Complications in paediatric anaesthesia Charles Lee and Linda Mason
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1 Complications in paediatric anaesthesia Charles Lee and Linda Mason Purpose of review This review identifies the most serious complications likely to be encountered in the current practice of paediatric anaesthesia. Recent findings The findings of the ASA Closed Claims Project, published in 1993, showed a higher proportion of closed paediatric malpractice claims related to respiratory events than to cardiovascular events. The Pediatric Perioperative Cardiac Arrest Registry an offshoot of the American Society of Anesthesiologists Closed Claims Project reviewed cardiac arrest data collected between 1994 and 1997, revealing a shift in the aetiology of cardiac arrest during paediatric anaesthesia over the past 20 years. The study found that reported cardiac arrests were now more prevalent from cardiovascular causes than respiratory causes, unlike the findings in the previous Closed Claims Project. Follow-up data collected by both the Pediatric Perioperative Cardiac Arrest Registry and the American Society of Anesthesiologists Closed Claims Project confirm this trend. Summary Outcomes for paediatric patients undergoing anaesthesia have improved over the years as a result of advances in monitoring and equipment, safer and more easily titratable anaesthetic agents, and possibly the practice of subspecialization. Preventable complications still, however, occur. An awareness of frequently encountered complications during paediatric anaesthesia may lead to the earlier detection and treatment of perioperative problems, leading to better outcomes. Keywords anaesthesia, cardiac arrest, complications, paediatric Curr Opin Anaesthesiol 19: # 2006 Lippincott Williams & Wilkins. Loma Linda University, Loma Linda, California, USA Correspondence to Linda Mason MD, Loma Linda University Medical Center, Loma Linda, CA 92354, USA Tel: ; fax: ; lmason@llu.edu Current Opinion in Anaesthesiology 2006, 19: Abbreviations ASA American Society of Anesthesiologists POCA pediatric perioperative cardiac arrest # 2006 Lippincott Williams & Wilkins Introduction Despite an overall improvement in mortality and morbidity rates for anaesthetized children over the past 50 years, the long-recognized fact [1] that anaesthesiarelated complications occur more frequently in the paediatric population still holds true. The most recent ASA Closed Claims data [2], published in 1993, and the initial findings of the Pediatric Perioperative Cardiac Arrest (POCA) Registry help define the most prevalent complications encountered in the current practice of paediatric anaesthesia. These two landmark studies identified respiratory and cardiac events as the two most significant categories of complication in paediatric anaesthesia. The ASA Closed Claims Project found that 43% of the closed paediatric malpractice claims were related to mostly preventable respiratory events, whereas 13% of cases were related to cardiac arrest from cardiovascular causes. The initial POCA study [3, 4], which examined cardiac arrest data submitted by participating panel members between 1994 and 1997, revealed a shift in the aetiology of cardiac arrest during paediatric anaesthesia over the past 20 years. The initial POCA study found that 32% of reported cardiac arrests were due to cardiovascular causes, whereas 20% of arrests were due to respiratory causes a significant change from the findings of the earlier ASA Closed Claims Project. This review will examine the anaesthetic complications identified in these studies, as they reflect the complications most likely to be encountered in paediatric anaesthesia practice today. Cardiac arrest in the paediatric patient Unexpected cardiac arrest in the perioperative period is the most serious and disastrous complication in paediatric anaesthesia. The higher incidence of cardiovascular causes of anaesthesia-related cardiac arrest may, in part, be due to the fact that the initiation of chest compressions was an inclusion criterion for the POCA Registry (such that arrests caused by adverse respiratory events were not included in the data unless chest compressions were required). Another factor that may play a role is that the use of pulse oximetry in 98% and capnography in 86% of the POCA cases may have been more effective in preventing respiratory than cardiovascular incidents before arrest occurred. Morray et al. [2] noted that 89% of the closed paediatric malpractice claims of inadequate ventilation could have been prevented with the use of pulse oximetry and/or capnography alone. 262
