You are a 3rd year medical student on your surgery clinical rotation currently on Trauma week. You receive an Epic chat message from your senior resident saying to evaluate a patient in ED room 23.
[[Patient details]]
Clinical Case: Minimally Invasive Lumbar Interbody Fusion (MIS-LIF) with Spineology’s OptiMesh® Implant for Spinal Trauma
[[Begin]]
Name: John Doe
• Age: 42
• Gender: Male
• Medical Record Number: 123456789
• Chief Complaint: severe lower back pain, bilateral lower extremity weakness, and numbness
What would you like to do next?
[[1. Talk to the patient and gather further history]]
[[2. Perform a physical exam]]
[[3. Order imaging studies]]
[[4. I am ready to present to the attending]]HPI
A 42-year-old male construction worker presents to the Carle ED after falling approximately 15 feet from scaffolding. He landed on his feet but experienced an immediate onset of excruciating lower back pain, followed by progressive weakness and numbness in both legs.
The patient describes the pain as 10/10 in intensity, sharp, and radiating bilaterally down to the posterior thighs. He reports difficulty standing and ambulating due to leg weakness but denies complete paralysis. There is no loss of bowel or bladder control. He denies head trauma or loss of consciousness.
Using your differential diagnosis as a guide, what further questions would you like to ask?
[[ROS pertinent positives]]
[[ROS pertinent negatives]]
[[Past medical history]]
[[Past surgical history]]
[[Medications]]
[[Allergies]]
[[Family history]]
[[Social history]]
Return back to [[Patient details]]Using your differential diagnosis as a guide, what parts of the physical exam would you like to assess?
Vital Signs: Blood Pressure: 135/88 mmHg, Heart Rate: 92 bpm, Respiratory Rate: 18 bpm, Temperature: 98.6°F (37°C), Oxygen Saturation: 99% on room air
General: Patient appears uncomfortable but alert and oriented. No signs of head trauma or distress.
[[Spine:]]
[[Neurological Exam:]]
You think back to your neuro clerkship and try to remember all the components of the neuro exam...
Return back to [[Patient details]]
What type of imaging study would you like to order?
[[CT lumbar spine]]
[[MRI lumbar spine]]
Return back to [[Patient details]]ROS Pertinent Positives:
• Inability to bear weight due to leg weakness
• Bilateral lower extremity numbness
• Worsening pain with movement
ROS Pertinent Negatives:
• No saddle anesthesia
• No bowel or bladder incontinence
• No recent infections, fever, or systemic symptoms
[[What neurosurgical emergency must be ruled out immediately, and why?]]
• Significant tenderness over the L4-L5 vertebra
• No obvious deformity, but pain worsens with palpation and movementMental Status: Alert and oriented to person, place, and time. Normal speech and comprehension
Cranial Nerves:
CN II: Visual fields intact.
CN III, IV, VI: Extraocular movements intact, no nystagmus.
CN V: Facial sensation intact.
CN VII: Symmetric facial movements.
CN VIII: Hearing intact bilaterally.
CN IX, X: Normal gag reflex, palate elevates symmetrically.
CN XI: Shoulder shrug and head rotation intact.
CN XII: Tongue midline, no fasciculations.
[[Why is it important to assess cranial nerves in a suspected spinal injury?]]
Motor:
Upper Extremities: 5/5 strength in all muscle groups bilaterally.
Lower Extremities:
• Hip flexion: 4/5 bilaterally
• Knee extension: 4/5 bilaterally
• Dorsiflexion: 2/5 bilaterally
• Plantarflexion: 2/5 bilaterally
[[Which spinal nerve roots correspond to dorsiflexion and plantarflexion? How does this help localize the lesion?]]
Sensation:
• Biceps, Triceps, Brachioradialis: 2+ bilaterally.
• Intact sensation in upper extremities and thoracic region
• Decreased pinprick and light touch in L4-L5 dermatomes.
[[What are the dermatomal distributions of L4 and L5, and how do they relate to this patient’s symptoms?]]
Reflexes:
• Patellar reflex: diminished (+1) bilaterally
• Achilles reflex: absent (0) bilaterally
[[How does the absence of the Achilles reflex help differentiate between upper motor neuron (UMN) and lower motor neuron (LMN) lesions?]]
