MANAGEMENT :
The first periority is to clear the upper airway and prevent asphyxia.
Whenever an aspiration is observed endotracheal suctioning should be attempt promptly even if difficult intubation precipitated the aspiration.
Bronchopulmonary lavage is not recomended for acidic aspirates because damage to the lungs occurs within 12 to 18 seconds(3).
In addition more extensive pulmonary damage may occur due to the spread of acidic aspirates to lower regions of the lung.
An immediate danger of particulate aspirates is mechanics obstruction.
Bronchoscopy to remove particulate materials should be performed in this situation. Bronchoscopy is indicated for any patients who shows clinical or rongentnologic signs of large airway obstruction.
Lobar and segmental collapse or atelectasis are the usual findings.
Large food particles may also cause a ball valve obstruction.
Expiratory film or fluoroscopy can confirm this diagnosis.
In these cases bronchoscopy with straight scope is the most effective means of removing aspirated material.a(5,6).
Postural drainage and respiratory therapy with bronchodilators may be useful.
It had been hoped that corticosteroid might interrupt the pulmonary inflamatory response to acid aspiration and ameliorate the subsequent clinical course. Unfortunately after decades of investigation no beneficial effect has been shown (3,5).
There is controversy about the value of systemic steroids in reducing bronchial odema and the alveolar exudate.
Although corticosteroid may attenuate inflamatory pneumonitis the immuno suprresant effect glucocorticoid may exacerbate any seondary bacterial pneumonia or sepsis (3,5).
Secondary bacterial invasion may be an additional threat to recovery and samples of bronchial aspirates should be cultured by bacteriologist.
The use of prophylactic antibiotics cannot be shown to improve the course of the disease or reduce mortality.(5)
The most important measure after pulmonary aspiration is maintainance of pulmonary gas exchange.
Often mechanical ventilation is instituted immediately after any major pulmonary aspiration.Although the prophylactic beneficities of positive pressure ventilation and positive end expiratory pressure on the development
of subsequent lung injury have been debated, such measures are often required merely to provide adequate oxygenation.
PREVENTION :(1,3,4)
Includes :
1.Save airway management
2.Cricoid pressure
3.Gastric tube the compression
4.Chemoprophylaxis
- Clear citrate antacids
- H2 receptor histamine antagonist
- Proton pump inhibitors
- Gastro prokinetic agents
Careful and skill airway management is very needed to reduced pulnary aspiration.
Cricoid pressure(Sellick's manouver) when properly applied can prevent the passage of gastric contents into oropharynx, however it may also provokes active vomiting in an unanesthetized patient.
In addition backward pressure on the cricoid cartilage facilitate laryngoscopy in some patients but interference with it in others. Infact in some patients pushing the larynx posteriorly,cephalad and to the right provides the best view of vocalcord but can also impede mask or larygeal mask airway ventilation.
Cricoid pressure during active vomiting has the potential to cause oesophageal rupture, Nasogastric tube permits gastric decompression,it also prevent lowoesopageal sphincter (LES) closure.
Chemoprophylaxis :
Antacids: Many investigators have demonstrated that particulate antacids are effective in raising gastric fluid pH in reasonably high precentage in both elective and emergent situation.
Indeed their effectiveness in raising fluid pH depends on :
1.The volume and pH of the gastric contents present at the time of their administration.
2.The frequency and timing of antacid administration.
3.The type and amount of antacid given.
4.What manouvers it any are done to promote mixing of antacid with gastric contents.
5.The intrinsix gastric motility present at the time of antacid administration.
6.The rate of ongoing gastric acid production.
The First :
Their administration may increase gastric volume. As example routine of 2-4 hour dosing with antacid became common practice on many obstetrical wards because of the unpredictability of emergency induction of anesthesia as well as concern over acid rebound(a decrease in pH over basal levels four or more hours following antacid neutralization). In the laboring patient(particularly those receiving narcotic for pain) gastric motility is slowed.
Thus such a practice could lead to significant increases in gastric volume.
The second :
Major criticism is that particulate aspirates result not only in as significant of initial pulmonary derangement as a highly acidic aspirate but also in histologic abnormalities that were present as long as one month following aspiration.
