Subarachnoid Hemorrhage And Pregnancy (PART 3)

Other consideration:(4)
Fluids and electrolyte changes occur as a result of the increase in interstitial fluid by as much as 6 litres.To maintain this isotonic hyperhydration sodium is retained. 
Although total body sodium is increased the serum sodium is 2-3 meq/L below non pregnant level.
The infusion of sodium free fluids such as 5% dextrose in water can lead to hyponatremia in mother and neonate (Lind,1983), potassium levels are also somewhat lower in pregnancy.

Plasma osmolality is reduced by as much as 10 mosm /kg H20(Hytten 78) within the first few weeks of pregnancy due to the fall in electrolyte and urea. Urea falls in early pregnancy to about a quarter of normal values and continues to fall slightly throughout pregnancy possibly due to the increased renal clearance.Similarly creatinine and uric acid levels falls.

Fasting glucose levels are decreased by the 10th week of pregnancy. Glycosuria however is common making the diagnosis of gestational diabetes dependent on fasting blood sugar levels.
Periods of starvation should be restricted to the minimum necessary for anesthetic safety as rapid increase in ketone production can occur.

Serum alkaline phosphatase rises to about 4 times normal in pregnancy as it produced by the placenta in normal women.

Marked leucocytosis occurs due to an increase in the neutrophil polymorphnuclear cells.The erythrocyte sedimentation rate is not value in pregnancy as a nonspesific sign of disease.It is usually very high possibly due to the high levels of plasma globulins and fibrinogen.

How the mother's immunological system deals with the fetal allograft is not known. Certainly she can still respond with anaphylactic reactions to drugs (Lund,1980,Bareka 1980).The hypotension and bronchospasm of such response can be lethal to the fetus eventhough the mothers survives.


The developing fetus and anesthethics:(4,5)
The risk of anesthesia for the mother is proportionate to gestation. The risk to the fetus of anesthesia are however in inverse proportion to its gestational age.(Broadsky et all 1980).

It is estimated that 30% of pregnancies abort 
spontaneously.It is not known wether anesthesia in early and as yet undiagnosed pregnancy does increase the rate of fetal loss. It seems certain that some drugs and enviromental factors can cause fetal loss during the first week of pregnancy before implantation has occured and its possible that anesthesia may also cause fetal death at this early stage.


Organogenesis takeplace in the fetus from second to the tenth week of gestation and during this period, when pregnancy is often not yet diagnosed teratogenic affects may occur.However even during this very vulnerable fetal stage,it seems possible that the most likely effect of drugs would be fetal death.

By the end of the first trimester the differentiation of embryonic cells into organ is completed and congenital malformations can no longer becaused by the drugs. But it is possible that fetal death may result from the action of drugs ,or the indirect effect of anesthesia or surgery. Fetal loss of 23% indiagnosed pregnancy has been reported following laparatomy (Saunders and Milton, 1973) and 30% following cervical sutures(Shinder and Loebster 1965).
Many different factors may play a part in these very high rates of fetal loss and there is no evidence that any particular anesthetic technique is involved.Teratogenic damage to the fetus is the most feared side effect of drugs during pregnancy.It is seems essential thay any drugs that does have teratogenics effects must cross the placenta (Beeley 1981).

But this is not an inevitable consequence of drugs that cross the placenta even at this stage of organogenesis.
All drugs that affect the mother's CNS must also cross the placenta and are thus treated with suspicion early in pregnancy.
Thalidomide cause congenital abnormalities in only a quarter of the cases at the same stage of development. 

Several factors may be involved in damage to the fetus including enviromental factors.
Other drugs are suspected of teratogenic potentially,such as alcohol,phenytoin,warfarin,lithium and quinine.
Many more have a lesser index of suspicion such as barbiturate,phenothiazine,diazepam and chronic low dose inhalational agents especially N20.

