Case of the Week (COW) #5

CC: Vomiting for 2 days

HPI: 47 year old female with PMHX of HTN and ETOH abuse presents with abdominal pain. Patient states that beginning two days ago she was woken up from her sleep with sudden onset non-bloody vomiting as well as epigastric pain which radiates to the back and is sharp in nature. She admits to over 15 episodes of vomiting. She is also having cramping of her feet bilaterally. She admits to daily ETOH use, and states her last intake was two days ago, denies illicit drug use. Denies taking any medication prior to arrival. Denies fever, chills, chest pain, SOB or dysuria. Denies recent travel or sick contacts. PMHX/PSHX: none Meds: none Allergies: none

Physical Exam: Vitals: BP 150/96 P 98 RR 16 O2 sat 98% RA General: Awake, alert, anxious Cardiac: Regular rate, no murmurs Lungs: CTAB, no rales, no rhonchi, no wheezing Abd: soft, non-distended, Mild tenderness to palpation epigastric area

Labs: Magnesium- 1.3 Potassium- 3.5 Troponin- 0.017

EKG:

DX: Prolonged QT interval with non-sustained polymorphic Ventricular tachycardia secondary to Hypomagnesemia

ED/Hospital course:  Upon arrival to ED patient had Epigastric pain with vomiting, Patient started on IVF and received Pepcid and Zofran. EKG at this time showed QT prolongation and patient found to have magnesium of 1.3. While waiting for magnesium, she started to have short runs of polymorphic ventricular tachycardia and during these times she complained of chest tightness. After 2 grams of magnesium patients repeat EKG showed normal QT and runs of ventricular tachycardia stopped. She received another 2mg of Magnesium and 40 mEq of Potassium Chloride. Patient was then admitted to Telemetry floor. Patient observed for 24hours and discharged to home with follow up with a cardiologist and Norvasc 5 mg 1tab PO daily, Losartan 100 mg 1tab PO daily, Ranitidine 150mg 1tab PO BI.

Pearls:

  • An abnormally prolonged QTc, especially >500 is associated with an increased risk of ventricular arrhythmias, Torsade’s de Pointes
  • Prolonged QT with prolonged T wave is due to: HypoK, HypoMg, Medications, Elevated ICP, Cardiac ischemia, Congenital.
  • Prolonged QT with prolonged ST-segment is due to: HypoCa, Hypothermia.
  • If EKG reveals long QT start by reviewing drug history and checking electrolytes. Stop any offending agents. Suppress early after depolarization with IV magnesium sulfate and keep potassium >4.5meq/L.
  • If non responsive to magnesium, may consider cardiac pacing and rarely isoproterenol infusion. Acceleration of the heart rate may produce suppression of arrhythmias, with a reduction in the QT interval.
  • Unstable patients should undergo non-synchronized electrical defibrillation.

Post by: Dr. Kerri Clayton, DO

 

Steroids for SJS and TEN?

Here’s a quick hit summary of the evidence regarding the use of systemic corticosteroids in the treatment of SJS/TEN

  • Small amount of evidence, NO RCT to date
  • Small retrospective study (n=30, groups comparable) in 1984 from a burn center found survival benefit (66% versus 33% survival) in NOT giving steroids. Also found decreased complications such as Candida sepsis & esophageal ulcer in patients who did NOT receive steroids.
  • Cohort of ~500 patients from RegiSCAR (International Registry of Severe Cutaneous Adverse Reactions to Drugs)
    • No statistical diff in Hazard Ratio among treatment groups (supportive care vs. corticosteroids vs. IVIG).
  • Systematic Review of literature from 2001-2009 (only used Pubmed, not great)
    • Pooled analysis demonstrated no statistically significant difference in Mortality Ratio among groups (supportive care vs. corticosteroids vs. IVIG).
    • B.: i2 statistic not reported but authors mention no problematic heterogeneity.
  • Very small study (n=12 over 10 years) demonstrated potential benefit to early pulse-dose IV steroids (1.5 mg/kg/day dexamethasone for 3 days) in the form of (1) disease halt at 3 days (2) 1 actual death versus 4 predicted deaths.
  • Interestingly, a case-control study (case n=92; control n=381) demonstrated that pre-existing chronic steroid use delayed onset of SJS/TEN in patients using high-risk drugs by 7 days but also prolonged disease course by 2 days.

Bottom line

  • Systemic corticosteroids have not been shown to consistently correlate or provide a survival benefit in patients with SJS/TEN.
  • Paucity of evidence may show benefit to pulse-dose IV steroids such as are used in the treatment of autoimmune diseases such as pemphigus vulgaris.
  • Supportive care is the standard of care.

Post by: Dr. Katrina D’Amore DO, MPH

Case of the Week #3 – Why my flap sunken?

