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Abstract
Sir,
Awake fiberoptic intubation (AFOI) is recommended for patients with anticipated difficult
airway, failed intubation, and unstable cervical spine injury where optimum positioning
for laryngoscopy is difficult to achieve. Preparation includes obtundation of airway
reflexes, adequate sedation, and anxiolysis along with preservation patent airway
and adequate ventilation. Dexmedetomidine produces hypnosis, amnesia, analgesia, anxiolysis,
sympatholysis, and antisialogogue effects; all of them are desired during AFOI.[1]
Administration of dexmedetomidine through inhalational route could be a new promising
noninvasive method. The bioavailability of dexmedetomidine is 65% and 82% through
nasal and buccal mucosa, respectively, following nebulization.[2]
Here, we reported a series of four cases of patients with difficult airway in which
dexmedetomidine was used as adjuvant to lignocaine nebulization before awake fiberoptic
bronchoscope-guided nasotracheal intubation. Written consent was taken from all patients.
All these patients were scheduled for mandibular excision and reconstruction under
general anesthesia. After shifting the patients to operating room, standard ASA monitor
was connected and baseline was taken. Injection glycopyrrolate 0.2 mg i.m., intranasal
xylometazoline 0.1%, was given 15 min prior to nebulization to each patient. Patients
were nebulized with mixture of 4% lignocaine 10 ml and dexmedetomidine 1 μg/kg by
using ultrasonic nebulizer for 15 min followed by fiberoptic bronchoscope-guided nasotracheal
intubation. All patients received supplemental oxygen (2 l/min) through the working
channel of the bronchoscope. Following intubation, general anesthesia was induced.
The parameters observed include heart rate, mean arterial pressure, oxygen saturation
at 0, 5, 10, 15 (end of nebulization), and 20 min (just after intubation). Other parameters
were observed such as cough and gag reflexes [severity graded as no cough, slight
≤2 coughs, moderate (3–5 coughs), severe (>5 coughs)], patient comfort (cooperative,
restless/minimal resistance, severe resistance/requirement for immediate general anesthesia),
and signs of lignocaine toxicity.
Discussion
There were bradycardia and hypotension noted during nebulization in case 2 and 3 as
shown in Table 1. Tachycardia was noted at 20 min in case 2 and 4. One episode of
cough and gag reflex was noted in case 2. No cough, gag, and other adverse effects
such as bronchospasm, seizures due to lignocaine toxicity, and oversedation were recorded
in rest of cases as shown in Table 1. Patients were comfortable throughout the procedure.
Table 1
Shows vitals parameter and cough/gag reflexes during intubation
Vitals of patients
Time (Min)
Case 1
Case 2
Case 3
Case 4
HR
MAP
SPO2
HR
MAP
SPO2
HR
MAP
SPO2
HR
MAP
SPO2
0
63
71
92
67
121
100
130
70
100
66
120
100
5
64
80
94
66
88
100
100
91
100
65
90
100
10
66
81
100
65
85
100
95
90
100
67
88
100
15
65
80
100
65
89
100
100
85
100
67
88
100
20
64
80
100
80
131
100
90
80
100
70
85
100
Complication during procedure
Episodes of cough reflex
Episodes of gag reflex
Patient comfort
Sign of lignocaine toxicity
Case 1
No
No
Co-operative
No
Case 2
One (Slight)
One (slight)
Co-operative
No
Case 3
No
No
Co-operative
No
Case 4
No
No
Co-operative
No
Brummett et al.[3] studied the effect after perineural dexmedetomidine injection and
they attributed to the increased duration of analgesia to the local action of dexmedetomidine.
The analgesic effect of dexmedetomidine was not reversed by a ∞2-adrenoceptor antagonist
(prazosin or idazoxan), hence confirming its local site of action.
