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Neurological Stressors I-IV

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Presentation on theme: "Neurological Stressors I-IV"— Presentation transcript:

1 Neurological Stressors I-IV
NUR240 Joy Borrero, RN, MSN

2 Assessment Family history and genetic risk Personal history
Level of consciousness and orientation Memory: remote or long term, recall, immediate Attention Language and copying

3 Assessment Cognition Cranial nerves Sensory function
Pain and temperature Touch Abnormal sensory findings

4 Assessment of Motor Function
Muscle strength Cerebral or brainstem integrity Abnormal motor findings

5 Assessment of Cerebellar Function
Coordination Gait and equilibrium

6 Rapid Neurologic Assessment
Glasgow Coma Scale Response to painful stimuli Level of consciousness Decortication Decerebration Pupil assessment

7 Laboratory Tests Blood cultures necessary Skull and spine x-ray tests
Cerebral angiography CT scan: possible use of contrast medium, assess for allergic response, fluids Positron emission tomography

8 Lumbar Puncture Insertion of spinal needle into the subarachnoid space (between the third and fourth lumbar vertebrae) Contraindicated in clients with increased intracranial pressure Empty bladder Position Spinal headache possible from spinal tap Sentence and phrases

9 Electroencephalography (EEG)
Graphically records the electrical activity of the cerebral hemispheres Sleep deprivation requirement Anticonvulsants possibly withheld S&P

10 Neurological Assessment of Intracranial Pressure
Normal ICP= <15mm Hg Increased intracranial pressure: Causes and mechanisms: Increases in intracranial blood volume Increases in cerebral spinal fluid volume (CSF) Increases in the bulk of brain tissue-swelling

11 ICP Signs & symptoms of increased ICP Changes in LOC Visual Motor
Headache Vomiting Restlessness

12 ICP Cushing’s triad: Increased MAP (D +1/3 S-D)
Increased pulse pressure (normally 40-50) Bradycardia

13 Causes of Increased ICP
Increase in blood volume Blood clot, edema, increased cerebral blood flow Increased BP, PaCO2 Decreased PaO2 Vasodilitation- NTG, Nitroprusside Increased intrathoracic pressure Impairment of Cerebral Venous return Increased intrathoracic pressure- coughing, straining, suctioning, PEEP Impaired cerebral venous return- supine, head low, twisted neck

14 Compensatory Mechanism for Increased ICP
Displacement and reduction of volume of CSF- increased absorption by arachnoid villi Reduction of volume of blood by vasoconstriction Displacement of the tissues of the brain

15 Increased ICP Treat pain, restrict fluid Monitor patient
Cluster nursing care to promote rest Moderate increase in ICP (20-30): Hyperventilate, maintain pCO Sedate, neuro checks. Severe Increase in ICP over 40: Constant hyperventilation, mannitol, barbituate coma (peds). Family teaching- child head injury- wake baby q4 Older fruit juice etc. Call MD if hard to arouse, return to ER, vomiting 8h after hit head, irritable, having convulsions. Goals of nsg intervention are: To protect brain from further injury, therefore the cause of change in mental status has to be assessed quickly. Stabilize VS. Keep pt. free from physical injury Support patient and family.

16 ICP Monitoring Facilitates continual assessment of ICP and is more precise than relying on vague parameters Devices include the intraventicular catheter, subarachnoid screw or bolt and epidural monitor. ICP levels should be <15mm Hg Assess client frequently for increasing ICP Assess device insertion site for s/s infection

17 Management of Patients with Increased ICP
Altered Cerebral Tissue Perfusion: Decrease brain edema- osmotic diuretics, Lasix, Steroids Control Temp Lower CSF volume- venticulostomy drain Positioning- avoid Trendelenberg and extreme hip flexion

18 Management of Patients with Increased ICP
5. Decrease blood volume Hyperventilation leads to resp alkalosis-vasoconstriction 6. Reduce cellular metabolic demands- Barbituates/ Barbituate Coma 7. Nursing implications of ICP monitoring

19 Neurosurgery-Craniotomy
Indications Surgical Approaches: 1. Supratentorial 2. Infratentorial 3. Transphenoidal 4. Burr holes

20 Pre-op Craniotomy Anticonvulsants I & O, foley Head shave prior to sx
Bowel prep only as ordered Explain procedure and ICU course Antiembolism stockings No narcotics or hypnotics

21 Post-op Craniotomy Adequate respiratory ventilation
Arterial pressure monitoring Evaluate for cerebral edema and increasing ICP Temp control Medicate for HA and anticonvulsant meds: Dilantin (phenytoin) and Valium (diazepam) Prevent aspiration Prevent complications Evaluate dsg for bleeding or leakage of CSF Stool softeners

