Category Archives: FOAMed


Author: Kristin E. Fontes, MD (Emergency Physician, Santa Barbara Cottage Hospital and Goleta Valley Cottage Hospital) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center)

Case presentation:

A 28-year-old female is brought to the emergency department by ambulance from home after her roommate found her disoriented and poorly responsive. The roommate reports finding a small container of antifreeze in the patient’s bedroom. Vital signs are as follows: T 37.0C, HR 65, BP 126/76, RR 32, and SpO2 98% on room air.  Venous blood gas shows pH 6.97, pCO2 21, pO2 38, HCO3 4.8, and lactate 6.75.


What are the laboratory abnormalities that can occur with toxic alcohol poisoning and how can it be treated?


Common features of toxic alcohol poisoning are elevated anion gap metabolic acidosis and elevated osmolar gap (the latter being a distinguishing feature from ethanol poisoning); osmolar gap usually elevated early after ingestion.(1,2)

Recall the toxic alcohol metabolites and their effects:

toxic alcohol metabolism

  • EG toxicity can cause significant renal failure due to oxalate crystal deposition in the kidneys and glycolic acid, which is directly nephrotoxic; hypocalcemia and tetany can also result due to oxalate binding to calcium.(1)
  • MeOH toxicity classically causes visual disturbances (“snowfield” vision) due to formic acid-induced optic neuropathy.(1)
  • Isopropanol toxicity causes ketosis without acidosis (no lactic acid formed!).  Usually benign clinical course but can occasionally cause hemorrhagic gastritis. Fomepizole and HD not usually indicated.(1)
  • Propylene glycol toxicity often due to intravenous medication preparations containing this alcohol (e.g., diazepam, lorazepam, esmolol, nitroglycerin, phenobarbital, phenytoin) can result in severe lactic acidosis.(1)
Treatment Approach:
  • Fomepizole competitively inhibits alcohol dehydrogenase, which is involved in the metabolism of all alcohols, including ethanol. It is given to prevent the buildup of toxic metabolites from ethylene glycol (glycolic acid, glyoxylic acid, and oxalic acid) and methanol (formic acid) whose deposition in tissues can cause irreparable damage.(1)
  • Fomepizole is indicated for MeOH or EG ingestion resulting in a metabolic acidosis with an elevated osmolar gap (not accounted for by ethanol) and a serum MeOH or EG level of at least 20 mg/dL.(1)
  • Fomepizole dosing: 1) Load: 15 mg/kg (max 1.5 g) IV, diluted in 100 mL of normal saline or 5% dextrose, infused over 30 minutes; 2) Maintenance: 10 mg/kg IV every 12 hours for 4 doses, then increase to 15 mg/kg until serum toxic alcohol level is less than 20 mg/dL.(1,3)
  • Hemodialysis is indicated for toxic alcohol poisoning with an elevated osmolar gap and/or severe metabolic acidosis refractory to standard therapy, refractory hypotension, or end organ damage (i.e. acute renal failure).(1,3)
  • Vitamin Supplementation: Give folic or folinic acid to patients with MeOH toxicity to divert metabolism away from formic acid to carbon dioxide and water. Give folic acid, pyridoxine, and thiamine to patients with EG toxicity to divert metabolism to nontoxic metabolites.(1,3)
Main points:

Consider toxic alcohol poisoning in a patient with an unexplained elevated anion gap metabolic acidosis and elevated osmolar gap. Consider fomepizole and/or HD in patients with severe toxic alcohol poisoning, especially if refractory to standard therapy.


  1. Olson KR & California Poison Control System. (2012). Poisoning & drug overdose. New York: Lange Medical Books/McGraw-Hill.
  2. Emmett M and Palmer BF. Serum osmolal gap. In: UpToDate, Forman JP (Ed), UpToDate, Waltham, MA, 2016.
  3. LeBlanc C, Murphy N. Should I stay or should I go?: toxic alcohol case in the emergency department. Can Fam Physician 2009 Jan;55(1):46-9.

