43 year old female with no previous medical history was brought to the hospital after a motor vehicle accident. She was found to be unresponsive at the scene. The patient was put on the ventilator and CT scan of her head was ordered. CT scan revealed some subarachnoid hemorrhage due to the head injury, otherwise no acute findings. No injuries to the chest, abdomen or pelvis were detected.

Traumatic brain injury (TBI) remains the leading cause of death in the US for individuals between the ages of 1 and 45 years. TBI often leads to significant disability and has a huge socioeconomic impact.

TBI is being classified depending on the prevailing pathological mechanism identified with neuroimaging – primarily CT scan of the head and MRI scan of the brain. Some head injuries, like subdural or epidural hematomas, may require neurosurgery.

The patient above remained unresponsive one week after the accident. Tracheostomy and a feeding tube were inserted. Repeat CT scan of the brain showed some improvement in the extent of the traumatic subarachnoid hemorrhage, yet no new pathology to explain the patient’s poor clinical status.

MRI of the brain was performed and revealed evidence of the Diffuse Axonal Injury (DAI). DAI is a common result of traumatic deceleration injuries and commonly seen after high-speed motor vehicle accidents. The leading pathological mechanism is the disruption of the axons – connections between the nerve cells in the brain.

DAI if often missed or underappreciated on the CT scan since the primary changes happen on the microscopic level. MRI brain is the study of choice to diagnose DAI.

Despite it’s “underwhelming” presentation on the neuroimaging studies, DAI remains a serious cause of morbidity. 90% of patients with DAI remain in a persistent vegetative state. DAI rarely causes death since the brainstem function remains intact.

The injury to the brain is most significant in the areas where the density difference is the greatest. Most DAI lesions, for this reason, occur at the gray-white matter junction. The primary injury often precipitates a cascade of adverse changes on the cellular level leading to further brain damage and atrophy.

The patient remained unresponsive and was transferred to a nursing facility for further treatment.

Middle aged female with no previous medical problems presented as a trauma patient after a motor vehicle accident. The patient had decreased level of consciousness. CT head revealed subdural hematoma as well as frontal lobe contusion. She was taken to the operating room for craniotomy and subdural hematoma evacuation.

Several days after the admission her condition improved and the patient was able to follow simple commands. She was taken off mechanical ventilation. Follow-up CT head revealed evolving contusions in the frontal lobes. (Click on the image above to see a larger version).

Later in her hospital state, she was able to communicate, yet her family noted a striking difference in her behavior. Previously energetic and an enthusiastic person, she was apathetic, inattentive and even inappropriate at times. She was being described by nurses as “not a very nice person”.

Several months after discharge her condition somewhat improved, yet she continued to struggle with a lack of drive, mood swings and distractibility. Neurocognitive evaluating and rehabilitation were warranted.

Frontal lobe, due to its anatomical location is often subjected to injury and trauma. In general, patients with frontal lobe damage suffer from attention disorder and impaired executive function. The patients exhibit difficulties with planning and completing a complex task. Many patients are unable to continue fruitful employment.

Depending on the affected portion of the frontal lobes (orbitofrontal syndrome) the patient could become disinhibited and impulsive. Patients suffer from inappropriate euphoria and poor judgment. Some patients exhibit a peculiar sexual behavior.

If frontal convexity is primarily affected (apathetic syndrome) the patients suffer from apathy, psychomotor retardation and indifference. The patients are generally less talkative and less social. Creativity and problem solving skills are impaired as well.

If the motor strip, located towards the back of the frontal lobes, is damaged the patient might suffer from weakness on the opposite side of the body.

Recognizing the long term emotional and behavioral consequences of the frontal lobe injury is very important for a successful rehabilitation of these patients. Even though they could be subtle, these changes might have a dramatic effect on the quality of life of the injured person.

Cerebral edema (brain swelling) is an “aftershock” of severe traumatic brain injury. Caused, primarily, by vasogenic edema, it usually peaks 48 to 72 hours after the injury. By itself cerebral edema could be detrimental and cause a significant deterioration in the patient’s condition.

The skull is a rigid structure with limited space within it. Once the brain starts expanding within the skull, secondary damage to the brain can occur, primarily, via vascular compromise.

The image above demonstrates the consequences of cerebral edema: loss of white-gray matter differentiation, loss of cerebral sulci, compressed ventricles. You can also see the brain is, literally, bulging out through the craniotomy defect.

The pressure inside the skull, in the patient with a head injury, should be closely monitored. Ventricular drains are being used to monitor the intracranial pressure (ICP) and administer therapeutic interventions like draining the cerebrospinal fluid (CSF) to decrease pressure in the brain. Medications, primarily osmotic diuretics, could also be use to alleviate elevated ICP.

