CCRN-PCCN Certification Review Course: Neuro

CCRN-PCCN Certification Review Course: Neuro

What’s on the Test? CCRN only CCRN and PCCN Neurologic infections
ICP monitoring Neurosurgery Musculoskeletal (immobility/immobility/falls) Brain death Brain tumours Traumatic brain injury CCRN and PCCN Aneurysm, AV Malformation Encephalopathy Intracranial hemorrhage (subarachnoid, epidural, subdural) Seizure disorders Stroke Stroke includes Ischemic (embolic), hemorrhagic, transient ischemic attack, (TIA)

What’s on the Test? Neuro is combined with musculoskeletal and psychosocial to make up 13% of the CCRN exam Neuro is combined with Multisystem and Behavioral to make up 15% of the PCCN exam Note for PCCN candidates This presentation includes discussions of advanced devices such at ICP monitoring and administration of vasoactive medications These topics will not be tested in the PCCN exam Note that the exam items for the PCCN begin on June 26, 2013

Intracranial Hypertension
Terminology Intracranial Pressure (ICP): Pressure normally exerted by CSF Obtained via direct measurement with intracranial monitor (bolt, ventriculostomy) NL: 0-15 mmHg Cerebral Perfusion Pressure (CPP) Blood pressure gradient across the brain CPP = MAP – ICP NL: > 60 mm Hg CPP – won’t have math on the exam. CPP of more concern than ICP (it’s all about adequate tissue perfusion in all systems). However, you need ICP to calculate CP

Monro-Kellie Doctrine
If there is an increase in the volume of one of the components, it must be offset by an equal decrease of one or both of the other components in order for the ICP to remain normal If an increase in the volume of one of the components is not offset by an equal decrease in one or both of the other components, the ICP will increase Information only. Will need to understand physiology for the exam, but won’t be tested on it directly. Basically, because the skull is a rigid box, volume is finite.

Components Brain = 80% Blood = 10% CSF = 10%
Normal percentage of each component. If brain swells, it will take up more room. In order to prevent an increase in ICP, one or both of the other components will have to decrease.

Compensatory Mechanisms
CSF displaced into spinal cistern (lumbar area of spine) and increasing CSF absorption Blood displaced into venous sinuses 90% Example: brain volume is increased to 90%, due to swelling, tumor, etc. To compensate, CSF is either displaced or decreased through a decrease in production or increase in absorption. Blood is displaced into the venous system

Volume/Pressure Curve
Flat portion: increases in volume are compensated Small increases in volume cause sharp increase in pressure when compensatory mechanisms are exceeded Until the compensation is at its maximum, small increased in volume will not result in an increase in ICP. Once the compensatory mechanisms are exhausted, very small increases in volume result in dramatic increases in ICP

Herniation Syndromes Cingulate Uncal Central Tonsillar
When the pressure becomes too great, either from increased volume of brain tissue, blockage in drainage of CSF (as in hydrocephalus), or increases in blood volume (such as ruptured aneurysm or trauma), the volume needs to move out through openings. Cingulate (1) Shift of brain tissue of one cerebral hemisphere under the falx cerebri to the other cerebral hemisphere Uncal (2) Lesion above tentorium forces uncus of temporal lobe to displace through the tentorial notch. Central (3) Downward shift of cerebral hemispheres, basal ganglia, and diencephalon through the tentorial notch Tonsillar (4) Cerebellar tonsils displaced through the foramen magnum

Causes of Increased ICP
Space occupying lesions Subdural, epidural, intracerebral hematomas Abscesses Tumors Cytotoxic edema Intracellular swelling Cellular hypoxia Acute hypo-osmolality Water intoxication (SIADH) Cytotoxic edema: due to failure of sodium and calcium pumps. Results in cellular retention of sodium and water. Seen with various intoxications and early ischemia.

Causes of Increased ICP
Vasogenic cerebral edema Direct injury Hypoxic injury Severe hypertension Inflammatory mediators May see with contusions, tumors, abscesses, meningitis, diffuse brain injury Normal processes that maintian an adequate blood-brain barrier fail. As a result, normally excluded intravascular proteins and fluid penetrate into cerebral parenchymal extracellular space. Occurs fast and is widespread. Seen in response to hemorrhagic contusion in cases of trauma, bleed, venous infarcts, late stages of cerebral ischemia where an associated hemorrhagic transformation occurs, tumors, focal inflammation, acute hypertensive encephalopathy. Image gallery:

Assessment of Increased ICP: LOC
Awareness of self and environment General behavior Appearance Appropriateness to the situation Attention span Long and short term memory, insight, orientation and calculation No additional information needed.

Emotional state, affect Thought content Illusions, hallucinations, delusions Execution of intentional motor activity Inability = apraxia Recognition and interpretation of sensations Apraxia = neurogenic impairment involving planning, executing, and sequencing motor movements

Language Fluency, clarity, content, comprehension of written and spoken word Ability to name objects and repeat phrases Patient awareness of language disorder Receptive aphasia Expressive aphasia Receptive & expressive aphasia described on next two slides

Receptive aphasia (Wernicke’s aphasia) Comprehension of speech impaired Able to make words, but will be nonsensical, rambling Unable to identify written words Damage to the temporal lobe

Expressive aphasia (Broca’s aphasia) Deficit in language output or speech production May be mild if due to weakness or lack of coordination of muscles of speech (dysarthria) Incorrect intonation or phrasing Most severe – inability to communicate thorough verbal and written means or gesturing Damage to the frontal lobe

