https://wikem.org/w/api.php?action=feedcontributions&feedformat=atom&user=Ncdavis 2026-05-07T02:54:35Z User contributions MediaWiki 1.38.2 https://wikem.org/w/index.php?title=Status_epilepticus&diff=15491 2013-12-29T16:11:19Z

<p>Ncdavis: </p> <hr /> <div>=Overview=<br /> *Seizures are abnormal neuronal activity with various neurological sequale.<br /> **Further defined by whether they involve 1 hemisphere (partial) or both hemispheres (generalized). While generalized seizures surely cause an alteration in mental status, seizures involving one hemisphere (partial) may further be subdivided by whether they maintain baseline mental status (simple) or an alteration (complex). <br /> *Epilepsy is defined a 2 or more epileptic seizures that occur unprovoked by any identifiable cause. This include all seizure events with the exception of febrile or neonatal seizures. <br /> **Further subclassified into cryptogenic (meaning unknown cause) or symptomatic (meaning associated with previous CNS insult). <br /> ***Symptomatic seizures further subdefined as acute or remote (depending on if &gt; or &lt; 1 week after CNS insult)<br /> *Status epilepticus is the persistence of seizure beyond 30 minutes. (includes either persistent clinical seizure activity OR no return to consciousness during that timeframe or between attacks. <br /> **Functionally presume people to be in status if clinically seizing beyond 5 minutes<br /> **Status Epilepticus can be defined as “convulsive” (meaning obvious clinical signs of seizure activity –tonic clonic/myoclonic/tonic) or “Nonconsulsive” meaning no obvious signs of activity but decreased level of consciousness. <br /> ***NCSE (Non consulsive status) is a critical and relevant consideration. Up to 50% of patients with generalized tonic-clonic seizures will have NCSE after convulsions have subsided.<br /> *Seizure type and associated EEG findings are at core of determining risk of recurrence and indication for antiepileptic therapy. Follow the “seizure” link (pending Jan 2014) for more information on the non-acute general treatment of seizures. <br /> <br /> ==Management of acute status epilepticus==<br /> Overview<br /> *The general theme of seizure treatment is to<br /> #Address immediate concerns (ABC’s) (primarily referring to airway/breathing) <br /> ##Constantly return to evaluate this for the duration of seizure episode<br /> ###continuously monitor O2 saturations via pulse oximetry<br /> ###periodic blood gases to evaluate for CO2 retention and lactic acidosis (q10-15mins- up to clinical judgement).<br /> #Manage the seizure activity with medications along with investigation/correction of causes. <br /> ##Treat quickly; Do not hold medications. Treatment initiated in first 30 minutes has 80% response. Drops to 40% around two hours<br /> ###Medication regimes include a benzodiazepine to terminate seizure in immediate term and an anti-epileptic drug (AED) to continue longer term neuronal suppression. Continued seizure activity is treated by additive AED’s and/or sedating medications.<br /> ###Very often phenytoin is used for AED (Cost and plethora of studies) however alternatives exist Leveteriacetam, lacosamide, valproate with lesser side effect profile. You may refer to pharmacy for assistance with typical protocol, otherwise phenytoin is acceptable and can always be changed to another AED later.<br /> ===Take a Stepwise Approach: Timeline===<br /> ====0-5 minutes====<br /> #Is this patient still seizing ? (look for return of consciousness) or if on EEG look to EEG (Reading EEGs link to come).<br /> ##If this is first episode, may await seizure to break however ready materials to be given should seizure persist greater than 5 minutes<br /> #Protect patient<br /> ##turn on side prn for airway protection if vomitting to attenuate aspiration events. Remove any obvious dangerous material that may hurt the patient. <br /> ##DO NOT, try to limit patient movement by holding extremities down. DO NOT place bite block (risk of occluding airway).<br /> #Obtain Diagnostic labs (CBC, CEM 10, LFT, coagulation, AED levels (If indicated: assess if therapeutic), ECG, troponins, toxicology screen, pregnancy test (preparation for possible CT), blood gas, continuous SaO2, BP and continuous ECG.<br /> #Ready medications to be given if seizure persists &gt; 5 minutes<br /> ##lorazepam (0.1mg/kg max given in 2-4 mg aliquots )<br /> ## AED loading agent (Fosphenytoin 20mg/kg)<br /> ## Thiamine 100mg IV along with 50ml D50IV.<br /> #Briefly familiarize patient H+P to help guide diagnostic causes<br /> ##PMHx: Sz History? (get AED levels/home dosages), CNS insults?<br /> ###description of previous seizures semiology (if applicable) – jerking/automatisms/gaze deviation<br /> ##Medications: anything that reduces seizure threshold?<br /> ##Physical Exam: Neuro evaluation <br /> ###while in convulsive status patient is obviously seizing and one should continue timeline for acute treatment. The neuro exam is primarily focused on identifying 1. Neuro signs to help localize seizure focus 2.identifying NCSE; focusing on recognizing an improvement of wakefulness/mental status.<br /> ####No improvement in wakefulness &gt;20 minutes or continued AMS &gt; 30-60 minutes prompts concern for NCSE and requires 24-48hr cEEG<br /> <br /> ====6-10 minutes (seizure persists)====<br /> #Administer thiamine 100mg IV along with 50ml D50IV (empirically for possible hypoglycemia)<br /> ##May forego if hypoglycemia ruled out with recent CEM panel.<br /> #Administer the 2-4mg lorazepam aliquot over 2 minutes. <br /> ##Repeat 1x (max dose 0.1mg/kg) if seizure continues another 5 minutes.<br /> ##If no IV access available. Diazepam may be given rectally (20mg PR) or Midazolam (10mg intrabucally/intranasally). <br /> ====10-20 minutes ====<br /> #Admin AED loading agent (Fosphenytoin 20mg/kg). MAX INFUSION RATE 150mg/min<br /> ##Phenytoin associated with hypotension. Fosphenytoin use attenuates some of this risk however still significant. Administer with frequent BP checks and ECG monitoring. <br /> ###Continue AED maintenance with target phenytoin level 2-3 G/mL after seizure subsides (typically qd checks). Defer to neurology for long term AED management.<br /> ##If seizure persists may rebolus 1x with additional Fosphenyoitn 10mg/kg bolus.<br /> #OTHER OPTION<br /> ##if patient on AED at home, may reload with home medication: Some examples below<br /> ###IV valproate: 20mg/kg over 10 minutes. May re bolus (same dose) 1x if seizure persists &gt; 5 minutes following<br /> ###IV keppra 1000-4000mg IV<br /> #Reassess ABC status<br /> #Make arrangements for possible ICU transfer ( If applicable - as next step is intubation).<br /> <br /> ====20-60 minutes (refractory status epilepticus====<br /> #Intubate for airway protection (As we will definitively sedate to the point of respiratory compromise) <br /> #Place arterial line (Continuous BP monitoring with propofol infusion)<br /> #Medications (May use propofol as pressure tolerates, otherwise midazolam; Typically start with propofol since may regain neuro exam faster, and add midazolam). <br /> ##IV propofol (causes hypotension)<br /> ### 1mg/kg bolus with continued boluses (same dose) every 3-5 minutes until seizures stop (As BP tolerates). <br /> ###May place on cIV infusion 1-15 mg/kg/h (Do not exceed &gt;5mg/kg/h in 24 hrs)<br /> ##IV midazolam (less hypotension, longer sedation than propofol)<br /> ###0.2mg/kg bolus with repeat boluses (Same dose) every 5 minutes until seizures stop (max dose 2mg/kg)<br /> ###May place on cIV 0.05-2.0 mg/kg/h (up to 200mg/h for 70kg patient).<br /> <br /> ====&gt; 60 minutes ====<br /> #Place in pentobarbital coma<br /> ##5 mg/kg up to 50mg/min. Repeat boluses (same dose) until seizure stop.<br /> ##cIV 1mg/kg/h titrated to suppression on cEEG.<br /> <br /> ==References==<br /> &lt;references/&gt;<br /> <br /> [[Category:Neuro]]</div>

Ncdavis https://wikem.org/w/index.php?title=Status_epilepticus&diff=15490 2013-12-29T16:08:05Z

