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Friday Refresher Courses

By Kate Gentry, MD
Seattle Children’s Hospital

Refresher Course: Physician Wellbeing
Haleh Sadaat MD (Nationwide Children’s Hospital, Columbus) spoke about the important yet under-appreciated issue of physician wellness during the Friday afternoon refresher course session. We all recognize that the practice of anesthesiology can be stressful; what can we do to foster resiliency and prevent burnout in ourselves and in our colleagues?

When we talk about “stress,” it can have many meanings—some positive and some negative. A good type of stress comes from challenges; without challenges we would never learn new concepts or develop new skills. Most often, though, we talk about stress in the context of “being stressed out.” This translates to an imbalance of demands compared to an individual’s (or a system’s) resources and capabilities. Exposure to a prolonged occupational stress can lead to burnout, characterized by the following triad: feelings of inadequacy, emotional exhaustion, and depersonalization/cynicism.  Burnout can manifest itself physically, mentally, emotionally, and behaviorally.

To be resilient is to thrive despite or even because of stressors. It is a dynamic process, not an inherent trait; to become resilient one needs to develop coping skills. Resilient individuals see challenges as opportunities for growth, and are able to establish equilibrium after a setback. Pathological responses to stress can occur when a stressor is so frequent that there is no time for recovery, when an individual fails to adapt their response to the same stressor, when there is a failure to dampen the stress response, or when there is a failure to even mount a stress response.

Depression and burnout are common in medical students, residents, and practicing physicians. Dr. Sadaat presented data from studies of individuals at each level of training that illustrate this point. Two serious consequences of depression and burnout include suicide and medical errors. Suicide is the leading cause of early death among physicians, with a rate ranging from 28-40 per 100,000, as compared to 12 per 100,000 in the general population. Particularly surprising was that female physicians have a suicide rate that is 3-4 fold higher than that of male physicians.

Studies have also found links between the depersonalization and emotional exhaustion characteristic of burnout, and increased rates of medical errors. We all acknowledge the negative effect medical errors can have on patients and their families; what we don’t necessarily recognize is the negative impact medical errors have on the involved health care providers. We are usually our own worst critics, and medical errors can lead to what is called the “second victim phenomenon.”  

There are several proposed solutions to the second victim phenomenon that aim to prevent and recognize burnout, promote team empathy, and encourage open discussion of errors. In a wellness initiative aimed at preventing burnout at Yale, Dr. Sadaat created an intervention that had three major components: (1) identify the problem(s), (2) analyze the pattern (of responses), and (3) explore resources to help one cope. A key feature of component two is modifying one’s cognitive and appraisal processes. Through cognitive restructuring and reframing of stressors and events, one can develop healthier responses. Some recommended tools included: listening to your own self-talk, challenge negative thoughts, building a personal network of social support, and engaging in activities shown to help with stress management such as exercise, eating well, doing breathing and muscle relaxation exercises, and practicing refusal skills when tempted by drugs and alcohol.

It is apparent that wellness needs to be taken seriously by individual practitioners as well as by employers.

Refresher Course: Neonatal Anesthesia
Julie Niezgoda, MD (Cleveland Clinic, Cleveland) provided a helpful refresher course on neonatal anesthesia. We all recognize that neonates are among our most fragile patients, and it is always worthwhile to review the pertinent physiology, pharmacology and anesthetic issues specific to this population.

Beginning with the cardiovascular system, Dr. Niezgoda reviewed the transitional circulation and the incremental decreases in PVR that occur at birth, then at 4-6 weeks, and finally leveling off by 6 months. Neonatal cardiac output is more dependent on heart rate than stroke volume, due to a number of factors. A higher proportion of Type 1 collagen makes the tissue less compliant, and the cellular components that are expressed in the neonatal myocardium handle calcium differently than in adults, making the neonate very dependent on extracellular calcium. While ventricular diastolic function improves significantly in just the first month of life, systolic function remains relatively unchanged during the first six months. Parasympathetic innervation is more developed in the neonate, and there is a predominance of cholinergic receptors on the myocardium. The newborn has high levels of circulating catecholamines, and as such the myocardium is already maximally sympathetically stimulated and has little reserve for increasing cardiac output in response to stress. Sources of cellular energy are mostly limited to glucose and glycolysis, whereas adults can utilize long chain fatty acids. Thus, low cardiac output syndrome should be addressed from multiple angles, including optimizing volume status, hemoglobin, glucose and calcium levels, and optimizing contraction/relaxation with the use of the PDE inhibitor milrinone.  

