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Approach to
altered mental status & seizure
DrHambaliHaironi
DIFFERENTIAL DIAGNOSIS
History and physical findings, may be influenced by factors
such as patient’s age & medical co-morbidities
PRIMARY/ CNS
• Tumors
– Primary
– Metastatic
Hemorrhage
– Spontaneous
– Traumatic
Edema
– HTN enceph
– Obstructive hydrocephalus
– Tumor
Seizure
– Post-ictal state
– Todd’s paralysis
Dementia
– Degenerative
– Multi-infarct
Metabolic/Autoregulatory Hypo/hyper
-glycemia
-natremia
-calcemia
-thyroid
-thermia
Hypercarbia
Hypoxemia
Pharmacologic/Toxic Medication effects
– HTN
– Steroids
– Sedatives
– Analgesics
– Sleep aids
– Anticholinergics
– Polypharmacy
Alcohols
– ETOH
– Methanol/ethylene glycol
Illicit drugs
Withdrawal
– Alcohol
– Benzodiazepine
– Narcotic
Infectious Primary CNS
– Meningitis
– Encephalitis
– Abscesses
Other site of infection
– UTI
– Pneumonia
– Skin/decub ulcer
– Intra-abdominal
– Viral syndrome
Other Hypoperfusion states
– Cardiogenic
– Hypovolemic
– Hemorrhagic
– Distributive
Complicated migraine
Psychiatric dosorder
– Acute
– Chronic
Sundown/ICU psychosis
DEMENTIA
• Typically is a slow progressively degenerative process that is managed
by primary care physicians rather than in the ED.
• Sometimes families bring a dementia patient to the ED and the true
“emergency” is that they are no longer able to care for the patient at
home.
DELIRIUM (CONFUSIONAL STATE)
• Delirium is brain dysfunction resulting in alterations of both level of arousal and
thought content.
• Normal consciousness requires both arousal and cognition. Arousal is mediated primarily by brainstem nuclei (reticular activating system) while cognition and organized thought is dependent on cortical functioning.
• is caused by an underlying medical problem that has toxic or metabolic affects on
the brain.
• Delirium has a very poor prognosis unless the underlying cause is recognized and
remedied.
TYPES OF DELIRIUM
Hyperactive delirium
-restlessness (for example, pacing), agitation, rapid mood changes or hallucinations, and refusal to cooperate
with care.
Hypoactive delirium
-inactivity or reduced motor activity, sluggishness, abnormal drowsiness, or seeming to be in a daze.
Mixed delirium
-includes both hyperactive and hypoactive signs and symptoms. The person may quickly switch back and forth
from hyperactive to hypoactive states.
Psychosis
• Functional (psychiatric) changes in behavior
• a condition in which there is a loss of reality testing, disturbance of
though processes, and consequently change in behavior
Initial Actions and Primary Survey
Airway
• airway is open and protected
• check pulse-oximetry
• provide supplemental oxygen if needed
• Hypoxia is a potentially reversible cause of
AMS
Breathing
• Assess breathing
• Inadequate ventilation will lead to elevated levels of CO2 (respiratory
acidosis) and can cause AMS.
• In a patient with AMS and a depressed respiratory status, consider narcotic
narcotic overdose as a possible cause.
Circulation
• Can you feel good distal pulses?
• Is the blood pressure very high or low?
• What is the cardiac rhythm?
• Hypoperfusion starves the brain of oxygen and glucose and leads to AMS.
• Nonperfusing rhythms require immediate CPR and ACLS.
• Hypotension should prompt IV fluid bolus and an immediate search for the
the cause.
Neurologic
disability
• Use Glasgow Coma Score (GCS) or Alert Verbal painful unresponsive (AVPU) scale for a quick assessment of
level of consciousness.
• Look for seizure activity.
• Are the pupils equal and reactive?
• Pay attention to spontaneous movements.
• -Lack of movement on one side of the body night indicate stroke
• -Lack of movement below a certain level of the body could indicate spinal cord injury.
• If there is any suspicion of trauma the cervical spine should be stabilized.
