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Table of Contents
ORIGINAL ARTICLE
Year : 2019  |  Volume : 35  |  Issue : 4  |  Page : 504-508

Hemodynamic response to tracheal intubation in postlaryngectomy patients


Department of Anaesthesiology, Amrita Institute of Medical Sciences, Amrita Vishwa Vidyapeetham, Kochi, Kerala, India

Date of Web Publication13-Dec-2019

Correspondence Address:
Dr. Sunil Rajan
Department of Anaesthesiology, Amrita Institute of Medical Sciences, Kochi, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/joacp.JOACP_207_18

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  Abstract 


Background and Aims: Endotracheal intubation in postlaryngectomy patients is usually accomplished by inserting endotracheal tube directly into the laryngectomy stoma. The primary objective of our study was to assess the systolic blood pressure (SBP) response to intubation in postlaryngectomy patients. Secondary objectives included assessment of changes in heart rate (HR), mean arterial pressure (MAP), and to estimate tracheal component of hemodynamic response to intubation in normal patients by finding out the relative reduction in hemodynamic response that might occur in postlaryngectomy patients.
Material and Methods: This was a prospective, observational study. Forty postlaryngectomy patients formed group L and 40 normal patients constituted group N. After induction of anesthesia and neuromuscular blockade, direct laryngoscopy and tracheal intubation were performed in group N, whereas an endotracheal tube was passed through the laryngectomy stoma directly into the trachea in group L. Hemodynamic responses were documented. Chi-square test, independent samples t-test, and analysis of covariance (ANCOVA) test were applied.
Result: Group L patients were significantly older with significantly lower baseline HR with higher SBP and MAP. As baseline values were not comparable, they were taken as covariates and ANCOVA was applied. Adjusted mean values were then compared. Immediately after induction HR, SBP and MAP were comparable in both groups. Subsequent comparison of adjusted mean values showed significantly higher HR, SBP, and MAP in group N immediately after intubation and 1,3,5, and 10 min later (P < 0.001). At 15 min, HR and SBP were significantly higher in group N with comparable MAP.
Conclusion: Hemodynamic stress response to endotracheal intubation is minimal or absent in postlaryngectomy patients. They mostly present with elevated blood pressure and develop hypotension following induction that persists despite intubation.

Keywords: Blood pressure, hemodynamic, hypotension, intubation, laryngectomy, tracheal


How to cite this article:
Rajan S, Chandramohan R, Paul J, Kumar L. Hemodynamic response to tracheal intubation in postlaryngectomy patients. J Anaesthesiol Clin Pharmacol 2019;35:504-8

How to cite this URL:
Rajan S, Chandramohan R, Paul J, Kumar L. Hemodynamic response to tracheal intubation in postlaryngectomy patients. J Anaesthesiol Clin Pharmacol [serial online] 2019 [cited 2020 Jan 27];35:504-8. Available from: http://www.joacp.org/text.asp?2019/35/4/504/272929




  Introduction Top


The hemodynamic stress response to laryngoscopy and endotracheal intubation is inevitable in patients undergoing surgeries under general anesthesia with endotracheal intubation, which results in tachycardia and hypertension. General anesthesia for postlaryngectomy patients coming for subsequent procedures is usually accomplished by inserting an endotracheal tube directly into the laryngectomy stoma after induction of anesthesia. Endotracheal intubation does not require laryngoscopy due to the absence of the larynx with an exteriorized trachea in these patients there will not be any laryngeal stimulation during intubation.

The primary objective of our study was to assess systolic blood pressure (SBP) response to laryngoscopy and tracheal intubation in postlaryngectomy patients. Secondary objectives included comparison of changes in heart rate and mean arterial pressure as well as to find out the tracheal component of hemodynamic stress response to intubation by finding out the relative reduction in hemodynamic response that might occur in these patients as compared with normal patients. Time to secure the airway as well as the changes in oxygen saturation were also compared.


  Material and Methods Top


This was a prospective, nonrandomized, observational study performed in 80 surgical patients of whom 40 were postlaryngectomy cases, at a tertiary care teaching institute during the period August 2016 to May 2018. Forty American Society of Anesthesiologists (ASA) physical status one to three patients, aged 20–70 years, with Mallampatti score of I and II, coming for surgery under general anesthesia requiring endotracheal intubation were included in group N. An equal number of postlaryngectomy patients of the same ASA physical status coming for subsequent surgeries requiring general anesthesia were included in group L. Exclusion criteria were anticipated difficult airway (group N), ischemic heart disease, patients on beta–blockers, and chronic obstructive pulmonary disease. The study was conducted after obtaining Hospital Ethical Committee approval and patients' consent.

