Mortalità in anestesia

Claudio Melloni

Anestesia e Rianimazione

Ospedale di Faenza(RA)

What lessons have the ASA closed claims

teached to us?

What is a claim?

Claim is a demand for financial compensation by an individual who has sustained an injury from medical care.

Once a claim is resolved the file is closed

Che cosa sono gli ASA Closed claims?

Collection of 35 USA insurance companies

14500 anesthesiologists covered 50-55% of all USA practicing

anesthesiologists

Closed claim

Medical records Narrative statement by the

involved health care personnel Deposition summaries Outcome and follow up reports Cost of the settlement or jury award

Utilità dei closed claims

Collection of “ sentinel” events

Identification of areas of risk(and litigation….)

Provides direction for further analysis

Demography and general characteristics

Adults(91%>16 years) Generally healthy:asa 1 & 2 69% Non emergency surgery 75% GA 67% The database is not a collection of medically or

surgically compromised patients in whom the underlying disease plays a major role in the outcome;for this reason the closed claim database offers the unique opportunity to discern how the process of care contributes to the genesis of adverse outcomes…..

Problemi nella interpretazione dei dati

Data collected to resolve claims Not collected for outcome research Total number of anesthesia and patients unknown Unknown denominator for risk calculation Retrospective Lag time in

publication;closure,availability,study,calculations…publication

Geographic imbalance ? Interrater reliability;bias… Claims selectivity;only 30-33% of claims available are

evaluated….

Definizioni

Complication;adverse outcome or injury sustained by the patient

Damaging event:the specific incident or mechanism that led to the adverse outcome(e.g.airway obstruction)

Risarcimenti (*1000 $) Outcome median range

Death(1725) 216 260-14700 Brain damage adults(676) 673 2750-23200

Brain damage newborns(129) 499 3333-6800

Relationships associated with

payment

Appropriateness /unappropriateness

of caregravity of injury standard of care

Frequency of paymentmagnitude of paymentBetter

monitoring

Relationships emerged form studies of closed claims:

Frequency of payment linked to appropriateness of care,but not to severity of injury

magnitude of payment linked to both severity of injury and to standard of care

adverse outcome judged preventable with better monitoring were far costlier than those which were not considered preventable with better monitoring.

Cheney FW et al. Standard of care and anesthesia liability. JAMA 1989;261:1599‑1603 Tinker JH et al. Role of monitoring devices in prevention of anesthetic mishaps: a closed claims analysis. 1999;71:535‑540.

Effect of outcome on physician judgements

Examination of the Closed Claims database suggests the presence of a recurrent association between the severity of an adverse outcome and accompanying judgments of appropriateness of care.

Caplan RA.Effect of outcome on physician judgement of appropriateness of care.JAMA 1991;265:1957-1960.

Severity of Severity of adverse outcomeadverse outcome

judgments ofjudgments of appropriatenessappropriateness of care. of care.

Effect of outcome on physician judgements:2

Specifically, non disabling iniuries are more often associated with ratings of appropriate care, while disabling injuries and death are more often associated with ratings of less than appropriate care.

Effect of outcome on physician judgements:3

This raises the possibility that highly unfavorable outcomes may predispose (bias) peer reviewers towards harsher judgments,while minor injuries may elicit less critical responses.

Study of peer review:1 cases from the Closed Claims database study of peer review with 112 practicing anesthesiologists

volunteered to judge appropriateness of care involving adverse anesthetic outcomes.

The original outcome in each case was either temporary or permanent.

For each original case, a matching alternate case was devised. The alternate case was identical to the original in every respect,

except that a plausible outcome of opposite severity was substituted. The original and alternate cases were randomly divided into two sets

and assigned to reviewers. The reviewers were blind to the intent of the study.

Study of peer review:2 The care in each case was independently rated by the

reviewers based upon the conventional criterion of reasonable

and prudent practice at the time of the event. Knowledge of the severity of injury produced a

significant inverse effect on judgments of appropriateness of care.

the proportion of ratings for appropriate care by 31 percentage points when the outcome was changed from temporary to permanent, and increased by 28 percentage points when the outcome was changed from permanent to temporary.

Effect of outcome on judgements of appropriate

care

0

10

20

30

40

50

60

70

actuallytemporary

changed topermanent

actuallypermanent

changed totemporary

% of appr

opriat

eness of

care

Schroeder SA et al. Do bad outcomes mean bad care? JAMA

199 1; 265:1995.

non disabling iniuries = appropriate care

disabling injuries and death = less than appropriate care.

Concern about peer review and bias

obstacle to objective evaluation of major medical risks….

Frequency and size of payments!!

Foster practices which result in minor but avoidable injuries….

If such injuries are pervasive…» Aggregate cost

Incidence % of claims related to the most common adverse

outcomes

0

5

10

15

20

25

30death

nerve damage

brain damage

airway trauma

pnx

eye injury

fetal/newborn injury

headache

stroke

awareness

aspiration

bckpain

myocardial infarction

burns

Most common damaging events:%

resp

cardiovasc

equipment

reg block techn.

surg.techn.

wrong drug dose

1382

717591

372278

209

Conclusioni Damaging events and adverse outcome show tight

clustering in a small number of specific categories; Damaging events:3 categories account for almost half of

claims;resp, equipment & cardiovascular account for 46% of claims:

Adverse outcome:death,nerve damage,brain damage account for almost 65% of claims

This clustering of damaging events and adverse outcome is of fundamental importance since suggests that research and risk management strategies directed at just a few areas of clinical practice could result in large improvements in professional liability.

Most common adverse outcomes Range of payments($*1000)

0

5000

10000

15000

20000

25000

deathnerve dam

age

brain damage

airway traum

a

eye in.

pnxfetal/new

born in,.

stroke

aspiration

back pain

headache

MI

burns

awareness

min

med

max

Most common adverse outcomes Median Payment:$*1000

0

100

200

300

400

500

600

700

median payment

deathnerve damagebrain damageairway traumaeye injurypnxfetal7newborn injurystrokeaspirationback painheadacheMIburnsawareness

Claims differ in different populations;

»FOR INCIDENCE

»FOR SERIOUSNESS

Morray J, Geiduschek J, Caplan R, Posner K, Gild W, Cheney FW: A comparison of

pediatric and adult anesthesia malpractice claims. ANESTHESIOLOGY 78:461-7, 1993

Chadwick,HS,Posner,K,Kaplan,RA,Ward,RJ,Cheney FW.A comparison of obstetric and

nonobstetric anesthesia malpractice claims.Anesthesiology 1991;74:242-249.

ob vs non ob:190 vs 1351» ob cases 67% CS,33% vaginal» 65% associati a anest reg,33% con

GA» 2 claims per non disponibilità

dell’anestesista!

ASA closed claims project Malpractice claims against

anesthesiologists:OB VS NON OB

0

5

10

15

20

25

30

35

40

%

ob nonob

morte (materna)danno cerebrale neonatalecefaleamorte neonataledolore dur.anestdanno neuraledanno cerebrale paz.distress emotivodolore dorso

Claims ostetrici:regionale vs GA.

0

5

10

15

20

25

30

35

40

45

%

reg GA

morte materna

danno cerebrale neonatale

cefalea

morte neonatale

dolore dur.anest

danno neurale

danno cerebrale paz

distress emoz

dolore dorso

*

*

*

*

Patogenesi del danno neonatale

45% attribuiti a cause anestetiche:

GA:4» 1 broncospasmo» 1 intub esofagea» 1 aspir polm» 1 ritardo anest.

» Regionale:13» 9 convuls da iniez

intravasc» 1 eclampsia» 1 ritardo disponibilità» 3 spinali alte

37% a probl ostetrici o congeniti,

13% con probl di rianimaz.

Dati relativi ai pagamenti:OB VS NON OB

claims non ob claims ob Claims obregionale generale

non pagati(%) 32 38 43 27

pagati(%) 59 53 48 63

pagamento mediano($) 85000 203000 91000 225000

range di pagamento($) 15000-6 milioni 675000-5.4 milioni 675-2.5 mil 750-5.4 mil

GA pagata il 63% vs 48% delle reg.

Conclusioni dai closed claims obs

Danno cerebrale neonatale è il claim più frequente,anche se solo il 50% è LEGATO ALL’ANESTESIA!.

Pagamento mediano per il danno cerebr. Neonatale:500.000 $ ,vs 120.000 $ dei danni ob;

Cefalea è il III problema: e risulta in pagamento il 56% delle volte……...

RESPIRATORY related events

Characteristics of respiratory related

claims high frequency of severe

outcomes:85% death or brain damage Costly payments($ 200.000 and +) 72% judged preventable by monitoring

(pulse oximetry and etCO2) Monitoring helpful in reducing

inadequate ventilation and inadeq.oxygenation

Classification of the most common respiratory system damaging events:% of 1382

cases.

diff intub

inadeq vent/O2

esoph intub

airway obstruct

aspiration

premat extub

bronchospasm

Trends in death and brain damage according to the basic

damaging event

05

101520253035404550

%

1980 1990

Resp eventcardiovasc eventequipment probl

Most common respiratory events associated with death and brain

damage

inadequate ventilationesophag intubdifficult intubother resp eventsadv resp events

inadequate ventilationesophag intubdifficult intubother resp events

1980

1990

Adv resp events

Other respiratory damaging events associated with death or

brain damage

0

2

4

6

8

10

12

%

1980 1990

air obsbronchospasmpremat extubaspir

Which is the impact of pulse oxymetry and

end tidal CO2 monitoring in death and brain damage?

Respiratory damaging events associated with death or brain damage by monitoring group

0

5

10

15

20

25

30

35

%

inadeq ventil esophag intub diff.intub

noneSpO2 onlySpO2+etCO2

799

102167

Cardiovascular damaging events associated with death or brain

damage

0

10

20

30

40

50

60

unexp./othercv event

neuraxcardiac arrest

inadeq fluid blood loss

19801990

Unexplained/other damaging cardiovascular events in the 90’s(137)(death and brain

damage)

arrhythMIpulm embstroke path abnormmultifactorial

How do end tidal CO2 and SpO2 monitoring affect the occurrence

of cardiovascular damaging events as the mechanism of brain damage or

death?

Cardiovascular damaging events associated with death or brain damage by monitoring group

0102030405060

none

SpO2 only

SpO2+etCO2

72194

192??

Conclusions from the data about the

future role of monitoring in the

prevention of severe anesthesia

related injury?

Better monitoring would have

prevented death or brain damage

Better monitoring would have prevented death or brain damage

in the 90’s

no

yes

Resp events:221

Cardiovascular events judged preventable by better monitoring

no

yes

Respiratory and cardiovascular events contribution to deaths and brain

damage(Cheney,FW Anesthesiology 1999;91:552-6)

0

10

20

30

40

50

60

70

80

%

'70 '80 '90

respcardiovascinadeq ventesoph.intub<standard of careplaintiff payment

Trends in death and brain damage

0

10

20

30

40

50

60

70

80

%

'70-79 '80-89 '90-94

nerve injurybrain damagedeath

“The fact that professional liability premiums for anesthesiologists have decreased significantly since the mid-1980s would imply an overall reduction in severe injuries.”

Emerging trends Claims fro death and permanent brain damage are

decreasing injuries attributed to inadequate ventilation and

oxygenation are decreasing;SpO2 and etCO2 monitoring are the most likely causes

relative increase in the proportion of cardiovascular damaging events and respiratory events not prevented by monitoring

better monitoring would not lead to further reductions in death and brain damage

Death associated with Regional anesthesia in the 90’s(97

cases):etiology

pain management

neuraxial block

notblock related

intravascinjectionother blockrelated

Neuraxial cardiac arrest

Sudden and unexpected severe bradycardia and /or

asystole occurring during neuraxial block with relatively stable

haemodynamics preceding the event.

Cardiac arrest associated with neuraxial block

900 cases in claims 1988; 14 cases of neuraxial cardiac arrest…..,all pts

were resuscitated,8 survived but only 1 regained a sufficient neurologic function…..

Hypothesis: poor cerebral perfusion pressures

engendered by closed chest cardiac massage in the presence of high sympathetic blockade.

Sudden cardiac arrest during regional anesthesia

Cardiac arrest during spinal anesthesia

Closed claim database:14/1000 (1978-86) Features consistent with a sentinel event:

» Young healthy adults for relatively minor surgery» Standard anesthetic techniques and monitoring» Arrest followed by prompt & brief CPR» All resuscitation successful» Death/severe brain damage;13/14 !!» Up tp the year 2000 other 41 cases were reported in the

literature(26 spi + 15 epid);but outcome much better…..

Risk factors for cardiac arrest during spinal anesthesia

Advanced age & high ASA physical status(Auroy)

baseline HR < 60 (Carpenter et al). ASA physical status I patients(ASA closed claims)

Current therapy with b-blockers block height >T6 patients who are <50 years old (Tarkkila)

patients with first-degree heart block (Liu)

Conclusions from cases of sudden bradycardia or asystole associated with

spinal anesthesia:

Cases do occur There are no clear clinical

predictors… Prompt recognition and treatment

keys to injury prevention.

Incidence of anesthesia related cardiac arrest/per 10.000

anesthetics

0

1

2

3

4

5

6

7

incidence mortality

BibouletOlssonAuroyNewland:directNewland: relatedNewland anesth.attribAubasAubas reg onlyTarkkilaGeffin

spinal

*10 !!

GA

GA

Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected cardiac arrest during spinal anesthesia: Anesthesiology 1988; 68:5–11.

