Tuesday, November 23, 2010
Sunday, November 14, 2010
Saturday, November 13, 2010
Wednesday, November 10, 2010
case report
Anaesthetic Management of a Patient with Sarcoidosis Presenting for Mastectomy
Rachel Cherian Koshy, Rajasree, Mary Thomas
Sarcoidosis is a rare condition, the reported incidence being
1-64 per 100000 population worldwide.1 There are anecdotal
reports of serious cardiac, pulmonary and airway problems
in patients with sarcoidosis undergoing surgical procedures
under anaesthesia.
CASE REPORT
A 48 year lady with sarcoidosis presented for mastectomy
for carcinoma breast. Prior to two years, she had
experienced difficulty in breathing even while carrying out
a conversation. A biopsy of cervical lymph node revealed
her disease to be sarcoidosis. She was treated with oral
steroids for a year, which improved her symptoms.
The patient became hypertensive since one year. She
was on Tab bisoprolol 2.5 mg and hydrochlorthiazide 6.25
mg once daily. She weighed 71kg, her blood pressure was
130/80 mm Hg and heart rate 68/minute. Her airway
examination showed a mouth opening of 5 cms, thryomental
distance of 3 fingers and Mallampatti Class 2. Both heart
sounds were normal with no added sounds. Chest was
clear and air entry equal bilaterally. Physical examination
revealed lumps in both breasts. Hematological & biochemical
investigations were all within normal limits. Chest X-ray PA
view showed calcified node in the right hilum. There was
no cardiomegaly. ECG showed sinus rhythm with a heart
rate of 70/minute, PR interval 0.16 sec and no significant
ST-T changes. Echo cardiograph showed normal sized heart
chambers and valves with good LV function and no wall
motion abnormality. A tricuspid regurgitation of 27mm Hg
was present. Pulmonary function test showed mild restriction
with FEV1 94% of predicted & FVC 90% of predicted, FEV1/
FVC ratio of 104. CT study of chest and abdomen did not
reveal any abnormality except the calcified node in right
hilum of lung.
The patient was premedicated with Tab Diazepam
10mg, Pantoprazole 40mg on the night before and 6.00 am
on day of surgery. In addition she was given inhaled
bronchodilators and Inj Hydrocortisone 100mg intravenously
an hour before induction of anaesthesia.
In the OR, monitoring of ECG, pulse oximetry, NIBP
was instituted. She was given Inj Midazolam 1mg and
Fentanyl 80mcg intravenously. This was followed by
Drs. Rachel Cherian Koshy, Additional Professor and Head, Rajasree, Post Graduate Trainee, Mary Thomas, Associate
Professor, Department of Anaesthesiology, Regional Cancer Centre, Trivandrum 695 011, Kerala, India.
Correspondence: Dr. Rachel Cherian Koshy, E-mail: rachelrcc@yahoo.co.in
precurarisation with 5 mg Atracurium and induction with
100mg Propofol and 100mg succinylcholine. Endotracheal
intubation was performed with size 7mm ID cuffed oral
endotracheal tube and cuff inflated with 6ml air. Patient was
connected to an anaesthesia work station and ventilated
with 1 % halothane in a mixture of air and oxygen with an
FiO2 of 0.35. A low dose propofol infusion was also started.
Vital parameters (heart rate, BP, ECG, SpO2, ETCO2, were
all kept stable and maintained throughout the surgical
procedure (left mastectomy and wide excision of lump right
breast) Muscle relaxation was achieved with Atracurium
45mg iv. At the end of surgery which lasted for 150 minutes,
neuromuscular blockade was reversed with Inj. Neostigmine
2.5mg and Atropine 1.2mg. Diclofenac 100mg was given
as rectal suppository. The patient recovered completely and
was awake with mild pain which was relieved in about 15
minutes. Post operative pain relief was achieved with
intravenous Injection Tramadol 50mg 6th hourly. The post
operative period was uneventful.
DISCUSSION
Sarcoidosis is an idiopathic multisystem granulomatous
disorder occurring commonly in the age group of 20-40
years with a slight preponderance in females.1 Sarcoidosis
results from an exaggerated cell mediated immune response
which can be inherited, acquired, or both.
The organ most frequently affected is the lung followed
by lymph nodes. Other organs such as skin, eye and liver
could also be affected. Sarcoidosis favours nonsmokers. In
the lung, the inflammatory cells and granulomas distort the
walls of the alveoli, bronchi and blood vessels.
Approximately 50% patients develop permanent pulmonary
abnormalities and 5-15% have progressive fibrosis of the
lung. There is an interstitial lung disease which presents
with dyspnea on exercise and dry cough with rales in the
lung fields on examination. Endobronchial sarcoidosis can
produce distal atelectasis. Large vessel pulmonary
granulomatous arteritis is common. Pleural involvement
occurs in 1 to 5% cases as unilateral pleural effusion.1 Cor
pulmonale may develop owing to sarcoidosis.
Intrathoracic lymphadenopathy occurs in 75 to 90% of
all patients. The most commonly involved are hilar and
J Anaesth Clin Pharmacol 2010; 26(4): 555-556
556
paratracheal nodes. Subcarinal, mediastinal nodes may
also involved. Nasal mucosal involvement occurs in 20%
patients who present with nasal stuffiness. Laryngeal
involvement occurs in 1-5% of cases. These individuals
have hoarseness of voice, dyspnea, wheeze and stridor.
Hypercalcaemia occurs in 1-2% cases.2 Neurologic findings
are observed in 5% of patients. Seventh nerve involvement
with unilateral facial paralysis is most common.3 The
hypothalamo- pituitary axis is involved and the condition
presents as diabetes insipidus. Nearly 5% of patients have
significant heart involvement with clinical evidence of cardiac
dysfunction. Arrhythmias and conduction disturbances can
occur. Papillary muscle dysfunction, pericarditis, CCF is
also observed. Myocardial sarcoidosis although rare may
manifest as heart block, cardiac arrythmias or restrictive
cardiomyopathy.2,4
Chest radiograph could show bilateral hilar adenopathy
with or without parenchymal changes and "ground glass
appearance" consistent with active alveolitis is seen on CT
scan.
Lung function tests show decrease lung volumes,
decreased diffusing capacity and normal or increased ratio
of FEV1/FVC. The therapy of choice is glucocorticoids. Initial
dose of prednisone is 20 to 40 mg /day for less than two
years.
Sarcoidosis appears to be associated with increased
risk for cancer in affected organs.5,6,7 This may be secondary
to immunological abnormalities associated with sarcoidosis8
Sarcoidosis may be improved or exacerbated by pregnancy.9
Anaesthetic problems in patients with sarcoidosis
Laryngeal involvement and tracheal stenosis may interfere
with passage of appropriate sized adult endotracheal tube.3,8
Stenosis of trachea and bronchi as a result of sarcoidosis
and symptomatic improvement following dilatation with
Fogarty catheter has been described.10
Anaesthesia may contribute to precipitating heart block
in a patient with sarcoidosis as is described in the case
report of a fit young man with sarcoidosis who developed
complete heart block during emergency mastoidectomy. The
case was managed with temporary transvenous pacemaker
and later insertion of permanent pacemaker11 Cardiac
sarcoidosis is a dreaded condition where left ventricular
dysfunction manifested as severe reduction in ejection
fraction and myocardial conduction defects occur. Cases of
sudden death during stable cardiac function have been
reported.4
In our case anaesthesia did not result in any additional
morbidity or problems.
In conclusion it is prudent to be prepared for cardiac
events, difficult intubation and respiratory compromise in
patients with known sarcoidosis.
Rachel Cherian Koshy, Rajasree, Mary Thomas
Sarcoidosis is a rare condition, the reported incidence being
1-64 per 100000 population worldwide.1 There are anecdotal
reports of serious cardiac, pulmonary and airway problems
in patients with sarcoidosis undergoing surgical procedures
under anaesthesia.
CASE REPORT
A 48 year lady with sarcoidosis presented for mastectomy
for carcinoma breast. Prior to two years, she had
experienced difficulty in breathing even while carrying out
a conversation. A biopsy of cervical lymph node revealed
her disease to be sarcoidosis. She was treated with oral
steroids for a year, which improved her symptoms.
The patient became hypertensive since one year. She
was on Tab bisoprolol 2.5 mg and hydrochlorthiazide 6.25
mg once daily. She weighed 71kg, her blood pressure was
130/80 mm Hg and heart rate 68/minute. Her airway
examination showed a mouth opening of 5 cms, thryomental
distance of 3 fingers and Mallampatti Class 2. Both heart
sounds were normal with no added sounds. Chest was
clear and air entry equal bilaterally. Physical examination
revealed lumps in both breasts. Hematological & biochemical
investigations were all within normal limits. Chest X-ray PA
view showed calcified node in the right hilum. There was
no cardiomegaly. ECG showed sinus rhythm with a heart
rate of 70/minute, PR interval 0.16 sec and no significant
ST-T changes. Echo cardiograph showed normal sized heart
chambers and valves with good LV function and no wall
motion abnormality. A tricuspid regurgitation of 27mm Hg
was present. Pulmonary function test showed mild restriction
with FEV1 94% of predicted & FVC 90% of predicted, FEV1/
FVC ratio of 104. CT study of chest and abdomen did not
reveal any abnormality except the calcified node in right
hilum of lung.
The patient was premedicated with Tab Diazepam
10mg, Pantoprazole 40mg on the night before and 6.00 am
on day of surgery. In addition she was given inhaled
bronchodilators and Inj Hydrocortisone 100mg intravenously
an hour before induction of anaesthesia.
In the OR, monitoring of ECG, pulse oximetry, NIBP
was instituted. She was given Inj Midazolam 1mg and
Fentanyl 80mcg intravenously. This was followed by
Drs. Rachel Cherian Koshy, Additional Professor and Head, Rajasree, Post Graduate Trainee, Mary Thomas, Associate
Professor, Department of Anaesthesiology, Regional Cancer Centre, Trivandrum 695 011, Kerala, India.
Correspondence: Dr. Rachel Cherian Koshy, E-mail: rachelrcc@yahoo.co.in
precurarisation with 5 mg Atracurium and induction with
100mg Propofol and 100mg succinylcholine. Endotracheal
intubation was performed with size 7mm ID cuffed oral
endotracheal tube and cuff inflated with 6ml air. Patient was
connected to an anaesthesia work station and ventilated
with 1 % halothane in a mixture of air and oxygen with an
FiO2 of 0.35. A low dose propofol infusion was also started.
