CNS Disorders

EMS Professions

Temple College

Pathophysiology of CNS Emergencies

Structural Changes Often due to Trauma but not always Circulatory Changes

Inadequate Perfusion Alterations of ICP

Response to insult

Toxic Metabolic states Alteration to blood chemistry or introduction of toxins

Psychiatric ‘mimicking’

ICP Review CBF is a factor of CPP & CVR

If CPP , then CBF If CVR , then CBF most likely

CPP = MAP - ICP MAP = Diastolic + 1/3 PP PP = SBP - DBP

PCO2 has greatest effect on CVR Sympathomimetics may CVR

ICP Review As PCO2 , CVR

Therefore, if PCO2 , CVR Then, as CVR , CBF

Normal ICP < 15 mm Hg As ICP , CPP then CBF Compensation for ICP via MAP

Cushing’s Reflex (Triad) Cushing’s triad with coma indicates possible

herniation

Altered Mental Status

Coma A decreased state of consciousness from

which a patient cannot be aroused Mechanisms

Structural lesions Toxic Metabolic states Psychiatric ‘mimicking’

Brain injury Recall that Brain injury is often

shown by: Altered Mental Status Seizures Localizing signs

Is unconsciousness itself an immediate life threat?

Loss of airway Vomiting, aspiration

YES, IT IS!

Altered Mental State

Manage ABC’s Before Investigating Cause!

Initial Assessment/Management Airway

Open, clear, maintain If trauma or + history, control C-spine

Breathing Presence? Adequacy (rate, tidal volume)? High concentration O2 on ALL patients with altered

mental status Assist ventilations prn

Circulation Pulses? Adequate Perfusion?

Investigate Cause DERM

D = Depth of Coma E = Eyes R = Respiratory Pattern M = Motor Function

D = Depth of Coma

What does patient respond to? How does he respond?

Avoid use of non-specific terms like “stuporous”, “semi-conscious”, “lethargic”,

“obtunded”

D = Depth of Coma

AVPU Glasgow Scale (later)

Describe level of consciousness in terms of reproducible findings

E = Eyes Pupils

Size - mid, dilated or constricted measurement - e.g. 4 mm

Shape - round, oval, pontine Equality - equal in size Symmetry - equal in reaction/response Response to light

Yes or No How?

R = Respiratory Pattern

Depth Unusually deep or shallow?

Pattern Regular or Unusual pattern

Can you identify the pattern?

M = Motor Function Paralysis?

Where? Muscle tone?

Rigid or Flaccid Movement?

Where? What is it like? Posturing?

How? Symmetrical Motor Function?

Physical Exam Vital Signs

Shock? Increased ICP? Hypoxia/Hypercarbia

Diagnostics Dysrhythmias? Blood glucose Oxygen saturation

Physical Exam Detailed (Head-to-Toe) Exam

Injuries causing coma? Injuries caused by coma? Clues to the cause

Probable Causes of AMS Not enough Oxygen Not enough Sugar Not enough blood flow to deliver oxygen, sugar Direct brain injury

Structural Metabolic

Differentiating AMS Causes Structural

Asymmetrical deficits

Unequal pupils Afebrile History of trauma,

structural abnormality

Often a rapid onset

Metabolic Symmetrical deficits Equal pupils

(? altered function) ? Fever History of metabolic

disorder or illness Rapid onset less

likely

Management Maintain ABCs Attempt to identify cause Mainstays of therapy

Oxygenation/Ventilation IV fluids appropriate for the patient D50 (if hypoglycemic) Narcan if possibility of opiate OD Flumazenil in known benzo only OD

AEIOU TIPS

Alcohol Epilepsy Insulin Overdose Uremia

(Metabolic causes)

Trauma Infection Psychogenic Stroke/Syncope

Cerebrovascular Accident AEIOU TIPS

Cerebrovascular Accident

Any disease process that disrupts blood flow to a distinct region of the brain

Transient Ischemic Attack (TIA) S/S less than 24 hours without

permanent neuro deficits

Cerebrovascular Accident 500,000/yr in US 25% die Survivors often socially, financially

devastated $20 billion in medical costs, lost

wages

Cerebrovascular Accident (CVA)

Pathophysiology Thrombosis (brain itself) Embolus (head, neck or heart) Hemorrhage (within brain) Ischemia (systemic blood flow)

