Neurological Disorders Part 1 (DJ).pdf

NEUROLOGICAL DISORDERS PRESENTER: DEREEKA JONES NEUROLOGICAL ASSESSMENT Health history- common clinical manifestations include pain, seizures, dizziness, weakness, visual disturbances, abnormal sensations, risk factors Physical examination- Level of consciousness (LOC), Pupil assessmen...

NEUROLOGICAL DISORDERS PRESENTER: DEREEKA JONES NEUROLOGICAL ASSESSMENT Health history- common clinical manifestations include pain, seizures, dizziness, weakness, visual disturbances, abnormal sensations, risk factors Physical examination- Level of consciousness (LOC), Pupil assessment Vital signs; temp, pulse, respiration, blood pressure, oxygen saturation Cranial nerves, Motor: strength and balance, Reflexes, NEUROLOGICAL ASSESSMENT Sensory function; touch, pain, pressure Meningeal irritation Posturing; Autonomic system; sympathetic/adrenergic responses, parasympathetic/cholinergic responses DIAGNOSTIC INVESTIGATIONS SKULL AND SPINAL RADIOGRAPHY- reveals size and shape, fractures, indentations calcification of skull bones. Shows fractures, dislocation, compression, curvature, erosion or degeneration of spine. Provide support for patients Maintain immobilization Remove metal and jewellery Always enquire about pregnancy before radiographic procedures COMPUTED TOMOGRAPHY CT Detects intracranial bleeds, Patient need to lie still and lesions, edema, flat hydrocephalus, infarctions Give antihistamine and May/not require dye corticosteroids before dye if Assess for iodine or shellfish allergy present and monitor allergy for dye Initiate IVA appropriate size Assess renal function Replacement fluid to remove Hot flushed sensation and dye, diuresis expected metallic taste when dye Assess for bleeding, injected perfusion and sensation ELECTROENCEPHALOGRAM (EEG). records electrical activity Allow breakfast of superficial layer of Premedicate with sedative cerebral cortex. Monitor post procedure Wash patient’s hair Electrodes attached to the head Withhold antidepressants, stimulants, antiseizure tranquilizers, medications 24-48 before procedure MAGNETIC RESONANCE IMAGING MRI identifies tissues, tumors, Assess for claustrophobia vascular and spinal and premedicate as abnormalities ordered Remove ALL metal Patient must be still Patients with pacemaker, Contraindicated in implanted defibrillator, pregnancy other metal implant (hip or Determine need for vascular clip) CANNOT do contrast agent MRI LUMBAR PUNCTURE LP Spinal needle inserted Maintain flat between L3 & L4 to obtain Encourage fluid intake cerebrospinal fluid CSF Monitor I/O Empty bladder Lateral recumbent position with knees to abdomen Assist with collection STRICT asepsis Monitor VS, neuro signs headaches CSF leak  CEREBRAL ANGIOGRAM Dye injected into carotid NPO 4-6 hrs before arteries via femoral or V/S & Neuro assessment other artery to assess cerebral arteries & for Bed rest 12 hrs post lesions Bed 15-30 degrees if Assess for allergy ordered flat if femoral artery was used Assess medication history- hold anticoagulant Assess peripheral pulses medication if prescribed Apply sandbag or other Increase fluid intake 2 immobilization device to days before test injection site Administer premedications Monitor for bleeding UNCONSCIOUSNESS UNCONSCIOUSNESS A state of depressed cerebral functioning with unresponsiveness to stimulation of sensory and motor functions. Commonly caused by head trauma, cerebral toxins, shock, haemorrhage, tumor or infections. ASSESSMENT Unarousable Assess LOC Primitive or no response to Pupils painful stimuli Glasgow coma scale Altered respirations Motor, sensory and Decreases cranial nerve reflexes and reflex activity Respiratory status Abnormal posture NURSING DIAGNOSES Ineffective airway clearance Risk for injury Deficient fluid volume Impaired oral mucosa Risk for impaired skin integrity Ineffective thermoregulation Impaired urinary elimination Bowel incontinence Disturbed sensory perception NURSING MANAGEMENT Elevate HOB Do not leave unattended Oropharyngeal suctioning Pad and keep up rails Maintain oxygenation Avoid use of restraints Chest physiotherapy Initiate seizure precautions if needed Auscultate breath sounds Monitor VS & blood Assume the patient can hear; speak positively gasses Remove dentures NURSING MANAGEMENT Maintain NPO until Reposition 2hrly conscious Provide passive ROM Maintain nutrition Use foot board & wrist IF/enteral splints Assess bowel sounds Monitor skin integrity Monitor elimination Maintain temperature patterns ; constipation Provide frequent mouth Monitor I/O weigh daily care INCREASED INTRACRANIAL PRESSURE  INTRACRANIAL PRESSURE ICP is the pressure exerted by the brain tissue, CSF, and cerebral blood within the intracranial vault. There is a delicate balance that exists between the volume of the intracranial contents within this rigid compartment (80% brain tissue, 10% blood, 10%CSF) The normal ICP is 0-15 mmHg (15 is the upper limit). Pressures over 20mm Hg represent severely increased ICP, which seriously impairs cerebral perfusion.  