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Aspiration of stomach contents into the lungs is a serious com-plication that may cause pneumonia and result in the following clinical picture: tachycardia, dyspnea, central cyanosis, hyperten-sion, hypotension, and finally death. It can occur when the pro-tective airway reflexes are decreased or absent from a variety of factors (Chart 23-11).
The primary factors responsible for death and complications after aspiration of gastric contents are the volume and character of the aspirated gastric contents. For example, a small, localized aspira-tion from regurgitation can cause pneumonia and acute respira-tory distress; a massive aspiration is usually fatal.
A full stomach contains solid particles of food. If these are as-pirated, the problem then becomes one of mechanical blockage of the airways and secondary infection. During periods of fasting, the stomach contains acidic gastric juice, which, if aspirated, may be very destructive to the alveoli and capillaries. Fecal contami-nation (more likely seen in intestinal obstruction) increases the likelihood of death because the endotoxins produced by intesti-nal organisms may be absorbed systemically, or the thick pro-teinaceous material found in the intestinal contents may obstruct the airway, leading to atelectasis and secondary bacterial invasion.
Aspiration pneumonitis may develop from aspiration of sub-stances with a pH of less than 2.5 and a volume of gastric aspirate greater than 0.3 mL per kilogram of body weight (20 to 25 mL in adults) (Marik, 2001). Aspiration of gastric contents causes a chemical burn of the tracheobronchial tree and pulmonary parenchyma (Marik, 2001). An inflammatory response occurs. This results in the destruction of alveolarâ€“capillary endothelial cells, with a consequent outpouring of protein-rich fluids into the interstitial and intra-alveolar spaces. As a result, surfactant is lost, which in turn causes the airways to close and the alveoli to col-lapse. Finally, the impaired exchange of oxygen and carbon diox-ide causes respiratory failure.
Aspiration pneumonia develops following inhalation of colo-nized oropharyngeal material. The pathologic process involves an acute inflammatory response to bacteria and bacterial products. Most commonly, the bacteriologic findings include gram-positive cocci, gram-negative rods, and occasionally anaerobic bacteria (Marik, 2001).
Prevention is the primary goal when caring for patients at risk for aspiration.
Aspiration is likely to occur if the patient cannot adequately co-ordinate protective glottic, laryngeal, and cough reflexes. This hazard is increased if the patient has a distended abdomen, is in a supine position, has the upper extremities immobilized by in-travenous infusions or hand restraints, receives local anesthetics to the oropharyngeal or laryngeal area for diagnostic procedures, has been sedated, or has had long-term intubation.
When vomiting, a person can normally protect the airway by sitting up or turning on the side and coordinating breathing, coughing, gag, and glottic reflexes. If these reflexes are active, an oral airway should not be inserted. If an airway is in place, it should be pulled out the moment the patient gags so as not to stimulate the pharyngeal gag reflex and promote vomiting and as-piration. Suctioning of oral secretions with a catheter should be performed with minimal pharyngeal stimulation.
Even when the patient is intubated, aspiration may occur even with a nasogastric tube in place. This aspiration may result in nosocomial pneumonia. Assessment of tube placement is key to prevent aspiration. The best method for determining tube place-ment is via an x-ray. There are other nonradiologic methods that have been studied. Observation of the aspirate and testing of its pH are the most reliable. Gastric fluid may be grassy green, brown, clear, or colorless. An aspirate from the lungs may be off-white or tan mucus. Pleural fluid is watery and usually straw-colored (Metheny & Titler, 2001). Gastric pH values are typically lower or more acidic that that of the intestinal or respiratory tract. Gastric pH is usually between 1 and 5, while intestinal or respi-ratory pH is 7 or higher (Metheny & Titler, 2001). There are dif-ferences in assessing tube placement with continuous versus intermittent feedings. For intermittent feedings with small-bore tubes, observation of aspirated contents and pH evaluation should be performed. For continuous feedings, the pH method is not clinically useful due to the infused formula (Metheny & Titler, 2001).
The patient who is receiving continuous or timed-interval tube feedings must be positioned properly. The patient receiving a con-tinuous infusion is given small volumes under low pressure in an upright position, which helps to prevent aspiration. Patients re-ceiving tube feedings at timed intervals are maintained in an up-right position during the feeding and for a minimum of 30 minutes afterward to allow the stomach to empty partially. Tube feedings must be given only when it is certain that the feeding tube is posi-tioned correctly in the stomach. Many patients today receive en-teral feeding directly into the duodenum through a small-bore flexible feeding tube or surgically implanted tube. Feedings are given slowly and regulated by a feeding pump. Correct placement is confirmed by chest x-ray.
A full stomach may cause aspiration because of increased intra-gastric or extragastric pressure. The following clinical situations cause a delayed emptying time of the stomach and may con-tribute to aspiration: intestinal obstruction; increased gastric secretions in gastroesophageal reflex disease; increased gastric se-cretions during anxiety, stress, or pain; or abdominal distention because of ileus, ascites, peritonitis, use of opioids and sedatives, severe illness, or vaginal delivery.
When a feeding tube is present, contents are aspirated, usually every 4 hours, to determine the amount of the last feeding left in the stomach (residual volume). If more than 50 mL is aspirated, there may be a problem with delayed emptying, and the next feeding should be delayed or the continuous feeding stopped for a period of time.
Prolonged endotracheal intubation or tracheostomy can depress the laryngeal and glottic reflexes because of disuse. Patients with prolonged tracheostomies are encouraged to phonate and exer-cise their laryngeal muscles. For patients who have had long-term intubation or tracheostomies, it may be helpful to have a reha-bilitation therapist experienced in speech and swallowing disor-ders work with the patient to assess the swallowing reflex.
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