CC: Altered mental status and frequent falls

HPI: 55 y/o male presents from rehab with altered mental status (lethargy and agitation) and frequent falls for the past 2 days. Patient has a PMHx of large traumatic subdural hematoma 9 months ago treated with a craniectomy, seizure disorder, and HTN. Patient complains of headache and is a difficult historian. Pt does answer some questions appropriately.

Pertinent PE and Vitals: BP 121/81 HR 98 RR 16 Temp 98.1 100% on RA

GCS=14 and in no acute distress

L pupil dilated at 4 mm and nonreactive. R pupil 1 mm and reactive.

Pt. with moderate R arm and leg weakness (patient has baseline weakness but this is worse).

Pertinent Labs (if any): Unremarkable workup

Imaging

Working Diagnosis at time of Disposition Sinking Skin Flap Syndrome (also known as Syndrome of the Trephined) with possible Paradoxical Herniation

ED & Hospital Course Patient was admitted and received neurology and neurosurgical consultations. Medications were adjusted to control agitation. It is questionable per the consultants if his symptoms were due to paradoxical brain herniation. Plan is for an outpatient cranioplasty.

Pearls & Takeaways

  • Sinking skin flap syndrome is a delayed complication of a decompressive craniectomy. As the herniated brain tissue recedes, the skin flap from the surgical site can become sunken.
  • Symptoms include headaches, dizziness, seizure, and mood changes.
  •  Symptoms worsen when is head elevated vs reclined; treatment option is cranioplasty. Symptoms are much worse in an upright posture.
  • If atmospheric pressure exceeds intracranial pressure, patients can get paradoxical herniation and midline shift. This is more of an emergency and symptoms include focal deficits, pupillary changes, and alterations in consciousness.
  •  Paradoxical herniation is a state of low intracranial pressures; therefore traditional measures to treat midline shift and ICP will worsen the condition such as mannitol, hyperventilation, etc.
  • Treatment of sunken skin flap with paradoxical herniation is to elevate the intracranial pressure, including Trendelenburg position, hydration, and clamping of any CSF drains. Definitive treatment is cranioplasty.

Antibiotics for chest tubes

Things to keep in mind:

Prophylactic antibiotics for surgical patients in tube thoracostomy is usually limited to 24hrs duration and is 1st generation cephalosporin. It is meant to cover s. aureus the most common organism found in post traumatic empyema

increasing antibiotic use is leading to increase incidence of drug resistance

Potential infectious complications of penetrating or blunt chest trauma:

  • Post Traumatic Empyema
  • Pneumonia

Literature is mixed on whether antibiotics should be given for chest tubes placed for trauma.

In 1998 EAST guidelines gave a level 3* recommendation to give antibiotics prophylacticly to reduce incidence of pneumonia based off of Class I and Class II** data. AND there was insufficient data to give prophylactic antibiotics for post traumatic empyema

This recommendation remains controversial because 

  •    In order for antibiotics to be prophylactic they have to be given prior to a procedure and must reach a steady state concentration in the tissue before an incision is made.
  •    In the case of antibiotics given after a trauma has already occurred, the pleura has already been violated regardless of whether it is penetrating or blunt trauma. Therefore antibiotics do not reach needed concentration before contamination has concerned so these antibiotics are considered presumptive antibiotics.
  •    Non standard definitions of pneumonia and empyema were used, as well as various antibiotics were used in the different studies

In 2012 EAST guidelines reviewed the use of presumptive antibiotics for chest tubes (Tube thoracostomy):

They decided that they cannot make a recommendation for or against the routine use of presumptive antibiotics for chest tubes placed for traumatic hemopneumothorax.

Nor are they able to recommend an optimal duration of antibiotic prophylaxis when antibiotics are administered for traumatic hemopneumothorax because there are insufficient published data to support the routine use of antibiotics.

They concluded:

No single published study has been powered to adequately address the practice of administering presumptive antibiotics in TT for traumatic hemopneumothorax to decrease the incidence of empyema or pneumonia. Until a large and likely multicenter, randomized, controlled trial can be performed, the routine practice of presumptive antibiotics in TT for chest trauma will remain controversial.

If you want to read the article it isn’t a long read:
Post by: Dr. Ashley Guthrie, DO

Case of the Week #1

CC Chest pain and palpitations

HPI Pt is a 23 y/o male with no PMHx presenting with c/o palpitations, chest pain since last night. Pt states the pain is localized to the mid sternal chest wall with radiation to b/l upper extremities at times. Pt states the pain came on suddenly last night and he didn’t think anything of it so he went to bed. He woke up this morning with same pain and now with associated nausea and dizziness prompting the visit to the ED. Pt has never had pain like this in the past. Denies vomiting, F/C, recent illness, sudden cardiac death in the family other than a 70 y/o uncle who was obese. Pt denies drug use and states he was drinking over the weekend 2 days ago.

