Emergency Department


Rapid sequence induction (RSI) for intubation is an effective method for securing the airway in combative or agitated patients.


If hypotension is detected at any time in the course of the emergent management of a head-injured patient, a cause should be sought other than the head injury. Hypotension is rarely caused by head injury except as a terminal event, but important exceptions include profound blood loss from scalp lacerations and pediatric patients with relatively small circulating blood volumes. In small children, hemorrhage into an epidural or subgaleal hematoma can produce profound hypovolemic shock. In the presence of concomitant spinal cord injury, spinal cord hypotension may occur. This is rare and can be differentiated from hypovolemic hypotension by its nonresponsiveness to fluid administration.

Recently, it has been suggested that hypotensive patients with penetrating abdominal trauma may have better outcomes if fluids are restricted before operation. These studies did not include head-injured patients. In the case of the head-injured patient, systematic hypotension cannot be tolerated without profound worsening of neurologic outcome; fluids should therefore be delivered to maintain a systolic blood pressure of at least 90 mm Hg. Several laboratory and clinical studies have investigated the effects of the delivery of large amounts of fluid to severely head-injured patients who are hypotensive from other injuries and have not demonstrated clinically significant increases in ICP. Fluids should not be withheld in the hypovolemic hypotensive head trauma patient for fear of increasing cerebral edema and ICP. Hypotension from any cause increases mortality from the head injury by 30%. Hypotension may interfere with the accurate neurologic assessment of the brain-injured patient. Often, when blood pressure is restored, an improved neurologic status is observed.

As many as 60% of patients with severe head injury are victims of multiple trauma. The dramatic presentation of the head injury should not distract the clinician from a thorough search for other life threats.

The ED neurologic assessment should be compared with the initial prehospital examination, focusing on evidence of neurologic deterioration or signs of increasing ICP. If the patient is deteriorating or has signs of increased ICP, active intervention must be initiated in the ED.


Hyperventilation to produce an arterial P CO2 of 25 to 30 mm Hg will temporarily reduce ICP by promoting cerebral vasoconstriction and subsequent reduction of CBF. The onset of action is within 30 seconds and probably peaks within 8 minutes after the P CO2 drops to the desired range. In most patients hyperventilation lowers the ICP by 25%; if the patient does not rapidly respond, the prognosis for survival is generally poor. Prolonged hyperventilation probably loses its effectiveness and therefore is of limited value beyond the acute phase. The partial pressure of carbon dioxide should not fall below 25 mm Hg because this may cause profound vasoconstriction and ischemia in normal and injured areas of the brain. Prophylactic hyperventilation has been associated with worsened neurologic outcome when measured at 3 and 6 months after severe trauma and is therefore not recommended in head-injured patients who are not exhibiting signs of increased ICP.

Central Transtentorial

Central Transtentorial.

The central transtentorial herniation syndrome is demonstrated by rostrocaudal neurologic deterioration caused by an expanding lesion at the vertex or the frontal or occipital pole of the brain. It is less common than uncal transtentorial herniation. Clinical deterioration occurs as bilateral central pressure is exerted on the brain from above. The initial clinical manifestation may be a subtle change in mental status or decreased level of consciousness, bilateral motor weakness, and pinpoint pupils (<2 mm). Light reflexes are still present but often are difficult to detect. Muscle tone is increased bilaterally, and bilateral Babinski signs may be present. As central herniation progresses, both pupils become midpoint and lose light responsiveness. Respiratory patterns are affected and sustained hyperventilation may occur. Motor tone increases. Decorticate posturing, initially contralateral to the lesion, is elicited by noxious stimuli. This progresses to bilateral decorticate and then spontaneous decerebrate posturing. Respiratory patterns that may initially include yawns and sighs progress to sustained tachypnea, followed by shallow slow and irregular breaths immediately before respiratory arrest.


Cerebellotonsillar herniation occurs when the cerebellar tonsils herniate downward through the foramen magnum. This is usually caused by a cerebellar mass or a large central vertex mass causing the rapid displacement of the entire brain stem. Clinically, patients demonstrate sudden respiratory and cardiovascular collapse as the medulla is impinged. Pinpoint pupils are noted. Flaccid quadreplegia is the most common motor presentation because of bilateral compression of the corticospinal tracts. The mortality resulting from cerebellar herniation approaches 70%.

