Читать книгу Concussion - Kester J Nedd DO - Страница 20
ОглавлениеIN THE CASE of a stroke in the settings of trauma, the compromise of blood supply to the brain requires immediate restoration in order to protect the nerve cells and the supporting cells. To illustrate, JL Saver published an article in a journal called “Stroke” in 2006, wherein he noted that when there are interruptions of major blood vessels to the brain, approximately 120 million neurons, 830 billion synapses (connections), and 714 kilometers (447 miles) of myelinated nerve fibers are lost each hour (Saver 2006).
A compromise in blood circulation, oxygen, and nutrition to the brain can result in the loss of brain cells and their connection if the circulation, oxygen, and nutrition are not restored rapidly following injury.
Secondary effects of trauma
“Time is Brain” deals with protecting neurons before and after an injury from dying and trying to restore their function in as short a time as possible. Once those neurons are lost, there is generally only limited nerve cell regeneration possible in the brain to where there can be significant difference. However, this depends on the severity of the injury, area of the brain involved, and age of the brain.
“Neuroprotection” is a term used to describe this form of protection in the nervous system.
| Image # 6 – Neuroprotection |
Estimates of the total amount of neurons in the brain depending upon age range from 10-100 billion neurons (Pakkenberg 1997).
Years of clinical research and experience gleaned from caring for patients in emergency situations have allowed us to develop some key principles to manage TBI and concussion in the field and in the hospital setting to allow for neuroprotection. While those principles are simple, they have a profound impact on the outcome. Employing these methods of early resuscitation can radically change the outcome of a critically ill patient. These principles have been established as part of the basic cardiac life support (BCLS), advanced cardiac life support (ACLS), and advance trauma life support (ATLS).
The key elements in the resuscitation of a traumatized unconscious patient are the ABCs, i.e., Airway and Breathing first, followed by the Circulation of blood. Although providing oxygen by establishing access through the breathing apparatus is critically important, it has been proven that keeping proper circulation by pumping on the chest to keep blood flowing from the heart, in situations where the heart fails to pump blood, is quite effective even if there is not an airway (Sathianathan 2016).
Addressing the critical intervention in Mario’s case (#1) in order to preserve the brain cells
The measures of neuroprotection were performed in the field by his friend and the first responders, which resulted in some degree of stabilization until Mario was transported to a major medical trauma center capable of further interventions.
Restoration of respiratory function
Mario was in a coma in the period immediately following his injury and could not breathe on his own. He needed to be intubated to ensure the cells in the brain received oxygen via his respiratory system (lungs). Oxygen is an important element in the combustion of the fuel sources, such as glucose, proteins, and fats to produce energy, and is critical for each cell in the body to stay alive and function. The energy produced by the cell is utilized to produce electric currents in the body responsible for the messaging system which allows us to function. If there is no oxygen, this combustion cannot take place, hence leading to no energy in the body. Those of you who know about engines understand that gasoline is the fuel that mixes with oxygen from the air and combusts by a spark plug to produce the energy that makes a vehicle move. The body utilizes oxygen and fuel (glucose) in the same manner to produce energy. In fact, some of the energy developed is dissipated immediately to make the vehicle move, while others are stored in a battery system for later use. In the body, when energy is produced, it is preserved in a chemical battery storage system present in every cell called adenosine triphosphate (ATP). You can only imagine now what would have happened to Mario if he was not intubated (Airway) and placed on a ventilator (breathing machine) so that his body system could continue working by acquiring oxygen. The importance of respiratory function following TBI/concussion is a critical factor in the resuscitation of patients, since the lack of oxygen prevents energy production. If not addressed early, this leads to cell death, ultimately disrupting the brain hierarchical organization and restoration process (Brenner 2012, Alai 2019).
Clinicians rarely get to see what happens in the moments following a TBI/concussion, except if you are a team doctor in the field at the time of the injury. I had the opportunity to see someone in the immediate period following a TBI/concussion and witness the events as they transpired thereafter.
