Which should the nurse monitor a client for that is receiving a salicylate? select all that apply!

Most adverse reactions are caused by the drug's mineralocorticoid activity (retention of sodium and water) and include hypertension, edema, cardiac enlargement, congestive heart failure, potassium loss, and hypokalemic alkalosis.

When fludrocortisone is used in the small dosages recommended, the glucocorticoid side effects often seen with cortisone and its derivatives are not usually a problem; however the following untoward effects should be kept in mind, particularly when fludrocortisone is used over a prolonged period of time or in conjunction with cortisone or a similar glucocorticoid.

Musculoskeletal-muscle weakness, steroid myopathy, loss of muscle mass, osteoporosis, vertebral compression fractures, aseptic necrosis of femoral and humeral heads, pathologic fracture of long bones, and spontaneous fractures.

Gastrointestinal-peptic ulcer with possible perforation and hemorrhage, pancreatitis, abdominal distention, and ulcerative esophagitis.

Dermatologic-impaired wound healing, thin fragile skin, bruising, petechiae and ecchymoses, facial erythema, increased sweating, subcutaneous fat atrophy, purpura, striae, hyperpigmentation of the skin and nails, hirsutism, acneiform eruptions, and hives; reactions to skin tests may be suppressed.

Neurological-convulsions, increased intracranial pressure with papilledema (pseudotumor cerebri) usually after treatment, vertigo, headache, and severe mental disturbances.

Endocrine-menstrual irregularities; development of the cushingoid state; suppression of growth in children; secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress (e.g., trauma, surgery, or illness); decreased carbohydrate tolerance; manifestations of latent diabetes mellitus; and increased requirements for insulin or oral hypoglycemic agents in diabetics.

Ophthalmic-posterior subcapsular cataracts, increased intraocular pressure, glaucoma, and exophthalmos.

Metabolic-hyperglycemia, glycosuria, and negative nitrogen balance due to protein catabolism.

Allergic Reactions-allergic skin rash, maculopapular rash, and urticaria.

Other adverse reactions that may occur following the administration of a corticosteroid are necrotizing angiitis, thrombophlebitis, aggravation or masking of infections, insomnia, syncopal episodes, and anaphylactoid reactions.

Therapeutic objectives include cardiopulmonary stabilization, prevention of absorption, correction of fluid deficits, correction of acid-base abnormalities, and enhancement of excretion and elimination. Large-bore vascular access catheters may be required to facilitate emergent hemodialysis.

Endotracheal intubation may be required for the following reasons:

• Ventilatory support in patients with severe hypoxemia from aspirin-induced pulmonary edema

• Maintenance of hyperventilation (as compensation for metabolic acidosis) - Hyperventilate a patient with severe salicylate poisoning who has just been intubated (when acid-base status had been maintained previously by the patient's own hyperventilation) to prevent lethal acidemia

• It must be emphasized that patients with severe salicylate overdose should only be intubated and placed on a ventilator if really needed, because it may be very difficult to hyperventilate these patients enough on a ventilator to compensate for their metabolic acidosis. As noted above, if they really require intubation and mechanical ventilation, they must be hyperventilated and closely monitored, including frequent checking of their blood gases, or they may rapidly deteriorate. In a recent article by Dr. Daniel J. McCabe patients who were intubated had much better survival if they had hemodialysis performed early [26] . 

• Protection of patients who are too agitated and delirious for central line placement, hemodialysis, and other necessary medical procedures without therapeutic sedation

• Protection of the airway against aspiration during lavage or activated charcoal administration or in obtunded patients who cannot protect their own airway

As with all significant overdoses the airway, breathing, and circulation (ABC) should be evaluated and stabilized as necessary. Dehydration and concomitant electrolyte abnormalities must be immediately corrected.

Some authorities recommend performing gastric lavage in all symptomatic patients regardless of time of ingestion. Gastric lavage may be beneficial, unless contraindicated, up to 60 minutes after salicylate ingestion. Warmed (38°C) isotonic sodium chloride solution may be used. Protect the airway before gastric lavage.

Initial treatment should include the use of oral activated charcoal, especially if the patient presents within 1 hour of ingestion. Activated charcoal can limit further gut absorption by binding to the available salicylates. The recommended initial dose of activated charcoal is 1 g/kg of body weight to a maximum of 50 g in children and 1-2 g/kg to a maximum of 100 g in adults. The minimum dose is 30 g.

Use of cathartics is not routinely indicated with activated charcoal; however, many clinicians administer the first dose of activated charcoal with sorbitol. Sorbitol should not be used in young children. Repeat cathartic dosing generally should be avoided because of concern over resultant electrolyte imbalances.

