Tag Archives: CORE EM

EM@3AM – Acute APAP Toxicity

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 14 year-old male with a history of major depressive disorder presents to the emergency department following a toxic ingestion. The patient reports consumption of approximately 40 extra strength Tylenol caplets (500mg each), two hours prior to arrival. The patient is nauseated and covered in non-bloody gastric contents. Upon initial examination: GCS 15. VS: HR 132, BP 128/84, RR 18, SpO2 98% on room air.

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?

Answer: Acute Acetaminophen Toxicity1-3

  • Recommended dosing: 3-4g QD; toxic dose: 150mg/kg
  • Presentation varies according to stage of toxicity:
    • Stage 1 (0.5-24 hrs): mild nausea, emesis, weakness
    • Stage 2 (24-72 hrs): hepatotoxicity +/- nephrotoxicity => RUQ abdominal pain
    • Stage 3 (72-96 hrs): hepatotoxicity peaks => nausea, vomiting, jaundice, coagulopathy
    • Stage 4 (4 days -2 wks): recovery or decompensation resulting in death
  • Evaluation:
    • Use the Rumack-Matthew nomogram for single ingestions occurring <24 hours prior to arrival:
      • Obtain AST level at 4 hours s/p ingestion: utilize nomogram to determine the appropriateness of N-acetylcysteine (NAC) treatment
    • If the time of ingestion is unknown:
      • Obtain AST level and a serum acetaminophen level => if AST is elevated or serum acetaminophen concentration >10mcg/mL = initiate NAC2,3
  • Treatment:
    • If patient presents within one hour of toxic ingestion, consider NG lavage if no contraindications.
    • NAC Loading dose: 150 mg/kg IV (max 15g) infused over 1 hr or 140 mg/kg PO
  • Pearls:
    • Rumack-Matthew nomogram should not be employed in the setting of unknown time of ingestion or chronic acetaminophen therapy.
    • NAC is most effective if initiated within 8 hours of acetaminophen ingestion.
    • Evaluate for co-ingestions: serum salicylate, serum ETOH; calculate an anion gap and an osmolar gap as appropriate. Consider UDS.
    • End point of NAC treatment: AST <100 U/L and acetaminophen <10mcg/mL or if extended therapy required: normalization of INR, resolution of encephalopathy, and decreasing AST (<1,000 U/L).3


  1. Tintinalli J, Kelen G, Stapczynski J, Ma O, Cline D, et al. Tintinalli’s Emergency Medicine. 8th ed. New York: McGraw-Hill; 2016. Chapter 190, Acetaminophen.
  2. Heard K. Acetylcysteine for acetaminophen poisoning. N Engl J Med. 2008; 359(3):285-292.
  3. Mottram A, Kumar A. Focus On: Acetaminophen Toxicity and Treatment. American College of Emergency Physicians Clinical and Practice Management. Available from: https://www.acep.org/Clinical—Practice-Management/Focus-On–Acetaminophen-Toxicity-and-Treatment/

EM@3AM – Abdominal Aortic Aneurysm

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 67 year-old patient with a history of smoking, hypertension, and hyperlipidemia presents for the evaluation of sudden onset, severe, right flank pain. ROS is remarkable only for right thigh pain and weakness of two weeks duration. Triage VS: HR 114, BP 101/78, RR 22, SpO2 92% on room air.

What is the patient’s diagnosis? What’s the next step in your evaluation and treatment?

Answer: Abdominal Aortic Aneurysm1-3

  • Risk Factors: smoking, hypertension, family history, atherosclerosis
  • Presentation: sudden onset, severe pain radiating to the back/flank +/- pulsatile abdominal mass, +/- hypotension
  • Unstable or Symptomatic:
    • Emergent vascular/general surgery consult
    • Bedside ultrasound
    • Type and screen 6-10U pRBCs
  • Stable:
    • CT abdomen/pelvis with IV contrast
  • Asymptomatic:
    • Aortic diameter > 3cm: requires follow-up for surveillance
    • Aortic diameter > 5cm (female) or >5 cm (male): surgical candidate
  • Pearls:
    • Consider in patients presenting with femoral neuropathy: indicative of a ruptured aneurysm with enlarging hematoma.2-3
    • Consider in the differential of the elderly syncope patient.


  1. Tintinalli J, Kelen G, Stapczynski J, Ma O, Cline D, et al. Tintinalli’s Emergency Medicine. 8th ed. New York: McGraw-Hill; 2016. Chapter 60, Aneurysmal Disease.
  2. Haddad F, Hatrick N, Shanahan D. An unusual presentation of a ruptured abdominal aortic aneurysm. J Accid Emerg Med. 1995; 12(3): 220-221.
  3. Razzuk M, Linton R, Darling R. Femoral neuropathy secondary to ruptured abdominal aortic aneurysms with false aneurysms. JAMA. 1967; 201(11): 817-820.

Penetrating Wounds in the Emergency Department: Considerations for Management

Authors: Darren Cuthbert, MD, MPH (EM Resident Physician at Rutgers Robert Wood Johnson University Hospital) and Joshua Bucher, MD (EM Attending Physician, Rutgers Robert Wood Johnson University Hospital) // Edited by: Erica Simon, DO, MHA (@E_M_Simon) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Emergency physicians encounter penetrating trauma on a regular basis. Beyond Advanced Trauma Life Support protocols, the assessment of a patient presenting with a penetrating wound requires careful thought and thorough examination. If it’s been a while since you’ve reviewed the basics, let’s take a minute to work through a few cases and discuss the pearls and pitfalls for the management of penetrating injuries.

Case I: A 69-year-old intoxicated male presents via EMS with what appears to be a penetrating wound to the neck. The patient is in no obvious distress. Speaking clearly to the room, he reports robbery by an unknown assailant, and a singular knife wound to his neck. Upon examination the patient has clear breath sounds bilaterally. His pulses are equal and bounding, and his initial vital signs are within normal limits. Secondary survey is remarkable for a 3 cm superficial laceration to the lateral aspect of the left neck, localized to zone II. There is no evidence of a rapidly expanding hematoma or pulsatile bleeding. There is no violation of the platysma.

Case II: A 20-year-old female presents to the trauma bay intubated, ventilated, and sedated. EMS details arriving on scene to find the young women diaphoretic, in respiratory distress, and covered in blood. While holding her chest, she reported her fiancé as having inflicted a knife wound to her upper abdomen. Given the patient’s appearance, EMS performed intubation on scene. Emergency room evaluation revealed diminished breath sounds on the left. Tube thoracostomy was performed and resuscitation initiated (2U PRBCs), however, the patient remained tachycardic and hypotensive.

Case III: During an early morning shift, you receive a phone call regarding a patient en route from scene: 32-year-old male involved in an altercation with a machete; intubated on scene secondary to altered mental status, wounds localized to the head and left upper extremity. Upon arrival, primary and secondary survey reveal a hemodynamically stable male with a 7 cm gaping wound localized to the posterior occiput (hemostatic), and a 3 cm gaping wound localized to the left forearm (hemostatic).

Case IV: A 21-year-old male presents to emergency triage with the chief complaint of injury to the neck and armpit. The patient, in no acute distress, speaks in clear sentences while detailing his recent fall over a nail gun, with subsequent gun discharge and trauma to his neck and chest. As he was “feeling fine,” the patient reports having removed two nails prior to seeking treatment. Emergency department primary and secondary surveys are significant for puncture wounds to the anterior midline neck (zone III), and left midaxillary line at the level of T4. Crepitus is noted on palpation of the left anterior chest wall.

Let’s move on to a review of the fundamentals before we address our cases:

 The Head

The initial approach to penetrating head wounds centers on attaining hemostasis. After addressing airway and breathing in a patient with head trauma, direct pressure should be applied to any actively bleeding wound as these injuries (specifically injuries to the highly vascular scalp) may result in hemodynamic instability.1 If hemostasis is not attained following the application of direct pressure, experts advise local wound infiltration with lidocaine with epinephrine, or the ligation, suture, or clamping of visibly damaged vessels.1

The majority of patients with head trauma will required advanced imaging to rule out intracranial pathology and foreign bodies.1-3  If no evidence of foreign body or underlying depressed skull fracture, irrigate wounds thoroughly, explore to the base, and remove any organic material.1,2 If the galea is involved, consideration should be made for repair as failure to do so may lead to frontalis muscle (facial expression) deficit.1


The Face

In patients with penetrating facial trauma, management of the airway if paramount. During assessment pay close attention to voice changes and tachypnea, and evaluate for cyanosis as these are precursors of airway compromise and respiratory demise.1 Facial fractures and active bleeding into the oropharynx increase the level of difficulty when performing endotracheal intubation, therefore equipment preparation is advised (bougie or surgical airway kit). CT scans of the head, facial bones, and neck may be required to evaluate for underlying injuries to the face and surrounding structures of the head and neck.1 For impaled objects, admission is often required for surgical intervention, monitoring, and administration of broad spectrum antibiotics.1


The Neck

Patients with trauma to the neck who present with signs of respiratory compromise, such stridor, expanding hematoma, pulsatile arterial bleeding, bruit/thrill, or altered mental status should be emergently intubated.1,2 After attaining a definitive airway, be prepared to address circulation: exsanguination is the most common cause of death in this patient population.1 Consider placing the patient with a penetrating neck injury in Trendelenburg position to prevent air embolism, while addressing all actively bleeding wounds with direct pressure (caution as excessive force may occlude the carotid arteries).1 Although randomized controlled trials in the setting of penetrating neck trauma are lacking, hemostatic dressings including QuikClot, Combat Gauze, and HemCon are commonly utilized in the emergency department and have demonstrated affectivity in the attainment of hemostasis in the setting of life threatening hemorrhage.1 Clamping vessels of the neck is not recommended in the emergency department, as anatomic structures are not easily identified upon visual inspection, and probing of a neck wound is not advised.1,3 If active bleeding continues despite direct pressure and the use of a hemostatic dressing, consider mechanical tamponade with a Foley catheter: insert the catheter into the tract of the wound and inflate until bleeding ceases.1,2 If these attempts are unsuccessful, emergent surgical intervention is required.

