Traumatic brain injury is the leading cause of death in North America for those between the ages of 1 and 45. Many TBI survivors have significant and often permanent disabilities, and much of the outcome is dependent on the extent of the injury itself, not initial ED interventions.
The intent of ED treatment is to use existing evidence to improve patient outcomes. Unfortunately, the lack of randomized clinical trials addressing many aspects of caring for the severe TBI patient makes the strength of supporting data for most treatment concepts relatively weak. Severe TBI ideally should be treated in large trauma centers that offer neurosurgical expertise and access to specialized neurocritical care, but many injured patients first present to nontrauma center facilities. Patients with severe head injury frequently have other traumatic injuries to internal organs, lungs, limbs, and the spinal cord that are more obvious and require immediate interventions. Clearly, initially managing the patient with severe TBI is complex and varied.
A variety of resuscitative fluids have been studied for hypovolemic shock, with many trials comparing albumin, Plasmanate, lactated Ringer's, hypertonic saline, and normal saline. Despite a surfeit of potential benefits or detriments of various fluids, normal saline appears to be the ideal initial ED fluid for the resuscitation of hypovolemic shock. It does have some minor caveats, such as worsening acidosis with normal saline, but overall, the emergency physician should probably not be concerned with infusing anything except normal saline. Lactated Ringer's is a reasonable alternate fluid for resuscitation during initial stages.
Despite an overall consensus on the use of fluids for hypovolemic shock, the proper fluid resuscitation for patients with traumatic brain injury remains unsolved. One should choose a fluid that would not cause harm and be a potential benefit to patients with cerebral injury. Specific questions about the optimal composition and volume of fluids to be administered to a patient with TBI still remain unanswered, however. This month's column puts into perspective current opinion on the ideal fluid for resuscitation. Unfortunately, this issue is not yet settled.
Intravenous Fluids and Traumatic Brain Injury: What's the Solution?
Gantner D, Moore EM, Cooper DJ
Curr Opin Crit Care
These authors state the obvious, that the goals of fluid resuscitation in patients with TBI are rapid reversal of hypovolemia by restoring intravascular volume, avoiding hypotension, maintaining cerebral blood flow, and limiting cerebral ischemia and hypoxia. Of course, this is all supposed to be accomplished while avoiding intracranial hypertension. Cerebral vascular and blood brain barrier changes in the presence of TBI can lead to pathological fluid passage by interrupting the normal protective mechanisms, resulting in cerebral edema. The brain is quite sensitive to changes in osmolality and systemic blood pressure during the initial phases of TBI, and one walks a fine line, especially when there are additional injuries, such as those producing hypovolemia.
There is an overlap between the infusion of intravenous fluids to resuscitate volume deficits yet maximize cerebral perfusion and minimize secondary brain injury. It had been shown that 4% albumin increases mortality, likely by increasing brain edema. One can manipulate intracranial pressure with the use of osmotic diuretics (mannitol) or hypertonic saline, but their actual impact on the outcome of TBI patients is not well established.
It's well appreciated that hypotension can worsen brain injury and that it is associated with a worse neurological outcome. It is detrimental to the brain to have a systolic blood pressure less than 90 mm Hg. Maintaining systolic blood pressure for initial resuscitation is a universal intervention for treating hypovolemic trauma patients. Specific initial fluid administration is often a ballpark guess, and can lead to substantial overinfusion of intravenous fluids in hypotensive patients with concomitant TBI. Overall, it appears to be exceedingly detrimental to long-term outcomes to use early excessive fluid resuscitation in trauma, so this is best avoided.
It had been shown that hypothermia, a common and probably helpful intervention post-cardiac arrest can increase intracranial hypertension in patients with multiple trauma.
These authors focus on which fluid is safe in traumatic brain injury. They note that isotonic crystalloid distributes equally into intravascular and interstitial spaces and can lead to whole body interstitial edema. One would think that adding colloid to maintain intravascular volume osmotically would be beneficial, but no benefit is seen with any colloid in any patient with traumatic brain injury, and it is generally recommended that albumin not be administered, but 4% albumin is particularly detrimental and should be avoided. Apparently, the theory that there would be less cerebral edema because of a better intravascular oncotic pressure does not occur, and there is a paradoxically greater net influx of fluid into the intracerebral or vascular spaces in patients who receive albumin. Details of this concept are found in a New England Journal of Medicine article. (2004;350:2247.) Synthetic colloids, such as hydroxyethyl starch, are generally considered similar to albumin and are not recommended for resuscitation of TBI. (New Engl J Med 2012;367:1901.)
The medical literature often talks about the use of hypertonic saline and mannitol for treating TBI. They can effectively but transiently lower intracranial pressure, but these are not usually emergency medicine interventions. Neither mannitol nor hypertonic saline have firm scientific evidence supporting improved survival or superior long-term neurological outcome, despite their common use. Many institutions limit mannitol except in time-critical situations where there is severe refractory intracranial hypertension and the surgical evacuation of a mass lesion is undertaken.
