Risk factors and outcomes associated with systolic dysfunction following traumatic brain injury

Jungen Li1, Yuzhu Miao2, Guoxing Zhang3

  • 1Department of Emergency, the First Affiliated Hospital of Soochow University, Suzhou, China.

Medicine
|July 26, 2024
PubMed

Insights

Early detection of systolic dysfunction after moderate-severe traumatic brain injury (Ims-TBI) is crucial. Higher heart rate, lower Glasgow Coma Scale (GCS) score, and elevated cardiac troponin T levels on admission predict this complication and impact patient survival.

Area of Science:

  • Neurology
  • Cardiology
  • Critical Care Medicine

Background:

  • Systolic dysfunction is a known complication following moderate-severe traumatic brain injury (Ims-TBI).
  • Early predictors and prognostic impact of post-Ims-TBI systolic dysfunction remain under-investigated.

Purpose of the Study:

  • To identify early risk factors for systolic dysfunction after Ims-TBI.
  • To assess the impact of systolic dysfunction on patient prognosis, including in-hospital mortality.

Main Methods:

  • Prospective observational study of 123 patients (aged 16-65) with Ims-TBI (GCS ≤12) and no cardiac comorbidities.
  • Systolic dysfunction assessed within 24 hours via echocardiography (LVEF <50% or regional wall motion abnormality).
  • Clinical data, including heart rate, GCS, Hs-cTnT, and outcomes, collected on admission and during hospitalization.

Main Results:

  • 18.7% of patients developed systolic dysfunction.
  • Independent predictors of systolic dysfunction: higher admission heart rate, lower GCS score, and higher Hs-cTnT.
  • A combination of these three factors demonstrated strong predictive performance (AUC=0.85).
  • Systolic dysfunction was associated with longer mechanical ventilation, ICU stay, and higher in-hospital mortality.
  • Lower GCS, lower oxygen saturation, and systolic dysfunction independently predicted in-hospital mortality.

Conclusions:

  • Admission heart rate, GCS score, and serum Hs-cTnT are significant early risk factors for systolic dysfunction post-Ims-TBI.
  • Combining these parameters enhances prediction of systolic dysfunction development.
  • Early identification and management of systolic dysfunction are vital for improving outcomes in Ims-TBI patients.

Related Concept Videos

Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Traumatic Brain Injury l: Introduction01:28

Traumatic Brain Injury l: Introduction

DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...