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Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 10  |  Issue : 2  |  Page : 207-211  

Influence of two anesthetic techniques on blood sugar level in head injury patients: A comparative study


1 Department of Anesthesia, Madan Mohan Malviya Hospital, New Delhi, India
2 Department of Anesthesia and Critical Care, Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
3 Department of Anesthesia and Critical Care, MLN Medical College, Allahabad, Uttar Pradesh, India

Date of Web Publication26-Apr-2016

Correspondence Address:
Manoj Tripathi
2/126 A, Vikrant Khand, Gomti Nagar, Lucknow - 226 010, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0259-1162.172335

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   Abstract 


Background: Head injury presents a major worldwide social, economic, and health problem. Hyperglycemia is a significant indicator of the severity of injury and predictor of outcome, which can easily be prevented. There has been a long-standing controversy regarding the use of inhalational or intravenous (i.v.) anesthetic agents for surgery of head injury cases and impact of these agents on blood sugar level.
Aims and Objectives: The aim of this study is to find out anesthetic drugs and technique having minimal or no effect on the blood sugar, and Glasgow Coma Scale (GCS) of patients with a head injury by comparing two types of anesthetic techniques in surgery of head injury patients.
Materials and Methods: This was a prospective, randomized, and comparative study, conducted on 60 adult head injury patients. The patients were divided into two groups of 30 each. Group I patients received induction with sevoflurane and then had O2 + air + sevoflurane for maintenance with controlled ventilation. Group II patients received induction with i.v. propofol and then had O2 + air + propofol for maintenance with controlled ventilation. Injection fentanyl was used in both the groups at the time of induction and in intermittent boluses in maintenance. In observation, blood sugar level and mean arterial pressure were assessed at different time periods perioperatively in both groups while GCS was analyzed pre- and post-operatively.
Statistical Analysis: Statistical analysis was performed by Microsoft Excel 2010 using t-test for comparison between the two groups and Z-test for comparison of proportions.
Results and Conclusion: Blood sugar level was found significantly higher in patients of sevoflurane group at 30 min after induction, at the end of surgery, and 1 h after the end of anesthesia than propofol group patients. This increase of blood sugar level did not have any significant alteration in the GCS profile of the patients in sevoflurane group as compared to propofol group patients. Nausea and vomiting were found more in sevoflurane group while hypotension and bradycardia were found more with propofol group.

Keywords: Head injury, hyperglycemia, propofol, sevoflurane


How to cite this article:
Kumar M, Tripathi M, Malviya D, Malviya P S, Kumar V, Tyagi A. Influence of two anesthetic techniques on blood sugar level in head injury patients: A comparative study. Anesth Essays Res 2016;10:207-11

How to cite this URL:
Kumar M, Tripathi M, Malviya D, Malviya P S, Kumar V, Tyagi A. Influence of two anesthetic techniques on blood sugar level in head injury patients: A comparative study. Anesth Essays Res [serial online] 2016 [cited 2019 Nov 14];10:207-11. Available from: http://www.aeronline.org/text.asp?2016/10/2/207/172335




   Introduction Top


Head injury presents a major worldwide social, economic, and health problem and is the leading cause of coma and disability. Traumatic brain injury (TBI) is a nondegenerative, noncongenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical, and psycho social functions, with an associated diminished or altered state of consciousness.[1] Classification of head injury consists of primary and secondary head injury. Primary injuries occur at the time of trauma and can be manifested as focal or diffuse. Secondary injury is a result of primary and it causes significant axonal damage. It is caused by ischemia, cerebral hypoxia, cerebral edema, hypotension, raised intracranial pressure, and hyperglycemia. Secondary brain damage is potentially preventable. Minimizing secondary brain injury is the key to the optimal management of head injured patients. The release of catecholamines and hyperglycemia are results of the stress response to head injury and are among significant extracranial factors causing secondary brain damage. Early hyperglycemia is a significant indicator of the severity of injury and predictor of outcome that can easily be prevented. Anesthetic drugs and techniques may also contribute to the problem of hyperglycemia.

