Published on May 3, 2014
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? l Claim is a demand for financial compensation by an individual who has sustained an injury from medical care. l Once a claim is resolved the file is closed
Che cosa sono gli ASA Closed claims? l Collection of 35 USA insurance companies l 14500 anesthesiologists covered l 50-55% of all USA practicing anesthesiologists
Closed claim l Medical records l Narrative statement by the involved health care personnel l Deposition summaries l Outcome and follow up reports l 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…pu blication 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 care gravity of injury standard of care Frequency of paymentmagnitude of payment Better 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 adverse outcome judgments of appropriateness 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 actually temporary changed to permanent actually permanent changed to temporary % of appro priate ness 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 30 death 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 717 591 372 278 209
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 death nerve dam age brain dam age airw ay traum a eye in. pnx fetal/new born in,. stroke aspirationback painheadacheM I burns aw areness min med max
Most common adverse outcomes Median Payment:$*1000 0 100 200 300 400 500 600 700 median payment death nerve damage brain damage airway trauma eye injury pnx fetal7newborn injury stroke aspiration back pain headache MI burns awareness
Claims differ in different populations; »FOR INCIDENCE »FOR SERIOUSNESS
Morray J, Geiduschek J, Caplan R, Posner K, Gild W, Cheney FW: A comparison of pediatric and adult anesthesia malpractice claims. ANESTHESIOLOGY 78:461-7, 1993
Chadwick,HS,Posner,K,Kaplan,RA,Ward,RJ,Cheney FW.A comparison of obstetric and nonobstetric anesthesia malpractice claims.Anesthesiology 1991;74:242-249. ob vs non ob:190 vs 1351 » ob cases 67% CS,33% vaginal » 65% associati a anest reg,33% con GA » 2 claims per non disponibilità dell’anestesista!
ASA closed claims project Malpractice claims against anesthesiologists: OB VS NON OB 0 5 10 15 20 25 30 35 40 % ob nonob morte (materna) danno cerebrale neonatale cefalea morte neonatale dolore dur.anest danno neurale danno cerebrale paz. distress emotivo dolore dorso
Claims ostetrici:regionale vs GA. 0 5 10 15 20 25 30 35 40 45 % reg GA morte materna danno cerebrale neonatale cefalea morte neonatale dolore dur.anest danno neurale danno cerebrale paz distress emoz dolore dorso * * * *
Patogenesi del danno neonatale 45% attribuiti a cause anestetiche: GA:4 » 1 broncospasmo » 1 intub esofagea » 1 aspir polm » 1 ritardo anest. » Regionale:13 » 9 convuls da iniez intravasc » 1 eclampsia » 1 ritardo disponibilità » 3 spinali alte 37% a probl ostetrici o congeniti, 13% con probl di rianimaz.
Dati relativi ai pagamenti:OB VS NON OB claims non ob claims ob Claims ob regionale generale non pagati(%) 32 38 43 27 pagati(%) 59 53 48 63 pagamento mediano($) 85000 203000 91000 225000 range di pagamento($) 15000-6 milioni 675000-5.4 milioni 675-2.5 mil750-5.4 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 0 5 10 15 20 25 30 35 40 45 50 % 1980 1990 Resp event cardiovasc event equipment probl
Most common respiratory events associated with death and brain damage inadequate ventilation esophag intub difficult intub other resp events adv resp events inadequate ventilation esophag intub difficult intub other 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 obs bronchospasm premat extub aspir
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 none SpO2 only SpO2+etCO2 102 167
Cardiovascular damaging events associated with death or brain damage 0 10 20 30 40 50 60 unexp./other cv event neurax cardiac arrest inadeq fluid blood loss 1980 1990
Unexplained/other damaging cardiovascular events in the 90’s(137)(death and brain damage) arrhyth MI pulm emb stroke path abnorm multifactorial
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 0 10 20 30 40 50 60 unexpect/othercvevent neuraxcardiacarrest inadeqfluids bloodloss none SpO2 only SpO2+etCO2 72 194 192??
