HeadHypothermia

CORE

Why the Treatments Work — The Physiology Behind TBI Interventions

Understand the chemistry and mechanics behind hyperventilation, TXA, head elevation, and hypertonic saline. Every TBI treatment exists to manipulate one of the three Monroe-Kelli compartments: brain tissue, blood, or CSF.

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The Core Concept — Monroe-Kelli in Plain English

The skull is a closed box. It holds three things: brain tissue, blood, and CSF. The total volume cannot change. If any one of these three expands, one of the others must shrink, or pressure rises. Every TBI treatment in the field attacks one of these compartments to lower the total volume inside the skull.

Treatment	Compartment Attacked	How It Shrinks It
Hyperventilation	Blood (arterial)	Constricts cerebral arteries; less arterial blood enters the skull
Head elevation 30°	Blood (venous) and CSF	Gravity drains venous blood and CSF out of the skull
Hypertonic saline	Brain tissue	Pulls water out of swollen brain cells into the bloodstream
Mannitol	Brain tissue	Pulls water out of brain; excretes it in urine
TXA	Blood (prevents expansion)	Stops the hematoma from getting bigger; does not shrink existing volume

Hyperventilation — The Chemistry of pH and CO2

Cerebral blood vessels are extremely sensitive to CO2 and pH. The arterioles in the brain have smooth muscle that constricts in alkaline conditions (low CO2) and dilates in acidic conditions (high CO2).

The chemical equation:

CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃^-

CO2 in solution is acidic. More CO2 means more hydrogen ions, which means lower pH (more acidic). When you hyperventilate, you exhale CO2 faster than the body produces it, blood CO2 drops, and the equation shifts left to replace the lost CO2. This consumes hydrogen ions. Fewer hydrogen ions means higher pH (alkaline).

Hyperventilation — The Numbers

Value	Normal	After Hyperventilation
pH	7.35 to 7.45	7.5 or higher
PaCO₂	35 to 45 mmHg	25 to 30 mmHg

Hyperventilation — The Physiology Chain

1

Hyperventilate → blow off CO₂ → PaCO₂ drops.

2

Lower CO₂ → equation consumes H⁺ ions → serum pH rises.

3

Higher pH (alkaline) → cerebral arteriole smooth muscle constricts.

4

Constricted arteries → less blood enters the cranial vault.

5

Smaller blood compartment → lower ICP.

Hyperventilation — The Trade-Off

Vasoconstriction lowers ICP, but it also lowers cerebral blood flow. Less blood flow means less oxygen delivery to brain tissue. Aggressive or prolonged hyperventilation causes cerebral ischemia. This is why hyperventilation is a temporizing measure for impending herniation only, NOT a routine treatment. The goal in non-herniating patients is normocapnia (PaCO2 35 to 40), not hypocapnia.

The Two-Way StreetIt also runs backwards: hypoventilation → CO₂ builds up → pH drops → cerebral vasodilation → more blood in the skull → higher ICP. This is why a TBI patient with depressed respirations from opioids, sedation, or brain injury itself spirals fast. Protecting the airway and ventilation rate is not optional in head injury.

Why We Give TXA in TBI

When blood vessels are damaged, the body forms a clot through a cascade ending in fibrin, the mesh that holds the clot together. The body also has a system to dissolve clots once healing begins, called fibrinolysis. The key enzyme is plasmin, which is converted from plasminogen.

In trauma, this clot-dissolving system gets switched on too early and too strongly. This is called hyperfibrinolysis. The body breaks down clots faster than it can form them. Bleeding worsens.

TXA Mechanism

TXA (tranexamic acid) is a lysine analog. It binds to plasminogen at the site where plasminogen normally attaches to fibrin. With TXA in the way:

1

Plasminogen cannot bind to fibrin.

2

Plasminogen cannot be activated into plasmin.

3

The clot cannot be broken down.

4

The clot stays intact.

TXA does not form clots. It protects clots that have already formed.

Why TXA Matters in TBI

A brain bleed (epidural, subdural, intracerebral) is a clot expanding inside a fixed skull. The faster it grows, the faster ICP rises and the faster herniation occurs. If hyperfibrinolysis is breaking down the developing clot at the bleeding site, the bleed keeps getting bigger. TXA stabilizes the clot and limits hematoma expansion.

The 3-Hour Window

The CRASH-3 trial showed TXA reduces head-injury-related death when given within 3 hours of injury. After 3 hours, the benefit disappears and may even cause harm. The clot dynamics change after that point: the early phase of hyperfibrinolysis ends, and giving an antifibrinolytic later may promote inappropriate clotting elsewhere.

Dose per JTS TCCC: 2 grams slow IV or IO push as soon as possible, not later than 3 hours after injury.

Why We Elevate the Head 30 to 60 Degrees

The brain sits inside a closed box. Blood comes in through arteries and leaves through veins. Arterial blood enters under high pressure driven by the heart, so it reaches the brain regardless of position. Venous blood leaves under low pressure and depends largely on gravity and the absence of obstruction.

How Elevation Helps

Flat position: venous blood pools in the cranial vault; jugular veins drain less efficiently when horizontal; more venous volume in the skull means higher ICP.
Elevated 30 degrees: gravity assists venous drainage out the jugular veins; less venous blood pools in the skull; the blood compartment shrinks slightly; ICP drops.
CSF also drains better with elevation: CSF moves from the cranial vault down into the spinal subarachnoid space; the CSF compartment shrinks slightly inside the skull; ICP drops further.

The 30 vs 60 Degree Distinction

Angle	When to Use
30 degrees	Standard target for general ICP management. Improves venous and CSF outflow without compromising cerebral perfusion.
60 degrees	Used when CSF is actively leaking from the ears or nose. The steeper elevation reduces the pressure gradient driving CSF out through the fracture and lowers meningitis risk.

The Hypovolemia ContraindicationDo NOT elevate the head of a hypovolemic casualty. If blood volume is already low, the heart is struggling to push blood up to the brain against gravity. Elevating the head forces the heart to work harder to perfuse the brain. Cerebral blood flow drops, causing ischemia. In hypovolemia, keep the patient flat until volume is restored.

Why We Give 250 mL of 3 to 5% Hypertonic Saline

Normal blood plasma has a sodium concentration around 140 mEq/L. Normal saline is 0.9% sodium chloride. Hypertonic saline at 3 to 5% has roughly three to five times the salt concentration of normal blood.

