loss of skin turgor and ulceration. An ulcer can also occur after a varicose vein opens and causes bleeding.
Consider a patient who presents with a venous ulceration. In most cases, these patients receive wound care and compression therapy. One does not usually perform an ultrasound. Ultrasound is crucial in finding out where the insufficiency lies and which veins lead to the ulceration. It is imperative that the physician or registered vascular technician evaluates both the deep vein and superficial vein systems for reflux. Just scanning the deep vein system for a thrombus would be incomplete and will not identify the pathology involved.
Direct attention to the lower extremities while the patient is standing. Evaluate the deep vein system, including the femoral, popliteal, tibial and peroneal veins, and look for the presence of a thrombus and reflux. In the superficial system, test the greater and small saphenous veins as well as anterior and posterior circumflex and perforating veins.
In general, one should utilize the following guidelines to identify insufficiency in the superficial system: a greater saphenous vein larger than 0.4 cm in diameter, longer than 0.5 seconds of reflux and a small saphenous or perforating vein larger than 0.3 cm in diameter and 0.5 seconds of reflux. If varicosities are present, one can follow the varicosities towards their tributary. This is called vein mapping.
With the presence of a venous ulcer, the ultrasonographer will be able to scan over the ulcer and trace it back to the insufficient vein. The ulcer is usually a direct extension from a superficial varicosity. However, the underlying etiology is a result of insufficiency of the superficial, deep or perforating vein system. By addressing the insufficient vein either through ultrasound guided chemical ablation or endovenous ablation, venous ulcerations heal on an average of four weeks barring that no infection is present.
Key Insights On Ultrasound Guided Chemical Ablation
Ultrasound guided chemical ablation is a treatment in which one injects a sclerosant into the refluxing vein. The two most common sclerosants are sodium tetradecyl sulfate (Sotradecol, Angiodynamics), which recently received FDA approval, and polidocanol (Asclera, Merz). Traditional saline injections are not strong enough to treat large veins and should be reserved for cosmetic spider and reticular veins only.
With ultrasound guidance, inject liquid sclerosant or foam sclerosant (sclerosant mixed with air or CO2) into the insufficient vein. Foam has become widely accepted for its advantages. Foam solution makes more contact with the vein wall due to increased surface area properties, disperses quicker and stays in the vein longer than liquid. Furthermore, one can easily visualize and follow the solution on ultrasound during treatment. With sclerotherapy treatment, the chemical damages the vessel wall. The vein hardens and the body breaks it down. Larger and deeper veins will harden, thicken and shrink but may not disappear altogether.
One does not directly inject the ulceration but rather the insufficient vein along its course. If one performs ultrasound chemical ablation alone, it will take a few treatments before treatment addresses the veins at the ulceration site. Accordingly, this method usually occurs after an ablative procedure. Only perform this treatment on the superficial and perforating vein systems. Do not inject the deep venous system.
A Closer Look At Endovenous Laser Ablation
Endovenous laser or radiofrequency ablation is a procedure that closes the long segment of the insufficient vein. First access the insufficient vein under the guidance of ultrasound. Through the access needle, insert a guide wire. Remove the needle and place a dilator and sheath over the wire and into the vessel. Remove the wire and the dilator, and leave the sheath in the vein. Proceed to instill a fiber optic laser or catheter for radiofrequency. Confirm the placement of the fiber or cathode exiting the end of the sheath. Be sure to avoid superficial/deep vein junctions by at least 1.5 inches.
Then deliver anesthetic agents mixed with saline, creating what is known as a sea of tumescence. After administering adequate anesthetic, remove the sheath along with the laser and/or catheter while delivering laser energy or radiofrequency. One must apply enough laser energy or radiofrequency to the vein in order to create appropriate closure and stop the flow through the insufficient portion. After the procedure, the patient wears compression stockings and bandages over the ulceration for approximately one week.
Follow-up with the patient includes the use of post-procedure ultrasound to confirm the success of the procedure (namely ensuring there is no deep thrombus) and mapping the vein to the ulcerated site.
Perform traditional debridement and have the patient wear compression dressings for two weeks. After the two-week period, if the ulceration has not already healed, ultrasound guided chemical ablation may close any remaining branches of veins that have reflux flow. Do not inject sclerosant directly through the ulceration. It is imperative to treat any and all vessels leading to the ulceration but it is not necessary to treat all superficial vein structures if insufficiency is not present.
Over the course of therapy, the ulceration will decrease in size and the vessels will become hardened. Perform injections every three to four weeks. Four to six sessions may be needed to complete the course of therapy. On ultrasound, these vessels will not be able to compress and there is no filling on color flow Doppler.
Final Thoughts
It is important to note that once an individual has venous insufficiency, it does not go away and may in fact affect other veins. Other veins may become insufficient due to increased load and hypertension, and new vessels can develop. This process is called neovascularization. It is necessary to perform maintenance and follow-up care to ensure a new ulceration does not develop.
Performing procedures to improve and control the chronic venous insufficiency should be the focus of venous ulcer healing. Depending on the size and healing potential of the patient, the wound healing time is significantly shorter. This positively affects all aspects of patient care including increased patient adherence, decreased risk of infection, decreased healthcare costs and more efficient medical care.
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