Episode 49 – The AAP BRUE (formerly ALTE) Guidelines


The Free Open Access Medical Education (FOAM)

We review the American Academy of Pediatrics guideline on Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants.

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Note: Some have voiced concerns that these guidelines potentially downplay the event. The concern is that the yield of these workups and admissions may be low, but possibly worthwhile.  At FOAMcast, we are not qualified to critique these guidelines but there are helpful tables and charts in them to realize that these recommendations really are only for specific events and children AFTER thorough history and physical.

Generously Donated Rosh Review Question

A 6-week-old boy is brought to the emergency room because of cyanosis. He was sleeping comfortably in a supine position right after a feeding when he suddenly choked, became limp and lips turned blue. The mother witnessed the event and blew to the face of the boy. The whole episode lasted for about two minutes. EMS was called and upon arrival at the house, the boy was back to his usual self. At the ER, he boy has normal vital signs with normal physical examination findings.


  1.  Admit for cardiorespiratory monitoring. The boy in the vignette had an apparent life-threatening event (ALTE) which is not a specific diagnosis but a description of an acute, unexpected episode that is frightening to the caretaker. ALTE includes one or more of the following features: apnea, color change (may be cyanotic, pallid, erythematous or plethoric), marked change in muscle tone (limpness or rigidity) and choking or gagging. A specific cause for ALTE can be identified in over one-half of patients after a careful history, physical examination, and appropriate laboratory evaluation. The remaining cases are considered idiopathic if no cause can be identified after a thorough assessment. Common etiologies for ALTE include gastroesophageal reflux, neurologic problems (such as seizures), and respiratory infection. The history of an ALTE must be taken seriously, even if the infant appears entirely well by the time he or she is evaluated. In-hospital observation with cardiorespiratory monitoring is indicated for infants whose initial evaluation suggests physiologic compromise. Hospital admission may provide important clinical information where additional episodes may be witnessed by medical personnel during the observation period. In addition, serious underlying medical conditions may become apparent.  Discharging the patient after reassuring the parents (B) and observing the patient for four hours in the ER (C) are not appropriate management strategies for the infant in the vignette who needs admission for cardiorespiratory monitoring. Requesting for complete blood count (D) is not routinely done in the evaluation of an ALTE and would not aid in the management for the infant in the vignette.


Tieder JS, Bonkowsky JL, Etzel RA, Franklin WH, Gremse DA, Herman B et al. Subcommittee on Apparent Life Threatening Events. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants: Executive Summary.  Pediatrics. In Press

Episode 48 – Urine Drug Screen, Cocaine, and PCP


The Free Open Access Medical Education (FOAM)

We review a post by Dr. Seth Trueger (@MDaware) on false positives of common medications in the urine drug screen.  We delve into posts by Dr. Bryan Hayes (@PharmERToxGuy) on false negatives for benzodiazepines and opioids in the urine drug screen.

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Core Content

We delve into core content on cocaine and phencyclidine (PCP) using Rosen’s (8th edition), Chapter 154 and Tintinalli (8th edition)




Note: Beta-blockers are contra-indicated in cocaine induced hypertension and chest pain.  Much of the ischemia induced by cocaine is thought to be due to vasospasm, predominantly from alpha-1 receptor effects.  Beta-blockers block the relaxation provided by beta-2 stimulus on muscles, leaving alpha-1 constricting vessels, “unopposed.”  This is largely theoretical/based on canine literature as there are only two human studies on this, (a) 10 humans given propranolol + cocaine with vasospasm and (b) 9 humans given labetalol + cocaine without vasospasm [4,5]. However, recent papers attempting to dispel this teaching don’t quite prove the point. One retrospective chart review looked at cocaine positive urine screens in patients with chest pain and found no worsened troponins. Cocaine stays positive in the urine for 3 days so it is not clear that these were patients presenting with cocaine associated chest pain [6].

Phencyclidine (PCP)

Generously Donated Rosh Review Questions

  1.  An 18-year-old man is brought to the ED by the police after being found running around a parking lot, screaming at bystanders. He reportedly smoked phencyclidine (PCP) earlier that day. His vital signs are notable for a heart rate of 130 beats per minute and a blood pressure of 150/86 mm Hg. On physical exam, he is diaphoretic, with vertical nystagmus and equal pupils and appears acutely agitated. 

2. A 39-year-old woman presents with chest pain and difficulty breathing that began shortly after smoking crack cocaine. Vital signs are BP 190/85 mm Hg, HR 105, RR 18, T 99.1℉. The ECG demonstrates ST segment depression and T wave inversions in the lateral leads. 


