Neurologic disorders

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CHAPTER 7 Neurologic disorders

General neurologic assessment

MUSCLE STRENGTH RATING
Score	Description of Strength
5/5	Patient moves joint with full ROM against normal resistance and gravity
4/5	Patient moves joint with full ROM against mild resistance and gravity
3/5	Patient moves joint with full ROM against gravity only
2/5	Patient moves joints with full ROM but not against gravity
1/5	Patient’s muscle contracts in an attempt to move joint; joint does not move
0/5	Patient does not visibly attempt to move; no muscle contraction; paralysis

ROM, Range of motion.

• Assess for abnormal motor movements unilaterally and bilaterally:

• Decorticate posturing (abnormal flexion)

• Decerebrate posturing (abnormal extension)

• Flaccidity

Motor deficits (weakness or paralysis) are caused by injury or edema to the primary motor cortex and corticospinal (pyramidal) tracts.

• Perform specific testing for abnormalities as appropriate:

• Grasp: Place two fingers within the patient’s palm and ask patient to squeeze your fingers. Ask the patient to let go. Abnormal grasp: Patient cannot let go once grasp is in progress. May reflect frontal lobe disease; observed occasionally with occipital lobe disease, Alzheimer disease, or bilateral thalamic disease.

• Babinski sign: Upward or dorsiflexion of the big toe when stroking the outer sole and ball of the foot) can indicate a lesion of the pyramidal tract.

• Kernig sign: Painful resistance to full extension of the leg at the knee when the hip is flexed; used in diagnosis of meningitis due to meningeal irritation

• Brudzinski sign: Flexion of the hip and knee involuntarily with neck flexion and used in diagnosis of meningitis due to meningeal irritation

Sensory assessment

Sensory deficits occur when the primary sensory cortex, the sensory association areas of the parietal lobe, or the spinothalamic tracts are injured or edematous. Sensory deficits include inability to distinguish objects according to characteristics (e.g., size, shape, weight) and inability to distinguish overall changes in temperature, touch, pressure, and position.

• Assess perception of touch, proprioception, pain, temperature, and vibration (if possible). Ask patient to close eyes while you apply stimuli. The patient should not be given the opportunity to anticipate your moves. Compare the same stimulus on the right side of the body to the identical location on the left side of the body. Note if patient perceives stimuli symmetrically and appropriately (sharp versus dull using a needle versus a cotton swab, or hot versus cold). Compare proximal and distal parts of arms and legs when testing pain and touch.

• Superficial and deep reflexes are tested on symmetrical sides of the body and compared noting the strength of contraction.

• Test vibratory sense (with vibrating tuning fork) distally (on the tip of big toe or finger) and ask when patient feels the vibration stop.

• For position sense, move distal joints about using very light touch and ask about the position the patient perceives of the joint.

• Two-point discrimination can be done using a bent paper clip. Note the smallest distance between the two points at which the patient senses two points are pressing on the skin. Document using a dermatome map.

Improvement in both motor and sensory perception may be seen as cerebral edema subsides.

Fundoscopic assessment

Generally done by the physician or midlevel practitioner and may reveal retinal hemorrhage(s) at the side of the optic disc. Hemorrhage is caused by blood from the subarachnoid space (SAS) being forced along the optic nerve sheath under high pressure. The patient may complain of blurred vision or blind spots (scotomata). Terson hemorrhage associated with vitreous and/or subhyaloid hemorrhage has been seen as a subarachnoid complication and its presence has been noted with increased mortality and morbidity rates.

Dysphagic screening

Should be performed early, particularly when stroke has occurred, to prevent complications of aspiration and to initiate appropriate nutritional therapy. People with neurologic dysfunction are poor judges of their own ability to swallow, so a thorough evaluation and intervention by a speech pathologist may be required, following routine screening procedures recommended by institutional protocol.