These chronic granulomatous response were not noted in groups with acid aspirates.
Particulate antacids are hazardous to the lungs and are therefore contra indicated preoperatively.
Because of these concerns an intense interest has been sparked in soluble antacids.
The propenderance of evidence suggest that soluble antacids are as effective as particulate antacids in raising gastric fluid pH in both elective or emergency surgical patients if given within 15-60 minute of induction of anaesthesia(4).
Work has demonstrated that soluble antacids mix with gastric contents more readily than particulate antacids.
Sodium citrate 0.5-1 ml/kg (30 ml max;1 hour preoperatively may increase gatric volume,but decreases gastric fluid pH and no changes in LES tone).
It must be kept in perspective that antacids remain the most rialable pharmacologic method of neutralizing gastric acid in emergent situation.
HISTAMINE H2 RECEPTOR ANTAGONIST :
(e.g.cimetidine,ranitidine and famotidine)(1,4).
The H2 blockers decrease gastric acid production by competitively inhibiting the action of histamine on the H2 receptor of gastric pariethal cell. In contrast they have no apparent effect on gastric emptying time or the lower esophageal sphincter(LES) pressure. Administration of cimetidine intravenously one hour before induction of anesthesia in patients presenting for elective surgery has been shown to signifantly decrease the acidity of gastric contents in samples taken immediately following the induction of anesthesia.
A delay onset of cimetidine ,60-90 minutes following intravenous administration limit its usefulness in emergence situation.
The cimetidine has been reported to inhibit the mixed function oxydase system and to decrease liver blood flow.
Co administration of cimetidine will prolonge the elemination half life of warfarin,diazepam,theophylline,phenythoin and propranolol.
That cimetidine therapy can agravate bronchospasm in asthmatics by allowing histamine to have an opposed H1 effect.
Rapid intravenous administration of relatively large doses(600 mg) of cimetidine in critically patients has been reported to cause hypotension and significant dysrythmia.
Ranitidine has greater potency, longer duration of gastric anti secretory effect (six to eight hours) than cimetidine (four to six hours) and lower incidence of side effects and lesser degree of inhibition of mixed function oxydase system but their clinical utility is limited in truly emergent surgical patients since its onset of action is no more rapid than that of cimetidine 45-60 minutes following intravenous administration.
Famotidine is propanimidamide derivative is the lattest H2 receptor antagonist. Clinical used dosages supress acids production for 10 to 12 hours intravenous administration may be ascociated with slightly faster onset of anti
secretory effect (30 minutes) compared to other H2 receptor antagonist thus offering a limited advantage of famotidine in emergent situation.
Systemic effect of famotidine in the CNS,cardiovascular,respiratory or endocrine system have been negligible to date and minimal drug interactions
have been identified in clinical trials.
PROTON PUMP INHIBITOR
(e.g omeprazole,lansoprazole,pantoprazole).
Similarly effective in reducing further gastric acids production but they have no demonstrable advantage over the H2 histamine receptor antagoinist. For aspiration prophylax.
GASTRO PROKINETIC (e.g.metoclopropamide).
A chlorbenzamide derivative which possesses three characteristic which make it potentially very useful in anestesia.
It increases the LES pressure,speeds gastric emptying time, and has anti emetic properties. It has no direct effect on gastric fluid pH.
Its action are mediated centrally via antidopaminergic effects and peripherally by facilitation of cholinergic stimulation, an action predominately limited
to the upper gastric intestinal tract.
Diabetes and others with known or suspected gastroparesis are likely the best candidate for gastroprokinetic medication.
A 10 or 20 mg intravenous dose of metoclopropamide can empty the stomach within 10-20 minutes whereas an oral dose taken 30-60 minutes.
But it is contraindicated to attempt to increase gastrointestinal motility in the presence of intestinal obstruction.
In the dose range commonly employed (0,15 to 0,3 mg)kg, metoclopropamide has proven relatively safe.
Higher dosages especially in children has been ascociated with agitation,irritability,confusion and extrapyramidal symptoms(4).
