Posts (14)

Jul 12, 2015 · Blunt Agonal Arrest

Presented at Joint Trauma Conference on December 17, 2013. Mayo Clinic, Rochester MN.
Authors: Rachelle Beste, Dustin Leigh, Ashley Martin, Diana Shewmaker, Cameron Wangsgard
Reviewed by: Daniel Cabrera

Update July 2015

shutterstock_69312310

Blunt Agonal Arrest

Blunt agonal arrest referes to the severely injured patient in extremis (Class IV Shock) not responding to fluid resuscitation. They may or may not have a palpable pulse.Markers include:
•    Heart rate < 60 bpm
•    Systolic blood pressure < 80
•    Any ventricular tachycardia, ventricular fibrillation, or PEA
•    Loss of signs of life
Trauma resuscitation of the patient in blunt agonal arrest includes a rapid assessment and treatment of reversible, life-saving traumatic etiologies of the arrest. This includes hemorrhage/hypovolemia, airway compromise, tension pneumothorax, and pericardial tamponade. ACLS and BLS in an the resuscitation of the blunt agonal arrest patient is classically thought to be of limited benefit due to the nature of the underlying injuries that lead to arrest in the trauma patient. The result is that a initial airway assessment, needle decompression/chest tubes, and rapid fluid resuscitation with blood products should take priority over chest compressions in the blunt trauma agonal arrest patient.Our normal trauma algorithm is followed with a few key steps taking place:
  1. Obtain a definitive airway (orotracheal vs. surgical)
  2. Bilateral needle thoracostomy followed by bilateral tube thoracostomy when able
  3. Initiate massive blood transfusion/resuscitation
  4. Attach cardiac leads and obtain an US of the heart to assess for pericardial effusion and cardiac kinetic activity (typically a subxiphoid or peristernal long view)

References:

  1. Trauma Center Practice Management Guideline: Traumatic Blunt Agonal / Arrest Algorithm. Mayo Clinic, Rochester. Last Reviewed: 10/2012.

 

Thoracostomy Tube Placement

Relative Contraindications:

Bleeding or coagulopathy, correct if possible.

Equipment:

  • Chest tube tray (see attached powerpoint)
  • Sterile gloves
  • Two packets 0-silk
  • Sterile gauze
  • Drainage system (Atrium Oasis)
  • Chest tube selection
  • Traumatic pneumothorax or hemothorax: 36-40 French to allow evacuation of clot
  • Large pneumothorax, unstable: 24-28 French
  • Large pneumothorax, stable: 16- 22 French

Preparation:

  • If time allows: pre-procedure CXR, informed consent, and consideration of procedural sedation
  • Optimize patient positioning with abduction of ipsilateral arm to patient’s head
  • Barrier precautions and sterile field
  • Locate triangle of safety (anterior border of latissimus dorsi, lateral border of pec major, line above nipple or inframammary crease)
  • Apply chlorhexidine
  • Insertion will be at 4th-5th intercostal space in the anterior axillary line
  • Incision site should be one intercostal space BELOW actual chest-tube insertion site
  • Skin wheal with 1% lidocaine and 25-gauge needle
  • Aspirate and anesthetize subcutaneous tissues,  intercostal muscle, periosteal surface with 20 cc lidocaine and 21-gauge needle
  • March up periosteal surface, continuing to aspirate and anesthetize to chest-tube insertion site
  • Confirm entry into pleural space with aspiration of air or flash of pleural fluid.  Inject any remaining lidocaine.

Incision and Disection:

  • Use scalpel to make 1.5-2 cm incision parallel to rib. Avoid making too small of an incision.
  • Use a kelly clamp to dissect subcutaneous tunnel cephalad to insertion site above rib.  Remember neurovascular bundle is inferior to rib.
  • Once at parietal pleura, gently push closed Kelly clamp through.  Open clamp to spread the intercostal muscle and parietal pleura while maintaining tract.  Space will need to accommodate clamped chest tube and index finger.
  • Use index finger to ensure proper position.  Confirm there are no adhesions between lung and pleural surface in order to proceed.

Insertion:

  • Clamp proximal and distal end of chest tube.
  • Insert end with side ports along finger tract until into pleural cavity.
  • Unclamp and advance manually.  Aim apically for pneumothorax and basally for evacuation of any fluid.
  • Note insertion of last port hole and total depth of insertion, usually 2-5 cm beyond last port, depending on body habitus.

Securing:

  • Use 0-silk sutures to secure chest tube.  Place two simple interrupted sutures on each side of the chest tube.  Each suture should be tightly tied and wrapped around chest tube several times prior to again tying.
  • Ensure securement by tugging chest tube with minimal displacement.
  • Tape tube to side of patient with mesentery fold and wrap petroleum-based gauze around tube.
  • Cover with sterile gauze, multiple pressure dressings, and silk tape.
  • Connect clamped end to drainage system, then unclamp.

Confirmation:

  • Obtain AP CXR and identify radio-opaque line which contains proximal drainage hole.  Ensure it is located inside pleural space.

