Page 493 - ACCCN's Critical Care Nursing

470 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

are a poor marker for intubation and ventilation main acute causes. The mortality in status epilepticus is
because these values change late in the decompensa- about 20%; most patients die of the underlying condition
tion cycle. Being able to recognise fatigue (inability to rather than the status epilepticus itself. SE can result in
speak, poor lung expansion, VC below 1 L, shoulder permanent neurological and mental deterioration, par-
and arm weakness) in patients with neuromuscular ticularly in young children; the risks of morbidity greatly
weakness and air hunger is important. 117 increase with longer duration of the status epilepticus
● Non-invasive ventilation can be difficult to administer episode. SE in the intensive care setting falls into two
safely, with the potential for aspiration due to insi- main groups: those transferred to the ICU because of
dious upper airway weakness, however the option uncontrolled SE (refractory SE), and those who are admit-
should be considered with careful assessment of gag, ted to the ICU for another reason and have SE as an
swallow and cough reflexes in order to prevent additional finding. 121
intubation. 116
● Neuromuscular blockade should be avoided (resid- Pathophysiology
ual long-term paralysis), with the use of glottal local
anaesthetic spray for emergency intubation and At a cellular level, status epilepticus results from a failure
ventilation. of normal inhibitory pathways, primarily mediated by
● Placement of small-bore duodenal tubes decreases the gamma-aminobutyric acid (GABA) acting via GABA (A)
risk of aspiration and may be more comfortable than receptors. This loss of inhibitory drive allows the activa-
regular nasogastric tubes for the patient. tion of excitatory feedback loops, leading to repetitive,
● Tracheostomy is generally not needed, as the duration synchronous firing of large groups of neurons. As seizure
of intubation is often less than 2 weeks. activity continues, there is further decline in GABAergic
● Cardiac assessment needs to include assessment for function. Continued excitatory input mediated primarily
119
arrhythmias of both atrial and ventricular origin due by glutamate leads to neuronal cell death.
112
to autonomic nerve dysfunction. These can be insid-
ious and can be provoked by subtle changes in Clinical Manifestations
electrolytes. Convulsive SE is a medical emergency. The initial conse-
● Nursing care will relate to the needs of long-term quence of a prolonged convulsion is a massive release of
immobilised, intubated, ventilated patients with neu- plasma catecholamines, which results in a rise in heart
romuscular alterations. rate, blood pressure and plasma glucose. During this
Myasthenia gravis patients have similar care needs to stage cardiac arrhythmias are often seen, and may be
those of patients with GBS (refer to Independent practice fatal. Cerebral blood flow is greatly increased, and thus
for GBS). Fatigue and the structure and timing of care are glucose delivery to active cerebral tissue is maintained. As
very important. Flexibility of care is important, as energy the seizure continues, hyperthermia above 40°C with
117
fluctuates on an hourly basis. Despite having a shorter lactic and respiratory acidosis continues to intensify espe-
recovery time than GBS, weaning and recovery in myas- cially without adequate resuscitation and control of the
thenia gravis is a still a slow process and impulsive extu- seizure. 122
bation is discouraged. Therapy should be tailored on The SE may then enter a second, late phase in which
118
an individual basis using best clinical judgment. cerebral and systemic protective measures progressively
fail. The main characteristics of this phase are: a fall
SELECTED NEUROLOGICAL CASES in blood pressure; a loss of cerebral autoregulation,
resulting in the dependence of cerebral blood flow on
STATUS EPILEPTICUS systemic blood pressure; and hypoglycaemia due to the
Status epilepticus (SE) has been generally defined as exhaustion of glycogen stores and increased neurogenic
enduring seizure activity that is not likely to stop spon- insulin secretion. Intracranial pressure can rise precipi-
taneously. The traditional SE definition is 30 minutes of tously in SE. The combined effects of systemic hypoten-
continuous seizure activity (which has recently been sion and intracranial hypertension may result in a
updated due to neurological alteration to 5 minutes only) compromised cerebral circulation and cerebral oedema.
or 2 or more seizures without full recovery of conscious- Intracranial pressure monitoring is advisable in pro-
119
ness between the seizures. There are as many types of longed severe SE when raised intracranial pressure is sus-
SE as there are types of seizures. The distinction between pected. Further complications that can occur include
convulsive and nonconvulsive SE depends on clinical rhabdomyolysis leading to acute tubular necrosis, hyper-
observation and on a clear understanding of several SE kalaemia and hyponatraemia. 122
types. Estimates of the overall incidence of SE have varied
from 10 to 60 per 100,000 person-years, depending on Nursing Practice
120
the population studied and the definitions used. Over
half the cases of SE are acute symptomatic, emphasising The following nursing practice should be undertaken.
the importance in management of identifying an acute
precipitant. Infections with fever are the major cause Resuscitation
of SE, accounting for 52% of cases, while in adults SE requires control of the seizure and then investigation
low antiepileptic drug levels, cerebrovascular accident, regarding the cause. Airway protection is often difficult in
hypoxia, metabolic causes and alcohol represent the the seizing patient, so the first line of treatment includes