Since almost in every case anesthesia is needed in some or other form during surgery of head injured patients, there has been a long-standing controversy regarding the use of inhalational or intravenous (i.v.) anesthetic agents for surgery of such cases. Hence, very few studies are there which compare total i.v. with inhalational anesthesia techniques to demonstrate major outcome difference in relation to their effect on blood sugar level. In this study, we have tried to compare i.v. technique of anesthesia (using propofol) with inhalational (sevoflurane) for their effect on blood sugar level in head injured patients.

Aims and objectives

This study was conducted with the aim to find out anesthetic drugs and technique having minimal or no effect on the blood sugar of patients with head injury. This was done with the following objectives:

  • To administer general anesthesia by two different techniques using a different combination of drugs
  • To assess and compare the blood sugar of the patients at different time intervals
  • Complications, if any were observed and noted.



   Materials and Methods Top


After approval from the Research Ethical Committee and informed consent from relatives, the study was conducted on 60 adult head injured patients of either sex who underwent various neurosurgical procedures admitted to the emergency of SRN Hospital (Associated to MLN Medical College) Allahabad and Dr. Ram Manohar Lohia Institute of Medical Sciences Lucknow over a period of 1 year.

Inclusion criteria

Adult patients of either sex, scheduled for various (emergency) neurosurgical procedures because of head injury.

Exclusion criteria

Patients having diabetes mellitus, renal disease, liver disease, lung disease, and patients having severe cardiovascular diseases making our anesthetic technique unsuitable.

Before surgery, all patients had a routine preoperative assessment. Routine preoperative investigations were done in all patients including liver function test, electrocardiogram (ECG), and X-ray chest. No premedication was given except in the cases showing bradycardia.

Patients were allocated randomly by computer generated tables into two groups of 30 each:

  • Group I received induction with sevoflurane and then had O2 + air + sevoflurane for maintenance with controlled ventilation
  • Group II received induction with i.v. propofol and then had O2 + air + propofol for maintenance with controlled ventilation.


Injection Rocuronium was used to achieve muscle relaxation in both groups.

In the Group I, anesthesia was induced with inhalational agent sevoflurane by face mask with a concentration of 8% and fresh gas flow of 6 L/min in a closed circuit. Anesthesia was maintained with sevoflurane up to 3.5%, and fresh gas flow of 2.5 L/min along with oxygen and air. Injection rocuronium was administered to achieve muscle relaxation for tracheal intubation in doses of 0.9 mg/kg in both the groups.

In the Group II anesthesia was induced i.v. with propofol in a dose of 1–2.5 mg/kg. Anesthesia was maintained with oxygen, air, and infusion of 100–200 µg/kg/min of propofol. Injection fentanyl 2 µg/kg was given before induction in both the groups. Intra-operatively fentanyl was used in increments of 50 µg and 100 µg. Muscle relaxation was maintained by injection rocuronium in 0.1 mg/kg increments as required. End tidal concentration of carbon dioxide (EtCO2) level was maintained around 30. Residual neuromuscular block was reversed by using neostigmine 0.05 mg/kg and glycopyrrolate 0.01 mg/kg when appropriate. Sevoflurane was discontinued approximately 5 min before the end of the surgery, and propofol infusion was discontinued 10 min before the end of surgery. Standard monitoring of vital signs was instituted, that include pulse oximetry, automated noninvasive blood pressure, ECG, respiratory rate, heart rate, and EtCO2.

