A bilateral, coarse movement, asterixis is characterized by sudden relaxation of muscle groups holding a sustained posture. This elicited sign is most commonly observed in the wrists and fingers, but may also appear during any sustained voluntary action. Typically, it signals hepatic, renal, or pulmonary disease.
To elicit asterixis, have the patient extend his arms, dorsiflex his wrists, and spread his fingers (or do this for him if necessary). Briefly observe him for asterixis. Alternatively, if the patient has a decreased level of consciousness (LOC) but can follow verbal commands, ask him to squeeze two of your fingers. Consider rapid clutching and unclutching indications of asterixis, or elevate the patient's leg off the bed and dorsiflex the foot. Briefly check for asterixis in the ankle. If the patient can tightly close his eyes and mouth, watch for irregular tremulous movements of the eyelids and corners of the mouth. If he can stick out his tongue, observe the patient for continuous quivering. (See Recognizing asterixis.)
Because asterixis may signal serious metabolic deterioration, quickly evaluate the patient's neurologic status and vital signs. Compare this data with baseline measurements, and watch carefully for acute changes. Continue to closely monitor his neurologic status, vital signs, and urine output.
If the patient has hepatic disease, assess him for early indications of hemorrhage, including restlessness, tachypnea, and cool, moist, pale skin. If the patient is jaundiced, check for pallor in the conjunctiva and mucous membranes of the mouth.
It's important to recognize that hypotension, oliguria, hematemesis, and melena are late signs of hemorrhage. Prepare to insert a large-bore I.V. catheter for fluid and blood replacement. Position the patient flat in bed with his legs elevated 20 degrees. Begin or continue to administer oxygen.
If the patient has renal disease, briefly review the therapy he has received. If he's on dialysis, ask about the frequency of treatments to help gauge the severity of disease. Question a family member if the patient's LOC is significantly decreased.
Then assess the patient for hyperkalemia and metabolic acidosis. Look for tachycardia, nausea, diarrhea, abdominal cramps, muscle weakness, hyperreflexia, and Kussmaul's respirations. Prepare to administer sodium bicarbonate, calcium gluconate, dextrose, insulin, or sodium polystyrene sulfonate.
If the patient has pulmonary disease, check for labored respirations, tachypnea, accessory muscle use, and cyanosis, which are critical signs. Prepare to provide oxygen via nasal cannula, mask, or intubation and mechanical ventilation.
Hepatic encephalopathy.A life-threatening disorder, hepatic encephalopathy initially causes mild personality changes and a slight tremor. The tremor progresses into asterixis—a hallmark of hepatic encephalopathy—and is accompanied by lethargy, aberrant behavior, and apraxia. Eventually, the patient becomes stuporous and displays hyperventilation. When he slips into a coma, hyperactive reflexes, a positive Babinski's sign, and fetor hepaticus are characteristic signs. The patient may also experience bradycardia, decreased respirations, and seizures.
Severe respiratory insufficiency.Characterized by life-threatening respiratory acidosis, severe respiratory insufficiency initially produces headache, restlessness, confusion, apprehension, and decreased reflexes. Eventually, the patient becomes somnolent and may demonstrate asterixis before slipping into a coma. Associated signs and symptoms of respiratory insufficiency include difficulty breathing and rapid, shallow respirations. The patient may be hypertensive in early disease but hypotensive later.
Uremic syndrome.A life-threatening disorder, uremic syndrome initially causes lethargy, somnolence, confusion, disorientation, behavior changes, and irritability. Eventually, signs and symptoms appear in diverse body systems. Asterixis is accompanied by stupor, paresthesia, muscle twitching, fasciculations, and footdrop. Other signs and symptoms include polyuria and nocturia followed by oliguria and, then, anuria; elevated blood pressure; signs of heart failure and pericarditis; deep, gasping respirations (Kussmaul's respirations); anorexia; nausea; vomiting; diarrhea; GI bleeding; weight loss; ammonia breath odor; and metallic taste (dysgeusia).
Drugs.Certain drugs, such as the anticonvulsant phenytoin, may cause asterixis.
▪ Provide frequent rest periods to minimize fatigue.
▪ Elevate the head of the bed to relieve dyspnea and orthopnea; administer oxygen therapy.
▪ Administer oil baths and avoid soap to relieve itching caused by jaundice and uremia.
▪ Provide emotional support to the patient and his family.
▪ If the patient is intubated or has a decreased LOC, provide enteral or parenteral nutrition.
▪ Closely monitor serum and urine glucose levels to evaluate hyperalimentation.
▪ Because the patient will probably be on bed rest, reposition him at least once every 2 hours to prevent skin breakdown.
▪ Because the patient's debilitated state makes him prone to infection, follow strict hand-washing and aseptic techniques when changing dressings and caring for invasive lines.
▪ Discuss end-of-life issues, as appropriate.
▪ Explain the underlying disorder and treatment plan.
▪ Teach the patient the importance of planning periods of rest.
▪ Explain measures to relieve itching.
▪ Discuss measures to reduce the risk of infection with the patient and his family.
![Asterixis [Liver flap, flapping tremor] - 5489.1.png](/bookimages/16/5489.1.png)
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Copyright Details: Nursing: Interpreting Signs and Symptoms, Copyright © 2008 Williams & Wilkins.
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Title: Nursing: Interpreting Signs and Symptoms Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 1-58255-668-7 
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