Migraine is a common complaint, accounting for about 1 million ED visits per year. It is characterized by a unilateral, pulsating headache that is moderate to severe in intensity and exacerbated by routine activities. [1] Most emergency physicians have their own "cocktail" they like to use. And because many different medications are effective, there are multiple approaches available. This review will be to provide evidence for common therapies and a word on some less common alternative medications. Most of the information comes from a well-done systemic review article evaluating random controlled trials of pharmacologic therapies for acute migraine headache in the ED or similar settings. [2]

Sumatriptan (Imitrex) [2]

• Selective 5-HT receptor agonist
• Dose: 6 mg subcutaneously
• More effective than placebo
• Inferior to metoclopramide and prochlorperazine
• Side effects: flushing, tingling, chest heaviness
• May be considered in select group of patients

Dihydroergotamine (DHE) [1,2]

• 5-HT receptor agonist
• Dose: 1 mg IV or IM, may be repeated in one hour
• Effective, especially in those with status migrainosis
• Contraindications include pregnancy, breast feeding, HTN, CAD, and PVD
• Side effects: nausea and vomiting are common
• May be considered in select group of patients

Ketorolac (Toradol) [1,2]

• NSAID
• Dose: 30 mg IV or 30-60 mg IM
• Safe and effective agent for acute migraine
• Cautions/contraindications would be for those with GI issues such as PUD, renal insufficiency (or diabetics), or before a pregnancy test is confirmed. This last point is important because migraines are more prevalent among women.
• Although the quality of evidence overall is poor, its safe side effect profile makes it an agent to consider in most cases of migraine.

Prochlorperazine (Compazine) [1-3]

• Phenothiazine in the class of antipsychotics, in an antagonist of the dopamine D2 receptors. It is unknown how this is effective in the treatment of migraines, but high quality evidence shows it is effective.
• Dose: 10 mg IV
• Although effective, it does carry side effects of akathsia, dystonic reactions and sedation. Overall, side effects are seen in 1 in 5 patients.
• Side effects attempted to be mitigated with diphenhydramine. This has been shown to be effective in reducing unwanted side effects, while increasing sedation. Both of these are positive effects when treating acute migraine patients.

Metoclopramide (Reglan) [1,2,4]

• Antiemetic, dopamine antagonist
• Dose: 10-20 mg IV
• It does not carry the same level of evidence as prochlorperazine, but nevertheless has been shown to be effective with moderate quality of evidence.
• It shares the same side effects as prochlorperazine (thanks to the dopamine antagonism), which again are counteracted by diphenhydramine.
• Interestingly, a recent RCT in the Annals of Emergency Medicine did not show a decrease in reported side effects or benefit of migraine reduction when metoclopramide with diphenhydramine was compared with metoclopramide with placebo.

Haloperidol (Haldol) [1,2,5,6]

• First generation antipsychotic, dopamine D2 antagonist
• Dose: 5 mg IV
• Less commonly used and not listed as option in Rosen's
• Although overall low quality of evidence has been shown to be effective
• Side effects are common and similar to those mentioned with other dopamine antagonists. Other clinically relevant side effect is QTc prolongation.
• Some of the best evidence was recently published in the Journal of Emergency Medicine, which was a well-done RCT that compared haloperidol to metoclopramide. Diphenhydramine (25 mg IV) was administered before the study medication. There was a statistically significant difference in the reduction of pain scores (primary outcome) for both agents, but there was no statistically significant difference between groups. Both were similarly effective at treating nausea.
• There were no significant side effects (restlessness and sedation) within each group or compared to each other.
• Less rescue medications needed in haloperidol group (statistically significant)
• No significant change in QTc interval in either group
• Considering the above, haloperidol is a safe and effective alternative to the treatment of acute migraine headache, and should be considered as a standard agent in its management. This is especially true now as prochlorperazine continues to be on shortage.

Droperidol [1,2,7,8]

• Antiemetic, dopamine antagonist (among other mechanisms of action)
• Dose: 2.5 mg IV
• Reportedly effective, however no evidence to support its use over other agents
• Rarely used due to Black Box Warning of proarrhythmic effects due to QTc prolongation
• Interestingly, data shows droperidol to not significantly effect the QTc even when high doses of 10 mg used (for sedation in acute agitation)
• Its use in smaller doses less than 2.5 mg are supported by the American Academy of Emergency Medicine
• Side effects similar to other dopamine antagonists

Others [2]

• Magnesium Sulfate: little side effects, but no good evidence for its use
• Muscle relaxers: no evidence to support use
• Dexamethasone: no evidence for acute migraine therapy but has been shown to be effective in preventing recurrence
• Opioids: no, just no!