Pharmacologic agents used for the prophylaxis of pulmonary aspiration in children.(3)
Antacids GV pH LES tone
=====================================================================
Sodium citrate 0,5 - 1 ml/kg I I 0
(30 ml max;1 hr BS )
Anti cholenergic:
Glycopyrolate 7,5-10 microgram/kg 1 hr BS ? ? 0
H2 blocker :
Cimetidine 7,5 mg/kg (PM/AM) D I 0
Ranitidin 1,5- 2mg/kg (1-2 hr BS) 0 I 0
Famotidine 0,5 mg/kg (PM/AM) D I 0
Prokinetic agents::
Metoclopropamide:0,1mg/kg (1 hr BS) D 0 I
Proton pump inhibitor :
Lansoprazole 1,5 mg/kg (PM/AM) D I 0
Omeprazole 0,3 mg/kg (PM/AM) D 1 0
Pantoprazole 1,4 mg/kg QID D I 0
======================================================================
hr=hour BS=before surgery PM=night before AM=morning of surgery
GV=gastric volume, pH=pH gastric contents LES=low esophageal sphincter
I=increase D=decrease 0=no effect.
======================================================================
Extubation in patient at high risk for pulmonary aspiration should be performed when the patient fully awake and has full return of neuromuscular functions (3).
SUMMARY :
Aspirations of gastric contents to the lungs account for at least 10 percent of deaths attributable to anaesthesia.
The likelihood of pulmonary aspiration is three to four times greater for emergency surgery than the elective surgery.
The preoperative factor most often ascociated with aspiration is gastrointestinal obstruction.
The classic symptoms complex associated with pulmonary aspiration is sudden in onset,with wheezing,shortness of breath, cyanosis and tachycardia.
Pneumonitis aspiration which result from chemically induced damage to lung tissue where pneumonia aspiration is caused by a bacterial infections.
The first periority of treatment is to clear the upper airway and prevent asphyxia. Endotracheal suctioning should be attempt promptly whenever an aspiration is observed.
Brochoscopy is indicated for any patients who shows clinical or rongentnologic signs of large airway obstruction.
Bronchopulmonary lavage is not recomended for acidic aspirate because damage to the lungs occurs within 12 to 18 seconds, in addition more extensive pulmonary damage may occur due to the spread of acidic aspirates to lower regions of the lungs.
The use of prophylactic antibiotics cannot be shown to improve the course of the disease or reduce mortality.
The use of corticosteroid not recomended because the immuno supressant effect of corticosteroid may exacerbate any secondary bacterial pneumonia or sepsis.
Particulate antacids are hazardous to the lungs and therefore contraindicated preoperatively.
The most important measure after pulmonary aspiration is maintainance of pulmonary gas exchange.
REFERENCES
1.Tasch D.Mark : Pulmonary Aspiration ;Atlee L.John: Complications in Anesthesia,2nd edit,Saunders Elsevier,2007. pp 186-88.
2.Meyer mark : Perioperative Aspiration Pneumonitis ;Atlee l.John: Complications in Anesthesia;2nd edit,Saunders Elsevier,2007. pp 641-43.
3.Schultetin.R.Ray : Aspiration Pneumonitis;Atlee.L.John:Complications in Anesthesia;2nd edit,Saunders Elsevier,2007,pp 157-60.
4.Mc Cammon L.Ri : Aspiration Pneumonitis Prophylaxis and Prevention; International Anesthesia Research Society,Review Course Lectures, San Diego california ,1988,pp.40-44.
5.Spence A.Alastair : Post operative Pulmonary Complication;Nun.FJ,Utting EJ Brown R.Burmell;General Anaesthesia,5th edit;Butterworths ,London,Boston,1989.pp.1153-4.
6.Wynne W.James : Aspiration Pneumonitis;Ravin B.Mark:Problems in Anesthesia; A Case Study Approach;Little Brown and Company,Boston.1981,pp 237-41.
7.Lebowitz W.Philip,:Emergency Complicating Anesthesia.Lebowitz.W.Philip Clark L.John. Clinical Anesthesia Procedures of the Massachusetts General Hospital,Little Brown and Company,Boston, 1978,pp.350-1.