Definitive management of wounds to the neck historically centers upon patient presentation and zone classification (see Figure 1). Patients experiencing hemorrhagic shock, airway obstruction, air discharge from their wound, active pulsatile blood flow, massive hemoptysis, and uncontrolled bleeding (the hard signs of neck trauma), regardless of zone classification, require surgical evaluation and treatment.1 Hemodynamically unstable patients with Zone I injury may require ED thoracotomy.1

  • Zone I => sternal notch to cricoid cartilage
    • CT angiography, endoscopy, and bronchoscopy are indicated for evaluation.1,2,5
      • Note: suspect hemothorax or pneumothorax in patients presenting with dyspnea or absent breath sounds (20% of patients with penetrating neck trauma have a pneumothorax or hemothorax on further examination1).
    • Zone II => cricoid cartilage to angle of the mandible
      • Violation of the platysma mandates surgical exploration.1
    • Zone III => angle of the mandible and above
      • CT angiography and endoscopy indicated for evaluation.1,2,5

Note: Importantly, esophageal injuries occur in up to 9% of patients with penetrating neck trauma. As the sensitivity of CT in the detection of early esophageal injury is reported as 53%,6 patients with esophageal perforation most commonly present with sepsis secondary to mediastinitis.1 If concern for esophageal perforation exists: initiate antibiotic therapy, obtain surgical consultation, and perform esophagograpy with a water-soluble contrast material.1

Figure 1. Zones of the Neck

A cervical collar may prevent adequate examination and stabilization of the patient with a penetrating neck injury. As vertebral and spinal cord injuries are rare in the setting of isolated penetrating neck trauma, current guidelines recommend against c-spine immobilization.1,5


The Thorax

Thoracic trauma is the third leading cause of traumatic death in the United States.2 Injury to the heart or major vessels should be assumed in all patients presenting with injury localized to the “cardiac box” – i.e. the area bordered by the sternal notch, bilateral nipples, and xiphoid process. Patients experiencing penetrating trauma at this anatomic locale may suffer right ventricular injury (most anterior mediastinal structure) and subsequent tamponade or exsanguination.1-3 On examination, the most reliable sign of developing tamponade physiology is a narrowed pulse pressure (Beck’s Triad is present in < 10% of cases).1

The FAST is a useful tool for evaluating cardiac injury and tamponade. Patients with tamponade secondary to cardiac trauma may require emergent pericardiocentesis prior to operative repair.1 Individuals who are hemodynamically unstable or become pulseless upon ED evaluation frequently undergo emergent thoracotomy.1

 Penetrating chest trauma that violates the pleura may also result in a pneumothorax or hemothorax.1,2,4 Pneumothorax should be presumed in patients with significant subcutaneous emphysema on examination.1,2,7 An EFAST may quickly identify the presence of a pneumothorax or hemothorax.1 All patients with evidence of tension physiology (hypotension, hypoxia, absent breath sounds, and tracheal deviation) should undergo needle decompression and subsequent thoracostomy.1 All patients with an identified hemothorax require thoracostomy to avoid the sequelae of fibrosis and empyema.1 An immediate indication for surgical intervention (versus ED thoracotomy) in the setting of a hemothorax is the release of greater than 1,500 mL of blood upon initial placement of a chest tube, or persistent drainage of at least 150-200 mL of blood for greater than 2 hours after chest tube placement.1,7


The Abdomen

Hemodynamically unstable patients with penetrating trauma to the abdomen, or those who present with frank evisceration, require exploratory laparotomy.1 Hemodynamically stable patients with a positive FAST are appropriate for advanced imaging (CT). If there is question regarding fascial penetration, bedside wound exploration should only be undertaken by a specialist (general/trauma surgeon).1,2


The Extremities

Similar to bleeding at other anatomic locations, initial management of extremity trauma concentrates on hemostasis through the application of direct pressure or pressure dressings.1 Tourniquet application should be considered in the setting of life threatening hemorrhage.1 In this patient population, the secondary survey should focus on the evaluation of injury to vascular, neurologic, and musculoskeletal structures.1 Similar to neck injuries, penetrating trauma localized to the extremities require attention to hard and soft signs (Figure 2).1 Hard signs which require surgical management are absent or diminished pulses, obvious arterial bleeding, expanding hematoma or pulsatile bleeding, audible bruit, palpable thrill, or distal ischemia.1 Soft signs requiring additional diagnostic evaluation include small hematomas, nerve injury, unexplained hypotension, history of hemorrhage, proximal vascular damage without hypotension, and complex fracture.1 As with neck injuries, avoid clamping vessels in the extremities as this intervention carries high risk of arterial or nerve damage.1

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Final Words

It is important to perform a thorough secondary examination of all patients presenting with a penetrating injury. Wounds hidden in skin folds, the axilla, or nape of the neck are easily missed. All impaled objects that remain in place upon arrival to the ED should not be removed, but rather stabilized.1,4

How should our patients in the cases be managed?

Case I: The patient is stable and does not require emergent surgical intervention as his wound is localized to zone II and does not violate the platysma. He is likely to undergo advanced imaging given his intoxication.

Case II: The patient should be taken to the operating room for diagnostic laparotomy given her persistent hypotension despite resuscitation.

 Case III: The patient is hemodynamically stable with gaping, hemostatic wounds to the skull and forearm. Given his altered mental status and absence of vital sign abnormalities, increased ICP should be assumed: head of bed elevated 30°, hyperventilated to a pCO2 of 35, and 3% NS delivered (+/- mannitol administered per institutional policy or in consultation with trauma surgery/neurosurgery). CT imaging subsequently revealed a large epidural hematoma with 3 mm of midline shift.

Case IV: The patient’s chest X-ray was notable for subcutaneous emphysema, and CT of the chest revealed significant subcutaneous emphysema with a large apical pneumothorax. A left sided chest tube was placed and the patient was admitted for further evaluation with bronchoscopy and EGD.



  • ED management of a patient with a penetrating injury begins with addressing the ABCs.
  • The first step in addressing active bleeding is the application of direct pressure.
  • Patients with head wounds commonly undergo advanced imaging to rule out foreign body and underlying trauma.
  • Hemorrhagic shock, airway obstruction, air discharge from a wound, active pulsatile blood flow, massive hemoptysis, and uncontrolled bleeding in patients with neck injuries mandate immediate surgical intervention.
  • Assume cardiac and great vessel injury in all patients with trauma to the cardiac box.
  • Hemodynamically unstable patients with abdominal trauma require operative intervention.
  • Patients with penetrating injuries to the extremities with absent or diminished pulses, obvious arterial bleeding, expanding hematoma or pulsatile bleeding, audible bruit, palpable thrill, or distal ischemia require operative intervention.


References / Further Reading

  1. Tintinalli, J.E., Stapczynski, O.J., Ma, D.M., Meckler, G.D., Cline, D.M. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8th www.accessmedicine.com. 2015.
  2. LoCicero, J., Mattox, K.L. Epidemiology of Chest Trauma. Surgical Clinics of North America. 69(1): 15-9. 1989. PMID: 2911786.
  3. Sormann, P., Wutzler, S., Sommer, K., Marzi, I., Lustenberger, T., Walcher, F. Gunshot and Stab Wounds: Diagnosis and Treatment in the Emergency Room. Emergency and Rescue Medicine. 2(1-9). 2016. DOI: 10.1007/s10049-016-0162-9
  4. Daya, N.P., Liversage, H.L. Penetrating Stab Wound Injuries to the Face. Europe PMC. 2004. 59(2):55-59. PMID: 15181702.
  5. White, C.C., Domeier, R.M., Millin, M.G. National Association of EMS Physicians and American College of Surgeons Committee on Trauma. EMS Spinal Precautions and the Use of the Long Backboard. Available from: http://www.naemsp.org/Documents/Position%20Papers/EMS%20Spinal%20Precautions%20and%20the%20Use%20of%20the%20Long%20Backboard_Resource%20Document.pdf
  6. Bothwell N. Acute Management of Pharyngoesophageal Trauma. Ch 30. Department of Defense. Otolaryngology/Head and Neck Surgery Combat Casualty Care in Operation Iraqi freedom and Operation Enduring Freedom. Army Borden Institute.
  7. Mowery, N.T., Gunter O.L., Collier, B.R., Diaz, J.J. Hemothorax and Occult Pneumothorax; Management of. Journal of Trauma. 2011. Feb; 70 (2): 510-8. Available from: https://www.east.org/education/practice-management-guidelines/hemothorax-and-occult-pneumothorax,-management-of

Healthy Patients with Potential to Crash

Authors: Daniel Ritter (Medical Student, The Ohio State University College of Medicine) and Mark J Conroy, MD (Assistant Professor of EM, The Ohio State University Wexner Medical Center, @mjconroy_md) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)


A 30-year-old healthy female presents to the emergency department (ED) complaining of nausea, vomiting, and diarrhea that have worsened over the last 24 hours. She admits to some lightheadedness and states that she feels “just out of it”.  She denies any abdominal pain or blood in her emesis and stool. Some coworkers have been out sick with similar symptoms following a company party over the weekend.  She takes “some pill” for a “gland problem”, but she lost the bottle a few days prior.

The patient’s initial vital signs include a heart rate of 105 beats per minute (bpm) and a blood pressure of 90/50 mmHg. The patient is physically fit and reports that her blood pressure always runs on the “low side”. Her examination reveals dry mucous membranes and tachycardia but it is otherwise normal.  The patient has no neck stiffness, cardiac murmurs, abdominal pain, or rashes. You order routine laboratory tests and and treat her symptoms with an antiemetic and intravenous (IV) fluids.

After about 30 minutes, the patient’s chemistry returns and demonstrates a marked hyperkalemia and hyponatremia. When you reassess the patient, you note that she has an altered mental status and her blood pressure is 72/40 mmHg.

Unhealthy healthy patients

One of the first steps in any ED evaluation is differentiating between those patients who are sick and those who are not sick. While a lifetime of patient care can make this a subconscious decision for most emergency providers, the process is still subjective. Criteria, algorithms, and/or clinical decision tools exist for many scenarios, but not all. It is especially difficult for clinicians to determine the severity of an illness in an otherwise young healthy patient with non-specific symptoms.

Among every group of nonspecific presentations is a new (or overlooked) diagnosis that, if missed, can seriously harm or even kill a patient. The goal of training and lifetime learning is for emergency physicians to become experts at teasing out those who are covertly sick. Several of the conditions discussed below can easily be overlooked because they may present, at least initially, with non-concerning symptoms. However, they have the ability to cause serious harm.

Acute Adrenal Insufficiency (Adrenal Crisis)


Adrenal insufficiency is divided into three categories: primary, secondary, and tertiary.1  Primary disease is due to intrinsic problem(s) with the adrenal cortex, while secondary adrenal insufficiency is due to pituitary failure or a lack of responsiveness of the adrenal glands to adrenocorticotropic hormone (ACTH). Tertiary adrenal insufficiency is due to the impaired hypothalamic production or action of ACTH, vasopressin or both.1

Adrenal crisis can occur as an exacerbation of any chronic cause of adrenal insufficiency, or as an abrupt injury to any component of a healthy adrenal axis.  Common causes include abrupt cessation of exogenous glucocorticoid use, bilateral adrenal infarction/hemorrhage, or acute stress in the setting of previously undiagnosed chronic adrenal insufficiency.2

How it presents

Acute adrenal insufficiency can present with hypotension, abdominal pain and/or rigidity, nausea, vomiting, and fever due to coexisting infection.  Hyperpigmentation may be a feature of those with chronic adrenal insufficiency.  A history of chronic fatigue or abrupt cessation of chronic glucocorticoid use could be present depending on the etiology.2

Why the diagnosis can be challenging

Acute adrenal insufficiency is rare. The risk of developing acute adrenal insufficiency in a patient with chronic adrenal insufficiency is about 6-10 per 100 patient-years.3  It can also be easily overlooked as a diagnosis early on in a patient’s presentation.  Furthermore, endocrine causes of hemodynamic instability are not generally considered to be one of the four main categories of shock (obstructive, cardiogenic, distributive, and hypovolemic).  These factors can delay diagnosis and lead to worsening crisis before appropriate treatment is initiated.

