Airway grand rounds WITH DR. carleton
A female in her 70’s presented to the emergency department with a complaint of tongue swelling. She described that it began approximately five hours prior to her arrival. She noted that she was recently started on lisinopril. Her ability to speak was markedly compromised by her protruding tongue and therefore the rest of her history was very limited. She was without significantly increased work of breathing, wheezing, stridor, or trismus. Her vital signs were within normal limits including a normal oxygen saturation on room air.
Applying our indications for airway management:
1. Failure to oxygenate?: No, she is with appropriate oxygenation saturation without supplemented oxygen.
2. Failure to ventilate?: Probably not. We don’t have a blood gas; however, nothing by exam suggests this.
3. Failure to protect her airway?: Her airway is certainly concerning; however, at this moment she is protecting it.
4. Predicted clinical course: Her presentation is at high risk for deterioration and we predict she will need advanced airway management.
Endoscopic nasal intubation was chosen as the airway management strategy.
Applying our Seven P’s of airway management for this endoscopic nasal intubation:
1. Preparation: Dry the mucosa. Glycopyrrolate was used.
2. Preoxygentation: Flush rate oxygen with a reservoir mask.
3. Patient optimization: Anesthesia with 4% lidocaine using a mucosal atomizing device.
4. Paralysis and Induction: An awake look was chosen for this procedure due to difficulty anticipated in rescuing a failed attempt. Instead, Ketamine was used for sedation.
5. Positioning: The patient was placed in an upright seated, sniffing position, to assist with advancement of the endoscope.
6 and 7. Place tube and Post intubation management: The patient was intubated successfully on first pass.
A male in his 20s presented to the emergency department with weakness, lethargy, and dyspnea. He has a complex medical history including micrognathia, immunosuppression, and frequent respiratory infections. He was unable to provide any direct history due to his medical condition. On EMS arrival to his home he was noted to be with an oxygen saturation of 57% that improved to over 94% with 15L oxygen by face mask. Despite the improvement in his oxygen saturation his work of breathing continued to be significantly labored.
On exam the patient had micrognathia, a narrow midface, limited mouth opening, small nostrils, and coarse lung sounds bilaterally.
A chest X-ray showed pneumonia. Patient was treated for pneumonia with sepsis appropriately with antibiotics and IV fluids. Over the course of the next few hours his work of breathing continued to worsening and he was started on BiPAP and did not improve significantly so the decision was made to intubate him.
He was preoxygenated on BiPAP with FiO2 at 100%. Sedated with ketamine. Placed on high flow nasal cannula as continued oxygenation during the first oral intubation. The video laryngoscope was used; however, the patient clenched his jaw limiting the providers ability to advance the video laryngoscope. This attempt was then abandoned but the patient continued to spontaneously breathe.
The next attempt was made by placing a Williams airway allowing for utilization of the fiberoptic endoscope for orotracheal intubation. This was done successfully
1. Endoscopy and video laryngoscopy are of equal efficacy in patients with predictors of difficulty.
2. When you anticipate a patient is at risk for rapid oxygen desaturation during intubation consider optimizing preoxygenation with BiPAP.
A male in his late 50’s presented after being found confused at home and had been immobile for several days per history. He had told his family he had been feeling “weak” and not able to leave the bed. At the point of arriving to the ED he was unable to provide additional reliable history. EMS noted him to have an oxygen saturation of 69% on room air at home which increased to over 94% on 15L by face mask.
On arrival to the ED his physical exam was remarkable for dry mucous membranes, a clear oropharynx, no hoarseness or stridor, but with increased work of breathing. Chest X-ray showed a left upper lobe consolidation. EKG showed sinus tachycardia. The patient was appropriately treated for his pneumonia with sepsis. He was admitted to the medicine service; however, his respiratory status worsened and was started on BiPAP while still in the Emergency Department.
Repeat venous blood gas showed worsening hypercarbia with increased work of breathing despite being on BiPAP. The decision was made to intubate the patient for failure to ventilate and failure to protect his airway. This was performed successfully with video laryngoscopy without difficulty.
