**Abstract**

Pulmonary aspiration in the perioperative period is one of the well-known complications under anesthesia and procedural sedation. A full stomach condition either due to non-adherence to fasting guidelines or due to various other factors that delay gastric emptying are the most common causes. Following aspiration, a patient may develop a wide spectrum of clinical sequelae. The key factors in preventing aspiration include proper pre-operative assessment, appropriate premedication and operating room preparations. Rapid sequence induction and intubation is the recommended technique for securing the airway in cases of full stomach. Management of aspiration depends on the nature of the aspirate. Pre-operative fasting guidelines have been established by various medical societies which may be modified in special circumstances of high risk of aspiration. Prediction of difficult airway in certain cases of full stomach necessitates clinical expertise in airway management.

**Keywords:** pulmonary aspiration, full stomach, gastric volume, rapid sequence induction, negative pressure pulmonary edema

## **1. Introduction**

Full stomach is a condition when a patient has ingested a certain amount of food or drink within a certain period prior to anesthetic induction or believed to have an anatomical, hormonal, metabolic or pathological condition that delays the gastric emptying. The amount of food or Full stomach poses a risk of pulmonary aspiration of gastric contents during the perioperative period more than if the patient had been fasting or definitive time has passed to allow the gastric emptying. Pulmonary aspiration poses a significant risk to each individual surgical patient, affecting the outcome of the surgical care and poses high costs for healthcare system. The incidence of pulmonary aspiration during anesthesia is around 1 in every 2000–3000 surgeries. The National Audit Project 4 (NAP4) by the Royal College of Anesthetists in the UK showed that aspiration was 23% among all reported cases to NAP4 either as a primary or secondary event. Unfortunately, more than 50% of the death related to anesthesia in NAP4 was because of aspiration [1].

#### **2. History**

The first case descriptions of aspiration under anesthesia had been reported in the late 19th century. In 1861, out of the first 51 reported cases that died under Chloroform, Dr. Sanom reported two cases died following sudden vomiting under anesthesia with an estimate of aspiration related mortality of 2%. In 1876 at the Guy's Hospital in UK, the first reported case of death related aspiration after recovery from anesthesia was reported, when a patient turned cyanotic after vomiting in the recovery area, later undigested meat was retrieved from the upper pharynx and trachea was full of vomitus. In U.S.A., the first case was reported in 1898, a 6-year-old boy who had his dinner 3.5 h before anesthesia, has died from aspiration in the recovery. The autopsy confirmed undigested spinach material in the main bronchus [2].

In the 50s of the twentieth century, the danger of a full stomach was realized based on high aspiration rate, but optimum fasting time was insufficiently recognized. The observational studies have found esophageal pooling of incomplete swallowing of fluid are very common under anesthesia. Aspiration risks were found in early 1950 to be high in hemorrhage, bowel obstruction, peritonitis and multiple abdominal surgeries, using of both narcotics and the belladonna alkaloids, and under obstetrics anesthesia, especially if pain and delivery are prolonged. In 1951, aspiration accounts for 4% of overall maternal death, and have reported that aspiration contributed to more than 50% of the mortality [3]. Surprisingly, the aspiration was not limited to inhalation anesthesia; but also, during spinal anesthesia. In 1946, Dr. Mendelson describes the relationship between aspiration of solid and liquid matter, and pulmonary sequelae in obstetric patients. Another tracer dye-based aspiration study 1950 by Dr. Weiss found the minor regurgitations were very common. Interestingly, the incidence rate of blue dye regurgitation was 26% in the pharynx, 16% in the bronchus as confirmed by bronchoscopy, but the frank vomiting occurred in only 8% [4].

Out of the historical recommendations were stomach decompression by a stomach tube pre induction, hyperventilation, head-up position during induction and recovery in lateral position, but no reliable and safe method has been recommended. Sellick's technique of cricoid pressure was introduced in 1961 to prevent regurgitation and aspiration during induction.

#### **3. Physiology of regurgitation and aspiration**

The physiological mechanisms preventing gastric content from regurgitation and aspiration are **lower esophageal sphincter, upper esophageal sphincter** and **protective airway reflex.**

**Upper esophageal sphincter** is the cricopharyngeal muscle acting on the transition zone between esophagus and hypopharynx. **Lower esophageal sphincter (LES)** is composed of circular muscle fiber at the junction of esophagus and stomach, acting as a true sphincter. The difference between Lower esophageal pressure (LOP) and gastric pressure is called the esophageal barrier pressure. Intragastric pressure is less than 7 mmHg, LOP in conscious patient is 15–25 mmHg higher than intragastric pressure. An incompetent LOS reduces barrier pressure and increase the risk of regurgitation. When esophageal pressure equals intragastric pressure, this will lead to a common cavity which in turn causes spontaneous gastroesophageal reflex. LOP decreases during peristalsis, vomiting, pregnancy and various drugs for instance anticholinergic, inhalational

**105**

*Airway Management in Full Stomach Conditions DOI: http://dx.doi.org/10.5772/intechopen.93591*

decrease upper esophageal sphincter tone.

