Eugenia Flouraki* DVM, PhD, Ioannis Savvas DVM, PhD, George Kazakos DVM, PhD, Tilemahos Anagnostou DVM, PhD,
Alexia Bourgazli DVM, MSc, PhD
Companion Animal Clinic, School of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece
*Current address: Surgery Clinic, School of Veterinary Medicine, University of Thessaly, Karditsa, Greece
aspiration pneumonia, dog, gastroesophageal reflux
A 4-year-old, female, English bulldog, referred for elective surgery developed gastro-oesophageal reflux and gastric content regurgitation, soon after induction of anaesthesia. After the end of surgery, the oesophagus was flushed with saline 0.9% and the animal was treated with prokinetics, proton pump inhibitors and mucosal protectants. Radiographic evaluation of the thorax was consistent with aspiration pneumonia in the cranial lung lobes and the patient was transferred to the Intensive Care Unit. The dog was treated with antibiotics and oxygen administration. After three days the animal was discharged from the Intensive Care Unit, on the basis of normal clinical examination and blood gases. Two months later, the dog was clinically healthy without any symptoms of cough, dyspnoea or dysphagia. Despite proper preoperative fasting, aspiration of gastric contents and/or pharyngeal secretions may still occur intraoperatively, as long as tracheal intubation may not fully protect the lungs.
The reduction of the lower oesophageal sphincter (LOS) pressure during anaesthesia is a wellknown mechanism of gastro-oesophageal reflux (GOR) development in dogs and cats (Gibbs & Modell 1990). The prevalence of GOR intraoperatively varies and percentages of up to 50% have been reported (Galatos & Raptopoulos 1995a, Galatos & Raptopoulos 1995b, Wilson & Walshaw 2004, Wilson et al. 2006). On most occasions, the refluxate does not reach the pharynx (“silent” reflux). In a retrospective study, aspiration was only witnessed in 2 out of 240 dogs with post-anaesthetic aspiration pneumonia (Ovbey et al. 2014). This refluxate, which is a mixture of ingested food, gastric chyme, and in some cases duodenal enzymes (duodeno-gastro-oesophageal reflux), is erosive to the oesophageal mucosa. As long as GOR remains unnoticed, the refluxate stays in contact to the oesophageal mucosa during anaesthesia, and this may cause oesophageal inflammation and potentially oesophageal stricture in due course. Stricture formation may have serious consequences to the animals, and it may lead to death or euthanasia (Wilson & Walshaw 2004). GOR is a major complication of anaesthesia in humans. If the refluxate reaches the pharynx before the airway is secured, it may be aspirated with potentially devastating complications. Indeed, one of the commonest causes of death related directly to anaesthesia is pulmonary aspiration of gastric contents (Engelhardt & Webster 1999)
It is interesting that a condition with the same underlying mechanism of development can produce two different clinical complications in two different species. As far as the authors are aware of the medical and veterinary literature, there is no report of oesophagitis or oesophageal stricture caused by GOR during anaesthesia in humans, although pulmonary aspiration at induction is the main complication. On the contrary, in dogs and cats there have been no case reports of pulmonary aspiration of gastric contents that occurred during general anaesthesia, whereas many cases of oesophageal inflammation and stricture have been reported. In this case report, we describe the aspiration of gastric contents after GOR in a dog under general anaesthesia resulting to pneumonia.