How to catch it

A more thorough history can be key in identifying the right track for the emergency physician. Routine laboratory analysis often reveals hyperkalemia and hyponatremia.2 Patients in adrenal crisis face significant morbidity and mortality. Immediate treatment with fluid resuscitation and steroid replacement (dexamethasone 4-10 mg IV when no prior diagnosis exists4, otherwise hydrocortisone 100 mg IV or IM, with 100-300 mg every day thereafter for the duration of treatment2) is necessary before receiving confirmatory diagnostic tests in patients who are at risk.2

Other pearls

Cessation of inhaled glucocorticoids can precipitate acute adrenal insufficiency.5

Acute Pancreatitis


A condition involving inflammation, and often hemorrhagic necrosis, of the pancreatic parenchyma. Several causes exist but gallstone obstruction of the pancreatic duct, metabolic/hereditary disorders, and alcohol use most commonly underlie this painful condition6.  In necrotizing pancreatitis, mortality can be as high as 17%.7 Severe cases can lead to marked hypotension and end-organ failure.6

How it presents

About 50% of the time, patients present with severe, persistent epigastric pain radiating to the back.8 Pain is usually associated with severe nausea and vomiting.6

Why the diagnosis can be challenging

The differential diagnosis for patients with abdominal pain is, unfortunately, very broad.  Epigastric pain could be the manifestation of intra-abdominal, cardiac, or intra-thoracic processes. In addition, pancreatitis due to alcohol or metabolic disorders can have a more gradual onset with poor localization of pain.  Degree of pain is also variable, and some patients may not be as uncomfortable as others.  In a patient who is otherwise healthy, and who presents with gradual onset, localized and unimpressive epigastric pain, acute pancreatitis could easily be missed.

How to catch it

Keeping broad differential diagnoses for patients with abdominal pain is key.  Consider abdominal computed tomography (CT) for lipase (+/ amylase) levels that are only mildly elevated, or with atypical presentations not otherwise explainable.

Other pearls

Acute pancreatitis on ultrasound appears enlarged and heterogeneous.  Hypoechoic fluid may be visualized, as well as gallstones in the gallbladder or common bile duct.9



Abnormal cardiac rhythms vary in pathophysiology, appearance on electrocardiogram (ECG), and lethality.  They can range from benign ectopic beats (like PVCs) to very dangerous (like atrial fibrillation in patients with Wolff-Parkinson-White).

How it presents

Presenting symptoms are variable and can include palpitations, anxiety, syncope, dizziness, chest pain, and shortness of breath.

Why the diagnosis can be challenging

The difficulty is not in obtaining the ECG but instead the interpretation. Outside of the overt arrhythmia, ECG signs of channelopathy or structural abnormality in asymptomatic patients can easily be overlooked.

 How to catch it

Key features on ECG for high-risk syndromes include:

  • Long QT interval: A sign of the aptly named Long QT Syndrome. It can be congenital or can be acquired in the setting of electrolyte abnormalities or certain pharmacologic agents.  A long QT interval puts patients at risk for sudden cardiac death due to Torsades de pointes.10
  • Delta wave: Classic for Wolff-Parkinson-White syndrome. The “slurring” of the R wave is a sign of an accessory pathway, which can lead to an unstable tachycardia (rate often greater than 200), cardiovascular instability and death.11
  • Q waves, atrial enlargement, left axis deviation, inverted T waves: In a young, healthy patient, any of these could be a sign of hypertrophic cardiomyopathy. Look for signs of structural changes, such as P wave abnormalities suggesting atrial enlargement.  Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death in young athletes.12
  • Pseudo-right bundle branch block and ST elevation in V1 and V2: Suggestive of Brugada syndrome, a sodium channelopathy. ST elevation can be divided into two patterns: type 1 features a convex, descending ST segment followed by an inverted T-wave, and type 2 features a “saddle-back” ST-T morphology.  A third type exists involving the criteria of Type 1 & 2 but with < 2 mm of elevation. Brugada syndrome predisposes patients to sudden-onset ventricular tachyarrhythmias.13

Other pearls

Often genetic, but not always, a family history is very helpful for assessing risk for different arrhythmias.

Substance Abuse


Overdoses and withdrawal are an increasingly large burden on emergency medical service (EMS) providers and emergency departments as newly synthesized illicit drugs are abused and opioid addiction across the United States grows.14

How it presents

Signs and symptoms of overdose or withdrawal depends on the substance in question.  Some common examples include:

  • Opioids
    • Intoxication: Respiratory depression, altered mental status, bradycardia, miotic pupils.15,16
    • Withdrawal: Dysphoria, restlessness, myalgias/arthralgias, nausea, vomiting, tachycardia, diarrhea.16
  • Cocaine
    • Intoxication: Hypertension, tachycardia, mydriatic pupils, agitation.16,17
    • Withdrawal: Depression/anxiety, fatigue, anhedonia, increased sleep.18
  • Amphetamines
    • Intoxication: agitation/psychosis, tachycardia, hypertension, mydriatic pupils, diaphoresis.19
    • Withdrawal: dysphoria, fatigue, increased sleep, anxiety.18,19
  • Phencyclidine (PCP)
    • Intoxication: Hypertension, hallucinations, nystagmus, tachycardia, agitation.20
    • Withdrawal: Confusion, anxiety, depression, memory loss.19
  • Alcohol
    • Intoxication: Slurred speech, nystagmus, unsteady gait, nystagmus, disinhibition.21
    • Withdrawal: Insomnia, tremulousness, hallucinations, headache, diaphoresis, seizures, delirium tremens.22,23

 Why the diagnosis can be challenging

Intoxication or overdose from alcohol or drugs can be easy to diagnose with sufficient history.  Otherwise, an acutely altered patient with little available history can be a diagnostic challenge. Additional conditions can also be overlooked in the patients – head trauma following opiate and alcohol abuse, myocardial infarction with cocaine intoxication, or delirium tremens in a patient with no known history of alcohol abuse.

 How to catch it

Whenever possible, accurately identify the substance in question in order to prepare for potentially dangerous sequelae.  Try to keep a wide differential in patients who are altered or agitated.

 Other pearls

Remember to ask about alcohol, tobacco, and drug use in all patients.

Crush Injury


The development of rhabdomyolysis and acute kidney injury in the setting of a crush injury is well-known. A more severe results of crush injury can occur in disaster victims who become trapped in fallen structures. In this case, these victims can often become hypotensive following extrication due to third-spacing of fluids into the freed crushed tissue. Thus, compartment pressures should be monitored closely in these patients.24,25

 How it presents

Providers in the field will most often encounter hypotensive patients following a crush injury.  However, providers in the ED should be aware of this possibility when caring for victims of natural or man-made disasters.

 Why the diagnosis can be challenging

Providers in the field must be aware of the dangers of crush injuries beyond the direct trauma to limbs.  If an IV is not placed and fluids not started before extrication, deterioration should be an ongoing concern. Additionally, it is possible that a provider in the emergency department setting could be unaware of a crush injury in a hypotensive trauma patient, prompting him or her to look for other causes of hypotension.

 How to catch it

When dealing with entrapped victims, an IV line and fluids should be started before extrication whenever possible.  This can prevent post-extrication hypotension as well as ameliorate the potential for acute kidney injury (AKI).25

 Other pearls

Bicarbonate and mannitol (1 amp and 10 g IV, respectively, during extrication) can be used to avoid AKI following crush injury.24

Heat Illness


Heat illness is considered a failure of the body’s thermoregulatory system to handle intrinsic and extrinsic heat. It can be further classified based on signs and symptoms. Syncope, muscle cramps, heat exhaustion are all part of the spectrum of heat related illness, with heat stroke having the highest rates of morbidity and mortality.26

How it presents

Heat illness can affect populations of all ages, from very young to very old. Typically, younger patients present following a period of exertion.  Any rectal temperature greater than 104° Fahrenheit (F) with mental status changes necessitates active cooling. For patients with a temperature less than 104° but still greater than 98.6°, active cooling (ice water immersion, cooling mattress, etc) should seriously be considered. Passive cooling (removing the patient from the warm environment, getting rid of wet clothing, and hydration) is still a must. Rechecking a rectal temperature to ensure improvement is also necessary as some patients can continue increasing early on before passive methods have taken effect.

Why the diagnosis can be challenging

Older patients often present with heat illness without any preceding exertion. Often left unattended in the heat as well as additional medications complicating the diagnosis, these patients present with little to no history to direct your evaluation and treatment. Additionally, these patients can suffer from secondary electrolyte and cardiovascular complications. 26

How to catch it

Obtaining a rectal temperature is the gold standard when evaluating patients for heat illness. Keep heat illness in your list of differential diagnoses, especially when working on days with high heat indices or an endurance event nearby.

Other pearls

Ice packs in the axillae and groin as well as evaporative cooling with misting and a fan are the most feasible cooling options in the ED. Cold water immersion is the gold-standard when working events. Goal rate for cooling is 1° (F) every 3 minutes.  Antipyretics are not useful for decreasing temperature in these patients.27,28

“Vitals are vital” and “Keep your differential broad”

Providers have heard these phrases repeated since beginning medical school, and nowhere are they more applicable than when dealing with young healthy patients.

Abnormal vital signs need to be explained within the clinical context.  Hydration status can be an easy go-to for tachycardia but anchoring can lead you down the wrong diagnosis and treatment pathways if other alternative causes are not considered. In the case at the start of this post, symptomatic hypotension and an unclear medication history are key red flags that should not be overlooked.

Finally, when a patient does not respond as you expect (improved heart rate with IV fluids, decreased pain with medication, etc.) emergency providers should step back and re-evaluate. Make sure you have considered all life threatening diagnoses and that you have adequately evaluated patients for these diagnoses. Not every potential diagnosis needs to be tested for. However, considering the diagnosis is important because it helps avoid bias and potentially, missed diagnoses.


Address abnormal vital signs or have a cohesive explanation as to why you are not addressing them.

Abnormal vital signs without a clear explanation, as well as vital signs that do not resolve with treatment, should prompt expanded consideration of the patient’s complaint, further investigation, and likely both.

-Bad things happen and even healthy people get sick.

References / Further Reading

1Charmandari E, Nicolaides NC, Chrousos GP. Adrenal insufficiency. The Lancet. 2014;383(9935):2152-2167.

2Puar TH, Stikkelbroeck NM, Smans LC, Zelissen PM, Hermus AR. Adrenal Crisis: Still a Deadly Event in the 21st Century. The American Journal of Medicine. 2016;129(3).

3Arlt W, Allolio B. Adrenal insufficiency. The Lancet. 2003;361(9372):1881-1893.

4Asare K. Diagnosis and Treatment of Adrenal Insufficiency in the Critically Ill Patient. Pharmacotherapy. 2007;27(11):1512-1528.

5Piédrola G, Casado JL, López E, Moreno A, Perez-Elías MJ, García-Robles R. Clinical features of adrenal insufficiency in patients with acquired immunodeficiency syndrome. Clinical Endocrinology. 1996;45(1):97-101.

6Lankisch PG, Apte M, Banks PA. Acute pancreatitis. The Lancet. 2015;386(9988):85-96.

7Banks PA, Freeman ML. Practice Guidelines in Acute Pancreatitis. The American Journal of Gastroenterology. 2006;101(10):2379-2400.

8Banks PA. Acute pancreatitis: Diagnosis. In: Pancreatitis, Lankisch PG, Banks PA (Eds), Springer-Verlag, New York 1998. p.75.

9Bollen TL, Santvoort HCV, Besselink MG, Es WHV, Gooszen HG, Leeuwen MSV. Update on Acute Pancreatitis: Ultrasound, Computed Tomography, and Magnetic Resonance Imaging Features. Seminars in Ultrasound, CT and MRI. 2007;28(5):371-383.

10Khan IA. Long QT syndrome: Diagnosis and management. American Heart Journal. 2002;143(1):7-14.

11Bhatia A, Sra J, Akhtar M. Preexcitation Syndromes. Current Problems in Cardiology. 2016;41(3):99-137.

12Elliott P, Mckenna WJ. Hypertrophic cardiomyopathy. The Lancet. 2004;363(9424):1881-1891.