<p>Ncdavis: </p> <hr /> <div>=Overview=<br /> *Seizures are abnormal neuronal activity with various neurological sequale.<br /> **Further defined by whether they involve 1 hemisphere (partial) or both hemispheres (generalized). While generalized seizures surely cause an alteration in mental status, seizures involving one hemisphere (partial) may further be subdivided by whether they maintain baseline mental status (simple) or an alteration (complex). <br /> *Epilepsy is defined a 2 or more epileptic seizures that occur unprovoked by any identifiable cause. This include all seizure events with the exception of febrile or neonatal seizures. <br /> **Further subclassified into cryptogenic (meaning unknown cause) or symptomatic (meaning associated with previous CNS insult). <br /> ***Symptomatic seizures further subdefined as acute or remote (depending on if &gt; or &lt; 1 week after CNS insult)<br /> *Status epilepticus is the persistence of seizure beyond 30 minutes. (includes either persistent clinical seizure activity OR no return to consciousness during that timeframe or between attacks. <br /> **Functionally presume people to be in status if clinically seizing beyond 5 minutes<br /> **Status Epilepticus can be defined as “convulsive” (meaning obvious clinical signs of seizure activity –tonic clonic/myoclonic/tonic) or “Nonconsulsive” meaning no obvious signs of activity but decreased level of consciousness. <br /> ***NCSE (Non consulsive status) is a critical and relevant consideration. Up to 50% of patients with generalized tonic-clonic seizures will have NCSE after convulsions have subsided.<br /> *Seizure type and associated EEG findings are at core of determining risk of recurrence and indication for antiepileptic therapy. Follow the “seizure” link (pending Jan 2014) for more information on the non-acute general treatment of seizures. <br /> <br /> ==Management of acute status epilepticus==<br /> Overview<br /> *The general theme of seizure treatment is to<br /> #Address immediate concerns (ABC’s) (primarily referring to airway/breathing) <br /> ##Constantly return to evaluate this for the duration of seizure episode<br /> ###continuously monitor O2 saturations via pulse oximetry<br /> ###periodic blood gases to evaluate for CO2 retention and lactic acidosis (q10-15mins- up to clinical judgement).<br /> #Manage the seizure activity with medications along with investigation/correction of causes. <br /> ##Treat quickly; Do not hold medications. Treatment initiated in first 30 minutes has 80% response. Drops to 40% around two hours<br /> ###Medication regimes include a benzodiazepine to terminate seizure in immediate term and an anti-epileptic drug (AED) to continue longer term neuronal suppression. Continued seizure activity is treated by additive AED’s and/or sedating medications.<br /> ###Very often phenytoin is used for AED (Cost and plethora of studies) however alternatives exist Leveteriacetam, lacosamide, valproate with lesser side effect profile. You may refer to pharmacy for assistance with typical protocol, otherwise phenytoin is acceptable and can always be changed to another AED later.<br /> ===Take a Stepwise Approach: Timeline===<br /> ====0-5 minutes====<br /> #Is this patient still seizing ? (look for return of consciousness) or if on EEG look to EEG (Reading EEGs link to come).<br /> ##If this is first episode, may await seizure to break however ready materials to be given should seizure persist greater than 5 minutes<br /> #Obtain Diagnostic labs (CBC, CEM 10, LFT, coagulation, AED levels (If indicated: assess if therapeutic), ECG, troponins, toxicology screen, pregnancy test (preparation for possible CT), blood gas, continuous SaO2, BP and continuous ECG.<br /> #Ready medications to be given if seizure persists &gt; 5 minutes<br /> ##lorazepam (0.1mg/kg max given in 2-4 mg aliquots )<br /> ## AED loading agent (Fosphenytoin 20mg/kg)<br /> ## Thiamine 100mg IV along with 50ml D50IV.<br /> #Briefly familiarize patient H+P to help guide diagnostic causes<br /> ##PMHx: Sz History? (get AED levels/home dosages), CNS insults?<br /> ###description of previous seizures semiology (if applicable) – jerking/automatisms/gaze deviation<br /> ##Medications: anything that reduces seizure threshold?<br /> ##Physical Exam: Neuro evaluation <br /> ###while in convulsive status patient is obviously seizing and one should continue timeline for acute treatment. The neuro exam is primarily focused on identifying 1. Neuro signs to help localize seizure focus 2.identifying NCSE; focusing on recognizing an improvement of wakefulness/mental status.<br /> ####No improvement in wakefulness &gt;20 minutes or continued AMS &gt; 30-60 minutes prompts concern for NCSE and requires 24-48hr cEEG<br /> ====6-10 minutes (seizure persists)====<br /> #Administer thiamine 100mg IV along with 50ml D50IV (empirically for possible hypoglycemia)<br /> ##May forego if hypoglycemia ruled out with recent CEM panel.<br /> #Administer the 2-4mg lorazepam aliquot over 2 minutes. <br /> ##Repeat 1x (max dose 0.1mg/kg) if seizure continues another 5 minutes.<br /> ##If no IV access available. Diazepam may be given rectally (20mg PR) or Midazolam (10mg intrabucally/intranasally). <br /> ====10-20 minutes ====<br /> #Admin AED loading agent (Fosphenytoin 20mg/kg). MAX INFUSION RATE 150mg/min<br /> ##Phenytoin associated with hypotension. Fosphenytoin use attenuates some of this risk however still significant. Administer with frequent BP checks and ECG monitoring. <br /> ###Continue AED maintenance with target phenytoin level 2-3 G/mL after seizure subsides (typically qd checks). Defer to neurology for long term AED management.<br /> ##If seizure persists may rebolus 1x with additional Fosphenyoitn 10mg/kg bolus.<br /> #OTHER OPTION<br /> ##if patient on AED at home, may reload with home medication: Some examples below<br /> ###IV valproate: 20mg/kg over 10 minutes. May re bolus (same dose) 1x if seizure persists &gt; 5 minutes following<br /> ###IV keppra 1000-4000mg IV<br /> #Reassess ABC status<br /> #Make arrangements for possible ICU transfer ( If applicable - as next step is intubation).<br /> <br /> ====20-60 minutes (refractory status epilepticus====<br /> #Intubate for airway protection (As we will definitively sedate to the point of respiratory compromise) <br /> #Place arterial line (Continuous BP monitoring with propofol infusion)<br /> #Medications (May use propofol as pressure tolerates, otherwise midazolam; Typically start with propofol since may regain neuro exam faster, and add midazolam). <br /> ##IV propofol (causes hypotension)<br /> ### 1mg/kg bolus with continued boluses (same dose) every 3-5 minutes until seizures stop (As BP tolerates). <br /> ###May place on cIV infusion 1-15 mg/kg/h (Do not exceed &gt;5mg/kg/h in 24 hrs)<br /> ##IV midazolam (less hypotension, longer sedation than propofol)<br /> ###0.2mg/kg bolus with repeat boluses (Same dose) every 5 minutes until seizures stop (max dose 2mg/kg)<br /> ###May place on cIV 0.05-2.0 mg/kg/h (up to 200mg/h for 70kg patient).<br /> <br /> ====&gt; 60 minutes ====<br /> #Place in pentobarbital coma<br /> ##5 mg/kg up to 50mg/min. Repeat boluses (same dose) until seizure stop.<br /> ##cIV 1mg/kg/h titrated to suppression on cEEG.<br /> <br /> ==References==<br /> &lt;references/&gt;<br /> <br /> [[Category:Neuro]]</div>

Ncdavis https://wikem.org/w/index.php?title=User_talk:Ostermayer&diff=15483 2013-12-29T06:07:17Z

<p>Ncdavis: </p> <hr /> <div>== software improvements ==<br /> <br /> Leave any suggestions below<br /> <br /> 1.any way we can integrate an automated calculation function into the wiki? (Ie for calculation of dosages based on kg weight)? unsure as to what effectively this would entail from a coding standpoint.</div>

Ncdavis https://wikem.org/w/index.php?title=Status_epilepticus&diff=15482 2013-12-29T06:04:30Z

<p>Ncdavis: </p> <hr /> <div>=Overview=<br /> *Seizures are abnormal neuronal activity with various neurological sequale.<br /> **Further defined by whether they involve 1 hemisphere (partial) or both hemispheres (generalized). While generalized seizures surely cause an alteration in mental status, seizures involving one hemisphere (partial) may further be subdivided by whether they maintain baseline mental status (simple) or an alteration (complex). <br /> *Epilepsy is defined a 2 or more epileptic seizures that occur unprovoked by any identifiable cause. This include all seizure events with the exception of febrile or neonatal seizures. <br /> **Further subclassified into cryptogenic (meaning unknown cause) or symptomatic (meaning associated with previous CNS insult). <br /> ***Symptomatic seizures further subdefined as acute or remote (depending on if &gt; or &lt; 1 week after CNS insult)<br /> *Status epilepticus is the persistence of seizure beyond 30 minutes. (includes either persistent clinical seizure activity OR no return to consciousness during that timeframe or between attacks. <br /> **Functionally presume people to be in status if clinically seizing beyond 5 minutes<br /> **Status Epilepticus can be defined as “convulsive” (meaning obvious clinical signs of seizure activity –tonic clonic/myoclonic/tonic) or “Nonconsulsive” meaning no obvious signs of activity but decreased level of consciousness. <br /> ***NCSE (Non consulsive status) is a critical and relevant consideration. Up to 50% of patients with generalized tonic-clonic seizures will have NCSE after convulsions have subsided.<br /> *Seizure type and associated EEG findings are at core of determining risk of recurrence and indication for antiepileptic therapy. Follow the “seizure” link (pending Jan 2014) for more information on the non-acute general treatment of seizures. <br /> <br /> ==Management of acute status epilepticus==<br /> Overview<br /> *The general theme of seizure treatment is to<br /> #Address immediate concerns (ABC’s) (primarily referring to airway/breathing) <br /> ##Constantly return to evaluate this for the duration of seizure episode<br /> ###continuously monitor O2 saturations via pulse oximetry<br /> ###periodic blood gases to evaluate for CO2 retention and lactic acidosis (q10-15mins- up to clinical judgement).<br /> #Manage the seizure activity with medications along with investigation/correction of causes. <br /> ##Treat quickly; Do not hold medications. Treatment initiated in first 30 minutes has 80% response. Drops to 40% around two hours<br /> ###Medication regimes include a benzodiazepine to terminate seizure in immediate term and an anti-epileptic drug (AED) to continue longer term neuronal suppression. Continued seizure activity is treated by additive AED’s and/or sedating medications.<br /> ###Very often phenytoin is used for AED (Cost and plethora of studies) however alternatives exist Leveteriacetam, lacosamide, valproate with lesser side effect profile. You may refer to pharmacy for assistance with typical protocol, otherwise phenytoin is acceptable and can always be changed to another AED later.<br /> ===Take a Stepwise Approach: Timeline===<br /> ====0-5 minutes====<br /> #Is this patient still seizing ? (look for return of consciousness) or if on EEG look to EEG (Reading EEGs link to come).<br /> ##If this is first episode, may await seizure to break however ready materials to be given should seizure persist greater than 5 minutes<br /> #Obtain Diagnostic labs (CBC, CEM 10, LFT, coagulation, AED levels (If indicated: assess if therapeutic), ECG, troponins, toxicology screen, pregnancy test (preparation for possible CT), blood gas, continuous SaO2, BP and continuous ECG.<br /> #Ready medications to be given if seizure persists &gt; 5 minutes<br /> ##lorazepam (0.1mg/kg max given in 2-4 mg aliquots )<br /> ## AED loading agent (Fosphenytoin 20mg/kg)<br /> ## Thiamine 100mg IV along with 50ml D50IV.<br /> #Briefly familiarize patient H+P to help guide diagnostic causes<br /> ##PMHx: Sz History? (get AED levels/home dosages), CNS insults?<br /> ###description of previous seizures semiology (if applicable) – jerking/automatisms/gaze deviation<br /> ##Medications: anything that reduces seizure threshold?<br /> ##Physical Exam: Neuro evaluation <br /> ###while in convulsive status patient is obviously seizing and one should continue timeline for acute treatment. The neuro exam is primarily focused on identifying 1. Neuro signs to help localize seizure focus 2.identifying NCSE; focusing on recognizing an improvement of wakefulness/mental status.<br /> ####No improvement in wakefulness &gt;20 minutes or continued AMS &gt; 30-60 minutes prompts concern for NCSE and requires 24-48hr cEEG<br /> ====6-10 minutes (seizure persists)====<br /> #Administer thiamine 100mg IV along with 50ml D50IV (empirically for possible hypoglycemia)<br /> ##May forego if hypoglycemia ruled out with recent CEM panel.<br /> #Administer the 2-4mg lorazepam aliquot over 2 minutes. <br /> ##Repeat 1x (max dose 0.1mg/kg) if seizure continues another 5 minutes.<br /> ##If no IV access available. Diazepam may be given rectally (20mg PR) or Midazolam (10mg intrabucally/intranasally). <br /> ====10-20 minutes ====<br /> #Admin AED loading agent (Fosphenytoin 20mg/kg). MAX INFUSION RATE 150mg/min<br /> ##Phenytoin associated with hypotension. Fosphenytoin use attenuates some of this risk however still significant. Administer with frequent BP checks and ECG monitoring. <br /> ##Continue AED maintenance with target phenytoin level 2-3 G/mL<br /> ##If seizure persists may rebolus 1x with additional Fosphenyoitn 10mg/kg bolus.<br /> #OTHER OPTION<br /> ##if patient on AED at home, may reload with home medication: Some examples below<br /> ###IV valproate: 20mg/kg over 10 minutes. May re bolus (same dose) 1x if seizure persists &gt; 5 minutes following<br /> ###IV keppra 1000-4000mg IV<br /> #Reassess ABC status<br /> #Make arrangements for possible ICU transfer ( If applicable - as next step is intubation). <br /> ====20-60 minutes - If still seizing despite 2 drug intervention - considered refractory status epilepticus ====<br /> #Intubate for airway protection (As we will definitively sedate to the point of respiratory compromise) <br /> #Place arterial line (Continuous BP monitoring with propofol infusion)<br /> #Medications (May use propofol as pressure tolerates, otherwise midazolam; Typically start with propofol since may regain neuro exam faster, and add midazolam). <br /> ##IV propofol (causes hypotension)<br /> ### 1mg/kg bolus with continued boluses (same dose) every 3-5 minutes until seizures stop (As BP tolerates). <br /> ###May place on cIV infusion 1-15 mg/kg/h (Do not exceed &gt;5mg/kg/h in 24 hrs)<br /> ##IV midazolam (less hypotension, longer sedation than propofol)<br /> ###0.2mg/kg bolus with repeat boluses (Same dose) every 5 minutes until seizures stop (max dose 2mg/kg)<br /> ###May place on cIV 0.05-2.0 mg/kg/h (up to 200mg/h for 70kg patient).<br /> ====&gt; 60 minutes ====<br /> #Place in pentobarbital coma<br /> ##5 mg/kg up to 50mg/min. Repeat boluses (same dose) until seizure stop.<br /> ##cIV 1mg/kg/h titrated to suppression on cEEG.<br /> <br /> ==References==<br /> &lt;references/&gt;<br /> <br /> [[Category:Neuro]]</div>