When you inject hypertonic saline into the bloodstream, the blood becomes saltier than the surrounding tissue. Water moves from areas of low salt concentration to areas of high salt concentration through osmosis. The salt acts as a magnet for water.

How Hypertonic Saline Lowers ICP

Brain tissue swelling after TBI is essentially water trapped inside and between brain cells (cerebral edema). The brain compartment has expanded with fluid. Per Monroe-Kelli, this expansion raises ICP.

1

Hypertonic saline enters the bloodstream; blood becomes hypertonic relative to brain tissue.

2

Water is pulled out of brain cells into the interstitial space.

3

Water then moves from the interstitial space into the blood vessels.

4

The brain compartment shrinks slightly as water leaves; ICP drops.

The Blood-Brain Barrier Requirement

The blood-brain barrier is normally selective about what crosses between blood and brain. Sodium does not cross easily. This is the key to why hypertonic saline works for the brain. The salt stays in the bloodstream and pulls water across the barrier without itself crossing. The osmotic gradient is maintained.

If sodium could cross freely (which it does eventually if equilibration is given time), the gradient would dissipate and the effect would end. This is why hypertonic saline has a finite duration of action.

Why 250 mL Specifically

You want enough salt to create a meaningful osmotic gradient but not so much volume that you overload an already injured patient with fluid. 250 mL of 3 to 5% saline delivers a high salt load in a small volume. Compare this to giving the same amount of sodium as normal saline, which would require liters of fluid and could worsen cerebral edema.

The Bonus — Blood Pressure Support

Hypertonic saline pulls fluid into the bloodstream from everywhere, not just the brain. The intravascular volume expands by more than the 250 mL infused, because water follows the salt out of cells and interstitial spaces throughout the body. This raises blood pressure. In a TBI patient who needs SBP above 90 (or above 110 per RMHB), this is a useful side benefit.

Hypertonic Saline vs Mannitol — Why HS Wins in Combat

Feature	Mannitol	Hypertonic Saline
How it pulls water from brain	Osmotic gradient	Osmotic gradient
What happens to the water	Filtered into urine; patient urinates it out	Stays in the bloodstream
Effect on blood pressure	Drops BP (diuresis)	Raises BP (volume expansion)
Effect on volume status	Worsens hypovolemia	Treats hypovolemia
Best use case	Hemodynamically stable patient	Hypovolemic, hypotensive, or both — the typical combat casualty

The Three Interventions Together

A casualty with severe TBI gets TXA to stop the bleed from expanding, head elevation to drain venous blood and CSF out of the skull, and hypertonic saline to pull water out of the swollen brain tissue. All three reduce the volume inside the cranial vault by attacking different compartments:

TXA limits the blood compartment from growing further.
Head elevation drains the blood and CSF compartments.
Hypertonic saline shrinks the brain tissue compartment.

Together they buy time until surgical decompression at a facility with a neurosurgeon. None of these treatments fix the primary injury. They all prevent secondary injury by manipulating the Monroe-Kelli compartments.

One Sentence SummaryEvery field intervention for TBI either shrinks one of the three intracranial compartments (brain, blood, CSF) or prevents one of them from expanding further. Understand which compartment each drug or maneuver attacks and the rest of TBI management makes sense.

1

Hypothermia Prevention & Management Kit Procedure

Identify the indications and step-by-step procedure for applying the Hypothermia Prevention and Management Kit.

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Indications

Prevention of heat loss in a trauma casualty.
Active re-warming of a hypothermia patient.

Procedure

1

Ensure hemorrhage is controlled and other injuries are managed per appropriate protocols.

2

Open the heat reflective shell and place it on a litter with the hood aligned to the patient’s head.

3

Place the patient inside the reflective shell.

4

Wrap the casualty’s head in the hood.

5

Remove wet clothing and replace with dry if possible.

6

Place the four-cell self-heating shell liner on the torso. Barrier MUST sit between casualty and liner.

7

Wrap and secure the reflective shell.

8

If environment permits, keep tourniqueted extremities external to the reflective shell.

9

Monitor per protocol. Continue trauma assessment and treatments.

Documentation

Detailed assessment, vital signs, oxygen saturation, skin color, complications encountered.

Barrier RequirementA barrier must sit between the casualty’s skin and the self-heating liner. Direct contact causes burns.

If HPMK Is Unavailable (MASCAL)Use blizzard blankets, clothing from uninjured personnel, blankets found on target. Whatever works.

2

TBI Definitions and Epidemiology

Identify the key definitions and epidemiology of traumatic brain injury.

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Definition of Traumatic Brain Injury

Traumatic brain injury (TBI) is an impairment in brain function as a result of mechanical force. Key features:

Can be temporary or permanent.
May or may not result in underlying structural changes in the brain.
Clinical severity ranges from very mild to profoundly impaired.

TBI in the Department of Defense

Over 80% of TBIs occur in a non-deployed setting.
Common causes: motor vehicle accidents, falls, sports and recreation, military training.

General TBI Epidemiology

Leading cause of death and disability in children and adults ages 1 to 44.
Twice as common in men.
Common mechanisms: falls, motor vehicle crashes, concussive weapons.
Mortality rises continuously with age.
More than 20% of combat personnel sustain TBI.

Trimodal Age Distribution

Peak	Age Range
1	0 to 4 years old
2	15 to 24 years old
3	Over 75 years old

Why This Matters in SOFThe 15–24 peak overlaps the population most likely to be in combat training and operations. Combine that with the “20% of combat personnel” statistic and TBI is one of the most likely injuries a medic will manage in a career.

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TBI Pathophysiology — Primary vs Secondary Injury

Identify the pathophysiology of traumatic brain injury, including the Monroe-Kelli Doctrine and the ICP cascade.

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Primary Injury — The Impact Itself

Primary injury (also called "impact injury") is tissue destruction that occurs as a direct result of physiologic trauma.

Very little can be done by providers to influence primary injury.
The severity and location of the primary brain injury will dictate the patient’s immediate level of consciousness, mental status, and focal neurologic signs.

Secondary Brain Injury — The Treatable Phase

Secondary brain injury is the focus of TBI treatment. It can be more damaging than the primary injury and continues for an indefinite period of time. The primary goal of head injury management is to prevent it.

