Category Archives: ultrasound

FOAMed Resource Series Part II: Ultrasound

Author: Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hosptial)

This is Part II of the FOAMed Resource Series. Part I evaluated the FOAMed world of the ECG, which can be found here: Today’s post will evaluate Ultrasound (US) resources. As EM has grown, so has US. This tool is now often considered an extension of the physical exam, providing key clinical data at the bedside. A great deal of resident curriculum is geared towards US use in the ED.

The following resources were chosen based on useful education pearls, validity of content, impact on clinical practice, and clear citation of references and authors. Similar to Part I in this series, this list is not all encompassing, but serves as an overview of several top education US resources. If you have found other great resources, please mention them in the comments below!


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The Ultrasound Podcast by Dr. Matt Dawson, Dr. Mike Mallin, and Dr. Mike Stone originally sought to fill a void, as at the time of this podcast introduction few US resources were available. Today, this resource has given the EM community so much more. From amazing, free podcasts with videos to a great app, this resource provides top-of-the-line ultrasound education. Also look for the free books “Intro to Bedside Ultrasound: Volume 1 and 2” at or iBooks, as well as the app One Minute Ultrasound for iPhone and Android.


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This US guide was originally published online by Dr. Beatrice Hoffmann and the ACEP Emergency US section. It serves as a comprehensive reference with still images and videos that educates those of all training levels. The explanations are second-to-none, with a variety of topics including primary EM scanning topics (FAST, aorta, cardiac, gall bladder, renal, DVT), critical care, small parts (ENT, testicular, ocular), and procedures (vascular access, pericardiocentesis, US guided nerve blocks, and many others). The videos have complete explanations, and the still images possess a roll-over function that explains specific anatomical areas of interest.


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LIFTL makes the FOAMed list again, providing a full database page with posts, critical care based ultrasound posts, clinical cases with US, and a library with over 40 videos demonstrating key US findings. This is a great reference to use while on shift or if the provider has a specific question in mind.


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Ultrasound Village is an online site containing several great features including US modules, lectures, worksheets, quizzes, and references. It also has an image library categorized by system with normal anatomy and pathology. The site provides high-quality education, produced by physicians passionate about education and medical ultrasound.


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This resource from Dr. Jacob Avila and Dr. Ben Smith provides a basic how-to video for specific US exams, though videos do not delve into subtle findings or much of the research behind the exam. A link on each video page demonstrates abnormal and normal findings. This resource also provides US reference values for many specific US exams. The creators do have a linked blog to the site ( that evaluates updates in scanning technique and new US exams, as well as the literature behind scans.


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ICU Sonography is a resource brought to you by Dr. Kishore Pichamuthu and Dr. George John, based on US use for the medical ICU. This resource contains tutorials with tremendous explanations and anatomical images, with videos. The echocardiogram and volume assessment sections are particularly thorough.


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This resource comes from the Sinai EM US division. It provides information for medical students, residents, fellows, and attendings on point-of-care US. The site has great tutorials on separate scans that are constantly being updated. One of the best features is a breakdown of the current machines on the market and how to actually use them in the ED.


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SonoSpot is truly one of the most comprehensive sites on this list. This resource contains tutorials on standard US examinations, as well as US of the appendix, airway, procedural, pelvic, and pleural examinations. Cases are provided based on anatomy and chief complaint. Best of all, each post contains links to primary literature, making this resource important for academic centers and those with desire for the evidence behind scanning.


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SonoWorld is a complete resource for learners of all levels. It contains full lectures, cases, tutorials, literature, and CME. If wanting to use this site in its full glory, registration is needed (which is free). The blog portion is updated daily with articles from around the world for US enthusiasts.


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This site from South Carolina is a great resource geared for all learners, but targeting residents, PA’s, nurses, and attending physicians. It provides full lectures, US cases, US still images, and videos on scanning. It contains an entire section of US literature, as well as pediatric centered scanning. If you’re interested in testing your knowledge, you can take three separate tests.


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Last, but not least, this blog by Dr. Ben Smith and Dr. Jacob Avila (yes, the same creators of provides posts with the mission “learn bedside ultrasound, one week at a time,” with weekly posts based on cases. Each post contains a patient case with high-quality US images, followed by an explanation and case resolution based on the most recent literature.

Thanks for reading, and comment below on other great resources. Stay tuned for our next post on Pediatric EM FOAMed!

A Case of Non-bacterial Thromboembolic Endocarditis

Authors: Captain William Dirkes (EM Resident Physician, Madigan Army Medical Center), Captain Joshua Kessler (EM Resident Physician, Madigan Army Medical Center), Lieutenant Colonel Jay Baker (EM Attending Physician, Madigan Army Medical Center), and Colonel Ian Wedmore (EM Attending Physician, Madigan Army Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021)


A 59 year-old male presented to the emergency department with a chief complaint of difficulty concentrating and loss of vision. He had presented to the same facility the day prior for chest pain, chills, and a cough. During his prior visit, the patient underwent a chest x-ray which demonstrated a consolidation suggestive of a lobar pneumonia and was subsequently discharged home with a prescription for Azithromycin as well as instructions to follow-up with his primary care doctor. However, he was unable to fill his prescription. Upon attempting to drive home, the patient was pulled over by law enforcement because he was acting “delirious.” Despite the traffic incident, he was allowed to return home. The patient reported that once he arrived at home he began bumping into furniture, experiencing difficulty with concentration, and suffered vision loss. In addition, he continued to experience chills, chest pain, and shortness of breath. He denied experiencing any abdominal pain, dysuria, focal numbness or weakness, headache, hematuria, hematochezia or melena, speech disturbances, or a rash. His medical history included diabetes, hypertension, hyperlipidemia, and an unprovoked DVT (deep venous thrombosis) approximately 5 months prior. He denied any surgical history. His medications included Atorvastatin, Lantus, Metformin, Rivaroxaban, Sitagliptin, and Telmisartan. He reported smoking a ½ pack of cigarettes per day for the last 15 years, consuming alcohol occasionally, and denied any current or prior illicit drug use.

His initial vital signs in the emergency department were a blood pressure of 150/95, a heart rate of 106, a respiratory rate of 24, an oxygen saturation of 95% on room air, and a temperature of 97.8F, taken temporally. His physical exam demonstrated a male appearing his stated age, in no apparent distress but with mild tachypnea, diminished breaths sounds in the left posterior lung fields, and no cardiac murmurs on auscultation. His neurologic examination demonstrated that he was alert and oriented, but had intermittent periods of confusion and difficulty with recall during the interview. His speech was normal and his cranial nerves were grossly intact. He had a right hemianopsia on visual confrontation. He had full strength in all of his extremities and normal sensation to light touch. No dysmetria on finger-nose testing and heel-shin was normal.

He underwent a non-contrasted computed tomography (CT) scan of his head which demonstrated multifocal cortical abnormalities concerning for embolic infarcts with a dense left middle cerebral artery sign indicative of an evolving territorial infarct. A portable chest x-ray demonstrated a moderate left lung pleural effusion and prompted further imaging to characterize the lesion. A CT pulmonary arteriogram demonstrated a segmental pulmonary embolism of the right lower lung lobe with an enhancing mediastinal mass concerning for malignancy in addition to the already visualized left-sided pleural effusion. Abnormal laboratory findings included a white blood cell count of 10.4 and a platelet count of 58. The remainder of the CBC was unremarkable and his lactate, liver function tests, coagulation panel, troponin, and urinalysis were within normal limits. His electrocardiogram demonstrated a normal sinus rhythm with a rate of 85 beats/minute.

CT chest
segmental pulmonary embolism of the right lower lung lobe with an enhancing mediastinal mass concerning for malignancy in addition to the already visualized left-sided pleural effusion
ct head
multifocal cortical abnormalities concerning for embolic infarcts with a dense left middle cerebral artery sign indicative of an evolving territorial infarct.

He was admitted to the inpatient medicine service which included a neurology consultation. An inpatient MRI of his brain was obtained which demonstrated an acute ischemic infarct in the left parieto-occipital lobes. These findings were consistent with multiple chronic infarcts versus vasogenic edema possibly representing metastatic disease. A trans-esophageal echocardiogram demonstrated tricuspid vegetations. He was subsequently diagnosed with Non-Bacterial Thromboembolic Endocarditis (NBTE) and discharged home on the following day.

Non-Bacterial Thromboembolic Endocarditis (NBTE)

NBTE is also known as Libman-Sacks Endocarditis or formerly, as Marantic Endocarditis. It is a rare condition, often diagnosed on autopsy, most often found between the fourth and eighth decades of life. [1, 2, 4] NBTE is the result of platelet and/or fibrin aggregation on a heart valve secondary to an underlying hypercoagulable state. Usually, the hypercoagulable state is induced by a metastatic process or rheumatologic condition such as Systemic Lupus Erythematosus (SLE), Anti-Phospholipid Syndrome, or Rheumatoid Arthritis. [1-3] These disorders are known to have a higher prevalence in female patient populations (approximately 5-9 times their male counterparts), more specifically in African American and Hispanic ethnicities. As such, the clinician should maintain a higher degree of suspicion when treating these patient populations. Unlike bacterial vegetations, the vegetations of NBTE are symmetric with a smooth or verrucoid texture and contain little evidence of polymorphonuclear leukocytes, microorganisms, or inflammation. The disease affects the heart valves with the following predilection: aortic valve > mitral valve > tricuspid valve > pulmonary valve. Clinically, the disease presents with embolic events including stroke, delirium, pulmonary embolism, renal/splenic infarction, acute myocardial infarction, digital ischemia, and/or rash. Because of the non-invasive nature of NBTE, clinical examination may or may not reveal a new cardiac murmur. An embolic stroke may be the initial presentation to suggest a diagnosis of NBTE and if the clinician is suspicious, an Echocardiogram should be obtained to assess for valvular lesions. Emergency Department management should include evaluation for Disseminated Intravascular Coagulation (obtaining coagulation panel, d-dimer, fibrinogen), as this complication has been found in 18% of cases of NBTE.


Treatment of NBTE consists of anti-coagulation and therapy directed at the underlying metastatic process or rhematoogical condition. Unfractionated heparin should be the anti-coagulant employed as warfarin is less effective and has been associated with increased rates of thromboembolic events. Novel anticoagulants, such as Dabigatran, Apixaban and Rivaroxaban, should also be avoided as they have not been evaluated for use in this disease process. Surgical intervention may be considered in select cases where the risk-benefit ratio is favorable. Anticoagulation should be continued indefinitely, since recurrent thromboembolism has occurred in patients following its discontinuation. [5] The indications for surgical intervention in NBTE are similar to those in infective endocarditis, namely heart failure, valve rupture, and most commonly recurrent embolization despite anticoagulation. Follow-up should be considered on an individual basis. However, patients should be monitored for known complications of NBTE, specifically infective endocarditis and emobilzation despite anticoagulation. Additionally, Echocardiogram 6 weeks to 3 months after initiation should be considered to follow the progression or resolution of valvular vegetations. Prognosis is generally grim despite anticoagulation due to the underlying predisposing medical condition rather than NBTE itself; a strong association between advanced malignancy and NBTE has been demonstrated in retrospective studies. Similarly, in patients with SLE, a longitudinal, cross-sectional study reports poor outcomes due to recurrent embolic events (25%), cognitive disability (24%) and death (9%). [6]

References/Further Reading

  1. el-Shami, K, Griffiths, E, and Streiff, M. Nonbacterial Thrombotic Endocarditis in Cancer Patients: Pathogenesis, Diagnosis, and Treatment. The Oncologist. 2007;12:518-23.
  2. Deppisch LM, Fayemi AO. Non-bacterial thrombotic endocarditis: Clinicopathologic correlations. Am Heart J 1976;92:723–729.
  3. Eiken PW, Edwards WD, Tazelaar HD, McBane RD, Zehr KJ (2001).“Surgical pathology of nonbacterial thrombotic endocarditis in 30 patients, 1985–2000”. Mayo Clin. Proc.76 (12): 1204–12. doi:4065/76.12.1204. PMID 11761501.
  4. Lopez JA, Ross RS, Fishbein MC, SIegel JC. Nonobacterial thrombotic endocarditis: a review. AM Heart J 1987; 113:773.
  5. Rogers LR, Cho ES, Kempin S et al. Cerebral infarction from non-bacterial thrombotic endocarditis: Clinical and pathological study including the effects of anticoagulation. Am J Med 1987;83:746 –756.
  6. Roldan CA, Qualis CR, Sopko KS, SIbbit WL Kr. Transthoracic versus tranesophageal echocardiography for detection of Libman-Sacks endocarditis: a randomized controlled study. J Rheumatol 2008; 35:224.