Blood glucose was measured preoperatively, after induction of anesthesia, ½ hr after induction of anesthesia and, after complete recovery from anesthesia using glucometer (Accu-Chek) that was calibrated daily. Finger prick capillary blood glucose was measured. Blood glucose unit is mentioned as mg/dl. Patient recovery was studied for 1 h after termination of anesthesia. The Glasgow Coma Scale (GCS) was used to assess patient's neurological status preoperatively, during recovery and postoperatively after 1 h. Intra-operatively, systolic blood pressure, and heart rate were maintained. Bradycardia was defined as heart rate <60 bpm, tachycardia as heart rate >100 bpm. Bradycardia was treated by the administration of atropine 0.6 mg. and tachycardia, or hypertension by first increasing the expired sevoflurane concentration, or increasing the rate of propofol infusion. Hypotension was first treated by decreasing the inspired sevoflurane concentration and propofol infusion and, if persistent by the administration of fluids then later by vasopressor drugs.

Statistical analysis was performed using Microsoft Excel 2010, Software using t-test for comparison between the two groups and Z-test for comparison of proportions. Inference of significant/nonsignificant were drawn at confidence limit 95% i.e., P = 0.05.


   Observations and Results Top


Demographic data

Since the P > 0.05, no significant statistical difference found between patient characteristics of age, sex, weight, and height [Table 1].
Table 1: Demographic data

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Blood glucose measurements at various time interval were compared between two groups, while no significant statistical difference was found preoperatively and after induction of anesthesia, significant statistical difference in blood sugar level was found ½ after induction of anesthesia, at the end of anesthesia and 1 h after end of anesthesia [Table 2].
Table 2: Blood glucose measurements (mg %)

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GCS was compared at various time intervals between two groups, and no significant statistical difference found [Table 3].
Table 3: GCS at various time interval

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Blood pressure (mean arterial pressure) in two groups was compared at various time interval, and no significant statistical difference was found (P > 0.05) [Table 4].
Table 4: Comparison of mean arterial pressure (mm Hg) in two groups

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In [Table 5], we can see that hypotension and bradycardia were more common with Group II, where propofol was used for induction and maintenance of anesthesia. Nausea and vomiting were more common with sevoflurane.
Table 5: Comparison of complications between two groups

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   Discussion Top


Head injury can cause stress response and release of catecholamines that may further aggravate the ischemic damage because of hyperglycemia.

Lam et al.[2] concluded in his study that severely head injured patients frequently develop hyperglycemia and the elevated serum glucose level may aggravate ischemic insults and worsen the neurological outcome in such patients. In a similar study, Rovlias and Kotsou (2000)[3] concluded that patients with severe head injury (GCS <8) had significantly higher serum glucose levels than those with a moderate injury. Early hyperglycemia is a frequent component of stress response to head injury.

In our study, we did not observe a significant rise in blood sugar preoperatively, since most of the cases that we included in our study was either of moderate or mild head injury and we, therefore, expected less chances of hyperglycemia. If we assess the trend of blood sugar level, preoperatively and at the time of induction both the groups had almost equal blood sugar levels, the difference was statistically insignificant. After ½ hr of induction, at the time of the end of anesthesia and after 1 h of the end of anesthesia, Group I had significantly increased blood sugar level than total i.v. Group II. Maximum blood sugar level was found at the end of surgery in Group I patients. In Group II patients, blood sugar level was found almost similar that showed minimal effect of propofol and fentanyl on blood sugar level. The study showed that sevoflurane caused the significant rise of blood sugar level in head injury patients. If we observe [Table 3], it depicts no significant change of GCS in both the group of patients at preoperative, at the end of anesthesia, and postoperative period. Therefore, now we can conclude that while sevoflurane caused the significant rise of blood sugar level in Group I patients, this rise was not sufficient to change in GCS of patients at preoperative, at the end of anesthesia, and 1 h after extubation period.

