Stellate ganglion block may prevent the development of neurogenic pulmonary edema and improve the outcome.

Nov 2012

Zhang L, Yao J, Zhang T, Jin J, Zeng X, Yue Z.

Source

Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, Heilongjiang Province, China.

Abstract

Neurogenic pulmonary edema (NPE) is an acute and serious complication after a central nervous system insult with high mortality. The pronounced activation of sympathetic nervous system and the release of vasoactive substances are necessary prerequisites for the development of NPE. We introduce a hypothesis that stellate ganglion block (SGB) may prevent NPE development on the basis of the inhibition of sympathetic overactivation, reduction of the concentration of norepinephrine and attenuation of baroreflex sensitivity, and improve the outcome by improving cerebral blood flow and pulmonary circulation and maintaining cardiovascular stability. In clinical practice, the guidance technique and close monitoring might guarantee the safety of SGB. If our hypothesis is supported by further experiments, this may open a new doorway for the treatment of NPE.

Elsevier

Neurogenic Pulmonary Edema and Acute Respiratory Distress Syndrome in a Healthy Child With Febrile Status Epilepticus.

August 2012

Nguyen TT, Hussain E, Grimason M, Goldstein J, Wainwright MS.

Abstract

Neurogenic pulmonary edema is a clinical syndrome that manifests as an acute onset of pulmonary edema in the setting of a central nervous system injury, without cardiac dysfunction. Neurogenic pulmonary edema is rare in children, and the mechanism is still not completely understood. The clinical pathology overlaps with acute lung injury and acute respiratory distress syndrome. The authors report a case of a 14-month-old previously healthy child who presented with febrile status epilepticus, fulminant neurogenic pulmonary edema, and acute respiratory distress syndrome. Neurogenic pulmonary edema should be considered in the differential diagnosis for the rapid progression of respiratory failure following an acute neurological injury such as status epilepticus in a child. Prompt respiratory support and treatment of the acute neurological insult can prevent further cerebral hypoxemic injury.

SAGE Journals

Neurogenic pulmonary edema associated with underlying lung disease after a breakthrough seizure.

2012

Dutta G, Demetis S.

Source

Department of Internal Medicine, Lutheran Medical Center, 150 55th Street, Brooklyn, NY 11209, USA.

Abstract

Neurogenic pulmonary edema (NPE) can result from various central nervous system disorders such as brain malignancies, traumatic brain injuries, infections, and seizures. Although the pathogenesis is not completely understood, NPE creates an increase in pulmonary interstitial and alveolar fluid. It has been reported with prolonged seizure activity. Treatment for NPE is largely supportive. If unrecognized, it can lead to hypoxia and respiratory arrest. We report a case of NPE in a middle-aged female patient following a breakthrough seizure in whom an immunological cause for respiratory findings was high on the differential list, based on her past medical history and chronicity of symptoms. Rapid symptomatic and radiological improvement following hospitalization led to the correct diagnosis.

NIH

Sudden Death in Toddlers with Viral Meningitis, Cerebral Edema, Lund Edema

Sudden Death in Toddlers with Viral Meningitis, Massive Cerebral Edema, and Neurogenic Pulmonary Edema and Hemorrhage: Report of Two Cases.
Pediatr Dev Pathol. 2007 Mar

Krous H,
Chadwick A,
Miller D,
Crandall L,
Kinney H.

Viral (lymphocytic) meningitis typically does not cause sudden death, especially in the absence of severe inflammation in the brain or other organs. We report two toddlers with clinical evidence of a viral infection who died unexpectedly and were found at autopsy to have lymphocytic meningitis associated with severe brain edema, transtentorial herniation, neurogenic pulmonary edema and hemorrhage, and cardiomegaly. Influenza A, demonstrated in tracheal epithelium by immunocytochemistry, is the presumed cause of the mild meningitis in one case; adenovirus was cultured from swabs of the brain and anus in the second case.

Current concepts of neurogenic pulmonary edema and acute cardiac dysfunction associated with intracranial disease are discussed in considering the mechanism of sudden death in these toddlers. These cases emphasize the possibility that mild intracranial viral infections may be a rare cause of sudden death via lethal cardiopulmonary complications. They also underscore the importance of a comprehensive autopsy, including detailed neuropathologic examination and viral testing, in determining of the cause of unexpected death in toddlers.

PMID: 17378656 [PubMed - as supplied by publisher]