  1. B. The most common cause of morbidity and mortality in patients with phencyclidine (PCP) intoxication is rhabdomyolysis. Fluid hydration with normal saline is the initial therapy for rhabdomyolysis. Creatinine kinase (CK) should be obtained in patients with PCP intoxication. If abnormal, serial levels should be obtained until a downward trend is noted. Serum creatinine should also be monitored for evidence of renal insufficiency. PCP is a dissociative anesthetic drug that works on the NMDA glutamate receptor. People who abuse PCP can have sensations of euphoria initially, but this can be followed by an emergence reaction that is characterized by dysphoria and psychosis. If initial calming measures such as placing the patient in a calm environment fail and chemical restraints are needed, benzodiazepines are the treatment of choice. Benzodiazepines are also the preferred medication for acute agitation. Haloperidol (A) may cause dysrhythmias and hypotension. It also lowers the seizure threshold and may precipitate PCP-induced movement disorders. PCP is a weak base and its excretion is increased in acidic urine. Physical restraints (C) may be required for patients with PCP intoxication, but they should be used in conjunction with chemical restraints (preferably benzodiazepines). An agitated patient fighting against physical restraints is at risk for worsening rhabdomyolysis, which, if unrecognized, can precipitate cardiac arrest. Traumatic injuries (D)frequently occur in PCP-intoxicated patients; however, rhabdomyolysis with subsequent renal insufficiency is the most common cause of associated morbidity and mortality. Patients with PCP intoxication should be evaluated for suspected trauma, and any injuries should be stabilized and treated. Acidification of the urine (E) can cause a metabolic acidosis, which is potentially harmful and has not demonstrated improved outcomes. For these reasons, urinary acidification is not routinely recommended.
  2. A. D  Diazepam, a benzodiazepine, should be administered to this patient who is hyperadrenergic from cocaine intoxication. Signs and symptoms of cocaine intoxication include, dilated pupils, diaphoresis, tachycardia, hypertension and hyperthermia. Many patients experience euphoria, though some will develop acute psychosis. Benzodiazepines decrease the cocaine-induced hyperadrenergic state. Reduction of sympathetic tone induces coronary and peripheral vasodilation. Coronary artery dilation directly improves myocardial blood flow. Peripheral vasodilation reduces preload and afterload. Reductions in preload and afterload decrease blood pressure and improve myocardial oxygen demand. Several factors, including, excess sympathetic stimulation, dehydration, hyperthermia, and cocaine-induced cardiac sodium channel blockade, may cause patients with cocaine intoxication to develop dysrhythmias. These contributing factors should be treated with benzodiazepines, IV fluid resuscitation and temperature management. In some patients, cocaine-induced cardiac sodium channel blockade may cause wide complex tachycardia that should be treated with sodium bicarbonate. Hyperthermia should be managed aggressively with a target temperature of less than or equal to 102.0℉. Severe agitation, aggression or psychosis should be initially managed with benzodiazepines. Most antipsychotic agents have pronounced anticholinergic side effects. This may worsen dysrhythmias.and decrease sweating, further complicating temperature management.
  1. Rao R, Hoffman RS.  Cocaine and other Sympathomimetics. Rosen’s Emergency Medicine (8e). Chapter 154, 1999-2006.e2
  2. “Cocaine and Amphetamines.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (8e). Chapter 187
  3. “Prison Medicine.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (8e). Chapter 301
  4. Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of cocaine, induced coronary vasoconstriction by beta adrenergic blockade. Ann Intern Med. 1990;112:897–90
  5. Boehrer JD, Moliterno DJ, Willard JE, Hillis LD, Lange RA. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993;94(6):608–610
  6. Ibrahim M, Maselli DJ, Hasan R, Hamilton A. Safety of β-blockers in the acute management of cocaine-associated chest pain. The American Journal of Emergency Medicine. 31(3):613-616.


Episode 47 – Left Bundles and Implantable Cardiac Devices


The Free Open Access Medical Education (FOAM)

We cover a post from Dr. Smith’s ECG blog investigating ways to read ischemia on a ventricular paced ECG.  In A Patient with Ischemic symptoms and a Biventricular Pacemaker, Dr. Smith asserts that the modified Sgarbossa criteria may work in ventricular paced rhythms as well as Left Bundle Branch Blocks (LBBB).



Core Content

We delve into core content on implantable cardiac devices using Rosen’s (8th edition), Chapter 80 and Tintinalli (8th edition)

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Generously Donated Rosh Review Questions

Question 1.  A 44-year-old man with an automatic implantable cardioverter-defibrillator (AICD) in place presents with weakness and palpitations. Vitals are HR 180, BP 83/53, RR 28. His ECG is shown below.  

rosh review

Question 2.  A 76-year-old woman presents to the Emergency Department with generalized weakness and fatigue. She had a pacemaker placed one month ago. 

