US researchers say they have identified how a high-fat diet interferes with the body's sugar sensors and triggers type 2 diabetes....
The authors argue that a deeper understanding of the processes involved could help them develop a cure. One of the main risk factors for type 2 diabetes is being overweight -- rising obesity levels have contributed to a doubling of diabetes cases in the last 30 years.
Sugar in the blood is monitored by pancreatic beta cells. If sugar levels are too high then the cells release the hormone insulin, which tells the body to bring the levels back down. Key to this is the enzyme GnT-4a. It allows the cells to absorb glucose and therefore know how much is in the blood.
Researchers at the University of California and the Sanford-Burnham Medical Research Institute say they have shown how fat disrupts the enzyme's production. Experiments on mice showed that those on a high-fat diet had elevated levels of free fatty acids in the blood. These fatty acids interfered with two proteins - FOXA2 and HNF1A - involved in the production of GnT-4a. The result: fat effectively blinded cells to sugar levels in the blood and the mice showed several symptoms of type 2 diabetes. The same process also took place in samples of human pancreatic cells.
Lead researcher Dr. Jamey Marth said, "The observation that beta cell malfunction significantly contributes to multiple disease signs, including insulin resistance, was unexpected."
He suggested that boosting GnT-4a levels could prevent the onset of type 2 diabetes: "The identification of the molecular players in this pathway to diabetes suggests new therapeutic targets and approaches towards developing an effective preventative or perhaps curative treatment." "This may be accomplished by beta cell gene therapy or by drugs that interfere with this pathway in order to maintain normal beta cell function."
Dr. Iain Frame, Director of Research at Diabetes UK, said, "The researchers have linked their results in mice to the same pathways in humans and although they did not show they could prevent or cure type 2 diabetes, they have shown it is a theory worth investigating further."
"We will watch this with great interest and hope this early work will eventually lead to some benefit to people with type 2 diabetes."
Wednesday, August 31, 2011
Tuesday, August 30, 2011
Obesity Ranking System Predicts Mortality
An obesity classification system that distinguishes between fat and lean tissue and takes into account functional status and the various comorbid conditions that can be associated with obesity may be a more effective mortality prediction tool than standard body mass index (BMI), according to new research....
Raj S. Padwal, MD, from the Department of Medicine, University of Alberta, Edmonton, Canada, explains, "Anthropometric-based classification schemes for excess adiposity do not include direct assessment of obesity-related comorbidity and functional status and thus have limited clinical utility." The new tool, called the Edmonton obesity staging system (EOSS), ranks obese and overweight people according to a 5-point scale based on factors relating to an individual's underlying health status and the presence or absence of underlying health conditions and, therefore, may be a better predictor of mortality.
A "0" on the EOSS scale, for instance, represents "no apparent risk factors (e.g., blood pressure, serum lipid and fasting glucose levels within normal range), physical symptoms, psychopathology, functional limitations and/or impairment of well-being related to obesity," according to the study authors.
A ranking of 2 indicates "the presence of established obesity-related chronic disease (e.g., hypertension, type 2 diabetes, sleep apnea, osteoarthritis), moderate limitations in activities of daily living and/or well-being," and the highest ranking indicates, "severe (potentially end-stage) disabilities from obesity-related chronic diseases, severe disabling psychopathology, severe functional limitations and/or severe impairment of well-being."
In determining efficacy of the tool, researchers with the University of Alberta applied it to data on 8143 people aged 20 years and older in the 1988-1994 and 1999-2004 US National Health and Human Nutrition Examination Surveys (NHANES).
The results indicated that 77.2% of overweight or obese people in the 1988-1994 survey and 90.3% of those in the 1999-2004 survey were classified as stage 1 or 2 in the EOSS, and their risk for death was significantly lower than that of overweight or obese people classified as stage 3.
In the NHANES 1988-1994 data, scores of 2 and 3 each were associated with a higher risk for dying (hazard ratio, 1.57; 95% confidence interval [CI], 1.16 - 2.13; hazard ratio, 2.69; 95% CI, 1.98 - 3.67, respectively) compared with scores 0 or 1.
The higher risk was seen even after adjustment for BMI, metabolic syndrome, and hypertriglyceridemic waist (i.e., waist circumference ≥ 90 cm and a triglyceride level ≥ 2 mmol/L for men or ≥ 85 cm and ≥ 1.5 mmol/L for women), as well as in a cohort eligible for bariatric surgery.
Measurements of BMI and waist circumference are typically among key factors in the assessment of appropriate treatments for obesity, such as bariatric surgery or anti-obesity therapies.
