Transcript Slide 1

Common
Neurologic
Emergencies
Tamer Belal, MD ,PHD 19 April
Lecturer of Neurology 2012
Mansoura University Hospitals
These are time sensitive situations in which
effective therapy may lessen or completely
reverse a potentially catastrophic insult to the
central nervous system
Stroke
Coma
Status
Eepilepticus
Coma
Definitions
Confusion.
Disturbance of consciousness characterised by impaired capacity
to think clearly and to perceive, respond to and remember current
stimuli; there is also disorientation.
Delirium
A state of much disturbed consciousness with motor restlessness,
transient hallucinations, disorientation and delusions.”
Obtundation A disturbance of alertness associated with psychomotor
retardation.
Stupor
A state in which the patient, though not unconscious, exhibits
little or no spontaneous activity.
Coma
A state of unrousable psychologic unresponsiveness in which the
subject lies with eyes closed and shows no psychologically
understandable response to external stimulus or inner need.
Case Report: Part 1
A 50-year-old man is found unconscious in the street. The patient is
transported to the emergency department. The paramedics report that the
patient is comatose with a Glasgow Coma Scale of 7 (no eye opening = 1;
unintelligible sounds = 2; nonspecific withdrawal movements = 4).
His breathing was noisy, but improved with a jaw thrust maneuver. He has
been placed on a backboard with spine precautions. His C-spine has been
immobilized. Vital signs are 140/90, 90 pulse, 24 respiratory rate, pulsoximetry
94%.
Oxygen at 6L/min by nasal cannula has been applied. An IV line is initiated.
Serum glucose level is 80. Cardiac monitor shows sinus rhythm. There was no
response to intravenous naloxone.
There is a nearly empty bottle of Thunderbird wine in his jacket along with a
full bottle of (phenytoin) Dilantin® capsules dated two weeks earlier
Case Report: Part 1
The patient smells of alcohol and his pants are urine stained. There are
numerous healed scars about the head with encrusted sutures along his right
parieto-occipital scalp.
His right pupil is 6 mm and does not appear to react, while the left is 3 mm
reactive. According to his buddies, he had been drinking more than usual
recently to alleviate a headache. He has been lying on the ground for several
hours.
Although the patient is a known alcoholic and appears to be in an alcoholic
stupor or perhaps in a postictal state, the history and physical examination
point to a more urgent situation.
The pupil asymmetry (presumably not due to a previous insult) suggests that
coma is due to brainstem compromise with herniation. Because acute or
chronic intracranial hematoma is the likely cause, the trauma team is notified.
History
A careful history, along with timely and appropriate interventions
is necessary in the management of patients presenting with an
altered level of consciousness
Obtain history from witnesses, friends, and family keeping in
mind that certain interventions must be performed while
gathering information.
Is there any history of trauma, seizures, diabetes, allergies or medical problem?
How long has the patient been unconscious?
Were there any bottles or medication containers at the scene?
Is the patient taking prescribed medications?
Is there anything special about the environment in which the patient was found?
Indoors or outdoors?
Any unusual odors?
Any others in the vicinity in a similar state?
Is the patient wearing a Medical Alert bracelet?
Interventions
Always assume there is a C-spine fracture
Ensure a patent airway maintaining C-spine precautions
If respirations are inadequate, a jaw-thrust or chin-lift maneuver
may assist respirations initially
Oxygen – Initially high- flow oxygen by nasal cannula or mask
Repeat and monitor vital signs including temperature
Intravenous line
ECG monitor
Thiamine –Wernicke’s encephalopathy may present as coma
In such patients, administer 100 mg of thiamine by intravenous
injection before giving glucose
Interventions
Glucose – If the patient is hypoglycemic, administer 50 cc
D50%W intravenously. In children give 2 cc/kg of D25W
NB: If the patient is not hypoglycemic, giving a glucose load to a patient with a
stroke or other brain injury may aggravate the brain damage
Naloxone - Give 2 mg. intravenously. Be prepared for the patient
who is a narcotic overdose individual to awaken in response to
the naloxone and to become combative and resist further medical
evaluation.
Review responses to glucose, thiamine, naloxone and oxygen
With the airway protected, an orogastric tube for gastric lavage is
inserted and activated charcoal is instilled when there is a
possibility of a toxic ingestion
Interventions
A Foley catheter is inserted for obtaining urine for laboratory
tests and monitoring urine output.
