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Peripheral leg oedema

Oedema is defined as palpable swelling caused by an increase in interstitial fluid volume ( John W Ely et al 2006 )

 

Chronic oedema ( CO ) is a general term used for leg swelling that has been present for atleast 3 months and this includes all form of edema irrespective of etiology and corresponding co-morbidities and risk factors It is a major clinical problem in the community and a challenging issue for primary care – management can be frustrating and time consuming The problem will only worsen as the population gets older , it is estimated that in the UK population will include 3.5 million people aged 85 or over with many older than 100 Moffatt et al in 2003 reported that chronic oedema is a common in community 
( 1.33/1000 ) with the prevalence increasing in those aged 64 yrs ( 5.4 / 1000 ) Heart failure affects approximately 1 % of the general population

 

Fluid balance between these compartments is maintained by hydrostatic pressure and oncotic pressure , these are governed by Starling’s law

 

Altered vascular dynamics Governed by Starlings law which can be -
- increased intravascular volume , decreased intravascular or oncotic pressure
- increased vascular permeability Vessel wall permeability Excess bodily fluids Lymphatic systems – excess protein rich interstitial fluid within skin and s/c tissue resulting from lymphatic dysfunction Local injury , infection Medications Pregnancy ,Physiological changes such as cyclical premenstrual changes.

 

Causes – systemic Cardiac Fluid overload Liver cirrhosis Kidney for e.g nephrotic syndrome , end stage renal failure , AKI Nutritional for e.g Hypoproteinemia Endocrine ( e.g hypothyroidism , Cushing’s ) Pregnancy Premenstrual disorder Medication related e.g Ca channel antagonists , NSAIDs , corticosteroids Malignancy – abdominal or pelvic Complex regional pain syndrome

 

Local – Venous causes e.g acute DVT , post thrombotic syndrome , trauma , severe varicose veins , chronic venous insufficiency Lymphoedema Lipedema Stasis Inflammation e,g cellulitis , allergic disorders Trauma Benign or malignant neoplasms.

 

Why important -high need of attention from community nursing teams patients with leg ulceration often suffer with peripheral oedema itt can adversely affect QOL , health and people’s ability to engage in normal daily activities patient who suffer with chronic oedema often have greater comorbidities than those without it- particularly diabetes , heart failure / IHD , peripheral arterial disease and presence of a wound people with CO are more likely not to be able to walk unaided people with chronic oedema suffer more from cellulitis people with CO are more likely to be obese

 

History -Onset Distribution Duration – arbitrary cut of 72 hours of is widely quoted in literature ie less than 72 hours is considered acute h/o limb trauma h/o skin infection pain less or painful use of medications for e.g prednisolone , NSAIDs , calcium channel blockers skin changes family h/o venous disease any symptoms suggestive of a systemic illness particularly indicting a dysfunction in functioning of ,pulmonary ,liver , heart or the kidneys occupation ( e.g prolonged standing ) sleep apnoea – its important to ask about this smoking status interests and limitations in activities that the patient is experiencing h/ o neoplasm particularly in pelvic / abdominal region h/o radiation therapy.

 

Examination –distribution ( b/l or unilateral ) tenderness general mobility , ankle movements pitting or non-pitting severity ( mild , moderate or severe ) skin changes as discoloration , hydration , pigmentation / lipodermatosclerosis , fragility , redness/ pallor / cyanosis , signs of infection , broken or ulcerated skin , presence of fungal infection varicose veins signs of systemic disease for e.g
JVP , crackles
ascites
spider haemangiomas if the swelling involves the feet as well how far does the oedema extends for e.g in relation to knee or ankles or involves the trunk.

 

Check – Check BMI Leg circumference at the thickest point Blood profile to include FBC , U/E , LFT , Blood sugar , TSH If a cardiac cause is suspected consider
ECG , Echocardiography , CXR and Brain Natriuretic peptide ( BNP ) Suspected DVT consider D-Dimer and Doppler If vascular disease is suspected consider ABPI Lymphoedema is suspected consider further testing with lymphoscintigraphy , CT , MRI or ultrasound abdominal /renal / pelvic ultrasound Urinalysis Consider a holistic assessment in patients with chronic oedema which includes peripheral pulses and ABPI.