PMHx: none

Meds: none

Allergies: none

PSHx: none

Social: occasional ETOH, (-) drugs

Pertinent PE and Vitals: BP 90/62 P 186 RR 22 O2 sat 100% RA

General: Awake, alert, mild distress Cardiac: (+) tachycardic; no murmurs Lungs: CTAB, no rales, no rhonchi, no wheezing Abd: soft, nontender, nondistended Skin: diaphoretic; mild pallor

Pertinent Labs (if any) Troponin: 0.439

DDX: SVT with aberrancy vs VTach

ED Course: Pt placed on cardiac monitor immediately and IVF bolus initiated. Adenosine 12 mg IVP given while rhythm strip running with no change. A second dose of Adenosine 12 mg IVP given again with no change. 150 mg Amiodarone given with improvement of HR from 190’s to 170’s still wide complex. Second dose of 150 mg Amiodarone given with improvement of HR from 170‘s to 150’s and eventually converted to a NSR rate 85. Pt remained in stable condition and BP responsive to IVF. Pt admitted to telemetry and Cardiology consulted. While still in the ED, pt reverted back to wide complex tachycardia. 3rd dose of 150 mg Amiodarone given and recommendation from Cardiology was to try a 20 mg IVP of Cardizem. Cardizem given and pt immediately converted to NSR. Pt started on Cardizem drip and upgraded to the CCU. Pt underwent EPS and AV dissociation was noted. Determination was Verapamil Sensitive Ventricular Tachycardia. Pt remained stable throughout hospital course and started on Verapamil. Discharged on hospital day #3 with follow up with cardiology clinic.

Final Dx:  Idiopathic Fascicular Left Ventricular Tachycardia AKA • Fascicular Tachycardia • Verapamil-sensitive VT • Belhassen-type VT

Discussion:  MC type of idiopathic tachycardia of LEFT ventricle ! It is a reentrant tachycardia typically seen in young patients without structural heart disease ! Verapamil is first line treatment • Dose: 10 mg IVP over 1 minute ! EKG features: • Monomorphic V tach • QRS 100-140 ms (narrower than other forms of Tach) • Short RS interval 60-80 ms • RBBB pattern • Axis deviation depends on anatomical site of re-entry circuit ! Often misdiagnosed as SVT with RBBB ! Keys to dx: • Observe features of VT such as caption/fusion beats, AV dissociation • Usually unresponsive to adenosine, vagal maneuvers, or beta blockers

Post by: Kristen Pena, DO

Getting ready to intubate? Let’s pray they don’t DESATurate!

You head over to bed 44 to meet the BLS crew as they start telling you about an 82 year old man who has been having trouble breathing and is “confused” as per his family.  His oxygen saturation when you check is 76% and quicker than you can say “sepsis”, the eager resident has popped the grey airway box open and is setting up to intubate.

You slap the NRB on and turn the O2 up all the way.  So why is the resident so focused on finding and placing a nasal cannula too?!

Apneic oxygenation (AO) is used to extend the time until critical arterial desaturation (SaO2 88-90%) following cessation of breathing/ventilation that occurs during intubation.  AO, similar to our other RSI preparation, premedication, and positioning, is used to optimize the patient prior to the first intubation attempt.

First demonstrated by anesthesiologists over 50 years ago, the alveoli of the lungs will continue to take up oxygen even in the absence of active breathing.  AO focuses on increasing a patient’s oxygen saturation through “nitrogen washout” in first the alveoli, and then throughout the circulation.  This effectively replaces the nitrogen one inhales in normal atmospheric air with oxygen and increases the patient’s overall oxygen storage in both the lungs (95% of a person’s natural reservoir) and bloodstream.  Maximizing pre-oxygenation provides us an additional buffer of time for “safe apnea” during oral intubation.  In a 2011 article in the Annals of Emergency Medicine, Weingart et al outline recommendations to reduce the risk of hypoxemia during emergency tracheal intubations which include emphasis on:

Pre-oxygenation for every patient

  • Nasal Cannula set at 15 L/min is the most effective method of AO
  • Non-rebreather mask at rates as high as possible
  • HOB elevated 20-30 degrees or Reverse Trendelenburg in suspected C-spine injuries
  • Minimum of 3 minutes total or 8 deep breaths, if possible

Take home:  Keep in mind the acronym “NO DESAT” which stands for “Nasal Oxygen During Efforts Securing A Tube”.  A nasal cannula with high flow rates should be placed on every patient prior to endotracheal intubation and left in place during attempts in order to reduce the risk of hypoxemia and deterioration.

Fat embolism syndrome

Typically when we start talking about anything related to fat embolisms our minds go immediately to trauma and long bone fractures as the cause, but this isn’t always the case. The constellation of signs and symptoms of respiratory insufficiency, neurologic dysfunction and petechial rash which are typically associated with fat embolism syndrome can also be caused by pancreatitis, sickle cell disease and liposuction; all of which show up regularly in the Emergency Department. With mortality rates as high as 20%, despite the fact that FES usually doesn’t present for at least 12 hours after the initial event, it should be something that we are aware of.