Vital parameters (heart rate, BP, ECG, SpO2, ETCO2, were
all kept stable and maintained throughout the surgical
procedure (left mastectomy and wide excision of lump right
breast) Muscle relaxation was achieved with Atracurium
45mg iv. At the end of surgery which lasted for 150 minutes,
neuromuscular blockade was reversed with Inj. Neostigmine
2.5mg and Atropine 1.2mg. Diclofenac 100mg was given
as rectal suppository. The patient recovered completely and
was awake with mild pain which was relieved in about 15
minutes. Post operative pain relief was achieved with
intravenous Injection Tramadol 50mg 6th hourly. The post
operative period was uneventful.
DISCUSSION
Sarcoidosis is an idiopathic multisystem granulomatous
disorder occurring commonly in the age group of 20-40
years with a slight preponderance in females.1 Sarcoidosis
results from an exaggerated cell mediated immune response
which can be inherited, acquired, or both.
The organ most frequently affected is the lung followed
by lymph nodes. Other organs such as skin, eye and liver
could also be affected. Sarcoidosis favours nonsmokers. In
the lung, the inflammatory cells and granulomas distort the
walls of the alveoli, bronchi and blood vessels.
Approximately 50% patients develop permanent pulmonary
abnormalities and 5-15% have progressive fibrosis of the
lung. There is an interstitial lung disease which presents
with dyspnea on exercise and dry cough with rales in the
lung fields on examination. Endobronchial sarcoidosis can
produce distal atelectasis. Large vessel pulmonary
granulomatous arteritis is common. Pleural involvement
occurs in 1 to 5% cases as unilateral pleural effusion.1 Cor
pulmonale may develop owing to sarcoidosis.
Intrathoracic lymphadenopathy occurs in 75 to 90% of
all patients. The most commonly involved are hilar and
J Anaesth Clin Pharmacol 2010; 26(4): 555-556
556
paratracheal nodes. Subcarinal, mediastinal nodes may
also involved. Nasal mucosal involvement occurs in 20%
patients who present with nasal stuffiness. Laryngeal
involvement occurs in 1-5% of cases. These individuals
have hoarseness of voice, dyspnea, wheeze and stridor.
Hypercalcaemia occurs in 1-2% cases.2 Neurologic findings
are observed in 5% of patients. Seventh nerve involvement
with unilateral facial paralysis is most common.3 The
hypothalamo- pituitary axis is involved and the condition
presents as diabetes insipidus. Nearly 5% of patients have
significant heart involvement with clinical evidence of cardiac
dysfunction. Arrhythmias and conduction disturbances can
occur. Papillary muscle dysfunction, pericarditis, CCF is
also observed. Myocardial sarcoidosis although rare may
manifest as heart block, cardiac arrythmias or restrictive
cardiomyopathy.2,4
Chest radiograph could show bilateral hilar adenopathy
with or without parenchymal changes and "ground glass
appearance" consistent with active alveolitis is seen on CT
scan.
Lung function tests show decrease lung volumes,
decreased diffusing capacity and normal or increased ratio
of FEV1/FVC. The therapy of choice is glucocorticoids. Initial
dose of prednisone is 20 to 40 mg /day for less than two
years.
Sarcoidosis appears to be associated with increased
risk for cancer in affected organs.5,6,7 This may be secondary
to immunological abnormalities associated with sarcoidosis8
Sarcoidosis may be improved or exacerbated by pregnancy.9
Anaesthetic problems in patients with sarcoidosis
Laryngeal involvement and tracheal stenosis may interfere
with passage of appropriate sized adult endotracheal tube.3,8
Stenosis of trachea and bronchi as a result of sarcoidosis
and symptomatic improvement following dilatation with
Fogarty catheter has been described.10
Anaesthesia may contribute to precipitating heart block
in a patient with sarcoidosis as is described in the case
report of a fit young man with sarcoidosis who developed
complete heart block during emergency mastoidectomy. The
case was managed with temporary transvenous pacemaker
and later insertion of permanent pacemaker11 Cardiac
sarcoidosis is a dreaded condition where left ventricular
dysfunction manifested as severe reduction in ejection
fraction and myocardial conduction defects occur. Cases of
sudden death during stable cardiac function have been
reported.4
In our case anaesthesia did not result in any additional
morbidity or problems.
In conclusion it is prudent to be prepared for cardiac
events, difficult intubation and respiratory compromise in
patients with known sarcoidosis.
Sunday, November 7, 2010
1- anesthetic management for nephroureterectomy in a patient with dilated cardiomyopathy
2- twin to twin trasfusion syndrome
3- blood products, derivatives and biologicals used to treat introperative coagulopathy
4-cauda eqina syndrome after regional anesthesia
5-postoperative complications after radical pneumonectomy
6-anesthetic consideration for endovascular management of cerebral aneurysm
these were questions for MD exam, ain shams 2010
what do you think? easy or difficult and how would you answer?
2- twin to twin trasfusion syndrome
3- blood products, derivatives and biologicals used to treat introperative coagulopathy
4-cauda eqina syndrome after regional anesthesia
5-postoperative complications after radical pneumonectomy
6-anesthetic consideration for endovascular management of cerebral aneurysm
these were questions for MD exam, ain shams 2010
what do you think? easy or difficult and how would you answer?
Friday, November 5, 2010
hi, I wish I can start a study group in a week or two. my next trial for MD will be after 5 months. I hope I will hear from any of you fellows to help me get started. any any idea, suggestions. I am in a country where we are evaluated based on how much knowledge you can momorize and cite at one time which is extremely difficult now after 40. I apperciate any comments of you. thanks
Wednesday, November 3, 2010
Intravenous Opioids for Severe Acute Pain in the Emergency Department (November)
Asad E Patanwala PharmD1*, Samuel M Keim MD MS2, Brian L Erstad PharmD3
1 Clinical Assistant Professor, College of Pharmacy, University of Arizona, Tucson, AZ
2 Professor, Department of Emergency Medicine, College of Medicine, University of Arizona
3 Professor, College of Pharmacy, University of Arizona
* To whom correspondence should be addressed. E-mail: Patanwala@pharmacy.arizona..
Abstract
OBJECTIVE: To review clinical trials of intravenous opioids for severe acute pain in the emergency department (ED) and to provide an approach for optimization of therapy.
DATA SOURCES: Articles were identified through a search of Ovid/MEDLINE (1948-August 2010), PubMed (1950-August 2010), Cochrane Central Register of Controlled Trials (1991-August 2010), and Google Scholar (1900-August 2010). The search terms used were pain, opioid, and emergency department.
STUDY SELECTION AND DATA EXTRACTION: The search was limited by age group to adults and by publication type to comparative studies. Studies comparing routes of administration other than intravenous or using non-opioid comparators were not included. Bibliographies of all retrieved articles were reviewed to obtain additional articles. The focus of the search was to identify original research that compared intravenous opioids used for treatment of severe acute pain for adults in the ED.
DATA SYNTHESIS: At equipotent doses, randomized controlled trials have not shown clinically significant differences in analgesic response or adverse effects between opioids studied. Single opioid doses less than 0.1 mg/kg of intravenous morphine, 0.015 mg/kg of intravenous hydromorphone, or 1 μg/kg of intravenous fentanyl are likely to be inadequate for severe, acute pain and the need for additional doses should be anticipated. In none of the randomized controlled trials did patients develop respiratory depression requiring the use of naloxone. Future trials could investigate the safety and efficacy of higher doses of opioids. Implementation of nurse-initiated and patient-driven pain management protocols for opioids in the ED has shown improvements in timely provision of appropriate analgesics and has resulted in better pain reduction.
CONCLUSIONS: Currently, intravenous administration of opioids for severe acute pain in the ED appears to be inadequate. Opioid doses in the ED should be high enough to provide adequate analgesia without additional risk to the patient. EDs could implement institution-specific protocols to standardize the management of pain.
Asad E Patanwala PharmD1*, Samuel M Keim MD MS2, Brian L Erstad PharmD3
1 Clinical Assistant Professor, College of Pharmacy, University of Arizona, Tucson, AZ
2 Professor, Department of Emergency Medicine, College of Medicine, University of Arizona
3 Professor, College of Pharmacy, University of Arizona
* To whom correspondence should be addressed. E-mail: Patanwala@pharmacy.arizona..
Abstract
OBJECTIVE: To review clinical trials of intravenous opioids for severe acute pain in the emergency department (ED) and to provide an approach for optimization of therapy.
DATA SOURCES: Articles were identified through a search of Ovid/MEDLINE (1948-August 2010), PubMed (1950-August 2010), Cochrane Central Register of Controlled Trials (1991-August 2010), and Google Scholar (1900-August 2010). The search terms used were pain, opioid, and emergency department.
STUDY SELECTION AND DATA EXTRACTION: The search was limited by age group to adults and by publication type to comparative studies. Studies comparing routes of administration other than intravenous or using non-opioid comparators were not included. Bibliographies of all retrieved articles were reviewed to obtain additional articles. The focus of the search was to identify original research that compared intravenous opioids used for treatment of severe acute pain for adults in the ED.
DATA SYNTHESIS: At equipotent doses, randomized controlled trials have not shown clinically significant differences in analgesic response or adverse effects between opioids studied. Single opioid doses less than 0.1 mg/kg of intravenous morphine, 0.015 mg/kg of intravenous hydromorphone, or 1 μg/kg of intravenous fentanyl are likely to be inadequate for severe, acute pain and the need for additional doses should be anticipated. In none of the randomized controlled trials did patients develop respiratory depression requiring the use of naloxone. Future trials could investigate the safety and efficacy of higher doses of opioids. Implementation of nurse-initiated and patient-driven pain management protocols for opioids in the ED has shown improvements in timely provision of appropriate analgesics and has resulted in better pain reduction.
CONCLUSIONS: Currently, intravenous administration of opioids for severe acute pain in the ED appears to be inadequate. Opioid doses in the ED should be high enough to provide adequate analgesia without additional risk to the patient. EDs could implement institution-specific protocols to standardize the management of pain.
Tuesday, November 2, 2010
case report
hi, I have added a new section, case report in anesthesia. feel free to read and give your valuble comments about the case and any other suggestions.