Ncdavis https://wikem.org/w/index.php?title=Status_epilepticus&diff=15481 2013-12-29T05:58:19Z

<p>Ncdavis: </p> <hr /> <div>==Overview==<br /> *Seizures are abnormal neuronal activity with various neurological sequale.<br /> **Further defined by whether they involve 1 hemisphere (partial) or both hemispheres (generalized). While generalized seizures surely cause an alteration in mental status, seizures involving one hemisphere (partial) may further be subdivided by whether they maintain baseline mental status (simple) or an alteration (complex). <br /> *Epilepsy is defined a 2 or more epileptic seizures that occur unprovoked by any identifiable cause. This include all seizure events with the exception of febrile or neonatal seizures. <br /> **Further subclassified into cryptogenic (meaning unknown cause) or symptomatic (meaning associated with previous CNS insult). <br /> ***Symptomatic seizures further subdefined as acute or remote (depending on if &gt; or &lt; 1 week after CNS insult)<br /> *Status epilepticus is the persistence of seizure beyond 30 minutes. (includes either persistent clinical seizure activity OR no return to consciousness during that timeframe or between attacks. <br /> **Functionally presume people to be in status if clinically seizing beyond 5 minutes<br /> **Status Epilepticus can be defined as “convulsive” (meaning obvious clinical signs of seizure activity –tonic clonic/myoclonic/tonic) or “Nonconsulsive” meaning no obvious signs of activity but decreased level of consciousness. <br /> ***NCSE (Non consulsive status) is a critical and relevant consideration. Up to 50% of patients with generalized tonic-clonic seizures will have NCSE after convulsions have subsided.<br /> *Seizure type and associated EEG findings are at core of determining risk of recurrence and indication for antiepileptic therapy. Follow the “seizure” link (pending Jan 2014) for more information on the non-acute general treatment of seizures. <br /> <br /> ===Management of acute status epilepticus===<br /> Overview<br /> *The general theme of seizure treatment is to<br /> #Address immediate concerns (ABC’s) (primarily referring to airway/breathing) <br /> ##Constantly return to evaluate this for the duration of seizure episode<br /> ###continuously monitor O2 saturations via pulse oximetry<br /> ###periodic blood gases to evaluate for CO2 retention and lactic acidosis (q10-15mins- up to clinical judgement).<br /> #Manage the seizure activity with medications along with investigation/correction of causes. <br /> ##Treat quickly; Do not hold medications. Treatment initiated in first 30 minutes has 80% response. Drops to 40% around two hours<br /> ###Medication regimes include a benzodiazepine to terminate seizure in immediate term and an anti-epileptic drug (AED) to continue longer term neuronal suppression. Continued seizure activity is treated by additive AED’s and/or sedating medications.<br /> ###Very often phenytoin is used for AED (Cost and plethora of studies) however alternatives exist Leveteriacetam, lacosamide, valproate with lesser side effect profile. You may refer to pharmacy for assistance with typical protocol, otherwise phenytoin is acceptable and can always be changed to another AED later.<br /> ====Take a Stepwise Approach: Timeline====<br /> # 0-5 minutes<br /> ##Is this patient still seizing ? (look for return of consciousness) or if on EEG look to EEG (Reading EEGs link to come).<br /> ###If this is first episode, may await seizure to break however ready materials to be given should seizure persist greater than 5 minutes<br /> ##Obtain Diagnostic labs (CBC, CEM 10, LFT, coagulation, AED levels (If indicated: assess if therapeutic), ECG, troponins, toxicology screen, pregnancy test (preparation for possible CT), blood gas, continuous SaO2, BP and continuous ECG.<br /> ##Ready medications to be given if seizure persists &gt; 5 minutes<br /> ###lorazepam (0.1mg/kg max given in 2-4 mg aliquots )<br /> ### AED loading agent (Fosphenytoin 20mg/kg)<br /> ### Thiamine 100mg IV along with 50ml D50IV.<br /> ##Briefly familiarize patient H+P to help guide diagnostic causes<br /> ###PMHx: Sz History? (get AED levels/home dosages), CNS insults?<br /> ####description of previous seizures semiology (if applicable) – jerking/automatisms/gaze deviation<br /> ###Medications: anything that reduces seizure threshold?<br /> ###Physical Exam: Neuro evaluation <br /> ####while in convulsive status patient is obviously seizing and one should continue timeline for acute treatment. The neuro exam is primarily focused on identifying 1. Neuro signs to help localize seizure focus 2.identifying NCSE; focusing on recognizing an improvement of wakefulness/mental status.<br /> #####No improvement in wakefulness &gt;20 minutes or continued AMS &gt; 30-60 minutes prompts concern for NCSE and requires 24-48hr cEEG<br /> #6-10 minutes (seizure persists)<br /> ##Administer thiamine 100mg IV along with 50ml D50IV (empirically for possible hypoglycemia)<br /> ###May forego if hypoglycemia ruled out with recent CEM panel.<br /> ##Administer the 2-4mg lorazepam aliquot over 2 minutes. <br /> ###Repeat 1x (max dose 0.1mg/kg) if seizure continues another 5 minutes.<br /> ###If no IV access available. Diazepam may be given rectally (20mg PR) or Midazolam (10mg intrabucally/intranasally). <br /> #10-20 minutes <br /> ##Admin AED loading agent (Fosphenytoin 20mg/kg). MAX INFUSION RATE 150mg/min<br /> ###Phenytoin associated with hypotension. Fosphenytoin use attenuates some of this risk however still significant. Administer with frequent BP checks and ECG monitoring. <br /> ###Continue AED maintenance with target phenytoin level 2-3 G/mL<br /> ###If seizure persists may rebolus 1x with additional Fosphenyoitn 10mg/kg bolus.<br /> ##OTHER OPTION<br /> ###if patient on AED at home, may reload with home medication: Some examples below<br /> ####IV valproate: 20mg/kg over 10 minutes. May re bolus (same dose) 1x if seizure persists &gt; 5 minutes following<br /> ####IV keppra 1000-4000mg IV<br /> ##Reassess ABC status<br /> ##Make arrangements for possible ICU transfer ( If applicable - as next step is intubation). <br /> #20-60 minutes - If still seizing despite 2 drug intervention - considered refractory status epilepticus<br /> ##Intubate for airway protection (As we will definitively sedate to the point of respiratory compromise) <br /> ##Place arterial line (Continuous BP monitoring with propofol infusion)<br /> ##Medications (May use propofol as pressure tolerates, otherwise midazolam; Typically start with propofol since may regain neuro exam faster, and add midazolam). <br /> ###IV propofol (causes hypotension)<br /> #### 1mg/kg bolus with continued boluses (same dose) every 3-5 minutes until seizures stop (As BP tolerates). <br /> ####May place on cIV infusion 1-15 mg/kg/h (Do not exceed &gt;5mg/kg/h in 24 hrs)<br /> ###IV midazolam (less hypotension, longer sedation than propofol)<br /> ####0.2mg/kg bolus with repeat boluses (Same dose) every 5 minutes until seizures stop (max dose 2mg/kg)<br /> ####May place on cIV 0.05-2.0 mg/kg/h (up to 200mg/h for 70kg patient).<br /> #&gt; 60 minutes <br /> ##Place in pentobarbital coma<br /> ###5 mg/kg up to 50mg/min. Repeat boluses (same dose) until seizure stop.<br /> ###cIV 1mg/kg/h titrated to suppression on cEEG.</div>

Ncdavis https://wikem.org/w/index.php?title=Status_epilepticus&diff=15480 2013-12-29T05:56:21Z

