Trauma Tuesday! The Cervical Collar

What is a C Collar?

 They come in a couple of different flavors, but the two extremes are hard and soft collars. The primary function of C Collars is to immobilize the C spine. Hard collars provide more immobilization and restriction of ROM compared to their soft brethren, but are generally more uncomfortable for patients.  

Why use a C Collar?

C Collars are placed to protect the spinal cord from the possibility of secondary injury in the unstable cervical spine. The theoretical risk is worsening an unstable fracture, and potentially causing devastating neurological injury.

When to use a C Collar? Who should be in a C Collar?

Following trauma, early immobilization of the cervical spine can be crucial if c-spine injury is suspected. This can be obvious in patients involved in MVA, falls, and assaults to the head or neck. On history and physical, the patient may be complaining of sensation changes, neck, and back pain. But cervical injury may not be so obvious in the patient found down and unresponsive, who cannot communicate what happened to them, and may have had signs of a recent fall and possible C spine injury.  C-collars are often placed on these patients too.

Protection of the C spine is considered so important, that a rigid C collar placement is reflexive in both the in and out of hospital environment. It's built into ATLS protocols. In many EMS protocols, if a patient is complaining of neck pain or any neurological symptom after trauma, they've bought themselves a C Collar.


This all sounds great....but then why is there debate around C-Collars?

The potential harm of C Collars:

C Collars are not benign interventions. The long term changes include muscular, bone, and tendon atrophy, but what about in the short term? Hard collars, like the C collars we place in the ED for our trauma patients, are associated with pain, breathing restriction, tissue ischemia, increase aspiration events, and adds barriers to medical care, including maintaining C spine when moving, exposing, and cleaning the patient. And that's only talking about the C collar in a vacuum: C Collars are notorious for hiding extent of trauma, such as soft tissue swelling and more commonly, bleeding of the occiput and neck. They also increase ICP- Stone et al. demonstrated that C collars increase ICP in healthy volunteers placed in C Collars, potentially worsening intracranial injury. Additional studies, like that of Kolb et al, found increased ICP measured by CSF pressure obtained through LP in a group wearing a c collar compared to a group that didn't.

What else does the literature say?

A lot of the benefits associated with C Collars are theoretical. Do they actually help and do what they're supposed to do?

Here's the problem with the existing literature: There are no prospective studies comparing an experimental C collar group with a no collar control group. And thus, a lot of research on C spine injury and c collars are done on cadavers and in analogous studies. 

Some studies looked at whether C collars are even able to immobilize the spine. One study looked at "lightly embalmed" cadavers with an induced C5-6 instability injury, and then put on different types of C collar. They tested for motion using EMG sensors, and tested all planes of cervical motion. They found no significant difference in motion between the C spine groups and the no c collar group. Another cadaver study with induced c spine instability even found increased motion in axial and cranial-caudal planes in a rigid C collar group compared to no c collar group, possibly through the creation of  "pivot points" from where the collar meets the TMJ and shoulders. 

What about the possibility of preventing secondary injury? Other studies (involving mostly cadavers, again) has shown that a considerable amount of force is required to fracture the spine, and that subsequent, low energy forces from patient's moving their neck is unlikely to cause additional spinal cord injury. Additionally, these and similar studies suggest that an unstable fracture existing without already devastating neurological injury is rare. Furthermore, it is also suggested in a retrospective study looking at neurological outcome between the USA (where we routinely immobilize with C collars) vs Malaysia (a country that does not routinely immobilize patients) and found that less neurological disability occurred in the unimmobilized group, suggesting that there may even be the potential of neurological harm. Obviously, a lot of this research is not perfect but it certainly does not favor the absolute benefit of using C collars routinely.

What should we do?

The real question at the end of the day. Placing C Collars is still the standard of care, though additional research may one day point us away from reflexively using it, and perhaps protocols detailing its use in trauma may become more sparing. In the meantime, for our trauma patients, we can decrease the time sensitive risks associated with these devices by clearing them as soon as we can, as we always have. This research at least opens my eyes to the potential of C collars causing harm, and that one day what has been drilled into my head regarding trauma management may not always be the case.

Thanks for sticking around till the end!

-SD

Sources:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481593/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684205/

http://www.emdocs.net/cervical-collars-for-c-spine-trauma-the-facts/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2751736/

https://pubmed.ncbi.nlm.nih.gov/511875/

https://pubmed.ncbi.nlm.nih.gov/22962052/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949434/

https://www.uptodate.com/contents/evaluation-and-initial-management-of-cervical-spinal-column-injuries-in-adults?search=Cervical%20spine%20trauma&source=search_result&selectedTitle=1~145&usage_type=default&display_rank=1


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POTD: Decubitus Ulcers in the ED

Here's a deep dive into decubitus ulcers, and more specifically the scope of the ED in staging, recognizing when you should be worried about infection, and management tips.

