Case Presentation by Dr. Justin Kessler
Patient B.B. a 17–year-old high school football player presenting to the emergency department via EMS after collapsing to the ground unresponsive approximately 3 hours after being struck in the head without a helmet on by another player’s helmet. Initially he was dazed but was able to stand up and joke about what a “hard head he had.” He complained of a headache throughout the rest of practice and vomited once per his coach who thought it was due to the heat. PMHx significant only for acne. Patient takes Tylenol for headaches PRN after football practice. On exam patient is not responsive to name, he makes gurgling mumbles, slowly opens his eyes to painful stimuli, and only has an abnormal flexed posture does not withdraw to pain.
Vitals: BP146/92, HR 98 , RR9, Sat87% Room, Temp 37.4
HEENT: HEAD: Slight boney stepoff along the patient’s right temporal area. No Scalp Lacerations.
EYES: The pupils are 7mmOD 3mm OS sluggish reactive to light,. fundoscopic exam shows evidence of swelling of optic disk ,hyperma, and loss of physiologic cupping on exam in OD only. Sclera were anicteric, conjunctiva were without palor.
EARS: Pinnae are intact bilaterally, TM are clear,no evidence of hemotympanum Bilaterally.
NOSE: No noticeable deformity, moist mucosa, no erythema, no epistaxis, discharge, no swollen turbinates.
MOUTH AND THROAT: Mucous membranes are moist,no erythema, no tonsillar exudates, no intraoral leisions of the gums, tongue, lips, or palates.
CV: S1 S2 present, regular rhythm and tachycardic rate~ 100bpm, no murmurs
Resp: Slow shallow breaths,
Abd: Soft, nondistended, BS all 4 Qs
Ext: Peripheral pulses present in all 4 limbs, cap refill <2 seconds ROM intact with passive movement of all 4 limbs. Tone increased.
Back: No tenderness to palpation throughout cervical, thoracic, and lumbar spine. No bony deformity, crepitus, or step-offs noted.
Neuro: Pt obtunded, Decorticate posturing, not opening eyes to command or name. Positive gag reflex. Absent ankle jerk bilaterally, Babinski negative bilaterally.
Electrolytes, BUN, creatinine, glucose, and CBC were all within normal limits.
12-lead ECG performed at 1550 is interpreted as revealing tachycardic normal sinus rhythm at a rate of 102 beats per minute. Axis was normal. There were no ST or T wave abnormalities to suggest myocardial ischemia or injury.
Diagnostic Studies: Head CT as Follows:
1. Following Injury in which there is later radiographic evidence on head CT of an epidural hematoma what is the estimated percentage in which there is a “lucid” period before deterioration?
2. In regards to a Minor Head Trauma which of the following patients would warrant CT scanof head or prolonged emergency department observation?
A. A 23 YO male that bumped his head on a door 2 days ago, currently asymptomatic, no LOC with intact orientation, memory.
B. A 30 YO male with a minor headache after being hit in the head from a falling telephone book(for Kansas City), no vomiting no LOC
C. A 45 YO female with fall to carpeted surface wearing high heels after drinking 2 glasses of wine with no change in consciousness, intact orientation and recall.
D.A 61 YO male who tripped over a shopping cart hit head into a car door with past history of epilepsy, last seizure was >20 years ago.
E. 5 YO female running away from her brother that hit her head on a coffee table complains of headache, witnessed by mother, child consolable on scene.
3.Which of the following factors has the greatest predictive value in the Development of seizures following head trauma?
A Patient Age
B. Occipial Lobe injury
C. Glasgow coma Score <8
D. Concomitant use of illicit drugs
E generalized brain injury.
4.Two of these Famous TBI patients are related other than the fact that they had Traumatic Brain injury which two?
This patient is suffering from an epidural hematoma with possible transtentorial herniation. Epidural hematomas are collections of blood between the skull and dura mater. Epidural hematomas that are large and rapidly expanding are usually caused by arterial bleeding. Classically these are due to damage of the middle meningeal artery or one of its branches sometimes caused by a temporal bone fracture. Without swift diagnosis and intervention, patient with arterial epidural hematomas name rapidly deteriorate and die.
In this patient B.B. underwent initial trauma and was experiencing secondary injury after a “lucid period.” Although lucid intervals only account for proximately 20% of all cases of epidural hematoma the history of a head injury minutes to hours before having declining neurological function are classic for epidural hematomas. Patient will often still complain of a progressive headache during these lucid intervals as in the case of patient B.B..
The pathophysiology lies in the increasing arterial bleed causing increased intracranial pressure. Because the craniospinal intradural space nonexpandable, some of the volume of brain, CSF, and blood are factors at which if any volume of these components increases the volume of another must decrease to maintain ICP. This is known as Monroe-Kellie Doctrine. In the case study, CFS may have been displaced from the intracranial vault to the spinal canal office setting increase of blood volume. When this compensatory mechanism is overwhelmed and volumes of blood are still increasing the brain matter may start herniate as it too will continue to swell due to congestive brain swelling as well cerebral edema.