2 Complications in paediatric anaesthesia Lee and Mason 263 During the initial POCA study period, the incidence of anaesthesia-related cardiac arrests was found to be 1.4 per instances of anaesthesia per year, with a mortality rate of 26%. The mortality rate in American Society of Anesthesiologists (ASA) physical status 3 5 patients was 37% compared with 4% in ASA physical status 1 and 2 patients. ASA physical status 3 5 was the strongest predictor of mortality, followed by emergency status. Thirty-three percent of all anaesthesiarelated cardiac arrests occurred in previously healthy ASA physical status 1 and 2 patients, and were mostly medication-related errors (64%). Infants younger than 1 year of age accounted for 55% of all anaesthesiarelated cardiac arrests. Overall, the POCA study [3] found medication-related (37%) mechanisms of cardiac arrest to be most common, followed by cardiovascular causes (32%), respiratory causes (20%) and equipmentrelated causes (7%). Since the initial study, over 300 additional cases have been submitted to the POCA Registry ( ), half of these being related to anaesthetic causes, but the demographic and etiologic profile has changed (Table 1) [5 ]. The percentage of ASA physical status 1 and 2 patients has decreased from 33 to 27%, and the proportion of patients less than 1 year of age has decreased from 55 to 36%. This change may be partially due to the decreased number of arrests caused by inhalational agents, which were more likely to occur in ASA physical status 1 or 2 patients who were less than 1 year of age. The mortality in the two time periods has not changed, being 27% in the new data [5 ]. Mechanisms of cardiac arrest The POCA study found that the predominant mechanism of arrest in this category was cardiovascular depression from inhalational agents. The administration of halothane, either alone or in combination with other drugs, was responsible for cardiovascular depression and arrest in 71% of all medication-related cases. Bradycardia and hypotension were the most common antecedent events. Several large studies [2,3,6 10] have consistently shown that the risk of anaesthesia-related cardiac arrest appears Table 1 Changing trends in anaesthesia-related complications [5 ] Primary cause of arrest (%) (%) Medication Cardiovascular Respiratory Equipment 7 5 to be inversely proportional to age, the incidence of cardiac arrest being highest in infants, and higher in children than in adults. Of the cases of cardiac arrest related to the administration of halothane (either alone or in combination with an intravenous medication), 50% occurred in infants 6 months of age or younger, and 50% had a reported inspired halothane concentration of 2% or less. This finding is consistent with the observation [3,11,12] that infants may exhibit a greater susceptibility to cardiovascular depression from even conventional doses of inhalational agents. Morray et al. [3] observed that cardiovascular depression by halothane might have been facilitated by the use of assisted or controlled ventilation, with a resulting accelerated rise in plasma halothane concentration, or a prolonged exposure to high inspired concentrations of halothane while attempting to gain intravenous access. More recent data [5 ] show a decline in the percentage of medication-related causes of cardiac arrest from 37 to 22% of the total, owing to a decrease in the number of cases of cardiovascular depression resulting from inhaled agents. This finding [13] may reflect the increasing use and popularity of sevoflurane in paediatric anaesthesia. Sevoflurane produces less myocardial depression and bradycardia in infants and children than does halothane [14 18], although induction with a high inspired concentration (8%) may be associated with an earlier onset of bradycardia than is seen with an incremental induction [19]. Sevoflurane does have a number of other advantages over halothane. Anaesthetic overdose in the newborn is less likely with sevoflurane because its minimum