Acute Aspiration of Gastric Contents (Mendelson Syndrome)
Aspiration is defined as the inhalation of oropharyngeal or gastric contents into the larynx and lower respiratory tract. Several pulmonary syndromes may occur after aspiration, depending on the amount and nature of the aspirated material, the frequency of aspiration, and the host’s response to the aspirated material.
Acute aspiration of gastric contents may be catastrophic. The pulmonary response depends on the characteristics and amount of gastric contents aspirated. The more acidic the material, the greater the degree of chemical pneumonitis. Aspiration of pure gastric acid (pH < 2.5) causes extensive desquamation of the bronchial epithelium, bronchiolitis, hemorrhage, and pulmonary edema. Acute gastric aspiration is one of the most common causes of ARDS.
- Reduced consciousness resulting in a compromise of the cough reflex and glottic closure.
- Neurological dysphagia.
- Disorders of the upper gastrointestinal (GI) tract, including oesophageal disease, surgery involving the upper airways or oesophagus, and gastric reflux.
- Disruption of the gastro-oesophageal junction due to tracheostomy, endotracheal intubation, bronchoscopy, upper endoscopy, and nasogastric feeding.
- General anaesthesia.
- Extremes of age.
Known as Mendelson’s syndrome, as described by the obstetrician in 1946, this condition involves lung tissue damage as a result of aspiration of non-infective but very acidic gastric fluid. This usually occurs in two phases – firstly desquamation of the bronchial epithelium causing increased alveolar permeability. This results in interstitial oedema, reduced compliance and VQ mismatch. The second stage, occurring within 2 to 3 hours, is due to an acute inflammatory response, mediated by proinflammatory cytokines such as tumour necrosis factor alpha and interleukin 8 and reactive oxygen products. Clinically, this may be asymptomatic, or present as tachypnoea, bronchospasm, wheeze, cyanosis and respiratory insufficiency.
This occurs either as a result of inhaling infected material or secondary bacterial infection following chemical pneumonitis. It is associated with typical symptoms of pneumonia such as tachycardia, tachypnoea, cough and fever, and may be evidenced by segmental or lobar consolidation (classically right middle lobe) on chest radiography. The disease process is similar to a community acquired pneumonia although the complication rate is higher, with cavitation and lung abscess occurring more commonly.
If particulate matter is aspirated, acute obstruction of small airways will lead to distal atelectasis. If large airways are obstructed, immediate arterial hypoxaemia may be rapidly fatal.
Signs and symptoms
The clinical picture is one of abrupt onset of respiratory distress, with cough, wheezing, fever, and tachypnea. Crackles may be audible at the bases of the lungs. Hypoxemia may be noted immediately after aspiration occurs.
Radiographic abnormalities, consisting of patchy alveolar opacities in dependent lung zones, appear within a few hours. If particulate food matter has been aspirated along with gastric acid, radiographic features of bronchial obstruction may be observed. Fever and leukocytosis are common even in the absence of infection.
The commonly quoted figures of a critical volume of 25ml of aspirate, with a pH < 2.5 being sufficient to cause aspiration pneumonitis are derived from unpublished work by Roberts and Shirely on Rhesus monkeys, and extrapolated to humans. In fact 50% of fasted patients have a residual gastric volume exceeding this, with an average pH of around 2.0. Unnecessarily prolonged nil by mouth (NBM) orders lead to dehydration and possibly hypoglycaemia, with resultant thirst, hunger, discomfort and irritability. Current guidelines are 2 hours for clear fluids, 4 hours for breast milk, and 6 hours for a light meal, sweets, milk (including formula) and non clear fluids.
Histamine (H2) antagonists and proton pump inhibitors (PPIs) are commonly used to increase gastric pH, although they do not affect the pH of fluid already in the stomach. Oral sodium citrate solution reliably elevates gastric pH above 2.5, but it increases gastric volume, and is associated with nausea and vomiting. H2 antagonists act by blocking H2 receptors of gastric parietal cells, thereby inhibiting the stimulatory effects of histamine on gastric acid secretion. PPIs on the other hand, block the ‘proton pump’ of the same cell, inhibiting the stimulatory actions of histamine, gastrin and acetylcholine.
An oral H2 antagonist must be given 1-2 hours before anaesthesia, and a PPI, 12 hours in advance. A recent meta-analysis by Clark et al suggested that ranitidine was superior to PPIs in both reducing gastric fluid volume and acidity. Its use is recommended in patients at risk of aspiration only, not routinely. Metoclopramide has a prokinetic effect promoting gastric emptying, but there is little evidence to support its use. It does however, remain part of the usual pre-medication for Caesarean section under general anaesthetic.
