Date post: | 21-Apr-2017 |
Category: |
Healthcare |
Upload: | faculty-of-nursing-alexandria-university-egypt |
View: | 1,016 times |
Download: | 4 times |
Guillain-Barré Syndrome, Myasthenia Gravis,
Dr. Nermine ElcokanyLecturer, Critical Care & Emergency Nursing Department
Alexandria, Egypt
Guillain-Barré SyndromeIt is an acute inflammatory demyelinating
polyneuropathy, is a rapidly evolving illness that
commonly presents as symmetrical weakness,
sensory loss, and areflexia. This condition is an
inflammatory peripheral neuropathy in which
lymphocytes and macrophages strip myelin from
axons.
ETIOLOGYThe etiology of Guillain-Barré syndrome is unclear, but an
autoimmune response is strongly suspected.
There is a preceding event or trigger that is often an
infection.
Occasionally, vaccinations have been known to trigger
Guillain-Barré syndrome.
The febrile infection is usually respiratory or
gastrointestinal.
Other predisposing factor (surgery, lymphoma,
trauma)
PATHOPHYSIOLOGYIn Guillain-Barré syndrome, the myelin sheath
surrounding the axon is lost.
Loss of the myelin sheath in Guillain-Barré
syndrome makes nerve impulse transmission is
aborted.
Demyelination is initiated by an antibody attack on
the myelin early in the course of the disease
Phases of Guillain-Barré syndrome
CLINICAL MANIFESTATIONS
Muscle weakness and diminished reflexes of the lower extremities.
Quadrilegia
Deep tendon reflexes are usually lost, even in the earliest stages.
Neuromuscular respiratory failure.
Paresthesias
N.B. Weakness usually begins in the legs and progresses upward.
DIAGNOSISSigns and symptoms include- motor weakness,
paresthesia.
A history of a viral illness
ascending weakness
Declining pulmonary function capacity
Lumbar puncture reveals elevated CSF protein level
Electromyography (EMG) Nerve conduction studies (NCS)
CLINICAL MANAGEMENTPreventive measures need to be established to
prevnt DVT and pulmonary embolism do not develop.
Heparin 5000 units subcutaneously may be given along with antiembolism stockings and sequential compression devices
The first therapy proven to benefit patients with Guillain-Barré syndrome is plasmapheresis.
This procedure mechanically removes humoral factors.
Intravenous immunoglobulin (IVIG) is also useful in managing Guillain-Barré syndrome.
Nursing managementGoals of management
1. Prevent infections and complications of immobility
2. Provide proper nutrition
3. Provide functional maintenance of body systems
Goals of management
4.Treat life threatening problems
5.Provide comfort and emotional support.
6.Patient education
Myasthenia GravisMyasthenia gravis (from Greek "muscle",
"weakness", and Latin gravis "serious"; abbreviated MG) is an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatigability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the post-synaptic neuromuscular junction, inhibiting the stimulative effect of the neurotransmitter acetylcholine.
ETIOLOGYMyasthenia gravis is an autoimmune disorder.
The factors that trigger the autoimmune process are not known, but the thymus gland is involved.
The thymus lies behind the sternum and may extend down to the diaphragm or up to the neck.
This gland plays a role in the responsiveness of T cells to foreign antigens.
The thymus gland is large in children and small in adults.
By adulthood, the gland has shrunken and has nearly been replaced by fat.
Abnormalities in the thymus gland frequently occur in patients with myasthenia gravis.
Eighty percent of patients with myasthenia gravis have thymal hyperplasia.
PATHOPHYSIOLOGYMyasthenia gravis is a result of circulating antibodies
directed toward the skeletal muscle acetylcholine
receptors.
This leads to a decrease in end plate depolarization,
which may be insufficient to generate an action potential.
This results in a failure of the muscle to contract.
CLINICAL MANIFESTATIONS
The hallmark of myasthenia gravis is fatigability. Muscles become progressively weaker during periods of activity and improve after periods of rest. Muscles that control eye and eyelid movement, facial expressions, chewing, talking, and swallowing are especially susceptible.
The muscles that control breathing and neck and limb movements can also be affected.
Symptoms, which vary in type and severity, may include asymmetrical ptosis (a drooping of one or both eyelids), diplopia (double vision) due to weakness of the muscles that control eye movements, an unstable or waddling gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, dysphagia (difficulty in swallowing), shortness of breath and dysarthria (impaired speech).
In myasthenic crisis a paralysis of the respiratory muscles occurs, necessitating assisted ventilation to sustain life. In patients whose respiratory muscles are already weak, crises may be triggered by infection, fever, an adverse reaction to medication, or emotional stress. Since the heart muscle is only regulated by the autonomic nervous system, it is generally unaffected by MG.
DIAGNOSISpatient’s history
Patients may present with complaints of double vision or drooping eyelids.
Also, myasthenia gravis causes weakness of the shoulder girdle muscles.
The cranial nerve examination may reveal ptosis and diplopia
Motor weakness may be exhibited
Blood is drawn for acetylcholine receptor antibodies
Electromyography (EMG)
CLINICAL MANAGEMENT• The clinical management of myasthenia gravis
includes the following strategies:
1. use of medications to enhance neuromuscular transmission; such as anticholinesterases (Pyridostigmine (Mestinon), and steroids (Prednisone)
Long-term immunosuppression with corticosteroids, azathioprine (Imuran), cyclophosphamide (Cytoxan), or cyclosporine;
Short-term immunomodulation with plasmapheresis or IVIG; or thymectomy.
Nursing management1. Assessment
2. Provide proper nutrition
3. Provide functional maintenance of body systems
4. Provide comfort and emotional support.
5. Patient education
THANK YOU