There are two competing theories as what causes FES. Some believe more in the mechanical-obstruction theory where the fat globules act similarly as other embolic events, showering throughout the end organs and wreaking havoc by those means. The new challenger to this theory is the biochemical theory where proponents support the notion that the fat is broken down into free fatty acids and the damage is caused by the endothelial damage and subsequent increased vascular permeability. No matter which theory you support, the clinical diagnosis is going to be equally as challenging. There are a few criteria/scores that have been developed in the past that are non-specific diagnostic tools to identify patients with FES, but they have not been compared head-to-head in their accuracy. In the Emergency Department we are limited with the tests that we can routinely order. Unfortunately, CXRs are going to be essentially useless in diagnosing FES, but MRI may hold more promise. The starfield pattern seen on MRI is not specific to FES, but has been seen routinely in patients who have disease processes associated with FES along with neurologic symptoms. Otherwise, in the ED this is going to essentially be a clinical diagnosis with a good history and a little bit of luck. There is some evidence that earlier fixation and specific orthopedic surgery techniques may decrease the rate of FES, but from an EM point-of-view it is essentially supportive care. Research seems to be lacking into the non-trauma causes of FES, so maybe there is somewhere for us to intervene in those patients…

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Fixed dose PCC?

In the past, vitamin K and FFP were the mainstays of reversing warfarin, but now we have fancy new drugs like four-factor prothrombin complex concentrate (4F-PCCs).  4F-PCCs can rapidly reverse the INR of warfarin induced coagulopathy with less volume and quicker than FFP.  Many of the dosing regimens base the dose on the patient’s presenting INR and body weight, with ranges from 25-50 IU/kg.  A few problems arise with this approach, first the INR is not immediately available.  Second, 4F-PCCs are not cheap; costing up to $7,000 per patient in some cases.  Is there a fixed-dose regimen that we can give to patients on vitamin K antagonists without having to wait for the INR?

Some studies have looked at using 500 IU and 1000 IU fixed dose regimens for reversing the INR.  The 500 IU only corrected the INR in 43% of the patients, whereas the 1000 IU fixed dose study showed better clinical outcomes in 83.5% of the patients, but there is concern that the obesity epidemic in the United States will dilute the IU/kg concentration of the 4F-PCC and not be as efficacious.  Klein et al looked at using a fixed dose of 1500 IU of 4F-PCC for reversal of warfarin in 2015.  It was a relatively small sample of 38 patients on warfarin with the vast majority of them presenting with an intracranial hemorrhage.  Each patient had their INR drawn and then 1500 IU given before the result of the INR returned.  92.3% of the patients had their INR lowered to less than 2.0 after the 1500 IU of 4F-PCC and they reported no thrombotic events within the subsequent 7 days.  The presenting INR median was 3.3 (2.5-4.0) which was reduced to 1.4 (1.2-1.6) after administration of the 4F-PCC.  Additionally, this saved $40,273 dollars when compared to the typical INR and weight based dosing regimen for their patient sample.

We’ll have to figure out whether this fixed dose regimen of 1500 IU is the way to go, or should we base the dose solely on the patient’s weight and not worry about waiting on the INR.  Does waiting the extra 20 minutes for the INR lead to improved clinical outcomes?  And if we are going to start using a standard dose, is there a role for pre-hospital administration of the 4F-PCCs?

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Abdominal CPR?

There was a case report published in the Western Journal of Emergency Medicine last year about interposed abdominal compression CPR (IAC-CPR).  Personally, I’ve never heard anything of the sort and had to take a deeper look into it.  Essentially, you need two people to do compressions, one for the chest and one for the abdomen.  The abdominal compressor performs CPR with their hands about 5cm above the umbilicus and compressing about as deep as you would need to palpate the abdominal aorta pulse.  Both compress at the same rate and alternate their compressions; chest-abdomen-chest-abdomen and so on.  Theoretically, the abdominal compressor is acting as an external intra-aortic balloon pump.  By compressing the aorta during diastole, there is retrograde blood flow back into the coronaries.  Additionally, this abdominal compression increases venous return and promotes forward flow of the intrathoracic blood pool.  There have been no intra-abdominal injuries noted in survivors besides one pediatric traumatic pancreatitis reported in 1984.  The most recent review of IAC-CPR in Resuscitation showed significant improvements in the probability of achieving ROSC in the pre-hospital and in-hospital cardiac arrests when compared to standard CPR.  The question for me is why are we not doing this more? Is there harm in trying it if the person is already in cardiac arrest?

Post by: Terrance McGovern DO, MPH (@drtmcg13)