nursing case study on head injury

Nursing Case Study for Head Injury

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Chad is a 22-year-old male patient brought to the emergency room after falling from a hotel balcony. He was visiting a resort town and, on a dare, tried to jump from one balcony to another falling three stories. Upon arrival to the ER, he is awake, alert, oriented x 4. There are various scrapes and bruises from head to toe noted upon triage and a large bump near his right temple

What assessments and initial check-in activities should the nurse perform to best assist the patient and law enforcement?

• Full head-to-toe assessment noting all injuries in the documentation. Focused neurological exam with a focus on Glasgow Coma Scale (GCS) and pupillary check. Also, assess for suicidal ideation in case his fall was intentional.

Question - What orders does the nurse expect the provider to give?

• CT of the head and spine to rule out spinal injury or intracranial bleed. BAC, UDS (BAC=blood alcohol content, UDS=urine drug screen) to determine baseline and help guide treatment. Orders for frequent neuro checks including GCS to monitor progression. Place on seizure precautions. No medications that may sedate the patient (i.e. pain meds) yet until the extent of head injury is determined.

Question - What should the nurse be cognizant of caring for this patient?

• How to identify immediate neurologic emergencies (i.e. concussion which may have early symptoms of headache, dizziness (vertigo or imbalance), lack of awareness of surroundings, and nausea and vomiting; these may immediately follow the head trauma or evolve gradually over several minutes to hours) Recognition and management of neurologic sequelae (following neurological injury; examples of sequelae include aphasia, ataxia, hemiplegia and quadriplegia) Prevention of further injury and deterioration

After screening and assessing the patient, the nurse has the following data.

The patient is able to follow instructions and complains of generalized pain but moves all extremities. His protective cervical spine collar remains in place, and he has 18 G IVs in each arm. Pupils are equal and reactive but sluggish. He converses appropriately, opening his eyes spontaneously when addressed. He is cleared to go to radiology for CT.

BAC: 0.5 percent UDS: NO INDICATION of amphetamines, methamphetamines, benzodiazepines, barbiturates, marijuana, cocaine, PCP, methadone, opioids (narcotics) CBC: WNL CMP: WNL EKG: sinus rhythm, no ectopy noted

BP 120/70 SpO2 98% on Room Air HR 62 bpm and regular Ht 175 cm RR 12 bpm Wt 75 kg Temp 36.9°C

What is the patient’s current GCS score? Why is this important before going to the radiology department?

• 15…4 for spontaneous eye-opening, 5 for being oriented, 6 for obeying commands. This is important to have a baseline and to make sure he is stable enough to go out of the department.

Radiology calls the ER at the conclusion of the diagnostic studies. The tech says, “The patient got this weird look on his face and is slow to answer our questions. He also talks like he is drunk. Please come get him.”

What should the RN do now?

• Reassess! Check GCS again. Alert the provider of the findings. Make sure patient is safe (cannot fall, watch for seizures, etc)

Neuro check gives a new GCS of 10. His eyes are closed and only open with noxious stimuli. His speech is garbled and he answers questions inappropriately although he still knows his name. He moans and moves his hand away when painfully stimulated but does not follow commands.

What is a complication may this patient be experiencing?

• Neurologic deterioration after mild TBI is highly suggestive of an evolving intracranial hematoma, which may be intracerebral, subdural, or epidural and usually occurs due to a tear in a blood vessel. Signs include worsening headache, focal neurologic signs, confusion, and lethargy, which may progress to loss of consciousness or even death. In the setting of substantive secondary hemorrhage with deterioration in the Glasgow Coma Scale (GCS), the TBI would be reclassified as moderate or severe.

Are there new orders the nurse might anticipate and/or suggest?

• The patient needs to be reassessed by the provider and/or a specialist. Radiological results may need to be expedited. There are more specialized tests for this injury and should be conducted by a provider since this could be a life-threatening emergency. It may be necessary to transfer to a neuro ICU (anticipate this).

The nurse receives orders to transfer the patient to an inpatient progressive care unit.

What is the best way to give report from one unit to another?

• SBAR: Situation, Background, Assessment, Recommendations. The Joint Commission, Agency for Healthcare Research and Quality (AHRQ), Institute for Health Care Improvement (IHI), and World Health Organization (WHO) recognize SBAR (Situation, Background, Assessment, Recommendation) as an effective communication tool for patients’ handoff. SBAR is a reliable and validated communication tool that has been shown to reduce adverse events in a hospital setting, improve communication among health care providers, and promote patient safety.

After giving a report, the nurse notes that Chad is once again able to follow commands and seems more alert. He says he does not remember going to radiology and complains of a dull headache rated 3/10 on a 1-10 scale with 10 being the worst. His transfer is completed without incident. The nurse documents he is fully alert and oriented x 4 prior to transfer.

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Nursing case studies.

This nursing case study course is designed to help nursing students build critical thinking.  Each case study was written by experienced nurses with first hand knowledge of the “real-world” disease process.  To help you increase your nursing clinical judgement (critical thinking), each unfolding nursing case study includes answers laid out by Blooms Taxonomy  to help you see that you are progressing to clinical analysis.We encourage you to read the case study and really through the “critical thinking checks” as this is where the real learning occurs.  If you get tripped up by a specific question, no worries, just dig into an associated lesson on the topic and reinforce your understanding.  In the end, that is what nursing case studies are all about – growing in your clinical judgement.

Nursing Case Studies Introduction

Cardiac nursing case studies.

• 6 Questions
• 7 Questions
• 5 Questions
• 4 Questions

GI/GU Nursing Case Studies

• 2 Questions
• 8 Questions

Obstetrics Nursing Case Studies

Respiratory nursing case studies.

• 10 Questions

Pediatrics Nursing Case Studies

• 3 Questions
• 12 Questions

Neuro Nursing Case Studies

Mental health nursing case studies.

• 9 Questions

Metabolic/Endocrine Nursing Case Studies

Other nursing case studies.

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Jamaica Amurao, Kenny Dadacay and Josh Perez

Sean is a 21-year-old male who was admitted to the emergency department after being involved in a motor vehicle accident with his sister Anna. Anna was pronounced dead on scene and Sean suffered mild loss of consciousness. Upon arrival to the emergency department, Sean was confused and complained of left upper quadrant pain, which radiated to his left arm. During physical examination, Sean’s vital signs were: BP 123/85 mmHg, HR 95 beats/min., RR 22 breaths/min, Temp, 98.6°F, and an Oxygen Saturation of 97%. Sean’s orders included strict spinal immobilization protocols, EKG, IV fluid bolus, morphine and zofran, ultrasound (FAST), and a CT scan. After the CT scan, Sean lost consciousness and vital signs significantly changed from baseline. Sean’s vital signs were: BP 93/56 mmHg, HR 132 beats/ min, RR 34 breaths/min. Temp, 95.6°F, and an Oxygen Saturation of 89%. The trauma team performed resuscitation interventions and then the patient was transferred to the operating room to treat the cause of bleeding. Sean was hemodynamically stabilized and transferred to the intensive care unit for further monitoring.

• which patient characteristics indicate altered hemodynamic stability and why?
• based on the signs/symptoms what organ might’ve been affected that led to the bleeding and why?
• What is the role of case management in this scenario?

Nursing Case Studies by and for Student Nurses Copyright © by jaimehannans is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License , except where otherwise noted.

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Head Injury Nursing Diagnosis and Nursing Care Plan

Last updated on May 18th, 2022 at 07:54 am

Head Injury Nursing Care Plans Diagnosis and Interventions

Head Injury NCLEX Review and Nursing Care Plans

Any concussion to the brain, skull, or scalp is considered a head injury. A traumatic brain injury can range from a minor bump or bruise to severe head trauma.

The implications and therapeutic interventions differ tremendously depending on what caused the head injury and its severity.

There are two common kinds of head injuries: closed and open.

Any head injury that does not damage the skull is referred to as a closed head injury.

An open (penetrating) head injury occurs when something permeates the scalp and skull, entering the brain.

It is hard to ascertain how severe a head injury is just by looking at it. Some minor head injuries bleed profusely, while others do not bleed at all.

All head injuries should be addressed medically and evaluated by a physician.

Types of Head Injury

• Hematoma. A hematoma is a blood clot formation outside the blood vessels. A hematoma in the brain can be incredibly dangerous. Pressure can build up inside the skull as a result of the clotting. It is indeed possible that the patient may lose consciousness or suffer permanent neurological damage.
• Hemorrhage. Uncontrolled bleeding is referred to as a hemorrhage. Subarachnoid hemorrhage is bleeding in the space around the brain, while intracerebral hemorrhage is bleeding within the brain tissue. Moreover, headaches and nausea are common symptoms of subarachnoid hemorrhages. The amount of bleeding measures the intensity of intracerebral hemorrhages, but any volume of blood can end up causing fluid to accumulate over time.
• Concussion . When an impact to the head is strong enough to cause brain trauma, it is called a concussion. A concussion transpires when the brain collides with the skull’s formidable walls or by sudden acceleration and deceleration forces. In most cases, the impairment of body functions caused by a concussion is only temporary. Multiple concussions, on the other hand, can cause irreversible damage.
• Edema. Also known as swelling, edema can result from any brain injury. Swelling of the surrounding tissues is joint in many injuries, but it is hazardous in the brain. As a result, the affected person cannot stretch the skull to accommodate the swelling. Edema leads to the accumulation of pressure in the brain, causing it to press against the skull.
• Fracture of the skull. Dissimilar to other bones in the body, the skull lacks bone marrow. As a result, the skull is highly resilient and tough to break. Since a broken skull cannot absorb the force of a blow, it is more highly probable that the brain will be damaged as well.
• Diffuse axonal injury. A diffuse axonal injury, commonly known as sheer injury, is a type of brain injury that does not result in hemorrhage but damages cells in the brain. Since the brain cells are severely damaged, they cannot function effectively. It can also lead to inflammation, aggravating the situation. Furthermore, a diffuse axonal injury is one of the most threatening head injuries. Thus, even though this is not as noticeable as other types of brain injury, it has a higher possibility to cause irreparable brain damage, as well as fatality.

Signs and Symptoms of Head Injury

Since the head has more blood vessels than any other part of the body, bleeding on the surface or within the brain during a head injury is a significant concern. However, not all head injuries result in bleeding.

The following are common symptoms of a minor head injury:

• Mild disorientation
• Temporary ringing in the ears
• Whirling sensation

Many of the symptoms of a severe head injury are similar to those of a minor head injury. They may also include the following:

• State of unconsciousness
• Convulsions
• Balance or coordination impairment
• Severe confusion
• Inability to focus one’s eyes for a moment
• Unusual eye movements
• Deterioration in muscle control
• Headache that persists or worsens
• Memory lapses
• Alterations in mood
• Clear fluid leaking from the ear or nose

Causes of Head Injury

The following are the most common causes of head injuries:

• Violent behavior
• Accidents involving cars or motorcycles
• Child abuse
• Fall incidents

When two athletes collide, or a player was hit in the head with a piece of sporting equipment, a concussion or other head injury can also occur.

As a result, the following sports-related activities cause the most significant number of head injuries in people of all ages:

• Riding powered recreational vehicles such as dune buggies, go-karts, and mini bikes
• Softball and baseball

Head injuries are not always the result of sports or trauma. Other causes of concussions or brain hemorrhages include:

• Bleeding disorders such as Hemophilia
• Improper usage of blood thinners or certain recreational drugs
• Long-term hypertension (in adults)

Risks Factors to Head Injury

The following groups are the most vulnerable to traumatic brain injury:

• Children, particularly newborn babies to four-year-olds
• Young adults, particularly those aged 15 to 24,
• Adults aged 60 and up
• Males of any age are eligible.

