Benzos, Bleeding, Burns. Case Conference Review, November 8, 2017

Welcome back to another edition of Case Conference Review here at Academic Medicine Pearls at THE Ohio State University! Old Man Adams starts us off with a 38-year-old male with known history of alcohol abuse presenting via EMS for suspected EtOH withdrawal. On walking into the room, Dr. Adams is greeted with choice expletives and the subsequently refuses any vitals or to participate in the examination. The patient then promptly starts to seize, sending Dr. Adams down his alcoholic withdrawal seizure pathway.

To treat the alcoholic withdrawal seizure, he recommends the following simple piece of advise: “Benzos, benzos, benzos.”

His initial treatment of choice is Ativan 4mg. If that doesn’t work, repeat it. Keep in mind that Ativan (and oxazepam) are also safe benzo choices for cirrhotic patients. Should the seizures be refractory to initial measures and status epilepticus is achieved, intubation may be necessary. RSI should be done using versed or propofol for their GABAnergic effects and your choice of paralytic. Dr. Aziz adds that you may require higher doses of versed than the standard 0.3mg/kg dosing given chronic alcohol abuse.

Other options for seizure control? Propofol and phenobarbital are both good options if benzos fail, with ketamine as a consideration as well. “What about phosphenytoin?” one resident asks. While this is a common secondary agent in any seizure algorithm, it will not be effective in the alcohol seizure. The reason for this lies in the neurotransmitters affected by chronic alcohol use. Withdrawal seizures are caused by reduced GABAnergic and increased glutaminergic activity, on which phenytoin will have no effect, but benzos and barbituates will.

Further workup for this patient should include a head CT and also an EEG if paralyzed. Dr. Rublee reminds us that if suspicious for Wernicke’s, the treatment dose of thiamine is 500mg TID for three days, which Dr. Aziz reminds us should be given IV if possible due to an absorption of only 50% orally.

Dr. Nagaraj then takes us to into procedure land with her patient presenting with headache, fever and maculopapular rash (Figure 1) suspicious for meningococcal meningitis. She asks the question, “When is a lumbar puncture safe in the anticoagulated patient?”

Unfortunately, clear guidelines are not available, though there does exist some information to help us make informed decisions.

When it comes to Coumadin, An INR > 1.4 is considered a relative contraindication. It is recommended to hold Coumadin for five days prior to performing an LP. What if you don’t have five days? Should we give PCC? Dr. Nagaraj comments on a retrospective study that addresses this. PCC can be safely used to reduce INR <1.5 within roughly two hours, creating a safe environment for LP from a bleeding standpoint. In this study, however, thromboembolic events occurred in 6% of patients who received PCC (PCC has 2% established acceptable thromboembolic event rate). While its use in hemorrhaging patients has long been established to be beneficial, its usage in nonemergent scenarios remains unclear.

Information on LPs in patients with NOACs is similarly unclear, with no guidelines in existence. LPs are commonly performed within 24h of a patient’s last dose of a NOAC. Anticoagulation is considered fully resolved after five half-lives have passed for a given drug

Half-lives for NOACs

  • Pradaxa – 3 days
  • Xarelto – 1.5 days
  • Eliquis – 2.25 days

What about low platelet counts? In one study of cancer patients, 199 LPs were performed on patients with platelet counts of 20,000/μL or less, and 742 LPs were performed with platelet counts between 21,000/μL and 50,00/μL, without any cases of major bleeding.

Bottom line: Consistent guidelines do not exist for LPs in patients at risk for bleeding. Use risks and benefit analysis to determine necessity of LP in these patients. Keep in mind that to date, there are only 35 case reports of iatrogenic spinal hematoma in the past 40 years.

Dr. Krystin Miller is up next, with a 33 year-old male who presents with burns to face and upper extremities after a can of PAM explodes after being set next to a hot grill. She started with IV, O2, monitor and ABCs, though had to use a lower extremity for her blood pressure cuff due to burns. She then walks us through standard management.