rosh review


  1. Electrical cardioversion.  This patient presents with unstable ventricular tachycardia and should immediately be electrically cardioverted. AICDs are placed for a number of indications but the goal is the treatment of ventricular dysrhythmias, particularly ventricular tachycardia (VT) and ventricular fibrillation (VFib). All AICDs have a right ventricular lead that is used for sensing. During insertion, the cardiologist determines the parameters for the device to deliver a shock. Despite the presence of these devices, patients may still present in ventricular dysrhythmias that have not been shocked if the device is malfunctioning. Patients may also experience inappropriate shocks. Regardless of the presence of the device, if a patient presents in an unstable dysrhythmia,electrical cardioversion or defibrillation (depending on the circumstance) should still be performed. This patient presents with ventricular tachycardia and hypotension and device failure. It is recommended that if a shock is to be delivered in a patient with an AICD that the pads not be placed over the device site. Otherwise, the presence of a device is not a contraindication to external electrical cardioversion/defibrillation.
    Amiodarone (A) and procainamide (D) are antidysrhythmic agents that can be used in the treatment of stable ventricular tachycardia. Placing a magnet over the AICD site (C) may be beneficial in treating patients who are receiving inappropriate shocks.
  2. A. Failure to capture can range from complete absence of pacemaker activity to pacemaker spikes being seen but not resulting in depolarization of the myocardium. Complete absence of activity can be due to battery depletion, fracture of the pacemaker lead (which is uncommon with today’s technology) or disconnection of the lead from the generator. Intermittent failure to capture is commonly due to lead displacement and is most likely to happen within the first month of placement. Failure to pace can also be due to impaired endocardium, which despite an intact and normally functioning pacemaker, will not depolarize properly. Causes include ischemia or infarction, hyperkalemia or use of class III antiarrhythmic drugs. Overpacing (B) can occur when atrial flutter develops during dual chamber pacing. The pacemaker may sense the atrial flutter waves resulting in a rapidly paced ventricular rate. A “runaway pacemaker”, a pacemaker that causes extreme increases in pacing rates due to malfunction, is very unlikely with current pacemaker technology. In both of these cases, placing a magnet over the pacemaker will switch it from demand to fixed mode and may terminate the tachycardia. Oversensing (C) occurs when the pacemaker senses electrical activity that is not of cardiac origin and erroneously inhibits the generator. This may result in bradycardia. Undersensing (D) occurs when the pacemaker can not adequately sense the intrinsic electrical activity of the heart. If the pacemaker is in an inhibit mode, this can result in the pacemaker firing inappropriately.


1. Sgarbossa EB, Pinski SL, Barbagelata et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med. 1996 Feb 22;334(8):481

2.  Smith SW, Dodd KW, Henry TD et al. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med. 2012 Dec;60(6):766-76.

3.Cai Q, Mehta N, Sgarbossa EB, Pinski SL, Wagner GS, Califf RM, Barbagelata A. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am Heart J. 2013 Sep;166(3):409-13. doi: 10.1016/j.ahj.2013.03.032.

Episode 36 – Pneumothorax


The Free Open Access Medical Education (FOAM)

HEFT EMcast has produced an excellent podcast summary of the literature demonstrating that needle decompression at the 2nd intercostal space at the midclavicular line (2ICS MCL) is likely to fail.  They review a systematic review and meta-analysis by Laan et al in 2015 that suggests the fifth intercostal space at the anterior axillary line (5ICS AAL) is less likely to fail [1].

Problems with the 2ICS MCL (For more detail on this, see this post) 

  • Chest Wall Thickness – to achieve a success rate >90% of the time with needle decompression at the 2ICS MCL, a [1,2]
  • The 2ICS MCL is Difficult to Find– one study of emergency physicians found that providers could find the 2ICS MCL 60% of the time. Similarly, a blinded cadaveric study in which naval corpsmen who had just had a refresher course in needle decompress were asked to needle decompress cadavers at the 2ICS MCL and 5ICS AAL.  They found 80% correct placement in the 5ICS AAL group compared with a mere 30% in the 2ICS MCL group [3,4].
  • Important vascular structures nearby – the heart and great arteries lie nearby the 2ICS MCL and given the frequent misplacement of these catheters, these structures may be injured. Of note, placement aiming for the 5ICS AAL, if too inferiorly placed, could result in liver or splenic injury.
Needle Thoracostomy: 5th ICS Anterior Axillary Line = Less Likely to Fail

Needle Thoracostomy: 5th ICS Anterior Axillary Line = Less Likely to Fail

Core Content

We delve into core content on pneumothorax and empyema using Rosen’s Medicine (8e),  Chapters 77 and Tintinalli’s Emergency Medicine: A Comprehensive Study Guide  (8e) Chapters 68


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Smaller bore percutaneous tubes (seldinger technique) are becoming increasingly common, even in traumatic pneumothorax.  These tubes have the advantage of smaller size, less pain, and reduced infection.  However, they may be more prone to kinking and may be less desireable for some fluid collections [6-19].  See this post for more on percutaneous tubes.

Open pneumothorax (“sucking chest wound”): communication between the surrounding environment and the pleural space, often due to penetrating trauma but may occur in its absence.

  • Treatment:  3 sided dressing (occlusive dressing could create tension) followed by chest tube (not inserted into wound).