13Littmann L, Monroe MH, Kerns WP 2nd, Svenson RH, Gallagher JJ. Brugada syndrome and “Brugada sign”: clinical spectrum with a guide for the clinician.  Am Heart J. 2003 May; 145(5):768-78.

14Rudd RA, Aleshire N, Zibbell JE, Gladden RM. Increases in Drug and Opioid Overdose Deaths — United States, 2000–2014. MMWR Morbidity and Mortality Weekly Report. 2016;64(50-51):1378-1382.

15Sporer KA. Acute Heroin Overdose. Annals of Internal Medicine. 1999;130(7):584.

16Hughes JR, Higgins ST, Bickel WK. Nicotine withdrawal versus other drug withdrawal syndromes: similarities and dissimilarities. Addiction. 1994;89(11):1461-1470.

17Merigian KS, Roberts JR. Cocaine Intoxication: Hyperpyrexia, Rhabdomyolysis and Acute Renal Failure. Journal of Toxicology: Clinical Toxicology. 1987;25(1-2):135-148.

18Lago JA, Kosten TR. Stimulant withdrawal. Addiction. 1994;89(11):1477-1481.

19Khantzian EJ. Acute Toxic and Withdrawal Reactions Associated with Drug Use and Abuse. Annals of Internal Medicine. 1979;90(3):361.

20Mccarron MM, Schulze BW, Thompson GA, Conder MC, Goetz WA. Acute phencyclidine intoxication: Incidence of clinical findings in 1,000 cases. Annals of Emergency Medicine. 1981;10(5):237-242.

21Camí J, Farré M. Drug Addiction. New England Journal of Medicine. 2003;349(10):975-986.

22Etherington JM. Emergency management of acute alcohol problems Part 1: Uncomplicated withdrawal. Canadian Family Physician. 1996;42:2186-2190.

23Ferguson JA, Suelzer CJ, Eckert GJ, Zhou X-H, Diffus RS. Risk factors for delirium tremens development. Journal of General Internal Medicine. 1996;11(7):410-414.

24Gonzalez D. Crush syndrome. Crit Care Med. 2005 Jan;33(1 Suppl):S34-41.

25Sever MS, Vanholder R, Lameire N. Management of Crush-Related Injuries after Disasters. New England Journal of Medicine. 2006;354(10):1052-1063.

26Leon LR, Bouchama A. Heat Stroke. Comprehensive Physiology. March 2015:611-647.

27Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care. 2007;11(3):R54

28Smith JE.  Cooling methods used in the treatment of exertional heat illness. Br J Sports Med. 2005;39:503-7.

Pelvic Inflammatory Disease: Pearls and Pitfalls

Authors: Marina N. Boushra, MD (EM Resident Physician, Vidant Medical Center) and Cassandra Bradby, MD (EM Attending Physician, Vidant Medical Center) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

A 24-year-old female with no significant past medical history presents to the emergency department (ED) with lower abdominal pain for five days. The pain has been associated with decreased appetite and nausea but no vomiting. It is exacerbated by sexual intercourse. Her last menstrual was period five days ago, and while she typically gets cramping, she states that this pain is more severe. Her vitals on arrival are temperature 101.2º Fahrenheit (F), heart rate (HR) 80 beats per minute (bpm), respiratory rate (RR) 14/minute, blood pressure (BP) 115/70 mmHg. Her physical examination is notable for diffuse tenderness to palpation of the abdomen, scant blood in the vaginal vault, yellow discharge from the cervical os, and severe bilateral adnexal tenderness on bimanual examination.


Pelvic inflammatory disease (PID) is infection of the upper genital tract (uterus, endometrium, fallopian tubes, ovaries) in women. PID may extend to involve adjacent structures, causing periappendicitis, pelvic peritonitis, and perihepatitis (Fitz-Hugh-Curtis syndrome). The majority of PID is caused by ascending sexually-transmitted infections (STI). Neisseria gonorrhea and Chlamydia trachomatis are the most commonly implicated pathogens in PID1. However, PID can also be caused by bacterial-vaginosis related organisms or, more rarely, enteric or respiratory pathogens that have colonized the lower genital tract1. Even more rarely, a chronic form of PID may be seen with tuberculosis in endemic areas or Actinomyces in women who have intrauterine devices2,3.

Any sexually active woman is at risk for PID but women with multiple sexual partners are at the highest risk4. Other risk factors include age younger than 25 years, herpes infection, HIV infection, a partner with an STI, prior PID, or prior STI. Barrier contraception is protective5. Pregnancy also decreases the risk of PID due to the mucus plug that can prevent ascending infection from the lower to the upper genital tract. Note, however, that PID can still develop in the first 12 weeks of pregnancy6. The spectrum of PID symptoms is wide with some patients going undiagnosed until they develop sequelae such as tubal factor infertility or an ectopic pregnancy. In symptomatic patients, lower abdominal pain, typically bilateral, is often the presenting symptom1. Dyspareunia and/or an onset of pain with, or shortly after, menstruation should also raise suspicion for PID7. A history of abnormal uterine bleeding, such as menorrhagia, metrorrhagia, or post-coital bleeding, is seen in one third of patients with PID8. Physical examination typically reveals lower abdominal pain, which may be unilateral or bilateral, although diffuse abdominal pain may also be seen. Cervical motion tenderness and the classic “chandelier sign” – severe pain with cervical motion such that the patient “jumps for the chandelier” on examination – may be present. Fever, rebound tenderness, and/or hypoactive bowel sounds are indicative of more severe disease and should increase suspicion for a pelvic abscess. Associated right upper quadrant pain is concerning for Fitz-Hugh-Curtis syndrome inflammation of the hepatic capsule. The most common cause of death in PID is rupture of a tubo-ovarian abscess (TOA), which has a mortality rate of 5-10%6. Serious complications include tubal factor infertility, tubal scarring leading to ectopic pregnancy, and chronic pelvic pain.

Differential Diagnosis

The differential diagnosis for pelvic and lower abdominal pain is extremely broad and varies by age. The differential in pre-menopausal women includes ectopic pregnancy, a complicated intrauterine pregnancy, ovarian cyst, ovarian torsion, endometriosis, urinary tract pathologies, appendicitis, and irritable bowel syndrome. Laboratory evaluation should include a pregnancy test in any pre-menopausal woman. In post-menopausal women, many of the gastrointestinal and urinary pathologies are still possible but there is lower risk for ovarian torsion and endometriosis. Diagnoses such as ovarian masses, endometrial cancer, and colon cancer should be considered.


There is no specific lab value, physical examination finding, or imaging study that is diagnostic of PID. The diagnosis of PID is often presumptive based on clinical findings. The clinical diagnosis is only 65-90% specific, but the addition of the criteria in Table 1 increases the specificity of the clinical diagnosis1,5,9. In patients with known or suspected PID, testing for STIs, including syphilis and HIV, should be obtained. Other helpful laboratory tests include a white blood cell count, C reactive protein (CRP), and erythrocyte sedimentation rate (ESR). A positive urinalysis does not exclude the diagnosis of PID, as inflammation in the pelvis can cause white blood cells in the urine6.

 Table 1: Findings suggestive of PID1

Oral temperature >101°F (>38.3°C)
Abnormal cervical or vaginal mucopurulent discharge
Cervical friability
Abundant white blood cells on saline microscopy of vaginal secretions
Documented infection with of N. gonorrhoeae or C. trachomatis

Imaging with pelvic ultrasound may be helpful in excluding other causes of pelvic pain, including ectopic pregnancy, ovarian cysts, and ovarian torsion. It is also helpful in the diagnosis of TOA. Computed tomography (CT) or magnetic resonance imaging (MRI) may also be used, with MRI being particularly useful in characterizing complicated soft-tissue masses as would be seen with TOA6.


While the clinical diagnosis is only 65-90% specific, even minimal symptoms without an alternative diagnosis warrant antibiotic therapy to reduce the risk of potentially serious complications due to the delay of or withholding therapy1. Women with IUDs do not need to have them removed prior to the start of treatment because they are rarely the cause of PID1. If symptoms fail to improve in 48-72 hours, removal of the IUD should be considered1.

Antibiotic selection should cover for N. gonorrhea and C. trachomatis. The importance of anaerobic coverage is controversial, since no trial has demonstrated improved outcomes and there is concern that the gastrointestinal side effects associated with metronidazole will lead to noncompliance10. There is currently an ongoing study on the role of anaerobic coverage in PID (Clinical Trials.gov, identifier NCT01160640).

Anaerobic coverage should be added, however, in patients who have a history of gynecologic instrumentation in the prior two to three weeks. Possible antibiotic regimens for inpatient and outpatient management are listed in Table 2.

 There has been a trend towards outpatient management of patients with mild to moderate disease. The Pelvic Inflammation Disease Evaluation Clinical Health Trial (PEACH Trial) showed similar short-term clinical and microbiologic and long-term reproductive outcomes between the inpatient and outpatient arms of the trial, with the inpatient arm experiencing high rates of phlebitis from IV doxycycline administration12.

Table 2: Inpatient and Outpatient Treatment Regimens1

Outpatient management Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)
Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)
Inpatient management Cefoxitin (2g IV q6 hours) plus doxycycline (100mg po bid for 14 days)
Cefotetan (2g IV q12 hours) plus doxycycline (100mg po bid for 14 days)
Clindamycin (900mg IV q8 hours) plus gentamicin (2mg/kg loading dose then 1.5 mg/kg q8 hours IV)

Indications for hospitalization and IV antibiotics include pregnancy, clinically severe disease, complicated PID (pelvic abscess), and intolerance to, noncompliance with, or failure of oral antibiotics1.

If a patient is treated as an outpatient, follow up in 72 hours should be arranged. Patient education is paramount, especially in adolescents where the risk of recurrence is higher and the time to pregnancy is shorter than in adult patients. Partner notification, evaluation and treatment should be encouraged. Patients should be educated about the use of barrier contraception and safe sex practices and instructed to remain abstinent from sexual activity until one week after the completion of treatment for them and their partner.


  • Even though the presumptive clinical diagnosis is only 65-90% specific, symptoms suggestive of PID should be treated with antibiotics immediately to avoid the risk of serious sequelae, including permanent scarring that may lead to infertility and ectopic pregnancy.
  • Obtain a pelvic ultrasound to assess for TOA in patients with asymmetrical pelvic findings or clinical signs of toxicity.
  • Fluoroquinolones should not be used in known or suspected gonorrhea infection due to increasing rates of resistance.
  • IUDs do not need to be removed prior to treatment of PID.
  • Antibiotics should cover both gonorrhea and C. trachomatis.
  • Anaerobic coverage is only suggested if there has been recent gynecologic instrumentation.


  • Dismissing the pelvic pain associated with PID for dysmenorrhea.
  • Assuming a positive UA excludes the diagnosis of PID (beware sterile pyuria)
  • Failing to do a pelvic exam and STI testing on a woman with lower abdominal pain.