Exposure
• Fully undress
• Perform a rapid head to toe
• -look for signs of trauma, dialysis access, infectious sources (such as catheters) or
• petechiae.
HISTORY
• Patients with an AMS are, by definition, difficult to derive a comprehensive and detailed history from. Family,
friends, caretakers, nursing home workers, witnesses are all invaluable sources of information. Make the
effort to contact them to ascertain the nature of the change in mental status.
• Can you tell me what you see different about your grandmother? → What’s she like on a good day? Does she
cook/do laundry for herself? Can she get around the house on her own? Can she be left alone? Can she hold
a conversation about current events?
• Can you describe how she is different? → Is she more quiet/agitated? Is she confused or forgetful? Is she
hallucinating?
• When did this change start? → Did this change come on suddenly or gradual? Is it continuous or does it wax
and wane (identify pattern)? Has it ever happened before (previous diagnosis)? Have there been any changes
in her medicines recently (polypharmacy)?
• What do you think might have caused this? → Does she administer her own medicines? Is she prone to falls?
Could she have gotten into someone else’s medicines or household poisons? Does she have parents or
siblings with similar conditions? Have there been any significant stressful events lately such as
hospitalization, loss of a love one or moving to an unfamiliar environment?
• Screen for delirium: → If the patient has an acute or fluctuating course, evidence of inattention and either
disorganized thinking or an altered level of consciousness (elevated or decreased), they have a very high
likelihood of having delirium.
• Medication
detailed review of medications (including nonprescription, health
supplements, home remedies) is critical. Has the patient recently
started or stopped any medications
PHYSICAL
• Head to toe
• GCS
• Vital signs
• Does the patient have a fever?
• Is the patient bradycardic or tacycardic?
• Is the patient bradypneic or tachypneic?
• Is the patient hypotensive or severely hypertensive?
• Neurologic status
• Level of alertness
• GCS score or AVPU scale (A=alert, V=responds to verbal stimuli, P=responds to painful stimuli,
U=unresponsive). A verbal description is helpful
• How difficult is it to keep the patient awake?
• Content of thought and speech
• Does the patient stay focused?
• Is their speech tangential?
• Is the patient appropriately oriented?
• Does the patient keep asking the same questions over and over (perseveration)?
• Are they reacting to internal stimuli?
• Assess for focal motor findings
• Is there weakness or pronator drift?
• Cranial nerve exam (especially pupils)
• Remember, the brainstem is where isolated structural or ischemic lesions can cause
decreased arousal. Decreased level of consciousness with cranial nerve findings is a
brainstem lesion until proven otherwise.
• Evaluate for tremulousness or abnormal reflexes
• Common in withdrawal states or metabolic derangements
• Cardiovascular exam
• Are there arrhythmias (a-fib) that predispose to embolic strokes?
• Is there a murmur? endocarditis?
• Is there evidence of good peripheral circulation?
• Are there pulmonary findings that indicate pneumonia (sepsis) or pulmonary edema
(hypoxia)?
• Are there bruits over the carotid arteries?
• Abdominal exam
• Is there ascites, caput medusa, liver enlargement or tenderness (hepatic encephalopathy)?
• Is the abdomen tender (appendicitis, intussusception, abdominal sepsis source, mesenteric
ischemia)?
• Genitourinary and rectal exam
• Is the patient making urine (uremic encephalopathy)?
• Are there signs or urinary, vaginal, prostatic or perineal infection?
• Is there melena or blood in the stool?
• Skin, extremity, musculoskeletal exam
• Are there petechiae (meningococcemia)?
• Is there a dialysis graft (uremic encephalopathy)?
• Are there track marks from injection drug abuse?
• Are there transdermal drug patches?
• Is the skin jaundiced (hepatic encephalopathy)?
• Is there nuchal rigidity or meningismus (CNS infection)?
• Are there signs of trauma (raccoon’s eyes, Battle ‘s sign, hemotympanum)?
• Are there infectious sources noted (decubitus ulcers, cellulitis, abscesses)?
• Are there masses or lymphadenopathy that might indicate cancer (paraneoplastic
syndromes)?
