Nursing Diagnosis: Application to Clinical Practice
11th Edition

Potential Complication: Neurologic/Sensory
PC: Neurologic/Sensory: Describes a person experiencing or at high risk to experience various neurologic or sensory dysfunctions
Significant Laboratory/Diagnostic Assessment Criteria
Cerebrospinal Fluid
Protein (increased in meningitis)
White blood cell (WBC) count (increased in meningitis)
Albumin (elevated with brain tumors)
Glucose (decreased with bacterial meningitis)
WBC count (elevated with bacterial infection, decreased in viral infection)
Alcohol level
Glucose calcium
Mercury, lead levels if indicated

Skull, spine x-rays
Computed tomography (CT)
Magnetic resonance imaging (MRI)
Cerebral angiography
Lumbar puncture
Electroencephalography (EEG)
Continuous bedside cerebral blood flow monitoring
PC: Increased Intracranial Pressure: Describes a person experiencing or at high risk to experience increased pressure (<15 mm Hg) exerted by cerebrospinal fluid within the brain’s ventricles or the subarachnoid space
High-Risk Populations
  • Intracerebral mass (lesions, hematomas, tumors, abscesses)
  • Blood clots
  • Blockage of venous outflow
  • Head injuries
  • Reye’s syndrome
  • Meningitis
  • Premature birth
  • Cranial surgery
Nursing Goals
The nurse will manage and minimize episodes of increased intracranial pressure (ICP).
General Interventions and Rationales
  • Monitor for signs and symptoms of increased ICP.
    • Assess the following:
      • Best eye opening response: spontaneously, to auditory stimuli, to painful stimuli, or no response
      • Best motor response: obeys verbal commands, localizes pain, flexion–withdrawal, flexion–decorticate, extension–decerebrate, or no response
      • Best verbal response: oriented to person, place, and time; confused conversation; inappropriate speech; incomprehensible sounds; or no response
      (Deficiencies of cerebral blood supply resulting from hemorrhage, hematoma, cerebral edema, thrombus, or emboli compromise cerebral tissue. These responses evaluate the client’s ability to

      integrate commands with conscious and involuntary movement. The nurse can assess cortical function by evaluating eye opening and motor response. No response may indicate damage to the midbrain.)
    • Assess for changes in vital signs:
      • Pulse changes: slowing rate to 60 beats/min or lower or increasing rate to 100 beats/minor higher (Bradycardia is a late sign of brain stem ischemia. Tachycardia may indicate hypothalamic ischemia and sympathetic discharge.)
      • Respiratory irregularities: slowing rate with lengthening apneic periods (Respiratory patterns vary depending on the site of impairment. Cheyne-Stokes breathing [a gradual increase followed by a gradual decrease, then a period of apnea] points to damage in both cerebral hemispheres, midbrain, and upper pons. Central neurogenic hyperventilation occurs with midbrain and upper pontine lesions. Ataxic breathing [irregular with random sequence of deep and shallow breaths] indicates pontine dysfunction. Hypoventilation and apnea occur with medullary lesions.)
      • Rising blood pressure and/or widening pulse pressure
      • Bradycardia, increased systolic blood pressure, and increased pulse pressure (These are late signs of brain stem ischemia leading to cerebral herniation.)
    • Assess pupillary responses. (Changes indicate pressure on oculomotor or optic nerves.)
      • Inspect the pupils with a bright pinpoint light to evaluate size, configuration, and reaction to light. Compare both eyes for similarities and differences. (The oculomotor nerve [cranial nerve III] in the brain stem regulates pupil reactions.)
      • Evaluate gaze to determine whether it is conjugate (paired, working together) or if eye movements are abnormal. (Conjugate eye movements are regulated from parts of the cortex and brain stem.)
      • Evaluate the ability of the eyes to adduct and abduct. (Cranial nerve VI, or the abducens nerve, regulates abduction and adduction of the eyes. Cranial nerve IV, or the trochlear nerve, also regulates eye movement.)
