Neurologic Dysfunction PDF Spring 2023-2024

Neurologic Dysfunction Marina Gharibian PhD, RN, N. 210B Spring 2023-2024  A fully conscious patient is aware of his surroundings Levels of consciousness exist on a continuum that Levels of includes:  Consciousness Consciousness  Conf...

Neurologic Dysfunction Marina Gharibian PhD, RN, N. 210B Spring 2023-2024  A fully conscious patient is aware of his surroundings Levels of consciousness exist on a continuum that Levels of includes:  Consciousness Consciousness  Confusion  Somnolence  Obtundation  Stupor  Coma Stupor and coma are signs of advanced brain failure Altered Level of Consciousness  Level of responsiveness and consciousness is the most important indicator of the patient's condition.  Altered LOC is not the disorder but the result of a pathology.  Coma, Persistent vegetative state  Is a clinical state of unarousable unresponsiveness in which there are no purposeful responses to internal or external stimuli, although no purposeful responses to painful stimuli and brain stem reflexes may be present.  Is a condition in which the unresponsive patient resumes sleep-wake cycles after coma but is devoid of cognitive or affective mental function. Glasgow Coma Scale An assessment tool called the Glasgow Coma Scale often is used to describe levels of coma. This scale uses 3 aspects of neurologic function: 1. EYE opening 2. VERBAL response 3. MOTOR response GCS Score= E + M + V. Best possible score is 15 and Worst possible score is 3.  Assessment Verbal response Orientation to time, person, and place Alertness: the ability to open the eyes spontaneously or in response to a vocal or noxious stimuli. Motor response: spontaneous, purposeful movement, movement only in response to painful stimuli, or abnormal posturing. Respiratory Status With further deterioration respirations change from Cheyne- Stokes breathing to neurogenic hyperventilation, in which the frequency of ventilation may exceed 40 breaths per minute. Intracranial pressure  The cranial cavity contains:  Blood (approximately 10%)  Brain tissue (approximately 80%)  Cerebrospinal Fluid (CSF: approximately 10%) in the rigid non-expandable skull.  Each of these three volumes contributes to the ICP, which normally is maintained within a range of 5 to 15 mm Hg. The volumes of each of This association is called the Monro-Kellie hypothesis which these components can states that the sum of intracranial vary slightly without volumes is constant and therefore an increase in any one of these causing marked changes compartments must be offset by an in ICP. equivalent decrease in the other two. Increased Intracranial Volume & Pressure The brain is enclosed in the rigid skull, or cranium, making it particularly susceptible to increases in Intracranial Pressure (ICP). Excessive ICP can: obstruct cerebral blood displace brain damage delicate flow and destroy brain cells tissue brain structures An increase in tissue volume can result from a brain tumor, brain edema, or bleeding into brain tissue. An increase in blood volume develops when there is a vasodilatation of cerebral vessels or obstruction of venous outflow. Excess production, decreased absorption of CSF affords the potential for an increase in the CSF component. Tissue volume is relatively restricted in its ability to undergo change; CSF and blood volume are best able to compensate for changes in ICP.  Intracranial mass lesions (eg, tumor, hematoma) Major Cerebral edema (large cerebral infarction, severe traumatic brain injury) causes of Increased CSF production (eg, choroid plexus increased papilloma) ICP Decreased CSF absorption (eg, arachnoid granulation adhesions after bacterial meningitis) Obstruction of venous outflow (e.g., venous sinus thrombosis, jugular vein compression) Compensatory Mechanisms  Autoregulation refers to the brain’s ability to change the diameter of its blood vessels to maintain a constant cerebral blood flow during alterations in systemic blood pressure.  Chamber 1: Normally, the intracranial components are in equilibrium.  Chamber 2: Initially, the volume of a space-occupying lesion is compensated for by displacement of blood and CSF and ICP remains normal.  Chamber 3: When the limits of this compensation is reached; any additional increase in the volume of the mass lesion is accompanied by a corresponding increase in ICP. Compensatory mechanisms allow volume to increase with minimal elevation in ICP. These mechanisms include:  Displacement of CSF into the thecal sac  Decrease in the volume of the cerebral venous blood via venoconstriction and extracranial drainage.  