INVESTIGATIONS
• Metabolic or Endocrine causes
• Rapid glucose
• Serum electrolytes (Na+, Ca+)
• ABG or VBG (with co-oxymetry for carboxy- or met-
hemoglobinemia)
• BUN/Creatinine
• Thyroid function tests
• Ammonia level
• Serum cortisol level
• Toxic or medication causes
• Levels of medications (anticonvulsants, digoxin,
theophylline, lithium, etc.)
• Drug screen (benzodiazepines, opioids, barbiturates, etc.)
• Alcohol level
• Serum osmolality (toxic alcohols)
• Infectious causes
• CBC with differential
• Urinalysis and culture
• Blood cultures
• Chest X-ray
• Lumbar puncture (with opening pressure)
• Always CT first if you suspect increased ICP.
• Traumatic causes
• Head CT/ cervical spine CT
• Neurologic causes
• Head CT (usually start without contrast for trauma or
CVA)
• MRI (if brainstem/posterior fossa pathology suspected)
• EEG (if non-convulsive status epileptics suspected)
• Hemodynamic instability causes
• ECG
• Cardiac enzymes (silent MI)
• Echocardiogram
• Carotid/vertebral artery ultrasound
MANAGEMENT
• Beyond interventions required for the immediate life threats such as impending
cardiopulmonary collapse,
treatment should be geared towards correcting / treating the underlying pathology.
This may include;
Dextrose for hypoglycemia
Naloxone for opioid toxicity
Supportive care and sedation for agitated withdrawal states
Intravenous fluids for dehydration, hypovolemia, hypotension or hyperosmolar states
such as HHNS or hypernatremia
Empiric antibiotics for suspected meningitis, urosepsis, pneumonia, etc.
Rewarming or aggressive cooling for temperature extremes
Controlled reduction of blood pressure with nitroprusside, labetolol or fenoldepam
for hypertensive encephalopathy
Hypertonic saline for profound hyponatremia with seizures or AMS
Consider thiamine for suspected Wernicke’s encephalopathy
SEIZURE
• Provoked
-Acute central nervous system (CNS) insults, toxins, or acute
metabolic derangements
• Unprovoked
- Epilepsy
Classification of seizure
Generalized Seizures:
• Primary generalized non convulsive seizure classification
1. Absence
• Primary generalized convulsive seizure classifications
1. Tonic-clonic
2. Clonic
3. Tonic
4. Myoclonic
5. Atonic
• Secondary generalized seizure classifications
1. Convulsive
2. Nonconvulsive
Partial Seizures:
• Simple partial seizure classification of symptoms
1. Motor
2. Somatosensory
3. Autonomic
4. Psychic
• Complex partial seizure classification
1. With focal onset prior to alteration in consciousness
2. Without focal onset prior to alteration in consciousness
DIFFERENTIAL DIAGNOSIS
• Hypoglycemia
• Central nervous system infection
• Central nervous system vascular event
• Drug toxicity
• Psychiatric disorder
• Metabolic encephalopathy
• Migraine
• Transient global amnesia
Acute Management
1. Stabilization(ABC)
2. Vital sign monitoring and reflo
3. IV access
4. Administration of IV diazepam(IV valium)
5. If, at any time, breathing or ventilation is compromised, rapid
sequence intubation is recommended
Status epilepticus
• Status epilepticus is a condition resulting either from the failure of
the mechanisms responsible for seizure termination or from the
initiation of mechanisms, which lead to abnormally, prolonged
seizures
• It is a condition, which can have long-term consequences including
neuronal death, neuronal injury, and alteration of neuronal
networks, depending on the type and duration of seizures
Refractory status epilepticus
• is defined as on-going seizures following first- and second-line drug
therapy.
Super – refractory status epilepticus
• SE that continues or recurs 24 hours or more after the onset of
anaesthetic therapy, including those cases where SE recurs on the
reduction or withdrawal of anaesthesia .
Management of SE
1. Initial supportive management
• Place the patient on a smooth surface, if possible.
• Remove any harmful objects.
• Loosen tight clothing.
