ASPIRATION PNEUMONIA

Dr Ameena Aslam
 INTRODUCTION

• Pulmonary consequences that follow abnormal entry of

fluid ,particulate matter or endogenous secretions from
the upper airways or gastric contents into the lower
airways

• Clinical features depend on:

• Quantity &nature of inoculum

• Frequency
• Predisposing host factors
 EPIDEMIOLOGY

• Aspiration pneumonia is the most common cause of death in pts

with dysphagia due to neurologic disorders

• 5_15%of the 4.5 million cases of CAP result from aspiration

• 18% in HAP

• Aspiration pneumonitis occurs in approximately 10% pts who are

hospitalised after a drug overdose
 PREDISPOSING FACTORS

• CONDITIONS WITH ALTERED OR REDUCED CONSCIOUSNESS:

• Alcoholism

• Drug overdose

• Seizures

• Stroke

• Head trauma

• General anesthesia
ESOPHAGEAL CONDITIONS:
• Dysphagia_ in elderly
• GERD
• Esophageal strictures,diverticula,neoplasm
• Tracheo esophageal fistula

NEUROLOGIC
DISORDERS:
• Multiple sclerosis
• Dementia
• Parkinson’s disease
• Myasthenia gravis
Mechanical conditions:
• Nasogastric tube
• Endotracheal intubation
• Tracheostomy
• Upper gastrointestinal endoscopy
• Bronchoscopy

OTHERS
• Protracted vomiting
• Prolonged recumbency
• General deconditioning & debility
• Periodontal disease
 CLASSIFICATION

• CHEMICAL PNEUMONITIS

• BACTERIAL PNEUMONIA

• MECHANICAL OBSTRUCTION
 CHEMICAL PNEUMONITIS

 Aspirate inoculum:acid,animalfats (milk),mineral oil,volatile

hydrocarbons

 Mendelson was the first to describe gastric acid pneumonitis in

humans in 1946

 PATHOPHYSIOLOGY:

 Rapid inflammatory response

 Ph of the inoculum must be 2.5 0r less,volume to be relatively large

a minimum of 0.3 to 0.6 ml/kg for the initiation

 Described in 2 phases
  FIRST PHASE:
 Peaks at 1 to 2 hrs after aspiration
 Due to the direct toxic effect of low ph on the alveolar walls
 Degeneration of bronchial epithelial cells, peribronchial
hemorrhage,atelectasis

 SECOND PHASE
 Peaks in 4 to 6 hrs
 Infiltration of neutrophils into the alveoli & interstitium
 Pulmonary edema,alveolar consolidation

Resolution begins by 3 rd day , may sometimes result in pulmonary

fibrosis
CLINICAL FEATURES:
 Abrupt onset of dyspnea, tachypnea, tachycardia
 Low grade fever
 Cyanosis ,hypoxemia
 Diffuse crackles on auscultation

Disease course varies ,in a retrospective review of 50 cases,

• 12%_ fulminant,ARDS
• 62%_ rapid clinical improvement
• 26%_ initial rapid improvement,then developed new infiltrates
• on the xray probably due to secondary infection or ARDS
 DIAGNOSIS:
• Presumptive,based on the clinical features
• Chest radiograph abnormalities appear within 2 hrs

NITRIC ACID POISONING

PARAFFIN PNEUMONITIS
TREATMENT
• Immediate tracheal suction to clear fluids &particulate matter

• Ventilatory support with PPV, mechanical ventilation

•
• Resuscitation with iv fluids

• Steroids :ineffective
• Antimicrobial agents: commonly given
empirical in severily ill

• It s appropriate to stop antibiotics ,if no infiltrates develop after

48 to 72 hrs
 ASPIRATION PNEUMONIA /BACTERIAL

• Inoculum:oropharyngeal bacteria

• Historically causative agents were less virulent

streptoccci & oral anerobes

• Normal oral anerobic flora :resides in the gingival

crevicae are:

• GRAM NEGATIVE COCCI:veillonella

• GRAM POSITIVE COCCI:peptostreptococci

• GRAM NEG BACILLI • GRAM POS BACILLI

• Pigmented prevotella • Clostridium species

• Fusobacterium nucleatum • Eubacterium

• Bacteroides fragilis • Propionibacterium

• Bacteroides ureolyticus • Lactobacillus

• bifidobacterium
Recent study in 95 hospitalised elders with severe aspiration pneum

Out of the 67 pathogens identified:

49%_Gram neg enteric bacilli

16%_ anerobes
12%_ staphylococcus aureus
CLINICAL PRESENTATION
• Variable

• Usually insidious in onset

• Cough ,fever, purulent sputum& dyspnea

• Radigraphic infiltrates in dependent pulmonary segments or

lobe
• With/without cavitation
C/F that are charecteristic of anerobic infection are:
• Indolent
• Compromised consciousness
• Absence of rigor
• Sputum with putrid odour
• Concurrent evidence of periodontal disease
• Failure to recover likely pulmonary pathogens in sputum
• Radiograph showing evidence of pulmonary necrosis with lung
Abscess or an empyema
DIAGNOSIS:

LABORATORY DIAGNOSIS:
1.Sputum ;Gram stain & culture
Uncontaminated specimens that are ideal for anerobic culture:

• Trans trachealaspirate,Trans thoracic aspirate

• Specimens obtained at thoracotomy
• BAL or with protected brush
Pleural fluid

2.Blood culture : in shock / sepsis

RADIOLOGICAL DIAGNOSIS

Pattern depends on pt position

• Supine:post seg of UL/sup seg
of LL
• Standing:B/L LL
• Prone: UL

• Right LL is the m/c site of

infiltration
TREATMENT
Antibiotics form the main stay of treatment

When anerobic bac are probable agents:

first line therapy:
Clindamycin600 mg iv TDS followed by 300mg (o)QID
Alternatives:
Amoxicillin clavulanate875mg (O)BD or metronidazole plus amoxicillin

DRUGS WITH POOR INVITRO ACTIVITY INCLUDE:

Trimethoprim_sulfamethoxazole,ciprofloxacin,aminoglycosides,aztr
eonam,ceftazidime

Moxifloxacin,macrolides, selected cephalosporins not used

In HAP:piperacillin _tazobactam or carbapenam is indicated

DURATION OF TREATMENT:
Cases not complicated by empyema or cavitation:7 to 10 days

Lung abscess, empyema need a longer course of antibiotic until

there is radiographic clearance or significant improvement
 MECHANICAL OBSTRUCTION

 Aspiration pneumonia involving fluid or particulate matter can

cause airway obstruction or reflex airway closure

 FLUIDS (aspirated but non toxic to lungs)

 Saline
 Barium
 Water
 Gastric contents with a ph >2.5

 Vagus mediated intrinsic pulmonary reflex closure occurs

CLINICAL FEATURES:
Acute dyspnea, cyanosis +/_ apnea ,pulmonary edema

TREATMENT:
Tracheal suctioning
Oxygen supplementation
Mechanical ventilation
SOLID PARTICLE ASPIRATION:
• Severity of obstruction depends upon:
 Relative size of the object aspirated & the calibre of the lower
airways
 Level of obstruction

• Foreign body asp m/c in children 1 to 3 yrs

• Usual objects recovered are peanuts,other vegetable

particles,inorganic materials &teeth

• Large objects that lodge in the larynx or trachea leads to sudden

resp distress, cyanosis ,aphonia &death
• Aspiration of smaller particles cause less severe obstruction

• Pts present with an irritative cough,chest radiograph shows

atelectasis or obstructive emphysema

• o/e wheeze in partial obstruction

• Bacterial superinfection is a fqt complication when obstruction

persists for > 1 week

• Primary treatment is removal of foreign object

 PREVENTION

 Position pts with altered consciousness in a semirecumbent

position with the head of the bed at a 30 to 45 degree angle or
upright position

 For pts with dysphagia, a soft diet reducing the bite size,keeping
the chin tucked & head turned, &repeated swallowing

 Using nectar or honey thickened fluids may prevent aspiration in

pts with dementia

 Tracheostomy, reducing gastric contents via suction,gastrostomy

tube feeding , neutralisation of gastric acid are the measures with
moderate efficacy
Patients who require nasogastric tube feeding are aspiration prone
,percutaneous endoscopic gastroscopy(PEG) is an alternative .but,
Studies are quite variable.

The incidence of pneumonia was no difft b/w the two groups

Alternative procedures:postpyloric feeding jejunostomy,Nissen fundo

plication
 PROGNOSIS

• If bacterial aspiration pneumonia not treated early,can lead to

lung abscess & BPF

• 30 day mortality rate in aspiration pneumonia is 21% overall&

29.7% in hosp acquired aspiration pneumonia

• Mortality rate for chemical pneumonitis :30 to 62%

Thank you