I was attending a function and was about to enter the building when a young boy (Hal, Case # 7), about 12 years old without looking to the right or left, ran across the street to catch up with his friends, who had already safely crossed the street. I saw the boy running into a moving vehicle (SUV) as it came around a corner. He was thrown about 12 feet from the vehicle and ended up on the sidewalk. The first to arrive on the scene, I had the rare opportunity to see what happens in the immediate period after a TBI/concussion. The 12-year-old boy was limp, unresponsive, and not breathing, but had a normal pulse indicating that the heart was working. Meanwhile, the ABC of resuscitation was first and foremost in my mind to ensure that Hal would not suffer hypoxia (lack of oxygen) to the brain. The ambulance was at least 10 minutes away, and there was no emergency management equipment available. Within 90 seconds, the patient was breathing and hyperventilating when he opened his eyes and started looking around. In Hal’s case, the impact caused a concussion to the brain that temporarily knocked out the reticular activating system (RAS) responsible for consciousness and arousal and the chemoreceptors system responsible for breathing.
The central chemoreceptor system responsible to sense high levels of carbon dioxide and hydrogen is a center located in the brain stem, at the point where the brain and spinal cord meet, called the Medulla Oblongata (Nattie 2012). There are also peripheral chemoreceptors located in the bodies of the carotid and aortic arteries that sense carbon dioxide, oxygen, and acidity (Detweiler 2018).
Without spontaneous breathing (when breathing stops), carbon dioxide accumulates in the blood and the oxygen levels plummet. Under such conditions, carbon dioxide is not expelled if there is no expiration (breathing out), and oxygen levels plummet if there is no inspiration (breathing in). Note that from the combustion of oxygen and glucose, the result is the production of carbon dioxide, which is the gas we breathe out from the lungs primarily (think of what comes out of the muffler in your car). These chemoreceptors (sensors) in the brain stem pick up such high levels of carbon dioxide when someone stops breathing. The stimulation of the carbon dioxide chemoreceptors serves to drive the desire to breathe without even thinking of breathing. The chemoreceptor system is part of a primitive system of breathing seen in mammals, which developed as a part of our survival. We often refer to this drive to breathe as the hypercarbia drive.
A similar system exists when there are low oxygen states called the hypoxic drive. The hypoxic drive is only responsible for 10% of the drive to breathe. This occurs when the partial pressure of oxygen (PaO2) falls below 70%. The hypercarbia or hypercapnic drive is responsible for 90% of our drive to breathe.
The goal of hyperventilating or the increased rate of breathing is to reduce the amount of carbon dioxide that accumulates and to restore normal levels of oxygen as a result of low oxygen states, such as when Hal stopped breathing for approximately 90 seconds. High levels of carbon dioxide and low oxygen states cause the bloodstream to become acidic, which is bad for the body. When there are low oxygen states in the body, the cells cease to produce ATP, the chemical energy storage battery system needed to keep us going.
When the chemoreceptors in the brain stem responsible for breathing and the systems responsible for arousal are suppressed or damaged, the will to breathe is reduced or completely suppressed. To ensure survival, an organism must rely on mechanical means to continue breathing, hence the need for ongoing mechanical ventilation (ventilator or breathing machine) in persons with severe TBI, where there is suppression of the chemoreceptors in the brain stem. Patients who are unable to restart their breathing due to severe TBI (causing damage to the hypercarbia chemoreceptors centers in the brain stem) will need external/mechanical or artificial respiratory support, such as mouth-to-mouth resuscitation or with an ambu-bag or ventilator. It should be noted that in Hal’s case, he was spontaneously hyperventilating after he came to himself.
These measures are critical to preserve brain function in severely brain-injured victims and avoid a cascade of further injury.
Another system that was important in Hal’s case was the RAS, located at the back of the brain stem (midbrain and pons), which allows for arousal and unconsciousness. This system was also temporarily injured due to Hal’s concussion, but within 90 seconds after injury, he was aroused from his state.
