NSG210 Hinkle Ch. 64: Management of Patients with Neurologic Infections, Autoimmune Disorders, and Neuropathies

Source: Hinkle & Cheever, Brunner & Suddarth’s Medical-Surgical Nursing 15e, Chapter 64, pp. 2087-2111 (textbooks/HINKLE_MS_CH64.pdf, also in textbooks/exam04/). Week 11 reading (multiple sclerosis); Exam 4 content (the course calendars end Exam 3 content with the October 28 OB lecture). Numbering note: the syllabus lists “Ch. 65” (16th edition); this is Ch. 64 in the 15th edition (see nsg210-textbook-chapter-crosswalk). Increased ICP care is in nsg210-hinkle-ch61-neurologic-dysfunction; cranial nerve exam is in nsg210-hinkle-ch60-neurologic-assessment.

Learning Outcomes

1. Differentiate infectious disorders of the nervous system by cause, manifestations, medical care, and nursing management.
2. Describe pathophysiology, manifestations, and management of multiple sclerosis (MS), myasthenia gravis, and Guillain-Barre syndrome (GBS).
3. Use the nursing process for the patient with MS or GBS.
4. Explain cranial nerve disorders, their manifestations, and nursing interventions.
5. Apply the nursing process to the patient with a cranial nerve disorder.

Key Terms

• Ataxia: impaired coordination during voluntary movement
• Diplopia: double vision
• Dysphagia: difficulty swallowing. Dysphonia: voice impairment
• Hemiparesis: weakness of one side. Hemiplegia: paralysis of one side
• Neuropathy: general term for a nervous system disorder
• Paresthesia: numbness, tingling, “pins and needles”
• Prion: pathogen smaller than a virus, resistant to standard sterilization
• Ptosis: drooping eyelid
• Spasticity: muscle hypertonicity with increased resistance to stretch, weakness, increased deep tendon reflexes, diminished superficial reflexes

I. Meningitis

A. Types and Risk Factors

• Inflammation of the meninges covering the brain and spinal cord.
• Septic (bacterial): Streptococcus pneumoniae and Neisseria meningitidis cause 80 to 90 percent of adult bacterial meningitis.
• Aseptic (viral, or secondary to cancer or immunosuppression such as HIV): enteroviruses most common; more frequent in summer and early fall.
• Meningococcal risk: unvaccinated first-year college students and military; peak in winter and early spring.
• Risk factors for bacterial meningitis: tobacco use and viral URI (more droplets), otitis media and mastoiditis (direct spread), immune deficiency.

B. Pathophysiology

• Spread through the bloodstream or directly (facial bone trauma, invasive procedures). Organism crosses blood-brain barrier, multiplies in CSF; inflammation of subarachnoid and pia mater raises ICP.
• N. meningitidis is acutely fulminant about 10 percent of the time: adrenal damage, circulatory collapse, widespread hemorrhage (Waterhouse-Friderichsen syndrome).

C. Clinical Manifestations

• Headache, fever (stays high), chills. Older adults: mental status changes, focal deficits.
• Nuchal rigidity: stiff painful neck, may be early.
• Kernig sign: thigh flexed on abdomen, leg cannot be fully extended; bilateral suggests meningeal irritation.
• Brudzinski sign: flexing the neck (after ruling out cervical injury) produces flexion of knees and hips; more sensitive than Kernig.
• Photophobia.
• Rash in about half of meningococcal cases: petechial to purpuric to large ecchymoses.
• Disorientation and memory impairment early; then lethargy, unresponsiveness, coma. Seizures. Increased ICP (first signs: decreased LOC, focal motor deficits); uncal herniation.
• Fulminant: abrupt high fever, extensive purpura on face and extremities, shock, DIC; death within hours.

D. Diagnosis (Table 64-1)

• CT before lumbar puncture if altered LOC, papilledema, neuro deficits, new seizure, immunocompromise, or CNS disease history (detect shift that could herniate).
• Key tests: bacterial culture and Gram stain of CSF and blood (Gram stain allows rapid targeted antibiotics).