Upward Transtentorial.

Upward transtentorial herniation is occasionally seen as a result of an expanding posterior fossa lesion. A rapid decline in the level of consciousness occurs. These patients may have pinpoint pupils because of compression of the pons. A downward conjugate gaze with the absence of vertical eye movements is also observed.

The Cushing Reflex.

The Cushing Reflex

Progressive hypertension associated with bradycardia and diminished respiratory effort is a specific response to acute, potentially lethal rises in ICP. This response is called the Cushing reflex, and its occurrence indicates that the ICP has reached life-threatening levels. The Cushing reflex can occur whenever ICP is increased, regardless of the cause. The full triad of hypertension, bradycardia, and respiratory irregularity is seen in only one third of cases of life-threatening increased ICP.


Cerebral herniation occurs when increasing cranial volume and ICP overwhelms the natural compensatory capacities of the CNS. Increased ICP may be the result of posttraumatic brain swelling, edema formation, traumatic mass lesion expansion, or any combination of the three. When increasing ICP cannot be controlled, the intracranial contents will shift and herniate through the cranial foramen.


The most common clinically significant traumatic herniation syndrome is uncal herniation, a form of transtentorial herniation (Fig. 31-5) (Figure Not Available) . Uncal herniation is often associated with traumatic extraaxial hematomas in the lateral middle fossa or the temporal lobe. The classic signs and symptoms are caused by compression of the ipsilateral uncus of the temporal lobe on the U-shaped edge of the tentorium cerebelli as the brain is forced through the tentorial hiatus. As compression of the uncus begins, the third cranial nerve is compressed. Anisocoria and a sluggish light reflex in the dilated pupil develop on the side ipsilateral to the expanding mass lesion. This phase may last for minutes to hours, depending on how rapidly the expanding lesion is changing. As the herniation progresses, compression of the ipsilateral oculomotor nerve eventually causes ipsilateral pupillary dilatation and nonreactivity.

Initially in the uncal herniation process, the motor examination can be normal, but contralateral Babinski’s responses develop early. Contralateral hemiparesis develops as the ipsilateral peduncle is compressed against the tentorium. With continued progression of the herniation, bilateral decerebrate posturing eventually occurs; decorticate posturing is not always seen with the uncal herniation syndrome. In up to 25% of patients, the contralateral cerebral peduncle is forced against the opposite edge of the tentorial hiatus. Hemiparesis is then detected ipsilateral to the dilated pupil and the mass lesion. This is termed Kernohan’s notch syndrome and causes false localizing motor findings.

As uncal herniation progresses, direct brain stem compression causes additional alterations in the level of consciousness, respiratory pattern, and the cardiovascular system. Mental status changes may initially be quite subtle, such as agitation, restlessness, or confusion. This is soon replaced with lethargy and progression to frank coma. The patient’s respiratory pattern may initially be normal, followed by sustained hyperventilation. With continued brain stem compression, an ataxic respiratory pattern develops. The patient’s hemodynamic status may change, with rapid fluctuations in blood pressure and cardiac conduction. Herniation that is uncontrolled progresses rapidly to brain stem failure, cardiovascular collapse, and death.

Cerebral edema

Cerebral edema is an increase in brain volume caused by an absolute increase in cerebral tissue water content.Diffuse cerebral edema may develop soon after head injury. Vasogenic edema arises from transvascular leakage caused by mechanical failure of the tight endothelial junctions of the BBB. Vasogenic edema is frequently associated with focal contusions or hematomas. It eventually resolves as edema fluid is reabsorbed into the vascular space or the ventricular system.

Cytotoxic edema is an intracellular process that results from membrane pump failure. It is very common after head injury and is frequently associated with posttraumatic ischemia and tissue hypoxia. Normal membrane pump activity depends on adequate CBF to ensure adequate substrate and oxygen delivery to brain tissue. If the CBF is reduced to 40% or less of baseline, cytotoxic edema begins to develop. If CBF drops to 25% of baseline, membrane pumps fail and cells begin to die. Congestive brain swelling can contribute to cytotoxic edema if it becomes severe enough to increase ICP and reduce CPP so that cerebral circulation cannot be maintained.