Diagnostic Tests for Neurologic Disorders

Test	Purpose	Abnormal Findings
Cerebral angiography	Digital subtraction angiography visualizes blood flow. Involves use of intravascular catheter The gold standard for evaluating cerebral vasculature Invasive procedure with minimal risk used to visualize the cerebral blood vessels	Areas of reduced cerebral blood flow, aneurysms, arteriovenous malformations (AVMs), vascular abnormalities Used with interventional neuroradiologic procedures such as coiling, AVM embolization (gluing) Provides specific information on the cause of stroke by identifying the blood vessel involved
Computed tomography (CT) of brain	Performed emergently, is the gold standard of differentiating ischemic from hemorrhagic stroke; may be done at intervals to monitor progress Assess details of structures of bone, tissue, and fluid-filled space. Detects exudate, abscesses, and intracranial pathology (e.g., tumors, brain injury) Assess for hydrocephalus.	Shift of structures due to enlarged mass, edema, exudate, abscesses, fresh hemorrhage, hematomas, infarction, hydrocephalus Can visualize facial skeleton and soft tissue structures for abnormalities (e.g., tumors, brain injury) Within the first few hours after an acute ischemic stroke, the scan may appear normal. Intracranial hemorrhage is easily diagnosed on CT—blood appears as a bright white signal.
Continuous electrocardiographic (ECG) monitoring	Evaluate cardiovascular status, especially during medication administration.	Phenytoin and other AEDs can cause dysrhythmias and hypotension.
CT angiography	Less invasive than cerebral angiography; involves use of contrast media injection into peripheral vein and use of CT scanner	Visualize intra-arterial clot, small intracranial aneurysm, AVM
CT perfusion or CT-xenon scan (CTP)	Provides information related to cerebral blood flow (CBF)and volume Used to guide clinical decision making regarding the use of thrombolysis or interventional procedures	Compromised blood flow; a limited test; cannot detect infarcted tissue
Electroencephalography (EEG)	Evaluate the brain’s electrical activity for ongoing seizures, even if there are no clinical signs of seizures.	Diagnosis of seizures and localization of structural abnormalities Also used as element of criteria for brain death
Electromyography (EMG) or nerve conduction velocity (NCV)	Assesses nerve conduction velocity deficit as a result of the demyelination of peripheral nerves	EMG and NCV demonstrate profound slowing of motor conduction velocities and conduction blocks several weeks into the illness.
Lumbar puncture (LP) with cerebrospinal fluid (CSF) specimen for analysis	Measures CSF pressures and obtains CSF specimen when infection, such as meningitis or neurosyphilis, is suspected May be performed when SAH is suspected and CT is normal	Elevated protein, low glucose, elevated WBC
Magnetic resonance imaging (MRI) of brain	Minute oscillations of hydrogen atoms in brain create graphic image of bone, fluid, and soft tissue Provides a more detailed image MRI is most useful for ischemic patients in identifying the cause and area involved. Provides detailed information regarding the area of injury or its vascular supply (MRA) Diffusion-weighted imaging (DWI) is a measurement of edema, whereas perfusion weighted imaging (PWI) is a measurement of global CBF.	Infarcts, areas at risk or ischemic areas, vascular defects, stenosis, occlusion
Positron emission tomography (PET) and single-photon emission computed tomography (SPECT)	To evaluate brain metabolism and blood flow using three-dimensional imaging produced using a radioactive tracer	Demonstrates abnormal function of the brain by revealing abnormal structures, metabolism, and perfusion Locates areas of brain causing seizures, head injury, and some disorders (e.g., Alzheimer’s)
Radioisotope brain scan	Examine areas of blood flow through concentration of isotope uptake in the brain.	Increased or decreased blood flow intraoperatively or assess for postoperative cerebral infarction Lack of uptake may indicate cerebral brain death.
Transcranial Doppler	Noninvasive and can be done serially at the bedside Evaluates the intracranial vessels and assesses the velocity of blood flow in the anterior and posterior cerebral circulation Also used to evaluate vasospasm, to determine brain death via detection of cerebral circulatory arrest, for intraoperative monitoring, and to locate emboli	Arterial narrowing vasospasm, cerebral circulatory arrest, emboli due to vasospasm Can also be used to confirm absent blood flow in brain death

Brain death

Pathophysiology

Brain death is defined as irreversible loss of function of the brain, including the brainstem and respiratory centers. Cardiac death is the cessation of mechanical action/pumping of the heart, resulting in absence of pulse, heart sounds, blood pressure, and respirations. Brain death is most frequently the result of increased intracranial pressure (ICP) caused by severe traumatic head injury or hemorrhagic stroke caused by ruptured cerebral aneurysm with subarachnoid hemorrhage (SAH) or intracranial hemorrhage (ICH). A significant number of patients with large acute ischemic strokes (AIS) experience cerebral edema and herniation. Hypoxic-ischemic encephalopathy with massive brain swelling after prolonged cardiopulmonary resuscitation or asphyxia and encephalopathy with cerebral edema resulting from fulminant hepatic failure may also result in increased ICP, herniation, and brain death.

