Acid aspiration is a serious complication of anesthesia and other forms of unconsciousness that can result in the adult respiratory distress syndrome (ARDS), which continues to have a very high mortality despite our current therapeutic interventions. This type of injury damages the alveolar epithelium, principally alveolar type I cells, and requires proliferation of alveolar type II cells to restore gas exchange units. Since keratinocyte growth factor (KGF) has been shown to be a potent mitogen for alveolar type II cells, we evaluated whether intrabronchial administration of KGF would minimize lung injury due to the unilateral instillation of 0.1 N hydrochloric acid (HCl). Rats were pretreated or post-treated by intrabronchial instillation of KGF (5 mg/kg) into the left lung before HCl instillation. All rats receiving KGF at 48 or 72 h before HCl instillation survived for the 7-day observation period, whereas the mortality rate for those receiving HCl alone or saline followed by HCl was 31% and 33%, respectively. Pretreatment with KGF at 72 h but not at 24 or 48 h considerably ameliorated morphologic damage produced by HCl. Inflammatory cells in bronchoalveolar lavage were markedly decreased 3 and 7 days after HCl instillation by the 72-h KGF pretreatment. Pretreatment with KGF at 72 h also attenuated the reduction of total lung capacity, decreased the alpha 1(I) procollagen mRNA levels, and diminished hydroxyproline accumulation due to HCl instillation. Saline pretreatment at 72 h had no significant effect on the HCl injury and subsequent physiologic abnormalities. Our attempts to improve outcome with post-treatment instillation of KGF were unsuccessful. We conclude that KGF pretreatment reduces lung injury due to acid instillation and can prevent subsequent pulmonary fibrosis.

Keratinocyte growth factor (KGF, FGF-7) is a potent mitogen for epithelial cells. We instilled recombinant human KGF to determine the effects of KGF on alveolar epithelial cells. Left lungs of adult rats were instilled intrabronchially with KGF (5 mg/kg) or normal saline. KGF instillation resulted in epithelial cell hyperplasia, and the alveolar bromodeoxyuridine (BrdU) labeling index peaked at 35% on day 2 after instillation. The mRNA levels for the surfactant proteins (SPs) SP-A, SP-B, and SP-D were increased in whole lung tissue on days 1 and 2 after KGF treatment and then returned to control levels on days 3-7. SP-C mRNA levels were increased on days 2-5 after KGF instillation. However, all surfactant protein mRNAs were reduced in type II cells isolated from rats instilled with KGF 2 or 3 days before isolation. These observations were confirmed by in situ hybridization. Instillation of KGF also increased the amount of SP-A and SP-D in lavage fluid. Transcripts for CC10, the 10-kDa Clara cell protein, were decreased. KGF increases the mRNA for the surfactant proteins per lung because of type II cell hyperplasia, but the mRNA per cell is slightly diminished as measured in isolated cells or estimated by in situ hybridization.

Background: Periarticular anesthetic infiltration (PAI) with a corticosteroid is a modality for pain control following total knee arthroplasty (TKA). Systemic corticosteroids are an established antiemetic for the prophylaxis of postoperative nausea and vomiting (PONV). The purpose of this retrospective observational study was to elucidate the relationship between dexamethasone added to PAI and PONV in patients who underwent TKA. Methods: Data from 435 patients who received PAI using ropivacaine with or without dexamethasone were reviewed. The primary outcome was the incidence of PONV within 24 h following TKA. The incidence of deep incisional and organ/space surgical site infection (SSI) within the first year was also assessed. Results: The overall incidence of PONV was 23.2%. A multivariate logistic regression analysis showed that dexamethasone added to PAI was independently associated with a reduced incidence of PONV (adjusted odds ratio, 0.23; 95% confidence interval, 0.12-0.44, P < 0.001). The incidence of PONV and rescue analgesic requirements within 24 h were lower in patients who received PAI with dexamethasone than in those who received PAI alone (19.5% vs 49.1%, P < 0.001, 7.9% vs 29.1%, P < 0.001, respectively). SSI developed in one out of the 55 patients who received PAI alone, but in none of those who received PAI with dexamethasone. Conclusions: Dexamethasone added to PAI for postoperative pain management was independently associated with a lower risk of PONV within 24 h of TKA.

We compared the intracuff pressure (ICP) of a laryngeal mask airway (LMA) in the lateral and prone positions with that in the supine position. One hundred and eight patients, weighing 50-70 kg, scheduled for elective orthopedic and plastic surgery, were assigned to three groups, based on their body position during surgery. General anesthesia was induced and then a size 4 deflated LMA was inserted in each patient in the supine (group 1; n = 42), lateral (group 2; n = 45), or prone position (group 3; n = 21). The LMA cuff was inflated with 15 ml of air. Anesthesia was maintained without nitrous oxide, and the ICP was measured until LMA removal in the supine position. ICP in groups 2 and 3 was significantly lower than that in group 1 from immediately after insertion to the end of surgery. After surgery, turning from the lateral (group 2) or prone (group 3) position to the supine position significantly raised the ICP. Because the ICP is related to the seal pressure of the LMA and postoperative pharyngolaryngeal morbidity, we recommend evaluating and adjusting the ICP appropriately in each body position.

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