The Crashing Trauma Patient

Author: Bryant Allen, MD (@bryantkallen, Assistant Profess of Emergency Medicine, Carolinas Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021, Senior Staff Physician, Henry Ford Hospital)

ABCDE: General principles for the resuscitation and treatment of the unstable trauma patient

Case 1: A 35-year-old male presents after a high-speed motor vehicle collision. He was the restrained driver of a vehicle traveling approximately 70 mph when it struck a tractor-trailer stopped in the roadway. First responders found him slumped in his seat, airbags deployed, with the seat fractured from the vehicle. The car had severe front-end damage. He was placed in a cervical collar by EMS and after a prolonged extraction was placed on a spine board. Obvious injuries included an open deformity to his right femur, a tender and distended abdomen, and multiple facial and scalp injuries. Vital signs per EMS included a maximum heart rate of 139 bpm, lowest blood pressure of 84/40 mmHg, respiratory rate of 30 bpm, and GCS of 6.


Accidental and traumatic injuries remain one of the leading causes of death worldwide, accounting for 5.8 million deaths annually and a large percentage of ED evaluations.1 Increasing disease severity creates an environment that makes patient care difficult. The American College of Surgeons has created a protocol driven framework, Advanced Trauma Life Support, in order to overcome this challenge and achieve success in the “Golden Hour”.

Management of the crashing trauma patient can be hectic and challenging. The primary role of the traumatologist is to create a calm environment in the trauma bay in order to effectively designate roles and provide cohesive, structured care. Preparing the trauma team prior to arrival can be helpful in order to obtain appropriate equipment, including an airway cart, RSI drugs, tube thoracostomy, ED thoracotomy tray, or a Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) catheter. Managing the room and all members of the trauma team can be difficult, but can often make a sloppy and potentially unsuccessful resuscitation more organized. As the Boy Scouts of America motto states, “Be prepared.”

After preparation for the resuscitation is complete, initial evaluation and management of the unstable trauma patient can be framed using the ATLS Primary Survey mnemonic ABCDE.

A – Airway maintenance and cervical spine precaution

Cervical spine precautions

Patients presenting with debilitating traumatic injury have been found to have a high prevalence of cervical spine injuries, with between 4-34% of polytrauma patients suffering from cervical spine injury.2 Given this high likelihood of injury, care should be taken with initial evaluation, transport and bed transfer of these patients, with use of appropriately sized and fitted cervical collars. Manual in-line stabilization methods during intubation are important as well, given stabilization with a cervical collar during intubation can limit jaw movement, increasing the difficulty of intubation.2 However, when such interventions limit laryngoscopic views, as has been seen in the setting of direct laryngoscope usage, relaxation of aggressive immobilization may be necessary to facilitate successful intubation.3 Efforts to limit flexion and extension, including usage of a supraglottic airway, gum-elastic bougie or video laryngoscopy, should be considered for every polytrauma patient requiring airway management.


In many cases, the unstable and crashing trauma patient will require securement of the airway through intubation. An extensive deep dive into this topic was covered recently (here). The trauma airway is an inherently difficult airway and should never be taken for granted. Patients present un-fasted and with pathology that often makes standard intubation approaches impossible. Additionally, they present with pathology that suffers greatly from even small periods of hypotension or hypoxia. As such, practitioners should have a well thought out airway management plan, with multiple backups and airway adjuvants available for immediate use at the bedside, including materials for a surgical airway.4

B – Breathing and ventilation


Traumatic pneumothorax may quickly develop tension physiology, resulting in devastating preload elimination, hypotension and hypoxia. As such, rapid identification and reversal are key to preventing decompensation or cardiac arrest. Several methods for decompression of pneumothorax are described. Needle decompression has been described and is still taught as part of ATLS; however, this method is often unsuccessful and has frequent complications, requiring the provider to be prepped for rapid conversion to finger thoracostomy.5 Recent literature has identified lack of appropriate placement of needle for decompression and inadequate angiocatheter length as potential causes of needle decompression failure.6 Given the timely need for reversal of tension physiology in the unstable trauma patient, efforts should be directed instead at performance of finger thoracostomy, a procedure used in the initial stages of tube thoracostomy placement.7  As resuscitation proceeds, immediate placement of a chest tube is reasonable over finger thoracostomy.

Several methods may be used to rapidly identify a pneumothorax, including X-ray, point-of-care ultrasound and auscultation of breath sounds. In the unstable trauma patient, auscultation of lung sounds can be extremely difficult with standard stethoscopes.8 Other components of the physical exam may point toward pneumothorax with tension physiology, such as tracheal deviation, subcutaneous emphysema with crepitus, and penetrating trauma. Supine radiographs of the chest certainly demonstrate large pneumothoraces, but there is growing literature to support improved identification of this pathology and other lung pathology with ultrasound.9-11 Examination of the intercostal spaces on the anterior chest wall with linear array probe may illustrate lack of lung sliding as evidence of pneumothorax, and in the setting of traumatic instability, should be acted upon.

In setting of rapid decompensation and pending cardiac arrest, many algorithms recommend immediate bilateral decompression in blunt, and ipsilateral decompression in penetrating trauma.5,12 Vigilance should be maintained in the post-intubation patient, given the propensity for worsening pneumothorax in the setting of positive-pressure ventilation.

C – Circulation with hemorrhage control

Hemorrhage identification and control

The most common etiology of hemodynamic collapse in the trauma patient is hemorrhagic shock. Given this, the trauma practitioner should quickly identify the shock state and determine the source of hemorrhage. ATLS teaches practitioners to look to “blood on the floor and then four more (chest, abdomen, pelvis/retroperitoneum, long bones)” as sources for major blood loss.

Superficial injuries

Blood from superficial and deep lacerations is often the most obvious source for blood loss. Despite the frequent overestimation of blood lost at the scene of a trauma, large volume exsanguination can occur without correction. Direct pressure to venous and arterial bleeding is often sufficient to prevent additional blood loss, but care should be made not to overpad dressings. Big, bulky dressings can be less effective that those that provide direct, pointed pressure to the site of hemorrhage. In the setting of continued blood loss despite pressure, the practitioner should be prepared to ligate bleeding vessels, either though whip-stitching of the vessel or closure of the wound with sutures/staples to provide tamponade. The key to a successful trauma resuscitation is exposure; a missed scalp laceration can result in severe hemorrhage that would have been easily addressed if the patient was rolled and scalp explored.


Large volume blood loss into the chest can result from both blunt and penetrating trauma, and can potentially result in tension physiology. After identification of hemopneumothorax in the unstable trauma patient, a chest tube should be placed on the affected side. ATLS recommends placement of large bore chest tubes in the setting of any traumatic hemothorax large enough to be identified on chest radiograph.1 Often hemothorax is secondary to a lung laceration or intercostal vessel injury, and decompression with placement of chest tube may be the definitive management, with patients often not requiring further intervention. However, should the patient have massive output (see below), further surgical intervention is necessary.

Indication for surgical intervention for hemothorax
>1,500cc immediate output
>200cc/hr output for 2-4 hours
Patient requires large volume transfusion

With large volume hemorrhage, early initiation of auto-transfusion of the patient’s own whole blood should be attempted. Patient’s with suspected diaphragmatic injury, concomitant gastric injury with violation into the thorax or associated chest malignancy are potential contraindications for autotransfusion.13 Commercially available devices can be used to ensure adequate filtration when used in-line with chest tube suction devices.

Intra-abdominal hemorrhage

Damage to intra-abdominal organs, both solid and hollow, can result in large volume blood loss without significant changes to the external appearance of the patient.1 Gross examination of the abdomen and review of the mechanism of injury can lend some information as to the presence of an abdominal injury. In the absence of obvious signs of injury, the addition of the Focused Assessment Sonography in Trauma (FAST) exam can help to identify presence of intra-abdominal free fluid suggestive of traumatic hemorrhage. Given the high sensitivity and specificity, FAST examination carries an EAST Level II recommendation as the initial study for identifying intra-abdominal free fluid. Diagnostic peritoneal lavage may also be employed to identify hemorrhage in this setting. Many algorithms exist for the use of these procedures in the unstable patient instead of CT imaging. Positive studies should result in immediate surgical intervention, unless a contraindication is present.

EAST Algorithm for evaluating for intra-abdominal injury in the hemodynamically unstable trauma patient.

Pelvic fractures

The pelvis also serves as a large cavity for blood loss, with a substantial increase in volume in the setting of acute pelvic ring fractures. In one cadaveric study, fracture of the pelvis resulting in a pelvic diastasis of 5cm resulted in a 20% increase in pelvic volume, with a high association of venous injury.14 As a result, large volumes of blood can rapidly accumulate in the pelvis. Binding the pelvis, either with commercially-available devices or with an appropriately fitted sheet, has been found to decrease the volume of the pelvis, but has not been shown to have a statistically significant decrease in blood loss.15 Given the potential for decreasing pelvic volume and blood loss, placement of a temporary pelvic binder is recommended in the setting of a potential pelvic source of hemorrhage. In the patient who has no other identifiable source for hemorrhage, pelvic angiography is the EAST recommended intervention over surgical intervention.


The compartments containing long bones can serve as a large vacuum for blood loss in the setting of acute fracture, in addition to blood lost externally in the setting of open fractures. One study illustrated an average blood loss of greater than 1,200cc in the setting of isolated femur fractures in adults.16 Rapid identification of and splinting of fractures can result in improved pain control and decreased blood loss.17 For most fracture related external hemorrhage, external direct pressure is sufficient to prevent additional hemorrhage. Some devices exist for rapid wound packing which may be of benefit in this patient population. However, in the setting of massive hemorrhage with suspected arterial source, placement of a tourniquet may be indicated. Tourniquet use has illustrated decreased hemorrhage rates and improved morbidity and mortality, even when placed by first responders in the out-of-hospital environment.18,19 If placing such devices, carefully document placement location and specific time of placement to prevent prolonged tourniquet times.

General hemorrhage

One intervention proven to decrease death from bleeding and all-cause mortality at 30-days is the early administration of an antifibrinolytic agent tranexamic acid.20 This medication has shown great success when administered in the first hour after injury, though it did illustrate a slight association with increased risk of bleeding death if administered after 3 hours post-injury.20 As such, this medication is recommended in the setting of transfusion-requiring severe traumatic injury and should be given early in the evaluation, potentially in the pre-hospital setting.21 Recommended dosing is 1g administered IV over 10 minutes, with additional infusion of 1g over 8 hours. For further details, go here:

Anticoagulant reversal

Use of anticoagulants and antiplatelet agents complicate the management of traumatic hemorrhage.22 Often the hemodynamically stable patient will be unable to provide medication history, and additional data may be necessary to know of concomitant anticoagulant use. Elderly patients, patients with history or evidence of atrial fibrillation and those with history of CVA should be considered at risk for usage of either anticoagulant or antiplatelet agents. Point-of-care PT/INR may help if the patient is using warfarin, but will otherwise be of little help to the practitioner.

In the setting of anticoagulant use, efforts should be made to reverse the anticoagulated state in the setting of life-threatening hemorrhage. Use of these agents has an associated increased injury severity and mortality in elderly patients, so rapid reversal of their effects is paramount.23 Several protocols exist for reversal in the trauma patient, but consensus statements do not exist. With the addition of new reversal agents, more work should be done to create reversal protocols.


Sample reversal protocols for anticoagulant agents in traumatic, life-threatening hemorrhage.