IMPORTANT PARAMETERS AFFECTING ICP  Cerebral perfusion pressure (CPP) is the amount of blood flow (pressure gradient ) from the systemic circulation that is required to provide adequate oxygen and glucose for brain metabolism. It is the difference between mean arterial pressure (MAP) and ICP. CPP = MAP – ICP Cerebral blood volume (CBV) is dependent on cerebral blood flow (CBF). Cerebral blood flow (CBF) depends upon cerebral perfusion pressure (CPP). If CBF increases, so does CBV. When MAP & ICP are equal there is no CPP & blood flow stops!  THE MUNRO-KELLIE HYPOTHESIS The Munro-Kellie Hypothesis states that a change in volume of any of the normal components (brain, cerebral blood volume and cerebrospinal fluid) of the intracranial vault must be accompanied by a reciprocal change in one or more of the other components. If this reciprocal change is not accomplished the result is an increase in intracranial pressure (ICP).  HOW DOES THE BODY COMPENSATE FOR CHANGES IN ICP? 1. Displacement of CSF into the spinal subarachnoid space, increased absorption or decreased secretion of CSF 2. Reduction of blood volume 3. Herniation ;displacement of brain tissue. Most lethal stage of compensation, often results in death from brain stem compression. Always an emergency!  COMMON CAUSES Increases in tissue volume Space occupying lesions: brain tumor, abscess, hemorrhage, Cerebral edema: infarction, interstitial edema, infection, metabolic disorders, toxins, electrolyte imbalances Abscess Trauma hypertension Increases in CSF hydrocephalus Deficient CSF absorption or overproduction of CSF (Hogan & Hill, 2004) NERVE COMPRESSION WITH IICP CUSHING’S TRIAD! A response involving three classis signs: widening pulse pressure: increased systolic BP with diastolic remaining the same or slightly elevated. Bradycardia Slowing respirations Cushing’s triad indicates increased severe ICP!  ASSESSMENT Restlessness Increased systolic pressure Altered level of with widened pulse slowed consciousness Headache heart rate Abnormal respirations Weakness to hemiplegia Increased blood pressure Positive Babinski reflex widening pulse pressure Slowing pulse Seizures Elevated temperature Cushing’s triad; Nausea & Vomiting hyperbradybrady Change in speech pattern Abnormal pupillary Abnormal posturing; reactions decerebrate, decorticate  Emergency Care ABCs Airway maintenance, intubation with oxygenation (PO2 > 90mmHg), mild hyperventilation – avoid hypercapnia. Ensure adequate fluid however avoid lowering the blood osmolarity. Initial neuro assessment and Glasgow Coma Scale Etiology of the brain injury will dictate further evaluation & treatment  EMERGENCY CARE CONT’D osmotic diuretics (mannitol IV) steroids (controversial) vasoactive medication (100-150mmHg systolic) elevate HOB (30 degrees) sedate as needed (barbituates IV) drain CSF (keep ICP < 20) maintain fluid status (normal serum Na & osmolality) NURSING DIAGNOSES Ineffective airway clearance rt diminished protective reflexes (cough and gag) Ineffective breathing pattern rt neurologic dysfunction Impaired cerebral tissue perfusion rt (cause of the IICP) Risk for/ deficient fluid volume rt fluid restriction Risk for injury rt altered level of consciousness  NURSING MANAGEMENT IN CONTROLLING ICP Elevate HOB 30 to 40 degrees Ongoing Glasgow Coma Scale Pulmonary management; prevent hypoxia, mechanical ventilation if prescribed Cardiovascular: monitor BP, CO, volume status Prevent Valsalva maneuver; exhale while moving Avoid straining activities like coughing and sneezing Maintain body temperature; prevent shivering Limit fluid intake (1.2L/day) monitor I/O  NURSING MANAGEMENT CONT’D Administer prescribed meds to reduce ICP: barbituates, mannitol analgesics, narcotics Maintain fluid and electrolyte balance with NaCl or RL solution Decrease environmental and noxious stimuli Group activities and allow rest Maintain intracranial pressure >20mmHg  MEDICATIONS Antiseizure; can be given prophylactically Antipyretics and muscle relaxants; prevents fever and shivering Blood pressure medications; maintain cerebral perfusion systolic 100-150 mmHg (above or below notify physician) Corticosteroids; reduces cerebral edema IVF; monitor closely to prevent cerebral edema and fluid overload Hyperosmotic Agent; increases intravascular pressure HEAD INJURY TYPES OF BRAIN INJURY TYPES OF HEAD INJURY Scalp injury: minor injury resulting in laceration, abrasion & hematoma Skull injury: may occur with or without damage to brain. Brain injury SKULL FRACTURES Linear Skull Fracture: is a break in the continuity of the bone, appear as thin lines