References / Further Reading

  1. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep 2015; 64:1.
  2. Namavar Jahromi B, Parsanezhad ME, Ghane-Shirazi R. Female genital tuberculosis and infertility. Int J Gynaecol Obstet 2001; 75:269.
  3. Kim YJ, Youm J, Kim JH, Jee BC. Actinomyces-like organisms in cervical smears: the association with intrauterine device andpelvic inflammatory  Obstet Gynecol Sci. 2014 Sep;57(5):393-6.
  4. Lee NC, Rubin GL, Grimes DA. Measures of sexual behavior and the risk of pelvic inflammatory disease. Obstet Gynecol 1991; 77:425.
  5. Ross, Johnson. Pelvic Inflammatory Disease: pathogenesis, microbiology, and risk factors. UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 12 October 2016.
  6. Shepherd SM, Weiss B, Shoff WH. Pelvic Inflammatory Disease in Tintinalli, Judith E., Gabor D. Kelen, and J. Stephan Stapczynski. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill, Medical Pub. Division, 2016. Ch 103:668-672.
  7. Korn AP, Hessol NA, Padian NS, et al. Risk factors for plasma cell endometritis among women with cervical Neisseria gonorrhoeae, cervical Chlamydia trachomatis, or bacterial vaginosis. Am J Obstet Gynecol 1998; 178:987.
  8. Wiesenfeld HC, Sweet RL, Ness RB, et al. Comparison of acute and subclinical pelvic inflammatory disease. Sex Transm Dis 2005; 32:400.
  9. Peipert JF, Boardman LA, Sung CJ. Performance of clinical and laparoscopic criteria for the diagnosis of upper genital tract infection. Infect Dis Obstet Gynecol 1997; 5:291.
  10. Walker CK, Wiesenfeld HC. Antibiotic therapy for acute pelvic inflammatory disease: the 2006 Centers for Disease Control and Prevention sexually transmitted diseases treatment guidelines. Clin Infect Dis 2007; 44 Suppl 3:S111.
  11. Wiesenfeld, HC. Pelvic Inflammatory Disease: Treatment. UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 12 October 2016.
  12. Ness RB, Soper DE, Holley RL, et al. Effectiveness of inpatient and outpatient treatment strategies for women with pelvic inflammatory disease: results from the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) Randomized Trial. Am J Obstet Gynecol 2002; 186:929.

Modern-Day Burn Resuscitation: Moving Beyond the Parkland Formula

Authors: Mary Ellen Billington, MD (EM Resident Physician, Parkland Memorial Hospital, Dallas, TX) and Brett D. Arnoldo, MD, FACS (Associate Professor, Department of Surgery, Parkland Memorial Hospital, Dallas, TX) // Edited by: Erica Simon, DO, MHA (@E_M_Simon) & Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW Medical Center / Parkland Memorial Hospital)

In the midst of a busy ED shift, a patient arrives by EMS. You immediately recognize the distinctive odor: a dry and unfortunately singed smell lingers in the air. As the catecholamines surge, you recognize your own tachycardia: it’s time to see a burn victim.

Thoughts race through your mind: What’s that  formula for fluid resuscitation? What rate do I use for the lactated ringers? What are the criteria that determine the need for burn center care? Where is my co-oximetry equipment?

Step away from your MDCalc – we’re going to calm that scorching stress-induced acid reflux with an update on the emergency department management of burns.

Mental Road Map

To adequately manage the burn victim, the emergency medicine physician must remember three key guidelines:

  1. The burn patient is a special type of trauma patient.
  2. The burn patient may be a toxicological patient.
  3. The burn patient requires comprehensive evaluation and management, and is best served by transferring to a burn center in accordance with ABA (American Burn Association) guidelines.

The Burn Patient is a Special Type of Trauma Patient

Begin with the ABCs: Is the airway intact? Is there concern that the airway may be lost? What is the patient’s projected course?

  • If the airway is not protected: intubate.
  • Signs of impending airway compromise include: stridor, wheezing, subjective dyspnea, and a hoarse voice.1
    • Severe burns to the lower face and neck may develop significant edema predisposing to airway obstruction.1
    • A history of the inhalation of superheated air, or steam in a confined space, is concerning for severe bronchial injury.1
    • Keep in mind that perioral burns and singed nasal hairs mandate an examination of the oropharynx for mucosal injury, however, these findings alone do not indicate airway involvement.2
    • Smoke inhalation victims may develop delayed respiratory failure: when in doubt, admit for observation and bronchoscopy.3
  • Projected Course: patients with burns involving >60% total body surface area (TBSA) tend to deteriorate rapidly: consider immediate intubation.1
  • Keep in mind that patients possessing burns involving a lower percentage of TBSA (e.g. < 40%), may require intubation if significant volume resuscitation is required.1
  • If the airway is intact, and the history and physical are not consistent with inhalational injury, it is prudent to administer oxygen by nasal cannula or face mask.1

Aside from airway concerns, complete your primary and secondary surveys and treat life-threatening emergencies as appropriate:

  • Consider a cervical collar if the mechanism is appropriate (blast injuries), or when doubt surrounds the circumstances of the injury.
  • Remember that full-thickness burns to the chest wall may lead to mechanical restriction of ventilation: consider escharotomy.1,3
    • Note: It is advised that escharotomies be performed in cooperation with a burn surgeon.4

In terms of fluid resuscitation:2

  • Burns <15% TBSA generaly require only PO fluid resuscitation.
  • Obtain large bore PIV access: two sites recommended for burns >40% TBSA.
  • Despite popular belief, IV access may be obtained through burned skin; ensure that lines are  well secured.
  • Obtain IO access if unable to obtain IV access.
  • Central lines equipped with invasive monitoring devices may provide useful volume-status metrics to guide resuscitation.

The What, When, and How Much of Fluids

  • In order to determine the volume of fluid resuscitation required for a burn patient, the Rule of Nines for adults and the Lund and Browder chart for children should be utilized (Figures 1 and 2 below).1,2
  • Remember: do not include first degree burns in the calculation of % TBSA.2
  • The over-estimation of % TBSA may result in hypervolemia, predisposing to a number of dangerous conditions:4
    • abdominal compartment syndrome
    • extremity compartment syndrome(s)
    • intraocular compartment syndrome
    • pleural effusions
Figure 1. Rule of Nines (Reference 5)
Figure 1. Rule of Nines (Reference 5)
Figure 2. Lund & Browder Chart (Reference 5)
Figure 2. Lund & Browder Chart (Reference 5)

Fluid Formulas:

  • The Parkland (or Baxter) Formula is possibly the most well-known and widely utilized formula:
    • 4 mL x weight in kg x % TBSA (up to 50%) = total volume of lactated ringers (LR) required for resuscitation
      • Half of the total volume is administered over the first 8 hrs post injury; the remaining, over the following 16 hours.
    • It is important to note that this formula is not universally accepted. Current trends in burn management literature emphasize a clinical assessment of volume status as essential in guiding fluid administration.1,2 Early consultation with a burn center is advised.1,2
  • The Advanced Burn Life Support (ABLS) handbook recommends the following for fluid resuscitation:
    • 2-4mL x kg body weight x % TBSA burn = volume of LR required for adult resuscitation (formula adjusted to 3-4mL x kg body weight x % TBSA burn for pediatric patients).6
      • Half of the total resuscitation volume is given over the first 8 hours, with administration of the remaining half titrated to patient response (urine output of 0.5mL/kg/hr for adults and 1mL/kg/hr for children).6
  • Inhalation injuries most commonly increase fluid resuscitation requirements.2
  • All resuscitation measures should be guided by perfusion pressure and urine output:4
    • Target a MAP of 60 mmHg, and urine output of 0.5-1.0ml/kg/hr for adults and 1-1.5mL/kg/h for pediatric patients.
    • The placement of a radial or femoral catheter is advised.4
    • Heart rate, pulse pressure, capillary refill, and mental status should also be assessed when determining resuscitation adequacy.
    • Additional markers, i.e. – lactate, base deficit, intestinal mucosal pH, and pulmonary arterial catheters are of limited use, and demonstrate varied mortality benefit.

We saw that the Parkland Formula and ABLS handbook recommend the use of LR, but are there recommendations regarding the use of other fluids for burn resuscitation?

  • Generally crystalloid solutions should be infused during the initial 18-24 hrs of resuscitation.1,4
  • It is recommended that 5% dextrose be added to maintenance fluids for pediatric patients weighing < 20kg.1
  • Hypertonic solutions tend to decrease initial resuscitation volumes, but are associated with increased renal failure and death, and therefore should be avoided.2,4,8
  • Colloid administration is a topic of debate.
    • Extensive heterogeneity exists regarding the recommendation for albumin utilization:
      1. Previous studies assessing albumin delivery in burn resuscitation (the most recent >15 years ago) demonstrated no statistically significantly improvement in patient outcomes.3  Today, however, a number of burn experts argue the value of albumin administration in the post capillary leak time frame (>18-24 hours post injury)given it’s ability to decrease third spacing.Further large scale, randomized control trials are needed.3
    • Blood transfusion is considered immunosuppressive, and is associated with increased mortality in burn patients. Blood products should be withheld unless there is an apparent physiologic need.2,4

The Burn Patient May be a Toxicological Patient

 In the evaluation of a burn patient, be sure to obtain a thorough history from EMS or from the patient. Victims of enclosed-space fires may be exposed to toxic levels of carbon monoxide and cyanide:

Your patient is the victim of an apartment fire. He has what appears to be red-tinged skin in areas absent burn; he is neurologically depressed, and suddenly decompensates into cardiac arrest. What toxic exposure do you suspect? How do you confirm your diagnosis? How will you treat your patient?

  • Carbon monoxide (CO) poisoning may manifest with persistent neurologic symptoms or even as cardiac arrest. Despite the board-style vignette stated above, cherry-red skin is a neither sensitive nor specific finding.3
  • If you suspect CO poisoning, order a carboxyhemoglobin level.1 In a patient with CO poisoning, pulse oximetry readings will be falsely normal, and the PaO2 and % hemoglobin saturation on ABG will be unaffected.1
  • How do you use a carboxyhemoglobin level? Subtract the carboxyhemoglobin level from the pulse oximetry level to determine true oxygen saturation.
    • Interpreting levels:3
      • Non-smokers: up to 1% normal
      • Smokers: 4-6% common
      • Any reading >10% = concern for significant exposure
    • To treat the toxic exposure administer 100% O2. Hyperbaric oxygen may be also be considered.2

Your burn patient, despite initial resuscitative efforts, maintains a persistent lactic acidosis and develops S-T elevation on EKG. What toxic exposure do you suspect? How do you treat your patient? 

  • The spectrum of the clinical presentation of cyanide poisoning varies from mydriasis,  to tachypnea and central apnea, to hypotension, to loss of consciousness and seizures.1
  • If concerned for cyanide toxicity, initiate 100% O2 therapy and administer hydroxocobalamin, with consideration for sodium thiosulfate (slower mechanism of action).1 Note: The commercially available cyanokit contains hydroxycobalamin.
  • Be sure to rule out other etiologies of lactic acidosis: under-resuscitation, CO poisoning, or missed traumatic injury.2

Additional Resuscitative Therapies and Considerations for Transfer

 What other resuscitative treatments may be indicated? When should you transfer a burn patient to a designated burn center?