2: Joshi GP, Shearer VE, Racz T. Ruptured aortic aneurysm and cardiac arrest associated with spinal anesthesia. Anesthesiology 1997; 86:244–7.

3: Geffin B, Shapiro L. Sinus bradycardia and asystole during spinal and epidural anesthesia: J Clin Anesth 1998; 10:278–85.

4: Tarkkila PJ, Kaukinen S. Complications during spinal anesthesia: Reg Anesth 1991; 16:101–6.

5: Auroy Y, Narchi P, Messiah A. Serious complications related to regional anesthesia. Anesthesiology 1997; 87:479–86.

6: Chopra V, Bovill JG, Spierdijk J. Accidents, near accidents and complications during anaesthesia: Anaesthesia 1990; 45:3–6.

Newland MC,Ellis SJ,Lydiatt CA, Peters KR,Tinker JH,Romberger DJ,Ullrich FA Anderson J.Anesthestic-related Cardiac Arrest and Its Mortality: A Report Covering 72,959 Anesthetics over 10 Years from a

US Teaching Hospital.

August 15, 1989 to August 14, 1999, 72,959 anesthetics University of Nebraska Hospital A total of 144 cardiac arrest (within 24-

h periop.) 19.7/ 10,000 anesthetics (95%

confidence interval [CI], 16.52-22.96)

Newland MC,Ellis SJ,Lydiatt CA, Peters KR,Tinker JH,Romberger DJ,Ullrich FA Anderson J.Anesthestic-related Cardiac Arrest and Its Mortality: A Report Covering 72,959 Anesthetics over 10 Years from a

US Teaching Hospital. : A prospective and retrospective case analysis study of all

perioperative cardiac arrests occurring during a 10-yr period from 1989 to 1999 was done to determine the incidence, cause, and outcome of cardiac arrests attributable to anesthesia.

Methods: One hundred forty-four cases of cardiac arrest within 24 h of surgery were identified over a 10-yr period from an anesthesia database of 72,959 anesthetics. Case abstracts were reviewed by a Study Commission composed of external and internal members in order to judge which cardiac arrests were anesthesia-attributable and which were anesthesia-contributory. The rates of anesthesia-attributable and anesthesia-contributory cardiac arrest were estimated.

Newland et al.Anesthestic-related Cardiac Arrest and Its Mortality: A Report Covering 72,959

Anesthetics over 10 Years from a US Teaching Hospital.

Results: Fifteen cardiac arrests out of a total number of 144 were judged to be related to anesthesia. Five cardiac arrests were anesthesia-attributable, resulting in an anesthesia-attributable cardiac arrest rate of 0.69 per 10,000 anesthetics (95% confidence interval, 0.085-1.29). Ten cardiac arrests were found to be anesthesia-contributory, resulting in an anesthesia-contributory rate of 1.37 per 10,000 anesthetics (95% confidence interval, 0.52-2.22). Causes of the cardiac arrests included medication-related events (40%), complications associated with central venous access (20%), problems in airway management (20%), unknown or possible vagal reaction in (13%), and one perioperative myocardial infarction. The risk of death related to anesthesia-attributable perioperative cardiac arrest was 0.55 per 10,000 anesthetics (95% confidence interval, 0.011-1.09).

Conclusions: Most perioperative cardiac arrests were related to medication administration, airway management, and technical problems of central venous access. Improvements focused on these three areas may result in better outcomes.

Risk factors for cardiac arrest(Newland et al.Anesthestic-related Cardiac Arrest and Its Mortality: A

Report Covering 72,959 Anesthetics over 10 Years from a US Teaching Hospital.)

As compared to controls, patients experiencing cardiac arrest were:more likely male (OR 0.71; 95% CI, 0.49-1.02;P = 0.07)» more likely to have a greater ASA physical status (P <

0.0001; 68% ASA IV or V vs. 14% for controls)» more likely to have emergency surgery (OR, 5.14; 95% CI,

3.49-7.56;P < 0.0001)– thoracic (including cardiac)-spine or upper abdominal surgery

(P < 0.0001),

» longer operations (OR, 1.00; 95% CI, 1.003-1.00;P = 0002)

» and surgery after 3 pm (OR, 0.45; 95% CI, 0.30-0.66;P < 0.0001).

Auroy et al.Serious Complications Related to Regional Anesthesia: Results of a

Prospective Survey in France.Anesthesiology 87:479-86, 1997

Self reporting by participating anesthesiologists

(736 /4,927 :14.9%) 103,730 regional anesthetics during the 5-

month study period:40,640 spinal anesthetics, 30,413 epidural anesthetics, 21,278 peripheral nerve blocks, 11,229 intravenous regional anesthetics.

Auroy et al;summary of results

103,730 regional anesthetic procedures:sufficient prospective data for investigators??

32 Cardiac arrest,28 radicular deficits,23 seizures,5 cauda equina,1 paraplegia,7 deaths

More Ko following spinal; » cardiac arrest 6,4/10.000,(6/26 deaths)» neurol Ko 6/10.000» permanent cauda equina assoc with lidocaine 5%

All 26 reported seizures were preceded by minor auditory symptoms and complaints of metallic taste;more frequent occurrence of seizures after peripheral block than after epidural anesthesia

Cardiac Arrest(da Auroy et al.Serious Complications

Related to Regional Anesthesia: Results of a Prospective Survey in

France.Anesthesiology 87:479-86, 1997 incidence of cardiac arrest was significantly

greater with spinal anesthesia (6.4 ± 1.2 per 10,000 patients) than with epidural anesthesia and peripheral nerve blocks combined (1.0 ± 0.4 per 10,000 patients; P < 0.05

During the 26 cardiac arrests occurring with spinal anesthesia, 15 patients were treated only with closed-chest cardiac massage and ephedrine; one patient was treated only with epinephrine (0.5 mg); and 10 patients were treated with closed chest cardiac massage and epinephrine (3.4 ± 3.6 mg).

Cardiac Arrest(da Auroy et al.Serious

Complications Related to Regional Anesthesia: Results of a Prospective Survey in France.Anesthesiology 87:479-86,

1997

Fatal outcome from cardiac arrest:6/26 Risk of death after cardiac arrest was significantly

associated with age and American Society of Anesthesiologists' (ASA) physical status class. The average age of survivors was 57 ± 20 yr, whereas the average age of nonsurvivors was 82 ± 7 yr. The difference in average ages was statistically significant (P < 0.05). Similarly, the breakdown of ASA physical status for survivors versus nonsurvivors was n = 13 versus n = 0 for ASA I; n = 5 versus n = 2 for ASA II; n = 2 versus n = 3 for ASA III; and n = 1 versus n = 0 for ASA IV.

Auroy et al.Serious Complications Related to Regional Anesthesia:

Results of a Prospective Survey in France.Anesthesiology 87:479-86,

1997

0

1

2

3

4

5

6

7

8

1/10.000

spinal epidural periph.reg i.v.reg Total

cardiac arrestdeathseizuresneurol.injuryradiculopathycauda equinaparaplegia

Cardiac Arrest(da Auroy et al.Serious Complications

Related to Regional Anesthesia: Results of a Prospective Survey in France.Anesthesiology 87:479-86, 1997

Two variables were statistically different regarding cardiac arrest in patients undergoing spinal anesthesia: (1) the time between onset of spinal blockade and occurrence of cardiac arrest was longer in nonsurvivors than in survivors (42 ± 19 min versus 17 ± 16 min, respectively; P < 0.05); and (2) total hip arthroplasty (THA) more frequently was the type of surgery in nonsurvivors than in survivors (5 of 6 THA among nonsurvivors compared with 2 of 20 non-THA surgeries in survivors; P < 0.05). During THA, three cardiac arrests happened at the time of cement insertion and were fatal. Blood loss at the time of cardiac arrest was 700 ml in nine cardiac arrest patients, with four arrests being fatal. Sedation was not performed nor was cyanosis or dizziness observed before any of the fatal cardiac arrests, although all cardiac arrests were reported to have been preceded by bradycardia.

3

Cardiac Arrest:epidural & peripheral nerve block(da Auroy et al.Serious Complications Related to Regional

Anesthesia: Results of a Prospective Survey in France.Anesthesiology 87:479-86, 1997

3 reversible cardiac arrest were reported with epidural anesthesia.

3 cardiac arrest were reported during peripheral nerve blocks. In each case, these appeared to be associated with inadequate analgesia. In two of the three cases, cardiac arrest also was associated with vasovagal responses, treated, and reversed. One fatal cardiac arrest resulted from a myocardial infarction. No neurologic sequelae were observed in the 25 patients who recovered from cardiac arrest.

Biboulet et al.Fatal and non fatal cardiac arrests related to anesthesia.General

Anesthesia*Can J Anesth 2001 / 48 / 326-332

0

0,1

0,2

0,3

0,4

0,5

0,6

0,7

1/10.000

AG epid spinl caudal ivra plexus nerve

cardiac arrestdeath

7182

6

4145

76562

08

1

330

8 922

2

323

1

Treatment of bradycardia/hypotension associated with neuraxial

block

Treat aggressively HR <60 ,>50:atropine 0.5-1 mg HR <50,>30;atropine 0.5-1

mg+ephedrine 10-20 mg HR<30 epinephrine 0.1 mg Asystole:epi 1 mg + chest

compressions

P waves without QRS;O2 + Atropine 1,2 mg

Repetitive chest thumping

After 30 sec of precordial thumping

;high grade AV block with occasional

supraventricular beats.

Precordial thumping resumed

at arrows again resulting in QRS and patient

awakening

Thumping stopped :pt

awaken and asks why he is beaten!

Resuscitation lasted 3 min..sinus bradycardia…NSR..ok.

Operation performed,no sequelae,pt discharged 24 hr later in good health.

Causative factors in asystole following spinal anesthesia

Cerebral deoxygenation?see article from reg anesth & turp…..univ of cairo….

Reflex;decreased venosu return..empty atrium..empty ventricle….bradycardia …. fall in CO?

Vasovagal reflex? Organize a study….Somanetics ,CO

impedance ,FC,NIBP,consciousneess,level of blockade…

Caplan RA, Ward R, Posner K, et al. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of the predisposing factors. Anesthesiology 1988; 68:5-11.

13 Caplan RA. The ASA closed claims project: lessons learned. Annual refresher course lectures, 1997. 242.

14 Auroy Y, Narchi P, Messiah A, et al. Serious complications related to regional anesthesia. Anesthesiology 1999; 87:47-86.

15 Krisner AC, Hogan QH, Wenzel W, et al. The efficacy of epinephrine or vasopressin for resuscitation during epidural analgesia. Anesth Analg 2001; 93:734-742.

 

Krisner AC, Hogan QH, Wenzel W, et al. The efficacy of epinephrine or vasopressin for resuscitation during epidural analgesia.

Anesth Analg 2001; 93:734-742 Cardiopulmonary resuscitation (CPR) during epidural anesthesia is considered difficult because

of diminished coronary perfusion pressure. The efficacy of epinephrine and vasopressin in this setting is unknown. Therefore, we designed this study to assess the effects of epinephrine versus vasopressin on coronary perfusion pressure in a porcine model with and without epidural anesthesia and subsequent cardiac arrest. Thirty minutes before induction of cardiac arrest, 16 pigs received epidural anesthesia with bupivacaine while another 12 pigs received only saline administration epidurally. After 1 min of untreated ventricular fibrillation, followed by 3 min of basic life-support CPR, Epidural Animals and Control Animals randomly received every 5 min either epinephrine (45, 45, and 200 mg/kg) or vasopressin (0.4, 0.4, and 0.8 U/kg). During basic life-support CPR, mean ± SEM coronary perfusion pressure was significantly lower after epidural bupivacaine than after epidural saline (13 ± 1 vs 24 ± 2 mm Hg, P < 0.05). Ninety seconds after the first drug administration, epinephrine increased coronary perfusion pressure significantly less than vasopressin in control animals without epidural block (42 ± 2 vs 57 ± 5 mm Hg, P < 0.05), but comparably to vasopressin after epidural block (45 ± 4 vs 48 ± 6 mm Hg). Defibrillation was attempted after 18 min of CPR. After return of spontaneous circulation, bradycardia required treatment in animals receiving vasopressin, especially with epidural anesthesia. Systemic acidosis was increased in animals receiving epinephrine than vasopressin, regardless of presence or absence of epidural anesthesia. We conclude that vasopressin may be a more desirable vasopressor for resuscitation during epidural block because the response to a single dose is longer lasting, and acidosis after multiple doses is less severe compared with epinephrine.