ToxCard: TCA Poisoning

Author: Tharwat El Zahran, MD (Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center) screen-shot-2017-01-08-at-11-30-27-pm
Case Presentation:

2 yo male child presented to the ED with status epilepticus. His parents found an empty bottle of amitriptyline at home. He was intubated, given benzodiazepines and antiepileptic drugs. VS: BP 70/30, T 106 F, RR 24, HR 98, sat 98% RA, glucose 100 mg/dl. EKG is shown below.



What EKG findings occur in tricyclic antidepressant (TCA) poisoning? And how are they treated?


TCAs alter the conformation of the sodium channel and slow the rate of rise of the action potential, which produces both negative dromotropic and inotropic effects. Sodium bicarb is the primary treatment for TCA poisoning.

  • All TCA are competitive antagonists of the muscarinic acetylcholine receptors and antagonize peripheral α1 adrenergic receptors.
  • Most prominent effects of TCA overdose result from binding to cardiac Na channels.
  • Acute ingestion 10-20 mg/kg of most TCAs cause cardiovascular and CNS toxicity. In children,  >5mg/kg results in toxicity.(1)
  • Signs of acute cardiovascular toxicity are refractory hypotension, acidosis, and arrhythmias. EKG indicators include intraventricular conduction delay (R shift of QRS axis and prolonged QRS), R in avR≥ 3mm, R/S>0.7 and arrhythmias. A QRS≥100 msec indicates increased incidence of serious toxicity, including coma, intubation, hypotension, seizures, and dysrhythmias. Sinus tachycardia is the most common EKG abnormality. (2)(3)
  • Acute neurological toxicity include AMS, delirium, agitation , seizures, and/or psychotic behavior with hallucinations, lethargy, coma.
Treatment approach
  • If the decision is made to intubate, avoid apnea, consider awake intubation, pretreat w benzos to raise seizure threshold and hyperventilate to promote alkalosis.(4)
  • If the EKG indicates signs of TCA poisoning as mentioned above,  give 1-2 meq/kg of sodium bicarb IV boluses at 3-5 min intervals.(4)
  • Continue bicarb drip until QRS duration <100, vitals stable, Na ~150, pH ~7.55. Watch for hypokalemia and hypocalcemia with bicarb drip.  Consider hypertonic saline (3%) if refractory or if serum pH>7.55.(4)
  • Hypotension unresponsive to sodium bicarb, or fluid boluses should be treated with vasopressors (norepi recommended).(4)
  • Treat dysrhythmias with lidocaine bolus of 1mg/kg IV followed by infusion of 20-50 mcg/kg/min.
  • Benzodiazepines, barbiturates, or propofol are recommended for seizures. Consider continuous EEG monitoring with neuromuscular blockade in refractory cases. Avoid phenytoin.(4)
  • For refractory cardiovascular poisoning consider intralipid or ECMO if available.(4)
Main point

TCAs are sodium channel blockers and primary treatment of TCA poisoning is sodium bicarb. The EKG abnormalities like QRS≥100,  R wave in avR ≥3mm, and R/S> 0.7 can predict significant toxicity.  Sodium bicarb displaces the TCA from the Na binding site by raising the Na+ gradient and increasing the pH.  Prolonged resuscitation might be necessary.

  1. Caksen et al. Acute amitriptyline intoxication: an analysis of 44 children. Human & Experimental Toxicology (2006) 25: 107-110
  2. Olgun et al. Clinical, Electrocardiographic, and Laboratory Findings in Children With Amitriptyline Intoxication. Pediatr Emer Care 2009;25: 170-173
  3. Paksu et al. Amitriptyline overdose in emergency department of university hospital: Evaluation of 250 patients. Human and Experimental Toxicology 2014;33:980–990
  4. Goldfrank’s Toxicologic Emergencies, 10th E, Chapter 71: Cyclic Antidepressants, p 972- 982.



