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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3050_Библиотеки_им_академика_М_И_Перельмана
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Intracranial pressure (mmHg)
120
100
80
Critical point
60
Compensation
20
0
Increasing size of space-occupying lesion (SOL)
240 Neurological observations (I)
Figure 11.19 The sudden rise in the intracranial pressure (RICP) occurs when the brain compensa-
tory mechanism fails. This critical point must be watched for very carefully.
i.e. life-threatening symptoms can occur within a few minutes, compared with the slower
subdural haematoma, which causes problems over several hours or even days. This indi-
cates two things:
1 The need for a scan or a 24-hour stay in hospital for head injuries to exclude the extra-
dural haematoma. If the subdural develops at home after that, there is time to get the
patient back to hospital.
2 The need for continuous observation since the patient may deteriorate rapidly and die
if vital symptoms of an extradural are missed.
The symptoms of RICP fall into two categories:
1 General symptoms: those that indicate the presence of RICP but give no clue to the
exact site of the pressure on the brain
2 Local (or focal) symptoms: those that indicate both the presence and the site of pres-
sure on the brain.
General symptoms are headache (which is worse on wakening), nausea, vomiting, altered
state of consciousness (see page 230, Figure 11.12), blurred vision, respiratory irregulari-
ties and papilloedema (see Chapter 13, page 283). Slow pulse rate (bradycardia) and raised
blood pressure may occur late as the patient deteriorates and should not be relied on.
Focal symptoms are:
• unilateral (one sided), ipsilateral (on the same side as the injury) xed dilated pupil
followed later by bilateral xed dilated pupils
• nystagmus (Chapter 13, Figure 13.13)
• visual eld defects (Chapter 13, p
• ts (page 233)
• aphasia (loss of speech)
age 271)
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Neurological observations (I) 241
• ataxia (unsteady walking)
• hemiparesis and/or hemiplegia (Chapter 14, page 300)
• specic sensory losses.
These symptoms will develop at different speeds depending on several factors. For extra-
dural and subdural haematomas, the factors include which blood vessel is bleeding, the
location of the bleed and the brain’s compensatory mechanism. These compensatory
mechanisms allow for a certain increase in the space occupying lesion (SOL), i.e. the
bleed, without undue change in the intracranial pressure (ICP).
As the SOL grows with further bleeding, the pressure it exerts is compensated at rst by
a reduction in the blood volume entering the skull and the CSF volume produced. These
account for 20% of the ICP (see page 239), and this percentage could drop to accommo-
date the growing SOL. This compensation only lasts for a while, after which the ICP will rise
sharply because the brain then comes under pressure (Figure 11.19). This is the critical point,
i.e. the change from compensation to decompensation, where the resultant RICP may prove
fatal if it is not noticed urgently. Increasing RICP will displace the brain, forcing it downwards
and/or sideways, referred to as herniation of the brain structures, with associated tearing of
membranes and crushing of nerves. As the brainstem is forced downwards, it impacts on
the foramen magnum, the large opening in the base of the skull through which the spinal
cord emerges. This impaction blocks the ow of CSF through the opening and puts pressure
on the vital centres of the brainstem: the cardiac and vasomotor centres (Chapter 3) and the
respiratory centre (Chapter 5). This is a life-threatening situation, called coning, and it is far
better avoided by accurate observation. The treatment for RICP is generally a surgical open-
ing made into the skull, called a burr hole, to let the haematoma out. This vital procedure,
combined with accurate neurological observation, can save the patient’s life. ICP is regularly
monitored in those patients who are at risk of RICP. This can be done by placing a probe
within the skull connected to an external monitor (Chitnavis and Polkey 1998).
Head injuries may also result in a fractured skull. The symptoms of this may be obvious
very soon after the accident, and they may get worse quickly. These symptoms include:
• an open wound on the scalp with varying degrees of blood loss. It may be the site of a
fracture below the wound
• bleeding into the eye socket (the orbit), i.e. a periorbital haematoma, which may be
either unilateral or bilateral, causing the soft tissue in and around the socket to swell
and making the lids difcult to open. The area around the eye becomes blackened
• blood or clear uid (cerebrospinal uid, CSF) coming from one or both ears
• bruising behind the ear
• clear uid (CSF) coming from the nose
• post traumatic deafness.