Predisposing Factors: Modifiable

Hypertension Cigarette smoking Diabetes Mellitus Heart disease Hyperlipidemia Cardiovascular

disease

Chronic atrial fibrillation

Sickle cell disease Polycythemia Hypercoagulability Birth control pill use Cocaine use

Predisposing Factors: Unmodifiable

Age Gender Race Prior stroke Heredity

CVA Mechanisms

Ischemic stroke--80 to 85% Hemorrhagic stroke--15 to 20%

Thrombus Embolus Aneurysm Arrhythmia Hypovolemia

CVA Origin

Ischemic Stroke Blood vessel occlusion

Thrombosis Embolism

Plaque fragments from carotids Chronic atrial fibrillation Fat particles IV substance abuse particulates

Systemic hypoperfusion Pump failure Hypovolemia

Ischemic Stroke Syndromes Transient Ischemic Attack (TIA)

Neurological deficits that resolve in 24 hours or less (most in 30 minutes)

Commonly result from carotid artery disease Same symptoms as CVA Often warning sign of impeding CVA 5% risk of stroke per year

Ischemic Stroke Syndromes Dominant Hemisphere Infarction

Contralateral weakness, numbness Contralateral blurring of vision of half the

visual field in both eyes Difficulty pronouncing words (dysarthria) Difficulty speaking or understanding speech

(dysphasia or aphasia)

Ischemic Stroke Syndromes Nondominant Hemisphere Infarction

Contralateral weakness, numbness Contralateral visual field cut Neglect of contralateral extremities Constructional apraxia (difficulty drawing

figures like a clock face) Dysarthria Usually NOT dysphasic or aphasic

Ischemic Stroke Syndromes Vertebrobasilar Syndrome

Involves blood flow to brainstem, cerebellum, and visual cortex

Dizziness, vertigo Diplopia Dysphagia Ataxia, bilateral limb weakness

Hemorrhagic Stroke 30 to 50% 30-day

mortality Younger patient

population Two subtypes:

Intracerebral, usually 2o to hypertension

Subarachnoid, usually from berry aneurysms

Hemorrhagic Stroke Syndromes Intracerebral Hemorrhage

Headache, nausea, vomiting precede deficits Patients commonly have decreased LOC with

extreme hypertension Contralateral hemiplegia, hemianesthesia Possible aphasia, extremity neglect depending

on hemisphere involved

Hemorrhagic Stroke Syndromes Subarachnoid HemorrhageGrade I Asymptomatic or mild headache and mild

nuchal rigidityGrade II Moderate to severe headache, nuchal

rigidity, cranial nerve dysfunction but noother deficits

Grade III Drowsiness, confusion, mild focal deficits

Grade IV Stupor, moderate to severe hemiparesis,possibly early decerebrate rigidity,vegetative response

Grade V Deep coma, decerebrate rigidity,moribund appearance

CVA Assessment

Presentation of CVA varies with area(s) of brain involved and type of CVA

CVA Presentation Brain can show injury in only three ways:

Decreased LOC Seizures Localizing signs

Hemiparesis or hemiplegia Dysphasia (Receptive or expressive) Visual disturbances Gait disturbances Inappropriate affect Bizarre behavior Incontinence

Cincinnati Prehospital Stroke Scale Have patient smile (“Facial Droop”)

Normal: Both sides of face move equally well Abnormal: One side does not move as well as other

Have patient close eyes and hold arms out (“Arm Drift”) Normal: Both arms drift same amount or do not drift Abnormal: One arm does not drift or one drifts down compared to

other or can’t move arms

Have patient say, “You can’t teach an old dog new tricks.” (“Speech”) Normal: Correct words, no slurring Abnormal: Slurs words, uses inappropriate words, or unable to

speak

Assessment Signs & Symptoms

Ischemic S&S usually of slower onset Hemiparesis or hemiplegia Numbness or decreased sensation of face

or unilateral Altered LOC or coma Convulsions Visual disturbances Slurred or inappropriate speech Headache or dizziness

Assessment Signs & Symptoms

Cerebral Embolus with rapid onset Emboli from valvular HD or Afib rapid onset Often with an identifiable cause (e.g.