But BMI fails to directly distinguish between fat and lean tissue, and neither measurement reflects underlying obesity-related functional status or health conditions, which can include diabetes, hypertension, dyslipidemia, osteoarthritis, liver disease or kidney disease, or metabolic syndrome.
In considering the broader range of factors, the EOSS is intended to provide more clinically relevant prognostic information in a manner similar to that of the tumor, node, metastasis system used in the staging of cancer, the authors write.
"The major incremental contribution of this staging system to anthropometric indices and cardiovascular risk equations is the direct measurement of the presence and severity of underlying obesity-related comorbidities, which enables a more comprehensive and individualized assessment of risk," they said.
"Such enhanced risk assessment may enable a greater understanding of obesity-related prognosis and may also assist in determining the urgency of intervention."
The system could be particularly beneficial in prioritizing patients for bariatric surgery according to ranking that reflects a broader assessment of obesity and obesity-related comorbid conditions than simply a BMI ranking, the authors added.
Canadian Medical Association Journal, August 15, 2011 cmaj.110387
Raj S. Padwal, MD, from the Department of Medicine, University of Alberta, Edmonton, Canada, explains, "Anthropometric-based classification schemes for excess adiposity do not include direct assessment of obesity-related comorbidity and functional status and thus have limited clinical utility." The new tool, called the Edmonton obesity staging system (EOSS), ranks obese and overweight people according to a 5-point scale based on factors relating to an individual's underlying health status and the presence or absence of underlying health conditions and, therefore, may be a better predictor of mortality.
A "0" on the EOSS scale, for instance, represents "no apparent risk factors (e.g., blood pressure, serum lipid and fasting glucose levels within normal range), physical symptoms, psychopathology, functional limitations and/or impairment of well-being related to obesity," according to the study authors.
A ranking of 2 indicates "the presence of established obesity-related chronic disease (e.g., hypertension, type 2 diabetes, sleep apnea, osteoarthritis), moderate limitations in activities of daily living and/or well-being," and the highest ranking indicates, "severe (potentially end-stage) disabilities from obesity-related chronic diseases, severe disabling psychopathology, severe functional limitations and/or severe impairment of well-being."
In determining efficacy of the tool, researchers with the University of Alberta applied it to data on 8143 people aged 20 years and older in the 1988-1994 and 1999-2004 US National Health and Human Nutrition Examination Surveys (NHANES).
The results indicated that 77.2% of overweight or obese people in the 1988-1994 survey and 90.3% of those in the 1999-2004 survey were classified as stage 1 or 2 in the EOSS, and their risk for death was significantly lower than that of overweight or obese people classified as stage 3.
In the NHANES 1988-1994 data, scores of 2 and 3 each were associated with a higher risk for dying (hazard ratio, 1.57; 95% confidence interval [CI], 1.16 - 2.13; hazard ratio, 2.69; 95% CI, 1.98 - 3.67, respectively) compared with scores 0 or 1.
The higher risk was seen even after adjustment for BMI, metabolic syndrome, and hypertriglyceridemic waist (i.e., waist circumference ≥ 90 cm and a triglyceride level ≥ 2 mmol/L for men or ≥ 85 cm and ≥ 1.5 mmol/L for women), as well as in a cohort eligible for bariatric surgery.
Measurements of BMI and waist circumference are typically among key factors in the assessment of appropriate treatments for obesity, such as bariatric surgery or anti-obesity therapies.
But BMI fails to directly distinguish between fat and lean tissue, and neither measurement reflects underlying obesity-related functional status or health conditions, which can include diabetes, hypertension, dyslipidemia, osteoarthritis, liver disease or kidney disease, or metabolic syndrome.
In considering the broader range of factors, the EOSS is intended to provide more clinically relevant prognostic information in a manner similar to that of the tumor, node, metastasis system used in the staging of cancer, the authors write.
"The major incremental contribution of this staging system to anthropometric indices and cardiovascular risk equations is the direct measurement of the presence and severity of underlying obesity-related comorbidities, which enables a more comprehensive and individualized assessment of risk," they said.
"Such enhanced risk assessment may enable a greater understanding of obesity-related prognosis and may also assist in determining the urgency of intervention."
The system could be particularly beneficial in prioritizing patients for bariatric surgery according to ranking that reflects a broader assessment of obesity and obesity-related comorbid conditions than simply a BMI ranking, the authors added.
Canadian Medical Association Journal, August 15, 2011 cmaj.110387
Monday, August 29, 2011
Venous ulcers: The role of compression therapy
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.
