Lisfranc Injuries

Inspiration:
Jacobi/Montefiore Follow-Up Rounds
Andrew Barbera, PGY-3


 

The Case

32M no PMH p/w left foot pain
Triage vitals: 98          117/80 RR: 97  RR: 17  T: 98    O2: 100%

HPI
32M p/w left foot pain x 3 days after dropping AC unit onto foot

  • Patient had to twist foot in order to remove it from underneath AC unit
  • Went to hospital immediately afterwards, X-rays at the time were negative
  • Discharged with ACE bandage and crutches
  • Patient’s foot continued to swell, extremely painful, unable to bear weight on left

Physical Exam
Gen: No apparent distress, using crutches to ambulate
HEENT: NCAT, MMM, EOMI, no facial asymmetry. Neck supple
Extremity: left food edematous, tender over 3rd, 4th, and 5th metatarsal. Able to range toes. 2+ DP bilaterally. Sensation intact to fine touch bilaterally. No point tenderness noted over the ankle. No lower leg swelling or tenderness
Neuro: no gross neurological deficit

X-ray: XR of left foot notes no visible fracture
CT foot: fracture at base of left 2nd metatarsal
Weight bearing XR of left foot: widening between base of 1st and 2nd metatarsal consistent with Lisfranc injury

Disposition: OR for ORIF on day 3 of admission

Lisfranc Injuries

Definition: a lis franc fracture is an injury of the tarsometatarsal joint (TMT) complex. It is a very easily missed/misdiagnosed fracture.

Normal anatomy: the lisfranc joint complex includes the bones (see below) and ligaments that connect the midfoot to the forefoot and includes the 5 tarsometatarsal joints. The lisfranc ligament connects the lateral aspect of the medial cuneiform to the medial aspect of the 2nd metatarsal. A lisfranc injury is anything from a sprain to a complete disruption of the midfoot.

Normal Foot

 

Mechanism of Lisfranc injuries:
Lisfranc injuries are common in direct trauma resulting in crush injuries. In patients who have injuries suggesting a crush mechanism (compartment syndrome, vascular injuries, etc.) keep lisfranc injuries in mind. Of note, the dorsalis pedis artery passes between the 1st and 2nd metatarsals.

They are also common in indirect trauma causing twisting of a pronated food (forced external rotation) or axial loading of the foot in a fixed equinus position. These injuries can also be associated with cuboid bone fractures caused by compression of the bases of the 4th and 5th metatarsal heads 

Presentation
Common symptoms of indirect lisfranc injuries include swelling and pain in the midfoot, bruising of the bottom of the foot (plantar echymoses is pathognomonic), swelling out of proportion with a normal X-ray, midfoot instability, tenderness over dorsal TMT joints. Any patient with a twisting or crush injury can have a lisfranc injury. This specific injury is especially common in athletes.

What to look for in plain films?

In the AP film, the medial border of the 2nd metatarsal should be collinear with the medial border of the 2nd (intermediate) cuneiform.

Normal Foot Xray

This AP film shows normal alignment. The 2nd metatarsal forms a straight line with the 2nd cuneiform bone.

Lisfranc X ray AP

AP radiograph of a Lisfranc injury. Notice the disallignment between the 2nd metatarsal (the yellow line) and the 2nd (intermediate) cuneiform bone (the red line). This is diagnostic of a Lisfranc injury.
This diagnosis can be missed on regular X-ray, so if suspicion is high, a weight-bearing AP radiograph is necessary to evaluate the space between the 1st and 2nd metatarsals

In an oblique plain film, evaluation of the lateral midfoot becomes possible. A normal oblique X-ray shows alligment of the 2nd through 4th TMT joints:

Lisfranc X ray oblique

An abnormal oblique film notes disallignment of the TMT joints (circle below)

Lisfranc X ray oblique abnormal

 

If, as in the above case presentation, a patient’s complaint is suspicious for a fracture and plain films are negative, CT is recommended. A 2012 study notes that X-rays correctly identified Lisfranc injuries in only 68.9% of cases with a sensitivity of 84.4% and a specificity of 53.3%.