Two Most Acute and Easily Treatable Mechanisms

Hypoxia (PaO2 less than 95)

Mortality of TBI patients with hypoxia is doubled. Increases brain cell death and edema.

Hypotension (SBP less than 90)

Hypotension → decreased cerebral perfusion → cerebral ischemia → mortality doubles.

Other Systemic Causes of Secondary Injury

Anemia from blood loss — decreases oxygen-carrying capacity.
Hypocapnia (decreased pCO2 from hyperventilation) → increased serum pH → cerebral vasoconstriction → decreased cerebral blood flow.
Hypercapnia (increased pCO2 retention) → cerebral vasodilation → increased intracranial blood volume.
Increased or decreased blood glucose — brain cells cannot function without glucose.
Seizures — seen in 30 to 40 percent of patients with penetrating brain injuries.

Intracranial Causes of Secondary Injury

Cerebral edema.
Hematomas.
Increased intracranial pressure.

Monroe-Kelli Doctrine

The brain is a semisolid organ that occupies 80% of the cranial vault. It uses 20% of the body’s oxygen supply and receives 15% of cardiac output.

The cranial vault is fixed in size by the rigid outer skull and contains three compartments:

Brain tissue
Blood vessels (and blood)
Cerebrospinal fluid (CSF)

The doctrine: Because the vault cannot expand, the expansion of one compartment MUST be accompanied by a compensatory reduction in the volumes of the other compartments to maintain a stable intracranial pressure. When this compensation fails, ICP rises.

The Increased ICP Cascade

Increased intracranial pressure is the most frequent cause of death and disability after severe head injury. Delayed cerebral swelling is the major cause of raised ICP and death.

1

ICP rises.

2

Cerebral perfusion pressure (CPP) decreases.

3

PO2 decreases (less oxygen reaches the brain).

4

PCO2 levels increase.

5

Cerebral vasodilation occurs in response to the rising CO2.

6

Cerebral blood volume increases.

7

ICP increases further. The cycle accelerates until herniation or death.

The Whole Point of TBI TreatmentEverything done for a TBI casualty in the field — oxygen, blood pressure support, head elevation, ventilation control, hypertonic saline — exists to interrupt this cascade. Primary injury is fixed. Secondary injury is what the medic can prevent.

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Types of Head Injuries — Classification

Identify the major categories of head injury (scalp, closed, open, fractures, blast, penetrating).

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Master Classification

Category	Subtypes
Scalp	Open (puncture, laceration, avulsion); Closed (contusion)
Closed	Blunt; Diffuse Axonal Injury (DAI); Intracranial hemorrhages; Cerebral contusions
Skull Fractures	Open; Closed; Classified by location and pattern (linear, depressed, comminuted, basilar)
Primary Blast	Overpressure central nervous system injuries
Penetrating	Fragments; Gunshot wound; Guttering (grooving the skull)

Open vs Closed Head Injury (RMHB Definitions)

Type	Defining Feature	Common Mechanism	Primary Concern
Open	Penetration of the skull	Missiles, blunt instruments	Direct brain damage + infection. Lethality scales with square of velocity.
Closed	No skull penetration; may have scalp laceration or facial fracture	Falls, motor vehicle accidents	Delayed deterioration from hematoma or swelling raising ICP

The HallmarkAcross every category, the hallmark of brain injury is alteration of consciousness. It may be mild or severe, immediate or delayed, brief or permanent.

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Scalp Injuries and Closed Skull Injuries

Identify the clinical presentation and management of scalp injuries, closed skull injuries, and diffuse axonal injury.

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Scalp Injury — Definition

Injury to the overlying skin of the scalp, which may be in combination with injury to the skull, brain, and/or face.

Scalp Injury Causes

Penetrating trauma — rifle, impaled objects, missile wounds.
Blunt trauma — motor vehicle accident, blast.

Types: Closed (contusion); Open (puncture, laceration, avulsion). Can lead to massive blood loss and hypovolemic shock due to high vascularity of the scalp.

Scalp Laceration Management

Hemorrhage control — direct pressure or pressure dressings.
Donut ring — used when a depressed skull fracture or impaled object is suspected, so pressure does not drive fragments inward.
Lidocaine with epinephrine infiltration — both anesthetizes and constricts vessels.
Clamp or ligate vessels for persistent bleeders.
Assess for fracture beneath the laceration.
Prevent contamination.
Repair galeal defects.

Closed Skull Injury — Definition

May or may not be lacerations of the scalp, but the skull is intact and there is no opening to the brain. Injury to the brain itself may be far more extensive in a closed head injury because more of the injuring force is transmitted deeper into the brain due to pressure build-up.

Closed Skull Injury Causes

Coup-contrecoup — brain bruised at site of impact and on the opposite side.
Blunt trauma.

Closed Skull Injury Signs and Symptoms

Crepitus around injury site
Headache
Neurological symptoms: altered level of consciousness, restlessness, unequal pupils
Bruising
Drainage of blood or CSF from ears, nose, or eyes
Bradycardia
Increased systolic blood pressure
Nausea / vomiting
Decreased respirations / Cheyne-Stokes breathing pattern
Deformity of the skull

Diffuse Axonal Injury (DAI)

DAI is a closed skull injury characterized by:

Stretching and shearing of white matter and axons.
Generated by sudden deceleration or rotational forces.
Edema develops rapidly.
Often produces devastating and irreversible deficits.
Common mechanisms: blunt trauma, motor vehicle accidents, shaken baby syndrome.

Bradycardia + Hypertension TogetherBradycardia plus rising systolic blood pressure in a head-injured patient is part of the Cushing reflex (covered in Increased ICP). It signals dangerously high intracranial pressure. Combined with irregular respirations (third component), herniation is imminent.

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Open Skull Injuries and Skull Fractures

Identify the classifications of skull fractures and the signs of basilar skull fracture.

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Open Skull Injury — Signs and Symptoms

Profuse bleeding no matter how minor the injury appears.
Crepitus
Edema
Depressions
Deformities
Visualization of skull or bony fragments

Classification of Skull Fractures

Axis	Categories
Open vs Closed	Open = scalp laceration over fracture site; Closed = intact overlying skin
Location	Specific skull bone (e.g. temporal); Basilar
Pattern	Linear; Depressed; Comminuted

Linear Skull Fracture

Accounts for about 69 percent of all open head injuries.
Injury does not penetrate brain tissue.
Most are minor and require little treatment.