Repeated doses of charcoal may enhance salicylate elimination and may shorten the serum half-life. [27] Although no convincing data support the administration of multi-dose activated charcoal, some experts strongly recommend this for patients with a very serious ingestion. Repeated doses of charcoal may remove salicylates from the circulation into the GI tract. Repeated doses of activated charcoal may assist in treating bezoars with ongoing absorption of salicylates, which should be suspected when salicylate levels continue to rise or fail to decrease, despite appropriate management. Repeated doses of activated charcoal have also been used to treat overdoses of enteric-coated or sustained-release aspirin; however, whole-bowel irrigation (WBI) with polyethylene glycol is probably more effective in this setting, as noted below.

The passage of stool with charcoal and the resolution of serious clinical manifestations may be the reasonable criteria for discontinuing multiple doses of activated charcoal.

WBI with polyethylene glycol was found to be more effective than single-dose activated charcoal in reducing salicylate absorption. The study was carried out in volunteer subjects 4 hours after they had ingested enteric-coated aspirin. [28] When enteric-coated aspirin has been ingested or when salicylate levels do not decrease despite treatment with charcoal, which may indicate that concretions are present, WBI should probably be used in addition to charcoal therapy. The American Academy of Clinical Toxicology advises that “WBI can be considered for potentially toxic ingestions of sustained-release or enteric-coated drugs, particularly for those patients presenting later than 2 h after drug ingestion when activated charcoal is less effective.” [29]

Provide treatment for correction of fluid deficits and enhancement of excretion and elimination. Administer lactated Ringer or isotonic sodium chloride solution for volume expansion at 10-20 mL/kg/h until a 1- to 1.5-mL/kg/h urine flow is established. Provide maintenance fluids to maintain urinary alkalization. Forced diuresis is not recommended. The greater the urine flow, the more difficult it is to alkalinize the urine. Be cautious of excessive fluid volumes in cases of salicylate-induced pulmonary edema.

Renal excretion of salicylic acid depends on urinary pH. Increasing the urine pH to 7.5 prevents reabsorption of salicylic acid from the urine. [30] Because acidosis facilitates transfer of salicylate into tissues, especially in the brain, it must be aggressively treated by raising blood pH higher than brain pH, thereby shifting the equilibrium from the tissues to the plasma.

Concomitant alkalization of blood and urine keeps salicylates away from brain tissue and in the blood, in addition to enhancing urinary excretion. When the urine pH increases to 8 from 5, renal clearance of salicylate increases 10-20 times. Raising the urinary pH level from 6.1 to 8.1 results in a more than 18-fold increase in renal clearance by preventing nonionic tubular back-diffusion, which decreases the half-life of salicylates from 20-24 hours to less than 8 hours. Because aspirin is a weak acid, it ionizes when exposed to a basic environment, such as alkaline urine. Ions are poorly reabsorbed in the tubules and are excreted more readily. This phenomenon is called ion trapping and also works well for overdoses of other weak acids, such as phenobarbital.

Most experts alkalinize the urine by giving an initial intravenous bolus of 1 mEq/kg of sodium bicarbonate and then start a sodium bicarbonate intravenous infusion. The continuous intravenous infusion is made by adding 3 ampules of sodium bicarbonate (each ampule containing 44 mEq of sodium bicarbonate) to a liter of D5W. The infusion is initially run at 2 times the maintenance rate and then titrated to keep the urinary pH greater than 7.5. Once the patient is putting out good amounts of urine, and it has been established that the patient is not in renal failure and is not hyperkalemic, then 40 mEq of potassium can be added to each liter of this solution. A simple regimen for the use of bicarbonate in pediatric salicylate poisoning has been described by Ong. [31]

Hypokalemia and dehydration limit the effectiveness of urine alkalization. Hypokalemia prevents excretion of alkaline urine by promoting distal tubular potassium reabsorption in exchange for hydrogen ions. Symptomatic patients typically have low or borderline-low serum potassium concentration. Treatment with sodium bicarbonate alone may produce further intracellular shift of potassium ions, which further impairs the ability to excrete alkaline urine. Repletion of potassium is often necessary, even when serum potassium levels are in the low reference range (eg, < 4.5 mEq/L).

Urinary alkalization should be continued at least until serum salicylate levels decrease into the therapeutic range (< 30 mg/dL). Although acetazolamide results in the formation of a bicarbonate-rich alkaline urine, it unfortunately also causes metabolic acidosis that can worsen toxicity and, therefore, should not be used.