 

Treatment
Stable injuries with minimal displacement/fractures can be managed nonoperatively. These patients should wear a short leg cast or walking boot for 6-10w and should be non-weightbearing initially. These patients need close followup and a repeat X-ray 2 weeks after the initial injury.
Unstable injuries with significant fractures or displacement require operative management (ORIF with screw fixation).


 

Sources:
Gotha, Heather E., MD, Craig R. Lareau, MD, and Todd A. Fellars, MD. “Diagnosis and Management of Lisfranc Injuries and Metatarsal Fractures.”Rhode Island Medical Journal (2013). Rhode Island Medical Journal. Web.

Trevino, Saul G., MD, John S. Early, MD, Allison M. Wade, MD, Santaram Vallurupalli, MD, David Flood, MD, Francisco Talavera, PharmD, PhD, Thomas M. DeBerardino, MD, and James K. Deorio, MD. “Lisfranc Fracture Dislocation.”Lisfranc Fracture Dislocation. Medscape, 4 Jan. 2016. Web. 05 Feb. 2016.

 

 

PCP Pneumonia

Inspiration:
Jacobi/Montefiore Conference
Edouard Coupet, MD PGY-4

The Case:
Triage: 63 y/o M complains of SOB and cough x 3 days
Nursing Assessment: alert, making grunting noise with breathing

HPI: 63M p/w SOB. Patient notes 2 days of increasing shortness of breath. Also notes a non-productive cough. Denies any pain, but does note subjective fevers and malaise. Denies recent travel.

PMH: HTN, asthma
Meds: amlodipine, albuterol

Physical Exam

T: 101, BP: 137/68, RR: 22, HR: 118, O2: 98% on NRB
General: moderate distress
Skin: WNL
Heart: tachycardic
Lungs: coarse rales
Abd: WNL
Ext: WNL

Labs

Na: 138, Cl: 101, BUN: 32, Glucose: 117
K: 4.9, CO2: 26, Cr: 1.4

WBC: 10.2, Hgb: 8.2, Hct: 24.2, Plt: 306

Emergency Department Course

  • O2 sat improved from initial 40% on RA to 90% on non-rebreather. He was then dstarted on non-invasive positive pressure ventilation (BiPAP) 8/5 @ 100% FiO2

PCP CXR

  • CXR report: diffuse hazy airspace opacity of both lungs, may be due to CHF or pneumonia
  • The patient was started on Ceftriaxone and Azithromycin for presumed community acquired pneumonia
  • Patient states he was recently tested for HIV and was negative

Three Hours Later

  • Patient becomes increasingly hypoxic on NIPPV. Patient was intubated, but course was complicated by multiple desaturations to 70s
  • After intubation, patient was noted to be very difficult to bag. Critical care consulted
  • “Patient is now intubated and requiring a lot of ventilator support, PEEP 12, and 100% FiO2. Hemodynamically stable. Sedated now. Reason for resp failure likely pneumonia progressing to ARDS. Will cover with Vanc, Zosyn, & Azithromycin. Send urine legionella & pneumococcal antigen. CXR findings could be PCP, send PCP smears. Send HIV study if possible.”

ICU Course

  • Patient developed ARDS likely 2/2 PCP and was treated accordingly. He eventually tested positive for HIV and required ECMO and pressors in the ICU. CD4 count was very low
  • Patient was deccanulated from ECMO 9 days after presentation and extubated 3 days later. He was started on HAART and PCP prophylaxis per ID recs. He was discharged 32 days after initial presentation