The use of anti-platelet agents also creates an unfavorable environment for hemostasis. Some protocols call for the transfusion of platelets to reverse effects. In the hemodynamically unstable patient, platelets should be added as part of standardized massive transfusion protocols, making this intervention less important for the specific reversal of the anti-platelet agent.

Resuscitative Thoracotomy

A third subset of shock that may present in the unstable and crashing trauma patient is that of cardiogenic shock. In the setting of blunt traumatic injury, this may be related to direct cardiac contusion or free wall rupture, resulting in pericardial tamponade. In the penetrating trauma patient, this may also be due to cardiac injury resulting in pericardial tamponade. As discussed in a prior post on traumatic cardiac arrest, emergency department thoracotomy can be considered in certain situations for correction of potentially reversible causes. Pericardiocentesis, though temporizing, may only have short-lived effects, given the nature of injuries that lead to pericardial tamponade in the setting of trauma. As such, rapid transition to thoracotomy is recommended.

New therapies

REBOA: A relatively new therapy for the management of traumatic hemorrhage of the trunk and torso is the use of resuscitative endovascular balloon occlusion of the aorta (REBOA). A technique initially described in 1950s, REBOA has been used in multiple arenas related to hemorrhage, from abdominal aortic aneurysm rupture to post-partum hemorrhage.24 Through the strategic placement of a balloon catheter in various zones of the aorta, a provider can selectively prevent distal blood flow to sites of hemorrhage, hopefully temporizing the patient until more definitive management can be performed. Several protocols have been proposed for initiation of REBOA in the ED, with more facilities introducing REBOA programs.25 Despite expanding its use, one review of REBOA use illustrated no improvement in hemorrhage-related mortality.26 REBOA remains a viable option in the age of damage control resuscitation of the patient with massive traumatic torso hemorrhage, though more research is needed to identify the best populations for usage.


After identifying the potential source of exsanguination, efforts should be directed at resuscitation. “Damage control resuscitation” protocols have been developed to reduce the dangers of the “lethal triad” of trauma: acidosis, hypothermia, and coagulopathy.27 Infusion of crystalloid in large volumes has been linked to worsening acidosis and hemodilution. After initial field resuscitation with crystalloid, the unstable patient should be transitioned to blood product. The Eastern Association for the Surgery of Trauma guidelines give Level I recommendation for the transfusion of packed red blood cells in the setting of trauma and hemodynamic compromise, with less emphasis placed on hemoglobin directed transfusion.28 Combat literature has shown that the ideal transfusion product would be whole blood, though this resource is not often held in supply. The PROMMTT study found that practitioners attempted to replicate whole blood in their transfusion patterns, approaching a 1:1:1 or 1:1:2 ratio of plasma to platelets to packed red blood cells. Further investigation into ideal transfusion ratios by the PROPPR trial showed similar outcomes with these ratios, but noted a slight improvement in achievement of hemostasis and 24-hour mortality related to exsanguination in the 1:1:1 group.29

Given that hemorrhage is the most common etiology of shock in the trauma patient, little emphasis should be placed on vasopressor agents. Blood product replacement remains the gold standard in management of traumatic hemorrhagic shock. An exception to this rule involves patients with traumatic spinal cord injuries presenting with hypotension secondary to neurogenic shock.30 While guidelines recommend aggressive reversal of hypotension with fluid resuscitation, there is no one specific vasopressor agent for additional support recommended.31 Norepinephrine, phenylephrine or dopamine are all mentioned as potential agents, though phenylephrine should be avoided in those patients presenting with simultaneous bradycardia secondary to neurogenic shock.32

D – Disability; neurologic status

GCS/neurologic examination

After initial assessment, efforts should be made to perform a neurologic examination and determine the Glasgow Coma Scale of the patient. In the unstable patient, efforts may often proceed quickly to rapid sequence intubation, which can prevent adequate neurologic examination. Though protection of the patient’s airway is paramount, a neurologic exam should be performed and short-acting paralytics should be considered for RSI if possible.

Spinal cord injuries

Spinal column and cord injuries may complicate the poly-traumatized patient, leading to further injury load and potential source for hemodynamic instability. Patients will often present in a cervical collar and on spinal immobilization boards, though recent review of the literature suggests that spinal motion restriction methods may be more beneficial than immobilization boards. Efforts to minimize spinal manipulation should be attempted, with knowledge that life-saving measures may limit the ability to do so. During initial resuscitation, some elements of the physical exam may suggest spinal cord injury: focal neurologic deficit, priapism, or shock refractory to standard transfusion methods. Careful attention should be made to prevent hypoxia and hypotension, which increase morbidity and mortality.

Intracranial hemorrhage (ICH) management

Traumatic intracranial injury can complicate the course of the poly-traumatized patient. Though CT examination may be performed after the patient reaches a more hemodynamically stable state, suspicion of severe ICH should remain high so that early intervention can occur. The practitioner should look for signs of expanding ICH: palpable skull crepitus/obvious skull fracture, signs of basilar skull fracture, scalp hematoma, and facial bone fractures. Additionally, patients with diminished GCS without obvious signs of head injury should be considered high risk for ICH.

Progressively worsening ICH and associated edema can quickly progress, resulting in herniation of intracranial contents. This is often heralded by a combination of vital sign changes and lateralizing physical exam findings. Cushing’s response is the combination of bradycardia and hypertension in the herniating patient. Additionally, a unilateral dilated and unreactive pupil may be observed. Hemodynamic instability due to severe ICH and herniation requires rapid intervention. Hypertonic saline or mannitol may be used in an effort to decrease intracranial pressure, though guidelines do not exist for preferential use. The practice of hyperventilation should be avoided, unless rapid surgical decompression is possible, given the associated cerebral vasoconstriction and decreased oxygen delivery. Neurosurgical consultants should be involved as early as possible. Please go here for further details:

E – Endpoints/Markers (ATLS uses “Exposure/environmental control” here)

The ultimate goal in the resuscitation of the unstable and crashing trauma patient is to preserve life and return the patient to a normal physiologic state. However, the severity of injury may require prolonged resuscitation and multiple interventions before an external sign of response is noted by the practitioner. Surrogate markers for injury severity are the serum lactate level and base deficit. Severely elevated base deficit has been linked to increased mortality and blood product requirements, while the rate at which the base deficit is corrected in the resuscitation is associated with improved survival.33-35 Base deficit may be slightly better than lactate at this prediction, but lactate has also shown utility.36 Both are recommended as markers of resuscitation response by the most recent EAST Guidelines. Hemoglobin measurement is known to be inherently flawed in the acutely hemorrhaging patient and should not be used as an initial risk stratifying tool or resuscitation goal. Aggressive efforts to improve oxygen delivery, through prevention of further hemorrhage, application of supplemental oxygen and transfusion of blood product may be linked to more rapid correction of these physiologic markers and improved outcomes.37

Ultimately, the crashing trauma patient may require definitive surgical intervention. The initial resuscitation should be aimed at rapid identification of potentially reversible causes of hemorrhage, protection of the airway, and aggressive resuscitation. If the facility does not have the potential for surgical intervention, then the patient should quickly be prepped for transfer. Intubation, placement of chest tubes, and fracture splinting can be performed quickly in most emergency departments; however, a “stay-and-play” approach to the trauma patient is often detrimental to the patient and transport should not be delayed if available.

Case Recap

35-year-old male presents after a high speed MVC. Patient unresponsive on scene, placed in cervical collar and on spinal board by EMS after prolonged extrication. 5 minutes prior to patient arrival, EMS alerts EM providers to current vital signs and mechanism of injury. Trauma surgery paged to ED, lead EM physician briefs nursing and support staff in trauma bay prior to arrival, assures adequate procedural supplies are present and alerts blood bank to likely massive transfusion protocol event. Airway setup prepped.

Primary Survey:

A: Airway intact and without obvious obstruction

B: Spontaneous but sonorous respirations, left chest wall crepitus with diminished lung sounds

C: Thready pulses in bilateral radial locations and left dorsalis pedis; absent pulse in right DP; large volume hemorrhage from posterior scalp wound; open right femur fracture with continued hemorrhage; distended abdomen

D: GCS 6 (Eye – 1, Verbal – 2, Motor – 3)

E: Cool to touch, worse in distal right lower extremity

Vitals: HR 139 bpm, BP 84/40 mmHg manual, RR 30 bpm, SpO2 78%

Patient identified as having multiple potential sources for shock on arrival. After initial assessment, he underwent endotracheal intubation using ketamine and rocuronium. Video laryngoscope was used primarily, and intubation was successful on first attempt with no worsening hypoxia. Lack of breath sounds with associated crepitus to the left chest wall raised concern for left hemopneumothorax, and a left chest tube was placed with return of air and 500cc blood immediately. An autotransfuser device was employed, and the massive transfusion protocol was initiated at 1:1:1 ratio with 1g TXA IV. Given an open deformity to the right femur, a tourniquet was requested, but after the patient was placed in a traction splint, hemorrhage ceased. The scalp laceration was stapled for rapid hemostasis. Chest radiograph confirmed appropriate ETT placement, chest tube placement with small residual hemothorax, and left sided rib fractures. Pelvic radiograph demonstrated a sacral fracture with associated anterior diastasis, resulting in the placement of a pelvic binder. FAST examination was performed, illustrating presence of anechoic fluid collection in Morison’s pouch and peri-splenic views. After interventions and blood product administration, vital signs were notable for persistent hypotension and minimal improvement in tachycardia, resulting in immediate transit to operating room for exploratory laparotomy.

Discharge problem list following 15-day hospitalization:

Right-sided subdural hematoma, status post surgical decompression
Right maxillary, frontal sinus fractures
Rib fractures (R 3-5, L 3-8)
Left hemopneumothorax
Liver laceration
Splenic laceration, status post splenectomy
Sacral fracture
Pelvic ring fracture
Right open femoral shaft fracture, status post ORIF