She reminds us that the first step is stabilization. She offers us the following tips:

  • Remember to check to oropharynx for any singed tissue or swelling. Also listen carefully for stridor, wheezing or any other signs of airway compromise. Intubation should be done early so as to decrease chance of a difficult airway due to swelling.
  • Don’t forget adequate pain control
  • For extremities, it is important to get a good neurovascular exam, especially in cases of circumferential burns that can lead to swelling and neurovascular compromise requiring
  • Cover the burns. Use saline moistened gauze (or dry with adaptic). Sterile drapes may be used for large burns
  • Update tetanus
  • Nutrition is important due to high protein losses with burns and large amount of tissue rebuilding that will take place.

Once stabilization has been completed, appropriate fluid administration must be initiated. The first step is calculating the total body surface area (TBSA) that sustained 2nd or 3rd degree burns. This is done using the “Rule of 9’s,” as seen in Figure 1.

Classification of burns goes according to the following scheme:

First degree: Superfiical, epidermis only. Think sunburns.

Second degree: Epidermis and part of the dermis. Blisters may be present and the wound is very painful.

Third degree: Entire epidermis and dermis are involved. Wound may appear charred, leathery and pale. This should be painless and nerve fibers in dermis have been destroyed.

Once you have the TBSA calculated, you can then use the Parkland Formula to determine fluid administration volumes.

Total fluid to be given within first 24 hours = TBSA x weight (kg) x 4mL

Recommendations are to give one half of this total within the first 8 hours and the rest during the subsequent 16 hours. Due to the large volume being administered, we recommend using lactated ringer’s instead of normal saline to prevent the development of hyperchloremic metabolic acidosis.

“Should You Find Yourself in Afghanistan.” A helpful tip from our Chief resident in this week’s Case Conference Summary

Conference moderator and forever resident Dr. Zach Adams leads off this week’s case conference with a 65-year-old female diabetic presenting with the always challenging chief complaint of a “room-spinning” dizziness, otherwise classified as vertigo. She describes it as worse with position, severe, and present intermittently for the past few days. Suspicious for peripheral vertigo, Dr. Adams performs the Dix-Hallpike maneuver (Figure 1). Seconds after placing the patient in the reclined position with head turned laterally, the patient displays strong rotary nystagmus and promptly vomits on Dr. Adams’ shoes. Confirming his suspicion for benign paroxysmal peripheral vertigo, Dr. Adams then successfully performs the Epley maneuver (Figure 2) to reposition the otoliths within the semicircular canal and relieve the patient’s vertigo.

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Figure 1: Dix-Hallpike Maneuver

 

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Figure 2: Epley Maneuver

 

However, what if this vertigo had not given a positive on the Dix-Hallpike test? Central vertigo needs to be ruled out.

 

This is done using the HINTS exam, or Head Impulse, Nystagmus, Test of Skew to diagnose, a beside examination that has been shown to be superior to early MRI in the detection of posterior strokes (Kattah et al., 2015).

 

Components

Head Impulse: Corrective saccade implies peripheral vertigo. Lack of corrective saccade means the vestibule-ocular reflex is intact, as you would find in central vertigo (or a person not actually suffering from vertigo at all, like you or me).

Nystagmus: unidirectional, horizontal nystagmus is suggestive of peripheral vertigo. If the nystagmus is bidirectional, torsional, or vertical, this is suggestive of a central cause

Test of Skew: Positive test is suggestive of central pathology

View the following video for instruction on how to correctly perform this maneuver!

https://www.youtube.com/watch?v=1q-VTKPweuk

Excellent article detailing the sensitivity of this test listed below. As Dr. Aziz pointed out, these tests were conducted by neuro-ophthalmologists, so be sure that you understand the tests themselves in order to be able to expect any sensitivity.

Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y.-H., & Newman-Toker, D. E. (October 26, 2009). HINTS to Diagnose Stroke in the Acute Vestibular Syndrome. Stroke, 40, 11, 3504-3510.