Saho et al. (1997)[4] investigated the effects of two different concentrations of sevoflurane, 0.4 minimum alveolar anesthetic concentration (MAC) and 1.0 MAC, on insulin secretion before, during, and after sevoflurane anesthesia and concluded that sevoflurane anesthesia has a rapidly reversible inhibitory effect on basal and glucose-stimulated insulin secretion, as do other inhaled anesthetics, and might induce insulin resistance. Tanaka et al.[5] compared the dose-dependent effects of sevoflurane and isoflurane anesthesia on glucose tolerance and concluded that sevoflurane anesthesia impairs glucose tolerance to the same degree as does isoflurane anesthesia. Glucose intolerance during sevoflurane or isoflurane anesthesia is independent of agent and dosage up to 1.5 MAC. We have used sevoflurane in the concentration of <3.5% during maintenance and found the same incidence of glucose intolerance. Kitamura et al.[6] examined changes in blood glucose levels in rats undergoing sigmoid colostomy under sevoflurane, sevoflurane/buprenorphine, propofol, and propofol/buprenorphine anesthesia. It was found that during surgery, hyperglycemia was observed under sevoflurane, and sevoflurane/buprenorphine anesthesia, but blood glucose levels were relatively stable under propofol and propofol/buprenorphine anesthesia. These studies have similar results and support our study. Ishii et al. (2002)[7] in their experiment on rats found that propofol suppresses glucose metabolism in the brain and possess neuroprotective properties in cerebral ischemia. Vandersteene et al. (1998)[8] found no changes in lactate and glucose metabolism during propofol anesthesia in man. Fentanyl is known to cause suppression of stress response; therefore, it is supposed to be the choice for head injury patients as it may not cause the rise of blood sugar during the perioperative period. Ellis and Steward [9] retrospectively analyzed that fentanyl dosage is associated with reduced blood glucose in pediatric patients after cardiopulmonary bypass. Verma et al.[10] found no significant difference in the baseline intra-operative and postoperative blood sugar values during propofol anesthesia in laparoscopic cholecystectomy. Bent et al. (1984)[11] concluded that the administration of high dose fentanyl has little effect on the established metabolic response to surgery, therefore, no significant differences in blood glucose values were found. As seen in earlier studies, propofol has very little impact on blood sugar level. That is the reason of blood sugar level in Group II was found stable.

Hyperglycemia is expected as a result of stress response to head injury. In our study, we compared any rise in intra-operative blood sugar with the preoperative value, it is, therefore, assumed that at the time of taking preoperative blood sugar sample, the stress response, and consequent rise of blood sugar were already “set-in” and the sample under consideration was representing raised blood sugar level. We did not observe any abnormal rise of blood glucose. There was a time difference between the event of head injury and operation. In majority of cases, it was few hours. Liu-DeRyke et al.[12] findings from their study suggest a glucose level ≥160 mg/dl within the first 24 h of admission following TBI is associated with poor outcome irrespective of severity of injury.

In order to maintain normal level of blood glucose, i.v. solutions containing glucose were avoided during perioperative period, and the normal saline infusion was given in our study.

Manorama [13] found that general anesthesia decreases the stress response to injury. We, therefore, presume that the observation of preoperative blood sugar itself showed a raised level of blood sugar in response to cortisol and other glucocorticoid mediated glucogenesis.[14],[15],[16] It can now be explained that no rise of blood sugar was seen after induction of general anesthesia using propofol and fentanyl in Group II patients.

Continuous hemodynamic monitoring allowed us to identify and quantify all episodes of various intra-operative and postoperative complications. Hypotension and bradycardia were more common with Group II where propofol was used while nausea and vomiting were more common with Group I where sevoflurane was used.


