2020-Nurs420 critical care Neurological Assessment and Disorders lecture notes PDF

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Neurological Assessment and Disorders

Fundamentals  Cerebral Circulation o Sufficient blood supply needed o Carotid and Vertebral Arteries  Brain Metabolism o Large amounts of energy needed o Role of glucose

Munro-Kellie Hypothesis  Rigid, limited space (closed vault)  Contents: Brain (80%), Cerebral Blood Volume (10%), CSF (10%)  If volume increases in one compartment, then one or both of the others must decrease- comply

Brain Herniation Fundamentals  Cerebral Blood Flow

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o Without adequate blood flow we have loss of membrane integrityèECF into cellècellular edema Autoregulation o Ability of cerebral vessels to adjust diameter to pressure changes in the brain.  Role of PCO2 and PaO2

Autoregulation  Autoregulation – the brain’s ability to change the diameter of its blood vessels automatically for maintenance of constant cerebral blood flow  Cushing’s response – the brain’s attempt to restore blood flow by increasing arterial pressure to overcome increased intracranial pressure Decompensation Phase  Exhibit changes in mental status & V/S – Cushing’s triad: something has to be done now!!! o Bradycardia o Widening pulse pressure/hypertension o Respiratory changes – decrease before complete apnea  Herniation of brain stem + occlusion of cerebral blood flow = cerebral ischemia & infarction = leading to brain death Fundamentals  Cerebral Perfusion Pressure CPP

CPP= MAP – ICP    

Pressure required to perfuse the brain at least 80 mmHg Normal is (70), 80-100 mmHg ICP – 0-15, cut off is 20, above 20 = intervene now MAP – 70 -100, 65 for vital organs

Focused Assessment – q 1 hour  Critical Care Nurse Neurological Assessment o Glasgow Coma Scale / LOC  Lowest category is 3, never below 3 o Pupillary Responses o Motor Function o Vital Signs o Reflexes o Brainstem function if appropriate o Sensory

pupillary response – consistency in the report you give ppl Classification of Abnormal Motor Function  Spontaneous

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o Occurs without regard to external stimuli and may not occur by request Localization o Occurs when the extremity opposite the extremity receiving pain crosses midline of the body in an attempt to remove the noxious stimulus from the affected limb Withdrawal o Occurs when the extremity receiving the painful stimulus flexes normally in an attempt to avoid the noxious stimulus Decortication o Abnormal flexion response that may occur spontaneously or in response to noxious stimuli (Figure 17-1, A and C ) Decerebration o Abnormal extension response that may occur spontaneously or in response to noxious stimuli (Figure 17-1, B and C ) Flaccid o No response to painful stimuli

Protective Reflexes Protective reflexes indicating brainstem function 1. Cornealblink 2. Gag reflex  suction far back enough 3. Swallowing reflex 4. Cough reflex Oculocephalic Reflex  Dolls eyes: The eyes move in the opposite direction you turn the head.  Awake person – dolls eyes reflex not present  Comatose person- this reflex IS normal  Absent dolls eyes reflex in a comatose patient is BAD. Indicates brainstem dysfunction. Damage in pons &/or medulla.  Would not test on pt with a C-spine injury Oculovestibular Reflex  Cold caloric  Iced caloric  Normal – Pt will look toward the ear injected, and be like that hurts  Absent reflex – BAD sign, usually a lesion in the pons or medulla  Abnormal – look away or opposite, if patient partially awake.

Intracranial Pressure    

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Monroe Kelly Hypothesis/Doctrine Brain is a closed vault Contents: Brain (80%), Cerebral Blood Volume (10%), CSF (10%) Monroe-Kellie Hypothesis - ↑ in any of the cranial vault components causes a change in the volume of the others by displacing or shifting CSF, ↑ CSF absorption or ↓ blood volume Combination of the 3 compartment volumes Measured via the CSF – pressure exerted by the CSF within the ventricles of the brain – catheter in ventricles, placed in OR or bedside Normal 0 – 15mm Hg Dynamic/fluctuates ICP greater than 20mmHg for more than 5 minutes – bc the ICP fluctuates Flattened ICP waveform = elevated ICP

Reduced cerebral blood flow results in ischemia Complete ischemia for > 3-5 mins. results in irreversible brain damage CO2 concentration regulates cerebral blood flow – rise causes dilation whereas a fall cause vasoconstriction – want to maintain regular co2 level Cerebral edema occurs when there is ↑ in “water” content of the brain tissue