Observe for status epilepticus . A rhythmical twitching of some of
the digits of either hand or a rhythmical small amplitude
horizontal jerking of the eyes may be the only clue that the
patient is in status epilepticus.
If meningitis is suspected, perform a lumbar puncture
If a unilaterally dilated pupil (sluggish or unresponsive to light) is
present, suggesting uncal cerebral herniation, the patient is
hyperventilated to a pCO2 of about 30 to 35mmHg and given
mannitol IV at 1 gram/kg as a temporizing measure for the
increased intracranial pressure. Obtain a head CT scan while
neurosurgery consultation is requested emergently
Physical Examination
Confirm the comatose state
Use the Glasgow Coma Scale to assess the degree of coma
prior to intubation and the use of paralytic or sedative
agents.
Components Of The Physical Examination
Vital Signs
Motor System
Head
Skin
Neck
Lungs, Cardiac,
Abdomen
·Eyes
Extremities
Glasgow Coma Scale
Eye Opening
Response
Verbal
Response
Motor
Response
Spontaneous--open with blinking at baseline
4
Opens to verbal command, speech, or shout
3
Opens to pain, not applied to face
2
None
1
Oriented
5
Confused conversation, but able to answer questions
4
Inappropriate responses, words discernible
3
Incomprehensible speech
2
None
1
Obeys commands for movement
6
Purposeful movement to painful stimulus
5
Withdraws from pain
4
Abnormal (spastic) flexion, decorticate posture
3
Extensor (rigid) response, decerebrate posture
2
None
1
Case Report: Part 2
On arrival at the emergency department, the rescue squad's findings were
confirmed. The patient was comatose with a nonreactive 6mm right pupil. In
response to noxious stimuli, his left side moved much less than the right.
Immediately, the C-spine was examined radiologically and the patient was
intubated, slightly hyperventilated, and placed on a ventilator with 100%
oxygen.
Mannitol 100 grams was given intravenously and a CT of the head obtained.
The neurosurgeon was at the bedside and the operating room staff were
notified of possible emergent surgery.
Preoperative laboratory and X-ray studies were performed
Differential Diagnosis
Is the coma due to a primary central nervous system disease or
the consequence of a systemic illness?
The first 10 items in the differential diagnosis list below are
the most life- and function threatening.
The first 10 items in the differential diagnosis list below are the most
life- and function threatening.
1) Shock or Hypertensive encephalopathy: decreased cardiac output,
myocardial infarction, congestive heart failure, and pulmonary embolus
2) CO2 Narcosis or Hypoxia: pulmonary disease, hypoventilation
3) Hyperthermia or Hypothermia
4) Hypoglycemia (insulin overdose)
5) Wernicke's encephalopathy (thiamine deficiency)
6) Exogenous toxins (eg, opiates, carbon monoxide, cyanide, barbiturates,
benzodiazepines, antidepressants, antihistamines, atropine, organic phosphates,
bromides, anticholinergics, ethanol, methanol, ethylene glycol, hallucinogens,
ammonium chloride, heavy metals, over the- counter drugs including salicylates)
7) Stroke (ischemic)
8) Intracranial hemorrhage (with or without trauma): subarachnoid
hemorrhage, intracerebral hematoma, epidural hematoma, subdural
hematoma
9) Meningitis: bacterial, syphilis, fungal, carcinomatous Encephalitis:
Herpes simplex
10)Reye's syndrome (pediatric )
The first 10 items in the differential diagnosis list below are the most
life- and function threatening.
11) Trauma: diffuse axonal injury to the brain without significant intracranial
hemorrhage
12) Tumor: CNS meningioma, glioma, and remote effects (e.g., lung cancer)
13) Toxin: mercury, arsenic, lead, and magnesium.
14) Infections: sepsis, any infection outside of CNS especially in elderly, AIDS,
subacute bacterial endocarditis (SBE).