alveolar concentration remains constant in the first 6 months of life [16], whereas the minimum alveolar concentration for halothane is lower in the newborn than in the 6-months-old [11]. Heart rate one of the main determinants of cardiac output in infants is maintained under sevoflurane anaesthesia but decreased by halothane [16]. Although sevoflurane certainly appears to be safer than halothane, numerous case reports and studies [20,21, 22 30] have associated it with epileptiform electroencephalogram activity and tonic-clonic seizure-like activity during anaesthesia in children without a history of epilepsy. The mechanism underlying the epileptogenic effect of sevoflurane currently remains unknown. Sevoflurane does share a similarity in molecular structure with enflurane, which is known [21,31] to induce electrocorticographic seizure activity. Epileptiform activity induced by anaesthesia is, however, not necessarily either ictal or epileptogenic, and there is no evidence that epileptiform EEG patterns induced by
3 264 Paediatric anaesthesia potent inhaled agents have caused cerebral injury in any patients; concerns [26] about sevoflurane s epileptogenic potential may therefore be unfounded. Another notable medication-related cause of arrest in the POCA study was the intravascular injection of local anaesthetic. This mishap occurred despite negative aspiration and a negative test dose. Cardiac arrest is a rare complication of caudal anaesthesia but can occur despite appropriate precautionary measures. The use of an epidural test dose in children is still a subject of debate. Factors such as basal heart rate, age, premedication and the general anaesthetic agent used can affect the reliability or interpretation of the test dose. Routine test dosing is, however, still useful as it has the potential benefit of identifying a significant number of inadvertent intravascular injections [32,33]. Pretreatment with atropine may improve the sensitivity of the test dose in patients under general anaesthesia [34]. All practitioners can probably agree that a slow incremental injection of the total dose of local anaesthetic, while closely monitoring the patient s vital signs, is essential. Bupivacaine is frequently used for caudal administration. Cardiac arrest resistant to resuscitation following systemic toxicity [35] and a prolonged effect on the cardiac conduction system [36,37] are drawbacks of bupivacaine. Infants are at greater risk of bupivacaine toxicity because the level of α1-acid glycoprotein, which binds bupivacaine, is decreased in infants compared with older age groups [38]. Adding epinephrine to bupivacaine solutions may slow vascular absorption, thereby reducing systemic toxicity, and provide beneficial positive inotropic cardiac effects in case of accidental intravascular injection [39]. A promising experimental treatment [40] for bupivacaine-induced cardiac toxicity is the infusion of a lipid emulsion (which theoretically extracts lipid-soluble bupivacaine molecules from tissue binding sites) during resuscitation. The intravenous delivery of a 20% lipid infusion for 10 min resulted in the resuscitation of 100% of dogs in which cardiovascular collapse had been induced with 10 mg/kg of bupivacaine. None of the dogs given an equivalent volume of saline was successfully resuscitated. The use of local anaesthetic agents with less myocardial toxicity, such as ropivacaine and levobupivacaine, may be safer for caudal anaesthesia in infants, but incremental dosing is still advisable. Succinylcholine-induced cardiac arrest is most often attributed to an acute, massive release of potassium. Unanticipated cardiac arrest caused by succinylcholineinduced rhabdomyolysis and hyperkalemia in the presence of an undiagnosed myopathy can occur [41 44]. When faced with sudden, life-threatening arrhythmias or cardiac arrest following succinylcholine administration at induction of anaesthesia in paediatric patients, especially males, occult myopathy and hyperkalemia should be considered in the differential diagnosis. The early, aggressive treatment and reversal of hyperkalemia may ensure good a neurologic outcome. Owing to its rapid onset and ultrashort duration, succinylcholine given intramuscularly is extremely useful for treating laryngospasm during inhalational induction in