Protein Deficiency Scenerio Discussion

Read the following scenario and discuss the questions that follow. I attached some article it may help, but you still can use any article that you preferred.

Frank Hershey is a 60-year-old male who is brought to the Emergency Department following an automobile accident. The car Frank was driving swerved off the road into the median, where the car’s front end hit a highway bridge. Frank is treated for minor injuries, and several lab tests are ordered. Frank’s blood alcohol level (BAL) is .20% (0.20%), and his liver enzymes are elevated. Assessment findings include lethargy, an enlarged liver on palpation, jaundiced skin and sclera, and ascites. Frank is admitted for further evaluation with a medical diagnosis of cirrhosis.

Discuss which lab values you anticipate will be elevated.
Explain how the symptoms displayed are connected to the lab values you anticipate. Choose at least two symptoms and explain in detail. (You may also discuss symptoms you might anticipate but that are not listed in the scenario, there are many. Please provide rationale).

ORDER CUSTOM, PLAGIARISM-FREE PAPER

THE MOST OVERLOOKED ELECTROLYTE IMBALANCE Long ignored as a cause of

potentially fatal arrhythmias, hypomagnesemia is now

receiving carefui attention. Find out what you need to

know to uncover this problem in your patients.

AVID WALLACE, A 73-YEAR-OLD RETIRED CON- struction worker, is admitted to your coronary care unit (CCU) with a di- agnosis of congestive heart failure (CHF). Although he denies having chest pain, he’s pale, diaphoretic, and dyspneic. You auscultate moist crack- les in his lungs and note that he’s pro- ducing frothy, pink-tinged sputum.

His vital signs are: pulse, 110; blood pressure, 100/64; respirations, 28; and temperature, 97.6° F (36.4° C). Car- diac monitoring shows sinus tachycar- dia, with four to five ventricular ec- topic beats per minute.

This is Mr. Wallace’s second episode

BY REBECCA P. YARNELL, RN, MSN Nursing Instructor Fort Sanders School of Nursing Knoxville, Tennessee

MARTHA P. CRAIG, RN, MSN Director of Department of Nursing Maryville College Knoxville, Tennessee

of CHF since he suffered a myocardial infarction 4 years ago. He’s remained otherwise healthy on a drug regimen of digoxin (Lanoxin), furosemide (La- six), and a potassium chloride supple- ment (K-Lyte/Cl). Other than a bor- derline low hematocrit of 39%, his lab results are within normal limits.

So what’s gone wrong? The answer isn’t immediately obvious because Mr. Wallace is suffering from hypomag- nesemia, an often overlooked and life- threatening- electrolyte deficiency, which affects many more patients than you might suspect. Recent research suggests doctors and nurses should be- come more aware of this potential problem. Protein Deficiency Scenerio Discussion

This article will tell you what you need to know — how to identify patients at risk for hypomagnesemia, what causes to consider, what signs and symptoms to look for, and how to ad-

Nursing91, July 55

minister treatment. We’ll also take you through Mr. Wallace’s therapy and postdischarge planning.

Associated with hypokalemia Studies show that 42% of hypokalemic patients also have hypomagnesemia — many of them experiencing ventricular ectopy, one of Mr. Wallace’s symp- toms. In these studies, ventricular ar- rhythmias persisted after hypokalemia was corrected and continued until hy- pomagnesemia was eliminated. The findings prove that magnesium is as important as potassium in the etiology and treatment of these cardiac prob- lems.

That’s because a magnesium deficit can lead to intracellular potassium loss and sodium accumulation, altering membrane excitability. This creates ab- normal areas of automaticity, which contribute to inefficient conduction in the heart. Of course, any changes in the normal sequence of conduction

usually result in symptomatic arrhyth- mias.

Diagnosing Mr. Wallace In Mr. Wallace’s case, as in so many others, no one recognizes his magne- sium deficit initially. Shortly after his admission, you insert an intravenous (I.V.) line and infuse furosemide (80 mg) and digoxin (0.25 mg) as ordered. Because Mr. Wallace is experiencing ventricular ectopy, the doctor also or- ders 250 ml of D,W with 40 mEq po- tassium chloride, infused at 25 ml/ hour, hoping to prevent the ventricular irritability from getting worse.

Over the next 24 hours, Mr. Wallace improves, his respirations slowing to 16 per minute, his chest sounds clear- ing. But the cardiac monitor reveals occasional premature ventricular con- tractions, so he’s transferred to the te- lemetry unit for continued electrocar- diogram monitoring. On the unit, he’s started on an oral regimen of digoxin.