  • In the evaluation of a burn patient, screening laboratory studies are appropriate.
    • Consider: ABG and CXR; cardiac enzymes, and a carboxyhemoglobin level.1,3
  • Administer a tetanus vaccination in the emergency department if indicated.
  • Control pain and administer anxiolytics as required.
  • Monitor resuscitation: bedside ultrasound is useful in the assessment of intravascular volume. Place a foley catheter or perform suprapubic cystotomy to monitor urine output and reduce the risk of abdominal compartment syndrome.3
  • Avoid hypothermia: warm the resuscitation room, administer warm inspired air, apply warm blankets, infuse warmed fluids, and cover wounds with clean dry sheets.2,4
  • Treat inhalation injury as indicated: intubate, order aggressive pulmonary toilet + bronchodilator (albuterol) +/- N-acetylcysteine, aerosolized heparin, aerosolized TPA, recombinant human antithrombin, surfactant, inhaled NO, or ECMO if required (the majority of this will be addressed in an ICU setting).2
  • Consider escharotomy or lateral canthotomy if concern for hypoventilation or compartment syndromes.4
  • After initial stabilization, follow the American Burn Association (ABA) Guidelines for the transfer of patients to designated burn centers. Suggested criteria for transfer can be found on the ABA webpage: http://www.ameriburn.org/BurnCenterReferralCriteria.pdf

A few words on steroids and antibiotics – Today there is no data to support steroid administration in the setting of inhalation injury.2 Prophylactic antibiotics are also withheld in the setting of burn injuries as several studies have demonstrated their administration as promoting systemic fungal infection.2

Morality – The Baux Score (% TBSA + Age) has historically been utilized as a predictor of mortality.2


In treating a burn patient:

  1. Follow ATLS guidelines in the initial evaluation and resuscitation of the burn patient, with special attention to unique airway considerations.
  2. Evaluate the patient for signs of toxic exposures, particularly carbon monoxide and cyanide.
  3. The burn patient requires comprehensive care. Follow ABA guidelines when considering transfer.


  1. DeKoning E. Thermal Burns. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. New York, NY: McGraw-Hill; 2016. http://accessmedicine.mhmedical. com.foyer.swmed.edu/content.aspx?bookid=1658&Sectionid=109438787.
  2. Friedstat J, Endorf FW, Gibran NS. Burns. In: Brunicardi F, Andersen DK, Billiar TR, Dunn DL, Hunter JG, Matthews JB, Pollock RE. eds. Schwartz’s Principles of Surgery, 10e. New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical. com.foyer.swmed.edu/content.aspx?bookid=980&Sectionid=59610849.
  3. Drigalla D, Gemmill J. Chapter 45. Burns & Smoke Inhalation. In: Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment Emergency Medicine, 7e.New York, NY: McGraw-Hill; 2011.http://accessmedicine.mhmedical.com.foyer.swmed.edu/content.aspx?bookid=385&Sectionid=40357261.
  4. Latenser BA. Critical Care of the Burn Patient. In: Hall JB, Schmidt GA, Kress JP. eds. Principles of Critical Care, 4e. New York, NY: McGraw-Hill; 2015.http://accessmedicine.mhmedical.com. foyer.swmed.edu/content.aspxbookid=1340&Sectionid=80027724.
  5. Remote Primary Health Clinic Manuals. Burns. 2014. Available from: https://rphcm.allette.com.au/publication/cpm/Burns.html
  6. American Burn Association. Advanced Burn Life Support Course Provider Manual. American Burn Association 2007.
  7. Lawrence A1, Faraklas I, Watkins H, Allen A, Cochran A, Morris S, Saffle J. Colloid administration normalizes resuscitation ratio and ameliorates “fluid creep”. J Burn Care Res. 2010 Jan-Feb;31(1):40-7. doi: 10.1097/BCR.0b013e3181cb8c72. PMID 20061836.
  8. Saffle JI. The phenomenon of “fluid creep” in acute burn resuscitation. J Burn Care Res. 2007 May-Jun;28(3):382-95. PMID 17438489

Geriatric Trauma and Medical Illness: Pearls and Pitfalls

Authors: Matthew R Levine, MD (Assistant Professor and Director of Trauma Services, Department of Emergency Medicine, Northwestern Memorial Hospital, Chicago, IL) and Lora Alkhawam, MD (Attending Physician, Duke Regional Hospital, Department of Emergency Medicine, Durham, NC) // Edited by: Erica Simon, DO, MHA (@E_M_Simon) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

An 85 year-old male is brought in by EMS status post MVC. He is confused and unable to detail the events surrounding his accident. When questioned, he has no recollection of his PMHx, but repeatedly states that he is in pain secondary to his c-collar and backboard. Vitals: HR 70 and irregular, BP 110/65, RR 16, O2 sat 94% on room air. Primary and secondary surveys are remarkable only for scant wheezing upon pulmonary auscultation. GCS is 14 without focal neurologic deficits. As you contemplate the next steps in your patient evaluation, you scan your knowledge bank: What critical diagnoses should you be considering? Let’s discuss some pearls and pitfalls in addressing the geriatric trauma patient.



According to 2010 US Census data, adults > 65 years of age account for 14% of the current U.S. population.1,2 It is estimated that nearly one in five Americans will be elderly by the year 2050.1,2 Why is this relevant to the practice of emergency medicine? Approximately 1 million persons aged 65 and older are affected by trauma each year.3  In fact, trauma in the elderly accounts for $12 billion in annual personal and institutional medical expenditures, and $25 billion in total annual healthcare expenditures.4 While elderly patients comprise a small percentage of total major trauma patients (8-12%) presenting to emergency care centers, they represent a disproportionate percentage of trauma fatalities and costs (15-30%).4

To date, numerous studies have demonstrated mortality related to trauma as increasing with advancing patient age.5-7 In fact, the Major Trauma Outcome Study published in 1989 (n = 3,833 > age 65 and 42,944 < age 65) demonstrated mortality as rising sharply between the ages of 45-55 and doubling by age 75.5 This pattern occurred at all Injury Severity Scores (ISS), mechanisms, and body regions.5

Screen Shot 2016-08-20 at 1.43.38 PM

Representation of Trauma Mortality Data5

Today, we also know that advancing age is an independent risk factor for morbidity and mortality, despite lesser severity of injuries.1,2,5 However, while age has value in mortality projections for geriatric trauma patients presenting to the ED, literature suggests favorable functional outcomes for those who survive to hospital discharge.8 Therefore, age alone is not a criteria to deny or limit care in the elderly.9



 This review will highlight important differences in elderly trauma patients with respect to:

  • Triage
  • Pathophysiology in the Elderly
  • Mechanisms and Patterns of Injury
  • Trauma Bay Approach
  • Special Considerations

There will be many citations throughout, but please keep in mind the limitations of research in geriatric trauma:8

  • Few prospective randomized controlled trials
  • No widely accepted age cut-off (“elderly” used to characterize patients ages 45-80)6
  • Lack of a uniform definition of an elderly trauma patient
  • Limited current studies (majority based in the 1980s-1990s)


Triage of the Elderly Trauma Patient

In its statement regarding trauma in the elderly, the CDC notes: “under triage of the older adult population is a substantial problem.”10 Under triage is defined as a failure to transport a trauma patient to a state-designated trauma center.10 Why is this important? Current studies (Zafar et al. and Maxwell et. al, 2015) have identified a significant mortality benefit for elderly patients presenting to trauma centers having had repeat exposure to geriatric trauma.11,12 Zafar et al. reported elderly patients as 34% less likely to die in these trauma centers.11 While it is true that level 1 trauma centers traditionally have longer lengths of stay and higher total costs of care, a large percentage of elderly trauma patients survive discharge from these facilities.11,12 Elderly patients with multiple injuries benefit from trauma center care.11,12 The difficulty here is that standard adult EMS triage guidelines provide poor sensitivity for detecting older adults that require trauma center care.13 The under triage rate is reported as 50%14,15 in patients older than 65, versus 17.8% for those under 65.14 Given this data, several experts have concluded that an age threshold should be established which mandates triage to a trauma center (various age ranges (55-70) have been recommended).6,9,16,17,18

What difficulties are encountered in identifying trauma severity in the elderly population? Potential explanations for under triage of elderly trauma patients are: significant injury secondary to low energy mechanisms, and altered physiologic response to injury with aging.

  • The CDC recommends direct transport to a trauma center for any trauma patient age >65 with SBP <11010
    • What affect does this have on triage of the elderly population? One that is substantial:
      • Substituting SBP < 110 instead of SBP < 90 for patients older than 65 reduced under triage by 4.4%, while only increasing over triage by 4.3%.19

Once an elderly patient arrives at a trauma center, trauma team activation occurs significantly less often for elderly patients (14% vs 29%) despite a similar percentage of severe injuries (defined as ISS>15).l

  • The Eastern Association for the Surgery of Trauma (EAST) recommends a lower threshold for trauma team activation for patients 65 and older evaluated at trauma centers (level 3 evidence).20
    • Some trauma centers use age as mandatory criteria for trauma team activation. This is supported by data that 63% of elderly trauma patients with ISS > 15 had no standard physiologic activation criteria.20

Clinical implications: Have a low threshold for recommending EMS transport of elderly trauma patients to a designated trauma center, especially for patients with SBP < 110. Have a low threshold for activating the trauma team for elderly trauma patients.


Pathophysiology Concerns in the Elderly

No other population is more susceptible to serious injury secondary to low-energy mechanisms (particularly falls) than the elderly. The elderly are less able to compensate for physiologic stresses occurring during injury, and are more likely to suffer complications during treatment and recovery. Key reasons for this are:

  • Less physiologic reserve
  • Occult shock/misleading picture of stability
  • Comorbid illnesses (See Figure below)

Screen Shot 2016-08-20 at 1.49.35 PM

Comorbid Illnesses Contributing to Morbidity and Mortality in the Elderly

It is important to note that in elderly patients, profound shock may be present even in the setting of “normal” vital signs.  Pharmaceutical therapy in the elderly (beta blockers and calcium channel blockers) may prevent typical tachycardic responses in shock states.  Also significant, aging myocardium exhibits decreased sensitivity to endogenous catecholamines.

Blood pressures considered normal in young patients may represent hypotension when compared to baseline BPs in an elderly patient. A landmark article by Scalea et al. assessing early invasive (PA catheter) monitoring in elderly trauma patients demonstrated that the majority of trauma patients experienced profound perfusion deficits despite “normal” vital signs.19 In fact, a HR>90 and SBP<110 have been correlated with increased mortality in the elderly trauma population.19,21 What does this mean for the EM provider? The window to intervene may be narrow; delayed recognition of shock may postpone life-sustaining resuscitation.

What about additional markers of perfusion?

Multiple studies have demonstrated that elevated lactate levels (>2) or abnormal base deficit (<-6) are associated with major injury and mortality in trauma patients.23-25 One such study, performed in 1987, identified a venous lactate > 2.5 as a marker of occult hypoperfusion in 20% of the included geriatric patients.26 Lactate levels or ABG base deficit should be used as an adjunct to vital signs for early identification of perfusion deficits in elderly trauma patients.

Clinical implications: Avoid being falsely reassured by normal vital signs in elderly trauma patients. Use lactate levels or ABG with base deficit as adjuncts to vital signs to detect occult shock and guide resuscitation in unclear cases. Also use ECGs as an adjunct to detect silent ischemia as a response to the physiologic stress of trauma. Have a low threshold for admitting elderly trauma patients to an ICU.


Mechanisms and Patterns of Injury

Which mechanisms and patterns of injury are more concerning in the elderly? They all are.

More specifically, falls from ground level, head trauma, chest wall injuries, pedestrian struck by vehicle, and cervical spine injuries have a disproportionate burden on elderly patients.

Screen Shot 2016-08-20 at 1.51.54 PM

Falls are the most frequent cause of injury in patients > 65 years of age, and are the most common fatal accident in patients > 80 years of age.27 More than one third of elderly patients presenting to the ED post fall return to the ED, or die within one year of initial evaluation.28 Same level falls must not be minimized – they are ten times more likely to cause death in an elderly vs. non-elderly patient (25% vs 2.5%).29 Even falls that seem purely mechanical can be a sign of occult illness. It is imperative that emergency physicians perform a complete H&P for all elderly patients having experienced a fall for:

  • Sudden disturbances in cardiovascular/neurologic function
  • New/progression of underlying conditions or emerging infection
  • Intoxicants/medication effects
  • Environmental safety
  • Impact of injury on functional status/ability to care for self

Why are falls so devastating in the elderly population?