Alteration in Consciousness

Consciousness is a state of awareness of the self and of the environment and requires intact functioning of the cerebral cortices and the reticular activating system (RAS) of the brain stem. An altered level of consciousness is the hallmark of brain insult from any cause and results from an interruption of the RAS or a global event that affects both cortices.

A patient who has sustained TBI commonly has an altered level of consciousness. Head-injured patients may be hypoxic from injury to respiratory centers or from concomitant pulmonary injury. Hypotension from other associated injuries can compromise CBF and affect consciousness. Global suppression may be present as a result of an intoxicating substance consumed before the injury. With increasing ICP from brain swelling or an expanding mass lesion, brain stem compression and subsequent RAS compression can occur.

Patients with altered levels of consciousness require careful monitoring and observation. Reversible conditions that can alter mental status, such as hypoxia, hypotension, hypoglycemia, should be corrected as they are identified.

Brain metastasis from an unknown primary

The last thing I’d like to just mention about, and it’s an important point, is the issue of brain metastasis from an unknown primary.If one looks at a series from M.D. Anderson, 220 patients with brain metastasis. Approximately 39 of those patients, or 18%, were without a known systemic site. The median age of these patients is approximately 55. Most of them had good performance status. About half of those lesions were multiple, however half of them were single. One actually looked at the histology of those tumors.

Approximately 31% were adenocarcinomas, representing by far the greatest number. In the few patients where a primary was eventually found, usually at autopsy, lung represented the most common primary site. The important thing to know about these tumors however is that there is a subset of these patients who can actually do quite well. All these patients were treated with whole brain radiation, 30 gray, and that intracranial disease-free survival at five years was 72% of these patients. And that the overall median survival of these patients was well over a year, whereas 12% of these patients surviving eight years and probably effectively cured of their disease.

What this says is that, particularly if you have a young middle aged person, good performance status, who has a solitary metastasis with no known primary, that that patient should indeed be treated very aggressively, both with surgery and radiation. Because that patient has a very good chance of having a long term disease-free survival, and potentially even cured.

Surgical resection of solitary lesions

There was a growing interest in the use of surgical resection of solitary lesions, and in fact there have now been two randomized trials that have shown a substantial benefit. But as far as local control, neurologic relapse and actual overall survival in patients who were randomized to surgical resection of solitary lesions compared to standard radiation therapy. The most famous of these is the Patrick study, published in the New England Journal where it was shown that patients did much better if they had surgical treatment. Women complaining about lack of desire find female viagra very helpful. Other positive prognostic signs were absence of extra-cranial disease, young age and a long time to CNS metastasis. A similar study was recently published that again showed a particularly significant survival advantage for surgery, also younger age and absence of extra-cranial disease were other important prognostic signs. Then of course came the question, if you do surgically resect a solitary brain metastasis should you radiate the patient’s brain again, particularly because of what we discussed; the issue of long term neuro-cognitive deficits? That study was recently published in JAMA and the answer is yes.

You probably should radiate the brain following removal of the lesion. There were patients who did receive radiation therapy compared to randomized patients who didn’t receive radiation following completion of their surgical resection had a much higher incidence of relapse in the brain, compared to the others who got radiation therapy. The relapses were local as well as distant. Although the median survival did not reach significant differences, there was a trend toward higher survival in patients who received radiation therapy. But at least from the point of view of neurologic sequelae and quality of life relative to neurologic symptoms, I think there clearly is a role for radiation therapy for most patients who have undergone resection for solitary brain lesions.

