Changes in consciousness after a fall in patients with spinal cord injury Clinical reasoning

How to diagnose and differentiate patients who have shortness of breath and then changes in consciousness after falling? The latest issue of the journal Neurology reported an 18-year-old patient with a history of complete traumatic spinal cord injury and a change in consciousness after a fall.

Translation: Reflections without a trace

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Part I

The patient is an 18-year-old man who presents with altered mental status following a fall
.
History
of complete traumatic spinal cord injury (SCI) 3 years ago.

Physical examination shows normal proximal arm muscle strength, but assistance with movement; Ability to self-feed with adaptive utensils; paralysis of both legs; Autonomic dysreflexia and neurogenic bowel/bladder; Cognitive function intact
.
On the day of the visit, the patient fell and hit his head on the floor while changing from sitting to standing, but did not initially lose consciousness
.
After 30 minutes of injury, the patient felt difficulty breathing and tingling in his hands, and for this purpose he took 10 mg of diazepam orally (taken regularly for anxiety).

When emergency medical services arrived, oxygen saturation was measured at 78%, so oxygen therapy
was given.
Patients arrive at the emergency room unresponsive, unable to open their eyes or follow orders, and their arms flex
in a harmful way.
No signs of
bruising or swelling.
Patients received the benzodiazepine antagonist flumazenil without improvement
.

Arterial blood gas analysis shows normal
pCO2.
Chest X-ray showed no obvious abnormalities
.
Plain head CT scan showed no obvious abnormalities
.
Head and neck CTA and CTP did not show large vessel occlusion, dissection, or hypoperfusion
.
CT of the cervical spine shows C4-C7 fusion
.
Rapid-response EEG shows β activity consistent with known diazepam administration, with no seizures or epileptiform activity
.
Urine toxicology screen is positive
for benzodiazepines, THC (marijuana), opioids, and cocaine.
The family described taking acetaminophen, codeine, and marijuana, but had no known history
of cocaine or intravenous drug use.
The patient was then transferred to the neurointensive care unit
.

Question Thinking:

1.
Location diagnosis?

2.
Differential diagnosis?

Part II

Coma and decortical posture are localized in the midbrain, thalamus, or bilateral hemispheres, so a more comprehensive neuropathy
is initially considered.
Naloxone is used to treat possible poisoning, but the test results show no new abnormalities
.
The toxicology department believes that known drugs and poisons do not adequately explain all symptoms
.
Because epilepsy remains a concern, the patient undergoes a video EEG showing global slowing with eruption suppression
.
Given the duration and severity of symptoms, post-shock syndrome is considered unlikely
.

The patient subsequently developed severe hypoxia and shortness of breath and required intubation
.
Chest x-ray shows aspiration pneumonia and bilateral pulmonary edema, transthoracic echocardiography shows ejection fraction of 25%, and overall ventricle movement is reduced
.
ECG shows normal sinus rhythm with incomplete right bundle branch block
.
Laboratory tests showed leukocytosis of 20,400/uL (predominantly neutrophils) and thrombocytopenia of 92,000/uL
.
An increase in procalcitonin of 2.
64 ng/mL (<0.
1) indicates infection
.
Cefepime and vancomycin are used for possible sepsis
.
CRP is 42 mg/L (<10), and D-dimer exceeds 10,000 ng/mL (<255), indicating an inflammatory response
.
Elevated BNP 142 pg/mL (< 100) and troponin I 0.
32 ng/mL (< 0.
04) suggest cardiac injury
.
Urine culture showing 20,000 CFU/mL Klebsiella pneumoniae; Both sputum and blood cultures are negative
.
Normal cerebrospinal fluid: glucose 100 mg/dL, protein 51 mg/dL, one nucleated cell, culture negative, and meningitis-encephalitis are negative
.

Consistent with initially possible bilateral cerebral hemisphere localization, non-contrast MRI scan of the head on day 1 after the fall shows extensive bilateral hemisphere injury, diffuse punctate diffuse restricted lesions (Figure 1), and massive microbleeding (Figure 2).

Figure 1: MRI images of patients
.
Diffusion-weighted imaging with high signal (DWI, A) and apparent dispersion coefficient sequence low signal (ADC, B) showed punctate diffusion-restricted lesions, and magnetic sensitivity weighted imaging showed low signal (SWI, C) indicating massive microbleeding
.

Figure 2: X-rays of both knees show mild incarceration, undisplaced, and incomplete fracture
of the metaphysis at the distal femur.

