practice updates

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? […]

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

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!

What to consider and keep in mind when confronted with the all-too-common violent patient in the ED…

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

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.

Ectopic pregnancy is a common and potentially fatal emergency in early pregnancy. Its prevalence is about 2% in the general population, but is as high as 16% in women presenting to the emergency department with concerning symptoms. Ectopic pregnancy is a cause of pregnancy-related death and can also lead to chronic pelvic pain, need for blood transfusions, and long-term infertility. Because of the potentially devastating outcomes, it is imperative that emergency physicians diagnose ectopic pregnancy early and refer patients to the proper specialist care. […]

It’s 4pm on a Wednesday. As per usual, the chart rack is full, and you’re trying to stay positive and keep up morale of the entire team. You pick up your next chart, and as you read the chief complaint, your heart sinks into your belly. The complaint is, “severe headache,” and you’re already trying to figure out how you’re going to fit an LP into your busy patient load.

Headaches are experienced in all types of ways by our patients. Many are benign – but we are in the catastrophe business. How do we know if the headache is actually a brain mass? Or what if it’s a raging intracranial hemorrhage? And if it is a brain bleed, what kind will it be? If we have a suspicion of subarachnoid hemorrhage (SAH), did our mouse click for “head CT (non-contrast)” just commit us and our patient to a lumbar puncture? […]

The transplant patient is always sicker than they appear. It is important to be aggressive in these patients since they are severely immunocompromised which not only puts them at greater risk of infection but also blunts their normal signs to infection. Always contact the transplant team to help with management as many centers have specific protocols for treatment of rejection and infection. Often it is very difficult to differentiate between rejection and infection. In these cases, treat on the side of infection as it would be the greatest immediate threat to life in the patient. […]