on X-ray. Depressed Skull Fracture - The broken piece of skull bone is pressed towards or embedded in the brain. Comminuted and Compound Skull Fracture - The scalp is cut and the skull is splintered, multiple fractures. Basilar Skull Fracture The skull fracture is located at the base of the skull and may include the opening at the base of the skull SOME SIGNS OF SKULL FRACTURES CSF or fluid draining from ear (“halo” sign) Blood behind tympanic membrane Raccoon Eyes: periorbital ecchymoses Battles Sign: bruise over mastiod process Cranial nerve and inner ear damage  Traumatic brain injury (TBI) is an insult to the brain, caused by an external physical force, that may produce physical, intellectual, emotional, social and vocational changes. Major causes of TBI motor vehicle accidents, falls, acts of violence, sports & recreational injuries, blows to head, child abuse (shaken baby syndrome). INJURIES Blunt Penetrating Coup-Contrecoup TYPES OF BRAIN INJURY Concussion: is a head trauma that may or may not result in loss of consciousness (for 5 minutes or less) and retrograde amnesia. Contusion: is a severe injury in which the brain is bruised resulting in swollen brain tissue, areas of hemorrhage, infarction, necrosis, edema. Results in loss of consciousness and symptoms of shock.  CONCUSSION May experience only dizziness and feel “dazed”. Retrograde amnesia Treatment involves observing patient for headache, dizziness, lethargy, irritability and anxiety. Client should resume normal activities slowly and the following should be watched for: difficulty in awakening or speaking, confusion, severe headache, vomiting or weakness on one side of the body. May or may not show up on CAT scan. Blood clot can occasionally occur causing death Months to years to heal  CONTUSION Depends on which areas of the brain damaged – cerebral hemispheres, brain stem (RAS) Can cause diffuse axonal type injury resulting in permanent or temporary damage If widespread injury, abnormal eye movement and motor function, increased intracranial pressure and herniation - poor outcome. May have residual damage, seizures  Diffuse Axonal Injury Extensive tearing of nerve tissue throughout the brain causing the release of chemicals, causing additional injury. Immediate coma, decerebrate & decorticate posturing, and global edema The tearing of the nerve tissue disrupts the brain’s regular communication and chemical processes producing temporary or permanent widespread brain damage, coma, or death. A person with a diffuse axonal injury could present a variety of functional impairments depending on where the shearing (tears) occurred in the brain. INTRACRANIAL HEMORRHAGE Intracranial hematomas are collections of blood that develop within the cranial vault. Three kinds: epidural, subdural & intracerebral TYPES OF CEREBRAL HEMORRHAGE  Epidural Meninges Hematoma: Scalp mostly Skull arterial Dura matter (blood Arachnoid collects b/t Pia the skull & Brain tissue the dura grey mater of the white brain)  Subdural hemorrhage - usually Scalp venous (blood Skull collects b/t the Dura matter dura & the arachnoid mater). May be classified as acute, subacute or chronic. ACUTE & SUBACUTE SUBDURAL HEMATOMA Usually result from brain or blood vessel laceration Symptomatic within 24 to 48 hours of injury Symptoms include loss or variable levels of consciousness, headache, irritability, increasing signs of increased ICP (increased BP, decreased pulse, slowing respiratory rates) Requires prompt treatment! INTRACEREBRAL HEMATOMA BLEEDING DIRECTLY INTO THE BRAIN TISSUE. POST HEAD INJURY Observe for 24 hrs Take to emergency if any of following:: decreasing LOC (confusion, drowsy) loss of consciousness/inability to wake vomiting convulsions bleeding or drainage from ears/nose weakness or loss of sensation in arm or leg blurring of vision/slurring of speech changes in pupil MEDICAL MANAGEMENT Prompt recognition and treatment of hypoxia & acid-base disorders (why?) Control of increasing ICP resulting from increased cerebral edema and expanding hematoma Surgical treatment Burr holes Craniotomy BURR HOLES CRANIOTOMY (PRE) CRANIOTOMY CRANIOTOMY NURSING MANAGEMENT  NURSING MANAGEMENT Maintaining airway Monitoring fluid and electrolyte balance Promoting adequate nutrition Preventing injury Maintaining body temperature Maintaining skin integrity Improving cognitive circulation Preventing sleep pattern disturbance Supporting family coping Monitoring/managing potential complications NURSING CARE AFTER CRANIOTOMY Ineffective cerebral tissue perfusion r/t cerebral edema PC: Ineffective thermoregulation r/t damage to the hypothalamus, dehydration, and infection. Disturbed sensory perception r/t periorbital edema, head dressing, e/t tube, & effects of ICP Body image disturbance r/t change in appearance or physical disabilities.