Adult Nursing II: Conditions of the Nervous System PDF

ADULT NURSING II Conditions of the Nervous System Presented by Keron Jones-Fraser; RN, BScN, Cert. Nsg. Ed. MScN, PhD Candidate  OBJECTIVES  At the end of the session, students should discuss the following conditions:  Altered level of consciousness - Un...

ADULT NURSING II Conditions of the Nervous System Presented by Keron Jones-Fraser; RN, BScN, Cert. Nsg. Ed. MScN, PhD Candidate  OBJECTIVES  At the end of the session, students should discuss the following conditions:  Altered level of consciousness - Unconsciousness  Increased intracranial pressure  Head injury  Meningitis  Encephalitis  Brain abscess  Stroke/CVA  Seizure disorder 2  Conditions  Altered level of consciousness - Unconsciousness  Increased intracranial pressure  Head injury  Meningitis  Encephalitis  Brain abscess  Stroke/CVA  Seizure disorders 3  INCREASED INTRA-CRANIAL PRESSURE  The rigid cranial vault contains brain tissue (80%/1,400 g), blood (10%/75 mL), and CSF (10%/75 mL).  The volume and pressure of these three components are usually in a state of equilibrium and produce the intracranial pressure.  ICP is usually measured in the lateral ventricles; normal ICP is roughly 10 - 15 mmHg (normal value ranges may vary slightly among different laboratories) 4  Increased intra-cranial pressure  ICP is the pressure exerted by the contents inside the cranial vault of the brain tissue (gray and white matter), CSF and the blood volume.  Increased ICP is a potentially life-threatening situation that results from an increase in any or all three components. Increased sustained ICP greater than 15 mmHg is considered abnormal. 5  Monro-Kellie hypothesis  States that because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others.  Because brain tissue has limited space to change, compensation typically is accomplished by displacing or shifting CSF, increasing the absorption of CSF, or decreasing cerebral blood volume. Without such changes, ICP will begin to rise. 6  Pathophysiology  The brain contents must be kept in equilibrium, and the ratio between volume and pressure must remain constant.  Any increase in the volume of one component must be accompanied by a reciprocal decrease in one of the other components.  When this volume-pressure relationship becomes unbalanced, ICP increases 7  Clinical manifestations When ICP increases to the point at which the brain’s ability to adjust has reached its limits, neural function is impaired;  earliest sign is LOC  slowing of speech and delay in response to verbal suggestions  restlessness, confusion, or increasing drowsiness. These signs may result from compression of the brain due to swelling from hemorrhage or edema, an expanding intracranial lesion or a combination of both. 8 Clinical manifestations 9  Complications Include:  Brain stem herniation  Diabetes insipidus  Syndrome of inappropriate antidiuretic hormone (SIADH). 10  Diagnostic evaluation  Cerebral angiography - to assess cerebral circulation.  Computed tomography (CT) scanning - three- dimensional view of the brain, distinguishes between soft tissues and water.  Positron emission tomography (PET) – permits study of brain’s function by evaluating the metabolism, blood flow and chemical processes. 11  Diagnostic evaluation  Magnetic resonance imaging (MRI) - provides information about electric function  Transcranial Doppler - measure the velocity of blood flow through cerebral arteries, providing information about the circulation to the brain.  Lumbar puncture is avoided in patients with increased ICP because the sudden release of pressure can cause the brain to herniate. 12  Medical Management  Increased ICP is a true emergency and must be treated promptly.  Invasive ICP monitoring - to identify increased pressure early in its course (before cerebral damage occurs), to quantify the degree of elevation, to initiate appropriate treatment, to provide access to CSF for sampling and drainage, and to evaluate the effectiveness of treatment. 