Anesthesia: Essays and Researches  Login  | Users Online: 425 Home Print this page Email this page Small font sizeDefault font sizeIncrease font size
Home | About us | Editorial board | Ahead of print | Search | Current Issue | Archives | Submit article | Instructions | Copyright form | Subscribe | Advertise | Contacts


 
Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 11  |  Issue : 4  |  Page : 834-841  

To evaluate the efficacy of intravenous infusion of dexmedetomidine as premedication in attenuating the rise of intraocular pressure caused by succinylcholine in patients undergoing rapid sequence induction for general anesthesia: A randomized study


1 Department of Anaesthesiology, NMCH, Sasaram, Bihar, India
2 Department of Anaesthesiology, ELMCH, Lucknow, Uttar Pradesh, India
3 Department of Anaesthesiology, Varun Arjun Medical College and Rohilkhand Hospital, Shahjahanpur, Uttar Pradesh, India

Date of Web Publication28-Nov-2017

Correspondence Address:
Raj Bahadur Singh
Department of Anaesthesiology and Critical Care, Narayan Medical College and Hospital, Sasaram
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aer.AER_100_17

Rights and Permissions
   Abstract 


Context: Laryngoscopy and intubation performed during RSI lead to choroidal blood volume increase and an eventual rise in intraocular pressure (IOP). Use of succinylcholine (SCh) causes an undesirable rise in IOP which is further aggravated by laryngoscopy and endotracheal intubation. Dexmedetomidine is a highly selective centrally acting α2adrenergic agonist that has IOP lowering properties. Aims: This study aims to evaluate the efficacy of intravenous (i.v.) infusion of dexmedetomidine (0.5 μg/kg) as premedication in attenuating the rise of IOP and adverse effect if any caused by SCh in patients undergoing RSI for general anesthesia. Settings and Design: This was a double-blind, randomized trial. Subjects and Methods: Sixty adult patients in the age group of 20–50 years scheduled for elective surgeries under general anesthesia. Group I (dexmedetomidine group) (n = 30) received i.v. infusion of dexmedetomidine (0.5 μg/kg) and Group II (control group) (n = 30) received i.v. infusion of 50 ml normal saline as premedication Statistical Analysis Used: The analysis was done using Statistical Package for Social Sciences Version 15.0 statistical Analysis Software. Results: It was observed that Group I (dexmedetomidine group) had a better attenuating effect over the increases in IOP in patients undergoing RSI for general anesthesia using SCh. An increase in IOP was seen in Group II (control group) patients with RSI. Conclusions: The findings in the present study indicate that i.v. dexmedetomidine effectively attenuates the increases in IOP with an additional advantage of control on hemodynamic responses following RSI.

Keywords: Dexmedetomidine, general anesthesia, intraocular pressure, laryngoscopy, succinylcholine


How to cite this article:
Singh RB, Choubey S, Mishra S. To evaluate the efficacy of intravenous infusion of dexmedetomidine as premedication in attenuating the rise of intraocular pressure caused by succinylcholine in patients undergoing rapid sequence induction for general anesthesia: A randomized study. Anesth Essays Res 2017;11:834-41

How to cite this URL:
Singh RB, Choubey S, Mishra S. To evaluate the efficacy of intravenous infusion of dexmedetomidine as premedication in attenuating the rise of intraocular pressure caused by succinylcholine in patients undergoing rapid sequence induction for general anesthesia: A randomized study. Anesth Essays Res [serial online] 2017 [cited 2017 Dec 13];11:834-41. Available from: http://www.aeronline.org/text.asp?2017/11/4/834/209977




   Introduction Top


Rapid sequence induction (RSI) is a medical procedure involving the prompt induction of general anesthesia and subsequent laryngoscopy and endotracheal intubation. It is typically used in an emergency setting for patients at the risk of regurgitation/aspiration or raised intracranial pressure (ICP). Laryngoscopy and intubation performed during RSI lead to choroidal blood volume increase and an eventual rise in intraocular pressure (IOP).[1]

Physiologic mechanisms maintain normal IOP between 11 and 21 mm Hg. Pressure must be maintained within this range to ensure constant corneal curvature and a proper refracting index of the eye.[2] Values higher than 25 mm Hg are considered to be pathologic and in case of a perforated globe could lead to the expulsion of intraocular contents.[3]

