BLUK017-Tjandra September 12, 2005 21:43
Textbook of Surgery
Edited by Joe J. Tjandra, Gordon J.A. Clunie, Andrew H. Kaye & Julian A. Smith
79 Post-traumatic confusion
John David Laidlaw
Introduction
Although confusion is particularly common after sig-
nificant head injuries, it is also not an uncommon oc-
currence after other types of trauma. It affects patients
of any age, very young and elderly patients being par-
ticularly prone. The clinical finding of post-traumatic
confusion should not be considered a diagnosis in itself,
and requires appropriate clinical assessment and inves-
tigation to diagnose the causative pathology before the
institution of a management regime appropriate to that
particular pathology.
Aetiology and pathogenesis
Relatively minor head trauma is not infrequently over-
looked in cases where there are significant other in-
juries. Although minor head injuries in themselves do
not typically cause significant confusion, the effects
of secondary brain injury in the post-traumatic pe-
riod can rapidly develop into a relatively dangerous
condition which often has confusion as its present-
ing symptom. Therefore, any post-traumatic confu-
sion warrants specific clinical assessment and investi-
gation to rule out potentially dangerous intracranial
pathology.
However, it must be stressed that the exclusion of sig-
nificant intracranial pathology is, in itself, insufficient
investigation in a patient with post-traumatic confu-
sion. Respiratory problems, metabolic derangements,
infections and drugs can all be significant and poten-
tially dangerous causes of post-traumatic confusion,
and must be recognized and appropriately managed
(Box 79.1).
© 2006 by Blackwell Publishing Ltd
Management of patient with post-traumatic
confusion
Clinical assessment
All patients with post-traumatic confusion require a
full physical examination, including full neurological
examination. Any suggestion of a reduction in con-
scious state of 2 or more GCS points (Table 79.1),
any focal neurological deficit, or any symptoms of
meningism indicate a potential intracranial emergency.
Particular attention must also be given to examination
of respiratory system and for clinical evidence of sepsis.
Investigation
Investigation is dictated by the clinical history and
examination findings. However, most cases of post-
traumatic confusion require the following (Box 79.2):
r CT scan brain (urgent if GCS drop >2, or focal neu-
rological signs)
r Arterial blood gas analysis (Pao2 , Paco2 , Bicarbon-
ate, pH, base excess). Note that any patient with con-
fusion must be suspected of having disturbances in
respiratory function, and this must be excluded with
arterial blood gas analysis. Skin oxygen saturation
monitoring (pulse-oximetry) is a useful adjunct to
monitor trends in patients with known ventilatory
parameters, but is not an alternative to initial ABG
analysis.
r Full blood examination (haemoglobin, RCC, WCC,
platelets)
r Urea and electrolytes
r Calcium/phosphate
r Consideration of septic work-up (if indicated clin-
ically, and which may include wound swabs, blood
cultures, urine analysis and culture, chest X-ray, lum-
bar puncture for CSF analysis).
671
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672 Problem Solving

Box 79.1 Causes of post-traumatic confusion

Head injury
Subdural empyema

• Primary brain injury
Intracerebral abscess
◦ Diffuse axonal injury
Septic venous sinus thrombosis
◦ Cerebral contusions
General/Metabolic
• Secondary brain injury
◦ Hypoxia
◦ Hypoxia
◦ Hypercapnia

Hypoxaemia due to respiratory causes
◦ Acid–base problems (particularly acidosis)
• Aspiration
Metabolic
• Pulmonary contusions
• Renal failure
• Pulmonary oedema
• Lactic acidosis
• Pulmonary thromboembolism
• Diabetic ketoacidosis
• Pulmonary fat embolism
Respiratory

Hypoxaemia due to anaemia
◦ Electrolyte imbalance
◦ Cerebral ischaemia

Sodium

Shock

Vascular injury (particularly arterial dissection)

• Hyponatraemia

Thromboembolism
• Hypernatraemia (unusual to cause confusion)

Calcium
• Thromboembolic
• Hypocalcaemia
• Cerebral fat emboli
◦ Glucose
• Disseminated intravascular coagulation
Diabetic hyperglycaemia/ketoacidosis

