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Brain Herniation Syndromes

major components of the brain Monroe-Kellie Doctrine types of Herniation Discuss nursing care and management of the patient with increased intracranial pressure

The definition of brain herniation is the protrusion of the brain tissue from one compartment (of higher pressure) to a compartment of lower pressure. With this shift of brain tissue, blood and oxygen supplies are diminished causing herniating tissue to suffer from ischemia, hypoxia and finally cell death. To better understand the different herniation syndromes, lets take a look at what the brain is comprised of and how it is divided. The components of the brain include:

Parenchyma - The essential tissue (Brain in this case) of an organ distinct from its surrounding connective tissue. This is the largest intracranial volume (80%). Blood vessel - The volume of blood in the cerebral arteries is an important determinant of intracranial pressure (10%). Cerebral Spinal Fluid - CSF is comprised of fluid in the ventricles and subarachnoid spaces and is produced by the choroid plexus. Approximately 500 cc is produced daily (10%).

The Monroe-Kellie Doctrine simply states that in a non-expandable, non-contractable, freely communicating space, the pressure of the fluid contents and the brain itself, must be directly porportional to eachother in order to maintain a constant pressure. If one of these pressures increases, another must decrease in order to compensate. In addition to the parenchyma, blood vessels and CSF, the brain is also comprised of several individual compartments that are separated by folds of fibrous and relatively rigid dura mater. Two of the major dura folds include: Falx Cerebri which is a double fold of dura mater that drops into the longitudinal fissure and partially, divides the supratentorial space into the left and right side. Tentoruim Cerebelli this is also a double fold of the dura mater that forms a tent like partition (higher in the middle), between the cerebrum and cerebellum. (The area above the tentorium is the supratentorium space and the area below is known as the infratentorial space). Note: Because it is surrounded by strong bone and it is comprised of several small compartments divided by dura mater, the brain is at greater risk then other body organs for herniation. Types and Location of Herniation Syndromes

Brain Herniation

OVERVIEW

brain herniation is the displacement of part of the brain through an opening or across a separating structure into a region that it does not normally occupy. TYPES Supratentorial 1. Uncal transtentorial herniation 2. Central tentorial herniation 3. Subfalcine herniation 4. Transcalvarial hernaiton Infratentorial 5. Upward transtentorial herniation (reverse coning) 6. Foraminal or tonsillar herniation (coning)

Click image for source UNCAL TRANSTENTORIAL HERNIATION

The uncinate process of the temporal lobe herniates into the anterior part of the opening of the tentorium cerebelli CT Features:

Shift of brainstem and distortion of adjacent cisterns

Dilatation of the contralateral temporal horn PCA territory infarct due to compression of the posterior cerebral artetry as it crosses the tentorium CENTRAL TENTORIAL HERNIATION

symmetrical downward movement of the thalamic region through the opening of the tentorium cerebelli SUBFALCINE HERNIATION

Displacement of the cingulate gyrus under the falx and across the midline. TRANSCALVARIAL HERNIATION

Aka external herniation Displacement of brain through a defect in the skull, such as a fracture site or following craniectomy. UPWARD HERNIATION

So-called reverse coning can occur if an EVD is inserted for hydrocephalus due to a posterior fossa mass lesion. This leads to upwards transtentorial herniation of posterior fossa contents. FORAMINAL HERNIATION

Aka tonsillar herniation Downward herniation of the cerebellar tonsils into the foramen magnum

Supratentorial Herniation (descending) There are three major types of herniation that are caused by expanding supratentorial lesions, these include: Cingulate Herniation This occurs when the cingulated gyrus is forced under the falx cerebri, displacing it to the opposite side. Cingulate herniation alone is not considered to be life threatening, but because it displaces the falx cerebri and can cause compression and/or loss to local blood supply and surrounding cerebral tissue, it can lead to increases in ICP, which can contribute other and more devastating forms of herniation. Signs and symptoms from Cingulate Herniation are not well defined, but thought to include:

Increased ICP Cerebral Edema Altered LOC Change in Neuro Exam

Note: Though Cingulate Herniation is without defined symptomatology; it is often thought to be a precursor to other more serious herniation syndromes. Central Transtentorial Herniation (Central Syndrome) This occurs when a downward shift or displacement, pushes the cerebral hemispheres, basal ganglia, diencephalons, mid-brain and finally the medulla through the tentorial incisura (notch). Progression of signs and symptoms vary depending on whether herniation is in the early (reversible) or late (irreversible) stage. These include: Early herniation to the diencephalons region (reversible):

Change in LOC (decreased alertness, agitation, drowsiness) Pupils are small (1-3mm) but reactive Conjugate or slightly disconjugate pupils at rest Early hemiparesis or hemiplegia develop bilateral signs Purposeful to painful stimuli Babinskis sign absent Respiratory will show deep sigh, yawns and occasional pauses

Herniation to the Midbrain/Upper Pons (Middle phase of Central Herniation):


Deep Coma Pupils midpoint (3-5mm) and non-reactive

Disconjugate pupils with limited horizontal movement Decorticate posturing changes to decerebrate posturing Babinskis sign present Gradual respiratory change to sustained hyperventilation Diabetes Insipidus (not seen early) Hyperthermia (not seen early)

Herniation to the Medulla (Late phase of Central Herniation and irreversible):


Deep Coma Pupils dilated and non-reactive Absent pupil movement Flaccid extremities at rest, occasional flexor response to deep pain Slow irregular respiratory rate, ataxia and periods of apnea Cushings Triad (Hypertension, Bradycardia, Irregular Respirations)

Note: The underlying pathophysiology is that in the early phase of Central Transtentorial Herniation, ischemia and compression, which are, both thought to be reversible conditions, are the basis for signs and symptoms of diencephalic involvement. In the later phase after the midbrain becomes involved, it is thought that infarction of brain tissue has begun and it is at this point that the damage is irreversible. Uncal Transtentorial Herniation (Uncal Syndrome) This occurs when the uncus or hippocampal gyrus (or both), shift from the middle fossa through the tentorial notch and into the posterior fossa. When this occurs, there is compression of the ipsilateral third cranial nerve, then contralateral third cranial nerve and finally the mesencephalon. When Uncal Herniation occurs, the diencephalons and mid-brain are shifted to the opposite side of the brain. As with Central Transtentorial Herniation, signs and symptoms of Uncal herniation are considered to be reversible in the early stages and irreversible in the late stages. These signs and symptoms include: Early herniation to the diencephalons region (potentially reversible):

LOC may not be impaired initially Unilateral sluggish, dilating pupil (Ipsilateral to primary lesion) Full extraocular movement Pupils react to Cold Carolics No motor function abnormality Babinskis sign absent Normal respiratory pattern and rate

Herniation to the Midbrain/Upper Pons (Middle phase of Uncal Herniation):

Deep Coma Pupils contralaterally fixed and either completed dilated or enlarged to 5-6mm No extraocular movement Bilateral decerebration Bilateral positive Babinskis sign Hyperventilation (usually with rate 20-4- per minute)

Herniation to the Medulla (Late phase of Uncal Herniation and irreversible):


Deep Coma Bilateral and fully dilated and fixed pupils No extraocular movement Flaccid extremities with occasional flexor response to deep painful stimuli Slow and irregular respirations with occasional gasps and periods of apnea Hyperthermia Cushings Triad (Hypertension, Bradycardia, Irregular Respirations)

Note: The result of continued and unresolved downward displacement from any of the supratentorial herniation syndromes is ultimate brainstem herniation. When the medulla, which controls such vital functions as respiration and cardiac function, herniates into the foramen magnum, death is immediate. Infratentorial Herniation (ascending) Lesions of the infratentorial compartment that contribute to herniation are much less frequent then supratentorial herniation syndromes. Included in the infratentorial compartment are the brainstem and the cerebellum. There are three possible effects of an expanding lesion in the infratentorial compartment and they include:

Direct compression of the brainstem, cerebellum or the vascular supply to each area Upward transtentorial herniation of the brainstem and cerebellum Downward herniation of one or both cerebellum tonsils through the foramen magnum, to the cervical spine. When this occurs, the medulla is compressed and death is immediate.