Even so the evidence seems to point to a possible rise in spontaneous abortion rate rather than congenital malformation (Vesseg and Nunn,1980) in those working in the theatre and also in women undergoing.
Anesthesia in the first trimester of pregnancy (Heinomen et al 1977). No anesthetic drugs other than N20 has been directly implicated in causing congenital abnormalities.
Many factors other than teratogenicity may be involved in the apparent rise of fetal loss associated with anesthesia.
Indirect effect such as a fall in placental perfusion,anoxia
relative hypercarbia,hyperpyrexia,acidosis and fluid and electrolyte imbalance may all cause the death of the fetus without apparent ill effects on the mother.Direct effects of anesthetic drugs on the fetus may cause exagerated effects on fetal physiology such as a reduction in fetal cardiac output resulting in death.

Monitoring maternal temperature between 37-37,5 C is important as fetal wastage is high following pyrexia from any cause.


Anesthetic consideration :(4)
All elective surgery should be postponed until after pregnancy. Anesthesia in the first trimester should be avoided whenever possible if fetal survival is desired.But if it does take place it seems more possible that fetal death rather than malformation will result.
Therapeutic abortion is therefore not advised.
Pregnancy should be excluded in all women in whom it is possibly before elective surgery is undertaken.

New drugs which of necessary have not been tested for teratogenicity should not be used in the first trimester if fetal survival is desired eventhough there is some benefit from the drug.
New sedatives,metoclopromide,and H2 antagonist have not been shown to be safe from teratogenic effects and should be avoided when possible.


Effects of Anesthetic and Analgesic drugs:(4,5,6)
Non anesthetic factors :
Anxiety: Morishima et al 1978 have experimentally established and reproduced fetal asphyxia induced by psychological maternal stress.


Pain:(5)
The pain of labor produces an increase in maternal blood cathecolamine and decrease in UBF and therefore in fetal oxygenation (Shnider 1971).
Maternal cathecolamines decrease intrauterine pressure and frequency of contractions.However it is still uncertain wether the small amount of epinephrine added to local anesthetic for epidural analgesia during labor affects the duration of labor (Albright et all 1981).
Epidural analgesia decreases the maternal cathecolamine level and restores UBF as well as a decreasing sympathetic activity and vasoconstriction caused by painful uterine contractions(Shnider et all 1980).


Drugs :(2,3,5,6)
Drugs administered during pregnancy can have fetal or maternal side effects and interact with anesthetic drugs.
Betamimetics are prescribed in obstetrics as tocolytic (Jouhet 1981). The drugs most often used in France
(salbutamol,ritodrine) have predominant beta-2 action but also have beta-1 actions,which can cause maternal side effects both cardiovascular (tachycardia,hyper or hypo
tension),fetal tachycardia and metabolic (hypoglycaemia,
maternal and fetal hyperinsulin,lipolysis).
Pulmonary edema and cardiac failure have been reported when betamimetics are used,especially when used with corticosteroids to accelarate fetal lung maturation (Millier,1980).

The interactions of these drugs with some anesthetics are known :
1.Cardiovascular effects of betamimetics can be poten
   tiated by halogenated anesthetics and produce cardiac 
   arrythmia.


2.Muscle relaxant such as succinylcholine can have cardio
   vascular side effects potentiated by betamimetics.


3.Regional anesthesia can produce hypotension,with 
   betamimetics these effect may be increased and induce 
   acute fetal distress.


Antihypertensive therapy :
Betablocker and especially propranolol increase fetal and neonatal vulnerability to hypoxia by preventing increases in cardiac output. After blockade of betareceptors,the neonate may have bradycardia and hypoglycaemia and delayed pulmonary fluid resorption after birth.
These effects can be correlated with the neonatal phar
macokinetics of the betablocker (Boutroy et all 1981).
The pharmacokinetics of propranolol are modified by cimetidine which is sometimes administered as a preme-
dication for emergency can to avoid the acid aspiration syndrome (Mc Coughey et all 1981).
If the propranolol and cimetidine are administered together the blood level is higher than otherwise(Howe et all 1980).
As cimetidine is transfered across the placenta neonatal side effects of propranolol could be increased although this is not yet been reported.