13  Invasive ICP monitoring Retrieved from drugline.org Retrieved from crashingpatient.com 14  Medical Management  Immediate management to relieve increased ICP involves decreasing cerebral edema, lowering the volume of CSF, or decreasing cerebral blood volume while maintaining cerebral perfusion  These goals are accomplished by administering osmotic diuretics and corticosteroids, restricting fluids, draining CSF, controlling fever, maintaining systemic blood pressure and oxygenation, and reducing cellular metabolic demands.  https://www.youtube.com/watch?v=9 mbiu315VMI 15  HEAD INJURY  Is a broad classification that includes injury to the scalp, skull, or brain.  Is the disruption of normal brain function due to trauma-related injury resulting in compromised neurologic function resulting in focal or diffuse symptoms. 16  Etiology  motor vehicle crashes  violence  falls  Types of traumatic brain injury 1. Concussion 2. Cerebral contusion 3. Intra-cerebral hematoma 4. Epidural hematoma 5. Subdural hematoma 6. Diffuse axonal injury (DAI) 18  Pathophysiology  Damage to the brain from traumatic injury takes two forms: primary injury and secondary injury.  Primary injury is the initial damage to the brain that results from the traumatic event. may include contusions, lacerations, torn blood vessels from impact, acceleration /deceleration, or foreign object penetration 19  Pathophysiology  Secondary injury evolves over the ensuing hours and days after the initial injury and is due primarily to brain swelling or ongoing bleeding.  Any bleeding or swelling within the skull increases the volume of contents within a container of fixed size and so can cause increased intracranial pressure (ICP) 20  Pathophysiology Brain suffers traumatic injury Brain swelling or bleeding increases intracranial volume Rigid cranium allows no room for expansion of contents so intracranial pressure increases Pressure on blood vessels within the brain causes blood flow to the brain to slow Cerebral hypoxia and ischemia occur Intracranial pressure continues to rise. Brain may herniate Cerebral blood flow ceases Producing ischemia, infarction, irreversible brain damage, and eventually brain death 21  Scalp injuries  Isolated scalp trauma is generally classified as a minor head injury. Because its many blood vessels constrict poorly, the scalp bleeds profusely when injured.  Trauma may result in an abrasion (brush, wound), contusion, laceration, or hematoma beneath the layers of tissue of the scalp (subgaleal hematoma). 22  Skull fracture  Is a break in the continuity of the skull caused by forceful trauma. It may occur with or without damage to the brain.  Are classified as linear, comminuted, depressed, or basilar. May be open, indicating a scalp laceration or tear in the dura (eg, from a bullet or an ice pick), or closed, in which the dura is intact 23  Clinical manifestation Depends on the severity and the distribution of brain injury  Disturbances in consciousness: confusion to coma  Headache, vertigo  Agitation, restlessness  Respiratory irregularities  Cognitive deficits  Coma and coma syndromes; persistent vegetative state 24 Clinical manifestation  Otorrhea may indicate leakage of CSF from ear due to posterior fossa skull fracture; rhinorrhea may indicate leakage of CSF from nares due to anterior fossa skull fracture  Raccoon eyes and Battle sign indicate skull fractures 25  Clinical manifestation  Pupillary abnormalities  Sudden onset of neurologic deficit  Episodes of altered LOC, tachycardia, tachypnea, hyperthermia, agitation due to sympathetic storming (aggravated stress response)  Abnormal bleeding due to coagulopathy  Cardiac arrhythmias due to increased release of catecholamines in stress response 26  Diagnostic evaluation  CT scan to identify and localize lesions, edema, bleeding.  Skull and cervical spine films to identify fracture, displacement.  Neuropsychological tests during rehabilitation phase to determine cognitive deficits. 27  Diagnostic evaluation  MRI to identify and diagnosis DAI (MRI is rarely performed as it does not affect medical treatment).  CBC, coagulation profile, electrolyte levels, serum osmolarity, ABG values, and other laboratory tests to monitor for complications and guide treatment. 