Which assessments would the nurse complete within an hour of administering a diuretic

References

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References
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Continuing Education Activity
Indications
Mechanism of Action
Administration
Adverse Effects
Contraindications
Enhancing Healthcare Team Outcomes
Review Questions
What to monitor after administering furosemide?
What should you check before giving diuretics?
What is a common side effect of diuretics?
Which of the following is an effect of a diuretic?

Austin J, Hockey D, Williams WR, Hutchison S. Assessing parenteral diuretic treatment of decompensated heart failure in the community. Brit J Community Nurs. 2013; 18:(11)528-534 https://doi.org/10.12968/bjcn.2013.18.11.528

Sankaranarayanan R, Kanagala P, Douglas H, Rawat A, Hassan S, Beleznai T, Lee C. Ambulatory management of acute decompensation in heart failure. Brit J Hosp Med. 2019; 80:(1)40-45 https://doi.org/10.12968/hmed.2019.80.1.40

Veilleux RP, Wight JN, Cannon A, Whalen M, Bachman D. Home diuretic protocol for heart failure: partnering with home health to improve outcomes and reduce readmissions. Perm J. 2014; 18:(3)44-48 https://doi.org/10.7812/TPP/14-013

02 December 2021

Volume 26 · Issue 12

ISSN (print): 1462-4753

ISSN (online): 2052-2215

Abstract

Chronic heart failure is a condition associated with ageing, affecting 1–2% of the adult population, raising to 70% of the adult population over 70 years of age. Diuretics are often the first-line treatment for patients with symptomatic heart failure, not just oedema. Traditionally, intravenous (IV) diuretic therapy has been administered only in hospitals. In 2012, the British Heart Foundation ran a pilot study investigating the effectiveness of IV diuretic administration within the home. Since then, there has been an increase in these services. This article examines the advantages and disadvantages of this service, whether community nurses are best placed to deliver this, and what the benefits to the patient might be.

In 2012, the British Heart Foundation (BHF) announced a pilot study to evaluate giving IV diuretics in the patient's home. It claimed that it would end weeks of hospital in-patient care for people with severe heart failure and could be rolled out across the UK if successful (BHF, 2012). We are now beginning to see this being provided for patients in the community, but it is not without its challenges.

For more than a decade, the Department of Health and Social Care has championed a policy of moving services from the hospital environment into the community setting, closer to where patients live (Barton, 2018). In 2017, the National Institute for Cardiovascular Outcomes Research (NICOR) called for improved and earlier detection and management of oedema in the community, to prevent the need for hospital admission (NICOR, 2017). Providing IV diuretics in the home environment meets both of these objectives, but there are far more benefits to this than mere compliance with these two polices.

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Continuing Education Activity

Furosemide is a loop diuretic that has been in use for decades. The Food and Drug Administration (FDA) has approved furosemide to treat conditions with volume overload and edema secondary to congestive heart failure exacerbation, liver failure, or renal failure, including the nephrotic syndrome. However, clinicians must be aware of updates related to the indications and administration of furosemide to ensure safe practices and minimize adverse effects. This activity reviews updates on the recommended use of furosemide, the mechanism of action, indications, contraindications, adverse effects, toxicity, and other key factors (e.g., off-label uses, dosing, pharmacokinetics, monitoring, relevant interactions) profile. It highlights the interprofessional team's role in caring for patients on furosemide therapy.

Objectives:

Identify the mechanism of action of furosemide.
Describe the contraindications to the use of furosemide.
Outline the monitoring necessary for patients on furosemide.
Explain how healthy collaboration and communication between interprofessional team members can optimize the use of furosemide and minimize adverse effects, thereby improving patient outcomes.

Access free multiple choice questions on this topic.

Indications

The Food and Drug Administration (FDA) has approved furosemide to treat conditions with volume overload and edema secondary to congestive heart failure exacerbation, liver failure, or renal failure, including the nephrotic syndrome.

