Section 9.2: Sensory-Perception and Neurologic/Coordination Disorders

Sensory-Perception Disorders

Sensory-perception and neurological disorders represent critical competencies on the Philippine Nurse Licensure Examination (PNLE). These conditions require a high degree of clinical vigilance, as errors in nursing management can lead to permanent disability, blindness, or death. Under the Philippine Nursing Act of 2002 (RA 9173), nurses must independently identify acute changes and implement evidence-based safety measures.

Cataracts

A cataract is an opacity or clouding of the crystalline lens of the eye, which normally focuses light onto the retina.

• Pathophysiology: Most commonly caused by the aging process (senile cataracts) due to clumping of lens proteins and water loss, leading to a loss of lens elasticity and transparency. Other risk factors include ocular trauma, maternal rubella, diabetes mellitus, prolonged corticosteroid use, and excessive ultraviolet light exposure.
• Visual Changes: Patients experience a gradual, painless, and progressive blurring of vision. Classic signs include:
  • Decreased visual acuity (especially at night).
  • Glare and abnormal sensitivity to bright light (e.g., headlights while driving).
  • Halos around lights.
  • Faded or yellowed color perception.
  • No pain or redness is associated with age-related cataracts.
• Post-operative Nursing Care: Following cataract extraction (usually via phacoemulsification with an intraocular lens implant), nursing care focuses on preventing infection and avoiding an increase in Intraocular Pressure (IOP), which can disrupt the suture line.
  • Patient Education to Prevent Elevated IOP: Instruct the patient to avoid bending at the waist (keep the head above the level of the chest), lifting objects heavier than 5–10 pounds, coughing, sneezing, vomiting, blowing the nose forcefully, and straining during bowel movements (Valsalva maneuver). Administer prescribed stool softeners (e.g., docusate sodium) to prevent straining.
  • Positioning: Position the client in a semi-Fowler's position. Instruct the patient to sleep on the back or on the unoperated side to prevent pressure on the surgical eye and reduce orbital edema.
  • Safety & Protection: Apply an eye patch and a metal shield as prescribed to protect the eye from accidental trauma, especially during sleep.
  • Eye Drops Instillation Technique: Teach the patient and family the correct method for administering eye drops (antibiotic and anti-inflammatory drops):
    1. Wash hands thoroughly.
    2. Tilt the head back, look upward, and gently pull the lower eyelid down to form a small conjunctival pouch.
    3. Instill the prescribed number of drops into the conjunctival sac, never directly onto the cornea.
    4. Close the eye gently; do not squeeze or rub the eye.
    5. Apply gentle pressure to the lacrimal duct (inner canthus) for 1 to 2 minutes to prevent systemic absorption of the medication.

Glaucoma

Glaucoma is a group of ocular disorders characterized by an increase in Intraocular Pressure (IOP), optic nerve atrophy, and progressive visual field loss. Normal IOP is 10 to 21 mmHg, maintained by a balance between the production of aqueous humor by the ciliary body and its drainage through the trabecular meshwork and Canal of Schlemm.

• Primary Open-Angle Glaucoma (POAG): The most common type. The drainage channel (trabecular meshwork) becomes clogged or narrow, but the angle remains open.
  • Manifestations: Slow, progressive, painless, and bilateral loss of peripheral vision (often described as tunnel vision). The patient is typically asymptomatic in the early stages, earning POAG the nickname "the thief in the night."
• Primary Angle-Closure Glaucoma (PACG): A medical emergency. The iris bulges forward, physically blocking the drainage angle, leading to a rapid, complete obstruction of aqueous humor drainage.
  • Manifestations: Sudden onset of excruciating eye pain, severe headache, nausea and vomiting, blurred vision, rainbow-colored halos around lights, a fixed, semi-dilated pupil, and a cloudy/hazy cornea. The IOP is extremely elevated (often $> 50 ext{ mmHg}$).
• Pharmacotherapy:
  1. Miotics (Cholinomimetics): E.g., Pilocarpine. Works by causing pupillary constriction (miosis). This pulls the iris away from the trabecular meshwork, opening the drainage angle and facilitating the outflow of aqueous humor.
  2. Beta-Blockers: E.g., Timolol. Decreases the production of aqueous humor by the ciliary body.
     • Nursing Responsibility: After instilling timolol, perform punctal occlusion (lacrimal pressure) for 2 minutes to prevent systemic absorption, which can cause bradycardia, hypotension, and bronchospasm (contraindicated in patients with asthma, COPD, or severe bradycardia).
  3. Mydriatics: E.g., Atropine, Epinephrine. These agents dilate the pupil (mydriasis). Mydriatics are strictly contraindicated in glaucoma, especially angle-closure, because dilating the pupil folds the iris back into the drainage angle, completely blocking outflow and causing a catastrophic spike in IOP.

