A short presentation regarding Neurogenic Pulmonary Edema - Pulmonary Edema following Neurological Insult

1. NEUROGENIC PULMONARY EDEMA
Dr. Muhammed Thasneem
K
Junior Resident, Dept. of General Surgery 1

2. CONTENT
Introductio
n
Epidemiolog
y
Pathophysiolog
y
NPE Trigger Zone
s
Pathogenesi
s
Clinical Feature
s
Diagnosi
s
Management 2

3. INTRODUCTION
Pulmonary Edema - Accumulation of fluid in the airspaces and
interstitium of the lun
g
Intrinsic or Systemi
c
Classified into Cardiogenic and Non Cardiogeni
c
Cardiogenic - MI > LV failure > elevated pulmonary
venous pressure > increased pulmonary hydrostatic
.
Non Cardiogenic - Acute Lung Injury ,ARDS
3

4. NEUROGENIC
PULMONARY EDEMA
Rare form of Pulmonary Edema, follows CNS insult
.
Caused by increase in pulmonary interstitial and alveolar fluid
.
Potential to increase the secondary injury to brain - fatal
.
SAH,Traumatic Brain Injury, Cervical Spinal Cord Injury,
Intracerebral Hemorrhage are associated with NPE.
4

5. 5

6. EPIDEMIOLOGY
Exact numbers not clear, most of available data derived from case
reports / few patients / different diagnostic criteri
a
2% - 42% in patients with SA
H
SAH with NPE have higher mortality approaching 10%
.
Increasing Age , delay in surgery, clinical and radiological
presentations (poor grade SAH) associated with higher incidence
of NPE
6

7. In TBI, reports of development of NPE is as high as 20
%
In large autopsy series by Rogers et al., the incidence of NPE was
32% in TBI who died at the scene,it increased to 96% within
96hours following TB
I
It is estimated that nearly one-third of patients with status
epilepticus develop NPE
7

8. PATHOPHYSIOLOGY OF
NPE
Poorly understood , common finding in these cases is the severity
of the CNS insult and sudden increase in ICP
.
Raised ICP level correlates with extravascular lung water (EVLW)
and occurrence of NP
E
Two probable mechanisms by which NPE develops following CNS
injury
8

9. 1. Damages to the neurons directly or indirectly affects the
pulmonary vascular bed, leading to increased permeability and
hence pulmonary edem
a
11. Overstimulation of the vasomotor center inflicts changes in
autonomic function.
9

10. Sudden increase in ICP leads to neuronal compression or
damage,which follows an intense activation of CNS
.
Increased secretion of Catecholamines > Systemic
vasoconstriction > Shift of blood from systemic to pulmonary
circulatio
n
Catecholamine Release + increased PulmonaryVascular
Permeability increases EVLW and NPE
10

11. 11

12. NPETRIGGER ZONES
Hypothalamus ,Brain Stem,Upper Cervical Spinal Cor
d
The imp. centres for triggering NPE are A1,A5 nuclei, nuclei of
solitary tract, area postrem
a
A1 nuclei - present inVentroLateral aspect of Medulla and
project in hypothalamu
s
A5 neurons are located in the upper brain stem and project into
centres for sympathetic flow in the spinal cord
12

13. 13

14. PATHOGENESIS
Sudden increase in ICP, in association with sympathetic discharge ,
has been associated with development of NPE , four mechanisms
have been proposed by which PE develop
s
1 . NEUROCARDIAC NP
E
directly inflicts myocardial injury, inturn lead to pulmonary
edema,characterised by cardiomyopathy with diastolic
dysfunction ,decreased contractility and global hypokinesia
14

15. histology-myocytolysis and contraction band necrosis
ECG - regional wall , motion wall abnormalit
y
Sudden surge of catecholamines is the causative factor in this
form of NPE
15

16. 2.NEUROHEMODYNAMIC THEOR
Y
Alteration in ventricular compliance is believed to cause abrupt
increase in pulmonary and systemic pressures after a CNS injur
y
Sudden increase in afterload causes altered LVF , blood shifts to
low resistance PulmonaryVascular System , increased pressure in
pulmonary circulation forms Hydrostatic Pulmonary Edema
16

