Colleen Bland, RN, BSN, Medical Science Liaison describes the impact of TTM on clinical outcomes of neonates; identifying scientific data supporting TTM in neonates, and helping health care practitioners understand their role in the delivery of TTM to a neonate.
This presentation covers the following learning objectives:
Identify scientific data supporting TTM in neonates
Describe the impact of TTM on clinical outcomes of neonates
Understand your role as a health care practitioner in the delivery of TTM to a neonate
welcome to today's presentation of the science behind targeted temperature management, specifically in the neonatal intensive care unit. My name is Colleen Bland, and I'm a nurse representing the medical affairs division. I hope you enjoy this presentation free of any commercial influence. Let's get started. Today's objectives of this course are going to focus on both identifying all the scientific data supporting targeted temperature management in the neonatal population, as well as describing the impact of temperature management on the clinical outcomes of neo neyts. All this should help you understand your role as a health care practitioner and delivery of targeted temperature management to this neonatal specific population. So why are we here today? You at the bedside play a critical role and both identifying opportunities where these events are going to be at high risk for both the mother or the child communicating in advance when we should be expecting injury because of some sort of hypoxic event, and then really focusing on that early assessment, gathering the team and having grading conversations about how we're going to evaluate the extent of this injury, knowing we have a small window of opportunity to adjust this that may impact an entire lifetime for this child and the family that care for them from birth through the 1st 28 days of life. The unique neuro anatomy of a neonatal helps us understand that even with profound risk of injury, and we are not able to prevent that from happening, this concept of neural plasticity allows us to come in and at least minimize the extent of that injury. Enhance cellular recovery with the goal of somehow impacting the lifeline course of this child, to allow them to meet cognitive milestones, and how that impacts both their quality of life and that of the family in which they are joining. The concept and risk of ischemia is not new to those that practice in the intensive care unit, the gravity associated with global ischemia as that this represents a complete lack of blood flow and the nutrients that it is delivering to both the lungs, the heart, the brain and basically, every cell in the body as there is zero chance of collateral flow in a global ischemic event. If this flow is not restored within minutes, widespread necrosis occurs hypoxic ischemic encephalopathy, or H i E. Is a type of brain damage that occurs when the infant's brain doesn't receive enough oxygen. Hypoxic, which leads to a lack of profusion esque emmick encephalopathy, resulting in brain dysfunction. It is a dangerous condition that requires immediate medical intervention. H i e. Caused by asphyxia is the leading cause of infant fatalities in the United States, as well as the primary cause of severe impairments. There is a broad range of causes of H i E. Any of which can occur before, during or after the baby is born. It is your role in the early recognition and implementation that will hopefully minimize these injuries and maximize neuro protection and recovery. The ante partum phase represents nine months when this developing fetus is at risk of initial pre birth injury. Maternal diabetes may affect micro vascular problems. In terms of profusion, there could be placental disruptions in blood circulation. Preeclampsia, where blood pressure, disturbances and or adhesions of the placenta to the wall, may impact delivery or flow of these nutrients, both cardiac disease in the fetus and in mom, congenital infections of the fetus, drug and alcohol abuse and the nutritional deficits that may be associated with that or respiratory depression that may have affected events in terms of hypoxia, severe fetal anemia and the babies of oxygen carrying capacity, as well as long malformations and profusion. Opportunities for risk. Statistics show that about 25% of all complications occur within that golden hour prior to delivery during delivery or intra partum is about 50% or greater for that percentage of deliveries where HIV is associated most of them from dramatic interruptions and flow, either from hemorrhage cord impairments due to positioning both of the baby and of the mother during delivery, even after the miracle of an event, free delivery risk continues. Postpartum. If there is severe cardiac or pulmonary disease, present infections, including sepsis and meningitis, increased risk, severe prematurity, low neonatal blood pressure, brain or skull trauma or congenital brain malformations. In some cases, however, there are no identical causes for this infant hypoxic ischemic encephalopathy. The damage, however, is real. Some of these risk factors are going to be much more obvious, like cardiac arrest, others specific to the high risk nature of the pregnancy and delivery. Some can only be noticed when they happen, such as shoulder dishdasha or cord prolapse, either way. The early recognition of these at risk will be essential in diminishing cerebral palsy, sensory disruption, learning and motor deficits. Whatever we can do to decrease any impairments in fetal cardiac output and enhance flow to the cerebral brain looking for signs of