E. Prevention

• Meningococcal conjugate vaccine at 11 to 12 years with booster at 16 (CDC ACIP).
• Close contacts of meningococcal patients: chemoprophylaxis with rifampin, ciprofloxacin, or ceftriaxone, started within 24 hours of exposure; consider vaccinating household members.
• Vaccinate at-risk children and adults for H. influenzae and S. pneumoniae.

F. Medical Management

• Early IV antibiotic that crosses the blood-brain barrier: penicillin G plus a cephalosporin (ceftriaxone, cefotaxime), given emergently.
• Dexamethasone as adjunct (acute bacterial and pneumococcal): before or with first antibiotic dose, then every 6 hours for 4 days; improves outcomes, no added GI bleeding risk.
• Fluid volume expanders for dehydration and shock; anticonvulsants for seizures; treat increased ICP.

G. Nursing Management

• Infection control precautions until 24 hours after antibiotics start (oral and nasal discharge infectious).
• Pain management (body aches, neck pain); rest in a quiet, darkened room.
• Fever: antipyretics, cooling blankets (fever raises cardiac workload, cerebral metabolism, and ICP).
• Hydration; close neuro monitoring; pulse oximetry and ABGs; intubation if brainstem compromised.
• BP (often arterial line) for early shock; rapid IV fluids but avoid fluid overload.
• Seizure and injury protection; daily weight, electrolytes, urine volume, specific gravity, osmolality (watch for SIADH); prevent immobility complications.
• Family support and information.

II. Brain Abscess

• Collection of infectious material in brain tissue; under 1 percent of space-occupying lesions; more common in immunosuppressed.
• Predisposing in immunocompetent adults: otitis media and rhinosinusitis (about 40 percent otogenic); also intracranial surgery, penetrating injury, tongue piercing, spread from lungs, gums, tongue, heart, wounds, abdominal infection.
• Manifestations: headache (often worse in the morning) is most common; fever only 53 percent; vomiting; focal deficits; then increased ICP (decreasing LOC, seizures).
• Chart 64-1 by location: frontal (expressive aphasia, frontal headache, hemiparesis, seizures); temporal (vision changes, facial weakness, localized headache, receptive aphasia); cerebellar (ataxia, nystagmus, occipital headache).
• Diagnosis: CT with contrast; MRI preferred (higher resolution); CT- or MRI-guided aspiration for culture; blood cultures if distant source.
• Treatment: control ICP, drain abscess (stereotactic aspiration), high-dose IV antibiotics (initially ceftriaxone plus metronidazole, adjusted to cultures); corticosteroids for increasing deficits; anticonvulsants.
• Nursing: neuro checks, response to meds; with steroids monitor blood glucose and potassium (insulin or replacement); safety; family support. About 70 percent have no or minimal permanent deficits.

III. Encephalitis

A. Herpes Simplex Encephalitis

• HSV is the most common cause of acute encephalitis in the US (10 to 15 percent).
• Local necrotizing hemorrhage, then edema.
• Signs: fever, headache, confusion, hallucinations, behavior change, focal seizures, dysphasia, hemiparesis, altered LOC.
• Diagnosis: MRI hyperintense areas; EEG temporal lobe changes; CSF high opening pressure, normal glucose, high protein; PCR of CSF is the standard (95 percent sensitive, 99 percent specific).
• Acyclovir is the drug of choice; start early; continue up to 3 weeks to prevent relapse; infuse slowly over 1 hour to prevent crystallization in urine; reduce dose in renal insufficiency.
• Nursing: neuro assessment; dim lights, limit noise and visitors, cluster care; analgesics (opioids cautiously, may mask neuro signs); seizure safety; monitor renal function and urine output.

