Abstract
Background and Aims:
Emergence agitation is a significant clinical issue during recovery from general anesthesia. Patients after intracranial operations are even more vulnerable to the stress resulting from emergence agitation. Due to the limited data available in neurosurgical patients, we evaluated the incidence, risk factors, and complications of emergence agitation.
Material and Methods:
317 consenting eligible patients undergoing elective craniotomies were recruited. The preoperative Glasgow Coma Scale (GCS)) and pain score were recorded. Bispectral Index (BIS) guided balanced general anesthesia was administered and reversed. Immediate postoperatively, the GCS and the pain score were noted. The patients were observed for 24 hours following extubation. The levels of agitation and sedation were evaluated by the Riker’s Agitation-Sedation Scale. Emergence Agitation was defined as Riker’s Agitation score of 5 to 7.
Results:
In our subset of the patient population, the incidence was 5.4%, mildly agitated in the first 24 hours and none required sedative medication as therapy. The sole risk factor identified was prolonged surgery beyond 4 hours. None of the patients in the agitated group had any complications.
Conclusion:
Early objective assessment of risk factors in the preoperative period with objective validated tests and shorter duration of surgery maybe the way forward in patients at high risk for emergence agitation, to reduce the incidence and mitigate the undesirable consequences.
Keywords: Agitation, emergence, neuroanesthesia
Introduction
Emergence agitation is a common complication in the early phase of recovery from general anesthesia.[1] It can range from agitation, confusion, delirium, or violent behavior. EA occurs in the operating room (OR) or the post anesthesia care unit (PACU) within 24–72 hours after surgery, while, Postoperative Cognitive Dysfunction (POCD) is measured at weeks to months after anesthesia.[2]
Emergence agitation can have serious consequences, such as self-extubation, accidental removal of catheters, and self-injury. Patients after craniotomy are more susceptible to stress resulting from emergence agitation during recovery from anesthesia.[3] Increased sympathetic activity may cause intracranial hemorrhage and brain edema. Elevated oxygen consumption disturbs the oxygen demand–supply balance, and may result in cerebral ischemia.[4]
The reported incidence varies from 3% to 21% in adult patients undergoing ENT, ophthalmologic, abdominal, urologic, and vascular surgeries.[5] The causes are multifactorial. Several risk factors have been identified; pain, endotracheal intubation, duration of surgery, and long-term anti-depressant use.[4,5]
There is a paucity lack of Indian literature on emergence agitation after elective craniotomies. Hence, we embarked on this study in neurosurgical patients to quantify the incidence, identify the risk factors, and, subsequently, attempt to identify the inherent complications ofemergence agitation, to prevent and mitigate them.
Material and Methods
After approval of the Institutional Review Board and written, informed consent from patients, a prospective observational cohort study was conducted on 317 adult patients undergoing elective craniotomy for brain tumor under general anesthesia. The study is registered with the Clinical Trial Registry of India (CTRI/2019/03/018176).
Data was collected from 317 consecutive patients undergoing craniotomies under general anesthesia in our institute from April 2019 through to March 2020. The study included consenting adult patients between the ages 18 to 80 years, ASA Grade 1–3. Exclusion criteria were preoperative documented impairment of consciousness, an unarousable state during the first 24 hours after surgery, reintubation within 24 hours, postoperative Glasgow Coma Scale (GCS) < 8, and patients on antipsychotic drugs.
All patients underwent a thorough preoperative anesthesia assessment. Data collected preoperatively were demographic characteristics including gender, age, and weight, in addition were documented the use of preoperative anticonvulsants, and diagnosis and location of the lesion.
In the OR, GCS was noted. The standard anesthesia monitors were supplemented by Bispectral Index (BIS) and neuromuscular blockade (NMB) monitoring. Invasive arterial blood pressure (IABP) monitoring and central venous pressure (CVP) monitoring was done as indicated. After adequate preoxygenation, general anesthesia was induced with intravenous Fentanyl 2 μg/kg, Propofol 2 mg/kg IV, Atracurium 0.5 mg/kg IV, and the airway secured with an endotracheal tube. Balanced anesthesia was maintained with a combined administration of Sevoflurane (MAC <1) and Propofol infusion (100–200 μg/kg/min) to maintain BIS between 40 to 60. Atracurium was titrated to maintain Train of Four (TOF) < 2. At the end of surgery, the patients were reversed with Glycopyrrolate 10 μg/kg and Neostigmine 0.05 mg/kg and extubated. Immediate postoperative GCS and visual analogue pain scores were noted. The level of agitation was evaluated in the first 1, 2, 3, 4, 5, 6, 8, 12, and 24 hours after surgery by Rikers Agitation-Sedation Scale [Figure 1]. Agitation was defined as a score of 5–7.