For patients with acutely decompensated heart failure (ADHF) with volume overload who have not received diuretics previously, the initial dose of furosemide should be 20 to 40 mg intravenously. Later, titrate the furosemide dose according to the clinical response of the patients. However, for those patients with ADHF with a normal kidney function on chronic diuretic therapy, the initial dose of furosemide can be equivalent to or greater than the total oral maintenance dose of furosemide the patient takes daily. Subsequently, the diuretic dose adjustments are according to the patient's clinical response. Nevertheless, starting with higher doses of furosemide, at a dose of 2.5 times the total daily oral dose of furosemide per day, has shown a significant trend toward a rapid improvement in the global assessment of patient symptoms.[1]

Although the FDA approved the use of loop diuretics alone or in combination with other anti-hypertensive medications as an alternative to thiazide diuretics to treat hypertension, however, the clinical guidelines panel report of the Eighth Joint National Committee (JNC-8) published in 2014 and the American College of Cardiology/American Heart Association (ACC/AHA) Task Force Panel Guidelines on hypertension treatment published in 2017 do not recommend the use of loop diuretic as a first-line medication to treat hypertension.[2][3] Nevertheless, Furosemide can be a second-line agent in heart failure patients with symptoms and advanced kidney disease with an estimated glomerular filtration rate of less than 30 ml per minute; loop diuretics (furosemide) are preferred over thiazide diuretics to treat hypertension.[4]

Diuretic therapy is recommended in patients with liver cirrhosis and ascites, accompanied by dietary sodium restriction. The recommended diuretics are a combination of spironolactone and furosemide, starting at a ratio of 100 mg of spironolactone and 40 mg of furosemide. They are titrated up to the dose of diuretics in an increment of the same ratio until achieving an adequate response to diuretic therapy or reaching a maximum dose of 400 mg of spironolactone plus 160 mg of furosemide.[5] However, in cases of intolerance to diuretics secondary to borderline blood pressure, the diuretics can be started at relatively lower doses of 50 mg of spironolactone with 20 mg of furosemide.

Mechanism of Action

Furosemide inhibits tubular reabsorption of sodium and chloride in the proximal and distal tubules and the thick ascending loop of Henle by inhibiting the sodium-chloride cotransport system resulting in excessive excretion of water along with sodium, chloride, magnesium, and calcium.[6]

Pharmacokinetics

Absorption: The onset of action of furosemide is usually within the first hour of oral furosemide intake, and it takes the first 1 to 2 hours to achieve a peak effect. The mean bioavailability of oral furosemide is 51% compared with the bioavailability of intravenously administered furosemide.[7]

Bioavailability: The furosemide absorption is slower than normal in patients with edema, particularly in patients with decompensated heart failure; however, the amount of loop diuretic absorbed is normal.[8] Oral and sublingual administration of furosemide achieves a peak concentration slower than the iv route. Although furosemide is more avidly absorbed with a bioavailability of 59% via the sublingual route compared with the oral route of administration, i.e., 47%, the half-life and time to peak concentration were not different between the oral and sublingual route of drug delivery. Also, the urinary excretion rate of furosemide and sodium and cumulative urine excretion rate was not different between the oral and sublingual administration of furosemide.[9].The bioavailability of furosemide is variable and relatively lesser than that of torsemide in patients with compensated congestive heart failure.[10][11]

Distribution: In healthy individuals, greater than 95% of furosemide is bound to plasma protein, mainly albumin. Only 2.3% to 4.1% of furosemide is existent in an unbound form in therapeutic concentrations.

Metabolism: Furosemide glucuronide is a major biotransformation active product of furosemide, having an active diuretic effect. Contemporary evidence indicates that furosemide is minimally metabolized in the liver.[12]

Excretion: The terminal half-life of furosemide is approximately 2 hours, and the total time of therapeutic effect is 6 to 8 hours. However, the half-life of furosemide will prolong in patients with chronic renal disease.[7] Although more furosemide gets excreted in the urine after IV administration, there is no difference in the amount of unchanged furosemide excretion in urine between the two formulations. After intravenous administration, furosemide achieves an early and high serum peak concentration and a higher peak excretion rate. A greater extent of furosemide is excreted in urine following the parenteral administration than oral administration.