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 resp cardiovasc inadeq vent esoph.intub <standard of care plaintiff payment
Trends in death and brain damage 0 10 20 30 40 50 60 70 80 % '70-79 '80-89 '90-94 nerve injury brain damage death “The fact that professional liability premiums for anesthesiologi have decreased significantly since th 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 intravasc injection other block related
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 Biboulet Olsson Auroy Newland:direct Newland: related Newland anesth.attrib Aubas Aubas reg only Tarkkila Geffin 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
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 arrest death seizures neurol.injury radiculopathy cauda equina paraplegia
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
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 arrest death 71826 4145 7656 2081 3308 9222 3231
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 beat Precordial thumping resumed at arrows again resulting in QR and patient awakenin 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.
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.
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
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
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
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
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
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
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,
13: Schultz CH, Rivers EP, Feldkamp CS. A characterization of hypothalamic- pituitary-adrenal axis function during and after human cardiac arrest. Crit Care Med 1993; 21:1339–47.<ldn>! 14: Vallotton MB. At the cutting edge: Mol Cell Endocrinol 1991; 78:C73–6. 15: Lindner KH, Prengel AW, Pfenninger EG. Vasopressin improves vital organ blood flow during closed- chest cardiopulmonary resuscitation in
Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Resuscitation 2000; 46:1–447. 26: Lindner KH, Ahnefeld FW, Bowdler IM. Comparison of different doses of epinephrine on myocardial perfusion and resuscitation success during cardiopulmonary resuscitation in a pig model. Am J Emerg Med 1991; 9:27– 31.<ldn>! 27: Brown CG, Werman HA, Davis EA.
Leclercq JF, Rosengarten MD, Kural S. Effects of intrinsic sympathetic activity of beta-blockers on SA and AV nodes in man. Eur J Cardiol 1981; 12:367– 75.<ldn>! 38: Noc M, Weil MH, Gazmuri RJ. Ventricular fibrillation voltage as a monitor of the effectiveness of cardiopulmonary resuscitation. J Lab Clin Med 1994; 124:421
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.
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
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
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
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
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
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
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
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
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.
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
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
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
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
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
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
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
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
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
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.
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
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
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.
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
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
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.
Kawamoto M, Tanaka N, Takasaki M. Power spectral analysis of heart rate variability after spinal anesthesia. Br J Anaesth 1993; 71:523-7.
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
Coronary perfusion pressure during cardiopulmonary resuscitation after spinal anesthesia in dogs.
Increase in coronary perfusion pressure with increase in epinephrine dose 0 0,5 1 1,5 2 2,5 3 3,5 4 CPP increase in mmHG 0,01 0,1 0,2 0,4 bupi spinal saline spinal
resuscitation 0 10 20 30 40 50 60 70 80 90 100 % 0,01 0,1 0,2 0,4 bupi spinal saline spinal
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
to cardiac arrest( from Rosember et al Mean noerpi change from baseline ng/mn 0 500 1000 1500 2000 2500 post 1 3 control bupi
Aromaa et al Vedi ref prtec
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
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
Cardiac arrest (or severe arrhytmia)cases... author drug Site of inj. level other matta Bupi 12,5 L2-3 T5 Done on l side bernard s Lido 60 mg 5% + epi 200 micr L4-5 T4-3 Left side
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
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.
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
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 .
Impaired 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
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)
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
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
Norepinephrine response to cardiac arrest Bupivicaine, closed circles black; control, open circlesred Rosenberg: Crit Care Med, 26(3). 1998.533- 537
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
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 : 1 +/- 2 (SD) vs. 0 +/- 2 mm Hg (p > .1). The mean arterial pressure was, however,
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 , 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
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.  regarding adrenalectomized dogs undergoing CPR  shows decreases in CPP similar in both profile and magnitude. Foley et al.  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.  is their finding of higher cortisol
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
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
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.
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.
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
Danno materno;CS vs vaginale 0 5 10 15 20 25 % CS vag morte materna danno cerebrale neonatale cefalea morte neonatale dolore dur.anest danno neurale danno cerebrale paz distress emoz dolore dorso *
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 0 2 4 6 8 10 12 14 % ob nonob ventilaz inadeguata iot difficile aspiraz intub esofag broncospasmo FiO2 inadeg ostruz vie aeree estubaz prematura convuls probl attrezz errore farmacol errore idrico.. perdite ematiche errore trasf * * * Probl.resp Probl cardiocirc
Outcome from literature All patients resuscitated;all neurologically intact Drugs: » Vagolytics » Vasopressors » Chronotropics » Pacing thumps » ECM
Calcification Inhibitors in CKD and Dialysis Patients
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