 

Background: Decubitus ulcers are soft tissue injuries formed from prolonged pressure on the skin. For the decubitus (or lying down) patient, the points under most prolonged pressure involve the tissue between any bony prominence and the patient's bed. Common places we see decubitus ulcers, depending on the patient's position, are shown in the pic below:

 

Pathophysiology: Multifactorial with a combination of internal and external factors. But the end pathway is always ischemia and necrosis of tissue.

 

Internal risk factors: Anything that decreases blood flow to pressure sites, promotes inactivity, or decreases sensation are risk factors for decubitus injury. This includes vascular disease, DM, neurological injury, surgical patients, malnutrition. It just so happens that most of these are present in the elderly, and explains why they are the most at risk for decubitus ulcers. Specifically with neurological injury: pressure ulcers are oftentimes very painful. If the patient has decreased sensation, they may not feel the discomfort caused by the increased pressure, and may not readjust to relieve pressure.

 

External risk factors: Constant external pressure exceeds capillary pressure supplying blood flow to and from tissue. Ischemic tissue eventually becomes necrotic and progresses to pressure injury. Hard static mattresses, physical objects left under patients, and side railings all exacerbate the amount of pressure on vulnerable tissue. Wet tissue from bodily fluids, as well as friction between skin and clothing/bedding also encourage skin breakdown and worsening of pressure injury.

 

Some evidence suggests that as little as 2 hours of immobility can lead to tissue breakdown from pressure injury.

 

Staging: 1-4

Stage 1: Skin is INTACT, usually with nonblanchable erythema.

Stage 2: Exposed dermis; partial thickness loss of skin. Erythematous and moist.

Stage 3: Exposed fat. Full thickness loss of skin. Ulceration and granulation tissue likely to be present. 

Stage 4: Exposed fascia, muscle, or bone. Erosion may form tracts deeper than what is initially visible. 

Unstageable: Full thickness skin loss, but depth is unstageable because of existence of eschar or sloughed tissue. If unstageable ulcer is present, there is at least a stage 3 or 4 pressure injury. If the eschar is stable, defined as dry, intact, and no obvious signs of overt infection, then management is to leave it alone with no plans for debridement.

 

When to Suspect Infection:

At baseline, pressure ulcers are colonized with low levels of polymicrobial bacteria, consisting of skin, urine, and fecal flora. Infection, at least when we refer to an "infected ulcer,"occurs when this bacteria spreads to surrounding, healthier tissue. Infection usually starts with local surround cellulitis and then progresses to involve deeper soft tissue infection, osteomyelitis, and sepsis. Therefore, the extent of an infected ulcer may not be all apparent on physical exam and a high clinical suspicion is needed. Findings include surrounding erythema or discoloration, warmth, fluctuance, exudate, and frank necrosis.


 

If decubitus ulcer is suspected as the reason for your patient's sepsis, urgent debridement is necessary. In the meantime, start the patient with your normal sepsis cocktail including fluid and antibiotics. Obtain blood cultures for disseminated infection, as well as ESR and CRP if worried about osteo. Choice of antibiotics depends on extent of suspected infection; for mild cellulitis, oral therapy is indicated, but when they arrive to the ED with overwhelming infection, big guns with IV vancomycin and zosyn is a good place to start.

 

Imaging is not always needed. If diagnostic scans are needed, CT can be a good initial test, but MRI may be needed to measure extent of necrotic tissue.

 

As far as identifying pathogens in the wound, swab cultures are limited in the information they provide as the infection is often deeper. In this case, a biopsy of the deepest tissue associated with the wound obtained during debridement is the most helpful for goal oriented treatment.

 

Hope you enjoyed all the fun pictures!

Stay well, friends;

-SD

 

Sources:

https://www.ncbi.nlm.nih.gov/books/NBK553107/

https://www.uptodate.com/contents/clinical-staging-and-management-of-pressure-induced-skin-and-soft-tissue-injury?search=sacral%20decubitus%20ulcer&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H21

https://www.uptodate.com/contents/infectious-complications-of-pressure-induced-skin-and-soft-tissue-injury

https://reference.medscape.com/slideshow/classifying-pressure-injuries-6005748#38

https://www.shutterstock.com/image-photo/pressure-injury-stageiv-pressuresore-bedridden-medical-1221772201

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Conference Summary 9/8/21

Today we had a wonderful conference (in person!) kicked off with a really cool case presented by the brilliant Dr. Yum.

