GUILLIAN-BARRE (GBS) LEWIS 1585-1587 CNs : III, V, VI, VII, X, XII
Etiology and Postinfectious polyneuropathy, ascending Drug Therapy Plasmapheresis-used in 1st 2
Pathophysiology polyneuropathic paralysis. weeks, ↓ length of hospital Acute, rapidly progressing, and potentially stay, length of time on a fatal form of polyneuritis. It affects the ventilator, and time peripheral nervous system and results in required to resume walking. loss of myelin (a segmental IV administration of high- demyelination) and edema and dose immunoglobulin inflammation of the affected nerves, (Sandoglobulin) has been causing a loss of neurotransmission to the shown to be as effective as periphery. plasma exchange and has Etiology: Unknown, but it is believed to the advantage of immediate be a cell-mediated immunologic reaction availability and greater directed at the peripheral nerves. Often safety. Make sure pt is well preceded by immune system stimulation hydrated and have adequate from a viral infection, trauma, surgery, renal function. 3 weeks viral immunizations, HIV. Campylobacter after disease onset, plasma jejuni is most recognized organism. exchange and Pathophysiology: These stimuli are immunoglobulin therapies thought to cause an alteration in the have little value. immune system, resulting in sensitization Acute phase: Vasopressor of T lymphocytes to the pt’s myelin and, agents and volume ultimately, myelin damage. Demyelination expanders are used to treat occurs, and the transmission of nerves low blood pressure. impulses is stopped or slowed down. The muscles innervated by the damaged peripheral nerves undergo denervation and atrophy. In recovery phase, remyelination occurs slowly, and neurologic function returns in a proximal-to-distal pattern.
Clinical Symptoms mild to severe: Surgical Therapy NA
Manifestation Symptoms develop 1-3 weeks after an upper respiratory or GI infection. Hours to days: weakness of the lower extremities, usually peaking about the 14th day. Distal muscles are more severely affected. Paresthesia (numbness & tingling) Hypotonia (reduced muscle tone) Areflexia (lack of reflexes) Objective sensory loss is variable, with deep sensitivity more affected than superficial sensations. Autonomic nervous system dysfunction: results from alterations in both the sympathetic and parasympathetic nervous systems: Most dangerous: orthostatic hypotension, hypertension, and abnormal vagal responses (bradycardia, heart block, asystole). Bowel and bladder dysfunction, facial flushing, diaphoresis. Syndrome of inappropriate antidiuretic hormone secretion. (SIADH) Progression of GBS include: CNs VII, VI, III, XII, V, X. : facial weakness, extraocular eye movement difficulties, dysphagia, and paresthesia of the face. Pain is common: paresthesias, muscular aches, cramps, and hyperesthesias. Pain is worse at night. Pain also may lead to a decrease in appetite and may interfere with sleep.
(which occurs as the paralysis Intervention paralysis progresses to the nerves that Assess respiratory function innervate the thoracic area) Monitor ABGs Fever: 1st sign of infection Assess gag reflex Immobility: from paralysis can Assess Corneal reflex cause problems such as paralytic Assess swallowing reflexes ileus, muscle atrophy, DVT, Monitor BP, Cardiac rate pulmonary emboli, skin and rhythm. breakdown, orthostatic Assess for autonomic hypotension, nutritional dysfunction: bradycardia, deficiencies. dysrhythmias. Assess for orthostatic hypotension secondary to muscle atony may occur in severe cases. If SIADH is present: fluid restriction is initiated. Diagnostic Studies CSF: normal or has a low protein Nursing Nutritional Therapy: content initially, but after 7-10 Management Soft mechanical diet days: shows ↑ protein level to Mild dysphagia is managed 700mg/dl (norm 15-45mg/dl) with by placing pt in upright normal cell count. position and flexing the EMG and nerve conduction: head forward during (electromyogram) abnormal feeding. reduced nerve conduction velocity Severe dysphagia: tube in the affected extremities. feeding may be required. Pts with paralytic ileus or intestinal obstruction: parenteral nutrition.
Nursing Diagnosis Impaired spontaneous Nursing The objection of therapy is to
ventilation r/t progression of support body systems until the disease process resulting in Implementation patient recovers. respiratory muscle paralysis. Monitor vital capacity and Risk for aspiration r/t dysphagia. ABG. Acute pain r/t paresthesias, If vital capacity drops to muscle aches and cramps, and <800ml (15ml/kg or 2/3 of hyperesthesias. pt’s normal vital capacity) Impaired verbal communication or ABCs deteriorate, r/t intubation or paralysis of the endotracheal intubation or muscles of speech. tracheostomy may be done. Fear r/t uncertain outcome and Meticulous suctioning seriousness of the disease. technique is needed to Self-care deficits r/t inability to prevent infection. use muscles to accomplish Bronchial hygiene and activities of ADLs. chest physiotherapy: to help clear secretions and prevent respiratory deterioration If fever exists: obtain sputum cultures to identify pathogen. Establish a communication system: difficult if cranial nerves are involved. Explain all procedures before doing, and reassure pt that muscle function will return. Intermittent cath since urinary retention is common for a few days. If pt is receiving >2.5 L/day: indwelling catheterization is safer. Physical therapy should be indicated early to help prevent problems r/t immobility ROM exercises to prevent contractures/ deformities. Meticulous eyes care should be provided to prevent corneal damage or irritation Check for gag reflex (note drooling) Assess tube feedings or parenteral nutrition since delayed gastric emptying exists. Monitor electrolytes Initiate a bowel program. Provide support and encouragement. Health Promotion Goal: Pt will be free from aspiration Maintain adequate ventilation Be pain free or have pain controlled Maintain adequate nutritional intake Maintain an acceptable method of communication Return to usual physical functioning.