The mechanism of neurogenic pulmonary edema in epilepsy

Zhao, Hong; Lin, Gui-jun; Shi, Mumu; Gao, Jingli; Wang, Yanming; Wang, Hongzhi; Sun, Hai‐Ying; Cao, Yonggang

doi:10.1007/s12576-013-0291-6

Cited by 21 publications

(21 citation statements)

References 39 publications

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“…[10] Moreover, these patients had more signifi cant neurogenic pulmonary edema. [11] Persistent and intense excitation of the sympathetic nerve resulted in high-pressure and highpermeability pulmonary edema, leading to refractory hypoxemia, and decreased local immunity and clearing ability of the respiratory tract. So, A2DS2 score provides a basis for risk stratification and treatment regimen of post-stroke pneumonia.…”

Section: Discussionmentioning

confidence: 99%

Risk assessment of ischemic stroke associated pneumonia

Li¹,

Zhang²,

Wu-ping³

et al. 2014

World Journal of Emergency Medicine

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BACKGROUND: Cerebral stroke is a disease with a high disability rate and a high fatality rate. This study was undertaken to assess the risk of stroke associated pneumonia (SAP) in patients with ischemic stroke using A2DS2 score. METHODS:Altogether 1 279 patients with ischemic stroke who were treated in our department from 2009 to 2011 were retrospectively analyzed with A2DS2 score. A2DS2 score was calculated as follows: age ≥75 years=1, atrial fi brillation=1, dysphagia=2, male sex=1; stroke severity: NIHSS score 0-4=0, 5-15=3, ≥16=5. The patients were divided into three groups according to A2DS2 score: 620 in score 0 group, 383 in score 1-9 group, and 276 in score ≥10 group. The three groups were comparatively analyzed. The diagnostic criteria for SAP were as follows: newly emerging lesions or progressively infiltrating lesions on post-stroke chest images combined with more than two of the following clinical symptoms of infection: (1) fever ≥38 °C; (2) newly occurred cough, productive cough or exacerbation of preexisting respiratory tract symptoms with or without chest pain; (3) signs of pulmonary consolidation and/or wet rales; (4) peripheral white blood cell count ≥10×10 9 /L or ≤4×10 9 /L with or without nuclear shift to left, while excluding some diseases with clinical manifestations similar to pneumonia, such as tuberculosis, pulmonary tumors, non-infectious interstitial lung disease, pulmonary edema, pulmonary embolism and atelectasis. The incidence and mortality of SAP as well as the correlation with ischemic stroke site were analyzed in the three groups respectively. Mean± standard deviation was used to represent measurement data with normal distribution and Student's t test was used. The chi-square test was used to calculate the percentage for enumeration data. RESULTS:The incidence of SAP was significantly higher in the A2DS2 score≥10 group than that in the score 1-9 and score 0 groups (71.7% vs. 22.7%, 71.7% vs. 3.7%, respectively), whereas the mortality in the score≥10 group was signifi cantly higher than that in the score 1-9 and score 0 groups (16.7% vs. 4.96%, 16.7% vs. 0.3%, respectively). The incidences of cerebral infarction in posterior circulation and cross-MCA, ACA distribution areas were signifi cantly higher than those in the SAP group and in the non-SAP group (35.1% vs.10.1%, 11.4% vs. 7.5%, respectively). The incidence of non-fermentative bacteria infection was signifi cantly increased in the score≥10 group.CONCLUSIONS: A2DS2 score provides a basis for risk stratifi cation of SAP. The prevention of SAP needs to be strengthened in acute ischemic stroke patients with a A2DS2 score≥10.