PCP Pneumonia

  • Overview:
    • Caused by Pneumocystis jiroveci, a fungi, in immunocompromised patients
    • This is an AIDS defining illness
    • History usually includes shortness of breath, low fever, cough
    • Patients with PCP pneumonia can decompensate very quickly and (as in this case) go into ARDS
  • How should we diagnose it?
    • CXR might show butterfly pattern ie findings in bilateral lungs. These findings are usually interstitial
    • PCP pnuemonia increases risk of pneumothorax, which can also be seen on CXR
    • CT chest show ground glass opacities
    • High LDH (>300 U/I)
    • Send sputum cultures to help out your medicine colleagues
      • Induced sputum cultures sent to the lab get giemsa and methenamine silver stains
      • PCR is also a mode of diagnosis
    • How should it be treated?
      • Emperic therapy immediately. PCP pneumonia has a very high morbidity and mortality
      • First line treatment is TMP-SMX either PO or IV (use IV for more severe cases)
        • Trimethoprim 20mg/kg/day and sulphamethoxazole 150mcg/kg/day in 4 divided doses for 21 days
      • Alternatives: primaquine + clindamycin, atovaquone, dapsone + trimethoprim
      • If patient is HIV positive, steroids will help
    • Propylaxis: If CD4 < 200 cells/mm or if HIV positive with history of oropharyngeal candidiasis

References
Coupet E. “M&M Conference: PCP Pneumonia.” Jacobi Medical Center. Jacobi/Montefiore Emergency Medicine Conference. Bronx. Dec 2015. Lecture

Nickson, Chris. “Pneumocystis Jiroveci Pneumonia.” Life in the Fast Lane. Web. 26 Jan. 2016. http://lifeinthefastlane.com/ccc/pneumocystis-jiroveci-pneumonia/

Journal Club: The Canadian Head CT Rule

The purpose of Journal Club is to review papers essential to emergency medicine. The aim is not to summarize the latest and most up-to-date literature recently released. Instead, Journal Club will review the methodology, data, and conclusions of landmark papers which are used in a day to day basis in modern Emergency Medicine. Oftentimes, the conclusions of these studies are used in treatment decisions, but the basics of the studies are not as well known by clinicians.

The Canadian Head CT Rule

The Canadian Head CT Rule is used in day to day practice in the emergency room. The paper was first published in 2001 by Stiell et al in The Lancet and sets down a clinical decision rule for use of CT scans in minor head traumas.

The Rule
In head trauma patients with GCS = 13-15 who lost consciousness, have amnesia to the trauma, or are confused upon initial presentation, a head CT is not necessary if all of the following criteria are negative:

  • GCS < 15 at 2 hours after the trauma
  • Suspected open or depressed skull fracture
  • Signs of basilar skull fracture i.e. hemotympanum, raccoon eyes, Battle’s sign, or otorrhea/rhinorrhea consisting of CSF
  • 2 or more episodes of vomiting
  • Age > 65
  • Retrograde amnesia > 30 minutes to the event
  • Dangerous mechanism

If the patient meets any of these criteria, he or she needs a head CT

Study Question

  • In patients suffering minor head trauma, which ones need a CT scan of their brain?

Study Design

  • Prospective cohort study
  • 10 large Canadian hospitals
  • Outcome: need for neurological intervention OR clinically important brain injury on CT
  • Number of patients: 3121
  • Common misconception: this rule doesn’t apply to head trauma patients who are at baseline, have no amnesia, and didn’t lose consciousness

Study Population

  • Inclusion criteria:
    • Blunt head trauma causing witnessed loss of consciousness, definite amnesia, or witnessed disorientation
    • GCS of 13-15 upon initial presentation
    • Head injury in the last 24 hours
  • Exclusion criteria:
    • < 16 years old
    • Minimal head injury (no LOC, amnesia, or disorientation)
    • No clear history of trauma as the primary event
    • Penetrating skull injury or obvious depressed skull fracture
    • Acute focal neurological deficit
    • Unstable vital signs
    • Seizure before assessment in the ER
    • Bleeding disorder or on anticoagulation
    • Patient who returns to the ER for the same head injury
    • Pregnant patients

Outcomes

  • Primary outcome: need for neurosurgical intervention. This is defined as:
    • death within 7 days secondary to head injury
    • need for craniotomy
    • elevation of depressed skull fracture
    • intracranial pressure monitoring
    • intubation for head injury shown on CT
  • Secondary outcome: clinically important brain injury on CT requiring hospital admission and neurological followup
    • All brain injuries found on CT were included In this group UNLESS the patient was neurologically intact and had one of the following minor injuries
      • solitary contusion < 5mm in diameter
      • localized subarachnoid hemorrhage less than 1mm thick
      • smear subdural hematoma < 4mm thick
      • isolated pneumocephaly
      • closed depressed skull fracture not through the inner table
    • This definition was standardized after surveys were given to 129 neurosurgeons, neuroradiologists, and ER physicians