Needle Thoracostomy Placement

  • Immediate decompression is necessary for high suspicion of tension pneumothorax.
  • 14-16 gauge angiocatheter attached to 5-10 mL syringe (found in drawer below chest tube tray)
  • Superior margin of 2nd- 3rd rib in midclavicular line or at location of standard chest tube (4th-5th intercostal space at the anterior axillary line)
  • Advance while aspirating until air aspirated
  • Withdraw needle from angiocatheter, rush of air indicates partial or complete conversion to simple pneumothorax
  • Place thoracostomy tube as above

Indications for Operative Thoracotomy

  • Immediate drainage of >1 L of blood or 20 mL/kg
  • Accumulation of >3 mL/kg per hour of blood or 150-200 mL/h for 2-4 hours
  • Persistent blood transfusions to maintain hemodynamic stability

Reference:

  1. NEJM Chest Tube Insertion (16 min video): http://www.youtube.com/watch?v=NiDFYGQts5c
  2. Doelken, Peter, MD. “Placement and Management of Thoracostomy Tubes.” Placement and Management of Thoracostomy Tubes. UpToDate, 7 Aug. 2013. Web. 08 Dec. 2013. <http://www.uptodate.com/contents/placement-and-management-of-thoracostomy-tubes?source=search_result&gt;.
  3. Brunett PH, Yarris LM, Cevik AA. Chapter 258. Pulmonary Trauma. In: Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011. http://www.accessmedicine.com/content.aspx?aID=6389704. Accessed December 10, 2013.

 

Resuscitation and IV Access

Intravenous Access

Establishing adequate venous access is prudent in any trauma patient, and is obviously more so for the unstable traumatic patient. Large-bore peripheral IVs may be adequate if two or more can be secured.[1] If peripheral access is not easily obtainable, there should be consideration of central access via large catheter introducer (8F to 9F) or intraosseous access. This can typically be the femoral vein as the subclavian and jugular veins may be partially collapsed with significant hypovolemia, and iatrogenic pneumothorax would cause further hemodynamic decompensation. However, vascular access above the diaphragm is preferred if there is concern of major vascular injury in the area of the abdomen or pelvis.[2]In general, the rate at which crystalloid can be infused is dependent on the catheter diameter and the driving pressure. [2] This is based on Poiseuille’s Law which is arguable not applicable to in-vivo use given the non-laminar flow.[3]Nevertheless, theoretical infusion rates are in the table below for comparison purposes. Flow rates via intraosseous access are less well established, but are thought to be comparable to peripheral access. Some studies have shown that the humeral site compared to tibial access allows for more rapid infusion; however, the studies are flawed and are either small, biased or based on animal models.[4-5]Theoretical Infusion Rates based on Poiseuille’s Law [2]:
References:
  1. Li SF, Cole M, Forest R, Chilstrom M, Reinersman E, Jones MP, Zinzuwadia S, King S, Yadav K. Are 2 smaller intravenous catheters as good as 1 larger intravenous catheter? Am J Emerg Med. 2010 Jul;28(6):724-7. doi: 10.1016/j.ajem.2009.05.003. Epub 2010 Mar 25. PubMed PMID: 20637391.
  2. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. Judith E. Tintinalli, J. Stephan Stapczynski, David M. Cline, O. John Ma, Rita K. Cydulka, and Garth D. Meckler. The American College of Emergency Physicians. 2011.
  3. McPherson D, Adekanye O, Wilkes AR, Hall JE. Fluid flow through intravenous cannulae in a clinical model. Anesth Analg. 2009 Apr;108(4):1198-202. doi: 10.1213/ane.0b013e3181966451. PubMed PMID: 19299786.
  4. Lairet J, Bebarta V, Lairet K, Kacprowicz R, Lawler C, Pitotti R, Bush A, King J. A comparison of proximal tibia, distal femur, and proximal humerus infusion rates using the EZ-IO intraosseous device on the adult swine (Sus scrofa) model. Prehosp Emerg Care. 2013 Apr-Jun;17(2):280-4. doi: 10.3109/10903127.2012.755582. Epub 2013 Jan 18. PubMed PMID: 23331182.
  5. Miller L, Philbeck T, Montez D and Puga T A two-phase study of fluid administration measurement during intraosseous infusion Annals of Emergency Medicine 2010; 56(3):S151

 

ED Thoracotomy

Indications for ED Thoracotomy

The potential benefits of an ED thoracotomy (EDT) need to be carefully balanced with the potential harmful exposure of health care personnel to blood-borne pathogens. [1] It is performed on patients who have just sustained or are on the verge of cardiac arrest, and is done to evacuate a pericardial tamponade, temporarily repair a myocardial wound, cross-clamp the descending thoracic aorta (to prevent exsanguinating abdominal hemorrhage and improve coronary/cerebral flow), and to allow for internal cardiac massage.Overall mortality is high, where only 1.4% of blunt trauma patients undergoing EDT will survive. Survival is higher for penetrating trauma, 16.8% and 4.3% for stab wounds and gunshot wounds, respectfully. According to the Practice Management Guidelines published by the American College of Surgeons Committee on Trauma, indications for EDT include the following: [2]
  • EDT is best applied to patients sustaining penetrating cardiac injuries who arrive at trauma centers after a short scene and transport time with witnessed or objectively measured physiologic parameters showing signs of life.
  • EDT should be performed in patients sustaining penetrating noncardiac thoracic injuries, but these patients generally experience a low survival rate. Because it is difficult to ascertain whether the injuries are noncardiac thoracic versus cardiac, EDT can be used to establish the diagnosis.
  • EDT should be performed rarely in the patient sustaining cardiopulmonary arrest secondary to blunt trauma because of its very low survival rate and poor neurologic outcomes. It should be limited to patients who arrive with vital signs at the trauma center and experience witnessed cardiac arrest.
  • EDT should be performed in patients sustaining exsanguinating abdominal vascular injuries, but these patients generally experience a low survival rate.