M+M with Dr. Yum:

28 year old M BIBEMS s/p suicide attempt. As per EMS drank antifreeze. Found in cemetery unresponsive. Currently on 10L NRB

Upon arrival:

ABCS- intact

BP 167/94, HR 81, RR 14, SPo2 94% T: afebrile Blood glucose: WNL

PE: Unresponsive, copious secretions in mouth, no external signs trauma. Neuro: not speaking, not opening eyes, not moving extremities. GCS 3.

Initial VBG: pH normal, glucose normal. Lactate 10.1

Intubate? Factors involved in making clinical decision:

  • GCS 3, copious secretions

  • Jaw thrust being applied, has decent capnography

  • Course of disease/management

Patient was intubated.

Wide DDX for AMS: AEIOUTIPS:

  • Highest on differential: Alcohol, infection, tox, icp, poisoning, seizure

Plan: Rainbow lab, utox, salicylate, acetaminophen levels, etoh/methanol/ethylene glycol level (send out), serum osmolarity, cxr, ekg

Start fomepizole pyridoxine, thiamine early for high clinical suspicion

Consults:

Poison control

Nephrology

MICU
Family arrived shortly after and provided additional history:
Patient had previous suicide attempts and psychiatric history. He had recently stopped taking his psych meds. New stressors in family, including recent passing of mother. Patient stated he went to cemetery to be with mother. Called family right after taking antifreeze.
Initial labs significant for:

  • CBC WNL, BMP: anion gap: 15

ED Course:

Nephrology asked for HD, started in ED

Accepted by MICU- started bicarb and folic acid on him

Osmolality: 311, Osmolar gap: 21

Osmolality: Normal 285-295. Number osmoles in kg of solvent

Osmolar gap: measured osmolarity – calculated osmolarity

Gap should be less than 10. IF gap >10, there is osmol that is not being accounted for, like possibly a toxic alcohol

*Urine placed under black light: patient’s urine glows positive after ingestion of ethylene glycol

Send out labs:

Methanol: none, Ethylene glycol: 588

Hospital course:

  • Extubated 2 days later in MICU

  • Evaluated and transferred to psych, started on abilify

  • 7/12 completed safety plan and discharged home

Toxic Alcohol Poisoning:

  • Seen with intentional suicidal attempt, accidental, recreational ingestion

  • All these alcohols get metabolized by alcohol dehydrogenase

Ethylene Glycol

  • Radiator fluid, antifreeze, brake fluid

  • Rapidly absorbed, eliminated by kidneys, 17 hours half life

  • Inebriated --> cardiopulmonary stage --> kidney failure --> neurological sequelae

Methanol

  • Windshield wiper fluid

  • Deicing products

  • Moonshine

  • Windex

  • Rapidly absorbed, eliminated by expiration

  • Little renal elimination

  • Inebriated -> visual symptoms, neurological sx, late neuro Parkinson’s like symptoms

Clinical clues:

  • Tachypnea in absence of respiratory illness, visual changes (if awake and able to communicate)

  • Not sobering up as expected

  • Seizures

Lab clues:

  • Low ethanol in intoxicated patient

  • Hypocalcemia with prolonged QT

  • Anion gap metabolic acidosis

  • High osmolality + osmolar gap

Get metabolic acidosis from build up of toxic metabolites

Our patient: had lactate of 10, but normal pH

The lactate gap: Glycolic acid --> glycolate from breakdown of ethylene glycol similar to lactate chemically, and mimics it on VBG lab

Can send serum lactate, which is more specific for serum lactate; can compare to VBG, which cannot differentiate between lactate and glycolic acid

**On initial ingestion: high osmolar gap, low anion gap. As metabolized, lower osmolar gap, but increasing anion gap

Important labs:

  1. Anion gap metabolic acidosis elevated osmolar gap/osmolarity

  2. Low ethanol level

  3. Send out labs of levels of toxic alcohols

  4. Testing urine for ethylene glycol:

    1. Calcium oxalate crystals in urine. Not specific for testing urine for toxic alcohol ingestion. Also not put in commercial toxic alcohols

    2. Fluorescence of urine under woods lamp

Management Goals:

  • Block toxic metabolites formation

  • Correct pH

  • Eliminate toxic metabolites formed

  • Get poison control and other consultants on board early

  • GI contamination: NG suction if within 30 min to 1 hour after ingestion, no role for activated charcoal