If brain death occurs quickly, cardiac death may occur immediately. If brain death occurs more slowly, with time to initiate mechanical ventilation prior to cardiac death, the heart can continue to beat/pump since the cardiac pacing cells operate independently from brain regulation. Mechanical ventilation provides the oxygen necessary to maintain the pacing cells if the patient is circulating adequate amounts of blood cells carrying oxyhemoglobin, acidosis is controlled, and electrolytes are managed. Over time, without a functional hypothalamus and pituitary gland, patients experience further instability of blood pressure due to loss of regulation of the thyroid and adrenal glands. Massive diuresis is common when the posterior pituitary gland ceases to function. If the patient is an organ donor, the organs must be sustained prior to removal, requiring management of all sequelae of brain death. Guidelines for managing brain dead organ donors have common elements internationally, with most controversy stemming from the need to provide additional hormones to help control endocrine-related crises associated with loss of function of the pituitary and hypothalamus and use of prophylactic antibiotics to prevent infection.

Neurologists or neurosurgeons may diagnose brain death approximately two to three times monthly in large referral centers. Herniation, or displacement of a portion of the brain through openings in the intracranial cavity, results from increased ICP. Herniation occurs when there is difference between the cranial compartment pressures above (supratentorial) and below (infratentorial) the tentorium, the rigid membrane that divides the skull. If additional blood or cerebrospinal fluid (CSF), edematous tissue, or tumor occupies space inside the skull, there is little ability to expand to “make room” for anything not normally present. These “mass lesions” or “space-occupying lesions” cause “crowding” within their cavity, which increases the pressure.

When pressure in one of the two compartments (supratentorial or infratentorial) is markedly elevated, the brain structures and blood vessels within the cavity are compressed, resulting in ischemia, hypoxia, and, if uncontrolled, cerebral anoxia. When blood flow is minimal to absent, the hypoxic/anoxic brain tissues become more edematous. Eventually, no space remains for further expansion. The skull cannot expand and the tentorium expands minimally, so the brain is forced through the available openings. The movement or displacement through an opening causes further compression of blood vessels, with possible laceration and destruction, which leads to necrosis of brain tissues and brain death (see Traumatic Brain Injury, Neurologic Herniation Syndromes, p. 333).

Neurologic assessment: brain death

Goal of system assessment

To validate absence of function of the brain and brainstem. According to the American Academy of Neurology (AAN) guidelines, if coma or unresponsiveness, absence of brainstem reflexes, and apnea are present, the patient is dead. If mechanical ventilation is terminated, natural death results. Severity of brain injury should be determined following two expert clinical assessments and diagnostic testing.

Apnea test

• Determines absence of respirations when mechanically induced ventilations cease. Must be done carefully to avoid cardiac death during the test. If the patient begins to deteriorate while off the ventilator, the patient should be placed back on the ventilator.

Vital signs

• Mild hypothermia: Core temperature must be greater than 32°C (90°F), but less than 36.5°C (97°F).

• Hypotension: With mechanical ventilation in place, blood pressure is greater than 90 mm Hg. Without mechanical ventilation, the heart rate will decrease, resulting in hypotension and eventually asystole.

• Apnea: No spontaneous respirations when mechanical ventilation is suspended. A formal apnea test is required to confirm the absence of respirations.

Observation/inspection/palpation

• Coma or unresponsiveness: Patient does not respond to verbal stimuli, touch, or deep pain induced by pressure exerted on nail beds, the supraorbital area of the skull, or the temporomandibular joint or rubbing the sternum.

• Brainstem reflexes/cranial nerve function: Absent

• Pupils: Unresponsive to bright light; size is 4 to 9 mm (dilated) in midposition.

• Ocular movement: No oculocephalic reflex (“doll’s eyes” negative). No oculovestibular reflex: no deviation of eyes toward irrigation of ear canal with 50 ml ice cold water within 1 minute following irrigation. Irrigation of each ear canal should be done at least 5 minutes apart (cold caloric test).

• Facial sensory and motor responses: No corneal reflex to touch with a cotton swab, no jaw reflex, no grimacing to deep pain

• Pharyngeal and tracheal reflexes: No coughing or gagging when posterior pharynx is stimulated by a tongue blade; no cough response to bronchial suctioning (See Appendix 1, Cranial Nerves.)