Both depolarizing and nondepolarizing muscle relaxants have been used for RSI. Nondepolarizing muscle relaxants when used for this purpose are required in very high doses leading to unnecessary prolongation of duration of action. Among depolarizing muscle relaxants, succinylcholine (SCh) is the drug of choice for RSI.[4] It is preferred in RSI because it has the fastest onset and shortest duration of action among all muscle relaxants. The former is a major point of consideration in the context of trauma care, where endotracheal intubation may need to be accomplished early. The latter means that, if attempts at endotracheal intubation fail and the patient cannot be ventilated, there is a prospect for neuromuscular recovery and the onset of spontaneous breathing before hypoxemia occurs. The use of SCh, however, causes an undesirable rise in IOP which is further aggravated by laryngoscopy and endotracheal intubation.[4] This may prove hazardous in patients with penetrating eye injuries and patients with preexisting high IOP.[5]

The mechanism of rise in IOP due to SCh is thought to be caused by the contraction of extraocular muscles although dilatation of choroidal vessels is a contributory factor.[6] Various methods have been used to attenuate the effects of SCh on IOP; they include self-taming with 1/10th dose of SCh,[7] pretreatment with nondepolarizing muscle relaxant [8] and the use of 300 μg per oral clonidine.[9] However, no modality has been devoid of drawbacks and limitations. With α2 receptor agonists, vasoconstrictor effects have been observed in several vascular beds, including the eye.[10]

Dexmedetomidine is a highly selective centrally acting α2 adrenergic agonist that has IOP lowering properties.[11] It exerts its effects by binding to α2 receptors pre- and postsynaptically in the locus ceruleus (a cluster of nerves that lies near the 4th ventricle of brain) and in the spinal cord.[12] The purpose of the present study is to evaluate the role of dexmedetomidine at a selective dose of 0.5 μg/kg for attenuation of the increase in IOP due to RSI using SCh.


   Subjects and Methods Top


The study was carried out in the Department of Anaesthesiology of a tertiary care teaching hospital after obtaining the clearance from Institutional Ethical Committee.

This study incorporated sixty adult patients in the age group of 20–50 years scheduled for elective surgeries under general anesthesia. All patients were examined for depth of anterior chamber and fundus of the right eye by an ophthalmologist. After assessing the patients for anesthesia, informed consent of patients for the proposed study, and anesthesia was obtained. Patients were kept fasting overnight, and no premedication was given. On arrival of patients in the operation theater, intravenous (i.v.) line was initiated with 18G cannula. Preoperative recording of heart rate (HR), noninvasive blood pressure, and arterial oxygen saturation (SpO2) were made.

Preoperative baseline IOP was measured with a Schiotz tonometer after installation of 4% lignocaine drops in the right eye by an ophthalmologist.

The patients were randomly allocated into two groups of thirty each:

  • Group I (dexmedetomidine group) (n = 30) received i.v. infusion of dexmedetomidine (0.5 μg/kg) diluted in normal saline to make a solution of 50 ml as premedication, over a period of 10 min
  • Group II (control group) (n = 30) received i.v. infusion of 50 ml normal saline as premedication, over a period of 10 min.


Standard anesthetic techniques were followed. All patients were preoxygenated with 100% oxygen for 3 min. Induction of anesthesia was carried out with injection propofol 1% 2 mg/kg intravenously. SCh was administered at a dose of 2 mg/kg to achieve muscular relaxation for intubation in both groups. After cessation of fasciculations, the trachea was intubated under direct vision laryngoscopy. Those patients who could not be intubated in the first attempt were excluded from the study. After securing the airway, anesthesia was maintained in both groups with oxygen (33.33%), nitrous oxide (66.67%), halothane (0.4%–1.2%), and intraoperative relaxation was maintained by rocuronium in a dose of 0.6 mg/kg bolus followed by incremental doses of 0.12 mg/kg. The lungs were ventilated to maintain the end-tidal carbon dioxide concentration between 23 and 35 mm Hg. The parameter recordings included were IOP in the right eye, mean arterial pressure (MAP), HR, and SpO2 and were done at the following time points.

  • T1: Just before premedication
  • T2: After conclusion of premedication
  • T3: Thirty seconds after induction of anesthesia
  • T4: Thirty seconds after SCh injection
  • T5: Immediately after intubation
  • T6: 2 min after intubation
  • T7: 4 min after intubation
  • T8: 6 min after intubation.


