Background and Clinical Situation
Traumatic brain injury (TBI), an acquired brain injury and not degenerative, takes place when there is an insult to the brain. TBI may result from a “sudden and violent blow to the head or it may occur when an object pierces the head and enters the brain tissue” (Mangat, 2012, p. 532). The first detailed analysis of TBI, for instance, was the case of “Phineas Gage, a construction worker who, in 1848, survived an accident in which an iron bar went through his skull, seriously damaging the frontal lobe” (Schwarzbold et al., 2008, p. 797). There are mild cases of TBI in which the person maintains consciousness or may show “loss of consciousness for a short duration, usually seconds or minutes” (Mangat, 2012, p. 532). Mild TBI is also associated with other adverse outcomes such as blurred vision, fatigue, poor sense of taste, headache, confusion, memory loss, notable changes in sleep behaviors, patterns or mood swings, and loss of concentration and attention among others. Moderate or severe cases of TBI may also express similar symptoms. However, the intensity of these symptoms is normally high and could get worse or persist for several days. For instance, the patient may suffer repeated vomiting, convulsions, slurred speech, poor or loss of coordination, weaknesses in body limbs, prolonged confusion, agitation, and restlessness among others.
Major interests have been shown on severe traumatic brain injury because it has challenged healthcare providers for many centuries. Once the condition has disrupted the normal functions of the brain, it is difficult to reverse. It is estimated that nearly 1.5 million cases of both mild and severe traumatic brain injury are registered each year in the US alone (Littlejohns, Bader, & March 2003). In addition, about 500,000 people with traumatic brain injury die while another 800,000 do not fully recover and suffer some forms of disabilities. At present, over 5.3 million individuals in the US live with some form of disability that results from traumatic brain injury (Littlejohns et al., 2003). The main injury that takes place immediately during the event results in “the disturbance of axons, body cells and other components of the cell membrane” (Littlejohns et al., 2003, p. 17). This condition results in enhanced deterioration of cell structures and impaired cell functions and finally, the death of the affected cells. Secondary injury takes place due to a lack of attention to “cerebral edema, ischemia, and the chemical changes associated with direct trauma to or systemic effects on the brain” (Littlejohns et al., 2003, p. 17).
One major example of traumatic brain injury is the decreased cerebral tissue perfusion, which results in intracranial regulation disturbances. The essay focuses on decreased cerebral tissue perfusion as an exemplar to demonstrate various processes associated with intracranial regulation disturbances in Traumatic Brain Injury in the context of a clinical situation.
Cerebral perfusion pressure (CPP) is the variation in pressure noted between the Mean Arterial Pressure (MAP) and the Intracranial Pressure (ICP). It is the pressure responsible for cerebral blood flow (CBF) and therefore facilitates the supply of oxygen and metabolite. Under normal conditions, the brain will automatically control these processes to ensure constant supply irrespective of blood pressure status by changing any potential resistance of cerebral blood vessels.
It involves the brain and the central nervous system and therefore effective function of neurons and transmitter is necessary to ensure neurological activities. The brain requires enough perfusion of oxygen, glucose, and blood to ensure normal functions. Intracranial regulation is reflected in movements, perfusion, cognitive abilities, and the exchange of gases. In this case, nurses must identify behaviors that reflect age-appropriate cognitive capabilities and highlight abnormal ones.
However, after any damage to the brain, individuals experience the loss of these normal homeostatic processes. Such damages result in increased cerebral vascular resistance and thus, the brain is much exposed to adverse effects of variations in blood pressure. Specific areas of the brain could be ischemic (inadequate blood supply) or at high risk of ischemia. Therefore, cerebral perfusion pressure results from such impairment in the brain tissues.
Pathophysiology
To determine changes in brain activities, various methods of diagnosis are used. It requires a thorough neurological assessment to ensure that evidence of brain damage can be obtained. Thus, brain imaging is conducted through PET scan, SPECT, MRI, and CAT scan. In addition, the cognitive assessment may be necessary for addition to other forms of physical and social capability assessments.
From a general perspective, the initial stages of TBI are shown through direct damages to tissues and derailed control of CBF and metabolic activities (Werner & Engelhard, 2007). In addition, characteristics associated with ischemia are noted and they can result in the accumulation of “lactic acid because of anaerobic metabolism, high rate of membrane permeability and subsequent edema development” (Werner & Engelhard, 2007, p. 4).