References

1. Kwiakowski T, Friedman, Benjamin W. Headache Disorders. In: Marx J, Hockenberger RS, Walls RM, et al, editor. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia: Elseveir Saunders; 2014.
2. Orr SL, Aube M, Becker WJ, et al. Canadian Headache Society systematic review and recommendations on the treatment of migraine pain in emergency settings. Cephalalgia. 2015 Mar;35(3):271-84.
3. Coralic Z. I am giving prochlorperazine. Should I give diphenhydramine too? Academic Life in Emergency Medicine; 2014.
4. Friedman BW, Cabral L, Adewunmi V, et al. Diphenhydramine as adjuvant therapy for acute migraine: an emergency department-based randomized clinical trial. Ann Emerg Med. 2016 Jan;67(1):32-9 e3.
5. Honkaniemi J, Liimatainen S, Rainesalo S, Sulavuori S. Haloperidol in the acute treatment of migraine: a randomized, double-blind, placebo-controlled study. Headache. 2006 May;46(5):781-7.
6. Gaffigan ME, Bruner DI, Wason C, Pritchard A, Frumkin K. A randomized controlled trial of intravenous haloperidol vs. intravenous metoclopramide for acute migraine therapy in the emergency department. J Emerg Med. 2015 Sept;49(3):326-34.
7. Perkins J, Ho J. Clinical practice statement: safety of droperidol use in the emergency department. AAEM Board of Directors; 2013.
8. Calver L, Page CB, Downes MA, et al. The safety and effectiveness of droperidol for sedation of acute behavioral disturbance in the emergency department. Ann Emerg Med. 2015 Sep;66(3):230-8 e1.

Submitted by Dr. Michael Craddick, PGY-2

Mucormycosis is the generic name of an invasive fungal infection. It is caused by a variety of fungi, but the most common are from either the genus Rhizopus or Mucor, which is where the disease gets its name. Theses are ubiquitous fungi and do not cause disease in immunocompetent individuals. Rather, it is seen in those with primary or secondary immunosuppression. (1-3)

The most important risk factors, and therefore the populations affected, are diabetics and those with hematologic malignancy. Diabetes, specifically with ketoacidosis, is the main risk factor. (1,2) Neutrophil dysfunction, along with hyperglycemia and an iron rich environment induced by ketoacidosis allows for the fungi to avoid the immune system and thrive in a substrate rich environment. (3) Retrospective studies have reported over 80% of cases in those with diabetes, and 40% of those who previously did not have known history of the disease. (1) Hematologic malignancy, especially those with acute myelogenous leukemia are also at increased risk. Other immunosuppressive states and burn victims without a protective skin barrier are also at risk.

The three most common forms of disease are rhinocerebral, pulmonary and cutaneous. The most common is rhinocerebral. This is the classic disease state seen in patients with DM or DKA. Inhalation of spores leads to invasion of the sinuses. This leads to typical symptoms of sinusitis. However the hallmark feature is a necrotic eschar on the palate, nasal turbinates or external skin. Seeing this feature does not rule out mucormycosis, but absolutely rules it in. If cerebral or orbital invasion occurs, cranial nerve or ophthalmologic symptoms can develop. If these are seen in combination, it should be considered mucormycosis unless proven otherwise. (1,2)

The pulmonary form of the disease is rapidly progressive and has a high mortality rate (76%). (1) Manifestations would be similar to other forms of pneumonia, specifically invasive pulmonary aspergillosis. It would be difficulty to sore this out in the emergency department, but could be considered in the right patient population or in those who are failing to improve while on broad-spectrum antibiotics. (1,2)

The cutaneous form of mucormycosis can have variable presentations, but again if nerotic eschars are present, this needs to be in the differential. If invasion of the underlying soft tissues, muscle and bone occur, it can cause significant pain or present similar to necrotizing fasciitis. (1)

Source control is an important component of treatment. Consultation with subspecialties such as otolaryngology, ophthalmology or pulmonology should occur promptly. If history and physical exam are suggestive this should occur prior to further studies because this is a highly fatal disease that is a time sensitive emergency, often requiring extensive debridement. CT scans of affected areas can help in the diagnosis but do not show specific findings. Anti fungal therapy with the lipid formulation of amphotericin B at 5 mg/kg/day is the agent of choice. (2)

This is a rare disease that may never be encountered in the career of the emergency physician. It nevertheless should remain in the differential because of its high mortality rate that approaches 80% in invasive disease. While other forms of the disease may be hard to distinguish, the rhinocerebral form has hallmark physical exam findings that can aid in the diagnosis. For a terrific review of a case of mucormycosis, please use this link to the EM:RAP Podcast.