Inclusion criteria are adult patients aged between 20 and 50 years, the American Society of Anesthesiologists physical status Class I and II, Scheduled for elective surgery under general anesthesia. Exclusion criteria are patients with ocular diseases with or without increased IOP, patients with anticipated difficult intubation: Mallampati grade III and IV, patients with history of cardiorespiratory illness, obesity (body mass index ≥30), contraindication to the use of SCh, refusal to enroll for the study.

The observations made during above study were recorded on a pro forma, and the results obtained were analyzed statistically by t-test, paired, and unpaired.

Statistical tools employed

The statistical analysis was done using Statistical Package for Social Sciences Version 15.0 statistical Analysis Software. The values were represented in number (%) and mean ± standard deviation and P < 0.05 is statistically significant.


   Results Top


The present study was undertaken in the Department of Anaesthesiology of a tertiary care teaching hospital to evaluate the efficacy of i.v. dexmedetomidine premedication 0.5 μg/kg in attenuating the rise of IOP caused by SCh in patients undergoing RSI for general anesthesia. Totally 60 adult patients in age group of 20–50 years scheduled for elective surgery under general anesthesia were randomly allocated into two groups, Group I (n = 30) and Group II (n = 30) [Table 1].
Table 1: Group-wise distribution of study population

Click here to view


Although proportion of patients aged 21–30 years was higher in Group II (33.33%) as compared to Group I (30.00%) and proportion of patients aged 41–50 years was higher in Group I (33.33%) as compared to Group II (30.00%), this difference was not found to be statistically significant (P = 0.949).

Out of sixty patients enrolled in the study, only 22 (36.67%) were females. The proportion of females was higher in Group I (40.00%) as compared to Group II (33.33%), but this difference was not found to be statistically significant (P = 0.592) [Table 2].
Table 2: Between-group comparison of demographic profile of study population

Click here to view


At baseline, all the above variables except SpO2 in Group II were found to be higher than that of Group I, but differences were not found to be statistically significant.

SpO2 levels of Group I and Group II were found to be similar with each other, and no difference was found between them [Table 3].
Table 3: Between-group comparison of hemodynamic variables at baseline (T1)

Click here to view


At baseline (T1), HR of Group I (73.37 ± 5.44 per min) was found to be lower than that of Group II (74.00 ± 4.50 per min) but difference in HR of both the groups was not found to be statistically significant (P = 0.625).

At all the time periods from T1 to T8 HR of Group II patients were found to be higher than that of Group I patients except at period T7 where HR of Group I (75.83 ± 5.08 per min) was found to be higher than that of Group II (75.03 ± 4.51 per min). Difference in HR of both groups was found to be statistically significant (P < 0.001) at all time intervals except at T1 (P = 0.625), T7 (P = 0.521), and T8 (P = 0.126) [Table 4].
Table 4: Between-group comparison of heart rate (per minute) at different time intervals

Click here to view


At baseline (T1), MAP of Group I (92.00 ± 5.91 mm Hg) was found to be lower than that of Group II (93.03 ± 5.43 mm Hg), but the difference in MAP of both the groups was not found to be statistically significant (P = 0.483).

At all the other time intervals from T2 to T8 MAP of Group II was found to be higher than that of Group I and difference at each of the time interval was found to be statistically significant (P < 0.001) [Table 5].
Table 5: Between-group comparison of mean arterial pressure (mm Hg) at different time intervals

Click here to view


At baseline (T1), IOP of the right eye of Group I (12.90 ± 1.94 mm Hg) was found to be lower than that of Group II (13.08 ± 1.91 mm Hg), and this difference was not found to be statistically significant.

At all other time intervals from T2 to T8, IOP of the right eye of Group I was found to be lower than that of Group II. The difference in IOP of right eye of both the groups was found to be statistically significant at T2 to T6 (P < 0.001) and statistically nonsignificant at T7 (P = 0.233) and T8 (P = 0.757) [Table 6] and [Figure 1].
Table 6: Between-group comparison of the right eye intraocular pressure (mm Hg) at different time intervals

Click here to view
Figure 1: Between-group comparison of the right eye intraocular pressure (mm Hg) at different time intervals

Click here to view


In Group I, at T2 a decline in HR (2.13 ± 0.57 per min) from its baseline value (T1) was observed, this change in HR from its baseline value was found to be statistically significant. Thereafter, between time intervals T3 to T7 HR were found to be above the baseline value and change in HR at all these time intervals was found to be statistically significant (P < 0.001). At T8, HR was found to be lower than that at baseline (2.80 ± 2.12 per min), and this change from its baseline value was found to be statistically significant (P < 0.001). Maximum change in HR from its baseline value was found at T5 (7.60 ± 1.69 per min), and minimum change was observed at T6 (1.47 ± 1.94 per min).

