121 Anaesthesia For VP Shunt Insertion
121 Anaesthesia For VP Shunt Insertion
121 Anaesthesia For VP Shunt Insertion
SELF-ASSESSMENT QUESTIONS
Before reading the tutorial consider the following questions and discuss them with your
colleagues
INTRODUCTION
This article aims to look at anaesthetic techniques which can be employed for the
insertion of ventriculoperitoneal (VP) shunts. It will also address the basic principles of
neurophysiology which are required to treat patients with raised intracranial pressure.
Prior to shunting being introduced as a treatment for hydrocephalus in the 1940s, those
children affected had a poor prognosis. Only 20% of those who did not receive surgery
reached adulthood and 50% of the survivors were brain damaged. The development of
valved and then silicone shunt systems have dramatically improved the outlook for these
patients.
Cerebral blood flow (CBF) determines cerebral blood volume and is higher in children
compared to adults (100 vs 50 ml/100g/min). It is coupled to the metabolic demands of
the normal brain and regulated via oxygen requirement, PaCO2 and intracerebral acidosis.
Autoregulation allows for a relatively constant blood flow across a wide range of arterial
pressures which can be as low as 40 mmHg in small children. This mechanism is not
available to premature neonates or during some pathological processes (e.g. infection)
where the relationship between CBF and arterial pressure is more linear. Reducing
PaCO2 causes vasoconstriction of the cerebral vessels, reducing CBF and hence blood
volume and ICP but at the expense of oxygen delivery. Therefore hyperventilation should
only be used as a short-term measure when ICP is dangerously high, prior to more
definitive treatment.
Cerebrospinal fluid (CSF) is continuously produced by the choroid plexus, and after
circulating through the ventricles is absorbed at the arachnoid villi. In children the rate of
production of CSF is 0.2-0.4 ml/min with around 250 ml produced and absorbed per day
and at any given time around 70 mls is present in the head. Any interruption to normal
flow, increased production or decreased reabsorption of CSF can manifest itself as
hydrocephalus which may lead to raised ICP. The classical distinction between
obstructive and communicating hydrocephalus is less useful clinically as the cause of
reduced absorption of CSF in communicating hydrocephalus is usually functional
obstruction at the arachnoid villi (e.g. by blood or protein).
Brain tissue, the largest component of the cranial contents, may be pathologically
enlarged by the presence of a space occupying lesion which if of insidious onset may lead
to a gradual increase in ICP.
Cerebral perfusion pressure is defined as the difference between the mean arterial
pressure (MAP) and the sum of intracranial pressure and the central venous pressure
(CVP).
The normal range of ICP in neonates is 2-4 mmHg (7-15 mmHg in adults). Increased ICP
gives rise to such symptoms and signs as: vomiting, irritability, drowsiness, bulging
fontanelle (if still present), increasing head circumference, downward gaze of the eyes
(setting sun sign), Cushings response (hypertension and bradycardia). At ICP >
20mmHg focal ischaemia occurs and at >50 mmHg global ischaemia occurs if CPP
remains constant (this is the reason MAP is raised therapeutically with the use of
vasoconstrictors in some cases of raised ICP). Long term increases in ICP can impair
neurological development, whilst in the acute setting, high ICP can cause distortion and
displacement of the cerebral contents through the foramen magnum - coning - leading
to coma, respiratory arrest and death. Most anaesthetic agents cause a reduction in MAP
but this potentially deleterious effect is usually offset by the corresponding reduction in
the cerebral metabolic demand for oxygen (CMRO2).
There are several causes of hydrocephalus which may necessitate the insertion of a VP
shunt (see Box 1). VP shunts are therefore required for a wide range of patients from
newborns to older children with the potential for a number of co-morbidities. The shunt
provides a route for the CSF to drain and decreases ICP. The proximal end is placed in
the ventricle and the distal end at a site where the CSF can be absorbed (most commonly
peritoneum but atria and pleura are also used). The complications associated with VP
shunts include blockage, infection and over drainage, all of which may necessitate
revision surgery.
The incidence of infantile hydrocephalus is estimated at 3-5 cases per 1000 live births.
The peak ages of presentation include the first weeks of life, 4-8 years and early
adulthood. An estimated 750,000 people have hydrocephalus, approximately 160 000
ventriculoperitoneal shunts are inserted worldwide each year, with over 56 600 children
under 18 years thought to have a shunt in place. Depending on the indication for VP
shunt insertion, the procedure may be urgent or an emergency with additional attendant
risks (full-stomach, abnormal electrolytes, hypovolaemia, precipitously high ICP).
Table 1: Causes of hydrocephalus
Congenital : Acquired :
Myelomeningocele Infection
Stenosis of the cerebral aqueduct Intraventricular haemorrhage
Arnold-Chiari malformation Tumour
Arachnoid cysts Trauma
Vascular malformations Nutritional deficiencies
Idiopathic
PREOPERATIVE ASSESSMENT
Blood results should be reviewed to ascertain the level of haemoglobin and clotting
function so that appropriate blood products can be ordered as indicated. Urea and
electrolytes should be checked if medical problems or drug treatment suggest that they
may be abnormal and require attention perioperatively.
The preoperative visit is an opportunity to apply topical anaesthesia over a suitable vein if
intravenous induction is planned. Sedative premedication should be considered carefully
as it may exacerbate or mask signs of neurological dysfunction conversely, an anxious
combative patient may have a detrimental rise in ICP during induction. The patient
should be carefully monitored whilst awaiting surgery for signs of neurological
deterioration as this can occur rapidly. If the preoperative assessment reveals a patient
with multiple co-morbidities, such as an ex-premature infant with chronic lung disease,
the need for additional respiratory support in the postoperative period should be
considered and organised in advance.