Depressed Skull Fracture

Typically occurs when significant force is applied over a small area.
Scalp lacerations should undergo sterile exploration.
Palpation may reveal an "ashtray" feel.

Basilar Skull Fracture

May occur anywhere along the skull base.
Significant risk factor for intracranial injury.
Basilar fractures typically do not have localizing symptoms.
Indirect signs often develop:

Indirect Signs of Basilar Skull Fracture

Sign	Description	Location
Battle’s sign	Retroauricular ecchymosis — discoloration of soft tissue behind the ear	Fracture of auditory canal and lower skull. Late sign; may not be readily seen.
Raccoon eyes	Bilateral periorbital ecchymosis	Fracture in the anterior portion of the skull base
Hemotympanum	Blood behind the tympanic membrane; fracture line communicates with auditory canal	May have associated vertigo, hearing loss, and CN VII (facial nerve) palsy
CSF leak	CSF can leak from nose (rhinorrhea) or ears (otorrhea)	Dextrose or halo test can assist confirmation but is not reliable. Patients can develop meningitis. Requires surgical repair. Head elevation and antibiotics are field treatment.

⚠ Battle’s Sign vs Raccoon EyesBoth indicate basal skull fracture, but the location is different. Battle’s sign is BEHIND the ear (mastoid bruising). Raccoon eyes are AROUND the orbits (periorbital). These get swapped on exams constantly.

7

Brain Injuries — Hemorrhages and Contusions

Identify the four types of intracranial hemorrhage and cerebral contusion patterns.

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Direct Brain Injury Categories

Type	Description	Examples
Focal	Occur at a specific location in the brain	Cerebral contusion; epidural, subdural, subarachnoid, intracerebral hemorrhage
Diffuse	Widespread brain involvement	Concussion; Diffuse Axonal Injury

Coup vs Contrecoup

Pattern	Location of Injury
Coup	The brain is injured directly under the area of impact.
Contrecoup	The brain is injured on the side opposite the impact.

Cerebral Contusion

Blunt trauma to local brain tissue with capillary bleeding into brain tissue.
Common with blunt head trauma.
Symptoms: confusion; neurologic deficit including personality changes, vision changes, speech changes.
Results from coup-contrecoup injury.

The Four Types of Brain Hemorrhage

Classified by location: epidural, subdural, subarachnoid, intracerebral (intraparenchymal).

Epidural Hematoma

Blood between the skull and dura mater.
Mechanism: blunt trauma to the temporal or temporoparietal area with associated skull fracture and middle meningeal artery disruption.
Arterial high-pressure bleed — can lead to herniation within hours after injury.
Classic symptom pattern: transient loss of consciousness, followed by a lucid interval, then rapid neurological decline. Not common but classic for testing.
Lucid interval usually lasts 6 to 18 hours.
As ICP rises, level of consciousness decreases.
Patient may only complain of headache and drowsiness in early stages.

Subdural Hematoma

Blood between the dura mater and the surface of the brain.
Mechanism: bleeding from bridging veins in the subdural space, due to sudden acceleration and deceleration.
Associated contusion or laceration of the brain is frequently present.
Often the result of blunt head trauma.
Commonly associated with skull fracture.

Subarachnoid Hemorrhage

Intracranial bleeding into the CSF resulting in bloody CSF and meningeal irritation.
Bleeding typically results from trauma or rupture of an aneurysm.
Classic presentation: "worst headache of life" — thunderclap headache.
Neck stiffness from meningeal irritation.

Intracerebral Hemorrhage

Greater than 5 mL of blood somewhere within the brain.
Causes: multiple lacerations from penetrating head trauma; high-velocity deceleration injury; compression and distortion from increased ICP.
Often associated with subdural hemorrhage and skull fracture.

Side-by-Side Comparison

Type	Anatomic Location	Source	Speed of Decline
Epidural	Between skull and dura	Middle meningeal artery (arterial)	Rapid (hours); classic lucid interval
Subdural	Between dura and brain	Bridging veins (venous)	Slower than epidural
Subarachnoid	Into the CSF space	Trauma or ruptured aneurysm	Sudden thunderclap headache
Intracerebral	Within brain tissue itself	Penetrating trauma, deceleration, or pressure	Variable

⚠ Epidural vs SubduralEpidural = arterial, fast, lucid interval, often temporal bone fracture and middle meningeal artery. Subdural = venous, slower, bridging veins, acceleration-deceleration mechanism. The lucid interval is the testable feature of epidural.

Worst Headache of LifeSudden onset thunderclap headache with neck stiffness in a trauma context (or even without one) is subarachnoid hemorrhage until proven otherwise. Treat as a neurosurgical emergency.

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Blast and Penetrating Brain Injuries

Identify the clinical presentation and complications of primary blast and penetrating head injuries.

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Primary Blast Injury

A direct injury to the brain or via a force transmitted by the great vessels of the chest to the brain.

Primary Blast Signs and Symptoms

Unconsciousness, confusion, headache
Tinnitus, dizziness, tremors
Increased startle response
Increasing intracranial pressure
Bleeding may occur from multiple orifices
May have no external signs of injury and only subtle signs of cognitive dysfunction in attention, concentration, reaction time, and balance

Penetrating Injury

Mechanisms: missiles and stab wounds.
Associated injuries: skull fracture, damage to cerebral vasculature, intracranial hemorrhage.
Complications include infection and post-traumatic epilepsy.
Pneumocephalus (air pockets in the skull) is a hallmark on imaging.

The Invisible Blast InjuryPrimary blast can cause significant brain dysfunction with no visible external trauma. A casualty within 150 meters of a blast who looks fine still requires MACE evaluation. The cognitive deficits are subtle and easily missed.

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TBI Assessment — GCS, Classification, and Examination

Identify the assessment of TBI including history, physical exam, neurological exam, and GCS classification.

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Three Primary Goals of TBI Management

1

Identify other life-threatening injuries.

2

Prevent further secondary brain injury by correcting or preventing hypoxia, hypotension, anemia, and hyperthermia.

3

Identify treatable mass lesions and evacuate intracranial masses (performed at surgical facility).