References

1. Petrikkos G, Skiada A, Lortholary O, Roilides E, Walsh TJ, Kontoyiannis DP. Epidemiology and clinical manifestations of mucormycosis. Clin Infect Dis. 2012 Feb;54 Suppl 1:S23-34
   
2. Long B, Koyfman A. Mucormycosis: what do emergency physicians need to know? Am J Emerg Med. 2015 Aug 28
   
3. Ibrahim AS, Spellberg B, Walsh TJ, Kontoyiannis DP. Pathogenesis of mucormycosis. Clin Infect Dis. 2012 Feb: 54 Suppl1:S16-22
   

Submitted by Dr. Michael Craddick, PGY-2

Sticking with the pediatric theme, this post is going to give an overview on the management of pediatric sepsis. We all feel relatively comfortable managing the adult patient with sepsis. Sure, some items will be case specific, but the management is well taught and a hot topic right now. Pediatrics, on the other hand, is not as mainstream. Just as with everything else, kids are not just small adults. As such I hope to provide some important differences in the management of this sick population.

Definitions and Epidemiology (1-3)
Approximately 100,000 pediatric patients are diagnosed with severe sepsis per year in the United States. That number drops to 75,000 for septic shock. 

The definitions of pediatrics, like everything else, are age based. While the values pertinent to each age are noted, remembering 140 (HR) and 40 (RR) gets you pretty close. Aside from that, the definitions of septic shock is important, because it does not just include hypotension. Rather, other signs of hypo perfusion can be used to make the diagnosis, and reliance on BP to drop can result in delayed recognition or management. The big pearl here is you do not need hypotension to be in shock.

SIRS - Dependent on Age, >/= 2 or more of the following

• Temperature < 36 C (96.8 F) or > 38.5 C (101.3 F)
  
• Tachycardia 

                Newborn - 1 year: HR > 180 bpm
                1 - 5 years; HR > 140 bpm
                5 - 12 years; HR > 130 bpm 
                12 - 18 years; HR > 110 bpm
                > 18 years; HR > 90 bpm

• Tachypnea 
  

                Newborn - 1 week: RR > 50
                1 week - 1 month; RR > 40
                1 month - 1 year; RR > 34
                1 - 5 years; RR 22
                5 - 12 years; RR 18
                12 - 18 years; RR 14

• WBC < 4,000 cells/mL3; > 12,000 cells/mL3; or > 10% bands
  

Sepsis
SIRS and suspect or present source of infection

Severe Sepsis
Sepsis with organ dysfunction, hypotension, and tissue hypoperfusion (altered mental status, acute renal failure, acute liver failure, decreased urine output, etc)

Septic Shock
Sepsis plus cardiovascular dysfunction despite 40 mL/kg fluid administration in one hour (not just defined by blood pressure)

• Hypotension
  

                0 - 28 days, < 60
                1 - 12 months, < 70
                1 - 10 years, < 70 + (age in years x 2)
                > 10 years, < 90

• Need for vasoactive medication to maintain blood pressure in normal range
  

                Two or more of the following
                Unexplained metabolic acidosis: base deficit > 5.0 mEq/L
                Increased arterial lactate > 2 times upper limit of normal
                Oliguria: urine output < 0.5 mL/kg/hr
                Prolonged capillary refill > 5 sec
                Core to peripheral temperature gap > 3C

Diagnosis (3,4)
Although the diagnosis of sepsis can eventually be straight forward, the initial assessment can be challenging. Histories can be limited in non-verbal children or if caregivers are not available. The most important clinical characteristics are tachycardia, fever, and mental status change, as well as respiratory rate and peripheral capillary refill. While all of these clinical findings are not unique to sepsis, they are nevertheless the most commonly used by most pediatric emergency physicians. Like an case of sepsis, your history, physical and workup can most often point toward a source.

Management (3, 5, 6)
The general approach of securing the airway, if needed, and administering early fluids and antibiotics applies to both adults and pediatric sepsis. Here are some specific differences though when if comes to kids.

Airway

• Give supplemental oxygen to all patients in septic shock
  
• Intubation and mechanical ventilation indicated if cannot reach oxygen saturation of 92% despite supplementation, or if pO2 < 65 mmHg
  
• No atropine pretreatment (dropped in new 2015 ACLS guidelines)
  
• Avoid etomidate (controversial)
  
• Ketamine or versed/fentanyl for RSI
  

Fluid Management

• 20 mL/kg and reassess
  
• Repeat 2-3 times if no evidence of rales, respiratory distress or hepatomegaly develop
  
• Crystalloid or colloid can be used (NS most common)
  
• Administer through 3-way stop cock or "push-pull" method (using a 60 mL syringe, draw fluid out of the bag and then either turn the stop cock or inject directly into the line as many times as needed to give desired quantity of fluid)
  

                Desired rate of infusion is at least 60 mL/kg in < 60 minutes
                Each bolus is to be given in 5-10 minutes to allow for reassessment

• Hypoglycemia may also occur and should be corrected (remember rule of 50's; dose of fluid and concentration of dextrose equal 50)
  

                Infants: 5-10 mL/kg D10W
                Children: 2-4 mL/kg D25W

Vasoactive Agents

• Dopamine 1st line
  

                Initial dose: 5-10 mcg/kg/min, max 20 mcg/kg/min

• "Warm Shock" (shock with vasodilation or flash cap refill)
  

                Norepinephrine 0.05-1 mcg/kg/min

• "Cold Shock" (shock with vasoconstriction)
  

                Epinephrine 0.05-1 mcg/kg/min

Antibiotics
Remember 15 for vancomycin, 50 for everything else, and look up acyclovir

• Neonates: ampicillin 50 mg/kg, cefotaxime 50 mg/kg, +/- acyclovir
  
• > 4 weeks: vancomycin 15 mg/kg and ceftriaxone 50 mg/kg
  

I know it is a quick and brief review, but hope it helps the next time you approach one of these patients. Until next time.