Administration

Furosemide is available in oral and intravenous formulations. The administration of oral furosemide can be in the form of tablets or an oral solution. Intravenous furosemide is twice as potent as oral furosemide.

In patients with normal renal function, the oral dose equivalence of furosemide relative to other oral diuretics is as follows[13]:

40 mg of furosemide = 20 mg of torsemide = 1 mg of bumetanide
Furosemide oral tablet formulations are available in 20 mg, 40 mg, and 80 mg.
Furosemide oral solution is available as 10 mg/ml or 8 mg/ml, i.e., 40 mg furosemide/5 ml of solution.

Breaking phenomenon and ceiling effect: Normally, when an individual receives furosemide either orally or intravenously, it increases sodium excretion in urine. In a patient with extracellular volume expansion who has never had exposure to furosemide, the first dose of the drug causes significant sodium excretion and diuresis within the first 3 to 6 hours. After that effect of furosemide weans off, the kidney starts retaining sodium and chloride; this is called "post-diuretic sodium retention." Therefore, it is imperative to repeat the furosemide dose at 6 to 8-hour intervals to avoid post diuretic sodium retention and achieve significant diuresis. When furosemide is prescribed chronically, the patient's weight loss correlates with urine volume. A discrepancy in weight loss and diuresis indicates excessive sodium intake by the patient, which can be detected by 24-hour urine sodium collection.

In a normal person and patient with extracellular fluid (ECF) expansion, there is a linear relationship between ECF expansion and natriuresis when receiving furosemide; this means that the patient will have higher natriuresis and urine output if ECF volume expands as compared to a person with normal ECF volume. As furosemide use becomes chronic in a patient, ECF volume shrinks, and the level of natriuresis also goes down. At that point, the amount of natriuresis equals sodium intake; this is called the "breaking phenomenon." This phenomenon is adaptive when it occurs at low ECF volume. But in chronic heart failure patients with persistent ECF volume expansion, this phenomenon is maladaptive. Natriuresis is lower even when ECF volume becomes expanded. The reason for these maladaptive changes is remodeling in the distal nephron. There are hypertrophy and hyperplasia of distal segments of the nephron. These results from increased salt delivery, increased aldosterone, angiotensin II, and a change in potassium concentration; as a result of distal segment hypertrophy, sodium transport capacity increases which rivals furosemide's sodium absorption inhibiting capacity at the level of the thick ascending loop of henley. Clinicians can overcome this phenomenon by adding thiazide diuretics which block sodium absorption in distal segments of the nephron.[14][15]

Use in Specific Population

Patients with Hepatic Impairment: In patients with hepatic cirrhosis and ascites, furosemide therapy should be initiated in the hospital. In hepatic coma and states of electrolyte depletion, therapy should not be started until the underlying condition is improved. Sudden fluid and electrolyte balance alterations in patients with cirrhosis may precipitate hepatic encephalopathy; therefore, stringent observation is necessary during diuresis.

Patients with Renal Impairment: GFR ≤30 mL/min; increased doses are required to achieve desired diuretic response. If increasing azotemia and oliguria occur during severe progressive renal disease treatment, furosemide should be discontinued.

