Chronic Lower Extremity Edema Research Articles

Chronic Edema Management of the Lower Extremities.

Peripheral edema is a prevalent condition affecting patients dealing with an assortment of health conditions, such as congestive heart failure (CHF), liver disease, venous insufficiency, and postoperative surgical complications. Edema can present in a variety of ways, ranging from mild localized symptoms to severely debilitating forms that impact patients' daily lives. Despite the vast number of publications addressing the underlying causes of peripheral edema, there seems to be an absence of literature that presents the effectiveness and compliance of current management techniques. This paper aims to condense the current literature on the effectiveness and compliance of current edema management approaches across various common etiologies, with the intentionof identifying alternative therapies that could enhance the quality of care for patients with chronic lower extremity edema. Several promising new therapies such as exogenous calf muscle stimulation, leg raise exercises, high-dose albumin injections, and device-based negative pressure lymph drainage (NPLD), deviate from the currentestablished standard of care. This scoping review revealed diverse treatment methods tailored to the specific underlying etiology of edema. The use of diuretics and vasodilators has shown benefits in treating CHF-induced edema but failed to alleviate and prevent the recurrence of edema in hospitalized and recently discharged patients. Albumin injections have emerged as a potential alternative treatment for edema due to liver disease, addressing hypoalbuminemia symptoms caused by liver failure. Patients with vascular causes of edema are efficaciously treated conservatively with compression stockings, although patient adherence remains a hurdle. For postoperative edema, device-based NPLD appears promising, with potential benefits over elastic bandage wraps and kinesiology taping.

Kronik Alt Ekstremite Ödemi Olan Hastalarda Sakroiliyak Eklem Disfonksiyonu Varlığı ve Postür Analizi

Abstract
 Background and Aim: Chronic lower extremity edema has been associated with postural impairment, sacroiliac joint dysfunction (SIJD), and abnormal gait. Lymphedema and lipedema are important chronic lower extremity causes. This study aimed to detect the presence of SIJD and postural disorders in patients with lower extremity edema and the relationship between them.
 Methods: This is a comparative, prospective cohort study. Fifty-three patients with lower extremity edema and 53 healthy subjects were included in the study. Pain provocation tests were used to determine SIJD. Postural analysis was conducted with PostureScreen® Mobile 11.2 (PostureCo, Inc., Trinity, FL) software. The life quality of participants was determined by the Lymphedema Quality of Life (LYMQOL) scale. The functional status of the patients was determined by the Oswestry Disability Index and Lower Extremity Functional Scale.
 Results: SIJD (18.9%) was more common in the edema group. There was a positive correlation between volume differences, percentages, and the development of SIJD. We found deviations in the head, shoulder, and hip angulations in the edema group. Q angle and lateral shoulder angulation were significantly higher in patients with SIJD in the edema group. In the edema group, LYMQOL-leg total score was higher in patients with SIJD.
 Conclusion: Chronic lower extremity edema was found to be associated with postural deviations and SIJD. Besides edema control, postural disorders and SIJD should also be considered in these patients.

Hypomagnesemia-Induced Hypocalcemia Successfully Treated With Sodium-Glucose Cotransport Inhibitor (SGLT-2i), a Case Report