• Apnea: No spontaneous respirations. Structured testing is required for diagnosis.

• Euvolemia: Patient does not exhibit signs of dehydration. If dehydration is present, patient must be hydrated prior to structured apnea testing.

Screening labwork

• Toxicology screen: Evaluates for presence of toxic doses of recreational drugs, medications, or poisons (see Drug Overdose, p. 868)

• Basic metabolic panel/blood chemistry: Identifies electrolyte imbalance, including hypoglycemia, hyperglycemia, and acidosis (using bicarbonate/CO₂). May also reflect patient’s volume status, including dehydration and hypovolemia (see Fluid and Electrolyte Disturbances, in p. 37).

• Arterial blood gas (ABG) analysis: Evaluates for hypoxia, acidosis, and hypercapnia (see Acid-Base Balance, p. 1).

Making the diagnosis of brain death

The three cardinal signs/symptoms in brain deat h are coma, absent brainstem reflexes, and apnea according to the AAN guidelines. Patients must have all three findings to be considered dead (brain dead patients are dead). There should be at least two separate clinical examinations, preferably by a neurologist, with at least 2 hours between examinations. If clinical uncertainty is present, two different physicians, preferably neurologists, should examine the patient following completion of appropriate diagnostic testing to ensure patient has not overdosed on a drug; has ingested a poison; has undiagnosed endocrine system dysfunction, electrolyte imbalance, or dehydration; and is free of untreated significant hypoxia, hypercapnia, or acidosis. Adherence to the AAN guidelines varies among the large medical centers in the United States. Diabetes insipidus, myxedema coma, and adrenal crisis may result from loss of the hypothalamic/pituitary regulatory axis as part of brain death. Large amounts of dextrose-containing IV fluids and insulin resistance may prompt hyperglycemia.

7-1 RESEARCH BRIEF

Guidelines for brain death determination are developed at an institutional level, according to the Uniform Determination of Death Act, which may lead to variability of practice. The authors evaluated the differences in brain death guidelines in major U.S. hospitals with strong neurology and neurosurgery services to determine variation from the guidelines of the American Academy of Neurology (AAN). Results revealed major discrepancies were present among institutions in the guidelines’ requirements for performance of the evaluation, prerequisites before testing, techniques used for the brainstem examination and apnea testing, and ancillary tests performed. Major differences exist in brain death guidelines used among the leading neurologic hospitals in the United States. Adherence to the AAN guidelines is variable. There may be substantial differences in practice, which might have consequences for the determination of death and initiation of transplant procedures.

From Greer DM, Varelas PN, Hague S, Wijdicks, EFM: Variability of brain death determination guidelines in leading US neurologic institutions. Neurology 70(4):284–289, 2008.

DIAGNOSTIC TESTS FOR BRAIN DEATH

Test	Purpose	Abnormal Findings
Arterial blood gas (ABG) analysis	Assesses for acidosis resulting from abnormal gas exchange or compensation for metabolic derangements	Low pH: Acidosis may reflect respiratory failure or metabolic crisis. Carbon dioxide: Elevated CO₂ or hypercapnia reflects respiratory failure; decreased CO₂ may reflect compensation for metabolic acidosis. Hypoxemia: PaO₂ less than 80 mm Hg Oxygen saturation: SaO₂ less than 92% Bicarbonate: HCO₃−less than 22 mEq/L Base deficit: less than –2
Apnea test • The ventilator is disconnected, the patient placed on 100% oxygen via T-tube and observed for apnea. Vital signs must be stable (mild hypothermia, normotensive BP, euvolemia, with normal Pao₂ and Pco₂) to begin the test. PaO₂, PCO₂, and pH are measured after approximately 8 minutes; the ventilator is reconnected after the ABG sample is drawn.

Test

Purpose

Abnormal Findings

Arterial blood gas (ABG) analysis

Assesses for acidosis resulting from abnormal gas exchange or compensation for metabolic derangements

Low pH: Acidosis may reflect respiratory failure or metabolic crisis.
Carbon dioxide: Elevated CO₂ or hypercapnia reflects respiratory failure; decreased CO₂ may reflect compensation for metabolic acidosis.
Hypoxemia: PaO₂ less than 80 mm Hg
Oxygen saturation: SaO₂ less than 92%
Bicarbonate: HCO₃−less than 22 mEq/L
Base deficit: less than –2

Apnea test

• The ventilator is disconnected, the patient placed on 100% oxygen via T-tube and observed for apnea. Vital signs must be stable (mild hypothermia, normotensive BP, euvolemia, with normal Pao₂ and Pco₂) to begin the test.