The first periority is to clear the upper airway and prevent asphyxia.
Whenever an aspiration is observed endotracheal suctioning should be attempt promptly even if difficult intubation precipitated the aspiration.
Bronchopulmonary lavage is not recomended for acidic aspirates because damage to the lungs occurs within 12 to 18 seconds(3).
In addition more extensive pulmonary damage may occur due to the spread of acidic aspirates to lower regions of the lung.
An immediate danger of particulate aspirates is mechanics obstruction.
Bronchoscopy to remove particulate materials should be performed in this situation. Bronchoscopy is indicated for any patients who shows clinical or rongentnologic signs of large airway obstruction.
Lobar and segmental collapse or atelectasis are the usual findings.
Large food particles may also cause a ball valve obstruction.
Expiratory film or fluoroscopy can confirm this diagnosis.
In these cases bronchoscopy with straight scope is the most effective means of removing aspirated material.a(5,6).
Postural drainage and respiratory therapy with bronchodilators may be useful.
It had been hoped that corticosteroid might interrupt the pulmonary inflamatory response to acid aspiration and ameliorate the subsequent clinical course. Unfortunately after decades of investigation no beneficial effect has been shown (3,5).
There is controversy about the value of systemic steroids in reducing bronchial odema and the alveolar exudate.
Although corticosteroid may attenuate inflamatory pneumonitis the immuno suprresant effect glucocorticoid may exacerbate any seondary bacterial pneumonia or sepsis (3,5).
Secondary bacterial invasion may be an additional threat to recovery and samples of bronchial aspirates should be cultured by bacteriologist.
The use of prophylactic antibiotics cannot be shown to improve the course of the disease or reduce mortality.(5)
The most important measure after pulmonary aspiration is maintainance of pulmonary gas exchange.
Often mechanical ventilation is instituted immediately after any major pulmonary aspiration.Although the prophylactic beneficities of positive pressure ventilation and positive end expiratory pressure on the development
of subsequent lung injury have been debated, such measures are often required merely to provide adequate oxygenation.
PREVENTION :(1,3,4)
Includes :
1.Save airway management
2.Cricoid pressure
3.Gastric tube the compression
4.Chemoprophylaxis
- Clear citrate antacids
- H2 receptor histamine antagonist
- Proton pump inhibitors
- Gastro prokinetic agents
Careful and skill airway management is very needed to reduced pulnary aspiration.
Cricoid pressure(Sellick's manouver) when properly applied can prevent the passage of gastric contents into oropharynx, however it may also provokes active vomiting in an unanesthetized patient.
In addition backward pressure on the cricoid cartilage facilitate laryngoscopy in some patients but interference with it in others. Infact in some patients pushing the larynx posteriorly,cephalad and to the right provides the best view of vocalcord but can also impede mask or larygeal mask airway ventilation.
Cricoid pressure during active vomiting has the potential to cause oesophageal rupture, Nasogastric tube permits gastric decompression,it also prevent lowoesopageal sphincter (LES) closure.
Chemoprophylaxis :
Antacids: Many investigators have demonstrated that particulate antacids are effective in raising gastric fluid pH in reasonably high precentage in both elective and emergent situation.
Indeed their effectiveness in raising fluid pH depends on :
1.The volume and pH of the gastric contents present at the time of their administration.
2.The frequency and timing of antacid administration.
3.The type and amount of antacid given.
4.What manouvers it any are done to promote mixing of antacid with gastric contents.
5.The intrinsix gastric motility present at the time of antacid administration.
6.The rate of ongoing gastric acid production.
The First :
Their administration may increase gastric volume. As example routine of 2-4 hour dosing with antacid became common practice on many obstetrical wards because of the unpredictability of emergency induction of anesthesia as well as concern over acid rebound(a decrease in pH over basal levels four or more hours following antacid neutralization). In the laboring patient(particularly those receiving narcotic for pain) gastric motility is slowed.
Thus such a practice could lead to significant increases in gastric volume.
The second :
Major criticism is that particulate aspirates result not only in as significant of initial pulmonary derangement as a highly acidic aspirate but also in histologic abnormalities that were present as long as one month following aspiration.