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Section: Discussionmentioning

confidence: 99%

Risk assessment of ischemic stroke associated pneumonia

Li¹,

Zhang²,

Wu-ping³

et al. 2014

World Journal of Emergency Medicine

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“…A physiologic right‐to‐left shunt may also occur in the setting of pulmonary edema, as blood in the pulmonary vasculature does not come into contact with alveolar air due to filling of the alveolar spaces with fluid. Pulmonary edema may occur after seizures, possibly through centrally mediated effects on pulmonary vasculature and alveolar cells . Pulmonary edema is a commonly reported autopsy finding in cases of SUDEP …”

Section: Respiratory Mechanismsmentioning

confidence: 99%

From unwitnessed fatality to witnessed rescue: Nonpharmacologic interventions in sudden unexpected death in epilepsy

et al. 2016

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Summary Sudden unexpected death in epilepsy (SUDEP) risk reduction remains a critical aim in epilepsy care. To date, only aggressive medical and surgical efforts to control seizures have been demonstrated to be of benefit. Incomplete understanding of SUDEP mechanisms limits the development of more specific interventions. Periictal cardiorespiratory dysfunction is implicated in SUDEP; postictal electroencephalography (EEG) suppression, coma, and immobility may also play a role. Nocturnal supervision is protective against SUDEP, presumably by permitting intervention in the case of a life‐threatening event. Resuscitative efforts were implemented promptly in near‐SUDEP cases but delayed in SUDEP deaths in the Mortality in Epilepsy Monitoring Unit Study (MORTEMUS) study. Nursing interventions—including repositioning, oral suctioning, and oxygen administration—reduce seizure duration, respiratory dysfunction, and EEG suppression in the epilepsy monitoring unit (EMU), but have not been studied in outpatients. Cardiac pacemakers or cardioverter‐defibrillator devices may be of benefit in a few select individuals. A role for implantable neurostimulators has not yet been established. Seizure detection devices, including those that monitor generalized tonic–clonic seizure‐associated movements or cardiorespiratory parameters, may provide a means to permit timely periictal intervention. However, these and other devices, such as antisuffocation pillows, have not been adequately investigated with respect to SUDEP prevention.

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“…The etiology of pulmonary edema in the present case remains unclear but could possibly result from HBOT, because the echocardiogram and electrocardiogram both yielded normal findings, and no other apparent reasons for the pulmonary edema such as infection, allergic reaction were detected. The other possible cause is neurogenic pulmonary edema secondary to the seizure because neurogenic pulmonary edema can occur following generalized seizure (8). In addition to adverse side effects and complications directly associated with HBOT, various unexpected events could occur because those who require emergent HBOT are generally critically ill.…”

Section: Discussionmentioning

confidence: 99%

Convulsive seizure and pulmonary edema during hyperbaric oxygen therapy:A case report

et al. 2018

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Hyperbaric oxygen therapy (HBOT) for carbon monoxide (CO) poisoning is widely performed to prevent delayed neuropsychiatric syndrome. Although HBOT can generally be performed with safety, the appropriate management of HBOT still remains unestablished. A 31-year-old man was transferred to our facility to undergo HBOT in a multiplace chamber with a diagnosis of CO poisoning. The first HBOT session ended uneventfully. During the second HBOT session, the patient suddenly experienced convulsive seizures. The accompanying doctor administered intravenous propofol to stop the convulsion and terminated the HBOT. Soon after the convulsion, the patient developed frothy secretions through the endotracheal-tube with impaired oxygenation. Head computed tomography scan showed no abnormalities, suggesting the seizure was associated with complications of HBOT. A chest X-ray revealed bilateral pulmonary edema, and echocardiography revealed normal cardiac function, indicating that the pulmonary edema resulted from HBOT or neurogenic mechanism secondary to the seizure. The patient's respiratory status improved without recurrence of the seizure and no delayed neurological sequelae was seen afterwards. Here we report unexpected rare adverse events during HBOT. Hyperbaric oxygen therapy for acute indications should be performed in multiplace chambers, with appropriate preparation and medical equipment.

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The mechanism of neurogenic pulmonary edema in epilepsy

Cited by 21 publications

References 39 publications

Risk assessment of ischemic stroke associated pneumonia

Risk assessment of ischemic stroke associated pneumonia

From unwitnessed fatality to witnessed rescue: Nonpharmacologic interventions in sudden unexpected death in epilepsy

Convulsive seizure and pulmonary edema during hyperbaric oxygen therapy:A case report

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