Neurogenic pulmonary edema
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Shaghayegh Habibi, M.D.[2]
Overview
Neurogenic pulmonary edema usually appears within minutes to hours after a cerebral injury. It is an acute life-threatening complication associated with many forms of central nervous system injury, such as brain or spinal cord hemorrhage, trauma, tumors, epilepsy and infections. The pathogenetic factors for the its onset include increased intracranial pressure and severe over-activation of the sympathetic nervous system. Neurogenic pulmonary edema must be differentiated from other diseases with same symptoms, include aspiration pneumonia, cardiogenic pulmonary edema, angioedema and asthma attack. NPE is characterized by dyspnea, bilateral basal pulmonary crackles and the other signs and symptoms of pulmonary edema, in the absence of cardiac failure. Arterial blood gas test shows hypoxemia, hypercapnia and acidosis. In treatment of neurogenic pulmonary edema, the main principle is supportive treatment and decreasing intracranial pressure as in acute respiratory distress syndrome.
Historical Perspective
- In 1908, W. T. Shanahan noted acute pulmonary edema as an adverse effect of epileptic seizures.
- During WWI, francois Moutier noted the sudden onset of pulmonary edema among soldiers shot in the head.[1][2]
- In the Vietnam War, alveolar edema and hemorrhage seen in the lungs of soldiers dying after isolated bullet head wounds.[3]
Pathophysiology
- Pulmonary edema may develop in the setting of a sudden neurologic event. Neurogenic pulmonary edema usually appears within minutes to hours after cerebral injury.[4][5]
- Neurogenic pulmonary edema is an acute life-threatening complication associated with many forms of central nervous system injury, such as:[5]
- Brain or spinal cord hemorrhage
- Trauma
- Tumors
- Epilepsy
- Infections
- The pathogenetic factors for the onset of neurogenic pulmonary edema include:[6]
- Increased intracranial pressure
- Severe over-activation of the sympathetic nervous system
- Neurogenic pulmonary edema may develop as a result of activation of specific CNS trigger zones in the brainstem, leading to a rapid sympathetic discharge, rise in systemic blood pressure, baroreflex-induced bradycardia, and enhanced venous return. These cause pulmonary vascular congestion characterized by interstitial edema, intra-alveolar accumulation of transudate and hemorrhages.[7]
- The initiating mechanism may be a marked, although brief, generalized vasoconstriction, followed by a shift of blood from the peripheral vascular bed to the pulmonary vascular bed.[8]
Differentiating neurogenic pulmonary edema from other Diseases
- Neurogenic pulmonary edema must be differentiated from other diseases with same symptoms, include:[9]
- For more information about differential diagnosis of pulmonary edema click here.
Epidemiology and Demographics
- The incidence of neurogenic pulmonary edema is approximately 2000 to 42900 per 100,000 individuals in patients with subarachnoid hemorrhage.[10][11]
- The incidence of neurogenic pulmonary edema is approximately 20000 per 100,000 individuals in patients with traumatic brain injury.[12]
- Age, gender, race and other epidemiologic and demographic features are based on underlying neurologic problem. Overall pulmonary edema commonly affects individuals older than 65 years of age.
Risk Factors
- Severe brain damage represents a risk factor for developing neurogenic pulmonary edema, which include:[13]
Natural History, Complications and Prognosis
- Misdiagnosis and inappropriate treatment may worsen cerebral damage because of hypoxemia or reduced cerebral perfusion pressure.[13]
- Common complications of neurogenic pulmonary edema are based on underlying neurological damage and pulmonary edema (include electrolyte disturbance, leg and/or abdominal swelling and respiratory arrest).
- Prognosis is generally poor and the associated mortality rate is high, but surviving patients usually recover very quickly.[14][15]
Diagnosis
Symptoms
- NPE is characterized by dyspnea, bilateral basal pulmonary crackles and the other signs and symptoms of pulmonary edema, in the absence of cardiac failure.[16]
- For more information about symptoms in pulmonary edema click here.
Physical Examination
- Patients with neurogenic pulmonary edema usually appear:
- Anxious
- Decrease in level of consciousness
- Physical examination is remarkable for the signs of underlying neurologic damage and pulmonary edema, include:
- Wheezing
- Prolonged expiratory phase
- Retraction of intercostal muscle
- Use of accessory muscles of respiration
- Nasal flaring
- Tachypnea
- Bradycardia
- High systemic blood pressure
Laboratory Findings
Arterial blood gas test:
- Hypoxia:
- Oxygen saturation < 90%
- PaO2 < 60 mm Hg
- Hypercapnia:
- CO2 > 45–55 mm Hg
- Acidosis:
- PH < 7.35 nEq/liter
- Early findings of pulmonary edema may be respiratory alkalosis because of hyperventilation
Imaging Findings
- Imaging findings are remarkable for the pulmonary edema and underlying neurologic damage.
- For more information about imaging findings in pulmonary edema click here.
Treatment
Medical Therapy
- In treatment of neurogenic pulmonary edema, the main principle is supportive treatment and decreasing intracranial pressure as in acute respiratory distress syndrome.[17]
- For more information about medical therapy in pulmonary edema click here.
