ACCCN's Critical Care Nursing

428 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


Parietal emissary
Superior sagittal sinus
Inferior sagittal sinus
Diploic


Superior ophthalmic

Straight sinus Cavernous sinus
Superior petrosal sinus

Transverse sinus Angular
Sigmoid sinus
Mastoid emissary
Inferior petrosal sinus

Retromandibular
Anterior facial
Maxillary

Internal jugular
External jugular
Vertebral
FIGURE 16.9 Cerebral venous drainage.
23
1
PaO 2 . This vasoconstriction will decrease the CBF. In
TABLE 16.5 Changes in cerebrovascular and addition, intrinsic factors can change the extrinsic factors
cerebrometabolic parameters when various cerebral by altering the metabolic mechanisms. These changes can
variables are reduced with and without intact lead to an alteration in the CBF. For example, there can
autoregulation be a change from aerobic to anaerobic metabolism,
which increases the concentrations of other end-products
Primary reduction in such as lactic acid, pyruvic acid and carbonic acid, which
these variables CBF CBV (ICP) AVDO 2 causes a localised acidosis. These end-products result in
a high pH which will cause an increase in CBF. Other
↑ ↓ —
factors that can affect CBF include pharmacological
CMRO 2
CPP (autoregulation intact) — ↑ — agents (anaesthetic agents and some antihypertensive
CPP (autoregulation defective) ↓ ↓ ↑ agents), rapid-eye-movement sleep, arousal, pain, sei-
zures, elevations in body temperature, and cerebral
Blood viscosity — ↓ — trauma.
(autoregulation intact)
Blood viscosity ↑ — ↓ Spinal Cord
(autoregulation defective)
The spinal cord is the link between the peripheral nervous
↓ ↓ ↑
PaCO 2
system and the brain. The spinal cord has a small, irregu-
Conductive vessel diameter ↓ ↑ ↑ larly shaped internal section of grey matter (unmyelin-
(vasospasm above ated tissue) surrounded by a larger area of white matter
ischaemic threshold)
(myelinated axons). The internal grey matter is arranged
CBF = cerebral blood flow; CBV = cerebral blood volume; ICP = intracranial so that a column of grey matter extends up and down
pressure; AVDO 2 = arteriovenous O 2 difference; CMRO 2 = cerebral metabolic dorsally, one on each side; another column is found in
rate of oxygen; CPP = cerebral perfusion pressure; PaCO 2 = arterial CO 2 1
tension; ↑ = increase; ↓ = decrease; — = no change. the ventral region on each side (see Figure 16.10).
The spinal cord is an essential component of both the
sensory and motor divisions of the nervous system. The
Intrinsic factors include PaCO 2 (pH), PaO 2 and ICP. The first of the primary functions of the spinal cord is to
vessels dilate with increases in PaCO 2 (hypercarbia) or transmit sensory impulses along the ascending tracts to
low pH (acidosis) and with decreases in PaO 2 (hypoxia). the brain as well as to transmit motor impulses down the
24
This vasodilation increases CBF. The vessels constrict with descending tracts away from the brain. The second
decreases in PaCO 2 or high pH and with increases in local primary function of the spinal cord is to house and

Neurological Assessment and Monitoring 429

White matter Grey matter


Ventral root Spinal nerve




Dorsal root Dorsal root
ganglion


Arachnoid Pia mater












Dura mater




A Posterior view



Dura mater
Vertebral Pia mater Subarachnoid
body Anterior Arachnoid space
Rami Autonomic
communicantes (sympathetic)
ganglion

Ventral root
of spinal
nerve

Ventral
ramus

Dorsal
Spinal cord ramus
Dorsal root
Adipose tissue ganglion
in epidural space Denticulate
ligament
Posterior
B Sectional view
FIGURE 16.10 The spinal cord and spinal meninges; (A) posterior view of the spinal cord, showing the meningeal layers, superficial landmarks, and dis-
tribution of grey matter and white matter; (B) sectional view through the spinal cord and meninges, showing the peripheral distribution of spinal nerves. 1


regulate spinal reflexes. Receipt of sensory impulses may activity, smooth muscle activity and secretion by both
cause a reaction anywhere in the body; alternatively, the endocrine and exocrine glands.
signal might be stored in the memory to be used at
some stage in the future. Within the motor division of Sensory neurons from all over the skin, except for the skin
the nervous system the spinal cord helps to control of the face and scalp, feed information into the spinal
the various bodily activities, including skeletal muscle cord through the spinal nerves. The skin surface can

430 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


C-2
C-2
C-3

C-3 C-4
C-4 C-5
T-2 C-6
C-5 T-3 T-2
T-4 T-6 T-3
T-5 T-7
T-6 T-8 C-7
T-7 T-9
T-1
T-8 T-10
T-9 T-11 C-8
C-6 T-10 T-12 T-1
T-11
T-12 C-6
C-7 L-1 L-1
L-1 S-3 L-1
S-3 S-3
L-2 L-2
S-4
C-8 L-2 L-2
L-3 L-3

S-2 S-2
L-5 L-5 L-4
L-4 L-4

L-5


S-1 S-1
FIGURE 16.11 (A) Anterior and (B) posterior distri- A B
25
butions of dermatomes on the surface of the skin. Anterior view Posterior view


be mapped into distinct regions that are supplied by a have previously been discussed regarding their role in
25
19
single spinal nerve (see Figure 16.11). Each of these brainstem function. The PNS has both motor and sensory
regions is called a dermatome. Sensation from a given components. The former includes the motor neuron cell
dermatome is carried over its corresponding spinal nerve. body in the anterior horn of the spinal cord and its
This information can be used to identify the spinal nerve peripheral axonal process travelling through the ventral
or spinal segment that is involved in an injury. In some root and eventually the peripheral nerve. The motor nerve
areas, the dermatomes are not absolutely distinct. Some terminal, together with the muscle endplate and the
dermatomes may share a nerve supply with neighbouring synapse between the two, comprises the neuromuscular
regions. For this reason, it is necessary to numb several junction. The peripheral sensory axon, beginning at
adjacent dermatomes to achieve successful anaesthesia. receptors in cutaneous and deep structures, as well as
muscle and tendon receptors, travels back through periph-
The blood supply to the spinal cord arises from branches eral nerves to its cell body located in the dorsal root
19
of the vertebral arteries and spinal radicular arteries. The ganglion. Its central process, travelling through the dorsal
midthoracic region, at approximately T4–T8, lies between root, enters the spinal cord in the region of the dorsal
the lumbar and vertebral arterial supplies and is a vulner- horn. All commands for movement, whether reflexive or
able zone of relatively decreased perfusion. This region is voluntary, are ultimately conveyed to the muscles by the
most susceptible to infarction during periods of hypo- activity of the lower motor neurons.
tension, thoracic surgery or other conditions, causing
decreased aortic pressure and potentially leading to isch-
aemic spinal injury with devastating consequences. 19 Motor Control
Movements can be divided into three main classes:
PERIPHERAL NERVOUS SYSTEM voluntary activity, rhythmic motor patterns, and reflex
The PNS consists of 12 pairs of cranial nerves and 31 pairs responses. The highest-order activity is voluntary move-
of spinal nerves, and includes all neural structures lying ment, which allows for expression of the will and a
outside the spinal cord and brainstem. The cranial nerves purposeful response to the environment (e.g. reading,

Neurological Assessment and Monitoring 431

1
speaking, performing calculations). Such activity is goal- exceptions, act on their effectors by releasing the neu-
directed and largely learned, and improves with practice. rotransmitter adrenaline and the related compound nor-
In rhythmic motor patterns, the initiation and termina- adrenaline. This system is therefore described as adrenergic,
1
tion may be voluntary, but the rhythmic activity itself which means ‘activated by adrenaline’. The autonomic
does not require conscious participation (e.g. chewing, regulation of several organ systems of particular impor-
walking, running). Reflex responses are simple, stereo- tance in clinical practice is illustrated in Figure 16.12. 15
typed responses that do not involve voluntary control
(e.g. deep tendon reflexes or withdrawal of a limb from NEUROLOGICAL ASSESSMENT
a hot surface). Motor control is carried out in a hierarchi- AND MONITORING
cal yet parallel fashion in the cerebral cortex, the brain-
stem and the spinal cord. Modulating influences are This section explores the complex issues surrounding
provided by the basal ganglia and cerebellum through the cerebral haemodynamics and assessment. The objective
thalamus. 1 of assessment is to determine the extent of neurological
injury, recognise fluctuations in condition and imminent
Sensory Control deterioration, and assist in maintaining cerebral perfu-
The somatic sensory system has two major components: sion as part of multimodal monitoring.
a subsystem for the detection of mechanical stimuli (e.g. PHYSICAL EXAMINATION
light touch, vibration, pressure, cutaneous tension), and
a subsystem for the detection of painful stimuli and tem- The neurological physical exam begins at the onset of
perature. Together, these subsystems give the ability to patient contact, and the priorities are defined by a primary
1
identify the shapes and textures of objects, to monitor the survey and vital signs. The history and contact with family
internal and external forces acting on the body at any can inform the clinical exam and should include the
moment, and to detect potentially harmful circumstances. patient’s normal baseline status, medications and other
Mechanosensory processing of external stimuli is initi- substance use, and past neurological symptoms such as
ated by the activation of a diverse population of cutane- syncope or seizures.
ous and subcutaneous mechanoreceptors at the body Specific areas tested during the initial physical exam
surface that relays information to the central nervous include level of consciousness, general behaviour,
system for interpretation and ultimately for action. Addi- memory, attention and concentration, abstract thought
tional receptors located in muscles, joints and other deep and judgement. Not every aspect of the examination will
structures monitor mechanical forces generated by the be relevant in all critical care situations and therefore may
musculoskeletal system, and are called proprioceptors. not be tested. Nevertheless, the clinician should under-
Mechanosensory information is carried to the brain by stand how all components are integrated and how they
several ascending pathways that run in parallel through influence priority decision making for patient care. At
the spinal cord, brainstem and thalamus to reach the change of shift, performing a physical exam with the
primary somatic sensory cortex in the postcentral gyrus incoming nurse ensures clear communication of the
1
of the parietal lobe. The primary somatic sensory cortex patient’s previous status. The patient’s ability to perform
projects in turn to higher-order association cortices in the should be taken into consideration, as it may be neces-
parietal lobe, and back to the subcortical structures sary to modify assessment techniques. For example, intu-
involved in mechanosensory information processing. bated patients who are otherwise awake and aware may
Autonomic Nervous System gesture or write answers to questions instead of verbalis-
ing them. In addition, when patients are the recipients of
The autonomic nervous system, with its three major divi- very frequent neurological assessment over an extended
sions (sympathetic, parasympathetic and enteric), is period of time (including arousal and awareness, pupil
largely an involuntary system and is part of the efferent and motor response) sleep and sensory rest deprivation
division, as we saw in Figure 16.1. It allows the body to is common. Sleep deprivation and sensory overload will
adjust to rapidly changing external events (the ‘flight or confound assessment accuracy. Therefore careful consid-
fight’ response of the sympathetic division), and to regu- eration needs to be given in regard to the priorities of
late internal activities (blood pressure, temperature, assessment and rest; a plan needs to implemented to
airway and breathing, urinary function, digestion by the promote rest as neurological injury requires rest and sleep
1
parasympathetic and enteric divisions). Whereas the for restoration. See Online resources for links to a full neu-
major controlling centres for somatic motor activity are rological assessment and physical examination protocol.
the primary and secondary motor cortices in the frontal
lobes and a variety of related brainstem nuclei, the major Conscious State
locus of central control in the visceral motor system is the Arousal and awareness are the fundamental constituents
hypothalamus and the complex circuitry that it controls of consciousness and should be evaluated and docu-
1
in the brainstem tegmentum and spinal cord. The status mented repeatedly for trend analysis. Changes in the con-
of both divisions of the visceral motor system is modu- scious state are the first to change in deterioration.
lated by descending pathways from these centres to pre-
ganglionic neurons in the brainstem and spinal cord, Arousal assessment
which in turn determine the activity of the primary vis- The evaluation of arousal focuses on the ability to be
ceral motor neurons in autonomic ganglia. The post- able to respond to a variety of stimuli and can be
ganglionic neurons of the sympathetic system, with few described using the AVPU scale or terms such as

432 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


Sympathetic division Parasympathetic division

Dilates pupil Constricts pupil

Oculomotor
Stimulates nerve (CN III)
salivation and
Inhibits lacrimation
salivation and Facial nerve (CN VII)
lacrimation
Cranial Glossopharangeal Cranial
nerve (CN IX)

Superior Constricts Vagus
nerve
Cervical airways (CN X)
ganglion
Dilates
airways
Cervical Cervical
Inferior
cervical
(stellate)
ganglion Accelerates
T1 heartbeat Slows
T2 Stimulates secretion heartbeat
T3 by sweat
T4 glands Stimulates glucose
production
T5 and release
Thoracic T6 Fibre-erection Liver Thoracic
T7
T8 Hair Inhibits Stimulates
follicle
digestion
T9 Coeliac digestion
ganglion
T10
T11 Stomach
T12
Stimulates gall bladder
L1 to release bile
Constricts Gall
L2 systemic bladder
Lumbar L3 blood vessels Lumbar
Pancreas
Superior
mesenteric Dilates blood
ganglion vessels in
Adrenal intestines S2
Sacral Constricts S3 Sacral
blood vessels
in intestines S4
Stimulates secretion
of adrenaline and
noradrenaline Relaxes urinary
bladder
Stimulates urinary
bladder to contract
Stimulates penile
Inferior erection
Sympathetic mesenteric
trunk ganglion
Stimulates Key
ejaculation Acetylchloline
Paravertebral Provertebral Parasympathetic ganglia Noradrenaline
ganglia ganglia in or near end organs
FIGURE 16.12 Sympathetic and parasympathetic divisions of the autonomic nervous system. Sympathetic outputs (left) arise from thoracolumbar spinal
cord segments and synapse in paravertebral and prevertebral ganglia. Parasympathetic outputs (right) arise from craniosacral regions and synapse in
15
ganglia in or near effector organs.


disorientated, lethargic, or obtunded. The advanced motor). If there is no response to voice or light touch,
26
trauma life support course recommends an initial painful stimulus is needed to assess neurological status.
assessment during initial resuscitation based on the Central pain should be used first and applied with care.
response to stimulation: Awake, Verbal, Pain, Unrespon- Sternal rub, supraorbital pressure (least used), trapezius
sive (AVPU). Observe the patient’s response (verbal or pinch (most used) or pinching the fleshy portion of the

Neurological Assessment and Monitoring 433

upper arm near the axilla are methods for introducing ● pinpoint non-reactive pupils are associated with
central pain. Hand grasp is a reflex and is a poor test for opiate overdose
motor strength. If the patient does not respond to verbal ● non-reactive pupils may also be caused by local
stimulus but moves spontaneously in a purposeful damage
manner (picks at linen, pulls at tubes), the patient is ● atropine will cause dilated pupils
localising. Painful stimulus is not required if spontane- ● one dilated or fixed pupil may be indicative of an
ous localisation has been observed. Watch for symmetry. expanding or developing intracranial lesion, com-
Localising is purposeful and intentional movement pressing the oculomotor nerve on the same side of the
intended to eliminate a noxious stimulus, whereas with- brain as the affected pupil
drawal is a ‘smaller’ movement used to ‘get away from’ ● A sluggish pupil may be difficult to distinguish from
noxious stimulus. Abnormal flexion differs from with- a fixed pupil and may be an early focal sign
drawal in that the flexion is rigid and abnormal looking. of an expanding intracranial lesion and raised intra-
Abnormal extension is a rigid movement with extension cranial pressure. A sluggish response to light in a
of the limbs. previously reacting pupil must be reported
immediately.
Assessment of awareness Assessment of pupillary function focuses on three areas:
If arousable, progress to assessment of awareness using (1) estimation of pupil size and shape; (2) evaluation of
27
the Glasgow Coma Scale (GCS). Teasdale and Jennett pupillary reaction to light; and (3) assessment of eye
designed the GCS to establish an objective, quantifiable movements. Metabolic disturbances rarely cause pupil-
measure to describe the prognosis of a patient with a lary changes, so abnormal pupillary findings are usually
30
brain injury and include scoring of separate subscales due to a nervous system lesion. Irregular-sized pupils
related to eye opening, verbal response and motor are normal for some people and eye prostheses are
response (Table 16.7). Originally, the GCS was developed common so it is important to establish and document
as three separate response areas and reported as such. these findings so a trend can be established to determine
Contemporary use of the GCS automatically adds the normal from altered states.
three best response scores and easily loses the informa-
tion given from the separate response areas. Reporting the Eye and eyelid movements
GCS as three numbers and then the total gives a broader Patients who are comatose will exhibit no eye opening.
assessment interpretation.
In patients with bilateral thalamic damage, there may be
The advantage of the GCS is that it allows rapid serial normal consciousness, but an eye opening apraxia may
comparisons and categorisation of basic neurological mimic coma. If the patient’s eyes are closed, the clinician
function over time. However, it has several recognised should gently raise and release the eyelids. Brisk opening
weaknesses, including poor prediction of outcome and closing of the eyes indicates that the pons is grossly
beyond survival, poor interrater reliability, and inconsis- intact. If the pons is impaired, one or both eyelids may
tent use in the prehospital and hospital settings. GCS close slowly or not at all. In the patient with intact frontal
accuracy will be affected if the patient is receiving anaes- lobe and brainstem functioning, the eyes, when opened,
thetic agents or sedation and noxious stimuli should be should be pointed straight ahead and at equal height. If
avoided. Furthermore, the rare event of a locked-in syn- there is awareness, the patient should look towards
drome where a patient is neurologically aware and awake stimuli after eye opening. Eye deviation indicates either
but not responding is poorly represented by the GCS. a unilateral cerebral or brainstem lesion. If the eyes
Also, interpretation of response in regard to language deviate laterally, gently turn the head to see if the eyes
used or a previous communication disability is important will cross the midline to the other side. A pattern of
for assessment accuracy. See Online resources for a link to spontaneous, slow and random movements (usually lat-
a full GCS procedure. erally) is termed roving-eye movements. This indicates
that the brainstem oculomotor control is intact but
awareness is significantly impaired. 31
Eye and pupil assessment
Pupillary responses, including pupil size and reaction Limb movement
to light, are important neurological observations and
localise cerebral disease to a specific area of the brain. Assessment of extremities and body movement (or motor
response) provides valuable information about the
32
The immediate constriction of the pupil when light is patient with a decreased level of consciousness. The
shone into the eye is referred to as the direct light clinician must observe the patient’s spontaneous move-
reflex. Withdrawal of the light should produce an ments, muscle tone, and response to tactile stimuli.
immediate and brisk dilation of the pupil. Introduction Decorticate (flexor) posturing is seen when there is
of the light into one eye should cause a similar con- involvement of a cerebral hemisphere and the brain stem.
striction to occur in the other pupil (consensual light It is characterised by adduction of the shoulder and arm,
reaction). 28 elbow flexion, and pronation and flexion of the wrist
while the legs extend. In terms of the GCS motor score,
Other points to consider when conducting pupillary the withdrawal flexor scores a higher (4/6) than a spastic
observations include the following: 29 flexor movement (3/6). Decerebrate (extensor) posturing

434 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

is seen with severe metabolic disturbances or upper have been assessed because this noxious stimulation may
brainstem lesions. It is characterised by extension and cause alteration in pupillary reactivity (hence one reason
pronation of the arm(s) and extension of the legs. Patients for the lack of preference for its use).
may have an asymmetrical response and may posture
spontaneously or to stimuli. Corneal reflexes
Motor tone is first assessed by flexing the limbs and noting The corneal reflex is assessed by holding the patient’s eye
35
33
increased or absent tone. If no tone is present, the open and lightly stimulating the cornea. The stimuli
hand is lifted approximately 30 cm above the bed and should result in a reflexive blink, best seen in the lower
carefully dropped while protecting the limb from injury. eyelid. The traditional assessment technique involves
The test is repeated with all extremities. Typically, the using a wisp of cotton, lightly brushed along the lower
lower the level of consciousness, the closer to flaccid the aspect of the cornea. An alternative, and less potentially
limb(s) will be. An asymmetrical examination may traumatic, method is to gently instil isotonic eye drops
indicate a lesion in the contralateral hemisphere or or saline irrigation ampoules onto the cornea. This reflex
brainstem. is dependent upon CN V for its sensation and CN VII for
its motor response. Loss of this reflex is indicative of
The next assessment, peripheral reflex response, is response lower brainstem damage, but may be absent due to
to tactile stimuli peripherally and usually elicits a reflex trauma, surgery, or long-term contact lens usage.
response rather than a central or brain response. It is
important to apply stimuli in a progressive manner, using
the least noxious stimuli necessary to elicit a response. If Oropharyngeal reflexes
there is no response to light or firm pressure, the clinician The oropharyngeal reflexes are controlled by CN IX and
36
must use noxious stimuli. Each extremity is assessed indi- CN X. The gag reflex is elicited by lightly stimulating the
vidually. The typical technique for peripheral noxious soft palate with a suction catheter or tongue blade. Clini-
stimuli involves pressure on the nail beds for asserting a cians should always avoid stimulating a gag reflex by wig-
peripheral stimulus. The triple-flexion response is a with- gling the endotracheal tube because doing so may result
drawal of the limb in a straight line with flexion of in an inadvertent extubation. A gag reflex is a forceful,
the wrist–elbow–shoulder or the ankle–knee–hip. This symmetrical lowering of the soft palate. The cough reflex
response is considered a spinal reflex and is not an indica- is usually assessed only in patients with an endotracheal
tion of brain involvement in the movement. The triple- tube. This reflex is elicited by gently passing a suction
flexion response is common in patients with severe catheter through the tube and stimulating a cough. Loss
neurological impairment. It is not uncommon in patients of these reflexes is indicative of lower brainstem damage. 37
who have become brain dead, and great care must be
taken to avoid confusion between brain and spinal- Post Traumatic Amnesia Scale
mediated responses. If the patient has any other motor Posttraumatic amnesia (PTA) is a disorder after brain injury
activity to peripheral extremity noxious stimuli, it is an that is classified as a traumatic delirium and may even
indication of higher brain function. 38
be found in patients who rate a GCS of 15. The inci-
If a noxious stimuli is applied centrally through a sternal dence of delirium after a brain injury event is high espe-
rub, trapezius pinch or supraorbital nerve pressure and cially with severe injuries and loss of consciousness.
the patient moves an extremity, it is an indication of brain Delirium is discussed in detail in Chapter 7, however,
involvement in the movement and not a spinal reflex. traumatic delirium historically has been referred to in
34
The movement should be noted as normal, decorticate the literature as posttraumatic amnesia. Posttraumatic
(flexor: either withdrawal or spastic) or decerebrate amnesia is defined as the ‘time elapsed from injury until
(extensor) and documented accordingly. It should be recovery of full consciousness and the return of ongoing
noted that careful consideration should be given to the memory’. 39,p.841 It is the initial stage of recovery from brain
choice of noxious stimuli with trapezius pinch the pre- injury and is characterised by anterograde (formation of
ferred choice as both sternal rub and supraorbital nerve new memory) and retrograde (memory before injury)
pressure can be traumatic when applied. In ventilated amnesia, disorientation and rapid forgetting. Brief periods
patients, endotracheal suction can also be a substitute for of PTA can occur after minor concussion and may be the
a central noxious stimulus, but the choice of stimulus only clinical sign of any brain injury. This is where PTA
needs to be consistent. is useful for defining severity of injury and alert the clini-
cian in regard to greater surveillance and investigation as
Facial symmetry described in Table 16.6. Patients often progress directly
Facial symmetry is often difficult to appreciate in, for from coma into delirium without a clearly-defined stupor
stage, so using a tool to measure PTA can be useful to
example, severely ill patients due to oedema, endotra- gauge the actual condition of the patient in the delirium
cheal tube tape and nasogastric tubes. An asymmetric state. Duration of PTA is extremely variable, ranging from
response is indicative of a lesion of CN VII. Complete minutes to months. Although the early stages of PTA are
hemi-facial involvement is typically seen in peripheral easily recognised, identifying the end point is difficult
dysfunction (Bell’s palsy), whereas superior division and complex. 40
(forehead) sparing weakness indicates a pontine/
medullary (central) involvement. It is important to refrain The duration of PTA is the best indicator of the extent of
from supraorbital pressure until after pupillary responses cognitive and functional deficits after TBI. In Australia,