Diagnosis of Head Injury

• Glasgow Coma Scale (GCS) – This 15-point test assists a doctor, or other urgent care personnel in determining the initial intensity of a brain injury by assessing a person’s ability to follow commands and the movement of their eyes and limbs. The consistency of speech also gives valuable data. The Glasgow Coma Scale rates abilities on a scale of three to fifteen. Higher scores indicate less severe injuries.
• Patient Interview – Evaluating the details about the injury and its symptoms. The answers to the following questions may be critical in identifying the intensity of the head injury:
• Did the individual pass out?
• How long was the individual unconscious?
• Did someone notice any other changes in alertness, speech, coordination, or other signs of the patient’s injury?
• What parts of the body, if any, were struck?
• Provide necessary information about the severity of the injury. For instance, what struck the person’s head, how far did he or she fall, or was the person thrown from a vehicle?
• Was the individual’s body thrown around or grievously shaken?
• Computerized Tomography (CT scan). This test is performed in an emergency room for a suspected traumatic brain injury. A CT scan creates a detailed image of the brain using a sequence of X-rays. A CT scan can accurately identify fractures as well as proof of internal bleeding (hemorrhage), blood clots (hematomas), lacerated brain tissue (contusions), and inflammation of brain tissue.
• Magnetic Resonance Imaging (MRI).  An MRI provides a comprehensive image of the brain using powerful radio waves and magnets. This test is beneficial once the patient’s condition has stabilized or if clinical manifestations do not rectify within a few days of the injury.

Treatment for Head Injury

• Medications. The following medications are used to treat various types of head injuries:
• Anti-seizure medication – may be prescribed within the first week of treatment to prevent any additional brain damage inflicted by a seizure. Seizures are only treated with anti-seizure medications as long as they occur.
• Coma-inducing medications – used to induce momentary comas since an unconscious brain requires less oxygen to function. This medication is incredibly beneficial if blood vessels in the brain are constricted by tremendous pressure and cannot deliver average amounts of essential nutrients and oxygen to brain cells.
• Diuretics – decrease the amount of fluid in the body tissue while increasing urine output. Diuretics minimize pressure within the brain if administered intravenously to people suffering from brain trauma.
• Surgery. Surgery may be an excellent choice to treat the following health issues:
• Removal of coagulated blood (hematomas) – Hemorrhage from the outside or inside the brain can cause blood clot collection, putting much pressure on the brain and damaging brain tissue.
• Repair of fracture/s in the skull – Surgery may be required to fix severe skull fractures or remove skull fragments from the brain.
• Cessation of bleeding in the brain – Head trauma that results in brain hemorrhage may necessitate surgery to cease the bleeding.
• Reduction of intracranial pressure (ICP) – Surgery may alleviate the pressure within the skull by depleting aggregated cerebrospinal fluid in the brain.

3. Rehabilitation. The majority of people who have suffered substantial brain trauma will need rehabilitation. They may need to relearn essential skills like walking and talking. The focus of rehabilitation is to enhance their ability to carry out daily tasks.

Prevention of Head Injury

Depending on the extent of damage, brain injury symptoms can be minor, tolerable, or severe. Sometimes even minor injuries can affect how the brain functions. Follow these prevention tips to lower the risk of traumatic brain injury:

• Put on the seat belt all the time when driving.
• Do not drive while intoxicated in liquor or drugs.
• Avoid using a cellular phone while driving.
• Always put on a helmet while riding a motorcycle.
• Perform actions to prevent slips and falls at home.
• Take good care of children to avoid head injuries at all costs.

Nursing Diagnosis for Head Injury

Nursing care plan for head injury 1.

Risk for Bleeding

Nursing Diagnosis: Risk for Bleeding related to tissue trauma or disturbance of the standard blood clotting mechanisms secondary to head injury as evidenced by petechiae, bruises, blood clot formation, or overflowing of blood.

Desired Outcome: The patient will learn how to prevent bleeding and recognize clinical manifestations of hemorrhage that must be disclosed to a health care professional instantaneously.

Nursing Care Plan for Head Injury 2

Acute Confusion

Nursing Diagnosis: Acute Confusion related to a pattern of memory impairment secondary to head injury as evidenced by changes in cognition, heightened agitation, or alterations in one’s level of consciousness.

Desired Outcome: The patient will have diminished hallucinations and recover normal reality orientation and consciousness.

Nursing Care Plan for Head Injury 3

Nursing Diagnosis: Nausea related to acute concussion secondary to head injury as evidenced by headache and vomiting.

Desired Outcome: The patient will report a reduction in the intensity or complete elimination of nausea.

Nursing Care Plan for Head Injury 4

Acute Pain (Headache)

Nursing Diagnosis: Acute Pain related to traumas and illnesses secondary to head injury as evidenced by severe migraine.

Desired Outcome: The patient will be able to cope with acute pain.

Nursing Care Plan for Head Injury 5

Risk for Seizure

Nursing Diagnosis: Risk for Seizure related to unwanted electrical firing or discharges from cerebral cortex nerve fibers secondary to head injury as evidenced by short, brief episodes of altered state of consciousness, motor functions, and sensory manifestations.

Desired Outcome: The patient will execute safety measures when seizure episodes occur suddenly.

Nursing References

Ackley, B. J., Ladwig, G. B., Makic, M. B., Martinez-Kratz, M. R., & Zanotti, M. (2020).  Nursing diagnoses handbook: An evidence-based guide to planning care . St. Louis, MO: Elsevier.  Buy on Amazon

Gulanick, M., & Myers, J. L. (2017).  Nursing care plans: Diagnoses, interventions, & outcomes . St. Louis, MO: Elsevier. Buy on Amazon

Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2018).  Medical-surgical nursing: Concepts for interprofessional collaborative care . St. Louis, MO: Elsevier.  Buy on Amazon

Silvestri, L. A. (2020).  Saunders comprehensive review for the NCLEX-RN examination . St. Louis, MO: Elsevier.  Buy on Amazon

Disclaimer:

Please follow your facilities guidelines, policies, and procedures.

The medical information on this site is provided as an information resource only and is not to be used or relied on for any diagnostic or treatment purposes.

This information is intended to be nursing education and should not be used as a substitute for professional diagnosis and treatment.

Anna Curran. RN, BSN, PHN

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Case Study: A Blow to the Head

By Tod Schimelpfenig

Mar 14, 2019

The Setting

You are the leader of a hiking group at a summer day camp. Today, you allowed some of your campers with good navigation skills and expedition behavior to walk 3 miles back to your camp on a well-marked trail without a camp leader present.

When the campers arrive, you notice one of them has a bandage on their forehead. You learn that about an hour ago and a mile back on the trail this camper tripped, fell, and knocked their head. You move the group off the trail and conduct a patient assessment. First, you focus on initial care, which means slowing the patient’s very fast breathing. This takes 20 minutes with focused coaching. Then, you move into a more in-depth assessment.

SOAP Report

The patient, a 15-year-old male, tripped and fell while hiking. He struck his forehead on a log. Group members report he did not talk for a few minutes. They say he was “knocked out.” The patient states he remembers the fall and was stunned, but did not lose responsiveness.

At present, the patient is breathing quickly and says his hands hurt. He is alert and oriented to person, place, time, and recent events (A+Ox4), calm, and not distracted. Except for the pain in his hands, he has good circulation, sensation and movement (CSM). The patient walked a mile from the incident site to this location.

The patient has a golf ball sized hematoma (local swelling) on his forehead. No other injuries found. The initial pain in his hands has resolved. Patient specifically denied spine pain, has no distractions, has normal mental status, and CSMs in all 4 extremities.

Vital Signs

Stop reading.

What is your assessment and plan? Take a few minutes to figure out your own assessment and make a plan. Don’t cheat—no reading on without answering this first!

• Low risk mechanism for spine injury. Patient has been ambulatory for a mile and meets criteria for no spine protection.
• Possible mild brain injury/concussion.
• Hematoma on forehead.
• Possible hyperventilation and an anxiety episode.
• Calm the patient and slow breathing.
• Monitor patient for signs and symptoms (S/S) of worsening head injury.
• Have patient walk, without pack, the 2 miles to the parking lot, then drive to clinic for evaluation.
• Stop and seek assistance if patient’s condition deteriorates.

Notes from NOLS on Evaluating and Responding to Minor Head Injuries

Ruling out spinal injury.

In the evolving approach to spine injury management, a simple fall from a standing height is not a mechanism for spinal cord injury. Also, walking a mile, as the patient did, strongly suggests there is no significant spine injury.

The pain in the hands could indicate spine injury, but the rescuer’s careful assessment showed the CSMs were otherwise normal. If you have reason to suspect a spine or spinal cord injury, then a Focused Spine Assessment is a good decision-making tool.

Responding to Hyperventilation

The patient was breathing faster than normal (hyperventilating), which probably explains the pain in his hands (hyperventilation can cause tingling and cramping as well). This very uncomfortable side effect of hyperventilation can be resolved by slowing the breathing, although this may take some time and focused coaching.

Symptoms and Decision-Making Tools for Head Injuries

It may be unclear, as in this scenario, whether someone was unresponsive after a blow to the head. Those present on the scene may not have the skill to make this determination and the "stunned" patient may appear to be unresponsive.

If you are unsure what might have happened, you can make your treatment decision based on the patient’s present mental status, which in this case is A+Ox4.

A blow to the head with subsequent headache, nausea, and fatigue indicates a possible concussion.

Not every head injury requires evacuation. There are situations in the wilderness where signs and symptoms following a blow to the head are minor. In those situations, an appropriate response can be simply to monitor the patient for developing signs of a serious head injury instead of evacuating. This may be reasonable from a medical perspective and practical from a wilderness perspective, especially if location, terrain or weather complicate the evacuation.

With the symptoms observed in this patient, it’s practical to try to walk to patient to the closest road with a backup plan of requesting evacuation support if the patient’s condition deteriorates.

End of the Tale

The patient’s condition does not change during the walk to the road. He urinates once (yellow, not dark) and is able to drink a liter of water and eat some trail mix.

The patient is then driven to a medical clinic for evaluation, diagnosed with a possible concussion, and referred to his family physician for follow-up.

Keep your skills fresh: Recertify with NOLS .  

Further Resources for Minor Head Injuries

Signs and symptoms of a mild head injury include:.

• Brief change in Level of Responsiveness (LOR)
• Temporarily blurred vision or “seeing stars”
• Nausea and/or isolated vomiting
• Headache, dizziness, and/or lethargy
• Personality changes, emotionally volatile

Signs of a more serious or worsening head injury include:

• Worsening headache, vision disturbances, protracted vomiting, lethargy, excessive sleepiness, ataxia (loss of balance) and seizures
• LOR: disoriented, irritable, combative, unresponsive
• HR: decreases and bounds
• RR: hyperventilation, erratic respirations
• SCTM: warm and flushed
• BP: increases and pulse pressure widens
• Pupils: unequal

Evacuation Guidelines for Head Injuries

Observe patient for 24 hours if:.

