Neurogenic pulmonary edema: Difference between revisions
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==Overview== | ==Overview== | ||
Revision as of 19:11, 14 March 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Shaghayegh Habibi, M.D.[2]
Overview
Historical Perspective
- [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
- In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
- In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
Classification
- [Disease name] may be classified according to [classification method] into [number] subtypes/groups:
- [group1]
- [group2]
- [group3]
- Other variants of [disease name] include [disease subtype 1], [disease subtype 2], and [disease subtype 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.[1][2]
- Neurogenic pulmonary edema is an acute life-threatening complication associated with many forms of central nervous system injury, such as:[2]
- Brain or spinal cord hemorrhage
- Trauma
- Tumors
- Epilepsy
- Infections
- The pathogenetic factors for the onset of neurogenic pulmonary edema include:[3]
- Increased intracranial pressure
- Severe over-activation of the sympathetic nervous system
- 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.[4]
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Clinical Features
Differentiating [disease name] from other Diseases
- Neurogenic pulmonary edema must be differentiated from other diseases with same symptoms, include:[5]
- Aspiration pneumonia
Epidemiology and Demographics
- The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
- In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].
Age
- Patients of all age groups may develop [disease name].
- [Disease name] is more commonly observed among patients aged [age range] years old.
- [Disease name] is more commonly observed among [elderly patients/young patients/children].
Gender
- [Disease name] affects men and women equally.
- [Gender 1] are more commonly affected with [disease name] than [gender 2].
- The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.
Race
- There is no racial predilection for [disease name].
- [Disease name] usually affects individuals of the [race 1] race.
- [Race 2] individuals are less likely to develop [disease name].
Risk Factors
- Severe brain damage represents a risk factor for developing neurogenic pulmonary edema, which include:[6]
- Cerebral hemorrhage
- Subarachnoid hemorrhage
- Head injuries
- Seizures
Natural History, Complications and Prognosis
- Misdiagnosis and inappropriate treatment may worsen cerebral damage because of hypoxemia or reduced cerebral perfusion pressure.[7]
- Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
- If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
- Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
- Prognosis is generally poor and the associated mortality rate is high, but surviving patients usually recover very quickly.[8][9]
Diagnosis
Diagnostic Criteria
- The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
- [criterion 1]
- [criterion 2]
- [criterion 3]
- [criterion 4]
Symptoms
- [Disease name] is usually asymptomatic.
- Symptoms of [disease name] may include the following:
- [symptom 1]
- [symptom 2]
- [symptom 3]
- [symptom 4]
- [symptom 5]
- [symptom 6]
Physical Examination
- Patients with [disease name] usually appear [general appearance].
- Physical examination may be remarkable for:
- [finding 1]
- [finding 2]
- [finding 3]
- [finding 4]
- [finding 5]
- [finding 6]
Laboratory Findings
- There are no specific laboratory findings associated with [disease name].
- A [positive/negative] [test name] is diagnostic of [disease name].
- An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
- Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
Imaging Findings
- There are no [imaging study] findings associated with [disease name].
- [Imaging study 1] is the imaging modality of choice for [disease name].
- On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
- [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
- There is no treatment for [disease name]; the mainstay of therapy is supportive care.
- The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
- [Medical therapy 1] acts by [mechanism of action 1].
- Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].
Surgery
Prevention
- Treating the underlying neurologic disease is the only way of preventing the recurrence of pulmonary edema.[10]
References
- ↑ Smith WS, Matthay MA (May 1997). "Evidence for a hydrostatic mechanism in human neurogenic pulmonary edema". Chest. 111 (5): 1326–33. PMID 9149590.
- ↑ 2.0 2.1 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.
- ↑ 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.
- ↑ Ridenti FA (March 2012). "Neurogenic pulmonary edema: a current literature review". Rev Bras Ter Intensiva. 24 (1): 91–6. PMID 23917719.
- ↑ 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.
- ↑ 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.