FUROSEMIDE

​

Furosemide, a loop diuretic, is not directly involved in anesthesia but can play an important role in the perioperative period for specific patient populations and clinical scenarios. Its importance can be highlighted by the following factors:

​

1. Fluid management: In patients with congestive heart failure, chronic kidney disease, or hepatic cirrhosis, careful fluid management is crucial during the perioperative period. Furosemide can help in maintaining an appropriate fluid balance and preventing complications such as pulmonary edema or worsening of the underlying disease.

2. Prevention of acute kidney injury: In certain high-risk patients or procedures, furosemide can be used to promote urine output and maintain renal perfusion to prevent acute kidney injury. However, its use in this context should be carefully considered, as excessive diuresis may potentially worsen renal function.

3. Treatment of acute pulmonary edema: Although not a routine scenario in anesthesia, acute pulmonary edema may develop perioperatively in high-risk patients. Furosemide can help alleviate pulmonary edema by promoting diuresis and reducing preload, thereby improving oxygenation and respiratory function.

4. Treatment of hyperkalemia: In the perioperative setting, hyperkalemia may pose a significant risk to the patient, as it can cause life-threatening arrhythmias. Furosemide can be used as part of a combination therapy to promote renal potassium excretion and lower serum potassium levels.

5. Contrast-induced nephropathy: In patients undergoing procedures involving the administration of iodinated contrast agents, furosemide may be used to reduce the risk of contrast-induced nephropathy by promoting diuresis and maintaining renal perfusion.

​​

.Here are the main steps in furosemide's mechanism of action:

​

1. Entry into the tubular lumen: Furosemide is secreted into the tubular lumen by the organic anion transporter (OAT) in the proximal tubule cells of the nephron. This process allows the drug to reach its site of action in the thick ascending limb of the loop of Henle.

2. Inhibition of the Na-K-Cl cotransporter: Furosemide specifically binds to and inhibits the Na-K-Cl cotransporter (NKCC2) on the luminal side of the thick ascending limb cells. This cotransporter is responsible for the active reabsorption of sodium, potassium, and chloride ions from the tubular fluid back into the blood.

3. Disruption of ion transport: By inhibiting the Na-K-Cl cotransporter, furosemide disrupts the normal transport of ions across the thick ascending limb cells. This leads to a reduction in sodium, potassium, and chloride reabsorption, resulting in increased excretion of these ions in the urine.

4. Osmotic diuresis: The decreased reabsorption of sodium and chloride ions creates an osmotic gradient that prevents the passive reabsorption of water in the loop of Henle, the distal tubule, and the collecting ducts. This effect results in an increased urine volume and promotes diuresis.

5. Enhanced excretion of other ions: The increase in tubular flow rate and urine output leads to the enhanced excretion of other ions, such as calcium and magnesium, due to a decreased opportunity for their reabsorption along the nephron.

​

​

                                                                                         Key points about Furosemide

​

• Loop diuretic that inhibits reabsorption of sodium, potassium, and chloride by impairing activity of the Na+ K+ 2 CL transport protein in the medullary portions of the thick ascending limb of the loop of Henle.

 

• It has a rapid onset, producing diuresis within 5 to 10 minutes of administration, with a peak effect at 30 minutes and duration of action of 2 to 6 hours.

 

• In patients with normal renal function, 40 mg of IV furosemide will produce maximal natriuresis.

 

• Hypokalemic metabolic alkalosis is one of the most common complications of chronic furosemide administration.

 

​​

 

​​

​

​

​

​

​

​

​

​

​

​

​

​

​

​

​

​

​

 

​​

​​