In Group II, HR at all time intervals except at T8 were found to be higher than its value at T1 (baseline), and at T8 time interval, the HR was found to be lower than its baseline value (T1). The maximum change was observed at T5 (19.17 ± 1.74 per min), and change was found to be minimum at T7 (1.03 ± 2.66 per min). Change in HR from its baseline value was found to be statistically significant at all the above time intervals [Table 7].
Table 7: Intragroup change in heart rate from baseline (T1) in the study population (paired t-test)

Click here to view


In Group I, at all time intervals, MAP was found to be lower than its value at Time T1. Minimum change in MAP was observed at T2 (7.07 ± 0.91 mm Hg), and maximum change was observed at T7 (22.00 ± 2.77 mm Hg). Change in MAP from its baseline value was found to be statistically significant at all time intervals.

In Group II, MAP was found to be higher than its value at baseline (T1) at time intervals between T2 and T5 and was found to be lower than its baseline value at time intervals T6, T7, and T8. Minimum change in MAP was found at T3 (0.10 ± 1.06 mm Hg), and maximum change was observed at T7 (12.97 ± 4.90 mm Hg). Change in MAP from its baseline value was found to be statistically significant at all time intervals except at T3 (P = 0.610) [Table 8].
Table 8: Intragroup change in mean arterial pressure from baseline (T1) in the study population (paired t-test)

Click here to view


In Group I, at all the time intervals, IOP of the right eye remained lower than its baseline value (T1). Maximum change from its baseline value was observed at T7 (4.16 ± 1.74 mm Hg), and minimum change was observed at T5 (0.26 ± 1.78 mm Hg). Change in IOP was found to be statistically significant at all time intervals except at T4 and T5.

In Group II, IOP of the right eye was found to be lower than its baseline (T1) value at time intervals at T2, T3, T6, T7, and T8 while it was found to be higher than its baseline value at T4 and T5 time intervals. Minimum change from its baseline value was found at T2 (0.67 ± 0.60 mm Hg), and maximum change was observed at T5 (4.81 ± 1.68 mm Hg). Change in IOP of the right eye was found to be statistically significant at all the time intervals [Table 9] and [Figure 2].
Table 9: Intragroup change in intraocular pressure of the right eye from baseline (T1) in the study population (paired t-test)

Click here to view
Figure 2: Intragroup change in intraocular pressure of the right eye from baseline (T1) in the study population (Paired t-test)

Click here to view



   Discussion Top


RSI is a process whereby pharmacological agents, specifically a sedative (e.g., induction agent) and a neuromuscular blocking agent, are administered in rapid succession to facilitate endotracheal intubation.[13]

The purpose of RSI is to make emergent intubation easier and safer, thereby increasing the success rate and decreasing the complications of intubation. The rationale behind RSI is to prevent aspiration and its potential problems including aspiration pneumonia and to counteract the increase in systemic arterial blood pressure, HR, plasma catecholamine release, ICP, and IOP that occur with endotracheal intubation. Avoiding an increase in IOP may be desirable, especially in the patients with glaucoma or acute eye injury.[14]

SCh, the only depolarizing neuromuscular blocking agent currently available, has been used in innumerable patients since its introduction as a neuromuscular blocking drug (NMBD) in 1952. It is the most commonly used NMBD for RSI.[15],[16]

SCh is the prototype of the depolarizing agents. Since its chemical structure (i.e., quaternary ammonium compound) is similar to that of acetylcholine (ACh), it binds to the ACh receptors (AChRs) on the motor end plate and depolarizes the postjunctional neuromuscular membrane, resulting in continuous stimulation of the motor end plate AChRs. The major advantages of Sch are its rapid onset with complete motor paralysis occurring within 45–60 s and short duration of action lasting only 6–10 min when given in the recommended 1.5-mg/kg i.v. dose. Despite its rapid onset, SCh has several side effects such as hyperkalemia, bradycardia, prolonged neuromuscular blockade, increased ICP, increased IOP, trismus, fasciculations, and malignant hyperthermia, which limit its use in RSI.