The second stage of TBI pathophysiological feature is noticeable through depolarization at the end of the membrane accompanied by the abnormal release of excitatory neurotransmitters, activation of N-methyl-d-aspartate among other chemicals in the brain. Together, these phenomena cause membrane impairment at the vascular and cellular structures. Finally, they cause the death of cells or apoptosis.
Cerebral blood flow is also a component of pathophysiology in cerebral perfusion pressure. In this case, patients may experience cerebral hyperfusion of CBF >55 ml 100 g−1 min−1 during the initial stage of the TBI (Werner & Engelhard, 2007). In a similar manner, hyperemia is most likely to occur soon after traumatic ischemia. The pathology of hyperemia is equally risky relative to ischemia based on consequences associated with increased CBF that goes above the normal range for metabolic use. Consequently, there is a resultant increase in the volume of the cerebral blood, which causes intracranial pressure (ICP).
At any given moment after the TBI, cerebrovascular autoregulation and CO2-reactivity can be used to offer enough CBF. They are therefore the best indicators for managing cerebral perfusion pressure and ICP. Any adverse effects on these regulatory processes could increase the risk of developing secondary brain damage.
Another factor for consideration in pathophysiological processes is post-traumatic cerebral vasospasm. This is secondary injury, which is responsible for showing the most likely outcomes for patients. The condition normally takes place in nearly one-third of individuals with TBI, and it shows severe brain damage. Differences are observed between the “temporal profile and extent of hypoperfusion with post-traumatic vasospasm and from vasospasm occurring after aneurysmal subarachnoidal hemorrhage” (Werner & Engelhard, 2007, p. 4).
Metabolic dysfunction of the cerebral, which is identified through cerebral oxygen and glucose utilization, and cerebral energy condition (depicted by the availability of phosphocreatine and ATP or through the lactate/pyruvate ratio indirectly) are normally lowered after traumatic events to the brain. They show significant sequential and spatial variations.
Cerebral oxygenation is also evaluated during pathophysiological processes. In this case, there is an imbalance between the supply and use of cerebral oxygen. It is imperative to note that the imbalance results from many various vascular and hemodynamic processes. However, the common result is a condition known as brain tissue hypoxia.
Stress associated with excessive release of excitatory amino acid neurotransmitters is also evaluated. The outcome indicates excitotoxicity and oxidative stress because of “excess extracellular glutamate, which affects neurons and astrocytes and results in over-stimulation of ionotropic and metabotropic glutamate receptors with consecutive Ca2+, Na+, and K+-fluxes” (Werner & Engelhard, 2007, p. 4).
Formation of edema is also considered because it is a common occurrence after traumatic brain injury. In this case, the approach will focus on structural brain damage. Alternatively, water and osmotic imbalance, which may result from either primary or secondary insult, is also assessed. A condition known as vasogenic brain edema, which results from physical or autodigestive impairment or impairment of endothelial cell layer, is also evaluated. These layers are the vital structure for creating the barrier between the blood vessels and brain vessels.
Traumatic brain injury causes several complex cases of immunological or inflammatory tissue reactions, which may be similar to ischemic reperfusion injury. In addition, both types of insults on the brain cause the release of cellular mediators.
Finally, it is imperative to assess different types of cell death that are most likely to take place after traumatic brain injury, which is mainly necrosis and apoptosis. Necrosis occurs because of extreme physical damages to the issue. In this case, the excitatory amino acid may be released while metabolic failure also occurs (Werner & Engelhard, 2007).
Typical and Actual Assessment Findings
Findings have shown that cerebral tissue perfusion results in decreased cerebral blood supply and lowered mean transit period. Hence, there is abnormal hyperintensity in the affected regions. These findings demonstrate vital signs about perfusion alteration after traumatic brain injury in cases of acute ischemia in the affected regions that display abnormality (Galvez, York, & Eastwood, 2004).
The most important objective for assessment is to determine the formation of cerebral tissue presented by evaluating two types of ischemic brain tissue, which include tissues that are most likely to be restored through interventions to ensure normal blood flow and tissues that may not be saved through a similar approach. One major challenge is the identification of these types of tissues from each other and from other nearest tissues that are not at any risk. Abnormalities may indicate severe conditions of ischemic tissue.
Cerebral tissue perfusion is an active field of study. However, hyperintense abnormalities on delicate tissues with decreased blood flow normally show that the conditions may be irreversible.
