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AccessPharmacy Quick Test
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Quick Test posted on 1.31.11:
| Treatment Selection in Open-Angle Glaucoma
| All patients with elevated IOP and characteristic optic disk changes and/or visual field defects not caused by other factors (i.e., glaucoma by definition) should be treated. Recent findings that 1 in 5 patients with "normal" IOP and glaucomatous retinal nerve findings (i.e., normal-tension glaucoma) do not have progression of visual field loss if left untreated have prompted recommendations to monitor normal-tension glaucoma patients without immediate threat of loss of central vision, and treat only when progression is documented. Some controversy exists as to whether the initial therapy of glaucoma should be surgical trabeculectomy (filtering procedure), argon laser trabeculectomy, or medical therapy. Presently, drug therapy remains the most common initial treatment modality.
Drug therapy of patients with documented glaucomatous change with either elevated or normal IOP is initiated in a stepwise manner (Fig. 97-5), starting with lower concentrations of a single, well-tolerated topical agent. The goal of therapy is to prevent further visual loss. A "target" IOP is chosen based on a patient baseline IOP and the amount of existing visual field loss. Typically, an initial target IOP reduction of 30% is desired. Greater reductions may be desired in patients with very high baseline IOPs or advanced visual field loss. Patients with normal baseline IOPs (normal-tension glaucoma) may have target IOPs of less than 10 to 12 mm Hg.
|  | | Figure 97-5. Algorithm for the pharmacotherapy of open-angle glaucoma.a Fourth-line agents not commonly used any longer.b Most clinicians believe laser procedure should be performed earlier (e.g., after three-drug maximum, poorly adherent patient). (CAI, carbonic anhydrase inhibitor.) |
| Sidebar: Clinical Controversy
How much should the IOP be reduced in patients who may have POAG? Although the major clinical trial (OHTS) required a 20% reduction in IOP for patients with ocular hypertension, many clinicians believe a further lowering of IOP may be more beneficial in preventing the progression of ocular hypertension to glaucoma. The American Academy of Ophthalmology Preferred Practice Guidelines suggest 20% to 30% IOP lowering. It remains to be seen if a more aggressive approach earlier in the treatment of the POAG suspect would be more beneficial.
| Pharmacotherapeutic Approach
Medications most commonly used to treat glaucoma are the nonselective β-blockers, the prostaglandin analogs (latanoprost, travoprost, and bimatoprost), brimonidine (an α2-agonist), and the fixed combination product of timolol and dorzolamide.
Before 1996, a β-blocker was used provided no contraindications existed, because this class of drugs has a long history of successful use, providing a combination of clinical efficacy and tolerability. The newer agents, in particular the prostaglandin analogs, brimonidine, and topical CAIs, are also considered suitable first-line therapy or alternative initial therapy in patients with contraindications to or other concerns with β-blockers (see Fig. 97-5). Pilocarpine and dipivefrin are used as third-line therapies because of their increased frequency of adverse effects or reduced efficacy.
Therapy optimally is started as a single agent in one eye (except in patients with very high IOP or advanced visual field loss) to evaluate drug efficacy and tolerance. Monitoring of therapy should be individualized: Initial response to therapy is typically done 4 to 6 weeks after the medication is started. A monocular trial of medication is recommended when possible. Once IOPs reach acceptable levels, the IOP is monitored every 3 to 4 months (more frequently after any change in drug therapy).
Visual fields and disk changes are typically monitored annually or earlier if the glaucoma is unstable or there is suspicion of disease worsening. Patients should always be questioned regarding adherence to and tolerance of prescribed therapy. Initial IOP response does not predict long-term IOP control. Using more than one drop per dose does not improve response, but increases the likelihood of adverse effects and the cost of therapy. When using more than one medication, separation of drop instillation of each agent by at least 5 to 10 minutes is suggested to provide optimal ocular contact for each agent.
