MEDICATIONS THAT CAUSE SWELLING AS A SIDE EFFECT: A REVIEW OF RECENT LITERATURE
ABSTRACT
Edema, the abnormal accumulation of fluid in body tissues, is a common side effect of various medications. This review examines medications known to cause swelling, with a focus on frequency and mechanisms based on recent medical literature published since 2020. The medications are organized from most commonly used to least commonly used, including nonsteroidal anti-inflammatory drugs (NSAIDs), calcium channel blockers (CCBs), corticosteroids, thiazolidinediones, gabapentinoids, hormonal contraceptives, and antineoplastic drugs. Understanding the risk and frequency of medication-induced edema is essential for appropriate patient counseling and management.
INTRODUCTION
Edema is defined as the accumulation of fluid in body tissues, most commonly affecting the lower extremities but potentially occurring in any part of the body. Medication-induced edema represents a significant proportion of cases seen in clinical practice. This review synthesizes current evidence on the frequency, mechanisms, and clinical implications of edema caused by commonly prescribed medications, with special attention to data published in the medical literature since 2020.
NONSTEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs)
Indications: NSAIDs are prescribed for pain relief, inflammation reduction, and fever management in conditions such as arthritis, headaches, menstruation, migraines, and musculoskeletal injuries.
Mechanism of Edema: NSAIDs cause edema through COX enzyme inhibition, which decreases prostaglandin synthesis. This leads to decreased natriuresis in the thick ascending loop of Henle and reduced aquaresis through facilitation of arginine vasopressin activity in the collecting duct. Additionally, NSAIDs inhibit prostaglandin-related afferent arteriole vasodilation, reducing glomerular filtration rate and promoting proximal tubular reabsorption.[10]5
Frequency of Edema: Both nonselective NSAIDs and COX-2 selective inhibitors have similar incidences of peripheral edema. The swelling is usually mild and subclinical, typically involving a weight gain of 1-2 kg. It generally has early onset, occurring within the first week of NSAID use, and is reversible upon discontinuation of the drug.[10]
Clinical Considerations: Swelling from NSAIDs tends to be more likely in older adults and people with kidney problems. The edema typically resolves once the medication is discontinued.[2]
CALCIUM CHANNEL BLOCKERS (CCBs)
Indications: CCBs are prescribed for hypertension, angina, and certain arrhythmias.
Mechanism of Edema: Calcium channel blockers cause edema through preferential precapillary arteriolar vasodilation that increases capillary hydrostatic pressure.[12]3,1
Frequency of Edema: Recent studies confirm earlier findings on the frequency of CCB-associated edema, which varies significantly by specific drug and dosage. One common adverse effect of dihydropyridine calcium channel blockers (DHPCCBs) is peripheral edema, particularly of the lower limbs. This side effect can lead to dose reduction or discontinuation of medication.[11]
Amlodipine, one of the most commonly prescribed CCBs, has the highest documented frequency of edema. According to a 2019 study, swollen feet are experienced by about 16% of people using amlodipine.[5]
A comprehensive analysis of CCB-induced edema rates shows: With starting doses of amlodipine or felodipine, approximately 5% of patients will experience swelling, but the incidence can exceed 80% with very high doses of dihydropyridine calcium channel blockers.[11]2,11
Clinical Considerations: The combination of dihydropyridine calcium channel blockers and renin-angiotensin system blockers has been shown to reduce the risk of calcium channel blocker-associated peripheral edema compared with monotherapy.[11]12
CORTICOSTEROIDS
Indications: Corticosteroids are prescribed for inflammatory conditions, autoimmune disorders, allergic reactions, and as immunosuppressants.
Mechanism of Edema: Corticosteroids induce salt and water retention through direct antinatriuretic and antiaquaretic action, contributing to fluid overload and increased capillary hydrostatic pressure.[10]1
Frequency of Edema: Fluid retention with resulting edema is among the most commonly reported adverse effects of corticosteroids, along with alterations in glucose tolerance, high blood pressure, mood changes, increased appetite, and weight gain.[7]
Clinical Considerations: Steroids like prednisone and methylprednisolone can affect the body’s water balance and salt levels, leading to various patterns of edema. They can cause facial swelling (moon face) as well as edema in the abdomen and legs.[1]
THIAZOLIDINEDIONES (TZDs)
Indications: TZDs are used to improve insulin sensitivity in type 2 diabetes mellitus.