Method

  • Enrolled patients were low risk head trauma patients as defined above who were evaluated by a clinician trained to identify 22 different criteria which were being studied.
  • Enrolled patients either had a head CT (if the ER physician felt it was indicated) OR had a telephone followup 14 days later. Patients were classified as either:
    • Having a need for neurosurgical intervention or clinically important brain injury on CT (as defined above)
    • OR as having a clinically insignificant or no brain injury
      • These patients either had a negative head CT OR met all of the following criteria in their telephone interview 14 days later
        • Mild or absent headache
        • No memory or concentration problems
        • No seizure or focal motor neurological findings
        • Return to daily activities
        • Error score < 10 out of 28 on the Katzman Short Orientation-Memory-Concentration-Test
      • Patient who failed the 14 day telephone interview were recalled to the hospital for a head CT
      • If the followup head CT was negative, the patient was classified as having a clinically insignificant injury

Results

  • Study population: 3121
  • CT scans: 2078
  • Two week follow up interview: 1043
  • 363 patients were excluded because they did not have a CT scan and were lost to followup
  • Patients requiring neurological intervention: 44
  • Clinically important brain injury: 254
  • Clinically unimportant lesion (as defined above): 94

Analyses

  • Each of the patients were evaluated by trained ER physicians for 24 primary predictor variables.
  • Logistic regression and recursive partitioning analyses were used to analyze the data
  • The analyses identified 5 high risk criteria and 2 medium risk criteria. When the high risk criteria were combined, one could identify all of the patients who were at risk for requiring neurological intervention. When the medium risk criteria were added, one could additionally identify patients who were at risk for having clinically important lesions

Conclusions

  • Patients who meet any of the high risk criteria are at risk for requiring neurological intervention.
  • Patients who meet the medium risk criteria are at risk for having clinically important lesions.

The Vent

Conference Lecture
10/7/2015
The Vent

Synopsis: A hands on, informal lecture given on vents and their alarms by Dr. Tom Perera