The value of an agent with which the patient has shown a drop in IOP following an initial response can be measured by discontinuing the medication completely and determining if an increase in IOP occurs. Patients responding to but intolerant of initial therapy may be switched to another drug or to an alternative dosage form of the same medication. For patients failing to respond to the highest tolerated concentrations of an initial drug, a switch to an alternative agent after 1 day of concurrent therapy should be considered. Alternatively, if only a partial response occurs, addition of another topical drug to be used in combination is a possibility. A number of drugs or drug combinations may need to be tried before an effective and well-tolerated regimen is identified. Because of the frequency of adverse effects, carbachol, topical cholinesterase inhibitors, and oral CAIs are considered last-line agents to be used in patients who fail less-toxic combination topical therapy.
|  | Treatment: Hypokalemia
Desired Outcome
The goals of hypokalemia management are to prevent the development of and to treat if present serious life-threatening complications, to normalize the serum potassium concentration, to identify and correct the underlying cause of hypokalemia, and to prevent overcorrection of the serum potassium concentration.
| General Approach to Therapy
The general approach to therapy depends on the degree and rapidity with which hypokalemia developed and the presence of symptoms. Serum potassium concentrations between 3.5 and 4 mEq/L are a sign of early potassium depletion. No pharmacologic therapy is recommended at this point; however, these patients should be encouraged to increase their dietary intake of potassium-rich foods. When the serum potassium concentration is between 3 and 3.5 mEq/L, it is debatable whether pharmacologic therapy should be initiated. Oral potassium supplementation should be initiated in patients with underlying cardiac conditions that predispose them to cardiac arrhythmias. This includes patients receiving concomitant digoxin therapy. Patients with serum potassium concentrations below 3 mEq/L should always be treated to achieve values between 4 and 4.5 mEq/L. In asymptomatic patients, oral therapy is the preferred route of administration. Intravenous potassium can be necessary in symptomatic patients with severe depletion, or in patients who are intolerant to oral supplementation. In patients with concomitant moderate to severe hypomagnesemia, the magnesium deficit should be corrected before potassium supplementation, to prevent refractory hypokalemia.
| Nonpharmacologic Therapy
Various nonpharmacologic therapies have been used to prevent and treat hypokalemia. The best and most abundant source of potassium supplementation comes from dietary sources, in particular, fresh fruits and vegetables, fruit juices, and meats. Table 54-2 lists foods that are excellent sources of potassium. Salt substitutes that contain potassium chloride are another effective, inexpensive source of potassium. Increased dietary intake of foods with high potassium content is not recommended long-term for many patients because it can add unwanted calories to the patient's diet. Moreover, dietary potassium is almost entirely coupled with phosphate, rather than chloride, so it is not as effective in correcting potassium loss associated with hypochloremic conditions such as vomiting, nasogastric suctioning, and diuretic therapy.
| | Table 54-2 Foods That Are High in Potassium | | Highest content (>1,000 mg/100 g) | | Dried figs | | Molasses | | Very high content (>500 mg/100 g) | | Dried fruits (dates, prunes) | | Nuts | | Avocados | | Bran cereals | | Lima beans | | High content (>250 mg/100 g) | | Vegetables | | Spinach | | Tomatoes | | Broccoli | | Squash | | Beets | | Cauliflower | | Carrots | | Potatoes | | Fruits | | Bananas | | Cantaloupe | | Kiwi | | Oranges | | Mangos | | Meats | | Ground beef | | Steak | | Pork | | Lamb | | Veal |
| Pharmacologic Therapy
Guidelines for potassium supplementation were last published by the National Council on Potassium in Clinical Practice in 2000 (Table 54–3). These guidelines provide a comprehensive framework for potassium prophylaxis and replacement in many distinct patient populations. When deciding on appropriate pharmacotherapy to replete potassium, five factors must be considered: (1) the patient's normal baseline potassium concentration; (2) underlying medical conditions that can affect potassium balance; (3) concomitant medications that can affect potassium balance; (4) the patient's dietary and salt intake; and (5) the patient's ability to comply with the therapeutic regimen.
| | Table 54-3 General Consensus Guidelines for Potassium Replacement | | Guideline | Comment | | Potassium replacement therapy should accompany dietary consumption of potassium-rich foods. | Potassium-rich foods often cannot completely replace potassium associated with chloride losses (vomiting, diuretics, or nasogastric suction) because it is almost entirely coupled to phosphate. Furthermore, increasing dietary intake of these foods can lead to unwanted weight gain. | | Potassium replacement is recommended for patients who are sodium sensitive, and hypertensive patients. | A high-sodium diet often results in excessive urinary potassium excretion. | | Potassium replacement is recommended in patients who are subject to vomiting, diarrhea, or diuretic/laxative abuse. | These conditions promote excessive renal and GI potassium loss. | | Potassium supplementation is best administered orally in divided doses over several days to achieve full repletion. | | | Laboratory measurement of serum potassium is convenient but not always accurate. | Clinicians should be aware of the factors that result in transcellular potassium shifts. Monitoring 24-hour urinary potassium excretion can be necessary in high-risk patients. | | Patient adherence to potassium replacement can be increased with compliance-enhancing regimens. | Microencapsulated products have no bitter smell or aftertaste and have much better GI tolerance. Regimens should be made as simple as possible to follow. | | A potassium dosage of 20 mEq/day is usually sufficient to prevent hypokalemia from occurring. Doses of 40-100 mEq are usually sufficient to treat hypokalemia. | |
| A general rule for potassium replacement is that for every 1-mEq/L decrease of potassium below 3.5 mEq/L, there is a corresponding total body potassium deficit of 100 to 400 mEq. Because of the wide variance in projected deficits, each patient's therapy must be individualized and adjustments made on the basis of the patients signs, symptoms, and frequent measurements of serum potassium. In patients receiving chronic loop or thiazide diuretic therapy, 40 to 100 mEq of potassium can correct mild to moderate potassium deficits. Doses up to 120 mEq can be required in more severe deficiencies. When providing oral potassium supplementation, the total daily dose should be divided into three to four doses to minimize the developement of GI side effects. Patients receiving diuretics can become chronically hypokalemic and can benefit from combination potassium-sparing diuretic therapy.
