Acute Lung Injury Associated With Systemic Inflammatory Response Syndrome Following Subarachnoid Hemorrhage: a Survey by the Shonan Neurosurgical Association

Abstract

Acute lung injury (ALI) associated with systemic inflammatory response syndrome (SIRS) is a systemic complication following subarachnoid hemorrhage (SAH), but the incidence and influence on prognosis are unclear. The incidences of SIRS and ALI were surveyed in a prospective multicenter study of 96 patients admitted for SAH between December 2004 and June 2007. Hunt and Hess grade and Glasgow Outcome Scale score were also investigated. Forty-eight patients were diagnosed with SIRS, and 26 developed ALI within 4 weeks of admission. Nineteen of the 26 patients with ALI were complicated by SIRS, and 7 developed only ALI. Thirteen of the 19 patients complicated by SIRS and ALI died, and this mortality was higher than for patients with only SIRS (3/29) and only ALI (1/7). Multivariate analysis of the development of SIRS and/or ALI and Hunt and Hess grade as risk factors associated with aggravation of the outcome showed that complication with SIRS and ALI had the highest risk. Half of the patients admitted for SAH developed SIRS, and more than 25% developed ALI. The prognosis for patients complicated by SIRS and ALI was poor, which indicates that prevention and active treatment of these two pathologies are important.

Association between ventilatory settings and development of acute respiratory distress syndrome in mechanically ventilated patients due to brain injury

“…ARDS was also associated with a significant increase in mortality, and it prolonged the duration of mechanical ventilation and the length of ICU stay. Similarly, in previous reports, ARDS has been identified as a major contributor to the morbidity and mortality of patients with brain injuries [2,3,5,15,17,18,30]. ARDS also worsens longterm neurologic outcome [1,2,3,32], and is associated with longer ICU and hospital length of stay [5,29].…”

“…In previous reports, ARDS occurs in up to 20-38% of cases of subarachnoid haemorrhage [13][14][15], traumatic brain injury [1,16] and spontaneous intracerebral haemorrhage [4,5,17,18], and 35% reported in a mixed cohort of neurologically ill patients [19]. Variability in ARDS incidence may reflect differences in study populations and in diagnosis approach, variable use of consensus approach.…”

Hypoxic–ischemic brain damage induces distant inflammatory lung injury in newborn piglets

“…Extracerebral impact of perinatal asphyxia has been uniformly attributed to the redistribution of blood flow and/or the effects of global hypoxia-ischemia (2,3). Observational studies from adults indicate that lung injury may develop after local brain damage such as intracranial hemorrhage, traumatic brain injury, or ischemic cerebral stroke (4)(5)(6). For these conditions, the incidence of lung injury is related to the severity of brain damage and represents an independent factor associated with poor clinical outcome (7).…”

“…In adult animal models and in patients suffering from subarachnoid hemorrhage, brain injury leads to a systemic inflammatory response with upregulation of inflammatory mediators such as TNF-α, intracellular adhesion molecule-1, IL-1β, and NF-kB and reactive oxygen species, microglial activation, and neutrophil accumulation (5,9,10). It has been hypothesized that lung injury might be triggered by the spread of that (such a systemic) response, favored by the disruption of the blood-brain barrier in the context of this inflammatory process (10).…”

Subarachnoid Hemorrhage Complicated With Neurogenic Pulmonary Edema and Takotsubo-Like Cardiomyopathy

“…Since the number of patients with SAH complicated with NPE-TCM is relatively small, a multi-center cooperative study may be required to clarify the issue. 17) The SAH grade on admission may be an important prognosticator, and so that outcome of grade IV patients was significantly better compared with that of grade V patients is not surprising. Most grade V patients died of primary brain damage incurred at the time of aneurysm rupture rather than cardiopulmonary dysfunction due to NPE-TCM.…”