History — Reconstruct the MOI

SAMPLE history.
Specific questions: nausea, vomiting, headache, memory impairment, visual/auditory symptoms, seizures, loss of consciousness.
Drug or alcohol intoxication.

Airway and Breathing

Early establishment of a definitive airway is imperative.
Suctioning; patient positioning; OPA/NPA use; endotracheal intubation; cricothyrotomy.
Avoid hypoxia by maintaining oxygen saturation greater than 95%.
Avoid vasoconstriction or vasodilation by maintaining PaCO2 between 35 and 40 mmHg.

Circulation

Hemorrhage control — cover open wounds securely enough to aid clotting without pressing skull fragments inward; use a donut O-ring.
Blood pressure maintenance: SBP must be maintained above 90.
Initiate fluid bolus as indicated. Do NOT let SBP go below 90 — this can double mortality.

Fluid Resuscitation

Goal: systolic blood pressure above 90.
Hypovolemia reduces cerebral perfusion and causes hypoxia.
Initiate IV/IO normal saline or Hextend; titrate to effect.
In TBI plus shock, use restoration of radial pulse or SBP greater than 90 mmHg as the resuscitation endpoint.

⚠ SBP Targets Differ Across SourcesThe SOMTRL1F lecture and original Tactical Trauma Protocols target SBP greater than 90. The 2025 Ranger Medic Handbook targets SBP greater than 110. The lower threshold (90) is the "do not fall below" floor; the higher threshold (110) is the resuscitation goal in newer guidance. Both numbers are correct — the RMHB is more aggressive. Know which source the exam is using.

⚠ SpO2 Targets DifferSOMTRL1F lecture: maintain SpO2 greater than 95%. RMHB: maintain greater than 92% and less than 100%. The newer RMHB number is lower because there is evidence that hyperoxia is also harmful in TBI.

Physical Examination — Head Exam

Scalp trauma.
Skull fractures.
Signs of basilar skull fracture: Battle’s sign, raccoon eyes, hemotympanum, otorrhea, rhinorrhea.
Assess for other injuries, especially C-spine and extremities.
All head trauma patients are assumed to have a cervical spine injury until proven otherwise.

Neurological Examination — Level of Consciousness

Level of consciousness is the best indicator of perfusion.
Document with AVPU and GCS.
Reevaluate several times during the encounter.
Deterioration in LOC is the best indicator of increasing ICP.

Glasgow Coma Scale

Category	Response	Score
Eye Opening	Spontaneous	4
	To voice	3
	To pain	2
	None	1
Verbal Response	Oriented	5
	Confused	4
	Inappropriate words	3
	Incomprehensible words	2
	None	1
Motor Response	Obeys commands	6
	Localizes pain	5
	Withdraws (pain)	4
	Flexion	3
	Extension	2
	None	1

TBI Severity Classification by GCS

Classified based on patient’s level of consciousness, not actual underlying injury. Patients with the same TBI severity classification may have dramatically different pathophysiology.

Severity	GCS Range
Mild TBI	14 to 15
Moderate TBI	9 to 13
Severe TBI	3 to 8

Pupillary Examination

Finding	Meaning
Fixed dilated pupil	Ipsilateral intracranial hematoma resulting in uncal herniation
Bilateral fixed and dilated	Poor brain perfusion, bilateral uncal herniation, or severe hypoxia. Indicative of very poor neurological outcome.

Alcohol and other drugs can cause abnormal pupillary reactions.

Cranial Nerves Affected by Rising ICP

Nerve	Function	Effect of ICP
CN III (Oculomotor)	Controls pupil size	Pressure paralyzes the nerve; pupil dilates and becomes unreactive
CN X (Vagus)	Supplies SA and AV nodes	Pressure on nerve stimulates bradycardia

Why the Pupil Dilates on the Same SideAn expanding intracranial hematoma pushes the temporal lobe (uncus) medially, compressing CN III against the brainstem. CN III controls the pupil constrictor. When it is compressed, the pupil dilates. The dilated pupil is on the SAME side as the hematoma. This is uncal herniation.

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Increased ICP — Clinical Presentation and Management

Identify the clinical signs and management of increased intracranial pressure including Cushing reflex, head elevation, mannitol, hypertonic saline, hyperventilation, and seizure prophylaxis.

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Early Warning Signs of Increasing ICP

Headache
Nausea and vomiting
Altered level of consciousness — the earliest sign of increasing ICP is a change in LOC
Decline in GCS score of 2 points or more

Cushing Reflex (Triad) — Late and Ominous

Acute entity seen in severely head-injured patients with significant increased intracranial pressure and impending herniation.

Hypertension
Bradycardia
Respiratory irregularity (e.g. Cheyne-Stokes)

Papilledema (swollen optic disc) is a late finding and is probably not going to be seen in acute head injury. Unilateral presentation is extremely rare.

Late Signs of Herniation

Rapidly unresponsive to verbal and painful stimuli
Neurological posturing — decorticate or decerebrate
Ipsilateral dilated and unreactive pupil

Herniation Syndromes

Eventually some part of the brain will push through an opening in the skull or dura. Various syndromes exist; uncal transtentorial is the most common.

Head Elevation Rules

Scenario	Action
CSF leak from ears or nose AND hemodynamically stable	Elevate head 30 to 60 degrees if other injuries permit
Signs of increased ICP AND hemodynamically stable	Consider elevating head 30 degrees to improve venous outflow and decrease ICP
Hypovolemic casualty	Do NOT elevate the head — this will reduce cerebral blood flow further

Mannitol (Osmotrol) — Osmotic Diuretic

Field	Detail
Mechanism	Large glucose molecule that does not leave the bloodstream; pulls fluid from brain into vasculature
Dose	1 gram per kilogram
Contraindications	Hypovolemia, hypotension, congestive heart failure
Cautions	Forms crystals at low temperatures. Reconstitute with rewarming and gentle agitation. Use an in-line filter and preflush the line.

Hypertonic Saline (3 to 5%)

Scenario	Treatment
Isolated TBI (hemodynamically stable)	3 to 5% HS, 250 mL IV or IO
TBI with controlled external hemorrhage	3 to 5% HS, 250 mL IV or IO, plus Hextend or other fluids per fluid resuscitation protocol if required

Controlled Hyperventilation — NOT Routine

Temporizing measure only for evidence of increasing ICP and herniation.