15) CNS Infections: progressive multifocal leukoencephalopathy, CreutzfeldtJakob disease
16) Seizures: status epilepticus, including non-convulsive; prolonged postictal state
17) Blood: anemia, sickle cell disease
18) Vascular: systemic lupus erythematosis (SLE)
19) Metabolic: hypercalcemia ,uremic encephalopathy , hepatic encephalopathy
hyperosmolar state, thyrotoxicosis or myxedema coma, Cushing's disease
pituitary apoplexy, porphyria
20) Psychiatric: especially depression; hysterical conversion reaction
21) Other: migraine, basilar (especially in children) intussusception in children
Diagnostic Adjuncts
Laboratory Evaluation
CBC, differential, platelets
Serum glucose, electrolytes, calcium, magnesium, phosphorus
Renal function tests
Hepatic function tests
Arterial blood gases; carboxyhemoglobin level
Urine for urinalysis and toxicology studies, myoglobin and porphobilinogen
ECG
CT scan
Thyroid function studies
Lumbar puncture for CSF cells, protein, sugar, India ink prep, fungal cultures,
and extra tubes as needed
EEG (immediately if suspect status epilepticus)
Alcohol level
Case Report: Part 3
The CT scan showed a large right parieto-occipital chronic subdural
hematoma, which probably explains the patient's recent headaches.
There was fresh blood within the chronic subdural. This recent bleeding
probably resulted in the patient's acute decompensation.
The patient was taken immediately to the operating room to have the subdural
hematoma evacuated
Case Report: Part 4
After evacuation of the subdural hematoma, the patient had an uneventful
course and recovered completely
Referral
Transfer should be considered when
The patient is stable enough to be transferred and definitive
care exists which your facility does not offer
If there is uncertainty regarding the diagnosis or management
If the clinician does not have privileges to provide the type of
care needed (e.g., surgery),
The clinician is ethically opposed to providing care (e.g.,
hospice care, or the opposite, definitive care at the patient’s/
family’s request when it would be futile).
Referral
Transfer should be considered when
When there is a conflict (e.g., personality conflict or the patient
is a close friend or family member) and the clinician feels they
cannot be objective.
As a second opinion may be wise when the diagnosis is
unexpected (e.g., young person with severe injury), serious, the
prognosis is grim or the patient is not getting better
If the patient requests a consultation.
There is inadequate equipment (e.g., no dialysis, CT or EEG)
or facilities (e.g., limited ICU) in your hospital
Specific examples of consultation for neurologic emergencies include
All neurologic emergencies requiring surgery,
Status epilepticus requiring general anesthesia,
For rehabilitation for neurological emergencies with sequelae
if the clinician is not comfortable.
Psychosocial Impact
Surviving a neurological emergency can be very stressful for
the patient and/or family members.
Survivors of neurologic emergencies with risk of recurrence go
through many of the same stages of any patient receiving bad
news:
denial,
anger,
bargaining, (depression )
resolution.
caregiver burnout
ISCHEMIC
STROKE
Incidence of Ischemic Stroke by Subtype
Stroke Subtype
Incidence
Cardioembolic
30%
Atherothrombotic (large vessel) disease
30%
Lacunar (small vessel) disease
25%
Other (vasculitis, dissection, hypercoagulable state)
10%
Cryptogenic
5%
Succinct Approach to the Stroke Patient
WHERE – Neuroanatomical localization
WHERE – Vascular localization
WHEN – Profile of onset
HOW – Vascular mechanism
Common conditions mimicking acute stroke
Hypoglycemia
Mass Lesion
Complex Migraine
Seizure with postical Todd’s paralysis
Ion channels dysfunctions (channelopathies)
Psychiatric disorders with functional focal defi cits
Is this a vascular event
Are the neurological symptoms focal rather than non-focal?
Are the focal neurological symptoms negative (that is, loss
of function) rather than positive (for example, pins and
needles rather than numbness)?
Was the onset of the focal symptoms sudden?
Were the focal symptoms maximal at onset (that is, coming
on over minutes to hours) rather than progressive (that is,
evolving over hours to days)?
