Furosemide Use in Medical Care - Essay Example

? Furosemide Use in Medical Care Introduction Furosemide is a potent loop diuretic benzoic acid. It primarily blocks sodium and chloride re-absorption in the loop of Henle. It helps minimize the risk of alkalosis, treat oedema in hepatic cirrhosis, and congestive heart failure. It helps reduce the fluid volume in the body to control heart disease, kidney and liver, and terminal illnesses (Tripathi, 2003). It can be aerosolized and used to reduce breathing difficulties in patients with lung cancer. In most cases, these aerosols are used for first aid in these patients (Physician’s desk reference, 1999). Furosemide has little side effects on users and health care providers as shown in various studies. Literature Review Furosemide is used for treating hypertension, renal diseases, and heart failure (Jacobson, Kokko and, Annu, 1976, Solanski, 2011). By conserving potassium, (Solanski, 2011) it minimizes the risk of alkalosis (Singh et al, 1992). It controls body fluids to reduce the symptoms of terminal diseases (Physicians desk, 1999, Rayyan and Allegaert, 2007). Intravenous furosemide is used in neonates after ECMO treatment (Vorst, 2007, Wernovsky et al. 1995). In a research by (Vorst, 2007) the patients have a high fluid accumulation in the body, and they require induced excretion (Martin and Danziger, 1994). Continuous administration of the drug stimulates the renal section of the kidney to excrete more urine (Vorst, 2007, Rayyan and Allegaert, 2007, Schoemaker et al, 2002). Furosemide can also protect individuals from noise induced hearing loss (de Jong et al 2012, Hirose and Sato, 2011). Administration of furosemide before exposure to noise can reduce hearing loss (Adelaman et al, 2008, Henderson et al, 2006). It suppresses the cochlear amplifier (Kopke et al., 2000) during exposure to protect the individual (Hirose and Sato, 2011). This drug can also induce reversible deafness to protect the individual (Henderson et al, 2006, Fraenkel et al, 2001). Aerosolized furosemide is also used in treatment of dyspnea (Bianco et al, 2000, Shimoyama, 2002). Patients have breath loss (Stein, 1995) and furosemide is administered to relieve them, and restore normal breathing (Campell, 1965). It stimulates the air sacs to hold more air, and the patient gets a better supply of oxygen in the blood (Chandler, 1999, Moosavi et al, 2007, Bruera, Schmitz et al, 2000). Search Methods The search process involved formulating questions using the PICO framework. The problem at hand was a critical appraisal for furosemide. This involved determining the importance of furosemide in medical practice. The intervention would be searching for medical journals from CINAHL, which outline the various uses of furosemide. This drug has several uses, and the search was narrowed down to fast life saving uses. These are uses that yield required results within a short time. This was the main alternative for the search process. The search question was; what is the importance of furosemide in medical practice? The outcome was journal articles outlining the use of furosemide to treat dyspnea and neonates after ECMO. Critical appraisal 1: From Kallet, H. R. 2007. Dyspnea is experienced in patients suffering from terminal diseases such as metastatic cancer, pulmonary fibrosis, congestive heart failure, and other neurological conditions. About 33% to 47% of cancer patients experience dyspnea (Dudgeon et al, 2001 and Hayes, Philip, and Spruyt, 2006). This percentage increases to 55-70% in terminal stages (Reuben, Mor, 1986). In patients with primary lung cancer, dyspnea increases in frequency and intensity, unlike pain which is well controlled (Bruera, Schmitz et al, 2000). This condition inhibits breathing and provokes psychological suffering. The patients gasp for breath due to terminal illness. Dyspnea treatment was carried out using opioids, but their use declined in the 1950s (Mercadante, Casuuccio, and Fulfaro, 2000). Breathlessness leads to an unpleasant urge to breath and a feeling of suffocation or breath holding (Stein, 1995). This condition results from multiple sensory inputs in the brain, which evoke action to the breathing muscles and corollary discharge (Peters and Donnel, 2006). The intensity of distress caused by dyspnea is individualized, and there is little resemblance between breathing difficulties experienced by patients (Chandler, 1999). Different signals from the brain cause the muscles and tendons in the airways to evoke different information. This information contains both the degree and velocity of displacement in the lungs and chest walls. A combination of discharge and displacement leads to breathing impairments. When tension in the ventilator muscles is excess due to the shortening of muscle fibers and stretching of lung tissues, dyspnea is evoked (Campell,1965). Muscle weakness and fatigue can also cause dyspnea. Elevated carbon dioxide can trigger other stimuli and cause dyspnea (Banzett et al, 1989). Aerosolized furosemide is used to treat dyspnea. Its effectiveness was first observed in a patient suffering from end-stage Kaposi’s sarcoma (Stone, Kurowska and Tookman, 1994). Recent studies have explored the potential of furosemide to treat or reduce dyspnea in patients with terminal cancer (Shimoyama, 2002). Three patients were reported by Shimoyama (Shimoyama 