Background: Severe hypomagnesemia can result in hypocalcemia as magnesium is a co-factor necessary for PTH production in the parathyroid glands. Calcium replacement alone can prove difficult in the setting of hypomagnesemia, therefore optimal treatment should also include repletion and normalization of magnesium levels. Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are a class of oral medications used in the treatment of type 2 diabetes and recently in heart failure which inhibit the sodium-glucose transporter in the proximal tubule of the kidney. A lesser known effect of SGLT-2i is renal tubular resorption of magnesium leading to increased serum magnesium levels. We report a case of refractory diuretic-induced hypomagnesemia and subsequent hypocalcemia which was successfully treated with SGLT-2i. Clinical Case: A 74-year-old male with uncontrolled type 2 DM, vitamin D deficiency, NASH cirrhosis, chronic lower extremity edema on furosemide therapy, and CKD stage III presented with unexplained hypocalcemia at 7.4–8.4 mg/dL (n: 8.8 – 10.4 mg/dL) and hypomagnesemia at 1.0–1.3 mg/dL (n: 1.5 – 2.5 mg/dL) for the past two years. He had been followed by his PCP who performed a workup revealing 25-OH vitamin D level 22.6 ng/mL, PTH 43 pg/mL (n: 10–55 pg/mL) with corresponding calcium 8.1 mg/dL. He was started on ergocalciferol 50,000IU, magnesium oxide 400mg daily, titrated up to 400mg BID, and calcium carbonate 400mg BID with no improvement in magnesium or calcium level. Later, he was admitted to the hospital with volume overload. During admission, magnesium was repleted with IV magnesium sulfate to a level of 2.1 mg/dL and serum calcium level normalized to 8.8 mg/dL without supplementation once magnesium level was replete. He was discharged with resumption of oral magnesium sulfate 400mg BID, but within 10 days his serum magnesium level dropped to 1.0 mg/dL. Endocrinology was consulted, and due to the severe hypomagnesemia, empagliflozin 10mg daily was started for the purpose of increasing the serum magnesium level and secondarily for improvement in glucose and edema control. After one week of treatment, the magnesium level increased to 1.4mg/dL and calcium level to 8.7mg/dL. Six months later, magnesium and calcium levels remained stable at 1.7 mg/dL and 9.1 mg/dL, respectively. The patient continues to now remain normocalcemic and normomagnesemic on empagliflozin 12.5mg daily. Conclusion: SGLT-2i represent a potent class of anti-hyperglycemic agents with the secondary effect of renal tubular absorption of magnesium which may help achieve appropriate PTH secretion in cases of treatment refractory hypocalcemia. This is one of the first cases to report the off-label use of SGLT-2i for refractory hypocalcemia due to hypomagnesemia. SGLT-2i should be considered in these cases especially in the setting of suboptimally controlled type 2 DM when other interventions have been unsuccessful.

Compression Therapy to Prevent Recurrent Cellulitis of the Leg

Lower extremity (LE) cellulitis is a common diagnosis in patients presenting to the emergency department and frequently becomes a recurrent issue for patients with chronic lower extremity edema. These patients frequently require hospital admission and if discharged, rarely have a long-term plan in place to address the underlying edema that increases their risk for recurrent cellulitis. This study evaluated the benefit of outpatient leg compression therapy in the prevention of recurrent LE cellulitis.

How often does pulmonary hypertension cause chronic lower extremity edema?

How often does pulmonary hypertension cause chronic lower extremity edema?

An Unusual Cause of Jaundice: Cholestasis-lymphedema Syndrome “Aagenaes Syndrome”: ACG/AstraZeneca Clinical Vignette Award: Presidential Poster