Coordination: Normal finger-to-nose and rapid alternating movements in upper extremities.
Gait: Unable to bear weight due to lower extremity weakness.
Babinski sign: Negative bilaterally
Rectal tone: NormalCT lumbar spine
IMPRESSION
• Comminuted burst fracture of L4 vertebral body
• Retropulsion of bony fragments into the spinal canal, causing significant narrowing
[[What are the key radiologic features of a burst fracture? How does it differ from other fracture types?]]
MRI lumbar spine
IMPRESSION:
• Spinal cord compression at L4-L5 with associated ligamentous injury and spinal cord edema
• No evidence of herniated discs at adjacent levels
[[What role does inflammation and edema play in secondary spinal cord injury?]]
[[What is the ASIA grading system for spinal cord injury, and how would you classify this patient?]]
Past Medical History (PMH):
• hypertension, well-controlled on medication
• type 2 DM
• No prior spinal injuries or surgeries
Past Surgical History (PSH):
• R knee arthroscopy for meniscal repair (10 years ago)
• appendectomy (childhood)
Medications:
• Lisinopril 10 mg daily
• Metformin 500 mg BID
Allergies:
• No known drug allergies
Family History (FH):
• Father: Hypertension, deceased from myocardial infarction at age 65
• Mother: Type 2 Diabetes Mellitus
• No history of spinal disorders or neurological diseases
Social History (SH):
• Occupation: Construction worker
• Smokes 1 pack per day for 15 years
• Occasional alcohol use, denies illicit drug use
Problem List:
1. Traumatic L4 vertebral fracture
2. Spinal cord compression
3. Bilateral lower extremity weakness and sensory deficits
4. Hyporeflexia concerning for LMN involvement
5. High-risk occupation (construction worker)
[[How do occupational factors contribute to the increased risk of spinal cord trauma in this population?]]
[[What is the likely diagnosis?]]Diagnosis:
• L4 burst fracture with retropulsed fragments causing spinal canal compromise and incomplete spinal cord injury (ASIA Grade C).
What would you like to do next?
[[1. Consult neurosurgery for surgical evaluation]]
[[2. Monitor conservatively and reassess]]
The neurosurgical team evaluates the patient and recommends minimally invasive lumbar interbody fusion (MIS-LIF) with the Spineology OptiMesh® expandable implant due to:
• Progressive neurological deficits
• Significant canal compromise with spinal cord compression
• Instability of the fractured segment requiring stabilization
The goal is to use Spineology’s OptiMesh® expandable implant to restore vertebral height, decompress the spinal canal, and stabilize the spine.
[[What is the difference between primary and secondary bone healing?]]
[[Why is mechanical stabilization important?]]
Would you like to proceed with surgery?
[[Yes]]
[[No]]
Close neurological monitoring is initiated.
The patient is started on a physical therapy regimen.
Follow-up imaging is scheduled in 2 weeks to reassess spinal stability.
[[Continue observation and reassess in follow-up]]You have reached the end of the module!
Please meet in the Everritt SIM center at your scheduled OR time
To prepare for the surgery, you can watch the following video: <iframe width="560" height="315" src="https://www.youtube.com/embed/mDpzRTi7vlY" frameborder="0" allow="accelerometer; autoplay; encrypted-media; gyroscope; picture-in-picture" allowfullscreen></iframe>
[[2. Monitor conservatively and reassess]]After 4 weeks of conservative management, the patient continues to experience persistent lower back pain, worsening numbness in the lower extremities, and difficulty ambulating despite physical therapy. He reports increased reliance on assistive devices and ongoing severe discomfort, significantly limiting daily activities.
Repeat Imaging Findings:
• MRI shows persistent spinal cord compression at L4-L5 with incomplete bony healing.
• Increased degenerative changes noted at adjacent levels.
Would you like to re-evaluate for surgical intervention?
[[1. Consult neurosurgery for surgical evaluation]]
Why is it important to assess cranial nerves in a suspected spinal injury?
To rule out concurrent head or bainstem injury: CN deficits may indicate intracranial pathology, such as a brainstem contusion, hemorrhage, or increased intracranial pressure.
