Woke up dead: A review on traumatic brain injuries

TBI risk factors, managing patient refusals and oxygenation tips for treating head injuries


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Sometime during the night of Jan. 8, 2022, comedian Bob Saget hit his head on something, went to bed in his hotel room and never woke up. He was found dead the next morning by hotel staff, and just like that, Danny Tanner, the surrogate dad to a generation of American kids who grew up watching “Full House,” was gone.

The circumstances of Saget’s death give rise to more questions than answers. The initial investigation ruled his death accidental, postulating that he fell and hit his head in the bathroom, and thinking nothing of it, just went to bed and fell asleep. However, the extent of his skull fractures – multiple skull fractures and even bilateral orbital fractures – make it implausible that Saget simply brushed off his injuries and went to bed. Also curious was the fact that investigators found no blood or hair on the floor, counters or tables in Saget’s hotel bathroom.

In 2009, Natasha Richardson, actress and wife of Liam Neeson, died from an epidural hematoma sustained in a skiing accident. On New year’s Eve 1997, Michael Kennedy, son of assassinated presidential candidate Robert F. Kennedy, died of massive head trauma after striking a tree while skiing in Aspen, Colorado.

Traumatic brain injuries are classified by whether they involve the brain parenchyma or not.
Traumatic brain injuries are classified by whether they involve the brain parenchyma or not. (Photo/Getty Images)

Most of us in our career will never care for a famous actress or the scion of a political dynasty, but we will encounter our share of fallen grandmas, car accident victims and the wobbly impaired who suffer similar injuries. It behooves us, therefore, to review the pathology of traumatic brain injuries.

Two broad classifications of TBI

Traumatic brain injuries are classified by whether they involve the brain parenchyma or not. Extra-axial injuries involve bleeding within the skull, but outside the brain tissue itself. Among these are subdural hematomas, epidural hematomas and subarachnoid hemorrhages. The symptoms experienced in these injuries usually result from swelling of an expanding hematoma putting pressure on the brain.

Intra-axial injuries, however, occur within the brain parenchyma itself, and are correspondingly more difficult to treat. Rather than a simple hematoma to evacuate or a craniotomy for the neurosurgeon to perform, intra-axial injuries are more diffuse, difficult to manage directly and potentially devastating. Even if the patient does survive, many of them suffer long-term or permanent cognitive impairment.

Epidural hematoma

An epidural hematoma occurs between the dura mater and the skull, typically from rupture of one of the meningeal arteries. Roughly 75% of the time, this occurs at the middle meningeal artery, which lies beneath the junction of the frontal, parietal, temporal and sphenoid bones. This area is a particularly thin section of the lateral skull known as the pterion, and a linear fracture in this area can cause devastating arterial bleeding within the skull. On a CT scan, an epidural hematoma looks like a lemon pressing into the brain. The dura mater is attached tightly to the sutures of the skull, leaving the expanding hematoma nowhere to go but push into the brain parenchyma itself.

The classic sign of an epidural hematoma is a temporary loss of consciousness at the moment of impact, followed by awakening, and then a rapid decline in level of consciousness shortly thereafter. This brief period of wakefulness is called a lucid interval. This may not be present in all epidural hematomas, but Natasha Richardson experienced a classic lucid interval after her head injury. She initially refused medical attention, but then complained of a severe headache about two hours later and died soon thereafter.

There’s a lesson to be learned for EMS providers from that incident, in how we ensure informed consent and more importantly, informed refusal of medical care.


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Should I stay, or should I go?

Managing high-risk/difficult refusals with the FEARS mnemonic


Subdural hematoma

Subdural hematomas, however, typically are venous bleeds resulting from rupture of the bridging veins connecting the cerebral venous sinuses to the superficial veins of the skull. This results in venous bleeding between the dura mater and the arachnoid membrane. A subdural hematoma often looks like a banana on a CT scan, and may cross the suture lines of the skull.

As subdural bleeds are slow venous bleeds, the onset of symptoms may be rather delayed, but no less serious. A significant number of patients with subdural hematomas do not seek medical attention until symptoms develop, and often these symptoms herald increased intracranial pressure. The elderly, chronic alcoholics and infants are particularly susceptible to subdural hematomas.

The classic subdural hematoma patient in EMS is the elderly patient taking anticoagulant medications who falls. Many of these patients claim to feel fine after the fall and insist only on lift assistance, but your index of suspicion for occult brain bleeds should be high.