Assessment: Muscle Strength
Able to follow commands Grade on 0-5 scale 0 = Absent, no muscle contraction 1 = Contraction of muscles felt or seen 2 = Movement through full range of motion with gravity removed 3 = Movement through full range of motion against gravity 4 = Movement against resistance but can be overcome 5 = Full strength against resistance As described

Unable to follow commands Observe which extremities move spontaneously or to noxious stimuli Hemiparesis or hemiplegia may be detect by lifting both arms off bed and releasing simultaneously Limb on hemiparetic side will fall more quickly and more limply

Pathologic movements: Primitive Grasp – in response to stimulation of palm Sucking – In response to lip stimulation Rooting – Mouth opens, head deviates toward a stimulus to lower lip or cheek These movements may occur in even severly damages patients. Most basic movements

Pathologic movements - Babinski Stroking the lateral sole of foot from heel up and across ball of foot Causes abnormal dorsiflexion of the great toe and extensor fanning of the other toes Normal Abnormal

Assessment: Pupil Abnormalities
Indicates area of brain affected Small, equal, reactive Nonreactive, midpositional Fixed and dilated Bilateral fixed and dilated Pinpoint, nonreactive One pupil smaller than other, both reactive

Assessment: Vital Signs
Temperature – neurogenic fever can be caused by damage to hypothalamus Respiratory patterns - Indicate area of brain affected Apneustic Cluster Ataxic Cheyne-Stokes Central neurogenic hyperventilation Cheyne-Stokes – regular cycles of respiration that gradually increase in depth to and then decrease to periods of apnea Central neurogenic hyperventilation – Deep, rapid respirations Apneustic – Prolonged inspiration followed by 2 to 3 second pause Cluster of irregular breaths followed by apneic period lasting a variable amount of time Ataxic – Irregular, unpredictable pattern of shallow and deep respirations and pauses

Assessment: Vital Signs
Pulse and blood pressure Not reliable Changes usually a late indication Cushing’s Triad Cushing’s described on next slide

Cushing’s Triad Compensatory response that attempts to provide adequate CPP in the presence of rising ICP Bradycardia, systolic hypertension, bradypnea Late and poor prognostic sign Systolic hypertension: systolic BP elevated; diastolic normal or low. Created a widened pulse pressure (SBP-DBP)

Glascow Coma Scale Total score ranges 3-15
As Cindy Blank-Reid says – patient gets 3 points just for being there. Humor: neuro doctor can tell you’re a novice if you say a brain-dead patient has a GCS of 0. Abnormal flexion = decorticate posturing Extension posturing = decerebrate posturing – more severe, but both are very bad

Posturing Decorticate Decerebrate
Decorticate – arms turned into the “core.” Decerebrate – arms at side, hands turned outward

Early Signs and Symptoms
Deterioration in LOC Visual changes Motor weakness Sensory deficits Headache Early visual changes = Blurred vision, diplopia (double vision)

Late Signs and Symptoms
Progressive deterioration in LOC Vomiting Pupillary changes Posturing Changes in vital signs (Cushing’s Syndrome) Impaired brain stem reflexes Late pupillary changes = Nonreactive, midpositional Fixed and dilated Bilateral fixed and dilated Pinpoint, nonreactive One pupil smaller than other As previously stated Brain stem reflexes – involuntary responses to stimuli mediated by the brainstem. Assessed with tests such as doll’s eye movement (turn head to one side, eyes stay straight ahead; should track opposite of turn), cold calorics (pour cold water into ear, look for movement of eyes; if none, evidence of brain death) , babinski (previously described) and eliciting cough when suctioning..

ICP Monitoring Epidural Subdural Subarachnoid Intraparenchymal
Intraventricular Epidural: Sensor placed in epidural space; Least invasive; Quick and easy to insert; Does not allow CSF drainage; Waveform accuracy and reliability poor Not commonly used Subdural: Catheter or probe placed in subdural space; Easy to insert; Less brain penetration; Does not allow CSF drainage; Waveform poor; Swollen brain may compress; Accuracy and reliability decreases over time Subarachnoid: Tip of a hollow bolt is placed into the subarachnoid space; Quick, easy to insert; Less brain penetration; Does not allow CSF drainage; Waveform fair; May cause CSF leak from insertion site; Easily occluded with blood clot, brain tissue, bone fragment, Intraparenchyma: Probe placed into brain tissue; Quick and easy to place; Few complications; Good waveform; Accurate and reliable; Does not allow CSF drainage; Some risk of infection Intraventricular: Cannula inserted through scalp, skull, meninges, and brain; tissue into the lateral ventricle; usually anterior horn of nondominant hemisphere; Accurate and reliable; Measures CSF pressure directly; Considered fold standard; Excellent waveform; Allows for therapeutic drainage of CSF and withdrawal of CSF for analysis;

Ventriculostomy Drainage System
Description Drain that is inserted into one of the ventricles of the brain Only can be used with intraventricular catheter Usually non-dominent ventricle Left – end connected to catheter Middle – CSF measured; port for sampling Bag – for output measurement

Uses for Ventriculostomy Drain
Drain CSF to manage ICP Obtain CSF sample for analysis Glucose White cells Protein Bacteria Viral antibodies Physician may order CSF to be drained when ICP reaches a set level; may order specific amount to be drained hourly, or may order drainage bag to be set at a specified level for consistant drainage Glucose decreased in presence of infection White cells present and elevated Protein will be increased

Nursing Care of the Patient with a Ventriculostomy
Document character, amount, and turbidity of drainage Monitor system for air bubbles Drain CSF as indicated for IICP Maintain sterility of system

Interventions for IICP
Goal: Maintain adequate CPP Quiet environment Normothermic/ hypothermic Optimize MAP Medications Surgical interventions Positioning Infection control Avoid increased intrathoracic/intra-abdominal pressure Intervene surgically Discussed in greater detail on following slides

Positioning Facilitate venous return
HOB elevated to level that minimizes ICP Usually 30o Avoid hyperextension, flexion, or rotation of head and neck Trach ties not wrapped tightly around neck Proper fit of cervical collar All of these can increase ICP. Think of patient with head slumped to side as we frequently see. This can increase ICP in a patient with an ICP problem.