To detect basilar skull fractures: CN deficits may suggest a basilar skull fracture, particularly in CN I (anosmia), CN VII (facial weakness), and CN VIII (hearing loss or vertigo).
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<table>
<tr>
<th>Cranial Nerve</th>
<th>Function</th>
<th>Type</th>
</tr>
<tr>
<td>I - Olfactory</td>
<td>Smell</td>
<td>Sensory</td>
</tr>
<tr>
<td>II - Optic</td>
<td>Vision</td>
<td>Sensory</td>
</tr>
<tr>
<td>III - Oculomotor</td>
<td>Eye movement, pupil constriction, eyelid elevation</td>
<td>Motor</td>
</tr>
<tr>
<td>IV - Trochlear</td>
<td>Eye movement (superior oblique muscle)</td>
<td>Motor</td>
</tr>
<tr>
<td>V - Trigeminal</td>
<td>Facial sensation, chewing (mastication)</td>
<td>Both</td>
</tr>
<tr>
<td>VI - Abducens</td>
<td>Eye movement (lateral rectus muscle)</td>
<td>Motor</td>
</tr>
<tr>
<td>VII - Facial</td>
<td>Facial expressions, taste (anterior 2/3 of tongue), salivation, tear production</td>
<td>Both</td>
</tr>
<tr>
<td>VIII - Vestibulocochlear</td>
<td>Hearing, balance</td>
<td>Sensory</td>
</tr>
<tr>
<td>IX - Glossopharyngeal</td>
<td>Taste (posterior 1/3 of tongue), swallowing, salivation, carotid body reflex</td>
<td>Both</td>
</tr>
<tr>
<td>X - Vagus</td>
<td>Autonomic control of heart, lungs, digestion, taste, swallowing, speech</td>
<td>Both</td>
</tr>
<tr>
<td>XI - Accessory</td>
<td>Shoulder shrug (trapezius) and head turning (sternocleidomastoid)</td>
<td>Motor</td>
</tr>
<tr>
<td>XII - Hypoglossal</td>
<td>Tongue movement</td>
<td>Motor</td>
</tr>
</table>
Mnemonic to Remember Cranial Nerve Names:
Oh Oh Oh, To Touch And Feel Very Green Vegetables, Ah Heaven
Mnemonic for Sensory/Motor/Both:
Some Say Marry Money, But My Brother Says Big Brains Matter More
Which spinal nerve roots correspond to dorsiflexion and plantarflexion? How does this help localize the lesion?
Dorsiflexion is controlled by L4-L5, while plantarflexion is controlled by S1. Weak dorsiflexion suggests L4-L5 involvement.
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<table>
<tr>
<th>Spinal Root</th>
<th>Myotome</th>
<th>Function</th>
</tr>
<tr>
<td>C1-C2</td>
<td>Neck flexion</td>
<td>Flexes the head and neck</td>
</tr>
<tr>
<td>C3</td>
<td>Neck lateral flexion</td>
<td>Tilts the head to one side</td>
</tr>
<tr>
<td>C4</td>
<td>Shoulder elevation</td>
<td>Elevation of the shoulders (e.g., shrugging)</td>
</tr>
<tr>
<td>C5</td>
<td>Elbow flexion</td>
<td>Bicep muscle control (flexing the elbow)</td>
</tr>
<tr>
<td>C6</td>
<td>Wrist extension</td>
<td>Extends the wrist and fingers</td>
</tr>
<tr>
<td>C7</td>
<td>Elbow extension</td>
<td>Triceps muscle (extends the arm)</td>
</tr>
<tr>
<td>C8</td>
<td>Finger flexion</td>
<td>Flexes the fingers</td>
</tr>
<tr>
<td>T1</td>
<td>Finger abduction</td>
<td>Abducts fingers (separating them)</td>
</tr>
<tr>
<td>L2</td>
<td>Hip flexion</td>
<td>Flexes the hip (lifting the leg)</td>
</tr>
<tr>
<td>L3</td>
<td>Knee extension</td>
<td>Extends the knee (quadriceps)</td>
</tr>
<tr>
<td>L4</td>
<td>Ankle dorsiflexion</td>
<td>Foot lifting (pointing the foot upward)</td>
</tr>
<tr>
<td>L5</td>
<td>Great toe extension</td>
<td>Extends the big toe (helps with walking and balance)</td>
</tr>
<tr>
<td>S1</td>
<td>Ankle plantarflexion</td>
<td>Pointing the foot downward (e.g., standing on tiptoe)</td>
</tr>
<tr>
<td>S2</td>
<td>Hip extension</td>
<td>Extends the hip (e.g., bending the knee behind you)</td>
</tr>
<tr>
<td>S3-S5</td>
<td>Pelvic floor muscles</td>
<td>Control of bowel and bladder, sexual function</td>
</tr>
</table>
What are the dermatomal distributions of L4 and L5, and how do they relate to this patient’s symptoms?