• Turn the patient to the left (or right, if left not possible) lateral position, and place
the head on a soft support (bundle of cloth or pillow).
• Avoid placing any objects in the patient’s mouth.
• Stay with the patient until he or she recovers fully, and gather information about
the patient’s background and epilepsy history.
• Get the patient to the nearest hospital if the seizure persists beyond 5 minutes, or
there is no recovery of consciousness after 30 minutes, significant fever, serious
injury, or a recent increase in seizure frequency.
2. Pre-hospital treatment
• The duration and recurrence rate of seizures may bereduced by proper
pre-hospital treatment by paramedical personnel including
buccal/intramuscular midazolam or rectal diazepam in the case
without venous access.
Treatment of convulsive SE
• In the event that the seizure does not stop vital parameters, including the blood
pressure, heart rate, oxygen saturation and ECG must be monitored.
• Oxygen is delivered through a high flow mask.
• Any suspicion of hypoglycaemia as the cause of the seizures, 50 ml of 50%
glucose should be given intravenously.
First line: Benzodiazepines (BDZ)
• IV diazepam is the principal first line AEDs used for prolonged seizures in
Malaysia.
• IV diazepam 0.15 mg/kg (10 mg for 60-70kg adult), repeated once after 10-20 min
if seizures continue
Second line: Phenytoin
• For sustained control or if seizures continue, phenytoin 15-18 mg/kg at an
infusion rate of ≤50 mg/min.
Refractory SE
• If the seizures persist, the patient should be referred to an anaesthesiologist for
ICU care and administration of barbiturates or other anaesthetic agents, including
thiopentone, midazolam, propofol or ketamine.
• Intubation will be necessary as respiratory depression and hypotension from the
seizure as well as the effects of the phenytoin or BDZ.
Thank You
Referrence :
1) Guide to the essential in emergency medicine , Shirley Ooi
2) Consensus Guideline on the management of epilepsy 2017
3) Emergency Medicine Practice ; Behavioral Emergencies ,Differintiating medical
from Psychiatric disease (Journal)

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altered mental state n seizure.pptx

  • 1. Approach to altered mental status & seizure DrHambaliHaironi
  • 3. History and physical findings, may be influenced by factors such as patient’s age & medical co-morbidities PRIMARY/ CNS • Tumors – Primary – Metastatic Hemorrhage – Spontaneous – Traumatic Edema – HTN enceph – Obstructive hydrocephalus – Tumor Seizure – Post-ictal state – Todd’s paralysis Dementia – Degenerative – Multi-infarct
  • 4. Metabolic/Autoregulatory Hypo/hyper -glycemia -natremia -calcemia -thyroid -thermia Hypercarbia Hypoxemia Pharmacologic/Toxic Medication effects – HTN – Steroids – Sedatives – Analgesics – Sleep aids – Anticholinergics – Polypharmacy Alcohols – ETOH – Methanol/ethylene glycol Illicit drugs Withdrawal – Alcohol – Benzodiazepine – Narcotic
  • 5. Infectious Primary CNS – Meningitis – Encephalitis – Abscesses Other site of infection – UTI – Pneumonia – Skin/decub ulcer – Intra-abdominal – Viral syndrome Other Hypoperfusion states – Cardiogenic – Hypovolemic – Hemorrhagic – Distributive Complicated migraine Psychiatric dosorder – Acute – Chronic Sundown/ICU psychosis
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  • 8. DEMENTIA • Typically is a slow progressively degenerative process that is managed by primary care physicians rather than in the ED. • Sometimes families bring a dementia patient to the ED and the true “emergency” is that they are no longer able to care for the patient at home.
  • 9. DELIRIUM (CONFUSIONAL STATE) • Delirium is brain dysfunction resulting in alterations of both level of arousal and thought content. • Normal consciousness requires both arousal and cognition. Arousal is mediated primarily by brainstem nuclei (reticular activating system) while cognition and organized thought is dependent on cortical functioning. • is caused by an underlying medical problem that has toxic or metabolic affects on the brain. • Delirium has a very poor prognosis unless the underlying cause is recognized and remedied. TYPES OF DELIRIUM Hyperactive delirium -restlessness (for example, pacing), agitation, rapid mood changes or hallucinations, and refusal to cooperate with care. Hypoactive delirium -inactivity or reduced motor activity, sluggishness, abnormal drowsiness, or seeming to be in a daze. Mixed delirium -includes both hyperactive and hypoactive signs and symptoms. The person may quickly switch back and forth from hyperactive to hypoactive states.
