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Summary

Traumatic brain injury (TBI): most likely to occur in adolescents and adults >65 yr of age; primary vs secondary injury — severe central nervous system (CNS) physiologic derangements are caused by the primary injury; the secondary injury is the focus of operative management during the “golden hour”; 40% of patients with TBI deteriorate after the initial injury; TBI is combination of metabolic failure, oxidative stress, and apoptotic cell death activation; the consequences for long- and short-term neurologic function may be severe; exacerbation of secondary injury is caused by hypoxemia, ischemia, and inflammatory responses; mitigation of secondary injury is dependent on timely diagnosis of TBI and initiation of care

Diagnosis of TBI: mild TBI causes concussion-like symptoms; signs and symptoms which indicate severe injury are decreasing consciousness, paralysis, fixed dilated pupils, abnormal posturing; Cushing triad (bradycardia, elevated blood pressure, respiratory depression) may be seen; Glasgow coma score (GCS) — 15-point scale based on eye movement and verbal response; 13 to 15 indicates a mild TBI, 9 to 12 is moderate, and ≤8 is a severe TBI; further deterioration is unlikely in patients who maintain GCS for 24 hr after initial injury; head computed tomography (CT) — strongly indicated for patients with moderate or severe TBI or deteriorating GCS; CT establishes diagnosis and determines the need for surgical intervention (eg, decompressive craniotomy) or invasive intracranial pressure (ICP) monitoring (eg, external ventricular drains [EVDs]); head CT is the modality of choice because it is rapid, special resolution is high, is noninvasive and free of contraindications, and sensitivity is high for diagnosing hemorrhage; however, head CT has low sensitivity for small traumatic lesions in the inferior and posterior fossa in the base of the skull and for small nonhemorrhagic lesions of the cerebral cortex, white matter, and brain stem

Other tools: include assessment of bone and soft tissues, CT angiography, and magnetic resonance imaging (MRI); MRI has a limited role for TBI due to longer examination times, limited availability, patient contraindications, and cost

Treatment of TBI: acute period — the aim in the “golden hour” is stabilization of the patient and prevention of secondary injury; oxygenation and adequate blood flow to the brain must be present and ICP must be controlled; chronic period — patients undergo rehabilitation with, eg, physiotherapy, speech therapy, cognitive rehabilitation, occupational therapy

Airway and ventilation: airway protection should be promptly established to prevent pulmonary aspiration and compromised respiratory function; intubation is indicated for GCS ≤8; oxygenation and arterial CO₂ levels must be maintained; arterial CO₂ is the most powerful determinant of cerebral blood flow; low levels of arterial CO₂ leads causes low cerebral blood flow, which results in cerebral ischemia; elevated CO₂ levels result in cerebral hyperemia and elevated ICP; hyperventilation — cerebral hyperemia was formerly thought to be more common than cerebral ischemia; partial pressure of arterial CO₂ should be maintained at 35 to 45 mmHg; the arterial CO₂ target in patients with elevated ICP and refractory to treatment is revised to 30 to 34 mmHg; hyperventilation should be avoided for the first 24 hr after injury; hyperventilation may be used as a temporizing measure; prolonged use should be avoided; oxygen should be maintained at a partial pressure of 80 to 120 mmHg; one episode of hypoxemia (<60 mmHg) doubles risk for mortality

Cerebral perfusion pressure (CPP): systolic blood pressure reduction triggers vasodilation of cerebral blood vessels to maintain CPP in patients with intact autoregulation; vasodilation causes brain volume to increase, which increases ICP and worsens edema; a reduction in systolic blood pressure in patients without intact autoregulation (eg, in patients with a disrupted blood-brain barrier) produces areas of cerebral ischemia; hypotension increases morbidity and mortality after TBI; secondary injury is reduced by maintaining blood pressure to improve delivery of oxygen and nutrients; cerebral perfusion therapy delivers glucose and oxygen to the brain; maintenance of target CPP of 60 to 70 mmHg has produced favorable outcomes in adults; low-dose vasopressors, eg, norepinephrine, phenylephrine, may be used in cases in which CPP is not maintained with intravenous (IV) fluid or blood transfusion

ICP threshold: normal ICP is 5 to 15 mmHg; >20 mmHg indicates mild intracranial hypertension; the goal ICP after TBI should be <22 mmHg for all ages; ICP <22 mmHg is associated with reduced mortality and <18 mmHg is associated with favorable outcomes in women and patients >55 yr of age; clinical examination and CT findings should be correlated with ICP, as select patients with low ICP require interventions; clinicians should consider EVDs for ICP monitoring in patients presenting with a GCS ≤8 and a concern for elevated ICP on head CT; EVDs allow removal of cerebrospinal fluid (CSF) to reduce ICP until other interventions are started and are preferred to bolt placement