Coronary perfusion pressure in pogs given epidural saline using

either epinephrine(+) or vasopressin(triangle) Krisner AC, Hogan QH, Wenzel W, et al. The efficacy of epinephrine or

vasopressin for resuscitation during epidural analgesia. Anesth Analg 2001; 93:734-742

Coronary perfusion pressure in pigs given epidural bupivacaine using either epinephrine(+) or

vasopressin(triangle) Krisner AC, Hogan QH, Wenzel W, et al. The efficacy of epinephrine or

vasopressin for resuscitation during epidural analgesia. Anesth Analg 2001; 93:734-742

Mean fibrillation frequency during VF and CPR with

epinephrine Krisner AC, Hogan QH, Wenzel W, et al. The efficacy of epinephrine or vasopressin for resuscitation during epidural analgesia. Anesth

Analg 2001; 93:734-742

Mean fibrillation frequency during VF and CPR with vasopressin and epidural

bupivacaine Krisner AC, Hogan QH, Wenzel W, et al. The efficacy of epinephrine or vasopressin for resuscitation during epidural analgesia. Anesth

Analg 2001; 93:734-742

Conclusions from KrisnerKrisner AC, Hogan QH, Wenzel W, et

al. The efficacy of epinephrine or vasopressin for resuscitation during epidural analgesia. Anesth

Analg 2001; 93:734-742

our results demonstrate that CPR during epidural anesthesia is possible, although the underlying pathophysiology has to be carefully considered. Epidural blockade profoundly decreases ventricular fibrillation mean frequency during basic life-support CPR and is reversed by both epinephrine and vasopressin. If our findings can be extrapolated to a clinical setting, advanced cardiac life support should be started immediately, and vasopressor drugs should not be withheld. In the context of epidural anesthesia, both epinephrine and vasopressin increase coronary perfusion pressure sufficiently during CPR. During epidural block, muscarinic blockade may be needed after vasopressin resuscitation. Vasopressin may be a more desirable vasopressor for resuscitation during epidural block because the response to a single dose is longer lasting, and acidosis after multiple doses is less severe compared with epinephrine.

Hogan QH, Stadnicka A, Stekiel TA. Effects of epidural and systemic lidocaine on sympathetic activity and mesenteric circulation in rabbits. Anesthesiology 1993; 79:1250–60.<ldn>!

2: Jacobsen J, Sofelt S, Brocks V. Reduced left ventricle diameters at onset of bradycardia during epidural anesthesia. Acta Anaesthiolol Scand 1992; 36:831–6.

3: Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected cardiac arrest during spinal anesthesia: Anesthesiology 1988; 68:5–11.<ldn>!

4: Rosenberg JM, Wahr JA, Sung CH. Coronary perfusion pressure during cardiopulmonary resuscitation after spinal anesthesia in dogs. Anesth Analg 1996; 82:84–7.<ldn>!

5: Rosenberg JM, Wortsman J, Wahr JA. Impaired neuroendocrine response mediates refractoriness to cardiopulmonary resuscitation in spinal anesthesia. Crit Care Med 1998; 2:533–7.

6: Ditchey RV, Lindenfeld JA. Failure of epinephrine to improve the balance between myocardial oxygen supply and demand during closed-chest resuscitation in dogs. Circulation 1988; 78:382–9.<ldn>!

7: Niemann JT, Haynes KS, Garner D. Postcountershock pulseless rhythms: Ann Emerg Med 1986; 15:112–20.<ldn>!

8: Tang W, Weil MH, Gazmuri R. Pulmonary ventilation/perfusion defects induced by epinephrine during cardiopulmonary resuscitation. Circulation 1991; 84:2101–7.<ldn>!

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5 Aromaa U, Lahdensuu M, Cozanitis DA. Severe complications associated with epidural and spinal anaesthesia in Finland 1987-1993: a study based on patient insurance claims. Acta Anaesthesiol Scand 1997; 41:445-452.

6 Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988; 68:5-11.

7 Carpenter RL, Caplan RA, Brown DL, et al. Incidence and risk factors for side effects of spinal anesthesia. Anesthesiology 1992; 76:906-916.

8 Pollard JB. Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention. Anesth Analg 2001; 92:252-256.

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10 Pollock JE, Neal JM, Liu SS, et al. Sedation during spinal anesthesia. Anesthesiology 2000; 93:728-734.

Pollard JB. Cardiac arrest during spinal

anesthesia: common mechanisms and

strategies for prevention. Anesth

Analg 2001; 92:252-256

Cardiac arrests during spinal anesthesia are described as “very rare,” “unusual,” and “unexpected,” but are actually relatively common . The two largest prospective studies designed to evaluate the incidence of complications during spinal anesthesia reported two arrests in 1881 patients and 26 arrests in 40,640 patients for an overall incidence of seven arrests for every 10,000 (0.07%) spinal anesthetics. A review of approximately 4000 regional anesthetics revealed six cases of severe bradycardia (pulse of 20 to 40 bpm) and six others (0.15%) with cardiac arrest after spinal anesthesia . These rates are high when compared with an incidence of three arrests from any cause for every 10,000 cases (0.03%) reported for patients undergoing noncardiac surgery . The incidence of cardiac arrest with spinal anesthesia is also frequent compared with the rate of one cardiac arrest for every 10,000 cases (0.01%) recently reported for epidural anesthesia

4: Tarkkila PJ, Kaukinen S. Complications during spinal anesthesia: Reg Anesth 1991; 16:101–6.<ldn>!

MEDLINEÒ RECORD:

AB - Complications during spinal anesthesia were studied prospectively in 1881 patients. Twenty-six percent of the patients suffered from one or more complications. The most common complications were hypotension (16.4%) and bradycardia (8.9%). The risk for hypotension was found to be higher with increasing age of patients (p less than 0.005). Higher peak sensory level significantly increased the risk for hypotension (p less than 0.0001), bradycardia (p less than 0.0001) and nausea (p less than 0.0001). Female patients suffered significantly more hypotension (p less than 0.001), nausea (p less than 0.001) and vomiting (p less than 0.001) than males. Cementation of prosthesis and deflation of the leg tourniquet were other risk factors demonstrated in this study.

Aubas S,Biboulet Ph,daures JP,Du Cailar J.Frequence et cause des arrets cardiaques

peroperatoires et en salle de reveil.A prpopos de 102468

anesthesies.Ann.Fr.Anesth.Reanim. 1991;10:436-442.

102468 anesthetics 189 CA 29 linked totally or partially to

anesth.;11 survived:mortality 1.1/10.000

8/29 during regional 7 pd &1 only under spinal:8/12981=6/10.000

Mackey DC, CARPENTER RL, THOMPSON GE, BRowN DL,

BODILY MN. Bradycardia and asystole during spinal anesthesia : a report of three

cases without morbidity. Anesthesiology, 70

: 866‑868, 1989.

3 cases not associted with hypoxemia full recovery

The most common serious cardiovascular side-effects from spinal anesthesia are hypotension and bradycardia, with an incidence of cardiac arrest said to range from 0.4 to 1.0 per 10 000 spinal anesthetics . Risk factors for hypotension include block height T5 or greater, age older than 40 years, baseline systolic blood pressure less than 120 mmHg, and spinal puncture performed above L3-L4. Hypotension occurs as a result of reductions in systemic vascular resistance and central venous pressure from sympathetic block triggering vasodilation and the redistribution of central blood volume to the lower extremities and splanchnic beds.

Interestingly, the first publication from the American Society of Anesthesiologists Closed Claims Project database in 1988 reported sudden cardiac arrest in 14 healthy patients undergoing spinal anesthesia. Six patients died, and of the eight survivors, seven had serious neurological damage. That initial report emphasized the suddenness of the bradycardia and asystole that can develop with spinal anesthesia, despite seemingly satisfactory vigilance and resuscitation efforts by the anesthesia providers. In that seminal publication, Caplan and colleagues admonished that the early treatment of bradycardia with epinephrine is indicated if conventional doses of atropine and ephedrine are ineffective. If asystole ensues, a full resuscitation dose of epinephrine should be administered immediately to reverse alpha blockade and direct perfusion to the heart and brain. They also postulated that prophylactic treatment of heart rates less than 60 beats per minute with vagolytic agents in patients with high spinal blockades may be an effective preventive strategy.

Prospective studies by Carpenter and colleagues as well as by Auroy et al. found no link between sedation and cardiac arrest during spinal anesthesia. Clearly, a circulatory etiology seems much more probable than a respiratory etiology, given the blockade of sympathetic efferents and the profound decrease in venous return associated with higher levels of spinal blockade. The reduced preload triggers bradycardia by three possible reflexes that may be operative: (i) decreased venous return results in reduced pacemaker stretch and slower heart rate; (ii) low pressure baroreceptors in the right atrium and vena cava may fire; and (iii) the Bezold-Jarisch reflex causes bradycardia when mechanoreceptors in the left ventricle are stimulated.

The fact that patients who have sustained cardiac arrest and poor outcome associated with spinal anesthesia have typically been young and previously healthy is deeply troubling and raises concern about patient selection and prevention strategies. A recent study by Pollard highlighted six possible risk factors for moderate bradycardia (<50 bpm) during spinal anesthesia. These were: baseline heart rate less than 60 bpm; American Society of Anesthesiologists physical status I; the use of beta-blocking drugs; a sensory level above T6; age less than 50 years; and a prolonged PR interval. The author warned that if two or more risk factors are present, the patient may be at high risk of bradycardia/cardiac arrest during spinal anesthesia. He offered several prevention strategies that emphasized rigorous patient selection (beware of young, vagotonic patients!), liberal fluid administration before initiating spinal anesthesia, and having a low threshold for additional fluids, vasopressors, or patient repositioning to augment venous return. Furthermore, he advocated rapidly escalating the treatment of moderate bradycardia: intravenous atropine, ephedrine (25-50 mg), and if necessary epinephrine (0.2-0.3 mg). For severe bradycardia, full resuscitation doses of epinephrine should be given immediately.

Another fascinating area in which our understanding of physiology has expanded recently is the appreciation of convergence in mechanisms of general and spinal anesthesia. For example, minimum alveolar concentration, a traditional measure of inhalational agent potency, appears to have a primary mechanism in the spinal cord . Alternatively, central neuraxial anesthesia may have direct effects on the suppression of consciousness, and several studies have observed that patients appear drowsy after spinal anesthesia despite the lack of sedative medications . In fact, greater sedation has been observed with higher blocks. The possible mechanisms include the rostral spread of local anesthetic agents, or a reduction in the function of the reticular activating system caused by an interruption of afferent input. The clinical take-home message is, of course, that patients undergoing spinal anesthesia have a reduced requirement for pharmacological sedatives.

Conclusions from closed claims analysis

90’sClaims for death and brain damage are decreasing compared to 80’s

Claims Inadeq ventilation/oxygenation and esophageal intubation decreased from 90’s to 80’s….

That happened thanks to the widespread use of Oxygenation and end tidal CO2 monitoring (and LMA????….)

Cardiovascular causes of death and brain damage increased;is this real or is because the relative reduction in the respiratory causes?

Could better monitoring decrease deaths and brain damage?

Recurrent patterns in the analysis of sudden cardiac arrest

during spinal anesthesia

Healthy adult patients Conventionally managed spinal(but often epi

i.t,fent & midaz i.v…..) Relatively minor surgery Block at T4 or higher Onset within 30 min from start of spinal Presence of apparent normal haemodynamics

and respiration in about 50% of cases

Although resuscitation was promptly initiated,epinephrine was nor administered until a median of 7 min had elapsed;bad outcomes(1989) suggest that insufficient restoration of peripheral tone in the setting of high sympathetic blockade may contribute to the severity of cardiac and neurologic outcome .Rosenberg 1996 & 1998)and colleagues have provided experimental results consistent with this hypothesis.:Using a canine model……they demonstrated that total spinal anesthesia decreased coronary perfusion pressure during CPR to levels below the threshold established for successfl resuscitation and that administration of epinephrine during CPR increase coronary perfusion above the critical threshold:moreover non spinalized animals had a significant increase in endogenous epinephrine and norepi levels at 1 & 3 min post carfdiac arrest.but catchoamien levels did not increade in spinaliozed animals

Conclusions from Rosenberg

These studies support the potential importance of exogenous earlier epinephrine administration when cardiac arrest occurs in the setting of central neuraxial blockade.

Jordi EM,Marsch SC U, Strebel S.Third Degree Heart Block and

Asystole Associated with Spinal Anesthesia

1998 ; 89:257-260

We present a case of spinal anesthesia-induced asystole in which onset and recovery could be recorded by means of Holter monitoring. Holter monitoring revealed that shortly after subarachnoid injection, a first degree heart block developed that, without any previous change in heart rate, progressed to a complete heart block. After successful resuscitation, a first degree heart block that persisted until 6 h after subarachnoid injection partly outlasted sensory and motor blockade.

68-yr-old patient was scheduled for elective total hip arthroplasty. Apart from arterial hypertension, treated with nifedipine, he had no history of cardiovascular disease. Physical examination and preoperative 12-lead electrocardiograph (ECG) revealed no abnormal condition. Premedication consisted of 7.5 mg oral midazolam administered 1 h before surgery. Intraoperative monitoring included pulse oximetry, noninvasive blood pressure measurement, and 2-lead ECG. On arrival in the operating room, blood pressure was 180/90 mmHg, and heart rate was 72 beats/min. A peripheral vein was cannulated, and 500 ml of Ringer's lactate solution was administered. The patient was turned to the left lateral decubitus position, and 4.0 ml of bupivacaine, 0.5%, in saline was injected into the subarachnoid space via a 22-gauge Quincke needle inserted at the L3—L4 interspace. Thereafter the patient was placed in the supine position. Approximately 5 min after the subarachnoid injection, the patient complained of nausea. Blood pressure at this time was 100/60 mmHg.

Our case suggests that a new first degree heart block during spinal anesthesia may be a warning sign of impending complete heart block or asystole. Moreover, a spinal anesthesia-induced first degree heart block may persist for a prolonged period of time after the level of spinal anesthesia has receded below the thoracic dermatomes associated with sympathetic innervation of the heart. However, the present case illustrates that the value of first degree heart block as a warning sign of impending complete heart block may be limited by the rapidity with which first degree heart block may progress to complete heart block or asystole and the difficulty in detecting first degree heart block on a bedside ECG screen. The diagnosis of first degree and third degree heart block was only made retrospectively by analyzing the Holter recordings.