general anaesthesia in paediatric patients without intravenous access. Succinylcholine should, however, be reserved for emergency intubation or instances in which immediate securing of the airway is necessary, such as laryngospasm, difficult airway and full stomach [44]. Cardiovascular causes of cardiac arrest Cardiovascular causes of arrest were the second most common mechanism of perioperative arrest in the POCA study. The exact cause of arrest could not be determined in many cases in the cardiovascular category; these were frequently children with congenital heart disease and an ASA physical status of 3 5. Of the clearly identifiable cardiovascular causes, the consequences of haemorrhage (e.g. hypovolemia and inadequate fluid replacement) or its therapy (transfusionrelated events, most commonly hyperkalemia) topped the list. The newer data [5 ] from the POCA Registry indicated an increase in the number of cases related to cardiovascular causes, from 32 to 35%. The most frequent known causes of arrest in this category remained the same. Intravascular fluid loss and current volume status are often underestimated in paediatric patients, especially in newborns and infants. Due to their smaller blood volume, paediatric patients are more sensitive to excessive as well as inadequate hydration. In children, heart rate may be a more sensitive guide to intravascular fluid status than blood pressure. By the time hypotension becomes apparent, severe hypovolemia is often already present, and cardiovascular collapse may soon ensue without appropriate volume resuscitation. Securing adequate intravascular access prior to surgery is a must for surgeries in which significant blood loss is expected. Failure to do so and failure to keep up with intraoperative blood loss are the most common reasons why cardiac arrests from hypovolemia are deemed to be anaesthesia-related [6]. Large-volume or exchange transfusions in neonates and small children can result in life-threatening hyperkalemia and cardiac arrest [45 49]. This is potentially preventable. Serum potassium levels can rise quickly during blood transfusions in children with a small blood volume. Blood components with the highest levels of
4 Complications in paediatric anaesthesia Lee and Mason 265 potassium include whole blood, irradiated blood and units approaching their expiration date. To reduce the risk of transfusion-related hyperkalemia in neonates and infants, washed or fresh (i.e. less than 7 days old) packed red blood cells should be used [6,50 ]. Packed red cells have a lower potassium load than whole blood because of the reduced amount of plasma. Life-threatening hyperkalemia can still occur with packed red blood cells if large volumes are rapidly transfused. Whole blood should be avoided, and irradiated blood should be given only as indicated in neonates and immunocompromised patients. Respiratory causes of cardiac arrest In the initial POCA study, the most common respiratory cause of arrest was airway obstruction due to laryngospasm. The additional data collected between 1998 and 2003 by the POCA Registry [5 ] show an increase in respiratory causes of cardiac arrest from 20 to 28%, with laryngospasm still the primary respiratory cause of arrest. Most of the cases occurred in children less than 2 years of age, but ASA physical status did not appear to be a contributing factor. Over one third of the cases, however, were associated with upper respiratory infection and copious secretions. Laryngospasm occurred most frequently during inhalation induction and in patients without intravenous access, but vigilance must be exercised during emergence and transport to the postanaesthesia care unit as laryngospasm may occur at these times as well. The early treatment of laryngospasm with airway manoeuvres [51] and/or succinylcholine may improve outcomes. Equipment-related causes of cardiac arrest In the POCA study, the most common equipment problems were complications of anaesthesiologist-placed central lines, either from induction of an arrhythmia or from creation of tamponade, hemothorax or pneumothorax. These numbers have remained fairly constant from 7% in 1994 to 1999 to 5% in the 1998 to 2003 periods [5 ]. Domino et al. [52] examined the closed malpractice claims collected through December 2002 in the ASA Closed Claims