But a bolus of esmolol (0,5 to 1mg/kg) may be critical in preventing aneurysm rupture. Methyldopa is very useful for antihypertensive therapy during pregnancy. 
A recent study has demonstrated that neonate from mothers who receive methyldopa have a significant decrease in systolic blood pressure(SBP) for two days after birth(Whitelaw, 1981).

Hazard of anesthetic drugs to both the mother and the neonate are increased by the use of antihypertensive drugs.
Drugs that are potentially toxic include nitropruside ,betablockers and mannitol. Although nitropruside may decrease UBF and cause fetal cyanide toxicity one or two boluses of 25 to 100 mcg may be extremely useful during laryngoscopy and intubation.
Both nitropruside and betablocker given briefly in bolus form before delivery are unlikely to produce fetal problem.


Mannitol has been shown to cross the placenta and it may accumulate in the fetus and lead to change in fetal osmolality,volume and the concentration of various electrolytes. In human study the administration of 200 g of mannitol to the mother before delivery altered 
the volume, osmolality and concentration of solutes in 
the fetus. 
However in dosage used clinically in aneurysm clipping (0,5 to 1 g/kg) mannitol is unlikely to cause severe fluid or electrolyte abnormalities on the fetus.
Mannitol is also not always essential for brain relaxation
however if it is required moderate doses should be used.


All drugs used for relief of apprehension and pain during labour and delivery cross the placenta and affect the baby who is markedly susceptible to the depressant effect of drugs used in labour.
Conway and Brackbill 1970 evaluated the neonatal effects of a number of anesthetic and analgesic drugs and described muscular hypotonia, decreased level response to auditory stimuli,and decreased visual attention and all these signs lasted for one month.
The most widely used narcotics is pethidine(mepheridine)
by im at a dose of 50 to 100 mg or intravenous 12,5  to 
30 mg, neonatal respiratory depression is slight unless there is fetal distress or other central depressant drugs have been administered before pethidine.
The use of narcotics whatever the way of administration carries a risk of respiratory depression to the neonate so an antagonist is essential in the delivery room. Naloxon is the agent of choice. Neonatal respiratory depression may occur after moderate maternal administration of narcotic
especially if there has been fetal asphyxia. 
Neonatal injection of naloxone (0,04 mg iv or 0,2 mg im) should be given after ventilation resuscitation (Lassner et all 1978).


Inhalation analgesia :(3,5,6)
N20 can be offered throughout labour for intermittent analgesia, selfadministered by the mother or administered by the midwife or doctor,70% of mothers have reasonable pain relief with a mixture of 50%N20 and 50% oxygen. The concentration is safe for the mother and fetus and does not cardiorespiratory depression or affect the progress of labour. A premix concentration of 50% N20 and 50% 02 (Entonox) is available in the VK and most of Europe 
 allowing self administration without the risk of oxygen failure.
Increasing the dose and duration of N20 anesthesia before delivery carries with the risk of producing diffusion hypoxia in the neonate.
If the induction delivery period exceeds 20 minutes,N20 should be stop.


Halothane used in 0,5% concentration is a good supple-
mental anesthetic to N20 for ceasarean section, in higher concentrations it depresses uterine tone.During vaginal delivery this effect may be used to treat uterine hyper
contractility or to facilitate intrauterine manipulation.
The halogenated agents do not cause important depres
sion of neonate. If absolutely necessary isoflurane seems  
a good choice because it maintains uterine blood flow in experimental animals at levels of 1,5 MAC.


Thiopental in less than a 250 mg dose does not produce an important degree of depression of the nonate.
Tranquilizers are administered iv and/or im for treat apprehension early in labour;promazine 25-50 mg,prome-   
thazine 25-50mg,propromazine 10-20 mg and hydroxyzine 25-50 mg. These drugs should be given carefully when combined with sedative or narcotics because ventilatory and cardiovascular depression in the mother and the baby.