Addressing the issue of blood supply
Mario (Case #1) experienced a common phenomenon that is seen in individuals with severe TBI called bradycardia. Bradycardia is the slowing down of the heart rate, usually to a level that impairs blood flow. Bradycardia in TBI is caused when there is an expanding mass in the brain, causing increased intracranial (inside the skull) pressure. The increased pressure in the brain caused the stimulation of the vagus nerve, which ultimately slowed down the heart rate. The vagus nerve originates in the brain stem (lower portion of the brain), and by its connection to the heart, it can influence the rate and extent of heart muscle contractility. When the heart rate is slow, it means the pumping capacity of the heart is reduced, and blood supply to the brain and other organs becomes compromised. In the normal human brain, cerebral blood flow (CBF) is approximately 50–60 cc/100 g/minute. When CBF drops between 20–30cc/100g/min, there is a loss of electrical activity due to diminished production of energy. Neuronal cell death occurs when the CBF falls below 10 cc/100g/min. (Bullock 1996) Low blood pressure and blood flow ultimately cause diminished tissue perfusion, which can be caused by bleeding, cardiac arrest, slow or irregular heart rate, diminished ability of the heart to pump (heart failure), medications, infections, and the lack of fluid intake.
Addressing increase intracranial pressure
While Mario was given drugs to speed up his heart and increase his blood pressure, relieving the intracranial pressure in the brain was the only assured way to gain control of the low heart rate (bradycardia) and prevent the continuous dropping of his heart rate and blood pressure in the period following his injury.
| Image # 7 – Vagus nerve ICP and the heart |
As a result, the next intervention to preserve the brain was performing a craniectomy to give the brain room to expand and reduce the pressure. Given the restricted space within the skull, there was not much room for the brain to accommodate the swelling. The increased pressure (increased intracranial pressure or increased ICP) was caused by massive swelling in the brain. Increased ICP was also the result of a subdural hematoma (bleeding in the space between the covering of the brain called the dura and the brain itself), causing the brain to shift from the right to left. The shift was due to the “mass effect,” i.e., the subdural hematoma caused it. Increased ICP results in diminished blood supply and oxygen to the brain cells, as the heart has to pump blood into a high-pressure system and has to work harder to do so. Mario’s emergency craniectomy was lifesaving, as it helped to mechanically relieve the pressure in the brain ultimately eliminating the bradycardia and allowing for the restoration of blood supply to the brain. In this case, the goal was to preserve nerve cells by mitigating further cell death. His heart rate and blood pressure improved to normal levels following the craniectomy as the vaso-vagal response caused by the vagus nerve stimulation ceased, and the additional work required by the heart to pump blood into a high-pressure system was reduced.
A review of the literature performed by Barthelemy et al. and published in World Neurosurgery showed decreased mortality (death) and improved outcomes in patients aged 50 and under when decompressive craniectomies were performed in less than 5 hours following TBI (Barthelemy 2016).
For persons with more severe injuries such as a TBI, where hemorrhaging causes the mass effect (pressing on other brain structures), an emergency craniectomy (removal of portion of the skull) or craniotomy (opening of skull) for the removal of blood products or a craniostomy, creating a hole for the placement of a catheter in the ventricular (fluid channel in the brain) can result in the reduction or elimination of increased intracranial pressure in the brain. These measures, if implemented in a timely manner, can reduce or eliminate cellular edema and cell death in the brain and preserve brain hierarchical organization.
Neuroprotection through primary and secondary prevention
You must have heard, “An ounce of prevention is better than a pound of cure”. Our ability to preserve the brain hierarchical organization starts with measures to prevent and mitigate injury in the first instance. Such preservation and prevention of injury are called primary prevention. In this fight, prevention is our first line of defense. Primary prevention includes safety education and prevention measures, such as the use of helmets and seat belts, the development of safer cars, and regulatory policies that promote personal safety and the safety of others to avoid injury or to mitigate the severity of any injury. Drunk driving, seatbelt, and helmet laws have heightened standards for safer cars and reduced the number of traffic accidents over the years. These laws have increased the chance of surviving an accident and preserving brain organization.
Primary prevention related to the wearing of helmets to really protect American football players was not established until 1973 by the National Operating Committee on Standards for Athletic Equipment (NOCSAE) (Clarke 1979).
Shortly thereafter, in 1976, rules for leading with the head when blocking and tackling were established. After helmet standards were adopted, fatalities dropped by 74%, decreasing head injuries from 4.5/100,000 to 0.69/100,000. So yes, contrary to popular beliefs, better helmet technology can make a difference (Levy 2004).
