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NEUROGENIC PULMONARY
EDEMA
Dr Kamal Bharathi. S
Case Report 1
• 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.
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
• 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.
• 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.
• 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.
• 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.
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.
Case 2
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..
• 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.
• CT pulmonary
angiography
demonstrated
bilateral, diffuse mixed
alveolar filling with
ground-glass opacities
of upper lobe
predominance, but
negative for acute
pulmonary embolism.
• 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.
Diagnosis: Neurogenic pulmonary edema
complicated by diffuse alveolar hemorrhage
secondary to seizure
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 %
• 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
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
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
Neurogenic Pulmonary Edema
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
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.
• 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
DIFFERENTIAL DIAGNOSIS
• Cardiogenic pulmonary edema
• Aspiration pneumonia
• Transfusion-related lung injury
• Sepsis
• Postairway obstruction edema,
• Ventilator-associated pneumonia
• Ventilation-induced lung injury
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.
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 %
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.
Thank You…!!!

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Neurogenic Pulmonary Edema

  • 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.
  • 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.