• The patient is A+O x 3 or 4
• only S/S of mild head injury are present

Evacuate the patient if:

• The patient had a loss of responsiveness or obvious altered mental status, even if they recover to A+O x 3 or 4
• Headache, nausea/vomiting, irritability, or other S/S of mild head injury are not improving after 24 hours

Rapidly evacuate the patient if:

• The patient is not A+O x 3 or 4
• There are distinct changes in mental status (disoriented, irritable, combative)
• There are S/S of serious head injury.
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Tod Schimelpfenig

As a NOLS Instructor since 1973 and a WEMT, volunteer EMT on ambulance and search and rescue squads since the 70s, Tod Schimelpfenig has extensive experience with wilderness risk management. He has used this valuable experience to conduct safety reviews as well as serve as the NOLS Risk Management Director for eight years, the NOLS Rocky Mountain Director for six years, and three years on the board of directors of the Wilderness Medical Society, where he received the WMS Warren Bowman Award for lifetime contribution to the field of wilderness medicine. Tod is the founder of the Wilderness Risk Manager’s Committee, has spoken at numerous conferences on pre-hospital and wilderness medicine, including the Australian National Conference on Risk Management in Outdoor Recreation, and has taught wilderness medicine around the world. He has written numerous articles on educational program, risk management and wilderness medicine topics, and currently reviews articles for the Journal of Wilderness and Environmental Medicine. Additionally, he is the author of NOLS Wilderness Medicine and co-author of Risk Management for Outdoor Leaders, as well as multiple articles regarding wilderness medicine. Tod is the retired curriculum director for NOLS Wilderness Medicine and is an active wilderness medicine instructor

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You are a Search and Rescue (SAR) volunteer working with a team to sweep a trail in the central Rocky Mountains in response to a vague cell phone report of an ill person somewhere on the trail. Eight miles from the trailhead at 8,800 ft. (2,680 m) you find the patient sitting on a log. After introducing yourselves, and with the patient's permission, you and the SAR team members begin an assessment.

The patient was intubated by EMS and brought by helicopter to your level 1 trauma center. A foley catheter is placed. She’s had  CT of her head, neck, chest and pelvis. Her initial assessment reveals the following:

• GCS 6 (No eye opening, no speech, withdraws to painful stimuli)
• Gross hematuria noted in urine drainage bag
• Profuse bleeding from head and open right tib/fib fracture

The patient is taken to emergency surgery for a decompressive craniotomy with bone flap, EVD placement and exploratory laparotomy with bladder repair. She is then brought to you in the surgical ICU. What do you expect to see and do for this patient? Let’s use LATTE!  If you don’t know what LATTE is, check it out here!

L = LOOK: After a decompressive craniotomy with a flap, your patient will have a large gauze dressing on her head. In this case she also has an EVD (extraventricular drain). She will be on a ventilator because her GCS is still 6. And, due to the exploratory laparotomy, she’ll also have an abdominal dressing and possibly a drain. If C-spine is involved, she’ll be wearing a collar, but our gal’s C-spine was cleared…yay!

A = ASSESS:  The main assessments you will be doing on this patient are neurological and hemodynamics. What is she doing neurologically? What is her GCS? Are her pupils equal? Are there signs of shock? Is she bleeding anywhere? And, because she’s vented, you’ll be keeping an eye on her respiratory status as well…is she compliant with the vent? How do her lungs sound? What’s her O2 saturation? Is she breathing spontaneously? What kind of tidal volumes are we getting?

T = TESTS: You’ll do an ABG at some point to make sure she’s being ventilated adequately. You’ll also want to keep a close eye on CBC and coags as you monitor for bleeding and infection. Other labs include a chem panel to keep those electrolytes optimized! Expect to be taking this patient to CT a few times to keep an eye on the bleeding into her brain and any hydrocephalus that may be present. She’ll get a chest X-Ray daily since she’s on a vent and has rib/clavicle fractures. She may also get cystogram studies to keep an eye on how her bladder is doing. Remember she had hematuria…so they’ll want to keep a close eye on that.

T = TREATMENTS: How will this patient be treated? If you read my book, Nursing School Thrive Guide, you’ll recall that I talk quite a bit about prioritizing continuously. The treatments you provide at 0300 could be vastly different from the treatments you’re providing at 0600, based on the patient’s condition. For a fresh post-op patient who’s had a decompressive craniotomy many of your treatments/interventions are going to be focused on keeping the ICP within normal limits. You’ll also be administering pain and sedation meds as well as antibiotics. Depending on blood loss, you may be giving packed red blood cells. Note that we haven’t fixed her open fracture yet…that has to wait until morning when the ortho doc can get to her. So for now we’re just adding additional dressings to the site and keeping an eye on bleeding.

E = EDUCATION: At this point, you’re not providing education to the patient with a GCS of 6. However, you will be educating the family. In this acute phase, you don’t want to overwhelm them with information…it’s going to go in one ear and out the other. The highlights to hit on include: ICP management, pain control and sedation.

It is now 0430 and your monitor alarm starts going off for elevated ICP. It’s 23. Whatcha gonna do? (For a refresher on ICP management, check out this post here!)

First things first…assess your patient, not the monitor. You enter the room and do a quick assessment…this is what you find: head crooked off to one side, knees gatched, temp elevated, tachypnea and dyssynchrony with the ventilator, no drainage since you last drained the EVD an hour ago. Hmmm….what’s wrong with this picture?

Step 1: Straighten the patient’s neck to allow CSF to drain more freely. Step 2: Un-gatch the knees to reduce intrathoracic pressure Step 3: Looks like she might be fighting the vent…increase sedation and pain medication Step 4: Check EVD…make sure there are no kinks in the tubing. In most facilities, policy states that you can BRIEFLY drop the level of the drainage bag to ensure patency…you do this and note drainage in the bag…so there are no kinks or clots. Hmmm… Step 5: Initiate cooling measures…IV Tylenol works great as do ice packs. Be careful of shivering, though! Shivering increases ICP. Step 6: Give it a few minutes and re-assess.

Thankfully the rest of your shift goes smoothly. You report off to Super Nurse, RN and head home for a day of blissful sleep. When you come back in that evening, this is what you hear in report:

• Pt went to surgery at 1000 that morning for ORIF of the right tib/fib fracture, right ulnar/radial fracture and right femur fracture.
• Hgb dropped from 8.5 to 7.2…you are now doing serial Hgb and Hct every six hours. Your next draw is due at 2200.
• Temp spiked to 39.1, cultures drawn, antibiotics continued.
• ICPs still hovering around 18-20. Neurosurgeon changed the height of the EVD from 10mm Hg to 5mm Hg…EVD drainage has been steady at 10ml/hr throughout shift.
• GCS remains at 6.
• Pt still on ventilator.
• Plan is for pt to have pelvic fracture fixed the next day.

Upon your initial assessment you note the following:

• BP lower than it was last night…hovering around 95 systolic.
• O2 sats a bit lower than the night before. They were 98% then, they’re 93-95% now.
• Temp is better…that’s good!
• Lung sounds are mildly coarse.
• ICP 19-20. EVD drainage is good and she’s adequately sedated.

An hour later, you’re at the nurse’s station doing an ungodly amount of charting, when your monitor alarm goes off. ICP is 22. You do all your checks…positioning, temp, EVD patency…all looks good. But her ICPs are still high. As you are doing your assessment, the ICP creeps up to 23-24. Time to notify the neurosurgeon on call.

SBAR Communication

“This is Nurse Sam, calling about your patient Ramirez in Trauma ICU bed 10. She had a decompressive craniotomy yesterday. Her ICPs are holding steady in the 23-24 range. She’s afebrile, well-sedated, compliant with vent. GCS remains at 6 and EVD drainage is averaging about 10ml/hr. What do you think about trying mannitol?”

So, your neurosurgeon thinks this is a fantastic idea and orders Mannitol q 4 hr prn ICP > 20; Check serum sodium prior to each dose; Hold for serum sodium > 146. You give your first dose and watch the monitor as the ICP drops down bit by bit to a more acceptable 14. Go you!

A few hours hours later, at 2230, you notice your patient’s O2 sats have dropped dramatically…they’re now 74%. What the heck? You hustle into the room and amp up the ventilator to give 100% FiO2. As you place your stethoscope into your ears, you quickly assess the ET tube to ensure it hasn’t become dislodged. You listen to her lungs and hear no lung sounds on the right…the same site as her rib fractures and lung contusion. You call for help and immediately take her off the vent and manually breathe for her using the BVM. When your nurse friends show up, you ask one to call RT, one to call the doc and another to put in an order for a stat Chest X-RAY. What is going on?

As you are bagging the patient, waiting for the RT to show up and take over, you notice tracheal deviation off to the left and BP has dropped to 83/54. You relay this to the nurse who is on the phone with the MD, stressing that she needs to get up there STAT! Your patient has a pneumothorax and seconds count. The respiratory therapist arrives to take over the airway and you ask one of your friends to obtain a large-bore needle.  You ask another to grab a chest tube kit…it’s time to get serious folks.

The MD arrives, agrees with your assessment of tension pneumothorax and, using the large-bore needle, performs an emergent pleural decompression. You watch in amazement as the patient’s O2 saturation levels quickly start to climb back to 93%. You prep the pleuravac and monitor the patient while the MD inserts a chest tube on the right side. Good catch!

While you have the doc there, you notify her that the 2200 H&H showed a hemoglobin of 6.9. She orders 2 units packed red cells. You give the blood and, happily, the patient’s O2 saturation and blood pressure both improve. And, with a couple of Mannitol doses your patient’s ICP hangs around 14 for the rest of the night. Nice job…you go home and sleep a beautiful sleep.

When you come on that night, the off-going nurse reports the following:

• Your patient had her pelvic fractures repaired that day, returning from surgery at 1120 with hemovac drain at surgical site.
• The tachycardia that has been present since admission has slowed to normal sinus rhythm, likely due to decreased pain now that all her fractures are repaired.
• Urine output averaging 75ml/hr.
• The biggest news is that her GCS has improved dramatically…she’s now a 9 (opens eyes to speech (3 points), no verbal response due to ETT (1 point) and localizes to pain (5 points). This is a massive improvement! Guess she likes that EVD and all that lovely Mannitol.
• The plan is to let her rest overnight, and lighten up her sedation early in the morning with the neurosurgeon rounds.

Your initial assessment reveals the following:

• ICP 11 (yay!) with 5ml CSF from last hour…looks like drainage is slowing down.
• BP 129/67; HR 85
• Surgical dressing across abdomen and at right hip. Both are clean, dry, intact. Belly is soft, flat; pt grimaces and moves hands toward abdomen as you palpate…likely very tender.
• All other dressings from prior surgeries also clean, dry, intact.
• Lung sounds equal bilaterally; chest tube is patent; O2 saturation 98% on 30% FiO2.
• GCS remains at 9…she is slowly but steadily improving. Whew!

At 2300, you notice that your patient’s  blood pressure is trending down and heart rate is trending up. You aren’t alarmed yet…though you are keeping a careful eye on things. Currently, her O2 saturation is 94%, BP is 109/63, HR is 104, urine output 45/hr. Nothing scary yet, but you don’t like how the trend is going. An hour later, at 0000 you notice O2 sat is now 92 %, BP is 98/62, HR is 115 and urine output for the past hour is 25. You definitely don’t like how this is going. At all. You perform your midnight assessment and notice that your hemovac is full…it was empty two hours ago…what’s going on? You drain the hemovac and pull back the patient’s gown. You immediately see that her belly isn’t quite as flat…and when you touch it it feels much more firm. You immediately go call the ortho surgeon…you’re getting pretty good at waking docs up in the middle of the night, so this SBAR should be a no-brainer!

“This is Nurse Sam, calling about your patient Ramirez in Trauma ICU bed 10. You performed an ORIF on her pelvis today and I’m concerned she may be bleeding into the abdomen. BP has dropped 30 points since 1900, most of the past hour. HR is up from 85 to 115, O2 sats are down to 91 from 98, and urine output is decreasing. Her belly is a bit rounded and more firm than on my initial assessment. I’d like to get a stat Abdominal scan, a stat CBC and coags, and ask you to come see this patient.”