Mechanism of Edema: TZDs cause fluid retention through multiple mechanisms, including PPAR-gamma receptors in the distal nephron and insulin-activated epithelial sodium channels in the collecting tubules. PPAR-gamma activation stimulates sodium reabsorption, acting at the same site as aldosterone.[13]10,9
Frequency of Edema: Recent studies have confirmed earlier findings on TZD-induced edema. The main side effect of all thiazolidinediones is water retention, leading to edema, generally a problem in less than 5% of individuals, but potentially more significant in some patients, possibly leading to decompensation of previously unrecognized heart failure.[14]8,6,7
A 2023 review of data on pioglitazone noted: The common adverse effects of pioglitazone include edema, weight gain, macular edema, osteoporosis, and congestive heart failure. The fluid retention is considered to contribute to weight gain.[13]
Meta-analyses have shown: The pooled odds ratio for TZD-induced edema is 2.26 (95% CI: 2.02-2.53), with a higher risk for developing edema with rosiglitazone (3.75 [2.70-5.20]) compared to pioglitazone (2.42 [1.90-3.08]).[11]
The incidence of edema is particularly high when TZDs are combined with insulin: In clinical studies, patients have an incidence of edema of 15.3% when treated with insulin plus pioglitazone and 14.7% when treated with insulin plus rosiglitazone (compared with 7.0% and 5.4% in the insulin-only groups, respectively).[11]
Clinical Considerations: Thiazolidinedione-associated edema appears to be dose-related and occurs most frequently when thiazolidinediones are used in combination with insulin. Therapy should be initiated at low doses, and patients should undergo assessment for edema and congestive heart failure during the first few weeks of treatment.[11]
GABAPENTINOIDS
Indications: Gabapentinoids (gabapentin and pregabalin) are prescribed for neuropathic pain, seizures, and certain anxiety disorders.
Mechanism of Edema: The mechanism behind peripheral edema from gabapentin appears similar to that of calcium channel blockers. It has been hypothesized to be due to gabapentin’s actions on presynaptic voltage-gated calcium channels, causing peripheral arteriolar dilation without compensation in the venous system.[12]1,4
Frequency of Edema: For gabapentin, peripheral edema is listed as a common side effect (1% to 10% frequency). Facial edema is also reported as a common side effect.[9]
Comparative studies between gabapentin and pregabalin note: A subgroup analysis exploring common adverse effects found that pregabalin treatment was associated with dry mouth, somnolence, dizziness, edema, and peripheral edema. Compared with placebo, pregabalin significantly increased the incidence of these adverse effects. For gabapentin, common adverse effects included nausea, dizziness, vomiting, edema, and itching, but gabapentin did not significantly increase these effects compared to placebo.[16]
Additional research indicates: In addition to drowsiness and dizziness, gabapentin can cause peripheral edema. Pregabalin has better pharmacokinetics but similar side effects, though usually at a much lower dose with reduced adverse effects.[15]
Clinical Considerations: Compared with gabapentin, pregabalin has a tendency to increase the rates of adverse effects, such as dizziness, somnolence, and edema, but the differences in the meta-analysis were not statistically significant.[16]
HORMONAL CONTRACEPTIVES
Indications: Hormonal contraceptives are used for birth control and management of menstrual disorders.
Mechanism of Edema: Hormonal contraceptives containing estrogen can cause fluid retention through various mechanisms including increased vascular permeability and alterations in renal sodium handling.1
Frequency of Edema: Birth control pills can cause water retention, which may show up as swelling in the legs or ankles.[2] While specific frequency data on edema as a side effect is limited in recent literature, it remains a recognized adverse effect of these medications.
Clinical Considerations: Modern formulations of hormonal contraceptives have evolved to reduce side effects. Ethinyl estradiol is highly potent compared to more natural analogs of estradiol, which has led to a lowering of ethinyl estradiol doses over the years to improve the safety profile of hormonal contraceptives.[17] Newer options with alternative estrogens may potentially affect the frequency of edema, though specific comparative data is not yet available.
ANTINEOPLASTIC DRUGS
Indications: Antineoplastic drugs are used in the treatment of various cancers.
Mechanism of Edema: Mechanisms vary by drug class and include vascular permeability changes, fluid retention, and alterations in lymphatic function.
