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									Status Epilepticus
         Status Epilepticus
   Σοβαρή επείγουσα ιατρική
    κατάσταση που χρήζει άμεσης
    παρέμβασης
           Status Epilepticus
   Επιπλοκές
     Αρρυθμίες
     Διαταραχές ΑΝΣ

     Νευρογενές πνευμονικό οίδημα

     Υπερθερμία

     Ραβδομυόλυση

     Εισρόφηση

     Μόνιμη νευρολογική βλάβη
              Ορισμός
 Συνεχής επιληπτική δραστηριότητα > 30
  λεπτών ή
 Αν μεταξύ 2 κρίσεων δεν υπάρχει πλήρης
  ανάληψη του επιπέδου συνείδησης
 Νέος ορισμός: επιληπτική κρίση > 5

  λεπτών ή ε επιληπτικές κρίσεις χωρίς να
  επανέλθει ενδιάμεσα το επιπεδο
  συνείδησης
 Υποτροπιάζουσα επιληπτική
          κρίση
 Διάρκεια πάνω από 2 ώρες
 2 ή περισσότερα επεισόδια μέσα σε 1
  ώρα παρά την θεραπεία ή
 μη ανταποκρινόμενη στην αγωγή

  επιληπτική κρίση
               Ταξινόμηση
   Electroclinical features,
     (convulsive status epilepticus)
     (nonconvulsive status epilepticus)

   Επηρεάζουν
     whole brain (generalized status
      epilepticus) ή
     part of the brain (partial status
      epilepticus).
         Επιδημιολογία
 150,000 cases of status epilepticus and
 55,000 deaths from it occur annually in
  the United States.
 An incidence of between 6.2 and 18.3

  per 100,000 population has been
  reported in the United States
Αιτιολογία
                           Στάδια
   The first stage generalized convulsive tonic-clonic
    seizures that are associated with an increase in
    autonomic activity that results in
       hypertension,
       hyperglycemia,
       sweating,
       salivation, and
       hyperpyrexia
   Second phase: 30 min of seizure activity,
    characterized by
       failure of cerebral autoregulation,
       decreased cerebral blood flow, an
       increase in intracranial pressure, and
       systemic hypotension.
   Electromechanical dissociation may occur
          Διάγνωση
 Κλινική εικόνα
 ΗΕΓ απαραίτητα
           Θεραπεία
 Επιθετική αντιμετώπιση
 Πρόληψη νευρολογικών βλαβών και
  συστηματικών επιπλοκών
 Διακοπή σπασμών

 Προστασία αεραγωγού

 Πρόληψη εισρόφησης

 Θεραπεία υποκείμενης πάθησης
         Γενικά μέτρα
 Επαρκής αερισμός – οξυγόνωση
 Σωστή θέση ασθενούς

 2 φλεβικές γραμμές: υγρά –

  φάρμακα
 Διασωλήνωση τραχείας
 Lorazepam
 Propofol,

 Midazolam, or

 Etomidate

 Rocuronium (1 mg/kg)

 Succinylcholine
                   Άλλα μέτρα
   Hypoglycemia
   100 mg IV thiamine
   50% dextrose
   BP, ECG, and temperature
   Hyperthermia (ie, temperature 40°C), then passive cooling
   Serum chemistry levels
   Myoglobin
   Hydration is necessary to prevent myoglobin-induced renal
    failure. urinary alkalinization
   Brain imaging with a CT scan and/or MRI
   Lumbar puncture
   Endotracheal intubation and
   Neuromuscular
                   Φάρμακα
 Diazepam,
 Lorazepam,

 Midazolam,

 Phenytoin,

 Fosphenytoin, and

 Phenobarbital

       have all been used as first-line therapy for
        the termination of status epilepticus.
                   Φάρμακα
   lorazepam, 0.1 mg/kg;
   diazepam, 0.15 mg/kg, followed by 18 mg/kg
    phenytoin;
   phenytoin, 18 mg/kg; and
   phenobarbital, 15 mg/kg

   Status epilepticus was terminated in 64.9% of
    patients randomized to lorazepam, 58.2% of those
    randomized to phenobarbital, 55.8% of those
    randomized to diazepam and phenytoin, and
    43.6% of those randomized to phenytoin (p 0.002
    for lorazepam vs phenytoin)
               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’
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?

              YES, IT IS!

 Loss of airway
 Vomiting, aspiration
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
          Yesor 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                   Metabolic
       Asymmetrical                 Symmetrical deficits
        deficits                     Equal pupils
       Unequal pupils                (? altered function)
       Afebrile                     ? Fever
       History of trauma,           History of metabolic
        structural                    disorder or illness
        abnormality                  Rapid onset less
       Often a rapid onset           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              Trauma
 Epilepsy             Infection

 Insulin              Psychogenic

 Overdose             Stroke/Syncope

 Uremia (Metabolic
  causes)
  Seizures
AEIOU 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                    Head trauma
 Hypoxia                Hypoglycemia

 Infection/Fever        Brain neoplasms

 Drug/alcohol           Psychiatric

  withdrawal              disorders
 Poisoning/OD           Eclampsia

 Thyrotoxicosis         Hypocalcemia
         Seizures Etiology

Most epileptic seizures
are idiopathic in origin
           Generalized Seizures

   Petit Mal         Grand mal
     Absence Sz        aka Convulsions
     Children          Common

     No LOC            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                          Complex
     Localized clonic                Change in
      activity                         behavior
     Abnormal sensory                Preceded by aura
      symptoms                        Repetitive motor
     Usually no LOC                   behavior
     May progress                    No recall
         Jacksonian   March          May progress
         (Seizure)
                       Partial Seizures
   Simple partial seizures
    (No loss of consciousness)
       Focal motor seizures
         Localclonic 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

         Postictalphase
         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
          LgBore, 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?
        Anti-seizure Medications
 Seizures caused by hyperactive brain
  areas
 Multiple chemical classes of drugs

     All have same approach
     Decrease propagation of action
      potentials
          Na+, Ca++ influx (delay
          depolarization/prolong repolarization)
          Cl- influx (hyperpolarize membrane)
     Anti-Seizure Medications
Benzodiazepines        Ion Channel Inhibitors
 diazepam (Valium)     carbamazepine

 lorazepam (Ativan)     (Tegretol)
Barbiturates            phenytoin (Dilantin)

 phenobarbital        Misc. Agents
  (Luminal)             valproic acid
                         (Depakote)
    Outline of Clinical Problems
   Altered mental status---most common consult
   Seizures
   Stroke
   Delirium/dementia
   Infections
   Focal weakness
   Diffuse weakness
   Trouble breathing
   Trouble swallowing
                               Seizures
 Gen tonic/clonic; complex partial;
  absence; myoclonic
 Causes usually metabolic
       Hypoxia, drugs, d/c AEDs
 Can be seen with strokes, infections
  (meningitis, encephalitis, abscess)
 Prolonged post-ictal phase

 Sub-clinical seizures--must use an EEG
       Cause of AMS

								
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