Fomepizole

  • Blocks alcohol dehydrogenase. Keeps toxic alcohol in parent compound

  • If suspicion high enough- give it

  • 15mg/kg initial dose à 10mg/kg q12h x 4 doses for 2 days

Ethanol

  • 2nd line after fomepizole

  • Alcohol dehydrogenase favors ethanol over toxic alcohol

  • Ethanol metabolized with zero order kinetics, nee to get levels, associated with longer ICU stays compared to fomepizole

Vitamins and Cofactors

Bicarb

  • Correct until pH >7.2

  • Normalization of pH keeps toxic metabolites in ionized form

    • More support for methanol poisoning

    • Less able to penetrate tissues

Hemodialysis

  • Takes out parent compound and toxic metabolites

  • Corrects metabolic acidosis and electrolyte abnormalities

  • Indications: if enough toxic alcohol/metabolites to have end organ damage, or pH <7.15,or anion gap >24

  • Ethylene glycol may not require HD, while methanol always does

Dr. Vasquez: Three Common Medical Ear Problems in Children

Ear anatomy: outer, middle, inner ear

Eustachian tube: connects nasopharynx to ear. Acts as a way to drain middle ear. In children, the tube is shorter, smaller, and easily clogged. Leads to infection

  • Otitis Media

    • Diagnosis and Management of acute Otitis Media

    • Definition: Needs

      • Moderate to severe bulging of TM (or new otorrhea not due to AOE)

      • Acute signs of illness

      • Signs of middle ear effusion

    • Bugs:

      1. Strep pneumo, H flu, Moraxella catarrhalis

    • How to examine ear:

      • Have child sit in moms lap, distract child

      • Parent holding head and arms against chest

      • Take elbows, hold them to patients ears to examine mouth then nose

      • Rest dominate hand against patient for stabilization

    • Characteristics of the TM

      • Color: translucent or opaque

      • contour : bulging or retracted

      • translucency

      • mobility

    • AOM Vs OME

      • OME: no signs of illness, but may see effusion

    • TM Rupture

    • Bullous AOM

    • ABX

      • Any child with otorrhea, signs of ear pain, signs of fever

      • Any child with severe symptoms

      • Uncertainty to follow up after visit

    • ABX or additional observation

      • >2 years old with BL AOM without otorrhea

      • Unilateral AOM without otorrhea

    • Strep pneumonia resistance

      • Penicillin binding proteins

      • Overcome by high dose amox

      • Failure after three days:

        • Amox clav

        • H flu and Moraxella produce beta lactamase

      • Ceftriaxone 50mg kg IM q day x 3days

    • Otitis conjunctivitis syndrome:

      1. Treat with amox clav

  • Mastoiditis

    • NNT of AOM to prevent 1 mastoiditis: 4800

    • Infection of mastoid air cells

    • Swollen area with ear turned forward

    • High fever, discharge from canal, swelling mastoid process, ear protrudes

    • Evaluation and treatment:

      • Consult with ent, consider CT scan

      • IV ceftriaxone and myringotomy

      • If fails, needs mastoidectomy

      • Can develop meningitis

  • Otitis Externa: Swimmers Ear

    • Swimmers ear

    • Ear pai, discharge, pruritis, hearing loss, lymphadenopathy

    • Treatment: topical abx ear drops, and pain

Small Groups:

Dr. Sokolovsky: Rashes

3 year old tachycardic out of proportion of fever. Rash disseminated, back of mouth

DDX: coxsackie, herpes, eczema herpeticum

Tx: fluids bolus, antipyretics, rainbow labs

Labs significant for: elevated wbc, low bicarb, mild thrombophilia

Diagnosis: Atypical Coxsackie aka disseminated coxsackie

If child appears well, PO well, has good follow up, can possibly go home

(But what if rash was more vesicular, given picture of similar looking rash)

Diagnosis: eczema herpeticum aka disseminated herpes

Needs to be admitted, needs IV acyclovir

But these rashes look so similar.

An RVP can help- if receive back a positive result such as enterovirus

If no RVP available, unsure if it is disseminated herpes or not, would need to admit


Rapid Fire Images and Questions:

Parvovirus: slapped cheek. Mom may develop fetal hydrops

Rash: pityriasis: tx Benadryl for itching

Dacryoadenitis: tx: warm compresses

Chicken pox: multiple stages of rash

Melanoma: screen for ABCDE

Osler nodes: endocarditis, admit

Erythema migrans with cardiac complaints/heart block: IV ceftriaxone à CCU

Roseola: the fever that rashes

Erysipelas: strep

Seborrheic keratosis: stuck on appearance

Basal cell carcinoma

Kawasaki: IVIG, aspirin, coronary aneurysms

Circumferential burn crosses joint lines. Parkland formula for fluids

Herpes ophthalmic, Hutchinson sign

Dendritic lesions on herpes. VZV has pseudo dendrites

Anaphylaxis: epinephrine IM

Pox virus

Dr.Kurbedin: Basic cutaneous rashes

Pox virus

  • not dangerous, + contagious, spread skin to skin.