The ortho surgeon agrees with your order requests and states she is going to call the general surgeon who is on site at the hospital right now. If the patient is bleeding, she’s going to need to go to surgery asap. You anticipate this happening, so you get ready:

• You assign a friend to draw a rainbow (this means you’re going to draw the three main studies…a chemistry panel, a CBC and a coagulation panel…these are in different colored tubes so we call it a “rainbow”).
• Another nurse calls blood bank to ensure the patient has units on hold and also calls CT to tell them they’ve got a stat patient coming in.
• You call RT so they can come put the patient on the portable ventilator.
• You get the patient packed up and ready to transport to CT. They quickly run the scan and a few minutes after you return to the room the general surgeon shows up. She assesses the patient, agrees with your findings, and logs into the computer to view the scan which has miraculously been processed amazingly fast! She notes blood in the abdominal space and says what you’ve been anticipating for the past hour…”We’re going to surgery.”
• You wheel the patient down to surgery, report off to the circulating RN and anesthesiologist and decide this is a perfect time for your lunch break.  Nice work,  you!

The patient comes back from the OR 90 minutes later. The surgeon tells you she’d had a large hematoma in one of her pelvic vessels that ultimately burst, causing the drop in pressure and distended abdomen. The patient received four units packed red blood cells in the OR and you’re back to doing q 6-hr H & Hs. BP has improved to 115/67, HR Is 94 and O2 saturation is 98%. That was a close one! Thankfully, the rest of your night goes off without a hitch. When the neurosurgeon rounds at 0600, you’ve had sedation off for about 20 minutes. The patient is moving much more and opening eyes spontaneously. She is not, however, following commands…but her total GCS is now 10. The neurosurgeon likes what he sees and states that if she continues to improve she could likely be weaned from the ventilator soon.

Your relief arrives right on time, you report off and tell her you’re back again that night for your fourth shift in a row. You feel like this patient has really put you through the wringer and hope your last night of the week is easier than the last three! Off you go to sleep.

When you arrive that night, you receive the following information in report:

• GCS is now 11…patient is following commands and trying to write notes! Sedation is minimal.
• Pt has been on CPAP for the past three hours and doing great with RR 14-22 and O2 saturation levels > 95%. She’s pulling good tidal volumes and on a measly 30% FiO2. Awesome!
• ICP has been 4-8 all day with minimal drainage from EVD.
• The PM doc is planning to be by around 2000 to assess pt. You are to have an ABG done at that time to assess for readiness to extubate. You cross your fingers!
• All other VS stable, all dressings CDI and hemovac draining an appropriate amount of serosanguinous fluid.

When the doc comes by at 2000,  you’ve got sedation completely off and your ABG done. After a review of that morning’s CXR and a glance at your patient’s fantastic ABG results, the MD decides to write an order to extubate. Finally some real progress!

You contact your respiratory therapist, grab a towel and a 12 ml syringe. You suction the patient’s mouth and oropharynx thoroughly, making sure you get all the secretions cleared from above the ET cuff. The RT loosens the ET holder from the patient’s face while you get the nasal cannula ready to go with 2L O2. The RT then deflates the cough, tells the patient to cough and pulls the tube. You place the nasal cannula on the patient and instruct her not to talk for a little while. You encourage her to take slow, deep breaths through her nose and cough periodically to keep her lungs clear. Her O2 saturation is 99% and when you ask her how she’s doing she gives you a thumbs up to indicate she is doing fine. You did it!

Now that you’ve got an awake pt who could potentially  move around a lot in bed, you need to be extra careful you don’t over drain through the EVD. You explain to the patient (and the patient’s family) that she is not to abruptly change position or move the head of the bed. She nods to indicate understanding and then mouths the words, “What happened?” You give her a brief synopsis…something along the lines of,

“You were in an accident four days ago and badly injured. You’ve had several surgeries for a head injury and broken bones. You currently have a drain in your head to keep the swelling in your brain under control. You also have a chest tube in place to keep your lungs expanding normally. You also have a catheter in your bladder draining urine. Currently everything looks good. Your vital signs are stable and your neuro status is improving. The short term plan is to keep your pain controlled and monitor your neuro status throughout the night. To do that I’ll have to wake you every couple of hours. Do you understand? Now, I know this is a lot to take in and I want you to try not to worry…that’s my job. I’ll be right out there all night and I’m watching over you continuously. You are hooked up to monitors that may occasionally make noise…a lot of times those noises are false alarms and nothing to be concerned about so try not to let it upset you. As long as I’m not alarmed, you don’t need to be alarmed. OK? Now, what is your pain level on a 0-10 scale?”

Throughout the rest of the night, you’re on dilaudid duty and neuro-assessment duty. The patient is scoring a 14 by the time morning rolls around and you report off to the oncoming nurse feeling like you’ve done an awesome job these past four nights. You rock!

I hope you enjoyed this scenario-based look at caring for a post-surgical trauma patient. Luckily I haven’t had a patient with this many complications, but the point is you are always on the lookout for what COULD go wrong. Being ready when the shizzle hits the fan can mean the difference between life and death…but you’re an awesome nurse and you got this!

Note I couldn’t cover every contingency, assessment, treatment, med and diagnostic test in this one case study…this is just an example and I sincerely hope it helped paint a picture for you! Got a story to share about how you caught a problem before it got too big? Got questions about post-op care? Let’s talk about it in our Facebook Group, Thriving Nursing Students .

____________________________________________________________

The information, including but not limited to, audio, video, text, and graphics contained on this website are for educational purposes only. No content on this website is intended to guide nursing practice and does not supersede any individual healthcare provider’s scope of practice or any nursing school curriculum. Additionally, no content on this website is intended to be a substitute for professional medical advice, diagnosis or treatment.

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Neurology Case Study: Episode 135

Trauma Case Study: Episode 31

Neuro Case Study

Successful outcome in severe traumatic brain injury: a case study

Affiliation.

• 1 Neurotrauma Intensive Care Unit, Hospital of the University of Pennsylvania in Philadelphia, PA, USA.
• PMID: 16379129
• DOI: 10.1097/01376517-200510000-00002

This case study describes the management of a 54-year-old male who presented to the Hospital of the University of Pennsylvania (HUP) with a traumatic brain injury (TBI) after being assaulted. He underwent an emergent bifrontal decompressive hemicraniectomy for multiple, severe frontal contusions. His postoperative course included monitoring of intracranial pressure, cerebral perfusion pressure, partial pressure of brain oxygen, brain temperature, and medical management based on HUP's established TBI algorithm. This case study explores the potential benefit of combining multimodality monitoring and TBI guidelines in the management of severe TBI.

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A case of head injury

• Related content
• Peer review
• Benjamin R K Smith , specialist registrar in radiology ,
• Aidan G Shaw , specialist registrar in radiology ,
• David C Howlett , consultant radiologist
• 1 Eastbourne District General Hospital, East Sussex Hospitals Trust, Eastbourne BN21 2UD, UK
• Correspondence to: B R K Smith brksmith{at}doctors.org.uk

An 82 year old man tripped on uneven paving and sustained a frontal head injury. A passer-by came to his aid and called an ambulance. The patient did not lose consciousness and was fully oriented at the scene.

On arrival at the emergency department he was fully oriented and remembered all events. He had been feeling nauseous in the ambulance and had vomited twice since his arrival. Apart from ongoing nausea and a mild headache he was feeling okay. Baseline observations were normal. Clinical examination showed no neurological deficit. He had extensive right periorbital swelling and a full thickness right forehead laceration that needed suturing.

The casualty officer was worried about the ongoing nausea and arranged for an urgent computed tomogram of the brain (fig 1 ⇓ ).

Fig 1 Axial computed tomogram of the brain (soft tissue windows)

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1 What is the most likely diagnosis?

2 what additional images would be helpful, 3 what injuries and complications are associated with this pathology, 4 how should this condition be managed, short answer.

Free intracranial air (pneumocephaly) is seen around the frontal lobes, sylvian fissures, and para-falcine region, with soft tissue swelling over the right frontal bone (fig 2 ⇓ ). The combination of frontal head injury and extensive pneumocephaly suggests a frontal sinus fracture.

Fig 2 Axial computed tomogram of the brain (soft tissue windows) showing free air around the frontal lobes (white arrows), falx, and sylvian fissures (white arrowheads)

Long answer

This is a case of frontal sinus fracture with intracranial extension. The non-contrast computed tomogram of the brain shows extensive pneumocephaly with pockets of air seen around the frontal lobes, sylvian fissures, falx, and quadrigeminal cistern (fig 2). Soft tissue swelling is seen overlying the right frontal bone. The brain parenchyma has normal a appearance, with no evidence of intra-axial or extra-axial haemorrhage. The basal cisterns are patent.

Bony reformats (fig 3 ⇓ ) show a linear fracture of the right frontal bone extending through the frontal sinus and inner table of the skull. This fracture cannot be seen on the standard soft tissue windows of fig 1, which shows how important it is to use the correct image windows.

Fig 3 Axial bony reformats at the same level as fig 1. The fracture site is indicated by the white arrow

Dedicated bone reformatted images through the skull are highly desirable for the evaluation of skull fractures—without them underlying fractures can be missed (fig 3 ⇑ ).

In the acute setting dedicated bone reformatted images through the skull are highly desirable for the evaluation of skull fractures. These can be extracted from the original scan data. Where possible a fine cut (1 mm) helical acquisition should be obtained and processed to include sagittal and coronal bony reformats. Figure 3 is an axial bony reformat at the same level as fig 1, and it clearly shows a linear frontal bone fracture passing through the frontal sinus.

In the past, plain skull radiographs were used for the evaluation of skull fractures, with Caldwell and lateral views being the most useful for frontal sinus fractures because air fluid levels may be seen in the sinus. However the sensitivity of skull radiographs for detecting fractures is low, and the routine use of skull radiographs in trauma is no longer advocated. 1

Where there have been more extensive facial injuries, a detailed high resolution volumetric computed tomogram of the facial bones is helpful for diagnostic and operative planning purposes.

These fractures are associated with many other injuries including neurological injury, ophthalmic injury, facial fractures, and cerebrospinal fluid leaks.

The frontal bone is the strongest component of the craniofacial skeleton. When serious fractures of the frontal bone occur, these can propagate easily along the adjacent orbital and nasoethmoid complexes, which have much weaker tolerances. 2 Severe ophthalmic injury is seen in about 25% of frontal sinus injuries, the most common of which is damage to the optic nerve and its associated sequelae. 3 Around a third of patients with frontal sinus injury have associated midface fractures, which can need complex surgical reconstruction.

More than half of patients who sustain a frontal sinus fracture will have some form of neurological injury, including cerebral contusions, haemorrhage, and diffuse axonal injury. 3 4 Around 10% of patients have an acute subdural or extradural bleed that requires neurosurgical intervention. 5

Leakage of cerebrospinous fluid (CSF) is a serious associated complication of frontal sinus fracture. It is caused by injury to the posterior wall and subsequent disruption of the attached dura. 6 Even without such a leak, patients who sustain frontal sinus fractures with underlying dural tears have a high risk of developing meningitis. The cumulative risk over 10 years is about 85%. 7

Pneumocephalus, as in this case, is often associated with frontal sinus injury, but its presence is not a reliable or consistent sign of neurological injury or the presence of a cerebrospinal fluid leak.

Urgent maxillofacial and neurosurgical input should be obtained. After basic resuscitation, the patient should be admitted for close neurological observation pending definitive management. Prophylactic antibiotics were given in this case because the patient has a compound fracture and dural tear. Patients are managed by observation or surgery, depending on the degree of injury and associated complications.

Frontal sinus fractures account for 5-15% of all maxillofacial fractures, 5 and they are associated with a high rate of morbidity and mortality. 3 In the emergency department the patient should receive standard trauma care according to advanced trauma life support guidelines. 8 Once airway, breathing, and circulation have been controlled, the next step is to assess the neurological injury and proceed to urgent computed tomography of the brain as required. 1 Keep the patient under strict neurological observation to enable early detection of complications and involve neurosurgeons and maxillofacial surgeons from the outset.