1. Induction agents are cardio-depressants
2. A state of hypoxia is a negative inotrope and is arrythmogenic
3. A state of acidosis is a negative inotrope and is arrythmogenic
4. To help prevent peri-intubation mortality, before intubating you should try to optimize your patients physiologic and hemodyanamic status. Consider the following before you intubate: volume resuscitation, pressors as needed, push-dose epinephrine, preoxygenate optimally, treat acidosis, and minimize laryngoscopy time.
Global health grand rounds WITH DRs. owens, sabedra, murphy-crews, and ventura
Uganda with Dr. Sabedra
In Uganda, thousands of people die annually from easily treated conditions (diarrhea, pneumonia etc)
Our trips focus on teaching providers to provide emergency care in these settings and teach future generations of EM providers
Global Emergency Care is an organization formed in 2007 with one of their goals being to provide a 2 year training program for non-physician clinicians to become emergency care providers. Additionally, they have implemented a ‘“train the trainer” system in which graduates of their program can then go on to provide education for the next group of participants in the program to help create a sustainable system. Since 2009 they have now seen over 80,000 patients.
Tanzania with Drs. Ventura, Murphy-Crews, and Owens
A 9 year old female presents to a clinic with fever, headache and malaise. She had previously been treated for malaria without any improvement in her symptoms. Today, her rapid malaria test is negative.
In Tanzania this constellation of symptoms is most commonly associated with Malaria; however, this patient was negative and had been treated without improvement and today was negative for Malaria by testing.
Ultimately, this patient was diagnosed with Typhoid Fever. Typhoid is caused by Salmonella typhi. Classically, it presents as a constant fever that is worse in the evenings with the patient complaining of malaise, body aches, and anorexia. You can also see abdominal pain, headache, and diarrhea. The “Rose Spots” that are commonly described in textbooks are very difficult to see in individuals with darker skin.
The major complications of Typhoid are intestinal perforation, hemolytic anemia (especially in G6PD deficiency), lobar pneumonia, meningitis, abscesses in the spleen, liver, brain, and osteomyelitis.
The treatment is with chloramphenicol or amoxicillin; however, emergency resistance patterns have led to new recommendations for fluoroquinolones or 3rd generation cephalosporins.
A 14 year old female presents to clinic with cough, fever, tachycardia, and tachypnea. Her physical exam reveals right lower lobe crackles on pulmonary auscultation. An ultrasound is performed showing pneumonia.
The sensitivity and specificity of ultrasound for the detection of pneumonia rivals that of the commonly used chest X-ray. Ultrasound is also a readily portable, accessible, imaging modality commonly used in Emergency Medicine global health trips. Although many providers embarking on global health ventures anticipate that they will manage many conditions not commonly seen in the United States it is important to remember that many of the same common conditions (pneumonia, diarrhea, trauma etc) are just as common in patients from other countries. Additionally, there are more pediatric deaths from pneumonia than diarrhea or HIV/AIDS in sub-Saharan areas.
A male in his 70s with general aches and pains presents to a clinic. He ambulates with the use of two crutches under his arms and drags his legs behind him. He states that at around 15 years of age he remembers developing a fever and subsequently losing the ability to walk and since has had use the crutches for ambulation.
This patient had likely suffered from Poliomyelitis. This is caused by an enterovirus transmitted by the fecal-oral route. Many patients will develop only a flu-like illness that is self limited lasting less than one week. A smaller proportion of patients will go on to develop significant symptoms affecting the brain and spinal cord and in severe cases leading to irreversible paralysis. Can be prevented by vaccination; however, this is not readily available in many developing countries.
Qi/KT : upper GI bleeding WITH DRs. skrobut and C. Shaw
Upper gastrointestinal bleeding is defined as a bleeding source proximal to the ligament of Treitz. It classically presents with hematemesis, melena, and much less commonly bright red blood per rectum.
There are approximately 250,000 hospitalizations per year for upper GI bleed with an estimated 8-20% mortality rate.
Differential diagnosis: Ulcers, esophagitis, gastritis, varices, aorto-enteric fistula, swallowed blood (epistaxis etc)
Factors suggesting an upper GI bleeding source instead of a lower GI bleeding source:
Age greater than 50
Prior upper GI bleed
Melena on digital rectal exam or a patient provided history of melena
Assessment Tools in the Emergency Department:
Fecal occult blood testing: This test is only validated as a screening tool to detect occult bleeding for colorectal cancer. Emerging data suggests against its routine use in the Emergency Department for evaluation of possible upper GI bleed, we encourage the utilization of visible melena .
