injuries poisoning
Traumatic Brain Injury (TBI)
Pathophysiology of Traumatic Brain Injury
Brain function may be immediately impaired by direct damage (eg, crush, laceration) of brain tissue. Further damage may occur shortly thereafter from the cascade of events triggered by the initial injury. Traumatic brain injury (TBI) of any sort can cause cerebral edema and decrease brain blood flow. The cranial vault is fixed in size (constrained by the skull) and filled by noncompressible CSF and minimally compressible brain tissue; consequently, any swelling from edema or an intracranial hematoma has nowhere to expand and thus increases intracranial pressure (ICP). Cerebral blood flow is proportional to the cerebral perfusion pressure (CPP), which is the difference between mean arterial pressure (MAP) and mean ICP. Thus, as ICP increases (or MAP decreases), CPP decreases. When CPP falls below 50 mm Hg, the brain may become ischemic. Ischemia and edema may trigger various secondary mechanisms of injury (eg, release of excitatory neurotransmitters, intracellular calcium, free radicals, and cytokines), causing further cell damage, further edema, and further increases in ICP. Systemic complications from trauma (eg, hypotension, hypoxia) can also contribute to cerebral ischemia and are often called secondary brain insults. Excessive ICP initially causes global Pathophysiology . If excessive ICP is unrelieved, it can push brain tissue across the tentorium or through the foramen magnum, causing Injury to the hypothalamus, subfornical organ, and nucleus tractus solitarius, which regulate the overall sympathetic tone, blood flow circulation, and baroreflex response, can lead to profound changes in cardiac and renal function. Hypothalamic dysfunction affects the hypothalamic-pituitary-adrenal axis, causing hemodynamic instability, hypertension, and tachycardia from a sympathetic "storm" that upregulates cardiac contractility and induces fluid retention in the kidney. These changes can subsequently cause Acute Kidney Injury (AKI) (AKI) and Takotsubo cardiomyopathy (sometimes termed neurogenic stress myocardium or stunned Hyperemia and increased brain blood flow may result from concussive injury in adolescents or children. Second impact syndromeis a rare and debated entity defined by sudden increased ICP and sometimes death after a second traumatic insult that is sustained before complete recovery from a previous minor head injury. It is attributed to loss of autoregulation of cerebral blood flow that leads to vascular engorgement, increased ICP, and herniation. 