The treatment options for frontal sinus fractures are controversial but are essentially observation or surgery. This decision should be guided by the maxillofacial surgeons and the neurosurgeons, and local practice may differ. In general, minimally displaced anterior table fractures with no concurrent injury or involvement of the frontonasal duct can often be managed conservatively. In patients with complex facial bone injuries or complications (such as a cerebrospinal fluid leak, dural tear, infection, or mucocoele) surgical reconstruction is generally advocated. In the event of neurological injury, including haemorrhage, urgent neurosurgical management may be needed.

The nasofrontal outflow tract provides drainage of the frontal sinus to the nasal cavity. When it is injured, the sinus may not drain properly, which increases the risk of infection. The management of frontal sinus fractures therefore depends on whether or not this tract is injured. With modern multidetector computed tomography scanning these tracts can be well visualised and should be formally assessed and commented on.

Recent studies have led to the development of a treatment protocol based on fracture displacement and involvement of the nasofrontal outflow tract. 9 10 When the tract is injured surgery is advocated. If the posterior table is intact and the dura is not injured, surgery may include sinus obliteration and anterior table repair. If the posterior table is displaced or the dura is injured then cranialisation of the frontal sinus and anterior table repair are generally recommended. If there is a displaced fracture but the tract is not injured, surgical reconstruction of the frontal sinus can be considered.

Patients who have sustained a compound head fracture (as in this case) are at an increased risk of meningitis (5%), extradural abscesses (<0.05%), subdural empyema (<1%), and brain abscesses (with a 40-60% mortality rate). 11 When a frontal sinus fracture is associated with a dural tear the risk of meningitis is even higher. 7 Despite this, the routine use of prophylactic antibiotics remains controversial, and only limited evidence supports their use. 12 13 Treatment should therefore be guided by local protocol.

A major concern with frontal sinus injury is the development of a cerebrospinal fluid leak and subsequent intracerebral infection, including meningitis and empyema. As such, it is normal practice to treat patients with a cerebrospinal fluid leak with prophylactic antibiotics, as guided by local protocol. Treatment would typically continue for the duration of the leak.

Patient outcome

The patient was managed conservatively and developed no complications. He went on to make a full recovery without neurological deficit.

Cite this as: BMJ 2011;343:d4155

Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.

Provenance and peer review: Not commissioned; externally peer reviewed.

Patient consent obtained.

• ↵ National Institute for Health and Clincal Excellence. Head injury: triage, assessment, investigation and early management of head injury in infants, children and adults. CG56. 2007. www.nice.org.uk/nicemedia/pdf/CG56NICEGuideline.pdf .
• ↵ Nahum AM. The biomechanics of maxillofacial trauma. Clin Plast Surg 1975 ; 2 : 59 -64. OpenUrl PubMed
• ↵ Manolidis S, Hollier LH Jr. Management of frontal sinus fractures. Plast Reconstr Surg 2007 ; 120 (7 suppl 2): 32S -48S. OpenUrl CrossRef PubMed Web of Science
• ↵ French JG. Extensive fracture of the walls of the frontal sinus. Proc R Soc Med 1909 ; 2 : 19 . OpenUrl PubMed
• ↵ Gerbino G, Roccia F, Benech A, Caldarelli C. Analysis of 158 frontal sinus fractures: current surgical management and complications. J Craniomaxillofac Surg 2000 ; 28 : 133 -9. OpenUrl PubMed
• ↵ Stanley RB Jr. Management of severe frontobasilar skull fractures. Otolaryngol Clin North Am 1991 ; 24 : 139 -50. OpenUrl PubMed Web of Science
• ↵ Eljamel MS, Foy PM. Acute traumatic CSF fistulae: the risk of intracranial infection. Br J Neurosurg 1990 ; 4 : 381 -5. OpenUrl PubMed
• ↵ Price SJ, Suttner N, Aspoas AR. Have ATLS and national transfer guidelines improved the quality of resuscitation and transfer of head-injured patients? A prospective survey from a regional neurosurgical unit. Injury 2003 ; 34 : 834 -8. OpenUrl CrossRef PubMed Web of Science
• ↵ Stanwix MG, Nam AJ, Manson PN, Mirvis S, Rodriguez ED. Critical computed tomographic diagnostic criteria for frontal sinus fractures. J Oral Maxillofac Surg 2010 ; 68 : 2714 -22. OpenUrl CrossRef PubMed Web of Science
• ↵ Bell RB, Dierks EJ, Brar P, Potter JK, Potter BE. A protocol for the management of frontal sinus fractures emphasizing sinus preservation. J Oral Maxillofac Surg 2007 ; 65 : 825 -39. OpenUrl CrossRef PubMed Web of Science
• ↵ Miller JD, Jennett WB. Complications of depressed skull fracture. Lancet 1968 ; 2 : 991 -5. OpenUrl CrossRef PubMed Web of Science
• ↵ Ali B, Ghosh A. Antibiotics in compound depressed skull fractures. Emerg Med J 2002 ; 19 : 552 -3. OpenUrl Abstract / FREE Full Text
• ↵ Mendelow AD, Campbell D, Tsementzis SA, Cowie RA, Harris P, Durie TB, et al. Prophylactic antimicrobial management of compound depressed skull fracture. J R Coll Surg Edinb 1983 ; 28 : 80 -3. OpenUrl PubMed

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Pediatric Head Injury: A Study of 403 Cases in a Tertiary Care Hospital in a Developing Country

Abrar ahad wani.

Department of Neurosurgery, Sher-I Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

Arif Hussain Sarmast

2 Department of Neurosurgery, Jawaharlal Nehru Medical College, AMU, Aligarh, Uttar Pradesh, India

Muzaffar Ahangar

Nayil khursheed malik, sarabjit singh chhibber, sajad hussain arif, altaf umar ramzan, bashir ahmed dar.

1 Department of Anaesthesiology, Sher-I Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

Zulfiqar Ali

Introduction:.

Traumatic brain injury (TBI) in children is a significant cause of morbidity and mortality worldwide. Falls are the most common type of injury, followed by motor vehicle-related accidents and child abuse.

Aims and Objectives:

The aim and objective of this study was to elucidate the various modes of injury, prognostic factors, complications, incidence of various modes of injury, and outcome in TBI in pediatric population.

Materials and Methods:

Patients with TBI, 18 years or less in age, managed in our Department of Neurosurgery, over a period of 2 years, were studied prospectively. Detailed history, general physical examination, systemic examination, and central nervous system examination including assessment of Glasgow Coma Scale score (GCS) and pupillary size and reaction were noted in every patient. Based on GCS, patients were divided into mild head injury (GCS 13–15), moderate head injury (GCS 9–12), and severe head injury (GCS ≤8) categories. All the patients were subjected to plain computed tomography (CT) scan head, and CT findings were noted. Patients were managed conservatively or surgically as per the standard indications. The outcome of all these patients was assessed by Glasgow outcome scale and divided into good (normal, moderate disability) and poor (severe, vegetative, dead) outcome. Outcome was assessed in relation to age, sex, GCS, pupil size and reaction, CT scan features, intervention, and associated injuries.

A total of 403 patients aged between 1 day and 18 years were included in the study comprising 252 males (63%) and 151 females (37.75%). The common modes of injury were fall 228 (56.6%) followed by road traffic accidents 138 (34.2%), assault 10 (2.5%), and others 27 (6.7%) which include sports injury, hit by some object on head, and firearm injury. Majority of our patients had a GCS of 13–15 (mild head injury), 229 (57.3%), followed by 9–12 (moderate head injury) 119 (29.8%), followed by 8 or less (severe head injury) 52 (13%). In group of patients in the category of GCS ≤ 8, poor outcome was seen in 65.3%, followed by patients in group GCS 9–12 at 2.45% succeeded by group of patients with GCS 13–15 at 2.6%, which was statistically significant ( P < 0.0001). A total of 354 (87.8%) patients had normal pupils, 37 (9.2%) had anisocoria, and 12 (3%) patients had fixed dilated pupils. Fixed dilated pupil had poor outcome (100%) followed by anisocoria (40.5%) and normal pupils (16%), which was statistically significant ( P < 0.0001).

Conclusion:

Majority of children who suffer from TBI do well although it still continues to be a significant cause of morbidity and mortality in them. The outcome is directly related to the neurological status in which they present to the hospital.

I NTRODUCTION

Severe traumatic brain injury (TBI) in children is Sa significant cause of morbidity and mortality worldwide.[ 1 ] Falls are the most common type of injury, followed by motor vehicle-related accidents.[ 2 ] Furthermore, child abuse remains a major cause of head trauma in children under 2 years of age. The percentage of each contributing factor differs between studies, and the distribution varies according to age group and sex. Infants and young children are more vulnerable to abuse because of their dependency on adults.[ 3 ] A force applied to the skull may be distributed evenly throughout the skull without causing a skull fracture (closed head injury) but damaging the less rigid brain tissue. When the skull vault is fractured, it is described as an open head injury. Open head injuries are much less common in children.[ 4 ] TBI is classified as mild (Glasgow Coma Scale [GCS] 13–15), moderate (GCS 9–12), or severe (GCS 3–8).[ 5 ] Children ≤10 years of age with a GCS of ≤8 or a strong suspicion of injury despite normal plain films (anteroposterior [A/P] and lateral views for children <10 years of age, without an A/P peg view), or if plain films are inadequate, should undergo computed tomography (CT) scanning of the cervical spine within an hour of presentation or when sufficiently stable.[ 6 ] Responsiveness is assessed with the Alert, Verbal, Pain, Unresponsive system and with the GCS[ 5 ] and its modified Paediatric GCS.[ 7 ]

CT is the most helpful and most definitive way to assess the severity of TBI. CT provides all essential information necessary to make a decision regarding the presence or absence of significant intracranial injury and whether emergency operative intervention is required.[ 8 , 9 , 10 ]

Although clinicians usually attempt to take a wide range of factors into account when making clinical decisions and assessing prognosis, there is probably a redundancy in this effort to be complete. In practice, relatively few features have been found to contain most of the prognostic information.[ 11 , 12 , 13 ] These include the patient age, clinical indices indicating the severity of brain injury (e.g., the depth and duration of coma and other neurological abnormalities), and the results of investigation and imaging studies, particularly intracranial pressure (ICP) and CT scanning, which disclose the nature of brain injury and its effects on intracranial dynamics.[ 14 ]

M ATERIALS AND M ETHODS

Four hundred and three (403) patients with TBI, 18 years or less in age, managed in the Department of Neurosurgery, Sher-i-Kashmir Institute of Medical Sciences, Srinagar, over a period of 2 years from August 2011 to September 2013, were enrolled in the study.

The patients were evaluated on the basis of a predetermined pro forma. Detailed history of the patients was taken (including patients’ bio data, age, and mode of injury). Patients were subjected to detailed general physical examination, systemic examination, and central nervous system (CNS) examination including GCS and pupil size and reaction. Based on GCS, the patients were divided into mild head injury (GCS 13–15), moderate head injury (GCS 9–12), and severe head injury (GCS ≤ 8) categories All the patients were subjected to plain CT scan head, and CT findings were noted.

After the preliminary resuscitation and workup, the patients were managed conservatively or surgically as per indications. The outcomes of all these patients were assessed by Glasgow Outcome Scale and divided into good (normal, moderate disability) and poor (severe, vegetative, dead) outcome. Outcome was assessed in relation to age, sex, GCS, pupil size and reaction, CT scan features, intervention, and associated injuries.