Infection between the visceral pleura which covers the lung and the parietal pleura which covers the thoracic wall.


  • Parapneumonic effusions (i.e. effusions that came as a result of an underlying pneumonia)- most common causes of pneumonia (s. pneumo or s. aureus. or H flu if not vaccinated)
  • Trauma (iatrogenic or otherwise, i.e. retained hemothorax):  gram negative bacilli.

Clinical symptoms:

  • Fever
  • Cough
  • Pleuritic chest pain
  • Decreased breath sounds.


  • Exudative (early) – drainage, antibiotics
  • Fibropurluent (middle) – fibrinolytics +/- video assisted thorascopic surgery (VATS)
  • Organizational (late) – VATS and/or surgery

Generously Donated Rosh Review Questions

Question 1. A 22-year-old woman with a history of asthma presents with chest pain. Over the last several days, the patient has been coughing due to an asthma exacerbation. Today she developed sharp chest pain in the middle of her chest.  A chest X-ray is shown below.

Question 2. You are caring for an intubated patient diagnosed with sepsis that is awaiting a bed in the intensive care unit. The patient has peripheral intravenous access, however you decide to place a right-sided subclavian central venous catheter in order to measure central venous pressure, assess volume status and determine if vasopressors are indicated.  Shortly after successful line placement, the patient becomes hypotensive and develops high peak airway pressures.

  1.  D. Pneumomediastinum is free air contained within the mediastinum of the chest, most commonly due to air originating in the alveolar space. Air escapes from ruptured alveoli along the peribronchial vascular sheaths to the hilum and into the mediastinum. However, other causes like Boorhaeve’s syndrome and traumatic chest injury can lead to pneumomediastinum. The patient’s outcome is typically related to the underlying cause. In most cases, patients are hemodynamically stable and only require supportive care and observation. The condition rarely progresses to become tension pneumomediastinum and therefore surgical intereventions are not necessary. Approximately 14% of patients with pneumomediastinum have an associated pneumothorax. CT scan of the chest (A) may identify other pathology causing pneumomediastinum. However, in this patient with a history of asthma and recent coughing, a ruptured alveolus is the likely culprit. Additional investigation with CT scan is not necessary. High flow oxygen therapy (B) is often used for nitrogen washout in the treatment of a pneumothorax. In patients with pneumomediastinum, this is not necessary. A pig tail catheter (C) has been reported in some case reports however, surgical intervention with a catheter is rarely needed in the condition because of its stability. This differs from isolated peumopericardium because pneumocardium should not rise above the level of the pericardial reflection which it does in this case. In addition, the history of chest pain after coughing due to asthma is also consistent with pneumomediastinum.
  2. C. The patient likely has a tension pneumothorax that resulted from subclavian central line placement combined with the fact that the patient is on positive pressure ventilation (PPV). The patient requires emergent needle thoracostomy in the right second intercostal space midclavicular line to alleviate the tension. Pneumothorax is a common complication associated with subclavian venipuncture and occurs in up to 6% of attempts. Patients on positive pressure ventilation are more likely to develop a tension pneumothorax due to increased intrapleural pressures.Tension pneumothorax is a clinical diagnosis not a radiographic diagnosis. Clinical signs and symptoms include hypotension, absent breath sounds on the affected side, trachea deviation away from the affected side and sudden resistance to ventilation for patients on PPV. This is life threatening and requires immediate attention. Waiting for radiology to come and perform a chest X-ray (A) can result in patient death. Patients may develop hypotension as a result of intubation and positive pressure ventilation. This generally occurs immediately following initiation of PPV and is secondary to decreased venous return. This is treated with an IV fluid bolus (B) however would not cause elevated peak airway pressures as in this scenario. Emergent pericardiocentesis (D) is performed for treatment of cardiac tamponade, which manifests as hypotension, muffled heart tones and jugular venous distention. This is unlikely to be the problem in this scenario.