Nasogastric lavage: Performed by irrigating the stomach and subsequently removing the aspirate to evaluate for visible blood/coffee ground appearance. The literature suggests that this is not helpful in our population and expert local opinion agrees to not perform this routinely.
TEG: With variceal bleeding increased volume is associated with increased rates of bleeding. The TEG allows providers to target their resuscitation with specific products aimed at reversing the coagulopathy. TEG guided targeted treatment has been shown to decrease total volumes administered and therefore is thought to have a positive contribution to the management of these patients.
Treatment Modalities in the Emergency Department:
Proton pump inhibitor bolus vs. drip: Literature and expert local opinion suggests equal efficacy for both.
Antibiotics: In the setting of variceal bleed, literature shows prophylactic antibiotics decrease infection rates, decrease rates of re-bleeding, decrease total hospital days. Ceftriaxone is the recommended antibiotic in Cincinnati, fluoroquinolones may also be appropriate depending on your sensitivities to E. Coli.
Blood Products: Literature suggests that for stable patients a more conservative approach using a hemoglobin cut-off of 7 when considering transfusion of packed red blood cells. There is no good literature to guide the use of platelet transfusions; however, expert consensus seems to target transfusing only when platelet count falls below 40,000.
Octreotide: Literature suggests a possible mortality benefit in upper GI bleeding caused by variceal bleeding. Additionally, there is a demonstrated benefit with its use by decreasing re-bleeding episodes and decreasing number of required hospital days.
Balloon Tamponade: The literature is difficult to interpret on this subject. Patients who undergo this procedure trend towards worse outcomes, and increased mortality; however, they are likely inherently more ill to begin with for this procedure to be considered. Literature does suggest patients that undergo this procedure do have delays in other standards of care including antibiotics, octreotide, PPI, and EGD)
Endoscopic intervention by GI: This is recommended to occur within 12 hours of presentation for variceal bleeding.
taming the sru : ace-Inhibitor induced angioedema WITH DR. ham
A pre-notification call was received from EMS stating that they were en-route with a patient with significant facial swelling concerning for angioedema. The patient arrived and was noted to have a protruding tongue, significant facial swelling, and in marked respiratory distress. He was rapidly moved to the resuscitation bay and decompensated to cardiopulmonary arrest within one minute of arrival.
An attempt was made to perform endotracheal intubation during compressions but the laryngoscope could not be entered into the mouth and the patient could not receive sufficient bag-valve mask ventilation due to his significant oropharyngeal swelling. The decision was made to perform a cricothyrotomy, which was performed successfully. Shortly thereafter the patient achieved return of spontaneous circulation. He was admitted and later underwent conversion to a tracheostomy. It was later discovered in discussion with family that approximately one week ago he had been started on lisinopril.
There are two main categories of angioedema: mast cell mediated and bradykinin induced. ACE-I induced angioedema is a type of bradykinin induced.
Epidemiology: Only 0.1 to 0.7% of all people on ACE-I develop ACE-I induced angioedema. However, there is a very large amount of people prescribed ACE-I and so the potential for emergency department providers to see this complication is high.
Risk Factors: Elderly, Female, African American, and a personal history of ACE-I induced angioedema.
Medical Management: Standard therapy includes H1/H2 antagonists, steroids, and epinephrine, although will data lacking. There are a number of evidence based therapies for hereditary angioedema such as C1 esterase inhibitors, Icatibant, and Ecallantide that do not have good evidence behind their use in ACE-I induced angioedema. Ensure adequate airway management and consider more aggressive interventions such as intubation early when appropriate.
ClinicoPATHOLOGICAL conference : Addison’s disease WITH DRs. gleimer and faryar
A pediatric patient in her early teens presented to a community emergency department with nausea, vomiting, and fever (Tmax 101 at home) for a few days. She otherwise had no complaints and her review of systems was negative. On physical exam she appeared dehydrated and her vitals were within normal limits aside from a mild tachycardia. Her laboratory studies were remarkable for a mild hypochloremic hyponatremia with a pH of 7.31 and a glucose of 73. She was provided IV fluids, felt better and requested discharge.
