Recurrent Acute Neurogenic Pulmonary Edema after Uncontrolled Seizures

Abstract

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.

Neurological Perspectives of Neurogenic Pulmonary Edema

“…There are no systematic, prospective studies about the frequency of triggers of NPE available, but according to retrospective studies, the most frequent CNS disorders causing NPE include EV-71-associated brainstem encephalitis (myelitis), SAB (> 50% of cases) [1], open or closed TBI, and epilepsy with generalized seizures or epileptic states [1,4]. When screening the literature about NPE for CNS triggers between 2012 and 2019 (last 6 years), the trigger was EV-71-associated brainstem encephalitis in 621 cases, SAB in 97 cases, ICB in 34 cases, TBI in 32 cases, and seizure in 8 cases (Table 1).…”

“…Another argument for a common trigger is the study of Inamasu et al [34] in which 14 patients with NPE after SAB also had TTS. Diagnosis NPE is diagnosed upon clinical presentation, with a chest X-ray, and after exclusion of various differential diagnoses [4]. NPE is frequently diagnosed at the time of postmortem at autopsy, particularly in patients who die from sudden unexplained death in epilepsy (SUDEP) or in patients with TBI [1].…”

“…Proposed criteria for diagnosing NPE include pulmonary edema, bilateral opacities (infiltrates) on X-ray of the lungs, rapid resolution of the opacities, pink, frothy sputum or occasionally hemoptysis, PaO 2 :PiO 2 < 200 mm Hg, acute CNS compromise severe enough to increase the intra-cranial pressure, absence of left atrial hypertension on echocardiography, and absence of other common causes of respiratory distress or acute respiratory distress syndrome. Differential diagnoses of NPE that have to be excluded before diagnosing NPE include cardiogenic pulmonary edema, aspiration pneumonia, pneumonitis, sepsis, negative pressure pulmonary edema, post-airway obstruction edema, ventilator-associated pneumonia, ventilation-induced lung injury, and transfusion-related lung injury [1,2,4,13]. If heart failure was excluded and if pulmonary edema develops rapidly and bilaterally, and without a definite cause, NPE is quite likely [4].…”

“…Differential diagnoses of NPE that have to be excluded before diagnosing NPE include cardiogenic pulmonary edema, aspiration pneumonia, pneumonitis, sepsis, negative pressure pulmonary edema, post-airway obstruction edema, ventilator-associated pneumonia, ventilation-induced lung injury, and transfusion-related lung injury [1,2,4,13]. If heart failure was excluded and if pulmonary edema develops rapidly and bilaterally, and without a definite cause, NPE is quite likely [4]. If clinical or radiological abnormalities resolve within 48-72 h after onset, NPE should be strongly suspected [4].…”

“…If heart failure was excluded and if pulmonary edema develops rapidly and bilaterally, and without a definite cause, NPE is quite likely [4]. If clinical or radiological abnormalities resolve within 48-72 h after onset, NPE should be strongly suspected [4].…”