It has been reported that SCh increases the IOP by 6–8 mm Hg. Various methods have been used to attenuate the effects of SCh on IOP. They included self-taming, where a 1/10th dose of SCh is given initially followed by the remaining amount of SCh and pretreatment with nondepolarizing neuromuscular blocking agents, lidocaine, opioids, nifedipine, or nitroglycerin.[17] However, no modality was devoid of drawbacks and limitations. Rocuronium, an intermediate-acting nondepolarizing muscle relaxant used commonly, provides good intubating condition after 60–90s, but it is not preferred in patients with anticipated difficult airway.[18],[19]

Dexmedetomidine is a highly selective α2-adrenergic agonist that has sedative and analgesic effects.[14] α2-adrenergic agonists provide potentially beneficial effects in ophthalmic surgery because of their IOP-lowering properties.[14],[20] Recent studies have shown its successful use for attenuation of suxamethonium and SCh-induced IOP among patients undergoing rapid sequence intubation.[5],[11],[14],[20] However, some authors have expressed reservations on the use of dexmedetomidine owing to its hemodynamic effect.[11] Hence, the present study was carried out with an aim to evaluate the efficacy of i.v. infusion of dexmedetomidine premedication with 0.5 μg/kg in attenuating the rise of IOP caused by SCh in patients undergoing RSI for general anesthesia and to monitor and manage the side effects of dexmedetomidine.

For this purpose, a total of sixty adult patients in the age group of 20–50 years scheduled for elective surgeries under general anesthesia were enrolled in the study and were randomly allocated to one of the two groups – Group I included thirty patients who were given i.v. infusion of dexmedetomidine (0.5 μg/kg) diluted in normal saline to make a solution of 50 ml as premedication, over a period of 10 min and comprised the study group whereas the remaining 30 patients were given i.v. infusion of 50 ml normal saline as premedication, over a period of 10 min and comprised the control group of the study.

At baseline, both groups had matched mean values with mean IOP right eye of Group I being 12.90 ± 1.94 mm Hg as compared to 13.08 ± 1.91 mm Hg in Group II (P > 0.05).

At all the other time intervals from T2 to T8, IOP of the right eye of Group I was found to be lower than that of Group II. The difference in IOP of right eye of both the groups was found to be statistically significant at T2 to T6 (P < 0.001) and statistically nonsignificant at T7 (P = 0.233) and T8 (P = 0.757).

With respect to change in IOP, in study group just after the conclusion of premedication, a decrease (−2.83 ± 0.65 mm Hg) in mean IOP was observed. Thirty seconds after the induction of anesthesia the decline reached to −3.58 ± 0.93 mm of Hg. Thirty seconds after SCh injection a slight increase in IOP was observed taking the difference to −0.52 ± 1.63 mm of Hg. Immediately after intubation, another increase in IOP was observed which led to take the gap from baseline to be −0.26 ± 1.78 mm of Hg. However, at 2 min and 4 min, postintubation intervals a declining trend of IOP was observed followed by a slight incline at 6 min. At 6 min postintubation interval, mean IOP was lower than baseline value by −4.03 ± 1.63 mm of Hg. At all the time intervals except 30 s post SCh injection and postintubation intervals, the difference from baseline was significant statistically (P < 0.001).

In control group, premedication a decrease (−0.67 ± 0.60 mm Hg) in mean IOP was observed. Thirty seconds after induction of anesthesia, the decline reached to −2.67 ± 0.77 mm of Hg. Thirty seconds after SCh injection a slight increase in IOP was observed taking the difference to 2.87 ± 1.81 mm of Hg. Immediately after intubation, another increase in IOP was observed which took the gap from baseline to 4.81 ± 1.68 mm of Hg. However, at 2 min postintubation interval onward a declining trend of IOP was observed. At 6 min postintubation interval, mean IOP was lower than baseline value by 4.06 ± 1.64 mm of Hg. At all the time intervals, the difference from baseline was significant statistically (P < 0.001).

On comparing the mean IOP levels in the two groups, at all time intervals except at baseline, 4 and 6 min postintubation intervals, mean IOP was significantly higher in control group as compared to the dexmedetomidine group.