References / Further Reading

  1. ATLS Student Course Manual, 10th edition
  2. Aoi Y, Inagawa G, Hashimoto K, Tashima H, Tsuboi S, Takahata T, Nakamura K, Goto T. Airway scope laryngoscopy under manual inline stabilization and cervical collar immobilization: a crossover in vivo cinefluoroscopic study. J Trauma. 2011; 71(1): 32-6.
  3. Manoach S, Paladino L. Manual in-line stabilization for acute airway management of suspected cervical spine injury: historical review and current questions. Ann Emerg Med 2007; 50(3): 236-45.
  4. Stephens CT, Kahntroff S, Dutton RP. The success of emergency endotracheal intubation in trauma patients: a 10-year experience at a major adult trauma referral center. Anesth Analg. 2009 Sep;109(3):866-72.
  5. Leigh-Smith S. Tension pneumothorax – time for a re-think? Emerg Med J 2005; 22:8-16.
  6. Chang SJ, Ros SW, Kiefer DJ, Anderson WE, Rogers AT, Sing RF, Callaway DW. Evaluation of 8.0cm needle at the fourth anterior axillary line for needle chest decompression of tension pneumothorax. J Trauma Acute Care Surg 2014; 76(4):1029-34.
  7. Aylwin CJ, Brohl K, Davies GD, et al. Pre-hospital and in-hospital thoracostomy indications and complications. Ann R Coll Surg Engl 2008; 90:54-7.
  8. Gaydos S. Clinical auscultation in noisy environments. J Emerg Med. 2012; 43(3): 492-3.
  9. Zanobetti M, Poggioni C, Pini R. Can chest ultrasonography replace standard chest radiography for evaluation of acute dyspnea in the ED? Chest. 2011; 139(5):1140-7.
  10. Zhang M, Liu ZH, Yang JX, Gan JX, Xu SW, You XD, Jiang GY. Rapid detection of pneumothorax by ultrasonography in patients with multiple trauma. Crit Care. 2006; 10(4): R112.
  11. Tasci O, Hatipoglu ON, Cagli B, Ermis V. Sonography of the chest using linear-array versus sector transducers: Correlation with auscultation, chest radiography, and computed tomography. J Clin Ultrasound. 2016 Feb 11 [Epub ahead of print]
  12. Sherren PB, Reid C, Habig K, Burns BJ. Algorithm for the resuscitation of traumatic cardiac arrest patients in a physician-staffed helicopter emergency medical service. Crit Care 2013; 17(2): 308.
  13. Salhanick M, Corneille M, Higgins R, Olson J, Michalek J, Harrison C, Stewart R, Dent D. Autotransfusion of hemothorax blood in trauma patients: is it the same as fresh whole blood? Am J Surg 202(6):817-822, 2011
  14. Baque P, Trojani C, Delotte J, et al. Anatomical consequences of “open-book” pelvic ring disruption: a cadaver experimental study. Surg Radiol Anat. 2005;27:487–490.
  15. Sadri H, Nguyen-Tang T, Stern R, Hoffmeyer P, Peter R. Control of severe hemorrhage using C-clamp and arterial embolization in hemodynamically unstable patients with pelvic ring disruption. Arch Orthop Trauma Surg. 2005;125:443–447.
  16. Lieurance R; Benjamin JB; Rappaport WD. Blood loss and transfusion in patients with isolated femur fractures. J Orthop Trauma. 1992; 6(2):175-9.
  17. Wood SP, Vrahas M, Wedel SK. Femur fracture immobilization with traction splints in multisystem trauma patients. Prehosp Emerg Care, 2003 Apr–Jun; 7(2): 241–3.
  18. Kragh JF, Littrel ML, Jones JA, et al. Battle casualty survival with emergency tourniquet use to stop limb bleeding. J Emerg Med 2011;41:590-597.
  19. Callaway DW, Robertson J, Sztajnkrycer MD. Law enforcement-applied tourniquets: a case series of life-saving interventions. Prehosp Emerg Care. 2015 Apr-Jun;19(2):320-7.
  20. Roberts I, Shakur H, Coats T, et al. The CRASH-2 trial: a randomized controlled trial and economic evaluation of the effects of tranexamic acid on death, vascular occlusive events and transfusion requirement in bleeding trauma patients. Health Technol Assess. 2013; 17(10).
  21. Napolitano J. et al. Tranexamic acid in trauma: how should we use it? J Trauma Acute Care Surg. 2013 Jun;74(6):1575-86.
  22. Pieracci FM, Eachempati SR, Shou J, Hydo LJ, Barie PS. Use of long-term anticoagulation is associated with traumatic intracranial hemorrhage and subsequent mortality in elderly patients hospitalized after falls: analysis of the New York State Administrative Database. J Trauma. 2007 Sep;63(3):519-24.
  23. Boltz MM, Podany AB, Hollenbeak CS, Armen SB. Injuries and outcomes associated with traumatic falls in the elderly population on oral anticoagulant therapy. Injury. 2015 Sep;46(9):1765-71.
  24. Stannard A, Eliason JL, Rasmussen TE. Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) as an adjunct for hemorrhagic shock. J Trauma. 2011; 71(6): 1869-72.
  25. Biffl WL, Fox CJ, Moore EE. The role of REBOA in the control of exsanguinating torso hemorrhage. J Trauma Acute Care Surg. 2015; 78(5): 1054-8.
  26. Morrison JJ, Galgon RE, Jansen JO, Cannon JW, Rasmussen TE, Eliason JL. A systematic review of the use of resuscitative endovascular balloon occlusion of the aorta in the management of hemorrhage shock. J Trauma Acute Care Surg. 2016; 80(2): 324-34.
  28. EAST Guidelines Napolitano LM, Kurek S, Luchette FA, et al. Red Blood Cell Transfusion in Adult Trauma and Critical Care. J Trauma. 2009; 67(6): 1439-42.
  29. Holcomb JB, Tilley BC, Baraniuk S, Fox EE, et al; PROPPR Study Group. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA. 2015 Feb 3;313(5):471-82.
  30. Atkinson PP, Atkinson JL. Spinal shock. Mayo Clin Proc. 1996 Apr;71(4):384-9.
  31. Stein DM, Roddy V, Marx J, Smith WS, Weingart SD. Emergency neurological life support: traumatic spine injury. Neurocrit Care. 2012 Sep;17 Suppl 1:S102-11.
  32. Wing PC, et al. Early Acute Management in Adults with Spinal Cord Injury. J Spinal Cord Med. 2008; 31(4): 403–479.
  33. Davis JW, Kaups KL, Parks SN: Base deficit is superior to pH in evaluating clearance of acidosis after traumatic shock. J Trauma 1998;44:114-118.
  34. Davis JW, Shackford SR, MacKersie RC, Hoyt DB: Base deficit as a guide to volume resuscitation. J Trauma 1988;28:1464-1467.
  35. Rixen D, Raum M, Bouillon B, et al: Base deficit development and its prognostic significance in posttrauma critical illness: an analysis by the trauma registry of the Deutsche Gesellschaft für unfallchirurgie. Shock 2001;15:83-89.
  36. Shoemaker WC, Appel P, Bland R: Use of physiologic monitoring to predict outcome and to assist in clinical decisions in critically ill postoperative patients. Am J Surg 1983;146:43-38.
  37. Abramson D, Scalea TM, Hitchcock R, Trooskin SZ, Henry SM, Greenspan J: Lactate clearance and survival following injury. J Trauma 1993;35:584-589.

Additional FOAMed resources:

Ultrasound-Guided Peripheral Intravenous Access – Tips for Success

Authors: Marc Zosky, DO (LSUHSC Emergency Medicine Residency, Chief Resident, Baton Rouge, LA) and Emilio Volz, MD (LSUHSC Emergency Ultrasound Fellowship Director, Baton Rouge, LA) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Stephen Alerhand, MD (@SAlerhand)

Obtaining intravenous (IV) access is a basic necessity in the emergency department. So what do you do when you are unable to place a peripheral IV, and your go-to external jugular line is not an option? You certainly do not want to place an IO in a stable patient, and you definitely want to avoid placing a time-consuming and potentially dangerous central line.

Ultrasound guided peripheral IVs are quickly becoming the standard of care for patients with difficult IV access. This article will review the skills needed for successful placement.

Step 1: Prepare & position

First, gather all your materials and have them arranged for easy access. You will need a tourniquet, skin cleaning solution, angiocatheter, IV tubing, saline flush, and bandage to secure the newly placed IV. We recommend you use an angiocatheter which is long enough for at least 1/3 of the catheter to sit inside the selected vessel as this will increase the longevity of your line’s functionality. There are many “long” 1.8 – 2 inch commercially available products made for this purpose. Twenty gauge or larger catheters, graded for power injection, are usually easily visualized under ultrasound guidance. Position the patient to maximize both operator and patient comfort. One common novice mistake is forcing yourself to lean over and sit/stand in a position that may cause fatigue or back straining quite quickly. If your ultrasound machine has a high frequency vascular probe, it will facilitate visualization of superficial vessels. Make sure to follow your own institutional recommendations regarding peripheral IV placement.

Step 2: Find a vein

Start scanning in the short axis view until you see the largest and most superficial vein available. Practice scanning with your non-dominant hand. When placing lines, you should use your dominant hand to drive the needle and your non-dominant hand to scan. Once visualized, scan a few centimeters proximally and distally to see the direction in which the vein courses. You do not want to insert an IV into a vein that changes angle acutely. Also, evaluate the vessel for abnormalities. If the vessel is not compressible or has a hematoma around it, find a different site.

Step 3: Make sure your vein… well, is actually a vein

How do you determine the vessel you are looking at is actually a vein? There are many techniques; however, we recommend two methods. First, compress the vessel. Arteries typically continue to pulsate, while veins should easily collapse with minimal pressure (Video 1). Remember that with sufficient pressure one can completely occlude an artery. If you are still not sure, we recommend using spectral Doppler (the one which gives you a waveform (Figure 1). Arterial waveforms will be peaked when compared to the flat waveform of peripheral veins.

 Video 1. Observe the easily compressible vein. There is an adjacent artery which is seen pulsating.

 fig 1

 Figure 1. Spectral doppler of an artery, showing peaked waveforms.

Step 4: Cannulate the vessel

Now that you have found an easily compressible vein in the short axis view, turn the probe 90 degrees to get the long axis view (Figures 2, 3). We believe that a long axis approach is safer and helps to develop ultrasound techniques necessary for safe central line cannulation as well. Ideally, learn to use both long and short axis approaches, making sure to visualize the needle tip all the way through. Advance the catheter under direct visualization until you see the catheter (not just the needle) tip in the vessel (Videos 2, 3). As needed, level off your angle with the skin to maximize the amount of catheter in the vessel before you advance. At this point, let go of the ultrasound probe and advance the catheter into the vessel until it is hubbed at the skin. The catheter should advance easily. If there is resistance, the catheter may not be in the vessel. If this is a possibility, do not force it. Some catheters have a wire within them which can be used to guide the catheter in the vessel. If you are using one of these catheters, you may not get flash when accessing the vessel and should confirm wire position in the vein before advancing the catheter. Once this step is completed, secure the IV in place and get ready to confirm placement.

fig 2

Figure 2. Proper positioning for cannulating the vein in the long axis.

fig 3

Figure 3. Visualization of the vein in the long axis.

Video 2. Under direct ultrasound visualization in the long axis, the needle is seen making contact with the vein.

Videos 3. The needle is slowly advanced until it enters the vein.

Step 5: Confirm placement

Just because your angiocatheter chamber filled with dark blood, and you saw your needle tip make contact with the vein, this does not mean you are necessarily secured in a good position in the vein. How do you check? First, scan the vein in the long axis and visualize the catheter inside the vein (Video 4). Second, under ultrasound guidance inject 10cc of normal saline, and you can directly visualize turbulence within the vein (Video 5).

Videos 4. Long axis view visualizing the majority of the catheter in the vein.

Videos 5. Long axis view of a 10cc saline injection, showing turbulence within the vein.


References/Further Reading
  1. Costantino, Thomas G. et al. Ultrasound-Guided Peripheral Venous Access vs. the External Jugular Vein as the Initial Approach to the Patient with Difficult Vascular Access. Journal of Emergency Medicine. 2010;39:462-467
  2. Costantino, T.G., Parikh, A.K., Satz, W.A., Fojtik, J.P. Ultrasonography-guided peripheral intravenous access versus traditional approaches in patients with difficult venous access. Ann Emerg Med. 2005;46:456–461.
  3. Gregg, SC, Murthi SB, Sisley AC, et al. Ultrasound-guided peripheral intravenous access in the intensive care unit. J Crit Care. 2010;25:514-519.
  4. Stein J, George B, River G, et al. Ultrasonographically guided peripherall intravenous cannulation in emergency department patients with difficult intravenous access: a randomized trial. Ann Emerg Med. 2009;54:33-40.



Pneumonia Mimics: Pearls and Pitfalls

Authors: Drew A. Long, BS (@drew2232, Vanderbilt University School of Medicine, US Army) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021, Senior Staff Physician, Henry Ford Hospital)

It’s a busy day in the ED. You have a full waiting room and multiple patients who have been roomed but not seen. You force your exhaustion to the back of your mind as you see your next patient: a 52-year-old male with cough and shortness of breath for three days. He states he has felt warm at home, but he denies chest pain, abdominal pain, vomiting, and diarrhea. He has experienced several episodes of nausea.  His past medical history includes hypertension and hyperlipidemia.

His vital signs include HR 103, RR 24, BP 128/72, T 99.8, and SpO2 95% on room air. He has some crackles in the lower lung bases, but has an otherwise normal physical exam. You order a chest x-ray, which demonstrates a right lower lobe infiltrate. As you write the diagnosis of “pneumonia” on the discharge form and write a prescription for antibiotics, you pause. Is there something else you could be missing? Are there other diagnoses you should consider?


Pneumonia is defined as an acute infection of the pulmonary alveoli.  Pneumonia can be life-threatening, most commonly in older patients with comorbidities or immunocompromised patients.  It is the 7th leading cause of death in the U.S. and the number one cause of death from infectious disease in the U.S.1   The annual incidence of community acquired pneumonia (CAP) ranges from 2 to 4 million, resulting in an estimated annual 500,000 hospitalizations.1  Pneumonia is broken into several categories: community-acquired (CAP), hospital-acquired, healthcare-associated (HCAP), and ventilator-associated (VAP) (Table 1).