L4 affects the anterior thigh and medial leg; L5 affects the lateral thigh, lateral leg, and dorsum of the foot. Sensory deficits align with L4-L5 compression.
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<tr>
<th>Spinal Root</th>
<th>Dermatome Area</th>
<th>Location</th>
</tr>
<tr>
<td>C2</td>
<td>Posterior scalp</td>
<td>Back of the head, upper neck</td>
</tr>
<tr>
<td>C3</td>
<td>Neck</td>
<td>Neck area, upper trapezius</td>
</tr>
<tr>
<td>C4</td>
<td>Lower neck, upper shoulder</td>
<td>Across the clavicle area, upper shoulder</td>
</tr>
<tr>
<td>C5</td>
<td>Lateral arm</td>
<td>Upper outer arm (shoulder to elbow)</td>
</tr>
<tr>
<td>C6</td>
<td>Lateral forearm, thumb</td>
<td>Forearm and thumb (radial side)</td>
</tr>
<tr>
<td>C7</td>
<td>Middle finger</td>
<td>Middle finger and back of the hand</td>
</tr>
<tr>
<td>C8</td>
<td>Little finger, medial hand</td>
<td>Little finger, medial side of the hand, and forearm</td>
</tr>
<tr>
<td>T1</td>
<td>Medial elbow</td>
<td>Medial side of the forearm and elbow</td>
</tr>
<tr>
<td>L2</td>
<td>Anterior thigh</td>
<td>Upper anterior thigh</td>
</tr>
<tr>
<td>L3</td>
<td>Medial knee</td>
<td>Medial side of the knee, anterior thigh</td>
</tr>
<tr>
<td>L4</td>
<td>Medial lower leg</td>
<td>Medial lower leg and foot</td>
</tr>
<tr>
<td>L5</td>
<td>Lateral lower leg, dorsum of foot</td>
<td>Lateral side of the leg, dorsum of the foot</td>
</tr>
<tr>
<td>S1</td>
<td>Lateral foot, heel</td>
<td>Lateral foot and outer edge of the heel</td>
</tr>
<tr>
<td>S2</td>
<td>Posterior thigh</td>
<td>Posterior thigh, medial calf</td>
</tr>
<tr>
<td>S3-S5</td>
<td>Perineum, buttocks</td>
<td>Genital region, anal area, perineum</td>
</tr>
</table>
How does the absence of the Achilles reflex help differentiate between upper motor neuron (UMN) and lower motor neuron (LMN) lesions?
A diminished or absent Achilles reflex suggests a LMN lesion at S1. A lesion in the LMN (nerve root, peripheral nerve) disrupts communication from spinal cord to muscles. Example causes include radiculopathy or peripheral neuropathy.