Any suspect skull fracture requires urgent removal to hospital (Table 11.5).
Other causes of loss of consciousness
There are many other causes of unconsciousness. Here are a few important examples:
1 Lack of oxygen, either in the air or through strangulation, choking, drowning or airway
obstruction
2 Various poisons and toxins
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242 Neurological observations (I)
3 Central nervous system infections, such as meningitis (inammation of the meninges)
or encephalitis (inammation of the brain substance).
4 Intoxication by alcohol or drug abuse or drug overdose
5 Electric shock
6 Loss of blood pressure, temporarily as in fainting (also known as syncope) or more
profound as in severe shock
7 Metabolic disorders, such as diabetes (see Chapter 8), where both high and low blood
sugar levels induce coma in response to instability in the blood insulin level.
Fainting is possibly the most common cause of unconsciousness, the one most people
may suffer or encounter. The temporary drop in blood pressure causes a transient loss of
blood supply to the brain, which then causes the brain to go unconscious. It is usually
temporary because it tends to treat itself. The problem is caused by the brain being verti-
cally above the heart, which then has the job of pumping blood uphill, against gravity,
to the brain. This requires a good arterial blood pressure, and if the left ventricle fails to
deliver this blood, the brain suffers. It is normally self-treating because fainting causes
the person to collapse and this puts the brain horizontally in line with the heart, and the
pressure then required to supply blood to the brain is much reduced. In short, fainting
does away with gravity. Now the left ventricle can happily supply blood to the brain at the
new lower pressure, and the brain recovers. The fall can cause injury since the head (and
therefore the brain) has furthest to fall. The casualty must remain at until the ventricular
pressure is high enough to supply the brain once more in the upright position. If the per-
son faints while pinned in an upright position, i.e. unable to fall to the ground, such as
standing in a tightly packed train on a long, hot journey, the drop in blood pressure results
in the blood being unable to ow uphill to reach the brain. If the person is unable to fall
down, the brain is starved of blood for longer.
The anaesthetic drugs
Anaesthetic drugs may be local or general. Local anaesthetics cause loss of sensation,
including pain, at the site where they are administered. They do not affect conscious-
ness. General anaesthetics (Table 11.4) cause loss of consciousness and therefore loss of
awareness.
They can be given by inhalation or by intravenous routes. Some general anaesthetics
also provide a degree of pain relieve after consciousness has returned, i.e. they have an
analgesic effect (see Chapter 12).
Currently, it is not possible to say exactly how most of the general anaesthetic drugs
create unconsciousness. Lipid solubility is a common feature of these drugs and correlates
well with their anaesthetic properties, i.e. the more lipid-soluble, the greater their power
of anaesthesia. One theory suggests that they may get incorporated into cortical neurone
cell membranes, which are themselves lipid-based. Distortion of these membranes by
the drugs may disrupt ionic movement across the membrane and cause the neurone to
fail temporarily. However, growing evidence is now supporting the notion that general
anaesthetics block the passage of neuronal impulses necessary for conscious connectivity
(Figure 11.1, see page 220). They do this by targeting specic proteins in the cell body
membrane or at the pre- and postsynaptic membranes (Figure 11.10). These proteins then
fail to move or function properly and connectivity is lost. Different drugs appear to act
in different ways and may often need to be used in combination (Table 11.4). This makes
isolating the mechanism of function in any single drug difcult to achieve.
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Neurological observations (I) 243
Of concern are the post-operative problems that may be linked to anaesthetics, espe-
cially in the elderly. These include post-operative delirium (temporary disorientation,
hallucinations and memory losses) and post-operative cognitive dysfunction (POCD;
learning difculty, memory losses and short attention spans). While there is no direct
evidence that these are caused by the drugs, there is circumstantial evidence that the
anaesthetics may be involved (Anderson 2017).
Table 11.4 General anaesthetics
Drug Possible side effects Use and other notes
Etomidate Depresses breathing, nausea,
hypotension, skin reactions.
Propofol Depresses breathing, nausea,
hypotension, arrhythmias, headache.
Desurane Blood clots, conjunctivitis, abdominal
pain, malaise.
Isourane Skin reactions, dyspnoea, delirium,
mood changes.
Nitrous oxide Addiction, disorientation, dizziness,
euphoria, nausea.
