Grand Rounds Recap 3.6.19

Airway Grand Rounds WITH DR. CARLETON

An elderly year old male presents after his “throat feels swollen.” He has a history of ACEI-induced angioedema. He took some leftover enalapril today because he was out of amlodipine. He is drooling and unable to speak on presentation. Vital signs show a respiratory rate of 6, oxygen saturation of 100% on a non-rebreather. His exam reveals no swelling of the tongue, but he has significant pharyngeal edema.

This patient has significant predicted difficulty when the universal airway algorithm is applied, but we are not yet forced to act (although he is dangerously close). In this particular scenario, the providers chose a double set up: RSI with D-blade and they prepared the patient’s neck with the cricothyrotomy tray out. The initial attempt was unsuccessful, and he was rescued with an iGel. A second attempt was performed with endoscopy through the iGel, but no view could be obtained due to significant airway edema. On the third attempt, nasal endoscopy was attempted but was again unsuccessful. At that point, he was a failed airway, so a cricothyrotomy was performed.

Trouble shooting difficulty with nasal/oral endoscopy:

If secretions are the enemy, dry them up in advance by using glycopyrrolate. Recall that it takes 10-20 minutes for this to work. Additionally, performing a jaw thrust can open the airway significantly during endoscopy, and it helps distribute the secretions such that a view might be attainable. If you cannot see anything recognizable, aim for the bubbles. Sometimes this will guide you towards the airway even if the anatomy is not recognizable.

Predicting Difficulty with Cricothyrotomy:

Recall the SMART mnemonic. Surgically altered airway, Mass, Access/Anatomy, Radiation, Trauma. A common error is to place the ET tube too deep. Remember that you are already entering the airway below the cords, so the tube does not need to be too deep.

Complications of Surgical Airways:

The most frequent error in performing cricothyrotomy is performing it too high and causing a thyrohyotomy which results in numerous potential complications down the line. There was one study reporting up to 34% of cricothyrotomies end up being thryohyotomies. In fact, many studies have shown varying success rates of providers (including anesthesiologists) in identifying the cricothyroid membrane.1 The laryngeal handshake method should prevent this because you are holding onto the thyroid cartilage with your hand and will make the incision inferior to this. Hemorrhage is also common. It is possible to cut through the thyroid isthmus which will cause significant bleeding. Utilize a bougie for tactile reassurance that you are in the airway.


  1. Aslani A., Ng S., Hurley M., McCarthy K., et al. Accuracy of identification of the cricothyroid membrane in female subjects using palpation: an observational study. Anesth Analg, 2012; 114(5): 987-992.

QI/KT: Infective Endocarditis  WITH DRS. JENSEN AND MAKINEN

Endocarditis develops after an insult to the endocardium which creates a thrombus. This thrombus acts as a nidus for infection. Bacteremia then seeds the thrombus and results in endocarditis. Endocarditis can be diagnosed using the Modified Duke Criteria.

Major Criteria:

  1. The presence of a vegetation, abscess, valvular dehiscence, or new regurgitation on echocardiography.

  2. Positive blood culture with an organism typical for endocarditis or a single culture positive for C. burnetti.

Minor Criteria:

  1. The presence of a predisposition: intravenous drug use (IVDU), prosthetic valve, etc.

  2. Fever >100.4.

  3. The presence of vascular phenomena (Janeway lesions, mycotic aneurysms, etc).

  4. The presence of immunologic phenomena (Roth spots, glomerulonephritis, Osler nodes, etc).

  5. Other microbiological evidence (other positive blood cultures not meeting major criteria).

The sensitivity of these criteria have been reported to be about 80% and 90% respectively.1 Four findings have been shown to enhance the sensitivity of these criteria. These include an elevated ESR or CRP, new clubbing of the digits, splenomegaly, and microscopic hematuria. Risk factors for the development of endocarditis include age >60, IVDU, presence of a prosthetic valve or other intracardiac device (pacemaker, AICD), diabetes, chronic hemodialysis use, immunosuppression, previously treated endocarditis, and structural heart disease. The prevalence of each of these risk factors is on the rise in today’s population, resulting in an increased incidence of endocarditis.