<p>Ncdavis: /* Take a Stepwise Approach: Timeline */</p> <hr /> <div>==Overview==<br /> *Seizures are abnormal neuronal activity with various neurological sequale.<br /> **Further defined by whether they involve 1 hemisphere (partial) or both hemispheres (generalized). While generalized seizures surely cause an alteration in mental status, seizures involving one hemisphere (partial) may further be subdivided by whether they maintain baseline mental status (simple) or an alteration (complex). <br /> *Epilepsy is defined a 2 or more epileptic seizures that occur unprovoked by any identifiable cause. This include all seizure events with the exception of febrile or neonatal seizures. <br /> **Further subclassified into cryptogenic (meaning unknown cause) or symptomatic (meaning associated with previous CNS insult). <br /> ***Symptomatic seizures further subdefined as acute or remote (depending on if &gt; or &lt; 1 week after CNS insult)<br /> *Status epilepticus is the persistence of seizure beyond 30 minutes. (includes either persistent clinical seizure activity OR no return to consciousness during that timeframe or between attacks. <br /> **Functionally presume people to be in status if clinically seizing beyond 5 minutes<br /> **Status Epilepticus can be defined as “convulsive” (meaning obvious clinical signs of seizure activity –tonic clonic/myoclonic/tonic) or “Nonconsulsive” meaning no obvious signs of activity but decreased level of consciousness. <br /> ***NCSE (Non consulsive status) is a critical and relevant consideration. Up to 50% of patients with generalized tonic-clonic seizures will have NCSE after convulsions have subsided.<br /> *Seizure type and associated EEG findings are at core of determining risk of recurrence and indication for antiepileptic therapy. Follow the “seizure” link (pending Jan 2014) for more information on the non-acute general treatment of seizures. <br /> <br /> ===Management of acute status epilepticus===<br /> Overview<br /> *The general theme of seizure treatment is to<br /> #Address immediate concerns (ABC’s) (primarily referring to airway/breathing) <br /> ##Constantly return to evaluate this for the duration of seizure episode<br /> ###continuously monitor O2 saturations via pulse oximetry<br /> ###periodic blood gases to evaluate for CO2 retention and lactic acidosis (q10-15mins- up to clinical judgement).<br /> #Manage the seizure activity with medications along with investigation/correction of causes. <br /> ##Treat quickly; Do not hold medications. Treatment initiated in first 30 minutes has 80% response. Drops to 40% around two hours<br /> ###Medication regimes include a benzodiazepine to terminate seizure in immediate term and an anti-epileptic drug (AED) to continue longer term neuronal suppression. Continued seizure activity is treated by additive AED’s and/or sedating medications.<br /> ###Very often phenytoin is used for AED (Cost and plethora of studies) however alternatives exist Leveteriacetam, lacosamide, valproate with lesser side effect profile. You may refer to pharmacy for assistance with typical protocol, otherwise phenytoin is acceptable and can always be changed to another AED later.<br /> ====Take a Stepwise Approach: Timeline====<br /> # 0-5 minutes<br /> ##Is this patient still seizing ? (look for return of consciousness) or if on EEG look to EEG (Reading EEGs link to come).<br /> ###If this is first episode, may await seizure to break however ready materials to be given should seizure persist greater than 5 minutes<br /> ##Obtain Diagnostic labs (CBC, CEM 10, LFT, coagulation, AED levels (If indicated: assess if therapeutic), ECG, troponins, toxicology screen, pregnancy test (preparation for possible CT), blood gas, continuous SaO2, BP and continuous ECG.<br /> ##Ready medications to be given if seizure persists &gt; 5 minutes<br /> ###lorazepam (0.1mg/kg max given in 2-4 mg aliquots )<br /> ### AED loading agent (Fosphenytoin 20mg/kg)<br /> ### Thiamine 100mg IV along with 50ml D50IV.<br /> ##Briefly familiarize patient H+P to help guide diagnostic causes<br /> ###PMHx: Sz History? (get AED levels/home dosages), CNS insults?<br /> ####description of previous seizures semiology (if applicable) – jerking/automatisms/gaze deviation<br /> ###Medications: anything that reduces seizure threshold?<br /> ###Physical Exam: Neuro evaluation <br /> ####while in convulsive status patient is obviously seizing and one should continue timeline for acute treatment. The neuro exam is primarily focused on identifying 1. Neuro signs to help localize seizure focus 2.identifying NCSE; focusing on recognizing an improvement of wakefulness/mental status.<br /> #####No improvement in wakefulness &gt;20 minutes or continued AMS &gt; 30-60 minutes prompts concern for NCSE and requires 24-48hr cEEG<br /> #6-10 minutes (seizure persists)<br /> ##Administer thiamine 100mg IV along with 50ml D50IV (empirically for possible hypoglycemia)<br /> ###May forego if hypoglycemia ruled out with recent CEM panel.<br /> ##Administer the 2-4mg lorazepam aliquot over 2 minutes. <br /> ###Repeat 1x (max dose 0.1mg/kg) if seizure continues another 5 minutes.<br /> ###If no IV access available. Diazepam may be given rectally (20mg PR) or Midazolam (10mg intrabucally/intranasally). <br /> #10-20 minutes <br /> ##Admin AED loading agent (Fosphenytoin 20mg/kg). MAX INFUSION RATE 150mg/min<br /> ###Phenytoin associated with hypotension. Fosphenytoin use attenuates some of this risk however still significant. Administer with frequent BP checks and ECG monitoring. <br /> ###Continue AED maintenance with target phenytoin level 2-3 G/mL<br /> ##If seizure persists may rebolus 1x with additional Fosphenyoitn 10mg/kg bolus.<br /> ##OTHER OPTION<br /> ###if patient on AED at home, may reload with home medication: Some examples below<br /> ####IV valproate: 20mg/kg over 10 minutes. May re bolus (same dose) 1x if seizure persists &gt; 5 minutes following<br /> ####IV keppra 1000-4000mg IV<br /> ##Reassess ABC status<br /> ##Make arrangements for possible ICU transfer ( If applicable - as next step is intubation). <br /> #20-60 minutes - If still seizing despite 2 drug intervention - considered refractory status epilepticus<br /> ##Intubate for airway protection (As we will definitively sedate to the point of respiratory compromise) <br /> ##Place arterial line (Continuous BP monitoring with propofol infusion)<br /> ##Medications (May use propofol as pressure tolerates, otherwise midazolam; Typically start with propofol since may regain neuro exam faster, and add midazolam). <br /> ###IV propofol (causes hypotension)<br /> #### 1mg/kg bolus with continued boluses (same dose) every 3-5 minutes until seizures stop (As BP tolerates). <br /> ####May place on cIV infusion 1-15 mg/kg/h (Do not exceed &gt;5mg/kg/h in 24 hrs)<br /> ###IV midazolam (less hypotension, longer sedation than propofol)<br /> ####0.2mg/kg bolus with repeat boluses (Same dose) every 5 minutes until seizures stop (max dose 2mg/kg)<br /> ####May place on cIV 0.05-2.0 mg/kg/h (up to 200mg/h for 70kg patient).<br /> #&gt; 60 minutes <br /> ##Place in pentobarbital coma<br /> ###5 mg/kg up to 50mg/min. Repeat boluses (same dose) until seizure stop.<br /> ###cIV 1mg/kg/h titrated to suppression on cEEG.</div>

Ncdavis https://wikem.org/w/index.php?title=Status_epilepticus&diff=15479 2013-12-29T05:53:46Z