Tox Cards: CO Poisoning

Author: Patrick C. Ng (Chief Resident, San Antonio Military Medical Center) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center)
Case Presentation:
It is a cold day in the middle of December. A 56 yo female and her 29 yo daughter who is 8 months pregnant present to your ED with a chief complaint of generalized weakness and headache for 2 days. They mention that they think they both caught the flu due to the cold temperatures despite turning their heater on high and using oil lamps for extra heat in their apartment. Their vital signs are normal.
What are the most common signs/symptoms of carbon monoxide (CO) poisoning, and what are the general management plans?

CO poisoning presents with nonspecific symptoms that can be mistaken for other diagnosis such as the flu. Initial treatment includes high-flow supplemental O2. Hyperbaric oxygen therapy (HBOT) may or may not be the “standard of care” (controversial).

  • CO poisoning can be an elusive diagnosis, as non-specific symptoms such as headache, dizziness, nausea, fatigue, and chest pain are non-specific and can be consistent with many other disease processes.(1,2)
  • Key historical clues include people from the same household presenting with symptoms of headache and flu-like symptoms that improve throughout the course of the day (i.e. when patients leave their dwellings for work, school, etc.) and history of exposure to CO sources such as heaters and enclosed garages.(1,2)
  • A co-oximetry is a spectrophotometer that uses many different wavelengths to measure oxygenated hemoglobin (oxyHb), deoxygenated hemoglobin (deoxyHb), as well as carboxyhemoglobin (COHb) and methemoglobin (MetHb) concentrations.(3)
  • The use of greater number of wavelengths in a co-oximeter as compared to a standard pulse oximeter allows the co-oximeter to distinguish between other types of hemoglobin,  whereas a standard pulse oximetry can only distinguish between oxyHb and deoxyHb.(3)
  • Blood COHg levels commonly reaches a level of 10 % in smokers and may even exceed 15 %, as compared with 1 to 3 % in nonsmokers.(2)
  • Standard treatment includes  high-flow O2  via NRB mask (or intubation in severe cases) until symptoms resolve and CO levels return to baseline; pregnant patients should continue for at least 24 hours with fetal wellbeing assessment. Patients also require follow up at 1-2 months for neuropsychiatric assessment.(1,2)
  • Normal half life of Hb-CO is 4-6 hrs with room air oxygen, 40- min with high-flow O2, and 15-30 min with HBOT.(2)
  • Although the indications for HBO are controversial, some recommend HBO for any CO-poisoned patient with mental status change or history of syncope, signs of cardiac ischemia or arrhythmia, history of ischemic heart disease and CO level > 20%, symptoms that do not resolve with normobaric O2 therapy after 4-6 hours, or any pregnant patient with CO > 15%. Coma is generally an undisputed indication for hyperbaric-oxygen therapy.(2)
  • The use of HBO has been reported to reduce the risk of neurological/cognitive sequelae thought to be associated with carbon monoxide poisoning.(4,5)
Main Point:
Carbon monoxide poisoning can be a deadly diagnosis associated with significant morbidity and long-term permanent neurological damage. It can present with very non-specific symptoms. Specific historical clues as well as co-oximetry can help the emergency physician quickly make the diagnosis. High-flow O2 therapy is the initial standard therapy with some advocating HBOT for select severe or at risk cases.
1. Piantadosi CA. Diagnosis and treatment of carbon monoxide poisoning. Respir Care Clin N Am. 1999;5:183-202.
2. Ernst A, Zibrak JD. Carbon Monoxide Poisoning. N Engl J Med 1998;339:1603-1608.
3. Hampson NB. Noninvasive pulse CO-oximetry expedites evaluation and management of patients with carbon monoxide poisoning. Am J Emerg Med. 2012 Nov;30(9):2021-4.

4. Tibbles PM, Perrotta PL. Treatment of carbon monoxide poisoning: a critical review of human outcome studies comparing normobaric oxygen with hyperbaric oxygen. Ann Emerg Med. 1994;24:269-276.
5. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347:1057–1067

Treatment for Salicylate Poisoning

Author: Sean Kolowich (Emory University School of Medicine) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)


Case presentation:

A 53 year-old previously healthy female is brought into the ED by family members 4 hours after ingesting 100 tablets of aspirin (325mg, unknown formulation). She has no complaints and denies any co-ingestions. VS: Temp 98.1 (oral), HR 93, BP 136/87, RR 20, pulse ox 98% on room air. CMP and ECG are unremarkable, ASA 47.1 mg/dL, ABG pH 7.48, pCO2 20, pO2 122.


