Abstract

The aim of the present study was to test the hypothesis that blockade of nociceptive input with bupivacaine during tonsillectomy can decrease pain beyond the immediate postoperative period. Fourteen patients between the ages of 6 and 18 years scheduled for tonsillectomy (with or without adenoidectomy) were randomly divided into two groups. The patients of both groups received 0.006 mg/kg atropine and anesthesia was induced by inhalation of halothone. Atracurium 0.5 mg/kg was used for myorelaxation. After oral intubation anesthesia was maintained with isoflurane plus nitrous oxide 67% in oxygen. In the bupivacaine group, 5 min before incision the tonsillar fossae were infiltrated with 0.25% bupivacaine with epinephrine (1 : 200,000). In the control group, the tonsillar fossae were infiltrated with normal saline with epinephrine (1 : 200,000). All patients received morphine 0.07 mg/kg (in the recovery room) and oral elixir with codeine 0.05 mg/kg plus acetaminophen 5 mg/kg every 4 h. Pain assessments were made using the visual analog (100 mm scale) self-rating method. Two types of pain were assessed: constant incisional pain and pain caused by drinking 100 ml of water. In the bupivacaine group, the constant pain score on the second day after surgery was 19 ± 6 compared to 74 ± 8 in the saline group ( P < 0.0002). By the 4–5th day after surgery almost no constant pain occurred in the bupivacaine group, but the pain score remained at the 40–60 level in the saline group. The difference in pain intensity on swallowing between the bupivacaine and saline groups was present even on the 10th postoperative day ( 1 ± 1 vs. 14 ± 5, P < 0.05 ). The results indicate that pre-incisional infiltration of the tonsils with bupivacaine markedly decreased the intensity of pain following tonsillectomy well beyond the immediate postoperative period. An explanation for the long-lasting pain relief might be that neural blockade prevents nociceptive impulses from entering the central nervous system during and immediately after surgery and thus suppresses formation of the sustained hyperexcitable state that is responsible for the maintenance of postoperative pain.

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