Whereas hyperreflexia would suggest an UMN lesion. UMNs are located in the brain or spinal cord and send signals down to the LMNs to initiate muscle movement. Lesions to the UMN can result in the loss of normal inhibitory control on the LMNs, leading to hyperreflexia. Example causes include stroke, brain injury
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<table>
<tr>
<th>Reflex</th>
<th>Nerve Root(s)</th>
<th>Innervated Area</th>
</tr>
<tr>
<td>Patellar Reflex (Knee Jerk)</td>
<td>L2, L3, L4</td>
<td>Quadriceps (knee extension)</td>
</tr>
<tr>
<td>Achilles Reflex (Ankle Jerk)</td>
<td>S1, S2</td>
<td>Gastrocnemius, Soleus (plantar flexion)</td>
</tr>
<tr>
<td>Biceps Reflex</td>
<td>C5, C6</td>
<td>Biceps brachii (elbow flexion)</td>
</tr>
<tr>
<td>Triceps Reflex</td>
<td>C6, C7</td>
<td>Triceps brachii (elbow extension)</td>
</tr>
<tr>
<td>Plantar Reflex</td>
<td>L5, S1</td>
<td>Flexion of the toes (normal response is toe flexion)</td>
</tr>
<tr>
<td>Cremasteric Reflex</td>
<td>L1, L2</td>
<td>Cremaster muscle (elevation of the testicle)</td>
</tr>
<tr>
<td>Abdominal Reflex</td>
<td>T8-T12</td>
<td>Abdominal muscles (contraction when the abdomen is stroked)</td>
</tr>
<tr>
<td>Babinski Reflex (abnormal response)</td>
<td>L5, S1</td>
<td>Toe extension (in response to foot stimulus)</td>
</tr>
<tr>
<td>Hoffmann's Reflex</td>
<td>C7, C8</td>
<td>Finger flexion (involuntary, caused by flicking of the nail)</td>
</tr>
<tr>
<td>Clonus</td>
<td>Multiple segments (most commonly L5, S1)</td>
<td>Repetitive muscle contractions (often in the ankle or knee)</td>
</tr>
</table>
What are the key radiologic features of a burst fracture? How does it differ from other fracture types?
Burst fractures involve compression failure of the vertebral body with retropulsed fragments into the canal, unlike wedge fractures, which do not affect the posterior column.
<img src="https://radiologyassistant.nl/assets/1-tab-type-a.jpg" alt="Description of the image" />
to read more: https://radiologyassistant.nl/musculoskeletal/spine/ao-classification
[[What is on your problem list?]]What role does inflammation and edema play in secondary spinal cord injury?
Inflammation and edema increase ischemia and excitotoxicity, worsening neural damage beyond the initial trauma. The swelling from edema can lead to mechanical compression of the spinal cord.
Primary spinal cord injury: occurs immediately following the traumatic event, typically from mechanical damage (ie. compression, contusion, laceration)
Secondary spinal cord injury: series of biological and physiological processes that occur after the initial injury, leading to further damage to the spinal cord tissue over time. Includes inflammation, edema, oxidative stress, and ischemia.What is the ASIA grading system for spinal cord injury, and how would you classify this patient?
The ASIA (American Spinal Injury Association) grading system is a standardized tool used to assess and classify the severity of spinal cord injuries. It categorizes spinal cord injuries based on motor/sensory function. This patient likely falls into ASIA C (incomplete motor function preservation).
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<tr>
<th>Grade</th>
<th>Description</th>
<th>Key Features</th>
</tr>
<tr>
<td>A</td>
<td>Complete (No Sensory or Motor Function Below the Level of Injury)</td>
<td>No motor or sensory function below the injury level.</td>
</tr>
<tr>
<td>B</td>
<td>Sensory Incomplete (Sensory Function Preserved, but No Motor Function)</td>
<td>Sensory function below injury level, no motor function.</td>
</tr>
<tr>
<td>C</td>
<td>Motor Incomplete (Motor Function Preserved, but Weak)</td>
<td>Some motor function, but strength below grade 3.</td>
</tr>
<tr>
<td>D</td>
<td>Motor Incomplete (Some Motor Function with Strength 3 or More)</td>
<td>At least half of key muscles below injury grade 3 or more.</td>
</tr>
<tr>
<td>E</td>
<td>Normal (Full Function with No Neurological Deficits)</td>
<td>No deficits in motor or sensory function.</td>
</tr>
</table>
What is the difference between primary and secondary bone healing?