Awake craniotomy is becoming more popular as a neurosurgical
technique that allows for increased tumor
resection and decreased postoperative neurologic morbidity.
This technique, however, presents many challenges
to both the neurosurgeon and anesthetist. An
ASA class II, 37-year-old man with recurrent oligodendroglioma
presented for repeated craniotomy. Prior
craniotomy under general anesthesia resulted in residual
neurologic deficits. An awake craniotomy was
planned to allow for intraoperative testing for maximum
tumor resection and avoidance of neurologic morbidity.
The patient was sedated with propofol, and bupivacaine
was infiltrated for placement of Mayfield tongs and
skin incision. Following exposure of brain tissue, propofol
infusion was discontinued to allow for patient cooperation
during the procedure. Speech, motor, and sensory
testing occurred during tumor resection until resection
stopped after onset of weakness in the right arm.
The propofol infusion was resumed while the cranium
was closed and Mayfield tongs removed. The patient was
awake, alert, oriented, and able to move all extremities
but had residual weakness in the right forearm.
Awake craniotomy requires appropriate patient
selection, knowledge of the surgeon's skill, and a thorough
anesthesia plan. This case report discusses the
clinical and anesthetic management for awake craniotomy
and reviews the literature.
Keywords: Anesthesia, awake craniotomy, opioid,
propofol.
Nonopioid Anesthesia for Awake Craniotomy:
A Case Report
Diane L Wolff, CRNA, MS
Robert Naruse, MD
Michele Gold, CRNA, PhD
Awake craniotomy for tumor resection presents
many challenges for the neurosurgeon
and anesthetist. Surgery performed on brain
tissue poses an inherent risk of permanent
neurological deficit, especially for tumor
resection involving the eloquent cortex. Awake craniotomy
allows for intraoperative speech, motor, and sensory
testing, with the goal of maximum tumor resection
while avoiding postoperative neurological morbidity.1-4
The anesthetic management for this surgery must provide
sedation, analgesia, respiratory and hemodynamic control,
and a responsive, cooperative patient for neurologic
testing intraoperatively.1
Case Report
A 37-year-old, 69-kg male was scheduled for a left frontal
awake craniotomy for resection of recurrent grade 2 oligodendroglioma.
The patient was diagnosed 5 months earlier
after sudden onset of seizures, and the initial resection of
tumor was done under general anesthesia 4 months earlier.
Postoperatively the patient suffered weakness of the right
hand and right-sided facial numbness. Current preoperative
assessment revealed residual facial numbness, but the
patient was otherwise neurologically intact. Medications included
levetiracetam, 5 mg twice a day, for seizure prophylaxis.
The patient reported a minor seizure 16 days earlier.
Laboratory results were reviewed and were within normal
limits. Preoperative vital signs were a pulse rate of 78/min
and blood pressure of 110/58 mm Hg. An 18-g intravenous
(IV) catheter was inserted in the right hand. Premedication
included glycopyrrolate, 0.2 mg IV; metoclopramide, 10 mg
IV; and ranitidine, 50 mg IV. The right naris was prepared
with phenylephrine drops, and a 7.5-mm nasal airway with
5% topical lidocaine was placed in case tracheal intubation
would be needed during the operation.
The patient was transported to the operating room
(OR). Standard monitors were placed, including electrocardiography
(ECG), noninvasive blood pressure monitoring,
pulse oximetry, and capnography. A simple
oxygen face mask was placed, with 6 L/min of oxygen.
Propofol, 100 mg IV, was administered, followed by continuous
infusion at 150 μg/kg per minute titrated to a respiratory
rate of 12 to 14/min. A 20-gauge right radial arterial
line was placed for continuous intraoperative
monitoring of blood pressure. An indwelling urinary
catheter was inserted for patient comfort during the
lengthy operation and for diuretic administration.
Cefazolin, 1 g IV, was given for infection prophylaxis.
Somatosensory and motor evoked potential monitoring
was instituted. Ten minutes before pinning of the
patient’s head in Mayfield tongs, 0.25% bupivacaine with
epinephrine was infiltrated by the neurosurgeon at the pin
sites. The patient was positioned with a right tilt and sniff
position was achieved to help facilitate a patent airway. A
tent was created under the drapes to allow visualization
and communication with the patient. The surgeon infiltrated
0.25% bupivacaine with epinephrine into the scalp
surrounding the entire surgical site before incision.
Dexamethasone, 10 mg IV, and mannitol, 1 g/kg IV, were
administered to help facilitate surgical exposure of the
brain. Vital signs before incision were a pulse rate of
73/min and blood pressure of 95/57 mm Hg. Blood pressure
after skin incision and during craniectomy remained
stable, with a systolic range of 95 to 108 mm Hg over a diastolic
range of 50 to 60 mm Hg; pulse rates were 70 to
80/min. The propofol infusion was stopped after craniectomy
and the brain tissue was exposed. Stereotactic monitoring
was employed to help identify tumor margins.
A neuropsychologist performed speech testing after
the patient awakened. The patient was asked to squeeze
the anesthetist’s hand intermittently and move his feet.
The patient remained alert and oriented throughout the
awake portion without speech impairment. Blood pressure
remained 98 to 110/51 to 62 mm Hg, and pulse rate
ranged from 71 to 79/min. Seventy minutes into resection
the patient complained of persistent weakness of the
right hand and arm, prompting the neurosurgeon to stop
tumor resection. The propofol infusion was resumed and
continued until the cranium was closed and the Mayfield
tongs removed. Ondansetron, 4 mg IV, was administered
for prophylaxis of postoperative nausea. The patient was
awake by the time the head dressing was complete.
Immediate neurologic assessment was completed in the
OR and was repeated on arrival to the recovery room.
The patient was alert and oriented to person, place, time,
and situation, and he was able to move all extremities but
had residual weakness in the right hand and forearm. The
patient had no pain, and vital signs remained stable, with
blood pressure 114/56 mm Hg and pulse rate 81/min.
Oxygen saturations throughout the entire case were 100%.
No airway obstruction or complications occurred. The
patient remembered portions of the intraoperative testing
but stated he was comfortable throughout the operation.
The patient’s postoperative course was uncomplicated,
with the exception of residual right hand and forearm
weakness. Vital signs remained stable and the patient
complained of minor head pain on postoperative day 1
that was treated with hydrocodone initially and then
acetaminophen until discharge. The patient was discharged
home on postoperative day 4.
Discussion
Resection of tumor in the eloquent cortex of the brain has
an inherently high risk of postoperative neurologic morbidity.
Modern technological advances in magnetic resonance
imaging (MRI) and the use of intraoperative motor
strip testing, ultrasound, and stereotactic monitoring
have helped to decrease postoperative neurologic
deficits.2-4 Intraoperative wake-up testing or awake craniotomy
is becoming increasingly more popular to aid in
resection of tumors within the eloquent cortex.
Historically, awake craniotomy was used for epilepsy
surgery, which often involves resection of the temporal
region of the brain where the eloquent cortex is located,
but additional surgical procedures have shown benefit
from this technique1 (Table 1).
Awake craniotomy poses unique challenges, especially
for the anesthetist, who is faced with an unprotected
airway and limited access to the patient due to positioning
and pinning of the head. Therefore, appropriate
patient selection is of utmost importance for this method.
Patients must be cooperative, have a thorough understanding
of the procedure, able to lie still for an extended
time, and not have profound existing neurologic
deficit. Patients who are obese, have esophageal reflux,
sleep apnea, and difficult airways are not good candidates
for this type of craniotomy procedure (Table 2). Lastly,
patients must desire to proceed with this plan.1
Patients require sedation or general anesthesia until the
brain is exposed and again at the end of surgery while the
cranium is closed. Multiple anesthetic techniques have
been described in the literature without identification of a
superior technique.1-4 The anesthetic technique used
must provide adequate sedation and analgesia, maintenance
and control of respiratory and hemodynamic parameters,
and an awake and cooperative patient during
neurologic testing.1 Early techniques employed local
anesthetic at the incision site or scalp nerve blocks with
the addition of IV fentanyl or midazolam. Variations of
this technique use droperidol or a propofol infusion.
Patients were given oxygen via nasal cannula or face
mask. This combined local anesthetic and IV sedation
technique has a high potential for complications related to
an unprotected airway, including obstruction and desaturation
as reported in the literature.1-4 This technique is
Table 1. Operative Considerations
Awake craniotomy indications
Supratentorial tumors, eloquent cortex (motor strip cortex,
Broca and/or Wernicke area; sensory cortex)
Intractable epilepsy
Deep brain nerve stimulator
Arteriovenous malformation
Aneurysms
Benefits
Optimal tumor resection
Improved tumor diagnosis
Resection of tumor that is otherwise inoperable
still used by some, with increasing use of propofol infusion
and opioids together.1,3 Propofol decreases the cerebral
metabolic rate, reduces cerebral blood flow, and also
has anticonvulsant and antiemetic effects. All of these
factors benefit patients undergoing craniotomy surgery.
Dexmedetomidine, a selective α2 adrenoreceptor
agonist, is being increasingly used to provide sedation and
analgesia for awake craniotomy. Benefits of dexmedetomidine
are that it does not cause respiratory depression, as is
possible with other anesthetic agents, and it reduces intraoperative
and postoperative anesthesia requirements;
however, hypotension and bradycardia have been noted.
Case studies report that patients are easily aroused by
verbal stimuli, whereas some report concerns of impaired
neurocognitive testing, even after stopping the dexmed -
etomidine infusion for extended periods, delaying tumor
resection or resulting in cancellation of the case. These
reports also use a wide dose range of dexmedetomidine
infusion and various combinations of other drugs, including
opioids and midazolam. A case report by Moore and
colleagues discussed the successful use of dexmedetomidine
as a rescue drug during awake craniotomy that
avoided conversion to general anesthesia in a restless
patient. The literature reveals no consistent use pattern for
dexmedetomidine, which may explain the wide variability
of clinical outcomes.
Another technique known as asleep-awake-asleep uses
a laryngeal mask airway (LMA) or an endotracheal tube
(ETT).1 Recent retrospective case review shows an increased
use of LMAs for awake craniotomy surgery.