Indications and Contraindications for ICP Monitoring  Possible Indications o Trauma, TBI (traumatic brain injury) o Stroke o Brain tumor o Post-cardiac arrest o Craniotomy o Coma o Subarachnoid Hemorrhage o Systemic infarction o Hydrocephalus  Contraindications o Coagulopathy o Systemic infection o CNS infection o Infection at the site of device insertion

Types of ICP Monitoring Systems  Intraventricular (ventriculostomy) – most common one, monitor and provide drainage for ICP  Subarachnoid  Epidural/subdural  Fiberoptic transducer tipped catheter ICP Monitoring Sites  Subarachoid bulb – measures ICP from outside the brain, not as accurate  Intraventricular – inside the ventricles, very accurate ICP measurements, monitor and drain ICP, not all pt can get this bc the brain can be so swollen the ventricle on CT scan disappears they don’t have a landmark  Intrparenchymal – great option in place of intraventricular if the brain is swollen, goes straight to the brain tissue  Epidural – for epidural bleeds, not as good of the reading Normal ICP Waveform  P1 = percussion wave (originating from the pulsations of the choroid plexus)  P2 = tidal wave (most directly linked to the stated of decreased compliance)  P3 = dicrotic wave (pressure usually tapers down to the diastolic position)

Ventriculostomy

Zero at Level of Tragus of the Ear, HOB 30!!

zero, adjust height, Zero the ICP transducer  Then return drainage buretrol to the ordered number of cm of pressure – empty hourly  Remember this is a gravity driven drainage system – so don’t leave it at 0

external drainage setup

Nursing Measures for ICP Monitoring  Sedation/analgesia  Neuro assessments (hourly & PRN)  VS/Temperature – want normal to low temp, very closely monitor temp with VS  Monitor drainage  Monitor ICP/CPP  Monitor Waveforms  Strict aseptic technique  Know how high to have drainage system – has to be an order in for that (normal 10-15)  Monitoring system/tubing  Drain CSF as ordered  Monitor insertion site  Level/zero – tragus of the ear  Notify physician when appropriate  Medications  Labs: Na+ and serum osmolality levels, coags – might give FFP to let then still have ICP monitoring Nursing Care of Patients Receiving ICP Monitoring  Diligent nursing monitoring  Prevent complications  Maintain integrity of system  Drain CSF appropriately – open vs. closed system o Open – pt waiting for organ donation or if ICP is still really high after everything DOC might just tell u to leave open o Closed – during turns and repositioning  Troubleshoot  Gather, document, report accurate data Brain Tissue Oxygen Pressure – NOT ON EXAM  PbtO2> 20 mmg Hg- Licox

Causes of Increased ICP  Increased Brain Volume: o Cerebral edema, mass  Increased Cerebrospinal Fluid (CSF): o Hydrocephalus  Increased CBF: o Impaired autoregulation o Hypoxemia/hypercapnia o Hyperthermia – want normal to low temp o Clustering of nursing activities  Physical activity  Pain/noxious stimuli  Seizures – increase ICP  Increased intrathoracic pressure  Increased intraabdominal pressure Assessment and Diagnosis of Intracranial - Hypertension  Assessment Techniques o Early Symptoms – diligent neuro checks!!  Decreased LOC (earliest)  Vomiting/headache – that wakes u up from sleep  Late signs  Decreased pupil reaction to light and unequal pupil size  Cushing’s triad (herniation) o Systolic Hypertension o Bradycardia o Bradypnea  Diminished brainstem reflexes  Abnormal flexion (decorticate posturing)  Abnormal extension (decerebrate posturing)  Change in respiratory patterns Nursing Measures – Aimed at Decreasing/Managing ICP • Calm, quiet, dark room (low stim) • Proper patient positioning, HOB 30° - make sure they family knows as well • Sedation – Propofol • Osmotherapy – Mannitol • CSF Drainage – open vs. closed • Hyperventilation (no longer recommended) • Barbituate Therapy –Pentobarb coma, maybe • Maintain CPP • Hypertonic Saline (3%) IV via central line Management of Intracranial Hypertension  Cerebrospinal fluid drainage o Ventriculostomy/VP Shunt  Pliable catheter into anterior horn of lateral ventricle