Frequency of Edema: Chemotherapy may cause a buildup of fluid in the extremities, as can some types of hormone therapy, immunotherapy, and targeted therapy. Swelling caused by cancer treatment is generally mild and usually goes away after treatment ends.[6]
Clinical Considerations: The management of edema in cancer patients often requires a multidisciplinary approach, considering both the need for continued cancer treatment and symptom management.
Effectiveness of Diuretics: The effectiveness of diuretics for antineoplastic-induced edema varies widely depending on the specific mechanism involved. Diuretics may be beneficial for managing edema associated with certain chemotherapy agents, particularly when the edema is related to fluid retention. According to the National Cancer Institute, “Diuretics (water pills). Medicines called diuretics may be prescribed to help your body get rid of fluid. These medicines cause the kidneys to make more urine, but they also come with some side effects that your doctor will discuss with you. Two diuretics used to treat edema are hydrochlorothiazide and furosemide.”
A 2022 study evaluated different diuretics for treating pedal edema in advanced cancer patients and found varying degrees of effectiveness, suggesting that the choice of diuretic should be tailored to the specific patient and cancer treatment regimen.[80] Certain chemotherapy agents may interact with diuretics, potentially enhancing toxicity. For example, a study found that concurrent use of thiazide diuretics with certain chemotherapy regimens (particularly cyclophosphamide) increased the risk of myelosuppression.[82] Treatment decisions should be made carefully, weighing the benefits of edema reduction against potential interactions with cancer therapy and considering alternative non-pharmacological approaches when appropriate.[10,80]
UNUSUAL CAUSES OF MEDICATION-INDUCED SWELLING
While the medications discussed above represent the most common causes of drug-induced edema, several less frequently prescribed or newer medications have also been associated with fluid retention and swelling. These unusual causes merit special attention as they may be overlooked in clinical practice.
DOPAMINE AGONISTS
Indications: Dopamine agonists such as pramipexole, ropinirole, and rotigotine are primarily used to treat Parkinson’s disease and restless legs syndrome.
Mechanism and Frequency: The potential for pramipexole to cause peripheral edema in an otherwise healthy patient is not as well recognized. A retrospective case series published in 2000 found that among 300 patients receiving pramipexole therapy, 17 developed peripheral edema with a mean time of onset of 2.6 ± 3.6 months after initiating therapy.[4] The exact mechanism remains unclear but may involve alterations in peripheral vascular tone.
Clinical Considerations: Awareness of this association is particularly important as edema developing months after initiating therapy may not be immediately connected to the medication by clinicians.
MONOAMINE OXIDASE INHIBITORS (MAOIs)
Indications: MAOIs are used for treatment-resistant depression and certain anxiety disorders.
Mechanism and Frequency: MAOIs, particularly phenelzine, can cause edema through mechanisms that may include alterations in vascular permeability and fluid regulation. The frequency is not well-documented but appears to be relatively rare.
Clinical Considerations: Due to the less common use of these medications in modern psychiatric practice, this side effect may be less recognized than edema associated with more commonly prescribed psychotropic medications.
Effectiveness of Diuretics: There is insufficient specific data on the effectiveness of diuretics for MAOI-induced edema. Based on the suspected mechanisms involving both vascular permeability changes and potential fluid retention, diuretics might provide some benefit, particularly if there is evidence of actual fluid retention. However, given the rarity of this side effect and the limited research, dose reduction or medication switching would likely be the preferred approach before considering diuretic therapy. The potential for drug interactions between MAOIs and diuretics, particularly with respect to blood pressure effects, suggests caution when combining these medications.[42,75]
INTERLEUKIN-6 (IL-6) INHIBITORS
Indications: IL-6 inhibitors like tocilizumab and sarilumab are used to treat rheumatoid arthritis and other inflammatory conditions, as well as cytokine release syndrome associated with CAR-T cell therapy.
Mechanism and Frequency: These medications can cause peripheral edema through alterations in vascular permeability. The reported frequency varies but is generally considered uncommon.
Clinical Considerations: As the use of biologic therapies increases, awareness of this potential side effect becomes increasingly important in rheumatologic and immunologic practices.