Although the occurrence of severe bradycardia and asystole during spinal anesthesia has been repeatedly reported, the underlying mechanism remain a matter of debate. Proposed theories include (1) reflex-induced bradycardia resulting from a decreased venous return; and (2) an unopposed vagal tone by spinal anesthesia-induced thoracic sympathectomy. Current knowledge favors the former hypothesis: lumbar epidural anesthesia, confined to the lower spinal segments, induced an enhancement of cardiac vagal tone resulting from venous pooling. Likewise, clinical, biochemical, and echocardiographic findings in healthy volunteers, suffering from a decrease in blood pressure and heart rate during lumbar epidural anesthesia, conform to central blood volume depletion, leading to an increase in vagal tone. Anzai and Nishikawa showed that head-up body tilt induced similar increases in heart rate during either low (analgesic level T10) or high level (analgesic level T4) of spinal anesthesia. This indicates that a T4 sensory level of spinal anesthesia does not produce total sympathetic blockade and, therefore, challenges the concept of spinal anesthesia-induced thoracic sympathectomy.

Although the mechanism of lumbar neuraxial anesthesia-induced bradycardia or asystole is presently unknown, the final pathway is most likely an absolute or relative increase in parasympathetic activity. It is noteworthy that nausea, a parasympathomimetic event, was the first symptom in our patient. An increase in parasympathetic activity slows conduction through the nodal region of the AV node. Higher degree heart blocks have been described to occur during spinal anesthesia in the presence or absence of preexisting conduction abnormalities. Thus, in keeping with these previous reports, our case emphasizes that spinal anesthesia may seriously affect atrioventricular conduction. Moreover, our case illustrates that a first degree and even a third degree heart block may be missed on line. Thus heart blocks may occur more frequently during spinal anesthesia than presently thought, and impairment of atrioventricular conduction, induced by an increase in parasympathetic activity, might be an important cause of asystole during spinal anesthesia. In the present case, asystole occurred in a patient treated with the calcium antagonist nifedipine. Unlike verapamil, nifedipine does not affect atrioventricular conduction. It is therefore unlikely that nifedipine promoted or aggravated the development of heart block;

Our case reemphasizes that in a witnessed cardiac arrest, prompt treatment is crucial. This implies strict adherence to established safety standards, i.e., the presence of qualified anesthesia personnel throughout the procedure and the continuous monitoring of the electrocardiogram. The initial treatment of asystole consists in precordial chest thumping and the administration of vagolytic and sympathomimetic drugs.

It is noteworthy that previous reports indicate that acute bradycardia or asystole may occur at any time during neuraxial anesthesia. In our case, first degree heart block persisted longer than the sensory blockade of the upper thoracic dermatomes. Liguori and Sharrock reported a case of severe bradycardia 210 min after epidural injection, when sensory and motor modalities had considerably receded. Both their observation and our case suggest that neuraxial anesthesia-induced bradycardia or alterations in atrioventricular conduction may, at least partly, outlast sensory or motor blockade. If this hypothesis were to be confirmed, this would have important implications for postoperative monitoring and timing of discharge of patients to the ward.

Brooker R F,Butterworth JF IV, Kitzman DW,Berman JM, Kashtan H,McKinley AC.Treatment of Hypotension after

Hyperbaric Tetracaine Spinal Anesthesia: A Randomized, Double-blind, Cross-over

Comparison of Phenylephrine and Epinephrine.Anesthesiology 1997; 86:797-

805

Background: Despite many advantages, spinal anesthesia often is followed by undesirable decreases in blood pressure, for which the ideal treatment remains controversial. Because spinal anesthesia-induced sympathectomy and management with a pure alpha-adrenergic agonist can separately lead to bradycardia, the authors hypothesized that epinephrine, a mixed alpha- and beta-adrenergic agonist, would more effectively restore arterial blood pressure and cardiac output after spinal anesthesia than phenylephrine, a pure alpha-adrenergic agonist.

Methods: Using a prospective, double-blind, randomized, cross-over study design, 13 patients received sequential infusions of epinephrine and phenylephrine to manage hypotension after hyperbaric tetracaine (10 mg) spinal anesthesia. Blood pressure, heart rate, and stroke volume (measured by Doppler echocardiography using the transmitral time-velocity integral) were recorded at baseline, 5 min after injection of tetracaine, and before and after management of hypotension with epinephrine and phenylephrine. Cardiac output was calculated by multiplying stroke volume x heart rate.

Results: Five min after placement of a hyperbaric tetracaine spinal anesthesia, significant decrease in systolic (from 143 +/- 6 mmHg to 125 +/- 5 mmHg; P < 0.001), diastolic (from 81 +/- 3 to 71 +/- 3; P < 0.001), and mean (from 102 +/- 4 to 89 +/- 3; P < 0.001) arterial pressures occurred. Heart rate (75 +/- 4 beats/min to 76 +/- 4 beat/min; P = 0.9), stroke volume (115 +/- 17 to 113 +/- 13; P = 0.9), and cardiac output (8.0 +/- 1 l/m to 8.0 +/- 1 l/m; P = 0.8) did not change significantly after spinal anesthesia. Phenylephrine was effective at restoring systolic blood pressure after spinal anesthesia (120 +/- 6 mmHg to 144 +/- 5 mmHg; P <0.001) but was associated with a decrease in heart rate from 80 +/- 5 beats/min to 60 +/- 4 beats/min (P < 0.001) and in cardiac output from 8.6 +/- 0.7 l/m to 6.2 +/- 0.7 l/m (P < 0.003). Epinephrine was effective at restoring systolic blood pressure after spinal anesthesia (119 +/- 5 mmHg to 139 +/- 6 mmHg; P < 0.001) and was associated with an increase in stroke volume from 114 +/- 12 ml to 142 +/- 17 (P < 0.001) and cardiac output from 7.8 +/- 0.6 l/m to 10.8 +/- 1.1 l/m (P < 0.001).

Conclusions: Epinephrine management of tetracaine spinal-induced hypotension increases heart rate and cardiac output and restores systolic arterial pressure but does not restore mean and diastolic blood pressure. Phenylephrine management of tetracaine spinal-induced hypotension decreases heart rate and cardiac output while restoring systolic, mean, and diastolic blood pressure.

Comparison of Phenylephrine and Epinephrine

Sedative medications before spinal anesthesia were limited to 2 mg of midazolam and 100 mg of fentanyl intravenously. Fluid administration was limited to 3 ml/kg before spinal anesthesia.

Comparison of Phenylephrine and Epinephrine

After spinal anesthesia, when a 15% reduction in systolic arterial pressure was observed, treatment was initiated with a bolus of either epinephrine (4.0 mg) or phenylephrine (40.0 mg) followed by an infusion of either epinephrine (0.05 mg×kg-1×min-1) or phenylephrine (0.5 mg×kg-1×min-1), respectively. If systolic blood pressure did not increase with the initial infusion, repeat bolus doses could be given and the infusion rate could be doubled until systolic blood pressure increased to the value measured before spinal anesthesia. Then, after measurements were completed, the infusion was discontinued. A 10-min washout period was used, and the second drug was given in a similar manner. The drugs were administered in a random order. Patients and physicians were blinded to the identity of the drugs. The drug infusions were prepared as follows: 10 mg of phenylephrine was dissolved in 250 cc normal saline (40 mg/ml), and 1.0 mg epinephrine was dissolved in 250 cc normal saline (4.0 mg/ml). Based on this preparation, bolus volumes and infusion volumes were similar for each drug.

Lumbar puncture was performed at either the L3—L4 or L4—L5 interspace using a midline approach. Ten mg of tetracaine diluted in an equal volume (1 ml) of 10% dextrose was injected in every patient. Drug injections were made with patients in a lateral decubitus position. Patients were turned supine immediately after drug injection.

Our data show that epinephrine restored systolic blood pressure and increased heart rate and cardiac output after spinal anesthesia, but it did not restore MAP and diastolic blood pressure. Phenylephrine restored systolic, MAP, and diastolic blood pressure in all patients, but it decreased heart rate and cardiac output. Using the Doppler transmitral flow—velocity integral as an approximation of stroke volume, we observed that epinephrine significantly increased stroke volume, whereas phenylephrine had no effect on stroke volume.

Liguori GA,Sharrock NE. Asystole and Severe Bradycardia during Epidural

Anesthesia in Orthopedic Patients.Anesthesiology 1997;89:250-257

This is a report of 7 cases of severe bradycardia and 5 cases of asystole that occurred during orthopedic surgery under epidural anesthesia during the past 9 yr at our institution. These include one case of asystole and one case of severe bradycardia that occurred in the post anesthesia care unit (PACU). Although this report does not provide data on the incidence of bradycardia, these individual cases provide the greatest experience on patterns of onset of acute bradycardia and asystole during epidural anesthesia yet published, and may provide insight into potential etiologic mechanisms.

Asystole and Severe Bradycardia during Epidural Anesthesia in

Orthopedic Patients

Asystole and Severe Bradycardia during Epidural Anesthesia in

Orthopedic Patients

Asystole and Severe Bradycardia during Epidural Anesthesia in

Orthopedic Patients

Asystole and Severe Bradycardia during Epidural Anesthesia in

Orthopedic Patients

Bernards CM,Hymas NJ.Progression of first degree heart block to high grade second degree block during

spinal anesthesia

ABSTRACT: A case is presented in which a patient with pre-existing first degree heart block developed high-grade second degree heart block during spinal anaesthesia. Progression of the block was associated with blockade of cardiac sympathetic neurons induced by spinal anaesthesia. This suggests that patients with pre-existing heart block may be at increased risk for development of higher grade block during spinal anaesthesia.

CAN J ANAESTH 1992 / 39: 2 / pp173-5

Progression of first degree heart block to high grade second degree block during spinal

anesthesia

Progression of first degree heart block to high grade second degree block during spinal

anesthesia

An 18-gauge intravenous catheter was placed and 600 ml Ringer's lactate and 4 mg morphine were given iv. The blood pressure was 118/58, and heart rate was 84 beats per minute (sinus rhythm). She was placed in the left lateral decubitus position and 60 mg 5% lidocaine in 10% dextrose with 200 mg epinephrine was injected into the subarachnoid space at the L4

Progression of first degree heart block to high grade second degree block during spinal

anesthesia

She remained in the left lateral decubitus position for two minutes and was then turned supine. Seven minutes later sensory block was evaluated by pin prick and found to be at the level of T4 on the right and T3 on the left. Over the next several minutes she developed Type I second degree heart block (Wenckebach) with a 4:3 conduction ratio which progressed within 15 sec to high-grade second degree block with a 2:1 conduction ratio (). Blood pressure decreased to 90/48. Atropine (0.6 mg) was administered iv and the second degree heart block converted to a junctional tachycardia (110 bpm) which changed over the next one to two minutes to sinus tachycardia (125 bpm) with resolution of her first degree AV block (PR interval 0.2 msec) ().

Carpenter RL,Caplan RA,Brown DL,Stephenson C,Wu R. Incidence and risk factors for side effects

of spinal anesthesia Anesthesiology 76:906-916, 1992

We prospectively studied 952 patients to identify the incidence of hypotension (systolic blood pressure < 90 mmHg), bradycardia (heart rate < 50 beats/min), nausea, vomiting, and dysrhythmia during spinal anesthesia. Historical, clinical, and physiologic data were correlated with the incidence of these side effects by univariate and multivariate analysis. Hypotension developed in 314 patients (33%), bradycardia in 125 (13%), nausea in 175 (18%), vomiting in 65 (7%), and dysrhythmia in 20 (2%). Variables conferring increased odds of developing hypotension include peak block height ³ T5 (odds ratio 3.8, P < 0.001), age ³ 40 yr (2.5, P < 0.001), baseline systolic blood pressure < 120 mmHg (2.4, P < 0.001), combination of spinal and general anesthesia (1.9, P = 0.01), spinal puncture at or above the L2–L3 interspace (1.8, P < 0.001), and addition of phenylephrine to the local anesthetic (1.6, P = 0.02). Variables conferring increased odds of developing bradycardia include a baseline heart rate < 60 beats/min (odds ratio 4.9, P < 0.001), ASA physical status classification of 1 versus 3 or 4 (3.5, P < 0.001), current therapy with b-adrenergic blocking drugs (2.9, P < 0.001), and peak block height ³ T5 (1.7, P = 0.02). Variables conferring increased odds of developing nausea or vomiting include addition of phenylephrine or epinephrine to the local anesthetic (3.0–6.3, P £ 0.003), peak block height ³ T5 (odds ratio 3.9, P < 0.001), use of procaine (2.6–4.4, P £ 0.003), baseline heart rate ³ 60 beats/min (2.3, P = 0.03), history of carsickness (2.0, P = 0.01), and development of hypotension during spinal anesthesia (1.7, P = 0.009). Our results indicate that the incidence of side effects during spinal anesthesia may be reduced by 1) minimizing peak block height; 2) using plain solutions of local anesthetics; 3) performing the spinal puncture at or below the L3–L4 interspace; and 4) avoiding the use of procaine in the subarachnoid space.

Incidence and risk factors for side effects of spinal anesthesia.

Incidence and risk factors for side effects of spinal anesthesia.

Incidence and risk factors for side effects of spinal anesthesia.