CURRENT EAST GUIDELINES ON RESUSCITATIVE THORACOTOMY IN TRAUMA (JULY 2015, FREE OPEN ACCESS)

thorac4

References:

  1. Mollberg NM, Glenn C, John J, Wise SR, Sullivan R, Vafa A, Snow NJ, Massad MG. Appropriate use of emergency department thoracotomy: implications for the thoracic surgeon. Ann Thorac Surg. 2011 Aug;92(2):455-61. doi: 10.1016/j.athoracsur.2011.04.042. Epub 2011 Jun 25. PubMed PMID: 21704969.
  2. Practice management guidelines for emergency department thoracotomy. Working Group, Ad Hoc Subcommittee on Outcomes, American College of Surgeons-Committee on Trauma. J Am Coll Surg. 2001;193(3):303.

 

Further Reading:

Should Advanced Life Support be Initiated or Continued?

Research Arguing For or Against Currently Accepted Guidelines
Traumatic cardiac arrest:  Should advanced life support be initiated?According to the article by Leis et al. (J Trauma Acute Care Surg, Volume 74 Number 2, Pages 634-638), ALS should be initiated regardless of the initial cardiac rhythm in a traumatic cardiac arrest (TCA), realizing that the highest survival rates are those presenting in VF or PEA and children.His group performed a retrospective cohort study between 2006-2009 of an urban-based EMS two-tier response system, meaning that both BLS and ALS ambulances were present at each scene with a rapid response time of 7-9 minutes.  A physician-in-charge as well as an ambulance physician were also present on-scene and during transfer to level 1 trauma reference centers.  All TCA patients received ALS on-scene including intubation, IV access, fluid and drug therapy, POC blood analysis, and procedures such as chest drain insertion, pericardiocentesis, and FAST exam.  The study objective:  describe survival results and compare them with other published series to determine which factors could be associated with return of spontaneous circulation (ROSC) and complete neurological recovery (CNR).They evaluated patients at three points in time:  when initial patient contact was made; when ALS was terminated; and when the patient was discharged from the ICU.  They found that of 167 patients included in the study, ROSC was obtained in 49.1% with 6.6% achieving CNR.  The survival rate was 23.1% in children, 5.7% in adults, and 3.7% in the elderly.   The etiology included 40.1% traffic accidents, ; 15.6% assaults, stab wounds, or GSWs; 16.8% falls; and the other group being drowning, electrocution, self-harm, railroad or underground accidents, etc.  There was no significance in ROSC regarding the type of ambulance to arrive first.  There was, however, a significant difference between response times and survival with CNR; if >10 minutes passed, none of the patients achieved CNR.  They also found that the rate of ROSC was greater if TCA was witnessed or patients received more fluid replacement.  These, along with other findings, led them to conclude that ALS should be initiated in TCA regardless of the initial cardiac rhythm.

When Should Efforts be Terminated in Resuscitation of Blunt Agonal Arrests?

The Consequences of Noncompliance With Guidelines for Withholding or Terminating Resuscitation in Traumatic Cardiac Arrest in Patients

Mollberg, et al. would argue otherwise (The Journal of TRAUMA Injury, Infection, and Critical Care, Volume 71, Number 4, October 2011, Pages 997-1002).  They studied the consequences of violating the published guidelines by The National Association of Emergency Medical Services Physicians and American College of Surgeons Committee on Trauma (NAEMSP/ACS-COT) for withholding or terminating resuscitation in prehospital traumatic cardiopulmonary arrest (TCPA).  Also studied was whether EMS personnel were able to accurately identify patients in TCPA.  This was done via a retrospective review of all patients with TCPA managed by the Chicago Fire Department and transported to Mount Sinai Hospital during an eight year time period, composing the largest series to date on this topic.

Of the 294 patients identified who met criteria for withholding or terminating resuscitation, 0.3% survived with a GCS of 6.  Their outcomes were dismal with four being declared brain dead, one having life support withdrawn, two passing away in <24 hours, and the lone survivor being discharged to a long term care facility.  Total costs incurred were $3,852,446.65, excluding those associated with intubation and ACLS medications in the field and ambulance transportation.  There was 100% agreement between BLS and ACLS teams on the presence or absence of a pulse for 39.8% of patients.  The study excluded those patients younger than 18, those who arrested secondary to drowning, strangulation, hypothermia, electrocution, fire, when a nontraumatic cause proceeded the arrest, as well as anyone transported by another agency.

They concluded that strict adherence to the current guidelines should be maintained with little risk of loss of neurologically intact survivors in a system where no physicians are on scene to provide advanced care such as a thoracotomy or pericardiocentesis.  Upholding the guidelines will result in significant cost savings within the medical system and for the patients’ families as well as reduce the burden placed on families and care facilities whom must provide for individuals no longer capable of performing activities of daily living.

Image from Shutterstock used under license 

Mar 15, 2015 · Accidental Hypothermia

hypothermia_EMBlog

Rewarming

  • Most important:
    • Remove clothes
    • Cover with dry warm blankets and bedsheets
    • Bair hugger and/or Arctic sun (no real difference between the two. Bair hugger easier to initiate in ED. Cover up everything, including face too)
    • Warm room / heat lamps
  • Second most important:
    • Warmed humidified O2
    • Warmed IVF (but each 1L at 42 degrees will only raise body temp ~0.3 degrees C)
  • Generally initiate these measures above for anyone less than 34 degrees (moderate hypothermia)
  • Other considerations: NG lavage, bladder irrigation, thoracic lavage, peritoneal lavage are all invasive and time consuming with only at best being moderately effective. The easiest to perform – NG lavage and bladder irrigation are really minimally effective.