22 Intervention Don’ts: Suction nose Lower HOB Restrain Take rectal temp
Heavily sedate patient Administer narcotics unless Double Checked

23 Post-op Transphenoidal Approach
PC Hemorrhage: Check nasal packing and frequent swallowing Risk for infection- antimicrobials Pain analgesics Steroids Assess visual acuity Oral care q4h HOB up, do not blow nose, bend or strain Monitor for CSF leakage, postop meningitis, SIADH Vaporizer and HOB up for 2 weeks postop Visual acuity- Close proximity of optic chiasm

24 Head Injury- Skull fracture
Assessment Fracture of the base of the skull nose- cerebrospinal fluid-rhinorrhea ears- cerebrospinal fluid-otorrhea Ecchymosis or bruising seen over the mastoid ( Battle’s sign) Bloody spinal fluid

25 Traumatic Brain Injury
Result of an external force applied to the head and brain causing disruption of physiologic stability Diffuse axonal injury (shearing injuries) locally, at the point of injury, as well as globally with elevations in ICP and potentially dramatic changes in blood flow within and to the brain

26 Primary Brain Injury Open head injury occurs when there is a skull fracture or when the skull is pierced by a penetrating object; the integrity of the brain and the dura is violated and exposure to outside contaminants occurs. Closed head injury is the result of blunt trauma; the integrity of the skull is not violated. Physical force of either an open or closed trauma Open- depressed fracture, open fracture, penetrating wounds, gun shot Closed- blunt trauma

27 Open Head Injury (Continued)
Comminuted fracture: involves fragmentation of the bone, with depression of bone into brain tissue Open fracture: scalp is lacerated, creating a direct opening to brain tissue

28 Basilar Skull Fracture
Occurs at the base of the skull Usually extends into the anterior, middle, or posterior fossa and results in cerebrospinal fluid leakage from the nose or ears Potential for hemorrhage, damage to cranial nerves, and infection

29 Types of Closed Head Injuries TBI- Traumatic Brain Injury
Mild concussion-transient disorder with momentary LOC followed by complete recovery Contusion (coup and contrecoup injury)- bruising without tearing of vessels, results of brain hitting the skull Laceration Head movement during acceleration- deceleration injury typically seen in MVA Coup- site of impact to frontal area of brain and contercoup injury to frontal and temporal areas of brain Concussion- Home Care- observe for HA, dizziness, irritablity, insomnia, impaired memory and concentration-return to ER

30 Head trauma Concussion- jostling brain Contusion= bruising
Increased intracranial pressure- change in LOC first seen, lethargy, slowed speech, delayed responses, later change in VS Establish airway, hyperoxygenate. Proper positioning, HOB 30 degrees. Minimal noise and stimulation Concussion- most common brief reversible, no long term effects. Concussion with or without post traumatic seizures. There may or may not be brief LOC, no structural injury seen on CT or MR. After concussion- memory loss, headache, visual disturbances, irritable, slowed responses. Contusion= bruising, rapid acceleration/deceleration coup/contracoup injury- car accident, shaken baby syndrome Trauma can be the result of injury to the scalp, skull, or brain tissue. The skull is a fixed compartment. Within the skull is brain tissue (80%), blood (10%) and CSF (10%). Skull fractures – surgery neede if fracture is deeper then thickness of skull. Basilar skull fracture – High speed impact- blood in external auditory canal or behind tympanic membrane. CSF draining from ear or nose (test for glucose). Bruise on mastoid bone behind ear (Battle’ssign). Periorbital discoloration racoon eyes. Within 1 hour- post traumatic seizure. Vs in ICP- increase in systolic BP- widening pulse pressure, to increase blood flow to brain. Increased ICP any increase in ICP affects cerebral perfusion may lead to ischemia and eventual permanent brain damage and death.

31 Types of Force Acceleration injury is caused by an external force contacting the head, suddenly placing the head in motion. Deceleration injury occurs when the moving head is suddenly stopped or hits a stationary object.