Introna, Robert, MD*; Yodlowski, Edmund, PhD*; Pruett, Jack, PhD*; Montano, Nicola, MD†;

Porta, Alberto, MS†; Crumrine, Robert, MD*

Sympatovagal effects of spinal anesthesia assessed by heart

rate variability analysis

Heart rate variations (HRV) result from moment-to-moment changes in sympathetic and parasympathetic activity in response to many conditions. These two neural inputs to the heart can be identified by analyzing power spectra of HRV for frequency components at the vasomotor (low-frequency [LF]) and the respiratory (high-frequency [HF]) rhythms. HRV analysis has been used successfully in humans to noninvasively evaluate the autonomic responses to specific maneuvers and drugs, as well as responses to more chronic preexisting pathologic conditions. The effects of an isolated "acute" withdrawal of sympathetic activity in humans, however, have not as yet been evaluated using an autoregressive (AR) technique. We examined HRV using this technique in a group of patients receiving subarachnoid block for abdominal surgery. The sensory levels achieved were within the range of those reported to interrupt sympathetic outflow to the heart. Electrocardiograms were recorded and subjected to AR analysis. AR analysis of HRV after spinal anesthesia revealed significant decreases in both dominant frequency components (LF and HF) that occur between 0.03 Hz and 0.5 Hz. These reductions coincided with blockade of cardiac sympathetic outflow after cephalad spread of the spinal block. The power spectra were almost abolished in patients with sensory blocks reaching T1-2. The decreases in amplitude of the LF and HF components, therefore, act as markers of diminished sympathetic and parasympathetic activity to the heart, while the ratio of LF:HF indicated that sympathovagal balance was predominantly maintained during most of the block. Only during the onset of spinal block in the lumbosacral area was cardiac sympathetic activity (LF) initially increased while parasympathetic activity (HF) reflexly decreased. AR power spectral analysis of HRV provided a quantitative measure of sympathovagal activity during spinal anesthesia.

Anesth Analg 1995; 80:315-21

Sympatovagal effects of spinal anesthesia assessed by heart

rate variability analysis

Assessment of autonomic function in a clinical setting has been difficult to accomplish, depending on the techniques used . Normally, the autonomic nervous system maintains a sympathovagal balance that modulates heart rate to accommodate bodily demands subsequent to physiologic and environmental changes. Oscillations in heart rate that result from this modulation can reveal markers for sympathetic and parasympathetic function . Various algorithms including approximate entropy , fast Fourier transform (FFT), and autoregressive (AR) analysis have been used to analyze and display these oscillations. Most studies have relied on FFT, including prior work in our laboratories . However, the AR technique has the advantages of obtaining the number, amplitude, and center frequencies of the oscillatory components without the need for a priori selections, and provides reliable information even on shorter series of data than FFT . The disadvantage of the AR technique is its dependence on model order determination with possible loss of information from frequency components not contained in the model fit.

Of all the untoward effects of spinal anesthesia, the most important, from a physiologic standpoint, is the paralysis of preganglionic sympathetic fibers . Sympathetic innervation to the sinoatrial node exits from the spinal cord between T1 and T4 . Sympathetic block below these segments results in arterial and venous vasodilation in the lower extremities and reflex compensatory increased sympathetic activity above the block . Blocks reaching the T1-4 segments would then interrupt the sympathetic flow to the heart. Parasympathetic innervation to the heart, on the other hand, originates in the brainstem, travels via the vagus nerve and should not be blocked, even during high levels of spinal anesthesia .

Subarachnoid block (spinal anesthesia) is a popular anesthetic technique. It has a long history of successful use for many types of surgical procedures. However, Caplan et al. reported a series of cases in which unexpected cardiac arrests occurred during spinal anesthesia. These authors formulated a hypothesis that the unrecognized presence of a high sympathetic block may have been responsible for the arrest as well as its poor outcome.

At higher levels of somatosensory block, e.g., T3-4, sympathetic block may exceed the somatosensory block by two or more dermatomes . Furthermore, the onset and duration of sympathetic block by local anesthetics may not correlate with somatosensory block since sympathetic fibers are more sensitive to local anesthetics than either sensory or motor nerves . Although the patients in the report by Caplan et al. did not appear to develop excessively high sensory levels of spinal block prior to cardiac arrest, one can speculate, as these investigators did, that cardiac arrest resulted from sympathetic block and unopposed parasympathetic activity. These results have since been supported by the work of Kawamoto et al. .

Spectral analysis of heart rate variations (HRV) using FFT or AR can reveal characteristic frequency peaks that represent changing sympathetic and parasympathetic input to the heart . Furthermore, the relationship between the low-frequency (LF) and high-frequency (HF) components can serve as markers of sympathovagal balance . Many factors influence this balance . We therefore investigated the effects of spinal anesthesia on sympathetic and parasympathetic activity using an autoregressive algorithm to analyze HRV. The relationship of sympathetic block to the level of sensory block and the existence of unopposed increased parasympathetic activity during spinal anesthesia were specifically investigated.

Sympatovagal effects of spinal anesthesia assessed by heart

rate variability analysis

The cephalad progression of spinal block to higher dermatome levels after injection of the local anesthetic into the lumbar space was accompanied by a quantitative reduction of HRV, as reflected by changes in the power of all components between 0.03 and 0.5 Hz within the HRV power spectra. In those patients whose spinal blocks were adequate for surgery, the reduction in total HRV power became significant when sensory blocks reached T3-4. HRV was almost totally eliminated when the blocks reached T1-2. The loss of HRV that occurred resulted from block of sympathetic outflow to the heart, as reflected by a significant reduction (P < 0.016) in the LF component of the HRV power spectrum . A reduction in parasympathetic activity also contributed to the total reduction in HRV power and was reflected by a diminished HF component . Unlike the spinal anesthetic block of the cardiac sympathetic outflow, decreased cardiac parasympathetic outflow probably resulted from reflex conditions, not from direct spinal block of the vagus nerve . In most physiologic conditions, activation of either outflow is accompanied by inhibition of the other . However, when the spinal anesthetic rises to the level of cardiac sympathetic outflow, the acute interruption of sympathetic activity results in a depression of both LF and HF components and provides support that both components depend on the interaction of the two neural outflows. This demonstrates the reciprocal relationship between sympathetic and parasympathetic outflows as described by Malliani et al. .

General markers for sympathetic and parasympathetic activity are linked to LF and HF oscillations in R-R variations . Total power, identified as the area under the spectral components between 0.03 and 0.5 Hz, reflects autonomic tone. Spectral analysis of these variations reveal two main components; a LF component, with a central frequency between 0.03 and 0.15 Hz, and a HF component between 0.15 and 0.5 Hz . The HF component correlates well with the respiratory signal and is generally considered a marker of vagal activity while the components within the LF range have been associated with sympathetic autonomic tone . There is some disagreement about the contributions of the parasympathetic system in the LF range .

The relationship between LF and HF components serves as an indicator of sympathovagal balance . The HRV power spectra obtained from patients before spinal anesthesia contained frequency components consistent with those previously described by other investigators . During the control period, the LF:HF ratio was approximately unity, based on nu. As the block spread to the T3-4 level, the LF:HF ratio increased to approximately two and then returned toward unity when the block reached T1-2. In this case, sympathovagal balance appeared unchanged; however, examination of the power spectrum reveals a significant reduction in total power () that is not obvious from nu or ratios alone, as shown in . illustrates these power spectral changes in a single patient. These observations suggest that, in the case of acute block of sympathetic fibers supplying sympathetic ganglia, nu and LF:HF ratios (derived from nu) did not convey the quantitative information provided by the power spectrum in absolute values.

The results of the present study support the existence of a reciprocal relationship between sympathetic and parasympathetic activity as proposed by Malliani et al. . The possibility of direct effects of spinal block on the vagus nerve is unlikely. Other investigators were unable to measure significant concentrations of anesthetics in the cerebrospinal fluid of the fourth ventricle during spinal anesthesia . Unlike epidural anesthesia, the dose of local anesthetic injected into the subarachnoid space for spinal anesthesia is very small, and does not result in systemic blood concentrations great enough to cause physiologic effects . This may represent a situation where central sympathetic activity continues to be reflexively activated while conduction to the end-organ, i.e., the heart, is interrupted. The parasympathetic outflow would then continue to be reflexively inhibited even though it remained physically unblocked.

In both the current study and our earlier work, which used Fourier analysis instead of an AR technique , spinal anesthesia resulted in diminution of both the LF and HF components of HRV. We did not observe an increase in the HF components of the power spectra as reported by Kawamoto et al. . However, we did observe a relative shift toward HF dominance during the later stages of spinal block, i.e., during the recovery period. These results suggest that during the acute phase of spinal block, disruption of sympathetic neural pathways leads to a loss of sympathetic activity (LF components) as well as a reflex reduction of parasympathetic activity (HF components) in an effort to maintain homeostasis. With time, eventual hemodynamic stabilization of the sympathectomized state and/or elimination of anesthetic from the subarachnoid space could result in a withdrawal of the reflex parasympathetic inhibition and result in a relative increase in the HF components of the power spectra.

The use of HRV analysis by anesthesiologists in research and clinical practice is increasing. The present study supports the prospect of using HRV spectral analysis to monitor autonomic function during spinal anesthesia. It also may prove clinically useful as a means for assessing the efficacy of a spinal block. For example, in this study, a "target" level for spinal block was the T4 dermatome level. Progression of the block to the T1-2 level or higher, although unintentional, occurred in approximately half of our patients. A T3-4 spinal block is typically considered adequate for postpartum tubal ligation. Yet four of our patients who lost sensation to pinprick at this level required additional anesthetics for surgery to continue. Interestingly, the power spectra of those patients who required further anesthetic intervention were not significantly reduced from control, unlike those power spectra of patients for whom spinal block was adequate for surgery. We cannot definitively explain why a sensory level of T3-4 was inadequate for anesthesia at the T10 surgical site nor can we explain why the power spectra of these same patients was unchanged. We can postulate, however, that due to the inherent subjectivity of both patient and anesthesiologist in pinprick determination of anesthetic levels, a state of unrecognized incomplete sensory and autonomic block must have existed.

In conclusion, this study clearly demonstrates that block of cardiac sympathetic neural pathways, while leaving parasympathetic neural pathways intact, results in a decrease of both LF and HF components of HRV. This supports the concept that both power spectral components depend on the interaction of sympathetic and parasympathetic neural outflows. These data also support the concept of a reciprocal relationship between the sympathetic and parasympathetic components of cardiac autonomic regulation as proposed by Malliani et al. . Furthermore, these results suggest that analysis of HRV during spinal anesthesia may be useful as an alternative clinical tool to assess the level and efficacy of spinal block.

Kawamoto M, Tanaka N, Takasaki M. Power spectral analysis of heart rate variability

after spinal anesthesia. Br J Anaesth 1993;

71:523-7.

Rosenberg JM,Wahr JA,Sung CH,Oh YS,Gilligan LJ. Coronary perfusion pressure during cardiopulmonary resuscitation after

spinal anesthesia in dogs.Anesth Analg 1996; 82:84-7

Cardiac arrest during spinal anesthesia is a rare event, but when it does happen cardiopulmonary resuscitation (CPR) is often ineffectual. This study examines the effect of spinal anesthesia on coronary perfusion pressure (CPP) during CPR and the subsequent response of CPP to epinephrine administration. Twenty mongrel dogs were anesthetized, and randomly assigned to a spinal injection with either 0.5 mg/kg bupivacaine or with an equivalent volume of normal saline. 20 minutes later, ventricular fibrillation was electrically induced and after 1 min CPR was started. CPP was measured every minute. After 4 min of CPR, epinephrine 0.01 mg/kg was given followed by 0.1, 0.2, and 0.4 mg/kg epinephrine intravenously (IV) at 6, 8, 10 min of CPR, respectively. The bupivacaine (n = 11) group had significantly less CPP than the sham spinal (n = 8) group, 12–13 mm Hg as compared to 27–34 mm Hg. Only 4/11 dogs (36%) in the bupivacaine group had CPP ³ 15 mm Hg during the first 4 min after arrest as compared to 8/8 (100%) in the sham spinal group. This increased to 7/11 dogs (64%) after 0.01 mg/kg epinephrine and to 9/11 after 0.1 mg/kg epinephrine. Total spinal anesthesia decreases CPP and thus the efficacy of CPR in dogs below the threshold previously established for predicting successful resuscitation. Epinephrine is effective in increasing CPP during CPR above the critical threshold. These data suggest that if cardiac arrest occurs during spinal anesthesia, epinephrine should be given in doses of 0.01–0.02 mg/kg IV initially and then increasing to 0.1 mg/kg IV. When this does not work, and ineffective CPR is suspected, alternative resuscitative measures should be considered.

Coronary perfusion pressure during cardiopulmonary

resuscitationafter spinal anesthesia in dogs.