  1.  Laan D V., Vu TDN, Thiels CA, et al. Chest wall thickness and decompression failure: A systematic review and meta-analysis comparing anatomic locations in needle thoracostomy. Injury. 2015:14–16. doi:10.1016/j.injury.2015.11.045.
  2. Hecker M, Hegenscheid K, Völzke H, et al. Needle decompression of tension pneumothorax. J Trauma Acute Care Surg. 2016;80(1):119–124. doi:10.1097/TA.0000000000000878.
  3. Aho JM, Thiels CA, El Khatib MM, et al. Needle thoracostomy. J Trauma Acute Care Surg. 2016;80(2):272–277. doi:10.1097/TA.0000000000000889.
  4. Ferrie EP, Collum N, McGovern S. The right place in the right space? Awareness of site for needle thoracocentesis. Emerg Med J. 2005;22(11):788–789. doi:10.1136/emj.2004.015107.
  5. Inaba K, Karamanos E, Skiada D, et al. Cadaveric comparison of the optimal site for needle decompression of tension pneumothorax by prehospital care providers. doi:10.1097/TA.0000000000000849.
  6.  Laws D et al. BTS guidelines for the insertion of a chest drain. Thorax. 2003 May;58 Suppl 2:ii53-9.
  7.  Benton IJ, Benfield GF. Comparison of a large and small-calibre tube drain for managing spontaneous pneumothoraces. Respir Med. 2009 Oct;103(10):1436-40.
  8. Dull KE, Fleisher GR. Pigtail catheters versus large-bore chest tubes for pneumothoraces in children treated in the emergency department. Pediatr Emerg Care. 2002 Aug;18(4):265-7.
  9. Gammie JS et al. The pigtail catheters for pleural drainages: a less invasive alternative to tube thoracostomy. JSLS. 1999 Jan-Mar;3(1):57–61.
  10.  Kuo HC, et al. Small-bore pigtail catheters for the treatment of primary spontaneous pneumothorax in young adolescents. Emerg Med J. 2013 Mar;30(3):e17.
  11. Repanshek ZD, Ufberg JW, Vilke GM, Chan TC, Harrigan RA. Alternative Treatments of Pneumothorax. J Emerg Med. 2013 Feb;44(2):457-466.
  12. Hassani B, Foote J, Borgundvaag B. Outpatient management of primary spontaneous pneumothorax in the emergency department of a community hospital using a small-bore catheter and a Heimlich valve. Acad Emerg Med. 2009 Jun;16(6):513-8.
  13. Kulvatunyou N, Vijayasekaran A, Hansen A, et al. Two-year experience of using pigtail catheters to treat traumatic pneumothorax: a changing trend. J Trauma. 2011 Nov;71(5):1104-7.
  14. Rivera L, O’Reilly EB, Sise MJ, et al. Small catheter tube thoracostomy: effective in managing chest trauma in stable patients. J Trauma. 2009 Feb;66(2):393–9
  15. Kulvatunyou N, et al. A prospective randomized study of 14-French pigtail catheters vs 28F chest tubes in patients with traumatic pneumothorax: impact on tube-site pain and failure rate. EAST Annual Surgical Assembly, Oral paper 12, Jan 17, 2013.
  16. Kulvatunyou N, Joseph B, Friese RS, et al. 14 French pigtail catheters placed by surgeons to drain blood on trauma patients. J Trauma Acute Care Surg. 2012;73(6):1423–1427.
  17. Russo RM, Zakaluzny SA, Neff LP, et al. A pilot study of chest tube versus pigtail catheter drainage of acute hemothorax in swine. J Trauma Acute Care Surg. 2015;79(6):1038–1043.
  18.  Liu YH, et al. Ultrasound-guided pigtail catheters for drainage of various pleural diseases. Am J Emerg Med. 2010 Oct;28(8):915-21
  19.  Inaba K, Lustenberger T, Recinos G. Does size matter? A prospective analysis of 28-32 versus 36-40 French chest tube size in trauma. The journal of trauma and acute care surgery. 72(2):422-7. 2012.


Episode 45 – Diverticulitis


The Free Open Access Medical Education (FOAM)

Life in the Fast Lane Research and Reviews (LITFL R&R) #121  featured a section on the new American Gastroenterology Association (AGA) guidelines on diverticulitis. The game changer?  Antibiotics aren’t a requirement in select patients with uncomplicated acute diverticulitis [1].

The guidelines based this recommendation on two studies, previously covered by Dr. Ryan Radecki on Emergency Medicine literature of note over the past 3 years. This post details a prospective observational study on antibiotics for acute diverticulitis [2].  In another post, Dr. Radecki discusses an RCT of antibiotics (ABX) vs IV fluids only.

  • 623 patients with an episode with a short history and with clinical signs of diverticulitis, with fever (>38 Celsius) and inflammatory parameters, verified by computed tomography (CT), and without any sign of complications (fistula, perforation, abscess) or signs of sepsis
  • Randomized to IVF only or IVF + antibiotics
  • Primary Outcome – 6 patients (1.9%) developed complications in the no ABX arm vs 3 patients (1.0%) in the ABX arm (not statistically significant). Overall study complication rate was 1.4% [3].

Of note, since 2012, the Cochrane Review suggests that antibiotics may not be necessary in uncomplicated appendicitis [4].

A note on LITFL R&R – every week this blog post features 5-10 high yield articles, culled from contributors across the globe from all kinds of literature – pediatrics, critical care, emergency medicine, etc. It is difficult to keep up with the literature and some have estimated that the number needed to read (NNR) to of 20-200, depending on the journal [5].  Those looking for high yield articles may find their time well spent focused on this cherry picked selection of articles.

Core Content

We delve into core content on diverticula and clostridium difficile using Rosen’s Medicine (8e),  Chapters 31, 173 and Tintinalli’s Emergency Medicine: A Comprehensive Study Guide  (7e) Chapters 76, 85.