Raised ICP (CPP = MAP – ICP)

Hypoglycaemia (usually seen in treated diabetics)
• Intracranial haemaotoma
◦ Infection
◦ EDH

Septicaemia
◦ Acute SDH
• Primary (iatrogenic, i.v. lines, etc)
◦ Intracerebral haematoma and enlarging
• Secondary (to other infection)
contusions
Pulmonary
◦ Chronic SDH

Urinary
• Hydrocephalus
Wound
◦ Obstructive
◦ Nutritional
◦ Communicating

Vitamin B
12 deficiency
• Brain swelling
◦ Vascular Drug intoxication/withdrawal

Vasodilatation ◦ Medication
• Post-traumatic (usually children)
Sedatives and tranquilizers

• Hypercapnia
Analgesics (particularly narcotics)

Venous engorgement
Steroids (although not usually indicated

• Jugular compression or obstruction in trauma)

• Sinus thrombosis or obstruction
Anticonvulsants

◦ Oedema
Hypoglycaemic agents

Vasogenic ◦ Non-medicinal

Cytotoxic
Alcohol

Hyponatraemia
Narcotic

◦ Infection
Hallucinogens

Meningitis
Cocaine

Epidural abscess
Solvents

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79: Post-traumatic confusion 673

Table 79.1 Glasgow coma score

Best eye
Score opening (E) Best verbal (V) Best motor (M)

6 Obeys
5 Orientated Localizes pain
4 Spontaneous Confused Withdraws to pain
3 To speech Inappropriate words Abnormal flexion to pain (‘decorticate’)
2 To pain Incomprehensible sounds Extension to pain (‘decerebrate’)
1 None None None

Notes on GCS:
• GCS = E + V + M.
• Worst score is 3, best is 15.
• Use best response if differences between sides for eye opening or motor function.
• GCS measures only conscious state, not neurological deficit.

Box 79.2 Management of post-traumatic confusion

Clinical assessment • Analgesia if required

• Physical examination ◦ If narcotic, only small frequent i.v. doses (e.g.
◦ Airway, breathing, circulation immediately, then 1–2 mg morphine p.r.n.) titrated carefully, with
general examination the patient closely supervised (not intramuscular
• Neurological examination or subcutaneous)
◦ Particularly note GCS, papillary inequality ◦ Recognition of legal incompetency
or other focal neurological deficit, and ◦ Relevancy to consent and refusal of treatment
meningism
Specific management of the cause of confusion
Investigation • Intracranial Lesions
• CT scan brain (urgent if GCS drop >2, or focal ◦ Immediate neurosurgical opinion for all
neurological signs) ◦ Usually surgical decompression if mass effect,
• Arterial blood gas analysis (Pao2 , Paco2 , and relatively urgent if a patient is developing
bicarbonate, pH, base excess). lateralising signs or deteriorating GCS
• Full blood examination (haemoglobin, RCC, WCC, • Hypoxia and respiratory disturbance
platelets) ◦ Oxygen supplementation
• Urea and electrolytes ◦ Immediate intubation if
• Calcium/Phosphate
Airway not patent and protected (cough and gag)

• Septic work-up (wound swabs, blood cultures,
Respiratory failure

urine analysis and culture, chest X-ray, ± CSF
Note spinal precautions for all intubations, but