B. Arthropod-Borne (Arbovirus) Encephalitis

• Mosquitoes main vector in North America; summer and fall. Five US types: eastern equine, western equine, St. Louis, La Crosse, West Nile.
• St. Louis and West Nile mostly affect adults. Unique feature: SIADH with hyponatremia.
• Abrupt fever, headache, dizziness, nausea, malaise; CNS spread: stiff neck, confusion, tremors, coma. Eastern equine has highest mortality (50 percent).
• Diagnosis by presentation, location, travel dates; MRI (basal ganglia in St. Louis; periventricular in West Nile); EEG.
• No specific medication: supportive; control ICP.
• Prevention teaching: covering clothing, insect repellent with 20 to 35 percent DEET, stay indoors at dawn and dusk, screens, remove standing water. Report all cases to the local health department.

C. Creutzfeldt-Jakob Disease (CJD) and Variant CJD (vCJD)

• Transmissible spongiform encephalopathies caused by prions; no CNS inflammation; spongy vacuoles with amyloid plaque.
• CJD: sporadic (about 85 percent, 1 per million), familial (5 to 10 percent), acquired (under 1 percent, contaminated tissue or neurosurgical instruments). Mean onset 65 years; survival under 1 year. Mental deterioration, ataxia, visual disturbance, then memory loss, involuntary movement, paralysis, mutism; psychiatric symptoms late.
• vCJD: from eating prion-infected beef (mad cow disease); mean onset 27 years; psychiatric (behavioral) symptoms early, sensory disturbance, limb pain; survival about 14 months.
• Blood donation deferral: over 3 months in UK 1980-1996, or transfusion in France or UK since 1980.
• Diagnosis: brain biopsy not recommended; CSF 14-3-3 protein, EEG (periodic activity, burst suppression), MRI (basal ganglia hyperintensity).
• No treatment: supportive and palliative; hospice.
• Standard precautions (isolation not needed); institutional protocols for brain, spinal cord, pituitary, eye tissue; disposable surgical instruments incinerated, or bleach and extended sterilization.

IV. Multiple Sclerosis

A. Overview

• Immune-mediated, progressive demyelinating disease of the CNS; nearly 400,000 in the US. Peak onset 20 to 50 years; women 3 times more than men.
• Higher prevalence in northern colder latitudes (Europe, northern US, southern Canada, New Zealand, southern Australia); less in Asians.
• Risks: genetic variations (about 200), possible viral molecular mimicry; obesity, low vitamin D, high-salt diet in teens.
• Forms: radiologically isolated syndrome (MRI lesions, no symptoms; about one third diagnosed with MS within 5 years); clinically isolated syndrome (symptoms at least 24 hours; optic neuritis, focal symptoms, partial myelopathy).
• Main clinical forms: relapsing-remitting (RRMS, about 85 percent; most later become secondary progressive), primary progressive (PPMS, about 15 percent; steady worsening), progressive-relapsing (about 5 percent).

B. Pathophysiology

• Sensitized T cells stay in CNS, causing inflammation that destroys white matter myelin and oligodendroglia. Plaques on demyelinated axons; axons eventually degenerate (permanent damage).
• Common sites: optic nerves, chiasm, tracts; cerebrum; brainstem; cerebellum; spinal cord.

C. Clinical Manifestations

• Fatigue (60 to 90 percent; most disabling, main reason patients stop working); worsened by heat, depression, anemia, deconditioning, medications.
• Depression, weakness, numbness, incoordination, loss of balance, spasticity, pain.
• Visual: blurring, diplopia, scotoma, blindness.
• Pain and sensory: paresthesias, dysesthesias, loss of proprioception; perimenopausal women at risk of osteoporosis pain (estrogen loss, immobility, steroids); bone density testing.
• Spasticity in 90 percent, mostly legs; loss of abdominal reflexes.
• Cognitive changes in about half (memory, concentration); dementia rare. Emotional lability, euphoria.
• Ataxia and tremor (cerebellum, basal ganglia).
• Bladder, bowel, sexual dysfunction; complications: UTI, constipation, pressure injury, contractures, pedal edema, pneumonia, osteoporosis.
• Exacerbations and remissions; relapses linked to emotional and physical stress.
• Older adults: life expectancy 7 to 14 years shorter; drug interactions, altered metabolism, osteoporosis from steroids, medication cost.