compensatory mechanisms  The main compensatory mechanisms are increased drainage of blood or cerebrospinal fluid from the cranial cavity, in turn allowing for space to be created for this new lesion. This means that the intra- cranial pressure remains normal. Intracranial compensation in the presence of pathology to maintain a normal intracranial pressure However, if the tumor continues to grow, it will reach a certain size where these compensatory mechanisms will become exhausted, whereby no further drainage of blood or CSF will be possible. At this point, the equilibrium becomes disrupted, and the patient enters a decompensated state where intracranial pressure will begin to rise. Intracranial decompensation in the presence of pathology causing a rise in intracranial pressure Cerebral Compliance and the Impact of ICP The shape of the curve demonstrates effects of intracranial volume changes on ICP.  Volume-pressure relationship The intracranial volume-pressure curve (1) No pathology (2) Small volume pathology in a compensated state with normal ICP The (3) intracranial Large volume-pressure volume pathology curve (1) No pathology in a decompensated state with(2) Small volume pathology elevated ICPin(4) a compensated statepathology Very large volume with normal ICPa (3) with Large volume significantly pathology elevated ICPinand a decompensated brain herniationstate with elevated ICP (4) Very large volume pathology with a significantly elevated ICP and brain herniation  Key Points The Monro- In non- Kellie Doctrine pathological Small volume Larger volume describes the states, three changes can be changes can lead components exist accommodated to the relationship in equilibrium to compensatory between the maintain by compensato mechanisms being contents of the normal ICP, ry mechanisms exhausted, leading cranium and the brain tissue, to maintain to significant intracranial the blood, and the the ICP increases in ICP CSF pressure  Cerebral blood flow — Following a significant increase in ICP, brain injury can result from brain stem compression Why Is ICP and/or a reduction in CBF. Raised ICP leads to death or disability in most acute cerebral conditions. Important? Cerebral perfusion pressure (CPP) is a It is also potentially treatable. clinical surrogate for the adequacy of cerebral perfusion. The 2 major consequences of increased ICP are: Brain Shifts and Ischemia  CPP=MAP-ICP  Normal ICP = 10-20mmHg  Normal CPP= 70-100mmHg  CPP=MAP-ICP  MAP= SBP+2DP divided by 3 Example: BP 90/45 mm Hg and ICP= 5 mm Hg  What is the MAP and CPP? mmHg MAP=1/3PP+DBP  The CPP is the pressure perfusing the brain. Impact of ICP The MAP and ICP are monitored frequently in persons with brain conditions that on CPP increase ICP and impair brain perfusion. Brain ischemia develops at CPP levels between 50 to 70 mm Hg. The continued cellular hypoxia leads to general neurologic deterioration; the level of consciousness may deteriorate from alertness through CONFUSION, LETHARGY, OBTUNDATION, STUPOR, and COMA Irreversible damage to the brain neurons occurs after 3-10 minutes of hypoxia. The concentration of Carbon Dioxide in the blood and in the brain tissue also plays a role in the regulation of cerebral blood flow. An increase in PaCO2 causes cerebral vasodilation, leading to increased cerebral blood flow and increased ICP. A decrease in PaCO2 has a vasoconstrictive effect, limiting blood flow to the brain. Decreased venous outflow may also increase cerebral blood volume, thus raising ICP.   A clinical phenomenon known as the Cushing’s response is seen when Cushing’s cerebral blood flow decreases Response significantly.  When ischemic, the vasomotor center triggers an increase in arterial pressure to overcome the increased ICP.  Increase in the systolic BP, a widening of the pulse pressure and cardiac slowing.  Perfusion may be recoverable if the Cushing’s response is treated rapidly. Clinical Manifestations Reductions in CBF are Headache, which is probably mediated via the responsible for pain fibers of cranial nerve (CN) V in the dura the clinical and blood vessels manifestations of elevated Decreased LOC due to either the local effect ICP. of mass lesions or pressure on the midbrain Vomiting Papilledema, characterized by Papilledema secondary to impaired blurring of the optic disc axonal transport and congestion margins A triad of bradycardia, respiratory depression, and hypertension (Cushing triad). Cheyne–Stokes respiration Central neurogenic hyperventilation  Cheyne–Stokes respiration is an abnormal pattern of breathing characterized by progressively deeper, and sometimes faster, breathing followed by a gradual decrease that results in a temporary stop in breathing, apnea. The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes.  Central neurogenic hyperventilation (CNH) is an abnormal pattern of breathing characterized by deep and rapid breaths at a rate of at least 25 breaths per minute. Increasing irregularity of this respiratory rate generally is a sign that the patient will enter into coma.  CNH is the body's response to reduced carbon dioxide levels in the blood. This reduction in carbon dioxide is caused by contraction of cranial arteries from damage caused by lesions in the brain stem. However, the mechanism by which CNH arises as a result from these lesions is still very poorly understood.  