Purpose: A 61-year-old Caucasian male of Norwegian descent presented to the emergency department with complaints of progressive jaundice, pruritus, dark urine, clay-colored stools, and lower extremity edema for one month. This patient had history of intermittent jaundice all of his life, with chronic lower extremity edema. As an infant, he had an exploratory laparotomy for biliary atresia, but no definitive intervention was done. There was no family history of liver disease, no history of alcohol use, and his only medication was furosemide. On examination, he had no stigmata of chronic liver disease, reduced air entry in both lower lung fields, a healed laparotomy scar, and 2 + bilateral pedal edema. Initial labs showed a normal complete blood count and renal function, but a total bilirubin of 6.7 (Direct 4.2), alkaline phosphatase of 422 with AST 41, and ALT 32. A chest X-ray done in the ED revealed bilateral pleural effusions. Subsequent work-up for chronic liver disease was negative, and liver ultrasound with Dopplers and MRI of the liver were negative. A liver biopsy showed chronic lymphocytosis. Thoracentesis demonstrated chylothorax with triglycerides of 815 mg/dl. In summary, this is a 61 year-old Caucasian male of Norwegian heritage with recurrent, intermittent, cholestatic jaundice with chronic lymphedema, pruritus, and chylothorax. Given this constellation of findings, we diagnosed our patient with Aagenaes syndrome. This syndrome was first described in six large Norwegian families, and is characterized by chronic lymphedema and cholestasis. Its inheritance is autosomal recessive, with a prevalence of < 1 in 100,000. Pathogenesis involves a defect in lymphangiogenesis with generalized hypoplasia of lymphatics and the abnormal development of lymphatics around small biliary tracts. Patients present with severe neonatal cholestasis, which decreases during early childhood and becomes episodic later. Lymphedema is present at birth, but is usually noticed later, and affects the small bowel and thoracic soft tissue leading to chylothorax. Liver histology may show non-specific inflammation (as in our patient), giant cell transformation, fibrosis, or cirrhosis. Prognosis for liver disease is good. Management involves eating a fat-reduced diet during cholestasis, with supplementation of fat-soluble vitamins. We used subcutaneous octreotide for the chylothorax, with resolution of his pleural effusions. The patient is doing well currently, and is being followed in the hepatology clinic.

Predictive Factors for Chronic Lower Extremity Edema After Multimodality Limb-sparing Therapy of Soft-tissue Sarcoma of the Proximal Lower Extremity

Predictive Factors for Chronic Lower Extremity Edema After Multimodality Limb-sparing Therapy of Soft-tissue Sarcoma of the Proximal Lower Extremity

A Case of Fulminant Hepatic Failure and Chronic Lower Extremity Edema

INTRODUCTION: Acute liver failure refers to the rapid development of severe acute liver injury with impaired synthetic function and encephalopathy in a person who previously had a normal liver or had well-compensated liver disease. In the United States, the leading cause is acetaminophen ingestion (39 percent), indeterminate (17 percent), idiosyncratic drug reactions (13 percent), and viral hepatitis A or B (12 percent). Budd-Chiari syndrome is a relatively uncommon cause of acute liver failure.

Natriuretic Peptide Testing in Heart Failure

Case presentation 1: A 78-year-old woman with a history of morbid obesity, coronary artery disease, chronic obstructive pulmonary disease, and chronic kidney disease (serum creatinine 2.0 mg/dL) presented to the emergency department with worsening dyspnea. Her ECG shows no acute ischemic changes; her chest radiograph reveals chronic emphysematous changes with mild bilateral infiltrates. Her lung examination is notable for diffuse wheezing, and she has chronic lower extremity edema. Her amino-terminal pro-B-type natriuretic peptide ( NT-proBNP) level is 5500 pg/mL (upper limit of normal is 75 years). Does this patient have acutely decompensated heart failure (ADHF)? Many patients presenting with acute dyspnea (including those with ADHF) have multiple coexisting medical disorders that may complicate their diagnosis and management. Diagnostic uncertainty in the setting of acute dyspnea is associated with longer hospital length of stay, more diffuse diagnostic and therapeutic efforts, increased healthcare costs, and higher likelihood for repeat heart failure (HF) hospitalization or death.1 The addition of testing for brain natriuretic peptide (BNP) or NT-proBNP to standard clinical assessment has been shown to be valuable for an accurate and efficient diagnosis and prognostication of HF, and the use of BNP or NT-proBNP may be associated with improved clinical outcomes.2,–,4 Circulating levels of BNP/ NT-proBNP are normally very low in healthy individuals. In response to increased myocardial wall stress due to volume- or pressure-overload states (such as in HF), the BNP gene is activated in cardiomyocytes. This results in the production of an intracellular precursor propeptide (proBNP108); further processing of this propeptide results in release of the biologically inert amino-terminal fragment ( NT-proBNP) and the biologically active BNP (Figure 1). In addition, a significant portion of BNP or NT-proBNP detected by current assays includes uncleaved proBNP108, whereas BNP concentrations …

Resection of the Inferior Vena Cava Without Reconstruction for Urologic Malignancies