Approximately one month later she presents with the family also noting that she has lost approximately four pounds over the last few weeks. Review of her growth chart shows that she has been having progressive slow weight loss over the last few months. Her physical exam was remarkable for appearing ill and pale. Her review of systems was otherwise negative. She had no known past medical or surgical history. Her family history was significant for hypothyroidism in her mother and melanoma in her maternal grandfather.
Vital Signs: HR: 105 BP: 91/45 RR: 18 SpO2: 100% on room air
IV access was established and IV fluids were initiated. Her finger-stick glucose was 62. Her laboratory studies were remarkable for a normal white blood cell count and normal hemoglobin. Her electrolytes showed a mild hypochloremic hyponatremia. She had an elevated lactate at 4.4.
Approximately 1 hour into her visit the provider was called to bedside by the patient’s nurse for evaluation of change in mental status. When the provider arrived they found the patient acting strangely and the patient was only oriented to self. A finger-stick blood glucose was 41 at this time and the patient was provided an amp of D50.
And then a diagnostic test was ordered …
Diagnostic Test: Cortisol / ACTH
Diagnosis: Addison’s Disease
Addison’s disease (primary adrenal insufficiency) is most commonly caused by autoimmune destruction of the adrenal glands. This results in in the inability to produce hormones such as cortisol and aldosterone. Classic presenting symptoms include extreme fatigue, weight loss and anorexia, hyperpigmentation of the skin, hypotension and orthostasis, nausea/vomiting and abdominal pain, and depressed mood. Acute onset of severe symptoms is referred to as an adrenal (addisonian) crisis. Laboratory findings often show a hypochloremic hyponatremia with kyperkalemia and a non-gap acidosis. The management consists of glucose containing resuscitation fluids and steroids.
Clinical diagnostics : HEART SCORE WITH DR. hunt
A 54 year old male presents to the emergency department with chest pain that started approximately three hours prior while he was playing with his grandchildren. The pain is located on the left side of his chest, is stabbing in nature, and is made worse with movement of his left upper extremity. The pain does not radiate, nor is it associated with nausea, vomiting, or diaphoresis. He has never had this pain before. He has no family or personal history of coronary artery disease; however, he also does not regularly see a physician. He has never smoked tobacco, does not use illicit drugs, and only rarely consumes alcohol.
Vitals: BP 150/90 but otherwise within normal limits.
Physical Exam: Remarkable for reproducible tenderness of the left anterolateral chest wall.
EKG shows a normal sinus rhythm. Laboratory studies are remarkable for a negative troponin times two and glucose at 250. Chest X-ray is unremarkable.
Developed in the emergency department setting to help risk stratify patients with chest pain for major adverse cardiac events.
Major adverse cardiac events are defined as all-cause mortality, myocardial infarction, or need for coronary revascularization.
The score is calculated based on the history provided by the patient, EKG evaluation, age, risk factors, and the initial troponin.
This patient provides a history that is only slightly suspicious for acute coronary syndrome (0 points). His EKG is normal sinus rhythm (0 points). His age is 54 (1 point). His troponin was negative (0 points).
He declares no past medical history and denies smoking tobacco or having a family history of coronary artery disease; however, this is complicated by him not seeing a physician on a regular basis. Initially, you would give this patient 0 points for risk factors based solely on the information he provides. In reality, he has a glucose of over 200 suggesting diabetes and is hypertensive as well suggesting possible diagnosis of hypertension. He may also have hypercholesterolemia but we would not know since he has no recent evaluation for this. He likely has at minimum 1-2 risk factors (1 point). Even with this consideration he would still fall in the 0-3 low risk category and is likely safe for outpatient This case highlights the importance of considering undiagnosed or undisclosed risk factors when calculating the HEART score.
A female in her 70’s presents via EMS to the emergency department with chest pain that began thirty minutes prior while watching television. The pain is centrally located on her chest and does not radiate. There are no alleviating or exacerbating factors. She has no family history of coronary artery disease. She has a past medical history of breast cancer status post mastectomy and hypertension. She has never smoked tobacco, does use illicit substances, and never drinks alcohol. She only takes lisinopril for her hypertension.
Vitals: Mild tachycardia at 104, hypertensive at 138/86 but otherwise within normal limits
Physical Exam: Mild tachycardia but otherwise unremarkable
EKG shows precordial T wave prominence but no overt ST segment elevation. Initial troponin was negative.