2002) with dyspnea. The patients had shown resistance to treatment involving parenteral morphine sulfate, and they received treatment using 20 mg of aerosolized furosemide. Within 20-30 minutes, dyspnea effect and the respiratory rate had reduced. This improvement lasted for more than four hours. In some of the patients, the respiratory rate and use of accessory muscles diminished. According to Kohara et al (2003), dyspnea can be effectively reduced in 12 out of 15 patients who receive 20 mg of the aerosol. However, some patients show no response to the drug since there is no change on arterial blood gases, heart rate, or respiratory rate. In another study, there was insignificant worsening in patients with cancer who received aerosolized furosemide. Aerosolized furosemide prevents bronchospasm (Bianco et al, 2000). Its bronchodilatory effect helps ameliorate dyspnea (Ono et al, 1997). Administering 40 mg of aerosolized furosemide increases the breath-holding time for patients with hypercapnia and reduces dyspnea. It suppresses pulmonary C-fibers in the bronchial epithelium, reducing breathing difficulties. Inhaling the drug reduces cough and bronchospasm when the patient is exposed to low chloride solutions. The ionic changes in the environment are circumvented by furosemide, which prevents irritant receptors from being stimulated (Moosavi et al, 2007). Inhaling furosemide stimulates pulmonary stretch receptors (Kim, Stolar, 2000). Deep lung inflation is enabled by the stimulation, which reduces the effect of breathlessness. Large tidal volumes of air are caused in the lungs, and the patient receives enough supply of air (Ventresca et al, 1990). Aerosolized furosemide inhibits the mechanisms of cellular ionic transport increasing the concentration of sodium. This stimulates the pulmonary stretch receptors (Nishino et al, 2000). In most of the performed studies, the researchers have not observed renal effects caused by aerosolized furosemide (Shimoyama, 2002). This makes the drug safe for use by medical practitioners. Cases of brisk dieresis have however been reported in patients. The effects of inhaled furosemide can only emanate from reduced pulmonary edema. This reduces the respiratory stimulation of the J-receptors. Other effects of furosemide effects observed in patients include nausea, sleeplessness, cough, frequent urination, and substernal irritation. Inhaling this drug has minimal effects on health care practitioners. Medical staff and paramedics are exposed to the aerosol fumes, but studies have not reported any significant addiction to the chemicals. Medics can develop chemical dependencies when exposed to these chemicals. Exposure to these substances and job stress increase the risks for health care providers. Exhalation from patients caused secondary exposure, but it has minimum effects on the medical staff. Critical Appraisal 2: From Vorst, M. V, Hartigh, J. D., Wildschut, E., Tibboel, D., and Burggraaf, J. 2007. Intravenous furosemide is effectively adaptable for controlling urine output in neonates treated with extracorporeal membrane oxygenation. In this study, seven neonates received continuous intravenous furosemide, which was adjusted according to the target urine production. ECMO is used to treat several cardio-respiratory problems in neonates. These include pulmonary hypertension, pneumonia, and meconium aspiration syndrome (Journois, 1998). The ECMO circuit triggers inflammatory reaction and is associated with capillary leakage syndrome (Singh et al,1992). This results to intravascular hypovolaemia and renal hypoperfusion. Loop diuretics are enhanced to mobilize fluid excess. Continuous administration of intravenous furosemide is necessary in such cases. Adequate urine production was achieved within 24 hours after the onset of furosemide administration (Rayyan and Allegaert, 2007). ECMO and CPB result fluid overload and models developed for treating infants after cardiac surgery are applicable to neonates after ECMO treatment. The main aim of this study was to achieve a urine output of 6 ml/kg per hour. This was to be achieved without the neonates developing toxicity due to the drug. Neonates who have undergone ECMO treatment can receive Furosemide infusion at a rate of 0.2 mg/kg per hour. The amount of drug administered depends on the required output, and the infusion rate can be increased or decreased depending on the urine production. In most cases, patients receive about 400 ml of ECMO treatment and furosemide can be administered for 72 hours. Continuous furosemide infusion is started after ECMO treatment followed by a loading bolus of 1 mg/kg per hour. The age determines the dosage administered, and a high dose can lead to excessive urine production. Urine production at the start of the infusion is usually low but increases as the infusion rate increases. The drug requires some time for full absorption to take place before high volumes of urine can be produced. Normal urine production is realized within seven hours from the onset of infusion. The cardiovascular aspects like blood pressure and heart rate are usually within the normal range when the infusion begins. The patients remain with cardiovascular stability during the infusion period, and the inotropic support can be decreased gradually during the observation period. Intravenous furosemide infusion has