Sevourane Drowsiness, fever, confusion, asthma
attack.
Thiopental sodium Arrhythmias, poor appetite, cough,
skins reactions.
Given by injection.
Given by injection.
Volatile liquid halogenated
inhalation vapour.
Volatile liquid halogenated
inhalation vapour.
Inhalation gas.
Volatile liquid halogenated
inhalation vapour.
Slow intravenous injection
Table 11.5 Red and amber ag warnings of deteriorating consciousness
O Red Flag = serious situation which needs urgent medical attention.
O Amber Flag = important to get a medical assessment as soon as possible.
Flag Details
warning
O Red Flag
Sudden drowsy, fainting, confusion or seizure for unknown reason.
Fainting in a xed upright position, i.e. unable to lay the patient at; get the
patient at urgently.
Fainting with symptoms or a known past history of diabetes or heart condition.
Symptoms of stroke: F.A.S.T. = sudden Facial or Arm weakness on one side;
rapid Speech impediment; Time for urgent medical care.
Symptoms associated with a head injury:
• loss of consciousness
• drowsiness
• confusion
• convulsion
• amnesia for longer than 5 minutes
• increasing or persistent headache
• vomiting
• unilateral or bilateral xed dilated pupils
• bleeding or clear uid from the ear
• periorbital bleeding
• history of anticoagulation medication, illicit drug or alcohol consumption.
O Amber Fainting that does not recover consciousness after 15 minutes.
Flag Fainting in patient with known hypotension (Chapter 3).
Signs of epilepsy.
(After Hill-Smith and Johnson 2021, with permission)
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244 Neurological observations (I)
Key points
The nature of consciousness
• The cerebral cortex, particularly the prefrontal cortex, is part of a network of connectiv-
ity in the brain to achieve alertness and maintain consciousness.
• Awareness of the environment and control of activities are qualities of consciousness.
• The cortex is made up of nerve cells called neurons.
• Neurons have a cell body with dendrites and an axon that is often myelinated.
• Grey matter is cell bodies packed together and white matter is axons packed
together.
• Neurons connect to each other through synapses. These tiny gaps require a neurotrans-
mitter, the most important of which for consciousness is glutamate.
• The left and right hemispheres of the cortex are further divided into lobes: the frontal,
parietal, temporal and occipital lobes.
• The motor cortex is in the frontal lobe and the sensory cortex is in the parietal lobe. The
cells are carefully arranged in a layout that matches the body plan.
• Sensations coming into the brain from the body must rst pass to the thalamus, a sen-
sory relay station that sends sensations on to the correct part of the cerebral cortex.
Unconsciousness assessment
• Consciousness can be considered as a spectrum, from fully conscious at one end
to coma at the other. The various points on this spectrum are the altered states of
consciousness.
• Painful stimuli are achieved by applying pressure to the ngernails and toenails, which
are dead tissue and therefore will not be damaged. The response to pain is motor, i.e.
limb movements.
• Purposeful responses are signs of trying to stop painful stimuli; non-purposeful
responses are limb movements without any attempt to stop painful stimuli.
• The Glasgow Coma Scale is the most widely adopted scale. This denes coma as
unable to open the eyes, unable to obey commands and unable to speak.
Epilepsy
• The cause of epilepsy can be a small area of damaged or disturbed brain tissue, the
epileptogenic focus.
• The grand mal t involves collapse, tonic rigidity, clonic convulsions and then full
recovery.
• Minor ts (petit mal or vacancies) are short periods of aimless staring with fumbling,
followed by complete recovery.
Strokes
• Strokes, or cerebrovascular accidents (CVAs), are sudden, unpredictable disruptions to
the blood supply to the brain, bleeding into the brain (intracerebral bleed) or sudden
arterial obstruction (cerebral thrombosis or embolus).
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Neurological observations (I) 245
Head injury
• Unconsciousness in head injury is caused by shaking of the brain (concussion), dam-
age or pressure on the brain (compression, e.g. raised intercranial pressure).
• Some protection to the brain is afforded by the meninges, the pia mater next to the
brain, the arachnoid mater and, beneath the skull, the dura mater and by the cerebro-
spinal uid or CSF.
• The development of unconsciousness with an extradural haematoma is rapid, e.g.
within minutes, compared with the slower subdural haematoma, which takes several
hours or days.