Ergot alkaloids and vasopressors administered together or following one another may lead to severe hypertension and cerebrovascular accidents.The only agents that do not cross the placenta (except gallamine) are muscle relaxant.


Drugs in Breast milk :(4)
Analgesia and anesthesia in the puerperium cause concern when the mother is breast feeding as the effect of the drugs on the neonate may be undesirable. Analgesic and anesthetics are all lipid soluble drugs that are distributed throughout the body and in the milk.
For similar pharmacokinetics reason drugs in the milk would be absorbed by the neonate.Therapeutic doses of analgesic and anesthetic drugs used for short periods of time do not result in neonatal sedation of prolonged duration.These drugs are highly protein bound in the mother and only very small quantities of free drug are able to cross to the milk.

Here futher protein binding occurs but less in plasma. 
Milk has a lower pH than plasma so weakbases such a narcotics, benzodiazepines and phenothiazines can reach higher concentrations in the milk than weak acids such as barbiturate. However,although these lipid soluble drugs diffuse into the milk already present in the breast between feeds, incomplete equilibration occurs because of the changing plasma levels and rate of milk production.The volume of milk the baby ingest is small and the low level of drug in the milk prevents therapeutic level being obtained in the baby's plasma.
However it is possible that the baby may have an allergy to a drug in less than therapeutic dose.
Breast feeding is no justification for following the mother poor analgesic in the puerperium when pain can be considerable from abdominal of perineal wounds.

to be continued

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Management of Status Epilepticus (PART 3)

ANESTHETIC CONSIDERATION IN SE:(1)
After all standard therapy has failed or has been determined to have unacceptable side effects most neurology textbooks recomend consulting an anesthesiolo
gist for administration of general anesthesia to manage SE.Under these situations what anesthetic should be given ?
Unfortunately no controlled clinical studies have been conducted to adequately answer this question.
Anesthetic drugs that have been used successfully to stop SE include barbitutates,benzodiazepine,propofol,etomidate ketamine,isoflurane,enflurane,and halothane. 
If general anesthesia is needed to manage SE a patient outcome is thought to corelate more with the underlying diseases than the success in terminating seizures.

One factor in this is the delay in beginning general anesthesia caused by the need to first try less potent drugs and the logistic problems in starting an anesthetic in an intensive care unit.
Prolonged used of high dose of barbiturate (i.e.for days or weeks) has been associated with barbiturate tolerance which may exacerbate the underlying seizure problem.
In one case report,isoflurane was used to facilitate the withdrawal of barbiturate.In addition,the neurochemical effects of such prolonged anesthetic used can result in substantial increases in brain glycogen after only a few hours. Moreover the potential for prolonged volatile anesthesia to be organotoxic or to induce tolerance is unknown.

The effects of isoflurane,thiopental,ketamine and midazo 
lam were assessed in rats undergoing mercaptopropionic acid induced or flurothyl induced seizures. 
Midazolam resulted in less damaged in the substantia nigra after seizures.
No protective effect was suggested with isoflurane or thiopental and although a protective effect was suggested with ketamine,it was statistically unsignificant.  
Unfortunately this study revealed nothing about the anes
thetic effects or seizure induce damage in the lymbic system.The ketamine data however are supported by other reports of anticonvulsant or neuroprotective of ketamine in the lymbic system during seizures in rodents. 
For the reasons previously given the therapeutic approach in choosing an anesthetic agent for SE should first involve increasing dosis of benzodiazepine or barbiturate. 
Only after this therapy failed should volatile anesthetic drugs be considered.

Volatile anesthetics have the advantage of allowing continuous realtime titration to maintain a spesific blood anticonvulsant level based on entidal gas monitoring.
In one patient the monitoring of end tidal volatile anesthetic concentration facilitated titration of the anti
convulsant anesthetic against EEG.
In another patient,isoflurane use facilitated withdrawal of a prolonged barbiturate infusion on which the patient was thought to be dependent.
Thus volatile anesthetics may have a role in closely titrating anticonvulsant therapy for seizures in situation where a general anesthesia is to use as little as possible while observing the patient closely for cessation of seizure and for hemodynamic compromise.