analysis) do not delay for spinal investigation

• Electrolyte disturbance
General management of confused patient
◦ Appropriate fluid and electrolyte therapy
• Environmental
• Infection
◦ Close monitoring and supervision
◦ Appropriate antibiotic therapy instituted
◦ Protection
immediately after cultures, and modified when
◦ Quiet environment if possible
culture and sensitivities known
• Sedation avoided if at all possible
• Medications and non-medicinal drugs
◦ If absolutely required, best to use only short-acting
◦ Medications scrutinised
parenteral (i.v.) sedatives in small doses titrated to
◦ Drug and alcohol history determined
effect, closely supervised
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674 Problem Solving
General management of confused patient
Environmental
Confused patients are generally best managed in a quiet
environment, but need to be closely monitored by ex-
perienced nursing and medical staff. Agitated patients
need to be protected from falls, etc., and bedsides are
therefore essential. Padding to the bedsides, or even
nursing on the floor on a thick mattress may provide
more protection. On occasions physical restraints may
be needed to protect the patient; however these must be
checked regularly to ensure they do not cause pressure
or pain or subject the patient to a risk for entanglement.
It is essential that restraints are not used as a means to
avoid close supervision; all confused patients need such
supervision and those requiring restraint should be su-
pervised even more diligently.
Familiar faces, such as family or close friends, may
help relax a confused patient, although visitors and un-
familiar contacts should be kept to a minimum. Busy
wards and noisy areas will often cause a confused pa-
tient to become quite agitated and are best avoided if
possible.
Sedation
Sedation is best avoided in confused patients if at all
possible. The aim is to identify and treat the cause of the
confusion rather than sedate the patient. Sedation may
rarely be needed in an agitated patient where there is the
risk of self-harm or injury. However, very often close su-
pervision in a calm environment will allow sedation to
be avoided. Sedation should only be used if significant
intracranial and metabolic (particularly hypoxic) prob-
lems have been excluded. Sedation should never be used
simply to facilitate easier nursing care. On the few occa-
sions where sedation is needed it is most appropriate to
use only short-acting parenteral (i.v.) sedatives in small
doses titrated to effect. The clinician must constantly
be aware of the potential for wrongly attributing
decreased conscious state to sedative use, and missing
a worsening and dangerous intracranial pathology or
metabolic event.
Analgesia
Many patients with post-traumatic confusion have sig-
nificant pain from other injuries. The pain often causes
severe agitation, and the patient can be much better
managed if appropriate analgesia is used. Narcotics
have the side effects of altering conscious state, causing
pupillary constriction and depressing ventilation, all of
which are potentially catastrophic in a patient with a
significant intracranial pathology. They have therefore
historically been shunned by neurosurgeons. However,
most modern neurosurgeons and traumatologists rec-
ognize the effective analgesic properties and the short
and predictable action of narcotics when used by the
i.v. route, and are prepared to use them cautiously. It
must be stressed that only small, frequent i.v. doses
(e.g. 1–2 mg morphine p.r.n.) should be used and these
must be titrated carefully, with the patient closely super-
vised. Intramuscular doses have a more unpredictable
and delayed action and should be avoided. The his-
torical anachronism of using codeine instead of nar-
cotics should be discarded; codeine is a narcotic with
the same side effects as other narcotics when used in
the same analgesic dose, but has the disadvantage of
not being available in i.v. preparation. A note should
be made that tramadol, which has recently been used
increasingly in the management of severe pain, does
increase the risk of seizures, and therefore is probably
best avoided following head injury.
Legal competency
A confused patient is not competent to make appro-
priate important decisions. This of course includes giv-
ing consent for surgical procedures, and most coun-
tries have legal avenues which allow the clinician to
undertake emergency medical procedures without con-
sent. It must also be understood that a confused patient
cannot competently discharge himself or herself from
hospital against medical advice. The clinician must un-
derstand that the refusal of a confused patient to follow
the clinician’s advice is not done from a position of le-
gal competency, and therefore the clinician maintains
significant responsibility for consequences of these ac-
tions. On occasions, formal declaration of incompe-
tency is required to allow appropriate care or restraint.
However, in most cases even very confused patients can
be quietly reasoned with and will follow gentle calm
advice, particularly if people familiar to them are in-
volved.
Specific management of the cause of confusion
The primary rule in management of a confused patient
is to correct the primary cause of the confusion.
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Intracranial lesions