Neurological Assessment and Monitoring 435



TABLE 16.6 PTA scale used to determine severity of TABLE 16.8 The brain and related structures in CT
brain injury
Structure/Fluid/Space Grey Scale
PTA Score Severity Bone, acute blood Very white
1–4 hours Mild brain injury Enhanced tumour Very white
Subacute blood Light grey
≤1 day Moderate brain injury Muscle Light grey
Grey matter Light grey
2–7 days Severe brain injury White matter Medium grey
1–4 weeks Very severe brain injury Cerebrospinal fluid Medium grey to black
Air, Fat Very black
1–6 months Extremely severe brain injury
>6 months Chronic amnesia state
than 2 weeks had a good recovery, compared with 46%
42
for those with a PTA duration between 4 and 6 weeks.
A person is said to be absolved of PTA if they can achieve
TABLE 16.7 Glasgow Coma Scale a perfect score for three consecutive days.
The Glasgow Coma Scale is scored between 3 and 15, 3 being the
worst, and 15 the best. It comprises three parameters: best eye ASSESSMENT OF THE INJURED BRAIN
response, best verbal response and best motor response. The The primary aim of managing patients with acute brain
definition of these parameters is given below. injury in the critical care unit is to maintain cerebral
43
perfusion and oxygenation. There is little that can be
The Glasgow Coma Paediatric version of
Scale for adults the Glasgow Coma Scale done to reverse the primary damage caused by an insult.
Secondary insults may be subtle and can remain unde-
Best eye response (4) Best eye response (4) tected by routine systemic physiological monitoring.
1. No eye opening 1. No eye opening Continuous monitoring of the central nervous system in
2. Eye opening to pain 2. Eye opening to pain 44
3. Eye opening to verbal 3. Eye opening to verbal the ICU serves three functions:
command command 1. determine the extent of the primary injury
4. Eyes open spontaneously 4. Eyes open spontaneously
2. early detection of secondary cerebral insults so that
Best verbal response (5) Best verbal response (5) appropriate interventions can be instituted
1. No verbal response 1. No vocal response 3. monitoring of therapeutic interventions to provide
2. Incomprehensible sounds 2. Occasionally whimpers and/
3. Inappropriate words or moans feedback.
4. Confused 3. Cries inappropriately Although serial cranial imaging such as computerised
5. Orientated 4. Less than usual ability and/or
spontaneous irritable cry tomography (CT) or functional magnetic resonance
5. Alert, babbles, coos, words or imaging (fMRI) provides useful information, these are
sentences to usual ability neither continuous nor can they be undertaken at the
Best motor response (6) Best motor response (6) bedside. Continuous invasive arterial blood pressure
1. No motor response 1. No motor response to pain monitoring in addition to pulse oximetry, temperature,
2. Extension to pain 2. Abnormal extension to pain end-tidal carbon dioxide and urine output should be
3. Flexion to pain (decerebrate) included as part of standard general monitoring of brain-
4. Withdrawal from pain 3. Abnormal flexion to pain
5. Localising pain (decorticate) injured patients. In addition, techniques specific to the
6. Obeys commands 4. Withdrawal to painful stimuli CNS are required. The commonest and most easily per-
5. Localises to painful stimuli or formed clinical assessment tool is the GCS. Brain-specific
withdraws to touch methods of monitoring reflect pressure in the cranial
6. Obeys commands or cavity, changes in brain oxygenation and metabolism
performs normal
spontaneous movements (brain oxygen saturation), jugular venous oxygen satura-
tion, near-infrared spectroscopy, brain tissue monitoring,
cerebral haemodynamics (transcranial Doppler) and
electrical activity of the CNS (EEG).
the most common means of assessing PTA is the West-
41
mead PTA scale. In this scale, four pictures, one with the Brain Imaging Techniques
examiner’s face and name, are to be recalled by the patient
on the next day. Those with severe PTA will have difficulty Computed tomography
recalling such short-term memory tasks. Often, patients CT is the primary neuroimaging technique in the initial
will have a GCS of 15 but have moderate to severe PTA evaluation of the acute brain injury patient and uses a
and can be overlooked by inexperienced clinicians who computer to digitally construct an image based upon the
fail to watch for secondary insults. The duration of PTA measurement of the absorption of X-rays through the
correlates well with the extent of diffuse axonal injury brain. Table 16.8 generally summarises the white to black
and with functional outcomes. For example, one study intensities seen for selected tissues in CT. The advantages
found that 80% of patients with a PTA duration of less of CT are: (1) it is rapidly done, which is especially

436 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



TABLE 16.9 A comparison of various imaging techniques for assessing brain structure haemodynamics

Imaging Technique Bedside use Spatial resolution Temporal resolution Scope of use Ease of interpretation
CEEG excellent good excellent excellent poor
Evoked potentials good fair Fair fair poor
Transcranial Doppler good fair Fair fair poor
MRI poor excellent poor good fair
Functional MRI poor excellent good poor poor
CT poor excellent poor good fair
Xenon CT poor good poor fair poor
ICP monitoring excellent poor good fair good
CEEG, continuous EEG; MRI, magnetic resonance imaging; CT, computed tomography; ICP, intracranial pressure.



important in neurological emergencies; (2) it clearly function, monitor the growth and function of brain
shows acute and sub-acute haemorrhages into the men- tumours and guide the planning of surgery or radiation
ingeal spaces and brain; and (3) it is less expensive than therapy for the brain. 49
45
a MRI. Disadvantages include: (1) it does not clearly
show acute or sub-acute infarcts or ischaemia, or brain Cerebral angiography
oedema, only established injury; (2) it does not clearly Cerebral angiography involves cannulation of cerebral
differentiate white from grey matter as clearly as an MRI; vessels and the administration of intraarterial contrast
and (3) it exposes the patient to ionising radiation. agents and medications for conditions involving the arte-
Despite these limitations it is still the most prevalent rial circulation of the brain. This procedure also has the
form of neurological imaging. 46 benefit of using non-invasive CT or MRI with or without
contrast to guide the accuracy of the procedure. For
Magnetic resonance imaging example, intracranial aneurysms and arteriovenous mal-
The tissues of the body contain proportionately large formations can be accurately diagnosed and repaired
amounts of protons in the form of hydrogen and func- without surgical intervention. 50
tion like tiny spinning magnets. Normally, these atoms Cerebral perfusion imaging techniques
are arranged randomly in relation to each other due to
the constantly changing magnetic field produced by the Numerous imaging techniques have been developed and
associated electrons. Magnetic Resonance Imaging (MRI) applied to evaluate brain haemodynamics, perfusion and
uses this characteristic of protons to generate images of blood flow. The main imaging techniques dedicated to
the brain and body. The advantages of MRI are: (1) it can brain haemodynamics are positron emission tomogra-
be manipulated to visualise a wide variety of abnormali- phy (PET), single photon emission computed tomogra-
ties within the brain; and (2) it can show a great deal of phy (SPECT), xenon-enhanced computed tomography
47
detail of the brain in normal and abnormal states. The (XeCT), dynamic perfusion computed tomography (PCT),
disadvantages of MRI are: (1) it does not show acute or MRI dynamic susceptibility contrast (DSC) and arterial
sub-acute haemorrhage into the brain in any detail; (2) spin labelling (ASL). All these techniques give similar
the time frame and enclosed space required to perform information about brain haemodynamics in the form of
51
and prepare a patient for the procedure is not advanta- parameters such as CBF or CBV. They use different
geous for neurological emergencies; (3) relatively more tracers and have different technical requirements. Some
expensive compared to CT; (4) the loud noise of the are feasible at the bedside and others not (see Table 16.9).
procedure needs to be considered in the patient manage- The duration of data acquisition and processing varies
ment; and (5) equipment for life support and monitoring from one technique to the other. Brain perfusion imaging
needs to be non-magnetic due to the magnetic nature of techniques also differ by quantitative accuracy, brain
the procedure. 48 coverage and spatial resolution. 52
Figure 16.13 is a scan from a traumatic brain injury
Functional magnetic resonance imaging patient and demonstrates a brain perfusion scan radio-
Functional magnetic resonance imaging (fMRI) is similar nuclide imaging. In the image the cerebral cortex is dark,
to MRI but uses deoxyhaemoglobin as an endogenous indicative of no CBF or perfusion confirming brain death.
contrast, and serves as the source of the magnetic signal
for fMRI. It can determine precisely which part of the Intracranial Pressure Monitoring
brain is handling critical functions such as thought, Invasive measures for monitoring intracranial pressure
speech, movement and sensation, help assess the effects (ICP) are commonly used in patients with a severe head
of stroke, trauma or degenerative disease on brain injury or after neurological surgery. Normal ICP varies

Neurological Assessment and Monitoring 437















FIGURE 16.13 Brain death confirmed with brain per-
fusion scan radionuclide imaging. The cerebral cortex
is dark, indicative of no CBF. Permission received from
patient’s next of kin (patient brain dead).

with age, body position, and clinical condition. The insertion of the ventriculostomy catheter may be diffi-
normal ICP is 7–15 mmHg in a supine adult, 3–7 mmHg cult. Importantly, bleeding or ventricular collapse may
56
in children, and 1.5–6 mmHg in term infants. The defini- occur if CSF is drained too rapidly. For this last reason,
tion of intracranial hypertension depends on the specific many clinicians set the ventriculostomy drainage system
pathology and age, although ICP >15 mmHg is generally to drain CSF when the ICP is greater than 15–20 mmHg
considered to be abnormal. Increased ICP causes a critical by adjusting the height of the drip chamber. In addition,
reduction in CPP and CBF and may lead to secondary a limit of ventricular drainage per hour using gravity and
ischaemic cerebral injury. A number of studies have three-way taps to 5–10 mL/h has been used to avoid
shown that high ICP is strongly associated with poor excessively rapid CSF drainage. Using a ventriculostomy
outcome, particularly if the period of intracranial may allow lifesaving CSF drainage and control of intra-
53
hypertension is prolonged. ICP is not a static pressure cranial hypertension and secondary injury. 57
and varies with arterial pulsation, with breathing and Whilst routine ICP monitoring is widely accepted as a
during coughing and straining. Each of the intracranial mandatory monitoring technique for management of
constituents occupies a certain volume and, being essen- patients with severe head injury and is a guideline sug-
tially liquid, is incompressible. ICP cannot be reliably gested by the Brain Trauma Foundation, there is some
estimated from any specific clinical feature or CT finding debate over its efficacy in improving outcome from severe
and must actually be measured. Different methods of TBI. A review of neurocritical care and outcome from
58
monitoring ICP have been described but two methods are TBI suggested that ICP/cerebral perfusion pressure (CPP)-
commonly used in clinical practice: intraventricular cath- guided therapy may benefit patients with severe head
eters and intraparenchymal fibreoptic microtransducer injury, including those presenting with raised ICP in the
systems. absence of a mass lesion and also patients requiring
The reference point for the transducer is the foramina of complex interventions. 59
Monro (the duct joining the lateral and third ventricle
that is in alignment with the middle of the ear), although, Pulse waveforms
in practical terms, the external auditory meatus is Interpretation of waveforms that are generated by the
often used.
cerebral monitoring devices is important in the clinical
Currently, ventriculostomy is the most accurate (although assessment of intracranial adaptive capacity (the ability
the intraparenchymal fibreoptic is now similar in accu- of the brain to compensate for rises in intracranial
60
racy), cost-effective and reliable method of monitoring volume without raising the ICP). Brain tissue pressure
ICP and is associated with low infection risks if the dura- and ICP increase with each cardiac cycle and, thus, the
54
tion of placement is less than 72 hours. The ventricu- ICP waveform is a modified arterial pressure wave. See
lostomy catheter is part of a system that includes an Figure 16.14. The cardiac waves reach the cranial circula-
external drainage system and a transducer. The drainage tion via the choroid plexus and resemble the waveforms
system and transducer are primed on insertion with transmitted by arterial catheters, although the amplitude
preservative-free saline. The transducer can easily be cali- is lower.
brated or zeroed against a known pressure. Advantages of 61
using an indwelling ventricular catheter include allowing There are three distinct peaks seen in the ICP waveform:
CSF drainage to effectively decrease ICP and using the ● P1: the percussion wave, which is sharp and reflects
catheter as a means to instil medications. Access to CSF the cardiac pulse as the pressure is transmitted from
drainage allows serial laboratory tests of CSF and deter- the choroid plexus to the ventricle;
mination of volume–pressure relationships. Disadvan- ● P2: the tidal wave, which is more variable in nature
tages of ventriculostomy include risk of infection, which and reflects cerebral compliance and increases in
is higher than that associated with other ICP-monitoring amplitude as compliance decreases;
55
techniques. In addition, the catheter may become ● P3: which is due to the closure of the aortic valve and
occluded with blood or tissue debris, interfering with is known as the dicrotic notch. Of recent importance
CSF drainage or ICP monitoring. Also, if significant cere- is that the elevation of the P3 may indicate low global
bral oedema is present, locating the lateral ventricle for cerebral perfusion. 62

438 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

threshold in adults especially those who are pressure-
63
P1 active (i.e. ICP varies inversely with MAP). Higher CPP
P2 has been associated with increased lung water and acute
respiratory distress syndrome. Furthermore, mortality
P3
rises approximately 20% for each 10 mmHg loss of CPP.
In those studies where CPP was maintained above
70 mmHg, the reduction in mortality was as much as
64
35% for those with severe head injury. The Brain Trauma
Foundation recommends a CPP goal of 50–70 mmHg
A despite the lack of definitive data, such as from ran-
domised controlled trials and intention-to-treat clinical
65
P2 trials. In the paediatric population a CPP >40 mmHg is
the recommended guideline. 66,67 Utilising cerebral oxy-
P3 genation monitoring in combination with pressure has
been associated with better outcomes for brain-injured
P1 patients, and is part of the multimodal assessment for
brain injury.

ASSESSMENT OF CEREBRAL OXYGENATION
Jugular Venous Oximetry
B
Jugular venous catheterisation is used for deriving oxygen
68
based variables. It facilitates the assessment of jugular
venous oxygenation (SjvO 2 ), cerebral oxygen extraction
(CEO 2 ), and arteriovenous difference in oxygen (AVDO 2 ).
All of these variables indicate changes in cerebral metabo-
lism and blood flow, and therefore the catheter generates
continuous data that reflect the balance between supply
and demand of cerebral oxygen.
C
The catheter is inserted in the right jugular vein, as it is
FIGURE 16.14 The intracranial pressure waveforms. ‘A’ depicts the situa- slightly larger than the left and provides readings that are
tion of a compliant system, ‘B’ A high pressure wave recorded from a more representative of overall brain function. The cath-
non-compliant system in which P2 exceeds the level of the P1 waveform, eter tip is advanced so that the tip sits in the bulb of the
due to a marked decrease in cerebral compliance. The lower tracing (C) is
an example of an ICP waveform from a patient monitoring system in which internal jugular vein.
can be identified the three distinct components, as indicated in the text.
The normal requirement for cerebral oxygen delivery is
consumption at 35–40% of available oxygen, giving a
normal SjvO2 of 60–65%. Changes in SjvO 2 reflect
It is important that the waveform be continuously changes in cerebral metabolic rate and cerebral blood
observed, as changes in mean pressure or in waveform flow; however, as it is a global measure it does not detect
shape usually require immediate attention. In acute states regional ischaemia. A high SjvO 2 is indicative of increased
such as head injury and subarachnoid haemorrhage, the cerebral blood flow, reduced oxygen consumption, and
value of ICP depends greatly on the link between moni- hyperventilation. Low SjvO 2 levels suggest that cerebral
toring and therapy, so close inspection of the trend of the perfusion is reduced, with levels below 40% indicative of
69
ICP and the details derived from the waveform is global cerebral ischaemia. However, caution must be
extremely important. Simple ongoing visual assessment used when interpreting values generated using this
of the ICP waveform for increased amplitude, elevated P2 method, as high values might also imply an increase in
and rounding of the waveform provides non-specific arteriovenous shunting secondary to vasoconstriction,
information suggestive of decreased intracranial adaptive maldistribution of blood flow or lack of oxygen con-
capacity and altered intracranial dynamics. sumption as in brain death. Because SjvO2 monitoring is
70
a global measure of cerebral oxygenation, smaller areas
Assessment of Cerebral Perfusion of ischaemia are not detected unless these are of sufficient
Cerebral perfusion pressure is calculated as the mean magnitude to affect global brain saturation. SjvO2
arterial pressure minus the intracranial pressure (ICP) requires special care such as frequent recalibration to
and represents the pressure gradient across the vessel that ensure accurate measurements, observing for catheter
drives cerebral blood flow (CBF): migration that interferes with signal quality, and often,
medical intervention is required to reposition the cathe-
−
CPP = MAP ICP ter. The position of the patient also affects signal quality,
and ideally the patient should be nursed supine with a
CPP is a pressure-based indicator of oxygen and meta- head elevation of 10–15° and at least a neutral head
bolite delivery. There is no evidence for the optimum alignment. It is important that measurement errors be
level of CPP, but 70–80 mmHg is probably the critical excluded when abnormal readings are noted; algorithms

Neurological Assessment and Monitoring 439

have been developed to assist nurses when caring for evaluating cerebral circulation and haemodynamics.
patients with jugular bulb oximetry. 71 Pulses of ultrasound are directed using a handheld trans-
ducer towards the vascular formations in the base of the
Partial Brain Tissue Oxygenation Monitoring skull. Velocities from the cerebral arteries, the internal
Changes in ICP values alone do not accurately depict carotids, the basilar and the vertebral arteries can be
poor cerebral blood flow or oxygenation deficits to brain sampled by altering transducer location, angle and the
tissue. Consequently brain tissue hypoxaemia is often instrument’s depth setting. The commonest windows in
observed during the first 24 hours after injury despite the cranium are located in the orbit (of the eye), and in
controlled brain pressures. Monitoring partial pressure of the temporal and suboccipital regions. TCD measures
oxygen in brain tissue (PbtO 2 ) can be used to collect systolic, diastolic and mean middle cerebral artery (MCA)
more accurate and timely information about cerebral flow velocities and a derived value, the pulsatility index
oxygen delivery and demand than ICP allows. A tissue (PI). Changes in the PI can be used to identify the thresh-
oxygen value of less than 10 mmHg for more than 10 old of autoregulation or cerebral perfusion pressure break
minutes carries a higher risk of death. Normal brain point in individual patients. In subarachnoid haemor-
oxygen levels (PbtO 2 between 20 and 25 mmHg) emerge rhage (SAH) and TBI this may be due to vasospasm, or
as a critical determinant of outcome, with values below impaired autoregulation or abnormal intracranial com-
20 mmHg carrying a higher risk. 69 pliance. TCD is a simple, portable and non-invasive tool,
well suited to serial monitoring, that can be used at the
Regardless of ICP, brain tissue oxygenation falls with a bedside to detect relative changes in CBF in brain-injured
decrease in cerebral blood flow below an ischaemic patients. 76
threshold of 18 mL/100 g/min. ICP may respond to the
changes but often several hours later when the damage Continuous Electroencephalography
can not be reversed. Alterations in cerebral metabolic rate Electroencephalography (EEG) is the recording of electri-
can also change tissue oxygen levels. Reducing the cal activity by sensors along the scalp produced by the
patient’s energy consumption via reduced noise and/or firing of neurons within the brain. Continuous EEG
distractions, and increasing their protein caloric intake to (cEEG) has the advantage of being continuous, noninva-
complement their increased stress state can improve sive and carrying the potential to detect alterations in
tissue oxygenation. 72 brain physiology at a reversible stage, which may trigger
treatment before permanent brain injury occurs. The
Microdialysis invention of digital EEG has made cEEG monitoring fea-
77
Cerebral microdialysis (using a catheter ideally placed in sible for ICU patients. Currently, the main applications
the frontal lobe) is a tool for investigating the metabolic of cEEG are diagnosing nonconvulsive status epilepticus,
status of the injured brain and is part of multimodal monitoring and guiding the treatment of status epilepti-
monitoring. The microdialysis probe is inserted into the cus and detecting delayed cerebral ischaemia from vaso-
cerebral tissue where substances in the extracellular fluid spasm in subarachnoid haemorrhage patients. Other
surround the semipermeable membrane at the tip of the applications may include monitoring of reperfusion after
catheter. Following equilibration of the tissue metabolites tissue plasminogen activator in acute stroke patients and
with the perfusion fluid, the dialysate can be analysed for detection of intracranial hypertension. Clinically unrec-
concentrations of products of energy metabolism (glucose, ognised electrographic seizures and periodic epileptiform
lactate, pyruvate) as indicators of hypoxia and ischaemia. discharges have been shown to be frequent and associ-
In addition, interstitial glycerol can be determined, which ated with poor outcome in patients with severe brain
is a parameter of lipolysis and/or cell membrane damage. injury from different aetiologies, including TBI, ischaemic
78
In theory, the microdialysis catheter acts like a blood and haemorrhagic strokes and CNS infection. The EEG
73
capillary. Thereby, it is proposed that microdialysis pro- becomes substantially abnormal (suppressed) when cere-
vides information regarding events that take place in the bral blood flow declines to 20–30 mL/100 g/min. More
tissue before any chemical events are reflected by changes subtle abnormalities accompany lesser degrees of hypo-
74
in systemic blood levels of indicator substances. These perfusion, including initial loss of beta activity, slowing
molecules diffuse across the membrane part of the cath- to the theta range, and then to the delta range. Irreversible
eter and equilibrate with the perfusion fluid, which is injury to brain tissue occurs at cerebral flows of about
pumped through the probe at very low rates of flow. 10–12 mL/100 g/min. Thus, the EEG sensitivity to isch-
Changes in the concentration of a substrate in the sur- aemia allows its use in situations where cerebral perfu-
79
rounding milieu are reflected by subsequent changes in sion is at risk. To facilitate interpretation, digital EEG
75
the dialysate. Rather than inserting an instrument into data can be transformed into power spectra by fast Fourier
the tissue, microdialysate is extracted and later analysed transformation. Changes over time in these quantitative
in the laboratory or clinically at the patient’s bedside. EEG (qEEG) parameters can trigger remote reading,
focused neurological examination, imaging studies and
NON-INVASIVE ASSESSMENT early treatment. Subtle EEG changes may be difficult to
Transcranial Doppler interpret in isolation, but may be better understood when
interpreted in concert with other components of a mul-
Transcranial Doppler (TCD) ultrasound has proven to be timodality monitoring paradigm, which may include
a safe, reliable and relatively inexpensive technology microdialysis, brain tissue oxygen and cerebral perfusion
for measuring cerebrovascular blood velocities and pressure.