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.
Extended wear of high heels can cause foot damage
High heels make you look great, improve your figure, and are the final touch to a fashionable look, but if high heels do wonders for your appearance, they don't do a lot for foot health.
Dr. Michael Nirenberg, a podiatrist at Friendly Foot Care in Crown Point, says he doesn't discourage women from wearing high heels occasionally. "Once or twice a week is going to do minimal damage to your feet," he says. "If you wear heels over a long period of time, then you can do permanent damage to your feet and your body."
Dr. Nirenberg says that although high heels make you look taller in the short term, in the long term they cause you to become shorter as your body adapts to the shoes. He says your back will begin to curve and your buttocks expand out and you end up the same height you were without heels.
High heels also put all your weight on the front of the foot, which compresses the toes and the ball of the foot, leading to injuries such as the unlovely bunions, hammertoes or painful pinched nerves called neuromas.
And don't think you can wear high heels until you begin having a problem. Studies have shown that if you wear high heels and stop wearing them, later on you're more likely to have foot problems.
"Constant wearing of high heels change the feet permanently," Dr. Nirenberg says. "They also change the way all your joints in your body are aligned. Heels, even the small ones, cause you to fall forward, and the body compensates by contorting the back and changing the positioning of the shoulders and neck, making you prone to herniated discs. You also use the joints and muscles incorrectly, because you're not walking in a natural way. The Achilles tendon also shortens and you'll have pain whenever you wear a flat shoe. You can lengthen that tendon over time, but it depends upon how long you've been wearing high heels. A podiatrist can help."
When wearing heels, Dr. Nirenberg says the lower the heel the better. The platform sole is better than stilettos because they spread the weight more evenly over the ball and heel of the foot. "The high heel inserts help, too," Dr. Nirenberg says, "because they spread the weight and provide cushioning. Shoes should not hurt, even high heels. Make sure yours is the right size, and if your high heels begin to hurt your feet, you've worn them long enough."
Dr. Michael Nirenberg, a podiatrist at Friendly Foot Care in Crown Point, says he doesn't discourage women from wearing high heels occasionally. "Once or twice a week is going to do minimal damage to your feet," he says. "If you wear heels over a long period of time, then you can do permanent damage to your feet and your body."
Dr. Nirenberg says that although high heels make you look taller in the short term, in the long term they cause you to become shorter as your body adapts to the shoes. He says your back will begin to curve and your buttocks expand out and you end up the same height you were without heels.
High heels also put all your weight on the front of the foot, which compresses the toes and the ball of the foot, leading to injuries such as the unlovely bunions, hammertoes or painful pinched nerves called neuromas.
And don't think you can wear high heels until you begin having a problem. Studies have shown that if you wear high heels and stop wearing them, later on you're more likely to have foot problems.
"Constant wearing of high heels change the feet permanently," Dr. Nirenberg says. "They also change the way all your joints in your body are aligned. Heels, even the small ones, cause you to fall forward, and the body compensates by contorting the back and changing the positioning of the shoulders and neck, making you prone to herniated discs. You also use the joints and muscles incorrectly, because you're not walking in a natural way. The Achilles tendon also shortens and you'll have pain whenever you wear a flat shoe. You can lengthen that tendon over time, but it depends upon how long you've been wearing high heels. A podiatrist can help."
When wearing heels, Dr. Nirenberg says the lower the heel the better. The platform sole is better than stilettos because they spread the weight more evenly over the ball and heel of the foot. "The high heel inserts help, too," Dr. Nirenberg says, "because they spread the weight and provide cushioning. Shoes should not hurt, even high heels. Make sure yours is the right size, and if your high heels begin to hurt your feet, you've worn them long enough."
Monday, August 22, 2011
Pain of Gout Hits More Americans: Study
Greg Hannoosh's battle with gout began 10 years ago with a severe pain in his foot in the middle of the night.
"I remember waking up in the night with soreness and pain in my right foot," said 51-year-old Hannoosh of West Newbury, Mass. "The pressure from my sheets was even causing pain."
The next morning, Hannoosh recalled, "The pain had spread [from my right toe] to the point that my whole foot was not useable. I couldn't walk and couldn't wear shoes. It was pretty debilitating."
Hannoosh saw his doctor, and lab tests revealed high levels of uric acid in his blood. The bad news followed -- doctors diagnosed him with gout, an incapacitating condition in which crystal forms within the joints, causing inflammation and pain.
In gout, the pain is not constant, but rather presents in episodes called gout attacks -- a fitting term, according to Hannoosh.