Increase in coronary perfusion pressure with increase in

epinephrine dose

0

0,5

1

1,5

2

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CPP increase in mmHG

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% of dogs with CPP > 15 mmHg durinmg cardiopulmonary

resuscitation

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2030

4050

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Thgese dta demonstarte that spinal anesthesia decrease CPP during CPR to levels below the threshold established for successful resuscitation ant that epinephrine is effective in increasing CPP during CPR above the critical threshold

Norepinephrine response to cardiac

arrest( from Rosember et al

Mean noerpi change from baseline ng/mn

0

500

1000

1500

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Aromaa et al

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Clòaims in Finland

Patient Iniry Act(PIA) from May 1 1987 23500 claims up to 31/12/1993 86 claims associated with spinaòl/peidural anesth;estimated at 550.000 spinal & 170.000

epid. SPINAL 25(/550.000)0,45/10.000: Cardiac arrest 2 paraplegia 5 permamnet cauda equina 1 peorneal nerve paresis 6 neurological deficits 7 bacterial infect0n 4 epidural 9(170.000):0,52/10.000 paraparesis 1 permamnet cauda equina 1 peroneal nerve oaresis 1 neurol deficits 1 bacteroial infection 2 acute tox reaction 2 overdoseof epidural opioid 1

Matta BF,Magee P.Wenckebach type heart block following spinal anesthesia for

caesarean section. CAN J ANAESTH 1992 / 39: 10 / pp1067-8

ABSTRACT: A case is described of complete heart block during spinal anaesthesia for Caesarean section in a fit 23 yr-old-woman. This developed shortly after the institution of the block(left side,L2,3 iuntespace,bupi 12,5 mg!!), with the height of the block below T5 and in the absence of hypotension. The patient was resuscitated successfully with vagolytic and alpha-agonist drugs. A Wenckebach block persisted for a short period postoperatively. The importance of instituting monitoring before the beginning of anaesthesia and the immediate availability of atropine and alpha-agonists before the initiation of spinal anaesthesia is stressed.

Cardiac arrest (or severe

arrhytmia)cases...

author drug Site ofinj.

level other

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L2-3 T5 Doneon lside

bernards

Lido 60mg 5%+ epi200micr

L4-5 T4-3 Leftside

Cardiac arrest associated with neuraxial block

900 cases in claims 1988;14 cases of neuraxial cardiaca rrest…..,all pts were resuscitated,8 survived but only 1 regained a sufficiemnt neurologic function…..

Geffin B, Shapiro L. Sinus bradycardia and asystole during spinal and epidural anesthesia: J Clin Anesth 1998; 10:278–85.<ldn>!

MEDLINEÒ RECORD:

AB - STUDY OBJECTIVE: To characterize the clinical features that predispose to sinus bradycardia and cardiac arrest during spinal and epidural anesthesia. DESIGN: Retrospective clinical review. SETTING: University affiliated medical center. PATIENTS: 13 patients, aged 26 to 76 years, who suffered severe sinus bradycardia or asystole over a 5-year period, during which approximately 4,000 regional anesthetics were administered. MEASUREMENTS AND MAIN RESULTS: Case histories of 13 patients who developed severe sinus bradycardia or asystole during spinal or epidural anesthesia are summarized. Twelve cases occurred during spinal anesthesia, and the thirteenth, during epidural anesthesia. In all but one case, the acute event occurred 15 minutes or longer from the time of the anesthetic injection. Resuscitation was successful in all cases, with no postoperative sequelae. CONCLUSION: The clinical picture suggests a reflex cause, possibly associated with low right-sided cardiac filling pressure. No common precipitating cause or high-risk patient profile was noted.

Pollard

Pollard

This consistent pattern suggests that the risk factors for bradycardia may help identify patients who are more susceptible to vagal predominance leading to circulatory collapse and asystole during spinal anesthesia.

Pollard

Could such reflex responses to decreases in preload cause more than bradycardia? Studies of the hemodynamic effects of graded hypovolemia have demonstrated progressive vagal symptoms including sweating, nausea, and syncopeMurray RH, Thompson LJ, Bowers JA, Albright CD. Hemodynamic effects of graded hypovolemia and vasodepressor syncope induced by lower body negative pressure. Am Heart J 1968; 76:799–809.

. The resulting decreases in central venous pressure were comparable to those observed during spinal anesthesiaKennedy WF, Bonica JJ, Akamatsu TJ. Cardiovascular and respiratory effects of subarachnoid block in the presence of acute blood loss. Anesthesiology 1968; 29:29–35.

11: Sancetta SM, Lynn RB, Simeone FA, Scott RW. Studies of hemodynamic changes in Humans following induction of low and high spinal anesthesia. Circ 1952; 6:559–71.

. One of the seven healthy subjects progressed from vagal symptoms to abrupt sinus arrest . Murray RH, Thompson LJ, Bowers JA, Albright CD. Hemodynamic effects of graded hypovolemia and vasodepressor syncope induced by lower body negative pressure. Am Heart J 1968; 76:799–809.

In a separate study, two healthy subjects experienced vagal arrests after they had 10 mL/kg of blood withdrawn to simulate acute blood loss with sensory epidural block levels of T4 to T6

Bonica JJ, Kennedy WF, Akamatsu TJ, Gerbershagen HU. Circulatory effects of peridural block: Anesthesiology 1972; 36:219–27.

Pollard

Taken together, these studies demonstrate that decreases in preload can precipitate not only classic vagal symptoms, but also full cardiac arrest. Although one might assume that maintaining preload during spinal or epidural anesthesia is a uniform practice of anesthetists, the literature demonstrates otherwise. Geffin and Shapiro reported that prophylactic preloading with a bolus of 300 to 750 mL was not practiced during the 5-yr period when they experienced 13 cases of severe bradycardia or cardiac arrest during spinal or epidural anesthesia. Cardiac arrests have also been reported in settings where decreases in afterload are added after epidural anesthesia has been initiated. A report of bradycardia/cardiac arrest during epidural or spinal anesthesia revealed that five of these events were associated with initiating sodium nitroprusside infusions and in two cases pulmonary artery pressures were noted to decrease just before the onset of bradycardia

Pollard

Often two or more of these factors are present in patients who receive spinal or epidural anesthesia for labor analgesia or for cesarean delivery. With the similarities between spinal and epidural anesthesia one might expect a comparable rate of cardiac arrest during epidural anesthesia. The decreased incidence of cardiac arrest associated with epidural anesthesia compared with spinal anesthesia is a relatively new finding that has not been explained . One possibility is that the incremental dosing and slower onset of epidural anesthesia may allow time for compensatory mechanisms (e.g., upper body vasoconstriction) to compensate for the decrease in preload. Alternatively, the physiologic changes associated with pregnancy may help explain the small rate of cardiac arrest observed in these settings. Pregnancy is associated with changes in autonomic control and at-term heart rates of 90–95 bpm are typical. This may be attributable to decreased parasympathetic tone during pregnancy . If vagal predominance plays a key role in the cardiac arrests that occur during spinal or epidural anesthesia, then the weaker vagal tone associated with pregnancy may decrease this risk.

Lovstad RZ, Granhus G, Hetland S.

Bradycardia and asystolic arrest during

spinal anaesthesia: Acta Anaesthesiol

Scand 2000; 44:48–52.<ldn>!

Rosenberg et alImpaired neuroendocrine response

mediates refractoriness to cardiopulmonary resuscitation in spinal anesthesia.Crit.care

Med.26; 533-537: 1998  Objective: To determine the extent of neurogenic control on

adrenal secretion in a canine model of high spinal anesthesia and cardiac arrest.

Design: Randomized, controlled, acute intensive study. Setting: University intensive care laboratory. Subjects: Nineteen healthy, anesthetized, mongrel dogs. Interventions: Cardiac arrest was induced in 11 spinally

anesthetized dogs and 8 sham-control animals; cardiopulmonary resuscitation (CPR) was started 60 secs later. Epinephrine was injected at 4 mins and every 2 mins thereafter. Arterial blood samples were obtained before anesthesia, before arrest, and after 1, 3, 5, 7, 9, and 11 mins of CPR.

Rosenberg JM, Wortsman , Wahr JA, Cryer PE,Gomez-Sanchez CE.

Impaired neuroendocrine response mediates refractoriness to cardiopulmonary resuscitation in spinal anesthesia.Crit.care

Med.26; 533-537: 1998  Measurements and Main Results: At 1 and 3 mins after cardiac

arrest, the control group exhibited significant increases of epinephrine and norepinephrine concentrations (p < .05) that were absent in the spinal anesthesia group. Plasma renin increased in both groups whereas aldosterone and cortisol remained unchanged.

Conclusions: Spinal anesthesia abolishes the catecholamine release that follows cardiac arrest, while a previously postulated direct adrenal effect of hypoxia stimulating catecholamine release was not confirmed in these experiments. Since epinephrine treatment restores coronary perfusion pressure (CPP) during CPR, we conclude that catecholamine deficiency is the most likely mechanism for inadequate CPP during CPR conducted in the presence of spinal anesthesia. (Crit Care Med 1998; 26:533-537)

Rosenberg JM, Wortsman , Wahr JA, Cryer PE,Gomez-Sanchez CE.

Impaired neuroendocrine response mediates refractoriness to cardiopulmonary resuscitation in spinal anesthesia.Crit.care

Med.26; 533-537: 1998 

Introduction The central role of the central nervous system (CNS) in the generation of the hormonal responses to maximal stress has been examined in human and animal models of cardiac arrest [1-7]. The main target organ of the endocrine reaction to stress is the adrenal

gland, which is under the control of neurogenic and humoral factors. The importance of adrenal activation in cardiac arrest is underlined by the results of experiments performed on adrenalectomized animals that led to the suggestion that the release of adrenal hormones plays a major role in determining a positive outcome for resuscitation maneuvers [1].

Neurogenic blockade with spinal anesthesia may have uncovered an additional modulatory role for the CNS in the humonal adrenal responses as it ablates not only epinephrine and norepinephrine, but also the aldosterone and cortisol release that follow major surgical procedures [8-13]. Concordantly, recovery from cardiac arrest in the presence of spinal anesthesia is also impaired [14].

We [15] have previously demonstrated that dogs with spinal anesthesia and subsequent cardiac arrest exhibit significantly lower coronary perfusion pressure (CPP), a major determinant of cardiopulmonary resuscitation (CPR) outcome, as compared with CPR without spinal anesthesia. Moreover, the low CPP of anesthetized animals is restored to the levels of controls by administration of epinephrine [15]. We then hypothesized that total spinal anesthesia could interfere with the adrenal hormonal responses and, in turn, would be responsible for the decrease in CPP seen in our canine model. This investigation was therefore designed to examine the hormonal changes after cardiac arrest and during CPR in dogs with and without spinal anesthesia.

RESULTS Eleven of the twenty dogs were included in the bupivacaine spinal group and eight dogs were included in the sham-spinal group. One dog was excluded from the study because of the technical difficulties which occurred during placement of the spinal needle.

Before arrest, the central venous pressure was similar in both groups [15]: 1 +/- 2 (SD) vs. 0 +/- 2 mm Hg (p > .1). The mean arterial pressure was, however, significantly lower in the group receiving spinal bupivacaine (81 +/- 18 vs. 110 +/- 27 mm Hg; p < .05). Spinal injection alone (sham or bupivicaine) had no significant effect on the epinephrine, norepinephrine, aldosterone, cortisol, or renin concentrations, as determined at 15 mins after the injection. As already reported [15], after cardiac arrest and before epinephrine administration, the CPP during CPR in the bupivacaine group was significantly lower than in the control group (12 to 13 vs. 27 to 34 mm Hg; p < .01).

Profile analysis showed that the control group exhibited a significant tenfold increase in norepinephrine concentrations over the first 3 mins of CPR, while the spinal bupivacaine anesthesia group had significant blunting of this response (p = .04 for difference between groups; Figure 1). Similar evaluation of the epinephrine data (Figure 2, top) showed that the two groups did not differ by profile analysis. However, independent time point comparison, using the Mann-Whitney U nonparametric test (because of high variability), disclosed that the plasma epinephrine concentrations were significantly higher in the control group immediately before the first epinephrine injection (p = .01). Overall, in the control group, epinephrine increased 100-fold over baseline before exogenous epinephrine was administered. Cortisol concentrations were similar between groups and did not change over time (p = .06). Likewise, aldosterone was similar between groups (p = .33) and did not change over time ( Figure 2, middle). Renin increased significantly over time (p < .001) and with similar magnitude in both groups (p = .74, Figure 2, bottom).

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Figure 1. Norepinephrine response to cardiac arrest. The changes depicted represent the mean +/- SEM from baseline over the first 3 mins of cardiopulmonary resuscitation (CPR). The differences between groups were significant (see text). Time points after 3 mins are not shown because expected contribution from analytical crossover (by the exogenous epinephrine administered) exceeded the observed norepinephrine concentrations. Bupivicaine, closed circles; control, open circles.

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Figure 2. Epinephrine response to cardiac arrest (top). The log mean change in serum epinephrine +/- SEM from baseline is shown. Epinephrine levels increased in both groups over time (p < .001). Mann-Whitney U testing demonstrated a significant difference between groups after 3 mins of cardiopulmonary resuscitation (CPR) (p = .014). Aldosterone response to cardiac arrest shown as mean change in serum concentration +/- SEM from baseline (middle). There was no significant difference between groups or over time. Renin response to cardiac arrest shown as mean change in serum concentration +/- SEM from baseline (bottom). Renin increased in both groups over time (p < .0001). There were no differences between groups. Bupivicaine, closed circles; control, open circles.DISCUSSION

The present work demonstrates that spinal anesthesia produces significant suppression of the norepinephrine and probably epinephrine responses to maximal stress, as represented by cardiac arrest. Since CPP is restored after epinephrine injection [15], the data herein confirm that catecholamine deficiency is an important physiologic mechanism for refractoriness to CPR during spinal anesthesia. Thus, the significant reduction in catecholamine release in the bupivacaine group strongly suggests that low catecholamine concentrations would be associated with relaxation or poor constrictory response of aortic root vascular tone thereby decreasing coronary perfusion. While the increase in cortisol of the sham group showed a trend toward statistical significance (p = .06), the magnitude of the changes does not appear physiologically important in effecting the outcome of cardiac arrest.