Diverticula are small herniations through the wall of the colon (small outpouchings). Often this is asymptomatic, identified incidentally on imaging or colonoscopy. Most common cause of lower gastrointestinal bleeding (LGIB) in adults in the U.S.


Diverticulitis Algorithm

Diverticulitis Algorithm

Clostridium Difficile (c. diff)

C. Difficile


Note on testing – asymptomatic carriage rates of c.diff vary based on the population but may be between 3-50%.  Textbooks quote a 3% carriage rate in newborns and rates of 20%-50% in hospitals and long term care facilities, respectively [10,11].

C. diff historically has a unique odor, refrains of “it smells like c. diff” echo in the halls.  Yet this does not perform very well, essentially a coin flip based on a 2013 study by  Rao and colleagues.  They  had 18 nurses smell 10 stool samples (5 c. diff positive and 5 c. diff neg) and found the median percent correct identification of c. diff positive vs negative was 45% [6]. 

Rosh Review Questions

Question 1.

Question 2.A 75-year-old woman presents with several days of voluminous watery stools. She was discharged from the hospital one week ago following treatment for pneumonia. Stool studies reveal C. difficile toxin


  1. C. Patients who present with uncomplicated diverticulitis should be treated with oral antibiotics for 7-10 days. Diverticulitis is an inflammation of the diverticulum in the large intestine. In uncomplicated cases of diverticulitis, patients present with abdominal pain typically in the left lower quadrant with tenderness to palpation in the same area. Patients should not have peritoneal signs or masses on examination. Complicated diverticulitis is defined as the presence of either extensive inflammation or complications such as abscess, peritonitis or obstruction. Patients with uncomplicated diverticulitis can be empirically treated with antibiotics (typically as an outpatient) for 7-10 days. Patients with uncomplicated diverticulitis typically do not require CT imaging (A). Patients with complicated diverticulitis should be treated with intravenous antibiotics (B) and admitted to the hospital. Ultrasound (D) has shown promise in diagnosing diverticulitis but CT is the imaging modality of choice.
  2. C.C. difficile infection is caused by a spore-forming obligate anaerobic bacillus that causes a spectrum of disease ranging from diarrhea to pseudomembranous colitis. C. difficile is the most common cause of infectious diarrhea in hospitalized patients in the United States. Risk factors for infection include broad-spectrum antibiotic use, particularly clindamycin, though other antibiotics have also been implicated. Additional risk factors include prolonged hospitalization, advanced age, and underlying comorbidities. The spectrum of clinical manifestations includes frequent watery stools to a more toxic clinical presentation with profuse stools (up to 20-30 per day), crampy abdominal pain, fever, leukocytosis, and hypovolemia. C. difficile colitis should be suspected in patients who develop diarrhea while taking or after recent cessation of antibiotics, or among recently discharged patients who develop diarrhea. Diagnosis is confirmed by identification of C.difficile toxin in the stool. Colonoscopy, while not usually necessary for diagnosis, reveals characteristic yellowish plaques in the intestinal lumen, confirming pseudomembranous colitis. Treatment for C. difficile infection depends on disease severity. Previously healthy patients with very mild symptoms may be managed by cessation of the offending antibiotic and close clinical monitoring. Oral metronidazole, 500 mg po every 6 hours for 10-14 days is the treatment for moderately severe colitis. Severely ill patients should be hospitalized and treated with oral vancomycin, 125 mg po every 6 hours for 10-14 days.


  1. Stollman N, Smalley W, Hirano I, AGA Institute Clinical Guidelines Committee. American Gastroenterological Association Institute Guideline on the Management of Acute Diverticulitis. Gastroenterology. 2015;149(7):1944–9. doi:10.1053/j.gastro.2015.10.003.
  2. Isacson D, Thorisson A, Andreasson K, Nikberg M, Smedh K, Chabok A. Outpatient, non-antibiotic management in acute uncomplicated diverticulitis: a prospective study. Int J Colorectal Dis. 2015;30(9):1229–1234. doi:10.1007/s00384-015-2258-y.
  3. Chabok A, Phlman L, Hjern F, Haapaniemi S, Smedh K. Randomized clinical trial of antibiotics in acute uncomplicated diverticulitis. Br J Surg. 2012;99(4):532–539. doi:10.1002/bjs.8688.
  4. Shabanzadeh DM1, Wille-Jørgensen P.Antibiotics for uncomplicated diverticulitis.  Cochrane Database Syst Rev. 2012 Nov 14;11:CD009092. doi: 10.1002/14651858.CD009092.pub2. 
  5. McKibbon KA, Wilczynski NL, Haynes RB. What do evidence-based secondary journals tell us about the publication of clinically important articles in primary care journals? BMC Med. 2004;2:33.
  6. Rao K, Berland D, Young C, Walk ST, Newton DW. The Nose Knows Not: Poor Predictive Value of Stool Sample Odor for Detection of Clostridium difficile. Clinical Infectious Diseases. 56(4):615-616. 2012.
  7. “Chapter 85: Diverticulitis.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e.New York, NY: McGraw-Hill; 2011. p 578-581.
  8. “Disorders of the Large Intestine.” Rosen’s Emergency Medicine, 8th e. p 1261-1275.
  9. “Gastrointestinal Bleeding.”  Rosen’s Emergency Medicine, 8th e. p 248-253.
  10.  “Infectious Diarrheal Disease and Dehydration.” Rosen’s Emergency Medicine, 8th ep 2188-2204.
  11. “Chapter 76: Disorders Presenting Primarily with Diarrhea.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e.New York, NY: McGraw-Hill; 2011. p 534-535