440 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

Near-Infrared Spectroscopy haemorrhage, episodes of angiographic cerebral vaso-
Near-infrared spectroscopy (NIRS) is a non-invasive spasm were strongly associated with reduction in trend
81
method of monitoring continuous trends of cerebral in the ipsilateral NIRS signal. Furthermore, the degree
oxygenated and deoxygenated haemoglobin by utilising of spasm (especially more than 75% vessel diameter
an infrared light beam transmitted through the skull. reduction) was associated with a greater reduction in
Oxygenated and deoxygenated haemoglobin have same-side NIRS signal demonstrating real-time detection
different absorption spectra and cerebral oxygenation of intracerebral ischaemia.
and haemodynamic status can be determined by their
relative absorption of near-infrared light. NIRS allows SUMMARY
interrogation of the cerebral cortex using reflectance
spectroscopy via optodes, light transmitting and This chapter provides an overview of anatomy and physi-
detecting devices, placed on the scalp. Normal satura- ology in the context of and in application to neurological
tion is 70%. Because NIRS interrogates arterial, venous, assessment of the critically ill. Priorities of clinical assess-
and capillary blood within the field of view, the derived ment are described in terms of the critically ill patient.
saturation represents a regional tissue oxygenation (rSO 2 ) Imaging techniques and assessment incorporate the
measured from these three compartments and can be therapeutics of intracranial pressure, cerebral perfusion
used to identify tissue hypoxia and ischaemia in the pressure and partial brain tissue oxygenation monitor-
brain cortex. ing, cEEG, transcranial Doppler and cerebral perfusion
imaging. The research vignette reports how alcohol
The clinical and bedside use of NIRS is constrained by intoxication impacts upon clinical assessment using the
potential sources of error, which include contamination Glasgow Coma Scale score. The clinical case examples
of the signal by the extracerebral circulation (such as in neurological assessment priorities in an unstable, trau-
the scalp), extraneous light, and the presence of extravas- matic brain injury patient. Clinical, non-invasive and
cular blood arising from subarachnoid or subdural haem- invasive assessment techniques are described within the
80
orrhage. In a recent study in patients with subarachnoid context of this patient’s care.

Case study
On the 30th August, a 24-year-old male, Daniel, was riding his trail skin pink in colour, peripherally cold and pale; capillary refill
bike on a dirt road. Whilst negotiating a corner he collided at high >4 seconds.
speed with a truck and was dragged under the truck for approxi- ● Disability: He was unresponsive, GCS 3; pupils: left 3 mm and
mately 60 metres. He was wearing a helmet. At the scene his GCS right 5 mm non-reacting. Daniel was intubated using thiopen-
was 3 and his pupils, sized 3 mm in diameter, were reacting sequen- tone, fentanyl and rocuronium and mechanically ventilated in
tially to light. Rib and severe bilateral femur fractures were evident combination with physiological fluid resuscitation.
to the attending paramedics who applied compression to the
profusely-bleeding femur. Daniel’s helmet was removed; his airway Secondary survey
was maintained and the cervical spine immobilised, his chest The secondary survey revealed the following details.
decompressed by needle thorocentesis on the left side. Intrave- ● Head: scalp clear, nil abrasions. CT revealed widespread
nous access was obtained and normal saline infused. Oxygen was petechial haemorrhages consistent with diffuse axonal injury,
administered and Daniel was transferred to the nearest trauma acute subdural haemorrhage with midline shift of the ventri-
tertiary centre by helicopter. cles, hairline base of skull fracture and cerebral oedema with
poor differentiation between grey and white matter.
● Face: No oedema; rhinorrhoea and otorrhoea from both
Emergency Department
Arrival to the Emergency Department (ED) was 20 minutes later. nostrils and ears.
Daniel bypassed triage and was admitted to the resuscitation area ● Neck: Stiff neck collar left in situ; no obvious lacerations
where members of the trauma team conducted primary and sec- observed around neck area; no evidence of tracheal deviation.
ondary surveys. On presentation, Daniel’s vital signs were: heart Cervical spine CT reported no bony injury, spine not cleared;
rate 134 beats/min, respirations 8 breaths/min with paradoxical with a stable L4 pedicle fracture.
chest rise and fall, blood pressure 93/65 mmHg, mean arterial pres- ● Chest: Obvious chest deformity and instability of sternum and
sure (MAP) 74 mmHg, SaO 2 unable to obtain, temperature 34.9°C, ribs; paradoxical chest rise and expansion; decreased air entry
with a GCS of 3. bilaterally, no subcutaneous emphysema. Bilateral pulmonary
contusions, left haemopneumothorax diagnosed on review of
Primary survey the chest X-ray; a left sided chest drain was inserted.
Daniel’s primary survey revealed the following details. ● Abdomen: Firm, no abnormal distension, some bruising. IDC
● Airway: Upper airway cleared. Cervical spine: Status unknown, insertion revealed haematuria.
collar in situ. ● Pelvis: Bruising bilaterally with no obvious deformity.
● Breathing: Hand ventilated on 12 L/min at 14 breaths/min, ● Back: Marked flank bruising, no lacerations, right perinephric
paradoxical chest rise and fall, generalised poor air entry, haematoma on CT; rectal tone present. Upper limbs: Obvious
decreased bilaterally, no tracheal deviation. deformity of right arm; X-ray revealed right radial and ulna
● Circulation: Tachycardic, hypotensive, and hypovolaemic; fractures, lacerations and bruising present; pulses present.
pulses present on palpation except for the right popliteal ● Lower Limbs: Bilateral femur fractures – right one compound;
and dorsalis pedis; temperature centrally warm, well perfused, lacerations and extensive bruising; pulses absent right side.

Neurological Assessment and Monitoring 441



Case study, Continued
Emergency surgery noradrenaline support for a CPP of 65; SaO 2 97%; temperature
Due to his continued bilateral pupil enlargement and non reac- 35.5°C; his pupils returning to a stabilised 3/3 mm (R/L), sluggish
tivity, Daniel was transferred to the operating theatre within the sequential reaction; he was heavily sedated, not paralysed initially,
hour for a craniotomy and insertion of external ventricular drain and unresponsive with a Glasgow Coma Scale score (GCS) of 3T
(EVD) and evacuation of the subdural haematoma. A repeat CT (eye opening 1, verbal 1 [T = intubated], motor 1). The initial
scan revealed reduced cerebral oedema and repositioning of the opening intracranial pressure of 28 mmHg was indicative of the
ventricular midline shift. Widespread petechial hemorrhages cerebral oedema from the diffuse injury. The EVD was positioned
remained. In terms of his further injuries, a right femur external at 15 cm above the tragus and remained opened during episodes
fixation, right femoral artery repair, lateral right thigh fasciotomy, of increased ICP exceeding 20 mmHg and drained 26 mL of blood-
and right forearm fracture stabilisation by plaster cast were per- tinged cerebral spinal fluid in the first 24 hours. He required para-
formed in conjunction with his neurosurgery due to a large lysing and increased sedation to control his ICP and CPP. Pain
amount of blood loss mainly from the right femur. The right peri- stimulation for neurological assessment under these conditions
nephric haematoma had stabilised and was managed conserva- was only assessed during endotracheal suction. Noradrenaline
tively. A left subclavian central venous catheter was placed and a infusion fluctuated throughout the day and Daniel required hypo-
radial arterial cannulation for arterial blood pressure monitoring. tonic saline boluses for intracranial hypertension. Normal saline
was infused to maintain euovolemia.
Daniel received a massive blood transfusion:
● 34 units packed red blood cells Days 2–7
● 17 units fresh frozen plasma Daniel’s clinical parameters and assessment are shown in Table
● 10 units cryoprecipitate 16.10. His condition remained variable and on days 3 and 4 his
● 5 units platelets ICP and CPP were unstable with increasing need for sedation and
● 7 L voluven (hydroxyethyl starch/normal saline) paralysis. His pupils enlarged to size 5 and became unreactive.
● 4.5 L Hartmans solution He was stabilised with boluses of hypertonic saline and increased
● 2.5 L normal saline drainage from the EVD which totalled 35 mL for the day. A repeat
CT determined a diffuse injury with global cerebral oedema. The
Following surgery, he was admitted to the Intensive Care Unit (ICU) ventricles were effaced but not compressed. After stabilising on
for further management day 4, Daniel’s sedation was turned off the morning of day 5 for
ICU management neurological assessment. His GCS was 5 (E2 V1(T)M3) with normal
Day 1 flexion to pain and remained unchanged until day 7. His GCS
On arrival to the ICU, Daniel’s condition was critical but stable: may have increased but it was difficult to assess his verbal response
heart rate = 132 beats/min; intubated and ventilated at 14 breaths/ whilst intubated. The EVD was removed on day 6 and he remained
min, Vt 500 mL, FiO 2 = 0.7, Positive End Expiratory Pressure sedated and ventilated to support his chest injuries. Daniel con-
(PEEP) = 10 cmH 2 O; blood pressure 160/65 mmHg (MAP 93) with tinued to slowly recover.



TABLE 16.10 Overview of Daniel’s clinical parameters and assessment, Days 1–7
Day of Admission
Parameter 1 2 3 4 5 6 7
Pupils (mm)
Right 3+ 2+ 5- 3+ 3+ 3+ 3+
Left 3+ 2+ 5- 3+ 3+ 3+ 3+
GCS 3T (E1V1(T) 4 T (E1V1(T) 3 T (E1V1(T) 3 T (E1V1(T) 5 T (E2V1(T) 5 T (E2V1(T) 5 T (E2V1(T)
M1) M2) M1) M1) M3) M3) M3)
CSF drainage (mL/24hr) 26 19 35 38 20 15*
ICP range mmHg 15–35 20–28 22–42 21–45 18–34 15–26
Sedation infusion fentanyl/ fentanyl/ fentanyl/ fentanyl/ Fentanyl/ Fentanyl/ Fentanyl/
midazolam midazolam midazolam midazolam Midazolam Midazolam Midazolam
propofol propofol propofol
Paralysing agent rocuronium rocuronium rocuronium
intermittent intermittent intermittent
Noradrenaline (µg/min) 9–29 5–22 28–45 26–44 18–32 15–22 12–18
Heart rate range 108–140 98–118 82–128 89–135 95–122 98–118 102–112
MAP mmHg range 65–98 67–89 65–87 63–94 65–90 65–83 63–80
CPP mmHg range 48–68 53–68 41–66 43–70 58–70 60–67*
E = eye opening, V = verbal, [T = intubated], M = motor, * ICP EVD removed.

442 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



Research vignette
Lange RT, Iverson GL, Brubacher JR, Franzen MD. Effect of blood GCS scores will likely over-estimate the severity of brain injury in
alcohol level on Glasgow Coma Scale scores following traumatic patients with abnormal head CT scans and BALs greater than
brain injury. Brain Injury 2010; 24(7–8): 919–27. 200 mg dl( ).
−1
Abstract Critique
Objective This study provides insight into what decision making trauma clini-
It is a common clinical perception that alcohol intoxication system- cians face on a daily basis: the confounding of alcohol intoxication
atically lowers Glasgow Coma Scale (GCS) scores when evaluating on neurological assessment including different levels of injury
traumatic brain injury (TBI). However, the research findings in this severity. Overall, the finding that GCS can be used in the majority
area do not uniformly support this notion. The purpose of this of trauma patients at face value gives confidence in assessment
study is to examine the effects of blood alcohol level (BAL) on GCS findings. Probably this confidence can be also applied to those
scores following TBI. patients with abnormal CT scans as in this study the GCS is over-
Method estimated rather than underestimated. It also reports that in higher
−1
Participants were 475 patients (64% male) who presented to a BALs (>200 mg dl ) the GCS is overestimated; this can also be
Level 1 trauma centre following a TBI. Patients were selected if they affirmed by experienced clinicians demonstrating the clinical
were injured in a motor vehicle accident and had an available day- validity of the study.
of-injury GCS, BAL and Computed Tomography (CT) brain scan. In terms of study design, it was a well-structured observational
Results study with well-defined inclusion and exclusion criteria, unpow-
Overall, acute alcohol intoxication did not significantly affect GCS ered, but with a strong sample (475) selected prospectively with
scores, even in patients with BALs of 200 mg dl( ) or higher. When retrospective follow up of vital sign and GCS documentation and
−1
controlling for the effects of injury severity, acute alcohol intoxica- CT results. However, there was no discussion relating to different
tion affected GCS scores only in those patients with BALs greater gender responses to alcohol despite 172 of the cohort being
−1
than 200 mg dl( ) who also had intracranial abnormalities female. Certainly this may be a question for further work in the
detected on CT scan. same area.
Conclusions
These findings suggest that GCS scores can be interpreted at face
value in the vast majority of patients who are intoxicated. However,




Learning activities

1. What effect would decreasing the concentration of extracel- patient elicits a flexion withdrawal response of the wrist, arm
lular potassium ions have on the transmembrane potential of and shoulder. Explain what this response means in terms of
a neuron? central or peripheral response.
2. Which brain structure coordinates endocrine and nervous 6. What is the pathophysiological basis for the rise in ICP? How
system activities? would this manifest on the ICP waveform?
3. Which component of the brain controls the cardiac centres, the 7. Explain the physiological mechanism for dilated (size 5), non
vasomotor centres and the respiratory rhythm centre? reactive pupils.
4. What information does the GCS provide? What does GCS 8. A patient recovering from a subarachnoid haemorrhage can
predict? not remember events prior to the haemorrhage event. What
5. During the testing of motor response a noxious stimulus is type of amnesia is this?
applied to the nail bed of the middle finger. The unconscious



ONLINE RESOURCES mulus%2520in%2520relation%2520to%2520glasgow%2520coma%25
20scale%2520observations.pdf
American Association of Neuroscience Nurses (AANN), http://www.aann.org Head Injury Society of New Zealand, http://www.head-injury.org.nz
Australasian Neuroscience Nurses’ Association, http://www.anna.asn.au Neuroscience tutorials, http://thalamus.wustl.edu/course/
The Brain Trauma Foundation, http://www.braintrauma.org Neurological Exam, http://www.neuroexam.com/neuroexam/
Brain Explorer, http://brainexplorer.org/ Neurological Foundation of New Zealand, http://www.neurological.org.nz/
Brain Injury Association Inc, http://www.biausa.org. Official Journal of the American Academy of Neurology (AAN), http://
GCS protocol, http://intensivecare.hsnet.nsw.gov.au/five/doc/gcs_R_am_rpa.pdf; neurology.org/
GCS procedure 1, http://www.nursingtimes.net/neurological-assessment-part-3- Physical Examination and Neurological Assessment, http://www.neurologyexam.
glasgow-coma-scale/1735582.article com/
GCS procedure 2,http://www.nursingtimes.net/neurological-assessment-part-4- Post traumatic amnesia protocol, http://www.psy.mq.edu.au/pta/
glasgow-coma-scale-2/1768984.article Rural Neurotrauma Assessment, http://www.racs.edu.au/media/16138/PUB_
GCS and use of painful stimulus, http://www.mpdgp.com.au/files/docs/laos%25 090824_-_Neurotrauma_(Standard_Version).pdf
20recommendations/the%2520use%2520of%2520painful%2520sti Society for Neuroscience, http://web.sfn.org/

Neurological Assessment and Monitoring 443

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S65–70.

Neurological Alterations


and Management 17





Di Chamberlain
Wendy Corkill



of diseases such as stroke, brain and spinal cord injury,
Learning objectives and status epilepticus. This chapter discusses the concepts
that underlie neurological abnormalities and addresses
After reading this chapter, you should be able to: current management techniques and modalities.
● differentiate cerebral hypoxia from cerebral ischaemia and
focal from global ischaemia CONCEPTS OF NEUROLOGICAL
● differentiate between primary and secondary brain injuries DYSFUNCTION
due to brain injury
● relate the procedures of selected neurodiagnostic tests to This section discusses the concepts of neurological
dysfunction including altered levels of consciousness,
nursing implications for patient care motor and sensory function and cerebral metabolism
● discuss the rationale for medical and nursing management and perfusion.
in the care of the brain-injured patient.
ALTERATIONS IN CONSCIOUSNESS
In critical illness, impaired consciousness is often the first
sign of a severe pathological process. Consciousness is
Key words defined as recognition of self and the environment, which
requires both arousal and awareness. There are different
coma types of depressed consciousness through to coma, the
cerebral perfusion most severe form of absolute unconsciousness.
neuroprotection
intracranial hypertension Altered Cognition and Coma
seizures Coma is a state of unresponsiveness from which the
traumatic brain injury patient, who appears to be asleep, cannot be aroused by
stroke verbal and physical stimuli to produce any meaningful
spinal cord injury response; therefore, the diagnosis of coma implies the
absence of both arousal and content of consciousness.
1
meningitis Coma must be considered a symptom with numerous
subarachnoid haemorrhage
causes, different natural modes, and several management
modes.
Stupor is a state of unconsciousness from which the
INTRODUCTION patient can be awakened to produce inadequate responses
to verbal and physical stimuli.
There are numerous conditions encountered in critical
care areas that relate to serious neurological dysfunction. Somnolence is a state of unconsciousness from which the
While most are associated with critical illness, or at least patient can be fully awakened. Although there are many
well defined, several others are very infrequent and specific causes of unconsciousness, the sites of cerebral
not addressed extensively in this chapter. One problem affection are either the bilateral cerebral cortex or the
arises in that the onset of an abrupt neurological com- brainstem reticular activating system. The commonest
plication is frequently obscured by the effects of the causes of bilateral cortical disease are deficiencies of
primary illness. For example a metabolic disorder pro- oxygen, metabolic disorders, physical injury, toxins, post-
2
ducing encephalopathy can delay recognition of an intra- convulsive coma and infections. The reticular activating
cerebral haemorrhage, or by its treatment, such as using system maintains the state of wakefulness through
sedation to allow greater synchrony with a mechanical continuous stimulation of the cortex. Any interruption
ventilator. However, neurological alterations are generally may lead to unconsciousness. The reticular activating
defined by problems that derive from the acute aspects system can be affected in three principal ways: by 445

446 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

supratentorial pressure, by infratentorial pressure, and by of a partial seizure patient is the preepileptic event, the
intrinsic brainstem lesions. Supratentorial lesions produce aura. The patient will describe the aura as a virtually
impaired consciousness by enlarging and displacing identical sensation every time.
tissue. Lesions that affect the brainstem itself damage the
reticular activating system directly. Aetiology of seizures
Seizures may either prompt the patient’s admission to ICU
Aetiology of altered cognition (because of status epilepticus) or develop as a complica-
6
Recently gained confusion, severe apathy, stupor or coma tion of another illness. Seizures can be due to vascular,
implies dysfunction of the cerebral hemispheres, the infectious, neoplastic, traumatic, degenerative, metabolic,
3
diencephalon and/or the upper brainstem. Focal lesions toxic or idiopathic causes. Factors influencing the develop-
in supratentorial structures may damage both hemi- ment of posttraumatic epilepsy include an early post-
spheres, or may produce swelling that compresses the traumatic seizure, depressed skull fracture, intracranial
diencephalic activating system and midbrain, causing haematoma, dural penetration, focal neurological deficit
transtentorial herniation and brainstem damage. Primary and posttraumatic amnesia (PTA) over 24 hours with the
subtentorial (brainstem or cerebellar) lesions may com- presence of a skull fracture or haematoma. Seizures in
press or directly damage the reticular formation anywhere critically ill patients are most commonly due to drug
between the level of the midpons and, (by upward pres- effects; metabolic, infectious or toxic disorders; and intra-
sure), the diencephalon. Metabolic or infectious diseases cranial mass lesions although they may be due to trauma
7
may depress brain functions by a change in blood com- or neoplasm. Conditions producing seizures tend either
position or the presence of a direct toxin. Impaired con- to increase neuronal excitation or to impair neuronal
sciousness may also be due to reduced blood flow (as inhibition. A few generalised disorders (e.g. non-ketotic
in syncope or severe heart failure) or a change in the hyperglycaemia) may produce partial or focal seizures.
brain’s electrical activity (as in epilepsy). Concussion,
anxiolytic drugs and anaesthetics impair consciousness ALTERATIONS IN MOTOR AND
without producing detectable structural changes in the SENSORY FUNCTION
brain.
Alterations of motor and sensory function include skeletal
Many of the enzymatic reactions of neurons, glial cells, muscle weakness and paralysis. They result from lesions
and specialised cerebral capillary endothelium in the in the voluntary motor and sensory pathways, including
brain must be catalysed by the energy-yielding hydrolysis the upper motor and sensory neurons of the corticospinal
of adenosine triphosphate (ATP) to adenosine diphos- and corticobulbar tracts, or the lower motor and sensory
phate (ADP) and inorganic phosphate. Without a con- neurons that leave the CNS and travel by way of the
stant and generous supply of ATP, cellular synthesis slows peripheral nerve to the muscle and sensory receptors.
or stops, neuronal functions decline or cease, and cell Muscle tone, which is a necessary component of muscle
4
structures quickly fall apart. The brain depends entirely movement, is a function of the muscle spindle (myotatic)
on the process of glycolysis and respiration within its system and the extrapyramidal system, which monitors
own cells to provide its energy needs. Even a short inter- and buffers input to the lower motor neurons by way of
ruption of blood flow or oxygen supply threatens tissue the multisynaptic pathways. Upper motor neuron lesions
8
vitality.
produce spastic paralysis, and lower motor neuron lesions
produce flaccid paralysis. Damage to the upper motor
Seizures and sensory neurons of the corticospinal, corticobulbar
A seizure is an uninhibited, abrupt discharge of ions from and spinothalamic tracts is a common component of
a group of neurons resulting in epileptic activity. The stroke. Polyneuropathies involve multiple peripheral
9
5
majority of patients experiencing seizures in the ICU do nerves and produce symmetrical sensory, motor, and
not have preexisting epilepsy, and their chances of devel- mixed sensorimotor deficits:
oping epilepsy in the future are usually more dependent
on the cause than on the number or intensity of seizures ● Lesions of the corticospinal and corticobulbar tracts:
that they experience. However, because of other deleteri- result in weakness or total paralysis of predominantly
ous neuronal and systemic effects of seizures, their rapid distal voluntary movement, Babinski’s sign (i.e. dorsi-
diagnosis and suppression during a period of critical flexion of the big toe and fanning of the other toes in
illness is necessary. response to stroking the outer border of the foot from
heel to toe), and often spasticity (increased muscle
Seizures are classified depending on how they start as (a) tone and exaggerated deep tendon reflexes).
partial or focal seizures, (b) generalised or full body sei- ● Disorders of the basal ganglia: (extrapyramidal dis-
zures involving both cerebral hemispheres, or (c) partial orders) do not cause weakness or reflex changes.
seizures with secondary generalisation. A patient may still Their hallmark is involuntary movement (dyskinesia),
be conscious during a partial seizure whereas in gener- causing increased movement (hyperkinesias) or
alised seizures they are not. As partial seizures may not decreased movement (hypokinesia) and changes in
always progress to tonic-clonic movement or alteration muscle tone and posture.
in consciousness, partial seizure represents one of the ● Cerebellar disorders: cause abnormalities in the range,
most elusive diagnoses in neurology and is often misdi- rate and force of movement. Strength is minimally
agnosed. One of the most helpful points in the history affected.