<p>Ncdavis: Created page with &quot;==Overview== *Seizures are abnormal neuronal activity with various neurological sequale. **Further defined by whether they involve 1 hemisphere (partial) or both hemispheres (...&quot;</p> <hr /> <div>==Overview==<br /> *Seizures are abnormal neuronal activity with various neurological sequale.<br /> **Further defined by whether they involve 1 hemisphere (partial) or both hemispheres (generalized). While generalized seizures surely cause an alteration in mental status, seizures involving one hemisphere (partial) may further be subdivided by whether they maintain baseline mental status (simple) or an alteration (complex). <br /> *Epilepsy is defined a 2 or more epileptic seizures that occur unprovoked by any identifiable cause. This include all seizure events with the exception of febrile or neonatal seizures. <br /> **Further subclassified into cryptogenic (meaning unknown cause) or symptomatic (meaning associated with previous CNS insult). <br /> ***Symptomatic seizures further subdefined as acute or remote (depending on if &gt; or &lt; 1 week after CNS insult)<br /> *Status epilepticus is the persistence of seizure beyond 30 minutes. (includes either persistent clinical seizure activity OR no return to consciousness during that timeframe or between attacks. <br /> **Functionally presume people to be in status if clinically seizing beyond 5 minutes<br /> **Status Epilepticus can be defined as “convulsive” (meaning obvious clinical signs of seizure activity –tonic clonic/myoclonic/tonic) or “Nonconsulsive” meaning no obvious signs of activity but decreased level of consciousness. <br /> ***NCSE (Non consulsive status) is a critical and relevant consideration. Up to 50% of patients with generalized tonic-clonic seizures will have NCSE after convulsions have subsided.<br /> *Seizure type and associated EEG findings are at core of determining risk of recurrence and indication for antiepileptic therapy. Follow the “seizure” link (pending Jan 2014) for more information on the non-acute general treatment of seizures. <br /> <br /> ===Management of acute status epilepticus===<br /> Overview<br /> *The general theme of seizure treatment is to<br /> #Address immediate concerns (ABC’s) (primarily referring to airway/breathing) <br /> ##Constantly return to evaluate this for the duration of seizure episode<br /> ###continuously monitor O2 saturations via pulse oximetry<br /> ###periodic blood gases to evaluate for CO2 retention and lactic acidosis (q10-15mins- up to clinical judgement).<br /> #Manage the seizure activity with medications along with investigation/correction of causes. <br /> ##Treat quickly; Do not hold medications. Treatment initiated in first 30 minutes has 80% response. Drops to 40% around two hours<br /> ###Medication regimes include a benzodiazepine to terminate seizure in immediate term and an anti-epileptic drug (AED) to continue longer term neuronal suppression. Continued seizure activity is treated by additive AED’s and/or sedating medications.<br /> ###Very often phenytoin is used for AED (Cost and plethora of studies) however alternatives exist Leveteriacetam, lacosamide, valproate with lesser side effect profile. You may refer to pharmacy for assistance with typical protocol, otherwise phenytoin is acceptable and can always be changed to another AED later.<br /> ====Take a Stepwise Approach: Timeline====<br /> # 0-5 minutes<br /> ##Is this patient still seizing ? (look for return of consciousness) or if on EEG look to EEG (Reading EEGs link to come).<br /> ###If this is first episode, may await seizure to break however ready materials to be given should seizure persist greater than 5 minutes<br /> ##Obtain Diagnostic labs (CBC, CEM 10, LFT, coagulation, AED levels (If indicated: assess if therapeutic), ECG, troponins, toxicology screen, pregnancy test (preparation for possible CT), blood gas, continuous SaO2, BP and continuous ECG.<br /> ##Ready medications to be given if seizure persists &gt; 5 minutes<br /> ###lorazepam (0.1mg/kg max given in 2-4 mg aliquots )<br /> ### AED loading agent (Fosphenytoin 20mg/kg)<br /> ### Thiamine 100mg IV along with 50ml D50IV.<br /> ##Briefly familiarize patient H+P to help guide diagnostic causes<br /> ###PMHx: Sz History? (get AED levels/home dosages), CNS insults?<br /> ####description of previous seizures semiology (if applicable) – jerking/automatisms/gaze deviation<br /> ###Medications: anything that reduces seizure threshold?<br /> ###Physical Exam: Neuro evaluation <br /> ####while in convulsive status patient is obviously seizing and one should continue timeline for acute treatment. The neuro exam is primarily focused on identifying 1. Neuro signs to help localize seizure focus 2.identifying NCSE; focusing on recognizing an improvement of wakefulness/mental status.<br /> #####No improvement in wakefulness &gt;20 minutes or continued AMS &gt; 30-60 minutes prompts concern for NCSE and requires 24-48hr cEEG<br /> #6-10 minutes (seizure persists)<br /> ##Administer thiamine 100mg IV along with 50ml D50IV (empirically for possible hypoglycemia)<br /> ###May forego if hypoglycemia ruled out with recent CEM panel.<br /> ##Administer the 2-4mg lorazepam aliquot over 2 minutes. <br /> ###Repeat 1x (max dose 0.1mg/kg) if seizure continues another 5 minutes.<br /> ###If no IV access available. Diazepam may be given rectally (20mg PR) or Midazolam (10mg intrabucally/intranasally). <br /> #10-20 minutes <br /> ##Admin AED loading agent (Fosphenytoin 20mg/kg). MAX INFUSION RATE 150mg/min<br /> ###Phenytoin associated with hypotension. Fosphenytoin use attenuates some of this risk however still significant. Administer with frequent BP checks and ECG monitoring. <br /> ###Continue AED maintenance with target phenytoin level 2-3 G/mL<br /> ##If seizure persists may rebolus 1x with additional Fosphenyoitn 10mg/kg bolus.<br /> ##OTHER OPTION<br /> ###if patient on AED at home, may reload with home medication: Some examples below<br /> ##IV valproate: 20mg/kg over 10 minutes. May re bolus (same dose) 1x if seizure persists &gt; 5 minutes following<br /> ##IV keppra 1000-4000mg IV<br /> ##Reassess ABC status<br /> ##Make arrangements for possible ICU transfer ( If applicable - as next step is intubation). <br /> #20-60 minutes - If still seizing despite 2 drug interventionconsidered refractory status epilepticus<br /> ##Intubate for airway protection (As we will definitively sedate to the point of respiratory compromise) <br /> ##Place arterial line (Continuous BP monitoring with propofol infusion)<br /> ##Medications (May use propofol as pressure tolerates, otherwise midazolam; Typically start with propofol since may regain neuro exam faster, and add midazolam). <br /> ###IV propofol (causes hypotension)<br /> #### 1mg/kg bolus with continued boluses (same dose) every 3-5 minutes until seizures stop (As BP tolerates). <br /> ####May place on cIV infusion 1-15 mg/kg/h (Do not exceed &gt;5mg/kg/h in 24 hrs)<br /> ###IV midazolam (less hypotension, longer sedation than propofol)<br /> ####0.2mg/kg bolus with repeat boluses (Same dose) every 5 minutes until seizures stop (max dose 2mg/kg)<br /> ####May place on cIV 0.05-2.0 mg/kg/h (up to 200mg/h for 70kg patient).<br /> #&gt; 60 minutes <br /> ##Place in pentobarbital coma<br /> ###5 mg/kg up to 50mg/min. Repeat boluses (same dose) until seizure stop.<br /> ###cIV 1mg/kg/h titrated to suppression on cEEG.</div>

Ncdavis https://wikem.org/w/index.php?title=Elevated_intracranial_pressure&diff=15408 2013-12-24T21:13:29Z

<p>Ncdavis: </p> <hr /> <div>=Overview=<br /> *Cranial vault is a fixed volume made up of 3 main components<br /> **brain tissue (80%) blood (10% or 150L) and CSF (10% or 150mL). <br /> *While brain parenchyma is a relatively fixed volume, the blood and CSF are fluids with entranace and egress points into and out of the skull and are primarily affected with changes in ICP. <br /> **CSF is created at a rate of 20mL/hr or 500mL/day. <br /> *Neuronal injury occurs secondary to vascular compromise to brain cells either by a reduction in cerebral blood flow or direct ischemia <br /> **This is an ''' emergency''' and requires emergent intervention if sustained &gt; 5-10 minutes<br /> <br /> ==Clinical Signs and Symptoms==<br /> *Increased ICP generally causes headache (from increased pressure on heavily innervated meninges), Nausea/vomiting, and occasionally optic abnormalities (most notably ocular palsies (CN6 particularly long course intracranially) along with AMS and optic atrophy.<br /> *Morning headaches are pathomnemonic (mild hypoventilation during sleeping hours causes increases in cerebreal blood flow)<br /> <br /> ==Causes==<br /> *As the cranial vault is a fixed volume, Increases in ICP are either due to increased brain tissue (edema), blood (increase inflow or decreased outflow) and CSF (increased inflow/production or decreased outflow) in addition to abnormal mass lesions.<br /> #Mass lesions<br /> ##tumor, hematoma, air, abscess,foreign body<br /> #CSF accumulation<br /> ##Hydrocephalus(obstructive or communicating)<br /> ###Most often obstrcutive via tumor, intraventricular hemorrhage, ventriculutus/meningitis) with compression of CSF outflow<br /> #Vascular<br /> ##Either input or output failure<br /> ###Input failure: increased CBF or CBV due to failed autoregulatoin<br /> ###Outflow failure: venous congestion or sinus thrombosis<br /> #Cerebral edema<br /> ##vasogenic (vessel damage due to tumor/infection abscess<br /> ##Cytotoxic (ischemia)<br /> ##Hydrostatic: Increased transmural pressure with hydrocephalus<br /> ##Hypo osmolar<br /> <br /> ==Management==<br /> #Ensure data accurate<br /> ##observe for accurate waveforms in arterial and ICP monitors <br /> ###EVD zeroed at ear, changes with coughing/positioning<br /> ###Arterial line zeroed at ear (for accurate CPP measurement; although typically level at heart reasonably accurate<br /> #Assess ABC (as increased ICP often accompanies decline in mental status<br /> ##If need to intubate - ensure measures to avoid coughing/bucking (increases ICP).<br /> ###Lidocaine 1% 1ml/kg 1x IV bolus as premedication. <br /> ====Goals====<br /> #Keep CPP 60-110mmHg<br /> ##If &lt;110 utilize pressors (levophed or neosynephrine; levophed preferred)<br /> ##Levophed: start at 4 mcg/min; maximum 20 mcg/min.<br /> ##Phenylepherine: start at 0.4 mcg/kg/min; maximum 9 mcg/kg/min.<br /> #Keep ICP &lt; 20mmHg (nonsustained temporary elevateions ~&lt;5 minutes ok<br /> <br /> ====Take Stepwise approach to treatment==== <br /> *1st (conservative)<br /> #Elevate HOB 30-to 45 deg; keep head midline<br /> ##May &quot;sandbag&quot; head of those in c-collar to promote venous drainage(c-collar can restrict venous outlfow)<br /> #Control agitation/pain<br /> ##narcotics, benzodiazepines, sedative hypnotics<br /> ###Attempt to favor short acting medications to allow neuro exam checks. Versed, Fentanyl and propofol are often appropriate.<br /> #Maintain Normocapnia (pCO2 35-40)<br /> #Maintain normothermia.<br /> ##Treat shivering<br /> ###Bear hugger (warms skin temperature)<br /> ###APAP 650q6prn for temp &gt;38.5 <br /> #Maintain euvolemia (Input = output)<br /> *2nd (Intervention-short term)<br /> #hyperventilate to pCO2 ~30mmHg<br /> ##This is short term as patient will equilibrate; is only meant as a temporizing measure. Attempt to wean to normocapnia as soon as able. Further do not overventilate past 25mmHg as may exacerbate damage via cerbral hypoxia (CO2 is primarily involved in autoregulation of cerebral vasculature).<br /> #Hypertonic fluids<br /> ##Mannitol 20% 1-1.5g/kg rapid IV bolus (no need for central line) OR<br /> ## 23% 30mL over 15 minutes (Needs central line)<br /> #Consult Neurosurgery (urgent) for possible evacuation or ventricular drainage. <br /> ##This is especially relevant for mass lesions causing mass effect or in hydrocephalus. <br /> *3rd (Intervention- long term)<br /> #Hypertonic fluid maintenance<br /> ##Iatrogenic hypernatremia. Use 3% NaCl to maintain na &gt;145 with q6hr serum Na cks. <br /> ###3%NS at 1mL/kg/hr appropriate (typically start at 50mL/hr).<br /> ###May continue to push Na &gt; 145, then &gt;150 then &gt;155 prn to manage ICP<br /> ####Eventually osmotic pressures will equilibrate over days. requiring higher Na values (rationale behind pushing Na slowly upward as needed rather than pushing hypernatremia to maximum). <br /> ##Iatrogenic hyperosmolar maintenance <br /> ###Mannitola 20% 0.5g/kg q4 hrsth seurm Osm checks q6hrs. (Goal Osm 300-320 mOsm/L)<br /> *4th (Intervention - Refractory elevation)<br /> #Pentobarbital coma<br /> ##loading dose: 5-20mg/kg bolus then 4mg;kg/hr titrated to burst supression on EEG.<br /> #Induced hypothermia (32-34deg)<br /> ##Arctic Sun<br /> ###Must perform surveillance cultures (routine blood culture, UA, CXR) every 48 hours since artificially supressing fever.<br /> ##Shivering protocol<br /> #Paralytics<br /> ##Risk of ICU myopathy/neuropathy with long term use.</div>