It has been shown that most cases of aspiration occur on induction and laryngoscopy, hence the following is of the utmost importance. For patients at high risk of aspiration, a RSI is the induction of choice unless presented with a sufficiently difficult airway to warrant an awake fibreoptic intubation. The patient should be on a tilting trolley, with suction to hand. Three minutes of pre-oxygenation precede the administration of an induction agent, cricoid pressure (discussed below) and the rapidly acting muscle relaxant succinylcholine. This avoids the need for bag-mask ventilation and the possibility of gastric insufflation. Adequate depth of anaesthesia is important to avoid coughing, laryngospasm and vomiting. Cricoid pressure is not released until confirmation of appropriate placement of the tracheal tube with the cuff inflated.
First described by Sellick in 1961, cricoid pressure remains an essential manoeuvre performed as part of RSI despite significant controversy. The aim is to compress the oesophagus between the cricoid ring cartilage and the sixth cervical vertebral body thus preventing reflux of gastric contents. The force recommended is 30N, or that required to close the oesophagus without distorting the airway. This latter complication is the greatest limiting feature of the manoeuvre, causing malalignment, distortion of the cricoid ring and possible closure of the vocal cords. Even when applied correctly there is doubt as to its efficacy, simply causing anatomical displacement of the oesophagus in some people, and non compression in others. In addition, manometry studies have shown it to reduce LOS tone thus reducing barrier pressure. Cricoid pressure should be released in the case of active vomiting to avoid oesophageal rupture.
Patients for emergency theatre with intestinal obstruction frequently have a nasogastric tube in situ. There is evidence from cadaver studies that this does not alter the efficacy of cricoid pressure. Furthermore it can be useful to empty the stomach before induction of anaesthesia. Studies have shown that there is no significant difference between the incidence of gastroesophageal reflux with large or small bore tubes.
A cuffed endotracheal tube is considered the gold standard device used for airway protection. However, it has disadvantages – cardiovascular and respiratory instability, postoperative hoarseness, sore throat, increased length of stay in recovery to name but a few. It has also been suggested that microaspiration of secretions occuring between the cuff and tracheal mucosa plays a role in ventilator acquired pneumonia. Alternative supraglottic devices include the classic Laryngeal Mask Airway (LMA) and the Proseal LMA, the latter providing a higher seal pressure (up to 30cmH20) and a drainage channel for gastric contents. These have excellent safety records, and can be used for positive pressure ventilation although the main contraindication to their use is an increased risk of regurgitation.
It should be remembered that those patients at risk of aspiration on induction are similarly at risk on emergence. Care should be taken to ensure that their airway reflexes have fully returned before extubation occurs.
Patients with an observed aspiration should be placed in the head-down position on the right side and should have also immediate tracheal suction to maintain a clear airway. However, this manoeuvre will not protect the lungs from chemical injury, which occurs instantly in a manner that has been compared with a ‘flash burn’. The acid inoculum is rapidly neutralized by the physiological response. Pulmonary lavage is futile, since the full extent of injury has usually occurred by the time the diagnosis is recognized.
The major therapeutic approach is to correct hypoxia and support pulmonary function by assisted ventilation or positive-pressure oxygen. Endotracheal intubation should be considered for patients who are unable to protect their airways.
The use of corticosteroids in the treatment of chemical pneumonitis is controversial. Studies in animals have failed to demonstrate beneficial effects of corticosteroids on pulmonary function, lung injury, alveolar–capillary permeability, or outcome after acid aspiration. Furthermore, given the failure of two multicentre, randomized controlled trials to demonstrate a benefit of high-dose corticosteroids in patients with ARDS, the administration of corticosteroids cannot be recommended.
Although it is common practice, the prophylactic use of antibiotics in patients in whom aspiration is suspected or witnessed is not recommended. Similarly, the use of antibiotics shortly after aspiration in patients in whom a fever, leukocytosis, or a pulmonary infiltrate develops is discouraged, since the antibiotic may select for more resistant organisms in patients with an uncomplicated chemical pneumonitis.
However, empirical antibiotic therapy is appropriate for patients who aspirate gastric contents, and who have small-bowel obstruction or other conditions associated with colonization of the gastric contents. Antibiotic therapy should be considered for patients with aspiration pneumonitis that fails to resolve within 48 hours following aspiration.
Empirical therapy with broad-spectrum agents is recommended; antibiotics with anaerobic activity are not routinely required. Sampling of the lower respiratory tract (with a protected specimen brush or by broncho-alveolar lavage) and quantitative culture in intubated patients may allow targeted antibiotic therapy, or in patients with negative cultures, the discontinuation of antibiotics.