Question Thinking:

1.
What are the new differential diagnoses given the findings of MRI?

2.
What are the next steps for the assessment?

Part III

Punctate diffusion restriction and microbleeding suggest that the lesion involves small blood vessels, and differential diagnoses include vasculitis, microangiopathy, or embolism
.
Given the acute course, vasculitis seems unlikely
.
The absence of splinter cells on the peripheral smear suggests thrombotic thrombocytopenic purpura or disseminated intravascular coagulation
.
Very small infarction patterns with diffuse punctate microbleeding are inconsistent with cardioembolism, which often results in large infarcts without bilateral hemispheric microbleeding
.
Transesophageal echocardiography shows no intracardiac emboli or patent foramen ovale
.
Ultrasound of the extremities has found no evidence
of deep vein thrombosis.

Air or fat emboli cause acute microemboli, followed by cerebral emboli, which seem to reasonably explain the patient's symptoms, as the patient has respiratory symptoms
prior to acute neurological changes after a fall.
However, initially there is no obvious source of embolism, there are no obvious signs of bruising indicating a fracture
.
On the second day of hospitalization, petechiae appeared in the armpits and groin
.
Further examination reveals new cortical detachment on the lateral side of the metaphysis at the distal femur of both femurs, and a mild incarcerated, non-displaced, incomplete fracture
is suspected.
Orthopedic surgery places a knee fixator
.
Patients are diagnosed with lipoembolic syndrome (including cerebral lipoembolism).

Although data on efficacy are limited, patients were treated with a daily injection of 100 mg of methylprednisolone for one week and then tapered
.
However, the course is complicated by cerebral edema and hydrocephalus, requiring osmotherapy and EVD placement
.

During hospitalization, the patient remains minimally conscious, ventilator-dependent, and requires tracheostomy and percutaneous gastrostomy tubes
.
After treatment at a rehabilitation facility, alertness and a sense of direction are restored, and vocalization is maintained using letter boards, communicating by speech, and performing tracheostomy in indoor air
.
Patients also received intrathecal baclofen pumps for arm spasms; It is possible to straighten the body, but it requires maximum assistance to maintain
.

discuss

After SCI, patients are prone to fractures
due to a severe decrease in bone density.
Bone loss is characterized by decalcification of trabecular lattice structures in the distal femur and proximal epiphysis of the tibia, replaced by adipose, marrow
.
Factors that affect bone mass include the extent and location of injury, muscle spasms, age, sex, weight-bearing activity, and duration
after injury.
Common causes of fracture, as seen in this patient, include wheelchair mobility, collisions with invisible objects, and other low-impact activities
.
In these injuries, the knee is often the first point of contact and is particularly prone to fractures
.
Bilateral femoral fractures increase the risk of lipoembolism, which occurs when fat embolism leads to multisystem organ failure and typically includes pulmonary, cutaneous, and neurological complications
.
Neurologic manifestations include headache, behavioral changes, seizures, and altered
consciousness.
More rare findings include cortical posture, cerebral oedema, hydrocephalus, and paroxysmal hypersympatheticism
.
Systemic effects include fever, tachycardia, retinal involvement, jaundice, renal insufficiency, anaemia, thrombocytopenia, and elevated
inflammatory markers.
In this patient, myocardial fat embolic injury may lead to new heart failure
.

A pathophysiological theory of fat embolism holds that trauma increases intramedullary pressure, causing bone marrow to enter the sinuses and release fat droplets into the veins, blocking blood flow
to small blood vessels.
Therefore, given the increased bone marrow fat content, the incidence of post-traumatic fat embolism is expected to increase
in patients with spinal cord injury.
However, data on fat emboli after minor trauma in patients with the spinal cord are limited
.
Fat embolism is more common in patients with Duchenne muscular dystrophy (DMD), another group
with significant bone mineral density.
Fatal FES following minor trauma has also been reported in patients with DMD, but no significant fractures
have been found on imaging and/or autopsy.

Cerebral fat embolism is usually a self-limiting process that eventually leads to complete recovery
.
Supportive care and symptom management remain the mainstay
of treatment.
Corticosteroids are commonly used to prevent fat embolism, and some studies have reported that treatment measures such as limiting the rise in free fatty acid levels after injury and slowing the inflammatory response may benefit
patients.
There is limited or conflicting evidence for other treatments, including anticoagulation, sodium dehydrocholate 20%, low molecular weight dextrans, albumin, 5% alcohol-glucose solution, dehydrating agents, cooling therapy, and hyperbaric oxygen
.
However, poor prognosis for cerebral fat embolism is also common, with a mortality rate of up to 10%.

Therefore, lipoembolization
must be considered in patients at high risk of bone mineral density reduction, including those with SCI.