"They called it a gout attack because it is just like an attack; you are being invaded," he said.
Now, new research suggests more and more Americans may be sharing Hannoosh's struggle against the pain of gout. A new study published Thursday in the journal Arthritis & Rheumatism reveals that the prevalence of gout in the United States has risen over the last 20 years and now affects 8.3 million Americans -- compared to just 6.1 million two decades ago.
The study was supported by Takeda, the pharmaceutical company that makes the gout drug Uloric. Researchers compared data collected from a survey of Americans in the latest U.S. National Health and Nutrition Examination Survey (NHANES) between the periods of 2007-2008 to a previous NHANES surveys conducted in 1988-1994. When the study took into account factors such as obesity or hypertension away from the results, the numbers of people with gout lessened -- a hint that lifestyle choices may be at least part of the problem.
"The burden of gout and hyperuricemia continues to be substantial in the U.S. population," said lead study researcher Dr. Hyon Choi, a rheumatologist and professor of medicine at Boston University School of Medicine.
"The prevalence of gout rose from 2.7 percent two decades ago to an increase of 3.9 percent. Although that seems like a small number, it is actually a 44 percent increase," Choi said. "Obesity and hypertension are main contributing factors."
But though obesity and hypertension may be contributing factors, they are not the only factors involved. High uric acid blood levels, diabetes, high cholesterol, dehydration, alcohol intake, a high-protein diet and the side effects of certain medications such as diuretics can add to a person's risk. Genetics can also play a role.
"Certainly a key take away [from this study] is that many patients with gout have multiple other conditions, such as obesity, hypertension, kidney disease, diabetes mellitus, coronary disease or metabolic syndrome, which must be considered in the management of gout," said Dr. Theodore Fields, rheumatologist at the Hospital for Special Surgery in New York.
"The public needs to realize that this is one more nail in the coffin about the importance of obesity and cardiovascular disease." said Dr. Eric Gall, rheumatologist and director of the Arizona Arthritis Center in Tucson."They need to also know that the treatment for gout is not just lowering the uric acid but also paying attention to diet and exercise."
For Hannoosh, treatment meant going off of his blood pressure medication, as doctors believe it may have contributed his gout. And he made lifestyle changes as well.
"I don't drink beer anymore and don't eat near as much red meat as I used to," he said. "I also drink a lot more water than I did before."
The measures may be working; Hannoosh said his last gout attack was about two and a half years ago.
By MERCY EDIONWE, M.D.
July 28, 2011
"I remember waking up in the night with soreness and pain in my right foot," said 51-year-old Hannoosh of West Newbury, Mass. "The pressure from my sheets was even causing pain."
The next morning, Hannoosh recalled, "The pain had spread [from my right toe] to the point that my whole foot was not useable. I couldn't walk and couldn't wear shoes. It was pretty debilitating."
Hannoosh saw his doctor, and lab tests revealed high levels of uric acid in his blood. The bad news followed -- doctors diagnosed him with gout, an incapacitating condition in which crystal forms within the joints, causing inflammation and pain.
In gout, the pain is not constant, but rather presents in episodes called gout attacks -- a fitting term, according to Hannoosh.
"They called it a gout attack because it is just like an attack; you are being invaded," he said.
Now, new research suggests more and more Americans may be sharing Hannoosh's struggle against the pain of gout. A new study published Thursday in the journal Arthritis & Rheumatism reveals that the prevalence of gout in the United States has risen over the last 20 years and now affects 8.3 million Americans -- compared to just 6.1 million two decades ago.
The study was supported by Takeda, the pharmaceutical company that makes the gout drug Uloric. Researchers compared data collected from a survey of Americans in the latest U.S. National Health and Nutrition Examination Survey (NHANES) between the periods of 2007-2008 to a previous NHANES surveys conducted in 1988-1994. When the study took into account factors such as obesity or hypertension away from the results, the numbers of people with gout lessened -- a hint that lifestyle choices may be at least part of the problem.
"The burden of gout and hyperuricemia continues to be substantial in the U.S. population," said lead study researcher Dr. Hyon Choi, a rheumatologist and professor of medicine at Boston University School of Medicine.
"The prevalence of gout rose from 2.7 percent two decades ago to an increase of 3.9 percent. Although that seems like a small number, it is actually a 44 percent increase," Choi said. "Obesity and hypertension are main contributing factors."
But though obesity and hypertension may be contributing factors, they are not the only factors involved. High uric acid blood levels, diabetes, high cholesterol, dehydration, alcohol intake, a high-protein diet and the side effects of certain medications such as diuretics can add to a person's risk. Genetics can also play a role.
