F.

What drugs would you and by what route would you administer them to control
MJ’s pain
Opioid administration via the IV route, particularly in the emergent and acute phases of
burn management, remains the mainstay for pharmacologic management of burn pain
(DeBoer & O'Connor, 2004). Use of opioids is complicated by the fluctuation in the
bioavailability of a drug, protein binding of the drug, and drug clearance related to the
hemodynamic and fluid volume shifts that occur with a burn injury. Absorption of the
opioid also may be affected. Titration of analgesic agents to obtain pain relief while
minimizing side effects is crucial. The patient's requirements for analgesia are often
high, but fear of addiction on the part of the patient and the health care provider
hampers adequate opioid administration.
Morphine sulfate remains the analgesic of choice for treatment of acute burn pain. It is
titrated to obtain pain relief based on the patient's self-report of pain using a
standardized pain rating scale (Carrougher et al., 2003; Martin-Herz et al., 2003).
Fentanyl is another useful opioid for burn pain, particularly procedural burn pain. It has
been shown to be effective for management of intense pain of short duration. Fentanyl
has a rapid onset, high potency, and short duration, all of which make it effective for use
with burn wound procedures. However, its anticholinergic metabolite properties increase
the risk of delirium. Appropriate cardiac and respiratory monitoring must be carried out
during its administration
Sustained-release opioids, such as MS Contin or oxycodone (OxyContin), have also
been used successfully in the treatment of burn pain. These medications can effectively
treat the resting pain that is often associated with burn injury. Additional medications
must be prescribed with these medications to cover breakthrough pain.
Some burn units use self-administered nitrous oxide during burn wound procedures.
The need for proper ventilation and monitoring equipment and the availability of
qualified personnel to monitor administration of nitrous oxide limit its use.
Anxiety and pain go hand in hand for burn patients. The entire burn experience can
produce severe anxiety, which can, in turn, exacerbate pain. Therefore, the ideal pain
management
regimen
must
incorporate
the
treatment
of
pain
and anxiety and must be individualized for each patient. Sedation with anxiolytic
medications such as lorazepam (Ativan) and midazolam (Versed) may be indicated in
addition to the administration of opioids

as water shifts from the interstitial space to the vascular space Injury: Immediately after burn injury.K.0 meq/L.0 mEq/L Interpretation During burn shock: serum sodium levels vary in response to fluid resuscitation. K – 6.0 mEq/L 3. What is the rationale of these lab and ABG findings? What would be your next step? Day 2 lab test revealed Lab values – Na-126 meq/L. Hyponatremia is also common during the first week of the acute phase. hyponatremia (sodium depletion) is present.5-5. hyperkalemia (excessive potassium) results from massive cell destruction. Lab test Sodium Result 126 mEq/L Normal Value 136-145 mEq/L Potassium 6. Usually. Hypokalemia (potassium depletion) may occur later with fluid shifts and inadequate potassium replacement Dehydration: The potassium becomes more concentrated in dehydrated .

potassium is expelled from the cell. When the patient is rehydrated. because sodium is consumed abundantly in a normal diet. lactated Ringer's solution or isotonic saline (0. hydrogen ions are driven from the blood and into the cell. Serum sodium must not be increased by more than 12 mEq/L in 24 hours. as well as assessment of the patient's actual serum sodium value (Elgart. . For patients who can eat and drink.9% sodium chloride) solution may be prescribed. or a parenteral route. For those who cannot consume sodium. nasogastric tube. to avoid neurologic damage due to osmotic demyelination. potassium levels may in fact be reduced. Hsu & Chiu. 2003).patients. Potassium level rise Hyponatremia Medical Management The key to treating hyponatremia is assessment. and serum levels appear to be elevated. Acidosis: To maintain physiologic pH during acidosis. 2004). To maintain electrical neutrality. This condition may occur when the serum sodium concentration is overcorrected (exceeding 140 mEq/L) too rapidly or in the presence of hypoxia or anoxia (Lin. this includes assessment of the speed with which hyponatremia occurred. sodium is easily replaced. It may produce lesions in the pons that cause paraparesis. dysarthria. Sodium Replacement The obvious treatment for hyponatremia is careful administration of sodium by mouth.