28  Management  Airway - assess and maintain patent airway intubate for GCS less than 8 (comatose) placement of nasogastric tube with intubation to prevent aspiration  Breathing - all intubated patients should have ventilatory support Oxygen as needed Avoid use of hyperventilation 29  Management  Circulation - prevent hypotension Maintain SBP above 90 mm Hg through use of vasopressors and albumin Maintain normovolemia Treat symptomatic anemia with packed RBC and iron supplements Treat symptomatic arrhythmias  Management of increased ICP and cerebral edema 30  Management  Supportive care - nutritional support, rehabilitative care, skin care…  Antibiotics to prevent infection with open skull fractures or penetrating wounds  Surgery to evacuate intracranial hematomas, debridement of penetrating wounds, elevation of depressed skull fractures or repair of CSF leaks 31  Management  Treatment of hypernatremia with fluid replacement, pitressin therapy  Treatment of hyponatremia by monitoring daily fluid status, fluid restriction, oral salt replacement, and IV saline  Seizure prophylaxis – phenytoin (Dilantin) 32  Complications  Infections: systemic (respiratory, urinary), neurologic (meningitis, ventriculitis)  Increased ICP, hydrocephalus, brain herniation  Post-traumatic seizure disorder  Permanent neurologic deficits: cognitive, motor, sensory speech  Neurobehavioral alterations; impulsivity, uninhibited aggression, and emotional lability  Persistent sympathetic storming  Disseminated Intravascular Coagulation (DIC), Diabetes Insipidus (DI), Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), Death 33  MENINGITIS  Meningitis is a disease caused by the inflammation of the protective membranes (pia mater and arachnoid membranes) covering the brain and spinal cord known as the meninges.  The subarachnoid space between these two meninges contains CSF that may reflect the signs and symptoms of meningitis. 34  Classifying Meningitis Classified as aseptic or septic.  In aseptic meningitis, bacteria are not the cause of the inflammation; the cause is viral or secondary to lymphoma, leukemia, or brain abscess.  Septic meningitis refers to meningitis caused by bacteria, most commonly Neisseria meningitidis, although Haemophilus influenzae and Streptococcus pneumoniae are also causative agents. 35  Types of Meningitis  Viral Meningitis most common form; usually self-limiting; management is supportive; usually caused by a nonpolio enterovirus (90%); targets children and the elderly; spread by the fecal-oral route and through sewage. 36  Types of Meningitis  Bacterial Meningitis usually more serious than viral meningitis; cause damage to the CNS from the inflammatory process rather than the pathogen; typically caused by: 1.Streptococcus pneumoniae (pneumococcal meningitis), a gram-positive diplococci; 2.Neisseria meningitidis (meningococcal meningitis), a gram-negative diplococci. 37  Types of Meningitis  Parasitic Meningitis usually cause by flukes, worms, or amoeba.  Fungal meningitis particularly Cryptococcus neoformans, affects immunosuppressed patients (eg, HIV) through soil contaminated with excrement from pigeons and chickens. 38  Pathophysiology Meningeal infections generally originate in one of two ways:  through the bloodstream as a consequence of other infections, or  by direct extension, such as might occur after a traumatic injury to the facial bones, or secondary to invasive procedures. 39  Pathophysiology  Once the causative organism enters the bloodstream, it crosses the blood–brain barrier and causes an inflammatory reaction in the meninges.  Independent of the causative agent, inflammation of the subarachnoid space and pia mater occurs. Since there is little room for expansion within the cranial vault, the inflammation may cause increased intracranial pressure. 40  Pathophysiology  Cerebrospinal fluid (CSF) flows in the subarachnoid space, where inflammatory cellular material from the affected meningeal tissue enters and accumulates in the subarachnoid space, thereby increasing the CSF cell count 41  Clinical manifestation  Classic symptoms are fever, headache, nuchal rigidity  Altered mental status; confusion in older patients  Petechial or purpuric rash from coagulopathy, especially with N. meningitidis  Photophobia 42  Clinical manifestation  Nuchal rigidity, neck tenderness, or a bulging the anterior fontanelle in infants  Children may exhibit behavioral changes, arching of the back and neck, a blank stare, refusal to feed, and seizures. Viral meningitis can cause a red, maculopapular rash in children. 