Project database for injuries and liability related to central vascular catheters. Sixteen claims were related to cardiac tamponade, and onethird of these claims involved paediatric patients ranging in age from 2 months to 6 years. The risk of cardiac tamponade with central venous catheters is particularly high in infants [53] (especially premature infants and infants younger than 6 months of age) because the infant s thin-walled right atrium and right ventricle are more susceptible to trauma [54,55]. The primary cause of tamponade associated with central venous catheter use is the inappropriate placement of the catheter tip within the heart [54,56 60]. Perforation of the heart can happen during catheter insertion but is more typically delayed and is probably due to migration of the catheter tip into the right atrial or right ventricular wall, with subsequent mural necrosis [54]. Another predisposing factor for cardiac tamponade may be a catheter angle that is not parallel with the wall of the superior vena cava [61 63]. Domino et al. [52] concluded that nearly half of all central catheter claims were possibly preventable by either ultrasound guidance or pressure waveform monitoring. Confirmation of catheter tip position by chest radiographs and adjustment of catheter position if intracardiac or at an acute angle to the wall of the superior vena cava might also have prevented many of the tamponade claims. As each pass of a needle carries the risk of a complication such as pneumothorax, two-dimensional ultrasonography may be a safer technique than the landmark approach by allowing fewer passes of the needle to successfully locate the internal jugular vein and by identifying anomalous internal jugular venous anatomy [64,65]. Conclusion Jiminez [66,67 ] recently examined trends in ASA paediatric anaesthesia closed malpractice claims over the past three decades (1970s to 1990s). Approximately half of the claims involved patients 3 years of age or younger. The newer data reveal a significant decrease in the proportion of respiratory events (25%) and a rise in cardiovascular claims (27%), paralleling the trends seen by the POCA Registry (especially those preventable with monitoring such as inadequate oxygenation or ventilation, with no significant change for events not easily preventable with monitoring, such as laryngospasm). Despite substantial advances in paediatric anaesthesiology, anaesthesia-related cardiac arrest continues to occur. The majority of complications leading to arrest may be preventable [2,66 ]. The risk of cardiac arrest in paediatric patients can be reduced by placing high-risk children in experienced hands, selecting safer inhalational agents, the incremental injection of local anaesthetics, the early treatment of laryngospasm, avoiding old and irradiated blood that can cause hyperkalemia, limiting the use of succinylcholine to circumstances in which immediate securing of the airway is necessary, keeping up with blood and fluid losses, using safer techniques for central venous pressure line insertion (such as ultrasonography), and the preferential use of epinephrine to treat bradycardia in the presence of hypotension.
5 266 Paediatric anaesthesia References and recommended reading. Papers of particular interest, published within the annual period of review, have been highlighted as: of special interest of outstanding interest Additional references related to this topic can also be found in the Current World Literature section in this issue (pp ). 1 Beecher HT, Todd DP. A study of the deaths associated with anesthesia and surgery. Ann Surg 1954; 140: Morray JP, Geiduschek JM, Caplan RA, et al. A comparison of pediatric and adult anesthesia closed malpractice claims. Anesthesiology 1993; 78: Morray JP, Geiduschek JM, Ramamoorthy C, et al. Anesthesia-related cardiac arrest in children: initial findings of the Pediatric Perioperative Cardiac Arrest (POCA) Registry. Anesthesiology 2000; 93: Mason LJ. An update on the etiology and prevention of anesthesia-related cardiac arrest in children. Paediatr Anaesth 2004; 14: Bhananker S, Ramamoorthy C, Posner K, et al. Changing profile of anesthesia-related cardiac arrests in children: update from Pediatric Perioperative Cardiac Arrest (POCA) Registry. Anesthesiology 2005; 103:A1310. Update of POCA Registry data. 6 