Valvular dysfunction is common with endocarditis. Regurgitation of the valves is most common, but the pulmonic valve is rarely affected. Heart failure often results due to chronic valvular dysfunction. Mycotic aneurysms may develop as well and cause ischemic cardiomyopathy. Bedside echocardiogram can be useful early in a patient’s course to evaluation for obvious valvular dysfunction. Interestingly, transthoracic and transesophageal echocardiography may miss cardiac abscesses. Cardiac CTA may actually be necessary if this is suspected.2

Roth spots are retinal hemorrhages that can be seen in endocarditis but are a poorly specific finding. Osler nodes are painful nodes usually seen on the palms and soles. These are also poorly specific. Janeway lesions are uncommon but are actually quite specific for endocarditis. Splinter hemorrhages are also poorly specific and can be seen in other immunologic conditions.

CNS manifestations of endocarditis include sub-clinical brain emboli, with one study reporting up to 80% of patients with endocarditis have some sort of acute brain embolism.3 The incidence of mycotic aneurysms is reported to be up to 2-4%. This is important to keep in mind when evaluating patients with altered mental status or even acute stroke symptoms, as this can significantly increase the possibility of intracranial hemorrhage.

Blood cultures are a crucial test when evaluating for endocarditis. The more blood obtained for a blood culture, the better the sensitivity. 60 ccs of blood for a blood cultures has a sensitivity of about 96%. Classically, three blood cultures are obtained because there is better discrimination of contaminants and improved sensitivity for intermittent bacteremia. However, one may consider a single large volume culture prior to initiation of antibiotics in critically ill or unstable patients. Studies have shown that straight sticking for cultures has less contamination than obtaining them from a venous access site.

The workup for suspected endocarditis should include a renal panel to evaluate for renal embolic phenomenon, CBC to evaluate for hematologic consequences, troponin and BNP to evaluate for myocardial injury, and urinalysis to evaluate for microscopic hematuria. An EKG should also be obtained. The presence of a new bundle branch block or new atrioventricular blocks are often indicative of extension into the valvular area, and para-valvular abscess should be considered.

The sensitivity of echocardiography is directly proportional to the size of the vegetation: it is estimated to be about 25% for vegetations < 5mm, 70% for vegetations 6-10mm, and 84% for vegetations >10mm, although this has not been shown in POCUS. Additional imaging should be considered depending on the patient’s presentation. Right-sided lesions should prompt concern for pulmonary manifestations. Left-sided lesions in patients with altered mental status should prompt concern for embolic phenomena to the brain. New abdominal pain, renal failure, or new anemia should prompt evaluation with CT abdomen/pelvis. The presence of back pain should prompt evaluation for spinal imaging.

The use of anticoagulation in infective endocarditis has mixed results in the literature. It is likely very high risk to start anticoagulation in the ED given the possibility of occult mycotic aneurysm. Therefore, the IDSA recommends discontinuation of all forms of anticoagulation. There is one randomized controlled trial looking at antiplatelet use.4 Antiplatelets were not found to reduce the risk of embolic events and was associated with an increased bleeding risk.

Per the IDSA, it is recommended to talk with local infectious disease specialists to determine appropriate antibiotic therapy for patients with infective endocarditis. Staph and strep are very common causative organisms. Our infectious disease department recommends empiric treatment with vancomycin and ceftriaxone. Gentamycin should be given only if the patient is in septic shock, neutropenic, or receiving chemotherapy. Pseudomonas actually causes a very miniscule portion of cases of infective endocarditis locally, so unless the a patient has a history of positive pseudomonas cultures, empiric pseudomonal depends on your local patterns. This is similar with empiric fungal coverage.


  1. Cecchi E., Trinchero R., Imazio M., Forno D., et al. Are the Duke criteria really useful for the early bedside diagnosis of infective endocarditis? Results of a prospective multicenter trial. Ital Heart J, 2005; 6(1): 41-48.

  2. Habets J., Tanis W., van Herwerden L., van den Brink R., et al. Cardiac computed tomography angiography results in diagnostic and therapeutic change in prosthetic heart valve endocarditis. Int J Cardiovasc Imaging, 2014; 30(2): 377-387.

  3. Cooper H., Thompson E., Laureno R., Fuisz A., et al. Subclinical brain embolization in left-sided infective endocarditis: results from the evaluation by MRI of the brains of patients with left-sided intracardiac solid masses (EMBOLISM) pilot study. Circulation, 2009; 120(7): 585-591.

  4. Chan K., Dumesnil J., Cujec B., Sanfilippo A., et al. A randomized trial of aspirin on the risk of embolic events in patients with infective endocarditis. J Am Coll Cardiol, 2003; 42(5): 775-780.