Anesthesia is initially induced with propofol and an
opioid infusion, such as remifentanil, and an LMA is
placed. This allows for spontaneous breathing and for
positive pressure ventilation should it be needed. At the
appropriate time during the surgery, anesthesia is
stopped, the LMA is removed, and intraoperative neurologic
testing is performed. After the awake portion is
completed, anesthesia is induced once again, and the
LMA is reinserted until the end of surgery.1 Patients not
appropriate for LMA may have a nasal ETT placed, which
is removed for the wake-up period and then reinserted
with the use of a fiberoptic bronchoscope. The advantage
of this technique is that it does provide airway protection
and an ability to provide a deeper level of anesthesia for
the patient during the most painful and stimulating parts
of the surgery. This is beneficial if the surgeon
Table 3. Anesthesia Considerations
OR indicates operating room; ETT, endotracheal tube; LMA, laryngeal mask airway; ETCO2, end-tidal carbon dioxide; CVP, central venous
pressure; ECG, electrocardiography; BP, blood pressure.
Goals = 4 As
Adequate sedation
Analgesia
Awake cooperative
Airway, respiratory, and hemodynamic control
Anesthesia options
SAS = sedate-awake-sedate
AAA = asleep-awake-asleep
With or without local anesthetic infiltration
Emergency preparedness/OR setup
Airway: available ETT, oral/nasal airways, LMA, fiberoptic scope
Breathing: ETCO2, O2 delivery, direct visualization of patient
Circulation: ± arterial line/CVP, hemodynamic support,
transfusion ready
Monitors: ECG, oximetry, BP, ETCO2, temperature, CVP, Foley
catheter
Additional OR setup
Patient comfort: pillows, padding, temperature control
Minimize noise/movement
Sign on door “Awake Patient”
Table 2. Patient Selection Criteria
BMI indicates body mass index; GERD, gastroesophageal reflux disease.
Inclusions
Normal airway examination
Able to lie still for extended period
Cooperative
Relative exclusions
Obesity, BMI > 40 kg/m2
Obstructive sleep apnea
Symptomatic GERD
Altered mental status
Communication barrier (language, profound dysphagia)
Extreme anxiety
Large vascular tumor or substantial dural involvement
does not provide adequate infiltration of local anesthetic
at the sites of the incision or Mayfield tongs.1
The use of opioids is controversial owing to the sedative
and respiratory depressant effects that occur with
their administration. This can interfere with providing an
awake, cooperative patient and lead to brain swelling due
to hypercarbia.1,5,9 In clinical practice, some anesthesia
professionals believe intraoperative opioids are unnecessary
in craniotomy surgery because manipulation of brain
tissue is painless.10 Pain associated with craniotomy is
superficial at the incision site and meninges, suggesting a
somatic versus visceral origin for this pain. Therefore, it
could be inferred that hemodynamic changes normally
attributed to pain, such as increased heart rate and blood
pressure, may in fact be caused by catecholamine release
from sympathetic fiber stimulation of the brain parenchyma.
10,11 Hence, during tumor resection patients can be
awake and performing various speech and motor tests
without pain. This physiology supports the use of an
awake craniotomy technique in which analgesia is administered
during scalp incision and craniectomy, the
time when pain fiber stimulation occurs.
Anesthetic management of this case followed a traditional
awake craniotomy by administering a propofol infusion
for sedation and administering oxygen through a
simple face mask. No sedative or opioid drugs were given
and the patient was pain free, which further supports that
brain parenchyma may lack pain receptors. The surgeon
did an extensive and thorough infiltration of local anesthetic
before head pinning and incision. This provided
anesthesia at the incision, where nerves are located.
Avoidance of opioids and sedatives decreased the risk of
airway complications from concomitant use with propofol.
The patient still received analgesia but without the
respiratory depressant effects of systemic opioids. The
technique used also provided for a very fast intraoperative
wake up and an alert and cooperative patient with no
anesthetic complications to facilitate the extensive intraoperative
neurologic testing during tumor resection.
Several factors influenced the decision to choose this
approach to awake craniotomy versus the asleep-awakeasleep
technique. Patient factors included a good airway
on examination, appropriate weight, no history of
esophageal reflux, and willingness to cooperate with directions
from the anesthesia care team. Additional important
factors included a surgeon known to be very
skilled at performing this surgery, good local anesthetic
infiltration at the incision site, and additional attention to
patient needs and OR setup (see Table 3). Lastly, the
surgeon, anesthesia team, and patient all had a thorough
understanding of the surgical and anesthesia plan and
agreed to proceed.
technique that allows for increased tumor
resection and decreased postoperative neurologic morbidity.
This technique, however, presents many challenges
to both the neurosurgeon and anesthetist. An
ASA class II, 37-year-old man with recurrent oligodendroglioma
presented for repeated craniotomy. Prior
craniotomy under general anesthesia resulted in residual
neurologic deficits. An awake craniotomy was
planned to allow for intraoperative testing for maximum
tumor resection and avoidance of neurologic morbidity.
The patient was sedated with propofol, and bupivacaine
was infiltrated for placement of Mayfield tongs and
skin incision. Following exposure of brain tissue, propofol
infusion was discontinued to allow for patient cooperation
during the procedure. Speech, motor, and sensory
testing occurred during tumor resection until resection
stopped after onset of weakness in the right arm.
The propofol infusion was resumed while the cranium
was closed and Mayfield tongs removed. The patient was
awake, alert, oriented, and able to move all extremities
but had residual weakness in the right forearm.
Awake craniotomy requires appropriate patient
selection, knowledge of the surgeon's skill, and a thorough
anesthesia plan. This case report discusses the
clinical and anesthetic management for awake craniotomy
and reviews the literature.
Keywords: Anesthesia, awake craniotomy, opioid,
propofol.
Nonopioid Anesthesia for Awake Craniotomy:
A Case Report
Diane L Wolff, CRNA, MS
Robert Naruse, MD
Michele Gold, CRNA, PhD
Awake craniotomy for tumor resection presents
many challenges for the neurosurgeon
and anesthetist. Surgery performed on brain
tissue poses an inherent risk of permanent
neurological deficit, especially for tumor
resection involving the eloquent cortex. Awake craniotomy
allows for intraoperative speech, motor, and sensory
testing, with the goal of maximum tumor resection
while avoiding postoperative neurological morbidity.1-4
The anesthetic management for this surgery must provide
sedation, analgesia, respiratory and hemodynamic control,
and a responsive, cooperative patient for neurologic
testing intraoperatively.1
Case Report
A 37-year-old, 69-kg male was scheduled for a left frontal
awake craniotomy for resection of recurrent grade 2 oligodendroglioma.
The patient was diagnosed 5 months earlier
after sudden onset of seizures, and the initial resection of
tumor was done under general anesthesia 4 months earlier.
Postoperatively the patient suffered weakness of the right
hand and right-sided facial numbness. Current preoperative
assessment revealed residual facial numbness, but the
patient was otherwise neurologically intact. Medications included
levetiracetam, 5 mg twice a day, for seizure prophylaxis.
The patient reported a minor seizure 16 days earlier.
Laboratory results were reviewed and were within normal
limits. Preoperative vital signs were a pulse rate of 78/min
and blood pressure of 110/58 mm Hg. An 18-g intravenous
(IV) catheter was inserted in the right hand. Premedication
included glycopyrrolate, 0.2 mg IV; metoclopramide, 10 mg
IV; and ranitidine, 50 mg IV. The right naris was prepared
with phenylephrine drops, and a 7.5-mm nasal airway with
5% topical lidocaine was placed in case tracheal intubation
would be needed during the operation.
The patient was transported to the operating room
(OR). Standard monitors were placed, including electrocardiography
(ECG), noninvasive blood pressure monitoring,
pulse oximetry, and capnography. A simple
oxygen face mask was placed, with 6 L/min of oxygen.
Propofol, 100 mg IV, was administered, followed by continuous
infusion at 150 μg/kg per minute titrated to a respiratory
rate of 12 to 14/min. A 20-gauge right radial arterial
line was placed for continuous intraoperative
monitoring of blood pressure. An indwelling urinary
catheter was inserted for patient comfort during the
lengthy operation and for diuretic administration.
Cefazolin, 1 g IV, was given for infection prophylaxis.
Somatosensory and motor evoked potential monitoring
was instituted. Ten minutes before pinning of the
patient’s head in Mayfield tongs, 0.25% bupivacaine with
epinephrine was infiltrated by the neurosurgeon at the pin
sites. The patient was positioned with a right tilt and sniff
position was achieved to help facilitate a patent airway. A
tent was created under the drapes to allow visualization
and communication with the patient. The surgeon infiltrated
0.25% bupivacaine with epinephrine into the scalp
surrounding the entire surgical site before incision.
Dexamethasone, 10 mg IV, and mannitol, 1 g/kg IV, were
administered to help facilitate surgical exposure of the
brain. Vital signs before incision were a pulse rate of
73/min and blood pressure of 95/57 mm Hg. Blood pressure
after skin incision and during craniectomy remained
stable, with a systolic range of 95 to 108 mm Hg over a diastolic
range of 50 to 60 mm Hg; pulse rates were 70 to
80/min. The propofol infusion was stopped after craniectomy
and the brain tissue was exposed. Stereotactic monitoring
was employed to help identify tumor margins.
A neuropsychologist performed speech testing after
the patient awakened. The patient was asked to squeeze
the anesthetist’s hand intermittently and move his feet.
The patient remained alert and oriented throughout the
awake portion without speech impairment. Blood pressure
remained 98 to 110/51 to 62 mm Hg, and pulse rate
ranged from 71 to 79/min. Seventy minutes into resection
the patient complained of persistent weakness of the
right hand and arm, prompting the neurosurgeon to stop
tumor resection. The propofol infusion was resumed and
continued until the cranium was closed and the Mayfield
tongs removed. Ondansetron, 4 mg IV, was administered
for prophylaxis of postoperative nausea. The patient was
awake by the time the head dressing was complete.
Immediate neurologic assessment was completed in the
OR and was repeated on arrival to the recovery room.
The patient was alert and oriented to person, place, time,
and situation, and he was able to move all extremities but
had residual weakness in the right hand and forearm. The
patient had no pain, and vital signs remained stable, with
blood pressure 114/56 mm Hg and pulse rate 81/min.
Oxygen saturations throughout the entire case were 100%.
