Transcript Posttraumatic Pulmonary Insufficiency

Posttraumatic Pulmonary
Insufficiency
Bradley J. Phillips, M.D.
Burn-Trauma-ICU
Adults & Pediatrics
Definition
Clinical state in which gas exchange
in the lungs
is inadequate to maintain body function
without mechanical support
Incidence

Pulmonary complications 11% ( Hoyt, 1993)





Pneumonia 7.5%
Atelectasis 3.4%
ARDS 2.8%
Aspiration 1.5%
PE 0.7%
Predictors







Injury Severity Score > 16
Blunt trauma
Shock on admission
Chest surgery
Pedestrian vs MVC
Head injury
Age > 55 years
Causes

Disease-related







Shock
Pulmonary contusion
Fat emboli
CNS injuries
Sepsis
PE
Smoke inhalation

Iatrogenic



Fluid overload
Massive blood transfusion
Ventilator-induced
Pulmonary contusion




Evident on CXR within 24 hours
Worsen within 24-48 hrs
Increased risk of infection
Flail chest induced hypoxia result of contusion
Fat Embolism

Syndrome characterized by cerebral and pulmonary
dysfunction after long bone injury




asymptotic 12-48 hrs post injury
increasing tachypnea, restlessness, and confusion
“full blown” - severe hypoxia/coma mortality 10-20%
Assume in all patient with pelvic and long bone
fractures

quantified by platelet count and A-a gradient
Fat Embolism

Origin



Platelet adhere to fat particles



long bone
in situ blood formation with increased lipolysis
thrombocytopenia
petechiae on chest/conjunctiva/axilla
Increased risk with immobilized fracture

Early fixation recommended
CNS Injuries

Greatly increased risk




aspiration
atelectasis
prolonged ventilation
Neurogenic pulmonary edema



frequently pre-mortem spinal cord/head injury
increased pulmonary tone
increased capillary leak
Pneumonitis


Risk in ventilated patients 1-4% per day
Diagnosis






Fever ( > 101)
Leukocytosis ( > 12 K)
New infiltrate
Sputum with PMN’s
Bacteria on gram stain and culture
Stress ulcer prophylaxis

no difference in ventilated patients on sulcrafate,
antiacids, or ranitidine
Pulmonary Embolism


Significant risk in trauma patients
Risk assessment profile of thromoembolism (RAPT) by
Greenfield
 5 or more (out of 14) increases risk 3 times

Underlying condition


Iatrogenic factors


CVL, operations > 2 hrs, major venous repair
Injury-related factor


Obses, malignancy, hx of thromboembolism
Spinal factures, coma, pelvic fx, plegia
Age

> 40 (highest risk > 75)
Other Causes

Shock
 decreases ciliary function and surfactant
hypotension alone  ARDS
Fluid Overload
 increased interstitial edema
Massive blood transfusions
 controversial
 main risk is increased infections



Other Causes

Smoke inhalation injury
36 hrs
2-6 days
bronchospasms
airway edema
bronchitis

Ventilator-induced injury


pulmonary edema
Volume not pressure etiology
Sepsis
 increased risk of ARDS
 severe persistent infections
1-2 weeks
bronchopneumonia
airway cast formation
Adult Respiratory Disease Syndrome

First described in 1967 (12 patients)




cyanosis refractory to oxygen
decreased lung compliance
diffuse infiltrates on CXR
Modern definition (1994)





Acute onset
Bilateral infiltrates on CXR
Wedge < 18 mmHG or absence of L atrial HTN
PaO2/FiO2 < 200 ( if > 200, acute lung injury)
Not predictive of outcome within 24-72 hrs
ARDS

Incidence




15- 75 /100,000
depends on definition
prospective study underway
Phases of Pathophysiology



Acute (0-6 days)
Proliferative (4-10 days)
Chronic or fibrosis (8-14 days)
Risk Factors

Direct

Common




Indirect

Pneumonia
Aspiration


Less common





Pulmonary contusion
Fat emboli
Near drowning
Inhalation injury
Reperfusion injury
Common

Sepsis
Severe trauma with shock
and transfusions
Less common




Cardiopulmonary bypass
Drug overdose
Acute pancreatitis
Transfusion of blood
products
Mediators of Injury





Vasoactive substances
Leukocyte activation
 oxygen radicals
 neutrophil proteases
 arachidonic acid metabolites
Complement activation
Platelets
Cytokines
 TNF, IL-1, IL-8
Anatomical Consequences

Capillary endothelium




gap junctions wider
“leaky” = fluid and protein interstitium
Proliferation of type II pneumocytes
Vascular occlusion


capillaries and small vessels
75-80% occlusion for increase in PA pressures (moderate-severe
ARDS)


poor prognosis
Pulmonary fibrosis (late)
Gas Exchange


Hypoxemia
V/Q abnormalities
 atelectasis and alveolar flooding
 shunting (20%)


most sensitive for impending early respiratory failure
Increased dead space
 dead space fraction of .6-.65 = severe dysfunction
Physiologic Changes

Most consistent and frequent hemodynamic evidence
of poor prognosis after trauma



early secondary to neurohumoral activity
late secondary to microemboli and edema
Decreased compliance (< 50 ml/cm H2O)




interstitial and alveolar edema
tachypnea is usually first sign
if not correctable = poor prognosis
TV and PEEP adjusted to provide best static compliance
Treatment


Eradicate all underlying infection
General supportive measures
 frequent position changes
 elevation of head/chest
 chest physiotherapy
 pain control
 relief of gaseous distension
 reduce O2 requirements
Treatment