Ncdavis https://wikem.org/w/index.php?title=Elevated_intracranial_pressure&diff=15407 2013-12-24T21:10:08Z

<p>Ncdavis: </p> <hr /> <div>=Overview=<br /> *Cranial vault is a fixed volume made up of 3 main components<br /> **brain tissue (80%) blood (10% or 150L) and CSF (10% or 150mL). <br /> *While brain parenchyma is a relatively fixed volume, the blood and CSF are fluids with entranace and egress points into and out of the skull and are primarily affected with changes in ICP. <br /> **CSF is created at a rate of 20mL/hr or 500mL/day. <br /> *Neuronal injury occurs secondary to vascular compromise to brain cells either by a reduction in cerebral blood flow or direct ischemia <br /> **This is an ''' emergency''' and requires emergent intervention if sustained &gt; 5-10 minutes<br /> <br /> ==Clinical Signs and Symptoms==<br /> *Increased ICP generally causes headache (from increased pressure on heavily innervated meninges), Nausea/vomiting, and occasionally optic abnormalities (most notably ocular palsies (CN6 particularly long course intracranially) along with AMS and optic atrophy.<br /> *Morning headaches are pathomnemonic (mild hypoventilation during sleeping hours causes increases in cerebreal blood flow)<br /> <br /> ==Causes==<br /> *As the cranial vault is a fixed volume, Increases in ICP are either due to increased brain tissue (edema), blood (increase inflow or decreased outflow) and CSF (increased inflow/production or decreased outflow) in addition to abnormal mass lesions.<br /> #Mass lesions<br /> ##tumor, hematoma, air, abscess,foreign body<br /> #CSF accumulation<br /> ##Hydrocephalus(obstructive or communicating)<br /> ###Most often obstrcutive via tumor, intraventricular hemorrhage, ventriculutus/meningitis) with compression of CSF outflow<br /> #Vascular<br /> ##Either input or output failure<br /> ###Input failure: increased CBF or CBV due to failed autoregulatoin<br /> ###Outflow failure: venous congestion or sinus thrombosis<br /> #Cerebral edema<br /> ##vasogenic (vessel damage due to tumor/infection abscess<br /> ##Cytotoxic (ischemia)<br /> ##Hydrostatic: Increased transmural pressure with hydrocephalus<br /> ##Hypo osmolar<br /> <br /> ==Management==<br /> #Ensure data accurate<br /> ##observe for accurate waveforms in arterial and ICP monitors <br /> ###EVD zeroed at ear, changes with coughing/positioning<br /> ###Arterial line zeroed at ear (for accurate CPP measurement; although typically level at heart reasonably accurate<br /> #Assess ABC (as increased ICP often accompanies decline in mental status<br /> ##If need to intubate - ensure measures to avoid coughing/bucking (increases ICP).<br /> ###Lidocaine 1% 1ml/kg 1x IV bolus as premedication. <br /> ====Goals====<br /> #Keep CPP 60-110mmHg<br /> ##If &lt;110 utilize pressors (levophed or neosynephrine; levophed preferred)<br /> ##Levophed: start at 4 mcg/min; maximum 20 mcg/min.<br /> ##Phenylepherine: start at 0.4 mcg/kg/min; maximum 9 mcg/kg/min.<br /> #Maintain normothermia.<br /> ##Treat shivering<br /> ###Bear hugger (warms skin temperature)<br /> ###APAP 650q6prn for temp &gt;38.5<br /> ====Take Stepwise approach to treatment==== <br /> *1st (conservative)<br /> #Elevate HOB 30-to 45 deg; keep head midline<br /> ##May &quot;sandbag&quot; head of those in c-collar to promote venous drainage(c-collar can restrict venous outlfow)<br /> #Control agitation/pain<br /> ##narcotics, benzodiazepines, sedative hypnotics<br /> ###Attempt to favor short acting medications to allow neuro exam checks. Versed, Fentanyl and propofol are often appropriate.<br /> #Maintain Normocapnia (pCO2 35-40)<br /> #Treat shivering<br /> #Maintain euvolemia (Input = output)<br /> *2nd (Intervention-short term)<br /> #hyperventilate to pCO2 ~30mmHg<br /> ##This is short term as patient will equilibrate; is only meant as a temporizing measure. Attempt to wean to normocapnia as soon as able. Further do not overventilate past 25mmHg as may exacerbate damage via cerbral hypoxia (CO2 is primarily involved in autoregulation of cerebral vasculature).<br /> #Hypertonic fluids<br /> ##Mannitol 20% 1-1.5g/kg rapid IV bolus (no need for central line) OR<br /> ## 23% 30mL over 15 minutes (Needs central line)<br /> #Consult Neurosurgery (urgent) for possible evacuation or ventricular drainage. <br /> ##This is especially relevant for mass lesions causing mass effect or in hydrocephalus. <br /> *3rd (Intervention- long term)<br /> #Hypertonic fluid maintenance<br /> ##Iatrogenic hypernatremia. Use 3% NaCl to maintain na &gt;145 with q6hr serum Na cks. <br /> ###3%NS at 1mL/kg/hr appropriate (typically start at 50mL/hr).<br /> ###May continue to push Na &gt; 145, then &gt;150 then &gt;155 prn to manage ICP<br /> ####Eventually osmotic pressures will equilibrate over days. requiring higher Na values (rationale behind pushing Na slowly upward as needed rather than pushing hypernatremia to maximum). <br /> ##Iatrogenic hyperosmolar maintenance <br /> ###Mannitola 20% 0.5g/kg q4 hrsth seurm Osm checks q6hrs. (Goal Osm 300-320 mOsm/L)<br /> *4th (Intervention - Refractory elevation)<br /> #Pentobarbital coma<br /> ##loading dose: 5-20mg/kg bolus then 4mg;kg/hr titrated to burst supression on EEG.<br /> #Induced hypothermia (32-34deg)<br /> ##Arctic Sun<br /> ###Must perform surveillance cultures (routine blood culture, UA, CXR) every 48 hours since artificially supressing fever.<br /> ##Shivering protocol<br /> #Paralytics<br /> ##Risk of ICU myopathy/neuropathy with long term use.</div>

Ncdavis https://wikem.org/w/index.php?title=Elevated_intracranial_pressure&diff=15406 2013-12-24T20:44:36Z

<p>Ncdavis: </p> <hr /> <div>=Overview=<br /> *Cranial vault is a fixed volume made up of 3 main components<br /> **brain tissue (80%) blood (10% or 150L) and CSF (10% or 150mL). <br /> *While brain parenchyma is a relatively fixed volume, the blood and CSF are fluids with entranace and egress points into and out of the skull and are primarily affected with changes in ICP. <br /> **CSF is created at a rate of 20mL/hr or 500mL/day. <br /> *Neuronal injury occurs secondary to vascular compromise to brain cells either by a reduction in cerebral blood flow or direct ischemia <br /> **This is an ''' emergency''' and requires emergent intervention if sustained &gt; 5-10 minutes<br /> <br /> ==Clinical Signs and Symptoms==<br /> *Increased ICP generally causes headache (from increased pressure on heavily innervated meninges), Nausea/vomiting, and occasionally optic abnormalities (most notably ocular palsies (CN6 particularly long course intracranially) along with AMS and optic atrophy.<br /> *Morning headaches are pathomnemonic (mild hypoventilation during sleeping hours causes increases in cerebreal blood flow)<br /> <br /> ==Causes==<br /> *As the cranial vault is a fixed volume, Increases in ICP are either due to increased brain tissue (edema), blood (increase inflow or decreased outflow) and CSF (increased inflow/production or decreased outflow) in addition to abnormal mass lesions.<br /> #Mass lesions<br /> ##tumor, hematoma, air, abscess,foreign body<br /> #CSF accumulation<br /> ##Hydrocephalus(obstructive or communicating)<br /> ###Most often obstrcutive via tumor, intraventricular hemorrhage, ventriculutus/meningitis) with compression of CSF outflow<br /> #Vascular<br /> ##Either input or output failure<br /> ###Input failure: increased CBF or CBV due to failed autoregulatoin<br /> ###Outflow failure: venous congestion or sinus thrombosis<br /> #Cerebral edema<br /> ##vasogenic (vessel damage due to tumor/infection abscess<br /> ##Cytotoxic (ischemia)<br /> ##Hydrostatic: Increased transmural pressure with hydrocephalus<br /> ##Hypo osmolar<br /> <br /> ==Management==<br /> #Ensure data accurate<br /> ##observe for accurate waveforms in arterial and ICP monitors <br /> ###EVD zeroed at ear, changes with coughing/positioning<br /> ###Arterial line zeroed at ear (for accurate CPP measurement; although typically level at heart reasonably accurate<br /> #Assess ABC (as increased ICP often accompanies decline in mental status<br /> ##If need to intubate - ensure measures to avoid coughing/bucking (increases ICP).<br /> ###Lidocaine 1% 1ml/kg 1x IV bolus as premedication. <br /> ====Goals====<br /> #Keep CPP 60-110mmHg<br /> ##If &lt;110 utilize pressors (levophed or neosynephrine; levophed preferred)<br /> ##Levophed: start at 4 mcg/min; maximum 20 mcg/min.<br /> ##Phenylepherine: start at 0.4 mcg/kg/min; maximum 9 mcg/kg/min.<br /> #Maintain normothermia.<br /> ##Treat shivering<br /> ###Bear hugger (warms skin temperature)<br /> ###APAP 650q6prn for temp &gt;38.5<br /> ====Take Stepwise approach to treatment==== <br /> *1st (conservative)<br /> #Elevate HOB 30-to 45 deg; keep head midline<br /> ##May &quot;sandbag&quot; head of those in c-collar to promote venous drainage(c-collar can restrict venous outlfow)<br /> #Control agitation/pain<br /> ##narcotics, benzodiazepines, sedative hypnotics<br /> ###Attempt to favor short acting medications to allow neuro exam checks. Versed, Fentanyl and propofol are often appropriate.<br /> #Maintain Normocapnia (pCO2 35-40)<br /> #Treat shivering<br /> #Maintain euvolemia (Input = output)<br /> *2nd (Intervention-short term)<br /> #hyperventilate to pCO2 ~30mmHg<br /> ##This is short term as patient will equilibrate and is only meant as a temporizing measure. Attempt to wean to normocapnia as soon as able. Further do not overventilate far past 30mmHg as may exacerbate damage via cerbral hypoxia (CO2 is primarily involved in autoregulation of cerebral vasculature).<br /> #Hypertonic fluids<br /> ##Mannitol 20% 1-1.5g/kg rapid IV bolus (no need for central line OR<br /> ## 23% 30mL over 15 minutes (Needs central line)<br /> #Consult Neurosurgery (urgent) for possible evacuation or ventricular drainage. <br /> ##This is especially relevant for mass lesions causing mass effect or in hydrocephalus. <br /> *3rd (Intervention- long term)<br /> #Hypertonic fluid maintenance<br /> ##Iatrogenic hypernatremia. Use 3% NaCl to maintain na &gt;145 with q6hr serum Na cks. <br /> ###3%NS at 1mL/kg/hr appropriate (typically start at 50mL/hr).<br /> ###May continue to push Na &gt; 145, then &gt;150 then &gt;155 prn to manage ICP<br /> ####Eventually osmotic pressures will equilibrate over days. requiring higher Na values (rationale behind pushing Na slowly upward as needed rather than pushing hypernatremia to maximum). <br /> ##Iatrogenic hyperosmolar maintenance <br /> ###Mannitola 20% 0.5g/kg q4 hrsth seurm Osm checks q6hrs. (Goal Osm 300-320 mOsm/L)<br /> *4th (Intervention - Refractory elevation)<br /> #Pentobarbital coma<br /> ##loading dose: 5-20mg/kg bolus then 4mg;kg/hr titrated to burst supression on EEG.<br /> #Induced hypothermia (32-34deg)<br /> ##Arctic Sun<br /> ###Must perform surveillance cultures (routine blood culture, UA, CXR) every 48 hours since artificially supressing fever.<br /> ##Shivering protocol<br /> #Paralytics<br /> ##Risk of ICU myopathy/neuropathy with long term use.</div>