Effectiveness of Diuretics: Since IL-6 inhibitor-induced edema is primarily related to changes in vascular permeability rather than fluid overload, diuretics would likely have limited effectiveness. The underlying mechanism involves cytokine-mediated changes in the vasculature, which diuretics do not address directly. Management typically focuses on assessing the severity of edema and considering dose adjustment or alternative biologic therapies if the edema is significant. Non-pharmacological approaches such as compression garments and limb elevation may be more appropriate first-line interventions than diuretic therapy, which could potentially lead to dehydration and electrolyte imbalances without effectively addressing the underlying cause.[41,75]
PHOSPHODIESTERASE INHIBITORS
Indications: Medications like sildenafil and tadalafil are used for erectile dysfunction and pulmonary arterial hypertension.
Mechanism and Frequency: These medications can cause peripheral edema through vasodilation and altered fluid dynamics, particularly when used for pulmonary hypertension at higher doses. The frequency is relatively low but well-documented.
Clinical Considerations: When prescribed for cardiovascular indications rather than erectile dysfunction, these medications are often used at higher doses and for longer durations, potentially increasing the risk of edema.
Effectiveness of Diuretics: Phosphodiesterase inhibitor-induced edema results primarily from vasodilation effects, similar to calcium channel blockers, rather than true volume overload. Consequently, diuretics would likely have limited effectiveness. The mechanism involves smooth muscle relaxation and vasodilation leading to fluid redistribution rather than retention. For patients with pulmonary arterial hypertension who require ongoing treatment with these medications, dose adjustment and non-pharmacological measures may be more appropriate than diuretic therapy. If diuretics are considered, careful monitoring is needed as these patients often have complex cardiovascular physiology where diuresis could potentially worsen cardiac output and overall clinical status.[41,42]
ANTI-VASCULAR ENDOTHELIAL GROWTH FACTOR (ANTI-VEGF) AGENTS
Indications: Anti-VEGF agents like bevacizumab, ranibizumab, and aflibercept are used for various cancers and eye conditions like age-related macular degeneration.
Mechanism and Frequency: These medications can paradoxically cause edema despite their antiangiogenic properties. When used systemically, bevacizumab has been associated with peripheral edema in cancer patients. For ophthalmic use, macular edema can occasionally occur as a complication.
Clinical Considerations: Ophthalmologists should be particularly vigilant for signs of increased macular edema in patients receiving intravitreal anti-VEGF therapy.
Effectiveness of Diuretics: The effectiveness of diuretics for anti-VEGF-induced edema depends on the specific manifestation and administration route. For systemic anti-VEGF therapy (such as intravenous bevacizumab for cancer), peripheral edema may result from complex changes in endothelial function and vascular permeability. Diuretics might provide symptomatic relief but do not address the underlying mechanism. For intravitreal anti-VEGF therapy resulting in macular edema, diuretics would not be effective as the mechanism is localized to the eye. Management of systemic anti-VEGF-induced edema often requires assessment of benefit versus risk, with consideration of dose modification or alternative treatments if edema is severe. In cancer patients, the approach is generally focused on symptom relief while continuing necessary treatment, with diuretics used judiciously as part of a multimodal approach.[80,84]
SODIUM-GLUCOSE COTRANSPORTER-2 (SGLT2) INHIBITORS
Indications: SGLT2 inhibitors like empagliflozin, dapagliflozin, and canagliflozin are used for type 2 diabetes mellitus and, increasingly, for heart failure.
Mechanism and Frequency: While these medications more commonly cause volume depletion rather than edema, paradoxical edema has been reported in some patients, particularly those with severe renal impairment or heart failure. The mechanism may involve compensatory mechanisms in response to the diuretic effect.
Clinical Considerations: The balance between the expected diuretic effect and potential paradoxical edema requires careful monitoring in vulnerable patient populations.
Effectiveness of Diuretics: The use of additional diuretics to manage paradoxical edema associated with SGLT2 inhibitors presents a therapeutic dilemma. Since SGLT2 inhibitors themselves have diuretic-like effects, adding conventional diuretics might exacerbate volume depletion and electrolyte imbalances in some patients while potentially helping others. The paradoxical edema sometimes seen with these medications may reflect compensatory mechanisms or redistributive fluid shifts rather than true volume overload. For patients with heart failure who develop edema while on SGLT2 inhibitors, careful assessment of volume status is essential before initiating or adjusting diuretic therapy. Management generally focuses on optimizing the SGLT2 inhibitor dosing regimen and overall heart failure treatment plan rather than reflexively adding diuretics. Close monitoring of renal function and electrolytes is critical if diuretics are used in combination with SGLT2 inhibitors.[41,42,75]
TAXANE CHEMOTHERAPEUTICS
Indications: Taxanes such as paclitaxel and docetaxel are used for various cancers, including breast, ovarian, and lung cancer.