All patients who were recruited into the study received general anesthesia as per a standardized protocol. After obtaining an intravenous line and attaching the monitors, all patients were preoxygenated for 3 min, induced with propofol 2mg/kg body weight after administering fentanyl 2μg/kg, glycopyrrolate 0.2mg, and midazolam 1mg intravenously. After induction of anesthesia, suxamethonium was given at a dose of 2mg/kg. At the end of 1 min, direct laryngoscopy and tracheal intubation were performed in group N, whereas a lubricated appropriate sized endotracheal tube was passed through the laryngectomy stoma into the trachea in group L.

Correct endotracheal tube placement was confirmed with auscultation and capnography. Anesthesia was continued with isoflurane 1% in oxygen–nitrous oxide mixture (1:2) with mechanical ventilation. Vecuronium 0.1 mg/kg was given after intubation for muscle relaxation. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressures (MAP) were documented before induction of anesthesia, after induction, immediately after intubation, then 3, 5, 10, and 15 min later. The time required to secure the airway and SpO2 values at these time points were also noted.

As there were no similar studies published in the past, we conducted a pilot study with 20 cases in each group. Considering changes in systolic blood pressure from baseline to immediately after intubation as primary objective with a standard deviation of 19.76 in group L and 11.86 in group N, with a power of 99% and confidence interval of 99%, a sample size of 3 was calculated to obtain statistically significant results. However as the study period extended to 22 months and since the study was conducted at a high volume center treating head and neck malignancy cases, we were able to recruit 40 patients in each group.

Chi-square test was used to compare gender and ASA in both groups. Independent t-test was used to compare age, height, weight, intubation time, and SpO2. Analysis of covariance (ANCOVA) test with Bonferroni adjustment (for multiple comparisons) was used to compare the hemodynamic variables at different time points in groups N and L as baseline hemodynamic parameters were not comparable. Statistical analysis was done using IBM SPSS Statistics 20 Windows (SPSS Inc., Chicago, IL, USA).


  Results Top


Patients in both groups were comparable with respect to height, weight, as well as in the distribution of gender and ASA physical status. Patients in group L were significantly older in comparison with those in group N ([Table 1]).
Table 1: Comparison of demographics, gender, and ASA

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Preinduction HR was significantly lower in group L as compared to group N. Preinduction SBP as well as MAP were significantly higher in group L HR, SBP, and MAP were comparable in both groups immediately after induction of anesthesia. Subsequent comparison of adjusted mean values showed a significantly higher HR, SBP, and MAP in group N at immediately after intubation and 1, 3, 5, and 10 min later. At 15 min, HR and SBP were significantly higher in group N, but MAP was comparable in both groups [Table 2], [Table 3], [Table 4].
Table 2: Comparison of changes in heart rate

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Table 3: Comparison of changes in systolic blood pressure

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Table 4: Comparison of changes in mean arterial pressure

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Time taken to secure the airway was significantly shorter in group L (4.0 ± 0.1 vs 14.9 ± 4.3 sec P < 0.001). SpO2 was significantly lower in group L before induction and immediately after induction (P < 0.001), but it became comparable immediately after intubation and at the later time points.


  Discussion Top


In this study, it was seen that postlaryngectomy patients had a lower heart rate with higher blood pressure before induction of anesthesia, but after induction, they developed profound hypotension which persisted despite intubation. Normal patients responded to laryngoscopy and intubation with significant tachycardia and hypertension. Instead of hemodynamic stress response, hypotension was observed in group L. Intergroup analysis had revealed a significantly lower HR, SBP, and MAP in postlaryngectomy patients as compared with normal.

Laryngoscopy and intubation cause hemodynamic stress response.[1],[2],[3] The response begins within seconds of direct laryngoscopy and further increases with the passage of the endotracheal tube. The response is observed within 5 s of laryngoscopy, usually peaks in 1-2 min and returns to normal levels by 5 min.[4] Hemodynamic stress response to laryngoscopy and intubation occur due to (a) stimulation of tongue which is directly related to the force applied and duration of laryngoscopy, (b) laryngeal stimulation, and (c) tracheal stimulation due to passage of the endotracheal tube.