"Certainly a key take away [from this study] is that many patients with gout have multiple other conditions, such as obesity, hypertension, kidney disease, diabetes mellitus, coronary disease or metabolic syndrome, which must be considered in the management of gout," said Dr. Theodore Fields, rheumatologist at the Hospital for Special Surgery in New York.
"The public needs to realize that this is one more nail in the coffin about the importance of obesity and cardiovascular disease." said Dr. Eric Gall, rheumatologist and director of the Arizona Arthritis Center in Tucson."They need to also know that the treatment for gout is not just lowering the uric acid but also paying attention to diet and exercise."
For Hannoosh, treatment meant going off of his blood pressure medication, as doctors believe it may have contributed his gout. And he made lifestyle changes as well.
"I don't drink beer anymore and don't eat near as much red meat as I used to," he said. "I also drink a lot more water than I did before."
The measures may be working; Hannoosh said his last gout attack was about two and a half years ago.
By MERCY EDIONWE, M.D.
July 28, 2011
Saturday, August 20, 2011
New papers revisit, rekindle flexible flatfoot controversy
“Other considerations” spark debate
Two recent literature reviews have reignited the debate over treatment options for pediatric flexible flatfoot.
In January 2010, when LER first covered the controversy, Australian podiatrist and researcher Angela Evans, PhD, had recently published a paper in the Journal of the American Podiatric Medical Association suggesting that children whose feet were flatter than expected, but asymptomatic, should be monitored rather than automatically treated with orthoses.1 This provoked the ire of some American pediatric foot specialists, who thought the approach downplayed important pathologies. Not everyone agreed, however; for example, Edwin Harris, DPM, the lead author of guidelines from the American College of Foot and Ankle Surgeons, concurred with the basic premise of Evans’s approach, and said it provided a practical direction for further investigation.2
More recently, Evans and a colleague, Keith Rome, DPM, professor of podiatry at Auckland University of Technology in New Zealand, published two literature reviews revisiting the topic—and rekindling the debate. In the first, comprising three trials involving 305 children, they concluded that the evidence was too limited to draw definitive conclusions about use of nonsurgical interventions for pediatric pes planus.3 The more recent review broadened the inclusion criteria for studies, reviewing 15 and proposing an algorithm for managing flexible flat feet.4
Part of the goal, Evans told LER, was to further develop the “yellow zone” in the original JAPMA paper—the asymptomatic children who, as mentioned, should simply be monitored.
“That seems to have been interpreted in an absolute sense of monitoring only,” she said. “But monitoring is a dynamic process; within that yellow zone, if a clinician sees a foot that’s not painful, but that also isn’t functioning well, that should direct some form of treatment. That may mean changing their shoes or using an inexpensive foot orthotic. Our criticism has been of the excessive use of expensive customized orthoses. But it also came out of the review that in children with arthritis and foot pain, customized orthoses are indicated because they improve both pain and function.”
Alan Ng, DPM, who practices with Advanced Orthopedics and Sports Medicine Specialists in Denver and is on the board of directors for the American Board of Podiatric Surgery, concurs with the monitoring approach in asymptomatic children.
“I think a lot of pediatric flatfoot can be treated conservatively, as long as there’s no coalition,” he said. “The initial evaluation should include weight-bearing, x-rays, gait analysis, resting calcaneal stance position, and mobility. Most of the time, initial treatment is physical therapy, muscle strengthening, functional orthotics, or good, supportive shoes, and eighty or ninety percent of the time they do fine. But if a kid is asymptomatic and can do full activity with no issues, I don’t touch them; putting them into an orthotic just because they have flat feet is inappropriate.”
Russell Volpe, DPM, who teaches at the New York College of Podiatric Medicine, said that the evaluation and treatment parameters in Evans and Rome’s most recent paper don’t go far enough.
“It’s an exemplary review and analysis of what’s been published, but it doesn’t cover the complicated topic of what makes asymptomatic flat feet a potential issue,” he said.
What Evans and Rome refer to passingly in the paper as “other considerations” are, to Volpe, a big issue and a significant part of his practice. They include superstructural and pedal influences on all three body planes.
“They miss the point about the huge role of lower extremity residual torsions, equinus, genu or tibial varum, calcaneal varus, and the like,” he said. “There’s a lot that goes into identifying the foot that is at risk to become dysfunctional and symptomatic over time, and the big tool for evaluating it is the biomechanical integrity of that lower extremity. In their paper I see one sentence about it in twenty pages. That’s the problem.”
