The incidence of perioperative regurgitation and aspiration in surgical patients is likely higher than is commonly appreciated by practising anesthesiologist.That this phenomen occurs and often may go unrecognized is inconvertible. On the otherhand wether such unrecognized aspiration lead to a higher incidence of perioperative respiratory complications is a matter of debate.
Nevertheless it is stark reality that clinically significant aspirations do on occasion occur resulting in markedly increased patient morbidity(4).
However not all who aspirate during or after anesthesia suffer damage to the lungs while sometimes there may be a mild bronchopneumonia with only slight systemic upset.(5)
However,the aspiration pneumonitis threatens life more than of these and will be considered in greater detail.
DEFINITION :
Pulomary aspiration is defined as the presence of bilions secretions or particulate matter in the tracheobronchial tree.(3)
Aspiration pneumonitis is the lung's reaction to the pulmonary aspiration which result from chemically(gastric contents) induced damage to lung tissue.(3)
Pulmonary aspiration of pharyngeal liquid is fairly common and usually is without squelae. However when the aspiration exceeds a certain frequency or volume and contained pathogenic organism,aspiration pneumonia result.
Aspiration pneumonitis(Mendelson Syndrome) and aspiration pneumonia may progress to the Adult Respiratory Distress Syndrome(ARDS).
The process must be bilateral on chest radiograph and acute in onset.
There must be a known risk factor such as shock ,sepsis or trauma.
The patient must have hypoxaemia and must have a left atrial pressure less than 19mmHg to differentiate congestive heart failuire(CHF) as a primary cause.(3)
Pulmonary aspiration has two basic component (1)
First : Gasric contents must either escape or be propelled
from the stomach into the oropharynx.
Second: They must enter the lung.
The pulmonary aspiration of gastric contents can produce a variety of hazardous squelae,depending on the nature of the aspirate.
Aspiration may include the following :
- Large food fragment,which can obstruct the airway
rapidly causing asphyxia.
- Small particles (e.g.particulate antacids) which can
produce severe granulomatous infection.
- gastric acids, which can induce chemical pneumonitis
- blood and digestive enzymes which relatively innocuous.
- excrementious material which can cause severe infectious
pneumonia.
INCIDENCE :
The most current retrospective study by Olsson et all noted an incidence as aspiration 1 of in 2131 or 0,05%.(4)
The likelihood of pulmonary aspiration is three to four times greater for emergency surgery than the elective surgery.(1)
Aspiration of gastric contents to the lungs account for at least 10% of deaths attributable to aneaesthesia.(5)
Children and elderly are more likely to aspirate than are patients of intermediate age.(1).
76% of pediatric patients have gatric content whose pH is less than 2,5 and whose volume is greater than 0,4 ml/kg versus 32% to 55% of adults who meet these criteria.(3).
Onethird to onehalf of manifest pulmonary aspiration occurs during anesthesia induction or laryngoscopy, onefifth to onethird occurs during emergence from anesthesia and extubation.(1)
Pediatric who aspirate during anesthesia 40% actively vomit and remainder passively regurgitation.
When anesthetized patients aspirate, 80% do so during induction, 14% during emergence, 4% during procedure and 2% post operatively.(3)
The preoperative factor most often ascociated with aspiration is gastrointestinal obstruction.
Absence of predisposing factors,two third of such episodes are complication of unanticipated difficult in airway management.(1)
PATHOPHYSIOLOGY MECHANISM :
Multiple mechanism are involved including reflex airway closure, alteration of surfactant,and interstitial and alveolar odema as well as in somecases obstruction of
small airways.(6)
For regurgitation to occur,the intragastric pressure must exceed the barrier pressure in the lower oesophageal(the barrier pressure=the lower oesopha geal sphincter(LES) pressure minus the intragastric pressure).(3)
Following aspiration,reflex laryngospasm and bronchospasm result because of chemical and physical irritation of the airway.
These changes are usually most severe in the first one and onehalf hours after aspiration.
When highly acidity materials are aspirated loss of capillary permeability as well as intensive inflamatory reactions with odem,hemorrhage and necrosis account for continued hypoxia.