Positioning Avoid sharp hip flexion
Ensure proper placement of external transducer and intraventricular catheter drainage chamber after position change Sharp hip flexion transfers increased pressure to cerebral arteries ICP measurement may be inaccurate if placement has been changed

Infection Control Strict sterile technique during monitor insertion and when accessing intraventricular catheter system Connections snug Dressing dry and intact As described. No further discussion needed

Avoid Increased Intrathoracic/Intra-Abdominal Pressure
Coughing Straining Valsalva maneuver Avoid full bladder or bowel Suctioning PEEP Abdominal Compartment Syndrome Increased pressure transferred to cerebral arteries, increasing ICP Suctioning: Limit suction passes to 1-2 times Hyperoxygenate to 100% FiO2 Hyperinflate for four breaths Consider sedation, NMB, lidocaine Midazolam (Versed) or propofol (Diprivan) for sedation Vecuronium (Norcuron) or atacurium (Tracrium) for NMB

Quiet Environment Seizure prevention Barbiturate coma Limit stimuli
Avoid clustering of nursing care Control family/visitor interaction Encourage family/visitor involvement Excess stimulation increases ICP Barbiturate coma only if other interventions unsuccessful Limit stimuli – TV, lights, calling out to colleagues Provide rest between nursing care. Space care out Instruct families to speak in low voices, control emotional outbursts. Describe monitor indications of increased ICP when that happens At the same time, promote family involvement: softly stroking patient, talking to patient in soft, calm manner

Normothermic/ Hypothermic
Avoid fever – increases cerebral metabolism and increased blood flow Antipyretics Cooling devices Mild hypothermia between 320 and 350 Reduces cerebral metabolism As stated

Hyperventilation Elevated CO2 dilates cerebral blood vessels
Lowered CO2 constricts cerebral blood vessels Too low, can decrease CPP Goal: pCO2 ~ 35 mm Hg As stated

Optimize MAP Aggressive volume replacement Vasopressors
NSS, Ringer’s Vasopressors Phenylephrine (Neosynephrine) if fluids not effective Only pressor that crosses blood-brain barrier Vasodilators if pressure too high As stated

Other Medications Mannitol Lasix Steroids
Creates osmotic gradient to pull fluid from brain in presence of cerebral edema Lasix May use alternating with Mannitol Steroids Indicated for edema due to brain tumor Not indicated for TBI or stroke As stated

Surgical Intervention
Evacuation Debulking Lobectomy Trauma flap Evacuation = removal of blood Debulking = decreasing size of mass Lobectomy = removal of lobe in which pathologic condition is occurring Trauma flap = removal of piece of skull to allow for swelling (TV journalist Bob Woodward). Replaced with titanium plate after recovery.

Neuro Trauma Traumatic brain injury (TBI)

Traumatic Brain Injury
Any injury to the scalp, skull, or parenchyma GCS is divided into three categories of severity

Mechanism of Injury Deformation Acceleration-Deceleration Rotational
Deformation = ex: hit with baseball bat Acceleration-deceleration = ex: car accident. Head goes forward and back. Brain hits front and back of skull.. Cous contre cous injury and bruising of brain Rotational = brain twists; May cause tearing of bridging veins

Normal CT Scan of Brain Need to have idea of what normal brain looks like on cat scan to understand injury. Note that hemispheres are divided evenly at midline. Ventricles (dark, crescent shaped areas) are equal and located on either side of midline.

Scalp and Skull Injuries
Scalp injuries “Bark is worse than the bite” Extensive vascularity and poor contractility of vessels Diagnosis made on physical exam Treatment range dependent on severity and mechanism of wound Fractures Observation or Surgery depending on degree of injury Scalp injuries bleed a lot. Usually not serious, but can be fatal from blood loss in instances of “scalping.” Classic example is indian scalping. Those who died were as a result of massive blood loss. Today, seen in machine accidents.

Scalp and Skull Injuries
Example here of hematoma and fractured skull; no apparent injury to brain.

Basilar Skull Fractures
Account for 20% of all fractures Base of skull fracture What is wrong with this picture? (the patient has an NG tube. It should be an OG tube)

This is why you don’t put an NG tube in patients with head injury
This is why you don’t put an NG tube in patients with head injury. If the cribiform plate, which is a fragile bone that separates the nose from the skull, is broken, the NG tube can go into the brain, as shown here.