Neurological Alterations and Management 447

Autonomic Nerve Dysfunction parenchyma. Accordingly, reduction of ICP is usually
Dysfunctions of the autonomic nervous system (ANS) argued for restoration of previously compromised cere-
or autonomic dysreflexia are recognised by the symptoms bral perfusion for improvement of cerebral metabolism.
that result from failure or imbalance of the sympathetic Although uncontrolled ICP elevation has been shown
or parasympathetic components of the ANS such as (i) to be responsible for reduced oxygen delivery, non-
increased (>120/min) or decreased (<50/min) heart rate, ischaemic impairment of oxidative metabolism and
(ii) increased respiratory rate (>24/min), (iii) raised mitochondrial damage has only recently been recog-
temperature (>38.5°C), (iv) increased (>160 mmHg) or nised as a prominent source of energy crisis triggered
decreased (<85 mmHg) systolic blood pressure, (v) by brain injury in the presence of adequate cerebral
12
increased muscle tone, (vi) decerebrate (extensor) or decor- blood flow. Accumulating evidence has shown that the
ticate (flexor) posturing, and (vii) profuse sweating. For mitochondrion has a pivotal role in post traumatic neu-
example, in spinal injury the presence of a noxious sti- ronal death by integrating numerous noxious signals
mulus can be transmitted from the periphery to the spinal responsible for both structural and functional damage
cord and activates dysfunctional sympathetic response. on one hand and by amplifying these signals through
activation of several cellular signalling events leading
There is strong evidence for numerous interactions among to cell death. In addition, more complex processes
the central nervous system (CNS), peripheral nervous with the alteration of cerebral perfusion, such as
system (both sympathetic and parasympathetic branches), cerebral hypoperfusion, ischaemia, reperfusion injury,
the endocrine system, and the immune system, hence inflammation and oedema result in increased intracra-
10
ANS dysfunction is related to that complex triad. Auto- nial pressure (ICP).
nomic nerve (AN) dysfunction ranges from alterations
in the sympathetic–parasympathetic balance to almost Cerebral Ischaemia
complete cessation as occurs in spinal cord injury. As the
ANS controls organ function AN dysfunction is related to Ischaemia is the inadequate delivery of oxygen, the inad-
all-organ alteration and failure. The immune system is equate removal of carbon dioxide from the cell, and an
connected to the nervous system through the ANS with increase in the production of intracellular lactic acid.
many of the patients with infections, systemic inflamma- Ischaemia can be caused by an increase in nutrient utilisa-
tory response and multi-organ failure exhibiting AN dys- tion by the brain in a hyperactive state, a decrease in
function. AN dysfunction is closely related to systemic delivery related to either cerebral or systemic complica-
13
inflammation hence those with conditions with increased tions, and/or a mismatch between delivery and demand.
levels of inflammatory markers such as chronic disease The ischaemic cascade is described in Figure 17.1. Inflam-
and obesity have predisposing AN dysfunction. AN mation, together with oxidative stress, excitotoxicity, dis-
dysfunction is assessed by time and spectral domain heart rupted calcium homeostasis and energy failure, is one of
14
rate variability and is currently being researched as a the key pathological changes in ischaemic brain damage.
neurological assessment technique. 11 There is a significant inflammatory response in ischaemic
brains, including leucocyte and monocyte infiltration
into the brain, activation of microglia and astrocytes,
ALTERATIONS IN CEREBRAL METABOLISM elevated production of inflammatory cytokines and che-
mokines and increased expression and activity of adhe-
AND PERFUSION sion molecules, complement and metalloproteinases.
For decades, impairment of cerebral metabolism has Of importance, brain ischaemia can lead to significant
been attributed to impaired oxygen delivery, mediated inflammatory responses in the central nervous system
by reduced cerebral perfusion in the swollen cerebral and can also cause significant changes in the peripheral




Cerebral ischaemia Inflammation
Cytokines
ATP depletion Chemokines Neuronal death

Ion pump failure Brain oedema

Depolarisation Protease Breakdown
Na +
Nuclease DNA damage
Ca + +
Phospholipase Free radicals
NO Mitochondrial damage
Glutamate release
Transcription Gene expression
FIGURE 17.1 Ischaemic cascade. In cerebral ischaemia, energy failure causes depolarisation of the neuronal membrane, and excitatory neurotransmitters
such as glutamate are released together. A marked influx of Ca into neurons then occurs, which provokes the enzymatic process leading to irreversible
2+
neuronal injury. Inflammation is also a contributing factor in the development of ischaemic damage.

448 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

immune system. There are two phases. In the relatively passages connecting the ventricles become blocked, pre-
early phase, activated spleen cells and lymph nodes and venting movement of CSF to its drainage sites in the
21
blood mononuclear cells secrete significantly enhanced subarachnoid space just inside the skull. This type of
levels of TNF-α, IL-6 and IL-2. This then results in global hydrocephalus is called ‘non-communicating’. Reduction
immunosuppression affecting the spleen, lymph nodes, in absorption rate, called ‘communicating hydrocepha-
thymus and a significant decrease in the number of lus’ can be caused by damage to the absorptive tissue.
15
immune cells in the circulation. When cerebral blood Both types lead to an elevation of the CSF pressure within
flow (CBF) falls to about 40% of normal, EEG slowing the brain. A third type of hydrocephalus, ‘normal pres-
occurs. When CBF falls below 10 mL/100 g/min (20%), sure hydrocephalus’, is marked by ventricle enlargement
the function of ionic pumps fails, which leads to mem- without an apparent rise in CSF pressure, which mainly
brane depolarisation. Cerebral ischaemia and reperfusion affects the elderly.
injury contri bute to the cascade of physiological events,
termed secondary brain injury. Recent studies have shown Hydrocephalus may be caused by: congenital brain
that low-dose paracetamol reduces inflammatory protein defects; haemorrhage, in either the ventricles or the sub-
release from brain endothelial cells exposed to oxidant arachnoid space; CNS infection (syphilis, herpes, menin-
16
stress and that propofol protects against neuronal gitis, encephalitis or mumps); and tumours. Irritability is
apotosis. 17 the commonest sign of hydrocephalus in infants and, if
untreated, may lead to lethargy. Bulging of the fontanelle,
Cerebral Oedema the soft spot between the skull bones, may also be an
early sign. Hydrocephalus in infants prevents fusion of
Cerebral oedema is defined as increased brain water the skull bones, and causes expansion of the skull. Symp-
content. The brain is particularly susceptible to injury toms of normal pressure hydrocephalus include demen-
from oedema, because it is located within a confined tia, gait abnormalities and incontinence. Tre atment
22
space and cannot expand, and because there are no lym- includes ventriculostomy drainage of CSF in the short
phatic pathways within the CNS to carry away the fluid term, or a surgical shunt for those with chronic condi-
that accumulates. The white matter is usually much more tions. Either is predisposed to blockage and infection.
involved, as myelinated fibres have a loose extracellular
space, while the grey matter has a much higher cell
density with many connections and much less loose Intracranial Hypertension
extracellular space. The two main subdivisions of cere- Intracranial pressure is the pressure exerted by the con-
18
bral oedema are extracellular and intracellular. tents of the brain within the confines of the skull and
the BBB. The Munro–Kelly hypothesis states that the
Intracellular (cytotoxic) oedema contents of the cranium (60% water, 40% solid) are
Cellular swelling, usually of astrocytes in the grey matter, not compressible and thus an increase in volume causes
a rapid rise in pressure and changes to the compen-
is generally seen after cerebral ischaemia caused by cardiac satory reserve and pulse amplitude, as illustrated in Figure
19
arrest or minor head injury. The blood–brain barrier 17.2. Normal ICP is 0–10 mmHg, and a sustained
23
(BBB) is intact and capillary permeability is not impaired. pressure of >15 mmHg is termed intracranial hyperten-
The cause of intracellular oedema is anoxia and isch- sion, with implications for CBF. Areas of focal ischaemia
24
aemia; it is usually not clinically significant, and is revers- appear when ICP is >20 mmHg and global ischaemia
ible in its early phases.
occurs at >50 mmHg. ICP waveform contains valuable
information about the nature of cerebrospinal patho-
Extracellular (vasogenic) oedema physiology. ICP increased to the level of systemic arterial
Extracellular oedema involves increased capillary perme- pressure extinguishes cerebral circulation, which will
20
ability, and had been termed ‘BBB breakdown’. Rises restart only if arterial pressure rises sufficiently beyond
in brain water content with extracellular oedema are the ICP to restore cerebral blood flow. Autoregulation
often quite dramatic, because the fluid that results from of cerebral blood flow and compliance of the cerebro-
increased capillary permeability is usually rich in pro- spinal system are both expressed in ICP. Methods of
teins, resulting in the spread of oedema and brain isch- waveform analysis are useful, both to derive this infor-
aemia. This can lead to cytotoxic oedema, and to the mation and to guide the management of patients. 25
19
progressive breakdown of both astrocytes and neurons.
While the classification of oedema is useful to define Initially, intracranial compliance allows compensation
specific treatments, it is somewhat arbitrary, as cytotoxic for rises in intracranial volume due to autoregulation.
and vasogenic oedema often occur concurrently. In fact, During a slow rise in volume in a continuous mode, the
each of these processes may cause the other. Ultimately, ICP rises to a plateau level at which the increased level
these changes can lead to raised intracranial pressure and of CSF absorption keeps pace with the rise in volume
herniation. with ample compensatory reserve. This is expressed as
an index, as shown in Figure 17.3. Intermittent expan-
26
sion causes only a transient rise in ICP at first. When
Hydrocephalus sufficient CSF has been absorbed to accommodate the
Hydrocephalus is the result of an imbalance between the volume, the ICP returns to normal. The ICP finally rises
formation and drainage of cerebrospinal fluid (CSF). to the level of arterial pressure which itself begins to rise,
Reduced absorption most often occurs when one or more accompanied by bradycardia or other disturbances of

Neurological Alterations and Management 449


Intracranial pressure (mmHg) 50 Cerebral blood flow (mL/min) 100 (partial pressure of
60
PaCO 2
40
carbon dioxide)
30
50
20
10
0
Volume (mL) 0 0 5 10 15
PaCO (kPa)
Relationship between ICP and intracranial volume 2
Relationship between CBF and PaCO 2



Cerebral blood flow (CBF) mL/min Cerebral blood flow (mL/min) 100 (partial pressure 2




PaO
50
50
of oxygen)


50 mmHg 150 mmHg 0 0 5 10 15
Mean arterial pressure (MAP) PaO (kPa)
2
Relationship between CBF and MAP Relationship between CBF and PaO 2
FIGURE 17.2 The volume–ICP curve relationship.
21





heart rhythm (termed the Cushing’s response). This is NEUROLOGICAL THERAPEUTIC
accompanied by dilation of the small pial arteries and MANAGEMENT
some slowing of venous flow, which is followed by pul-
satile venous flow. This section explores cerebral perfusion, oxygenation and
assessment. The objective of assessment is to identify and
The respiratory changes depend on the level of brainstem
involved. A midbrain involvement results in Cheyne- then initiate strategies in an attempt to prevent secondary
Stokes respiration. When the midbrain and pons are insults and ischaemia. ICP monitoring is discussed in
involved, there is sustained hyperventilation. There are terms of therapeutic management.
rapid and shallow respirations with upper medulla
involvement, with ataxic breathing in the final stages (see OPTIMISING CEREBRAL PERFUSION
Figure 17.4). 27 AND OXYGENATION

Often, neurogenic pulmonary oedema may occur due to Intracranial hypertension and cerebral ischaemia are
increased sympathetic activity as a result of the effects of the two most important secondary injury processes that
elevated ICP on the hypothalamus, medulla or cervical can be anticipated, monitored and treated in the ICU.
spinal cord. The causes of intracranial hypertension are This applies to all aetiologies of brain injury including
classified as acute or chronic. Acute causes include brain trauma. This section discusses the modalities of neu-
trauma, ischaemic injury and intracerebral haemorrhage. roprotection, including the management of intracranial
Infections such as encephalitis or meningitis may also lead hypertension, vasospasm and cerebral ischaemia. Nursing
to intracranial hypertension. Chronic causes include many interventions for the prevention of secondary insults and
intracranial tumours, such as ependymomas, or subdural promotion of cerebral perfusion are described in Table
bleeding that may gradually impinge on CSF pathways 17.1. Imp ortantly, the aims of nursing management are
and interfere with CSF outflow and circulation. As the ICP based on published guidelines and are directed at opti-
continues to increase, the brain tissue becomes distorted, mising cer ebral perfusion and metabolism by various
leading to herniation and additional vascular injury. 28 initiatives.

450 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

ICP RAP < 0
Deranged
cerebrovascular
RAP = 0 RAP = 1 reactivity
Good Poor
compensatory compensatory
reserve reserve
‘Critical’ ICP pulse amplitude Pressure response-ICP
















Volume







Pulsatile cerebral blood
volume RAP = index of compensatory reserve.
FIGURE 17.3 In a simple model, pulse amplitude of intracranial pressure (ICP) (expressed along the y-axis on the right side of the panel) results from
pulsatile changes in cerebral blood volume (expressed along the x-axis) transformed by the pressure–volume curve. This curve has three zones: a flat zone,
expressing good compensatory reserve, an exponential zone, depicting poor compensatory reserve, and a flat zone again, seen at very high ICP (above
the ‘critical’ ICP) depicting derangement of normal cerebrovascular responses. The pulse amplitude of ICP is low and does not depend on mean ICP in the
first zone. The pulse amplitude increases linearly with mean ICP in the zone of poor compensatory reserve. In the third zone, the pulse amplitude starts
to decrease with rising ICP. RAP, index of compensatory reserve.
26














Cheyne-Stokes
breathing

Central neurogenic
hyperventilation

Apneusis

Cluster breathing

Ataxic breathing
One minute

27
FIGURE 17.4 Injury to the brainstem can result in various abnormal respiratory patterns.

Neurological Alterations and Management 451



TABLE 17.1 Nursing interventions for the promotion of cerebral perfusion in acute brain injury

Aim Goal Interventions
Maintain SaO 2 98%, PaO 2 ● Maintain airway.
oxygenation 100 mmHg, ● Use 100% O 2 during initial resuscitation phase.
PbtO 2 >20 ● Intubate as soon as possible for Glasgow Coma Scale less than 8 or diaphragmatic
respiratory insufficiency (C – spine number).
● Obtain arterial blood gas and manipulate set FiO 2 to meet parameter goal.
● Suction patient as needed.
● Consider need for kinetic therapy, e.g. rotation/percussion therapy bed within spinal
precautions. Use frequent subglottal suctioning, and maintain head of bed elevation at 30°
or more to prevent VAP.
● In recovery: assess for upper airway weakness and reflex (prevent aspiration), sputum
retention and atelectasis.
PaCO 2 35–40 mmHg ● ABG assessment.
Maintain PaCO 2
● Adjust ventilator settings to obtain PaCO 2 of 35–40 mmHg.
● Ensure optimal PaCO 2 for your patient: observe PbtO 2 and ICP during manipulation of
PaCO 2 .
● Monitor end-tidal CO 2 continuously.
● Observe for hypoventilation.
Maintain mean MAP 90 mmHg ● Maintain euvolaemia.
arterial ● Give IV volume as prescribed to maintain CVP and PCWP within parameters.
pressure ● Use noradrenaline once euvolaemic in order to optimise MAP.
(MAP) ● Observe PbtO 2 for sedation-induced hypotension.
● Transfuse to haematocrit of 33% or haemoglobin content 80–100 g/L.
● Stroke: thrombolytic, embolic and ICH, MAP 90–120 mmHg
Maintain CPP 50–70 mmHg ● Effectively reduce ICP while preserving or improving CPP
cerebral ● Position body with neck straight and no knee elevation in order to maintain venous outflow.
perfusion ● Make sure cervical collar and endotracheal tube ties are not too tight, especially behind the
pressure neck.
50–70 mmHg ● If patient has a ventriculostomy, drain per doctor’s orders.
Maintain ICP <20 mmHg ● Elevate head of bed above the level of the heart to obtain optimal level of ICP and CPP.
intracranial Monitor ICP, CPP and PbtO 2 to ensure optimal level for your patient (15–30°).
pressure (CP) ● Sedate using propofol, morphine, fentanyl and/or lorazepam/midazolam
<20 mmHg ● Mannitol prescription at 0.25–1.0 g/kg IV for ICP sustained at less than 20 mmHg (watch
serum osmolality and consider holding for values >320 mOsmol/kg) OR Hypertonic Saline
7.5% prescription
● Consider paralytics if positioning, cooling, sedation and mannitol does not resolve
increased ICP.
● Maintain the brain temperatures at 36–37°C, using cooling measures; prevent shivering
(increases cerebral metabolic demands)
● Prepare for surgical craniotomy if indicated.
Maintain SjO 2 50–75% PbtO 2 ● Group necessary interventions in a timely manner to allow for rest periods.
environment/ >20 ● Screen visitors.
reduce ● Minimise noise and lighting.
stimulation ● Avoid stimulation and prioritise interventions if ICP precarious.
● Sedation as prescribed.
Maintain PbtO 2 <20 ● Optimise CPP to prescribed levels (60–70 mm Hg).
cerebral ● Optimise PaCO 2 as indicated to increase CBF.
blood flow ● Optimise sedation and consider paralytics.
● Consider barbiturate prescription if above measures are not successful.
● PaO 2 100 mmHg and SaO 2 98%.
● Maintain CVP of 5–10 mmHg, and a PCWP of 10–15 mmHg.
● Administer normal saline and/or colloids as prescribed to maintain parameters.
● Transfuse to haematocrit of 33% or haemoglobin content 80–100 g/L. (Prescription to
correct coagulopathies).
● Monitor closely for signs and symptoms of neurogenic pulmonary oedema, especially in
patients with cardiac history.
● Maintenance of brain temperature at 36–37°C, with active cooling if necessary.
● Transcranial Doppler image to check for vasospasm.
● Non-traumatic SAH, administer IV nimodipine or magnesium infusion to prevent vasospasm
as prescribed; consider components of HHH therapy.
● Ischaemic stroke, administer tPA within 3 hours of event.
● ICH, prevent rebleeding; administer prescribed recombinant factor VII, reduce hypertension.
Maintain ● Ensure early enteric feeding.
nutrition ● Oral enteric feeding tube (nasogastric contradicted in TBI).
● Dietitian referral for metabolic requirements.
● Stress ulcer prophylaxis.