Afib, Valvular heart disease, recent long bone fracture)

Assessment Signs & Symptoms

Cerebral hemorrhage associated with rapid onset

high mortality rate Often with severe HA (“Worst headache

ever”) N/V Rapid decrease in LOC or seizure Coma, Cushing’s and Herniation

Assessment History Associated Altered LOC or Seizure? Onset/Precipitating factors? Initial symptoms and progression?

Dizziness, Severe HA, N/V Previous CVA or TIA? Previous neuro deficits? Concomitant illnesses?

Sickle Cell Disease Atrial fibrillation

Risk factors for stroke & thrombus formation? BCP, Smoking HTN, CVD

Assessment Physical Exam

Mental Status & Behavior Extremity Motor & Sensory

Gait Pupils & Vision Cincinnati Prehospital Stroke Scale Evidence of Cushing’s or Herniation Blood glucose level

CVA Management

Basic ObjectiveImprove cerebral blood flow

and oxygenation

CVA Management Airway

If no gag reflex, intubate Otherwise, position to ensure drainage of

secretions Suction prn

Breathing Oxygen via NRB Ventilate with BVM and O2 if rate or tidal volume

inadequate Intubate if herniating

CVA Management Controlled hyperventilation if intracranial

hemorrhage suspected with increased ICP and neurologic deterioration

Indicators Sudden onset Headache Rapid loss of consciousness Seizures Unequal pupils

CVA Management Circulation

Check blood glucose level Hypoglycemia may mimic CVA Treat hypoglycemia with D50

Establish IV Access Draw blood samples TKO avoid solutions with glucose

Monitor ECG 10% of CVAs are associated with cardiac event 12 Lead ECG if suspected ischemia

CVA Management

Do not assume patient cannot understand because they cannot talk

Position appropriately: If hypertensive, semireclined (head slightly

elevated) If normotensive, on affected side If hypotensive, supine

CVA Management Increased Blood pressure treated ONLY

if strongly suggestive of ischemic stroke If systolic >220 or diastolic >120 consider

gradual blood pressure reduction Labetalol Nitropaste Nitroprusside

Controlled reduction Return to pre-CVA levels, NOT to “normal”

CVA Management Thrombolytic agents

Consider for all patients with ischemic CVA presenting within 3 hours of onset

Early recognition of ischemic stroke and administration of thrombolytics can prevent/limit loss of neurologic function

Requires CT scan!!!

CVA Management Think like AMI of the Brain

Time is tissue Therapy Mainstays

Oxygenation/Ventilation IV Access Rapid assessment & differential

Treat associated conditions (hypoglycemia, hypoxia, hypotension)

Rapid Transport to appropriate facility CT Scan & Thrombolytics vs. CT Scan &

Neurosurgery

SyncopeAEIOU TIPS

Syncope aka Fainting Pathophysiology

Brief loss of consciousness caused by transient cerebral hypoxia

May be caused by lack of glucose or seizure activity in the brain

Syncope Types

Postural Inadequate blood flow to brain due to

position Vasovagal

Excessive vagal stimulation Carotid Sinus stimulation/pressure

Cardiogenic Dysrhythmia, usually bradycardia Stokes-Adams Syndrome

Syncope Types

Tussive “coughing spell” resulting in

intrathoracic pressure causing venous return to the heart

most often in overweight male smokers with chronic bronchitis

Micturation associated with urination, usually in

patients who have consumed EtOH and compounded by increased vagal stimulation

Syncope Assessment

History of the event Often preceded by sensation of light-

headedness Rapid return of consciousness is most

common

Past History History of vertigo Similar past episodes

Many possible causes

Syncope Management

Manage ABCs Clear airway and Assist ventilations as

needed Oxygen NRB (initially) Calm & Reassure Assess for underlying cause

ECG Blood glucose History (present and past) Physical Exam

Treatment based on underlying cause

SeizuresAEIOU TIPS

Seizures Alteration in behavior/consciousness 2°

unstable, uncoordinated electrical activity in the brain Often a result of altered membrane

permeability Manifested by sudden, brief episodes of:

altered consciousness altered motor activity altered sensory phenomena unusual behavior

