Edema is characterized by a noticeable swelling caused by the expansion of interstitial fluid volume. Pitting edema is identified by a depression in the tissue that remains for at least five seconds after applying pressure to the swollen area. This type of edema indicates the movement of excess interstitial water in response to pressure. A number of conditions affecting the circulatory and/or lymphatic system can cause pitting edema, most often in peripheral areas. Signs of pitting edema indicate potential risk factors for surgery and anesthesia and the need for the OR team to investigate the patient’s condition and medical history.
Peripheral edema typically occurs in dependent areas, appearing mainly in the lower extremities of ambulatory patients and over the sacrum in bedridden patients. It can also occur in the upper extremities, though less frequently. Several clinical conditions are linked to the development of edema, including heart failure, cirrhosis, nephrotic syndrome, and other conditions such as venous and lymphatic diseases. Determining the cause of edema depends on whether it is unilateral or bilateral. The sudden onset of unilateral leg edema often raises concerns about deep vein thrombosis (DVT). In addition to edema, DVT patients may experience calf tenderness, pain, or firmness along a vein, or unilateral warmth or erythema. The most common cause of chronic unilateral or asymmetric edema is chronic venous disease in the lower extremities. Acute bilateral leg edema is rare and may be due to medications, acute heart failure, or acute nephrotic syndrome. Chronic bilateral leg edema is usually caused by chronic venous disease, although heart failure and pulmonary hypertension are often underdiagnosed. Less common causes of chronic bilateral leg edema include renal and liver diseases.
If present, pitting edema should be assessed by the OR team before surgery due to its association with increased perioperative complications. For instance, patients with pitting edema caused by a DVT need anticoagulation therapy to lower the risk of recurrent DVT, heart attack, and stroke. However, while on blood thinners, these patients face an increased risk of surgical bleeding. Therefore, it is advisable to delay surgery if the patient is clinically stable or to consider withholding anticoagulation during the perioperative period.
In patients with bilateral edema due to liver disease, evaluating surgical risk involves assessing the severity of liver disease, the urgency of surgery (and alternatives to surgery), and any coexisting medical conditions. Surgery is contraindicated in patients with acute liver failure, alcoholic hepatitis, and severe chronic hepatitis, as the risks surpass the benefits. For patients with less severe liver disease, physicians commonly use surgical risk calculators, such as the Child-Turcotte-Pugh score, to determine if the benefits of surgery outweigh the risks.
Finally, for patients with pitting edema due to heart failure, obtaining a chest X-ray can help determine the presence of pulmonary edema (fluid accumulation in the lungs), which significantly increases surgical risk. Patients experiencing an acute exacerbation of heart failure may have shortness of breath due to pulmonary edema, and this condition should be managed with diuretics before surgery to prevent cardiopulmonary complications.
Lastly, the OR and PACU teams should recognize that pitting edema may worsen after surgery due to the release of inflammatory signals that increase capillary permeability, allowing more fluid to accumulate in the interstitial space. Additionally, patients often receive IV fluids during the perioperative period, which can further exacerbate edema. Ultimately, the decision to proceed with surgery is influenced by the urgency of the procedure (emergency, urgent, or elective), the severity of symptoms, the presence of comorbid conditions, and the specific risks associated with the proposed surgery.
References
Lawenda BD, Mondry TE, Johnstone PA. Lymphedema: a primer on the identification and management of a chronic condition in oncologic treatment. CA Cancer J Clin. 2009 Jan-Feb;59(1):8-24. doi: 10.3322/caac.20001. PMID: 19147865.
Hull R, Hirsh J, Sackett DL, Taylor DW, Carter C, Turpie AG, Powers P, Gent M. Clinical validity of a negative venogram in patients with clinically suspected venous thrombosis. Circulation. 1981 Sep;64(3):622-5. doi: 10.1161/01.cir.64.3.622. PMID: 7261292.
Gorman WP, Davis KR, Donnelly R. ABC of arterial and venous disease. Swollen lower limb-1: general assessment and deep vein thrombosis. BMJ. 2000 May 27;320(7247):1453-6. doi: 10.1136/bmj.320.7247.1453. PMCID: PMCID: PMC1127644.
Blankfield RP, Finkelhor RS, Alexander JJ, Flocke SA, Maiocco J, Goodwin M, Zyzanski SJ. Etiology and diagnosis of bilateral leg edema in primary care. Am J Med. 1998 Sep;105(3):192-7. doi: 10.1016/s0002-9343(98)00235-6. PMID: 9753021.
Guazzi M, Polese A, Magrini F, Fiorentini C, Olivari MT. Negative influences of ascites on the cardiac function of cirrhotic patients. Am J Med. 1975 Aug;59(2):165-70. doi: 10.1016/0002-9343(75)90350-2. PMID: 1155476.
Matthay MA. Resolution of pulmonary edema. Thirty years of progress. Am J Respir Crit Care Med. 2014 Jun 1;189(11):1301-8. doi: 10.1164/rccm.201403-0535OE. PMID: 24881936; PMCID: PMC4098087.