Such patient must be intubated and mechanical ventilated .
Optimally continuous EEG shoul be monitored through anesthetic procedure.If thiopental is used 50 to 500 mg iv can be given as a loading dose in adult,followed by an iv infusion,the infusion rate initially should be higher
and then should be decreased as indicated by EEG.
After the loading dose the infusion rate could be set initially at 500-1000 mg/h and then decreased as indicated to the lowest rate feasible.
Repeated boluses,100-500 mg,might be needed initially to mantain close titration.
If isoflurane is used it should be started at 0,2-0,3% inspired concentration (6L/min gas flow initially) and inreased over 10 to 20 min as indicated by EEG and hemodynamic tolerance.

Determining the end point to guide drug titration can be difficult. For example,burst occuring within a burst suppression pattern on EEG can resemble epileptic discharges.
The decision about seizure control and EEG interpretation should be jointly with the refering neurologist or epileptologist.
After seizures are controlled and if the source is still unclear reversible causes should be sought and corrected,
after which,anesthesia should be stopped. 
Otherwise the anesthetic dose should be decreased periodically to permit assessment. 
If seizures continue to recur on anesthetic discontinuation the next decision is wether to continue anesthesia considering the many unknown effects,bioethical concerns and logistic and economic issues of prolonged anesthetic administration compared with drawing life support. Nothing,the trend toward end tidal concentrations at which seizures recur,a real time seizure thresold,over such 
assessment may contribute to such decision.

Summary :
Status epilepticus can be defined as a condition in which prolonged or recurrent seizures or epileptic events persist for more than 30 minutes.
SE is most often seen with drug withdrawal (including antiepilepticmedication and alcohol),drug intoxication
metabolic disarray and structural lesion from stroke,tumor,
abscess and trauma.

Morbidity and mortality from SE are related to three factors 
1.the damage to the CNS caused by the acute insult 
    precipitating the SE.
2.systemic stress from repeated seizures.
3.the injury from repetitive electrical discharges with the 
   CNS.

The most important clinical factors determining outcome are etiology, and the time from onset of SE until treatment is initiated.
The worst prognosis is found in those in whom status results from a serious intracranial process such as encephalitis, 
stroke or cerebral hemorhage.The best prognosis is seen in patients without structural lesions.

Generalized convulsive status epilepticus is considered  
a neurologic emergency.
To prevent brain damage seizure must be stopped as soon as possible optimally within 30 minutes of onset.
Initial treatment of SE starts with basic life support.
In addition the management of SE is best carried out using a predetermined protocol.
After all standard therapy has failed or has been deter mined unacceptable side effects neurology textbooks recomend consulting anesthesiologist for administration of general anesthesia to manage status epilepticus.

Reference :
1.Koffke Andrew W et all: Status Epilepticus,Anesthesia for 
   Epileptic Patients ;Cottrell E James;Anesthesia and 
   Neurosurgery;4th edit,Mosby Company,St Louis, 
   London,Philadelphia,2001,pp 477-8.

2.Trop Davy,Oliver Andre:The Problem of Status Epilepti
    cus,Albin S M;Textbook of Neuroanesthesia ,The McGraw 
    Hill Company,Newyork,1997,pp.684-7.

3.Chang JW,Bleck P Thomas:Status epilepticus;Stone DJ
   Sperry JR;the Neuroanesthesia Handbook,Mosby,St louis
   Baltimore,1966.pp.452-5

4.Namara MC Brian,Boniface J Simon:The EEG in Status   
   Epilepticus;Matta F Basil;Textbook of Neuroanesthesia 
   and Critical Care,Greenwich Medical Media Ltd,London
   2000,pp.78-80.