    • Note any other signs and symptoms:
      • Vomiting (Vomiting results from pressure on the medulla, which stimulates the brain’s vomiting center.)
      • Headache: constant, increasing in intensity, or aggravated by movement
      • Straining (Compression of neural tissue increases ICP and causes pain.)
      • Subtle changes (eg, lethargy, restlessness, forced breathing, purposeless movements, changes in mentation; These signs may be the earliest indicators of cranial pressure changes.)
    • Elevate the head of the bed 30 to 45 degrees unless contraindicated. (Slight head elevation can aid venous drainage to reduce cerebrovascular congestion, thereby decreasing ICP.)
    • Avoid the following situations or maneuvers, which can increase ICP (Porth, 2002):
      • Carotid massage (This slows the heart rate and reduces systemic circulation, which is followed by a sudden increase in circulation.)
      • Neck flexion or extreme rotation (This inhibits jugular venous drainage, which increases cerebrovascular congestion and ICP.)
      • Digital anal stimulation, breath-holding, straining (These can initiate the Valsalva maneuver, which impairs venous return by constricting the jugular veins, thus increasing ICP.)
      • Extreme flexion of the hips and knees (Flexion increases intrathoracic pressure, which inhibits jugular venous drainage, increasing cerebrovascular congestion and, thus, ICP.)
      • Rapid position changes
    • Teach client to exhale during position changes. (This helps prevent the Valsalva maneuver.)
    • Consult with the physician or nurse practitioner for stool softeners, if needed. (Stool softeners prevent constipation and straining during defecation, which can trigger the Valsalva maneuver.)
    • Maintain a quiet, calm, softly lit environment. Schedule several lengthy periods of uninterrupted rest daily. Cluster necessary procedures and activities to minimize interruptions. (These measures promote rest and decrease stimulation, both of which can help decrease ICP.)
    • Avoid sequential performance of activities that increase ICP (eg, coughing, suctioning, repositioning, bathing). (Research has validated that such sequential activities can cause a cumulative increase in ICP [Porth, 2002].)
    • Monitor temperature. As indicated, initiate external hypothermia or hyperthermia measures per orders and institutional protocol. (Impaired hypothalamic function can interfere with temperature regulation, necessitating intervention. Hypothermia may reduce ICP, whereas hyperthermia may increase it.)
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    • Limit suctioning time to 10 s at a time; hyperoxygenate and hyperventilate client both before and after suctioning. (These measures help prevent hypercapnia, which can increase cerebral vasodilation and raise ICP, and prevent hypoxia, which may increase cerebral ischemia.)
    • Consult with physician or advanced practice nurse about administering prophylactic lidocaine before suctioning. (This measure may help prevent acute intracranial hypertension [Thelan et al., 1998].)
    • Maintain optimal ventilation through proper positioning and regular suctioning. (These measures help prevent hypoxemia and hypercapnia.)
    • Monitor arterial blood gas (ABG) values. (ABG values help evaluate gas exchangein the lungs and determine circulating oxygen level and arterial CO2. It isrecommended that arterial O2 be between 90 and 100 torr, and that arterial CO2 be between 25 and 30 mm Hg, to prevent cerebral ischemia and cerebrovascular congestion, which increase ICP.)
    • If indicated, initiate protocols or collaborate with physician or advanced practice nurse for drug therapy, which may include the following (Thelan et al., 1998):
      • Sedation, barbiturates (These drugs reduce cerebral metabolic rate, contributing to decreased ICP.)
      • Anticonvulsants (These agents help prevent seizures, which increase cerebral metabolic rate.)
      • Osmotic diuretics (These agents draw water from brain tissue to the plasma to reduce cerebral edema.)
      • Nonosmotic diuretics (These agents draw sodium and water from edematous areas to reduce cerebral edema.)
      • Steroids (These drugs can reduce capillary permeability, limiting cerebral edema.)