43  Clinical manifestation  Positive Brudzinski's and Kernig's signs  Onset may be over several hours or several days depending on the infectious agent, the patient's age, immune status, comorbidities, and other variables. 44  Diagnostic evaluation  Complete blood count  Blood cultures are obtained to indicate the organism  CSF evaluation for pressure, leukocytes, protein, glucose  MRI/CT scan with and without contrast rules out other disorders.  CT scan with contrast must be done to detect abscesses. 45  Diagnostic evaluation  Low CD4+ counts indicate immunosuppression in HIV-positive patients and other patients with immunosuppressive disorders.  In patients with acquired immunodeficiency syndrome (AIDS), MRI is used to detect meningeal irritation, evidence of a sinus infection, or brain abscess. 46  Management  Cultures should be taken before initiating antibiotics.  I.V. antibiotics until the laboratory findings determine the type of meningitis. Penicillin antibiotics (eg, ampicillin, piperacillin) or one of the cephalosporins (eg, ceftriaxone sodium [Rocephin], cefotaxime sodium) may be used. 47  Management  Dexamethasone (Decadron) to manage inflammation  Antifungal agent (Amphotericin B, Flucanazole, Intraconazole) are indicated for cryptococcal meningitis  Antitubercolosis drugs if infection by Mycobacterium tubercolosis is suspected 48  Management  Dehydration and shock are treated with fluid volume expanders.  Seizures, which may occur in the early course of the disease, are controlled with phenytoin (Dilantin).  Increased ICP is treated as necessary 49  Complications  Bacterial meningitis, particularly in children, may result in deafness, learning difficulties, spasticity, paresis, or cranial nerve disorders.  Increased ICP in AIDS patients with cryptococcal meningitis has resulted in severe visual losses.  Seizures occur in 20% to 30% of patients. 50  Complications  Increased ICP may result in cerebral edema, decreased perfusion, and tissue damage.  Severe brain edema may result in herniation or compression of the brain stem.  Purpura may be associated with disseminated intravascular coagulation 51  ENCEPHALITIS  Encephalitis is an inflammation of cerebral tissue, typically accompanied by meningeal inflammation.  Meningoencephalitis is most commonly caused by a viral infection.  Like meningitis, encephalitis can be infectious or noninfectious and acute, subacute, or chronic. 52  Clinical manifestations  Fever, headache, nausea and vomiting  Altered mental status to coma  Motor weakness such as hemiparesis  Increased deep tendon reflexes  Bizzarre behaviour and personality changes  Tremors, seizures  Memory impairment, amnesia & dysphagia 53  Diagnostic evaluation  Lumbar puncture with evaluation of CSF  Electroencephalography (EEG)  CT scan  MRI  Brain tissue Biopsy 54  Management  Determine the type of encephalitis: viral, noninfectious, fungal…  Patients with cytomegalovirus may be treated with ganciclovir (Cytovene) and foscarnet (Foscavir), commonly used to treat cytomegalovirus retinitis in HIV-positive patients. 55  Management  Pyrimethamine (Daraprim) and sulfadoxine (Fansidar) are commonly used to treat Toxoplasma encephalitis.  I.V. acyclovir over 10 to 21 days is indicated for herpes simplex virus.  Anticonvulsants manage seizures. 56  BRAIN ABSCESS  A brain abscess is a free or encapsulated collection of infectious material of brain parenchyma, between the dura and the arachnoid linings (subdural abscess) or between the dura and the skull (epidural abscess).  Although relatively rare, it is a complication encountered increasingly in patients whose immune systems have been suppressed either through therapy or disease. 