What treatments should a salicylate poisoned patient receive?


Patients with salicylate poisoning should receive IV bicarb to alkalinize the urine. Indications for hemodialysis include cerebral edema, pulmonary edema, renal failure, intractable acidosis, clinical deterioration, or ASA level > 100 mg/dL or > 70 mg/dL if chronic.

  • Support ABCs, prevent further organ toxicity by encouraging salicylate elimination
    • Alkalinize the serum/urine
      • 1-2 mEq/kg sodium bicarb. IV bolus followed by sodium bicarb. infusion (3 amps into 1L D5W) @ 1.5-2 X maintenance rate
        • goal serum pH ~7.5
        • goal urine pH >7.5
  • Salicylate overdose + IV sodium bicarbonate therapy = potential hypokalemia
    • Avoid hypokalemia because it prevents alkalization of the urine ® prolonged elimination of salicylate
      • goal K+ 4.0 to 4.5 mEq/L
    • Monitor calcium levels (ionized/total); IV NaHCO3 can cause hypocalcemia
  • Consider glucose supplementation if altered mental status
    • Serum glucose may be normal but CNS levels may be low 2/2 effects of salicylates
  • Indications for extracorporeal treatment (intermittent hemodialysis is ECTR of choice):
    • Salicylate level > 100 mg/dL (> 90 mg/dL if impaired kidney function) or > 70 md/dL if chronic.
    • Cerebral edema (altered mental status, seizures)
    • Renal failure
    • Pulmonary edema or new hypoxemia requiring supplemental O2
    • IF standard therapy fails AND:
      • Salicylate level > 90 mg/dL (> 80 mg/dL if impaired kidney function)
      • Systemic pH < 7.20
  • Continue IV sodium bicarb therapy b/w ECTR sessions
Main Point:

Patients presenting with acute salicylate toxicity should receive supportive care and alkalinization with IV sodium bicarbonate. Hemodialysis should be considered early in treatment and is indicated if there is evidence of end organ damage (AMS, ARDS), failure of standard therapy, or severely elevated salicylate levels.



  1. Lugassy DM. Salicylates. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR. Eds. Goldfrank’s Toxicologic Emergencies, 10e. New York, NY: McGraw-Hill; 2015.
  2. Levitan R, Lovecchio F. Salicylates. 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.
  3. Juurlink DN, Gosselin S, Kielstein JT, et al. Extracorporeal Treatment for Salicylate Poisoning: Systematic Review and Recommendations From the EXTRIP Workgroup. Ann Emerg Med 2015; 66:165

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

Screen Shot 2017-01-29 at 5.56.37 PM


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 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:
  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:,-management-of

Limitations of CIWA score

Author: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)


Case Presentation:

You are working a busy ED shift and are also managing a handful of boarded patients admitted to your ICU. Nursing resources are especially strained today. One of your intubated patients that you admitted for alcohol withdrawal starts having a seizure. His vitals are T 101F, HR 135, BP 175/100, RR 16, O2 sat 89% on 40% O2.


What are some of the limitations of using the CIWA score?


Although the CIWA score is a widely cited example of symptom-triggered therapy it has several important limitations and can be difficult to properly execute in the emergency department setting.

