Raised intracranial pressure levels increases the risk for secondary brain ischemia and is highly correlated with poor outcome, which highlights the importance of aggressive ICP‐directed treatment 1) 2) 3) 4) 5) 6) 7).
The definition of a secondary insult can be intracranial pressure > 20 mm Hg.
Cerebral perfusion pressure < 60 mm Hg.
Systolic blood pressure < 100 mm Hg for 5 minutes or more.
Secondary injury is an indirect result of the insult. It results from processes initiated by the trauma.
Microglial inflammation plays a vital role in intracerebral hemorrhage (ICH)-induced secondary brain injury. IL-17A has been identified to promote microglia activation, but the role in the pathology following ICH remains unclear.
Unlike in most forms of trauma a large percentage of the people killed by brain trauma do not die right away but rather days to weeks after the event.
In addition, rather than improving after being hospitalized as most patients with other types of injuries do, about 40% of people with TBI deteriorate.
This is often a result of secondary injury, which can damage even neurons that were unharmed in the primary injury. It occurs after a variety of brain insults including subarachnoid hemorrhage, stroke, and traumatic brain injury and involves metabolic cascades.
Secondary injury can result from complications of the injury:
Changes in the blood flow to the brain
In addition, alterations in the release of neurotransmitters (the chemicals used by brain cells to communicate) can cause secondary injury. Imbalances in some neurotransmitters can lead to excitotoxicity, damage to brain cells that results from overactivation of biochemical receptors for excitatory neurotransmitters (those that increase the likelihood that a neuron will fire). Excitotoxicity can cause a variety of negative effects, including damage to cells by free radicals, potentially leading to neurodegeneration. Another factor in secondary injury is loss of cerebral autoregulation, the ability of the brain's blood vessels to regulate cerebral blood flow.
Other factors in secondary damage are breakdown of the blood–brain barrier, edema, ischemia and hypoxia.
Ischemia is one of the leading causes of secondary brain damage after head trauma.
Similar mechanisms are involved in secondary injury after ischemia, trauma, and injuries resulting when a person does not get enough oxygen. After stroke, an ischemic cascade, a set of biochemical cascades takes place.
Secondary brain injury starts after the initial traumatic impact and marked by an increase in the intracellular calcium concentrations.This cascadeeventually results in membrane lipid peroxidation and neuronal cell death.
A study included 18 patients, seven women and 11 men, aged 36-76 years with different neurosurgical diagnoses. The total number of nursing interventions analyzed was 1,717. The most common kind of secondary insults after a nursing measure was high intracranial pressure (n = 93) followed by low cerebral perfusion pressure (n = 43) and low systolic blood pressure (n = 14). Repositioning (n = 39) and simultaneous interventions (n = 32) were the nursing interventions causing most secondary insults. There were substantial variations between the patients; only one patient had no secondary insult. There were, overall, a limited number of secondary insults related to nursing interventions when a standardized management protocol system was applied to reduce the occurrence of secondary insults. Patients with an increased risk of secondary insults should be recognized, and their care and treatment should be carefully planned and performed to avoid secondary insults 8).