Morray JP. Unexpected cardiac arrest in pediatric anesthesia: causes and prevention. American Society of Anesthesiologists: Annual Meeting Refresher Course Lectures, Las Vegas, Nevada. Abstract 2004; 309: Salem MR, Bennett EJ, Schweiss JF, et al. Cardiac arrest related to anesthesia: contributing factors in infants and children. JAMA 1975; 233: Rackow H, Salanitre E, Green LT. Frequency of cardiac arrest associated with anesthesia in infants and children. Pediatrics 1961; 28: Tiret L, Nivoche Y, Hatton F, et al. Complications related to anaesthesia in infants and children: a prospective survey of anaesthetics. Br J Anaesth 1988; 61: Cohen MM, Cameron CB, Duncan PG. Pediatric anesthesia morbidity and mortality in the perioperative period. 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Anesthesiology 1994; 80: Johannesson GP, Floren M, Lindahl SG. Sevoflurane for ENT-surgery in children: a comparison with halothane. Acta Anaesthesiol Scand 1995; 39: Russell IA, Miller Hance WC, Gregory G, et al. The safety and efficacy of sevoflurane anesthesia in infants and children with congenital heart disease. Anesth Analg 2001; 92: Green DH, Townsend P, Bagshaw O, Stokes MA. Nodal rhythm and bradycardia during inhalation induction with sevoflurane in infants: a comparison of incremental and high-concentration techniques. Br J Anaesth 2000; 85: Akeson J, Didriksson I. Convulsions on anaesthetic induction with sevoflurane in young children. Acta Anaesthesiol Scand 2004; 48: Constant I, Seeman R, Murat I. Sevoflurane and epileptiform EEG changes. Pediatr Anesth 2005; 15: A recent study examining the epileptogenic potential of sevoflurane. 22 Haga S, Shima T, Momose K, et al. Anesthetic induction of children with high concentrations of sevoflurane. Masui 1992; 41: Jaaskelainen SK, Kaisti K, Suni L, et al. Sevoflurane is epileptogenic in healthy subjects at surgical levels of anesthesia. Neurology 2003; 61: Baines D. Convulsive movements with sevoflurane. Anaesth Intensive Care 1998; 26: Messeri A. Reflections on sevoflurane. Paediatr Anaesth 2000; 10: Politis GD, Quigg MS. Is fast induction with sevoflurane associated with an increased anesthetic risk in pediatric patients? In response. Anesth Analg 2003; 96: Komatsu H, Taie S, Endo S, et al. Electrical seizures during sevoflurane anesthesia in two pediatric patients with epilepsy. Anesthesiology 1994; 81: Adachi M, Ikemoto Y, Kubo K, Takuma C. Seizure-like movements during induction of anaesthesia with sevoflurane. Br J Anaesth 1992; 68: Bosenberg AT. Convulsions and sevoflurane. Paediatr Anaesth 1997; 7: Holzki J, Kretz FJ. Changing aspects of sevoflurane in paediatric anaesthesia: [editorial]. Paediatr Anaesth 1999; 9: Niejadlik K, Galindo A. Electrocorticographic seizure activity during enflurane anesthesia. Anesth Analg 1975; 54: Dalens B, Hasnaoui A. Caudal anesthesia in pediatric surgery: success rate and adverse effects in 750 consecutive patients. Anesth Analg 1989; 68: Cladis FP, Litman RS. Transient cardiovascular toxicity with unintentional intravascular injection of 3% 2-chloroprocaine in a 2-month-old infant [case report]. Anesthesiology 2004; 100: Desparmet J, Mateo J, Ecoffey C, Mazoit X. Efficacy of an epidural test dose in children anesthetized with halothane. Anesthesiology 1990; 72: Albright GA. Cardiac arrest following regional anesthesia with etidocaine or bupivacaine. Anesthesiology 1979; 51: Groban L, Deal DD, Vernon JC, et al. Cardiac resuscitation after incremental over-dosage with lidocaine, bupivacaine, levobupivacaine, and ropivacaine in anesthetized dogs. Anesth Analg 2001; 92: Clarkson CW, Hondeghem LM. Mechanism for bupivacaine depression of cardiac conduction: fast block of sodium channels during the action potential with slow recovery from block during diastole. Anesthesiology 1985; 62: Mazoit JX, Denson DD, Samii K. Pharmacokinetics of bupivacaine following caudal anesthesia in infants. Anesthesiology 1988; 68: Moore DC, Scurlock JE. Possible role of epinephrine in prevention or correction of myocardial depression associated with bupivacaine. Anesth Analg 1983; 62: Weinberg G, Ripper R, Feinstein DL, Hoffman W. Lipid emulsion infusion rescues dogs from bupivacaine-induced cardiac toxicity. Reg Anesth Pain Med 2003; 28: Sullivan M, Thompson WK, Hill GD. Succinylcholine-induced cardiac arrest