Page 494 - ACCCN's Critical Care Nursing

Neurological Alterations and Management 471

basic life-support measures followed by the administra- its recurrence. The best regimen for an individual patient
tion of IV propofol, midazolam or, in refractory cases, will depend on the cause of the seizure and any history
phenytoin. Neuromuscular blockade will be required to of antiepileptic drug therapy. A patient who develops SE
facilitate intubation in patients who continue to have in the course of alcohol withdrawal may not need anti-
tonic–clonic seizure activity despite these pharmacologi- epileptic drug therapy once the withdrawal has run its
cal interventions. Rocuronium (1 mg/kg), a short-acting, course. In contrast, patients with new, ongoing epilepto-
non-depolarising muscle relaxant that is devoid of sig- genic stimuli (e.g. encephalitis or trauma) may require
nificant haemodynamic effects and does not raise intra- high doses of antiepileptic medication to control their
cranial pressure, is the preferred agent. Succinylcholine seizures.
should be avoided if possible, as the patient may be
hyperkalaemic as a consequence of possible rhabdomy-
olysis. Prolonged neuromuscular blockade should be INTRACEREBRAL HAEMORRHAGE
avoided as it only stops the motor response hence
123
masking the altered neuronal activity. Once the sei- Intracerebral haemorrhage (ICH) is an acute and sponta-
zures are controlled, intubation and ventilation can neous extravasation of blood into the brain parenchyma
protect the airway and potentially reverse the acidosis. In and is one of the most serious subtypes of stroke, affect-
the patient who already has an airway secured, urgent IV ing over a million people worldwide each year, most of
administration of propofol, midazolam or phenytoin is whom live in Asia. About one-third of people with ICH
indicated. 124 die early after onset. The majority of survivors are left
with major long-term disability. ICH accounts for 10–
30% of all stroke admissions to hospital, and leads to
Specific post-SE patient assessment catastrophic disability, morbidity, and a 6-month mortal-
ity of 30–50%. 126 Long-term outcomes are poor: only
Post-SE, the patient remains intubated, ventilated and 20% of patients regain functional independence at 6
sedated. Neurological assessment is limited in the sedated months. ICH is most common in men, in elderly people,
patient. Pupillary response is usually sluggish and reflects and in Asians and African–Americans. The annual crude
the medication prescribed. Routine monitoring in an incidence of stroke in Australia has been estimated at
ICU is essential, with CT and MRI to exclude mass lesions. 17.8 per 100,000 126 and in 2006 there were 8484 deaths
The blood glucose level should be checked immediately attributable to stroke. 127
by bedside testing. Blood should be tested for electro-
lytes, magnesium, phosphate, calcium, liver and renal There are several modifiable risk factors for spontaneous
function, haematocrit, WBC count, platelet count, anti- ICH. Hypertension is by far the most important and
epileptic drug levels, toxic drugs (particularly salicylates) prevalent risk factor, directly accounting for about 60–
and alcohol. 70% of cases. 128 Chronic hypertension causes degenera-
tion, fragmentation, and fibrinoid necrosis of small
EEG monitoring in the ICU for refractory SE is essen-
tial, as a patient may enter a drug-induced coma with penetrating arteries in the brain, which can eventually
little outward sign of convulsions yet have ongoing result in spontaneous rupture. Hypertensive ICH typi-
electrographic epileptic activity. Furthermore, continu- cally occurs in the basal ganglia (putamen, thalamus or
ous reco rding will give an indication of worsening of caudate nucleus), pons, cerebellum, or deep hemispheric
generalised convulsive status epilepticus regardless of white matter.
the presence or absence of sedating drugs or paralysing
agents. This can be monitored only by EEG and mani- Pathophysiology
fests as bilateral EEG ictal discharges. Deeper sedation
and anaesthesia is then indicated and can be titrated to Understanding of the pathophysiology of ICH has
EEG results. 124 changed in recent years. What was thought to be a simple
and rapid bleeding event is now understood to be a
dynamic and complex process that involves several dis-
Collaborative practice tinct phases. The two most important new concepts are
Because only a small fraction of seizures go on to that many haemorrhages continue to grow and expand
over several hours after onset of symptoms – a process
become SE, the probability that a given seizure will known as early haematoma growth – and that most of
proceed to SE is small at the start of the seizure and the brain injury and swelling that happens in the days
increases with seizure duration. The goal of pharmaco- after ICH is the result of inflammation caused by throm-
logical therapy is to achieve the rapid and safe termina- bin and other coagulation end-products. 129
tion of the seizure, and to prevent its recurrence without
adverse effects on the cardiovascular and respiratory On rupture of a pathologically altered artery, blood
systems or without altering the level of consciousness. extravasates into the surrounding parenchyma. The
Diazepam, lorazepam, midazolam, phenytoin and phe- blood appears to dissect tissue planes, compressing
nobarbitone have all been used as first-line therapy for adjacent structures. Serial imaging has shown that 20–
the termination of SE. 125 The antiseizure activity of phe- 38% of ICH haematomas enlarge within 36 hours of
3
nytoin is complex; however, its major action appears to onset. Hae matomas larger than 25 cm are more likely
block the voltage-sensitive, use-dependent sodium chan- to grow in the first six hours after symptom onset. In
nels. Once SE is controlled, attention turns to preventing addition, elevated systolic blood pressure and serum