  • Tx self limiting, can have derm follow up. Catharidin

  • Popular growths, dome shaped, flesh colored

Shingles

  • Dermatomal. If in more than 1 dermatome: disseminated. If it crosses midline: disseminated This person needs to be admitted, IV meds

  • Reactivation of vzd

  • Can have pain and itching at site before vesicles appear

  • Tx: acyclovir, vaclyclovir PO within 72 hours, or if new lesions still occurring

  • Gabapentin for post herpetic neuralgia

  • If disseminated or including eye: IV acyclovir, or if cannot tolerate PO

  • Disseminated zoster requires airborne precautions

Zoster Ophthalmicus (shingles)

  • Risk of blindness

  • PE: look in ear, slit lamp, fluorescein dye, look for dendritic pattern

    • If present, admit, give IV acyclovir, ophthalmology consult

Cold sore. Herpes 1 and 2

  • +contagious

  • Tx: initial episode, recurrence, suppressive therapy are different doses

  • Acyclovir vs valacyclovir vs famciclovir

Herpetic Whitlow

  • Don’t I+D, contagious

  • Can give acyclovir, follow up

Necrotizing Fasciitis

  • Can be missed if not careful

  • Severe pain, crepitus, pain out of proportion

  • Fast evolving on history

  • Needs IV ABX, broad spectrum, +clinda for antitoxin properties, OR, debridement

  • Multimicrobial in nature

  • High mortality 30-50% with treatment

  • Xray, CT, MRI, US not sensitive enough compared to clinical suspicion

  • If concern for vibrio- water based, fish take, recent vacation, add doxycycline

Dr. Cueva: Dermatology Bizz Buzz

Basal Cell Carcinoma: irregular, heterogenous, raises edges, sun soaked edges. Pearly. Telangiectasia. Locally invasive. Not metastatic. Follow up dermatology.

Squamous Cell Carcinoma: scabby, transformation actinic keratosis, metastatic, derm follow up for biopsy. Associated with hypercalcemia

Melanoma: Asymmetry, irregular borders, colorful, diameter, evolving and elevation. Refer to biopsy. Most common mets to brain

Shingles: unilateral, one dermatome, painful and itchy, then rash. Pain control. When sores open, they are still infectious. Contact precautions. Check eye, nose, ears.

Bullous pemphigoid: chronic, autoimmune disorder. Older patients, antibodies to basement membrane. Negative Nikolsky.

Pemphigoid vulgaris: autoimmune, drug induced, +nikolsky, mucosal involving, high mortality, tx steroids, a/p burn center

Sacral decubit ulcers: stage 2 with intact skin. Black eschar on decubiti: this is unstable, needs debridement to be able to stage. Stage 4: bone visible


Trauma Conference:

Trauma panel: Drs Marshal, King, Patel, Chen, Zapolsky

Hemothorax/Pneumothorax

  • Traditionally taught to use large bore chest tube for hemothorax

  • Some literature suggests no difference between pigtail and large chest tube for hemothorax

  • Additionally can consider pigtail for

    • pneumothorax- for obvious ones, for patients who are stable, no respiratory distress, can be prep and draped, anesthetic, sterile pigtail procedure

    • Occult pneumothoracies on CT but not on xray- is patient stable/resp distress? How busy is team? If can't perform serial exams/monitor patient, if the patient is going to floor, then likely important to put chest tube due to risk of worsening pneumothorax

  • If no improvement, then can escalate with a second chest tube/larger chest tube

  • If several days passed, hemothorax found on imaging, but now has fibrosis and clotted, consider OR; chest tube may not be of use

  • Delayed chest tubes have their own risks

  • Consider putting large bore in unstable patients, patients in the trauma bay where oyu have limited histroy/timeline of assessment, prior history of pneumothorax/hemothorax with possibility of old scarring

  • Time outs in chest tube placements are important. Easy to mix up side of placement, etc.

Delayed brain bleeds

  • Still need period of observation once found, serial imaging. Still need interval imaging to prove stability.

  • Unlikely for neurosurgical intervention in delayed presentation, depending on multiple factors, including length of delayed presentation, baseline functional status

Have a fantastic rest of your Wednesday!

-SD

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