A total of 403 patients aged between 1 day and 18 years with a mean age of 8.398 years with SD of ± 5.5228 were included in the study comprising 252 males (63.25%) and 151 females (37.75%), with a male-to-female ratio of 5:3. It was evident from our series that age ( P = 0.478) and sex ( P = 0.165) had no statistical significance in outcome [ Table 1 ].

Relationship of age, gender, mode of trauma, and Glasgow Coma Scale score with outcome

The most common modes of injury were fall 228 (56.6%) followed by road traffic accidents (RTAs) 138 (34.2%), assault 10 (2.5%), and others 27 (6.7%) which include sports injury, hit by some object on head, and firearm injury. RTAs had a poor outcome in 16.6% while patients with fall had a poor outcome of 7.8% ( P = 0.052) [ Table 1 ].

Majority of our patients had a GCS of 13–15 (mild head injury), 229 (57.3%) followed by 9–12 (moderate head injury) 119 (29.8%), followed by 8 or less (severe head injury) 52 (13%). In group of patients in the category of GCS ≤8, poor outcome was seen in 65.3%, followed by patients in group GCS 9–12 at 2.45% succeeded by group of patients with GCS 13–15 at 2.6%, which was statistically significant ( P < 0.0001) [ Table 1 ].

Out of the 403 patients, 354 (87.8%) patients had normal pupils, 37 (9.2%) had anisocoria, and 12 (3%) patients had fixed dilated pupils. Fixed dilated pupil had poor outcome (100%) followed by anisocoria (40.5%) and normal pupils (16%), which was statistically significant ( P < 0.0001). CT scan findings were noted as normal in 86 patients (21.3%), isolated skull fracture in 89 (22%), contusion or hematoma in 98 (24.3%), extradural hemorrhage (EDH) in 66 (16.4%), subdural hemorrhage (SDH) in 35 (8.7%), pneumocephalus or aerocele in 13 (3.2%), brain edema in 8 (2%), and subarachanoid hemorrhage in 8 (2%). Among the mode of injury, it is evident that diffuse brain edema had poor outcome in 50%, SDH in 25.7%, contusion in 13%, while in EDH, it was 4.5% [ Table 2 ]. .

Relationship of pupillary status, computed tomography findings, and midline shift with outcome

From our series, we inferred that poor outcome was associated with the highest (60%) being midline shift (MLS) >3 mm and it was 13.6% with MLS of <3 mm and it was 8.5% in patients with no MLS ( P < 0.001) [ Table 2 ]. Out of the 403 patients, 276 (69%) were managed conservatively and 124 (31%) patients were managed surgically. The various surgical procedures performed in patients include fracture debridement and elevation in 44 (35.48%), hematoma or contusion removal in 38 (30.64%), decompressive craniotomy in 9 (7.25%), hematoma or contusion removal with fracture debridement in 12 (9.67%), and hematoma removal with decompressive craniotomy in 21 (16.93%) [ Table 3 ]. We followed up our patients for 10 days to 12 months, with a mean of 4.63 months. In the operated group, wound infections occurred in 22 (5.5%), cerebrospinal fluid (CSF) leak in 21 (5.3%), aspiration or hospital-acquired pneumonia in 15 (3.8%), CNS infections (meningitis or subdural abscess, etc.) in 6 (1.5%), and recollection of hematoma after surgery (SDH) in 6 (1.5%) cases.

Relationship of mode of treatment with outcome

While doing the survey for associated injuries, fractures of face were noted in 42 (10.5%), limb fractures in 27 (6.8%), abdominal trauma in 16 (4%), spinal trauma in 11 (2.8%), chest trauma in 9 (2.3%), multiple traumas in 12 (3.1%), and isolated head trauma in 286 (70.9%). It was noticed that chest, spinal, and multiple injuries were associated with a poor outcome ( P < 0.0001) [ Table 4 ].

Relationship of associated injuries with outcome

D ISCUSSION

Although in the developed world, with the advent of highly specialized Intensive Care Units and a high level of multidisciplinary approach, the outlook of the TBI has improved dramatically, it still continues to be a major challenge for the neurosurgery units in our part of the world. A pediatric TBI as is true in adults occurs due to a variety of reasons and generally has a good prognosis. These injuries more often than not are not isolated and are associated with polytrauma and are treated more or less on the same lines as the adults.[ 15 , 16 , 17 , 18 ]

There are discrepancies in the literature when defining the age point where prognosis significantly worsens. For example, there has been disagreement regarding the pediatric age group. One group of reports has indicated that outcome tends to be better in children under 10 years of age,[ 19 , 20 ] while others report that children under five have a higher mortality rate.[ 21 ] Although in our series there was no difference in poor outcome in children below 5 years or above 5 years as was reported by Suresh et al .,[ 22 ] there was slightly higher poor outcome above 12 years that was not statistically significant. The importance of age as a prognostic factor has been a subject of controversy. Luersson et al .[ 23 ] and Braakman et al .[ 11 ] have reported age as the strongest factor for mortality and morbidity. Although literature supports age as the stronger factor of mortality and morbidity in severe head trauma, these studies compare adults with children. In our series, we had compared only children and all grades of trauma were taken into consideration.

In our series, the most common modes of TBI were fall 228 (57%) with good outcome in 210/228 (92%) patients, followed by RTAs 135 (33.8%) with good outcome in 115/135 (83%), followed by assault in 10 (2.4%) with good outcome in 100%, followed by other modes in 27 (6.7%) with good outcome in 92.5%.

The patients with low GCS had a poor outcome as is expected. The patients who had a GCS of 13–15 (229 [57.3%]) had a poor outcome in 6 (2.6%), followed by GCS of 9–12 (119 [29.8%]) who had a poor outcome in 3 (2.52%), followed by GCS of 8 or less (52 [13%]) who had a poor outcome in 34 (65.4%). Suresh et al .[ 22 ] reported poor outcome in the group of GCS 3–5 as 58.5%, GCS 6–8 had 35.2%, GCS 9–12 had 11.4%, and GCS 13–15 had 1.3%. Beca et al .[ 24 ] and Kuday found that the initial GCS score was the single most important factor affecting outcome ( P < 0.00001).[ 25 ] Astrand et al .[ 26 ] reported poor outcome in GCS 14–15 in 0%, in 9–13 as 6.2%, and < 8 had 22% poor outcome. Ong et al .[ 27 ] and Aldrich et al .[ 4 ] reported that low GCS did not always accurately predict the outcome in the absence of hypoxia or ischemia. In our series, we found a significant impact of GCS on outcome. The developing and underdeveloped areas like ours have poorer outcome due to lack of prehospital resuscitation and late presentation to hospital.

Out of the 403 patients, 351 (87.8%) patients had normal pupils, 37 (9.3%) had anisocoria, and 12 (3%) patients had fixed dilated pupils. Poor outcome in patients with normal pupils was 4.55%, patients with anisocoric pupils was 40.5%, and with fixed dilated pupils was 100%. Astrand et al .[ 26 ] reported 100% poor outcome in dilated pupils unresponsive to light. Suresh et al .[ 22 ] reported poor outcome of 49.3% in patients of abnormal pupils and 7.4% in normal pupils. Jennett et al .[ 12 ] reported poor outcome of 96% in fixed dilated and 50% in normal pupils. Francel et al .[ 28 ] stated that papillary response is not a good predictor of outcome. In our series, we found abnormal pupillary response being the strongest predictor of outcome.

Out of the 403 patients in our series, CT scan findings were noted as normal in 86 patients (21.3%) [ Table 2 ], with good outcome in 71/86 (88%) and poor outcome in 11.6%. These results closely match those of Van Dongen et al .[ 29 ] in whose series patients with normal CT were 12% and good outcome was seen in 78% and poor outcome in 22%. Lobato et al .[ 30 ] reported normal CT in 10% patients. The extent of a skull fracture is proportional to the severity of brain injury which clearly does not apply to the pediatric age group.[ 28 ]

We found isolated skull fracture in 89 (22%) patients with good outcome in 97.8% and poor outcome in 2.2%. Suresh et al .[ 22 ] had 17% patients with isolated skull fracture with good outcome in 94.1% and poor outcome in 5.9%. The probability of associated intracranial hematoma with skull fracture in children is half of that of adults.[ 31 ]

Extradural hematoma is significantly less common in children than in adults and is even more rare in infants.[ 32 ] EDH can occur without fracture in children more commonly.[ 28 ] We had noticed EDH in 66 (16.4%) patients with good outcome in 95.5% and poor outcome in 4.5%. EDH reported by Suresh et al .[ 22 ] was at 28% with poor outcome in 8.4%. Astrand et al .[ 26 ] reported 48% of patients of EDH with good outcome in 98% and poor outcome in 2%. The mortality rate in children with EDH ranged from 7% to 15%, 5%–10% of patients also had residual neurological deficits.[ 28 ]

In our series, contusions/hematoma was seen in 98 (24.3%) with good outcome in 86.8% and poor outcome in 13.2%. Suresh et al .[ 22 ] reported 16.7% with poor outcome in 18.2% and Lobato et al .[ 30 ] reported that outcome was better in EDH. The outcome was unfavorable in patients with intracerebral hematomas and hemorrhagic contusions.[ 33 ]

SDH is seen six times more often in infants than in toddlers.[ 28 ] The outcome of patients with SDH is significantly worse than that of patients with EDH, mainly because of the underlying brain damage accompanying SDH and the resultant intracranial hypertension. In our series, SDH was seen in 35 (8.7%) patients and out of those poor outcome was noted in 9 (25.7%) patients. Suresh et al .[ 22 ] had recorded SDH in 10.33% of patients out of whom 35.3% had poor prognosis. Yi et al .[ 34 ] and Tomberg et al .[ 33 ] recorded 25% and 17.1% of patients having SDH and none of them had good prognosis. In our series, EDH was seen more common than SDH and possibly it is because of higher incidence of fractures in our series, i.e. 89 (22%) patients and EDH was mainly because of fracture line hematoma.

Diffuse brain swelling occurs in approximately 50% of children with severe head injury. The outcome is significantly better in children as compared to patients with operable mass lesion.[ 33 ] Diffuse swelling of brain may develop more readily in children because of the lack of CSF available for displacement. Children with CT scan indicating of diffuse axonal injury but without diffuse cerebral edema generally did not have sustained increased ICP and more than two-thirds attained a favorable outcome. Diffuse brain swelling with or without diffuse axonal injury demonstrated by the first CT scan was related to high mortality. In our series, diffuse brain edema was observed in 8 (2%) with poor outcome in 4 (50%) patients. Suresh et al .[ 22 ] reported the incidence of diffuse brain edema as 30% with poor outcome in 25%.

Quattrocchi et al .[ 35 ] found a prognostic significance of the presence or absence of MLS on the admission CT. Athiappan et al .[ 36 ] found the prognostic value of MLS to be more important in patients with single contusions or intracerebral hematoma than for those with multiple lesions and extra-axial or subdural hematoma. In our series, we found poor outcome in 8.5% and good outcome in 91.5% patients without MLS, patients with MLS <3 mm had poor and good outcome of 13.7% and 86%, respectively, and patients with MLS >3 mm had poor outcome and good outcome of 60% and 40%, respectively. The presence of MLS was associated with a poor outcome in 50% of cases, whereas the absence of MLS was associated with a poor outcome in only 14% of cases ( P < 0.05).[ 35 ] Lobato et al .[ 30 ] reported that bad outcome can be predicted correctly as 68% when MLS >1.5 cm.