On vital sign examination this patient has to have progressive hypertension associated with bradycardia and diminished respiratory effort. These are specific responses to ICP increase known as the Cushing reflex; usually indicating ICP is that critical levels.
Management ED and this case should include rapid sequence intubation for airway protection since the patient’s GCS is 7. Lidocaine 1.5-2 mg per kilogram IV push may be used to attenuate the cough reflex with intubation since his patient’s gag reflex is still intact.
Hyperventilation may prevent further herniation in the early phases, hyperventilation works by causing cerebral vasoconstriction. Onset is within 30 seconds and peaks at 8 minutes after pCO2 drops to arrange of 30-35 mmHg. However, continued cerebral vasoconstriction also leads to ischemia.
More often hypertonic saline (HTS) is being used to reduce ICP however it is controversial whether it really has an effect. These studies are using the 3% drip however probably not including the 24% bolus that is given by our cavalier neurointensivists.
Further management to prevent herniation and tissue damage would include osmotic agents such as manitol as well as possible barbiturate coma to decrease metabolic demand of the injured brain tissue. Mannitol at 0.25-1g/kg can effectively reduce ICP and prevent further herniation onset 60minutes and lasting for 6-8hrs. However, with such a large bolus of osmolytes you could overwhelm the kidneys. Early seizure prophylaxis of benzodiazepines may also be needed, as up to 12% of patients with traumatic brain injury will develop early posttraumatic seizures. The patient having a depressed skull fracture is indication for acute seizure prophylaxis in his head trauma.
Only after the patient stabilized well CT imaging be required to complete the final diagnosis.
#1 Answer: B.) 20% Although Tintinalli’s along with was every other study or reference quotes this 20% estimation of the number of the epidural hematomas that will have a heralding lucid interval, if you look back to the original paper below where this estimation came from is actually estimation of 20 up to 50% which has given way to more recent articles stating that the ” lucid period” of epidural hematomas is a “classical finding” when doing a workup for epidural hematomas.
However, one must realize that traumatic brain injury that it comes from many different degrees and levels of injury. Therefore, a quantifiable estimation based on a study set of patients must be taken with a grain of salt.
I believe the original author accounted for this wide variation by giving a range in his estimation based on data available. I wrote the question before going to the first source of this statistic sorry.
Liau LM, Bergsneider M, Becker DP. Pathology and pathophysiology of head injury. In: Youmans JR, ed. Neurological Surgery. 4th ed. Philadelphia, Pa: WB Saunders Co; 1996:1549-1594.
#2 Answer: D.) Validated prospective studies have shown that High-risk patients with minor head trauma with any criteria including presence of headache, (mainly a progressive headache), vomiting, age >60, drug or ETOH intoxication, short-term memory deficit, post-traumatic seizures, or evidence of trauma above the clavicals are indicative of increased likelihood of intracranial injuries. Further high risk factors are also considerations for CT scan which include:
Focal neurologic findingsAsymmetrical pupilsSkull fracture on clinical examinationMultiple traumaSerious, painful, distracting injuriesExternal signs of trauma above the claviclesInitial Glasgow Coma Scale score of 14 or 15Loss of consciousnessPost-traumatic confusion/amnesiaProgressively worsening headacheVomitingPost-traumatic seizureHistory of bleeding disorder/anticoagulationRecent ingestion of intoxicantsUnreliable/unknown history of injuryPrevious neurologic diagnosisPrevious epilepsySuspected child abuseAge >60 yr, <2 yr
– For this reason one could argue that choice (E) may be a likely answer since the child is unable to give an accurate history anyway and might be having a progressive worsening headache, or that the Lady in (C) might be trashed from her two glasses of wine. The key rebuttal from the author of this question is “might.”
#3 Answer : C) GCS<8. The factor that is most predictive of posttraumatic head injury seizures is a GCS<8. 38.7 % of patients in the studies below developed seizures compared with 3.8% of patients with GCS> or equal to 8. Patient age, occipital lobe injury, concomitant use of illicit drugs, and generalized brain injury had not been shown to be predictive of posttraumatic seizures. Again, every case is different in traumatic brain injury and every study set of patients in different institutions will also be different. However, this is the data that is available.
Varon J, Marik PE Management of head trauma in children Crit Care Shock 2002;5:133-43.
Varon J, Marik PE Management of head trauma. Chest Aug 2002 vol.122 669-771
#4 Answer: A&D Ken Norton fought Muhammad Ali in the 1970’s however his disability of sounding “punchy” with his speech is due to a TBI from an auto accident.
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