In the state of Florida, there was a time when helmet laws were fully enforced. Effective July 1st, 2000, Florida’s Universal Helmet Law was amended to exclude riders ages 21 and older with insurance coverage of at least $10,000. I still cannot fathom how legislators could respond to the pressures of financial gain in this way. Word on the street has it that the short-sighted legislators in Florida felt threatened that bikers would pull out of the famous “bike week” during which riders from all over the world came to Florida and pour a significant amount of dollars into the state’s coffers. A study by Kyrychenoko and McCartt in 2006 showed that helmet use declined from almost 100% in 1998 when the helmet law was fully in effect to 53% when the law was amended. The rates of death from motorcycle crashes in Florida before the law changed (1998–1999) was 30.8 per 1000 crash, and that changed to 38.8 deaths per 1000 crash between 2001 and 2002 after the law was changed (Kyrychenko 2006).
In this period, in the trauma center at Jackson Memorial Hospital, we saw a decline in the number of motorcyclists reaching the hospital for medical attention after the law was changed. We attributed this to the fact that many of the motorcyclists declined the use of helmets, and thus, many of them died following an accident before reaching the hospital. State and Federal Laws have in the past 5 decades weakened motorcycle helmet laws. According to a paper published by the Journal of Public Health Policy, “universal motorcycle helmet laws effectively promote helmet use compliance, reduce morbidity and mortality in motorcycle crashes, and lower the health care costs and associated societal burdens of these crash victims. In road traffic accidents due to motorcycles, helmets clearly saved lives.”
Secondary prevention entailed avoiding a second injury or the reoccurrence of the same or similar injuries. The issue of secondary prevention arose in the case of Mario, the patient with severe TBI. For athletes who feel the pressure to return to play before completely recovering from a concussion, second impact syndrome (SIS) can be their fate. Today, the entire sports medicine world is involved in preventing SIS, and clinicians have become sensitive to this issue. Experiencing a second injury before the brain fully recovers can cause a devastating cascade of physiologic events that ultimately result in massive brain swelling with the death of critical brain cells (McCrory 2001, Prins 2013).
Neuroprotection through secondary prevention
| Image # 8 – Secondary prevention |
Secondary prevention measures are also utilized to prevent the worsening of a current injury, and this includes the administered treatment interventions. Whenever there is an injury, our most important early treatment goal should be aimed at preserving the brain hierarchical organization, utilizing various methods to allow for neuroprotection. This can be achieved by the timely implementation of interventions that prevent the death of nerve cells by reducing the impact of the cascade of negative physiological events that occur after brain injury.
Various measures can be implemented per emergency and on an ongoing basis to prevent further injury or to prevent the negative cascade of physiological events that occur in the brain following injury. These secondary prevention methods also include early rescue measures to prevent or reduce further injury. In the case of Mario, his friend removed him from the water to prevent drowning and then made the critical phone call to the emergency medical response team. The paramedics were the first medical responders; they instituted early life-saving measures to protect and preserve the brain cells and brain architecture important for maintaining the hierarchal organization of Mario’s brain.
Let us now examine the events as they transpired to provide secondary prevention and neuroprotection in the case of Mario.
The “first responder” in the field were paramedics, and they performed the following secondary prevention measures:
• Early intubation measures to ensure adequate oxygen going to the lungs
• Intravenous (IV) fluids to support his blood pressure
• The administration of life-saving medications to stop his seizures
Despite the early intervention by the first responders, the emergency medical management team in the trauma center, neurosurgical intervention and management in an ICU equipped to handle critically ill neurosurgical patients, and neuroprotection measures to restore cerebral blood flow and oxygen and manage the increased intracranial pressure, Mario’s brain function couldn’t be sufficiently restored. Without those measures, however, he would not be alive today.
Even with all the measures taken, Mario’s brain was severely disorganized with the functional disruption that rendered him to stay in an unconscious comatose state, as he was not responsive to the external or internal environment. When I first evaluated him some three months after the initial injury, his nervous system was disrupted to the degree that he could not maintain physiological homeostasis. Physiological homeostasis refers to the body systems working together in a balanced manner.
In neuroscience we say, “Time is brain,” and the faster we provide definitive intervention, the more likely we are to preserve nerve cells, thus preventing cell death. With the preservation of nerve cells, the likelihood of recovery and preservation of function and hierarchical organization significantly improve.
