Keywords
optic nerve sheath diameter - end-tidal carbon dioxide - intracranial pressure - hypocapnia
- hypercapnia
Introduction
Intracranial pressure (ICP) monitoring is an essential component in the management
of traumatic brain injury (TBI). The clinical signs of raised ICP may be unreliable
and may reflect relatively late cerebral decompensation. Similarly, papilledema and
pupillary signs are late to develop and may not appear for hours after TBI. Moreover,
in a sedated patient, clinical assessment may not be possible. Many studies have shown
that early detection of elevated ICP with timely intervention is associated with improved
outcome of a TBI patient.[1] ICP may be monitored by invasive or noninvasive techniques. Though invasive techniques
show the real-time values of ICP, they are associated with many complications, such
as intracranial bleeding and infection, occlusion of the catheter tip by blood, debris,
and difficult to locate ventricle in presence of cerebral edema. Moreover, invasive
monitoring is contraindicated in presence of coagulopathies (which often accompanies
the TBI patients). All these drawbacks of invasive methods can be averted by using
noninvasive techniques of ICP monitoring. Although they do not show a real-time value,
they are excellent tools to detect presence or absence of raised ICP. Elevated ICP
can be detected by computed tomographic (CT) scan or magnetic resonance imaging (MRI);
however, these techniques are time consuming and require transportation of patients
who may be unstable. The quick and noninvasive nature of ultrasonography is fast becoming
popular for rapid detection of elevated ICP at bedside in emergency and intensive
care unit (ICU) by monitoring the optic nerve sheath diameter (ONSD). Its limitations
notwithstanding, ultrasonographic ONSD monitoring is likely to be more reliable than
clinical assessment in the diagnosis of intracranial hypertension, especially when
the patient is under sedation that precludes proper clinical examination.[2] Therefore, in recent years, among noninvasive methods, bedside ocular ultrasonography
to monitor ICP has gained popularity.[3]
[4] Owing to direct communication with brain, intraorbital subarachnoid space around
the optic nerve is subjected to the same pressure changes as intracranial compartment.
Distension of optic nerve sheath increases its diameter in response to elevated ICP.
Carbon dioxide (CO2) is a potent modulator of cerebral vascular tone, alters the ICP by changing the
size of cerebral vasculature, and thereby cerebral blood flow (CBF), and this action
occurs very rapidly over a period of few minutes. In a range of partial pressure of
carbon dioxide (PaCO2) 20 to 80 mm Hg, the CBF changes in a linear manner. End-tidal carbon dioxide (EtCO2) concentration is a surrogate measure of PaCO2 (especially in a hemodynamically stable patient with healthy lungs) and is routinely
monitored continuously in patients subjected to general anesthesia. To date there
is very little literature on the effects of changing EtCO2 on ONSD. This prompted us to conduct this study to find out the effects of different
levels of EtCO2 on ONSD.
Materials and Methods
This observational study was performed after obtaining approval from the institutional
ethics committee (Ref no.—IEC 128/05.02.2016, RP-23/2016). The study included American
Society of Anesthesiologists (ASA) class I patients in age group of 18 to 65 years
undergoing surgery for brachial plexus injury under general anesthesia. Patients with
history of cardiopulmonary disease, smoking, eye disease/injury, and nonconsenting
patients were excluded from the study. This was a crossover study, and the sequence
of normocapnia, hypocapnia, and hypercapnia was randomized using a computer-generating
program. Allocation concealment was done with the help of a sealed opaque envelop
technique.
Preanesthesia checkup was performed a day prior to surgical procedure. Premedication
consisted of oral ranitidine 50 mg and metoclopramide 10 mg orally 1 hour prior to
induction of anesthesia. In the operating room, electrocardiogram (ECG), pulse oximeter
(SpO2), and noninvasive blood pressure (NIBP) cuff were attached. Anesthesia was induced
with 2 μg/kg of intravenous (IV) fentanyl and 2 mg/kg of propofol. An appropriately
sized laryngeal mask airway (LMA) was inserted without administering muscle relaxant.
Anesthesia was maintained with continuous infusion of 100 to 300 μg/kg/min of propofol
with oxygen and air (1:1) along with intermittent fentanyl (1 μg/kg) administered
hourly.
Mechanical ventilation was initiated with a fixed tidal volume of 8 mL/kg and adjusting
respiratory rate (RR) to obtain the desired EtCO2. Patients were given approximately 30-degree head-up tilt. After approximately 10
minutes, ONSD was measured by using 6 to 13 MHz linear probe of ultrasound machine
(Sonosite S-Nerve; Bothell, Washington, United States) at EtCO2 30, 40, and 50 mm Hg. Sequence of measurement was determined by randomization. Ultrasonography
was performed by the author (IK) who had sufficient experience of performing this
procedure. The patients’ eyes were covered with a transparent film, and a water-soluble
jelly was applied over the probe. The probe was gently placed on the eyelid paying
careful attention to exert minimal pressure on the eyeball. The probe was slid from
temporal to nasal end to find a suitable angle for displaying the entrance of the
optic nerve into the globe. The probe was adjusted to bring optic nerve in the center
of ultrasound screen for measurement of size. The diameter was measured 3 mm behind
the globe in fixed transverse plane. The diameter was measured 5 minutes after achieving
the desired EtCO2 level. Three measurements were taken at each EtCO2 level in an eye, and average of the three readings was taken as final ONSD value.
The person conducting the ultrasound was blinded to the EtCO2 values. Other parameters such as SpO2, heart rate (HR), and BP were also recorded simultaneously.