D. Diagnosis

• Plaques disseminated in space and time on MRI with no better explanation; 2017 McDonald criteria (Table 64-2).
• CSF oligoclonal bands (IgG); evoked potentials; urodynamic studies; neuropsychological testing; sexual history.

E. Medical Management

• No cure. Goals: delay progression, manage chronic symptoms, treat exacerbations.
• Disease-modifying therapies reduce relapse frequency, duration, and MRI plaques in RRMS (not effective in PPMS); start early:
  • Interferon beta-1a and beta-1b (subcut every other day; IM weekly form; pegylated every 14 days): flulike symptoms, elevated LFTs, leukopenia, headache, depression, skin necrosis.
  • Glatiramer acetate (subcut daily): injection-site reactions, brief flushing; no monitoring.
  • Oral: teriflunomide, fingolimod, dimethyl fumarate.
  • Ocrelizumab: for PPMS.
  • Mitoxantrone IV every 3 months: secondary progressive or worsening RRMS; cardiotoxicity; lifetime maximum dose.
• Acute exacerbation: IV methylprednisolone 1 g daily for 3 to 5 days, then oral prednisone taper; shortens relapse, no long-term benefit; mood swings, weight gain, electrolyte imbalance.
• Symptom management:
  • Spasticity: baclofen (GABA agonist; drug of choice; oral or intrathecal); diazepam, tizanidine, dantrolene; nerve blocks or surgery.
  • Fatigue: amantadine, pemoline, dalfampridine.
  • Ataxia (most resistant): propranolol, gabapentin, clonazepam.
  • Bladder and bowel: anticholinergics, alpha-adrenergic blockers, antispasmodics; fluids and perineal care to prevent UTI.

F. Nursing Process: MS

• Assess mobility and balance (fall risk) both rested and fatigued; weakness, spasticity, vision, incontinence, swallowing, speech; coping; adherence.
• Diagnoses: impaired mobility, risk for falls, fatigue, difficulty coping. Complications: bowel problems, communication and aspiration (cranial nerves), cognitive changes, home management, sexuality, urinary incontinence.
• Promoting mobility: relaxation and coordination exercises; progressive resistive exercise; walking to improve gait.
• Spasticity and contractures: daily stretching (hamstrings, gastrocnemius, hip adductors, biceps, wrist and finger flexors); stretch-hold-relax; swimming, stationary bike; warm packs OK but avoid hot baths (burns from sensory loss, heat worsens symptoms); avoid extreme cold; do not hurry the patient.
• Activity and rest: work and exercise to just short of fatigue; avoid strenuous exercise (raises body temperature); frequent short rests; air conditioning in at least one room.
• Nutrition: weight management; avoid alcohol and smoking.
• Falls: walk with feet apart (wide base); watch feet if position sense lost; assistive devices; wrist weights for intention tremor; pressure injury prevention.
• Fatigue: limit electronic devices before sleep, sleep hygiene (Chart 64-2).
• Coping: no two patients alike; many have near-normal lifespan; family stress; referrals; National MS Society.
• Monitor for suicide risk: 50 percent have major depression; suicide rate twice the general population.
• Home care (Chart 64-3): injection technique, symptom management, complication prevention, fatigue strategies, bowel and bladder, exercise.

V. Myasthenia Gravis

A. Overview and Pathophysiology

• Autoimmune disorder of the myoneural junction: antibodies to acetylcholine (ACh) receptors (found in 85 percent) reduce available receptors, so voluntary muscle weakness worsens with activity and improves with rest.
• Incidence 9 to 30 per million; women in 2nd-3rd decades; men more after 50.
• Most have thymic hyperplasia or thymoma (thymus thought to make the antibodies).
• Purely motor: no effect on sensation or coordination.

B. Clinical Manifestations

• Ocular form: diplopia, ptosis.
• Generalized: facial weakness (bland expression), bulbar weakness (dysphonia, dysphagia; choking and aspiration risk), limb weakness, respiratory weakness; decreasing vital capacity leads to myasthenic crisis.