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What do you do after the lift assist?

Helping a fall patient back into bed, a chair or onto the ambulance cot should launch risk mitigation in the patient’s home to prevent future falls


Subarachnoid hemorrhage

Subarachnoid hemorrhages (SAH) occur beneath the arachnoid membrane and the pia mater, the microscopic meningeal layer covering the brain parenchyma itself. The most common cause of SAH is trauma, but spontaneous subarachnoid hemorrhage may result from rupture of a berry aneurysm in the Circle of Willis, or from arteriovenous malformations. Individuals with connective tissue disorders like Marfan’s Syndrome and vascular Ehlers-Danlos Syndrome have weakened arterial walls and are at particularly high risk for spontaneous hemorrhagic strokes of this nature, even at young ages. The classic complaint of spontaneous SAH is the “thunderclap” headache, often described as the worst headache of the patient’s life. Signs and symptoms of SAH closely mimic those of migraines – headache, light sensitivity, nausea and vomiting – and care should be taken to not dismiss symptoms as a simple migraine. Even frequent migraine sufferers can have a SAH, so be sure to ask if the current episode is more severe or different in any way from their normal migraine pattern.

Intra-axial Injury

Diffuse Axonal Injury is an intra-axial injury that results from stretching and shearing of axons in the white matter of the brain. Such an injury has very subtle findings on a CT scan, and is often diagnosed by a coma lasting six hours or more in the absence of a significant brain lesion. Many of the patients who awaken from their coma may have impairments of memory or language skills, or impairments in higher-order thinking or planning, such as executive dysfunction disorder.

Herniation

Brain herniation is defined as a portion of the brain pushed out of place or out of the skull itself, usually a result of inflammation and edema of injured brain tissue. In uncal herniation, the medial portion of the temporal lobe is pressed downward, putting pressure on the oculomotor nerve and brainstem. This may result in a dilated pupil on that side, and that pupil will often look down and out due to oculomotor nerve palsy. Compression of the posterior cerebral artery may result in a peripheral visual field deficit on the contralateral side.

Central herniation results from downward displacement of the brainstem. It may result in fixed and dilated pupils, and a downward deviation of gaze known as “sunset eyes” sign.

Increased intracranial pressure

It is important to remember that the intracranial vault is a non-expandable space, and the three fluid levels within this space – brain, blood and cerebrospinal fluid – have a fixed total volume. If the fluid volume of one increases, one or both of the other two must correspondingly decrease. This principle is known as the Monro-Kellie Doctrine, and illustrates the delicate balance we must strike in managing the patient’s cerebral perfusion pressure. Hyperventilation may reduce arterial carbon dioxide resulting in vasoconstriction, thus decreasing the space blood occupies in the cranium, but at the cost of impairing blood flow to already damaged brain tissue. Do not hyperventilate head injury patients, even those with signs of increased intracranial pressure. Instead, aim for restoring as close to “normal” oxygenation and ventilation as you can get – keep spO2 at 94% or better and keep etCO2 on the physiologically low end of normal, at roughly 35 mmHg.

Risk factors for TBI

Aside from the obvious mechanisms, like a whack on the head from a car, a baseball bat, the ground or a tree, we need to be aware of the subtler risk factors for intracranial hemorrhage that can result in a brain hemorrhage from a relatively minor traumatic insult:

  • Elderly patients – their brains shrink, stretching those cerebral bridging veins
  • Infants – shaken baby syndrome is a major risk factor for SAH and other brain hemorrhages
  • Anticoagulant use, for the obvious reasons
  • Patients with connective tissue disorders
  • Chronic alcohol abuse – the brain of an alcoholic atrophies much like an elderly patient. If your patient is an elderly alcoholic who takes a blood thinner and recently fell, obtain a refusal on this patient at your own peril

Odds are, you’ll encounter plenty of patients with traumatic brain injury in your career, and the cases that will bite you (metaphorically, not literally, but never stick your fingers in a head injury patient’s mouth) are the ones that you missed. When you recognize head injury, transport the patient in a semi-Fowler’s position unless protocol dictates otherwise, keep their mean arterial pressure (MAP) at 65 mmHg if you can, maintain oxygen and ventilation as close to physiologically normal as possible, and transport the patient to an appropriate facility.

That’s the best starting point for managing head injuries.

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