Data analysis was performed using software Stata 11.0 (College Station, Texas, United
States). Data were summarized as mean ± standard deviation (SD). The effect of various
levels of EtCO2 on ONSD was compared using generalized estimating equation (GEE)—population averaged
model with exchangeable correlation. The stability of hemodynamic parameters over
various levels of EtCO2 was also analyzed using GEE method. A p-value < 0.05 was considered significant.
Results
Total 30 patients participated in the study conducted over a period of 4 months, and
data from all were analyzed. All patients were male with a mean age of 29.8 (8.84)
years and mean weight of 65.6 (8.81) kg. Different hemodynamic parameters at all three
values of EtCO2 such as HR30 (73), HR40 (74), HR50 (72), SBP30 (105), SBP40 (109), SBP50 (105) and DBP30 (62), DBP40 (65), DBP50 (63) were comparable ([Table 1]).
Table 1
Demographic and clinical profile (baseline)
|
Patient characteristics
|
Mean (SD)
|
|
Abbreviations: DBP, diastolic blood pressure; HR, heart rate; SBP, systolic blood
pressure; SD, standard deviation.
|
|
Age (y)
|
29.8 (8.84)
|
|
Weight (kg)
|
65.6 (8.81)
|
|
HR (beats/min)
|
75.7 (9.67)
|
|
SBP (mm Hg)
|
121.8 (10.44)
|
|
DBP (mm Hg)
|
74.7 (10.22)
|
The calculated 95% confidence interval (CI) for the difference of two measures (Thypocarbia, EtCO2 40 and 30 mm Hg) on ONSD was −0.056 to −0.036, and the calculated CI for the difference
of other two measures (Thypercarbia, EtCO2 40 and 50 mm Hg) on ONSD was 0.044 to 0.077, and thus were observed to be significant
(p < 0.0001) ([Table 2]).
Table 2
Change in ONSD in response to different EtCO2 levels
|
Mean (cm) (SD±)
|
Coefficient (95% CI)
|
p-Value
|
|
Abbreviations: CI, confidence interval; EtCO2, end-tidal carbon dioxide; ONSD, optic nerve sheath diameter; SD, standard deviation.
|
|
ONSD (40 mm Hg)
|
0.34 (0.04)
|
|
|
|
ONSD (30 mm Hg)
|
0.29 (0.05)
|
−0.05 (−0.06, −0.04)
|
< 0.0001
|
|
ONSD (50 mm Hg)
|
0.40 (0.05)
|
0.06 (0.04, 0.08)
|
< 0.0001
|
Discussion
In this study, we monitored the effect of hypocarbia and hypercarbia on ONSD. We observed
a rapid response in ONSD with changes in EtCO2. This again highlights the fact that optic nerve being in direct communication with
the brain, the pressure changes in the latter are reflected in the ONSD. The alteration
in ONSD was immediate in response to EtCO2 changes; moreover, changes in ONSD were parallel to the EtCO2 changes. Since CBF and cerebral blood volume change in response to changes in PaCO2, the ONSD also changes accordingly.
Over the years, advancements in monitoring of ICP have enabled the diagnosis of elevated
ICP reliably by noninvasive techniques.[5] ONSD measurement using bedside ultrasound has been shown to correlate with clinical
and radiologic signs and symptoms of raised ICP.[6]
[7]
[8]
[9] Despite the association between ONSD and PaCO2,[10] there is scanty literature on ONSD responsiveness to a more dynamic surrogate of
PaCO2, that is, EtCO2. The pertinent advantages of EtCO2 over PaCO2 measurement is that the former is continuously monitored under anesthesia and avoids
time-consuming process of arterial blood gas sampling.[11]
[12] Moreover, the sensitivity of ICP to even small fluctuations in EtCO2 has been reported in the literature.[13] Animal studies have estimated that the rate of this increase in ONSD by 0.0034 mm/mm
Hg increase in ICP.[14]
The ONSD was minimum (0.29 cm) at EtCO2 30 mm Hg and maximum (0.40 cm) at EtCO2 50 mm Hg, whereas it was 0.34 cm at EtCO2 40 mm Hg. These changes in ONSD are direct representation of changes in ICP brought
about by changes in CBF due to PaCO2 changes. Our results correlate well with the study by Kim et al.[15] They studied ONSD responsiveness at two levels of EtCO2, 40 and 50 mm Hg, each measured at 1 and 5 minutes, and observed significant changes
in the diameter of ONSD. According to the available literature, the upper limit of
ONSD used to define ICP greater than 20 mm Hg (raised ICP) ranges from 0.48 to 0.57
cm.[6]
[9]
[16] In our study, the upper limit of ONSD at EtCO2 level 50 mm Hg was average of 0.40 cm, which implies that even at EtCO2 50 mm Hg, intracranial hypertension is a remote possibility in healthy non-neurosurgical
patients with normal brain compliance, and thus it may not be clinically significant.
Factors such as position of patients, time of measurement after achieving target EtCO2, measuring ONSD in a single plane (transverse), and involving same experienced operator
were kept constant, thereby avoiding any confounding factors.
The limitation of this study is that it was conducted in non-neurosurgical patients
with normal brain compliance. Thus these results cannot be applied to patients with
disturbed brain compliance in whom ONSD may behave in different manners in response
to EtCO2 alterations.
We conclude that ONSD changes significantly in response to different EtCO2 levels in healthy non-neurosurgical patients under general anesthesia.