Comparison of the CPP data in this work regarding dogs with spinal anesthesia with the results reported by Foley et al. [1] regarding adrenalectomized dogs undergoing CPR [1] shows decreases in CPP similar in both profile and magnitude. Foley et al. [1] observed a 30% increase in norepinephrine in sham-adrenalectomized dogs as compared with 100% (ten-fold) seen in control animals in the current work. This difference is probably the result of the different anesthetic agents that were used in the two sets of experiments (barbiturate as compared with chloralose). An additional difference with the work of Foley et al. [1] is their finding of higher cortisol concentrations after sham adrenalectomy as compared with the unchanged value in the animals used in this experiment. Again, methodologic differences are the likely explanation for this discrepancy since abdominal surgery performed almost immediately before cardiac arrest is expected to stimulate cortisol release [11,22].

It is still unclear whether the norepinephrine plasma response to stress originates from the adrenal medulla or from peripheral sympathetic nerve endings. Our experimental model with both widespread sympathetic blockade and suppression of afferent adrenal neurogenic stimulation could not differentiate between those sources. However, if norepinephrine released into the blood was derived from the peripheral sympathetic system, as suggested by its release in adrenalectomized animals [1], then the present results would have additional connotations. Thus, at least in quantitative terms, the norepinephrine response would appear to be just as important, or more so, as the epinephrine response to cardiac arrest, and the norepinephrine response would also be an important determinant of CPP and presumably outcome of CPR. This conclusion is based on the observation that the apparently larger increase in plasma epinephrine during CPR (100-fold of baseline concentration), compared with the plasma norepinephrine response (ten-fold increase), may not give a true estimate of the stimulatory drives. While epinephrine is released directly into the blood from the adrenal medulla, the norepinephrine concentration at the nerve endplate (release and effector site) may be 10 3 to 105 larger than that overflowing into plasma [23].

It has been suggested that hypoxia, a contributing mechanism in our preparation, may be directly responsible for catecholamine release. In this regard, combined oxygen and glucose starvation has been shown to release catecholamines from heart preparations; this process has, however, a latency of [approximately]10 mins [24,25], a period longer than the 3 mins observed for the catecholamine responses seen in the present experiment. Nevertheless, a hypoxic mechanism for catecholamine release has been recently described in neonates, but it may represent a unique developmental phenomenon. Further experiments, using neonate puppies, are needed to confirm this observation. Regardless, the present data obtained in spinal-anesthetized, fully mature dogs demonstrate the absence of a prompt norepinephrine secretory response to the intense low flow/hypoxic state of CPR.

The effects of norepinephrine in CPR have been tested in animal models that have shown significant improvements in myocardial and cerebral perfusion compared with the effects of epinephrine [26-29]. This finding was confirmed by Lindner et al. [30] who compared 1 mg of norepinephrine to an equivalent dose of epinephrine in a randomized, prospective protocol in humans. They found better outcomes in the former group; the respective rates of return of spontaneous circulation were 56% and 24%, while hospital discharges were 24% and 16% [30]. However, in another large clinical trial, Callaham et al. [31] were not able to detect a difference been the resuscitation rates of humans resuscitated with either high-dose epinephrine or norepinephrine.

In absolute terms, the magnitude of the norepinephrine response is smaller after the stress of major surgery than cardiac arrest [4,22]. Another difference with the long-term effects of major surgery was the present observation of absence of significant increases of cortisol or aldosterone in our shortterm experiments. Most likely, enlarging the size of the experimental pool to increase the statistical precision of our results could have shown a statistically significant but still minuscule release of those factors in cardiac arrest with spinal anesthesia. While these results would have theoretical interest, the physiologic significance is doubtful since epinephrine alone equalized the outcome in the two groups. Our results therefore indicate that the neurogenic supply to the adrenal cortex is of minimal physiologic significance in the setting of acute, intense stress. The data also emphasize that extreme hypoperfusion can directly stimulate renin release, as opposed to the blunted plasma renin response observed during surgical hypotension under spinal anesthesia [9,10]. Epinephrine is a known stimulus for renin release and perhaps it contributed as such to the present results. Regarding epinephrine-stimulated releases of aldosterone and cortisol, it is still possible that such effects could have been elicited by a longer period of CPR/perfusion than used in the present work.

While previous studies of cardiac arrest have largely focused on the cardiovascular involvement, the present investigation provides a basis for further research into the role of the CNS as an integral component, rather than an affected end organ in resuscitation. Norepinephrine deserves reconsideration as an important factor in resuscitation as it may be the native, resuscitative catecholamine. Functional studies of the neural centers supplying the excitatory stimulus for activation of the sympathetic system (hypothalamus and brainstem) may provide new approaches for improving the recovery from cardiac arrest.

Rosenberg JM, Wortsman , Wahr JA, Cryer PE,Gomez-Sanchez CE.

Impaired neuroendocrine response mediates refractoriness to cardiopulmonary resuscitation

in spinal anesthesia.Crit.care Med.26; 533-537: 1998 

MATERIALS AND METHODS Twenty, 18 to 35 kg, fasted, flatchested, mongrel dogs of random sex were anesthetized with 20 mg/kg of thiopental and 2 [micro sign]g/kg iv of

fentanyl, followed by 50 mg/kg of chloralose (0.8% in normal saline) in an intravenous bolus and continued at 20 mg/kg/hr (0.4% in normal saline), according to the protocol approved by the Animal Care Committee at the University of Michigan School of Medicine. The total amount of saline administered was 11 mL/kg over a 1-hr period. The trachea was intubated and the dogs were mechanically ventilated with air flow adjusted to keep the end-tidal CO2 between 35 and 45 torr (4.7 and 6.0 kPa). A 7-French, 100-cm, multiorifice, midthoracic catheter was inserted in the ascending aorta via the femoral artery; a double lumen, 7-French, 16-cm catheter was inserted in the superior vena cava via the right external jugular vein. Pressures were measured with calibrated Gould P23 transducers (P23XL, Spectramed, Oxnard, CA). The dogs were then randomized into two groups. One group received a 0.5-mg/kg bupivacaine spinal anesthetic, bupivacaine 0.75% in dextrose 8.25%, and up to a total volume of 15 mL of preservative free normal saline with 1 mL of a solution of 0.5% Evans blue in normal saline was added as a marker. This bupivacaine dose was previously demonstrated to adequately block spinal conduction in these animals [16]. The control group received a spinal injection with an equivalent volume of normal saline with Evans blue. The contents of the syringe as well as hemodynamic data were unknown to the investigator directing the CPR.

Twenty minutes after the spinal injection, ventricular fibrillation was induced by electrical shock (30 volts, 60 Hz) delivered through a 100-cm, right external jugular pacing wire (USCI Bard, Billerica, MA). After 60 secs, CPR was started, using a mechanical resuscitator (Thumper, Michigan Instruments, Grand Rapids, MI) at a depth of 20% to 25% anterior-posterior diameter, 60 cycles/min. Ventilation with 100% oxygen was set at 1 for every five compressions. Epinephrine (1 mg/mL) at a dose of 0.01 mg/kg was injected in the right superior vena cava at 4 mins after the beginning of CPR. Additional intravenous doses of 0.1, 0.2, and 0.4 mg/kg of epinephrine were given sequentially every 2 mins thereafter (after 6, 8, and 10 mins of CPR). As previously defined in the approved protocol, the experiment was terminated by stopping CPR and administering barbiturate and potassium chloride.

Intrathecal injection of bupivacaine or saline was confirmed at autopsy by anterior laminectomy at high thoracic levels (T1 - T4) to determine the presence of Evans blue in the spinal cord. Dogs without dye in the thoracic spinal cord were excluded from the study.

Arterial blood samples were collected before the spinal injection, at baseline before arrest, and after 1, 3, 5, 7, 9, and 11 mins of CPR. As the blood sample was removed, it was simultaneously replaced with equal volumes of normal saline. These blood samples were immediately mixed with 5 mM of glutathione, placed on ice, and centrifuged. Plasma was separated and stored at -70[degree sign]C until analysis.

The following determinations were performed: epinephrine, norepinephrine, aldosterone, cortisol, and renin. Plasma norepinephrine and epinephrine concentrations were determined by a single-isotope derivative (radioenzymatic) method [17]. Epinephrine to norepinephrine crossover was determined to be 3% to 4% in dog serum in the presence of epinephrine concentration of 500,000 to 1,000,000 pg/mL. Since in the postepinephrine injection norepinephrine concentrations calculated from the effect of assay crossover were significantly higher than the observed concentrations, norepinephrine data obtained after 3 mins of CPR (the time of the first epinephrine injection) were not included in the statistical analysis.

Plasma renin activity was measured, using the method of Poulsen and Jorgensen [18]. Serum (or plasma) aldosterone concentration was measured by ELISA using a monoclonal antibody [19,20]. Serum cortisol was measured by ELISA by a modification of a previously described method [21].

Statistical Analysis. Data were expressed as change from the baseline values by subtracting the individual measurements obtained 15 mins after spinal injection. The results were evaluated by profile analysis (two factor ANOVA, one factor crossed) followed by Student's t-test; where indicated, the Mann-Whitney U nonparametric test was used. Statistical significance was set at the 5% level (p <>

Norepinephrine response to cardiac arrestBupivicaine, closed circles black;

control, open circlesred  Rosenberg: Crit Care Med, 26(3). 1998.533-

537

Rosenberg JM, Wortsman , Wahr JA, Cryer PE,Gomez-Sanchez CE.

Impaired neuroendocrine response mediates refractoriness to cardiopulmonary resuscitation in spinal anesthesia.Crit.care

Med.26; 533-537: 1998  Epinephrine response to cardiac arrest (top). The log mean

change in serum epinephrine +/- SEM from baseline is shown. Epinephrine levels increased in both groups over time (p < .001). Mann-Whitney U testing demonstrated a significant difference between groups after 3 mins of cardiopulmonary resuscitation (CPR) (p = .014).

Aldosterone response to cardiac arrest shown as mean change in serum concentration +/- SEM from baseline (middle). There was no significant difference between groups or over time.

Renin response to cardiac arrest shown as mean change in serum concentration +/- SEM from baseline (bottom). Renin increased in both groups over time (p < .0001). There were no differences between groups. Bupivicaine, closed circles; control, open circles.

Rosenberg JM, Wortsman , Wahr JA, Cryer PE,Gomez-Sanchez CE.

Impaired neuroendocrine response mediates refractoriness to cardiopulmonary resuscitation

in spinal anesthesia.Crit.care Med.26; 533-537: 1998 

RESULTS Eleven of the twenty dogs were included in the bupivacaine spinal group and eight dogs were

included in the sham-spinal group. One dog was excluded from the study because of the technical difficulties which occurred during placement of the spinal needle. Before arrest, the central venous pressure was similar in both groups [15]: 1 +/- 2 (SD) vs. 0 +/- 2 mm Hg (p > .1). The mean arterial pressure was, however, significantly lower in the group receiving spinal bupivacaine (81 +/- 18 vs. 110 +/- 27 mm Hg; p < .05). Spinal injection alone (sham or bupivicaine) had no significant effect on the epinephrine, norepinephrine, aldosterone, cortisol, or renin concentrations, as determined at 15 mins after the injection. As already reported [15], after cardiac arrest and before epinephrine administration, the CPP during CPR in the bupivacaine group was significantly lower than in the control group (12 to 13 vs. 27 to 34 mm Hg; p < .01).

Profile analysis showed that the control group exhibited a significant tenfold increase in norepinephrine concentrations over the first 3 mins of CPR, while the spinal bupivacaine anesthesia group had significant blunting of this response (p = .04 for difference between groups; Figure 1). Similar evaluation of the epinephrine data (Figure 2, top) showed that the two groups did not differ by profile analysis. However, independent time point comparison, using the Mann-Whitney U nonparametric test (because of high variability), disclosed that the plasma epinephrine concentrations were significantly higher in the control group immediately before the first epinephrine injection (p = .01). Overall, in the control group, epinephrine increased 100-fold over baseline before exogenous epinephrine was administered. Cortisol concentrations were similar between groups and did not change over time (p = .06). Likewise, aldosterone was similar between groups (p = .33) and did not change over time (Figure 2, middle). Renin increased significantly over time (p < .001) and with similar magnitude in both groups (p = .74, Figure 2, bottom).

Discussion from Rosenberg: Crit Care Med, Volume 26(3).March

1998.533-537 The present work demonstrates that spinal anesthesia produces

significant suppression of the norepinephrine and probably epinephrine responses to maximal stress, as represented by cardiac arrest. Since CPP is restored after epinephrine injection [15], the data herein confirm that catecholamine deficiency is an important physiologic mechanism for refractoriness to CPR during spinal anesthesia. Thus, the significant reduction in catecholamine release in the bupivacaine group strongly suggests that low catecholamine concentrations would be associated with relaxation or poor constrictory response of aortic root vascular tone thereby decreasing coronary perfusion. While the increase in cortisol of the sham group showed a trend toward statistical significance (p = .06), the magnitude of the changes does not appear physiologically important in effecting the outcome of cardiac arrest.