Figure 1.
Rikeræs agitation sedation scale
Intraoperatively, the approach for craniotomy, duration, blood loss, and anesthesia technique were recorded. Serum sodium, glucose, and potassium were also recorded every 2 hours.
Postoperatively, we recorded GCS, Riker’s agitation sedation score, continued mechanical ventilation, presence of an external ventricular drain, and visual analogue pain scores. All complications and use of sedatives (Midazolam or Propofol) and analgesics (Fentanyl) were noted.
Statistical analysis was performed using SPSS software version 26 (IBM, Chicago, IL, USA). The categorical variables were presented as frequency and percentages. The continuous variables were presented as mean and standard deviation. Chi-square test was applied to test for statistical differences in categorical variables and student t-test was applied to test for significant differences in continuous variables. P value < 0.05 was considered statistically significant for all comparison.
Results
The incidence of postoperative agitation in our patients occurred within the first 2 hours of surgery [Table 1].
Table 1.
Incidence of postoperative agitation
| Agitation | Frequency | Percentage |
|---|---|---|
| Yes | 17 | 5.4 |
| No | 300 | 95.6 |
Incidence of postoperative agitation was 5.4%.
The age distribution was comparable between the two groups [Table 2].
Table 2.
Age distribution in agitated and nonagitated patients
| Age (years) | Agitated (n=17) | Non-agitated (n=300) | P |
|---|---|---|---|
| Mean±SD | 45.8±14.7 | 48.4±13.7 | 0.441 |
| Age groups | |||
| ≤30 | 3 (17.6) | 30 (10.0) | |
| 31 to 40 | 4 (23.5) | 63 (21.0) | 0.848 |
| 41 to 50 | 4 (23.5) | 69 (23.0) | |
| 51 to 60 | 3 (17.6) | 73 (24.3) | |
| >60 | 3 (17.6) | 65 (21.7) |
There was no difference in the mean age of patients from the agitated and nonagitated groups (45.8±14.7 vs 48.4±13.7 respectively, P=0.441). The distribution of patients from two groups in different age groups was also non-significant (P=0.848).
Gender distribution in both the agitated and non-agitated groups was not significant. The mean weight among agitated patients was 73 ± 13.9 kg and in non-agitated was 71.3 ± 13.8 kg (P = 0.536). The majority of the patients in both groups were in ASA Grade I (A 70.6% and NA 64%, respectively). Distribution of patients from the two groups according to ASA grade was statistically not significant (P = 0.842). Although a P value of 0.052 was not statistically significant, it does indicate that there is a difference of serum sodium values between the groups. Similarly, there was a difference in serum potassium (P = 0.386) and blood glucose (P = 0.941) values, though not significant. All patients in the agitated group and 89.7% in the non-agitated group had a preoperative pain score of zero, with no statistically significant between the groups (P = 0.583). Preoperative use of anticonvulsant in both groups [Table 3] was not significant (A 47.1% as compared to NA 50.7%, respectively, P = 0.772). The majority of surgeries were done in the supine position (A 70.6%, NA 74.0%) followed by sitting position (A 17.6%, NA 11.7%). The distribution was not statistically significant (P = 0.715). Location of the lesion was highly variable in both groups.
Table 3.
Preoperative anticonvulsant use
| Anticonvulsant use | Agitated (n=17) | Non-agitated (n=300) | P |
|---|---|---|---|
| Yes | 8 (47.1) | 152 (50.7) | 0.772 |
| No | 9 (52.9) | 148 (49.3) |
Preoperative use of anticonvulsant showed no difference in proportion of patients using these drugs from the agitated and non-agitated groups (47.1% vs 50.7% respectively, P=0.772).