C. Diagnosis

• Edrophonium (acetylcholinesterase inhibitor) test: IV; 30 seconds later facial weakness and ptosis resolve for about 5 minutes = positive. Keep atropine available (bradycardia, asystole, bronchoconstriction, sweating, cramping).
• Ice test (for patients with cardiac disease or asthma): ice pack over eyes 1 minute; ptosis temporarily resolves.
• ACh receptor antibody blood tests; repetitive nerve stimulation (decreasing action potentials); single-fiber EMG (about 99 percent sensitive, uncomfortable); MRI for enlarged thymus.

D. Medical Management

• No cure; treatments do not stop antibody production.
• Pyridostigmine (anticholinesterase): first line; inhibits ACh breakdown; divided doses, usually four times a day; adverse effects diarrhea, abdominal cramps, excess saliva.
• Immunosuppression: prednisone daily 1 to 2 months then taper (allows lower anticholinesterase dose); azathioprine if steroids insufficient (effect in 3 to 12 months; leukopenia, hepatotoxicity; monthly LFTs and WBC).
• IVIG: exacerbations or long-term adjunct; improvement in days to a week; lasts about 28 days; headache, migraine, aseptic meningitis, flulike symptoms.
• Therapeutic plasma exchange (plasmapheresis): large-bore double-lumen central catheter; temporarily lowers circulating antibodies; daily or alternate days.
• Contraindicated medications can worsen MG; avoid procaine; inform dentist.
• Thymectomy: antigen-specific immunosuppression; best if under 60 and diagnosed within 3 years; only treatment that can produce complete remission (about 35 percent); entire gland removed; preop IVIG or plasma exchange shortens postop ventilation; ICU monitoring of respiratory function; benefit may take up to 3 years; elective when disease stable.

E. Complications: Crises

• Myasthenic crisis: exacerbation with severe generalized, respiratory, and bulbar weakness leading to respiratory failure. Most common trigger: respiratory infection; also medication change, surgery, pregnancy, exacerbating drugs.
• Cholinergic crisis: overmedication with cholinesterase inhibitors; rare.
• Neuromuscular respiratory failure is the critical complication in both. First sign: downward trend in negative inspiratory force and vital capacity.
• Management: ICU; ventilatory support takes precedence; intubation or noninvasive vest ventilation; stop cholinesterase inhibitors during respiratory failure, restart gradually after plasma exchange or IVIG improves patient; nutrition support.
• Nursing in crisis: respiratory rate, depth, breath sounds, vital capacity, NIF; ABGs; chest physiotherapy and postural drainage (not within 30 minutes after feeding); suction; ABGs, electrolytes, I&O, daily weight; tube feeding if unable to swallow; avoid sedatives and tranquilizers (worsen hypoxia and hypercapnia).

F. Nursing Management and Teaching

• Quality and Safety Alert: give anticholinesterase medications ON TIME; delay may worsen weakness so much the patient cannot swallow pills.
• Symptom diary to time doses; know signs of myasthenic vs cholinergic crisis.
• Energy conservation: rest periods, items on each floor, handicapped plate, schedule activity at peak strength.
• Aspiration prevention: meals at peak medication effect; rest before meals; sit upright with neck slightly flexed; soft foods in gravy or sauce; larger meals in the morning; speech-language pathology evaluation; home suction.
• Eyes: tape eyes closed briefly and use artificial tears if lids do not close; eyelid “crutches” on glasses; patch one eye or prism glasses for diplopia.
• Avoid triggers: emotional stress, infections (especially respiratory), vigorous activity, some medications, high environmental temperature. Myasthenia Gravis Foundation of America.