Basilar Skull Fractures
Specific associated signs Raccoon’s eyes (Anterior fossa) Battle’s sign (Middle and Posterior fossa) Ottorhea Rhinorhea Specific associated signs a. Raccoon’s eyes (Anterior fossa) = ecchymosis around eyes (seen in first picture) b. Battle’s sign (Middle and Posterior fossa) = ecchymosis behind ear c. Ottorhea = CSF coming out of ear d. Rhinorrhea = CSF coming out of nose

Diagnosis and Treatment
CT poor for detecting Plain skull x-rays and clinical criteria more sensitive Treatment of fracture itself not necessary Treatment of potential complications associated with fracture At risk for intracranial hematoma, meningitis CT is not effective for detecting a basilar skull fracture. Plain skull x-rays and clinical criteria are better. The treatment of fracture itself is not necessary, unless it is causing injury to the brain. Treatment of potential complications including hematoma and meningitis

Parenchymal Injuries Concussion Contusion Subdural hematoma
Epidural hematoma Intracerebral hematoma Discussion of each to follow

Concussion Transient, temporary neurogenic dysfunction without parenchymal abnormality Classified as mild or classic Signs and symptoms vary in time and sequelae CT brain recommended Observation Parenchymal = functioning tissue (as opposed to structural tissue, ie, connective tissue) Everybody gets a CT scan Usually on requires observation, including frequent neuro checks (as discussed)

Contusion Bruising of the surface of the brain
Signs and symptoms dependent on size of contusion and associated edema Treatment CT brain Observation Admit Dependent on degree of abnormality May only require observation, rest; with significant neuro symptoms, may require more

Contusion Note small areas of lighter grey (top, left) at arrows

Subdural Hematoma Collection of blood within the subdural space
Usually caused by venous bleeding from tearing of bridging veins Subdural space is beneath the dura mater, where CSF baths the brain. A rotational injury (twisting, see slide no. 46), pulls at the veins that connect to the lining of the brain and the lining of the dura mater (bridging veins), causing the bleed. Subdural hematomas are always venous bleeds. This may very well be a question on the test.

Subdural Hematoma Note that, although the brain itself is not bleeding, the blood accumulating from the subdural bleed is pushing on the brain (white area on left). This causes pressure on the brain, and increases ICP. Note also that the ventricles are no longer equal; in fact, the left ventricle can hardly be seen. If the blood is not evacuated quickly, the patient can develop a brain herniation.

Diagnosis by non-contrast CT of brain Treatment varies depending on size, location and symptoms present Surgery Burr holes Craniotomy Why a non-contrast CT of brain (answer: because the contrast would leak out into the subdural space). If the bleed is small, it will be allowed to be reabsorbed; no surgery or other treatment is necessary. The patient would be closely watched for progression of neuro symptoms. Subsequent CT scans may be ordered to evaluate the bleed. If the bleed is significant, surgery will be done to remove the blood and reduce the pressure on the brain. This can be done by drilling a burr hole and evacuating the blood. It may also be done by performing a craniotomy, where a portion of the skull is removed.

Epidural Hematoma Bleeding into the potential space between the inner periosteum and the dura mater Brief LOC Lucid period followed by rapid neurologic deterioration High index of suspicion following blows to tempoparietal area (middle meningeal artery) Neurosurgical emergency There will definitely be at least one question on epidural hematoma, because of its dramatic and classic presentation. They are most often seen after trauma to the tempoparietal area. The middle meningeal artery is very close to the surface at this point, and can be ruptured by a severe enough blow. The actress Natasha Richards died after sustaining a significant blow to this area while skiing. She presented in the classic manner: she had a brief loss on consciousness, followed by complete lucidity. During her lucid period, she insisted she was fine and went to her room. There, she had a sudden and quick deterioration of her level of consciousness and neuro status. This is a medical emergency and must be treated immediately. Because she was in a location that was not near a hospital equipped to deal with the emergency, she required a helicopter to transport her to a hospital that was prepared for this type of injury. As a result of the time lost before definitive treatment could be provided, Ms. Richards died of a herniation. This the classic pattern of an epidural hematoma: brief LOC, period of lucidity, quick neurologic deterioration. Epidural hematomas are always arterial in nature.

Epidural Hematoma Note the blood pressing in on the left brain (white area). The left ventricle is almost imperceptible.

Diagnosis by non-contrast CT scan Usually emergent surgical intervention is necessary Non contrast CT for same reason as before. Surgical emergency. Best outcome if treated at a hospital that offers high quality neuro care.

Intracerebral Hematoma
Hemorrhage occurs in the parenchyma Signs and symptoms related to mass effect Treatment CT scan Surgical intervention may be necessary Associated with poor outcomes and mortality Because the bleed is in the brain itself, it is difficult to treat without causing more harm to brain tissue. If the bleed is small, symptomatic treatment may be all that’s needed. If bleeding is significant, surgery may be required, but the outcomes have a poor prognosis.

Intracerebral Hematoma
Note the two white areas on the right. These represent an intracerebral hematoma.

Penetrating Injury Missile injuries Impalement injuries
Missile injuries most often are caused by gunshot, but they can also be caused by shrapnel and flying debris. These are very damaging, as the object can traverse a large area. The gunshot wound on the left transverses the two hemispheres, which would have a very poor prognosis. On the left is a knife wound. With knives, the wound is only as long as the knife, and so may not cause as much harm. It can also kill. Would you remove the knife in the ER or ICU? (No. Should be removed in a controlled area, such as an OR). This particular impalement did not enter the brain. As bad as it looks, it did not pierce the skull. The patient was discharged after only one day.

Seizure Definition A single event of abnormal discharge in the brain that results in an abrupt and temporary altered state of cerebral function No additional information needed.