increasingly been used in patients after CPB surgery (Rayyan and Allegaert, 2007). It is increasingly used in neonates after EMCO treatment to reduce the amount of body fluids. In recent studies, continuous intravenous furosemide has been administered in about 78% of neonates after ECMO. This administration occurs in continuous or intermittent dosages. Adequate urine production is achieved within 24 hours of administration. The ECMO and CPB procedures are comparable; therefore the PK/PD model used in CPB is also applicable in ECMO (Wernovsky et al. 1995). Doses administered in ECMO treatment can be as low as 0.12 mg/kb per hour compared to doses of 0.2 and 0.3 mg/kg per hour required to produce 6 ml/kg per hour in CPB model. This indicates that relatively low doses of furosemide can be used to achieve the same results. Loading bolus required depends on the stimulated urine production profiles after the regimen administration. Within the first 24 hours, positive effects of loading bolus are observed as the target urine production is realized. Therefore, one loading bolus is sufficient to overwhelm the effects of the ECMO circuit (Schoemaker et al2002). The tender age of the neonates may lead to excess urine production. The renal functions are not fully developed, which causes excess production. In ECMO, renal functions of the patients remain normal while renal failure is reported in some patients after CPB. Furosemide is excreted in the renal section and becomes active in the tubular lumen. This prevents renal failure in the neonates. In CPB, renal clearance related to drug response causes the renal failure experienced (Wernovsky et al, 1995). This is the reason high doses are required in patients after CPB surgery. In infants, phase II reactions are better developed, therefore higher doses of furosemide are required. The effects of ECMO circuit are attributed to the decrease in doses required after loading bolus (Van et al, 2006). Neonates treated with ECMO have a better distribution of steady state volume and an elimination of half-life loop diuretic (Van et al, 2006). An addition of exogenous blood volume causes the large distribution volume. A 63-87% reduction in serum furosemide is observed within a 4 hour period in the ECMO circuit (Zuppa et al, 2004). The use of other drugs such as morphine has a decreased clearance in patients treated with ECMO, but furosemide clearance is not greatly affected (Martin and Danziger, 1994). The furosemide loading bolus compensates for the increased volume distribution. The effects of furosemide on renal functions are at a minimum, and the low doses required do not cause any impairment in the renal functions. Patients treated with ECMO have a higher renal clearance than those treated with CPB (Schoemaker et al, 2002). Loop diuretics are not observed in some patients after furosemide infusion. This means that furosemide therapy is highly effective in neonates after ECMO treatment. Serum furosemide levels remain below the accepted safety ototoxicity levels (Wells et al, 1992). This proves that furosemide infusion is a safe method for treating patients after ECMO. The fluid balance in the neonates is also contained within the acceptable range. A small variance in urine output may be observed during the infusion period, and the output can remain relatively low after furosemide administration in some patients. Infants also exhibit little variance in urine production after CPB surgery (Brater, Anderson and Brown, 1986). The neonates withstand the forced dieresis as indicated by the stable hemodynamic parameters. The only side effect of furosemide therapy is hypochloraemic metabolic alkalosis. The infusion therefore provided an effective means of dieresis without any cardiovascular instability. Conclusion Furosemide is an effective drug for relieving patients the discomfort caused by breathing difficulties. It stimulates the air sacs to hold more breath, and the chest muscle contraction is reduced. The stretching in lungs and chest muscles is reduced by inhaling the aerosol. The patients experience relieves within a short period, and the effect lasts for a long time. There are minimum side effects reported by such patients and medical workers. In the case of ECMA, small doses are required to help neonates excrete excess fluids from their bodies. The patients require treatment for 72 hours only before their bodies can stabilize. There are little side effects, which are not reported in all patients. 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Pharmacokinetics and pharmacodynamics of bumetanide in neonates treated with extracorporeal membrane oxygenation. J Pediatr, 121, PP.974-980. Zuppa, A. F., Nadkarni, V., Davis, L et al. 2004. The effect of a thyroid hormone infusion on vasopressor support in critically ill children with cessation of neurologic function. Crit Care Med, 32, PP. 2328-2322. Appendices Kallet, H. R.2007. The Role of Inhaled Opioids and Furosemide for the Treatment of Dyspnea. Respiratory care, 52, 900-908 PICO framework. Problem, Intervention, comparison, and outcome. Vorst, M. V, Hartigh, J. D., Wildschut, E., Tibboel, D., and Burggraaf, J. 2007. An explaratory study with an adaptive continuous intravenous furosemide regimen in neonates treated with extracorporeal membrane oxygenation. From http://www.ccforum.com/content/11/5/R111. Read More