The ancient Greek physician, Hippocrates, first discussed cerebrovascular injuries 2400 years ago. He described them as the onset of sudden paralysis.800 years later; this sudden onset of paralysis was termed apoplexy. During this time, the Swiss pathologist Johann Jakob Wepfer discovered that apoplexy (i.e. cerebrovascular injury) was caused by a disturbance in the blood supply to the brain.
Traumatic brain injury causes more than 80,000 emergency department visit in the elderly population (aged 65 years or older) each year (Gangavati et al., 2009). While motor vehicle accidents are the leading cause of traumatic brain injury (TBI) in the younger population (Susman et al., 2002), studies have concluded to other findings for the older population. More than 50% of TBI in the elderly are due to fall-related injuries, while this population constitutes 20% of all TBIs (Yap, & Chua, 2008).
These numbers are especially important when considering the fact that the population aged 65 years or older is constantly growing (Susman et al., 2002). With this change in the population’s demographics, the number of fall-related TBIs is expected to increase. In addition, this population has several risk factors that predispose them to TBI such as: muscle weakness, impaired balance (Yap, & Chua, 2008), anticoagulant use (Gangavati et al., 2009), comorbid conditions, and age related physiological changes. In fact, with older age, the dura’s adherence to the skull increases, the vessels become more brittle, and cerebral atrophy occurs (Thompson, McCormick, & Kagan, 2006).Thus, it is becoming increasingly important to acquire knowledge about this type of trauma and its respective management. The application of preventive measures and teaching this category of the population is also crucial, when taking into account that falls is one of the most preventable causes of TBI (Thompson, McCormick, & Kagan, 2006) (other causes include: MVAs, assaults…etc).
After presenting the case of a patient who was admitted to the American University of Beirut-Medical center with a diagnosis of intracranial hemorrhage, the pathophysiological process of his injury will be explained, along with the appropriate medical and nursing management, in addition to special considerations and issues.
H.S is a 79 year old male known to have hypertension, diabetes mellitus type II, and prostate cancer since 13 years. His previous surgeries include a cardiac catheterization 20 years ago. He takes Aspirin, Glucophage, Amlor, and Duactin. On 18/11/2010, patient H. was going up the stairs in his building when he fell and hit his head. He lost consciousness for a time that was not identified since no witness was immediately present at the scene.
In the Emergency room
One hour later, at 8:45 pm, he was brought to the emergency department. Upon arrival, the patient was conscious and oriented. He was anxious and agitated, and he reported a pressure pain over his head with an intensity of 9/10 for duration of 10 min. He also vomited upon arrival and after complaining of a stiff neck, a neck collar was applied. His vital signs were as follows: temperature= 36.8C, heart rate= 100 beats/ min, blood pressure= 148/75 mm Hg, respiratory rate= 20 breaths/min. In addition, his blood glucose level was 197 mg/dL. An intravenous line was initiated, blood tests were taken, and a Computed Tomography (CT) of the brain was done. 5 mg of Dormicon were given IV push, and 70 mg of Mannitol were given IV Drip. The CT revealed large right temporal contusion, parietal contusion, large right subdural hematoma and midline shift.
Afterwards, the patient desaturated and he became hemiparetic on the left side. Intubation was immediately done, a nasogastric tube was inserted, and the patient was rushed to the operating room (OR).
In the Operating room
The patient underwent a craniectomy and urgent evacuation of subdural hematoma. Surgery however was complicated by severe bleeding and hypoperfusion. He received fluids and 2 units of platelets were transfused, in addition to 2 packs of red blood cells. After the operation was completed, the patient was transferred to the intensive care unit (ICU).
In the Intensive Care Unit
The patient was semi-comatose, he was withdrawing to painful stimuli, and his pupils were sluggishly reactive. His Glasgow coma scale was 5T. He had a hemovac draining bloody fluid from the surgery site, two peripheral IV lines, one left radial arterial line, and an orogastric tube to dependent drainage. He was intubated on mechanical ventilator (assist control mode) and had an indwelling catheter. A head CT done on 19/11/2010 revealed intraparenchymal bleed, a fractured ethmoid bone, and a basal skull fracture.
The patient had family members visiting him on a daily basis who provided emotional and psychological support. They showed interest and concern over the care that the patient was receiving and participated in the decision making process.