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Neurologic and Coordination Disorders

Cerebrovascular Accident (CVA) / Stroke

A stroke is a sudden disruption of blood flow to the brain, causing oxygen deprivation and rapid cell death.

• Ischemic Stroke: Caused by occlusion of a cerebral artery by a thrombus or embolus. Accounts for approximately 85% of cases.
• Hemorrhagic Stroke: Caused by the rupture of a cerebral blood vessel (e.g., ruptured aneurysm, arteriovenous malformation [AVM], or chronic uncontrolled hypertension), leading to bleeding into the brain parenchyma or subarachnoid space. tPA is strictly contraindicated due to the risk of fatal hemorrhage.
• Tissue Plasminogen Activator (tPA) Protocol (for Ischemic Stroke):
  • tPA is a thrombolytic agent that dissolves clots and restores perfusion.
  • Time Window: Must be administered within 3 to 4.5 hours of the "last known well" (LKW) time.
  • Inclusion Criteria: Measurable neurological deficit; onset of symptoms within the time window.
  • Exclusion Criteria (Contraindications):
    • Active internal bleeding or bleeding diathesis.
    • History of hemorrhagic stroke or intracranial neoplasm.
    • Recent intracranial or intraspinal surgery, head trauma, or stroke within the past 3 months.
    • Uncontrolled hypertension (systolic BP $> 185 ext{ mmHg}$ or diastolic BP $> 110 ext{ mmHg}$); blood pressure must be lowered below this threshold before tPA can be administered.
    • Platelet count $< 100,000/ ext{mm}^3$ or elevated INR.
  • Nursing Management: Monitor blood pressure every 15 minutes during infusion. Maintain blood pressure below 180/105 mmHg post-tPA. Monitor for signs of bleeding (hematuria, epistaxis, gingival bleeding, mental status changes). Avoid invasive procedures (NG tube, Foley catheter, venipunctures) for 24 hours post-infusion.
• Motor and Speech Deficits:
  • Contralateral Deficits: Due to decussation of motor pathways in the medulla, a stroke in the left hemisphere causes right-sided hemiplegia (paralysis) or hemiparesis (weakness), and vice versa.
  • Left-Hemisphere Stroke: Associated with speech and language deficits, as the dominant speech centers (Broca's and Wernicke's areas) are typically in the left hemisphere. The patient is often cautious, slow, and anxious.
    • Broca's (Expressive) Aphasia: Damage to the frontal lobe. The client understands spoken language but cannot produce meaningful speech. Speech is effortful, slow, and telegraphic.
    • Wernicke's (Receptive) Aphasia: Damage to the temporal lobe. The client cannot comprehend spoken or written language. Speech is fluent but lacks meaning (word salad).
    • Global Aphasia: Severe loss of both expressive and receptive abilities.
  • Right-Hemisphere Stroke: Associated with spatial-perceptual deficits, neglect syndrome (ignoring the left side of the body), impulsivity, poor judgment, and lack of awareness of deficits (anosognosia), making them a high safety risk.
• Rehabilitation Phase:
  • Dysphagia Screening: Keep the patient NPO until a formal swallowing screen is passed. Sit the patient at a 90-degree angle during meals, place food on the unaffected side of the mouth, tuck the chin down when swallowing, and monitor for coughing or pocketing of food.
  • Unilateral Neglect Care: For patients with left-sided neglect, initially place objects within their right visual field. As rehab progresses, encourage them to scan the environment to the left and place items on the left to promote awareness.
  • Positioning: Use splints and hand rolls to prevent contractures. Use footboards or high-top sneakers to prevent foot drop.