32 Brain Injury Complications
Increased ICP Hemorrhage Epidural hematoma Subdural hematoma Intracerebral hemorrhage Loss of autoregulation Hydrocephalus Herniation

33 Epidural Hematoma Occurs between the skull and the dura
Generally an arterial bleed Classic picture- pt unconscious immediately after head trauma, awakens lucid and then lapses into coma Goal is to relieve pressure and decrease ICP

34 Subdural Hematoma Collection of blood between dura(outer meninges and arachnoid (middle layer meninges) Generally venous Acute- occurs within 24 hrs of injury Subacute- symptomatic 2-14 days later Chronic- weeks to months later S&S depends on size of vessel involved and amount of bleeding Management: Burr holes and craniotomy to remove clot As blood organizes into a clot the blood cells within the clot membrane lyse forming a fluid of high osmotic pressure. Water from surrounding subarachnoid space is drawn into clot producing an increasing mass-lead to cerebral herniation and death

35 Subarachnoid Hemorrhage (SAH)
Bleeding into the subarachnoid space Most common cause is rupture of aneurysm Berry aneurysm- congenitally associated with smoking, ¼ die before reaching ER More common in females + Kernig’s sign + Brudzinski reflex Kernig- nurse flexes leg at the hip and brings the knee to 90 degree angle and then attempts to extend the knee Brudzinski- flex the head and hips and knees

36 SAH Clinical Manifestations
Change in LOC Sudden severe HA Photophobia Nuchal rigidity Low back pain N & V Fever, elevate dWBCs Cranial nerve deficits Motor weakness EKG changes-bradycardia, AV block, PVCs

37 SAH TREATMENT Surgery- metal clip for aneurysms Amicar
Antifibrinolytics- controversial Nimodipine (Nimtop)- to reduce risk of vasospasm Phenytoin (Dilantin)- to tx seizures

38 Intracerebral Hemorrhage
Bleeding directly into brain tissue CAUSES ARE SIMILAR TO SUB/EPIDURAL HEMATOMA Tx- surgical- high mortality Head trauma that compromises the function of the pituitary gland may lead to DI and SIADH

39 Head Trauma Factors that predict a poor outcome:
The presence of an intracranial hematoma Increasing age of the patient Impaired or absent eye movements or pupil light reflexes Abnormal motor responses Early sustained hypotension Hypoxemia or hypercapnia ICP greater that 20mm Hg

40 Clinical Care following a Head Injury
Airway Establish baseline data Prevent aspiration Cardiovascular complications Skull and scalp injuries Infection prevention Prevention of straining Maintain normothermia

41 Clinical Care following a Head Injury
Fluid and electolyte, acid-base maintenance Monitor restlessness, pain and disorientation Pain management with mild analgesics Assess for seizures Positioning in bed to prevent stasis Stress ulcers Rest- prevent complications of inactivity Space activities to prevent increase in ICP

42 Tumors of the Nervous System
All intracranial tumors can be fatal, no room for expansion Classification: A. Intracranial tumors: Primary Metastatic Granulomas B. Spinal tumors C. Tumors of the peripheral nerves Granulomas- granulation tissue production in response to chronic infection, inflammation, foreign body or to unknown cause

43 Types of Intracranial Tumors
Gliomas Neuromas Meningiomas Various blood vewssel tumors Developmental tumors Miscellaneous

44 General Symptoms of Intracranial Tumors
Caused by generalized disturbances of cerebral function HA N&V-no relation to meals Papilledema Seizures Dizziness and vertigo Changes in mental status

45 Management of Brain Tumors
Surgical excision Brain mapping with steriotatic approach Brachytherapy Gamma knife for radiosurgery Radiation Chemotherapy Mannitol to allow more chemotherapy across blood brain barrier Thalidomide- decrease vascular supply Growth Factor inhibitor tx- shrink tumor size Decrease ICP Assess for seizure activity and early signs of motor function impairment Steriotatic approach- allows for precise location of tumor

46 Intracranial Aneurysms
Berry aneurysm is most common congenital aneurysm Aneurysms result from: - a congenital defect in the middle layer of the vessel wall - degenerative changes in the vessel wall at the same site - constant stress caused by the force of the flow of blood particularly at the bifurcattion

47 Symptoms of Intracranial Aneurysm
Caused by compression of surrounding brain tissue or cranial nerves Usually sudden onset of symptoms Severe HA (occipital) and usually accompanied by vomiting May lose consciousness immediately or initially present with confusion, lethargy Generalized seizures Meningeal irritation, stiff neck and back and leg pain, motor weakness, monoparesis, hemiparesis

48 Management Surgical-evacuation of hemorrhage if life is threatened by increased pressure Medical- antihypertensives antifibrinolytics decrease ICP prophylactic anticonvulsants After an aneurysm ruptures, a clot forms at the site of the hemorrhage and for a few days rebleeding is prevented. As the clot begins to dissolve, the chance of rebleeding increase, with the greatest risk of rebleeding occuring at about the 7th day


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