Acute Neurogenic Pulmonary Edema Research Articles

Acute Neurogenic Pulmonary Edema After Unanticipated Challenging Airway in A Case of Pediatric Cystic Craniopharyngioma

Acute Neurogenic Pulmonary Edema After Unanticipated Challenging Airway in A Case of Pediatric Cystic Craniopharyngioma

Acute Neurogenic Pulmonary Edema: The Unaddressed Mechanism of Death

Impaired pulmonary function is a frequent but poorly understood complication of acute head injury. A potential early contributor to the pulmonary dysfunction seen in Head injury patients is neurogenic pulmonary edema (NPE). Neurogenic Pulmonary Edema is pulmonary edema that is associated with neurological diseases in patients in whom no other cardiac or pulmonary cause for the edema is apparent. It is associated with several acute neurological catastrophes; including spontaneous intracranial haemorrhage in general and Sub-arachnoid haemorrhage secondary to aneurysmal rupture in particular, sudden unexpected death in epilepsy, and traumatic brain injuries of various types. Often, very less described in the literature, this can be an immediate cause of death in patients with head injuries. Its pathophysiology is multifactorial but largely unknown. It‘s not only for the clinician to be aware of this clinical entity but it‘s also important for the Forensic Medicine expert to know about the pathophysiology, clinical presentation and autopsy findings of NPE. This paper aims to review the current concepts on pathophysiologic mechanisms involved in the development of NPE and discuss the facts which are relevant for a Forensic expert.

Acute neurogenic pulmonary edema following electroconvulsive therapy: a case report

ObjectiveWe report the case of a 47-year-old man with depression who developed acute dyspnea, hypoxemia, and mild hemoptysis after electroconvulsive therapy (ECT). MethodIntravenous carbazochrome sodium sulfate hydrate as a hemostatic drug (100 mg/day) was prescribed for 2 days. On the day of ECT, oxygen inhalation (4 L/min) was continued, and SpO2 was maintained at 94–96%. ResultsChest radiography showed improvement in alveolar infiltration. Chest CT 6 days after ECT also confirmed the disappearance of ground glass opacities in the lung fields. Conclusion(s)NPE is lifethreatening and should be recognized as an uncommon adverse event associated with ECT.

Acute Neurogenic Pulmonary Edema After Depth Electrode Placement for Epilepsy Surgery

Acute Neurogenic Pulmonary Edema After Depth Electrode Placement for Epilepsy Surgery

Posictal neurogenic pulmonary edema secondary to acute poisoning by organochlorine pesticide in an adolescent suicide attempt

We reported the case of an adolescent, without neurological background, who attempted suicide by organochlorine pesticide ingestion. The acute intoxication was expressed as a convulsive status epilepticus followed by an acute neurogenic pulmonary edema with rapid recovery within 48 hours. The diagnosis of neurogenic pulmonary edema in pediatrics, and particulary after a seizure, is unusual and often an exclusion one. Its evolution tends to be favorable, but can be fatal if it is not recognized and treated early. An acute nervous system injury associated with signs and symptoms of respiratory failure suggests the diagnosis. Other causes of pulmonary edema must be ruled out in order to avoid evaluation and treatment mistakes.

Autonomic dysreflexia and associated acute neurogenic pulmonary edema in a patient with spinal cord injury: a case report and review of the literature

A case report of a patient with spinal cord injury with autonomic dysreflexia and associated acute neurogenic pulmonary edema. To further describe autonomic dysreflexia as a potential cause of acute neurogenic pulmonary edema; specifically in a population with spinal cord injury. James A Haley Veterans Hospital, Tampa, FL, USA. A patient with a prior history of C5 AIS (ASIA impairment scale) B spinal cord injury was admitted for bowel preparation before a screening colonoscopy. During the 2-day bowel preparation, the patient developed severe autonomic dysreflexia. Due to persistent hypertension and acute onset respiratory failure, he required transfer to the intensive care setting. Following a complicated course, the patient expired without a definitive cause of death. Autopsy findings showed gross and microscopic evidence of pulmonary edema. To date, the association between autonomic dysreflexia and acute neurogenic pulmonary edema is not described in the spinal cord or rehabilitation literature. The purpose of this case report is to further describe the overlooked and/or under reported incidence of acute neurogenic pulmonary edema associated with episodes of dysreflexia in a population with spinal cord injury.