Increased Intracranial Pressure (ICP)

The Monro-Kellie Doctrine states that the cranial vault is a rigid container with a fixed volume. It contains three components: brain tissue (80%), blood (10%), and cerebrospinal fluid (CSF) (10%). An increase in the volume of any one component must be compensated by a decrease in another, or the intracranial pressure will rise. Normal ICP is 5 to 15 mmHg.

• Clinical Presentation:
  • Earliest Sign: A change in the Level of Consciousness (LOC). Restlessness, agitation, irritability, or mild confusion are the first indicators of cerebral hypoxia.
  • Other Early Signs: Constant, generalized headache (worsened by coughing or straining); pupillary sluggishness.
  • Late Signs: Progressive lethargy, stupor, and coma. Fixed, dilated, nonreactive pupils ("blown pupil"). Abnormal motor posturing:
    • Decorticate (Flexion): Internal rotation and adduction of arms, flexion of elbows, wrists, and fingers. Indicates damage to the cerebral hemispheres.
    • Decerebrate (Extension): Adduction and rigid extension of arms, pronated forearms, legs stiffly extended with plantar flexion. Indicates damage to the brainstem (ominous sign).
  • Cushing's Triad: A late, classic sign of impending brain herniation:
    1. Systolic hypertension with a widening pulse pressure (systolic BP rises while diastolic BP drops/stays constant).
    2. Bradycardia (slow, bounding pulse).
    3. Irregular respirations (Cheyne-Stokes or biot breathing).
• Nursing Management to Promote Venous Drainage:
  1. Elevate the head of the bed (HOB) to 30 degrees (never flat, and avoid raising above 45 degrees as hip flexion increases intra-abdominal pressure).
  2. Maintain the head and neck in a neutral, midline alignment. Avoid neck flexion or lateral rotation, which compresses the jugular veins and impedes venous outflow from the brain.
  3. Avoid hip flexion (e.g., knee gatch, bending legs) to prevent increased intra-abdominal and intrathoracic pressure.
  4. Space out nursing activities to allow the ICP to return to baseline.
  5. Limit endotracheal suctioning. Hyperoxygenate with 100% $O_2$ before and after, perform no more than 2 passes, and restrict suctioning to less than 10 seconds per pass. Suctioning triggers coughing, which spikes ICP.
  6. Maintain normocapnia ($PaCO_2$ between 35 and 45 mmHg). Hypercapnia ($PaCO_2 > 45 ext{ mmHg}$) causes cerebral vasodilation, increasing blood volume and ICP. Hypocapnia ($PaCO_2 < 35 ext{ mmHg}$) causes cerebral vasoconstriction, which reduces ICP but can induce cerebral ischemia.
  7. Administer osmotic diuretics (e.g., Mannitol) through an in-line filter to pull water out of brain tissue into blood vessels.

Spinal Cord Injury (SCI)

Spinal cord injuries are classified by the level of injury. Cervical injuries (C1-C8) cause tetraplegia (quadriplegia); thoracic and lumbar injuries cause paraplegia. Injuries at or above C3-C5 involve the phrenic nerve and cause respiratory paralysis, requiring immediate intubation and mechanical ventilation.