    • Carefully monitor hydration status; evaluate fluid intake and output, serum osmolality, and urine specific gravity and osmolality. (Dehydration from diuretic therapy can cause hypotension and decreased cardiac output.)
    • If intravenous (IV) fluid therapy is prescribed, carefully administer IV fluids with an infusion pump. (Careful IV fluid administration is necessary to prevent overhydration, which increases ICP.)
    • If using an ICP monitoring device, refer to the procedure manual for guidelines (eg, ventriculostomy, subarachnoid bolt, epidural monitor).
PC: Seizures: Describes a person experiencing or at high risk to experience paroxysmal episodes of involuntary muscular contraction (tonus) and relaxation (clonus)
High-Risk Populations
  • Perinatal injuries
  • Family history of seizure disorder
  • Cerebral cortex lesions
  • Head injury
  • Infectious disorder (eg, meningitis)
  • Cerebral circulatory disturbance (eg, cerebral palsy, stroke)
  • Brain tumor
  • Alcohol overdose or withdrawal
  • Drug overdose or withdrawal (eg, theophylline)
  • Electrolyte imbalances (eg, hypocalcemia, pyridoxine deficiency)
  • Hypoglycemia
  • High fever
  • Eclampsia
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  • Metabolic abnormalities (renal, hepatic, electrolyte)
  • Poisoning (mercury, lead, carbon monoxide)
Nursing Goals
The nurse will manage and minimize seizure episodes.
General Interventions and Rationales
  • Determine whether the client senses an aura before onset of seizure activity. If so, reinforce safety measures to take during an aura (eg, lie down, pull car over to roadside and shut off ignition).
  • If seizure activity occurs, observe and document the following (Hickey, 2002):
    • Where seizure began
    • Type of movements, parts of body involved
    • Changes in pupil size or position
    • Urinary or bowel incontinence
    • Duration
    • Unconsciousness (duration)
    • Behavior after seizure
    • Weakness, paralysis after seizure
    • Sleep after seizure (postictal period)
    (Progression of seizure activity may assist in identifying its anatomic focus.)
  • Provide privacy during and after seizure activity. (To protect the client from embarrassment)
  • During seizure activity, take measures to ensure adequate ventilation (eg, loosen clothing). Do not try to force an airway or tongue blade through clenched teeth. (Strong clonic/tonic movements can cause airway occlusion. Forced airway insertion can cause injury.)
  • During seizure activity, gently guide movements to prevent injury. Do not attempt to restrict movements. (Physical restraint could result in musculoskeletal injury.)
  • If the client is sitting when seizure activity occurs, ease him or her to the floor and place something soft under his or her head. (These measures help prevent injury.)
  • After seizure activity subsides, position client on the side. (This position helps prevent aspiration of secretions.)
  • Allow person to sleep after seizure activity; reorient on awakening. (The person may experience amnesia; reorientation can help him or her regain a sense of control and can help reduce anxiety.)
  • If person continues to have generalized convulsions, notify physician or advanced practice nurse and initiate protocol:
    • Establish airway.
    • Suction PRN.
    • Administer oxygen through nasal catheter.
    • Initiate an IV line.
    (Status epilepticus is a medical emergency with a 10% mortality rate. Impaired respiration can cause systemic and cerebral hypoxia. IV administration of a rapid-acting anticonvulsant [eg, diazepam] is indicated [Hickey, 2002].)
  • Keep the bed in a low position with the siderails up, and pad the siderails with blankets. (These precautions help prevent injury from fall or trauma.)
  • If the client’s condition is chronic, evaluate the need for teaching self-management techniques. Use the nursing diagnosis Risk for Ineffective Therapeutic Regimen Management related to insufficient knowledge of condition, medication regimen, safety measures, and community resources (see Section II).

PC: Increased Intraocular Pressure: Describes a person experiencing or at high risk to experience increased aqueous humor production or resistance to outflow, which can cause compression of nerve fibers and blood vessels in the optic disc (Schremp 1995a)
High-Risk Population
  • Glaucoma
  • Corneal transplant
  • Radiation therapy
  • Eye trauma
  • Ophthalmic surgery
Nursing Goals
The nurse will manage and minimize increased intraocular pressure.