PaO₂, PCO₂, and pH are measured after approximately 8 minutes; the ventilator is reconnected after the ABG sample is drawn.

Validates absence of spontaneous respirations while ventilator is disconnected; test is designed to be completed safely, to avoid inducing cardiopulmonary instability during the procedure: Confirmatory findings
The apnea test is positive if:

• No spontaneous chest or abdominal excursions that produce reasonably normal, effective tidal volumes occur.

• The arterial Pco₂ is either more than 60 mm Hg or increased 20 mm Hg from the baseline Pco₂.

• The ventilator must be reconnected before 8 minutes due to instability/intolerance of test.

The apnea test is negative if:

• Effective respiratory movements are observed.

• Pco₂ does not increase by 20 mm Hg above baseline or is not more than 60 mm Hg.

Note: If the patient has severe facial trauma, preexisting abnormal pupils, sleep apnea, severe lung disease resulting in chronic hypercapnia (CO₂ retention), or toxic levels of any sedative drugs, aminoglycosides, tricyclic antidepressants, anticholinergics, antiepileptic drugs, chemotherapeutic agents, or neuromuscular blocking agents, additional testing may be required to confirm brain death. Additional confirmatory tests are not mandatory if the clinical diagnosis is positive (patient is unresponsive/in a coma, brainstem reflexes are absent, apnea test is positive). Cerebral angiography Assesses if cerebral perfusion is present Absent perfusion: No intracerebral blood filling is present at the level of the carotid bifurcation or circle of Willis. Electroencephalography (EEG) Assesses level of electrical activity of the brain (brain wave analysis) No signs of viability: No electrical activity during at least 30 minutes of recording, which meets the minimal technical criteria of EEG recording for brain viability; test adheres to American
Electroencephalographic Society criteria for those with suspected brain death. Transcranial Doppler ultrasonography Assesses for presence of cerebral perfusion and degree of vascular resistance using Doppler signals
Positive findings indicate very high vascular resistance resulting from markedly increased ICP. No functional blood flow: Small systolic peaks corresponding with early systole without diastolic flow or reverberating flow. Note: 10% of patients do not have temporal windows appropriate for transmitting ultrasound signals. Initial absence of Doppler signal does not confirm brain death. Cerebral perfusion scan using technetium-99m hexamethapropyleniamineoxime Assesses for cerebral circulation and brain cell viability using uptake of isotope as the criteria No circulation/no uptake: No uptake of isotope by brain cells (“hollow skull phenomenon”) Somatosensory evoked potentials Assesses for normal brain responses to electrical stimulation No response: Bilateral absence of N20-P22 response with median nerve stimulation

Collaborative management

ORGAN DONOR MANAGEMENT FOLLOWING BRAIN DEATH

Once brain death has been diagnosed, the organ removal team may begin preparations for organ removal within 5 minutes under ideal conditions. If the death was unanticipated, or organ donation was not discussed or controversial, additional time is needed for approaching the donor’s family/significant other(s) regarding donation. The parameters below must be managed in order to provide the best opportunity to recover viable organs from the donor.
Physiologic Parameter	Intervention
Maintain blood pressure.	MAP 60 to 70 mm Hg: maintain euvolemia; administer vasopressor agents (e.g., norepinephrine) if needed.
Monitor organ perfusion.	Monitor urine output and lactate level; consider hemodynamic monitoring with a pulmonary artery catheter.
Balance electrolytes.	Monitor electrolytes (Na⁺, K⁺) every 2 to 4 hours; correct to normal range.
Control diabetes insipidus.	Suspected diabetes insipidus (urine output more than 200 ml/hr, rising serum sodium): administer DDAVP (e.g., 2 to 4 mcg IV in adults) and replace volume loss with 5% dextrose.
Manage hyperglycemia.	Treat hyperglycemia: keep blood glucose 100 to 180 mg/dl.
Control hypothermia.	Keep temp greater than 35°C. Early use of warming blankets to prevent declining temperature is helpful; hypothermia is difficult to reverse once developed.
Ventilate and oxygenate.	Provide ongoing respiratory care: frequent suctioning, positioning/turning, PEEP, alveolar recruitment strategies.
Manage anemia.	Maintain hemoglobin at greater than 8 g/dl.
Control hormonal imbalances causing hemodynamic instability.	Consider hormonal replacement therapy if volume resuscitation and low-dose inotropes are ineffective for maintaining BP and/or if cardiac ejection fraction is less than 45%. Typical regimens include: Triiodothyronine (T₃): 4 mcg IV bolus, then 4 mcg/hr by IV infusion Arginine vasopressin (AVP): 0.5 to 2.4 units/hr to maintain MAP 60 to 70 mm Hg Methylprednisolone: 15 mg/kg IV single bolus

