Often, the dreaded complications that we are taught to look for don’t present to us in the Emergency Department, but develop and evolve during the hospitalization that began with the patient seeing us in the ED. Our skill can help the child in distress, but our vigilance can detect the evolving Acute Chest Syndrome and perhaps even prevent it.
Thanks to Sean M. Fox, MD (@PedEMMorsels) for this gem with significant clinical relevance.
Acute Chest Syndrome Read More »
Questions addressed by EM Lyceum and bulleted by emDocs:
1. When do you use tranexamic acid in trauma?
2. When you can’t get peripheral access in a trauma patient, do you prefer subclavian, femoral, or IO?
3. Which trauma patients do you give PCC to over FFP?
4. In blunt abdominal/flank trauma, do you send a urinalysis or simply look for gross hematuria?
Lyceum Bullets: Trauma Read More »
A discussion of can’t miss life threatening complications in the postpartum period
HELLP!!! Pregnancy Complications in the Postpartum Period Read More »
Stress testing: a beginner’s guide Author: Jason Brown, Capt, USAF, MD (EM Resident Physician, University of Maryland) // Editor: Alex Koyfman, MD Stress tests are aptly named in that the goal is to cause a physiologic stress and to, through a variety of modalities, detect that stress’ impact on the myocardium. There are three major modes of stressing the patient: Exercise – either treadmill or supine bike Vasodilation – adenosine, dipyridamole, regadenoson Inotropy – dobutamine There are five different ways to detect stress on the myocardium: EKG *all modalities employ Echocardiography Radionuclide imaging – Thallium201, Technetium99M PET MRI Treadmill stress testing is the most common form of stress test that you will see as a direct extension of the ED. It employs the Bruce protocol (starting at 1.7mph and 10% grade with increases in both every 3 minutes to a maximum heart rate of 85% (220-age)) while the patient wears an EKG. Tests are positive if the patient has early chest pain, hyper-/hypotension, ST changes, or arrhythmia. Supine bike exercise testing allows for real-time echocardiography. This provides an excellent option for patients with valvular disease and are functional but cannot use a treadmill. The vasodilatory stress tests use agents which increase coronary blood blow. They work on the principle that diseased arteries are already maximally dilated and that there will be no further perfusion of their vascular territories when under stress. A variety of detectors can be used to detect the difference between rest and stress phases. Vasodilation is contraindicated in patients with hypotension, high AV block, or bronchospasm No caffeine (12 hours), Cialis (72 hours), nitrates (48 hours), or calcium channel blockers (48 hours) prior to the test Dobutamine stress tests use the positive inotropic effects of dobutamine to increase the heart rate and elicit perfusion deficits in lieu of actual exercise. There are a variety of protocols but the main goal is to achieve 85% of maximal heart rate (220-age) and to use a detector to examine the myocardium. Contraindicated in patients with arrhythmias, significant hypertension, or LV outflow obstruction. Must hold beta-blockers and calcium channel blockers 24 hours prior. Detection of myocardial perfusion deficits The EKG is the most common modality for detection of ischemic changes. Consistent horizontal or down-sloping ST depressions in contiguous leads is considered positive. In patients that have known CAD or prior revascularization, an abnormal EKG, or a need for functional examination of the heart structures (valvular function, LVEF, etc) then imaging should be considered. There are four major imaging modalities: SPECT, ECHO, PET, MRI. Dobutamine is used in conjunction with echocardiography to evaluate function under stress. New wall motion abnormalities are considered positive for flow-limiting disease. Drawbacks include: technologist-dependent images and difficult interpretation in patients with baseline wall motion abnormalities and/or the obese. All three of the above vasodilators can be used with SPECT, PET, and MRI; deemed myocardial perfusion imaging. All three of these imaging modalities attempt to detect perfusion deficits between rest and stress states. These tests are generally used in patients which need investigations which are beyond the scope of the emergency department. Recommendations: Personally, when I am evaluating a patient in our clinical decision unit (CDU, observation unit) I use either: An EKG treadmill stress for low-intermediate risk ACS patients with normal initial and serial EKGs who can exercise. A supine bike ECHO for any patient that is low-intermediate risk who has an abnormal but nonischemic EKG who can exercise. A dobutamine stress ECHO for any patient with an abnormal EKG who cannot exercise. Any patient with CHF, known CAD, previous PCI/CABG, BBB, or congenital cardiac issue should be evaluated by a staff cardiologist. REFERENCES -Anderson KM, Murphy DL, Balaji M. Essentials of noninvasive cardiac stress testing. J Am Assoc Nurse Pract. 2014;26(2):59-69. -Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update for exercise testing: summary article. J Am Coll Cardiol 2002; 40:1531. -Hendel RC, Berman DS, Di Carli MF, et al. ACCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging. J Am Coll Cardiol 2009; 53:2201. -ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography. J Am Soc Echocardiogr 2011; 24:229. -Douglas PS , Khandheria B, Stainback R. et al. ACCF / ASE / ACEP / AHA / ASNC / SCAI / SCCT / SCMR 2008 Appropriateness Criteria for Stress echocardiography. Circulation. 2008;117:1478‐1497 -Fraker TD Jr, Fihn SD, et al. Chronic Stable Angina Writing Committee: focused update of the ACC/AHA 2002 guidelines for the management of patients with chronic stable angina: J Am Coll Cardiol. 2007;50(23):2264. – https://www.ncbi.nlm.nih.gov/pubmed/24730402 – https://www.ncbi.nlm.nih.gov/pubmed/24211281 – https://www.ncbi.nlm.nih.gov/pubmed/23517258 – https://www.ncbi.nlm.nih.gov/pubmed/21908137
Stress testing: a beginner’s guide Read More »
Scenario: You receive a call from EMS stating they are on the way to your emergency department with a 60 year-old male in acute respiratory distress. VS: HR 105, RR 30, BP 126/68, SpO2 83%. No further information is provided.