It has been shown that avoiding laryngoscopy during intubation results in less stress response. Here, response to stimulation of tongue and oropharynx is avoided. But, the response to laryngeal and tracheal stimulation are present. This could be observed with use of I gel, PLMA, or a flexible bronchoscope-aided tracheal intubation.[5],[6],[7] Intubation through an intubating laryngeal mask airway (LMA) also avoids the stimulus from laryngoscopy. From the attenuated hemodynamic response, effect of laryngoscopy had been documented.[8],[9] However, the role of laryngeal and tracheal stimulation has not been separately quantified so far.

The hemodynamic response to tracheal intubation using either direct laryngoscopy or Intubating LMA was studied by Siddiqui et al.[8] who found that intubation through intubating LMA had resulted in minimal hemodynamic responses in comparison with intubation accomplished with direct laryngoscopy. Kahl et al.[9] also compared stress response to tracheal intubation following direct laryngoscopy and intubating LMA and made similar observations. Through these studies, it could be inferred that the act of laryngoscopy mainly contributes to hemodynamic stress response.

But a contradicting observation was made by Barak et al.,[10] who assessed hemodynamic and catecholamine response to tracheal intubation following direct laryngoscopy and fiberoptic intubation after induction of general anesthesia and concluded that both techniques produced a comparable stress response. But catecholamine levels did not correlate with the hemodynamic changes.

Singh et al.[11] studied the cardiovascular changes after the three stages of nasotracheal intubation and found that nasopharyngeal intubation caused a significant pressor response. They suggested that stimulation of the larynx and trachea by the passage of the tracheal tube, but not direct laryngoscopy, caused significant increase in this response. The results of our study were not in agreement with their observations. This could be because of differences in patient population. One group of patients in our study constituted postlaryngectomy cases.

Most of our patients in group L had presented with higher baseline blood pressure. This could be because of damage to nerve supply to carotid bodies during total laryngectomy with radical neck dissection. Postoperative hypertension is commonly observed after carotid endarterectomy or radical neck dissection and carotid sinus denervation leading to baroreceptor failure is the commonly proposed mechanism.[12],[13] Baroreceptor function tends to deteriorate with advancing age also. The patients in group L were significantly older than group N. Most of the patients in group L had received radiation therapy which might also had contributed to attenuated baroreflex sensitivity.[14],[15] All these factors could have contributed to the baseline hypertension observed in group L.

The absence of hemodynamic response observed in group L could be due to baroreceptor failure, profound hypotension following administration of a fixed dose of propofol as hypertensives commonly have a contracted intravascular volume. As group L patients were postlaryngectomy and most were post radiation as well, many had swallowing disorders including esophageal strictures and had varying degrees of dehydration and malnutrition preoperatively. This might also have contributed to the severe postinduction hypotension. We used a calculated dose of propofol rather than a sleep dose because induction had to be rapid as preoxygenation as well as mask ventilation were difficult in group L. Moreover, they did not have tracheostomy tube in place to attach the breathing circuit. So, induction as well as securing airway had to be done in a short time frame for fear of inability to ventilate in case of desaturation. A significantly shorter intubation time could be another reason for the attenuated response in group L. All these factors could have contributed in masking the hemodynamic stress response to tracheal stimulation during intubation in these patients.

The strong point of our study was that no attempt at quantifying the tracheal component of hemodynamic stress response to laryngoscopy and intubation was done so far. The major drawbacks were lack of randomization as postlaryngectomy patients were recruited to one group. Baseline hemodynamic parameters were not comparable between the groups. So, ANCOVA was used to analyze adjusted values. Group L patients were significantly older, probably because incidence of malignancy increases with age. This might have possibly added a certain degree of error, while results of this group were compared with a younger population. We were not able to estimate the tracheal component of the hemodynamic response to intubation due to the observation of an absent to minimal stress response in group L.


