Neurogenic pulmonary edema (NPE) is a potentially life-threatening condition which has been noted in head injury, subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH) and others.

It is a relatively rare form of pulmonary edema caused by an increase in pulmonary interstitial and alveolar fluid. Neurogenic pulmonary edema develops within a few hours after a neurologic insult.

The incidence of NPE in subarachnoid hemorrhage was 8% (39 of 477 patients). Most patients with NPE were severely impaired and all of them presented with radiologically severe hemorrhage. The incidence of NPE was significantly higher in patients with ruptured aneurysm in the posterior circulation. Elevated intracranial pressure was found in 67%, pathologically high cardiac biomarkers in up to 83% of patients with NPE. However, no patient suffered from persistent cardiac dysfunction. Compared with patients without NPE, patients with NPE showed poor neurologic outcome (Glasgow outcome scale 1 to 3 in 25% vs.77% of patients). In conclusion, patients with NPE have a high mortality rate more likely due to their severity grade of the bleeding. Morbidity and mortality due to cardiopulmonary failure might be reduced by appropriate recognition and treatment. The awareness of and knowledge about occurrence, clinical presentation, and treatment of NPE, are essential for all those potentially confronted with patients with SAH in the acute phase ¹⁾.

Neurogenic pulmonary edema (NPE) occurs frequently after aneurysmal subarachnoid hemorrhage (SAH), and excessive release of catecholamines (epinephrine/norepinephrine) has been suggested as its principal cause.

Elevated plasma norepinephrine may have more active role in the pathogenesis of SAH-induced NPE compared with epinephrine, although both catecholamines may be involved via multiple signaling pathways ²⁾.

Systemic manifestations of traumatic brain injury ³⁾.

Neurogenic pulmonary edema occurs as a complication of acute neurologic illness and may mimic acute lung injury of other etiology. Its presence is important to recognize in patients due to its impact on clinical course, prognosis, and treatment strategies ⁴⁾.

Neurogenic pulmonary edema (NPE) is an acute and serious complication after subarachnoid hemorrhage (SAH) with high mortality.

The incidence of clinical symptoms was correlated with pulmonary index. P2X7R and the marker of alveolar type I epithelial cells (the mucin-type glycoprotein T1-α) immunoreactivities were generally co-localized. BBG administration decreased mature interleukin-1β, myeloperoxidase, and matrix metallopeptidase-9 activation, but increased tight junction proteins, such as ZO-1 and occludin, which ameliorated pulmonary edema via anti-inflammation and improved neurological deficits.

P2X7R inhibition prevented NPE after SAH by attenuating inflammation. Thus, BBG is a potential therapeutic application for NPE after SAH and warrants further research ⁵⁾. Pulmonary complications occur in about 80% of patients with aSAH. Massive catecholamine release during ictus can cause pulmonary hypertension, increased hydrostatic pressure and pulmonary edema, increasing the risk of morbidity and mortality ⁶⁾.

Myocardial dysfunction and treatment for vasospasm with hypervolemia can aggravate this complication. Poor grade patients can aspirate oro-pharyngeal and gastric contents into the lungs due to depressed consciousness. Intubation and ventilation may be required in such patients to both protect the airway and to stabilize respiratory parameters ⁷⁾.

Diagnosis requires exclusion of other causes of pulmonary edema (eg, high-altitude pulmonary edema).

Includes myocardial infarction, myocarditis, and nonischemic cardiomyopathy ⁸⁾.

In a study Saracen et al., retrospectively reviewed medical records of 250 consecutive patients with aneurysmal subarachnoid hemorrhage (SAH) for the frequency and treatment results of NPE. The following factors were taken under consideration: clinical status, aneurysm location, presence of NPE, intracranial pressure (ICP), and mortality. All patients had plain- and angio-computer tomography performed. NPE developed most frequently in case of the aneurysm located in the anterior communicating artery. The patients with grades I-III of SAH, according to the World Federation of Neurosurgeons staging, were immediately operated on, while those with poor grades IV and V had only an ICP sensor's implantation procedure performed. A hundred and eighty five patients (74.4 %) were admitted with grades I to III and 32 patients (12.8 %) were with grade IV and V each. NPE was not observed in SAH patients with grade I to III, but it developed in nine patients with grade IV and 11 patients with grade V. Of the 20 patients with NPE, 19 died. Of the 44 poor grade patients (grades IV-V) without NPE, 20 died. All poor grade patients had elevated ICP in a range of 24-56 mmHg. The patients with NPE had a greater ICP than those without NPE. Gender and age had no influence on the occurrence of NPE. We conclude that the development of neurogenic pulmonary edema in SAH patients with poor grades is a fatal prognostic as it about doubles the death rate to almost hundred percent ⁹⁾.

A total of 204 patients with SAH were included in a multicenter prospective cohort study to investigate hemodynamic changes after surgical clipping or coil embolization of ruptured intracranial aneurysms by using a PiCCO-plus device. Changes in various hemodynamic parameters after SAH were analyzed statistically.

Fifty-two patients (25.5%) developed pulmonary edema. Patients with pulmonary edema (PE group) were significantly older than those without pulmonary edema (non-PE group) (p = 0.017). The mean extravascular lung water index was significantly higher in the PE group than in the non-PE group throughout the study period. The pulmonary vascular permeability index (PVPI) was significantly higher in the PE group than in the non-PE group on Day 6 (p = 0.029) and Day 10 (p = 0.011). The cardiac index of the PE group was significantly decreased biphasically on Days 2 and 10 compared with that of the non-PE group. In the early phase (Days 1-5 after SAH), the daily water balance of the PE group was slightly positive. In the delayed phase (Days 6-14 after SAH), the serum C-reactive protein level and the global end-diastolic volume index were significantly higher in the PE group than in the non-PE group, whereas the PVPI tended to be higher in the PE group.

Pulmonary edema that occurs in the early and delayed phases after SAH is caused by cardiac failure and inflammatory (i.e., noncardiogenic) conditions, respectively. Measurement of the extravascular lung water index, cardiac index, and PVPI by PiCCO-plus monitoring is useful for identifying pulmonary edema in patients with SAH ¹⁰⁾.

A 33-year female involved in a motor vehicular accident had a GCS of 14/15 and CT scan showed a moderate-sized unilateral Posterior fossa epidural hematoma (PFEDH). She had sudden deterioration in her haemodynamic status with drop in sensorium 2 hours after admission. There was a copious amount of frothy secretions noted on intubation and she was diagnosed as having neurogenic pulmonary edema.

Subocciptial craniectomy (SOC) with haematoma evacuation was performed and was managed with PEEP mechanical ventilation post-operatively. Excellent outcome was obtained and was discharged with a GOS of 5 ¹¹⁾.