Seizure Categories Generalized

Tonic-Clonic (grand mal) AKA Convulsions

Absence (petit mal) Partial

Simple partial Complex partial

Hysterical

Seizure Etiology CVA Hypoxia Infection/Fever Drug/alcohol

withdrawal Poisoning/OD Thyrotoxicosis

Head trauma Hypoglycemia Brain neoplasms Psychiatric

disorders Eclampsia Hypocalcemia

Seizures Etiology

Most epileptic seizures are idiopathic in origin

Generalized Seizures

Petit Mal Absence Sz Children No LOC

Grand mal aka Convulsions Common Often w/Aura Sudden LOC Tonic / Clonic Postictal phase Status epilepticus

Generalized Seizures

Symmetrical No local onset Irritable focus difficult to identify

Near simultaneous activation of entire cortex

Focus may begin deep in brain and spread outward

Generalized Seizures Tonic-Clonic Seizures (Grand Mal)

Aura (preictal phase) Loss of consciousness/postural tone Tonic phase Hypertonic (tetanic) phase Clonic phase Post-ictal phase May experience transient neurologic deficits

(Todd’s paralysis)

Generalized Seizures Absence Seizure (Petit Mal)

Brief loss of awareness (10 - 30 seconds) Usually no loss of postural tone May occur 100+ times a day Primarily pediatric problem Often described as “daydreaming”, not

paying attention Usually disappear as child matures

Partial Seizures

Seizure begins locally May remain localized or spread to

entire cortex Result from focal structural lesion

in brain

Partial Seizures Simple

Localized clonic activity

Abnormal sensory symptoms

Usually no LOC May progress

Jacksonian March (Seizure)

Complex Change in

behavior Preceded by aura Repetitive motor

behavior No recall May progress

Partial Seizures

Simple partial seizures (No loss of consciousness) Focal motor seizures

Local clonic activity May display Jacksonian march

Sensory seizures Autonomic seizures

Partial Seizures Complex partial seizure (psychomotor or

temporal lobe seizures) Distinctive aura Loss of consciousness Automatisms May be mistaken for drunks or

psychotics May experience episodes of rage

Hysterical “Seizures” Usually in front of audience Usually follow interpersonal stress Movements asymmetrical or purposeful Does not fall, hit head, bite tongue Incontinence rare Recalls things said, done during

“seizure”

Assessment Seizure Assessment

Duration Seizure Postictal phase Typical for the patient?

Onset Events before HA Aura Trauma Vision Disturbances

Assessment Recent History

Trauma to the head/brain HA / Neck Pain Pregnancy Brain tumor Recent Infection/Illness CVA Symptoms Introduction of Poisons into body

Assessment Past History

Diabetes Mellitus Seizure Disorder Tumor CVA Medications Recreational Drug Use Alcohol abuse

Assessment Physical Exam

Evidence of trauma Evidence of alcohol, drug abuse Rash, stiff neck Pregnant CVA Signs Incontinence

Status Epilepticus Two or more seizures without

intervening conscious period Usually due to medication non-

compliance Management same as for other

Seizures just more aggressive

Seizure Management Patient actively seizing

Do NOT restrain Do NOT put anything in mouth Oxygen NRB if possible ECG Monitor when possible IV Access

Lg Bore, NS Assess blood glucose

Seizure Management Patient actively seizing

If hypoglycemic: Assess IV patency FIRST!! Dextrose 50% 12.5 - 25 grams IV push Consider Thiamine 100 mg slow IV push

Diazepam, slow IV administration until seizure stops or until ~ 10 mg

Usually aimed at 2.5 mg doses, one after another

Phenobarbital, 100 mg/min IV push to a total ~390 mg or seizure stops

Barbiturate coma NMB & Intubation

Seizure Management Current Mainstays of Therapy for Actively Seizing

Patient Diazepam Lorazepam Phenobarbital

“New” Therapy Phosphenytoin

Other Considerations Glucose MgSO4

Paraldehyde Dilantin (phenytoin) 18mg/kg at 25 mg/min

Seizure Management After seizure stops:

Open -Clear- Maintain airway O2 via NRB Assist ventilations if needed Roll patient onto side protecting head Reassess ABCDs Assess blood glucose Physical Exam and History

Most seizure deaths are due to anoxia

Seizure Management

If the patient is epileptic, do these

seizures match what is “normal”

for him? Just because the patient is

epileptic, he does NOT have to be

having an epileptic seizure!