In this case, the role of the nurse is to monitor and record patients’ neurological conditions and vital signs and rate them against the normal or standard measures. Nurses must also observe key critical changes related to visual activities and speech. At the same time, they must ensure that patients remain comfortable at all times by avoiding straining positions. In addition, nurses must ensure collaboration among members of a multidisciplinary team that offers care to traumatic brain injury patients. This is critical in oxygen and dosage monitoring.
Presenting Signs and Symptoms
The Glasgow Coma Scale is important in assessing patients’ signs and symptoms in cases of brain injury and decreased cerebral tissue perfusion. The Scale assists in estimating and classifying the patient’s conditions related to outcomes of the TBI. The overall scale outcome reflects the patient’s social abilities or dependence on care providers. The measures include verbal/speech capabilities, eye-opening, and motor activities.
Severe brain injuries can be determined through a loss of consciousness for more than six hours with a rating between three and eight on the Glasgow Coma Scale. In such cases, the diagnosis is clear for nurses. However, in other situations with life-threatening injuries, it may not be simple to identify closed head injuries. Lifesaving measures are vital in this process.
Patients may be put on a ventilator and then sedated. During the initial stages, assessment of the brain injury could be restricted because of sedation but can be conducted once the patient has emerged from medications and the ventilator removed. In addition, mild cases of brain injury can only be determined in a later stage once the patient displays difficulties with certain familiar social activities and tasks.
Brian’s injuries that affect specific areas reflect certain symptoms. For instance, clinicians can evaluate any loss in higher cognitive abilities. Insults that affect intracranial regulation, including gas exchange, heart rates, and arousal inhibit vital processes and cause further damages.
Treatment Modalities
After the brain insult has occurred, and specifically in cases of multiple injuries, cerebral blood flow may be impaired to the level of ischemic. Thus, initial interventions focus on the restoration of the normal flow of cerebral blood with highly oxygenated blood. This would inhibit any possible neural death from secondary insults. The critical threshold ranges between 70 and 80 mmHg, and the rate of mortality increases by nearly 20 percent for every 10 mmHg loss of cerebral perfusion pressure. CPP sustained beyond 70 mmHg is responsible for reducing the rate of mortality by as much as 35 percent in cases of severe insults.
It is possible to sustain cerebral perfusion pressure by increasing the Mean Arterial Pressure or by reducing the intracranial pressure. Usually, intracranial pressure is maintained at optimal levels (less than 20 mmHg) while the Mean Arterial Pressured is increased. It is not clear if ICP has any effect when CPP is sustained at an optimum level beyond the critical threshold.
Interventions should focus on increasing blood pressure because available evidence suggests that early hypotension (below 90 mmHg) has been linked with high rates of morbidity and mortality in patients with severe brain insults. A single case of low blood pressure in the ICU could imperatively reduce the prognosis.
Restricting hemorrhage is also important for the patient to ensure oxygenation.
Any attempts to inhibit brain cell death after TBI normally strive to improve cerebral perfusion pressure and manage intracranial pressure. Nurses can rely on brain tissue oxygenation devices to ensure early evaluation and detection of decreased cerebral oxygenation and finally ischemia. It is imperative for nurses to recognize that early detection of brain tissue oxygenation is a more critical assessment of cerebral blood flow and oxygenation. For prevention and treatment of secondary cerebral ischemia, both brain tissue oxygenation and cerebral perfusion pressure should be monitored (Hession, 2008).
In fact, current practices of treatment modalities focus on efficient maintenance of cerebral perfusion pressure after brain injury.
Pharmacology
Decreased cerebral perfusion pressure requires medications to sedate and induce coma in patients after traumatic brain injury to control chances for secondary insults and restrict agitation. Patients may also require seizure medication early enough, particularly if the patient has seizures.
Patients may also need medications for controlling spasticity during recovery of normal functions while behavioral challenges may be controlled through medications. Patients may be given medications for attention issues (amantadine and methylphenidate, bromocriptine, and antidepressants) and any displayed aggressive behaviors (carbamamazapine and amitriptyline) (Dolen, 2010).
Collaborative Interventions
Traumatic brain injury interventions require a team of multidisciplinary professionals. The trauma surgeon must lead and direct other professionals to provide care for the patient. The patient may undergo resuscitation procedures, observe vital functions, focus on life-threatening emerging issues, and ensure care coordination with nurses (Lewis, Dirksen, Heitkemper, & Bucher, 2013).
There are also specific nursing interventions for traumatic brain injury patients, which require evaluations, rationales, and collaborative approaches (Giddens, 2013).