How do I get warmed IVF?

How do I get warmed humidified O2?

  • Patient breathing on own?
    • Ask for a “blender”. RTs can get this from upstairs. You can attach it to a facemask and provide high flow O2. This is the same device that we use to initiate high flow NC for our peds patients.
    • Many BiPAP machines have a warmer/humidifier attached in line. Check with your own department before to find out if this is the case.
  • Patient intubated?
    • Modern ventilators can provide warmed/humidified air. However, many EDs only have access to older ventilators so again, know what’s in your own department.

Rewarming in critically ill/hemodynamically unstable/peri-code/code

  • ECMO (best option when able, but not available most places)
    • Page ECMO team early!
  • CVVH (way easier than dialysis to initiate. You need to be able to place a Meherker and a nephrology nurse able to bring and operate the machine. That’s basically it.
  • Hemodialysis (hard to initiate – unlikely to be a feasible option)
  • Cardiac bypass (hard to intitiate – unlikely to be a feasible option)
    • All these methods can raise body temp at least 2-4 degrees C per hour.

Patient is bradycardic? Should I pace them?

  • In general, pacing is not indicated in the hypothermic patient. If they have a pulse, continue to rewarm and the bradycardia should resolve.
  • Atrial fibrillation is the most common arythmia of hypothermia. Will convert to sinus with rewarming.
  • Classic board exam question is bradycardia with osborn waves but only see this in ~30% if severe hypothermic patients.

CPR/Defibrillation

  • Somewhat controverial. Some say no CPR for PEA as you could induce a dysrhythmia. Some say shock only once and if it doesn’t work, don’t shock again until at least 2 degrees warmer.
  • Most would say if there is no pulse, you should be doing CPR.
  • Every 2 minutes, if there’s a shockable rhythm… shock! If it’s still a shockable rhythm 2 minutes later on rhythm check, shock again! It doesn’t take that long to do. Just make sure you continue to re-warm them during the code.
  • Be careful with meds. Consider only giving 1mg epi ONCE rather than repeat dosing over the course of the code. As they re-warm, they will vasodilate. If they have a bunch of epi from multiple rounds sitting in their vasoconstricted extremity, they could get a huge surge of epi all at once.

When should I call the code? When is the patient truly warm and dead?

  • Most textbooks would say 32 degrees – if there is still no pulse, resuscitation efforts should be terminated.
  • Alternatively K > 12 mmol/L warrants termination of resuscitation efforts.

What other interventions/testing should be done?

  • Does the patient have frostbite?
    • Patient needs aggressive rewarming of areas of frostbite. Consider NSAIDS, calcium channel blockers, and if there are signs of decreased perfusion in the hands or toes, they may be a candidate for tPA/heparin.
  • Was there trauma?
    • If patient was found down, consider imaging of head/c-spine if altered and obviously, perform a thourough physical exam.
  • Was this an intentional self-harm attempt?
    • Consider checking acetaminophen, salicylate, ethanol, EKG.
      • Incidentally, ethanol causes vasodilation making hypothermia more severe and re-warming techniques potentially less effective.
  • How long was the patient down?
    • Consider checking a Creatine Kinase – typical symptoms of rhabdomyolysis can be clouded by hypothermia.
  • Is this for sure accidental hypothermia? Could the patient have just incidentally been found outside for another reason? Maybe they were confused or just incidentally picked up outside.
    • Differential for hypothermic patient:
      • Accidental hypothermia (environmental exposure)
      • Hypoglycemia
      • Myxedema coma
      • Adrenal insufficiency
      • Sepsis
    • For these secondary causes, your goal is not active re-warming, but to treat the underlying cause. For example, treating myxedema coma primarily by active rewarming will result in vasodilation and secondary cardiovascular collapse. Focussed treatment would be removing cold clothes + warm blankets but not other active rewarming techniques + medical treatments (T3/T4, steroids, fluids, etc)

Further reading?

 

Oct 15, 2014 · The Crashing Patient with Pulmonary Artery Hypertension

The Diagnosis of Pulmonary Artery Hypertension (PAH) Carries with it a Very Poor Long Term Survival

  • Without treatment, most patients, both children and adults, will die within 1–3 years.
  • Treatment does improve survival, but long term survival is still poor:
    • Pediatric patients have a 1 year survival of 89% and 5 year survival of 75%. [1]
    • Adult patients have a 1 year survival of 85% and 5 year survival of 57% from time of diagnosis. [2]
  • Similar to LVAD patients, pulmonary vasodilator therapy may be destination therapy or a bridge for a transplant (typically heart and lung) depending on the underlying etiology of the patient’s pulmonary artery hypertension and the patient’s other co-morbid medical conditions. It’s important to try and figure this out when the patient arrives in the ED.