Mandatory Transports First time seizures Seizure patient off medications Change in seizure pattern Associated with trauma Pregnant patient Status epilepticus Associated with increased body temperature

Not always; Seldom in young children Has infection been diagnosed and treatment initiated?

Insulin: Hypo/Hyperglycemia AEIOU TIPS

Insulin

Hypoglycemia Hyperglycemia

DKA HHNC

Insulin Assessment

Medical Alert Tag/Bracelet Evidence of DM Medications Fruity breath odor Signs of repeated SQ injections Blood glucose level (See Endocrine for further assessment)

Insulin Management

Hypoglycemia Management ABCs: Oxygen/IV/ECG Dextrose 50% (adult), 12.5 - 25 grams IV

push via patent line Consider Thiamine 100 mg slow IV push Dextrose 25% (children), 0.5 - 1 grams

IV push (2-4 cc/kg) via patent line Carbohydrate meal Assess for underlying cause Consider transport

Insulin Management

DKA/HHNC Management ABCs: Oxygen/IV/ECG Ventilate/Intubate prn Fluid administration titrated to signs of

shock 250 cc boluses and reassess

Consider administration of Regular Insulin (consult medical control)

Assess for underlying cause Transport

Alcohol AEIOU TIPS

Alcohol

“Dead drunk” Mixed overdose May be associated with

Head trauma Hypoglycemia

EtOH present in up to 40% of AMS patients

Alcohol

Is it alcohol or is it something

else?A patient is never “Just

Drunk”

Alcohol Management

Manage ABCs Clear airway and ventilate as needed Oxygen IV access prn

Assess for other causes of AMS ECG Monitor Blood glucose level History of mixed poisoning or EtOH poisoning Physical exam

Treat other causes

Overdose/PoisoningAEIOU TIPS

Overdose/Poisoning Possible Overdose/Poisonings resulting

in AMS Alcohol: Ethanol/Methanol Narcotics Sedative-hypnotics Solvent inhalation Stimulants

Overdose Assessment

Needle marks? Pupil responses? Slow respirations?

Associated hypotension Odd behavior? Breath odors? Color of oral mucosa, vomitus? History of Recent Drug/Poison use?

Uremia/Metabolic CausesAEIOU TIPS

Uremia (Metabolic Causes) Uremia/Renal Failure Hyperthyroidism Hypothyroidism Addisonian Crisis Hepatic Coma/Encephalopathy

Uremia (Metabolic Causes) Assessment

Med Alert? Patient medications? Physical findings? The Physical Exam and History (recent

and past) are most useful

TraumaAEIOU TIPS

Trauma Concussion Cerebral contusion Intracranial hematoma Hypovolemia Hypoxia

Trauma

Assessment Physical findings?

Evidence of brain injury

History of recent or remote trauma?

Trauma

Altered Mental Status = Head Injury

Until Proven Otherwise

Trauma

Head injury severity cannot be evaluated

accurately in presence of shock

Trauma Management

Manage ABCs Spinal motion restriction if indicated Clear airway and secure prn Ventilate prn Oxygen Establish IV access, NS

Fluid to titrate BP to ~ 90 mm Hg systolic Assess for other causes: ECG, Blood glucose Transport to trauma center

Infection/FeverAEIOU TIPS

Meningitis Encephalitis Brain abscess Sepsis Fever

Infection

Infection Assessment

Headache? Fever? Sore throat? Stiff neck (nuchal rigidity)? Rash? Associated symptoms of systemic

infection

Infection Management

Infection Control Measures Manage ABCs

clear airway and ventilate prn oxygen IV access prn

Consider acetaminophen for fever fluid / rehydration

PsychogenicAEIOU TIPS

Hysterical faking Catatonia

“psychomotor disturbances characterized by physical rigidity, negativism, or stupor”

may occur in schizophrenia, mood disorders or organic mental disorders

Psychogenic

Psychogenic

Assessment Circumstances?

Events leading up to this point Prior behavior?