Source	Target EtCO2 (Herniation)	Without Monitor
SOMTRL1F lecture	30 to 35 mmHg	Ventilate at 20 BPM, tidal volume approximately 500 mL, highest oxygen concentration possible
RMHB 2025	25 to 30 mmHg for 15 to 20 minutes	Same: 20/min, tidal volume approximately 500 mL

⚠ EtCO2 Targets DifferThe lecture gives 30 to 35 mmHg for hyperventilation in herniation. RMHB 2025 gives a more aggressive 25 to 30 mmHg. Both target the same physiology — reducing cerebral blood volume by causing vasoconstriction. RMHB is the newer and more aggressive number.

Seizure Prophylaxis Options

Drug	Dose	Notes
Fosphenytoin (Cerebyx)	18 mg/kg IV or IO at 100 to 150 mg/min (slow IVP); repeat 100 mg IV/IO every 8 hours for maintenance	WARNING: do not administer faster than 150 mg/min — may cause hypotension. Refrigerate at 2 to 8 degrees C. Not stable at room temperature beyond 48 hours.
Levetiracetam (Keppra)	4 grams IV (RMHB-preferred)	Newer RMHB protocol agent for TBI seizure prophylaxis

⚠ Two Different Seizure ProphylacticsThe older SOMTRL1F lecture uses fosphenytoin (Cerebyx). The newer 2025 RMHB uses levetiracetam (Keppra) 4 grams IV. Levetiracetam is preferred operationally because it does not require refrigeration and has a wider therapeutic margin.

Active Seizure Management

Drug	Dose
Diazepam (Valium)	5 to 10 mg IV/IO every 5 minutes, max dose 20 mg
Midazolam (Versed)	5 mg IV/IO every 5 minutes (no maximum dose)
Fosphenytoin	18 mg/kg IV/IO at 100 to 150 mg/min for seizures refractory to benzodiazepines

Monitor casualty closely for apnea when administering benzodiazepines.

Sedation for Agitation

Agitation is a common finding and may result from pain, delirium, or difficulties with oxygenation and ventilation. Painful stimuli and stress increase metabolic demands, blood pressure, and ICP. Minimizing agitation limits ICP rises and improves oxygenation.

Midazolam (Versed) — 1 to 2 mg IV/IO if no evidence of shock or hypotension.
Diazepam (Valium) — 5 to 10 mg IV/IO if no evidence of shock or hypotension.

Antibiotics for Penetrating Head Trauma

Source	Drug	Dose
SOMTRL1F lecture	Ertapenem (Invanz) OR Ceftriaxone (Rocephin)	1 gram IV/IO
RMHB 2025	Ceftriaxone (Rocephin)	2 grams IV/IO

⚠ Ceftriaxone Dose DiffersSOMTRL1F lecture: 1 gram. RMHB 2025: 2 grams. The newer 2 gram dose reflects improved CNS penetration evidence.

Evacuation

If possible, evacuate the casualty to a facility with a neurosurgeon available. Generally, head injuries should be evacuated by air using low altitude or pressurized cabin.

11

Mild TBI (Concussion) — MACE and Red Flags

Identify the definition, assessment, MACE evaluation, and red flag symptoms of mild traumatic brain injury.

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Mild Traumatic Brain Injury Definition

Physiologic changes in brain functioning resulting from trauma to the head without radiographic evidence of structural damage.

Does not require loss of consciousness.
Clinical symptoms and cognitive deficits linked to brain-related changes in physiology.
Normal structural neuroimaging.

Core Concerns with mTBI

Period of vulnerability after the first injury.
During this period, less biomechanical force results in more serious injury.
Physical and cognitive exertion protracts and complicates recovery.

Consider mTBI in Anyone Who Is...

Dazed, confused, "saw stars," lost consciousness (even momentarily), or has memory loss from a fall, explosion, motor vehicle crash, or any event involving abrupt head movement, direct blow to the head, or other head injury.

mTBI Assessment Components

History
Physical exam
Neurocognitive testing (MACE, ImPACT)

mTBI History Findings

Loss of consciousness
Drowsiness, restlessness, confusion, anxiety
Amnesia — retrograde (unable to recall events before injury) or antegrade (unable to recall events after injury)
Abnormal speech; repetitive questioning
Vomiting

mTBI Physical Exam Findings

Ruptured tympanic membranes
Trauma to the head or neck (penetrating and non-penetrating)
Cranial nerve deficits
Sensory deficits
Motor deficits
Inability to do rapid alternating movements
Visual field deficits
Abnormal mini-mental status evaluation
Abnormal vestibular screening: inability to maintain balance, persistent nystagmus, tracking and convergence problems

mTBI Red Flags — Comprehensive List

Category	Red Flag
Neurological	Witnessed loss of consciousness
	Amnesia and memory problems
	Unusual behavior or combative
	Seizures
	Worsening headache
	Cannot recognize people
	Abnormal speech
Eyes	Double vision
General	Two or more blast exposures within 72 hours
	Repeated vomiting
	Weakness
	Unsteady on feet

Military Acute Concussion Evaluation (MACE)

Can be easily used by medics to confirm a suspected diagnosis of concussion.
Can be administered in 5 minutes.
Assesses four cognitive domains: orientation, immediate memory, concentration, delayed recall.

MACE Scoring

Result	Interpretation
Total possible	30 points
Mean for non-concussed	28
Below 25	May represent clinically relevant neurocognitive impairment; requires further evaluation for the possibility of a more serious brain injury

Serial assessments document either decline or improvement in cognitive functioning.

Mandatory Events Requiring MACE

Personnel in a vehicle associated with a blast, collision, or rollover
Personnel within 150 meters of a blast
Personnel with a direct blow to the head
Command-directed evaluation

ImPACT — Immediate Post-Concussion Assessment and Cognitive Testing

Computerized neurocognitive assessment.
Assists in determining a patient’s ability to return to duty after concussion.
All SOF personnel should have a baseline.
Retest after injury.

When to Test (ImPACT Timing)

1

Baseline testing — before injury, ideally for all personnel.

2

24 to 72 hours post-injury.

3

Days 5 to 10 post-injury.

4

Beyond if necessary for protracted recovery.