To present our experience with inferior vena cava (IVC) resection in 6 patients. Complete surgical excision of tumors within the retroperitoneum may afford patients their best chance at long-term disease-free survival. In rare instances, surgical therapy may require resection of the IVC. Between 2005 and 2008, a total of 6 patients underwent caval resection. The median age of the patients was 47 years (range 26-66 years). Three patients had metastatic germ cell tumors within the retroperitoneum and underwent postchemotherapy retroperitoneal lymph node dissection. Two patients had transitional cell carcinoma and 1 had renal cell carcinoma of the right kidney, which were treated by radical nephrectomy. The infrarenal IVC was removed in 5 patients and the infrahepatic cava in the remaining patient. The IVC was not reconstructed in any patient. Mean length of stay was 10 days (range 7-17 days). Five complications were noted in 2 patients. Complications included pneumothorax, lower-extremity compartment syndrome, right upper-extremity brachial plexus stretch injury, and respiratory failure in 1 patient and atrial fibrillation in another. No complications occurred in the remaining patients. Chronic lower extremity edema was not encountered in any patient. At present, all 3 patients with testicular cancer are disease-free. Of the 3 patients with kidney cancer, 2 died of disease progression and the remaining patient has metastatic disease. IVC resection without reconstruction is well tolerated in patients with large retroperitoneal masses because most patients have well-established collaterals before surgery due to pre-existing caval obstruction. Multiple variables have been correlated with improved prognosis in cancer patients. One of the factors most important to surgical oncologists is complete tumor resection at the time of initial extirpative surgery. Complete excision of tumors within the retroperitoneum may require resection of major vascular structures, including the IVC.

The incidence of symptomatic lower-extremity lymphedema following treatment of uterine corpus malignancies: A 12-year experience at Memorial Sloan-Kettering Cancer Center

Objectives. To describe the incidence of symptomatic postoperative lower-extremity lymphedema in women treated for uterine corpus cancer, and to evaluate its relationship to regional lymph node removal and postoperative therapy. Methods. A retrospective chart review of all patients with uterine corpus cancer managed over a 12-year period (1/93–12/04). All patients had a hysterectomy as part of their therapy. We identified patients with leg lymphedema – as described by the physician or reported by the patient – through medical records. We excluded cases of leg edema that developed secondary to medical conditions such as cardiovascular and renal disease, venous thrombosis, and end-stage recurrent malignancy. Lymphedema dermal changes and related fibrosis were graded using the common terminology criteria for adverse events. Results. In all, 1289 patients with uterine corpus malignancy were evaluated. We excluded other chronic lower-extremity edema that was related to a variety of medical conditions in 74 patients (5.7%). With a median follow-up of 3 years (interquartile range, 1.1–5.4 years), new symptomatic post-treatment lower-extremity lymphedema was noted in 16 patients. Patients who had lymph nodes removed at initial surgery had a higher rate of developing lymphedema (16/670, 2.4%) than those who did not (0/619, 0%) ( P = 0.0001). Furthermore, symptomatic lymphedema was limited to patients who had 10 or more regional lymph nodes removed 16/469 (3.4%). Lymphedema was noted at a median of 5.3 months after surgery (range, 1–32 months). Lymphedema was unilateral in 11 patients (69%) and bilateral in 5 (31%); moreover, it was considered grade 1 in 12 patients (75%) and grade 2 in 4 (25%). Age, weight, stage, type of hysterectomy, and type of postoperative adjuvant therapy were not associated with lymphedema. Conclusions. To date, this is the largest series evaluating symptomatic lower-extremity lymphedema in women with uterine corpus cancer. Patients who had 10 or more regional lymph nodes removed at initial surgery appeared to be at higher risk for developing new symptomatic leg lymphedema. Patients undergoing surgery with lymphadenectomy for uterine corpus malignancy should be informed about the possibility of postoperative new symptomatic leg lymphedema. A prospective evaluation of leg lymphedema is needed to accurately determine the incidence, severity, and risk factors of this complication.