Keywords
delayed emergence - lumbar spine - pneumocephalus
Introduction
Delayed recovery from anesthesia always poses a diagnostic challenge for the anesthesiologist
because multiple factors need to be considered. This is particularly true in short
surgeries using newer anesthetic agents where delayed recovery is not anticipated.
Some of its causes are easy to identify and temporary, whereas others may have serious
long-term effects.
Lumbar spine surgeries are routinely performed in most neurosurgical set-ups around
the world, and most of these patients are extubated in the operating room. Pneumocephalus
has a high incidence after craniotomies and cervical spine surgeries, but its occurrence
is rare in uncomplicated lumbar spine surgeries.[
1
]
,
[
2
]
Case Report
A 2-year-old male child, weighing 10 kg, with no known comorbid illness was scheduled
to undergo lumbar laminectomy (L2–L3) and excision of an intramedullary spinal cord
tumor. The child was brought by the parents to the hospital with a brief history of
difficulty in walking. Pre- operative evaluation was unremarkable, and all laboratory
parameters were within normal limits.
Anesthesia was induced with fentanyl 20 µg and propofol 20 mg. Tracheal intubation
was facilitated with rocuronium 10 mg, and a standard-sized microcuffed endotracheal
tube was inserted. Intraoperative monitoring was done with pulse oximetry, noninvasive
blood pressure, electrocardiogram, nasopharyngeal temperature, end-tidal gases and
CO2. Forced warmair blanket was used to maintain normothermia. Anesthesia was maintained
with oxygen with nitrous oxide (40:60), sevoflurane (1%–1.5%) and boluses of rocuronium
and fentanyl as required. After laminectomy and tumor excision, the dura was repaired
and its adequacy was confirmed by valsalva manoeuvre. The total duration of surgery
was 3 h. At the end of the surgery, the child did not regain consciousness even after
1 h of discontinuing sevoflurane and adequate neuromuscular reversal. Hemodynamic
parameters, as well as body temperature were normal. The pupils were bilaterally constricted,
equal and reacting to light; ventilatory efforts were adequate. The child was not
extubated and shifted to the Intensive Care Unit (ICU) for further investigations.
Immediately after reaching the ICU, the child had a sudden episode of generalized
tonic-clonic seizure lasting for around 10 s with spontaneous cessation. Loading dose
of 150 mg (15 mg/kg) phenytoin was administered to the patient. Post-seizure investigations
including arterial blood gases, serum electrolytes and glucose were normal. A computed
tomography (CT) scan revealed the presence of pneumocephalus in the pre-pontine cistern
([
Fig. 1
]). The patient had full recovery of consciousness and followed commands after 3 h
in the ICU. The trachea was extubated 12 h later. Further course in the ICU was uneventful,
and he was discharged from the ward on the seventh postoperative day without any neurological
deficit.
Fig. 1 A noncontrast computed tomography scan showing pneumo cephalus in the prepontine
cistern.
Discussion
Delayed emergence from anesthesia is multifactorial and warrants close attention.
The most common cause of delayed emergence from anesthesia is pharmacological – drugs
that are used in the perioperative period – their overdose, interactions or residual
effects. Other common causes include hypothermia, electrolyte disturbances, hypercarbia,
acidosis, hypoglycemia, obesity and advanced age. In most instances, the etiology
is readily identifiable and is promptly reversible. More serious and unexpected causes
after general anesthesia include cerebral hypoxia, seizure, central anticholinergic
syndrome, cerebral hemorrhage, embolism or thrombosis. Pneumocephalus is a rare cause
that is not encountered too often outside neurosurgical operating rooms. Pneumocephalus
is formed once cerebrospinal fluid flows out of a surgical or traumatic defect in
the dura and air takes its place to equilibrate the pressure differential.
The incidence of pneumocephalus is extremely high following craniotomies. Most of
these cases are benign and resolve spontaneously. Sometimes, it may manifest as tension
pneumocephalus with severe headache, altered sensorium, seizure or focal neurological
deficit. In our patient, pneumocephalus close to the prepontine cistern manifested
in generalised tonic–clonic seizure. Although the exact mechanism of seizure in this
case is difficult to ascertain, possible causes include sudden rise in intracranial
pressure, alteration in cerebrovascular fluid homoeostasis and change in neuronal
membrane excitability because of the air pocket. Pneumocephalus has been reported
after traumatic injuries, spinal anesthesia and accidental dural puncture whilst performing
epidural analgesia and epidural steroid injections.[
3
]
,
[
4
]
,
[
5
]
,
[
6
]
,
[
7
] However, there are only a few case reports that describe it after lumbar spine surgery.
Akyüz et al described a case of delayed pneumocephalus and pneumorrhachis 2 months
after lumbar spinal fusion surgery secondary to infection.[
6
] Karavelioglu et al reported a case of pneumocephalus after lumbar disc surgery with
pedicle screw fixation, where they postulated that they may have inadvertently torn
open the arachnoid layer while trying to retrieve a large disc fragment.[
7
] In another case, diffuse pneumocephalus after posterior lumbar surgery for spinal
stenosis was seen, where dural tear was noted intraoperatively and repaired.[
8
] Turgut and Akyüz reported a case of symptomatic tension pneumocephalus after a repeat
surgery for L5 to S1 discectomy.[
9
] Pirris and Nottmeier reported pneumocephalus after lumbar arthrodesis, which they
attributed to intraoperative reverse Trendelenburg position with an unintended durotomy.[
10
]
The use of nitrous oxide has been implicated in the enlargement of pneumocephalus.
Nitrous oxide dissolves into the bloodstream and enters closed spaces at a rate faster
than the rate of absorption of nitrogen present in that space. Even though nitrous
oxide use is contraindicated if pneumocephalus is already present, there is no strong
evidence to discontinue its use in usual neurosurgical procedures. Nitrous oxide was
used in this case and may have been contributory.
Continuous positive airway pressure ventilation has also been implicated in the development
of pneumocephalus by increasing positive pressure in the upper airway and causing
a slow entry of air into the intracranial space. Similarly, coughing, sneezing, Valsalva,
forceful blowing and even positive pressure during bag-mask ventilation can enlarge
the size of pneumocephalus.
The treatment of pneumocephalus is mostly supportive with gradual resorption of the
air over several days. However, tension pneumocephalus, caused by large volume of
air, can result in sudden mass effect with major neurological sequelae. It is a neurosurgical
emergency that needs to be promptly diagnosed and decompressed with interventions
such as craniotomy, burr role evacuation, needle aspiration or ventriculostomy placement.
High FiO2 may be helpful in treating pneumocephalus.[
11
]
,
[
12
] When high concentration of oxygen is used, it reduces blood and brain nitrogen concentrations,
increasing the nitrogen concentration gradient across the pneumocephalus-containing
cavity, promoting its absorption.
To conclude, pneumocephalus is a rare presentation after uncomplicated lumbar spine
surgery and may not be suspected by many anesthesiologists. Pneumocephalus should
be a differential diagnosis following any spinal surgery when unanticipated complications
such as delayed recovery from anesthesia, failure of extubation and neurological manifestations
are present that is not explained by any other usual cause. A head CT-scan is warranted
in such cases.