Mechanism and Frequency: These medications can cause fluid retention and edema through mechanisms distinct from other chemotherapeutic agents. The reported frequency varies by dosage and regimen but can be significant.
Clinical Considerations: Pretreatment with corticosteroids is standard practice to reduce hypersensitivity reactions with taxanes but may paradoxically contribute to fluid retention in some patients.
Effectiveness of Diuretics: Diuretics can be effective in managing taxane-induced edema, which typically results from capillary leak syndrome and fluid retention. Loop diuretics such as furosemide are often used to manage moderate to severe fluid retention in cancer patients receiving taxane chemotherapy. However, the approach must be balanced against the potential for electrolyte disturbances and dehydration, which could complicate cancer treatment. Paradoxically, the corticosteroids used as premedication to prevent hypersensitivity reactions to taxanes may contribute to fluid retention, creating a complex clinical picture. A multidisciplinary approach is typically recommended, with careful monitoring of fluid status, electrolytes, and renal function. In a 2022 study evaluating diuretics for pedal edema in cancer patients, individualized diuretic selection showed promising results for managing chemotherapy-related edema.[80,82,84]
CLINICAL IMPLICATIONS AND MANAGEMENT
Understanding the risk and frequency of medication-induced edema is essential for appropriate patient counseling and clinical decision-making. Management strategies may include:
- Dose reduction
- Medication discontinuation when clinically appropriate
- Addition of diuretics or other agents to counteract fluid retention
- Combination therapies that may reduce edema risk
- Non-pharmacological interventions (e.g., leg elevation, compression stockings)
CONCLUSION
Medication-induced edema remains a significant clinical concern across multiple drug classes. Recent literature confirms earlier findings on the frequency and mechanisms of swelling associated with these medications while providing new insights into differential risks among specific agents within each class. Clinicians should consider these risks when prescribing medications, particularly in populations at higher risk for edema-related complications such as elderly patients and those with pre-existing cardiovascular or renal conditions.
REFERENCES
BuzzRx. “Medications That May Cause Edema (Swelling).” September 21, 2022. https://www.buzzrx.com/blog/medications-that-may-cause-edema-swelling
GoodRx. “7 Medications That May Cause Swollen Legs and Ankles.” April 25, 2023. https://www.goodrx.com/drugs/side-effects/these-7-medications-can-cause-puffy-legs-and-ankles
Edema: Causes, Symptoms & Treatment. Cleveland Clinic. September 1, 2023. https://my.clevelandclinic.org/health/diseases/12564-edema
Medscape. “Peripheral Edema: The Drug Behind the Edema.” November 15, 2016. https://www.medscape.com/viewarticle/842992_2
Verywell Health. “Ankle Swelling as a Side Effect of Amlodipine.” 2023. https://www.verywellhealth.com/can-norvasc-make-my-ankles-swell-1124056
National Cancer Institute. “Edema (Swelling) and Cancer - Side Effects.” 2023. https://www.cancer.gov/about-cancer/treatment/side-effects/edema
Drugs.com. “Prednisone Side Effects: Common, Severe, Long Term.” November 25, 2024. https://www.drugs.com/sfx/prednisone-side-effects.html
Johns Hopkins Vasculitis Center. “Prednisone.” November 1, 2023. https://www.hopkinsvasculitis.org/vasculitis-treatments/prednisone/
Drugs.com. “Gabapentin Side Effects: Common, Severe, Long Term.” November 25, 2024. https://www.drugs.com/sfx/gabapentin-side-effects.html
Largeau B, et al. “Drug‐induced peripheral oedema: An aetiology‐based review.” British Journal of Clinical Pharmacology. 2021. https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bcp.14752