| Sidebar: Clinical Controversy
The replacement of potassium intravenously can be accomplished by IV piggyback or Buretrol administration. A pharmacist usually prepares the potassium IV piggyback, double checks the concentration and fluid, and then dispenses the final product to the medical unit. However, with Buretrol administration, essentially any clinician (e.g., nurse or physician) can prepare the solution on the medical unit, and infuse the potassium solution into the patient. The Joint Commission and the United States Pharmacopeia 797 Standards now advocate that all parenteral products be compounded in a sterile, laminar flow environment, and be double-checked by a pharmacist to assure patient safety. Many hospitals to date have not adapted these recommendations, which were developed to improve patient safety.
Whenever possible, potassium supplementation should be administered by mouth. Three salts are available for oral potassium supplementation: chloride, phosphate, and bicarbonate. Potassium phosphate should be used when patients are both hypokalemic and hypophosphatemic; potassium bicarbonate is most commonly used when potassium depletion occurs in the setting of metabolic acidosis. Potassium chloride, however, is the primary salt form used because it is the most effective treatment for the most common causes of potassium depletion (i.e., diuretic-induced and diarrhea-induced) as these conditions are associated with potassium and chloride losses.
Potassium chloride can be administered in either tablet or liquid formulations (Table 54-4). The liquid forms are generally less expensive; however, patient compliance can be low because of their strong, unpleasant taste. Two sustained-release solid dosage forms are currently available in the United States: a wax-matrix formulation, and a microencapsulated formulation. The microencapsulated tablet is generally preferred because it disintegrates better in the stomach and is associated with less GI irritation. | | Table 54-4 Differentiation of Available Potassium Supplements | | Supplement | Comment | | Controlled-release microencapsulated tablet | Disintegrates better in GI tract; fewer GI erosions as compared to wax-matrix tablets | | Encapsulated controlled-release microencapsulated particles | Fewer erosions as compared to wax-matrix tablets | | Potassium chloride elixir | Inexpensive, poor taste, poor compliance, immediate effect | | Potassium chloride effervescent tablets for solution | More expensive than elixir, convenient | | Wax-matrix extended-release tablets | Easier to swallow; more GI erosions as compared to other therapies |
| Intravenous potassium use should be limited to: (1) severe cases of hypokalemia (serum concentration <2.5 mEq/L); (2) patients exhibiting signs and symptoms of hypokalemia such as ECG changes or muscle spasms; or (3) patients unable to tolerate oral therapy. Intravenous supplementation is more dangerous than oral therapy because it is more likely to result in hyperkalemia, phlebitis, and pain at the site of infusion.
The vehicle in which IV potassium is administered is important. Whenever possible, potassium should be prepared in salinecontaining solutions (e.g., 0.9% or 0.45% sodium chloride [NaCl]). Dextrose-containing solutions stimulate insulin secretion, which can cause intracellular shifting of potassium worsening the patient's hypokalemia, and should be avoided whenever possible. Generally, 10 to 20 mEq of potassium is diluted in 100 mL 0.9% NaCl for intravenous administration. These concentrations are safe when administered through a peripheral vein over 1 hour. When infusion rates exceed 10 mEq/h, ECG monitoring should be performed to detect cardiac changes. The serum potassium concentration should be evaluated following the infusion of each 30 to 40 mEq, to direct further potassium replacement requirements. Multiple doses of potassium can be repeated as needed until the serum potassium concentration normalizes. To allow adequate time for the potassium to equilibrate between the intra- and extracellular spaces, the clinician should wait at least 30 minutes from the end of each infusion before obtaining a serum concentration. Care should be taken to avoid sampling from the same line in which the potassium was infused, as this can result in a spuriously high potassium concentration.