Protracted Recovery Risk Factors

Age
History of migraine headache
Exertion during recovery
Gender
History of previous concussion

Amnesia Outweighs LOCAmnesia is approximately 10 times more predictive than loss of consciousness for deficits on ImPACT testing. A casualty who never lost consciousness but cannot remember the event is at high risk. Do not be falsely reassured by an alert, oriented patient who has gaps in memory.

12

mTBI Management, Second Impact, and Return to Duty

Identify the management of mTBI, second impact syndrome, the 5-stage rehabilitation protocol, and return-to-duty criteria.

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mTBI Management Principles

Symptomatic treatment and prevention of secondary injury.
All patients with mild traumatic brain injury should be observed for 24 hours after injury.

Protect from Further Injury

Controlled environment — come out of the fight, no contact activities.
Limit exertion — both physical and mental.
Find the "sweet spot" — enough activity to feel useful, not enough to slow healing.
Do not allow a patient with mTBI to return to duty prior to full recovery.

Risks of Premature Return to Duty

PTSD; depression
Prolonged recovery
Post-concussive syndrome
Second impact syndrome

Second Impact Syndrome

Additional injury during the period of vulnerability after a first concussion. Mechanism:

The first head injury disrupts normal cerebral vascular autoregulation.
This causes increased cerebral blood flow.
The brain becomes vulnerable to a second impact.
When the second impact occurs, rapid malignant swelling develops.
Less biomechanical force is required to cause severe injury in susceptible individuals.

Treat the Headache

Choice	Reason
Tylenol (acetaminophen) is the best choice	No effect on platelets, no sedation
Avoid COX-1 NSAIDs (ibuprofen, naproxen)	Effects on platelets and potential increased bleeding risk. If they are the only option and no red flags are present, they may be used.
Avoid tramadol (Ultram)	Alters level of consciousness; lowers seizure threshold
Avoid diphenhydramine (Benadryl)	Alters level of consciousness
Avoid narcotics	Alter level of consciousness, mask deterioration

Evacuation Criteria

Red flags present — consult with medical provider for possible urgent evacuation.
MACE less than 25 or persistent symptoms despite rest and treatment — consult with medical provider for possible priority evacuation.

Educate, Reevaluate, Rehabilitate

1

Educate the patient about expected recovery.

2

If MACE is normal, recommend 24-hour rest and reevaluation.

3

Perform ImPACT testing during the 24- to 72-hour post-injury window.

4

Graded return of cognitive and physical exertion through the 5-stage rehabilitation protocol.

5-Stage Rehabilitation Protocol

Stage	Target Heart Rate	Focus
Stage 1	30 to 40% of max exertion	Quiet area, no impact, balance and vestibular as needed, limited head movement, 10 to 15 min light cardio
Stage 2	40 to 60% of max exertion	Gym environment, light to moderate aerobic, light weights, active stretching, 20 to 30 min cardio
Stage 3	60 to 80% of max exertion	Moderately aggressive aerobic, all strength forms, impact activities (running, plyometrics), challenging balance, 25 to 30 min cardio
Stage 4	80% of max exertion	Non-contact physical training, aggressive strength, impact and plyometrics, job-specific training
Stage 5	Full exertion	Full activities and combat training, contact resumed, job-specific (shooting, CQB, fast-roping)

Return to Duty Criteria

Completed Stage 5 rehabilitation protocol.
Symptom-free.
Consider additional ImPACT exam.
If you do not feel the patient is back to baseline, do not allow RTD — consult a medical provider.
All return-to-duty must be evaluated and approved by an MD or PA.

Post-Concussion Syndrome

A set of symptoms develops within 4 weeks of injury and may persist for months.

90% of patients are symptomatic at 1 month.
25% are symptomatic at 1 year.

Common symptoms: chronic migraine-type headache, photosensitivity, nausea, neurobehavioral changes, sleep deficits, cognitive deficits, academic difficulties.

mTBI and PTSD — Support Resources

Warrior 2 Warrior (warrior2warrior.org)
Veterans Crisis Line (veteranscrisisline.net)
22Kill (22kill.com)

Second Impact Syndrome Is CatastrophicThe lesson of second impact syndrome: a casualty who feels "mostly fine" 24 hours after a blast is NOT cleared. Their cerebral autoregulation is still impaired. A second hit during this window — even a minor one — can produce rapid malignant brain swelling and death. This is the core reason mandatory 24-hour rest is non-negotiable.

The "Sweet Spot"Complete bed rest delays recovery. So does aggressive return. The goal is the minimum activity level that maintains morale and physical conditioning without exacerbating symptoms — the "sweet spot."

13

Eye Injury and Lateral Canthotomy

Identify the assessment, management, and lateral canthotomy procedure for penetrating eye injury and retrobulbar hematoma.

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Eye Injury — The Primary Rule

Rigid eye shield, never a pressure patch. Avoid any manipulation of the eye or globe if penetrating injury is suspected.

Rapid Field Visual Acuity Test (Best to Worst)

1

Able to read print.

2

Can count fingers held up.

3

Can see hand motion.

4

Can see light.

Red Flags for Penetrating Globe Injury

Large subconjunctival hemorrhage with chemosis
Dark uveal tissue projecting through cornea or limbus
Distorted pupil
Leak from corneal defect (fluorescein exam)
Hyphema — blood in anterior chamber
Mechanism with visible object or facial injury
Impaled object

Eye Injury TCCC Management

Phase	Action
Care Under Fire	Stop life-threatening bleeding
TFC / TACEVAC	Rapid visual acuity test; rigid shield; ondansetron 4 to 8 mg IV/IM/ODT/PO to prevent vomiting-induced IOP rise; moxifloxacin 400 mg PO or ertapenem 1 g IV/IM; tetanus if available

Retrobulbar Hematoma — Bloody, Blind, Bulging

If intraocular pressure rises above 21 mmHg, central retinal artery occlusion or optic nerve damage may occur with permanent vision loss. Optic nerve ischemia develops within 45 to 90 minutes.

Signs: pain, periorbital ecchymosis, progressive proptosis, decreased vision, diffuse subconjunctival hemorrhage, afferent pupillary defect.

Lateral Canthotomy Procedure

Indication: retrobulbar hematoma (Bloody, Blind, Bulging). Contraindication: globe rupture.