• The symptoms of raised intracranial pressure (RICP) are general, i.e. those that indicate
RICP is present but do not identify the site or focal, i.e. those that indicate both RICP
and the site of pressure. A slow pulse rate and raised blood pressure may occur late and
should not be relied on.
• Coning, i.e. death by the medulla impacting on the foramen magnum, is avoidable
with accurate observation.
• Symptoms of possible fractured skull fracture includes, unilateral or bilateral periorbi-
tal bleeding, blood or cerebrospinal uid coming from the ears or cerebral spinal uid
coming from the nose and post-traumatic deafness.
Fainting
• Fainting is a common cause of unconsciousness caused by a temporary drop in blood
pressure with loss of blood supply to the brain.
• It can be self-treating because collapse puts the brain level with the heart and the pres-
sure required to supply blood to the brain is much less.
• If a person faints while pinned in an upright position, i.e. unable to fall, it could be
fatal.
Notes
1 Constantin von Economo (1876–1931) was an Austrian neurologist and psychiatrist.
2 Reticular means it appears as a network of bres.
3 This ‘Nature rst’ concept also applies to many other things in biology, including the wheel!
4 Extra means outside of... . In this case its outside the dura mater between the dura and the skull.
This space does not normally exist and must be created by the bleed. The dura gets xed rmly
to the inside of the skull with increasing age.
References
Anderson A. (2017) The risk of going under. Scientic American, 28(2): 61–65.
Blows W.T. (2022) The Biological Basis of Mental Health (4th edition). Routledge, Abingdon.
Carlson N.R. and Birkett M.A. (2017) Physiology of Behavior (12th edition). Pearson Educational,
Harlow, Essex.
Chitnavis B.P. and Polkey C.E. (1998) Intracranial pressure monitoring. Care of the Critical Ill, 14(3):
80–84.
Fischer D.B., Boes A.D., Demertzi A., Evrard H.C., Laureys S., Edlow B.L., Liu H., Saper C.B.,
Pascual-Leone A., Fox M.D. and Geerling J.C. (2016) A human brain network derived from coma-
causing brainstem lesions. Neurology, 87(23): 2427–2434.
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246 Neurological observations (I)
Hickey J. (2013) The Clinical Practice of Neurological and Neurosurgical Nursing (7th edition). Lip-
pincott Williams & Wilkins, Philadelphia, PA.
Hill-Smith I. and Johnson G. (2021) Little Book of Red Flags. National Minor Illness Centre,
Bedfordshire.
Juarez V. and Lyons M. (1995) Interrater reliability of the Glasgow Coma Scale. Journal of Neurosci-
ence Nursing, 27(5): 283–286.
Koch C. (2015) Closing in on consciousness. New Scientist: The Collection, 2(1): 84–85.
Koch C. (2017) The footprints of consciousness. Scientic American Mind, 28(2): 53–59.
McCance K.L. and Huether S.E. (2014) Pathophysiology: The Biological Basis for Disease in Adults
and Children (8th edition). Elsevier, St. Louis, Missouri.
Williams C. (2015) The consciousness connection. New Scientist: The Collection, 2(1): 87–89.
Young E. (2021) Is consciousness detectable in the brain? In Consciousness expanded (part 8). New
Scientist, 10 July, 251(3342): 41–42.
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12 Neurological observations (II)
Pain
• Introduction
• Nature and causes of pain
• Pain pathways
• Observation of pain
• Genetic inuence over pain
• Pain in children
• Pain management
• Key points
• Notes
• References
Introduction
Observing pain is one of the most difcult assessments to make, but it is important to
get pain assessment as accurate as possible. One way of assessing a patient’s pain is to
ask them. But this type of assessment is not measurable, so there is no hard data upon
which pain treatment can be based. People have different pain thresholds, and staff could
interpret a patient’s pain while unconsciously adding their own pain perceptions. This
becomes evident when carers say things such as, ‘Come on, it can’t hurt that much!’ Pain
observations are an attempt to overcome these problems (
D’Costa 2011).
Nature and causes of pain
There are three physiological types of pain:
1 Nociception, caused by actual or potential tissue injury or irritation
2 Neuropathic pain caused by nerve damage (Meijler 2006)
3 Nociplastic pain caused by the brain’s pain centres becoming overactive (Lawton
2022). Every individual adds an emotional (or affective) component to their pain
which is derived from complex neuroanatomy. It amounts to a pain network in the
brain which is poorly understood.