Table 1.  Classification of Pneumonia (Adapted from Maloney G, Anderson E, Yealy DM.  Tintinalli’s Emergency Medicine:  A Comprehensive Study Guide.  Chapter 65:  Pneumonia and Pulmonary Infiltrates.  McGraw Hill Professional 2016.  8th ed.)



Community-acquired pneumonia



Acute pulmonary infection in a patient who is not hospitalized or residing in a long-term care facility 14 or more days before presentation



Hospital-acquired pneumonia


New infection occurring 48 hours or more after hospital admission




Healthcare-associated pneumonia


Patients hospitalized ≥ 2 days within past 90 days

Nursing home/long-term care residents

Patients receiving home IV therapy

Dialysis patients

Patients receiving chronic wound care

Patients receiving chemotherapy

Immunocompromised patients



Pneumonia can be caused by bacteria, viruses, or fungi.  However, it is often challenging to differentiate between these in the ED, and many patients will not have an etiologic agent identified even after inpatient evaluation.   It is estimated that a microbial agent cannot be identified in nearly half of cases of CAP.1 The “typical” pathogens in patients hospitalized with pneumonia include S. pneumoniae and H. influenza, with S. pneumoniae being the most common.  The “typical” pathogens are thought to account for about half of cases.1 “Atypical” pathogens include Legionella, Mycoplasma, and Chlamydia.  The most common identified viral causes of pneumonia are influenza and parainfluenza viruses.  Fungal pneumonia is often associated with patients who are immunocompromised or possess other risk factors.1,2

History and Physical Examination

The classic presentation of pneumonia is a cough productive of purulent sputum, shortness of breath, and fever.  The most common signs of pneumonia include cough (79%-91%), fever (up to 75%), increased sputum (up to 65%), pleuritic chest pain (up to 50%), and dyspnea (approximately 70%).3 There are many patterns of presentation with a variety of these symptoms and physical findings, making the diagnosis at times difficult. Elderly or debilitated patients in particular can present with non-specific complaints, such as altered mental status without the classic symptoms.1,2 In addition, pneumonia may cause lightheadedness, malaise, weakness, headache, nausea/vomiting, joint pain, and rash.  The examination may reveal bronchial or decreased breath sounds, dullness on percussion, rales, rhonchi, or wheezing. This wide variation in symptoms and presentation provides potential for misdiagnosis, especially if other conditions are not considered.

The chest x-ray in patients with pneumonia can vary greatly.  Radiologic findings in pneumonia are used in conjunction with the physical exam to identify any area of consolidation.  The most common cause of pneumonia, S. pneumoniae, classically presents with a lobar infiltrate visualized on chest x-ray.  Other organisms, such as Staphylococcus aureus pneumonia can be seen on chest x-ray as extensive infiltration and effusion or empyema.  Klebsiella may present with diffuse, patchy infiltrates.  Other findings on chest x-ray found in various organisms include pleural effusions, basilar infiltrates, interstitial infiltrates, or abscesses.1,2,4 However, each agent can present multiple ways on chest x-ray, and many patients may not demonstrate the classic radiographic findings, especially elderly and immunocompromised patients with weakened immune systems.

PA chest radiograph showing left upper lobe pneumonia.  (Image from Marx JA.  Rosen’s Emergency Medicine:  Concepts and Clinical Practice.  Saunders 2014.  8th ed.)

 While it is tempting to diagnose pneumonia in a patient with a classic presentation (fever, cough, shortness of breath) and a supportive chest x-ray, what else should be considered?  As Table 2 shows, many conditions can be confused for pneumonia based on the history, physical exam, and radiographic findings.

Table 2.  Mimics of Pneumonia (Adapted from Marx JA.  Rosen’s Emergency Medicine:  Concepts and Clinical Practice and Maloney G, Anderson E, Yealy DM.  Tintinalli’s Emergency Medicine:  A Comprehensive Study Guide.  Chapter 65:  Pneumonia and Pulmonary Infiltrates.)

Pulmonary Embolism
Septic Emboli
Congestive Heart Failure
Cancer and leukemic infiltrates
Acute Respiratory Distress Syndrome
Bronchiolitis obliterans organizing pneumonia
Granulomatous disease
Drug induced pulmonary disease
Pulmonary fibrosis
Eosinophilic pneumonia
Allergic/hypersensitivity pneumonitis
Radiation pneumonitis
Foreign body obstruction


Unfortunately, many of these diagnoses are not even considered in a patient with a classic presentation for pneumonia until the patient fails to improve with initial antibiotic management.  Of the diagnoses listed in Table 2, several of these carry high potential for morbidity and mortality.  These include pulmonary embolism, endocarditis, vasculitis, acute decompensated heart failure, tuberculosis, primary lung cancer, and acute respiratory distress syndrome.  The remainder of this discussion will focus on differentiating each of these from pneumonia.

*Bonus: What can potentially assist providers? Ultrasound (US)!

US has demonstrated tremendous utility differentiating pneumonia from other conditions. X-ray has a sensitivity of 46-77% in diagnosing pneumonia. US findings with pneumonia include air bronchograms, b-lines, consolidations, pleural line abnormalities, and pleural effusions. Dynamic air bronchograms (those that move) are considered pathognomonic for pneumonia.  Positive likelihood ratios (LR) for these findings range from 15.6 to 16.8, with negative LR’s of 0.03 to 0.07.5,6  Please see a prior post on the use of US in pneumonia:

Air bronchograms in pneumonia (From

Pulmonary Embolism

Pulmonary embolism (PE) occurs when a thrombus, most commonly from the venous system, embolizes to the pulmonary vasculature.7,8 Like pneumonia, the clinical presentation of a PE can vary greatly, ranging from an asymptomatic patient to an ill-appearing, dyspneic patient.  PE can be easily confused with pneumonia, as the most common presenting symptom is dyspnea followed by pleuritic chest pain and cough.8,9 Fever can also be present in pulmonary embolism. The most common symptoms and their frequency are shown in Table 3.

Table 3.  Signs and Symptoms Of Pulmonary Embolism (adapted from Stein PD, Beemath A, Matta F, et al.  Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med. 2007;120(10):871.)

Sign/Symptom Frequency
Dyspnea 73%
Tachypnea 70%
Pleuritic Chest Pain 66%
Rales 51%
Cough 37%
Tachycardia 30%
S4 heart sound 24%
Accentuated P2 23%
Hemoptysis 13%
Circulatory collapse 8%


A PE most commonly has non-specific chest x-ray findings (atelectasis, pleural effusion, peripheral infarct/consolidation, elevated hemidiaphragm) or is normal.2  That being said, while a normal chest x-ray is helpful in distinguishing PE from pneumonia, a normal chest x-ray does not definitively exclude pneumonia or pulmonary embolism.  Hampton’s Hump (peripheral wedge-shaped opacity with base against pleural surface) and Westermark’s Sign (focus of oligemia and vessel collapse distal to the PE) are classic findings in the PE radiograph, but they lack sensitivity.

The important aspect of not missing PE is first considering it. As the presentation of PE is nonspecific, clinical gestalt and risk stratification are useful. Evaluate the patient for signs/symptoms of PE including shortness of breath with pleuritic chest pain, tachypnea, and leg swelling in the setting of risk factors such as recent travel history, prior history of thrombosis, family history of thrombosis, or history of cancer.  If signs and/or symptoms are present and concerning, do not hesitate to begin the workup for PE.

In PE, US may reveal RV strain with dilated RV and free wall hypokinesis and normal RV apical contractility (McConnell Sign). On short axis view, the LV will appear “D” shaped, with RV bowing into the LV due to elevated right-sided pressures.10-12

Enlarged RV when compared to LV in setting of acute PE (from


Endocarditis is most commonly caused by a bacterial agent, with a one-year mortality of 40%.13 The most common symptoms are intermittent fever (85%) and malaise (80%).1  Additionally, endocarditis can present with dyspnea, chest pain, cough, headache, weakness, and myalgias.  Infective endocarditis (IE) can easily be confused with pneumonia in a patient presenting with fever and dyspnea or chest pain.  Risk factors for IE are shown below in Table 4.  Diagnosis includes the Duke Criteria. A patient with flu-like symptoms (cough, myalgias, etc.) with the risk factors shown in Table 4, warrants further evaluation for IE. 13-17

Table 4.  Risk factors for IE

Age ≥ 60 (over half of cases occur in this population)
History of IV drug use
Poor dentition or dental infection
Structural heart disease (e.g. valvular or congenital)
Presence of prosthetic valve
Presence of intravascular device
Chronic hemodialysis


One of the most important aspects to not miss is the patient with multiple infiltrates on chest x-ray, as a dreaded complication of IE is septic emboli.  This has been described in 13 to 44% of patients with IE.18,19 Septic emboli can lead to damage in the systemic or pulmonary artery circulation, depending on left vs. right-sided disease.  Specifically, embolization can lead to stroke, paralysis, blindness, ischemia of the extremities, splenic or renal infarction, pulmonary emboli, or an acute myocardial infarction.18 In particular, septic emboli from the right heart to the pulmonary arteries can lead to a toxic-appearing patient with fever and shortness of breath.  Again, the chest x-ray may demonstrate multiple infarcts or consolidations. This patient may originally be worked up for pneumonia.  In the patient with IE risk factors described above and multiple consolidations/infarcts on chest x-ray, strongly consider IE and obtain multiple blood cultures and echocardiogram.  US may reveal valvular vegetation(s) and/or regurgitation.

Multiple emboli with consolidations from R sided IE (From
Valvular Regurgitation with Vegetation in Endocarditis (From Journal of Medicine Cases,

Vasculitis (Systemic Lupus Erythematosus)

A vasculitis that often manifests with pulmonary involvement is systemic lupus erythematosus (SLE).  SLE is an autoimmune disorder that leads to inflammation of multiple organ systems.  Pulmonary involvement is common and has been observed in up to 93% of patients with SLE.20,21 Lung involvement in SLE often manifests as pleurisy, coughing, and/or dyspnea.21-23 The most common respiratory condition among patients with SLE is pleuritis, thought to be due to autoantibodies damaging the pleura itself.1 Pneumonitis may also occur in the setting of SLE. Patients with acute lupus pneumonitis present with a rapid onset of fever, cough, and dyspnea, with elevation of serum antinuclear antibodies and anti-DNA antibodies.22,23

Patients with SLE (either diagnosed or undiagnosed) and lung involvement should be worked up for infection.  Since patients with SLE are often immunosuppressed due to immunomodulatory therapy and the disease itself, they are at a much higher risk of infection with both typical and opportunistic agents.  The patient with extrapulmonary features of SLE (e.g. malar rash, oral ulcers, polyserositis, renal insufficiency, cytopenia, thrombophilia, lymphadenopathy, splenomegaly, or arthritis) and signs of lung involvement warrants treatment for infection and worsening vasculitis. Consultation with rheumatology and the ICU is recommended due to the potential for rapid decompensation.