The mean intraoperative blood loss [Figure 2] did not differ significantly (A 379.4 ± 192.9 in comparison to NA 333.9 ± 266.6 ml, P = 0.489). Also, the distribution of blood loss categorized as ≤250, 251–500, and >500 did not show statistically significant difference in the proportion of patients in two groups (P = 0.318).
Figure 2.
Blood loss distribution in agitated and nonagitated patients
The mean duration of surgery [Table 4] did not differ in the two groups significantly (P = 0.673). However, the number of patients who had a duration of surgery of >4 hours was significantly higher in the agitated group than those in the non-agitated group (A 88.2% compared to NA 63.7%, respectively, P = 0.039).
Table 4.
Duration of surgery distribution in agitated and non-agitated patients
| Duration of surgery (hours) | Agitated (n=17) | Non-agitated (n=300) | P |
|---|---|---|---|
| Mean±SD | 5.0±0.8 | 4.9±1.1 | 0.673 |
| Groups | |||
| ≤4 | 2 (11.8) | 109 (36.3) | 0.039 |
| >4 | 15 (88.2) | 191 (63.7) |
Mean duration of surgery did not differ in two groups significantly (P=0.673). However, proportion of patients who had duration of surgery of >4 h was significantly higher in agitated group than those in non-agitated group (88.2% vs 63.7% respectively, P=0.039).
None of the patients from both the groups had pain score of 0 till 6 h postoperation.
None of our patients reported any complications due to EA.
Discussion
Emergence from anesthesia is the stage of anesthesia featuring the transition from unconsciousness to complete wakefulness and recovery of consciousness (RoC). Neurobiologically emergence and RoC processes should not be simply considered as reverse events occurring in the induction of anesthesia. Mathematically, this non-linear system anesthesia can be ideally compared as a travel with a forward way (induction), which differs from that of return (emergence). Data demonstrate that the neurobiology of the two processes are not passive and may not be mirror images but rather under the control of distinct neural circuits, which may be actively controlled in the future. This has given rise to the concept of neural inertia, which can have genetic and pharmacological influence, and may account for variations in emergence patterns.[6]
Our study is congruent with contemporary literature that emergence agitation is seen in adult patients undergoing craniotomies for brain tumor under general anesthesia. In our study, 5.4% of patients had an episode of agitation in first 2 hours of postoperative period. Among those, agitated 100% are graded as mild, and none required analgesics or sedatives.
The current published data on postoperative emergence agitation has shown an incidence of 3%–21% in patients undergoing non-neurosurgical operations.[5,7–9]
Lepouse et al.[8] reported the incidence of emergence agitation as 4.7% (64/1359 patients) in the post anesthesia care unit (PACU). Radtke et al.[7] investigated the prevalence of delirium in non-intubated adult patients after general anesthesia. 8.2% of patients, exhibited inadequate emergence: 5% positive for emergence delirium, and 3.2% hypoactive emergence. Rim et al.[1] in 2014, studied 5358 adult patients in the PACU of which 245 patients (4.6%) developed emergence agitation. Chen et al.[4] assessed patients in the first 12 hours after surgery and determined that agitation developed in 35 patients (29%); 28 (80%) of these were graded as dangerously agitated. Liu et al.[10] retrospectively examined 792 patients with an overall incidence of emergence agitation of 22.2%. In 2019, Makarem et al.[11] found inadequate emergence in 20.3% of patients, including 13.9% with Emergence Agitation and 6.4% with hypoactive emergence. Ramroop et al.[12] in their study of patients who received general anesthesia with sevoflurane found the incidence of emergence delirium was 11.8%. In van den Boogaard[13] group study, delirium was assessed in ICU patients using the Confusion Assessment Method-ICU (CAM-ICU). This study found that the incidences of hyperactive, hypoactive, and mixed delirium were 0%, 5.4%, and 4.1%, respectively.