Fluids


maintain adequate perfusion
excessive fluid greatly aggravates tendency toward
ARDS
Central venous monitoring
 ? Role of colloid ( risk of leaking into interstitium)


maintain hemoglobin
accept > 10 g/dl
 trend in survival if Hgb > 12 g/dl

Treatment

Optimizing DO2 and VO2


Shoemaker (1988) reduced incidence of pulmonary
complications in high-risk surgery for 27% to 4%
Fleming (1992) fewer deaths (14% vs 44 %) and
respiratory failure (39% vs 68%)
supranormal CI (>4.5)
 DO2 (> 670 ml/min/m2)
 VO2 (160 ml/min/m2)

Treatment


Nutrition
 early, aggressive enteral nutrition
 ? enteral vs no feeding
 ? benefit of fish oil, arginine, glutamine
Drugs
 bronchodilators
 inotropics
 diuretics
Ventilatory Support


Oxygenation
 > 60% usually required
 oxygen toxicity not an issue if PaO2 < 50
PEEP
 ability to reduce oxygen
 risks
CO2 retention
 high airway pressures/
 hemodynamic instability

Ventilatory Support
Type
Year
Type
Outcome
High PEEP
1975
Observe
High PTX
ECMO
1979
Phase III
No benefit
Jet Vent
1983
Phase III
No benefit
PC/Inverse
1994
Observe
Inconclusive
Liquid
1996
Observe
Safe, ? Benefit
Oscillatory
1997
Observe
Safe, ? Benefit
Prone
1997
Observe
Inconclusive
Prone
2000
Observe
Inconclusive
Open Lung
1998
Phase III
dec. 28 day mortality
Low tidal
1999-2000
Phase III
No benefit/dec. mortality
Problems

High airway pressures
 sedation and/or paralytics
 pressure control ventilation
 permissive hypercapnea
reduce tidal volume (5-7 ml/kg)
 in general maintain pH > 7.2

? permissive hypoxemia
Hypoxia
 acidemia
 reverse I:E ratio


Recommendation



Minimize FiO2 and PEEP to maintain PaO2 > 60
Low tidal volumes (5-7 ml/kg)
Pressure regulated or control ventilation



PIP < 30
Permissive hypercapnea
Reverse I:E ratio
Other Therapies

Steroids


Nitric Oxide


no benefit
Surfactant replacement


possible benefit in late ARDS with difficulty weaning
successful in neonates only
Triiodothyronine


experimental in animals
improved compliance, histologic integrity, and surfactant
Other Therapies
Treatment
Year
Type
Findings
Steroids (acute)
Steroids (acute)
Steroids (late)
1987
1988
1998
Phase III
Phase III
Phase III
No benefit
No benefit
dec. mortality
Surfactant
Nitric Oxide
Nitric Oxide
Ketoconazole
1996
1998
1999
2000
Phase III
Phase II
Phase III
Phase II
No benefit
No benefit
No benefit
No benefit
Nonconventional Methods

Unilateral pulmonary insufficiency (isolated pulmonary
contusions or aspiration pneumonitis)



“Down with the good lung”
Independent lung ventilation
Bilateral pulmonary insufficiency





Permissive hypercapnia
I:E reversal
High –frequency Ventilation
Prone positioning
ECMO
Unilateral Pulmonary Insufficiency

Lateral positioning



Allow redistribution of V/Q mismatch
Good lung down – increased blood flow to normal lung parenchyma
Independent lung ventilation



Two separate ventilators using double lumen ET
Deliver TV to each lung based on pathology
Numerous disadvantages



Monitoring tube position (tube dislogdes often)
Heavy sedation/paralysis
Increased cost
Bilateral Pulmonary Insufficiency

Permissive hypercapnia


Minimize peak inspiratory pressure with low TV while
maintaining acceptable oxygenation
Acceptance of hypoventilation/hypercapnia
Slow increase in CO2 tolerated very well
 Often maintain pH 7.10 to 7.20 range
 ? Use of bicarb to buffer pH


Contraindicated in head injury
Bilateral Pulmonary Insufficiency

I:E reversal



Normal I:E is 1:2 TO 1:4
Allows more time for recruitment of alveoli and oxygen diffusion
Disadvantages



Often leads to permissive hypercapnia
Auto-PEEP
High-frequency ventilation



Small TV (1-3 ml/kg) at 100-3000/min)
Adequate oxygenation with reduced airway pressures
Disadvantages


Necrotizing tracheobronchitis
No difference in outcomes compared to conventional methods
Bilateral Pulmonary Insufficiency

Prone positioning

Physiology


Disadvantages





Better V/Q matching anteriorly
More intensive nursing care
Risk of tube and line dislodgement
? Increase skin breakdown
Cannot use in open abdomens, spinal fractures etc
Outcomes

Reduced FiO2 and PEEP




> 2/3 of patients
PaO2/FiO2 improved by 50%
Reduced shunt 50% to 34%
? Improved mortality

Small studies show increased survival using combined prone ventilation, low
tidal volumes, and permissive hypercapnia
Ventilatory Strategies
Hirvela, E, Archives of Surgery, 2000.
Volume-Pressure Curve
Outcomes

Mortality rates 40-60% (Historical)




Mortality rates 30-40 %(recent)




sepsis
MSOF
not usually primary respiratory causes
? more effective treatments of sepsis
changes in mechanical ventilation
improvement in supportive care
Risk factors for death


chronic liver disease, sepsis, age, MSOF
failure to improve in first week
ARDS Consequences


After 1 year, most not restricted in activities
Permanent restrictive changes and pulmonary
HTN develop if prolonged need for oxygen > 60%
Questions…?