Browse Category: Cerebral edema

Osmotic Agents

Additional therapy for increased ICP includes the use of osmotic diuretics, such as mannitol. In the face of deepening coma, pupil inequality, or other deterioration of the neurologic examination, mannitol may be life saving. Mannitol (0.25 to 1.0 gm/kg) can effectively reduce cerebral edema by producing an osmotic gradient that prevents the movement of water from the vascular space into the cells during membrane pump failure and draws tissue water into the vascular space. In effect, this reduces brain volume and provides increased space for an expanding hematoma or brain swelling. The osmotic effects of mannitol occur within minutes of its administration and peak at about 60 minutes after the bolus has been administered.

The ICP-lowering effects of a single bolus may last for 6 to 8 hours. Mannitol has many other neuroprotective properties. It is an effective volume expander in the presence of hypovolemic hypotension and therefore may maintain systemic blood pressure required for adequate cerebral perfusion. It also promotes CBF by reducing blood viscosity and microcirculatory resistance. Mannitol reduces RBC deformity and therefore improves oxygen carrying capacity. It is an effective free radical scavenger, reducing the concentration of oxygen free radicals that may promote cell membrane lipid peroxidation.

Pancreatic cancer information

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.