Diffuse alveolar hemorrhage (DAH) is one of the most life-threatening conditions in SLE. Diffuse alveolar damage is a more common presentation in patients who already have a documented history of lupus and rarely presents as the initial manifestation of lupus.  These patients present with severe shortness of breath, hemoptysis, and diffuse patchy infiltrates on chest x-ray. Patients often require intubation, ICU admission, and high dose steroids.24-26

Heart Failure Exacerbation

A patient with heart failure exacerbation can present similarly to a patient with pneumonia, particularly if a patient has undiagnosed heart failure.  Patients with acute decompensated heart failure most commonly present with cough, shortness of breath, fatigue, and/or peripheral edema.  The history and physical exam may be enough to differentiate a heart failure exacerbation from pneumonia.  A history of orthopnea and/or paroxysmal nocturnal dyspnea leading up to the patient’s presentation is sensitive and specific for heart failure.  Furthermore, many of these patients will have a cardiac history, history of cardiac procedures, and comorbid conditions for CHF (such as diabetes, hypertension, hyperlipidemia, or a history of smoking).  Physical exam may reveal an S3 or S4 heart sound, elevated jugular venous pressures, lower extremity edema, and crackles indicating interstitial pulmonary edema on auscultation of the lungs.  These patients often have nonspecific EKGs showing left-ventricular hypertrophy, bundle branch block, or signs of a previous MI such as prominent Q waves or T wave inversions.  BNP will more likely be elevated in CHF exacerbations, though sepsis from pneumonia can also increase BNP.1,27

The chest x-ray findings in CHF may include prominent interstitial markings, cardiomegaly, and pleural effusions.2

CXR in a patient with CHF depicting cardiomegaly, alveolar, and interstitial edema (From

US in the setting of CHF will reveal b-lines in 3 or more lung fields bilaterally, which has a +LR of 20. The IVC will often reveal significant distension, with 2-2.5cm in size and < 50% collapse. Echocardiogram may reveal depressed contractility if systolic dysfunction is present.28

Multiple b-lines in the setting of acute CHF (From,


Tuberculosis (TB) is currently the world’s second leading infectious cause of death.1 The lungs are the major site for infection with Mycobacterium tuberculosis.  TB can occur in multiple forms, including primary TB, reactivation TB, laryngeal TB, endobronchial TB, lower lung field TB infection, and tuberculoma.29 As TB affects the lungs and can present with fever, cough, or dyspnea, it is often misdiagnosed as viral or bacteria pneumonia.  There are a wide array of nonspecific signs and symptoms associated with the multiple forms of TB, shown in Table 5.30

Table 5.  Symptoms and Signs of Tuberculosis (Adapted from Barnes PF, et al:  Chest roentgenogram in pulmonary TB: new data on an old test. Chest. 94:316, 1988.)

Symptom or Sign Frequency
Cough 78%
Weight loss 74%
Fatigue 68%
Tactile fever 60%
Night sweats 55%
Chills 51%
Anorexia 46%
Chest pain 40%
Dyspnea 37%
Hemoptysis 28%


In differentiating TB from pneumonia, it is important to assess the patient for risk factors for TB.  The most commonly reported behavioral risk factor among patients with TB in the U.S. is substance abuse (including drugs, tobacco, and alcohol).31 Other risk factors include malnutrition, systemic disease (silicosis, malignancy, diabetes, renal disease, celiac disease, or liver disease), or patients who are immunocompromised or homeless.32  Additionally, TB should be considered when a patient has a history of recent travel to an area where TB is endemic (Africa, the Middle East, Southeast and East Asia, and Central and South America).33

 As TB has many forms, the chest x-ray in TB can vary and may not be all that helpful in differentiating TB from pneumonia.  In summary, TB should be suspected in a patient with vague symptoms who possesses risk factors for TB, particularly in patients who are homeless, immunosuppressed, have a history of drug use, or have recently traveled to a TB endemic area.

Primary Lung cancer

In 2012, lung cancer worldwide was the most common cancer in men and the third most common cancer in women.34 In the U.S., lung cancer occurs in an estimated 225,000 patients every year and is responsible for over 160,000 deaths.35 There are many risk factors for cancer, the most notorious of which is smoking.

A patient with a primary lung cancer can easily be confused with pneumonia due to the similarity of symptoms (Table 6).  What is key in primary lung cancer is these symptoms have a more insidious onset than the relatively more acute onset of symptoms in pneumonia. Furthermore, these symptoms will progress over time and may include symptoms less commonly seen in pneumonia (weight loss, bone pain, or voice hoarseness).

Table 6.  Symptoms of lung cancer at presentation.  (Modified from: Hyde, L, Hyde, CI. Chest 1974; 65:299-306 and Chute CG, et al. Cancer 1985; 56:2107-2111).

Symptom Percent of Patients Affected
Cough 45-74%
Weight Loss 46-68%
Dyspnea 37-58%
Chest pain 27-49%
Hemoptysis 27-29%
Bone pain 20-21%
Hoarseness 8-18%


The chest x-ray in patients with lung cancer varies depending on the type and stage of cancer.  The chest x-ray in patients with a primary lung cancer may display a solitary nodule, an interstitial infiltrate, or may be normal.2

Non-small cell lung cancer.  (Image from

 If considering a primary lung malignancy in a patient whose presentation is consistent with pneumonia, more definitive imaging including CT of the chest may be warranted. Discussion with the oncology service is advised.

Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome (ARDS) is acute, diffuse, inflammatory lung injury that carries high rates of morbidity, ranging from 26 to 58%.35,36 ARDS stems from diffuse alveolar damage and lung capillary endothelial injury, leading to increased capillary permeability and pulmonary edema.1 This disease manifests with respiratory distress, with patients often displaying tachycardia, tachypnea, hypoxemia, and dyspnea.37 Arterial blood gas analysis shows hypoxemia in addition to acute respiratory alkalosis and increased alveolar-arterial oxygen gradient (though ABG is usually not required in the ED).  A chest radiograph will typically reveal bilateral alveolar infiltrates, and classically, no cardiomegaly is seen.2

Chest radiograph depicting bilateral lung opacities in a patient with ARDS.  (Image from

When considering ARDS, several factors come into play.  The diagnosis of ARDS is complicated, as the most common cause or ARDS is sepsis. Thus, ARDS may result from a prior pneumonia leading to sepsis. The patient with ARDS will appear sick and will likely require high levels of FiO2 or positive pressure ventilation if not intubated, while the severity of pneumonia varies greatly based on the patient and infectious microbe.  Risk factors such as sepsis, aspiration, and multiple transfusions are commonly seen with ARDS.38 Other risk factors for ARDS include alcohol abuse, trauma, and smoke inhalation.  On physical exam, patients with ARDS often have diffuse crackles on auscultation of the lungs.  The chest x-ray shows more diffuse involvement than would be expected in a patient with pneumonia.2 US will reveal b-lines in multiple lung fields.  If concerned for ARDS, be ready to intubate the patient for clinical course/oxygenation and admit to the ICU.

Case resolution

As you return to this 52-year-old gentleman’s room with his prescription for antibiotics, you notice that he remains tachycardic, tachypneic, and hypoxic (HR 105, RR 24, SpO2 93%).  You perform a more complete review of systems and find out this gentleman has been experiencing pain in his right calf over the past week after returning from an overseas business trip.  On exam, you notice that his right lower extremity is slightly edematous compared to the left.  In addition to pneumonia, you decide to begin to work up this gentleman for a possible deep venous thrombosis and pulmonary embolism.  A chest CT reveals a large right-sided segmental PE.


Many potentially deadly conditions can be confused for pneumonia.  Unfortunately, many of these conditions are not considered until the patient fails to improve after treatment with antibiotics.  The following should be considered in a patient presenting with signs of pneumonia:

  • Pulmonary embolism: suspect when a patient has signs/symptoms of PE including shortness of breath with pleuritic chest pain, tachypnea, and leg swelling in the setting of risk factors for DVT/PE.
  • Endocarditis/septic emboli: consider in febrile patients with risk factors including history of IV drug use, poor dentition, structural heart disease, or the presence of a prosthetic valve. Septic emboli leading to pulmonary infarction can present with multiple infiltrates on chest x-ray.
  • Systemic Lupus Erythematosus: pulmonary involvement is very common in lupus. Patients with SLE and lung involvement must always be evaluated for infection, and diffuse alveolar hemorrhage is a life-threatening complication.
  • Heart Failure exacerbation: suspect in a patient with cardiac history and signs/symptoms of heart failure (orthopnea, PND, peripheral edema, elevated jugular venous distension, etc.).
  • Tuberculosis: suspect in patients with risk factors for TB including substance abuse, malnutrition, systemic diseases, immunocompromise, or recent foreign travel.
  • Lung cancer: suspect in patients with insidious onset of symptoms and in patients complaining of constitutional symptoms such as weight loss or fatigue.
  • Acute Respiratory Distress Syndrome: suspect in toxic-appearing patients with white-out on chest x-ray who require high levels of FiO2 or positive pressure ventilation.


References/Further Reading

  1. Marx JA. Rosen’s Emergency Medicine:  Concepts and Clinical Practice.  Saunders 2014.  8th
  2. Maloney G, Anderson E, Yealy DM. Tintinalli’s Emergency Medicine:  A Comprehensive Study Guide.  Chapter 65:  Pneumonia and Pulmonary Infiltrates.  McGraw Hill Professional 2016.   8th
  3. Fine MJ, Stone RA, Singer DE et al. Processes and outcomes of care for patients with community-acquired pneumonia:  results from the Pneumonia Patient Outcomes Research Team (PORT) cohort study.  Arch Intern Med 159:  970, 1999.
  4. Bartlett JG. Diagnostic approach to community-acquired pneumonia in adults.  UpToDate.  Jan 2016.
  5. Hu QJ, Shen YC, Jia LQ, et al. Diagnostic performance of lung ultrasound in the diagnosis of pneumonia: a bivariate meta-analysis. Int J Clin Exp Med. 2014;7(1):115-21. [pubmed]
  6. Chavez MA, Shams N, Ellington LE, et al. Lung ultrasound for the diagnosis of pneumonia in adults: a systematic review and meta-analysis. Respir Res. 2014;15:50. [pubmed]
  7. Thompson BT. Overview of acute pulmonary embolism in adults.  UpToDate.  Jan 2016.
  8. Thompson BT. Clinical presentation, evaluation, and diagnosis of the adult with suspected acute pulmonary embolism.  UpToDate.  Jan 2016.
  9. Stein PD, Beemath A, Matta F, et al. Clinical characteristics of patients with acute pulmonary embolism:  data from PIOPED II.  Am J Med.  2007;120(10):871.
  10. Perera, T. Mailhot, D. Riley, and D. Mandavia, “The RUSH exam: rapid ultrasound in Shock in the evaluation of the critically ill,” Emergency Medicine Clinics of North America, vol. 28, no. 1, pp. 29–56, 2010.
  11. P. Borloz, W. J. Frohna, C. A. Phillips, and M. S. Antonis, “Emergency department focused bedside echocardiography in massive pulmonary embolism,” Journal of Emergency Medicine, vol. 41, no. 6, pp. 658–660, 2011.
  12. Madan and C. Schwartz, “Echocardiographic visualization of acute pulmonary embolus and thrombolysis in the ED,” American Journal of Emergency Medicine, vol. 22, no. 4, pp. 294–300, 2004.
  13. Murdoch DR, Corey GR, Hoen B. Clinical Presentation, Etiology and Outcome of Infective Endocarditis in the 21st Century:  The International Collaboration on Endocarditis-Prospective Cohort Study.  Arch Intern Med.  2009 Mar 9;169(5):463-473.
  14. Sexton DJ. Epidemiology, risk factors, and microbiology of infective endocarditis.  UpToDate.  Jan 2016.
  15. Hill EE, Herijgers P, Claus P. Infective endocarditis:  changing epidemiology and predictors of 6-month mortality:  a prospective cohort study.  Eur Heart J.  2007;28(2):196.
  16. Cantrell M, Yoshikawa TT. Infective endocarditis in the aging patient.  Gerontology.  1984;30(5):316.
  17. Castillo FJ, Anguita M, Castillo JC, et al. Changes in the Clinical Profile, Epidemiology and Prognosis of Left-sided Native-valve Infective Endocarditis Without Predisposing Heart Conditions.  Rev Esp Cardiol (Engl Ed).  2015 May;68(5):445-8.  Epub 2015 Mar 16.
  18. Spelman D, Sexton DJ. Complications and outcome of infective endocarditis.  UpToDate.  Jan 2016.
  19. Steckelberg JM, Murphy JG, Ballard D, et al. Emboli in infective endocarditis:  the prognostic value of echocardiography.  Ann Intern Med.  1991;114(8):635.
  20. Dellaripa PF, Danoff Sonye. Pulmonary manifestations of systemic lupus erythematosus in adults.  UpToDate.  Jan 2016.
  21. King Jr. TE, Kim EJ, Kinder BW. Connective tissue diseases:  In:  Interstitial Lung Disease, 5th, Schwartz MI, King TE Jr. (Eds), People’s Medical Publishing House-USA, Shelton, CT 2011.
  22. Matthay RA, Schwarz MI, Petty TL, et al. Pulmonary manifestations of systemic lupus erythematosus:  review of twelve cases of acute lupus pneumonitis.  Medicine (Baltimore).  1975;54(5):397.
  23. Wiedemann HP, Matthay RA. Pulmonary manifestations of systemic lupus erythematosus.  J Thorac Imaging.  1992;7(2):1.
  24. Zamora MR, Warner ML, Tuder R, Schwarz MI. Diffuse alveolar hemorrhage and systemic lupus erythematosus.  Clinical presentation, histology, survival, and outcome.  Medicine (Baltimore).  1997;76(3):192. 
  25. Andrade C, Mendonca T, Farinha F, et al. Alveolar hemorrhage in systemic lupus erythematosus:  a cohort review.  Lupus.  2016 Jan;25(1):75-85.  Epub 2015 Sep 18.
  26. Collard HR, Schwarz MI. Diffuse alveolar hemorrhage. Clin Chest Med 2004;25:583–592, vii.
  27. Borlaug BA. Clinical manifestations and diagnosis of heart failure with preserved ejection fraction.  UpToDate.  Jan 2016.
  28. Ang S-H, Andrus P. Lung Ultrasound in the Management of Acute Decompensated Heart Failure. Current Cardiology Reviews. 2012;8(2):123-136.
  29. Pozniak A. Clinical manifestations and complications of pulmonary tuberculosis.  UpToDate.  Jan 2016.
  30. Barnes PF, et al: Chest roentgenogram in pulmonary TB:  new data on an old test.  94:316, 1988.
  31. Oeltmann JE, Kammerer JS, Pevzner ES, Moonan PK. Tuberculosis and substance abuse in the United States, 1997-2006.  Arch Intern Med.  2009;169(2):189.
  32. Horsburgh CR. Epidemiology of tuberculosis.  UpToDate.  Jan 2016.
  33. World Health Organization. Global Tuberculosis Report 2014.
  34. World Cancer Research Fund International. Worldwide Data.
  35. MacCallum NS, Evans TW. Epidemiology of acute lung injury.  Curr Opin Crit Care.  2005;11(1):43.
  36. Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury.  N Engl J Med.  2005;353(16):1685.
  37. Hansen-Flaschen J, Siegel MD. Acute respiratory distress syndrome:  Clinical features and diagnosis in adults.  UpToDate.  Jan 2016.
  38. Siegel MD. Acute respiratory distress syndrome:  Epidemiology, pathophysiology, pathology, and etiology in adults.  UpToDate.  Jan 2016.