The study findings showed that at all the time intervals dexmedetomidine had a better control on mean IOP. α-adrenergic blockers such as dexmedetomidine and clonidine have shown a good attenuating effect on IOP following SCh and suxamethonium use.[9],[14],[20] For IOP trends similar to the present study were also obtained by Pal et al.,[5] who reported the use of 0.4 μg/kg and 0.6 μg/kg dexmedetomidine infusion and found the comparable results for control of IOP following the use of suxamethonium as the muscle relaxant and rapid sequence intubation, for both the dosages and obtained significantly lower mean values in both groups as compared to control group. Mowafi et al.[11] in their study using 0.6 μg/kg dexmedetomidine found results exactly comparable to results in the present study. In the present study, maximum postintubation increase in IOP was nearly 36% in control group as compared to −2% decline at the same time in dexmedetomidine group, thus showing the difference between two groups to be almost 38%.

The intraocular hypotensive effect of dexmedetomidine in the present study is consistent with the previous several researches on α2-adrenergic agonists. Clonidine was effective in preventing the rise of the IOP in response to SCh and endotracheal intubation.[9],[21],[22] Similar effects were shown in elderly patients during cataract surgery.[23],[24] Only two studies till date have examined the effect of dexmedetomidine on the SCh-induced ocular hypertension.[11]

According to explanation given by Mowafi et al.,[11] the effect of dexmedetomidine on the IOP may be caused by a direct vasoconstrictor effect on the afferent blood vessels of the ciliary body, which results in reduction of aqueous humor production.[25] Moreover, it could increase outflow of the aqueous humor caused by a reduction of the sympathetically mediated vasomotor tone of the ocular drainage system.[26] In addition, its associated hemodynamic response could contribute to the IOP lowering effect.[27]

The study findings showed that at all the time intervals dexmedetomidine had a better control on HR. Dexmedetomidine is an α2-adrenoceptor, presynaptic activation of the α2-adrenoreceptors inhibits the release of norepinephrine, terminating the propagation of pain signals. Postsynaptic activation of α2-adrenoreceptors in the central nervous system inhibits sympathetic activity and thus can decrease blood pressure and HR.[17] For HR trends, similar to the present study were also obtained by Pal et al.,[5] who reported the use of 0.4 μg/kg and 0.6 μg/kg dexmedetomidine infusion and found the comparable results for control of HR following the use of suxamethonium as the muscle relaxant, for both the dosages and obtained significantly lower mean values in both the groups as compared to control group. Mowafi et al.[11] in their study using 0.6 μg/kg dexmedetomidine found results exactly comparable to results in the present study. In the present study, maximum postintubation increase in HR was 10% lower in dexmedetomidine group as compared to control group. The study findings showed that at all the time intervals, dexmedetomidine had a better control on MAP. Dexmedetomidine has a known blood pressure-lowering effect. It is a fast-acting blood pressure attenuating agent and has been shown to be quite successful in attenuation of hemodynamic reflex in endotracheal intubation and laryngoscopy for different procedures [28],[29],[30],[31] and has been shown to have comparable or better attenuating effect on pressor response as compared to a number of anesthetic drugs, namely, lidocaine, esmolol etc., at variable dosages ranging from 0.4 μg/kg to 1.0 μg/kg. For MAP trends similar to the present study were also obtained by Pal et al.,[5] who reported the use of 0.4 μg/kg and 0.6 μg/kg dexmedetomidine infusion and found the comparable results for control of MAP following the use of suxamethonium as the muscle relaxant and rapid sequence intubation for both the dosages and obtained significantly lower mean values in both the groups as compared to control group.

Dexmedetomidine is known to have a hypotensive effect.[19] However, in the present study, no such effect was observed. In none of the patients, any withdrawal from the study owing to hypotensive effect of dexmedetomidine was observed. Contrary to our observations, Pal et al.[5] reported hypotension in two patients to be the reason for their withdrawal from the study. This finding could only be incidental as even higher dosages of dexmedetomidine when used to attenuate hemodynamic reflex following endotracheal intubation did not result in any such hypotensive effect leading to withdrawal from study.

A limitation of this study was that the effect of dexmedetomidine on the IOP changes after SCh and intubation could not be isolated from its action on the hemodynamics since both effects are parallel and a causal relationship cannot be denied. However, this limitation should not decline the potential advantage of using dexmedetomidine as an alternative agent to obtund the IOP changes of SCh and intubation.