  • Symptom-triggered treatment for alcohol withdrawal using the CIWA score has many benefits including reduced progression to mechanical ventilation requirement, 4-fold decrease in benzodiazepine requirements, shorter duration of treatment, and shorter hospitalization stays by 2 days when compared to fixed-dosing scheduling.(1)
  • However, an important clinical limitation of CIWA as a tool to assess alcohol withdrawal is that it does not incorporate vital sign assessment, which can be an important and sometimes the only clue available in recognizing inappropriately treated DT patients.(2)
  • The CIWA score also does not address choice of benzodiazepines, frequency of administration, use of adjuvant medications and underlying medical conditions (renal failure, liver failure, respiratory failure, cardiac disease, age, etc.) in treating withdrawal.(2)
  • The CIWA score requires patients to be able to respond to questions and follow commands. This can be difficult in patients with language barriers, altered mental status or who are intubated.(2)
    • For example “Do you feel sick to your stomach, have you vomited?”; “Do you have any itching, pins-and-needles sensations, burnings, or numbness…?” and “Are you seeing anything that is disturbing you?” are some questions asked.
  • Many of the studies that have evaluated CIWA have excluded patients with seizures, which is an important sign of severe withdrawal and should be taken into consideration.(3)
  • Moreover, the CIWA score can be especially difficult to execute properly without adequate nursing staff. Many busy EDs are often understaffed and have limited nursing resources. Thorough staff training is required to appropriate use CIWA.(2) Studies have shown that the CIWA score tends to be administered irregularly by nursing staff, often used for patients who are not appropriate for symptom-guided treatment and can have a higher proportion of protocol errors.(4)
  • Scoring systems are important for symptom-triggered therapy and provide the ability for comparison analysis in clinical trials. However, many other scoring systems exist. An example is the Richmond Agitation Sedation Scale (RASS), which is observer based.(5) Many hospitals have their own scoring systems as well.
Main point:

Symptom triggered therapy has been shown to have better outcomes than fixed benzodiazepine scheduling in managing alcohol withdrawal. The CIWA score is a widely cited method of using symptom triggered therapy. However, physicians should not rely on just the CIWA score and other hospital and research protocols exist. The CIWA score has several important limitations including the exclusion of vital signs as an assessment, reliance of the patient’s ability to answer questions and follow commands, and can be time consuming in a busy ED environment.

  1. Daeppen J, Gache P, Landry U, et al. Symptom-triggered vs fixed-schedule doses of benzodiazepines for alcohol withdrawal. JAMA. 2002;162(10):1117-1121.
  2. Sankoff J, Taub J, Mintzer D. American College of Medical Quality: Accomplishing much in a short time: use of a rapid improvement event to redesign the assessment and treatment of patients with alcohol withdrawal. Am J Med Qual. 2013; 28(2):95-102.
  3. Saitz R, Mayo-Smith MF, Roberts MS, Redmond HA, Bernard DR, Calkins DR. Individualized treatment for alcohol withdrawal: a randomized double-blind controlled trial. JAMA. 1994;272:519-523.
  4. Hecksel KA, Bostwick JM, Jaeger TM, Cha SS. Inappropriate use of symptom-triggered therapy for alcohol withdrawal in the general hospital. Mayo Clin Proc. 2008;83:274-279. 10.
  5. Sessler CN. The Richmond Agitation-Sedation Scale” validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med. 2002; 166:1338-1344.

FOAMed Resources Part IX: Residency Program-Sponsored FOAMed

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

Welcome back to the FOAMed Resource Series with Part IX. We have discussed a wide variety of topics including critical care, ultrasound, pediatrics, and toxicology. Today we focus on FOAMed coming to you from residency programs. These sites provide some of the best education out there, so hold on tight for more great educational content!



CORE EM comes straight from FOAMed heavyweight Anand Swaminathan and the NYU EM program. This site focuses on yep, you guessed it, core content. The site provides regular blogposts (including cases, journal club, and core topics), videos, as well as a podcast. It provides free, bread and butter education that is second to none.




Taming the SRU (Shock Resuscitation Unit) from Cincinnati is another major contributor to core content. The site contains a blog focusing on several aspects of emergency medicine including procedures, ultrasound, cases, core content, and education. The site is associated with a podcast, and the “Annals of B-Pod” are downloadable journal-type articles on interesting cases and conditions.




Brown Emergency Medicine publishes great content on cases, core topics, journal reviews, procedural videos, images, and controversial topics in EM. Asynchrony EM is a FOAMed-guided tour of EM topics. The site also has an overview of 52 classic articles in EM.