The signs and symptoms of an Infratentorial Herniation vary widely depending on the brainstem involvement. In addition to medullary compression, an infratentorial lesion can also encroach on a portion of the ventricular system (3rd and 4th ventricle), which causes acute hydrocephalus. Nursing Care and Management of Increased Intracranial Pressure:

Monitor LOC using Glasgow Coma Scale (or other objective scale) Assess motor response (bilaterally) Check for positive Babinskis sign Assess sensory responses (place emphasis on side opposite of injury) Include the following in assessment of pupils:

Comparing pupil size, shape and equality bilaterally Check pupils with the direct light reflex (check each eye individually) Check that pupils are equal, round reactive to light accommodation (PERRLA) Assess 6 cardinal fields of gaze (Cranial Nerves 3, 4 and 6) Assess for Dolls eye phenomenon in unconscious patients (indicates brain stem damage) Monitor vital signs (Notify MD for deviation from set parameters) Provide nursing measures r/t respiratory care including: Suctioning ABGs Providing O2 Monitoring O2 saturation Monitoring ventilator settings Position pt to maintain venous outflow from brain Elevate HOB to 30 degrees (except for dural tear) No pillow under head (can interfere with venous flow) Turn by logrolling q 2 hrs Administer prescribed medications Control noise and stimuli Provide rest/activity balance (stagger tasks) Maintain desired temperature range (use antipyretics or hypothermia blanket) Provide nursing care to prevent damage to eyes, skin, oral mucous Provide education and emotional support to family

Nursing Diagnosis

Altered tissue perfusion r/t impaired cerebral circulation Altered sensory perception Impaired gas exchange Self-care deficits Altered body image Potential for skin breakdown Potential for injury Ineffective coping (family) Knowledge deficit Anxiety (fear) Altered Nutrition

Major Goals

Maintain normal ICP Vital signs and ABGs normal for patient Improvement in LOC

References Marini, J., J. & Wheeler, A., P. (2006). Critical care medicine: the essentials.(3rd ed.). Lippencott, Williams and Wilkes. Philadelphia Arbour, R., (2004). Intracranial hypertension: Monitoring and nursing assessment. Critical Care Nurse. Oct. 2004. Hickey, J., V., (2002). The Clinical Practice of Neurological and Neurosurgical Nursing. (5th ed.) Lippencott. Philadelphia S Peterman, G., M.D., & Smirniotopoulos, J., G., M.D. (2005). Brain herniation. Retrieved on December 5, 2006 at: http://rad.usuhs.mil/rad/herniation/herniation.html Neurological Nursing NU 454. (2000). Retrieved on December 20, 2004 at: http://www.muw.edu/nursing/acuteneuro.html

Sub-Arachnoid Hemorrhage - 2 Nursing CEs Author: Kristi Hudson RN MSN CCRN Course Objectives Upon completion of this course, the student will be able to:

Describe the pathophysiology involved with a sub-arachnoid hemorrhage List 3 signs and symptoms of sub-arachnoid hemorrhage Have a better understanding of how the Hunt-Hess Grading scale is used Discuss 3 risk factors for vasospasm Describe 3 signs and symptoms of vasospasm Explain methods used to diagnose vasospasm Discuss the benefits of daily Transcranial Doppler studies to rule out vasospasm Explain the risk vs. benefit of using Nimodipine for treatment of vasospasm

What is a Sub-Arachnoid Hemmorhage? Subarachnoid hemorrhage occurs when there is bleeding into the space between the brain and the arachnoid membrane (the middle membrane covering the brain). This may occur either by a spontaneous or traumatic rupture of a cerebral aneurysm, an arteriovenous malformation, or from other unidentified causes. Risks include: disorders associated with aneurysm or weakened blood vessels, including a history of polycystic kidney disease, fibromuscular dysplasia (FMD), other connective tissue disorders, aneurysms in other blood vessels, high blood pressure and smoking.

Signs and Symptoms:


Headache: sudden onset and very severe Meningeal Signs A warning leak may occur in 50% of the cases several days or weeks prior to the onset of hemorrhage (Headache, Dizziness, Nausea and/or Vomiting).