References

1. Goldstein B, Giroir B, Randolph A. International Consensus Conference on Pediatric S. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005 Jan;6(1):2-8.
   
2. Singhal S, Allen MW, McAnnally JR, Smith KS, Donnelly JP, Wang HE. National estimates of emergency department visits for pediatric severe sepsis in the United States. PeerJ. 2013;1:e79.
   
3. Silverman AM. Septic shock; recognizing and managing this life-threatening condition in pediatric patients. Pediatr Emerg Med Pract. 2015 Apr;12(4):1-25;quiz6-7.
   
4. Thompson GC, Macias CG.Recognition and management of sepsis in children: practice patterns in the Emergency department. J Emerg Med. 2015 Oct;49(4):391-9.
   
5. Association AH. Pediatric Advanced Life Support. 2015 [cited 2015 November 18]; available from https://eccguidelines.heart.org/index.php/circulation/cpr-ecc-guidelines-2/part-12-pediatric-advanced-life-support/
   
6. Associate AH. Pediatric Advanced Life Support. United States of America: First American Heart Association Printing; 2010.
   

Submitted by Dr. Michael Craddick, PGY-2

References
1 Mick NW. Pediatric Fever. In: Marx J, Hockenberger RS, Walls, RM, et al, editor. Rosen's Emergency Medicine: Concecpts and Clinical Practice. 8th ed. Philadelphia: Elseveir Saunders; 2014.

2 Nadkarni MD. Fever and Serious Bacterial Illness. In: Cline DM, Ma OJ, Cydulka RK, Thomas SH, Handel DA, Meckler GD, editors. Tintinalli's Emergency Medicine: Just The Facts. 3rd ed. China: McGraw-Hill; 2013.

3 Morley EJ, Lapoint JM, Roy LW, et al. Rates of positive blood, urine, and cerebrospinal fluid cultures in children younger than 60 days during the vaccination era. Pediatr Emerg Care. 2012 Feb;28(2):125-30.

4 American College of Emergency Physicians Clinical Policies C, American College of Emergency Physicians Clinical Policies Subcommittee on Pediatric F. Clinical policy for children younger than three years presenting to the emergency department with fever. Ann Emerg Med. 2003 Oct;42(4):530-45.

5 Martinez E, Mintegi S, Vilar B, et al. Prevalence and predictors of bacterial meningitis in young infants with fever without a source. Pediatr Infect Dis J. 2015 May;34(5):494-8.

6 Sloas A. PEM ED Podcast.  Fever of Unknown Source - Part 1; 2011.

7 Sloas A. PEM ED Podcast.  Fever of Unknown Source - Part 2; 2011.

8 Baker MD, Bell LM, Avner JR. Outpatient management without antibiotics of fever in selected infants. N Engl J Med. 1993 Nov 11;329(20):1437-41.

9 Jaskiewicz JA, McCarthy CA, Richardson AC, et al. Febrile infants at low risk for serious bacterial infection--an appraisal of the Rochester criteria and implications for management. Febrile Infant Collaborative Study Group. Pediatrics. 1994 Sep;94(3):390-6.

10 Dagan R, Powell KR, Hall CB, Menegus MA. Identification of infants unlikely to have serious bacterial infection although hospitalized for suspected sepsis. J Pediatr. 1985 Dec;107(6):855-60.

11 Baskin MN, O'Rourke EJ, Fleisher GR. Outpatient treatment of febrile infants 28 to 89 days of age with intramuscular administration of ceftriaxone. J Pediatric. 1992 Jan;120(1):22-7.


Submitted by Dr. Michael Craddick, PGY-2

Postural modification to the standard Valsalva maneuver for emergency treatment of SVT (REVERT): a randomized controlled trial

This was a randomized controlled, parallel group trial at Emergency Departments in England. The study compared the well known standard Valsalva maneuver to attempt conversion of SVT to sinus rhythm, to a modified Valsalva maneuver. The primary outcome was return to sinus rhythm at 1 minute after the chosen intervention. The standard maneuver required participants in a semi-recumbent position to perform the standardized strain to a pressure of 40 mmHg sustained for 15 seconds by forced expiration, and remain in that position for 60 seconds. In the modified maneuver, participants performed the standardized strain in the same semi-recumbent position but immediately after were laid flat and had their legs raised to 45 degrees for 15 seconds. They were then returned to the semi-recumbent position for the remaining 45 seconds prior to re-assessment of their rhythm. At the conclusion of the study, the results were that 17% of the participants assigned to the standard Valsalva achieved sinus rhythm, compared to 43% of participants who achieved sinus rhythm with the modified Valsalva. A major benefit of the modified Valsalva is that it can be easily taught to patients and appears to be more effective than the standard. Another benefit of discovering a more efficacious maneuver for conversion to sinus rhythm is that the effects of adenosine can be extremely unpleasant to patients, and this may decrease that rate at which it is administered. This can be easily implemented in our ED.