Causes of deterioration after stroke
Neurological
Non-neurological:
Progression/completion of stroke
Infection*
Extension/early recurrence
Metabolic derangement
Haemorrhagic transformation of an infarct
Drugs*
Developing cerebral oedema
Hypoxia*
Obstructive hydrocephalus*
Hypercapnia*
Epileptic seizures*
Incorrect diagnosis
*Potentially reversible causes
Algorithm for Management of Acute Ischemic Stroke
Clinical Evaluation
History
Time of onset (for patients who cannot provide
information, use the time when they were last
seen normal) and circumstancesHistory
Time of onset (for patients who cannot provide
information, use the time when they were last
seen normal) and circumstances
Recent events: strokes, chest pain, MI, trauma,
surgery, bleeding
Comorbidities: HTN, DM, Cardiac disease,
hyperlipidemia, smoking, allergies (iodine)
Medications: anticoagulants, antihypertensives,
antiplatelets, antidiabetics, antiarrhythmics
Exam
GENERAL:
ABC, Oxg Sat, temperature, signs of trauma or
seizures, carotid bruits, CHF, arrhythmias,
abdominal and skin exam to identify comorbities
(hepatic dysfunction, coagulopathies and etc)
Use NIH Stroke Scale
NEUROLOGICAL:
Localize and Identify Stroke Syndrome
Labs/Imaging Evaluation
All Patients
Brain imaging: CT or MRI (preferably multimodal)
Fingerstick glucose, CBC, BMP
ECG
Cardiac enzymes
PT/PTT/INR
Oxygen saturation
Selected Patients
LFT
CXR
Urinalysis
Tox Screen
Blood ETOH levels
AED levels
ABG
CSF (if SAH is suspected and HCT is negative)
B-HCG (for all women of child bearing potential)
Candidate for Recanalization? > refer to recanalization algorithm
Algorithm for Management of Acute Ischemic Stroke
Candidate for Recanalization? > refer to recanalization algorithm
Yes
Contact Acute Stroke team and proceed per
recanalization algorithm
No
Pt stable for stroke unit (no risk of
malignant edema, not intubated and no
severe comorbidities)?
Recanalization performed?
No
Yes
Yes
No
Admit to Neuro ICU and follow early subacute stage
algorithm plus specific instructions from Neuro ICU team
Admit to telemetry bed and
follow early subacute stage
algorithm
Recommended Target time points for evaluation of
acute stroke patients.
Time from ED arrival
Action
10 minutes
Evaluate potential stroke patient (ED physician)
15 minutes
Notify stroke team or physician with stroke expertise
25 minutes
Initiate head CT
45 minutes
Interpret head CT
60 minutes
Administer IV tPA
Case Report
You have just completed your morning rounds at the hospital, and are informed
that a long-time patient has notified your office that her husband (a 65-year-old
man who has always been in excellent health and on no medications) is en route to
the Emergency Department (ED).
You go directly to the ED where the paramedics arrive at 8AM. They report that
the patient’s wife called 911 when she noticed upon awakening at 7:30 AM her
husband was having difficulty speaking, his face was crooked and his right arm
was limp at his side.
They had established an intravenous line, obtained a blood glucose measurement of
120 mg/dL, and placed the patient on low-flow oxygen by nasal canulae. Blood
pressure in the field was 200/100 mm Hg, and it was the same in the ED, heart rate
was 82 and regular, with a respiratory rate of 18. The patient's temperature was
recorded along with the initial vital signs in the ED as 37°C.
Case Report
You examine the patient and the key findings are neurologic.
There is no speech output but he seems to follow some simple commands (close
your eyes, lift up your arm),
There is right facial asymmetry, a right field cut to threat, a flaccid right arm with
no withdrawal to a painful stimulus to the nailbed digits of the right hand, and
spontaneous weak movement of the right leg compared to the left.
You join the Emergency Physician in providing care.
Question 1
Your initial management includes
Sublingual nifedipine
Chewable aspirin
Obtain an emergency head computerized tomography (CT) scan
All of the above
The patient goes to CT scan, monitored, with a nurse, and returns from the CT scan
15 minutes later.
The radiologist's preliminary report is that the CT scan is negative.
Reassessment shows that there is no change in the patient's clinical state, except
the BP is now 150/80 mmHg
Question 2
Your management includes
Ordering tissue plasminogen activator (t-PA) at 0.9 mg/kg
Ordering a heparin infusion at 10 units/kg/hour
Performing a lumbar puncture before either 1 or 2
None of the above
None of the above
Case Report
Minutes later the patient’s wife arrives. She states that she and her husband had
arisen early that morning, awakening in time to catch a beautiful sunrise. At that
time her husband was perfectly normal. They returned to bed at 6:30 AM, and
when they awoke at 7:30 AM, he was noted to have the neurologic deficit. She
knows he's having a stroke and is asking that you do something.
You re-evaluate the patient. He's neurologically the same.
The radiologist states the CT scan shows no hemorrhage and there are no early
infarct signs.
The nurse provides you with the blood test results from clinical laboratory. A
complete blood count including platelets, glucose, electrolytes, renal function tests,
prothrombin time and partial thromboplastin time are all within normal limits.