452 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

Management of Cerebral Oxygenation potential to become established as a key component of
and Perfusion multi-modality monitoring during management of acute
Cerebral monitoring in brain-injured patients has focused brain injury during neurointensive care.
on the prevention of secondary injury to the brain owing Management of Intracranial Hypertension
to impaired perfusion. However, ICP monitoring and ICP
29
manipulation does not equal cerebral oxygenation. Raised ICP is treated by removing mass lesions and/or
There are currently four techniques that can be used to increasing the volume available for expansion of injured
assess cerebral oxygenation: jugular venous oxygen satu- tissue. This may be achieved by reducing one of the other
ration, positron emission tomography, near-infrared available intracranial fluid volumes:
spectroscopy, and brain tissue oxygenation monitoring 1. CSF by ventricular drainage (as discussed
(PbtO 2 ). Their strengths and weaknesses are the subject previously)
of several recent reviews. 30,31 The selection among these 2. cerebral blood volume by hyperventilation,
forms of oxygenation monitoring is focused on the osmotic diuretic therapy or hypothermia
appropriateness of focal or global monitoring, the loca- 3. brain tissue water content by osmotic diuretic
tion of the monitor in relation to the injury, and the therapy
intermittent or continuous nature of the monitoring. The 4. removing swollen and irreversibly injured brain
use of PbtO 2 , as assessed by the intraparenchymal polaro- 5. increasing cranial volume by craniotomy
graphic oxygen probe, has the advantage of directly moni- decompression.
toring the zone of injury and thus earlier detection of
perfusion abnormalities that may impact global cerebral Each modality will be discussed in terms of its physiologi-
oxygenation later. This may also allow the rescue of cal effect, efficacy and potential use for prevention of
watershed areas of perfusion. However, there is contro- secondary brain injury.
versy regarding the appropriate placement of such moni-
tors. Insertion of the probe into non injured areas yields Hyperventilation
data equivalent to global assessments of cerebral oxygen- Hyperventilation reduces PaCO 2 and will reduce ICP by
ation. Consequently, close attention should be paid to vasoconstriction induced by alkalosis but it also decreases
35
the location of the catheter in relation to the injury in cerebral blood flow. The fall in ICP parallels the fall in
interpretation and use of PbtO 2 results. Jugular venous CBV. Hyperventilation decreases regional blood flow to
oxygen saturation (SjO 2 ) is representative of global cere- hypoperfused areas of the brain. Thus, generally PaCO 2
bral oxygen metabolism, but technically it is difficult to should be maintained in the low normal range of about
obtain reproducible results. Cerebral tissue oxygenation 35 mmHg. Hyperventilation should be utilised only
values of <20 mmHg are targeted for intervention based when ICP elevations are refractory to other methods and
on Brain Trauma Foundation (BTF) guidelines but only when brain tissue oxygenation is in the normal range.
36
32
at level III evidence. PbtO 2 can be increased by increas- The BTF Guidelines recommend hyperventilation therapy
ing the FiO 2 /PaO 2 ratio and by reducing cerebral meta- only for brief periods when there is no neurological dete-
bolic requirements for oxygen (CMRO 2 ) using brain rioration or for longer periods when ICP is refractory to
temperature control with active cooling and metabolic other therapies. 32
rate control with sedation and adequate feeding. Addi-
tional interventions such as volume infusion, transfu- Osmotherapy
sion, and inotropic support directed at improving cardiac
output can also be used to increase oxygen delivery. 33 Acute administration of an osmotic such as mannitol or
hypertonic saline produces a potent antioedema action,
Brain inflammation after injury contributes to impaired primarily on undamaged brain regions with an intact
oxygenation and perfusion, but currently its management BBB. This treatment causes the movement of water from
has not translated to successful clinical management. the interstitial and extracellular space into the intravascu-
However, the use of cerebral microdialysis (MD) and the lar compartment, thereby improving intracranial compli-
measurement of biochemical markers (lactate, glutamate, ance or elastance. In addition to causing ‘dehydration’ of
pyruvate, glycerol and glucose) of cerebral inflammation the brain, osmotic agents have been shown to exert ben-
and metabolism do contribute towards early warnings of eficial non-osmotic cerebral effects, such as augmentation
impending hypoxia/ischaemia and neurological deterio- of cerebral blood flow (by reducing blood viscosity,
ration, and this may allow timely implementation of resulting in enhanced oxygen delivery), free radical scav-
neuroprotective strategies. Elevation of the lactate/ enging, and diminishing CSF formation and enhancing
pyruvate ratio is typically seen in cerebral ischaemia and CSF reabsorption. 37
mitochondrial dysfunction, and has been used to tailor
34
therapy. However, MD reflects only local tissue bio- The BTF recommends mannitol in intracranial hyperten-
chemistry and the accurate placement of the catheter is sion in bolus administration, keeping the serum osmolari-
+
crucial. Furthermore, because there are wide variations in ties greater than 320 mOsm/L, plasma Na <160 mmol/L
measured variables, trend data are more important than and avoiding hypovolaemia. Urine output after mannitol
absolute values. Although MD is used routinely in a few administration needs to be replaced, generally with
centres it has not yet been introduced into widespread normal saline. Brain free water is increased with 5% dex-
clinical practice and, at present, should be considered a trose and hyperglycaemia; hence these need to be avoided.
research tool for use in specialist centres. MD has the The use of frusemide in conjunction with mannitol

Neurological Alterations and Management 453

promotes a synergistic action, particularly in patients Corticosteroids
refractory to mannitol alone. Recent studies now suggest Excessive inflammation has been implicated in the pro-
that mannitol and frusemide have antiepileptic proper- gressive neurodegeneration that occurs in multiple
38
ties and that mannitol has a role in ischaemic stroke.
neurological diseases, including cerebral ischaemia. The
Intravenous hypertonic saline (HTS) increases cerebral efficacy of glucocorticoids is well established in amelio-
perfusion and decreases brain swelling and inflammation rating oedema associated with brain tumours and in
more effectively than conventional resuscitation fluids. improving the outcome in subsets of patients with bacte-
HTS behaves like 20% mannitol in acute cerebral oedema rial meningitis. Despite encouraging experimental results,
but maintains haemodynamic status. However, unlike clinical trials of glucocorticoids in ischaemic stroke, intra-
HTS, mannitol induces a diuresis, which is relatively con- cerebral haemorrhage, aneurysmal subarachnoid haem-
traindicated in patients with both TBI and hypovolaemia orrhage and traumatic brain injury have not shown a
as it may worsen intravascular volume depletion and definite therapeutic effect. Furthermore, the CRASH (cor-
decrease cerebral perfusion. Therefore, despite theoretical ticosteroid randomisation after significant head injury)
advantages of HTS resuscitation in patients with TBI, an trial demonstrated an increased risk of death from use of
39
Australian randomised controlled trial found no differ- steroids from all causes within two weeks of injury, and
48
ence in outcome between HTS and other resuscitation was stopped early. Consequently, the BTF Guidelines
fluids in prehospital resuscitation. However, in many Aus- state that the use of steroids is not recommended
tralian and New Zealand intensive care units, HTS is used for TBI. 32
as a preferred alternative to mannitol in patients with The evidence supporting glucocorticoid therapy for spinal
raised ICP. cord injury is controversial; however, methylpredniso-
lone continues to be widely employed in this setting
Normothermia (this is discussed further below under Spinal injury
Hyperthermia occurs in up to 40% of patients with isch- management).
aemic stroke and intracerebral haemorrhage and in
40–70% of patients with severe TBI or aneurysmal sub- Barbiturates and sedatives
arachnoid haemorrhage. Hyperthermia is independently The BTF Guidelines state that high-dose barbiturate
associated with increased morbidity and mortality after therapy may be considered in haemodynamically-
ischaemic and haemorrhagic stroke, and in subarachnoid salvageable severe TBI patients with intracranial hyper-
haemorrhage and TBI patients temperature elevation tension refractory to maximal medical and surgical
49
has been linked to raised intracranial pressure. Tempe- interventions. The utilisation of barbiturates for the
rature elevations as small as 1–2°C above normal can prophylactic treatment of ICP has not been indicated.
aggravate ischaemic neuronal injury and exacerbate Barbiturates exert cerebral protective and ICP-lowering
brain oedema. Mild hypothermia protects numerous effects through alteration in vascular tone, suppression
40
41
tissues from damage during ischaemic insult. The use of of metabolism and inhibition of free radical-mediated
paracetamol, cooling blankets, ice packs, evaporative lipid peroxidation. Barbiturates may effectively lower
cooling and new cooling technologies may be useful cerebral blood flow and regional metabolic demands.
in maintaining normothermia. Hyperaemia (increased The lower metabolic requirements decrease cerebral
blood flow) may occur during rewarming, resulting in blood flow and cerebral volume. This results in benefi-
acute brain swelling and rebound intracranial hyperten- cial effects on ICP and global cerebral perfusion. Barbi-
42
43
sion. In an original study, Marion and colleagues. turates within the BTF guidelines are now included
demonstrated a higher mortality rate than in more recent under the heading of Anaesthetics, Analgesics and Seda-
trials, possibly due to rapid rewarming and rebound tives and these also recommend (Level II) that it is ben-
44
hyperaemia and cerebral oedema. eficial to minimise painful or noxious stimuli as well as
agitation as they may potentially contribute to eleva-
Maintenance of body temperature at 35°C may be tions in ICP. Therefore propofol is recommended for the
45
optimal. Intracranial pressure falls significantly at brain control of ICP, but does not improve mortality or six-
temperatures below 37°C but no difference was observed month outcome. High dose propofol should be avoided
at temperatures below 35°C. Cerebral perfusion pressure as it can produce significant morbidity. 49
peaks at 35–36°C and decreases with further falls in
45
temperature. At a temperature below 35°C, both oxygen Surgical interventions
delivery and oxygen consumption decrease. Cardiac The European TBI Guidelines suggest that operative man-
output decreases progressively with hypothermia. There- agement be considered for large intracerebral lesions
fore, cooling to 35°C may reduce intracranial hyperten- within the first four hours of injury. The use of unilateral
sion and maintain sufficient CPP without associated craniectomy after the evacuation of a mass lesion, such
46
cardiac dysfunction or oxygen debt. As the temperature as an acute subdural haematoma or traumatic intracere-
is lowered from 34°C to 31°C, the volume of IV fluid bral haematoma, is accepted practice. Surgery is also
infusion and inotrope requirements increase substan- recommended for open compound depressed skull frac-
tially and, despite such interventions, mean arterial pres- tures that cause a mass effect. 50
sure decreases. At 31°C serum potassium, white blood
47
cell count and platelet counts are diminished. Thus, it Decompressive craniectomy, for refractory intracranial
seems that hypothermia to 35°C may be optimal. hypertension, has been performed since 1977, with a

454 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

50
significant reduction in ICP for both TBI and ischaemic cerebral vasospasm occurs in approximately 10–15%
51
stroke. In 2011 a multi-centre prospective randomised of patients.
trial of early decompressive craniectomy in patients with
severe traumatic brain injury reported that in adults Calcium antagonists, such as nimodipine, have not been
with severe diffuse traumatic brain injury and refractory effective in TBI subarachnoid haemorrhage with vaso-
intracranial hypertension, early bifrontotemporoparietal spasm, and recent studies have suggested that calcium
decompressive craniectomy decreased intracranial pres- antagonists even prevent neurogenesis after TBI. Nimo-
sure and the length of stay in the ICU but surprisingly dipine has demonstrated effectiveness in the treatment of
was associated with more unfavorable outcomes at both vasospasm in aneurysmal SAH and is now an option for
6 and 12 months using the Extended Glasgow Outcome recommended practice. An initial study of nimodipine in
Scale. 52 patients with TBI demonstrated no difference in out-
come, and a Cochrane Systematic Review supports this
Prevention of Cerebral Vasospasm conclusion. 53
Cerebral vasospasm is a self-limited vasculopathy that Magnesium may prevent cerebral vasospasm through
develops 4–14 days after subarachnoid haemorrhage several mechanisms. Increased ATP entry into cells could
(SAH) and/or TBI (see Figure 17.5). Oxyhaemoglobin, decrease ischaemic depolarisation and limit infarction
a product of haemoglobin breakdown, probably initi- size. Magnesium also both inhibits the presynaptic
ates vasoconstriction, leading to smooth-muscle pro- release of excitatory amino acids and is a non-competitive
liferation, collagen remodelling and cellular infiltration antagonist to postsynaptic NMDA receptors. The drug
of the vessel wall. The resulting vessel narrowing can also cause vasodilation by inhibiting calcium
can lead to ischaemia. SAH patients develop cerebral channel-mediated smooth muscle contraction. Finally,
va sospasm, and about one-third develop symptomatic magnesium increases cardiac contractility, which may
vasospasm, which is associated with neurological signs improve cerebral perfusion in dysautoregulated brain
and symptoms of ischaemia. Posttraumatic brain injury tissue. TBI animal studies have demonstrated promising




Injury






Primary brain injury Extracranial injury
Mediator release Haemorrhage Sympathetic surge
Alteration in BBB permeability Haematoma
Neuronal damage Contusion
Microvascular changes
Neurogenic hypertension
Neurogenic pulmonary oedema


Cerebal Impaired Decreased
oedema autoregulation consciousness Hypoxia



Hypercapnia
Decreased cerebral Raised intracranial
blood flow pressure Secondary
brain injury


Decreased cerebral
perfusion pressure Hypotension



Neuronal ischaemia



Neuronal death
FIGURE 17.5 Pathophysiology of traumatic brain injury.

Neurological Alterations and Management 455

neuroprotection, but this is still to be confirmed in clini- population. Approximately 90,211 Australians 58,59 and
54
60
cal trials. Magnesium, however, does not cross the 16,000–22,500 New Zealanders are hospitalised for
intact BBB easily, limiting its effect to injury and disease TBI every year. Males aged 15–19 years have the highest
with leaky BBB. A randomised clinical trial of aneurys- incidence rates and suffer TBI at a rate almost three times
mal SAH patients receiving magnesium found that IV that of women. The very young (0–4 years) and the
61
magnesium infusion reduced the frequency of delayed very old (over 85 years) are also at increased risk. Indig-
cerebral ischaemia in patients with aneurysmal SAH and enous Australians suffer TBI at almost three times the rate
62
subsequent poor outcome. 55 (410 per 100,000) of non-Indigenous Australians. It is
estimated that 40,000 Australians are living with a dis-
In SAH, more aggressive intravascular volume expansion ability as a result of TBI. Despite definition issues relat-
63
and induced hypertension are used in conjunction with ing to TBI epidemiology, there was an average annual
haemodynamic monitoring. By maintaining haematocrit decline of 5% in the TBI rate to 1997/98 but the inci-
at 30–33%, a shift in the oxygen dissociation curve is dence has increased since then. An Australian and new
56
avoided. Haemodilutional therapy increases collateral Zealand epidemiological study of TBI (see Research
64
circulation at the site of haemorrhage, while reducing vignette) found that the mean age was 41.6 years; 74.2%
aggregation of erythrocytes where small vessel spasm has were men; 61.4% were due to vehicular trauma, 24.9%
occurred. However, there is some emerging physiological were falls in elderly patients, and 57.2% had severe TBI
data suggesting that normovolaemic hyperten sion may (Glasgow Coma Scale score ≤8). Twelve-month mortality
be the component most likely to increase cerebral blood was 26.9% in all patients and 35.1% in patients with
flow after subarachnoid haemorrhage. In contrast, hyper- severe TBI.
volaemic haemodilution is associated with increased
complications and might also lower the haemoglobin
56
to excessively low levels. Also in aneurysmal SAH, Aetiology
endovascular therapies, such as intra-arterial papaverine In Australia, motor vehicle-related trauma accounts
infusion, are employed. Papaverine acts immediately and for about two-thirds of moderate and severe TBI, with
increases arterial calibre and cerebral blood flow, but its falls and assaults being the next most common causes.
effects are short-lived. Balloon angioplasty is particularly New Zealand has a higher proportion of recreational
effective as a durable means of alleviating arterial nar- in juries compared to vehicle-related trauma. Sporting
rowing and preventing stroke in patients with symptom- accidents and falls account for a far greater percentage
atic vasospasm after aneurysmal SAH. The timing of of mild injuries. Alcohol is associated with up to half of
endovascular intubation and use of inotropes in patients all cases of TBI. In Australia and New Zealand, blunt
with cardiac dysfunction are unresolved issues. 57 trauma (falls and vehicle-related), rather than penetrat-
ing (stabbing and firearms) or blast, is the predominant
63
Other Neuroprotective Measures mechanism of injury. The transfer of energy to the
brain tissue actually causes the damage and is a signifi-
Many promising animal studies have not transferred cant determinant in the severity of injury (and routinely
to successful human clinical trials and there have been noted in ED on admission). In the past 10 years, the
a plethora of different mechanisms that block single introduction of safer car designs, airbags and other road
molecular processes but do not address the complex traffic initiatives (e.g. redesigning hazardous intersec-
molecular processes involved in brain injury. Currently tions, driver education campaigns, random breath
there is interest in antioxidants (Tirilazad mesylate), leu- testing and reducing speed limits) have decreased the
kocyte adhesion inhibition (Enlimomab), and continued overall number of road fatalities; improvements in
interest in erythropoietin, progesterone and their meta- retrieval, neurosurgery and intensive care in the past few
bolites and receptors as neuroprotective targets and decades have enabled many people to survive injuries
treatments. that would previously have been fatal. Research into
and prevention of falls and shaken-baby syndromes has
CENTRAL NERVOUS SYSTEM had a small impact on incidence reduction. 65,66
DISORDERS
Pathophysiology of TBI
CNS disorders include brain and/or spinal injury from
trauma, infection or immune conditions. The pathophys- TBI is a heterogeneous pathophysiological process (see
iology and aetiology of these disorders are discussed here, Figure 17.5). The mechanisms of injury forces inflicted
including management of these conditions. on the head in TBI produce a complex mixture of diffuse
67
and focal lesions within the brain. Damage resulting
TRAUMATIC BRAIN INJURY from an injury can be immediate (primary) or secondary
in nature. Secondary injury results from disordered
Head injury is a broad classification that includes injury autoregulation and other pathophysiological changes
to the scalp, skull or brain. Traumatic brain injury (TBI) within the brain in the days immediately after injury.
is the most serious form of head injury. The range of Urgent neurosurgical intervention for intracerebral, sub-
severity of TBI is broad, from concussion through to post dural or extradural haemorrhages can mitigate the
coma unresponsiveness. The Australian age-standardised extent of secondary injury. Scalp lesions can bleed pro-
incidence rate of TBI in 2004/5 was about 150 per 100,000 fusely and quickly lead to hypovolaemic shock and brain

456 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

Defend CPP Optimise CPP Maintain CPP
Restore MAP Normalise MAP Maintain MAP
Reduce ICP Reduce ICP
120



30
Cerebral blood flow (mL/100 g/min) 40 C 10 Intracranial pressure (mmHg)
B
A
80

20












Hypoperfusion Hyperaemia Vasospasm
0

0 1 2 3 4 6 8 10 12 14
Days post-injury

FIGURE 17.6 Conceptual changes in cerebral blood flow and intracranial pressure (ICP) over time following traumatic brain injury: (A) cytotoxic oedema;
(B) vasogenic oedema; (C) cerebral blood flow CPP = cerebral perfusion pressure; MAP = mean arterial pressure.





ischaemia. Cerebral oedema, haemorrhage and bio- Contact phenomena are commonly superficial and can
chemical response to injury, infection and increased ICP generate superficial or contusional haemorrhages through
are among the commonest physiological responses that coup and contrecoup mechanisms. Cerebral contusions
71
can cause secondary injury. Tissue hypoxia is also of are readily identifiable on CT scans, but may not be
major concern and airway obstruction immediately after evident on day 1 scans, becoming visible only on days 2
injury contributes significantly to secondary injury. Poor or 3. Deep intracerebral haemorrhages can result from
cerebral blood flow, as a result of direct (primary) vas- either focal or diffuse damage to the arteries.
cular changes or damage, can lead to ischaemic brain
tissue, and eventually neuronal cell death. Systemic Diffuse injury
68
changes in temperature, haemodynamics and pulmonary
status can also lead to secondary brain injury (Figure Diffuse (axonal) injury (DAI) refers to the shearing of
17.6). In moderate to severe and, occasionally in mild, axons and supporting neuroglia; it may also traumatise
injury, cerebral blood flow is altered in the initial 2–3 blood vessels and can cause petechial haemorrhages,
71
days, followed by a rebound hyperaemic stage (days deep intracerebral haematomas and brain swelling.
4–7) leading to a precarious state (days 8–14) of cerebral DAI results from the shaking, shearing and inertial
vessel unpredictability and vasospasm. More than 30% effects of a traumatic impact. Mechanical damage to
64
of TBI patient have AN dysfunction characterised by small venules as part of the BBB can also trigger the for-
episodes of increased heart rate, respiratory rate, tem- mation of haemorrhagic contusions. This vascular
perature, blood pressure, muscle tone, decorticate or damage may increase neuronal vulnerability, causing
70
decerebrate posturing, and profuse sweating. Lack of post-traumatising perfusion deficits and the extravasa-
insight into these processes and implementing early tion of potentially neurotoxic blood-borne substances.
weaning of supportive therapies can lead to significant The most consistent effect of diffuse brain damage, even
secondary insults. when mild, is the presence of altered consciousness. The
depth and duration of coma provide the best guide to
the severity of the diffuse damage. The majority of
Focal injury patients with DAI will not have any CT evidence
Because of the shape of the inner surface of the skull, to support the diagnosis. Other clinical markers of
focal injuries are most commonly seen in the frontal DAI include the high speed or force strength of injury,
and temporal lobes, but they can occur anywhere. absence of a lucid interval, and prolonged retrograde

Neurological Alterations and Management 457

in Table 17.2 and is an adaptation of the current guide-
32
lines (see Table 17.3) to clinical practice (see Online
resources for TBI-related protocols). In all TBI multitrauma
patients, disability and exposure/environmental control
assessment includes the routine trauma series of X-rays,
namely chest, pelvis and cervical spine (lateral, anter-
oposterior and odontoid peg views). These should be
reviewed by a radiologist and areas of concern, parti-
FIGURE 17.7 Extradural haematoma and a subtle subdural haematoma cularly in the upper and lower regions of the cervical
(left), subdural haematoma (middle left), diffuse axonal injury (middle spine, should be clarified with further investigations such
right), and combination injuries (right).
as CT scans. Isolated TBI requires CT scanning of the head
and upper spine. The management of TBI should include
and anterograde amnesia. Figure 17.7 contrasts CT scans spinal precautions until spinal injury is definitively
with haematoma formation and DAI. excluded.

SPINAL CORD TRAUMA
Mild TBI
In Australia, nearly 11,000 people live with a disability
Mild TBI often presents as a component of multitrauma from spinal cord injury (SCI), with an age-adjusted inci-
or sports injury and can be overlooked at the expense of dence rate of 13.6 per million of the population. In
75
other peripheral injuries. Risk factors such as vomiting, 2007–08 there were 362 new spinal cord injuries, the
dizziness, facial and skull fractures; including the loss of majority of which (79%) were due to traumatic causes.
CSF from the nose or the ear, will categorise those needing SCI were most frequent in the 15–24 year age group
further surveillance. Routine head CT and assessment of (30%), although trends show a significant increase in the
PTA are recommended to exclude mass lesions and DAI. average age at injury from 38 years in 1995–96 to 42 years
Diagnosis and management in the acute phase of mild in 2007–08. Males accounted for 84% of traumatic SCI.
TBI is as crucial to functional outcome and rehabilitation Transport-related injuries (46%) and falls (28%) were the
as in moderate-to-severe TBI. 72 main contributors to traumatic SCI.