primary energy failure is going to be focusing on the acidosis after the profound increase in lactic acid from the anaerobic shift in metabolism, as well as the cerebral oedema that may impair respirations, consciousness, tone and reflexes that direct cellular injury and potential necrosis signal screening for the consideration of cooling within that six hours after birth. The goal of timing cooling prior to secondary failure is to both limit global neuronal damage that occurs with the secondary energy failures. This second phase, occurring after six hours of birth, is more associated with the oxidative industry injury of increased cerebral edema, seizures and both side a toxic edema. As we can see, hypoxic, ischemic encephalopathy is not the result of a single event, but rather an evolving process of delayed cell death. By concentrating on the primary causes, we can normalize cerebral blood flow and prevent primary energy failures by instituting targeted temperature management in this latent phase. What we do is enhance brain recovery on no longer able to rely on an intact cerebral auto regulation system. What we have enter ischemic brain injury is that that zone of intact cerebral blood flow shrinks. So by controlling metabolic demand, we're enhancing the mean arterial blood flow in a continued regulatory state and minimizing the amount of oxygen blood flow that needs to go to the head in an already cerebral oedema are swollen brain phase. If we can optimize cerebral oxygen delivery prior to this tertiary phase, our goal is to minimize the chemical messaging that changes during apoptosis. What benefit does it have to your child if you can stop the pre programmed message of cell death to be delivered when we look at how complex just one cell is, it's easy to see how just a small amount of injury can translate into such dysfunction. Imagine, after a global ischemic event where every one of these cells has had some form of impairment, the role that targeted meant temperature management plays provides hope and that it broadly acts in both reducing the amino acid accumulation, reducing the production of nitric oxide protecting and staving off secondary energy failures. The cooler temperatures offload metabolism and preserve those energy chains. They inhibit free radical activity, prevent oxidative injury and stave off cell death. Imagine what this can do to both supporting injured cells and promoting the growth of healthy ones. Yeah, the recognition of injury associated with hypoxic ischemic injury is usually spoken to in terms of two distinct phases of care. The primary or acute phase is an energy failure. Stage depletion of the metabolites leads to anaerobic metabolism. That lack of oxygen and glucose can lead to immediate cell necrosis site. A toxic Kadima shifts in electrolytes, resulting in both acidosis and low. Apgar scores in between primary and secondary phases is considered the ideal therapeutic window in which to optimally time hypothermia. The goal of neonatal cooling is to reduce neurologic injury. Between the primary phase, there is a re profusion that occurs. This return of cerebral blood flow actually causes some oxidative stress, and the secondary or latent phase of injury occurs hours. Two days following the primary phase in this area site, a toxic death can occur both from an inflammatory response. Direct cerebral oedema viso spasm associated with seizures, increase free radical release, excessive calcium exposure and an accumulation of excited oh Tori amino acids. Increasing the work of the brain after the primary ischemic event. Moving on to pre programmed messaging for further cell death and apoptosis, This injury cascade starts quickly and gains momentum by the time the secondary air injury or re profusion injury begins after the first few minutes, it will continue up to 72 hours or longer. The immature respiratory and circulatory systems of premature babies may lend to a more impaired cerebral auto regulation. At what gestational age would you consider cooling at your hospital? Have you had these conversations? So what criteria must be considered for the selection of infants that would benefit from hypothermia? Previous guidelines recommend infants must be 36 weeks gestation or more, targeting the first six hours of age scoring with a SAR net scale. Considering the story of what led up to these events. Checking cord blood gases, checking out acid based deficits all within the golden hour of birth, monitoring for seizure activity, categorizing the level of encephalopathy, determining agreed and realistic goals of therapy. Targeting that first six hours for cooling to be initiated. Yeah, hoping to offload the metabolic demand down to a targeted body temperature of 33.5 degrees Celsius for the next 72 hours where secondary injury would continue, allowing the rewarming from that offloaded temperature back to normal. Neonatal temperature no faster than 0.5 degrees Celsius per hour. Longstanding studies have followed babies greater than or equal to 36 weeks gestation and also equal or below that six hour age limit to be eligible for H i E. Treatment with cooling to be considered. Prior to that, the more immature bait it may be at higher risk of decreased hemoglobin levels. Increased fluctuations in cerebral blood flow. If minimizing this hyper Arcoxia exposure can be offloaded with some demand control with cooling. Could this possibly impact any intracranial hypertension, ischemic lesions or development impairments that could occur based on this most newer studies, as supported by the NAN guidelines, consider cooling beginning at 35 