Decerebrate posture [Decerebrate rigidity, abnormal extensor reflex]
Decerebrate posture is characterized by adduction (internal rotation) and extension of the arms, with the wrists pronated and the fingers flexed. The legs are stiffly extended, with forced plantar flexion of the feet. In severe cases, the back is acutely arched (opisthotonos). Decerebrate posture indicates upper brain stem damage, which may result from primary lesions, such as infarction, hemorrhage, or tumor. Other causes include metabolic encephalopathy, head injury, and brain stem compression associated with increased intracranial pressure (ICP).
Decerebrate posture may be elicited by noxious stimuli or may occur spontaneously. It may be unilateral or bilateral. With concurrent brain stem and cerebral damage, decerebrate posture may affect only the arms, with the legs remaining flaccid. Decerebrate posture may also affect one side of the body and decorticate posture the other. The two postures may also alternate as the patient’s neurologic status fluctuates. Generally, the duration of each posturing episode correlates with the severity of brain stem damage. (See Comparing decerebrate and decorticate postures.)
Act Now: Upon initial assessment of the decerebrate posture, your first priority is to ensure a patent airway. Insert an artificial airway and institute measures to prevent aspiration. (Don’t disrupt spinal alignment if you suspect spinal cord injury.) Suction the patient as necessary.
Next, examine spontaneous respirations. Give supplemental oxygen, and ventilate the patient with a handheld resuscitation bag, if necessary. Intubation and mechanical ventilation may be indicated. Keep emergency resuscitation equipment handy. Be sure to check the patient’s chart for a do-not-resuscitate order.
Assessment
History
After the patient’s airway has been stabilized, assess the history of the patient’s coma. If a family member is available, ask about any accident or trauma responsible for the coma, and find out when the patient’s level of consciousness (LOC) began deteriorating. Did it occur abruptly? Did the patient express presence of any symptoms, such as headache, nausea, or visual or behavioral changes, before he lost consciousness? Does he have a history of diabetes, liver disease, cancer, blood clots, or aneurysm? If you’re unable to obtain this information, look for clues to the causative disorder, such as hepatomegaly, cyanosis, diabetic skin changes, needle tracks, or obvious trauma.
Physical examination
After taking the patient’s vital signs, determine his LOC. Use the Glasgow Coma Scale as a reference. Evaluate the pupils for size, equality, and response to light. Test deep tendon reflexes and cranial nerve reflexes, and check for doll’s eye sign. (See Testing for absent doll’s eye sign, page 104.)
Pediatric pointers
Children younger than age 2 may not display decerebrate posture because the nervous system is still immature. However, if the posture occurs, it’s usually the more severe opisthotonos. In fact, opisthotonos is more common in infants and young children than in adults and is usually a terminal sign. In children, the most common cause of decerebrate posture is head injury. It also occurs with Reye’s syndrome — the result of increased ICP causing brain stem compression.
Medical causes
Brain stem infarction.
When brain stem infarction — a primary lesion — produces a coma, decerebrate posture may be elicited. Associated signs and symptoms vary with the severity of the infarct and may include cranial nerve palsies, bilateral cerebellar ataxia, and sensory loss. With deep coma, all normal reflexes are usually lost, resulting in absence of doll’s eye sign, a positive Babinski’s reflex, and flaccidity.
Brain stem tumor
With brain stem tumor, decerebrate posture is a late sign that accompanies coma. Commonly, the posture is preceded by hemiparesis or quadriparesis, cranial nerve palsies, vertigo, dizziness, ataxia, and vomiting.
Cerebral lesion
Whether the cause is trauma, tumor, abscess, or infarction, any cerebral lesion that increases ICP may also produce decerebrate posture. Typically, this posture is a late sign. Associated findings vary with the lesion’s site and extent but commonly include coma, abnormal pupil size and response to light, and the classic triad of increased ICP — bradycardia, increasing systolic blood pressure, and widening pulse pressure.
Hepatic encephalopathy
A late sign in hepatic encephalopathy, decerebrate posture occurs with coma resulting from increased ICP and ammonia toxicity. Associated signs include fetor hepaticus (foul-smelling breath), a positive Babinski’s reflex, and hyperactive deep tendon reflexes.
Hypoglycemic encephalopathy
Characterized by extremely low blood glucose levels, hypoglycemic encephalopathy may produce decerebrate posture and coma. It also causes dilated pupils, slow respirations, and bradycardia. Muscle spasms, twitching, and seizures eventually progress to flaccidity.
Hypoxic encephalopathy
Severe hypoxia may produce decerebrate posture — the result of brain stem compression associated with anaerobic metabolism and increased ICP. Other findings include coma, a positive Babinski’s reflex, absence of doll’s eye sign, hypoactive deep tendon reflexes and, possibly, fixed pupils and respiratory arrest.
Pontine hemorrhage
Typically, pontine hemorrhage — a life-threatening disorder — rapidly leads to decerebrate posture with coma. Accompanying signs include total paralysis, absence of doll’s eye sign, a positive Babinski’s reflex, and small, reactive pupils.
Posterior fossa hemorrhage.
Posterior fossa hemorrhage is a subtentorial lesion that causes decerebrate posture. Early signs and symptoms include vomiting, headache, vertigo, ataxia, stiff neck, drowsiness, papilledema, and cranial nerve palsies. The patient eventually slips into coma and may experience respiratory arrest.
Other causes
Diagnostic tests
Relief of high ICP by removal of spinal fluid during a lumbar puncture may precipitate cerebral compression of the brain stem and cause decerebrate posture and coma.
Nursing considerations
Help prepare the patient for diagnostic tests that will determine the cause of his decerebrate posture; these can include skull X-rays, computed tomography scan, magnetic resonance imaging, cerebral angiography, digital subtraction angiography, electroencephalogram, brain scan, and ICP monitoring.
Monitor the patient’s neurologic status and vital signs every 30 minutes or as indicated. Also, be alert for signs of increased ICP (bradycardia, increasing systolic blood pressure, and widening pulse pressure) and neurologic deterioration (altered respiratory pattern and abnormal temperature).
Patient teaching
Inform the patient and his family that decerebrate posture is a reflex response, not a voluntary response to pain or a sign of recovery. Offer emotional support. Refer the patient and his family to a mental health worker or spiritual counselor, if indicated.
Pictures
![Decerebrate posture [Decerebrate rigidity, abnormal extensor reflex] - 4923.png](/bookimages/13/4923.png)
![Decerebrate posture [Decerebrate rigidity, abnormal extensor reflex] - 4923.1.png](/bookimages/13/4923.1.png)
Book Source Details
- Book Title: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series
- Author(s): Springhouse
- Year of Publication: 2007
- Copyright Details: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, Copyright © 2007 Lippincott Williams & Wilkins.
Other Book Chapters Related to Posture symptoms
Read excerpts from these other book chapters related to Posture symptoms:
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- "Professional Guide to Diseases (Eighth Edition)" (2005)
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Copyright Details: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, Copyright © 2008 Williams & Wilkins.
More About Causes of Posture symptoms
» Next page:
Decorticate posture [Decorticate rigidity, abnormal flexor response] (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
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