Pulmonary injury can occur within 12-18 seconds,and extensive atelectasis by 3 minutes. By 1 hour after pulmonary aspiration, pulmonary injury has progressed to the bronchial epithelial degeneration, pulmonary edema and hemorrhage. The consequent increased pulmonary capillary leak is followed by neutrophil response. As a result of alveolar cell damage,fluid and protein move into the alveoli and interstitium and reduce pulmonary surfactant
activity and the large fluids shift may also cause loss of intravascular volume. Hypotension occuring after aspiration usually indicates extensive lung damage and has been shown to be a poor prognostic sign.
CLINICAL FEATURES :
Signs and symptoms can appear immediately or after several hours.
If the patient has been breathing spontaneously there is an initial periods of apnoe followed by rapid shallow breathing and obvious distress.
A potentially fatal asthma like syndrome,showed cyanosis,
cough and dyspnoe ascociated with bronchospasm;
scattered moist sounds in the lung and tachycardia
(Mendelson's syndrome).(6)
Rales and ronchi may audible in affected lung regions where a whezing may be prominent in only onethird of patients with pulmonary aspiration.(5)
Pulmonary odema may also be ascociated with pink,frothy sputum.
Both brochial obstruction and pulmonary edema can induce profound hypoxaemia.The arterial PO2 is reduced markedly usually sufficiently to cause cyanosis, but the arterial PCO2 may be unchanged or increased.(5).
Tachycardia can result from respiratory distress and hypotension from intravascular hypovolemia due to massive leakage of fluid through damaged pulmonary capillaries probably neurogenic origin.(1,5)
Following aspiration,the intrapulmonary shunt may be as much as 50% of cardiac output (Cameron et all 1972)(5).
Initially X ray of the lungs reveal patchy opacities which may be uni or bilateral. No particular radiographic pattern is specific to pulmonary aspiration it depend on the volume of material inhaled and the patient's position during aspiration. In supine adult patients the bronchial anatomy most commonly directs foreign matter into the right lower lobe and less frequently into the left upper lobe.(5,7)
The clinical and radiological changes in the lung in advanced form of aspiration pneumonitis are undistinguishable from ARDS.
RISK FACTORS :
I.ESCAPE OF GASTRIC CONTENTS :
Due to
1. Active vomiting can provoked by:
- gastrointestinal obstruction
- opioids
- cricoid pressure
- hypotension
2. Passive regurgitation is promoted by:
- gastrointestinal obstruction
- diabetic gastroparesis
- gastroesophageal reflux
- increased intragastric pressure
- decreased lower oesophageal sphincter(LES)
tone is weakened by nicotine,caffeine,fatt and gastric
acid.
3. Other factors :
- Impaired laryngeal protective reflex can result from
neurologic or neuromuscular
disorders, sedative/narcotic or anesthesia.
- Difficult airway management.
II. VOLUME AND CHARACTER OF GASTRIC VOLUME :
- Increased volume of gastric contents
- Increased of acidity of gastric contents
- Particulate matter in stomach
- Feculent matter in aspirate
As a rule the larger the volume aspirate the poorer the prognosis. Increased volume alone may overcome any protection efforded by strength of LES tone (aspirate volume greater than 0,4 ml/kg(20-25 ml) in adult is fatal.(4)
Although the normal stomach appearently passes clear liquids within 2-3 hours,clearance of solids may require 6 hours or longer.
Gastic emptying may be inhibited by diabetic gastroparesis. Gastric acids secretion is thought to be stimulated by ethenol, hypoglycaemia and anxiety.
Indeed the acidity of the aspirate is probably the most important factor contributing to the severity of pneumonitis (Mendelson 1946).(5)
For many years it has been held that gastric contents must have pH less than 2,5 in other cause lung damage bur recent studies shown that gasric contents with pH greater than 2,5 also cause respiratory distress and pneumonitis especially when there is food matter in the aspirate.(6)
The risk of pulmonary aspirates due to high gastric residual volume in morbidity obese patients appears to be exaggerated.
Remarkably,there is little evidence that obese patients have a higher incidence of gastroesophageal reflux as aspiration pneumonitis.
In fact a study of 256 fasted patients revealed significantly gastric residual volume in obese patients(BMI > 30) compared with controls.
Patients with BMI>30 who drank 300 ml of clear fluid 2 hours preoperatively had no increase in gastric residual volume or decrease in gastric pH compared to fasting controls and therefore rapid squence induction for airway protection is unnecessary for most the obese patients.(2)
to be continued
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