PREPARATION, EQUIPMENT AND MONITORING
Prior to induction all anaesthetic equipment and drugs should be checked to ensure they
are available and in good working order. This should include a means of delivering
oxygen and volatile anaesthetic agent, suction, a tilting trolley and monitoring.
Equipment such as facemasks, oropharyngeal airways, tracheal tubes and laryngoscopes
should be available in a range of sizes appropriate for the patient. A weight appropriate
breathing circuit should be checked for correct configuration and patency. Standard
monitoring should include pulse oximetry, electrocardiogram, non-invasive blood-
pressure, oxygen concentration, and capnography.
INDUCTION OF ANAESTHESIA
The method of induction is determined by the circumstances of the case and the
preference of the patient and the anaesthetist.
Intravenous induction allows for rapid control of the airway in emergency situations if
the patient is not fasted and if no difficulties with the airway have been anticipated. This
may be achieved using a suitable induction agent in a carefully titrated sleep dose.
(proprofol 2-4 mg/kg, thiopentone 3-5 mg/kg) Hypotension should be avoided because of
the risk of decreasing CPP in the face of raised ICP. Ketamine should not be used as it
can increase ICP. Muscle relaxation can be achieved with the use of a neuromuscular
blocking agent (NMB). Suxamethonium can be used if the risk of aspiration outweighs
the problems of transient increases in ICP, otherwise non-depolarising NMB are
preferable.
The patient should be positioned to allow good access for the surgeon and to avoid any
undue pressure on vulnerable areas. Consideration should be given to optimizing venous
drainage to increase CPP, reduce venous bleeding and improve the surgical field. The
core temperature of the patient should be monitored (rectal or oesophageal) and warming
devices (e.g. warm air blankets) used as required to maintain normothermia.
MAINTENANCE OF ANAESTHESIA
Anaesthesia can be maintained with a volatile agent and a mixture of oxygen and air. The
aim is to maintain CPP until the raised ICP is relieved by positioning of the VP shunt. To
do this hypotension should be avoided and minute ventilation controlled to maintain
normocarbia (end tidal CO2 4-4.5 kPa) to optimise CPP and avoid increases in ICP.
Positive end-expiratory pressure (PEEP) should be minimised to avoid venous congestion
in the head but may be used if there are difficulties in maintaining oxygenation.
The most stimulating parts of the surgery include the initial incision and tunnelling under
the skin. A short acting opioid, such as fentanyl (1-3 mcg/kg) or remifentanil (1 mcg/kg),
or increased depth of anaesthesia, can be used to attenuate the increase in heart rate and
ICP. Post-operative analgesia can be provided by a combination of infiltration of local
anaesthetic such as bupivicaine 0.25% (0.5-0.75 ml/kg) and paracetamol (15 mg/kg)
either intravenous or per rectum. High doses of long acting opioids should be avoided
because of potential detrimental effects on conscious level.
POSTOPERATIVE MANAGEMENT
Preoperative assessment should look for problems associated with neonates and
prematurity such as anaemia, coagulopathy, jaundice, respiratory disease and congenital
cardiac problems. Additional investigations such as an echocardiogram may therefore be
indicated. Blood and any other required products should be readily available prior to
surgery.
Gaseous induction of anaesthesia with sevoflurane provides good cardiovascular stability.
Neonates are a more technically challenging group of patients and particular attention
must be paid to securing tracheal tubes and intravenous cannulae as endobronchial
intubation and extravasation are commonly encountered problems. Congenital
hydrocephalus may have distorted the anatomy of the skull which can make management
of the airway more difficult. Often a pillow placed under the body of the neonate can
facilitate laryngoscopy. The use of a naso-gastric tube is an important component of
managing the neonatal airway and ventilation. Handling should be careful and minimal to
reduce the risks of complications (e.g. pneumothoraces).
Neonates have a high surface area to volume ratio and so lose heat quickly and their
mechanisms for maintaining thermal homeostasis are poorly developed. Core temperature
must be recorded and active measures taken to maintain body heat. These include,
increasing the ambient temperature, warm air blankets, overhead heaters, heat-moisture
exchangers to warm inspired gases, warming intravenous fluids and covering of exposed
areas.
Drug metabolism is different in neonates with an immature liver but a relatively higher
volume of distribution. Paracetamol, local anaesthetics, volatile anaesthetic agents and
opioids are all used in relatively lower doses. Careful attention must be paid to fluid
balance as renal function is also immature in the neonate. An infusion of 10% glucose
may be required to maintain blood glucose within the normal range but hypo and
hyperglycaemia should be avoided. Regular monitoring of blood glucose and electrolytes
allows for adjustment of fluid regimens as required.
Postoperatively some neonates will require further respiratory support (especially pre-
term infants with bronchopulmonary dysplasia). Patients that can be extubated will need
apnoea monitoring for 24-hour hours postoperatively in addition to regular neurological
observations.
CONCLUSION
ANSWERS TO SELF-ASSESSMENT
Kramer LC, Management of Spina Bifida, Hydrocephalus and Shunts eMedicine 2007
http://www.emedicine.com/ped/TOPIC2976.HTM
Hill L, Cerebral Blood Flow and Intracranial Pressure. Parts 1 and 2 Tutorial of the week.
www.worldanaesthesia.org