Such influences, Volpe said, are better corrected with custom orthoses, and he took particular umbrage at the paper’s suggestion that custom approaches “desist.”
“I will not desist; in fact I will insist!” he said. “For the cohort with biomechanical comorbidities, I need to incorporate postings and modifications that allow me to manage both the primary structural comorbidity and the compensation in the foot, and for that I need to use a custom orthosis.”
By Cary Groner
Two recent literature reviews have reignited the debate over treatment options for pediatric flexible flatfoot.
In January 2010, when LER first covered the controversy, Australian podiatrist and researcher Angela Evans, PhD, had recently published a paper in the Journal of the American Podiatric Medical Association suggesting that children whose feet were flatter than expected, but asymptomatic, should be monitored rather than automatically treated with orthoses.1 This provoked the ire of some American pediatric foot specialists, who thought the approach downplayed important pathologies. Not everyone agreed, however; for example, Edwin Harris, DPM, the lead author of guidelines from the American College of Foot and Ankle Surgeons, concurred with the basic premise of Evans’s approach, and said it provided a practical direction for further investigation.2
More recently, Evans and a colleague, Keith Rome, DPM, professor of podiatry at Auckland University of Technology in New Zealand, published two literature reviews revisiting the topic—and rekindling the debate. In the first, comprising three trials involving 305 children, they concluded that the evidence was too limited to draw definitive conclusions about use of nonsurgical interventions for pediatric pes planus.3 The more recent review broadened the inclusion criteria for studies, reviewing 15 and proposing an algorithm for managing flexible flat feet.4
Part of the goal, Evans told LER, was to further develop the “yellow zone” in the original JAPMA paper—the asymptomatic children who, as mentioned, should simply be monitored.
“That seems to have been interpreted in an absolute sense of monitoring only,” she said. “But monitoring is a dynamic process; within that yellow zone, if a clinician sees a foot that’s not painful, but that also isn’t functioning well, that should direct some form of treatment. That may mean changing their shoes or using an inexpensive foot orthotic. Our criticism has been of the excessive use of expensive customized orthoses. But it also came out of the review that in children with arthritis and foot pain, customized orthoses are indicated because they improve both pain and function.”
Alan Ng, DPM, who practices with Advanced Orthopedics and Sports Medicine Specialists in Denver and is on the board of directors for the American Board of Podiatric Surgery, concurs with the monitoring approach in asymptomatic children.
“I think a lot of pediatric flatfoot can be treated conservatively, as long as there’s no coalition,” he said. “The initial evaluation should include weight-bearing, x-rays, gait analysis, resting calcaneal stance position, and mobility. Most of the time, initial treatment is physical therapy, muscle strengthening, functional orthotics, or good, supportive shoes, and eighty or ninety percent of the time they do fine. But if a kid is asymptomatic and can do full activity with no issues, I don’t touch them; putting them into an orthotic just because they have flat feet is inappropriate.”
Russell Volpe, DPM, who teaches at the New York College of Podiatric Medicine, said that the evaluation and treatment parameters in Evans and Rome’s most recent paper don’t go far enough.
“It’s an exemplary review and analysis of what’s been published, but it doesn’t cover the complicated topic of what makes asymptomatic flat feet a potential issue,” he said.
What Evans and Rome refer to passingly in the paper as “other considerations” are, to Volpe, a big issue and a significant part of his practice. They include superstructural and pedal influences on all three body planes.
“They miss the point about the huge role of lower extremity residual torsions, equinus, genu or tibial varum, calcaneal varus, and the like,” he said. “There’s a lot that goes into identifying the foot that is at risk to become dysfunctional and symptomatic over time, and the big tool for evaluating it is the biomechanical integrity of that lower extremity. In their paper I see one sentence about it in twenty pages. That’s the problem.”
Such influences, Volpe said, are better corrected with custom orthoses, and he took particular umbrage at the paper’s suggestion that custom approaches “desist.”
“I will not desist; in fact I will insist!” he said. “For the cohort with biomechanical comorbidities, I need to incorporate postings and modifications that allow me to manage both the primary structural comorbidity and the compensation in the foot, and for that I need to use a custom orthosis.”
By Cary Groner
Friday, August 19, 2011
Early research characterizes gait associated with autism
Results could have clinical implications
Little research has been published about gait patterns in children with autism, but that could be changing. One recently published study, although small, appears to lay the foundation for more focused research and could have clinical implications as well.