Hyperosmolar therapy: consists of mannitol and hypertonic saline (usually 3% sodium); the choice of agent depends on the individual’s clinical circumstances and medical history; both agents reduce ICP by reducing blood viscosity, which improves microcirculation and decreases cerebral blood volume; the effects are most notable in the pial vessels which give rise to smaller penetrating arteries and are surrounded by CSF; improvement in microcirculation improves outcomes; mannitol scavenges free radicals and inhibits cellular apoptosis; the target serum osmolarity is 300 to 320 mOsm/L when using 20% mannitol; the dose is 0.25 to 1.5 g/kg every 6 hr as needed; alternative treatments (eg, emergent hemodialysis) to mannitol should be considered in patients with end-stage renal disease; the diuresis produced by mannitol may not be desirable in patients with polytrauma, hypotension, or severe heart failure; no significant differences between mannitol and hypertonic saline have been observed for length of stay or mortality; hypertonic saline is a volume resuscitant and is useful for initial treatment for patients with TBI and polytrauma; hypertonic saline increases the intravascular space by 8- to 10-fold more than isotonic saline; hypertonic saline may be given as a bolus of 4 mL to 6 mL/kg of ideal body weight over 14 min; the goal is to raise plasma sodium by 1.5 to 2 meq/L per hr for the first 3 to 4 hr of resuscitation (≤12 meq/L in 24 hr)

Steroids: used for brain edema but are contraindicated in patients with trauma and TBI; data from the CRASH-1 trial (Edwards et al, 2005) showed higher mortality in patients given steroids at 2 wk (21% vs 18%) and 6 mo (25.7% vs 22.3%) compared with placebo; the steroid group had a higher incidence of gastrointestinal bleeding and infection; use of steroids should be avoided in the acute period in patients with trauma and TBI

Hypotonic solution: data from the SAFE trial (SAFE Study Investigators, 2007) showed increased mortality in patients with trauma and head injury given albumin compared with patients given saline (24.5% vs 15.1%); the increase in mortality was thought to be caused by increased ICP; albumin should be avoided in initial resuscitation for patients with TBI; transfusion and hypertonic solution are preferred

Hemoglobin transfusion goals: Hébert et al (1999) established 7 g/dL as the threshold for transfusions in critically ill patients; the threshold differs in patients with TBI because elevated hemoglobin concentration may be beneficial in maintaining cerebral oxygen delivery; Sekhon et al (2012) reported increased mortality in patients with a mean 7-day hemoglobin concentration <9 g/dL; however, other studies have reported no benefit of attaining liberal transfusion goals; Elterman et al (2013) reported that patients with suspected TBI with transfused hemoglobin goals >10 g/dL have reduced 28-day survival and increased incidence of acute respiratory distress syndrome; transfusion for acute management of patients with TBI with hemoglobin levels ≥7 g/dL should be considered safe

Coagulopathy: should be corrected with reversal agents; reversal is essential in cases of life-threatening intracranial bleeding; platelet count, fibrinogen, and partial thromboplastin time and thromboelastrography should be taken on arrival of the patient in the ED; patients on warfarin and factor Xa inhibitors or with international normalized ratio >2 should have coagulopathy corrected with fresh frozen plasma or anti-inhibitor coagulant complex (eg, FEIBA, Autoplex T); platelet transfusion or IV desmopressin (eg, DDAVP, Nocdurna) should be considered in patients with platelet dysfunction or taking antiplatelet medication; platelet administration in patients on antiplatelet agents with TBI reduces mortality; transfusion with platelets may cause complications; Prodan et al (2016) reported negative outcomes with platelet transfusion in patients with cerebral hemorrhage; the incidence of death was higher in the group receiving platelets on arrival compared with standard of care; increased mortality may have been caused by lesion expansion from thrombosis, ischemia, and inflammation; IV desmopressin reduces expansion of hematomas in patients with mild TBI taking antiplatelet medications, and improves platelet function in patients with intracranial hemorrhage; the dose is ≈0.3 to 0.4 μg/kg

Prophylactic hypothermia: intended to preserve cells and tissues during metabolic challenge and provide nerve protection after cardiac arrest; however, studies have reported no statistically significant difference in mortality; prophylactic hypothermia is associated with risk for, eg, immunosuppression, coagulopathy, cardiac dysrhythmia; Todd et al (2005) found no strong evidence for reduced mortality with cooling and reported increased bacteremia; periods of hyperthermia increase the cerebral metabolic rate and ICP and should be avoided

Overall goals: Morano et al (2021) summarizes treatment for patients with TBI, including maintaining oxygenation, cerebral perfusion pressure, glucose control, and normothermia

New therapy goals: the brain and heart may be directly linked; early myocardial injury and cardiac systolic dysfunction (SD) are increasingly recognized after moderate to severe TBI; SD may be caused by inflammation and catecholamine excess after injury, and is associated with early hemodynamic instability after TBI which contributes to cerebral hypoperfusion; TBI causes acute worsening of global longitudinal strain, delayed worsening of ejection fraction, and elevated cardiac enzymes; Ley et al (2018) found lower mortality in patients receiving β blockers after TBI (13.8% vs 17.7%); propranolol was superior to other β blockers