MANAGING COMPLICATIONS OF MAGNESIUM THERAPY With the clinical significance of hy- pomagnesemia finally being recog- nized, you can expect to administer magnesium supplements more of- ten to your patients. Here are some guidelines to help you detect com- plications during magnesium re- placement therapy: • Monitor the patient’s vital signs, checking for an irregular or de- creased heart rate, lowered blood pressure, and depressed respira- tions. Also watch ECG tracings closely, looking for peaked T waves and widened QRS complexes, both of which may indicate too mucti magnesium. • Magnesium infusions can be toxic for patients with renal problems, so keep in mind that decreased car- diac output could signal a problem. Also monitor intake and output carefully before, during, and after the infusion. • Assess the patient for impaired neuromuscular reactions, which may indicate an increased magne- sium level. Look for muscle weak- ness, respiratory depression, and, ultimately, flaccid paralysis. On- going evaluation of deep tendon re- flexes before and during magne- sium infusions will help you identify any problem before it gets too se- vere.

• Keep calcium gluconate and cal- cium gluceptate on hand for rapid reversal of toxic effects. Also keep resuscitation equipment available. As you’re watching for potentially toxic magnesium levels, remember that your patient’s level may also re- main normal despite continuous in- fusion. That’s because serum levels are a poor indicator of intracellular magnesium levels, which fluctuate independently from serum levels.

• You may also be asked to admin- ister I.M. magnesium, usually or- dered as magnesium sulfate (20 grams in 2 ml). But some experts question the effectiveness of this therapy because many patients show no change in serum levels af- ter injection. One reason may be that the injectable concentration of magnesium exceeds the renal tubu- lar threshold. You can address this problem by getting an order to ad- minister injections more frequently.

• Oral magnesium therapy poses problems too. Because of its laxa- tive effect, magnesium hydroxide can exacerbate the deficiency through gastrointestinal loss. Mag- nesium chloride avoids this problem but is unpalatable. Timed-release tablets of magnesium chloride are available, but using them for contin- uous therapy is expensive.

furosemide, and a potassium supple- ment — the same medications he’d been taking at home. He starts to feel en- ergetic and is allowed to resume a full activity level.

But his progress doesn’t last long. On the morning of the fourth day, he com- plains of vague discomfort and fatigue. A nurse on the telemetry unit notes that he seems nervous and uneasy. A few hours later, he develops ventricular tachycardia, with its characteristic wide QRS complexes, missing P waves, and a heart rate of 150 to 158 beats/ minute. The nurse gives a stat order of lidocaine (50 mg I.V. bolus), followed by an infusion administered at 3 mg/ minute. Mr. Wallace is transferred back to the CCU, where you’re at a loss to explain what went wrong again.

Hypomagnesemia discovered The reason isn’t apparent until the car- diologist asks for stat serum magne- sium and potassium levels. The results show a potassium level of 3.9 mEq/ liter (normal is 3.8 to 5.5) and a mag- nesium level of 1.3 mEq/liter (normal is 1.5 to 2.5). He orders replacement therapy —5 grams of magnesium sul- fate and potassium chloride, 15 mEq in 250 ml of D,W, to be administered over 10 hours.

You use a controller to administer the infusion and monitor the infusion site carefully for signs of infiltration. You also check and document Mr. Wal- lace’s heart rate and blood pressure hourly, aware that a drop in either vital sign could mean that excess magne- sium is slowing conduction in the myo- cardium, compromising cardiac out- put. This is possible because hyper- magnesemia, like hypomagnesemia, slows conduction in the myocardium. (See Managing Complications of Mag- nesium Therapy.)

Two hours after starting the infusion, you find Mr. Wallace’s vital signs are stable. A rhythm strip reveals a normal sinus rhythm with an occasional but rare premature ventricular contraction.

Mr. Wallace returns to the telemetry unit after spending 24 hours oh the CCU. His serum magnesium and po- tassium levels are checked daily. Dis- charge is planned within a few days because his electrolyte levels return to normal and his CHF resolves.

His diuretic is changed from furose- mide to triamterene/hydrochlorothiazide (Maxzide), which spares potassium and magnesium. He’ll no longer need to take potassium supplements but will

56 Nursing91, July

CAUSES OF HYPOMAGNESEMIA GASTROINTESTINAL • Alcoholism • Protein-calorie malnutrition • Prolonged I.V. therapy (without

magnesium replacement) • Gastric suction • Intestinal bypass for obesity • Diarrhea • Colonic neoplasms • Laxative abuse • Bulimarexia • Short-bowel syndrome • Malabsorption

RENAL • Diuretics • Antibiotics (ticarcillin, gentamicin,

carbenicillin) • Cispiatin • Cyclosporine • Hypercalcemic states (including

malignancies) • Postobstructive diuresis • Acute tubular necrosis (diuretic

phase) • Hereditary renal magnesium Protein Deficiency Scenerio Discussion