17. 3. BLAST THEOR
Y
Explains the presence of RBCs and exudative fluid in alveolar
space
The Shift in the blood from systemic circulation to pulmonary
circulation causes altered permeability and forms exudative
pulmonary edem
a
The sudden increase in pulmonary circulation also leads to
damage of alveolar - capillary membrane, explains presence of
RBCs and protein rich PE.
17

18. 4.ADRENERGIC HYPERSENSITIVITY of pulmonary venules to
catecholamines . Catecholamine surge leads to endothelial injury
irrespective of systemic changes
18

19. CLINICAL FEATURES
Depending on onset of symptoms and signs , two forms of NP
E
1. Early Onset - onset of symptoms within minutes to hour
s
2. Delayed Onset - following 12-24 h of CNS insult
.
Severity of Neurologic Insult = Severity of NPE
19

20. Typically , patient may complain of difficulty in breathin
g
Acute Onset Dyspnea ,Tachypnoea and Hypoxia - onset of NP
E
Auscultation - B/l Crackle
s
Pink, Frothy Sputu
m
Sympathetic Hyperactivity - Tachycardia,Hypertension and Fever
Spikes.
20

21. DIAGNOSIS
No specific diagnostic test for NP
E
neurologic origin is a diagnosis of exclusio
n
ECG changes and elevated Cardiac enzymes may be asso. with
SA
H
high degree of suspicion to rule out cardiogenic PE
21

22. 22

23. DIFFERENTIAL DIAGNOSIS
LV
F
Community Acquired Pneumoni
a
Aspiration Pneumoni
a
Pulmonary Contusio
n
NB; More than one condition can co-exist
23

24. MANAGEMENT
Treatment of NPE is mainly supportive care
focus should be on the management of CNS disorder and its
associated complication
s
generally NPE resolves in 48-72 hours
24

25. GENERAL SUPPORTIVE CARE
1.Airway and Breathin
g
Supplemental Oxygen , Intubation depending on Neurologic statu
s
In severe distress - Intubation & MechanicalVentilatio
n
In conscious patient - Non invasive PPV
desaturation and hypoxia - higher PEE
P
higher PEEP >10cmH20 should be avoided in raised ICP
25

26. in cases which require higher PEEP, ICP should be monitore
d
Permissive hypercapnia should be avoided in patients with raised
IC
P
In patients with refractory hypoxemia - High Frequency
OscillatoryVentillation
26

27. 2. CIRCULATION
:
Choice of drug depends on associated injuries and preexisting
patholog
y
Cardiac Index should be maintained >2.5L / min / M^
2
SystemicVascular Resistance < 1000dynes/second/cm-
5
Dobutamine is the first line of drug
addl, beta1 agonists and alpha adrenergic blockers have been
tried
27

28. SPECIFICTHERAPY
Pharmacological agents not routinely used in the management of
NP
E
beta blockers and alpha adrenergic blockers have been trie
d
NPE is self limiting and resolves spontaneously , care should be
ensured for adequate Cerebral Perfusion Pressur
e
EFforts to reduce ICP like Decompression, Hematoma
Evacuation, anti epileptics ,tumor resection and steroids -
improvement in Oxygenation
28

29. CONCLUSION
SUDDEN ONSET OF HYPOXEMIC RESPIRATORY FAILURE IN
ASSOCIATION WITH A CNS CATASTROPHE ,WHICH
CANNOT BE ATTRIBUTED TO ANY OTHER CAUSE , POINTS
TOWARDS NPE
.
SUPPORTIVE CARE OF PATIENTS TO PREVENT HYPOXIA IS
THE MAINSTAY OF TREATMENT
29

30. REFERENCE
Complications in Neuroanaesthesia - Hemanshu Prabhaka
r
Rosen's Emergency Medicine
30

31. –Wilder Penfield
“The brain is the organ of destiny. It holds within its
humming mechanism secrets that will determine the
future of human race .”
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32. THANKYOU
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