Features of the neonatal respiratory system include a compliant chest wall and stiff lungs, and a flat diaphragm that contains only 25% slow twitch fatigue resistant fibers. Closing capacity is higher than FRC, meaning that even at normal tidal breathing small airways are prone to collapse, resulting in intrapulmonary shunting. This is why PEEP is so helpful when ventilating neonates. Decreased respiration or apnea is a common neonatal response to a number of stimuli. The response to hypercapnea is depressed, and the response to hypoxia is biphasic, with initially increased ventilatory drive, followed by a decrease. Other pathophysiologic states that trigger apnea include hypoglycemia, hypocalcemia, hypothermia, and anemia. Vagal stimulation of the airways, as well as lung inflation, also can cause apnea.

Anesthesiologists rely on oxygen a great deal to provide a margin of safety when caring for our patients. However, there is significant evidence suggesting that high O2 concentrations are not good for neonates. In the late 1980s, Saugstad proposed that many of the complications experienced by premature infants such as bronchopulmonary dysplasia, retinopathy of prematurity, periventricular leukomalacia, necrotizing enterocolitis, and patent ductus arteriosus are all different organ systems’ manifestations of an “oxygen free radical disease of the newborn.” What is still not clear is how detrimental brief exposures to high oxygen tensions may be, as can occur during neonatal anesthetic exposures.

Key points about newborn renal physiology include a low GFR, probably due in part to low systolic blood pressure, and high renal artery resistance. GFR increases incrementally in the first two years of life, and by 2 years urine concentrating ability is nearly equal to that of adults. The net effect of the neonatal renal state is that the infant has a decreased ability to clear medications and handle volume and electrolyte loads.

In terms of the liver, nearly everything about neonatal liver function is decreased, including Phase 1 and Phase 2 drug metabolism, blood flow, insulin responsiveness, total protein and albumin, alpha-1 acid glycoprotein, and clotting factor synthesis.

Dr. Niezgoda introduced the “conundrum” of neonatal coagulopathy that was described in a 2012 paper by Revel-Villk (1). Basically, although there are deficiencies in many clotting factors in premature infants and neonates, the system is “balanced” such that in healthy neonates, hemostasis is normal.

We all know that babies are prone to hypothermia under general anesthesia. The reasons are multifactorial, including a baseline vulnerability to heat loss due to large body surface are to volume ratio, thin skin, and low subcutaneous fat reserves. Heat production is primary performed by metabolism of brown fat, but this response is attenuated by general anesthesia. The most effective strategies for preventing neonatal hypothermia in the O.R. are aimed at reducing radiant heat loss. The consequences of not keeping a neonate warm include norepinephrine release, pulmonary vasoconstriction and increasing PA pressures, resulting in right to left shunting.

Time in the lecture was running short, so the final piece covered in this lecture was how to make neonatal anesthesia safer. Dr. Niezgoda recommended adoption of a checklist with reminders regarding the preoperative history, surgical issues likely to be encountered, and elements of good O.R. set-up. Other advice included having a go-to reference text on syndromes and their anesthetic implications, implementing policies to ensure that neonates receive PRBCs that are less than seven days old to prevent hyperkalemia, and using code sheets and drug calculators to minimize simple math errors that can occur when administering drugs to neonates.

Obviously, entire textbooks are written about neonates and their anesthetic issues. This refresher course effectively incorporated important basic concepts and pertinent scientific data to make for an interesting and enjoyable review at the end of a full conference day.

Revel Villk, S. Hematology Am. Soc. Hematol. Educ. Program, 2012, 12: 450.

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