weeks, whether your hospital considers patients at 36 whether they look or consider patients younger to 35 or may even be active in a pre me trial as low as 34 weeks. When the decision has been made to institute cooling. There are trends what's recommended According to neonatal resuscitation. It is to actively and continuously monitor body temperature, maintaining precise temperature management Throughout the therapy, Conversations about cooling should be done early so that the commencement of cooling can be started. An active offloading of body temperature is started within the first six hours. The maintenance of this cooling continues for the next 72 hours. According to clearly defined protocols. Remember never to rewarm the infant faster than four hours from point A to point B or from offloaded temperature to normal. Body temperature should never exceed 0.5 degrees Celsius per hour. Once normal body temperature is reached, it must be actively kept within that normal Rome for the next 24 hours with a strict avoidance of fever. As I mentioned, there is no definitive test for H i e. What we're left with is to rely on tools, tools of assessment tools of piecing together the story of all of the components that went on during this course of events incorporating objective scales. PH Apgar scores. What we tend to look for with an objective scale for encephalopathy is trying to match the impact of that primary injury. With that degree of dysfunction, you may be utilizing an impasse. Finnegan or Sartet scale to figure out which category of encephalopathy your neon eight falls in. We've seen so much hope in what T T. M has shown for the severely injured infants in terms of surviving more and going on to meet more developmental milestones. We do know that 35% of infants with diagnose mild H i e still went on to develop a deleterious short term outcomes. What can we do if incorporating the tools that we know for neural protection and neuro development to enhance the story for these Children? Incorporating high touch with high tech, maybe maternal holding and feeding Early express milk Music story Dr Shank Rin authored some of the landmark trials associated with HIV and cooling. However, to date there is no clear diagnostic test that is positive to whether H. I e. Has occurred. Abnormal Finding the first few days after birth could be a useful predictor that an insult has occurred in the Para Natal period, but with such a small window in which to institute cooling, we can't underscore the importance of the neuro exam. E G, whether it be amplitude integrated or continuous, can be very useful in predicting if there's sub convulsive or any sort of seizure activity going on with the infant. How does your hospital categorize abnormal behavior? Do you do continuous E G. Do you integrate nearest monitoring? Do you have ability of an M R I? So the determination of HIV treatment eligibility is not going to come from the lab. It's going to be a careful conversation, including the infants. Gestational age, current metabolic acidosis, any early onset of enamel abnormal behavior in terms of respirations, consciousness tone or reflex with the goal of limiting further brain injury or multi system organ dysfunction. Neonatal resuscitation drills are practiced. Assessment skills need to be honed. Conversations need to include multidisciplinary specialists and need to be expedited urgently. How does your hospital decide who and went to cool in these critical link? Are you a level three or a level four? Nick, you Do you deliver in house? Do you have to move from our delivery unit to a separate tower for neonatal care? Or will you be working with transport teams to deliver this baby away from their family. Yeah. Either way, you want to immediately commence temperature monitoring either directly or axillary. Babies can easily be cooled by turning off the incubator, opening up the portholes documenting temperature at a minimum every 15 minutes, knowing that large shifts can occur in far less time. As your temperature is falling, you want to make sure that your baby temperature remains above 33 degrees Celsius. If you do not have access to advance cooling mechanisms with a feedback loop, make sure that you are continually checking and either adding a blanket to prevent accidental cooling or removing a blanket or adding a fan until transport can be salt consulted. Ideally targeting a temperature of 33.5 degrees Celsius, there are four distinct phases of targeted temperature management, the first time to initiation. Once the decision has been made to cool, how long before you are actively offloading baby's temperature? The induction should be quick. There's no need to program in a rate of cooling. The goal is to offload below 34.5 degrees Celsius as soon as possible, avoiding any overshoot that would get you below 33.5, maintaining that offloaded hibernation phase for the next 72 hours of the baby's life, followed by a controlled slow rewarm phase never faster than the half degree Celsius per hour as talked about earlier. Maintaining strict temperature control in the next 24 hours following offload in rewarm ensuring that there is an active prevention of fever. Knowing time is brain. What is your goal for managing temperature? Once the decision has been made to prescribe a metabolically offloading cooling protocol, what should you see on your monitors? Heart rate should come down. We want to minimize any stress to the infant throughout therapy, and we want to see that the baby is following down in their cardiac workload up to 15 beats per minute. We should see a degree Celsius correlation. The