Surgery may be recommended for specific brain insults. Thus, trauma surgeons must also collaborate with surgical staff, including neurosurgeons during interventions. An orthopedic surgeon will focus on skull fractures and other fractures while the general surgeon will perform normal procedures.
Physicians will focus on the patient’s general condition and response to interventions. The trauma team must conduct resuscitation, stabilize and provide supportive care, and nurses have the greater responsibility of coordinating and offering communication support for families and the multidisciplinary team.
After the patient has been stabilized, the team at the specialized trauma care unit will provide subsequent care. This is where the critical care nursing team has a greater role in assessing, monitoring, and interpreting the patient’s vital body or physiologic functions, communicating changes to physicians, conducting regular assessments and communicating with family members, as well as offering required therapies (Mangat, 2012). In addition, critical care nursing must monitor the patient for possible pain or infections.
Respiratory care specialists are also a part of the multidisciplinary team. They conduct resuscitation, ensure oxygen therapy, set up the ventilator, and ensure that they function effectively.
It is necessary to recognize that nurses who provide supportive care for patients in critical care units are highly trained, and they comprehend their roles for traumatic brain injury patients.
Related Concepts
Traumatic brain injury is not restricted to specific individuals or populations. Instead, it can affect any person of any age involved in traumatic events that affect brain functions and leads to decreased cerebral perfusion pressure.
The processes for disease involving traumatic brain injury and cerebral perfusion pressure remain highly complex. Currently, the focus of the study has been on maintaining cerebral perfusion pressure and intracranial pressure to prevent adverse effects on intracranial regulation. Care provided aims to prevent further adverse effects (Haddad & Arabi, 2012).
A traumatic brain injury requires effective care from nurses, physicians, and other family members (Dolen, 2010).
Conclusion
Decreased cerebral perfusion pressure is an exemplar of adverse effects on intracranial regulation after traumatic brain injury. Decreased CPP is most likely to impair gas exchange, cerebral blood flow, and supply of glucose to the body for severe traumatic brain injury cases. Therefore, interventions have often focused on maintaining optimum cerebral perfusion pressure and intracranial pressure and ensuring blood flow to prevent secondary insults and ischemic and other complications. This is the most complex process for a multidisciplinary team, and it, therefore, requires effective care.
The role of nurses, particularly critical care nurses is important because they must coordinate all aspects of care provision with various medical teams and communicate with family members. Sufficient care would ensure improved patient outcomes.
References
Dolen, C. E. (2010). Brain Injury Rewiring for Survivors: A Lifeline to New Connections. Enumclaw, WA: Idyll Arbor.
Galvez, M., York, G. E., & Eastwood, J. D. (2004). CT Perfusion Parameter Values in Regions of Diffusion Abnormalities. American Journal of Neuroradiology, 25, 1205-1210.
Giddens, J. F. (2013). Concepts for nursing practice. St. Louis, MO: Mosby Elsevier.
Haddad, S. H., & Arabi, Y. M. (2012). Critical care management of severe traumatic brain injury in adults. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 20, 12. doi: 10.1186/1757-7241-20-12.
Hession, D. (2008). Management of traumatic brain injury: nursing practice guidelines for cerebral perfusion and brain tissue oxygenation (PbtO2) systems. Pediatric Nursing, 34(6), 470-2.
Lewis, S. L., Dirksen, S. R., Heitkemper, M. M., & Bucher, L. (2013). Medical-Surgical Nursing: Assessment and Management of Clinical Problems (9th ed.). St. Louis: Mosby.
Littlejohns, L. R., Bader, M. K., & March, K. (2003). Brain Tissue Oxygen Monitoring in Severe Brain Injury, I Research and Usefulness in Critical Care. Critical Care Nurse, 23(4), 17-25.
Mangat, H. S. (2012). Severe traumatic brain injury. Continuum, 18(3), 532-46. doi: 10.1212/01.CON.0000415426.76524.e1.
Schwarzbold, M., Diaz, A., Martins, E. T., Rufino, A., Amante, L. N., Walz, M. E… Thais, R. (2008). Psychiatric disorders and traumatic brain injury. Neuropsychiatric Disease and Treatment, 4(4), 797–816.
Werner, C., & Engelhard, K. (2007). Pathophysiology of traumatic brain injury. British Journal of Anaesthesia, 99(1), 4-9. doi: 10.1093/bja/aem131.