Key Differential in the Crashing Patient with PAH [3]

  • Flolan pump dysfunction
    • Patient’s may be on this at home. Similar to an insulin pump in diabetes, it is providing a constant infusion of Epoprostenol, a prostaglandin that causes pulmonary vasodilation.
    • As opposed to an insulin pump which is SQ, a flolan pump administers a constant infusion through an indwelling CVC or a PICC line.
  • Lethal triad of PAH:
    • Hypoxia
    • Hypercarbia
    • Acidosis
      • All 3 lead to pulmonary vasoconstriction which will worsen underlying PAH.
      • Causes include:
        • Acute decompensated heart failure
          • Fluid retention/overload is common due to poor cardiac output with underlying PAH, causing RV dysfunction and often times RV failure.
        • Sepsis
          • Of any type, but in particular worry about pneumonia or if Flolan pump, consider line infection.
        • PE
          • Patients are at increased risk for venous thromboembolism.
          • Often times on anti-coagulation or have an IVC filter placed.
        • RV ischemia/infarction
          • Due to fluid retention/overload leading to increased stress on an already strained RV from the PAH.
        • Mesenteric ischemia
          • Due to chronically poor cardiac output
        • GI Bleed
          • Can be due to mesenteric ischemia (as mentioned above)
          • Patients may be anti-coagulated (as mentioned above)

How to Manage the Crashing Patient with PAH

  1. Look for a Flolan Pump. If it’s there, make sure it’s functioning. Consider battery failure, lack of Epoprostenol in the pump, or a clot in the line. If there is any evidence of Flolan pump failure, priority number one is getting Epoprostenol infusing again! You can run it through a regular PIV if you need to. The half life of is Epoprostenol very short (minutes) and a patient that is dependent on this infusion, will not survive long without it.
  2. Correct the lethal triad.
    • Keep the spO2 > 92%. Like patients with COPD, patients with PAH may have a normal spO2 around 92–94%, but any saturation lower than needs to be managed aggressively including intubation if necessary.
    • Check a blood gas. Ensure the patient is not hypercarbic due to respiratory failure, pulmonary edema, PE, etc. If they are, initiate non-invasive ventilation or intubate if this won’t be tolerated.
    • Correct the acidosis. Correct the acidosis by correcting the underlying cause whether it be sepsis, fluid overload, etc. If giving fluids consider a balanced fluid like Lactated Ringers or plasmolyte. Normal saline is an acidic solution and can cause a hyperchloremic metabolic acidosis which is not likely to be tolerated as well in these patients.
  3. Initiate a gentle fluid bolis, ~500cc, and reassess if more volume is warranted. These patients are tricky. They have RV dysfunction at baseline. While they may benefit from fluids, they may also already be in a fluid overloaded state. I would not rely on IVC US to determine if they will benefit from fluids as it will likely always have some component of dilation. As discussed above, consider a balanced solution, not normal saline.
  4. Maintain a MAP > 65mm Hg. Initiate norepinephrine early, even if fluids are ongoing or aren’t being given. Poor perfusion will lead to worsening acidosis, cardiac output, and end organ dysfunction.
  5. Initiate dobutamine or milrinone for ionotropy. Particularly if signs of cardiac dysfunction, either by bedside Echo, signs of poor perfusion despite MAP >65 mmHg, etc.
  6. Do a Bedside US. Interpretation is tricky and needs to be taken into the context of the patient’s underlying PAH. They will likely have an enlarged RV at baseline, so don’t jump straight to PE as the diagnosis if you see a large RV. Don’t jump straight to fluid overload either just because the RV is large and IVC isn’t collapsing. These patient’s may benefit from fluids still (mentioned above)
    • B-lines? Septal bowing? (see image below for septal bowing [3]) Either more likely to be seen with fluid overload (but far from perfect in these patients). Consider positive pressure ventilation and fluid restriction or at least very cautious use of fluids. Initiate norepineprhine and ionotropy as discussed above.
      Septal bowing
    • Decreased cardiac c contractility Initiate dobutamine / milronone. (have norepi started or on hand… either of these can precipitate hypotension)
    • Non-compressible femoral vein? If evidence of DVT, consider thrombolytics.
  7. Consider Nitric Oxide. Or any pulmonary artery vasodilator… but nitric oxide is easiest due to it’s short half-life and that it is easily titratable. If this isn’t available in your ED (it’s not here at Saint Marys ED… yet), consider getting Anesthesia involved early. The patient may benefit from being taken up to the OR to be put on Nitric where it is readily available.
  8. Consider ECMO. Last resort if the patient is not improving with other interventions. Certainly depends on the patient’s underlying cause of PAH and the etiology of their acute illness. Regardless, something to consider on a case by case basis.

  1. Moledina, S., et al. “Childhood idiopathic pulmonary arterial hypertension: a national cohort study.” Heart (2010): hrt–2009.  ↩
  2. Benza, Raymond L., et al. “An evaluation of long-term survival from time of diagnosis in pulmonary arterial hypertension from the REVEAL Registry.” CHEST Journal 142.2 (2012): 448–456.  ↩
  3. Rubenfire, Melvyn, Melike Bayram, and Zachary Hector-Word. “Pulmonary hypertension in the critical care setting: classification, pathophysiology, diagnosis, and management.” Critical care clinics 23.4 (2007): 801–834.  ↩

Oct 10, 2014 · When is CT + LP indicated in the patient with HIV / AIDS

HeadCTLPHIVAIDS

Quick tip for estimating CD4 count in ED

CD4 < 200 significantly raises risk for opportunistic infections.