  • 10. Psychosis • Functional (psychiatric) changes in behavior • a condition in which there is a loss of reality testing, disturbance of though processes, and consequently change in behavior
  • 11. Initial Actions and Primary Survey Airway • airway is open and protected • check pulse-oximetry • provide supplemental oxygen if needed • Hypoxia is a potentially reversible cause of AMS Breathing • Assess breathing • Inadequate ventilation will lead to elevated levels of CO2 (respiratory acidosis) and can cause AMS. • In a patient with AMS and a depressed respiratory status, consider narcotic narcotic overdose as a possible cause. Circulation • Can you feel good distal pulses? • Is the blood pressure very high or low? • What is the cardiac rhythm? • Hypoperfusion starves the brain of oxygen and glucose and leads to AMS. • Nonperfusing rhythms require immediate CPR and ACLS. • Hypotension should prompt IV fluid bolus and an immediate search for the the cause.
  • 12. Neurologic disability • Use Glasgow Coma Score (GCS) or Alert Verbal painful unresponsive (AVPU) scale for a quick assessment of level of consciousness. • Look for seizure activity. • Are the pupils equal and reactive? • Pay attention to spontaneous movements. • -Lack of movement on one side of the body night indicate stroke • -Lack of movement below a certain level of the body could indicate spinal cord injury. • If there is any suspicion of trauma the cervical spine should be stabilized. Exposure • Fully undress • Perform a rapid head to toe • -look for signs of trauma, dialysis access, infectious sources (such as catheters) or • petechiae.
  • 13. HISTORY • Patients with an AMS are, by definition, difficult to derive a comprehensive and detailed history from. Family, friends, caretakers, nursing home workers, witnesses are all invaluable sources of information. Make the effort to contact them to ascertain the nature of the change in mental status. • Can you tell me what you see different about your grandmother? → What’s she like on a good day? Does she cook/do laundry for herself? Can she get around the house on her own? Can she be left alone? Can she hold a conversation about current events? • Can you describe how she is different? → Is she more quiet/agitated? Is she confused or forgetful? Is she hallucinating? • When did this change start? → Did this change come on suddenly or gradual? Is it continuous or does it wax and wane (identify pattern)? Has it ever happened before (previous diagnosis)? Have there been any changes in her medicines recently (polypharmacy)? • What do you think might have caused this? → Does she administer her own medicines? Is she prone to falls? Could she have gotten into someone else’s medicines or household poisons? Does she have parents or siblings with similar conditions? Have there been any significant stressful events lately such as hospitalization, loss of a love one or moving to an unfamiliar environment? • Screen for delirium: → If the patient has an acute or fluctuating course, evidence of inattention and either disorganized thinking or an altered level of consciousness (elevated or decreased), they have a very high likelihood of having delirium.
  • 14. • Medication detailed review of medications (including nonprescription, health supplements, home remedies) is critical. Has the patient recently started or stopped any medications
  • 15. PHYSICAL • Head to toe • GCS • Vital signs • Does the patient have a fever? • Is the patient bradycardic or tacycardic? • Is the patient bradypneic or tachypneic? • Is the patient hypotensive or severely hypertensive? • Neurologic status • Level of alertness • GCS score or AVPU scale (A=alert, V=responds to verbal stimuli, P=responds to painful stimuli, U=unresponsive). A verbal description is helpful • How difficult is it to keep the patient awake? • Content of thought and speech • Does the patient stay focused? • Is their speech tangential? • Is the patient appropriately oriented? • Does the patient keep asking the same questions over and over (perseveration)? • Are they reacting to internal stimuli?