Classification Generalized Partial
Initial involvement of both cerebral hemispheres Tonic-Clonic Myoclonic Partial Seizures limited to part of one cerebral hemisphere Described on following slides

Generalized Seizure: Tonic-Clonic
Loss of consciousness followed by brief period of muscle rigidity (tonic phase) and then rhythmic muscle jerking (clonic phase) May see incontinence, diaphoresis Post-ictal phase Period following seizure May see H/A, amnesia, confusion, fatigue No additional information needed

Generalized Seizure: Myoclonic
Sudden, brief muscular contractions, either generalized or localized to extremities or face No additional information needed

Partial Seizure Seizures limited to part of one cerebral hemisphere
Simple partial – patient conscious Complex partial – LOC May progress to general No additional information needed

Partial Seizure Symptoms related to area of brain affected
Motor – face twitching, limb jerking Automatisms – lip smacking, blinking Sensory – numbness, tingling May be visual, auditory, gustatory (taste) or vertiginous (vertigo, dizziness) Psychic – Hallucination, illusion Autonomic – diaphoresis, vomiting No additional information needed

Causes Inadequate levels of seizure medications
Withdrawal from seizure medications Acute withdrawal from chronic use of sedatives or depressants Alcohol Benzodiazepines Barbiturates Drug toxicity or adverse reaction No additional information needed

Causes Metabolic disorders Neurologic conditions Uremia Hypoglycemia
Electrolytes Fever Neurologic conditions Traumatic brain injury CNS infections Brain tumors Cerebral edema Stroke Cerebral anoxia AV malformation Increased ICP No additional information needed

Intervention Observation Prevent injury Anti-seizure medication
Many seizures will stop without intervention Prevent injury Anti-seizure medication Surgery Observation should include noting behavior prior to the onset of the seizure, removing anything that might harm the patient, timing the duration of the seizure, noting anything that occurred during the seizure (such as incontinence), and describing the presentation in the post-ictal phase. Anti-seizure medication will be discussed shortly Surgery is required only in extreme cases where the seizures cannot be controlled by medication, where the quality of life is significantly affected, and when the location of the initiating tissue can be identified.

Status Epilepticus More than 30 minutes of continuous seizure activity
Two or more sequential seizures without full recovery of consciousness between seizures No additional information needed

Status Epilepticus: Treatment
ABC’s Stop the seizure Ativan (up to 8 mg IV) Propofol Barbituate coma (loading dose followed by infusion) Look for causes Prevent recurrence Prevent complication No additional information needed

Anti Epileptic Drugs (AEDs)
To treat or not to treat Circumstances of the seizure Patient medical condition Response to treatment Quality of life Duration between seizures Not all seizures required medication. If the patient only has a seizure rarely, there is no way to tell if the medication is preventing the seizure. Seizures caused by a specific event (fever, trauma, anoxia, etc) may not require seizure medication.

AEDs Specific for type of seizure Begin with monotherapy
Polytherapy or different agent if monotherapy not effective Titrate does to therapeutic blood level or clinical control Consider side effects AEDs = Anti-Epileptic Drugs

AEDs Phenytoin (Dilantin) Fosphenytoin (Cerebyx)
Valproic acid (Depakote) Carbamazepine (Tegretol) See table in handout for indications, dose, and adverse effects Don’t go into medication in detail. Although important for the test, they can read them in their notes. A full page is dedicated to AEDs.

AEDs May require glucose due to large amounts used during seizure
All siderails up and padded Jewelry, clothing that can injure or restrict airway removed If in chair when seizure begins, lower to floor No restraints, no tongue blade Seizures utilize a great deal of glucose because of the involuntary movements commonly seen. Patients may use up glucose faster than it can be delivered. Finger sticks do not require a physician’s order, so obtain one in order to ascertain the patient’s status. Restraints and tongue blades can be harmful, even breaking bones and teeth.

Stroke Definition: Neurological changes brought about by an interruption in blood supply to the brain

Non-Modifiable Risk Factors
Age Sex Race/Ethnicity Genetics Risk factors are similar to MI, PAD, abdominal aneurysm, other cardiac events. Age: older patient is, more at risk Male more than female, but females have a higher mortality African-American more than Caucasian kAs with other cardiac diseases, a family history puts a patient at greater risk

Modifiable Risk Factors
Cardiac Risk Non- Cardiac Risk HTN Cholesterol Heart-bypass Angioplasty AFib Smoking Illicit drugs HRT Alcohol Modifiable factors are those that the patient can decrease their risk with a healthy lifestyle, diet, exercise, not smoking, taking medications as prescribed, and seeing physician regularly. HRT = hormone replacement therapy

Stroke Classification
Primary ischemic (80%) Due to thrombosis or embolism which lodges in cerebral artery causing ischemia of distal tissue Primary Hemorrhagic (20%) Due to ruptured cerebral artery with subsequent pressure on surrounding tissue Intracerebral hemorrhage Subarachnoid hemorrhage As described. Good news is that we now have effective treatment for ischemic strokes.

Presentation Hemiplegia (paralysis) Hemiparesis (weakness) Aphasia
Dysarthria (motor speech disorder) Visual Changes Hemiplegia is paralysis of one side, Hemiparesis is weakness of one side. As previously discussed, aphasia can be Wernicke’s or Broca’s. Dysarthria is not caused by ischemia to the speech center in the brain. It is due to paralysis of the structures in the throat that control speech.

Initial Work-Up Non contrast CT scan Quick History and physical
Start IV line Non-contrast because contrast does not visualize any better, but also because, if the stroke is hemorrhagic, contrast can flow into the brain tissue. Quick H&P – Time is of the essence. Only determine those facts that directly affect the situation. We are not interested in the leg they broke skiing two years ago, or the appendectomy from childhood. Will most likely want to start several IVs. Once the fibrinolytic is administered, any puncture is at risk of bleeding.