From the Australasian Transplant Coordinators Association Inc: National guidelines for organ and tissue donation, ed 3. 2006. http://www.atca.org.au/files/ATCAguidelinesonlineoct06.pdf

Care priorities

1. Confirm a clinical diagnosis of brain death:

Unresponsiveness or coma, absence of brainstem reflexes and apnea. Complete additional diagnostics as needed.

2. Allay doubts about the diagnosis:

When patient manifests the three cardinal findings of brain death recognized by the AAN, the health care team should educate the patient’s family members about signs and symptoms that may be present. The following findings commonly cause doubt about the diagnosis of brain death in both care providers and the patient’s family:

• Spontaneous movement of limbs: spinal reflex movements may occur.

• Respiratory-like movements of the chest and abdomen: shoulder elevation and adduction, back arching, intercostal expansion, which do not produce effective tidal volume

• Sweating, blushing, and tachycardia: residual autonomic responses

• Normal blood pressure without vasopressors or sudden increases in blood pressure: residual autonomic responses

• Absence of diabetes insipidus: does not occur in some patients

• Reflexes are present: deep tendon, superficial abdominal, triple flexion, Babinski

3. Discuss organ donation only after the clinical diagnosis of brain death has been made and the family understands the patient is dead.

Contact with the organ procurement organization should be done in a timely manner when death is imminent. Collaborate with the organ procurement organization to enhance the experience of the donation process. Do not broach the subject of donation or hint about donation prior to the time the patient has been pronounced dead, unless the patient had resolved the issue of organ donation with the family prior to death. The subject of organ donation is generally better discussed after the patient has been pronounced dead and the family understands that despite the patient having a beating heart, without mechanical ventilation, cardiac death will ensue. Choose a quiet, private, comfortable place to discuss organ donation, ideally leaving the lead role to a professional from the organ procurement agency. The family requires privacy, so they can express their grief regarding the death and can be left alone to discuss donation, if needed. Ensure all members of the team participating in the discussion are introduced to family members. All family members/significant others should be introduced to the team by name, and their role in the family/life of the deceased should be explained. Only those whom the next of kin requests to be present should participate in the discussion. Adequate time should be given asking/answering questions. The words used during the discussion are very important:

• Words to avoid: harvest, cadaver, remains, breathing, respirator, corpse, or any complex medical terminology

• Phrases to avoid: artificial life support, will live on in others, deeply comatose

• Words to include: the deceased patient’s name, ventilator, procurement, retrieval, donation, dead

• Phrases to include: time of death, wishes regarding organ donation, reasons for declining the opportunity, religious beliefs on organ donation

4. Maintain organs for donation if the family/significant others agree.

If the family agrees to donation, the next of kin/others chosen by next of kin are interviewed by the organ procurement team regarding the patient’s medical and social history. Reassure the family that the patient’s body will be handled with utmost care/respect to maintain dignity and will not be visibly disfigured. Offer the opportunity to view the patient’s body following donation. Major immediate threats to organ donation are development of pulmonary edema, hypotension, polyuria leading to dehydration from diabetes insipidus, and infection. Initiate measures discussed in the table on p. 626.

5. Discontinue life support after the family has had time to visit the patient, if the family declines the opportunity to donate the patient’s organs.

Weaning of mechanical ventilation and vasoactive drugs is unnecessary because the patient is dead. Reasons for declining donation generally relate to the wishes of the patient, religious convictions, fear of disfigurement/mutilation of the patient’s body, and mistrust of the motives or anger with the procurement team members. Mistrust and anger often ensue if the family is improperly approached regarding organ donation. Involving the experienced health care professionals from the organ procurement team has been shown to yield a higher success rate with donation.

CARE PLANS FOR BRAIN DEATH

Decreased intracranial adaptive capacity

Goals/outcomes

Patient is maximally supported for reduction of ICP until efforts are proved futile, when brain herniation ensues, resulting in brain death. Following brain death, hemodynamic status is supported until decisions are made regarding organ donation and/or discontinuation of life support.