Any intracranial mass lesion (haematoma, hydro-
cephalus, brain swelling) identified on CT scan war-
rants an immediate neurosurgical opinion. Even pa-
tients managed in rural hospitals who are considered
to have a relatively small lesion deserve the potential
benefits of a telephone consultation between the man-
aging clinician and a neurosurgeon. Whether the le-
sion requires surgical treatment (craniotomy in the
case of an acute haematoma or burr-hole drainage of
chronic subdural haematomas or hydrocephalus) de-
pends primarily on the patient’s clinical condition and
the amount of mass effect of the lesion. Therefore, in
a telephone consultation the most important informa-
tion the neurosurgeon requires is the patient’s GCS
score, whether this has deteriorated and if so the rapid-
ity of change, any focal neurological signs (e.g. pupil-
lary inequality or unilateral change in motor function)
and the amount of midline shift and asymmetry on the
CT scan. Teleradiology can be a major benefit in these
cases. Most neurosurgeons would generally advise sur-
gical decompression of an accessible intracranial lesion,
which causes more than a millimeter or two of midline
shift, and would consider this to be relatively urgent if
a patient is developing lateralising signs or has a dete-
riorating conscious state.
Hypoxia and respiratory disturbance
Oxygen supplementation must be used on confused pa-
tients until blood gas analysis results are available. Al-
though relatively mild hypoxia or hypercarbia do not
usually in themselves cause confusion, following a head
injury they can seriously potentiate secondary brain
injury and most neurosurgeons would advise mainte-
nance of Pao2 of more than 100 mm Hg and Paco2
30–35 mm Hg. Hyperventilation is not usually recom-
mended now following head injury as it has the poten-
tial to exacerbate cerebral ischaemia.
In a confused patient with a deteriorating conscious
state it must be determined that not only is the airway
patent and the patient has appropriate blood gases, but
it needs to be ensured that the airway is protected by an
intact and strong gag and cough reflex. If there is any
doubt about the adequacy of airway patency or protec-
tion then endotracheal intubation becomes an immedi-
ate priority. If intubation is required in a trauma pa-
tient this must be done immediately, with the head and
neck held in a neutral position by an assistant (spinal
79: Post-traumatic confusion 675
precautions), and should not be delayed for cervical
radiology, brain scans or other investigations.
Electrolyte disturbance
Electrolyte disturbances, particularly sodium anoma-
lies, must be corrected with appropriate fluid and elec-
trolyte therapy. A point of caution is that the rapid
correction of long-standing hyponatraemia can cause
central pontine myelinosis, and in this case the aim
should be to correct slowly over 24–48 hours. More
rapid correction of acute hyponatraemia (e.g. that
caused by iatrogenic water intoxication) can be safely
performed. Similarly, acute hyponatraemia caused by
either SIADH or cerebral salt-wasting syndrome can be
safely done relatively quickly. It needs to be recognised
that while fluid restriction is appropriate for SIADH,
salt-wasting syndromes are associated with total body
water deficit. Expert endocrinology advice can be in-
valuable in these cases.
Infection
Infections, particularly pulmonary, urinary, wound or
i.v.-line associated, are the most common causes of
post-traumatic confusion after the first 24–48 hours.
These must be considered in all cases, and a septic
work-up performed. Meningitis must be suspected if
confusion is associated with decreasing conscious state
or meningism. In these cases lumbar puncture is manda-
tory. However, in a post-traumatic case an urgent cere-
bral CT is always advisable prior to lumbar puncture;
intracranial mass lesions can mimic meningitis and can
cause lumbar puncture to be a fatal procedure. If infec-
tion is clinically suspected, appropriate antibiotic ther-
apy should be instituted after cultures are collected,
and modified when culture and sensitivity results are
known.
Medications and non-medicinal drugs
All confused patients must have their current medica-
tions scrutinised, and drug and alcohol history deter-
mined. Narcotics and sedatives can in themselves cause
confusion, particularly in the elderly, and in these cases
their use needs to be reconsidered. Anticonvulsant tox-
icity can also cause an acute confusional state, and their
levels should be checked if appropriate. Similarly, with-
drawal of chronically ingested substances (sedatives,
alcohol, recreational drugs) can cause a potentially
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676 Problem Solving

dangerous acute confusional state. Usually, in these c hypoxia

cases it is not appropriate to reinstitute the drug, and d hypernatraemia
in those cases management is usually supportive with e venous engorgement
judicious sedative use.
2 Post-traumatic confusion may require the following
treatments except:
MCQs a i.v. sedatives
b i.v. codeine
Select the single correct answer to each question. c i.v. morphine
d physical restraint
1 Post-traumatic confusion commonly occurs due to the
e oxygen supplementation
following conditions except:
a cerebral contusion
b intracerebral haematoma