General Interventions and Rationales
  • Reinforce prescribed postoperative activity restrictions, which may include avoiding the following:
    • Bending at the waist
    • Making sudden head movements
    • Valsalva maneuver (eg, straining during bowel movements)
    (These activities can increase intraocular pressure.)
  • Reinforce the need to wear eye protection (patch and shield). (These protect the eye from trauma.)
  • Monitor for bleeding, dehiscence, and evisceration. (Ocular tissue is vulnerable to these problems because of its high vascularity and fragile vessels.)
  • Monitor for signs and symptoms of increased intraocular pressure:
    • Eyebrow pain
    • Nausea
    • Halos around lights
    (Intraocular pressure may increase in response to surgery or owing to medications, such as steroid eye drops [Schremp, 1995b].)
  • Administer an antiemetic if nausea develops. (Vomiting increases intraocular pressure and must be avoided.)
  • Monitor visual acuity and note any changes (eg, halos around lights). (Factors that can alter vision include blood in the vitreous or from the incision, infection, dislocation of the lens implant, redetachment of the retina, and increased intraocular pressure.)
  • Position client on the back with the head elevated; turn on the unaffected side. (This positioning can help reduce pressure in the affected eye.)
  • Maintain a quiet environment; limit external stimuli and activities. (These measures can help reduce stress and may promote a decrease in intraocular pressure.)

PC: Neuroleptic Malignant Syndrome (NMS): Describes a person experiencing or at high risk toexperience an acute, life-threatening reaction to neuroleptic medication. The pathophysiology of NMS is poorly understood, but like other forms of extrapyramidal symptoms, there appear to beneuroleptic-induced dopaminergic blockade and dopamine depletion in the CNS, particularly in the basal ganglia and hypothalamus, which causes the various symptoms. It is most often characterized by the rapid onset of severe muscular rigidity, autonomic instability, hyperthermia, and deteriorating mental state. It occurs in 1% of clients receiving neuroleptic agents.
High-Risk Populations
  • Use of neuroleptics, especially the higher-potency drugs haloperidol, fluphenazine, and chlorpromazine
  • Use of long-acting depot neuroleptics
  • Use of neuroleptic medications in combination with:
    • Concurrent lithium therapy
    • Physiologic stress
    • Nutritional deficiencies
    • Concurrent organic brain syndrome
    • Physical exhaustion
    • Dehydration
    • Acquired immunodeficiency syndrome (AIDS)
    • Restraints
    • Anticholinergic drugs
    • Agitation
    • Mood disorders
    • High temperature and humidity
  • High doses of neuroleptics
  • Concurrent use of two or more neuroleptics
  • Previous history of NMS
  • Male gender, younger than 40 years of age (80% of cases)
  • Undergoing “rapid neuroleptization,” especially if administered by injections
  • Initial 2 weeks of therapy, although it can occur at any point in neuroleptic therapy (eg, 16% within 24 h of administration)
  • Discontinuation of antiparkinsonian drugs
Nursing Goals
The nurse will manage and minimize NMS episodes.
General Interventions and Rationales
  • Hold doses of all neuroleptic drugs and drugs with anticholinergic properties, and notify physician.
  • Maintain airway. Provide a calm environment. (Any client with altered level of consciousness is at risk for airway compromise and hypoventilation. Chest wall muscle rigidity also contributes.)
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  • Recognize and treat promptly cardiac dysrhythmias and blood pressure instabilities as necessary.
  • Monitor for signs and symptoms.