Several studies have shown the benefit of decompressive craniectomy – removing part of the patient’s skull to make more room for the injured brain to expand.

Recombinant Factor 7 (Factor 7) is a synthetic version of the naturally circulating coagulation enzyme. Factor 7 exerts a potent hemostatic effect. Originally, it was developed for the treatment of hemophilia. Factor 7 has been used off label to stop bleeding in trauma patients and to correct coagulopathy in patient taking anticoagulants (Warfarin aka Coumadin).

I like to think of Factor 7 as tPA (thrombolytic) with the reverse action. It is a very potent medicine when used appropriately, yet the side effects could be devastating. With a potent procoagulant action, Factor 7 can cause thrombosis (clotting) in the cerebral arteries causing strokes and coronary arteries causing myocardial infarction. Thrombosis in the mesenteric and peripheral arteries was also reported.

The use of factor 7 for patients with blunt trauma showed reduced blood transfusion and massive transfusion requirements. There was no benefit when Factor 7 was used for penetrating trauma. In both groups of patients there was no mortality benefit.

In my personal experience, I used Factor 7 in an elderly patient with a massive blunt chest injury and uncontrolled bleeding. We were able to control the bleeding, yet the patient developed a disabling stroke attributed to Factor 7.

The application of Factor 7 for the treatment of intracerebral hemorrhage (ICH) is controversial as well. One study found that the use of Factor 7 may limit the progression of hemorrhage, yet there was no improve in survival or functional outcome. Factor 7 in this study was used regardless of the pre-administration coagulation profile. The patients not taking anticoagulants prior to Factor 7 administration may have limited benefit and potentially develop thrombotic complications, offsetting the beneficial effects of Factor 7.

A recent small study out of Texas published in the Journal of Trauma looked at the use of Factor 7 for patients with a traumatic brain injury and preexisting coagulopathy. The study indicates that when used in the appropriate setting (administered to coagulopathic patients with a head injury), Factor 7 was associated with an effective correction of coagulopathy, decreased transfusion rates with blood and plasma, as well as savings associated with the reduction in blood transfusions.

The fact that the cost savings were documented in this study is quite remarkable. Factor 7 is considered very expensive. The cost of 1mg is about 1000 dollars. I have been using Factor 7 in doses ranging from 90 to 120mcg per kilogram. A 70kg patient will get a dose of 7mg on average, costing about 7000 dollars. This is not cheap but any measure.

Having reviewed the literature and having some experience with using Factor 7 I came to the conclusion that Factor 7 has it’s role in the Intensive Care Unit primarily as a rapid coagulopathy reversal agent to facilitate the management of massive bleeding or life-threatening intracerebral hemorrhage.

I have attended multiple meetings in the hospital to facilitate the process of rapid coagulopathy correction with fresh frozen plasma in the patients with intracerebral hemorrhage. At the end of the day, I found that nothing beats Factor 7 when you need to reverse coagulopathy. The same goes for patients on Coumadin with traumatic subdural/epidural hematomas that require urgent craniotomy. In these circumstances it’s not just about saving money by transfusing less blood products, it’s about saving lives.

Riding a bike could be a lot of fun. It could also be dangerous. According to the official statistics, motorcyclists are 37 times more likely than car occupants to die in a crash (per vehicle mile traveled) and 8 times more likely to be injured. There is no surprise here – when riding a bike the protective shell of an automobile is not around you!

What about the age of a motorcycle rider? Does that affect your chances of being injured or even dying in a motorcycle crash?

According to a study conducted in California, yes, the age could be a problem as well.

All motorcycle accidents victims were divided into three age groups in this study:
There were patients younger than 18 years, 18 to 55 years and older than 55 years.

The incidence of severe injury was 23.5% (<18 years), 30.3% (18 to 55 years), 36.2% (>55 years) and the critical injuries occurred in 6.5%, 12.3% and 13.8% respectively.
So, being older does increase your risk of a severe and critical injury in a motorcycle crash.

Older patients were more likely to sustain severe head and chest injury and spinal trauma as well.

The mortality due to motorcycle accidents was also affected by age.
Mortality was increased twofold in the 19 to 55 year old group and threefold in the older than 55 year group compared with the <18 year-old group. Being an older motorcycle rider increases your chances of dying as well.

The study also emphasized the use of helmets to protect passengers from head injury. According to a recent review, wearing a helmet might reduce head injuries by 69% and may decrease the risk of death by 42%. Surprisingly, only 20 states in the Union have helmet laws.

So, if you are getting an AARP card, it might be time to start thinking about ditching that motorcycle. If riding a bike is your thing and you can’t live without it, at least wearing a helmet might help.