The patient’s management during his stay in the ICU consisted of administration of Mannitol, Kefzol, Epanutin, Nexium, Perfalgan, and Humulin R. He received several blood transfusions when his Hematocrit was too low, and his blood osmolality was monitored. The head of bed was kept elevated to 45. Feeding was started on 22/11/2010 with Fresubin original/NG and on 26/11/2010 he was transferred to the Neurological Intensive Care Unit (NCU).
In the Neurological Intensive Care Unit
On 30/22/2010 he had a tracheostomy inserted and on 01/12/2010 he had a Percutaneous Endoscopic Gastrostomy (PEG). The following days, the patient further deteriorated, he became comatose, he no longer had a response to painful stimuli and his pupils were non reactive. On 5/12/2010, the patient arrested while transportation to CT, the procedure was cancelled and he was returned to the unit after successful resuscitation. The possibility of a Do Not Resuscitate (DNR) order was discussed with the family members, however, they refused. The following day, at 4:45 am, he had an episode of bradycardia that reached 36 beats/min. The code team was informed and ACLS protocol for sinus bradycardia was initiated. The patient however did not pick up and resuscitation was stopped due to medical futility. A flat ECG was recorded, all lines were discontinued, and the body was sent to the morgue.
Pathophysiology and diagnostics
Traumatic brain injury is:”any injury to the scalp, skull or brain” (Mavin, 2008). However, for the purpose of this paper, the pathophysiological process will solely focus on what is pertinent to the previously presented case. When dealing with a patient with TBI, it is important to remember that the consequences do not only include those of a primary injury but of a secondary insult as well.
Primary brain injury
Primary brain injury is the result of the direct impact. The blunt force that occurs (when someone falls down the stairs and hits his head for example) causes a disruption in the cerebral tissue and the brain’s vascular supply. For a detailed explanation of this type of injury refer to figure 1. The movement of the brain inside the skull and the resulting injury is termed coup contrecoup. Coup refers to the area of the direct impact against the object, whether contrecoup refers to the area of the impact of the brain against the skull as a result of movement (Sise, 2001). This process leads to contusion which is accompanied with bruising and hemorrhage into the brain tissue (This was obvious on the first CT that was performed to the patient upon admission).
Acute subdural hematoma
When the surface vessels of the brain are torn as a result of an injury that involves contusion and laceration, subdural hematoma develops. Acute subdural hematoma is defined as the accumulation of blood between the dura and the brain within 48 hours of an injury (Reddy, 2006). An immediate CT scan and blood studies are ordered for diagnosing subdural hematoma. Older age is considered a risk factor for the tearing of the bridging veins and thus for the formation of subdural hematoma (Madden, 2008). Refer to figure 2 for an illustration.
Intraparenchymal hemorrhage refers to bleeding in the brain tissue itself. It is accompanied with a poor prognosis and includes the formation of hematoma and edema which will compress the brain parenchyma and cause neurological dysfunction (Madden, 2008). The shifting of the brain tissue will lead to increased intracranial pressure, if left untreated the latter may be fatal. Refer to figure 2 for an illustration.
Secondary brain injury
As a result of the primary injury, an inflammatory process is initiated: Released cytokines lead to increased vascular permeability and a resulting vasogenic cerebral edema occurs (Mavin, 2008). Biochemical disturbances impair cellular metabolism with neuronal dysfunction as a consequence. Decreased cerebral perfusion may also occur and further increase the extent of the secondary injury (Mavin, 2008).
Symptoms of intracranial bleeding depend on the location of the hemorrhage and its extent. However, important signs include a change in the level of consciousness from a previous state, headache, seizures, focal neurological symptoms, and vomiting (Reddy, 2006). When reviewing these symptoms, it becomes apparent that the patient in the case study exhibited all of them excluding seizures.
In terms of diagnostic tools a CT scan and magnetic resonance imaging (MRI) are ordered to visualize any structural changes in the brain tissue and to identify any hematoma or hemorrhage (Madden, 2008). An angiography may be useful to visualize cerebral vasculature. Blood tests are also ordered, these include: a complete blood cell count (CBC), prothrombin time, activated partial thromboplastin time, and serum chemistry (Reddy, 2006). If the patient’s CT and MRI are negative and he does not show any signs of increased intracranial pressure, a lumbar puncture can be performed (Mavin, 2008). It allows analysis of cerebrospinal fluid and assesses pressure.