Tissue Perfusion: Cerebral; Neurological Status: Consciousness.

Cerebral perfusion promotion

1. Consult with physician or midlevel practitioner to determine hemodynamic parameters.

2. Maintain hemodynamics within set parameters.

3. Administer osmotic diuretics/rheologic agents (e.g., mannitol, dextran) as ordered.

4. Administer vasopressin as ordered if diabetes insipidus ensues.

5. Keep blood glucose level within ordered range, avoiding hyperglycemia unless using medications which induce osmotic diuresis.

6. Avoid neck flexion or extreme hip/knee flexion.

7. Consult with physician regarding optimal elevation of the head of bed.

Cerebral edema management

1. Monitor neurologic status closely and compare with baseline.

2. Monitor respiratory status: rate, rhythm, depth of respirations, PaO₂, PCO₂, pH, and bicarbonate.

3. Monitor ICP and cerebral perfusion pressure (CPP) at rest and in response to patient care activities. Minimize activities that result in further increases in ICP.

Decisional conflict

Goals/outcomes

Family/support system is maximally supported in making judgments, and choosing between immediate discontinuation of life support, organ donation, or possibly continuing life support until information about brain death can be processed and accepted.

Decision Making; Information Processing; Dignified Life Closure; Acceptance: Health Status

Dying care

1. If cerebral perfusion promotion measures fail and brain death ensues, provide care appropriate for the dying.

2. Encourage family to share feelings about death.

3. Monitor deterioration of patient’s physical (and mental) capabilities.

4. Facilitate obtaining spiritual support for the family/significant others.

5. Facilitate discussion of funeral arrangements.

Coping enhancement

1. Assess the impact of the patient’s life situation on roles and relationships within family/support system.

2. Use a calm, reassuring approach.

3. Provide factual information concerning diagnosis, treatment, and prognosis.

4. Seek to understand the family’s perception of the stressful situation.

5. Acknowledge the patient and significant others’ religious, spiritual, and cultural beliefs surround death, dying, and organ donation.

6. Encourage gradual mastery of the situation if resistance or denial is impacting the family’s ability to accept the diagnosis of brain death.

7. Ensure the family understands brain dead patients are dead. Patients are no longer able to breathe without mechanical ventilation, will experience cardiac death when removed from mechanical ventilation, will never regain consciousness, will never interact with others, and have no ability to experience joy related to human life.

8. Explain the difference between brain death, persistent vegetative state, and cardiac death. The family and significant others may have difficulty understanding why brain dead patients are different than those in coma who can recover from their insult/injury and those in a vegetative state who can recover brainstem function to begin breathing spontaneously. Families may not be able to comprehend why when the brain is dead, the heart still functions unless mechanical ventilation is removed. Guilt may be associated with removal of mechanical ventilation since the patient appears “alive” with mechanical ventilation in place.

Emotional Support; Environmental Management; Fluid/Electrolyte Management; Fluid Monitoring; Hypovolemia Management; Infection Control; Intravenous Therapy; Mechanical Ventilation; Positioning; Surveillance; Respiratory Monitoring; Spiritual Support; Vital Signs Monitoring

Additional nursing diagnoses

As appropriate, see nursing diagnoses and interventions in Nutritional Support (p. 117), Acute Respiratory Failure (p. 383), Mechanical Ventilation (p. 99), Prolonged Immobility (p. 149), and Emotional and Spiritual Support of the Patient and Significant Others (p. 200).

Cerebral aneurysm and subarachnoid hemorrhage

Pathophysiology

An aneurysm is a localized dilation of an arterial lumen caused by weakness in the vessel wall—90% of cerebral aneurysms are berry or saccular, while the other 10% are fusiform, traumatic, septic, dissecting, and Charcot-Bouchard aneurysms. Recent research suggests that cerebral aneurysms result from degenerative vascular diseases complicated by hypertension and atherosclerosis. Aneurysms most often occur at the bifurcation of the blood vessels of the circle of Willis, with 85% in anterior cerebral circulation and 15% in posterior cerebral circulation. Approximately 25% of patients have multiple aneurysms.