The patient arrives, awake, alert and oriented in visible respiratory distress and to your surprise has a tracheostomy in place! How does this change your management? […]
Management of Acute Respiratory Distress in a Tracheostomy Patient Read More »
Author: Jennifer Robertson, MD (EM Attending Physician, Cleveland Clinic) // Edited by: Alex Koyfman, MD (@EMHighAK) Featured on #FOAMED REVIEW 30TH EDITION – Thank you to Michael Macias from emCurious for the shout out! Introduction Cavernous sinus thrombosis (CST) is a rare condition, defined as a septic thrombophlebitis of the cavernous sinus. It is caused by a bacterial infection that typically originates in the face, sinuses, ears, or orbits (1). Prior to the discovery of antibiotics, mortality was nearly 100% (2). It still causes significant morbidity and mortality today, even with treatment (3,4,5). Due to the rarity of CST, data is limited as randomized control trials will likely never be conducted (4). Thus, some proposed treatments, such as anticoagulation and steroids, remain controversial (1,4,6). Antimicrobial therapy, however, is paramount and due to the potentially severe complications from CST, physicians should have a low threshold for initiating antibiotics as early as possible (1,7). Pathophysiology The two cavernous sinuses are located on both sides of the sella turcica. Important structures are located in, or run through, the cavernous sinus, including the pituitary gland, cranial nerves III, IV, V and VI, and the internal carotid arteries (ICA) (6,8). The cavernous sinuses receive blood from the superior ophthalmic and cerebral veins, the sphenoparietal sinuses, and emissary veins. The cavernous sinuses also communicate with the deep facial and inferior ophthalmic veins. Many of these veins have no valves and blood can flow in either direction, depending on pressure gradients. It is hypothesized that this is the reason why infection spreads and thromboses form (2,6). In addition, the thrombus itself is a good growth medium for bacteria and the bacteria, in turn, stimulate thrombosis by releasing substances that cause tissue damage (1,9). Risk Factors Sphenoid and ethmoid sinusitis are the most common causes of CST (3,4,5,6). Other risk factors include dental infections, facial cutaneous infections, otitis media, maxillofacial surgery, and trauma (1,3,4, 5,6,10). Even bacterial seeding from a distant site of infection has been a reported cause of CST (11). Staphylococcus aureus is the primary organism that causes CST, but many other bacteria can be involved (4,10). Presentation CST can present acutely or sub-acutely. Most patients will have fever, headache, proptosis, periorbital edema and/or chemosis. Most will also have external ophthalmoplegia, due to venous congestion of orbital tissues, extra-ocular muscle inflammation and/or inflammation of cranial nerves III, IV and VI (1,5,6,12). Other symptoms include eyelid erythema, autonomic dysfunction, sensory changes in the ophthalmic and maxillary trigeminal nerve distributions, pupillary abnormalities, and papilledema (1, 3, 4, 6). Vision loss is rare as the orbital nerve lies outside the cavernous sinus but it can occur via other mechanisms such as occlusion of the ICA, ophthalmic or central retinal arteries, orbital congestion, or arteritis (1,13). CST commonly spreads from one eye to both within 24 to 48 hours (4,6). Differential Physicians should keep a wide differential, especially in patients with pain with extra-ocular movements and ophthalmoplegia. Differential diagnoses include orbital cellulitis, orbital apex syndrome, ICA aneurysm, malignancy of the CS, trauma, carotid-cavernous fistula (CCF), Tolosa-Hunt Syndrome, and ischemic stroke (6,14) Workup If CST is suspected, imaging should be ordered. Either computed tomography (CT) or magnetic resonance imaging (MRI) may be obtained, but CT tends to be the initial test of choice, as it is better than MRI in detecting thrombus directly in the cavernous sinus (1, 15,16). MRI, however, is better at detecting dural venous sinus thromboses (1,16). On CT, various direct and indirect findings of CST may be found. Direct signs include enlargement of the cavernous sinuses, convex bowing of the lateral wall of the cavernous sinus and/or abnormal filling defects. Indirect signs include dilation of the superior ophthalmic vein, exophthalmos, and/or increased dural enhancement along the lateral wall of the sinus (1,6,15,16). Treatment Antibiotics are primary in the treatment of CST (1,3,7). Empiric therapy should consist of a third generation cephalosporin, nafcillin, and metronidazole. Vancomycin can be substituted for nafcillin if methicillin-resistant Staphylococcus aureus (MRSA) is a concern (4,6). Along with antibiotics, surgery