Skull fractures In 2001–02 New Zealand had an unadjusted rate of 27
Skull fractures are present on CT scans in about two- per million and has one of the highest SCI incidences in
thirds of patients after TBI. Skull fractures can be linear, the Western world, related mostly to snowboarding and
60
depressed or diastatic, and may involve the cranial vault rugby. SCI occurs three times more often in men, and
or skull base. In depressed skull fractures the bone the incidence among those aged 15–34 years is roughly
fragment may cause a laceration of the dura mater, result- double the rate in those 35 years and over. More than half
ing in a cerebrospinal fluid leak. Basal skull fractures of the SCIs are due to vehicular trauma and a quarter due
73
include fractures of the cribriform plate, frontal bones, to motorcycle crashes. Falls account for nearly a third of
sphenoid bones, temporal bone and occipital bones. the injuries, with nearly half occurring in older people.
The clinical signs of a basal skull fracture may include: Recreational and sporting injuries account for 15% of
CSF otorrhoea or rhinorrhoea, haemotympanum, post- SCI, and 19% are work-related. Of all SCI cases, 51%
auricular ecchymoses, periorbital ecchymoses, and injury resulted in complete tetraplegia (loss of function in the
to the cranial nerves: VII (weakness of the face), VIII (loss arms, legs, trunk and pelvic organs). The predominant
of hearing), olfactory (loss of smell), optic (vision loss) risk factors for SCI include age, gender, and alcohol and
and VI (double vision). drug use. The vertebrae most often involved in SCI are
the 5th, 6th and 7th cervical (neck), the 12th thoracic,
and the 1st lumbar. These vertebrae are the most suscep-
Nursing Practice tible because there is a greater range of mobility in the
76
The surveillance and prevention of secondary injury is the vertebral column in these areas. Damage to the spinal
69
key to improving morbidity and mortality outcomes cord ranges from transient concussion or stunning (from
(see Table 17.1). It should be noted that in a post hoc in which the patient fully recovers) to contusion, laceration
analysis of saline critically ill patients with TBI, fluid and compression of the cord substance (either alone or
resuscitation with albumin was associated with higher in combination), to complete transection of the cord
74
mortality rates than was resuscitation with saline. Inter- (which renders the patient paralysed below the level of
ventions are targeted at maintaining adequate cerebral the injury).
blood flow and minimising oxygen consumption by the
brain in order to prevent ischaemia. The anticipation and Mechanisms of Injury
prevention of systemic complications are also of vital
importance. Assessment is vital to establish priorities in Cervical injury can occur from both blunt and penetrat-
care and is discussed in Chapter 16. ing trauma but in reality is a combination of different
mechanisms of acceleration and deceleration with and
77
Nursing management of the neurologically impaired, without rotational forces and axial loading. An illustra-
immobilised, mechanically ventilated patient is described tive example is a diving injury, caused by a direct load

458 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



TABLE 17.2 Nursing management of the neurologically impaired, immobilised, mechanically-ventilated patient

Nursing domain Nursing outcome Nursing interventions
Ventilation and ● Airway patent. ● Assess ventilation parameters: ensure ET patency and position.
oxygenation ● Arterial pH, PaO 2 , PbtO 2 , SaO 2 within ● Assess bilateral chest movement: listen for airway obstruction or
normal range. ET cuff leak; auscultate for air entry.
● PaCO 2 & ETCO 2 within normal range. ● Assess chest X-ray.
● Lungs clear to auscultation. ● Adequate sedation and ventilation to maintain PbtO 2 , ICP, CPP.
● No evidence of atelectasis or aspiration. ● Suction only as necessary: preoxygenate, avoid prolonged
● Chest X-ray clear of pathology. coughing; effective technique.
● Avoid ICP complications of PEEP.
● Position to avoid aspiration.
● Provide meticulous oral hygiene.
Mobility/safety ● Cerebral blood flow uncompromised. ● Haemodynamic stability maintained. Brain ischaemia and
● Minimal and transient changes in intracranial hypertension controlled.
PbtO 2 –ICP–CPP and return to desired ● Nursing interventions planned for minimal disturbance; efficient
parameters within 5 min of nursing intervention.
intervention. ● Pressure-relieving mattress: allows minimal position changes for
● Patient integument maintained and integument protection, with minimal CMRO 2 requirement,
infection free: skin, mucous membranes, sequential compression device for venous return.
cornea, wounds, invasive lines ● Hygiene maintained: assess integument, assess cornea, assess
● Complications of immobility prevented: mucous membranes.
DVT, pneumonia, muscle strength. ● Maintain infection control interventions with invasive devices
● Patient safety enabled, preventing and wounds.
nosocomial infection, secondary brain ● Administer preventive plan of treatment with vigilance and
injury, self-harm. prediction.
● Nutrition prescribed according to ● Enable communication with other health professionals.
patient need. ● Chemical and physical restraint applied per assessment and
● Healing defined and uneventful. prescription, within institutional policy.
Psychological/ ● Family and significant others informed ● Refer and coordinate information and service provision from
family and supported. other health professionals.
● Psychological wellbeing of patient in ● The provision of quality, informed and inclusive care to the
recovery patient provides family and significant others with the
● The patient will feel safe. confidence that the nurse advocates for the patient in their place.
● Ensure psychological assessment and administer prescribed
therapy for delirium and post traumatic stress.
● Nursing interventions planned to allow for rest and recovery.
● Administer coordinated rehabilitation strategies.



through the head and cervical spine. In reality, cervical ● Extension–rotation: Rotational injuries result from
trauma is produced by a combination of these mecha- forces that cause extreme twisting or lateral flexion of
nisms as listed below. the head and neck. Fracture or dislocation of vertebrae
may also occur. The spinal canal is narrower in the
● Hyperflexion: These injuries usually result from force- thoracic segment relative to the width of the cord, so
ful decelerations and are often seen in patients who when vertebral displacement occurs it is more likely
have sustained trauma from a head-on motor vehicle to damage the cord. Until the age of 10, the spine has
collision (MVC) or diving accident. The cervical increased physiological mobility due to lax ligaments,
region is most often involved, especially at the C5–C6 which affords some protection against acute SCI.
level. Elderly patients are at a higher risk due to osteophytes
● Vertical compression or axial loading: This typically and narrowing of the spinal canal.
occurs when a person lands on the feet or buttocks
after falling or jumping from a height. The vertebral
column is compressed, causing a fracture that result Classification of Spinal Cord Injuries
in damage to the spinal cord. SCIs can be broadly classified as complete or incom-
78
● Hyperextension: This is the most common type of plete. The diagnosis of complete SCI cannot be made
injury. Hyperextension injuries can be caused by a until spinal cord shock resolves. If the bulbocaverno-
fall, a rear-end MVC, or hit on the head (e.g. during a sus reflex (BCR) is present (involuntary contraction of
boxing match). Hyperextension of the head and neck the rectal sphincter after squeezing the glans penis
may cause contusion and ischaemia of the spinal or clitoris or tugging on an indwelling urinary cathe-
cord without vertebral column damage. Whiplash ter) it indicates a complete injury. If, after the return
injuries are the result of hyperextension. Violent of the BCR, the patient has some sensation below the
hyperextension with fracture of the pedicles of C2 level of injury, he/she is considered to be sensory-
and forward movement of C2 on C3 produces the incomplete. If the BCR has returned and the patient
‘Hangman’s fracture’. has some motor function and sensation below the

Neurological Alterations and Management 459



TABLE 17.3 Summary of guidelines of the management of severe traumatic brain injury from the Brain
Trauma Foundation 32

Item Level I Level II Level III
Blood pressure None Blood pressure should be monitored and Oxygenation should be monitored and
and hypotension (SBP <90 mmHg) avoided. hypoxia (PaO 2 < 60 mmHg or O 2 saturation
oxygenation < 90%) avoided
Hyperosmolar None Mannitol is effective for control of raised Restrict mannitol use prior to ICP monitoring
therapy intracranial pressure at doses of 0.25 gm/kg to patients with signs of transtentorial
to 1 g/kg body weight. Arterial hypotension herniation or progressive neurological
(SBP <90 mmHg) should be avoided deterioration not attributable to
Hypertonic saline evidence is limited on the extracranial causes
use, concentration and method of
administration for the treatment of
traumatic intracranial hypertension
Prophylactic Insufficient data Insufficient data Prophylactic hypothermia is not significantly
hypothermia associated with decreased mortality
Prophylactic hypothermia is associated with
significant higher Glasgow Outcome Scale
scores
Infection Insufficient data Periprocedural antibiotics for intubation Routine ventricular catheter or prophylactic
prophylaxis should be administered to reduce the antibiotic use for ventricular catheter
incidence of pneumonia – but does not placement is not recommended to reduce
change length of stay or mortality. infection
Early tracheostomy – reduces mechanical Early extubation in qualified patients,
ventilation days without increased risk of pneumonia
Deep vein Insufficient data Insufficient data Graduated compression stockings or
thrombosis intermittent pneumatic compression
prophylaxis stockings until ambulatory
Low molecular weight heparin or low
unfractionated heparin in combination
with above.
Risk of expansion of intracranial
haemorrhage
Indications for Insufficient data ICP monitoring recommended for patients Normal CT with 2 or more of the following:
ICP with GCS score of 3–8 with abnormal CT. ● Age 40+ years
monitoring ● Motor posturing
● BP <90 mmHg
● GCS score 9–15 with abnormal CT at
prescription discretion
ICP monitoring Insufficient data Insufficient data Insufficient data
technology The ventricular catheter with external strain
gauge; most accurate low-cost, reliable ICP
device.
Can also be recalibrated in situ.
Parenchymal ICP cannot be recalibrated.
Negligible drift.
ICP treatment Insufficient data Treatment initiated ICP above 20 mmHg A combination of ICP values, clinical and
threshold brain CT should be used to determine the
need for treatment.
Cerebral Insufficient data Aggressive attempts to maintain CPP above CPP of <50 mmHg should be avoided
perfusion 70 mmHg with fluids and pressors due to The CPP value to target lies within the range
risk of ARDS of 50–70 mmHg
Patients with intact pressure autoregulation
tolerate higher CPP values
Ancillary monitoring of cerebral parameters
that include blood flow, oxygenation, or
metabolism facilitates CPP management
Brain oxygen Insufficient data Insufficient data Jugular venous oxygenation (<50%) or brain
Monitoring tissue oxygen tension (< 15 mmHg) are
and treatment thresholds and are to be
thresholds avoided

460 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



TABLE 17.3, Continued

Item Level I Level II Level III
Anaesthetics, Insufficient data Manage pain and agitation None advised
analgesics High-dose barbiturate may be used in
and sedatives haemodyamically stable patients refractory
to other ICP treatments.
Propofol for the control of ICP. High dose
propofol can produce significant morbidity.
Nutrition Insufficient data Full caloric replacement by day 7 post injury None advised
Antiseizure Insufficient data Phenytoin or valproate is not recommended None advised
prophylaxis for preventing late post traumatic seizures.
Anticonvulsants are indicated to decrease the
incidence of early post traumatic seizures.
Hyperventilation Insufficient data Prophylactic hyperventilation (PaCO 2 Use hyperventilation for temporary
<25 mmHg) is not recommended. reduction of elevated ICP.
Hyperventilation should be avoided during
the first 24 hrs after injury when CBF is
often critically reduced.
If hyperventilation used; SjO 2 or PbrO 2
measures recommended to monitor
oxygen delivery
Steroids Not None advised None advised
recommended




level of injury, he/she is considered to be sensory- and decreased cutaneous sensation of pain, temperature
motor-incomplete. There are four incomplete SCI syn- and touch on the same side of the spinal cord at the
dromes as follows: level of the lesion. Below the level of the lesion on
the same side, there is complete motor paralysis. On
● Anterior cord syndrome: Injury to the motor and the patient’s opposite side, below the level of the
sensory pathways in the anterior parts of the spine; lesion, there is loss of pain, temperature and touch,
thus patients are able to feel crude sensation, but because the spinothalamic tracts cross soon after
movement and detailed sensation are lost in the pos- entering the cord.
terior part of the spinal cord. Clinically, the patient
usually has complete motor paralysis below the level
of injury (corticospinal tracts) and loss of pain, tem- Pathophysiology
perature, and touch sensation (spinothalamic tracts), SCIs can be separated into two categories: primary inju-
with preservation of light touch, proprioception and ries and secondary injuries. Primary injuries are the
position sense. The prognosis for anterior cord syn- result of the initial insult or trauma, and are usually per-
drome is the worst of all the incomplete syndrome manent. The force of the primary insult produces its
prognoses. initial damage in the central grey matter of the cord.
● Posterior cord syndrome: This is usually the result of Secondary injuries are usually the result of a contusion
a hyperextension injury at the cervical level and is or tear injury, in which the nerve fibres begin to swell
not commonly seen. Position sense, light touch and disintegrate. Secondary neural injury mechanisms
and vibratory sense are lost below the level of the include ischaemia, hypoxia and oedema. Ischaemia, the
injury. most prominent post-SCI event, may occur up to 2 hours
● Central cord syndrome: Injury to the centre of the post-injury and is intensified by the loss of autoregula-
cervical spinal cord, producing weakness, paralysis tion of the spinal cord microcirculation. This will
78
and sensory deficits in the arms but not the legs. decrease blood flow, which is then dependent on the
Hyperextension of the cervical spine is often the systemic arterial pressure in the presence of hypotension
mechanism of injury, and the damage is greatest to or vasogenic spinal shock. Oedema develops at the
the cervical tracts supplying the arms. Clinically, the injured site and spreads into adjacent areas. Hypoxia
patient may present with paralysed arms but with no may occur as a result of inadequate airway maintenance
deficit in the legs or bladder. and ventilation. Immune cells, which normally do not
● Brown-Séquard syndrome: This involves injury to the enter the spinal cord, engulf the area after a spinal cord
left or right side of the spinal cord. Movements are injury and release regulatory chemicals, some of which
lost below the level of injury on the injured side, are harmful to the spinal cord. Highly reactive oxidising
but pain and temperature sensation are lost on the agents (free radicals) are produced, which damage the
opposite side of injury. The clinical presentation is cell membrane and disrupt the sodium–potassium
one in which the patient has either increased or pump.

Neurological Alterations and Management 461

Free-radical production and lipid peroxidation lead to hypercapnia occur, both of which promote neuronal and
vasoconstriction, increased endothelial permeability and glial acidosis, oedema and neuroexcitation.
increased platelet activation. A secondary chain of events
produces ischaemia, hypoxia, oedema and haemorrhagic
lesions, which in turn result in the destruction of myelin Nursing Practice
and axons. Autoregulation of spinal cord blood flow may Spinal cord injury should be suspected in patients with
be impaired in patients with severe lesions or substantial neck pain, sensory and motor deficits, unconsciousness,
oedema formation. These secondary reactions, believed intoxication, spondylitis or rheumatoid arthritis, head
to be the principal causes of spinal cord degeneration at injury and facial fractures. If spinal cord injury is
the level of injury, are now thought to be reversible 4–6 suspected or cannot be excluded, the patient must be
hours after injury. Therefore, if the cord has not suffered placed on a spine board with the head and neck immo-
irreparable damage, early intervention is needed to bilised in a neutral position using a rigid collar to reduce
prevent partial damage from developing into total and the risk of neurological deterioration from repeated
permanent damage. 80 mechanical insults. Spinal injury patients are susceptible
to pressure insults, so time must be considered when
Spinal shock occurs with physiological or anatomical
transection or near-transection of the spinal cord; it occurs hard surfaces are used for immobilisation. Total neck
immediately or within several hours of a spinal cord immobilisation should not interfere with maintenance of
injury and is caused by the sudden cessation of impulses the airway, and inadequate respiratory function must be
82
79
from the higher brain centres. It is characterised by the avoided.
loss of motor, sensory, reflex and autonomic function
below the level of the injury, with resultant flaccid paral- Resuscitation
ysis. Loss of bowel and bladder function also occurs. In Initial treatment aims for decompression of the spinal
addition, the body’s ability to control temperature (poi- cord and reversal of neurogenic shock and respiratory
kilothermia) is lost and the patient’s temperature tends failure. Spinal shock is associated with decreases in sys-
to equilibrate with that of the external environment. temic vascular resistance, arterial hypotension, venous
Neurogenic spinal shock occurs as a result of mid- to pooling, severe bradycardia and decreased myocardial
upper-level cervical injuries and is the result of sympa- contractility. Consequently, treatment of neurogenic
thetic vascular denervation and peripheral vasodilation. shock includes fluid replacement using crystalloid or
The loss of spinal cord vasculature autoregulation occurs, colloid solutions to maintain arterial blood pressure, cir-
causing the blood flow to the spinal cord to be depen- culatory volume, renal function and tissue oxygenation.
dent on the systemic blood pressure. Signs and symptoms Infusion of free water must be avoided, as this decreases
include hypotension, severe bradycardia, and loss of the plasma osmolarity and promotes spinal cord oedema.
ability to sweat below the level of injury. The same Atropine may be administered to reverse bradycardia and
clinical findings pertaining to disruption of the sympa- increase cardiac output. Administration of vasopressors
thetic transmissions in spinal shock occur in neurogenic (e.g. noradrenaline) prior to correction of the intravascu-
shock. 78 lar volume status may increase systemic vascular resis-
tance (left ventricular afterload) and further impair
Systemic effects of spinal cord injury myocardial contractility. Therefore, volume replacement
The traumatic insult causing the spinal cord injury is is the first step, and administration of vasopressors the
associated with an immediate stimulation of central second step in the treatment of arterial hypotension and
79
and peripheral sympathetic tone. Initially, the elevated low cardiac output after acute cervical spinal cord injury.
sympathetic activity raises systemic arterial blood pres- The major early cause of death in patients with acute
sure and induces cardiac arrhythmias. At the stage of cervical SCI is respiratory failure. Tracheal intubation may
spinal shock with loss of neuronal conduction, the sym- be indicated in unconscious patients, during shock, in
pathetic excitation is closely followed by decreases in patients with other major associated injuries, and during
systemic vascular resistance, arterial hypotension and cardiovascular and respiratory distress. It is also indicated
venous pooling. Lesions above the level of T5 addition- in conscious patients presenting with the following
ally present with severe bradycardia and cardiac dysfunc- criteria: maximum expiratory force below +20 cmH 2 O,
tion. The decreases in cardiac output combined with maximum inspiratory force below −20 cmH 2 O, vital
systemic hypotension further aggravate spinal cord isch- capacity below 1000 mL, and presence of atelectasis, con-
aemia in tissues with defective autoregulation. tusion and infiltrate. 81
Spinal cord injury may produce respiratory failure. The
extent of respiratory complications is related to the level Investigations and alignment
of the injured segments. Injuries above the level of C4–C5 Following the initial assessment of the patient, detailed
produce complete paralysis of the diaphragm, with diagnostic radiography defines the bone damage and
substantial decreases in tidal volume and consecutive compression of the spinal cord. First, lateral, ante-
hypoxia. With lesions below C6, the function of the dia- roposterior, odontoid and possibly oblique cervical
phragm is maintained and there is incomplete respiratory spine radiographs are obtained. If there is no evidence
failure due to paralysed intercostal and abdominal of injury, flexion and/or extension views may be con-
musculature. As a consequence, arterial hypoxia and sidered. If any of these radiographs suggest cervical spine

462 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

abnormalities, specific radiological procedures such as ● Hyperglycaemia is associated with increased inflam-
cervical myelography, high-resolution CT scan or mag- mation and must be controlled to less than 10 mmol/
netic resonance imaging will identify fractures, disloca- Hg, avoiding hypoglycaemia. 84
82
tion of bony fragments, and spinal cord contusion. ● The concept of pain relief and sedation in patients
In patients with a dislocated cervical fracture, decom- with spinal cord injury is based on the maintenance
pression and anatomical bony realignment may be of coupling between metabolism and spinal cord
achieved with traction forces applied manually, or with blood flow while achieving hypnosis, analgesia and a
halo or Gardner–Wells systems under radiological control. ‘relaxed cord’. This concept includes maintenance of
If the anatomical bony alignment procedures and trac- normal to high systemic perfusion pressures, nor-
tion forces fail to decompress the cord, surgical inter- moxia and normocapnia.
vention to remove the lesion is required. The timing ● Psychological and empathetic support is essential and
of surgical intervention remains controversial. While appropriate referral for grieving and stress is para-
urgent surgical decompression or internal stabilisation mount. Rehabilitation counselling and planning starts
should be performed in all patients with deteriorating at the acute stage in order to give the family unit some
neurological status, some centres tend to defer surgical future focus and hope.
treatment in patients with spinal cord injury but stable
neurological deficit. See the Online resources for specific protocols related to
spinal injury.
Concepts of Neuroprotection CEREBROVASCULAR DISORDERS
and Regeneration
Cerebral vascular disorders include cerebrovascular
There have been many negative SCI clinical trials in disease and cerebral vascular accidents (stroke). A stroke
regard to neuroprotection with the exception of methyl- (acute brain injury of vascular origin) may be either isch-
prednisolone within 8 hours after SCI, which has shown aemic or haemorrhagic and is defined as an interruption
77
some beneficial effect. The failure of these neuroprotec- of the blood supply to any part of the brain, resulting in
tive agents has been attributed to the attempt of blocking damaged brain tissue.
only one molecular pathway of a complex range of SCI
molecular mechanisms. However, there has been renewed
interest in regeneration which involves stem cell trans- Stroke
plantation or similar restorative approaches designed to Stroke is the primary cerebrovascular disorder in Australia
optimise spontaneous axonal growth and myelination and New Zealand and is still the third-leading cause of
but is still in its infancy in Australia and NZ due to limit- death. Every year approximately 40,000 people in Austra-
ing legislation in regard to stem cell research. lia are admitted to hospital with a diagnosis of stroke;
approximately 6000 New Zealanders suffer from a stroke
every year and approximately 2000 deaths each year are
Collaborative Management attributable to stroke. 85,86 The prevalence of stroke is
Patients with acute cervical spinal cord injury require ICU higher among men than women (1.4% versus 1.0%).
monitoring, observation and support of ventilation, Almost 60% of people who have had a stroke are aged
a nasogastric tube to reduce abdominal distension 65 years and over, while 18% are under the age of 55
and risk of aspiration, a urinary catheter and thermal years. Indigenous Australians have higher rates of death
maintenance. and illness from heart, stroke and vascular diseases than
other Australians. In 2007–08, death rates were 2.6 times
● Tracheostomy is indicated in high cervical spine injury as high and hospitalisation rates 1.4 times as high as for
and ischaemia, sometimes only while the early other Australians. Stroke is currently the biggest single
85
oedema is resolving. cause of adult disability in Australasia. Strokes can be
● Spinal alignment and immobilisation requires careful divided into two major categories: ischaemic (85%), in
positioning with dedicated neck support by experi- which vascular occlusion and significant hypoperfusion
enced clinicians. occur; and haemorrhagic (15%), in which there is extra-
● Shoulder and lumbar support pillows are often pre- vasation of blood into the brain. Although there are some
scribed. Pressure-relief mattresses must be suitably similarities between the two broad types of stroke, the
designed for spine immobilisation and when pre- aetiology, pathophysiology, medical management, surgi-
scribed can be tilted to facilitate ventilation. cal management and nursing care differ.
● Meticulous integument and bowel care are indicated
with daily protocols for regular stool softeners and
peristaltic stimulants essential for the prevention Aetiology
of autonomic dysreflexia and autonomic nerve Hypertension is the leading risk factor for stroke. Other
dysfunction. risk factors include diabetes, cardiac disease, previous
● Early nutritious feeding is essential, whether oral or cerebrovascular disease (transient ischaemic attack
enteric; however, aspiration must be prevented. The or stroke or myocardial infarction), age, sex, lipid disor-
supplementation of feeding with high-energy protein ders, excessive ethanol ingestion, elevated hematocrit,
fluids to match the catabolic state assists with recovery elevated fibrinogen and cigarette smoking. Cerebral arte-
(see Chapter 19). riosclerosis predisposes indiuiduals to both ischaemic

