Peripheral Neuropathies in Critical Care Nursing

1. Guillain-Barré Syndrome,
Myasthenia Gravis,
Dr. Nermine Elcokany
Lecturer, Critical Care & Emergency Nursing Department
Alexandria, Egypt

2. Guillain-Barré Syndrome
It 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.

3. ETIOLOGY
The 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.

4. The febrile infection is usually respiratory or
gastrointestinal.
Other predisposing factor (surgery, lymphoma,
trauma)

5. PATHOPHYSIOLOGY
In 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

8. Phases of Guillain-Barré
syndrome

9. 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.

10. DIAGNOSIS
Signs 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)

11. CLINICAL MANAGEMENT
Preventive 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

12. 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.

13. Nursing management
Goals of management
1.Prevent infections and complications of immobility
2.Provide proper nutrition
3.Provide functional maintenance of body systems

14. Goals of management
4.Treat life threatening problems
5.Provide comfort and emotional support.
6.Patient education

15. Myasthenia Gravis
Myasthenia 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.

16. ETIOLOGY
Myasthenia 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.

17.  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.

19. PATHOPHYSIOLOGY
Myasthenia 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.

21. 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.

24. 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).

25. 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.

26. DIAGNOSIS
patient’s history
Patients may present with complaints of double vision or drooping
eyelids.
 Also, myasthenia gravis causes weakness of the shoulder girdle
muscles.

27. The cranial nerve examination may reveal ptosis and
diplopia
Motor weakness may be exhibited
Blood is drawn for acetylcholine receptor antibodies
Electromyography (EMG)

28. 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)

29. Long-term immunosuppression with corticosteroids,
azathioprine (Imuran), cyclophosphamide
(Cytoxan), or cyclosporine;
 Short-term immunomodulation with
plasmapheresis or IVIG; or thymectomy.

30. Nursing management
1. Assessment
2. Provide proper nutrition
3. Provide functional maintenance of body
systems
4. Provide comfort and emotional support.
5. Patient education

31. THANK YOU