    • Severe extrapyramidal symptoms:
      • Muscular rigidity
      • Dysarthria
      • Dysphagia (difficulty swallowing)
      • Excess salivation
      • Myoglobinuria (urine turning red)
      • Akinesis
      • Cogwheel rigidity
      • Muteness
      • Waxy flexibility
      • Exaggerated deep tendon reflexes
    • Autonomic dysfunction:
      • Tachycardia
      • Diaphoresis
      • Urinary incontinence
      • Labile or sustained hypertension
      • Hypotension (abnormal blood pressure)
      • Dyspnea
      • Tachypnea
      • Pallor
      • Cardiac dysrhythmias
    • Fever above 100°F
    • Behavioral changes or fluctuations (eg, confusion, delirium, agitation, coma, catatonic-like posturing, combativeness)
    • Dehydration
    • Malnutrition
    (The underlying pathophysiology is not well understood but appears to be related to the blockage or depletion of the CNS neurotransmitter dopamine. Signs and symptoms of NMS appear to be related to the degree and sites of involvement of dopamine blockade. For example, dopamine blockade in the nigrostriatal pathway appears to cause muscular rigidity; dopamine impairment in the preoptic anterior hypothalamus, which regulates temperature, appears to cause fever; dopamine disturbance in the spinal cord may cause autonomic dysfunction.)
  • Monitor for abnormal laboratory findings:
    • Elevated creatine phosphokinase
    • Elevated WBC count
    • Elevated liver functions
    • ABG
    • Electrolytes
    (As the body reacts to dopamine depletion, WBC count rises, creatine phosphokinase is elevated because of micronecrosis of the skeletal muscles, and hepatic enzymes are elevated. Blood gas determinations measure the degree of autonomic instability. Electrolytes measure the effect of autonomic instability and micronecrosis on the body systems.)
  • Assess vital signs frequently (blood pressure; temperature, pulse, respiration; and electrocardiogram) for signs of respiratory and cardiovascular decompensation.
  • Monitor degree of rigidity through deep tendon reflexes. If rigidity is worsening, further measures must be taken because it can affect the muscles of the vital organs. (Deep tendon reflexes indicate objectively whether the rigidity is worsening or improving.)
  • Institute seizure precautions.
  • Monitor fluid intake and output and for signs of renal decompensation. (Excessive muscle breakdown [micronecrosis] can cause myoglobinuria and renal failure.)
  • Auscultate and evaluate lungs for pulmonary stasis and embolus. (Dysphagia can lead to aspiration pneumonia. Immobility places a person at risk for pulmonary stasis or embolus.)
  • If dantrolene is ordered to help decrease muscle rigidity, remain alert for:
    • Liver toxicity
    • Phlebitis and tissue damage (if administered IV)
    (Dantrolene, a skeletal muscle relaxant, acts at the level of the sarcoplasmic reticulum, complementing the effects of a dopaminergic agent.)
  • Apply cooling blankets, antipyretic medications, and cool sponge baths (to control fever).
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  • If dysphagia is present:
    • Monitor food intake closely.
    • Provide soft or liquid diet.
    • Tube feedings or total parenteral nutrition if nutritional status continues to decline
    • Refer also to Impaired Swallowing.
  • Refer to Risk for Impaired Skin Integrity to prevent pressure ulcers. (Profuse diaphoresis, dehydration, urinary incontinence, and contracted limbs set the stage for skin breakdown.)
  • Provide mouth care and suctioning as needed. (Dysphagia can cause increased salivation.)
  • Apply eye patches and lubricants as needed. (These prevent exposure keratitis secondary to inadequate blinking.)
  • After recovery:
    • Teach client and significant others the importance of maintaining proper nutrition, sleep, and exercise. (Physiologic depletion predisposes the person to NMS.)
    • Review manifestations of NMS and teach client and significant others to seek immediate medical help if stiffness, fever, excess sweating, and racing pulse occur. (Early detection can prevent serious complications; NMS has an 11.6% mortality rate.)
  • Institute seizure precautions.
PC: Alcohol Withdrawal: Describes a person experiencing or at high risk to experience the complications of alcohol withdrawal (eg, delirium tremens, autonomic hyperactivity, seizures, alcohol hallucinosis, and hypertension)
High-Risk Populations
Nursing Goals
The nurse will manage and minimize alcohol withdrawal complications.