The question often comes up for patients who have already had radiation therapy or who have potentially chemotherapy-sensitive tumors, what is the role for chemotherapy for the treatment of brain metastases, particularly multiple brain metastases? One of the important things to understand about brain metastasis is the issue of the blood-brain barrier. It’s often said, “Oh, you can’t get drugs into a brain metastasis because of blood-brain barrier.” However, it should be recognized that the blood-brain barrier in brain metastasis is virtually destroyed by the tumor, particularly in the middle of those metastases. This is in contradiction to what we see with primary gliomas where in fact the blood-brain barrier remains very much intact, or at least to a variable extent intact. So actually drug delivery is a much bigger problem for the treatment of gliomas than it is for brain metastasis. And generally, if you have a chemotherapy-sensitive tumor, whether it be in the lungs or whether it be in the brain, you have a very high likelihood of obtaining a response to chemotherapy.

I think the perfect examples of that are the experience in breast cancers. So for instance, here is one experience with the treatment of breast cancer metastasis to the brain where patients were treated with either CMF or CAF in patients who had previously not received chemotherapy, and the objective tumor responses in the brain were between 50-76% with a median duration of neurologic remission being 30 weeks. So it does appear that patients who have chemotherapy-sensitive tumors can significantly benefit from chemotherapy, even though their disease is in their brain. A similar type of experience has been seen with small cell lung cancer, where 116 patients from 12 series were treated with chemotherapy for brain metastases from small cell lung cancer, with an overall response rate of 76% in patients who had not received prior radiation therapy, compared to only 43% in those who had failed standard radiation therapy. So again, if you have a chemotherapy-sensitive disease it’s very possible that you can obtain very significant responses in the brain in treating brain metastasis. The problem is most diseases, like lung cancer and melanoma that have metastasized to the brain are intrinsically chemotherapy-resistant and thus if they are chemotherapy-resistant systemically they are going to likewise be chemotherapy-resistant in the brain.

The management of patients with brain metastases

As far as the management of patients with brain metastases, generally we don’t instantly go to the use of steroids unless the patient needs them. If the patient needs them, meaning that they have significant symptoms of increased cerebral edema, then we recommend starting out at high doses of steroids, such as 4 mg four times a day, but within an aggressive taper. The patients are going to need to be on long term steroids. Viagra professional works faster and lasts longer than you’ve ever known. If you are not able to wean them off the steroids then one should consider Pneumocystis prophylaxis which usually consists of a double strength Bactrim three times per week. There is no data to support the routine use of anticonvulsants and thus we only recommend anticonvulsants in patients who have already had a seizure. If patients are on anticonvulsants, one has to worry about a relatively high rate of Dilantin/Tegretol reactions, particularly in the setting of receiving radiation therapy where there is this syndrome of Dilantin-steroid taper where patients develop this inflammatory red rash on their skin which tends to progress to a Stevens-Johnson-like syndrome. So anticonvulsants are not a benign drug.

As far as the standard treatment for patients with brain metastases, particularly multiple brain metastases, radiation therapy remains the main form of treatment. There have been a number of studies, including several RTOG studies, that have tried to define the optimal dose. It appears that the optimal dose is somewhere between 20-40 gray. What has become clear however is that the standard way that radiation therapy used to be given – which is in 3 gray fractions or higher – can result in a significant amount of neuro-cognitive deficits if patients live long enough; meaning usually at least a year. Thus for patients who have relatively good prognostic factors, who you think might otherwise actually live for a year or longer, if you are going to treat them with external beam radiation therapy as far as whole brain radiation, one should significantly consider the use of lower fraction sizes, such as 2 to 2.5 grays in order to try to reduce the chances of long term significant neuro-cognitive sequelae.

How about the treatment of single brain metastasis? That represents a more questionable and changing area of management in these patients. If one looks at the data by CT scan one can see that approximately 50% of patients have brain metastasis of single lesions. However, when one uses more selective MRI scans the number reduces down to approximately 30% of patients with brain metastasis. The average or median diameter of these lesions is approximately 2.5 centimeters. About 5-10% of these are invasive, which means that 90-95% of these tumors are that type I CNS lesion that I talked about earlier, where almost all the tumor cells reside locally. This is the reason that surgery can offer a significant benefit for patients with brain metastasis. Another important area to recognize is that approximately 11% of patients with brain metastasis have no known systemic primary and just as importantly, approximately 15% of lesions seen on MRI scans in patients with known systemic cancer are not brain metastasis so one cannot just innocently assume that an abnormality on a scan represents metastasis in the brain.

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