No airway obstruction or complications occurred. The
patient remembered portions of the intraoperative testing
but stated he was comfortable throughout the operation.
The patient’s postoperative course was uncomplicated,
with the exception of residual right hand and forearm
weakness. Vital signs remained stable and the patient
complained of minor head pain on postoperative day 1
that was treated with hydrocodone initially and then
acetaminophen until discharge. The patient was discharged
home on postoperative day 4.
Discussion
Resection of tumor in the eloquent cortex of the brain has
an inherently high risk of postoperative neurologic morbidity.
Modern technological advances in magnetic resonance
imaging (MRI) and the use of intraoperative motor
strip testing, ultrasound, and stereotactic monitoring
have helped to decrease postoperative neurologic
deficits.2-4 Intraoperative wake-up testing or awake craniotomy
is becoming increasingly more popular to aid in
resection of tumors within the eloquent cortex.
Historically, awake craniotomy was used for epilepsy
surgery, which often involves resection of the temporal
region of the brain where the eloquent cortex is located,
but additional surgical procedures have shown benefit
from this technique1 (Table 1).
Awake craniotomy poses unique challenges, especially
for the anesthetist, who is faced with an unprotected
airway and limited access to the patient due to positioning
and pinning of the head. Therefore, appropriate
patient selection is of utmost importance for this method.
Patients must be cooperative, have a thorough understanding
of the procedure, able to lie still for an extended
time, and not have profound existing neurologic
deficit. Patients who are obese, have esophageal reflux,
sleep apnea, and difficult airways are not good candidates
for this type of craniotomy procedure (Table 2). Lastly,
patients must desire to proceed with this plan.1
Patients require sedation or general anesthesia until the
brain is exposed and again at the end of surgery while the
cranium is closed. Multiple anesthetic techniques have
been described in the literature without identification of a
superior technique.1-4 The anesthetic technique used
must provide adequate sedation and analgesia, maintenance
and control of respiratory and hemodynamic parameters,
and an awake and cooperative patient during
neurologic testing.1 Early techniques employed local
anesthetic at the incision site or scalp nerve blocks with
the addition of IV fentanyl or midazolam. Variations of
this technique use droperidol or a propofol infusion.
Patients were given oxygen via nasal cannula or face
mask. This combined local anesthetic and IV sedation
technique has a high potential for complications related to
an unprotected airway, including obstruction and desaturation
as reported in the literature.1-4 This technique is
Table 1. Operative Considerations
Awake craniotomy indications
Supratentorial tumors, eloquent cortex (motor strip cortex,
Broca and/or Wernicke area; sensory cortex)
Intractable epilepsy
Deep brain nerve stimulator
Arteriovenous malformation
Aneurysms
Benefits
Optimal tumor resection
Improved tumor diagnosis
Resection of tumor that is otherwise inoperable
still used by some, with increasing use of propofol infusion
and opioids together.1,3 Propofol decreases the cerebral
metabolic rate, reduces cerebral blood flow, and also
has anticonvulsant and antiemetic effects. All of these
factors benefit patients undergoing craniotomy surgery.
Dexmedetomidine, a selective α2 adrenoreceptor
agonist, is being increasingly used to provide sedation and
analgesia for awake craniotomy. Benefits of dexmedetomidine
are that it does not cause respiratory depression, as is
possible with other anesthetic agents, and it reduces intraoperative
and postoperative anesthesia requirements;
however, hypotension and bradycardia have been noted.
Case studies report that patients are easily aroused by
verbal stimuli, whereas some report concerns of impaired
neurocognitive testing, even after stopping the dexmed -
etomidine infusion for extended periods, delaying tumor
resection or resulting in cancellation of the case. These
reports also use a wide dose range of dexmedetomidine
infusion and various combinations of other drugs, including
opioids and midazolam. A case report by Moore and
colleagues discussed the successful use of dexmedetomidine
as a rescue drug during awake craniotomy that
avoided conversion to general anesthesia in a restless
patient. The literature reveals no consistent use pattern for
dexmedetomidine, which may explain the wide variability
of clinical outcomes.
Another technique known as asleep-awake-asleep uses
a laryngeal mask airway (LMA) or an endotracheal tube
(ETT).1 Recent retrospective case review shows an increased
use of LMAs for awake craniotomy surgery.
Anesthesia is initially induced with propofol and an
opioid infusion, such as remifentanil, and an LMA is
placed. This allows for spontaneous breathing and for
positive pressure ventilation should it be needed. At the
appropriate time during the surgery, anesthesia is
stopped, the LMA is removed, and intraoperative neurologic
testing is performed. After the awake portion is
completed, anesthesia is induced once again, and the
LMA is reinserted until the end of surgery.1 Patients not
appropriate for LMA may have a nasal ETT placed, which
is removed for the wake-up period and then reinserted
with the use of a fiberoptic bronchoscope. The advantage
of this technique is that it does provide airway protection
and an ability to provide a deeper level of anesthesia for
the patient during the most painful and stimulating parts
of the surgery. This is beneficial if the surgeon
Table 3. Anesthesia Considerations
OR indicates operating room; ETT, endotracheal tube; LMA, laryngeal mask airway; ETCO2, end-tidal carbon dioxide; CVP, central venous
pressure; ECG, electrocardiography; BP, blood pressure.
Goals = 4 As
Adequate sedation
Analgesia
Awake cooperative
Airway, respiratory, and hemodynamic control
Anesthesia options
SAS = sedate-awake-sedate
AAA = asleep-awake-asleep
With or without local anesthetic infiltration
Emergency preparedness/OR setup
Airway: available ETT, oral/nasal airways, LMA, fiberoptic scope
Breathing: ETCO2, O2 delivery, direct visualization of patient
Circulation: ± arterial line/CVP, hemodynamic support,
transfusion ready
Monitors: ECG, oximetry, BP, ETCO2, temperature, CVP, Foley
catheter
Additional OR setup
Patient comfort: pillows, padding, temperature control
Minimize noise/movement
Sign on door “Awake Patient”
Table 2. Patient Selection Criteria
BMI indicates body mass index; GERD, gastroesophageal reflux disease.
Inclusions
Normal airway examination
Able to lie still for extended period
Cooperative
Relative exclusions
Obesity, BMI > 40 kg/m2
Obstructive sleep apnea
Symptomatic GERD
Altered mental status
Communication barrier (language, profound dysphagia)
Extreme anxiety
Large vascular tumor or substantial dural involvement
does not provide adequate infiltration of local anesthetic
at the sites of the incision or Mayfield tongs.1
The use of opioids is controversial owing to the sedative
and respiratory depressant effects that occur with
their administration. This can interfere with providing an
awake, cooperative patient and lead to brain swelling due
to hypercarbia.1,5,9 In clinical practice, some anesthesia
professionals believe intraoperative opioids are unnecessary
in craniotomy surgery because manipulation of brain
tissue is painless.10 Pain associated with craniotomy is
superficial at the incision site and meninges, suggesting a
somatic versus visceral origin for this pain. Therefore, it
could be inferred that hemodynamic changes normally
attributed to pain, such as increased heart rate and blood
pressure, may in fact be caused by catecholamine release
from sympathetic fiber stimulation of the brain parenchyma.
10,11 Hence, during tumor resection patients can be
awake and performing various speech and motor tests
without pain. This physiology supports the use of an
awake craniotomy technique in which analgesia is administered
during scalp incision and craniectomy, the
time when pain fiber stimulation occurs.
Anesthetic management of this case followed a traditional
awake craniotomy by administering a propofol infusion
for sedation and administering oxygen through a
simple face mask. No sedative or opioid drugs were given
and the patient was pain free, which further supports that
brain parenchyma may lack pain receptors. The surgeon
did an extensive and thorough infiltration of local anesthetic
before head pinning and incision. This provided
anesthesia at the incision, where nerves are located.
Avoidance of opioids and sedatives decreased the risk of
airway complications from concomitant use with propofol.
The patient still received analgesia but without the
respiratory depressant effects of systemic opioids. The
technique used also provided for a very fast intraoperative
wake up and an alert and cooperative patient with no
anesthetic complications to facilitate the extensive intraoperative
neurologic testing during tumor resection.
Several factors influenced the decision to choose this
approach to awake craniotomy versus the asleep-awakeasleep
technique. Patient factors included a good airway
on examination, appropriate weight, no history of
esophageal reflux, and willingness to cooperate with directions
from the anesthesia care team. Additional important
factors included a surgeon known to be very
skilled at performing this surgery, good local anesthetic
infiltration at the incision site, and additional attention to
patient needs and OR setup (see Table 3). Lastly, the
surgeon, anesthesia team, and patient all had a thorough
understanding of the surgical and anesthesia plan and
agreed to proceed.
Neuroleptic Malignant Syndrome and Anaesthesia: A Case Report
Pramendra Agrawal1, Abha Agrawal2, Ishwar Singh3
1. DNB Resident Presently working as Senior Resident, JPNATC, AIIMS, New Delhi
2. Consultant, 3. Head of the Department
Department of Anaesthesiology and Intensive Care
Jaipur Golden Hospital, Rohini, New Delhi.
Correspondence: Pramendra Agrawal (pramendraagrawal@yahoo.com)
About the Author: Dr Pramendra Agrawal passed
DNB in Anaesthesiology in the year 2008. He is
presently working as Senior Resident in Jai Prakash
Narayan Apex Trauma Centre, All India Institute of
Medical Sciences [AIIMS], New Delhi, India. His field
of interests include trauma care, regional
interventional techniques and intensive care.
Neuroleptic Malignant Syndrome (NMS) is a life threatening, neurological disorder most
often caused by an adverse reaction to neuroleptic or anti psychotic drugs. We report a case
of Neuroleptic Malignant Syndrome who was posted for an incidental surgery and its
anaesthetic management.
Key Words: Neuroleptic Malignant Syndrome, anti psychotics, hyperthermia
Neuroleptic Malignant Syndrome (NMS) is a rare but potentially life threatening
idiosyncratic reaction to neuroleptic drugs. It causes hyperthermia, muscular rigidity, altered
mental status, elevated creatine phosphokinase (CPK) and autonomic dysfunction. The
underlying pathological abnormality is thought to be the central dopamine D2 receptor
blockade or dopamine depletion in the hypothalamus, nigrostriatal and spinal pathways.