57  Pathophysiology It may occur by:  direct invasion of the brain from intracranial trauma or surgery;  by spread of infection from nearby sites, such as the sinuses, ears, and teeth (paranasal sinus infections, otitis media, dental sepsis);  or by spread of infection from other organs (lung abscess, infective endocarditis) 58  Prevention  To prevent brain abscess, otitis media, mastoiditis, sinusitis, dental infections, and systemic infections should be treated promptly. 59  Clinical manifestations  Result from alterations in intracranial dynamics (edema, brain shift), infection, or the location of the abscess.  Headache, usually worse in the morning, is the most prevailing symptom.  Vomiting is also common. 60  Clinical manifestations  Focal neurologic signs (weakness of an extremity, decreasing vision, seizures) may occur, depending on the site of the abscess.  May be a change in mental status, as reflected in lethargic, confused, irritable, or disoriented behaviour.  Fever may or may not be present. 61  Diagnostic evaluation  CT scan, MRI with contrast locate the sites of abscess  Blood cultures are obtained to identify the organism, positive Gram's stain, leukocytosis, and elevated erythrocyte sedimentation rate (ESR). 62  Diagnostic evaluation  Cultures are obtained from the suspected source of infection, using stereotaxic needle aspiration or brain surgery, to identify the organism and sensitivity to antimicrobials.  EEG detects seizure disorders.  Findings in cerebral subdural empyema include increased WBC and increased pressure of the CSF. 63  Management  With cerebral subdural empyema or intracranial epidural abscesses, management consists of trephining (drilling through skull to evacuate purulent material), systemic antibiotics, and treatment of cerebral edema.  Closed stereotaxic needle biopsy, under CT guidance, may be used for drainage evacuation instead of craniotomy. 64  Management  Antimicrobial therapy – Penicillin G & chloramphenicol (Chloromycetin) is directed toward the most common etiologic agents: streptococci, anaerobic bacteria (eg, Bacteroides species).  Multiple abscesses may be treated with appropriate antimicrobial therapy alone, with close monitoring by CT scans. 65  Management  Antiseizure medications (phenytoin, phenobarbital) may be prescribed to prevent seizures.  Antifungal therapy, such as amphotericin B, is initiated for candidiasis and other fungal infections. 66  Management  Antituberculosis pharmacotherapy, such as rifampin, isoniazid, and pyrazinamide, should be used to treat abscesses containing AFB.  Adjunctive therapy includes corticosteroids and osmotic diuretics to reduce cerebral edema, and anticonvulsants to manage seizures 67  STROKE/CVA  Stroke, cerebrovascular accident (CVA), or brain attack is the onset and persistence of functional abnormality of the CNS lasting longer than 24 hours and resulting from disruption of blood supply to the brain and indicates infarction rather than ischemia. 68  Definitions  Transient Ischemic attack (TIA) is a clinical syndrome of rapid onset of focal deficits of brain function which resolves within 24 hours.  Progressive Stroke - a stroke in which the focal neurological deficits worsen with time. Also called stroke in evolution.  Completed Stroke - a stroke in which the focal neurological deficits persist and do not worsen with time. 69  Types  Two types are: 1. Ischemic 2. Hemorrhagic 70  Risk factors  Fixed  Modifiable 1. Advanced age (>55yrs) 1. Hypertension 2. Heart disease (Atrial fibrillation, 2. Gender (male>female) endocarditis) 3. Race (higher risk for afro- 3. Diabetes mellitus caribbean) 4. Hyperlipidaemia 4. Heredity 5. Smoking 5. Previous vascular event eg. 6. Excess alcohol consumption MI, peripheral embolism 7. Oral contraceptives 6. High fibinogen 8. Overweight and obesity 9. Physical inactivity 71  Pathophysiology Ischemic stroke  Partial or complete occlusion of a cerebral blood flow to an area of the brain due to: Thrombus (most common) due to arteriosclerotic plaque in a cerebral artery, usually at bifurcation of larger arteries; occurs over several days. Embolus a moving clot of cardiac origin (frequently due to atrial fibrillation) or from a carotid artery that travels quickly to the brain and lodges in a small artery; occurs suddenly with immediate maximum deficits. 