Intercepting wrong-patient orders in a computerized provider order entry system

Even though there are many safety benefits of computerized provider order entry, there are still errors that can be made, such as ordering on the wrong patient. This study evaluated the short and long term effects of a computerized provider order entry based patient verification intervention to reduce wrong patient orders in 5 emergency departments. The goal of this study was to reduce wrong-patient orders. Prior to implementing the intervention, monthly measurements of wrong-patient ordering rates were obtained, and then compared to the rates after the implementation of the verification process. The intervention focused on providing some sore of visual cues about the patient to the provider, immediately prior to placing an order. A dialog box was displayed at the beginning of every ordering session, requiring providers to verify the patient for whom they were placing an order. The short term results were that wrong patient orders were reduced by 30% immediately after implementation of this dialog box intervention. The long term results showed that after 2 years, the rate of wrong patient orders remained 24.8% less than before intervention. One down-side of this type of intervention is the effect of alert fatigue on providers. However, the effect of alert fatigue on the response rate to alerts was analyzed and the slight decline in the effect of the patient verification module in the study was less severe and not statistically significant. Overall this was a though provoking study and in our discussion we agreed that spending an extra few seconds to verify a patient is worthwhile when compared to the potential risks of harming a patient with incorrect orders, and the time spend having to undo certain orders even if the mistake w

Fluid overload in patients with severe sepsis and septic shock treated with early goal directed therapy is associated with increased acute need for fluid related medical interventions and hospital death

This was a retrospective cohort study of adults admitted with severe sepsis and septic shock to the MICU of a tertiary care academic hospital. The goal of the study was to determine the potential morbidity and mortality associated with fluid overload in those receiving adequate EGDT for both sepsis and septic shock on days 1 and 3, regardless of vasopressor use. Early fluid resuscitation through EGDT has been shown to decrease in hospital mortality and improve morbidity by decreased occurrence of organ dysfunction. However, there are adverse effects of fluid overload such as pulmonary edema and increased cardiac, that are detrimental to the patient. The study found that the clinical evidence of fluid overload was common and associated with increased medical interventions such as thoracentesis and diuretics, and increased hospital mortality. Interestingly, the study found that patients with fluid overload did not have a statistical difference in fluid administration. Additionally, BMIs were significantly higher in the fluid overload group, leading the reader to believe that those patients were at a higher risk of fluids overload in the first place. There were several limitations to the study, such as clinical evidence of overload being subjective, quality of documentation, and the retrospective nature of the study, which led to some gaps in the data. A major limitation was that the study was non-randomized. Since the study was not randomized, it is possible that certain patient factors may have been responsible for the development of fluid overload rather than the resuscitation approach. Since it is impossible to tell if the method of resuscitation caused the fluid overload or the patient's risk factors, we agreed in our discussion that we should not alter the way we resuscitate our patients at this time, but that we should be meticulously reassessing our patients for improvement v. deterioration and adjusting our therapies accordingly.

Slaminen P, et al. Antibiotic therapy vs appendectomy for treatment of uncomplicated acute appendicitis. The APPAC randomized clinical trial. JAMA. 2015;313(23):2340-2348.

This was a noninferiority randomized clinical trial that compared outcomes between antibiotic therapy and appendectomy in CT confirmed acute appendicitis.  Antibiotic therapy was IV ertapenem, 1 gram a day for 3 days while inpatient, followed by 7 days of levofloxacin and metronidazole. Primary endpoints were successful appendectomy and successful discharge from the hospital without need for surgery or recurrent appendicitis within a year. In the antibiotic group, 70/257 required open appendectomy within one year. The study had a prespecified noninferiority margin of 24% and the results yielded at 27% difference in treatment efficacy between the two groups. By their criteria, noninferiority of antibiotic therapy was not demonstrated. After discussion, there were a few questions that arose. Were the groups truly comparable? There was no mention of health or comorbidity equality between the groups that might effect outcome. Also, the secondary outcome, complication rates was better in the antibiotic group. Furthermore, it would have been nice to have some comparison of cost difference between the two groups. Which may provide another avenue for research. Our take is that this is interesting information but will not affect our standard practice of consulting surgery.