In the February issue of Clinical Biomechanics, researchers at the University of New Brunswick in Fredericton, New Brunswick, Canada, published what they describe as the first comprehensive analysis of 3-D joint and muscle gait patterns in children with autism. The study found that a group of autistic children, compared to controls, had a significantly higher cadence, increased upper flexion of the ankle in swing phase, decreased peak ankle joint angles, and significantly smaller peak plantar reflex moments.
The study included 12 children with autism, ages 5 to 9, plus 22 age-matched control participants. However, the researchers excluded toe-walkers and children with Asperger syndrome or pervasive developmental disorder not otherwise specified (who typically would fall under the definition of full autism spectrum disorder [ASD]). Many children with ASD have sensory sensitivities that make them behave less than ideally when researchers use markers, tape, and Velcro to capture patterns for wave form analysis, explained senior author Victoria Chester, PhD, associate professor of kinesiology at UNB’s Andrew and Marjorie McCain Human Performance Laboratory.
“We were successful in getting them through,” she added, probably because of the exclusion of some children from the study.
The researchers used an eight-camera motion capture system to track 3-D trajectories of reflective markers placed on the children’s skin. They used custom software to compute cadence, velocity, and percent cycle spent in single limb stance for every gait cycle. They used parameterization techniques and principal component analysis to analyze their data and then compared the two sets.
“We actually managed to get kinematic and kinetic data sets for a group of kids with autism,” Chester said. “And you really need both sets of data to get a better understanding of what their gait patterns are like. I was surprised that the children could actually be grouped this way for a study. They often appear to the naked eye to be very different from one another.”
So what do the study results mean to practitioners?
“Given our small sample size, we remain fairly conservative in terms of our clinical relevance,” Chester said. “However, the findings may be important in terms of treatment planning for children with autism [plantar flexor strength training, stretching, and orthotics]. Gait analysis can provide clarification in terms of identifying gait deviations and treatment planning. The effects of treatment on gait can also be monitored. Practitioners should know that children with autism may benefit from the objective data made available from gait analyses for treatment planning. We still need to learn more about the autism spectrum and associated gait disorders, and this paper is a start in that direction.”
Whether gait pattern analysis could be used to screen for possible autism disorders is a “huge topic, very controversial,” Chester said. And while some people are looking into that possibility, it was not a focus of the UNB research, she said.
Dawn-Marie Ickes, PT, a physical therapist at Core Conditioning PT in Studio City and Burbank, CA, agreed that gait analysis screening is not close to being ready for prime time.
“I wouldn’t say it is something that is a clinically objectifiable screening program for autism. Symptoms do overlap, but not all children with sensory integration dysfunction have autism. However, it could be a predictor of other things that look like autism but aren’t,” Ickes said. “The best takeaway from this study for practitioners is that these abnormalities can pose value for predicting ASD if they’re coupled with sensory integration screening.”
Although other symptoms and aspects often are given priority when managing autism, Chester encouraged practitioners to remember that there is a physical component to autism as well, making it necessary to treat the whole child.
“A child who can’t keep up with others on the playground from a motor perspective is also affected socially,” she said.
Larger studies are now needed that include children from all autistic-related groups, Chester said, to facilitate an understanding of how gait differs across the autism spectrum
By Larry Hand
Little research has been published about gait patterns in children with autism, but that could be changing. One recently published study, although small, appears to lay the foundation for more focused research and could have clinical implications as well.
In the February issue of Clinical Biomechanics, researchers at the University of New Brunswick in Fredericton, New Brunswick, Canada, published what they describe as the first comprehensive analysis of 3-D joint and muscle gait patterns in children with autism. The study found that a group of autistic children, compared to controls, had a significantly higher cadence, increased upper flexion of the ankle in swing phase, decreased peak ankle joint angles, and significantly smaller peak plantar reflex moments.
The study included 12 children with autism, ages 5 to 9, plus 22 age-matched control participants. However, the researchers excluded toe-walkers and children with Asperger syndrome or pervasive developmental disorder not otherwise specified (who typically would fall under the definition of full autism spectrum disorder [ASD]). Many children with ASD have sensory sensitivities that make them behave less than ideally when researchers use markers, tape, and Velcro to capture patterns for wave form analysis, explained senior author Victoria Chester, PhD, associate professor of kinesiology at UNB’s Andrew and Marjorie McCain Human Performance Laboratory.
“We were successful in getting them through,” she added, probably because of the exclusion of some children from the study.
The researchers used an eight-camera motion capture system to track 3-D trajectories of reflective markers placed on the children’s skin. They used custom software to compute cadence, velocity, and percent cycle spent in single limb stance for every gait cycle. They used parameterization techniques and principal component analysis to analyze their data and then compared the two sets.
