Neurologic Trauma Bryan E. Bledsoe, DO, FACEP
Neurologic Trauma “Suppose you were an idiot. And suppose you were a member of Congress. But I repeat myself.” Mark Twain
Traumatic Brain Injury (TBI) • Defined as a blow or jolt to the head or a penetrating head injury that disrupts the function of the brain.
Statistics • 1.4 million people sustain a TBI each year in the United States: • 50,000 die, • 235,000 are hospitalized, • 1.1 million are treated and released from the ED.
Statistics • Causes: • Falls (28%) • MVCs (20%) • Struck by/against events (19%) • Assaults (11%) Blasts are the leading cause of TBI for active duty military personnel in war zones.
Statistics • Males are about 1.5 times more likely to sustain a TBI as a female.
Statistics • Highest risk for TBI: • 0-4 years • 15-19 years • African Americans have the highest death rate from TBI.
Statistics • Estimated $60 billion lost from TBI (medical costs and lost productivity).* * 2000
Physiology • Brain Metabolism: • Like all tissues, the brain requires a constant supply of oxygen and nutrients.
Physiology • Brain accounts for 2% of total body mass. • Brain accounts for 15% of total metabolism in the body. • Brain metabolic rate 7.5 times the rate of other neurological tissues.
Physiology • Almost all of the brain’s energy needs are supplied by glucose. • Provided by capillaries in the brain.
Physiology • Insulin NOT needed for glucose delivery to brain tissues.
Physiology • The brain is among the most oxygen dependent organs in the body. • The brain is not capable of much anaerobic metabolism. • Primarily due the high metabolic rate of the neurons.
Physiology • Because of this, sudden cessation of blood flow to the brain can cause unconsciousness within 5-10 seconds.
Physiology • Neuroglobin: • Intracellular hemeprotein. • Reversibly binds oxygen with an affinity greater than that of hemoglobin. • Increases oxygen availability to brain tissue and provides protection under hypoxic or ischemic conditions, potentially limiting brain damage.
Physiology • Brain requires: • Oxygenation • Glucose • Perfusion • Any deficit in these results in immediate dysfunction.
Intracranial Pressure • The cranial vault is effectively a closed container. • Largest opening is the foramen magnum. • Limited room for brain swelling.
Intracranial Pressure • There is always some pressure in the brain. • Referred to as intracranial pressure (ICP). • Normal ICP: • Children: 0-10 mm Hg • Adults: 0-15 mm Hg
Intracranial Pressure • Volume of the cranial vault defined by the Monro-Kellie doctrine: Intracranial Volume (fixed) = Brain Volume + CSF Volume + Blood Volume + Mass Lesion Volume
Intracranial Pressure • Normally: • Brain = 80% of cranial vault space • Blood = 10% of cranial vault space • CSF = 10% of cranial vault space Space Available for Blood or MASS = 0%
Intracranial Pressure • To perfuse the brain, the pressure of blood delivered to the brain MUST be greater than the intracranial pressure. CPP = MAP - ICP
Intracranial Pressure • Mean Arterial Pressure: MAP DP + 1/3 (SP–DP)
Intracranial Pressure • Perfusion of the brain is driven by the CPP. MAP - ICP = CPP • - 30 = 40 CPP of 60 is the critical minimum threshold. CPP of 40 is the critical minimum threshold for children < 8 years of age.
Intracranial Pressure • Injury to brain tissue causes: • Swelling • Bleeding • Edema • All cause an increase in the size and mass of the brain.
Intracranial Pressure • As the brain swells, it will eventually reach a critical volume where ICP increases to a point that perfusion is compromised.
Brain Injury • Etiology of TBI: • Primary injury: • Damage to the brain from mechanical effects of trauma causing: • Ischemia • Anoxia/hypoxia • Shear injury
Brain Injury • Secondary Injury: • Results from a traumatic event and changes in the brain or in the brain vasculature. • Hypoxia • Hypotension ( cerebral blood flow) • ICP • Hyperglycemia/Hypoglycemia • Metabolic disturbances • Seizures
Brain Injury • 12-24 hours post-injury: • Hypoperfusion and decrease in CBF. • Results from increases in distal microvascular resistance and intravascular clot formation.
Brain Injury • 1-5 days post injury: • Increased CBF > CMRO2. • Vascular engorgement • Swelling • Increased ICP • Induction of free radicals and oxidative stress.
Brain Injury • 5/6-14 days post injury: • CBF slows due to vasospasm • Brain vulnerable to changes in ICP.
Brain Injury • Secondary Injury: • Impaired autoregulation: • Autoregulation is the ability of the brain to maintain CBF in light of changes in BP and CPP. • Impaired autoregulation causes: • O2 delivery to the brain and cerebral ischemia. • Cerebral metabolism altered due to loss of, or a decrease in, CBF. • Conversion from aerobic to anaerobic metabolism.
Brain Injury • Secondary Injury (extracranial causes): • Hypotension (SBP < 90 worsens outcomes) • Hypoxia (significantly associated with increased morbidity and mortality) • Hypocapnia: • Low CO2 causes vasoconstriction • 1 mm Hg decrease on CO2 = 3% decrease in CBF. • Anemia • Hyperthermia
Brain Injury • Compensatory mechanisms: • Brain shifts or is compressed. • Venous blood is shunted to heart. • CSP shunted to spinal SAS.
Signs and Symptoms • Early ( ICP): • Altered mental status • Agitation • Nausea and/or vomiting • Hemiparesis
Signs and Symptoms • Late ( ICP): • Coma • Hemiplegia • Posturing • Cushing’s Triad: • Widening pulse pressure • Bradycardia • Respiratory abnormalities