Global Health Grand Rounds: Malaria Updates WITH DRS. BRYANT AND LAGASSE

Possible or probable malaria is a medical emergency. Obtaining a travel history is crucial, but it involves asking more than just where someone traveled. Providers should inquire about pre-travel preparation (was malaria prophylaxis indicated/taken), specific travel itinerary, and exposure history. The CDC Yellow Book is a very helpful resource for patients with a recent travel history. It can help build a differential and develop a diagnostic plan.

Types of Malaria:

  1. Falciparum: Incubation period is 7-14 days.

  2. Vivax: Incubation period is 12-17 days.

  3. Ovale: Incubation period is 9-18 days.

  4. Malariae: Incubation period is 13-40 days.

  5. Knowlesi: New, primarily found in Southeast Asia.

The work-up should include blood cultures, CBC, BMP, and LFTs. Exam should include palpation of the liver and spleen. A blood smear should be ordered as well. The thick smear evaluates for the presence of a parasite; the thin smear helps to identify exactly which parasite it is and what is the percentage of parasitemia.

The treatment of malaria varies depending on the specific type of malaria and where the patient was exposed (chloroquine-resistant areas, for example). Malarone and Coartem are both weight-based medications and are a good initial option. They cover malaria regardless of the strain acquired in areas of chloroquine resistance. P. vivax and P. ovale can remain dormant in the liver, so patients with these strains need the addition of primaquine or tafenoquine. If a patient has G6PD deficiency, these two medications can cause hemolysis, so admission may be required in this scenario.

Pediatric malaria often mimics sepsis, gastroenteritis, pneumonia, or meningitis. Fever patterns are rarely present. Children often present much more ill with acidosis, altered mental status, or respiratory distress. The mortality of severe malaria is exceedingly high, 100% untreated and about 20% if treated. Any patient with severe malaria should be admitted to an intensive care unit. This means patients with malaria and one of the following: depressed GCS, seizures, acidosis, jaundice, hypoglycemia, anemia, hypoxemia, DIC, shock, and p. falciparum parasitemia >10%.

Cerebral malaria is a complication specifically of p. falciparum infection. It results in cerebral edema leading to death. The pathophysiology of this is unclear. Head CT and LP should be obtained in addition to the standard work-up. Empiric antibiotics and malaria treatment should be given in this scenario. Inpatient malaria management for severe malaria includes intravenous artesunate. When in doubt, admit the patient because they can decompensate quickly.


The patient is an elderly female with a couple hours of abdominal pain, nausea, and vomiting. She was somnolent on arrival and is found to be a very difficult historian. Her abdomen is distended and slightly firm. Vitals reveal tachycardia, tachypnea, hypoxia, hypothermia, and hypotension. A bedside ultrasound reveals intra-abdominal free fluid. She ultimately was found to have a cecal volvulus with perforation.

Evaluation and management of the undifferentiated hypotensive patient is a crucial skill for emergency physicians. One tool that can be very helpful in this is point-of care ultrasound (POCUS) and the RUSH exam. One study showed that the use of POCUS for hypotensive patients allowed providers to create a very accurate diagnosis within a very short time period.1 More recently, the SHoC-ED trial was a non-blinded, multi-center trial looking at POCUS use and its effect on mortality.2 They found no difference in mortality, length of stay, use of CT scan, inotrope use, or fluid administration. Nonetheless, the study had many limitations including using a convenience sample, many incomplete POCUS studies, and it was stopped early. Ultimately, POCUS in shock is a diagnostic tool that may be helpful, but thorough evaluation through a variety of testing modalities may still be indicated.

Information on how to perform the RUSH exam can be found here.

R4 Case Follow Up WITH DR. LIEBMAN

The patient is a 78 year old female who was found down in a fire. Initial saturations were 80%, so she was placed on a non-rebreather in route but had no evidence of external burns. She ended up having an extensive smoke inhalation injury.

The presence of smoke inhalation injury has been reported to be up to 1/3 of patients hospitalized with burns. Mortality increases up to 20% over having burns alone. 31% of patients with inhalation injuries will die.

Upper airway injuries usually are a result of direct thermal injury. This is the least common type of smoke inhalation injury. Lower airway/parenchymal injuries are an effect of particulate and chemical exposure. It results in an inflammatory process which may result in a delayed presentation. Finally, carbon monoxide (CO) and cyanide (CN) toxicity can also result in a chemical asphyxiation.

