scholarly journals Recurrent Acute Neurogenic Pulmonary Edema after Uncontrolled Seizures

2018 ◽  
Vol 2018 ◽  
pp. 1-4 ◽  
Author(s):  
Daniel C. Sacher ◽  
Erika J. Yoo

Acute pulmonary edema following significant injury to the central nervous system is known as neurogenic pulmonary edema (NPE). Commonly seen after significant neurological trauma, NPE has also been described after seizure. While many pathogenic theories have been proposed, the exact mechanism remains unclear. We present a 31-year-old man who developed recurrent acute NPE on two consecutive admissions after experiencing witnessed generalized tonic-clonic (GTC) seizures. Chest radiographs obtained after seizure during both admissions showed bilateral infiltrates which rapidly resolved within 24 hours. He required intubation on each occasion, was placed on lung protective ventilation, and was successfully extubated within 72 hours. There was no identified source of infection, and no cardiac pathology was thought to be contributory.

2001 ◽  
Vol 29 (6) ◽  
pp. 1222-1228 ◽  
Author(s):  
Ossama Hamdy ◽  
Hiroshi Maekawa ◽  
Yasuhiro Shimada ◽  
Guo Gang Feng ◽  
Naohisa Ishikawa

2018 ◽  
Vol 21 (1) ◽  
pp. 49-52
Author(s):  
Carlos Eduardo Romeu De Almeida ◽  
Eberval Gadelha Figueiredo ◽  
Bernardo Assumpção De Monaco ◽  
Arthur Maynart Pereira Oliveira ◽  
Manoel Jacobsen Teixeira

Neurogenic Pulmonary Edema (NPE) is defined as the acute onset of dyspnea or a decrease in PaO2/FiO2 ratio, following an acute central nervous system (CNS) insult, in the absence of other obvious causes of lung injury. The most important cause of NPE is subarachnoid hemorrhage (SAH), followed by cerebraltrauma and epilepsy. The incidence of NPE after SAH in the literature may vary from 4 to 23% in greater studies, with SAH accounting for 43-73% of cases of NPE. It is postulated that an excessive adrenergic discharge would lead to pulmonary vasoconstriction and a rapid increase in pulmonary capillaryhydrostatic pressure, thus promoting fluid leakage to the alveolar space. NPE is generally treated in a supportive and conservative fashion, and patient management should be focused in the primary insult.


2008 ◽  
pp. 499-506
Author(s):  
J Šedý ◽  
J Zicha ◽  
J Kuneš ◽  
P Jendelová ◽  
E Syková

Neurogenic pulmonary edema is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. This review summarizes current knowledge about the etiology and pathophysiology of neurogenic pulmonary edema. The roles of systemic sympathetic discharge, central nervous system trigger zones, intracranial pressure, inflammation and anesthesia in the etiopathogenesis of neurogenic pulmonary edema are considered in detail. The management of the patient and experimental models of neurogenic pulmonary edema are also discussed.


Author(s):  
Pawan Gupta

An infectious disease, as the name implies, is caused by pathogenic microorganisms such as bacteria, viruses, parasites, and fungi, and it spreads from one person to another through various ways, directly or indirectly. Most, but not all, of such diseases present to the ED with fever. Septic shock, respiratory failure, or central nervous system involvement may occur following an infection and threaten life. Such a situation presenting with tachycardia, reduced BP, tachypnoea, or depressed GCS requires immediate assessment and resuscitation. Following the principles of ABCDE, promptly carry out airway protection, oxygenation, and IV access with collection of blood samples for investigations, and fluid resuscitation. The aetiology of fever may be wide ranging, but a careful history and a detailed physical examination should help in determining the cause in majority of cases presenting to the ED. In addition to this, the initial investigations may help further in establishing the diagnosis. In elderly patients, the source of such infections may be the respiratory system, the genitourinary system or the involvement of the soft tissues, and they are often serious. In the otherwise healthy younger patient, one must keep in mind the other systems such as the central nervous system, as well as abdominal and soft tissue infections. Patients may often present in septic shock. Even if the cause of a fever may not be evident at the outset, the best ‘guestimate’ often helps in determining which antibiotics to start with, which should be given as soon as the culture samples have been collected. One must make every effort to collect appropriate samples of body fluids (blood, urine, stool, sputum, etc.) to find the source of infection so that targeted antimicrobial therapy may be started if the empirical treatment has not worked. A discussion with the on-call microbiologist to properly direct the empirical antibiotic therapy is often most rewarding. A patient with an infectious disease may put others at risk as well, resulting in devastating effects, particularly in hospitals.


1957 ◽  
Vol 190 (1) ◽  
pp. 84-88 ◽  
Author(s):  
Richard N. Matzen

Massive pulmonary edema, varying degrees of alveolar hemorrhage and tracheo-bronchial inflammation occur in animals exposed to high concentrations of ozone. Initial exposures to low concentrations of ozone can prevent the formation of edema and death on subsequent severe exposures in mice. This tolerance was shown to be detectable in 24 hours and present for as long as 102 days. Protection is rendered against a challenging dose as high as 2 1/2 times the ld50. The signs caused by exposure suggest that the central nervous system may be affected as well as the lungs.


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