Ncdavis https://wikem.org/w/index.php?title=Elevated_intracranial_pressure&diff=15405 2013-12-24T20:40:26Z

<p>Ncdavis: ICP management</p> <hr /> <div>=Overview=<br /> *Cranial vault is a fixed volume made up of 3 main components<br /> **brain tissue (80%) blood (10% or 150L) and CSF (10% or 150mL). The pressure inside this space is summi<br /> *While brain parenchyma is a relatively fixed volume, the blood and CSF are fluids with entranace and egress points into and out of the skull and are primarily affected with changes in ICP. <br /> **CSF is created at a rate of 20mL/hr or 500mL/day. <br /> *Neuronal injury occurs secondary to vascular compromise to brain cells either by a reduction in cerebral blood flow or direct ischemia <br /> **This is an ''' emergency''' and requires emergent intervention if sustained &gt; 5-10 minutes<br /> <br /> ==Clinical Signs and Symptoms==<br /> *Increased ICP generally causes headache (from increased pressure on heavily innervated meninges), Nausea/vomiting, and occasionally optic abnormalities (most notably ocular palsies (CN6 particularly long course intracranially) along with AMS and optic atrophy.<br /> *Morning headaches are pathomnemonic (mild hypoventilation during sleeping hours causes increases in cerebreal blood flow)<br /> <br /> ==Causes==<br /> *As the cranial vault is a fixed volume, Increases in ICP are either due to increased brain tissue (edema), blood (increase inflow or decreased outflow) and CSF (increased inflow/production or decreased outflow) in addition to abnormal mass lesions.<br /> #Mass lesions<br /> ##tumor, hematoma, air, abscess,foreign body<br /> #CSF accumulation<br /> ##Hydrocephalus(obstructive or communicating)<br /> ###Most often obstrcutive via tumor, intraventricular hemorrhage, ventriculutus/meningitis) with compression of CSF outflow<br /> #Vascular<br /> ##Either input or output failure<br /> ###Input failure: increased CBF or CBV due to failed autoregulatoin<br /> ###Outflow failure: venous congestion or sinus thrombosis<br /> #Cerebral edema<br /> ##vasogenic (vessel damage due to tumor/infection abscess<br /> ##Cytotoxic (ischemia)<br /> ##Hydrostatic: Increased transmural pressure with hydrocephalus<br /> ##Hypo osmolar<br /> <br /> ==Management==<br /> #Ensure data accurate<br /> ##observe for accurate waveforms in arterial and ICP monitors <br /> ###EVD zeroed at ear, changes with coughing/positioning<br /> ###Arterial line zeroed at ear (for accurate CPP measurement; although typically level at heart reasonably accurate<br /> #Assess ABC (as increased ICP often accompanies decline in mental status<br /> ##If need to intubate - ensure measures to avoid coughing/bucking (increases ICP).<br /> ###Lidocaine 1% 1ml/kg 1x IV bolus as premedication. <br /> ====Goals====<br /> #Keep CPP 60-110mmHg<br /> ##If &lt;110 utilize pressors (levophed or neosynephrine; levophed preferred)<br /> ##Levophed: start at 4 mcg/min; maximum 20 mcg/min.<br /> ##Phenylepherine: start at 0.4 mcg/kg/min; maximum 9 mcg/kg/min.<br /> #Maintain normothermia.<br /> ##Treat shivering<br /> ###Bear hugger (warms skin temperature)<br /> ###APAP 650q6prn for temp &gt;38.5<br /> ====Take Stepwise approach to treatment==== <br /> *1st (conservative)<br /> #Elevate HOB 30-to 45 deg; keep head midline<br /> ##May &quot;sandbag&quot; head of those in c-collar to promote venous drainage(c-collar can restrict venous outlfow)<br /> #Control agitation/pain<br /> ##narcotics, benzodiazepines, sedative hypnotics<br /> ###Attempt to favor short acting medications to allow neuro exam checks. Versed, Fentanyl and propofol are often appropriate.<br /> #Maintain Normocapnia (pCO2 35-40)<br /> #Treat shivering<br /> #Maintain euvolemia (Input = output)<br /> *2nd (Intervention-short term)<br /> #hyperventilate to pCO2 ~30mmHg<br /> ##This is short term as patient will equilibrate and is only meant as a temporizing measure. Attempt to wean to normocapnia as soon as able. Further do not overventilate far past 30mmHg as may exacerbate damage via cerbral hypoxia (CO2 is primarily involved in autoregulation of cerebral vasculature).<br /> #Hypertonic fluids<br /> ##Mannitol 20% 1-1.5g/kg rapid IV bolus (no need for central line OR<br /> ## 23% 30mL over 15 minutes (Needs central line)<br /> #Consult Neurosurgery (urgent) for possible evacuation or ventricular drainage. <br /> ##This is especially relevant for mass lesions causing mass effect or in hydrocephalus. <br /> *3rd (Intervention- long term)<br /> #Hypertonic fluid maintenance<br /> ##Iatrogenic hypernatremia. Use 3% NaCl to maintain na &gt;145 with q6hr serum Na cks. <br /> ###3%NS at 1mL/kg/hr appropriate (typically start at 50mL/hr).<br /> ###May continue to push Na &gt; 145, then &gt;150 then &gt;155 prn to manage ICP<br /> ####Eventually osmotic pressures will equilibrate over days. requiring higher Na values (rationale behind pushing Na slowly upward as needed rather than pushing hypernatremia to maximum). <br /> ##Iatrogenic hyperosmolar maintenance <br /> ###Mannitola 20% 0.5g/kg q4 hrsth seurm Osm checks q6hrs. (Goal Osm 300-320 mOsm/L)<br /> *4th (Intervention - Refractory elevation)<br /> #Pentobarbital coma<br /> ##loading dose: 5-20mg/kg bolus then 4mg;kg/hr titrated to burst supression on EEG.<br /> #Induced hypothermia (32-34deg)<br /> ##Arctic Sun<br /> ###Must perform surveillance cultures (routine blood culture, UA, CXR) every 48 hours since artificially supressing fever.<br /> ##Shivering protocol<br /> #Paralytics<br /> ##Risk of ICU myopathy/neuropathy with long termed use.</div>

Ncdavis https://wikem.org/w/index.php?title=Brain_death&diff=15401 2013-12-23T20:53:38Z

