Prevention of Cardiac Arrest During Pediatric Anesthesia

Prevention of Cardiac Arrest in Pediatric Anesthesia

From the first analysis of deaths associated with anesthesia in 1954, there have been a substantial percentage of cardiac arrests reported in children, most of these under the age of one year. In this report, 14 children died for every 10, 000 anesthetics performed. Over the last forty years, these statistics have improved dramatically until today the rate of arrest in children is about .3/10,000 anesthetics. In some series, representing ASA 1 and 2 patients in outpatient settings the number is closer to 0/10,000. This is an incredible improvement; how and why has this occurred?

In 1954 and up through the late 1980s the primary volatile agents used in anesthetizing infants and children were highly soluble – ether, cyclopropane, and then halothane. Because of the physicochemical properties of these agents, they were rapidly taken up and distributed. Each was characterized by significant cardiac depression. Mask induction and positive pressure ventilation together were responsible for many cardiac arrests due to reduction in cardiac output. Palliation and/or repair of congenital heart disease was in its infancy in the 1950s. Patients with serious pulmonary hypertension were often unresuscitatible. Monitoring for any patient was primitive at best. No SPo2, no end tidal carbon dioxide monitoring. Technology to visualize the airway in an infant with a congenital abnormality of the head and neck were not available. Training in the care of infants and children in the operating room were not yet available.

In 2013 we can anesthetize an infant with agents that are much less toxic. We can monitor oxygenation, carbon dioxide and blood pressure in every child. Clinicians with specific training and experience care for the sickest infants. We have eliminated many if not most of the problems that increased mortality in infants and children forty years ago.

 Despite the rosy statistics above, in 2013, cardiac arrests still occur in children and many are in children less than one year of age. Current statistics relate most of these arrests to increases in ASA physical status with healthy children much less likely to have a cardiac arrest. Many of these arrests are associated with massive transfusion. Massive transfusion in infants carries the risk of hyperkalemia, hypothermia, and hypocalcemia, which cannot be managed easily once established. Hypovolemia is a significant issue in children that have large tumor loads or trauma. Maintaining an appropriate intravascular volume must be planned for before it starts if one is to maintain any semblance of homeostasis.

The administration of anesthetic drugs is still responsible for a large number of arrests in children. In the past, halothane has been the major offender but has been replaced by sevoflurane in the last twenty years and is not used anymore in the US. Over the forty years that it was marketed halothane was a cause of many deaths in infants. Mask induction with 4% halothane is quite rapid and controlled ventilation without reducing agent concentrations causes rapid uptake of the drug. Because of the reduced volume of contractile myocardium in the heart, uptake in the contractile elements produces a substantially greater reduction in contractility than in an adult. This aspect of its action, associated with bradycardia caused by the drug will reduce cardiac output, often to dangerous levels. Thus, mask induction is more risky in infants. The need to do CPR , especially in training programs, was quite common. Sevoflurane has characteristics that are more protective of the cardiac output. It is a less potent drug, has a MAC value that is stable in the first year of life and maintains the heart rate

Intravascular injection of local anesthetic during caudal block or other regional techniques has been reported on five different occasions to the POCA registry. Training in the recognition of intravascular injection, and the appropriate management of resuscitation should reduce the incidence of morbidity and mortality associated with intravascular injection in infants and children.

Anaphylaxis associated with latex exposure or the use of other anesthetic medications is a medical issue that seems to be eternally with us. Though the re-exposure of patients that have been sensitized to drugs and latex seems to be reasonably well incorporated into the fabric of the operating room, initial exposure with anaphylaxis in patients not known to have been exposed continues to occur. 

Early reports of cardiac arrests in children included many from aspiration and airway obstruction. Current NPO guidelines have reduced the incidence of vomiting on the induction of anesthesia in children and adults. Dissemination of difficult airway pathways, the use of improved equipment, and the introduction of the LMA into clinical practice have reduced the incidence of airway obstruction.

How do we prevent cardiac arrest in infants and children?

1.     The clinical guidelines promulgated by the ASA and other safety organizations (e.g. NPO guidelines) protect many patients from disastrous interventions by the uninformed. We are asked to bend these guidelines daily. Be very careful about second guessing approaches that have been demonstrated to be effective in reducing morbidity and mortality.

2.     Protect the airway if there is any question.

3.     Consider carefully the hemodynamic consequences of a surgical procedure. More IV access is better if there is doubt.

4.     Ask the questions: Is this patient dehydrated? Is this patient profoundly anemic?

5.     Understand the cardiovascular physiology of infants and the problems caused by hypovolemia and low heart rate

6.     For infants and children that require massive transfusion, hyperkalemia will likely be a result. Be prepared to deal with it.

7.     When performing a caudal block use the most benign local anesthetic that can be used. Ropivacaine and levo bupivacaine are much more forgiving than bupivacaine. The dose of intralipid is 1.5 ml/kg rapidly as a bolus followed by an infusion of 0.25ml/kg/min for 30 – 60 minutes

8.     Some children are sensitive to latex. Many have been exposed to latex on multiple occasions.

9.     If it seems to be anaphylaxis, it probably is.

10. Be aware of the issues associated with an anterior mediastinal mass and malignant hyperthermia.

11. Don’t inject anything that you didn’t draw up and label.

12. Be very suspicious of the clinical stability of patients with demonstrated pulmonary hypertension. Hypotension in the face of pulmonary hypertension is very dangerous.

Rae Brown, M.D.
February 8, 2014