may be necessary; it is rarely needed for drainage of the primary infection (1,4,5,6,17). The use of anticoagulation and corticosteroids remains controversial (1,4). Some studies have found improved cranial nerve function with steroid use, but there is currently no data to support its routine use (1,4,6). Regarding anticoagulation, data is also limited given the rarity of CST and the lack of prospective trials (1,6). It is theorized that anticoagulation may prevent the spread of the thrombus to other sinuses (1,5) as well as help dissolve the clot, allowing the antibiotic to reach the infected thrombus more readily (13,17). On the other hand, there is a risk of systemic and intracranial bleeding and some authors state it may result in dissemination of septic emboli (4,5,13). Most authors recommend considering anticoagulation only if there is no evidence of severe bleeding risk or current hemorrhage by history, exam, and imaging (1,4,5). It is always best to consult with specialists regarding treatment regimens. Complications Even with appropriate treatment, the complications of CST can be devastating and mortality still remains high at 20-30% (6,7). In addition, nearly half of patients have residual sequelae including cranial nerve lesions, weakness of extraocular muscles, impaired vision, hemiparesis, or hypopituitarism (5,6,13,18). Because of the high mortality and devastating consequences of CST, physicians need to keep a high level of suspicion for the condition, image liberally, and administer antibiotics as soon as possible. References/Further Reading: 1 Bhatia K, Jones NS. Septic cavernous sinus thrombosis: are anticoagulants indicated? A review of the literature. J Laryngol Otol 2002; 116: 667-76. 2 Singh Y, Singh M, Saxena S R, et al. Pansinusitis, cavernous sinus thrombosis and cerebral infarction. J Med Investig Pract 2014;9:95-7 3 Pavolvich P, Looi A. Septic thrombosis of the cavernous sinus: two different mechanisms. Orbit 2006; 25: 39-43. Orbit, 25:39–43, 2006 4 Desa V, Green R. Cavernous sinus thrombosis: current therapy. J Oral Maxillofac Surg 2012; 70: 2085-2091. 5 Southwick FS, Richardson EP, Swartz MN. Septic thrombosis of the dural sinuses. Medicine 1986; 66
Cavernous Sinus Thrombosis Read More »
Our ongoing intern report series is the product of first-year EM residents at UT Southwestern exploring clinical questions they have found to be particularly intriguing. For med students & junior residents – if you haven’t encountered these issues yet, you will!
Intern Report Collection Read More »
What to consider and keep in mind when confronted with the all-too-common violent patient in the ED…
Ketamine for the Agitated/Violent Patient Read More »
Featured on #FOAMED REVIEW 28TH EDITION – Thank you to Michael Macias from emCurious for the shout out! Author: Joe Rogers, MD (Senior EM Resident, Rutgers-NJMS) // Editor: Alex Koyfman, MD & Justin Bright, MD The following is a compilation of helpful tips for managing the airway in the emergency department. **EAR TO STERNAL NOTCH POSITIONING** Why do it? -Position yourself (and your patient) for success! -Universal position for both ventilation and intubation – Facilitates maximal jaw distraction and mouth opening – Independent of age and size, though especially helpful in obese patients Of note: – Contraindicated in context of known or suspected cervical spine pathology Technique: – Horizontally align the sternal notch with the external auditory meatus – The facial plane should be parallel to the ceiling; hyperextending the neck may worsen your view – In adults, the head usually needs to be raised; in infants, the torso may need to be raised **NASAL OXYGEN** Why do it? – Administration of high-flow nasal oxygen during pre-oxygenation and after RSI improves arterial oxygenation during apnea – High-flow nasal oxygen saturates the nasopharynx with oxygen, patients inhale a higher percentage of oxygen, and the oxygen reservoir in the lungs increases prior to apnea – Oxygen saturation can be maintained without respirations if a continuous path of oxygen is supplied from the pharynx to the glottis because alveolar oxygen absorption continues during paralysis (“apneic oxygenation”) – “NO DESAT”: Nasal Oxygen During Efforts Securing A Tube Technique: – During pre-oxygenation apply high-flow nasal oxygen at 15 lpm as well as a face mask at 15 lpm – 3 minutes is an acceptable duration of pre-oxygenation – Leave on high-flow nasal cannula during intubation attempts **BIMANUAL LARYNGOSCOPY** Why do it? -External laryngeal manipulation by the laryngoscopist is the easiest, fastest, and most effective modification to improve view Of note: This is not B.U.R.P or cricoid pressure (both of which are done by an assistant, neither of which are