Question 3
Your management includes
Ordering t-PA at 0.9 mg/kg, 10% initial bolus, and the remainder over an hour because
the patient has a greater likelihood of functionally independent recovery with minimal
or no disability than without t-PA therapy, despite a 6% increase in the likelihood of a
symptomatic intracerebral hemorrhage.
Ordering 1,000,000 units of streptokinase (SK) since SK is minimally more effective
compared to t-PA for acute stroke and is less expensive
Withholding thrombolytic therapy for the acute ischemic stroke since the patient
cannot give informed consent
Withholding thrombolytic therapy for acute ischemic stroke until the patient's private
physician arrives since it is now only just over 2 hours from stroke onset and the
patient may still be suffering only a transient ischemic attack.
Case 1
A 72-year-old woman with a past medical history of arthritis, diabetes mellitus,
coronary artery disease, and stroke presented to the ICU in a coma. Apparently, she
had been found slumped over in a chair earlier in the day by her husband.
At the time he found her, she was confused and combative. By the time emergency
medical services arrived at the home, she was comatose. They quickly intubated
her, supported her low blood pressure, and transported her to the ICU.
The neurologist was called to see the patient to determine the cause of the coma.
In further discussion, the husband denied that the patient had hit her head,
complained of chest pain, or had an obvious seizure. He claimed she had been
feeling ill for a few days and had not had much of an appetite. According to him,
she had never had an episode like this before.
Review of her medications showed medicines appropriate for her disease history
without any narcotics. The husband denied any illegal drug use.
The neurologist was asked to comment on the cause of the coma and order more
tests if necessary.
Case 1
Comment
This type of coma, preceded by an episode of combativeness and delirium, is
commonly associated with seizures or metabolic problems.
The most important entity to rule out here is hypoglycemia. Since the patient is
taking hypoglycemic medications for her diabetes and she has had a suppressed
appetite, it is likely she is hypoglycemic.
It is critical to search for this condition because the correction of the blood
glucose level can lead to significant recovery.
Hypoxia is the second derangement that could lead to rapid recovery.
Other entities, including seizures, encephalitis, stroke, intracerebral hemorrhage,
and metabolic derangements, can be investigated in turn after hypoglycemia and
hypoxia are ruled out.
STATUS
EPILEPTICUS
Definition
Patient does not recover to a normal alert state between two or
more tonic clonic seizures or duration of seizures greater than
20 minutes.
Although most epileptic seizures are self-limited, some go on
for prolonged periods, whereas others recur so rapidly that the
condition is referred to as status epilepticus.
The most serious form of this disorder is generalized
convulsive status epilepticus, in which convulsive seizures are
repeated without return of consciousness in between.
Treatment of the premonitory stages is likely to be more successful
than treatment in the later stages and so treatment should commence
as soon as it is apparent that the seizure is persisting (a tonic-clonic
seizure of more than five minutes duration) or there is a significant
worsening of a patient’s normal seizure pattern
Status epilepticus to account for about 4% of admissions to
neurological intensive care, and 5% of all visits to a university
hospital casualty department
The mortality of status epilepticus is about 20%.
Permanent neurological and mental deterioration may result from
status epilepticus, particularly in young children, the risks of
morbidity being greatly increased the longer the duration of the status
epilepticus episode
Medical complications in tonic-clonic status epilepticus
Cerebral
Hypoxic/metabolic cerebral damage
Seizure-induced cerebral damage
Cerebral oedema and raised intracranial pressure
Cerebral venous thrombosis
Cerebral haemorrhage and infarction
Hypotension
Hypertension
Cardiac failure, tachy- and bradyarrhythmia, arrest
Cardiovascular Cardiogenic shock
Respiratory failure
respiratory
autonomic
Disturbances of respiratory rate and rhythm, apnoea
Pulmonary oedema, hypertension, embolism
Pneumonia, aspiration
Hyperpyrexia
Sweating, hypersecretion, tracheobronchial obstruction
Peripheral ischaemia
Medical complications in tonic-clonic status epilepticus
Metabolic
Other
Dehydration
Electrolyte disturbance (especially hyponatraemia,
hyperkalaemia,
hypoglycaemia)
Acute renal failure (especially acute tubular necrosis)
Acute hepatic failure
Acute pancreatitis
Disseminated intravascular coagulopathy/multiorgan failure
Rhabdomyolysis
Fractures
Infections (especially pulmonary, skin, urinary)
Thrombophlebitis, dermal injury
Goals of Treatment
Terminate seizure activity as soon as possible, preferably within 30
minutes of onset
Prevent recurrence of seizures.