Neurological Alterations and Management 463

and haemorrhagic stroke. Smoking is the strongest risk by uncontrolled hypertension. Secondary intracerebral
factor for aneurysmal SAH. Atrial fibrillation, endocardi- haemorrhage is associated with arteriovenous malforma-
tis and medications containing supplemental oestrogen tions (AVMs), intracranial aneurysms, or certain medica-
are risk factors for embolic stroke. Seizures develop in tions (e.g. anticoagulants and amphetamines). Symptoms
approximately 10% of cases, usually appearing in the first are produced when an aneurysm or arteriovenous mal-
24 hours and more likely to be focal than generalised. formation (AVM) enlarges and presses on nearby cranial
Most patients with aphasia will have a cerebral infarction nerves or brain tissue or, more dramatically, when a
in the distribution of the left middle cerebral artery. 87 blood vessel, aneurysm or AVM ruptures, causing intra-
cerebral or subarachnoid haemorrhage. When an aneu-
Ischaemic Stroke rysm ruptures, arterial pressure forces blood into the
subarachnoid space between the arachnoid mater and
Ischemic stroke compromises blood flow and energy
supply to the brain, which triggers mechanisms that lead the surface of the brain. Free blood then travels through
to cell death. Infarction occurs rapidly in the region of the fissures into the basal cisterns and across the surface
most severe ischaemia (termed ischaemic penumbra) of the brain. When clotted, this blood can interfere with
and expands at the expense of the surrounding hypoxic the circulation and reabsorption of cerebrospinal fluid
tissue, from the centre to the periphery. Therapeutic strat- (CSF), potentially causing obstructive hydrocephalus and
egies in acute ischaemic stroke are based on the concept raised intracranial pressure. The commonest cause is a
of arresting the transition of the penumbral region into leaking aneurysm in the area of the circle of Willis or a
infarction, thereby limiting ultimate infarct size and congenital AVM of the brain. Blood in the subarachnoid
improving neurological and functional outcome. Isch- space is a powerful meningeal irritant, and it is this irrita-
aemic stroke can be further categorised as middle cerebral tion that causes most of the initial signs and symptoms
artery occlusion, acute basilar occlusion, and cerebellar of SAH.
infarcts. 88 In intracerebral haemorrhage the bleeding is usually arte-
rial and occurs most commonly in the cerebral lobes,
The management of an ischaemic stroke comprises four
primary goals: restoration of cerebral blood flow (reper- basal ganglia, thalamus, brainstem (mostly the pons) and
fusion), prevention of recurrent thrombosis, neuropro- cerebellum. Occasionally, the bleeding ruptures the wall
tection, and supportive care. The timing of each element of the lateral ventricle and causes intraventricular haem-
89
of clinical management needs to be implemented in a orrhage, which is often fatal.
decisive manner. Refer to Table 17.4 for classification and Normal brain metabolism is disrupted by the brain being
treatment strategies and to Online resources for specific exposed to blood. The sudden entry of blood into the
ischaemic stroke protocols. subarachnoid space or brain parenchyma results in a rise
in ICP, which then leads to compression and ischaemia
Haemorrhagic Stroke resulting from the reduced perfusion pressure and vaso-
spasm that often accompany intracerebral and subarach-
Haemorrhagic strokes are caused by bleeding into the noid haemorrhage. Depending on the severity, clinical
89
brain tissue, the ventricles or the subarachnoid space. findings include severe headache, nuchal rigidity, photo-
Primary intracerebral haemorrhage from a spontaneous phobia, nausea and vomiting, hypertension, ECG
rupture of small vessels accounts for approximately changes, pyrexia, cranial nerve deficits, visual changes,
80% of haemorrhagic strokes and is primarily caused sensory or motor deficits, fixed and dilated pupils, sei-
zures, herniation and sudden death.
The Factor Seven for Acute Hemorrhagic Stroke (FAST)
multicentre international clinical trial recently reported
that haemostatic therapy with recombinant activated
TABLE 17.4 Classification and type of ischaemic stroke factor VII (rFVIIa) reduced growth of the haematoma but
and treatment options did not improve survival or functional outcome after
intracerebral haemorrhage. 90
Classification Treatment options
Middle cerebral Intravenous or intra-arterial tissue
artery occlusion plasminogen activator (tPA). Subarachnoid Haemorrhage
Exclusion criteria: >3 hours elapsed from
stroke onset and widespread early Admission to ICU is indicated for subarachnoid haem-
infarct changes on CT scan. orrhage Hunt-Hess SAH severity Scale III (see Table
Tolerate autoprotective hypertension for 17.5) and greater to manage systemic complications,
perfusion of the ischaemic penumbra. recognise and treat clinical deterioration, investigate the
Acute basilar Anticoagulation with intravenous heparin. cause of the haemorrhage and to treat any underlying
occlusion Thrombolysis up to 12 hours after onset. aneurysm or arteriovenous malformation. Resuscitation
Cerebellar infarcts May be difficult to recognise because of is directed towards maintaining cerebral perfusion pres-
the slow evolution of brainstem and sure by ensuring adequate arterial blood pressure (often
cerebellar signs. with the use of inotropes to produce relative hyperten-
Aspirin, antihypertensives and sion although reactive hypertension is often present),
conventional cerebral oedema strategies.
ensuring a relatively high circulating blood volume

464 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

Cerebral Venous Thrombosis
TABLE 17.5 Hunt-Hess scale for SAH Cerebral venous thrombosis is particularly important to
recognise because there is general consensus that early
Score Description anticoagulation can result in good clinical outcomes.
96
0 Unruptured; asymptomatic discovery MR and CT vascular imaging has made it easier to estab-
lish the diagnosis, but close monitoring of the patient is
I Asymptomatic or minimal headache with slight
nuchal rigidity essential, as late deterioration can occur.
II Moderate to severe headache, nuchal rigidity; no
neurological deficit other than cranial nerve Collaborative Management of Stroke
deficit
Expected outcomes for patients with acute ischaemic and
III Drowsiness, confusion, or mild focal deficit (e.g. haemorrhagic stroke include prevention of secondary
hemiparesis), or a combination of these findings
injury, of airway and respiratory complications, and
IV Stupor, moderate to severe deficit, possibly early the maintenance of haemodynamic stability. Timely
decerebrate rigidity and vegetative disturbances
assessment and intervention is paramount in the man-
V Deep coma, decerebrate rigidity, moribund agement of ischaemic stroke, especially regarding inter-
appearance ventional pharmacology and prevention of cerebral
haemorrhage. See Online resources for specific protocols
related to stroke.
(hypervolaemia), and producing relative haemodilution Atrial fibrillation and deep vein thrombosis (DVT) pre-
(’triple H therapy’). 91 vention (in ischaemic stroke) requires anticoagulation
Hypovolaemia occurs in 30–50% of patients, as does control. In haemorrhagic stroke, sequential compression
excessive hyponatraemia in 30% of patients. In the first device and stockings are indicated for DVT prophylaxis as
six days, plasma volume decreases of greater than 10% anticoagulants are a risk factor for rebleeding. Mainte-
can occur following SAH, thus increasing the risk of vaso- nance of bowel and bladder function and prevention of
spasm and ischaemia. Women have been found to have integument complications, malnutrition, seizures and
more significant drops in blood volume than men fol- increasing neurological deficits are important goals. Envi-
92
lowing SAH. ‘Third space’ loss, insensible losses and ronmental precautions are implemented to provide a
blood loss account for this drop in fluid volume, as well non-stimulating environment, preventing rises in ICP
as electrolyte disturbances. and further bleeding.
Sensory perceptual and motor alterations need to be
Other aspects of management in the acute stages include assessed in regard to effective communication and pain
suitable analgesia, seizure control, and treatment with management. Rehabilitation and psychological support
nimodipine to prevent secondary ischaemia caused by for the patient and significant others are integrated into
vasospasm. Vasospasm often occurs 4–14 days after the acute care phase for a smooth transition.
initial haemorrhage when the clot undergoes lysis (dis-
solution), increasing the chances of rebleeding. It is
believed that early surgery to clip the aneurysm prevents INFECTION AND INFLAMMATION
rebleeding and that removal of blood from the basal The CNS infections of major interest in the ICU are
cisterns around the major cerebral arteries may prevent divided into those which affect the meninges (meningi-
vasospasm. 93,94 (See previous section on Management of tis) and those which affect the brain parenchyma
vasospasm.) (encephalitis). They may be viral or bacterial in aetio-
logy. There are also numerous medical conditions that
ICP monitoring and drainage of CSF via ventricul ostomy may produce an encephalopathic illness which may
89
is indicated in SAH but not in cerebral haemorrhage. mimic viral encephalitis. In patients recently returning
SAH causes increased sympathetic activation from the from abroad, particular vigilance must be paid to the
presence of haemoglobin in the subarachnoid space. This possibility of such non-viral infections as cerebral
results in elevated catecholamine levels, which may result malaria, which may be rapidly fatal if not treated early.
in focal myocardial necrosis, expla ining the presence of A number of metabolic conditions, including liver and
inverted T waves, ST dep ression, prominent U waves, and renal failure and diabetic complications, may also cause
Q-T intervals in more than 50% of pati ents. As cardiac confusion due to the manifestation of cerebral oedema.
function is one of the determinants for adequate cerebral The possible role of alcohol and drug ingestion must
blood flow, it is essential to identify such occurrences always be considered.
95
early and treat them acco rdingly. Hyponatraemia occurs
from alte rations in atrial natriuretic factor (ANF) in
response to sympathetic nervous system activation. The Meningitis
syndrome of inappropriate secretion of antidiuretic The incidence of disease caused by Neisseria meningitidis
hormone (SIADH) is primarily responsible for hypona- remains an issue of public health concern in Australia
traemia in those with SAH, as is cerebral salt-wasting and New Zealand. The introduction of a publicly funded
syndrome; however, both mechanisms are still relatively program of selective vaccination with conjugate sero-
misunderstood. 90 group C meningococcal vaccine in 2004 has resulted in

Neurological Alterations and Management 465

a significant reduction in the number of cases of menin- development of subdural empyema, brain abscess and
97
gococcal disease. Nationally in 2008 only 15 serogroup acute hydrocephalus may require surgical intervention.
C infections were identified and serogroup B accounted Bacterial meningitis with accompanying bacteraemia can
for 88% of all infections. New Zealand has one of the lead to a marked systemic inflammatory response with
highest rates of meningococcal B disease in the developed septic shock, respiratory distress syndrome and dissemi-
world but the incidence has declined. There were 132 nated intravascular coagulation.
cases of meningococcal disease notified in 2009, which
equates to a rate of 3.8 per 100,000 population. The Collaborative care
number of confirmed cases was 117, giving a confirma-
tion rate of 88.6% which is the third-equal-highest con- Neurological derangement often coexists with circulatory
firmation rate since 1991. Five deaths occurred in 2009, insufficiency, impaired respiration, metabolic derange-
giving a case-fatality rate of 3.8%. Since 1991 a total of ment and seizures. Protecting the patient from injury
265 deaths have been recorded, an overall case-fatality secondary to raised ICP and seizure activity is essential.
rate of 4.2%. The policy of giving antibiotics prior to Prevention in relation to complications associated with
hospital admission, implemented in 1995, reduced the immobility, such as decubitus and pneumonia, is
case-fatality rate for those receiving antibiotics. In addi- required. It is important to institute droplet infection
tion this rate has reduced from 470 cases in 2001, prior control precautions in those attending the patient until
to the immunisation for meningococcal B commencing 24 hours after the initiation of antibiotic therapy (oral
98
in 2004. The incidence of meningococcal disease varies and nasal discharge is considered infectious). See Online
seasonally, rising in June and peaking in October each resources for infection control protocols relating specifi-
year. The highest incidence of meningococcal disease was cally to meningitis.
for children aged 4 years and under. A secondary peak in
the incidence of meningococcal disease is seen in adoles- Encephalitis
99
cents and young adults. However, during the H1N1
influenza epidemic there were several cases of H1N1 Encephalitis implies inflammation of the brain substance
influenza-related meningitis. See Table 17.6 for CSF pro- (parenchyma), which may coexist with inflammation
files for acute meningitis and encephalitis and Table 17.7 of the meninges (meningoencephalitis) or spinal cord
for the classification, treatment and clinical presentation (encephalomyelitis). Encephalitis may be mild and self-
of meningitis. limited, or may produce devastating illness.
Complications Aetiology
Complications of meningitis vary according to the Herpes simplex virus (HSV) is the commonest cause
aetiological organism, the duration of symptoms prior of non-seasonal encephalitis in Australia. Without tre-
to initiation of appropriate therapy, and the age and atment, HSV encephalitis is fatal in up to 80% of cases,
100
immune status of the patient. Temporary problems and leaves up to 50% of survivors with long-term
include development of haemodynamic instability sequelae. 101
and disseminated intravascular coagulopathy, particu- ● In the absence of particular risk factors, other
larly in meningococcal infection, SIADH or other common causes are enteroviruses, influenza virus and
dysregulation of the hypothalamic–pituitary axis (e.g. Mycoplasma pneumoniae. However, the likely patho-
diabetes insipidus) and an acute rise in ICP.
gens in encephalitis are dramatically influenced by
Focal neurological signs may develop in the early stages geographic location, history of travel and animal
of meningitis, but are more common later. The exposure, and vaccination.



TABLE 17.6 Typical profiles of cerebrospinal fluid in acute meningitis and encephalitis

Meningitis Encephalitis
Investigation Reference range Bacterial Viral Bacterial/Viral
Opening pressure <30 mmH 2 O Raised Normal Raised
White cells
6
Total count <5 × 10 /L Greatly raised Moderately raised Moderately raised
Differential Lymphocytes (60–70%), Neutrophils predominate Lymphocytes Lymphocytes
monocytes (30–50%), no predominate predominate
neutrophils or red blood cells
Glucose concentration 2.8–4.4 mmol/L Lowered Normal Normal
CSF: serum glucose ratio >60% Lowered Normal Normal
Protein concentration <0.45 g/L Raised Normal or slightly raised Normal or slightly raised

466 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



TABLE 17.7 Classification of acute meningitis

Acute meningitis Bacterial – notifiable disease Viral
Aetiology Neisseria meningitis Enteroviruses: 85–95% of cases
● Serogroups A,B,C – 90% invasive isolates Herpes simplex 1 & 2
● Serogroup B – most disease Varicella zoster
● Serogroup A – epidemic disease and indigenous Cytomegalovirus
haemophilus influenzae type B Epstein–Barr
streptococcus pneumoniae HIV infection can also present as aseptic meningitis
listeria monocytogenes Postinfectious encephalomyelitis: may occur following a
variety of viral infections, usually of the respiratory tract.
Cryptococcus neoformans
Fungal isolates
Pathophysiology Rapid recognition and diagnosis of meningitis is The physical signs are not so marked and the illness is not
imperative. as severe and prolonged as bacterial meningitis.
Quick and insidious progress of disease Viral infection of mucosal surfaces of respiratory or
Colonisation of mucosal surfaces (nasopharynx) gastrointestinal tract
Haematogenous or contiguous spread Virus replication in tonsillar or gut lymphatics
Specific antibodies important defence Viraemia with haematogenous dissemination to the CNS
Bacterial invasion of meninges: inflammatory response, Meningeal inflammation, BBB breakdown, cerebral
breakdown of the BBB, cerebral oedema, intracranial oedema, vasculitis and spasm
hypertension
Vasculitis, spasm and thrombosis in cerebral blood vessels
Clinical Presents with sepsis: headache, fever, photophobia, Presents with non-specific symptoms, viral respiratory
presentation and vomiting, neck stiffness, alteration of mental status. illness, diarrhoea, fever, headache, photophobia,
progression Meningococcaemia is characterised by an abrupt onset of vomiting, anorexia, rash, cough and myalgia.
fever (with petechial or purpuric rash). Occurs in summer or late autumn.
Progresses to purpura fulminans, associated with the Enteroviral, pleurodynia, chest pain, hand-foot-mouth
rapid onset of hypotension, acute adrenal disease
haemorrhage syndrome, and multiorgan failure. HSV-2: acute genital herpes
Kernig’s sign
Brudzinski’s sign
Cranial nerve palsy (III, IV, VI, VII) uncommon and develop
after several days
Focal neurological signs in 10–20% cases
Seizures in 30% of cases
Signs of intracranial hypertension: coma, altered
respiratory status
Leads to hypertension and bradycardia before herniation,
or brain death, leads to irreversible septic shock
Treatment If meningococcal infection is suspected, the best way to Administer intravenous aciclovir.
reduce mortality is to administer Dexamethasone may be prescribed: reduces BBB
Empirical IV therapy immediately permeability.
Ceftriaxone 2g IV 12hrly or Supportive treatment and resuscitation
Cefatoxime 2g IV 6hrly or immediately Management of intracranial hypertension/ischaemia
Consequent dose, times and type of antibiotic need to be
modified after full investigation and a detailed
examination have taken place.
Dexamethasone may be prescribed: Needs to be at same
time of antibiotic as outcome neurologically is reduced
if given after antibiotic. Reduces BBB permeability.
Supportive treatment and resuscitation
Management of intracranial hypertension/ischaemia


● Murray Valley encephalitis (MVE) virus causes sea- ● Mycobacterium tuberculosis, the yeast Cryptococcus
sonal epidemics of encephalitis at times of high neoformans and Treponema pallidum (syphilis) may
regional rainfall. This arthropod-borne virus is the also affect the brain parenchyma but usually
commonest flavivirus to cause encephalitis in produce chronic or subacute meningitis in such
Australia. circumstances.
● Since 2005, the distribution of Japanese B ence phalitis
virus has expanded into Australia via the Torres Strait
102
Islands. It causes disease clinically similar to MVE. Pathophysiology
In addition, two novel encephalitis viruses were In the majority of encephalitis cases, the offending organ-
recently identified in Australia, the Hendra virus and ism finds access to the brain via the nasopharyngeal epi-
Australian bat lyssavirus. These should be considered thelium and the olfactory nerve system. Arboviruses are
if there is a history of animal exposure, or if no other transmitted from infected animals to human through bite
103
pathogen can be implicated. of infected animals. The cytokine storm results in

Neurological Alterations and Management 467

neural cell damage, as well as the apoptosis of astrocytes. Guillain–Barré Syndrome
The disruption of the blood–brain barrier progresses to Guillain–Barré syndrome (GBS) is an immune-mediated
the systemic cytokine storm, resulting in septic shock, disorder resulting from generation of autoimmune anti-
disseminated intravascular coagulopathy (DIC) and mul- bodies and/or inflammatory cells which cross-react with
tiorgan failure (MOF).
epitopes on peripheral nerves and roots, leading to demy-
elination or axonal damage or both, and autoimmune
Clinical features and diagnosis insult to the peripheral nerve myelin. In Australia,
Encephalitis may present with progressive headache, fever Guillain–Barré has an average incidence of about 1.5 per
and alterations in cognitive state (confusion, behavioural 100,000, in men slightly higher than in women. Of all
106
change, dysphasia) or consciousness. Focal neurological patients, 85% recover with minimal residual symptoms;
signs (paresis) or seizures (focal or generalised) may also severe residual deficits occur in up to 10%. Residual defi-
occur. Upper motor signs (hyperreflexia and extensor– cits are most likely in patients with rapid disease progres-
plantar responses) are often present, but flaccid paralysis sion, those who require mechanical ventilation, or those
and bladder symptoms may occur if the spinal cord is 60 years of age or over. Death occurs in 3–8% of cases,
involved. Associated movement disorders or the SIADH resulting from respiratory failure, autonomic dysfunc-
secretion may be seen. In northern Australia, it may be tion, sepsis or pulmonary emboli. 107
desirable to distinguish MVE from Japanese encephalitis
clinically. Both conditions often affect the brainstem and Aetiology
basal ganglia, but MVE often involves the spinal cord,
while Japanese encephalitis may produce striking menin- The diagnosis of GBS is confirmed by the findings of
geal signs, with or without thalamic involvement. Both cytoalbuminological dissociation (elevation of the CSF
have high mortality (25–33%) and high rates of chronic protein without concomitant CSF pleocytosis), and by
sequelae in survivors (~50%). 101 neurophysiological findings suggestive of an acute
(usually demyelinating) neuropathy. These abnormalities
106
The most sensitive type of imaging for diagnosis of may not be present in the early stages of the illness.
encephalitis is MRI; in HSV encephalitis, CT scans may There are two forms of GBS. The demyelinating form, the
initially appear normal, but MRI usually shows invol- more common one, is characterised by demyelination
vement of the temporal lobes and thalamus. 103,104 Exa- and inflammatory infiltrates of the peripheral nerves and
mination of CSF can assist in differential diagnosis. roots. In the axonal form the nerves show Wallerian
Electroencephalography is less sensitive but may be degeneration with an absence of inflammation. Discrimi-
helpful if it shows characteristic features (e.g. lateralising nation between the axonal and demyelinating forms
periodic sharp and slow-wave patterns). Refer to Table relies mainly on electrophysiological methods. There is a
17.6 for CSF profiles. close association between GBS and a preceding infection,
suggesting an immune basis for the syndrome. The com-
Collaborative management monest infections are due to Cambylobacter jejuni, cyto-
Support in an ICU is often required in encephalitis to megalovirus and Epstein–Barr virus.
maintain ventilation, protect the airway and manage
complications, such as cerebral oedema. The man- Pathophysiology
agement of acute viral encephalitis includes aggressive GBS is the result of a cell-mediated immune attack on
airway, ventilation, sedation, seizure, haemodynamic, and peripheral nerve myelin proteins. The Schwann cell is
fluid and nutritional support. Clinical deterioration in spared, allowing for remyelination in the recovery phase
encephalitis is usually the result of severe cerebral oedema of the disease. With the autoimmune attack there is an
with diencephalic herniation or systemic complications, influx of macrophages and other immune-mediated
including generalised sepsis and multiple organ failure. agents that attack myelin, cause inflammation and
The use of ICP monitoring in acute encephalitis remains destruction and leave the axon unable to support nerve
controversial but should be considered if there is a conduction. This demyelination may be discrete or
rapid deterioration in the level of consciousness, and if diffuse, and may affect the peripheral nerves and their
imaging suggests raised ICP. Prolonged sedation may be roots at any point from their origin in the spinal cord to
necessary. Decompressive craniotomy may be successful the neuromuscular junction. The weakness of GBS results
in cases where there is rapid swelling of a non-dominant from conduction block and concomitant or primary
temporal lobe, as poor outcome is otherwise likely. 105 axonal injury in the affected motor nerves. Pain and par-
aesthesias are the clinical correlates of sensory nerve
NEUROMUSCULAR ALTERATIONS involvement.