Ischemic Stroke Drug of choice is r-TPA
Patients eligible if presentation within 3 hours of symptom onset Lengthy exclusion criteria Greater than 3 hours from time of symptom onset Current or recent use of anticoagulants Coagulopathy Uncontrolled hypertension Rapidly improving neurologic signs Severe stroke NIHSS>22 NIHSS: National Institutes of Health St

Exclusion Criteria Other reasons Inform patient and family of risks
Previous stroke, ICH or serious head injury in the past 3 months Major surgery within last 14 days GI or urinary bleeding within the preceding 21 days Blood glucose <50 mg/dl or >400mg/dl Seizure at the onset of stroke Recent MI Inform patient and family of risks These reasons are not in outline; most likely won’t be on the test. Informative only.

Post r-TPA Care Avoid invasive procedures (Foley, NG tubes, etc)
Monitor closely for intracerebral hemorrhage (ICH) Monitor BP and treat according to AHA guidelines

Medical Management: if not Eligible for TPA
Heparin Platelet Anti-Aggregation ASA Persantine Plavix

Surgical Management Carotid endarterectomy Indication
Objective is to restore normal perfusion pressure to internal carotid system and removal of emboli Indication Carotid stenosis > 70% and symptomatic

Hemorrhagic Stroke

Intracerebral Hemorrhage
Onset usually during activity Sx: based on location, progressive onset Diagnosis and treatment Non-contrast CT BP control Correct coagulopathy Medical vs. non-medical management dependent on size and location Non-contrast CT to differentiate from ischemic stroke Frequently due to uncontrolled HBP Coagulopathy from anticoagulants

Subarachnoid Hemorrhage (SAH)
“Worst headache of my life”

Causes of Subarachnoid Hemorrhage
Blood vessel in subarachnoid space, just outside the brain, ruptures Rapidly fills with blood Most common cause is cerebral aneurysm Blue area is subarachnoid space. You can see that, if there was a bleed there, it would put terrific pressure on the brain itself.

Locations of Cerebral Aneurysms
Bifurcations and branches of the large arteries located at the Circle of Willis Approximately 85% of aneurysms develop in the anterior part of the circle The Circle of Willis encircles the brain, and is fed by vessels such as the internal carotid, basilar artery, anterior and middle cerebral arteries and the anterior and posterior communicating arteries. They form a circular pathway around the brain. Aneurysms are most commonly found at bifurcations. Almost 50% of them are anterior.

Risk Factors and Presentation
Sudden, intense headache Sometimes described as the worst headache of one’s life Neck pain (nuchal rigidity) N/V. Rapid LOC or death Family history.. Previous aneurysm. Gender Women more than men Race African Americans more than whites History of hypertension History of smoking Risk factors are similar to cardiac risk factors in MI. The rapid build up of blood in the subarachnoid space is responsible for the severe headache.

Non-contrast CT If no space-occupying lesion→ LP Angiogram Definitive treatment Clipping vs. coiling Non-contrast, again, to differentiate between ischemic and hemorrhagic stroke. An angiogram can locate the aneurysm. Clipping is surgery, while coiling is interventional. The decision on which to do depends on the aneurysm’s size, location, and neck geometry. doiling is likely to be favored in patients who are older, are in poor health, have serious medical conditions, or have aneurysms in certain locations.

Aneurysm Clipping Clipping involves surgical access to the aneurysm. A clip is placed over the base of the aneurysm to prevent blood from entering and putting pressure on the walls of the aneurysm

Aneurysm Coiling Coiling uses a catheter placed in the femoral artery, as with cardiac catheterization. It is advanced to the brain, to the area of the aneurysm. Platinum coils are placed inside the aneurysm to reduce pressure from blood.

Blood Pressure Management
Tolerate higher BP for secured aneurysm Antihypertensives for unsecured aneurysms to reduce risk of rupture Hypertension plays a role in hemorrhagic stroke. If the aneurysm hasn’t yet been treated with clipping or coiling, blood pressure will have to be maintained and a lower rate. It may require antihypertensive drugs to control the BP. Once the aneurysm has been successfully treated, a higher blood pressure can be tolerated.

Complications Re-bleeding Hydrocephalus Acute neurologic deterioration
Peak: 24 hours after initial bleed Treatment = clipping Hydrocephalus Acute requiring ventriculostomy Chronic requiring ventriculo-peritoneal shunt Rebleeding is the greatest cause of mortality and morbidity after a bleed. It requires clipping. Hydrocephalus can develop as a result of the bleed, and requires either a temporary external ventriculostomy or an internal V-P shunt.

Complications Vasospasm
Narrowing of vessel lumen Progressive neurologic deterioration Most significant cause of M&M in patients surviving long enough to reach medical care Onset Peak 7-14 days post SAH Up to 21 days The blood in the surarachnoid space is irritating to the vessels of the brain. The patient will present as if they are having another stroke. Patients are at risk for vasospasm for 21 days after their initial bleed.

Prevention and Treatment
Triple H therapy Hypertension, hypervolemia, hemodilution Hct > 40: Albumin, IV fluids Keep SBP ~150 mmHg May require vasopressors Calcium channel blocker: Nimodipine Interventional treatment Selective cerebral angioplasty In triple H therapy, IV fluids are administered to force the blood through the narrowed artery. Blood pressure, particularly the MAP, is kept higher for the same reason. The increased volume will dilute the blood, making it easier to pass through the vessels. Nimodipine, a calcium channel blocker that is not effective for any other purpose, is the drug of choice to stop the spasming. The patient may require angioplasty of the vessel. Triple H and Nimodipine are the most common treatments, and most likely will be on the test.