A 4-year-old, intact female, obese English bulldog, weighing 21 kg (body condition score 7), was referred for elective resection of a tail fold. The patient was clinically healthy. A complete blood count and basic biochemistry profile were performed and found to be within normal limits. The patient had a 3-hour pre-operative fasting. In particular, half of the daily requirements of a commercial canine canned diet was given in the evening before surgery, followed by a fasting period of 12 hours until the next morning, when the dog was administered another half of the daily requirements. Three hours later the dog was premedicated with acepromazine (Acepromazine, Alfasan, Netherlands) 0.05 mg kg-1 and butorphanol (Butador, Richter Pharma AG, Austria) 0.1 mg kg-1, intramuscularly (IM), in the quadriceps femoris muscle. Twenty minutes after premedication, an indwelling catheter was introduced into the cephalic vein. Carprofen (Rimadyl, Pfizer, Scotland, UK) was also administered at a dose of 4 mg kg-1 intravenously (IV) as pre-emptive analgesia. Anaesthesia was induced with propofol (Propofol, Fresenius Kabi, Greece) at 2 mg kg-1 IV and the trachea was intubated with an endotracheal tube (Lo-Contour Murphy, Mallinckrodt, Ireland) with an internal diameter of 6.5 mm. The cuff of the tube was inflated at a pressure of about 20 cmH2O, using the technique of inflating the cuff while squeezing the breathing bug at about 20 cmH2O pressure (anaesthetic machine manometer) and listening for leaks from the mouth of the dog. Anaesthesia was maintained with isoflurane (Isoflurane, Merial, Italy) in oxygen through a circle rebreathing system, with a 1 L min-1 oxygen flow rate. A Lactated Ringer’s solution was being administered peri-operatively at a rate of 10 ml kg-1 h-1.
During anaesthesia the patient was placed into sternal recumbency. Five minutes after induction of anaesthesia, a pH electrode (52-00/pH meter 507, Crison Instruments S.A., Spain) was introduced into the oesophagus 5 cm cranially to the LOS and the oesophageal pH was constantly monitored, as a procedure of a clinical study on GOR. Just after the placement of the pH electrode, the oesophageal pH was found to be 3.5 and the patient was considered to have a reflux episode. Fifteen minutes later, gastric contents were regurgitated into the oropharyngeal and nasal cavities and also leaking from the mouth and the nostrils. The outflow of gastric contents from the mouth lasted for about 2.5 hours and regurgitated material from the nasal cavity, the pharynx and the oesophagus were being suctioned during this time. The oesophageal pH ranged from 3 to 3.8 throughout the surgical procedure.
When the surgical procedure was finished, the oesophagus was flushed with aliquots of normal saline and aspirated. Saline flushing and aspiration were repeated several times until the oesophagus was free of gastric content and the pH was recorded to be approximately 5. Moreover, treatment with prokinetics, proton pump inhibitors and mucosal protectants was initiated. In particular, metoclopramide (Primperan, Sanofi Aventis, Greece) and ranitidine (Zantac, Glaxo Smithkline, Greece) were used at 0.5 mg kg-1 and 2 mg kg-1 IV, respectively.
After oesophageal lavage and before recovery, the patient was also evaluated for aspiration. Radiographic evaluation revealed alveolar infiltration with air bronchograms at the cranial lung lobes compatible with aspiration pneumonia and the patient was transferred to the Intensive Care Unit (ICU). The dog was extubated in head-down position with the endotracheal tube cuff partially deflated. Treatment included the administration of antibiotics: marbofloxacine (Marbocyl, Vetoquinol, France) 2 mg kg-1 every 24 hours, combined with clindamicin (Dalacin, Pfizer, Greece) 10 mg kg-1 and cephazolin (Vifazolin, Vianex SA, Greece) 30 mg kg-1 every 12 hours, were administered IV for the next three days. Sucralfate (Peptonorm, Uni-Pharma, Greece) administration was also administered, at 30 mg kg-1 per os, every 8 hours. After extubation, arterial oxygen tension was 89 mmHg. However, a nasal catheter was also introduced for oxygen supplementation preventively, for 24 hours. Haemoglobin saturation (pulse oximetry) remained above 92% thereafter. Administration of Lactated Ringer’s solution was initiated at 80 ml h-1 for the first 2 hours and then at 40 ml h-1 for the next 24 hours. On the next day the animal was discharged from the ICU, on the basis of normal clinical examination and blood gases. The patient was hospitalized for three days in total. Two months later, the dog was clinically healthy without any symptoms of cough, dyspnoea or dysphagia.