These chronic granulomatous response were not noted in groups with acid aspirates.
Particulate antacids are hazardous to the lungs and are therefore contra indicated preoperatively.
Because of these concerns an intense interest has been sparked in soluble antacids.
The propenderance of evidence suggest that soluble antacids are as effective as particulate antacids in raising gastric fluid pH in both elective or emergency surgical patients if given within 15-60 minute of induction of anaesthesia(4).
Work has demonstrated that soluble antacids mix with gastric contents more readily than particulate antacids.
Sodium citrate 0.5-1 ml/kg (30 ml max;1 hour preoperatively may increase gatric volume,but decreases gastric fluid pH and no changes in LES tone).
It must be kept in perspective that antacids remain the most rialable pharmacologic method of neutralizing gastric acid in emergent situation.
HISTAMINE H2 RECEPTOR ANTAGONIST :
(e.g.cimetidine,ranitidine and famotidine)(1,4).
The H2 blockers decrease gastric acid production by competitively inhibiting the action of histamine on the H2 receptor of gastric pariethal cell. In contrast they have no apparent effect on gastric emptying time or the lower esophageal sphincter(LES) pressure. Administration of cimetidine intravenously one hour before induction of anesthesia in patients presenting for elective surgery has been shown to signifantly decrease the acidity of gastric contents in samples taken immediately following the induction of anesthesia.
A delay onset of cimetidine ,60-90 minutes following intravenous administration limit its usefulness in emergence situation.
The cimetidine has been reported to inhibit the mixed function oxydase system and to decrease liver blood flow.
Co administration of cimetidine will prolonge the elemination half life of warfarin,diazepam,theophylline,phenythoin and propranolol.
That cimetidine therapy can agravate bronchospasm in asthmatics by allowing histamine to have an opposed H1 effect.
Rapid intravenous administration of relatively large doses(600 mg) of cimetidine in critically patients has been reported to cause hypotension and significant dysrythmia.
Ranitidine has greater potency, longer duration of gastric anti secretory effect (six to eight hours) than cimetidine (four to six hours) and lower incidence of side effects and lesser degree of inhibition of mixed function oxydase system but their clinical utility is limited in truly emergent surgical patients since its onset of action is no more rapid than that of cimetidine 45-60 minutes following intravenous administration.
Famotidine is propanimidamide derivative is the lattest H2 receptor antagonist. Clinical used dosages supress acids production for 10 to 12 hours intravenous administration may be ascociated with slightly faster onset of anti
secretory effect (30 minutes) compared to other H2 receptor antagonist thus offering a limited advantage of famotidine in emergent situation.
Systemic effect of famotidine in the CNS,cardiovascular,respiratory or endocrine system have been negligible to date and minimal drug interactions
have been identified in clinical trials.
PROTON PUMP INHIBITOR
(e.g omeprazole,lansoprazole,pantoprazole).
Similarly effective in reducing further gastric acids production but they have no demonstrable advantage over the H2 histamine receptor antagoinist. For aspiration prophylax.
GASTRO PROKINETIC (e.g.metoclopropamide).
A chlorbenzamide derivative which possesses three characteristic which make it potentially very useful in anestesia.
It increases the LES pressure,speeds gastric emptying time, and has anti emetic properties. It has no direct effect on gastric fluid pH.
Its action are mediated centrally via antidopaminergic effects and peripherally by facilitation of cholinergic stimulation, an action predominately limited
to the upper gastric intestinal tract.
Diabetes and others with known or suspected gastroparesis are likely the best candidate for gastroprokinetic medication.
A 10 or 20 mg intravenous dose of metoclopropamide can empty the stomach within 10-20 minutes whereas an oral dose taken 30-60 minutes.
But it is contraindicated to attempt to increase gastrointestinal motility in the presence of intestinal obstruction.
In the dose range commonly employed (0,15 to 0,3 mg)kg, metoclopropamide has proven relatively safe.
Higher dosages especially in children has been ascociated with agitation,irritability,confusion and extrapyramidal symptoms(4).
