Name two potential early secondary injuries after TBI.

Name two potential early secondary injuries after TBI.

• A. Fractured skull and nasal polyps
• B. Peripheral neuropathy and myelopathy
• C. Migraine and tension headache
• D. Hypoxic/ischemic injury and intracranial hypertension (or seizures)

Answer: (D)

After a TBI, secondary injuries are the evolving problems that worsen brain damage after the initial impact. The most important early ones are hypoxic/ischemic injury and intracranial hypertension (which can be associated with seizures). Hypoxic/ischemic injury happens when brain tissue doesn’t get enough oxygen or blood flow, often due to systemic issues like hypotension, respiratory failure, or impaired autoregulation, leading to added neuronal injury beyond the primary insult. Intracranial hypertension arises from brain edema and swelling that increase pressure inside the skull, reducing cerebral perfusion and risking herniation; seizures can also begin early because the injured cortex becomes highly irritable. These fit as early secondary injuries because they reflect rapid, evolving brain physiology after the initial trauma, unlike fractures, peripheral neuropathy, or typical post-traumatic headaches, which are not the classic early secondary processes.

After a TBI, secondary injuries are the evolving problems that worsen brain damage after the initial impact. The most important early ones are hypoxic/ischemic injury and intracranial hypertension (which can be associated with seizures). Hypoxic/ischemic injury happens when brain tissue doesn’t get enough oxygen or blood flow, often due to systemic issues like hypotension, respiratory failure, or impaired autoregulation, leading to added neuronal injury beyond the primary insult. Intracranial hypertension arises from brain edema and swelling that increase pressure inside the skull, reducing cerebral perfusion and risking herniation; seizures can also begin early because the injured cortex becomes highly irritable. These fit as early secondary injuries because they reflect rapid, evolving brain physiology after the initial trauma, unlike fractures, peripheral neuropathy, or typical post-traumatic headaches, which are not the classic early secondary processes.