General Interventions and Rationales
  • Carefully attempt to determine if the client abuses alcohol. Consult with the family regarding their perception of alcohol consumption. Explain why accurate information is necessary. (It is critical to identify high-risk people so potentially fatal withdrawal symptoms can be prevented.)
  • Obtain history of previous withdrawals.
    • Delirium tremens:
      • Time of onset
      • Manifestation
    • Seizures:
      • Time of onset
      • Type

    (Withdrawal occurs 6 to 96 h after drinking ends. Withdrawal can occur in people who are considered “social drinkers” [6 oz of alcohol daily for a period of 3 to 4 weeks]. Withdrawal patterns may resemble those of previous episodes. Seizure patterns unlike previous episodes may indicate another underlying pathology.)
  • Obtain a complete history of prescription and nonprescription drugs taken. (Benzodiazepine or barbiturate withdrawal may mimic alcohol withdrawal and complicate the picture.)
  • Consult with the primary provider regarding the risk of the client and initiation of benzodiazepine therapy, with dosage determined by assessment findings. (Benzodiazepine requirements in alcohol withdrawal are highly variable and client specific. Fixed schedules may oversedate or undersedate.)
  • Observe for the desired effects of benzodiazepine therapy:
    • Relief from withdrawal symptoms
    • Peaceful sleep but rousable
    (Benzodiazepines are the drugs of choice in controlling withdrawal symptoms. Neuroleptics cause hypotension and lower seizure threshold. Barbiturates may effectively control symptoms of withdrawal but have no advantages over benzodiazepines.)
  • Monitor for indicators of a drop in blood alcohol level and determine the time of onset:
    • Anxiety
    • Insomnia
    • Mild tachycardia
    • Tremors
    • Sensory hyperacuity
    • Low-grade fever
    • Disorientation
    • Dehydration
    (Once a level drops 100 mg/dL below the person’s normal, withdrawal typically occurs. These symptoms can last up to 5 days. Withdrawal results in a hypermetabolic state from adrenergic excess and possible alteration of prostaglandin E1 levels.)
  • Monitor for withdrawal seizures.
    (Withdrawal seizures can occur 6 to 96 h after drinking ends. They are usually nonfocal and grand mal, last minutes or less, and occur singly or in clusters of two to six.)
  • Monitor for and intervene promptly in cases of status epilepticus. Follow institution’s emergency protocol. (Status epilepticus is life-threatening if not controlled immediately with IV diazepam.)
  • Monitor for delirium tremens.
    • Delirium component (vivid hallucinations, confusion, extreme disorientation, and fluctuating levels of awareness)
    • Extreme hyperadrenergic stimulation (tachycardia, hypertension or hypotension, extreme tremor, agitation, diaphoresis, and fever)
    (Delirium tremens appears on either the 4th or 5th day after cessation of drinking and resolves within 5 days.)
  • Monitor and determine onset of alcohol hallucinosis, which involves visual, auditory, and tactile hallucinations (however, the person senses that the hallucinations are not real and is aware of surroundings). (Alcohol hallucinosis occurs 6 to 96 h after abstinence and can last up to 3 days.)
  • Monitor vital signs every 2 h:
    • Temperature, pulse, and respiration
    • Blood pressure
    (Clients in withdrawal have elevated heart rate, respirations, and fever. Clients experiencing delirium tremens can be expected to have a low-grade fever. Rectal temperature greater than 37.7°C (99.9°F) is a clue to possible infection.)
  • Maintain the client’s IV running continuously. (This is necessary for fluid replacement and dextrose, thiamine bolus, benzodiazepine, and magnesium sulfate administration. Chlordiazepoxide and diazepam should not be given IM because of unpredictable absorption.)
  • Refer to the nursing diagnosis Ineffective Denial for interventions for substance abuse.