In our series, we found that 80% of patients had pure TBI, 10% had facial trauma, 7% had limb fractures, 4% had abdominal solid organ injury, 3% had spinal injuries, 3% had chest trauma, and 3% had multiple injuries. Jagannathan, et al .[ 1 ] reported orthopedic (50%), abdominal (27%), thoracic (20%), facial (20%), and multiple injuries (48%).  Paret et al .[ 37 ] reported chest trauma in 62%, limb fracture in 32%, facial fractures in 29%, abdominal solid organ lesions in 20%, spinal cord injuries in 5% and multiple in 67%. This difference is because we had taken all patients into consideration irrespective of grade of injury, while others have taken severe TBI patients into consideration.[ 1 , 37 ]

The overall outcome of our series of patients irrespective of their grade revealed a mortality of 5.7% and normal outcome of 81.9% with 4.7% patients being completely dependent for their day-to-day activities and 7.4% patients have moderate disability [ Table 5 ].

Glasgow Outcome Scale in the study group

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Conflicts of interest.

There are no conflicts of interest.

R EFERENCES

CASE REPORT article

Case report: an mri traumatic brain injury longitudinal case study at 7 tesla: pre- and post-injury structural network and volumetric reorganization and recovery.

• 1 Cambridge Intellectual and Developmental Disabilities Research Group, Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom
• 2 Department of Rehabilitation and Human Performance, Brain Injury Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, United States
• 3 Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, United States
• 4 Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States
• 5 Department of Computer Science, Mathematics, Physics, and Statistics University of British Columbia, Kelowna, BC, Canada

Importance: A significant limitation of many neuroimaging studies examining mild traumatic brain injury (mTBI) is the unavailability of pre-injury data.

Objective: We therefore aimed to utilize pre-injury ultra-high field brain MRI and compare a collection of neuroimaging metrics pre- and post-injury to determine mTBI related changes and evaluate the enhanced sensitivity of high-resolution MRI.

Design: In the present case study, we leveraged multi-modal 7 Tesla MRI data acquired at two timepoints prior to mTBI (23 and 12 months prior to injury), and at two timepoints post-injury (2 weeks and 8 months after injury) to examine how a right parietal bone impact affects gross brain structure, subcortical volumetrics, microstructural order, and connectivity.

Setting: This research was carried out as a case investigation at a single primary care site.

Participants: The case participant was a 38-year-old female selected for inclusion based on a mTBI where a right parietal impact was sustained.

Main outcomes: The main outcome measurements of this investigation were high spatial resolution structural brain metrics including volumetric assessment and connection density of the white matter connectome.

Results: At the first scan timepoint post-injury, the cortical gray matter and cerebral white matter in both hemispheres appeared to be volumetrically reduced compared to the pre-injury and subsequent post-injury scans. Connectomes produced from whole-brain diffusion-weighted probabilistic tractography showed a widespread decrease in connectivity after trauma when comparing mean post-injury and mean pre-injury connection densities. Findings of reduced fractional anisotropy in the cerebral white matter of both hemispheres at post-injury time point 1 supports reduced connection density at a microstructural level. Trauma-related alterations to whole-brain connection density were markedly reduced at the final scan timepoint, consistent with symptom resolution.

Conclusions and Relevance: This case study investigates the structural effects of traumatic brain injury for the first time using pre-injury and post-injury 7 Tesla MRI longitudinal data. We report findings of initial volumetric changes, decreased structural connectivity and reduced microstructural order that appear to return to baseline 8 months post-injury, demonstrating in-depth metrics of physiological recovery. Default mode, salience, occipital, and executive function network alterations reflect patient-reported hypersomnolence, reduced cognitive processing speed and dizziness.

Introduction

Traumatic brain injury (TBI) is a leading cause of disability worldwide, particularly in young and military populations, with well-documented links to psychiatric and neurodegenerative pathology ( 1 ). Patients who experience mild traumatic brain injury (mTBI) typically report vestibular, sensory, cognitive or emotional symptoms that persist for several months after injury ( 2 ). Patients experiencing mTBI typically show low frequency of positive MRI findings at 6 months post-injury, highlighting the need for more sophisticated and sensitive imaging techniques in the clinical investigation of mTBI ( 3 , 4 ). Previous studies have reported the utility of diffusion-weighted imaging and tractography methodology in determining the presence of neuronal injury in cases where conventional neuroimaging findings are negative ( 5 , 6 ), as they allow examination of fiber- and tract-related pathology. Tracking of the spinothalamic tract in a mTBI case demonstrated thinning and discontinuation of fibers at the subcortical white matter in mTBI patients with no conventional radiological abnormalities ( 6 ), and the corticobulbar tract and fornix exhibited similar narrowing and discontinuations in an mTBI case study caused by violence ( 5 ). It is probable that white matter damage, common in TBI due to both indirect shearing forces and direct damage, may be a pertinent but often undetected pathophysiology in this population ( 7 ). Moreover, it is generally appreciated that injury to the brain resulting from trauma often arises globally, as axons crossing areas of differing tissue density react differently to the mechanical force of the trauma ( 8 ). This can cause widespread damage, which may be explored using network and connectivity analyses that draw directly upon anatomically accurate estimations of white matter connection density. A connectomic network approach allows data integration of distinct regions of brain anatomy and connection strength, which makes it a useful methodology for examining both localized and global effects of mTBI on white matter ( 9 ).

In this case study, unique due to the rare availability of pre- and post-injury 7 Tesla high-resolution data, we investigated the trajectory of structural changes attributed to mTBI. The multiple time-point pre-injury data is an uncommon strength to the present research, as longitudinal data can be examined in both healthy and post-injury settings. Moreover, we aimed to investigate and characterize disparities between conventional structural MRI and diffusion-weighted connectomic findings. In this report, we hope to illustrate how recent developments in the field of computational neuroimaging, such as morphometric subcortical segmentations and network theory, may aid in the identification of suitably sensitive biomarkers of brain injury.

Case Description

A 38-year-old female was involved in a motor vehicle accident in which she was a pedestrian hit by a car turning into the intersection she was crossing. She was thrown across the road where her head hit the curb. She was transported to the nearby hospital where acutely, the patient was dizzy, faint and mildly confused. Head CT revealed subcutaneous soft tissue swelling over the right parietal bone. There was no evidence of acute territorial infarction or intracranial hemorrhage. Ventricles and sulci appeared normal in size and configuration for the patient's age. There was no midline shift or other mass effect, and gray-white matter differentiation was maintained throughout the brain. The patient received surgical staples to close a laceration over the right parietal bone and was discharged home. The patient reported minimal headaches or nausea, but dizziness, daytime fatigue, hypersomnolence, reduced problem-solving skills and slowed cognitive processing persisted for several weeks following the injury. She returned to work the day after the injury, working slightly reduced hours to accommodate fatigue. Full recovery, defined as full symptom resolution and return to baseline function, was achieved ~6 months post-injury. The patient gave fully informed consent for participation in the presented research. Institutional Review Board (IRB) approval for human research was obtained for this experiment from the Program for Protection of Human Subjects at the Icahn School of Medicine at Mount Sinai.

Longitudinal Data Acquisition

The patient had undergone two scanning sessions at 7 Tesla prior to the head injury as a healthy control. Two more scans were acquired post-injury. The scan times in relation to injury were as follows: 23 months prior to injury, 12 months prior to injury, 2 weeks post-injury, and 8 months post-injury. All MRI scanning was performed using the same Siemens 7T scanner. Clinical assessment and an initial head CT were carried out immediately after injury, and neurocognitive testing was administered by a trained clinician 18 months post-injury.

Clinical Neurocognitive Data Acquisition

A brief battery of performance-based neurocognitive tests was administered to estimate premorbid intellectual functioning and quantitatively confirm cognitive recovery 18 months post-injury ( 10 ).

MRI Acquisition

Included in each MRI protocol was a T 1 -weighted Magnetization Prepared 2 Rapid Acquisition Gradient Echo (MP2RAGE) ( 11 ), a T2-weighted Turbo Spin Echo (TSE), and a diffusion MRI.

The MP2RAGE sequence obtains improved gray-white contrast at high field compared to the classic MPRAGE acquisition ( 11 ). High spatial resolution voxel size was 0.8 mm isotropic, TR/TE = 6,000/3.2 ms, TI1(θ 1 )/TI2(θ 2 ) = 1,050(5°)/ 3,000(4°) ms and total acquisition time was 7:26 minutes. From the MP2RAGE dataset, a total of four images were reconstructed from (a) data acquired after inversion time (TI) of 1,050 ms, (b) data acquired after TI of 3,000 ms, (c) T1 relaxation maps calculated from (a) and (b), and (d) uniform-denoised (UNIDEN) images calculated from (a) and (b). An in-plane acceleration factor of 3 was used.

Two TSE structural images were obtained at high in-plane resolution (0.4 × 0.4 mm 2 ), a slice thickness of 2 mm, TR/TE = 6,900/69 ms and θ = 150°. An in-plane acceleration factor of 2 was used. The first T2-TSE was obtained with a 6:14 min acquisition time in a coronal-oblique orientation where the imaging plane was aligned perpendicular to the long axis of the hippocampus. The second T2-TSE was obtained in an axial orientation; the imaging plane alighted along the axis connecting the anterior commissure and the posterior commissure (AC-PC). The acquisition time for the second T2-TSE scan was 6:50 min.

Diffusion MRI data were collected using a single-shot spin-EPI sequence aligned axially with an isotropic resolution of 1.05 mm, an in-plane acceleration factor of 3, a multi-band acceleration factor of 2 and TR/TE = 6,900/67 ms. The diffusion sequence was a paired acquisition with reversed phase encoding in the AP/PA direction, and each pair had 64 diffusion encoding directions ( b = 1,200 s/mm 2 ) and 4 unweighted scans ( b = 0 s/mm 2 ). Total scan time for the paired acquisition was 20 min.

Structural MRI Analysis

The FreeSurfer “recon-all” pipeline (version 6.0) ( 12 ) was used to carry out the following processing steps on T1-weighted structural data: motion correction, intensity correction, transform to Talairach space, intensity normalization, skull strip, subcortical segmentation, neck remove, subcortical labeling, segmentation statistics, a second intensity correction using brain only (after skull strip), white matter segmentation, subcortical mass creation, brain surface creation, surface inflation, automatic topology fixer, cortical thickness/pial surfaces, cortical ribbon mask, spherical inflation of the brain surface, ipsilateral surface registration, contralateral surface registration, resampling of the average atlas curvature to subject, cortical parcellation, and creation of summary table for parcellation statistics. As the T1-weighted data had a submillimeter isotropic voxel size, the “-hires” flag was used to preserve enhanced spatial resolution ( 13 ).

Hippocampal subfield ( 14 ) and amygdala subnuclei segmentation ( 15 ) was carried out using FreeSurfer 6.0 development version. A multi-spectral approach was used, utilizing both the T1-weighted and T2-weighted images, leveraging the enhanced resolution of the T2-weighted image to provide additional anatomical information. This subcortical segmentation is visualized in Figure 1 .

Figure 1. (a) Multi-spectral hippocampal subfield segmentation (CA1, CA3, CA4, dentate gyrus, and subicular complex) with underlay of axial T1-weighted data. (b) Hippocampal subfield segmentation with underlay of axial T2-weighted data. (c) Multi-spectral amygdala subnuclei segmentation (lateral, basal, accessory basal, central, cortical, medial nuclei, and corticoamygdaloid transition area (CATA) with underlay of axial T1-weighted data. (d) Amygdala subnuclei segmentation with underlay of axial T2-weighted data.

To investigate test–rest variability, blinded re-runs of the imaging processing were carried out, and pairwise coefficients of variation were calculated per measure by dividing the standard deviation by the mean and multiplying by 100 to produce a percentage.