Discussion from Rosenberg: Crit Care Med, Volume 26(3).March

1998.533-537

Comparison of the CPP data in this work regarding dogs with spinal anesthesia with the results reported by Foley et al. [1] regarding adrenalectomized dogs undergoing CPR [1] shows decreases in CPP similar in both profile and magnitude. Foley et al. [1] observed a 30% increase in norepinephrine in sham-adrenalectomized dogs as compared with 100% (ten-fold) seen in control animals in the current work. This difference is probably the result of the different anesthetic agents that were used in the two sets of experiments (barbiturate as compared with chloralose). An additional difference with the work of Foley et al. [1] is their finding of higher cortisol concentrations after sham adrenalectomy as compared with the unchanged value in the animals used in this experiment. Again, methodologic differences are the likely explanation for this discrepancy since abdominal surgery performed almost immediately before cardiac arrest is expected to stimulate cortisol release [11,22].

Discussion from Rosenberg: Crit Care Med, Volume 26(3).March

1998.533-537

It is still unclear whether the norepinephrine plasma response to stress originates from the adrenal medulla or from peripheral sympathetic nerve endings. Our experimental model with both widespread sympathetic blockade and suppression of afferent adrenal neurogenic stimulation could not differentiate between those sources. However, if norepinephrine released into the blood was derived from the peripheral sympathetic system, as suggested by its release in adrenalectomized animals [1], then the present results would have additional connotations. Thus, at least in quantitative terms, the norepinephrine response would appear to be just as important, or more so, as the epinephrine response to cardiac arrest, and the norepinephrine response would also be an important determinant of CPP and presumably outcome of CPR. This conclusion is based on the observation that the apparently larger increase in plasma epinephrine during CPR (100-fold of baseline concentration), compared with the plasma norepinephrine response (ten-fold increase), may not give a true estimate of the stimulatory drives. While epinephrine is released directly into the blood from the adrenal medulla, the norepinephrine concentration at the nerve endplate (release and effector site) may be 10 3 to 105 larger than that overflowing into plasma [23].

It has been suggested that hypoxia, a contributing mechanism in our preparation, may be directly responsible for catecholamine release. In this regard, combined oxygen and glucose starvation has been shown to release catecholamines from heart preparations; this process has, however, a latency of [approximately]10 mins [24,25], a period longer than the 3 mins observed for the catecholamine responses seen in the present experiment. Nevertheless, a hypoxic mechanism for catecholamine release has been recently described in neonates, but it may represent a unique developmental phenomenon. Further experiments, using neonate puppies, are needed to confirm this observation. Regardless, the present data obtained in spinal-anesthetized, fully mature dogs demonstrate the absence of a prompt norepinephrine secretory response to the intense low flow/hypoxic state of CPR.

The effects of norepinephrine in CPR have been tested in animal models that have shown significant improvements in myocardial and cerebral perfusion compared with the effects of epinephrine [26-29]. This finding was confirmed by Lindner et al. [30] who compared 1 mg of norepinephrine to an equivalent dose of epinephrine in a randomized, prospective protocol in humans. They found better outcomes in the former group; the respective rates of return of spontaneous circulation were 56% and 24%, while hospital discharges were 24% and 16% [30]. However, in another large clinical trial, Callaham et al. [31] were not able to detect a difference been the resuscitation rates of humans resuscitated with either high-dose epinephrine or norepinephrine.

In absolute terms, the magnitude of the norepinephrine response is smaller after the stress of major surgery than cardiac arrest [4,22]. Another difference with the long-term effects of major surgery was the present observation of absence of significant increases of cortisol or aldosterone in our shortterm experiments. Most likely, enlarging the size of the experimental pool to increase the statistical precision of our results could have shown a statistically significant but still minuscule release of those factors in cardiac arrest with spinal anesthesia. While these results would have theoretical interest, the physiologic significance is doubtful since epinephrine alone equalized the outcome in the two groups. Our results therefore indicate that the neurogenic supply to the adrenal cortex is of minimal physiologic significance in the setting of acute, intense stress. The data also emphasize that extreme hypoperfusion can directly stimulate renin release, as opposed to the blunted plasma renin response observed during surgical hypotension under spinal anesthesia [9,10]. Epinephrine is a known stimulus for renin release and perhaps it contributed as such to the present results. Regarding epinephrine-stimulated releases of aldosterone and cortisol, it is still possible that such effects could have been elicited by a longer period of CPR/perfusion than used in the present work.

Discussion from Rosenberg: Crit Care Med, Volume 26(3).March

1998.533-537

While previous studies of cardiac arrest have largely focused on the cardiovascular involvement, the present investigation provides a basis for further research into the role of the CNS as an integral component, rather than an affected end organ in resuscitation. Norepinephrine deserves reconsideration as an important factor in resuscitation as it may be the native, resuscitative catecholamine. Functional studies of the neural centers supplying the excitatory stimulus for activation of the sympathetic system (hypothalamus and brainstem) may provide new approaches for improving the recovery from cardiac arrest.

AuthorAromaa, U.; Lahdensuu, M.; Cozanitis, D. A.

Severe complications associated with epidural and spinal

anaesthesias in Finland 1987-1993. A study based on patient

insurance claims Acta Anaesthesiologica Scandinavica.

41(4):445-452 1997

The Patient Injury Act has been in effect in Finland since 1 May 1987. This legislation is a no-fault compensation scheme and implies that if a patient during the course of medical treatment suffers any injury as a result of that treatment he or she may file a claim to the Patient Insurance Association (PIA). From 1 May 1987 to 31 December 1993, 23 500 claims for compensation were made.

Methods: All claims made to PIA involving spinal and epidural anaesthesias during the above period were collected and reviewed and a data base was prepared. The total number of anaesthetics given during this period was estimated by sending questionnaires to every hospital in the country.

Results: Eighty-six claims were associated with spinal and/or epidural anaesthesia. Respectively, the total the number of spinal and epidural anaesthesias administered was 550 000 and 170 000. There were 25 serious complications associated with spinal anaesthesia: cardiac arrests ( 2), paraplegia ( 5), permanent cauda equina syndrome ( 1), peroneal nerve paresis ( 6), neurological deficits ( 7), and bacterial infections ( 4). The 9 serious complications which were associated with epidural anaesthesia were: paraparesis ( 1), permanent cauda equina syndrome ( 1), peroneal nerve paresis ( 1), neurological deficit ( 1), bacterial infections ( 2), acute toxic reactions related to the anaesthetic solution ( 2), and overdose of epidural opioid ( 1).

Conclusions: According to this material the incidence of serious complications was 0.45:10 000 following spinal and 0.52:10 000 following epidural anaesthesia.

Atraumatic technique, careful patient selection and early diagnosis and treatment of complications are essential in avoiding permanent injury.

Tinker JH et al. Role of monitoring devices in prevention of anesthetic mishaps: a closed

claims analysis. 1999;71:535‑540.

Caplan RA et al. Adverse respiratory events in anesthesia: a closed claims analysis. Anesthesiology 1990;72:828

6. Kroll DA et al. Nerve injury associated with anesthesia. Anesthesiology 1990;73:202‑7. Cheney F et al, Nerve injury associated with anesthesia. Anesthesiology 1999;90:1062‑9. Prielipp RC et al. Ulnar nerve pressure: influence of arm position and relationship to somatosensory evoked p

Anesthesiology 1999; 91:345‑54. Contreras MG et al. The anatomy of the u1nar nerve at the elbow: potential relationships of acute u1nar

neuropathy differences. Clinical Anatomy 1998;11:372‑8. Caplan RA et al. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing

Anesthesiology 1988;68: 5‑11. Rosenberg JM et al. Coronary perfusion pressure during cardiopulmonary resuscitation after spinal anesthesia.

and Analgesia 1996;82:84‑7 Rosenberg JM et al. Impaired neuroendocrine response mediates reftactoriness to cardiopulmonary

resuscitation' anesthesia. Critical Care Medicine 1998;26:533‑7. Cheney FW. High‑severity injuries associated with regional anesthesia in the 1990's. ASA Newsletter 2001;

65(6)j Biboulet P. Fatal and nonfatal cardiac arrests related to anesthesia. Can J Anaesth 2001;48:326‑332. Lee LA. Postoperative visual loss data gathered and analyzed. ASA Newsletter 2000; 64(9): 25‑27. Lee LA. ASA postoperative visual loss (POVL) registry. APSF Newsletter 2001; 16(4):56‑7. Fitzgibbon DR. Liability arising from anesthesiology‑based pain management in the nonoperative setting. ASA N

2001:65:6‑8. Cheney FW. The ASA Closed Claims Project: what have we learned, how has it affected practice, and how will

it practice in the future? Anesthesiology 1999; 91:552‑6.

32 y,110 kg for repair of ventral hernia 700 m l preload,16 gauge,Ecg,NIBP;SaO2

monit fent 100 microgr premed(rekease of

vasopressin inhibited by low dose morphine left lat dec;at L2-3 15 mg of bupi 0.75%

+d8,25%2 min later supine,nause+ tingling hands;C5-C6 block!--15 sec…lost consciousenne no carortid pulse

Danno materno;CS vs vaginale

0

5

10

15

20

25

%

CS vag

morte materna

danno cerebrale neonatale

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morte neonatale

dolore dur.anest

danno neurale

danno cerebrale paz

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Biblio ASa closed claims and others…..

Posner KL, Sampson, PD, Caplan RA, Ward RJ, Cheney FW: Measuring interrater reliability among multiple raters: An example of methods for nominal data [published erratum appears in Stat Med 1992; 11:1401]. Stat Med 9:1103-15, 1990<ldn>!

2: Caplan RA, Ward RJ, Posner K, Cheney FW: Unexpected cardiac arrest during spinal anesthesia: A closed claims analysis of predisposing factors. ANESTHESIOLOGY 68:5-11, 1988<ldn>!

3: Frerichs RL, Campbell J, Bassell, MB: Psychogenic cardiac arrest during extensive sympathetic blockade. ANESTHESIOLOGY 68:943-4, 1988

4: Chester, WL: Spinal anesthesia, complete heart block, and the pericardial chest thump: An unusual complication and a unique resuscitation. ANESTHESIOLOGY 69:600-2, 1988

5: Liguori GA, Sharrock NE: Asystole and severe bradycardia during epidural anesthesia in orthopedic patients. ANESTHESIOLOGY 86:250-7, 1997

6: Caplan RA, Posner KL, Ward RJ, Cheney FW: Adverse respiratory events in anesthesia: A closed claims analysis. ANESTHESIOLOGY 72:828-33, 1990<ldn>!

7: Tinker JH, Dull DL, Caplan RA, Ward RJ, Cheney FW: Role of monitoring devices in prevention of anesthetic mishaps: A closed claims analysis. ANESTHESIOLOGY 71:541-6, 1989<ldn>!

8: American Society of Anesthesiologists Task Force on Guidelines for Management of the Difficult Airway: Practice guidelines for management of the difficult airway. ANESTHESIOLOGY 78:597-602, 1993

9: Cheney FW, Domino KB, Caplan, RA, Posner KL: Nerve injury associated with anesthesia: A closed claims analysis. ANESTHESIOLOGY 90:1062-9, 1999 <ldn>!

10: Morray JP, Geiduschek JM, Caplan RA, Posner KL, Gild WM, Cheney FW: A comparison of pediatric and adult anesthesia closed malpractice claims. ANESTHESIOLOGY 78:461-7, 1993<ldn>!

Safety in anesthesia

Leape LL: Error in medicine. JAMA 272:1851–1857, 1994 2: Lagasse RS: Anesthesia safety. Anesthesiology 97:1609–17, 2002 <ldn>! 3: Derrington MC, Smith G: A review of studies of anaesthetic risk, morbidity and mortality. Br

J Anaesth 59:815–33, 1987<ldn>! 4: Lunn JN, Devlin HB: Lessons from the confidential enquiry into perioperative deaths in

three NHS regions. Lancet 2:1384–6, 1987 5: Beecher HK, Todd DP: A Study of the Deaths Associated With Anesthesia and Surgery.

Based on a study of 599,518 anesthesias in ten institutions 1948–1952, inclusive. Ann Surg 140(1):2–35, 1954

6: Marx G, Mateo C, Orkin L: Computer analysis of postanesthetic deaths. Anesthesiology 39:54–8, 1973

7: Memery HN: Anesthesia mortality in private practice. JAMA 194:127–30, 1965 8: Eichhorn JH: Prevention of intraoperative anesthesia accidents and related severe injury

through safety monitoring. Anesthesiology 70:572–7, 1989<ldn>! 9: Arbous MS, Grobbee DE, van Kleef JW, de Lange JJ, Spoormans HHAJM, Touw P,

Meursing AEE: Mortality associated with anaesthesia. Anaesthesia 56:1141–53, 2001<ldn>! 10: Fasting S, Gisvold SE: Serious intraoperative problems. Can J Anesth 49:545–58,

2002<ldn>! 11: Macintosh R: Deaths under anaesthetics. Br J Anaesth 21:107–36, 1948 12: ReasonJ: Managing the risks of organizational accidents. Aldershot, England, Ashgate

Publishing Limited, 1997 13: Gaba DM: Anaesthesiology as a model for patient safety in health care. BMJ 320:785–8,

2000

Eventi dannosi nei claims ostetrici

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8

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12

14

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intub esofag

broncospasmo

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estubaz prematura

convuls

probl attrezz

errore farmacol

errore idrico..

perdite ematiche

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Probl.resp

Probl cardiocirc

Outcome from literature

All patients resuscitated;all neurologically intact

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