Primary healing occurs with rigid fixation and direct osteonal remodeling. Secondary healing relies on callus formation and is less stable
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<tr>
<th>Characteristic</th>
<th>Primary Healing</th>
<th>Secondary Healing</th>
</tr>
<tr>
<td>Fixation</td>
<td>Rigid fixation (e.g., plates, screws)</td>
<td>No rigid fixation, often with some movement (e.g., cast)</td>
</tr>
<tr>
<td>Healing Process</td>
<td>Direct osteonal remodeling (minimal callus formation)</td>
<td>Callus formation followed by remodeling (longer process)</td>
</tr>
<tr>
<td>Stability</td>
<td>More stable, minimal movement at the fracture site</td>
<td>Less stable, some movement is allowed at the fracture site</td>
</tr>
<tr>
<td>Healing Time</td>
<td>Faster and more organized healing</td>
<td>Slower and involves several stages (callus formation)</td>
</tr>
<tr>
<td>Example</td>
<td>Surgical fracture fixation (plate and screws)</td>
<td>Fracture treated with a cast or splint</td>
</tr>
<tr>
<td>Risk of Malunion</td>
<td>Lower risk of malunion or nonunion</td>
<td>Higher risk of malunion or nonunion</td>
</tr>
<tr>
<td>Role of Osteoblasts and Osteoclasts</td>
<td>Osteoblasts form new bone, osteoclasts remove excess bone tissue for remodeling</td>
<td>Osteoblasts form callus, osteoclasts remodel the callus to mature bone</td>
</tr>
</table>
Why is mechanical stabilization important?
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<tr>
<th>Objective</th>
<th>Importance of Mechanical Stabilization</th>
</tr>
<tr>
<td>Immediate Stabilization</td>
<td>Prevents further injury and ensures proper alignment of the spine.</td>
</tr>
<tr>
<td>Preventing Neurological Damage</td>
<td>Reduces compressive forces on the spinal cord and nerve roots.</td>
</tr>
<tr>
<td>Promoting Bone Healing</td>
<td>Ensures proper fusion of vertebrae and prevents nonunion or delayed healing.</td>
</tr>
<tr>
<td>Preventing Deformities</td>
<td>Reduces the risk of long-term deformities (kyphosis, scoliosis) by maintaining alignment.</td>
</tr>
<tr>
<td>Enabling Rehabilitation</td>
<td>Provides a stable environment for early mobilization and physical therapy.</td>
</tr>
<tr>
<td>Reducing Pain</td>
<td>Alleviates pain caused by abnormal spinal motion and instability.</td>
</tr>
</table>
What neurosurgical emergencies must be ruled out immediately, and why?
The following require urgent surgical decompression to prevent permanent neurologic damage.
• Conus medullaris and cauda equina syndrome: compression of the spinal cord and nerves/nerve roots arising from L1-L5 levels, leading to saddle anesthesia, bladder/bowel dysfunction, and progressive motor deficits.
• Spinal cord compression at higher levels (above L1) can lead to UMN signs (hyperreflexia, Babinski sign) and paralysis.How do occupational factors contribute to the increased risk of spinal cord trauma in this population?
Falls are a leading cause of traumatic occupational death. Construction workers are high-risk occupational groups for spinal cord injuries due to frequent falls, heavy lifting, and exposure to unsafe working conditions.
• In 2021, the construction industry accounted for 46.2% of all fatal falls, slips, and trips across all industries.
• Scaffold-related accidents result in approximately 60 deaths and 4,500 injuries annually, accounting for about 25% of fatal falls from all working surfaces.
• Falls are the leading cause of death in construction, with 351 fatal falls to a lower level out of 1,008 construction fatalities in 2020.
The National Spinal Cord Injury Statistical Center estimates the average yearly health care costs and living expenses for spinal cord sufferers to be as follows:
$1,065,980 for the first year with high tetraplegia and $185,111 for every subsequent year.
$770,264 for the first year with low tetraplegia and $113,557 for every subsequent year.
$519,520 for the first year with paraplegia and $68,821 for every subsequent year.
$347,896 for the first year with motor function affected at any level $42,256 for every subsequent year.
This does not include lost income, pain, suffering, and other damages.
''to read more:''
https://www.bls.gov/opub/ted/2023/construction-deaths-due-to-falls-slips-and-trips-increased-5-9-percent-in-2021.htm
https://www.enjuris.com/construction-accidents/scaffold-accidents-injuries-deaths/
https://www.osha.gov/stop-falls
https://www.cdc.gov/niosh/docs/92-108/default.html