Age-related atrophy of the brain leads to increased potential space and shearing forces on the intracranial bridging veins when exposed to trauma. The risk of intracranial bleeding is also markedly increased with medications commonly prescribed to the elderly (anticoagulants and anti-platelets).30,31 Keep in mind that older patients are excluded from studies that attempt to identify populations in which imaging is low yield = IMAGE the elderly.

 Outside of head trauma, are there any other areas for EM docs to be on the lookout?

Even “minor” chest injuries impair the elderly. Thoracic cage trauma is poorly tolerated secondary to decreased compliance, loss of alveolar surface area, impaired lung defenses, and increased pulmonary bacterial colonization with aging. A rigid C-collar and backboard can further impair chest wall expansion. Elderly patients with rib fractures are at increased risk for pneumonia (31% vs. 17% with 16% increase per rib fractured), pulmonary contusion, and delayed hemothorax.32 Mortality also increases 19% per rib fractured.32

 The elderly spine is vulnerable to fracture from minor mechanisms due to conditions such as cervical stenosis, osteoporosis, and degenerative, rheumatoid, and osteoarthritis.33 High cervical fractures (type 2 odontoid being the most common), and central cord syndromes are also more frequent in the elderly.34

Pedestrian struck by a vehicle is perhaps the most devastating mechanism of injury to disproportionately affect this population. Patients age > 65 account for 22% of pedestrian vs. MVC deaths.33 Current statistics report 46% of these accidents as occurring in crosswalks.33 Factors that predispose the elderly to increased severity of injury include decreased ability to raise or turn the head due to cervical arthropathy, and reduced speed and agility (crosswalk timers often allow for a pedestrian speed of 4 ft/sec).33

Clinical implications: Maintain a heightened suspicion for significant injury (especially intracranial and C-spine pathology) even from ground level falls. Assess elderly patients for medical impairments that may have precipitated the fall. Be liberal with CT scanning for elderly head and neck trauma, and always inquire regarding the use of anticoagulant and antiplatelet medications. Ensure adequate analgesia and oxygenation for chest wall injuries. Remove the collar and backboard as early as safely possible. Maintain a low threshold for admitting elderly patients with rib fractures.


Special Considerations

 ABCs in the Elderly

  • A – Early airway control. Edentulous patients may be difficult to bag; remove dentures for intubation.
  • B – Avoid respiratory decompensation by use of O2; analgesia for chest injuries; suction/pulmonary toilet; clear the C-spine, and remove the backboard as early as possible to prevent respiratory impairment.
  • C – Early transfusion to minimize fluid overload from crystalloids. Recognizing that “normal” BP may be relative hypotension for an elderly patient. Question patients regarding anticoagulant use and consider reversal early in the course.
  • D – Liberal use of head and C-spine CT; GCS is not a sensitive indicator in the elderly trauma patient.
  • E – Assess for signs of comorbidities that may not have been reported (i.e. surgical scars, pacemakers, medications or med lists in patient belongings, medical alert tags, bruising from anticoagulants).

Elder Abuse

No report on elderly trauma is complete without mention of elder abuse. Elder abuse can be very difficult to detect for several reasons:

  • Patient reluctance to identify a loved one
  • Patient dependence on the abuser
  • Perceived frailty limiting the patient from feeling empowered in seeking help
  • Patient mental or memory impairment limits the history
  • Abuse in the form of neglect can mimic cachexia from comorbidities

Clinical implications: When the scenario has stabilized, assess the patient’s social situation. Be wary of wounds or injuries that are suspicious for abuse or do not match the reported mechanism of injury. And of course, ask the patient, preferably in private!

A Quick Word on Anticoagulants

Anticoagulant use is far more prevalent in the elderly population. An increasing portion of the elderly population are being prescribed novel oral anticoagulants, which are not as readily reversible as warfarin. An elderly trauma patient should be questioned regarding anticoagulants ASAP. An irregular heartbeat may be a clue to chronic atrial fibrillation and anticoagulant use. Know your institution’s reversal protocol for the novel anticoagulants. If your institution does not have a protocol, then have a plan in mind. Know which prothrombin complex concentrates are available to you. Know if Praxbind is stored by your pharmacy.

Back to the Case

The patient in the initial case presentation may have been exhibiting his normal baseline mental status or could have been confused secondary to the emotional distress pertaining to the accident, but the provider must assume the confusion secondary to intracranial bleeding until proven otherwise. The patient’s irregular heart rate should alert the clinician to the possibility of aspirin or anticoagulant use, necessitating a plan for reversal should it be needed. In terms of the rest of the vital signs: the patient’s “normal” blood pressure may actually represent relative hypotension. The borderline hypoxia (and wheezing discovered on exam) is likely related to lung injury, aspiration, or an underlying comorbidity (i.e. COPD or CHF). This should serve as a warning – the patient is high risk for respiratory decompensation from chest injury and impaired chest wall motion from the C-collar and backboard. The backboard should be removed as soon as possible, pain from the chest injury treated as applicable, and supplemental oxygen employed. Suction may be considered as an adjunct. If and when the C-spine is cleared, the patient should be placed in an upright position to facilitate gas exchange and decrease work of breathing. The patient may have critical injuries and blood loss despite minimal symptoms so a lactate or ABG for base deficit should be sent. Imaging to rule out internal injuries is a must. Initial diagnostic work-up and resuscitation should be aggressive until the patient’s prognosis and wishes are clear. Volume resuscitation should be minimized, with blood products being the fluid of choice. The clinician should have a low threshold for trauma team activation vs. consultation and admission.



  • Resuscitation of the elderly trauma patient must be thoughtful but aggressive:
    • Heighten awareness that with age, signs and symptoms may be minimal, and that the outcome is often initially unclear, and commonly, but not necessarily poor.
    • Up to 85% of elderly trauma survivors return to baseline or independent function.9
      • This justifies initial aggressive approach which can be reassessed later when patient/family wishes and prognosis becomes increasingly clear.9
    • Less physiologic reserve leaves little time for delays in diagnosis and under- or over- resuscitation.
    • Blood is the fluid of choice.
    • The principles of diagnosis and management in trauma are the same regardless of age, but the incidence of physiologic changes and disease states mandates a different overall approach.
    • You may be the only one in the room who knows how sick the patient really is.


References / Further Reading

  1. Hashmi A, Ibrahim-Zada I, Rhee P et al. Predictors of mortality in geriatric trauma patients: A systematic review and meta-analysis. J Trauma Acute Care Surg. 2014;76:894-901.
  2. Vincent GK, Velkoff VA, U.S. Census Bureau. The next four decades the older population in the United States: 2010 to 2050. Population estimates and projections P25-1138. Washington, DC: U.S. Dept. of Commerce, Economics and Statistics Administration, U.S. Census Bureau; 2010. Available from http://purl.access.gpo.gov/GPO/LPS126596.
  3. CDC National Center for Health Statistics (NCHS), National Vital Statistics System. http://www.cdc.gov/nchs/nvss.htm.
  4. CDC Data and Statistics (WISQARSTM): Cost of Injury Reports Data Source: NCHS Vital Statistics System for Numbers of Deaths. http://wisqars.cdc.gov/8080/costT/.
  5. Champion HR, Copes WS, Buyer D et al. Major trauma in geriatric patients. Am J Public Health. 1989;79:1278-1282.
  6. Bonne S, Schuerer D. Trauma in the Older Adult – Epidemiology and evolving geriatric trauma principles. Clin Geriatr Med. 2013;29:137-150.
  7. Goodmanson NW, Rosengart MR, Barnato AE et al. Defining geriatric trauma: When does age make a difference? Surgery. 2012;152:668-675.
  8. Grossman MD, Ofurum U, Stehly CD et al. Long-term survival after major trauma in geriatric trauma patients: The glass is half full. J Trauma. 2012;72:1181-1185.
  9. Jacobs DG, Plaisier BR, Barie PS et al. Practice Management Guidelines for Geriatric Trauma. The EAST Practice Management Guidelines Work Group. J Trauma. 2003;54:391-416.
  10. Sasser SM, Hunt RC, Faul M et al. Guidelines for field triage of injured patients: recommendations of the National Expert Panel on Field Triage, 2011. MMWR Recomm Rep. 2012 Jan 13;61(RR-1):1-20.
  11. Zafar SN, Obirieze A, Schneider EB et al. Outcomes of trauma care at centers treating a higher proportion of older patients: The case for geriatric trauma centers. Acute Care Surg. 2015;78:852-859.
  12. Maxwell CA, Miller RS, Dietrich MS et al. The aging of America: a comprehensive look at over 25,000 geriatric trauma admissions to United States hospitals. Am Surg. 2015;81(6): 630-636.
  13. Ichwan B, Subrahmanyam D, Shah MN et al. Geriatric-specific triage criteria are more sensitive than standard adult criteria in identifying need for trauma center care in injured older adults. Ann Emerg Med. 2015;65:92-100.
  14. Chang DC, Bass RR, Cornwell EE et al. Undertriage of elderly trauma patients to state-designated trauma centers. Arch Surg. 2008;143:776-781.
  15. Kodadek LM, Selvarajah S, Velopulos CG et al. Undertriage of older trauma patients: is this a national phenomenon? J Surg Research. 2015;199:220-229.
  16. Caterino JM, Valasek T, Werman HA. Identification of an age cutoff for increased mortality in patients with elderly trauma. Am J Emerg Med. 2010;28:151-158.
  17. Lehmann R. The impact of advanced age on trauma triage decisions and outcomes: a statewide analysis. Am J Surg. 2009 May; 197(5):571-4.
  18. American College of Surgeon Committee on Trauma. Geriatric Trauma. In: ATLS: student course manual. 8th Chicago. 2008:247-257.
  19. Scalea TM, Simon HM, Duncan AO et al. Geriatric blunt multiple trauma: improved survival with early invasive monitoring. J Trauma. 1990; 30: 129–136.
  20. Brown JB, Gestring ML, Forsythe RM et al. Systolic blood pressure criteria in the National Trauma Triage Protocol for geriatric trauma: 110 is the new 90. J Trauma Acute Care Surg. 2015;78:352-359.
  21. Calland JF, Ingraham AM, Martin N et al. Evaluation and management of geriatric trauma: An Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73:S345-S350.
  22. Heffernan DS,Thakkar RK, Monaghan SF, et al. Normal presenting vital signs are unreliable in geriatric blunt trauma victims. J Trauma. 2010;69(4):813-820.
  23. Zehtabchi S, Baron BJ. Utility of base deficit for identifying major injury in elder trauma patients. Acad Emerg Med. 2007;14:829-831.
  24. Callaway DW, Shapiro NI, Donnino MW et al. Serum lactate and base deficit as predictors of mortality in normotensive elderly blunt trauma patients. J Trauma. 2009;66:1040-1044.
  25. Paladino L, Sinert R, Wallace D et al. The utility of base deficit and arterial lactate in differentiating major from minor injury in trauma patients with normal signs. Resuscitation. 2008;77:363-368.
  26. Salottolo KM, Mains CW, Offner PJ et al. A retrospective analysis of geriatric trauma patients: venous lactate is a better predictor of mortality than traditional vital signs. Scan J Trauma Resusc Emerg Med. 2013;21:1-7.
  27. Labib N,Nouh T, Winocour S et al. Severely injured geriatric population: morbidity, mortality, and risk factors. J Trauma. 2011;71(6):1908-14.
  28. Liu SW, Obermeyer Z, Chang Y et al. Frequency of ED revisits and death among older adults after a fall. Am J Emerg Med. 2015;33:1012-1018.
  29. Sterling DA,O’Connor JA, Bonadies J. Geriatric Falls: injury severity is high and disproportionate to mechanism. J Trauma. 2001;50(1):116-119.
  30. Rathlev NK, Medzon R, Lowery D et al. Intracranial pathology in elders with blunt head trauma. Acad Emerg Med. 2006;13(3):302-7.
  31. Li J, Brown J, Levine M. Mild head injury, anticoagulants, and risk of intracranial injury. Lancet. 2001; 357(9258):771-2.
  32. Bulger EM. Rib fractures in the elderly. J Trauma. 2000;48(6):1040.
  33. Bonne S, Schuerer DJ. Trauma in the older adult: epidemiology and evolving geriatric trauma principles. Clin Geriatr Med. 2013;29(1):137-50.
  34. Reinhold M, Bellabarba C, Bransford R et al. Radiographic analysis of type II odontoid fractures in a geriatric patient population: description and pathomechanism of the “Geier”-deformity. Eur Spine J. 2011. Nov;20(11):1928-39

Core EM: Life-Threatening Asthma

Originally published at CoreEM.net, who are dedicated to bringing Emergency Providers all things core content Emergency Medicine available to anyone, anywhere, anytime. Reposted with permission.