deeper you cool, the slower the heart rate will continue. Yeah, with the peripheral vaso constriction associated with cooling, you might want to consider placing your lines as soon as possible, depending on how much resuscitation occurred with volume or fluids. You want to pay attention to the intake and output of your neo Nate as renal clearance may speed up because of recently volume resuscitation and enhanced kidney filtration. With the visa construction, the protective trends continue. Not only will you see an offload in cardiac workload, a protection of the neuro functioning, but you'll also see some respiratory components. Most infants will require assisted ventilation during cooling. That temperature may promote more viscosity, and secretions tend to be more sticky. More frequent suctioning with saline and or regular positioning may be necessary. This is a great time to consult with your respiratory team and depending on the degree of encephalopathy, maybe incorporating your family into these maneuvers. Overall, the benefit of cooling is in the reduction of oxygen consumption and c 02 production. The physiological effects of cooling continued to the GI system as well. Spow motility is slowed, although caloric demands are also minimized during cooling. Talk with your care team to find out what the metabolic nutrients are for your newborn. Depending on painful procedures, seizure activity and whether they need to be addressed with TPN or expressed milk, we want to make sure that there's enough fuel available to the cells so the preventing of hypoglycemia will be constantly monitored as cooling continues. We may also see some inhibited insulin secretion, so the prevention of hyperglycemia as just as integral. We want to minimize any opportunities that would cause bleeding in the neon eight. If procedures are deemed acute, unnecessary monitor for using and follow up with blood work. Monitoring white count alone is not going to be the fastest way to screen for infections. Actively preventing fever and slowed metabolism can delayed. These responses continue to screen for a BGS, follow lactic acid, continue with cultures when warranted, and knowing that whatever drugs are ordered for these neon eight's, the metabolism of these drugs may be prolonged. 70% of heat is produced by the neonatal brain. Even with advanced systems, one cannot discount that heat is lost to cooler objects in the room or water evaporating from the skin. Assess your environment in an incubator or not to evaluate for excessive heat and how it may be lost. Do neonatal shiver. Ask a different person and you may get a different answer. Babies rely on brown adipose tissue to help with heat generation. Non shivering Thermo Genesis. It is the primary defense against cold, and it doubles the heat production in neo neyts. However adequate oxygenation is necessary in non shivering thermogenesis. Others have reported that babies with impaired oxygenation have witnessed shivering. Either way, you're going to be monitoring for the skeletal muscle movement if there is no movement, but you're picking up on excessive heat production monitor for the possibility of seizure activity, physical movements like swimming or bicycling of their legs. A temperature management protocol relies heavily on the data that's being supplied to it. A soft vaginal probes have been shown to display the most accurate temperature reading in neo neyts. However, placement may have certain risks to based on the individual. A rectal or esophageal temperature probe is recommended, ensuring that they are monitoring a secondary source to ensure correct placement and valid temperature. When cooling to hypothermia, you may see a cold induced diary sis closely monitor intake and output and see what may be affecting the location of your temperature. Probe. Such large temperature swings in neonatal requiring active support enhanced with an immature central thermo regulatory control, most of this metabolic heat is lost from the skin surface. The focus on the warm chain as well known in neonatal worlds. However, the point of cooling is to reduce the apoptosis of the micro glia, thereby preventing some of the behavioral changes down the road and enhancing mortality. If we're going to support maternal holding, which is feasible, we need to ensure what may affect babies temperature at any one of these links in the warm chain. With so many adjuncts available to help US control temperature, we must continue to meet the baby's demand for high touch during these high tech environments. Way risk versus benefit and time. These interactions synergize ng to allow one and maybe controlling any overshoot with another Routine skin care and assessment are essential. We want to monitor all skin integrity, including the dependent areas where repositioning may cause enhanced pressure. Pressure Ulcers from devices are the most common pressure related injuries in the neonatal period. Avoiding injury Allowing Sarah Thema to resolve keeping the infants clean screening for subcutaneous fat necrosis or cyanosis. Early assessment of calcium derangement may be most beneficial in correcting the effects of morning off subcutaneous fat necrosis. In summary, it is important to properly recognize and manage neonatal patients eligible to receive targeted temperature management. You must be dedicated to patient management in order to effectively cool patients, all sources of heat generation should be assessed and monitored. This 72 hours of neuro advocacy will best to determine the lifetime of neuro disability or delay in the healthy development of this child.