**Protective upper airway reflexes**

the false cord.

10 seconds.

infiltrates [6, 7].

bronchospasm [8].

increasing the risk of aspiration [5].

**3.1 Pathology of lung aspiration**

anesthetics, Thiopentone and opioids. Intragastric pressure increases if gastric volume is more than 1000 ml and with raised intra-abdominal pressure. Gastric volume is influenced by the rate of gastric secretion; approximately 0.6 ml/ kg/h, swallowing of saliva 1 ml/kg/h, ingestion of solid and food and the rate of gastric emptying. LES can be affected by food as (Chocolate, Ethanol and Caffeine), hormones (as Progesterone, Glucagon, Secretin, Cholecystokinin, and Somatostatin), drugs (as Anticholinergic, alpha-adrenergic antagonist, Beta adrenergic agonist, Calcium channel blocker, Diazepam and Morphine) and smoking. All anesthetic agents except Ketamine as well as muscle relaxants

1.Coughing which is forceful expiration after brief inspiration.

2.Laryngospasm is a closure of both false and true vocal cords with apnea.

3.Expiration reflex which lead to sudden opening of the glottis and the closure of

4.Spasmatic panting which involve a rapid closing and opening of the glottis and shallow breathing of around 60 breath per minute for less than

Opioids can blunt all these reflexes except laryngospasm. Reduced consciousness

level in perioperative period including after emergence will affect these reflexes

Pulmonary aspiration is defined by the inhalation of oro-pharyngeal or gastric contents into the larynx and the respiratory tract or the presence of bilious secretions or particulate matter in the tracheobronchial tree. Time frame of perioperative pulmonary aspiration starts from preoperative period until 2 h after termination of anesthesia. Diagnosis of perioperative pulmonary aspiration is made by direct examination of the oral-pharynx, bronchoscopy assessment of the tracheobronchial tree, or postoperative chest X-rays showing new

During the induction of anesthesia, as the patient loses consciousness and the protective airway reflexes are obtunded, the gastric contents, in case of full stomach, may regurgitate through the esophagus and get aspirated into the lungs. Clinical outcomes of pulmonary aspiration range from benign hypoxia and desaturation, to fatal course of Acute Respiratory Distress Syndrome (ARDS), respiratory failure, cardiopulmonary collapse and death (**Figure 1**). The severity of these pulmonary complications depends on the acidity and the volume of gastric contents as well as the immune response of the patient. Small particulate aspiration induces a foreign body reaction of inflammation and consequently results in granuloma formation. Aspiration of acidic content induces acute inflammatory response and progresses rapidly to pneumonitis over 24–48 h. Hypoxia is common due to either upper airway obstruction or obstructed lower airway by debris, thus leading to high airway resistance and vicious cycle of alveolar collapse, alveolar edema and reflex

*Airway Management in Full Stomach Conditions DOI: http://dx.doi.org/10.5772/intechopen.93591*

*Special Considerations in Human Airway Management*

The first case descriptions of aspiration under anesthesia had been reported in the late 19th century. In 1861, out of the first 51 reported cases that died under Chloroform, Dr. Sanom reported two cases died following sudden vomiting under anesthesia with an estimate of aspiration related mortality of 2%. In 1876 at the Guy's Hospital in UK, the first reported case of death related aspiration after recovery from anesthesia was reported, when a patient turned cyanotic after vomiting in the recovery area, later undigested meat was retrieved from the upper pharynx and trachea was full of vomitus. In U.S.A., the first case was reported in 1898, a 6-year-old boy who had his dinner 3.5 h before anesthesia, has died from aspiration in the recovery. The autopsy confirmed undigested spinach material in