Hence, it can be concluded that the rise of IOP with SCh and rapid sequence intubation can be blunted with i.v. dexmedetomidine premedication. The hemodynamic stability is an additional advantage. Further studies are recommended to corroborate the findings.


   Conclusion Top


The findings in the present study indicate that i.v. dexmedetomidine effectively attenuates the increases in IOP with an additional advantage of control on hemodynamic responses following RSI. Hence, dexmedetomidine can safely be recommended as i.v. premedication for attenuation of rise in IOP.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Sinclair RC, Luxton MC. Rapid sequence induction. Contin Educ Anaesth Crit Care Pain 2005;5:45-8.  Back to cited text no. 1
    
2.
Shields MB. Intraocular pressure and tonometry. Shield's Textbook of Glaucoma. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2010.  Back to cited text no. 2
    
3.
Wu TH, Acquadro MA. Anaesthesia for head and neck surgery. Clinical Anaesthesia Procedures of the Massachusetts General Hospital. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2007.  Back to cited text no. 3
    
4.
Lee C, Katz RL. Clinical implications of new neuromuscular concepts and agents: So long, neostigmine! So long, sux! J Crit Care 2009;24:43-9.  Back to cited text no. 4
    
5.
Pal CK, Ray M, Sen A, Hajra B, Mukherjee D, Ghanta AK. Changes in intraocular pressure following administration of suxamethonium and endotracheal intubation: Influence of dexmedetomidine premedication. Indian J Anaesth 2011;55:573-7.  Back to cited text no. 5
[PUBMED]  [Full text]  
6.
Jantzen JP. Anesthesia and intraocular pressure. Anaesthesist 1988;37:458-69.  Back to cited text no. 6
    
7.
Verma RS. “Self-taming” of succinylcholine-induced fasciculations and intraocular pressure. Anesthesiology 1979;50:245-7.  Back to cited text no. 7
    
8.
Katz RL, Eakins KE. The actions of neuromuscular blocking agents on extraocular muscle and intraocular pressure. Proc R Soc Med 1969;62:1217-20.  Back to cited text no. 8
    
9.
Polarz H, Böhrer H, Martin E, Wolfrum J, Völcker HE. Oral clonidine premedication prevents the rise in intraocular pressure following succinylcholine administration. Ger J Ophthalmol 1993;2:97-9.  Back to cited text no. 9
    
10.
Wikberg-Matsson A, Simonsen U. Potent alpha (2A)-adrenoceptor-mediated vasoconstriction by brimonidine in porcine ciliary arteries. Invest Ophthalmol Vis Sci 2001;42:2049-55.  Back to cited text no. 10
    
11.
Mowafi HA, Aldossary N, Ismail SA, Alqahtani J. Effect of dexmedetomidine premedication on the intraocular pressure changes after succinylcholine and intubation. Br J Anaesth 2008;100:485-9.  Back to cited text no. 11
    
12.
Bustillo MA, Lazar RM, Finck AD, Fitzsimmons B, Berman MF, Pile-Spellman J, et al. Dexmedetomidine may impair cognitive testing during endovascular embolization of cerebral arteriovenous malformations: A retrospective case report series. J Neurosurg Anesthesiol 2002;14:209-12.  Back to cited text no. 12
    
13.
Murphy MF, Walls RM. Rapid sequence intubation. In: Mace SE, Ducharme J, Murphy MF, editors. Pain Management and Sedation Emergency Department Management. New York: McGraw-Hill Company; 2006. p. 211-8.  Back to cited text no. 13
    
14.
Mace SE. Challenges and advances in intubation: Rapid sequence intubation. Emerg Med Clin North Am 2008;26:1043-68, x.  Back to cited text no. 14
    
15.
Sagarin MJ, Chiang V, Sakles JC, Barton ED, Wolfe RE, Vissers RJ, et al. Rapid sequence intubation for pediatric emergency airway management. Pediatr Emerg Care 2002;18:417-23.  Back to cited text no. 15
    
16.
Sagarin MJ, Barton ED, Chng YM, Walls RM; National Emergency Airway Registry Investigators. Airway management by US and Canadian emergency medicine residents: A multicenter analysis of more than 6,000 endotracheal intubation attempts. Ann Emerg Med 2005;46:328-36.  Back to cited text no. 16
    
17.
Chidiac EJ, Raiskin AO. Succinylcholine and the open eye. Ophthalmol Clin North Am 2006;19:279-85.  Back to cited text no. 17
    