72  Pathophysiology Ischemic stroke  Area of brain affected is related to the vascular territory that was occluded. Subtle decrease in blood flow may allow brain cells to maintain minimal function, but as blood flow decreases focal areas of ischemia occur, followed by infarction to the vascular territory. 73  Pathophysiology Ischemic stroke  An area of injury includes edema, tissue breakdown, and small arterial vessel damage. The small arterial vessel damage poses a risk of hemorrhage. The larger the area of infarction, the greater the risk of hemorrhagic conversion.  Ischemic strokes are not activity dependent; may occur at rest. 74  Pathophysiology Hemorrhagic stroke  Leakage of blood from a blood vessel and hemorrhage into brain tissue, causing edema, compression of brain tissue, and spasm of adjacent blood vessels.  May occur outside the dura (extradural), beneath the dura mater (subdural), in the subarachnoid space (SAS or subarachnoid), or within the brain substance (intracerebral). 75  Pathophysiology Hemorrhagic stroke  Causal mechanisms include: Increased pressure due to hypertension. Head trauma causing dissection or rupture or vessel. Deterioration of vessel wall from chronic hypertension, diabetes mellitus, or cocaine use. Congenital weakening of blood vessel wall with aneurysm or arteriovenous malformation (AVM). 76  Pathophysiology Hemorrhagic stroke  The intracranial hemorrhage becomes a space-occupying lesion within the skull, further compromising brain function. The mass effect causes pressure on brain tissue. The hemorrhage irritates local brain tissue leading to surrounding focal edema. SAH or hemorrhage into a ventricle can block normal CSF flow, leading to hydrocephalus.  Hemorrhage commonly occurs suddenly while a person is active 77  Clinical manifestations Clinical manifestations vary depending on the vessel affected and the cerebral territories it perfuses. Symptoms are usually multiple. Headache may be a sign of impending cerebral hemorrhage or infarction; however, it is not always present. Numbness (paresthesia), weakness (paresis), or loss of motor ability (plegia) on one side of the body. Loss of balance and coordination 78  Clinical manifestations Difficulty in swallowing (dysphagia). Aphasia (expressive, receptive, global). Visual difficulties of inattention or neglect (lack of acknowledgment of one side of the sensory field), loss of half of a visual field (hemianopsia), double vision, photophobia. Altered cognitive abilities, change in mental status and psychological affect. Self-care deficits 79  Comparison of Lt. & Rt. Hemispheric strokes Left Right  Paralysis/weakness on  Paralysis/weakness on Lt. Rt. side of body side of body   Lt. visual field deficit Rt. visual field deficit   Spatial-perceptual deficits Aphasia (expressive, receptive, or global)  Increased distractibility  Altered intellectual ability  Impulsive behaviour & poor  judgment Slow, cautious behavior  Lack of awareness of deficits 80  Diagnostic evaluation  Carotid ultrasound to detect carotid stenosis.  CT scan to determine cause and location of stroke.  MRA or CT angiogram noninvasive evaluation of cerebrovascular structures. 81  Diagnostic evaluation  Cerebral angiography to determine extent of cerebrovascular insufficiency and to evaluate for structural abnormalities.  PET, MRI with diffusion-weighted images to localize ischemic damage. 82  Management Ischemic stroke 1. Maintain airway, breathing, oxygenation, circulation 2. Neurological assessment 3. IVF (NS) until pt. is able to tolerate oral diet 4. Maintain BP within prescribed parameters (SBP 100mmHg) to promote adequate cerebral perfusion to prevent further ischemia 5. Thrombolytic treatment 83  Management Ischemic stroke 6. Maintain normal blood glucose as hyperglycemia is associated with poor outcome 7. Maintain normothermia because hyperthermia is associated with poor outcome 8. DVT prophylaxis – compression stockings and low molecular-weight Heparin 9. Focus on early rehabilitation 84  Management Hemorrhagic stroke 1. Maintain airway, breathing, oxygenation, circulation 2. Neurological assessment 3. IVF (NS) until pt. is able to tolerate oral diet 4. Maintain BP within prescribed parameters (SBP