Diffusion MRI Analysis

Denoising of the diffusion weighted data was performed using MRTrix two-shell phase-reversed processing ( 16 , 17 ). Segmented and parcellated structural images from the FreeSurfer “recon-all” pipeline were used for whole brain masking ( 12 ). B 1 field inhomogeneity correction was carried out ( 18 ) and the fiber orientation distributions (FODs) were created from the diffusion data using constrained super-resolved spherical deconvolution ( 19 ). Estimation of the diffusion tensor was done using iteratively reweighted linear least squares methodology ( 20 ). The tensor image was used to create a whole brain map of fractional anisotropy (FA) ( 21 ). Mean FA was extracted from cerebral white matter hemispheric masks created by the FreeSurfer pipeline.

Co-registration of anatomical images into diffusion space was then carried out using Statistical Parametric Mapping software (SPM12). Degree of spline interpolation was 4. The MRTrix command “5ttgen” was used to generate a five tissue-type segmentation image, utilizing the FreeSurfer outputs, to use in anatomically constrained tractography ( 22 ). A segmented mask image was then created for the seeding of tractography streamlines at the gray-white matter interface ( 22 ). The fiber orientation distributions were then used to create whole brain tractograms for each participant ( 23 ). Ten million streamlines were generated from the probabilistic tractography per brain. Individual step size for the streamlines was 0.1 mm × voxel size, the fiber orientation distribution amplitude cut-off was 0.05 and the maximum angle between successive steps was 90° × step size × voxel size. Seeds were placed in the gray white matter interface. Spherical deconvolution informed filtering (SIFT2) was applied to the tractograms, the purpose of which was to weight streamlines based on likelihood of anatomical accuracy, remove spurious streamlines from further analysis and ensure data that is highly representative of ground-truth biology ( 24 ). A structural connectome, based on node-to-node connection density, was created using MRTrix ( 25 ).

Structural connectomes at different timepoints were compared by custom functions that performed elementwise subtraction of the matrices in MATLAB. Similarly, variability of the connectomes was assessed by stacking matrices into a 3-dimensional array and computing the mean and standard deviation along the z -axis for each network edge. To investigate variability between scan timepoints, specifically to examine test–retest variation, the two pre-injury connectomes were compared using co-efficients of variation, calculated elementwise for each edge of the connectivity matrix by dividing the standard deviation by the mean and multiplying by 100 to produce a percentage. The mean co-efficient of variation was calculated by averaging the co-efficients of variation across the whole matrix. To determine a streamline threshold of the connectome with an acceptable level of variability, mean matrix co-efficients of variation were calculated for the following streamline thresholds: 25, 50, 100, 200, 400, 800, 1,600, 3,200, 6,400, 12,800, and 25,600. Actual streamline thresholding was subsequently set at 15,000, discarding edges consisting of streamline bundles with less density than the threshold.

Clinical Neurocognitive Data

This high-achieving woman with a history of academic excellence throughout 20 years of formal education had an estimated premorbid intellectual ability in the high average-superior range ( 10 ). At the time of testing her performance-based intellectual quotient (IQ) was in the superior range, consistent with expectation. She demonstrated a relative strength in verbal comprehension (96th percentile) as compared to perceptual reasoning (>99th percentile). Performance on tests of contextual and non-contextual verbal memory was consistently above the 98th percentile, while visual memory performance was at the 34th percentile (Average range). Tests of complex attention and working memory were generally above the 85th percentile (High Average range), and tests of verbal fluency were variable (semantic fluency 38th percentile; phonemic fluency 96th percentile). Performance on timed tests of sequencing and task-switching were below expectation (<1st percentile – 62nd percentile) while untimed tests of these higher order executive functions were well within expectation (>96th percentile). Overall, performance on neurocognitive tests indicate superior intellectual ability with performance 18 months post-TBI largely consistent with expectations; impaired performance on select timed tests suggest a tendency to sacrifice speed to ensure accuracy which may reflect a compensatory strategy.

The subcortical segmentation of the amygdala nuclei and hippocampal subfields did not reveal any clear changes between the scanning timepoints. The average test-retest coefficient of variation for the hippocampal subfield segmentation was 1.4%, and 5.2% for the amygdala nuclei. Considering this estimation of variability within the image processing, the data did not reveal evidence of volumetric change to the hippocampus or amygdala post-injury, either at a whole or substructure level.

At post-injury timepoint 1, the right and left hemispheric brain segmentation revealed lower cortical gray matter and cerebral white matter volume compared to other scanning timepoints. No change was apparent in ventricle volume ( Figure 2 ). The average test-retest variation co-efficient for each of these variables was <0.001%, significantly less than the observed change post-TBI.

Figure 2 . Volumes of choroid ventricles, hemispheric gray matter, and hemispheric white matter and fractional anisotropy of the hemispheric cerebral white matter across scanning timepoints.

Concurrent with the changes in the structural volumetrics, FA of the cerebral white matter was markedly reduced in both hemispheres in the first scan following the head trauma. In both the left and right hemispheres, the final timepoint scan revealed a subsequent increase of FA to levels similar to those pre-injury ( Figure 2 ).

Averaging of the structural diffusion MRI connectomes pre- and post-injury revealed a widespread decrease in connectivity after the patient’s head trauma, mainly involving connections between cortical regions ( Figure 3A ). To a lesser degree, mean pre- to post-injury comparison also revealed some increased connectivity, primarily in subcortical areas and the forebrain ( Figure 3B ). A comparison between the first and second post-injury connectome matrices was then carried out, to investigate if changes to the patient's structural connectivity post-TBI were consistent over time. The results showed that at post-injury timepoint 1, connection density was extensively reduced, but this decrease in connectivity was partially reduced by post-injury timepoint 2.

Figure 3. (a) Areas of decreased connection density of the structural network mean post-injury compared to mean pre-injury. (b) Regions of increased connection density of the structural network mean post-injury compared to mean-pre-injury.

Structural high-resolution neuroimaging data in this mTBI case study revealed reduced cerebral white matter and cortical gray matter volumes post-injury that appeared to restore to pre-injury quantifications by the 8-month post-TBI MRI acquisition. Whole brain white matter fractional anisotropy demonstrated a concurrent pattern of change, with marked short-term reductions post-injury returning to a baseline level by the 8-month following TBI. The structural connectome, derived from tractography-based connection density metrics, showed that post-injury connectivity was reduced extensively between cortical nodes, in particular in the right parietal injury site. To a lesser degree, limbic, and forebrain regions were intra-hyperconnected. The final post-injury scanning timepoint showed globalized increases in connection density compared to the primary post-injury data, suggestive of recovery of the network. We highlight here the rare availability of pre-injury data, which gives significant benefits to interpretability compared to post-injury only research into mTBI.

Interestingly, subcortical segmentation and analysis of regional brain volumetrics did not reveal changes post-TBI, indicating a robustness of the limbic structures in this case. This is in contrast to previous reports of the hippocampal and amygdala structures being promising predictors of outcome when analyzed at a gross level ( 26 ); however, severity and type of TBI are significant contributors to heterogeneity. Our results suggest that subcortical volumetrics may not be a sensitive measure of mTBI pathology in all cases. At a whole brain level, it appeared that quantification of hemispheric white and gray matter volumes was a more effective metric of brain changes post-TBI in this case, especially when considering the minimal test–retest variability.

The mechanical properties of the white matter make it particularly vulnerable to injury in TBI ( 5 ), which was a prominent motivation for the use of high spatial resolution diffusion-weighted MRI in this case investigation. Our findings show that primary post-injury connectivity is reduced in a widespread manner, mainly between cortical nodes. Similarly, a study of mTBI patients and matched controls revealed decreased fractional anisotropy in the association, commissural and projection white matter tracts, indicative of reduced connectivity, which partially resolved 6 months post-injury ( 27 ). In addition, our results identified increased white matter connectivity in the limbic and forebrain regions post-injury compared to pre-injury data. Resting-state investigation into mTBI has shown comparable hyperconnectivity in the limbic system post-injury ( 28 ), and thalamic circuitry, in particular, has been shown to be a key underlying factor in mTBI recovery ( 29 ). Alterations of the connectome post-mTBI in the present case were further substantiated by widespread corroborative changes in fractional anisotropy, suggesting that after injury, white matter microstructure was changed in a way highly indicative of axonal damage ( 30 ).

The involvement of the posterior cingulate, precuneus and prefrontal cortices in the decline of structural network density implicates decreased cohesiveness of the default mode system. Decreased functional coupling of the default mode network, in particular in the frontal regions, has been shown to occur during sleep in both humans and primates, suggesting that default mode cohesiveness may be required to maintain conscious states ( 31 ). The default mode white matter damage detected in the present study; therefore, may be a contributory factor in the patient's reported hypersomnolence and fatigue post-injury. Similarly, the superior frontal and orbitofrontal regions are integral sites for executive processing ( 32 ), and the observed decreases in network connection density here tally closely with the patient's symptomology of delayed cognitive processing post-injury. Decreased white matter connectivity of the insular cortex implicates decreased salience network integration, which may be another possible physiological correlate of cognitive slowing via diminished attentional regulation ( 33 ). Alterations to the thalamic-occipital lobe circuitry, which forms the posterior portion of the primary visual pathway ( 34 ), may also underlie symptomatic dizziness post-TBI. Localized increases in the mean connection density of the thalamus post-injury, a factor previously reported as a protective feature against long-term pathological effects in mTBI ( 29 ), is also seen in this patient, and may reflect compensatory plasticity promoting sensory relay and upstream network integration ( 35 ).

Additionally, consistent with previous studies of diffusion-weighted imaging in TBI ( 27 ), the current data show recovery of the brain white matter, which is consistent with symptomatic recovery per subjective report at ~6 months post-injury. However, the structural network at post-injury timepoint 2 exhibits some evidence for enduring TBI-related change, given that compared to pre-injury data, the final timepoint connectivity shows some disorganization, albeit markedly improved compared to the initial post-injury network. The functional implications of long-term reorganization of the network appear to be minimal, although may account for the few isolated areas of cognitive performance that were lower than expected in patient at 18 months post-injury. Taken together, our findings show that diffusion MRI connectomics and microstructural measurements may be sensitive to clinical status.

This 7 Tesla case report demonstrates novel evidence of widespread connectivity and microstructural changes at a highly granular level after mTBI, where conventional neuroimaging at a clinical level showed no radiological abnormalities. Moreover, we demonstrate the disparity between T1- and T2-weighted acquisition-derived information and diffusion MRI and suggest that diffusion-weighted investigation of TBI symptomology may be of significant use in clinical practice.

Data Availability Statement

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

Ethics Statement

The studies involving human participants were reviewed and approved by Regional ethics committee, Icahn School of Medicine at Mount Sinai. The patients/participants provided their written informed consent to participate in this study.

Author Contributions

SB, KD-O'C, PB, and RF contributed substantially to the study conception and design, drafted, and revised the article for important intellectual content and gave final approval of the version to be published. EW provided guidance for cognitive assessment. SB carried out all data processing and neuroimage analyses. All authors contributed to the article and approved the submitted version.

This work was funded by DOD-IDA W81XWH-19-1-0616 and NIH R01 MH109544.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Keywords: 7T MRI, diffusion MRI, traumatic brain injury, structural connectivity, case study

Citation: Brown SSG, Dams-O’Connor K, Watson E, Balchandani P and Feldman RE (2021) Case Report: An MRI Traumatic Brain Injury Longitudinal Case Study at 7 Tesla: Pre- and Post-injury Structural Network and Volumetric Reorganization and Recovery. Front. Neurol. 12:631330. doi: 10.3389/fneur.2021.631330

Received: 19 November 2020; Accepted: 15 April 2021; Published: 17 May 2021.

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Copyright © 2021 Brown, Dams-O'Connor, Watson, Balchandani and Feldman. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Stephanie S. G. Brown, sb2403@medschl.cam.ac.uk

† These authors have contributed equally to this work

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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