Ultrasound for Confirmation of Endotracheal Tube Placement During CPR

Stephen Alerhand MD (Emergency Medicine Resident Physician, Icahn School of Medicine at Mount Sinai (@SAlerhand), Edited by Alex Koyfman MD (@EMHighAK)


There are several ways to confirm correct placement of the endotracheal tube after intubation:

  • Visualizing the tube passing through the vocal cords
  • Fog within the endotracheal tube on expiration
  • Auscultating bilateral breath sounds, absence of sounds in the epigastrum, and thoracic movement with respiration
  • Endotracheal tube palpation in the neck or suprasternal notch
  • Pulse oximetry
  • Qualitative and/or quantitative end-tidal CO2 measurement

Quantitative end-tidal CO2 measurement is considered the best method at present to evaluate correct placement of the ET tube. It indirectly reflects real-time changes in CO2 production in the tissues, along with the circulatory system’s delivery of that CO2 to the lungs.

However, this method is less accurate in patients with decreased circulatory perfusion such as those in cardiac arrest, recent return of spontaneous circulation (ROSC), or other low-flow states. Simply put, the delivery of carbon dioxide to the lungs may not be sufficient. This issue may also present in: obese patients, those with air in the esophagus or stomach, and those with copious amounts of gastric or pulmonary secretions.

Let us present the following scenario in which all of the above confirmatory methods are utilized, but where their accuracy may be suboptimal. Then an additional confirmational adjunct for precisely these situations will be introduced as a useful tool in trained hands.


The red phone arrives with a notification alert: “68 year-old male in cardiac arrest, ACLS performed for 15 minutes, ETA 5 minutes.”

The team leader assigns you to the airway role, and 5 minutes later the EMS team wheels the patient into the room.

The first things you notice: The patient is obese, chest compressions are in progress, and the patient has been intubated in the field. You next notice that there are some dark gastric secretions pooled up around the endotracheal tube.

Sequence of Actions

You take the following actions (as written above):

  • You attach a quantitative end-tidal CO2 connector between the ETT and the BVM (or ventilator)
    •      However, as described above, the low-flow state of cardiac arrest limits this method’s reliability.
  • You attach the pulse oximetry probe to the patient’s finger.
    •      However, you are not seeing a good waveform on the monitor, thus the number alongside the waveform is unreliable.
  • You attach a qualitative colormetric end-tidal CO2 device between the ETT and the BVM (or ventilator).
    •      However, the device may turn from purple to yellow (end-tidal CO2 >2%) when contaminated by gastric secretions or other acidic substances, and may not function when clogged by secretions.
  • You try using the video laryngscope to confirm correct placement of the ETT through the vocal cords.
    •      However, the patient’s body habitus and gastric secretions may this difficult.
  • You look for fog within the ETT.
    •      However, the gastric secretions make this unreliable.
  • You try to auscultate bilateral breath sounds, absence of sounds in the epigastrum, and thoracic movement with respiration.
    •      However, this is also made unreliable by the patient’s body habitus, as well as by the crowd of noisy providers circled around the patient performing chest compressions, attaching monitor leads, acquiring peripheral or central access, and/or administering medications.
  • You try to feel for the ETT in the neck or suprasternal notch.
    •      However, the patient’s large neck makes this unreliable.

The team leader asks: “ Did you confirm the airway?”

You start to mumble and bumble, when suddenly your Ultrasound Fellowship-trained attending grabs the linear probe, sticks it on the patient’s neck, and within 15 seconds declares that the correct ETT placement is confirmed.

How did he do that? The attending states that the method is by no means perfect and certainly technically difficult, but that with enough practice and repetition he has been able to harness US as a helpful tool for similar situations as the one presented.

Using Ultrasound to Confirm Proper ETT Placement
  1. Gently place the high-frequency linear probe just superior to the suprasternal notch in the transverse plane.
  1. The trachea will appear as a hyperechoic curvilinear structure with shadowing. A comet tail, or reverberation rings, appear deep to that structure.

ACEP trachea
Chao A, Gharahbaghian L.

  1. The esophagus will appear distally and to the right. It has a hyperechoic wall and hypoechoic center.
  1. Tracheal intubation: Visualize the second hyperechoic curvilenar structure within the trachea. You can also gently shake the ETT and visualize tracheal movement on the screen. Using Doppler, a color ray will also appear within the trachea.

ETT confirmation pic

  1. Esophageal intubation: The “double tract sign” (in which there seemingly appears to be two tracheas) indicates esophageal intubation.

ACEP double tract
Chao A, Gharahbaghian L.

  1. Pitfall: If the esophagus is anatomically located just posterior to the trachea, then the trachea’s shadowing may obscure an esophageal intubation.


Supporting Literature

Chou EH, Dickman E, Tsou PY, et al. Ultrasonography for confirmation of endotracheal tube placement: a systematic review and meta-analysis. Resuscitation. 2015 May;90:97-103.
Objective: To summarize evidence of diagnostic value of US for assessment of ETT placement in adults.
Design: Meta-analysis
Results: 12 studies. In detecting esophageal intubation, pooled sensitivity 0.93 (95% CI 0.86-0.96) and specificity 0.97 (95% CI 0.95-0.98).
Conclusions: Current evidence shows US has high diagnostic value for identifying esophageal intubation, especially when capnography may be unavailable.

Chou HC, Chong KM, Sim SS, et al. Real-time ultrasonography for confirmation of endotracheal tube placement during cardiopulmonary resuscitation. Resuscitation. 2013 Dec;84(12): 1708-12.
Objective: To evaluate accuracy of tracheal US for assessing ETT position during CPR.
Design: Prospective observational study. Gold standard of correct ETI was combination of clinical auscultation and quantitative waveform capnography.
Results: n=89 patients. 7 had esophageal intubation. Sensitivity of tracheal ultrasonography 100% (95% CI 94.4-100), specificity 85.7% (42.0-99.2), positive predictive value 98.8% (92.5-99.0), negative predictive value 100% (54.7-100).
Conclusions: Real-time tracheal US is accurate for identifying ETT position during CPR without need for interruption of chest compressions. Tracheal US in resuscitation may serve as powerful adjunct in trained hands.

Das SK, Choupoo NS, Haldar R, Lakhar A. Transtracheal ultrasound for verification of endotracheal tube placement: a systematic review and meta-analysis. Can J Anaesth. 2015 Apr;62(4):413-23.
Objective: To evaluate diagnostic accuracy of transtracheal US in detecting ETI.
Design: Meta-analysis
Results: 11 studies, 969 intubations. Pooled sensitivity 0.98 (95% CI 0.97-0.99), specificity 0.98 (95% CI 0.95-0.99). In emergency situations, those values were 0.98 (95% CI 0.97-0.99) and 0.94 (95% CI 0.86-0.98).
Conclusions: Transtracheal US is useful for confirming ETI with acceptable sensitivity/specificity. Can be used in emergency situations as preliminary test before final confirmation by capnography.

Gottlieb M, Bailitz JM, Christian E. et al. Accuracy of novel ultrasound technique for confirmation of endotracheal intubation by expert and novice emergency physicians. West J Emerg Med. 2014 Nov;15(7):834-9.
Objective: To evaluate the accuracy of a novel, simplified, 4-step (4S) technique (see article for steps)
Design: Blind, randomized trial of 4S technique sing adult cadaver, randomized to tracheal or esophageal intubation. Three experts and 45 residents performed 150 scans.
Results: Experts had sensitivity 100% (95% CI 72-100) and specificity 100% (77-100) on thin cadavers, 93% (66-100) and 100% (75-100) on obese cadavers. Residents had sensitivity 91% (69-98) and specificity 96% (76-100) on thin cadavers, 100% (82-100) and 48% (27-69) on obese cadavers. Overall mean time to detection of 17 seconds (13-20) for experts and 29 seconds (25-33) for residents. Statistically significant decrease in specificity on obese cadavers between residents and experts, as well as increased time to detection for residents.
Conclusions: The simplified 4S technique was accurate and rapid for US experts. Among residents, the 4S technique was accurate in thin cadavers, less so in obese cadavers.

Abbasi S, Farsi D, Zare MA, et al. Direct ultrasound methods: a confirmatory technique for proper endotracheal intubation in the emergency department. Eur J Emerg Med. 2015 Feb;22(1):10-6.
Objective: To assess diagnostic accuracy of US for detection of proper ETT placement.
Design: Prospective study. Two phases: 1) dynamic: as intubation being performed 2) static: after intubation.
Results: n=60 patients. For dynamic phase, sensitivity for determining correct ETI 98.1% (95% CI 88.8-99.9), specificity 99% (51.6-100), positive predictive value 100% (91.5-100), negative predictive value 85.7% (42-99.2%). For static phase, all testing characteristics were 100%.
Conclusions: Acceptable sensitivity, specificity, positive predictive value, and negative predictive value for prediction of tracheal ETT placement with use of dynamic and static US.

Chenkin J, McCartney CJ, Jelic T, et al.. Defining the learning curve of point-of-care ultrasound for confirming endotracheal tube placement by emergency physicians. Crit Ultrasound J. 2015 Dec 7(1):14.
Objective: To determine amount of practice required by ED docs to develop proficiency at interpreting clips of tracheal and esophageal intubations.
Methods: Physicians and residents completed a baseline interpretation test, then a 10-minute tutorial. They then took 10-question tests.
Results: n=66. Means core on baseline test: 42.9% (SD 32.7%). After tutorial, 90.9% answered all ten questions correctly after one attempt, 100% after two attempts. Sensitivity of 98.3% and specificity of 100% for detecting correct ETT location.
Conclusions: After brief online tutorial and only two practice attempts, physicians quickly and accurately interpreted US intubation clips of esophageal and endotracheal intubations.