Traumatic brain injury is an emergency and it requires immediate intervention. Paramedic reporting of the details of the incident is especially important and can warrant the healthcare providers to the type and location of the injury (Sise, 2001). However, when a paramedic or an eye witness is not present at the time of the incident, the patient’s own recall may be useful. Observation for orientation during questioning is also used for identification of symptoms (Sise, 2001). Immediate assessment and interventions are crucial influencers of the patient’s prognosis and outcome (Madden, 2008).
If a subdural hematoma is apparent on CT, immediate surgical evacuation is needed. According to the surgical guidelines issued on 2006 by the congress of neurological surgeons, the recommendations for surgical management of acute subdural hematoma include: (only the recommendations pertinent to the patient previously presented are mentioned)
> Presence of a subdural hematoma that is thicker than 10 mm on CT
> Presence of a midline shift that is greater than 5 mm on CT
> After assessing the need for a surgical evacuation, it should be performed as soon as possible
> Surgical evacuation is performed using a craniotomy (with or without cranial flap removal)
(Bullock et al., 2006)
For the management of intraparenchymal hemorrhage, surgical evacuation is not recommended as no evidence has been found that it improves patient outcome (Madden, 2006). Treatment is nonsurgical with close monitoring and prevention of complications.
An article published by Lourdes Reddy on 2006 in addition to: The guidelines for the management of severe traumatic brain injury, issued by The Brain Trauma Foundation in 2007 will constitute the basis of the medical and nursing care in the intensive care unit.
Reddy published the following recommendations for nurses when caring for a patient with cerebral bleed:
> Monitor for any arrhythmias on the electrocardiogram (ECG) that may reflect an increase in intracranial pressure (such as bradycardia).
> Maintain the SpO2 above 94% by administering supplemental oxygen.
> Manage hyperthermia with antipyretics and cooling measures (e.g cooling mattress) as it can exacerbate a hypermetabolic state.
> Administer isotonic intravenous fluids to maintain normal volume.
> For the reduction of intracranial pressure: Osmotic diuretics (Mannitol) and antihypertensives (Nitroprusside)
> For preventing/reducing seizures: Anticonvulsants and barbiturates (Phenobarbital)
> To decrease the risk of gastric ulcers: Proton pump inhibitors (Nexium) and Histamine2 blockers
In addition, Reddy gave special importance for increased ICP, since if left untreated; it may prove to be detrimental for the patient. To decrease ICP, Reddy advises nurses to: Elevate the head of bed to 30, prevent hyperextending the head, limit suctioning and procedures as possible, hyperoxygenate the patient before suctioning, prevent seizures, and finally administer neuromuscular blockers as needed to decrease agitation (Reddy, 2006).
After a review of literature, The Brain Trauma Foundation released its 3rd edition of: The guidelines for the management of severe traumatic brain injury. A brief summary of only the main findings is going to be presented:
> Hypotension and Hypoxia are deemed imperative to be corrected by nurses and physicians even with the absence of supporting data.
> Evidence reveals the effectiveness of Mannitol in reducing ICP, while it is not as supportive for the use of hypertonic solutions.
> Data gathered from ICP monitoring is a predictor of the prognosis of patients with TBI. In addition, it has been proven that when decreasing ICP, better management would result if it is coupled with ICP monitoring (knowing that the upper threshold of ICP is 20-25 mm Hg).
> Feeding should be initiated by a maximum of 1 week following injury (Early nutritional support has been found to improve outcome).
> Seizure prophylaxis is not beneficial if it is started more than 1 week after the injury.
> Steroids are not recommended in the management of TBI
Special considerations and conclusion
After comparing these findings with the care that the patient received, it may be noted that his care followed nursing and medical research (although not to a full extent). He underwent a craniectomy with evacuation of subdural hematoma; anticonvulsants (Epanutin) were introduced since his first day of admission to prevent seizures, and feeding was initiated five days after admission. In addition, the patient was receiving Mannitol, and not hypertonic saline, with his osmolality observed. He also received gastric ulcer prophylaxis, DVT prophylaxis, and his head of bed was elevated above 30. The patient’s management however did not follow recommendations in terms of ICP monitoring. His ICP in fact was not monitored.
In conclusion, with the management of TBI being multifaceted and requiring the input of all the members of the healthcare team, standardized clinical pathways and unified guidelines may be recommended. By coordinating patient care and management, they would therefore improve care and eventually lead to a better outcome.