Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system (CNS) insult. The etiology is thought to be a surge of catecholamines that results in cardiopulmonary dysfunction. A myriad of CNS events, including spinal cord injury, subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), intracranial hemorrhage, status epilepticus, meningitis, and subdural hemorrhage, have been associated with this syndrome.

1. NEUROGENIC PULMONARY
EDEMA
Dr Kamal Bharathi. S

2. Case Report 1

3. • Moderate sedation during bronchoscopy is safe with
serious complications in < 1/10,000 cases. Reports of
seizures with status epilepticus or neurogenic pulmonary
edema with moderate sedation are equally rare. This
report is of a patient undergoing bronchoscopy with
moderate sedation who developed both complications.

4. Case report
• A 58 year-old woman
• Evaluation of generalized mediastinal lymphadenopathy.
• She had well-controlled diabetes and CAD, but otherwise
asymptomatic.
• she was scheduled for outpatient bronchoscopy and EBUS

5. • She was given 1% nebulized lidocaine and received
additional topical lidocaine during bronchoscopy (total 14
mL).
• Moderate sedation was achieved with midazolam (3 mg),
fentanyl (75 mcg), and diphenhydramine (25 mg) given
over ten minutes.
• Vital signs were stable during the initial unremarkable
bronchoscopic survey with bronchoalveolar lavage
performed of the RLL and RML.
• Then she developed tonic-clonic seizures lasting several
minutes. terminating with additional benzodiazepines.

6. • Bronchoscopy was aborted and she was transferred to the
ICU where she deteriorated with hypoxic respiratory
failure. pulseless electrical activity (PEA) arrest, shock, and
oliguria.
• Chest imaging showed diffuse vascular congestion, and
echocardiography demonstrated severe global hypokinesis
(LV EV < 20%, bubble study negative). Head CT scan was
unremarkable and EEG demonstrated no epileptiform
activity.

7. • Her hypoxia persisted despite continuous renal
replacement therapy, rescue ventilatory
maneuvers, triple vasopressors, and she was then
transferred to an outside facility for ECMO.
• After 72 hours, her oxygenation, hemodynamics
and sensorium improved to permit
discontinuation of ECMO and ventilator support.

8. • A repeat echocardiogram showed normal
cardiac function. She was discharged home
neurologically intact one week after her
initial event.
• On outpatient follow-up, an enlarged
supraclavicular lymph node was noted and
biopsied, demonstrating well-formed non-
caseating granulomas establishing a
diagnosis of sarcoidosis.

9. Discussion
• This patient developed two extremely rare
complications during moderate sedation, seizures which
are rare in patients without known epilepsy and
profound neurogenic pulmonary edema.
• Neurogenic pulmonary edema occurs following an acute
neurologic insult resulting in hypoxic respiratory failure
not attributable to a cardiac event or other causes of
ARDS.
• This illustrates the importance of recognizing that
severe, life threatening complications can occur even
with moderate sedation.
• Prompt recognition and aggressive support are crucial
for recovery.

10. Case 2

11. Case report
• 49-year-old woman with a medical history
of epilepsy presented to the ED 1 h after a
single, 15-min, witnessed, tonic-clonic
seizure.
• While being evaluated by the neurology
service, the patient complained of sudden-
onset chest pain and cough with associated
hypoxemia..

12. • On physical examination,
• Temp 36.7 C, HR 111 beats/ min, BP 132/69 mm Hg, RR
24 breaths/min, Spo2 88% on room air, which recovered
to 97% on 3 L/m oxygen by nasal cannula.
• The patient appeared comfortable and oriented;
however, she was experiencing intermittent,
nonproductive paroxysms of cough.
• Auscultation of the chest revealed posterior bilateral
diffuse crackles on inspiration without wheezing that
did not clear with cough.
• CVS revealed tachycardia with regular S1 and S2 absent
of murmurs.

13. • CT pulmonary
angiography
demonstrated
bilateral, diffuse mixed
alveolar filling with
ground-glass opacities
of upper lobe
predominance, but
negative for acute
pulmonary embolism.

14. • Right upper lobe alveolar BAL and TBLB were performed.
• Three serial lavage aliquots demonstrated an RBC count of
267,500 with 133 WBCs; 302,000 RBCs with 111 WBCs;
and 197,500 RBCs with 78 WBCs.
• BAL infectious studies, including Gram stain with culture,
respiratory viral panel, direct fluorescence assay for PCP,
MRSA, polymerase PCR, and galactomannan, were
unremarkable.
• The transbronchial biopsies- nondiagnostic.
• Rheumatologic evaluation: ANA and ANCA screen-negative.
• C-reactive protein was undetectably low as <0.5 mg/dL
and ESR was 5 mm/h.