   Conclusion Top


An inhalational group where sevoflurane was used causes an increase in blood sugar in head injury patients in comparison total intravenous anesthesia group where propofol was used. However, this increase of blood sugar level was insufficient to cause a change in GCS scale of patients. Sevoflurane causes more incidence of nausea and vomiting, and propofol causes more incidence of hypotension and bradycardia.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Dawodu ST. Traumatic Brain Injury (TBI) – Definition, Epidemiology, Pathophysiology; 2009. Retrieved from: http://emedicine.medscape.com/article/326510-overview 3.  Back to cited text no. 1
    
2.
Lam AM, Winn HR, Cullen BF, Sundling N. Hyperglycemia and neurological outcome in patients with head injury. J Neurosurg 1991;75:545-51.  Back to cited text no. 2
    
3.
Rovlias A, Kotsou S. The influence of hyperglycemia on neurological outcome in patients with severe head injury. Neurosurgery 2000;46:335-42.  Back to cited text no. 3
    
4.
Saho S, Kadota Y, Sameshima T, Miyao J, Tsurumaru T, Yoshimura N. The effects of sevoflurane anesthesia on insulin secretion and glucose metabolism in pigs. Anesth Analg 1997;84:1359-65.  Back to cited text no. 4
    
5.
Tanaka T, Nabatame H, Tanifuji Y. Insulin secretion and glucose utilization are impaired under general anesthesia with sevoflurane as well as isoflurane in a concentration-independent manner. J Anesth 2005;19:277-81.  Back to cited text no. 5
    
6.
Kitamura T, Ogawa M, Kawamura G, Sato K, Yamada Y. The effects of sevoflurane and propofol on glucose metabolism under aerobic conditions in fed rats. Anesth Analg 2009;109:1479-85.  Back to cited text no. 6
    
7.
Ishii H, Arai T, Segawa H, Morikawa S, Inubushi T, Fukuda K. Effects of propofol on lactate accumulation and oedema formation in focal cerebral ischaemia in hyperglycaemic rats. Br J Anaesth 2002;88:412-7.  Back to cited text no. 7
    
8.
Vandersteene A, Trempont V, Engelman E, Deloof T, Focrouf M. Effect of propofol on cerebral blood flow and metabolism in man. Anaesthesiology 1998;43:42-3.  Back to cited text no. 8
    
9.
Ellis DJ, Steward DJ. Fentanyl dosage is associated with reduced blood glucose in pediatric patients after hypothermic cardiopulmonary bypass. Anesthesiology 1990;72:812-5.  Back to cited text no. 9
    
10.
Verma RK, Jaiswal S, Rao PB, Singh N. Total intravenous anesthesia in laproscopic cholecystectomy: Comparison of butorphenol and fentanyl. Internet J Anaesthesiol 2007;14 (1).  Back to cited text no. 10
    
11.
Bent JM, Paterson JL, Mashiter K, Hall GM. Effects of high-dose fentanyl anesthesia on the established metabolic and endocrine response to surgery. Anesthesia 1984;39:19-23.  Back to cited text no. 11
    
12.
Liu-DeRyke X, Collingridge DS, Orme J, Roller D, Zurasky J, Rhoney DH. Clinical impact of early hyperglycemia during acute phase of traumatic brain injury. Neurocrit Care 2009;11:151-7.  Back to cited text no. 12
    
13.
Manorama S. Stress response and anaesthesia altering the peri and post-operative management. Indian J Anaesth 2003;47:427-34.  Back to cited text no. 13
    
14.
Griesdale DE, Tremblay MH, McEwen J, Chittock DR. Glucose control and mortality in patients with severe traumatic brain injury. Neurocrit Care 2009;11:311-6.  Back to cited text no. 14
    
15.
Zuurbier CJ, Keijzers PJ, Koeman A, Van Wezel HB, Hollmann MW. Anesthesia's effects on plasma glucose and insulin and cardiac hexokinase at similar hemodynamics and without major surgical stress in fed rats. Anesth Analg 2008;106:135-42.  Back to cited text no. 15
    
16.
Tanaka K, Kawano T, Tomino T, Kawano H, Okada T, Oshita S, et al. Mechanisms of impaired glucose tolerance and insulin secretion during isoflurane anesthesia. Anesthesiology 2009;111:1044-51.  Back to cited text no. 16
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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