  • Absolute lymphocyte count < 1000 correlates to CD4 count < 200.
    • Predictive value 91% [1]
  • Absolute lymphocyte count > 2000 correlates to CD4 count > 200.
    • Predictive value 95% [1]

Patient with CD4 <200 or ALC <1000

  • Even vague complaints including fever, headache, and/or malaise may have CNS infections. [2]
  • Obtain CT followed by LP.
    • CSF WBC counts and glucose may appear normal despite a concomitant CNS infection [3]
    • Initiate empiric treatment until cutlures and antigen testing returns.
    • Consider CT with and without contrast
      • Contrast shows ring-ehanching lesions of toxoplasmosis.

Patient with CD4 >200 or ALC >2000

  • Clinical decision rule developed in cohort of 110 HIV positive patients.
    • 100% sensitivity in ruling out new intracranial lesions [4]
      • New or different headache than usual?
      • Headache lasting more than three days?
      • Focal neurologic deficit?
      • Altered mental status?
      • New-onset seizure?
    • If none of these are present, it is considered safe to forego CT and LP.

Special considerations in differential for HIV pt w/ CNS symptoms

  • Includes fever, malaise, headache, focal weakness, etc.
    • Cryptococcal meningitis
    • Toxoplasma gondii
    • Progressive multifocal leukoencephalopathy
    • CNS lymphoma
    • Guillain-Barré

  1. Shapiro, Nathan I., et al. “Absolute lymphocyte count as a predictor of CD4 count.” Annals of emergency medicine 32.3 (1998): 323–328.  ↩
  2. Graham III, Cole Blease, et al. “Screening CT of the brain determined by CD4 count in HIV-positive patients presenting with headache.” American journal of neuroradiology 21.3 (2000): 451–454.  ↩
  3. Clark, Rebecca A., et al. “Spectrum of Cryptococcus neoformans Infection in 68 Patients Infected with Human Immunodificiency Virus.” Review of Infectious Diseases 12.5 (1990): 768–777.  ↩
  4. Rothman, Richard E., et al. “A Decision Guideline for Emergency Department Utilization of Noncontrast Head Computed Tomography in HIV‐infected Patients.” Academic emergency medicine 6.10 (1999): 1010–1019.  ↩

Oct 6, 2014 · Abdominal Pain vs. Chest Pain in the Elderly

Chest pain vs abdominal pain

2 patients present to the ED at the same time.

  • In room 1, there is an 80 year old male. T 37.0, HR 70, BP 120/80, RR 20, spO2 99%. The chief complaint is “abdominal pain”.
  • In room 2, another 80 year old male. T 37.0, HR 70, BP 120/80, RR 20, spO2 99%. The chief complaint is “chest pain”.

 

Which patient is more likely to be sick and have a an acute life threatening illness?

 

Which patient is more likely to be hospitalized?

  • Chest pain in the elderly (>75 years old): 77% are admitted (1)
  • Abdominal pain in the elderly (>60 years old): 60% are admitted (2)

Which patient has the greater likelihood of undergoing an operative or invasive procedure?

  • Abdominal pain in the elderly (>60 years old): 20% undergo operative or invasive procedures (2, 3)
  • Chest pain in the elderly (>75 years old): 20% undergo cardiac catheterization. (1)

Which patients has the greater likelihood of 14 day mortality?

  • Chest pain in the elderly (>75 years old): 2.7% 14 day mortality (1)
  • Abdominal pain in the elderly (>60 years old): 5% 14 day mortality (2, 3)

 

14 day mortality for elderly patients presenting with abdominal pain is 5%!

 

Elderly patient presenting with abdominal pain in the ED is 1.85 times as likely to die in the next 14 days compared to the elderly patient with chest pain. Yet the ESI level for a chest pain patient is generally 2, while the ESI level for abdominal pain is 3.

 

There is little you can do prior to imaging to predict the likelihood of an acute life threatening etiology as well.

  • Regarding vital signs:
    • Fever is often absent despite a serious bacterial infection or surgical condition (4)
    • Elderly patients often have suppressed tachycardia from medications or intrinsic cardiac disease (5)
  • With labs:
    • WBC often normal despite a surgical condition (4)
  • On physical exam, elderly patients have:
    • An altered pain perception from chronic pain medications; coexistent disease (5)
    • A four times higher likelihood of hypothermic response with a significant intra-abdominal process lower likelihood of localized tenderness despite a focal surgical condition (5)
    • Reduced rebound and guarding from decreased abdominal wall musculature (5)

 

 

Summary

Abdominal pain in the elderly is more likely to be life threatening compared to chest pain in the elderly. In addition, there’s no great way to be reassured based on vitals, laboratory findings, or physical exam alone. Given this, it is important to have a very low threshold to obtain CT imaging in the elderly patient presenting to the ED with abdominal pain and even if negative, have a low threshold to either have the patient admitted for observation or ensure close follow up and reassessment is available.

 

 

Update November 9

 

References:

  1. Han, Jin H., et al. “The elder patient with suspected acute coronary syndromes in the emergency department.” Academic Emergency Medicine 14.8 (2007): 732-739.
  2. Lewis, Lawrence M., et al. “Etiology and clinical course of abdominal pain in senior patients: a prospective, multicenter study.” The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 60.8 (2005): 1071-1076.
  3. Marco, Catherine A., et al. “Abdominal pain in geriatric emergency patients: variables associated with adverse outcomes.” Academic emergency medicine 5.12 (1998): 1163-1168.
  4. Potts FE 4th, Vukov LF. Utility of fever and leukocytosis in acute surgical abdomens in octogenarians and beyond. J Gerontol A Biol Sci Med Sci. 1999;54:M55–8
  5. Bryan ED, et. al. Abdominal Pain in Elderly Persons. (2013): eMedicine. Web. 4 Oct. 2014.