 

Common causes

Cardiac -heart failure – can be left or right sided, right heart failure can cause peripheral oedema , pleural effusions and at times ascites Constrictive pericarditis and restrictive cardiomyopathy both can present with a raised JVP , dyspnoea , hepatic congestion , ascites and peripheral oedema
Constrictive pericarditis can cause cause cardiac tamponade cardiac causes of peripheral oedema are almost always accompanied by other symptoms for e.g dyspnoea , orthopnoe, rapid weight gain.

 

Liver cirrhosis -end stage liver disease causes ascites but often also causes b/l pedal oedema the cause of the edema is multifactorial and includes
- hypoalbuminemia ( in later stages )
- profound salt and water retention
- AV fistula formation throughout the body cardiac output is normal or elevated in this form of high output failure

 

Lymphoedema -due to an abnormality in the locoregional lymphatic drainage lymphoedema can be primary or secondary secondary lymphoedema is due to an acquired cause like trauma , recurrent infection , malignancy , surgery ,radiotherapy , filariasis early lymphoedema may be difficult to distinguish from venous insufficiency painless swelling, distal part of the leg is affected initially and proximal extension happens later

 

New onset renal disease -nephrotic syndrome may present with b/l lower limb and peri-orbital oedema ( proteinuria , low albumin + high cholesterol )
can be caused by diabetes or from primary glomerular disease acute renal failure ( AKI )

 

Venous insufficiency- due to venous hypertension – can be multifactorial this can be caused by venous valve reflux , venous flow obstruction or both cause can be primary or secondary primary happens without a precipitating event and is due to congenital defects or changes that happen in venous wall biochemistry ( eg.g reduced elastic content , increased extracellular matrix remodeling and inflammatory infiltrate ) secondary happens after a DVT which causes an inflammatory response which leads to injury of the venous wall presentation is with dependent pitting edema , leg discomfort , fatigue and itching skin changes.

 

Idiopathic oedema -also known by other names as cyclical oedema , periodic edema , fluid retention syndrome or orthostatic edema aetiology is poorly understood and this mainly affects premenopausal women periodic episodes with weight changes that are clearly not related to the menstrual cycle.

 

Clues to diagnosis-

 

Pain -Lymphoedema is painless DVT and reflex sympathetic dystrophy can be painful Chronic venous insufficiency can cause mild low grade ache.

 

Overnight improvement -In venous insufficiency the swelling improves overnight but not in lymphedema

 

Pitting or non-pitting -Non-pitting lymphoedema is very uncommon

 

Distribution –Unilateral leg oedema is due to a local disease process whereas B/L peripheral oedema is often due to a systemic illness

 

Age –venous insufficiency is very common is people over 50 where it can affect 30 % of the population in women less than 50 the most common cause of edema is idiopathic edema ( previously known as cyclical edema )

 

Skin changes -in early stages of venous disease patients may have spider veins ( ankle flare ) advanced disease can lead to more apparent and severe skin changes like hemosiderin staining

 

Acute unilateral- Acute is considered < 72 hours. Always consider the following when the patient presents with a unilateral swelling of acute nature
 Deep vein thrombosis Cellulitis Ruptured Baker’s cyst Superficial thrombophlebitis

 

Medications -calcium channel blockers ( common – dose limiting ) NSAIDs ( up to 5 % ) anti-depressants beta blockers direct vasodilators ( minoxidil ) thiazolidinediones ( e.g pioglitazone ) oestrogens ,progesterone’s , testosterone

 

Management strategies -often poorly managed ( diuretics are commonly user erroneously in all forms of oedema it is important to evaluate for underlying cause which will guide management 
( once it is understood why the Starling’s law was disrupted – its correction is the only way to halt the cycle and reverse the process ) in many cases a resolution of edema may not be possibly despite being a frequent complain in primary care globally no guidelines exist to aid physicians in management of this common condition a simplified approach is presented below for your consideration