The condition shares many features with the serotonin syndrome and malignant
hyperthermia. Anaesthesia for an incidental surgery in such a patient poses unique
challenges to an anaesthesiologist.
Case Report: An 18 year old male, a known case of Bipolar mood disorder on antipsychotics
was admitted to our Intensive Care Unit with complaints of high grade fever (1060F) for 2
days, agitation and involuntary movements for 8 days and vomiting with altered sensorium
for 1 day. Patient was immediately intubated to protect his airway, intensive measures to
bring down temperature commenced and investigations including haematological, biochemical,
brain imaging and cerebrospinal fluid sent for evaluation. Investigations revealed:
The Indian Anaesthetists’ Forum – (http://www.theiaforum.org) Online ISSN 0973-0311
January 2010(4)
Agrawal P,Agrawal A, Singh I: Neuroleptic Malignant Syndrome and Anaesthesia : A Case Report 2
leukocytosis (TLC 19,000/mm3), elevated liver enzymes (SGOT 477 IU/l, SGPT 190 IU/l);
progressively increasing Creatine Kinase (1004; 2040; 3270; 39794 U/l), Serum Creatinine
(1.3; 1.5; 1.8 mg/dl) and Serum K+ (4.8, 4.9, 5.5 meq/l). Computed tomography of brain and
cerebrospinal fluid examination were normal. So a diagnosis of neuroleptic malignant
syndrome was made. All antipsychotic medications were then stopped. Tab. Bromocriptine
1.25 mg thrice daily and Tab. Alprazolam 0.25 mg four times daily were started and other
intensive care measures continued. Patient was gradually weaned off ventilator support and
extubated on 6th day.
Unfortunately patient developed a bed sore on the buttock which needed a flap
cover He was posted for surgery on 15th day of admission. A pre-anaesthetic check up
revealed a responsive patient, hypertonia present in all limbs and restricted mouth opening
(just 2 fingers due to hypertonia). Investigations revealed elevated CPK 829 U/l, S. K+ 4.9
meq/l, INR = 1.54; rest of examination and investigations were within acceptable limits.
Anaesthetic management included avoidance of following drugs perioperatively: Inj.
droperidol, succinylcholine, prochlorperazine, promethazine and metoclopramide. Patient
received premedication with alprazolam 0.25 mg at 10 p.m. before the day of operation and
at 6 a.m. on day of surgery. Consent taken and patient shifted to operation theatre. Drip
started with 16 G intravenous cannula and standard monitoring established. Fentanyl 1.5
μg/kg and midazolam 1 mg IV was administered. Anaesthesia induced by thiopentone
sodium 4 mg/kg IV slowly, after pre-oxygenation or 5 minutes and adequacy of mask
ventilation confirmed, muscle paralysis achieved with atracurium 0.5mg/kg. Airway secured
with 34Fr cuffed armoured endotracheal tube orally and anaesthesia maintained with 50%
of O2 + N2O + Isoflurane < 0.4%, fentaynl was used for analgesia and atracurium for muscle paralysis assisted by neuromuscular monitoring. Surgery was conducted in prone position; procedure lasted 2½ hours during which 2 units of whole blood, 2 units of FFP and 1.5 litres crystalloid were infused. Patient remained haemodynamically stable throughout procedure. At end of surgery, neuromuscular blockade was reversed with neostigmine and glycopyrrolate. Trachea was extubated in prone posture itself as requested by surgeons to avoid pressure on flap after patient was awake; Ondansteron 4mg IV was used as antiemetic. Post operatively patient was shifted to post anaesthesia care unit with O2 supplementation and then towards after 2 hrs. Patient was discharged from hospital on 7th post operative day with psychiatry referral. Discussion: Neuroleptic Malignant Syndrome (NMS) was first described by Delay et al during early trials of haloperidol1. The incidence is estimated to range from 0.02–2.4% with The Indian Anaesthetists’ Forum – (http://www.theiaforum.org) Online ISSN 0973-0311 January 2010(4) Agrawal P,Agrawal A, Singh I: Neuroleptic Malignant Syndrome and Anaesthesia : A Case Report 3 conventional anti-psychotics and a much lower incidence for atypical antipsychotics2 The Diagnostic criteria are: • Administration of neuroleptics • Hyperthermia (> 38oC)
• Muscle rigidity
• Five of following: mental status change, tremor, tachycardia, incontinence, labile
blood pressure, metabolic acidosis, tachypnoea/hypoxia, CPK elevation,
diaphoresis/sialorrhea, leukocytosis.
• Exclusion of other central and systemic causes of hyperthermia.
Although NMS has a variable onset and sometimes evolves rapidly, rigidity and
altered mental status usually occur early, followed by autonomic changes and
hyperthermia3. No laboratory tests are pathognomonic of diagnosis. Serum creatine kinase
is frequently elevated reflecting rhabdomyolysis, with resultant risk of myoglobinuric renal
failure. CT scan brain and cerebrospinal fluid examination and sepsis evaluation are negative
in NMS and allow for the exclusion of other causes of fever and neurological deterioration.
Other frequently described laboratory abnormalities include metabolic acidosis, hypoxia,
low serum iron, electrolyte abnormalities, elevated serum catecholamines and
coagulopathies
Differential Diagnosis of NMS: Infectious encephalitis4,5, structural lesion of brain, rare
cases of status epilepticus6, lethal catatonia7, heat stroke, endocrinopathies, drugs,
autoimmune disorders, thyrotoxicosis, phaeochromocytoma, malignant hyperthermia,
serotonin syndrome8. Volatile anaesthetics and succinylcholine are associated with
malignant hypertherma during surgery, which can be confused with NMS if neuroleptics are
administered9
The basic management of NMS remains risk reduction, early diagnosis, cessation of
neuroleptic medications and institution of Intensive, medical and nursing care10,11.
Benzodiazepines, bromocriptine, amantadine or other dopamine agonists may be a
reasonable next step in patients with moderate symptoms of NMS. Dantrolene may be
beneficial in cases of NMS with extreme rigidity and hyperthermia. Electro convulsion
therapy (ECT) is used if NMS is refractory to other measures or who remain psychotic after
NMS is resolved. Since a common pathophysiology has been suggested between NMS and
malignant hypertherima (MH)12,13 the possibility that patients with a history of NMS may be
vulnerable to developing MH is an important factor when considering general anaesthesia,
especially succinylcholine administration. To date, there is no report in the literature of
(MH) as a complication of ECT in NMS patients. However, until the association between
The Indian Anaesthetists’ Forum – (http://www.theiaforum.org) Online ISSN 0973-0311
January 2010(4)
Agrawal P,Agrawal A, Singh I: Neuroleptic Malignant Syndrome and Anaesthesia : A Case Report 4
NMS and MH is conclusively disproved, careful metabolic monitoring of general anaesthesia
is necessary.
Conclusion: Neuroleptics are highly effective medications that have achieved wide spread
use in medicine and psychiatry. However they have been associated with NMS in about 0.2
percent of patients. Awareness of diagnosis, cessation of medications, early medical
intervention and consideration of specific remedies can reduce morbidity and mortality
when NMS occurs.
Pramendra Agrawal1, Abha Agrawal2, Ishwar Singh3
1. DNB Resident Presently working as Senior Resident, JPNATC, AIIMS, New Delhi
2. Consultant, 3. Head of the Department
Department of Anaesthesiology and Intensive Care
Jaipur Golden Hospital, Rohini, New Delhi.
Correspondence: Pramendra Agrawal (pramendraagrawal@yahoo.com)
About the Author: Dr Pramendra Agrawal passed
DNB in Anaesthesiology in the year 2008. He is
presently working as Senior Resident in Jai Prakash
Narayan Apex Trauma Centre, All India Institute of
Medical Sciences [AIIMS], New Delhi, India. His field
of interests include trauma care, regional
interventional techniques and intensive care.
Neuroleptic Malignant Syndrome (NMS) is a life threatening, neurological disorder most
often caused by an adverse reaction to neuroleptic or anti psychotic drugs. We report a case
of Neuroleptic Malignant Syndrome who was posted for an incidental surgery and its
anaesthetic management.
Key Words: Neuroleptic Malignant Syndrome, anti psychotics, hyperthermia
Neuroleptic Malignant Syndrome (NMS) is a rare but potentially life threatening
idiosyncratic reaction to neuroleptic drugs. It causes hyperthermia, muscular rigidity, altered
mental status, elevated creatine phosphokinase (CPK) and autonomic dysfunction. The
underlying pathological abnormality is thought to be the central dopamine D2 receptor
blockade or dopamine depletion in the hypothalamus, nigrostriatal and spinal pathways.
The condition shares many features with the serotonin syndrome and malignant
hyperthermia. Anaesthesia for an incidental surgery in such a patient poses unique
challenges to an anaesthesiologist.
Case Report: An 18 year old male, a known case of Bipolar mood disorder on antipsychotics
was admitted to our Intensive Care Unit with complaints of high grade fever (1060F) for 2
days, agitation and involuntary movements for 8 days and vomiting with altered sensorium
for 1 day. Patient was immediately intubated to protect his airway, intensive measures to
bring down temperature commenced and investigations including haematological, biochemical,
brain imaging and cerebrospinal fluid sent for evaluation. Investigations revealed:
The Indian Anaesthetists’ Forum – (http://www.theiaforum.org) Online ISSN 0973-0311
January 2010(4)
Agrawal P,Agrawal A, Singh I: Neuroleptic Malignant Syndrome and Anaesthesia : A Case Report 2
leukocytosis (TLC 19,000/mm3), elevated liver enzymes (SGOT 477 IU/l, SGPT 190 IU/l);
progressively increasing Creatine Kinase (1004; 2040; 3270; 39794 U/l), Serum Creatinine
(1.3; 1.5; 1.8 mg/dl) and Serum K+ (4.8, 4.9, 5.5 meq/l). Computed tomography of brain and
cerebrospinal fluid examination were normal. So a diagnosis of neuroleptic malignant
syndrome was made. All antipsychotic medications were then stopped. Tab. Bromocriptine
1.25 mg thrice daily and Tab. Alprazolam 0.25 mg four times daily were started and other
intensive care measures continued. Patient was gradually weaned off ventilator support and
extubated on 6th day.