To date, there is no standard instrument for the evaluation of Emergence Agitation after general anesthesia. Many sedation and agitation scales have been used to measure the depth of sedation and to identify agitation in patients, such as the Richmond Agitation Sedation Scale, Motor Activity Assessment Scale, as well as Riker’s Agitation Sedation Scale. In 2013, the revised Society for Critical Care Medicine clinical practice guidelines for the management of pain, agitation, and delirium suggested that the Richmond’s Agitation and Sedation Score and the Riker’s Agitation Sedation Scale were the most valid and reliable assessment tools for detecting agitation and for measuring the quality and depth of sedation in adult ICU patients.[14] The advantage of the Riker’s scale is the precise grading of agitation and ease of use. No studies have investigated the reliability and validity of the Riker’s scale in the evaluation of agitation in patients after craniotomy; however, we believe that it is comparable to using it in ICU patients. Khan et al.[15] performed 2469 concomitant Riker’s and Richmond’s scale assessments in 975 admissions to the ICUs and found that both scales led to similar rates of delirium assessment using the CAM-ICU. The Nu-DESC is an observational screen for delirium that assesses disorientation, inappropriate behavior, inappropriate communication, hallucination, and psychomotor retardation over 12 hours. Hargrave et al.[16] seeking to validate this score in 405 hospitalized patients assessed every 12 hours for 2 consecutive days found NU-DESC was highly specific but not very sensitive.
Univariate analysis revealed a significant association between the incidence of EA and 12 variables (male gender, older age, neuropsychiatric disease, abdominal, spine, head and neck surgery, TIVA, use of N2O, longer duration of anesthesia, PONV, postoperative pain).
In 2014, Rim et al.[1] (OR = 1.626, P = 0.001) and Chen et al.[4] in their studies of adult patients after undergoing general anesthesia concluded that male gender could be an independent predictor for EA. The distribution of gender in our study (P = 0.333) and weight (0.536) was not statistically significant. The distribution of patients from two groups according to ASA grade was also statistically non-significant (P = 0.842).
There was also no difference in the mean age of patients in the 2 groups (P = 0.441). Some earlier studies found the incidence of EA significantly higher in older patients. Radtke et al.[7] classified three age groups (18–39, 40–64, and ≥65 years) and showed that younger and older patients were at a higher risk for EA compared to middle-aged patients. In 2011, Pol et al.[17] evaluated 142 vascular patients and determined that the Groningen Frailty Indicator has a positive predictive value for postoperative delirium (P = 0.03). Rim et al.[1] in 2014, also found that older age (OR = 1.010, P = 0.035) was associated with a higher incidence of EA. In 2015, Liu et al.[10] evaluated that younger age was also a strong risk factor (odds ratio, 0.975 for each 1-year increase; 95% confidence interval, 0.964 to 0.987). In 2019, Ramroop et al.[12] concluded that age (>65 years) (P = 0.04) was associated with postoperative EA.
In their review of published literature, Evered et al.[18] found that there was a higher incidence of POCD with older patients, and in those with preoperative documented cognitive impairment.
The function of the frontal lobes involves cognition and emotional behavior; therefore, damage during a frontal approach for craniotomy could result in abnormal behaviors. Yan et al.[3] and Chen et al.[4] did find that a frontal approach to be an independent factor to predict postoperative EA. Our study did not find any increase in incidence; in fact, none of the patients with frontal lobe tumors included in our study had EA.
Bilotta et al.[19] identified already established risk factors and categorized them by occurrence and clinical outcome. They divided predictors and preoperative risk factors into four groups: demographics, comorbidities, surgery, and anesthesia-related such as age, education, laboratory anomalies, smoking habits, benzodiazepines premedication, cardiac surgery, thoracic surgery. Intraoperative risk factors were categorized into two groups: surgery and anesthesia-related such as anemia, duration and type of surgery, selected opioid, as well as intraoperative hypotension.
Electrolyte imbalance especially hyponatremia, and hypoglycemia may contribute to confusion and disorientation in postoperative patients, which maybe mistaken for emergence agitation In our study, there was no significant difference in the two groups with regards to the mean levels of serum sodium (P = 0.052), potassium (P = 0.386), and blood glucose (P = 0.941).
Preoperative use of antidepressants and benzodiazepines increases chances of emergence agitation. In our study, preoperative use of anticonvulsant was similar in both patient groups (P = 0.772). In 2004, Kudoh et al.[20] studied 328 patients undergoing orthopedic surgery and found postoperative confusion occurred in 15 (26%) of 57 benzodiazepine users and in 34 (13%) of 271 nonusers (P < 0.01). Chen et al.[4] Radtke et al.,[7] and Lepousé et al.[8] concluded preoperative benzodiazepines as a risk factor was emergence agitation.