  • 16. • Assess for focal motor findings • Is there weakness or pronator drift? • Cranial nerve exam (especially pupils) • Remember, the brainstem is where isolated structural or ischemic lesions can cause decreased arousal. Decreased level of consciousness with cranial nerve findings is a brainstem lesion until proven otherwise. • Evaluate for tremulousness or abnormal reflexes • Common in withdrawal states or metabolic derangements • Cardiovascular exam • Are there arrhythmias (a-fib) that predispose to embolic strokes? • Is there a murmur? endocarditis? • Is there evidence of good peripheral circulation? • Are there pulmonary findings that indicate pneumonia (sepsis) or pulmonary edema (hypoxia)? • Are there bruits over the carotid arteries? • Abdominal exam • Is there ascites, caput medusa, liver enlargement or tenderness (hepatic encephalopathy)? • Is the abdomen tender (appendicitis, intussusception, abdominal sepsis source, mesenteric ischemia)?
  • 17. • Genitourinary and rectal exam • Is the patient making urine (uremic encephalopathy)? • Are there signs or urinary, vaginal, prostatic or perineal infection? • Is there melena or blood in the stool? • Skin, extremity, musculoskeletal exam • Are there petechiae (meningococcemia)? • Is there a dialysis graft (uremic encephalopathy)? • Are there track marks from injection drug abuse? • Are there transdermal drug patches? • Is the skin jaundiced (hepatic encephalopathy)? • Is there nuchal rigidity or meningismus (CNS infection)? • Are there signs of trauma (raccoon’s eyes, Battle ‘s sign, hemotympanum)? • Are there infectious sources noted (decubitus ulcers, cellulitis, abscesses)? • Are there masses or lymphadenopathy that might indicate cancer (paraneoplastic syndromes)?
  • 18. INVESTIGATIONS • Metabolic or Endocrine causes • Rapid glucose • Serum electrolytes (Na+, Ca+) • ABG or VBG (with co-oxymetry for carboxy- or met- hemoglobinemia) • BUN/Creatinine • Thyroid function tests • Ammonia level • Serum cortisol level • Toxic or medication causes • Levels of medications (anticonvulsants, digoxin, theophylline, lithium, etc.) • Drug screen (benzodiazepines, opioids, barbiturates, etc.) • Alcohol level • Serum osmolality (toxic alcohols) • Infectious causes • CBC with differential • Urinalysis and culture • Blood cultures • Chest X-ray • Lumbar puncture (with opening pressure) • Always CT first if you suspect increased ICP. • Traumatic causes • Head CT/ cervical spine CT • Neurologic causes • Head CT (usually start without contrast for trauma or CVA) • MRI (if brainstem/posterior fossa pathology suspected) • EEG (if non-convulsive status epileptics suspected) • Hemodynamic instability causes • ECG • Cardiac enzymes (silent MI) • Echocardiogram • Carotid/vertebral artery ultrasound
  • 19. MANAGEMENT • Beyond interventions required for the immediate life threats such as impending cardiopulmonary collapse, treatment should be geared towards correcting / treating the underlying pathology. This may include; Dextrose for hypoglycemia Naloxone for opioid toxicity Supportive care and sedation for agitated withdrawal states Intravenous fluids for dehydration, hypovolemia, hypotension or hyperosmolar states such as HHNS or hypernatremia Empiric antibiotics for suspected meningitis, urosepsis, pneumonia, etc. Rewarming or aggressive cooling for temperature extremes Controlled reduction of blood pressure with nitroprusside, labetolol or fenoldepam for hypertensive encephalopathy Hypertonic saline for profound hyponatremia with seizures or AMS Consider thiamine for suspected Wernicke’s encephalopathy
  • 21. • Provoked -Acute central nervous system (CNS) insults, toxins, or acute metabolic derangements • Unprovoked - Epilepsy
  • 22. Classification of seizure Generalized Seizures: • Primary generalized non convulsive seizure classification 1. Absence • Primary generalized convulsive seizure classifications 1. Tonic-clonic 2. Clonic 3. Tonic 4. Myoclonic 5. Atonic • Secondary generalized seizure classifications 1. Convulsive 2. Nonconvulsive
  • 23. Partial Seizures: • Simple partial seizure classification of symptoms 1. Motor 2. Somatosensory 3. Autonomic 4. Psychic • Complex partial seizure classification 1. With focal onset prior to alteration in consciousness 2. Without focal onset prior to alteration in consciousness