15. Diagnosis: Neurogenic pulmonary edema
complicated by diffuse alveolar hemorrhage
secondary to seizure

16. NEUROGENIC PULMONARY EDEMA
• Neurogenic pulmonary edema (NPE) is a
clinical syndrome characterized by the acute
onset of pulmonary edema following a
significant central nervous system (CNS) insult.
• The etiology is thought to be a surge of
catecholamines that results in cardio-
pulmonary dysfunction.
• Can be considered as a form of ARDS
• Prevalence: 2-8 %

17. • In 1903, Harvey Williams Cushing, described
the connection between CNS injury and
hemodynamic dysfunction.
• reported 11 cases of acute pulmonary edema
as a complication of epileptic seizures.
• Similar reports exist of observed alveolar
edema and hemorrhage in the lungs of 17
soldiers dying after isolated bullet head
wounds in the Vietnam War

18. ETIOLOGY
• Subarachnoid
hemorrhage (SAH)
• Intracranial
hemorrhage (ICH)
• Traumatic brain injury
• Stroke
• Acute hydrocephalus
• Seizures and status
epilepticus
• Meningitis
• Subdural hemorrhage
• Cervical medulla
injury
• Cerebral thrombosis
• Cerebral gas embolism
• Medication overdose
• Multiple sclerosis
• Arteriovenous
malformation

19. PATHOPHYSIOLOGY
• Central sympathetic discharge
• The hemodynamic theory is based on
systemic and pulmonary vasoconstriction
following the sudden increase in circulating
catecholamines
• This vasoconstriction and hypertension may
cause increased pulmonary blood volume
through a shift of blood from the systemic to
the pulmonary circulation

21. CLINICAL PRESENTATION
• Signs of oxygenation failure, such as
dyspnea, tachypnea, tachycardia, cyanosis,
pink frothy sputum, and crackles and rales
on auscultation.
• Hypoxia is reflected by low PaO2 and a
PaO2/FiO2 ratio below 200
• Chest radiogradiograph (CXR) usually
shows features of pulmonary edema with
bilateral diffuse alveolar infiltrates

22. CLINICAL COURSE
• Early: minutes to hours after CNS insult (in
most cases: 30-60 minutes)
• Delayed: 12-24 hours after CNS insult
• The abrupt nature of respiratory distress is an
impressive feature of NPE.
• the patient becomes acutely dyspneic,
tachypneic, and hypoxic within minutes. Pink,
frothy sputum is commonly seen and bilateral
crackles and rales are appreciated on
auscultation.

23. • Chest radiograph will reveal bilateral
hyperdense infiltrates consistent with acute
respiratory distress syndrome (ARDS)
• Symptoms usually resolve within 48–72
hours after onset, but may subside as
rapidly as they developed

24. DIFFERENTIAL DIAGNOSIS
• Cardiogenic pulmonary edema
• Aspiration pneumonia
• Transfusion-related lung injury
• Sepsis
• Postairway obstruction edema,
• Ventilator-associated pneumonia
• Ventilation-induced lung injury

25. Diagnostic criteria
1) Bilateral infiltrates;
2) PaO2/FiO2ratio < 200;
3) no evidence of left atrial hypertension;
4) presence of CNS injury (severe enough to have
caused significantly increased ICP);
5) absence of other common causes of acute
respiratory distress or ARDS (e.g., aspiration,
massive blood transfusion, sepsis).
 a trial of an α-adrenergic blocking agent, such
as phentolamine, can be considered.

26. TREATMENT & PROGNOSIS
• Treatment of the underlying neurologic
condition focused on reduction of ICP
(decompression and clot evacuation, osmotic
diuretics, anti-epileptics, tumor resection, and
steroids) in order to halt the sympathetic
discharge that is presumed to be the culprit for
the lung injury
• Supportive treatment for pulmonary edema.
(volume management, ventilation strategies)
• Mortality: 50-100 %

27. SUMMARY
• NPE occurs as a complication of acute
neurologic illness and may mimic acute lung
injury of other etiology
• Central sympathetic role
• Treatment strategies are mainly supportive
and must target both the neurologic
condition and NPE.

28. Thank You…!!!