Pregnancy Considerations: Furosemide was a pregnancy category C drug under the old FDA categories, and clinicians should use caution in pregnant women after discussion with the patient about risks and benefits.[16] Furosemide is known to cross the placenta, and animal reproduction studies have shown adverse events. Although pregnant women with heart failure have had treatment with furosemide, a risk and benefits discussion should occur with the pregnant patient, and caution is necessary with the decision to take furosemide during pregnancy; fetal growth will require close monitoring.[17][18]

Breastfeeding Considerations: Because little information is available on using furosemide during breastfeeding and because intense diuresis might decrease lactation, an alternate drug may be preferred, especially while nursing a newborn or preterm infant. Low doses of furosemide may not suppress lactation.[19]

Adverse Effects

Adverse reactions are categorized below by the system organ classification system(soc) and listed by decreasing severity. The following are potential adverse effects associated with furosemide use[10][20]:

Gastrointestinal System

Hepatic encephalopathy in patients with cirrhosis[21]
Pancreatitis
Jaundice (intrahepatic cholestatic jaundice)
Increased liver enzymes
Anorexia
Oral and gastric irritation
Cramping
Diarrhea
Constipation
Nausea
Vomiting

Systemic Hypersensitivity Reactions

Severe anaphylactic or anaphylactoid reactions (e.g., with shock)
Systemic vasculitis
Interstitial nephritis
Necrotizing angiitis

Central Nervous System:

Paresthesias
Vertigo
Dizziness
Headache
Blurred vision
Xanthopsia

Hematologic Reactions

Aplastic anemia
Thrombocytopenia
Agranulocytosis
Hemolytic anemia
Leukopenia
Anemia
Eosinophilia

Dermatologic-hypersensitivity Reactions

Toxic epidermal necrolysis
Stevens-johnson syndrome
Erythema multiforme
Drug rash with eosinophilia and systemic symptoms
Acute generalized exanthematous pustulosis
Exfoliative dermatitis
Bullous pemphigoid
Purpura
Photosensitivity
Rash
Pruritus
Urticaria

Cardiovascular System

Alcohol, barbiturates, or narcotics may aggravate orthostatic hypotension.
Increase in cholesterol and triglyceride serum levels

Renal Disorders

Acute kidney injury due to fluid loss[23]

Metabolic Disorders

Hyperglycemia
Hyperuricemia
Hypokalemia
Hypomagnesemia[24]

Contraindications

Contraindications to furosemide use include patients with documented allergies to furosemide and patients with anuria.

A boxed warning suggests the cautious use of furosemide as it is a potent diuretic, which can predispose to excessive loss of water and electrolytes, resulting in dehydration with electrolyte depletion.

According to Beers Criteria, caution is necessary when administering diuretics to patients 65 years and older to avoid potential adverse effects of inducing hyponatremia by causing or exacerbating syndrome of inappropriate antidiuretic hormone secretion (SIADH); therefore, close monitoring of serum sodium is advisable at initiation or during the dose adjustment in older adults.[25]

Ototoxicity can occur with the use of furosemide, but the following conditions predispose patients to a higher risk of reversible or irreversible hearing impairment[26]:
- Use of a higher than the recommended dose of furosemide or a fast infusion rate of the drug,
- Hypoalbuminemia comorbid illnesses
- The concomitant use of ethacrynic acid, aminoglycosides, or other ototoxic drugs
- Patients with underlying severe renal impairment

Caution is also necessary for patients with underlying liver disease, especially those with decompensated liver disease, as rapid electrolytes imbalance secondary to furosemide use can precipitate hepatic encephalopathy and hepatic coma. In patients with hepatic coma, the prescriber should delay giving furosemide until there is an improvement in the patient's mental status.[5]

Patients with the advanced renal disease with fluid overload should be closely monitored for oliguria, azotemia, and volume status. If either oliguria or azotemia develops, furosemide should be discontinued to prevent kidney injury.

In patients with primary adrenal insufficiency with hypertension, diuretics are a practice clinicians should avoid to treat hypertension. Alternatively, the dosage of glucocorticoid/mineralocorticoid requires adjustment, and, if needed, the Clinician should prefer other classes of antihypertensive agents over diuretics to treat hypertension.[27]

High-risk patients for radiocontrast-induced nephropathy are more predisposed to having a worsened kidney function if furosemide is given before contrast administration than high-risk patients receiving gentle hydration before contrast exposure.