A Seven-Month-Old Infant With Acute Onset of Neurologic Deterioration

A Seven-Month-Old Infant With Acute Onset of Neurologic Deterioration

Stereotactic biopsy complicated by pneumocephalus and acute pulmonary edema

Background The aim of this study was to describe pneumocephalus as a rare complication of stereotactic biopsy and as a possible cause of acute neurogenic pulmonary edema. Case Description A case of frameless stereotactic biopsy complicated by pneumocephalus presenting with acute lung injury 48 hours after the procedure. A frameless stereotactic procedure was performed in the standard fashion. Immediate postoperative CT showed no intracranial air except for a gas inclusion at the biopsy site within the lesion. The skin staple placed at the end of surgery on the skin incision was removed 36 hours later. A CT scan performed 48 hours postoperatively showed new pneumocephalus. The patient exhibited acute respiratory distress but no new neurologic symptoms. There was no detectable systemic cause for the pulmonary edema. The patient received supportive respiratory treatment and fully recovered. Conclusion Pneumocephalus is apparently a rare complication of stereotactic brain biopsy and one that may result from early removal of the skin staple or suture. The occurrence of acute neurogenic pulmonary edema may be attributed to the pneumocephalus.

Neurogenic Pulmonary Edema Due to Traumatic Brain Injury: Evidence of Cardiac Dysfunction

Acute neurogenic pulmonary edema, a common and underdiagnosed clinical entity, can occur after virtually any form of injury of the central nervous system and is a potential early contributor to pulmonary dysfunction in patients with head injuries. To explore myocardial function in patients with evident neurogenic pulmonary edema after traumatic head injury. During a 1-year period in a university hospital in Sfax, Tunisia, information was collected prospectively on patients admitted to the 22-bed intensive care unit because of isolated traumatic head injury who had neurogenic pulmonary edema. Data included demographic information, vital signs, neurological status, physiological status, and laboratory findings. All of the patients had computed tomography and plain radiography of the neck and determination of cardiac function. All 7 patients in the sample had cardiac dysfunction. Evidence of myocardial damage was confirmed by echocardiography in 3 patients, pulmonary artery catheterization in 3 patients, and/or postmortem myocardial biopsy in 4 patients. Echocardiography studies, repeated 7 days after the initial study in one patient and 90 days afterward in another, showed complete improvement in wall motion, with a left ventricular ejection fraction of 0.65. All patients who had neurogenic pulmonary edema due to traumatic head injury had myocardial dysfunction. The mechanisms of the dysfunction were multiple. The great improvement in wall motion seen in 2 patients indicated the presence of a stunned myocardium. Further studies are needed to understand the mechanisms of this cardiac dysfunction.

Acute Neurogenic Pulmonary Edema

Survey of Anesthesiology: April 2004 - Volume 48 - Issue 2 - p 80-81 doi: 10.1097/01.sa.0000119062.14209.9b

Effect of neonatal capsaicin treatment on neurogenic pulmonary edema from fluid-percussion brain injury in the adult rat

The frequent occurrence of acute death from pulmonary failure in experimental head injury studies on Sprague-Dawley rats prompted an investigation into the manner in which acute neurogenic pulmonary edema develops in these animals as a result of an applied fluid pressure pulse to the cerebral hemispheres. Studies were performed in adult animals using histamine H1 and H2 blocking agents, or in adult animals treated as neonates with capsaicin to destroy unmyelinated C-fibers. Recordings were made of either the pulmonary arterial or the right ventricular pressure, and the left atrial and femoral arterial pressures before, during, and after injury to provide a record of the hemodynamic response throughout the development of neurogenic pulmonary edema. Head injury triggered the almost immediate development of pressure transients with and without neurogenic pulmonary edema. All rats, regardless of treatment, reacted with nearly identical systemic arterial pressure responses; however, the pulmonary responses followed a time course that was independent of systemic arterial pressure changes. Acute neurogenic pulmonary edema was always associated with a substantial increase in pulmonary arterial and left atrial pressures; conversely, pressure increases of similar magnitude were not always associated with edema. Histamine H1 and H2 blockers significantly reduced the pulmonary pressure surges only in rats free of neurogenic pulmonary edema. All capsaicin-treated rats showed suppressed pulmonary pressure responses, normal lung water content, elevated lung surface tension, and significantly reduced levels of immunoreactive substance P in the spinal cord and vagus nerve. While the pressures cannot clarify how edema influences the observed hemodynamics, they do not support the view that edema is the direct consequence of pulmonary hypertension. It is proposed that neurogenic pulmonary edema is a functional disturbance provoked by adverse stimuli from outside the lungs and that in the rat the primary afferent fiber is essential to the production of this entity.

Neurogenic Pulmonary Edema after Trigeminal Nerve Blockade

Acute neurogenic pulmonary edema developed immediately after injection of bupivacaine hydrochloride into the trigeminal cistern of a 32-year-old man with atypical facial pain and no prior history of cardiopulmonary problems. This complication of trigeminal nerve blockade has not been reported previously, to our knowledge. Associated neurologic deficits suggest a key role for the brain stem in the pathogenesis of this disorder.

重症クモ膜下出血に伴う急性肺水腫

重症クモ膜下出血に伴う急性肺水腫