UMEM education pearls provide almost daily updates on classic EM topics and cutting edge research. The site is easy to use and follow, and all posts are referenced so you can gather more information if needed. The UMEM educational hub contains video lectures from some of the best in EM and critical care –




The residents of Kings County Hospital ED bring you an up-to-date, evidence-based blog on board review topics, ECGs, clinical cases, critical care, toxicology, pediatrics, radiology, and many others. Content is almost released daily, and oh yeah, they have lectures from grand rounds for those visual learners.




Washington University in St. Louis has put together a great combination of FOAMed content. This sites contains case-based learning, FOAM supplement (a combination of great FOAMed topics), EMS cases (brought in by ambulance), consultant teachings, challenging cases, and classic and challenging ECGs. The residency’s journal club is also available, with discussions on key topics vital to everyday practice.




NUEM comes from Northwestern University EM. This blog contains content on new literature, dogma in EM, and interesting cases, broken down by organ system. Each post is well written and referenced, as well as peer reviewed by a staff expert in the subject.




Sinai EM is a great blog that provides several posts per week focusing on imaging, cases, controversy, and literature updates. The vast majority of EM content is well represented. They also cover the core literature, focusing on one article in one week.




Carolinas Core Concepts comes from the CMC EM residency program. The blog contains several categories, each providing valuable content. Core Concepts provides you with the basics for success in EM through bullet point reviews. The site also contains resident driven blogs including ortho, cardiology, tox, and peds, as well as attending blogs on coding/billing, ultrasound, and health policy.




EM DAILY from Cooper University Health Care gives you great educational pearls. Every day of the week focuses on a specific topic, with basics on Monday, advanced techniques on Tuesday, radiology on Wednesday, conference on Thursday, critical care on Friday, Wellness on Saturday, along with several others. A weekly summary is provided on Sunday for those who desire an all-in-one stop.




The EMBlog from the Mayo Clinic EM Program provides a platform for FOAMed focusing on new and controversial studies, resident education, social medicine, shared decision making, and disposition. This blog’s strength is in its coverage of topics not covered elsewhere in FOAMed, specifically the social aspects of our care in the ED. You don’t want to miss this resource.




Las Vegas EMR contains posts including bread and butter topics in EM, while also evaluating myths and dogma in daily EM practice. Conference videos on lectures are provided on the site, giving learners of all levels access to more content. All posts are well referenced as well.




HQMedED comes from Hennepin County Medical Center. This site is a collection of online videos and lectures on EM topics ranging from procedures, ECG, pediatrics, critical care, and toxicology, as well as core content. This is a great resource for visual learners.




The Temple EM Residency blog provides regular updates in common EM topics through an evaluation of the most current literature. Posts are provided at least once per week, though more commonly this occurs several times per week. If you want to stay up to date on relevant literature, this is the blog for you.

This is not an all-encompassing list, and if you like other resident-run blogs, please comment below! Stay tuned for more in the series.

#EMConf: Live Tweeting?

Author: Vidya Eswaran, MD (EM Resident Physician, Northwestern University Feinberg School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

It’s no secret that the #FOAMed movement is strong on Twitter. Blogs, articles, and opinions are shared on a nearly 24/7 basis. Within minutes, clinical questions can be answered, connections can be made, and knowledge can be shared among physicians from around the world. Increasingly, Twitter use at conferences has also grown. An analysis of tweets sent from an Australian Emergency Medicine Conference from 2011 to 2014 showed a 920% increase in the number of tweets from 460 to 4694, and an increase in number of tweet generators from 54 to 572.[1] This phenomenon is not limited to Emergency Medicine, and specialties such as Family Medicine,[2] Urology, Oncology,[3] and Surgery[4] have all participated in this trend. It has even been posited that “Global twitter conferences could be a cost-effective and low-carbon complement to traditional conferences”.[5]  Beyond tweets from large-scale meetings, residency programs are increasingly tweeting ‘pearls’ from their weekly educational conferences using the hashtag #EMConf.[6] From Dec 28, 2016 to Jan 6, 2017, 277 tweets were sent with the hashtag #EMConf by 145 users, reaching an audience of 135,835. I myself have sent numerous tweets from national conferences as well as from my own residency program’s weekly conference and have found myself asking the questions: Are my tweets serving any purpose, or am I merely adding to the background noise on the Twitter-sphere? Could my tweets serve more harm than good?