• Neurogenic Shock: A temporary loss of sympathetic vasomotor tone occurring in cervical or high thoracic injuries (above T6). It is characterized by the triad of hypotension, bradycardia, and poikilothermia (loss of temperature regulation; skin is warm and dry due to peripheral vasodilation).
• Autonomic Dysreflexia (Hyperreflexia): A life-threatening, uncoordinated sympathetic nervous system response that occurs in patients with spinal cord injuries at or above the T6 level, usually after spinal shock has resolved.
  • Pathophysiology: A noxious (painful or irritating) stimulus below the level of injury sends sensory signals up the spinal cord. These signals trigger a massive, uncontrolled sympathetic reflex, causing severe vasoconstriction of blood vessels below the injury. This leads to acute, life-threatening hypertension. The brain detects the high BP via baroreceptors and attempts to compensate by sending parasympathetic signals down, but these signals are blocked by the spinal lesion. Consequently, parasympathetic effects (vasodilation, bradycardia) only occur above the level of injury, while sympathetic effects (vasoconstriction) persist below the level of injury.
  • Clinical Manifestations:
    • Extreme, sudden hypertension (systolic BP can reach $200-300 ext{ mmHg}$).
    • Pounding, severe headache.
    • Bradycardia (heart rate drops to 30–40 bpm due to vagal stimulation).
    • Profuse sweating and flushing of the skin above the level of injury (face, neck, shoulders).
    • Nasal congestion.
    • Goosebumps (piloerection) and pale, cool, clammy skin below the level of injury.
  • Common Triggers:
    • Bladder distension (the most common cause, due to a blocked or kinked urinary catheter, or urinary retention).
    • Bowel impaction (fecal mass in the rectum).
    • Skin irritation (pressure ulcers, tight clothing, folded bedsheets, ingrown toenail).
  • Immediate Nursing Interventions (Priority Sequence):
    1. Elevate the HOB to 90 degrees (high-Fowler's) or place the patient in an upright sitting position. This immediately utilizes orthostatic gravity to help lower the blood pressure.
    2. Loosen or remove tight clothing, shoes, or binder straps to eliminate constrictive skin stimuli.
    3. Assess and eliminate the primary trigger:
       • Bladder: Palpate the bladder or scan for distension. If an indwelling catheter is present, check the tubing for kinks or obstruction. If no catheter is in place, insert an indwelling catheter immediately as prescribed. Apply an anesthetic gel (e.g., lidocaine) to the urethra before insertion to prevent triggering further sympathetic discharge.
       • Bowel: If the bladder is not distended, perform a digital rectal examination to check for fecal impaction. Apply lidocaine ointment to the rectum 5–10 minutes before checking to desensitize the area and prevent worsening the autonomic spasm.
    4. Monitor blood pressure and heart rate closely (every 2 to 5 minutes).
    5. Administer prescribed fast-acting antihypertensives (e.g., IV hydralazine, sublingual nifedipine) if the BP remains critically elevated after addressing the physical triggers.

Parkinson's Disease

Parkinson's disease is a slowly progressive, degenerative neurological movement disorder.

• Pathophysiology: Characterized by the destruction of dopamine-producing neurons in the substantia nigra of the basal ganglia. Under normal conditions, dopamine (an inhibitory neurotransmitter) and acetylcholine (ACh) (an excitatory neurotransmitter) exist in a delicate balance to coordinate smooth muscle movements. The loss of dopamine results in a relative excess of acetylcholine, leading to involuntary motor activity and rigidity.
• Classic Triad of Symptoms:
  1. Resting Tremor: Often the first sign, characterized as a "pill-rolling" motion of the thumb and fingers at rest. It decreases or disappears with purposeful movement and sleep.
  2. Muscle Rigidity: Increased resistance to passive joint movement. It is often described as "cogwheel rigidity" (a jerky, rhythmic resistance when rotating a joint).
  3. Bradykinesia: Extreme slowness of active movements. Manifestations include a mask-like facial expression (flat affect), drooling (due to impaired swallowing), a shuffling, propulsive gait (short, rapid steps with no arm swing), and difficulty initiating movement (freezing).
• Pharmacotherapy:
  • Levodopa-Carbidopa: The gold standard treatment. Levodopa is a precursor to dopamine that crosses the blood-brain barrier and is converted to active dopamine. Carbidopa does not cross the barrier but inhibits the peripheral breakdown of levodopa, allowing more drug to reach the brain.
  • Dietary Education: Avoid consuming high-protein meals at the same time as taking levodopa-carbidopa. Amino acids from digested protein compete with levodopa for absorption in the small intestine and transport across the blood-brain barrier, reducing the drug's effectiveness.
  • Side Effects: Monitor for orthostatic hypotension, dyskinesias (involuntary writhing movements, indicating toxicity), hallucinations, and harmless darkening of urine and sweat.