Hence, we hypothesize that dexmedetomidine nebulization provides surface analgesia
to airway mucosa in addition to its systemic effect due to its effects on peripheral
nerve endings. We could not measure systemic levels of the drugs due to lack of this
facility in our institute. Hence, we limited the maximum dose of lignocaine to 400
mg and dexmedetomidine 1 μg/kg. For validation of our hypothesis, we further require
randomized controlled studies.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
This research determined the safety and efficacy of two small-dose infusions of dexmedetomidine by evaluating sedation, analgesia, cognition, and cardiorespiratory function. Seven healthy young volunteers provided informed consent and participated on three occasions with random assignment to drug or placebo. Heart rate, blood pressure, respiratory rate, ETCO(2), O(2) saturation, and processed electroencephalogram (bispectral analysis) were monitored. Baseline hemodynamic measurements were acquired, and psychometric tests were performed (visual analog scale for sedation; observer's assessment of alertness/sedation scale; digit symbol substitution test; and memory). The pain from a 1-min cold pressor test was quantified with a visual analog scale. After a 10-min initial dose of saline or 6 microg. kg(-1). h(-1) dexmedetomidine, volunteers received 50-min IV infusions of saline, or 0.2 or 0.6 microg. kg(-1). h(-1) dexmedetomidine. Measurements were repeated at the end of infusion and during recovery. The two dexmedetomidine infusions resulted in similar and significant sedation (30%-60%), impairment of memory (approximately 50%), and psychomotor performance (28%-41%). Hemodynamics, oxygen saturation, ETCO(2), and respiratory rate were well preserved throughout the infusion and recovery periods. Pain to the cold pressor test was reduced by 30% during dexmedetomidine infusion. Small-dose dexmedetomidine provided sedation, analgesia, and memory and cognitive impairment. These properties might prove useful in a postoperative or intensive care unit setting. IMPLICATIPNS: The alpha(2) agonist, dexmedetomidine, has sedation and analgesic properties. This study quantified these effects, as well as cardiorespiratory, memory and psychomotor effects, in healthy volunteers. Dexmedetomidine infusions resulted in reversible sedation, mild analgesia, and memory impairment without cardiorespiratory compromise.
The current study was designed to test the hypothesis that the increased duration of analgesia caused by adding dexmedetomidine to local anesthetic results from blockade of the hyperpolarization-activated cation (I(h)) current. In this randomized, blinded, controlled study, the analgesic effects of peripheral nerve blocks using 0.5% ropivacaine alone or 0.5% ropivacaine plus dexmedetomidine (34 μM or 6 μg/kg) were assessed with or without the pretreatment of α(1)- and α(2)-adrenoceptor antagonists (prazosin and idazoxan, respectively) and antagonists and agonists of the I(h) current (ZD 7288 and forskolin, respectively). Sciatic nerve blocks were performed, and analgesia was measured by paw withdrawal latency to a thermal stimulus every 30 min for 300 min postblock. The analgesic effect of dexmedetomidine added to ropivacaine was not reversed by either prazosin or idazoxan. There were no additive or attenuated effects from the pretreatment with ZD 7288 (I(h) current blocker) compared with dexmedetomidine added to ropivacaine. When forskolin was administered as a pretreatment to ropivacaine plus dexmedetomidine, there were statistically significant reductions in duration of analgesia at time points 90-180 min (P < 0.0001 for each individual comparison). The duration of blockade for the forskolin (768 μM) followed by ropivacaine plus dexmedetomidine group mirrored the pattern of the ropivacaine alone group, thereby implying a reversal effect. Dexmedetomidine added to ropivacaine caused approximately a 75% increase in the duration of analgesia, which was reversed by pretreatment with an I(h) current enhancer. The analgesic effect of dexmedetomidine was not reversed by an α(2)-adrenoceptor antagonist.
More than 200 studies and reports have been published regarding the use of dexmedetomidine in infants and children. We reviewed the English literature to summarize the current state of knowledge of this drug in children for the practicing anesthesiologist. Dexmedetomidine is an effective sedative for infants and children that only minimally depresses the respiratory system while maintaining a patent airway. However, dexmedetomidine does depress the cardiovascular system. Specifically, bradycardia, hypotension, and hypertension occur to varying degrees depending on the age of the child. Hypertension is more prevalent when larger doses of dexmedetomidine are given to infants. Consistent with its 2-hour elimination half-life, recovery after dexmedetomidine may be protracted in comparison with other sedatives. Dexmedetomidine provides and augments analgesia and diminishes shivering as well as agitation postoperatively. The safety record of dexmedetomidine suggests that it can be used effectively and safely in children, with appropriate monitoring and interventions to manage cardiovascular sequelae.
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