In the 50s of the twentieth century, the danger of a full stomach was realized based on high aspiration rate, but optimum fasting time was insufficiently recognized. The observational studies have found esophageal pooling of incomplete swallowing of fluid are very common under anesthesia. Aspiration risks were found in early 1950 to be high in hemorrhage, bowel obstruction, peritonitis and multiple abdominal surgeries, using of both narcotics and the belladonna alkaloids, and under obstetrics anesthesia, especially if pain and delivery are prolonged. In 1951, aspiration accounts for 4% of overall maternal death, and have reported that aspiration contributed to more than 50% of the mortality [3]. Surprisingly, the aspiration was not limited to inhalation anesthesia; but also, during spinal anesthesia. In 1946, Dr. Mendelson describes the relationship between aspiration of solid and liquid matter, and pulmonary sequelae in obstetric patients. Another tracer dye-based aspiration study 1950 by Dr. Weiss found the minor regurgitations were very common. Interestingly, the incidence rate of blue dye regurgitation was 26% in the pharynx, 16% in the bronchus as confirmed by bronchoscopy, but the frank

Out of the historical recommendations were stomach decompression by a stomach tube pre induction, hyperventilation, head-up position during induction and recovery in lateral position, but no reliable and safe method has been recommended. Sellick's technique of cricoid pressure was introduced in 1961 to prevent

The physiological mechanisms preventing gastric content from regurgitation and aspiration are **lower esophageal sphincter, upper esophageal sphincter** and

**Upper esophageal sphincter** is the cricopharyngeal muscle acting on the transition zone between esophagus and hypopharynx. **Lower esophageal sphincter (LES)** is composed of circular muscle fiber at the junction of esophagus and stomach, acting as a true sphincter. The difference between Lower esophageal pressure (LOP) and gastric pressure is called the esophageal barrier pressure. Intragastric pressure is less than 7 mmHg, LOP in conscious patient is 15–25 mmHg higher than intragastric pressure. An incompetent LOS reduces barrier pressure and increase the risk of regurgitation. When esophageal pressure equals intragastric pressure, this will lead to a common cavity which in turn causes spontaneous gastroesophageal reflex. LOP decreases during peristalsis, vomiting, pregnancy and various drugs for instance anticholinergic, inhalational

**2. History**

the main bronchus [2].

vomiting occurred in only 8% [4].

**protective airway reflex.**

regurgitation and aspiration during induction.

**3. Physiology of regurgitation and aspiration**

**104**

anesthetics, Thiopentone and opioids. Intragastric pressure increases if gastric volume is more than 1000 ml and with raised intra-abdominal pressure. Gastric volume is influenced by the rate of gastric secretion; approximately 0.6 ml/ kg/h, swallowing of saliva 1 ml/kg/h, ingestion of solid and food and the rate of gastric emptying. LES can be affected by food as (Chocolate, Ethanol and Caffeine), hormones (as Progesterone, Glucagon, Secretin, Cholecystokinin, and Somatostatin), drugs (as Anticholinergic, alpha-adrenergic antagonist, Beta adrenergic agonist, Calcium channel blocker, Diazepam and Morphine) and smoking. All anesthetic agents except Ketamine as well as muscle relaxants decrease upper esophageal sphincter tone.

## **Protective upper airway reflexes**


Opioids can blunt all these reflexes except laryngospasm. Reduced consciousness level in perioperative period including after emergence will affect these reflexes increasing the risk of aspiration [5].

#### **3.1 Pathology of lung aspiration**

Pulmonary aspiration is defined by the inhalation of oro-pharyngeal or gastric contents into the larynx and the respiratory tract or the presence of bilious secretions or particulate matter in the tracheobronchial tree. Time frame of perioperative pulmonary aspiration starts from preoperative period until 2 h after termination of anesthesia. Diagnosis of perioperative pulmonary aspiration is made by direct examination of the oral-pharynx, bronchoscopy assessment of the tracheobronchial tree, or postoperative chest X-rays showing new infiltrates [6, 7].

During the induction of anesthesia, as the patient loses consciousness and the protective airway reflexes are obtunded, the gastric contents, in case of full stomach, may regurgitate through the esophagus and get aspirated into the lungs. Clinical outcomes of pulmonary aspiration range from benign hypoxia and desaturation, to fatal course of Acute Respiratory Distress Syndrome (ARDS), respiratory failure, cardiopulmonary collapse and death (**Figure 1**). The severity of these pulmonary complications depends on the acidity and the volume of gastric contents as well as the immune response of the patient. Small particulate aspiration induces a foreign body reaction of inflammation and consequently results in granuloma formation. Aspiration of acidic content induces acute inflammatory response and progresses rapidly to pneumonitis over 24–48 h. Hypoxia is common due to either upper airway obstruction or obstructed lower airway by debris, thus leading to high airway resistance and vicious cycle of alveolar collapse, alveolar edema and reflex bronchospasm [8].