Aspiration pneumonia develops after the inhalation of oropharyngeal or gastrointestinal contents into the airways. It is a common clinical condition in dogs, which is associated with oesophageal disease, vomiting, neurologic disorders or laryngeal disease. It may also develop post-anaesthesia (Ko-gan et al. 2008). Aspiration pneumonia is a severe condition, which may lead to acute respiratory distress syndrome. With the appropriate therapy and hospitalization, the disease has a good prognosis in dogs, with an overall survival rate of 68-81% (McConnell et al. 2007, Kogan et al. 2008). In a large, multicentre, randomized, case-controlled retrospective study in dogs, the estimated overall prevalence of post-anaesthetic aspiration pneumonia was 0.17% and ranged from 0.04% to 0.26% among the institutions (Ovbey et al. 2014). Interestingly, in the same study, in the patients which developed aspiration pneumonia, a large-volume GOR occurred either during the period of tracheal intubation (at induction of anaesthesia) or in the recovery period.
The risk of aspiration is well recognized in clinical practice. In two clinical studies, 1/240 and 2/270 dogs that underwent surgery developed regurgitation of gastric contents from the mouth (Galatos & Raptopoulos 1995a, Galatos & Raptopoulos 1995b). In human medicine, aspiration pneumonia occurs in about 10-20% of the GOR cases at induction of anaesthesia (Gibbs & Modell 1990). A major factor that may affect the prevalence of GOR is the volume of gastric contents. However, the concept that fasting guarantees an “empty stomach” has been shown to be incorrect (Engelhardt & Webster 1999, Watson & Rinomhota 2002). As the stomach continues to secret gastric juices, it can never be completely empty even after an overnight fast (Engelhardt & Webster 1999).
In veterinary clinical practice, there are several studies reporting the prevalence of GOR in small animals. The administration of propofol which is associated with a much higher prevalence of GOR than the administration of thiopental (Raptopoulos & Galatos 1997), may contribute to high prevalence of GOR, probably due to the greater decrease of LOS pressure induced by propofol than by thiopental in dogs. Other factors include prolonged preoperative fasting (Galatos & Raptopoulos 1995b) and the administration of an opioid (Wilson et al. 2005) thiopental, and isoflurane. Morphine decreases LOS pressure and increases the probability of reflux in rhesus monkeys and humans (Hall et al. 1975). In a study (Savvas et al. 2009), it has been shown that canned food at a half daily rate administered 3 hours before anaesthesia does not increase significantly the gastric content volume. According to this study, it seems that within the range of the usual duration of preoperative fasting, including a 2 to 4 hours fast, gastric content volume does not play an important role in affecting the occurrence of GOR. In contrast, it may be that in dogs, low gastric content pH is a more important risk criterion for identifying patients at increased risk for intraoperative GOR, given that canned food at a half daily rate administered 3 hours before anaesthesia did not increase significantly the gastric content volume. However, in our case, despite the application of a short preoperative fasting, GOR occurred, showing that reflux may still develop.
In our case, a tube with a high-volume low-pressure cuff was used. This type of cuff is floppy and easily deformed, and it has a large resting volume and diameter and a thin compliant wall that allows a seal to be achieved without stretching the wall of the trachea. If the residual diameter of the cuff is much greater than the diameter of the trachea, cuff infolding may occur, with the possibility of aspiration along the folds. Aspiration can occur past low-pressure cuffs with folds or wrinkles. This will be increased with spontaneous respiration, while continuous positive airway pressure and positive end-expiratory pressure are protective (Dorsch & Dorsch 2008).
In our case, a tube with 6.5 mm internal diameter was used and it is unlikely that infolding occurred. Moreover, the appropriate inflation pressure of the cuff had been applied. A possible explanation for the aspiration may be that the manipulations of the obese dog are difficult and might have resulted in dislodgment of the cuff. This in combination with the fact that GOR had already occurred just after induction, may have led to the aspiration. Another explanation could be that aspiration had already occurred before the introduction of the tube and it was unnoticed.
In clinical veterinary practice, premedication with an opioid can dramatically increase the possibility for GOR, despite the application of proper preoperative fasting to reduce this prevalence. Moreover, complications associated with the endotracheal tubes may occur. In particular, the possibility that pharyngeal secretions or stomach contents could be aspirated before a secure airway is established or may seep through the incompetent larynx during anaesthesia in the presence of a cuffed endotracheal tube into the lungs is not null, and the clinician must always be aware of such a possibility.
Conflict of interest
The authors declare no conflicts of interest.
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