VI. Guillain-Barre Syndrome

A. Overview

• Acute idiopathic polyneuritis: autoimmune attack on peripheral nerve myelin; rapid segmental demyelination of peripheral and some cranial nerves; ascending weakness, hyporeflexia, paresthesias.
• Antecedent event (usually viral) in 60 to 70 percent, 1 to 3 weeks before symptoms: Campylobacter jejuni (40 percent of US cases), CMV, Epstein-Barr, Mycoplasma, H. influenzae, Zika.
• Incidence 1 to 2 per 100,000; males and females equal. Death in 5 to 10 percent (respiratory failure, autonomic dysfunction, sepsis, PE). 70 percent full recovery; 30 percent some disability.
• Molecular mimicry. Schwann cell may be spared, allowing remyelination; axonal damage regrows slowly and incompletely.
• Variants: classic ascending; purely motor; descending (head and neck first); Miller-Fisher (ocular paralysis, ataxia, areflexia).

B. Clinical Manifestations

• Begins with leg weakness and diminished reflexes, ascends; may reach tetraplegia and neuromuscular respiratory failure.
• Paresthesias of hands and feet; pain.
• Peak severity within 2 weeks, no longer than 4 weeks (longer = chronic inflammatory demyelinating polyneuropathy).
• Cranial nerves: optic (blindness), IX and X (cannot swallow or clear secretions).
• Vagus involvement: autonomic dysfunction (tachycardia, bradycardia, hypertension, orthostatic hypotension), comes and goes rapidly.
• Cognition and LOC are NOT affected.

C. Diagnosis

• Symmetric weakness, diminished reflexes, ascending weakness, recent viral illness.
• Monitor vital capacity and negative inspiratory force.
• CSF: elevated protein without increased cells. Nerve conduction velocity progressively decreases. Serum labs not useful.

D. Medical Management

• Medical emergency; often ICU. Mechanical ventilation as needed; some recommend elective intubation before extreme respiratory muscle fatigue (emergent intubation can trigger autonomic dysfunction).
• VTE prevention: anticoagulants, sequential compression boots.
• Plasma exchange and IVIG lower antibody levels and shorten immobility and ventilation time.
• Continuous ECG; short-acting alpha-adrenergic blockers for tachycardia and hypertension; IV fluids for hypotension.

E. Nursing Process: GBS

• Diagnoses: impaired breathing, impaired mobility, impaired nutrition (cannot swallow), impaired verbal communication, anxiety, fatigue. Complications: respiratory failure, autonomic dysfunction.
• Respiratory: incentive spirometry, chest physiotherapy; monitor vital capacity and NIF; discuss possible ventilation early so it can be planned, not emergent; suction for bulbar weakness.
• Impending respiratory failure signs: breathlessness while speaking, shallow irregular breathing, accessory muscle use, tachycardia, weak cough, changed pattern.
• Frequent BP and HR (autonomic dysfunction); medications or temporary pacemaker for significant bradycardia.
• Mobility: functional positioning; passive ROM at least twice daily; VTE prevention (ROM, turning, anticoagulation, stockings, SCDs, hydration); pad bony prominences.
• Nutrition: paralytic ileus possible (IV fluids, parenteral nutrition, listen for bowel sounds); gastrostomy if bulbar paralysis; check gag reflex and bowel sounds before oral feeding.
• Communication: cognition intact; picture cards, eye blink system; speech therapy.
• Anxiety: information, relaxation, distraction, diversional activities, family participation in care; support groups.
• Fatigue: pace activities with rest as recovery proceeds.
• Other complications: arrhythmias, transient hypertension, orthostatic hypotension, DVT, PE, urinary retention.
• Home care (Chart 64-4); most recover completely; rehabilitation may be long.

VII. Cranial Nerve Disorders

• Table 64-3 summarizes disorders of CN I-XII and nursing interventions (for example CN I anosmia after head trauma: assess smell, check for CSF rhinorrhea; CN VIII: vertigo, change positions slowly, fall prevention; CN IX-X: dysphagia, aspiration prevention, upright for eating; CN XII: tongue weakness, swallowing, possible tube feeding).