o CSF drainage o Monitoring device for ICP o Treatment to lower ICP o Aseptic technique  Maximize CPP o Diuretics and Volume Maintenance  Osmotic diuretics  Mannitol  Non-osmotic diuretics  Furosemide (Lasix) o Serum osmolality 300 to 320 mOsm/L o Fluid volume maintenance (limited) o Sodium want a little higher – 145-155 Control of Metabolic Demand • Maximize CPP – Noxious Stimuli • Reduce noxious stimuli/pain/pressure • Reduce metabolic demand • Patient care activities (cluster care) – as tolerated – Sedation and Pain Control • Benzodiazepines (alters neuro exam) – short acting • Propofol – drip pt is on when sedated • Narcotics – manage pain • Neuromuscular blockade (NMB) (maybe) • Barbiturate therapy Collaborative Management for Intracranial Hypertension  Therapy aimed at reducing volume of one or more of the components  Head elevation positioning -now it is individualized to minimize ICP and maximize MAP o (use to be 30 degrees) – head is midline, no pillow = skin breakdown  Avoid positions that decrease venous return from the brain  Keep PEEP less than 20 cm H2O  Coughing/suctioning – allow adequate rest time inbetween  Trach ties—not too tight!!!! – tight obstruct venous outflow  Hyperventilation – keep CO2 low normal now (hypervent-no longer recommended)  Temperature control; normothermic – cerebral metabolic rate  BP control o MAP usually between 70-90 mm Hg to achieve needed CPP o How to treat hypo or hypertension?  Seizure Control o Anticonvulsants prophylactically o Seizures increase metabolic requirements – may have ischemia  Dilantin (phenytoin); Kepra  Ativan A word about CO2  Davis et al (2006) determined that patients that were hypercarbic or hypocarbic had WORSE outcomes  Postulated low pCO2=vasoconstriction=cerebral ischemia  High pCO2=vasodilation=increased ICP  Improved survival occurred when pCO2 was between 30 & 49 and SpO2 was greater than 95%

Herniation Syndromes • Goal of neurologic evaluation, ICP monitoring, and treatment of increased ICP is to prevent herniation. • Herniation of intracerebral contents results in: – Shifting of tissue from one compartment of the brain to another. – Places pressure on cerebral vessels and vital centers of the brain. • Herniation rapidly causes death as a result of cessation of cerebral blood flow. Causes of Increased ICP – Traumatic Brain Injury (TBI)  Mild Injury GCS  13-15  Moderate Injury GCS  9-12  Severe Injury GCS  less than 8 – intubate!!! Missile Injuries  Bullet wounds of the head. Bullet wound or other penetrating missile wounds cause an open (compound) skull fracture and damage to brain tissue.  Shock wave effects are transmitted throughout the brain.  A, Perforating injury. – exit wound much bigger than the entrance wound  B, Penetrating injury – sometimes they would just leave it in Types of Cerebral Hematomas  A, Subdural hematoma.  B, Epidural hematoma.  C, Intracerebral hematoma Subdural  usually a venous bleed, slow onset – can develop s/s a whole week later

Epidural  Arterial Bleed-fast decompensation (middle meningeal artery), can be venous-slower onset of symptoms  Hit their head, loss consciousness, wake up and be fine and then suddenly die

Coup-Countercoup Mechanism of Injury  Coup and contrecoup head injury after blunt trauma.  A, Coup injury: impact against object. a, Site of impact and direct trauma to brain; b, shearing of subdural veins; c, trauma to base of brain.  B, Countercoup injury: impact within skull. a, Site of impact from brain hitting opposite side of skull; b, shearing forces throughout brain.  These injuries occur in one continuous motion—the head strikes the wall (coup), then rebounds (countercoup).  Mechanism of injury – be concerned about how they are injuried Diffuse Axonal Injury-Shear  No way to fixed it  Diffused injury  A – the bleed can be removed  B – the bleed is everywhere, there is no way to evaluate the bleed, catoptric

Assessment of the Patient with a TBI  GCS  Pupillary response  Motor function  Vital signs  Reflexes/Pain  Brainstem function if required  Respiratory

Diagnostics  CT – fast and the go to  MRI/MRA  Transcranial Doppler  EEG  Angiography Vital Signs  Hyperdynamic State o Increased BP, HR, CO o What happens to autoregulation? o What does this do to the ICP? o What about the RR and pattern? o Cushing’s Triad – elevated BP, bradycardia, irregular respirations Medical Management of TBI  Surgical management – if it can be removed  Nonsurgical management – supportive care, stabilize pt as much as possible  Seizure control  Nursing priorities in management of TBI focus on: o Stabilizing vital signs o Preventing further injury o Reducing increases in ICP and maintaining adequate cerebral perfusion pressure o Always be ready to travel to CT or OR emergently.  Management of secondary injuries  Brain trauma foundation protocol o Early intubation 145 mEq/L o High Urine Output  Syndrome of Inappropriate Antidiuretic Hormone (SIADH) o Producing too much ADH – holding on to too much fluid o SIADH is LOW o Na...