Neurogenic pulmonary edema

Davison, Danielle; Terek, Megan; Chawla, Lakhmir S.

doi:10.1186/cc11226

Cited by 234 publications

(266 citation statements)

References 37 publications

(56 reference statements)

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“…This clinical syndrome is characterized by an increase in interstitial and alveolar fluid in response to an acute central nervous system injury (e.g., SAH or severe head injury). 4 Neurogenic pulmonary edema occurs as a result of a surge in the levels of endogenous serum catecholamines, which may result in changes in cardiopulmonary hemodynamics. 3 We evaluated patient hemodynamics after SAH by using a PiCCO-plus device and found that the cause of pulmonary edema differed according to the timing of its onset.…”

Section: Discussionmentioning

confidence: 99%

A multicenter prospective cohort study of volume management after subarachnoid hemorrhage: circulatory characteristics of pulmonary edema after subarachnoid hemorrhage

Obata

Takeda

Sato

et al. 2016

JNS

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S ubarachnoid hemorrhage (SAH) from a ruptured aneurysm is accompanied by several complications, including electrolyte abnormalities, vasospasm, hydrocephalus, cardiac dysfunction, and pulmonary edema. 15,16,18 Among these complications, delayed cerebral ischemia (DCI) remains an important cause of morbidity and death. 15 Many studies have investigated the prevention or treatment of DCI after SAH.Triple-H therapy (i.e., hypertension, hypervolemia, and hemodilution) has reportedly been an effective approach abbreviatioNs CI = cardiac index; CRP = C-reactive protein; DCI = delayed cerebral ischemia; ELWI = extravascular lung water index; GEDI = global end-diastolic volume index; PVPI = pulmonary vascular permeability index; SAH = subarachnoid hemorrhage; SVRI = systemic vascular resistance index; WFNS = World Federation of Neurosurgical Societies. obJective Subarachnoid hemorrhage (SAH) is often accompanied by pulmonary complications, which may lead to poor outcomes and death. This study investigated the incidence and cause of pulmonary edema in patients with SAH by using hemodynamic monitoring with PiCCO-plus pulse contour analysis. methods A total of 204 patients with SAH were included in a multicenter prospective cohort study to investigate hemodynamic changes after surgical clipping or coil embolization of ruptured cerebral aneurysms by using a PiCCO-plus device. Changes in various hemodynamic parameters after SAH were analyzed statistically. results Fifty-two patients (25.5%) developed pulmonary edema. Patients with pulmonary edema (PE group) were significantly older than those without pulmonary edema (non-PE group) (p = 0.017). The mean extravascular lung water index was significantly higher in the PE group than in the non-PE group throughout the study period. The pulmonary vascular permeability index (PVPI) was significantly higher in the PE group than in the non-PE group on Day 6 (p = 0.029) and Day 10 (p = 0.011). The cardiac index of the PE group was significantly decreased biphasically on Days 2 and 10 compared with that of the non-PE group. In the early phase (Days 1-5 after SAH), the daily water balance of the PE group was slightly positive. In the delayed phase (Days 6-14 after SAH), the serum C-reactive protein level and the global end-diastolic volume index were significantly higher in the PE group than in the non-PE group, whereas the PVPI tended to be higher in the PE group. coNclusioNs Pulmonary edema that occurs in the early and delayed phases after SAH is caused by cardiac failure and inflammatory (i.e., noncardiogenic) conditions, respectively. Measurement of the extravascular lung water index, cardiac index, and PVPI by PiCCO-plus monitoring is useful for identifying pulmonary edema in patients with SAH.Clinical trial registration no.: UMIN000003794 (clinicaltrials.gov)http://thejns.org/doi/abs/10.3171/2015.6.JNS1519

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Section: Discussionmentioning

confidence: 99%

A multicenter prospective cohort study of volume management after subarachnoid hemorrhage: circulatory characteristics of pulmonary edema after subarachnoid hemorrhage

Obata

Takeda

Sato

et al. 2016

JNS

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“…Catecholamines can cause significant pulmonary and peripheral vascular changes by provoking a rapid shift of blood to the central circulation mediated through systemic (Lord et al 1975;Davison et al 2012;Drobatz and MacIntire 2012) and pulmonary vasoconstriction ("blast theory") (Bachman and Waldrop 2012;Davison et al 2012), in turn leading to systemic and pulmonary hypertension (Bachman and Waldrop 2012). This increases the pressure in the left atrium as a result of a reduced cardiac output and increased peripheral vascular resistance (Davison et al 2012), producing an increase in hydrostatic pulmonary pressure and damage to the alveolo-capillar epithelium, which ultimately results in vascular disruption and fluid escape (Bachman and Waldrop 2012).…”

Section: Discussionmentioning

confidence: 99%

“…This increases the pressure in the left atrium as a result of a reduced cardiac output and increased peripheral vascular resistance (Davison et al 2012), producing an increase in hydrostatic pulmonary pressure and damage to the alveolo-capillar epithelium, which ultimately results in vascular disruption and fluid escape (Bachman and Waldrop 2012). All these mechanisms can be followed by lymphatic vasoconstriction and insufficient lymphatic circulation (Glaus et al 2010) worsening oedema formation.…”

Section: Discussionmentioning

confidence: 99%

“…With the exception of hypoglycaemia all these findings were evident in this case. It is suspected that the mechanism of NCPO involves massive central neural sympathetic stimulation in the medulla oblongata (Davison et al 2012), which promotes the release of a large amount of catecholamines (Malik 1985;Glaus et al 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Massive central sympathetic doi: 10.17221/8419-VETMED neural stimulation releases large amounts of catecholamines into the bloodstream. The consequences of the release of catecholamines are not entirely clear, but they seem to involve significant pulmonary and peripheral vasoconstriction, which ends in pulmonary and systemic hypertension (Malik 1985;Glaus et al 2010;Davison et al 2012). This paper describes a hunting dog that developed pulmonary oedema after chasing prey.…”

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Pulmonary oedema in a hunting dog: a case report

Agudelo¹,

Schánilec²

2015

Vet. Med. - Czech

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This case report describes an episode of acute dyspnoea after hunting in a Dachshund dog. Thoracic radiographs confirmed pulmonary oedema. Echocardiography, electrocardiography and cardiac markers were within normal limits. Based on the history, clinical signs and other diagnostic tests this case could have been neurogenic non-cardiogenic pulmonary oedema-like syndrome as described in Swedish dogs also after hunting and probably the first case detected in Central Europe. The dog survived with intense oxygen, diuretic and bronchodilator therapy. The pathological mechanisms of neurogenic non-cardiogenic pulmonary oedema are also discussed.Keywords: neurogenic lung oedema; diuretic therapy; oxygen; catecholamines List of abbreviations ARDS = acute respiratory distress syndrome, CBC = complete blood count, ECG = electrocardiogram, NCPO = non-cardiogenic pulmonary oedema, NP = natriuretic peptides, NT-proBNP = N-terminal pro-brain natriuretic peptide, SAS = sympatico-adrenal system, VHS = vertebral heart size

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What caused this subarachnoid hemorrhage?

Maas

Naidech

2019

Warlow's Stroke

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Neurogenic pulmonary edema

Cited by 234 publications

References 37 publications

A multicenter prospective cohort study of volume management after subarachnoid hemorrhage: circulatory characteristics of pulmonary edema after subarachnoid hemorrhage

A multicenter prospective cohort study of volume management after subarachnoid hemorrhage: circulatory characteristics of pulmonary edema after subarachnoid hemorrhage

Pulmonary oedema in a hunting dog: a case report

What caused this subarachnoid hemorrhage?

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