18.
Abou-Arab MH, Heier T, Caldwell JE. Dose of alfentanil needed to obtain optimal intubation conditions during rapid-sequence induction of anaesthesia with thiopentone and rocuronium. Br J Anaesth 2007;98:604-10.  Back to cited text no. 18
    
19.
Molina AL, de Boer HD, Klimek M, Heeringa M, Klein J. Reversal of rocuronium-induced (1.2 mg kg-1) profound neuromuscular block by accidental high dose of sugammadex (40 mg kg-1). Br J Anaesth 2007;98:624-7.  Back to cited text no. 19
    
20.
Scheinin B, Lindgren L, Randell T, Scheinin H, Scheinin M. Dexmedetomidine attenuates sympathoadrenal responses to tracheal intubation and reduces the need for thiopentone and peroperative fentanyl. Br J Anaesth 1992;68:126-31.  Back to cited text no. 20
    
21.
Ghignone M, Noe C, Calvillo O, Quintin L. Anesthesia for ophthalmic surgery in the elderly: The effects of clonidine on intraocular pressure, perioperative hemodynamics, and anesthetic requirement. Anesthesiology 1988;68:707-16.  Back to cited text no. 21
    
22.
Kumar A, Bose S, Bhattacharya A, Tandon OP, Kundra P. Oral clonidine premedication for elderly patients undergoing intraocular surgery. Acta Anaesthesiol Scand 1992;36:159-64.  Back to cited text no. 22
    
23.
Virkkilä M, Ali-Melkkilä T, Kanto J, Turunen J, Scheinin H. Dexmedetomidine as intramuscular premedication for day-case cataract surgery. A comparative study of dexmedetomidine, midazolam and placebo. Anaesthesia 1994;49:853-8.  Back to cited text no. 23
    
24.
Virkkilä M, Ali-Melkkilä T, Kanto J, Turunen J, Scheinin H. Dexmedetomidine as intramuscular premedication in outpatient cataract surgery. A placebo-controlled dose-ranging study. Anaesthesia 1993;48:482-7.  Back to cited text no. 24
    
25.
Macri FJ, Cevario SJ. Clonidine. Arch Ophthalmol 1978;96:2111-3.  Back to cited text no. 25
    
26.
Vartiainen J, MacDonald E, Urtti A, Rouhiainen H, Virtanen R. Dexmedetomidine-induced ocular hypotension in rabbits with normal or elevated intraocular pressures. Invest Ophthalmol Vis Sci 1992;33:2019-23.  Back to cited text no. 26
    
27.
Georgiou M, Parlapani A, Argiriadou H, Papagiannopoulou P, Katsikis G, Kaprini E. Sufentanil or clonidine for blunting the increase in intraocular pressure during rapid-sequence induction. Eur J Anaesthesiol 2002;19:819-22.  Back to cited text no. 27
    
28.
Yildiz M, Tavlan A, Tuncer S, Reisli R, Yosunkaya A, Otelcioglu S. Effect of dexmedetomidine on haemodynamic responses to laryngoscopy and intubation: Perioperative haemodynamics and anaesthetic requirements. Drugs R D 2006;7:43-52.  Back to cited text no. 28
    
29.
Saǧıroǧlu A, Celik M, Orhon Z, Yüzer S, Sen B. Dıfferent doses of dexmedetomidine on controlling haemodynamic responses to tracheal intubation. Internet J Anesthesiol 2010;27:2.  Back to cited text no. 29
    
30.
Singhal SK, Malhotra N, Kaur K, Dhaiya D. Efficacy of esmolol administration at different time intervals in attenuating hemodynamic response to tracheal intubation. Indian J Med Sci 2010;64:468-75.  Back to cited text no. 30
  [Full text]  
31.
Gogus N, Akan B, Serger N, Baydar M. The comparison of the effects of dexmedetomidine, fentanyl and esmolol on prevention of hemodynamic response to intubation. Rev Bras Anestesiol 2014;64:314-9.  Back to cited text no. 31
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
   Introduction
   Subjects and Methods
   Results
   Discussion
   Conclusion
    References
    Article Figures
    Article Tables

 Article Access Statistics
    Viewed185    
    Printed21    
    Emailed0    
    PDF Downloaded23    
    Comments [Add]    

Recommend this journal