Neurological and Neurosurgical emergencies
these including the following items
1-Raised intracranial pressure
2-Brain stem compression
3-Cerebral Stroke
4- Seizure
5- Trauma as Head Trauma
Raised Intracranial Pressure ICP
ICP normally varies between 4 and 14 mm Hg. Sustained ICP levels above 20 mrn Hg can injure the brain. The Monro-Kellie doctrine states that the cranial vault is a rigid structure, and therefore the total volume of the contents determines ICP.The three normal contents of the cranial vault are brain, blood, and CSF. The brain's contents can expand due to swelling from traumatic brain injury . stroke or reactive edema. Blood volume can increase by extravasation to form a hematoma, or by reactive vasodilation in a hypoventilating, hypercarbic patient. CSF volume increases in the setting of hydrocepbalus. . Addition of a fourth element, such as a tumor or abscess, will also increase ICP
Increased ICP can injury the brain in several ways. Focal mass lesions cause shift and herniation. Temporal lesions push the uncus medially and compress the midbrain. This is known as uncal herniation. Tbe posterior cerebral artery passes between the uncus and midbrain and may be occluded, leading to occipital infarct, Masses higher up in the hemisphere can push the cingulate gyrus under the falx cerebri. This is known as subfalcine herniation. The anterior cerebral artery branches run along the medial surface of the cingulate gyrus and may be occluded, leading to medial frontal and parietal infarcts. Diffuse increases in pressure in the cerebral hemispheres can lead to central, or transtentorial, herniation. Increased
pressure in the posterior fossa can lead to upward central herniation or downward tonsillar herniation through the foramen magnum. Uncal, transtentorial, and tonsillar herniation can cause direct damage to the very delicate brain stem Patients with increased ICP, also called intracranial hypertension (ICH), will often present with headache, nausea, vomiting, and progressive mental status decline. Cushing's triad is the classic presentation of ICH: hypertension, bradycardia, and irregular respirations. This triad is usually a late manifestation. Focal neurologic deficits may also be present if there is a focal mass lesion causing
the problem. Patients with these symptoms should have a head CT as soon as possible
Initial management of ICH includes airway protection and adequate ventilation. A bolus of mannitol up to 1g/kg causes free water diuresis, increased serum osmolarlity, and extraction of water from the brain. The effect is delayed by about 20 minutes and has a transient benefit. Driving serum osmolality above 300 mosm|L is of indeterminate benefit and can have deleterious cardiovascular side effects, such as hypovolemia that leads to hypotension and decreased brain perfusion. Cases of ICH usually need rapid neurosurgical evaluation. Ventriculostomy or craniotomy may be needed for definitive decompression.
It is critical to note that lethargic or obtunded patients often have decreased respiratory drive. This causes the partial pressure of arterial carbon dioxide (Paco2) to increase, resulting in cerebral vasodilation and worsening of lCH. This cycle causes a characteristic crashing patient, who rapidly loses airway protection, becomes apneic, and herniates. Emergent intubation and ventilation to reduce to roughly 35 mm Hg can reverse the process and save the patient's life
Brain Stem Compression
Disease in the posterior fossa (brain stem and cerebellum) requires special consideration. The volume of the posterior fossa is small. Hemorrhage or stroke in the posterior fossa causes mass effect and can rapidly kill the patient in two ways. Occlusion of the fourth ventricle causes acute obstructive hydrocephalus, leading to raised ICP, herniation, and then death, .The mass effect can also lead directly to brain stem compression . Symptoms of brain stem compression include progressive obtundation and hypertension, followed rapidly by brain death. A patient with evidence of either or both needs emergent neurosurgical evaluation for possible ventriculostomy and suboccipital craniectomy (removal of the bone covering the cerebellum). This situation is especially critical, as expeditious decompression can lead to significant functional recovery of patients who present near brain death
Stroke
Patients who present with acute focal neurologic deficits for whom the time of onset of symptoms can be clearly defined (i.e., when the patient was last seen in a normal state of health) must be evaluated
as rapidly as possible. An emergent head CT scan should be done. This is often normal, because CT changes from ischemic stroke may take up to 24 hours to appear . A patient with a clinical
diagnosis of acute stroke less than 3 hours old, without haemorrhage on CT may be a candidate for thrombolytic therapy with tissue plasminogen activator TPA.
Seizure
A seizure is defined as uncontrolled neuronal electrical activity. New-onset seizure often signifies an irritative mass lesion in the brain. Tumors commonly present with seizure. Patients with traumatic intracranial hemorrhage are at risk for seizure. A seizure patient is at risk for neural damage if the seizure is not stopped, as well as airway and ventilation problems. Any patient with new onset seizure should have imaging of the
brain. such as a head CT scan, after the seizure is controlled and the patient resuscitated.
Trauma will be discussed separately
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