Sepsis: Redefined


The Society of Critical Care Medicine (SCCM)  and the European Society of Intensive Care Medicine (ESICM) redefined sepsis with the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). Sepsis is life-threatening organ dysfunction due to dysregulated host responses to infection.  Septic shock is a subset of sepsis where underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality [2]. 

2003 vs 2016 Definitions of Sepsis [1-4]

Sepsis Definitions: Old vs. 3.0

Sepsis Definitions: Old vs. 3.0   —- @FOAMpodcast

Systemic Inflammatory Response Syndrome (SIRS) is out.  

  • Includes normal responses to infection (eg. fever and tachycardia is not dysregulated infection; it’s just infection)
  • SIRS even MISSES up to ⅛ very septic ICU pts (NEJM 2015) [5]. 

qSOFA is in. a qSOFA score of 2 or 3 or a rise in the SOFA score of 2.  The SOFA score requires a ton of lab values so the authors wanted something that could be assessed at triage, hence the quick SOFA score (qSOFA). The authors derived and retrospectively validated this score and compared it to SIRS in a cohort of 148,907 patients [3]

qSOFA scoring

qSOFA scoring   —@FOAMpodcast


  • Unclear how to interpret studies (EGDT through ProCESS, PROMISE, ARISE) with new definitions.
  • CMS is not going to adapt.
  • Not endorsed by ACEP or SAEM as emergency providers were not included.
  • qSOFA has not been prospectively validated. It’s unclear how it will perform in this fashion

Notes: Sepsis rates have increased over the past 10 years and it appears that mortality has decreased.  However, less sick patients are included  in this. It appears that the Sepsis 3 authors were hoping for a more specific definition.


  1. Levy MM, Fink MP, Marshall JC. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Critical care medicine. 31(4):1250-6. 2003.
  2.  Singer M, Deutschman CS, Seymour CW, et al: The Sepsis Definitions Task Force The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3).
    AMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287.
  3.  Seymour CW, Liu V, Iwashyna TJ, et al. Assessment of clinical criteria for sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3).JAMA. 2016;315(8):762-774. doi:10.1001/jama.2016.0288.
  4. Shankar-Hari M, Phillips G, Levy ML, et al.Developing a New Definition and Assessing New Clinical Criteria for Septic ShockFor the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) (JAMA, Feb 22, 2016).
  5. Kaukonen KM, Bailey M, Bellomo R. Systemic Inflammatory Response Syndrome Criteria for Severe Sepsis. The New England journal of medicine. 373(9):881. 2015.

Episode 43 – Alcohols


The Free Open Access Medical Education (FOAM)

The Skeptic’s Guide to Emergency Medicine Episode 144, “That Smell of Isopropyl Alcohol for Nausea in the Emergency Department.” This podcast reviews an article by Beadle et al, an RCT on the use of inhalational isopropyl alcohol for nausea.

Population – Adults in the Emergency Department

Intervention – Nasal inhalation of an isopropyl alcohol pad for ~ 60 seconds (time 0 and, if still nauseated, at 2 minutes and 4 minutes)

Comparison – Nasal inhalation of an identical pad soaked in saline.

Outcome -Nausea score at 10 minutes post treatment using an 11-point verbal numeric response scale (0:“no nausea”; 10:“worst nausea imaginable”)

  • Lower in the isopropyl group (Median score of 3 vs. 6 on an 11 point scale, p<0.001). This gave an effect size of 3 (95% CI 2 to 4).

Limitations – single center, convenience sample, unclear blinding as isopropyl likely has a particular smell to it, outcome nausea score, not vomiting

Eagerton-Warburton et al conducted an RCT of intravenous ondansetron 4mg, metoclopramide 20mg, or saline (placebo) of adult patients with nausea and found  no significant difference in nausea scores on a visual analog scale between groups (n=270).

Core Content

We delve into core content on vertigo using Rosen’s Medicine (8e),  Chapter 155 “Toxic Alcohols”  and Tintinalli’s Emergency Medicine: A Comprehensive Study Guide  (7e) Chapter 179“Alcohols.”