Ensure adequate cardiorespiratory function and brain oxygenation by
establishment and maintenance of an adequate airway and support of
blood pressure.
Correct any precipitating factors (e.g., hypoglycemia, hyponatremia,
hypocalcemia, or fever).
Prevent or correct any systemic complications, especially
hyperpyrexia, which may exacerbate neuronal damage cased by the
continuous seizure activity.
Evaluate and treat possible causes of the episode of status epilepticus.
Management of tonic-clonic status epilepticus (General measures)
First stage
(0–10 minutes)
Assess cardiorespiratory function
Secure airway and resuscitate
Administer oxygen
Second stage
(0–60 minutes)
Institute regular monitoring (see text)
Emergency antiepileptic drug therapy (see text)
Set up intravenous lines
Emergency investigations (see text)
Administer glucose (50 ml of 50% solution) and/or
intravenous thiamine (250 mg) as high potency intravenous
Pabrinex where appropriate
Treat acidosis if severe
Management of tonic-clonic status epilepticus (General measures)
Third stage
(0–60/90) minutes)
Forth stage
(30–90 minutes)
Establish aetiology
Identify and treat medical complications
Pressor therapy where appropriate
Transfer to intensive care
Establish intensive care and EEG monitoring (see text)
Initiate seizure and EEG monitoring
Initiate intracranial pressure monitoring where appropriate
Initiate long term, maintenance, antiepileptic therapy
These four stages should be followed chronologically; the first and second
within 10 minutes, and stage 4 (transfer to intensive care unit) in most
settings within 60–90 minutes of presentation.
An ideal antiepileptic drug should
Have no active metabolites (diazepam, midazolam, lidocaine (lignocaine),
and thiopentone have active metabolites)
Not interact with other medication
Not have saturable metabolism (both phenytoin and thiopentone have
saturable pharmacokinetics at therapeutic levels)
Not be unduly affected by hepatic or renal blood flow or disease
(chlormethiazole is an example of a drug whose metabolism is greatly
affected by both hepatic disease and changes in hepatic blood flow)
Show no tendency to autoinduction (thiopentone, phenobarbitone, and
phenytoin are all subject to strong autoinduction)
Have strong antiepileptic action (the non-barbiturate anaesthetics have little
or no intrinsic antiepileptic action – a conundrum for their use in status
epilepticus, the implications of which have not been fully considered)
Be stable in solution and unreactive with giving sets (a problem with
paraldehyde, diazepam, and thiopentone).
Management of tonic-clonic status epilepticus (Drug treatment)
Premonitory stage
(pre-hospital)
Early status
Diazepam 10–20 mg given rectally, repeated once 15 minutes
later if status continues to threaten
If seizures continue, treat as below
Lorazepam (IV) 0·07 mg/kg (usually a 4 mg bolus, repeated
once after 10–20 minutes; rate not critical)
If seizures continue 30 minutes after first injection, treat as
below
Management of tonic-clonic status epilepticus (Drug treatment)
Established status
Phenytoin infusion at a dose of 15–18 mg/kg at a maximum rate
of 50 mg/min or fosphenytoin infusion at a dose of 15–20 mg
PE/kg at a maximum rate of 100 mg PE/minute
and/or
Phenobarbitone bolus of 10 mg/kg at a rate of 100 mg/min
(usually 700 mg over seven minutes in an adult)
Refractory status
General anaesthesia, with propofol, midazolam, or thiopentone.
Anaesthetic continued for 12–24 hours after the last clinical or
electrographic seizure, then dose tapered
In the above scheme, the refractory stage (general anaesthesia) is reached
60/90 minutes after the initial therapy. This scheme is suitable for usual
clinical hospital settings. In some situations, general anaesthesia should be
initiated earlier and, occasionally, should be delayed.
Common reasons for the failure of emergency drug therapy to
control seizures in status epilepticus
Inadequate emergency antiepileptic drug therapy (especially the
administration of drugs at too low a dose)
Failure to initiate maintenance antiepileptic drug therapy (seizures will recur
as the effect of emergency drug treatment wears off)
Hypoxia, hypotension, cardiorespiratory failure, metabolic disturbance
Failure to identify the underlying cause
Failure to identify other medical complications (including hyperthermia,
disseminated intravascular coagulation, hepatic failure)
Misdiagnosis (Pseudostatus epilepticus is a common differential diagnosis
that is often missed)
Thank you