CIRCULATION Once the airway is secured, aggressive fluid resuscitation may be required to prevent hypotension and the resulting secondary brain injury. Studies have shown an increase in mortality from 27 to 50 percent for patients with isolated TBI who had a single episode of systolic blood pressure of less than 90 mmHg. Adequate fluid resuscitation has not been shown to increase ICP. Guidelines recommend that the MAP be maintained at 90 mmHg (systolic blood pressure of 120 to 140 mmHg) to achieve adequate cerebral perfusion.20 Hypotension in the setting of trauma should generally be addressed with vigorous fluid and blood replacement. The use of pressors is potentially dangerous and seldom indicated. However, in the absence of shock from volume loss, pressors may be used in an effort to maintain adequate cerebral perfusion. In these cases, monitoring should include cardiac output, continuous arterial blood pressure, and, optimally, intracranial pressure measurement. The pressors indicated for raising MAP to maintain cerebral perfusion are norepinephrine and phenylephrine. Norepinephrine dosages range from 2 to 80 pg/min and should be begun low and titrated slowly to the desired effect. Phenylephrine doses range from 40 to 180 pg/min and are similarly titrated.
Hypertension is a critical finding and must be taken as a Cushing's response in the setting of head injury. The finding of hypertension and bradycardia should initiate measures to decrease intracranial pressure. If hypertension exists independent of increased intracranial pressure, then the systemic pressure should be lowered by no more than 30 percent of the mean arterial blood pressure by using nipride. Pressor agents may be needed to maintain the MAP, although this has not been formally studied. Anemia is also associated with increased mortality. Therefore, external and internal bleeding need to be controlled quickly and the hematocrit should be kept above 30. Head injury alone rarely produces hypotension (except as a preterminal event). Exceptions to this include hypovolemic shock in infants due to epidural bleeding or subgaleal hematoma, or massive blood loss from scalp lacerations in any age group.
DISABILITY The Glasgow Coma Scale The initial neurologic examination of ATLS is to assess the level of consciousness using the AVPU system: Alert, responds to Verbal stimuli, responds to Painful stimuli or is Unresponsive. This same assessment provides most of the information needed to calculate the Glasgow Coma Scale. The GCS taken at any time does not replace an appropriate neurologic exam.
The Neurologic Exam Other important aspects of the neurologic examination in the initial trauma evaluation include assessing pupils for size, reactivity, and anisocoria. Motor function, cranial nerve function, deep tendon reflexes, and evaluation of sensory changes are also useful to indicate the presence of an intracranial injury. Brainstem function in the unresponsive patient is assessed by observing respiratory pattern and eye movements. Oculovestibular (cold calorics) and oculocephalic (doll's eyes) responses are not checked until the cervical spine has been fully cleared.
Pupils are assessed for size and reactivity. A fixed and dilated pupil is highly suggestive of an ipsilateral hematoma with uncal herniation that requires rapid operative intervention. Direct ocular trauma should also be assessed. Bilateral fixed and dilated pupils suggest poor tissue perfusion, (i.e., hypoxemia) bilateral uncal herniation or drug effect, whereas bilateral pinpoint pupils suggest either opiate use or a pontine lesion.
Altered motor function can indicate brain, spinal cord or peripheral nerve injuries. Careful attention is paid to signs of increasing ICP and herniation. Movement in unresponsive patients is assessed by the application of painful stimuli. Decorticate posturing (abnormal upper extremity flexion and lower extremity extension) is indicative of an injury above the midbrain. Decerebrate posturing (abnormal arm extension and internal rotation with wrist and finger flexion and internal rotation and extension of the lower extremities) is a result of a more caudal injury and a worse outcome.
After the primary survey a secondary survey is needed to identify other significant injuries. Up to 60 percent of patients with severe TBI will have other major injuries.
DIAGNOSTIC RADIOGRAPHY FOR TBI All patients with moderate to severe TBI require urgent head CT scan after stabilization. Delays in obtaining a CT scan can lead to a catastrophic delay in emergent neurosurgical interventions. Therefore, if the patient with moderate TBI is uncooperative or combative, intubation using RSI is often the best option. If this is undertaken, the best neurologic exam possible just prior should be performed, and may be valuable to subsequent neurosurgical consultation. Prior to the availability of CT scanning, skull films were the standard diagnostic test. Skull films will be positive in 5 percent of patients with mild TBI. Unfortunately, they often miss basilar skull fractures and do not reliably detect underlying intracranial pathology. CT scans are much more accurate and useful.
There is increasing agreement about the need to scan patients with a GCS of less than 14, but debate remains regarding the indicators for CT scanning for patients with a GCS of 15. Specific signs and symptoms can be indicative of intracranial lesions in these patients. These include a history of loss of consciousness, seizure, vomiting, alcohol use, or physical findings of large subgaleal swelling or amnesia. If any of these findings is present, patients shall have a less than 5 percent chance of having an intracranial lesion and a less than 1 percent chance of requiring neurosurgical intervention. Those with a GCS of 15 and none of these findings have not been shown to have adverse outcomes. Patients on anticoagulants or with coagulopathies are also at higher risk and should be scanned.
Control of the agitated patient with head injury is critical in the evaluation and stabilization of these cases. Haloperidol easily crosses the blood-brain barrier, has few adverse respiratory or cardiac effects, and does not interfere with the neurologic exam. However, contraindications to haloperidol include coma and severe toxic CNS depression. This limits its utility in severely inebriated patients and those patients whose mental status changes may deteriorate to coma. Haldol's slow onset of 10 to 30 min, even when given IV, diminishes it's utility in the more severely agitated patients.
Midazolam has sedative, hypnotic, anxiolytic, and amnestic effects. It easily crosses the blood brain barrier, reduces intracranial pressure and augments cerebral perfusion pressure.22 Midazolam also causes skeletal muscle relaxation and is an effective anticonvulsant. However, it will not control psychotic symptoms. Its use is contraindicated in severe hypotension and may be limited by respiratory depression. Admission of a continuous infusion may allow maintenance of adequate sedation while preserving an intact airway. However, close monitoring is required for patients on midazolam infusion; airway protection by intubation is often indicated. Midazolam's rapid clearance allows for an adequate neurologic exam within minutes of discontinuation.
Propofol is an intravenous sedative hypnotic with onset of action less than 1 min with a duration of less than 10 min. Propofol decreases elevated intracranial pressure while not significantly decreasing cerebral perfusion pressure. 23 For conduction and maintenance of sedation, a variable rate infusion method is preferable over intermittent bolus doses. Patients will generally require maintenance rates of 20 to 75 pg/kg/h during the first 10 to 15 min. Dose may be decreased to 25 to 50 pg/kg/h and titrated to clinical response. Propofol is contraindicated with cardiovascular instability and hypotension. It is recommended for use in patients who are intubated and mechanically ventilated.
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