  • 24. DIFFERENTIAL DIAGNOSIS • Hypoglycemia • Central nervous system infection • Central nervous system vascular event • Drug toxicity • Psychiatric disorder • Metabolic encephalopathy • Migraine • Transient global amnesia
  • 25. Acute Management 1. Stabilization(ABC) 2. Vital sign monitoring and reflo 3. IV access 4. Administration of IV diazepam(IV valium) 5. If, at any time, breathing or ventilation is compromised, rapid sequence intubation is recommended
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  • 27. Status epilepticus • Status epilepticus is a condition resulting either from the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms, which lead to abnormally, prolonged seizures • It is a condition, which can have long-term consequences including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures
  • 28. Refractory status epilepticus • is defined as on-going seizures following first- and second-line drug therapy. Super – refractory status epilepticus • SE that continues or recurs 24 hours or more after the onset of anaesthetic therapy, including those cases where SE recurs on the reduction or withdrawal of anaesthesia .
  • 29. Management of SE 1. Initial supportive management • Place the patient on a smooth surface, if possible. • Remove any harmful objects. • Loosen tight clothing. • Turn the patient to the left (or right, if left not possible) lateral position, and place the head on a soft support (bundle of cloth or pillow). • Avoid placing any objects in the patient’s mouth. • Stay with the patient until he or she recovers fully, and gather information about the patient’s background and epilepsy history. • Get the patient to the nearest hospital if the seizure persists beyond 5 minutes, or there is no recovery of consciousness after 30 minutes, significant fever, serious injury, or a recent increase in seizure frequency.
  • 30. 2. Pre-hospital treatment • The duration and recurrence rate of seizures may bereduced by proper pre-hospital treatment by paramedical personnel including buccal/intramuscular midazolam or rectal diazepam in the case without venous access.
  • 31. Treatment of convulsive SE • In the event that the seizure does not stop vital parameters, including the blood pressure, heart rate, oxygen saturation and ECG must be monitored. • Oxygen is delivered through a high flow mask. • Any suspicion of hypoglycaemia as the cause of the seizures, 50 ml of 50% glucose should be given intravenously. First line: Benzodiazepines (BDZ) • IV diazepam is the principal first line AEDs used for prolonged seizures in Malaysia. • IV diazepam 0.15 mg/kg (10 mg for 60-70kg adult), repeated once after 10-20 min if seizures continue
  • 32. Second line: Phenytoin • For sustained control or if seizures continue, phenytoin 15-18 mg/kg at an infusion rate of ≤50 mg/min. Refractory SE • If the seizures persist, the patient should be referred to an anaesthesiologist for ICU care and administration of barbiturates or other anaesthetic agents, including thiopentone, midazolam, propofol or ketamine. • Intubation will be necessary as respiratory depression and hypotension from the seizure as well as the effects of the phenytoin or BDZ.
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  • 36. Referrence : 1) Guide to the essential in emergency medicine , Shirley Ooi 2) Consensus Guideline on the management of epilepsy 2017 3) Emergency Medicine Practice ; Behavioral Emergencies ,Differintiating medical from Psychiatric disease (Journal)

Editor's Notes

  1. Is a symptom which may range from slight confusion to coma Family came and tell that their dad become less responsive this morning General changes in brain function eg confusion Amnesia-loss memory Loss of alertness Disorientated-tie place person Defects in judgment or thought Unusual or strange behaviour Poor regulation of emotions Disruption of perception
  2. Simultaneous onset of electrical discharge throughout cortex ABSENCE -brief <10s, suddenly stop taking then resume back …childhood TONIC-CLONIC -x consciousness….limbs stiffen(tonic), then jerk(clonic)….post ictal: confuse+drowsy MYOCLONIC - Sudden jerk of limb -