Follow Dr. Swaminathan and CORE EM on twitter at @EMSwami and @Core_EM

Written by: Anand Swaminathan, MD (@EMSwami)


Acute severe asthma or status asthmaticus refers to an episode of bronchoconstriction that is unresponsive to standard management. Patients with acute severe asthma will present with significant respiratory distress and it is critical to rapidly treat them to avoid significant morbidity and mortality. Patients will present with tachypnea, retractions, diaphoresis, ability to only speak 1-2 words at a time, abdominal breathing, cold extremeties. and wheezing (although the most severe may have a “quiet chest” indicating the absence of any significant air entry).

Immediate Management:

There are three main goals of immediate management of the severe asthma exacerbation:

  1. Stave off intubation while your medications have time to act. Intubation is associated with increased morbidity and mortality.
  2. Maximize pre-intubation parameters in case the patient doesn’t turn around and intubation is required.
  3. Reverse bronchoconstriction to decrease work of breathing and prevent respiratory failure from exhaustion of respiratory muscles.


ABCs, IV, supplemental O2. Patient should be provided with all of the therapies used in mild to moderate asthma exacerbations but will require more aggressive management

Oxygenation + Respiratory Support

  • Hypoxia only occurs late in a patient with a severe asthma exacerbation. Do not wait for hypoxia before supplying supplemental O2.
  • Standard Nasal Cannula – Turn up to 15-20 L/min
  • High-Flow Nasal Cannula (HFNC)
    • Allows for increased flow (40-60L/min of humidified O2
    • May be difficult to administer nebulizer treatments via facemask does not fit over HFNC
  • Non-Rebreather with Beta-Agnoist Reservoir
  • Non-invasive Positive Pressure Ventilation (NIPPV)
    • Decreases work of breathing and improves gas exchange
    • The evidence demonstrating a benefit to NIPPV is limited but available studies do not show substantial adverse events (Pollack 1995, Soroksky 2003, Lim 2012)
    • Bilevel Positive Airway Pressure (BPAP) preferred over Continuous Positive Airway Pressure (CPAP)
      • Difference in inspiratory (IPAP) and expiratory (EPAP) pressure aids in increasing tidal volume delivered
      • Start at IPAP 10 mm Hg, EPAP 5 mm Hg (or less) and titrate IPAP up (Typically no need to increase EPAP).

Intravenous Fluids

Close up of Intravenous drip

  • Patients with severe asthma exacerbations have enormous insensible losses from increased respirations and work of breathing.
  • Lung hyperinflation decreases pulmonary venous return, which can lead to hypotension. This is exacerbated by mechanical ventilation as the patient converts from negative pressure ventilation to positive pressure ventilation thus increasing intrathoracic pressure which can further decrease venous return.
  • Aggressive IV fluids (30 cc/kg) should be given early to replete intravascular volume.


  • Epinephrine is a non-selective beta agonist that causes bronchodilation, vasoconstriction, increased cardiac contractility and increased heart rate
  • Patients with severe asthma may have minimal benefit from inhaled beta agonists (i.e. albuterol) due to severe bronchoconstriction limiting delivery of medication to distal bronchioles.
  • Intramuscular (IM) / Subcutaneous(SQ) Epinephrine
    • Dose: 300-500 mcg
    • Limited evidence demonstrates minimal significant side effects at this dose (Cydulka 1988)
  • Intravenous (or Intraosseous) Epinephrine
    • More rapidly reaches target tissue than IM/SQ especially if patient hypotensive
    • Has effect of bronchodilation as well as vasoconstriction, which can reduce airway edema (Grandordy 1995)
    • Dose: 1 – 5 mcg/min and titrate to effect
    • Multiple retrospective studies demonstrate minimal adverse events with IV epinephrine (Smith 2003, Putland 2006)
  • Contraindications: Epinephrine can theoretically cause uterine vasoconstriction and should be used with caution in pregnant patients.
  • Terbutaline
    • Selective, parenteral beta 2 agonist that causes bronchodilation without effecting heart rate or cardiac output
    • Subcutaneous (SC) Terbutaline: 0.5 mg SC every 4 hours


  • Mechanism: Bronchial smooth muscle relaxation
  • Impact:
    • Modest decrease in hospital admission rate in patients refractory to standard management (Levy 2014). However, the sickest subset of patients were excluded from this study
    • The 3Mg trial (Goodacre 2013) demonstrated only a weak benefit to IV Magnesium in severe asthma however, this study did not include patients with life-threatening asthma.
    • In the absence of robust evidence, it is reasonable to administer magnesium to severe asthma exacerbations as there are minimal side effects of the drug and a potential for benefit
  • Dose: The dose in severe asthma is not established. 2 g IV over 15 minutes is a reasonable first dose and this may be repeated


  • Mechanism: Improved laminar flow of inhaled has which may allow better airflow through the constricted airways; allows better gas exchange and transport of medications to flow down to distal airways and alveoli
  • A mixture of helium and oxygen(multiple possible rations – 60:40, 70:30, 80:20). Only give the minimum FiO2 necessary to achieve goal O2saturation
  • Evidence of utility limited but has not been extensively studied in the sickest subset of asthmatic patients and may still be beneficial in this group.
  • Heliox may be used both via NIPPV and mechanical ventilator
  • Limitation: If patient markedly hypoxic, may not give an adequate amount of FiO2.


  • Only about 2% of asthma exacerbations require intubation with 10-30% of those admitted to the ICU requiring invasive ventilation (Rosen’s 2014)
  • Intubation is an inherently dangerous intervention in asthma because it does not fix the underlying problem (bronchoconstriction) and can cause dynamic hyperinflation (see below under ventilation), and rapid acidosis if respiration is not matched during RSI or post-intubation
  • There is no specific vital sign, lab value or other diagnostic test result, which determines the necessity for intubation. The decision to intubate is based on a number of factors including the patients overall appearance, work of breathing, perceived ability to maintain their effort of breathing, mental status etc.
  • Prior to intubation, be sure to maximize pre-oxygenation and intravascular volume
  • Rapid Sequence Intubation (RSI) Medications
    • There is no optimal set of agents for RSI in the severe asthmatic
    • Ketamine
      • Preferred agent because it does have hypotension as a side effect and it has bronchodilatory properties.
      • Dose: 1-2 mg/kg
    • Paralytic
      • Common options are rocuronium and succinylcholine
      • Rocuronium offers the advantage of longer paralysis which avoids vent asynchrony early in management

Mechanical Ventilation

  • Appropriate mechanical ventilation relies on ensuring that the patient has an adequate time to fully expire the delivered breath and avoid hyperinflation
  • Permissive Hypercapnea: Decreasing respiratory rate and allowing PaCO2 to rise to supranormal levels.
    • This strategy avoids breath stacking which leads to hyperinflation
    • Hyperinflation leads to increased airway pressures and can lead the development of a tension pneumothorax
    • Hyperinflation can also lead to marked decrease in venous return leading to decreased cardiac output and cardiac arrest
    • Hyperinflation leads to increased pulmonary vascular resistance and right ventricular dysfunction
  • Post-intubation meds (A full discussion of post-intubation care will appear in a future post)
    • Analgesia
      • Fentanyl (1-2ug/kg/hr) preferred over morphine or hydromorphone as it has minimal histamine effects
    • Sedation Options: Ketamine, propofolScreen Shot 2015-07-20 at 10.54.34 AM
    • Consider short-term paralysis if difficulty ventilating the patient
  • Initial Ventilator Settings
    • RR: 6-10 breaths/min
    • VT: 6-8 ml/kg (ideal body weight
    • PEEP: 0-5 cm H2O
    • FiO2: Minimum necessary to maintain O2 sat > 93%
    • Inspiratory Flow Rate: (suggest 100-120 L/min)
  • Check Plateau Pressures and maintain at < 30 mm Hg
    • Plateau pressure reflects the pressure experienced by alveoli
    • Maintaining Pplat < 30 mm Hg helps to avoid alveolar damage
    • If plateau pressure is > 30 mm Hg, consider lowering the RR and VT.

Mechanical ventilation does not fix the underlying bronchoconstriction. Be sure to continue maximal medical management.

Trouble Shooting the Ventilator

  • Hemodynamic instability and hypoxia after intubation and mechanical ventilation are common and life-threatening. Rapid recognition of the underlying problem and treatment are critical
  • DOPES Mnemonic – describes the most common causes of instability
    • Displacement of the endotracheal tube (ETT)
      • Direct visualization with laryngoscope preferred (US confirmation another option)
    • Obstruction of the endotracheal tube
      • Pass ETT suction catheter
    • Pneumothorax (tension)
    • Equipment failure
      • Disconnect the vent and deliver manual BVM breaths
    • Stacked Breaths
      • Forcibly exhale patient (gently push down on anterior chest wall with two hands until no further exhalation detected)

Trouble Shooting – Severe Acidemia

  • A pH < 7.15 can lead to physiologic issues
  • Check plateau pressure and if < 30 mm Hg, consider increasing ventilation (increase RR/TV)
  • Invasive Treatment
    • Inhaled Anesthetics (i.e. sevoflourane)
    • Veno-Venous (VV) ECMO

Take Home Points

  • Consider parenteral epinephrine in patients with severe asthma exacerbations as inhaled beta agonists are unlikely to penetrate into the distal airways.
  • Intravenous epinephrine is life-saving and safe when used appropriately.
  • Use NIPPV and high-flow nasal cannula to appropriately pre-oxygenate patients and avoid critical desaturations during intubation.
  • Use a strategy of permissive hypercapnea for mechanical ventilation to avoid breath stacking, hyperinflation and high airway pressures. Aim for plateau pressures < 30 mm Hg.
  • Use the DOPES mnemonic to troubleshoot hemodynamic instability after initiation of mechanical ventilation.

Read More:

EMCrit Podcast 15: The Severe Asthmatic

EMCrit Podcast 16: Coding Asthmatic, DOPES and Finger Thoracostomy

REBELCast: The Crashing Asthmatic


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