Diagnostic tests include a blood gas which can indicate CO poisoning. An EKG should be obtained because CO can worsen pre-existing cardiac disease. CXR is often not revealing, but it can be helpful to have a baseline. Nasopharyngoscopy/bronchoscopy can be useful in identifying the extent of injury. One study developed a grading score of inhalation injuries seen on bronchoscopy and found grades 0-1 had improved mortality compared with bronchoscopic grades 2-4.1

Management includes early airway management with intubation in upper airway injuries. Some animal studies suggest that empiric bronchodilator use may help avoid lung injury down the line. Supplemental oxygen should be administered if CO poisoning is a concern. If cyanide toxicity is suspected, an empiric cyanokit should be given. Unfortunately, the decision of who will require intubation can be somewhat difficult. One retrospective chart review showed a positive correlation with the presence of soot in the oral cavity, facial burns, body burns.2 As mentioned above, bronchoscopy can be very helpful in identifying patients with a risk of increased mortality and may be useful in predicting those who will require mechanical ventilation.

The evidence has shown no benefit for immediate removal of debris by bronchoscopy and no role for prophylactic antibiotics. In general, fluid resuscitation should actually be increased in patients with inhalation injury with an average of 6.6 ml/kg/TBSA given to patients with inhalation injuries and concomitant burns >4% total body surface area.


  1. Endorf F., Gamelli R. Inhalation injury, pulmonary perturbations, and fluid resuscitation. J Burn Care Res, 2007; 28(1):80-83.

  2. Madnani D., Steele N., de Vries E. Factors that predict the need for intubation in patients with smoke inhalation injury. Ear Nose Throat J, 2006; 85(4): 278-280.

Spontaneous Bacterial Peritonitis WITH DR. ROBLEE

Spontaneous bacterial peritonitis (SBP) is a spontaneous infection of the peritoneal fluid without an intra-abdominal source. The prevalence is about 2-5% in the outpatient setting, but the inpatient prevalence is up to 18%. It caries an in-hospital mortality of 20% with a 1-year mortality rate anywhere from 31-90%.

The pathophysiology is thought to be due to intestinal bacterial overgrowth. Patients with ascites often have significant edema and increased permeability of the intestinal wall, and bacteria are able to translocate through the wall, seeding the ascitic fluid. The clinical presentation often includes fevers, abdominal pain/tenderness, increasing ascites, and encephalopathy. Nonetheless, a significant proportion of patients are actually asymptomatic, up to 18%.1

The diagnosis is made with paracentesis. This is a procedure that caries with it the possibility of bleeding, bowel puncture, and introduction of infection. However, it is a safe procedure overall. It should be performed as soon as possible because delayed paracentesis has been shown to have increased in-hospital mortality.2 Every hour in delay to paracentesis is associated with a 3.3% increase in mortality in patients with SBP. The diagnosis is made in the presence of >250 neutrophils/mm3 or a positive gram stain. The presence of polymicrobial organisms should prompt evaluation for secondary bacterial peritonitis because SBP is rarely polymicrobial.

The treatment is a third generation cephalosporin (Ceftriaxone or Cefotaxime). A fluoroquinolone or ertapenem can be considered if the patient is cephalosporin allergic. Albumin may also be considered. One study found a significant reduction in renal impairment in patients who received albumin. In-hospital and 3-month mortality also was significantly decreased in the patients who received albumin.3 More recently, a retrospective study only found an improvement in patients who were considered higher risk.4 Because of this, the AASLD recommends albumin only for patients with creatinine >1, BUN > 30, or a total bilirubin >4. These patients should receive 1.5 g/kg of albumin within 6 hours of detection of SBP.


  1. Thanopoulou A., Koskinas J., Hadziyannis S. Spontaneous bacterial peritonitis (SBP): clinical, laboratory, and prognostic features. A single center experience. Eur J Intern Med, 2002; 13(3): 194-198.

  2. Kim J., Tsukamoto M., Mathur A., Ghomri Y., et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis. Am J Gastroenterol, 2014; 109(9): 1436-1442.

  3. Sort P., Navasa M., Arroyo V., Aldeguer X., et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. NEJM, 1999; 341: 403-409.

  4. Sigal S., Stanca C., Fernandez J., Arroyo V., et al. Restricted use of albumin for spontaneous bacterial pertonitis. Gut, 2007; 56(4): 597-599.