Management of Elevated Intracranial Pressure by zjm11893

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									The management of raised intracranial pressure
Complications of thiopentone therapy

Case

A 17 year old man was admitted under the neurosurgeons following a road traffic
accident, during which the vehicle he was driving struck a tree at high speed. His
GCS on scene had 8/15 (E2, M4, V2), and on arrival in the accident and emergency
department this had fallen to 6/15 (E1, M3, V2). His trachea was intubated following
a rapid sequence induction of anaesthesia using alfentanil 1mg, propofol 100mg and
suxamethonium 100mg, with full manual in line stabilisation of the neck. Anaesthesia
was maintained using a propofol infusion, with vecuronium administered as required
to maintain meuromuscular relaxation.
Secondary survey revealed a fractured right femur, fractured right radius and ulna,
and a CT scan of his abdomen revealed a burst fracture of L1. A CT scan of his head
showed loss of grey white differentiation consistent with diffuse axonal injury.
He was taken to theatre that night for the insertion of an external ventricular drain,
and subsequent femoral nailing and open reduction and external fixation of his right
radius and ulna. Fixation of his lumbar spine did not take place at this time.


Relevant management
He was transferred to the intensive care unit, where control of his intracranial pressure
(ICP) rapidly became a problem. He was treated as per our unit protocol. This
involves, sequentially, careful control of ventilation and CO2, hypertonic saline,
frusemide, cooling to 35°C and neuromuscular paralysis as required to control
shivering, and finally a thiopentone infusion. This was commenced on day three
(following a repeat CT scan to exclude surgical pathology), with
electroencephalographic monitoring to ensure burst suppression. An infusion of
noradrenaline was commenced to maintain his cerebral perfusion pressure >70mmHg.
His intracranial pressure was rapidly controlled on commencing thiopentone,
obviating the need to perform a decompressive craniotomy.
He required the thiopentone infusion for ten days, during which time 3 attempts were
made to transfer him to theatre for stabilisation of his lumbar spine. Each attempt was
aborted, twice because his intracranial pressure became elevated to approximately
35mmHg on transfer onto the transport ventilator, and once because his intracranial
pressure became uncontrollably elevated after he was turned prone on the operating
table. This demonstrated the brittleness of his condition, as only minor elevations in
his arterial PaCO2 lead to large rises in ICP.
On day seven his gas exchange deteriorated. This was associated with the presence of
purulent sputum, an increase in his white cell count and a difficulty maintaining
hypothermia. A diagnosis of ventilator associated pneumonia was made, and he was
treated with high dose intravenous cephalosporins.
At ten days his thiopentone was successfully weaned, and he underwent definitive
fixation of his lumbar spine, along with percutaneous tracheostomy (in view of poor
predictors for weaning). However, on day 17 his neurological state rapidly improved,
along with his oxygenation. By day 24 he was alert and orientated, with only minimal
objective impairment of mental fuction. He was discharged to the ward, where he
continued to make good progress, and subsequently had his tracheostomy
decannulated and was discharged home with minimal impairment of his short term
memory being the sole neurological sequela at that time.


Further information
Complications of thiopentone therapy

In our neurosurgical unit, thiopentone is used on approximately twenty patients a year
for post traumatic head injury, with raised intracranial pressure refractory to other
standard therapy. Barbiturates reduce intracranial pressure by both acting directly as a
cerebral vasoconstrictor, and by decreasing the metabolic demands of the brain. There
is also some theoretical benefit resulting from their actions as free radical scavengers,
although this is unlikely to influence intracranial pressure directly.
Thiopentone’s use remains controversial. Randomised studies have demonstrated
wildly differing results – from a doubling in mortality, to a fourfold reduction in
mortality. Certain subgroups of patients seem to benefit most i.e. those with increased
cerebral blood flow, and those with cerebral hypervasoreactivity. However, these
measurements are difficult to perform in most units, and pervading opinion in most
units is that the benefits outweigh the risks in traumatic brain injury patients with
cerebral hypertension not controllable by other measures.
The risks, however, are not insignificant, and I shall summarise them here. This data
is from a sequential study of 38 patients in Lund, Sweden in 19921.

   a. Hypotension. This is almost ubiquitous on induction. A fall in cerebral
      perfusion pressure (CPP) occurred in half the patients, and in 58%
      vasopressors had to be commenced to maintain CPP. Patients commenced on
      vasopressors were twice as likely to die as those who self maintained their
      CPP.
   b. Electrolyte disturbances. Hypokalaemia occurred in 82%, and was profound
      (<3 mmol/l) in 60%. In my experience, this is much less likely today, given
      the ease and rapidity of serial electrolyte measurements using ward based
      analysis.
   c. Infections. 20 of the 38 patients developed pyrexia greater than 39ºC, however
      therapeutic hypothermia was not undertaken in this unit. 37 patients were
      commenced on cefuroxime, however this was prophylactic in many cases.
      Lower respiratory tract infections were diagnosed in 20 patients, on the basis
      of two of i. positive cultures from protected tracheal aspirates, ii. pyrexia and
      iii. chest x ray changes. Staphylococcus aureus was the most frequently
      implicated organism, infecting 13 patients. Barbiturates are known to suppress
      lymphocyte activation, and also lung mucociliary clearance.
   d. Hepatic dysfunction. This was common (87%), but was of doubtful
      significance in most. However, 3 patients developed acalculous cholecystitis,
      2 requiring surgery.
   e. Renal dysfunction. This occurred in half, but it is unsure whether this was
      related to the thiopentone.

As this group of patients are already at a high risk of developing pneumonia, the
added effect of thiopentone is significant. The incidence of acalculous cholecystitis is
interesting, and this needs to be carefully watched for, especially given the difficulties
in diagnosis that exist in a deeply obtunded patient.

How would I change my future management?
Thiopentone is certainly an effective method of controlling elevated intracranial
pressure, and improves outcome in certain cases. Our patient, whilst initially
appearing to be a futile case, had a very good neurological outcome. This is almost
certainly largely due to his age, but the thiopentone may well have played a
significant part in minimising his brain injury. However, this treatment does not occur
without risk, and I will very aware of all the potential complications in future.

References

   1. Schalen W, Messeter K, Nordstrőm C-H. Complications and side effects
      during thiopentone therapy in patients with severe head injuries. Acta
      Anaesthesiol Scand 1992;36:369-77
   2. Eisenberg HM, Frankowski RF, Contant CH et al. High dose barbiturate
      control of elevated intracranial pressure in patients with severe head injury. J
      Neurosurg 1988;69:15-23
   3. Miller JD. Head injury and brain ischaemia – implications for therapy. Br J
      Anaesth 1985;57:120-9
   4. Ward JD, Becker DP, Miller JD et al. Failure of prophylactic barbiturate coma
      in the treatment of severe head injury.J Neursurg 1985;62:383-8

								
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