Patients with a known history of urinary retention due to, for example, benign prostatic hyperplasia, neurogenic bladder with bladder evacuation abnormalities, or urethral and ureteral strictures should be observed closely during the initial days of furosemide treatment. After that, they require observation for worsening symptoms as excessive diuresis and urine retention can lead to acute urinary retention leading to acute kidney injury.

The risk of hypokalemia increases with a high dose of furosemide, decreased oral potassium intake in patients with hyperaldosteronism states (liver abnormalities or licorice ingestion), or concomitant use of corticosteroid, ACTH, and laxatives.

Furosemide at high doses, i.e., more than 80 mg per day, inhibits thyroid hormone binding to thyroid binding protein leading to a transient increase in free thyroid hormones that subsequently causes a mild decrease in total thyroid hormone.[28]

Monitoring

Fluid status, BUN and creatinine to prevent oliguria and azotemia
Obtain potassium before and during rapid diuresis
Observe for signs of ototoxicity at the higher dose
Clinicians should check the chart for fluid intake and output.
NT-proBNP
Vitals: Orthostatic hypotension[29]

Toxicity

Toxicity with furosemide manifests as extensions of its diuretic activity. The main signs and symptoms of overdose with furosemide are blood volume reduction, dehydration, electrolyte imbalance, hypotension, hypochloremic alkalosis, and hypokalemia.[10]

Treatment of overdosage is supportive, and it consists of replacing excessive fluid and electrolyte losses. Clinicians should frequently determine serum electrolytes, arterial blood gas analysis, and blood pressure. In addition, providers must assure adequate drainage in patients with urinary bladder outlet obstruction (such as prostatic hypertrophy). Hemodialysis does not accelerate furosemide elimination.

Enhancing Healthcare Team Outcomes

American Heart Association (AHA) estimated that there were 6.2 million people with HF in the United States between 2013 and 2016.[30] Managing patients with hypervolemia requires an interprofessional healthcare team depending upon the healthcare setting, outpatient vs. inpatient care. For symptomatic patients with hypervolemia secondary to any of the following conditions; heart failure, liver cirrhosis, or nephrotic syndrome/chronic kidney disease, patients usually need aggressive diuresis. Hospitalized patients requiring aggressive diuretics need care by an interprofessional team that includes a nurse, laboratory technologists, pharmacists, and clinicians, including advanced heart failure specialists.

Careful monitoring of the patient's clinical condition, daily weight, fluids intake, urine output, electrolytes, i.e., potassium and magnesium, kidney function monitoring with serum creatinine and serum blood urea nitrogen level is vital to monitor the response of furosemide. For example, if indicated for diuresis with furosemide, replete electrolytes lead to electrolyte depletion, and adjust the dose or even hold off on furosemide if laboratory work shows signs of kidney dysfunction. Similarly, patients who are on furosemide treatment in an ambulatory care setting need close monitoring to evaluate the response to treatment, intermittent electrolytes and kidney function monitoring to replete electrolytes and manage the dose of furosemide as indicated, and to assess for other adverse effects of the furosemide treatment and manage it accordingly.

While the clinician, NP, or PA will make the initial decision to treat with furosemide, the entire healthcare team must put forth an interprofessional effort to maintain therapy. Nursing will be on the front lines for inpatient or outpatient monitoring. They can also be the first to assess therapeutic effectiveness and watch for adverse drug reactions. Pharmacists should verify that dosing is appropriate, and to do so, they will need to have received renal and liver function testing results from the team. The pharmacist should also look for drug-drug interactions and alert the clinician or nurse if any are present. The pharmacy can also assist the clinician with therapy changes to address the braking phenomenon and ceiling effect. Clinicians can optimize furosemide therapy with a coordinated interprofessional team effort for positive patient results. [Level 5]

Review Questions

References

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James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, Lackland DT, LeFevre ML, MacKenzie TD, Ogedegbe O, Smith SC, Svetkey LP, Taler SJ, Townsend RR, Wright JT, Narva AS, Ortiz E. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014 Feb 05;311(5):507-20. [PubMed: 24352797]