Unfortunately patient developed a bed sore on the buttock which needed a flap
cover He was posted for surgery on 15th day of admission. A pre-anaesthetic check up
revealed a responsive patient, hypertonia present in all limbs and restricted mouth opening
(just 2 fingers due to hypertonia). Investigations revealed elevated CPK 829 U/l, S. K+ 4.9
meq/l, INR = 1.54; rest of examination and investigations were within acceptable limits.
Anaesthetic management included avoidance of following drugs perioperatively: Inj.
droperidol, succinylcholine, prochlorperazine, promethazine and metoclopramide. Patient
received premedication with alprazolam 0.25 mg at 10 p.m. before the day of operation and
at 6 a.m. on day of surgery. Consent taken and patient shifted to operation theatre. Drip
started with 16 G intravenous cannula and standard monitoring established. Fentanyl 1.5
μg/kg and midazolam 1 mg IV was administered. Anaesthesia induced by thiopentone
sodium 4 mg/kg IV slowly, after pre-oxygenation or 5 minutes and adequacy of mask
ventilation confirmed, muscle paralysis achieved with atracurium 0.5mg/kg. Airway secured
with 34Fr cuffed armoured endotracheal tube orally and anaesthesia maintained with 50%
of O2 + N2O + Isoflurane < 0.4%, fentaynl was used for analgesia and atracurium for muscle paralysis assisted by neuromuscular monitoring. Surgery was conducted in prone position; procedure lasted 2½ hours during which 2 units of whole blood, 2 units of FFP and 1.5 litres crystalloid were infused. Patient remained haemodynamically stable throughout procedure. At end of surgery, neuromuscular blockade was reversed with neostigmine and glycopyrrolate. Trachea was extubated in prone posture itself as requested by surgeons to avoid pressure on flap after patient was awake; Ondansteron 4mg IV was used as antiemetic. Post operatively patient was shifted to post anaesthesia care unit with O2 supplementation and then towards after 2 hrs. Patient was discharged from hospital on 7th post operative day with psychiatry referral. Discussion: Neuroleptic Malignant Syndrome (NMS) was first described by Delay et al during early trials of haloperidol1. The incidence is estimated to range from 0.02–2.4% with The Indian Anaesthetists’ Forum – (http://www.theiaforum.org) Online ISSN 0973-0311 January 2010(4) Agrawal P,Agrawal A, Singh I: Neuroleptic Malignant Syndrome and Anaesthesia : A Case Report 3 conventional anti-psychotics and a much lower incidence for atypical antipsychotics2 The Diagnostic criteria are: • Administration of neuroleptics • Hyperthermia (> 38oC)
• Muscle rigidity
• Five of following: mental status change, tremor, tachycardia, incontinence, labile
blood pressure, metabolic acidosis, tachypnoea/hypoxia, CPK elevation,
diaphoresis/sialorrhea, leukocytosis.
• Exclusion of other central and systemic causes of hyperthermia.
Although NMS has a variable onset and sometimes evolves rapidly, rigidity and
altered mental status usually occur early, followed by autonomic changes and
hyperthermia3. No laboratory tests are pathognomonic of diagnosis. Serum creatine kinase
is frequently elevated reflecting rhabdomyolysis, with resultant risk of myoglobinuric renal
failure. CT scan brain and cerebrospinal fluid examination and sepsis evaluation are negative
in NMS and allow for the exclusion of other causes of fever and neurological deterioration.
Other frequently described laboratory abnormalities include metabolic acidosis, hypoxia,
low serum iron, electrolyte abnormalities, elevated serum catecholamines and
coagulopathies
Differential Diagnosis of NMS: Infectious encephalitis4,5, structural lesion of brain, rare
cases of status epilepticus6, lethal catatonia7, heat stroke, endocrinopathies, drugs,
autoimmune disorders, thyrotoxicosis, phaeochromocytoma, malignant hyperthermia,
serotonin syndrome8. Volatile anaesthetics and succinylcholine are associated with
malignant hypertherma during surgery, which can be confused with NMS if neuroleptics are
administered9
The basic management of NMS remains risk reduction, early diagnosis, cessation of
neuroleptic medications and institution of Intensive, medical and nursing care10,11.
Benzodiazepines, bromocriptine, amantadine or other dopamine agonists may be a
reasonable next step in patients with moderate symptoms of NMS. Dantrolene may be
beneficial in cases of NMS with extreme rigidity and hyperthermia. Electro convulsion
therapy (ECT) is used if NMS is refractory to other measures or who remain psychotic after
NMS is resolved. Since a common pathophysiology has been suggested between NMS and
malignant hypertherima (MH)12,13 the possibility that patients with a history of NMS may be
vulnerable to developing MH is an important factor when considering general anaesthesia,
especially succinylcholine administration. To date, there is no report in the literature of
(MH) as a complication of ECT in NMS patients. However, until the association between
The Indian Anaesthetists’ Forum – (http://www.theiaforum.org) Online ISSN 0973-0311
January 2010(4)
Agrawal P,Agrawal A, Singh I: Neuroleptic Malignant Syndrome and Anaesthesia : A Case Report 4
NMS and MH is conclusively disproved, careful metabolic monitoring of general anaesthesia
is necessary.
Conclusion: Neuroleptics are highly effective medications that have achieved wide spread
use in medicine and psychiatry. However they have been associated with NMS in about 0.2
percent of patients. Awareness of diagnosis, cessation of medications, early medical
intervention and consideration of specific remedies can reduce morbidity and mortality
when NMS occurs.
CASE REPORT - TOTAL SPINAL ANAESTHESIA
L.M. Dijkema and H.J. Haisma, Department of Anesthesiology, University Hospital Groningen, P.O.Box 30001, 9700 RB Groningen, the Netherlands., e-mail: l.m.dijkema@anest.azg.nl
--------------------------------------------------------------------------------
This is a report of a patient who suffered an unexpected high level of block during spinal anaesthesia. This review will describe the symptoms, predictive factors and the management of a “total spinal”.
Case Report
A 35-year old primigravida was scheduled for caesarean section because of expected difficult delivery due to a narrow pelvis. She had no relevant medical history. Her height was 1.58m. and she weighed 85kg. After discussion with the patient spinal anaesthesia was planned.
In the theatre electrocardiography, blood pressure monitoring, pulse oximetry and peripheral venous access were established and 500ml of normal saline was given. The spinal anaesthesia was performed in the sitting position at L4/L5 with 2.4ml. bupivacaine 0.5% in hyperbaric dextrose solution - “Heavy Marcaine”. Immediately following the block the patient was put back in the supine position, and the operating table altered with left lateral tilt to diminish aorto-caval compression.
About 5 minutes later the patient complained of nausea and “not feeling well” and experienced progressive difficulty to breathe. The blood pressure fell to 65/40mmHg.
Definition of total spinal
Total spinal is a local anaesthetic depression of the cervical spinal cord and the brainstem. It may follow excessive spread of an intrathecal injection of local anaesthetic, or inadvertent spinal injection of an epidural dose of local anaesthetic.
Predicting factors
Spread of block is influenced by many factors:
Local anaesthetic dose - volume, dosage and baricity of local anaesthetic.
Position of the patient - especially important when a hyperbaric solution of local anaesthetic is used.
Patient characteristics - height, age, gender, intra-abdominal pressure and anatomical configuration of the spinal cord.
Technique - type of needle, site of injection, direction of needle, velocity of injection and use of barbotage.
The patient in our case was a pregnant woman. Pregnant women have a raised intra-abdominal pressure and a diminished volume of the lumbar spinal canal caused by distension of the epidural veins. We therefore gave her a reduced dose of local anaesthetic (2.4ml bupivacaine 0.5% hyperbaric).
The spread of spinal block is sometimes very rapid. The level of the block should be tested within 4 minutes after the injection of local anaesthetic. Commonly used methods of assessing the block are: loss of temperature sensation, loss of pinprick sensation and loss of light touch sensation. Temperature sensation is lost first and light touch sensation last. A block may continue to extend for at least 30 minutes after injection.
Clinical symptoms
Early recognition is the key to management in case of total spinal.
The first signs of high spinal block are hypotension, bradycardia and difficulty in breathing. Before hypotension is detected, the patient often complains of nausea or “not feeling well”. Tingling in the fingers indicates a high block at the level of T1 (occasionally anxious patients who are hyperventilating may complain of this).
Hypotension is due to venous and arterial vasodilation resulting in a reduced venous return, cardiac output and systemic vascular resistance. It should be treated with volume infusion and vasopressors. The head-down (Trendelenburg) position should be used with caution because it may raise further the level of blockade. A better alternative is to raise the legs.
Bradycardia is caused by several factors. Extensive spread results in a widespread sympathetic block leading to unopposed vagal tone and blockade of the cardio-accelerator fibres arising from T1-T4. Heart rate may also decrease as a result of a fall in right atrial filling. Bradycardia can be treated with anticholinergic agents, like atropine, or ك-adrenergic agonists, like ephedrine.
Cardiac output is the product of heart rate and stroke volume. As we have seen, heart rate and stroke volume decrease. The most important reason for the decrease in stroke volume is the decreased volume of blood in the ventricle at the end of diastole (end-diastolic volume), often called “preload”. This is due to a reduction in venous return because of marked venous dilatation following spinal anaesthesia and compression of the vena cava by the pregnant uterus. Venous return is reduced further, if the patient is ventilated, due to the increase in intra-thoracic pressure during the inspiratory phase. Any bleeding which reduces blood volume is poorly tolerated, (see Cardiovascular Physiology and also the Pharmacology of Inotropes and Vasopressors in Update in Anaesthesia No 10).
Respiratory difficulty is caused by loss of chest wall sensation caused by paralysis of the intercostal muscles. Patients often describe their breathing as feeling abnormal, but can demonstrate a good inspiration and can cough and speak normally. When a total spinal occurs the nerve supply to the diaphragm (cervical roots 3-5) is blocked and respiratory failure develops rapidly. Early warning signs include poor respiratory effort, whispering and an inability to cough. Sudden respiratory arrest is usually caused by hypoperfusion of the respiratory centres in the brainstem.
Cardiac arrest may occur due to hypotension and hypoxaemia. Prevent this by adequate ventilation and use of vasopressors.
Other symptoms of total spinal are upper extremity weakness, loss of consciousness and pupillary dilatation.
Pregnant patients in this situation are at risk of aspiration and severe reductions in placental blood flow.