 

 

Oct 6, 2014 · Pediatric GI Foreign Body Management

Author: Dustin Leigh, M.D.

This is a lecture from Pediatric noon lecture series at the Mayo Clinic by Dr. Dustin Leigh, Emergency Medicine Attending Physician at the Mayo Clinic.

 

 

 

Oct 3, 2014 · Septic Arthritis: Myth Busting

Septic Arthritis

Note: “Septic arthritis” in this post and discussion refers to non-gonococcal septic arthritis.

What’s the big deal with septic arthritis? It’s not really an emergency is it?

  • Within days of onset, septic arthritis destroys cartilage and can leave the joint with permanent joint disability occurring in 25-50% of the cases.
  • The mortality rate for in-hospital septic arthritis ranges from 7% to 15%, despite antibiotic use.
 

Ok ok. So that’s pretty bad. How do I make sure I don’t miss a septic arthritis?

 
Unfortunately, there are no physical examination findings or maneuvers, such as range of motion or degree of swelling, that have been studied that can help the clinician discriminate between etiologies of the monoarthritis.

 

Basically in any patient presenting with a single painful joint, there is no way to rule out a septic arthritis without an arthrocentesis and synovial culture.

 

That said, even synovial culture is not a perfect test.

 

Granted, we don’t tap every painful joint, because we often have an alternative diagnosis that results in a very low pre-test probability for a septic joint, and other risk factors or lack-of risk factors lowers the probability of disease even more. However, just keep in mind that you can never exclude a septic joint in a painful joint completely by physical exam and history alone. It can only be truly excluded with an arthrocentesis.

 

Below are some risk factors/likelihood ratios to definitely raise your suspicion for septic arthritis (1). But remember, that just because they have zero risk factors, doesn’t mean that they won’t  have a septic joint. It can happen to anyone.

 

  • Age >80 (+LR 3.5)
  • Diabetes (+LR 2.7)
  • Rheumatoid arthritis (+LR 3.5)
  • Joint surgery within past 3 mo (+LR 6.9)
  • Hip/knee prosthesis (+LR 3.1)
  • Skin infection (+LR 2.8)
  • Skin infection + prosthesis (+LR 15)
 

List of common myths and dogma regarding septic arthritis:

 
“The patient doesn’t have a fever, so it’s not a septic joint”
  • Fever Sensitivity 46%. Specifificity 31% (1)
  • So you’d only miss 54% of septic joints relying on fever.

 

“If the serum WBC isn’t elevated, it’s not a septic joint.”

  • Sensitivity WBC >10,000 is 90% (1)
  • If you’re ok with missing 10% of septic joints.

 

“If the CRP and ESR aren’t elevated, it’s not a septic joint”

  • Sensitivity ESR >30 is 95% (1) – miss 5% of septic joints relying on a very low cutoff for ESR
  • Sensitivity CRP >100 is 77% (1) – miss 23% of septic joints relying on CRP

 

“If the synovial WBC <50,000 it’s not a septic joint” (My personal favorite)

  • Sensitivity WBC >50,000 is 62% (1)
  • So 38% of septic joints are missed relying on a synovial WBC >50,000

 

“If the neutrophile count is <90% it’s not a septic joint”

  • Sensitivity PMN >90% is 73% (1)
  • Missing 27% of septic joints

 

“If the gram stain is negative, it’s not a septic joint”

  • Sensitivity of gram stain 50-80% (2)
  • Missing 20-50% of septic joints.
  • You have to follow the culture for 48 hours.
  • Depending on their risk factors, your clinical suspicion, and synovial WBC, you may or may not start antibiotics until the cultures come back

 

“If there are crystals, it’s not a septic joint”

  • 5% of crystal monoarthritis have a concomitant septic arthritis (3)
  • Crystals have also been found in asymptomatic patients, so crystals definitely can’t exclude an infection

 

“Synovial fluid culture is the gold standard rule out test for septic arthritis. If the culture is negative, it’s not septic arthritis.”

  • Synovial fluid culture is the most important test we have to rule out septic arthritis, but it’s not perfect. There have been multiple reports of cases of septic arthritis where other diagnostic tests (such as imaging), clinical course, etc resulted in a definitive diagnosis of septic arthritis despite an initial negative culture from synovial fluid. (4, 5)
  • The incidence of culture-negative septic arthritis is certainly small, but incredibly difficult to give a number too since there is no true gold-standard test to compare a 48 hour synovial culture to. 
  • The take home message is that when septic arthritis is suspected, empiric antimicrobial therapy is warranted following arthrocentesis until culture data are available. Even if the gram stain and culture are negative, if the patient seems to be responding to empiric therapy, continuing a full treatment course of antibiotics may be necessary given the lack of any true gold standard diagnostic test.

 

 

How do I perform an arthrocentesis?