Pharmacologic agents used for the prophylaxis of pulmonary aspiration in children.(3)
Antacids GV pH LES tone
=====================================================================
Sodium citrate 0,5 - 1 ml/kg I I 0
(30 ml max;1 hr BS )
Anti cholenergic:
Glycopyrolate 7,5-10 microgram/kg 1 hr BS ? ? 0
H2 blocker :
Cimetidine 7,5 mg/kg (PM/AM) D I 0
Ranitidin 1,5- 2mg/kg (1-2 hr BS) 0 I 0
Famotidine 0,5 mg/kg (PM/AM) D I 0
Prokinetic agents::
Metoclopropamide:0,1mg/kg (1 hr BS) D 0 I
Proton pump inhibitor :
Lansoprazole 1,5 mg/kg (PM/AM) D I 0
Omeprazole 0,3 mg/kg (PM/AM) D 1 0
Pantoprazole 1,4 mg/kg QID D I 0
======================================================================
hr=hour BS=before surgery PM=night before AM=morning of surgery
GV=gastric volume, pH=pH gastric contents LES=low esophageal sphincter
I=increase D=decrease 0=no effect.
======================================================================
Extubation in patient at high risk for pulmonary aspiration should be performed when the patient fully awake and has full return of neuromuscular functions (3).
SUMMARY :
Aspirations of gastric contents to the lungs account for at least 10 percent of deaths attributable to anaesthesia.
The likelihood of pulmonary aspiration is three to four times greater for emergency surgery than the elective surgery.
The preoperative factor most often ascociated with aspiration is gastrointestinal obstruction.
The classic symptoms complex associated with pulmonary aspiration is sudden in onset,with wheezing,shortness of breath, cyanosis and tachycardia.
Pneumonitis aspiration which result from chemically induced damage to lung tissue where pneumonia aspiration is caused by a bacterial infections.
The first periority of treatment is to clear the upper airway and prevent asphyxia. Endotracheal suctioning should be attempt promptly whenever an aspiration is observed.
Brochoscopy is indicated for any patients who shows clinical or rongentnologic signs of large airway obstruction.
Bronchopulmonary lavage is not recomended for acidic aspirate because damage to the lungs occurs within 12 to 18 seconds, in addition more extensive pulmonary damage may occur due to the spread of acidic aspirates to lower regions of the lungs.
The use of prophylactic antibiotics cannot be shown to improve the course of the disease or reduce mortality.
The use of corticosteroid not recomended because the immuno supressant effect of corticosteroid may exacerbate any secondary bacterial pneumonia or sepsis.
Particulate antacids are hazardous to the lungs and therefore contraindicated preoperatively.
The most important measure after pulmonary aspiration is maintainance of pulmonary gas exchange.
REFERENCES
1.Tasch D.Mark : Pulmonary Aspiration ;Atlee L.John: Complications in Anesthesia,2nd edit,Saunders Elsevier,2007. pp 186-88.
2.Meyer mark : Perioperative Aspiration Pneumonitis ;Atlee l.John: Complications in Anesthesia;2nd edit,Saunders Elsevier,2007. pp 641-43.
3.Schultetin.R.Ray : Aspiration Pneumonitis;Atlee.L.John:Complications in Anesthesia;2nd edit,Saunders Elsevier,2007,pp 157-60.
4.Mc Cammon L.Ri : Aspiration Pneumonitis Prophylaxis and Prevention; International Anesthesia Research Society,Review Course Lectures, San Diego california ,1988,pp.40-44.
5.Spence A.Alastair : Post operative Pulmonary Complication;Nun.FJ,Utting EJ Brown R.Burmell;General Anaesthesia,5th edit;Butterworths ,London,Boston,1989.pp.1153-4.
6.Wynne W.James : Aspiration Pneumonitis;Ravin B.Mark:Problems in Anesthesia; A Case Study Approach;Little Brown and Company,Boston.1981,pp 237-41.
7.Lebowitz W.Philip,:Emergency Complicating Anesthesia.Lebowitz.W.Philip Clark L.John. Clinical Anesthesia Procedures of the Massachusetts General Hospital,Little Brown and Company,Boston, 1978,pp.350-1.
