Page 492 - ACCCN's Critical Care Nursing

Neurological Alterations and Management 469

Patients who require mechanical ventilation typically neuromuscular transmission is markedly affected by
present with rapidly progressive weakness. Of interest, small and subtle changes in acetylcholine release and
PaCO 2 may remain constant until just before intuba- other triggers (as above), and this gives rise to the decre-
tion, emphasising the importance of not relying on ment in transmission with repetitive stimulation and the
arterial blood gas analysis to make decisions regarding characteristic fatiguable muscle weakness. Pharmacologi-
intubation. cal management for myasthenia gravis includes the use
of anticholinesterases (pyridostigmine), steroids, azathi-
The side effects of IVIg administration include low-grade oprine and cyclophosphamide. Thymectomy reduces the
fever, chills, myalgia, diaphoresis, fluid imbalance, antibodies responsible for acetylcholine blockade and is
neutropenia, nausea and headaches, and at times acute often performed early in the disease. Plasmapheresis
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tubular necrosis. Administration and assessment require and IVIg are used in the short term for myasthenic crisis
adherence to transfusion protocols. Plasmapheresis is and are especially useful for preventing respiratory col-
performed by transfusion nurse specialists in collabora- lapse or assisting with weaning.
tion with the patient care nurse. Multidisciplinary case
management is utilised after stabilisation in the acute
phase, especially when the level of severity is determined. Clinical manifestations
Recovery and rehabilitation process information is pro- In a myasthenic crisis, vital capacity falls, cough and
vided to the patient and family so that consultation and sigh mechanisms deteriorate, atelectasis develops and
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communication is effective in recovery. hypoxaemia results. Ultimately, fatigue, hypercarbia
and ventilatory collapse occur. Commonly superim-
Myasthenia gravis posed pulmonary infections lead to increased morbid-
ity and mortality. Assessment for triggers begins with
Myasthenia gravis is an autoimmune disorder caused by a careful review of systems, with attention to recent
autoantibodies against the nicotinic acetylcholine rec- fevers, chills, cough, chest pain, dysphagia, nasal regur-
eptor on the postsynaptic membrane at the neurom- gitation of liquids and dysuria. Detailed history-taking
uscular junction. It is characterised by weakness and should note any trauma, surgical procedures and medi-
fatiguability of the voluntary muscles. It peaks in the cation use. General assessment includes vital signs; ear,
third and sixth decades of life. Its prevalence in Western nose and throat inspection; chest auscultation; and
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countries is 14.2/100,000. Prevalence rates have been abdominal check. In addition to supportive care and
rising steadily over the past decades, probably due to the removal of triggers, management of myasthenic
decreased mortality, longer survival, and higher rates of crisis includes treatment of the underlying myasthenia
diagnosis. The development of respiratory failure, pro- gravis. An experienced neurologist, who will ultimately
gressive bulbar weakness leading to failure of airway provide the patient’s care outside the ICU, should be
protection and severe limb and truncal weakness causing part of the care team. Options for treatment during
extensive paralysis, as in a myasthenic crisis, all may crisis include: use of AChE inhibitors, plasma exchange,
result in admission to ICU. IV immunoglobulins, and immunosuppressive drugs,
including corticosteroids. Median duration of hospi-
Aetiology talisation for crisis is 1 month. The patient usually
spends half of this time intubated in the ICU. About
Myasthenic crisis occurs when weakness from acquired 25% of patients are extubated on hospital day 7, 50%
myasthenia gravis becomes severe enough to necessitate by hospital day 13, and 75% by hospital day 31. The
intubation for ventilatory support or airway protection. mortality rate during hospitalisation for crisis has
At some point in their illness, usually within 2–3 years fallen from nearly 50% in the early 1960s to between
after diagnosis, 12–16% of myasthenic patients experi- 3% and 10% today. With the incidence of crisis
ence crisis. This occurrence is most likely in patients remaining stable over the past 30 years, this fall in
whose history includes previous crisis, oropharyngeal mortality rates probably reflects improvements in the
weakness or thymoma. Possible triggers include infec- intensive care assessment and management of these
tions, aspiration, physical and emotional stress and patients. 114
changes in medications. Most antibiotics have a trigger
effect and should be carefully prescribed by an informed
physician. Nursing practice
Careful and accurate assessment by the nurse in the pre-
Pathophysiology senting myasthenic crisis patient determines the triggers
of the event and incorporates a history, including infec-
In myasthenia gravis both structural changes in the tions and prescribed medications. These medications can
architecture of the neuromuscular junction and dynamic exacerbate the acetylcholine receptor blockade, and respi-
alterations in the turnover of acetylcholine receptors ratory demand proves too much for the myasthenic
erode the safety margin and efficiency of neuromuscular patient. Awareness by the nurse of trigger medications
transmission. Of all patients with myasthenia gravis, 80– ensures advocacy for the patient when the prescription is
85% have an identifiable and quantifiable antibody uncertain. 114
found in the IgG fraction of plasma, which is responsi-
ble for blocking receptors to the action of acetylcholine ● Respiratory and cardiovascular assessment incorpo-
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at the neuromuscular junction. Therefore, successful rates upper and lower airway muscle weakness. ABGs