Brain Herniation  If the ICP continues to rise OR the tumor continues to grow without intervention, the ICP will rise to such a degree that occlusion of the cerebral blood flow will occur, and the brain parenchyma, will shift in position and become displaced, this is termed herniation. Because herniation puts extreme pressure on parts of the brain and cuts off the blood supply to various parts of the brain, it is often fatal. Brain Herniation  There are several types of herniation depending on which part of the brain is being displaced, the most serious of which are uncal and tonsillar herniation: Uncal herniation refers to displacement of the medial part of the temporal lobe (uncus) below the tentorium cerebelli Tonsillar herniation occurs when the cerebellar tonsils are forced downwards through the foramen magnum, causing compression on the brainstem (fatal if left untreated) The tentorium is an extension of the dura mater that separates the cerebellum from the cerebrum. There are two major classes of herniation: supratentorial and infratentorial. Supratentorial refers to herniation of structures normally found above the tentorial notch, and infratentorial refers to structures normally found below it. Transtentorial herniation  Supratentorial herniation 1.Uncal (transtentorial) 2.Central 3.Cingulate (subfalcine/transfalcine) 4.Transcalvarial 5.Tectal(posterior) Infratentorial herniation 5.Upward (upward cerebellar or upward transtentorial) 6.Tonsillar(downward cerebellar)  The best therapy for intracranial hypertension (ICH) is resolution of the proximate cause of elevated ICP. Examples include evacuation of a blood clot, resection of a tumor, CSF diversion in the setting of hydrocephalus. Regardless of the cause, ICH is a medical emergency, and treatment should be undertaken as expeditiously as possible. Management The urgent assessment and support of oxygenation, blood pressure (BP),and end-organ perfusion Large shifts in BP should be minimized, with particular care taken to avoid hypotension. Although it might seem that lower BP would result in lower ICP, this is not the case. Hypotension, especially in conjunction with hypoxemia, can induce reactive vasodilation and elevations in ICP. Management Osmotic diuretics: (Intravenous mannitol). reduce brain volume by drawing free water out of the tissue and into the circulation, where it is excreted by the kidneys, dehydrating brain parenchyma, reducing brain edema. Hypertonic saline has increasingly been employed as a first-line agent, supplanting mannitol at numerous institutions. Mannitol and hypertonic saline have been compared in several studies. The results indicated that hypertonic saline appears to have greater efficacy in managing elevated ICP, but clinical outcomes have not been systematically examined. Further clinical trials are required to clarify the appropriate role of hypertonic saline infusion versus mannitol in the management of elevated ICP. Hyperventilation — Use of mechanical ventilation to lower PaCO2 to 26 to 30 mmHg has been shown to rapidly reduce ICP through vasoconstriction and a decrease in the volume of intracranial blood. Sedation: Keeping patients appropriately sedated can decrease ICP by reducing metabolic demand, ventilator asynchrony. Position: Patients with elevated ICP should be positioned head elevated to maximize venous outflow from the head. Important maneuvers include reducing excessive flexion or rotation of the neck, and minimizing stimuli that could induce Valsalva responses, such as endotracheal suctioning. Fever: Elevated metabolic demand in the brain results in increased cerebral blood flow and can elevate ICP by increasing the volume of blood in the cranial vault. Conversely, decreasing metabolic demand can lower ICP by reducing blood flow. Fever increases brain metabolism and has been demonstrated to increase brain injury. Therefore, aggressive treatment of fever, including acetaminophen should be implemented. Ventriculostomy: Valsalva Maneuver  The Valsalva maneuver is a breathing technique that increases pressure in the chest. It can be used to normalize some abnormally fast heart rhythms. People may also use this technique regularly without knowing it, such as when they push to induce a bowel movement.  From the neurological perspective, this maneuver causes sudden expulsion of blood from the thoracic vessels into the carotid vessels causing a rise in the intracranial pressure (ICP), altering the brain perfusion. Effect of High temperature on ICP Elevated elevated ICP by increased increasing the metabolic Fever demand in cerebral volume of blood flow blood in the the brain cranial vault. Removal of CSF: Ventriculostomy  An external ventricular drain (EVD) is a small catheter inserted through the skull usually into the lateral ventricle, which is typically connected to a closed collecting device to allow for drainage of cerebrospinal fluid. The EVD can also be connected to a transducer that records intracranial pressure.