Surgery
- The mainstay of treatment for pulmonary edema is medical therapy. Surgery may be reserved for underlying neurological damage.
Prevention
- Treating the underlying neurologic disease is the only way of preventing the recurrence of pulmonary edema.[18]
References
- ↑ Davison DL, Terek M, Chawla LS (December 2012). "Neurogenic pulmonary edema". Crit Care. 16 (2): 212. doi:10.1186/cc11226. PMC 3681357. PMID 22429697.
- ↑ Izumida H, Homma K, Sasaki J, Hori S (April 2017). "Pulmonary edema following tonic-clonic seizure". Acute Med Surg. 4 (2): 221–222. doi:10.1002/ams2.251. PMC 5667274. PMID 29123866.
- ↑ Simmons RL, Heisterkamp CA, Collins JA, Genslar S, Martin AM (July 1969). "Respiratory insufficiency in combat casualties. 3. Arterial hypoxemia after wounding". Ann. Surg. 170 (1): 45–52. PMC 1387602. PMID 5789529.
- ↑ Smith WS, Matthay MA (May 1997). "Evidence for a hydrostatic mechanism in human neurogenic pulmonary edema". Chest. 111 (5): 1326–33. PMID 9149590.
- ↑ 5.0 5.1 Kim JE, Park JH, Lee SH, Lee Y (October 2012). "Neurogenic pulmonary edema following intracranial coil embolization for subarachnoid hemorrhage -A case report-". Korean J Anesthesiol. 63 (4): 368–71. doi:10.4097/kjae.2012.63.4.368. PMC 3483499. PMID 23115693.
- ↑ Kim JE, Park JH, Lee SH, Lee Y (October 2012). "Neurogenic pulmonary edema following intracranial coil embolization for subarachnoid hemorrhage -A case report-". Korean J Anesthesiol. 63 (4): 368–71. doi:10.4097/kjae.2012.63.4.368. PMC 3483499. PMID 23115693.
- ↑ Šedý J, Kuneš J, Zicha J (August 2015). "Pathogenetic Mechanisms of Neurogenic Pulmonary Edema". J. Neurotrauma. 32 (15): 1135–45. doi:10.1089/neu.2014.3609. PMID 25496372.
- ↑ Piatti L, Locatelli V, Ferracini C, Sozzi G (August 1984). "[Neurogenic pulmonary edema. Description of a case occurring after an epileptic crisis]". G Ital Cardiol (in Italian). 14 (8): 602–5. PMID 6437896.
- ↑ Pender ES, Pollack CV (1992). "Neurogenic pulmonary edema: case reports and review". J Emerg Med. 10 (1): 45–51. PMID 1629591.
- ↑ Fontes RB, Aguiar PH, Zanetti MV, Andrade F, Mandel M, Teixeira MJ (April 2003). "Acute neurogenic pulmonary edema: case reports and literature review". J Neurosurg Anesthesiol. 15 (2): 144–50. PMID 12658001.
- ↑ Solenski NJ, Haley EC, Kassell NF, Kongable G, Germanson T, Truskowski L, Torner JC (June 1995). "Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study". Crit. Care Med. 23 (6): 1007–17. PMID 7774210.
- ↑ Bratton SL, Davis RL (April 1997). "Acute lung injury in isolated traumatic brain injury". Neurosurgery. 40 (4): 707–12, discussion 712. PMID 9092843.
- ↑ 13.0 13.1 Ridenti FA (March 2012). "Neurogenic pulmonary edema: a current literature review". Rev Bras Ter Intensiva. 24 (1): 91–6. PMID 23917719.
- ↑ Baumann A, Audibert G, McDonnell J, Mertes PM (April 2007). "Neurogenic pulmonary edema". Acta Anaesthesiol Scand. 51 (4): 447–55. doi:10.1111/j.1399-6576.2007.01276.x. PMID 17378783.
- ↑ Fontes RB, Aguiar PH, Zanetti MV, Andrade F, Mandel M, Teixeira MJ (April 2003). "Acute neurogenic pulmonary edema: case reports and literature review". J Neurosurg Anesthesiol. 15 (2): 144–50. PMID 12658001.
- ↑ Tu YF, Lin CH, Lee HT, Yan JJ, Sze CI, Chou YP, Ho CJ, Huang CC (May 2015). "Elevated cerebrospinal fluid endothelin 1 associated with neurogenic pulmonary edema in children with enterovirus 71 encephalitis". Int. J. Infect. Dis. 34: 105–11. doi:10.1016/j.ijid.2015.03.017. PMID 25820093.
- ↑ Sarı MY, Yıldızdaş RD, Yükselmiş U, Horoz ÖÖ (December 2015). "Our patients followed up with a diagnosis of neurogenic pulmonary edema". Turk Pediatri Ars. 50 (4): 241–4. doi:10.5152/TurkPediatriArs.2015.1411. PMC 4743867. PMID 26884694.
- ↑ Piatti L, Locatelli V, Ferracini C, Sozzi G (August 1984). "[Neurogenic pulmonary edema. Description of a case occurring after an epileptic crisis]". G Ital Cardiol (in Italian). 14 (8): 602–5. PMID 6437896.