DOI: 10.4324/9781003389118-12
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248 Neurological observations (II)
Nociceptive pain
Nociception is pain caused by everyday injuries or disease, (e.g stings, burns etc) and is
important for localising the site of the pain. There are several types of nociception:
• Acute pain has recently occurred and is of relatively short duration. It identies that
something is wrong and needs attention, and it can protect the individual against fur-
ther tissue injury, such as withdrawing quickly from burning.
• Chronic pain has a longer duration, lasting for more than 3 months (Wood 2002;
Osborne-Crowley 2022). Chronic pain changes some synaptic connections in the
brain in a manner that makes the brain’s pain centres more sensitive to future pain or
continues the pain long after any tissue damage is healed. This brain centred cause of
pain is known as central sensitisation. It can be referred to as intractable pain which
is chronic pain with no detectable reason causing it, and it may never have had any
physical cause. It can result from a combination of physical effects, emotional trauma
and memory of previous injury. It is very difcult to treat such pain when no cause can
be found (Osborne-Crowley 2022).
• Inammatory pain is caused by inammation which is caused by local trauma or irrita-
tion, e.g. infections, stings and mechanical or thermal injury (Figure 12.1). The immune
system could not function adequately without inammation. The increase in capillary
wall permeability that occurs in inammation causes more water to leak into the tissues
from blood plasma, along with proteins and white blood cells. Extra protein in the tissue
uid attracts more water from the capillaries. This causes a local oedema (see page 129).
Pain mediators, i.e. chemicals causing pain, are released at the site, notably histamine,
prostaglandins and bradykinins (Figure 12.2). These bind to receptor sites on nociceptors,
H
2
O
H
2
O
Thicker
wall
Thinner
wall
Protein
Protein
Protein
Nor
mal
Dilation
Blood vessel
Blood vessel
A
B
H
2
O
Immune cells
Local oedema
and antibodies
Figure 12.1 Inammation. (A) The non-inamed blood vessel is normal width and has a wall thick
enough to prevent inappropriate leakage of blood contents into the surrounding tissues.
(B) In inamed tissues, blood vessels are dilated and the walls are stretched and thinner,
and leakage of water, proteins, immune cells and antibodies can take place. Protein that
has escaped into the tissues attracts further water out of the blood, causing local tissue
oedema. This oedematous swelling puts pressure on nociceptors (pain receptors). Pain is
generated by this swelling and locally released pain mediators (Figure 12.2).
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Pain mediator
molecules
3
1
2
To Brain
Histamine
Mast cell
Infammation
Bradykinin
Kallikreins
(enzymes)
Kininogens
(plasma globulins)
Pain
Prostaglandins
Arachidonic
acid
Cell membrane
COX
phospholipids
Neurological observations (II) 249
Figure 12.2 P ain mediators. Histamine is released from mast cells (found in most tissues), bradykin-
ins are derived from the plasma globulins kininogens, and prostaglandins are formed
from arachidonic acid.
Figure 12.3 Pain mediator molecules bind to nociceptors (1, 2 and 3). Number 1 has bound a lot of
molecules and sends rapid impulses to the brain, and pain is experienced. Number 2
has fewer molecules and sends a slower rate of impulses, which the brain interprets as
irritation. Number 3 has no molecules and sends no impulses to the brain.
which are pain nerve endings. Two types of nociceptors occur: mechanoreceptors and
polymodal receptors. Mechanoreceptors are pain receptors that respond to mechanical
injury, while polymodal receptors caused pain from many types of tissue injury.
Conscious perception of pain requires certain criteria. First, sufcient chemical media-
tors must bind to the nociceptors to raise the level of stimulation to the pain threshold
point or beyond. Threshold means the amount of chemical stimulation necessary to gen-
erate strong enough impulses from the nociceptors that are recognised as pain by the
brain. With less chemical binding, i.e. below threshold level, weaker impulses can still be
generated from the nociceptor, and these are recognised by the brain as irritation. Itch-
ing is one form of irritation caused by mediators binding to nociceptors in concentrations
below that needed to activate the pain threshold level (Figure 12.3).
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