Arteriovenous Malformation (AVM)
Abnormal collection of blood vessels Congenital Average age: 33 years Most common presentation Hemorrhage (small AVMs) Seizure (large AVMs) AVMs are congenital, but don’t usually become problematic until the patient is at least in their teens or older. Normally, capillaries separate the arterial vessels from the venous vessels. With AVM, the capillaries are missing; the arteries and veins are directly connected. As a result, the veins receive the high pressure of the arterial system. The thin walls of the veins cannot tolerate this and can rupture, leading to hemorrhagic shock.

MRI and angiography Treatment based on size and appearance of AVM Surgery Radiosurgery Interventional Neuroradiology (INR) The vessels require MRI and angiography to be visualized. AVMs may be treated surgically, in which they are removed, or interventionally, in which surgical “crazy glue” is placed in the vessels to prevent blood from passing through. They may be sealed off using a gammaknife or cyberknife, two types of radiotherapy.

Neuro Infections Guillian-Barre Syndrome Meningitis Encephalitis
Miscellaneous infections Discussion of each follows

Guillain-Barré Syndrome
Acute inflammatory polyneuropathy Believed to be an autoimmune response to a viral infection Destruction of myelin sheath Pt hx significant for acute infection (ie URI, pneumonia) within 2 weeks of onset of GBS As described

Guillain-Barré Syndrome
Rapidly progressive motor loss Most often ascending and symmetrical Autonomic dysfunction Cardiac arrhythmias/BP fluctuations Paralytic ileus Urinary retention SIADH As described

Patient hx Presentation LP EMG Treatment Plasmapheresis Respiratory support Supportive therapy As described

Meningitis Viral Not usually fatal Occurs more often in children
As described

Meningitis neisseria meningitidis
Bacterial: Meningococcal meningitis: neisseria meningitidis Highest incidence in children and young adults May cause rapid (within hours) circulatory collapse due to overwhelming septicemia Requires treatment of close contacts and healthcare personnel As described

Signs and Symptoms Adult Child HA: usually presenting sign
Fever, change in LOC, nucchal rigidity Meningeal irritation: check Kernig’s and Brudzinski’s signs Child Fever, vomiting, bulging fontanels, crying Nuchal rigidity – chin bent to chest causes pain

Brudzinski and Kernig’s Signs
Brudzinski sign – knees flexed, head forward Kernig’s sign – lig brought up and knee bend Both cause pain

Dx made based on hx and LP findings Early recognition and isolation Organism specific antibiotic therapy for bacterial meningitis Symptomatic and supportive care for viral meningitis As described

Encephalitis Inflammation of the brain caused by viruses, bacteria, fungi or parasites Arthropod-borne viruses West Nile virus Herpes Simplex As described

Encephalitis West Nile Virus Herpes Simplex
Varying degrees of severity Mosquito transmission Prevention! Treatment supportive Herpes Simplex Acute onset Flu-like symptoms Propensity for temporal lobes Poor prognosis if treatment not initiated before coma As described

Treatment Medical vs. Surgical Steroids for cerebral edema
Dependent on pt condition, cause of infection, location of lesion Steroids for cerebral edema Control of ICP Antibiotics or anti-parasitics As described

Encephalopathy Hypoxic-ischemic (anoxic) Metabolic
Cardiac arrest Exsanguination Drop in pO2 Metabolic Hepatic/Renal failure Hypo/ hyperglycemia Sepsis Hypoxic caused by insufficient blood to brain for significant period of time Metabolic caused by inflammatory mediators, toxins (liver and kidneys can’t remove). Hypoglycemia causes insufficient carbohydrate for metabolism; hyperglycemia can cause osmotic shifts.

Exam Question Mr. Jones is in the intensive care unit following a motor vehicle crash. He is oriented to person, place, and time; can move all extremities; and follows commands. His pulse is 75 beats/min, his blood pressure is 120/70, and his respirations are 18 breaths/min and regular.

Exam Question Which of the following is the earliest indicator that Mr. Jones' intracranial pressure is increasing? A. He exhibits decorticate posturing B. He is oriented to person only C. His blood pressure is 130/60 and his pulse is 58 beats/min D. His respirations are 10 per minute and irregular Answer: B. Confusion to place and time is a commonly seen early sign of increased ICP. Patients rarely are unable to identify themselves, which, when it occurs, is a very late sign of increased ICP. Decorticate posturing (A) is a late sign of increased ICP. A blood pressure of 130/60, with a widened pulse pressure > 30 mmHg and bradycardia, is referred to as Cushing’s sign, and is also a late sign of increased ICP. Changes in respiratory patterns are also a late sign.

Exam Question A patient has survived a severe traumatic brain injury with a basilar skull fracture but has now developed an elevated temperature. Although the nurse’s plan for managing fever in this patient population will be multifactorial, the most important aspect will center on identifying:

Exam Question A. Deep vein thrombosis, a frequently neglected complication of immobility B. Meningitis, a potential complication of basilar skull fractures C. Hypothalamic dysfunction or “storming”, a potentially lethal febrile syndrome after head trauma D. Foreign bodies still embedded in the skull base, a common course of infection Answer B. Because basilar skull fractures can include a tearing of the dura layer of the skull, the patient is a risk for meningitis. Although the patient may be at risk for DVT due to immobility (A), there is no indication of signs of DVT and subsequent PE, such as pain (Homen’s sign), redness and swelling of the calf, or SOB. Hypothalamic dysfunction (C) usually occurs in the setting of severe TBI associated with diffuse axonal injury where there is global injury to the white matter of the brain. Foreign bodies (D) may be embedded in the skull, but is not related to fever in a basilar skull fracture.