Repeat EKG was performed approximately 30 minutes later now showing ST segment elevation. Additionally, her repeat troponin is now 0.07.
Initially, before the repeat EKG and troponin, the patient had a HEART score of 5. This case highlights the importance of repeat EKGs in these patients. Her initial EKG showed hyperacute T wave changes that with time developed into overt ST segment elevations. Her initial troponin was negative due to the very early course of her myocardial infarction.
A 42 year old male presents to the emergency department with chest pressure that began yesterday while climbing some stairs. It is made slightly worse with exertion, but is not associated with nausea, vomiting, or diaphoresis. It has somewhat improved, but is still located in the center of his chest without radiation. The patient is homeless and does not have a primary care provider. He has an unknown family history and does not see a physician regularly. His past medical history is documented as hypertension and obesity. He has a 20 year smoking history, uses cocaine and alcohol regularly. He takes no daily medications.
Vitals: Mild tachycardia (110) and hypertensive (155/93)
Physical Exam: tachycardia and obesity but otherwise unremarkable.
EKG shows sinus tachycardia. His laboratory studies are unremarkable with a negative troponin. CXR shows no acute cardiopulmonary process.
This patient provides a history that is moderately suspicious for acute coronary syndrome (1 point). His EKG is normal (0 points). His age is under 45 (0 points). He has at least 3 risk factors and likely has more that are undiagnosed (2 points). His initial troponin is negative (0 points). His HEART score is calculated at 3 and is considered low risk.
This case highlights the importance of clinical gestalt and social considerations when determining disposition. The low risk category (based on the HEART score) is usually recommended for outpatient evaluation; however, this patient does not have reliable outpatient follow up. Additionally, his homelessness and frequent drug and alcohol abuse put him at higher risk for being lost to follow up. Many providers would agree that even though this patient is considered “low risk” he would still benefit from admission/observation for performance of further cardiac risk stratification.
Case Follow up: Refractory SVT WITH DR. I. Shaw
A male in his 60s with a past medical history of AVNRT status post ablation in 2016 and stage IV lung cancer presents for shortness of breath. The patient had been subacutely dyspneic for 2 weeks. However, on the day of presentation, he suddenly developed the onset of sharp, right sided chest pain that then became intermittent for 1-2 hours before he decided to present to the emergency department.
On arrival he was tachycardic to 166, with a normal blood pressure requiring a non-rebreather mask to maintain oxygen saturation at 87%. EKG showed SVT without signs of ischemia. Ultrasound showed only a mild pericardial effusion. Chest X-ray showed a large R pneumothorax. The providers place a pig tail chest tube prior to attempted cardioversion successfully.
Despite 6mg, 12mg, and then another 12mg of adenosine, the patient did not cardiovert out of SVT. Therefore, the providers gave him a diltiazem bolus of 5mg and he was then put on a drip. Within 5 minutes, the patient cardioverted out of SVT and was admitted to the hospital.
Consider using a pneumocath for spontaneous pneumothorax
Small-bore chest tubes (14F) have been shown to have equivalent success with much less pain than standard chest tubes
Pay special attention to the Heimlich valve orientation on the chest tube circuit as reversal of this can lead to tension pneumothorax
The most common form of paroxysmal SVT, which is from a reentrant current in the AV nodal cells
Unstable Patients (typical sounding chest pain, altered mental status, hypotension)
Valsalva maneuvers are the first line treatment
Consider doing the “REVERT Maneuver” (having the patient valsalva and then placing them supine with their legs up)
The REVERT Maneuver has had up to three times the success rate of valsalva alone
6mg is your starting dose, then 12mg if this does not work, and 12mg again
Higher doses may be needed in those who have consumed caffeine (12mg, 18mg, 18mg)
Lower doses may be used in patients with central access (3mg, 6mg, 6mg) as a higher concentration can get to the heart
The AHA recommends a trial of IV calcium channel blockers (CCB) as a second line therapy for SVT in those without evidence of acute heart failure
Diltiazem has been shown to have a higher success rate at cardioversion than Adenosine (98% vs 86%), but is slower than adenosine (6 minutes vs 1 minute)
Esmolol can also be considered, but has a much lower success rate of cardioversion compared to CCB (25% vs 100%)