Hunt-Hess Grading System The Hunt-Hess classification is used to help guide the physician in diagnosing the severity of a Sub-Arachnoid Hemorrhage secondary to aneurysmal bleeding, as well as assist in the timing surgical intervention. It can also be used to judge the risk of vasospasm. The patient is assigned to a category on admission to the hospital. Changes in the patients condition are then monitored according to the baseline.

Grade Grade O Grade 1 Grade 2 Grade 3 Grade 4 Grade 5

Hunt Hess Grading Scale Clinical Appearance Asymptomatic and have unruptured aneurysms. Mildly symptomatic with headache. Severe headache associated with Nuchal rigidity and possibly a cranial nerve deficit. Drowsy or confused and may have a mild focal Neurologic deficit. Stuporous with a moderate to severe hemiparesis and possibly early decerebrate rigidity. Comatose with decerebrate rigidity or flaccidity.

Note: Surgical risk increases with the clinical grade, which predicts eventual Neuro outcome. A second scale that is gaining momentum as a clinical indicator scale is the World Federation of Neurological Surgeons (WFNS). The WFNS is based on the sum score of the Glasgow Coma Scale (a very reliable method for evaluating the level of consciousness) and the presence of focal neurologic signs. The higher the grade; the worse the prognosis.

Grade 1 2 3 4

Clinical Grading Scale of the World Federation of Neurological Surgeons Score on Glasgow Clinical Appearance Coma Scale 15 No motor deficit 1314 No motor deficit 1314 Motor deficit 712 With or without motor deficit

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With or without motor deficit

Vasospasm Of the estimated 21,000 persons annually who survive initial aneurysmal rupture, 4,000 either die or are seriously disabled from cerebral vasospasm. Vasospasm is most frequently reported within 4 to 14 days post aneurysm bleed. Clinically significant vasospasm rarely occurs before day 4 and vasospasm is most likely to occur between days 7 through 10. Risk factors for vasospasm include:

Amount of Blood that was in the Subarachnoid space Age Hydrocephalus Antifibrinolytics (Increases risk by 50%) Grade upon admission Timing of Surgery (Early surgery has shown decreased mortality from vasospasm).

Signs and Symptoms (Depending on Location of Vasospasm) Middle Cerebral Artery:


Hemiparesis affecting the arm more than the leg Facial weakness Dysphagia (difficulty swallowing) Aphasia (difficulty speaking) if the brain's left hemisphere is involved Anosognosia (denial of paralysis) if the right hemisphere is affected

Anterior Cerebral Artery:


Hemiparesis (one sided weakness affecting the leg more than the arm) Flat affect

Posterior Cerebral Artery:

Visual deficits

Vertebrobasilar Arteries:

Cranial nerve palsies Ataxia (difficulty walking)

Diagnosis of Vasospasm Frequent Neuro assessment because vasospasm is often seen as a gradual neurologic deterioration. 50% of patients can remain asymptomatic during vasospasm and approximately 20% to 30% will have some delayed neurological ischemia. Decreased LOC or confusion is often the first signs of vasospasm. Transcranial Doppler Study (TCD) is a non-invasive ultrasound technology used to assess blood flow velocity in the major basal intracranial arteries on a real time, beat-to-beat basis. Blood flow velocity is calculated and used to make determinations about intracranial hemodynamics. Transcranial Doppler Studies are used in early (sub-angiographic) bedside detection of vasospasm in Subarachnoid hemorrhage patients, evaluation of stroke and transient ischemic attack, as an adjunct in the assessment of cerebral circulatory arrest, and as a monitoring tool for patients undergoing intracranial interventional procedures. Blood Flow Velocity (BFV) increases as flow volume increases or the diameter of the vessel decreases. Velocity readings are as follows:

80cm/sec = no vasospasm 80 120 cm/sec = non-critical spasm 120 cm/sec = critical vasospasm

Note: Initial CT scans that show blood clots that 3x5mm or a 1mm layer of blood in the basal cisterns can be an early predictor that the patient will later vasospasm. Nursing Assessment for Vasospasm Clinically, vasospasm can be recognized when nurses doing frequent neuro exams report subtle changes. It is important to make sure a well-documented base line neuro exam is present so it can be used for comparison. Some of the more subtle or gradual changes that can occur and should be frequently assessed include:

Level of consciousness Complaints of headache Periods of disorientation Inappropriate behavior Language impairment Hemiparesis

Note: Nurses must quickly detect and report changes as these deficits if undetected, can cause permanent disability. Treatment of Vasospasm The cause of vasospasm is a decreased blood flow to the clinically affected arterial territory. Therefore treatment for symptomatic vasospasm is directed at increasing Cerebral Perfusion Pressure using Triple H therapy, which is comprised of Hypertension, Hypervolemia and

Hemodilution. Hypertension Therapy is aimed at keeping the heart rate greater than 70 beats per minute and maintaining a 30% increase in the patients mean arterial blood pressure for the duration of the vasospasm. This can be induced with vasopressors such as Dopamine, Neosynephrine, Levophed or Dobutamine. Hypervolemia Central venous pressure (CVP) should be maintained at approximately 8 to 10mmHg and Pulmonary Artery Wedge Pressure should be maintained at approximately 14 to 18 mmHg. This is done with fluid resuscitation on a regular schedule, often a colloid (5% albumin) to allow for the expansion of the intravascular space. Hemodilution The balance of oxygen-carrying capacity and viscosity is optimized with lower then normal Hematocrit (around 25%). In order to attain this decreased concentration of cells and solids in the blood, volume expanders again can be used, or in critical situations removing blood and replacing it with plasma can achieve a decreasing blood volume. Note: Careful assessment for pulmonary edema, electrolyte imbalances (especially hyponatremia and hypokalemia) and cerebral edema must be done frequently when using Triple H therapy. Other Treatment Options for Vasospasm Fibrinolytics The most common used drug is recombinant tissue plasminogen activator (rt-PA) or streptokinase. These and other Fibrinolytic agents act by lysing the clot in the subarachnoid space. Angioplasty Spastic intracerebral vessels can be dilated to improve cerebral perfusion. This is done by passing a balloon through the carotid artery, and inflating and deflating it into the vessels that are in spasm. Medications for the Treatment of Vasospasm: Mannitol Which is an osmotic diuretic, has been shown to increase cerebral blood flow in the setting of vasospasm, with improvement in neurological function. Nimodipine Is a calcium channel blocker that that has been a standard treatment for nearly a decade and has been shown to have a beneficial effect on stroke and cerebral blood flow after Sub-Arachnoid Hemorrhage. It dilates collateral arteries around the vasospasm. This therapy seems reasonable as long as the hypertension treatment of Triple H therapy is not compromised. If hypotension results from the use of Nimodipine, the dose can be divided in two and given twice as often. If hypotension continues after this, the practitioner should consider discontinuing its use. References Finn, S., RN, BSN, (2003). Traumatic Brain Injury. Dynamic Nursing Education. Orange California

Hickey, J., V., (2002). The Clinical Practice of Neurological and Neurosurgical Nursing. (5th ed.) Lippencott. Philadelphia Kazzi, A., A., M.D. (2006). Subarachnoid Hemorrhage. Retrieved on December 3, 2006 at: http://www.emedicine.com/emerg/topic559.htm Medline Plus Medical encyclopedia (2006). Intracranial pressure monitoring. Retrieved on December 3, 2006 at: http://www.nlm.nih.gov/medlineplus/ency/article/003411.htm Giraldo, E., A. MD. Subarachnoid Hemorrhage (SAH). (2007). Retrieved on March 10, 2009 at: http://www.merck.com/mmpe/sec16/ch211/ch211d.html Oyama, Katie, RN, BSN, CCRN & Criddle, Laura, RN, MS, CCRN, CCNS. (October 2004). Vasospasm after aneurysmal sub-arachnoid hemorrhage. Critical Care Nurse. Vol. 24, No. 5, October 2004. Suarez, J., I., M.D., Tarr, R., W., M.D., & Selman, W., R., M.D. (2006). Aneurysmal Subarachnoid Hemorrhage. N Engl J Med 2006;354:387-96. Retrieved on December 3, 2006 at: med.unc.edu/obgyn/direct/residents/documents/Aneurysmal_subarachnoid_hemorrhage.pdf