  • You have to know the two types of ventilation out there used in the ER:
    • Volume A/C
    • Pressure A/C
      • This is wonderful theoretically, but as an emergency medicine physician you rarely use pressure A/C in the ER; these are “extreme” patients:
        • Failed volume A/C
        • Peak pressures are too high
        • Difficult asthmatics who are not doing well on volume A/C
  • Volume Assist Control
    • Volume based ventilation where you set a baseline breath volume
    • If the patient wants to take a bigger breath, the ventilator will not let them; keep patients on this setting more sedated than not
    • Basic settings for airway protection (i.e. no underlying lung disease)
      • Respiratory rate: Calculate the minute ventilation you want the patient to get
        • The great thing: The vents can be set to do all the calculations for you (i.e. no math)
        • You’ll likely start at 12-14 bpm
      • Volume: Most patients start at 450mL-500mL
        • 6-7mL/kg of ideal body weight (calculated based on height)
      • FiO2: Start at 100% — “crank it all the way up”
        • As an ER doc, you’re not going to affect a patient’s COPD by giving them 100% oxygen on a vent, because they’re on a vent
        • Intubating somebody is a traumatic procedure and leads to hypoxia
        • Start at 100%, titrate down
        • If no lung damage, no trouble intubating; you can start at 40%
      • PEEP: Start at 5, which is about physiologic
        • What is PEEP? For most cases, PEEP is a good thing
        • PEEP keeps a non-compliant lung more open, helping alveolar ventilation and decreasing V/Q mismatch
      • With all of these settings: Wait 5 minutes and look at the different alarms going off, and titrate
  • Making changes to vent settings: Special clinical scenarios
    • Let’s say the first ABG shows a low pO2. What changes can you make?
      • Obvious: Increase FiO2
      • Not as obvious: Increase PEEP
      • What you should do: Incrementally increase oxygen and PEEP together
    • Let’s say the patient is a bad asthmatic/COPD. What changes do you make?
      • Change the inspiratory/expiratory ratio. How?
      • The best way to do this is decrease the respiratory rate and to change the inspiratory peak flow rate
        • Most people start at an inspiratory peak flow rate of 60. If you increase this to 80, the inspiratory time decreases and the time spent on expiration increases
        • NB: If you do significantly decrease respiratory rate, make sure to have an adequate tidal volume
      • Decrease PEEP
        • These patients generally have so much auto-PEEP on board, that the thorax is kept in an “out-position” rather than fully collapsed
        • If you’re still fighting oxygenation with no PEEP, you can add a small amount of PEEP to see if that helps
      • Let’s say the patient has ARDS. What changes do you make?
        • Lung-protective ventilation: higher respiratory rate, smaller tidal volume
        • Large lung expansions worsen ARDS
        • Tidal volume: 4-6 ml/kg of ideal body weight
          • NB: This creates a higher percentage of dead space
        • Start RR at 18 and increase as needed
        • Wait 5 minutes, get an ABG and change settings as needed
  • Vent alarms
    • When an alarm starts to sounds: Think DOPE
      • Disconnect the vent:
        • Start bagging the patient every time you are confused, you think there’s a problem, or the patient is not getting ventilated
        • Make sure the bag is attached to oxygen
      • Obstruction
        • Check for obstruction in tube, plugging in lung, kinking in the line
        • Suction the tube
      • Pneumothorax
        • First, listen to the lungs
        • Next: E-FAST. It used to be get a chest X-ray, but ultrasound is faster and might be more accurate
      • Equipment failure
    • High pressure limit alarm
      • What do you do? Disconnect and bag
      • By bagging them, you’ll know if the problem is in the lung (i.e. if it is difficult bagging them, you know the high pressure is caused by the lung)
      • Look through the tube and find out where air flow is obstructed
      • This might indicate that you need a larger diameter ET tube
      • Coughing and gagging can also cause a high pressure alarm. You should be able to figure this out by watching the patient. They might need more sedation
    • Low pressure alarm
      • What do you do? Disconnect the bag
      • What causes low pressure?
        • ET tube leak/rupture or a disconnect of the system
      • Apnea alarm
        • This occurs when you haven’t set a baseline rate and the patient is not initiating enough breaths
      • Loss of O2
        • The vent is not connected to the wall O2
        • “Some of these alarms are really simple…”
      • High tidal volume/high minute ventilation/high respiratory rate
        • The patient is freaking out (i.e. not sedated enough air)
        • Increase sedation
      • Low tidal volume/low minute ventilation
        • Causes: Loose connection or a leak, disconnected from vent, ET tube leak
      • Ventilator inoperative or low battery
        • “Some of these alarms are really simple…”

Cases

  • Case 1: Recently intubated patient on SIMV with tidal volume = 500, FiO2 = 100%, respiratory rate = 12, PEEP = 5. The patient looks very uncomfortable, O2 = 93%, EtCO2 = 35. What do you do?
    • a) paralyze the patient
    • b) increase PEEP
    • c) increase ventilation
    • d) sedate the patient
  • Case 2: Recently intubated patient on volume AC, RR = 18, PEEP = 5, FiO2 = 100%, tidal volume = 6cc/kg. Currently overbreathing the vent at 28 breaths/minute. The ABG shows pH = 7.65. What do you do?
    • a) increase PEEP
    • b) increase tidal volume
    • c) give NaHCO3
    • d) decrease tidal volume

 

Answers:

Case 1 Answer: D (sedate the patient)

  • Do not paralyze without sedating, you lose a lot of information when you paralyze somebody
  • O2 = 93% is acceptable, FiO2 is already 100%
  • EtCO2 can’t be used as a substitute for PCO2, but it gives you an idea of what’s going on. In this case, EtCO2 is acceptable, and increasing ventilation will decrease the EtCO2 even more

Case 2 Answer: D (decrease tidal volume)

  • pH = 7.65 means the patient is very alkalotic and likely hyperventilating (blowing off their CO2). Decreasing the tidal volume will decrease their minute ventilation which will prevent hyperventilation
  • Another option would be sedation which would decrease the overbreathing of the vent