 

Unilateral -Once DVT excluded consider other causes as infection lymphoedema ruptured Baker’s cyst compartment syndrome

 

Bilateral –Patient has symptomatic peripheral oedema and JVP elevated. Consider cardiac cause , pulmonary hypertension , cor pulmonale , acute renal failure / volume overlaod if already on diuretics consider acute decompensation. Patient is asymptomatic and 
JVP normal Investigate and act per findings and consider causes as medications lymphoedema idiopathic malnutrition

References

  1. Peripheral Edema- A review
    Shaun Cho, MD, J. Edwin Atwood, MD 0002-9343/02/$–see front matter
    PII S0002-9343(02)01322-0 http://www.medecine.unige.ch/enseignement/apprentissage/module2/circ/apprentissage/intranet/pb2/cho_2002.pdf
  2. Chronic peripheral oedema:
    the critical role of the lymphatic system
    Peter S Mortimer and J Rodney Levick Clinical Medicine Vol 4 No 5 September/October 2004 https://www.rcpjournals.org/content/clinmedicine/4/5/448.full.pdf
  3. Venous edema of the lower limbs Pascal PRIOLLET Vascular Medicine
    St Joseph Hospital Foundation Paris, France https://www.phlebolymphology.org/venous-edema-of-the-lower-limbs/

  4. Powell AA, Armstrong MA. Peripheral edema. American Family Physician. 1997 Apr;55(5):1721-1726. ( Abstract )
  5. Goyal A, Cusick AS, Bansal P. Peripheral Edema. [Updated 2020 Jul 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554452/
  6. A guide to peripheral oedema
    GAYATHRI KUMARASINGHE MB BS, FRACP
    GERARD CARROLL AM, MB BS(Hons), FRACP, FCSANZ MedicineToday 2015; 16(6): 26-34 https://medicinetoday.com.au/sites/default/files/cpd/MT2015-06-026-KUMARASINGHE.pdf
  7. Trayes KP, Studdiford JS, Pickle S, Tully AS. Edema: diagnosis and management. Am Fam Physician. 2013 Jul 15;88(2):102-10. PMID: 23939641. https://pubmed.ncbi.nlm.nih.gov/23939641/
  8. Leg oedema EBM Guidelines Article ID: ebm00099 (003.045) https://www.ebm-guidelines.com/ebmg/ltk.free?p_artikkeli=ebm00099
  9. Approach to Leg Edema of Unclear Etiology
    John W. Ely, MD, MSPH, Jerome A. Osheroff, MD, M. Lee Chambliss, MD, MSPH, and
    Mark H. Ebell, MD, MS 148 JABFM March–April 2006 Vol. 19 No. 2 https://www.jabfm.org/content/jabfp/19/2/148.full.pdf
  10. Tiwari A, Cheng K, Button M, Myint F, Hamilton G. Differential Diagnosis, Investigation, and Current Treatment of Lower Limb Lymphedema. Arch Surg. 2003;138(2):152–161. doi:10.1001/archsurg.138.2.152 https://jamanetwork.com/journals/jamasurgery/fullarticle/394351
  11. Lower Extremity Edema by Editor https://ddxof.com/lower-extremity-edema/

  12. BMJ Best practice Assessment of peripheral oedema
  13. Epstein BJ, Roberts ME. Managing peripheral edema in patients with arterial hypertension. Am J Ther. 2009 Nov-Dec;16(6):543-53. doi: 10.1097/MJT.0b013e3181afbf9f. PMID: 19636244. ( Abstract )
  14. Bromage DanielMayhew JosephSado DanielManaging heart failure related peripheral oedema in primary care 
  15. Patel SK, Surowiec SM. Venous Insufficiency. [Updated 2020 Aug 15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430975/
  16. Chronic venous insufficiency and varicose veins
    of the lower extremities
    Young Jin Youn1,2 and Juyong Lee2 pISSN 1226-3303
    eISSN 2005-6648
    http://www.kjim.org

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