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Management of Status Epilepticus (PART 2)

MANAGEMENT OF TONIC- CLONIC  SE:(1,2)
Time from initiation
of observation and
treatment (min)          Procedure
=================================================
        0                         Assesss cardiorespiratory function
                                   as the presence of tonic clonic sta
                                   tus is verified.If ensure of diagnosis
                                   observe one tonic-clonic attack and
                                   verify the presence of unconcious
                                   ness after the end of the tonic clo
                                   nic attack.Insert oral airway and ad
                                   minister 02,if necessary.Insert an in
                                   travenous catheter.Draw venous 
                                   blood to determine anticonvulsant
                                   levels,glucose,BUN,electrolytes,and
                                   complete blood count stat.Draw ar
                                   terial blood for stat pH,PO2,PCO2,
                                   HCO3-.Monitor respiration,blood 
                                   pressure,and electrocardiograph.
                                   If possible monitor encephalograph.


        5                         Start iv infusion with NS contain- 
                                   ing with B complex. Give a bolus    
                                   injection of 50 ml of 50% glucose.


     10                          Infuse 1 mg lorazepam over 5 mi  
                                  nutes also give fosphenytoin to a
                                  total of 17 mg/kg(level >20 mcg
                                  per ml). If hypotension develops
                                  slow infusion rate.Phenytoin 50
                                  mg/ml in propyleneglycol may be
                                  placed in a 100 ml volume control
                                  set and diluted with normal saline.     
                                  the rate of infusion should be 
                                  watched. Alternatively phenytoin  
                                  may be injected slowly by iv.


    20                         If seizures persist give 1mg lorazepam 
                                 intravenously.


    30                         If seizures persist consider pseudo 
                                seizures if no CNS infection or   
                                trauma.Otherwise, phenobarbital 20 
                                mg/kg iv no faster than 100 mg/min  
                                until seizures stop or to a loading of 20 
                                mg/kg(level > 40 mcg/ml).


  60                          If seizure continue, general anesthesia  
                               with pentobarbital is instituted.


120                          If SE continue a neurologist and 
                               anesthesiologist with expertise in SE    
                               should be consulted. Advice from a 
                               regional epilepsy center on the 
                               management of intractable SE also 
                               should be sought Push pentobarbital      
                               until seizures stop or hypotension 
                               arises.With cessation of seizures if
                               still twitching assess EEG to rule out
                               subtle SE.


Generalized convulsive SE is considered a neurologic emergency.
Treatment to secure the airway, provide oxygen,and maintain circulation must be initiated within the first fiew minutes to prevent complications such as hypoxaemia,
systemic hypertension,tachydysrythmia.


Protocols for the treatment of convulsive SE remain somewhat individualized by institution and specialty.
Recent trends have pushed aggressive treatment beginning as soon as 10 minutes into continuous convulsive state. 
In practice this intervention can rarely be effected except in hospital. One of many approaches to control SE is shown as mention above. 
This protocol reflects the current widespread use of lorazepam titrated to effect (0,03 to 0,22 mg/kg) as a subtitute for diazepam.
Parke Davis has withdrawn phenytoin(Dilantin) in favor of the prodrug fosphenytoin(Cerebyx).This a water soluble preparation with pH of 9 is converted in 15 minutes to the active drug phenytoin by tissue phosphatases. It is equally as effective as phenytoin but without complications of the propyleneglycol solvent and higher alkalinity (pH 12).
It can be delivered intramuscularly and more stable in the iv form but it can also precipitate hypotension if adminis-
tered too rapidly.


Phenobarbital as alternative drug when seizure persist after lorazepam. Physicians are using thiopental much earlier in the treatment of SE when phenobarbital is not available.
When phenytoin and phenobarbital are ineffective, a benzodiazepine is often suggested. Midazolam and diazepam have a shorter onset time than lorazepam although lorazepam generally has a longer duration of action with a lower likelihood of severe respiratory depression making it the preferred agent of some clinicians.