The critical care nurse may care for a patient with an unruptured aneurysm or a patient who is post rupture and has a diagnosis of subarachnoid hemorrhage (SAH). Unruptured aneurysms may be asymptomatic, but nearly half of the affected population experiences some warning sign or symptom prior to rupture as a result of expansion of the lesion and compression of cerebral tissue. When rupture occurs, an SAH into the subarachnoid space (SAS) and basal cisterns results. If the patient survives the initial compromise of cerebral circulation from the force of hemorrhaging arterial blood, with sharply increased ICP, the next challenge is the possibility of rebleeding and cerebral arterial vasospasm. The greatest incidence of rebleeding is between 3 and 11 days after SAH, with the peak at day 7. Mortality is about 70% overall from aneurysmal SAH. Theories regarding the cause(s) of rebleeding involve the normal process of clot dissolution coupled with fluctuations in arterial pressure.

The major complication for which the critical care nurse monitors post rupture is the occurrence of delayed cerebral ischemia from cerebral arterial vasospasm, in which the constriction of the arterial smooth muscle layer of the major cerebral arteries causes a dramatic decrease in cerebral blood flow and leads to cerebral ischemia and progressive neurologic deficit. Vasospasm occurs in as many as 60% of patients 4 to 14 days following SAH, with incidence peaking between 7 and 10 days. The pathogenesis of cerebral vasospasm is poorly understood, but ongoing research indicates it may be directly related to the amount of blood in the SAS and basal cisterns. The greater the volume of blood, the more pronounced is the risk of vasospasm. As clots in the basal cisterns begin to hemolyze, substances may be released that precipitate vasospasms. Current treatments include careful fluid balance, “triple H” (hypervolemia-hemodilution-hypertension) therapy, calcium antagonists, balloon or chemical angioplasty, and possibly cisternal fibrinolytic drugs. The patient with a ruptured cerebral aneurysm and SAH is also at risk for communicating or obstructive hydrocephalus, hypothalamic dysfunction, and hyponatremia.

Some patients present with an obstructive hydrocephalus from intraventricular blood, but communicating hydrocephalus develops in approximately 20% of patients with SAH as a result of the presence of blood in the SAS and ventricular system. The hydrocephalus may be acute (occurs within less than 24 hours), subacute (occurs within less than 4 hours to 1 week), or delayed (beginning 10 or more days after SAH). Blood in the SAS and ventricles obstructs the flow of CSF, interferes with circulation and resorption of CSF, and causes increased ICP, with concomitant worsening of neurologic status. In some patients, the hydrocephalus produces minimal symptoms and resolves without medical intervention, while others may require temporary or permanent diversion of CSF circulation to achieve symptom relief.

Hypothalamic dysfunction, seen in approximately one-third of patients with hydrocephalus after SAH, may result from mechanical pressure on the hypothalamus from a dilated third ventricle. The increased pressure causes an increase in the releasing hormones from the hypothalamus, which activates the hypothalamic-pituitary axis of the anterior pituitary as well as stimulating the production of antidiuretic hormone (ADH) by the posterior pituitary gland. The response to the increased adrenocorticotropic hormone (ACTH) from the anterior pituitary gland mimics an exaggerated stress response, which includes a marked increase in serum catecholamines leading to overstimulation of the sympathetic nervous system. The vasoconstrictive response is severe enough in a subset of patients to cause “stunned myocardium,” similar to what is seen with an acute myocardial infarction.

The surge of ADH from the posterior pituitary results in SIADH, which may include hyponatremia caused by cerebral salt-wasting syndrome, or a combination of factors influencing sodium and water metabolism (Table 7-1). Fluid management strategies in this patient population may be difficult (see Syndrome of Inappropriate Antidiuretic Hormone, p. 734). Hyponatremia may occur in 10% to 50% of patients with SAH. Untreated hyponatremia may lead to intracranial hypertension, cerebral ischemia, seizures, coma, and death.

Table 7-1 CLINICAL PRESENTATION WITH CEREBRAL SALT-WASTING SYNDROME VS SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)

Cerebral Salt-Wasting Syndrome	SIADH
Hypotension	Normotension
Postural hypotension	Normotension
Tachycardia	Normal pulse rate or bradycardia
Elevated hematocrit	Normal or low hematocrit
Decreased glomerular filtration rate	Increased glomerular filtration rate
Normal or elevated BUN and creatinine	Normal or decreased BUN and creatinine
Normal or low urine output	Normal or low urine output
Hypovolemia	Normovolemia or hypervolemia
Dehydration	Normal hydration
True hyponatremia	Dilutional hyponatremia
Hypo-osmolality	Hypo-osmolality
Decreased body weight	Increased body weight