Claveau D, et al. Complications associated with nitrate use in patients presenting with acute pulmonary edema and concomitant moderate or severe aortic stenosis. Ann Emerg Med. 2015 Oct; 66(4):355-362 e1.

This was a cohort designed retrospective chart review study that evaluated the incidence of complications that occurred in patients who presented with acute cardiogenic pulmonary edema who were treated with nitrates, specifically between patients with moderate or severe aortic stenosis (AS) and those without AS. Patients were chosen if they had been given nitrates and had an echocardiography report available. They used data from two Canadian hospitals. They had a total of 195 that qualified, 65 in each category. Primary outcome was clinically relevant hypotension that required the nitrate discontinuation, IV fluid bolus, use of vasopressors or cardiac arrest. Secondary outcome was < 90 mmHg systolic hypotension that was sustained greater or equal to 30 minutes. This study found that nitrate administration was not associated with clinically relevant hypotension in the severe or moderate AS group when compared to those without AS. There were more significant outcomes with regards to the secondary outcome with more incidences occurring with higher disease presence. In discussion, it was interesting that this study excluded the patients that died in the ED. Also, it did not address whether or not the ED physician knew the patient's diagnosis, which might have affected the amount of nitrates given, thereby skewing the results. How would this information affect our practice? We think it is appropriate to consider nitrates as part of the treatment while taking into account disease burden and BP values on presentation. Also, it would probably be best with slower infusions to see how the patient is handling the treatment.




Pollack CV, et al. Idarucizumab for dabigatran reversal. N Engl J Med. 2015 Aug 6; 373(6):511-520.

This was a prospective cohort study to determine the safety of idarucizumab in patients who needed reversal of dabigatran therapy. They compared the outcome of two different groups; patients who had an overt, uncontrollable or life threatening bleeds and patients that required an urgent procedure or surgery that could not wait longer than 8 hours. Cohorts were given 5 grams of idarucizumab IV and looked for maximum percentage reversal of the anticoagulant effect of dabigatran within 4 hours of administration. Primary outcome measured percentage reversal by measuring the dilute thrombin time or ecarin clotting time. Secondary end point was restoration of hemostasis. Blood samples were taken at 10 and 30 minutes, and 1, 2, 4, 12 and 24 hours after administration. The results showed that administration of idarucizumab normalized test results in 98% of participants within minutes, with median maximum percent reversal of 100% in both groups. Clinical hemostasis, secondary measure, was 11.4 hours. After discussion, it would be helpful if there were more participants in this study. However, the patients in need of this treatment are in life threatening situations and given the results, this looks like it would be a viable treatment in patients taking dabigatran in need of emergent intervention.

Submitted by Dr. Christopher Branham, PGY1

A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters
 
This review article evaluated adverse events associated with giving vasopressors through peripheral IV catheters versus central lines, as it is standard practice not to give vasopressors through peripheral lines. The majority of the 85 articles examined were case reports. 318/325 adverse events were events that occurred with peripheral administration of pressors, most of which were at sites distal to the antecubital or popliteal fossa and administered for a longer period of time, with a median time of 24 hours. The results of the study showed that more investigation should be done regarding peripheral administration of pressors to determine whether peripheral administration is a safe practice. After discussion, our conclusions were that while a central line is still preferred for pressor use, it may be acceptable to give pressors through a more proximal peripheral line for a short period of time, such as <6 hours, until central access can be obtained.
 
 
The Diagnostic Accuracy of Bedside Ocular Ultrasonography for the Diagnosis of Retinal Detachment: A Systematic Review and Meta-analysis
 
This review article of 3 small prospective observational studies evaluated the diagnostic accuracy of ED bedside ultrasound in identifying retinal detachment. In all three trials, the examiner was at the very least given a lecture on how to perform the ultrasound examination of the posterior chamber to identify retinal detachment. Exams were performed by residents, fellows, and attendings. Sensitivity ranged from 97-100% and specificity was 83-100% in the three trials. Our discussion concluded that this is an exam worth doing on a patient with an ocular complaint that is concerning for retinal detachment or other posterior chamber abnormality.
 
 
Thrombectomy within 8 Hours after Symptom Onset in Ischemic Stroke
 
This article outlines a Randomized Controlled Trial that aimed to compare ischemic stroke patients treated within 8 hours of symptom onset with medical therapy (alteplase) alone versus medical therapy plus thrombectomy. Only individuals who had persistent proximal large-vessel occlusion 30 minutes after alteplase administration were included in the randomized groups. The study was concluded prior to reaching its goal of participants due to clear data from this trial and others published at the time that thrombectomy improves outcomes, so it was unethical to randomize patients to not receive the thrombectomy.  Despite the incomplete set of data, there was a significant difference in disability between the group that received medical therapy (lower disability) plus thrombectomy compared to medical therapy alone (more disability). Based on this study, patients that can be treated within 8 hours of symptom onset should be treated with medical therapy (if the patient qualifies for such treatment) plus thrombectomy for proximal large-vessel occlusion ischemic strokes.