 

Dr. Yeh then shares the case of a schizophrenic gentleman, previously admitted the psych hospital, presenting back from psychiatry to the ED with the somewhat ironic chief complaint of altered mental status. Per report, he has had increasing fatigue and lethargy. His physical exam is significant for slow, one-word responses, slow gait without any focal neurologic deficits. A quick medication review revealed the recent addition of 1500mg of Depakote. His blood valproic acid level was found to be 130 mg/L, only slightly elevated, but given its recent addition to his medication list and coupled with the clinical scenario, the likely culprit in his altered mental status.

How to treat?

Discontinue the offending medication immediately. In order to treat hyperammonemia, lactulose should be given. How much you ask? “It should be given until the patient poops,” as Dr. Martinez reminds us. Additionally, in the case of severe toxicity where the patient is at risk for coma and death, dialysis should be considered. Dr. Rublee advises that this is most likely to be beneficial in the setting of high serum Depakote levels, as you can expect a high percentage of drug not already bound to serum protein.

 

Next up, is Dr. Schwab with a case of a friendly wrestling match gone wrong. Our patient comes in after feeling a “pop” sensation in his left arm while wrestling his roommate. His XR can be seen below:

postdisloc

Diagnosis? Posterior dislocation of the elbow without fracture. This needs to be reduced. But first, Dr. Schwab took a moment to discuss his sedation, which he accomplished with propofol.

 

He offers the following advice:

  • Ensure sedation is adequate. Do not be afraid to pause the reduction to do so.
  • When using propofol, start with a 1mg/kg bolus followed by 20mg ever 30s until desired sedation is achieved
  • Consider pre-medicating with fentanyl to decrease amount of propofol needed (though be wary of increased potential for adverse events from a respiratory standpoint)
  • Consider ketamine as adjunct – independent subdissociative doses vs ketofol

 

Once adequate sedation was ensured, reduction was accomplished using traction-counter-traction while applying firm pressure over the olecranon.

reduction

Video of proper reduction technique can be found here.

 

Dr. Rublee is up next with her case of a 29-year-old inmate whose face was on the receiving end of a flaming bowl of lit baby oil and chili powder. He presents in agonizing eye pain with concern for chemical and thermal damage to his eyes. Dr. Rublee quickly tested eye pH, finding it elevated (7-8 normal). Realizing the need for irrigation, she obtained a Morgan lens and began irrigation, choosing then to discuss its proper usage, as seen below.

  • Anesthetize with tetracaine, with care to ensure that pH has already been tested, as tetracaine may alter the pH.
  • Connect the Morgan lens to irrigation (LR preferred but normal saline works) and insert in a fashion similar to that of a contact lens
  • First irrigate under the upper eye lid for 30 minutes and then move to under the lower lid for an additional 30 minutes

 

When in doubt, the official instructions can be found on the manufacturer’s website:

 

morganlens

Dr. Carrol took this opportunity to remind us that this may not be a suitable option in young children as their eyes may be too small, in which case manual irrigation is the preferred option. Dr. Adams, before closing out the day, advises a quick and useful alternative to the Morgan lens, “should you find yourself in Afghanistan.” He recommends as a substitute placing the prongs of a nasal cannula on either side of the bridge of the nose. The NC can then be hooked up to a saline bag, providing continuous irrigation to both eyes.

This wraps up another week of AMP at The Ohio State University. Thanks for reading and check back next week!

 

 

 

 

 

Case Conference Summary, October 11, 2017

Some rapid fire review of cases presented by our residents this week:

Leslie Adrian presented a pediatric case with a young male complaining of abdominal pain after sustaining a handle bar injury to the abdomen after falling off his bike.  Initial vital signs showed tachycardia and age adjusted hypotension.  He had RUQ abdominal pain on examination and a FAST was positive.  He was stable enough for CT scan which showed a large liver laceration and ultimately taken to the OR for definitive management.  She did an excellent job of reviewing the literature on management of blunt pediatric abdominal trauma.  In particular, management has changed dramatically recently, with hemodynamic and clinical status guiding management of solid organ injury versus grade of injury.  In particular, for blunt liver trauma the following algorithm applies:

  • Hemodynamically unstable patient or with signs of peritonitis = OR
  • Hemodynamically stable patient = abdominal CT versus labs and serial exams
    • Stable + “blush” = consider angiography
    • Stable without blush and no peritoneal signs = non-operative management, serial exams and labs
      • Non-operative management should only be provided in an environment that provides appropriate monitoring and an OR

Grace Rodriguez discussed management of suspected upper GI bleeding.  In particular, in patient’s with cirrhosis with or without known varices considering broadening management with the following:

  • Close hemodynamic monitoring
  • Resuscitate:
    • Hb goal >7
    • Platelet goal >50,000
    • Correct coagulopathies
      • Coumadin, DOAC – consider vitamin K (especially in cirrhotics), PCC or FFP
      • Remember that the INR in cirrhosis does not correlate with underlying coagulopathy
        • Consider TEG to guide management
        • Check a fibrinogen
          • Consider cryoprecipitate to maintain fibrinogen level >150-200
          • Consider tranexamic acid if hyperfibrinolysis is suspected
    • Ovoid over resuscitation, especially with crystalloids to prevent worsening bleeding
  • Administer a PPI
    • No mortality benefit but may prevent rebleeding
    • Bolus dosing non-inferior to bolus and an infusion
  • Give a third-generation cephalosporin (i.e ceftriaxone) if they have cirrhosis
    • Mortality benefit
    • Treats underlying precipitant (i.e. SBP) of variceal bleeding
  • Consider octreotide
    • No mortality benefit
    • Decreases transfusion requirement
  • Consult GI
  • Intubate for airway protection if massive bleeding

Other considerations we can utilize in our hospital’s clinical guidelines include the modified Glasgow-Blatchford Score to discharge low-risk risk patients with a score of zero (no GI bleeding mortality at 6 month follow-up).

Lalitha Kunduru presented the management of superficial venous thrombosis, which most commonly occurs in the long saphenous vein (50-60%), short saphenous vein (11-15%) and tributaries of both (30-40%).  Risks for complication include being male, a history of VTE, cancer, recent surgery, involvement above the knee, SVT in non-varicose veins, thrombosis >5 cm and thrombosis involving the saphenofemoral junction.  Importantly, the rate of concomitant DVT is 25% and PE is 5%, which must remain on the differential.   The CALISTO Study Group and other sources recommend consideration for anticoagulation, especially for thrombosis >5 cm or within 5 cm of the saphenofemoral or saphenopopliteal junction.  Recommended medications include fondaparinux at 2.5 mg SQ daily, lovenox at 40 mg SQ daily, or a DOAC.  Otherwise, patients should be followed closely as an outpatient for progression and managed with NSAIDs and compression stockings (20-30 mmHg).

Finally, a case of angioedema was presented which reviewed some of the current literature in how to manage.  If anaphylaxis is suspected or considered, IM epinephrine, H1/H2 blockade, and steroids might be considered.  However, these treatments are unlikely to be successful in hereditary or ACE inhibitor induced angioedema.  While hope was given to icatibant as a potential treatment option, studies have not shown great benefit, and it’s pretty pricey.  Less expensive options include consideration for FFP, which may show benefit but is poorly studied.  Factor replacement with C1 esterase inhibitor is first line in patients with hereditary angioedema.  If the airway looks eminent or worsening, intubate early!  If stable, observation for 4-6 hours is appropriate and if swelling is isolated or improving consider discharge.  ED work-up is often limited, but consider checking a C4 level to screen for hereditary angioedema if suspected and if you have the resources.  If low, send off a C1INH protein level for outpatient follow-up.

Lastly, we reviewed a recent EM:Rap topic on the reasons we intubate which we really liked and is easy to remember – ABCDEF!

  • Airway – obstruction (i.e. FB, angioedema, etc.)
  • Breathing – not oxygenating (type 1 respiratory failure), not ventilating (type 2 respiratory failure)
  • Circulation – shock with impending respiratory failure (type 4 respiratory failure)
  • Disability – altered mental status (i.e. airway protection)
  • Expected course – anticipated worsening of ABC or D
  • Feral – when your patient is that altered and combative either from intoxication or trauma that you can’t get the studies you need to do to rule out life threatening illness.