Individual institution protocols continue to direct the prescription of intravenous fluids despite numerous studies and various opinions. The choice of resuscitation fluids has considerable variation in various hospitals, however. Intravenous fluids in managing shock and TBI have overlapping goals and objectives, but dramatic new therapies are not anticipated. These authors have no specific recommendations other than careful application of existing therapy.
Comment: It is extremely difficult to study any single intervention, such as initial fluid choices in multiple trauma patients who also have TBI. Patients have diverse pathology, numerous interventions, and a variety of physicians directing their care. Emergency clinicians in particular have minimal knowledge and data on the exact pathology of their patient, and significant TBI can be present without any external signs of head trauma. Trauma surgeons also often intervene early, and their perturbations can be somewhat enigmatic.
Certainly the emergency clinician can evaluate and initially treat for hypoxia and initial hypotension with proven and safe interventions. The long-term use of high concentrations of oxygen can be detrimental to the brain, but hypoxia should be prevented by the best means possible in the initial hours of resuscitation. Numerous causes of hypoventilation and lung pathology that can produce hypoxemia can interfere with proper oxygenation of the brain, and these should be addressed. The emergency clinician can rarely distinguish between diffuse brain injury, diffuse axonal injury, focal brain contusions, or intracranial hemorrhage on first evaluation. It is axiomatic that intracranial hematomas be evaluated with a CT scan in a rapid fashion because they will often require surgical intervention. This is often not immediately possible in the unstable patient, and the omnipresent potential for cerebral spine injury is still always extant.
Hypoxia is often best treated with tracheal intubation and mechanical ventilation. Because cerebral ischemia increases with hyperventilation (Pco2 less than 35 mm Hg), ventilated patients should have a Pco2 maintained between 35 and 38 mm Hg unless signs of impending herniation are present. Hypotension during the initial evaluation typically prognosticates a poor outcome, but volume must be restored. It's best to limit fluids once the systolic blood pressure rises above 90-100 mm Hg, a difficult concept to adopt. Corticosteroids were once a common intervention, but their use has not been supported in head-injured patients and should be avoided. Hypothermia should also be avoided.
The emergency clinician's formidable tasks in patients with TBI are to evaluate and categorize the injury pattern, rule in or out surgically amenable trauma, avoid hypoxemia, and maintain systolic blood pressure above 90 mm Hg. It is generally safe and considered standard that normal saline be used to maintain euvolemia in patients with TBI. Subsequent management is out of the realm of emergency medicine, but one should eschew the temptation to intervene with exotic and unproven agents in an attempt to salvage the brain. Cerebral edema is highest at 24 hours, and the patient should be in a trauma center or undergoing ICU manipulations and evaluations by that time.
Elevating the head of the bed to 30 degrees for those with TBI is a simple measure that can be instituted in the ED. The neck should be maintained in a neutral position, but cervical collars should not be so tight that they interfere with venous drainage of the brain. The value of monitoring intracranial pressure is debatable. It is commonly performed in the United States, and its benefit in long-term survival is still in question.
Appropriate sedation is indicated in agitated patients with a severe head injury. The rationale is that appropriate sedation can lower intracranial pressure by reducing metabolic demand. Sedation is also often required in ventilated patients, and propofol is preferred by many because of its short duration of action that allows for intermittent assessment. Some evidence suggests that propofol can decrease intracerebral pressure, and it may have some neuroprotective effects. Little clinical data support the use of barbiturate coma, a prior popular intervention, so EPs need not be concerned with this aspect of treatment. It appears also that the short-term use of fentanyl, benzodiazepine, and morphine are also appropriate to sedate the ED patient initially.
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Is Syncope from Ruptured Ectopic Ever Occult?
Dr. Roberts: As usual, I read and enjoyed your column, this time the one in the August issue regarding pediatric syncope. (“Identifying Life-Threatening Syncope in Children,” EMN 2014;36:14; http://bit.ly/1qNUkt0.) The paper you reviewed had quite a few flaws, but I think the take-home messages were reasonable.
I do wonder, however, about your admonition that “a urine pregnancy test should be collected in all menstruating adolescents.” I've been told similarly, substituting “women” for “adolescents” through the years, but, really, is syncope associated with a ruptured ectopic ever going to be so occult that the patient has no abdominal pain, no abdominal tenderness, and no vaginal bleeding?
Trying to be a practical-sense clinician, it would seem to me that in a well-appearing woman s/p syncope with none of the above, ruptured ectopic could be stricken from the differential without the pregnancy test. Any literature to the contrary? — David Hoyer, MD, Houston
Dr. Roberts responds: Thank you for your comments. As you know, a normal intrauterine pregnancy can cause syncope without the woman knowing she is pregnant, good information for the clinician to know in the ED. The vast majority of patients with a ruptured ectopic pregnancy will have abdominal symptoms (but sometimes only back pain or rectal pain). If the woman is totally asymptomatic after she recovers from syncope, a ruptured ectopic can most likely be dismissed from the differential, but you cannot rule out an unruptured ectopic or intrauterine pregnancy.
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