helpful) Technique: – Manipulation is most effective at the thyroid cartilage, where vocal cords attach anteriorly – Once the view is optimized, an assistant can maintain pressure at the right location, freeing the right hand to place the tube **HEAD ELEVATION** Why do it? – Improves visualization by enlarging space beneath tongue and epiglottis – Less force required for full laryngeal exposure – After bimanual laryngoscopy, head elevation is the second easily performed manipulation to improve laryngeal view Of note: – Like ear to sternal notch positioning, head elevation is contraindicated in context of known or suspected cervical spine pathology Technique: – Performed while holding the laryngoscope with the left hand – Lift the patient’s head at the occiput with the right hand, keeping the face parallel to the ceiling – When ideal view is achieved, release the right hand – If possible, briefly suspend the head with the laryngoscope and attempt intubation – If the head is too heavy, have an assistant support the patient’s head and shoulders **STRAIGHT-TO-CUFF STYLET SHAPE** Why do it? – Narrower long-axis dimension allows greater visibility – Better maneuverability within the hypopharynx Technique: – Ideal shape of styletted tracheal tube is straight to the proximal cuff, then ≤ 35 degree angle bend at the proximal cuff (> 35 degrees increases likelihood of mechanical impaction) – Use far right corner of mouth to insert and pivot tube – Tube stays below the line of sight until tracheal insertion – Keep tip visible as it approaches target – If tube catches on tracheal rings after insertion, rotate clockwise and advance tube **EPIGLOTTOSCOPY** Why do it? – The epiglottis is the first reliable anterior landmark at the top of the laryngeal inlet Technique: – Prepare suction to maximize anatomical clarity – Slide blade gently and slowly down tongue – Once the epiglottis is in view, move the tongue to the left and lift epiglottis edge off the posterior pharynx – If the epiglottis is not seen, blade may be too deep: slowly pull back until epiglottis drops into view – Advance blade fully into the vallecula – Create anterior pressure at the hyoepiglottic ligament, causing the ligament to pull the epiglottis forward to expose the glottis – Optimize glottic view with bimanual laryngoscopy and/or head elevation **PREDICTORS OF DIFFICULT AIRWAY IN ED** Most Helpful – Thyroid-to-hyoid less than two fingers Somewhat Helpful – Hyoid-to-mental less than three fingers – Airway obstruction – Poor neck mobility, cervical collars, spinal immobilization – Trauma, facial distortion, secretions, mandibular injury – Obesity – Large tongue, large teeth – Grade 4 Cormack and Lehane score – Correlates to hyoid-mental distance, thyroid-hyoid distance Not Helpful – Mallampati classification not practical in ED setting Bottom line: – Beware the short fat neck – Mallampati not helpful – “LEON” – Look externally – Evaluate 3-3-2 – Obstruction – Neck mobility **PEDIATRIC AIRWAY ANATOMY** The unique features of the pediatric airway persist until about age 8 or 9 years, then become more adult-like: Occiput – The head and occiput in children are proportionally larger than in adults – In supine position may cause neck flexion and airway obstruction – To achieve ear to sternal notch positioning, a blanket may be placed under the shoulders and torso Tongue – Child’s tongue is relatively larger – Lower muscle tone increases risk of passive airway obstruction; MCC airway obstruction in children – Can be managed by better positioning or use of an adjunct device such as oropharyngeal airway or nasopharyngeal airway Larynx – Larynx is more anterior and cephalad in children, C4 vs. C6 in adults – Vocal cords slant anteriorly – Bimanual laryngoscopy more likely necessary to visualize the cords; alternatively, the fifth finger of the left hand can be used to improve glottic visualization – Also may be helpful to lower oneself to below the level of the patient and look up at an angle when intubating Epiglottis – The pediatric epiglottis is floppy, long, and narrow – A straight blade (Miller) can more easily pick up the epiglottis to facilitate intubation in
Novel Tips for Airway Management Read More »
Treat the patient, not the number. A blood pressure of 120/80 mmHg in a chronically hypertensive patient can be dangerously low. Whatever the HPI may suggest, unbiased implementation of the bedside physical examination and sonography are crucial in the workup of unexplained hypotension. This four step systematic approach of sequentially assessing heart rate, volume status, cardiac performance, and systemic vascular resistance can narrow the differential and guide management.
The Hypotensive ED Patient: A Sequential Systematic Approach Read More »