Any alcohol can be “toxic,” the ramifications depend on the dose. Toxic alcohols typically refer to ethylene glycol (EG) and methanol.  In these cases, the parent compound (EG or methanol) is inebriating but not particularly toxic. These compounds are metabolized, like any alcohol, but unfortunately the metabolites (oxalic acid – EG, formic acid – methanol) have unique toxic properties. For example, the oxalic acid produced from EG metabolism combines with calcium.  These deposit into tissues causing renal failure and neurologic sympotms. The formic acid has a predilection for the retina, causing visual symptoms.

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Toxic Alcohols

Osmolal Gap (calculator) – One of the touted features of toxic alcohols is the elevated anion gap, that is, the difference between the measured serum osmolality and the calculated osmolarity.

Calculated Osmolarity: 2[Sodium] + [Glucose]/18 + [BUN]/2.8 + [ETOH]/4.6    (Note: Some references use ETOH/3.7)

  • Problems:  A normal osm gap does not exclude the presence of toxic alcohols as the osm gap decreases as the alcohol is metabolized.  Also, other disease processes can increase the osm gap, including shock, diabetic ketoacidosis, etc [2,3].
Osm Gap vs Anion Gap As Toxic Alcohols Metabolize

Osm Gap vs Anion Gap As Toxic Alcohols Metabolize

A common pearl exists that urine can be placed under a Wood’s lamp for fluorescence due to the fluorescein in ethylene glycol antifreeze (to detect leaks). Unfortunately this is neither sensitive nor specific [4,5].


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Rosh Review Questions

Question 1. 

Question 2. 


1. A. Hypocalcemia. Most laboratories do not have the capability to measure serum levels of toxic alcohols in a timely fashion. As a result, physicians must use other clinical markers to determine the presence of these unmeasured toxins. The classic laboratory abnormality is an elevated serum osmolality with an osmolar gap since the actual toxic alcohol is not measured in its own quantity but contributes to the osmolality of the blood. When calculating the osmolar gap, it is important to have a measured serum ethanol level as this is a large contributor to the final osmolality.Ethylene glycol ingestion leads to the formation of calcium oxalate crystals. As a result, serum calcium levels will decrease and hypocalcemia is a surrogate marker for ethylene glycol toxicity.Hypoglycemia (B) is not characteristic of a toxic alcohol ingestion. Hypoglycemia is often seen in chronic alcoholics due to poor nutritional intake. In children, ethanol may induce hypoglycemia. Other toxic ingestions which may lead to hypoglycemia include beta-blockers, sulfonylureas and insulin. Hypokalemia (C) is not associated with any toxic alcohol ingestions. As patients become more acidemic from alcohol ingestions, hyperkalemia may develop. Hyponatremia (D) is not associated with toxic alcohol ingestions. Evidence of hyponatremia on laboratory analysis should prompt further investigation for other underlying causes.

2.C.  Glycolic acid level greater than 8 mmol/L. A glycolic acid level greater than 8 mmol/L is an indication for emergent hemodialysis following an acute ethylene glycol overdose. Ethylene glycol is found in automobile coolants, antifreeze, hydraulic brake fluid, de-icing agents and industrial solvents. Symptoms progress through 4 stages: inebriation and intoxication, cardiopulmonary symptoms (tachycardia, hypertension, pulmonary edema), renal symptoms (acute renal failure), and delayed neurologic symptoms (cranial neuropathy). Treatment includes 1.) Alcohol dehydrogenase (ADH) enzyme blockade with fomepizole or ethanol to prevent toxic and acidic metabolite production, 2.) Correction of the metabolic acidosis with sodium bicarbonate, and 3.) Hemodialysis for removal of the parent compound and toxic metabolites. Although somewhat controversial with the advent of fomepizole other indications for hemodialysis following ethylene glycol ingestion include severe metabolic acidosis, renal failure, deterioration despite intensive care, and electrolyte disturbances.Other indications for emergent hemodialysis following an acute ethylene glycol overdose include: ethylene glycol level greater than 50 mg/dL (B), anion gap greater than 20 mmol/L (A)and initial pH less than 7.3 (D).


  1.  Beadle KL, Helbling AR, Love SL, April MD, Hunter CJ. Isopropyl Alcohol Nasal Inhalation for Nausea in the Emergency Department: A Randomized Controlled Trial. Annals of emergency medicine. 2015. [pubmed]
  2. Chapter 155.  “Toxic Alcohols. ” In: Marx JA, Hockberger RS, Walls RM eds.  Rosen’s Emergency Medicine, 8th e.
  3. Chapter 179. Alcohols. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e.New York, NY: McGraw-Hill; 2011.
  4. Tobe TJM, Braam GB, Meulenbelt J, et al: Ethylene glycol poisoning mimicking Snow White. Lancet 2002; 359: pp. 444
  5. Wallace KL, Suchard JR, Curry SC, et al: Diagnostic use of physicians’ detection of urine fluorescence in a simulated ingestion of sodium fluorescein–containing antifreeze. Ann Emerg Med 2001; 38: pp. 49