Equipment: mosquito clamp/hemostats/needle driver; lidocaine 1% with epi preferred; 25g 5/8″ needle; iris scissors; tissue forceps.

1

Prep equipment.

2

Inject 1 to 2 mL lidocaine in the lateral canthus area.

3

Crimp the lateral canthus area with hemostats for 60 to 120 seconds.

4

Incise the lateral canthus at the crimped area with iris scissors, laterally about 1 to 2 cm.

5

Pull the inferior lid away to visualize the inferior lateral canthal tendon.

6

Incise the inferior crus of the lateral canthal tendon.

7

Gently pull tissue for global pressure release.

8

If symptoms have not improved, incise the superior crus.

9

Apply loose protective dressing material (no pressure).

Caution: all aspects of the procedure should be performed lateral to the eye.

Why Ondansetron for Eye InjuryVomiting raises intraocular pressure. In a compromised globe or developing retrobulbar hematoma, that pressure spike can extrude eye contents or worsen optic nerve ischemia. Ondansetron is protective, not just for comfort.

14

Seizures — Assessment and Management

Identify the assessment, differential diagnosis, and management of seizures including status epilepticus.

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Definition

A seizure is characterized by abrupt onset of abnormal muscle activity or a prodrome of confusion, peculiar behavior, automatisms, or vivid sights or smells. Most are brief and self-limited.

Assessment

Sudden onset of loss of consciousness
Tonic rigidity, clonic rhythmic movements
Urinary incontinence, frothing at mouth, biting tongue
Duration: seconds to minutes
Followed by postictal state: weakness, somnolence, confusion lasting hours
After focal motor seizures: Todd’s paralysis — focal weakness of the affected limb

Differential Diagnosis

Idiopathic epilepsy
Alcohol or drug associated seizures
Post-concussive syndrome
Convulsive syncope
Heat stroke
Infection (meningitis)
Brain mass lesions
Nerve gas exposure
Metabolic abnormalities
Eclampsia in pregnancy

Medications that lower seizure threshold: Wellbutrin, INH, tramadol.

Initial Management

Remove patient from areas where injury can occur.
Pad objects; keep sharp and breakable objects away.
Do NOT put anything in the patient’s mouth.
Never put fingers in the patient’s mouth.

Status Epilepticus — Seizure Lasting More Than 5 Minutes

Life-threatening event that may produce significant brain injury. Protocol triggers benzodiazepines after 2 to 5 minutes.

Drug	Dose / Route / Frequency
Midazolam	5 mg IV/IO every 2 to 3 minutes, or 10 mg IM every 15 minutes
Diazepam	5 mg IV/IO every 5 to 10 minutes, or 10 mg IM every 15 minutes (for 2 doses)

Seizure Prophylaxis After Seizure Stops (RMHB)

If available, administer levetiracetam 4 grams IV over 5 to 15 minutes to prevent recurrence. If evacuation is delayed more than 12 hours after loading, give 1 gram IV every 12 hours until higher level of care.

Meningitis Pathway

If the seizing patient has recent history of headache, neck stiffness, or fever: initiate saline lock and administer ceftriaxone 1 gram IV or ertapenem 1 gram IV every 8 hours. Evacuate as soon as possible.

Extended Care

No driving, weapons handling, or other dangerous activities until medically cleared. Urgent evacuation is not normally required for a single seizure that spontaneously resolved. Refer for routine neurological consultation.

⚠ Five Minutes Is StatusA seizure lasting longer than 5 minutes is status epilepticus. The protocol gives benzodiazepines after 2 to 5 minutes to prevent progression. Do not wait for the 5-minute mark.

15

Spinal Cord Injury Management

Identify indications for cervical immobilization, NEXUS criteria, and TCCC application for spinal cord injury.

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Combat Considerations

IED blasts and jump injuries have a high risk for lumbar fractures. Physical exam is essential for C-spine clearance; most patients require imaging.

Spine Boards — Limited Role

Spine boards cause harm through prolonged pressure.
No more than 10 minutes on a spine board.
Move to a padded rigid litter as soon as possible.
Do NOT place a suspected spine-injured patient on a SKEDCO or flexible litter.

NEXUS Criteria for C-Spine Clearance

If all five are NO, a cervical collar is not necessary.

Focal neurologic deficit?
Midline spinal tenderness?
Altered level of consciousness?
Intoxication?
Distracting injury?

TCCC Application

Phase	Action
Care Under Fire	Manage life-threatening hemorrhage. Preservation of life is paramount. Evacuation takes precedence over spine immobilization.
Tactical Field Care	Consider cervical collar for blunt mechanisms if tactical situation allows. Spinal stabilization only AFTER all other lifesaving interventions.
Tactical Evacuation	Urgent if gross neurological deficits. Priority if no other significant injuries and no deficit. Pad litter; ensure hypothermia prevention.

Mechanisms Warranting Cervical Collar (Blunt)

Major explosive or blast injury
Violent impact on head or neck
Sudden acceleration, deceleration, or lateral bending forces
Fall from height (not standing)
Ejection or fall from motorized vehicle

Penetrating Cervical Injury — The Autopsy Data Rule

Patients with penetrating cervical injury in war almost never survive.
Patients with isolated penetrating cervical injury, conscious, with no neurological signs — do NOT place a cervical collar prehospital.
Patients with isolated penetrating brain injury do not require a cervical collar unless trajectory suggests C-spine involvement.

Field Expedient Cervical Immobilization

IV bags, rolled poncho liner, stacked or taped MRE package, rolled uniform shirt, snivel gear.

Extended Care for Immobilized Patients

Pad litter to prevent pressure ulcers.
Be prepared for emergency suction (aspiration risk).
Use prophylactic antiemetics.
High cord injuries may affect diaphragm — be prepared for ventilation.
Neurogenic shock: hypotension + bradycardia. Hypovolemic shock: hypotension + tachycardia. If a spine-injured patient is tachycardic, look for blood loss.
Use Foley catheterization or tipping for urination management.

⚠ Neurogenic vs Hypovolemic ShockBoth cause hypotension. Heart rate is the differentiator. Neurogenic = bradycardia. Hypovolemic = tachycardia. A spine-injured patient with tachycardia is bleeding somewhere, not in neurogenic shock.

Head Trauma & Hypothermia