Mean intraoperative blood loss did not differ significantly in the agitated and nonagitated groups in our study. In 2019, Makarem et al.[11] associated intraoperative blood loss (P < 0.001) with increased postoperative agitation.
Our study did identify one independent predictor for emergence agitation after craniotomy under general anesthesia—the duration of surgery. The patients undergoing surgery for >4 hours were significantly higher in agitated group as compared to the non-agitated group (88.2% in comparison to 63.7%, respectively, P = 0.039). Previous studies have shown that the duration of surgery[1,3,5,7] and the anesthetic technique, i.e., general anesthesia with inhalational agents,[9,21–23] are risk factors for postoperative emergence agitation. Radtke et al.[7] found a longer duration of anesthesia was a risk factor for postoperative emergence agitation. Ramroop et al.[12] also concluded that a longer duration of surgery and anesthesia was a predictive factor for emergence agitation (P = 0.007).
Magni et al.[24] comparing the use of sevoflurane and desflurane in craniotomy patients found similar emergence from anesthesia, whereas the mean extubation time and recovery time were longer in sevoflurane (15.2 ± 3.0 min and18.2 ± 2.3 min) compared to desflurane (11.3 ± 3.9 min and 12.4 ± 7.7 min). Several randomized controlled trials measured agitation with the use of inhalational anesthetic agents and propofol in nonneurosurgical patients and found that propofol might decrease the incidence of emergence agitation. In 2012, Citerio et al.[22] conducted NeuroMorfeo trial conclude equivalence for inhalational and intravenous maintenance anesthesia in times to reach an Aldrete score > 9 after tracheal extubation. In a multicenter trial in Europe in adult patients undergoing elective supratentorial intracranial surgery under general anesthesia, Emergence agitation was compared among three different anesthesia maintenance methods (sevoflurane-remifentanil, sevoflurane-fentanyl, and propofol-remifentanil). No significant differences in agitation were found among the three groups. However, incidences of agitation reported in the study (3.7%–6.5%) were much lower than those in our study. We used both propofol and sevoflurane for maintenance of anesthesia. Further investigation is needed to clarify the influence of the anesthetic technique on emergence agitation in neurosurgical patients.
Pain is an independent risk factor for emergence agitation in nonneurosurgical patients.[7,9] By using the patient’s self-report pain scales, such as visual analog scale or numerical rating scale (NRS), several studies have found that 37%–63% of patients undergoing craniotomy experience moderate to severe pain during the first postoperative day. In our study, the distribution of pain scores in two groups did not show statistical significance (P = 0.583). Radke et al.[7] (NRS 6–10) and Liu et al.[10] (NRS >5) found that a higher postoperative pain score correlated with increased incidence of postoperative emergence delirium.
There were some limitations to our study. Preoperative psychological testing for depression and cognitive impairment using scales, such as the Groningen fatality indicator, and objective tests for frailty testing, which may help identify risk factors as suggested by ongoing research, were not available or implemented in our study. As our patients are referred to us for evaluation, any additional costs for further referrals and testing were a constraint in our institution. Specific history of substance abuse or addictions was not obtained from the patients unless volunteered and being a risk factor it could have assisted in identifying patients at risk. Makarem et al.[11] found that substance-dependent patients had higher risk for agitation (21.1%, P = 0.019) and hypoactive emergence (10.5%, P = 0.044).
Emergence agitation is an undesirable event that occurs in the postoperative period in patients undergoing general anesthesia. The paucity of evidence in Indian patients undergoing elective craniotomies under general anesthesia provoked our investigation, which concluded that the incidence of emergence agitation in our subset of neurosurgical patients was significantly relevant but minimal as compared to other contemporary studies.
The sole risk factor identified was prolonged surgery beyond 4 hours. This is a coincidental correlation we found in our study. It may not be extrapolated to a cause and effect relationship. However, it may help identify patients at risk of emergence agitation, assist in early intervention, and treatment preventing further complications.
Early objective assessment of risk factors in the preoperative period with objective validated tests and shorter duration of surgery maybe the way forward in patients at high risk for emergence agitation, to reduce the incidence and mitigate the undesirable consequences.
Financial Support and Sponsorship
Nil. No sponsor.
Conflicts of Interest
There are no conflicts of interest.
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