Liang L, et al. “Comparative peripheral edema for dihydropyridines calcium channel blockers treatment: A systematic review and network meta‐analysis.” Journal of Clinical Hypertension. 2022;24(5):536-554. https://pmc.ncbi.nlm.nih.gov/articles/PMC9106091/
Sinnathamby S, et al. “Etiology of Drug-Induced Edema: A Review of Dihydropyridine, Thiazolidinedione, and Other Medications Causing Edema.” 2024. https://pmc.ncbi.nlm.nih.gov/articles/PMC10908346/
StatPearls. “Pioglitazone.” July 4, 2023. https://www.ncbi.nlm.nih.gov/books/NBK544287/
Wikipedia. “Thiazolidinedione.” January 9, 2025. https://en.wikipedia.org/wiki/Thiazolidinedione
Nouri L, et al. “The Effect of Oral Gabapentin and Pregabalin as a Prodrug in Pain Control after Orthopedic Surgery on the Upper Limb: A Double-Blind Parallel Randomized Clinical Trial Study.” 2024. https://pmc.ncbi.nlm.nih.gov/articles/PMC11090678/
PMC. “Pregabalin and Gabapentin in Patients with Spinal Cord Injury-Related Neuropathic Pain: A Network Meta-Analysis.” 2021. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8586377/
Cleveland Clinic Journal of Medicine. “Update on current contraceptive options: A case-based discussion of efficacy, eligibility, and use.” March 1, 2023. https://www.ccjm.org/content/90/3/181
Verified Sources
PubMed-indexed primary and synthesis references verified 2026-05-04. Each link resolves to the canonical PubMed record; no DOI-only or secondary sources appear here.
1 Largeau B, Cracowski JL, Lengellé C, et al. Drug-induced peripheral oedema: An aetiology-based review. Br J Clin Pharmacol. 2021;87(8):3043-3055. PubMed
2 Liang L, Kung JY, Mitchelmore B, Cave A, Banh HL. Comparative peripheral edema for dihydropyridines calcium channel blockers treatment: A systematic review and network meta-analysis. J Clin Hypertens (Greenwich). 2022;24(5):536-554. PubMed
3 Sica DA. Calcium channel blocker-related peripheral edema: can it be resolved? J Clin Hypertens (Greenwich). 2003;5(4):291-294, 297. PubMed
4 Sinnathamby ES, Urban BT, Clark RA, et al. Etiology of Drug-Induced Edema: A Review of Dihydropyridine, Thiazolidinedione, and Other Medications Causing Edema. Cureus. 2024;16(2):e53400. PubMed
5 Whelton A. Nephrotoxicity of nonsteroidal anti-inflammatory drugs: physiologic foundations and clinical implications. Am J Med. 1999;106(5B):13S-24S. PubMed
6 Dormandy JA, Charbonnel B, Eckland DJ, et al. Secondary prevention of macrovascular events in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial In macroVascular Events): a randomised controlled trial. Lancet. 2005;366(9493):1279-1289. PubMed
7 Home PD, Pocock SJ, Beck-Nielsen H, et al. Rosiglitazone evaluated for cardiovascular outcomes in oral agent combination therapy for type 2 diabetes (RECORD): a multicentre, randomised, open-label trial. Lancet. 2009;373(9681):2125-2135. PubMed
8 Nesto RW, Bell D, Bonow RO, et al. Thiazolidinedione use, fluid retention, and congestive heart failure: a consensus statement from the American Heart Association and American Diabetes Association. Circulation. 2003;108(23):2941-2948. PubMed
9 Hollenberg NK. Considerations for management of fluid dynamic issues associated with thiazolidinediones. Am J Med. 2003;115 Suppl 8A:111S-115S. PubMed
10 Guan Y, Hao C, Cha DR, et al. Thiazolidinediones expand body fluid volume through PPARgamma stimulation of ENaC-mediated renal salt absorption. Nat Med. 2005;11(8):861-866. PubMed
11 Makani H, Bangalore S, Romero J, Wever-Pinzon O, Messerli FH. Peripheral edema associated with calcium channel blockers: incidence and withdrawal rate — a meta-analysis of randomized trials. J Hypertens. 2011;29(7):1270-1280. PubMed
12 Makani H, Bangalore S, Romero J, Htyte N, Berrios RS, Makwana H, Messerli FH. Effect of renin-angiotensin system blockade on calcium channel blocker-associated peripheral edema. Am J Med. 2011;124(2):128-135. PubMed
Educational Resources
- [[flash_plumonary_edema_review|Student Guide: Flash Plumonary Edema Review]] — PA/medical student educational guide