Lung Injury, Myocardial Injury, Subarachnoid Hemorrhage
Conditions
Keywords
myocardial injury, lung injury, SAH, subarachnoid haemorrhage, metanephrine, catecholamine-induced injury, Intensive Care Unit, neurocritical care
Brief summary
Up to this day, little is known whether the extent of brain damage in patients with SAH correlates with the degree neurogenic myocardial injury and neurogenic lung injury. This is a prospective observational study designed to asses relationship between catecholamine surge and development of myocardial and lung injury in subarachnoid haemorrhage patients.
Detailed description
Multiple forms of brain damage, primarily, subarachnoid haemorrhage (SAH) are frequently accompanied by neurogenic myocardial injury with changes in the electrocardiogram, accompanied by the release of markers of myocardial injury. This form of cardiac dysfunction is thought to be mediated by cellular toxicity associated with catecholamine release. Central nervous system damage in the course of intracranial haemorrhage may, in a similar pathogenic pathway, lead to neurogenic lung injury. Up to this day, little is known whether the extent of brain damage in patients with SAH correlates with the degree of neurogenic myocardial injury. Moreover, it remains unknown what is the full clinical picture and duration of this type of myocardial injury and how often it co-occurs with neurogenic lung injury. Such analysis is a fundamental and most important step in optimising the treatment of these patients. Methods: In this prospective observational study the authors aim to recruit 30 patients with subarachnoid haemorrhage, requiring hospitalization in the Intensive Care Unit. The patients will be monitored for elevation in cardiac damage markers (hs-TnT, CPK, CK-MB, NT-proBNP) and worsening of respiratory conditions, defined by need for more invasive ventilation parameters, and subsequent changes in arterial blood gas. The above mentioned parameters will be assessed every 12 hours. Additionally, the patients will be screened for an elevation in catecholamine metabolite (metanephrine) concentration in 12-hour urine collection. Hypothesis to be tested: Myocardial and lung injury in SAH patients is timely-associated with an increase in metanephrine concentration in urine.
Interventions
DIAGNOSTIC_TESThs-TnT (high-sensitive cardiac troponin T) plasma concentration
hs-TnT plasma concentration measured once every 12 hours
DIAGNOSTIC_TESTCK-MB (creatine kinase myocardial band) plasma concentration
CK-MB plasma concentration measured every 12 hours
DIAGNOSTIC_TESTCPK (creatine phosphokinase) plasma concentration
CPK plasma concentration measured every 12 hours
DIAGNOSTIC_TESTNT-proBNP (N-terminal prohormone of brain natriuretic peptide) plasma concentration
NT-proBNP plasma concentration measured every 12 hours
DIAGNOSTIC_TESTMetanephrine concentration in urine
Metanephrine concentration measured in 12-hour urine collection using spectrophotometry.
Sponsors
Medical University of Silesia
Study design
Observational model
COHORT
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No
Inclusion criteria
* patients with subarachnoid haemorrhage (both aneurysmal and non-aneurysmal) with acute consciousness disturbances (Glasgow Coma Scale \< 8 pts) requiring intubation and mechanical ventilation, hospitalized in the ICU for over 24 hours
Exclusion criteria
* severe prior pulmonary diseases * severe prior cardiac diseases * death in the first 72 hours of ICU stay * need for any extracorporeal life-saving techniques
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| In-hospital death (number of patients) | 7 days | Death of the patient during the first 7 days of hospitalization. |
| Number of Patients with elevation in hs-TnT levels | 7 days | hs-TnT treated as myocardial injury biomarker |
| Number of Patients with elevation in NT-proBNP levels | 7 days | NT-proBNP treated as myocardial injury biomarker |
| Number of Patients with elevation in creatine kinase levels | 7 days | Creatine kinase treated as myocardial injury biomarker |
| Number of Patients with elevation in creatine kinase MB levels | 7 days | Creatine kinase MB treated as myocardial injury biomarker |
| Number of Patients with a decrease in Horowitz index | 7 days | The decrease in Horowitz index treated as a sign of need for more invasive ventilation parameters with subsequent blood gas changes |
| Number of Patients with need of increased FiO2 | 7 days | Need of increased FiO2 treated as a sign of need for more invasive ventilation parameters with subsequent blood gas changes |
| Number of Patients with need of increased PEEP values | 7 days | Need of increased PEEP values treated as a sign of need for more invasive ventilation parameters with subsequent blood gas changes |
| Number of Patients with need for the use of neuro-muscular blocking agents | 7 days | Need for the use of neuro-muscular blocking agents treated as a sign of need for more invasive ventilation parameters with subsequent blood gas changes |
Countries
Poland
Contacts
Primary ContactNatalia Rachfalska
Outcome results
None listed