A. Trigeminal Neuralgia (CN V; formerly tic douloureux)

• Paroxysms of sudden, unilateral, shooting, stabbing, or burning pain in any of the three branches (ophthalmic V1, maxillary V2, mandibular V3); ends abruptly; facial twitching.
• Thought due to demyelination from vessel compression or MS. Usually 50s-60s; more in women and in MS. Onset before 50: evaluate for MS.
• Triggers: washing face, shaving, brushing teeth, eating, drinking, cold air, pressure on trigger points. Patients avoid touching or washing the face (diagnostic clue).
• Medications: carbamazepine (first line; take with meals; monitor serum levels; nausea, dizziness, drowsiness, aplastic anemia; monitor for bone marrow depression); gabapentin, baclofen; phenytoin as adjunct.
• Surgery: microvascular decompression (intracranial; lift artery loop off nerve); radiofrequency thermal coagulation (dysesthesia, loss of corneal reflex possible); gamma knife radiosurgery; percutaneous balloon microcompression.
• Nursing: avoid triggers; cotton pads and room-temperature water to wash face; mouthwash after eating if brushing hurts; hygiene in pain-free intervals; room-temperature soft foods, chew on unaffected side; address anxiety, depression, insomnia.
• Postop: assess each branch for motor and sensory deficits; if face numb, do not rub the eye; inspect eye; artificial tears; do not chew on affected side until numbness diminishes.

B. Bell’s Palsy (CN VII)

• Unilateral facial nerve inflammation causing facial weakness or paralysis; possible viral reactivation (HSV, zoster) or autoimmune; ages 15 to 45.
• Facial distortion, drooping mouth, drooling, excessive tearing, pain in face, behind ear, and eye; speech and eating difficulty on affected side.
• Most recover completely in 3 to 5 weeks; rarely recurs. Reassure that it is not a stroke.
• Prednisone started within 72 hours of onset reduces severity, pain, and denervation. Analgesics; electrical stimulation to prevent atrophy; surgical decompression controversial.
• Nursing: protect the eye (incomplete closure, decreased blink): shield at night, moisturizing drops by day and ointment at bedtime, manually close the lid before sleep, wraparound sunglasses or goggles. Eye patch may abrade cornea. Once tolerated, gentle upward facial massage several times daily; facial exercises (wrinkle forehead, blow out cheeks, whistle) with a mirror; avoid cold and drafts.

VIII. Peripheral Nervous System Disorders

A. Peripheral Neuropathies

• Bilateral, symmetric disturbance of motor and sensory nerves, usually starting in feet and hands. Most common cause: poorly controlled diabetes; also drugs such as antineoplastics.
• Loss of sensation, atrophy, weakness, diminished reflexes, pain, paresthesia.
• No specific treatment; control the cause. Risks: falls, thermal injury, skin breakdown. Inspect feet; walker or cane; check bathwater temperature; properly sized footwear; driving may be limited.

B. Mononeuropathy

• Single peripheral nerve: compression or entrapment (carpal tunnel), trauma, overstretching, injection injury (often permanent), adjacent inflammation; common in diabetes.
• Treatment: remove cause; local steroid injection; aspirin or codeine; gabapentin for chronic pain. Protect limb; PT and OT (splints).

High-Yield Numbers

Priority Nursing Actions and Red Flags

• Suspected bacterial meningitis: antibiotics emergently; CT first if altered LOC, papilledema, focal deficits, new seizure, or immunocompromise.
• Petechial or purpuric rash with fever and stiff neck: meningococcal infection; watch for shock and DIC.
• Infection control precautions for 24 hours after antibiotics; prophylaxis for close contacts within 24 hours.
• Acyclovir infused slowly over 1 hour; monitor renal function.
• MS: avoid heat (hot baths, overexertion); assess for depression and suicide risk.
• Myasthenia gravis: give pyridostigmine on time; falling vital capacity or NIF is the first sign of respiratory compromise; keep atropine at bedside during edrophonium testing; avoid sedatives in crisis.
• GBS: track vital capacity and NIF; plan intubation electively; watch for autonomic swings in HR and BP; cognition is intact, so communicate.
• Trigeminal neuralgia and Bell’s palsy: protect the eye (corneal injury).
• Peripheral neuropathy: inspect feet, test bathwater temperature, fall prevention.

Medications

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