However. lithium or demeclocycline can antagonize the osmotic effect of ADH on the medullary collecting tubule. calcium antagonizes the action of hyperkalemia on the heart. The usual daily sodium requirement in adults is approximately 100 mEq. Excess sodium would be excreted rapidly in a highly concentrated urine. Incorrect use of these fluids is extremely dangerous. 2000). Hyperkalemia Medical Management An immediate ECG should be obtained to detect changes. it may also cause sodium retention and fluid overload (Rose & Post. In SIADH. eliminating the use of potassiumcontaining salt substitutes in a patient who is taking a potassium-conserving diuretic may be all that is needed to deal with mild hyperkalemia. Kayexalate) may be necessary in patients with renal impairment. Shortened repolarization and peaked T waves are seen initially. it may be necessary to administer small volumes of a hypertonic sodium solution. of cation exchange resins (eg. it may be necessary to administer IV calcium gluconate. Infusion of calcium does not reduce the serum potassium concentration. Within minutes after administration. urine is not concentrated and isotonic urine is excreted to effect a change in water balance. Emergency Pharmacologic Therapy If serum potassium levels are dangerously elevated. if edema and hyponatremia occur together. in whom water restriction is difficult. Water Restriction In a patient with normal or excess fluid volume. provided there are no abnormal losses. If edema exists alone. hyponatremia is treated by restricting fluid to a total of 800 mL in 24 hours. In nonacute situations. Prevention of serious hyperkalemia by the administration. the administration of hypertonic saline solution alone cannot change the plasma sodium concentration. and coma. Calcium chloride and calcium gluconate are not interchangeable: calcium . because intestinal perforation can occur. restriction of dietary potassium and potassiumcontaining medications may suffice. In patients with SIADH. sodium is restricted. because 1 L of 3% sodium chloride solution contains 513 mEq of sodium and 1 L of 5% sodium chloride solution contains 855 mEq of sodium.dysphagia. but it immediately antagonizes the adverse cardiac conduction abnormalities. if neurologic symptoms are present. both sodium and water are restricted. it is also prudent to obtain a repeat serum potassium level from a vein without an IV infusing a potassium-containing solution. such as 3% or 5% sodium chloride. For example. To verify results. Cation exchange resins cannot be used if the patient has a paralytic ileus. This is far safer than sodium administration and is usually effective. either orally or by retention enema. With the addition of the diuretic furosemide (Lasix). Kayexalate can bind with other cations in the GI tract and contribute to the development of hypomagnesemia and hypocalcemia.

Monitoring the blood pressure is essential to detect hypotension. the appearance of bradycardia is an indication to stop the infusion. this may be accomplished by using cation exchange resins. HCO3 neturalizes these . are highly effective in decreasing potassium but remain controversial. Ventolin). Administration of these medications is a stopgap measure that only temporarily protects the patient from hyperkalemia. such as furosemide (Lasix). Loop diuretics. The myocardial protective effects of calcium are transient. Also. HCO3 – 18 meq/L Lab Test ABG pH Result Normal Values Interpretation 7.gluconate contains 4. hemodialysis. If the hyperkalemic condition is not transient. which may result from the rapid IV administration of calcium gluconate.35-7. Extra caution is required if the patient has been “digitalized” (ie. and chloride reabsorption in the ascending loop of Henle and distal renal tubule.5 mEq of calcium and calcium chloride contains 13. IV administration of sodium bicarbonate may be necessary to alkalinize the plasma and cause a temporary shift of potassium into the cells. because parenteral administration of calcium sensitizes the heart to digitalis and may precipitate digitalis toxicity. Beta-2 agonists also move potassium into the cells and may be used in the absence of ischemic cardiac disease. however. sodium bicarbonate furnishes sodium to antagonize the cardiac effects of potassium. increase excretion of water by inhibiting sodium. 2005). they are temporary. Glucose and insulin therapy has an onset of action within 30 minutes and lasts for several hours. because they can cause tachycardia and chest discomfort (Porth.Acute Renal Failure: Ketoacids are built up. such as albuterol (Proventil. lasting about 30 minutes. Effects of this therapy begin within 30 to 60 minutes and may persist for hours. or other forms of renal replacement therapy ABG revealed – pH-7. Beta-2 agonists. actual removal of potassium from the body is required.30 7. The ECG should be continuously monitored during administration.30. peritoneal dialysis.45 Acidosis – Renal Failure: Important base ions are lost. pCO2-35mmHg.6 mEq of calcium. potassium. caution must be used. has received accelerated dosages of a digitalis-based cardiac glycoside to reach a desired serum digitalis level rapidly). Acid ions are relatively increased and acidosis occur pCO2 HCO3 35 18 35-45 mmHg 22-26 mmHg Ketoacidosis Normal Low . therefore. IV administration of regular insulin and a hypertonic dextrose solution causes a temporary shift of potassium into the cells.

Therefore. hypokalemia may occur with reversal of the acidosis and subsequent movement of potassium back into the cells. treatment is aimed at eliminating the source of the chloride. bicarbonate is administered if the pH is less than 7.1 and the serum bicarbonate level is less than 10 mEq/L. Although hyperkalemia occurs with acidosis. In chronic metabolic acidosis. If the problem results from excessive intake of chloride. Treatment modalities may also include hemodialysis or peritoneal dialysis . low serum calcium levels are treated before the chronic metabolic acidosis is treated. and hypokalemia is corrected as acidosis is reversed. the serum potassium level is monitored closely.acids. HCO3 levels therefore drop Interpretation: Uncompensated Metabolic Acidosis Treatment is directed at correcting the metabolic defect (Kee et al. Alkalizing agents may be administered if the serum bicarbonate level is less than 12 mEq/L. 2004). When necessary. to avoid tetany resulting from an increase in pH and a decrease in ionized calcium..