<p>Ncdavis: fontera neurocritical care edit</p> <hr /> <div>==Criteria==<br /> # Known proximate cause of condition<br /> # Exclusion of complicating medical conditions (severe electrolyte, acidbase, or endocrine disturbance)<br /> # No drug intoxication/poisoning<br /> # Core temp &gt;32C (90F)<br /> # Cerebral unresponsiveness<br /> # Absence of brain stem relexes (see below)<br /> # Apneic (see below)<br /> # Irreversible condition (+/- repeat exam in 6hrs)<br /> <br /> ==Brain Stem Reflexes==<br /> # Pupils<br /> ##no response to light (fixed and mid-dilated)<br /> # Ocular movement<br /> ##Oculocephalic reflex (+Doll's Eyes)<br /> ###eyes should move to maintain forward fixation as head is turned.<br /> ##Oculovestibular reflex (aka &quot;Calorics&quot;)<br /> ###(irrigation w/ 60cc cold water to ears on intact tympanic membrane and observe for deviation of eyes/fast beat nystagmus. Allow 5 minutes between either side.<br /> #corneal reflex (CN 5)<br /> ##drip saline flush into eye<br /> ##progress to direct stimulation on sclera with gauze if no response above (DO NOT scrape cornea)<br /> #Paryngeal (CN 9/10)<br /> ##gag (tounge blade) or suction.<br /> #Tracheal (CN 10)<br /> ##endotracheal suction (In intubated patients only)<br /> ==Apnea Testing==<br /> # Prerequisites:<br /> ##Clinical Criteria<br /> ##Core temp &gt;32 C (actual temp value &gt; 32 varies by institution) with corrected electrolytes. &gt; 36.5C is preferred.<br /> ##SBP &gt;90<br /> ##Nl PCO2 (&gt;40)<br /> ##Nl PO2 (preoxiginate &gt;200)<br /> # Test:<br /> ##check baseline ABG (ensure PCO2 &lt;40mmHg to maximate target PCO2 rise)<br /> ##Connect pulse ox, disconnect ventilator, place nasal cannula in ET (at carina), and place on 100% O2 @ 6LPM.<br /> ##Physician able to declare brain death (typically neurology/neurosurgery) will observe for resp movements<br /> ##Draw [[ABG]] @ 8 min. Observe for PCO2 rise &gt;20mmHg over 8 minutes with no respiratory movement --&gt;positive apnea test (supports brain death) <br /> ###Pos test = 20 increase over baseline (typically 60) ensure to blow down CO2 to ~40 to enable 20mmHg rise. Typical rise is 3mmHg per minute<br /> #Considerations<br /> ##Abort the test (reconnect ventilator) if SBP &lt;90 or sig O2 desat (can draw [[ABG]] @ that time, with same criteria as above).<br /> ##Must perform 2 exams 6 hours apart in addition to apnea test.<br /> <br /> One-Legacy 800-338-6112<br /> <br /> ==Organ Donation==<br /> *Decisions over suitability of a donor typically are left to established organizations that differ for each hospital.<br /> *General contraindications <br /> #any kind of cancer (EXCEPT skin cancers other than melanoma, certain primary brain tumors). Essentially this means only cancers with very low risk of metastasis are acceptable.<br /> #Any kind of systemic infection or communicable incurable disease.<br /> ##Active Fungal disease (Cryptoccous, Aspergillus, Histoplasma, Coccidioides, Candidemia, invasive yeast<br /> ##Active Bacterial infection (Tb, sepsis)<br /> ##Viral infections HIV, HTLV, rabies, reactive HbsAg, West nile, SARS, enterovirus, HSV, VZV, EBC etc)<br /> <br /> *The general goals with organ donation are organ preservation by maintaining 1. physiologic levels of neuro mediated hormones 2. blood pressure 3. Obtaining Screening labs<br /> #Pan hypopituitary state<br /> ##Diabetes insipidus<br /> ###Clinical: DI typically presents with UOP &gt;5cc/kg/hr. Urine Spec Grav: &lt; 1.005, serum Na &gt; 145 or serum osmolality &gt; 305mg/dL. <br /> ###Treatment: Frequent Na monitoring. Bolus vasopressin 0.5U IV then gtt with goal of 0.5U/h. Titrate to UOP 1-2 ml/kg/h. <br /> ##Hypothyroid - T4 20 microgram T4 IV bolus then T4 at 10 micrograms/hr. (This causes hyperkalemia so administer 10U regular insulin with 1 amp 50% detrose before IV bolus)<br /> ##Hypoinsulinemia- Insulin gtt, titrate to maintain gluciose 80-110 with q1hr checks<br /> ##Hypocortisol - Tx - 15mg/kg IV bolus qd empirically.<br /> #Hypotension <br /> ##Place a- line with goal SBP &gt; 90 MAP &gt; 60<br /> ###If goals are not met a continuous caridac index monitor (Vigileo or PICCO) may be indicated. Goals are CI &gt; 2.5 and UOP &gt;1ml/kg/hr start dobutamine/milrinone gtt. <br /> ###If MAP &lt; 60 despite adequate CI, start peripheral pressor (phenylephrine or norepinepherine).<br /> ##Place central line with CVP goals &gt;5<br /> ##Maintain fluids at 1.5-2ml/kg/hr. Choice of fluids include NS for Na &lt; 155, 1/2NS for Na 156-165, D5W if Na &gt; 165.<br /> #Screening labs<br /> ##HIV 1/2, HTLV 1,2, RPR, Toxo IgG, CMV IgG, EBV IgV, VZV IgG, HSV 1-2, Hepatitis A,B,C. <br /> ##LFT's,amylase, lipase, CBC, coagulation profile. <br /> <br /> *Special Considerations<br /> #Heart - often experiences stunning myocardium secondary to neurogenic sympathetic surge. Often will lower EF with some myocyte necrosis and troponin leak. Order q6hr serial cardiac enzymes then repeat echo. Very often heart will recover after initial stunning period. <br /> <br /> ==See Also==<br /> *[[ACLS (Main)]]<br /> *[[Post Cardiac Arrest]]<br /> *[[Altered Mental Status]]<br /> <br /> ==Source ==<br /> 2/8/07 DONALDSON (adapted from One-Legacy)<br /> <br /> [[Category:Neuro]]</div>

Ncdavis https://wikem.org/w/index.php?title=Brain_death&diff=15400 2013-12-23T19:44:11Z

<p>Ncdavis: Neurocritical care edit</p> <hr /> <div>==Criteria==<br /> # Known proximate cause of condition<br /> # Exclusion of complicating medical conditions (severe electrolyte, acidbase, or endocrine disturbance)<br /> # No drug intoxication/poisoning<br /> # Core temp &gt;32C (90F)<br /> # Cerebral unresponsiveness<br /> # Absence of brain stem relexes (see below)<br /> # Apneic (see below)<br /> # Irreversible condition (+/- repeat exam in 6hrs)<br /> <br /> ==Brain Stem Reflexes==<br /> # Pupils<br /> ##no response to light (fixed and mid-dialated)<br /> # Ocular movement<br /> ##no oculocephalic reflex (+Doll's Eyes)<br /> ##no vestibulocochlear (deviation of eyes to irrigation w/ 50mL cold water to ears - allow 1 min after and 5 min b/t)<br /> # Facial motor response/sensation<br /> ##jaw reflex (grimacing to deep facial pressure)<br /> ##corneal reflex (touch eye w/ swab)<br /> # Paryngeal/tracheal<br /> ##gag (tounge blade)<br /> <br /> ==Apnea Testing==<br /> # Prerequisites:<br /> ##Clinical Criteria<br /> ##Core temp &gt;32 C (actual temp value &gt; 32 varies by institution) with corrected electrolytes. &gt; 36.5C is preferred.<br /> ##SBP &gt;90<br /> ##Nl PCO2 (&gt;40)<br /> ##Nl PO2 (preoxiginate &gt;200)<br /> # Test:<br /> ##check baseline ABG (ensure PCO2 &lt;40mmHg to maximate target PCO2 rise)<br /> ##Connect pulse ox, disconnect ventilator, place nasal cannula in ET (at carina), and place on 100% O2 @ 6LPM.<br /> ##Physician able to declare brain death (typically neurology/neurosurgery) will observe for resp movements<br /> ##Draw [[ABG]] @ 8 min. Observe for PCO2 rise &gt;20mmHg over 8 minutes with no respiratory movement --&gt;positive apnea test (supports brain death) <br /> ###Pos test = 20 increase over baseline (typically 60) ensure to blow down CO2 to ~40 to enable 20mmHg rise. Typical rise is 3mmHg per minute<br /> #Considerations<br /> ##Abort the test (reconnect ventilator) if SBP &lt;90 or sig O2 desat (can draw [[ABG]] @ that time, with same criteria as above).<br /> ##Must perform 2 exams 6 hours apart in addition to apnea test.<br /> <br /> One-Legacy 800-338-6112<br /> <br /> ==See Also==<br /> *[[ACLS (Main)]]<br /> *[[Post Cardiac Arrest]]<br /> *[[Altered Mental Status]]<br /> <br /> ==Source ==<br /> 2/8/07 DONALDSON (adapted from One-Legacy)<br /> <br /> [[Category:Neuro]]</div>

Ncdavis https://wikem.org/w/index.php?title=Brain_death&diff=15399 2013-12-23T19:11:22Z

<p>Ncdavis: changes per neurocritical care - fontera</p> <hr /> <div>==Criteria==<br /> # Known proximate cause of condition<br /> # Exclusion of complicating medical conditions (severe electrolyte, acidbase, or endocrine disturbance)<br /> # No drug intoxication/poisoning<br /> # Core temp &gt;32C (90F)<br /> # Cerebral unresponsiveness<br /> # Absence of brain stem relexes (see below)<br /> # Apneic (see below)<br /> # Irreversible condition (+/- repeat exam in 6hrs)<br /> <br /> ==Brain Stem Reflexes==<br /> # Pupils<br /> ##no response to light (fixed and mid-dialated)<br /> # Ocular movement<br /> ##no oculocephalic reflex (+Doll's Eyes)<br /> ##no vestibulocochlear (deviation of eyes to irrigation w/ 50mL cold water to ears - allow 1 min after and 5 min b/t)<br /> # Facial motor response/sensation<br /> ##jaw reflex (grimacing to deep facial pressure)<br /> ##corneal reflex (touch eye w/ swab)<br /> # Paryngeal/tracheal<br /> ##gag (tounge blade)<br /> <br /> ==Apnea Testing==<br /> # Prerequisites:<br /> ##Clinical Criteria<br /> ###Must be diagnosis compatabile with brain death (SAH/ICH/TBI etc.)<br /> ##Core temp &gt;32 C (actual temp varies by institution) with corrected electrolytes. &gt; 36.5C is preferred.<br /> ##Exclusion of iatrogenic drug effects<br /> ###check urine tox fo ropiates or benzodiazepines and illicit drugs. Review med rec for sedating/paralytic meds (recent intubation/propofol infusion etc).<br /> ####if drug cannot be quantified. Patient observed for 4x half life of drug (drug levels ~5% of previous)<br /> ##SBP &gt;90<br /> ##Nl PCO2 (&gt;40)<br /> ##Nl PO2 (preoxiginate &gt;200)<br /> #Physical Exam (when to perform brain death)<br /> ##must have no mention, no motor or sensory response. (no movement or hemodynamic response(increased tachycardia) to noxious stimulation).<br /> # Test:<br /> ##Connect pulse ox, disconnect ventilator, place nasal cannula in ET (at carina), and place on 100% O2, observe for resp movements, draw [[ABG]] @ 8 min.<br /> ##Pos test = 20 increase over baseline (typically 60) ensure to blow down CO2 to ~40 to enable 20mmHg rise.<br /> ##reconnect ventilator if SBP &lt;90 or sig O2 desat (can draw [[ABG]] @ that time, with same criteria as above).<br /> ##Must perform 2 exams 6 hours apart in addition to apnea test.<br /> <br /> One-Legacy 800-338-6112<br /> <br /> ==See Also==<br /> *[[ACLS (Main)]]<br /> *[[Post Cardiac Arrest]]<br /> *[[Altered Mental Status]]<br /> <br /> ==Source ==<br /> 2/8/07 DONALDSON (adapted from One-Legacy)<br /> <br /> [[Category:Neuro]]</div>

Ncdavis