  Conclusion Top


Hemodynamic stress response to intubation is minimal or absent in postlaryngectomy patients. This group of patients mostly presents with elevated blood pressure and develops hypotension following induction of general anesthesia, which persists despite tracheal intubation, and this hypotension possibly masks the stress response.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ahmed MS, Qureshi MN, Uddin SS, Hussain RM. Intravenous lignocaine 2 percent (plain) efficacy in attenuation of stress response to laryngoscopy and endotracheal intubation with impact on in-hospital morbidity and mortality. Pak Armed Forces Med J 2016;66:520-4.  Back to cited text no. 1
    
2.
Subbarao P, Vijayalakshmi V, Nirmaladevi Y. Attenuation of haemodynamic response to laryngoscopy and tracheal intubation in adult patients with a single intravenous bolus dose of 0.6 mg/kg body weight of dexmedetomidine - A prospective, randomised, double-blind controlled clinical study. J Evid Based Med Healthc 2017;4:2534-40.  Back to cited text no. 2
    
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Rani R, Nesargi SS, Evaluation of oral clonidine as premedicant in attenuating hemodynamic stress response to laryngoscopy and intubation - A clinical study. Karnataka Anaesth J 2015;1:50-4.  Back to cited text no. 3
    
4.
Henderson J. Airway management in the adult. In: Miller RD, editor. Miller's Anaesthesia. 7th ed. Philadelphia: Churchill Livingstone; 2010. p. 1573-610.  Back to cited text no. 4
    
5.
Tang C, Chai X, Kang F, Huang X, Hou T, Tang F, et al. I-gel laryngeal mask airway combined with tracheal intubation attenuate systemic stress response in patients undergoing posterior fossa surgery. Mediators Inflamm2015; Article ID 965925, 12 pages 1-12.  Back to cited text no. 5
    
6.
Kishnani PP, Tripathi DC, Trivedi L, Shah K, Patel J, Ladumor J. Hemodynamic stress response during insertion of proseal laryngeal mask airway and endotracheal tube-A prospective randomized comparative study. Int J Res Med 2016;5:34-8.  Back to cited text no. 6
    
7.
Gill N, Purohit S, Kalra P, Lall T, Khare A. Comparison of hemodynamic responses to intubation: Flexible fiberoptic bronchoscope versus McCoy laryngoscope in presence of rigid cervical collar simulating cervical immobilization for traumatic cervical spine. Anesth Essays Res 2015;9:337-42.  Back to cited text no. 7
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8.
Siddiqui NT, Khan FH. Haemodynamic response to tracheal intubation via intubating laryngeal mask airway versus direct laryngoscopic tracheal intubation. J Pak Med Assoc 2007;57:11-4.  Back to cited text no. 8
    
9.
Kahl M, Eberhart LHJ, Behnke H, Sänger S, Schwarz U, Vogt S,et al. Stress response to tracheal intubation in patients undergoing coronary artery surgery: Direct laryngoscopy versus an intubating laryngeal mask airway. J Cardiothorac Vasc Anesth 2004;18:275-80.  Back to cited text no. 9
    
10.
Barak M, Ziser A, Greenberg A, Lischinsky S, Rosenberg B. Hemodynamic and catecholamine response to tracheal intubation: Direct laryngoscopy compared with fiberoptic intubation. J Clin Anesth 2003;15:132-6.  Back to cited text no. 10
    
11.
Singh S, Smith JE. Cardiovascular changes after the three stages of nasotracheal intubation. Br J Anaesth 2003;91:667-71.  Back to cited text no. 11
    
12.
VenkatesanT, Pillai R, Subramani K. Postlaryngectomy hypertensive crisis: A manifestation of perioperative acute baroreflex failure? J Clin Anesth 2007;19:539-42.  Back to cited text no. 12
    
13.
Ketch T, Biaggioni I, Robertson RM, Robertson D. Four faces of baroreflex failure. Circulation 2002;105:2518-23.  Back to cited text no. 13
    
14.
Sharabi Y, Dendi R, Holmes C, Goldstein DS. Baroreflex failure as a late sequela of neck irradiation. Hypertension 2003;42:110-6.  Back to cited text no. 14
    
15.
Timmers HJ, Karemaker JM, Wieling W, Kaanders JH, Folgering HT, Marres HA, et al. Arterial baroreflex and peripheral chemoreflex function after radiotherapy for laryngeal or pharyngeal cancer. Int J Radiat Oncol Biol Phys 2002;53:1203-10.  Back to cited text no. 15
    



 
 
    Tables

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



 

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