Whelton PK, Carey RM, Aronow WS, Casey DE, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, Smith SC, Spencer CC, Stafford RS, Taler SJ, Thomas RJ, Williams KA, Williamson JD, Wright JT. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018 Jun;71(6):e13-e115. [PubMed: 29133356]

Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004 May;43(5 Suppl 1):S1-290. [PubMed: 15114537]

Runyon BA., AASLD. Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology. 2013 Apr;57(4):1651-3. [PubMed: 23463403]

Shankar SS, Brater DC. Loop diuretics: from the Na-K-2Cl transporter to clinical use. Am J Physiol Renal Physiol. 2003 Jan;284(1):F11-21. [PubMed: 12473535]

Hammarlund MM, Paalzow LK, Odlind B. Pharmacokinetics of furosemide in man after intravenous and oral administration. Application of moment analysis. Eur J Clin Pharmacol. 1984;26(2):197-207. [PubMed: 6723758]

Vasko MR, Cartwright DB, Knochel JP, Nixon JV, Brater DC. Furosemide absorption altered in decompensated congestive heart failure. Ann Intern Med. 1985 Mar;102(3):314-8. [PubMed: 3970471]

Haegeli L, Brunner-La Rocca HP, Wenk M, Pfisterer M, Drewe J, Krähenbühl S. Sublingual administration of furosemide: new application of an old drug. Br J Clin Pharmacol. 2007 Dec;64(6):804-9. [PMC free article: PMC2198789] [PubMed: 17875188]

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Brater DC. Diuretic therapy. N Engl J Med. 1998 Aug 06;339(6):387-95. [PubMed: 9691107]

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Vargo DL, Kramer WG, Black PK, Smith WB, Serpas T, Brater DC. Bioavailability, pharmacokinetics, and pharmacodynamics of torsemide and furosemide in patients with congestive heart failure. Clin Pharmacol Ther. 1995 Jun;57(6):601-9. [PubMed: 7781259]

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Ponto LL, Schoenwald RD. Furosemide (frusemide). A pharmacokinetic/pharmacodynamic review (Part I). Clin Pharmacokinet. 1990 May;18(5):381-408. [PubMed: 2185908]

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Brater DC, Chennavasin P, Day B, Burdette A, Anderson S. Bumetanide and furosemide. Clin Pharmacol Ther. 1983 Aug;34(2):207-13. [PubMed: 6872415]

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Ellison DH, Felker GM. Diuretic Treatment in Heart Failure. N Engl J Med. 2017 Nov 16;377(20):1964-1975. [PMC free article: PMC5811193] [PubMed: 29141174]

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Huxel C, Raja A, Ollivierre-Lawrence MD. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 25, 2021. Loop Diuretics. [PubMed: 31536262]

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Greenberg A. Diuretic complications. Am J Med Sci. 2000 Jan;319(1):10-24. [PubMed: 10653441]

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What to monitor after administering furosemide?

Monitor daily weight, intake and output ratios, amount and location of edema, lung sounds, skin turgor, and mucous membranes. Notify health care professional if thirst, dry mouth, lethargy, weakness, hypotension, or oliguria occurs. Monitor BP and pulse before and during administration.

What should you check before giving diuretics?

Lab Test Considerations: Monitor electrolytes (especially potassium), blood glucose, BUN, and serum uric acid levels before and periodically throughout course of therapy.

What is a common side effect of diuretics?

Diuretics are generally safe. Side effects include increased urination and sodium loss. Diuretics can also affect blood potassium levels. If you take a thiazide diuretic, your potassium level can drop too low (hypokalemia), which can cause life-threatening problems with your heartbeat.

Which of the following is an effect of a diuretic?

Diuretics bring down blood pressure because they help your blood vessels get wider. Also, there's a smaller amount of fluid in your blood to pump. Diuretics also help your body clear out extra fluids.