Rosen’s did a good job introducing us to the ventilator and approaches to its troubleshooting. I wanted to build upon that from some other sources, with a limited focus on problems we should know how to fix. This will help in the ED, but also on other critical care months. This is longer than some other posts, but review of the physiology and pathophysiology of the ventilator is included to help understand these concepts.

Problem 1: High Airway Pressures

When in the commonly used volume controlled ventilation setting, the tidal volume is set but the pressure varies. This is because positive pressure is applied until the goal tidal volume is reached. The amount of pressure that is needed to deliver a breath through the entire airway system (ETT, trachea, bronchi, etc) is known as the Peak Airway Pressure (Pap). There are two things that can affect this. One, there could be resistance in the system. This would cause the ventilator to work harder against this resistance and therefore require a higher pressure, which would trigger the ventilator to alarm this is happening. It could also mean that the lungs are becoming less complaint. What this basically means is that the lungs/chest wall have a restriction that does not allow them to inflate/expand. Similarly, a higher pressure is required to inflate the lungs, which again triggers the vent.  So, high peak airway pressures could be due to a lung problem or an airway problem.

To figure this out, you need to determine if there is high resistance (airway problem), or decreased compliance (lung problem). To do this, you first make note of the Pap. The next step is to determine a Plateau pressure (Pplat). Recall that the plateau pressure represents the peak pressure in the alveoli. If this number is > 30 mmHg it puts the alveoli at risk for barotrauma. To measure this, you need to perform an “inspiratory hold” at the end of inspiration. The pressure will then plateau and leaves you this important value.  

From there you can look at the difference between these two values. At baseline, the difference should be < 5 mmHg. If there is an increase in the Pap without a corresponding increase in Pplat, then the problem is due to increased resistance in the system. This is important because it does not mean you have to worry about the potential for barotrauma, but instead have to focus on decreasing the resistance. Common problems that may cause this could be:

• Kinked or obstructed ETT
• Mucous plugging
• Bronchospasm
• Too narrow of an ETT

 All of these problems have a potential fix:

• Pass a suction catheter and clear secretions. Unkink the tube at the tube holder.
• Again suction the ETT and/or trachea. Obtain a CXR to evaluate for an opacified lung indicating mucous plugging which requires aggressive pulmonary toilet or bronchoscopy.
• Administer inhaled bronchodilators
• Exchange the ETT, or accept a higher Pap

If when you perform an inspiratory hold and the Pplat is also elevated, it indicates there is decreased compliance and the problem is in the lungs. Common problems may be:

• Mainstem bronchus intubation
• Atelectasis
• Cardiogenic pulmonary edema
• ARDS
• Pneumothorax
• Developing or worsening pneumonia

Again, all of these have a potential solution:

• Pull the ETT back
• Aggressive pulmonary toilet or bronchoscopy
• Administer diuretics or inotropes as necessary
• Use a lung protective strategy (lower tidal volumes of 4-6 mL/kg)
• Insert a chest tube
• Maximize antibiotic therapy

If none of these problems are present and the Pplat is still elevated, then decrease the tidal volume until this value is < 30 mmHg.

Problem 2: Hypoxia

Another problem that can be encountered is hypoxia. This can be caused by multiple reasons. A commonly used mnemonic used to ensure a systematic approach is DOPES and DOTTS. DOPES is for the differential and DOTTS includes what actions to take.

Differential for the Alarming Ventilator: DOPE(S)

D – Dislodged tube
O – Obstructed tube (mucous plug, blood, kink)
P – Pneumothorax
E – Equipment failure (ventilator, tubing, etc)
S – Breath Stacking [breath] (Auto-PEEP)

This is certainly helpful for diagnosing an alarming ventilator, but it does not provide an approach to dealing with these problems. While it’s still a mnemonic that I am going to keep in the back of my mind, I really liked the DOTTS mnemonic that he (referring to the EM:RAP post linked to below in references) offered to outline the things that you should do. While it could certainly be argued that if you know what you’re doing, DOPES will result in a similar approach, I liked the order and direction of DOTTS.

Approach to the Alarming Ventilator: DOTTS

D – Disconnect the patient from the ventilator , listen for a hiss to imply release of trapped air, +/- provide gentle pressure to the chest (assess for and treat breath Stacking and Equipment failure)
O – Oxygen (100%) and manual ventilation with a bag (check compliance by squeezing the bag: difficult bagging suggests Pneumothorax or Obstructed tube, very easy bagging suggests Dislodged tube or Equipment failure due to a deflated cuff)
T – Tube position/function (see if the tube has migrated to assess for Dislodged tube; pass a bougie or suction catheter through to see if the tube is Obstructed)
T – Tweak the vent (prevents breath Stacking by decreasing respiratory rate, decreasing tidal volume or decreasing inspiratory time)
S – Sonography (assess for pneumothorax, mainstem intubation, plugging)


This was borrowed from the blog “Boring EM” (its OK in the interest of FOAM). This is a great blog that I encourage you to take a gander at to see if you like what it has to offer.