“We actually managed to get kinematic and kinetic data sets for a group of kids with autism,” Chester said. “And you really need both sets of data to get a better understanding of what their gait patterns are like. I was surprised that the children could actually be grouped this way for a study. They often appear to the naked eye to be very different from one another.”
So what do the study results mean to practitioners?
“Given our small sample size, we remain fairly conservative in terms of our clinical relevance,” Chester said. “However, the findings may be important in terms of treatment planning for children with autism [plantar flexor strength training, stretching, and orthotics]. Gait analysis can provide clarification in terms of identifying gait deviations and treatment planning. The effects of treatment on gait can also be monitored. Practitioners should know that children with autism may benefit from the objective data made available from gait analyses for treatment planning. We still need to learn more about the autism spectrum and associated gait disorders, and this paper is a start in that direction.”
Whether gait pattern analysis could be used to screen for possible autism disorders is a “huge topic, very controversial,” Chester said. And while some people are looking into that possibility, it was not a focus of the UNB research, she said.
Dawn-Marie Ickes, PT, a physical therapist at Core Conditioning PT in Studio City and Burbank, CA, agreed that gait analysis screening is not close to being ready for prime time.
“I wouldn’t say it is something that is a clinically objectifiable screening program for autism. Symptoms do overlap, but not all children with sensory integration dysfunction have autism. However, it could be a predictor of other things that look like autism but aren’t,” Ickes said. “The best takeaway from this study for practitioners is that these abnormalities can pose value for predicting ASD if they’re coupled with sensory integration screening.”
Although other symptoms and aspects often are given priority when managing autism, Chester encouraged practitioners to remember that there is a physical component to autism as well, making it necessary to treat the whole child.
“A child who can’t keep up with others on the playground from a motor perspective is also affected socially,” she said.
Larger studies are now needed that include children from all autistic-related groups, Chester said, to facilitate an understanding of how gait differs across the autism spectrum
By Larry Hand
Thursday, August 18, 2011
The Medical Evolution of Chronic Venous Insufficiency
Chronic Venous Insufficiency (CVI) can now be better identified than it had been previously by using advanced in-office vascular testing systems. These systems are easy to use and their collaborative care platforms offer increased accuracy. Full patient data is compiled, processed, analyzed and stored in order to deliver a thorough patient history that is utilized for more reliable diagnoses and continuous care.
These diagnostic systems, along with increased patient awareness and use of CVI testing procedures by physicians, allow CVI to be recognized earlier than ever. This makes proper management and treatment of the condition easier. Common treatment plans may include instructing patients to:
Avoid long periods of standing or sitting
Exercise on a regular basis
Lose weight
Elevate their feet[1]
As CVI can lead to serious infections of the lower extremities, it is important to check all at-risk patients for possible symptoms. Symptoms may include:
Aching
Heaviness
Leg-tiredness
Cramps[2]
CVI has been a known medical ailment for thousands of years. Until recently, ascending phlebography, the recording of the venous pulse, has been the method of choice to demonstrate patency of the veins[3]. The ancient Greek physician, Hippocrates, used a primitive bandaging method to manage this condition that affects the venous walls of the leg veins. By 1676, stockings were used to control humors, the normal functioning bodily semifluid or fluid, impacted in the leg[4]. Although both of these treatment techniques are still used to this day, there are now more effective means of detecting and treating CVI.
With modern medical technology, CVI can be better detected using non-invasive, easy-to-perform procedures.
These diagnostic systems, along with increased patient awareness and use of CVI testing procedures by physicians, allow CVI to be recognized earlier than ever. This makes proper management and treatment of the condition easier. Common treatment plans may include instructing patients to:
Avoid long periods of standing or sitting
Exercise on a regular basis
Lose weight
Elevate their feet[1]
As CVI can lead to serious infections of the lower extremities, it is important to check all at-risk patients for possible symptoms. Symptoms may include:
Aching
Heaviness
Leg-tiredness
Cramps[2]
CVI has been a known medical ailment for thousands of years. Until recently, ascending phlebography, the recording of the venous pulse, has been the method of choice to demonstrate patency of the veins[3]. The ancient Greek physician, Hippocrates, used a primitive bandaging method to manage this condition that affects the venous walls of the leg veins. By 1676, stockings were used to control humors, the normal functioning bodily semifluid or fluid, impacted in the leg[4]. Although both of these treatment techniques are still used to this day, there are now more effective means of detecting and treating CVI.
With modern medical technology, CVI can be better detected using non-invasive, easy-to-perform procedures.
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