  1. Sterile prep
  2. Consider using ultrasound. (I’m a big fan of ultrasound as an adjunct to look for the effusion… especially for small joints like wrists and ankles.)
  3. Lidocaine injection
  4. 18 or 20 gauge needle to aspirate fluid
  5. Location of needle entry for ankle, elbow, knee, shoulder via very photo from @ClinicalEMed below:

 

 

https://twitter.com/ClinicalEMed/status/456453031899693057

 

 

References:

  1. Margaretten, Mary E., et al. “Does this adult patient have septic arthritis?.” Jama 297.13 (2007): 1478-1488.
  2. Genes, N., and M. Chisolm-Straker. “Monoarticular arthritis update: Current evidence for diagnosis and treatment in the emergency department.” Emergency medicine practice 14.5 (2012): 1-19.
  3. Papanicolas, Lito Electra, Paul Hakendorf, and David Llewellyn Gordon. “Concomitant septic arthritis in crystal monoarthritis.” The Journal of rheumatology 39.1 (2012): 157-160.
  4. Ryan, M. J., et al. “Bacterial joint infections in England and Wales: analysis of bacterial isolates over a four year period.” Rheumatology 36.3 (1997): 370-373.
  5. Sharff, Katie A., Eric P. Richards, and John M. Townes. “Clinical management of septic arthritis.” Current rheumatology reports 15.6 (2013): 1-9.

 

 

Editor’s note.

A piece of comic relief.

It is always gout by @zdoggmd

 

Sep 30, 2014 · Don’t Forget TXA in the Trauma Bay

Author: Michael  A. Schwarz, Pharm.D., R.Ph.

tran_man

 

Tranexamic Acid (TXA)

  • Tranexamic Acid (TXA) is a competitive inhibitor of plasminogen activation to plasmin and a noncompetitive inhibitor of plasmin, which produces antifibrinolytic effects and stabilizes clot structure.
  • Mayo Clinic TXA protocol for Trauma : TXA is indicated for any acutely injured adult presenting within 3 hours of trauma who is meeting criteria for mass transfusion (2 of the following: Single SBP ≤ 90 mmHg, Single HR ≥ 120 bpm, Lactate ≥ 5 mmol/L, INR ≥ 1.5)
    • Tranexamic Acid (TXA) 1 gram IV Loading Dose over 10 minutes, immediately followed by an infusion of 1 gram over 8 hours.
    • TXA Exclusion Criteria:
      • < 18 years old
      • > 3 hours from injury
      • Current Anticoagulation (warfarin, heparin, LMWH, dabigatran, rivaroxaban, apixaban, etc.)
      • Known Thromboembolic Disease History (DVT, PE, ACS)
      • Evidence of clotting (DVT, PE, embolic stroke)
      • History of retinal vein or artery occlusion
      • Administration of PCCs, Factor VIIa

 

Studies Supporting Mayo TXA Protocol in Trauma:

  • CRASH-2 (Lancet 2010): Prospective, randomized control trial with 20,211 patients in 40 different countries. Patients presenting within 8 hours of injury who were determined by their provider to be at significant risk of bleeding were randomized to receive TXA (n= 10,096) or placebo (n= 10,115). TXA dosing 1 gram over 10 minutes, then 1 gram over 8 hours infusion
    • RESULTS:
      • TXA significantly reduced all-cause mortality from 16% to 14.5% (RR 0.91, 95% CI 0.85-0.97; p = 0.0035)
      • TXA significantly reduced death due to bleeding from 5.7% to 4.9% (RR 0.85, CI 0.76-0.96; p = 0.0077)
    • CONCLUSION:
      • TXA shows reduces all-cause mortality in trauma patients at significant risk of bleeding
  • CRASH-2: Timing of TXA Dosing (Lancet 2011): Retrospective analysis of CRASH-2 trial to determine if early timing of TXA from injury improves outcomes
    • RESULTS:
      • TXA ≤ 1 hour from injury reduced risk of death due to bleeding from 7.7% to 5.3%
      • TXA between 1-3 hours from injury reduced risk of death due to bleeding from 6.1% to 4.8%
      • TXA > 3 hours from injury increased risk of death due to bleeding 3.1% to 4.4%
    • CONCLUSION:
      • TXA is beneficial at reducing all-cause mortality in patients with significant risk of bleeding if given within the first 3 hours of a traumatic injury
  • MATTERs (JAMA – 2012): Retrospective observational study of military combat injuries in Afghanistan presenting to a surgical center at Camp Bastion. Included were injuries requiring ≥1 unit PRBC and a subset group that received ≥ 10 units PRBC. 896 combat injuries qualified and 293 received TXA (1 gram IV bolus, with discretional repeat)
    • RESULTS:
      • Main Group (≥ 1 PRBC) Mortality: non-TXA 23.9% vs TXA 17.4% (P=0.03)
      • Subset Group (≥ 10 PRBC) Mortality: non-TXA 28.1% vs TXA 14.4% (P <.003)
    •  CONCLUSION:
      • The largest benefit with TXA was seen in the most severe combat injuries which required massive transfusion

 

 References:

  • Effects of Tranexamic Acid on Death, Vascular Occlusive Events, and Blood Transfusion in Trauma Patients with Significant Haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet 2010; 376:23-32
  • The Importance of Early Treatment with Tranexamic Acid in Bleeding Trauma Patients: an exploratory analysis of the CRASH-2 Randomised Controlled Trial Lancet 2011; 377:1096-101
  • Morrison J et al. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation Study. JAMA 2012; 113-119
  • http://mayoweb.mayo.edu/traumacenter/documents/TranexamicAcidUse.pdf
  • Photo from: http://www.lshtm.ac.uk/newsevents/news/2011/tran_man.html

 

 

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