Emergence from Anesthesia
Most practitioners of neuroanesthesia believe that a premium should
be placed on "smooth" emergence, that is, one free of coughing/straining and arterial
hypertension. Avoidance of arterial hypertension is seen as desirable because of
the belief that arterial hypertension can contribute to intracranial bleeding and
increased edema formation.[166]
[167]
[168]
[169]
In
the
face of a poorly autoregulating cerebral vasculature, hypertension also has the potential,
through vascular engorgement, to contribute to elevation of ICP. Much of the concern
with coughing/straining has a similar basis. The sudden increases in intrathoracic
pressure are transmitted to both arteries and veins, and the transient increases
produced in both cerebral arterial and venous pressure have the same potential consequences:
edema formation, bleeding, and elevation of ICP. Coughing is a specific concern
with certain individual procedures. In the circumstances of transsphenoidal pituitary
surgery
in which the surgeon has opened and subsequently taken pains to close the arachnoid
membrane to prevent leakage of CSF, it is believed that coughing has the potential
to disrupt this closure because of sudden and substantial increases in CSF pressure.
Opening a pathway from the intracranial space to the nasal cavity conveys a substantial
risk of postoperative meningitis. In other procedures, notably those that have violated
the floor of the anterior fossa, there is also the potential for air to be driven
into the cranium and, in the event of a flap valve mechanism, cause a tension pneumocephalus.
This latter event can take place only when coughing occurs after the endotracheal
tube has been removed.
It should be acknowledged that there is a paucity of systematically
obtained clinical data to give a perspective to the actual magnitude of the risks
associated with an emergence that is not "smooth." One clinical investigation confirmed
the association of increased CBF velocity and hypertension occurring during emergence.
[170]
A second retrospective study revealed that
elevated postoperative blood pressure was a correlate of intracerebral bleeding after
craniotomy.[171]
However, there is in fact no proof
to show that it is specifically hypertension occurring at emergence that is correlated
with postoperative intracerebral bleeding. The same acknowledgment must be made
with the matter of edema formation. It has been demonstrated in anesthetized animals
that sudden substantial increases in arterial pressure can result in breech of the
blood-brain barrier with extravasation of tracers such as Evan's blue.[167]
However, no data have confirmed that the hypertensive pressure transients associated
with the typical coughing episode or with emergence are in fact associated with increased
edema formation. Nonetheless, it seems reasonable to take measures, to the extent
that these measures do not themselves add potential patient morbidity, to prevent
these occurrences.
A common method for the management of systemic hypertension during
the last stages of a craniotomy is the expectant or reactive administration (or both)
of vasoactive drugs, most commonly labetalol and esmolol.[172]
Other drugs, including enalapril and diltiazem, have been used to good effect.
Administration of dexmedetomidine during the procedure and up to 30 to 60 minutes
before conclusion of the procedure has also been reported to lessen the requirement
for antihypertensives during emergence.[173]
There
are also many approaches to the prevention of coughing and straining. We have several
biases, however. We encourage trainees to include in their anesthetic technique
"as much narcotic as is consistent with spontaneous ventilation at the conclusion
of the procedure." That practice is based on the same physiologic effect that justifies
the administration of codeine and related compounds as antitussive medication, specifically,
the depression of airway reflexes by narcotics. We also have the bias that patients
emerge more rapidly and smoothly when the last inhaled anesthetic to be withdrawn
is nitrous oxide and that clinicians should seek to avoid the "neither here nor there"
phase of anesthesia that occurs in patients who are stimulated in the face of residual
exhaled concentrations of volatile anesthetic on the order of 0.2 to 0.3 MAC. A
common practice among neuroanesthetists near the conclusion of a craniotomy is the
relatively early discontinuation of the volatile anesthetic and supplementation of
residual nitrous oxide with propofol by either bolus increments or infusion at rates
in the range of 25 to 100 µg/kg/min.
An additional principle relevant to emergence from neurosurgical
procedures that practitioners will learn either from a book or by bad experience
is that emergence should be timed to coincide, not with the final suture, but rather
with the conclusion of the application of the head dressing. Many a good anesthetic
for neurosurgery has been spoiled by severe coughing and straining that occur in
association with endotracheal tube motion during application of the head dressing.
Another nuance of our practice has been to withhold the administration of neuromuscular
antagonists as long as possible as a hedge against misjudgment while lightening anesthesia
in a patient in the later stages of the procedure. An additional popular and apparently
effective technique for reducing airway responsiveness and the likelihood of coughing/straining
while reducing the depth of anesthesia is the administration of lidocaine. Bolus
doses on the order of 1.5 mg/kg, often given as application of the head dressing
begins, are appropriate for this purpose.
The premium placed on minimizing coughing/straining and hypertension
will result, in most instances, in patients being extubated very expediently once
extubation is appropriate. In some instances, one may be tempted to extubate patients
before complete recovery of consciousness. This practice may be acceptable in some
circumstances. However, it should be undertaken with caution when the circumstances
of the surgical procedure make it possible that neurologic events may have occurred
that will delay recovery of consciousness or when lower cranial nerve dysfunction
may be present. In these circumstances, it will generally be best to wait until
the likelihood of the patient's recovery of consciousness is confirmed or until patient
cooperation and airway reflexes are likely to have recovered (or until both).