Additionally you may need to apply additional PEEP to increase the functional residual capacity and “recruit” more alveoli to participate in gas exchange. Also, always consider PE as a potential diagnosis.

Problem 3: Dynamic Hyperinflation

This problem occurs when there is inadequate time for exhalation, and can be exacerbated by high airway resistance. When this happens, residual air is trapped in the lungs and leads to autoPEEP/breath stacking. This increases the alveolar and intrathroacic pressure and can cause pneumothorax or decreased venous return. These both can lead to hypotension and circulatory collapse. Aside from that, this also will create more dead space ventilation and lead to worsening hypoxia and/or hypercapnea. This can be measured by performing an expiratory hold (measuring the pressure present at the end of expiration). This value would normally be equal to the PEEP setting, but in the case of autoPEEP, the value will be much higher. Subtract the preset PEEP from the pressure value obtained at the end expiratory hold to calculate the autoPEEP.

The management goes back to the DOPES/DOTTS mnemonic. However specific management steps are:

• Disconnect the patient from the ventilator and allow the trapped air to escape.
• Allow for a longer expiratory time by decreasing the respiratory rate
• Shorten the inspiratory time to allow for an inspiration:expiration (I:E) ratio of 1:3-1:5 (ask RT)
• Decrease the tidal volume
• Increase the inspiratory flow from the standard 60 L/min to 80 L/min
• Treat bronchospasm to reduce airway resistance

·      Disconnect the patient from the ventilator and allow the trapped air to escape.

·      Allow for a longer expiratory time by decreasing the respiratory rate

·      Shorten the inspiratory time to allow for an inspiration: expiration (I:E) ratio of 1:3 – 1:5 (ask RT)

·      Decrease the tidal volume

·      Increase the inspiratory flow from the standard 60 L/min to 80 L/min

·      Treat bronchospasm to reduce airway resistance.

Well that was a quick review to add a little more on how to troubleshoot the ventilator. I hope it helps you understand how to approach this situation better. I encourage you to seek out other sources for further reading and understanding on this important topic.

Thanks for reading.

References

1.     Boring EM

2.     EM:RAP Episode 147 (Near minute 16)

3.     Marino, Paul L. Chapter 25: Positive Pressure Ventilation. In: Marino’s ICU Book. 4th ed. Philadelphia: Lippincot Williams & Wilkin – a Wolters Kluwer Business; 2014: 487 – 503

4.     Owens, William. Ventilator Management and Troubleshooting in the Emergency Department. EB Medicine: EM Critical Care. Volume 4, Number 5. September/October 2014.

Vinson DR, Zehtabchi S, Yealy DM. Can Selected Patients With Newly Diagnosed Pulmonary Embolism Be Safely Treated Without Hospitalization? A Systematic Review. Ann Emerg Med. 2012;60 651-662
 
This review article evaluated a key issue in treating patients with pulmonary embolisms without hospitalization. Overall, it was a good article as it analyzed a frequently encountered disposition for EM physicians.  It concluded that patients with PE could possibly be treated without hospitalization in low-risk patients. Based on our discussion the observational setting is best for these patients. However, this article acknowledged the lack of data on outpatient management of PE patients and the studies selected for this were primarily observational studies.
 
Motov S. et al. Intravenous Sub-dissociative Ketamine vs. Morphine for Analgesia in the Emergency Department: A Randomized Controlled Trial. Ann Emerg Med. 2015
 
This article evaluated the use of ketamine vs. morphine in the ED setting. This was an excellent article with a double blind RCT that concluded that ketamine (0.3mg/kg) can be used with similar efficacy to IV morphine for acute pain control. Based on our discussion the use of ketamine could be useful for chronic pain patients.
 
Weekes AJ, et. al. Central Venous Catheter Placement Evaluation Using Saline Flush and Bedside Echocardiography. Academic Emerg Med. 2013 21 ;65-72
 
This study evaluated the use of saline flush and bedside echocardiography to monitor CVC placement. It was a good article that illustrated a different technique to evaluate CVC placement than the traditional chest X-ray.  It concluded that this technique using the Rapid Atrial Swirl Sign (RASS) on echocardiography could be used to evaluate the correct position of the CVC. This can be especially useful for a R IJ according to the article which indicated 100% sensitivity and specificity. Based on our discussion, this technique is beneficial due to the decreased time, cost, and radiation exposure versus a chest Xray. However, the article lacked more incorrect placements in their evaluation and this technique could not differentiate between arterial and venous placement. Thus, the discussion concluded that this technique could serve as an adjunct and the chest Xray remains as the standard of care.


Submitted by Dr. Ammar Ahmed, PGY-1