Exam Question A patient is admitted to the ICU for neurologic monitoring, after sustaining a linear left temporal skill fracture in a motor vehicle collision. The EMTs reported a transient loss of consciousness at the scene. Within 2 hours of admission, the patient’s neurological status deteriorates. The nurse suspects the patient has developed a

Exam Question A. Epidural hematoma B. Subdural hematoma C. Subarachnoid hemorrhage D. Intracerebral hemorrhage Answer A. A linear fracture of the temporal area of the brain places the patient at high risk of epidural hemorrhage due to tearing of the middle meningeal artery. Brief loss of conscious, following by a lucid period that can last as long as 48 hours, is then followed by a rapid deterioration of consciousness. This patient must be emergency taken for surgery for removal of blood and repair of the artery. None of the other choices present with the scenario as given.

Exam Question When providing nursing care for a patient with suspected stroke, the most important factor related to the use of fibrinolytic therapy is to:

Exam Question Begin the therapy within 90 minutes of the patient’s arrival B. Obtain a detailed history of the patient’s allergies C. Establish the nature and time of symptom commencement D. Start a large-bore central IV line Answer: C. Patients with sudden onset of neurologic deficiencies and persistence focal neurologic deficits should be considered for rt-PA therapy. Patients with persistent symptoms after one hour have an 85% risk of stroke with only a 15% chance of full recovery. Patients whose symptoms resolve rapidly are most like having a TIA and should not receive rt-PA. It is essential to determine the time of onset of symptoms or at least the last time the patient was seen without deficits. For therapy to be effective, it must begin within 3 hours of symptom onset, not arrival to the hospital (A). Patient allergies are important to identify (B), but are not the most important factor. The time window of treatment options is the primary timing factor in treatment of these patients. Bleeding at a noncompressible site such as a central line (D) should be avoided, so a peripheral IV line is preferred over a central line.

Exam Question A nurse has just admitted a patient with a diagnosis of acute ischemic stroke to the ICU. Which of the following assessment findings should alert the nurse to a contraindication for rt-PA therapy? A. NIH stroke scale score of 1 B. History of seizure disorder C. A mild traumatic brain injury from a motor vehicle collision 6 months ago D. INR great than 1.3 Answer: A. Isolated, mild deficits, (NIH score ≤1) represent a contraindication to rt-PA therapy. While a seizure at the beginning of a stroke is a contraindication, a history of epilepsy or seizure disorder (B) in itself, would not be a contraindication. Another stoke, intracranial surgery, or severe head trauma within the past 3 months would exclude a patient from receiving rt-PA, a mild TBI 6 months earlier would not (C). Current use of anticoagulants, or an INR ≥1.7 would qualify as a contraindication, an INR of 1/3 would be acceptable (D).

Exam Question During an initial neurologic assessment, the nurse finds that the patient has a positive Brudzinski’s sign and a positive Kernig’s sign. Otherwise, the patient’s assessment is nonfocal. Since the lumbar puncture performed earlier shows high protein and low glucose in the CSF, the nurse’s most appropriate action at this time is to:

Exam Question A. Prepare the patient for brain MRI to rule out mass lesion B. Arrange for administration of plasmaphoresis C. Prepare to administer IV antibiotics D. Prepare the patient for a repeat LP to withdraw accumulating CSF Answer C. The patient is exhibiting signs of meningitis, which include headache, chills, fever, nausea, vomiting, photophobia, back pain and generalized seizures. Sign of meningeal irritation may include stiff neck (nuchal rigidity), Brudzinki’s sign and Kernig’s sign. Common CSF findings in meningitis include high protein, low glucose, and elevated white blood cell count. Meningitis is diagnosed with lumbar puncture for CSF evaluation after CT scan is obtained. CT scan is the preferred scan in this population. MRI is not indicated (A). Plasmaphoresis is indicated for patients with Guillian-Barre Syndrome (B). There is no indication for serial LPs in this scenario (D).

Exam Question A patient was admitted to ICU yesterday evening after being found on the pavement following an apparent assault. The patient has not yet been identified, and his medical history is unknown. He has been clinically stable and maintained on mechanical ventilation with satisfactory ABGs.

Exam Question During a mid-morning assessment, the nurse notes that the patient demonstrates a rhythmic movement of his extremities and begins clenching his jaw on the endotracheal tube. He has not demonstrated this type of activity since admission, but was placed on prophylactic anticonvulsants after traumatic brain injury. The nurse hypothesizes that the patient is most likely experiencing:

Exam Question A. Hypoxia B. Delirium tremens C. Substance withdrawal D. Post-traumatic seizures Answer: C. Rationale: all of the options are possible reasons for seizures, but substance withdrawal is the most likely choice among these possibilites. Hypoxia (option A) is less likely because the patient just started this activity of clenching on his endotracheal tube (and, his ABGs were satisfactory). Delirium tremens (option B) is another possibility, but DTs usually occur hours after cessation of alcohol intake. The patient received seizure prophylaxis for post-traumatic seizures (option D), so while this is possible, it is a less likely cause.

CCRN-PCCN Certification Review Course: Neuro

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