Similar past episodes Medications & PMHx

Assessment & Management of AMS

Primary Assessment Onset

Mechanism (Kinematics) Preceding S/S

Level of Consciousness AVPU GCS (later)

Airway obstruction or compromise Fluid Unprotected airway (e.g. coma)

Primary Assessment Ventilatory ability

Adequate Ventilatory rate and depth? Respiratory Insufficiency 2° to ICP? (e.g.

irregular patterns) Cardiovascular compromise

Shock /hypotension /hypovolemia Hypertension

Primary Assessment Neuro Exam (motor & sensory)

Posturing? Muscle Tone? Pupillary Reflexes? Extraocular Movements? Symmetry

History Present and Recent Past

Management of AMS Goals:

Airway control/ maintenance Avoid hypoxia

Cardiovascular stabilization Avoid hypotension/shock

Interruption of cerebral injury Fix the root cause problem

Protection from further harm Avoid secondary brain injury

Other Neurologic Conditions

Headache Common complaint

Many persons experience regularly ~ 1/3 due to migraine HA May be associated with significant pathology

Characteristics Sudden vs Constant vs Recurring Generalized vs Localized Mild to Moderate to Severe Intensity of Pain

Cause is often unknown

Headache Vascular

Migraines Last minutes to hours to days Usually very intense, throbbing pain Photosensitivity N/V Often unilateral May be preceded by aura (not common) Occur commonly in women

Headache Vascular

Cluster Series of headaches Usually last for a few minutes or a few

hours Sudden, intense pain Usually unilateral May be accompanied by nasal congestion,

irritated or watery eye (same side) Occur commonly in men

Headache Tension

Most common headache Occur regularly Often awake in a.m. and worsens throughout

the day Dull, ache Feels like pressure on neck and/or head

Headache Organic

Not very common Due to some specific cause (illness/injury) in

the body Tumor Infection Meningitis Hypoglycemia etc.

Headache Potentially Serious Pathologies

Complaint “Worst headache ever” “It hurts right here” May localize at posterior neck at base of

skull Possible subarachnoid hemorrhage

Concern for possible intracranial hemorrhage

Neoplasms Less common neoplasm Risk factors

genetic exposure to radiation tobacco use occupational exposure to toxins medications/drugs/poisons diet

Neoplasms Pathophysiology

Most often a result of metastasis from another cancer (malignant)

Assessment focused on the detailed neuro exam not a diagnosis diagnosis BUT should be

included in the differential dx

Muscular Dystrophy Genetic disorder Results in degeneration of muscle fibers Types

Duchenne Fascioscapulohumeral Limb Girdle Myotonic

Muscular Dystrophy Duchenne dystrophy

most common childhood muscular dystrophy

onset usually by age 6 symmetrical weakness and wasting of

first the pelvic and leg muscles then pectoral and proximal upper

extremities progresses and results in early death

usually in adolescence

Multiple Sclerosis Common demyelinating disorder of the CNS Results in patches of sclerosis (patches) in brain

and SC Occurs primarily in young adults Typical S/S

visual loss, diplopia nystagmus weakness, paresthesias symptoms may have periods of exacerbation and

remission

Parkinson’s Disease Degenerative changes in the basal ganglia

result in deficiency of dopamine Characterized by rhythmical muscular

tremors, rigidity of movement, and droopy posture

Usually occurs after 40 years of age Leading cause of neuro disability > 60 years Estimated 500,000 in US

Central Pain Syndrome Known as Trigeminal Neuralgia paroxysmal bursts of pain in one or more

branches of the trigeminal nerve Often induced by touching trigger points in or

about the mouth Causes

tumor some medications (phenothiazines)

Bell’s Palsy Paresis or paralysis of the facial muscles

usually unilateral Occurs in 23 of 100,000 persons Caused by dysfunction of the 7th cranial nerve

cause is usually a viral infection other causes

post trauma herpes simplex lyme disease idiopathic

Amyotrophic Lateral Sclerosis

Progressive motor neuron disease aka ALS or Lou Gehrig disease disease of the motor tracts of the lateral

columns and anterior horns of the SC results in progressive muscular atrophy, increased

reflexes, and spastic irritability of muscles

Spina Bifida

An embryolgic failure of fusion of one or more vertebral arches results in spinal cord exposure spinal cord may protrude outward various types based upon type of deformity

Child requires frequent surgeries increased risk of latex allergies

Poliomyelitis

An inflammatory process of the Spinal Cord’s gray matter

May be caused by the poliomyelitis virus Enters bloodstream and nervous system results in paralysis of the limbs

Uncommon today in the US due to polio vaccine