Management
Our patient was immediately treated with 100% oxygen by mask, volume infusion and ephedrine. However she remained hypotensive despite a total of 30mg ephedrine IV and her condition continued to deteriorate. A rapid sequence induction was performed with thiopentone (100mg) and succinylcholine (100mg) and mechanical ventilation was started. After further volume loading with 1500mls crystalloid and 500mls of colloid solution she became haemodynamically stable without the further use of vasopressors. Anaesthesia was continued using isoflurane 0.6 % and nitrous oxide in oxygen (50/50%). A baby boy was born who had a good Apgar scores (7-9-10 after 1-5-10 minutes). Our patient was mechanically ventilated during 30 minutes in the recovery room under propofol sedation until her breathing pattern had normalized. When she was fully awake we explained her what had happened.
Treatment of a total spinal
A total spinal has to be treated symptomatically. Oxygen and intravenous vasopressors (ephedrine 5-10mg or metaraminol 1- 2mg, and if necessary adrenaline 50-100microgram (0.5 - 1ml of 1:10,000 solution) will always be needed. If the airway and breathing are satisfactory, the patient should be given oxygen and the blood pressure restored with vasopressors and intravenous fluid.
If the patient experiences progressive difficulty in breathing and speaking, the level of block is around C3-C5, the patient should be gently ventilated and the airway secured. Cricoid pressure should be used if practical.
If apnoea develops, ventilation should be started immediately and the patient intubated. In this case we used thiopentone because it was immediately available. Some anaesthetists prefer a less cardiovascularly depressant agent like etomidate or ketamine, but a small dose of thiopentone is also safe. When the patient has been intubated and mechanically ventilated it is important to sedate the patient until they can breathe effectively.
Outcome
The patient in our case recovered without harm and also the baby suffered no ill effects. The outcome of a total spinal is good when it is recognised early and treated effectively. All the clinical problems associated with a high spinal will reverse when cardiovascular and respiratory support are provided. After some time the level of the block will recede and wear off. It is important to start treatment immediatelyto prevent damage and harm to the patient. Afterwards explain to the patient and family what happened because a total spinal can be a very frightening experience.
The length of time that the block will last depends on the dose of local anaesthetic injected. With a spinal anaesthetic which spreads unexpectedly high, the block should start to recede after 1 - 2 hours. After a total spinal due to an epidural injection being delivered into the intrathecal space (subarachnoid or spinal) the block may last several hours due to the increased amounts of local anaesthetic injected. During the whole time of the high block the patient will need to be ventilated, if necessary by hand, until the anaesthetic wears off. Since the patient will recover consciousness before being able to breathe effectively some sedation (diazepam, midazolam or propofol) will be useful. Indications for extubation will include a good cough reflex on the endotracheal tube and effective spontaneous respiratory effort.
L.M. Dijkema and H.J. Haisma, Department of Anesthesiology, University Hospital Groningen, P.O.Box 30001, 9700 RB Groningen, the Netherlands., e-mail: l.m.dijkema@anest.azg.nl
--------------------------------------------------------------------------------
This is a report of a patient who suffered an unexpected high level of block during spinal anaesthesia. This review will describe the symptoms, predictive factors and the management of a “total spinal”.
Case Report
A 35-year old primigravida was scheduled for caesarean section because of expected difficult delivery due to a narrow pelvis. She had no relevant medical history. Her height was 1.58m. and she weighed 85kg. After discussion with the patient spinal anaesthesia was planned.
In the theatre electrocardiography, blood pressure monitoring, pulse oximetry and peripheral venous access were established and 500ml of normal saline was given. The spinal anaesthesia was performed in the sitting position at L4/L5 with 2.4ml. bupivacaine 0.5% in hyperbaric dextrose solution - “Heavy Marcaine”. Immediately following the block the patient was put back in the supine position, and the operating table altered with left lateral tilt to diminish aorto-caval compression.
About 5 minutes later the patient complained of nausea and “not feeling well” and experienced progressive difficulty to breathe. The blood pressure fell to 65/40mmHg.
Definition of total spinal
Total spinal is a local anaesthetic depression of the cervical spinal cord and the brainstem. It may follow excessive spread of an intrathecal injection of local anaesthetic, or inadvertent spinal injection of an epidural dose of local anaesthetic.
Predicting factors
Spread of block is influenced by many factors:
Local anaesthetic dose - volume, dosage and baricity of local anaesthetic.
Position of the patient - especially important when a hyperbaric solution of local anaesthetic is used.
Patient characteristics - height, age, gender, intra-abdominal pressure and anatomical configuration of the spinal cord.
Technique - type of needle, site of injection, direction of needle, velocity of injection and use of barbotage.
The patient in our case was a pregnant woman. Pregnant women have a raised intra-abdominal pressure and a diminished volume of the lumbar spinal canal caused by distension of the epidural veins. We therefore gave her a reduced dose of local anaesthetic (2.4ml bupivacaine 0.5% hyperbaric).
The spread of spinal block is sometimes very rapid. The level of the block should be tested within 4 minutes after the injection of local anaesthetic. Commonly used methods of assessing the block are: loss of temperature sensation, loss of pinprick sensation and loss of light touch sensation. Temperature sensation is lost first and light touch sensation last. A block may continue to extend for at least 30 minutes after injection.
Clinical symptoms
Early recognition is the key to management in case of total spinal.
The first signs of high spinal block are hypotension, bradycardia and difficulty in breathing. Before hypotension is detected, the patient often complains of nausea or “not feeling well”. Tingling in the fingers indicates a high block at the level of T1 (occasionally anxious patients who are hyperventilating may complain of this).
Hypotension is due to venous and arterial vasodilation resulting in a reduced venous return, cardiac output and systemic vascular resistance. It should be treated with volume infusion and vasopressors. The head-down (Trendelenburg) position should be used with caution because it may raise further the level of blockade. A better alternative is to raise the legs.
Bradycardia is caused by several factors. Extensive spread results in a widespread sympathetic block leading to unopposed vagal tone and blockade of the cardio-accelerator fibres arising from T1-T4. Heart rate may also decrease as a result of a fall in right atrial filling. Bradycardia can be treated with anticholinergic agents, like atropine, or ك-adrenergic agonists, like ephedrine.
Cardiac output is the product of heart rate and stroke volume. As we have seen, heart rate and stroke volume decrease. The most important reason for the decrease in stroke volume is the decreased volume of blood in the ventricle at the end of diastole (end-diastolic volume), often called “preload”. This is due to a reduction in venous return because of marked venous dilatation following spinal anaesthesia and compression of the vena cava by the pregnant uterus. Venous return is reduced further, if the patient is ventilated, due to the increase in intra-thoracic pressure during the inspiratory phase. Any bleeding which reduces blood volume is poorly tolerated, (see Cardiovascular Physiology and also the Pharmacology of Inotropes and Vasopressors in Update in Anaesthesia No 10).
Respiratory difficulty is caused by loss of chest wall sensation caused by paralysis of the intercostal muscles. Patients often describe their breathing as feeling abnormal, but can demonstrate a good inspiration and can cough and speak normally. When a total spinal occurs the nerve supply to the diaphragm (cervical roots 3-5) is blocked and respiratory failure develops rapidly. Early warning signs include poor respiratory effort, whispering and an inability to cough. Sudden respiratory arrest is usually caused by hypoperfusion of the respiratory centres in the brainstem.
Cardiac arrest may occur due to hypotension and hypoxaemia. Prevent this by adequate ventilation and use of vasopressors.
Other symptoms of total spinal are upper extremity weakness, loss of consciousness and pupillary dilatation.
Pregnant patients in this situation are at risk of aspiration and severe reductions in placental blood flow.
Management
Our patient was immediately treated with 100% oxygen by mask, volume infusion and ephedrine. However she remained hypotensive despite a total of 30mg ephedrine IV and her condition continued to deteriorate. A rapid sequence induction was performed with thiopentone (100mg) and succinylcholine (100mg) and mechanical ventilation was started. After further volume loading with 1500mls crystalloid and 500mls of colloid solution she became haemodynamically stable without the further use of vasopressors. Anaesthesia was continued using isoflurane 0.6 % and nitrous oxide in oxygen (50/50%). A baby boy was born who had a good Apgar scores (7-9-10 after 1-5-10 minutes). Our patient was mechanically ventilated during 30 minutes in the recovery room under propofol sedation until her breathing pattern had normalized. When she was fully awake we explained her what had happened.
Treatment of a total spinal
A total spinal has to be treated symptomatically. Oxygen and intravenous vasopressors (ephedrine 5-10mg or metaraminol 1- 2mg, and if necessary adrenaline 50-100microgram (0.5 - 1ml of 1:10,000 solution) will always be needed. If the airway and breathing are satisfactory, the patient should be given oxygen and the blood pressure restored with vasopressors and intravenous fluid.
If the patient experiences progressive difficulty in breathing and speaking, the level of block is around C3-C5, the patient should be gently ventilated and the airway secured. Cricoid pressure should be used if practical.
If apnoea develops, ventilation should be started immediately and the patient intubated. In this case we used thiopentone because it was immediately available. Some anaesthetists prefer a less cardiovascularly depressant agent like etomidate or ketamine, but a small dose of thiopentone is also safe. When the patient has been intubated and mechanically ventilated it is important to sedate the patient until they can breathe effectively.
Outcome
The patient in our case recovered without harm and also the baby suffered no ill effects. The outcome of a total spinal is good when it is recognised early and treated effectively. All the clinical problems associated with a high spinal will reverse when cardiovascular and respiratory support are provided. After some time the level of the block will recede and wear off. It is important to start treatment immediatelyto prevent damage and harm to the patient. Afterwards explain to the patient and family what happened because a total spinal can be a very frightening experience.
The length of time that the block will last depends on the dose of local anaesthetic injected. With a spinal anaesthetic which spreads unexpectedly high, the block should start to recede after 1 - 2 hours. After a total spinal due to an epidural injection being delivered into the intrathecal space (subarachnoid or spinal) the block may last several hours due to the increased amounts of local anaesthetic injected. During the whole time of the high block the patient will need to be ventilated, if necessary by hand, until the anaesthetic wears off. Since the patient will recover consciousness before being able to breathe effectively some sedation (diazepam, midazolam or propofol) will be useful. Indications for extubation will include a good cough reflex on the endotracheal tube and effective spontaneous respiratory effort.
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