In cases of severe potassium depletion, patients can require as much as 300 to 400 mEq/day. In this instance, it is common practice to dilute 40 to 60 mEq in 1,000 mL 0.45% NaCl and infuse at a rate not exceeding 40 mEq/h. When possible, this should be performed in an intensive care unit under continuous ECG monitoring. Because of the high potassium concentration, and the risk for burning pain and peripheral venous sclerosis, the infusion should be through a central intravenous line into a large vein (e.g., superior vena cava). Given the volume required to infuse this dose of potassium, this infusion strategy might be impractical in certain clinical situations (e.g., patients requiring fluid restriction). A reasonable alternative is to split the potassium dose between the oral and intravenous routes. For example, if a symptomatic patient requires 120 mEq of potassium, the clinician can give 60 mEq as the immediate-release potassium liquid, and the other 60 mEq can be given via the intravenous route (20 mEq/100 mL/h in three doses). When giving large potassium doses, serum monitoring should be performed following the administration of half the dose to guide the clinician as to the need for additional potassium. This can also help avoid the development of hyperkalemia.
| Alternative Therapies
Potassium-sparing diuretics are an alternative to chronic exogenous potassium supplementation, especially when patients are concomitantly receiving drugs that are known to deplete potassium (e.g., diuretics or amphotericin B). Spironolactone inhibits the effect of aldosterone in the distal convoluted tubule, thereby decreasing potassium elimination in the urine. Spironolactone is especially effective as a potassium-sparing agent in patients with primary or secondary hyperaldosteronism. Amiloride and triamterene act by an aldosterone-independent mechanism; however, the precise mechanism of their potassium sparing is unknown.
Spironolactone is available as 25-mg, 50-mg, and 100-mg tablets. The usual starting dose is 25 to 50 mg daily, and can be titrated to a maximum dose of 400 mg/day. The potassium-retaining effects generally take approximately 48 hours to occur. Important side effects include hyperkalemia, gynecomastia, breast tenderness, and impotence in men.
Triamterene is available as 50-mg and 100-mg capsules. The usual starting dose is 50 mg twice daily, which can be titrated to 100 mg twice daily. Triamterene 50 mg is available as a combination product with hydrochlorothiazide 25 mg and is commonly used for the treatment of hypertension. Common side effects include hyperkalemia, sodium depletion, and metabolic acidosis.
Amiloride is available as a 5-mg tablet. The usual starting dose is 5 mg daily; however, 10 mg can be given in those with severe hypokalemia. This is also available as a combination product with hydrochlorothiazide 50 mg. The most common side effects are hyperkalemia and metabolic acidosis.
Generally, concomitant use of potassium supplementation with potassium-sparing diuretics is not necessary. There is a significant risk of hyperkalemia during combination therapy, especially in patients with underlying renal insufficiency or diabetes mellitus.
To date, there have been no pharmacoeconomic evaluations of the different pharmacotherapeutic alternatives to manage hypokalemia. The most economical source of chronic potassium supplementation is to increase the amount in the diet. Thus patients receiving diuretic therapy should be instructed to increase their dietary intake of potassium-rich foods. By doing so, they can often avert the need for exogenous potassium therapy.
| Evaluation of Therapeutic Outcomes
Serum potassium concentrations should be monitored regularly while the patient is receiving potassium supplementation. For patients receiving prophylactic potassium supplementation during diuretic therapy, the serum potassium and magnesium concentrations, as well as renal function should be monitored every 1 to 2 months in stable patients. In hospitalized patients receiving oral therapy for mild hypokalemia, the potassium concentration should be monitored every 2 to 3 days. Generally, the potassium concentration begins to increase within 72 hours. If it does not increase by at least 1 mEq/L within 96 hours, the clinician should suspect concomitant magnesium depletion. If present, correcting the magnesium deficit generally results in normalization of potassium. Patients receiving IV potassium supplementation require close ECG monitoring if the infusion rate is greater than 20 mEq/h. Doses greater than this should be administered only in the presence of continuous ECG monitoring. Additionally, the patient should have potassium concentrations obtained halfway through, and 30 minutes following completion of the total potassium dose to guide further potassium dosing. Finally, the patient should be assessed for adverse effects such as burning pain at the infusion site or phlebitis.
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