The Case for Live-Tweeting

Attending conferences is expensive – the flight, hotel, and food expenses can add up, especially for residents on a limited income. The core behind the entire FOAMed movement is to break down barriers to accessing medical education, and tweeting conferences is another means to this end. By attending conferences-by-proxy via Twitter, physicians can learn what is on the forefront of clinical innovation as well as review the fundamentals. This makes us better physicians, and thereby can improve the care we give our patients – our ultimate goal.

One thing I’ve learned in my, albeit short, time as an EM physician, is that practice variation abounds – regionally, hospital-wide, and even amongst providers in the same department. By sharing information from conferences we encourage engagement and discourse from physicians around the world. From this there is the possibility to learn how different physicians practice, and with careful consideration, physicians could apply a new practice pattern to their patient care through further education on the topic.

One might question the percentage of conference tweets which actually hold educational value. One study, at least, seems to show the majority does. The authors analyzed data from 2014 European Public Health Conference held in Glasgow. 1066 tweets were retrieved, of which 60% had session-related content while social/logistic-related tweets were only 16%.[7]

While providing free access to educational content to emergency physicians is a very benevolent task, I would be remiss to say that live-tweeting a conference is without any personal benefit. The conference attendee who sends out tweets has the potential to expand his or her personal network on social media. For some an increase in the number of followers is in itself an achievement, and as the case with networking of any kind, can lead to increased opportunities in the future. Benefits also exist for the speaker whose lecture is being tweeted. Live-tweets of your presentation can serve as free publicity of your research or of your presentation skills and could lead to opportunities to speak at other institutions or conferences. Finally, conferences themselves benefit from live-tweeting of their events. By raising awareness of their conference, Twitter serves as a free source of advertising and branding, and might encourage those not in attendance to register in the future. Additionally residency programs which tweet their conferences may find their tweets to be a source of advertising to residency applicants.

The Case against Live-Tweeting

A common criticism of FOAMed in general is that the content published is not as rigorously assessed for accuracy as more traditional sources of education. FOAMed proponents have responded by emphasizing that peer-review does in fact occur both prior-to and after publication of FOAMed pieces. Live-tweeting magnifies this issue. Tweets are often sent rapidly, as the tweet writer sits in the conference – opening potential for mistakes not only from the conference speaker but from the transcriber as well. One study analyzed tweets sent from an emergency medicine conference where speakers were asked to assess the level to which tweets from their talk accurately represented what they intended to convey. The investigators found that speakers believed that 43.2% tweets represented, 43.2% partly represented, and 8.1% misrepresented what they intended to convey.[8] While likely a genuine mistake on the part of the tweet generator, the implications could be grave if wrong information were applied in a clinical situation. Along these lines, it is possible that comments made by the speaker may be taken out of context leading to sensationalization and misrepresentation, which can be harmful not only in terms of the veracity of the tweet but may have negative repercussions for the speaker him/herself.

FOAMed is often criticized because its content is not broad. One study found that topics such as airway techniques, ECG interpretation, resuscitation, ultrasonography, and analysis of literature were overrepresented while cutaneous, hematologic, obstetric and gynecologic, and non-traumatic musculoskeletal disorders were rarely covered.[9] A similar case could be made for tweets from conferences. Just as we will never know if an unattended tree in the forest makes a noise as it hits the ground, we cannot glean information from a talk at which nobody tweets. A larger number of tweet generators may attend talks at conferences about popular or exciting topics, and other, perhaps more mundane, but equally important topics may not be broadcasted.