Generalised muscle weakness can manifest in several
disorders that require ICU admission or complicate the Clinical manifestations
course of patients. These may involve motor neuron Onset is rapid, and approximately 20% of cases lead to
disease, disorders of the neuromuscular junction, peri- total paralysis, requiring prolonged intensive therapy
pheral nerve conduction and muscular contraction. with mechanical ventilation. The therapeutic window for
These disorders manifest as Guillain–Barré syndrome, GBS is short, and the current optimal treatment with
myas thenia gravis, and critical illness polyneuropathy whole plasma exchange or IV immunoglobulin (IVIg)
and myopathy. therapy lacks immunological specificity and only halves

468 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

108
the severity of the disease. GBS has three phases – acute, muscles, presence of paradoxical respiration and
plateau, and recovery – each stage lasting from days to integrity of upper airway reflexes), ABG data and chest
weeks and in recovery to months and years. The patient radiography determine levels of fatigue in both the
presents with: acute stage (for intubation and ventilation) and
rehabilitation (weaning) stage. Long-term ventilation
● symmetrical weakness, diminished reflexes, and
upward progression of motor weakness. A history of increases the risk of ventilator-acquired pneumonia
a viral illness in the previous few weeks suggests the (VAP), and routine surveillance for VAP is vital.
diagnosis ● Cardiovascular assessment is important, as serious
● changes in vital capacity and negative inspiratory tachyarrhythmias and bradyarrhythmias and destabi-
force, which are assessed to identify impending neu- lising fluctuations in blood pressure caused by
romuscular respiratory failure. autonomic impairment are prevalent. This feature is
common during fatigue, sleep and states of dehydra-
Indications for ICU admission include the following: tion. Often, autonomic dysfunction is worst in the
ventilatory insufficiency, severe bulbar weakness threat- early stages of a nosocomial infection. 112
ening pulmonary aspiration, autonomic instability, or ● Cranial nerve assessment and dermatome (for sensory)
109
coexisting general medical factors, and often a combi- and muscle strength assessment assist in mapping the
nation of factors, are present. The incidence of respiratory progression, severity and rehabilitation of the disease
failure requiring mechanical ventilation in GBS is approxi- and determining the risk of aspiration. Pain (espe-
mately 30%. cially neuropathic) is particularly common in GBS
during changes in myelination, and can be difficult to
Ventilatory failure is primarily caused by inspiratory 113
muscle weakness, although weakness of the abdominal treat. Assessment will include all aspects as indi-
and accessory muscles of respiration, retained airway cated for the long-term immobile, intubated, venti-
secretions leading to pulmonary aspiration and atelecta- lated and neuromuscular-impaired patient.
sis are all contributory factors. The associated bulbar
weakness and autonomic instability reinforce the need Independent practice
for control of the airway and ventilation. When caring for a neuromuscular-impaired patient, a
Acute motor and sensory axonal neuropathy, the acute structured care plan is essential for continuity of care and
axonal form of GBS, usually presents with a rapidly devel- should involve the patient and family. This is of particular
oping paralysis developing over hours, and a rapid devel- importance in the long-term recovery phase, where the
opment of respiratory failure requiring tracheal intubation provision of sleep, good nutrition and prevention of the
and ventilation. PaCO 2 may remain constant until just complications of immobility (noso comial infections,
before intubation, emphasising the importance of not DVT, integument and muscular we akening, adequate
relying purely on arterial blood gas analysis to make deci- nutrition and constipation) is important:
sions regarding intubation. ● Endotracheal and pharyngeal suction can be demand-
Recently sensory involvement in relation to pain has been ing (weakened upper airway reflexes), and sputum
studied asserting the clinical observation of pain ranging plugging and retention requires frequent reposition-
from mild to severe in the acute and rehabilitant phases. ing and physiotherapy.
Chronic pain is often present in survivors of GBS. 110 ● Routine daily gentle exercise as part of a flexible
program improves wellbeing and strength.
There may be total paralysis of all voluntary muscles of ● Fatigue must be avoided, as autonomic nerve dysfunc-
the body, including the cranial musculature, the ocular tion, deafferent pain syndromes, muscle pain and
muscles and the pupils. Prolonged paralysis and incom- depression can be exacerbated.
plete recovery are more likely, and prolonged ventila- ● Suctioning, coughing, bladder distension, constipa-
tory support may be necessary. Walgaard and colleagues tion and the Valsalva manoeuvre can also aggravate
found that GBS patients who experience rapid disease autonomic nerve dysfunction instability.
progression, bulbar dysfunction, bilateral facial weak- ● Therapeutic massage, warm and cold packs and
ness or autonomic nerve dysfunction were more likely careful positioning contribute to comfort and pain
111
to require mechanical ventilation. Tracheostomy is management.
usually performed within 2 weeks, and mechanical ven- ● The patient’s surroundings should be pleasant and
tilation is delivered in a supportive mode with minimal presentable, especially during long recovery.
yet adequate sedation and pain management. ● Communication techniques need to be refined to
prevent fatigue and frustration.
Nursing practice ● Patience, tolerance, empathy, humour and family
Assessment and understanding of neuromuscular weak- involvement assist the patient in psychological resil-
ness through motor and sensory neurological assess- ience and recovery.
ment is vital in the acute care and rehabilitation of GBS
patients: Collaborative management
● Comprehensive respiratory assessment (level of In the acute phase, accurate diagnosis and timely ven-
overall patient comfort, frequency and depth of tilatory support are provided by effective communica-
breathing, forced vital capacity, use of accessory tion between primary and in-hospital care providers.

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
115
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
115
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
114
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-
113
at the neuromuscular junction. Therefore, successful rates upper and lower airway muscle weakness. ABGs

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

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

472 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

glucose levels are independently associated with enlar- which might precipitate ischaemia in the region sur-
gement of the haematoma. About half of spontaneous rounding the haematoma.
ICH cases originate in the basal ganglia, a third in the The Australian Stroke Foundation’s current guidelines
cerebral hemispheres, and a sixth in the brainstem or recommend a target systolic BP below 180 mmHg or a
cerebellum. 130
mean arterial blood pressure of 130 mmHg. 133 Mana-
There is growing evidence that more than a simple mass gement of BP is particularly important in ICH and
effect compromises the region surrounding the haema- is currently the subject of a large Australian RCT
toma. The haematoma induces an inflammatory response (Interact-2). 134
from plasma that is rich in thrombin and other coagula-
tion end-products released by the clotted haematoma.
Activation and expression of cytotoxic and inflammatory Prevention of cerebral ischaemia
mediators, induction of matrix metalloproteases, leuco- and secondary brain injury
cyte recruitment and disruption of the blood–brain Intravenous therapy should be aimed at maintaining
barrier are all implicated in the inflammation response. euvolaemia with an isotonic fluid, such as normal
Both vasogenic and cytotoxic oedema contribute to saline. Potassium supplementation is often necessary,
ischaemia. although glucose should be avoided, except in rare
cases of hypoglycaemia. Emergency measures for ICP
Clinical manifestations control are appropriate for stuporous or comatose
patients, or those who present acutely with clinical
In 40% of cases, ICH is accompanied by intraventricular signs of brainstem herniation (see the section on
haemorrhage, which can cause acute hydrocephalus and Management of intracranial hypertension and ischaemia).
high ICP, and lessens the chance of a good outcome. The head should be elevated to 30 degrees for optimal
Rapid onset of a focal neurological deficit with clinical balance between perfusion and intracranial pressure
signs of high ICP – such as an abrupt change in level of and to prevent aspiration. Warfarin increases the risk
consciousness, headache, and vomiting – suggest a diag- of ICH 5–10 times, and presenting patients should have
nosis of ICH. However, these symptoms can also take this reversed with fresh frozen plasma, prothrombin-
place after acute ischaemic stroke. For this reason, CT or complex concentrates and vitamin K. Early in the
MRI is essential for confirming dziagnosis. Rapid progres- course of patients with ICH, even with exclusion of
sion to coma with motor posturing suggests massive coagulopathy, injection of activated factor VII results
supratentorial haemorrhage, bleeding into the brainstem in significant reduction in the rate of haematoma
or diencephalon, or acute obstructive hydrocephalus due expansion. 90
to intraventricular haemorrhage. Over 90% of patients
have acute hypertension exceeding 160/100 mmHg,
whether or not there is a history of pre-existing hyper- SUMMARY
tension. Dysautonomia in the form of central fever,
hyperventilation, hyp er glycaemia, and tachycardia or bra- Support of neurological function commences with an
dycardia is also common. 131 overview of specific pathophysiological alterations of
consciousness, seizures, motor and sensory function,
cerebral perfusion, ischaemia, cerebral oedema and
Nursing Practice intracranial hypertension. Therapeutic management of

The following nursing practice should be undertaken. intracranial hypertension and vasospasm are applied to
brain injury in general. Central nervous system dis orders
include traumatic brain and spinal injury, their aetio-
Intubation logy, clinical pathophysiology and management. Cere-
Patients with ICH, especially those with infratentorial brovascular disorders focus on intracerebral ha emorrhage
bleeding, may require intubation for protection of the and subarachnoid haemorrhage. Ischaemic stroke is dis-
airway as well as sometimes to acutely lower ICP. The cussed briefly.
decision to intubate should be based on the individual’s Meningitis and encephalitis are presented in infection
level of consciousness, ability to protect the airway and inflammation with Guillain–Barré syndrome, myas-
and arterial blood gas levels, rather than on an arbitr- thenic crisis in neuromuscular alterations. The selected
ary GCS score. neurological cases include caring for a potential organ
donor patient, status epilepticus and intracerebral haem-
Specific blood pressure management orrhage. A traumatic brain injury case is presented with
clinical questions.
There is a high risk of deterioration, death or dep-
endency with raised blood pressure after ICH; thus it The research vignette is an Australian and NZ TBI epi-
and should be corrected immediately to minimise the demiological study that defines the burden of TBI
potential for haematoma expansion and to maintain and compares clinical practice with the published TBI
adequate cerebral perfusion pressure. 132 Extreme hyper- Guidelines. ICP monitoring practice was deficient in
tension within the first six hours is common and comparison to the guidelines at the time of the study,
should be aggressively but carefully treated to avoid but a later study reported an improvement in this
excessive reduction of the cerebral perfusion pressure, practice.

Neurological Alterations and Management 473



Case study
Sam, a 21-year-old male driver was involved in a high-speed motor haemothorax, fractures 1st to 10th right ribs, transverse spinal T7
vehicle accident on the outskirts of a regional town; car versus a to T10 and L 1 to L5. The CT of the abdomen showed extensive
telegraph pole at high speed with two other people. Sam was subcutaneous gas extending from the lumbar spine into the peri-
partially ejected but his head was trapped between the steering toneal cavity and was in communication with the caecum.
wheel and the seat. When the ambulance officers arrived on Following the X-rays, Sam returned to the OT for further explora-
the scene, he was unconscious (GCS 3) and pupils non-reactive. tion of abdomen and insertion of ICP monitor. Intraoperatively he
His breathing was obstructed with stridorous respirations and remained hypotensive despite intravenous titration of triple
decreased air entry to the right lung. He was bleeding profusely therapy inotropes. On return to the ICU, Sam’s ICP was 10. Blood
from his nose, mouth and open head lacerations. Ambulance staff pressure remained labile and cerebral perfusion pressure fluctu-
cleared his airway, fitted a C spine collar, administered oxygen, ated between 50 and 70. Sam had to be paralysed as he began
obtained IV access and transported him to hospital within thirty shivering from attempts to reduce his temperature (39°C) with a
minutes. Of the two other occupants one was deceased and the related rise in his ICP to 25 mmHg. His GCS remained at 3 through-
other had life-threatening injuries that required transportation to out, sedated with midazolam and fentanyl. 3% saline boluses were
hospital.
initiated to reduce elevated ICP (25) in an attempt to improve his
On arrival in the Emergency Department (ED) at 0130h, Sam had a CCP to >60 mmHg.
GCS 5 (Eyes opening 1, Verbal response 1, Movement 3), pupils Days 2 and 3
were midpoint and sluggish (size 2). Rapid sequence induction For the next two days, Sam remained paralysed and sedated. His
intubation was performed due to an obstructing airway. Initial GCS remained at 3. His ICP ranged from 8 to 15. Interventions were
observations were: HR 130, BP 130/60, SpO 2 100% on FiO 2 1.0. Prior- related to a rise in ICP up to 30, but returned to baseline shortly
ity was given to the other injured occupant to go to X-ray for afterwards. CCP was maintained at 60–65 with noradrenaline and
trauma series of N-rays first. The X-ray department at this regional vasopressin. Pupils reacted sequentially to light size 2.
hospital had one CT scanner and was staffed with only one techni-
cian after midnight. Sam continued to be tachycardic (130) and remained febrile (38.8)
despite aggressive attempts to lower his temperature. A DIC
Within the second hour of being in ED, Sam became haemody- picture was developing evident by the drop in platelets and
namically unstable. His HR increased to 150, SBP dropped to 70 and increase in INR. The paralysing medication prescription was ceased.
Hb dropped from 150 to 108 g/L. The second FAST scan revealed GCS remained at 3 (E1, V1(ETT), M1) with IV infusions of fentanyl
fluid in the left internal flank region adjacent to penetration injury and midazolam. Noradrenaline and vasopressin infusion were
to L groin. The decision was made to forgo further trauma series weaned off over the day.
of X-rays and transport Sam to the operating theatre for an emer- Day 4
gency laparotomy. In OT Sam remained unstable. He was tachy- Sam’s sedation was ceased to facilitate a neurological assessment.
cardic with HR 130–150, blood pressure maintained with packed He achieved a GCS of 5 (E1, V1 (ETT), M3). ICP fluctuated between
red cell transfusion (10 units), fresh frozen plasma (4 units), plate- 9 and17 with CPP maintained at 60–65. A repeat CT showed new
lets (1 unit) (only one unit of platelets available at this regional small parafalcine subdural, left temporal bone fracture, diffuse con-
hospital; if more was required it needed to be ordered from inter- tusions in frontal and occipital regions with extensive oedema. He
state) and colloids. Oxygenation was maintained but EtCO 2 ranged was re-sedated with fentanyl and propofol infusions.
from 50–70.
Weeks 1–3
The operating theatre had one team on at this hour of night, and Daily neurological assessment occurred with gradual reductions in
due to the complexity and instability of patient, the EtCO 2 was sedation requirements. Sam began to open his eyes spontaneously
not able to be managed aggressively with resources available at but was increasingly agitated and restless. ICP monitoring was
the time. Surgical repairs were made to perforations in caecum, removed on day 6 and seizure activity was suspected. Phenytoin
colon and liver and the groin wound was explored, cleaned and was prescribed and commenced.
sutured.
Sam had a tracheotomy performed to facilitate weaning from
Vital signs on arrival in ICU mechanical ventilation. The weaning process was delayed due to
Temperature 37.8°C, HR = 155, BP = 90/40 MAP 61, EtCo 2 50, Pupils a further eight visits to OT for removal of necrotic tissue and
size 2 and reacting. Sam remained ventilated (SIMV VC 18 × 450, PS abdominal washouts related to intra-abdominal and right flank
10, PEEP 10, FiO 2 0.95) and sedated with an IV infusion of fentanyl injuries.
and midazolam. Spinal precautions were maintained with hard
collar and neck in neutral position. Noradrenaline, adrenaline and Eventually Sam was discharged to a surgical ward with impending
vasopressin were commenced to support his MAP which remained transfer to a rehabilitation facility interstate. GCS was at 13 (E4,
labile (range 49 to 60 mmHg). V1 4, M 5) at the time of discharge to ward.
Five hours after admission to ICU, Sam was taken to the CT On discharge (16 weeks later)
department to have the full trauma series of X-rays completed. Sam was decannulated and his GCS was 14 (E4, V1 5, M 5). He was
The brain CT showed diffuse oedema and foci of haemorrhage transferred to a rehabilitation facility interstate to continue his
related to the splenium or posterior portion of the corpus callosum rehabilitation. Rehabilitation service at the regional hospital was
and right frontoparietal cortex. Sam’s other injuries included: R not equipped to deliver the amount of rehabilitation services that

474 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



Case study, Continued
Sam required. Sam’s mother relocated with Sam to support him a car, due to his cognitive impairment. His speech and language is
through his rehabilitation. impaired and requires both visual and auditory formats for him
to make judgements on more complex information formats. He
One year later appears to have acquired dyslexia. Sam has reduced higher level
Upon leaving hospital, Sam was discharged home into the care of physical coordination required for dynamic tasks but this should
his mother who is now his principal carer. He remains interstate continue to improve with therapy. Sam is confident that he can
with his mother to continue on as an outpatient at the Brain Injury overcome his disabilities and has commenced studying through
Rehabilitation Community and Home Centre. Sam is a young man TAFE. He will only be able to do this with maximum support from
and prior to his accident was studying. He is no longer able to drive his immediate and extended family.








Research vignette

Myburgh, John A. PhD, FJFICM; Cooper, D James MD, FJFICM; strategies and interventions to minimise secondary brain injuries
Finfer, Simon R. FJFICM; Venkatesh, Balasubramanian MD, FJFICM; in the prehospital period.
Jones, Daryl MBBS; Higgins, Alisa MPH; Bishop, Nicole MSc; Higlett,
Tracey MPH; the Australasian Traumatic Brain Injury Study (ATBIS) Critique
Investigators for the Australian; New Zealand Intensive Care This is a remarkable study in terms of the Australian and New
Society Clinical Trials Group. Epidemiology and 12-month out- Zealand intensive care unit multicentre collaborative effort that
comes from traumatic brain injury in Australia and New Zealand. was largely unfunded and achieved prospective epidemiological
Journal of Trauma-Injury Infection & Critical Care 2008; 64(4): research that benchmarked a detailed profile of prevalence, injury
854–62. patterns, management strategies and outcomes of patients with
brain injuries admitted to intensive care units (ICUs) in Australia
Abstract and New Zealand. Sixteen units participated in this study, repre-
Background senting 76% (16 of 21) of eligible trauma centres in both countries
An epidemiologic profile of traumatic brain injury (TBI) in Australia at the time of the study. It included not only prospective admission
and New Zealand was obtained following the publication of inter- and ICU management daily data but also prehospital and pre ICU
national evidence-based guidelines.
data. Also there was extensive follow-up at 6 and 12 months using
Methods: Adult patients with TBI admitted to the intensive care the Glasgow Outcome Score to assess not only mortality but mor-
units (ICU) of major trauma centres were studied in a 6-month bidity in terms of outcome. The findings of this study represented
prospective inception cohort study. Data including mechanisms of those of a well-resourced society that possessed an integrated
injury, prehospital interventions, secondary insults, operative and national health care system, sophisticated prehospital and emer-
intensive care management, and outcome assessments 12-months gency systems, and highly developed, standardised training and
postinjury were collected. certification of the relevant health professionals. The study results
should also be interpreted in the context of a high degree of public
Results: There were 635 patients recruited from 16 centres. The health awareness about vehicular trauma, increased legislation
mean (±SD) age was 41.6 years ± 19.6 years; 74.2% were men; regarding violations for speeding, restraining devices, helmets and
61.4% were due to vehicular trauma, 24.9% were falls in elderly drink-driving, improvements in roads, technological advances in
patients, and 57.2% had severe TBI (Glasgow Coma Scale score ≤8). motor vehicle design, and low levels of interpersonal violence and
Secondary brain insults were recorded in 28.5% and 34.8% under- firearm ownership.
went neurosurgical procedures before ICU admission. There was
concordance with TBI and ICU practice guidelines, although intra- Interestingly, this study did not suggest a substantial improve-
cranial pressure monitoring was used in 44.5% patients with severe ment in outcomes following dissemination of evidence-based
TBI. Twelve-month mortality was 26.9% in all patients and 35.1% guidelines for the management of TBI in comparison to historical
in patients with severe TBI. Favourable outcomes at 12 months controls in America, Europe and Australia, despite during the ICU
were recorded in 58.8% of all patients and in 48.5% of patients with admission, there was concordance with evidence-based guide-
severe TBI. lines concerning systemic monitoring and supportive measures
such as nutrition, thromboprophylaxis and gastric ulcer prophy-
Conclusions: In Australia and New Zealand, mortality and favour- laxis. Similarly, there were consistent practices in the participat-
able neurologic outcomes after TBI were similar to published data ing ICUs concordant with management guidelines for TBI. This
before the advent of evidence-based guidelines. A high incidence was typified by the low incidence of the use of ‘brain-specific
of prehospital secondary brain insults and an ageing population therapies’ such as osmotherapy, barbiturates, hypothermia,
may have contributed to these outcomes. Strategies to improve hyperventilation and corticosteroids. However ICP monitoring
outcomes from TBI should be directed at preventive public health was employed in less than half of patients admitted with severe

Neurological Alterations and Management 475



Research vignette, Continued
TBI, for which intraparenchymal pressure tipped catheters were In terms of study design and methodological implications, there
most commonly used. It should be noted that since then were limitations relating to the missing elements in the data set.
improvement has been noted in an Australasian study with the However, this resulted in minor quantitative, rather than major
72
SAFE study in patients with TBI demonstrating higher ICP qualitative changes to the findings. Similar degrees of missing data
monitoring rates more in line with the TBI guidelines, using ven- were reported in the European historical controls study, which
tricular catheters (~75%) and conversely lower mortality (24.56%) emphasises the difficulties inherent in assessing the epidemiology
overall and (29.24%) in severe TBI. of TBI.





Learning activities

1. What clinical signs are indicative of a fractured base of skull? ● What are the clinical signs of coma?
Are the injuries noted on CT focal or diffuse? ● Where does the source of coma localise in the brain?
2. Reading the Case Study, interpret Sam’s vital signs in relation ● Which complications of TBI might lead to coma?
to cerebral perfusion. Are management changes required? ● What are the key treatment options to prevent cerebral
3. Ischaemia prevention requires a PbtO 2 >20. How can this be ischaemia?
achieved? 7. A child is taken to the emergency room with lethargy, fever and
4. What is the pathophysiological basis for the rise in ICP? How a stiff neck on examination.
would this manifest on the ICP waveform? ● What findings on initial lumbar puncture indicate bacterial
5. A 20-year-old man suffered spinal cord injury at the C2–C3 versus viral meningitis?
level as the result of a motorcycle accident. Explain the ● In the case of bacterial meningitis, what are the most likely
effects of this man’s injury on ventilation and communica- organisms?
tion; sensorimotor function; autonomic nervous system func- 8. Your patient had symptoms of an ischaemic stroke approxi-
tion; bowel, bladder and sexual function; and temperature mately 2 hours ago and is undergoing a confirmatory CT scan
regulation. in 30 minutes. You know tPA must be administered within 3
6. A 25-year-old-man is an unbelted driver involved in a motor hours of the symptoms. What actions would you take? What is
vehicle accident and presents in a coma. your rationale for these actions?





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