Diazepam is the fastest onzet (1-3 minutes) and hystoricaly was the treatment of choice because is known as the fastest  medication to terminate seizures. However because of its lipholicity diazepam has a very short duration in CNS (10-20 min). For this reason lorazepam has replaced diazepam as the drug of choice. Its onset in only slower (2-3 min) but its anticonvulsant action typically last for more than 4 hours.
Diazepam has been reported to be effective rectally, and midazolam to be effective intramuscularly and intranasally in children.
If seizures continue to be refractory to treatment with the previously noted drugs, pentobarbital  usually can be used some times thiopental.


Alternatively,volatile anesthetics can also be used. 
Intravenous valproate (depakene) is now available which being tried in refractory status. Any of the other non iv formulated AEDs can be administered via nasogastric tube.
Propofol has been used in ambulances for patient refractory to iv benzodiazepine, given in 30 mg boluses every 30 seconds until the seizure are terminated.There may be a future role for alpha 2 agonist therapy as such drugs become clinically available. 
Dexmedetomidine confered brain protection in an animal
seizure model.


Other protocol for tonic clonic generalized SE based on stage :


Stage             General measures            AEDs  Usual route of adm
Premonitory   Continued neurolo           Diazepam 10mg iv bolus                                                                
                     gic observation,dia         max 5mg/min
                     agnostic SE by ob           Lorazepam 4mg iv bolus                                       
                     serving continued           max 2mg/min                                                    
                     seizure activity of          Midazolam 5mg iv bolus                                                                                               
                     one additional sei           max 4m/min 
                     zure.                             Paraldehyde 5- 10 ml in
                                                         5- 1 ml water or oil
                                                         by rectal First line


Early              Ensure adequate           Diazepam 10mg iv bls
(0-30 mins)     cardiorespiratory          Lorazepam 4- 8mg iv
                     function,iv line,ad-             
                     minister 02,initiate      Second line
                     regular ECG,and BP      Midazolam  5-10 mg iv
                     monitoring,draw         Phenytoin 15-18 mg/kg
                     blood for emergen-     iv loading                  
                     cy investigations,in-    dose(max.               
                     tubation may be          50mg/min.
                     considered.                Paraldehyde solution 4%                                        
                                                      in saline,50-100ml/h                                                                                  
                                                      iv solution
                                                      Lidocaine:iv bolus and
                                                      short infusion.


Established     Set second iv line         First line                 
                     (large veins)admi-        Phenytoin repeate                        
                     nister thiamine 100       7mg /kg iv.                                
                     mg iv and glucose         Phenobarbital                                    
                     D50W-50 ml iv,           10-20 mg/kg iv         
                     treat acidosis,estab      loading dose                                         
                     lished etiology,admis-  (<100mg/m)
                     sion to ICU,intubation   second line        
                     ICU,intubation has to    Diazepam iv infusion       
                     be considered,EEG/     Midazolam iv infusion
                     ECG monitoring.          Paradeldehyde iv infusion


Refractory   Full anesthesia needed    First line
(>120 min)   EEG/ECG monitoring,ar-  Pentobarbital iv/infus
                   terial line,initiate pres-   Propofol iv/infusion           
                   sor therapy when requi-        
                   red monitoring of AEDs    Second line
                   levels intracranial pres-    Isoflurane inhalation      
                   sure monitoring where 
                   appropriate.


In a patient who is actively seizing a lateral position may help prevent aspiration.The choice of iv fluids should include normal saline if phenytoin will be used because phenytoin will precipitate in glucose containing solution 


After 8 mg of lorazepam if seizures have not been aborted
use of another anticonvulsant medication is indicated.
If benzodizepine are effecive in seizure control further seizures need to be prevented with a long acting anticonvulsant.


A loading dose of phenytoin is 18-20 mg /kg ,even at the recomended rate of administration (50mg/min),hypotension is the most common side effect and mandates decreasing the infusion rate.


to be continued

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