We can all remember a lecture in which we have found our minds wandering, or had the experience of being in a thoroughly engaging presentation, only to forget what was taught the next day. Those who tweet during conferences have two tasks: they must both pay attention to the content being delivered as well as expend mental energy to summarize important points into 140 character ‘pearls’. It seems inevitable that some content will be missed in the process. Not only is the tweet generator missing out on educational content, but their Twitter followers are also not gleaning the entirety of the presentation. Of all the critiques regarding live-tweeting, I think this to the most dangerous and in need of the most investigation. The primary goal for any learner, whether it be in a residency program setting or at a national conference, is to fill his or her own personal educational needs. Only then can one focus on spreading that knowledge to others. If live-tweeting prevents active engagement in the course, then it can be argued that the ‘risks’ of tweeting outweigh the benefits. On the other hand, others may find tweeting to be in line with their personal learning style by encouraging them to listen, synthesize, and summarize the main points of a lecture in real-time. Additionally, the act of typing may in itself serve as further ‘active learning’ to cement key topics.

To Tweet or Not to Tweet?

There are many questions yet to be answered – can learning from tweets be quantified, is there a way to ensure the greatest degree of accuracy in live-tweets, can we ensure that learners aren’t distracted from lecture content while tweeting? At this point in time I think I will continue to live-tweet. I enjoy being a part of the FOAMed community both as a generator of tweets as well as an enthusiastic reader of others’. As I ride the bus into shifts on Thursday mornings I find myself skimming through tweets from residency programs around the country, saving the ones I find interesting for further investigation. As with most things on the internet, however, I approach everything I read with a healthy dose of skepticism. It is on me to trust, but verify, what others tweet before implementing it into my clinical practice.

To those of you considering live-tweeting your next conference, I encourage you to pay close attention to how tweeting affects your learning. If you feel it is a distraction, perhaps take notes during the lecture and then tweet afterwards, when you have more time summarize and synthesize the material. If you wonder about the veracity of a statement or if you are unclear about whether you are representing the speaker’s point, perhaps wait to send the tweet until you can confirm your doubts with the speaker him/herself.

Will Twitter completely obviate the need to attend conferences? I doubt it. There are many benefits, both tangible and intangible to being physically present: from engaging in discourse, to asking the speaker questions directly, networking with other conference participants and having fun with friends, new and old, in different locales.  But for those who cannot attend, with a bit of caution, Twitter can offer an invaluable avenue to be a part of the clinical dialogue.

For more on Twitter use at conferences, see these great sites:

References/Further Reading:

[1] Udovicich C, Barberi A, Perera K. Tweeting the meeting: A comparative analysis of an Australian emergency medicine conference over four years. J Emerg Trauma Shock 2016;9:28-31.

[2] Mishori R, Levy B, Donvan B. Twitter use at a family medicine conference: analyzing #STFM13. Fam Med. 2014 Sep;46(8):608-14.

[3] Wilkinson S, Bastro M, Perovic G, Lawrentschuk N, Murphy D. The social media revolution is changing the conference experience: analytics and trends from eight international meetings. BJU International 2015: 115(5):839-846.

[4] Logghe H, Maa J, Schwartz J. Twitter usage at Clinical Congress rises markedly over two years. Bull Am Coll Surg. 2013 Feb;98(2):22-4.

[5] S Avery Gromm, S Hammer, G Humphries. The age of the Twitter conference. Science 2016: 352(6292): 1404.

[6] MR Haas et al. #EMConf: utilizing Twitter to increase dissemination of conference content. Medical Education 2016; 50: 564-591.

[7]  Bert F, Paget DZ, Scaioli G. A social way to experience a scientific event: Twitter use at the 7th European Public Health Conference. Scandinavian Journal of Public Health, 2016; 44: 130–133

[8] Roland D, May N, Body R, et al. Emerg Med J 2015;32:412–413.

[9] Stuntz R, Clontz R. An Evaluation of Emergency Medicine Core Content Covered by Free Open Access Medical Education Resources. Ann Emerg Med. 2016 May;67(5):649-653.e2. doi: 10.1016/j.annemergmed.2015.12.020. Epub 2016 Feb 11.