in children with undiagnosed myopathy. Can J Anaesth 1994; 41: Rosenberg H, Gronert GA. Intractable cardiac arrest in children given succinylcholine [letter]. Anesthesiology 1992; 77: Linter SP, Thomas PR, Withington PS, Hall MG. Suxamethonium associated hypertonicity and cardiac arrest in unsuspected pseudohypertrophic muscular dystrophy. Br J Anaesth 1982; 54: Larach MG, Rosenberg H, Gronert GA, Allen GC. Hyperkalemic cardiac arrest during anesthesia in infants and children with occult myopathies. Clin Pediatr (Phila) 1997; 36: Baz EM, Kanazi GE, Mahfouz RA, Obeid MY. An unusual case of hyperkalaemia-induced cardiac arrest in a paediatric patient during transfusion of a fresh 6-day-old blood unit. Transfus Med 2002; 12: Brown KA, Bissonnette B, McIntyre B. Hyperkalaemia during rapid blood transfusion and hypovolaemic cardiac arrest in children. Can J Anaesth 1990; 37: Scanlon JW, Krakaur R. Hyperkalemia following exchange transfusion. J Pediatr 1980; 96: Chen CH, Hong CL, Kau YC, et al. Fatal hyperkalemia during rapid and massive blood transfusion in a child undergoing hip surgery: a case report. Acta Anaesthesiol Sin 1999; 37: Buntain SG, Pabari M. Massive transfusion and hyperkalaemic cardiac arrest in craniofacial surgery in a child. Anaesth Intensive Care 1999; 27:
6 Complications in paediatric anaesthesia Lee and Mason Barcelona SL, Thompson AA, Cote CJ. Intraoperative pediatric blood transfusion therapy: a review of common issues. Part I. Hematologic and physio- logic differences from adults; metabolic and infectious risks. Pediatr Anesth 2005; 15: A current review of paediatric blood transfusion therapy and its associated complications. 51 Larson CP Jr. Laryngospasm: the best treatment. Anesthesiology 1998; 89: Domino KB, Bowdle TA, Posner KL, et al. Injuries and liability related to central vascular catheters: a closed claims analysis. Anesthesiology 2004; 100: Bar-Joseph G, Galvis AG. Perforation of the heart by central venous catheters in infants: guidelines to diagnosis and management. J Pediatr Surg 1983; 18: Leech RC, Watts AD, Heaton ND, Potter DR. Intraoperative cardiac tamponade after central venous cannulation in an infant during orthotopic liver transplantation. Anesth Analg 1999; 89: Musumeci R, Hickey PR. Anesthesia in a neonate with tamponade due to massive pericardial effusion. Anesth Analg 1994; 78: Byard RW, Bourne AJ, Moore L, Little KE. Sudden death in early infancy due to delayed cardiac tamponade complicating central venous line insertion and cardiac catheterization. Arch Pathol Lab Med 1992; 116: Cherng YG, Cheng YJ, Chen TG, et al. Cardiac tamponade in an infant: a rare complication of central venous catheterization. Anaesthesia 1994; 49: Collier PE, Blocker SH, Graff DM, Doyle P. Cardiac tamponade from central venous catheters. Am J Surg 1998; 176: Collier PE, Goodman GB. Cardiac tamponade caused by central venous catheter perforation of the heart: a preventable complication. J Am Coll Surg 1995; 181: Fioravanti J, Buzzard CJ, Harris JP. Pericardial effusion and tamponade as a result of percutaneous silastic catheter use. Neonatal Netw 1998; 17: Defalque RJ, Campbell C. Cardiac tamponade from central venous catheters. Anesthesiology 1979; 50: Sheep RE, Guiney WB Jr. Fatal cardiac tamponade: occurrence with other complications after left internal jugular vein catheterization. JAMA 1982; 248: Jiha JG, Weinberg GL, Laurito CE. Intraoperative cardiac tamponade after central venous cannulation. Anesth Analg 1996; 82: Verghese ST, McGill WA, Patel RI, et al. Comparison of three techniques for internal jugular vein cannulation in infants. Paediatr Anaesth 2000; 10: Alderson PJ, Burrows FA, Stemp LI, Holtby HM. Use of ultrasound to evaluate internal jugular vein anatomy and to facilitate central venous cannulation in paediatric patients. Br J Anaesth 1993; 70: Jimenez N. Trends in pediatric anesthesia malpractice claims over the last three decades. ASA Newsletter 2005; 69:8 9. A review of closed paediatric anaesthesia malpractice claims over the past three decades. 67 Jimenez N, Posner KL, Domino KB, Cheney FW. Trends in pediatric anesthesia malpractice claims over three decades. Anesthesiology 2005; 103: A1309. An analysis of the changing liability profile of paediatric anaesthesia.
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