Additional References

Chao A, Gharahbaghian L.

Galvagno , SM. Kodali, BS. Capnography educational website. Use of Capnography in Emergency Medicine and Prehospital Critical Care.

O’Conner RE, Swor RA. Verification of Endotracheal Tube Placement Following Intubation. National Association of EMS Physicians, 1999.—Practice-Management/Verification-of-Endotracheal-Tube-Placement/

Ultrasound for Optic Nerve Sheath Diameter

Author: Stephen Alerhand, MD (EM Resident Physician, Icahn School of Medicine at Mount Sinai) (@SAlerhand) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)


A 21 year-old heavy-set female with no prior medical history presents to your emergency department complaining of dull intermittent frontal headaches for the past 3 months. These headaches have no identified triggers, aggravators, or alleviators. They occur about three times daily, irrespective of position or time of day. They are associated with occasional nausea and transient binocular vision loss. She denies fever/chills, chest pain/shortness of breath, diarrhea, syncope, weakness. She has taken Ibuprofen 400 mg for these headaches but the medicine is bringing her less relief as time goes on. No other family members at home have had similar headaches.

Vital signs are within normal limits.

On exam, the patient is very well appearing without any visual deficits or other neurological findings.

The resident does not believe that this patient’s headache constitutes one of the acute dangerous headaches that must be ruled out immediately in the ED. Even if the resident had ordered a CT scan, he/she would have found it to be normal. In all likelihood, these headaches simply represent migraines that are not responding to Motrin anymore.  That being said, the resident tells the attending, could these headaches possibly represent pseudotumor cerebri… or benign intracranial hypertension… or idiopathic intracranial hypertension…or whatever they are calling it these days? Should he/she perform an LP and go down that path?


Blaivas M, Theodoro D, Sierzenski PR. Elevated intracranial pressure detected by bedside emergency ultrasonography of the optic nerve sheath. Acad Emerg Med 2003 Apr;10(4):376-81.

Type of Study: prospective blinded observational
Objective: to determine whether ONSD could accurately predict elevated intracranial pressure (EICP)
Results: n=35. 14 had EICP, all correctly predicted by ONSD >5 mm. Mean ONSD with EICP 6.27 mm versus 4.42 mm w/o EICP (p=0.001).
Conclusion: Bedside US may be useful for diagnosis of EICP

Irazuzta JE, Brown ME, Akhtar J. Bedside Optic Nerve Sheath Diameter Assessment in the Identification of Increased Intracranial Pressure in Suspected Idiopathic Intracranial Hypertension. Pediatr Neurol. 2015 Aug 28.

Type of Study: single-center, prospective, rater-blinded
Objective: to determine whether bedside OUS could identify elevated intracranial hypertension in patients aged 12-18 suspected of having idiopathic intracranial hypertension
Results: 13 patients in study, 10 of whom had elevated intracranial pressure. ONSD was able to predict or rule it out in all 13 patients.
Conclusion: Non-invasive assessment of ONSD could help identify patients with elevated intracranial pressure when idiopathic intracranial hypertension is suspected

Tayal VS, Neulander M, Norton HJ, et al. Emergency department sonographic measurement of optic nerve sheath diameter to detect findings of increased intracranial pressure in adult head injury patients. Ann Emerg Med. 2007 Apr;49(4):508-514.

Type of Study: prospective blinded observational
Objective: to determine whether bedside OUS of ONSD can accurately predict CT findings of elevated intracranial pressure in adult head injury patients
Results: n=59, 8 w/ ONSD > 5 mm that also had elevated intracranial pressure. Sensitivity 100% (68%-100%), specificity 63% (50%-76%).
Conclusion: Bedside ONSD has potential as sensitive screening test for elevated intracranial pressure in adult head injury.

Kimberly HH, Shah S, Marill K, Noble V. Correlation of optic nerve sheath diameter with direct measurement of intracranial pressure. Acad Emerg Med. 2008 Feb;15(2):201-4.

Type of Study: prospective blinded observational
Objective: to evaluate association between ONSD and ICP and to validate 5 mm threshold
Results: 38 OUS on 15 individual patients. ONSD > 5 mm detected ICP > 20 mmHg w/ sensitivity of 88% (47%-99%) and specificity 93% (78%-99%).
Conclusion: Study directly correlates ventriculostomy measurements of ICP w/ US ONSD measurements. Provides further support for use of ONSD as a noninvasive test for elevated ICP.

Dubourg J, Javouhey E, Geeraerts T, Messerer M, Kassai B. Ultrasonography of optic nerve sheath diameter for detection of raised intracranial pressure: a systematic review and meta-analysis. Intensive Care Med. 2011 Jul;37(7):1059-68.

Type of Study: meta-analysis
Objective: to evaluate diagnostic accuracy of US ONSD for assessment of intracranial hypertension
Results: n=231. Pooled sensitivity 0.90 (0.80-0.95), pooled specificity 0.85 (0.73-0.93)
Conclusion: ONSD showed good accuracy for diagnosing intracranial hypertension.

Karami M, Shirazinejad S, Shaygannejad V, et al. Transocular Doppler and optic nerve sheath diameter monitoring to detect intracranial hypertension. Adv Biomed Res. 2005 Oct 22;4:231.

Type of Study: cross-sectional case-control
Objective: To determine whether transocular Doppler and ONSD monitoring could reliably identify increases in ICP
Results: mean ONSD of 4.8 mm in patient with raised ICP vs 3.2 mm in healthy volunteers
Conclusion: US as alternative safe technique to invasive ICP methods


How to Perform the Ultrasound
  1. Use the high-frequency linear transducer.
  2. Cover the closed eyelids with a tegaderm and apply ultrasound gel.
  3. Have the patient stare straight ahead without squinting.
  4. Adjust the depth so that the eye fits within the entire screen.

eye in screen

  1. Measure the optic nerve sheath diameter at a distance 3 mm posterior to the globe, where the US contrast is greatest.

ONSD diagram





  1. Measure the ONSD twice. Determine the average.
  2. An ONSD > 5 mm suggests elevated intracranial pressure.

The optic nerve sheath contains fluid in which sits the optic nerve. The sheath attaches to the posterior aspect of the globe and is contiguous with the subarachnoid space. Accordingly, the ONSD can act as a surrogate for intracranial pressure.


Other References

Ultrasound for Appendicitis

Ultrasound for Appendicitis

by Stephen Alerhand MD (@SAlerhand)
EM Resident Physician, Icahn School of Medicine at Mount Sinai
Edited by Alex Koyfman MD (@EMHighAK)


A 27 year-old G1P1 female with no past medical history presents to the emergency department on a busy late-night shift complaining of lower abdominal pain since the morning. The pain is dull and intermittent, and though she cannot identify any aggravators or alleviators, the pain has steadily progressed over the course of the day to its current severe state. She has not eaten anything since the morning. She denies fever/chills, nausea/vomiting/diarrhea/constipation, dysuria/hematuria/discharge. Her last menstrual period was 3 weeks ago. She denies recent sexual intercourse.

Vital signs are within normal limits.

On exam, the patient moves within the stretcher with discomfort and is hunched over. Her abdomen is thin, soft, with tenderness to palpation in the right lower quadrant. Psoas sign is positive.

Note about Lower Abdominal Pain in Female Patients

You are concerned for appendicitis, though in most females with lower abdominal pain, the work-up is not complete without consideration for pelvic complaints such as pelvic inflammatory disease or ovarian torsion. For example, you may progress as far down the appendicitis pathway as you want, but you will never find the profuse yellow-green discharge and inflamed cervical os if you do not perform the pelvic – and by that time, the patient will have been sitting in the ED for several hours and gotten an expensive, radiating, non-diagnostic CT scan as well. Therefore, as part of the work-up, you perform a pelvic exam and find it unremarkable.

Urine pregnancy test is negative.
Urine dip shows no leukocytes or nitrates.
Basic labs including WBC are unremarkable.

Further Thought Process

At this point, given the initial RLQ tenderness, appendicitis sits atop your differential like it did at the initial presentation. Though some Surgical teams take presumed appendicitis patients to the operating room based on exam alone, this is not common. A diagnostic CT scan is called for most of the time.

These are the obstacles in your mind at this time:

  • Your ED is extremely crowded on this Monday after the holiday weekend.
  • Your team is working hard to manage all of the patients.
  • The patients due for the CT scanner are backed up, not only because of the large queue but because there is less staffing late at night.
  • On that matter itself, the young female has already expressed concern about the effects of radiation on her body.
  • The possible appendicitis patient in front of you has already required multiple rounds of pain medicine, has now spiked a fever, and is looking worse than when she initially came in.
  • You feel like the patient has an inflamed appendix, possibly even rupture. Knowing that the definite therapy is surgical removal, you need to figure out what steps are needed to go from Point A (presumed appendicitis) to Point B (laparoscopic appendectomy).


At that moment, an ultrasound fellowship-trained attending coming in for shift takes sign-out and prints out a few papers for you to scan briefly.

Mallin M, Craven P, Ockerse P, et al. Diagnosis of appendicitis by bedside ultrasound in the ED. Am J Emerg Med. 2015 Mar;33(3):430-2.
Study Design: Prospectively collected US data (by trained residents with attending supervision) for 97 cases of suspected appendicitis, 34 of which were confirmed by surgical or pathology report. Compared with review by fellowship-trained physician.
Results: 67% (24/34) sensitivity, 98% (23/24) specificity. 12% reduction in CT utilization.
Conclusion: Bedside US may be an appropriate initial test to eval patient with suspected appendicitis.

Fox JC, Solley M, Anderson CL, et al. Prospective evaluation of emergency physician performed bedside ultrasound to detect appendicitis. Eur J Emerg Med. 2008 Apr;15(2):80-5.
Study Design: Prospectively enrolled 132 patients with suspected appendicitis. Received work-up as deemed appropriate by attending.
Results: Sensitivity 65%, specificity 90%, PPV 84%, NPV 76%.
Conclusion: Insufficient evidence to support POC US use to rule out appendicitis. However, the high specificity may support US use to rule in the diagnosis.

Elikashvili I, Tay E, Tsung JW. The effect of point-of-care ultrasonography on emergency department length of stay and computed tomography utilization in children with suspected appendicitis. Acad Emerg Med. 2014 Feb;21(2):163-170.
Study Design: Prospective observational convenience sample of children with suspected appendicitis. Of 150 enrolled, 50 had appendicitis (33.3%).
Results: Those who had POC US had a significantly decreased ED length-of-stay compared with those requiring radiology US or CT scan. CT rate decreased during the study from 44 to 27%. For POC US, sensitivity 60% and specificity 94%. For radiology US, sensitivity 63% and specificity 99%. For CT, sensitivity 83% and specificity 98%.
Conclusion: May be feasible to reduce ED length-of-stay and avoid CT scan when using POC US in children with suspected appendicitis. High specificity to rule in appendicitis, similar to radiology US. Safe to use prior to radiology US, as there were no missed cases or negative laparoscopies.

Benefits of Ultrasound for Appendicitis

  • Avoidance of ionizing radiation
  • More readily available and cheaper than CT
  • Quicker than CT (which in many institutions requires a 2+ hour contrast drinking period, which patients often do not tolerate anyway)
  • Faster diagnostic time for Surgeons, who can take patient to OR


  • Lesser diagnostic capability on adults and larger children
  • Excellent specificity to “rule in”, but only moderate sensitivity to “rule out”, thus the patient may end up needing a CT anyway
  • Convincing your hospital’s Surgical team to “buy in” to the idea of appendicitis diagnosis via ultrasound
  • Training emergency physicians in bedside ultrasound for appendicitis rather than having it be performed by the radiology tech or resident
How to Perform the Ultrasound

Courtesy of Ee Tay, MD
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